Abstract

Attenuating postreperfusion syndrome during orthotopic liver transplant is very important for transplant anesthesiologists because of the syndrome's complications. Oxygen-derived free radicals play an important role in the genesis of postreperfusion syndrome, but the effect of mannitol (a free radical scavenger) on attenuating the syndrome is unclear.OBJECTIVES-To investigate the effectiveness of infusing mannitol during the anhepatic phase in preventing postreperfusion syndrome, as indicated by postreperfusion cardiac output and central venous oxygen saturation. In a randomized clinical trial, 53 patients who had undergone orthotopic liver transplant were allocated to 2 groups. During the anhepatic phase, patients in the mannitol group received 1g/kg mannitol, whereas those in the control group received physiological saline. Mean arterial pressure, cardiac output, and central venous oxygen saturation were measured before and after the portal vein was declamped. Serum levels of sodium and potassium were recorded at baseline and after portal vein declamping.Setting-Shiraz Organ Transplant Center, Shiraz, Iran. In the mannitol group, no significant change was found in mean arterial pressure, cardiac output, and central venous oxygen saturation before and after declamping of the portal vein (P= .78, P= .59, and P= .83, respectively). However, after declamping in the control group, mean arterial pressure, cardiac output, and central venous oxygen saturation were significantly lower than before declamping (P=.003, P=.001, and P<.001, respectively). No significant change in serum levels of sodium and potassium from baseline to after declamping were found in either group. Infusion of mannitol 1 g/kg during the anhepatic phase was effective in attenuating postreperfusion syndrome without stress about hyperkalemia or hyponatremia during anesthesia.

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