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Amebic Dysentery
Medical Clinics of North America January, 1937. Chicago Number
CLINIC OF DR. FRED M. DRENNAN MERCY HOSPITAL
AMEBIC DYSENTERY
I AM going to start this clinic with a brief history of the case being demonstrated as it is fairly typical. A young man, twenty-eight years old, came to my office a few months ago complaining of diarrhea. His work has been that of a salesman in the southern part of the United States. While in North Carolina, six months previously, he had been "upset by food" taken and had a severe though short duration diarrhea with abdominal cramps, tenderness, nausea and vomiting, mucus but no blood seen in the bowel movements. He did not know about temperature but felt he probably had no fever. He felt weak and "played out" but went on about his work and in a few days was seemingly all right. Following this, he had recurring short duration diarrheal attacks becoming more frequent, so that during the two months before examination he had continual loose movements, three to six daily, watery in consistency, with associated rumbling and gurgling, cramplike pain at times severe during defecation, marked generalized abdominal tenderness, mucus and blood in the bowel movements. There was only a slight loss in weight, though he felt tired and worn out. He complained of nausea and lack of appetite, but had no vomiting after the first attack. At our examination the blood pressure was 114/86, temperature 98° F. Urine was negative as to albumin, sugar and casts. Hemoglobin was 80 per cent. Ewald meal showed free acid 45, total 81; benzidine test for blood negative. Bowel movements were mushy to watery, and on examination showed benzidine Physical examination was essentially
++++.
159
160
FRED M. DRENNAN
negative except for a markedly spastic, ropelike, and tender colon. Rectal examination caused no particular pain, and no masses were felt. A second stool examination showed mucus and blood; on warming specimen for microscopical examination amebic organisms were demonstrated. A clinic on "amebic dysentery" is always an interesting subject for the teacher because it must deal with a condition concerning which medical investigation has had a great deal of uncertainty. In this clinic I am going to mention only things that seem at the present time to be fairly stable. By the term "amebic dysentery" we mean a disease caused specifically by the Endamoeba histolytica, the lesions originating and being chiefly in the large intestine though liver complications are present; clinically characterized by diarrhea with blood, pus and mucus in the bowel movements. There is a tendency for the symptoms to be intermittent which perhaps increases the difficulty in diagnosis, the locating of carriers, and the development of complications. Many cases are seriously disabling if allowed to develop, so that any diarrhea should be investigated thoroughly even though we may feel it is a relatively simple condition. The first intimation of amebae being associated with dysentery was made by Losch in 1875, but because similar organisms were found in healthy individuals and in other conditions associated with diarrhea, it was not taken seriously. Later investigators noted the association regularly and also found the organisms at postmortem in the ulcerative lesions in the mucous membrane of the gut. Then Schaudinn suggested the presence of 2 distinct organisms of similar morphology, both parasitic, but one (Endamoeba coli) nonpathogenic, the other (Endamoeba histolytica) pathogenic and the cause of the condition known as amebic dysentery. For the purpose of this clinic and of practical medicine we may only mention in passing the other endameba found in bowel movements and the types that grow freely in bowel movements, ice cream and simple media, which are not a cause of serious pathology. ft is readily seen then that a diagnosis of endamebic dys-
AMEBIC DYSENTERY
161
entery must rest, as in our case, on two important factors, first the clinical story which may be that of acute attacks of diarrhea or mild attacks -which are not severe enough to keep the . patient from his .work but which recur or persist for a few weeks and then clear up without definite treatment. Regularly, the colon is spastic and tender to pressure; cramplike pain may be severe with relief by passing gas and by bowel movements; temperature moderately raised, appetite lessened and nausea present, as might be seen in a simple diarrhea. During the intermittent stage the patient may feel normal. In severe or complicated cases symptoms are varied by the complications present as liver abscess, etc.; on examination of the bowel movement usually one finds fecal material mixed with mucus, pus and blood (not the watery secretion found in bacillary dysentery) . In this mucous and bloody material the active organisms are found. Fresh warm specimens give best results, though specimens which are kept cold and warmed just before examination are very satisfactory as the organisms become active on warming. It is to be noted that in specimens kept at body temperature the organisms deteriorate rapidly so that they are not visible. Specimens for examination for the trophozoites may be mounted in saline solution or a dilute aqueous solution of eosin so that the organism will appear white on a pink background. The movement is sluglike, likely to be fairly active, red cells are ingested and the nucleus almost invisible unless stained in some way. If direct examination does not show organisms, saline cathartics may be given or material may be secured directly from the ulcers by rectal tube or proctoscopic examination. Single examinations with negative findings do not rule out a positive diagnosis. The finding of other organisqls in material from the ulcers is to be expected because in the gut wall there is regularly a secondary infection. This may be responsible for difficulty in diagnosis in some cases in which an ulcerative colitis (idiopathic) is diagnosed, yet the case improves on emetin or similar treatment. In looking for carriers one must find encysted forms, usually by staining methods. Culture methods are technically difficult as are the VOL. 2I-II
FRED M. DRENNAN
complement fixation methods. Though both may be of value
if done by experts, neither is practical for a physician.
