Abstract

S INCE the advent of major abdomina1 surgery the probIem of postoperative peritonitis has been an extremeIy important one and stiI1 presents itseIf as a chaIIenge to the surgeon from the standpoint of both prevention and cure. During the past fifty years there has been a Iarge amount of work done on the production of peritonitis in various experimenta animaIs, and attempts have been made to correIate the findings in animaIs with the peritonitis which occurs in the human being. Such attempts have been far from satisfactory and there is stiI1 need for more carefuIIy controIIed Iaboratory and cIinica1 investigation in the fieId. The earIy workers on experimenta peritonitis found it diffrcuIt to produce a true fibrinopurulent peritonitis by the intraperitonea1 injection of bacteria. They couId eariIy produce a bacteremia, or, with more viruIent organisms, couId get a IethaI effect, but not a peritonea1 exudate. It therefore occurred to them that peritonitis per se was probabIy not the cause of death, but was in reaIity a protective mechanism, and that the animaIs, paradoxicaIIy enough, died from a want of inflammatory reaction rather than as a resuIt of it. Herrman, in 1927, at the Mayo CIinic, showed that in order to produce a peritonea exudate in the rabbit it was first necessary to buiId up an immunity before injecting the infecting materia1. This was successfuIIy carried out by using repeated smaI1 intraperitonea1 doses of a vaccine prepared from the coIon baciIIus and Streptococcus viridans. At autopsy the animaIs showed a true fibrinopuruIent peritonitis, but contro1 animaIs which received no such immunizing vaccine died promptIy with no visibIe evidence of peritonitis. Today, this concept regarding the production of peritonitis is generaIIy accepted, and comes to our attention every time we perform an abdomina1 operation. We know that the degree of resistance of the peritoneum wiI1 vary with the extent to which the peritoneum has been previously immunized. In cases of regressing acute choIecystitis, in which pus is spiIIed into the peritonea1 cavity at operation, there is no grave danger from a subsequent severe peritonitis. This resistance of the peritoneum to a limited amount of infection is probabIy not due to any “natura1” or “inherent” immune quaIity, but is more IikeIy the resuIt of an exceIIent bIood and Iymphatic suppiy. Attempts to immunize the peritoneum by the intraperitonea1 injection of vaccines and various foreign substances are by no means new. As earIy as 1887 PawIowsky used croton oi1 to produce peritonitis in experimenta animals. The probIem was more activeIy studied by Issaef in 1894 when he introduced the idea of vaccination to prevent postoperative peritonitis. PierraIini, in 1897, found that a Ieucocytic exudate couId be produced by the intraperitonea1 injection of sodium chloride and other inert substances. In the same year GarniCr demonstrated that bacteria were rapidIy destroyed in the presence of such a Ieucocytic exudate in the peritoneal cavity, and his researches reveaIed a new concept regarding the mechanism of protection from an otherwise fatal peritonitis, nameIy phagocytosis. In 1902, Soheri, working on the theory that “immunity” was a resuIt of phagocytosis, produced a peritonea1 Ieucocytic exudate, and found that animaIs

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