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Vol. 38. Issue 1.
Pages 44-47 (January - March 2021)
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Vol. 38. Issue 1.
Pages 44-47 (January - March 2021)
CASO CLÍNICO
Hipertensión arterial por hiperactividad simpática tras traumatismo craneoencefálico grave
HYpertension due to sympathetic hyperactivity after severe head injury
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T. Vázquez Sánchez
Corresponding author
teresavs89@hotmail.com

Autor para correspondencia.
, J.P. Gámez España, M.D. Martínez Esteban
Unidad de Gestión Clínica de Nefrología, Hospital Regional Universitario de Málaga, Universidad de Málaga, Instituto Biomédico de Investigación de Málaga (IBIMA), REDinREN (RD16/0009/0006), Málaga, España
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Tabla 1. Método de evaluación de la hiperactividad simpática paroxística
Resumen

Presentamos el caso de un paciente de 34 años que sufre un traumatismo craneoencefálico grave con afectación cerebral severa. Evoluciona de manera tórpida precisando varias reintervenciones por sangrado y herniación de masa encefálica. Nos interconsultan desde Neurocirugía por irregular control de cifras de presión arterial a pesar de tratamiento con calcioantagonistas. El paciente asocia diaforesis, taquipnea y taquicardia, junto a fiebre de alto grado de forma persistente sin evidencia microbiológica. Analítica con función renal normal, sin proteinuria y sin datos de hipertrofia de ventrículo izquierdo que sugieran hipertensión arterial previa. Esto nos hace plantearnos como primera posibilidad diagnóstica un síndrome de hiperactividad simpática debido al daño neurológico severo. Se inicia terapia antihipertensiva orientada a esta sospecha, entre los que se incluyen betabloqueantes no cardioselectivos, alfa-2-agonistas, benzodiacepinas y agonistas de los receptores GABA. Así se consigue mejorar la labilidad de las cifras de presión arterial, lo que apoya el diagnóstico.

Palabras clave:
Hipertensión arterial
Hiperactividad simpática
Traumatismo craneoencefálico grave
Abstract

We present the case of a 34-year-old patient with severe head trauma and severe brain involvement. The patient deteriorated progressively and required several reinterventions for bleeding and brain herniation. We were consulted by neurosurgery due to irregular blood pressure control despite treatment with calcium antagonists. The patient had associated diaphoresis, tachypnoea and tachycardia, together with persistent high-grade fever with no microbiological evidence. Laboratory tests showed normal kidney function, with no proteinuria and no signs of left ventricular hypertrophy to suggest previous arterial hypertension. This led us to consider sympathetic hyperactivity syndrome as a first possible diagnosis due to severe neurological damage. In line with this suspicion, antihypertensive therapy was initiated which included non-cardioselective beta-blockers, alpha-2 agonists, benzodiazepines and GABA receptor agonists. Thus, we were able to improve the labile blood pressure levels, which supports the diagnosis.

Keywords:
Arterial hypertension
Sympathetic hyperactivity
Severe head trauma

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