Case Presentation: A 49-year-old male presented for evaluation of an umbilical hernia. Past medical history was remarkable for alcohol misuse; the patient had ceased all alcohol consumption three years earlier. Physical exam revealed a protuberant, non-tender abdomen with a 4×4 cm reducible umbilical hernia. Pre-operative laboratory exam was remarkable for serum sodium of 137 mmol/L, bilirubin of 1.7 mg/dL, alkaline phosphatase of 143 U/L, AST of 66 U/L, and ALT of 66 U/L. The patient was scheduled for elective repair. During surgery, upon opening of the umbilical hernia sac, an immediate flood of chylous fluid was described. Approximately one liter of fluid was immediately evacuated. Laparoscopy was then performed, which disclosed a cirrhotic appearing liver surface and the presence of a large volume of chylous ascites (triglyceride level 915 mg/DL). Due to concern for wound dehiscence under pressure, a Jackson-Pratt (J-P) drain was placed in the left upper quadrant. A patch was then deployed through the umbilical defect and sutured into position, followed by closure of the wound. On post-operative day 10, the patient was admitted to the medical service with complaints of nausea, headache, and dizziness. He reported copious fluid output through his J-P drain and poor oral intake. Physical exam was remarkable for a soft, mildly distended abdomen and for the presence of chylous fluid in the J-P bulb. Laboratory exam was remarkable for serum sodium of 113 mmol/L, urine osmolality of 361 mosm/kg, serum osmolality of 251 mosm/kg, and urine sodium < 5 mmol/L. Ultrasound demonstrated a cirrhotic liver morphology and peri-hepatic ascites. Peritoneal acid-fast bacilli studies were negative, as was stool for ova and parasites. J-P drainage volumes of up to 5 liters per 24 hours were recorded. The patient was assessed as suffering from hyponatremia secondary to copious drain loss in association with inadequate oral solute replacement. He was treated with cautious normal saline infusion and removal of the J-P drain. Sodium corrected to 137 and he was discharged on oral furosemide, spironolactone and ciprofloxacin prophylaxis, to be followed in outpatient hepatology clinic.
Discussion: Chylous ascites (defined as triglyceride level > 110 mg/DL) is rare, occurring in 0.5-1.0% of cases of cirrhotic ascites, and in 1/20,000 hospital admissions (1). Chylous ascitic fluid has a predictable sodium concentration that approximates that of the plasma level (2). Hyponatremia secondary to copious peritoneal catheter drainage of malignant ascites has been reported. Hyponatremia secondary to excessive loss of chylous fluid from a pleural catheter has also been previously described (3). This case represents the unique situation of severe hyponatremia secondary to the profuse loss of chylous ascites through an abdominal surgical drain in the setting of alcoholic cirrhosis.
Conclusions: Excessive loss of ascitic fluid, including the rare variant of chylous fluid, in the absence of appropriate solute replacement may lead to severe hyponatremia. Careful monitoring of drain volume, attention to serum sodium, cautious solute replenishment, and control of the source of loss are all important elements of care in the hospitalized patient with an active abdominal drain in place.