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Multiple drugsHypokalaemia, rebound hyperkalaemia and lack of efficacy: case report A 17-year-old boy developed hypokalaemia during treatment with pentobarbital for refractory intracranial hypertension. Subsequently, he developed rebound hyperkalaemia following withdrawal of pentobarbital, and exhibited lack of efficacy during treatment with potassium for hypokalaemia and during treatment with calcium gluconate and sodium polystyrene sulfonate for hyperkalaemia [routes not stated; not all dosages, time to reactions onset and outcomes stated].The boy was admitted and intubated due to severe traumatic brain injury after a road traffic accident. CT scan showed multiple intracranial haemorrhages. Despite receiving unspecified analgesia, paralysis, sedation and hyperosmolar therapy, his intracranial pressure (ICP) remained high. For the treatment of intracranial hypertension, he received three boluses of pentobarbital 100mg over a period of half a day, which was followed by a continuous infusion of pentobarbital at a rate of 0.5 mg/kg/h, which was escalated to 2 mg/kg/h. After the initiation of pentobarbital, stabilisation of ICP was observed. However, 7 hours after the pentobarbital infusion, he developed hypokalaemia.The boy was treated with potassium. However, despite receiving treatment with potassium (a total of 220mmol), his hypokalaemia persisted for 24 hours with the lowest potassium level of 1.3 mmol/L (lack of efficacy). Pentobarbital was discontinued. Twelve hours after pentobarbital withdrawal, he developed rebound hyperkalaemia (5.3-6.2 mmol/L). His hyperkalaemia was treated with sodium polystyrene sulfate and calcium gluconate. Despite receiving treatment, his hyperkalaemia persisted for 3 days (lack of efficacy) with no dysrhythmia.
Multiple drugsHypokalaemia, rebound hyperkalaemia and lack of efficacy: case report A 17-year-old boy developed hypokalaemia during treatment with pentobarbital for refractory intracranial hypertension. Subsequently, he developed rebound hyperkalaemia following withdrawal of pentobarbital, and exhibited lack of efficacy during treatment with potassium for hypokalaemia and during treatment with calcium gluconate and sodium polystyrene sulfonate for hyperkalaemia [routes not stated; not all dosages, time to reactions onset and outcomes stated].The boy was admitted and intubated due to severe traumatic brain injury after a road traffic accident. CT scan showed multiple intracranial haemorrhages. Despite receiving unspecified analgesia, paralysis, sedation and hyperosmolar therapy, his intracranial pressure (ICP) remained high. For the treatment of intracranial hypertension, he received three boluses of pentobarbital 100mg over a period of half a day, which was followed by a continuous infusion of pentobarbital at a rate of 0.5 mg/kg/h, which was escalated to 2 mg/kg/h. After the initiation of pentobarbital, stabilisation of ICP was observed. However, 7 hours after the pentobarbital infusion, he developed hypokalaemia.The boy was treated with potassium. However, despite receiving treatment with potassium (a total of 220mmol), his hypokalaemia persisted for 24 hours with the lowest potassium level of 1.3 mmol/L (lack of efficacy). Pentobarbital was discontinued. Twelve hours after pentobarbital withdrawal, he developed rebound hyperkalaemia (5.3-6.2 mmol/L). His hyperkalaemia was treated with sodium polystyrene sulfate and calcium gluconate. Despite receiving treatment, his hyperkalaemia persisted for 3 days (lack of efficacy) with no dysrhythmia.
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