COLUMBIA LIBRARIES OFFSITE HEALTH SCIENCES STANDARD HX00034339 ^D S] ^^ T39 Columbia ®tttbet:!e(ftp l^partm^ttt of Bnt^tti^ (Sift of Ir. Soarplr A. Ikkr MANUALS FOK Students of Medicine. ELEMENTS OF Surgical Pathology. BY AUGUSTUS J. PEPPEE, M.S., M.B. LOND., F.E.C.S. Eng., FELLOW OF UNIVERSITY COLLEGE, LONDON ; SURGEON TO ST, MAET'S HOSPITAL; AND TEACHER OF PRACTICAL AND OPERATIVE SURGERY AT THE MEDICAL SCHOOL. ILLUSTRATED WITK 81 ENGBAVINQS. HENRY C. LEA'S SON & CO,: PHILADELPHIA, PA, ^0 GEOKGE VINER ELLIS, Esq., F.R.C.S., Emeritus Professor of Anatomy in University College, London, THIS WORK IS DEDICATED, IN GRATEFUL ACKNOWLEDGMENT OF MANY ACTS OF KINDNESS ; BY HIS FORMER FI'PIL, THE AUTHOR. PEEFACE My aim has been to supply what has long been felt as a desideratum, a small work on Surgical Pathology suited to the requirements of Students preparing for the final examinations. The following pages embody some of the con- clusions arrived at after many years of study and teaching. An attempt has been made to render in a practical form the knowledge conveyed, and to give an explanation of the causes and methods of pathological processes. My thanks are due to Mr. Charles Berjeau, who has drawn the figures on wood, for the most part from coarse preparations and sketches made by myself. Of the eighty-one figures with which the book is illustrated, sixty-six are original, the others have been copied from standard works and formally viii Surgical Pathology. acknowledged. The tables of "Urinary Deposits and Calculi " have been taken from the " Index of Surgery," by my friend Mr. C. B, Keetley. In conclusion, I have to express my indebtedness to A. B. Shepherd, Esq., M.D., late Dean of St. Mary's Medical School, for permission to make use of the material furnished by the Museum of that Institution. Augustus J. Pepper. Octoler, 1883. CONTENTS. CHAPTER PAGE I. -Inflammation and Abscess ...... 1 II.— Pain 13 III.— Ulceration 16 IV.— Gangrene 34 v.— Fever 41 VI.— Simple Surgical or Traumatic Fever . . . 47 VII.— Septicemia and Pyemia 50 VIII.— Erysipelas 69 IX.— Furuncle, Carbuncle, and Malignant Pustule 76 X.— Hypertrophy 81 XI.— Atrophy 85 xn.— Fatty Infiltration— Fatty Degeneration . . 92 Xin.— Mucoid and Colloid Degeneration . . . .100 XIV.— Pigmentation— Pigmentary Degeneration . . 106 XV.— Calcareous Degeneration 112 XVI.— Albuminoid Infiltration : Synonyms— Amyloid, Lardaceous, Waxy 117 XVn.— Trophic Le jions 121 XVIII.- Syphilis 128 XIX.— Rickets 145 XX.— Tubercle and Scrofula 153 XXI.— Lupus .162 XXII.— Tetanus 164 XXIII.— Union of Wounds 167 XXIV.— Fractures of Bone and Pseudarthrosis . . 178 XXV.— Injuries and Diseases of the Scalp . . .193 X Surgical Pathology. CHAPTEE PAGE XXVI.— Hernia Cerebri— Hemorrhage between the Skull and Dura Mater 196 XXVII.— Intracranial Suppuration 198 XXVIII.— Suppuration in the Mastoid Cells . . .202 XXIX.— Pulsation of the Eye-ball 203 XXX.— Inflammation op Bone 205 XXXI.— Rarefying Ostitis— Caries 207 XXXII.— Osteoplastic or Formative Ostitis and Peri- ostitis 219 XXXHI. —Acute Suppurative Periostitis, Ostitis, and Osteomyelitis 225 XXXIV.— Osseous Lesions in Congenital Syphilis . 228 XXXV.— Necrosis 232 XXXVL— Bone Abscess 244 XXXVH.— MoLLiTiES OssiUM— Osteomalacia . . .245 XXXVin.- Diseases of the Joints 249 XXXIX.— Strumous Arthritis 251 XL.— Chronic Rheumatic Arthritis . . . .256 XLL— Acute Serous Synovitis— Hydrops Acutus . 261 XLH.- Chronic Serous Synovitis . . . . .262 XLIIL— Phlegmonous or Suppurative Arthritis . 263 XLIV.— Gonorrhceal Arthritis, Gonorrhceal Rheu- matism 265 XL v.— Hemorrhage into Joints 266 XL VI.— Loose or Movable Bodies in Joints . , .266 XL VII.— On Deformities 268 XL VIII.— Curvature of the Spine 272 XLIX.— Deformities op the Foot, Knee, and Hip . 274 L.— Spina Bifida ' . . .278 LI.— Cerebral Meningocele and Meningo-Ence- phalocele 282 LIL— Cleft Palate and Hare-Lip 282 LIIL— Extroversion of the Bladder— Ectopia Vesica- Hypospadias 284 Contents. xi CHAPTER PAGE LIV.— Fatty Degeneration of Arteries, and Arteritis 285 LV.— Aneurism 290 L VI.— Ligature of Arteries . . . . . .298 LVII.— Yarix 300 LVni.— Embolism 304 LIX.— Thrombosis and Phlebitis . . . . .310 LX.— Acute Orchitis and Epididymitis . . . 319 LXI.— Chronic Enlargements of the Testicle . 321 LXn.— Atrophy of the Testicle 337 LXIII.— Hydrocele 337 LXIV.— Gonorrhoea and its Consequences . . .341 LXY.— Stricture of the Urethra 346 LXVI.— Urinary Abscess— Extravasation of Urine —Urinary Fistula . ... . .350 LX VII.— Hypertrophy of the Bladder . . . .354-^ LX VIII.— Cystitis : Ulceration of the Bladder . . 356 LXIX.— Tumours of the Bladder 360 LXX— Hematuria .364 LXXL— Diseases of the Prostate Gland . . .366 LXXIL— Surgical Kidney 370 LXXIIL— Urinary Deposits and Calculi . . . .375 LXXIV.— Ulcers of the Anus and Rectum . . .379 LXXV.— Stricture of the Rectum 382 LXXVL— Tumours of the Rectum 385 LXXVII.— Prolapse, Hemorrhoids, and Fistula . . 389 LXXVIII.— Peritonitis 392 LXXIX.— Strangulated Hernia ...... 399 LXXX.— Intussusception of the Bowel . . . .403 LXXXL— Tumours . . .405 LXXXH.- The Fibromata . 408 LXXXIII.— The Lipomata 412 LXXXIV.— The Enchondromata 415 LXXXV.— The Osteomata 419 xii Surgical Pathology. CHAPTER PAC4E LXXXYL— The Myxomata . . . . . . .427 LXXXVII— The Neuromata 430 LXXXVIII.— The Angiomata .434 LXXXIX.— The Sarcomata 437 XC— The Lymphadenomata 449 XCI.— The Papillomata 454 XCII.— Adenoid Tumours 458 XCIII.-Cysts 464 XCIV.-The Carcinomata 474 Index . • . * 495 Surgical Pathology. CHAPTER I. INFLAMMATION AND ABSCESS. So long as tissue elements retain their vitality they possess the property termed irritability; that is, they are capable of undergoing nutritive and formative changes on the application of a physical or chemical stimulus. This varies in degree in the different tissues, but is much more marked in those where there is a perpetual physiological succession of new cells which take the place of those whose term of life and function has expired, as in the epidermis and mucous epithelium. This increase of activity, whether showing itself by enlargement, and multiplication by division, or endogenous formation of cells, is always a sign of lowered vitality ; for the more rapid the rate of nutrition and reproduction, the less the stability, and so inflammation must of itself always be a destructive process. Redness, pain, heat, and swelling, the four stereo- typed factors of inflammation, may severally or in combination be met with in other conditions. Thus, redness, pain, and heat may be observed in joints, the seat of nervous mimicry of disease (Paget), swelling from exudation, as in transient erythema, and pain so momentary as not to admit of inflammation as a cause. B 2 Surgical Pathology. [Chap. i. In inflammation itself these signs are associated in difierent degrees ; thus, a joint may be filled with pus in purulent infection, with but little redness of the synovial membrane, or it may be intensely congested in rheumatism with only a slight amount of exudation. The redness is mainly due to dilatation of the vessels. In very acute cases the exudation of red corpuscles shares in its production, and in some diseases there is considerable discharge of the haemo- globin from the corpuscles, which, passing out in a state of solution, stains the bodies with which it comes in contact ; e.g.^ the brick-dust colour of the lymph in syphilitic iritis; and lastly, in long-standing hypersemia the blood pigment is taken up and fixed by the cells. The pain is caused chiefly by the tension on the filaments of the nerves from the pressure of the exudation, but partly by a chemical irritation of the inflammatory products acting upon the ends of the nerves; for it is not always proportionate to the extent of the stretching. The local heat depends upon the increased amount of oxygenated blood, and the active chemical changes going on in the part. The swelling is the result of the liypersemia and exudation. There is no new anatomical factor in inflammation. It is an exaggeration of the normal physiological forces ; for in health the calibre of the blood-vessels is frequently varying, exudation of fluids by osmosis is in constant process, and the white blood-corpuscles habitually wander to and from their vascular abodes. The stimulus is more intense than natural, and the changes induced less controlled ; and one phase of nutrition is substituted for another, as when cartilage cells expend their energy in growth and multiplication at the expense of the elaboration of chondrin. The Chap. I.] Inflammation and Abscess. 3 first thinsf noticed at the seat of irritation is contraction of the vessels rapidly followed by dilatation, then stasis gradually sets in, partly from this dilatation, partly from the tendency of the white corpuscles to cling to the walls of the vessels, increasing the " still layer." The walls of the capillaries being formed of protoplasmic cells, held together by a soft ground substance, allow of the ready passage of leucocytes through them. These bodies may be seen in different stages of transit, their amoeboid offshoots always being directed from the lumen of the vessel. Whether they pass through open spaces or stomata between the epithelioid cells, or make channels for themselves, is not certain. Cornil and Hanvier assert that minute openings through which the leucocytes have passed can be shown by the aid of nitrate of silver, but this view is highly speculative. Having cleared the vessels they make off into the surrounding tissues, and collect in groups, attracted probably by the fixed corpuscles. It was this aggTe- gation that led Yirchow to believe that the small groups of cells were derived from segmentation of the connective tissue corpuscles. In some tissues (e.^., cartilage) this does occur, for the cartilage cells may be seen in different stages of growth and multiplica- tion ; the nuclei enlarge, and the protoplasm swells up, division ensues, and, the capsules being dissolved, the broods of cells are set free, and, joining adjacent groups, a layer of embryonic tissue is formed on the surface. As to how far this happens in other forms of connective tissue, authors differ. In bone the corpuscles appear perfectly passive, even when the lacunse are opened up by absorption. In the cornea and areolar tissue the great majority of the cells have wandered from the vessels. Red corpuscles also traverse the walls of the capillaries, but not by amoeboid movements. They 4 Surgical Pathology. [chap. i. are driven through by the intravascular pressure, the change in walls of the vessels and the previous passage of leucocytes favouring this transportation. With the diapedesis of leucocytes there is rapid exosmosis of serum containing albumin, and one or more of the factors of fibrin, either plasmin, or fibrinogen which unites with the globulin of the cells outside the vessels, probably under the influence of a ferment. Fibrin, as such, does not exude from the vessels. In the exudation is a quantity of mucin. This has either escaped from the blood stream or it is derived from a mucoid transformation of the protoplasm of the cells. It is- best seen in discharges from inflamed mucous membranes, in the glairy secretion from some ulcers, and in the layer of embryonic tissue on the surface of articular cartilage in white swelling. There are important changes in the tissues themselves; the intercellular matrix, whether fibrillated or homogeneous, liquefies from mucoid softening (Rind- fleisch). The epithelioid cells of the blood-vessels swell, and help to obstruct the lumen ; and thus, aided by the pressure from without^ and the adhesion of leucocytes to the interior of the vessels, thrombosis ensues. Even yet resolution may happen, but a step farther takes us to actual destruction of tissue by suppuration or gangrene. Scrapings from an acutely inflamed tissue contain cells of different size and form : — {a) Embryonic, with a single nucleus. (6) Pus cells in which the nuclei, varying from two to five, are brought into relief by the action of acetic acid, which clears up the albuminoid particles that render the cells granular. (c) The so-called compound inflammatory cor- puscles of Gluge are only ordinary cells, enlarged and loaded with fat molecules ; they are most plentiful in Chap. I.] Inflammation and Abscess. 5 tissues rich in fatty matter, and hence are seen in numbers in softening of the brain and spinal cord. {d) Multinucleated niofcher-cells. Filaments of fibrin are also seen enclosing the cells in their meshes, and if the specimen have been hardened, coagulated strings of mucin are present. The majority of the cells are undoubtedly migratory corpuscles that have escaped from the blood-vessels ; some are derived from endogenous formation and subsequent dissociation, as in inflam- mation of cartilage and mucous membranes ; and a feW; perhaps, are obtained by gemmation and fission of multinucleated masses of protoplasm. Cohnheim supports the doctrine of migration pure and simple ; Cornil and Ranvier maintain that segmentation of connective tissue corpuscles is an important factor in the production of cells. Inflammation may terminate in resolution or absorption, organisation or new formation, or in death of the tissue by suppuration, gangrene, or caseation. Reigolution. — Some of the cells pass back into the blood-vessels, others undergo molecular disintegra- tion and capillary absorption by the lymphatics, whilst a few may remain as fixed connective tissue corpuscles. The fibrin becomes granular, it disinte- grates, and is then removed. The same change occurs in any capillary thrombi that have formed. The endothelial cells of the capillaries shrink to their former size, or, if degenerated past repair, are replaced by others. The vitality of the contractile walls of the capillaries and arterioles is re-established, and the vessels assume their proper calibre. It may be here remarked that the expression " venous absorption " is often used erroneously ; of course the walls of veins are permeable to fluids, and leucocytes may traverse theiji ; but still the chief part of absorption is capil- lary, be it blood vascular, or lymphatic. 6 Surgical Pathology. [Chap. i. Org'anisatioii. — Should the inflammation be prolonged, and moderate in degree, organisation takes place in the exudation without visible loss of tissue. JSTew blood-vessels are formed by a looping of the old ones, the softened walls of the capillaries allowing protrusion here and there. The channels of contiguous offshoots merge by absorption of the intervening walls and so a vascular network is established. There is, besides, a separate development of new vessels in the inflammatory embryonic tissue. This may be effected in two ways; firstly, by the loosening and disintegra- tion of the central cells of columns, whilst the peripheral elongate and become fixed, and so construct the walls of capillaries ; secondly, vasoformative cells send out canalicular processes which anastomose. The cells expand, the protoplasm liquefies, and the nuclei possibly grow into the first blood corpuscles. Be this as it may, these newly-built capillaries coalesce with the pre-existing vessels. Exactly the same changes are observed in the growth of tumours, such as sarcomas, the type of which is embryonic connec- tive tissue. This vascularised lymph' constitutes granulation tissne, which is merely a mass of indifferent cells, cemented by a scanty amount of ground substance, and traversed by capillary blood-vessels. It is termed granulation tissue^ because when formed on an inflamed surface the centrifugal pressure directs the loops of vessels in the path of least resistance, and the exudation corpuscles accumulate and arrange them- selves about them. The old tissue disappears before this inflammatory neoplasia, which, when the irrita- tion ceases, organises into connective tissue. The majority of the exudation cells disappear by dis- integration; some travel back into the vessels, others in surface inflammation are washed off in the discharges, and, lastly, a few persist as fixed Chap. I.] Inflammation and Abscess. 7 co.rpuscles. The intercellular substance fibrillates and contracts, tlius obliterating many of the vessels, so that a scar, which is at first more vascular than the surrounding tissue, becomes smaller and paler with the lapse of time, and eventually (unless pigmented) quite white. As a rule it is depressed ; but if the irritation be prolonged, as sometimes happens in the case of burns, the cicatricial tissue is so abundant as to project above the surface as a keloid mass. There is always a tendency during organisation to reproduce the original tissue of the part, as will be seen when we come to treat of the mode of union of wounds. The more highly developed the tissue, the less does this tendency become developed ; thus, in the human subject, at least, the ends of divided muscles are probably cemented by fibrous tissue only, and cicatrices of the skin do not contain sebaceous or sweat glands. Suppuration. — If this takes place with loss of tissue on the surface, the process is described as ulceration ; if in the substance of tissues or organs, an abscess is the result. We have only to suppose an intensified irritation to see that not only will the exudation of leucocytes and liquor sanguinis be increased, but the liquefaction of the cells and inter- cellular substance will be complete. Moreover, there will be extensive occlusion of vessels by pressure from without and coagulation within. The tissues sufiering acute starvation quickly disintegrate. These changes are more rapid if the inflammation be infec- tive, for then active chemical decomposition results from the influence of minute organisms — micrococci^ bacteria, etc. Here we have the mode of formation of an acute atoscess, i.e., a closed cavity filled with the debris of broken-down tissue, and fluid and cells derived from the vessels. This is the final sta2;e of an 8 Surgical Pathology. [Chap, I. acute inflammation. The wall of the abscess consists of a highly vascular granulation tissue, the so-called fyogenic mertibrane. From the vessels of this layer exudation passes into the cavity. Add to this, a continuous melting away of the lining wall itself as the inflammation spreads, and the picture of an c- V4^ Fig. 1. — Suppurative Inflammation of tlie CereT3ram ( x 250). The section was made half an inch away from the situation of numerous visible abscesses, a, blood-vessels, showing leucocytes collected within and without the walls ; h, " microscopical abscess ; " c, the same in the midst of a capillary extravasation ; d!, brain substance, showing delicate fibres and granules, the result of inflammatory softening and fatty degeneration. The normal histological characters have disappeared. enlarging abscess is complete. It may be noted that the suppuration does not start from one focus, for under the microscope numerous minute centres of pus -formation may be observed (Fig. 1). These micro- scopical abscesses increase in size, and coalesce. In addition to the original cause of the inflam- mation there is the added tension from the retained products of suppuration. This tension is afterwards removed by the bursting of tlie abscess. The importance of early relief from the pressure, in order Chap. I.] Inflammation AND Abscess. 9 to check the destruction of tissue and the absorption of intoxicating or septic material, is obvious. Blood-vessels and nerves resist the action of these inflammatory changes longer than oth^? tissues, except tendons and the calcified framework of bone. When an acute abscess has been opened its "walls collapse, and the granulating surfaces adhere more or less, and thus the suj)purating area is greatly diminished. When an acute abscess is opened, a thick creamy fluid escapes, mixed with blood from ruptured and divided vessels. The yellowish-white colour is due to the suspension of refractive bodies (pus cells) in a fluid termed liquor puris. To see that this is so, we have only to allow the pus to stand for a time in a glass vessel, when two distinct layers will be observed, the lower a yellowish-white deposit with uniform surface, the upper a clear fluid. Chemical analysis proves this fluid to be practically identical with liquor sanguinis, which is no doubt its source. If some of the lower layer be examined with the microscope, it will be found to consist mainly of corpuscles from -awo*^ *^ wb^"o*-^^ ^^ ^^ rn.c)i in diameter. These bodies are for the most part round, but some are crenated or otherwise misshapen. No boundary wall can be seen. They look cloudy or granular, from minute fatty and albuminoid particles. Acetic acid causes the cells to swell up and become clear. Many of the older cells are coarsely granular from fat molecules which are soluble in ether. The fat is chiefly derived from degeneration of the proto- plasm of the cells, but some, probably, has been taken up from the debris of perished tissue. The so-called compound inflammatory corpuscles of Gluge are of this nature. Pus cells occasionally contain pigment. There are also numberless free granules, the product of disintegration of the cells. Healthy or laudable lo Surgical Pathology. [Chap. t. pus is alkaline in reaction. It forms a viscid gela- tinous mass on the addition of liquor potassse. Origin of pus corpttscles. — The majority are leucocytes that have migrated from the blood-vessels, though it cannot be denied but that^ in interstitial inflammations, their number is increased by prolifera- tion of connective tissue corpuscles, and still more in the discharges from mucous membranes, and the exudation from serous surfaces. In the two latter situations there is a constant physiological reproduc- tion of cells. They resemble white blood-corpuscles, in that whilst living they possess the property of spontaneous movement. Their vitality, however, is low, and they soon become motionless and degenerate. The fact of their containing two or more nuclei is, perhaps, a sign of declining nutritive activity, the segmentation of the protoplasm ceasing before that of the nuclei. Oaiigrene. — Inflammation is the most common cause of gangrene or death of visible portions of tissue. The blood current is obstructed by the pressure of the exudation, and the vessels are blocked by coagula ; hence the tissues perish from acute starvation before there is time for complete disinte- gration of their individual elements. In the necrosed masses or sloughs the original structure is recognis- able. Caseation* — In chronic inflammations, especially of the lungs, bone, and lymphatic glands, the exuda- tion, together with the affected tissue, undergoes fatty degeneration and disintegration, the more liquid portion is absorbed, and a putty-like substance re- mains ; this consists chiefly of granular debris, in which crystals of stearic acid and plates of cholesterine are formed. The process often terminates in calcifi- cation. It may be remarked that the discharge from gouty to Chap. I.] Inflammation and Abscess. ii abscesses is loaded with what is often erroneously sjDoken of as chalky matter, but which in reality is urate of soda in the formof acicular crystals, scattered or in stellate groups. Cliroiiic inflamiiiatioii is the result of long- continued local irritation, or of some constitutional weakness. The inherent defect in nutrition may be g;eneral, or centred in certain organs or tissues ; e.g.^ in scrofula the bones, joints, lymphatic glands, and the lungs suflfer most. The predisposing condition is called a diathesis. It was believed by the humoral pathologists that a special materies morbi existed in the blood, and that this was the cause of the local disorder ; hence the origin of the expression " cancerous deposit^" malignant " growths " being regarded as exudations of caco- plastic lymph. On the other hand, the solidists laid the foundation of all disease in the tissues themselves, considering the blood as being secondarily affected. We know, how- ever, that it is a "flesh and blood" malady, for it is difficult to conceive how one can be affected without the other. It is true the specific nature of a blood poison may disappear, as shown by the failure of inoculation, and by the non-transmission of syphilis from parents to offspring in the tertiary stage ; and yet how often do very grave inflammatory lesions crop up in after years. Some pathologists look upon these as sequelae of syphilis, and, in so far as a repro- duction of the same disease in others is concerned, they may be ; yet it cannot be supposed that the blood is free from taint. The final result of a chronic inflammation turns mainly upon whether the latter proceeds from a local or constitutional cause. If purely local and only moderately severe, the lymph organises into connective tissue pure and simple, or with the admixture of a 12 Surgical Pathology. [Chap. i. more highly-developed product, such as bone. If constitutional, there may be loss of substance at one part with increase at another, as where the end of a bone is gradually worn away from softening and friction, whilst around it numerous osteophytes are thrown out ; e.g., in chronic rheumatic arthritis. When the individual is strumous, caseation and abscess are very common ; e.g. , in the cervical glands. Chronic abscess is also called congestive, from the presence of passive rather than acute hypersemia, and cold, from the fact that there is little or no elevation of temperature of the part, for the blood current is sluggish and the chemical changes are not very active. It is often consecutive, as when cervical glandular abscess follows caries of a tooth, or psoas abscess de- pends upon disease of the spine. From the persistence of the original cause, together with the continued tension, chronic abscesses frequently attain a great size ; and when deeply-seated and the resistance of the tissues around is unequal^ they follow well-known anatomical paths j thus, a spinal abscess may open at the groin or knee, or even at the ankle. And, inas- much as the line of least obstruction is usually in the long axis of the body, they gravitate to more dependent parts. The structures around become condensed. The cicatricial tissue, as it shrinks, diminishes its own vascularity, and makes the walls of the abscess rigid, so that they can only imperfectly collapse when the cavity is laid open. As the contents escajDe, germ- laden air too often enters and leads to decomposition of what remains. This is favoured by the retention of pus in offshoots from the main cavity. The badly- nourished walls are slow in constructing granulations for the obliteration of the space within, and are apt to absorb infective matter, the source of chronic and acute pyaemia. Hence the force of Billroth's remark, Chap. II.] Pain. 13 when speaking o£ psoas abscesses, " Be thankful for every day they remain closed." Chronic abscesses should be left to open themselves, unless (1) they are about to burst, and the vitality of the skin over them is threatened, as in the neck ; or (2) they encroach upon some important organ or structure, as in retro- pharyngeal abscess ; or (3) they would subsequently open in a less advantageous position, as when a psoas abscess, having reached the thigh, still shows signs of spreading. The contents of chronic abscesses vary much. Sometim.es the fibrinous portion of the exuda- tion remains in solution ; at others it separates in the form of flakes or curds. On absorption of the serum the pus is reduced to the consistence of clotted cream or of soft putty. The so-called " inspissated pus " is made up of fibrin and cells in a state of fatty degeneration. When the abscess has formed in connection with diseased bone, the pus contains an excess of lime salts, and not unfrequently minute sequestra. Abscesses arising at the seat of a previous in- flammation are termed "residual" (Paget). The vitality of the tissues has remained defective, and unable to cope with further irritation. The part is a "locus resistentise minoris." CHAPTER II. PAIN. Pain is always a symptom of diminished functional, and, therefore, nutritive, power, whether it be the headache from a tired brain or the smarting from a scald. We say functional 'power ; for excessive 14 Surgical Pathology. [Chap. ii. functional activity is one of tlie first indications of exhaustion (C. Bernard). It is purely subjective, and is, therefore, difficult to estimate ; for its existence, nature, and extent can be simulated, and it may appear out of all pro.- portion to the intensity of any assignable cause. It is the fashion to give but little heed to the suflferings of hysterical patients, but their nervous mimicry of pain is to them a real disease. There are three factors in the production of pain : (1) Extrinsic irritation, physical or chemical; (2) in- herent susceptibility of the implicated nerve-centre ; (3) emotion. It is well to assume that all pain is organic (it is termed functional when no correspond- ing tissue-change can be seen, but "cell " and " fibre" are only coarse expressions of molecular structure), for then there will be no excuse for considering the less obvious cases as ^'idiopathic." The irritation may be of peripheral or central origin. Wh-en cen- tral, it is referred to the whole or some part of the area of distribution of the corresponding nerve. When peripheral, it is usually referred to the seat of irritation, but not rarely to the terminal part of some other branch of the same nerve, as in the knee when the hip is diseased, or in the ear when a tooth-pulp is inflamed 3 or the pain is felt in some nerve asso- ciated in function, origin, or distribution, as when ascarides in the rectum lead to discomfort about the penis, or a stone in the bladder causes painful tenes- mus. If the stimulus be applied in the course of a nerve-trunk, as in neuritis, there is local tenderness to the touch, accompanied by pains radiating along the derivative branches. In some cases the pain is experienced only at the distal end ; e.^., at the back of the head in atlo-axoid disease, in which the great occipital nerve is caught as it passes between the bones. Chap. II.] Pain. ■ 15 In any case of localised pain the nerve should be examined as far back to its origin as practicable, and then the trunk and all its branches, and also the associated nerves, taken in review. Types of pain. — There are two primary types of pain: (1) continuous; (2) intermittent. The former is either aching^ which is symptomatic of tension beneath very resisting structures, as in ostitis, peri- ostitis, and subfascial inflammation, and in the erosion of vertebrae by an aneurism ; in all these instances the nerves are constantly on the stretch ; or it is smarting, which is characteristic of surface irritation, as in burns and scalds. (Perhaps the latter is in reality an intermittent pain, the impulses succeeding one another so rapidly as to make it appear con- tinuous, the analogy being that of tonic to clonic spasm.) Intermittent pain is either neuralgic or throbbing. In the former case it is indicative of recurring dis- charges of a diseased nerve-centre, as in the " lighten- ing pains " of locomotor ataxia ; or of varying vascular tension, as when the pulp of a tooth is inflamed. In throbbing pain, the nerve endings are over- sensitive from inflammation, and the tissues are softened, and so allow considerable latitude for expan- sion of the vessels ; hence the pulsation of the arteries is felt by the patient, and this gives the peculiar character to the pain. It is suggestive of the forma- tion of pus. The shooting pains felt in cancer are probably due to the implication of fresh nerve-fibres by the growth. A combination of continuous and spasmodic pain is well seen in the passage of a biliary or renal calculus, the continuous character depending upon the resisting nature of the walls of the duct, and the spasmodic upon the intermittent contractions of the muscular coat. 1 6 Surgical Pathology. [Chap. hi. Effects of pain on nutrition. — There can be no doubt but that nutritive changes are more marked where pain is severe, the atrophy of the muscles in hip-joint disease being proportionate {ceteris paribus) to the patient's suffering ; for local, like general, dis- turbance of rest prevents the natural repair of tissues wasted during activity. Keflex subdual of pain. — As pain can be induced by reflex action, so it may be subdued, hence, the use of powerful local sedatives applied to the skin ; e.g., in the deep-seated inflammation of joints. The relief given by counter-irritants, though apparently contradicting this theory, really supports it, for the peripheral irritation produces an exhaustion of the nerve-centre, and makes it less sensitive to a stimulus applied to the deep-seated nerves. CHAPTER III. ULCERATION. Ulceration is a surface solution of continuity from molecular death of the tissues. In this way it differs from gangrene, or molar death. (Molecular disinte- gration is not limited to ulceration, for it is met with in primary interstitial degeneration.) Whatever the primary cause of ulceration may be, there is at some period inflammation of the part ; thus, in cancrum oris the most important factor is progressive capillary thrombosis, but the coagula irritate the walls of the vessels, and cause them to inflame, and the inflammation spreads to the tissues around. An ulcer may begin as a surface lesion, or be the consequence of suppuration beneath the skin Chap. III.] Ulceration. 17 or a mucous membrane. An abscess may be defined as a closed ulcer. Oaiises of iilceration. — The irritation is either physical or chemical, or both ; in any case the result is vascular dilatation and exudation, and the tension thus increased acts as a further cause of inflammation, by obstructing the flow of blood and stretching the tissues. As physical causes, we may mention wounds, continued pressure and friction, as in bed sores, extreme heat and cold, and rupture of a varicose vein. Chemical irritants may be applied locally to the surface or beneath the skin, or they may be diffused in the circulation ; e.y., the specific poisons of typhoid and syphilis. Mode of formatioo of a simple ulcer. — We will take the case of the heel pinched by a shoe. In the first place, the friction causes dilatation of the vessels and exudation of liquor sanguinis and leu- cocytes ; hence the redness and swelling. The exuda- tion increases to such an extent that the tissues can no longer retain it wdthin their interstices, and some, escaping between the cells of the softened epidermis, oozes from the surface, as in eczema. If it be more rapid, the epidermis is raised in the form of a bleb. In the meantime the cells of the rete are being excited to greater formative activity. They divide and subdivide, but no longer undergo cornification. The embryonic corpuscles thus derived mingle with the discharge from the vessels. The epidermis becomes soddened, and is swept away by the outward current, or is brushed off* by the slightest friction. In this way the tips of the papillse become exposed, and the ulcer is fully formed. The papillse themselves are rendered succulent by the exudation and mucoid softening of their constituent elements. This, to- gether with the cellular infiltration, causes them to lose their natural histological features. They are, in c 1 8 Surgical Pathology. [Chap. hi. fact, converted into granulation tissue. The exuda- tion now Hows from the surface in the form of pus. The extent of the changes in the subcutaneous tissue varies as the severity of the inflammation. The stages of an ulcer. — There are two oppo- site processes in the course of an ulcer, destruction and repair. These pass so gradually into each other that it is diffi<5ult to say where one ends and the other begins. But, during the time that elapses from the commencement to the close, an ulcer may be said to pass through three stages : (1) spreading ; (2) stationary ; (3) healing. These are sometimes erroneously described as varieties of ulcers, whereas they really refer to their condition at a given time. Spreadiog- stag-e. — This is well exemplified in a soft chancre. The same changes that led to the formation of the ulcer are still in active progress. The margin is surrounded by a zone of hypersemia, is more or less swollen, is sharply defined and steep, and, if the ulceration be spreading more rapidly in the subcutaneous tissue than in the skin, it is under- mined. As to the hase., there will probably be no granu- lations in the floor of the ulcer, for the inflammatory neoplasia is destroyed too quickly to allow of its assuming the granular form. It has a gray, or yellowish-gray appearance, and is covered with pus and the debris of the disintegrating tissues. The colour is due to fatty matter and softened blood- clot, for thrombosis precedes the loss of vitality and subsequent dissolution ; and this is the reason why haemorrhage is not more common. If the ulceration be very active, the cellular tissue is destroyed before the more resisting structures, such as vessels and nerves, have had time to melt away into mole- cular debris. The base then appears somewhat floc- culent and the margin fringed ; in fact, gangrene is Chap. III.] Ulceration: 19 added to true ulceration. There is usually consider- able pain in the part. Stationary period. — This is best observed in chronic varicose ulcers of the leg, whose margins are indurated by condensation of the exudation. This always takes place when the healing is long deferred. The margin is usually thickened and rounded. It is rarely so precipitous or undermined as when the ulcer is spreading, nor is the surrounding inflammatory redness so marked. The base consists of small, un- healthy, or pale exuberant granulations. The dis- charge is subject to much variation as to character and amount ; at times it is scanty and highly fibrinous, and coagulates on the surface ; or, again, it is thin and serous ; or these conditions may alternate. The causes of ulcers being stationary are (1) obstruction to the return of blood ; e.g., where the veins are varicosed (the granulations are then' often large and oedematous) ; (2) continued slight irritation, as in an issue ; (3) fixation of the margin to some rigid underlying structure, which prevents cicatrisa- tion, as in ulcers over the malleoli and crest of the tibia, and over tendons where there is movement in addition. Healiug'period. — Under ordinary circumstances, when the source of irritation has been removed the ulcer begins to heal. In the first place, the inflamma- tion tends to resolution, the blood-vessels contract, there is less exudation from the surface of the sore, and that efiused into the interstices of the tissues is re-absorbed. The margin is fairly on a level with, or slopes towards, the base. Two zones may be dis- tinguished ; an outer, where the epidermis is heaped- up, opaque, white, and soddened ; and an inner, more transparent, where the epithelial cells are only one or two deep, on the surface of the granulation tissue. It has a slightly clouded purplish hue. There is a 2 Surgical Pathology. [Chap. hi. gradual transition from one zone to the other. The base is made up of bright florid granulations dis- charging healthy pus. Histology of the gi^aBiiilatioiis. — The granu- lations consist of migratory leucocytes held together by a scanty fibrinous intercellular substance. The deeper cells have greater cohesion than the more superficial ones. Those immediately on the surface are floated off by the fluid that bathes it, and are then known as pus corpuscles. Capillary blood-vessels traverse the cellular mass. They form overarching loops with the convexity towards the surface. This arrangement is based upon the plan laid down in healthy skin and mucous membrane. It becomes more marked in the granulations of an ulcer, on account of the pressure of the outflowing stream of exudation and the diminished resistance of the softened tissues. Granulations contain no lymphatics, and probably no nerves of new formation. Cicatrisation of an nicer. — This is quite as essential to the healing as the precedent growth of granulations. Many of the cells undergo fatty degeneration, and are absorbed; some probably return to the blood-vessels by their amoeboid movements ; the remainder develop into fixed connective tissue cor- puscles. As the inflammation subsides the deeper cells elongate and become fusiform, and the intercellular substance increases and fibrillates. This highly vascular and corpuscular connective tissue at length contracts, and in so doing obliterates many of the vessels ; nor does it stop until the scar is denser and whiter than the normal tissue around. Several months elapse ere the process is completed. As the ulcer heals the epithelial cells grow inward over the granulations, which at the margin cease to secrete pus. Eventually the entire surface is "skinned over." During this time the contraction may be so great as to cause Chap. III.] Ulceration. 21 serious deformity, especially where wide tracts of skin have been destroyed, as in extensive burns. The chin may be drawn down and fixed to the sternum. Ectropion or eversion of the eyelid often follows the cicatrisation of an ulcer of the face. In annular ulcer of the leg, there being no skin to glide in the circum- ference of the limb, the effect of contraction in this direction is to keep up continued irritation of the granulation tissue, hence these ulcers rarely heal. Reprodiietion of epithelmm. — As the ulcer heals the epithelium grows over the granulations. The cells are chiefly derived from segmentation of those at the margin, but it is possible that some are furnished by the granulations. Now and then islets spring up at a distance from the marginal zone of epithelium ; in these cases the cells of the rete must have escaped destruction by the ulceration, for there is nothing to show that they arise spontaneously from the granulations exce]:)t under the immediate influence of pre-existing epithelium. Kever din's skin gi^aftmg'. — All that is neces- sary is to transplant snippings from the deep proto- plasmic cells of the rete to the healthy granulations, and to fix and protect them there. This, by furnishing fresh centres of cicatrisation, greatly hastens the healing, and by so doing lessens the after contraction. These grafts are sufiiiciently fixed, after a few days, to hold of themselves. IVoineiielatiire. — The ordinary features of an ulcer may be so modified as to give to the condition a Fpecial appellation. This may arise from a local hindrance to healing, or depend upon some constitu- tional taint ; or both causes may act at the same time. Symptomatic ulcers are those that point to a disease of wider distribution than the part immediately under observation, such as syphilis, scrofula, lupus, epithelioma, venous varicosity, etc. In describing 2 2 Surgical Pathology. [Chap. iii. ulcers it is usual to direct attention to the granulations that do or should form the base, the edge, the tissues around, including the vessels that supply and return the blood, and lastly the discharge. The particular designation of an ulcer is drawn from the state of the part that shows the widest departure from the normal; hence we speak of "diseases of the granulations," of an "undermined" or "indurated margin," and so forth. But observation that is limited to any one of these is too exclusive, for it cannot be said that an ulcer is healthy as regards the edge, and not so in respect to the base ; the whole should be passed in review. L.ocality of ulcers. — There are three factors that determine this : (1) Exposure to injury, whether it be from direct violence or continued irritation ; (2) the local effect of a materies morbi, either at the seat of inoculation, or in some remote part, or both ; thus syphilis leads to primary, secondary, and tertiary ulceration. Typhoid fever attacks the intestine, and sometimes the throat ; scarlet fever and diphtheria the throat ; and small-pox the skin ; (3) inherent or acquired weakness of certain tissues, or, as it is termed, the liability or predisposition to this or that form of ulceration ; e.g., lupus is very prone to occur in the face, and tubercular disease in the small intestine. Varicose ulcers are practically confined to the lower extremities. Bearing these facts in mind, we have, apart from the characters of the ulcer, a valuable aid to regional diagnosis ; thus the majority of ulcers of the leg are either varicose, traumatic, or syphilitic. The widely destructive ulcers of the face are due to lupus, syphilis, rodent ulcer, and epithelioma. In the mouth and rectum malignant disease, syphilis, and local irritation take the lead. In the small intestine typhoid fever and tuberculosis head the list. In the case of the Chap. III.] Ulceration. 23 loenis the inquiry is very limited after excluding chancres, herpes, and epithelioma. Again, in the leg most ulcers begin on the front aspect, and this is notably the case in the traumatic and varicose varieties. Yaricose ulcers are nearly always found in the lower third; syphilitic fre- quently about the knee ; whilst strumous are more confined to the skin over the epiphyses and about the foot, since these parts are very subject to caries. Diseases of tlie granulations. — 1. Croupous; 2. Fungous ; 3. Hsemorrhagic ; 4. Diphtheritic. 1. Croupous disease, — The only way in which the condition resembles croup is in the existence of a rind covering the base of the ulcer. This may be likened to a false membrane, for it can be peeled off with the forceps. Its presence is compatible with good general health, and it is not contagious. It has a bright yellow or grayish yellow colour. Under the microscope it is seen to be composed of indifferent cells firmly held together by a highly fibrinous material. The formation of this probably depends upon a purely local cause. There is an alteration in the nutrition of the granulations, but whether the result of this is a degenerative change in the cells themselves, or a modified exudation of liquor sanguinis, is uncertain. We know that it can be artificially produced by the repeated application of a sharp irritant, such as blistering fluid, and that after a time it will disappear of itself. The actual cause of its spontaneous origin is to be sought perhaps in the properties of. the chemical products of decomposition of the exudation that escapes from the vessels of the granulations. The rational treatment of the ulcer is to remove all sources of irritation by protecting it from friction, and counter- acting the effects of unhealthy discharges by the use of detergent dressings. The fibrinous rind is quickly 24 Surgical Pathology. [Chap. hi. reformed, hence its simple removal will not suffice for a cure. 2. Fungous disease. — There are two forms of this, the one depending upon an interference with the return of blood from the part where it may be con- sidered much after the nature of a local oedema; the other upon excessive formative activity and defec- tive organising power of the granulations, kept up by continued slight irritation. Yery often both causes work together. The granulations are large, pale, and gelatinous, and secrete a thin muco-purulent matter. They may be so exuberant as to rise for some distance above the level of the margin of the ulcer, and even to overlap it. They have but little tendency to recede of them- selves, and this is notably the case when the veins of the part are dilated and varicosed, and the margin of the ulcer indurated. Besides the excess of watery exudation, there is softening of the granulations from mucoid degeneration ; this is shown by the nature of the discharge. The treatment consists in removing all obstacles to the return of blood from the ulcer, by attention to position, and artificial support of the veins, and in applying pressure directly to the granulations ; this relieves the fulness of the capillaries, and by making the extravascular greater than the intravascu- lar tension, tends to reverse the osmotic current, or, in more familiar but less explicit terms, favours absorp- tion. The cells of the granulations, robbed too of a part of their blood supply, undergo fatty degeneration prior to removal. Healing may be hastened by de- stroying the superficial granulations by an escharotic. Stimulant applications, as we have seen, promote a more fibrinous or plastic exudation, and this gives better support to the vessels. Astringents act both as irri- tants and desiccantsj they diminish the calibre of the granulation capillaries more by extracting water than Chap. III.] Ulceration. 25 Ly increasing the functional contractility of the walls of the vessels. 3. Hsemorrlftsigic condition of tbe grsiiiiila- tionis. — This may be solely due to the tension on the venous side of the capillaries being so great as to burst the delicate walls of the latter, as when the veins of the leg are dilated and varicosed, or the veinlets returning from the ulcer are compressed by its callous indurated walls, and perhaps thrombosed as well. On the other hand, the capillaries may be unable to with- stand the normal pressure, owing to a primitive weak- ness in construction or fatty degeneration of their walls. Then there are some ulcers that are essentially hsemorrhagic, e.g.^ those due to malignant disease, scurvy, etc. The result of haemorrhage is to delay the healing, esi:»ecially when it occurs in -the depths of the granulations, as well as on the surface, for vessels are not only destroyed by rupture, but some are obliterated by the compression of the extravasated blood. In extensive burns the granulations readily bleed ; even the removal of external support involved in changing the dressings, or the mere dependent position of the part^ may be sufficient to effect this. 4. Diphtlieria of tlie g'rauulatious. — This phrase is unfortunate in its application to the condition of an ulcer, for it implies that the latter is necessarily the seat of true diphtheria, either by direct inoculation with the virus of that specific fever, or by infection of the wound through the blood. JSTo doubt an ulcer offers a favourable surface for absorption, and especi- ally when it is spreading ; and there is no reason why there should be immunity from the action of the poison of diphtheria, nor why we should decline to recognise a true diphtheritic disease of the granulations. But what we wish to insist upon is, that the expression 26 Surgical Pathology. [Chap. hi. ''diphtheria of wounds," as commonly employed, is used to describe in general terms the local appearances that closely resemble those following true diphtheritic infection, without the expressed or implied belief that in all cases such infection has really happened. It. would certainly be better to restrict the application to the specific disease, diphtheria, but long usage stands in the way of this. The difficulty in arriving at a satisfactory nomenclature lies in the fact that many organisms possess the property of causing similar local manifestations, although each one differs from the rest in its real nature. Some pathologists consider the disease in question as identical with hospital gangrene. Billroth, whilst admitting a resemblance between the two affections, says they are quite distinct from one another, and expresses the belief that each one is dependent upon a specific poison. This coincides with our own views. Diphtheria, when it attacks an ulcer, gives rise to excessive fibrinous exudation, that infil- trates the granulations, and forms a thick rind on the surface. The vessels of the granulations become thrombosed, and this aids in the molecular disintegra- tion. The tissues around show inflammatory hyper- semia, and are in their turn destroyed. Other conditions of an ulcer : 1. Eiiflaiuma.tiou. — The usual signs of inflam- mation are seen in the skin around, and in addition there is often some catarrhal exudation, and occasion- ally a number of small acute eczematous ulcers. All this will depend upon the severity and duration of the inflammation. If the ulcer has been previously healing, the process is arrested, and the marginal zone of newly formed epithelium is destroyed. The granu- lations lose their florid hue and change to ashen gray. The superficial layer at least is destroyed, for the cir- culation in the delicate capillary loops is quickly arrested. After this the surface of the ulcer is more Chap. III.] Ulceration. 27 or less smooth, and covered with pus and the debris of broken-down granulations. There are great pain and tenderness. Should the inflammation continue, the ulcer spreads. 2. Irritable ulcer. — An inflamed ulcer is neces- sarily an irritable one, but the burning pain may be out of proportion to any visible cause. It is in some way due to the state of the nerves supplying the part, and is not always co-extensive with the ulcerated sur- face, but may be limited to a particular part corre- sponding to the known distribution of a nerve. By some it is supposed that the nerve-fibres are exposed in the floor of the ulcer. Billroth suggests that they may undergo bulbous enlargement, like the nerve- trunks involved in the cicatrix of an amputation stump ; but this is mere surmise. It seems to us that the nerve-fibres are subject to irritation in one of two ways : either chemically by the discharge, or physi- cally by being stretched in the base or margin of the ulcer. The latter is more probable^ since it accords with the fact that the pain is sometimes limited to a certain area. There is usually evidence of slight in- flammation. The granulations are very small, and the secretion scanty. Whilst this condition lasts re- pair is at a standstill. It is noteworthy that circum- cision of the ulcer, or subcutaneous division of the aflected nerve, may at once remove the pain, and with it the cause that prevents healing (Hilton). 3. Callous ulcer. — This is as much the conse- quence as the cause of delay in healing. It is mostly seen in varicose ulcers of the leg. The return of blood is prevented by the over-full veins, and the result is that the granulations are deprived of their proper supply of arterial blood, and the tension in them is increased. Moreover, as these ulcers are situated in the front of the leg, they are liable to friction; and as but little areolar tissue intervenes between the base 2 8 Surgical Pathology. [Chap. in. and margin of the ulcer and the underlying bone, adhesion takes place, and this prevents cicatrisation. The margin of the ulcer is thick and indurated, almost cartilaginous in consistence. It may be more than an eighth of an inch deep. It usually forms a steep declivity; it is rarely undermined. Microscopical sections of the walls show a coarsely fibrillated or homogeneous substance, in which leucocytes are im- bedded. The number of the latter varies inversely as the induration. The granulations at the base are unhealthy; they may be large and cedematous, or almost wanting. The papillse of the surrounding skin are hypertrophied ; they may be hidden by the exudation, or give a warty appearance to the surface. The skin itself is congested, and often deeply pigmented. Symptomatic ulcers. 1. Varicose ulcers. — No other variety passes through so many phases of the ulcerative process. They are of great interest on account of their fre- quency, and the difficulty that attends their cure. AVe class them with the symptomatic ulcers, since their origin or extension depends upon a diseased state of the veins. They are almost confined to the lower extremity, for in this part varix of the cutaneous veins reaches its highest development; and besides this, the leg is much exposed to injury, the skin is in close proximity to the bone, and therefore liable to become adherent to it, and the force of gravity adds to the difficulty of the venous circulation. Mode of oi^igin. — Varicose ulcers begin in one of four ways : — (1) By rupture of the attenuated walls of a dilated vein. (2) By thrombosis of a cutaneous vein and its capillary tributaries. Now there is but little vascular communication between contiguous capillary areas of the skin, and Chap. III.] Ulceration. 29 consequently the part, cut off from its direct supply, dies, and is cast off as a slough, or it undergoes mole- cular softening. In either case a circular or oval ulcer is left. (3) By an abrasion. (4) By the gradual transition of eczema to ulceration. The inflammation for a time causes only a catarrhal exudation, but sooner or later the true skin is exposed by the destruction of the rete. If on the first appearance of a varicose ulcer it be kept clean and protected from injury, and the pressure in the veins be lessened by raising the limb, it will readily heal. On the other hand, the deleterious effect of decomposing discharge, the continual fretting, and the congested state of the ulcer and skin around, increase and perpetuate the impairment of nutrition. The venous distension is the chief cause of cedema of the granulations, of rupture of capillaries, and pig- mentation of the skin. It also explains the failure at cicatrisation, for whilst it prevents healthy granulation, it gives time for the lymph effused into the base and edge of the ulcer to become indurated, and so to act as a secondary barrier to the circulation. The inflammation that extends for some distance beyond the ulcer causes eczema of the skin. Apart from the general treatment applicable to any ulcer, the special indication is to support the vessels by pressure and position, and thus remove the prime cause of the ulcer spreading or remaining stationary. Of the remaining symptomatic ulcers, some are due to a diathetic state, and others to a specific poison. In the former group we place malignant, lupous, and scrofulous ulcers ; in the latter, syphilitic, typhoid, etc. 2. Malignant ulcers. — {Vide Encephaloid, scirrhous, and epithelial cancer, and rodent ulcer.) 30 Surgical Pathology. [Chap. iii. 3. Liimmis]ied penspiration. — In simple fever the skin is hot and dry, which means that there is a check upon the cutaneous perspiration, or, in other words, a quantity of heat that should be extracted from the body by evaporation from its surface is retained. This of itself must of necessity tend to raise the temperature, but that it is not the sole cause is proved by the fact of a patient remain- ing feverish throughout prolonged perspiration. Thus, if the secretion of sweat be forced by pilocarpine during the hot stage of malarial fever, the tempera- ture continues to rise for some time afterwards. This is not inconsistent with a fall of temperature during the sweating stage of this disease, and after the rigors of pyaemia. By a physical law, rapid evaporation must get rid of a quantity of heat, but the production meanwhile may be greater than the removal. 2. Increased, production of lieat. — (a) Some have asserted that, at the seat of local inflammation (say an acute abscess), the heat derived from increased destruction of tissue raises the temperature of the part, and that the blood, as it courses through, is made hotter. This, too, is true as far as it goes, but then there is no constant ratio between the intensity of the local inflammation and the height of the general fever. A mere bead of pus beneath the skin may increase the body heat by five or six degrees. (b) The influence of the nervous system. — It is well known that there is a heat-regulating centre in the medulla oblongata, and that this may be dis- Chap, v.] Fever. 43 turbed in various ways : {a) through the cerebrum, as the result of emotional excitement ; (6) reflexly, from irritation of the peripheral nerves ; (c) from the action of pjrogenous matter absorbed from the seat of inflammation. The rise of temperature from cerebral excitement, though it may amount to several degrees, is very transient. Billroth disbelieves the reflex irri- tation theory. He says that if a wound be inflicted upon the foot of a dog, after all the nerves going to the limb have been divided, the temperature will still rise to the same degree as if the nerves had been left intact. This proves nothing ; for the nerves can- not be divided without causing a wound, and the inflammatory products from this must be in contact with the central end of the nerve ; besides, the opera- tion itself must cause considerable irritation of the nerves. Other observers have shown that a rise in temperature is directly connected with nerve irrita- tion. At a focus of inflammation the irritation may be mechanical, from stretching of the nerves, or chemical, from the action of the inflammatory pro- ducts. In either case the stimulus is conveyed to the centre in the medulla, and there transmitted into a fresh stimulus, which is sent to the tissues through- out the body, exciting them to increased combustion. (c) The action of infective matter. — By infec- tive matter we do not mean the products of pu- trescent decomposition of the tissues and discharges of a wound, but merely the outcome of the chemical changes that take place in all cases of inflammation. This may be modified by decomposition, or the pre- sence of a specific poison, circumstances which explain the great variety of fevers. . Absorption goes on through the capillaries and lymphatics, and thus the blood becomes charged with poisonous material, which then acts upon the medulla, and possibly on the other tissues through which it circulates. 44 Surgical Pathology. [Chap. v. Other sig^iis of fever. — All the tissues of the body suffer more or less. This is shown by disordered function, and markedly in the secretory organs. The work done by them is much diminished. The blood is charged with noxious matter in a threefold way : — there is the morbid material furnished by the local inflammation ; to this is added the results of a general increase in the oxidation of the tissues, and the nega- tive effect of partial arrest of secretion and excretion. Though many of the symptoms are in part due to the direct action of the pyrogenous matter on the organs which fail to carry out their functions, much is explained by the disturbed state of the vaso-motor, secretory, and trophic nerves of the glands. The first of these explains, to a great extent, the diminution in the watery constituents ; for, the lower the pressure, the less the filtration ; the second, perversion of the special function of the secreting cells ; and the third, disorderly metabolism of the tissue elements. The urine is high-coloured, of high sp. gr. ; it deposits urates. The water is scanty ; urea and uric acid are increased. The chlorides are diminished ; in acute pneumonia they are often absent. In simple fever the perspiration is diminished ; it is very acid, notably so in rheumatic fever. In this disease, and in hectic fever and pysemia, profuse sweating is a pro- minent symptom. The secretion of saliva is checked, and the discharge from the mucous glands is more tenacious than natural ; hence the clamminess and thirst. There is more or less anorexia, perhaps vomiting. The furred condition of the tongue is an index to the state of the stomach. Constipation is the rule ; but, in certain fevers that have a specific effect on the intestines ie.g.^ cholera, typhoid, and some cases of septicaemia) there is diarrhoea. Whether there be flux or drought depends upon the vascular tension, the condition of the walls of the vessels, and Chap, v.] Fever. 45 the chemical and physical nature of the fluids that dialyse. The nervous system. — There are symptoms directly referable to the nervous system, such as headache and delirhtm. These are explained rather by the pyrexia and toxic influence upon the brain than by the extent of vascular congestion ; and hence the futility of excessive depletion by blood-letting. Such treatment might do actual harm by adding the effects of anaemia to those of the fever. Sir W. Jenner has shown that in the specific fevers, and particularly in typhoid, headache ceases with the onset of delirium, whereas in tubercular meningitis it persists. The explanation is this : the poison of the specific fever at first excites the nervous system, and one of the chief signs of this is headache j but, later, it deadens the perceptive centres, and gives full play to disorderly and uncontrollable discharge of nerve energy — deli- rium. In tubercular meningitis the cause of the headache is twofold ; there is the pyrexia, and the irritation of the brain by local inflammation. The latter is so intense that it is only when the exhaustion from the fever and subsequent compression has super- vened that the headache is abolished. The ph^^sical conditions of headache are constant throughout the course of the two diseases ; but by the time the toxaemia of the specific fever has caused delirium, it has masked the headache. The musGidar system. — There is increased activity at the expense of diminished power. In slight cases this may not be evident during rest, but it becomes manifest on exertion ; there is the sense and sign of weakness in the tremulous state of the patient. This is mainly nervous, but the state of the muscular fibres themselves (for pyrexia causes fatty degeiiera- tion) has some share in the process. When the fever is high or the toxaemia intense, and, above all, when 46 Surgical Pathology. ■ [Chap. v. the blood is suddenly charged with infective matter, the natural tonic contraction of the muscles is replaced by a succession of rapidly repeated contractions, over which the patient has little or no control. There are four degrees of this : 1. Fibrillar tremor. — This can be better felt than seen; like the subsultus tendinum, it indicates extreme nervous exhaustion. 2. Rigor. — Here the contraction is more pro- nounced and more general. It is accompanied by a sensation of cold which is subjective, for before the rigor sets in the temperature has generally risen several degrees. It is the relative coldness of the atmosphere to the heat of the patient's body, which in his febrile state is a highly sensitive thermometer. The mind remains clear, firstly because the disturbance is mainly confined to the motor centres, and secondly because the contractions are not sufficiently vigorous and sustained to fix the chest walls, and so cause cerebral congestion from asphyxia. There may be only an initial rigor ; or a succession of rigors. They vary in degree from chattering of the teeth to shaking of the whole body. They are usually followed by profuse perspiration, not alone as a consequence of the rigors, but as a later link in the chain of toxic effects. 3. Eclamptic convulsions. - — These in children take the place of rigors in the adult, for in them there is greater excitability of the nerve centres. Not that adults are exempt from convulsions as the result of high fever. Primary convulsions usually usher in some acute fever, pneumonia ; e.g., when they occur later some grave lesion should be suspected — cerebral embolism, thrombosis, etc. The contractions are more violent than in rigors. There is loss of consciousness and more or less asphyxia. There are many causes of convulsions, but here we are only considering those dependent upon the pyrexial state. Chap. VI.] Surgical or Traumatic Fever. 47 4. Tetanic or tonic spasm. — In reality it is clonic, but the contractions are so minute and follow one another so rapidly that without the aid of the myograph they appear fused. In a minor degree it is seen in "cramp" and "stiffness," but it is the sympto- matic essence of two pyrexial diseases, tetanus and hydrophobia. It probably depends upon a more con- tinuous irritation than either a rigor or " clonic spasm." The discharge of nerve energy is not so violent as in ordinary convulsions, and therefore the nerve cells are not so quickly exhausted. CHAPTER YI. SIMPLE SURGICAL OR TRAUMATIC FEVER. After an operation of any magnitude, e.g., an ampu- tation of the leg, or removal of a breast, the patient becomes feverish. Eor some little time subsequent to the infliction of the wound, the temperature of the body is generally lowered. This is due to the shock of the injury and the depressing effects of the ansesthetic. After an apyrexial interval, varying in uncomplicated cases from twelve to thirty-six hours, the usual signs of fever show themselves ; the heat of the body is increased ; the patient looks somewhat flushed ; he complains of feeling hot and thirsty ; his appetite is indifferent, and his tongue moist and furred. In addition there are headache and general restlessness. The pyrexia varies within a range of three or four degrees; the temperature is rarely below 100° Fahr. or above 102-5°. If we now examine the wound we shall find very 48 Surgical Pathology. [Chap. vi. much, as follows : a certain amount of hypersemia, incidental to the injury. Tlie surfaces, which become glazed after the cessation of the bleeding, now look moist from effusion of liquor sanguinis from the dilated vessels. There are, in fact, the signs of traumatic inflammation, and, other things being equal, the height of the fever is proportionate to the extent of the local disturbance. Cause of the fever. — Allowing for the check on the cutaneous perspiration, and the possible effects of nerve irritation in the wound, there can be no doubt but that the general symptoms (the fever) depend mainly upon something absorbed from the wound : (1) Because whatever prevents a free escape of discharge causes an accession to the fever, and this in two ways; it affords a favourable condition for putrefaction, and increases the liability to absorption of the decomposed products. Per contra, the temperature falls on estab- lishing efficient drainage ; (2) because the measures taken for keeping a wound aseptic minimise the height of the fever curves. *The latter proves something more, viz., that the so-called traumatic fever is to a great extent a state of septic intoxication. We do not say entirely, for the chemical products of inflam- mation are themselves pyrogenous ; as witness the j^yrexia from a simple subcutaneous phlegmon. In all wounds the injury destroys the vitality of a certain amount of tissue, and the necrosed structures are resolved into simpler compounds. In open and exposed wounds these compounds further decompose, and furnish secondary products, which on being absorbed induce fever. The coiKlitioii of tlie wound favours absorp- tion, for there are a large number of blood-vessels and lymphatics, which take up fluids from the surface and transmit them to the blood and lymph streams beyond. As these vessels become firmly occluded, by Chap. VI.] Surgical or Traumatic Fever. 49 consolidation of the clots within and compression of the inflammatory exudation without, the fever declines, even whilst the wound is bathed with " discharges." A well-formed layer of granulations is a strong pro- tection against absorption, for the direction of the osmotic current is away from the blood-vessels, .and granulations have no lymphatics. Traumatic fever is generally more severe when it follows operations upon tissues indurated by chronic inflammation, for the vessels, being imbedded in dense exudation, cannot collapse. To return to the course of the fever. In ordinary circumstances it subsides in a few days, it rarely lasts beyond a week ; if so, we begin to suspect there is something wrong with the wound, and to fear that the simple traumatic fever may pass into the graver forms of blood-poisoning. It rises somewhat sharply at the beginning; for a day or two it oscillates about the maximum, with slight morning remissions. It terminates by lysis, or more rarely by crisis. In some cases it is so slight that its existence is only revealed by the thermometer. When a large wound unites by the first intention fever may be entirely absent; hence, as Billroth observes, it may be considered as a "pathological accident," but an accident so common as scarcely to deserve the name. We would once more repeat that it is the result of local inflammation and absorption of decomposing secretions and tissues. The latter may justly be considered as "an accident," for the presence of a slough on the surface of an aseptic wound neither excites local inflammation nor causes fever. Billroth distinguishes two forms or stages of surgical fever : (1) That due to absorption of the products of decomposition of necrosed tissues on the surface of the wound — primary wound fever ; (2) secondary suppurative fever, which depends on the taking up by the lymphatics of inflammatory 50 " Surgical Pathology. [Chap. vii. products — pus. He says that primary traumatic fever may go on to septicsemia, and secondary suppurative fever to pyaemia. We have not attempted to separate traumatic from inflammatory or suppurative fever, for in practice they overlap. CHAPTER YII. SEPTICEMIA AND PYEMIA. On attempting to define what is meant by the terms septicsemia and pyaemia one is met with this difficulty, that pathologists are by no means agreed as to the distinctive characters and relationships of the two conditions. ^ Some authorities make the word pyaemia cover all the cases of septic absorj)tion from wounds or inflam- matory foci that furnish products of decomposition, whether such absorption results in a general blood- poisoning with the occurrence of secondary metastatic infarctions and abscesses, or without them. They say that the variations observed in the symptoms, and post-mortem signs, depend upon the virulence or intensity of the poison, the state of nutrition of the tissues, and certain accidental circumstances likely to modify the course of the disease, rather than upon any specific character of the poison in different instances. Thus the absence of secondary metastatic lesions is explained by supposing that death or recovery occurs before sufficient time has elapsed for their develop- ment. We cannot admit this explanation, because, on the one hand, multiple secondary abscesses sometimes * The different views are set forth with great clearness in the Transactions of the Pathological Society, vol, xxx., pp. 8—10. Chap. VII.] Septicemia and Pyemia. 51 form very quickly after the injury or inflammation, e.g., the lungs may be full of them within a week of the onset of " acute necrosis"; and^ on the other, un- complicated fatal cases of septic poisoning are occa- sionally of much longer duration. Billroth considers that the two afi'ections are quite distinct, though they may exist together (septopysemia). He regards septicaemia as a severe form of primary traumatic fever, due to the putrefactive decomposition of necrosed tissue and exudation, prior to or after the occurrence of suppuration ; and pysemia as essentially dependent on absorption of pus : " reabsorption of pus is the cause ; intermittent course of the fever, with rapidly increasing marasmus, the chief symptom ; and the metastatic inflammations very essential anatomical conditions." Dr. Burdon Sanderson looks upon septicaemia as a non-infective process, or one in which there is no multiplication of the poison in the system. Since the poison necessarily becomes greatly diluted in the blood and tissues, successive inoculations or injections from animal to animal produce less and less eflfect, or they may fail altogether. In any individual case the result depends (1) upon the power of resistance to the action of the septic material ; some animals are more suscep- tible than others, and, ceteris 'paribus, the smaller the animal the smaller will be the dose necessary to kill it ; (2) upon the strength of the dose ; and (3) whether it be repeated or not. The tendency is to recovery, but the animal may be so overpowered as to succumb before the poison can be got rid of. The materies morbi consists of the chemical products of decomposition of organic matter. It is obviously such as would be furnished by a large wound {e.g., the placental surface of the uterus), and probably some of the cases of puerperal fever are of this nature. But if we thus 52 Surgical Pathology. [Chap. vii. limit the application of the term septicaemia, a large number of cases will be excluded, in whicli there is general blood-poisoning, also without secondary metastatic abscesses. It has been proposed to de- signate these by the term " septic infection^'' in con- tradistinction to " se'ptic intoxication " applied to the former group. In septic infection all the signs and symptoms of septic intoxication, or simple septic poisoning, may be present ; but there is this very important difference, that in the former the poison is multiplied in the system to an indefinite extent, and the disease can be communicated from animal to animal without any diminution in its virulence, in fact its intensity is often increased thereby. This is the nature of many cases met with in practice, and notably in post-parturient women. The ease with which puerperal fever can be in- duced by infinitesimal quantities of the infecting material is too well known. If we conclude, with Billroth, that Jt9^/cem^a is essen- tially due to reabsorption of pus — decomposed, thin, and ichorous pus (for a considerable quantity of freshly secreted healthy pus may be injected into the veins without causing any serious local or general conse- quences) — purulent infection, as it is called, we must also conclude that there are three distinct forms of blood-poisoning : (1) Septic intoxication (without metastases) from the absorption of the chemical pro- ducts of decomposition of tissues and fluids, products incapable of undergoing multiplication in the system, and therefore of being transmitted from animal to animal with unimpaired virulence ; (2) septic infec- tion (without metastases), in which the poison is hot only multiplied, but to a certain extent developed in intensity as it passes from one field of culti- vation to another; (3) pyaemia or septic infection Chap. VII.] Septicemia- AND Pyemia. 53 with metastases derived from one peculiar source — pus. But we are at a loss to understand what there can be in pus — which is only " fluid, as it were, melted, dissolved inflammatory new formation" (Billroth) — that it should furnish material for infection, of an altogether specific character. Simple septic, non-infective intoxication, or the septicaemia of Dr. Sanderson, explains most of the cases of severe blood-poisoning that recover without the formation of secondary abscesses. But it does not follow that all cases are of this nature ; nor, judging from the analogy between septic infection and malig- nant pustule, which is an essentially infective disease, and yet fatal in only about one-third of the subjects attacked (Greenfield), does it seem improbable that a certain number of patients may survive the death of the micro-organisms, or ferments, or whatever the cause of infection may be, providing that whilst active these agents do not give rise to widespread or deep-seated metastases. The nature of the poison. — The immediate cause of the blood-poisoning seems to be due to the unorganised products of decomposition, and not to the organisms that determine the decomposition ; for the virulence of a fluid known to be intensely septic is not lessened by destruction of the organisms (Ander). Several observers have shown that an amorphous substance can be extracted from the fluid that causes septic intoxication. Bergmann believed its composi- tion to be definite^ and he named it " sepsin " accord- ingly. Billroth doubts its specific nature, and thinks that there may be several products of decomposition capable of causing the symptoms. What is the cause of septic decomposition 1 Is the agency of living microscopical bodies essential to the process 1 probably so, for in all decomposing animal 54 Surgical Pathology. [Chap. vii. fluids they are there in abundance, and Dr. Sanderson has shown that the products of decoroYJOsition capable of inducing septic intoxication are only formed in their presence. What, then, is the reason of simple septic intoxica- tion occurring in one instance, and septic infection in another % This is not clear. It may be that the organisms that set up ordinary putrefaction are de- stroyed by the liAdng tissues, whilst those which cause septic infection have a much greater power of resis- tance. This would of course imply that there is a specific " germ " in each case, or that the circumstances under which any one form develops vary in difierent instances. From the intrinsic difficulty attending the necessary observations, and the small size of the organisms, and the number of transitional forms, it is not surprising that the results obtained should in many cases be directly opposite. Por the most part these organisms conform to one of two types, rod-shaped, single or pointed bacteria, possessed of a vibratory onward movement ; and micrococci consisting of mere rounded, specks of pro- toplasm, isolated, or linked to form strings or clumps, and quiescent, or capable only of oscillation, which is difficult to distinguish from the Brownian movement, common to all minute particles suspended in fluids. But these characters are scarcely sufficient to determine their individuality; still, judging from what we know of the bacillus of malignant pustule, we cannot deny the existence of specific germs in the difierent forms of septicaemia, although we are far from understanding their modes of life and action. W. Cheyne concludes from his observations {vide Trans. Path. Soc, vol. xxx., p. 557, et seq.) : (1) That the micrococci are comparatively harmless, and that they are quickly destroyed by the tissues when they gain access to the organism ; and (2) that it is Chap. VII.] Septicemia and Pyemia. 55 the bacterial form that is so potent in causing putre- faction and septic infection. On the other hand, in the report on " Septicsemia " contained in the same volume, pp. 50, 51, it is stated with regard to pyae- mia that micrococci were observed "in a large number of cases " in all or some of many organs, and that " bacteria were found in three cases." Koch asserts that " organisms are not found in the blood of animals suffering from septic intoxication," but that they are invariably present in septic infection. Billroth, who does not seem to draw a clear distinction between the two processes, denies that their presence is necessary. When speaking of pyaemia, which is an infective disease, he says, " I can entirely agree to the miasmatic origin of pysemia, if by miasm is understood what I understand by it , namely, dust-like, dried constituents of pus, and possibly also accompanying minute, living, very small organisms.' Is putrefaction necessary to blood - poisoning ? Certainly not, if the evolution of stinking gases be taken as the indication and measure of it, as the following case shows : Mr. J. Lane amputated a thigh for disease of the knee-joint with all antiseptic precautions. The discharges remained aseptic and the flaps to all appearance healthy, and post mortem no offensive smell could be detected in or about the wound. The symptoms were those of deep septic intoxication. Cadaveric decomposition set in early, and was very rapid. There were no metastases. The blood and discharges were not examined micro- scopically. Nor need the local irritation caused by the poison manifest itself in destructive inflammation, although the infection may cause secondary circumscribed and diffuse abscesses. The writer once lost a case of lithotomy, in which post mortem the wound in the 56 Surgical Pathology. [chap. vii. bladder, which had nearly healed, appeared quite healthy. There were no signs of cystitis, peritonitis, or pelvic cellulitis, or thrombosis of the local veins. The lungs were riddled with small abscesses, and there was a tract of diffuse suppuration between the scajjular muscles in the back. Yet although putrefaction, in the ordinary accep- tation of the term, is not a necessary condition in all cases, it is so exceedingly common that it is safe to infer that the circumstances likely to give rise to it are much the same as those which underlie the occurrence of blood-poisoning, whatever form the latter may take ; whether it be simple intoxication, or intoxication with infection, or infection with metas- tases (pysemia), or one or other combination of these phenomena. Excluding the theory of spontaneous generation, and admitting that the organisms found in the dis- charges from wounds and in closed inflammatory foci are the cause and not the consequence of the de- compositions attended with the formation of septic matter, and also that they are introduced from with- out, we can understand why blood-poisoning should be so closely associated with the overcrowding of wards, and the neglect of measures calculated to keep a wound healthy. The part played l>y tlie tissues. — This is very important, both as regards the wound and the body generally. The greater the bruising and lacera- tion, the more likely is a patient to suffer from primary traumatic fever, and its more severe form, septicaemia. There are several factors that work to this end : (1) A considerable portion of tissue being killed outright, it quickly undergoes putrefaction if germ-laden air be allowed access to it; (2) a large number of blood- vessels and lymphatics are opened, and thus an ex- tensive tract for absorption is provided ; (3) short of Chap. VII.] Septicemia and Pyemia. 57 actual death, the vitality of the tissues about the wound is greatly impaired by the injury itself and the inflammation it sets up. Dr. Sanderson has shown that bacteria "are incapable of producing the poison of septicaemia" (septic intoxication) " in the healthy organism." From this statement we must not infer that they do not gain admission to the body by the wound or some of the natural passages, but that the tissue elements destroy them, or are at least able to resist their action. Yirchow long since observed that the animal tissues tend to get rid of matters obnoxious to them. What is called susceptibility or predis- position of the tissues to be affected by specific poisons (e.^., those of the exanthematous fevers) is only another way of expressing inherent weakness, or im- paired vitality in a certain direction. In erysipelas, which is an infectious disease, the liability of communication from one individual to another is greatly influenced by the state of health. If two patients with similar wounds, the one a healthy young man, the other old and broken down by chronic kidney disease, be placed beside a case of erysipelas, the chances of immunity from, infection, and recovery if infected, are greatly in favour of the former (De Morgan). Further, closed abscesses and, notably, empyemata often contain the most foetid pus laden with bacteria, and yet the symptoms of septic intoxication and infection may be almost nil. Considering the minute size of the organisms, it is difficult to suppose that the wall of granula- tion tissue bounding the abscess is so germ-proof as to completely close all the possible paths of transit. The explanation then turns upon the innocuous- ness of these organisms, or the vital strength of the 58 Surgical Pathology. [chap. vii. tissues being able to destroy them, Tliu? much for the absence of infection. As to intoxication, the pro- ducts of decomposition, though offensive to the sense of smell, must be taken as being not very strongly pyrogenous, or as being so slowly absorbed that the tissues and excretory organs are able to get rid of them as fast as they pass into the system. When the tissues have been undermined by long- standing disease, and especially when they enclose large collections of pus (as in a psoas abscess) they offer but little resistance to the absorption of septic matter. A patient may be apyrexial so long as such an abscess remains closed, but once opened there is an almost certainty of fever, perhaps of fatal inten- sity, unless the ingress of germs be guarded against. Mr. Savory has shown that the virulence of a blood- poison is increased by the introduction of putrescent material from another source. In " acute necrosis," it may be that the infective matter developed at the seat of the local inflammation is of itself sufficient to account for the ulterior con- sequences, but it is by no means certain that the tissues generally are not strongly predisposed to its- action. ]>iagi[iosis of septic intoxication and in- fection. — As septic intoxication is a concomitant of septic infection, the diagnosis of the latter must be made (1) from a knowledge of the transmission of the blood-poisoned state from one subject to another by means of a very small dose of the poison, or such as would appear inadequate to cause the symptoms, except on the theory of multiplication in the system (take, e.g., a case of post-mortem inoculation with the fluid from acute peritonitis) ; (2) by the discovery of microscopic organisms in the blood and secretions. It has been shown that the presence of these bodies in decomposing or putrefying discharges from a wound Chap. VII.] Septicemia and PvyEMiA. 59 is in itself no proof that they must lead to general infection. On the other hand, one would suspect septic intoxi- cation alone where a patient becomes rapidly poisoned by absorption from a large surface of gangrenous tissue, and partic^darly if the escape of the decom- posing fluids be prevented. Pyaemia, or purulent infection, is accompanied by more or less septic intoxication, but the course of the fever is generally indicated by certain well-defined signs and symptoms. On pathological grounds, septic intoxication and septic infection may be considered as distinct, and on clinical, so far as the power of transmission from one patient to another is concerned ; yet, as the two con- ditions usually arise under similar circumstances, and as septic infection implies septic intoxication, they may be described together as SepticsBmia, or "an acute blood-poisoning by the products of decomposition of the animal tissues and fluids ; with or without the development and multiplication of infective organisms in various parts of the body." The exact mode of action of the poison is not well understood. In the main it is probably chemical. The blood is profoundly affected, so that it is unable to nourish the tissues. At the same time, the tissues themselves are so altered as to be unfitted to carry on their healthy functions. Character and course of the symptoms. — The symptoms are chiefly referred to the nervous system, but the effects of the poison are manifested to a greater or less degree in the respiratory and circu- latory organs and the alimentary canal. Cases differ somewhat from one another in the relative frequency and extent with which the different structures are affected. In the artificially-induced septicaemia of 6o Surgical Pathology. [Chap. vii. dogs the intestinal tract suffers considerably. The nervous symptoms are those of rapidly-increasing prostration and narcotism. The patient becomes apathetic and somnolent. In many instances there is low muttering delirium, gradually passing into coma. More rarely the mind is quite clear until the fatal end. Headache is not prominent. There are either no rigors, or only an initial cliill that ushers in the other symptoms. Muscular weakness quickly supervenes. This is shown by failing power of the heart, the inability to sustain exertion, and, it may be, general tremor of the body. The teinperature varies considerably. Sometimes it is very high, 104° F. or more ; in others there is but little change ; or. again, it may be subnormal from the first, and this often in the worst cases. Hence, taken alone, it helps very little in the prognosis. We do not find the steep fever curves as in pyaemia. It may rise considerably after death. I have known it to reach 108° P. This is due to rapid destruction of the tissues, and the non-conversion of heat into functional power. The respirations become quick and shallow from muscular weakness, and hurried still more, perhaps, from pulmonary congestion and stasis. The bowels are constipated in some cases, relaxed in others. Blood and mucus may be passed in the stools. There is sometimes uncontrollable vomiting. State of the blood and urine. — If a drop of blood be placed on a slide, the red corpuscles will be seen to gather into clumps rather than rouleaux, but they show nothing definite in outline. The white corpuscles are relatively and absolutely increased. Micrococci and bacteria may be present. The urine is high-coloured ; it is acid, but quickly becomes alkaline when passed. The urea and uric acid are increased. The phosphates, potash salts, Chap. VII.] Septicemia and Pyemia. 6i and chlorides are diminished. Biliary constituents are occasionally present. Colour of the skin. — The skin has a dusky earthy tint, or it is distinctly yellow. This may be from bile-staining, but it is probably tinted with blood pigment set free by disintegration of the red corpuscles. Post-mortem sigrms. — Rigor mortis sets in early and soon disappears. Decomposition is very rapid. The blood coagulates imperfectly. It may be almost fluid. It is said sometimes to be tarry, but I have never seen this. Disintegration of the red corpuscles goes on during life ; this is shown by the staining of the endo- cardium and the intima of the vessels, observed directly after death. The serum, too, is more or less deeply tinged, and dark from deoxidation of the haemoglobin. Micro- cocci are sometimes present (septic infection). The internal organs show marked congestion, especially at the most dependent parts. Thrombosis is very common, and capillary ex- travasation far from rare. The latter is most marked in the mucous and submucous coats of the intestine, and beneath the serous membranes in the form of pelechise or more diffuse extravasations. Meningeal haemorrhage is less frequent. There are several factors at work in causing the coagulation in the vessels : 1. A ferment is supposed to be liberated by the breaking up of the white corpuscles (Kohler). 2. The chemical composition of the blood is greatly altered. 3. Stasis from weak pro- pelling power of the heart. 