Volume 2 — DISEASES OF THE DIGESTIVE SYSTEM. (continued 28)

Metastatic suppurative inflammation leads to the formation of a single large abscess or to multiple minute purulent collections.

SYMPTOMS AND COURSE.—Parenchymatous degeneration gives rise to no distinctive symptoms. Its occurrence in typhoid fever or other infectious disease may be suspected when after prolonged hyperpyrexia there are enlargement of the liver and spleen and albuminuria. The appearance of jaundice (from pressure) increases the probability of involvement of the pancreas in the general gland-change.

The development of rigors, alternating with flushing, during the course of one of the lesions liable to be attended with metastatic abscesses in the pancreas might suggest the formation of pus in the gland, but an absolute diagnosis is impossible.

Several cases are on record pointing to the possibility of a metastasis of mumps from the parotid gland to the pancreas. In these the disappearance of the parotiditis was followed by symptoms resembling those of idiopathic pancreatitis—namely, thirst, fever, loss of appetite, anxiety, and burning in the epigastrium, with deep-seated pain extending toward the right side; in addition there was diarrhoea, with numerous, yellowish, watery stools. In one case that resulted fatally the secondary diarrhoea suddenly ceased and the parotid swelling reappeared. At the autopsy the pancreas was found to be swollen, reddened, engorged with blood, and indurated. Such a metastasis, however, must be very infrequent, and more extended observations are necessary to establish its course and clinical features.

The first form of acute secondary pancreatitis may be a comparatively unimportant complication of the acute infectious diseases, or, together with the parenchymatous degeneration of other organs, may form a distinct element in the fatal issue of these diseases.

Metastatic abscesses are prone to be followed by ulceration and the formation of fistulous communications with the neighboring viscera.

TREATMENT.—The management of secondary inflammation of the pancreas is regulated solely by the indications derived from the originating disease.

Chronic Interstitial Pancreatitis.

Inflammation of the connective tissue of the gland usually occurs after adult life, and depends upon a variety of causes.

The secondary form, due to long-continued venous engorgement resulting from lesions of the cardiac valves and from chronic disease of the lungs or liver, is the most frequently observed.

Other causes are closure of the duct of Wirsung, the retained secretion producing pressure upon the glandular tissue; the extension of inflammation from adjacent organs, as the bile-duct when there is an impacted gall-stone, or the stomach and duodenum, especially in cancer and perforating ulcer, where the floor of the ulcer is formed by the pancreas; the pressure of tumors, as aneurisms of the abdominal aorta and coeliac axis; chronic alcoholism; and syphilis.

ANATOMICAL APPEARANCES.—The lesion may be limited to the head or to isolated portions of the gland, or be uniformly distributed. The general changes are a hyperplasia of the interacinous connective tissue, with subsequent contraction and atrophy, or, in extreme instances, entire destruction of the glandular elements proper, the organ becoming granular and firmer and tougher than normal. A section shows a pale surface, studded at intervals with white spots, from which little cheese-like and fatty masses may be squeezed, and, when there has been intense hyperæmia, with minute collections of reddish pigment and small hemorrhagic cysts, indicating previous interstitial hemorrhages.

When the contraction causes closure of the small excretory ducts or of the duct of Wirsung itself, the section shows secondary cysts and beaded canals.

In exceptional instances of acquired syphilis the pancreas is the seat of gummata or sclerosis, but in congenital syphilis hyperplasia of the glandular connective tissue frequently occurs, being usually associated with specific lesions of the lungs, liver, kidneys, and general glandular system.

SYMPTOMS AND COURSE.—As chronic pancreatitis rarely attains a sufficient degree of development to interfere seriously with the function of the organ, the disease is usually latent, or masked by the symptoms of the originating lesion in secondary hyperplasia, or by the associated diseases of the abdominal viscera in alcoholism and acquired syphilis.

When due to hereditary syphilis, the foetus is stillborn or death takes place soon after birth, and there are no characteristic symptoms.

Occasionally, however, especially when it depends upon a complete obstruction of the duct of Wirsung, a diagnosis may be made from the presence of emaciation, fatty stools, and melituria, with epigastric pain of a neuralgic character, and the discovery of a deep-seated, dense tumor extending transversely across the epigastrium.

The duration is indefinite, and varies greatly with the cause. While a return to the healthy condition is possible during the early stage of the lesion, the usual course is similar to that of chronic interstitial inflammation in other organs.

TREATMENT.—The management, when a diagnosis can be made, must be guided mainly by the etiological indications. The restoration of the functions of the heart, lungs, or liver when these organs are at fault, the abstinence from alcohol in the drunkard, and an energetic use of mercurials or iodide of potassium in syphilis, are of the first importance in arresting the disease. A persistent course of mild purgatives and of cathartic mineral waters is serviceable. Pain should be relieved by belladonna or opium. The diet must be simple and digestible, and if an arrest of the pancreatic secretion be indicated by the appearance of fat in the stools, an effort should be made to supply the deficiency. For this purpose pancreatin, prepared by precipitation by alcohol from a watery extract of a calf's or pig's pancreas, may be used.¹ The pancreatin may be given in doses of from five to fifteen grains, in the form of a pill or in capsules, and at an interval of two hours after food is taken, or the same quantity of pancreatin may be added to the food a few moments before it is eaten. Probably the best substitute is a watery infusion of the gland containing all its soluble principles. To prepare an active infusion the pancreas must be taken from the animal during the act of digestion. It is then freed from its surrounding fat, and macerated for two hours in four times its weight of water at a temperature ranging between 25° and 30° C. (58.3° and 61.1° F.). Another plan is to beat a calf's pancreas in a mortar with six fluidounces of water until a milk-like fluid is obtained, and strain. One-third of the infusion obtained by either method is administered after each meal, an entire pancreas being thus used every twenty-four hours.

¹ One gramme of pancreatin is sufficient to emulsify fifteen grammes of fatty substances, to convert eight grammes of starch into glucose, to digest fifty grammes of fibrin, twenty grammes of syntonine, and thirty-three grammes of boiled albumen (Raymond).

The extractum pancreatis,² as it is now furnished to the profession, is a very useful preparation. It may be employed to peptonize milk, milk-gruel, and broth, or be given in combination with bicarbonate of sodium at a fixed interval after each meal, as in the following formula:

Rx. Ext. pancreatis, drachm j;

Sodii bicarbonatis, drachm ij;

M. et. ft. Chart No. XII.

S. One powder to be taken two hours after each meal.

² That prepared by Fairchild Brothers & Foster of New York has proved the best in my hands.

Peptonized milk is prepared by putting into a clean quart bottle 5 grains of extractum pancreatis, 15 grains of bicarbonate of sodium, and a gill of cool water; shake, and add a pint of fresh cool milk. Place the bottle in water not so hot but that the whole hand can be held in it without discomfort for a minute, and keep the bottle there for exactly thirty minutes. At the end of that time put the bottle on ice to check further digestion and keep the milk from spoiling.

Peptonized milk-gruel is made of equal parts of any farinaceous gruel and fresh cold milk. To a pint of this combination 5 grains of extractum pancreatis and 15 grains of bicarbonate of sodium are added, and the whole allowed to stand in a warm place for thirty minutes, when the process of digestion must be arrested by placing on ice.

Peptonized broth is made in the following way: Take one-fourth of a pound of finely-minced raw lean beef or mutton or chicken, and one-half pint of cold water; cook over a slow fire, stirring constantly, until it has boiled a few minutes. Then pour off the liquor, beat the meat to a paste, and put both into a bottle with a half pint of cold water. Add 30 grains of extractum pancreatis and 20 grains of bicarbonate of sodium; shake well, and set in a warm place (110-115°) for three hours, shaking occasionally; then boil quickly. Finally, strain or clarify in the usual way and season to taste.

MORBID GROWTHS OF THE PANCREAS.

Carcinoma.

Cancer is probably the most common of the chronic affections of the pancreas. It is usually secondary, being due to an extension of carcinoma of the stomach, duodenum, liver, or abdominal lymphatic glands, but there are enough cases on record to show that it may be primary. It has been discovered in the foetus at birth, but the vast majority of cases occur after the age of forty. Men are more frequently affected than women. Nothing is known as to the influence of inherited tendency in the production of the disease, and as little of the exciting causes, though some authors attach much importance to prolonged pressure upon the epigastrium and to blows and contusions on the upper part of the abdomen.

ANATOMICAL APPEARANCES.—Primary carcinoma may be either scirrhous, encephaloid, or colloid, the first being the variety most frequently observed.

The lesion begins in the head of the gland in the form of several small nodules which gradually coalesce. Sometimes the whole gland becomes involved in the new formation; again, isolated nodules may be scattered throughout its substance, and exceptionally the growth is limited to the tail or middle portion. When the head alone is involved, the remainder of the gland either remains healthy, undergoes fatty degeneration, or becomes indurated. The tumor is rounded in outline and nodular, and varies in size, density, and color according to the form of carcinoma present. The duct of Wirsung is ordinarily obstructed, large retention cysts, containing a yellowish-red liquid, are formed, and the changes already described under the head of Chronic Interstitial Pancreatitis take place in those portions of the gland which are free from carcinoma. The disease is very prone to extend to the surrounding organs, particularly the neighboring lymphatic glands, the duodenum, and the liver, rarely to the stomach. When the contiguous organs are not directly implicated in the carcinomatous changes, they are subjected to pressure by the tumor, and in the case of the stomach and duodenum adhesions often form, and are followed by perforation. There seems to be a tendency also to infiltration of the adjacent subperitoneal connective tissue and to hyperplasia of the fibrous tissue of the viscera, even when they are not secondarily involved in the morbid growth, leading to narrowing of the aorta, thickening of the walls of the stomach and duodenum, and a sclerosis of the liver. Obstruction of the common bile-duct, with dilatation of the gall-bladder from retention of bile, is a frequent result of the disease.

