The syndrome of bacteremic shock has long been recognized as a serious clinical problem. While the most common offending microorganisms belong to the coliform group, this usually fatal malady can be precipitated by Gram-positive bacteria, by rickettsiae, by viruses, and by spirochetes.1 The pathophysiology is generally pictured as vascular failure or collapse and is believed to be due directly or indirectly to endo- or exotoxins.2,3 The pattern of physiologic dysfunction is essentially similar with both toxins. It is estimated that about 12%-15% of clinical bacteremias develop hypotension and the shock syndrome.1 At one time the mortality rate was 100%. With the introduction of antibiotics, supportive therapy, and proper surgical intervention, the mortality rate has been reduced to 60%-70% in Gramnegative bacteremic shock and to 75%-80% in Gram-positive shock.
The management of bacteremic shock ideally is directed to the offending agent. The complex changes in the host which
BLAIR E, HENNING G, HORNICK R, COWLEY RA. Hypothermia in Bacteremic Shock. Arch Surg. 1964;89(4):619–629. doi:10.1001/archsurg.1964.01320040035006
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