Objectives: In accidental hypothermia the underlying physiological mechanisms responsible for poor outcome during rewarming through 32°C remain obscure, although possible associations include changes in acid-base balance, divalent cations, and inflammatory markers. This study investigated the metabolic and inflammatory changes that occur during the rewarming of hypothermic patients.
Methods: Eight patients, four men and four women, age 45 to 85 years, admitted with core temperatures <35°C were included in the study. Patients were rewarmed with dry warm blankets and fluid replaced by crystalloid at 40°C. Bloods for pH, ionised calcium (Ca2+) and magnesium (Mg2+), parathyroid hormone (PTH), interleukin 1 (IL1), interleukin 6 (IL6), tissue necrosis factor α (TNFα), were collected at presentation, during rewarming, and at 24 hours.
Results: Four patients were admitted with mild (32°–35°C) and four with moderate (28°–32°C) hypothermia. Rewarming to 32°C had no significant effect on the presenting acidosis (p=0.1740), although above 32°C pH increased with temperature (p<0.0001). There was a negative correlation between pH and both Ca2+ (p=0.0005) and Mg2+ (p=0.0488) below 32°C; above this temperature the relation was significant only for Ca2+ (p=0.0494). PTH and Ca2+ correlated positively (p=0.0041) and negatively (p=0.0039) below and above 32°C respectively. There was no relation between IL1 or TNFα with Ca2+ during rewarming, but IL6 and Ca2+ correlated positively (p=0.0039) and negatively (p=0.0018) when presentation temperature was below and above 32°C respectively.
Conclusions: During rewarming pH remains unchanged until patient temperature approaches 32°C. Ca2+ and Mg2+ decline is associated with the pH increase above 32°C. Poor outcome is associated with presentation temperature (<32°C), non-physiological correlation between IL6-PTH-Ca2+, and age (≥84 years).
- divalent cations
- parathyroid hormone
- PTH, parathyroid hormone
- IL1, interleukin 1
- IL6, interleukin 6
- tissue necrosis factor α
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