Abstract

Introduction Hyperlactataemia is associated with adverse outcomes in trauma cases. It is thought to be the result of anaerobic respiration during hypoperfusion. This produces much less energy than complete aerobic glycolysis. Low body temperature in the injured patient carries an equally poor prognosis. Significant amounts of energy are expended in maintaining euthermia. Consequently, there may be a link between lactate levels and dysthermia. Hyperlactataemia may be indicative of inefficient energy production and therefore insufficient energy to maintain euthermia. Alternatively, significant amounts of available oxygen may be sequestered in thermoregulation, resulting in anaerobic respiration and lactate production. Our study investigated whether there is an association between lactate levels and admission body temperature in hip fracture patients. Furthermore, it looked at whether there is a difference in the mean lactate levels between hip fracture patients with low (<36.5°C), normal (36.5-37.5°C) and high (>37.5°C) body temperature on admission, and for patients who have low body temperature, whether there is a progressive rise in serum lactate levels as body temperature falls. Methods The admission temperature and serum lactate of 1,162 patients presenting with hip fracture were recorded. Patients were divided into the euthermic (body temperature 36.5-37.5°C), the pyrexial (>37.5°C) and those with low body temperature (<36.5°C). Admission lactate and body temperature were compared. Results There was a significant difference in age between the three body temperature groups (p=0.007). The pyrexial cohort was younger than the low body temperature group (mean: 78 vs 82 years). Those with low body temperature had a higher mean lactate level than the euthermic (2.2mmol/l vs 2.0mmol/l, p=0.03). However, there was no progressive rise in serum lactate level as admission temperature fell. Conclusions The findings suggest that in hip fracture patients, the body attempts initially to maintain euthermia, incurring an oxygen debt. This would explain the difference in lactate level between the low body temperature and euthermic cohorts. The fact that there is no correlation with the degree of temperature depression and lactate levels indicates that the body does not fuel thermohomeostasis indefinitely with oxygen. Instead, in part, it abandons thermoregulatory mechanisms. Consequently, in this population, active rewarming may be indicated rather than depending on patients' own thermogenic ability.

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