Secondary carcinoma of the pancreas usually first appears in, and is limited to, the head of the gland. It seldom occurs in isolated nodules, but the growth is generally continuous with the primary cancerous mass. The form is either scirrhous or encephaloid. Wagner records a case of cylindrical-celled epithelioma following a simple epithelioma of the mucous membrane of the duodenum; and a similar instance has come under the author's own observation;³ but this variety of morbid growth is rare. The primary growth is almost uniformly situated in the stomach, duodenum, liver, or gall-bladder, though occasionally it may be seated in some distant organ; in such cases the pancreatic tumor appears as an isolated nodular mass.

³ Transactions of the Pathological Society of Philadelphia, vol. ix. 13.

SYMPTOMS AND COURSE.—The symptoms may be divided into two classes—namely, first, those which arise from the lesion of the gland itself; and, secondly, those which depend upon the effect of this lesion on the neighboring viscera.

The features belonging to the first class are general marasmus, pain, the appearance of fat and perhaps undigested muscular fibres in the fecal evacuations and of fat in the urine, and the physical signs of an abdominal tumor.

Loss of flesh is one of the earliest symptoms: it is generally progressive, and is at times so great that the spine can be distinctly traced through the abdominal walls. Together with this emaciation there is debility, often extreme, but sometimes not so marked as might be expected from the degree of wasting. The skin is commonly pale and dry, and before jaundice is developed has the ordinary sallow hue of cancerous cachexia. The features are pinched, and the face wears an expression of anxiety and suffering. In cases uncomplicated by peritoneal inflammation the temperature remains about normal, or it may be lowered as the general exhaustion increases. The pulse is feeble and slightly increased in frequency.

Pain is the most uniformly present and the earliest symptom. It is always situated deep in the epigastrium, and from thence extends to the back, to the right or left side, downward to the umbilicus or lower part of the abdomen, and upward into the chest. It is generally continuous, but is subject to remissions and paroxysmal exacerbations. During the remissions sensations of distress, of burning, or of dull pain are experienced at the pit of the stomach; during the exacerbations, which may last several days, the pain becomes extremely acute and lancinating and extended in distribution. The ingestion of food and pressure upon the epigastrium have no constant effect upon the pain. Quick movements of the body from side to side often increase it and excite exacerbations. The suffering is greatest in the erect posture, and on this account the patient bends his body forward so as to relax the abdominal muscles. The paroxysmal and neuralgic character of the pain indicates implication of the coeliac plexus.

The appearance of fat in the stools is an important symptom, unless there be at the same time an obstruction to the passage of bile into the duodenum, indicated by jaundice. Lipuria has been noticed in a few cases only.

In many instances (nearly one-half of the number of recorded cases) physical exploration reveals the signs of enlargement of the organ. At times there is merely a sense of fulness and resistance to the touch, and a modified tympanitic percussion note in one of the three regions of the upper segment of the abdomen. But usually when a tumor is present it is readily mapped out by palpation. The tumor is seated in the epigastrium, and may extend into the right or left hypochondrium or downward into the umbilical region. It varies much in size, is rounded, nodulated, firm, slightly movable or fixed, and tender, though sometimes painless, to the touch. Percussion yields dulness or a dull-tympanitic sound. On auscultation a blowing murmur may be heard when the tumor presses upon the aorta; and when this murmur is present there is usually also transmitted pulsation.

The symptoms belonging to the second class arise when the adjacent viscera become involved in the cancerous disease, or when their functional activity is disturbed by the encroachment and pressure of the enlarged pancreas.

From the association of a catarrhal condition of the mucous membrane of the stomach, particularly when the pyloric orifice is obstructed, several prominent symptoms of gastric catarrh are frequently observed—namely, sialorrhoea, pyrosis, acid eructations, flatulence, abnormal sensations, such as burning, weight and oppression in the epigastrium after taking food, and increased thirst. The tongue varies in appearance: it may be dry and covered with a brown or yellow fur, but when the flow of saliva is increased it is peculiarly clean and moist; and this condition is rather characteristic. The appetite is also variable; sometimes it remains good until the end, and occasionally it is perverted. Hiccough in some cases is an obstinate and annoying symptom.

Nausea and vomiting are late but moderately constant features. Their relation to the ingestion of food is not fixed. The vomited matter may consist of food, of glairy mucus more or less tinged with bile, of colorless liquid, or of a fluid resembling a mixture of bran and water. If there is marked pyloric obstruction with dilatation of the stomach, large quantities of frothy and fermenting material containing sarcina ventriculi are rejected at intervals. In the rare cases in which secondary sarcoma of the viscus is developed the ejecta are bloody or have the coffee-ground appearance, and the vomiting occurs several hours after eating, as the new growth is generally situated at the pylorus. When there is adhesion of the pancreatic tumor to the stomach, with perforation, both blood and pus are vomited. Dilatation of the stomach is attended by prominence of the epigastrium and an extended area of gastric tympany, and in cancer of the pylorus a tumor is often appreciable on palpation. The bowels are usually constipated. The fecal evacuations are hard, and when the biliary secretion is absent from the intestine they are clay-colored, and often contain fat. When there is ulceration of the mucous membrane of the duodenum following secondary cancer or adhesion, the stools become black and tar-like from the presence of altered blood. Complete obstipation occurs in mechanical obstruction of the gut from direct pressure or from bands of lymph. Occasionally, just before death there is diarrhoea, and there may be an alternation of vomiting and diarrhoea.

The symptoms and signs of secondary carcinoma or sclerosis of the liver may be present, but the most commonly observed indications of impaired hepatic function depend upon pressure-obstruction of the common bile-duct. These are jaundice, fatty and clay-colored stools, and the appearance of a tumor in the region of the gall-bladder. Jaundice is a very common symptom. It occurs late in the disease as a rule, is progressive and persistent, resisting all treatment, and is extreme in degree, the skin becoming deep-yellow or greenish in color. The tumor of the distended gall-bladder is pyriform in shape, firm and elastic to the touch, yields a dull percussion sound, and occupies a position opposite the extremity of the tenth rib on the right side of the abdomen.

Dropsy occurs in a large proportion of cases (nearly one-half) during the advanced stages of the disease. It is due to vascular obstruction occasioned by the pressure of the enlarged pancreas itself or of the secondarily degenerated coeliac glands, and finally by secondary lesions of the liver. The dropsy appears either in the form of ascites or anasarca, is not often extreme in degree, and is subject to variations, disappearing and reappearing at intervals. Ascites is the more common form, but both conditions may exist in the same patient.

It is impossible in the majority of instances to definitely fix the date of onset of a pancreatic cancer, but the average duration of the disease may be stated to be about one year. The uniformly fatal termination usually takes place slowly from gradual exhaustion or with the symptoms of an adynamic fever, but death may occur suddenly from hemorrhage.

DIAGNOSIS.—The principal features of carcinoma of the pancreas are extreme emaciation, loss of strength, dyspepsia, pain of a neuralgic character in the epigastrium, constipation, obstinate jaundice, moderate ascites or anasarca, the appearance of fat in the stools, lipuria, occasional vomiting, and the physical signs of an epigastric tumor.

These symptoms are not pathognomonic, however, and the diagnosis can be certainly established only when it is possible to exclude primary disease of the surrounding organs, especially of the stomach and liver.

Cancer of the stomach may be excluded by the less-marked character of the functional disturbances of the viscus; by the absence of frequent vomiting, hæmatemesis, and the rejection of coffee-ground material; by the somewhat different situation and greater immobility of the tumor, by the seat, distribution, and constancy of the pain; and by the presence of jaundice and of fat in the stools and urine.

Diseases of the liver attended with alterations in the size of the organ, as cancer, abscess, albuminoid and fatty degeneration, sclerosis and hydatid tumor, have sufficiently characteristic physical signs and symptoms to be readily distinguished from cancer of the pancreas. On the other hand, the tumor of an enlarged gall-bladder is often confusing. The situation of this tumor opposite the tenth rib and its pyriform shape are important; other distinguishing points depend upon the cause of the enlargement. In enlargement from accumulated bile the tumor is elastic and fluctuating; from accumulation of gall-stones, hard and nodulated, movable, painless on palpation, and often the seat of crackling fremitus, produced by manipulation and due to the rubbing together of several calculi; from cancer, hard, nodular, the size of an orange, tender on pressure, rapid in growth, preceded by attacks of biliary colic, and attended by fistulous communications with the intestines and the passage of gall-stones per anum.

In aneurism of the aorta or coeliac axis the tumor may present in the epigastrium and produce analogous pressure symptoms. But the pain is more of the character described as wearing, and is usually augmented at night: on grasping the tumor a uniform expanding pulsation is felt in place of the to-and-fro movement appreciable in a tumor resting upon a healthy blood-vessel and receiving a transmitted impulse, while the constitutional symptoms and course are quite different.

The tumor of malignant disease of the omentum, although it appears in the epigastrium or upper part of the umbilical region, is much more movable, and is accompanied by ill-defined symptoms very dissimilar to those of pancreatic cancer.

In cancer of the transverse colon the mass may occupy nearly the same position as a pancreatic growth, but the pain occurs several hours after food is taken; vomiting is absent, and there is frequently hemorrhage from the bowels.

Chronic pancreatitis is accompanied by symptoms simulating those of cancer; the enlargement of the gland, however, is not so great, nor are the indications of pressure upon adjacent organs so prominent. The pain is less severe, the general failure in health more gradual, the progress slower, and constipation less common.

TREATMENT.—The indications are to maintain the strength of the patient, to provide a diet that is nutritious and at the same time easily digested, to allay pain by the employment of narcotics, and to relieve as far as possible the various symptoms as they arise. The plan of administering a calf's pancreas or extractum pancreatis will prove serviceable when the fecal evacuations contain fat. Nutritious and peptonized enemata may be of service in some cases.