The life cycle of the Endamoeba histolytica is simple, consisting of two stages, first the trophozoites or motile forms which mUltiply rapidly in the large intestine producing the lesions and the symptoms of the disease. These motile forms are passed in large numbers but they die quickly when exposed to the air or stomach content and so do not transmit the disease. In the gut, conditions that are not compatible with growth of the trophozoites develop and they reproduce less rapidly and finally become encysted and are passed out of the bowel. These cysts when swallowed are broken up in the small intestine and a fournucleated ameba is freed .. These are held at points of stasis in the gut, divide into typical trophozoites and the usual lesions of amebic dysentery result. This makes the source of infection a carrier, who though passing cysts may be free from symptoms, perhaps may never have had enough diarrhea to fix it in his memory as being important, yet be the cause of epidemics as a handler of food, etc. The practical point is that any patient who has had amebic dysentery should be checked at regular intervals for months to be sure he is not a carrier. The pathology of the disease is primarily that of the intestinal ulcers, commencing in the cecal region though the entire large gut may be involved; the lesions start as a small inflammatory area, surrounded by a hemorrhagic area. In the center necrosis of the epithelium takes place, into this the amebae pass destroying tissue, undermining the submucosa, giving an oval undermined erosion. Usually enough inflammatory reaction takes place so that perforation does not happen; between the ulcers are areas of fairly normal mucous membrane. As healing takes place, marked scar tissue develops which produces obstruction and, if the gut is pliable, dilatation above the point of obstruction. The organisms are found in the submucosa, in muscle layers and in small venules, in which they may be carried to the liver giving the complication of liver abscess. These abscesses are usually single, may be in any portion of th~ liver; occasionally there may be multiple abscesses or
AMEBIC DYSENTERY
numerous miliary lesions. Usually there is a destructive necrosis of liver tissue without liquefaction or marked inflammatory reaction in surrounding tissue. The lesion is walled off by granulation tissue and if secondary infection takes place, as it usually does, one gets the reactions due to the invading organisms, plus the findings of the amebae. These abscesses may be fairly quiescent for weeks, may gradually increase in size, may rupture into surrounding tissue, lung, pleura, peritoneum, or externally. If walled off and drained, they may heal readily. While liver abscess is noted as a part of the pathology and may be thought of as a complication, it must be remembered that intestinal ulcers followed by liver abscess normally indicate amebic infection. Liver abscess may be present without demonstrable lesions in the gut. Other pathology as complications include peritonitis from perforation or near perforation, appendiceal involvement, very infrequently urinary tract infection by transplanting or perforation, partial or complete intestinal obstruction. In all locations the ulcers are prone to become secondarily infected, giving a changed symptomatology and pathology and frequently increasing the danger to the patient. Certain authors go so far as to state that all ulcerative colitis is likely to have been primarily amebic, later being complicated by the secondary invading organisms. This gives the basis for anti-amebic treatment in all such cases with improvement resulting in a considerable number. We began our history with the statement that our patient worked in the South and it is a fact that amebic dysentery is more common in tropical countries, not as an epidemic, but generally present. It is endemic in temperate zones, as our Chicago infection of a few years ago. Probably it is fair to say that we have cases quite regularly with us, that could be diagnosed if more frequent and careful microscopical examination of the bowel movements were made. Carriers, especially those who may handle food, vegetables that have been grown on ground fertilized by human excreta, contaminated water or milk supply, etc., must all be considered in the insidious extension of the disease. Careless laboratory technic is a possible
FRED M. DRENNAN
