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Hyponatremia in Guillain-Barre Syndrome: A Review of Its Pathophysiology and Management
Published online by Cambridge University Press: 16 February 2024
Abstract:
Guillain-Barre syndrome (GBS) is the commonest cause of acute polyradiculoneuropathy that requires hospitalization. Many of these patients experience systemic and disease-related complications during its course. Notable among them is hyponatremia. Though recognized for decades, the precise incidence, prevalence, and mechanism of hyponatremia in GBS are not well known. Hyponatremia in GBS patients is associated with more severe in-hospital disease course, prolonged hospitalization, higher mortality, increased costs, and a greater number of other complications in the hospital and worse functional status at 6 months and at 1 year. Though there are several reports of low sodium associated with GBS, many have not included the exact temporal relationship of sodium or its serial values during GBS thereby underestimating the exact incidence, prevalence, and magnitude of the problem. Early detection, close monitoring, and better understanding of the pathophysiology of hyponatremia have therapeutic implications. We review the complexities of the relationship between hyponatremia and GBS with regard to its pathophysiology and treatment.
Résumé :
Hyponatrémie dans le cas du syndrome de Guillain-Barré : une analyse de sa physiopathologie et de sa prise en charge.
Le syndrome de Guillain-Barré (SGB) est la cause la plus fréquente de polyradiculoneuropathie aiguë nécessitant une hospitalisation. Plusieurs des patients atteints présentent des complications systémiques liées à une maladie au cours de l’évolution de ce syndrome. L’hyponatrémie est l’une de ces complications. Bien que reconnue depuis des décennies, l’incidence, la prévalence et le mécanisme précis de l’hyponatrémie dans le cas du SGB ne sont pas bien connus. On le sait, l’hyponatrémie chez les patients atteints de SGB est associée à une évolution plus sévère de ce syndrome à l’hôpital, à une hospitalisation prolongée, à une mortalité plus élevée, à des coûts accrus, à un plus grand nombre d’autres complications survenant à l’hôpital et à un état fonctionnel moins favorable au bout de six mois et d’un an. Bien que le manque de sodium ait été fréquemment associé au SGB, nombre d’études n’ont pas inclus la relation temporelle exacte du sodium ou ses valeurs sérielles dans le cas du SGB, sous-estimant ainsi l’incidence, la prévalence et l’ampleur exacte du problème. Une détection précoce, une surveillance étroite et une meilleure compréhension de la physiopathologie de l’hyponatrémie ont pourtant des implications thérapeutiques. Dans cet article, nous entendons donc passer en revue les complexités de la relation entre l’hyponatrémie et le SGB en ce qui concerne sa pathophysiologie et son traitement.
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- Review Article
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- © The Author(s), 2024. Published by Cambridge University Press on behalf of Canadian Neurological Sciences Federation
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