Sarcoma and Tubercle of the Pancreas.

Sarcoma of the pancreas occurs with extreme rarity. It is impossible during life to distinguish it from carcinoma.

Tubercle of the gland is infrequently met with. Some pathologists deny its occurrence, and believe that the cases recorded as such are merely instances of caseous degeneration of the neighboring glands. When it does occur, it is always secondary, the primary disease being situated in the lungs or intestines. The alterations in the gland consist in the development of cheesy masses or of miliary granulations in the connective tissue between the acini. The condition gives rise to no definite symptoms, and its diagnosis during life is impossible.

DEGENERATIONS OF THE PANCREAS.

Fatty Disease of the Pancreas.

Two forms of fatty degeneration occur, either separately or combined—namely, fatty infiltration and fatty metamorphosis.

Fatty infiltration consists of a true hypertrophy of the fat-tissue normally existing in the gland, or of an increase and extension into the gland of the peripancreatic adipose tissue. Yellow bands and masses of fat-tissue appear between the acini, and by constantly increasing in size lead gradually to a total atrophy of the cells of the acini. The canal of Wirsung contains a fatty liquid. These changes are found associated with fatty liver, heart, and omentum, in drunkards especially.

Fatty metamorphosis of the gland consists of a change analogous to fatty metamorphosis of other organs. When hyperplasia of the interstitial connective tissue is absent, the organ is flaccid, soft, and diminished in size; the acinous structure remains distinct, though the acini and ducts are filled with a fatty emulsion: after this is discharged or absorbed the gland appears as a flaccid band, and finally becomes entirely atrophied. Fatty metamorphosis occurs in drunkards, in diabetes, in advanced age, in cancer, phthisis, and other wasting diseases.

Neither form of fatty disease gives rise to symptoms by which it can be recognized during life.

Albuminoid Degeneration of the Pancreas.

This is only found in combination with amyloid change in other organs of the body, and a diagnosis cannot be made.

Hemorrhages into the Pancreas.

Hemorrhages into the pancreas may be divided into three classes.

The most common form depends upon passive hyperæmia, the result of chronic diseases of the heart, lungs, or liver. In this condition the effusion of blood coexists with chronic inflammatory changes in the interstitial connective tissue. The appearance at first is of minute bloody points scattered throughout the areolar tissue; later, these change into round or oval pigment masses, or spaces containing reddish serum and surrounded by thickened, rust-colored, irregular walls.

The second class includes the rare cases of hemorrhage resulting from the rupture of one of the large blood-vessels of the gland, and due to some pre-existing change in the vessel walls. In these the pancreas is enlarged, may be converted into a sac containing blood, either fluid or coagulated or partially crystallized according to the duration of life after the hemorrhage has taken place, and a ruptured blood-vessel may be readily discovered on dissection.

The condition in which, without any evidence of passive hyperæmia or gross vascular lesion, the entire pancreas become hemorrhagic, constitutes the third class. The gland is then dark-red or violet in color, the meshes of the interstitial tissue are filled with recent or altered blood, and the acini are stained of a dull-gray hue. The hemorrhage may extend to the connective tissue surrounding the gland. Finally, the organ becomes soft, the peritoneal covering sloughs, and fragments of broken-down gland-tissue escape into the peritoneal cavity. These lesions are so analogous to those which attend thrombosis occurring in other organs that their dependence upon the same cause seems probable.

The first form of hemorrhage is unattended by special symptoms. In the second a pulsating tumor may suddenly appear in the epigastrium, and the ordinary indications of hemorrhage—vomiting, fainting fits, cold extremities, feeble pulse, and general exhaustion—are present. Death may occur suddenly or the patient may linger on for months. In the third condition death usually occurs very suddenly, probably from pressure upon the sympathetic ganglia. There are no symptoms, and the rapid termination prevents the development of general peritonitis, which would otherwise occur from the sloughing of the peritoneum.

There are no indications for treatment.

OBSTRUCTION OF THE PANCREATIC DUCT.

Obstruction of the excretory duct is a frequent occurrence in pancreatic disease, and is due to two classes of causes—namely, 1st, pressure from without; and, 2d, closure of the canal by catarrhal swelling of its mucous membrane or by calculi.

In the first class may be placed obstruction depending upon contraction occurring in sclerosis of the gland, upon carcinoma of the head of the gland, upon peripancreatic adhesions and indurations, upon the presence of large gall-stones in the ductus choledochus, and upon carcinoma of the pylorus and duodenum and enlargement of the neighboring lymphatic glands.

In catarrh of the canal of Wirsung the obstruction results either from simple swelling of the mucous membrane or from the presence of a plug of tough mucus.

The formation of pancreatic concretions is by no means a rare event, though these calculi are met with far less frequently than either gall-stones or salivary concretions. They result from precipitation of the inorganic ingredients of the pancreatic juice, and are usually seated in the main duct, although they may be situated in the smaller branches. They may be single or multiple, as many as twenty having been counted in one gland. In shape they are spherical, oval, or branched, with sometimes a smooth, at others a spiculated, surface; their size varies from that of a minute granule to a small walnut; they are usually white or grayish-white in color, but may be black; and are composed of the carbonate of lime or of a combination of the carbonate and phosphate with oxalate of lime. Coincidently with these calculi it is common to find concretions in the kidneys and gall-bladder.

Concretions composed of insoluble protein substances have also been found in the pancreatic ducts (Virchow).

The most probable causes of the formation of pancreatic calculi seem to be catarrhal conditions of the mucous membrane of the ducts and an alteration in the chemical composition of the secretion.

Whatever the cause, the obstruction, when complete, leads to retention of the secretion and the formation of retention cysts.

When the obstruction is situated at the duodenal extremity of the duct, the canal and its secondary branches are either uniformly dilated or sacculi are formed. These sacculi are round or oval, vary greatly in size, sometimes reaching the dimensions of the fist or of a child's head; they may be single, or several of them may be present, differing in size and causing irregular projections of the outer surface of the gland. When the obstruction occurs at some point in the course of the duct, the dilatations and sacculi are found only behind the point of occlusion. The small cysts contain a fluid resembling the pancreatic juice; the larger, a whitish, chalky fluid, which in old cases may contain white friable concretions composed of carbonate and phosphate of lime, and become purulent, or be stained bright red or chocolate-colored from the occurrence of hemorrhage. In such instances hæmatoidin crystals can be discovered by the microscope. The interior of the dilated ducts and of the retention cysts is lined by a single layer of thin flat cells, with irregular edges and with oval flat nuclei. The walls are thickened, and composed of superimposed layers of laminated connective tissue separated from one another by flat nucleated cells. The secreting structure of the gland undergoes atrophy from pressure, or fatty metamorphosis takes place, and, although the gland is increased in size from the presence of the cysts, its functional power is lost.

In addition to causing obstruction of the duct of Wirsung and the changes mentioned, pancreatic calculi may produce induration, atrophy, acute inflammation, or even suppuration of the surrounding glandular tissue.

SYMPTOMS AND COURSE.—The main feature is the presence in the epigastrium of a rounded, smooth, fluctuating, painless tumor. There are also indications of the absence of the pancreatic secretion from the digestive tract—notably, emaciation, general debility, and the appearance of fat in the stools. Jaundice resulting from a coincident obstruction of the bile-duct is a frequent symptom, and melituria has been noted in some cases. It is probable, too, that the passage of a calculus along the duct may give rise to pain resembling in character and distribution the pain of hepatic colic.

The duration is indefinite. Sometimes the termination is sudden from the rupture of a cyst into the peritoneal cavity or into the stomach or duodenum, with hemorrhage.

DIAGNOSIS.—The absence of pain, of tenderness, and of cachexia, together with the physical characters of the tumor, distinguishes it from carcinoma of the gland.

Though not likely to be confounded with this disease, both hydatid tumor of the liver and distension of the gall-bladder must be borne in mind in making the diagnosis of a fluctuating tumor situated in the upper third of the abdomen.

TREATMENT must be entirely symptomatic. Attention to the general health, proper regulation of the diet, and the employment of pancreatin or an infusion of calf's pancreas to supply the place of the deficient pancreatic juice, are the important steps. Attacks of pancreatic colic indicate the use of anodynes.

In two reported cases in which the cysts were very large paracentesis for the removal of the fluid contents was resorted to, and there are two cases on record in which the cysts were extirpated after abdominal section. Kulenhampff of Bremen records a case of a man, thirty-nine years of age, in whom, after a succession of severe blows upon the abdomen, a tumor appeared in the epigastrium. An exploratory incision was made, and a few ounces of pancreatic fluid evacuated by aspiration. Six days afterward the abdomen was opened, the peritoneum united to the incision, and antiseptic gauze inserted to produce adhesive inflammation between the sac and the abdominal wall. Adhesion taking place after four days, the cyst was opened, a liter of fluid evacuated, a tent inserted, and an antiseptic dressing applied. For sixteen days fluid constantly escaped in slowly diminishing quantities, and the tumor disappeared, a fistulous tract remaining. This completely closed under the use of tincture of iodine and nitrate of silver at the end of the seventh week. Thiersch opened a pancreatic cyst and evacuated three liters of chocolate-colored fluid; recovery with a fistula followed.

From a patient supposed to be suffering from ovarian dropsy Rokitansky partially extirpated a cyst connected with the tail of the pancreas; death from suppurative peritonitis occurred on the tenth day.

N. Bozeman⁴ on December 2, 1880, successfully removed from a woman forty-one years old a pancreatic cyst weighing, with its contents, twenty and a half pounds. In this instance also the operation was undertaken for the removal of a supposed ovarian tumor, the diagnosis not being established until after the abdomen was opened.