though probably not a frequent cause of infection. It is very difficult to establish an incubation period, inoculation experiments placing it at from thirty to one hundred days with the probability being that only a small percentage of people ingesting cysts actually develop amebic dysentery. Intestinal stasis and constipation on a basis of obstruction seem to increase the probability of pathology. I am going to list definite cases in discussing the differential diagnosis, because in each the diagnosis of an amebic dysentery was considered during the course of the disease. First, a twenty-five-year-old school teacher gave a history of acute and persisting diarrhea for several months, mucus and blood in the bowel movements, marked loss in weight, severe generalized abdominal cramps, and tenderness over the entire colon particularly in the right lower quadrant. At the time of examination her temperature was 102 0 to 103 0 F. in the afternoon. On fluoroscopic examination with a barium enema there was a definite filling defect in the cecum; the rest of the gut was spastic but not obstructed. No amebae were found on stool examination, nor were tubercle bacilli, though operation confirmed the probable diagnosis of tuberculosis. The second patient was seen at the age of fifty years, with a history of cramplike pain in the lower abdomen, generalized but worse on the left side, frequent desire for bowel movements, 4 to 6 movements daily, with the passage of soft material frequently containing mucus and blood, and spastic and tender colon. The patient sat on the toilet to empty bladder because of the passage of bowel movement on straining. Appetite was diminished. He had slight nausea, but no vomiting, and had lost 10 pounds' in weight. On examination temperature was 98.6 0 F., blood pressure 128/70, hemoglobin 90 per cent, and urine negative for sugar and albumin. Stomach secretions were normal and no blood was found. Bowel movements were mushy, with small amount of pus and persistent blood, but no amebae .. Rectal examination revealed a small firm nodule, like a polyp, about 4 inches from the rectum. Fluoroscopic examination w.it~ barium enema showed partial obstruction in pelvic loop
AMEBIC DYSENTERY
16 5
of gut. The barium, however, passed in sufficient amount to fill the gut, showing no further filling defects. There was a definite delay in expelling the enema which caused the patient considerable distress. Proctoscopic examination revealed the polyp felt by rectal examination but could not reach the region of partial obstruction. A diagnosis of malignancy was made and operation advised. At surgery, resection revealed numerous flat polypi with broad bases; 2 large ones separated by a distance of 3 inches had undergone malignant degeneration, giving the findings of blood in the bowel movements. The mucous membrane between these lesions was normal The patient has remained well following resection. Third, a man, fifty-five years old, came in complaining of abdominal cramps for a period of three months, COining in attacks, associated with desire and straining at bowel movements. The material passed was mushy to watery in consistency. There was some rumbling, with relief of cramp by water enema; he sometimes used 2 to 4 enemas during twenty-four hours. Mucus was seen in the bowel movements and frequently there was a rather profuse amount of bright red blood. He had lost 10 pounds in weight but was working regularly. On examination he weighed 144% pounds; temperature was 98.4° F. and blood pressure 150/104. Urine was negative for albumin and sugar. Hemoglobin 80 per cent. Ewald meal showed free acid 18, total 30, and negative benzidine test. Rectal examination was negative. The left side of the abdomen and the descending colon were tender to pressure. The first bowel movement examined was mushy in consistency, but negative to blood. A second series of bowel movements showed clots of blood, not digested, but no amebae. During hospital examination bowel movements at one time might be free from blood, but within an hour the patient would have a desire for movement and pass a large amount of fresh red blood, very definitely different from the usual occurrence in carcinoma, bleeding polyp, tuberculosis, or ulcerative colitis. Fluoroscopic examination with barium enema revealed a definite obstruction in the lower portion of the descending colon tight
r66
FRED M. DRENNAN
enough so that only a small stream of barium would pass through. The enema caused a great deal of pain. A diagnosis of malignancy was made, mention being made of the fact that certain of the bowel movements were free of blood which is not usual in a cancer of the colon, particularly the descending portion. At operation a palpable mass was felt at the location described; it was not hard, but the lumen of the gut was almost obstructed so resection was done. The mass was about 1 inch in diameter and cauliflower-like in appearance; on microscopic examination it was found to be a rare nodular hemangioma. The patient made an uneventful recovery following resection. Other conditions which may give the same picture as the cases cited are infected diverticulitis, infected