Septic shock (endotoxic shock).

: The pathophysiology, clinical aspects, medical, and surgical management of endotoxin shock are reviewed. In the primate, the pathophysiology of endotoxin shock is contributed to by selective vasopasm, disseminated intravascular coagulation, and reduced myocardial response to sympathetic stimuli. Studies in the baboon measured various parameters of hemodynamics and coagulation, catecholamines, and some biochemical changes following the injection of a single bolus of endotoxin. Hemodynamic studies pointed to the kidney as a primary target organ. Coagulation changes included alterations in factor XII and XIII (and others) and plasminogen. Deposition of fibrin was also noted. Neurohormonal studies using tritiated norepinephrine showed a sharp rise in catecholamines 3 minutes after injection of endotoxin followed by a return to normal within 120 minutes, confirming the role of vasopasm in reducing renal perfusion early in shock. Prevention of septic shock is the best way to eradicate the extremely high reported mortality rates; infected abortion, chorioamnionitis, and pyelonephritis should all be warning signals. Methods of monitoring the patient in septic shock with special attention to blood pressure, central venous pressure, blood volume changes, and urinary output are discussed. Early surgical intervention and the proper use of vasomotor drugs and corticosteroids enhance patient survival.