⁴ New York Medical Record, Jan. 14, 1882.

PERITONITIS.

BY ALONZO CLARK, M.D., LL.D.

Italian physicians in the later years of the seventeenth century and in the early ones of the eighteenth had acquired some knowledge of the symptoms of the disease we now call peritonitis, but known to them as inflammation of the intestines. Indeed, it is claimed by some of the admirers of Hippocrates that there are passages in his writings that indicate some knowledge of the disease. But this claim will probably be always received with many doubts as to its validity.

In confirmation of the first statement I will transcribe certain passages from Morgagni's thirty-fifth letter: In inflammation of the intestines "Albertini had observed the pulse to be low and rather weak, such as you will find it to have been in general in the foregoing letter under Nos. 9, 11, 18, and 25." He also observed the abdomen to be tense and hard, the face and eyes to have something unusual in their appearance. "Medical writers, indeed, agree in the tension of the abdomen, but they add many other symptoms, which prove beyond a doubt the intestines to be inflamed; yet they mean that evident inflammation which all may easily ascertain, and not that obscure disorder which we now speak of, and which few suspect" (gangrene of the intestines). "By the same writers it is also supposed that there is an obstinate costiveness and continual vomiting."

Morgagni refers to the assistance rendered by Albertini, Valsala, Van Swieten, Rosa, and others in elucidating this subject. It is singular, considering the clearness of his perception of the symptoms of inflammation of the intestines, that he should be so greatly confused regarding gangrene and sphacelus of the same parts. He looks on these as the result of inflammation, and when the two classes of cases are considered and compared, the result is a contrast and not a resemblance. Yet he supposes that the differences are to be accounted for by the different modes in which the same disease may be developed in different persons.

Another thing obtrudes itself on the attention in these letters: that while a number of post-mortem examinations are reported of those who had died of inflammation of the intestines, of gangrene and sphacelus of the intestines, of hepatic abscess opening into the peritoneal cavity, there is no record of finding in the abdomen anything corresponding to what is now known as the inflammatory effusions from serous membranes.

Sydenham died in 1689. I have searched his works, not for peritonitis, for the word was not in use in his day, but for some account of inflammation of the intestines or of some disease in the description of which symptoms are named that distinguish or belong to peritonitis, and with the single exception of pain the search has been fruitless.

Cullen in 1775 mentions the disease, but says that so little is known about it that he will not attempt a description of it.

Bichat died in 1802 in the thirty-eighth year of his age. I am not able at present to lay my hand on his Pathological Anatomy; I therefore quote from Chomel's article on peritonitis in the Dictionnaire de Médecine to show his claim to important studies regarding that disease: "For a long time peritonitis was confounded under the name of inflammation du bas ventre with inflammations of the abdominal viscera; and it is to Bichat belongs the merit of having proved that inflammation of the peritoneum is a disease distinct, and that it ought to be separated from enteritis, gastritis, etc., as pleurisy is separate from pneumonia. The studies of Gasc and of Laennec soon confirmed the opinion of Bichat, and assured to peritonitis the important place which it ought to occupy in all nosological tables. It has become since then a subject of numerous observations and of interesting researches regarding the causes de sa marche and the lesions it causes."

The references are not given by Chomel, but they are probably these: Laennec, Histoire des Inflammations du Peritoine, 1804; and Gasc, Dictionnaire des Sciences Méd., p. 490, 1809.

Gasc says that the twenty years next preceding his publication witnessed the first stage of the true history of peritonitis. Walther in 1786 had contributed some facts, and S. G. Vogel in 1795, but the rounding off and completing their work was left for Bichat.

Acute Diffuse Peritonitis.

MORBID ANATOMY.—The first thing that strikes the observer in the post-mortem examination of a person who has died of this disease is the tendency of the intestines to protrude through the cut made in the abdominal wall. This is produced by their dilatation generally, both small and large, by gas. No gas, under these circumstances, ever escapes from the peritoneal cavity unless there has been perforation of the alimentary canal somewhere. While the intestines are in this manner dilated, the stomach is small and usually empty.

On the surface of the intestines there will be found a layer of coagulated fibrin, often very thin and delicate, requiring a scraping of the surface of the peritoneum to demonstrate it, but commonly obvious enough, and sometimes quite abundant. This same false membrane can be found on the viscera covered by the peritoneal membrane, on its anterior extension, and most at the point of contact of one coil of the intestine with another. Incorporated with this new membrane or lying under it will often be seen blood-spots, thin, translucent, diffused, and having ill-defined boundaries.

The blood-vessels themselves are not remarkably congested. Here and there may be spots where some redness remains, and the vessels are larger than natural. But the congestion and redness, which analogy leads us to believe belong to the active stages of the disease, have in great degree disappeared after death.

The peritoneal membrane itself has hardly become thickened, certainly not in marked degree, but it has lost its lustrous surface, is, at least in parts, of an opaline color, as if it had absorbed diluted milk, and there is an effusion of serum or slight oedema on its attached surface. Whatever may be the popular opinion regarding the termination of inflammation of the bowels in mortification, whatever the opinion of the older physicians, it is safe to say that gangrene of the peritoneum has never been the result of uncomplicated, diffuse, acute peritonitis. Peritonitis from strangulation of the intestine or analogous causes is of course excepted. But in puerperal peritonitis I have noticed a fact to which I have nowhere seen an allusion. The parietal peritoneum is at two points in the abdomen but loosely attached to the wall. One of these is on the anterior wall, anterior to and a little above the iliac fossa; the other is above and below the kidney on each side of the body. In these parts I have seen the membrane forced off from its attachment to the walls, which with it made a sac containing pus. Such an abscess, if the patient live long enough, would doubtless cause the death of the membrane.

There is in almost every case of peritonitis more or less of serous effusion, commonly not seen at first on opening the abdomen, for it has sunk into the pelvis. It is transparent, of a yellowish hue, and sometimes flocculi of lymph are found in it.

Whether the inflammation of the peritoneum extends to organs covered by it is a question that has been much discussed; but it is admitted that these organs, to a shallow depth on their surface, have an unnatural color; and when it is remembered that the peritoneum is nourished by vessels not exclusively its own, but running along its attached surface, and distributed as well to the surface of the organs it covers, it is easy to admit that to a very limited depth the organs partake of the inflammatory disease. This supposition gives an easy explanation of the constipation which is so prominent a feature among the symptoms of the disease.

The manner in which the false membrane is disposed of in those who recover is an interesting question. Forty or more years ago Vogel described the process by which the new effusion became a living tissue, and the manner in which blood-corpuscles and blood-vessels were formed in it; and another author had found that the time needed to complete this vascularization was twenty days. But now Bauer and most of the German writers inform us that the coagulated fibrin is converted into fatty matter and is absorbed, and that when adhesions occur they result from the coalescence of a new formation of the connective-tissue elements built up into granules. The question, then, arises, Will the chemical constitution of fibrin permit its conversion into oil? If it will, then the further question presents itself, By what chemical action is the change effected within the body? I do not intend to discuss these questions, but propose them by way of expressing some doubt regarding the accuracy of this statement.

I have always supposed that the epithelial layer of the peritoneum was pushed off by the first of the effusions in peritonitis, and that this was one of the causes of the lustreless appearance of the membrane. This opinion I have never attempted to confirm or correct by the microscope. Bauer confounds this idea. He says: "The deposition of fibrin occurs before the endothelium presents any changes. This fibrinous effusion encloses, primarily, hardly any cellular elements, and only a few cast-off endothelial cells are to be found in it. The endothelium itself is swollen and turbid; the cell-body is increased in size; the contents are granular; multiplication of the nuclei is apparent; the cells are, in fact, in active division. In the tissue of the serous membrane itself, soon after the deposition on its surface, an accumulation of indifferent (?) cells takes place, especially around the vessels, so that the spaces between the vessels are thus completely filled up. The fixed connective-tissue corpuscles take part in the inflammatory process."

Delafield says: "If the autopsy is made within a few hours after death, we find the entire peritoneum of a bright-red color from congestion of the blood-vessels; but that is all: there is no fibrin, no serum, no pus; epithelial cells are increased in size and number." For this kind of peritonitis he proposes the term cellular. He finds it in cases of local abscess of the abdominal cavity in which inflammatory action has extended over the whole membrane, and particularly on the omentum also, in the first two days of puerperal peritonitis. "The ordinary form of acute peritonitis is attended with changes in the endothelium and fixed connective tissue, and with the production of serum, fibrin, and pus." He describes the migration of white corpuscles of the blood through the walls of capillaries to become pus-cells, and then says: "Minute examination shows that two distinct sets of changes are going on at the same time: first, a production of fibrin, serum, and pus; second, swelling and multiplication of the endothelial cells. If the inflammation is very intense, the pus and fibrin are most abundant; if milder, the changes in the endothelium are more marked."

I have said above that the epithelium is early washed off by the inflammatory effusions. In opposition—or, perhaps better, in correction—of this idea, Delafield says: "There may be a considerable amount of pus produced, and yet the layer of endothelium remains in place." "If, however, the pus and fibrin are produced in large amounts, the endothelium falls off and leaves the surface of the peritoneum bare." The connective-tissue cells of peritoneum, he says, undergo but little change in the first three days of the inflammation, "but by the seventh day these cells are marked by increase in size and number in all parts of the peritoneum."