4. Swelling and shedding of the endothelium of the vessels, the debris obstruct- ing the lumen. 5. Encroachment of the thickened intima upon the vascular channels. The hyperplasia is found in the small arteries f" obliterative end- 62 Surgical Pathology. [Chap. vii. arteritis ") not in the venules ; these, however, may- show inflammatory changes secondary to thrombosis.* 6. Aggregation of micrococci. The mechanism of the haemorrhage is thus ex- plained : 1. The walls of the vessels are degenerated through {a) starvation, from the blood supply being cut off by coagulation ; (6) fatty metamorphosis, from high temperature, and the blood-poisoning. 2. Capil- lary thrombosis leading to venous reflux, and conse- quent rise of tension in the congested areas. But " frequently the internal organs present no morbid appearances " (Billroth), or at least none that are characteristic. More often the above-described congestions, thromboses, and haemorrhages, singly or in combination, are met with, and as a rule the parenchyma is softer than natural from acute granulo- fatty change. The siileen is enlarged, soft, and congested. The liver is greasy, of a dirty yellowish gray colour. Its blood-vessels are full, esj)ecially those of the hepatic venous system. The tissue may be bile-stained. Crystals of tyrosin have been found. The kidney is enlarged ; the epithelium is granular and swollen. Exudation is occasionally seen between the Malpighian glomeruli and capsules. The sub- capsular stellate veins are injected, and the whole organ is more or less congested. There may be capil- lary extravasations between and into the tubes. The latter are often choked with epithelial debris. The lungs are congested, and oedematous. Patches of collapse and diffuse thrombosis, with or without extravasation, may be noticed. The loleura and pericardium sometimes contain blood-stained serum. The brain is congested ; more rarely it is the seat of meningeal extravasation. If * Vide Trans. Path. Soc, vol. xxx,, p. 53. Chap. VII.] Septicemia and Pyaemia. 63 the skin presented a dusky jaundiced tint during life, this will be found in the cadaver. In septic infection groups of micrococci often crowd the different tissues. They occupy the vessels and the intervascular spaces in the various organs. The above-described symptoms and post-mortem signs may be taken as those of a constructive case of septicaemia, rather than as constant and necessary phenomena. Many of them are rarely absent, and most or all may be present. They are also found with undiminished intensity in acute pysemia ; but anatomically pyaemia is septicaemia plus metas- tases. Fysemia. synonyms. — Purulent diathesis, puru- lent infection. Pus disease. Ichorhaemia (Yirchow). Pyohaemia simplex et multiplex, i.e., pyaemia with or without metastases (Hueter). The last-mentioned designation corresponds to what we regard as septi- caemia and pyaemia respectively. History and current views of pyaemia. — The name pyaemia was given to the disease by Piorry. The supposed necessary dependence upon absorption of pus seemed indicated (1) by the constant association of pus formation and the characteristic lesions; (2) by the discovery of cells and granular bodies in the blood, which were believed to be de- rived from segmentation of connective tissue cor- puscles (the leucocyte migration theory was not then in vogue). We now know that, whether the pus cells do or do not pass back into the vessels, they come from them in the first instance. Probably the corpuscular and granular masses thought to be simply altered pus were in many instances decolorised thrombi, set free by disintegration. (Vide Thrombosis.) Billroth insists that " reabsorption of pus is the cause " of pyaemia ; but his statements with regard to metastases are somewhat 64 Surgical Pathology. [Chap. vit. at variance; thus, lie says, "metastatic inflammations are very essential anatomical conditions;" and, again, ^' purulent infection " (pyaemia) sometimes occurs "without a trace of metastases." The latter condition corresponds to what we have described as septic infection, with this difference, that we did not consider pus to be a necessary factor in the process. Koch, who states that "pysemia does not arise, as was formerly supposed, from the entrance of pus into the vessels," looks upon the disease as a general one, accompanied by metastatic inflammations. This is the light in which we regard it, viz,, that pyaemia is septic infection with metastases. Although the simple absorption of pus does not express the exact truth, it must be remembered that suppuration is a very constant coincidence, for it is found in those extremely rapid cases where pyaemia follows acute necrosis, and, h fortiori^ where a longer time is given for the development of the primary and secondary inflammations. Causes of metastases. — The occurrence of metastases may be explained in three ways : (1) On the assumption that pyaemia is a distinct and specific affection ; (2) by the products of decomposition, local and disseminated, being unusually irritating to the tissues, which, in their turn, may be prone to undergo inflammatory changes ; (3) by embolism, from venous thrombi soaked in septic matter. In favour of the first of these views is the fact of the disproportion of the tissue changes to the degree of septic intoxication in all but very acute cases. But then a poison may be highly phlogogonous, whilst its intoxicating and pyrogenous qualities are comparatively slight. Koch says that the terms pyaemia and septicaemia " have only remained in use as general names for a number of symptoms which most probably belong to a series of different diseases." Chap. VII.] Septicemia and Pymmia. 65 Course and character of the symptoms. — Pyaemia is a continuous fever with very decided inter- missions. This seems to show that the pyrogenous matter thrown into the blood is largely derived from the foci of the secondary or metastatic inflammations, for the intervals and accessions appear too marked to be explained by absorption from the primary wound, or phlegmon, which may to all appearance be taking a steady continuous course. Billroth, however, believes that " extensive progressive inflammation about the wound must be regarded as the chief source of such repeated purulent infection." The fever is ushered in by symptoms of general malaise, or by an initial chill. The temperature rises before the occurrence of the rigor. Both are due to the same cause, viz., a charging of the blood with poisonous matter, which first induces increased meta- bolism of the tissues, and then disturbs the equilibrium of the motor centres. The sensation of cold is caused either by (1) the rapid elevation of the surface tem- perature, or by (2) " the blood being driven from the capillaries by the spasm of the cutaneous muscles " (Billroth). The heat of the body may rise to 105" F., or even higher; it is to some extent proportionate to the nervous irritability of the patient, and so is the severity of the rigor. At the end of this stage profuse perspiration occurs and the temperature falls, some- times below the normal, but even then it rises again, so that the fever is practically continuous. In this way it difiers from ague, which in some respects it greatly resembles. The chills and exacerbations are repeated at varying intervals. This is characteristic of the disease. The severity of the nervous and other symptoms depends in great measure upon the acuteness of the fever. In pyaemia from "acute necrosis" all the signs of septic intoxication are well marked. In the p 66 Surgical Pathology. [Chap. vii. sub-acute and chronic forms the mind is generally quite clear. Meanwhile the patient rapidly loses flesh, for whilst his tissues are being burnt up they are not replaced, owing to defective assimilation. The countenance assumes a cachectic hue, the features are drawn, and are expressive of extreme exhaustion rather than acute suffering. Towards the end the tongue becomes dry and brown, and the tainted sweetness of the breath more marked. Bed-sores are common. The jjrogyiosis turns upon (1) the possibility of getting rid of the primary source' of infection; (2) the extent and situation of the metastases; (3) the duration of the fever. Every day that passes adds to the probability of recovery. €hang:e$ in tlie ground. — The suppurative inflammation at first increases, in direct continuity, and by the formation of abscesses at some little distance beyond. The pus is thin — ichorous, as it is termed. Later on, the wound becomes drier. Any granulations that have formed are destroyed. The neighbouring veins are frequently thrombosed, and on cutting into them they are found to contain clots in various stages of formation and disintegration. The nearest lymphatic glands are enlarged. Metastases. — During life localised and diffuse suppurations may be met with ; especially in the joints, viscera, and the subcutaneous, subfascial, and inter- muscular connective tissue. The rapidity with which these abscesses form is often remarkable. Then, again, there may be evidence of pneumonia, pleurisy, and pericarditis. In rarer cases the eye-ball is destroyed, and cerebral abscess or suppuration in the arachnoid may ensue Post-mortem appearances. — Except in very acute cases, where during life the signs of septic Chap. VII.] SePTICMMIh AND PyMMIA. 67 intoxication were well marked, there may be nothing very striking to be seen post-mortem in the state of the blood j and the internal organs do not show such extensive congestions, thromboses, haemorrhages, and softenings as described under septicaemia. But there are quite characteristic lesions in the form of multiple circumscribed metastatic abscesses, and red infarctions in various stages of softening and suppuration. These are for the most part wedge-shaped, and are then evidently the result of septic embolism. The contents of the abscesses consist of disintegrated tissue and blood clot, mingled with pus. They are most fre- quently seen in the lungs, but they are not uncommon in the spleen, kidney, and other organs. More rarely the abscesses are scattered, appa- rently irrespective of the course of the circulation. These, and the occasional diffuse suppurations, are probably the consequence of primary thromboses, and of the phlogogonous action of the poison upon tissues predisposed to inflammation. The same may be said of suppuration in the joints. The primary wound will be found infiltrated with pus, and the veins usually filled with disintegrating clots. Such is a typical case of pyaemia j but the signs of septicaemia and pyaemia may be found in almost endless combinations ; " for instance, se'pticcemia occurs without a trace of metastases, with metastases, with thrombosis and embolism ; 'purulent infection (pyaemia) without a trace of metastases, with diffuse metastases and thrombi, with thrombi alone, with thrombi and emboli ; there are thrombi with local sequences with- out emboli, with emboli, with haemorrhagic effusions, with apoplexies, etc. (Billroth). Idiopatbic pysBinia. — Sometimes numerous abscesses attended with other pyaemic symptoms are met with, without our being able to trace their origin ; 6^8 Surgical Pathology. [Chap. vii. but then the source of infection may be some poison that has gained access to the organism by the re- spiratory tract, or through some minute focus of in- flammation in the alimentary canal. " Acute necrosis " seems to form the link in the etiological chain between these and the ordinary cases of traumatic pysemia. • Suppression of Urine — Urethral Fever. Suppression of iirine is obstructive or non- obstructive. In the former case it generally follows impaction of a calculus in one ureter, the kidney on the other side having previously been incapacitated by disease. The condition of the patient is peculiar, for whilst the suppression may last a week or more, the urinous odour of the breath is usually absent, and there is no dropsy. The passage of a catheter has been known to cause death within a feAV hours. The pathology of such cases is somewhat complex. It cannot be ex- plained by simple reflex congestion of the kidney, for the organ may not be flooded with blood to the extent that one would sujopose necessary to account for the total abrogation of function. It may be that the nerve irritation affects the secreting cells directly. The suddenness of onset and the absence of a large wounded surface preclude the assumption of acute septic intoxication being the cause ; but probably all the above-mentioned factors combine in their action. Uretliral fever is the name given to the general state caused by some injury to the urethra, such as internal urethrotomy, or forcible dilatation, or even simple catheterism. It is frequently ushered in by a rigor which may be repeated. The temperature rises rapidly. The other symptoms of fever are present. Then there is sweating, and with it a quick decline in the body-heat. Whilst the fever lasts, but Chap. VIII.] Erysipelas. 69 little urine is passed ; witli its disappearance there is often a copious flow. Sometimes a considerable amount of blood is lost, and this seems to come from the kidney, for it is well mixed with the urine, unless in such quantity as to coagulate in the bladder, a circumstance which has happened twice in the author's practice (once after Holt's dilatation and once after easy catheterism), and its effusion is attended with decided relief from pain in the back. The cause of the fever is apparently fourfold : (1) Keflex congestion and consequent im- pairment of function of the kidney ; (2) stimulation of the nerves of an unusually sensitive tract ; (3) absorption of poisonous matter, though this must be very slight in those cases where but little or no injury is done to the urethra j (4) nervous irritability of the patient. I have known it ensue more than once in the same case upon the withdrawal of a catheter which had lain in the bladder for 48 hours without causing the least disturbance. CHAPTER YIII. ERYSIPELAS. Erysipelas is generally described as existing under three forms : (1) Simple cutaneous erysipelas ; (2) phlegmonous or cellulo-cutaneous erysipelas ; (3) cellulitis ; though it is by no means certain that the poison is the same in each case. Those who believe in the unity of the disease explain the difierent results, (1) By the- mode of introduction of the virus ; (2) by the degree of its concentration ; (3) by the extent to which the cuta- yo Surgical Pathology. [Chap. viii. neous and subcutaneous tissues are predisposed to its action. There is also the fact of one variety taking on the characters of another. This is especially the case in the cutaneous and cellulo-cutaneous forms. The former may end in suppuration, and the latter spread superficially as a capillary lymphangitis ; and both may arise without the previous existence of a broken surface of skin or mucous membrane. Cellu- litis appears to be always preceded by a wound, although this is often very slight. Moreover, it may be excited by poisons of widely different nature ; e.g.., that of venomous animals, unhealthy matter from inflammatory foci, or cadaveric fluids. Simple cutaneous erysipelas is generally due to inoculation or infection of a wounded surface (Billroth, Trousseau); for the so-called idiopathic variety usually attacks the exposed parts of the body, particularly the face, or those most subject to scratches or abrasions, which may be so small as to pass unnoticed. The general predisposing causes are bad hygienic conditions and impaired health of the patient. The actual cause is the specific poison com- municated by direct inoculation, or infection. The disease is not highly infectious, but there can be no doubt as to this mode of transmission, as shown by the occurren prostate gland; ti, ureter; e, A'as deferens ;/, hydatid cyst. The essential cysts are collapsed and folded up within the adventitious cyst. (Reduced one-half. muscles, there is scarcely any limit to hypertrophy so long as there is no interference with the supply of properly oxygenated blood. Thus there is nothing to show that thickening of the muscular coat of the intestine above a stricture ceases of itself whilst the resistance continues. 84 Surgical Pathology. [Chap. x. The same holds good in all other instances where the natural stimulus is intermittent; e.g.^ in the glandular organs, such as the testicles. If one kidney be crippled or destroyed by disease, the other undergoes considerable enlargement. There is undoubtedly an increase in the size of the tubules, but whether new ones are formed is a disputed point. Paget asserts there are. If the tibia be short from arrested growth, from injury or disease of the epiphysis, the length of the limb may be preserved partially or entirely by an elongation of the femur. Allied to these forms are the associated hyper^ trophies, where the changes follow others in parts intimately connected with them; e.g., eccentric hyper- trophy of the bones of the skull, when the contents of the latter are increased, and concentric when they are diminished. The thickening in these cases is best seen at the seat of the original centres of ossification. The irritative hypertrophies are caused by intermittent pressure, for continuous pressure leads to atrophy. Thus the papillae become enlarged, and the epidermis is thickened in the form of corns and callosities ; and beneath these bursse may develop to diffuse the abnormal pressure from a tight shoe, or that misdirected in club foot. In all cases of hypertrophy there is an increased supply of blood, and the more active the renewal the more nearly do the new-formed elements con- form to the physiological type. Thus in the preg- nant uterus the circulation is very active, and there is a rapid and perfect reproduction of in- voluntary muscular fibres, and also an enlargement of pre-existing fibres from excessive nutrition. As the necessity for the hypertrophy is withdrawn after delivery, atrophy sets in ; the firm contraction of the muscular walls itself diminishing the blood supply. Chap. XL] Atrophy. 85 But let some mechanical cause interfere with the natural involution of the uterus, and the organ will remain enlarged for an indefinite period, not from mere failure of the atrophic change in the muscular fibres, but from overgrowth of connective tissue (areolar hyperplasia), the result of mechanical congestion. These cases show how a chronic inflammatory enlargement may overlap and simulate a triie physio- logical hypertrophy ; and there can be no doubt but that the latter may be maintained to some extent by the increment of nutrition set up by the local me- chanical hypersemia. When the original stimulus, instead of being physiological and simply calling for increased func- tional power, is an artificial one (e.^., friction against the skin, or the irritation of the hair follicles and papillae and subjacent bone in a case of chronic ulcer), the plastic exudation is not all used up in fashioning tissues after the likeness of the normal histological elements of the part. Some at least pass no farther from the embryonic type than indurated connective tissue. It would be a distinct gain if the word hyper- trophy were reserved for cases where there is a call for increased functional activity and compensation, and the term irritative overgroioth employed to desig- nate those arising from accidental stimulation. . CHAPTER XI. ATROPHY. Development and growth ; discharge of healthy function, with maintenance and repair; and finally a decline and death, make up the sum total of the life- history of all the tissues. The wasting of old age can scarcely be looked upon as evidence of disease ; 86 Surgical Pathology. [Chap. xi. but it rarely happens that the individual passes through his existence free f;:om abnormal change. People grow old before their time ; some in one structure, others in another. This premature agedness may show itself in blanching and loss of hair, decay of teeth, loss of the elastic tread of youth, senile atrophy of the brain, or weak and fatty heart. All these conditions are attended with a diminution in the nutrition of the tissues whereby their proper constituents lose in bulk and function. Atrophies are simple or essential, or secondary to some more actively destructive process. The former we see in the arcus senilis and degenerated arteries of the aged, the latter in wasting of a bone by pressure of an aneurism or its interstitial absorption by inflammation, cancer, rickets, or mollities ossiurn. Inflammatory difiers from simple atrophy in that it is often followed or accompanied by constructive or organising changes. Thus osteophytes are almost always found in the neighbourhood of joints destroyed by caries. Causes and varieties of atrophy. — (1) Natural or physiological atrophies ; e.g., of the uterus after parturition, of the breast after lactation, of the testicles of the deer after the rutting season. To these may be added the spontaneous withering of the thymus and the thyroid glands, and simple senile wasting. (2) A part may waste for want of its proper amount of functional stimulus, as in the case of paralysed muscles, of the optic nerve from blindness, and of amputation stumps. (The natural stimulus to the nutrition of a bone is the contraction of the muscles attached to it ; and after an amputation the muscles have less work to do.) (3) Atrophies of nervous origin. — The loss of Chap. XL] Atrophy. "87 nutrition may be largely influenced by disease of the nervous system. The secondary descending degenerations of the spinal cord, consequent on lesions in its substance higher up, or in the brain ; the wasting of the distal portion of a divided nerve ; and the absorption of the articular ends of the bones in locomotor ataxia, are instances in point. (4) Partial deprivation of hlood-sujoply, as when, in fracture of the shaft of a long bone, the nutrient artery is torn ; or the brain and heart soften from obstruction in their vessels. Then there are numerous instances showing the result of continuous pressure. Absorption of the hard palate by a badly fitting obturator ; erosion of the vertebrae by an aneurism or tumour (Fig. 3) ; changes of shape of the ends of bones in unreduced disloca- tions ; the ball-and-socket pseudartbrosis of an ununited fracture; and, lastly, shrinking of the testicle from varicocele. (5) Excessive functional activity tells its tale in the form of atrophy of overworn jaded brains. The waste from the great expenditure of nutritive force is not repaired for want of the natural term of rest. When, exceeding the ratio of general emaciation, the heart grows smaller, to accommodate itself to a diminished amount of blood, the atrophy is called "purposive." This is sometimes masked by a relative hyper- trophy, when opposite causes are at work in the same patient. Thus the organ may retain its normal weight, though atrophied, as it were, from the wasting of phthisis or cancer, or hypertrophied from the obstruc- tion of arterio-capillary fibrosis (Sibson.) Modes of atrophy. — The process may work out its effect by a simple diminution in the size, and 88 Surgical Pathology. [Chap. xi. eventual loss in number, of the tissue elements, tliose that remain being natural in appearance and con- sistence ; e.g.^ the fibres of striated muscle. But more often obvious degenerative changes can be seen, the chief being those due to fatty metamorphosis and infiltration. Muscles that have lain fallow for a long time from paralysis, or from forced rest in joint disease, as a rule become pale and soft. The bones which in the latter case are the seat of interstitial absorption, have their spaces filled with fat, and readily fracture when attempts are made to break down adhesions in the articulations. Perhaps the best example of fatty atrophy is the arcus senilis of the cornea, which commences in a degeneration of the stellate corpuscles. It is a con- dition of great pathological and clinical importance, from its frequent association with wide-spread vascular decay. Probably some of the deaths from chloroform are caused by acute distention of the degenerated walls of the right cavities of the heart during the struggling stage, rather than by the direct effect of the poison. In addition to fatty transformation of the proper elements, the connective tissue cells become loaded with fat from infiltration ; and in this way an organ or tissue in an advanced stage of essential atrophy may retain or exceed its normal bulk ; e.g., the en- lai'ged calves in pseudo-hypertrophic paralysis. In certain structures pigment granules are de- posited. This is particularly the case with the ganglion cells of the nerve centres ; e.g., those in the anterior comua of the grey matter of the spinal cord in infantile paralysis. As nutrition fails in the muscular coat of the small and medium-sized arteries, in the rib cartilages, and in many other situations, the parts become petrified with lime salts. Inflammatory deposits waste by a fatty and a Chap. XI.] Atrophy 89 mucoid or " liquef active degeneration." The latter change is best observed in caries of bone. There the protoplasm of the cells becomes fluid, and lactic acid is formed (Cornil and Ranvier). Atrophy of Ibone. — That continuous pressure causes atrophy, and intermittent pressure hypertroiDhy, are sometimes seen in the same preparation. In the museum, of St. Mary's hospital there is a portion of the dorsal spine in which the vertebrae have Pig. 3. — Vertebrae absorbed by an Aneurism. a. Cancellous ^0116 forming floor of cavity ; 6, compact hone forming floor of cavity ; c, new bone Ijy which the vertebrae are anchylosed. (Reduced one-third). been hollowed out by an aneurism of the descending thoracic aorta. The floor of the cavity is quite uniform. 90 Surgical Pathology. [chap. xi. contrasting with the irregularity produced by caries or cancer. On the right side these vertebrae have become anchylosed by the formation of a considerable amount of new bone j i.e., there is loss of substance on the left side and central portions where the pressure was constant, whereas the right margin, which was sub- ject only to the intermittent pulsation of the aneu- rismal sac, is hypertrophied (Fig. 3). According to Paget, the cancellous tissue is not exposed in these cases, a layer of compact bone covering the surface. The specimen in question, how- ever, shows in some parts the open fretwork of the interior of the vertebrae, though not so plainly as in caries or cancer. The modus operandi of the pressure is obvious — the blood-vessels of the adjacent layer are com- pressed, and the bone wastes from want of its proper nutritive supply. The bones in old age undergo a rarefaction, and the earthy salts are increased ; hence they easily break. Intracapsular fracture of the neck of the femur from slight force indirectly applied is an in- stance of this. The atrophy in these cases is eccentric. The size and shape of the bones are not necessarily altered. The medullary canal is enlarged. In eden- tulous jaws, however, the alveolar margin is absorbed, and the bones are in every way smaller. Atropliy of muscle. — The various causes of atrophy are well illustrated in the muscles, voluntary and involuntary, plain and striped. Disuse leads to wasting of the muscular coat of the bowel below an artificial anus. The muscles of an amputation stump gradually shrink and shorten from interstitial atrophy, and not from functional contraction. This is one reason why artificial socket-limbs are not ordered for some months Chap. XI.] Atrophy. 91 after operation, for they take their bearing chiefly from the general surface. If the flaps are too short, the atrophic shortening may stretch the cicatrix over the end of the stump, and cause obstinate ulceration. If muscles be kept habitually shortened, as in flexion and adduction of the thigh from hip-joint disease, they will shrink. This may ofier a serious bar to the straightening of the limb, and may necessi- tate division of the tendons. In acute inflammation of joints, the irritation of the articular nerves seems reflexly to impair the nutrition of the associated muscles, and to lead to a wasting out of proportion to the disuse. Disease of the motor ganglion cells of the spinal cord in progressive muscular atrophy and in infantile paralysis causes a corresponding wasting of the muscles supplied by them. In infantile paralysis, where the loss of power is often sudden and complete, the subsequent wasting from disuse may to some extent be averted or re- moved by an artificial stimulus, such as passive move- ment or electricity. When there is advanced general fatty degenera- tion of the muscular system, no operation should be undertaken that is not absolutely necessary, for the nutritive activity, which is. at a very low ebb, would not unlikely fail to repair an extensive wound. Atrophy of nerves. — In addition to what has been already said, we may cite softening of the brain from ligature of the carotid, embolism, etc., degeneration of nerves whose function has been annulled or impaired; e.^., in amputation stumps. According to Dickinson, the bulk of the nerve may be retained but the fibres wasted, fat and connective tissue taking their place. 92 CHAPTER XII. FATTY INFILTRATION FATTY DEGENERATION. Physiologically, fat exists in tlie animal tissues in two forms, firstly, in combination with albuminoid constituents, and secondly, in tlie free state, as granules or drOplets in the cells. In like manner we find it in pathological states either as a mere infiltra- tion, or as the result of metamorphosis of cell proto- plasm. Fatty infiltration.— The cells of the liver, and especially those forming the outer zone of the lobules, always contain a certain amount of fat, elaborated and stored uj) by the functional and nutritive activity of their proto^^lasm. This is notably increased during digestion. The excess is used up in the intervals of feeding to supply the requirements of the system, both for maintenance and repair. By its combustion heat is given off, and this keeps up the normal temperature, and, being transmuted into physical force, works the complicated machinery of the body. The villi of the intestines and the lacteals are also loaded with fat during digestion. Under ordinary conditions the balance between waste and supply is maintained ; but this may be lost on either side. Thus, if the amount of food be in- sufficient, fat quickly disappears from the cells, and the animal emaciates. On the other hand, obesity is the consequence of overfeeding and inaction. (The question of demand and supply is too often lost sight of in the treatment of patients taken from active life and suddenly confined to bed. Apart from indiscre- tion in diet, such a condition is sufficient in itself to Chap. xii.j Fatty Infiltration. 93 cause furred tongue, indigestion, headache, and a rise of one or two degrees in the body temperature. Hence the advantage of complete rest and modified regimen for some days prior to the performance of any severe operation.) It is impossible to say where a physiological becomes a pathological adiposity, but certain it is that the secretory function of an orsan may be strained by excess of work, just as much as a muscle used beyond certain limits will tire and waste. There can be no doubt but that overfeeding long- continued is a cause of organic disease of the liver, and this again of the whole of the digestive system. The connection between the "pleasures of the table " and haemorrhoids is well known. Although fatty degeneration and infiltration are quite distinct processes, they are not uncommonly associated; e.g., in "fatty heart" the muscular fibres have undergone a retrograde change, their constituent fat having been liberated. At the same time a con- siderable accumulation of fat in the cells of the connective tissue beneath the pericardium and between the muscular fasciculi is far from rare. Again, in certain paralytiG states, and especially in " pseudo-hypertrophic paralysis," the muscles are enlarged in the gross in spite of the wasting from fatty atrophy of their fibres. There is an infiltration within the sarcolemma and between the muscular bundles. The mere disuse of a part is often followed by a marked fatty infiltration; thus, if a limb be kept fixed for a long time, the bones become rarefied from simple atrophy, and the cells in the enlarged cancellous spaces filled with fat. A similar change is observed in the muscles. The bones are rendered more fragile, and so easily break on applying force to overcome stiffness in the joints. The muscles are less contractile, 94 Surgical Pathology. [Chap. xii. and hence amputation flaps retract but little, and their state of lowered vitality does not conduce to rapid healing. In phthisis a noteworthy feature is enlargement of the liver from fatty infiltration. The reason of this is not clear. It may be from the impaired function of the lungs, but it must not be forgotten that high temperature leads to a general absorption of adipose tissue, and it may be that the blood thus overloaded is relieved of its incubus by the liver. • Finally, although fatty infiltration may mechani- cally impede the contraction of muscle, and hamper the secretory function of glands such as the liver, it is not incompatible with the continued life and activity of the tissue elements affected. Fatty deg:eiieratioii. — Here there is a true metamorphosis of the cell protoplasm. By some it is alleged that albuminoid bodies are converted directly into fat, but it is more probable that fat normally exists as a constituent of cell composition in intimate combination with nitrogenous substances. As the result of chemical decomposition, the constituent fat is set free, and appears as minute particles, giving a granular appearance to the cells. Physiologically, fatty degeneration occurs in the mamma, and the sebaceous and ceruminous glands. The functional activity of the cells involves an end to their vitality. They become loaded with fat, then disintegrate and set free their contents. In the meantime new cells replace those that have dis- appeared, and so the balance of nutrition of the secreting structures is maintained as long as sufficient pabulum is afforded, and the secretion is carried on within natural limits. Over-action leads to exhaustion and wasting. During the involution of the uterus after par- turition the hyperfcrophied muscular fibres undergo Chap. XII.] Fatty Degeneration. 95 retrograde fatty metamorphosis prior to absorption ; and the same happens in the corpus luteum in the ovary. In old age fatty degeneration plays an important part in the natural decay of the tissues. Of such nature is the arcus senilis of the cornea. As a rule, this first appears in the upper segment as a dull, whitish crescent, at a short distance from the sclero- corneal junction. A second crescent is formed below, and these two extending, the circle is completed. It is of little clinical importance in itself, but it serves as an index to similar changes in other parts of the body, and particularly the vascular system. It points to the likelihood of fatty degeneration of the heart and arteries, and thus to the dangers of syncope and apoplexy. It is an interesting fact that in an eye that has been the seat of organic disease, even though all visible signs have disappeared, the fatty degeneration of the corneal corpuscles will come on earlier than in the pre\dously sound eye. This is a good example of lowered vitality constituting a "locus resistentise minoris." Another instance of fatty degeneration and natural decay of tissue elements is seen in the epithelioid cells lining the large arteries, which we have observed in children only three years of age (Fig. 4, a). This, and the senile changes above referred to, can scarcely be regarded as signs of disease. (Vide Atrophy.) At the same time, these fatty degenerations from old age are of the greatest moment in the consideration of surgical pathology, bearing so directly as they do upon the prognosis of disease, and the repair of wounds. They would count in the scale against the performance of operations that are not absolutely necessary. Causes of fatty deg^eneration. — The cir- cumstances that conduce to fatty degeneration are, g6 Surgical Pathology. [Chap. xii. (1) Inherent disposition to decay; (2) defective vas- cular supply; (3) rapid growth; (4) high temperature ; (5) the action of poisons. There may be a combination of causes, as in inflammation and the acute fevers, especially those of infective origin : (1) This was discussed when speaking of true physiological degenerations, and the allied changes dependent on old age. To these may be added cataract of the crystalline lens, and notably the fluid and soft varieties. (2) There are several ways in which deficient sufply of hlood entails fatty degeneration. It is seen in its simplest form in diseases that diminish the elasticity and lessen the calibre of the arteries, either by a primary calcification of the middle coat, or thickening and irregularity from chronic and sub- . acute arteritis. This is well illustrated in the heart. At times the orifices of the coronary arteries are greatly narrowed from atheroma of the first part of the aorta ; more frequently the walls of the arteries themselves are extensively afiected as well. Anaemia (in its physiological sense) over wide tracts follows obstruc- tion from embolism and thrombosis and their conse- quent infarctions, the extent of it depending upon the freedom of the collateral circulation. In the brain, where this is very limited, softening is sure to ensue if a vessel of considerable size be blocked. Althous^h three varieties of cerebral softening are described {red, yellow, and white), there are two factors only that contribute to the result : firstly, the suddenness and completeness of arrest of the blood stream ; and secondly, by implication, the amount of blood in the part. In all three there is fatty degeneration of the brain substance and of the products of exudation. If a good-sized vessel be plugged by an embolus, the venous reflux and capillary stagnation and rupture Chap. XII.] Fatty Degeneration. 97 reach their limit. The colouring matter of the dis- integrating infarct mingles with the fatty debris, and a semi-diffluent red pulp obtains. If, on the other hand, the arrest be gradual, there will be sufficient force to drive the blood through the obstructed artery and its capillaries and veins beyond ; but the current will be slow and small, and inadequate to the maintenance of the tissue it supplies, which will consequently waste from fatty atrophy. Between the red and the white softening stands the yellow, but it represents only one shade out of the many passing from white to red. At times a steady degeneration goes on for a period, giving rise to white softening, and this is subsequently modified by capillary rupture at the margin. Fatty degeneration of the heart and atheroma of the cerebral arteries are the precursors of white softening ; sudden occlusion by embolism or throm- bosis, of red. Cerebral softening is never sharply defined, but passes gradually into the surrounding healthy brain substance. Under the microscope, there will be observed, in variable quantity according to the kind of softening, blood corpuscles, pigment granules and crystals, large compound granule cells, free fat particles, crystals of fatty acids, and cholesterine, and, if the process have been rapid, shreds or sloughs of brain tissue. Fatty degeneration is a constant feature in all infianfimatory exudations. It is chiefly due to the insufficiency of blood supply from the tension on the capillaries ; but the increased temperature of the blood in general, and of the inflamed part in particular, and probably also the deleterious effect of the chemical products of decomposition of the exudation, have much to do with it. It involves not only the pus H pS Surgical Pathology. [Chap. xii. corpuscles, but the walls of the blood-vessels, and, in fact, all the elements that make up the inflamed tissue. (3) In rapidly growing tumours^ such as cancers and sarcomas, fatty degeneration often reaches such a degree that large tracts break down into a diffluent pulp, constituting "softening cysts." There are two reasons for this extensive fatty change : 1st, the formation of blood-vessels cannot keep pace with the growth of the tumour, and^ from the softness of the latter, capillary ruptures are common ; and 2nd, the vital activity of the cells is expended in their multiplication, to the exclusion of a higher develop- ment, hence, being unstable, they wither and die. (4) Hyperpyrcexia is a powerful cause of fatty degeneration, and cannot well be overrated, whether it be considered from a pathological standpoint, or in its practical application to the treatment of disease. Post mortem all the organs are found softened, and break down readily under the finger. They feel greasy, and are of a dirty yellow colour. The rapid transformation of protoplasm into fat explains the danger of fatal syncope from intrinsic failure of the heart. The beneficial efiect of bringing down the tempera- ture by the cold bath, or large doses of certain drugs, such as quinine, is very marked. The heart acts more powerfully, and the pulse becomes slower, and head- ache and delirium are decidedly checked. (5) The action of poisons. — Poisons causing fatty degeneration naturally fall into two groups : — (a) The materies morbi of infective fevers, in- cluding the acute specifics, and septicaemia. (h) Certain mineral poisons. The chief of these is phosphorus, then come antimony, arsenic, and mercury. How they act is uncertain. It may be that they diminish or destroy the vitality of the tissues, and Chap. XII.l Fatty Degeneration. 99 that these, no longer restrained by the conditions of life, fall a prey to chemical decomposition, of which Fig. 4. A, Eatty defeneration of the tunica interna in a flake of this membrane. In the midst of the flbrillated tissue, b, are seen masses of fat granules, a, resulting from the fatty degeneration of the flat ramifying cells of this layer (x 200). B, Secondary products of fatty degeneration; a, plates of cholesterine ; 6, crystals of stearic acid (Cornil and Ranvier). fat is the chief product. That death is the cause, and not the consequence, of fatty degeneration, is supported by the fact that when dead bodies are allowed to decompose slowly, under the influence of moisture, 100 Surgical Pathology. [Chap. xiii. ordinary putrefaction is arrested, and the tissues are converted into a fatty body termed adipocere. Microscopy and chemistry of fatty degene- ration. — Fat granules appear first around the nuclei of the cells. This can be easily observed in muscle, where the nuclei are large and elongated. The fat particles are here deposited in parallel streaks. They are very numerous, dark, and highly refractive. The smaller ones merge, but the cell is not distended by a large drop, as in fatty infiltration. After the cells break up the granules are dispersed, and are then more readily absorbed. Absorption is extensive and very constant, and hence it is not surprising that fatty degeneration is the principal mode of atrophy. If the fat be in large amount, or long retained, it breaks up into the fatty acids and cholesterine. Stearic acid crystals are rhomboidal, acicular, and stellate. Cholesterine appears as plates, with pieces chipped out of the corners (Fig. 4). Fat granules are dissolved by ether and strong solution of caustic alkali ; they are turned black by osmic acid, but do not take the staining from logwood or carmine. If iodine be added to cholesterine, and then strong sulphuric acid, a blue colour is obtained. Sulphuric acid alone gives a deep red colour. CHAPTEU XIII. MUCOID AND COLLOID DEGENERATION. These changes are very closely allied, and are found under similar circumstances. It is difficult, without the aid of chemical reagents, to distinguish between them. Mucoid deg:eneration. — This alteration in the Chap. XIII.] Mucoid Degeneration. ioi composition of the tissues does not appear to depend, like fatty degeneration, upon a mere diminution in nutritive supply, but to be an essential factor in the life-history of many new growths and other morbid products. Physiologically., mucoid tissue is widely distributed in the fcetus, where it marks the transitional stage from embryonic to more fully developed structures, and particularly connective tissue. In the mucous membranes the transformation of the protoplasm of the epithelial cells into mucin constitutes the natural secretion. In the main, the cells are destroyed by the pro- cess, and are replaced by others formed beneath them ; but it seems probable that a dehiscence or discharge of their contents may occur without a necessary loss of vitality. Mucous tissue is permanent in the Whartonian jelly of the umbilical cord, and in the vitreous humour of the eye. Pathogeny. — In the majority of cases this form of degeneration is found either in tissues, where it is a physiological constant, or in those that are but little removed from the embryonic type. In inflammation of the mucous membranes there is an exaggerated secretion. We see evidence of this in the flux of nasal catarrh, and in the ropy mucus from an inflamed bladder. It may be stated that anything which tends to render the vitality of the tissues unstable tends also to the formation of mucin in the cells and intercellular substance. Hence it is far from rare in inflammatory products and new growths. Tumours that spring from the mucous membranes are commonly gelatinous ; e.g., the simple polypi of the posterior nares. In them the mucoid transformation goes on ^^aH fassib with the increase of tissue, so that there is a uniform glistening throughout. Growths of similar structure I02 Surgical Pathology. [Chap. XIII. are found springing from connective tissue in various situations — beneath the skin and fasciae, and in the parenchyma of organs, the parotid gland, for example. There are some tumours in which the mucoid change is not generally diffused, but scattered in Fig. 5. — Multiple Cystic Epithelioma of Lower Jaw ; Cyst Develop- ment in process. Ac a, the central round epithelial cells are undergoing distension from mucoid metamorphosis • at h and c, this is further advanced ; at d, all the central cells of the loculi have disappeared. The peripheral columnar cells remain as an epithelial lining to the cysts, e, interlobular tissue, composed for the most part of spindle-shaped cells ; in other parts of the growth they had developed into fibrous tissue. patches as a secondary degeneration and softening. By the fusion of contiguous droplets cysts are formed, the walls of which are smooth or rugged, and the contents semifluid, and either clear or turbid, colour- less or stained. If coloured or turbid, it is due to admixture with granular fatty matter or blood pig- ment, and not to alteration in the chemical composition of mucin (Fig, 5). Chap. XIII.] Mucoid Degeneration. 103 Of this nature are many cystic sarcomata and en- chondromata. The costal and articular cartilages and the inter- vebral discs are liable to undergo this form of de- generation. It is seen in the rib cartilages of old people, in joints affected by "white swelling," and in the spinal column, the seat of caries. The glairy discharge and gelatinous granulations of many ulcers are explained in the same way. It is said that in mucoid degeneration the inter- cellular substance is attacked in preference to the cells, the reverse of colloid degeneration. The existence and general distribution of mucoid degeneration rest upon a physiological basis ; but there seems to be no satisfactory explanation why gelatinous polypi should be common in the nose and i^re in the rectum and bladder, nor why some growths sliould be riddled with mucous cysts whilst others of like structure remain free. Microscopy. — The fibres of connective tissue swell up, and their outline becomes obscured and finally lost. Elastic tissue resists the change much better than the white variety. When the cells are affected, a drop of mucin appears in the protoplasm (Fig. 5, 6). It enlarges and pushes the nucleus to one side. Eventually all signs of cell wall and nucleus disa,ppear. In the myxomata and in the umbilical cord, the outrunners of the branched cells unite to form a delicate network, spun, as it were, through the homogeneous gelatinous matrix. [Vide Figs. 61, b, 62, b.) The secretion from inflamed mucous membranes contains granular cells, probably leucocytes. Chemistry. — Mucin is only found in alkaline fluids. It is precipitated by alcohol, alum, and dilute mineral and acetic acids. The precipitate redissolves in excess of mineral acid, but this is not the case with I04 Surgical Pathology. rchap. xiir. acetic. It swells up in water, but is not soluble in it. Mucin reduces cupric sulphate. It is converted into acid- albumin by the mineral acids. Though closely allied to albumin, it differs from it in not being precipitated by bichloride of mercury, tannin, nor by boiling j and in the absence of sulphur from its composition. Its congeners^ gelatine and chondrin, contain a small percentage of sulphur, and are precipitated by alum and mercuric chloride. Mucin may be con- sidered as the chemical product of the retrograde metamorphosis of these bodies, a reversion to the embryonic state. Colloid de§-eiieratioii is closely related to mucoid. It affects chiefly the cells, but the inter- cellular substance is not exempt. Physiologically it is sometimes met with in the thyroid gland, even in very young children. It is conspicuous in many cases of bronchocela In them the change may be confined to individual glandular acini ; but very commonly, by the coalescence of the latter, cysts are formed, which contain a semi- gelatinous colourless or yellow fluid. It gives the characteristic appearance to colloid cancer, which has a special tendency to affect the intestines, omentum, and ovaries. We have also observed this variety of malignant disease in the breast and spermatic cord. It is found in other growths ; e.^., the sarcomata and enchondromata. The essential structure of tumours is not altered by its presence, though it modifies their physical and chemical characters. The colloid material is not precipitated by alcohol ; mucin is. Zeiakerism.— This term has been applied to a peculiar form of degeneration, allied to colloid. Chap. XIII.] Colloid Degeneration. 105 described by Zenker as occurring in tbe voluntary muscles in typhoid fever , notably the adductors of the thigh, the diaphragm, and abdominal recti. It has been observed in other febrile disorders. Cornil and Ranvier met with a similar condition in the muscles around centres of inflammation and new growths. It has also been detected post mortem in muscles that had undergone injury during life. Whether it be a distinct and peculiar form of degeneration, or, as Cohnheim supposes, a modification of post-mortem coagulation of myosin, is not certain. The fibres affected necessarily lose their contrac- tility, and become soft. From want of support the blood capillaries may rupture, the resulting haemorr- hages causing pain and tenderness, and even swelling along the course of the muscles. Microscopy. — The alteration in structure is by no means general in the same muscle. Patches appear here and there in the midst of what looks like healthy tissue. Even individual fibres can be seen lying side by side with others that have entirely escaped, re- minding one of the partial distribution of lardaceous degeneration in the muscle cells of the blood- vessels. The fibres affected are greatly swollen. They look glistening, having lost their natural striation. The sarcolemma is wrinkled irregularly from transverse cleavage of its contents. Regeneration takes place by absorption of the diseased fibres and the development of new ones. Myxcedema. — In this disease the connective tissue, especially of the hands, feet, and face, becomes swollen. Its constituent gelatine and chondrin un- dergo a chemical reversion to the embryonic condition, being converted into mucin. There may or may not be disease of the kidneys. The disease is slowly progressive, and the patients io6 Surgical Pathology. [Chap. xiv. evince a dullness of intellect and gradual diminution of bodily vigour. Tiie etiology is involved in ob- scurity. CHAPTER XIY. PIGMENTATION PIGMENTARY DEGENERATION. The term pigmentation is of wider application tban pigmentary degeneration. It is true there is a tendency to the deposit of pigment in structures that are losing their vitality; but there are many instances that do not fall under this category ; such, e.g., are the melanotic tumours, in which the process of fixation and storage of colouring matter is as much an essential part of the life-history of these growths as the formation and arrangement of the tissue elements that compose them. False pig-mentation. — In the first place, a dis- tinction should be drawn between true and false pig- ments, or rather, between those that are derived from the blood (primarily or secondarily) and those that are introduced from without. Of the latter the most common form is carbon suspended in the air in the form of minute particles. These are carried to the respiratory mucous membrane, to which they adhere. Eventually they becjome fixed in the pulmonary tissue, partly by their mechanical action, and partly by the agency of the protoplasm of the cells, in the same way that granules are appropriated by amoebae from the fluids in which they live. Not only do these particles invade the parenchyma of the lungs, but they find their way into the lymphatics, and are arrested in the bronchial and mediastinal glands. Such accidental pigmentation is Chap. XIV.] Pigmentation, 107 well exemplified in (1) tlie lungs of miners, which are very liable to be ajBfected with a form of fibroid phthisis, the overgrowth of connective tissue being due to the irritating action of the sharp angular pieces of carbon inhaled. (2) Lead workers and others who are the sub- jects of chronic poisoning by the metal, show a hlue line in the gums. Here the lead is probably deposited in combination with the albuminoid constituents of the tissues, although it is supposed by some that it takes the form of sulphide, sulphuretted hydrogen evolved from the decomposition about the teeth com- bining with a soluble salt of the metal carried by the capillaries. (3) Of like nature is the occasional discoloration of the skin from long-continued internal use of silver nitrate. (4) From tattooing and gunpowder explosions. We have a good instance of the former in the intentional pigmentation of the cornea for the purpose of hiding the unseemly appearance of indelible scars (leucomata). True pigmentation consists of the liberation of the colouring matter of the red blood-corpuscles, and its fixation by the tissues in the granular or crystalline form, not as haemoglobin^ but as some derivative, the product of chemical decomposition. The pigment may be derived directly from the blood, or through the medium of some natural secretion as the hile or urine. There are certain tissues of the body of which it is a natural constituent. Such are the skin, choroid coat of the eye, liver, spleen, muscle, and nerve cells. Physiologically, it is temporarily increased in the skin from sunburn and pregnancy; and standing midway, as it were, between physiological and pathological pigmentation is the mottling of the skin in freckles, and the melanosis of congenital moles. io8 Surgical Pathology. [Chap. xiv. In whatever tissues pigment naturally exists, there will it appear in excess in most morbid changes that affect them, even though the immediate seat of the disease become paler than normal ; e.^., the effect of choroiditis is often to leave whitish patches surrounded by dense black irregular zones. Cicatrices of the skin would at first sight appear an exception to this rule, but as a matter of fact they support it, the issue mainly turning upon the point whether the rete be entirely destroyed or no, for the rete is the natural seat of the cutaneous pigment. 8oiu'ces of true pigmeutatioii and stain- ing. 1. The hile. — In jaundice the conjunctiva, skin, and urine show the characteristic colour, and so do coincidental inflammatory exudations, such as pneu- monic sputa. In these cases it is more a staining than real pigmentation, for the bile pigment is in. the liquid state, and is quickly reabsorbed when the cause of the jaundice is removed. In gall stones pigment is always present. It varies much as to colour and amount, and somewhat as to composition. 2. The urine. — The colouring matter of the urine gives the " cayenne pepper " appearance to gravel, and the pink colour to deposits of urate of soda. Urinary calculi, again, have different hues indicative or suggestive of their composition ; e.g., the brown and fawn colour of uric acid ; and the yellow of cystic oxide (changing to green on long exposure). 3. The blood, however, is the chief immediate source. The pigment is either extracted and stored Lip by the activity of living cells without any lesion of blood-vessels, as in melanotic growths, or it is the remains of extravasation or thrombosis. In both cases the haemoglobin as set free from the corpuscles Chap. XIV.] Pigment A tion. 109 is in solution; it afterwards undergoes chemical decomposition, and this furnishes the variation in tint seen; e.g., in an ordinary bruise. It does not remain diffused for long, but assumes the granular or crystalline form. The colour of the granules may be yellow, orange, dark brown, or black, and no doubt the composition varies accordingly. There is no proof that any definite compound, which has been described under the name of melanin^ has any real »|f t*'^!>- J^. T: ^-. # '^m^ ••i«v'-^ B Fig. 6, — A, Melanotic Sarcoma of Muscle ; b, Granular and Crystalline Pigment from a case of old Cerebral Hsemorrliage. existence ; the dense black pigment so termed is one of the last products of a series of chemical changes. It does not necessarily follow, however, that change of colour always implies a change in composition- The greater part of the colouring matter of blood clots is absorbed by the vessels, and the extent of absorption depends upon the freedom of the circula- tion; hence, in the brain (Fig. 6, b), where anastomoses are scanty, we meet with permanent deposits of pigment, and the crystalline variety is more common in this situation than elsewhere. We have seen these crystals in the fluid of hydrocele, in ovarian cysts, and in the debris of liver tissue in acute yellow atrophy. It is noteworthy that granules and crystals are some- times found in vessels that have been blocked by coagula. no Surgical Pathology. [Chap. xiv. Apart from antecedent extravasation or thrombosis, pigmentation occurs {a) as an essential feature of some 1WW growths (Fig. 6, a), especially sarcoma of the choroid and skin. We know that sarcomas are based upon the type of embryonic or developmental tissue, and that nutritive changes occur in them in greater variety than in other new formations, Cancers are much less liable to pigmentation than sarcomas. Encephaloid takes the lead, there 'being comparative immunity in scirrhus and epithelioma. Pigmenta- tion is not confined to malignant growths, for it is far from rare in warty excrescences of the skin. In any case, the presence of pigment marks only a nutritive modification in the elements of a tumour, and has no direct reference to structural pecu- liarity as suggested by the expression melanoma. Melanotic growths, like natural pigment, are more widely distributed in the lower animals than in the human subject. As would be expected, the granules are for the most part contained within the cells of the growth, but some are found, both scattered and aggregated, in the intercellular substance. It is more than likely, however, that many of these collections were originally intracellular, and that they were left in situ after the atrophy and disappearance of the cells that held them. (h) In long-standing passive congestions pigmenta- tion is very constant, whether it has its origin in thrombosis, or capillary extravasation, or the escape of blood-corpuscleswithout recognisable rupture of vessels. We see it around varicosed veins, and in the liver cells. (c) In injiamifnatoTy exudations, and, notably, the lymph effused in syphilitic shin eruptions and syphili- tic iritis. The staining in this disease is out of pro- portion to the extent and duration of the vascular congestion. The difference can be explained by the supposition that the poison of syphilis is peculiarly Chap. XIV. J Pigment A tiox. Ill destructive to the red blood-corpuscles, and this view is supported by the fact that general anaemia is one of the obvious signs of constitutional syphilis. It is v^^orthy of remark that in syphilitic stains the pigment is confined to the rete and the tissue beneath, the superficial horny layer of the epidermis being quite Fig. 7. — Section of Skin at site of an old Syphilide. a. Lowermost layer of rete, deeply pigmented ; h, epidermis devoid of pigment ; c, sebaceous gland; d, groups of pigment granules in thickened corium ; e, hair. free (Fig. 7). Either the pigment must be decom- posed as the cells become cornified, fresh deposit going on meanwhile in the retej or it is taken over by the younger cells that replace the old ones lost by desquamation. These phenomena are not confined to syphilitic stains nor to any inflammatory pigmentation of the skin ; for they are found on a minor scale in the natural growth and decay of the epidermis ; another proof that pathological changes are only distorted forms of physiological nutrition. 112 Surgical Pathology. [Chap. xv. {d) The 'pigmentation of the skin around patches of leucoderma, and the bronzing of the skin and buccal mucous membrane in Addison's disease, are of uncertain origin; possibly they are instances of trophic lesions from perversion of nerve function. CHAPTER XY. CALCAREOUS DEGENERATION. Physiologically calcification occurs in the de- velopment of bone, where it serves the definite pur- pose of giving stability to the osseous framework. But even there it marks the limit of nutritive activity of the matrix, and corresponds to the final stage of formative activity of the bone corpuscles imprisoned within the lacunae. In caries it can be shown that granulation tissue, the anatomical product of rarefying ostitis, is of direct vascular origin, and not the result of proliferation of the bone corpuscles. Functionally, then, ossification must be considered a change to a higher state ; but from a nutritive point of view it is lower than chondrifi cation. It may be primary, as in calcification of the tunica muscularis of the medium-sized arteries ; it may be secondary and localised, as in the formation of calcareous plates in the aorta and the other large arteries afiected with atheroma ; or it may be secondary and widely diffiised, as when several organs are infiltrated with lime salts absorbed from the osseous system. Thus, then, calcification takes place under two widely different conditions : (a) from an inherent or accidental diminution in the nutrition of a tissue. Chap. XV.] Calcareous Degeneration, 113 without there being any evidence of excess of lime- salts in the blood ; (6) or as an act of relief, much in the same way that " chalk-stones " composed of urate of soda are formed about the joints and in the cartilages of the ear in gout, or as "dealkalised fibrin" is deposited from the blood as a depui'ative infiltration in lardaceous disease. In this case it is found in one or more organs. The lime salts pass through the walls of the blood-vessels in a state of solution, and are deposited outside in the interstitial tissue of the parts invaded, in the lung around the lobules_, in the kidney between the tubuli uriniferi. As before said, calcification implies tissue weak- ness. In rickets, it is true, there is excessive growth about the very parts where the cartilage capsules are undergoing calcification, but this in itself is evidence of perverted nutrition, growth, and development. In old age it is rarely absent, and here it la chiefiy met with in the arteries and the cartilages of the ribs and larynx. Anything that tends to diminish the vitality of a tissue predisposes to calcification ; thus we can under- stand why it is so frequently found in inflammatory deposits, and notably in those that are old, and the outcome of constitutional weakness, e.g., in strumous glands, and phthisical nodules in the lungs. Fatty degeneration is often found associated with it ; not that one entails the other, for both alike are the consequence of impaired nutrition. Finality in the series of degenerative changes is reached in calcification, which preserves the tissue elements or their debris from further decomposition. It is a conservative process, but not necessarily by design, since in the arterial system it is a cause of embolism, thrombosis, and gangrene. If calcification sets in whilst the tissues retain their structural in- tegrity, the lime salts are deposited first in the inter- I 114 Surgical Pathology. [Chap. xv. cellular substance, and then in the prot<3plasni of the cells. This is especially the case in new growths, e.g., sarcoma. The cells which are hidden by the opacity of the calcareous granules, can be again brought into view by dissolving out the salts with a dilute mineral acid. Calcification may be partial or complete ; in the former case it gives a roughness,, and adds to the friability of the mass, which feels something like soft mortar; in the latter the part is completely petrified and brittle. Compare the partially calcified remains of a chronic abscess with the dense plates from a large atheromatous artery. The salts are composed for the most part of carbonate and phosphate of lime; but when calcification happens in a tissue that possesses any characteristic chemical compounds, these will be found mingled with the salts of the earthy bases. Thus, in calcareous nodules of the kidney there are urinary constituents. Under the microscope the calcified patches appear black by transmitted light; they are for the most part angular in outline and composed of granules. Some- times crystals can be seen ; this is the more likely when calcification has taken place whilst the afiected part retained a considerable amount of moisture. On the addition of a mineral acid the carbonate of lime is decomposed, and the carbonic acid, set free, escapes in the form of minute bubbles. Calcification in the vascular system. 1. In the heart. — Vegetations on the aortic and mitral valves often become calcified. The rigidity thus acquired renders them more liable to be detached, and the liability is increased if there be a secondary ulcerative endocarditis. They are a fertile source of arterial embolism, and since the cohesion of these detached vegetations is increased by the calcification, large arteries (e.^., the middle cerebral) are not un- commonly blocked. Chap. XV.] Calcareous Degeneration. 115 2. In the arteries. — Here it occurs as a 'primary and secondary change. The former is seen in the medium-sized arteries, such as the tibials and cerebrals. This primary calcification, one of the signs of advanc- ing age, begins in the middle coat. The deposit commences around the nuclei ; it then spreads throughout the cells, which lie at right angles to the axis of the vessels, and as the calcification is unevenly distributed, it takes the form more or less of an irregular succession of rings. Portions of the arteries are sometimes so brittle that they can readily be fractured transversely. The process is not confined to the muscular coat, it spreads to the internal and external. In this way the surfaces become very irregular, and the lumen considerably diminished. The loss of elasticity and the increased friction, together with the diminution in vitality, favour localised or difiused thrombosis, and so become important factors in the production of senile gangrene. Other forms of dege- neration, fatty and fibroid, often accompany calcifi- cation. In the case of the cerebral arteries, if the process be slow, a partial anaemia sets in, and the brain, thereby impoverished, gradually wastes, at the same time becoming firmer. Most instances of so-called senile softening are really the reverse — sclerosis. If the obstruction be great and localised, especially if the heart be fatty, and still more if the blood coagulate within the rigid vessels, portions of the brain are cut off" from all nutritive supply, and con- sequently degenerate and soften. Secondary calcification. — This is found in the aorta and other large arteries. It assumes the shape of irregular plates, and is the final stage of athero- matous disease. It afiects chiefly the inner coat, for in the large vessels the muscular is but little ii6 Surgical Pathology. [Chap, x v. developed. The calcareous plates protect the vessel from further change, and even serve as safeguards against dilatation at their immediate seat. They often split away at their borders from the surrounding non-calcified portion of the vessel, and may even be bodily detached and swept along as emboli by the blood stream. They also act as foreign bodies, and cause the blood to coagulate upon them ; and the thrombi thus formed are very liable to be detached, being unable to withstand the force of the current that rushes by. 3. In the veins. — Calcification occasionally afiects the walls of the veins. It is also seen as phleboliths in their interior. In new growtlis it is by no means rare. It has a predilection for those that arise in connection with bone, and especially sarcoma and enchondroma. The intercellular substance is first infiltrated, and then the cells. In enchondroma it is often mixed with true ossification. In some cases the distinction can only be made out with the microscope ; but, as a rule, calcification is more patchy and irregular, and the absence of vessels gives to the naked-eye appearances a greater opacity. It rarely radiates from the surface of a bone, a common occurrence in ossifying sub- periosteal sarcomas. Other tumours, e.g.., ovarian fibroids and dermoid cysts, sometimes calcify. We have met with calcification in the membranes of the brain in old people, and as the sequel of trau- matic, spinal, and cerebral meningitis. Calcification of the adventitious fibrous capsules of hydatid cysts after the death of the parasite is not rare. We have seen such a shell a third of an inch in thickness. It may even occur between the collapsed cysts contained within the adventitious one. 117 CHAPTER XYI. ALBUMINOID INFILTRATION I SYNONYMS — AMYLOID, LARDACEOUS, WAXY. In some chronic wasting diseases there is found an enlargement of the liver, spleen, kidneys, and lymphatic glands. The causes in the order of frequency run thus : — 1. Protracted suppuration in caries and necrosis, empyema, and chronic phthisis. 2. Tertiary syphilis. 3. Cancer. 4. The cachexia produced by long resi- dence in hot climates and exposure to malarial in- fluence. The above-named organs may be severally or collectively diseased. The same change is sometimes met with in the mucous membrane of the intestine. The general characters are these : increase of size and density of the organ, a peculiar lustrous, waxy appearance on section, and a readiness with which the lardaceous substance takes the staining of certain reagents, such as iodine and methaniline violet. With iodine it turns a deep walnut colour, changing to a blackish violet tint on the addition of sulphuric acid. It was this reaction that led Virchow to term it amyloid, though from chemical analysis it is now known not to belong to the starchy group, but to the nitrogenous, and to be allied to albu- minous bodies. If caustic potash be added to a section stained with iodine, the colour vanishes, and it reappears on the addition of an acid. If a portion be soaked for some time in potash, it no longer gives the reaction ii8 Surgical Pathology. [Chap. xvi. with iodine even when acidulated, for the alkali dissolves out the new material, and to a much greater extent than it does the similar constituents of healthy- tissue. Whether the change be an infiltration or a degeneration, opinions are divided. Dr. Dickinson supports the former view, and adduces in support of it the enormous increase in bulk attained by the liver and spleen, and the early distribution of the disease in the walls of the arterioles. He believes that the material is dealkalised fibrin, which infiltrates the walls of the vessels and exudes from them, and that it is the result of a depurative process whereby the alkalinity of the blood is diminished. In protracted suppuration there is a great loss of potash by the discharge. The albuminoid substance is deficient in potash and phosphoric acid, whereas it contains an excess of sodium chloride and earthy salts. It must not be forgotten that there is an enormous loss of white blood-corpuscles by suppuration, although they are not diminished in number in the blood ; and this may be by no means an unimportant factor. Other observers take excejDtion to these views, both as to the exact nature of the substance and its origin. They say that other bodies, the albumins, ordinary fibrin, etc., will give a similar colour reaction with iodine, and that against its being a form of fibrin (which is a colloidal substance), is the fact that, in inflammation, filrin, as such, does not exude from the vessels. They also argue that the special liability of certain organs to be affected, and that not in a uniform way, is opposed to the theory of mere in- filtration. One fact must not be lost sight of, and that is, the tissues afi'ected play an important part in the process, whether it be an infiltration or de- generation, and the selection may be as much on the part of nutriendum as nutriens. Those who main- tain that it is a degenerative change, refer it to a ciiap. XVI.] Albuminoid Infiltration. 119 want of power to properly nourish certain tissues from a vitiated condition o£ the blood, whether it be due to a waste of alkali and corpuscles, from suppuration, or to the materies morbi of certain diseases, such as syphilis, cancer, and malaria. Anatomy. — The change begins in and about the walls of the arterioles. The muscularis is first affected. The fibres swell and look glistening. In the kidney the walls of the vessels of the Malpighian bodies and the vasa recta of the pyramids are notably diseased. Soon the epithelium becomes involved, and it is said exudative casts of the same substance may be found in the tubes, but these are perhaps cast-off degenerated epithelium. In the liver the intermediate arterial zone fi.rst suffers. In the spleen the Malpighian bodies stand out in bold relief, looking like boiled sago grains, hence the term "sago spleen." In the intestine (particularly the small), the tips of the papillae first present the waxy change. Statistics show that this disease does not appear within three months of the commencement of sup- puration. Fatty degeneration is found associated with the lardaceous change ; in fact, the albuminoid substance may itself undergo that transforma.tion. There is not sufficient evidence to show that it organises, nor that it disappears when far enough advanced to be diagnosed during life. The possibility of its occurrence must always be borne in mind in the treatment of chronic suppuration. Other reasons apart, it would point to amputation in preference to excision of diseased joints. Yessels affected by the change are more permeable to fluids ; he;nce the polyuria from affection of the kidney, and intractable diarrhoea when the villi of I20 Surgical Pathology. [Chap. xvi. the intestine are involved. The enlargement of the liver does not cause jaundice jjer se. When this is present, it depends either upon catarrh of the bile ducts, or pressure of enlarged glands in the transverse fissure (Murchison). Corpora ainylacea. — These are for the most part minute round or oval bodies. They have been termed amyloid on account of the colour reaction they give with iodine, or with iodine and sulphuric acid ; but several authorities believe that they are nitrogenous in composition. The colour test cannot be relied upon as an absolute indication of their nature, for it led to an erroneous interpretation in the case of lardaceous disease, which, however, is widely difierent in its pathology from the bodies in question. Lardaceous disease is the outcome of a general dys- crasia, whilst the corpora amylacea are purely local phenomena, and from the frequency with which they are found apart from other morbid changes (e.g., in the prostate gland) they are of very little clinical import. They are most common in the prostate, and in the central nervous system, but they have been met with in the lungs, in the mucous and serous mem- branes, and many other situations. In the nervous system they are by no means rare as a sequel of chronic degenerative changes. They are met with in the grey and white matter of the brain and cord, in the choroid plexuses of the cerebral ventricles, in the pineal and pituitary glands, and in the optic nerve and retina. They are liable to undergo calcareous infiltration. Structurally they consist of a homogeneous material frequently arranged in concentric laminae. The lamination is probably due to successive depositions from without. With iodine they give a blue, yellow, green, or Chap. XVII.] Trophic Lesions. 121 brown colour. The extent of the three latter tints is dependent on the amount of albuminoid matter present. Iodine stains starchy substances blue, and albuminoid yellow or brown. Sulphuric acid brings out or heightens the effect of iodine. Amyloid bodies have not been converted into glucose, a fact which tells against theh^ being closely affined to starch. CHAPTER XYII. TROPHIC LESIONS. The causes of deviations from normal nutrition must be sought (1) in the life processes of the tissues themselves ; (2) in modifications of nutriti^^e supply, qualitative and quantitative ; and (3) in morbid states of innervation. The tissues, like individuals, have an allotted period of healthy existence, after which they waste and die, apparently independent of vascular change or deprivation of nervous influence ; e.g.^ fatty de- generation of the corneal cells and coats of the blood vessels. ( Yide Atrophy. ) Many lesions owe their origin to abnormal con- ditions of the blood and vessels. Long-standincf venous congestion leads to atrophy, pigmentation, and fibroid induration, acute hypersemia to exudations and haemorrhages. The composition of the blood is also of great moment. On this depend the so-called cachexias of syphilis and pyaemia, and the rapid fatty softenings of protoplasm in the acute specific fevers and septicaemia. But from the very intimate connection betiveen 122 Surgical Pathology. [Chap. xvii. nerve endings and the elements of the tissues, and the evidence of physiological relationship between a healthy state of the nervous system and the proper discharge of functions of organs, it is not surprising that any wide divergence from the normal state of the one should show itself in a corresponding modifi- cation of nutrition and function of the other. Trophic nerves. — Probably there are special trophic fibres. If so, in the case of the spinal nerves they take the same course, and, in fact, are blended with the motor, sensory, and sympathetic bundles. Meissner has shown, that if the innermost fibres of the fifth cranial nerve be divided, inflammation of the eye will result, although sensation remain intact ; whereas if only the outer fibres be cut (sensa- tion being to a great degree lost) no such lesion is observed. In a case of inflammation of the fifth nerve that came under my notice, there was severe trifacial neuralgia, perforating ulcer of the cornea, and rapid wasting of the masseter muscle. The cutaneous system presents numerous in- stances of the effect of perverted function of the nervous system, both as to degree and kind. Thus, temporary or permanent blanching, or loss of hairy has been known to follow mental strain and severe neuralgia. Irregular pigmentation, as in leucoderma, is believed to be of neurotic origin. But the more frequent lesions are those where the disordered nutrition of the epidermis and true skin shows itself in the forms of glossy smoothness, eruptions, and ulcerations. Here it may be remarked that these lesions are more decided when the nerves are irritated, than when completely divided. In the latter case the nutrition is defective, and there is loss of power of with- standing injuries and repairing their consequences ; the process is passive rather than active. Vesicular eruptions are the most common; e.^., Chap. XVII.] Trophic Lesions. 123 heroes zoster.^ from perineuritis of the spinal nerves, and herpes labialis and frontalis in affections of the fifth cranial. The same is true of traumatic irritation. The skin supplied by the affected nerve often becomes glossy, like a polished scar, though at others it is rougher than natural, presenting a desquamating, branny appearance, analogous to the unilateral furring Cb Fig. 8. — Portion of Shot embedded in Posterior Tibial Nerve. a. Nerve fasciculi ; 5, blood-vessel ; c, the foreign body. The inflammatory exudation has organised. In some fasciculi the nerve fibres are fewer than normal. of the tongue, from irritation of the gustatory nerve or its trunk. Injuries of the nerve-centres^ leading to ulceration and sloughing, as seen in the formation of hed-sores, from fracture of the spine. Here the de- struction of tissue is out of proportion to the extent of continued pressure on one part, from inability to shift position. Moreover, in paraplegia the sores form over the sacrum, whereas in hemiplegia there is sloughing of the buttock, on the side opposite the cerebral lesion. Painful irritable ulcers, in the floor of which the terminal fibres of the nerves are probably exposed, 124 Surgical Pathology. [Chap. xvii. are very intractable, and often refuse to heal until those fibres have been destroyed by caustics, or the fasciculi supplying them have been divided (Hilton). Profuse sweating has been observed over the area of nerve disturbance. Although paralysis of the vaso-motor nerves, and in some cases active vaso-motor dilatation, from stimu- lation (Strieker), may play a conspicuous part in the causation of extensive cedema, and alteration of tem- perature, it is probably of secondary importance as compared with affection of the trophic fibres. Such oedema occurs in some cases of injury to the spinal cord, and also in certain diseases, e.g.^ locomotor ataxia. It may be transient or permanent. Perforating ulcer of tlie foot. — Mr. Savory and others have pointed out that this is the conse- quence of nerve lesion, sometimes local, more often central. The interstitial tissue of the nerves is increased, chiefly relatively, for the nerve fibres are fewer and smaller than normal. The smaller fibres, which are probably trophic and sensory, suffer more than the larger ones. There is abundant evidence of disordered nutrition. The skin is cold, frequently congested, and liable to profuse paralytic perspiration. At times, too, it is thickened, especially about the toes ; and the sensi- bility is diminished. The ulcer is often seated at the base of a corn, over the ball of the great toe, or outer part of the foot, i.e., where the greatest pressure is brought to bear. It leads to a deep, but usually narrow, sinus, which may traverse the whole thickness of the foot, or terminate at a diseased bone. It is very intractable, and liable to return after it has healed. It has been found in anaesthetic leprosy, locomotor ataxia, caries of the spine, and in congenital deformities of the feet, which are known to be some- times associated with disordered innervation, from Chap. XVII.] Trophic Lesions. 125 defective development of the spinal centres and nerves. Connective-tissue hypertrophy. — Short of ulceration, the soft tissues of the foot and leg may undergo hypertrophy, giving the part a coarse, clubbed, distorted look. The thickening is due to an overgrowth of an ill-developed connective tissue, similar to that seen in elephantiasis. It is more than probable that many cases looked upon as spontaneous local perversions of nutrition are really the outcome of nerve lesions. Muscular system. — Paralysed muscles waste from want of their proper physiological stimulus; but in addition to this there is a more rapid atrophy, accompanied by a speedy decline in electric contrac- tility where the trophic nerves are involved. Compare the state of the muscles of the face when palsied in an ordinary case of hemiplegia with that observed in injury to the trunk of the seventh nerve, whether directly from fracture of the base of the skull, or from the pressure of inflammatory exudation, from syphilis, or exposure to cold, or caries of the petromastoid bone. Osseous system. — The repair of a fracture is liable to be imperfect, or indefinitely delayed, when the nerve or nerve-centre supplying the part is injured ; thus, if the cord be crushed in the dorsal region, and a femur and humerus broken at the same time, union will occur in the latter, perhaps not in the former. Occasionally bone is deposited in unusual situations. Dr. Buzzard ("Clinical Lectures on Diseases of the Nervous System," p. 225) describes a case of locomotor ataxia, in which "a bony process appeared to occupy the position of the right rectus f emoris muscle ; it stretched obliquely downwards, and somewhat inwards, for a length of about nine inches." The hip joint was affected on the same side. Fracture of the bones sometimes occurs in locomotor ataxy; this is no doubt 126 Surgical Pathology. [chap. xvii. traumatic, but it is rendered more easy by reason of atrophy from disease (the patient being paralysed) and trophic erosion, when this is present. The joints. — The joints are subject to remark- able errors of nutrition from lesions of the nerve- centres, acute or chronic, traumatic or spontaneous. Injury of the cord from fracture of the spine some- times induces rapid inflammatory eflrusion. Charcot's disease. — Ataxic arthropathy. Charcot has described cases of the most extensive disorganisation of the joints in persons affected with sclerosis of the spinal cord, especially of the posterior columns — locomotor ataxy. During life the physical signs simulate those of chronic rheumatic arthritis, for which, in fact, they have been mistaken; but there are many important differences, so that one need never be left in doubt. In locomotor ataxia there is often considerable effusion into the joint ; in rheumatic arthritis little or none. This is one of the factors of dislocation, the other being absorption of the head of the bone, e.g.^ the femur. In locomotor ataxia the onset is more sudden and the course more irregular, and the process may subside partially or entirely, whereas in rheu- matic arthritis the disease is slowly and surely pro- gressive. In locomotor ataxia the formation of osteophytes is quite the exception ; in rheumatic arthritis it is constant. The joints are affected in the following order of frequency in locomotor ataxia : — knee, shoulder, hip. Monarticular rheumatism is most commonly met with in the hip. The absorption of the cartilages may be complete ; even the head and neck of a long bone (e.^., the femur) may disappear (Fig. 9). Other parts of the Chap. XVII.] Trophic Lesions. 127 bone may also be eroded, e.g.^ the iliac expansion of the hip. The disease affects one or more joints. In a case described by M. Fere several were involved. A patient between fifty and sixty years of age came under the care of the writer, complaining of '•' lameness from rheumatics of the great toe." On Fig. 9. — Osseous and Articular Lesions, from a case of Locomotor Ataxy. A, Left iliac bone : erosion of acetabulum and neighbouring part ; b, left femur, showing complete absorption of head (Fere). examination, the metatarso-phalangeal articulation of the right great toe was found to be the seat of con- siderable effusion, which had slowly developed during a period, of several months ; the skin over the joint was deeply congested ; there was absence of patellar reflex; the " Argyll -Robertson pupil" was well marked ; there had been lightening pains on and ofi* for seven years ; no other joint was affected ; there was no history of gout, either personal or family. Oenito-iirmary system. — Attacks of profuse 128 Surgical Pathology. [Chap, xviii. hsematuria, synchronous with lightening pains, have been observed by my colleague, Mr. Page, in a case of locomotor ataxia ; the urine was quite normal in the intervals {^Brit. Med. Journal, vol, i., p. 772, 1883). The writer has seen painless swelling of the testicles along with transient attacks of cystitis. Perhaps these phenomena were chiefly due to in- creased blood-capillary pressure from active vaso- motor dilation referred to by Strieker. There can be little doubt but that trophic and vaso-motor paralyses, from crushing of the spinal cord, cause a perversion of nutrition of the urinary tract, and play an important part in the causation of cystitis and surgical kidney. The eye. — In addition to what has been said of acute inflammatory destruction of the eye-ball in aflfections of the fifth nerve, there may be added that double descending optic neuritis is frequently seen in coarse lesions of the brain and spinal cord ; e.g., meningitis (simple, tubercular, and syphilitic), intra- cranial tumours, and cerebral and spinal scleroses. Then there is grey atrophy of the disc in locomotor ataxia, etc. CHAPTEH XVIII. SYPHILIS. Syphilis is a specific, contagious, non-infectious disorder, characterised by a period of incubation varying from one to seven weeks, by the deve- lopment of an indurated sore at the seat of inocula- tion in the "acquired " disease, and by an efiiorescence or rash, and usually by other inflammatory lesions. It is so strongly protective against subsequent attacks that the immunity conferred lasts for the whole, or Chap. XVIII.] Syphilis. 129 the greater j)art, of a lifetime, It can be comiDuni- cated from parent to offspring by indirect contagion. The local sores have been described in chapter iii., but there remain for discussion the rival theories of:— The unity aud duality of sypMlitic cliaii- cres. — Some syphilographers maintain that there is but one sore, though this may manifest itself in a non-infective or purely local form, or, on the other hand, give rise to constitutional symptoms. According to this view, soft and hard chancres, so-called, are relatively pathological accidents ; and the difference in the results is explained by the supposed absence or presence of the germs of syphilis. But, arguing from the analogy offered by other specific diseases, these germs must be considered as the essential elements concerned in the reproduction of the poison, and consequently in the propagation of the disease. On etiological grounds, no greater mark of distinc- tion between an ulcer caused by simple chemical irrita- tion and one produced by a specifi.c virus can be well conceived. To meet this objection, the supporters of the " unity " theory suppose, that either the germs of syphilis are destroyed by the local ulcerative process, or that they do not find in the system a fitting soil for their development. The former hypothesis is untenable ; for the poison is absorbed by the lympha- tics long before any destructive action can be set up at the seat of inoculation, as shown by the fruitless attempts to prevent infection by early excision of the sore. From the nature of things, it is next to impossible to prove the latter, since no one would think of inoculating a number of persons to see if any were proof against infection. The tenacity of life possessed by the germs is probably too great for them to succumb to the action of chemical products of decomposition in the sore ; for constitutional J 130 Surgical Pathology. [Chap. xviii. syphilis may certainly be conveyed by tlie secretions of most actively pliagedsenic chancres. Mr. Savory considers that the evidence afforded by gonorrhoea, which is in most cases only a local affection, but which, in a few, leads to general dis- turbance, upholds the unity theory. But the specific nature of gonorrhoeal pus is denied by some of the greatest authorities (Ricord, Lane) ; so the grounds for analogical inference are untrustworthy. Attention has also been drawn to the fact that scarlatina does not always give rise to the usual con- stitutional symptoms. But this by no means shows that the poison is one whit the less specific, for an individual infected from such a modified source may develop all the characteristic features of the disease. It is not the absence of constitutional symptoms, but the degree of manifestation. Again, it is said that there are many intermediate forms between soft and hard chancres. No doubt there are ; but the simulation of one morbid process by another does not prove an essential relationship between them; e.g.., syphilitic acne and acute lichen imitate the papular state of small-pox ; but each is distinct from the others. There is also a likeness between the symptoms of vaccinia, variola, and varicella ; still these diseases are none the less specific. Those who believe in the dualism of syphilitic sores explain the apparent transitional forms by the effects of local irritation, or by some peculiarity of the tissues in different individuals. By sharf) or continued irritation a hard chancre may be made to suppurate, and a soft one to indurate, to a certain extent. The subsequent induration of a previously soft suppurating chancre may also be due to double inoculation at the same time, each virus producing its own results in its own appointed time. Although there are pathological grounds for this Chap. XVIII.] SVPHILIS. I3I conflict of opinions, the practical rule is never to let a patient suSering from a venereal sore pass from notice until sufficient time has elapsed for the appear- ance of constitutional symptoms, whether this seems likely to be the case or not. J. Hunter maintained that gonorrhoea and syphilis were due to the same poison, from the fact that he could induce syphilitic infection by inoculation with the pus of acute " specific " urethritis ; but he did not take into account the existence of urethral chancres and the infectivity of the blood and secretions of the subjects of constitutional syphilis. Secondary and tertiary sypMlis. — Syphilis differs from other exanthematous fevers by the long tiaie through which the poison remains active. The group of secondary symptoms, including the eruption, mucous tubercles, ulceration of the mouth and throat, loss of hair, indurations of the lymphatic glands, iritis, and rheumatic affections of the muscles and joints, usually pass away within the first twelve or eighteen months. Then there is a period of quiescence which may occupy months or years, or extend through the patient's lifetime. In the latter case, the disease may be considered as eradicated ; in the former, the poison has lain dormant, or incapable of manifesting itself by obvious signs. After this interval it again acquires activity, and then we arrive at what is called the tertiary stage. In favour of the view of the continued potency of the virus is the uncertainty as to when the power of transmission from parent to offspring ceases, and the fact that a woman may bear an apparently healthy child between the births of two syphilitic ones, all by the same father. But many pathologists regard tertiary syphilis as the sequel, and not the direct result, of by-gone infection. They consider that the vitality of the tissues was lowered during the secondary period, and that, as in scrofula. 