Tamer Çelik1, Orkun Tolunay2, Ilknur Tolunay3, Ümit Çelik4. 1. Department of Pediatric Neurology, Adana Numune Training and Research Hospital, Adana, Turkey. 2. Department of Pediatrics, Adana Numune Training and Research Hospital, Antalya, Turkey. Electronic address: orkuntolunay@yahoo.co.uk. 3. Department of Pediatrics, Antalya Training and Research Hospital, Antalya, Turkey. 4. Department of Pediatric Infection, Adana Numune Training and Research Hospital, Adana, Turkey.
Abstract
BACKGROUND: Cerebral salt wasting is a hypovolemic hyponatremia state, caused by natriuresis and diuresis. The most important element of treatment is to replace the volume and sodium loss and improve the current clinic. PATIENTS: We present two children who were treated in the intensive care unit who subsequently developed cerebral salt wasting. Diagnosis was based on hyponatremia associated with high urinary sodium excretion and inappropriately high urine output in the presence of dehydration. As part of the treatment, one patient was given fluid and sodium replacement, measures that were insufficient in the other patient, who also required fludrocortisone treatment. CONCLUSION: The status epilepticus may be involved in the etiology of cerebral salt wasting. In both patients, cerebral salt wasting was detected in the posttreatment follow-up evaluations. Cerebral salt wasting is particularly likely to occur in individuals with status epilepticus, and the electrolyte and hydration status of these patients should be monitored closely, even after the convulsions are taken under control.
BACKGROUND:Cerebral salt wasting is a hypovolemic hyponatremia state, caused by natriuresis and diuresis. The most important element of treatment is to replace the volume and sodium loss and improve the current clinic. PATIENTS: We present two children who were treated in the intensive care unit who subsequently developed cerebral salt wasting. Diagnosis was based on hyponatremia associated with high urinary sodium excretion and inappropriately high urine output in the presence of dehydration. As part of the treatment, one patient was given fluid and sodium replacement, measures that were insufficient in the other patient, who also required fludrocortisone treatment. CONCLUSION: The status epilepticus may be involved in the etiology of cerebral salt wasting. In both patients, cerebral salt wasting was detected in the posttreatment follow-up evaluations. Cerebral salt wasting is particularly likely to occur in individuals with status epilepticus, and the electrolyte and hydration status of these patients should be monitored closely, even after the convulsions are taken under control.