Septic shock (Part 1).
Septic shock is a distinct clinical entity with an overall mortality of 30% to 40%. Gram-negative organisms are the most frequently identified causal agents. The shock syndrome appears to result from activation of complement, coagulation, kinin, endorphin, and other hormonal systems. Physiologic abnormalities include hypotension, metabolic acidosis, increased cardiac index, and decreased tissue extraction of oxygen. Clinicians must entertain the diagnosis of septic shock in a variety of settings, as prognosis is affected by early institution of therapy. Treatment is directed toward control of infection with antibiotics and surgical drainage and cardiorespiratory support utilizing fluids and pressor agents. Future therapeutic options may include naloxone, cyclooxygenase inhibitors, and antiserum to endotoxin.
D000255:Adenosine Triphosphate / Q000096:biosynthesis; D000596:Amino Acids / Q000378:metabolism; D001777:Blood Coagulation; D003167:Complement Activation; D004723:Endorphins / Q000502:physiology; D004731:Endotoxins / Q000494:pharmacology; D006439:Hemodynamics; D006801:Humans; D008099:Liver / Q000378:metabolism; D008954:Models, Biological; D011453:Prostaglandins / Q000378:metabolism; D012772:Shock, Septic / Q000276:immunology / Q000378:metabolism / Q000382:microbiology / Q000503:physiopathology*
D000596:Amino Acids; D004723:Endorphins; D004731:Endotoxins; D011453:Prostaglandins; D000255:Adenosine Triphosphate