132 Surgical Pathology. [Chap, xviii. these tissues then readily pass into a state of chronic inflammation. The non-transmissibility of the dis- ease in the advanced tertiary stage seems to lend weight to this supposition ; but against it are those cases in which the secondary symptoms pass without a break into the tertiary. Moreover, some ^ of the tertiary lesions are anatomically characteristic of syphilis (notably, gummy tumour), whereas the " sequelse " of other specific disorders {e.g., scarlet fever) are far from being so ; and, even in them, there is no absolute proof that the so-called " after results " are not, as far as causation is concerned, the direct outcome of specific irritation. The dogmatic assertions, "syphilis once, syphilis ever," and " syphilis is a flesh and blood disease," imply not only a belief that the tertiary symptoms are specific, like the secondary, but that the patient is never freed from the original taint. The latter is opposed to the experience of many surgeons. The type of the inflammatory processes changes considerably, for whilst the lesions of secondary syphilis tend to spontaneous cure, those of the tertiary period are much more permanent, and show a greater liability to relapses. Secondary syphilis, as regards tissue selection, expends the greater part of its virulence upon the cutaneous and mucous structures. Tertiary syphilis affects these parts as well, but it is also very prone to attack the viscera and the osseous and nervous systems. Another argument advanced in support of the view that secondary syphilis is chiefly a blood disease, and tertiary an induced morbid state of the tissues, is the symmetrical disposition of the local manifestations in the former, and the irregular distribution in the latter. But whilst this holds good in the majority of cases, there are too many exceptions to warrant its general a>pplication. Chap. XVIII.] Syphilis. 133 The characteristic lesions of tertiary syphilis (gum- mata) are by some classed among the tumours, or new growths, but for no good reason. They are simply masses of inflammatory exudation, and differ from many tumours in that they cannot be enucleated, and from the malignant ones further that they do not generalise ; moreover, they follow the course of inflam- matory exudations in general in their tendency to arrive at some typical end — -absorption, disintegration, caseation, etc. They are chiefly found in the skin and subcutaneous tissue ; in the mucous and submucous tissues, particularly in the mouth and pharynx ; in the internal organs, e.g.^ the liver, kidney, and brain; and lastly in bone. They vary in size from that of a hempseed to a large wahiut. They may be looked upon as aggregates of microscopical foci of inflammation, which, at first vascular throughout, subsequently, from de- generative and indurative changes, show three fairly distinct zones : an in- ternal, composed of fatty and granular debris de- void of vessels ; a middle one, where the cells are round and oval and under- going atrophy; and an external, highly vascular and exudative. No hard and fast line is to be drawn between these zones ; they shade into one another, since they represent overlapping stages of growth and decay. The cells are imbedded in a ground substance of lymph, sometimes fibrillated, giving a spun-glass appearance, but more often so thickly set with cells as to be scarcely visible (Fig. 10). ^^' 17 Fig, 10. — Syphilitic gimima of the Liver. a. Centres of nodes in which the cells have became granular ; 6, periphery of the nodfs: c, vessel (x 100). {After Cornil and Ranvier.) 134 Surgical Pathology. [Chap. xviii. An old gumma appears to tlie naked eye as a greyish yellow mass, surrounded by a zone of fibrous tissue. It is quite firm, and has less tendency than tubercle or infarctions to soften in the centre. In the internal organs it rarely breaks down, but the pro- ducts of its degenerations, and those of the tissue destroyed by its invasion, are slowly absorbed, deep puckered cicatrices marking the spot where it had existed. In the superficial structures, where it is more exposed to irritation, it very often ulcerates, causing widespread serpiginous sores, the discharge from which is at first glairy from mucoid or colloid degeneration of the lymph and cells. This may begin by superficial ulceration and gradual disintegration, or the whole mass may slough out. The caseation is dependent firstly upon an inherent low vitality of the exudation (aplastic), and secondly upon capillary thrombosis, the consequence of in- flammation of the walls of the vessels. Amongst the amorphous debris may be seen stellate crystals of stearic acid, and plates of cholesterine. Giant cells are occasionally present at the periphery, but they are not so common as in tubercle. Syptiilitic eruptions. — Unless rupiabe regarded as essentially of syphilitic origin, all the forms of cutaneous eruptions in syphilis are modifications of non-specific varieties. There are certain peculiarities, however, that, taken in the aggregate, give to syphilitic eruptions a well-defined character. They are ; 1. Polymorijhism. — The same patient may exhibit at once what is known as a mixed syphilide, i.e., an association of different types of cutaneous rash; e.g., papular, scaly, tubercular, etc. This is often seen in the secondary or exanthematous stage. It is also met with in the tertiary period. But it should be understood that this polymorphism depends rather upon the degree of local inflammation, than upon any Chap. XVIII.] Syphilis.. 135 well-marked variation in the morbid process. Thus papular passes insensibly into tubercular syphilide, the latter indicatino- a more extensive exudation, and therefore a greater obstruction to the capillary cir- culation, and liability to ulceration and interstitial destruction of tissue. Again, syphilitic psoriasis par- takes very much of the nature of an inflammatory desquamation, as well as of epithelial hyperplasia. 2. Selection of site. — Though no part of the skin is exempt from the efflorescence or secondary roseola, the trunk, and fronts of the axillse and elbows, are favourite situations for this form of eruption. Tubercular syphilide has a proclivity for the face, and especially the forehead — '' the mark of the beast," as it has been aptly termed. Squamous syphilide in the shape of palmar and plantar psoriasis is well known. The special liability of certain parts of the skin to the action of the virus is observed in other speciflc fevers. 3. Pigmentation is more marked in syphilitic than in simple eruptions. For the pathology of this staining, see chapter xiv. 4. Aberration from type. — Whereas simple psoriasis has a decided tendency to aflfect the back of the limbs, notably at the knees and elbows, the syphilitic form is more often observed on the flexor aspect. 5. Absence of itching is the rule, but there are many exceptions. It does not depend upon the state of tension of the nerves, for there is no certain relationship between the amount of exudation and the degree of hypersesthesia of the skin. Either the chemical products of the inflammatory changes are but slightly irritating, or the poison of syphilis has a sedative efiect upon the tissue elements of the nerves. iSecondary and tertiary eruptions. — The exanthem of syphilis, which is rarely or never absent, though frequently so slight as to pass unnoticed by 136 Surgical Pathology. [Chap. xviii. the patient, is a jjapular roseola or lichen. The spots vary from the size of a pin's head to the size of a split pea. The exudation is effused into the papillary layer of the skin. The rash generally makes its appearance from the fifth to the eighth week after inoculation. It is not all thrown out at once, but in an irregular series ; whilst some spots are fading away others are formed. At this time the joatient is somewhat feverish, the thermometer recording a rise of from one to two degrees. As before said, the natural efilorescence is often modified by other varieties of syphilide, of which the squamous is the most common, whilst the vesicular is comparatively rare. The more severe the cutaneous lesion, the more likely is it to assume the squamous and tubercular form. Though no hard and fast line can be drawn between the secondary and tertiary manifestations, it may be said that the former are less prone to suppurate and leave indelible cicatrices in the skin. In persons of pyogenic tendency, par- ticularly those of strumous diathesis, destructive ulceration may commence quite early. Syphilitic p§oria,§is. — Squamous syphilide. Small discrete patches are very frequently inter- spersed with lichenous papules in the primary eruption. The scales are less numerous and silvery than in the simple eruption. In some cases they form a fine circlet at the periphery of the spots, and are thinly scattered on the surface. In others the epithelial cells, imbedded in fibrinous exudation, form quasi- scabs, which split here and there, giving a fissured appearance. Syphilitic lepra is an inveterate kind of psoriasis. It occurs in patients who are broken down in health, and manifest the earthy cachexia ; hence it is an indication of profound constitutional disturbance. It assumes a circular or sinuous outline, so common in Chap. XVIII.] Syphilis. 137 syphilitic affections of the skin. The surface is more or less thickly coated with exudative and desquamative products ; but as the latter predominate it presents a coarse scaly aspect. Plantar and palmar psoriasis is generally of syphilitic origin. As the exudation spreads beneath the thick epidermis it raises it, and causes it to split into flakes. The heel cuticle, being very dense, resists this for some time, so that it is frequently undermined for a considerable distance, and when stripped off it leaves a moist raw surface. Cutaneous eruption of the sole is at once suggestive of syphilis and scabies, the same as ulceration between the toes. The syphilitic nature of palmar psoriasis is often confirmed by the existence of squamous patches, or superficial ulcers on the tongue. It is a late secondary or tertiary symptom. Tubercular syphilide. — The specific term has no reference to the microscopical anatomy of the lesion, as in tuberculosis. It relates only to the naked- eye appearance of the eruption. The " tubercles" are firm hard nodules raised above the surface of the skin. When they form about sebaceous glands the disease is known as syphilitic acne. They have a tendency to ulcerate ; but whether this is developed or not, the tissue elements are often destroyed, so that when the inflammation subsides and the exudation and softeninof products are absorbed, pale depressed cicatrices are left. This is all the more likely when the eruption occurs in the tertiary stage, for then there is less probability of its speedy disappearance. Histologically the tubercles consist of inflammatory neoplasia, without any very definite disposition of the constituents. They may be considered as gummata in miniature. Bullous and vesicular sypliilides. — Bullous eruptions occur both in acquired and congenital syphilis. In acquired, as rupia ; in congenital, as pempJiic/us. 138 Surgical Pathology. [Chap. xviii. Rujna is characterised by heapecl-up incrustations on the surfaces of patches which are usually occupied by bullae in the first instance. The bulla bursts or dries up, and the exudation and ej)idermis form a scab, which increases in depth by addition to its base. Meanwhile the area of inflammation widens, and consequently the scabs are somewhat conical, and as there is more or less lamination they resemble oyster- shells. Pempliigus. — Children are sometimes born with a bullous eruption upon them ; but most frequently it appears after birth. In the latter event it breaks out within the fi.rst few days, or, what is more usual, it shows itself about the time of the other manifestations of cutaneous syphilis ; viz., from the fifth to the eighth week. It shows that the tissues and blood are profoundly imbued with the poison, and betokens a fatal issue, very few cases recovering. "Vesicular syphilide occasionally constitutes a part of the general exanthem. When it occurs late in the disease it may correspond with the distribution of certain nerves, and then it is probably the result of syphilitic peri- neuritis. Visceral sypMlis. — Yery little is known of the visceral changes in the secondary stage of acquired syphilis. In the tertiary period they are among the best understood lesions. For the most part they are met with as chronic inflammatory thickenings, and lardaceous degeneration. The latter is more likely to develop when there has been long-continued suppura- tion, but it is not confined to these cases. The general cachexia is sufficient to account for its occurrence. The abdominal organs are the chief seat of the morbid process, especially the liver, kidneys, and spleen. As regards the essentially inflammatory exudations (e.^., in the liver) they are met with in four forms : (1) gummy tumours, (2) difiuse interstitial hyperplasia, Chap. xviiL] Syphilis. 139 (3) capsular indurations, (4) fibrous bands or seams, that divide the parenchyma into irregular nodular masses which simulate cancerous projections ; but the latter are generally somewhat umbilicated in the centre, whereas syphilitic elevations are wanting in this feature. Syphilis is one cause of fibroid phthisis. Intracramal syphilis includes (1) gummata, which are generally found in the cortical portions of the brain ; (2) chronic thickening of the meninges (pachymeningitis); (3) disease of the arteries {q.r}.\ which may lead to aneurism ; or to thrombosis, and consequent cerebral softening. The symptoms to be looked for are severe continued headache, some localised paralysis or spasm, and double optic neuritis. Syphilitic paralyses {e.g., of the cerebral nerves) are for the most part irregular and total. luti'aspiiial sypMlis. — Here also we find inflammatory induration, and occasionally gummata. Locomotor ataxy and lateral sclerosis are believed in many cases to owe their origin to syphilis. The peculiarity of these afiections consists in their being to a great extent confined to certain columnar systems of the cord, in this way contrasting strongly with the generally irregular distribution of tertiary syphilitic lesions. The localisation seems to point to these so-called " scleroses " being dependent on degeneration of the nerve -fibres and fibroid substitution, rather than on ordinary infiammatory exudation. This view is further strengthened by the extremely chronic nature of the morbid process. Syphilis of tlie larynx. — In the secondary stage we meet with an erythematous condition as in the fauces, mucous tubercles, and sometimes follicular ulcers. The inflammation subsides, or it passes into a more obstinate and destructive form, such as arises in the course of other tertiary manifestations. Tertiary ulceration of the larynx usually begins at the 140 Surgical Pathology. [Chap. xviii. base of the epiglottis. It is accomj)anied by a good deal of swelling in the mucous and submucous tissues. The vocal cords and epiglottis may be entirely eaten away. The perichondrium suffers as well, it may be to such an extent that the cartilao^es necrose. SypMlitic eye a^ffectioiiji. — Of these, the one of most frequent occurrence is iritis, a rather late secondary lesion. Although the disease is centred in the iris it involves other structures, e.g., the choroid, and sometimes the retina. The effused lymph, which is in considerable quantity, is more lumpy, and darker in colour than in simple iritis. Permanent adhesions to the lens capsule (posterior synechia) are liable to form, and by maintaining a constant state of tension predispose to recurrent attacks of inflammation. The natural hue and lustre are lost. The colour is a compound of the normal tint and that of the exuded reddish yellow lymph ; so that in a patient with dark eyes it becomes a rusty brown ; and in one with blue it assumes a dirty greenish appearance. Choroiditis syphilitica is characterised by dis- seminated whitish patches, surrounded by a zone of accumulated pigment. The pallor of these spots is due to absorption of the epithelial and stromal pigment, and to the vascular exudation. The re-deposit of the colouring matter follows the general law that guides inflammatory processes in highly pigmented tissues, e.g., the skin. It is not limited to syphilis, though in it it is unusually well marked. The subse- quent changes consist of atrophy of the choroidal cells and vessels. The retina is more or less affected at the same time as the choroid, to which it becomes adherent. Retinitis syphilitica presents itself as a diffuse exudation, which extends from the margin of the optic disc in an irregular manner along the course of retinal vessels. The outline of the cloudy whiteness Chap. XVIII.] Syphilis. 141 is indistinct. Tliis disposition contrasts strongly with the brilliant, highly refractive patches of albuminuric retinitis. Capillary haemorrhages are not infrequent. The lymph is partly absorbed, and partly organised with imperfectly filtrated tissue. Meanwhile, the proper elements of the retina waste ; and the vessels get smaller and smaller, until only a few attenuated streaks can be seen traversing the optic disc, on their way to the fundus. When the atrophy has reached this degree the disc is small and pale. Scattered patches of choroiditis, as above described, may be seen in different parts of the f and us. Double-descending opHc neuritis is one of the symptoms of intracranial lesions, which are frequently of syphilitic origin. Congenital sypliilis. — The embryo may be syphilised from the first, through one or both parents suffering from the disease at the time of impregnation. Or the mother may become infected during pregnancy. In either ease abortions are very common, but they are of greater frequency in the former. The placenta is often found to be extensively diseased, especially the foetal portion. The chorionic villi are imbedded in inflammatory exudations, which take the form of pale gummatous consolidations. This, together with the action of the virus upon the developing tissues, causes the death of the foetus and consequent abortion, which is most common about the third month of pregnancy. Should the foetus survive until it attains viability, it may then be born alive or perish in utero. In the latter case it generally shows unmistakable evidence of the disease. The skin is discoloured* The epidermis may be raised in blebs, or be under- going desquamation subsequent to bursting of the bullae of what was probably intra-uterine pemphi- gus. This must be distinguished from post-mortem 142 Surgical Pathology. [Chap. xviii. maceration. When the child is born alive, it may die immediately after birth, or within the first few days of life. As a rule, however, nothing unusual is noticed until it is from three to eight weeks old. It is noteworthy that the secondary symptoms of con- genital syphilis generally appear at about the same period after birth as those of the acquired disease after inoculation. Cutaneous eruptions. — These for the most part tend to be moist. They usually consist of deep- red or copper-coloured blotches upon the palms and soles, and about the anus and genital organs. Scaly and tubercular syphilides are not so well-marked as in the acquired affection. At the same time, the rash is liable to be polymorphous. Pemphigus has been referred to. Mucous tubercles {loide Ulcers) are very com- mon. They are chiefly found near the verge of the anus, in the flexures of the groins, on the bucco- pharyngeal mucous membrane, and in the larynx. Affections of tlie mouth and nose. — The mouth is subject to diffuse erythematous inflammation of the mucous membrane. It is also the seat of mucous tubercles and superficial fissured ulcers, which extend from the angles to the skin of the cheek. As these heal, they leave radiating pale cicatrices which may persist throughout life. The faulty de- velopment of the permanent teeth is the result of specific stomatitis. The mucous membrane of the nose is thickened, and gives off a muco-purulent discharge. The perios- teum and bones also suffer, hence imperfect growth and flattening of the bridge. ( Vide Diseases of bone. ) Affections of tlie eye. — (1) Acute iritis is more frequent than is supposed. It is often not observed because not looked for. It is generally symmetrical, and occurs about the same time as the Chap. XVIII. 1 Syphilis. T43 other early secondary symptoms, rarely beyond the sixth month. Since the anterior chamber is very shallow in infants, adhesions are liable to form between the lens capsule and the posterior surface of the cornea. There may be lasting evidence of this in the shape of a fine filament connecting the two structures, or of a central opacity on the front of the lens capsule (pyramidal cataract) ; but this is more common as a sequel of ophthalmia neonatorum than of congenital syphilitic ii'itis. (2) Interstitial keratitis {keratitis 'punctata^ is a tertiary phenomenon. Most common about the age of puberty, it attacks both eyes, though there may be an interval of several months. Lymph is deposited between the corneal laminse instead of upon the surface. It is first seen as hazy spots in the substance of the cornea. As these enlarge, a more diffused or nebulous appearance is presented. Loops of capil- lary blood-vessels form in the exudation in connection with the conjunctival and sclerotic circulation. As the inflammation subsides, the cornea* clears up, first at the periphery, then more or less throughout ; but, as a rule, there is a certain amount of haziness left, and, in severe cases, very considerable opacity. Whilst the lymph is being absorbed or organised, the vessels shrink and finally disappear. (3) Kerato-iritis is an inflammation of the cornea and iris. It is likewise a tertiary symptom, making its appearance from about the fifth to the eighth year. (4) Choroiditis and retinitis are said to affect one or both eyes with about equal degrees of frequency. The pathology is the same as in acquired syphilis. Affections of the ear.— Mucous tubercles are occasionally seen in the external auditory meatus, but they do not lead to any after results. Congenital syphilis is the most common cause of permanent 144 Surgical Pathology. [Chap. xviii. double deafness in children. This is du3 to chronic inflammation of the mucous membrane of the middle ear, and thickening of the membrana tympani. The tympanum is blocked with granulation tissue, which contracts and overcups the drum. Moreover, the ossicles become anchylosed, or even absorbed. Otitis media may be accompanied by catarrh of the external meatus. This form of ear disease is liable to supervene on the subsidence of a kerato- iritis, but it also occurs alone. Osseous lesions. ( Vide Diseases of bone). Visceral lesiosas consist of cono;estive and fibroid enlargement of the liver, spleen^ etc., and gummata. Swelling of the spleen is very common. It may be temjDorary or permanent. The capsular investments of the liver and spleen are sometimes much thickened. It is said that perihepatitis from congenital syphilis is one cause of infantile jaundice and ascites. " Abscesses " have been described in the lung and thymus gland. I have seen a gumma in the livsr of a child twelve months old at the time of death. In the brain one meets with chronic inflam- mation of the cerebral arteries, meningitis, and hydro- cephalus from " irritative dropsy " of the ventricles. Oeneral considerations. — The secondary and tertiary symptoms of congenital syphilis are more frequently associated than in the acquired disease. Thus g-ummata may be met with at a very early age. Still, as a rule, there is a well-marked interval between the time of disappearance of the rash, mucous tuber- cles, snuffles, etc., and the outbreak of graver lesions, such as phaged^enic ulcers, caries, and necrosis of bones. Considering that congenital syphilis exerts its morbid action on young and growing tissues, it is not to be wondered that 75 per cent, of the recorded cases of death from syphilis should happen in children Chap. X1X.J Rickets. 145 under one year of age. How profoundly the whole system is steeped in the virus is shown by the rapid wasting of the body, and the earthy, cachectic look of the skin. CHAPTER XIX. RICKETS. Ricketis is a constitutional disease. Its chief manifestation is a lesion of bone tissue, occurring at a time of great developmental activity. It is looked upon by some as a symptom of scrofula, but it differs from it by the usual absence of other signs of that disease, such as suppuration and caseation, and by the whole osseous system being affected. In some of its features it resembles congenital syphilis.^ e.g., the fibroid induration of parenchymatous tissues, such as the liver, and the enlargement of the epiphyses of bones. In fact, inherited syphilis is considered a cause of rickets. The balance of opinion, however, is in favour of the two diseases being distinct. Natiu'al ossification. — To rightly understand the morbid changes occurring in bones in rickets, we may briefly state what takes place in normal ossifica- tion at the epiphysis of a long boue. In a vertical section there may be seen : (1) A layer of hyaline cartilage ; (2) a cartilaginous matrix impregnated with lime salts forming trabecular spaces, or alveoli which contain embryonic medulla and blood-vessels. This layer constitutes the ossiform tissue of Broca ; (3) true bone. The cartilage cells lodged in primary capsules enlarge and divide, and become surrounded by secondary capsules. A further segmentation occurs, K 146 Surgical Pathology. [Chap. xix. and the secondary capsules undergo solution ; broods of embryonic cells are thus formed, which quickly join adjacent groups by absorption of the matrix. The embryonic tissue becomes vascular by blood- vessels shooting in from the canals in the true bone, which latter increases by the filling in of the alveoli. These changes succeed one another so rapidly that the intermediate ossiform layer only attains a thickness of about \\ mm. The growing part is softer than cartilage, and hence gives way in " fracture through the epiphysis." JYSodilied ossifieatioii in rickets. — Let us now look at a similar section of a rickety bone. The layer between the cartilage and the bone is many times thicker than normal. The tissue of which it is composed has been termed spongeoid by Guerin, on account of its porosity and consistence. Unlike the healthy ossiform layer, it is irregular in outline, sending processes into the bone continuous with it. It is highly vascular, and sometimes contains islets of hyaline cartilage, partly explaining the isolated cal- cified patches seen along the line of the epiphyses. This spongeoid tissue at the surface joins with the subperiosteal osteoid tissue of Yirchow, which is converted into a soft, thick, vascular substance, that at a later stage becomes firmer and more adherent to the underlying bone. The central marrow loses a good deal of its fat. Microscopy. — The primary cartilage capsules are unusually large, and the secondary capsules are very numerous and compressed ; in fact, there is evidence of greatly increased activity in the initial process of ossification, whilst the later stages are not only delayed, but are for the time abortive. Instead of the secondary capsules becoming dis- solved, they are invaded by the calcifying process of the matrix, and thus the cells they contain are cut ofi" Chap. XIX.] Rickets. 147 from further active change. They become angular, are larger than bone corpuscles, and have no anastomatic canaliculi (Fig. H)- No lamination is seen in the trabeculse of the spongeoid tissue. The vascular channels of the old bone are continued into the cartilage, where they enlarge by absorption of the calcified tissue, and there, Fig. 11. — Zone of Proliferating Cartilage in Eachitis. a. Cells pressed together and stained brown-violet with an aqueous solution of iodine, which stain is due to the glycogenic matter they contain ; &, secondary capsule ; section made in the fresh state and examined in water (Cornil and Ranvier). by joining together, form a system of intersecting canals filled with vascular embryonic marroAv. In normal ossification the alveoli become occupied by fully developed bone ; but in rickets there is defective calcification, which occurs where it is not wanted, and fails where it is. The corpuscles become angular, and the intercellular substance finely fibrillated. A similar condensation and fibrillation are noticed in the medulla of the cancellous bone, in the Haversian canals of the compact bone, and in the subperiosteal formation. 148 Surgical Pathology. [Chap. xix. The spaces everywhere containing this medulla enlai-ge by absorption of their walls, and thus, whilst the constructive process falls short, the destructive is actively at work, and so the whole bone is rendered soft, and is readily bent by pressure. In the osteoid tissue beneath the periosteum trabeculse form, and both in these and the osteoid basis the cells become stellate and anastomatic. Immediately surrounding the old bone in the more advanced stages are laminae of true bone, separated by a delicate connective tissue. This appearance is due to the increase and subsequent fibrillation of the medulla between the laminae, which have been attenuated by absorption (Comil and Ranvier). When the morbid changes in the bones cease, ossification proceeds at a rapid rate, and at the epi- physis is completed before the usual time, accounting for the undue shortness of the limbs, since it is chiefly by the growth at the epiphysial cartilages that the bones increase in length. Fracture. — The callus thrown out in fractures of rickety bones consists of osteoid tissue, and does not pass through the intermediate stage of cartilage. It is large, and ossifies readily. Deformities. — Even after all morbid action has ceased and ossification is completed, there is evidence more or less of the arrest of growth of the bones, which, coupled with the secondary deformities from pressure, make up the sum total of a rickety skeleton. It is true, as time goes on a re-moulding of the bones takes place, so that curvatures partially or entirely disapjDear. Where they remain in the long bones, a buttress of compact bone is formed in the concavity of the curve, acting as a support, and so diminishing the liability to fracture. It is not uncommon for a long bone (e.^., the tibia, which is curved on account of its elongation from diffuse or general ostitis) to be Fig. 12.— Tibia affected with Eickets. a, Butti'ess of compact hone support- ing tbe arch formed liy thehenfling of the shaft, h. Small osteophytes (One-third natural size.) 13. — Tibia affected with Ostitis Deformans. The sclerosed bone is thiclcer on the convex than on the concave side of the curve. The epiphyses ai-e hut little altered. The curve was single— antero-posterior. (One-third natural size.) 150 Surgical Pathology. [Chap. xix. mistaken for a rickety bone. A rickety tibia bends from inability to sustain the weight of the body, and the fibula follows its curve ; whereas, in addition to this cause, an elongated tibia becomes curved from the constant tension acting from the points of fixation at the ends of the fibula, the latter bone being healthy ; and this is not so much the result of actual bending, as re-absorption of bone in the concavity, and deposit along the convexity of the curve ; for, contrary to rickets, on vertical section we notice the compact tissue is much thicker in front than behind. There are other points of difference which may be noticed here : the curve is single ; in rickets it is in two planes. The surface of the bone is rough ; in rickets smooth. The epiphyses are not so wide, perhaps, as the shaft ; in rickets they are much larger. The circumference of the shaft is more rounded ; in rickets flattened. The bone is longer than it should be ; in rickets shorter. (Comp. Figs. 12 and 13.) Fracture simulated.- — Sometimes, in rickets, when the curvature is very marked in the leg, the shaft of the fibula is ossified to the tibia, simulating an old badly-set fracture of both bones. In the latter, however, the curve is less general and uniform, and the other signs of a rickety bone are absent. Although in rickets the whole skeleton is affected by the disease, the secondary deformities are more marked in some bones than in others, according to where the greater strain habitually falls ; and this, it is clear, will depend upon a variety of circumstances. If the child lie much upon the back, the occipital bone is flattened, and there is a corresponding promi- nence of the forehead ; for the bones of the cranium are easily displaced, since the delay in ossification protracts the time of closing of the fontanelles and the fixation of the sutures. Moreover, chronic Chap. XIX.] Rickets. 151 hydrocephalus is by no means infrequently present, and this aggravates the cranial deformity. The pres- sure from without and within acting upon softened yielding bone, we see why there is absorption here and there of the parietal and occipital bones (craniotahes). In the spine there is usually antero-posterior and lateral curvature, with their resultant twisting. There will be a forward cervical curve and one large posterior dorso-lumbar if the child have been unable to walk, the body having been arched forwards from want of power of support ; or the natural curves may be simply exaggerated. In some the lateral curve is in excess of the antero-posterior ; occasion- ally it is so marked that one vertebra may eventually be half an inch deeper on one side than the other. A rickety spine with dorsal curvature can be told from the kyphosis of past caries by its more uniform curve, by the less complete (if any) consolidation of the vertebrae, and the smooth surface of their bodies. It is obvious that this alteration in the shape of the spine must entail a displacement of the ribs and sternum, and so the general conformation of the chest. The sternum is thrown forward and keeled, and the adjacent part of the rib cartilages prominent, the more so as there is some lateral depression arising from the sinking in of the cartilages nearer the ribs. There is considerable thickening of the ribs at their junction with the cartilages, giving rise to the " beading," and these nodes lying in a curve on either side constitute the festooned " rickety rose-garland." The down-slanting of the ribs during life must thrust down the liver (frequently enlarged), and so encroach on the abdominal cavity. The pelvis is diminished at its inlet, having assumed a trefoil shape ; the weight of the body dis- places forwards the promontory of the sacrum and lumbar vertebrae, and the counter-pressure through 152 Surgical Pathology. [Chap. xix. the acetabula drives in those parts, A more irregu- lar deformity, or lateral twisting, depends upon an inequality of these forces. The femora show an exaggeration of the forward and outward curves ; the forward, in particular, if the child have been carried much with the thighs across the arms of a nurse ; the tibiae are curved forwards, and either inwards or out- wards ; the fibulse follow the tibise. In the upper extremity, we have in the same way to bear in mind the natural curves and the usual and unusual causes and direction of pressure. The joints are frequently distorted, especially the knees, in the form of bandy-leg or knock-knee. This is the result of the weak state of the ligaments, and perhaps also the alteration in the shape of the bones. The milli teetli are cut late, owing to arrested growth, the dental enamel being very deficient. When cut, they crack, and decay earlier than natural. Visceral cliaiig-es. — The spleen, liver, and lym- phatic glands may be found indurated, the two former, at the same time, being sometimes notably enlarged. The change is dependent upon a general increase in the interstitial tissue. The enlargement has been thought to be due to lardaceous change ; but it seems not to be identical, for fibrous tissue rarely, if ever, develops from the albuminoid substance found in the same organs in cases of protracted suppuration, cancer, syphilis, etc. ; and, further, the new material in rickets is deficient in earthy salts ; in lardaceous disease it is rich in them. '53 CHAPTER XX. TUBERCLE AND SCROFULA. So many different views have been held as to the structure and nature of tubercle that it is impossible to give a satisfactory definition. When first employed, it signified no more than that in certain diseased structures solid bodies could be seen ^vith tolerably well-marked naked-eye appearances. No allusion was made to microscopical characters ; in fact, the term was used in a loose generic sense, with a prefix to indicate its specific origin ; hence the ex- pressions "scrofulous tubercle," "cancerous tubercle," and the like. But later on it received a more restricted appli- cation, and came to be synonymous with the phrase " anatomical product of scrofulous inflammation ; " and to this day the same is understood in the de- scription of many surgical diseases, e.g.^ " tubercular testis," "tubercle of bone," etc. Tiiljercle. — The lungs of phthisical patients were, by the older pathologists, found post mortem to contain nodules varying in size, colour, and con- sistence. These they grouped under two heads : (a) minute, hard, semi-translucent bodies^ from the size of a millet to a hemp-seed {grey miliary granula- tions) ; (b) yellow caseous masses, the component elements of which had undergone fatty metamor- phosis (yellow tubercle). Yirchow proposed that the term " tubercle " should be limited to the grey miliary granulations, wherever found, whether in the form of a wide-spread out- break, or confined to the lungs as a part of the 154 Surgical Pathology, [Chap. xx. lesions of chronic phthisis ; whilst Bastian and others hold that it would be better either to abolish the term altogether, or reserve it only for the cases of acute general tuberculosis. Histology. — ISTor has a study of the histology of grey granulations led to any generally accepted definition. Thus, at one time pathologists were con- tent with describing tubercle as composed of a reti- form tissue like that of a lympliatic gland ; and the more so, as the grey granulations were mostly found where lymphoid tissue naturally exists, e.g.,, beneath the serous membranes and in the parenchyma of many organs, notably the lungs. Cornil and Kanvier assert that the fibrillar character of the meshwork enclosing the small embryonic cells is not natural, but is formed by the action of re-agents used for harden- ing sections, e.g.., alcohol. The next step was the discovery of multinucleated and multipolar giant cells, the outrunners from which freely unite with one another and with the delicate fibres of the lymphoid tissue in which they are imbedded. These giant cells cannot, however, be held by themselves to be charac- teristic, since they are not always present ; and they have been found in other tissues, e.g.., myeloid sar- coma, syphilitic gummata, and the granulations of simple ulcers. There can be no doubt but that the minute struc- ture of tubercle is subject to variation. Thus it may be reticular, or not ; it may contain giant cells, or net. A good deal depends upon the stage of growth and the extent of degeneration. The general arrangement is this : — The giant cells, which may be -o^o^h of an inch in diameter and con- tain as many as thirty or forty nuclei, occupy the centre of the tubercles. Their processes unite into a fine net-work of themselves, and this is continuous with that of the adenoid tissue. The adenoid tissue Chap. XX.] Tubercle and Scrofula. 155 varies in amount, constituting the greater part of the tubercle, or forming only a narrow zone around the giant cells. The alveoli or spaces between the fibres are filled with small lymph cells (Fig, 14). The whole is extravascular, or if vessels exist at all they become obliterated very early. The centre soon becomes caseous (a constant feature), and this depends (1) upon the ansemia of the Fig. 14. — Grey Granulation of the Liver, from a case of Acute Miliary Tuberculosis. In the centre of the tnhercle is a multinucleated and multipolar giant cell Its offshoots join the stroma of the retiforui adenoid tissue (6) ; a, liver cells. invaded tissue caused by the pressure of the over- crowding cells, and (2) upon an inherent low vitality. Orig:iii of the lymplioid or adenoid tissues. — Whether it be an irritative overgrowth of pre- existing adenoid tissue, as seems probable, from the tendency for tubercle to a^Dpear at the seats of natural distribution of the former ; or a mere inflammatory exudation which organises on the adenoid type, is not certain, and is of little moment. 156 Surgical Pathology. [Chap. xx. Origin of the giant celts. — According to Klein, they start from the epithelial cells of the alveoli in the case of the Inng, either by fusion of the protoplasm of contiguous cells, or by the continuous growth and arrested segmentation of individual cells. Another source is said to be the epithelioid lining of the lymphatics and even of the blood-vessels. It may be remarked that caseation, formerly con- sidered as characteristic of tubercle, is not confined to that morbid product, but occurs wherever the vitality of a tissue is slowly impaired, especially in scrofulous inflammations, and notably in the case of bone, testicle, lymphatic glands, and in the lungs of patients the subjects of catarrhal pneumonia. Again, it is well marked in syphilitic gummata, and in quickly growing tumours such as sarcoma and cancer, where the pro- duction of cells outstrips the development of blood- vessels. In all these instances the elements undergo fatty atrophy from slow starvation. Oemeral patliology of tutoercle. — 1. Infec- tive origin. — Without doubt tubercle arises from infection ; that is to say, it is the product of irritation of the tissues. The irritant consists for the most part of the debris from some caseous focus, as a scrofulous gland or carious bone. But the results of artificial inoculation of the lower animals show that whilst this material is more potent than any other (Sanderson), it is not essential. Thus in guinea-pigs tubercle can be induced by inserting a simjjle seton into the sub- cutaneous cellular tissue. The products of the local inflammation are carried by the lymphatics and blood- vessels, and set up secondary changes in various parts of the body. It is a significant fact that in most, if not all, the instances of tuberculosis in the human subject, a collection of caseous matter can be found. It may be situated in the immediate neighbourhood of the Chap. XX.] Tubercle and Scrofula. 157 tubercular deposit, as when a caseous pneumonia is the starting point of pulmonary tubercle ; or the source of infection may be more remote. I have known tuber- cular meningitis arise from strumous inflammation of the OS calcis. At the present time attention is being directed to the investigation of tubercle infection, and especially as to its dependence upon a microscopical organism (bacillus). Before this point can be satisfactorily settled, it must be shown that the bacillus is invariably present, and that it is the cause and not the consequence or coin- cidence of tubercular inflammation. If these alleged facts be established, they will go far to dispel the theory of '• caseous infection," for it seems improbable that a living: ora:anism should be dormant for months or years, and then, without any recognisable cause, start into active life. 2. Disposition of the tissues affected. — It must be allowed that there is something more than a mere local irritation. There is a tendency in the tissues themselves to undergo a special modification of nutri- tion (dyscrasia), just as in the specific fevers the poison of each " selects " one or more parts for its local manifestation; in typhoid it is the mucous mem- brane of the alimentary canal; in diphtheria, the throat. But there is this difference, that whereas tubercle usually arises spontaneously or is autogenetic, the specific fevers always depend upon infection from without. 3. Tubercle compared with pycemia. — In some respects tubercle resembles pysemia, especially in its mode of production, and more particularly in that form where it is artificially induced by exciting local in- flammation. But the contrasts are many and important. Thus, in tubercle there is (a) the absence of embolic infarction and abscess ; (&) the greater chronicity of 158 Surgical Pathology. [Chap. xx. its course ; (c) comparatively little tendency to rapid softening of the disseminated products ; {d) the un- doubted fact of hereditary taint; or, in other words, the transmitted tendency to scrofulous inflammation. Scrofula. — A patient is said to be scrofulous when he is subject to chronic inflammations of a low type, inflammations that arise without an adequate local cause, and show a tendency to persist and progress. The evidence of a low vital condition of the tissues is strengthened by the changes that occur in the inflammatory exudation. This is prone to undergo a slow fatty degeneration and caseation rather than organisation. The older pathologists termed the lymph in such cases " aplastic," in contradistinction to that efi'used under a more healthy state of the constitution. That there is a " scrofulous diathesis " in the sense of a specific materies morbi in the blood is improbable. All we can say with certainty is that there is a weakness of the tissues, an instability that renders them unable to resist the ordinary causes of inflammation and to rally for repair. ISTo doubt in many cases it is hereditary, but not in the sense of a specific transmission of disease as in syphilis, but as a repetition of a morbid condition of tissue, just as in any other simple disorder of nutrition. Besides, the child may be born strong, and of healthy parents, and yet afterwards become strumous through exposure to bad hygienic conditions. From the above statements it follows that we should meet with every degree of scrofula, from slight affection of one tissue to the serious implication of many ; and hence there is no reason for discarding the term simply because the local signs of the disorder are not more pronounced. There are some cases of disease of bones and joints which no surgeon would hesitate to speak of as scrofulous, and yet several authors argue that the Chap. XX.] Tubercle and Scrofula. 159 milder types of these affections are not of this nature ; a false conclusion, wo think, for between the most destructive form of caries and the mildest case of non-traumatic rarefying ostitis there is every grade of severity. And, again, the less severe the lesion, the less likely it is to show itself in several parts of the body. The difficulties in the way of clearly defining scrofula and tubercle and their mutual relationships have led some pathologists to evade the question by denying the scrofulous nature of hip-joint disease and allied disorders. The old idea that " tubercle is the anatomical product of scrofulous inflammation," in spite of all drawbacks, still remains the simplest and most com- prehensive explanation of the disease. According to this, the term " tubercle " includes every phase of the inflammatory exudation, whether this be in the form of diffuse gelatinous tissue, or grey miliary granulations, or either of these converted into yellow caseous matter by fatty degeneration ; take, e.^., the testis or bone. On anatomical grounds it would be better to describe miliary tuberculosis apart from diffuse chronic inflammation, but for the fact that they are often associated, and not merely by accident, for they depend, directly or indirectly, upon the same constitutional condition ; e.g.^ a child had strumous inflammation of the os calcis, and in the diseased bone neither giant cells nor retiform adenoid tissue could be found ; but it died from an acute outbreak of miliary tuberculosis in the lungs, pleurae, and pia mater. It is certain that grey granula- tions are met with in the bones and testes, but in by far the greater number of cases described as tubercular disease of these tissues, there is nothing more than the products of simple inflammatory exudation. We are inclined to use the word scrofula in a gen- eric sense descriptive of the constitutional condition, i6o Surgical Fathology. [Cnap. xx. and to speak of its products under two lieads : (I) the primary essential inflammatory exudation which may exist alone, or be followed by (2) secondary infective miliary tubercle. In some individuals there is a strong tendency to the development of the latter, whilst in others the tissues are destroyed by scrofulous inflammation extending over months or years without giving rise to a single grey granulation. Scrofulous inflammations are peculiarly liable to end in suppuration and caseation, either singly or more often in combination. Tissues affected. — The parts most prone to be aflected are, the skin, mucous membranes, bones, joints, testes, lymphatic glands, and the lungs. In the skin we meet with (1) simple catarrh, or eczema ; (2) limited superficial ulceration ; (3) wide- spread ulceration. In some cases there is extensive undermining from destruction of the subcutaneous cellular tissue. The skin becomes purple and con- gested in parts from obliteration of the lumen of the vessels that feed it. This form is exceedingly ob- stinate, and leaves thin broad cicatrices. Catarrhal inflammation and ulceration of the mucous membrane of the nose is very common. It causes snuffling and offensive discharge (ozoena). It is most marked at the back of the nasal fossae. Some- times it extends to the soft palate, which may be fenestrated by ulceration. Children are very liable to catarrhal ophthalmia, and also to pustular conjunctivitis and phlyctenular corneitis. These aflfections are apt to recur again and again. Scrofulous inflammation of the hones may only go so far as to cause a rarefying ostitis without suppura- tion (caries fungosa), but more often pus is freely formed. The bone is destroyed by the carious pro- cess, and it may be by necrosis as well. The cancellous Chap. XX.] Tubercle and Scrofula. i6i tissue is the favourite situation; e.g., the vertebrae, ends of the long bones, carpus and tarsus. Strumous disease of the joints commences either in the synovial membrane or in the bone. In '■^strumous or tubercular orchitis" the epididymis is first afiected ; both organs usually suffer sooner or Fig. 15.— Chronic Interstitial Epididymitis (Scrofulous Testicle). a, Intertubular tissue thickened and infiltrated with leucocytes; the vessels, c, ai'tiflcially injected; 6, epithelium lining tubules; cJ, epithelium m process of disintegration. later. The inflammation begins between the tubules (Fig. 15). Caseation and suppuration are common. The cord is thickened. The vesiculse seminales may be enlarged. Of the lymphatic glands, the submaxillary, cervical, mesenteric, and bronchial take the lead. The disease is rarely limited to one gland. It may lead to fibrous induration, but more likely to caseation and abscess. In the event of suppuration, the sores are slow to heal, and leave indelible scars in the skin. In the neck i62 Surgical Pathology. [Chap. xxi. they cause great deformity. Scrofulous inflammation of the mesenteric glands is kno^^ii as "tabes mesen- terica. " In the lungs the greater part of chronic phthisis is a scrofulous catarrhal pneumonia. Period of life. — Scrofula is most common in childhood and youth, but no age is exempt. Those who have had scrofulous glands, or bones, or joints in their earlier years, often die of phthisis at a later period. Sir J. Paget has described a senile scrofula of the bones, joints, and other parts, in which the patho- logical changes closely correspond to strumous disease of young subjects. It may be that such patients had an undeveloped tendency to scrofulous inflammation in childhood, but that it only showed itself in old age, when senile decay was added to the original weakness of the tissues. CHAPTER XXL LUPUS. Lupus is probably a disease jf:>er se. The family and ])ersonal history show it to be more often associated with scrofula than any other morbid state. Some authors describe it as one of the symptoms of scrofula ; but as it is frequently the only visible lesion, and as most scrofulous subjects are free from it, we are justified in assuming that it is modified rather than caused by scrofula. It manifests itself in a peculiar form of chronic inflammation of the skin and mucous membrane. It is sometimes hereditary. It has a special proclivity for the first two decades of life. Its course and duration are alike indefinite. The face is its favourite seat, but it is by no means confined to Chap. XXI.] Lupus. i6 «) that part. It also attacks the mucous membrane of the mouth, nose, and eyelids, and usually by spreading from the skin. Several forms are described, but these ai'e modifications of a common type, and not distinct varieties. If the hypersemia be in marked contrast to the degree of destruction of tissue it is called lupus erythematosus ; if the disease go on to ulceration it is known as lupus exedens ; if it stop short of this, lupus non exedens ; if the ulceration be rapid and extensive, the word vorax is affixed, and so on. It begins as a, small red inflammatory nodule or thickening in the skin. This may disappear, and others form, or it may continue to enlarge. There are usually several outlying tubercles, and as these increase in size they join one another and the central growth.. The exudation is firm, and to the unaided eye looks like " apple-jelly," an appearance which is due to mucoid transformation of the inflammatory products. Some suppose that capillary thrombosis precedes the other changes, but it is difficult to say how far it is the cause or consequence of the inflammation. Tlie microscope reveals a decided overgrowth of epithelium, both on the surface and in the glandular involutions ; and an infiltration with leucocytes and homogeneous gelatinous material. The exudation on the surface dries up and forms an adherent scab, or it escapes as a purulent discharge ; in the latter case the skin is as a rule ulcerated. As the inflammation subsides in the older parts, there is a tendency to cicatrise, to a greater extent than in rodent ulcer, but less than in tertiary syphilis. But whilst the central part is healing, the peri- pheral may continue to spread, and in this way very extensive thin cicatrices may be formed. Whether there be ulceration or not, there is always loss of tissue, and, as a consequence, a certain amount of pitting or depression of the surface. t64 Surgical Pathology. [Chap. xxii. Ulcerative lupus, lupus exedens. — The tendency of lupous ulceration is to spread widely, rather than deeply; but there are exceptions to the rule. The enlarged papillae are exposed, and then destroyed, and with them the glandular structures. In the more severe forms there is considerable secre- tion of pus, and molecular debris of the neoplasia. In these cases the edges are sharply defined, and the skin around is deeply congested, and the pain is often severe. Cicatrisation goes on slowly, for the inflam- matory new formation has little power of organising. That there is something peculiar in the nature of the morbid products is shown by the comparative readiness with which simple irritative exudation, caused by the means taken to destroy the lupus tissue, forms healthy granulations. The ulcers are mostly circular or sinuous in outline. There may be one or more. The cheek, the nose, and the eyelids are the parts most affected. The treatment consists essentially in the removal of the diseased tissue by caustic, or better still by scraping or scarification. After the wound has completely healed fresh tubercles are very likely to spring up in the neighbourhood of the scar, and then the whole pro- cess is repeated, unless checked by surgical interference. When it attacks the face the ulceration is usually confined to the skin, subcutaneous tissue, and cartilages of the nose; but the bones may be extensively affected. CHAPTER XXII. TETANUS. Tetanus is characterised by tonic contractions of the muscles, commencing about the face and neck and spreading to the trunk and extremities. Chap. XXII.] Tetanus. 165 Etiology and general pathology. — In the majority of cases tetanus arises in connection with wounds, especially those of the limbs. The liability to the disease is in no way dependent on the severity of the injury ; in fact, it is remarkable that in many instances the most acute onset and progress follow the slightest scratch. In hot climates it is often idio- pathic. Some consider that traumatic tetanus is due to irritation of the nerves implicated in the wound, and that the muscular spasms result from reflex irritation. In support of this view is the statement that an attack has now and then been cut short by division, or stretching of the nerves supposed to be at fault ; but some cases recover without treatment, whilst the greater number die, whatever is done for them. I once stretched the median and radial nerves in a patient whose thumb and fore-finger had been crushed by an engine-wheel ; but witliout the slightest benefit. The evidence in favour of its being a blood disease seems very strong. (1) It is greatly dependent on climatic influences, and is sometimes epidemic, though there is no proof that it is contagious. (2) The resemblance to strychnia poisoning, and still more to hydrophobia, is well marked, (3) The spasms commence in muscles having no anatomical connection with the injured nerves. (4) Some cases arise spontaneously. It is true the nerves have been found more or less locally congested and inflamed, but this must happen in all cases of wounds. I failed to find anything unusual in the median nerve in the case hereafter stated. Condition of tlie spinal cord. — Clifford AUbutt and others have described certain oro:anic changes, which in the main consisted of structureless exudation, and hyperplasia of the neuroglia. Cornil and Kanvier failed to detect anything abnormal. Of i66 Surgical Pathology. [Chap. XXII. four cases examined by myself, two were to all appearance quite healthy ; the third was simply con- gested; this might have been from asphyxial death; the Eig. 16. — Transverse Section of Spinal Cord (cervical region), from a case of very acute Tetaniis. A portion of one of the anterior cornua of the grey matter, with the surrounding antero-lateral column, is seen. a, Pia mater; J, anterior white column traversed by hundles of fibres going to form anterior root of spinal nerve ; c, grey matter ; d, blood-vessels ; e, patches of exudation and softening, x 85. fourth is represented by Fig. 16. The entire spinal cord, medulla oblongata, pons, and cerebellum (the cerebrum was not examined), were thickly strewn with patches easily visible to the naked eye. They were most numerous in the cervical part of the cord. They were readily stained with logwood and carmine. Under the microscope they appeared as roundish homogeneous masses, distributed equally in the grey and white constituents of the centres. The nerve- Chap. XXIII.] Tetanus. 167 fibres were in some places pushed aside by the exuda- tion, in which, at the margin of the foci, delicate fringes of softening tissue were seen to be imbedded (Fig. 16a). There was moderate congestion. The perivascular lymphatic sheaths were in some places dis- tended with a clear substance. There was singularly ^^#!f<^^>,<^:'(0^ I'^^^^^y Fig. 16a.— Portion of Fig. 16, x 260. a, MeduUated flhres in cross section ; 6, focus of softening : the nerve fl^bres and neuroglia completely absorbed in the centre ; c, exudation into perivascular lymphatic sheatli ; d, anterior cornual fibres. little cell-migration. The motor ganglion cells were healthy. The patient, a negro boy, cat. 11, under the care of Mr. Boon, of St. Kitts, had a gun-shot fracture of the left humerus, and laceration of the median nerve. Tetanus appeared on the seventh day, and death oc- curred on the tenth. The spasms were chiefly confined to the right side of the body. Sections of the median nerve an inch above the seat of injury showed nothing abnormal. CHAPTER XXITL UNION OF WOUNDS. Modes of union.— 1. By first intention or plas- tic adhesion. 2. By open granulation. ( Vide Healing 1 68 Surgical Pathology. [Chap, xxiii. nicer.) 3. By the union of opposed granulating surfaces. 4. By scabbing. There is no such thing as immediate union, for however perfectly the edges of a wound are brought , together, it is impossible for the open ends of the divided vessels to meet so accurately as then and there to re-establish the lumen. Besides this, the irritation caused by the injury sets up thrombosis in the mouths of the vessels, and the coagula must be absorbed before healing is complete. 1. Healiog- t>y Urst iiitention. — Take, e.g., a simple incised wound in the skin and subcutaneous tissue. The edges of the wound gape on account of the elasticity of the skin. Bleeding takes place from the divided vessels until arrested by the formation of clots. It usually stops of itself, for exposure leads to spontaneous coagulation of the blood, and the vessels shrink from contraction of their muscular elements, and retract somewhat within their sheaths or bed of areolar tissue. On wiping the clot away from the wound, its small w^orm-like processes occupying the ends of the vessels are often drawn out, whereupon the bleeding recommences. It is immediately arrested, however, if the sides of the wound be brought together. There is now a thin layer of blood between the cut surfaces, and thrombi fill the vessels for a short distance around. Very soon a faint blush is observed at the margin of the wound, fading away into the healthy tissue. The visible redness, which is due to paralysis of the vessels consequent on the injury, is an indication of a like condition in the deeper parts. Hxuclatioii stage. — Leucocytes infiltrate the tissues and collect in the space between the divided surfaces, first occupying and then replacing the clot, which liquefies, and undergoes absorption. By this time there is slight tumefaction of the part, and the line of incision is covered with a film of fibrin Chap. XXIII.] Union OF Wounds. 169 entangling blood corpuscles. In the meanwhile, the connective tissue becomes swollen, and its fibres less defined. As the inflammation subsides, the vessels regain their former calibre ; numbers of leucocytes break up from fatty degeneration, and the debris is taken up by the capillaries, whilst others remain to take part in the process of cicati'isation. As yet, the blood-vessels and lymphatics are blocked on each side of the column of leucocytes lying between the side walls of the incision. The blood clot has disappeared, and the wound to all external appearance has healed, for at the end of two or three days there is well- marked cohesion between its edges. The firmness of the part is due to the condensation of plastic lymph (fibrin), that glues the inflammatory cells together. Tasciilarisation of tlie neoplasia. — Loops and buds are given oflT from the vessels surrounding the wound, mainly in a direction at right angles to the latter. These approach from opposite sides, and, meeting midway, join by absorption of their contiguous walls. It is also possible that there is a free vascular new formation in the exudation, especially when there is a considerable tract of cells. In the meanwhile, the inflammatory corpuscles elongate. The wound is now united by vascularised lymph or granulation tissue, the capillaries of which are larger and more numerous than in the surrounding structures. Cicatrisatioii. — The fusiform granulation cells remain as connective tissue corpuscles. The inter- cellular substance fibrillates and contracts, and con- tracting obliterates many of the vessels ; nor does this cease until the scar is firmer and whiter than the normal tissue. Numbers of cells also disappear through atrophy from chronic starvation. If the adaptation of the edges of the wound have been accurate, and union unimpeded, the scar may entirely vanish in time. lyo Surgical Pathology. [Chap. xxiii. Failure of imion is brought about by any cir- cumstance that adds to the necessary amount of trau- matic inflammation. 1. Poisoning of the wound, as in post-mortem cuts. 2. Mechanical obstacles to close apposition of the edges ; {a) presence of foreign bodies or large blood-clots ; (6) tension on the supports from muscular contraction, etc. 3. Bruising of the edges at the time the injury was inflicted, or subsequent irritation. Mealiiag: toy graiiMlatioii. — There is no essential factor in this mode of healing that was not found in union by the first intention. The difierence is one of degree and disposition rather than of kind. Taking the case of an incised wound, where the edges are allowed to gape, the following signs are observed. Firstly, there is bleeding, which continues until the blood coagulates in the open vessels up to the next collateral branches. Then follow inflammatory hypersemia and exudation. The transuded fluid is so rich in fibrin that it gelatinises on the surface, giving it a glazed appearance. But about the second day the exudation is too copious to be retained within the interstices of the tissues and on the surface of the wound ; it therefore flows away as a pink serous fluid, the colour of which is due to suspended red blood-corpuscles and dissolved hsemogiobin. In a short time the discharge alters to a dirty yellowish- gray, in consequence of a greater proportion of pus cells, and the granular or flocculent debris of tissue elements that have died from the embarrassment of the circulation in the superficial layer. It passes insensibly into a genuine suppuration; but before the latter is quite established, the wound has under- gone a decided alteration ; small bright red elevated spots have made their appearance. These are inflam- matory granulations, or groups of cells heaped up Chap. XXIII.] Union of Wounds. 171 around festooned vascular loops given off by the under- lying vessels (Fig. 17). Suppose this pus-secreting layer to be folded up by bringing the opposite edges and surfaces together, and the same arrangement is obtained as in healing by the first intention. The granulations continue to grow until at length they reach the level of the surrounding surface, or Fig. 17. — Diagram of Granulation of a Wound. The laj'er of pus cells is represented as having heen acted on hy acetic acid, to distmsTLiish the pus cells in the figure more accurately from the grauulatlon cells (.Billroth). pass beyond it. As the inflammation subsides the secretion of pus diminishes, and organisation of the granulation tissue takes place. Henceforth the case is one of a healing ulcer {q.v.). The pus is derived from two sources : direct exudation from the vessels, and liquefaction of the uppermost stratum of the granulations. The drying up of the secretion is not simply the result of removal of the cause of irritation. 172 ' Surgical Pathology. [Chap. xxiii. There is an inlierent tendency to a typical end by organisation of the neoplasia, the same as obtains in normal development from embryonic tissue. In lacerated wounds portions of tissue are killed outright, for the vessels are twisted and bruised, besides being ruptured. Before union can take place, the dead parts must be thrown off; this is effected partly by the vital absorbent action of the granulation cells, partly by molecular disintegi'ation of the sloughs (post-mortem decomposition). Lacerated wounds inflame more than incised ones, for the injury to the tissues is greater, and the irritation is increased by the chemical products of the breaking up of necrosed shreds ; hence suppuration is more profuse and prolonged, and wider tracts are left to cicatrise. Although the cicatrisation is a conserva- tive process, it may entail serious consequences from displacement of certain parts by traction. Ectropion, or eversion of the eyelid, is an instance of this. Besides the extent of the injury, the nature of the tissue wounded has much to do with the rate of healing ; as, for instance, in tendon, where the vessels are few, the anastomoses scanty, and the density of structure prevents a ready opening up of collateral channels. In the last respect it resembles bone. Union of opposed granulating surfaces. — This is much rarer than healing by the first intention or by open granulation. A sinus or blind fistula has only one opening on the surface. Its walls may be formed of healthy granulations, and yet union may be indefinitely delayed from the tension of pent-up dis- charge, progressive disease at the botton of the sinus, or the friction of the opposed surfaces; the last keeping up irritation and preventing the granulations from lying in contact in a state of rest. Instances of this ai'e met with in sinuses beneath the scalp and pectoral muscles, and in the groin. Fixation of the muscles Chap. XXIII.] Union OF Wounds. 173 and external pressure are often sufficient to cause them to close. Tlie discliarge from the granulations having been greatly diminished, the opposed surfaces are no longer kept apart. What little fluid lies between them is taken up by the vessels. Fibrinous exudation glues the granulations together, and henceforth the mode of union is that of healing by the first intention, except at the orifice, which is reduced to a small surface ulcer that cicatrises in the usual way. Healiog: by scabbing*. — The epidermis is grazed off, and the tips of the papillae are bruised and slightly lacerated. There is very little bleeding. The coagulum which forms on the surface is increased by subsequent fibrinous exudation. As the inflammation subsides the scab dries up and breaks away at the margin; but before it is detached a new layer of epithelium covers the exposed papillae. The wound is well before there is time for development of new vessels in the scanty effusion. We have yet to explain the mode of healing in wounds of certain tissues — tendon, muscle, nerve, cartilage, and bone. TTouuds of tendons. — The simplest case is subcutaneous division of a tendon, say that of the heel. The muscular end is drawn away so that a gap is formed; this is immediately filled up by sinking in of the skin and effusion of blood. The clot is quickly absorbed, and its place taken by plastic lymph, which exudes from the vessels of the tendon-sheath and adjacent areolar tissue. The tendon itself, on account of its density and defective vascular supply, takes but a minor share in the earlier repara- tive changes. The lymph, which is thickly set with leucocytes, not only joins the tendon end to end, but overlaps the edges, giving rise to a fusiform swelling. Vascular loops from the vessels of the surrounding 174 Surgical Pathology. [Chap. xxiii. tissue lie athwart the axis of the tendon, and, passing inwards, join with those of the opposite side, and, later on, with similar loops from the cut surfaces of tendon. In some respects this is a repetition of the growth of provisional and definitive callus in bone fractures. The vascular cementing medium organises to connective tissue, and this undergoes cicatricial con- traction. The scar-like tissue reverts pretty closely to the normal histological type, parallel bundles of fibres with interfascicular connective-tissue corpuscles. Lacerated wounds are slow to heal, for they always cause death of a considerable portion of tissue, and it takes some time to throw off the softened shreds on account of the small supply of vessels in tendon. The superficial ulceration left after the deeper part is healed is troublesome, for the skin is bound down at the margin, and the contraction of the muscle keeps up irritation ; hence the need of mechanical appliances to restrain movement. TVounds and injuries of muscle.— Voluntary muscle is highly vascular, and its anastomoses are free and extensive. When incised, muscle retracts more than any other tissue ; the gap between the divided ends is quite large. Bleeding, thrombosis to arrest it, and subse- quent absorption of the clot, occur as in wounds of connective tissue. Granulation tissue is plentifully produced. The cells are mostly derived from the blood-vessels, but it seems probable that the nuclei of the muscular fibres are aroused by the local irritation to renewed formative activity. On division or rupture of the muscular fibres the contractile substance coils up somewhat within the sarcolemma, so that the ends become more or less club- shaped. The ends of the fibres degenerate and split up longitudinally, and the nuclei to the same extent Chap. XXIII.] Union of Wounds. 175 become granular from fatty metamorphosis. The degenerated products are absorbed, and the muscular Fig. 18. — Ends of Divided Muscular Fibres, from the Biceps Muscle of a Eabbit, eight days after the inj ury, a, 6, c, Old muscular fibres ; a, the contractile substance rolled up and balled together ; the same way in the bundle above d ; into the pointed cornet- shaped sarcolemma tube, c, there extends a series of young muscular nuclei, between which there is very delicate transversely-striated substance ; e, young free muscle cells ; /, two young ribbon-like muscular filaments ; g, the same, of various sizes, isolated, x 450 (From Billroth ; after O. Weber.) fibres are seen to be lying in a bed of proliferating granulation tissue. In the lower animals fusiform cells derived from the old muscle nuclei (Weber and Gussenbauer) and wandering corpuscles (Maslowsky) have been found to enlarge and become transversely striated, so that to 176 SURGICA L Fa THOLOGY. Chap. XXI 1 1 . some extent the union is by muscular fibre. Observa- tions are wanting to show if this occurs in the human subject. Connective tissue cicatrisation is certainly the rule, but from what we know of the repair of injured nerves there seems no reason why muscular fibres should not be regenerated. If the divided ends of a muscle be approxi- mated, a narrow seam of fibrous tissue is left. If there be much loss of substance, or the ends be allowed to separate, union is effected by a tendinous band, and the muscle remains more or less digastric. Wounds and injuries of nerves. — There are two remarkable facts connected with wounds and injuries of nerves. (1) The range of influence of nerve tissue over the mode of repair is very limited ; the divided ends must be in close proximity to insure union by other than connective tissue. (2) Extensive destruction of nerve cells and fibres is compatible with continued function of the parts supplied by them. A patient may be but little incapacitated by partial absorption and annular sclerosis of the spinal cord from caries of the vertebrae (Charcot) ; and haemorrhages, softening, and cysts of i3he optic thalami and corpora striata may leave very little impairment of function. In these cases it seems more probable that the remaining elements take on increased action, than that new ones are formed. As in muscle, the power of repair is greater in the lower animals than in man. Brown- Sequard found that the paralysis caused by division of the spinal cord in pigeons disappeared after a time. The approximated ends of a divided nerve will unite quite well if disturbing influences be excluded. This is seen after certain accidents and operations ; e.^., the sensibility of the skin of the lower lip and chin may be restored after laceration of the mental Chap. XXIII, ] Union of Wounds. 177 nerve from fracture of the jaw, and the conductivity of the superficial cervical is re-established in the case of ligature of the carotid artery. Again, portions of transplanted skin become sensitive as nerve-fibres pass through the cicatrix to pick up or replace those in the graft. Upon division of a nerve, degenerative changes ensue to a limited extent, less in the proximal than in the distal end, for it maintains its connection with the central ganglion cells. The white substance of Schwann breaks up, and the primitive sheath is ap- plied to the axis-cylinder, the most durable part of a nerve-fibre. Leucocytes infiltrate the part, and possibly the nerve nuclei increase in number. Some of the in- difierent cells become fusi- form, and, growing into nerve-fibres with double con- tour, pick up the ends of the old axis-cylinders, and the nerve cicatrix is fully formed (Fig. 19). Short of this, the newly-formed fibres remain embedded in the con- nective tissue scar, and the distal end of the divided nerve undergoes progressive atrophy, a reason for early operation in cases where nature has failed to effect the required union. According to some authors, the proximal part of the axis-cylinder elongates and joins directly with the distal. M Fig. 19. — Eegeneration of Nerve. From the Frog ten weeks after division. Development of young Nerve-cells from Spindle-cells. X 300. {After Hjelt. 'Erom Bill- roth's " Surgical Pathology.") J 78 Surgical Pathology. [Chap. xxiv. '^''©Iliads or fractures of cartilage unite by connective tissue, and in the case of the costal cartilages, occasionally by bone. There is little, if any, reproduction of cartilage cells. (In ununited fractures of bone the ends of the fragments are sometimes capped with hyaline cartilage ; this is in accord- ance with the fact that the enchondromata spring from bone or periosteum.) If a piece be split off an articular cartilage, the remaining portion proliferates at the seat of injury, the corpuscles divide and sub- divide, and the capsules and matrix soften. The granulation layer thus formed organises to fibrous tissue. The loss of substance is never completely repaired, but a depressed cicatrix remains. When the injury implicates the synovial membrane vascular loops grow into the granulation tissue, but they disappear as cicatrisation advances. CHAPTER XXIY. FRACTURES OF BONE AND PSEUDARTHROSIS. Simple fractiu-e. — When the shaft of a long bone is broken, there is bleeding from the vessels in the central medulla, Haversian canals, and periosteum, and also from the soft tissues round about, if these be lacerated by the displacement of the fragments. If the bleeding has been excessive, fluctuation, or bogginess, may be felt over the seat of fracture, and there is ecchymosis of the skin, and perhaps also bullse fi.lled with blood-stained serum. The staining of the skin becomes more marked after a while, for the blood corpuscles break up, and the colouring matter is diffused through the tissues. Chap. XXIV.] Fracture of Bone. 179 When the bone is deeply placed, or the break in it is a mere fissure, there may be no discoloration of the skin, or, at the most, only a light-yellow tinting from haemoglobin that has passed through the usual changes before it has reached the surface. Such may be seen in Scarpa's triangle a few days after intra- capsular fracture of the neck of the femur. Possibly a portion of the coagulum around the ends of the fragments organises, but certainly the greater part is re-absorbed. Inflammatory changes. — The swelling of the part is increased by exudation, which often causes oedema of the soft structures. There may be redness of the skin from hypersemia. The inflammatory changes set in immediately after the injury, and the products at first mingle with the extravasated blood, which, together with the serous portion of the exudation, is removed by absorption. Then it is that the more plastic fibrinous material can be felt as a firm sub- stance imbedding the broken ends of the bones. This will be about the end of the first week, when it is said the callus begins to form. It must not be supposed that up to the present there has been a simple sequence of three events : — • haemorrhage and absorption of blood, serous eflfusion and absorption, and the beginning of callus-formation. These processes overlap one another, as it were, and it is only the maximum development of each that is noted as a distinct phase. The result of the inflammation is that the medulla (subperiosteal, central, and interstitial or Haversian) has been converted into embryonic tissue, the cells of which lie fixed in a bed of firm inter- cellular substance. The early induration, which is more marked than in any other situation, takes place under the physio- logical law that rules the natural growth of bone. i8o Surgical Pathology. TChap. xxiv. The cells of the callus are derived from the blood-vessels, the bone corpuscles probably taking no active part in the process. So far as the bone is concerned, the embryonic or granulation tissue is limited externally by the peri- osteum. It forms a thin layer between the ends of the fragments, and fills up for a short distance the open ends of the Haversian canals. It also blocks the medullary canal. The fat cells of the central medulla are broken up and their contents absorbed. The inflammatory new formation is in greatest amount opposite the fracture, i.e., where the irritation from the injury is most intense ; from this point it subsides gradually, so that, if the broken ends be in accurate coaptation, they will be ensheathed by a regular fusiform collar or ferrule. Cartilaginous tramsformation of the cal- lus. — Some bones are developed directly from embry- onic tissue, and all grow in thickness from the same ; but many, e.g., the long bones, ossify from a carti- laginous basis until their full length is attained. So, in fractures, the callus formed of indurated granula- tion tissue may ossify forthwith, or pass through the intermediate state of cartilage. The reason why one fracture should unite through the medium of carti- lage, and another without it, is no clearer than that of the corresponding variation in normal development and growth. According to Cornil and Ranvier, the callus of simple fractures is converted into cartilage ; that of compound fractures is not. Billroth, ignoring this absolute distinction, says : — " In rabbits, the callus is always changed to cartilage before ossification, as it also is in children. In old dogs the callus usually ossifies directly, as in the human adult." The irritation in a compound frac- ture, where there is more or less suppuration, may be Chap. XXIV.] Fracture of Bone. i8i too great to allow of the necessary conditions (o£ which one is rest) for the transformation of exuda- tion into cartilage cells, and plasma into cartilage matrix. Age is likely to influence the event ; for in adults the natural formative activity of cartilage is almost m/, and cartilage tumours do not often show themselves late in life. On the other hand, car- tilage is always present in the growth of osteophytes about the joints in chronic rheumatic arthritis. Cartilage first appears at the upper and lower borders of the callus, both in the peri- osteal and central portions. It continues to grow until the chondrification is complete. Vascularization of the callus. — The blood-vessels of the bone and periosteum give off loops into the young peri- pheral callus; those of the bone ^IracwTildfurAbtt only into the central callus. The new vessels lie at right after the angles to the axis of the bone three weeks injiory. a. Compact bone of shaft; 6, callus ; c, cartilage formed In the callus; d, cartilaginous epiphyses ; the callus is chiefly deposited in the concavity lif the fracture-curve. (Natural size.) From a preparation by Dr. Silc .ck. in each case. Yascularisation of the callus between the opposed fragments is much slower than on the surfaces ; for the old vessels are pent up in the Haversian canals (except at the torn ends, which are plugged with clots), the rigid walls of which retard dilatation and lateral looping ; and hence it is some time before the i82 Surgical Pathology. [Chap. xxiv. continuity of the vessels in the two fragments is re- established. Ossification of tlie callus. — "Whether carti- lage be formed or not, lime salts are deposited around the blood-vessels imbedding the immediate granulation cells (osteoplasts). This follows in close order upon the growth of the vessels, and, in the superficial callus, advances from the bone and periosteum at the same time. The primary trabecul{« of bone form moulds around the vessels. As ossification advances, the osteal and periosteal spiculfe meet and widen, but the ossified callus never attains the density of compact bone ; for, before that stage is reached, retrogressive or absorptive changes set in. The osseous columns in the central and external callus lie, like the vessels, parallel to the transverse axis of the shaft of the bone. By the end of the first week, or a little later, ossification has commenced ; by the end of the third it is sufficiently extensive to enable the callus to support the bone without fear of bending or re- fracture. If the callus be changed to cartilage, ossification goes on after the physiological type. The primary capsules contain secondary capsules, which, dissolving, set free broods of embryonic cells derived from proli- feration of the cartilage cells. By absorption of the capsules and matrix, festooned passages filled with indifferent cells are opened up. Into these blood- vessels grow, whilst lime salts are deposited in the matrix. So far there is only calcification. True ossification is established by the inclosure of osteo- plasts as bone corpuscles in the ossifying matrix, corpuscles which unite by their processes, and lie in lacunar spaces that join one another and the central canals of the new Haversian systems. Chap. XXIV.] Fracture of Bone. 183 Provisional and definitive callus. — Du- puytren gave the name 'provisional to the callus formed about the ends of the fragments (that which causes the fusiform swelling on the surface, and blocks the medullary canal) since it provided for the union and support of the fracture pending the construction of the final or definitive callus between the broken surfaces. The amount of provisional callus depends chiefly upon the extent of the injury to the bone and soft parts. In comminuted simple fractures it is quite large, and welds the fragments into a continuous mass. In children it is more largely developed than in adults. If there be no displacement of the fragTnents, which require but little support, as in fissured fracture of the skull, it may be so small as to escape detection. The provisional callus so far disappears that the central canal is re-established and all external signs of the fracture lost, providing there has been little or no displacement of the fragments. Its complete absorp- tion requires months. Definitive callus^ though slow in forming, far exceeds the provisional in density ; indeed, it becomes more compact than the old bone, hence the saying, " A bone does not break twice in the same place." As the result of the injury a rarefying ostitis (5'. v.) is set up in the ends of the fragments. This goes on until the bone is quite porous, and the canals, enlarged by absorption, are filled with vascular fungous granulation tissue. The blood-vessels from the op- posite fragments m^eet and unite. Lime salts are deposited around them, so that the new bony tra- becules, unlike those of provisional callus, lie in the long axis of the bone ; and the continuity of the Haversian canals is once more established. The rarefjdng or destructive ostitis subsides into 184 Surgical Pathology. [Chap. xxiv. a sclerosing or constructive ostitis, and when this ceases repair is complete. The provisional callus is absorbed fari passu with the formation of the de- finitive. The amount of provisional callus formed, and the extent of the rarefying ostitis, vary as the intensity of the inflammation, and this as the degree of injury. Cliaug^es in the periosteiim, etc, — The me- dullary layer is converted into granulation tissu.e, and thence to callus. The fibrous layer becomes indefinite in outline, and commonly lost in the softened mass. In the latter event, a new periosteum is formed from the superficial cells of the callus. The development of new bony callus is not con- fined to the periosteum and bone ; the tendons and connective tissue of the muscles are likewise osteo- plastic. In simple fracture without displacement they do not enter into the process of repair, but where there is much laceration of the soft structures they are very active. The muscular fibres undergo absorp- tion corresponding in extent to the osteoplastic change in the interstitial tissue. When a fracture passes through a strong ten- dinous insertion, the callus at that part is increased by the physiological tension upon the tendon ; and when ossified, it may remain as a permanent osteo- phyte, whilst in the other parts it is completely absorbed. Fracture tlirougli epiphyisial cartilage is in reality fracture at the line of junction of the cartilage with the bone, so that one fragment carries the whole or greater part of the cartilage with it. This is the reason why epiphysial fractures, so common in children, do not, as a rule^ lead to a stunted growth of the bone. Severe injury may cause the cartilage to be entirely converted into embryonic tissue, and Chap. XXIV.] Fracture of Bone. this again into ossified callus, so that at one end the bone is arrested in its growth length- wise, but, as a rule, a part of the cartilage escapes the inflam- matory change. The cartilage developed in the callus probably ossifies throughout. It does not appear to possess the physiological pro- perty of continuous segmentation and reproduction (Fig. 21). In fracture through the epi- physis of the lower end of the humerus, the provisional callus partly fills the coronoid and olecranon fossae, and for a time checks the movements at the joint. The crepitus is not so hard and grating as in fracture through bone. Failure of ossific union. — The causes of non-union are constitutional and local. The con- stitutional causes are those that impair the healthy nutritive and formative activity of the tissues in general, and in one disease (molli- ties ossium) bone tissue in par- ticular. Chronic Bright's disease, tertiary syphilis, and cancerous cachexia may be cited as systemic defects likely to prevent bony Fig.21.— Defec- union, and permanently so. Frac- o/EaSusS^ t ures are slow to unite during: acute specific fevers, and afterwards if convalescence be protracted. result of frac- ture of tlie Lower Epiphysis. A ridge of bone is seen at the seat of union. (Reduced one- half.) 1 86 Surgical Pathology. [Chap. xxiv. The local causes are : (1) Tliose tliat prevent coaptation of the fragments ; (2) movement of the fragments one upon the other ; (3) defective vascular supply. Separation of tlie frag-ineiits may be effected by (a) muscular action, as in fracture of the patella and olecranon ; (6) the hydrostatic pressure of the effusion into the neighbouring joint, e.g., the knee ; (c) the interposition of a foreign body, such as muscle tendon, a detached portion of bone, a tooth in fracture of the jaw, or the necrosed end of one of the frag- ments. Wide separation by muscular action means that the new formation connecting the fragments is, at the part most distant from the bone, removed from the sphere of influence of the physiological stimulus to ossification possessed by the bone and periosteum. Movemeiit of tlie fragments entails more than the absence of coaptation. In a case of trans- verse fracture of the patella where the patient died from cellulitis of the limb set up by the use of Mal- gaigne's hooks, I found the fractured surfaces thickly studded with needle-like processes of new bone, a sixth of an inch in length. Now movement would tend to break off the tips of these minute stalactites, but would not prevent their fusion into a continuous layer by lateral growth. It seems strange at first sight that movement should cause an exuberance of callus, and yet in some cases prevent osseous union. The explanation is pro- bably in the degree and continuance of movement. If the callus sufiices to lock the fragments together, it will ossify ; if it fails to do this, it will not. Defective vascnlar smpply. — I believe this has little to do with the failure of union in the case of the patella and olecranon. In fracture through the anatomical neck of the humerus, the blood supply Chap. XXIV.] FSE UDA R THR OSIS. 187 can only come from one surface ; and in intracapsular fracture of the neck of the femur, the cervical liga- ment (periosteum) is usually torn, and the head of the bone gets very little nutriment through the liga- mentum teres, even if the latter is not ruptured by the accident. Pseudartlii'oses, or false joints. — Causes.