Two or three times in my life I have met with a peculiar arrangement of the false membrane and serum of peritoneal inflammation, of which I do not remember to have seen a description. It is this: the serum is enclosed or encysted in bladders, the walls of which are the false membrane. There may be two or three layers of these bladders, one upon another, all more or less flattened, and each holding from two to six ounces of fluid. It would seem that in these cases the inflammatory activity rose and fell in its progress, early reaching the point at which coagulable lymph was effused, then falling to the stage in which serum alone escaped. This serum lifted the false membrane irregularly, so that several pools were formed. After this the inflammation returns to the fibrous exudation stage, and gives to these bladders a floor which blends with the roof at the edges, and thus makes a complete sac. Once more the inflammatory action is changed in its intensity, so that the only effusion is serum; and this serum again raises the new layer of false membrane into bladders—not always or generally in the exact position of the first series. Still again, the inflammation may be so changed as to make a fibrinous flow to this second series of bladders. I am not certain that I have seen a third series of these rare productions. They have doubtless been seen by other persons, and may have been described. I have not been an exhaustive reader on the subject, but I can well understand how they may have been called hydatids on examination of the sacs without looking at the contents. The fluid in the cysts is simply serum, with no echinococcus sacs, and then the number of these inflammatory sacs greatly exceeds the probable number of the fibrous sacs of hydatids.

Pus in large quantity is not often a product of simple acute diffusive peritonitis, although it is frequently found in that form of the disease that attends puerperal fever, septicæmia, or erysipelas. Yet I have seen it a few times. The pus is not generally pure, but is mixed with serum in different proportions, and there will be seen at the same time deposits of lymph attached to the peritoneum or scales of it floating in the fluid effusion, or both. There is reason to believe that in the cases of this class a very large proportion are fatal in the acute stages, but in the cases that live for a few weeks the pus is disposed to collect in pools and become abscesses by adhesions around them at their borders. These abscesses are disposed to find an exit from the body. In one case four abscesses that were found in this way in different parts of the abdominal cavity had each burrowed toward the umbilicus, and were actually discharging their contents at this point when I saw the case. In another case one abscess only was formed, and in four weeks it had perforated the colon. The opening was nearly an inch in diameter.

Kalantarians says, in eight examinations of the solar and hypogastric plexus in persons who had died of acute peritonitis changes which he regards as inflammatory had occurred, with subsequent opaque swelling of the nerve-cells, ultimate fatty degeneration, brown pigmentation, and atrophy. In chronic peritonitis the cells are often converted into amorphous pigment matter, with increase and sclerosis of the ganglionic connective tissue. Still, it is worthy of notice that these changes do not express themselves in symptoms in those that recover.

ETIOLOGY.—Numerous writers have expressed a doubt whether a spontaneous acute peritonitis ever occurs, or if it is ever primary its occurrence in this way is very rare. Habershon¹ has presented the case with more apparent force than any other writer. He studied the record of five hundred autopsies of peritonitis made at Guy's Hospital during twenty-five years, but he "cannot find a single case thoroughly detailed where the disease could be correctly regarded as existing solely in the peritoneal serous membrane."

¹ Medico-Chirurgical Trans., vol. xliii. p. 5.

This statement must be received with some caution. In twenty-five years the records were probably made by a number of different persons, and persons of varying views and varying capacity and judgment. It is possible that the quotation may embrace some of the changes already referred to as the consequences of peritonitis. It does embrace the cases "when inflammation of the serous membrane occurs in the course of albuminuria, pyæmia, puerperal fever, erysipelas, etc." It also includes "peritonitis caused by general nutritive changes in the system," as seen "in struma, cancer, etc.," "comprising also those cases in which the circulation of the peritoneum has been so altered by continued hyperæmia (modifying its state of growth) that very slight existing causes suffice to excite mischief, as in peritonitis with cirrhosis, disease of the heart, etc."

With these explanations the statement differs widely from what it would seem to mean without them. It is far from saying that peritonitis always follows some abdominal lesion and is caused by that lesion.

Habershon's paper was published twenty-three years ago, and during all these years the curative treatment of peritonitis, to which the paper itself gave currency, has enabled us to study our cases after recovery as well as before the sickness, and it can hardly be doubted that a much larger proportion of the cases are primary and idiopathic than either Louis or Habershon found reason to admit. That a large number are produced by preceding lesions and constitutional conditions no one will be likely to doubt.

Among the 500 post-mortem examinations of peritonitis reported by Habershon, he found preceding disease or injury recognizable in the abdominal cavity in 261. The following is his table, viz.:

From hernia, of which 19 were internal obstruction 102

From injuries or operations 35

From perforation of the stomach, ileum, cæcum and appendix, colon, etc. (other 13 mentioned with hernia, or with cæcal disease) 43

And leading to fecal abscess (2 otherwise mentioned) 17

From typhoid ulceration without perforation 5

From disease or operation on bladder and pelvis, viscera, etc. 42

From disease of the liver and gall-bladder 11

From acute disease of the colon (3 others enumerated with perforation) 3

From disease of the cæcum or appendix (9 others previously mentioned) 3

261

Habershon says that in the (his) second and third divisions of the cases the causes were as follows:

From Bright's disease 63

From pyæmia, 13; erysipelas, 5; puerperal fever, 10; with pneumonia, 3 31

From strumous disease 70

From cancerous disease 40

From hepatic disease 27

From heart disease 9

240

I have drawn thus liberally from Habershon's paper because it is the only paper that I know, in any language, founded on the analysis of a large number of cases (for five hundred post-mortem examinations is a large number for a disease no more frequent than peritonitis), in the belief that he dealt with facts and that his conclusions must be of great value. He may differ with other physicians regarding what constitutes strumous disease and in the agency of heart disease. He may have mistaken coincidence for consequence, but the paper bears the marks of honesty and good faith from the beginning to the end.

In Habershon's second division, under which he ranks the cases of peritonitis caused by "a changed condition of the blood," he ascribes 63 to albuminuria. Every physician knows how often meningitis or pericarditis or pleurisy may occur under these circumstances, especially in young persons; but, for myself, I cannot but express surprise at these figures. In one capacity or another I have been connected with large hospitals for forty-eight years, and have seen many cases of albuminuria in private practice, and can recall but few instances in which kidney disease, excepting cancer and other tumors, has terminated in peritonitis. In modification of this statement, however, it is proper to add that the hospital physician cannot know how half the diseases he treats terminate, on account of the American plan of interrupted service, and even less can he know of the mode of death in cases which he sees in consultation. Even with this admission, from my standpoint it is not easy to believe that one-eighth of the cases of peritonitis are caused by albuminuria.

The word pyæmia used by Habershon, it seems to me, ought to be replaced by septicæmia, and it has been by many of the profession. Sédillot many years ago proved that laudable pus injected into the blood-vessels of the dog produced no signs of disease, but that septic pus, so used, was followed by grave symptoms, even death. Among the author's cases thirteen were associated with the septic poison. He also found five which he thinks were independent of erysipelas. One in one hundred is a proportion hardly large enough to establish the relation of cause and effect against the chances of concurrence.

I can make a remark with reference to the inquiry by C. Dubacy in the October number (1881) of the American Journal of Medical Sciences, whether diphtheria produces peritonitis. When diphtheria became epidemic among us in 1860 or 1861 for several years, I saw a great deal of it, but did not recognize any relation between it and peritonitis.

The relations of hernia, injuries, and operations to peritonitis need no commentary.

Perforations of the alimentary canal may require some illustrative statements. These occur most frequently in the vermiform appendix of the cæcum, and are almost invariably caused by some irritating substance imprisoned in its tube. In some cases it is a seed of some fruit, as the orange or lemon; in others, a cherry-pit; in one that I remember it was a small stone, such as is sometimes found in rice; in others, a hard fecal concretion; in one, a child, a singular formation: a strawberry-seed was the centre; around this a layer of fecal matter, around the fecal matter a calcareous layer, on this, again, a fecal layer, and so on to the number of six layers, the external one being calcareous. This body was about one-fourth of an inch in diameter, and may have been years in forming. In this connection I may state, per contra, that I am informed that in a pathological museum in Boston is preserved an appendix that contains, and did contain, a large number of bird-shot, which did no mischief except to enlarge the appendix. This was from the body of a man who had shot and eaten many birds. My observation has led me to the belief that a large proportion of the cases of peritonitis occurring in children are due to perforation of the appendix.

Of the diseases of the liver producing acute diffuse peritonitis, the foremost, I think, is abscess, single or multiple. The different modes in which gall-stones may produce it may be illustrated by the following cases: (1) A lady died of acute peritonitis. At post-mortem examination a large abscess was found, bounded above by the liver, in other directions by adherent intestines; it contained nearly a quart of pus: at the bottom of the sac was a single gall-stone, very large and very black; the gall-bladder was perforated and very much shrunken. The gall-stone had caused an ulceration of the gall-bladder, but none of the intestines, in this respect differing from the process known as painless transit of a gall-stone. So the calculus caused the abscess, and the abscess caused the general peritonitis. (2) A lady between fifty and sixty years of age had an attack of gall-stone pains; she had had them before. In a few hours symptoms of peritonitis were manifest, and she died. The post-mortem examination showed the ductus cysticus was ulcerated and perforated. Two gall-stones of large size had been formed in the gall-bladder, and had been pushed forward into the duct about halfway to the common duct, leaving it enlarged as they advanced. The foremost one had caused an ulcer on the anterior or lower side of the duct, and bile had escaped, staining all the right half of the abdominal cavity, and throughout this half only the parts were covered with false membrane and stained with bile.

These cases are not so very uncommon. John Freeland of Antigua had a patient, a colored woman sixty-five years of age, who had been suffering from intermittent fever, gastric disorder, and retching. In one of the vomiting spells she experienced great pain, which, being relieved by an opiate, soon returned and was attended by tympanitic and tender abdomen. Death occurred in collapse about eight hours later. The cavity of the abdomen was found filled with blood and bile, the intestines inflamed and gangrenous in spots, and there was general peritonitis. The gall-bladder was empty; the hepatic duct was lacerated, and contained pouches in which gall-stones were encysted. One of these bags was lacerated. This laceration was surrounded by evidences of recent inflammation, and caused the general peritonitis.²

² The Medical Record, Dec. 9, 1882.

