of the case, or the patient's own story of his present trouble. Let the patient tell in his own. words the story of his present trouble, take note of the important points and then check up these points and see whether or not the physical findings fit the history of the case. Don't try to lead the patient by asking what our legal friends term "leading questions"; in other words, approach each case with an open verdict, and listen and weigh the evidence in every case. The early symptomatology of chronic cholecystitis is charcterized by a long continued indigestion and flatulency, belching, sometimes vomiting and more or less intestinal indigestion. This stage is followed by a second stage, which may be characterized by the movement of calcali or colicky pains. It is during this stage that the colic is often brought on by indiscretions in diet. The attacks frequently occur at night and last but a few hours, but may last for several days. The ages of this second stage vary from 30 to 50 years of age. The final stage of cholecystitis is characterized by intense pain, often jaundice, and dangerous complications, such as empyema and gangrene of the gall bladder, obstruction of the common duct, acute pancreatitis, carcinoma, and intestinal obstruction from stones. These complications usually occur after 45 years of age, but, of course, may occur much earlier. The pain is usually referred to the right hypochondrium. Vomiting after meals and jaundice are present in about 41 per cent of the cases. In the diagnosis of gall stone disease, or cholecystitis, the x-ray should be considered only a support to the clinical history, as in the great majority of cases the diagnosis of gall stones cannot be made by the x-ray alone, and the majority of diagnoses of cholecystitis can and should be made before the occurrence of gall stones. It is estimated that when gall stones are present, the x-ray will reveal them in about 50 per cent of the cases. In the differential diagnosis of cholecystitis those diseases which must be excluded are appendicitis, stone in the kidney, recurrent chills and fever of ague and in the beginning stages of gall bladder disease and tuberculosis. Cholecystitis can be differentiated from tuberculosis by first, the history of the case; second, the lack of the tubercle bacillis in the sputum, and third, the absence of any great reduction of weight. In malaria the differential diagnosis will be made by the leukocyte count; the septic cholangeitis always produces a leukocytosis. In appendicitis the tenderness is located over McBurney's point. In the case of the kidney stone, the pain and tenderness are located over the affected kidney, radiating downward along the course of the ureter. The soreness following an attack of colic, due to the movement of a stone in the kidney or ureter rapidly disappears after the cessation of pain, and the attack is practically always followed by blood in the urine for a time. The soreness following the gall bladder attack will last much longer than the soreness following a case of stone in the kidney or ureter. In the diagnosis and treatment of all cases of cholecystitis we should not wait for jaundice and cholelithiasis to make their appearance nor does it matter so far as the treatment is concerned whether there are present in the gall bladder, gall stones or a cholecystitis. The treatment in both cases is purely surgical, and an operation is indicated whether the disease has progressed to stone formation or not. Now let us inquire into the cause of gall duct diseases. This pathology is brought about in every case by infection. The first stage of gall duct diseases is always an infection, followed by stagnation of the bile, which stagnation leads to stone formation; these stones cause the colic which results in the jaundice, so you see the chain of events, one following upon the other from the infection to the jaundice. The majority of observers believe that because of the failure in the functions of the liver, all the bacteria which the liver receives through the portal circulation are not destroyed, and that living organisms gain entrance to the gall bladder by direct invasion of the mucous membrane. This direct route, however, is probably the less frequent route of infection. According to Rosenow, the greater number of infected gall bladders results from bacteria brought through the capillary circulation of the walls of the gall bladder. This fact is borne out by cultures taken from the contents of the gall bladder, and found to be sterile, while a portion of the same gall bladder ground up would yield colonies of bacteria, which when injected into the blood stream of animals will produce acute inflammation of the gall bladder in 80 per cent of them. This would seem to prove that the infecting agent reaches the gall blad a third. der by at least two different routes, and probably der or bile passages, a great advantage will be derived from the use of a sandbag or air cushion of considerable thickness, placed at or a little above the level of the liver. In addition to this, it will be found convenient to so tilt the table as to raise the head of the patient from 4 to 6 inches; by these procedures the intestines fall away from the field of operation, and the liver is made to present itself forward, and the gall bladder and gall ducts become more accessible to the operator. As to the incision of choice, I shall have nothing to say, there being almost as many incisions, or modifications of the classic incisions as there are operators. This much, however, I will say: it is advisable whatever incision may be used that it be of sufficient length to enable the operator to work with freedom and dispatch. Many operators and investigators claim that jaundice has no appreciable effect upon the coagulation time of the blood, and therefore jaundice does not form a contrindication to operation. As to whether the gall bladder should be removed or not in a given case must be left to the discretion of the