Reversible hypophosphatemia during moderate hypothermia therapy for brain-injured patients

Citation
M. Aibiki et al., Reversible hypophosphatemia during moderate hypothermia therapy for brain-injured patients, CRIT CARE M, 29(9), 2001, pp. 1726-1730
Citations number
23
Categorie Soggetti
Aneshtesia & Intensive Care
Journal title
CRITICAL CARE MEDICINE
ISSN journal
00903493 → ACNP
Volume
29
Issue
9
Year of publication
2001
Pages
1726 - 1730
Database
ISI
SICI code
0090-3493(200109)29:9<1726:RHDMHT>2.0.ZU;2-I
Abstract
Objective: Because plasma potassium, which may similarly change as plasma p hosphate (P), decreases during moderate hypothermia, plasma P, a requisite electrolyte for the cell function, may alter during therapeutic moderate hy pothermia for brain-injured patients. In 22 such patients who underwent mod erate hypothermia or were treated with normothermia, plasma concentrations of P and other chemicals were examined. Design: A prospective study. Setting: The intensive care unit of a medical university hospital. Patients and Interventions: In 15 consecutive patients with brain injury wh o underwent moderate hypothermia and 7 serial patients treated with normoth ermia, plasma concentrations of P, potassium, glucose, blood gas tension an d pH, daily urine volume, and water balance were examined. Inequality in th e numbers of patients of the two groups was the result of patient exclusion because of multiple trauma, aluminum hydroxide administrations, hyperventi lation, preexisting diabetes mellitus, or administration of insulin. Daily blood sampling was done around 8 am. Inclusion criteria included a Glasgow Coma Scale score assessment less than or equal to8 at admission to the emer gency room and evidence of injury on computerized tomography scanning of th e brain. Measurement and Main Results: Hypothermia decreased plasma P levels as comp ared with those of normothermia within 4 days after the injury (this period was similar to the duration of the hypothermic phase in the hypothermia gr oup). Such reduction related to changes in blood glucose levels, but not to any in the urine volume, or water balance. The P decrease occurred during the hypothermic phase, but subsequently there was a recovery of P after the rewarming phase. The changes in plasma potassium levels were similar to th ose in plasma P concentrations during the course. Such changes were accompa nied by a recovery of decreased heart rate that occurred during the hypothe rmic phase. Conclusion. The results suggest that moderate hypothermia of 32-33 degreesC decreases plasma P levels. Further studies are required to examine whether P repletion may overcome certain hemodynamic derangements during moderate hypothermia in brain-injured patients.