Definitions of systemic inflammatory response syndrome (SIRS), sepsis, septic shock, and multiple organ dysfunction syndrome Systemic inflammatory response syndrome Two or more of the following clinical signs of systemic response to endothelial inflammation: • Temperature > 38°C or < 36°C?x Heart rate > 90 beats/min • Tachypnoea (respiratory rate > 20 breaths/min or hyperventilation (Paco2 < 4. 25 kPa)) • White blood cell count > 12 · 109/l or < 4 · 109/l or the presence of more than 10% immature neutrophils?In the setting (or strong suspicion) of a known cause of endothelial inflammation such as: Infection (bacteria, viruses, fungi, parasites, yeasts, or other organisms)
• Pancreatitis?x Ischaemia?x Multiple trauma and tissue injury?x Haemorrhagic shock?x Immune mediated organ injury?x Absence of any other known cause for such clinical abnormalities Sepsis Systemic response to infection manifested by two or more of the following: • Temperature > 38°C or < 36°C?x Raised heart rate > 90/min • Tachypnoea (respiratory rate > 20 breaths/min or hyperventilation (Paco2 < 4. 25 kPa)) • White blood cell count > 12 × 109/l or < 4 × 109/l or the presence of more than 10% immature neutrophils
Septic shock Sepsis induced hypotension (systolic blood pressure < 90 mm Hg or a reduction of >40 mm Hg from baseline) despite adequate fluid resuscitation Multiple organ dysfunction syndrome Presence of altered organ function in an acutely ill patient such that homoeostasis cannot be maintained without intervention Pathogenesis Systemic sepsis may complicate an obvious primary infection such as community acquired pneumonia or a ruptured abdominal viscus. Frequently, however, an infective source cannot be identified and the type of organism cultured may provide no clue to its anatomical origin.
Infections that complicate critical illness may arise from the gastrointestinal tract. This region is particularly sensitive to poor perfusion, which may lead to increased bowel permeability and translocation of organisms and endotoxin from the lumen of the gastrointestinal tract into the portal venous and lymphatic circulations. The subsequent release of cytokines and other inflammatory mediators by hepatic Kupffer cells and circulating monocytes may then initiate a sequence of events that culminates in the clinical signs of sepsis and multiple organ failure.