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

To investigate the role of the splanchnic region in the hyperlactatemia of septic patients.

Prospective, observational study.

Thirty-one-bed mixed medicosurgical intensive care unit.

Ninety invasively monitored and mechanically ventilated patients with severe sepsis.

Splanchnic lactate balance was measured in all patients. Splanchnic blood flow was determined by using the primed continuous indocyanine green infusion technique in 69 patients. In 71 patients, gastric mucosal Pco2 and the Pco2 gap (the difference between gastric and arterial Pco2) also were determined by using gas tonometry with an automated gas analyzer. In each patient, arterial, mixed-venous, and hepatic venous blood samples were obtained to determine hemoglobin oxygen saturations and lactate concentrations. Arterial and hepatic venous lactate concentrations were determined in triplicate and were averaged, and the arterial hepatic venous difference in lactate and lactate consumption were calculated. The splanchnic region produced lactate in only six of the 90 patients. Mean arterial pressure, cardiac index, arterial lactate, hepatic venous oxygen saturation, and catecholamine use were similar in the six patients with splanchnic lactate production and in the 84 others. The arterial hepatic venous differences in lactate and splanchnic lactate consumption were related directly 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 not related to Pco2 gap, to the gradient between mixed-venous and hepatic venous oxygen saturations, or to bilirubin concentrations.

Splanchnic lactate release is uncommon in septic patients, even when hyperlactatemia is severe.