Inappropriate Antidiuresis and Hyponatremia with Suppressible Vasopressin in Guillain-Barré Syndrome

Abstract

Studies in which plasma osmolality was altered acutely by oral water loading and hypertonic sodium chloride infusion were performed to further identify the mechanisms involved in the pathogenesis of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) in a patient with Guillain-Barré syndrome. Although resetting of the osmotic threshold for vasopressin release was demonstrated in these studies, this does not seem to have been a primary factor in the development of SIADH in this patient. Downward resetting of the osmotic threshold by sustained hypoosmolality has been previously demonstrated, and it is possible that this may account for the initially low osmotic threshold identified by our studies. These studies suggest that inappropriate antidiuresis, as shown by the absence of a diuretic response to low threshold suppression of the plasma arginine vasopressin concentration was due either to a vasopressin-independent mechanism or to markedly increased renal tubular sensitivity to vasopressin.

Posterior reversible encephalopathy as the first manifestation of Bickerstaff’s brainstem encephalitis

“…SIADH has been reported in 7–48 % of patients with GBS [22, 23]. The mechanism of which was hypothesized to be downward osmotic resetting and enhanced renal tubular sensitivity to antidiuretic hormone [24–26]. Of note, SIADH has been associated with poor outcome in GBS as bulbar weakness and such as the need of ventilator support or longer hospitalization period [22].…”

Guillain-Barre Syndrome

“…Nutrition should be complemented with adequate intravenous hydration and increased insensible losses need to be taken into account in patients with profuse diaphoresis or diarrhea. Electrolytes should be monitored, especially sodium since patients with GBS may develop hyponatremia from inadequate secretion of antidiuretic hormone [46]. Parenteral nutrition should be reserved for patients with refractory ileus.…”

Guillain-Barré-Syndrom und Syndrom der inadäquaten Adiuretinsekretion

“…Diskutiert wird einerseits eine Neuropathie der kardialen Volumenrezeptoren, die zu einer vermehrter ADH-Sekretion führt [7], andererseits wird eine vermehrte Responsivität der Niere bezüg-lich ADH vermutet [3]. Zusätzlich kann auch eine Erniedrigung des Osmostats eine wichtige Rolle bei der Entstehung des SIADH bei GBS spielen [3,6]. Hierbei kommt es zu einer Erniedrigung des Sollwerts der Serumosmolalität.…”