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Hypokalaemia in severe head trauma.

作者信息

Pomeranz S, Constantini S, Rappaport Z H

机构信息

Neurosurgery Department, Hadassah University Hospital, Jerusalem, Israel.

出版信息

Acta Neurochir (Wien). 1989;97(1-2):62-6. doi: 10.1007/BF01577741.

DOI:10.1007/BF01577741
PMID:2718795
Abstract

Forty-six consecutive patients with severe isolated head trauma (GCS less than or equal to 7) had significant hypokalaemia averaging 3.1 +/- 0.4 (S.D.) mmol/litre upon admission to the emergency room. This electrolyte imbalance occurred within hours of the trauma and resolved under treatment within the first day. There was no correlation between serum potassium and pH, glucose, urine electrolytes, patient age or sex, admission Glasgow Coma Score or the Glasgow Outcome Score. Sixteen patients with multiple trauma but without head trauma had an average serum potassium of 3.5 +/- 1.1 mmolar. Mechanisms of serum potassium level control and their correlation with brain trauma are addressed in a search for an explanation of this phenomenon. We believe that the most appropriate explanation for this hypokalaemia is the large catecholamine discharge that is known to accompany severe head trauma, with resultant beta 2-adrenergic stimulation of the Na+ -K+ pump. The formation of a prospective on-going study to clarify the basic mechanism of hypokalaemia in severe head trauma is presented.

摘要

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Adrenergic control of Na+-K+-homoeostasis.钠钾稳态的肾上腺素能控制
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