ulcerative polyp (nonmalignant), etc. Idiopathic ulcerative colitis furnishes the most difficult differentiation. The symptoms are more persistent and have all the earmarks of severe amebic dysentery. Except for the causative organisms, the clinical and laboratory findings are similar. One cannot be criticized too much for using anti-amebic medication in cases where the organism may not have been found, yet clinical or proctoscopic examination may be suggestive of amebic infection. Bacillary dysentery, food irritation, toxemias as from the thyroid or uremia, etc., also may be mentioned in connection with the differential diagnosis. The treatment of amebic dysentery should take into consideration the entire clinical picture and should include the nourishment and general condition of the patient as well as the elimination of the. causative organism. This means rest in bed, sufficient bland waste material, free food to provide nourishment, preparations of opium like deodorized tincture, 10 to 15 drops five times daily, paregoric, etc., to control the diarrhea. Bismuth preparations also help to control the diarrhea. As to specific treatment we have the arsenic preparations, such as stovarsol, in 3- or 4-grain doses three times a day for four to seven days, with a rest period of seven days and then resumption -of treatment, treparsol, 5 grains, three times a day for
AMEBIC DYSENTERY
seven days with a seven-day rest period, yatren, 4 grains three times a day for seven to eight days, carbarsone, 4 grains twice daily for seven to ten days, and emetin which is given by intramuscular injection, % to 1 grain daily, for five to seven days, with a corresponding period without medication. With all arsenic preparations one must watch for symptoms of arsenic poisoning, and when noted promptly stop the drug, whatever it may be, until certain that the accumulative effect has had time to wear off. With emetin the toxic effect on the heart muscle is probably the greatest danger, making it a drug which requires greater attention even than the arsenic preparations. I have been partial to stovarsol, as I used it early and find that if one watches for arsenic poisoning, it gives very satisfactory results. One must be cognizant of the fact that patients react differently; one patient may be influenced very little clinically or in the laboratory findings in the bowel movement by one drug, yet will get rapid clinical improvement and freedom from organisms from another type of D?edication. Each patient must be considered as an individual entity and clinical improvement, clearing of bowel movements from cysts and active organisms, and healing of ulcers must all result if treatment is satisfactory. Liver abscesses and other complications must be treated surgically as the condition demands, in addition to the regular medication outlined. In the final analysis, one must remember and impress upon the patient that recurrences are frequent, to be expected, and dangerous, when present, to him as well as to his associates. This means repeated examinations and, if necessary, repeated and varied treatments with no immunity established from previous attacks.
CLINIC OF DR. FRED M. DRENNAN MERCY HOSPITAL
AMEBIC DYSENTERY
I AM going to start this clinic with a brief history of the case being demonstrated as it is fairly typical. A young man, twenty-eight years old, came to my office a few months ago complaining of diarrhea. His work has been that of a salesman in the southern part of the United States. While in North Carolina, six months previously, he had been "upset by food" taken and had a severe though short duration diarrhea with abdominal cramps, tenderness, nausea and vomiting, mucus but no blood seen in the bowel movements. He did not know about temperature but felt he probably had no fever. He felt weak and "played out" but went on about his work and in a few days was seemingly all right. Following this, he had recurring short duration diarrheal attacks becoming more frequent, so that during the two months before examination he had continual loose movements, three to six daily, watery in consistency, with associated rumbling and gurgling, cramplike pain at times severe during defecation, marked generalized abdominal tenderness, mucus and blood in the bowel movements. There was only a slight loss in weight, though he felt tired and worn out. He complained of nausea and lack of appetite, but had no vomiting after the first attack. At our examination the blood pressure was 114/86, temperature 98° F. Urine was negative as to albumin, sugar and casts. Hemoglobin was 80 per cent. Ewald meal showed free acid 45, total 81; benzidine test for blood negative. Bowel movements were mushy to watery, and on examination showed benzidine Physical examination was essentially
++++.