operator. His decision in the matter will depend upon the general condition of the patient, the power to withstand the operation, the condition of the associated organs, namely, stomach, duodenum and pancreas. These factors, along with the experience of the operator, should have more weight in arriving at the decision whether or not to remove the gall bladder than the examples or practices of the more eminent surgeons in this field of work. Now let me illustrate just what I mean by the foregoing statement. Almost all gall stones are formed in the gall bladder. Ninety-eight per cent of all gall stones by weight is cholesterin, which is the product of the epithelial cells lining the gall bladder. In the formative stage gall stones are soft and putty like, and then they begin to crystallize, just as maple syrup crystallizes, and accumulate in the gall bladder. Gall stones differ from urinary calculi, which calculi are many times the result of precipitation of urinary salts. Gall stones begin to produce trouble, first, and most commonly, in the gall bladder. One has pain in the gall bladder region, and this pain may be recurrent for years. Secondly, they cause trouble when they begin to pass through the cystic duct, which gives rise to typical colic without jaundice. Colic is the result of a foreign body passing through a living tube. When the stone has progressed far enough from the cystic to the common duct, then, for the first time jaundice occurs, and if the stone is large enough to produce obstruction of the common duct, the jaundice will continue as long as the stone is in motion and the obstruction remains. If the stone is small enough to allow some bile to pass around it the icterus will slowly subside to a mild bronze color, which may be present for 2 to even 10 years, or until the stone begins to move again, and again obstructs the common duct. Cholelithic jaundice never occurs unless the stone gets into the common duct. Every gall stone is primarily an infection sequence, these foreign bodies by their presence in a more or less infected zone stimulate the production of cholesterin, which in turn keeps increasing the number of gall stones. These gall stones do not cause colic until they begin to pass through the duct; after reaching the common duct the stone may or may not produce jaundice. If the jaundice is not preceded by colic, the chances are 96 per cent that it is not jaundice due to cholelith. If, on the other hand, the jaundice was preceded by colic or recurrent colicky pains the chances are 90 per cent that it is a cholelithic jaundice. Now as to the treatment of gall duct diseases: The treatment in every case of gall duct disease, whether it is in the beginning or final stages, is surgical. Every case of gall duct disease is a surgical case. In all operations on the gall blad Mrs. M., aged 68 years, operated on January, 1919, with only drainage of the gall bladder. In this case we found the general condition of the patient poor and unable to withstand a long, tedious operation; her trouble was of long duration, and many adhesions between the colon and stomach and liver obstructed a free and easy access to the gall bladder. Judging from the pathological condition of the gall bladder only, this gall bladder should have been removed, but we satisfied ourselves, and the after course of the patient proved the wisdom of the decision, that it was wise to only drain. In fact, my experience received at Deaver's clinic some two years ago, stood me in good stead in this case. In his clinic, Deaver drains all complicated cases, and the mortality of his drainage cases is apparently higher than his cholecystectomys. As I do not wish to make this paper a compilation, I shall not enter into a discussion of the relative values of cholecystectomy and cholocystostomy; however, it is my belief that many gall bladders are drained when the patient would have benefited by their removal, and I might also add that many cases of cholecystosomy fail to be relieved, not because the gall bladder was not removed but because the drainage tube was removed too soon. We have come to believe that the drainage tube should be left in the gall bladder for a period of at least three weeks. As to the method of choice of removing a gall bladder, whether one begins at the fundus or neck, is of little importance, the important thing being the complete removal of the gall bladder and cystic duct down to the common duct, and the patient, thorough search for stones in the common duct. The removal of the gall bladder does not prevent the drainage of the common duct, although it is a safer procedure if one wishes to establish thorough drainage of the common duct, and wishes to relieve the pressure on the pancreatic duct, to leave the gall bladder in place, and drain through this structure. At this point, it might be well to emphasize one of the dangers of removing the gall bladder, and that is injury to the common duct. Again, let me illustrate this by a mishap that occurred to me some time ago. At the operation the gall bladder was removed by our usual method, the incision closed with iodoform gauze drainage down to the stump of the cystic duct, near where it joins the common duct. This gauze was removed on the second day following the operation, and all went well until about the tenth day. The patient at this time developed an intense jaundice, which we were unable to account for, as we had examined the common duct and were morally certain that no stones had been overlooked in this structure. In about 24 hours bile began to escape from the incision and we then saw the cause of the jaundice. The jaundice cleared up in due time, but there was a biliary fistula that would not heal. At the second operation we found a considerable opening in the common duct above where the cystic duct had entered. This opening was undoubtedly caused by some injury to the common duct at the previous operation. This defect was closed over a small T-shaped drainage tube, which