In the setting of moderate to severe pulmonary artery hypertension, orthotopic liver transplantation (OLT) may be complicated by pulmonary hemodynamic instability and cardiopulmonary mortality. We retrospectively studied the relationship between cardiopulmonary-related mortality and initial (untreated) pre-OLT pulmonary hemodynamics in 43 patients with portopulmonary hypertension who underwent attempted OLT. Thirty-six patients were reported in 18 peer-reviewed studies, and 7 patients underwent OLT at our institution since 1996. Transplantation procedure outcome, mean pulmonary artery pressure (MPAP), pulmonary vascular resistance (PVR), cardiac output, pulmonary capillary wedge pressure, and transpulmonary gradient (TPG) are summarized. Overall mortality was reported in 15 of 43 patients (35%). Fourteen of the 15 deaths (93%) were primarily related to cardiopulmonary dysfunction. Two deaths were intraoperative, 8 deaths occurred during the transplantation hospitalization, and 4 patients died of cardiopulmonary deterioration posthospitalization. In 4 patients, the transplantation procedure could not be successfully completed. Cardiopulmonary mortality was associated with greater pre-OLT MPAP (49 ؎ 14 v 36 ؎ 7 mm Hg; P F .005), PVR (441 ؎ 173 v 261 ؎ 156 dynes·s·cm Ϫ5 ; P F .005), and TPG (37 ؎ 13 v 22 ؎ 10 mm Hg; P F .005). MPAP of 50 mm Hg or greater was associated with 100% cardiopulmonary mortality. In patients with an MPAP of 35 to less than 50 mm Hg and PVR of 250 dynes·s·cm Ϫ5 or greater, the mortality rate was 50%. No mortality was reported in patients with a pre-OLT MPAP less than 35 mm Hg or TPG less than 15 mm Hg. Cardiopulmonaryrelated mortality in OLT patients with portopulmonary hypertension was frequent and associated with significantly increased pre-OLT MPAP, PVR, and TPG compared with survivors. Treated or untreated, we recommend intraoperative cancellation or advise against proceeding to OLT for an MPAP of 50 mm Hg or greater. Patients with an MPAP of 35 to less than 50 mm Hg and PVR of 250 dynes·s·cm Ϫ5 or greater appear to be at high risk for cardiopulmonary-related mortality after OLT. A prospective study is needed to define optimal pretransplantation treatments and pulmonary hemodynamic criteria that minimize OLT mortality associated with portopulmonary hypertension. (Liver Transpl 2000;6:443-450.) P ortopulmonary hypertension is defined as pulmonary artery hypertension (mean pulmonary artery pressure [MPAP], Ͼ25 mm Hg and pulmonary capillary wedge pressure [PCWP] less than 15 mm Hg) in association with portal hypertension. 1-3 Several investigators adhere to the additional criteria of increased pulmonary vascular resistance ([PVR] Ͼ120 dynes·s·cm Ϫ5 ). [4][5][6] A unifying hypothesis explaining the cause of this liver-lung relationship has yet to be proven. 2 Patients with portopulmonary hypertension have a high mortality rate. Within 15 months from the time pulmonary hypertension was diagnosed, death was reported in 38% (10 of 26 patients) to 41% (32 of 78 patients) of the patients describ...

Cirrhotic cardiomyopathy (CCM) is cardiac dysfunction in patients with end‐stage liver disease in the absence of prior heart disease. First defined in 2005 during the World Congress of Gastroenterology, CCM criteria consisted of echocardiographic parameters to identify subclinical cardiac dysfunction in the absence of overt structural abnormalities. Significant advancements in cardiovascular imaging over the past 14 years, including the integration of myocardial deformation imaging into routine clinical practice to identify subclinical cardiovascular dysfunction, have rendered the 2005 CCM criteria obsolete. Therefore, new criteria based on contemporary cardiovascular imaging parameters are needed. In this guidance document, assembled by a group of multidisciplinary experts in the field, new core criteria based on contemporary cardiovascular imaging parameters are proposed for the assessment of CCM. This document provides a critical assessment of the diagnosis of CCM and ongoing assessment aimed at improving clinical outcomes, particularly surrounding liver transplantation. Key points and practice‐based recommendations for the diagnosis of CCM are provided to offer guidance for clinicians and identify gaps in knowledge for future investigations.

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We review contemporary coagulation management for patients undergoing liver transplantation. A better understanding of the complex physiologic changes that occur in patients with end-stage liver disease has resulted in significant advances in anesthetic and coagulation management. A group of internationally recognized experts have critically evaluated current approaches for coagulopathy detection and management. Strategies for blood component and factor replacement have been evaluated and recommended therapies proposed. Pharmacologic treatment and prevention of coagulopathy, management of patients receiving antiplatelet medications, and the role of transesophageal echocardiography for early detection and management of thromboses are presented.

The effect of an aprotinin infusion on blood and blood product transfusion during adult primary orthotopic liver transplantation (OLT) was investigated in a prospective, randomized, double-blind study. Sixty-three patients were enrolled; 33 patients were administered an aprotinin regimen of a 1,000,000-KIU loading dose, followed by a 250,000-KIU/h infusion during surgery, and 30 patients were administered equivalent volumes of normal saline. O rthotopic liver transplantation (OLT) is a procedure associated with a substantial risk for massive hemorrhage and consequent massive transfusion. When this occurs, it entails considerable use of blood and blood products, with the attendant risks and use of resources. In addition, greater transfusion requirements are associated with greater incidences of both mortality and postoperative morbidity, 1 possibly related to modifications of the inflammatory response. 2 The coagulopathy that occurs during OLT is multifactorial, resulting from a combination of insufficient procoagulants and thrombocytopenia of end-stage liver disease, along with fibrinolysis occurring during the anhepatic phase and at reperfusion. 3,4 Aprotinin, a naturally occurring nonspecific serine protease inhibitor, inhibits fibrinolysis, may reduce platelet dysfunction, and inhibits the inflammatory response. 5 It has been shown to decrease blood loss in cardiac surgery. 5 For these reasons, it has been investigated as an agent to potentially reduce blood and blood-product transfusion requirements during OLT. Although several studies have reported decreased blood and/or blood-product use with aprotinin during OLT, the majority of these have been either nonrandomized or retrospective in nature. [6][7][8][9][10][11][12] Placebo-controlled randomized studies published to date have shown either significant decreases in transfusion requirements with aprotinin 13,14 or no beneficial effect. 15,16 Thus, the clinical efficacy of aprotinin during OLT remains to be determined: a recent editorial accompanying the study of Porte et al 14 noted that further clinical studies are required. 17 The aim of this investigation is to assess the effects of a continuous infusion of aprotinin on blood and bloodproduct transfusion requirements during OLT and evaluate effects on measured intraoperative coagulation parameters. MethodsAfter institutional review board approval and written informed consent were obtained, candidates for primary OLT were recruited between 1996 and 1998. Patients with a pre-OLT diagnosis of hepatorenal syndrome or established renal failure requiring dialysis were excluded because of concerns of worsening renal dysfunction with aprotinin use. Anesthesia was induced with thiopental and lorazepam, then maintained with fentanyl and isoflurane. Succinylcholine was administered to facilitate tracheal intubation, followed by pancuronium for intraoperative neuromuscular blockade. Dopamine (2 g/kg/min) was administered to all patients throughout the procedure. OLT was accomplished using a vena cava preservation te...