Septic peritonitis

Echtenacher B. Mannel DN. Hultner L Critical protective role of mast cells in a model of acute septic peritonitis. Nature 1996 381 75-77. 

Murine Model of Polymicrobial Septic Peritonitis Using Cecal Ligation and Puncture (CLP)... 

Key words Septic peritonitis, cecal ligation and puncture, polymicrobial sepsis. 

Zaloga G P, Sager A, Black K W et al 1992 Low dose calcium administration increases mortality during septic peritonitis in rats. Circulatory Shock 37 226-229 Ziemer E L, Parker H R, Carlson G P et al 1987 Clinical features and treatment of renal tubular acidosis In two horses. Journal of the American Veterinary Medical Association 190 294-296... 

Matsukawa A, Hogaboam CM, Lukacs NW, Lincoln PM, Stricter RM, Kunkel SL. Endogenous monocyte chemoattractant protein-1 (MCP-1) protects mice in a model of acute septic peritonitis cross-talk between MCP-1 and leukotriene B4. J Immunol 1999 163 6148-6154. 

O Primary peritonitis develops in up to 25% of patients with alcoholic cirrhosis.3 Patients undergoing continuous ambulatory peritoneal dialysis (CAPD) average one episode of peritonitis every 2 years.4 Secondary peritonitis may be caused by perforation of a peptic ulcer traumatic perforation of the stomach, small or large bowel, uterus, or urinary bladder appendicitis pancreatitis diverticulitis bowel infarction inflammatory bowel disease cholecystitis operative contamination of the peritoneum or diseases of the female genital tract such as septic abortion, postoperative uterine infection, endometritis, or salpingitis. Appendicitis is one of the most common causes of intraabdominal infection. In 1998, 278,000 appendectomies were performed in the United States for suspected appendicitis.5... 

The fluid and protein shift into the abdomen (called third-spacing) may be so dramatic that circulating blood volume is decreased, which causes decreased cardiac output and hypovolemic shock. Accompanying fever, vomiting, or diarrhea may worsen the fluid imbalance. A reflex sympathetic response, manifested by sweating, tachycardia, and vasoconstriction, may be evident. With an inflamed peritoneum, bacteria and endotoxins are absorbed easily into the bloodstream (translocation), and this may result in septic shock. Other foreign substances present in the peritoneal cavity potentiate peritonitis, notably feces, dead tissues, barium, mucus, bile, and blood. 

To induce peritoneal sepsis, a clot infected with bacteria is placed into the peritoneal cavity of rabbits. This method was first described in a canine model of septic shock (17). 

UK studies report mortality rates for adult patients hospitalised with community-acquired pneumonia ranging from 6% to 12%. Mortality increases to over 50% in patients admitted to the intensive care unit. Parapneumonic effusions develop in up to half of patients hospitalised with community-acquired pneumonia, requiring chest tube drainage it may be the cause of persisting pyrexia. Lung abscess is a relatively rare complication of community-acquired pneumonia, and metastatic infection such as meningitis, peritonitis, endocarditis and septic arthritis can occasionally develop. 

Riche FC, Cholley BP, Panis YH, et al. Inflammatory cytokine response in patients with septic shock secondary to generalized peritonitis. Crit Care Med 2000 28 433-437. 

Studies conducted in our laboratories examined the effects of such conjoint therapy with antibiotics on eicosanoid levels and survival in septic shock. In the rat faecal peritonitis model, improved survival time was observed with early treatment with steroids. However, this protection appears to be independent of inhibition of arachidonic acid metabolism. Corticosteroid pretreatment effected no more than a 30 and 40% inhibition of plasma levels of iTxB2 and i6-keto-PGFi3( respectively, compared with 100% inhibition with the cyclo-oxygenase inhibitors. Conjoint steroid and NSAID treatment improved survival time compared with each drug employed individually. The combination of steroid, NSAID and gentamicin produced the most significant effect on survival. 

Although there are reports of spontaneous reduction of intussusception (Swischuck etal. 1994 Navarro and Daneman 2004a), chronic and recurrent intussusceptions, and rare cases of spontaneous sloughing of the gangrenous intussusceptum through the rectum (Ravitch 1986), the usual course of an untreated intussusception is bowel obstruction followed by bowel perforation with peritonitis and septic shock. Currently, the overall perforation rate in developed countries is low (0%-3%). 

A 72-year-old man was given thiopental 303 mg/kg over 48 hours and 36 hours later developed abdominal tenderness, peritonism, and hyperlactatemia (11 mmol/1). At emergency laparotomy there was extensive fresh necrosis of the terminal ileum extending to the retro-sigmoid junction. Histology showed no vascular or inflammatory changes. He developed septic shock and died 12 hours postoperatively. 

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