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