Continuous Infusion Ranitidine in Postoperative Pediatric Liver Transplant Patients: Effects on Intragastric pH, Gastrointestinal Bleeding and Metabolic Alkalosis.

The effects of ranitidine, an H(2)-receptor antagonist, on gastric pH, incidence of upper gastrointestinal hemorrhage and postoperative metabolic alkalosis were evaluated in 23 pediatric liver transplant recipients. Intragastric pH probes were inserted postoperatively and pH was monitored for 48 h. Ranitidine was infused for 48 h at 0.2 mg kg(minus sign1) h(minus sign1) (0.15 with renal impairment) and increased once by 0.05 mg kg(minus sign1) if the pH was less than 4.0 for 4 h. The pretreatment gastric pH was 2.1 plus minus 0.7; ranitidine infusion raised the pH to 6.8 plus minus 0.6 (p greater-than-or-equal 0.05). An intragastric pH > 4 was achieved in 64 plus minus 36 min, with a median ED(50) (50% of maximum response) of 0.24 mg kg(minus sign1). The pH was < 4 for 5.3 plus minus 4.8% of the time after the initial response. Loss of pH control occurred in three patients, two of whom had bacterial sepsis. The incidence of upper gastrointestinal bleeding and metabolic alkalosis was evaluated by comparing the study patients to age- and weight-matched historic controls from our center. Bleeding occurred in 1 of 23 (4%) study patients compared to 7 of 23 (30%) controls (p greater-than-or-equal 0.05). Metabolic alkalosis did not develop in the study patients at 24 or 48 h postoperatively (p greater-than-or-equal 0.05 versus controls). Whole blood cyclosporine levels and hepatocellular enzymes were similar in the two groups. We conclude that continuous intravenous infusion of ranitidine in the postoperative pediatric liver transplant recipient raises intragastric pH, decreases the incidence of upper gastrointestinal hemorrhage and prevents the development of metabolic alkalosis.