Race, sex, age and occupation. These features appeared in conformity with the character of the population from which they were derived.
Treatment. A very small portion of these fatal cases were given the present-day methods of treatment.
Past medical history of cases. This was negative or unknown in all but 27 cases.
Causes of death. There were 27 cases which died of other causes than amebiasis, and which had but a few amebic ulcers at some point in the colon. Most of the deaths due to amebic infection resulted from the secondary extension of the disease to the liver, and sometimes to lung and brain. Another large group had a peritonitis that developed from either a perforation of amebic ulcers in the intestine, or from pyogenic extension through the thin base of an ulcer or of ulcers.
Distribution of primary amebic lesion. About 60 per cent of the series possessed amebic ulcers more or less all through the colon, while about 40 per cent had a local distribution in the more dependent parts of colon and appendix. The local incidence for age and number of lesions can be placed in the following order of importance: the cecum and ascending colon, the rectum and sigmoid, and the appendix. The results are in conformity, more or less, with the report of Kartulis (1) except in regard to the appendix, which was described as follows: “The appendix was seldom affected (only 9 times out of several hundred cases).”
It is quite true that the appendix is seldom involved alone, but it may take the lead in the clinical picture in some cases and be the cause of some time lapse before the disease of primary importance is discovered. This is a rudimentary organ that tends to become more or less obliterated in adult life, and is subject to congenital kinks, bands, malposition, etc., all of which make it a dangerous position in many cases for an ulcerative process. It seems to me that it might be a more difficult part of the intestinal tract to treat successfully, and this would make its possibilities as a “carrier pocket” even more important in the management of such cases.
Complications of primary amebic lesions. Perforations, single or multiple, occurred in amebic ulcers of the gut or appendix in 10.7 per cent of the series. The majority of these accidents occurred in the cecum, rectum, sigmoid, and appendix. There were 2 cases showing appendiceal abscesses, two more with perirectal abscesses, and 2 cases with fistulae of an amebic nature. A spontaneous fecal fistula through the right abdominal wall was found once.
Secondary lesions of an amebic nature. Liver abscesses of major or minor degree occurred in 51 per cent of the series. Woodward (2) reports 21 per cent in 3680 dysentery autopsies performed in various tropical countries, while Byam and Archibald (3) state that the liver abscess probably occurs in at least 30 per cent of the cases.
A solitary abscess occurred in 42 per cent, and multiple abscesses in 58 per cent, of the cases. The local distribution of the abscesses was as follows: right lobe, 55.7 per cent; 2 lobes or all lobes, 25.2 per cent; left lobe, 8.4 per cent; unstated location 2.1 per cent.
Peri-hepatitis of an acute plastic nature was present in a focal manner over abscess locations in 83 per cent.
An amebic colitis, focal or general, was present in nearly all the cases of liver abscess.
Important complications of liver abscesses. Rupture of one or more abscesses into the greater or lesser peritoneal cavity, happened in 14.7 per cent of the cases.
Rupture of an abscess through a wing of the diaphragm, or formation of an abscess between the liver and the diaphragm, happened in 12.6 per cent of the cases.
Rupture of an abscess into the stomach occurred once.
Spontaneous rupture of an abscess through the body wall was found once.
Pressure from an abscess once obstructed the duodenum and the stomach; there was another instance in which the gallbladder was stretched out as thin as a ribbon over the prominence of an abscess.
Exclusive of focal areas of acute plastic peri-hepatitis, there was a soiled or infected peritoneal cavity from ruptured abscesses in 17.8 per cent of the cases.
Other forms of secondary amebic lesions. Including all cases of peritonitis from ruptured liver abscesses, all cases resulting from perforations of the gut or appendix, and those cases in which a pyogenic peritonitis developed through the thin base of an unruptured amebic ulcer, there were 28.6 per cent that showed a serious degree of peritonitis.
The lungs and the brain were the seat of amebic abscesses 4 times.
Thrombosis, amebic, of large venous channels happened twice, and each time was associated with a liver abscess case.
Cecostomy wounds were extensively invaded in 3 cases by amebae.
Decline in mortality rate of amebiasis. There was a sharp decline in the number of autopsies showing amebic lesions, after the years 1914 and 1915. Possible factors that might have been an influence were, population changes, sanitary education, more effective methods of treatment and the installation of a good water-system.