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Objective: To assess clinical safety of a low central venous pressure (CVP) fluid management strategy in patients undergoing liver transplantation., Design: Retrospective record review comparing 2 transplant centers, one using the low CVP method and the other using the normal CVP method., Setting: University-based, academic, tertiary care centers., Participants: Patients undergoing orthotopic cadaveric liver transplantation., Interventions: Each center practiced according to its own standard of care. Center 1 maintained an intraoperative CVP <5 mmHg using fluid restriction, nitroglycerin, forced diuresis, and morphine. If pressors were required to maintain systolic arterial pressure >90 mmHg, phenylephrine or norepinephrine was used. At center 2, CVP was kept 7 to 10 mmHg and mean arterial pressure >75 mmHg with minimal use of vasoactive drugs., Measurements and Main Results: Data collected included United Network for Organ Sharing status, surgical technique, intraoperative transfusion rate, preoperative and peak postoperative creatinine, time spent in intensive care unit and hospital, incidence of death, and postoperative need for hemodialysis. Principal findings include an increased rate of transfusion in the normal CVP group but increased rates of postoperative renal failure (elevated creatinine and more frequent need for dialysis) and 30-day mortality in the low CVP group., Conclusions: Despite success in lowering blood transfusion requirements in liver resection patients, a low CVP should be avoided in patients undergoing liver transplantation.

Liver transplantation has become the procedure of choice for a wide variety of patients with end-stage liver disease. Perioperative morbidity and mortality have decreased dramatically over the past two decades, and superior graft and patient survival rates are now routine. Despite these advances, however, there remain several potentially lethal possibilities that may complicate the immediate postoperative period. Failure of the graft to regain any useful metabolic activity is known as primary nonfunction, and almost uniformly requires retransplantation for any hope of survival. Lesser degrees of immediate dysfunction require experienced clinical judgment as to the probability of sustaining long-term patient viability. Another potentially catastrophic development is thrombosis of the grafted hepatic artery. This is sometimes successfully managed by surgical reconstruction. It may develop immediately, or present insidiously much later. Thrombosis of the portal vein, while not usually fatal, can significantly complicate the immediate course, carrying with it a significant risk of sepsis. Close monitoring of patients in the period following liver transplantation is crucial, as prompt diagnosis and early intervention directly affects the patient's chances of survival.

The management of the liver transplant (OLT) candidate with portopulmonary hypertension (PPHTN) has dramatically changed in the past 3 years. Careful preoperative evaluation with functional characterization of right ventricular function plays a critical role. The pulmonary vascular response to epoprostenol infusion serves as a deciding factor for OLT candidacy. Careful perioperative attention to avoid right ventricular failure from acutely elevated pulmonary artery pressures or sudden increases in right ventricular preload is a key physiologic tenet of management. With increased surgical expertise, anesthetic sophistication, and availability of epoprostenol, PPHTN is no longer considered an absolute contraindication for OLT.

Pulmonary hypertension, defined as mean pulmonary artery pressure (mPAP) greater than or equal to 25 mmHg, is a recognized complication of hepatic dysfunction with portal hypertension and is considered a relative contraindication to liver transplantation. To characterize pulmonary hemodynamic responses in OLT candidates without pre-existing primary pulmonary hypertension, 22 consecutive patients referred for OLT at the Stanford University Hospital underwent prospective right heart catheterization with pressure determinations at baseline and following infusion of 11 crystalloid over 10 min. In addition, EKG, chest X-ray and transthoracic echocardiograms were performed as a part of the routine evaluation. Eleven non-cirrhotic patients served as controls. At baseline, 1/22 (4.5%) OLT patients had pulmonary hypertension while 9/22 (41%) developed pulmonary hypertension following volume infusion (p < 0.0001). In contrast, 0/11 controls manifested elevated pulmonary pressures at baseline or following volume challenge. OLT candidates were found to have significant increases in mean pulmonary pressure and capillary wedge pressure (PCWP) compared to controls, suggesting intravascular volume overload or left ventricular dysfunction as potential causes. OLT candidates who manifested volume-dependent pulmonary hypertension (a) had a 2-fold higher baseline PCWP, (b) currently smoked, and (c) had previously undergone portosystemic shunts. Aggregate analysis of EKG, echo and CXR for determination of volume-mediated pulmonary hypertension revealed a sensitivity of 25%, specificity of 75% and a positive predictive value of 40%. Preoperative identification of patients with a predisposition to manifesting elevated pulmonary pressures in the context of rapid volume infusion offers the potential for improved risk stratification and optimized clinical management.