Is gastric malperfusion and endotoxemia one motor of the systemic inflammatory response syndrome following cardiac surgery?

cc318 CCJ Meeting abstract Is gastric malperfusion and endotoxemia one motor of the systemic inflammatory response syndrome following cardiac surgery? Groetzner JP Graeter T Lauermann I Demircan L Jockenhövel S Vazquez-Jimenez JF Messmer BJ HJ Schäfers HJ

Department of Thoracic and Cardiovascular Surgery, RWTH University Hospital Aachen, Germany

Department of Cardiothoracic and Vascular Surgery, University Hospital Homburg, Saar, Germany

Critical Care International Symposium on the Pathophysiology of Cardiopulmonary Bypass Meeting abstracts International Symposium on the Pathophysiology of Cardiopulmonary Bypass Aachen, Germany

12 December 1998

1364-8535 1999 3 Suppl A P07 10.1186/cc318 2 3 1999 1999 Current Science Ltd cc-3-2-p001-p07

Introduction

Gastric mucosal acidosis and endotoxemia seems to be responsible for cytokine activation and development of the systemic inflammatory response syndrome (SIRS) in patients with congestive heart failure. In a retrospective study we previously concluded that patients with congestive heart failure (CHF) and a low preoperative cardiac index had a higher incidence of SIRS following cardiopulmonary bypass (CPB) than patients without CHF. In a prospective study we tried to prove our hypothesis that CHF leads to malperfusion of the gut and subsequently to endotoxin release with cytokine activation.

Methods

We evaluated one group with low risk for developing SIRS (Group1: coronary artery bypass grafting without CHF) and a high risk group (Group 2: mitral valve surgery with CHF) with 10 patients each for clinical and laboratory signs of SIRS as defined by BONE. Intramucosal gastric pH, endotoxin was detected using a tonometric gastric tube (Baxter Inc.), TNFα and interleukin 6 (IL6) were measured with an ELISA at nine different times pre-, intra- and postoperatively.

Results

Groups were similar with regards to age and sex. Cardiac Index was lower in Group 2 (1.7 ± 0.3 l/min/cm³) than in Group 1 (2.8 ± 0.5 l/min/cm³; P < 0.05). In Group 2 the aortic cross clamping time was longer (Group 1: 59.6 ± 15.2 min, Group 2: 42.7 ± 19.4 min) and norepinephrine requirements for maintenance of vascular resistance were higher (8.2 ± 12.6 mg) than in Group 1 (1.7 ± 2 mg; P < 0.05).

At the end of CPB gastric pH dropped to 7.33 ± 0.34 in Group 2 whereas the other group remained stable between 7.47 and 7.5 (P < 0.05). Endotoxin levels were significantly elevated and significantly higher in Group 2 (37.2 ± 3.2 pg/ml) than in Group 1 (20.6 ± 3.7 pg/ml; P < 0.05) after aortic cross clamp was opened. In Group 1 only in 1 of 3 patients (33%) with gastric acidosis endotoxin was detected, whereas in Group 2 8/9 patients (88%) endotoxemia occurred.

TNFα was elevated in both groups during CPB and significantly higher in Group 2 at aortic declamping (Group 1: 19.6 ± 2.9 pg/ml; Group 2: 39 ± 4.8 pg/ml; P < 0.05) and after protamin application (Group 1: 27.3 ± 4.2 pg/ml; Group 2: 62.8 ± 8.1 pg/ml; P < 0.05). After protamin application IL6 raised postoperatively and was significantly higher in Group 2 (653 ± 75 pg/ml) than in Group 1 (547 ± 439 pg/ml). SIRS occurred more often in Group 2 (9/10) than in Group 1 (6/10) postoperatively. All patients with detected endotoxemia developed SIRS (13/13). (see Figure).

Figure

Conclusion

SIRS is more common in patients with CHF undergoing CPB than in others. This seems to be related to a drop of gastric pH as a sign of malperfusion. Consecutively endotoxemia occurs more often and seems to be a trigger of cytokine activation (TNFα, IL6) making higher norepinephrine application necessary. Our study emphasize the role of splanchnic malperfusion and endotoxemia as one mechanism responsible for the development of SIRS.