횡문근융해증이 합병된 중증 저나트륨혈증 환자에서 발생한 삼투성 탈수초 증후군 1예
A Case of Osmotic Demyelination Syndrome in a Patient with Severe Hyponatremia Complicated by Rhabdomyolysis
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초록
Hyponatremia, the most common electrolyte disorder, has been rarely reported as causing rhabdomyolysis. Osmotic demyelination syndrome (ODS), a demyelinating disease of the central pons and/or other areas of the brain, is infrequently reported as associated with rapid correction of hyponatremia. This paper reports a case of ODS after correction of severe hyponatremia complicated by rhabdomyolysis. A 47-year-old female with a history of chronic alcoholism presented herself at the hospital with altered consciousness after three days of nausea and vomiting. She was on a thiazide diuretic for essential hypertension. Her blood tests upon her hospital admission showed hyponatremia (Na+ 98 mEq/L), hypokalemia (K+ 3.0 mEq/L), and elevation of her serum creatine phosphokinase (3,370 IU/L) with an increase in her serum myoglobin level 11,267 ng/mL). She was treated with intravenous fluid therapy that included isotonic and hypertonic salines along with potassium chloride. She became more alert, and her neurological condition gradually improved after the first five days of her therapy. On the ninth day after her admission, she developed progressive quadiaresis associated with dysarthria, dysphagia, and dystonia despite the resolution of her hyponatremia. Magnetic resonance imaging of her brain on 16th day revealed symmetrical areas of signal hyperintensity in her central pons, basal ganglia, and precentral gyrus in T2-weighted images, which are consistent with ODS. Her neurological symptoms steadily improved after six weeks with only supportive treatment and rehabilitation.
Abstract
Hyponatremia, the most common electrolyte disorder, has been rarely reported as causing rhabdomyolysis. Osmotic demyelination syndrome (ODS), a demyelinating disease of the central pons and/or other areas of the brain, is infrequently reported as associated with rapid correction of hyponatremia. This paper reports a case of ODS after correction of severe hyponatremia complicated by rhabdomyolysis. A 47-year-old female with a history of chronic alcoholism presented herself at the hospital with altered consciousness after three days of nausea and vomiting. She was on a thiazide diuretic for essential hypertension. Her blood tests upon her hospital admission showed hyponatremia (Na+ 98 mEq/L), hypokalemia (K+ 3.0 mEq/L), and elevation of her serum creatine phosphokinase (3,370 IU/L) with an increase in her serum myoglobin level 11,267 ng/mL). She was treated with intravenous fluid therapy that included isotonic and hypertonic salines along with potassium chloride. She became more alert, and her neurological condition gradually improved after the first five days of her therapy. On the ninth day after her admission, she developed progressive quadiaresis associated with dysarthria, dysphagia, and dystonia despite the resolution of her hyponatremia. Magnetic resonance imaging of her brain on 16th day revealed symmetrical areas of signal hyperintensity in her central pons, basal ganglia, and precentral gyrus in T2-weighted images, which are consistent with ODS. Her neurological symptoms steadily improved after six weeks with only supportive treatment and rehabilitation.
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