The effects of methylene blue infusion on gastric tonometry and intestinal fatty acid binding protein levels in septic shock patients.

OBJECTIVE

We prospectively studied the effect of methylene blue (MB) infusion on gastric mucosal metabolism perfusion ratio, assessed by gastric tonometry, and on mucosal cell damage, assessed by urinary levels of intestinal fatty acid binding protein, in septic shock patients.

METHODS

Methylene blue (MB) infusion (1 mg/kg per hour) during 4 hours in 10 consecutive patients with a proven or suspected bacterial infection and with severe vasodilatory shock, defined as a mean arterial pressure 70 mm Hg or lower for at least 1 hour despite adequate volume resuscitation and norepinephrine infusion at a rate >or=0.2 microg/kg per minute.

RESULTS

Methylene blue infusion did not significantly change the P(g-a)CO(2) gradient (P = .16). Post hoc analysis of the subgroup of patients with an elevated baseline P(g-a)CO(2) gradient, defined as >or=20 mm Hg, showed that the median P(g-a)CO(2) gradient (interquartile range [IQR]) decreased from 45 (41-56) mm Hg before infusion to 41 (28-52) at the end of the 4-hour infusion and decreased further to 32 (26-36) mm Hg 2 hours after cessation of MB infusion (P = .012). The median urinary intestinal fatty acid binding protein concentration at baseline was elevated (210 [79-437] pg/mumol creatinine) and did not change significantly after 24 hours (116 [53-601] pg/mumol creatinine, P = .15). The median mean arterial blood pressure (IQR) increased from 70 (69-71) mm Hg at baseline to 77 (67-83) mm Hg after 1 hour (P = .04), the norepinephrine dose did not change significantly. The median (IQR) cardiac index decreased from 4.4 (3.2-5.5) L min(-1) m(-2) at baseline to 3.6 (3.3-4.7) L min(-1) m(-2) after 2 h, returning back to baseline values after cessation of MB infusion P = .02).

CONCLUSION

Although MB infusion in patients with septic shock and advanced multi-organ failure increases mean arterial blood pressure and decreases cardiac index, it does not compromise the gastric mucosal perfusion metabolism ratio as indicated by tonometry, and by the release of a mucosal cellular injury marker.