摘要
We report a case of a 50-year-old malnourished African American male with hiccups, nausea and vomiting who was brought to the Emergency Department after repeated seizures at home. Laboratory evaluations revealed sodium(Na+) 107 mmol/L, unmeasurably low potassium, chloride < 60 mmol/L, bicarbonate of 38 mmol/L and serum osmolality 217 m Osm/kg. Seizures were controlled with 3% saline Ⅳ. Once nausea was controlled with iv antiemetics, he developed large volume free water diuresis with 6 L of dilute urine in 8 h(urine osmolality 40-60 m Osm/kg) and serum sodium rapidly rose to 126 mmol/L in 12 h. Both intravenous desmopressin and 5% dextrose in water was given to achieve a concentrated urine and to temporarily reverse theacute rise of sodium, respectively. Serum Na+ was gradually re-corrected in 2-3 mmol/L daily increments from 118 mmol/L until 130 mmol/L. Hypokalemia was slowly corrected with resultant auto-correction of metabolic alkalosis. The patient discharged home with no neurologic sequaele on the 11 th hospital day. In euvolemic hyponatremic patient, controlling nausea may contribute to unpredictable free water diuresis. The addition of an antidiuretic hormone analog, such as desmopressin can limit urine output and prevent an unpredictable rise of the serum sodium.
We report a case of a 50-year-old malnourished African American male with hiccups, nausea and vomiting who was brought to the Emergency Department after repeated seizures at home. Laboratory evaluations revealed sodium(Na+) 107 mmol/L, unmeasurably low potassium, chloride < 60 mmol/L, bicarbonate of 38 mmol/L and serum osmolality 217 m Osm/kg. Seizures were controlled with 3% saline Ⅳ. Once nausea was controlled with iv antiemetics, he developed large volume free water diuresis with 6 L of dilute urine in 8 h(urine osmolality 40-60 m Osm/kg) and serum sodium rapidly rose to 126 mmol/L in 12 h. Both intravenous desmopressin and 5% dextrose in water was given to achieve a concentrated urine and to temporarily reverse theacute rise of sodium, respectively. Serum Na+ was gradually re-corrected in 2-3 mmol/L daily increments from 118 mmol/L until 130 mmol/L. Hypokalemia was slowly corrected with resultant auto-correction of metabolic alkalosis. The patient discharged home with no neurologic sequaele on the 11 th hospital day. In euvolemic hyponatremic patient, controlling nausea may contribute to unpredictable free water diuresis. The addition of an antidiuretic hormone analog, such as desmopressin can limit urine output and prevent an unpredictable rise of the serum sodium.