— (1) Ununited fracture; (2) unreduced dislocation. There are two varieties of false joint as the result of ununited fracture : ia) ligamentous, (6) diarthrodial. L.ig'ameiitous pseiidartlirosis is seen in frac- tures of the patella, olecranon, acromion, and neck of the femur within the capsule. Unless the fragments be separated by serous effusion into the neighbouring joint, e.g., in the knee, in many cases of fracture of the patella, the interval between them is soon filled up with soft granulation Fi^". 22. — Ununited Fracture of Olecranon. a. Upper fragnu'iu; h, litramentoiis band joining the two fragments; c, humerus ; d, orbicular ligament ; e, triceps tendon. tissue, the vessels of which are derived from the broken surfaces and the surroundino- tissues. As the granulation tissue oro^anises the fibrous bundles lie })arallel to the line of greatest tension, i.e., from fragment to fragment. Surgical Pathology. [Chap. xxiv. The clistensit)ility of tlie young connective tissue accounts for the separation of the fragments subse- quent to their having been in pretty close apposition. Cartilage cells may sometimes be found in the meshes of the fibrous tissue at the fractured surfaces. l>iarttirodial pseudartlirosis. — The move- ment of one fragment upon the other may be so free as to prevent the growth of granulation tissue between the surfaces, or, if it have formed, to cause its re - absorption. This variety of false joint is found in the long bones. The medullary cavity on each side of the fracture is filled with callus, which may or may not I change to cartilage. The callus ossifies, but instead of being re- absorbed, as is the case when bony union occurs, it remains as a permanent compact mass. S This result is due to the fric- tion kept up between the frag- ments, whereby a condensing ostitis is maintained. Mean- while the granulation tissue formed from the soft tissues around the fracture organises, and the broken ends are en- Fig. 23 —Ununited Fiao- closcd within a dense fibrous cap- tSo£l?r™Toint''"" sule. When the cartilaginous a. Medullary cavity of the callus witMu the medullary caual bone; 6, compact bone clos- • n • i i u ing the medullary cavity OSSltieS, an HTCgular Jaycr 01 next " the joint ;" c, layer nf in- im • ,' cartilage ; d, fibrous capsule nyaime Cartilage IS sometimes containing a nodule of bone. ^ oi xi, £ /XT'* oo\ left upon the surrace (.rig. 23). A natural joint is further simulated by the change in shape of the fragments as they rub together, the cup- Chap. XXIV.] PSEUDARTHROSIS. 1 89 shaped hollow of one receiving the rounded, extremity of the other. The cavity of the false joint contains a little serum (not synovia) exuded from the vessels of the capsule. Pseiidarthrosis from imrecluced disloca- tion. — This may happen from disease or injury. In the former case the cartilage of the old joint is removed before the dislocation occurs. In caries of the hip pint the head of the femur is more or less absorbed, as is also the rim of the acetabulum, on the side of the dislocation where there is softening from caries, and atrophy from the continued pressure of the head of the femur ; hence the luxation usually takes place gradually. The capsule of the hip joint, softened by inflammation, is readily stretched by the localised tension upon it ; and at last it gives way, or is entirely destroyed by the disease at this part. Subsequent to the dislocation the caries may subside, and the granulation tissue become fibrous, and form a new capsule around the displaced bone. Then the cotyloid cavity becomes shallow, from atrophy of its margin and filling in of the hollow with connective tissue. The hip-bone is rough from osteophytes for some distance beyond the primary seat of disease. Where there is greatest movement (inter- niittent jjressitre) of the femur upon the hip, the irri- tation causes a buttress of bone to be thrown out, which serves as a support to the dislocated femur. This constructive process may go on even whilst the caries of the bones round about is progressing (Fig. 36). In Charcofs disease two factors may be concerned in the dislocation : (1) Erosion of the bones ; (2) stretching of the capsule from serous efi'usion into the joint. Pseudartlirosis from traumatic disloca- tion. — Here the dislocated bones are healthy at the time of the accident. The subsequent changes are : 190 Surgical Pathology. [Chap. xxiv. (1) Construction of a fibrous capsule about the false joint ; (2) alteration in the shape of the bones from mutual pressure ; (3) partial or complete absorption of the articular cartilages; (4) diminution in depth of the old articular depressions (glenoid, cotyloid, etc.); (5) formation of a buttress of support for the dis- located bone. Union of Compound Fractures. A compound fracture may be converted into a simple one by immediate closure of the wound in the skin or mucous membrane. The laceration of the soft structures, which is con- siderable, gives rise to a good deal of extravasation, and may possibly cause suppuration about the fracture after the external opening has closed. Besides the extent of the injury to the soft tissues, splinters of bone may be detached, and the ends of the fragments may necrose from stripping off of the periosteum, or consecutive inflammation. Taking an uncomplicated case of compound fracture, with suppu- ration, the bone, periosteum, and soft tissues implicated are acutely inflamed. The purulent exudation is at first mixed with disintegrating blood-clot. It bathes the broken ends of the bones, which are quite bare at the bottom of the wound. As the inflammation sub- sides a layer of vascular granulation tissue lines the whole interior of the wound. This for a time con- tinues to secrete pus, but at length the granulations from opposite sides come in contact and their vessels join. The inflammatory new formation passes through the usual changes. The cells that remain are imbedded in firm intercellular substance, in fact, the whole is converted into a mass of callus. The callus organises into bone without the intermediate formation of cartilage (Cornil and Eanvier). It rarely ends in Chap. XXIV.] PSE UDA R THR OSIS. 191 fibrous union of the fracture. The bone, periosteum, and fibrous structures in the vicinity are all active in the osteoplastic process, so that the amount of pro- visional callus is very great. The rarefying ostitis of the ends of the fragments is more extensive than in simple frac- ture, and this delays the time of comple- tion of the definitive callus. Compound fracture, with n e c r o s i s. — Por- tions of bone may be cut ofi* at once from all vascular supply, and lie loose at the seat of frac- ture ; or necrosis Fi?. 24.- Diagram of Fracture of a Loii? of the ends of the Bone, with external Wound; longitudinal section. (Natural size. ) fragments may en- sue from the vio- lence of the injury, stripping ofi" the pe- riosteum and caus- ing extravasation into the Haversian canals, or from arrest of the circulation, consequent on acute inflam- mation. Loose splinters of bone may retain their connection "with the periosteum, and, surviving the effects of the injury, help in the process of repair. Necrosed por- tions of bone, unless removed, keep up irritation, and whilst they stimulate to increased bone formation they e, e, bone ; /, /, /, /, soft parts of the limh ; a, a, ne- crosed ends of the hone ; the darkly-shaded part represents the granulations which line d, the wound that opens outwardly, and secrete pus ; b, b, internal callus in the two dislocated ends of the bone ; c, c, external callus. (,After Billroth.) 192 Surgical Pathology. [Chap. XXIV. prevent closure of the sinuses. If the ends of the fragments lose their vitality, union of the fracture is greatly delayed, but it may take place sufficiently to allow of restoration of the function of the bone whilst the sequestra are retained ; i.e., the mass of new bone thrown out from the outer surface of the living por- tions of the frag- ments and the soft tissues around, may bridge over the gap that holds the sequestra, so extensively as to leave but one or more narrow aper- tures (cloacse) for the escape of the purulent dis- charge from the granulations within. So long as the sequestra remain Fig. 25.— Diagram of Detacliment of a Necrosed ^ \ .^^ ^ Portion of Bone magnified 300 diameters. puratlOn Will COn- o, Necrosed portion of hone; 6, living bone ; c, new tinue \ but if formation in the Haversian canals by wJiicJi the ^ bone is detached. iAfter Billroth.) sequestrotomy be performed, even after the lapse of years, the sinuses will close and the case end favourably. Nature is unequal to the liberation of the dead pieces, for before they are detached a mantle of new bone has been de- posited around them, and the sinuses have con- tracted too much to allow of their extrusion by the pressure of the granulations. The casinsf of new Chap. XXV.] Spontaneous Fracture. 193 bone becomes very thick and dense, and the cavities left after removal of the sequestra fill up slowly on account of the dearth of vessels. The sequestra are quite characteristic. They present at one end a brittle fracture, at the other a worm-eaten appearance. Sponta-neous fracture. — By this we mean that the fracture results from an injury wholly inadequate to the breaking of a healthy bone. The force is almost always applied indirectly. The fracture sometimes occurs without the knowledge of the patient. Causes. — (a) More or less general. 1. Senile osteoporosis. Here the bones are very brittle, the compact tissue is wasted, and the spaces of the cancellous tissue are large and filled with fat. 2. MoUities ossium. In this disease the fractures are usually multiple. 3. Rickets. 4. Cha,rcot's disease. (b) Local causes. 1. Absorption of the bone by a new growth, or the pressure ayi an aneurism. 2. Congenital syphilitic dystrophia, causing separation of the epiphyses. 3. Syphilitic gummata. 4. Fatty atrophy from disease, e.g., in long-standing joint- afiections. 5. Alteration in the angle that the neck of the femur makes with the shaft in old people. This places the bone at a mechanical disadvantage when force is applied to the long arm of the lever. (The fulcrum is at the hip. joint, and the resistance at the seat of fracturei) CHAPTER XXY. INJURIES AND DISEASES OF THE SCALP. Cirsoid aneurism, nsevus, atheromatous cysts, and subaponeurotic cellulitis are described elsewhere. The parasitic diseases are beyond the scope of this work. N 194 . Surgical Pathology. [Chap. xxv. HeEematoma. — Hsematoma is an extravasation of blood sufficient in quantity to give rise to a boggy or fluctuating swellinsf. There are two forms of cephalhcematoma, subpericranial and subaponeurotic. In the former the effusion is beneath the periosteum ; in the latter, beneath the tendinous expansion of the occipito-frontalis muscle. Subpericranial hjematoma is limited to the bone over which it commences, for the periosteum is too firmly fixed at the sutures to allow of its further separation. Subaponeurotic hsematoma, whilst usually confined to a circumscribed area, is occasionally difiused over the cranial vertex from the superior curved line behind to the brow and root of the nose in front. It is impossible to tell by manipulation whether a localised haematoma is beneath the pericranium or aponeurosis. Necrosis is more likely to follow the former, but it is not common in either case, unless the bone is severely injured, for the vascular supply is chiefly derived from the meningeal arteries. The extravasated blood passes through the usual process of disintegration prior to absoi-p- tion. But whilst there is yet fluctuation, inflammatory lymph is efi'used at the base and margin of the swelling, so that the latter is surrounded by a vascular granulation membrane. The exudation from this mingles with the liquefying clot, and it may end in suppuration but more frequently it is reabsorbed. The inflammatoi'y induration terminates abruptly on the side of the hsematoma, whereas it gradually sub- sides into the soft structures beyond. As the finger is passed from without in, it comes upon a sharp declivity at the edge of the crateriform inclosure. This gives one the idea of a depressed fracture ; but it will be found that the floor of the apparently sunken space lies in the natural curve of the skull. In the end there is complete levelling by absorption Chap. XXV.] Diseases of the Scalp. • 195 of the superabundant lymph, and the normal condition is restored. Pott's pufiy tiimoiir. [Vide Necrosis.) Scalp wounds. — The large number of arteries in the scalp, and their very free anastomosis, explain at once the profuse bleeding, the wonderful power of repair of wounds, and the great rarity of sloughing. As the divided vessels are embedded in firm, closely- woven tissue, contraction and retraction are impeded, and hence mechanical means are usually required to / stop the haemorrhage. Erysipelas of tlie scalp is either idiopathic or traumatic. It is accompanied by a good deal of oedema, which causes marked bogginess. It may lead to sup- puration beneath the aponeurosis. Unless accompanied by fracture of the skull, meningitis is a rare sequel, but it may arise from spreading of the inflammation in the course of the communications between the cerebral sinuses and the external veins. The severe nervous symptoms frequently exhibited are in the majority of cases dependent on functional disturbance set up by the poison circulating in the vessels. It is thought by some that the tissues of the scalp are peculiarly liable to erysipelatous inflammation, but the explanation probably lies in the frequency of scalp wounds. Simple inflammatory redness and oedema may be mistaken for the specific disease, Tumoiu'S of the scalp. — The most common are nsevus, sebaceous cysts, and epithelioma. When a sebaceous cyst suppurates, obstinate ulceration with the growth of fungoid granulations may simulate epithelioma, but the history of the case, and the presence of other unbroken cysts, are points that serve to clear up the diagnosis. The ^pulsating svjellings comprise hernia cerebri, meningocele and encephalo-meningocele, cirsoid aneurism, malignant tumours communicatinsr or not with the interior of 196 * Surgical Pathology. [Chap. xxvl the skull, and, very rarely, subaponeurotic collections of pus, blood, or cerebro-spinal fluid, receiving the pulsations of the brain through the cleft of a fracture. (Pulsation of the scalp without tumour is seen at the fontanelles, and very rarely where the bone is exten- sively absorbed in craniotabes. ) CHAPTER XXVI. HERNIA CEREBRI HAEMORRHAGE BETWEEN THE SKULL AND DURA MATER. Hernia cerebri is a protrusion through an open- ing in the cranial walls of a soft mass, composed of highly vascular granulation tissue and softened brain substance. It essentially depends on inflammation of the meninges and cerebral cortex. It is most common after compound fracture with laceration of the dura mater. The idea that pressure of the dura mater against the edge of the inner table is sufficient of itself to set up ulceration is erroneous ; for this does not happen in cases of trephining, where the operation is performed for other than depressed fracture or intracranial suppuration ; or, in other words, where the soft structures are neither torn, nor weakened by acute inflammation. The outward pressure of the brain intermits with its pulsations, and the only result is moderate thicken- ing, the same as when a corn is produced by friction. In hernia cerebri the cerebral membranes are destroyed by inflammatory softening, and the underlying portion of brain is infiltrated with liquor sanguinis and leuco- cytes. New capillary blood-vessels are developed in the embryonic tissue. Inasmuch as absorption does Chap. XXVI.] Hernia Cerebri. 197 not keep pace with exudation, and tlie capacity of the cranium is a constant quantity, the surplus matter escapes where there is least resistance, just as in hernia testis {(l-v.). The difficulty with which the local circulation is carried on accounts for strangula- tion and rupture of the thin-walled capillaries. The congestion and interstitial extravasation may be so great that the hernial protrusion closely resembles a blood clot. Microscopical examination reveals vast numbers of leucocytes, dilated capillaries, apoplectic effusions, and disintegrating nerve-cells. The last- named are recognised by their size and shape. As a rule, the morbid process only ceases with the death of the patient. If recovery takes place the mass shrinks and undergoes cicatricial contraction. The fibrous tissue forms a scar, and fills up the opening ; sometimes it is partially converted into bone. Should the patient survive the loss of a con- siderable portion of the brain, the skull adajjts itself to its diminished contents by hypertrophy of the diploe and retrocession of the inner table, or by re- modelling without increase in the thickness of its walls. In the latter case the cranium loses its symmetrical outline. Hernia cerebri pulsates synchronously with the beats of the heart. Hsemorrliage between the skull and dura matei\ — This is met with in many cases of injury. Separation of the dura mater is effected in the first instance by the violence of the blow, but from this cause alone it is not very extensive. It is necessarily accompanied by haemorrhage from the torn vessels ; but unless there be fracture of the skull, the bleeding is seldom profuse. In due course the extravasated blood is absorbed, or suppuration is established about the clot. When the middle meningeal artery is wounded, the consequence is far more serious, since 198 SUR GICA L Fa T ho logy. [Chap . XXV 1 1 . the pressure under which the blood is poured out is sufficient to strip up the dura mater to a very consider- able extent, and the bleeding may not cease until a large effusion has taken place. The appearance of the clot when removed with the dura mater is quite characteristic. It is saucer- shaped, the outer convex surface corresponding with the con- cavity of the skull. The whole preparation bears a resemblance to a placenta with a portion of the membranes attached. The size varies in most in- stances from two to five inches in diameter, and from half an inch to an inch and a half in thickness. The colour depends upon the time that elapses between the injury and the death of the patient, upon the degree of post-mortem change, and upon the mode of preserving the specimen. It may be dark - red, greenish-black, or jet-black. The likeness to a melanotic malignant tumour is sometimes very striking, but it need never be mis- taken for this if the uniform shape of the mass and the presence of a broad expanse of fibrous membrane (dura mater) be borne in mind. As the large meningeal vessels are more intimately connected with the dui-a mater than the subjacent bone, they are carried inwards by the clot ; and the greatest difficulty may be experienced in detecting the situation of a wound in the bleeding artery at the bottom of the cavity ; in fact, this may be impossible. CHAPTER XXVIL INTEACRANIAL SUPPURATION. May be located : — (1) between the dura mater and the skull ; (2) in the arachnoid space : (3) on the surface of the brain, beneath the arachnoid ] (4) in Chap. XXVII.] Intracranial Suppuration. 199 the substance of the brain (cerebral abscess). It has been ah-eady noted that pus may be formed as a con- sequence of injury separating the dura mater. This is quite certain to be the case if the bone becomes necrosed. Fracture is not essential for its occurrence. It not infrequently happens that a patient recovers from the immediate effects of the concussion, and remains free from any marked symptom for several days, or even two or three weeks ; and that then headache, fever, and local tenderness and swelling, point to the probability of intracranial suppuration. The exact situation of the lesion as to its depth from the surface cannot be determined with certainty by the symptoms alone. If, at the bottom of a scalp- wound or abscess, the bone is dead and bare, the chances are that there is pus between the skull and dura mater, with or without more deeply-seated mis- chief. If the inner table has preserved its vitality, there may still be suppuration immediately beneath it; or, the dura mater remaining adherent, localised or diffuse abscess may be found in the arachnoid cavity. In a case of gun-shot injury to the skull, without fracture, I found a few drops of pus external to the dura mater, and a collection between the parietal and visceral layers of the arachnoid over a surface of about three inches in diameter. Interarachnoid suppuration is either local or gene- ral. The event turns mainly on the intensity and rapidity of the inflammatory process. Where these are moderate in degree, the opposed surfaces at the periphery of the inflamed area are united by plastic lymph, and a boundary wall is thus formed which prevents the diffusion of the pus. Abscess of the brain, the result of injury, is sometimes found with- out a trace of suppuration in the arachnoid or outside the dura mater. Purulent effusion between the bone and dura 2 00 Surgical Pathology. [Chap.xxvii. mater in the majority of cases is due to injury, with or without fracture or necrosis. When syphilitic caries attacks the inner table of the cranial vault, a certain amount of pus exudes from the granulations, and either remains locked-up between the bone and the thickened dura mater, or escapes through a crevice by the side of a sequestrum. In meningitis from disease of the middle ear and petro-mastoid cells, the dura mater is generally found in a sloughy condition ; there can, however, be little doubt but that, previously to its perishing in this manner, suppuration to a limited extent occurs be- neath it. Siippisrattve aractiiiitis is extremely rare, except as a consequence of inflammation spreading from the bone and dura mater ; hence a careful search should always be made for some local injury or disease, such as caries of the middle ear, or syphilitic caries. Now and then it occurs as a metastasis, from bed-sore or other form of pyaemia, but the liability to septic infection of the arachnoid is much less than is the case with the pericardium or pleura. There is sometimes increased secretion in the arachnoid as a result of irritation from pia-meningitis ; but, whilst the fluid may be cloudy, it never attains the purulent character, as it does in inflammation from the above- mentioned causes. Although the pus is occasionally confined to the region of some local centre of disease, it is generally difiused through the whole or greater part of the cavity. It usually escapes in some quantity on incising the dura mater ; and, when that membrane is removed, the brain is seen to be covered with a thick layer of exudation, creamy or yellowish-green in colour. Fia-]aieiiing:eal suppuration occurs as an idiopathic disease in many instances. This is notably Chap, xxvii.] Cerebral Abscess. 201 the case in very young children, who seem to be pecu- liarly predisposed to it. The term "idiopathic" is used, since the actual cause is not well ascertained. There appears to be reason for the belief that it is occasionally the manifestation of the action of the poison of an acute specific fever. Those circum- stances that combine to produce general marasmus also aid in its causation. In tubercular meningitis there is always a con- siderable amount of exudation ; this, in the ventricles and subarachnoid space, is cloudy and serous, and, in the meshes of the pia mater, highly fibrinous, and sometimes quite purulent. In the latter situation it appears as a sulphur-like layer beneath the visceral arachnoid. Tubercular meningitis is most marked at the base of the brain, idiopathic at the vertex. Another cause of pia-meningitis is abscess in the cerebral cortex. Ceretoral abscess is found as the sequel of injury to the skull. It also follows acute and chronic suppuration in the middle ear and mastoid cells. In pyaemia it is comparatively rare. The symptoms depend much more upon the locality than the size of the abscess. I have known the anterior lobe of the brain to be in great measure destroyed without there being any indication of such an extensive lesion. The situation of the abscess may be suggestive of its cause. Thus, the cerebellum is the usual seat of the suppuration set up by spreading of the inflammatory process from the mastoid cells ; next to this comes the temporo-sphenoidal lobe. As a rule, traumatic abscess forms beneath the x>art injured by a blow. The contents of the abscess consist of exudative material and the debris of the brain substance, together with a certain amount of blood extravasated from the capillaries. They are prone to decomposi- tion, and so the blood pigment is rapidly transformed 202 Surgical Pathology. [Chap. xxviii. into derivative compounds, and the pus variously coloured — deep yellow, reddish-brown, or dirty green. The odour is often very offensive, and this, too, where there has been no communication with the external air. The walls are composed of brain tissue, infiltrated with inflammatory products and blood that has escaped from rupture of degenerated vessels. On pouring water over the surface, fine flocculi float out from the disintegrating tissues^ except in cases of long standing, where there is a kind of pyogenic membrane. CHAPTER XXYIII. SUPPURATION IN THE MASTOID CELLS. By far the most common cause is disease of the middle ear, but it may arise in connection with strumous or syphilitic caries of the bone. In the former case there is generally some discharge from the external auditory meatus through a perforation in the membrana tympani. The process may develop with great rapidity, or, on the other hand, it may be exceedingly slow. Not unfrequently months or years elapse from the onset of otitis media before there is any external evidence of implication of the mastoid cells. The usual signs are pain and tenderness at the back of the ear, followed by redness and swelling, headache, and other cerebral disturbance. The facial nerve is liable to irritation and compression as it lies in its narrow channel. This will be evinced by twitching or paralysis of the muscles of the face. Although the osseous compartments communicate with one another, the pus does not all escape at once when the external plate of bone is destroyed by Chap. XXIX.] Pulsation of the Eye-Ball. 203 ulceration or removed by operation, for soft granulation tissue blocks more or less the openings from the cells. Free discharge by way of the tympanum is checked by swelling of the lining membrane ; and thus, from want of relief of the inflammatory tension, there is great danger of the disease spreading through the thin laminae that separate the mastoid cells from the dura mater, and setting up meningitis and cerebral abscess. On breaking down the avails of the cells in acute suppurative ostitis, pus escapes like honey from the comb j but in caries the softened bone contains not only pus, but a quantity of granulation tissue and caseous debris. CHAPTER XXrX. PULSATION OF THE EYE- BALL. Pulsation of the eye-ball is accompanied by more or less prominence. It is caused by (1) several varieties of aneurism, circumscribed, diffuse, ruptured, and cirsoid ; (2) very vascular sarcomatous growths ; and (3) rarely by pulsation of the vessels in exoph- thalmic goitre. Circumscribed aneurism results from direct wound of the ophthalmic artery or one of its branches, or it arises spontaneously. Cirsoid aneurism (g. v.) is some- times produced by blows, or concussion of the skull, though this cause cannot always be assigned. The morbid process is probably a subacute inflammatory thickening and softening of the walls of the arteries with secondary dilatation. In sacculated and cirsoid aneurism there is usually marked bruit, and there may be distinct thrill. 2 04 Surgical Pathology. [Chap. xxtx. Prominence op the Eye-ball, Exophthalmos. The causes of prominence of the eye-ball may be tabulated thus : (1) Enlargements of the globe : {a) intraocular tumours, e.g., glioma of the retina and sarcoma of the choroid and iris ; (h) acute glau- coma. (2) Orbital tumours: (a) vascular, including aneurisms, venous nsevus, and dilatation of the vessels in exophthalmic goitre ; (b) solid tumours. These may arise in the orbit, or invade it from other parts, e.g., the maxillary antrum, and the naso-pharynx and contiguous sinuses. (3) Orbital cellulitis and abscess. (4) Absorption or depression of the orbital plate of the frontal bone in chronic hydrocephalus. (5) Para- lysis of the ocular muscles, as when a gumma presses on the third nerve. (6) Dilatation of the frontal sinus from accumulated secretion or chronic abscess. Orbital cellulitis and abscess may be due to fracture, or syphilitic periostitis, or metastasis in pysemia. It occasionally follows suppurative inflammation of the eye-ball in rheumatic or traumatic ophthalmitis. It is recognised by the severe throbbing pain, and redness and oedema of the eyelids. The continuous pressure of the cerebro-spinal fluid in chronic hydrocephalus induces atrophy of the orbital plate, and at the same time causes depression of the bone. In this way the cavity of the orbit is encroached upon, and the contents driven forwards. In extreme cases the eyelids are unable to cover the front of the globe. The straight and oblique muscles of the eye by their tonic contraction maintain a gentle compression on the globe, which keeps it steadily in its place. When several of them are paralysed, the pressure of the blood-vessels in the orbit, no longer balanced by the usual support given to the eye-ball, causes the latter slightly to advance. 205 CHAPTEE, XXX. INFLAMMATION OF BONE. On account of its stability bone tissue presents a favourable field for the study of inflammation and other diseases. Dried specimens preserve indefinitely coarse altera- tions in form and structure ; and by softening and staining, preparations can be made that faithfully picture the more minute changes in nutritive and formative activity. Bone consists essentially of a rigid calcified frame- work, passive, but none the less important in the production of morbid states ; and of soft tissues modified here and there according to the function they are called upon to perform. Taking a long bone, there is a layer of cartilage covering the articular ends ; a highly vascular periosteum subserving nutrition and growth ; a soft medulla accumulated in the central canal, continuous with that which forms a bed for the vessels, in the open network of the cancellous tissue and the narrow channels of the Haversian canals. All this in the foetal state is red, but at a later period the cells of the central medulla and of the cancellous tissue become loaded with fat, giving these structures a yellow appearance. Then there is, up to a certain age, a layer of developmental cartilage between epiphysis and shaft. It may be noted that the marrow of certain bones {e.g.^ vertebrae, sternum, and ribs) retains more or less its foetal condition throughout life. For the main part the red medulla consists of embryonic cells, in which are imbedded huge multinucleated corpuscles and delicate-walled blood-vessels. 2o6 Surgical Pathology. [Chap. xxx. The relative porosity of different parts of the same bone will to a great extent determine the issue of inflammatory and other processes ; thus, in the open fretwork of the cancellous tissue, passive congestions, chronic exudations, caseation, and absorption of the osseous lamellae (the sum total of which is caries), find a more suitable nidus than in the compact bone, whose channels are so small that the blood-vessels readily become compressed, with consequent immediate death of the part (necrosis). Causes. — Ostitis may be caused by traumatism, or by some morbid material in the blood irritating the medullary constituent of bones, e.g., of syphilis, the acute specific fevers, pyaemia, and rheumatism. In struma the carious process often follows some slight injury, though frequently no local origin can b© assigned, and when it can the destructive changes are out of proportion to the intensity of the irritation. Then there are the so-called idiapathic inflamma- tions that are attributed to exposure to wet and cold, or some more obscure source ; the real cause being pro- bably what we term a predisposition, i.e., some diseased state of the blood, or bone, or both, suflicing to start the inflammation, but recognised only by its results. Terminations. — Ostitis may terminate (1) in molar death, or necrosis ; (2) molecular death, or caries ; (3) sclerosis, or condensation. The same specimen often shows all three; e.g., the lower end of the femur in strumous arthritis, where the articular surface, denuded of its cartilage, looks woiTQ-eaten, and the cancellous structure of the epi23hysis appears rarefied from absorption by granulation tissue, whilst occupying a cavity in the interior may be seen a sequestrum, and on the surface numerous stalactitic deposits of new bone. As to which shall predominate, one has to look (1) to the intensity of the inflammation; (2) to the cause, whether it be local or general ; (3) to Chap. XXXI.] Rarefying Ostitis — Caries. 207 the density of tlie bone. The exudation may he so excessive as to lead to an acute interruption in nutrition by strangulation of the vessels, and this will occur the more readily if the spaces that contain the latter are small, as in the Haversian canals of com- pact bone; hence the frequency of necrosis from sup- purative inflammation of the shafts of long bones. Constitutional states are a frequent cause of necrosis, as seen in the rapidly destructive inflammation of the growing part of bone in children, and in the more chronic lesions of syphilis and scrofula ; but the part that they play in the history of caries is all important, for the same conditions that favour the onset act also against the possibility of repair ; if the vitality of the tissues is so low as to be unable to meet the physio- logical calls for maintenance and repair, how can it be expected to be equal to the extra task of re-construction after the ravages of disease 1 C ceteris paribus, the same cause (e.^., syphilis), varying in intensity at difierent times, will lead to corresponding results; thus, an ossifying node of the tibia, caries of the skull, and necrosis of the nasal bones, may form a natural sequence in the same subject, or each may be found alone. Again, the outcome of one source of irritation may in its turn create another, as when a sequestrum sets up a formative ostitis, or caries entails necrosis, or necrosis, caries. CHAPTER XXXI. RAREFYING OSTITIS CARIES. Next to necrosis in order of severity is that form of destruction of bone commonly known as " caries," " molecular death," or '' ulceration," in which the 2o8 Surgical Pathology. [Chap. xxxi. earthy and animal constituents are slowly disintegrated and removed. This is effected by the absorbent action of granulation tissue. The word " caries " usually implies something more than mere inflammatory softening and porosis ; it raises the question of caseation and chronic sup- puration, with their local and general consequences. I£ the terms caries and rarefying ostitis are considered as synonymous, several forms of inflammatory rarefaction of bone (simple, scrofulous, tubercular, and syphilitic) more or less distinct in their origin, course, and ter- mination, are included in the same category. It would be well to discard the word " caries " alto- gether, and to describe separately each variety of rarefying ostitis. Cornil and Ranvier maintain that rarefying ostitis is only a stage of caries, and secondary to a charac- teristic lesion, viz., " a fatty change destructive of the cells contained in the lacunae," They recognise two distinct periods in caries ; "in the first the bone cells undergo fatty degeneration without there being previously the least sign of in- flammation ; in the second, the osseous trabeculse, killed by the death of their cellular elements, form so many foreign bodies which determine suppurative inflammation around themselves." But they do not assign any reason for the primary degeneration of the bone corpuscles, nor explain why their death should kill the osseous trabeculse. It is not usual for fatty degeneration to set up in- flammation, it is more often the result of it ; and I am inclined to believe that the degeneration of the bone corpuscles- is the consequence of their death, and that this depends on precedent inflam- mation. The heart, arteries, and cornea, when far advanced in fatty decay do not become inflamed. Chap. XXXI.] Rarefying Ostitis — Caries. 209 Simple rarefying ostitis, or caries*— When a bone is injured the blood-vessels dilate, and there is exudation of liquor sanguinis and leucocytes. Here the process may end, the simple ostitis subsiding, and the bone returning to its normal condition. If the irritation is more intense, as in the case of fracture, or if it is more prolonged, as when a seques- trum is imprisoned, the inflammation becomes chronic and the exudation continuous. The vessels, from their elongation, can only be accommodated within the rigid walls of the Haversian canals by forming loops, or curves. Around these curves migratory cells accumulate, giving rise to the first appearance of granulations or buds of embryonic tissue, which enlarge and destroy the bone. Hence, instead of an even absorption, the osseous trabeculse are excavated here and there in a festooned manner. The crypts or recesses filled with granulation tissue are called Howship's lacunae. It is supposed by some that the bone corpuscles take an active part in the process, dividing and sub- dividing ; but most pathologists agree that the in- difierent granulation-cells (osteoclasts) are merely leucocytes that have wandered from the blood-vessels ; and that the stellate bone-corpuscles show little or no sign of formative activity ; that, in fact, they undergo retrograde changes, as may easily be seen where opened lacunae are setting free their degenerated contents. There may or may not be suppuration and purulent discharge; the event depends mainly upon the intensity of the irritation. A spongy bone may be honeycombed by absorj)tion, so that it can be divided with a knife, and yet not a drop of pus be formed ; in fact, the shell of compact bone may contain little but granulation tissue. This is what Billroth terms caries fungosa, or caries non-suppurativa. Such a case, whether it be o 2IO Surgical Pathology. [Chap. XXXI. started by injury or arise spontaneously, shows that the granulation tissue has sufficient vitality to sur- vive, and that, instead of undergoing liquefaction or caseation, it may at any time (the inflamma- tion subsiding) organise and ossify until the de- posit of new bone exceeds in density the original structure. The rarefying ostitis has passed insensibly into a sclerosing or condensing ostitis. Strumous rarefying ostitis (struuious caries). — This differs from simple traumatic rarefying rig. 2'\ — I?arefying Fungous Ostitis, from a case of Strumous Dactylitis. The inflammation was very chronic. There is no caseation, but here and there an attempt at organisation. 4, Bone undergoing absorption by the granulation tissue, 6 ; e, granulation bud that has perforated the ' sseous lamellis ; d, blood-vessel. The bone cor- puscles show no signs of segmentation. ostitis, in that it arises from a constitutional cause alonSj or from local irritation too slight to set up Chap. XXXI.] StRUAWUS C ARIES. 211 destructive inflammation in a healthy subject. More- over, it rarely begins in compact bone. The most common situations are the tarsus and carpus, the vertebrae and the cancellous ends of the long bones. The sternum, ribs, and petromastoid bone are also frequently affected. Some cases are so slight that the disease runs its coarse without suppuration or caseation (Fig, 2Q). The granulation tissue which fills the Haversian canals, and medullary spaces, and eats out the bony trabecules, is exuberant, semi-gelatinous, and firm, and as the inflammation subsides it organises into connective tissue and bone. This is caries fungosa (fungating ostitis). But far oftener the exudation is purulent, and the granulation tissue breaks down ; and the pus and debris collect in an abscess cavity in the interior of the bone. The walls of the abscess are composed of inflamed disintegrating bone, and are lined with caseous pus. The abscesses may remain closed indefinitely, but, as a rule, they open into a contiguous joint, or ex- ternally. This is one way in which white swelling, or strumous arthritis, commences. Now and then the granulation tissue undergoes fatty degeneration and caseation without suppuration. The disease may be divided into three stages : (1) that of congestion; the bone is of a deep red or violet hue, giving one the idea of extravasation. This stands in marked contrast with the surrounding* pinkish-yellow colour of the healthy medulla ; (2) the growth of soft vascular granulation tissue ; (3) de- generation and softening of the neoplasia, purulent exudation, and absorption of the osseous trabeculse. The bone corpuscles wither and break up into fat molecules. The fat cells are destroyed. Caseation of the inflammatory products results from an inherent 2 12 Surgical Pathology. [Chap. xxxi. low vitality, and strangulation and thrombosis of the vessels. When the disease is very rapid, the cancellous spaces and Haversian canals are filled with pus. The bone may be absorbed in such a manner, that a portion is isolated from the rest by a zone of granu- lation tissue ; then it usually dies (caries necrotica), but it may retain its vascular connection, and survive as a " living sequestrum." A section through a carious bone {e.g., the head of the tibia) often shows the A^arious stages of the morbid process ; simple congestion at the periphery ; next to this, a tract of softened bone infiltrated with a pinkish-grey soft gelatinous material ; and then a pultaceous collection of j^^s and caseous debris, and in its midst a sequestrum. In central caries the surface of the bone varies j it may be simply thickened from deposit of new bone, or it may be worm-eaten for some distance, from extension of the i-arefying ostitis \ but even then osteophytes are thrown out at the borders. Superficial rarefying ostitis, or caries, is due to the same causes as the central variety, but it more often follows injury. The periosteum and superficial part of the bone are attacked at the same time. The subpeiiosteal medulla is converted into a red pulp, which extends into the Haversian canals of the compact bone. The osseous trabeculse are thinned, so that a probe can be driven through them. The further progress of the case depends upon the intensity of the initial irritation, and the state of health of the patient. It may pass at once into sclerosing repara- tive ostitis, or proceed to suppuration and caseation. When a periosteal abscess is opened, the bone beneath, unless necrosed, is found to be more or less porous. But most cases of superficial caries are chronic from the first, for acute exudation strangulates the vessels Chap. XXXI.] Tubercle of Bone. 213 ill tlie narrow Haversian canals of compact bone, so that it dies. Superficial caries from injury may occur in any bone. When of strumous origin it is found in the same situations as central caries. It is not uncommon in the malar bone, about the lachrymal sac, and in the mastoid process. Syphilitic caries has a special proclivity for the cranial vault, a place where stru- mous caries is rarely seen. Nature of tlie «liscliar§^e ia caries. — In strumous caries it is seropurulent, or curdy. The liquor puris holds in susjDension caseous flakes, pus cells, granular debris, and crumbs of necrosed bone set free by the melting down of the granulation tissue ; in solution, lactic acid, and the usual alkaline, earthy, and organic constituents. There is an excess of lime salts. Tiitoercle of bone. — Some authors consider all the products of strumous caries as tubercle ; but reference is here made to miliary granulations in bone ; small, hard nodules, composed of groups of cells, set in a granular, homogeneous, or fibrillated matrix. The vessels of the medullary spaces and Haversian canals are obliterated by the growth, which is extravascular. This takes place before the neoplasia has time to absorb the bone, hence those portions im- bedded in the tubercles do not appear notched, as in rarefying ostitis. There are two forms, discrete and confluent. The latter is the result of the fusion of isolated tubercles. The tubercles, together with the products of rarefying ostitis around them, undergo fatty degeneration, and are lost to sight in the caseous debris ; but the true nature of the case is shown by the existfince of isolated tubercles at the periphery, and by examination of the bony trabeculse. The vertebrae, sternum, and the bones of the 214 Surgical Pathology [Chap. XXXI. carpus and tarsus are the most likely situations. It is said the cranial bones are not affected. The deposits form part of a general tuberculosis, or they result from local infection by the caseous Fig. 27 (one-half natural size). — Caries of the Vertebrae, with Angular Curvature of the Spine. a. Body of vertebra, eroded and rarefied by granulation tissue ; 6, bodies of two vertebra in wbicb sclerosing ostitis has succeeded to carious rarefaction; c, neural arches aucbylosed. Many intervertebral discs have been removed by absorption, and the bodies of the corresponding vertebra fused together. products of strumous ostitis (caries atonica). They are thus at once the cause and consequence of rare- fying ostitis. Caries of the spine. — Pott's disease is usually of strumous oriein. It is often started by a blow or Chap. XXXI. 1 Caries of the Spine. 215 strain. It is essentially a rarefying ostitis of the cancellous tissue of the vertebrse. It rarely iDegins in the intervertebral discs. Whilst the bodies of the vertebrae are being absorbed, an osteoplastic ostitis is taking place about the neural arches. This is a con- servative process, for it prevents sudden dislocation, and so saves the spinal cord from being crushed. As the disease is more extensive at the anterior than the posterior parts of the bodies, the excavated bones fall together, hence the prominent spines and curvature. Appearance of tlie boues. — Compare them with the regular, circumscribed excavations from the pressure of an aneurism (Fig. 3), or an encapsuled tumour, and with a spine eaten into by an infiltrating sarcoma. A carious spine in the fresh state is quite soft, so that a probe can be driven into it. The enlarged medullary spaces are filled with a confused mass of granulation tissue, caseous matter, and pus. In a dried unmacerated specimen the desiccated debris Ivine- in the razored hollows looks like half -set mortar. By maceration all this is removed, and then the open fretwork of rarefied bone gives a rough representation of the festooned outline of microscopical fragments (Fig. 27). Then, again, there may be an abscess by the side of the spine. In sarcoma the bone is quite healthy close up to the margin of the growth ; and there are no firm caseous patches in the interstices of the cancellous tissue. Fixity of the spiue. — The rigidity during life is due (a) to loss of the elastic discs, (6) anchylosis, and (c) reflex spastic contraction of the spinal muscles. State of tSie spinal cord. — The cord usually escapes even when the disease of the bones is far advanced. It may be compressed by the displaced 2i6 Surgical Pathology. [Chap. xxxi. vertebrae ; or the inflammation may spread to the membranes and set up a localised sclerosis of the cord; or serous effusion into the theca may compress the cord. As the motor columns lie near the bodies of the v-ertebrse, paralysis of motion comes on earlier, is more marked, and often occurs without paralysis of sensation. The ciu'vatiire of the spine (kyphosis) is angular, for the disease is mostly confined to a few vertebrae. In rickets and chronic rheumatic disease the curves are uniform. ISpiiial a.fescesses (retropharyngeal, mediastinal, psoas, lumbar, etc.) are often very large. They m.ay dry up, leaving a cheesy residuum. At a later period suppuration may start afresh at the seat of the previous disease — residual abscess. {Vide Chronic abscess.) Process of cure. — As the disease subsides osteoplastic ostitis succeeds the caries, and in the end the eroded vertebrae are fused into a mass of bone much denser than the original cancellous tissue. Less commonly bars are seen to bridge over the hollows caused by absorption, which are not entirely filled in. It differs from united fracture of the bodies of vertebrae, for whilst in caries the intervertebral discs are to a great extent destroyed, in fracture they remain quite healthy close up to the circumscribed compact ossified callus. Sypliilitic caries and necrosis. — Syphilitic caries affects principally the tibia, cranium, nasal, bones, palatine arch, and sternum. It begins as a periostitis and superficial ostitis, or as a gummatous tumour in the substance of the bone. The osseous traV)eculae are absorbed in the same manner as in simple rarefying ostitis. In the cranial vault there are frequently a number of these deposits, which are slowly absorbed either spontaneously or as the result Chap. XXXI.] Syphilitic Caries and Necrosis. 217 of treatment. The loss of substance is not made good, so that permanent depressions are left in the outer table, and these are increased in depth by the heaping up of new bone around them. But there is a more formid- able form, in which the caries spreads over a wide surface, and gives it a pecu- liar, worm-eaten appearance. Like the nodular form of the disease, it ma J occur with or without sup- puration. It sometimes ex- tends throucrh the entire thickness of the bone, so that the inner plate is as irregu- lar as the outer. When the inflammation is more intense the vessels are obliterated to such an extent that the affected portion dies. Fig. 28 shows a carious sequestrum. It is surrounded by a narrow trench, which in the recent state was filled with granulation tissue. According . to Yirchow these sequestra are invari- ably the consequence of acute strangulation of the vessels. Cornil and Eanvier maintain that they sometimes result from an excessive interstitial de- posit of new bone, which goes on until the Haversian canals are completely filled. It seems Fig, 28. — Syphilitic Disease of the Craninm, a, Ossified node ; 6, sequestrum ; c, carious surface of settuestrum ; d, apertures formed by detachment of sequestra. 2i8 Surgical Pathology. [Chap. xxxi. strange that an osteoplastic ostitis should entail necrosis. Total necrosis of the diaphysis of a bone as the result of syphilis is very rare. Fig. 33 represents two tibiae from the same leg. The original shaft (a) separated sjjontaneously after necrosis. It was re- placed by a new one. (b) The patient, a woman cet. 22, died from acute yellow atrophy of the liver ten years later. Necrosis coBitrasted witli caries. — 1. The part affected. — Caries is more common in cancellous tissue^ necrosis in compact. The blood-vessels are better supported in compact bone, and so less liable to passive congestion ; but from the narrowness of the canals they are quickly strangulated by the pressure of the exudation, and so the bone is rapidly and completely deprived of its vitality. In cancellous bone there is room for dilatation and exudation, without their causing a sudden stasis in the vessels. Moreover, as the inflammation is less intense, more time is given for the enlargement of the vascular channels by absorption of the bone. 2. Result cf probing. — In necrosis the probe is suddenly arrested by striking against hard bone, and without giving rise to pain ; whereas in caries it can be felt to pass through soft inflamed bone, and this is quite sensitive. 3. Nature of the discharge. — In necrosis the dis- charge is mostly purulent ; in caries it is more watery or serous, and contains a greater amount of lactic acid. 4. Granulations along the sinus and at its orifice. — In necrosis they are comparatively healthy, often fungous and florid. In caries they are small : or large, pale, and cedematous. But they are subject to so much variation that little reliance can be placed upon their evidence. 5. Cause. — The more acute the cause, whether it be Chap, xxxii.j Osteoplastic Ostitis. 219 a local injury, or constitutional state such as an acute specific fever, the more likely is the inflammation to eacl in necrosis. In scrofula caries is more common than necrosis. In syphilis both necrosis and caries are frequent. CHAPTER XXXIL OSTEOPLASTIC OR FORMATIVE OSTITIS AND PERIOSTITIS. It has been shown that inflammation of bone, according to its severity, leads to necrosis, rarefaction, or new formation, and that these results may be seen side by side in the same specimen. The ossific deposit is either superficial or interstitial (internal). From the intimate connection between the perios- teum and adjacent bone, it is impossible for one to be affected without the other being involved sooner or later. It is true the morbid process may go on in the periosteum for some time without appreciable alteration in the bone. Acute inflammation ends in resolution, suppura- tion, necrosis, or it becomes chronic ; chronic leads to caseation, cold abscess, caries, or the formation of osteophytes alone. Chronic osteopla stic oistitis and periostitis occurs under many conditions. It may indicate a deep- seated destructive inflammation, as central caries ; or arise from injury, or the irritation of a chronic ulcer, or some constitutional state such as syphilis, rheumatism, etc. Anatomical changes. — The periosteum is at first succulent and thicker and redder than natural. 2 20 Surgical Pathology. [Chap. xxxii. Tlie fibrous and medullary layers lose their distinctive outline. The Tvhole is infiltrated with exudation cells, and can be easily separated from the bone. The connective tissue around the blood-vessels in the Haversian canals of the compact bone is increased in like manner. It is probable that in most cases rarefaction of the bone takes place to a slight extent. As organisation advances the periosteum acquires a greater density, it has fewer cells, and these are more elongated. Lime salts are deposited around the vessels as they pass from the bone to the periosteum, and the embryonic cells are imprisoned in the matrix as bone corpuscles. The new osseous trabeculse stand at rio-ht anoies to the surface of the old bone. Whilst there is continuity of structure between the osteophytes and subjacent bone, the former can be easily detached at this early period. The new bone is at the first quite porous, and it may remain so; but in some cases the deposit does not cease until it is as dense as ivory. Varieties of osteopliytes. — 1. In an unreduced dislocation a false joint is constructed, and to give security to this new bone is deposited where the pi-essure is intermittent, i.e., where it is exerted only in certain positions of the more movable bone. Thus, in subspinous dislocation of the shoulder the buttress of support is situated on the dorsum of the scapula. Here it is seen as an isolated compact mass, looking as though it had been soldered on to the healthy surface from which it springs, there being no sign of caries or necrosis. Such an osteophyte is coarsely furrowed and convex on one side, somewhat smooth and concave on the other. Its isolation at once dis- tinguishes it from chronic rheumatic arthritis, which at first sight it resembles. 2. In chronic rheumatic arthritis each bone entering into the formation of a joint has rounded outgrowths Chap. XXXII.] Osteophytes. 221 about tlie whole articular margin. They appear as if they had once been in a softer condition, and had become gradually solidified, for they droop like melted tallow or wax that has congealed on cooling. They really sjrow in aireat measure from cartilacje. The articular surfaces are eburnated from the same sclerosing ostitis (Fig. 38). 3. In strumous arthritis and caries the extent of bony deposit fluctuates widely in different prepara- tions ; it may amount to a mere roughening of the surface, or form closely- packed hard craggy masses, that bear the same contrast to the osteo- phytes of dry arthritis as do stalactitic rocks to water - beaten boulders. The articular surface is usually porous from caries (Fig. 36), 4. In chronic ulcers of the soft parts, lying near to a bone {e.g., vari- cose ulcer of the leg), the deposit, from irrita- tion of the periosteum, forms a flattish mass, gently sloping to the healthy bone. The sur- face is porous, but fairly uniform. 5. In rickets, when the curvature of a lono- bone IS very decided, the concavity is occupied by a beam of compact bone thrown out to support the arch (Fig. 12). %■ Fig. 29. — Acicular Outgrowths of Bone in the Base of a Sub- periosteal Sarcoma springinsr from the Epiphysis of a Long Bone. 22 2 Surgical Pathology. Chap, xxxii. 6. In ossifying 'peripheral sarcortias of bone, the new bone radiates from the surface of attachment in the shape of long delicate needle or spray-like pro- cesses, that bear the impress of a centrifugal growth so characteristic of these tumours. They are, in fact, easts of the intervascular spaces. 7. Bony tumours. (Vide Osteomata.) 8. In locomotor ataxia. (Vide Trophic lesions.) Nodes. — A node is a localised inflammatory thickening of bone. At first it consists merely of a soft vascular swelling of the periosteum and surrounding tissues. This may disappear, or break down and ulcerate, or ossify. It is very tender on pressure, and usually gives rise to tensive aching pain (vide Pain), especially at night, when increased warmth causes a fluxion to the part, and the patient's attention is concentrated more upon himself. Varieties of nodes. — Nodes are classified as to their anatomical condition, ossified, carious, etc. ; or as to their cause. The latter basis is here em- ployed. (1) Simjole nodes are due to injury, and hence they are most common in the bones that are least pro- tected, e.g., the tibia. (2) Syphilitic nodes are met with both in acquired and congenital syphilis. In the acquired form they may be located on any of the bones, but the seats of election are the tibiae, cranium, clavicles, and ulnse. As a rule, they ossify ; but, if left untreated, they frequently break down. They belong to the tertiary stage of syphilis. They are simulated by erythema nodosum ; but the latter disease afiects younger peoj^le, generally females ; it is more transient ; the part is movable over the bone ; and it never suppurates. (For de- scription of congenital syphilitic nodes, vide Osseous lesions of congenital syphilis.) Chap. XXXII.] Internal Osteoplastic Ostitis. 223 (3) Eheumatic nodes. Besides the masses of bone thrown out around the joints in dry arthritis, small painful nodes occasionally form in other parts. (4) Typhoid nodes. During an attack of typhoid fever, or whilst convalescence is being established, the periosteum may inflame over localised areas. These nodes, like most others, are generally situated on the tibiae. Their tendency is to disappear ; they rarely suppurate, and still more rarely end in necrosis. In a case I was called to at the London Fever Hospital, the patient, a young adult male convalescent from typhoid, was the subject of several recent nodes, which disappeared after a short time. On the same bones (tibise), were old ossified syphilitic thickenings. Internal osteoplastic ostitis. Synonyms. — Diffuse hypertrophy, condensing ostitis, sclerosis ossium. Causes. — In many cases no cause can be ascer- tained. In some there is a history of syphilis. I lately had under observation two patients, the sub- jects of congenital syphilis, in whom the hypertrophy of bone was most marked. In one, a male aged eighteen, there was characteristic notching of the teeth ; the tihice were enlarged throughout, much elongated, and curved forwards ; the osseous lesion had existed for years. The mother of this patient was under treatment at the same time for syphilitic nodes of the tibise. The second case was that of a woman aged twenty-two ; the teeth were notched and the cornese nebulous from past keratitis ; the left radius was uniformly rounded, thickened, elongated, and bent in a strong outward curve. There can be no doubt but that these two patients suffered from diffuse interstitial ostitis ; for peri- ostitis alone, whilst it would accoim.t for the circum- ferential enlargement, would not explain the marked elongation and curvature. 2 24 Surgical Pathology. [Chap, xxxii. Ostitis deformans. — We are indebted to Sir James Paget for a description of this remarkable affection of the osseous system, which is usually found in persons past the prime of life. It does not appear to be due to syphilis, as, in some cases, there is an absence of specific history, and the malady runs its course unchecked by treatment. It attacks several bones at the same time or in sequence ; those of the skull and lower extremities are particularly liable to suffer. From the multiplicity of the lesions, the disease may be considered as one of the osseous system in general, and not a chance affection of one or more bones. The long bones, e.g., the femora, are curved in spite of the increase in thickness ; this can be ex- plained by the fact that during the early stages the bone is rarefied and weakened by the inflammation. At the end of the process, however, there is marked increase in density, and the medullary cavity of the hollow bones is obliterated. The surface is roughened from periosteal deposit (Fig. 13). The skull may be three-quarters of an inch in thickness ; there is general hypertrophy of the tables, with filling-in of the diploe and obliteration of the sutures. The disease is very chronic, lasting through many years, and during this time the general health may not suffer. It is noteworthy that, after the lapse of years in several instances, the bones have been found to be the seat of malignant tumour (sarcoma). Butlin's observations show that the initial lesion is inflammatory. Hypertrophy of tlae facial bones, pelvis, etc. — Billroth says, " In such cases the bony deposits are spongy, puffed, nodular, so that the bone acquires a resemblance to skin affected with elephantiasis." The etiology is quite obscure Chap. XXXIII.] Acute Periostitis. 225- Senile thick ening^ of the skull. — In old people the cranial bones are often thicker and denser than normal j the diploe is replaced by solid bone. It is probably of the nature of a nutritive degeneration (like enlargement of the prostate), with increased formative activity. CHAPTER XXXIIL ACUTE SUPPURATIVE PERIOSTITIS, OSTITIS, AND OSTEOMYELITIS. When it is remembered that there is direct structural continuity between the periosteum and the medulla contained in the Haversian canals of compact and cancellous bone, and, in the case of the hollow bones, that of the central cavity as well, it is no matter of surprise that acute inflammation begin- ning in one or other of these situations should spread through the entire tract. Acute suppurative or phlegmonous periostitis can- not occur without ostitis ; osteomyelitis almost to a certainty entails periostitis ; yet, for clinical purposes, it is found convenient to treat of them separately. Acute periostitis and periosteal abscess. — The periosteum consists of two layers. " The deeper, which is applied to the bone, is formed of delicate fibres of elastic and white connective tissue ; it forms a kind of aponeurosis. The superficial stratum is much looser in texture, and i*s made up of an areolar meshwork, in which the vessels ramify and anastomose before penetrating the bone. It is in this tissue that acute periostitis usually begins. At first it is swollen and red from vascular congestion ; this is quickly followed by a rapid exudation of leucocytes and liquor p 2 26 Surgical Pathology. [Chap. xxxiii. sanguinis, so that the membrane is converted into a purplish pulp. The formed elements melt away, and the debris mingling with the purulent exudation from the vessels, the abscess is fully formed. Thus we see that the periosteum is destroyed by the inflammatory process, which meanwhile has spread to the surround- ing soft parts (muscle, cellular tissue, skin, etc.), and has made them highly oedematous. The wall of the abscess is bounded below either by bare bone or granulations, and superficially by a layer of inflamed tissue. At the same time, the superficial portion of the bone is infiltrated with pus cells, and part of the exudation, collecting on the surface, raises the periosteum ere the fibrous layer has completely softened (periosteal abscess). This is the explanation of the so-called "burrowing of pus and stripping-ofi" of the periosteum." When the bone is deeply seated, an enormous accumulation of pus may form around it. When superficial (e.^., the anterior part of the tibia) the abscess usually points quite early. In some cases the process is so acute that beads of pus may be seen on cutting into the inflamed part within thirty-six hours from the onset of the disease. When due to injury, the abscess is usually localised. When arising from constitutional causes, it is often very difiuse ; this is notably the case in children. Terminations. — The periosteum may be de- stroyed over a considerable area, and yet the bone survive ; but the cutting off of the blood supply from the surface, and the great tension on the vessels in the compact tissue, place it in imminent peril of death. Early and free incisions by draining off the exudation and unloading the engorged vessels may prevent suppuration. Even when pus has formed, resolution is some- Chap. XXXIII.] Osteomyelitis^ Osteophlebitis. 227 times rapid and complete after the bursting or opening of the abscess. In such cases the granulation tissue that bounded the purulent collection superficially applies itself to the bone, and organises into a new periosteum. There is probably in all cases a certain amount of new bone deposited on the surface of the old, and in the Haversian canals of the compact tissue. Necrosis is not rare. Acute osteomyelitis. — Acute osteomyelitis forms part of a general inflammation of the soft tissue of bone ; or it is set up by destructive disease of a contiguous joint, or it arises as a primary affec- tion. As the exudation is pent up under high pressure, and there is no possibility of an early spontaneous evacuation, necrosis is almost certain to follow. The patient often dies poisoned by the septic matter before the sequestrum is loosened. The inflammation may lapse into a chronic state, an exit for the pus being provided by operation, or the opening up of channels in the bone by rarefying ostitis. Osteophlebitis, or osteo-thrombosis is a concomitant of osteomyelitis, whether pathological or traumatic. The coagula are very liable to dis- integrate and break up into emboli, for they are steeped in a highly irritative or infective fluid. Moreover, as the veins lie in rigid canals, to the walls of which they are adlierent, thej are unable to collapse when divided or torn. 228 CHAPTER XXXIY. OSSEOUS LESIONS IN CONGENITAL SYPHILIS. Affections of the osseous system in congenital syphilis stand midway between those of the skin and the viscera in order of frequency. Our knowledge of the subject has been mainly derived from the researches of Wegner and Parrot abroad, and Drs. Barlow and Lees in this country.* In one way or another, every part of the skeleton is liable to be diseased, but the points of greatest interest are centred in the long hones, the cranium, and the teeth. Cranial bones. — The lesions here are of two kinds (1) atrophic; (2) osteophytic. Localised wasting of the cranial vertex is met with in the parts most subject to pressure from de- cubitus, and it is all the more marked if at the same time there is an increase of fluid in the cerebral ventricles. The usual situation is the parietal bone behind the eminence, but it has been observed in the occipital and squamous bones. The bone is gradually absorbed until nothing is left but a thin plate, or membrane, of parchment-like consistence, wliich readily yields under the pressure of the finger. The same condition occurs in rickets, but not so frequently as in congenital syphilis. The absorption leads to a well- marked depression of the inner surface of the bone. It is a case of atrophy from continued pressure acting upon a tissue preternaturally soft and weak. The process is designated craniotabes. It is found * An admirable account of the lesions is contained in the Transactions of the Pathological Society, vol. xxx. Chap. XXXIV.] Parrot's Nodes. 229 in very young infants. M. Parrot has described another form of atrophy, which he terms "gelatino- form." As the name denotes, it consists of conversion of the bone into a soft material. It begins beneath the pericranium, but rarely spreads as far as the dura mater. It cannot be diagnosed during life. Parrot's osteophytes or nodes are subperiosteal de- posits of new bone (Fig. 30). They are situated upon the four processes that bound the anterior fontanelle, to which they give a natiform appearance. Other de- posits are usually found upon the parietal bones, and chiefly along the co- ronal and saojittal sutures. It will be seen that they affect neither the frontal nor jDarietal eminen- ces, nor the sites of craniotabes, or only in very severe cases. The new bone is very vascular and porous when first formed. It consists of a series of trabe- culse, between which are spaces filled with a pulpy marrow. The vessels run at rio-ht angles to the Fig. 30.-View of Outer Surface of Cranium surface of the skull. afEected with. Congenital Syphilis. Tbp "KnmT- f»T>Ti « and 6 point respectively to a frontal and parietal j-Aic KJKixiy ciiii- nodeorhoss. These nodes are composed of bone of a coarser texture than that which bridges over the anterior fontanelle, d; c, fronto-parieral suture ; throughout the greater part of its extent It is obliterated by ossiflc deposit ; e, i)arietal eruinence. The natiform nodes bounding the anterior fontanelle are somewhat too sharply defined in the diacrara. The preparation is in the Museum of the Hospital for Sick Children, Gre.-it Ovmond Street, and is represented here by permission of Dr. D. Lees. nences may attain a thickness of more than half an inch at their centres. The f r o n t o - 230 Surgical Pathology. [Chap. xxxiv. parietal sutures are sometimes obliterated by an extension of ossification from one bone to the other. These osteophytes are quite characteristic of con- genital syphilis. In the majority of cases they form between the sixth and twelfth month. Ulcerating nodes, though common in acquired syphilis, are ex- cessively rare in congenital ; Barlow records one such case. The long- bones. — As in the cranium, the disease shows itself in two forms, atrophic and productive. The atrophic changes are seen in the growing layer of the tissue on the diaphysial side of the epiphysial cartilage. It is sometimes described as an osteo- chondritis, but it appears to consist essentially of a deviation from normal development. The inflammatory changes are secondary, and dependent upon injury. There are two distinct changes : (1) an excessive deposit of lime-salts in the cartilage matrix and capsules, and imprisonment of the cartilage cells. This, whilst it increases the brittleness of the part, puts a stop to the ossification ; (2) an overgrowth of gela- tinous medulla or spongeoid tissue in the ossiform layer (that next the cartilage) ; this absorbs the pre- formed bone, and may end in complete separation of the epiphysis. The fragility due to calcification, and the softening caused by " gelatiniform atrophy " render the bone liable to bend or break on the slightest injury. Then the irritation caused by the injury sets up a veritable inflammation, which may end, though rarely, in suppuration. If the child survives the cachexia of the disease, the epiphysial lesion subsides, and ossification goes on in the normal way. When the morbid process is in progress the limb hangs helj)lessly from the trunk. Parrot calls this condition "syphilitic pseudo-paralysis," to distinguish it from essential or infantile paralysis, of nervous Chap. XXXIV.] Syphilitic Teeth. 231 origin, in which there is actual powerlessness of the muscles. Osteophytes form, as a rule, after the sixth month of extra-uterine life. The bones most frequently affected are the tibia and humerus. I have seen symmetrical osteophytes on the upper ends of the ulnse. They consist of highly vascular spongy bone, the trabeculse of which stand perpendicularly to the axis of the limb. They are usually constructed of a number of superposed lamellae, united by narrow bars or columns, imbedded in a soft medulla. Sometimes the osteo- phytes are quite soft, and are made up of fibro- vascular tissue. Between the two forms there is every gradation. The tibial, ulnar, and radial osteophytes are mostly situated at the upper epiphyses; the humeral at the lower. In the scapula they are found in the spinous fossse ; in the hip, the external iliac fossa. Maxillae and teeth. — The characters of the teeth described by Mr. J. Hutchinson consist of mal- formation and defective structure. Those most commonly affected are the upper permanent central incisors. Instead of the borders of the cutting edges being in contact, they are separated by a gap. There is a central indentation or notch in the place that should be occupied by the middle tubercle. The lower incisors are sometimes pegged, and the canines (upper and lower) more pointed than natural. The inilk teeth are subject to early decay and premature shedding. The date of eruption is not deferred, as it is in rickets (Eustace Smith). Mr. Hutchinson attributes the mal- development to specific stomatitis, which affects the gums, periosteum, and bone in infancy. The above- described lesions, which are incidental to the early stages of congenital syphilis, are sometimes associated with falling in of the bridge of the nose from defective growth of the nasal bones, the result of inliammatory 232 Surgical Pathology. [Chap. xxxv. changes. There may also be rarefaction of the diaphyses of the long bones coincidental with atrophy and enlargement of the epiphyses. In the tertiary period serious lesions are met with; to wit, caries and necrosis of the nasal and other bones, hypertrophy of the long bones from diffuse interstitial osteoplastic ostitis, and localised thicken- ings from osteo-periostitis (nodes) CHAPTER XXXV. NECROSIS. Necrosis happens when the circulation in a portion of bone is permanently arrested, from injury or disease. In the former case, if many vessels be ruptured by violent concussion or fracture, the current through them is arrested by thrombosis in the torn ends, and by the pressure of extravasated blood. In fracture, too, with considerable displace- ment of the fragments, and especially if there be much splintering, portions may be entirely denuded of periosteum. Should the bone survive these accidents, it has to cope with the obstruction from inflammatory exudation, so that it is not surprising that necrosis is often of traumatic origin. Syphilitic ostitis leads to necrosis, either imme- diately, by occlusion of the vessels from the pressure of the effusion, or more remotely through the Haversian canals becoming narrowed by deposit of new bone within them, until at last they become entirely, or all but, obliterated, so that the blood supply is too scanty to support the life of the affected part. Chap. XXX V. ] Super ficia l Necr osis. 233 When discussing the subject of abscesses in carious epiphyses it will be shown that they often contain sequestra of considerable size, the result of acute ostitis, or of caseation of tracts of granulation tissue, with thrombosis of the vessels. According to Cornil and Ranvier, caries is essentially due to primary fatty degeneration of the bone corpuscles, which entails a death of the osseous laminse within their territories. They assert that these laminse then act as irritants, and set up a rarefying ostitis which gradually absorbs the bone, accompanied or not by further necrosis. Lastly, whatever the cause of arrested circulation, bone succumbs with other tissues in a general gangrene. Superficial necrosis, exfoliation. — A good example of this is seen in injuries to the cranial vertex, where the pericranium is destroyed, with probably some slight extravasation into the diploe and external plate. Unless the dura mater be detached, the inner table escapes death, for it is plentifully supplied by the meningeal vessels. Inflammatory effusion completes the stasis in those parts already crippled, but it must not be supposed that the inflammation is limited to the part that dies, for it gradually subsides into the healthy bone. The layer that is continuous with the necrosed portion becomes rarefied by absorption, the granulations thrusting their buds through the walls of contiguous Haversian canals, so that the latter open into one another. Finally the attenuated osseous laminae disappear, and the dead part is cast off. These changes take place chiefly in the tissue that has re- tained its vitality, but that the inflammatory new formation is able to absorb dead bone is proved by the erosion of ivory pegs employed in ununited fractures. Moreover, it is not rare to find perforations of thin superficial sequestra by pink granulations, a welcome sign to the surgeons, for it tells at once of the shallow depth of the necrosis. It is this riddling of the bone 234 Surgical Pathology. [Chap. xxxv. that causes it to crumble down during detachment. The source of irritation being removed, the layer of florid embryonic tissue that covers the surface begins to organise. The new bone is deposited around the vessels. It acquires considerable density. A new periosteum is constructed from the outer layer of granulations. The exact method of absorption of bone is not known. Virchow believes that cells (osteoclasts), derived from proliferation of bone corpuscles, are the active agents. E/indfleisch suggests that the blood in the congested vessels containing an excess of carbonic acid may dissolve the lime salts, forming an acid carbonate. Others suppose that lactic acid is de- veloped, and that this, combining with the earthy base, forms soluble calcic sarco-lactate. The two latter hypotheses are improbable, for bone exposed to the action of pus for months or years loses little or none of its substance, and it retains its smoothness of surface from the time when it becomes sequestrated. Whilst denying the origin of the bone-destroying cells ascribed by Yirchow, I believe his view of absorption by the vital action of living matter to be quite rational. An exfoliated lamina of bone is smooth on the outer surface, where it undergoes no change of structure in the osseous framework, but it looks worm-eaten on the under surface, the indentations having been formed and occupied by vascular granulations. If vertical sections of artificially-softened bone be made during the process of separation of a sequestrum, it will be seen that the Haversian canals of the necrosed portion are empty, or contain nothing but the debris of disintegrated marrow, whilst the spaces of the living bone are filled with embryonic cells and blood- vessels in a state of active proliferation. Picro- carmine stains the osseous trabeculse yellow, and the granulation tissue red, and shows a beautiful layer of Chap. XXXV.] A^ECROSIS. 235 S 3. -—b demarcation which ends abruptly, and is most intense in colour next the dead bone, but gradually fades away into the living. The adjacent periosteum is infiltrated with indifferent cells, especially in the deeper part. Pus escapes from the vessels of the granulations at the margin, and also beneath the sequestrum when this is loose. Necrosis of an amputation stump. — Am- putation through a long bone is a good example of compound fracture, and the wonder is that necrosis does not more frequently result, for the vessels of the me- dulla and periosteum are severed, and their ends compressed by ex- travasated blood, and necessarily plugged by clots. At the same time, the vitality of the bone may be impaired from disuse or existing in- flammation, both of which conditions readily allow of detachment of the periosteum if trac- tion be made upon the flaps. Without exception, the injury inflicted by the operation sets up an inflammatory reac- tion ; the medulla of the central canal, that contained in the substance of the bone, and the periosteum, all show acute hypersemia — c •a Fig. 31.— ISTecT'osis of Femtir after Amputation of Tliigh. a, dead bone more extensive on medullary aspect ; c, new bone deposited from periosteum, adherent to h, the living por- tion of the shaft, hut free from the necrosed portion, a; d, medulla deeply congested andhsemorrhagic ; e, the same, decolorised and purulent, in process of disintegration. 236 Surgical Pathology. [chap. xxxv. and exudation, and return to the embryonic state. This is followed by a rarefying ostitis. In ordinary cases the inflammation does not go beyond this, but, subsiding, ends in a condensation from deposit of new bone, which greatly narrows the vascular channels, and fills the open end of the medullary canal. Upon the completion of these changes, atrophy from partial loss of function sets in, and the end of the bone there- by becomes conical. In the event of necrosis, one or more of the hindrances to the circulation is increased ; thus, the periosteum is stripped off to such an extent that the bone cannot recover itself, or a central osteomyelitis destroys the medulla (Fig, 31). The sequestriun. — Stasis from the latter cause usually exceeds that from the former, and so the necrosis is more extensive on the inner aspect, account- ing for the sequestrum appearing in the shape of a truncated cone, whose outer surface is excavated into shallow pits and grooves by the granulation tissue during the process of separation. Whilst the rarefy- ing ostitis is going on in the substance of the bone, in order to set free the dead portion, ossification is pro- gressing in and beneath the periosteum, so that the outer surface becomes incrusted with soft spongy bone. "When once the sequestrum is removed, and it usually requires an operation to effect this, the subsequent changes differ in no way from those occurring in the healing of a stump by granulation without necrosis. These sequestra vary much in size. They may be many inches in length, and of great thickness, or so small as to break in pieces during attempts at removal. Their lower ends are sometimes smooth on the outer surface for a short distance, showilng that the periosteum was destroyed to a like extent, and that the granulations left untouched the denuded bone. In other cases the outer surface is smooth, and the Chap. XXXV.] Central Necrosis. 237 inner rough throughout, the loss of vitality being more of periosteal than medullary origin; it is, in fact, superficial, and not central necrosis. Whatever the variety, the general shape is quite characteristic, ending abruptly below ^vith a sawn surface, tapering above. The cavities from which they are removed are never bare, but are lined by a soft, vascular, pyogenic membrane, which, increasing, soon fills up the spaces and ossifies. Central or internal necrosis may ensue from osteomyelitis, without a previous loss of continuity in the bone, the osteomyelitis being either primary, or forming a part of a more widespread lesion of periosteum and medulla. In the former case it begins (1) as an acute suppurative inflammation in the central canal, when it is often fatal before the sequestrum is loose ; or (2) as an ostitis of the can- cellous tissue of an epiphysis, which spreads to the interior of the shaft. In young people the epiphysial cartilage is perforated by the advancing disease. In this variety the march of events is less rapid, so that there is time for the inflammation to subside, and the dead bone to be thrown ofi" into the medullary canal. Relief is given to the tension by the bursting of an abscess which communicates directly with the exterior, or in a more roundabout way by the con- tiguous joint. Scrofula is often at the root of the evil, so it is not surprising that caries and joint disease complicate this form of necrosis. The medullary canal becomes flUed with granulation tissue and pus, in which the sequestrum is imbedded. Outlets to the purulent exudation are made here and there by absorption of the osseous trabeculse, where the tension is greater than elsewhere. These outlets, which in the case of bone are called cloacce, correspond to sinuses in the soft tissues. 238 Surgical Pathology, [Chap. xxxv. Central can always be told from total necrosis by the se- questrum appearing rough and worm- eaten in the former, smooth in the latter. The encasing shell of bone is entirely of new formation in total necrosis, where- as in central necrosis it is composed of the outer portion of the original shaft, thick- ened by external de- posit. Sequestrotomy is necessary for the liberation of the se- questrum, which, so long as it is retained, keeps up suppura- tion, a cause of hectic fever, phthisis, and lardaceous disease. Nature, unaided, seems content with lowering the tension to the level of chronic inflammation. Acute total It necrosis. is Fig. 32. — Necrosis of the Femur. The sequestrum, a, liad been locked up f oi- eight years, and had by its weight and friction bored a passage through the epiphysis into the knee-joint (atrophy from continuous pressure) ; the articular cartilages are but little affected ; h, cloaca through which the pus escaped from the sequestrum cavity, which in the fresh state was lined with granulation tissue ; c, new hone ; d, osseous deposit that bas filled in the medullary canal; e, patella ; behind this, the tibia and fibula. (Half natural size. ) Chap. XXXV.] Acute Necrosis. 239 impossible, clinically, to draw a hard and fast line between so-termed partial and total necrosis ; indeed, such a division is unnatural, for many of the cases com- plete in the pathology of the disease in question fall short of death of an entire diaphysis. The symptoms and morbid signs are, notwithstanding, so marked as to justify a special description. Stripped of its details, the history runs thus : An often unaccountable onset, rapid progress, tendency to end in a fatal pyaemia, with secondary lesions, and liability to select the periods of childhood and youth. It is an acute sup- purative or phlegmonous inflammation of the growing part of bone, at one time limited to a periostitis and superficial ostitis, at another involving the destruction of the epiphysial cartilage, and even the entire medulla. The epiphyses themselves, as a rule, escape, or, at any rate, are not affected past recovery, although the inflammation may spread through them to the con- tiguous joints. Causes. — Injury, acute specific diseases, such as scarlet fever and measles, and exposure to wet and cold, have been assigned as the causes, but at most they can only be considered as exciting agents. There must be some underlying disposition on the part of the tissues attacked. Diagnosis. — The severity of the constitutional symptoms and the obscurity of origin account for many of the mistakes in diagnosis. Children are sometimes brought to hospital because a supposed erysipelas or acute rheumatism has not run an expected course, the first idea of the real state of things being aroused perhaps by the evidence of fluctuation over a bone ; and even this may be overlooked, the enigma being solved on the post-mortem table. A previously healthy girl of fourteen was treated for rheumatism, but getting rapidly worse, with high fever, wide-spread 240 Surgical Pathology. [Chap. xxxv. muscular spasm, and delirium, was taken to the medical ward of a hospital, where at first the possibility of cerebro-spinal meningitis was entertained, there being no apparent sign by which to localise the disease. After death, the right clavicle was found lying in a bed of pus, and the lungs riddled with small metastatic abscesses. Subject to these important exceptions, the local signs can scarcely be mistaken. The tensive pain and exquisite tenderness, the redness of the skin, and the fluctuation or bogginess of the part, tell their own tale. Dissection. — Tlie skin and cellular tissue appear congested and highly cedematous, the periosteum is detached to a variable extent, and the bone over the same area is bathed in pus. The epiphyses may be found loose, and the joints healthy or inflamed; in the latter case, either by the spreading of the local disease or by metastatic infection. If the bone be sawn vertically, the central medulla will present a deep red colour from congestion, with here and there patches of capillary extravasation, interspersed, perhaps, with collections of pus, which are generally situated at the periphery, the canal for the nutrient artery forming a purulent tract, that connects the superficial with the central suppuration. The compact and cancellous tissue presents a mottled appearance in place of the difiused pinkish- white tint of healthy bone, for the spaces are occupied by purulent exudation and dilated vessels, which are filled with dark deoxydised clots. Later on, of course, the contents of these spaces disintegrate, and leave the bare osseous framework v/hite or yellowish-white, and lustreless. Venous thrombi within and without the bone may be softened, and ready to develop a septic embolism. If any part of the bone escape death, it be- comes encrusted with ossific deposit, which forms an Chap. XXXV.] ACUTE Necrosis. 241 appreciable layer within ten days, provided the tension has been relieved by incision. Should the necrosis not be total, it is the deeper portion of the bone that survives, for this receives its vascular supply more directly from the large vessels, the higher arterial pressure tending to check blood stasis ; and being deeply seated, it is better supported and less exposed to injury. The tibia is affected more often than any other bone. Complicated l>y pysemia. — In this disease the blood becomes charged with infective matter, but how it originates is uncertain ; not necessarily by contagion through a wound, for, as before said, all the signs of virulent pysemia may arise without the local abscess having been opened. The theory of autogenetic origin is not borne out by facts, and this being granted, we are driven to suppose that whatever the materies morbi may be, it is introduced by the skin, or, more likely, by the mucous membranes. The analogy furnished by the acute specific diseases supports this view. At the same time, there can be no doubt but that it finds a suitable nidus for development and reproduction in the products of the local in- flammation. The living structures strive to get rid of matter obnoxious to themselves, and do their best to destroy any organisms that infest the blood and tissues ; but they may be overpowered by the intensity of the initial infection, or succumb to the continued absorp- tion under high pressure from the seat of primary suppuration. Early and free incisions, by lowering the tension, check the progress of the inflammation, and diminish the risk of blood-poisoning by providing for the escape of the exudation. Repair. — The loss of the whole or greater portion of a shaft is replaced by new bone, deposited from Q 242 Surgical Pathology [Chap. XXXV. \-l a any of the original j)eriosteum that may have remained, and from the fibrous structures around; nor is it necessary, as was formerly supposed, that the necrosed bone should be left for a long time to act as a stimulus to ossifica- tion, recent practice having shown that early " subperiosteal I I iiii resections " are suc- cessful. I have seen complete restoration of the diaphysis of a tibia that was re- moved on the tenth day from the onset of the disease (Mr. W. Pye'scase).* The younger the patient the greater is the developmental acti- vity, and the more rapid the reconstruc- tion. If the epiphysial ToteTNlo^olis cartilages have been oiailS clestroyed the result of acute Syphi- litic Ostitis and Peri- ostitis. The .sequestnmi separated natu- Mlly, a.s shown hy the irregular worm-eaten ap- pearance of its ends. (One- third natural size.) the new shaft will not attain to the length it other- wise would have done. Phosphorus necrosis of the jaws— The disease is less common than * Lanret, vol. ii., 1879, p. 654. — ShoTvs complete Re- storation of the Shaft of the Bone after original one had been destroyed by Necrosis. From the same subject as A. a, Caries of the new bone ; 6, hridee of bone un itiug th e tibia with tiie fibula. (One-lhird natural size. yide\\. 218.) Chap. XXXV.] Quiet Necrosis. 