Does N-Acetylcysteine Alter Prothrombin Index in Acetaminophen Poisoned Patients Admitted to the Intensive Care Unit without Hepatocellular Injury?

Objective: N-acetylcysteine (NAC) reduces the severity of acetaminophen poisoning-related liver damage. However, it may interact with clotting factors containing disulphide bonds. Our objective was to study the effect of NAC on prothrombin index (PI) in NAC-treated poisoned patients. Methods: Retrospective data collection, including PI, V-fector, and liver enzymes, measured before and during NAC administration; descriptive analysis (median [25%, 75%-per-centiles]); comparison of paired data using Wilcoxon tests. Results: During a 10 year-period, 171 patients (123F/48M, 28 years [21-41]) were admitted to our ICU for acetaminophen poisoning and treated with intravenous NAC (150 mg/kg in 1 h followed by 50 mg/kg in 4 h, 100 mg/kg in 16 h and, if necessary in case of liver damage, by 300 mg/kg/day). Acetaminophen concentration was 317 mu mol/l [149-708] with a 9 h [5-14]-delay from ingestion. Nine patients suffered from previous liver disease. Eighty percent were multidrug ingestions, mainly including propoxyphene and codeine. On admission, PI was 75 % [64-90], V-factor 66 % [45-82], AST 22 IU/1 [16-44], ALT 20 IU/1 [12-33], alkaline phosphatase 55 IU/1 [39-70], bilirubin 8 mu mol/l [6-13], and creatinine 66 mu mol/l [56-81]. The following complications were observed: cytolytic hepatitis (ALT>50 IU/1, 26%), acute liver failure (4%), acute renal failure (1%), and multiorgan failure (2%, leading to death). In patients without hepatocellular injury (ALT 60%, N=115), there was a significant decrease in PI under NAC (82% [72-92] before versus 73 % [66-79] at 11 h [10-19] following NAC administration, p