tube was removed at the end of 3 weeks, leaving a sinus that closed in a few days. After the removal of the gall bladder the ducts hypertrophy and overcome the action of Archibald's muscle and keep the bile moving into the intestines as it is secreted by the liver. There is almost always a dilatation of the hepatic and common ducts following the removal of the gall bladder. There seems to be no ill effects from this continuous flow of bile into the intestines. In closing, let me earnestly urge you as surgeons to do all within your power to destroy the false notion among the laity and some physicians that gall stones are the essential factors in calling for surgery of cholecystic diseases. It would be a great step forward if it were understood generally that the infection is the major issue in this, the greatest of the upper abdominal troubles. There would be less difficulty for the surgeon and fewer cases reaching the stage where a cholecystectomy is necessary, and a great saving in the surgical mortality of these cases. Upon these points all surgeons are agreed, and it is our duty to teach our medical brethren this very important lesson. Diseases of the biliary passages are essentially surgical and not medical, and the most common cause of failure to cure or relieve your patient is late operation. Until this fact has impressed itself upon the physicians, as well as upon the laity, we cannot expect to improve our percentages of cures of cholecystic diseases. Let us establish the fact that cholecystic diseases are surgical, first, last and always, until it becomes as well known by the laity as is the fact that appendicitis means operation. When we have succeeded in making cholecystic diseases mean operation, then there is no excuse for a failure to improve our percentage of cures. EPIDEMIC ENCEPHALITIS* S. S. WINNER, M. D., (LETHARGIC ENCEPHALITIS-SLEEPING SICKNESS-NONA.) The first case of epidemic encephalitis to occurin the State of Illinois, as far as we can ascertain Read at the Sixty-ninth Annual Meeting of the Illinois State Medical Society, at Peoria, May 22, 1919. at the present time, appeared some time in the latter part of October, 1918, in the vicinity of the Great Lakes Naval Training Station, with a history strongly suggestive of epidemic encephalitis, although it was not diagnosed as such at the time by the attending physician. This case, from the data obtained, was mild in character and recovered in a comparatively short time. It is significant that this very locality was the very first to be affected by the influenza epidemic in September, 1918. The first definite case to be reported to the State Department of Public Health of Illinois, and diagnosed as epidemic encephalitis by Ticken of Chicago, occurred in that city in November, 1918, Ticken reporting 14 cases of this disease up to the end of February, 1919, eleven of whom died; Bassoe 7, four of whom died, and Elliott 4, two of whom had died, for the same period. In all there had been reported, up to the time of the compilation of this paper, some 90 cases in the State. There have been undoubtedly a number of cases, most of them of a mild character, that occurred in this state since the fall of 1918, that have not been reported, the true nature of the disease not having been recognized. I am led to make this statement from the information received from physicians in the various parts of the State. Before proceeding with an analysis of the cases that occurred in Illinois, I will endeavor to present a brief summary of the literature on the subject, with some of the conclusions arrived at by investigators here and abroad: Briefly mentioning the "sleeping sickness" in connection with the grippe epidemic in 1718, recorded by Camerarus, the "Coma Somnolentum" of the grippe epidemic recorded by Lecoque de la Cloture in 1768, and the "Catarrhal Fever with somnolence," recorded by Ozanann as having occurred in Germany in 1745, in Lyons in 1800 and in Milan in 1802, all of which records are indistinctive, and may or may not have been the morbid entity known as epidemic encephalitis we are dealing with at the present time, we pass on to the period of the fairly well recorded epidemic of 1889-1890, when "Nona" made its appearance first in Italy, then in Hungary, and thereafter in Germany and France, following the course and sequence of the influenza epidemic. The disease, as described by the writers of that period, followed in the wake of the grippe, was characterized by somnolence and paralysis of some of the cranial nerves, with most of the cases running a very mild course. In an article read before the Chicago Medical Society in 1891, Archibald Church, analyzing the nervous complications and sequelae of the epidemic in this country does not mention any cases as having occurred here, so we may take it for granted that prior to 1918 the morbid entity known as epidemic encephalitis had not been recognized or encountered here. At a meeting of the Vienna Medical Society of Psychiatry, held in April, 1917, von Economo described a group of cases of a disease occurring in an epidemic form at that time in Austria, and to which he applied the term of "Encephalitis Lethargica." From the data presented by von Economo, it is evident that the disease occurred in epidemic form in Vienna in the winter of 1916-1917. A discussion concerning the same subject was held the following month in Paris by the Academy of Medicine, and Prof. Netter there expressed the opinion that the disease was not a form of acute poliomyelitis. A large number of case reports and discussions appear in the transactions of the French Medical Societies at this time. The first case to be noted in England occurred February 11, 1918, the largest number of cases in one week being 18, which occurred in the last week of April. The number of cases thereafter, and the epidemic, which never attained large proportions, came, at least temporarily, to an end in June. The disease had been made reportable in England, under