Managing combined critical hypothermia, diabetic ketoacidosis and cocaine intoxication noninvasively

Freundt, Miriam; Obaji, Adel; Hix, John K.

doi:10.1016/j.ajem.2013.10.042

Cited by 1 publication

(2 citation statements)

References 9 publications

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“…The cause of hypothermia associated with DKA is presumed to be the lack of insulin preventing the intracellular movement of glucose to be used as a substrate for heat production [ 7 ]; other causes of hypothermia in diabetic patients include impairment of heat conservation methods due to autonomic dysfunction failing to induce effective peripheral vasoconstriction, as well as reduced muscle mass producing insufficient heat output [ 8 , 9 ]. Severe hypothermia may indeed also exacerbate the worsening diabetic state by inhibiting the endogenous release of insulin as well as impairing the cellular effect of exogenously administered insulin [ 6 , 10 ]. These factors are the basis for the imperative to rapidly warm a DKA patient to >30-32 0 C [ 10 , 11 ].…”

Section: Discussionmentioning

confidence: 99%

“…Severe hypothermia may indeed also exacerbate the worsening diabetic state by inhibiting the endogenous release of insulin as well as impairing the cellular effect of exogenously administered insulin [ 6 , 10 ]. These factors are the basis for the imperative to rapidly warm a DKA patient to >30-32 0 C [ 10 , 11 ]. When dropping below this same temperature threshold (30-32 0 C), shivering stops typically allowing for core temperature to fall further at a faster rate.…”

Section: Discussionmentioning

confidence: 99%

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Brief Report: Diabetic Keto-Acidosis (DKA) Induced Hypothermia May Be Neuroprotective in Cardiac Arrest

Shiber

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2023

The Journal of Critical Care Medicine

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Despite the decreased survival associated with diabetes with out-of-hospital cardiac arrest and the overall low survival to hospital discharge, we would like to present two cases of OHCA in diabetics who despite prolonged resuscitation efforts had complete neurological recovery likely due to concomitant hypothermia. There is a steady decreasing rate of ROSC with longer durations of CPR so that outcomes are best when <20 minutes compared to prolonged resuscitation efforts (>30-40 minutes). It has been previously recognized that hypothermia prior to cardiac arrest can be neurologically protective even with up to 9 hours of cardiopulmonary resuscitation. Hypothermia has been associated with DKA and although often indicates sepsis with mortality rates of 30-60%, it may indeed be protective if occurring prior to cardiac arrest. The critical factor for neuroprotection may be a slow drop to a temperature <250C prior to OHCA as is achieved in deep hypothermic circulatory arrest for operative procedures of the aortic arch and great vessels. It may be worthwhile continuing aggressive resuscitation efforts even for prolonged periods before attaining ROSC for OHCA in patients found hypothermic from metabolic illnesses as compared to only from environmental exposures (avalanche victims, cold water submersions, etc.) as has been traditionally reported in the medical literature.

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