243 formerly ; for red amorphous phosphorus is used instead of the yellow variety, and workers in phos- phorus look more after the state of their teeth. It is caused by the acid fumes of phosphorus (probably phosphorus acid) acting upon exposed or unhealthy bone in the vicinity of carious teeth. The disease may begin as an acute osteo-periostitis, which rapidly ends in necrosis ; or it may be preceded by an osteo- plastic inflammation. This depends on the intensity of the cause, and the extent of caries of the teeth and exposure of the alveolar process of the jaw. The final result is death of the whole, or a large portion, of the jaw. An exuberance of spongy vascular bone is deposited around the sequestrum, which often takes a long time to separate. Sequestrotomy has been known to cause severe bleeding; in one case the carotid had to be tied to arrest it. " Quiet necrosis." — Sir J. Paget has desciibed a form of necrosis in which the death of the bone and separation of the sequestrum take place without manifest signs of inflammation. In fact, the patient may be quite ignorant of there being anything wrong. This "quiet necrosis" is sometimes internal; more often superficial. The sequestra lie in cavities lined by granulation tissue, but they excite so little irrita- tion that no external openings are formed. The periosteum is "thickened, tough, and little vascular." A similar process is occasionally observed in connec- tion with articular cartilage ; slight injury appears to be the exciting cause. 244 CHAPTER XXXYI. BONE ABSCESS. Bone abscess is either tlie result of an injury, or constitutional disease, such as struma or syphilis. The favourite locality is the end of a long bone ; but it may be found wherever there is a wide tract of cancellous tissue, as in the tarsal bones and the verte- brae. Commencing in a rarefying ostitis, a cavity is formed by the gradual absorption of the bony trabe- culse by granulation tissue ; this granulation tissue, in its turn degenerating, mingles its debris with more recent exudation of pus, and the abscess is completed. At first its walls are composed of soft carious bone, which, if the inflammation spreads, gradually becomes disintegrated, the cavity enlarging at its expense. But here the destructive process may end, and an organising one begin. New bone is deposited around the vessels of the granulation tissue, and this goes on until a zone of hard sclerosed bone has replaced that previously softened. The layer of granulation tissue immediately lining the cavity is converted into fibrous tissue (a kind of end- osteum) ; all formed elements found in the contents of the abscess break down from fatty degeneration, and only a serous or seropurulent fluid remains. In some cases it would appear that the granulation tissue having completely absorbed the bone for a consider- able distance, does not liquefy, but undergoes caseation, the bone around becoming condensed, as described above. More frequent than either of the above modes of termination is a progressive absorption of the bone, Chap. XXXVII.] Mo L LI TIES OSSIUM. 245 until the abscess opens by a narrow orifice, either upon the surface, or into the contiguous joint, or both. At the outset the obstruction to the circulation in the bone may be so great that a portion becomes necrosed, and is afterwards set free in the cavity formed by the more gradual destruction (rarefying ostitis). Bone abscess forms a conspicuous feature in the pathology of many cases of strumous disease of joints. Care should be taken in probing them through a sinus opening externally, as they are often bounded next the joint by the articular cartilage alone, and this might be inadvertently detached. When confined to the interior of the bone, and very chronic, the only symptom perhaps is localised aching, and the chief sign a fixed spot of tenderness to touch. Once opened, they rarely close spontaneously, or, , if so, only for a time. The tension being relieved by discharge, the sinus leading to the abscess cavity shrinks until the re-accumulation of pus again raises the pressure and renders the orifice patent. Tre- phining, by giving a free exit, removes the tension which is the chief local cause of non-obliteration of these cavities. Granulation tissue then encroaches upon the space without hindrance, and organisa- tion into fibrous tissue or bone puts an end to further trouble. CHAPTER XXXYII. MOLLITIES OSSIUM OSTEOMALACIA. This disease is more common in females than in males. It affects chiefly the periods of early and mid-adult life ; it is not found in children. By some 246 Surgical Pathology. [Chap. xxxvii- it is supposed to be a premature senile decay ; but atrophy of the bones of old people does not as a rule assume this form. We may safely conclude that its real cause is unknown. Like rickets, it seems to be the expression of a general disease, or, at least, a morbid state of the osseous system, and not a mere local or accidental disturbance of nutrition in one bone or group of bones. The greater part of the skeleton may be involved ; the vertebrae, ribs, pelvis, and long bones suffer most ; the bones of the cranium, carpus, and tarsus enjoy a much greater immunity. Morbid anatomy. — In the long bones the dis- ease commences in the medullary canal, and then extends to the medullary spaces and Haversian systems of the cancellous, and finally the compact bone. The periosteum seems to take little or no part in the process ; in fact, Rindfieisch ascribes to it a con- servative roZe, and says that, by nourishing the peri- pheral layers of compact bone, it checks, and even prevents, the outermost laminae from being absorbed The disease is a progressive one, and rarely stops before the long bones are hollowed out into mere shells, encased in a parchment-like layer of bone, or riddled with cystic cavities (" cystic degenera- tion "). Billroth mentions two cases of local osteomalacia in the long bones of the extremity ; but, as both were the subjects of caries of the joints, the osteoporosis was probably caused by rarefying ostitis and fatty atrophy from disuse ; the microscopy is not given. In the vertebrae, pelvis, sternum, and ribs it com- mences in several parts of the cancellous tissue at the same time, as shown by the numerous scattered exca- vations. Chap XXXVII.] MOLLITIES OSSIUM. 247 Naked-eye appearances, etc. — In the early stage there is very marked congestion of the medulla, in the central canals of the long bones, and the medul- lary spaces of the cancellous tissue generally. The dark-red colour seems to point to the congestion being passive rather than active. As the vessels are imper- fectly supported, capillary ruptures take place. Later ^•sir-- '^^i>-^^' ~^^^^ "-^^1^ Fig. 34.— Mollities Ossiuni, — Splinter of Bone from the Spongy Substance of an affected Eib. a, Normal Tjone tissue ; 6, decalciQed bone tissue : c. Haversian canal ; d, medul- lary spaces, the one on the left filled with red marrow. Tiie capillary vessels are gaping widely. l-300th. {.After Rindfleisch.) on, cystic cavities are formed by absorption of bony trabeculse and liquefaction of the medulla. These are filled with an albuminous fluid, clear, or turbid from fatty debris, and blood pigment the remains of ex- travasations. When the cysts cease to enlarge they Ijecome lined "with a fibrous membrane, but little vascular. This is derived from organisation of the outer portion of medullary tissue that originally filled 248 Surgical Pathology. [Chap. xxxvii. the spaces, and from fibrous transformation of tlie decalcified bone. The attenuated softened osseous trabeculfe are so soft that they may be bent or cut quite easily. Yery scanty osteophytes are occasionally deposited beneath the periosteum (Billroth). ITlicroscopy. — The capillaries of the afiected medulla in the central canals, cancellous spaces, and Haversian canals, are greatly enlarged. They are embedded in a soft gelatinous substance composed of a homogeneous basis containing embryonic cells, some of which are filled with large fat-drops. The cells are much less numerous than in caries. There are, be- sides, pigment granules and free blood-corpuscles. The natural fat cells disappear. The bony trabeculse bounding the spaces are some- what festooned, but to nothing like the extent as one sees in the form of Howship's lacunae from caries. The lime salts are absorbed before the animal con- stituents, so that there are two distinct zones around the medullary spaces, the one composed of soft de- calcified bone, homogeneous from obliteration of the lacunse and canaliculi, the other of healthy osseous laminae (Fig. 34). Billroth defines the disease as a "fungous fatty osteomyelitis." Cheniisti'y of tlie disease. — Rindfleisch suggests that the actual cause of absorption of the calcareous salts may \)% free carbonic acid contained in the blood of the congested medulla. This seems very doubtful. Weber has demonstrated the presence of lactic acid in the urine and bones, but this is more likely the con- sequence than the cause of osteomalacia. Deformities. — As the morbid process causes rarefaction and softening, the bones are rendered liable to curvatures and partial and complete fracture, the sum total of which is the wide- spread deformities of the skeleton. The mere weight of the super- Chap. XXXVIII.] Diseases of Joints. 249 incumbent parts and the natural muscular contractions is sufficient to produce the most striking results ; thus the ribs are bent by the pressure of the arm in the axillary line. They fall in near their sternal ends and along the attachment of the diaphragm. The weight of the trunk increases the natural curves of the spine, and the vertebrae at the same time undergo more or less rotation. The pelvis assumes a trefoil shape under the action of three forces : the weight of the body, which thrusts the sacral promontory forwards and downwards, and the counter pressure through the acetabula. The long bones may be the seat of many fractures, partial and complete. Mollities ossium contraisted with caries. — (1) Mollities ossium attacks many bones at the same time ; (2) each bone is the seat of scattered foci of absorption and excavation ; (3) the lime salts are absorbed before the organic constituents ; (4) the neoplasia softens and liquefies, but does not caseate ; (5) the cavities formed in the bones have regular walls, which are sometimes lined with a fibrous mem- brane ; (6) the disease has but little tendency to subside ; and (7) it does not begin nor spread beneath the periosteum. In caries the reverse of the above obtains. CHAPTER XXXYIIL DISEASES OF THE JOINTS. When studying the pathological changes going on in an inflamed joint, it is well to direct a systematic attention to the character of the secretion, the synovial membrane, articular cartilage and bones, the fibrous 250 Surgical Pathology. [Chap, xxxviii. capsule, and interarticular ligaments where these exist. It will be found that the anatomical components of a joint are modified individually or collectively, in different degrees and in varying manner, according to the nature of the cause that sets up the morbid pro- cess ; e.g.^ Simple traumatic ai^thritis is characterised by the large amount of serous exudation, with but little tendency to the secretion of pus, whilst the cartilage and bone are practically untouched. Strumous arthritis commonly ends in suppuration and "ulceration of cartilage and bone." Gouty arthritis is marked by a slow, but perma- nent, change in the articular cartilage, deposit of crystals of urate of soda, and recurrent attacks of very painful effusion. Pycemic arthritis causes a marvellously rapid purulent effusion from the synovial membrane, often with comparative freedom from pain. In chronic rheumatic arthritis the most noteworthy features, from a clinical point of view, are the extreme chronicity and steady downward course ; from an anatomico-pathological, the scantiness of the exudation (dry arthritis), the absorption of the articular car- tilages, the eburnation of the bones, and the exuberant growth of osteophytes. Gonorrhaeal rheumatism, is often verv intract- able, and liable to recur again and again. etiology. — The causes of arthritis may be classified as follows : — 1. Traumatism, including the cases that arise from the spreading of inflammation in the continuity of tissue from other parts ; e.g., Si diseased bone. 2. Acute blood-poisoning : (a) the acute specific fevers; and (b) pyaemia and syphilis, gonorrhoea (1). 3. Diathetic states: gout, rheumatism, scrofula, haemophilia. Chap. XXXIX.] Strumous Arthritis. 251 4. Trophic lesions and vaso-motor paralyses : loco- motor ataxia. 5. Degeneration from old age : " senile scrofula." Notice of the previous state of nutrition of the articular structures must not be omitted. When we say that a certain poison selects a certain tissue for its local manifestation, the truth is only half expressed. The tissues play a very important part in the history of the causation of their morbid states. This is nowhere better exemplified than in the joints. In gout there is a great predilection for the metatarsal articu- lation of the great toe. In scrofula it is the hip, knee, and the joints of the hands and feet ; in dry arthritis the hip, shoulder, knee, and temporo-maxil- lary articulation, and the digits ; in gonorrhceal rheumatism the knee and wrist. Previous disease, whilst it increases the liability to subsequent attacks, seems to confer a quantitative protection in some cases. Thus, if a healthy joint be wounded, there is great danger of acute destructive inflammation, gene- ral constitutional disturbance, and high fever. It is very diflferent in the case of one damaged by chronic strumous arthritis. A parallel case is that furnished by the normal peritoneum and an old thickened her- nial sac. CHAPTER XXXIX. STRUMOUS ARTHRITIS. Synonyms. — White swelling ; fungous disease or pulpy degeneration of the synovial membrane ; ulcera- tion of cartilage. Causes. — The disease is common in patients of obvious strumous diathesis. It is likewise met with where there is no other departure from good health. 252 Surgical Pathology. [Chap. xxxix. It may be traceable to an injury as the exciting cause. (Vide Scrofula.) Morbid anatomy. — The disease begins in the synovial membrane or the bone, never in the cartilage. Pathologists differ as to the relative degree of frequency of the two sources. Many believe that in a great majority of cases it starts in the synovial membrane. My own observations lead me to conclude that in not a few instances the bone is primarily affected, especi- ally in the carpus and tarsus. In the hip joint the ligamentum teres is sometimes held to be the seat of the initial lesion, but then it is really the synovial membrane that surrounds the ligament. At first the synovial memhrane is of a bright pink colour ; it looks glistening, and is slightly swollen. The microscope shows dilatation of the capillaries and some leucocytes. Later on, the swelling becomes more marked ; the surface endothelium is shed, and the meshwork of areolar tissue is no lonoer visible. Its fibres have softened, melted away, and the whole is overrun with wandering cells. In short, the folds and fringes have been converted into a pulpy reddish grey mass of gelatinous granulation tissue. By this time the cartilage is involved at the periphery ; it has lost its pearly lustre and firm consistence. The change consists of a mucoid lique- faction of the matrix and a proliferation of the cells. Vertical sections show successively from the free surface a layer of indifferent cells, broods of cells in process of joining one another, cartilage corpuscles in various stages of segmentation, and healthy cartilage. The fiuid in the joint is now thin and cloudy, or seropurulent from the presence of leucocytes and fat particles. The fungous granulation tissue goes on increasing by the development of new vessels and continued exudation until it fills all the crevices of the joint, Chap. XXXIX.] Strumous Arthritis. 25; pushing its way between the bones, and rooting its vessels in the softened cartilage as it passes over it. At length the entire thickness of cartilage is destroyed in patches, and the bone is attacked with rarefying ostitis (caries). In some cases the cartilage is absorbed on the articular and osseous surfaces at the same time, so Fig. 35. — Diagram of a Section of a Knee-joint (the Interarticular Carti- lages have been left out, the Articular Cartilages shaded), with Fungous Inflammation. a, a. Fibrous capsule ; 6, crucial ligament ; c, femur; d, tihia ; e, e, fungous syno- A'ial membrane growing into tlie cartilage ; at/ it even grows into the bone ; at f/ are isolated proliferations of the granulations into the bone on the border between bone and cartilage. {After Billroth.) that flakes are set free in the j oint, whilst other por- tions are so loosened from their attachment to the bone, that the handle of a scalpel can be readily thrust between the two structures (Fig. 35). The older pathologists, struck by this state of things, named the disease " ulceration of cartilage," but, as before said, this is always secondary to fungous synovitis or ostitis. 254 Surgical Pathology. [Chap. xxxix. " Starting " pains indicate not only that the car- tilage is "ulcerated, but that the bones are exposed in the joint. By this time the joint usually contains pus, and molecular and shreddy debris of broken-down granula- tion tissue and cartilage. Instead of diffuse sup- puration, localised abscesses may form in succession in different parts of the joint, open externally, discharge for a while, and then close, leaving the permanent cicatrices in the soft parts, so often seen about partially dislocated, stiff, or anchylosed joints. When the bones are diseased, either primarily or as the result of extension of inflammation from the joint, they are affected with fungous, atonic, and not seldom necrotic caries {q.v.). The capsule is softened and thickened. On section it looks gelatinous. It is stretched by the pressure from within, except on the aspect of flexion, where it is more or less contracted. The tissues around suffer considerably. The muscles waste from disuse. They become fatty, and undergo interstitial cicatricial absorption ; hence the shortening. The subcutaneous tissue is congested and oedem- atous. Except in very acute cases, tJie skin retains its white appearance (tumor albus). The ends of the hones appear enlarged, but this is fallacious. It is due to swelling of the soft parts and the shrinking of the muscles. Abscesses not unfrequently form outside the arti- cular capsule. Flexion and dislocation of tlie joint; e.g., the knee. Flexion is caused by reflex contraction of the muscles (Hilton), and by the hydrostatic pres- sure of the effusion within the joint (Bonnet). The head of the tibia is rotated out, and displaced back- wards and outwards. Several forces concur in effecting Chap. XXXIX.] StRUAWUS ARTERITIS. 255 this — atrophic contraction of the muscles, shrinking of the capsule and external ligaments, destruction of the crucial ligaments, and the weight of the limb. Fig. 36. — Hip joint affected with Strumous Arthritis. Theliead of the femur, a, has lost its cartilage ; the articular surface is composed of porous, rarefied, cancellous tissue; the upper and posterior part of the acetabular rim has been absorbed by the joint action of the carious process and the continuous pressure of the head of the femur; 6, buttress of bouf-, composed of sharp stalactitic osteophytes thrown out to support the dislo- cated head. (One-third natural size.) Terminations of the disease. — It may be arrested at any stage, perfect movement may be re- stored ; more often stiffness remains. Anchylosis is not uncommon. In this case, the granulation tissue between the bones organises to fibrous tissue or bone. Suppuration and complete destruction of the joint 256 Surgical Pathology. [Chap. xl. with extensive disease of the bones is far from rare. Hip-joint disease. — In some works the minute anatomy of hip-joint disease is given at great length, as though it constituted a special disease. This is not the case. It is fungous arthritis (white swelling), and begins, as before said, either in the synovial mem- brane or the bone, as implied in the enumeration of the " articular," " femoral," and " acetabular " varie- ties. What makes the affection of so much importance is its frequency, anatomical complexity, and clinical gravity. The abscesses that form in connection with the disease, open above and behind the great trochanter, or in the groin, following the course from the joint taken by the internal circumflex artery. When the acetabulum is extensively diseased, pus often collects within the pelvis, and the head of the femur, or what remains of it, is sometimes forced through the bottom of the cavity by the functional and atrophic contraction of the muscles. CHAPTER XL. CHRONIC RHEUMATIC ARTHRITIS. Synonyms. — Arthritis deformans, proliferating arthritis, dry arthritis, nodular rheumatism, malum coxae senilis, rheumatic gout. These terms refer to some points in the clinical or pathological history of the disease, which, although in the gross it presents wide structural variations, is sufficiently well defined in its general features and anatomical lesions. Causes. — The etiology is obscure as regards the immediate cause of the particular tissue change. It Chap. XL.] Chronic Rheumatic Arthritis. 257 is met with chiefly in persons beyond mid-life, and in those exposed to inclemencies of climate. The disease occurs under two forms, according as it is localised in one or more points. In the former case it attacks the large joints, especially the hip, and as it is incidental to advanced age it has been called morbus coxae senilis. It is chronic from the first, and is rarely traceable to injury. The polyarticular variety is found in the small and medium-sized points, those of the digits in particular. It affects the young and middle-aged rather than the old, women more often than men. It begins as a distinct affection, or it is the sequel of acute articular rheumatism. Tflorbid anatomy. — In the majority of cases the cartilages are first affected, but the synovdal mem- brane, bones, and ligaments soon become involved. However extreme the lesion, it never ends in sup- puration. In this way it stands in marked contrast to strumous arteritis. The disease is characterised by (1) a proliferation and subsequent destruction of the articular cartilage ; (2) by eburnation of the ends of th€ bones ; (3) by the formation of ecchondroses and massive rounded osteophytes ; (4) by chronic inflammatory hypertrophy of the synovial membrane. The joints of the fingers and, less frequently, the toes become knobbed, stiff, and contracted — rheu- matismus nodosus. Chang^es in the cartila§:e. — These are essen- tially proliferating or constructive ; but, inasmuch as the consistence is diminished, the new-formed cells and softened matrix are gradually worn away and finally destroyed altogether, leaving the bone exposed and condensed. The surface layer of cells is first affected. The R 258 Surgical Pathology. [Chap. XL. cells multiply by segmentation, but so slowly that instead of forming small round unstable granulation corpuscles, as is the case in white swelling, they assume more or less the characteristics of cartilage elements. The primary capsules enlarge and fill with numerous secondary cap- sules. The secondary cap- sules are contained one within another, forming a series of concentric rings, or they remain iso- lated within the primary capsules, or, if this has disappeared, in one large capsule. By softening of the Fig. 37. — Nodular Eheumatism. Surface of the Cartilage. a, Primary capsule filled with second- matrix, the SpaCCS filled ar>- capsules about to open into the ',^ i i articulation ; b, segmented matrix. With UCW CapSUiCS and Magnified 200 diameters. [After ,, . ■*■ , Cornil and Ranvier.) CCliS OpCU mto OnC another, constituting alveolar spaces perpendicular to the articular surface ; very similar to what takes place at the border of normal ossi- fication of bone, and in the epiphysial cartilages in rickets. The superficial capsules dissolve and set their contents free into the joint, leaving soft wavy villous processes of the matrix. The more or less parallel and vertical arrange- ment of the cells, groups, and bands of matrix is due (1) to the lateral resistance to expansion of the en- larging capsules ; (2) to the normal construction of cartilage, which, although it appears homogeneous on section, is seen on fracture to consist of columns set at right angles to the bone, i.e., in the direction of greatest pressure. At length the bone is exposed. Chap. XL.] Chronic Rheumatic Arthritis. 259 Chang^es in the subcai^tilaginous bone. — This also undergoes inflammatory absorption, but as the vascularisation and initial rarefaction are out- stripped by the condensation immediately below the surface, the spongy cancellous tissue is not exposed. The sclerosinf; ostitis causes ebumation. The bone is gradually worn away and polished by friction, either. uniformly or in fuiTOws. Cliang^es in tlie synovial membrane. — The synovial membrane becomes more vascular, and stand out swollen and thickened, as club-shaped protru- sions. I^Tew processes are given off from the The villi or fringes so that a appearance old ones, branched is produced ( " arbor- escent budding"). The fat cells dis- appear, and their place is taken by exudation corpuscles, some of which escape into the joint, and render the fluid, now increased in quantity, more or less turbid. But the greater part of the in- flammatory neoplasia organises into dense connective tissue. Some of the indiffer- ent corpuscles develop into cartilage, so that nodules are formed, and these remain isolated, or coalesce into thick tuberculated laminEe. Meanwhile, the lateral portions of the articular Fig. 38. -Hip joint affected with Chronic Eheiimatic Arthritis. rt. Articular surface of the femur denuded of its cartilage, t)ut smooth from the ehurna- tion consequent on sclerosing ostitis; 6, rounded osteophytes. Compare this figiire with Fig. 36. (One-third natural size.) 26o Surgical Pathology. [Chap. xl. cartilages, less subject to pressure and friction than the central part, whilst they proliferate, are not worn away, but, being soft, they yield like indiarubber to a force insufficient to cause their destruction. Thus the articular surface of the bone is greatly widened. In the case of the hip joint the cartilage (subsequently bone) droops, like a mantle with wavy border, from the head of the femur. The cartilaginous growths in the synovial mem- brane sometimes form pedunculated masses. They frequently calcify, and ossify into spongy bone. They are liable to be detached and roll free in the joint as foreign bodies. They sometimes appear as though " glued on to the bone." The i^ecretiou in the joint is thin, and clear or cloudy, never purulent. In some instances it is con- siderably increased, especially in the earlier stages of the inflammation. In others there is scarcely any at all ; this is notably the case in the polyarticular variety, which aflects the digits (dry arthritis). The exti'a-articiiiar structures. — The muscles of the limb waste from disuse. The ligaments become dense and contracted, frequently ossified ; so also the tendons attached to the bones around the affected joint. Osteophytes spring up from the periosteum, and grow into the articular capsule. Many are isolated, and lie at some little distance from the joint. The absorption of the head and shortening of the neck of the bone, together with the extensive out- growths, give to the hip joint, e.g.., a remarkable appearance, justifying the name, arthritis deformans. 26l CHAPTEK XLI. ACUTE SEROUS SYNOVITIS HYDROPS ACUTUS. Take, &.g.y the knee joint that has been injured by a blow or strain, or that has inflamed from exposure to wet and cold ; it soon becomes painful, especially on movement, so that walking is diificult. The pain is of an aching character, from stretching of the nerves. Swelling comes on very cjuickly, and so rapid is the effusion that the lateral depressions by the patella and patellar ligament, and the pouch beneath the triceps muscle, may be raised into pro- minences in a few hours. The skin over the joint retains more or less its natural colour. The joint is somewhat flexed, but not to the extent that is found in acute suppurative arthritis, although the amount of fluid it contains may be much greater than in the more severe affection. This seems to prove conclusively that the chief cause of the flexion lies in the reflex contraction of the muscles set up by the irritation of the nerves supplied to the synovial membrane. If the fluid be drawn off by the aspirator it will be found to be clear, or slightly cloudy, from shedding of the synovial endothelium, exudation of leucocytes, and it may be coagulation of fibrin in fine flakes, and for- mation of strings of mucin. If such a joint be opened the synovial membrane will be found to be uniformly pink, puffy, and gela- tinous, showing few or no signs of suppuration or disintegration. Under the microscope the fibrous element looks glassy, and is seen to contain exudation cells. 262 Surgical Pathology. [Chap. xlil The articular cartilage is cloudy on the surface, perhaps a little softened. The superficial cells are granular and swollen, and sometimes in process of segmentation. The primary cartilage capsules are enlarged ; the secondary ones more numerous. The matrix is somewhat fibrillated. Such a case resembles inflammation of the large serous membranes (pleurae, pericardium) in the rapidity with which the synovial membrane pours out large quantities of fluid. Unless the articular lesion is the result of acute rheumatism, the constitutional disturbance is not great. As the inflammation resolves the pain goes, and the function of the joint is restored. Frequently, however, it subsides into the chronic form, the fluid remaining in excess. CHAPTER XLII. CHRONIC SEROUS SYNOVITIS. This disease, called also hydrops articulorum, is either the sequel of acute or subacute synovitis, or it is chronic from the first. It is generally met with in the knee joint, and it affects by preference young adult males. The signs of inflammation (save one, swelling) are so little marked that some pathologists rega.rd the inflammation as a simple dropsy, analogous to hydrocele of the tunica vaginalis testis ; but from the fact that it is often the remains of a more acute process, and that in a series of cases every gradation may be met with, from a slow painless effusion to a fairly rajoid exudation, accompanied by increased heat of the joint, this view seems untenable. Morbid anatomy. — The jiiiid may be slightly viscid, but as a rule it is thin and serous. The synovial Chap. XLiii.] Suppurative Arthritis. 263 membrane is slightly swollen and cedematous. In old cases it is somewhat indurated from the growth of a low form of connective tissue, but it never presents the gelatinous fungous appearance of white swelling, and the tendency to suppurate is almost nil. The capsule is stretched, but the joint, though crippled me- chanically, is very little, if at all, painful. The spon- taneous form of the disease is often symmetrical. This points to an inherent weakness of tissue, or to some constitutional disorder. CHAPTEE, XLIII. PHLEGMONOUS OR SUPPURATIVE ARTHRITIS. Causes : (1) Severe injury, especially wound of the joint ; (2) spreading of acute inflammation from the bones or soft parts ; (3) some infective material in the blood, that of pyaemia, or, more rarely, acute rheumatism, or the specific fevers. Suppurative artliritis firom purulent in- feetiou sets in very rapidly ; the joint may be dis- tended with pus in a few hours. In these cases the synovial membrane is injected and swollen, but not to the extent that one would expect from the amount of exudation. The cells are mainly derived from the vessels of the synovial membrane. Segmen- tation of the cells of the articular cartilage furnishes others when this structure is softened and eroded. There may be embolic infarctions and localised dis- integrations of synovial membrane; but this is the exception. Traumatic suppurative arthritis. — Here the joint is intensely painful, sharply flexed, and 264 Surgical Pathology. [Chap. xliii. immovable from spastic contraction of the muscles. The outline is more or less globular ; for the capsule, subcutaneous cellular tissue, and skin are all injected and inflamed ; hence the elevations caused by the dis- tention of the synovial pouches are lost in the general swelling. The synovial membrane is intensely red, puffed, and pulpy. It may contain yellowish foci of minute interstitial suppuration. The vessels are dilated and pouched ; in some stasis has occurred. The surface has lost its polish. The cartilage. — This is obviously affected; the superficial portion is softened, pulpy, and either granular or slightly villous. The microscope shows an active proliferation of the cells, and a homoge- neous or fibrillar appearance of the matrix. The secon- dary capsules are dissolved, and the primary ones filled with granulation cells. Next the joint, no trace can be seen of the original structure ; nothing but a layer of indifferent cells imbedded in the liquefied matrix. The inflammation of the cartilage is secondary to that of the synovial membrane, and is set up by the irritation of the secretion poured out by the latter. The articular cajosule is thick and gelatinous, and the surrounding cellular tissue congested and oedema- tose. The contents of the joint consist at first of an increased synovial secretion. Very soon the cavity is filled with pus. If the inflammation is allowed to go on unchecked, the cartilages are entirely destroyed and the bones exposed ; the capsule softens, and is converted into granulation tissue ; the suppuration is no longer con- fined to the joint, but extends rapidly beneath the fascia around, or an external opening is formed, and so the tension is relieved. Chap. XLIV.] GONORRHCEAL RHEUMATISM. 265 There is severe constitutional disturbance, with high fever, the result of absorption of pyrogenous material and the acute pain. CHAPTEPv XLIY. GONORRHCEAL ARTHRITIS, GOXORRHCEAL RHEUMATISM. GoNORRHCEAL rheamatism is generally considered to be a mild form of pyaemia, due to purulent absorption from the inflamed urethra. Many eminent authorities hold that gonorrhoea itself is not a specific disease, but a simple acute suppurative urethritis. It occurs in only a fractional percentage of persons aflfected with gonorrhcea, and must therefore be sup- posed to result from some accidental alteration in the composition of the secretion; or, what is far more probable, from a disposition of the synovial membrane in certain individuals to become inflamed on slight irritation. Painful swelling of the joints is far from rare in many inflammatory diseases, particularly those attended with suppuration. The simple passage of a catheter has been known to produce the same result. The disease is sometimes very obstinate, and is liable to recur long after the original cause has disappeared, and is almost certain to do so if it be renewed. It may be accompanied by inflammation of the sclerotic coat of the eye-ball. The pathological changes are the same as in acute and subacute synovitis arising from other sources. The knee joint is more often affected than any other ; the writer has seen it in the elbow and wrist. The inflammation generally subsides after a time, but it may go on to complete destruction of the arti- culation. 266 CHAPTEK XLV. HEMORRHAGE INTO JOINTS. Causes : (1) Injury ; (2) rupture of a popliteal aneurism, into the knee joint ; (3) haemophilia ; (4) some blood diseases, e.g., scurvy. Traiamatic lisemartlu^osis. — This follows blows on the joint. The extravasation takes place fi-om the capillaries of the synovial membrane, and, in the knee joint, from the broken surfaces of a fractured patella. It is diagnosed from serous effusion by the fluctuation being less marked, and the rapidity with which the swelling follows the injury. As a rule, the blood is entirely absorbed, but occa- sionally fibrinous coagula remain. Msemorrtiag^e from liseinopliiliaL is most common in the knee joint. It is followed by a certain amount of synovitis. Haemophilia is eleven times as fi-equent in males as in females, though the latter usually transmit the disease (W. Legg). Beyond its consequences, the morbid anatomy is unknown. CHAPTER XLYI. LOOSE OR MOVABLE BODIES IN JOINTS. These are of different kinds : (1) The most common are termed melon-seed bodies, on account of their prevailing shape, rounded at one end, somewhat acuminate at the other, and flattened. Some are as small as a hemp seed, others are many times as large. A healthy synovial membrane is finely fimbriated ; Chap. XLVL] MOVABLE BODIES IN JOINTS. 267 the primary fringes consist of delicate areolar tissue, covered by a layer of endothelial cells ; and loops of capillary vessels. The secondary fringes are sometimes extravascular (Rainey). Kolliker has shown that the synovial pro- y<^^Jp^^^ cesses occasion- ally contain a few cartilage cells. Whe ther from chronic inflammation or a pure hy- pertrophy, part or whole of synovial mem- bi-ane of a joint may be covered with small pe- d u n c u 1 a t e d bodies(Fig.39). The pedicles are often ex- tremely fine, and the least force suffices to rupture them. The melon-seed bodies, then, are clearly en- larged synovial fringes. Their microscopical structure varies ; in most cases they show nothing but a dense homogeneous fi.bri- nous material ; sometimes there is a faint concentric lamination ; very rarely cartilage cells can be seen. (2) Rounded or nodular masses of a gelatinous Fig. 39. — Hypertrophy of the Synovial Fringes of the Knee Joint. a, Articular surface of the femur; &, patella; c, liga- mentum patellae ; d, portion of capsule. 2 68 Surgical Pathology. [Chap. xlvii. substance, devoid of any trace of organised structure. They are either fibrinous exudations from the synovial membrane, or swollen degenerated synovial fringes (1 and 2 are also found in synovial sheaths, ganglia, and mucous bursse). (3) Bodies of much larger size than any of the foregoing, consisting of hyaline or fibrous cartilage, either in the natural state, or ossified, or calcified. They are detached from arborescent outgrowths of the synovial membrane, and nodular thickenings of the lateral portions of the articular cartilages in chronic rheumatic arthritis. (4) Lipomatous bodies, hypertrophies of the cellulo-adipose tissue of the synovial membrane. (5) Portions of articular cartilage split off by accident, or set free by ulceration (white swelling). (6) The remains of blood-clots. Groups 1, 2, and 3 are chiefly met with in the knee joint. CHAPTER XLYII. ON DEFOEMITIES. Amongst the deformities of greatest interest to the surgeon are those involving : (1) Malposition of the bones entering into the articulations of the extremities ; and (2) curvatures of the spine. The shape of the bones may remain unaltered ; or it may deviate widely from the normal, as a part of the initial lesion, or as a secondary result of mis- directed and excessive pressure. Causes, — The causes of deformities are numerous : (1) Arrested or perverted development during intra- uterine life. Such are the congenital defects in the different varieties of club-foot, dislocation of the hip. Chap. XL VI I.] On Deformities. 269 spina bifida, and meningocele (cerebral). That most of the forms of club-foot are due to abnormal fcetal evolution is shown by the great regularity of disposi- tion of the structures implicated ; thus we come to arrange them in certain well-defined groups. Again, the most common (talipes equino- varus) is mainly an exaggeration of the position assumed during complete rest, ^.e., when all voluntary muscular action is with- drawn, as in the cadaver. Diefienbach says " that all children are born with the first stage of club-foot." This is only true in a physiological sense, for when the child comes to walk the foot takes its natural position without let or hindrance from alteration in the form of the articular surfaces of the bones, or contraction of ligaments, or paralysis or shortening of muscles. In early fcetal life the back of the lower extremity lies in contact wdth the belly, and in very rare cases it has been known to be fixed there by integument common to it and the trunk. As develop- ment goes on the limh rotates, so that the calf comes to look backwards, and the sole of the foot downwards. Talipes equino-varus may be considered as the result of imperfect rotation. It is not uncommon for spina bifida to be associated with some variety of club-foot, and pathologists have sought to connect the two, by supposing that the latter is due to perverted innerva- tion. But club-foot usually occurs without any other sign of disease of the spinal centres or nerves. In one case I found the brain and cord absent, adhesion of certain fingers to the palm, extroversion of the bladder, and talipes calcaneus. It seems far more probable that the spinal and pedal deformities are mere coincidences, than that they stand in relation of cause and effect, at any rate during intra-uterine life. The only structural changes are those due to an-ested development and growth ; there is nothing of an inflammatory nature. 270 Surgical Pathology. [Chap, xlvii. Intra-uterine pressure may explain certain irregular defects, but not those of constant and definite type. (2) Paralysis and contraction of muscles. — The theory of antagonistic contractions holds good in but a limited number of cases. (We refer to the physio- logical contraction, and not the atrophic shrinking from forced rest in unnatural position.) After disease of the hip joint, especially if complicated with disloca- tion on to the dorsum ilii, the heel is drawn up (talipes equinus) to compensate for the shortening of the limb and tilting of the pelvis. In this instance there is both dynamic and static contraction of the calf muscles. In infantile paralysis certain groups of muscles often remain permanently pa,ralysed or weak, but the opponents do not drag the foot in the opposite direc- tion ; the position assumed is that caused by the weight of the foot, and any accidental pressure that may bear upon it. Both in this and the congenital forms of club-foot the deformity is afterwards increased by misdirected pressure, as when the patient comes to walk upon the outer part of the dorsum in the latter case, or drags the limb after him in the former. The position taken by the hand and fore-arm in injury of the musculo-spiral nerve also tells strongly against the theory of muscular antagonism. Unless the patient voluntarily uses the flexor muscles, the limb hangs in a state of rest, slight flexion and semi- pronation ; and further, instead of the flexors con- tracting to their usual extent, the grasping power of the hand is greatly diminished from want of the sense of resistance by the extensors, so that at the first one might think there was some actual loss of power in the flexors. The full efiect of the extensor-paralysis is brought out by placing the upper arm in the horizontal position, and the fore-arm in that of flexion; Chap. XLVIL] On DEFORMITIES. 27 1 then it is seen that extension of the elbow, wrist, and fingers is impossible. Again, if the tendo Achillis be divided, say, for overcoming the contraction of the calf muscles in oblique fracture of the tibia, the foot remains some- what extended, whereas on the theory of antagonistic contraction it ought to become flexed (Volkmann). Physiological contraction of the muscles alone, whether arising from central or peripheral irritation of the nerves, is rarely continued long enough to cause permanent deformity. It is seen in the "late rigidity " of the muscles following gross lesions of the brain ; but here, too, the muscles undergo interstitial atrophic shortening as well. (3) Cicatricial and atrophic shortening of the muscles and tendons. The contraction of inflammatory lymph sometimes causes deformity of the joints, e.g.^ the thigh may be left permanently flexed as the result of psoitis. I have known talipes equinus follow deep - seated phlebitis in the calf of the leg. If a joint, e.^., the knee or hip, be allowed to remain flexed for a long time, the muscles and liga- ments will shorten up to the distance between their attachments by a process of interstitial absorption. In Pott's fracture one takes care to place the foot at a right angle with the leg before putting on a plaster casing. If this be neglected, some difficulty will be afterwards experienced in overcoming the resistance of the shortened tendo Achillis. From what has been said it will be gathei-ed that the chief causes of deformity lie outside the joints. In curvature of the spine a softened state of the bones and intervertebral discs greatly aids, and in fact may be the chief cause of, the permanent alteration in shape. 272 CHAPTER XLVIII. CURVATURE OF THE SPINE. The nature of the curvature depends (1) upon tlio disease wliich causes it ; (2) upon the distribution of the morbid process, whether it extends through the entire length of the cohimn, or is limited to a certain region or part ; (3) upon the condition of the support- ing structures, muscles, and ligaments ; (4) upon any extrinsic pressure or traction brought to bear upon the spine ; e.g., in disease of the hip joint the lumbar curve is exaggerated, together with a certain amount of rotation. Unilateral pleurisy may alter the natural curves, either during the effusion stage, or when tjiis has passed away and given place to retraction of the same side of the chest wall. Curvature in one region, such as that which follows Pott's disease, so alters the position of the centre of gravity that unless some means of compensa- tion were provided the body would be in a state of unstable equilibrium. The effect of kyphosis in the dorsal spine is counteracted by secondary lordosis in the lumbar. Diseases causing: curvature. — 1. Certain congenital defects. The lateral portions of the ver- tebrse may be imperfectly formed with or without coincidental defect in the ribs. The writer once saw a case in a girl aged about ten years, in which there was a firm nodule over the lower dorsal spine, apparently a cured spina bifida. Opposite this, two or three of the ribs on one side were fused into a solid plate. ' There was lateral curvature of the spine. 2. Caries {q.v.) Chap. XLViii.] Curvature of the Spine. 273 3. Kickets {q.v.), 4. Osteomalacia (q-v.). 5. In aneurism^ of the descending thoracic, or ab- dominal aorta, the bodies and contiguous parts of the neural arches of the vertebrae may be absorbed, and Fig. 40. — Fracture of the Spine. a, Wedge-sbaped mass, forming double-inclined plane. Which has been driven backward upon the cord, c ; 6, detritus of the anterior portion of the bodies of two vertebrae. this may lead to projection with lateral deviation of the spine. 6. Chronic rheiimatis'in sometimes affects the ver- tebral column. In these cases the anterior common ligament is usually ossified, and the vertebrae anchy- losed. The spine is generally thrown into one uniform dorsal curve, and there are compensatory curves in the lumbar and cervical regions. 7. Fracture of the bodies of the vertebrae (Fig. 40). '274 Surgical Pathology. [Chap. xlix. The history of an injury and the concomitant signs and symptoms suflSce to make the diagnosis easy, although a long time may have elapsed since repair took place. 8. One of the most important forms is that known as " lateral curvatwreT It is doubtful where the fault lies in the first instance. Billroth believes that the primary cause is a weakness -of the back muscles, and that the ligaments and discs are soft and yielding, and the bones affected with a ''mild form of rachitis." It is most common in girls about the age of puberty, and in those compelled to sit or stand for a long time in a constrained position. This causes a sense of fatigue, and to gain relief th^ spine is supported un- equally, e.g.^ by the hand against the object on which the patient is sitting. This gives the initial curve, which soon becomes exaggerated and permanent. If the dorsal curve is to the right^ there is compensatory lumbar curve to the left ; compensatory, but not secondary, for in all probability both arise together. When the lateral curve is at all marked, a certain amount of rotation or twisting is also observed After a time the bodies of the vertebrae become unequal in depth on the two sides, and sometimes they are more or less anchylosed by new bone. I have known the lumbar vertebrse to be a third of an inch deeper on one side than the other. CHAPTER XLIX. DEFORMITIES OP THE FOOT, KNEE, AND HIP. Talipes eqiiino-variis is the most common variety of congenital deformity of the foot. The extension is due to a contracted state of the tendo Chap XLix.] Talipes. 275 Achillis ; the inversion to a like defect in the tibiales, especially the tibialis posticus. The ball of the great toe is aj^proximatecl to the heel, and the plantar fascia is shortened. The dorsum and outer border of the foot are more convex than natural. The tarsal bones are more or less wedge-shaped, the base of the wedge being outwards. In well-marked cases the astragalus is partially dislocated outwards. After the patient has learned to walk, the deformity increases, for the pres- sure exerted by the weight of the body is misdirected. Being greater on the inner portions of the tarsal bones than on the outer, growth is checked in the former direction ; and as the movement of the bones one upon the other is greatly restricted, they inay become anchylosed. The liability to this is increased by the irritation caused by walking and standing on parts ill-adapted to receive and transmit pressure. For the same reason callosities and subcutaneous bursse are developed. The fore 9,nd n]iddle parts of the foot are stunted in growth. Talipes eqiiiniis is more often the result o| injury or acquired disease than a congenital deformity, In the case from which Fig. 8 was taken, it followed cicatrisation of a gun-shot wound of the tendo Achillis. There is shorteninsj of the calf muscles or the heel tendo^. A dense callosity forms over the balls of the toes. The toes themselves are pressed and drawn upwards, so that they become partially dislocated on to the heads of the metatarsal bones. Talipes valgxis et calcaneo-valgxis. — In the former the peroneal tendons are shortened and the tibials elongated. When the heel is depressed (cal- caneus) the extensors are contracted and the tendo Achillis leng-thened. Pes plaiins et plano-valg^is. — These de- formities are usually met with in youth and early adult life. They are comparable to genu valgum and 276 Surgical Pathology. [Chap. xlix. lateral curvature of the spine. As tlie consequence of long standing, the muscles and ligaments give way. Both arches of the foot, antero-posterior and intero- external, are lowered. The ligaments failing to support the strain upon them, the muscles are in a constant state of tension, and this causes the symptom complained of, viz., aching pain, referred at one time to the instep or sole of the foot, at another to the muscles of the leg. Oeiiu valgTim is the result of rickets in children, or continued strain upon the knees in youths and young adults, and more rarely in later life. The internal lateral ligament is stretched. The external and the biceps tendon shortened. The inner condyle of the femur is said to be hypertrophied. What really happens is this : if the bending of the knee occurs after the bones are fully grown, the external condyle atrophies from pressure ; if it comes on during childhood or youth, there is unequal growth of the two condyles : that of the outer is checked by the weight of the body transmitted through it, whilst that of the inner is unrestrained. In rickets there is sometimes knock-knee of one limb and bandy-leg of the other, the convexity of the former fitting into the concavity of the latter. This is due to the way in which the child is carried by the nurse. Bandy-leg' occurs in rickets. The pathology is the same as in genu valgum. The anatomy is simply reversed. It is simulated by outward curvature of the femur. Deformities of the liip consist of congenital dorsal dislocation, and malposition from contraction of the muscles, ligaments, and fasciae. Deformity from infantile paralysis. — As before said, the foot, when in a state of rest, is partially extended and slightlj inverted. The position Chap. XLix.] Infantile Paralysis. 277 is assumed and maintained by the weight of the foot and the tone of the muscles. In iofantile paralysis of marked degree the muscles are not only placed beyond the influence of the will, but there is"^a want of tone as well. The paralysis is rarely so extensive as to involve all the muscles of a limb ; usually only a group of muscles or individual ones are affected. ISTow although paralysis of one set does not at once cause displacement by the con- traction of the antagonists, still, when the patient uses the foot, the want of power of support in the direction of the j^aralysed muscles must greatly in- fluence the development of the deformity. This, however, is chiefly eff'ected by other agencies. The foot being allowed to remain in the position assigned to it by its own weight, the soft structures (muscles, tendons, ligaments, and fascise) undergo an atrophic shortening, which serves to perpetuate the malposition. And, again, the weight of the body thrown upon the foot thus displaced aggravates the deformity or alters its direction. In extreme cases, the affected foot is dragged after the other ; and the inner border and fore part coming in contact with the ground, the extension is increased, whilst any original inversion is removed, or even replaced by eversion. If, on the other hand, the patient is able to use the limb fairly well, the equinus is still well marked, for the limb is always more or less stunted in growth, so that the sole of the foot cannot properly be brought to the ground in progTession. The tendency is also to roll in or out according as the want of support is greater on one side or the other. Thus the deformity from infantile paralysis is not a definite one. In depends upon several factors : the weight of the foot, loss of tone in the paretic muscles, secondary contractions and elongations of the muscles and ligaments, and the direction of pressure. 278 Surgical Pathology. [Chap. l. Infantile paralysis is Lelieved to be due to atrophy of the motor ganglion cells in the anterior cornua of the grey matter of the spinal cord, though it may be that the nerve endings in the muscles are primarily at fault. Unless the power of the paralysed muscles is restored within a short time (say a month or two) it will probably never be regained. Subsequent improvement in the contractility is then chiefly confined to fibres that have wasted from simple disuse. When the paralysis is thoroughly established, the treatment consists of measures taken with a view of improving the nutrition of the limb in general, and the muscles in particular, such as electricity and massage ; and in preventing and correcting deformities by the use of surgical apparatus. Otlier deformities arise from congenital absence or contraction of muscles ; e.g.^ the sterno-mastoid, arrested development of a bone or limb, persistence of a branchial cleft in the neck, etc. There remains for description the pathology of spina bifida, cerebral meningocele and encephalocele, cleft palate, and extroversion of the bladder. CHAPTER L. SPINA BIFIDA. Spina bifida is a congenital deformity that owes its origin to arrested development of the neural arches of the vertebree. The absence of coalescence of the laminae allows the spinal membranes to protrude, and carry with them the cord or nerve roots ; and in the case of the sacral spine the beginnings of the nerve trunks. Chap. L.] Spina Bifida. 279 The tiimoiir is situated in the mid-line of the back. It is usually globular in shape, and about the size of an orange. When obloug, the long axis is parallel to the spinal column. The extent in this direc- tion depends upon the number of vertebrae involved. The lumbo-sacral region is the most common seat of the affection, i.e., where the laminse of the neural arches are naturally late in completion ; but no part of the spine is exempt ; in fact, the entire neural canal may remain open. It is not certain whether the arrest in development is always primary, or whether, in some instances at least, it may not be due to the pressure of fluid ac- cumulated in the canal. The occasional coincidence of other congenital defects {e.g., talipes) seems to tell in favour of the former hypothesis. The \Fall of the sac is composed of the in- teguments, the dura mater and parietal layer of the arachnoid, and generally also the visceral layer of that " membrane,'' so that the jiiiid is contained in a cavity continuous with the subarachnoid, or "internal arachnoid," space. More rarely the sac is lined by the parietal layer of the arachnoid, and the fluid contained between the parietal and visceral portions. In each case the condition is known as "hydro- meningocele." In other cases the central canal of the cord is dilated, and the cord itself, or what remains of it, spread out over the fluid (hydro-myelocele), which in this instance, and also in internal hydro-meningocele, presents all the characters of cerebro-spinal fluid. The sac is unilocular, or divided into compart- ments by partial dissepiments. The skin over the tumour is sometimes very thin, and the laminae forming the sac fused into a semi-translucent membrane, sometimes of such tenuity as to rupture spontaneously. 28o Surgical Pathology. [Chap. L. Now and again a central dimple can be seen in the swelling marking the attachment of the spinal cord to the inner surface of the sac. It is clear that a Fig. 41. — LumlDO-sacral Spina Bifida, from the Body of a Subject aged 29. A portion of the sac has heen removed to expose the nerves, 6, which, after running for a short distance iu the cavity, can he seen to enter its walls ; o, bodies of vertebriB in antero-posterior section. There is lateral curvature and rotation of the spine. (One-third natural size.) this, and the existence of hydro-myelocele, can only be met with in the dorsal, cervical, and lumbar regions, and rarely in the lower part of the last-mentioned situation; for, before the tumour has reached any size, the cord has already receded in an upward Chap. L.] Spina Bifida. 281 direction, as tlie result of its growth being out- stripped by that of the spine. The cereTbro-spinal fluid found in the sac is usually quite clear and colourless j but it may be blood-stained from capillary rupture, or slightly turbid from eflpQsion of inflammatory lymph and cells. Wilks and Moxon describe the process of secretion as an "irritative dropsy." Relation of tlie nerve-roots, nerves, and spinal cord to the sac. — When the central canal is dilated, the cord may be spread out over the inner surface of the sac, or it may have entirely atrophied from the centrifugal pressure. The cords of the cauda equina (nerve-roots) usually course through the centre of the sac, and "those which would naturally correspond to the vertebrae implicated in the tumour pass through the membranes to their distribution, while the lower ones return into the spinal canal " (Holmes) . The nerve- roots may end in the wall of the sac, or they may be altogether absent. In the case before alluded to (page 269) there was no trace of the spinal cord, or of the roots of the nerves, in the neural canal. Associated deformities. — The most common is chronic hydrocephalus ; next to this some variety of club-foot. Pressure applied to the hydrocephalic skull will sometimes increase the tension of the sac of the spina bifida ; but frequently the fluid collected in the ventricles is confined there by obliteration of the Sylvian aqueduct, or closure of the communication between the fourth ventricle and the subarachnoid space (Hilton). The latter condition I found in a case of lumbar spina bifida and chronic hydroce- phalus. 252 CHAPTER LI. CEREBRAL MENINGOCELE AND MENINGO-ENCEPHALOCELE. Cerebral meningocele and meningo-encephalocele are the analogues of spinal hydro-meningocele and hydro- myelocele ; i.e., the protrusion is either of the cere- bral membranes alone, or of these together with the brain substance surrounding the ventricles. The opening in the skull is most commonly found in the occipital bone ; it has been seen at the root of the nose, and the tumour mistaken for a nsevus. More rarely the parietal and squamous bones are perforated, and, still more rarely, the base of the skull. In the latter case one would expect, on developmental grounds, to find the floor of the pituitary fossa absent. The cranial sutures are generally spared. CHAPTER LII. CLEFT PALATE AND HARE-LIP. In the human being, that portion of the upper jaw which carries the incisor teeth never remains separate from the rest, except as the result of arrested development and growth ; but in the lower mammals, e.g., the dog, it exists throughout life as two distinct bones, called "intermaxillary" or " prem axillary." And, even in congenital malformation of the palate and alveolar arch, the fissure never runs straight through in the middle line, but diverges near the Chap. LiL] Cleft Palate and Hare Lip. 283 anterior part of the jaw, and passes out between the portions of bone that carry respectively the incisor and canine teeth. That is to say, although the osseous continuity between the maxillae and pre- maxillse may be wanting, the premaxillse themselves are always united into one piece of bone. In early fcetal life there is one large cavity, called the " naso- bucco-pharyngeal ; " this is subsequently partitioned off into four communicating compartments, the mouth, pharynx, and nasal fossae, by the growth of two septa, the hard and soft palate and the septum nasi. The roof of the mouth is completed by the union in the middle line of two laminae advancing from the sides of upper jaw and palate bones, and the un- ossified structures behind. If this union fails to take place, cleft palate is the result. It may consist merely of a bifid u^oila, or extend through the soft palate, or through the whole or any portion of the hard palate ; but, as before said, it never passes out in the middle line in front. When the cleft reaches the posterior part of the intermaxillary nodule, it may bifurcate, and the two limbs of the fissure isolate that piece of the jaw. This is known as "double-cleft palate." Single or double, when complete, it is almost invariably con- tinuous with a split in the upper lip. Cleft of the soft palate often exists alone ; so also hare-lip ; but cleft of the hard palate is rarely found without the velum being implicated. As the roof of the mouth is wanting in the middle line, it is clear that the septum nasi, unless its lower border remains free, must deviate to one side or the other, in order to join the hard palate j and this is what usually happens. When the cleft in the alveolar arch is double, the intermaxillary nodule can be swayed backwards and 284 Surgical Pathology. [Chap. liii. forwards, and the rudiments of the incisor teeth which it contains do not, as a rule, develop to the normal extent. This is one reason why, in operations for the cure of the deformity, the surgeon often elects to remove the piece of bone. In hare-lijy the fissure is to the side of the middle line j in the hare it is situated in the centre of the lip. It may be partial, or extend into the nostril. In the latter case, the ala nasi is flattened, for the muscles draw it and the corresponding part of the lip outwards. CHAPTER LIII. EXTROVERSION OF THE BLADDER ECTOPIA VESICA HYPOSPADIAS. Here the anterior part of the abdominal wall and the anterior wall of the bladder are wanting. At birth they are usually present in the form of a thin membrane, which afterwards dries up and is cast off as a slough by the development of a ring of granula- tions at its periphery. When the defect reaches its highest grade, the proximal part of the umbilical cord, instead of being inserted as usual into the wall of the abdomen, is spread out as a membranous lamina con- tinuous with the attenuated structures below, and, after ligature, separates with them. The posterior wall of the bladder is thus exposed, and, having lost its support in front, is thrust for- wards by the underlying viscera, so that, instead of a cavity, there is a bright-red elevation covered with mucous membrane. The symphysis pubis, too, is often imperfectly deve- loped, the pubic bones being united by a ligamentous Chap. Liv.j Hypospadias. 285 band, and more or less everted by tlie resultant of two forces exerted by the adductors of the thigh and the oblique muscles of the abdomen. The urethra is wanting. There is a groove on the dorsal surface of the penis, commencing at the lower part of the unnatural opening in the bladder. When tliis opening is confined to a small aperture above the pubes, the condition is known as epis-padias. In ectopia vesicae the urine constantly escapes from the exposed orifices of the ureters, and, coming in contact with the skin of the abdomen, causes con- siderable irritation. The transition from skin to mucous membrane is imperceptible. Hypospadias is due to imperfect development and union of the lateral lappets that go to form the normal urethra. It may extend the whole length of the penis, but it is generally confined within a short distance from the end of the gians. In the former case the scrotum may be cleft. Instead of the urethra being wanting in its anterior part, as described above, there may be a small opening at the peno- scrotal angle or in the perinaeum. CHAPTER LIY. FATTY DEGENERATION OF ARTERIES, AND ARTERITIS, Many terms more or less misleading have been used in the description of arterial .pathology; e.g.^ atheroma^ which is merely the consequence of prece- dent inflammation, and degeneration, is often used to indicate the substantive disease. In this work the 286 • Surgical Pathology. [Chap. liv. morbid processes and tlieir results will be described as they occur separately or in combination. Fatty degeneratioii is met with under two conditions : (1) As a primary and solitary change; (2) as the sequel of inflammation. (1) Primary fatty degeneration is best seen as it affects the endothelial and subendothelial layers of the internal coat. It is most common in the first part of the aorta, and although it increases in frequency as age advances, it is by no means rare in early life. It causes small, slightly elevated yellowish white patches. The fat granules are for the most part arranged in groups, still retaining the outline of the stellate endo- thelial cells (Fig. 4a). The tissue beneath may be quite healthy; so that these cases have no clinical significance. The fat granules are absorbed or swept off by the blood stream, and new cells replace the old ones. But the degeneration may be more wide-spread in the coats of the vessel. Tliis is very constant in senile decay. Hounded and bead-like collections are seen in the middle coat, following the course of the elastic laminae and muscular fibre-cells. (2) As the sequel of inflammation, fat molecules are never absent. The greater part of the contents of " atheromatous abscesses " is composed of them. Acute endarteritis. — Diffuse suppm-ative or phlegmonous arteritis is unknown. The disease in question affects chiefly the large arteries, especially the aorta. In some cases there is a history of syphilis, but in most the cause is obscure. The inner surface of the vessel has an irreg-ular gTeyish semi-translucent appearance, as if melted gelatine had been sprinkled upon it, and then set. Some patches are yellowish from fatty change. Calci- fication is rare. When cut into, the inflamed spots are found to be elastic and gelatinous-looking. The swollen intima may be many times thicker than Chap. LI v.] Atheroma. 287 natural. The middle coat is more or less involved, but never to the extent as in chronic arteritis . (atheroma). Under the microscope the diseased struc- ture is found to be infiltrated with small cells, which < lie parallel to the laminae. The cells are partly derived from the vasa-vasorum, partly from segmentation of the subendothelial corpuscles. In old cases the cells ~,^--^ Fig 42. — Sectioa of the Tumca Interna of the Aorta, in a case of Acute Endarteritis. This section, made after desiccation of tbe artery, shows the proliferation of the elements of the internal membrane. (Afte)- Comil and Ranvier.) may almost -entirely have disappeared, leaving a dense cartilaginiform homogeneous substance, and a few fat molecules. The most pronounced €ase I have seen was in a subject Vkdth aneurism of the aorta and both -popliteal and the right femoral arteries. The entire aorta was studded with hard, smooth, grey elevations, from the size of a pin's head to a pea. Chronic endarteritis..— Atheroma. This disease is said to begin in the deeper portion of the internal coat. Small cells accumulate in the midst of a homogeneous or granular matrix of exudation matter, and softened coat of the vessel. This goes on until there is bulging into the vessel, which here appears of a dull, yellowish-white colour. Should the inflamma- tion stop at this stage, the products of it will be partially absorbed subsequent to fatty degeneration, and the remaining portion of the intima will come m. 288 Surgical Pathology. [Chap. liv. contact with the middle coat ; or, if the latter has been destroyed, the internal and external coats will blend, forming together a slightly depressed fibrous cicatrix. But, meanwhile, lime-salts are frequently deposited, and then a brittle calcareous plate serves as a mark of the previous arteritis. During the slow progress of the inflammation the cells are transformed into fat, and this again into its chemical derivatives ; so that a so-called athero'matous abscess is filled with degenerating cells, granular debris, carbonate of lime, and crystals of cholesterine and the fatty acids, and, perhaps, hsematoidin crystals. If the pellicle, which bounds the atheromatous focus next the lumen of the vessel, gives way, the contents of the cavity are washed out by the blood stream, and the remaining excavation is termed an atheromatous ulcer. The base of the "ulcer" usually calcifies, or becomes fibrous. The calcareous plates above mentioned sometimes split away at the margin, and pigment is deposited beneath them from the blood undergoing coagulation as it trickles through the fissures. They also act as foreign bodies, and cause extensive thrombosis. They may be detached, and give rise to embolism. Arteritis deformans. — In old people, chronic inflammatory and degenerative changes are widely spread. Homogeneous thickening of the internal coat, atheromatous patches, calcified plates in the large arteries, and calcified rings in the small and medium- sized ones, may all be found in the same subject. On the whole these senile arteries are dilated, but the inner coat may be so thickened as to cause serious obstruction to the blood current, and cause thrombosis and gangrene. Like varicose veins, the arteries are elongated, so that they are thrown into permanent curves. Syphilitic disease of the arteries. (1) Syphilis, by impairing the nutrition of the Chap. Liv.] Diseases of Arteries. 289 tissues generally, may lead to early senile changes — fatty degeneration and atheroma. (2) But there is a specific syphilitic inflammation of the arteries, more or less acute in its progress. It begins in the internal coat, but the entire thickness of the walls may be converted into a glassy or slightly fibrillated substance containing small cells. In the arteries of the brain there is a good deal of exuda- tion into the perivascular sheaths as well, so that the lumen is narrowed from swelling within and com- pression without. It is one of the chief causes of cerebral thrombosis. The softened state of the vessels renders them very liable to aneurismal dilatation. In the case of the aorta and other large arteries the inner coat is enormously thickened and uneven. Atheroma and calcification are less common than in senile disease. Arterio-capillary li1>rosis enters largely into the pathology of granular gouty kidney. It is not limited to that organ, but is widely distributed throughout the various tissues (skin, nerve-centres, etc.). The walls of the vessels are thickened by a hyalin-fibroid material (Gull and Sutton) and hyper- trophy of the middle coat (Johnson). The lumen of the vessels is lessened. The obstruction it causes induces hypertrophy of the left ventricle of the heart. Other causes of arteritis need only be mentioned. They are chronic alcoholism and rheumatism. Inflamiiiatioii of the middle and external coats. — It is doubtful if this occurs as a primary disease. The middle coat may be destroyed by inflam- mation reaching it from either side. The external is involved in like manner, but it especially suffers in periarteritis. Periarteritis consists of an inflammation of the external coat and its areolar sheath. They rarely T 290 Surgical Pathology. [Chap. lv. escape altogether in acute and chronic endarteritis. It has been shown that in syphilitic disease of the cerebral arteiies the perivascular sheaths are ex- tensively infiltrated ; in fact, several vessels are occasionally imbedded in a continuous mass of exudation. In thrombosis of the deep veins the periphlebitis extends to the companion arteries. Not only may the areolar sheath and external coat of an artery be softened by inflammation until bulging takes place, as in aneurisms of branches of the pulmonary arteries skirting phthisical cavities, but the tension upon the vasa-vasorum may be so great that the entire thickness of the wall of a large artery may slough away; e.g.., the femoral in spreading perilymphatic abscesses of the groin. Periarteritis, by causing canalisation, serves as a dangerous check upon hsemostasis in wounded vessels; it prevents contraction, and retraction within the sheath. CHAPTER LY. A-ifEURISM. Varieties of alieiirism. — Aneurisms are either traumatic, or pathological (spontaneous). The term traumatic is limited to those cases that form directly as the result of injury. Many pathological aneurisms can be traced to some local strain, but of such a degree that had the vessel been healthy it would not have given way. Dilfiise traumatic aneiirlsms.— Blood escapes from the wounded vessel into the interstices of the surrounding structures, and in the direction of Chap. Lv.] Aneurism. 291 least resistance, e.g.^ in the intermuscular planes and beneath fasciae. The distending force is too great to allow of an adventitious sac of inflammatory tissue being formed. Thus a traiTmatic aneurism of the popliteal artery may spread up the thigh, or the blood from a ruptured axillary fill the arm-pit. The only treatment likely to avail is ligature of the artery on each side of the wound, or amputation. The cause is usually a stab, or rupture during the attempt to reduce an old dislocation. Sacculated or circuinscribed traumatic aneiu'ism. — These are either simple, or arterio- venous. In the former case the sac is variously constituted. (1) It may be formed by a yielding cicatrix, after the wound in the artery has closed; this can only happen when the artery is small, or the opening in it very minute. (2) It may consist of a protrusion of the internal, or internal and middle, coats through a wound in the external (hernial aneurism). (3) It may be formed of the external coat, the internal and middle having been lacerated by bruising against a bone. (4) The sac may be purely adventitious, all the coats having been divided \ in such cases the blood escapes very slowly ; the inflammatory induration around suffices to prevent a rapid extension of the aneurism. Arterio-vetioiis aneiu'ism results from the simultaneous wounding of an artery and neighbouring vein, e.g.^ the brachial and median basilic in blood- letting at the head of the elbow. If the inflammatory exudation caused by the injury fixes the vessels in contact, the blood will pass directly from the artery to the vein, and the latter will become dilated and tortuous, and will have its walls thickened from the irritation of the strain (cineurismal varix). But the cementing lymph may yield and form a sac between the two vessels {varicose aneurism). This 292 Surgical Pathology. [Chap. LV. is the more dangerous variety, since the sac is usually thin, and the tension upon it is more concentrated than on the resilient walls of vein. The pulsation, bruit, and thrill are also stronger than in aneurismal varix. Pathological or spoiitaiieous aneui'tsms are divided into true and false. The sac of a true aneurism is said to be formed of all the coats of the vessel, but on pathological grounds the distinction is not well founded ; for the disease of the vessel ere it Fig. 43.— Section through Femoral Artery, just below an Aneurism. a. Tunica intima, rugged and greatly thickened. allows of dilatation has caused at least the middle coat to disappear. Syphilitic and idiopathic arteritis (atheroma) are the causes of the weakness of the vessel. In chronic arteritis the deeper layers of the internal coat and the middle coat are destroyed, so that what remains of the internal coat is blended Avith the external, and both are so diseased that their natural structure cannot be made out. Frequently, also, the aneurism develops at the seat of an atheromatous ulcer, when nothing but the external coat remains. In most cases the irritation kept up causes the sac to be thickened by the interstitial deposit of lymph and inflammatory condensation of the areolar tissue outside. From want of elasticity Chap. LV.] Aneurism. 293 the sac continues to dilate in spite of its thickness. But usually there comes a time when the dilatation is so rapid that the sac is greatly thinned, and finally it gives way {imjjtured aneurism). The clot witliiii tUe aiieiirism is more or less laminated. The first formed laminse lie at the bottom of the sac, but do not reach its neck, whereas the Fig. 44. — Aneurism of Femoral Artery. a. Thickened walls of ttie artery forming the sac of the aneurism ; the coats are indistinguishable ; &, semi-detached clot. more recent ones do. This is explained by the increase in size of the aneurism. The lamination is due to variations in the rate of coagulation, or to a succession of coagulations, so that the superficial layer of the last deposit has undergone change by the time coagulation sets in again. Moreover, there is some- times an alternation of j)ale and coloured clots (Fig. ■ 45), the former consisting chiefly of fibrin, the latter of coagulated blood. The darker strata become paler as time goes on, from disintegration of the red corpuscles and diffusion and absorption of the hsemo- giobin. 294 Surgical Pathology. [Chap. LV. The laminse can be easily separated from one another, and the outermost from the sac of the aneurism. Irregular softening cavities occasionally form in the clots of large aneurisms, and in this way fragments may be detached and plug the vessel Fig. 45. — ^Aneurism of Middle Cerebral Artery. (Natural size.) a, Sac of aneurism laid open, and showing the laminated clot, & and d, within ; c, black coagulnm ; e, ai'tery ; /, space left hy clot shrinking from hardening in alcohol. The older periphei'al part of the clot was of a dark reddish-hrown colour, interspersed with two pale streaks. Tne more recent part of the clot was of a pale fawn colour, with the exception of that last formed, which was black. beyond, and possibly cause gangrene. If the laminse are loosened at their free borders blood j^asses into the clefts, and, meeting with little resistance between the layers, separates them more or less. Then the interlaminar spaces fill with dark coagula. This is another explanation of the alternation of pale and coloured clots ; but in such cases the disposition is very irregular. From natural causes, or as the result of treatment, the blood in the sac may coagulate en masse. However extensive the lamination, the final oblitera- tion is always effected by simple coagulation, which extends into the artery on each side of the aneurism. The irritation of the clot causes the artery to inflame, and this ends in its permanent obliteration by Chap. Lv.] Aneurism. 295 organised connective tissue. Tlie danger from subse- quent softening of the coagulum in the aneurismal sac is not great, for by the time it occurs the artery is pretty firmly plugged. IJnder the microscope, scrapings from the laminated clot show fibrin filaments, fatty debris, granular and crystalline hs&matoidin, and plates of chloresterine. Changes outside the aneiirism. — The irri- tation from expansion of the sac sets up inflammation around it. This causes a thickening of the sac at the expense of the tissues, which undergo gradual absorp- tion, partly from inflammatory softening, partly from diminution in the blood supply, through continuous pressure. Where the irritation is slight, the exudation organises, so that in the same specimen new tissue formation and atrophy may be seen side by side (Fig. 3). No structure is able to withstand the expanding force of an aneurism \ thus, the sternum, ribs, and vertebrae become excavated in aneurism of the aorta. Cornil and Ranvier assert that rarefying ostitis caused by the pressure of the sac is the sole cause of the absorption of bone. No doubt it is an important factor, but simple atrophy from sustained pressure must not be forgotten. In some cases the inflammation in and around the sac goes on to suppuration. This inevitably causes rupture, unless in the meantime coagulation has taken place in the aneurism and artery beyond, but even then the clot will probably disintegrate, so that the final result is the same. The superficial veins of the part are generally dilated, from obstruction to the current through the main trunk. There may also be oedema. The resistance ofiered to the blood stream as it passes through the aneurism increases the tension in the side branches of the artery, and so opens up the collateral circulation. For this reason gangrene of 296 • Surgical Pathology. [Chap. lv. the leg is less likely to follow ligature of the femoral, for a large or medium-sized than for a small aneurism. Hence also the value of compression preliminary to ligature. The existence of a spontaneous aneurism is evidence of arterial disease, which renders the vessels rigid and slow to expand. The pulsation of the artery on the distal side of the aneurism is usually weak ; at the same time, the artery may be fuller than normal, from blood entering it in many collateral streams. The bruit produced in the sac may be conducted for a considerable distance along the artery ; e.g.., in the case of a femoral aneurism it may sometimes be heard in the tibials. This is an important diagnostic sign between aneurism and a pulsating malignant tumour, where the bruit arises in many vessels and away from the main trunk. Varieties of patlioSog^ieal aneurism. — These are named : (1) From the composition of the sac — • true and false ; (2) from their shape — sacculated, fusiform, cylindrical, and racemose or cirsoid ; (3) from their primary origin — syphilitic, embolic ; (4) from some peculiarity in size, course, or distribution — miliary, dissecting, etc. Fusiforan aneurisms only attain a large size in the case of the aorta. They are not uncommon in the popliteal arteries. There is uniform dilatation of the entire circumference of the vessel. They generally yield at one part, and become sacculated. Cirsoid aneiirism. — Racemose aneurism. — Aneurism by anastomosis consists of a dilatation of a connected series of arteries, or of a single artery and its branches. They are most common in the scalp and orbit, but- they are met with in other parts, e.g., the buttock. The vessels are enlarged in every way, they are lengthened, tortuous, and varicosed ; their walls Chap. Lv.] Aneurism. 297 are thickened, and their lumen increased. Billroth believes these aneurisms to be of inflammatory origin, since they sometimes follow injury, and their walls contain many new-formed cellular elements. In one case I found two circumscribed aneurisms of the internal carotid, one just outside the skull, and the other in the cavernous sinus; and also uniform dila- tation of the ophthalmic artery and its branches. There was protrusion of the eye-ball. The patient had shortly before been kicked by a horse on the side of the head. Ligature of the common carotid failed to cure or arrest the disease, and death ensued from cerebral congestion. In another patient all the arteries of the scalp were dilated, and the occipital was as large as the little finger. By their pressure they had hollowed out the cranial bones into furrows. Emtooiic aneurisms are mostly intracranial. Vegetation from the cardiac valves arrested in the cerebral vessels set up a localised arteritis. Dilatation takes place at these spots. Such aneurisms are relatively common in children. Miliary aneurisms are found in the cerebral vessels. They are quite small, often no larger than a pin's head. Some are microscopical. They are usually multiple, and are met with in the pia mater and in the substance of the brain. Atheroma or syphilis is the cause. By their rupture they cause apoplexy, but previous hsemorrhage or thrombosis may in some cases be the exciting cause of the dilatation, the obstruction in front throwing strain on the diseased arteries. Hissecting: aneurism. — An " atheromatous abscess " bursts ; blood is forced between the middle and external coats, or more probably between the layers of the middle coat (Peacock). The channel thus formed opens again into the lumen of the artery, when it meets with a softening focus or another ulcer ; or it ends in a sacculated aneurism of 298 Surgical Pathology. [Chap. LVI. the internal or external coat, and then it obstructs the artery, or ruptures externally. Dissecting aneurism is not met with in the small arteries. It is most common in the aorta. CHAPTEE LVI. LIGATURE OF AETERIES. When an artery is tied the internal and external coats are cleanly divided, but they do not curl up as in torsion. The external coat is thrown into folds, and the convolutions are welded together by the ligature. The injury in- flicted on the vessel induces coagulation, which extends on each side to the next collateral branch. The clot is pyramidal, ^vith its base at the seat of ligature. At first it fills the artery for some little distance, but it shrinks as the con- tracting fibrin the expresses This allows serum. Fig. 46.— Common ,1111, , , Carotid Artery tlie Diood to pass between of a Child, on.. -,.■■ ^ , ,, , which a Catgut it ancl tlie vessci wall, and Ligature was ap- /> , i -, • ■ , i i plied three days lUrtlier QOpOSlt takCS place, The clot has Until the clot is more or been removed. , • n i • , i a points to the fur- ^^^s spu^ally laminated. Hga^u^t \^hlc^ When fully formed it is tiTlnte^afand fii^mly adhcreiit to the wall mMcUe coats of the ^f ^j^^ ^^^^^j^ Within a Fig. 47.— Portion of Femoral Artery examined on the fourth day after the application of a Ligature. a. Cardiac extremit:? ; 6, division of the internal and middle coats by the ligii- ture ; c, proximal thrombus ; d, distal thrombus ; e, origiu of prof nil da f emori^ {After Maneg.) Chap. LVi.] Ligature of Arteries. 299 fortnight it is quite pale from solution and diffusion of the colouring matter. The proximal is said usually to be larger than the distal clot, since the latter is formed under greater pressure, and is more disturbed by the inrush of blood from the collateral branches. The so-called secondary clot consists of inflammatory lymph, and cells exuded from the wall of the vessel under the irritation of the ligature. The exudation joins the primary clot about its base and sides, and is in fact incorporated with it. Organisation ensues, and the lumen of the vessel is obliterated by dense cicatricial tissue. Most observers agree that the clot is partly absorbed and partly organised. Cornil and Kanvier say that it is wholly absorbed, and that the young vascular connective tissue that fills the vessel is entirely derived from an ingrowth of granulations from the inflamed walls. The process is exactly the same as in occlusion by spontaneous thrombi (Tig. 50). As the vasa-vasorum run for a short distance within the sheath before penetrating the coats of the vessel, it is clear that the vascular supply to the arterial walls will be somewhat defective immediately on the distal side of the ligature. Moreover, as the collateral circulation is being established the tension is constantly being raised on the distal side and lowered on the proximal. The better nutritive supply and the greater quiescence explain why the artery on the proximal side of the ligature is more firmly occluded than on the distal ; and why in the case of secondary haemorrhage the blood more often issues from the distal portion. Cutting: through of the ligature. — What happens is as follows : The portion of external coat gripped by the ligature is killed outright, and has to be cast ofi" like any other slough. This is efi'ected by a true process of ulceration. A layer of granula- tion tissue forms on each side, the ligature holding ^3oo Surgical Pathology. [Chap. lvii. the necrosed portion of the artery. It is true the latter is not seen on examining the loop of the liga- ture, for it disintegrates whilst it is being set free. Catgut ligature melts awaj after a few daj'S, and whatever portion of the artery has lost its vitality is removed by absorption. If the artery be loosely tied with catgut ligature, occlusion may be effected without loss of tissue, exactly as in spontaneous thrombosis. CHAPTEU LYII. VARIX. Definition. — Yarix is an uneven or pouch-like dilatation of the veins, the walls of which are thickened, and the lumen widened and lengthened. Causes. — The exciting and sufficient cause is the strain from obstruction to venous circulation ; but besides this there is often a predisposition to the disease from inherent weakness of the coats of the veins. The obstruction may be temporary, e.g.^ the pressure of a tumour ; recurrent, as in repeated preg- nancies ; or permanent, as in aneurismal varix. Consequences. — (1) Thrombosis and phlebitis, as in inflamed piles ; (2) ulceration (in the leg) ; (3) atrophy of structures, e.g., the testicle, from vari- cocele, this arising partly from pressure and partly from deprivation of projDerly oxygenated blood. Usnal seats of varix. — The • lower extremity ; the prostatic, spermatic, and hsemorrhoidal plexuses ; and the neighbourhood of arteries (aneurismal varix and varicose aneurism). The veins of the lower extremity suffer more than those of the upper: (1) Because the force of gravity acts more continuously against the direction of the Chap. LVII.] VaRTX. 30I venous blood-stream ; (2) because contraction of the muscles of the lower limb is greater and more con- tinuous, and the blood from the deep intermuscular veins is forced into the superficial ones to a corre- sponding extent (advantage is taken of this compen- satory dilatation, in the operation of venesection); (3) accidental pressure upon the inferior vena cava and iliac veins is more common than upon the superior vena cava and innominates. Oeneral pattiology. — By some the initial change is described as inflammatory, whereas others look upon it as a mere fibroid substitution, that is to say, the normal elements of the coats are to a great extent replaced by a low form of connective tissue, the same as is seen in nutmeg cirrhosis of the liver. In both cases the increase of fibrous tissue follows chronic obstruction to the flow of blood through the veins. Formerly these changes were considered as inflammatory, now it is the fashion to speak of them as " cirrhoses," "scleroses," or "fibroses." It is diffi- cult to diflerentiate the two, for whilst the usual signs of inflammation are not marked, because they are very slight and spread over a long period, the final result is the same as one of the typical terminations of undoubted chronic inflammations, that isj the pro- duction of cicatricial tissue. Those who reject the inflammatoty theory assert that the stagnation in the veins prevents their coats from being properly replenished (for if the current through the veins is obstructed it is clear that the tributary vasa-vasorum cannot discharge their" contents with natural freedom). They say that the deoxydised blood suffices for the nourishment of con- nective tissue, but is not equal to the support of more highly organised structures such as muscular fibre. We refuse to accept this as the entire explanation^ (1) because the efiect of strain, which is traumatism. 302 Surgical Pathology. [Chap. lvii. long drawn out, perhaps, but none the less traumatism, is ignored ; (2) because the areolar tissue around the veins is much condensed and thickened by material that is more vascular and corpuscular than normal. There is degeneration from chronic starvation, and inflammatory thickening from strain. As before said, there is general increase in the width and length of the veins. They dilate in spite of the thickness of the walls, for the intravascular pressure is raised ah initio, and the altered structure is less able to bear the strain thrown upon it. On account of the great elongation the veins become curved in a remarkable manner. Then follows varicosity, (1) because the obstruction tells most at the seat of the valves ; (2) because the blood stream is diverted from its rectilinear course, and its impact is greater on the convex side of each curve as seen from without, like as a river hollows its banks here and there in its winding channel. Histology. — On opening a varicosed vein the inner surface looks rough from a longitudinal striation. Under the microscope this is seen to be due to coarse bundles of connective tissue interlacing with the elastic fibres of the inner portion of the middle coat, and greatly obscuring them. The muscular fibres at first undergo a compensatory hypertrophy, and on section lengthwise of the vein appear, if stained with logwood, as pale circles with dark central spots — muscular fibre-cells and their nuclei respectively. Eventually the muscular and elastic elements are so overrun by fibroid overgrowth that nothing can be seen but a partly fibrillated, partly homogeneous, scar- like tissue, in which are embedded granules oi ingment, scattered, or in groups. The vasa-vasorum are dilated and their coats thickened. Chap. LVIL] VaRIX. 