The hepatosplanchnic area is not a common source of lactate in patients with severe sepsis

Objective: To investigate the role of the splanchnic region in the hyperlac tatemia of septic patients. Design:Prospective, observational study. Setting: Thirty-one-bed mixed medicosurgical intensive care unit; Patients: Ninety invasively monitored and mechanically ventilated patients with severe sepsis. Measurements and Main Results: Splanchnic lactate balance was measured in a ll patients. Splanchnic blood flow was determined by using the primed conti nuous indocyanine green infusion technique-in 69 patients. In 71 patients, gastric mucosal Pco(2) and the: POD, gap (the difference between gastric an d arterial Pco(2) alsb were determined by using gas tonometry with an autom ated gas analyzer. In each patient, arterial, mixed-venous, and hepatic ven ous blood samples were obtained to determine hemoglobin oxygen saturations and lactate concentrations. Arterial and hepatic venous lactate concentrati ons were determined in triplicate and:were averaged, and the arterial hepat ic venous difference in lactate and lactate consumption were calculated. Th e splanchnic region produced lactate in only six of the 90 patients. Mean a rterial pressure, cardiac index, arterial lactate, hepatic venous oxygen sa turation, and catecholamine use were similar in the six patients with splan chnic lactate production and in the 84 others. The arterial hepatic venous differences in lactate and splanchnic lactate consumption were related dire ctly to arterial lactate concentrations (y = 0.073x + 0.209, r(2) =.06, p < .05, and y = 0.06x + 0.183, r(2) = .08, p < .05, respectively) but were no t related to Pco(2) gap, to the gradient between mixed-venous and hepatic v enous oxygen saturations, or to bilirubin concentrations. Conclusions: Splanchnic lactate release is uncommon in septic patients, eve n when hyperlactatemia is severe.