Intravascular and/or intracardiac thrombus formation followed by pulmonary thromboembolism with right ventricular dysfunction immediately after graft reperfusion during orthotopic liver transplantation (OLT) is described in 7 patients. This complication may have been related to excessive activation of the coagulation system by graft reperfusion, which overwhelmed anticoagulation mechanisms and was disproportionate to fibrinolysis. Activation of the coagulation system may be more pronounced in patients who receive less than optimal grafts, require massive transfusion, or have septic complications at the time of OLT. It is unclear whether antifibrinolytic therapy during the anhepatic stage had a role. Transesophageal echocardiography was useful in diagnosing and managing intracardiac thrombus and pulmonary thromboembolism. (Liver Transpl 2001;7:783-789.) P ulmonary air embolism or thromboembolism may occur during major vascular surgery. However, this complication is expected to be more common during orthotopic liver transplantation (OLT) because of several factors inherent to the procedure: excessive activation of the coagulation system secondary to injury to a large capillary bed, venous stasis during clamping of the portal vein and inferior vena cava (IVC), ischemic insult to the intestines, activators released from the grafted liver, and massive blood transfusion.A few case reports have documented intravascular and/or intracardiac thrombus formation during the dissection or anhepatic stage of OLT. 1-6 However, to date, the occurrence of intravascular and/or intracardiac thrombus formation within the first few minutes after reperfusion, followed by clinically significant pulmonary thromboembolism, has not been documented. In the 7 patients presented here, hemodynamic instability within minutes after graft reperfusion was associated with clinical signs of pulmonary embolism, evidenced by dramatic increases in pulmonary artery (PAP) and central venous pressures (CVP), as well as right ventricular (RV) dysfunction on transesophageal echocardiography (TEE), evidenced by acute right atrial and RV dilatation and hypokinesia, severe tricuspid regurgitation, and leftward shift of the interatrial and interventricular septa. These changes coincided with the observation of blood clots in the right atrium (RA) and pulmonary artery (PA) by TEE. These cases were encountered over a period of 2.5 years, during which time 577 OLTs were performed at the University of Pittsburgh (Pittsburgh, PA). During this period, coagulation management in the operating room was guided by thromboelastography and platelet count. Thromboelastography was performed on native blood and blood samples with the in vitro addition of ⑀-aminocaproic acid (EACA; 0.1% solution) and protamine (0.01% solution) for differential diagnosis of fibrinolysis and heparin effect, respectively.Transfusion and coagulation management guidelines of the liver transplant program were as follows. 7 Hemoglobin level was maintained at 8 to 10 g/dL; approximately an equal numbe...
We describe a new preservation modality combining machine perfusion (MP) at subnormothermic conditions (21°C) with a new hemoglobin‐based oxygen carrier (HBOC) solution. MP (n = 6) was compared to cold static preservation (CSP; n = 6) in porcine orthotopic liver transplants after 9 h of cold ischemia and 5‐day follow‐up. Recipients' peripheral blood, serial liver biopsies, preservation solutions and bile specimens were collected before, during and after liver preservation. Clinical laboratorial and histological analyses were performed in addition to mitochondrial functional assays, transcriptomic, metabolomic and inflammatory mediator analyses. Compared with CSP, MP animals had: (1) significantly higher survival (100% vs. 33%; p < 0.05); (2) superior graft function (p < 0.05); (3) eight times higher hepatic O2 delivery than O2 consumption (0.78 mL O2/g/h vs. 0.096 mL O2/g/h) during MP; and (4) significantly greater bile production (MP = 378.5 ± 179.7; CS = 151.6 ± 116.85). MP down‐regulated interferon (IFN)‐α and IFN‐γ in liver tissue. MP allografts cleared lactate, produced urea, sustained gluconeogenesis and produced hydrophilic bile after reperfusion. Enhanced oxygenation under subnormothermic conditions triggers regenerative and cell protective responses resulting in improved allograft function. MP at 21°C with the HBOC solution significantly improves liver preservation compared to CSP.
Thirty-two patients with coronary artery disease who underwent liver transplantation between 1990 and 1994 were identified. Coronary artery disease was managed medically (n = 9), by angioplasty (n = l), or surgically (n = 22) prior to liver transplantation. Two patients underwent simultaneous coronary artery bypass gralting and liver transplantation. Complete preoperative cardiac evaluation was performed in all patients. Perioperative and postoperative morbidity and mortality were retrospectively determined. Overall mortality was 50%, whereas morbidity was 81 %. Follow-up was between 1 and 3 years after liver transplantation.Subgroup analysis revealed that medically managed patients had a 56% mortality and a 100% morbidity. The patient who underwent angioplasty survived without morbidity. One patient who underwent simultaneous coronary artery bypass grafting and liver transplantation died intraoperatively. The second patient survived but required pacerthotopic liver transplantation (OLT) has be-
The purpose of this retrospective study was to examine the potential role of cerebral hemodynamic and metabolic factors in the outcome of patients with fulminant hepatic failure (FHF). Based on the literature, a hypothetical model was proposed in which physiologic changes progress sequentially in five phases, as defined by intracranial pressure (ICP) and cerebral blood flow (CBF) measurements. Seventy-six cerebral physiologic profiles were obtained in 26 patients (2 to 5 studies each) within 6 days of FHF diagnosis. ICP was continuously measured by an extradural fiber optic monitor. Global CBF estimates were obtained by xenon clearance techniques. Jugular venous and peripheral artery catheters permitted calculation of cerebral arteriovenous oxygen differences (AVDO 2 ), from which cerebral metabolic rate for oxygen (CMRO 2 ) was derived. A depressed CMRO 2 was found in all patients. There was no evidence of cerebral ischemia as indicated by elevated AVDO 2 s. Instead, over 65% of the patients revealed cerebral hyperemia. Eight of the 26 patients underwent orthotopic liver transplantation-all recovered neurologically, including 6 with elevated ICPs. Of the 18 patients receiving medical treatment only, all 7 with increased ICP died in contrast to 9 survivors whose ICP remained normal (P < 0.004). Hyperemia, per se, was not related to outcome, although it occurred more frequently at the time of ICP elevations. Six patients were studied during brain death. All 6 revealed malignant intracranial hypertension, preceded by hyperemia. In conclusion, the above findings are consistent with the hypothetical model proposed. Prospective longitudinal studies are recommended to determine the precise evolution of the pathophysiologic changes. (Liver Transpl 2005;11:1353-1360.)
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