Luminal lactate in acute pancreatitis - validation and relation to disease severity
1 Departments of Critical Care Medicine, Tampere University Hospital, Teiskontie 35, Tampere, 33520, Finland
2 Department of Gastroenterology and Alimentary tract Surgery in Tampere University Hospital, Teiskontie 35, Tampere, Finland
3 Department of Intensive care, Copenhagen University Hospital, Rigshospitalet, Blegdamsvej 9, Copenhagen, 2100, Denmark
4 Critical Care Medicine Research Group Tampere, Department of Critical Care Medicine, Tampere University Hospital, Teiskontie 35, Tampere, 33520, Finland
5 Department of Surgical Sciences/Anaesthesiology and Intensive Care, University of Uppsala, Akademiska Sjukhuset ing 70, 1tr, Uppsala, 75185, Sweden
BMC Gastroenterology 2012, 12:40 doi:10.1186/1471-230X-12-40Published: 30 April 2012
Increased rectal luminal lactate concentration may be associated with the severity of the septic shock and high dose of vasopressors. It suggests hypoperfusion of the gut mucosa. This is potentially associated with bacterial translocation from the gut leading to local and systemic inflammation. In acute pancreatitis (AP) bacterial translocation is considered as the key event leading to infection of necrotic pancreatic tissue and high severity of illness.
We used rectal luminal equilibration dialysis for the measurement of gut luminal lactate in 30 consecutive patients admitted to hospital due to acute pancreatitis to test the hypothesis that a single measurement of rectal luminal lactate predicts the severity of acute pancreatitis, the length of hospital stay, the need of intensive care and ultimately, mortality. We also tested the physiological validity of luminal lactate concentration by comparing it to luminal partial tension of oxygen. Additionally, a comparison between two different L-lactate analyzers was performed.
High rectal luminal lactate was associated with low mucosal partial tension of oxygen (R = 0.57, p = 0.005) thereby indicating the physiological validity of the method. Rectal luminal lactate at the hospital admission was not associated with the first day or the highest SOFA score, CRP level, hospital length of stay, length of stay in intensive care or mortality. In this cohort of unselected consecutive patients with acute pancreatitis we observed a tendency of increased rectal lactate in the severe cases. Low precision and high bias was observed between two lactate analyzers.
The association between rectal luminal lactate and oxygen tension indicates that luminal lactate is a marker mucosal anaerobiosis. Comparison between two different analyzers showed poor, non-constant precision over the range of lactate concentrations. Rectal luminal lactate concentration at the time of hospital admission did not predict the severity of pancreatitis.