“Agglutinated point of rupture at the median periphery of the cecum near the ileo-cecal valve.  The perityphlitic pus appeared to be sacculated by adherent intestinal coils, but beyond the adhesions in the free abdominal cavity below the omentum there was diffuse, fresh, fibrinous peritonitis and distributed here and there small quantities of thin, putrid pus (many bacteria, large quantities of streptococci and cold bacilli).  The peritoneum was injected. of a delicate rose-red color, here and there covered with fine, mucus-like pseudo-membranes.  Heart flabby.”

[The autopsy showed nothing more than would be expected.  The fresh peritonitis confirms what I say that a reinfection was forced because of the character of the food.  The meteorism opposed relaxation and rest, two conditions positively necessary and without which healing can not take place.  What was to hinder the heart from being flabby, Drugs and systemic infection are quite enough.

In proper hands this young man would not have been very sick; possibly his trouble would have been thrown off and the inflammation passed off by resolution.

The following should be of interest for it is a very scientific explanation of how the young man came to die:]

“The clinical history is in every respect typical and instructive.

“It shows us that the origin of peritonitis which is by far the most common, is in a diseased appendix.  At the autopsy this was found necrotic and perforated.  It is questionable whether the perforation existed from the onset of the disease; it is possible that at first an ulcer extending to the serosa caused an infection of the peritoneum; at all events this occurred acutely, and produced the sharply defined disease.”

[I agree.  The perforation brought on the relapse and the collapse.]

“The clinical abdominal symptoms in the first period of the malady pointed to the fact that at the onset there had been a diffuse inflammation of the peritoneum, and that later, by the adhesions to the appendix which were found at the autopsy an early encapsulation of pus had taken place in the ileo-cecal region; this produced a purulent softening in the wall of the cecum and led to the favorable rupture of pus into the intestine and to an immediate amelioration of the acute peritonitis.  The point of rupture, however, then closed, and partly perhaps to the action of fresh infectious and toxic material, perhaps only to the perforation of the appendix, may be ascribed the exacerbation of the peritonitis, that is, a renewed attack which caused the death of the patient.”