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Vol. 31. Issue 5.
Pages 216-222 (September - October 2020)
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Vol. 31. Issue 5.
Pages 216-222 (September - October 2020)
Clinical Research
Severe hypokalemia and rebound hyperkalemia during barbiturate coma in patients with severe traumatic brain injury
Hipopotasemia grave e hiperpotasemia de rebote durante el coma terapéutico inducido por barbitúricos en pacientes con lesiones cerebrales traumáticas
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Hande Gurbuz Aytuluka,b,
Corresponding author
handegrbz@gmail.com

Corresponding author.
, Hulya Topcuc
a Department of Anesthesiology and Reanimation, University of Health Sciences, Derince Training and Research Hospital, Kocaeli, Turkey
b Formerly: Department of Anesthesiology and Reanimation, Kocaeli State Hospital, Kocaeli, Turkey
c Department of Anesthesiology and Reanimation, Hitit University, Erol Olcok Training and Research Hospital, Corum, Turkey
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Tables (3)
Table 1. Patient demographics and characteristics.
Table 2. Analysis of patients with severe hypokalemia.
Table 3. The relevance of barbiturate therapy and other predisposing factors to serum potassium concentrations.
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Abstract
Objectives

To evaluate the incidence of severe potassium disturbances during barbiturate coma therapy in patients with severe traumatic brain injury (TBI), and the characteristics of these patients.

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

Severe hypokalemia refractory to medical treatment and rebound hyperkalemia is a serious adverse effect of thiopentone coma therapy in patients with severe TBI. Excessive and aggressive potassium replacement during the barbiturate-induced hypokalemia period must be avoided. Weaning barbiturate treatment over time may be advantageous in the management of severe serum potassium disturbances.

Keywords:
Barbiturates
Brain injuries
Traumatic
Hyperkalemia
Hypokalemia
Potassium
Thiopental
Resumen
Objetivos

Evaluar la incidencia de alteraciones graves de los niveles de potasio durante el coma terapéutico inducido por barbitúricos en pacientes con lesiones cerebrales traumáticas (LCT) graves y las características de estos pacientes.

Métodos

El estudio incluyó 37 pacientes con LCT grave que habían sido tratados mediante coma terapéutico inducido por barbitúricos entre 2015 y 2017 en unidades de cuidados intensivos de nivel 3 de dos hospitales.

Resultados

En 14 pacientes no se observaron alteraciones de los niveles de potasio. Diecisiete pacientes desarrollaron hipopotasemia leve o moderada (2,6-3,5 mEq/l), y 6 pacientes desarrollaron hipopotasemia grave (<2,5 mEq/l) después de la inducción de la terapia con barbitúricos. La incidencia de hipopotasemia de leve a grave inducida por barbitúricos fue del 62,2% y la tasa de hipopotasemia grave fue del 16,2%. El aporte medio de potasio al día durante el tratamiento con tiopentona fue diferente de forma estadísticamente significativa entre los pacientes con hipopotasemia leve o moderada y entre los que tenían hipopotasemia grave (p<0,001). Cuatro de los 6 pacientes con hipopotasemia grave desarrollaron hiperpotasemia de rebote que superó los 6mEq/l después de la suspensión de la infusión de barbitúricos. La concentración mínima de potasio fue de 1,5mEq/l y el valor máximo de potasio fue de 6,8mEq/l. El tiempo medio hasta alcanzar las concentraciones mínimas de potasio fue de 2,8 días. La tasa de mortalidad de los 6 pacientes fue del 66,7%. En los 2 supervivientes con hipopotasemia grave, los resultados de la Escala de Resultados de Glasgow (Glasgow Outcome Scale, GOS) en el alta y la GOS extendida un año después del traumatismo fueron 5 y 8, respectivamente.

Conclusiones

La hipopotasemia grave resistente al tratamiento médico y la hiperpotasemia de rebote suponen un efecto adverso grave de coma terapéutico inducido con tiopentona en pacientes con LCT grave. Debe evitarse una sustitución excesiva y agresiva del potasio durante el periodo de hipopotasemia inducida por barbitúricos. La retirada gradual del tratamiento con barbitúricos puede resultar ventajosa en la gestión de las alteraciones graves de los niveles de potasio sérico.

Palabras clave:
Barbitúricos
Lesiones cerebrales
Traumático
Hipercalemia
Hipocaliemia
Potasio
Thiopental

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