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Updated: May 21, 2026

Use of a Wireless Video-EEG System to Monitor Epileptiform Discharges Following Lateral Fluid-Percussion Induced Traumatic Brain Injury
Published on: June 21, 2019
[Water and electrolytes disorders after brain injury: mechanism and treatment]
G Audibert1, J Hoche, A Baumann
1Service d'anesthésie-réanimation, hôpital Central, CHU de Nancy, 29, avenue du Maréchal-de-Lattre-de-Tassigny, 54000 Nancy, France. g.audibert@chu-nancy.fr
Abstract:
Electrolyte disturbances are frequent after brain injuries, especially dysnatremia and dyskalemia. In neurological patients, usual clinical signs of hyponatremia are frequently confounded with clinical signs of the underlying disease. Natremia absolute value is less important than speed of onset of the trouble. Most often, hyponatremia is associated with hypotonicity and intracellular hyperhydration, which may exacerbate a cerebral edema. Distinction between inappropriate secretion of antidiuretic hormone (SIADH) and cerebral salt wasting syndrome (CSWS) may be difficult and is mainly based on assessment of patient's volemia, SIADH being associated with normal or hypervolemia and CSWS with hypovolemia. After subarachnoid haemorrhage, the most common disorder is CSWS. In this case, fluid restriction is strictly prohibited. Treatment of CSWS needs to compensate for the natriuresis and may justify the use of mineralocorticoid. It is important to avoid excessively rapid correction of hypernatremia, with a maximal speed of correction of 0.5 m mol/l/h. Serum sodium monitoring should be mandatory for the first ten postoperative days after pituitary adenoma surgery. Therapeutic barbiturate may be responsible for life threatening dyskalemia.
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