Gastrointestinal injury following cardiopulmonary bypass

The gastrointestinal (GI) tract may be the source of a number of bacterial and non-bacterial mediators, which may contribute to the development of morbidity and mortality following episodes of gut hypoperfusion/ ischaemia. The aim of this thesis has been to identify the changes in gut blood flow, oxygenation and function following cardiopulmonary bypass (CPB) and their relationship to the development of post-CPB morbidity. The findings are summarised below: The retrospective study identified age (>65 yr) and CPB time as risk factors for the development of post-CPB intra-abdominal complications . Tonometrically determined values for intramucosal pH (pHi) need temperature correction to avoid calculation of erroneously high values during hypothermic CPB. Considerable hypoperfusion occurs during hypothermic CPB, with laser Doppler flowmetry (LDF) falling to approximately 45% of pre-CPB values. The gastric and colonic pHi becomes acidotic (<7.35) during the re-warming and immediate post-CPB period. Intramucosal acidosis occurs at a time when mucosal LDF blood flow is normal or supranormal. CPB increases gut permeability and reduces the absorption of the monosaccharides, 3-O-m-D-glucose, D-xylose & L-rhamnose. Post-CPB gut permeability has a temporal relationship with the CPB time. Pulsatile flow attenuates the increase in post-CPB gut permeability. Endotoxaemia occurs during CPB but is not associated with the production of TNFα; pulsatile flow attenuates this endotoxaemia. When examining perfusion and patient factors, the best predictor for a protracted ventilation & ICU stay for patients was a low gastric pHi (