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Diuretic Abuse and Central Pontine Myelinolysis

机译:Diuretic Abuse and Central Pontine Myelinolysis

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Patients with eating disorders often use diuretics to eliminate fluid to achieve lower body weight. Diuretic abuse can lead to severe hyponatremia. Central pontine myelinolysis, a disruption of the myelinated neurons of the pons, has been associated with rapid correction of severe hyponatremia. A case is presented of a 35-year-old woman who was brought to the emergency service by ambulance complaining of vomiting for 7 days and that she could not hear well because she was ‘worn out’. Initial laboratory values included serum Na 91 mEq/l, K 1.6, Cl 46, bicarbonate 33, BUN 4 mg/dl, glucose 306 mg/dl. After 32 h of intravenous fluids, the serum Na was 126, K 4.0, Cl 89, bicarbonate 25, glucose 118 mg/dl. On the 3rd hospital day the serum Na was 139. On the 4th hospital day she was alert and appropriate. On the 5th hospital day, however, she was confabulating and chatty. The serum Na was 139. She progressed to develop a spastic quadriparesis, speech and swallowing difficulties. A magnetic resonance imaging scan showed central pontine myelinolysis. She acknowledged taking 400 mg daily of furosemide and drinking much water. She had a past history of anorexia nervosa. She had a residual weight phobia and strove to keep her weight below 106 lb. Her height was 5 feet, 6 inches. As illustrated by this case, diuretic abuse can cause severe hyponatremia and the subsequent risk of central pontine myelinolysis. In patients with severe chronic or subacute hyponatremia, a safe restoration rate for serum Na has been less than 0.55 mEq/l/h. Serum Na should be below 135 within the first 48 h and hypernatremia should be avoi

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