This paper will present an actual case record, taken from one of the foremost university hospitals in the United States, with comparative therapeutics of the allopathic and homoeopathic methods of treatment.
PRESENTATION OF CASE.
A 33-year-old American factory hand was admitted complaining of abdominal pain and vomiting.
The patient had been perfectly well until five months before entry, when he suddenly became ill with “intestinal grippe”, characterized by nonradiating, colicky, lower abdominal pain which was sufficiently severe to require the use of hypodermic medication. At the onset of the illness the temperature was 101 F., but this rapidly subsided. The patient was confined to bed for ten days. There was no nausea, vomiting or diarrhoea. Subsequently the patient returned to work but continued to feel rundown and became fatigued more rapidly than usual. There was no recurrence of the abdominal pain. Three days before coming to the hospital the patient took a mild laxative before going to work.
During the morning he had repeated shaking chills, headache and severe pain in the back and loins. There were several loose bowel movements, the color of which was not noted. His appetite was poor, but he had a bowl of soup for lunch. Subsequently he felt very sick and returned to his home, where the soup previously ingested was vomited. He felt hot and restless, and his temperature was found to be 102.5 F. He slept fitfully, and on the following day felt quite fatigued. There were anorexia and nausea, but no vomiting. A mild laxative was again taken, and throughout the remainder of the day there were frequent loose bowel movements. He felt alternately hot and chilly, but there were no further chills.
His skin was livid or purplish with face dark as mahogany and hot; sordes. He was white about mouth and nose with a thin, copious, ichorous, bloody nasal discharge. His temperature at that time was 104 F., and a physician stated that he had a septic throat, although his throat was not sore. It was swollen, purple and livid. There were ulcerations of the mouth with a gray membrane. Also burning in the mouth.
Necrotic destruction of soft parts of the palate and fauces with dark blood from the nose. Fauces red and covered with exudation. The throat was inflamed and oedematous. There was an irregular, patchy, livid eruption. Patient was semiconscious and delirious with weak pulse, general torpor and great and rapid prostration. There was a tendency toward haemorrhages from different orifices, of dark fluid blood; cyanosis, rapid respiration and heart action. The symptoms continued unchanged during the day preceding admission, but at two oclock on the following morning he began to vomit repeatedly. The vomiting was non-projectile. The vomitus was variously brown, yellow and green in appearance. He felt feverish and again took a laxative which was followed by a series of loose bowel movements, the character of which was not noted. During the day he developed epigastric soreness, worse when moving about, which he attributed to straining when vomiting.
The patient had received typhoid vaccine thirteen years ago, while in the navy. During a one-year period, twelve years before his entry, four members of his family contracted typhoid fever. There were no related illness in his family since that time. He last visited his family four weeks before the onset of his illness. Four years preceding entry the patient had attacks of burning mid-epigastric pain. This was thought to be due to an ulcer, but x-ray studies were negative. Subsequently the symptoms subsided.
Physical examination showed a well developed and nourished, pale young man, who was obviously acutely ill. The lips and nail- beds were slightly cyanotic and the mucous membranes dry. The pharynx was moderately injected and there was a small amount of mucoid exudate. The cervical lymph nodes were slightly enlarged but not tender. Questionable dullness was elicited at the right base and right lower axilla. In this region tactile fremitus and vocal resonance were slightly diminished and questionable distant bronchial breathing was heard. There were also a few transient crackling inspiratory rales, which were dispelled by cough. The heart was not enlarged. A systolic murmur was heard in the apical region. The blood pressure was 120/75. There were tenderness and muscle spasm in the epigastrium, more evident to the right of the midline. Peristaltic sounds were normal.
Rectal examination elicited slight tenderness on the right side.
The temperature was 104 F., the pulse 75. The respirations were 30.
The urine showed a specific gravity of 1.028 to 1.042, with a slight trace of albumin. The sediment was negative. The blood showed a red cell count of 4,600,000 with a hemoglobin of 86 per cent. The white cell count was 7,000, with 78 per cent poly- morphonuclears. The non-protein nitrogen of the blood serum was 15 milligrams per cent and the serum protein was 3.8 grams per cent. A Widal test showed agglutination of bacillus typhosus up to a dilution of 1:320. Agglutination test for bacillus abortus was negative. Three blood cultures were done; one was negative; the second showed staphylococcus albus in one flask and hemolytic streptococcus in the other, and the third showed no growth in one flask and nonhemolytic streptococcus in the other.
