Septic shock: Dx
Advanced, Clinical Subspecialties
Septic shock is typically defined by the combination of sepsis (SIRS criteria with evidence of infectious source) with severe hypotension despite resuscitation. Sepsis is a type of distributive shock, and the primary pathology is a depleted intravascular volume due to diffuse capillary leakage. Identifying sepsis is of course driven by identification of infectious etiology with culture results and clinical, imaging, or lab findings suggestive of infection.
Although not highly specific, clinical signs including fever, nausea/vomiting, altered mental status, hypoxemia related to ARDS, and tachycardia in the setting of hypotension are consistent with septic shock. Lab findings include leukocytosis with left shift and hyperglycemia due to insulin resistance. Lactate accumulates with worsening hypoperfusion, resulting in metabolic acidosis with respiratory compensation. In the hospital setting, culture findings suggest pulmonary and urinary tract infections with gram-negative bacteria are the most common offenders; of note however, no organism is isolated from blood cultures in up to 50% of septic shock cases.
Distinguishing a shock state to be of septic origin is made more challenging due to its variable presentation. Septic shock is often said to be hyperdynamic with normal or increased cardiac output even with simultaneous reduced cardiac contractility. Increased mixed venous oxygen saturation can be a useful marker- potentially reflecting both a high cardiac output state and metabolic dysfunction at the cellular level affecting utilization of oxygen.
Patients with pre-existing cardiac disease or severe extent of hypovolemia may also have more of a hypodynamic shock with reduced CO, reduced mixed venous O2, and pulmonary hypertension which is driven by vasoactive inflammatory markers and the formation of microthrombi in the pulmonary circulation.