303 Calcification may take place, (1) in tlie form of plates in the walls of tlie veins ; (2) as phleholitJis in. the interior, and probably in the remains of blood- clots that have formed about the valves. They are most common in the prostatic veins. The valves, which are merely reduplications of the lining membrane, suffer in the same way as the walls of the veins ; that is, they become thicker and less pliant. Their function is soon lost, for they undergo cicatricial contraction, whilst the lumen of the vein is increased. In the end they shrink to mere caruncles, or even disappear. Should one of the ampuUary dilatations of a greatly distended super- ficial vein rupture, blood will issue from the proximal and distal sides of the opening. The more dangerous bleeding often comes from the proximal side, for the valves no longer suffice to support the column of blood above them (it may be from the vena cava down- wards) ; and the weight of this column causes a con- tinuous downpour, which may end fatally in a few minutes, unless checked by pressure or by elevation of the limb. Clianges around the veins. — The areolar tissue in which the veins lie is congested and infil- trated with inflammatory exudation. The exudation becomes indurated and firmly united to the veins, so that the latter are more or less fixed. This accounts for the feeling of a shallow trench in the skin and subcutaneous tissue when the finger is pressed fiiTuly along the course of a dilated vein. *' The fixation of the veins, together with the thickening and rigidity of their walls, prevents them from collapsing when wounded, and so favours heemorrhao-e. Pigmentation of the skin and cellular tissue results from capillary extravasation, and transudation of red corpuscles. The discoloration around varicosed veins of the leg is often very marked. 304 Surgical Pathology. [Chap. lviii. The localised thinnings that lead to rupture are due to extreme distention of varicosities behind the valves, and to want of support from without. Thus we often find that the superficial part of the vein, together with the atrophied skin over it, is not so thick as the deeper portion of the vein alone. CHAPTER LYIIL EMBOLISM. Embolism, or the conveyance and subsequent arrest of foreign bodies in the blood current, begins either on the arterial or venous side of the circulation. The soiu'ces of arterial esiibolisiii are : vegetations from the cardiac valves, clots dislodged from the sac of an aneurism, the contents of an " athero- matous abscess," and calcified plates and thrombi from the walls of the large arteries. Venous embolism usually results from the detachment of clots. In fracture of bones, and laceration of adipose tissue, liquid fat sometimes makes its way into the open veins. The entrance of air in the case of wounds of veins within the " dangerous region " is well known, and the symptoms in these cases are probably the consequence of plugging of the pulmonary vessels by aerial emboli. Less common causes of embolism are, aggrega- tions of pigment granules, portions of new growths swept off" from the interior of vessels which they have invaded, pus from the bursting of an abscess, and parasites. The effects of embolism. — The immediate effect of embolism is anaemia of the part supplied by the obstructed vessel; but inasmuch as there is in Chap. LVIIL] Embolism. 305 most cases a free collateral circulation, blood makes its way in by the side channels, and if the embolus be rigid only partial occlusion may occur ; this also happens when it is arrested at the point of bifurcation of an artery, for then it may not be large enough to completely close either branch. Where the collateral circulation is but little developed, as in the intermediate- sized vessels of the brain, a venous reflux ensues, which soon leads to stasis, since the pressure in front is no longer over- come by the force of the current in the artery. The embolus, act- ing as a foreign body, Fig. 4S, -Diagram of Embolic Congestion of the Lung. a. Small artery rlngsed at e by an eraholiis ; v, small vein filled with a clot, wliirli extends as far as its trunk ; the shaded portion of the capillary network is the area of distribution of the artery, in a state of passive congestion, and about to be the seat of a hemorrhagic exudation. The arrows show the collateral channels through which the abnormal tur- gescence is effected (Rindfleisch). causes coagulation of the blood upon it. This reaches to the first collateral branch, where its progi^ess is arrested, provided the anastomosis is sufficiently free. When it is defective, and especially if a number of contiguous branches of the same vessel be occluded, the blood stagnates, and the whole area becomes the seat of secondary thrombosis. This, however, takes some time to become complete; and in the meanwhile, the walls of the capillaries, suffering from impaired nutrition, readily allow the passage of blood corpuscles, and pro- bably many capillaries actually rupture, the more so u 3o6 Surgical Pathology. [Chap. lviii. as the strain upon them is increased by the disten- tion of the congested vessels around. This is what is termed hcemorrhagic infarction. The size of the embolus will depend upon its source and its consistence. If it be derived from a calcified cardiac vegetation, or an atheromatous plate from an artery, it will withstand the impact against the walls of the vessels. Should it consist of a softened venous thrombus it will very likely be broken up in its onward course, the several portions being scattered in an embolic shower. A vessel may not be completely blocked by an embolus, but later on occlu- sion may ensue from coagulation of the blood upon the embolus. The effect upon tlie Tvall of tlie vessel will vary as to the nature and duration of the plugging. If the embolus consist of a healthy thrombus it may be quickly absorbed, leaving the structure of the vessel intact ; or it may become adherent and organise, the lumen in this way being permanently obliterated. A rough body, such as a calcified vegetation, will irritate mechanically, and cause thickening of the coats of the vessel. A portion of a tumour may infect the part at which it is arrested, and form the centre of a fresh growth. Lastly, from whatever source, a septic embolus invariably leads to acute inflammation and necrosis. Paths of transit. — Since as a rule the emboli are comparatively small, and tend to take a direct course, it is clear that the periphery of an organ will be more often the seat of the lesion than the centre, hence in the lungs the posterior bases suffer most. Inasmuch as they are carried along the main course of the blood stream, they will pass into the thoracic aorta rather than travel through the innominate, carotid, and subclavian orifices. So, again, they will be found in the left carotid, renal, and iliac arteries Chap. LVIIL] H.EMORRHAGIC INFARCTION. 307 more often than in the right. In a few instances, e.g.^ in the middle cerebral, coronary of the heart, and branches of the coeliac axis, their course is almost at a right angle to that of the parent vessel. When the embolus starts on the venous side of the circulation (which it usually does, and in the form of detached clots) its arrest usually takes place in the lungs, and the pulmonary capillaries filtering the blood prevent the distribution of the solid particles in other organs or tissues. But these capillaries are comparatively large, and are still further dilated in any disease that raises the pulmonary pressure ; hence, it is not very uncommon to find that some of the smallest emboli make their way through the lungs and left side of the heart into the aortic system. Still there is no doubt that many of the metastatic abscesses found in other organs than the lungs in pyaemia are the sequel of primary thrombosis, and not of embolic infarction. In cases where the abscesses are found only in the liver (excluding those of portal origin), the same explanation seems more probable than that which ^supposes the emboli to have passed from one or other cava into the hepatic veins, or, in other words, against the blood current \ although in severe obstruc- tive disease of the chest the systemic venous pressure may be so increased as to become positive. Thrombi, or portions of new growth set free from branches of the portal vein, will be conveyed to the liver, and there probably entirely arrested. Hsemorrliagit^ infarction has been already adverted to. It consists of secondary thrombosis, startino- from an embolus and extending throusfh a part or the whole of the area supplied by the obstructed artery, and, as a result, exudation from the vessels, extravasation of blood from rupture of capillaries, and the formation of an intense hyper£emic inflammatory zone around. These infarctions are mostly wedge- 3o8 Surgical Pathology [Chap. LVIII. shaped, for the vessels divide again and again, the area of distribution gradually widening (Fig. 49). The pathological changes that ensue depend : (1) Upon the size of the infarction; (2) upon the degree of freedom of anastomosis ; (3) upon the nature of the plug, whether it be simjole or septic. " If the embolus be small and the colla- teral circulation free, a quick absorption of the clot in the throm- bosed vessels is the usual result, and the part is thus restored to its healthy condi- tion. If the embolus be large, but not septic, the area of infarction is too wide for the thrombosed vessels to be cleared before fatty degenera- tion takes place in the tissues (including the walls of the vessels themselves) cut off from their blood supply. In this case the colouring matter of the coagulated and extravasated blood is discharged from the cor- puscles, and, with the more fluid portion, is absorbed by the surrounding vessels, leaving a firm yellowish- white putty-like mass, composed of degenerated tissue and blood clot, closely resembling a syj)hilitic gumma, for which, indeed, it is sometimes mistaken ; but a gumma is harder, and is not conical in shape, nor is it surrounded by such an intensely congested zone. This mass, in its turn, is gradually reduced in size by absorption of the debris resulting from the disintegra- tion, until at last a contracted puckered cicatrix, Fig. 49. — Embolic Infarction of Spleen. The wedge-shaped masses are partially de- colorised. This is farther advanced at the periphery, 6, than in the central portion, c. Each block is surrounded by a zone of hype- ragmia, a ; d, outer surface of the organ. Chap. LViii.] Embolism. 309 infiltrated, perhaps, with lime-salts, and containing some pigment granules, and, in the case of the brain, hsematoidin crystals, is all that remains. If the infarction start from a septic embolus, whether it be large or small, the intense irritation will invariably lead to the formation of a circumscribed metastatic abscess, the contents of such abscess con- sisting of inflammatory exudation, disintegrated clot, and broken-down tissue. Oeneral effects of emboHsm. — The original embolus may be so small, or it may crumble into such minute fragments, that only the capillaries are blocked, and unless in this case it be septic, or some vital organ, such as the brain or heart, be involved, it will probably lead to no further trouble. On the other hand, it may be of such a size as to cause almost instant death, as when large vegetations from a cardiac valve find their way into the cerebral vessels, or a thrombus loosened from an iliac vein plugs the trunk or main branches of the pulmonary artery. Besides the immediate danger in such cases, and the almost certainty of death in septic embolism of the internal organs, there are others of great gravity. Gangrene of the leg may follow the accidental plugging of the popliteal artery by a clot from an aneurism seated on the same A^essel, the opening up of the collateral circulation being too long impeded by the rigidity of the diseased vessels, AneitrisTii of the cerebral arteries often owes its origin to the degeneration consequent on the pressure of an embolus ; the walls softening from inflammation give way at first on the proximal side of the obstruc- tion. The source of the embolism is frequently de- tachment of vegetations from the cardiac valves after rheumatic fever, and this explains the apparent anomaly of pathological aneurisms occurring in children. CHAPTER LIX. THROMBOSIS AND PHLEBITIS. Thrombosis is a clotting of the blood in the vessels. Concerning the coagulation of blood drawn from the vessels, it can be shown that it is due to the interaction of three bodies, fibrinoplastin, fibrinogen, and a ferment resulting in a combination of the two former ; that is to say, fibrin which does not exist in the blood comes to be formed under certain ascertain- able conditions as the latter becomes solid. There is, so to speak, a constant antagonism between two sets of influences, between those that favour and those that retard or prevent coagulation. Amongst the former are : 1. Rapid motion, as in whipping, or, in other w^ords, multiplication of points of contact. 2. Exposure to not living matter. Amongst the latter we have : (1) The addition of a third of the bulk of some neutral salt ; (2) a temperature of about 32° Fahr. ; (3) moderate heat ; (4) the abstraction of haemoglo- bin ; (5) the absence of a neutra.l salt, whose presence, accordinof to Schmidt, is essential to coao-ulation. Now blood, whilst in the vessels, is known to clot more easily when the current is slowed, just the reverse of what is found in shed blood ; but this is only an apparent anomaly, for slowing of the blood current means a diminution in the nutrition of the coats of the vessel, and this brings it to a state of lower vitality, and so the question of slowness or rapidity of motion is resolved into that of contact with foreign matter. As to the so-called ferment, the conditions under which the consequences of its action are brought about in the living body cannot be doubted ; and it is here that the antiseptic treatment- Chap. Lix.] Thrombosis. 311 of wounds shows itself to advantage, for when decomposition of the discharges is allowed to take place unchecked, how much more likely is thrombosis to extend beyond the immediate seat of injury, how much more likely a rapid softening of the clot, and, as a natural consequence, detachment of emboli rife with mischief, by reason of their mechanical action, and still more so from their being saturated with septic matter. The two prominent features of thrombosis are : (.1) Its causation ; (2) the fate of the clot. Causes of tlirombosis. — To gain some clue to an answer to the question, why does the blood coagulate in the vessels'? the diseased states not seldom complicated with this result must be considered. Amongst others, the following cases have occurred in the experience of the author : thrombosis of the cerebral veins in phthisis and marasmus ; of the veins of the upper limb, in septicaemia, from compound fracture of the jaw; of the pulmonary artery, fatal when the aseptic wound from amputation of the breast was all but healed; of the varicose veins of the lower extremity ; of axillary and femoral veins in post-parturient women ; of the axillary vein in rheumatic fever ; of the brachial artery, from bruising. To these may be added, the plugging of the cerebral arteries in syphilis ; capillary thrombosis, as the essential pathology of cancrum oris, and as the explanation of the multiple openings in carbuncle (Billroth) ; not forgetting those cases where coagulation is intentionally induced, as in the ligation of arteries and the operations for varicosed veins. The conclusion to be drawn from the foregoing statements is, that there are two diseased conditions, one of the vessels, the other of the blood, that act as the proximate causes of thrombosis. Slowing: of the blood current from weakness of the heart is a subsidiary factor. 312 Surgical Pathology. [Chap. lix. Causeis foioid. in tlie tolood. — The blood may be so vitiated that it can no longer maintain its fluidity, from {a) increase in the fibrin factors, (6) excess of excrementitious matter, from defective elimination, as in gout, or the introduction of infective material, as in septicaemia. Causes in tiae vessels. — Alteration in the structure of the vessels from defective nutrition can be explained in three ways : 1. Those conditions that tend to slow the blood current ; such as («) varicosed veins ; (6) atheromatous and calcareous arteries, and aneurismal sacs ; (c) obstruction from without, as by ligature, or the pressure of a tumour, or inflammatory exudation, causing great capillary tension ; {d) venous reflux into capillary areas, from embolism of the arteries feeding them ; (e) feeble cardiac action, either from fatty degeneration, or acute myocarditis, or a deficient output of energy from want of the proper amount of stimulus, as when a person of active habits is suddenly confined to bed by an accident. 2. {a) The influence of inflammatory states, such as occur in subacute and chronic arteritis ; (6) simple degeneration of the vessel walls. 3. The immediate efiect of injury, that is, before there is time for inflammatory action to supervene. The state of nutrition of the tissues to be nourished must necessarily affect the quality of the blood, and so indirectly lead to its clotting. Relation of tliromtoosis to plilebitis. — The microscopical changes that are found in thrombosis have been studied chiefly in the veins, where coagula- tion is much more common than in the arteries, and for a long time phlebitis was considered the cause of thrombosis ; the order of things is now reversed, for, except in rare instances, there can be no doubt but that coagulation precedes inflammation. Some patho- logists ignore the existence of an endophlebitis, Chap. Lix.] Phlebitis. 313 admitting only a periphlebitis in the aclventitia and in the areolar tissue around the vein. Formerlj, the si^ns of inflammation aloni^ the course of a vein during life, and the redness of the intima, and ofttimes puriform contents found post-mortem, were looked upon as proofs that the disease was primarily and essentially a phlebitis. The first criterion is useless, since a periphlebitis would equally well explain the symptoms ; the second in many cases admits of another interpretation, since it can be shown that the discoloration of the inner coat is often due to staining by the hsemogiobin of the clot, and not to inflammatory hyperEemia ; and the third is practically valueless, for in most cases the material looked upon as a mixture of pus and blood is in reality but partially decolorised, softened, disintegrated clot, consisting of fatty and granular debris, but few leucocytes re- maining. Again, thrombosis follows so quickly upon injury to a vein that it is impossible in these cases for inflammation to have intervened. It cannot be denied, however, that phlebitis does occasionally precede and cause the thrombosis ; e.g.^ in cellulitis, where the vessels are attacked from without : moreover, the walls of veins are sometimes infiltrated with the anatomical evidences of pus, that is to say, cells which cannot be told from pus corpus- cles, and the same may be said of the clots which those veins contain. Signs of phlebitis. — When a subcutaneous vein is inflamed the signs are very manifest : redness of the skin over it, a hard cord with nodular swellings, i.e., the occluded vein still further thickened by the exudation of lymph around, the nodules marking the position of varicosities and the valves. It may be noted that as the clot shrinks or is absorbed more quickly from the internodal portions, small, hard lumps for a time remain, which in certain situations 314 Surgical Pathology. [Chap. lix. {e.g., Scarjja's triangle) may be mistaken for indurated glands. Then there will be oedema from obstruction of the current, and as the clotting and inflammation spread, the point of greatest intensity of pain will shift along the course of the vessel from day to day. It is by no means rare in patients with shattered health for abscesses to form here and there around the veins that have become plugged. Post mortem it is a matter of some difficulty to dissect out these veins from tlieir bed of lymph, which later on is either organised, leaving the vessels blocked, or is absorbed, the normal condition being restored. When the deep veins are thrombosed there is often no redness of the skin, but the pain, oedema, and distention of the superficial veins point to the pathological chauges going on (phlegmasia alba dolens). When diffuse coagulation occurs in a main artery and its companion vein, it usually begins in the artery ; and, again, diffuse thrombosis of an artery is more frequently attended by that of the vein than mce versa, for when a vein is plugged, the nutrition of the walls of the contiguous artery is not necessarily much inter- fered with, but when the circulation in the artery is stopped, the vasa-vasorum that supply the walls of the vein are also obstructed, and so a starvation of that part of the vein ensues, and this causes a dimi- nution of vitality, and consequent coagulation. At the same time it is likely that the inflammatory state outside the artery thrombosed may have some share in effecting the clotting in the neighbouring vein; be- sides, it is certain that something more than a simple failure of nutrition is at work, else how comes it that coagulation occurs in only a small proportion of the cases of degenerated vessels. The fate of tlie clot. — Absorption, disintegra- tion, organisation, and suppuration are the secondary changes occurring in the thrombus. Except in the ch ap. L I X. ] Thr ombosis. 3 1 5 case of septic thrombosis, where, if life be sufficiently prolonged softening always ensues, ahsorjotion is per- haps the most common event. This is often seen in varicose veins that have been treated by simple com- pression, where after temporary occlusion the channel is re-established. Absorption may proceed by a gradual disintegration of the central part of the clot, the blood current passing through the latter, which in the end is entirely removed ; or wasting may slowly progress from the periphery until only a fine filamentous cord of fibrin entangling white corpuscles (for the red ones break up early) is all that can be seen ; and this finally disappears, leaving the lumen of the vessel completely free. Embolism in these cases is prevented by the clot in the main vessel being kept in position by offshoots into the tributary branches. After alDSorption is complete, staining of the intima persists for some time. Disintegration occurs in all septic thrombi and in large simple clots where the blood supply is defective : thus in aneurisms that have been consolidated by rapid coagulation of the blood en 7nasse, as in those of the popliteal artery treated by Esmarch's rubber and cord, it is by no means rare to find fluctuation after some days. It would be a grave error in practice to mistake this liquefaction in the centre of the clot for suppuration. Such cases require great care in the after-treatment, for it is difficult to say the exact extent of the softening, and in- judicious manipulation might dislodge a portion of the contents and force it into the trunk and branches beyond. Although a healthy clot projecting into a vein may be broken off by the impact of the blood stream, by careless handling, or by movement on the pari of the patient (particularly flexion of the hip when the ilio-femoral vein is thrombosed) ; still such an event rarely happens, unless there be loss of consistence and tenacity from disintegration. It is the existence of 3i6 Surgical Pathology, [Chap. LIX. this softening in pyaemia that explains the very fre- quent occurrence of embolic abscesses and infarctions. Org'aiiiisatioii of tlie clot. — In some text- books it is stated that after phlebitis the vein some- times shrmks to a " fibro - cellular cord ; " this is Fig, 50. — Organised Thrombus in Common Carotid Artery from a Case of Aneurism of tlie Aorta. a, Tunica adventitia ; 6, tunica media ; c, tunica intima ; ilfu departures : (1) Filling in of the cavity with lymph that organises and cicatrises, ^.e., spontaneous cure;. (2) progressive suppuration, and destruction of the remaining portion of the gland. The former is the exception. The latter in its progress develops Hernia testis — fiuig'oiis testis, like hernia cerebri, is essentially inflammatory. The mere open- ing in the tunica albuginea does not explain it ; if it did, this would be sufiicient ground alone to centra-indicate the treatment of acute orchitis by puncture. Nevertheless, the resistance offered by the unyielding fibrous capsule is an important factor in the process, for whilst the volume of the contents tends continuously to increase, by reason of the exu- dation from the vessels, accumulation is prevented by the rigidity of the inexpansile investment of the organ. Hence it follows that so long as exudation exceeds absorption the surplus must escape through o 28 Surgical Pathology. [Chap. l.xi. the opening established by the bursting of the abscess. But it is not simply a filtering of pus through the inflamed tissue, since this would not account for the protrusion. Fibrin separates from the liquor sanguinis and imbeds the migratory leucocytes ; and into the semi-solid product capillary loops shoot from the adjacent vessels ; and thus a vascular granulation tissue is, formed which constitutes the greater part of the fungus. Meanwhile the glandular tubules are broken up, but before their disintegration is complete, columns and isolated cells of epithelium are carried outwards by the advancing granulation tissue with which they are incorporated, and can be recognised with the microscope. The fungus does not attain a large size, for the superficial layer melts away whilst the growth is replenished from beneath. After a time it becomes stationary, and with the subsidence of the inflamma- tion it recedes. The secretion is at first purulent, then muco-purulent, or thin and serous. Its nature and quantity depend upon the degree of inflammation. The skin around is congested, and in long-standing cases the papillae and hairs are hypertrophied. There is a milder form of " fungous testis," in which the glandular structure seems to be but little, if at all, afiected. A small abscess forms beneath the scrotuui, and opens externally. This leaves a sinus, terminating in an orifice surrounded by pale gelatinous granulations. On manipulation an indu- rated cord can be felt, taking ih.Q direction of the sinus, and fixed to the testis or epididymis. It pro- bably begins as a localised infiammation in the tunica vaginalis, and in that case it is comparable to a sup- purating sebaceous cyst. Section of a striimoiis testis. — The appear- ance on section will depend upon the rate at which the Chap. LXL] Scrofulous Sarcocele. 329 structure has been undermined, and the time at which the examination is made. In comparatively acute cases the whole organ may be broken down into a semi-diffluent pulp ; suppuration having completed Fi^. 52. — Scrofulous Orchitis, showing the Formation of Abscess. The preparation was injected with Gelatin and Prussian-blue. a. Spermatic cord much enlarged, the vessels are embedded in indurated lymph; &, portions of the testicle apparently quite healthy, the tubules are seen presenting a fringed appearance on the surface of the section; c, irre- gular mass of cheesy matcri'il, the nrtificial injection has stopped alirujitly at the periphery ; rV, small abscess pointing at the front of the organ. The epididymis, which hns lost its outline, forms a solid mass at the upper and back parts of the testis, continuous with the thickened cord. (E.educed one quarter.) the destruction begun and continued by gradual obli^ teration of the vessels and consequent fatty degene- ration. But the testis undergoes considerable enlargement, and caseation is for the most part well advanced before the occurrence of suppuration. Large tracts 330 Surgical Pathology. [Chap. lxi. ai-e slowly deprived of tlieir vascular supply, and the constituent elements break up into molecular fat. Meanwhile a gradual desiccation takes place, with the result that the disorganised tissue and exudation are left as irregular firm cheesy masses, which appear granular or quite smooth on the cut surface. Artificial injection shows these masses to be entirely free from the circulation, and makes them stand out in marked contrast to the surrounding tissue, which is coloured by the fluid that finds its way into the as yet patent vessels. Mg. 52 represents a strumous testis removed from a man cet. 30. The other gland had been excised three and a half years before for the same disease. The cord is thickened. A portion of the secreting structure appears healthy. There is a yellowish- white caseous mass at the centre and to one side. Suppuration has commenced, and already destroyed the investing tunics, and caused the skin to bulge. During life fluctuation could be detected at this spot. Minute anatomy of scrofulous sarcoeele. — It was formerly supposed that the disease began as an inflammatory effusion into the tubuli seminiferi, and that as the walls of the latter became softened and distended, they ruptured and discharged their contents into the intertubular spaces. But this is not the case. The essential pathology is a chronic interstitial orchitis (JFig. 15). The con- nective tissue is increased by infiltration with liquor sanguinis and leucocytes. This may be very decided before there is any change in the epithelial lining of the tubes. After a time, however, the cells become granular, and, as they proliferate, are set free in the lumen, which eventually becomes choked with de- squamative and exudation products. The morbid processes can be studied better in the epididymis than in the testis proper, for in it the tubes are much wider. Chap. LXL] Tubercular Orchitis. 331 The blood-vessels get blocked by coagula and com- pressed by exudation. The result of this is a starva- tion of the tissues they supply, and, as a natural consequence, fatty degeneration and caseation. Or the interruption in nutrition may be more acute, as the effusion from the vessels is more rapid and copious. Then, instead of caseating, the neoplasia liquefies, and suppuration is established. On the other hand, the lymph may organise into a low form of cicatricial tissue. Bearino: these facts in mind we can understand the diversified appearances in the group of cases designated strumous testis. Disseminatecl tubercular orchitis. — This variety of strumous testis is generally seen in the course of a more wide-spread miliary tuberculosis, particularly through the genito-urinary tract. Even when the disease appears to be localised in the testis there is great liability to its subsequent outbreak in other organs. I have known tubercular meningitis follow disseminated tubercle of the testis in the adult. Fig. 55 depicts the bladder of a patient who had tubercular ulcers of the urethra, and in whom the kidneys, prostate, vesiculse seminales, and vasa deferentia were affected with caseating miliary granulations. But it must be remembered that the diffuse strumous orchitis before described is also prone to set up or be followed by true tubercular deposit in the same organ, or in distant parts ; and that chronic strumous inflammation is excited by the presence of tubercles. The so-called strumous, and tubercular orchitis are strictly analogous to strumous, and tubercular ostitis {q.v^. Anatomically the disease is characterised by the development of grey granulations between the tubules of the epididymis and testis. At first they are dis- crete, but subsequently they become more or less con- fluent by their own growth ; or by the intercalation 332 Surgical Pathology. [Chap. lxi. of fresh, tubercules ; or a number of granulations may be hidden in the exudation products of in- flammation between and around them. They soon undergo fatty degeneration and caseation, and as they soften in the centre small abscesses are formed; by the aggTegation and fusion of these abscesses irregular cavities with, festooned margins are made. Miliary tuberculosis of the testis is more common than is generally supposed, as the patients frequently die from the invasion of the more vital organs before the local lesion is sufficiently advanced to be recognised during life. Both testicles are u,sually involved, and the vasa deferentia and vesiculae seminales appreciably thickened (Fig. 55). The inflammatory changes set up around the tubercles differ in no way from what is observed in primary diffuse strumous orchitis. The usual characters of grey granulations can be demonstrated : viz., a delicate reticulum of homogeneous or finely fibrillated intercellular substance enclosing lymph corpuscles and giant cells. Malignant sarcocele, — Malignant disease of the testicle includes encephaloid cancer, sarcoma, and enchondroma. Colloid cancer is very rare. The features that serve to distinguish new growths involving the testicle from inflammatory enlargements are as follows ; — 1. Size. This may be quite decisive, for whilst a tumour may exceed in size the foetal head at full term, simple, syphilitic, and strumous sarcocele rarely attain a gTeater magnitude than a goose's ^gg. 2. Lobulation. Malignant growths are not un- commonly lobulated, not so much on the surface as in their internal structure, for the resistance offered by the tunica albuginea serves to difluse the pressure and maintain the even outline of the mass. The caseous patches of strumous orchitis and syphilitic Chap. LXL] Cancer of the Testicle. 333 gummata are irregular in shape, and contrast strongly with the surrounding tissue. 3. Smooth-walled cysts are quite characteristic of new growth. Thev cannot be mistaken for the cavities formed by softening and suppuration in strumous disease. 4. Malignant tumours that are very rapid in their development, especially encephaloid cancer, often appear fiocculent on the cut surface when the pre- paration is placed in fluid. Inflammatory deposits, on the other hand, are generally quite smooth on section. 5. As malignant growths are plentifully supplied with blood-vessels, injections of coloured jluid pene- trate the entire mass. The yellow caseous tracts of strumous orchitis and syphilitic gummata are ex- travascular, and consequently the injection stops short at their periphery. Whilst one or more of the above-mentioned cri- teria may fail in a given case, the evidence afforded by their collective consideration can never leave a doubt as to the nature of the enlargement. Enceplialoid cancer is usually met with be- tween the as;es of twenty - five and fortv - five. It commences in a proliferation of the epithelium of the seminiferous tubes. The growth is generally very rapid. The whole of the secreting stiTicture is destroyed before the tunica albuginea gives way. When this takes place the scrotal tissues are quickly involved J and the skin, at first simply adherent, gets deeply congested, and finally it ulcerates, and the unrestrained growth protrudes as a bleeding fungus, '■'■fungus hcew.atodes.^'' The uniform elasticity of the tumour goes a long way in differentiating it from strumous and syphilitic orchitis. On puncture, blood escapes quite freely, sometimes bringing with it minute portions 334 Surgical Pathology. [Chap. LXI. of growth, the structure of which can be recognised under the microscope. Cysts and nodules of cartilage are much less frequent than in sarcoma. rt Fig. 53. — Chondro-sarcoma of the Testicle. The normal structure has entirely disappeared. The new growth, a, presents a regular iobulated appearance. At c several small smooth-walled mucous cysts are seen. With the exception of the nodule h the cartilage is disposed in microscopical islets in the substance of the softer sarcomatous hase ; /, caseous dehris of inflammatory exudation in upper part of tunica vaginalis ; «, blood-vessels filled with artificial injection; d, spermatic cord enlarged, but free from invasion by the growth. (Reducedone quarter.) The spermatic cord is always enlarged by dilata- tion of the blood-vessels to meet the wants of the rapidly-growing mass. It may also be indurated by the deposit of cancer in the lymphatics ; but this I have found to be the exception rather than the rule. ^ If the glands are affected, they will be found to Chap. Lxi.] Cystic Sarcocele. 335 be the lumbar in connection with the testicle. As the integument becomes involved, those in the groin may suffer as well. Except in very rare cases, the disease attacks only one testicle. For an account of the naked-eye and microscopical characters, vide Encephaloid cancer. Sarcoma, occurs at the same period of life as cancer, but it is also met with in children under ten years of age. It begins in the connective tissue of the gland or in the tunica albuginea. I have known it attain a large size without invading the testicle at all, but this is very unusual. In clinical gravity it Ades with cancer. It has a great tendency to generalise in the internal organs. The cord and lymphatic glands are sometimes infiltrated. It is very frequently cystic. Its minute struc- ture varies between round, mixed, and spindle cells. Cartilaginous transformation is not rare (Fig. 53). Hiicliondroma is rather a chondrifying sar- coma than a primary cartilage growth. The greater portion of the neoplasia may be converted into cartilage. In such a case the term enchondroma is admissible on anatomical grounds, but its affinities with sarcoma should never be lost sight of. The cartilage may exist in the form of microscopical islets or in large sinuous tracts or clumps. On hardening these tumours in spirit the cartilage contracts less than the surrounding soft sarcomatous tissue, and thus the cut surface is rendered uneven. Secondary growths in the internal organs retain the characters of the primary. The cartilage is mostly of the hyaline variety. In these tumours there is sometimes a considerable amount of gelatinous or mucoid tissue. Cystic sarcocele. — It would appear that some cases of cystic testicle are developed from constriction and dilatation of the seminiferous tubes of the rete 336 Surgical Pathology. [Chap. lxi. testis and the body of the organ. The large majority- are, however, not of this nature, but are dependent upon mucoid or colloid degeneration of the cells and intercellular substance of some pre-existing solid growth. The presence of a number of cysts in a tumour of the testis at once raises the presumption of its sarco- matous structure, for experience shows that here, as in all other situations, cystic sarcoma is of much more frequent occurrence than cystic cancer. The entire mass may be riddled with small cysts, many of which are of microscopical dimensions, im- bedded in a soft greyish-white ground substance ; or the cysts may be of large size, and so numerous as to give a honeycombed appearance on section. The walls of the cysts are for the most part quite smooth, and the contents clear, and either pale or stained with the colouring matter of the blood from minute capillary haemorrhages. Other cavities or accidental cysts owe their origin to interstitial extravasations and fatty softening from deficient vascular supply. Secondary intracystic growths sometimes partially or entirely fill the spaces. In the latter event the nature of affairs is manifest from the absence of structural continuity, except at the base of attach- ment, between the proliferating buds and the inner surface of the walls of the cysts. When the tumour is of slow growth the neoplasia passes to a higher phase of organisation, so that the intercystic trabeculae appear quite fibrous. 337 CHAPTER LXIL ATROPHY OF THE TESTICLE. Smallness of a testicle does not necessarily imply atrophy. It may he a case of imperfect development. Undescended testicles are below the normal size, whether they occupy the inguinal canal or remain in the abdomen free from unusual pressure. It is true the resistance offered by the walls of the canal may hinder the growth of the organ, but defective develop- ment is rather the cause than the consequence of arrested descent. The causes of atrophy are (1) inflammatory lesions ; (2) excessive functional activity; (3) senile decay; (4) long-standing varicocele, by preventing the re- newal of a proper amount of nutritive fluid, and by the continuous pressure of the distended vessels upon the tubules ; atrophy from this source never amounts to impotence (Paget). CHAPTER LXIII. HYDROCELE. The term hydrocele is applied to, for the most part, watery or serous exudations into (1) the tunica vaginalis testis ; (2) the whole or some part of the funicular portion of the processus vaginalis peritonei ; (3) dilated tubes of the epididymis or rete testis, or the hydatid of Morgagni, or the vas aberrans of Haller; (4) loculi in the spermatic cord, which are w 33^ Surgical Pathology. [Chap. lxiii. said to correspond to free cystic formations in the cellular tissue of other parts. Hydi'ocele of tlie tunica vaginalis. — So far as one can tell, this often constitutes a disease per se, i.e., it arises without any precedent morbid condition of the testicle. In such cases it is gene- rally found at the two extremes of life, infancy and old age. In the former period it seems to originate in the locking np of peritoneal fluid in the tunica vaginalis, as this is shut off from the funicular process by the physiological closure of the canal at the top of the testicle. The tension upon the mem- brane jDrobably stimulates it to further secretion, for simple withdrawal of the contents is usually sufficient to effect a cure. The hydrocele of old people is said to be the result of degenerative changes in the tunica vaginalis, which shows itself in a " loss of balance between secretion and absorption." It is due, then, either to hypersecretion, or to obstruction of the lymph vessels that naturally carry off the fluid from the serous sac ; or it may to some extent be compensatory to the atrophy of the testicle incidental to advanced age, in the same way that fat fills up the spaces of wasting bone and serous effusion takes the place of a shrinking brain. The nature of the Jluid is primarily that of the normal secretion of serous membranes, though it is frequently modified by secondary changes consequent on increased irritation, and more rarely by the acci- dental rupture of blood-vessels into the sac. As a rule, it is quite clear and straw-coloured. It contains a considerable amount of fibrinogen. It is albumi- nous, as shown by coagulation by heat or nitric acid. Occasionally it holds in suspension numerous crystals of cliolesterine, the product of fatty metamorphosis. These may be so plentiful as to cause the fluid Chap. LXIII.] Hydrocele. to sparkle when it is viewed by transmitted light. Granules and crystals of hsematoidin are of rarer occurrence ; they are the permanent evidence of previous efifusion of blood. Condition of the sac. — The walls are nsually thin enough to allow of translucency of the swelling. Fig. 54. — Encysted Hydrocele of the Epididymis. a, Cavity of tunica vaginalis ; b, testicle ; c, liydrocele ; d, spermatic cord. (Reduced one quarter.) In some cases they are much thickened and indurated, especially after repeated tappings. The inner surface is smooth, or exceptionally irregular from chronic in- flammatory exudation. Vaginal hydrocele is often secondary to disease of the testicle, especially orchitis {q.v.). The measures taken to obtain a cure of simple chronic hydrocele aim at obliteration of the cavity by inflammatory adhesion, or by such alteration of the secreting surface as entails a cessation of the 340 Surgical Pathology. [Chap. lxiii. abnormal effusion. An analogous process is that set up by injection of iodine into joints the seat of hydrops or chronic serous synovitis. In all cases of acute inflammatory hydrocele the fluid is highly fibrinous. Encysted Hydrocele of the Epididymis. This is most commonly the result of obstruction and subsequent dilatation of oue of the vasa efFerentia. Now and then it consists of an enlargement of the vas aberrans. It may be simulated by distension of the organ of Morgagni, or encysted hydrocele of the contiguous part of the spermatic cord. In the first instance it is situate above the testicle, but as it increases in size it invaginates the tunica vaginalis, the cavity of which it may entirely fill (Eig. 54). The contents are either clear and serous or semi- opaque and opalescent, like water rendered slightly turbid from admixture with milk. In the latter case spermatic filaments are present in abundance, and the tumour is known as ^^ sperriiatocele.^^ According to Curling, the fluid is of this nature from the commence- ment, or what was originally limpid has become cloudy from rupture of a seminal tubule into the sac of the hydrocele. Congenital Hydrocele. Here the process of peritoneum brought down with the descent of the testicle remains patent throughout, and the passage opens into the abdominal cavity by a smaller or larger orifice. Reduction of the fluid is usually quite easy, but some part of the tract may be so narrowed that continued pressure is required to effect it. Hydrocele of the Cord. Hydrocele of the cord is either encysted, or diffuse. Encysted hydrocele is due to incomplete closure Chap. LXIV.] GONORRHCEA, 341 of the funicular process of tlie peritoneum. Wliem very tense, and occupying the inguinal canal, it may be mistaken for an enlarged gland. Diffuse funicular hydrocele is reducible or irre- ducible. In the former case the continuity of the funicular and vaginal sections of the serous tube is broken by adhesion of the opposed surfaces of the membrane above the testicle, but the communication with the general peritoneal cavity is maintained. In the irreducible variety this also is closed, so that there is an isolated sac co-extensive with the whole or greater part of the cord. Instead of one space, there may be a series of encysted hydroceles, giving a moniliform appearance. Some authors describe an- other form of diffuse hydrocele, in which the fluid is said to distend the hollows of the areolar meshwork of the cord ; a local cedema, in fact. The cause of this is difficult to understand, for there are none of the other signs of inflammation present, and simple mechanical congestive exudation would probably be associated with varicocele, a condition by no means constant. The walls of funicular hydroceles are thin, and the fluid the same in kind as in simple vaginal hydro- cele. CHAPTER LXIV. GONORRHCEA AND ITS CONSEQUENCES. Creneral pathology. — Some pathologists be- lieve that gonorrhoea is a specific disease, whilst others deny it this attribute, and maintain that it is merely a purulent urethritis capable of being set up by other conditions than impure intercourse. Abuse of alcohol and excessive indulgence of the sexual orgasm 342 Surgical Pathology. [Chap. lxiv. are deemed sufficient for its causation. Certain vaginal discharges, concerning which there is no reason to suppose a specific origin, not unfrequently excite acute and subacute catarrhal inflammation ; such, e.g.^ are the products of leucorrhoea and menstru- ation. The fact that the disease is contagious does not prove that it is specific^ for the chemical bodies formed in unhealthy inflammations have a cauterant action on the tissues. Moreover, constitutional infec- tion is the chief sign of a specific disease, and in the great majority of cases gonorrhoea is a purely local disorder. Even when constitutional symptoms do manifest themselves, they are not pathognomic of specific infective inflammation, for simple idiopathic suppuration in other parts is known to cause them in certain subjects. Morbid aoatomy. — Gonorrhoea, like acute in- flammation of other mucous membranes, first shows itself in increased secretion of mucus, -i.e., in unusual nutritive and functional activity of the epithelial cells. But soon the exudation of leucocytes becomes very active, and the migratory cells mingle with embryonic corpuscles derived from segmentation and endogenous multiplication of the epithelium. Pus is freely poured out. The submucous tissue is infiltrated with liquor sanguinis and cells, and the membrane in its entire thickness is swollen. There is considerable in- duration, and the corjDus spongiosum may feel quite firm and cord- like. The vessels are set as it were in a bed of plastic matter, which prevents them from expanding equally with those of the corpora caver- nosa; hence the chordee. In very acute cases the tension on the capillaries is so great that occasion- ally some of them burst, and blood escapes from the urethra. As the inflammation subsides, the discharge gets more watery. With proper treatment it disappears Chap. LXIV.] GONORRH(EAL CvSTITIS. 343 altogether, for the natural termination is in cure. Not one case in a hundred ends in chronic thickening and stricture. Nevertheless, the part remains a locus resistentise minoris, and subsequent attacks are very easily excited, though not usually v^ith the virulence of the primary one. CoMsequeiices of g'onorrliflea. — These are local and general, immediate and remote. The imme- diate local consequences include cystitis, orchitis, and retention of urine. The remote local consequences are stricture and its results, cystitis, orchitis, sur- gical kidney, hypertrophy of the bladder and ureters, extravasation of urine, urinary abscess, etc. The term " local " is here used to imply the structures in anatomical relationship with the urethra. The general consequences are dependent on absorption of some irritating matter from the seat of primary in- flammation. In very rare cases acute fatal pysemia is induced ; more often the symptoms are less severe, and then the constitutional state is designated " gonorrhoeal rheumatism," on account of the preva- lence wdth which articulations and fibrous investments are involved, rather than on any known character of the virus showing its analogy with the materies morbi of idiopathic rheumatism. Gonorrhoeal ophthalmia occurs as a generalised affectionj and as an accident from direct inoculation. Ooitorrhceal cystitis. — Gonorrhoea is the most common cause of cystitis. It is due to spreading of the inflammation in the continuity of the mucous membrane, and not to regurgitation of pus. Il; is possible that catheterism may be exceptionally the means of conveying the discharge. The cystitis is most marked about the neck of the bladder. Ifc is recognised symptomatically by pain and frequency of micturition ; and anatomically by swelling and muco- purulent catarrh of the mucous membrane. When 344 Surgical Pathology. [Chap. lxiv. gonorrlioea ends in pyaemia, it is generally by destruc- tive cystitis, for in these cases the mucous and sub- mucous tissues are infiltrated with pus, and the mem- brane may be hsemorrhagic and sloughy. On the supposition that gonorrhoea is not a specific disease, we must say that pyaemia is not due solely to the virulence of the products of the primary non-infective inflammation, but to a true infective process grafted on to the original simple urethritis. Oonorrlioeal orcbitis. (T'ic^e Acute orchitis.) Retentioii of lurine. — This is partly the result of the static obstruction offered by the swollen mucous membrane, and partly of the dynamic resistance due to spastic contraction of the sphincter vesicae. Reflex paralysis of the expelling muscles of the bladder will not account for it, since the most powerful volun- tary contractions of the abdominal muscles are unable to overcome the difficulty. The intolerable suffering of the patient contrasts with his passive endurance of retention from enlarged prostate and long-standing stricture. This is explained by the excessively sensi- tive condition of the inflamed structures, and by the fact that the bladder is not accustomed to acute dis- tension of its walls ; another exemplification of the law, that morbid states suddenly induced show them- selves much more by signs and symptoms than those of slow development. OoitorrEioeal stricture of tlie urethra will be treated of in the general description of organic stricture, since the pathological changes do not materially differ from those concerned in the pro- duction of other forms of fibrous contraction, and the remote results are the same. Ooiiorrlioeal affections of the eye. — These are: (1) Gonorrhoeal rheumatic sclerotitis; (2) double catarrhal conjunctivitis ; (3) purulent ophthalmia (generally unilateral) due to inoculation. Chap. LXIV.] GONORRHCEAL EyE AfFECTIONS. 345 (1) Sclerotitis. — Although the symptoms are mainly- referred to the sclerotic, it must not be supposed that the contiguous structures are not affected ; no more than that periostitis exists without a certain amount of ostitis. The physical signs are increased tension of the globe ; injection of the sclerotic vessels some- times localised or intensified at the place of attachment of the external muscles ; and congestion of the ocular conjunctiva, etc. In persons predisposed to rheu- matism, and especially those of mature or advanced age, the morbid changes and symptoms are those of ordinary rheumatic ophthalmitis. In fact, the diagnosis turns chiefly on a knowledge of the cause. Go7iorrh(£al conjunctivitis seems to be due to ab- sorption of some irritating substance from the ure- thra, and its diffusion in the general circulation ; for not only are both eyes affected, but the symptoms are liable to recur with recurrence of the urethritis. It can scarcely be a reflex nervous disorder, for there is neither physiological nor anatomical connection between the structures primarily and secondarily involved. The inflammation is shown by hypersemia, and mucous or muco-purul-ent discharge. Purulent ophthalmia is mostly, if not always, caused by direct inoculation. It is one of the most destructive diseases of the eye. In many cases the sight is lost, and in most it is permanently damaged. As a rule only one eye is affected. The palpebral conjunctiva is greatly swollen, and the ocular overlaps the edge of the cornea (chemosis). The cornea inflames and then ulcerates, the ulceration usually taking place at the periphery, for the pressure is greater there than at the centre on account of the chemosed conjunctiva. Sometimes it sloughs, owing to the stoppage of the circulation in the plasmatic canals. The interlaminar spaces are crowded with pus cells (onyx). In the worst cases the eye-ball is 346 Surgical Pathology. [Chap. lxv. destroyed by suppuration and sloughing, only a shrunken caruncular mass remaining ; short of this the cornea remains opaque, and perhaps bulged (anterior staphyloma), or it is collapsed owing to escape of the vitreous humour. CHAPTER LXY. STRICTURE OF THE URETHRA. Three kmds are generally described : (1) Organic; (2) congestive ; (3) spasmodic. Spasmodic strictiu'e. — Authors differ as to the frequency and degree of functional, dynamic, or spasmodic stricture. There seems no reason to doubt its actual occurrence, for there is the anatomical basis in the extrinsic and intrinsic muscles of the urethra ; and, moreover, a catheter may be grasped and tightly held during its passage at one time, whilst it slips into the bladder with great readiness at another. It may constitute a disease ijer se, or, rather, it may be the only symptom of undue nervous or muscular excitability ; or it may complicate congestive and oro-anic strictures. Congestive stricture is seen to perfection in retention from acute gonorrhoea. It adds to the difficulty of micturition caused by organic stricture and enlarged prostate, and so explains those cases where urine can be voided one day whilst it is re- tained the next. The irritation that causes it may be mechanical, chemical, or functional, and it may act directly upon the part, or at a distance. The passage of a catheter constitutes a mechanical irri- tant ; excessive use of alcohol, and other local and Chap. Lxv.] Organic Stricture. ^4^ general stimulants, a physico-clieniical irritant ; and forced retention of urine, or sexual excitement, a functional irritant. Exposure to wet and cold evi- dently acts in a reflex manner. Tlie modus operandi probably varies in different cases. The possible explanations are : (1) Paralysis of the muscular fibre cells or terminals of the nerves from immediate injury; (2) reflex vaso-constrictor paralysis ; (3) reflex vaso-dilator stimulation. Passive congestion of long-standing is at once the cause and consequence of organic stricture, for the irritation maintained by the stricture keeps the blood- vessels dilated ; and this is accompanied by more or less exudation, induration, and contraction, like nut- meg cirrhosis of the liver from passive hypersemia of the hepatic veins. After a time the vessels lose their tone, and are unable to contract, and this may remain long after the primary source of irritation has been removed. Org-aiiic stricture. — Gonorrhoeal urethritis is by far the most common cause of organic stricture ; but traumatism is not rare. The urethra may be injured from v^ithout by blows upon the perineum, or from within by forcible instrumentation, or impac- tion of a calculus. In any case the natural elastic tissues of the urethra are substituted by inflammatory exudation that undergoes cicatricial contraction. In the majority of instances the entire circle of the urethra is involved, and the stricture is consequently annular. This is the necessary result of complete rupture. Localised ulceration from the pressure of an impacted calculus, although it leads to a certain amount of contraction, may cause but little difficulty, as a considerable portion of the circumference of the walls remains intact. The canal of the urethra is only a potential one 34^ Surgical Pa thology. [Chap. lxv. for when the parts are at rest, the opposite surfaces are in contact. The expansion of the walls under the pressure of the column of urine during micturition is more than counterbalanced by the contraction of the newly-formed connective tissue ; and so great is the resistance offered by the stricture, that the powerful exertion of a hypertrophied bladder is unable to cope with it beyond the extent of keeping the passage permeable. Post mortem a stricture does not appear so tight as during life, for all vital contractility is abolished, and softening of the fibrous elements sets in soon after death. The so-called " resiliency " of a structure, which accounts for recontraction within a short period of mechanical dilatation, is probably due to combined elasticity and contractility. Whilst there are few or no muscular fibres in tte stricture itself, there is reason to believe that the difficulty experienced in catheterism is partly owing to the spastic contraction of the muscles outside. This view is supported by the fact that although a catheter may be tightly gripped soon after engaging an orga,nic stricture, if the parts be allowed a short period of rest, the instrument after- wards travels with comparative ease. Of course the blood-vessels are relieved at the same time, but their previous fulness does not seem sufficient to explain the difference in the degree of resistance. A toi'idle stricture is one where fibrous bands stretch from one part of the urethral wall to another. It is possible that in some cases these trabeculse are formed by the making of false passages through the base of the stricture ; but as a rule they are of natural construction. Absorption of the central or external portions (short of the entire length) of mem- branous projections into the canal of the urethra would leave the free edges as the cords in question ; Chap. Lxv.] Organic Stricture. 349 the same as occurs physiologically in the development of the chorclse tenuinese of the heart. The effects of treatment.— An organic stric- ture is never cured, for whatever treatment is adopted the patient cannot dispense with the occasional use of a catheter or bougie. The different methods employed aim at one or more of three attainments : (1) Stretching of the cicatricial tissue ; (2) absorption of inflammatory products ; (3) the interposition of new plastic matter (splicing). In the process of stretching by "gradual dilatation " the tissue elements are elongated, and in all probability dislocated from one another at the same time. In " forcible dilatation " this is undoub- tedly the case ; in fact, the mechanism may be described as multiple interstitial laceration, for it is doubtful if the stricture ever gives way in one place alone. Absorption of inflammatory products, which exist in the form of recent exudation, and partially or perfectly organised fibrous tissue, is effected by the pressure of a catheter, especially when this is allowed to remain in the stricture for some time. The blood-vessels are mechanically supported, endos- mosis is favoured, and the result is atrophy from continuous pressure. The process is analogous to the dispersion of chronic inflammatory thickening of a limb by strapping and bandaging. In internal ure- throtomy the stricture is divided, and the edges gape; the latter condition I verified by post-mortem examination in a case fatal soon after operation. Lymph is effused about the wound, and the interval is filled up by plastic matter; the same in kind, but less in degree, as when a tendon is elongated after tenotomy. Catheterism, subsequent to section, stretches the young connective tissue, and with it, though to a slighter extent, the material of which the stricture was originally composed. 3^o Surgical, Pathology. [Chap. lxvi. When there is much induration outside the urethra, internal urethrotomy may fail to divide the entire thickness of the stricture. It is in these cases that external urethrotomy is of such signal service. CHAPTER LXYL URINARY ABSCESS. EXTRA VASATIOX OF URINE. URINARY FISTULA. Urinary abscess is usually preceded by stric- ture, which is in fact its principal cause. The tension upon the urethra at and behind the stricture sets up inflammation, and this leads to ulceration through the walls, and consequent escape of a small quantity of urine under high pressure ; or the inflammation spreads to the cellular tissue outside the urethra, and there ends in suppuration. In the latter case a communication between the urethra and the abscess cavity is subse- quently established. It is not always easy to tell the order of sequence, but from the fact that the cavities of some perineal abscesses due to stricture are en- tirely free from the channel of the urethra, and that occasionally urine first makes its appearance at the wound some time after the abscess has burst, or has been opened, it seems clear that the second mode of formation is by no means infrequent. Whatever may be the exact mode of formation, a barrier of tymph is thrown out around the abscess, and this checks the sudden outrush of urine and extravasa- tion into the spaces of the areolar meshwork. The pressure of the inflammatory exudation outside the urethra adds to the difficulty of the urine escaping by the natural passage, and to the chances of its finding Chap. LXVL] UrINARY AbSCESS. 35 1 its way into the abscess. In this way the tension becomes so great that unless it is relieved by free incision there is great danger of the wall of the abscess breaking down, with consequent extravasation. The obstruction to the flow of urine may be lessened by ulceration and sloughing of the strictured part of the urethra. In very rare cases the relief thus aflbrded is sufficient to provide for discharge of the contents of the abscess per urethram. As a rule, however, an artificial opening is made in the perineum, and through this the pent-up matter escapes. Sub- sequently the cavity of the abscess shrinks, but its complete closure is often prevented by the pressure of the urine behind the stricture, and fistula is the result. The contents of the abscess consist of pus, urine, and the debris of tissue. They are very offensive from putrefactive decomposition. The pressure of an impacted calculus may cause an opening in the urethral wall by ulceration, and in this way the calculus may escape into the sub-urethral tissues, and there set up suppuration. The pus from such an abscess may make its exit entirely by the urethra, since with the disappearance of the calculus from the natural passage the chief source of obstruc- tion to the flow of urine is removed. Such cases prove that high tension is a far more potent cause of urinary abscess and extravasation than the chemical irritation of the tissues by urine. So long as the calculus remains in its new position it is subject to increase in size, from the deposit of urinary salts as the fluid bathes its surface, for it is very seldom that the orifice, by which the cavity lodging the stone com- municates with the urethra, closes. The incrustation of the calculus may lead to difficulty in micturition later on, in consequence of encroachment upon the urethral channel. 352 Surgical Pathology. [Chap. lxvi. Urinary abscess in connection with the penile portion of the urethra is usually the result of impacted calculus. Extravasation of urine. — Either the bladder or the urethra may give way. When the former ruptures through its serous covering acute peritonitis is set up. When the rent occurs below the attachment of the false ligaments pelvic cellulitis is the consequence. The causes of urethral extravasation are stricture, blows in the perineum, fracture of the pubic bone, and impacted calculus. In children the last-mentioned cause is the most common. " Extravasation " differs from " urinary abscess " in that the urine is rapidly diffused through the interstices of the cellular tissue, instead of being limited to a comparatively small space. This depends (1) upon the size of the opening in the urethra, (2) upon the degree of obstruction in its lumen. The loose areolar tissue in the perineum and scrotum offers but little resistance to the escape of urine, as the latter is forced along under high pressure. The irritative nature of the fluid and the great tension upon the blood-vessels soon lead to stasis and wide- spread thrombosis and gangrene. The parts become enormously swollen. At first they are tense and red, then they become boggy and discoloured ; for with the cessation of the circulation exudation is checked j and the haemoglobin of the blood is decom- posed. The derivative pigments variously tinted cause the skin to assume a mottled and variegated aspect — red, green, black, etc. Subcutaneous, emphy- sematous crackling can be felt. This is due to the evolution of gases of putrefaction. On cutting into the gangrenous tissues a sero-sanguinolent fluid escapes. If suppuration have preceded the general extravasa- tion, the discharge will contain much pus. The local treatment is directed to two ends : (1) Relief of Chap. Lxvi.] Urinary Fistula, 353 inflammatory tension, and escape of decomposing fluids ; (2) establishment and maintenance of a free passage from the bladder; or, in other words, the removal of the efi'ects of past extravasation, and the prevention of further mischief. So long as the lymphatics and blood-vessels remain exposed to putrescent matter the danger of septic absorption continues. Asthenia and septicaemia are the conse- quences to be feared and guarded against. The path of the extravasation is directed by the attachments of the deep membranous layer of the superficial fascia ; hence it passes from the perineum to the scrotum, and so on to the abdomen. Limited yet fatal extravasation has been known to follow tapping of the bladder through the rectum and above the pubes, UriMary fistula. — The bladder may communi- cate with the rectum or vagina, and the urethra with the external surface, rectum, or vagina. Recto- vesical fistula is generally the consequence of some operative measure, such as rectal lithotomy, or tap- ping of the bladder per rectum ; but it also arises during the progress of a pelvic abscess. In the latter case a direct passage is set uf) between the two viscera by ulceration or sloughing of their contiguous walls ; or a sinuous tract intervenes. Vesico-vaginal fistula results from long-continued pressure of the foetal liead during parturition, and from vaginal lithotomy. Ordinary perineal urinary fistula is a common sequel of urinary abscess and extravasation. These unna- tural passages remain open from one or both of two causes : obstruction to the flow of urine per via'ni natitralem ; and want of rest, which entails the absence of those conditions necessary to the union of two opposed granulating surfaces. No amount of treat- ment is likely to be successful in a case of perineal fistula whilst a stricture of the urethra remains 354 Surgical Pathology. [Chap. lxvii. undilated, for there is a frequently recurring dis- tention of the walls of the fistula by the stream of urine diverted from its proper course. The physio- logical contraction of the muscles of the bladder, vagina, and rectum causes one granulating surface to glide upon the other, and so keeps up continual irritation and exudation from the vessels. An impor- tant point in the management of these cases after operation is, as far as possible, to relieve the viscera involved of their functional activity. Where fistulous tracts are long and sinuous, it is often necessary to lay them freely open, otherwise the external openings may contract, or even close, before the granulations in the deeper recesses cease to secrete more than suffices for their agglutination. By this unequal contraction, cul-de-sacs, or segments of the main sinus, become filled with pus, which goes on accumulating until the tension is high enough to burst open the original orifice, or a gradual process of ulceration establishes a new one. CHAPTER LXYII. HYPERTROPHY OF THE BLADDER. Hypertrophy of the muscular coat of the bladder is the result of increased functional activity. As a rare event, this happens in children from excess of intrinsic nervous or muscular irritability of the organ. With this exception, hypertrophy may be considered as consequent on obstruction to the flow of urine in some part of the urethra. Enlargement of the pro- state and organic stricture are by far the most com- mon antecedents. In these cases the hypertrophy is Chap. Lxvii.] Hypertrophy of the Bladder. 355 purposive or compensatory. It is called into existence by the stimulus of increased resistance (Fig. 2). Up to a certain extent, hypertrophy is able to keep pace with the obstruction ; but, as a rule, sooner or later the pressure becomes so great that dilatation is superadded, the same as in " dilated hypertrophy " of the heart. The walls of the bladder may be so expanded that the hypertrophy is masked. The true index of its existence is the amount or bulk of the entire muscular coat, and not simply its thickness. When the distention is very great, there is compara- tive powerlessness, and the condition is known as atony. Ceteris paribus the atony is proportionate to the acuteness of the distention. There are several factors concerned in its production : (1) Exhaustion of muscular irritability from repeated futile efforts to overcome the resistance ; (2) deficiency of innerva- tion ; (3) degeneration of the muscular fibre cells. As long as the bladder is able to empty itself, the obstruction may be very great without causing atony ; for, in the intervals of physiological rest, repair takes place. Permanent tension means exhaustion. A consideration of these facts explains why, in most cases, dilatation succeeds hypertrophy from enlarged prostate, and why, as an exceptional circumstance, the hypertrophied bladder remains empty and con- tracted, and is smaller than the prostate. The difficulty interposed in the way of free circu- lation through the vessels of the mucous membrane leads to atrophy of the more highly developed elements and areolar hyperplasia of the submucous tissue. Hypertrophy and dilatation of the ure- ters. — The pathology and morbid anatomy are the same as in the corresponding states of the bladder. --6 0D° CHAPTER LXYIII. CYSTITIS : ULCERATION OF THE BLADDER. The causes of cystitis are (1) spreading of the inflammatory process from one of the neighbouring passages, as in gonorrhoea! urethritis ; (2) tension on the walls of the bladder, as in retention from stric- ture, enlarged prostate, and fracture of the spine ; (3) irritation of the mucous membrane by the chemical products of decomposition of urine ; (4) mechanical irritation from a calculus, etc. ; (5) vaso-motor and trophic changes consequent on injury or disease of the central nervous system; (6) new growths, e.g., cancer, and tubercle. It frequently happens that more than one cause is concerned in producing cystitis ; e.g., in fracture of the spine there is tension from the retention of urine ; perverted nutrition of the mucous membrane from disordered innervation ; acute congestion from para- lysis of the vaso-motor nerves ; and sometimes, though unwarrantably, septic decomposition of urine from the passage of an unclean catheter. Decomposition of urine is both a cause and con- sequence of cystitis. In the viscid mucus of chronic catarrh there exists a ferment capable of setting up the alkaline fermentation. In consequence of this, urea is con- verted into carbonate of ammonia. But this is not the only product of the decomposition, and, probably, not the chief one, in so far as the cause or increase of the inflammation is concerned. ^ Varieties of cystitis. — These may be arranged on two bases: (1) As to the intensity of the inflam- Chap, i^xviii.] Acute Cystitis. 357 mation, acute and chronic ; (2) as to the cause, e.g., calculous cystitis, tubercular cystitis, etc. The term ' catarrh " is somewhat misleading ; for clinically it refers to chronic and subacute inflamma- tion, whilst pathologically it receives its interpretation more or less in every case of cystitis. Acute cystitis consists of increased multiplica- tion, mucoid transformation, and shedding of the epithelial cells, and of exudation of liquor sanguinis and migration of leucocytes. The iwoducU vary in appearance and consistence according to the degTee of inflammation. At first th-ey are comparatively thin, the serum of the blood mingling with and diluting the mucus derived from dissolution of the distended epithelial cells. A number of corpuscles are held in suspension, but not. as yet in sufficient numbers to cause more than a cloudiness of the fluid. As the inflammation heightens, the discharge becomes muco- purulent and then purulent ; but in every stage it contains a considerable quantity of mucin. Then, as resolution takes place, it diminishes in quantity, and gets more glutinous, and finally the secretion returns to the normal. In comparatively rare cases the exudation is highly fibrinous, coagulating upon the surface of the mucous membrane, and forming a cast of the interior of the bladder. Anatomically, it resembles the false membrane of croup and the casts of plastic bronchitis. "When the inflammatory congestion is very intense, capillary haemorrhages occur both in the interstices of the membrane and on its surface ; the exudation is consequently more or less sanguinolent. Stasis and thrombosis may be so extensive as to entail death of portions of the mucous membrane. Flakes or shreds of slough are set free by liquefaction of their attachments, and floated ofi" by the stream of exudation and the urine with which they are bathed. 358 Surgical Pathology, [cimp. lxviii. It must be remembered that the fluid passed per urethram varies not only as the characters of the inflam- matory products, but as the amount of urinary admix- ture and the existence and degree of decomposition. Chronic and subacute cystitis is exceedingly common as the result of hypertrophied prostate, and stricture of the urethra. In both these diseases there is difficulty in completely emptying the bladder. Very often it amounts to impossibility, so that after each effort at micturition there is a residuum of urine. This is very liable to decompose, and increase and perpetuate the cystitis. When the urine is allowed to stand, it will be found that thick ropy mucus clings so tenaciously to the bottom of the vessel that inversion of the latter does not suffice to disengage it. It is frequently alka- line in reaction when passed ; if not, it A-^ery quickly becomes so. It has an offensive ammoniacal smell. Besides mucus, it contains pus and dirty grumous matter, consisting of epithelial cells, blood corpuscles, and amorphous debris. It deposits crystals of triple phosphate. The mucous membrane is deeply congested, much swollen, and sometimes pigmented to a marked degree. The summits of the temporary rugae, and even broader tracts, are often encrusted with sabulous material (inspissated mucus and pus impregnated with earthy salts). The greater part of the surface may appear of a dirty grey colour. The ureters and kidneys are generally diseased. {Vide Surgical kidney.) Cystitis varies from acute purulent infiltration and discharge to chronic mucous catarrh. The terms '^ acute," "subacute," and "chronic" do not denote fixed pathological landmarks. They are used to indi- cate groups of symptoms and morbid appearances of comparative but indeterminate intensity. Chap, Lxviii.] Ulceration of the Bladder. 359 Ulceration of the bladder is caused by (1) the mechanical irritation of a stone, etc. \ (2) the breaking down of tubercular deposits; (3) malignant disease; (4) destructive inflammation arising from other Fig. 55. — Tubercular Ulceration of the Bladder. a, Miliary granulations ; &, excavated ulcers ; c, vesicula seminalis; d, vas deferens, enlarged from tubercular inflammation. (Reduced one half.) sources ; e.g., gonorrhoea, septic infection of a litho- tomy wound, etc. Ulceration from the pressure and friction of a stone is generally situated about the neck of the bladder, since this is the part most subject to injury when the viscus empties itself of its urinary contents. 360 Surgical Pathology. [Chap. lxix. The ulcer is comparatively superficial, and without marked induration of the base. It is usually asso- ciated with advanced cystitis of the entire mucous membrane. Tubercular ulceration is due to the softening of miliary tubercles and consecutive destruction of the surrounding tissues. The ulcers are multiple, as a rule (Fig. 55). Though most common at the base, they are often indefinitely distributed. Their margins are sharply defined, and frequently undermined. By the coalescence of contiguous ulcers the mucous and sub- mucous tissues may be destroyed over a wide expanse. Tubercular ulcers of the bladder, ureters, and urethra may be found in the same subject, together with miliary granulations in the kidneys, testicles, and other organs. Malignant tumours of the bladder ulcerate early, for in addition to their intrinsic tendency to dis- integration, they are subject to injury by muscular contraction. When treating of acute cystitis it was remarked that the circulation might be so far arrested as to lead to ulceration and sloughing of the mucous membrane. This is all the more likely to occur where the inflammation is infective. CHAPTER LXIX. TUMOURS OF THE BLADDER. Tumours of the bladder, like those of other hollow viscera, are liable to assume the polypoid or villous form. This is notably the case with regard to benign growths, but the malignant ones are not exempt. Chap. LXI X . ] TUMO UR S OF THE BlA DDER . 'Z6l The peculiarity depends more upon unequal resistance than on a special predisposition of the new formation to enlarge in a certain direction. On account of the varying amount of support, consequent on the state of tension of the walls of the bladder, and the disturbance of the circulation in the tumour caused by contraction of the muscular coat, haemorrhage is usually a prominent symptom. It is more likely to occur, and in profusion, in those cases where the blood-vessels are large, numerous, thin-walled, and imbedded in soft loose tissue; e.g., in simple villous tumour and villous cancer. Bleeding may be the first, and for a long time the only, indication of a gro"wi:h. But the diagnosis may often be verified by a microscopical examination of the urine, and especially that drawn off by a catheter. In one case I found numerous delicate tufts of villous growth, and in another a minute fragment of columnar epithelioma. This method of investigation is of gTeat importance where the existence of a benign tumour is suspected ; since there is an absence of induration of the walls of the bladder. Malii^nant tiimoiirs of tlie bladder comprise villous cancer (encephaloid), epithelioma, and sarcoma. They are mostly primary, beginning in the bladder or neighbouring parts, vagina, rectum, or prostate. Villous cancer is very rapid in its growth. The surface of the tumour is flocculent from delicate out- growths and shreds of disintegrating tissue. The base is broad, and not limited to the mucous mem- brane. In fact, there is infiltration of the walls of the bladder. The trigone is the usual seat of the disease. The surrounding structures may be involved. Haemorrhage, and painful and frequent micturition, are the chief symptoms. Epithelioma, — Authors differ as to the relative frequency of epithelioma and encephaloid cancer of 362 Si'RGiCAL Pathology. [Chap. lxix. the bladder. There are two facts that help to explain the discrepancy ; firstly, cases of sarcoma have been included with soft cancers ; and secondly, both the tumours in question (epithelioma and encephaloid cancer) are of epithelial origin, and the disposition and relative amount of stroma and cells vary. The natural surface epithelium of the bladder is flattened, and the cells of the deeper layers are fusiform or columnar. Each variety may be represented in the new growth. I have met with pure columnar epithe- lioma. The tumour is of firmer consistence than encephaloid cancer, and the surface is generally smoother, it may be unevenly lobulated. Sarcoma. — The clinical and pathological cha- racters are those of round and spindle-celled sarcoma generally. Beiii§ii tumoio'S of the bladder are almost invariably polypoid, or villous. They have a special tendency to grow from the trigone near the orifices of the ureters. By far the most common variety is the simple villous tumour (Fig. 74.) This may be single or multiple. Occasionally it is diffuse, the greater part of the mucous membrane being covered with a shaggy, flocculent coa.t. The villi are arborescent in some cases, filiform in others. The mucous mem- brane appears healthy close up to the insertion of the outgrowths, or only unusually rough from fine villosities. There is no invasion of the deeper structures. This is also true of the other benign growths. It is an important feature, since it serves to distinguish "villous tumour " from "villous cancer" eA^en in the early stages of development of the latter, when the two formations have such a close surface resemblance to one another. The basis of the villous or papillary processes consists of a delicate stroma of fibrous, or mucous tissue richly supplied with large capillary vessels. The epithelium may be squamous, Chap. Lxix.j Tumours of the Bladder. or columnar, and disposed in few or many layers. Granules of blood pigment, scattered, or in groups, may frequently be seen in the substance of the growth. These are the "^ remnants of interstitial extravasations, Fig. 56. — Mucous Polypi of the Bladder of a Female Child, aged eighteen months. The majority are attached around the orifice of the right ureter. The urinaiy organs have heen removed in their entirety, together with the rectum and a portion of the pelvis, a, polypi ; 6, the same prolapsed, and congested from partial strangulation by the dilated urethra; c, vagina; d, rectum ; e, cut surface of divided symphysis pubis ; /, dilated ureter. (Reduced one half.) and not the result of true physiological pigmentation by the agency of the protoplasm of the cells. Next in order of frequency to villous tumour comes fibroma, or fibrous 'polypus. It is distinctly pedun- culated, and of firm fleshy consistence. 364 Surgical Pathology. [Chap. lxx. Mucous or gelatinous polypus is a great rarity. Paget records two cases. Figs. 56 and 64 were taken from one that came under my notice at University College Hospital. With the exception that the epithelium is squamous, these polypi differ in no essential particular from the common nasal variety. A pedunculated outgrowth from the prostate sometimes projects into the bladder.' Clinically it may be classed with the other vesical tumours, but pathologically it is quite distinct from them. CHAPTER LXX. HEMATURIA. Blood may escape from any part of the urinary tract, from the Malpighian glomeruli of the kidney down to the spongy portion of the urethra. In the diagnosis of its source one has to pay attention, amongst other points, to its quantity, colour, degree of admixture with the urine, and the period at which it makes its appearance during micturition. When the blood comes from the kidney it is usually quite dark, from reduction of the oxy-hsemo- globin by the urine ; but there are exceptions to the rule. I have known it to be florid in copious bleeding from a cancerous tumour. Yery large effusions generally come from the kidney or the bladder. Profuse hsemorrhage from the urethra is known by the fact of its escaping independent of the act of micturition. Heemorrliage Irom the liidney may be in small or dangerously large quantity. The causes of severe haemorrhage are (1) malignant tumour; (2) laceration of the kidney ; (3) congestion in acute Chap. LXX.] H.-^MATURIA. 365 Bright's disease ; (4) reflex hypersemia, from irrita- tion of some part of the urinary passages, e.g.^ by tbe dilatation of a stricture of the urethra ; (5) disturb- ance of the spinal nervous system. {Vide Trophic lesions.) Renal calculus, tubercular disease of the kid- ney, and other morbid states occasionally give rise to it. The bleeding from primary cancer and sarcoma of the kidney may be very profuse, but its occurrence is by no means certain. One cause of immunity is obstruction of the ureter by a projection from the growth. Secondary cancer is less vascular than primary, and it usually exists in the form of nodules, instead of a soft fungoid mass, so the chances of haemorrhage are more remote. In laceration of the kidney, the hsematuria is likely to be very great, unless the organ is completely crushed, or the ureter ruptured. In acute Bright's disease the bleeding is salutary within a certain range. It is nature's mode of giving relief to the over-distended vessels. The mechanism consists of high blood-pressure and diminished power of resistance from degeneration of the walls of the capillaries. The haemorrhage from reflex hypersemia can be explained in two ways : (1) a general flooding of all the vessels of the kidney, from vaso-motor paralysis ; (2) contraction of the renal arteries, and, as a con- sequence, venous reflux into the capillaries. Hseiiiorrliage from the lu^eters is never very great. The causes are (1) the passage of a calculus ; (2) simple and tubercular inflammation. Hsemorrliag^e from the bladder, when pro- fuse, is strongly suggestive of villous growth, or acute ulceration opening up a comparatively large vessel. Inter^nittent JtcBmaturia depends on the presence of an animal parasite, Bilharzia haematobia. It may extend over many years. Adults rarely get rid of the disease. 366 Surgical Pathology. [Chap. lxxi. Other causes of vesical hsematuria are calculus and cystitis. Heeniorrhag^e from the prostate and iiretlira. — Prostatitis, prostatic abscess, malignant disease, and catheterism should be inquired after in the former case. Traumatism from without and within, over-distention of the erectile tissue of the corpus spongiosum, acute urethritis, urethral chancre, and the passage of a calculus in the latter. In old men with enlarged prostates, haemorrhage from the veins and capillaries is at times sudden and copious. It must be borne in mind that "blood in the urine" is not synonymous with "hsematuria." The admixture may take place after the urine is voided, the blood being derived from some other source than the uri- nary tract. CHAPTER LXXI. DISEASES OP THE PROSTATE GLAND. Hypertrophy of the prostate is a disease incidental to advanced age. The morbid anatomy is sufficiently precise, but the etiology is unknown. The entire gland may be the seat of diffuse hyperplasia, or a portion of it only may be enlarged, or circumscribed nodules may form in its substance (the so-called " prostatic glandular tumours ") ; or, lastly, similar masses may project from its surface, as in the analo- gous case of the thyroid. What were formerly designated " fibrous tumours " of the prostate are now known to consist in the main of unstriped muscular fibre-cells. Histologically, nothing is observed that is not typified in the normal structure (Fig. 57). The nearest approach is made by " uterine chs.'p.uK.^i.] Hypertrophy of the Prostate. 367 fibroids," but the latter do not contain glandular elements. Hypertrophy of the prostate stands, as it were, on the border-land of new formations or growths, Fig. 57.— Section of a so-called Prostatic Glandular Tumour (Lobulated Hypertrophy). A nodule as large as a walnut was shelled out during the extraction of a vesical calculus, a, Glandular recess ; b, involuntary muscular flbre ; c, blood-vessel, x 265. and chronic inflammatory neoplasise ; but the general likeness does not imply intrinsic pathological affinity. So long as the prostatic urethra is not encroached upon, the gland may assume considerable proportions without giving rise to symptoms. t68 Surgical Pathology. [Chap, lx xi. J Cancer of tlie prostate is not common. The encephaloid variety is said to be that usually met with. The few cases that I have seen were hard enough to merit the name " scirrhus." The symptoms generally are those of stone in the bladder. At first the induration and enlargement simulate the signs of chronic prostatitis and prostatic hypertrophy. Later on, the acuteness of the patient's suffering, the wasting of the body, the repeated haemorrhages, and, it may be, the implication of surrounding structures, clear up the diagnosis. Prostatitis and prostatic abscess. — Acute prostatitis is mostly a sequel of gonorrhoeal urethritis, but it may be caused by instrumentation, impaction of a calculus, and other modes of injury. The gland is excessively tender. It is swollen and indurated. Pus may escape fi'om the inflamed prostatic urethra without the occurrence of parenchymatous suppuration. Prostatic abscess is recog-nised by throbbing pain, and by the detection of bogginess or fluctuation per rectum, and by the discharge of matter in considerable quantity. It usually bursts into the urethra, but it sometimes opens into the rectum, or in the perineum. Piles occasionally develop meanwhile. Inflammation and ]3us formation may occur around the gland (peri- prostatitis). Chronic prostatitis is the sequel of an acute attack, or the inflammation is of moderate degree from the first. Gleet, syphilis, vesical calculus, and catheterism are the chief causes. The morbid changes are the same in kind as in the acute disease. The gland may be left permanently hard and enlarged. On section it looks greyish and somewhat translucent, not unlike a moderately firm scirrhous tumour. The secreting glands and ducts are marked by pale yellow spots and streaks. Tubercle of tlie prostate is seldom seen Chap. Lxxi.] Prostatic Calculi. 369 except in conjunction with a similar affection of the epididymis, vasa deferentia, and vesiculse seminales. The kidney, ureters, bladder, and urethra may be involved at the same time. The tubercles are at first discrete, then they be- come confluent. Simple chronic prostatitis is set up around them. The tubercles, and the exudation pro- ducts in which they are embedded, caseate, and the mass sometimes breaks down, forming an abscess with purulent and cheesy contents, like as in a strumous lymphatic gland. Tubercle of the prostate is more common than is generally supposed. In all cases of tuberculosis of other parts the prostate should be examined. Corpora amylacea are said to be usually present in the prostates of adults. They are of microscopical dimensions, or of such a size as to be clearly visible to the naked eye. Individually they may attain a diameter of from y^ to \ of an inch. Collectively they sometimes form masses of consider- able magnitude, being embedded in some cementing substance, and enclosed in a common capsule. They are for the most part composed of concentric laminae. In their interior may be seen granular particles, or even nuclei and cells. They may be coloured brown or black. The chief alteration to which they are subject is calcification. They have been found in phleboliths in the prostatic veins. Prostatic calculi. — Those of intryisic prostatic origin probably begin as a deposit of organic matter in the glandular acini or ducts. This would be followed by calcareous infiltration and accretion. The constituent salts are phosphate and carbonate of lime, chiefly the former. These calculi may be single or multiple. By their pressure the tissue of the prostate is more or less absorbed Y 370 Surgical Pathology. [Chap. lxxii. They may be encapsuled, or lie loose in a cavity, or project into the prostatic urethra. When there are several in the same subject they are liable to be. facetted by mutual attrition ; and as felt per rectum they may give a grating sensation as they are made to rub one against the other. A vesical calculus may become impacted in the prostatic urethra, and ultimately embedded in the substance of the gland. CHAPTER LXXII. SURGICAL KIDNEY. Surgical kidney consists essentially of an inter- stitial or intertubular nephritis. It differs from granular or gouty kidney as follows : (1) The inflam- matory changes are more irregularly disposed ; (2) the progress of the disease may be very rapid ; if chronic, it is subject to repeated exacerbations \ (3) it frequently ends in suppuration; (4) it is usually accompanied by cystitis and pyelitis ; (5) the con- comitant and consequent organic changes are limited to the urinary apparatus ; there is no hypertrophy of the heart, nor a general systemic arterio-capillary fibrosis. Causes. — These come under two heads: (1) Those that raise the tension in the renal tubes and capillaries ; (2) septic poisoning. The tension may be increased by interference with the escape of urine from stricture of the urethra; enlarged prostate ; obstruction of one or both ureters, from ia) impacted calculus, (6) stricture from ulceration and compression by a tumour, or organised lymph from pelvic cellulitis {vide Lancet^ 1879, p. 769, Chap. Lxxii.] Surgical Kidney. 