A chest x-ray was negative. There was no free air beneath the diaphragm.
On the second hospital day the patient complained of severe upper abdominal pain. There was marked spasm in the right epigastrium, and peristaltic sounds were absent. On the following day he felt comfortable, peristalsis was again audible, and the abdomen was soft. Subsequently, similar episodes occurred and eventually the abdomen became distended, tense and tender, and peristaltic movement ceased.
Another x-ray film with the patient recumbent showed obliteration of both sides of the diaphragm by dullness in the lower lung fields. The dullness was hazy in outline and extended higher on the left than on the right side. The heart was transverse in position. Throughout the hospital course the temperature remained elevated between 102 F. and 106 F. and the pulse rose progressively to 160. The white cell count also rose to 17,000, with 96 per cent polymorphonuclears. The patients condition became progressively worse and he died on the seventh hospital day.
Dr. A.: I think that the findings in the chest were due solely to a high diaphragm in a man who was very distended. It is obvious from this history that in the final days of his hospital stay the mischief was in the abdomen. When it started in the abdomen and what it represents are our problems. The next question is whether this attack of so-called intestinal grippe that he had five months previously was intestinal grippe and whether by any chance it was related to his final illness.
There is only one suggestion that there might be any relation, and that is the fact that from that time on, up to the last illness, he was not up to scratch, did not have all the pep he would like, and, as he stated, he felt “a little run-down”. I am inclined to believe, however, that this attack of right lower quadrant abdominal pain was more likely something that might pass under the name of intestinal grippe, rather than something related to the present illness. Nevertheless, we must still consider the possibility of this being a manifestation of something related to the final illness. In this day and age we are all regional-ileitis-minded, and we might think of that as a possibility, but the subsequent course makes it seem unlikely.
A more reasonable thought would be some form of acute ulcerative colitis. We should think of either the idiopathic type or that due to one of the dysentery organisms. We can have fairly extensive colitis at times, with very little in the way of symptoms and signs to show for it. If this was the cause of his original illness, it had been silent for a period of some five months. Since he had right lower quadrant pain, one must entertain the possibility of appendicitis. It could be appendicitis, which may or may not have ruptured. I think it unlikely that he could walk around for five months with an appendiceal abscess without more in the way of signs, fever and the like.
I think that is quite remote. If he had had appendicitis one might wonder if he had an associated pylephlebitis; but, again, there is nothing to suggest it. I think it is reasonable to assume that the pathology was in the large bowel. One might think that we were dealing with an individual who had multiple diverticula, one of which had ruptured. I should think, again, that it subsided too rapidly for that. I would be inclined to say that the illness five months before was in no way related to the final illness.
Three days before coming into the hospital he had a shaking chill, with sudden, severe pain in the back and loins. To me this means nothing more than a man coming down with an acute infection. One might wonder, since he had so many chills, if he did not have an actual blood stream invasion at that time, and whether we are now dealing with a septicemia or bacteremia. Whether this diarrhoea that he had had for three days was any- thing more than that induced by catharsis, is again difficult to say.
I think that interpretation is much more reasonable than to say that he had a second flare-up of ulcerative colitis. It would be unusual for a man to be as sick as this, with his temperature going as high as 104, without more pain in his abdomen if he had a severe enough ulcerative colitis to give this picture. Furthermore, the possibility of colitis could not be entertained for long because we have no further information about the stools, tenderness along the colon, or anything of that sort, which would help to make such a diagnosis. So I would be inclined to throw out the possibility of this man having ulcerative colitis.
I suppose the one thing that is really striking and that we must either take seriously or throw out is the question of typhoid fever. He had a temperature of 104 F., and a pulse of 75, a white count of 7,000, and a positive Widal of 1:320. A positive Widal this early in typhoid is very unusual. On the other hand this man had been vaccinated. Did the Widal become positive nonspecifically because the individual was suffering from a severe infection of some sort? I personally would be inclined to interpret it that way.