The perforations of the stomach which I have seen have been attended by little inflammation of the peritoneum. Death has followed this accident in twenty to thirty-six hours. There has been little pain, little tumefaction of the bowels, little tenderness, but a sense of sinking and a peculiar feeling at the stomach which the patient finds it difficult to describe.

The ulcers of dysentery do at times perforate all the coats of the colon, and yet do not with any uniformity cause general peritonitis; but as the destructive process approaches the outer covering the latter becomes inflamed, and lymph enough is effused to close the opening and prevent the escape of the contents of the intestine; so that, while perforation is not uncommon, I have rarely seen diffuse peritonitis accompanying dysentery.

Habershon reports 5 cases in which incomplete typhoid ulcers of the intestines caused peritonitis, and 15 from the complete perforation. I believe that the physicians of this country and those of France have found the complete perforation much the most common.

I do not remember to have seen fecal accumulation in the intestines produce peritonitis at all general. I did see, years ago, a man of middle age in whom fecal impaction in the ascending colon had caused destruction of all the layers of the abdominal wall on the right side, so that the contents of the intestine were exposed to view in a space of three inches by two. This implies that there had been peritoneal inflammation enough to seal the intestine to the abdominal wall on all the borders of this extraordinary ulcer. The man recovered in about six months, and returned to his business.

The inconsiderable operation of tapping for abdominal and ovarian dropsy has sometimes been followed by acute peritonitis. In the early part of my professional life I met with several such cases, and have witnessed the same from time to time since. These were mostly cases of dropsy from cirrhosis of the liver. Habershon found 5 such cases, and 7 in the tapping of ovarian cysts.

The rupture of ovarian cysts has produced peritonitis, but in a larger number of cases such rupture, even when the result of violence, has not led to inflammation; but the kidney secretion has been greatly augmented and the fluid absorbed, so that the rupture has been beneficial rather than harmful.

Tumors, particularly those of a malignant character, are apt to grow to the surrounding structures by adhesions the result of chronic inflammation, but now and then they provoke an acute attack which becomes general. Benign tumors may, in rare instances, do this. In one case a man died of acute peritonitis, and the examination showed that a tumor noticed before death, a very large serous cyst standing out of the left kidney, downward-forward, was the only lesion that antedated the inflammation.

Infiltration of urine, in any of the several ways in which it can reach the peritoneum, is a cause of peritonitis. Pelvic cellulitis may also be a cause, though twenty or thirty cases in succession may run a favorable course with no secondary lesions; it is still recognized as one of the occasional causes of peritonitis.

Among the rare causes of diffusive peritonitis is perforation of the intestine by lumbricoid worms. In such cases the product of the inflammatory action is apt to be sero-purulent, with but a limited amount of fibrin. E. Marcus reports such a perforation, and it was called by Peris ascaridophagie. The worms were apparently not found in the peritoneal cavity, but in the intestines. The perforation had bloodless edges, which lay quite close upon one another, as if they had been separated by a piercing action of the attenuated extremity of the parasite not eaten through.³

³ N.Y. Med. Journal, Jan. 27, 1883.

Lusk finds that certain vaginal injections excite a local peritonitis. Sentey gives the details of a case in which a midwife undertook to procure an abortion by the douche. She used a tube that was large with a spreading mouth or opening, which probably received the neck of the uterus in such a way as to prevent the return of the water. It was, in consequence, forced into the uterus and through one of the Fallopian tubes into the peritoneal cavity. By this a rapidly-fatal peritonitis was developed. He refers to two other similar cases. It would seem that this mode of procuring abortion can be frightfully misused, however safe it may be in skilful hands.

There is a word still to be said regarding the difference between peritonitis produced by wounds, operations, violence, and internal growths, or what, with a little liberty, may be called traumatic causes, and that which arises spontaneously or without recognizable cause. The first shows a tendency to limit itself to the immediate neighborhood of the injury, and more frequently does not become general; while the latter spreads pretty quickly over the whole extent of the peritoneum.

SYMPTOMS.—There is, perhaps, no grave disease whose symptomatology is more easily interpreted, in which the diagnosis is more easily made, than the average case of acute diffuse peritonitis. Yet there are obscure cases which it is difficult to recognize.

In a well-marked case the first symptom is pain. Chomel and even some later writers believe that chill precedes the pain, but to the best of my recollection it has not generally so occurred to me; and the question arises, Have they kept the symptoms of puerperal peritonitis separated from those of simple peritonitis?

The pain is first felt in a somewhat limited space in the abdomen, and pretty rapidly spreads, so that it is soon felt in every part of the bowels. It may remain greatest in the part where it first began, but there are many exceptions to this statement. As the disease advances the pain and tenderness become more marked, and the patient will try to diminish the tension of the abdominal walls by lying on his back and by bending the hip- and knee-joints, often also for the additional purpose of lifting the bedclothes from his abdomen. Often the patient will resist the physician's movement to examine his bowel with the hand. In the last few hours of life the pain ceases.

The pulse in its frequency follows the advances in the disease. At the onset it is not much accelerated, but in two or three hours it may reach 100 to 120 in the minute. Besides becoming more frequent, it becomes smaller in volume and more tense. Toward the end of a fatal case it may reach 140 to 160 in the minute and be very small.

In the early hours of peritonitis the bowels begin to swell, and percussion shows that the swelling is caused by gaseous accumulation. This increases as the disease goes on, so that in some the bowels become greatly distended—so much, indeed, as to diminish the thoracic space and interfere with the respiration. As the disease advances the tympanitic resonance may give place to dulness on percussion on the sides and lower part of the abdomen. This is due to fluid effusion.

Before the introduction of opium in the treatment of peritonitis the green vomit was a marked feature of the disease. It occurs in other conditions, but rarely, and its occurrence in this disease was so common that it was regarded as almost diagnostic. The fluid vomited is of a spinach-green color, and the color is probably derived from the bile; at least, I have examined it repeatedly for the blood-elements, and have not found them. In these days this symptom of peritonitis is not often observed.

Constipation is absolute in uncomplicated peritonitis of ordinary severity, and I believe is caused by a temporary paralysis of the muscular layer of the intestine. It has already been stated that the blood-supply of the peritoneum is through vessels whose capillaries are shared by that membrane and the tissues which it covers. Inflammatory action in the peritoneum of average severity would naturally extend to this muscular layer and render it inactive. When the inflammation abates it recovers its contractile power. Thus, the intestines become entirely insensitive to cathartic medicines. This fact is not observed in puerperal peritonitis, probably because the large share which the uterus takes of the disease may act, in some degree, as a derivative; and then, so far as I know, the muscular layer of the intestines does not undergo the change of color and appearance in the latter disease that has been observed in the former. This obstinate constipation has been noticed from the first discovery of the disease, and during forty years in the first part of this century many physicians believed that if they could overcome it their patients would recover. The present interpretation of this conviction is that if catharsis, which was very rarely effected, did precede recovery, the disease was not of a grave type—if, indeed, it was peritonitis at all.

Sometimes peritonitis occurs in the course of a diarrhoea; then the constipation is not at once established, but the symptoms of the two diseases concur for one or two days, when the diarrhoea ceases.

Abdominal respiration ceases when peritonitis is established, either because the movements of the diaphragm produce pain or because the diaphragm is partly paralyzed, as is the muscle of the intestines. Then the gaseous distension of the bowels obstructs the action of this muscle. As a clinical fact it is important, and has often helped me in a diagnosis. Another kindred fact is that all the indications of peristaltic action cease. I have a great many times placed my hand on the abdomen and patiently waited for a sensation that would be evidence of intestinal movements, but did not discover any—have placed my ear on the surface of the abdomen, and have long listened for the gurgling which is so constant in healthy bowels, and have listened in vain. In this respect my observations differ from those of Battey, who reports that he has heard the friction of the newly-made false membrane in respiration, while I concur with him in the statement that the sensation of friction can be felt by pressure of the ends of the fingers into the abdominal wall so as to produce indentation. It should be said regarding the friction sound in respiration that Battey has the support of Chomel, and he in his turn quotes Barth and Roger; so that there may be in this sign more than I have thus far found. (See case hereafter related.)

The temperature of the body is not, considering the extent of membrane involved, remarkably high. I have recently attended a most carefully-observed case in which the temperature never rose above 104° F. It falls below the temperature of health as the disease approaches a fatal termination.

From the time this disease was recognized as a separate and distinct affection the countenance has fixed the attention of writers. The face is pale and bloodless and the features pinched, and the general expression is one of anxiety and suffering. I do not remember to have seen a flushed face in peritonitis, although the degree of paleness differs in different patients.

The mind is almost always clear, unless disturbed by the medicines used in the treatment. Yet cases are recorded in which a mild, and still more rarely a violent, delirium has been noticed. Subsultus tendinum, and even convulsions, have been witnessed, but whether these symptoms belong to the peritonitis or to an accompanying uræmia has not received the attention of those who have witnessed them.

The urine is usually scanty and high-colored, but it does not often contain either albumen or casts. This statement is presumably untrue of the cases in which Bright's disease preceded the peritonitis and is supposed to be the cause of it—a variety of the disease with which I have already declared my scanty acquaintance. The urine is often voided with difficulty, and sometimes retained, so that resort to a catheter becomes necessary.