159
160
FRED M. DRENNAN
negative except for a markedly spastic, ropelike, and tender colon. Rectal examination caused no particular pain, and no masses were felt. A second stool examination showed mucus and blood; on warming specimen for microscopical examination amebic organisms were demonstrated. A clinic on "amebic dysentery" is always an interesting subject for the teacher because it must deal with a condition concerning which medical investigation has had a great deal of uncertainty. In this clinic I am going to mention only things that seem at the present time to be fairly stable. By the term "amebic dysentery" we mean a disease caused specifically by the Endamoeba histolytica, the lesions originating and being chiefly in the large intestine though liver complications are present; clinically characterized by diarrhea with blood, pus and mucus in the bowel movements. There is a tendency for the symptoms to be intermittent which perhaps increases the difficulty in diagnosis, the locating of carriers, and the development of complications. Many cases are seriously disabling if allowed to develop, so that any diarrhea should be investigated thoroughly even though we may feel it is a relatively simple condition. The first intimation of amebae being associated with dysentery was made by Losch in 1875, but because similar organisms were found in healthy individuals and in other conditions associated with diarrhea, it was not taken seriously. Later investigators noted the association regularly and also found the organisms at postmortem in the ulcerative lesions in the mucous membrane of the gut. Then Schaudinn suggested the presence of 2 distinct organisms of similar morphology, both parasitic, but one (Endamoeba coli) nonpathogenic, the other (Endamoeba histolytica) pathogenic and the cause of the condition known as amebic dysentery. For the purpose of this clinic and of practical medicine we may only mention in passing the other endameba found in bowel movements and the types that grow freely in bowel movements, ice cream and simple media, which are not a cause of serious pathology. ft is readily seen then that a diagnosis of endamebic dys-
AMEBIC DYSENTERY
161
entery must rest, as in our case, on two important factors, first the clinical story which may be that of acute attacks of diarrhea or mild attacks -which are not severe enough to keep the . patient from his .work but which recur or persist for a few weeks and then clear up without definite treatment. Regularly, the colon is spastic and tender to pressure; cramplike pain may be severe with relief by passing gas and by bowel movements; temperature moderately raised, appetite lessened and nausea present, as might be seen in a simple diarrhea. During the intermittent stage the patient may feel normal. In severe or complicated cases symptoms are varied by the complications present as liver abscess, etc.; on examination of the bowel movement usually one finds fecal material mixed with mucus, pus and blood (not the watery secretion found in bacillary dysentery) . In this mucous and bloody material the active organisms are found. Fresh warm specimens give best results, though specimens which are kept cold and warmed just before examination are very satisfactory as the organisms become active on warming. It is to be noted that in specimens kept at body temperature the organisms deteriorate rapidly so that they are not visible. Specimens for examination for the trophozoites may be mounted in saline solution or a dilute aqueous solution of eosin so that the organism will appear white on a pink background. The movement is sluglike, likely to be fairly active, red cells are ingested and the nucleus almost invisible unless stained in some way. If direct examination does not show organisms, saline cathartics may be given or material may be secured directly from the ulcers by rectal tube or proctoscopic examination. Single examinations with negative findings do not rule out a positive diagnosis. The finding of other organisqls in material from the ulcers is to be expected because in the gut wall there is regularly a secondary infection. This may be responsible for difficulty in diagnosis in some cases in which an ulcerative colitis (idiopathic) is diagnosed, yet the case improves on emetin or similar treatment. In looking for carriers one must find encysted forms, usually by staining methods. Culture methods are technically difficult as are the VOL. 2I-II
FRED M. DRENNAN
complement fixation methods. Though both may be of value
if done by experts, neither is practical for a physician.
The life cycle of the Endamoeba histolytica is simple, consisting of two stages, first the trophozoites or motile forms which mUltiply rapidly in the large intestine producing the lesions and the symptoms of the disease. These motile forms are passed in large numbers but they die quickly when exposed to the air or stomach content and so do not transmit the disease. In the gut, conditions that are not compatible with growth of the trophozoites develop and they reproduce less rapidly and finally become encysted and are passed out of the bowel. These cysts when swallowed are broken up in the small intestine and a fournucleated ameba is freed .. These are held at points of stasis in the gut, divide into typical trophozoites and the usual lesions of amebic dysentery result. This makes the source of infection a carrier, who though passing cysts may be free from symptoms, perhaps may never have had enough diarrhea to fix it in his memory as being important, yet be the cause of epidemics as a handler of food, etc. The practical point is that any patient who has had amebic dysentery should be checked at regular intervals for months to be sure he is not a carrier. The pathology of the disease