The systemic inflammatory response syndrome (SIRS) and sepsis are complex syndromes resulting from an inciting insult that causes systemic inflammation, leading to widespread tissue injury. In the case of sepsis, the initial insult is an infection. Sepsis is the leading cause of death in critically ill patients. In the Unites States, sepsis occurs in 750,000 people every year, and more than 200,000 of them die. The incidence of sepsis is increasing, and it is especially common in the elderly. Both SIRS and sepsis may be seen in the perioperative period and are common causes of admission to the surgical intensive care unit.

The American College of Chest Physicians and the Society of Critical Care Medicine published consensus-derived definitions of SIRS, sepsis, and organ failure in 1992 (Table 232-1). In 2001, a list of signs and laboratory findings that should prompt a clinician to consider sepsis in the differential diagnosis was proposed. In addition to tachypnea, tachycardia, and alterations in temperature and white blood cell count, these findings include chills, poor capillary refill, decreased skin perfusion, thrombocytopenia, hypoglycemia, oliguria, alteration in mental status, and skin mottling.

SIRS occurs in the absence of infection and may be secondary to surgical insult, trauma, or inflammatory conditions, such as pancreatitis. Sepsis is the result of a complex interaction among the patient’s immune, inflammatory, and coagulation systems and an infecting organism. In both SIRS and sepsis, at the site of injury or infection, a local inflammatory response is antagonized by a local antiinflammatory response (Figure 232-1). Such proinflammatory and antiinflammatory responses often become systemic. Both excessive and inadequate host-immune responses can lead to progression of disease and organ dysfunction. Further, a large inciting stimulus or a virulent infectious agent may cause organ dysfunction even in the presence of a competent immune system. Neutrophils play a key role in the development of sepsis. An initial toxic stimulus (e.g., bacterial endotoxin) leads to production of proinflammatory cytokines, such as interleukin 1 and tumor necrosis factor. Migration of neutrophils to vascular endothelium subsequently occurs, with concomitant activation of clotting and generation of secondary inflammatory mediators.

Multiple organ dysfunction syndrome (MODS) may result from SIRS or sepsis. Organ dysfunction tends to follow a predictable course—independent of the inciting insult—unless the process is halted by therapeutic interventions. Intravascular volume depletion and vasodilation initially lead to hypotension. The acute respiratory distress syndrome (ARDS) may also occur relatively early. Subsequently, acute kidney injury, ileus, mental status changes, and hepatic dysfunction may occur. As the process continues, direct myocardial depression and bone marrow suppression may develop.

Common sites of infection, in descending order of frequency, include the lung, the abdominopelvic region, urinary tract, and soft tissue. In 20% to 30% of patients, a definite site of infection is not identified, and blood cultures may be positive only 30% of the time.

Sepsis and SIRS are associated with a vasodilated state; intravascular volume depletion results from “third spacing.” The classic picture shows a hyperdynamic, high cardiac output state with a low systemic vascular resistance. However, this hemodynamic pattern may be absent in the early stages before adequate volume resuscitation has taken place or when sepsis-associated myocardial depression leads to a decrease in stroke volume.

Severe sepsis and septic shock are medical emergencies requiring prompt intervention. Guidelines for management have been developed by a multinational multidisciplinary collaboration of experts as part of an education initiative known as the Surviving Sepsis Campaign, the latest iteration being the 2012 version. Many institutions have incorporated these therapies into “sepsis bundles” to promote best practice. Suggested algorithms for investigating potential sepsis and managing patients with sepsis are provided in Figures 232-2 and 232-3. Elements of sepsis management include initial resuscitation, diagnosis, antibiotic therapy, source control, and supportive therapy.