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Multiple organ failure occurs with the presence of altered organ function and when homeostasis cannot be maintained without intervention. Multiple organ dysfunction syndrome (MODS) is the severe end of the sepsis spectrum. MODS is classified as primary or secondary:

· Primary MODS is the result of a well-defined insult in which organ dysfunction occurs early and can be directly attributable to the insult itself.

· Secondary MODS is organ failure not in direct response to the insult itself, but as a consequence of a host response.

It’s imperative for SIRS and severe sepsis to be recognized as early as possible. Progression to septic shock and MODS results in poor patient outcomes (Kaplow & Hardin, 2007). Identifying populations susceptible to developing sepsis leads to early recognition and better outcomes. According to Kaplow and Hardin, 2007, the following patients are at risk:

· Ages less than 1 year and greater than 85 years

· Immunocompromised

· Severe community-acquired pneumonia

· Intra-abdominal surgery

· Meningitis

· Chronic diseases such as cardiovascular disease, renal disease, and diabetes

· Cellulitis

· Urinary tract infection

Pathophysiology

The pathophysiology of sepsis is complex and involves many factors. For the purpose of this article, a simplified version will be explained using the inflammatory, procoagulant, and antifibrinolytic process. Cytokines are released during the inflammatory response. The cytokines cause other proinflammatory mediators, such as myocardial depressant factor to be released. This results in a decrease in the ejection fraction, a decrease in response to fluid resuscitation, and a decrease in blood pressure. The endothelium becomes procoagulant in response to the cytokines. This causes damage to the endothelium and leads to capillary leakage. When capillary permeability is disrupted, fluid shifts into the cells and the inflammatory process is further activated. This continuous cycle makes achieving homeostasis difficult (Kaplow & Hardin, 2007).

Thrombin production is promoted by the endothelium injury induced by the cytokines. A decline of protein C and antithrombin III results in procoagulation. Thrombin changes fibrinogen into fibrin and when combined with platelets, clots are formed. These clots can block microvasculature and negatively impact cell and organ function (Kaplow & Hardin, 2007).

Endothelial injury results in substances being produced to impair fibrinolysis. When fibrinolysis is impaired, the balance between clot formation and clot removal is disrupted. This imbalance can lead to disseminated intravascular clotting (DIC). DIC ultimately leads to MODS (Kaplow & Hardin, 2007).

Recognition

Early identification of sepsis results in better patient outcomes. Septic patients can be seen in the outpatient and inpatient setting (O’Brien et al, 2007). The presentation of symptoms varies; however, some common symptoms exist for each body system. The following table illustrates the common symptoms seen for each body system:

System 

Symptoms

General 

Fever, chills, fatigue, malaise, rigors, warm pink periphery

Central Nervous System 

Confusion, anxiety, disorientation, apprehension, agitation, obtunded, comatose

Cardiovascular 

Tachycardia, increase pulse pressure, hypotension
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