COLD THERAPY IN BACTEREMIC SHOCK 

 Emil Blair 



University of Maryland 



School of Medicine 

 Baltimore 1, Maryland 



ABSTRACT 



Approximately 10-12 per cent of bacteremic patients go into shock. Mortality is 

 60-70 per cent despite aggressive therapy, including bacteria sensitive antibiosis. 

 The basic problem in all forms of shock appears to be a disparity between MRO2 and 

 CDO2 (circulatory delivery of oxygen to the cell). The rationale of hypothermia is 

 directed primarily at MROg and secondarily at CDO2. At 32° C, MRO2 is one-third 

 of normal, cold pressor effect elevates and sustains arterial blood pressure, heart 

 rate is slowed, and the renal and the CNS flow and ventilation are augmented. The 

 patient is brought into a metabolic environment more commensurate with the red'-aced 

 perfusion. No direct effect on the bacterial organism or on antibiosis was observed. 

 Similarly, leucocytic response was not altered. Patients were cooled only when they 

 had become refractory to therapy and were in dire straights. Salvage rate was 50 per 

 cent in 52 cooled. Excluding deaths from various causes, 14 (27 per cent) died of un- 

 remitting septic shock. In two of these, opsonin indices were found to reduce markedly. 

 Current studies in dogs with no therapy appear to confirm the view that hypothermia 

 (32° C) exerts no direct effect on the organism or on host mechanisms. Death is likely 

 due in part to crippling of the RES. 



The syndrome of bacteremic shock has been long recognized as a 

 serious clinical problem (Laennec, 1831), While the most common 

 offending micro-organisms belongtothecoliform group, this usually 

 fatal malady can be precipitated by gram positive bacteria, by 

 Rickettsiae and by viruses (Spink, 1960; Ebert and Abernathy, 1961), 

 The pathophysiology is generally pictured as vascular failure or col- 

 lapse (Romberg, 1899; Gilbert, 1960) and believed due directly or in- 

 directly to endo- or exotoxins (Spink, 1960; Thai and Egner, 1956; 

 Aub et al., 1947). The physiologic dysfunction pattern is similar with 

 both toxins. It is estimated that about 15 per cent of clinical bacter- 

 emias develop hypotension and the shocksyndrome (Ebert and Aber- 

 nathy, 1961). Antibiosis along with supportive therapy reduced a 100 



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