A 58-year-old male underwent elective left lower lobe resection via video-assisted thoracoscopic surgery (VATS) for a 9 mm lung nodule suspicious for malignancy. The patient's past medical history included hypertension, gastroesophageal reflux disease, depression, anxiety, chronic hepatitis C, and AUD. Liver biopsy and Fibroscan had not been performed to assess for cirrhosis, preoperatively. His last admission was six months prior to surgery for alcohol withdrawal syndrome. The patient reported drinking 10 beers a day with his last drink on the day before surgery. He denied tobacco, but reported using marijuana. He had no known allergies or adverse drug reactions.
His baseline liver function tests (LFTs) before surgery were: AST 111 U/L, ALT 50 U/L, total bilirubin (TBili) 0.5 mg/dl, INR 1.11 (Table 1). AST/ALT ratio suggested alcoholic hepatitis. Nutritional status was marginal, with albumin 3.1 g/dL. Platelet count was 120,000 k/cmm. Outpatient medications included aripiprazole, sertraline, and a multivitamin.
There were no hypotensive episodes or other complications during VATS. Blood loss was less than 50 ml. He received general anesthesia with sevofluorane. There were no other concomitant medications given intraoperatively or postoperatively that could have contributed to deteriorating hepatic function.
The following analgesics were given to optimize pain control postoperatively: APAP 1 g orally every six hours for three days, oxycodone 5-10 mg orally every four hours as needed, and hydromorphone 0.5 mg IV every four hours as needed for breakthrough pain.
On postoperative day 2 (POD 2), the patient remained hemodynamically stable. On POD 3, he developed nausea and discomfort in the right upper quadrant. LFTs were checked and noted to be elevated: AST 3169 U/L, ALT 758 U/L, TBili 2.8 mg/dL (Table 1, Figure 1). He had received a total of 9 g of APAP over a period of 3 days, with no more than 4 g over a 24-hour period. APAP was discontinued at this time due to LFT elevation and concern for iatrogenic hepatotoxicity.
On POD 4, LFTs peaked: AST 5417 U/L, ALT 1372 U/L, TBili 3.5 mg/dL; albumin 2.6 g/dL, INR 2.83, lactate 6.1 mmol/L; and glucose 58 mg/dl. Renal function and arterial blood gas remained within normal limits. Urine toxicology screen was negative. The patient reported right-sided abdominal pain and nausea, and had two episodes of emesis. He was noted to have scleral icterus and grade I encephalopathy. He had a syncopal episode secondary to hypoglycemia, which promptly responded to intravenous dextrose administration. A CT scan of the abdomen and pelvis was done, revealing fatty liver without portal vein thrombosis or other biliary tract abnormalities. Ischemic hepatitis (shock liver) was thought unlikely as the patient was never hypotensive.
The hepatology service was consulted and a diagnosis of acetaminophen-induced hepatotoxicity was suspected based on the clinical picture, laboratory values, and negative imaging. However, APAP level was within normal limits at 12.9 mg/L (normal therapeutic range 5-20 mg/L). Despite a nontoxic APAP level, NAC was recommended. On POD 4, he was treated with 3 weight-based doses of IV NAC: 9 g (150 mg/kg) over one hour, then 3 g (50 mg/kg) over four hours, followed by 6 g (100 mg/kg) over sixteen hours. A one-time dose of oral vitamin K 10 mg was also administered.
On POD 5, APAP level decreased to 0.5 mg/L and LFTs were noted to be declining. He was discharged on POD 7, at which time he was clinically stable and asymptomatic. LFTs continued to improve and the patient's renal function remained at baseline and within normal limits. One month after discharge, LFTs further decreased to: AST 427 U/L, ALT 82 U/L, TBili 2 mg/dL.
Throughout the patient's hospital stay, renal function remained at baseline (0.8-1.4 mg/dl).