Calcium/phenobarbital/valproic acid
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Persistent hypocalcaemia, recurrent seizures and drug ineffectiveness: 2 case reports In a case series, an approximately 3-month-old boy developed recurrent seizures secondary to persistent hypocalcaemia during treatment with phenobarbital for generalised subintrant convulsion and an approximately at the age of 5 months, he exhibited drug ineffectiveness while being treated with valproic acid for seizures and calcium for hypocalcaemia, and a 22-month-old boy developed recurrent seizures secondary to persistent hypocalcaemia during supplementation with calcium [durations of treatments to reactions onsets not stated; not all routes stated]. Case 1: The boy was hospitalised for generalised subintrant convulsion at the age of 15 days. An electroencephalogram (EEG) highlighted diffuse cerebral pain. Laboratory tests revealed hypocalcaemia (57 mg/L), hypomagnesaemia (2 mg/L) and a decreased circulating parathyroid hormone level (5 ng/L). Blood protein, glucose, and electrolytes, as well as the renal panel were all normal. He received phenobarbital 20 mg/day, calcium 250 mg/day and magnesium. On discharge, his seizures persisted. After 3 months, his magnesium level was low at 10 mg/L and calcium level was low at 88 mg/L. The treatment was then readjusted. Two months later, he was seen again because of the persistence of seizures and the absence of psychomotor skill acquisition. Physical examination showed axial hypotonia, poor social contact and pyramidal hypertonia of all the 4 limbs, and a head circumference of 44cm. A new EEG confirmed diffuse irritative cerebral pain and a computed tomography scan revealed severe cortico-subcortical atrophy and calcifications of the basal ganglia. On valproic acid (20 mg/kg/day), oral calcium (250 mg/day) and magnesium, the outcome was not favourable (i.e. drugs were ineffective) and he died at home in unspecified circumstances [cause of death not stated]. Due to the underlying defect in intestinal absorption of magnesium, ineffectiveness w.r.t. magnesium supplementation was not considered. Case 2: The boy was hospitalised at the age of 21 days for subintrant right hemicorporeal convulsions which had started 3 days prior to the admission. Physical examination revealed a head circumference of 39cm, inability to suck, lethargy and general hypotonia. An electroencephalogram (EEG) showed diffuse, predominantly left hemispherical irritative pain. A CT scan of the brain and CSF analysis were normal. Laboratory tests revealed hypocalcaemia (71 mg/L), hypomagnesaemia (6 mg/L), hyperphosphataemia (88 mg/L) and a decreased circulating parathyroid hormone level (8 ng/L). His ALP, blood protein and electrolyte levels were normal. Under IV calcium-based treatment, the seizures had ceased during the day, and after 5 days of hospitalisation he was discharged to his home with a prescription of sodium valproate, oral calcium 125 mg/day and magnesium. Despite the absence of seizures, his acquisition of psychomotor skills had slowed down and repeated testing revealed the persistence of hypomagnesae
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