Hypophosphatemia and hypomagnesemia induced by cooling in patients with severe head injury

Citation
Kh. Polderman et al., Hypophosphatemia and hypomagnesemia induced by cooling in patients with severe head injury, J NEUROSURG, 94(5), 2001, pp. 697-705
Citations number
39
Categorie Soggetti
Neurology,"Neurosciences & Behavoir
Journal title
JOURNAL OF NEUROSURGERY
ISSN journal
00223085 → ACNP
Volume
94
Issue
5
Year of publication
2001
Pages
697 - 705
Database
ISI
SICI code
0022-3085(200105)94:5<697:HAHIBC>2.0.ZU;2-H
Abstract
Object. Induced hypothermia in patients with severe head injury may prevent additional brain injury and improve outcome. However, this treatment is as sociated with severe side effects, including life-threatening cardiac tachy arrhythmias. The authors hypothesized that these arrhythmias might be cause d by electrolyte disorders and therefore studied the effects of induced hyp othermia on urine production and electrolyte levels in patients with severe head injury. Methods. Urine production, urine electrolyte excretion, and plasma levels o f Mg, phosphate, K, Ca. and Na were measured in 41 patients with severe hea d injury. Twenty-one patients (Group 1, study group) were treated using ind uced 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 cont rol Group 2 remained unchanged. Electrolyte depletion in Group 1 occurred d espite the fact that moderate and, in some cases, substantial doses of elec trolyte supplementation were given to many patients, and supplementation do ses were often increased during the cooling period. Average urine productio n increased during the cooling period, from 219 +/- 70 to 485 +/- 209 ml/ho ur. When the target ed con temperature of 32 degreesC was reached, urine pr oduction returned to levels that approximated precooling levels (241 +/- 10 2 ml/hour). Electrolyte levels rose in response to high-dose supplementatio n. In the control group, urine production and electrolyte excretion remaine d unchanged throughout the study period. Conclusions. Induced hypothermia is associated with severe electrolyte depl etion, which is at least partly due to increased urinary excretion through hypothermia-induced polyuria. This may be the mechanism through which induc ed hypothermia can lead to arrhythmias. When using this promising new treat ment in patients with severe head injury, stroke, or postanoxic coma follow ing cardiopulmonary resuscitation, prophylactic electrolyte supplementation should be considered and electrolyte levels should be monitored frequently .