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Neurology India, Vol. 54, No. 2, April-June, 2006, pp. 214-215 Letter To Editor Oxcarbazepine induced hyponatremic coma Paliwal Vimal, Garg RavindraKumar, Kar AlokMohan, Singh ManeeshKumar Department of Neurology, King George Medical University, Lucknow - 226 003 Code Number: ni06065 Sir, Hyponatremia is a common side effect of oxcarbazepine but is generally mild and asymptomatic. Symptomatic hyponatremia is less common with oxcarbazepine and rarely seen in children. We report a 7-year-old boy presenting with hyponatremic coma due to oxcarbazepine. A 7-year-old boy presented with 2 months history of generalized tonic-clonic seizures. He was prescribed oxcarbazepine 300 mg daily in two divided doses. The patient had 2 similar episodes of seizures 15 days later. Doses of oxcarbazepine were increased to 450 mg daily. Seizures were controlled. One day prior to admission, he developed lethargy, increased somnolence and over next 6 hours he became drowsy. After another episode of seizure he became unarousable. On examination, patient was comatose (E 1 M 2 V 1 ). Cranial nerves were normal. Patient had hypotonia of limbs. There was no focal deficit. Deep tendon jerks were normal. Planters were extensor. Signs of meningeal irritation were absent. Systemic examination was normal. Biochemical investigations revealed blood sugar 97.0 mg/dl, blood urea 2 mg/dl, serum creatinine 0.5 mg/dl, serum sodium 113 mmol/L, serum potassium 4.3 mmol/L and serum calcium 8.7 mg/dl. Cerebrospinal fluid examination was normal. Computed tomography of brain and electroencephalography did not reveal any abnormality. Over next 2 days patient was given 3% NaCl solution at 1 mmol/liter/hour. A total of 240 mEq NaCl (380 ml of 3% solution) was administered in 48 hours. During this period patient regained complete consciousness. Repeat serum sodium level was 137 mmol/L. Oxcarbazepine was stopped and patient′s was switched over to phenytoin sodium (150 mg per day) with complete control of seizures. There was no recurrence of hyponatremia after 4 months of follow-up. Several reviews suggest that hyponatremia does not appear to be a substantial issue during the treatment of childhood partial epilepsy.[1],[2] In a series of 2026 patients receiving oxcarbazepine, hyponatremia was induced in 0.4% of children aged ≤ 17 years (no cases reported in patients aged < 6 years), the incidence being considerably lower than that observed in older patients (3.8% in patients aged 18-64 years).[3] In another prospective study, Holtmann et al evaluated changes in serum electrolyte balance in 75 children with epilepsy before and during treatment with oxcarbazepine and after replacing carbamazepine therapy with oxcarbazepine therapy. During treatment with oxcarbazepine authors found hyponatremia (Na+ < 135 mmol/L) without clinical symptoms in 26.6% of the children (n=20), sodium levels below 125 mmol/L were observed only in 2 children (2.6%), symptomatic hyponatremia occurred in one girl only (1.3%). In a subgroup of 27 children, in whom carbamazepine was directly replaced with oxcarbazepine, asymptomatic hyponatremia was found in one child under carbamazepine (3.7%) and in six children on oxcarbazepine (22.2%).[4] Our report highlights that hyponatremia in children may, at times, be severe enough to make patient unconscious. Unless treating physician is aware of this complication this condition may be missed. References
Copyright 2006 - Neurology India |
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