Complications
Sepsis is defined as systemic inflammatory response syndrome (SIRS) resulting from a documented or presumed infection.
Criteria for SIRS is the presence of two or more of the following vital signs or laboratory results: temperature >100.4°F (>38.4°C) or <96.8°F (<36°C); heart rate >90 beats per minute; respiratory rate >20 breaths per minute, or PaCO₂ <32 mmHg; WBC >12,000/mm³ or <4000/mm³ or >10% immature neutrophils. This has fallen out of favor in consensus guidelines due to it being a poor predictor of mortality, and the nonspecific nature of these criteria in both infectious and noninfectious causes.[83]
Septic shock includes: meeting the definition for sepsis (Sequential Organ Failure Assessment [SOFA] score >2 points from baseline scores, with organ dysfunction), elevated lactate >18 mg/dL (>2 mmol/L), persistent mean arterial pressure <65 mmHg, despite adequate volume resuscitation, or the use of vasopressors in the absence of hypovolemia.[40][83] A quick SOFA score (qSOFA): respiratory rate of 22 breaths per minute, altered mental status, and systolic blood pressure <100 mmHg, could be used in noncritical situations. However, it lacks prospective evaluation for mortality prediction, and as such has not been part of the consensus definition for sepsis.[83]
These findings (previous sepsis definition using SIRS), plus skin infection accompanied with pain out of proportion, rapid progression, bullae formation, subcutaneous crepitus, and visible gas on imaging studies show an 85% sensitivity in detecting necrotizing skin infections.[23]
Septic shock is a persistent hypotension (previous definition: systolic blood pressure <90 mmHg or <40 mmHg from baseline; current consensus: mean arterial pressure <65 mmHg) despite adequate fluid resuscitation, elevated lactate 18 mg/dL (2 mmol/L), and meets sepsis definitions (SOFA score >2 points from baseline with organ dysfunction).[23][83]
The mechanism of shock in gangrene is poorly understood. Unconcentrated filtrate from Clostridium perfringens, purified alpha-toxin, and purified phi-toxins cause hypotension, bradycardia, and decreased cardiac output when injected into laboratory animals. Because alpha-toxins and phi-toxins are lipophilic and may remain locally bound to tissue plasma membranes, the toxins may stimulate synthesis of secondary mediators that cause cardiovascular abnormalities.[6] Shock is present in 50% of patients with gangrene at the time they present to the hospital.[5]
Alpha-toxin, a metalloenzyme that has phospholipase-C activity and causes cell destruction by hydrolysis of key cell membrane components, is produced in gas gangrene. It acts to cause lysis of erythrocytes, leukocytes, platelets, fibroblasts, and muscle cells.[5]
A substantial number of cases of gangrene result in partial or complete loss of a limb. Careful observation is required to ensure that there is adequate healing.
A clinical manifestation of inappropriate thrombin activation. The activation of thrombin leads to fibrinogen conversion to fibrin, platelet activation and consumption, activation of factors V and VIII, protein C activation, endothelial cell activation, and fibrinolysis. The leading causes are malignancy and infection that leads to gangrene. Sometimes DIC may be the presenting sign of the infection, and prompt recognition and appropriate management may be life-saving. It can occur at any age, and the reported mortality for this complication is near 35%, with a morbidity because of amputation as high as 85%.[84]
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