Management of septic peritonitis: more than surgery (Proceedings)


Management of septic peritonitis: more than surgery (Proceedings)

Aug 01, 2011

Sepsis is responsible for a large percentage of human deaths each year and the mortality has remained unchanged despite advances in critical care. In small animals, sepsis is also a frequent contributor to morbidity and mortality. Septic peritonitis in animals may be the presenting complaint to the emergency service, or may be a complication of a surgical procedure such as enterotomy or gastric resection.


In sepsis, the local systemic response to infection that is designed to be protective becomes systemic and affects other body systems. The classic scenario for the cascade of events that result in sepsis begins with exposure to endotoxin, a component of the cell wall of gram-negative bacteria (or lipoteichoic acid in the case of gram positive bacteria). Exposure to endotoxin activates neutrophils and macrophages to secrete inflammatory cytokines, the most well studied cytokines being tumor necrosis factor (TNF), interleukin-1 (IL-1), and interleukin 6 (IL-6). Under normal circumstances, cytokines and other inflammatory mediators are responsible for the early clinical signs of sepsis (fever, neutropenia) and normally interact to neutralize the infection and generate a mild inflammatory response. If this immune response is overwhelmed, excessive inflammatory mediators are released leading ultimately to organ failure, shock and death.

The key changes associated with massive release of inflammatory mediators have important therapeutic implications and include disruption of microvascular permeability, nitric oxide mediated vasodilation, activation of coagulation with consumption of endogenous anticoagulants, and myocardial depression.


Systemic Inflammatory Response Syndrome (SIRS) is described as the systemic response to a variety of clinical insults including bacteria, fungal, or tissue injury. In order for a dog to have SIRS, 2 out of the following 4 criteria should be present: Tachycardia, leukocytosis or leukopenia, hypo-or hyperthermia, and tachypnea. A big limiting factor to the clinical usefulness of these criteria is that dog, unlike people, pant and therefore the respiratory component of these criteria is subjectively evaluated. In cats, similar criteria have been proposed (but not validated), with a tentative diagnosis of SIRS if 3 out of 4 criteria are fulfilled. Cats have a tendency to be bradycardic when shock is present, so in cats tachycardia or bradycardia is included for the diagnosis of SIRS. It is important to note that these criteria are far from ideal. Sepsis is considered the systemic response to a documented infection. Animals are septic if they have an infection in addition to SIRS. Because of this, the definition of sepsis in people includes evidence of SIRS (2/4 criteria listed above), along with 'gross, histopathological, or microbiological evidence of infection or a strong suspicion of infection'.

Severe sepsis describes sepsis along with evidence of organ dysfunction (hyperbilirubinemia, thrombocytopenia, azotemia, altered mental state). Septic shock describes sepsis along with hypotension that is refractory to therapy and requires vasopressor therapy. Many dogs that present to the emergency room collapsed with evidence of sepsis are erroneously diagnosed with septic shock. They may be experiencing shock, and they may be septic, but they can only be diagnosed with septic shock if hypotension persists despite adequate fluid resuscitation. Parameters that can be used to guide fluid therapy include calculation of a shock dose of crytalloids or colloids, central venous pressure monitoring (difficult to use in an emergency situation due to the need for a central line), lactate concentration, and echocardiography to look for left ventricular filling.

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