Treatment. Lavage-carbonic acid water-lime water-vichy.Keep patient perfectly quiet until acute symptoms have disappeared. Dieting is the most important part of treatment. Patients should have no solid food, but plenty of milk if tolerated, often and in small quantities, and boiled; beef tea; soft boiled eggs; scraped beef and pancreatine per rectum. Among drugs the speaker mentioned acetate of lead nitrate of silver, morphine, creosote, tincture of iodine, etc. If hoematemesis actually occurs, give ice to suck and feed per rectum for a couple of days. After this begin with milk and lime water and increase gradually. Afterwards change the diet to soft bread and milk, and further to pounded chicken, custard, eggs and the ordinary diet. A sulphate of iron and magnesia mixture three times a day in purgative doses is not bad. (Saundby). (Saundby). Sulphate of soda or carlsbad salts remove all remains of food from stomach, and help the anemia and constipation. (Ziemssen and Leube.

Wm. H. Palmer, the President, mentioned a case of rupture of the duodenum seen by him in his capacity of Medical Examiner to the City of Providence.

Frank L. Day read a paper on DISEASES OF THE PANCReas.

The author of the paper wished to have a case of fatal pancreatic hæmorrhage put on record and thought it might be profitable to review this rather uncommon disease. The author had attended the case jointly with H. G. Miller and Robert F. Noyes as consultant, both of Providence. Prof. Frederick C. Shattuck and later Charles F. Folsom, both of Boston, had also seen the case in consultation.

The patient was a physician, forty-nine years old, with nervous temperament. Father died at fifty-from heart disease, it was thought. Patient had had indigestion for years, aggravated by the irregularities of a busy physician's life. Had dieted for years. Had an attack of syncope some three years ago while traveling abroad, from which he recovered after weeks of weakness and debility. Had been in poor health for a year previous to last illness. Worked hard and could only sleep by the aid of stimulants. Had had much pain and distress in epigastrium for months, which was relieved by chloroform externally and internally. Was somewhat addicted to the use of cocaine applied to the nose.

In the spring of 1892 he was very weak and stimulants did not stimulate. On April 6th he resolved to stop work and rest. Uncontrollable vomiting would set in at times, consisting of food, some mucus and greenish liquid-never hoematemesis. The painful spot in epigastrium grew more tender and he could not bear pressure over it.

The pain was also felt in the right hypochondrium. For months he had had much tenderness over the right lower ribs, corresponding to

the hepatic region, which he had considered due to peri-hepatitis. Was rapidly growing weaker and delirious at times, with attacks of syncope. Pulse usually sub-normal but quicker at times and very weak. Temperature never exceeded 99° F. Bowels very constipated. Stools mostly clay-colored; sometimes darker; at one time there was jaundice. Conjunctive and skin had a muddy color most of the time. Could bear neither sour or sweet food. Alkalies, codeia and other things would relieve the stomach. After vomiting had been controlled by opium in suppositories he retained food better.

Dr. Shattuck saw him in consultation at this time and concurred in the diagnosis of gastro-duodenitis. After this he gained some, and on the 19th of May the speaker removed some painful glands from the maxilla under choloroform narcosis. He recovered promptly from this operation. Remained better for two weeks, with occasional vomiting spells and was never entirely free from localized pain; bowels always constipated. First week in June pain got worse and he relieved it with chloroform. At 6 A. M., June 11th, he had a sudden attack of severe vomiting with agonizing pain over epigastrium.

After this he had collapse, was semi-conscious and perspiring; had a dusky color, cold extremities, very low temperature and high pulse (120). Much pain over usual place, but no evidence of tumor. Collapse increased and death followed at 10:30 p. m., sixteen and one-half hours after first attack.

