Hypophosphatemia and hypomagnesemia induced by cooling in patients with severe head injury.
OBJECTIVE
Induced hypothermia in patients with severe head injury may prevent additional brain injury and improve outcome. However, this treatment is associated with severe side effects, including life-threatening cardiac tachyarrhythmias. The authors hypothesized that these arrhythmias might be caused by electrolyte disorders and therefore studied the effects of induced hypothermia on urine production and electrolyte levels in patients with severe head injury.


METHODS
Urine production, urine electrolyte excretion, and plasma levels of Mg, phosphate, K, Ca, and Na were measured in 41 patients with severe head injury. Twenty-one patients (Group I, study group) were treated using induced hypothermia and pentobarbital administration, and 20 patients (Group 2, controls) were treated with pentobarbital administration alone. In Group 1, Mg levels decreased from 0.98+/-0.15 to 0.58+/-0.13 mmol/L (mean +/- standard deviation; p < 0.01), phosphate levels from 1.09+/-0.19 to 0.51+/-0.18 mmol/L (p < 0.01), Ca levels from 2.13+/-0.25 to 1.94+/-0.14 mmol/L (p < 0.01), and K levels from 4.2+/-0.59 to 3.6+/-0.7 mmol/L (p < 0.01) during the first 6 hours of cooling. Electrolyte levels in the control Group 2 remained unchanged. Electrolyte depletion in Group I occurred despite the fact that moderate and, in some cases, substantial doses of electrolyte supplementation were given to many patients, and supplementation doses were often increased during the cooling period. Average urine production increased during the cooling period, from 219+/-70 to 485+/-209 ml/hour. When the targeted core temperature of 32 micro C was reached, urine production returned to levels that approximated precooling levels (241+/-102 ml/hour). Electrolyte levels rose in response to high-dose supplementation. In the control group, urine production and electrolyte excretion remained unchanged throughout the study period.


CONCLUSIONS
Induced hypothermia is associated with severe electrolyte depletion, which is at least partly due to increased urinary excretion through hypothermia-induced polyuria. This may be the mechanism through which induced hypothermia can lead to arrhythmias. When using this promising new treatment in patients with severe head injury, stroke, or postanoxic coma following cardiopulmonary resuscitation, prophylactic electrolyte supplementation should be considered and electrolyte levels should be monitored frequently.
Polderman
K H
KH
Surgical Intensive Care Unit, University Hospital Vrije Universiteit, Amsterdam, The Netherlands. k.polderman@tip.nl
Peerdeman
S M
SM
Girbes
A R
AR
D000293:Adolescent; D000328:Adult; D000368:Aged; D001145:Arrhythmias, Cardiac / Q000209:etiology; D006259:Craniocerebral Trauma / Q000150:complications* / Q000628:therapy*; D003663:Decision Trees; D003919:Diabetes Insipidus / Q000209:etiology; D004573:Electrolytes / Q000097:blood / Q000652:urine; D006801:Humans; D007008:Hypokalemia / Q000209:etiology; D017674:Hypophosphatemia / Q000209:etiology*; D007036:Hypothermia, Induced / Q000009:adverse effects*; D007427:Intracranial Pressure; D008274:Magnesium / Q000097:blood*; D008875:Middle Aged; D017211:Treatment Failure; D014556:Urine
D004573:Electrolytes; D008274:Magnesium