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Abstract

Introduction: 16 year old female with history of depression was brought to our hospital after an intentional overdose of carbamazepine. The patient was found lying by the side of the bed in an unresponsive state. Patient's mother found approximately twenty (200 mg each) carbamazepine pills missing from her step-brother's medication bottle. EMS brought the girl to the emergency department. Enroute to the hospital, a dose of diphenhydramine was given for dystonic posturing. Carbamazepine level upon admission was 24.1mcg/ml and a CT scan of the brain was reported normal. EKG shows borderline QRS widening with possible right bundle branch block. Echocardiogram and cardiac enzymes were normal. She was started on activated charcoal and received multiple doses during her hospital stay. Two hours following the admission the child was intubated and placed on a mechanical ventilator for decreased sensorium. Sodium bicarbonate was added to intravenous fluids to correct metabolic acidosis. The carbamazepine levels were monitored every six hours and at six hours after the admission the level was 34.5 mcg/ml and decreased to 4.2 mcg/ml in three days. Urine toxicology screen was negative. On day two of admission, the patient was polyuric with urine output at 7ml/kg/hr with negative fluid balance of 3398 ml over a 12-hour period. Possibility of diabetes insipidus considered and work up was sent. Laboratory data showed hypernatremia (160 mEq/L) and serum hyperosmolality (329 mosm/kg) with a urine osmolality of 459 mosm/kg and a urine specific gravity of 1.000. Appropriate fluid therapy was initiated and hypernatremia corrected over next 48 hours and urine output normalized. Child was discharged from the PICU with normal electrolyte and acid-base balance, cardiovascular and neurologic condition. Although the fluid balance was positive for first 24 hours she never developed hyponatremia. The lowest sodium concentration during her stay was 141 mEq/L. Discussion Carbamazepine is a commonly used medication in children with seizure disorders. It shares structural similarity with tricyclic antidepressants. Carbamazepine toxicity mainly manifests with neurological and cardiac side effects. Rare but life threatening adverse reactions includes agranulocytosis, bone marrow suppression, multiorgan hypersensitivity reactions (DRESS- Drug rash with eosinophilia and systemic symptoms). Among the other uncommon side effects include hyponatremia due to inappropriately excess anti diuretic hormone secretion (SIADH) and abnormal thyroid function. SIADH characterized by hyponatremia, low serum osmolality and oliguria. SIADH state due to carbamazepine was thought to be by two mechanisms by increasing endogenous antidiuretic hormone (ADH) release and by increasing the sensitivity of renal tubules to the ADH. Carbamazepine is used to treat patients with central or lithium induced diabetes insipidus. However, our index patient developed transient diabetes insipidus (DI). High urine output, hypernatremia, low urine osmolality compared to plasma and low urine specific gravity suggest DI in our patient. Urine output decreased to normal range within 24 hours after the onset of diuresis without the use of vasopressin. The mechanism of development of DI is not known. Whether the DI was of central or peripheral in origin could not be determined in our patient. Conclusion SIADH is a commonly reported endocrine complication of carbamazepine toxicity. To our knowledge we are presenting the first case of transient diabetes insipidus with carbamazepine toxicity. The mechanism of development of DI with carbamazepine is not known.