If he has typhoid we have to presuppose that he has ruptured his small intestine, but again if this is typhoid it is far too early in the course of the disease for such a complication. There is absolutely nothing on physical examination that would point to typhoid. There are no rose spots, no enlargement of the spleen, and no lead whatsoever that would enable one to make that diagnosis. People with septicemia have chills and fever, and at certain times they have relatively slow pulse and low white count, whereas at some subsequent time a high pulse and an increased white count will develop. Therefore, I would throw out the possibility of typhoid fever. As I said before, he evidently died because of something very radically wrong with his abdominal cavity.
One of the first things we should think of is whether we are dealing with an individual with peritonitis subsequent to rupture of some viscus. But there is nothing here to enable me to say that he had a ruptured viscus. His last illness started without any abdominal pain or symptoms. For three days the only symptom he had, with reference to his gastrointestinal tract, was diarrhoea, which may have been due to frequent catharsis. They evidently suspected a ruptured viscus because several flat plates of the abdomen were taken. On no occasion did they find anything suggesting air under the diaphragm.
The question of whether he may or may not have had ulcer four years ago is thrown in for good measure, but again there is nothing in the history to allow me to believe that he has a ruptured ulcer and subsequent peritonitis.
The other possibility is whether we might be dealing with a man with multiple diverticula and associated diverticulitis with rupture and peritonitis or abscess formation. There is nothing in the physical examination which would allow one to state that that had been the case.
I would like to know if he had a septic throat. I think it is unusual without an antecedent sore throat, but his illness evidently started off with an acute infection and probably a blood stream invasion almost from the start. If he had had a septic sore throat, that could be the source of entry for such an infection. Of all the laboratory work, the only blood culture on which I think we can really place any reliance is the one which contained hemolytic streptococcus. It is unusual to get hemolytic streptococcus as a contamination, whereas the other two organisms could conceivably be contamination. So we can say that we have some laboratory evidence which enables us to state that we are dealing with an individual who does have a septicemia.
I would be inclined to take one long guess on this man and say that he probably had a peritonitis secondary to the septicemia, and he died of a hemolytic streptococcus peritonitis. If you want to call it idiopathic in origin, all well and good. I could go on and make a complete differential diagnosis, but I do not think I would get any farther than making this one guess. I cannot entertain the question of typhoid and the various other things very seriously. If he did not die of streptococcus peritonitis, I have no idea what he had.
Dr. B.: While you are guessing, I wonder why you lost interest in the appendix in the middle of your discussion. The point is, we have been tricked a great many times by the appendix, and this story could be perfectly well accounted for by an atypical appendix right from the start.
Dr. A.: The thing that intrigued me when I first went over the history was the fact that we might be dealing with a lesion that started five months ago as an attack of appendicitis.
It is possible that he had a ruptured appendix at that time and had been carrying an appendiceal abscess since then. You see an occasional individual walking about with an appendiceal abscess for some time, with very little in the way of symptoms; but such individuals are very rare. The other thing that intrigued me was whether he could have a pylephlebitis secondary to appendicitis; but he goes five months without chills, fever or jaundice, and no tenderness of the liver–never anything to suggest it. When we come to the final illness, it is hard for me to believe that the first three days represent anything more than an acute infection.
There is nothing in the history except diarrhoea to suggest anything in the abdomen, and for that diarrhoea we have a reasonable explanation, that he took a cathartic on these three days. Not until the fourth day were the symptoms referable to the abdomen, and then they do not sound much like appendicitis. I suppose there is a possibility that I may have missed a ruptured appendix with widespread peritonitis. He came in with a temperature of 102, a pulse of 75 and a white count of 7,000. I think that set-up with an acute appendix would be unusual, even if it had ruptured. I think that if it had ruptured he would have obvious signs of peritonitis. It was not until the fourth or fifth day that he presented evidence that made me feel certain of peritonitis. I think a pulse of 75 and a temperature of 102 in appendicitis with or without rupture is an unusual set-up.
Dr. B.: It is an unusual set-up under any circumstances.
Dr. A.: No one knows better than I.
Dr. C.: Idiopathic peritonitis is rare at that age.
Dr. A.: I appreciate that it occurs usually either in childhood or adolescence. I wish we knew whether he had a septic sore throat That is important, that plus the positive blood culture.
