Intracardiac thrombus formation and pulmonary thromboembolism immediately after graft reperfusion in 7 patients undergoing liver transplantation

Abstract

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...

Incidental intracardiac thromboemboli during liver transplantation: Incidence, risk factors, and management

“…4,7,9,10,12,13,17,18 Others are inherent to the OLT procedure: excessive activation of the coagulation system, venous stasis during clamping of the portal vein and inferior vena cava, and release of activators from the liver graft. 6,7,9 In addition, other conditions such as heparin-induced thrombocytopenia, factor V Leiden, and antithrombin deficiency can contribute to thrombosis and possibly ICTs during OLT. Finally, intraoperative management may play an important role: PA catheter placement; the administration of antifibrinolytics, anti-hepatitis B immunoglobulin, and blood products; and the intraoperative utilization of continuous venovenous filtration.…”

“…However, some authors have suggested that an intracardiac clot can grow rapidly and be followed by the development of massive thromboemboli and hemodynamic collapse. 6 Despite the potential risks, a systematic examination of incidental ICTs has not been reported, and the incidence of incidental ICTs is not known.…”

“…6,[9][10]13 Despite aggressive pharmaceutical or surgical interventions, the overall mortality rate for patients with thromboemboli during OLT remains high, and a majority of the patients die intraoperatively.…”

“…Systemic heparin or thrombolytics (tissue plasminogen activator and urokinase) can be given after the identification of thromboemboli. 6,10 Surgical interventions such as thrombectomy, with or without cardiopulmonary Additional Supporting Information may be found in the online version of this article.…”

“…The thromboemboli in these cases are usually described as large, massive, severe, or fatal; these terms refer to the clot size, the impact on hemodynamics, or the patient outcomes (the term massive is used throughout this report). [3][4][5][6][7][8][9][10][11][12][13][14] The diagnosis of massive thromboemboli can be made on the basis of a typical clinical presentation with or without transesophageal echocardiography (TEE) evidence. Several strategies have been reported for the management of massive thromboemboli during OLT.…”