The symptoms of this disease are not invariable. In one case the inflation of the bowels is only enough to be perceptible; in another, as I have said, it becomes a distressing symptom, while in most the bowels are obstinately constipated. A case may now and then occur in which evacuations can be procured by cathartics. Pain is regarded by all physicians as the most constant symptom, and it has existed in every case that I have seen, or at least tenderness; but the late Griscom stated to me that a man once came to his office for advice in whom he suspected peritonitis; but the man asserted that he had no pain, and the doctor placed his fist on the abdominal wall and pushed backward till he was resisted by the spinal column, the man asserting that the pressure did not hurt him; yet he died the next day, the doctor declared, of peritonitis. This may be credible in view of the fact that absence of pain in puerperal peritonitis is not very uncommon. The green vomit, which was expected in all cases forty years ago, for the most part, as I have intimated, disappears under the opium treatment. There are persons in whom peritonitis does not accelerate the pulse beyond 100 beats in the minute. The pain, in rare cases, remits and recurs with some degree of regularity, in this respect resembling intestinal colic. Andral reports such a case; I have also witnessed it.

MORTALITY.—Up to the time when the opium treatment was adopted, peritonitis was a fearful word; a large proportion of those attacked by it died of it. In 1832, I began to visit hospitals as a medical student, and for eight years, at home or abroad, was almost a daily attendant. The number of recoveries of those that I saw in that time can be counted on the fingers of one hand. This may be regarded as its natural mortality, for the treatment of that day seemed to exercise little or no control over it. (Farther on this matter will be referred to again.)

DURATION.—Chomel believed that the disease might prove fatal in eighteen hours, while he regards its average duration as seven or eight days. I very much doubt whether peritonitis, not caused by perforation, violence, or surgical operation, was ever fatal in eighteen hours. I do not remember any case of shorter duration than two or three days. Then, on the other hand, the period of seven or eight days in the fatal cases appears to me too long. In the early part of my professional life I remember to have looked for death in three or four days. At present, in the fatal cases, life is prolonged to double or more than double that time. In the majority of those that recover at present the duration of the symptoms is from two days to a week; in a few they have continued fourteen days; and lately I have assisted in the treatment of a case in which there was little amelioration for forty days, and yet the peritonitis was cured.

DIAGNOSIS.—When the symptoms are fully developed there are few diseases that are more easily recognized. It is when these symptoms are slowly or irregularly manifested, or when some other disease which may account for many of the symptoms occurs with it or precedes it, that there should be any real difficulty. It is customary to regard the danger of confounding the transit of a renal or hepatic calculus with peritonitis as worthy of comment. But if the reader will turn to the articles in this work which relate to these topics, he will find the symptoms so widely different from those enumerated in this article as belonging to peritonitis that he will be surprised that this item in the diagnosis should have occupied so much room.

In a case already referred to, in which peritonitis followed gall-stone pains, the transition was so marked by the rapid acceleration of the pulse and swelling of the abdomen that each of the three physicians in attendance at once appreciated the significance of the change. A physician who resided in the country called on me to report his own case. He had a little before had a very painful affection of the abdomen which continued for three days. The pain was paroxysmal, confined to the region of the liver, back and front, for one day; after that there was some tenderness over most of the abdomen, but no tympanitis. His pulse became frequent and his temperature advanced to 103°. His physicians believed that these symptoms justified them in treating him for peritonitis. Yet his position in bed was constantly changed, and no one attitude long continued—a restlessness which never occurs in peritonitis, but is common in calculus transits. Add to this the absence of gaseous distension and of the green vomit, the paroxysmal character of the pain (though I remember one case in which peritoneal pain increased and diminished somewhat regularly, but only one), and, finally, the sudden cessation of the pain, such as often happens in calculus transit when the calculus passes into the intestine,—it is plain that his sufferings were caused by a gall-stone. The elevation of temperature was the result of a long-continued worry of the nervous system, and the abdominal tenderness came from the many times repeated contraction of the abdominal muscles which occurs in hepatic colic. And then, to make the diagnosis more complete, this gentleman, after twelve or fourteen hours of pain, became jaundiced—in the end very much so. There was no absolute constipation, and the stools were of the color of clay from the absence of bile.

The points of difference between renal colic and peritonitis are even better defined and easier recognized than those between it and hepatic colic.

In intestinal colic there may be some inflation of the bowels, and if it continues a day or two there may be some tenderness; but it is for the most part distinguished from peritonitis by the intermittent or remittent character of the pain, by its greater severity while it lasts, by its courting, rather than repulsing, pressure, by the moderate acceleration of the pulse, by no or only slight elevation of temperature (exception being made for long continuance), by the absence of the green vomit, by the absence of the fixed position of peritonitis, etc.

There does not seem to me any need of spending time to distinguish gastritis or enteritis or neuralgia from peritonitis, their symptoms are so wholly different; and if, as is said, the mucous inflammation can penetrate all the coats of the stomach or intestine, and so cause inflammation of the peritoneal layer, that is peritonitis, and will be distinguished by the proper symptoms of peritonitis.

TREATMENT.—Chomel⁴ says: "If general peritonitis is intense, it should be attacked by the most powerful therapeutic agents. One should immediately prescribe a large bleeding from the arm—from 500 to 600 grammes, for example—and repeat according to the need once or even twice in the first twenty-four hours; apply to the abdomen, and particularly to the part of it where the pain was first felt, leeches in large number—fifty, even a hundred—as the violence of the disease may demand and the strength of the patient will permit." He recommends baths, presumably tepid, and describes an apparatus by which the patient can be put into the bath and lifted out of it without pain; prescribes a fixed posture, gentle laxatives, mercurial frictions, blisters; conditionally and doubtfully, paracentesis, emetics under certain circumstances—musk, etc. under others. In the treatment of general peritonitis there is no reference to opium. The word does not occur, but it does in the treatment of peritonitis following perforation. In this condition he would, among other things, give opium à haute dose, but he does not prescribe any repetition or give any details. It is probable that the idea was obtained from Graves, whose first use of opium in this accident was in 1821, although its first publication appears to have been by Stokes in 1832.

⁴ Dictionnaire de Médecine, 1841.

Wardell,⁵ who has written the latest treatise on the disease we are considering, relies greatly on bloodletting, but falls short of Chomel in the quantity of blood he would take—would bleed, not to withdraw a certain number of ounces, but to produce certain effects. The venesection is to be followed by the application of leeches—twenty, thirty, or forty—to the abdomen; after this turpentine applications to the bowels. After depletion, he says, opium should be given at once: "two or three grains may be given in urgent cases." Vesication he calls "another of our aids." He disapproves of cathartics, but when there is accumulation in the colon would use injections. "Opium in the asthenic form is the chief agent, and Graves and Stokes were among the first physicians who gave it very largely." "Two or three grains may at first be prescribed, and a grain every four or three, or even two, hours afterward." "In perforation there is sometimes great toleration of the drug. Murchison has known so large a quantity as sixty grains to be given in three days with impunity." Mercurials, he thinks, are of doubtful efficacy. In the paragraph devoted to the treatment of puerperal peritonitis the word opium does not occur, and it is only by a very doubtful inference that we can assume that he would ever use it. Chomel makes no allusion to the use of opium in the same disease.

⁵ Reynolds's System of Medicine.

For two years (1834-36) I was connected with the New York Hospital as house-physician or in positions by which that office is reached. The treatment of acute diffuse peritonitis then and there was formulated as follows: First, a full bleeding from the arm, commonly sixteen ounces, then a dozen or more leeches to the abdomen; following this, another bleeding or not, in the discretion of the physician. Meantime, the patient would take half a grain to a grain of calomel every two hours, with a little opium "to prevent the calomel acting on the bowels," of which there was no danger, in truth. Mercurial inunction was used at the same time. The belief was that after depletion the most important thing was "to establish mercurial action in the system;" in other words, "to diminish the plasticity of the blood." Under this plan I saw one recovery in these two years.

In 1840, I went to Vermont to give a course of lectures in the Vermont Medical College, and while there was called by the physicians to see with them several cases of peritonitis. I found that they were treating the disease on the Armstrong plan; that is, bleeding freely, and then administering a full dose of opium, as they said, "to prolong the effects of the bleeding." In most cases there was a second bleeding and a second administration of opium. Leeches were also used, and irritating applications to the abdomen, and in some cases purges. I found they were getting better results than we were in New York, and I studied their cases as closely as I could, and reached the conclusion that opium was the curative agent, and that it would be safe to omit the abstraction of blood. This conviction grew in strength with every new case, and I saw, with different physicians, several cases, the disease being more prevalent among the mountains there than in the city—at least that year. The idea then formed was that to establish the narcotic effects of opium within safe limits, and continue them by repeated administration of the drug, would cure uncomplicated peritonitis—that a kind of saturation of the system with opium would be inconsistent with the progress of the inflammation, and would subdue it. There was no theory to build the treatment on, and no explanation of the action of the drug in my mind. What I saw of the action of two full doses of opium was the only foundation for the idea. I had in the course of two years after those observations in Vermont 9 cases of general acute peritonitis, 8 of which were cured. All these were reported in succession, as they occurred, to the medical societies and in my college lectures. The plan was adopted by many members of these societies and by others with whom I had opportunity of conversing on the subject, so that soon there were several—I may say many—workers in the field; and in all instances where the practitioner had the courage to carry out the treatment favorable reports were returned. Not that every case of peritonitis was cured, but the recoveries generally exceeded those that followed any other plan ever before used. No physician tried it with a proper understanding of its details, and with courage to execute them, who if living does not practise it to-day.

The treatment of puerperal peritonitis is not allotted to me, and I am very reluctent to encroach in any degree on the province of the very competent and highly-esteemed gentleman to whom that disease was assigned. But the history of the opium treatment is very incomplete without the statement I am about to make, and I trust to his generosity to forgive this encroachment; and all the more confidently because he was not at the time acquainted with the manner in which opium was first introduced into the treatment of puerperal fever.