Post partem examination (eighteen hours after death). Nothing abnormal about heart, lungs, pleura, spleen, liver or kindeys. Stomach was enlarged, with thin walls and adherent mucus; in gall-bladder one small concretion of inspissated bile was found; two others were firmly lodged in duodenal extremity of the common duct, the lumen of which they almost completely filled. The pancreas was enlarged in every direction, one inch longer than usual and double the ordinary diameter. The organ was very hard and dense and filled with a light chocolate colored liquid; the body and tail of the organ approaching a chocolate color. Dark areas were found everywhere on the organ; on section they proved to be conical shaped, suggesting altered blood, from their look and color.

Small pea like nodules were also found, of light gray color, very hard to the knife and feel. Microscopical examination eight hours afterwards by Professor Fitz of Boston showed evidence of "hæmorrhagic infiltration, with areas of fat necrosis," which was also coincided in by Prof. Whitney of Harvard University. The author regretted that the specimen. did not reach Prof. Fitz sooner, for if traces of blood pigment had been found, all doubt would have been positively settled. He said further that there is very little written on this disease.

After going over the anatomy and physiology of the organ he thought it was not improbable that pancreatitis is more common than has been suspected, as for instance in many obstinate cases of impaired digestion, gastric and duodenal. The author afterwards recalled the symptoms of the disease and its diagnosis in a very interesting manner. He felt certain that the case in question was a case of pancreatic hæmorrhage and thought it dated back to the attack three years ago.

DISCUSSION BY PROF. R. H. FITZ, OF HARVARD MEDICAL SCHOOL.

The speaker thought the case confirmed the relation between pancreatitis and gall-stones, which seems analogous to that between gallstones and cholangitis, inspissated foeces and appendicitis. Most recent investigations show that suppurative cholangitis cannot occur from gall-stones alone, but from gall-stones and bacteria, especially the colon-bacillus. Drs. Ernst and Jackson had recently isolated four cases of bacteria in hoemorrhagic pancreatitis, and Prof. Welch had found pure cultures of the colon-bacillus in foci of fat necrosis. Many cases had been published recently, but very little light had been thrown on the subject. A case of traumatic origin was cited from the service of the Massachusetts General Hospital, and the familiar fat necrosis of the pancreas had pointed strongly to probable affection of the pancreas. A case reported in "Osler's Practice of Medicine" was also referred to, where a patient was operated on at the Johns Hopkins Hospital for supposed acute intestinal obstruction, but instead, a dense indurated mass was found about the pancreas, with foci of fat necrosis in the mesentery and omentum.

This case proved to be quite remarkable because it was the first one that ever recovered from laparotomy, done for probable acute pancreatitis. The frequent occurrence of multiple fat necrosis associated with hæmorrhagic and gangrenous pancreatitis, had satisfied the author that the former was the cause of the latter in opposition to the view of Balser, who maintains that fat necrosis is the cause of pancreatitis. The foci of necrosis found in the case cited by the speaker from Massachusetts General Hospital were directly suggestive of escape of fluids. from the pancreas and their causing a chemical change. Langerhan's explanation was referred to, that the necrotic process begins with decomposition of the neutral fat in the cells into fatty acids, which afterwards combine with lime, and go to make up the necrotic nodules. Such was the physiological function of the pancreatic juice in the intestine, namely: to bring about a decomposition of neutral fat, and why could not the same process take place elsewhere, outside of the intestine, and bring about necrosis in this manner? Ernst, Jackson and Welch's observations about bacteria and their presence in areas of fat necrosis

might, perhaps, suggest another cause for the production of the crystals. The speaker thought it was an established fact that intestinal bacteria and pancreatic juice did decompose neutral fats into acidular crystals, like those seen in fat necrosis.

Balser had found that fat necrosis occurred also in swine, and were surrounded by inflamed tissue sometimes. An organism resembling actinomyces-had been found by him in the nodules, and from this fact he (Balser) argued that fat necrosis was an independent, possibly infectious disease.

