Summary Medical records of 21 dogs and 2 cats treated for septic peritonitis were reviewed. Animals were between 1 and 12 years old, (mean, 6.5 years) and weighed between 6 and 51.4 kg (mean, 22.7 kg). Overall, 13 animals survived and were discharged from the hospital. Immediately after surgical correction of the underlying cause of peritonitis, most animals were tachycardic (mean heart rate, 148 beats/min; range, 80 to 204 beats/min), and many were hypotensive (mean arterial pressure, 84.4 mm of Hg; range, 44 to 156 mm of Hg). Hypotension was attributed to sepsis and hypovolemia secondary to extensive loss of fluid into the peritoneal cavity. Survivors did not differ from nonsurvivors with regard to mean arterial pressure immediately after surgery, and in most animals, hypotension could be corrected by iv administration of fluids. Three animals died after failing to respond to fluid treatment, despite concurrent administration of inotropic or pressor agents. Mean rate for crystalloid fluid administration was 12.8 ml/kg of body weight/h (range, 5 to 23.5 ml/kg/h) during the first 24 hours after surgery. Six of 23 animals had low urine output for a short time after surgery, but urine output increased when fluids were administered. Hypoalbuminemia developed in all animals (mean serum albumin concentration, 1.17 g/dl; range, 0.6 to 2.3 g/dl), and peripheral edema developed in 13. Neither lowest mean serum albumin concentration nor fluid administration rate was significantly different between animals that developed peripheral edema and those that did not. Fluid administration rates were significantly higher in nonsurvivors (15 ml/kg/h; range, 5.5 to 23.5 ml/kg/h) than in survivors (11 ml/kg/h; range, 5 to 17.5 ml/kg/h). Thirteen animals had evidence of pulmonary alveolar consolidation, and 9 had pleural effusions; however, fluid administration rates were not significantly different between animals that did and those that did not develop clinical respiratory disease. Eleven animals had pancreatitis at the time of surgery, or developed pancreatitis subsequently. Four animals developed disseminated intravascular coagulation, and only 1 survived. Indicators of a poor prognosis included refractory hypotension, cardiovascular collapse, and development of respiratory disease or disseminated intravascular coagulation. Development of pancreatitis, high serum concentrations of hepatic enzymes, high or low wbc count, hypo- or hyperglycemia, signs of abdominal pain, and abdominal effusion were not associated with outcome.
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