Resuscitation of critically ill patients based on the results of gastric tonometry: A prospective, randomized, controlled trial

Abstract

To determine whether additional therapy aimed at correcting low gastric intramucosal pH (pHi) improves outcome in conventionally resuscitated, critically ill patients.

Prospective, randomized, controlled study.

General intensive care unit (ICU) of a university teaching hospital.

A total of 210 adult patients, with a median Acute Physiology and Chronic Health Evaluation II score of 24 (range, 8-51).

All patients were resuscitated according to standard guidelines. After resuscitation, those patients in the intervention group with a pHi of <7.35 were treated with additional colloid and then dobutamine (5 μg/kg/min then 10 μg/kg/min) until 24 hrs after enrollment.

There were no significant differences (p > .05) in ICU mortality (39.6% in the control group vs. 38.5% in the intervention group), hospital mortality (45.3% in the control group vs. 42.3% in the intervention group), and 30-day mortality (43.7% in the control group vs. 40.2 in the intervention group); survival curves; median modified maximal multiorgan dysfunction score (10 points in the control group vs. 13 points in the intervention group); median modified duration of ICU stay (12 days in the control group vs. 11.5 days in the intervention group); or median modified duration of hospital stay (60 days in the control group vs. 42 days in the intervention group). A subgroup analysis of those patients with gastric mucosal pH of ≥7.35 at admission revealed no difference in ICU mortality (10.3% in the control group vs. 14.8% in the intervention group), hospital mortality (13.8% in the control group vs. 29.6% in the intervention group), or 30-day mortality (10.3% in the control group vs. 26.9% in the intervention group).

The routine use of treatment titrated against pHi in the management of critically ill patients cannot be supported. Failure to improve outcome may be caused by an inability to produce a clinically significant change in pHi or because pHi is simply a marker of disease rather than a factor in the pathogenesis of multiorgan failure.