Robert F. Noyes followed, saying he had never seen any case of the disease. The speaker cited William Lawrence's observations in 1831, that: "Morbid changes of all kinds are rare in the pancreas, lachrymal and salivary glands. It seems doubtful whether modern pathological anatomists who have had the most extensive opportunities have ever seen inflammation of this gland." Text books did not contain much about the disease; occasionally a case was reported in medical journals. The speaker mentioned Prof. R. H. Fitz as one of the foremost investigators in this line of thought, and his (Prof. Fitz) forcible presentation of this subject in the Middleton Goldsmith Lectures (1889), had been the chief cause of the admission by the profession of such things as acute, chronic and suppurative inflammation; abscess, fat-necrosis and apoplexies in the pancreas were a reality. These lectures had brought out such editorials as that of the Medical Record for March, 1890, and had set forth these pathological changes in the pancreas and neighboring organs as had never been set forth before, and Prof. Fitz's labors had clearly indicated that the pancreas is the site of disease very often. Clinical experience had demonstrated that the disease is more often found in men than in women, and most common after middle age. Heredity, syphilis, pregnancy, high living, excessive drinking and disturbed menstrual functions were important etiological factors.

Sialorrhoea is often met with in pancreatic disease, but is not diagnostic. A pyrosis, or excessive salivation is not necessarily connected with pancreatic disease, but occurs also in gastric disease.

Free fat in the fecal dejection is, however, a valuable sign of pancreatic disease, and is found whether constipation or diarrhoea is present or not. This free fat often exceeds that ingested and is also found when all fats have been excluded from the diet. In estimating the value of this sign one must not lose sight of the fact that an excessive amount of fats cannot be absorbed rapidly enough by the small intestines, but may be ejected with the forces. A deranged pancreatic secretion is further suggested by the inability to digest oleaginous, saccharine and amylaceous varieties of food.

Free fat in the urine should not be confounded with chylous urine.

If the fat is found in an emulsion in the urine it indicates pancreatic activity; if found in a free state it points to impaired physiological function of the pancreatic juice. Glycosuria sometimes precedes or follows pancreatic derangement. Diabitis has been produced by injury to the pancreas in animals (Lancereaux); diabitis is rather dependent upon disturbances of the solar plexus, however, and the presence of glycosuria in pancreatic disease must be referred to pressure on the solar plexus. Pain in pancreatic disease may be due to peritoneal inflammation, and is then constant, and usually situated between the ensiform cartilage and the umbilicus. It may also be paroxysmal and very severe, like hepatic colic, and probably due to pressure on the solar plexus. In pancreatic apoplexy the pain is spoken of as agonizing, severe and followed by collapse. Calculi are commonly found in the pancreatic ducts, and the sudden paroxysmal pain often found in the epigastric region and associated with hepatic colic or gastralgia, without jaundice, may be due to the passage of pancreatic calculi.

It is, however, difficult to distinguish oedema of the lower extremities, jaundice, ascites, stenosis of pylorus, intestinal hemorrhage caused by pressure on the common bile-duct, the vena porta, vena cava inferior or pylorus, from pressure of the pancreas or from the pressure of some other organ.

L. F. C. Garvin-What was the cause of the immediate collapse; hoemorrhage?

Prof. Fitz-Haemorrhage producing paralysis by irritating plexus.
Wm. A. Gorton-Diabitis?

Prof. Fitz-Extirpation of pancreas in dog has produced diabitis.
Geo. F. Keene---Any chills?

Prof. Fitz-Not very common; recurrent chills do not occur.
Frank L. Day-Do we not have chills in suppurative pancreatitis.
Prof. Fitz-Sometimes.

Wm. A. Gorton wished to express his thanks to Prof. Fitz for bringing up this important and interesting subject. We will probably know more about it soon. We did not use to examine pancreas in New York when I was a student.

Prof. Fitz spoke of the treatment. Abstain from much treatment if pancreatic disease is diagnosed. Intestinal obstruction has been mistaken for this disease and only one case has ever recovered where laparatomy was resorted to. Do not perform laparatomy too early.

C. O'Leary asked, whether a physician in certifying to the cause of death would be warranted in stating that death was caused especially by disease of the pancreas, as distinctly as he can state that pneumonia is the cause of death, and whether disease of the pancreas is found to exist not complicated with disease of the liver and surrounding organs?