is primarily that of the intestinal ulcers, commencing in the cecal region though the entire large gut may be involved; the lesions start as a small inflammatory area, surrounded by a hemorrhagic area. In the center necrosis of the epithelium takes place, into this the amebae pass destroying tissue, undermining the submucosa, giving an oval undermined erosion. Usually enough inflammatory reaction takes place so that perforation does not happen; between the ulcers are areas of fairly normal mucous membrane. As healing takes place, marked scar tissue develops which produces obstruction and, if the gut is pliable, dilatation above the point of obstruction. The organisms are found in the submucosa, in muscle layers and in small venules, in which they may be carried to the liver giving the complication of liver abscess. These abscesses are usually single, may be in any portion of th~ liver; occasionally there may be multiple abscesses or
AMEBIC DYSENTERY
numerous miliary lesions. Usually there is a destructive necrosis of liver tissue without liquefaction or marked inflammatory reaction in surrounding tissue. The lesion is walled off by granulation tissue and if secondary infection takes place, as it usually does, one gets the reactions due to the invading organisms, plus the findings of the amebae. These abscesses may be fairly quiescent for weeks, may gradually increase in size, may rupture into surrounding tissue, lung, pleura, peritoneum, or externally. If walled off and drained, they may heal readily. While liver abscess is noted as a part of the pathology and may be thought of as a complication, it must be remembered that intestinal ulcers followed by liver abscess normally indicate amebic infection. Liver abscess may be present without demonstrable lesions in the gut. Other pathology as complications include peritonitis from perforation or near perforation, appendiceal involvement, very infrequently urinary tract infection by transplanting or perforation, partial or complete intestinal obstruction. In all locations the ulcers are prone to become secondarily infected, giving a changed symptomatology and pathology and frequently increasing the danger to the patient. Certain authors go so far as to state that all ulcerative colitis is likely to have been primarily amebic, later being complicated by the secondary invading organisms. This gives the basis for anti-amebic treatment in all such cases with improvement resulting in a considerable number. We began our history with the statement that our patient worked in the South and it is a fact that amebic dysentery is more common in tropical countries, not as an epidemic, but generally present. It is endemic in temperate zones, as our Chicago infection of a few years ago. Probably it is fair to say that we have cases quite regularly with us, that could be diagnosed if more frequent and careful microscopical examination of the bowel movements were made. Carriers, especially those who may handle food, vegetables that have been grown on ground fertilized by human excreta, contaminated water or milk supply, etc., must all be considered in the insidious extension of the disease. Careless laboratory technic is a possible
FRED M. DRENNAN
though probably not a frequent cause of infection. It is very difficult to establish an incubation period, inoculation experiments placing it at from thirty to one hundred days with the probability being that only a small percentage of people ingesting cysts actually develop amebic dysentery. Intestinal stasis and constipation on a basis of obstruction seem to increase the probability of pathology. I am going to list definite cases in discussing the differential diagnosis, because in each the diagnosis of an amebic dysentery was considered during the course of the disease. First, a twenty-five-year-old school teacher gave a history of acute and persisting diarrhea for several months, mucus and blood in the bowel movements, marked loss in weight, severe generalized abdominal cramps, and tenderness over the entire colon particularly in the right lower quadrant. At the time of examination her temperature was 102 0 to 103 0 F. in the afternoon. On fluoroscopic examination with a barium enema there was a definite filling defect in the cecum; the rest of the gut was spastic but not obstructed. No amebae were found on stool examination, nor were tubercle bacilli, though operation confirmed the probable diagnosis of tuberculosis. The second patient was seen at the age of fifty years, with a history of cramplike pain in the lower abdomen, generalized but worse on the left side, frequent desire for bowel movements, 4 to 6 movements daily, with the passage of soft material frequently containing mucus and blood, and spastic and tender colon. The patient sat on the toilet to empty bladder because of the passage of bowel movement on straining. Appetite was diminished. He had slight nausea, but no vomiting, and had lost 10 pounds' in weight. On examination temperature was 98.6 0 F., blood pressure 128/70, hemoglobin 90 per cent, and urine negative for sugar and albumin. Stomach secretions were normal and no blood was found. Bowel movements were mushy, with small amount of pus and persistent blood, but no amebae .. Rectal examination revealed a small firm nodule, like a polyp, about 4 inches from the rectum. Fluoroscopic examination w.it~ barium enema showed partial obstruction in pelvic loop
AMEBIC DYSENTERY
16 5
