Secondary peritonitis pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Shivani Chaparala M.B.B.S [2]

Secondary bacterial peritonitis is caused by inoculation of bacteria from the (GI lumen or during surgical procedures) in the peritoneal cavity.

• Bacteria can reach the peritoneal cavity by a variety of pathologic processes:
  • Transmural inflammation with luminal obstruction
  • Perforation of the GI tract
  • Intestinal ischemia
• The initial inoculum of bacteria is determined by the normal flora in the involved portion of the GI tract.

Microbial organisms causing secondary peritonitis depends on the site of the gut perforation.^[1]

• Small bowel perforation: Consist mainly of enterococci and Escherichia coli
• Distal small bowel lumen perforation: Mostly Enterobacteriaceae and anaerobic organisms, including the Bacteroides spp.
• Colon: Mostly anaerobes (e.g. Peptostreptococcus, Clostridium, and most commonly Bacteroides sis)

Bacteria and digestive enzymes act on the peritoneal serosal surface resulting in enzymatic digestion, necrosis and an outpouring of serum protein and electrolytes from the blood into the peritoneal cavity, together with the formation of an exudate rich in granulocytes. The inflammatory process may be diffuse or confined to an abscess. Systemically, there is paralysis of the bowel, hemoconcentration, and decrease in the cardiac output due to the shift of fluids and later acidosis. Intrapulmonary shunting, hypo/hypercapnia, hypoxemia, progressive azotemia, acute tubular necrosis, weight loss by protein consumption, fall of body temperature, loss of heat production, and exhaustion are other complications that may lead to the death of the patient if the process is not interrupted.