Randomized controlled trial of laparoscopic gastric ischemic conditioning prior to minimally invasive esophagectomy, the LOGIC trial
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- Veeramootoo, D., Shore, A.C. & Wajed, S.A. Surg Endosc (2012) 26: 1822. doi:10.1007/s00464-011-2123-1
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Minimally invasive esophagectomy (MIE) is a viable alternative to open resection for the management of esophagogastric cancer. However, the technique may relate to a higher incidence of ischemia-related gastric conduit complications. Laparoscopic ischemic conditioning (LIC) by ligating the left gastric vessels 2 weeks before MIE may have a protective role, possibly through an improvement of conduit perfusion. This project was designed to evaluate whether LIC influenced ultimate conduit perfusion.
A randomized controlled trial was designed to compare MIE with LIC (L) against MIE without (N). The project began in May 2009 and was offered to consecutive patients with the objective of recruiting 22 in each arm. Sample size calculations were based on data from previous clinical series. The main outcome measure was perfusion recorded by validated laser Doppler fluximetry, at the fundus (F) and greater curve (G); performed at routine staging laparoscopy and every stage of an MIE. A perfusion coefficient measured as ratio at stage of MIE over baseline was used for statistical analysis.
Sixteen patients were recruited before an interim analysis of the trial data. At staging laparoscopy perfusion at F was higher than at G (p = 0.016). In the L cohort, an apparent rise in perfusion at G is observed post intervention (p = 0.176). At MIE, baseline perfusion is comparable for both arms; however, a significant drop is observed at both locations once the stomach is mobilized and exteriorized (p = 0.001). Once delivered at the neck, perfusion coefficient is approximately 38% of baseline levels. However, there was no discernible difference between the L (38.3 ± 12) and N (37.7 ± 16.8) cohorts (p = 0.798).
LIC does not translate into an improved perfusion of the gastric conduit tip. The benefits reported from published clinical series suggest that the resistance of the conduit to ischemia occurs through alternative possibly microcellular mechanisms.