371 vol. i.) ; and paralysis of the bladder in fracture of the spine. Although the urine does not regurgitate from the bladder into the ureters, the result is the same as if it did; for if the bladder is distended, it is clear the urine must be dammed back upon the ureters and renal tubules. The distention of the tubules compresses the vessels that encircle them, and so causes a venous reflux into the capillaries on the distal side of the obstruction. Again, the tension may be raised from reflex irritation of some part of the urinary tract, by a stone in the bladder, or operations upon the urethra ; or the vaso-motor paralysis may be of central origin, as in crushing of the spinal cord. Septic 'poisoning may take place : (1) By spreading of the inflammation in the continuity of the mucous membrane from the bladder, ureter, or pelvis of the kidney ; (2) by lymphatic absorption from these parts. Dickinson accounts for the nephritis, and the scattered foci of the inflammation, by embolism of the renal veins; but the limitation of the infarctions to the kidney, and their shape and local distribution, seem opposed to the theory of embolic pyaemia. Johnson's explanation of the dissemination of the abscesses and patches of inflammation is, that they are due to rupture of the renal tubules ; but if this were correct, suppuration should be more constant than it is. My own view is that primary thromboses occur here and there in the obstructed intertubular capillaries (cortical and medullary) and that the clots set up localised perivascular inflammation. ISTephritis following injury to the spinal cord may be due in some measure to trophic lesions of the kidney. Oeneral anatomy. — The appearance of the kidney varies, according to the cause and acuteness of the inflammation. 372 Sl^J^ GICA L Pa THOL OG \ \ [Chap. LXXI I . In clironic interstitial iiepbi^itis, from oto struct ion to the flow of urine, tlie effects of atrophy from pressure are combined with those of inflammation. The papillae are fl.attened. or entirely absorbed, their places being occupied by recesses con- tinuous with the calyces. In extreme cases the pyramids may disappear, and only a thin layer of cortical substance remain. If the disease be limited to one kidney, every vestige of secreting substance may vanish, and the capsule may then retain its natural outline, or be converted into a, large thin-walled cyst. I have known such mistaken during life for an ovarian tumour. Atrophy from pressure is more pronounced when the disease is unilateral, for then the other kidney hypertrophies^ and compensates for the impaired function of the crippled organ, which is thus relieved from its physiological work. The effects of inflammation are : (1) Induration from organisation and contraction of the exudation ; (2) an irregular nodulation or puckering of the surface from the same cause ; (3) adhesion of the kidney to the capsule, and the capsule to the peri- renal fat ; (4) cysts from obstruction of the secreting tubes. Acute interstitial nepbritis. — Here the kidney is paler and softer than normal, being infi.ltrated with leucocytes. It is spotted and streaked with dilated vessels and minute extravasations both in the cortex and p}Tamids. The small-celled infiltration may be uniform, but more often it is unequally distributed, and then there are pale nodules, and these in different stages of softening and abscess formation. The abscesses are usually multiple, but the greater part of the kidney may be occupied by one large abscess formed by the coalescence of smaller ones. The capsule is adherent, Vjut can be readily separated. There may Chap. Lxxii.] Surgical Kidney. 373 be suppuration beneath the capsule, and in rare cases outside it. Sometimes there are streaks of suppura- tion within the pyramids. Acute superveniiig on chronic inflamma- tion. — The appearances will consist of a mixture of the signs of the above-mentioned types. Condition of tlie iweters and pelvis. — Much will depend upon the cause, duration, and intensity of the disease. When due to chronic ob- struction they are dilated, and their walls thickened from inflammatory exudation and muscular hyper- trophy. They are often strictured from contraction following inflammation, or cicatrisation of ulcers. The mucous membrane is thickened and hypereemic. In acute cases the passage contains a mixture of pus and decomposed urine, often tinged with blood from capillary haemorrhages. They rarely contain clear acid urine. The mucous membrane is swollen and deeply congested, and it may show points of capillary extravasation, and slate-grey patches of degenerating lymph. Microscopy. — (1) Chronic inflammation. — In the early stages there is congestion, and exudation of leucocytes, mostly about the Malpighian bodies, the capsules of which are slightly swollen and homogeneous. The tubules are somewhat dilated (Fig. 08). The epithelium is but little altered ; at the most the cells are flattened, or show signs of commencing proliferation and cloudy swelling. In advanced cases there are wide tracts of cica- tricial tissue, in which but few vessels and no tubules can be seen. In other parts the disease is more active, there being a rich infiltration with cells, and increased structural change in the secreting epithe- lium ; but even yet some portions may appear fairly healthy. (2) Acute injiammation. — The whole organ may 374 Surgical Pathology. [chap.Lxxii. be in a state of diffuse inflammation, the interstitial tissue being everywhere crowded with cells. The tubules contain altered epithelium and casts of fibrin, and even of leucocytes. But the disease is usually concentrated upon certain points where nothing can be seen but groups Fig. 58. — Early stage of Interstitial Nephritis (Surgical Kidney), from si case of Polypus of th.e Bladder, in which the Orifices of the Ureters were obstructed. a. Glomerulus, tlie vessels are hidden by corpuscles stained with logwood ; 6, renal tubule : c, tubule containinsr epithelial debris and desquamated cells ; d, intertubular tissue increased and infiltrated with leucocytes ; e, capillaries. of cells, or abscesses in existence or in course of formation. There is a zone of hypersemia around these foci, and in some parts capillary extravasation as well. State of the urine. — In chronic cases the quantity is increased from the high vascular tension. It may be double the normal. It is pale, and of low Chap.LXXIII.] Urinary Deposits. 375 specific gravity. At first it contains but little or nc albumin. The secretion of urea is diminished. In aciite cases the amount of urine may still be greatly above the normal. In one instance, supposed during life to be diabetes insipidus^ I found post mortem both kidneys riddled with abscesses. But often the kidney is so crippled that the amount of water is diminished, and there is a daily decrease in the secretion of urea. When cystitis and pyelitis are present the urine contains pus and mucus, and sometimes blood. The patients usually succumb to a combination of septicaemia and urinsemia. CHAPTER LXXIII. URINARY DEPOSITS AND CALCULI. TABLE OF UEINAEY DEPOSITS. Name. a m o C3r75 Hi Chaeacteks. Pinkisli yellow, red, or lateritious (brick- dust) sediment ; urine scanty, acid, and high- coloured. The pre- cipitate, "before suh- siding, forms a cloud in the urine, which clears off when heated. Crystalhne form — uric acid, mostly rhombic prisms and plates. " Gravel." Causes, 1. Rapid waste of tissues, e.g., as in fevers ; 2, excess in nitrogenoiis food; 3, dyspepsia ; 4, ob- structed perspiration ; 5, congestion of the kidneys (Golding Bird). Also imper- fect respiration. Cold weather will precipi- tate urates sometimes from healthy urine. Symptoms. Those of the causes. Some- times also a slight burning feel in passing water. Urates. — Minute spheres with acicular spiculae of uric acid projecting from them. 376 Surgical Pathology. [Chap.Lxxiii. Name. Chaeacters. Cattses. SyMPTOMS. i -i-i 1 1 o Ci-ystalLiiie forms : 1, quadratic octahe- dra ; 2, dumb - bell crystals. " Nervous exhaus- tion;" dyspepsia; over - work ; mental distress ; excess of saccharine food or alcoholic liquors. Those of the causes. Occasionally, loss of sexual vigour, or dis- order of the sexual func- tions. 09 w o rd P4 1. Phosphate of Lime. — White, cloudy mass. Crystals : spherules, dumb-bells, rosettes, oblique hesagocal prisms. 2. PhosphsU of Ammonia and. Mag- nesia {triple phosphate). Crystals (large) : tri- angular, truncated prisms, four - sided prisms, irregular six- sided plates ; stellate crystals when am- monia has been added. Alkaline urine is the immediate cause. It is caused by injuries and diseases of the bladder, especially paralysis andcatarrhal inflammations ; renal inflammation ; spinal injury or disease. Nervous exhaustion ; excessive use of alka- lies ; the alkalinity of the ui-ine is said to result from the meta- morphosis of urea into carbonate of ammonia. Urine is offensive, and often contains muco -pus. Signs of cau- sative disease. Small and delicate crystalline spherules. Drum-sticks. The causes which determine the change of urea into carbonate of ammonia. No speciiil symptoms known. De- posit rare. 8 Urine a dirty -red colour; after standing, a slightly flocculent, brownish sediment. Heat coagulates the albumen. There may be blood enough to form a clot ; then the urine is dark brown- ish-red. Or the blood may be quite unmixed with the urine. 1. Kidney disease. Calculi, congestion, inflammation, injury, scurvy, the Bilharzia capensis. Malaria may cause intermittent hasmaturia. Blood from the kidney is generally mixed urd- f ormly with the urine, andforms blood-casts. 2. Bladder affections ; injuries, stone, tu- mours. Blood from bladder often flows pure after the urine. 3. Urethra: blood piu'e, and comes be- fore or with urine, or without urine at all. Those of cause. Use Heller's test for blood. Heat urine, then add KHO and heat again. The phos- phates then fall down with the colouring matter of the blood. The sediment has a dirty - red colour by re- flected, and a splendid blood-red col- our by trans- mitted Ught. Chap.LXXIII.] Urinary Calculi. 77 Name. Characteks. Causes. Symptoms. Pus. Pus-corpuscles, un- der the microscope, are spheroidal and granular. The pus generally subsides as a dense layer of a " pale greenish cream- colour," which can be mixed thoroughly with the urine by shaking. Not affected by acetic acid. Porms a translucent jelly when liquor potassse is added. The urine is albuminous. Abscess, uJceration, or merely catarrh of any part of the urinary passages. 1. Pus from the kidneys is usually diffused throughout urine passed. 2. Pus f lom. bladder is mostly mixed with mucus. •3. Pus from an abscess is usually variable in quantity, and not equally diffused. Those of the cause. 2 • Epithelial cells lin- ing urinary passages. See works on general A natomy. Often in torm of casts. Kidney disease. Ul- ceration or catarrh of bladder. Those of cause. TABLE OF CALCULI. Physical Characters, etc. Chemical Characters. Occurs rarely except in children. G-rey, smooth, dusty, non - laminated ap- pearance. Soluble in boiling water. Add HCl to solution and you get a precipitate of uric acid. Reat with potassium carbonate : am- monia escapes. Blow-pipe bums it away. < t3 Smooth or warty. Yel- lowish or brownish. Con- centric structure. Gives off no ammonia when heated with KHO. Evaporate to dryness with nitric acid. Cool, and add a Httle NH3; the characteristic deep purpl't;- red murexide is then obtained. Blow-pipe burns uric acid away. 6 i <4-l O 1 6 Eough, warty, " mul- berry "' appearance. Very hard. Dark "blood-stained." Easily soluble in nitric acid. Boil long in a solution of potas- sium bicarbonate, neutralise carefully with nitric acid ; then white precipitates can be formed with solutions of lime, lead, or silver. Blow -pipe reduces it, urst to calcium carbonate, then to quick-lime. Heat on platinum foil and it chars. Then add HNO3 and it f ftervesces. 378 Surgical Pathology. [Chap.Lxxiii. o rrt 1 DO ?i Physical Characters, etc. Has a wavy appearance, especially when fractured. Changes colour with age from pale yellow to brown, grey, or green. Extremely rare. Contains sulphur. Section, lustrous bright brown. Most extremely rare. Chemicai Characters. Dissolves, in great part, in ammonia : its solution then de- posits, by spontaneous evapora- tion, six - sided prismatic and tubular crystals. Dissolve in strong caustic potash. Boil, and add a little solution of lead ace- tate : a black precipitate of sul- phide of lead falls. Chalky, soft, brittle, lami- nated. Has a peculiar deep yellow colour, when its solution in nitric acid is evaporated to dry- ness : characteristic. " Fusible calculus : " melts in the blow-pipe flame. Dissolve in nitric acid and add excess of ammonia : whiite precipitate.* Oall stones compa^red with urinary calculi. — (1) G-all stones are mucli lighter, the majority, when dry, floating in water ; (2) they feel greasy to the touch ; (3) the colour of many differs from that of any known form of urinary calculus ; (4) the shape is often suggestive, sometimes conclusive, of their nature. The presence of many facets is in favour of biliary origin. If large and barrel-shaped, with terminal facet, there can be no doubt that they are not only gall stones, but that they were retained for a long time in the gall bladder, and were multiple. When granular on the surface they look like aggregations of minute calculi, which in fact they often are. (5) On fracture, glistening flakes or scales of cholesterine may be very obvious. * Copied by permission from Keetley's "Index of Surgery." 379 CHAPTER LXXIY. ULCEES OF THE ANUS AND RECTUM. Ulcers about the anus. — The principal varieties are: (1) Simple fissure; (2) syphilitic mucous tubercles; (3) epithelioma; (4) ulcerated piles; (5) ulcers in connection with fistulous openings and operation wounds. Primary venereal sores are occasionally seen in this situation. Painful fissure of the anus may exist alone, but it frequently starts from the base of a pile. It probably commences in an abrasion of the mucous mem- brane. The nerve-fibres are subject to more or less constant irritation, from contraction of the sphincter, and the tension upon them is greatly increased by the act of clefgecation. It seems likely that the terminal twigs are exposed in the floor of the ulcer. It may be that they are constricted by the contraction of inflam- matory lymph. An incision made in the axis of the fiijsure divides some of the muscular fibres of the sphincter, and with them the nerves. A certain amount of physiological rest is given to the parts, and tills promotes healing. E pithelioriiatous ulceration commences at the junc- tion of the skin with the mucous membrane. The base of the ulcer is granular or tuberculated, and greatly indurated. On rectal examination it will usually be found that the structures beyond the anus are invaded, and the extent of this may be sufiicient in itself to exclude ulcerated piles. External piles are rarely ulcerated beyond the surface ; and when internal piles are extensively o So Surgical Pathologw [Chap. lxxiv. destroyed it is by a comlDined process of ulceration and gangrene, their bases being strangulated by the sphincter ani. Such a protruded mass shows an ab- sence of marked induration ; and there is no infiltra- tion of the tissues about the base, which is limited by the folds of the tliickened anal mucous membrane and skin. Anal fistulce sometimes refuse to heal after being laid open. Then the margins and base of the ulcer become indurated, and the papillse of the surrounding skin hypertrophied. Tliis gives a warty appearance, something like epithelioma. But in epithelioma the induration is greater, and there is more outgrowth, the constructive process outstripping the destructive. The direction of an ulcer left after operation for fistula is strongly suggestive of its origin. It must be remembered that long-continued irritation of a simple ulcer may cause it to take on a malignant character. Ulcers of tlie rectuni. — Those of greatest surgical importance are (1) simple; (2) syphilitic; and (3) malignant. Simple rectal ulcer may be due to traumatic or spontaneous irritation; but their origin, is generally involved in obscurity, since, when small and free from the disturbing influence of the sphincter they give but little trouble. They are mostly situated ^vithin the lower two inches of the rectum. The floor or base shows but little induration ; in fact, it may almost be as free from it as the healthy mucous membrane ; but the margin is usually defined. An important sign, and one of especial value in the diagnosis of recent ulceration, is the bleeding occasioned by digital examination. This is usually slight, but one does not meet ^vith it when the mucous membrane is intact. Kectal ulcers are slow to heal, on account of the muscular contractions of the bowel, and the irritation Chap. Lxxiv.] Ulcers of the Rectum. -^Zv caused by the passage of fseces. Whilst cicatrisation goes on at one part the ulcer often spreads at another. Other things being equal, the liability to stricture is proportionate to the duration of the ulceration. As the destructive process tends to spread in a circular direction, the resulting stricture is crescentic or annular. Syphilitic rectal ulcer is in most cases a tertiary lesion ; but it sometimes appears during the secondary symptoms. Like other ulcers of the rectum, it is usually within reach of the finger. The occasional existence of scars about the anus has led some surgeons to conclude that the ulceration commences externally, and afterwards involves the rectum. This view at first sight appears strengthened by the fact that syphilitic disease of the rectum is many times more frequent in women than in men. (In women there is a greater liability of ulceration spreading from the genitals to the anus than in men.) The foregoing explanation may be true to a certain extent, but it does not apply to the maj ority of cases in which the ulceration undoubtedly begins internal to the sphincter. It is by no means rare for an inch or so of healthy mucous membrane to intervene between the anus and the seat of the disease. Reflex or sympathetic irritation of the rectum from disorders of the generative organs, and pi'otracted constipation, cannot go for much in explaining the greater liability to syphilitic ulceration of the rectum in women ; for the same conditions would also predispose to malignant disease, and this is more common in males. There is no certain sign by which we can tell simple from syphilitic ulceration of the rectum, so we always appeal to the history of the case, and seek for concomitant evidence of syphilis to make the diagnosis complete. Speaking generally, it may be said that syphilitic ulceration is more extensive, more rapid in 382 Surgical Pathology. [Chap. lxxv. its development, and more amenable to specific remedies, than simple inflammatory erosion. At the same time, it is ver}^ inveterate, and gives rise to great discomfort from the pain, profuse dis- charge, and the secondary troubles consequent on stricture. Malignant rectal ulcer. — Every form of malignant disease that attacks the rectum sooner or later causes ulceration. This either begins at the anus, from the disintegration of epithelial cancer, or quite clear of the orifice in connection with columnar epithelioma, or scirrhus, or less commonly sarcoma. The base of the ulcer is very indurated, and of unequal depth at different parts, depressions alternating with hard nodular elevations. The margin has an irregular outline. It is raised, and the tissues are infiltrated with growth for some distance beyond it. The dis- charge consists of pus, slimy mucus, blood, and the debris of the new formation. It is very foul from decomposition, and the foetor is in proportion to the rate of destruction of tissue. Malignant ulcer of the rectum has a proclivity for the male sex. It is met with chiefly beyond mid- adult life. Stricture is a certain sequel. CHAPTER LXXY. STRICTURE OP THE RECTUM. It has been already noted that simple, syphilitic, and malignant ulceration entails constriction of the calibre of the bowel. In the two former the cicatrisa- tion is purely inflammatory in nature. In cancerous disease it is partly due to contraction of the fibrous Chap. Lxxv.i Stricture of the Rectum. 383 stroma, the same as retraction of the nipple from atro- phying scirrhus of the mamma. Obstruction from cancerous stricture is increased by projecting nodules of the growth. Stricture of the rectum, independent of ulceration, is very rare, but it may arise from the shrinking of plastic lymph effused into the submucous tissue, or from traction on the gut by the organised products of pelvic cellulitis. It is difficult to conceive how long- continued irritation can lead to localised annular hypertrophy of the muscular coat of the rectum, without causing at the same time ulceration of the mucous membrane, or inflammatory thickening of the cellular tissue beneath it. Stricture may be simulated by an unusually- developed fold or valve of Houston. The stricture is crescentic or annular, according as the disease which causes it involves a part or the whole of the circumference of the orut. So Ions: as a segment of the circle of mucous membrane remains free, the contraction is not likely to give rise to dangerous obstruction, save in the case of malignant disease, where a mass of new growth may block the passage at the seat of stricture. Effects upon the too^ el above and below the stricture. — The calibre of the gut for a lonjr way on the proximal side (it may be through the whole or greater part of the intestine) is very much dilated, and the muscular coat is enormously liy^er- trophied to compensate for the increased resistance to its action. But, in spite of the hypertrophy, the bowel is distended with flatus, and scybalous masses collect in the upper part of the rectum and in the colon. Co'iistipation is the natural result, but this may be masked by constant or periodical diarrhoea ("the diarrhoea of constipation") ; for, in addition to the discharge from the ulcerated surface, the mucou.«* 384 Surgical Pathology. [Chap. lxxv. membrane is fretted by incarcerated faeces, and so kept in a state of congestion and catarrh. From time to time a quantity of fluid is poured out to relieve the over-distended vessels. The har- dened faeces are softened and diminished in size, they being churned, as it were, in the exudation. , Then there comes, perhaps, a period of quiescence, to be followed, in turn, by another attack of diarrhoea. The important point to note is that all this time con- stipation may exist. Perforation of the howel sometimes takes place at a distance from the stricture, but more commonly in its proximity. The perforation is either purely ulcerative, or ulcerative and gangrenous. I once performed colo- tomy for obstruction from malignant stricture of the rectum. At the post-mortem it was found that a mass of hardened faeces had, by its pressure, led to death of a considerable portion of the wall of the caecum, and consequent perforation and peritonitis. The patient bore a healthy scar of amputation of the breast practised for scirrhus four years previously. The perforation may take place into the peri- toneum, or into an adjoining viscus, or it may set up abscess, and this may remain localised, or travel along the bowel and open externally. In the last- mentioned event the fistula serves as an escape-pipe for the matters pent up above the stricture. If the stricture is an inflammatory one, the ulcera- tion often heals below whilst it spreads above it, for the distal portion of bowel is in a state of rest com- pared with the proximal. Malignant ulcer nevei completely cicatrises on either side of the stricture. The traction exerted by the stricture, and the pressure of the exudation about it, cause obstruction to the circulation through the haemorrhoidal veins; hence piles are likely to form. These, when indurated, as Chap. Lxxvi.] Tumours of the Rectvm. 385 they often are, may be mistaken for cancerous nodules, especially as they are associated with ulceration and stricture. Stricture entails straining at defsecation, and the mechanical effects of this are patulous anus^ and in the female procidentia uteri, cystocele, and rectocele. CHAPTER LXXVI. TUMOURS OF THE RECTUM. Malignant tumours of the rectum comprise certain forms of cancer and sarcoma. It is customary to speak of two varieties of rectal cancer, epithelioma, and scirrhus. With regard to epithelioma of the anus, there can be no difference of opinion as to its origin, structure, and place in the nomenclature of new growths. It commences at the junction of the skin with the mucous membrane, and spreads deeply and widely in the surrounding tissues. It is essentially a new formation on the type of squamous epithelium, and it has the characters common to epithelioma of the lip, tongue, and cutaneous surface, the most striking feature being the presence of globes or pearls made up of concentrically laminated cells." As the growth encroaches on the mucous membrane, where the epithelium is columnar, cells of transitional form may be observed. The inguinal glands are infected from the outward part of the growth, and the pelvic and lumbar from the rectal. On the assumption that all cancers start fi-om pre-existing epithelium, it would be illogical to assert, on strict pathological grounds, that there is a clear distinction betw^een scirrhus, and columnar epithelioma 386 Surgical Pathology. LChap. lxxvi. of tlie rectum. It is true the epithelial cells lining or filling the alveoli do not always preserve the cylindrical shape in its integrity, being sometimes subcolumnar, or more or less angular, or rounded. The stroma, too, varies greatly in amount and regu- larity of distribution. There can be no objection to retaining the terms " scirrhus " and " epithelioma 1 so long as the central Fig. 59. — Columnar Epithelioma of Eectum. a. Acinus lined by columnar epithelium ; 5. acinus from which the epithelium has dropped out during the preparation of the section ; c, interaciuose stroma, formed of delicate fibres strewn with indifferent cells, x 265. idea of epithelial origin is kept in view. One thing is certain, rectal cancers proper do not show a tendency to develop squamous epithelium ; nor would this be expected, when one considers that the physiological type of the cells is columnar. Rectal cancers are often so perfectly glandular in their minute structure that it is difficult, from a microscopical examination alone, to distinguish them from adenomas. ( Vide Figs. 59 and 75.) But should a doubt arise as to the malignancy of a given specimen, it can be dispelled by the knowledge that the mode of growth is infil- trating and deeply destructive. The same is true Chap. Lxxvi.] Sarcoma of the Rectum. 387 concerning simple villous tumour and villous cancer of the bladder (q-v.). "The boundaries between simple papilloma and villous cancer mav be just as difficult to define as those between adenoma and carcinoma " (Billroth). When the glandular arrange- ment is well defined these rectal cancers are appro- priately designated "adenoid."' It will generally be found that the superficial portions of the tumour conform more to the likeness of the normal anatomy of the mucous membrane than do the deeper. The naked-eye and microscopical appearances of cancerous disease of the rectum vary as the rate of cell multiplication and the relative extent of the funj^atin^ and infiltratinoj modes of growth. In some cases there is a marked tendency to invade the sub- mucous coat, and to develop a quantity of fibrous tissue. The latter, as it undergoes cicatricial con- traction, gives rise to great induration, and, as the hardening and proliferation are not uniformly diftused, the surface is tuberculated. On the other hand, the interstitial tissue may be scanty, and richly strewn with indifi'erent cells, whilst the epithelial formation is abundant. At the same time, the growth may sjDread more in the direction of the lumen of the bowel than in its walls, and conse- quently assume a tuberous form. The fonner varietv is tliat usuallv recognised as " scirrhus," the latter as " adenoid cancer " or " columnar epithelioma ; " but between the two there are tumours that represent every gradation. /Sarcoma of the rectum is less common than cancer. It either invades the bowel from without, or starts in the submucosa. Histologically it consists of round and spindle cells and a variable amount of mucous tissue (myxo-sarcoma). Clinically and patho- logicallv it conforms to the laws regulatincr the fn*owth of sarcomatous tumours in general. 2,SS Surgical Pathology. [Chap. lxxvi. Innocent tumours of the rectum are met with chiefly in the polypoid form, benign intramural growths being exceedingly rare. They are more com- mon in children than in adults, contrasting in this way with malignant disease. The base of attachment is in most cases within reach of the finger. Every variety of simple polypus may be found. The following may be enumerated : (1) Tibro-glandular, or adenomatous ; (2) villous ; (3) vascular ; (4) myxo- matous ; (5) warty. The foregoing classification is based partly upon the coarse anatomy and partly upon the microscopical structure of rectal polypi. Adenomatous polypus occurs as a soft, fleshy mass, with a rather broad peduncle. The interacinose tissue consists of a more or less gelatinous ground substance, through which is woven a network of fibres, cell ramifications, and blood-vessels. In some cases it is exactly like the tissue that makes up the entire mass of a simple mucous polypus ; in others it is more densely fibrous. It is richly vascular and cellular. But the characteristic feature is the presence of glan- dular acini and tubular recesses lined with columnar epithelium. The adenoid tracts are circular, oval, straight, or sinuous, and are distributed singly or in racemose clusters. The surface of the tumour is covered with the same kind of epithelium that lines the acini and crypts (Fig. 75). Villous polyf)us is seen as an arborescent, leafy, or filiform outgrowth, sessile, or distinctly pedunculated. Histologically it is composed of connective tissue in various stages of development — embryonic, mucous, and fibrous. The surface epithelial cells are columnar. Vascular polypus is almost confined to early life ; hence it is commonly known as the " vascular polypus of children." It is found singly or in groups. It is often no larger than a pea or bean. It has a florid appearance, something like a raspberry. Structurally Chap. Lxxvii.] Prolapse of the Rectum. 389 it is made up of a delicate stroma of connective tissue, which supports the numerous large capillary blood- vessels. It is very similar to the small caruncular growths about the orifice of the female urethra. It is very liable to bleed. Myxomatous or gelatinous polyiius has the same structure as common nasal polypus, with the exception that the epithelium is not ciliated. Warty 'polypus is so seldom met with that a detailed description is not needed. The mucous mem- brane of the rectum over a considerable area has been found covered with small papillomatous proliferations. The so-called " fibrous polypus " is generally a villous growth, or fibro-glandular tumour, as above described. The chief symptoms of rectal polypi are tenesmus, sanguineous and mucous discharge, prolapse of the bowel, and reflex disturbance of the genito-urinary organs, such as irritation about the penis and frequent micturition. CHAPTER LXXVII. PROLAPSE, HEMORRHOIDS, AND FISTULA. Prolapse of the rectum. — In slight cases the loose submucous tissue just above the anus is stretched, and this allows a ring or fold of mucous membrane to protrude ; but a more important variety is that where the entire thickness of the gut becomes prolapsed. The causes are the same in each case, viz., laxness of the sphincter ani and muscular coat of the bowel, and mechanical strain upon the parts from long- continued or oft-repeated tenesmus. The irritation may arise from some rectal disorder, such as piles. 390 Surgical Pathology. [Chap.LXXvii polypi, or ascarides ; or, reilexly, from phimosis, stone ill the bladder, enlarged prostate, or stricture. But, apart from reflex contraction, voluntary efforts to overcome obstruction to the flow of urine entail a bearing down upon the rectum. In women, the recto-vaginal sejDtum may yield, and form the wall of a broad-mouthed cul-de-sac (rectocele). The causes of this are, loss of support from rupture of the perineum, and straining at stool. {Vide Stricture of the rectum.) HceifnoQ^r holds. — The essential pathology of piles is a dilatation of the hsemorrhoidal vessels, and chiefly of the veins. When the vascular dilatation is limited to the skin around the anal orifice, the piles are called "external;" and, when it is confined to the mucous membrane of the rectum, they are termed "internal." It very frequently happens that the two co-exist ; but even then the division is marked by a shallow groove on the surface, which serves as a guide to the suro-eon as to what should be lis^atured and what excised in operations for the cure of the disease. In external piles the veins are dilated and their walls thickened, and the perivascular connective tissue is hypertrophied and indurated. The result of these structural alterations is the formation of firm nodular blueish-white masses, covered with thickened skin. Loose folds of integument, radiating from the anus, are frequently seen apart from, or in continua- tion of, the hsemorrhoidal tumours. In internal piles the same morbid changes are observed, but the arteries and capillaries often parti- cipate largely in the process. On account of the arterio-capillary dilatation, the lack of surface support from chronic inflammatory induration of the mucous membrane^ and the liability to injury from the jiassage of hardened faeces, internal piles are prone to bleed. Chap.LXXVIL] FiSTULA IN AiVO. 39! Ill those cases where the ectasia mainly afifects the veins, the piles are often pedunculated, and they present a somewhat livid appearance. Where, on the other hand, the ai-teries and capillaries are extensively enlarged, the piles are brighter in colour and more sessile. Anything that serves to determine blood to the part, or mechanically prevents its return, conduces to the development of hemorrhoids. Chemical or mechanical irritation of the rectum, and plethora of the portal circulation, are the principal points to be borne in mind. The ultimate causes are constipation, straining on account of diihcult micturition, and alcoholism and high feeding. Cirrhosis of the liver is an intermediate factor. Internal and external piles may become inflamed ; and internal piles strangulated by the sphincter ani. When inflamed they are very tense, livid, and painful. The veins are thrombosed, and their walls and the connective tissue around are infiltrated with lymph and leucocytes. Speaking generally, we may say that the morbid anatomy of piles consists mainly of venous dilatation and varicosity ; and that phlebitis is the essence of their inflammation. Fistula in ano. — A complete fistula has one orifice on the cutaneous surface and the other in the bowel. Of incomplete, or blind fistulae, there are two varieties, internal and external. The former com- municates only with the rectum ; the latter opens by the side of the anus. An incomplete fistula of either kind may become complete, and vice versa. As a rule the internal opening is just above the sphincter, and the external near its outer border ; and the passage between them pretty direct. But there are many exceptions; e.g., the sinus, after "coasting the bowel," may end on the opposite side ("horse- shoe fistula ") ; or from inefiiciency of drainage the 392 Surgical Pathology. [Chap. lxxviii. original tract may give off diverticula, or be extended for a long distance above the upper opening, or out- wards from the external. In stricture of the rectum ifl-v.) the fistula joins the proximal dilated portion of the bowel. Suppuration is the means by which the fistula is established. It may commence in an extra-rectal abscess, or in an ulcer of the mucous membrane. The cause of such ulcer or abscess is either constitutional or local. The frequent association of fistula and phthisis suggests an origin in scrofulous inflammation. Irritation from hardened faeces, or a foreign body, although it cannot often be proved to be an exciting cause, may still be such. I once removed a fishbone which had transfixed the bowel immediately above the internal sphincter ; one end could be felt per rectum, and the other by means of a probe passed through the outer orifice of the fistula. With regard to the propriety of an operation, it may be said that it turns upon the chances of the wound healing rather than upon the influence that a fistula has been supposed to have in checking the progress of tubercular disease of the lungs. Experience teaches that the getting rid of a sup- purating cavity or tract has a decidedly beneficial efiect upon a patient suffering from phthisis. CHAPTER LXXYIIL PERITOXITIS. Peritonitis is not common except as the result of injury or some other source of local irritation, such as substances derived from rupture of the underlying Chap. Lxxviii.] Peritonitis. 393 viscera or pathological cavities, or diseased states spreading by continuity ; e.g.^ cancer of the liver, and typhoid and tubercular inflammation of the intestines. Peritonitis is usually described as acute or chronic, but between the two forms there are many inter- mediate degrees of intensity. Chronic peritonitis is either general or partial. When general it is caused by Bright's disease, or disseminated cancer, or tubercle. Partial peritonitis occurs in connection with localised disease of the structures beneath the serous membrane, e.g.., an ulcer of the stomach or intestine, or inflammation of the pelvic organs ; or, as the consequence of long-continued friction, notably in old hernial sacs. The lymph poured out from the vessels organises to connective tissue, which binds together adjacent parts, and, con- tracting, causes constriction of the hollow viscera ; and various displacements. By continued stretching the adhesions may be elongated into fibrous bands, beneath which a portion of the bowel may slip, and become strangulated. The peritoneum is greatly thickened, as is seen in hernial sacs, where the contents have been allowed to remain habitually prolapsed. Aciite peritonitis is set up by rupture, or ulcerative perforation of some viscus, e.g.., the bladder, or intestine ; or by bursting of a hydatid cyst, or localised abscess ; or by a wound from without, as in the operations of gastrostomy, gastrotomy, and herniotomy. The pathological appearances vary greatly in different cases according to the rapidity of the process, the general health of the patient, and as to whether the peritoneum be healthy, or altered in structure by previous disease. One result of chronic thickening of the membrane is to diminish the liability to acute general inflammation, so that the sac of an old hernia 394 Surgical Pathology. [Chap, lxxviii. may be ojoened with less risk than that of a recent one. The inflammation is termed serous, plastic, puru- lent, or hgemorrhagic, according to the prevailing product of exudation ; the same as happens in pleurisy and pericarditis. In surgical practice it is usual to speak of two varieties : sthenic ; and asthenic, or latent. In acute sthenic peritonitis the signs and symptoms are most pronounced. They are : severe pain ; great abdominal tenderness ; marked tympanites ; knees drawn up to relax the abdominal muscles ; fast, wiry pulse ; and high fever. In the latent or asthenic form there are the same physical conditions that underlie the above-mentioned symptoms, but the depressed or exliausted state of the patient prevents a general response to the absorp- tion of the products of inflammation, and the irritation of a wide tract of visceral nerves. One is often struck by the contrast offered by the comparative immunity from suffering, and the revelations of the post-mortem room. An old man who has been operated upon for strangulated hernia may never rally sufficiently to manifest by general signs the pro- found structural alterations going on in the perito- neum. Morbid anatoaiiy. — Unless the peritonitis be caused by some irritant fluid poured more or less over the whole surface, the inflammatory changes are most marked at the seat of the original injury ; e.g., whilst there is a copious deposit of lymph, and it may be pus, upon and about the contents of a hernial sac after reduction ; the parts more remote may be only lightly glued together by a scanty fibrinous exudation. In some cases, however, and especially where a large wound has been inflicted, and the inflammation is of a septic nature, the inflammation spreads with great Chap. LXXVIIL] PERITONITIS. 395 rapidity, and soon becomes widely diffused; e.g.^ after ovariotomy. The first stage is that of vascular injection; the subserous vessels are dilated^ then there is exudation upon the surface of the membrane and into its inter- stices. As the natural secretion is highly fibrinogenous it is not a matter of surprise that, under the influence of the globulin-laden constituents of the blood, fibrin, which does not exude as such from the vessels, should be formed and deposited with great readiness. This really occurs before there is any striking alteration in the appearance of the membrane, and certainly before it has lost its lustre. But even at this early period it can be shown by gently drawing the coils of intestine apart, when it will be seen that instead of gliding over one another with the usual facility, they stick somewhat. Scraping, too, reveals the presence of a small quantity of semi-transparent glutinous matter. As the exudation becomes more profuse it collects in the furrows formed by adjacent coils of bowel. Here, also, the hypersemia is more marked than elsewhere. In fact, on separating the coils, it will be found that, whilst their mutual pressure had prevented the accumuldtion of blood in the vessels at the surfaces of contact, it had as a natural consequence increased the tension in the collateral branches, and given rise to the so-called suction-hands of congestion and exudation that skirt the confines of the more ansemic parts. By this time the surface has lost its brightness, owing to the loss of the endothelial layer, and the coagulation of fibrin. It looks minutely granular to the naked eye, and with a low magnifying-glass finely reticulate from the interlacing of fibrin filaments. Authors differ as to the share that the serous endothelium takes in the process. Those who believe in the formative quiescence of connective-tissue corpuscles generally, assert that here they become 396 Surgical Pathology. [Chap. lxxviii. loosened by the exudation, and softened by liquefactive degeneration ; and that the richly cellular neoplasia consists mainly of fibrin and migratory leucocytes. They look upon the multi-nucleated giant-cells found in the exudation as masses of homogeneous plasma, embedding white blood-corpuscles. Others state that the endothelial cells swell up, and, together with their nuclei, divide and subdivide, and thus add greatly to the vascular effusion. Meanwhile the subserous connective tissue becomes swollen, succulent, and infiltrated with liquor san- guinis and leucocytes. Nor does the process end here, for the muscular coat of the bowel loses its contractility, hence the tympanites from the un- restrained pressure of the gases within. It also softens, as shown by the readiness with which it tears on attempting to dissociate adherent coils of bowel. In pelvic peritonitis the bladder suffers in a similar way, and is unable to empty itself properly. So far only the plastic stage of peritonitis has been considered, but unless the inflammation resolves, or death of the patient supervenes at this period, further changes are observed. The exudation becomes more copious, and can no longer be retained upon the surface, and within the meshes of the membrane. The coating of lymph, some- times distinctly laminated, is raised from its bed by the pressure of the fluid beneath. It can be readily peeled off, leaving a granular surface composed of loops of capillary blood-vessels surrounded by leucocytes. The outward pressure of the osmotic current separates the visceral and parietal layers and the involutions of the former. The fluid accumulates in the potential cavity, where it takes the course directed by gravity and least resistance, so it is found in greatest abundance in the pelvis, flanks, between the liver and the diaphragm, and beneath the liver. Chap. Lxxviii.] Peritonitis. 397 At first it is serous, or seropurulent and cloudy, and generally contains some flakes of lymph washed off from the surface of the peritoneum. Then it becomes more turbid, as the number of leucocytes increases, and the fibrin in suspension augments in quantity, and as both pass through retrograde granulo-f atty changes. Finally it is quite purulent. Some cases scarcely go beyond a plastic exudation, some stop with extensive serous efi^usion, whilst others 2:)ass rapidly into suppuration. The last is common in the asthenic peritonitis of old and exhausted patients, where the inflammatory effusion which often smears over the viscera, and resembles " melted I'jutter," is more copious than one would suppose from the extent of the congestion observed post mortem. Acute purulent peritonitis follows the admission of highly irritating matter, such as would be derived from extravasation of the gastro-intestinal contents, rupture of an abscess containing very infective (locally) pus, or the admission of air laden with septic germs. Under the last-mentioned conditions the softening of the peritoneum and subserous tissue is so great, and the vascular tension so high, that capillary ruptures are exceedingly common on the surface of the peritoneum, and into the lymph which covers it and infiltrates its substance. This is known as hcemorrhagic 'peritonitis. The red corpuscles break up very rapidly, and the liberated hsemoglobin decom- poses into other hesmatin compounds, so that the inflammatory products are variously stained. Where the extravasation is recent they are deep red and sanguineous ; where it is older they are reddish-brown and ochre-coloured. The fluid contained in the peritoneal cavity, which is highly decomposable, sometimes gives off" gases of putrefaction. Inflation also happens when there is free communication with the stomach or intestines. 398 Surgical Pathology. [Chap. lxxviii. In either case the tympanitic note is more uniform than when the hyper-resonance depends upon disten- tion from gases imprisoned in the natural passages. microscopy of t!ie exudation. — The products of peritonitis will be found to vary as the intensity and duration of the inflammation. In simple plastic peritonitis there will be filaments of homogeneous fibrin, leucocytes, and swollen endothelial cells. In purulent hsemorrhagic peritonitis the fluid obtained from the cavity will contain flakes of fibrin in a state of granular degeneration, pus cells, granulo-fatty debris, blood corpuscles, pigment granules, and some- times crystals of hsematoidin, cholesterine, and the fatty acids. Bodies of extra-peritoneal origin may also be discovered, such as the contents of hydatid cysts, and of the gall bladder, and the intestines. Vasciilarisatiou and org^anisation ; adhe- sive peritonitis. — As in inflammation of other tissues, new blood-vessels are formed. These are pro- bably derived for the most part from loops and buds of pre-existing vessels ; but it is quite possible that some have a separate origin in vaso-formative cells, and that they subsequently join the general circulation. As the fluid is absorbed, the opposite surfaces adhere, and the organisation into connective tissue is the same in every respect as before described under " Healing of wounds." Although the peritoneum is very susceptible to the causes of inflammation, simple incised wounds heal very readily, provided the tension be not too great and the injured surfaces be kept free from all sources of irritation. As plastic lymph is quickly efiiised, it is the object of the surgeon to bring the cut edges of peritoneum closely together, so that any communication with the external air or subjacent cavities may be shut off as early as possible, Chap. Lxxix.] Strangulated Hernfa. 399 The young connective tissue undergoes cicatricial contraction, and in this way many of the vessels are obliterated. Band-like adhesions become further attenuated, and even broken through, by the con- tinued traction exerted upon them consequent on the movement of the parts. Thus, the pedicle of an ovarian tumour fixed in an operation wound may in course of time atrophy and lose its connection with the abdominal wall. CHAPTER LXXIX. STRANGULATED HERNIA. The symptoms of strangulated hernia are depen- dent more upon the nipping of the nerves and acute congestion ot' the vessels than upon obstruction of the bowel ; for in some cases of obturator and femoral hernia, where only a part of the calibre of the gut is involved, and where there is consequently but partial oljstruction, the local pain and the vomiting may be just as pronounced as when several coils are tightly constricted. The irritation of the visceral nerves is reflected through the abdominal "sympathetic" system, and shows itself as widely-distributed pain, reverted peristaltis, and increased secretion of the mucous glands. Brinton explained the stercoraceous vomiting by direct onward contraction of the alimentary canal, and not by its reversal. According to this view, a circumferential current is established, which, on meeting with obstruction at the seat of strangulation, is turned back in the long axis of the bowel. This would be possible so long as the propelling tube remained full, but could not take place when it 400 Surgical Pathology, ichap. lxxix. became practically collapsed and empty. Moreover, experiments on the lower animals show that acute constriction is followed by reversed peristaltis ; and no doubt this is what obtains in strangulated hernia. Mediaoism of i^tr angulation. — When the neck of the sac is narrow and inexpansile, and the surrounding structures are rigid, strangulation is effected immediately after the descent of the bowel ; hence this is likely to happen in recent hernise, and in old ones that have been kept habitually reduced by a truss. On the other hand, where the neck of the sac is wide, unless several coils of intestine, or a single knuckle and a piece of omentum, are forcibly driven through the orifice, the symptoms are developed more slowly as the veins and capillaries become gorged with blood. As in constriction of a limb, the current through the veins is arrested before that in the arteries. Subsequent serous effusion into the sac increases the tension ; for, although fluid pressure is equal in all directions, it tells most on the least resilient parts, i.e.., at the neck of the sac and aperture of exit in the abdominal walls. State of the bowel. — In the first instance there is intense venous congestion, which causes the protruded gut to present a dark red appearance. Then, if the tension be not relieved, it sets up inflam- mation. The effusion changes its character from serous to plastic, and the peritoneal coat loses its lustre from desquamation of the endothelial covering and coagulation of lymph on the surface. Mean- while the walls of the gut are much thickened by congestion and exudation, and at the same time they are softened. As the strangulation continues, stasis is followed by coagulation, and the parts cut off completely from their vascular supply lose their vitality and become Chap. Lxxix.] Strangulated Hernia. 401 gangrenous. AVlien this stage is reached the bowel is black. Later on the blood corpuscles are broken up, and the colouring matter is discharged, and then there are dirty slate-grey patches. The condition is, in factj typical of moist gangrene, and the tissues are so rotten that very little violence is necessary to break them down j hence the danger of forcible attempts at taxis. Rupture of the gut may take place into the sac or the abdominal cavity. In the latter case it gives way on the proximal side of the constricted coil; for, in addition to the uniform compression at the neck, there is the mechanical dis- tiu'bance from peristalsis, w^hereas the bowel on the distal side of the strangulation, after emptying itself of its contents, remains collapsed and comparatively quiescent. The effect of distention and softening of the walls of the capillaries is occasionally seen in the form of hcemorrhage into the hoicel after reduction of the hernia. Such an event at first suggests ulceration into a large vessel, for the bleeding may be very copious (I have knoAvn half-a-pint of blood passed per I'ectum) j but this is not the case. The capillaries of the mucous membrane, ha^ving lost their natural j)Ower of resistance,- burst under the force of the ai-terial cuiTent let in upon them after the strangula- tion has been rehevecl. Extravasation to any great extent is very rare, whereas mucous and submucous ecchymoses are common enough. Fluid contents of the sac. — In all cases of strangulated hernia there is a certain amount of serous exudation from the congested vessels of the bowel, or omentum, or whatever else may compose the hernia. Where the sac is large, and the rupture small, the fluid accumulation may be very extensive. The nature of the exudation varies with the degree and duration of strangulation : thus, it is clear and A A 402 Surgical Pathology. [Chap, lxxix. straw-coloured ; or pink, or deep red, from admixture with blood, and dissolved haemoglobin ; or turbid from pus and flakes of lymph, the result of peritonitis ; and lastly, it is sometimes mixed with the contents of ruptured gangrenous bowel, or the gaseous products of decomposition. Apart from strangulation, the sac of a hernia may be dropsical and distended with clear serous fluid, when it simulates funicular or congenital hydrocele. This condition is known as "hydrocele of the hernial sac." Artificial anus is an unnatural opening of the bowel on the surface of the body. It is made intentionally in the operation of colotomy. If a patient survive the occurrence of gangrene of the bowel from strangulated hernia, the peritoneal sac is laid open by incision, or by a com.bined process of sloughing and ulceration. On cutting into the gut, if it has not already ruptured, the contents escape, and a communication is established with the lumen of the intestine on each side of the seat of strangulation. Extravasation into the general peritoneal space is prevented by previous plastic adhesion between the visceral and parietal layers of the peritoneum. The pressure of the underlying abdominal viscera, together with the peristaltic action of the bowel on the proximal side of the artificial anus, forces down the partition formed by the adherent walls of the proximal and distal segments of the gut. The outward flow of intestinal contents from the proximal segment keeps its orifice dilated, whilst the pressure exerted by the escape of fseculent matter, coupled with the projection of the partition above referred to (Dupuytren's spur), causes the opening of the lower collapsed portion of bowel to remain practically closed. The treatment of artificial anus consists essentially in getting rid of the spur-like barrier. 403 CHAPTER LXXX. IXTUSSUSCEPTION OF THE BOWEL. When one portion of intestine is invaginated in another the condition is known as intassusce^otion. It is by no means rare to find one or more such involu- tions post mortem, in cases where no symptoms pointed to their existence during life. It is doubtful whether they are formed before or after death, for peristalsis can be excited in animals by direct or indirect stimulation for some time after the heart has ceased to beat. Tliese so-called " post-mortem invaginations " can be reduced quite easily. For their development there must be an irregular contraction of different portions of the bowel. Thus, if one segment is in a state of peristalsis whilst that immediately succeeding it remains relaxed, the former can readily glide into the latter. The sudden increase in the calibre of the intestine beyond the ileo-csecal orifice is the chief reason why intussusception is more common in this situation than elsewhere. Children are more liable to it than adults : (1) l)ecause in them the general reflex excitability is very marked, and the bowel is readily excited to irregular peristaltic action through irritation of its nerves by ascarides, or other oflfending matter; (2) on account of the disposition of the peritoneum. It should be remembered that the part first invaginated always remains the lowest, or in other words, that the ensheathed portion merely travels on, whilst the ensheathing tube is being continually rolled in ; so that if the invagination commences at the ileo-csecal valve, this will be found the most advanced part. 404 Surgical Pa thology. [Chap. lxxx. Now, in children the csecum is freely swung by the mesentery, instead of being fixed in the iliac fossa, as it is in the adult, and consequently there is less check upon its involution. The ensheathed portion of bowel acts as a foreign body, and stimulates the surrounding muscular walls to continued contraction. This may not cease until the ileo-csecal valve has reached the rectum, or even protruded from the anus. The attachment of the peritoneum hinders the descent of the bowel chiefly at its posterior aspect, so that the orifice of the invaginated tube looks somewhat backwards. This should be borne in mind on rectal examination, as otherwise the prolapse might be mistaken for a polypus, from which, however, it otherwise differs in not being fixed at one spot. The symptoms are dependent on the degree of strangulation, and not on the simple existence of invagination, just the same as in an ordinary external hernia. Chaug^es secoaidary to strang^ulation. — The blood-vessels of the prolapsed gut become engorged, then inflammation sets in, and the part is much swollen. The mucous membrane secretes a quantity of thick mucus, which, together with some blood derived from rupture of capillaries, is often discharged from the anus. Lymph is thrown out on the opposed peritoneal surfaces, which it glues together after the process of invagination is complete. As the result of acute strangulation the ensheathed bowel may slough away. Extravasation of intestinal contents into the peritoneal cavity is prevented by plastic exudation uniting the contained and containing portions of bowel at the base of the invagination. But before the gangrenous part has time to separate the patient usually dies from collapse or general peritonitis ; and where it is effected there is the Chap. Lxxxi.] Tumours. 405 certainty of an annular stricture from cicatrisation of the inflammatory products. CHAPTER LXXXI. TUMOURS. " A TUMOUR is a mass of new formation that tends to gi'ow and persist." This tendency is in marked contrast to that of inflammatory neoplasias, which is to arrive at a typical termination. Fatty tumours, it is true, frequently become arrested in their growth, and papillomata, as in the case of common warts, often disappear spontaneously \ but still the tendency is the other way. Again, although long- continued irritation may certainly be the exciting cause of a tumour, as in the case of epithelioma of the lip and tongue from friction against a pipe or tooth, and in the same disease sometimes starting at the seat of old chronic inflammatory lesions, such as syphilitic ulceration of the tongue and skin, yet, whilst we can produce inflammation at will, we have no absolute power of producing a tumour at all. In studying the anatomical basis of tumours, it will be found that they all have their " type in some natural tissue of the body, either in the embryonic or developed state." In other words, a tumour is not a parasite ; there is nothing truly alien in its nature ; it is the rebellious scion of a parent stock. If the elements of a new growth are like those of the tissue where they are found, they are said to be liomoflastic, e.g., osteoma growing from bone ; if they diJQfer, they are termed heteroplastic, e.g., enchondroma of the testicle. From a knowledge of the fact that any 4o6 Surgical Pathology. [Chap, lxxxi. anatomical or physiological peculiarity of a tissue is usually stamped upon the tumour springing from it, a great insight as to the probable nature of the latter, may be obtained ; thus one would expect osteoma, enchondroma, and sarcoma to be frequently connected with bone, myo-libroma with the uterus, and so on. Why also myeloid sarcoma should have its seat almost exclusively in bone, and why sarcoma of the choroid should be melanotic, and giio-sarcoma of the retina and nerve centres present a stroma, like that of the natural structure of these parts. A tumour is malignant in proportion to the rate at which it destroys the tissue and tends to shorten life. It is impossible to denote definitely where malig- nancy ends and benignancy begins, for not only are there forms of intermediate gravity, but in the history of a given growth it may so alter in character as scarcely to be described by the same name; e.g.^ a " recurrent fibroid " may at first consist largely of fibrous tissue, but each successive recurrence after operation is often marked by a great increase in the number of cells. The signs of isialigiiaucy are : (1) Local recurrence after apparently complete removal. (2) Dissemination or generalisation in other parts, either directly by associated lymphatics, or more i-emotely by the blood-vessels. Multiplicity of growth may in some cases be explained as a general outbreak from a common source, rather than a causative sequence. It is intei-esting to note that the secondary growths usually maintain the type of the primary ; thus alveolar cancer of the breast is reproduced in the lymphatic glands, liver, and other parts; columnar epithelioma of the rectum, in the liver ; squamous ejDithelioma of the lip, in the cervical Chap. LXXXL] CLASSIFICATION OF TUMOURS. 407 lymphatics ; melanotic sarcoma of the skin and colloid cancer of the omentum or ovary follow the same rule. (3) Infiltration of surrounding tissues by the ele- ments of the tumour. (4) Rapidity of increase, leading to destruction by ulceration or sloughing. The vital activity of the cells being expended more in multiplication than in development, leads to a deficient vascular supply, and great liability to sufier from injury. (5) Multiplicity, though suggestive of malignancy, does not necessarily imply it, for some benign new formations (e.^., fatty tumours and atheromatous cysts) are often multiple. (6) An apyrexial cachexia from impaired assimi- lation leading to general wasting. (7) The influence of heredity is certainly more marked in maligTiant than in simple tumours. (8) Direction of growth. Benign tumours spring- ing from a surface are centrifugal ; malignant, both centrifugal and centripetaL Compare the mere out- growth of a papilloma with the deeply-rooted invasion of an epithelioma. Classification of tiimours. — Formerly, when tumours Avere arranged on a clinical basis^ such terms as " medulloma," " encephaioma," "soft cancer," etc., were applied without distinction to any soft, rapidly- growing new formation. In like manner, the word " melanoma " was used to indicate a tumour contain- ing pigment. It is true the other attributes were implied, but it was none the less unscientific, for a soft wart on the skin may be as black as a virulent melanotic cancer or sarcoma. We now employ an anatomical classification, for it serves to point out the re- semblances and differences of allied growths, and to distinguish between their essential nature and their suboidinate nutritive modifications. Relying upon 4o8 Surgical Pathology, [Chap, lxxxti. tlie microscope, there is no fear of mistaking a dis- integrating infarct for a malignant tumour. CHAPTER LXXXIL THE FIBEOMATA. "VYhite fibrous tissue exists in abundance in many tumours. In some, e.g., the fibro- adenomata, the fibrous element far outstrips the glandular. But the term fibroma denotes the absence from the growth of any more characteristic structural constituent. The fibromata rank amongst the benign tumours. They arise from connective tissue, especially the sub- cutaneous and submucous, but they are met with in many other parts. The so-called " fibroid " tumours of the uterus belong more strictly to the myomata, with which they will be considered. We shall divide the fibromata into three groups : (1) The isolated encapsuled tumours situated beneath the surface ; (2) the more widespread overgrowths of the cutaneous and subcutaneous connective tissue, known as hyper- trophies or diffuse fibromata ; (3) fibrous polypi. It may be stated generally that when fibrous tumours commence either in the skin or immediately beneath it, or in the submucous tissue, the tendency is for them to become pedunculated. The fibromata naturally fall under two heads, ac- cording to their consistence and vascularity. Thus we speak of the firm and soft varieties. In structure the fibromata present the same variations of textural arrangement as attains in normal white fibrous connective tissue. The greater portion of the tumour consists of bundles of fibres interwoven Chap. Lxxxii.] The Fibromata. 409 ill various directions. The general disposition of these bundles is along the course of the blood-vessels ; very often thej form concentric layers around the latter, giving the section a lobulated appearance, and this is more marked when the bundles between the lobules are less closely packed than those which constitute the latter. In some cases the fibres are loosely interlaced, forming an open mesh-work ; in others they are so intimately connected as to partially obscure the fibrillation. The fibrillation itself varies much, so that microscopical sections appear like spun glass, or present wavy fibres with definite outline. Elastic tissue is usually absent. The cells show great diversity in number, size, and shape in different tumours,- and in different parts of the same tumour. The younger, too, the tissue, the larger and more numerous the cells ; in fact, it may be difficult in the earliest staQ-es to distino-uish between a developing fibroma, myoma, and spindle- celled sarcoma. For the most part, however, the cells are small. They are round, angular, fusiform, or branched. Some elongate, and become finally lost amongst the fibres with which they blend. We have examined specimens where not a single cell could be seen. On the whole, the fibromata are scantily supplied with blood-vessels ; some appear almost devoid of them. The softer forms are more vascular, and are sometimes permeated by a cavernous network. Secondary cliang-es. — The most constant is calcification, either confined to the septa or as a petrifaction of the entire tumour. ISText to this comes mucoid softening. True cystic formation is rare. The skin may ulcerate over them, and the inflamma- tion spread into the interior, but they are not subject to primaiy suppuration. The firm fibromata are very dense, creaking on being cut with a knife. The cut surface looks dead- 41 o Surgical Pathology. [Chap, lxxxii. white and coarsely fasciculated, or greyish and glis- tening, according to the degree of homogeneity of structure. They grow from fasciae, bone, periosteum, nerves, and other parts. Well - marked examples are the fibrous e'pulides of the jaws, which spring from the bone or periodontal membrane, not from the mucous membrane of the gums. They project by the side ,of the teeth, which frequently become loose. When they ossify (and this is not rare), the bone is deposited in the direction of the vessels, i.e., from the point of attachment toAvards the periphery. If completely removed there is almost entire immunity from recurrence. Ossification may advance to within a short distance of the surface, which is covered by mucous membrane. What are known clinically as neuromata consist either of mucous, or of firm fibrous tissue. {Vide Myxoma.) The fibrous neuromata, like the mucous, start from the connective tissue around the nerves and between the fasciculi. The nerve-fibres are stretched over the tumour. We have seen a fibrous neuroma the size of an egg. Under the microscope it showed minute cells distributed with great regularity through a delicately fibrillated stroma. Some nasal polypi belong to the firm fibromata. The soft fitoroMiata include the diffuse fibrous hypertrophies of the subcutaneous tissue, and many pedunculated tumours attached to the skin and mucous membranes. The diffuse fibromata consist of loosely woven bundles of connective tissue, in the interstices of which the vessels ramify; the latter are sometimes very large. They form doughy masses, which some- times hang in overlapping folds from the buttocks, thighs, and other parts of the body. From its struc- ture and consistence the new formation was called molluscum fi)rosum, or fibroma molluscum, a name Chap. Lxxxii.] Fibrous Polypi. 411 still in use, but now generally restricted to the fleshy librous polypi of the skin. When the subcutaneous soft fibromata project from the skin as sessile or broadly pedunculated masses they are known as wens. Like the other diifuse fibromata, they have no capsule. Elephantiasis Arabum bears a marked structural resemblance to diffuse fibroma, but instead of being a simple non-inflammatory overgrowth, it appears to be closely connected with, if not dependent upon, recurrent attacks of lymphangitis. The scrotum and legs are the parts usually afiected. The growth often assumes enormous dimensions, weighing as much as forty or fifty pounds. It is mostly found in Orientals. Circumscribed, encapsuled, soft fibromata are met with in the subcutaneous tissue, but they are much rarer than the difluse variety. Fibrous polypi occur on the cutaneous and mucous surfaces. They may be considered as localised overgrowths of the subcutaneous and submucous tissues. Those growing from the skin have been referred to under the name "molluscum fibrosum." They are usually multiple. Their number may in some cases be counted by tens and hundreds. In size they vary from a pea to a potato. T. Fox describes two forms, the simple and the fungoid ; the latter are very vascular, and liable to ulcerate and fungate. Soft fibrous polypi of the mucous membranes are met with in the uterus, vagina, stomach, and intestines ; but those of greatest surgical interest grow from the naso2:)harynx and contiguous sinuses — frontal, sphe- noidal, etc. Clinically, many of them are more nearly related to the sarcomata than to the fibromata, for they tend to continuous growth, absorb everything in their way, and often recur after removal. Others, 412 Surgical Pathology. [Chap, lxxxiii. however, are quite innocent in their nature, and between them there is every gradation. They contain a good deal of mucous tissue, and are more vascular and succulent than those attached to the skin. CHAPTER LXXXIII. THE LIPOMATA. The majority of fatty tumours are met with between the ages of thirty and fifty, when there is a general disposition to obesity. The local determination of the growth can in many cases be referred to some injury or long-continued friction. They are occa- sionally hereditary. They are situated chiefly on the trunk, especially about the shoulders and waist ; parts subject to the pressure of articles of dress, such as the braces, corset, etc. ; here they spring from the sub- cutaneous fatty tissue. Local collections of fat are seen now and again in the synovial fringes of joints and tendon sheaths, resembling the appendices epi- ploicse of the omentum. Fatty tumours mostly occur singly, but several may be found in the same subject, the more so when hereditary. Cceneral anatomy.— As a rule they form roundish projections on the surface of the body. The most constant feature is a lobulation ; this may be visible, or be made out only on manipulation, or after dissection. When pressure is made on the skin at the margin of the tumour, that over the surface becomes dimpled, from stretching of the interlobular bundles of fibrous tissue that are fixed to the under surface of the skin. The author has seen a polypus as large as an Chap. Lxxxiii.] The LiPOMATA. 413 orange attached by a narrow stalk to the buttock ; one half of the structure was composed of fat intermingled with the other, which consisted of dense fibrous tissue (fibrous lipoma). The lipomata are usually circumscribed and limited by a distinct capsule, which is fixed to the surrounding tissue by a loose meshwork and strong bands of fibrous tissue. The latter conduct the blood-vessels, which enter chiefly at the upper and deeper parts. The external attachment may be so slight that the tumour changes its position; the resistance met with in the subcutaneous cellular tissue being slight, the force of gravity is sufficient to cause the displacement. In such cases the fibro-vascular bands become stretched. Very rarely fatty tumours show no limitation, the fat composing them being continuous with the normal tissue around (difiuse lipoma). They have occasion- ally been found connected with the peritoneum, by a prolongation of the latter through a cleft in the abdominal wall, particularly at the linea alba ; they then grow from the retroperitoneal fat. The possible danger attending their removal is obvious. Fatty tiunours vary in consistence. They may be so soft and elastic as to simulate fluid collections; chronic abscesses and sebaceous cysts have been mis- taken for them. On the other hand, they may be very firm, resembling fibrous tumours. The lobules are sepa- rated by areolar tissue, in which the supplying vessels are embedded. The amount of this, together with the composition of the fat in a given case, explains the density. In colour they are bright yellow, or yellowish white. In children, especially, they often contain a considerable quantity of erectile tissue, so that by pressure their size can be much diminished ; and they bleed freely on removal (nsevoid lipoma). Compare a fatty tumour after enucleation with an enchondroma of a long bone or the peMs, and 414 Surgical Pathology, [dap. lxxxiii. an agglomeration of enlarged lymphatic glands in Hodgkin's disease. All these are lobulated, but the enchondroma is very hard, of a bluish -white colour, and is attached to bone. The glands are not so yellow as fatty tumour, but they are firmer, and large trunk vessels can usually be seen passing through the mass, for it is usually taken from the abdominal mediastinal or cervical regions. Lipoma forms compound tumours with myxoma, sarcoma, and fibroma. Microscopy. — The greater part consists of fat cells, which do not differ from the normal, except that they Fig. 60.— Fatty Tiunour. The cells a, exactly in focus, have a more strongly marked outline than those, b, immediately beneath them : c, blood-^vessel ; connective-tissue corpuscles lie between the fat cells, x 265. are somewhat larger. They are roundish or polygonal from mutual pressure. The cells just out of focus are seen in dim outline (Fig. 60). Bundles of areolar tissue and blood-vessels run between the lobules. Fine fibres and connective tissue cells may be found between the individual fat cells. This last phenomenon is explained by the mode of growth, for the cells do not contain fat at first; this is stored up later. The first cells of the tumour are derived from the connective tissue, and the tumour increases in size by the addition of new cells Cnap. LXXXIV.] ThE EnCHONDROMATA. 415 produced by vaciiolation and division of pre-existing ones, and probably also by the fixation of wandering cells. The interlobular_, and, to some extent, the intralobular, tissue is filirillated. Secondary cbaug^es. — Fatty tumours are not very prone to structural modifications. Calcification and even ossification are occasionally met vrith in the matrix. The fat may alter its com- position and become semifluid. The fatty acids may then be set free and crystallise ; this is often produced by the action of reagents used in the preparation of microscopical sections. The skin over them may be atrophied by the continuous pressure, and this, together with accidental injury, may cause ulceration of the mass. Central suppuration rarely or never occurs. Fatty tumours neither generalise nor recur locally after removaL CHAPTER LXXXIY. THE ENCHONDROMATA, These tumours, which have their type in cartilage, grow for the most part from bone, and that too in the ^^.cinity of diarthrodial joints and synchondroses. They are not, however, confined to these situations, but are found in tissues {e.g.^ the parotid gland and testicle), in which at no period of their natural existence is any trace of cartilage to be seen. They never sjmng from cartilage. It must be borne in mind that cartilage is a primary derivative of embryonic tissue, and hence it is not surprising that it should be developed where the latter forms the structural basis of new growths. The admixture of cartilage with embryonic and 4i6 Surgical Pathology. [Chap. lxxxiv. mucous tissue is thus readily explained, and hence the varieties, chondro-sarcoma, chondro-myxoma, etc. Most enchondromata are innocent in their nature, rarely giving rise to secondary deposits. When these occur it is chiefly in the lungs. If all the indifferent cells are used up in the production of cartilage, the tumour may fairly be designated an enchondroma ; but where there is only a limited conversion, it is better to — a Fig. 61. — Myxo-Cliondroma of Parotid Gland. a, Hyaline cartilage ; 6, nlucous tissue, -rtith stellate corpuscles atid slightly flbrillated gelatinous matrix ; c, cartilage capsule, containing a nucleated cell and a fat globule, x 265. speak of it as a chondrification, for the specific nature of the growth is not modified thereby. A sarcoma is none the less malignant because islets of cartilage are scattered through its substance. We have seen this in a testicle removed during life (Fig. 53). The patient died within six months, with secondary deposits in the lumbar and mediastinal glands, and nearly all the abdominal viscera. In another case the association of Chap. Lxxxiv.] The Eaxhondromata. 417 sarcoma with enclioudroma was delayed ; but what appeared at first to be an innocent tumour of the parotid (for it only attained the size of a small orange in twelve years), subsequently made such progress that it doubled its size in six months ; one half was composed of hyaline chondro-myxoma {vide Fig. 61), the other of large round-celled sarcoma. It may be said, then, that cartilaginous tumours of parenchymatous organs should always be regarded with suspicion. The same is true of those growing from the shafts of bones and the jaws. ( Vide Lancet^ Nov. 24th, 1877.) Classification. — Enchondromata may be divided into three groups : (1) Those growing from the metacarpal bones and phalanges; (2) those springing from the ends of the long bones and the pelvis ; (3) those found in soft tissues, e.^., the parotid gland, testicle, and lungs. 1. Metacarpal and 'phalangeal enchondromata are rarely single. They commence in the interior of the bones, usually at the ends. They seldom grow larger than a walnut. They may calcify, but they do not ossify. Their surface is smooth, or only very slightly lobulated. They select by preference the periods of childliood and youth. They are perfectly benign. The matrix is hyaline, or faintly fibrillated, and the cells are comparatively small, and polymorphous. 2. Enchondromata springing from the ends of the long hones and the pelvis often attain an enormous size. Coarsely lobulated like fatty tumours, they differ from them in every other respect, being hard and of a blueish-white opalescent appearance. They grow from the surface of the bones, which they absorb by pressure and destroy by meta- morphosis of tissue. They are encapsuled on the surface, but their structure is continuous with the osseous tissue. Coarse fibrous bands carrying the B B 4i8 Surgical Pathology. [Chap. lxxxiv. blood-vessels intervene between the lobules. Nutri- tive changes are very common, calcification and mucoid degeneration taking the lead. The former is recognised as dead white patches of irregular shape between the semi-translucent nodules of cartilage. The latter causes softening/ and so large anfractuous Fig. 62. — Cystic Ossifying Encliondroma of the Diaphysis of the Femur ; from a Girl cet. 17. %, Cyst bounded above by an osseous bar; 6, nincoid softening of matrix, anas- tomotic stellate corpuscles form a raeshwork through the space; c, hyaline cartilage, the capsules are distended with mucin, x 265. cavities. They may ossify, or remain free from this and all other secondary modifications of structure. In the pelvis they are attached near the sym- physis and the sacro-iliac synchondrosis. Unlike the smaller phalangeal variety, they tend to indefinite increase in size, but they resemble them in being generally benign. 3. Enchondromata of the soft tissues are seldom simple. Thus, mixed "parotid tumour" may contain cartilage along with glandular, mucous, or sarcomatous Chap. LXXXV.] ThE OsTEOMATA. 419 tissue, one or more of them. In the testicle sarcoma is rarelj absent. The association with tumours of a lower type of organisation renders this group more malignant than either of the others. Histology. — The matrix is hyaline or fibrous ; or it looks like spun glass. Considerable variation in this respect may be met with in the same tumour. If calcified, microscopical sections look granular and opaque by transmitted light_, but the capsules and cells can again be brought into view by the solvent action of a dilute mineral acid. The cells are round, oval, angular, or multipolar, with long branching offshoots. The protoplasm may be clear, or obscured by fat granules and drops of mucin (Fig. 62). The entire cell may be petrified along with the matrix. If lobulated, the mass is intersected by vascular fibrous tracts, thus differing from normal cartilage. The blood-vessels furnish the lime salts for calcifica- tion, and hence the infiltration is more advanced at the periphery of the lobules and between them than in their interior. In mixed tumours, e.g.^ chondro- sarcoma, the cartilage is sharply mapped off from tlie surrounding tissue (Fig. 53, h). CHAPTER LXXXY. THE OSTEOMATA. The osteomata proper are bony growths, not dependent upon precedent inflammation. Deposit of bone is an accidental or an integral part of many morbid processes : thus it is found as a nutritive modification in many tumours, especially those springing from the osseous framework, e.g.^ the sarcomata, enchondromata, and fibromata. Bone is 420 Surgical Pathology. [Chap lxxxv. usually present in subperiosteal sarcomas ; it is far from rare in the large lobulated cartilage tumours attached to the ends of the long bones and the pelvis j and it is almost constant in fibrous epnlides. Then, again, it is the final anatomical product of inflamma- tion of bone that goes on to a natural termination. In cases where the erosion has been local, and the loss of substance made up by protuberant granu- lations, the latter may ossify en masse, and the result simulate the true non-inflammatory exostoses ; but, on section, the base of the new formation is found not to be limited by the surface level of the bone, but to lie some distance in the interior. As in the osteomata proper, the Haversian canals of these inflammatory osteophytes lie at right angles to those of the old bone ; for ossification follows the direction of the capillary loops in the outwardly directed granulations. Muscles and tendons subjected to much strain or irritation are now and then extensively ossified, the bony deposit commencing as a rule next the points of attachment; e.g., in the deltoid and biceps muscles of infantry soldiers from pressure of the butt end of the rifle, and in the adductors of the thigh of cavalry, the " rider's bone " (Rokitansky). But in these cases there must be an inherent disposition to bone forma- tion, else it would be more common than it is. In like manner, the bones are sometimes the seat of multiple outgrowths at the points of origin and insertion of the muscles, without there being any ascertainable reason (O. Weber). In old age there is a marked tendency to ossifi- cation in certain tissues ; e.g. , the cartilages of the larynx, trachea and bronchi, the costal cartilages, and intervertebral ligaments. This is interesting, as showing that, whether the bone formation occurs as a new growth or a nutritive modification in pre-formed Chap. LXXXV.] ThE OsTEOMATA. 42 1 tissue, it is evidence of a physiological degeneration, and serves to explain the apparent anomaly of bony retrograde metamorphosis occuring mostly in old age, whilst the osseous tumours are rarely met with beyond mid-adult life. The plates of bone found in the meninges of the brain and cord are probably the consequence of chi'onic inflammation. Cornil and Kanvier say they have seen true bone in the calcified adventitious cysts of hydatid tumours^ but this must be very rare. The author has observed a nodule of bone in the centre of a simple hronchocele. Bone is one of the multiform contents of dermoid cysts. The osteophytes thrown out around the joints affected with tumor alhus and dry rheumatic arthritis are clearly irritative and inflammatory. In ataxic arthropathy they are now and again met with as part of a trophic articular lesion ; but M. Charcot informs me that they are quite the exception in this disease, and that he is uncertain whether they grow from cartilage or not. Having cleared the way of these irregular and secondary bone formations, the course is clear for the consideration of The osteomata, which almost invariably arise from pre-existing bone. The vast majority occur as outgrowths, or exostoses. A few occupy the interior ; e.g., the medullary cavities of the long bones, enostoses ; but even these cause projections from the surface in most instances, and as they are probably of inflammatory origin they will not be further discussed. Like normal bone, the osteomata vary in density, and it is customary to divide them into two groups, the compact and spongy. The former includes the ivory osteomata, and those that resemble in consistence the outer part of the shafts of the long bones. 42 2 Surgical Pathology, [chap. lxxxv. Tlie ivory osteomata, are mostly situated on the flat bones of the skull, and usually on the inner surface. They are found as plates, or roundish nodules, composed of concentric laminae parallel to the surface of the mass. They are found not to contain blood-vessels. If the latter existed at an earlier period of development, they must have become obliterated by the pressure of the bony deposit around them, in much the same way as syphilitic cranial osteophytes are rendered extra vascular {vide page 217). The bone corpuscles in these tumours have long outrunners, which are for the most part directed towards the surface, like those of the crusta petrosa of the tooth fangs (Cornil and Ranvier). Compact osteoraata are found in other situations than the cranium. In the College of Surgeons museum is a fine specimen attached to the lower jaw. The spongy osteomata range in density from an open cancellous fretwork to a closely set trabecular structure bordering on the compact variety. They grow chiefly from the ends of the long bones in the vicinity of the epiphysial cartilages. In all probability they start from the latter, or, at least, from the superjacent periosteum. For this reason their origin is limited to the term of existence of epiphysial growth of bone, and hence they are not found after the age of twenty-five or thirty. The spongy osteomata are occasionally met with at the rough muscular attach- ments on the diaphyses ; e.g.., in the femur near the opening in the adductor magnus, and in the humerus at the supracondylar ridges. (In some animals normal bony projections exist in these situations for the support and protection of the large vessels and nerves.) The epiphysial osteomata are in intimate connec- tion with the cancellous tissue of the ends of the bones. They consist of rounded or lobulated masses. Chap. Lxxxv.] The Osteomata. 423 They have a surface layer of hyaline cartilage, from which they continue to grow, and this is covered with periosteum. Bursal cysts not uncommonly develop over them, and by some pathologists it is asserted that these from the first are continuous with the articular synovial membranes, and thus constitute a source of danger attending operations upon the tu- mours in question. On account of their cartilaginous investment the spongy osteomata are sometimes spoken of as ossifying enchondroTnata ; but this is not quite correct, for when they cease to grow, the surface cartilage may completely ossify ; a circumstance, as far as my observations go, that never obtains in un- doubted enchondromata. During their development the cartilage capsules are dissolved, and the pro- liferating cells contained within are set free to form a layer of embryonic tissue, and in this the ossification goes on. Whilst the deeper portion of the cartilage is encroached upon and used up, the superficial layer is constantly being added to. Microscopy, — Sections made vertical to the surface show from without in : (1) A fibrous layer, richly corpuscular, next the cartilage; (2) a narrow band of hyaline cartilage ; (3) a stratum of osteogenic granulation cells; (4) fully -formed bone. The last has all the characteristics of true bone, viz., Haversian canals, lacunae, and canaliculi ; but the concentric lamination is less perfect than in the normal tissue. Hereditary multiple osteomata. — These form a notable exception to the rule that osseous tumours are rarely seen in children under ten years of age. Hereditary or not, the osteomata as a group are not uncommonly multiple ; but the variety under notice afiects many bones of the body, and that, too, at a very early age. Fig. 63 is a copy of a photograph of a boy aged ten years, in whom the disease is well marked. His father and brother are afiected in the Fig. 63.— Multiple Hereditary Exostoses. Chap. LXXXV.] ThE OdONTOMATA. 425 same way, though to a less degree. The tumours first appeared when he was very young. They are extremely hard, and greatl}^ interfere with the movements at the joints. Specimens taken from a similar case, in which nearly all the bones in the body were involved, presented a nodulated or craggy surface. The majority were seated near to or on the epiphyses, although there were several exceptions to this. Some were pedunculated, others had broad bases of attachment ; all were covered with translucent cartilage. They would seem to be the outcome of an excessive and ill- directed osseous development, comparing in this way with congenital growths ; e.g.