A prospective study of gastric mucosal ischaemia in paracetamol-induced acute liver failure.

Abstract

To evaluate the time course of changes in the gastric mucosal pH (pHi) and the gastric mucosal to arterial CO2 gap (CO2 gap) following paracetamol-induced acute liver failure and to relate these variables to the severity of illness. Clinical prospective study. A liver intensive care unit in a university teaching hospital. Twenty-three patients with paracetamol-induced acute liver failure. Gastric tonometer placement. Daily assessment of pHi and CO2 gap, the systemic organ failure assessment (SOFA) score for up to 9 days post-paracetamol ingestion. Both pHi and CO2 gap were within the normal range on entry into the study. The CO2 gap showed increases from the normal range on days 5-7 post-ingestion (P<0.01) and increases from study entry on days 4, 7, and 8 post-ingestion (P< 0.01). The pHi showed decreases from the normal range on days 4, 6, 7 and 9 post-ingestion (P< 0.01) and decreases from study entry on days 4, 5, 7, and 9 post-ingestion (P<0.01). There was no correlation found between pHi, CO2 gap, and the SOFA score. Paracetamol-induced acute liver failure is associated with increases in the CO2 gap and decreases in pHi between 4 to 9 days post-paracetamol ingestion. This may reflect changes in mesenteric blood flow related to hepatic regeneration. These changes may be in part responsible for some of the morbidity seen with this condition.