the name of lethargic encephalitis. In the early part of 1918, the local government board, with the assistance of the Medical Research Committee, instituted clinical and pathological investigations, the results being published by H. M. Stationery Office, London. The following data are abstracted from a review of the Government reports, published in a recent number of the British Medical Journal: The disease is an acute affection, due to a specific virus, which, like that of acute poliomyelitis, probably finds entrance through the nasopharynx and which, like it, has a special affinity for the nervous system, though for different areas and elements. Pathologically, lethargic encephalitis belongs to the class of polioencephalitic diseases, which are inflammatory in nature. Bacteriological investigations have not yielded any results. Clinically, the disease is a general infectious disease, characterized by manifestations originating in the central nervous system, of which the most fre quent and characteristic are the progressive lethargy, and lesions in and about the nuclei of the third pair of cranial nerves. Although a rise of temperature was not observed in all the 164 cases of which notes were obtained, there seems to be little doubt, that there always is a certain amount of fever in an early stage, although occasionally it may not be observed for several days after the onset of the symptoms. The common range is between 101-102, but temperature up to 104 are not uncommon. The pyrexia usually lasts from 2 to 5 days, but may continue for ten or even 14 days. It may fall gradually or suddenly with oscillations. Subnormal temperatures have been noted. A prodromal period is described, the symptoms being the early stage of the developed disease. The cardinal symptoms given are lethargy, masklike face, facial paralysis, catalepsy, rigidity of muscles, opthalmoplegia, ptosis, unilateral or bilateral and febrile reaction. Dr. McNalty of the committee recognized seven groups of cases: (1) Clinical affections of the third pair of cranial nerves. (2) Affections of the brain stem and bulb. (3) Affections of the long tracts. (4) The ataxic types. (5) Affections of the cerebral cortex. (6) Cases with evidence of spinal cord involvement; and (7) the polyneuritic type in which affection of the peripheral nerves is suspected. Among 168 cases 37 deaths were recorded. The duration of the stupor is very variable, occasionally it lasts two to three days, more often two to five weeks, and in one case, which eventually recovered, eight weeks. Certain manifestations have persisted after three months, like alterations in the mental condition, persistent cranial palsy (nerves), the appearance of paralysis, apparently of spinal cord origin, and athetosis. S. A. Kinnier Wilson, writing in the London Lancet of July 6, 1918, reports 13 cases, seven of which are related in his paper, two with necropsies. The clinical features are thus summarized by Wilson: Epidemic encephalitis is an acute nervous disease characterized by both general and localizing symptoms, in a minority of cases the latter not being prominent. The sexes are affected indifferently and there is no age incidence specially. Its onset is relatively acute, the conditions being established within a few days, occasionally it opens in a fulminant fashion. General symptoms consist of apathy, lethargy, drowsiness, pathological sleep, stupor, absence of initiative in one form or another being prominent from the onset and throughout at least the earlier stages of the disease. Some times the lethargy appears later in the disease; occasionally, it is not a noticeable feature. Wilson considers this epidemic in every way analagous to the one which occurred in Vienna in 1917, and the similar epidemic in Paris in the spring of 1918, as described by Netter, from a pathological as well as clinical view. The French cases were reported exhaustively by Netter, Saint-Martin, Lhermitte, Chauffara and Bernard and Paul Sainton, with two necropsies by P. Marie and C. Tretiakoff. Paul Sainton gives the following definition of the disease: A toxic, infectious, epidemic syndrome, characterized clinically by a triad of symptoms, consisting of somnolence, palsies of the motor nerves of the eyeball, and a febrile state, and anatomically by a more or less diffuse encephalitis, situated chiefly in the gray matter of the midbrain. In addition to the nerves supplying the eyeball the facial nerves are frequently involved, and sometimes the motor branch of the fifth and hypoglossal. There may be also analgesia of the face from involvement of the sensory portion of the fifth. Sainton does not consider this a new disease, nor a form of poliomyelitis, nor an entirely independent disease. He, too, identifies it with the "Nona" described during the great epidemic of 1890 and he considers it very significant that the disease has reappeared during a new pandemic of influenza. Although admitting that positive evidence, especially of a bacteriological nature, is lacking, he is inclined to look upon this as a special form of influenza. Saint-Martin and Lhermitte emphasize the diagnostic importance of the two chief symptoms, lethargy and oculomotor paresis. They also point out that the main pathological lesion is found in the gray matter beneath the Aqueduct of Sylvius. This region has long been recognized as peculiarly vulnerable to toxic and bacterial agents. Thus, it is the location involved in the acute hemorrhagic polioencephalitis, long ago described by Wernicke, in which, however, the involvement is more extensive and the symptomatology much more complicated. These two authors are not willing to deny the relationship between the encephalitis and poliomyelitis, and they did add the information that in the part of France where their observations were made, an epidemic among fowls, resembling human poliomyelitis, existed at the same time. The two necropsies reported by Marie and Tretiakoff, both show acute inflammatory changes in |