Abstract
AbstractAcetazolamide is an infrequently prescribed medication in the outpatient pediatric setting, as one of its major indications is for the treatment of glaucoma, which is a largely adult disease. Though incredibly rare, serious neurologic side effects such as stroke, flaccid paralysis, and coma can occur after its administration. This case presentation of acute flaccid paralysis with metabolic derangement underscores the unusual, yet possible, toxic-metabolic and neurologic sequelae that can occur in an already acidotic host (in this case, caused by gastroenteritis) with acetazolamide ingestion. Life-threatening conditions must always be ruled out in patients who present with encephalopathy, but a medication history was crucial in clinching this case's unifying diagnosis. While there are case reports highlighting the rare central nervous system toxicities associated with acetazolamide ingestion, to our knowledge, none exist in the pediatric literature.
Highlights
Acetazolamide is an infrequently prescribed medication in the outpatient pediatric setting, but it is commonly used in the critical care setting.[1]
Though there are adult case reports on the rare effects of acetazolamide on the central nervous system (CNS),[4,5] here we report the first pediatric case, with acetazolamide being implicated in the development of paralysis in a toddler
The patient is on long-standing dorzolamide-timolol (Cosopt, Akorn Inc., 2–0.5%, one drop in both eyes twice a day) and travoprost (Travatan Z, Novartis Inc., 0.004%, one drop in both eyes nightly) ophthalmic drops for her congenital glaucoma with the addition of acetazolamide (Diamox, Mutual Inc., 125 mg three times a day by mouth, $30 mg/kg/day) 4 days before her gastrointestinal symptoms began
Summary
Acetazolamide is an infrequently prescribed medication in the outpatient pediatric setting, but it is commonly used in the critical care setting.[1]. Lumbar puncture (LP) with infectious markers including meningoencephalitis (ME) polymerase chain reaction (PCR) panel, toxicology screen, CT of the brain/cervical spine, magnetic resonance imaging (MRI) of the brain/cervical/lumbar/ thoracic spine, and continuous video-EEG (electroencephalogram) monitoring are subsequently completed. Her opening pressure on the LP was 15 cm H20, with no evidence of inflammation or infection on cerebrospinal fluid studies. Video-EEG did not show epileptiform discharges and was discontinued after the patient’s mental status returned to baseline She began to eat, drink, and ambulate with assistance and was discharged after a short 2-day intensive care unit admission. Laboratory test White blood cell count (1,000/UL) Hemoglobin (g/dL) Hematocrit (%) Platelets (1,000/UL) Neutrophils (%) Lymphocytes (%) Eosinophils (%) pH venous pCO2 venous (mm Hg) pO2 venous (mm Hg) HCO3 venous (mmol/L) Base excess venous (mmol/L) Lactate (mmol/L) Urine ketones Glucose (mg/dL) Sodium (mmol/L) Potassium (mmol/L) Chloride (mmol/L) Carbon dioxide (mmol/L) Anion gap (mEq/L) Urea nitrogen (mg/dL) Creatinine (mg/dL) C-reactive protein (mg/L) Sedimentation rate (mm/hour) CSF RBC count (/UL) CSF WBC count (/UL) CSF PMN (%) CSF lymphocytes (%) CSF glucose (mg/dL) CSF protein (mg/dL)
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