of gut. The barium, however, passed in sufficient amount to fill the gut, showing no further filling defects. There was a definite delay in expelling the enema which caused the patient considerable distress. Proctoscopic examination revealed the polyp felt by rectal examination but could not reach the region of partial obstruction. A diagnosis of malignancy was made and operation advised. At surgery, resection revealed numerous flat polypi with broad bases; 2 large ones separated by a distance of 3 inches had undergone malignant degeneration, giving the findings of blood in the bowel movements. The mucous membrane between these lesions was normal The patient has remained well following resection. Third, a man, fifty-five years old, came in complaining of abdominal cramps for a period of three months, COining in attacks, associated with desire and straining at bowel movements. The material passed was mushy to watery in consistency. There was some rumbling, with relief of cramp by water enema; he sometimes used 2 to 4 enemas during twenty-four hours. Mucus was seen in the bowel movements and frequently there was a rather profuse amount of bright red blood. He had lost 10 pounds in weight but was working regularly. On examination he weighed 144% pounds; temperature was 98.4° F. and blood pressure 150/104. Urine was negative for albumin and sugar. Hemoglobin 80 per cent. Ewald meal showed free acid 18, total 30, and negative benzidine test. Rectal examination was negative. The left side of the abdomen and the descending colon were tender to pressure. The first bowel movement examined was mushy in consistency, but negative to blood. A second series of bowel movements showed clots of blood, not digested, but no amebae. During hospital examination bowel movements at one time might be free from blood, but within an hour the patient would have a desire for movement and pass a large amount of fresh red blood, very definitely different from the usual occurrence in carcinoma, bleeding polyp, tuberculosis, or ulcerative colitis. Fluoroscopic examination with barium enema revealed a definite obstruction in the lower portion of the descending colon tight
r66
FRED M. DRENNAN
enough so that only a small stream of barium would pass through. The enema caused a great deal of pain. A diagnosis of malignancy was made, mention being made of the fact that certain of the bowel movements were free of blood which is not usual in a cancer of the colon, particularly the descending portion. At operation a palpable mass was felt at the location described; it was not hard, but the lumen of the gut was almost obstructed so resection was done. The mass was about 1 inch in diameter and cauliflower-like in appearance; on microscopic examination it was found to be a rare nodular hemangioma. The patient made an uneventful recovery following resection. Other conditions which may give the same picture as the cases cited are infected diverticulitis, infected ulcerative polyp (nonmalignant), etc. Idiopathic ulcerative colitis furnishes the most difficult differentiation. The symptoms are more persistent and have all the earmarks of severe amebic dysentery. Except for the causative organisms, the clinical and laboratory findings are similar. One cannot be criticized too much for using anti-amebic medication in cases where the organism may not have been found, yet clinical or proctoscopic examination may be suggestive of amebic infection. Bacillary dysentery, food irritation, toxemias as from the thyroid or uremia, etc., also may be mentioned in connection with the differential diagnosis. The treatment of amebic dysentery should take into consideration the entire clinical picture and should include the nourishment and general condition of the patient as well as the elimination of the. causative organism. This means rest in bed, sufficient bland waste material, free food to provide nourishment, preparations of opium like deodorized tincture, 10 to 15 drops five times daily, paregoric, etc., to control the diarrhea. Bismuth preparations also help to control the diarrhea. As to specific treatment we have the arsenic preparations, such as stovarsol, in 3- or 4-grain doses three times a day for four to seven days, with a rest period of seven days and then resumption -of treatment, treparsol, 5 grains, three times a day for
AMEBIC DYSENTERY
seven days with a seven-day rest period, yatren, 4 grains three times a day for seven to eight days, carbarsone, 4 grains twice daily for seven to ten days, and emetin which is given by intramuscular injection, % to 1 grain daily, for five to seven days, with a corresponding period without medication. With all arsenic preparations one must watch for symptoms of arsenic poisoning, and when noted promptly stop the drug, whatever it may be, until certain that the accumulative effect has had time to wear off. With emetin the toxic effect on the heart muscle is probably the greatest danger, making it a drug which requires greater attention even than the arsenic preparations. I have been partial to stovarsol, as I used it early and find that if one watches for arsenic poisoning, it gives very satisfactory results. One must be cognizant of the fact that patients react differently; one patient may be influenced very little clinically or in the laboratory findings in the bowel movement by one drug, yet will get rapid clinical improvement and freedom from organisms from another type of D?edication. Each patient must be considered as an individual entity and clinical improvement, clearing of bowel movements from cysts and active organisms, and healing of ulcers must all result if treatment is satisfactory. Liver abscesses and other complications must be treated surgically as the condition demands, in addition to the regular medication outlined. In the final analysis, one must remember and impress upon the patient that recurrences are frequent, to be expected, and dangerous, when present, to him as well as to his associates. This means repeated examinations and, if necessary, repeated and varied treatments with no immunity established from previous attacks.