Objective: It has been postulated that in critically ill patients, splanchnic hypoperfusion may lead to cytokine release into the systemic circulation. The presence of cytokines could trigger an inflammatory response and cause multiple organ dysfunction syndrome. Although experimental studies support this hypothesis, humans studies remain controversial. The aim of the study was to determine the relationship between splanchnic hypoperfusion and cytokine release during septic shock.
Design: Human prospective study.
Setting: Medical intensive care unit at a university hospital.
Patients: A total of 30 patients with mean arterial pressure of <60 mm Hg after volume loading with either oliguria or hyperlactatemia.
Measurements: Gastric intramucosal measurements as an indicator of splanchnic hypoperfusion and blood samples were obtained at admission to the medical intensive care unit and repeated during 48 hrs. Cytokine (tumor necrosis factor-alpha and interleukin-6) values were evaluated by enzyme-linked immunoassays at the following periods: at the time of admission and 2, 4, 8, 12, 24, 36, and 48 hrs later.
Main results: High levels of interleukin-6 and tumor necrosis factor-alpha were observed at admission in survivors and nonsurvivors, without significant difference. At 48 hrs, cytokine levels were significantly higher in patients who died compared with the survivors (tumor necrosis factor: 163 +/- 16 for nonsurvivors vs. 34 +/- 9 ng/mL for survivors; interleukin-6: 2814 +/- 485 for nonsurvivors vs. 469 +/- 107 ng/mL for survivors). At 48 hrs, the PCO2 gap was significantly higher in the nonsurvivors compared with survivors (25.87 +/- 2.73 vs. 11.35 +/- 2.25 mm Hg), despite systemic hemodynamic variables in the normal range. A positive relationship was demonstrated between plasma levels of tumor necrosis factor-alpha and interleukin-6 and the PCO2 gap throughout the study. The PCO2 gap was not correlated with hemodynamic variables.
Conclusions: Our data suggest a relationship between gastric mucosal acidosis, as assessed by PCO2 gap, and cytokine levels in critically ill patients with septic shock. Gut injury may be a contributor of the inflammatory response in patients with septic shock.