^ nsevi. The osteomata are benign ; they do not recur after complete removal ; and although sometimes multiple, they do not generalise. After a time they cease to grow. In themselves they are painless They cause annoyance by their unsightliness, by the occasional occurrence of inflammation and ulceration of the skin over them, and by their impeding move- ment. They should not be removed except under urgent necessity, and this applies particularly to the spongy osteomata about the joints. The odontomata are made to include inflamma- tory exostoses growing from the crusta petrosa of the fangs; but the term should be confined to tumours of new formation, that consist of one or more of the dental tissues. Of these there are three varieties : (1) Enamel plates situated usually about the neck of the tooth. They are small, and look like pearly drops of congealed wax. They give rise to no symptoms. (2) Dentine tubercles projecting into the pulp cavity. They are only recognised after extraction for neuralgia. (3) " Warty teeth " or " dentinal odontomes " (Broca). These are the most important of dental tumours. They grow from the neck or fang, and form lobulated masses embedded in the jaw, which they absorb by 426 Surgical Pathology. [Chap. lxxxv. their pressure j or projecting from the teeth sockets. Billroth figures one more than an inch in diameter. Their structure is made up of one or more of the tooth elements. Usually there is an admix- ture of bone with irregularly disposed dentine or enamel. Osteoid tiimour. — Yirchow has described a new formation, the fundamental structure of which is identical with the " osteoid tissue " found beneath the periosteum in rickets. ( F^io^e Rickets. ) These growths are smooth or lobulated. They may attain considerable size. Clinically they are more nearly related to the sarcomata than to the osteomata, for they generalise in the internal organs. They consist of spongy bone tissue, with an uncertain amount of embryonic, fibrous, or cartilaginous material ; hence they may, by the unaided eye, be mistaken for tumours composed of one or other of these last-named tissues. Microscopy. — Trabeculse of various sizes and shapes alternate with layers of connective tissue. They consist of a homogeneous or faintly fibrillated matrix in which angular corpuscles are embedded. These corpuscles have only short processes, and do not form a lacunar inosculating system as in true bone, although the spaces in which they lie are said to join minute channels in the intertrabecular tissue. The matrix is often calcified in patches, or it may be in its entirety. The fibrous tissue between the trabecules carries the blood-vessels for the support and growth of the tumour. In it islets of cartilage are distributed, and when in large amount the name " osteoid chondroma" is given to it. According to Yirchow, the osteoid tissue is not confined to new growths and rickets, but is met with in a minor degree beneath the periosteum during the normal development of bone. If this be so, it goes to show that the tumours under consideration are built upon the type of embryonic Chap. Lxxxvi.] The Myxomata. 427 tissue of a specialised form, and to confirm the view of their histological relationship with the sarcomata. CHAPTER LXXXVI. THE MYXOMATA. When treating of mucoid degeneration it was pointed out that certain tumours, especially the sarcomata, were liable to undergo this change ; and that it lay at the foundation of true cystic development. {Vide Fig, 5.) But the term myxoma indicates thase growths in which the embryonic tissue necessarily passes to the next place of organisation, or that between indifferent cell - growth and fully formed connective tissue. Their physiological type occurs widely distributed in the foetus, and in the permanent mucous tissue of the vitreous humour and umbilical cord. The pure myxomata are generally benign, having but little tendency to recur after complete removal, or to generalise in distant parts. This does not hold good concerning some mixed tumours, of which mucous tissue is a constituent, e.g.^ myxo-sarcoma. The gravity of these cases depends upon the more malignant element and the proportion it bears to the whole tumour. And there is this to be said, that a myxoma, representing as it does develop- mental tissue, is more likely than other simple tumours to revert to the embryonic type and become malignant. The association may be manifested quite early, or it may only show itself after a long interval. To the naked eye the myxomata appear as semi- translucent gelatinous masses, of pretty uniform 428 Surgical Pathology. [Chap. lxxxvi. consistence and colour, unless perchance they be varied by patches of hsemorrhage, and softening from fatty degeneration and liquefaction of the inter- cellular substance. A glairy glutinous fluid is obtained by scraping ; this consists of mucin mixed with cells of the gro^vth, and blood corjDuscles. It is very different from the lactescent juice of cancers. The greater number grow from the mucous membranes in the form of polypi, or from connective tissue. They are also found in the voluntary muscles. According to Virchow, hydatid moles of the placenta are of the same nature. These monilif orm growths start from the chorionic villi, which consist normally of mucous tissue. Many of the so-called neuromata are really myxomata, springing from the connective tissue of the nerves, the fibres of which are usually spread over the surface of the tumour, though occasionally they pass through the centre. There may be one or more; when multiple they are distributed over the branches of a nerve or nerve plexus. They are exceedingly painful from stretching of the nerve-fibres. Similar growths implicate the nerve centres. We have met with them both in the brain and spinal cord, in each instance arising apparently from the membranes. The myxomata are chiefly found in early life, especially the polypoid variety. Nasal mucous polj-pi are nearly always mul- tiple. They are attached almost exclusively to the outer walls of the nasal foss?e. In aspect they are grey and glistening. A thin watery mucus exudes from their surface. They difler from the succulent fleshy •' nasopharyngeal polypi " as follows : (1) They grow from the mucous membrane and not from the periosteum ; (2) their pedicles are very narrow, often filamentous ; (3) when completely removed they do not recur; (4) they do not absorb and destroy Chap. LXXXVI.l The Myxomata. 429 neighbouring structures. Though one operation may not suffice for a cure, it does not point to a " recur- rence " in the ordinary acceptation of the term, but to the existence of other polypi too small to be grasped by the forceps. Microscopy.— All possess a homogeneous gelati- nous intercellular substance. The cells embedded in /^ Fig. 64. — Mucous Polypus of the Bladder. a. Squamous epithelium ; 6, blood-vessel ; c, stellate corpuscle ; d, nucleus of corpuscle. X 300. (.See Fig. 06.) this are round and oval in some specimens ; stellate, branched, anastomotic in others, the outrunners forming a delicate plexus of fibres throughout the growth. But in by far the greater majority the cells are polymorphous, round, oval, stellate in varying proportions. This is well seen in Fig. 64, taken from a rare specimen of mucous polypus of the bladder (Fig. 56). Unless the section be stained the cells are barely 430 Surgical Pathology. [Chap. lxxxvii. visible, since tlieir refractive index is nearly that of the ground substance. The myxomata growing in connective tissue have, as a rule, a thin capsule. Mucous polypi are covered with epithelium, like that of the region in which they are found. Thus, in the bladder the superficial cells at least are flattened. In the nose they are columnar and ciliated. The blood-vessels are easily observed. They have distinct walls, but, the lateral support being unstable, they easily rupture, hence the frequency of capillary haemorrhages into the growth. Elastic fibres and fat cells are sometimes present, so are cysts. Occasionally in mucous polypi glandular prolongations can be traced from the surface inwards. In them, too, subject as they are to physical injury, nutritive modifications are far from rare — haemorrhages, inflammation, and gangrene from bruising or twisting of their pedicles. CHAPTEU LXXXVII. THE NEUROMATA. Most of the tumours designated neuromata are either fibromata or myxomata growing from the con- nective tissue of the nerves. True neuromata are always homologous, and never generalise, although they may be multiple. They contain nerve- fibres of new formation. There are two varieties^ according as they contain medullated or non-meduUated fibres, the myeline and amyeline neuromata of Virchow. Nerve cells are only met with in the tumours springing from the cerebral or spinal centres, and in some dermoid cysts of the ovary. Chap. Lxxxvii.] TheMyomata. 43 1 Mediillated or fascicular neiu^oanata are much more common than the non-meclullated, but both are rare. The best example is seen in the clubbed extremities of the nerves in amputation stumps. In the regeneration of divided or wounded nerves, new fibres are developed either from the elongation of the proximal ends of the severed fibres or from the con- version of the fusiform cells of the granulation tissue. The latter is more probable, as it explains the mode of formation of cicatricial neuromata. Even here the greater part of the enlargement consists of dense fibrous-tissue. On strict pathological grounds these bulbous ends of nerves should be relegated to the inflammatory new formations. A similar develop- ment of nerve-fibres is now and then met with in the continuity of nerve trunks, where it gives rise to fusiform swellings. MeduUated nerve -fibres are occasionally met with in dermoid cysts. Non-mediillatecl or amyeline neuromata are described by Yirchow as occurring in connection with the brain and spinal cord. They contain Ee- mak's fibres, neuroglia, and nerve cells. The isolated patches of nerve tissue found in some congenital encephaloceles are probably the remains of herniated brain substance, and not new formations. The bulgings of the spinal cord on division of the mem- branes must not be mistaken for neuromata. Non-meduUated nerve-fibres are developed in some dermoid cysts. The so-called neuromata of the optic nerve are either mucous or gliomatous tumours. The Myomata. Tumours composed of muscular tissue alone are very rare, but complex growths of which it is a con- stituent are more common. There are two varieties^ striped and unstriped. 43.2 Surgical Pathology. [Chap. lxxxvii. (1) Myomata with smooth fibres. — These are always found in connection with the muscles of organic life. The best examples are those growing from the uterus and alimentary canal. In these situations they are cither embedded in the muscular walls, or project beneath the mucous or serous membrane in the form of polypi. The submucous and subperitoneal myo- mata are probably intramural in their origin, and are forced to the surface by the contraction of the muscles in which I they are developed. Uterine myomata are often very large, filling and distending the cavity of the uterus, or occupying the pehTLS and abdo- men external to that organ. Fibrous tissue enters largely into their composition, and eventually may so ex- ceed the muscular elements as apparently to obliterate them. On this account some pathologists class these tumours with the fibromata, or notify their doubtful nature by the term "fibroid." They are more cor- rectly described as fibro-myomata or myo-fibromata (Fig. 65), The muscular fibre-cells can be dissociated from the connective tissue by dissolving the latter in a 20 per cent, solution of nitric acid. These myomata are smooth or lobulated. On section they are seen to consist of interlacing bundles of fibres, which often form concentric nodules ; con- nective tissue carrying blood-vessels fills up the in- tervals between the muscular fasciculi. They are gene- rally circumscribed, and even when dififiise they are Fig. 65. — Myo-Fibroma of Uterus a, Transversa section of himdle of muscular fibres embedded in connective tissue, b. The tumour was as hard as cartilage. X 265. Chap. Lxxxvii.] The Myomata. 433 surrounded by a capsule. They are for the most part very firm, and creak on being cut with a knife ; but a few are more succulent and contain large dilated vessels. In the oesophagus, stomach, and intestine unstriped myomata are occasionally seen as small interstitial nodules or submucous polypi. Like the uterine growths, they may be single or multiple. Muscular fibre is largely developed in the prostate glands of old men, as part of a difFuise hypertrophy, or as a circumscribed tumour. (Vide Adenoid growths. ) Nuti^itive modifications. — (1) Calcification is very common, especially in "uterine fibroids." The author once saw a completely petrified uterine myo-fibroma. It was as large as a cricket ball, and was attached to the uterus by a fibrous pedicle a foot long. (By the twisting of such pedicle the vessels supplying the tumour may be strangulated.) (2) FcUty degeneration usually accompanies calcification. (3) Mucoid soften- ing occurs sometimes, and gives rise to regular cysts or large anfractuous cavities. Clinically these tumours are benign, but they may be serious on account of the haemorrhage they occasion and the mechanical interference with the functions of organs. In one case a uterine fibroid caused fatal obstruction of the bowels by clamping the rectum against the brim of the true pelvis. Myomata wdth striped fibre*. — These are in- finitely rarer than the preceding. They are seldom, if ever, found as simple tumours. Striped muscular fibres enter into the composition of some complex cystic formations in the ovary, and of some congenital tumours of other parts. The author was shown a sarcoma of the kidney by Mr. W. Pye, in which they were beautifully developed. The unstriped myomata are homologous in their origin, the striped variety usually heterologous. c c 434 CHAPTER LXXXYIII. THE ANGIOMATA. Type : blood-vessels. — They mTist be distingmshed from aneurisms and varices, which are only dilatations of pre - existing vessels. It is doubtful whether aneurism by anastomosis should be included in this group; probably not, for there is want of proof that they consist of other than general and varicose dilatation. There are two species of angioma : (1) simple, (2) cavernous. (1) Simple angiomata; telangiectases; congenital nsevi. — These affect the skin and subcutaneous tissue. They appear at or soon after birth, and increase by new formation of vessels. In colour they vary, being scarlet, purple, or blue, accord- ing to the proportion severally of arteries, capillaries, and veins that enter into their composition ; and to the rate of the blood current through them. They are most common about the face and neck. They form soft spongy swellings, imbedded in the skin, or raised from the surface as broad sessile elevations. They are composed of a number of flexuous intertwining vessels, held together by a scanty amount of areolar tissue. The vessels for the most part consist of capil- laries, marked here and there with lateral loops and ampuUary dilatations. Their walls, which are very delicate, are constructed of elongated cells. Muscular fibres are developed in some of the older and larger vessels ; in fact, there may be well-formed arteries and veins. Chap. LXXXVIIIJ ThE AnGIOMATA. 435 (2) Cavernous angiomsita ; venous naevi erectile tumours (Dupuytren). — They are situated chiefly in and beneath the skin, but they are also found in the orbit and in the internal organs, e.g., the liver (Yirchow). On the cutaneous surface they appear bluish. They can be greatly reduced in size by pressure. They sometimes pulsate. In children fat often enters largely into their composition (nsevoid lipomata). The vessels form a system of wide intersecting canals, alternating with trabeculse of connective tissue, reminding one of the alveolar arrangement in carcinoma. They are lined with fusiform endo- thelial cells. Their walls con- sist of the fibrous tissue of the stroma, and sometimes con- tain muscular fibres and fat cells, but there y\%. 66.— Subcutaneous Venous Nsevus. are no regularly «, Fibrous stroma ; h, vascular canal, x 200. arranged tunics. The stroma is said to possess vasa-vasorum and even nerves (Esmarch), but the latter are probably the remains of the normal tissue invaded by the growth. The blood spaces show a natural injection {vide Fig. 66) in sections hardened by alcohol. The cavernous system is formed by dilatation of the vessels and by absorption of their walls. Where development is active the vessels are small as compared with the width of the inter- vening connective tissue trabeculse, but subsequently 436 Surgical Pathology. I^chap. lxxxviii. this disparity is reversed. Kindfleisch explains it by assuming that of two sets of intersecting columns (in this case represented by blood and connective tissue respectively), if one shrinks the other becomes enlarged. But any contraction of the stroma must be interstitial, and pretty equal in all directions, and therefore cause a diminution in the calibre of the vessels; besides in cirrhosis of the liver, and in the cicatrisation of wounds, many of the capillaries are strangulated and finally obliterated. It seems more probable, then, that the enlargement of the vessels in angioma takes place at the expense of the stroma, and that the atrophy of the latter is due to the pressure of the blood in the cavernous spaces. New vessels are formed by csecal protrusions from those already in existence. It is possible that some are developed from formative cells, as in the organisa- tion of blood clots and inflammatory exudations, and that later on they join one another and the vessels of the initial growth. When the vessels increase rapidly in size and number they are surrounded by a richly corpuscular tissue, and the growth may then simulate a sarcoma. On the other hand, vascular pulsatile sarcomatous tumours of bone have been erroneously considered as ''aneurism " or angioma. Secondary cliang'es. — (1) Calcification occurs now and then in the walls of cavernous nsevi ; (2) cysts may form by the expansion of the walls of one or more of the vessels after the latter have been strangulated, and occluded by coagula. The contents of such cysts consist of liquefied clot and serous exudation (E. Wagner). (3) The tumour may cease to grow, and shrink to a fleshy fibrous mass, " degenerated nsevus ; " this is chiefly seen in the scalp. Chap. Lxxxix.] The Sarcomata. 437 It may be noted tliat "vascular tumour of tlie meatus urinarius " is nsevoid in its nature. CHAPTEE LXXXIX. THE SARCOMATA. The sarcomata are tumours that liave their type in embryonic connective tissue. The simplest form is that consisting of an aggregation of round cells held together by a scanty homogeneous sub- stance and traversed by capillary blood-vessels. It is impossible, from a microscopical examination alone, to tell it from inflammatory granulation tissue ; in fact, it is sometimes called "granulation sarcoma." More frequently, however, the growth is not so primitive in structure ; the cells enlarge and elongate, becoming spindle-shaped ; or fibrous tissue is found more or less abundantly; or nodules of cartilage spring up here and there, and so on, until the most diversified group of tumours is completed. Whatever modification they undergo, with a few I'are exceptions, they do not assume that regular alveolar arrangement so characteristic of cancers. Having their type in embryonic tissue, they tend to follow it in the same lines of development, but they differ from it in that they never reach finality of growth, for there is no end to their formative activity. The cells of which they are chiefly composed vary much in size and shape. Most commonly they are round or fusiform ; but in the central sarcomas of bone large numbers are naked masses of protoplasm, with, it may be, as many as twenty nuclei. They may become so attenuated that when closely 438 Surgical Pathology. [Chap. lxxxix. packed tliey appear at first sight like bundles of fibrous tissue. Yariouslj shaped cells are often found in the same section. The nutritive modifications are more numerous than in any other class of tumours; e.g., melanosis is much more common than in cancers. Mucoid de- generation accounts for the frequency of essential cysts ; essential, inasmuch as many arise, not from accidental rupture of vessels, nor from liquefaction by fatty degeneration from deficiency of nutriment, but from certain cells set a^oart for this inherent trans- formation. The intercellular substance varies much in amount and form. In some cases {e.g., the round and large spindle-celled varieties) the cells appear in actual contact ] in others, composed mainly of small spindle cells, the matrix is often very abundant, and is homogeneous or fibrillated. In lympho-sarcoma there is a delicate reticuluni of fibres between the cells, resembling the tissue of a lymphatic gland ; and in glioma of the nerve centres and retina a similar arrangement is found. It is subject to calcification aud other chansjes. Blood-vessels traverse the tumour in all direc- tions. Their walls are very thin, and are constructed by the cells of the growth, elongated perhaps, and arranged end to end, but never forming distinct coats. They readily dilate and rupture ; hence aneurismal pouches, haemorrhages, and disseminations. From the frequent admixture of other than em- bryonic elements, sarcomas form composite tumours ; the terms myo-sarcoma, fibro-sarcoma, and chondro- sarcoma explain themselves. Although any variety may be found in any tissue, there is still a well-marked tendency in many instances to affect certain structures ; thus, the pigmented form Chap. LXXXIX.] ThE SaRCOMATA, 439 is mostly found in the choroid and skin ; the cystic in the bones, testicle, and breast ; the myeloid in cancellous bone ; the round, mixed, and spindle- celled growing from bones and fascise. Sarcomas destroy the tissues in which they grow in three ways : (1) By direct pressure, causing atrophy in the same way as an aneurism ; (2) by infiltration ; (3) by compression or invasion of large vessels. When the growth in a bone is central, we often find expansion with the wasting, which accounts for the " egg-shell " crackling over such tumours, especially in the jaws ; and for some of the so-called spontaneous fractures of the long bones. When pulsatile, and situated in the regions of large arteries, e.g., the popliteal space or the pelvis, it may be difiicult to diagnose them from aneurisms, for they give a distinct bruit and thrill ; the latter signs, however, are more uniformly diffused in sar- coma, and the murmur is not conducted along the main artery ; again, they cannot be so easily emptied by pressure. They do not refill so suddenly as aneurisms. The pulsation is increased by the formation of aneurismal dilations of the vessels, and hence sarcomas of bone are often described as " aneurisms ofhone.^' Sarcomas springing from the surface of bones present a radiating appearance (Fig. 29), from the centrifugal direction of the blood pressure, and when ossification occurs the new bone often follows the same lines in the form of delicate feathery sprays. Varieties of sarcoma. — These are based, firstly, upon the shape of the cells that predominate in the tumour (round-celled, spindle-celled, myeloid) ; secondly, upon some modification of structure, either in the arrangement of the cells and disposition of the intercellular substance (lympho-sarcoma, alveolar sar- coma), or from admixture with other than embryonic tissue (chondro-sarcoma, osteo-sarcoma) ; thirdly, upon 440 Surgical Pathology. [Chap. lxxxix. some nutritive change (melanotic sarcoma, cystic sar^ coma). As to relative malignancy, round - celled sar- coma takes the lead ; for the whole of the vital energy of the tumour is expended in growth, to the exclusion of a higher development. Next .comes the large spindle-celled variety, the cells of which are closely packed, there being but little ground sub- stance. Then^ in order, are the mixed round and spindle-celled, the small spindle-celled, and the myeloid or giant-celled. The melanotic and alveolar are, as a rule, very malignant. Chondrifying and ossifying sarcomas are malignant in proportion to the amount of embryonic tissue they contain. (1) Round-celled sarcoma, embryo-plastic tumour (Lebert), enceplialoid sarcoma (Cornil and Ranvier). — Of this there are two varieties, small and large-celled. They are of very rapid growth, often ending fatally in a few months, especially in children, the formative activity of whose tissues is very great. They are of soft, brain-like consistence, of a pinkish-grey or yellowish-white colour. The walls of the vessels being very thin and badly supported, rupture spontaneously, or on the slightest pressure, giving rise to patches of extravasation, or even large blood cysts. Having gained the surface, they form the so-called " fungus hsematodes," from their rapidity of growth and tendency to bleed (the same name is applied to fungating encejDhaloid cancer). The multi- plication of the cells outstripping the formation of vessels for their support, and the acute interruption of nutrition from rupture of capillaries, lead to fatty degeneration and death of the cells, the softened debris mixed with blood forming a grumous pulta- ceous mass. Their elasticity may easily be mistaken Chap. LXXXIX.] SpINDLE-CELLED SaRCOMA. 44 1 for the fl actuation of an abscess, but on passing a trochar little but blood escapes. They infiltrate the surrounding tissues, so that remoTal is difficult and recurrence rapid and certain. They generalise in the internal organs, in the lymphatic glands, and even in bone ; but death may supervene so shortly that there may not be time for secondary growths to appear. They aflect almost all the tissues, but the skin, bones, and fascise are their seats of election. IMicroscopically, they consist for the most part of simple embryonic cells, embedded in a scanty homogeneous or granular matrix. Sometimes the cells are more voluminous, with large bright nuclei. (2) Spindle-celled sarcoma. — Of this there are two varieties, the large and the small-celled. The rig. 67. — Large Spindle-celled Sarcoma from the Fascia Lata of the Thigh. a, Spindle cells wltli fusiform nuclei : 6, bundle of spindle cells in transverse section, x 265. large spindle-celled consists of long, tapering cells (Fig. 67), closely packed in a scanty homogeneous substance. The cells contain one or more nuclei and nucleoli. As they show little or no tendency to form fibrous tissue, they are much softer and more malignant than the small-celled variety. The small spindle- celled sarcomas include the "fibroplastic tumour" of 442 Surgical Pathology. [Chap, lxxxix. Lebert and tlie " recurrent fibroid " of Paget. The relative amount of cells and intercellular substance varies greatly ; in some the cells constitute the main part of the tumour ; in others they are embedded in a large quantity of ground material, homogeneous, granular, or fibrillated. Their appearance on section, rate of growth, and malignancy will thus differ with- in very wide limits ; they may run closely the large- celled variety in gravity, or they may approach the simple fibromata. It may be here noted that the unstriped myomata and the fibromata in the early stages of their growth contain fusiform cells which cannot be distinguished from those of sarcomas ; we must then turn to other portions of the same specimen, or wait for the further development of the tumour, to decide upon its real nature. The majority of small spindle-celled sarcomas are firm in consistence, generally encapsuled, and thus non-infiltrating. On section, they appear of a greyish- white colour, and are seen to be traversed by inter- secting bands of what appears like fibrous tissue. However hard, they do not retract and cup in the centre like scirrhous cancer; for their density is more uniform throughout. They grow from the bones, fasciae, muscles, aiid connective tissue generally. When they recur after removal, succes- sive growths are liable to be softer and more cellular than their predecessors, so that it is not uncommon for the intervals of immunity to get shorter and shorter. They generalise in the internal organs, but the lymphatic glands are rarely affected. After several years, death may ensue from exhaustion from operations and ulceration of the tumour, and not a secondary growth be found. Finally, the cure may be complete after one or more removals. They may ossify or calcify, more frequently the latter. If the lime salts be dissolved out, the true Chap. LXXXIX.] The Sarcomata, 443 structure becomes manifest on section ; cells which were before hidden by the petrification are brought into view. (3) Mixed round and spindle-celled sar- comas are very common. Their characters depend to a great extent on the proportion of round to spindle cells. (4) Myeloid, or giant-celled sarcomas, with very few exceptions, grow from bone, and that too from the cancellous tissue. Their favourite seats are the jaws and the ends of the long bones, especially the upper end of the tibia and lower end of the femur, radius, and ulna. In the jaws they are either central, or they project from the sockets of the teeth as epulides. When central the pressure of the growth causes atrophy of the com- pact laminae ; but' this is partly com- pensated by tlie de- posit of new bone on the outside from the irritation of the peri- osteum. This con- tinuous absorption and deposit accounts for the hollow, per- ^ig. 68.- Cystic Myeloid Sarcoma of the forated shells some- lower end of the Femur. tiTTiPCi Gjppn nffAv «' Cyst; 6, medullary canal of the femur; c, uiiiica oeen aiuei patella: d, tibia: e, fat beneath the synovial TYi n pprfi +.1 An membrane of the knee-joint; /, remains of JUaoerailOn. ^j^^ femoral articular cartilage. -\- a 444 Surgical Pathology. [Chap. lxxxix. Their growth is slow, even when the skin or mucous membrane has ulcerated over them. Complete removal often effects a cure ; very rarely do they give rise to secondary deposits. They are often cystic, seldom extensively ossified. To the naked eye they appear reddish -brown, or ochre -coloured, or pale yellowish - white, with splashes of a ruddier tint. Their uniform firmness is broken by patches of ossifi- cation and fatty degeneration, or by cysts developing, or fully formed. When central their outline is regular, and they may appear encapsuled (Fig. 68) ; when springing from a surface lobulation is not uncommon. The essential structure consists of large, round, oval, or branched cells, with many nuclei embedded in Fig, 69. — Myeloid Epulis from Lower Jaw. a. Multinucleated giant cells; 6, oval cell, x 265. homogeneous or granular protoplasm. These giant cells, which are from -^^ to joVo ^^^^^ ^^ diameter, are like those of foetal marrow, hence the favourite situation of these tumours, and their name, myeloid. They may be sparsely scattered in a bed of round and spindle cells (Fig. 69). They may constitute the greater part of the tumour. When found in peripheral Chap. LXXXIX.] ThE SaRCOMATA. 445 sarcoma of bone, which, is comparatively rare, they do not confer any clinical significance. Subvarieties of sarcoma. — -1. Lympho-sarcoTYia, re- sembling the structure of a lymphatic gland, is really a modification of the round-celled variety. There is a delicate reticulum, in the meshes of vv^hich the cells are enclosed ; this is found in the malignant lymph- adenomata, and in some sarcomas of bone, especially in children. 2. Alveolar sarcoma is chiefly found in bone, muscle, and skin. It seems to form an anatomical link between Fig. 70. — Alveolar Sarcoma of Ileum. a. Stroma composed of branched cells ; b, round nucleated cells filling alveoli, x 265. sarcoma and cancer ; but its affinities, structural and clinical, cling to the former. It difiers from cancer (a) in that the fibres, which are often only the out- runners of cells, ramify between the individual cells as well as between the groups ; (h) in that the cells are on the connective tissue type, and are less easily removed from the stroma than in cancer; (c) the alveolar retiform arrangement is more uniform (Fig. 70), 446 Surgical Pathology. [Chap, lxxxix. 3. GlioTiut, gliosarcoma, attacks the nerve centres, nerves, and retina ; in the latter case it is sometimes congenital, and it usually occurs in early childhood. It is developed after the manner of the neuroglia or connective tissue of the nerve centres. A typical sec- tion shows a delicate reticulum between the cells, but often only a scanty homogeneous matrix exists (Fig. 71). The cells, mostly round, like lymph cells, are occasionally fusiform. It is subject to fatty and mucoid Fig. 71. — Glioma of the Betina. ;, Cells of tbe growtli, the greater iiumher of which are round. The rest are oat-shaped, or stellate. The ir tercel lular suhstance is faintly flbrillated. 6, blood-vessels. Their walls are composed of fusiform gliomatous cells, x 265. Fig. 72.— Glioma of tlie Eetina. a, Sclerotic ; 6, dislocated crystalline, lens (it was <]uite transparent^ ; e, ' remains of choroid ; d, gelatinous mass of glioma; e, patch of cheesy- lookiiig matter (fatty degeneration") ; /, cleft containing serous fluid. CNatural size.) degeneration. When it grows from the retina, the fundus oculi presents a lustrous bright-yellowish ap- pearance, quite characteristic. It destroys all the structures, perforates the tunics, and forms a bleeding fungus. If removed early it may not return; but recur- rence in the optic ner^'e is to be feared. 4. Melanotic sarcoma. — Melanosis is more common in sarcoma than cancer, and of the former the spindle- celled variety is its chief seat. These sarcomata are prone to occur where pigment is normally present ; hence the choroid, iris, and the skin are the structures Chap. Lxxxix.] The Sarcomata. 447 usually aifected ; though they may be found in muscle, lymphatic glands, and other tissues. The pigment is in the form of minute granules. It occupies chiefly the cells ; probably that seen in the matrix is merely the remnant of disintegrated cells. The granules are black from the first, and thus differ from those formed from extravasated blood (Cornil and Eanvier). The deposit commences around the nuclei, which for some time by their brightness contrast strongly with the dull, dark colour of the pigment. The amount of pigmentation varies in different tumours, and in different cells of the same tumour, so that to the naked eye these growths appear grey, sepia-coloured, or jet black. Secondary growths present the same characters. Melanosis does not add to the malignancy ; but inasmuch as these tumours are mostly round or large spindle-celled, the prognosis is grave. 5. Mucous sarcoma. — With the exception of growths essentially cystic, sarcomas are more subject to the formation of cysts than any other group of tumours. We have said that cavities arising from extravasations of blood and fatty degeneration are pathological accidents ; but a sarcoma may be honey- combed by spaces filled with gelatinous matter derived from mucoid degeneration. The coalescence of these cysts may so hollow out the tumour that but little solid matter is left except the septa and marginal portion, which show the change in progress. Fresh growths encroaching upon these spaces project into the interior, and give rise to the so-called intracystic tumours; and by the junction of papillary processes of the latter, secondary cysts are formed between them. The contents of the cysts are usually mucoid, but sometimes the fluid is clear and limpid, and then perhaps has been derived from serous exudation between the lobules and delicate capsules covering 448 Surgical Pathology, chap, lxxxix them ; and it may be coloured with blood derived from capillary rupture. Cystic sarcoma in the popliteal space may easily be mistaken for an enlarged bursa. 6. Ossifying sarcoma. — Osteosarcoma is found chiefly in the jaws and at the ends of the long bones. The bone may be deposited iii isolated patches, but more commonly it occurs as a radiating outgrowth from the base of the tumour, as in subperiosteal epiphysial sarcomas, and some epnlides (Fig. 29). The cells of the tumour are converted into bone corpuscles with long processes. Haversian canals and canaliculi are constructed, but lamellation is rare. Stibungual exostoses occasionally recur, and theii may be classed with the above. It may be impossible by the unaided eye to tell an ossifying from a cal- cifying sarcoma. 7. Chondrosarcoma by preference attacks the ends of the long bones and the testicles. The author once amputated at the hip joint for a cystic chondro- sarcoma involving the whole length of the shaft of the femur ; it stopped short at the level of the epiphysial cartilages. These tumours are by some placed with the enchondromas, but it is better to name them generi- cally from the more malignant constituent. Between the nodules of cartilage are round and spindle cells. They often ossify and calcify. When the islets of sarcoma cells are imbedded in mucous tissue the growth is termed myxosarcoma.. Surface sarcomas, whether growing from the skin or into cavities {e.g., the maxillary antrum), are habitually papillated. The cells of a sarcoma may be filled with globules of fat, not derived from degeneration, but from simple infiltration, lipomatous sarcoma. Contrasting the central with the subperiostal sarcomas of bone, Mr. Butlin, who has thoroughly studied the pathology of Chap, xc] The Lymphomata. 449 these tumours, says the former more often pulsate, do not show a radiated structure, rarely ossify or chondrify, are found in older subjects, and are less malignant than peripheral sarcomas, for they have a slower growth, and do not infiltrate the surrounding structures and lymphatic glands to the same extent. Multiplicity of groivth in sarcomas may be due : (1) To a common origin, especially when many bones are affected ; (2) to true dissemination ; (3) to infil- tration of lymphatic glands by a continuous invasion from the primary growth. The psanimoiitata. — These are small tumours found in connection with the membranes of the brain. They are impregnated with calcareous salts, hence the name. In structure they are composed of large flat angular cells, arranged in concentric laminae. Virchow describes them as epithelial conglomerations, or nests, derived from the cells lining the ependyma ventriculorum. Cornil and Ranvier, who place them among the sarcomas, have traced their development from vascular buds of the choroid plexuses, and other parts of the pia mater. They explain the flattened laminated character of the cells by the pressure of the blood in the early stages of growth. If formed in this way they subsequently become isolated by oblite- ration of the vascular pedicles. They are of no clinical significance. CHAPTER XC. THE LYMPHADENOMATA. The term lymphadenoma or lymphoma is commonly applied to any hyperplastic enlargement of a lym- phatic gland, whether it arises spontaneously, or from D D 450 Surgical Pathology. [Chap. xc. simple irritation. It is difficult to separate the two groups ; for, in the first place^ there is no reason why a peripheral irritation of the lymphatics should not excite the associated glands to renewed developmental activity ; and, again, hypertrophy of the gland may continue long after the primary cause has disappeared, so that one is left in doubt as to its true nature. On the other hand, the enlargements due to injury lead to a typical end : subsidence, caseation, or suppuration (the two latter are pretty constant in scrofulous subjects) ; whereas the non- inflammatory lymphomata tend to persist, and affect other structures besides the glands. The lymphomata may be arranged clinically under four heads: (1) The simple or benign lymphomata; (2) the malignant lymphomata, or lympho-sarcomata of Yirchow ; (3) multiple lymphomata of the viscera {e.g., the liver, spleen, kidney, etc.), Hodgkin's disease, anaemia lymphatica, adenie (Trosseau) ; (4) the last-mentioned group associated with a marked increase in the number of white blood-corpuscles (leucaemia, leucocythsemia). (1) The benigii lymphomata. are more nume- rous than the other varieties combined. They may or may not be traceable to injury or precedent disease. Rarely attaining a lai-ge size, they cease to grow after a time, and remain quiescent, or shrink from fibroid condensation. They never extend beyond the glands involved, and are consequently homologous. They are the expression of tissue weakness, but are com- patible with good general health. Their removal is not attended with any special danger. Usually only one gland or group of glands is affected. The neck is the seat of election, next to that the groin and axilla. General anatomy. — The simple lymphomata are enclosed within a fibrous capsule, and maintain the Chap, xci The Lymphomata. 451 general outline of the lymphatic glands, being round, oval, or kidney-shaped. They are mostly firm, some- times very hard, and the consistence is fairly uniform. On section they look greyish and semitranslucent, or dull white and opaque, according to the amount of fibrous tissue present. For the same reasons they are more or less homogeneous, or streaked with whitish trabeculse. Microscopy. — The ground substance looks glassy or fibrous, and forms meshes within which small uni- nucleated lymph -cells are enclosed. In pencilled sections nuclei may be seen here and there at the nodal points of the reticulum. (2) The maligiiaiit lympUomata (malignant scrofula, lymphadenomata) usually involve several glands, and sometimes several groups, cervical, mediastinal, abdominal, etc. Clinically they are sarcomas. At first homologous, they may become heterologous by invasion of surrounding tissues. They are often lobulated from adhesion of contiguous growths. In preparations, the large vessels of the part are frequently seen to be embedded in the mass, or stretched over it. The elasticity of these tumours is so great that it may be mistaken for the fluctuation of an abscess. I have seen them incised on that supposition. Progressive * anaemia complicates the disease, which is fatal from asthenia, or pressure upon some vital organ. Multiplicity of growth does not imply dissemination, as in carcinoma; it is the sign of wide-spread instability of tissue in the lymphatic gland system. If left alone it is quite the exception for these tumours to fungate, but if incised they pursue an intractable course. Attempts at removal are often futile, and certainly dangerous, for during the operation the disease is rarely found to be as limited as appeared from a surface examination ; and the deep dissections required may lead to cellulitis 452 Surgical Pathology. [Chap. xc. aud pyaemia ; besides, the patients are bad subjects for the repair of extensive injuries. General anatomy. — The mass is bounded by a thin capsule, or, more rarely, it is infiltrating. In the latter case the original capsule of the gland has disappeared before the ravages of the disease, or else the growth has started in some part other than a lymphatic gland; e.g., the upper jaw. The cut surface appears grey or yellowdsh-gTey throughout, or it is mottled and flecked with red from capillary extravasation. Patches of softening and caseation may be seen. The distinction between the medullary and cortical portions of the gland disappears. Microscopy. — Small lymph cells form the greater part of the tumour ; but there are also large multi- nucleated cells which indicate rapid growth, the nuclei having divdded more quickly than the proto- plasm. The stroma is very delicate ; to see it the specimen must be shaken in water or lightly brushed. It is largely made up of branched cells. (3) l;;>/^?c scirrhus (Fig. 78, b). In its march scirrhous cancer attacks all the structures in its course, so that it becomes adherent to the skin over it, and to the pectoral muscle, and, it may be, the ribs and pleura beneath. The cicatricial contraction accounts for the wrinkling and puckering of the skin, and for the retraction of the nipple. If left to itself the skin usually becomes inflamed Chap. XCIV.] SCIRRHUS OF THE BrEAST. 477 and then ulcerated, and tlie cancerous tissue covered by a layer of granulations is deeply excavated; or it forms a jorotuberant fungus. In some cases nodules are seen in the skin around the central growth ; in fact, the skin may bear the brunt of the mischief, being thickly studded with tubercles that, coalescing, constitute the cancer en cicirasse, hide-bound cancer, shield cancer, squirrhe pustuleux (Yelpeau). The more rapid the growth the more likely are the axillary, mediastinal and supraclavicular glands to Fig. 78. — Scirrhous Cancer of the Breast. A, Rapidly growing form ; b, atropliied or cicatricial scirrhiis. Both show alveolar structure. In a the stroma is scanty and the epithelial cells dis- tinct. In B the stroma is dense and extensive, the alveoli shrunken, and the contents in a state of degeneration, x 263. be affected* In atrophic scirrhiis they escape for a long time, but eventually they are involved, with wide-spread dissemination in the internal organs. The male breast is the seat of the disease in about two per cent, of the cases (Paget). Cancer of the breast is sometimes " acinous ;" tliat is, the original outline of the gland acini is more or less preserved; this accords with the lobulated outline of these growths. But there is a " tubular " variety, in which the cancer cells permeate the gland tissue in narrow columns ; the ditierence, I believe, 47^ Surgical Pathology. [Chap. xciv. depends upon tlie point of departure of the new- epithelial formation ; in the latter instance (tubular) it probably starts in a hyperplasia of the cells lining the ducts. An eczematous condition of the nipple may precede the development of duct cancer in the gland by months or years. The obstinacy of the eruption and its circumscribed margin show that it is not a simple eczema, and against its being primarily cancerous is its long duration ; but it may be that ordinary glandular cancer in some cases commences in a slow derangement of nutrition of the epithelium, not thought of because not seen, and that it is only later that it manifests itself in an open " rebellion of cells." Analogous to the above is epithelioma, as a sequel to " psoriasis " of the tongue. Microscopy. — To understand the minute anatomy of scirrhus, sections should be made of different tumours and different parts of each. In a rapidly growing scirrhus the stroma at the periphery is imperfectly fibrillated, sometimes quite homogeneous, but in the older portions the fibrous trabeculse are very distinct. There is a marked relative increase as we near the centre of the growth, for as the cicatricial contraction obliterates the vessels, the cells atrophy and the stroma shrinks, so that the alveoli get smaller and smaller. The more rapid and recent the growth tlie more is the stroma infiltrated with embryonic cells, which are sometimes so numerous as to hide the matrix. The alveoli vary in size and shape from the first, but are for the most part fusiform, and double the width of the trabeculse bounding: them. They are not closed spaces, as they at first sight appear, for they constitute a system of intersecting canals, which can be seen in thick sections by altering the focus of the microscope. As the stroma shrinks they necessarily diminish in size. The cells filling the alveoli Chap, xciv.] Encephaloid Cancer. 479 are variously shaped, round, angular, tailed, etc., ac- cording to the extent of the pressure upon them. Their size is in marked contrast with the indifferent corpuscles of the stroma. Except at the periphery, the blood-vessels can only be seen in injected specimens. They become throm- bosed through the contraction of the stroma. In the oldest portions of the growth they disappear, from atrophy of their walls. It is said that by the aid of nitrate of silver the lym^phatics can be traced in fresh specimens into the alveoli. Any fat cells met with in the tumour belong to the tissue invaded. The epithelial cells of cancer never become distended with fat drops. In this way they differ from some cases of sarcoma. Siiceplialoid cancers have exactly the same structural arrangement as scirrhous, but differ from the latter in the relative amount of stroma and cells. They are usually soft, brain-like tumours, though sometimes they are moderately firm in consistence. The alveoli are larger than in scirrhous, and the trabeculse for the most part more delicate. Moreover, -their tendency is to degenerate and soften; in fact, they may be diffluent in the older portions, or even throughout ; hence haemorrhages into their substance are common. When the surface becomes ulcerated the unrestrained growth protrudes in the form of '■'■fungus hcernatodesJ^ They are so elastic that they often give a sense of fluctuation. In colour they are yellowish-white, mottled, or flecked with red; here and there may be seen patches of modena hue, from capillary extravasations. Blood-cysts are not un- common. Usually of rapid growth, and very malignant, there is^ nevertheless, a wide range in morbid appear- ances and clinical course. In St. Mary's museum is a specimen of encephaloid can.cer of the testicle, removed during life; it is firm 48o Surgical Pathology. [Chap xciv. and fibrous in one half its bulk, pultaceous in tLe other. The tumour, as large as a foetal head, had been growing for four years without any signs of thickening of the cord, secondary growth, or con- stitutional taint. Both scirrhous and encephaloid yield a milky juice on scraping. Microscopy. — The alveoli are large, and round or oval in shape, rarely narrow and fusiform as in scirrhus. The stroma is subject to great variation both in nature and extent. It gene- rally forms delicate overarching bands (Fig. 79, h), but at times wide dense trabeculse can be seen ; but even then we do not find the shrunken alveoli so constant in scirrhus. It may be entirely fibril- lated, or consist of a few fine fibres traversing a homo- geneous matrix. It may be almost devoid of in- different cells, or thickly strewn with them. The epithelial cells filling the alveoli are large. They are not so multiform as in scirrhus, for the intercellular substance is less dense and more copious ; and hence the cells are not so liable to alterations in shape from pressure. They contain large nuclei, one or more in each cell, with bright highly refractive nucleoli. When the cells are undergoing degeneration fat particles make their appearance in the protoplasm. The vessels are wide, and have very thin walls, and I^ig. 79.— Encephaloid Cancer of the Testicle a. Epithelial cells ; b, flljrous stroma, x 265. Chap, xciv.] Adenoid Cancer. 48 1 from defective and unequal support they develop am- pullary dilatations. These frequently rupture, and give rise to extravasation of blood. Adenoid cancer; colunuiar epitlielioma. — This variety affects the stomach and intestines (especially the rectum), the bladder, ovary, cervix uteri, nasal fossae, and the jaws. In the last-mentioned situation it starts from the gums, or, in the case of the upper jaw, the lining membrane of the antrum. The pattern is exquisitely alveolar, like a piece of mosaic. The stroma is now scanty and delicate, and a^ain excessive and coarsely fibrillated, the variation being often marked in the same specimen. In some parts it is almost free from corpuscles, in others crowded with small round, indifferent cells. The epithelial cells line the acini with great regularity. They are large, columnar, and have bright elongated nuclei (Fig. 59). Sometimes they become distended with mucin, and present an inflated appearance. The tumour, when it reaches the surface, quickly ulcerates, and, being very vascular, bleeds profusely, the more so when subjected to mechanical irritation; e.g., by the passage of faeces over it. It has a less tendency than scirrhous or en- cephaloid to generalise in the lymphatic glands. In the case of the rectum secondary growths are disseminated in the liver. The path of infection would seem to be along the branches of the portal system. These secondary growths in the liver possess the same glandular disposition and shape of the epithelial cells as the primary lesion. I have observed a columnar epithelioma of the bladder in which the alveoli were separated by a very scanty stroma, and the cells, arranged in super- posed columns, completely filling the spaces. In the jaws, particularly the lower, the central cells are round, or angular by compression, and the F F 482 Surgical Pathology. [Chap. xciv. peripheral columnar. In this situation the new formation is almost invariably cystic, and it is note- worthy that only the central cells undergo mucoid degeneration, the columnar ones at the periphery remaining as an epithelial lining to the cysts (Fig. 5). Here, too, the interacinose tissue is fibrous, or composed of spindle-shaped cells; in the latter case the growth has for this reason been mistaken for sarcoma. Cystic epithelioma of the jaw is slow in its progress, and has but little tendency to involve either the lymphatic glands, or the internal organs. Colloid cancer is built upon the same structural type as scirrhous and encephaloid. It bears a close resemblance to the latter in its clinical features, being rapid in growth, and quickly fatal. It selects for its ravages many different tissues, but the bulk of the cases is met with in the abdominal viscera, especially the intestinal tract and the ovaries. The peritoneum is often seen to be infiltrated ; but on the assumption that all cancers start from pre-existing epithelium, it must be granted that these omental and mesenteric growths begin in the stomach, intestine, pancreas, or liver, since the epithelioid lining of the peritoneum belongs to the connective tissue series. The open meshwork of the serous membrane is a favourable ground for the spread of the disease, richly provided as it is with blood-vessels and lymphatics. The consistence of these tumours is subject to wide variation, but for the most part they are very soft, sometimes diffluent. When springing from the ovary they may be mistaken for simple cystic for- mations. Cancer is rare in the thyroid hody^ but when it occurs colloid matter is seldom absent. In this way it conforms to the rule that most of the morbid changes found in the gland are accompanied by colloid degener- ation. The alveoli are laro-er and less angular than in Chap. XCIV.] Colloid Cancer. 483 scirrhus, for the colloid transformation gives rise to an increase in bulk, and this expands the walls of the spaces, and renders the latter globular or ovoid. The degeneration commences in the cells. First a drop appears in the protoplasm, and as it enlarges the nucleus is thrust to the margin. Finally, nuclei and cell capsules disappear. The change advances from Fig. 80.— Colloid Cancer of tlie Ovary. a, Fibrous stroma; 6, eel! distended witb di'op of colloid material; c, alveolus. The cells that occupied the centre have disappeared, and in their place a semi-homogeneous mass marked hy concentric streaks can he seen. The periphei'al cells are flattened from the pressure of the colloid suhstance, X 365. the centre to the periphery, and the outside cells, prior to their destruction, become compressed and elongated, and occupy a concentric position (Fig. 80). The stroma undergoes a similar alteration, it softens and liquefies, so that contiguous alveoli run together, forming festooned cavities. These anfractuous spaces, bounded by tracts of fibrous tissue, give an alveolar disposition that can be seen by the naked eye. The secondary growths are of the same nature as the primary. 484 Surgical Pathology. . [Chap. xciv. Squamous epithelioma, also called epithelial cancer, in contradistinction to scirrhous and encepha- loid, which were formerly believed to be connective tissue tumours, and are so to this day by Cornil and Ranvier. The prevailing idea of their nature negatives this differentiation, since most pathologists maintain that all cancers start from pre-existing epitheliunL There can be no question but that this is the case with the growths under consideration. Whatever their strucr tural relationship may be to other forms of cancer, they possess certain well-defined anatomical and clinical characters. They are found for the most part in situations that admit of their operative treatment, and they illustrate the principle that local irritation is a noteworthy factor in the etiology of malignant growths, whether this be in the form of a precedent inflammatory lesion, e.g., syphilitic ulcer of the tongue, or mechanical friction, as from a sharp tooth or the stem of a pipe. Their tendency to develop at the junction of skin with mucous membrane is well known, but this is explained rather by the coincidence that these are the very places most exposed to irritation, than by any inherent disposition of the epithelium to perverted growth. That the surface epithelium pre- ponderates in the lips, e.g., as age advances, is no proof that its nutritive activity is greater. The increase is relative rather than absolute, for in old peojDle the connective tissue and muscular fibres waste. The favourite situations where skin and mucous membranes meet, are the lijjs, genital organs, and anus. The general cutaneous surface is by no means exempt; the face and back of the hand take the lead, unless, perhaps, we exclude the skin of the leg, where- some simple chronic ulcers at length become cancerous. The mucous membranes, naturally covered with laminated scaly epithelium (e.g., the tongue, cheek, Chap, xciv.] Squamous Epithelioma. ' 485 fauces, oesopliagiis, vagina, and cervix uteri), are all liable to the inroads of tlie disease. In the bladder the deep epithelial cells are columnar, and the super- ficial flattened ; hence in this viscus both squamous and columnar epithelioma are met with. Epithelioma of the scrotum is kno"svn as chimney-sweep's cancer, it being thought that the friction of the sharp par- ticles of soot keeps up a chronic irritation ; and some weight is given to this view by the fact that the dis- ease is less common than formerly, when chimneys were swept by climbing. The first efiect of the local irritation is to cause a simple inflammatory hyperplasia, and this may go on for a long time before any specific epithelial over- growth takes place. Eventually this does happen, and the multiplication of cells proceeds from the deeper layers of the epidermis and its involutions — the hair- follicles, sebaceous and sweat glands. In some cases this is mainly confined to the surface — in others it infiltrates the structures beneath. There is great variety in this respect. Rod-like masses of epithelium advance in the direction of least resistance, i.e., between the bundles of connective tissue, it is said, in the lymphatic spaces. If this be so, we have a ready explanation of specific infection of the lymphatic glands next in order to the primary growth. These epithelial cylinders send off buds in various directions, which increase at the periphery, and thus form the well-known " epidermal globes '^ or "epithelial pearls." Concentric lamination of the cells explains the characteristic " bird's nest " appearance on section (Fig. 81). This lamination is the result of pressure, aided by the shrinking of the older epithelial cells as they become horny ; the latter process is a repetition of what takes place physiologically in the superficial layers of the epidermis. The " globes " are not all isolated groups of cells, but many are the 486 Surgical Pathology. [Shap. xciv. transverse sections of the down-growing columns above referred to. Some are microscopical, but others can be seen by the naked eye as yellowish spots, embedded in the indifferent s^rowth that surrounds them. As the Fig. 81. — From an Epithelioma of the Thumb. a. Epithelial "nest " ; 6, large polj-gonal cells mai-ked hy fine striations at their borders ; c, indifEerent tissue ; d, sweat duct. X 265. epithelial cylinders increase in size they project from, the surface, giving it a granular appearance. By pressure they can be squeezed out like the contents of a sebaceous gland. The peculiar hardness of this form of epithelioma (useful in diagnosis) is due to the corni- fication of the older cells in the same way that the chnp. xciv.] Squamous Epithelioma. 487 epidermis, -vritli its appendages, the hairs and nails, becomes horny, Now picro - carmine with an excess of picric acid stains the rete mucosum red, and the cuticle bright yellow; and as the same chemical changes occur in the cell-columns of epithelioma as is found in the normal evolution of epidermis, and as these columns increase in width mainly by the addition of new cells to the periphery, it follows that the central cells of the epithelial nests should be stained yellow, and the outer ones red, and so it is found in the greater numbjr of cases. In some, however, the central cells continue to enlarge and multiply, whilst the peripheral ones become compressed ; the result is a collection of large spherical, polygonal, or oval cells, surrounded by laminae of flattened epithelium. The connective tissue and other structures invaded by the proliferating epithelium show an irritative liyperplasia. Indifferent cells crowd the stroma. The old blood-vessels dilate and new ones ai-e formed. The inflammatory new formation leads to softening and ulceration. The destruction progresses from without in. In some cases the gTowth has but little tendency to spread deeply, but gives rise to large branched projections, termed caulijiovjer excrescences. The blood-vessels being less compressed than in the infil- trating variety, the necrosis of tissue is not so gTeat ; in fact, at first sight it is diflicult to say whether the tumour be a papilloma or a papillary epithelioma. Closer examination reveals some invasion of the tissues beneath the base of attachment, and perh-aps also lymphatic enlargement. A parallel case is furnished by the simple villous tumour and villous cancer of the bladder. However great the ulceration and sloughing may be, the constructive process is always greater than the destructive ; the epithelial and inflammatory formation is heaped around the ragged margins of a 488 Surgical Pathology. rchap. xciv. deeply excavated ulcer, and projects in nodules from the indurated base. There is great variation in the degree of malig- nancy. Some cases recur rapidly after removal, infect the lymphatic glands early, break down into gangrenous sores with foul discharge, and end fatally within twelve montlis. Others take years to run their course, and some are completely eradicated by ope- ration. The more vascular the tissue affected the graver is the prognosis. In epithelioma of the tongue and mouth the general emaciation and discomfort are increased by the pain and difficulty in swallowing, and matters are not mended by the passage of decomposing discharges into the stomach and lungs. Capillary and even arterial bleeding from ulcerated epithelioma is a great source of distress. It is often difficult to stop, and it recurs after short intervals, for the blood-vessels cannot contract, and fresh ones are opened by ulceration and sloughing. The secondary deposits in the lymphatic glands have the same histological characters as the primary growth. Infection of the internal organs is rarely seen. Microscopy. — If a vertical section be made through the margin and base of an ulcerated cutaneous epithelioma, it will be observed that the cells pass in columns into the subjacent structures. These columns follow the course of the hair follicles, sweat ducts, and sebaceous glands. They are not, however, confined to them, but ramify in the interstices of connective tissue. Since the buddings from the columns lie in different planes many are divided transversely and obliquely, giving one the idea of isolated cell masses. The characteristic arrangement in concentric laminae has already been alluded to as the result of lateral pressure, and shrinking of the older cells from cornification. The flattening of the cells is in parts so complete that they look like fibres. Their real nature is manifest in Chap, xciv.] Squamous Epithelioma. 489 the gradations of size and shape, from the centre to the periphery of the "epithelial globes." Moreover, they can be isolated by the aid of liquor potassse and teazing. The epithelial cells adhere firmly to one another either directly or through the medium of a scanty intercellular substance. Many appear to interlock by fine serrations at their margins (stachel and riif cells) (Fig. 81, 6). The epithelial masses are surrounded by connective tissue studded with indifferent cells. In some cases it is very scanty, in others it exceeds in amount the epithelial portion of the growth. The ground substance appears homogeneous, or more or less perfectly fibrillated. The extent of the small-celled infiltration varies much in different cases : generally speaking it may be said to be directly proportionate to the rapidity of growth, and the tendency to ulceration, and so to the local malignancy of the disease. The epithelial columns enlarge by segmentation and endogenous formation of their own cells, and by the conversion and appropriation of indifferent cells at the margin. Blood-vessels ramify in the stroma, but do not enter the epithelial masses, which may therefore be said to be extravascular. The stroma is less distinctly alveolate than in the other forms of cancer. The individual cells are very large, averaging y^ inch in diameter. They do not show such diversity of outline as in scirrhous and encephaloid. Cornification of the cells is characteristic of this form of cancer. The intercellular substance is much more scanty than in alveolar cancer. Secondary changes in ejnthelioma. — Inflammation and ulceration are constant. Tatty, mucoid, and pigmentary degeneration of the epithelial cells com- paratively rare. 490 Surgical Pathology. [Chap. xciv. Rodent ulcer may be conveniently discussed here. Until lately it was considered to be distinct from epithelioma in its structure and clinical course. Paget says " it does not contain epidermal globes, nor any other elements of a cancerous nature ; " but later observations have shown that this view is not correct, and that too great a similarity exists between rodent ulcer and the more chronic forms of epithelioma to justify its being regarded as other than "the least ex- pressed form of malignant disease" (T. Fox). Rarely beginning before the fiftieth year, it pursues a steady and certain course, so slow that after several years it may not exceed the size of a florin. The lymphatic glands may become enlarged from simple irritation, and even suppurate (Moore), but they are not liable to specific deposit by infection from the primary growth. In its ravages rodent ulcer spares no tissue, not even bone. Disseminated nodules around the primary lesion are generally absent. The older central part of the ulcer may dry up, but there is little or no approach to cicatricial contraction. The face is the favourite locality, though the disease is met with in other situations. The cellular elements composing the walls and base are for the most part the same as in simple chronic ulcers, but there is in addition a decided epitlielial proliferation. It is true the cells are smaller than in ordinary epithelioma, but like them they show a disposition, remote though it be, to concentric lamination. The new formation commences as a hyperplasia of the epithelial cells of the sebaceous and sweat glands. The rete Malpighii becomes atrophied by the pressure of the growth beneath, but it manifests little tendency to active change ; this is in marked contrast to the part it Inlays in the common variety of epithelioma. Extensive local destruction of tissue is compatible with the most perfect general health. Chip, xciv.] Can'Cers axd Sarcomas. 491 Early and complete removal offers a reasonable expectation of a radical cure. Cancers contrasted Tv^ith sarcomas. — (1) According to Waldeyer^ Billroth, and most English pathologists, all cancers are develojDed from pre- existing e2:)ithelium. There is no difference of opinion as to the origin of epithelioma, but the alveolar form (scirrhous and encephaloid) is asserted by Cornil and Rmvier to commence in a proliferation of the con- njctive tissue cells. They say that if Prussian blue be injected into the tumour, it will pass along a continuous path formed by cancerous alveoli and lymphatic vessels, and that the same arrangement will be observed in fresh sections stained with nitrate of silver, the endothelial connective tissue lining of the lymphatics passing directly into the groups of cells filling the alveoli. In this way they account for the constancy of generalisation in the glands first in order from the primary growth ; but it is one tiring to show an anatomical connection between the cancerous elements and the lymphatics, and another to prove that one springs from the other. Besides, epithelioma, which they allow begins in a proliferation of epithe- lium, also proj^agates itself in the next absorbent glands. Dr. Thm has shown that beneath the basement membrane of duct cancer there is a delicate feltwork of interlacing elastic fibres, similar to that described by Henle around the milk ducts of the breast. Sarcoma has its type in embryonic connective tissue. (2) Arrangement of constituent elements. — In alveolar cancer this is very definite, the cells being contained in sj)aces which intersect in all directions, like a labyrinth, forming a cavernous structure. The stroma bounding these spaces consists of fibrous tissue, in which the blood-vessels are distributed. 492 Surgical Pathology. [Chap. xciv. In sarcoma the cells are embedded in a ground substance, homogeneous or fibrous. The bundles of fibres, when present, follow the course of the vessels, and do not arch over and construct alveoli. The vessels may be considered as one great system of capillaries, whose walls are formed of the cells of the tumour itself. (3) Mode of generalisation.-— CsiiiCGYS disseminate chiefly by the lymphatics, as might be inferred from the close anatomical connection between them. The infecting material of sarcomas is conveyed, in the majority of cases, directly by the blood-vessels, and the secondary growths are for the most part found in the internal organs. Even when the glands are affected, it may be through the blood-vessels, for the intermediate lymphatics are not always infiltrated. Moreover, the glands may be attacked by a con- tinuous invasion from the primary growth, and not specially through the lymph channels. And, again, the initial cause of the disease in some cases selects the lymphatic glands for its ravages, so that it is not a question of dissemination at all. (4) Encapsulation. — When sarcomas spring from fasciae, the sheaths of muscles, and some other struc- tures, they often present a well-defined capsule, and can he shelled out of their bed, except at their base of attachment, and the slower the growth the more easily can this be done. Cancers, on the other hand, infiltrate the surrounding tissue, showing a complete absence of a true capsule, unless it be by chance derived from the fibrous tissue of an organ destroyed by the growth, e.g., the testicle. In many cases sarcomas aj^pear as indefinite in outline as cancers. This is well seen in the bones and in the internal organs, so too much stress must not be laid on this difference between the two groups of tumours. (5) Taking them all together, it may be affirmed Chap, xciv.] Cancers and Sarcomas. 493 that sarcomas are less liable to recur after removal^ but the more malignant vie with cancers in this respect, whilst in the extent and the early period of their generalisation they sometimes outstrip them. (6) Cachexia. — It is by no means rare to find a sarcoma of enormous size, the patient being in good general health ; whereas the constitutional signs of cancer are generally well marked, and often at an early stage, so much so that a cachectic appearance is a valuable aid to diagnosis. When, however, the generalisation of sarcoma is extensive, and still more when the primary growth has ulcerated, the wasting of the body and sallowness of the skin are very manifest. (7) Age of the patient. - -Sarcomas are prone to occur earlier in life than cancers, which seems only natural, considering they are formed upon the type of embryonic tissue, which is indifferent in striicture, and possessed of great nutritive and formative activity. This difference only holds good within certain limits, for the majority of cases of malignant disease of the testis, both cancerous and sarcomatous, occur between the ages of thirty and forty-five (Butlin) ; but even here there is a greater liability to sarcoma than to cancer during the first decade of life. (8) Nutritive changes. — Sarcomas, consisting as they do of unstable developmental tissue, are liable to greater variation from secondary changes than cancers, whether it be towards a higher phase of evolution, as in the tendency to form cartilage or bone, or to a decline in vital activity, as in calcification and the formation of cysts from mucoid softening; or to a perversion of normal nutrition, as when they become melanotic in the tissues of organs that are naturally devoid of pigment. (9) When quite fresh, sarcomas do not yield a lactescent juice on scraping, but soon after removal 494 Surgical Pathology. [Chap. xciv. a liquefaction of tlie intercellular substance takes place, and the cells are thus loosened from one another. Then a milky fluid can be easily obtained, certainly within twelve hours. Speaking broadly, sarcomas are not so malignant as cancers, but they differ from them less in this respect than do the various forms of sarcoma amongst themselves ; e.g., a round-celled subperiosteal sarcoma of a long bone may end fatally, with all the signs of malignancy, within six months, whilst a central myeloid, after amputation of a limb, may neither recui locally nor in distant parts. INDEX. Abscess, Acute, 7. Acute aortic endarteritis, 287. endarteritis, 286. interstitial nephritis, 372. iritis, congenital syphilitic, 142. lichen, 130. necrosis, 58, 68. orchitis, 319. osteomyelitis, 227. — — periostitis, 225. peritonitis, 393. serous synovitis, 261. ■ total necrosis, 238. A'lenocele of the breast, -460. Adenoid cancer, 481. tumours, 458. Adenoma, 460. of the hreast, 461. parotid, 462. prostate, 462. Adenomatous polypus, 388. Adhesive peritonitis, 398. Adipocere, 100. Albuminoid infiltration, 1 17. , Anatomy of, 119. Alveolar cancer, 475. sarcoma, 445. Amyeline neuromata, 431. Amyloid infiltration, 117. Aneurism, 2£0. of the cerebral arteries, 309. of femoral artery, 293. of middle cerebral artery, 294. Aneiirismal varix, 291. Angiomata, The, 434. Anthracsemia, 81. Anthrax, 78. Anus, Ulcers of the, 879. Areolar hyperplasia, 85. Argyll-Robertson pupil, 127. Arteiio-capillai-y fibrosis, 289. venous aneurism, 291. Arteritis, 285. deformans, 288. Arthritis deformans, 256, 260. Artificial anus, 402. Ataxic arthropathy, 126. Atheroma of the cerebral arteries, 97. Atony of the bladder, 355. Atrophic scirrhus, 476. Atrophies from deprivation of blood, 87. from functional activity, 87. , Natural or physiological, 86. of nervous origin, 87. Atrophy, 85. , Fatty, 88. , Modes of, 87. of bone, 89. of muscle, 90. of nerves, 91. of testicle, 337. Bacillus anthracis of Cohn, 79, 80. Bacteridium of Davaine, 79. Bandy-leg, 276. Benign lymphomata, 450. tumours of the bladder, 362. Bile, Pigmentation from, 108. BLidder, Tumours of the, 360. , Ulceration of the, 359. Blanching of the hair, 122. Blind boil, 77. Blood, pigmentation from, 108. Blue line in the gums of lead- vForkers, 107. Boils, 76. Bone abscess, 244. Bridle stricture of the urethra, 348. Bullous and vesicular syphilides, 137. Bursal cysts, 423. Cachexia, 493. Calcareous degeneration, 112. Calcification in the arteries, 11-5. 496 Surgical Pathology. Calciftcation in the lieart, 114. • in the memhranes of the brain, 116. in new growths, 116. iu old age, 113. in the veins, 116. of hydatid cysts, 116. , Partial and complete, 114. , Secondary, 115. Calcified patches under the micro- scope, 114. Calculi, Table of, 377. Callo\is ulcer, 27. Calltis-formation, 179. Cancer of the prostate, 368. Cancerous depo-^it, 11. tubercle, 153. Cancers and sarcomas con- trasted, 491. Cancrum oris, 40. Carbuncle, 77. Carcinomata, The, 474. Caries, 2u7, 209. fiingosa, 160, 209, 211. , Nature of the discharge in, 213. necrotica, 212. non-suiipurativa, 209. of the iiip joint, 189. of the spine, 214. • of the vertebrae, 214. , process of ciire in the spine, 216. Cartilage wounds or fractures, 178. Cartilaginous transformation of the callus, 180. Caseation, 10. Caseous inflection, 157. Catarrh, The term, 357. Catarrhal ophthalmia, 160. Cauliflower excrescences, 455, 487. Cavernous augiomata, 435. Cells from inflamed tissue, 4. Cellulitis, 75. Central necrosis, 237. Cephalhsematoma, 194. Cerebral abscess, 201. meningocele, 282. softening, 96. Cerebro-spinai flmil, 281. Cerebrum, Suppurative inflamma- tion of the, 8. Chancres, 31. Charcot's disease, 126, 189, 193. Chimney-sweep's cancer, 485. Cholesterine, 100. Chondro-sarcoma, 448. . of the testicle, 334. Choroiditis syphilitica, 143. Chronic abscess, 12. endarteritis, 287. enlargements of the testicle, 321. inflammation, 11. interstitial nephritis, 372. osteoplastic ostitis and peri- ostitis, 219. peritonitis, 893. rheumatic arthritis, 12, 256. serous synovitis, 262. Cicatrisation, 169. of an ulcer, 20. Cirrhoses, 301. Cirsoid aneurism, 296. Cleft palate, 282. Clonic spasm, 47. Clot within the aneurism, 293. Colloid cancer, 482. of ovary, 483. degeneration, 104. Columnar epithelioma, 481. of rectum, 386. Compound f ractui-e with necrosis, 191. fractures. Union of, 190. Condensiug ostitis, 210, 223. Congenital hydrocele, 340. nsevi, 434. syphilis, 141. , secondary and tertiary symptoms, 144. Congestive stricture of the ure- thi-a, 346. Connective tissue hypertrophy, 125. Contagious carbuncle, 78. Continuous pain, 1.5. Corpora amy]acea, 120, 369. Corpuscles of Gluge, 4, 9. Counter-irritantsreHevingpain,16. Cranial bones. Lesions of, in con- genital syphilis, 228. Craniotabes, 151, 228. Cranium aif ected in syphilis, 229. Croupous disease of granulations, 23. Curvature of the spine, 272. Cutaneous eruptions in syphilis, 142. system in nervous affections, 122. Cystic degeneration, 246. epithelioma, multiple, of lower jaw, 102. myeloid sarcoma of the fe- miu', 443. ossifying enchondroma of the femur, 418. Index. 497 Cystic sarcocele, 335. Cystitis, 356. Cysts, 464. Dead tissues in gangrene, Changes in the, 35. Defective growth of radius after fracture, 185. • vascular supply in fractures, 186. Definitive callu=!, 183. Deformities, 268. in rickets, 148. Diarthrodial pseudarthrosis, 188. Diathesis, 11. Diffuse adenoma, 462. fibromata, 410. funicular hydrocele, 341. hypertrophy of hone, 223. strumous orchitis, 326. traumatic aneiirisms, 290. Diphtheria of the granulations in ulceration, 25. of wounds, 26. Discoloration of the skin by silver nitrate, 107. Diseases of the granulations in ulceration, 23. Dissecting aneurism, 297. Disseminated tubercular orchitis, 331. Double-descending optic neuritis, 141. Dry arthritis, 256. Dupuytren's spur, 402. Ear, Congenital sypbilitic affec- tions of the, 143. Echinococcus, 471. Eclamptic convulsions in fever, 46. Ectopia vesicae, 284. Elephantiasis Arabum, 411. Emboli, Paths of transit of, 306. Embolic aneurisms, 297. congestion of the lung, 305. infarction of the spleen, 308. Embolism, 304. Embryo-plastic tumour, 440. Encephaloid cancer, 333. of testicle, 480. cancers, 479. sarcoma, 440. Enchondroma, 335, 415. Enchondromata, Classification of, 417. Encysted hydrocele of the epi- didymis, 339, 340. Ends of divided muscular fibres, 175. Enostoses, 421. G G Epididymis, 326. Epididymitis, 319. Epiphysial fractures, 184. osteomata, 422. Epispadias, 285. Epithelioma, 361. of the anus, 385. of the thumb, 486. Erysipelas, 69. , Infectious, 57. , Phlegmonous or cellulo- cutaneous, 73. of the scalp, 195. Erysipelatous lymi)hangitis, 73. Erythema, 71. Exophthalmos, 201. Exostoses, 421, 424. Extravasation of urine, 350. Extroversion of the bladder, 284. Exudation stage in the union of wounds, 168. Eye, Congenital syphilitic affec- tions of the, 142. in lesions of the brain and spinal cord, 128. False joints, 1&7. Fascicular neuromata, 431. Fatty degeneration, 94. , Microscopy and chemis- try of, 100. of arteries, 285. of the heart, 97. infiltration, 92. tumour, 414. Fever, 41. Fibrillar tremor of the muscles in fever, 46. Fibroma molluscum, 410. Fibromata, The, 408. Fibroses, 301. Fibrous polypus, 363, 389, 411. Fistula in ano, 391. Flexion of the joints in inflam- mation, 254. Fracture of the spine, 273. simulated in rickets, 150. Fractures of bone, 178. of rickety bones, 148. Fungating ostitis, 211. Fungous inflammation in the knee-joint, 253. testis, 327. Fungus disease of granulations, 24. hsematodes, 333, 479. Furuncles, 76. Fusiform aneurisms, 296. Gall stones and urinary calculi, 378. 498 Surgical Pathology. Gall stones, pigmentation in, 108. Gangrene, 10, 34. _ Gangrenous stomatitis, 40. Gelatinoform atrophy, 229. Genito-urinary system in loco- motor ataxia, 127. Genu valgum, 276. Giant cells, Origin of the, in tubercle, 156. Glioma, 446. Gliosarcoma, 446. Gonorrhcea, 341. Gonorrhceal affections of the eye, 344. ■ arthritis, 265. conjunctivitis, 345. cystitis, .343. orchitis, 344. rheumatism, 265. stricture of the urethra, 344. Granular and crystalline pigment from cerehral basmorrhage, 109. Granulation of a wound, 171. sarcoma, 437. tissue, 6, Grey granulation of the liver, 155. miliary granulations, 153. Gummata, 133, 139. Gunpowder explosions. Discolour- ing by, 107. Hsematoma, 194. Hsematuria, 364. Haemorrhage between the skull and dura mater, 197. from the bladder, 365. — — from the kidney, 364. from the prostate and urethra, 366. from the ureters, 365. from hsemophilia, 266. into joints, 266. _ ■ Haemorrhagic condition of the granulations of an ulcer, 25. infarction, 308, 307. peritonitis, 397. Hgemorrhoids, 390. Hare-lip, 284. Healing by granulation, 170. by scabbing, 173. • stage of an ulcer, 19. Heat in inflammation, 2. Hereditary multiple osteomata, 423. Hernia cerebri, 196. • testis, 327. Hei-pes zoster, 123. Heteroplastic tumours, 405. Hip affected with strumotis arthri- tis, 255. . deformities, 276. joint affected with chronic rheumatic arthritis, 259. disease, 256. Histology of grey granulations, 154. of the granulations forming the base of an ulcer, 20. Homoplastic tumours, 405. Horse-shoe fistula, 391. Hospital gangrene, 26, 39. Hospitahsm, 40. Howship's lacunae, 209. Hyaline masses in joints, 268. Hydrocele, 337. of the cord, 340. of the hernial sac, 402. of the tunica vaginalis, 338. Hydro-meningocele, 279. myelocele, 279. Hydrops acutus, 261. articulorum, 262. Hygroma, 465. Hyperpyrsexia, 98. Hypertrophies, 81. Hypertrophy and dilatation of the ureters, 355. of the bladder, 354. of the facial bones, 224. of the prostate gland, 366. , Physiological, 85. Hypospadias, 284. Ichorbsemia, 63. Infantile paralysis. Deformities from, 276. Infective origin of tubercle, 156. Inflammation, 1. of an ulcer, 26. of bone, 205. Inflammatory changes in bone fracture, 179. Innocent tumours of the rectum, 3S8. Inspissated pus, 13. Interarachnoid suppuration, 199. Intermittent pain. 15. Internal anthrax, 81. necrosis, 237. Interstitial keratitis, 143. Intracranial suppuration, 198. * syphihs, 139. Intracystic tumours, 447. Intraspinal syphilis, 139. Intussusception of the bowel, 403. Irritable ulcer, 27, Irritative dropsy, 281. IXDEX. 499 Irritative overgrowth, 85. Iritis, 140. Itcliing in syphilitic eruptions, 135. Ivory osteomata, 422. Joint murrain, 78. Joints, Diseases of the, 249. , Trophic lesions of, 126. Keloid mass, 7. Keratitis punctata, 143. Kerato-iritis, 143, Kyphosis, 216. Lacerated wounds, 172, 174. Lardaceous infiltration, 117. Lateral curvature of the spiae, 274. Leucocytes, 3. , Diapedesis of, 4. Leucocythsemia, 453. Ligamentous pseudarthrosis, 187. Ligature of arteries, 298. , Cuctiag through of the ligature, 299. Lipomata, The, 412. Lipomatous bodies in joints, 288. sarcoma, 448. Liquor puris, 9. sanguinis, 9. Living sequestrum. A, 212. Locality of ulcers, 22. Locomotor ataxy, 126. Lociis resistentiae miuoris, 13. Long bones. Congenital syxihilitic lesions of, 230. Lumho-sacral spina bifida, 280. Lupoiis ulcer, 30. ulceration, 164. Lupus, 162. erythematosus, 163. exedens, 163, 164. vorax, 163. Lymphadenomata, The, 449. Ljmphangiomata, The, 454. Lymphatic nsevi, 454. Lymphatics affected by striunous disease, 161. Lymphoid or adenoid tissues, Oriain of, 155. Lymphomata of the viscera, etc., 452. Lympho-sarcoma, 445. Malignant anthrax oedema, 80. faci;d carbuncle, 78. growths, 11, 406. iympbomata, 451. pustule, 78. Malignant rectal ulcer, 382. sarcocele, 332. ulcers, 29. Malum coxae senilis, 256. Maxillae and teeth, Congenital syphilitic, 231. Medullated neiiromata, 431. Melanin, 109. Melanoma, 110. Melanotic sarcoma, 446. of muscle, 109. Melon-seed bodies in joints, 266. Meningo-encephalocele, 282. Metastases, Causes of, 64. in pyaemia, ^. Miliary aneurisms, 297. Milk teeth in riciets, 152. Modified ossification in rickets, 146. Moist gangrene, 37. Mollities ossium, 193, 245. contrasted with caries, 249. Molluscum fibrosum, 410. Mouth and nose. Congenital sy- philitic affections of the, 142. Movement of the fragments after fracture, 186. Mucin, 103. Mucoid degeneration, 100. Mucous papillomata, 456. - — - polypi of the bladder, 383, 364, 429. sarcoma, 447. tissue, Distribution of, 101. tubercles, 32, 142. Muscle wounds, 174, Muscular system in fever, 45. Myeloid epulis from the lowe'- jaw, 444. sarcoma, 443. Myo-fibroma of uterus, 432. Myomata, The, 431. with striped fibres, 433. Myxo-chondroma of parotid gland, 416. Myxoedema, 105. Myxomata, The, 427. Myxomatous, or gelatinous poly- pus, 389. Myxo-sarcoma, 448. Nasal mucous polypi, 428. Naso-bucco-pharyn.:eal cavity,283. -pharyngeal polypi, 428. Natural ossification, 145. Necrosed part in gangrene, 36. Necrosis, 232. contrasted with caries, 218. 500 Surgical Pathology. Necrosis of an amputation stnmp, 235. of the femur, 238. Nerve injuries and wounds, 176. Nervous system in fever, 45. Neuralgic pain, 15. Neuromata, 410, 430. Nodes, 222. , Varieties of, 222. Nodular masses in joints, 267. rheumatism, 256, 258. Nomenclature of ulcers, 21. Non-medullated neuromata, 4S1. Odontomata, The, 425. Opposed graniolating surfaces. Union of, 172. Orbital cellulitis, 204. Orchitis, following gonorrhoea, 319. Organic stricture of the urethra, 347. Osseous and articular trophic lesions, 127. ' Ossific union, Failure of, 185. Ossification of the callus, 182. Ossiform tissue of Broca, 145. Ossifying enchondromata, 423, sarcoma, 448. Osteoclasts, 209. Osteoid chondroma, 426. tissue of Virchow, 146. tumour, 426. Osteomalacia, 245. Osteomata, The, 419. Osteophlebitis, 227. Osteophytes, Formation of, in locomotor ataxia, 126. , Congenital syphilitic, of the long bones, 231. , Varieties of, 220. Osteoplastic ostitis. Internal, 223. Osteoplasts, 182. Osteo-thrombosis, 227. Ostitis, Causes of, 206. deformans, 224. , Terminations of, 206. Otitis media, 144. Pachymeningitis, 189. Pain, 13. , Elf ects of, on nutrition, 16. , Factors of, 14. in inflammation, 2. Papillomata, The, 454. of the serou& membranes, 457. Papular syphilide, 136. Paralysed muscles in trophic lesions, 125. Parrot's osteophytes or nodes, 229. Pathological aneurisms, 292. aneurism. Varieties of, 296. Pemphigus, 138. Perforating ulcer of the foot, 124. Periarteritis, 289. Perihepatitis, 144. Periosteal abscess, 225. Periosteum, Changes in, after fracture, 184. Peritonitis, 392. Perspiration in fever, 44. Pes planus et plano-valgus, 275. Phagedeeua, 33. Phagedsenic chancres, 31. Phlebitis, Signs of, 313. Phlegmasia alba dolens, 31+. Phlegmonous arthritis, 263. erysipelas, 37, 73. teno-synovitis, 74. Phlyctenular corneitis, 160. Phosphorus necrosis of the jaws, 242. Phthisis and fatty infiltration, 94. Pia-meningeal suppuration, 200. Pigment, Sources of, 107. Pigmentation, 106. , cases that it occurs in, 110. , False, 106. in syphilitic eruptions, 135. , True, 107. Piles, 379, 390. Plantar and palmar psoriasis, 137. Polymorphism of syphilitic erup- tions, 134. Posterior synechia, 140. Pott's disease of the spine, 214. puffy tumour, 195. Primary convulsions in fever, 46. syphilitic sores, 33. Prolapse of the rectum, 389. Proliferating arthritis, 256. Prominence of the eye -ball, 204. . Prostate gland, diseases of, 3o6. Prostatic abscess, 368. calculi, 369. glandular tumour, 367. Prostatitis, 368. Provisional callus, 183. Psammomata, The, 449. Pseud arthroses, 178, 187. Pseudarthrosis from traumatic dislocation, 189. from xinreduced dislocation, 189. Pseudo - hypertrophic paralysis, 93. Index. 501 Pulpy degeneration of synovial membrane, 251. Pulsating swellings in tlie scalp, 195. Pulsation of tlie eye-ball, 203. Purposive atropby, 87. Purulent diathesis, 63. infection, 63. oplithalmia, 345. Pus corpuscle?. Origin of, 10. disease, 63. Pustular conjunctivitis, 160. Pyaemia, 50. , changes in the wound, 63 , course and character of the symptoms, 65. , Idiopathic, 67. , Post-mortem signs of, QQ. , Synonyms for, 63. Pyogenic membrane, 8. Pyohsemia simplex et multiplex, 63. Pyramidal cataract, 143. Pyrexia, 42. Quarter evil, 79. Quiet necrosis, 243. Ea-cemose aneurism, 296. Earefying fungous ostitis, 210. ostitis, 207. Pecto-vesical fistula, 353. Eectum, Stricture of the, 332. , Tumours of the, 885. , TJlcers of the, 380. Eedness in inflammation, 2. Eeflex subdual of pain, 16. Eeproduction of epitheliiim, 21. Eesidual abscesses, 13. Eetinitis syphilitica, 140, 143. Eeverdin's skin-graftiLg, 21. Eheumatic gout, 256. Eickets, 113, 145, 193. Eickety joiats, 152. rose-garland, 151. spine, 151. tibia, 149. Eigor in fever, 46. Eodent ulcer, 490. Eound-celled sarcoma, 440. Eupia, 1.34, 138. Euptured aneurism, 293. Sacculated aneurism, 291. Sago spleen, 119. Saliva in fever, 44. Sarcocele, 321. Sarcoma, 335, 362. of the rectum, 387. Sarcomata, The, 437. Scalp injuries and diseases, 193. wounds, 195. Scirrhus of the prostate, 3G8. of the breast, 475. Scleroses, 301. Sclerosing ostitis, 210. Sclerosis ossium, 223. Sclerotitis, 345. Scrofula, 158. , Period of life for, 162 Scrofulous diathesis, 158. orchitis, 329. sarcocele, 326. , Minute anatomy of, 330. testicle, 161, 326. tubercle, 153. ulcers, 30. Secondary clot, 299. Senile osteoporosis, 193. scrofula, 162. thickening of the skull, 225. Separation of the fragments after fracture, 186. Sepsin, 53. Septic infection, 52. infection, Diagnosis of, c8. intoxication, 52. , Diagnosis of, 59. Seijticsemia, 50. , Character and course of the symptoms in, 59. Septopysemia, 51. Sequestrotomy, 2-38. Sequestrum, 34, 236. Serous cysts, 465. Shooting pains in cancer, 15. Simijle angiomata, 434. fracture of bone, 178. gi'eenstick fracture of radius, 181. rarefying ostitis, 209. sarcocele, 321. surgical fever, 47. Site of syphilitic eruptions, 135. Sloughing phagedsena, 40. ulcer, 33. Soft chancre, 18. Softening cysts, 98. Spasmodic stricture of theurethi-a, 346. Specific symptomatic ulcers, 31. Spermatocele, 340. Sphacelus, 34. Spina bifida, 278. Spinal absce.'ses, 216. cord in tetanus, 165. Spindle-celled sarcoma, 441. Spine, Fixity of, in caries, 215. 5o: Surgical Pathology. Splenic fever, 78. Spougeoid tissue, 146. Spongy osteomata, 422. Spontaneous aneurisms, 292. • fracture, 193. Spreading stage of an ulcer, 18. Squamous epithelioma, 484. sypliilide, 136. Stationary stage of an ulcer, 19. Stearic acid crystals, 99, 100. Strangulated hernia, 399. Strumous arthritis, 251. caries, 210. orchitis, 161. rarefying ostitis, 210. testis. Section of, 328. ulcers, 30. Subungual exostoses, 448. Superficial caries, 213. necrosis, 233. • rarefying ostitis, 212. Suppuration, 7. between the bone and dura mater, 199. • in the mastoid cells, 202. Suppurative arachnitis, 200. arthritis, 263. Surgical fever, Stages of, 49. kidney, 370. Symptomatic ulcers, 21, 28. Syphilis, 128. of the larynx, 139. , Secondary and tf rtiary, 131. SyphUitic acne, 130, 137. caries, 216. • chancres. Unity and duality of, 129. disease of arteries, 288. disease of the cranium, 217. eruptions, 134. - — - eye aftections, 140. gumma of the liver, 133. lepra, 136. orchitis, 323. pseudo-paralysis, 230. psoriasis, 135. rectal ulcer, 381. sarcocele, 322. ulcers, 31. , Secondary, 32. , , of the throat and motith, 32, , Tertiary, 32. Swelling in inflammation, 2. Tabes mesenterica, 162. Talipes equino-varus, 274. ■ equinus, 275. valgus et caleaneo-valgus, 275. Tattooing discolourings, 107. Telargiectases, 434. Tertiary phagedeenic ulceration, 33. Tetanic spasm, 47. Tetanus, 164. Throbbing pain, 15. Thrombosis, 310. — — in common carotid artery, 316. , Eelation of, to phlebitis, 312. Tibia affected with ostitis defor- mans, 149. Tissues attected in scrofula and . tubercle, 160. Tonic spasm, 47. Traumatic fever, 47. — , Cause of, 48. hgemarthrosis, 266. suppurative arthritis, 263. Trophic lesions, 121. nerves, 122. Tubercle, 153. . com]pared with pyaemia, 157. , General pathology of, 156. of bone, 153, 213. of the prostate, 368. Tubercular meningitis, 45, 201. orchitis, 161. syphihde, 135, 137. testis, 153, 326. ulcers of the intestine, 83. Tumours, 405. , Classification of, 407. of the scalp, 195. Tunica vaginalis in syphilitic orchitis, 325. Types of pain, 15. Typhoid ulcers, 33. Ulcer, Simple, mode of its forma- tion, 17. , Stages of an, 18. Ulceration, 16. of cartilage, 251, 253. Ulcerative form ot hospital gan« grene, 40. Ulcers in terminal nerve-fibres, 123. in the small intestine, 22. of the anus an 1 rectum, 379 of the face, 22. of the leg, 22. on the penis, 23. Union of wounds, 167. by first intention, 168. Ununited fracture of olecranon, 187. of humerus, 183. Index. 503 Urethra, Stricture of, 3 46. Uretliral fever, 68, Urinary absce.ss, 350. deposits. Table of, 375. fistula, 353. Urine in fever, 44. , Pigmentation of, 108. , Retention of, in gonorrhoea, 344. in surgical kidney, 374, , Suppression of, 68. Valve of Hoiiston, 383. Valves in varicose veins, state of, 303. Varicose aneurism, 291. ulcer, 28. , Mode of origin of a, 28, Varix, 300. , Calcification in, 303. , General pathology of, 301. , Histology of, 302. Vascular polypus of rectum, 38S. Vascularisation r.f lymph, 169. of callus, 181. Venous absorption, 5. embolism, 304. nsevi, 435. Vertebrae absorbed by an aneurism, 89. Vesico-vaginal fistula, 353. Vesicular eruptions, 122. Villous polypus of rectum, 388, tumour of bladder, 362. Visceral changes in rickets, 152. lesions in congenital syphilia, 144. syphilis, 138. Warts, 455. Warty cicatrix, 31. polypus of rectum, 389. Waxy infiltration, 117. Weus, 411. White swelling, 251. Wounds of tendons, 173. Yellow tubercle, 153. Zenkerism, 104. CASSEH AND COMPANY, LIMITED, BELLE SAUVAGE WORKS, LONDON, E.C. COLUMBIA UNIVERSITY LIBRARIES (hsi.stx) RD 57 P39 C.1 Elements of surnical patholoc 2002129418