Dr. D.: I do not believe that it is not an idiopathic peritonitis. I would have asked the same question Dr. B. did, why you abandoned appendicitis and diverticulitis so readily. I also wonder if one should not consider the possibility, at least, of a local and general sepsis due primarily to cancer some where in the colon.
Dr. A.: There is very little to suggest anything in the colon. My experience is that colitis cannot go on without any evidence.
Why do you say that he died of appendicitis with rupture and so forth? The way I interpret the history is that he has gone three days without any evidence of anything in his abdomen. I would like to have the reaction of one of the surgeons on that. Does his illness during the first three days sound like appendicitis to you, Dr. E.?.
Dr. E.: I would say not, on the evidence we have here.
Dr. A.: I should think that the same sort of reasoning would be correct if you are going to presuppose diverticulitis with rupture. I think that the abdominal examination on the fourth hospital day would be different from what it is. I grant you that I am making a long guess, but I have thought a great deal about this case, and I could not reason it out any other way. I do not believe that he had a ruptured viscus.
Dr. F.: The rectal examination rules out long-continued appendicitis. It is true that pelvic abscess and appendicitis could explain the story, but here we have a rectal examination that rules them out.
A Physician: Four members of the family have had typhoid fever. He perhaps was a typhoid carrier and was ill several days before he came down with an acute chill.
Dr. A.: You mean that he was a carrier for twelve years and then came down with typhoid? I could not make a diagnosis of typhoid because of the rapidity with which this mans illness goes from the time he became ill. In that case we would have to pre-suppose a rupture of a Peyers patch on about the fourth day of the illness.
Dr. G.: I think that he was ill before he had the chill. He was ill when he took the laxative.
Dr. A.: The only story we have is that he was run-down and not up to par. If he has had for five months the pre-symptoms of typhoid, it is unusual. I prefer to date his illness from three days before he entered. If he has typhoid he has ruptured on the fourth day, and that is too early; besides, there is no good evidence.
Dr. G.: I do not believe that the positive Widal of 1:320 would come from vaccination twelve years before.
Dr. A.: A positive Widal of 1:320 to 1:100 is pretty unusual for the fourth or fifth day of typhoid fever.
Dr. G.: I do not think it is the fourth day; I think it is the tenth day.
Dr. A.: Even the tenth day is unusual.
Dr. H.: Dr. I., would a Widal become positive in an individual who has been previously vaccinated if he subsequently falls ill with an acute infection?.
Dr. I.: Yes, we have good evidence that it does. In typhus patients, if they come from surroundings where typhoid fever is prevalent, the Widal reaction often becomes positive in the first few days of the disease, before the development of the Weil-Felix reaction. In rabbits the antibodies which have disappeared from the serum sometimes are recalled by intravenous injections of non-related antigens. The early presence of agglutinins, as Dr. A. pointed out, speaks probably for the nonspecific nature of the agglutination.
Dr. A.: May I ask one question, Dr. I.? Which of these three positive blood cultures is the most significant?.
Dr. I.: I agree that the hemolytic streptococcus is the most significant. I cannot remember a single case in which we obtained hemolytic streptococci from the blood as a contaminant, while staphylococcus albus is a common contaminant of blood cultures. I believe that if he had typhoid fever the culture would be positive for the typhoid bacillus and not for hemolytic streptococcus.
DR. K.: I was asked to see this patients three or four days before he died and to transfer him because of typhoid fever. At that time he had, and I thought, definite tenderness in the lower quadrant with spasm, and although there were peristaltic sounds it seemed to me obvious that he had peritonitis. A great deal to comment occurred in regard to the presence of peristaltic sounds in this man, the commentators feeling that this ruled our peritonitis. In view of the fact that he had general peritonitis, and we felt that it was probably due to some inflammation of some viscus, I followed my fathers dictum, that he probably had Atypical appendicitis with peritonitis.
Atypical appendicitis with peritonitis?.
DR. A.S DIAGNOSES.
Acute hemolytic streptococcus peritonitis.
Septicemia, streptococcus hemolyticus.
Acute generalized peritonitis, streptococcus hemolyticus.
Septicemia, streptococcus hemolyticus.
Acute peritonitis with effusion, streptococcus hemolyticus.