Abstract | OBJECTIVES: METHODS: The study comprised 37 patients with severe TBI who were treated for barbiturate coma between 2015 and 2017 in level 3 intensive care units of two hospitals. RESULTS: No potassium disturbance occurred in 14 patients. Seventeen patients developed mild-moderate hypokalemia (2.6-3.5mEq/L), and 6 patients developed severe hypokalemia (<2.5mEq/L) following the induction of barbiturate therapy. The incidence of mild-to-severe barbiturate-induced hypokalemia was 62.2% and the rate of severe hypokalemia was 16.2%. The mean potassium supply per day during thiopentone therapy was statistically significantly different between patients with mild-to-moderate hypokalemic and those with severe hypokalemic (p<0.001). Four of 6 patients with severe hypokalemia developed rebound hyperkalemia exceeding 6mEq/L following the cessation of barbiturate infusion. The nadir potassium concentration was 1.5mEq/L and the highest value was 6.8mEq/L. The mean time to reach nadir potassium concentrations was 2.8 days. The mortality rate of the 6 patients was 66.7%. Of the 2 survivors of severe hypokalemia, the Glasgow Outcome Scale (GOS) on discharge and the extended GOS one year after the trauma were 5 and 8 respectively. CONCLUSIONS:
|
Authors | Hande Gurbuz Aytuluk, Hulya Topcu |
Journal | Neurocirugia (English Edition)
(Neurocirugia (Astur : Engl Ed))
2020 Sep - Oct
Vol. 31
Issue 5
Pg. 216-222
ISSN: 2529-8496 [Electronic] Spain |
PMID | 32146086
(Publication Type: Journal Article)
|
Copyright | Copyright © 2020 Sociedad Española de Neurocirugía. Publicado por Elsevier España, S.L.U. All rights reserved. |
Chemical References |
|
Topics |
- Barbiturates
(adverse effects)
- Brain Injuries, Traumatic
(complications, drug therapy)
- Coma
(chemically induced)
- Humans
- Hyperkalemia
(chemically induced, epidemiology)
- Hypokalemia
(chemically induced)
|