After the curative action of the drug was demonstrated in general peritonitis, I was anxious to try it in puerperal fever, of which peritonitis forms a part. But I had no hospital and no obstetrical practice. In 1847, I was appointed one of the physicians to Bellevue Hospital, to which an obstetrical department was attached. After one or two years a single case occurred and was sent to my division. I gave her 100 grains of opium in four days, with more or less of calomel—I have forgotten how much. She recovered, but after the symptoms of puerperal fever passed away she had secondary abscesses of the lungs. These kept her ill for several weeks. At length her recovery was complete.

In 1840 there was a very fatal visitation of puerperal fever in this hospital, and on invitation of Vaché, who then had charge of the whole institution, I was a daily visitor and took notes of all the cases. It was from these notes that Vaché compiled his report of the epidemic published in the Medical and Surgical Journal. The disease was fearfully fatal, although every known mode of treatment was tried in different cases, including Brenan's plan by turpentine, but all, with one or two exceptions, with the same result. At this time the opium plan was on its trial, and I had not acquired a confidence in it that authorized me to try it in these cases. The time for it came in 1851. Then a sudden, vigorous attack occurred. One woman was sent to me in whom the disease was well advanced. I instructed my house-physician not how much opium to give, but what effects to produce by it. I found this woman dying the next day, and that she had taken only three grains of opium in three doses. In three or four days seven cases were sent me from the lying-in wards. One was returned for error in diagnosis, and six put under treatment. Having found that prudence in my house-physician was so much more conspicuous than courage, another house-officer, who combined them both, was selected to be in almost constant attendance. The instruction I gave him was in these words: "I want you to narcotize those women to within an inch of their lives." He did it, and saved every one of them. This gentleman is now known over the whole land as a learned and distinguished surgeon. I feel called upon to give his name in this connection, that he may be a witness to the facts I state, and for the admiration with which his nerve and prudence impressed me. One of these patients took first two grains, then three grains, then four, and so on till she took twelve grains of opium at a dose, the intervals being two hours. The state into which the patient was to be brought I have denominated a state of semi-narcotism. The quantity of the drug necessary to produce this state varied surprisingly in different persons. One of these women was pretty fully narcotized by four grains every two hours. She was watched with anxiety; restoratives were kept in readiness, but nothing was done but to suspend the administration of the medicine and to wait. In seven hours the consciousness was fully restored, and the improvement in her condition was wonderful. The disease seemed to be cured. But in a few hours more the symptoms recurred, and the same medicine was again given in three-grain doses, and again narcotism was produced. Taught by the experience of the day before, we waited, and when she recovered from this second narcotism her disease was completely cured. She took no more medicine of any sort. This case was very instructive, as it taught me that over certain cases of puerperal fever opium has absolute control.

From the time here referred to, so long as the obstetrical service was maintained at Bellevue Hospital, a large proportion of cases of this fever, as they occurred, were sent to my wards, and in all these years I have not lost faith in opium. This statement, however, requires an explanation. Puerperal fever is a compound disease. Its great inflammatory lesions are found in the uterus and its appendages and in the peritoneum. When the inflammation of the uterus is the dominant lesion, and is purulent, opium has little or perhaps no control over its fatality; but in the cases in which peritonitis is the ruling lesion, if begun early, it will show its power. In this connection I will only add that in private practice the drug has been perhaps more curative than in the hospital. I have seen many cases in consultation, and a decided majority have recovered. In some instances the patient has fallen into a pleasant sleep, only broken by some administration, and ending with her recovery. In one instance a very eminent physician had undertaken to treat a case by the opium plan, but he had administered the drug so timidly that for fourteen days he had done no more than hold the disease in check. After trial, I found that I could not induce him to give the drug in my way, and I asked him to give me sole charge of the patient for twenty-four hours. To this he assented, remarking, "If you cure her, doctor, I will have it announced to the profession that she was the sickest person I ever saw get well." In half the time allowed me I was able to establish the opium symptoms as given farther on, and the lady slowly recovered.

The treatment of any form of peritonitis by opium permits the use of the drug itself, or of any extract or preparation of it which contains its narcotic qualities, but it is wise to persevere with that one first chosen unless there is strong reason for a change. This caution is based on the fact that we cannot change from one to another and be certain to obtain the same drug activity. For example, we begin with laudanum, and find what it will do. We cannot take in its place the sulphate of morphia with the certainty that we can so graduate it as to get precisely the same effects. Then the quantity which will be effectual in one case may be quite inadequate for the next. The tolerance of opium in different persons varies remarkably, and probably the disease itself increases the tolerance in all. This will be illustrated by some of the details of this paper.

The drug symptoms to be produced are as follows: Subsidence or marked diminution of the pain; some or considerable tendency to sleep; contraction of the pupils; reduction of the breathing to twelve respirations in the minute; in the favorable cases a considerable reduction in the frequency of the pulse; a gentle perspiration; an itchy state of skin, or oftener of the nose; absolute inactivity of the bowels, and after a time a subsidence of the tumor and tenderness in them; some suffusion of the eyes.

Of these several signs of opiumism there is none more easily observed and none more valuable than the frequency of the respiration; and while the physician aims to reduce it to twelve in a minute, there are chances that he will see it fall to something below that. I have often counted it at seven, and in perhaps two cases it fell to seven in two minutes; and yet these cases of marked oppression from opium all recovered. In the cases in which the respiration has fallen so low there has been considerable obtuseness of the mind; but in no case except in the hospital patient already referred to have I seen unconsciousness. Then the sleepiness, so long as the patient is easily awakened, is wholly within the limits of safety.

As to the quantity of opium to be given, I have known two grains every two hours do the work, and in other cases many times this quantity was necessary to produce this condition of semi-narcotism. The plan is to begin with a dose that is safe—say two or three grains of opium or its equivalent of sulphate of morphia—and in two hours notice its effects. If any of the opium symptoms have appeared, repeat the dose; if none, increase by one grain, and so on at intervals of two hours till the degree of tolerance in the patient is ascertained. After that the case can be treated by a diminished occupation of the physician's time—two or three visits a day. The dose is to be increased if the opium symptoms diminish before the disease yields, but always to be diminished or discontinued if narcotism is approaching. The duration of the treatment will be sometimes no more than two or three days; it may be a week, or even a fortnight, and in one case already mentioned the symptoms persisted mildly for forty days, and then yielded. In this case the medicine used was the sulphate of morphia, and the enormous dose reached by steady and graduated increase was one grain and a quarter every forty minutes in a boy ten years old.

In some puerperal cases the doses have been so large as to require witnesses to make the statement of them credible, and the administration of them criminal had not the effect of each dose been carefully studied and the amount of each measured by the action or inadequate action of the next preceding one.

Here are the doses given a woman who fell sick October 13, 1857; the record was made by C. H. Rawson during the treatment, and was kindly given me two or three years ago: On the first appearance of her disease, while the diagnosis was uncertain, 10 grains of Dover's powder gave her a quiet night. The next day the disease was more manifest, and she took of Magendie's solution (2 grains of sulphate of morphine to a drachm of water) x minims every hour; growing worse, at night she took xxx minims every hour; the next day, xl minims every hour, and no change of symptoms. She took in twenty-four hours 32 grains of sulphate of morphia; slept, but was awakened by the slightest noise. On the fourth day 3¹/3 drachms of the solution, and opium as follows: at 4 P.M., 3 gr.; at 5 P.M., 4 gr.; at 6 P.M., 5 gr.; at 7 P.M., 6 gr., and 6 gr. hourly after 7 P.M. Sleep light. Fifth day, in twenty-six hours took in opium and morphine the equivalent of 208 gr. of opium. The sixth day, 212 gr. of opium; on the seventh day, 221 gr. of opium; on the eighth, 224 gr.; on the ninth, the same quantity; on the tenth, the same; on the eleventh, 247 gr., pulse subsiding; on the twelfth, 261 gr., other symptoms better; on the thirteenth, 144 gr.; fourteenth day, 4 gr. hourly; slept for the first time heavily, all other symptoms improving, bowels moved freely, ate well, tympanites subsiding; fifteenth day, 1 gr. of opium every two hours, and at night the last dose. Recovery was complete. The woman denied the opium habit, and the medicines were tested by the apothecary. Such doses can only find their justification in the demonstrated fact that smaller doses will not produce the degree of narcotism desired.

In Keating's edition of Ramsbotham's Midwifery a case is reported by myself in which a woman, by pretty rapidly increasing doses, reached forty-eight grain doses of opium, with the effect of curing her disease and substituting a temporary active delirium.

A word of caution is probably necessary regarding the use of opium in high doses when peritonitis and Bright's disease coexist. I have already said that I have but scanty personal knowledge of such a concurrence, but in Bright's disease alone I have known a large, non-heroic dose of an opiate fatal. For example: A young man had a felon on his finger, and did not sleep, so great was his pain. His physician prescribed 40 drops of laudanum at bedtime. Not sleeping on this, he took another portion of 40 drops, and in the morning he was found in a comatose condition, and in the course of the day he died. A post-mortem examination revealed Bright's disease, which was not before suspected. A woman took half a grain of the sulphate of morphine—for what reason I do not know. I was called to see her when she was in a semi-comatose state. The time between my seeing her and that of taking the morphine was fourteen or fifteen hours; its removal from the body was therefore hopeless. Her limbs were swollen with oedema, and the urine contained albumen and casts. Although the usual means of opposing the poisonous effects of opium were resorted to, they were of little use, and the patient died in the course of the day. These are selected from a considerable number of similar cases that show a similarity in their action on the brain of opium and urea. It seems that opium precipitates the uræmic coma, yet the coma produced by these agents combined is not so profound as that produced by opium alone. There is in it some movement of the limbs or body or some imperfect utterances, yet it seems to be more fatal than the coma of opium unaided. Notwithstanding all this, I have met with several cases of cardiac disease combined with Bright's—perhaps I should say many—in which half a grain of morphia sulphate has been taken every night to procure sleep with only beneficial results. This has been observed several times when physicians have been the patients.