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...

Summary. Background: Pulmonary embolism (PE) and intracardiac thrombosis (ICT) are rare but potentially lethal complications during orthotopic liver transplantation (OLT). Methods: We aimed to review clinical and pathological correlates of PE and ICT in patients undergoing OLT. A systematic review of the literature was conducted using MEDLINE and ISI Web of Science. Results: Seventy-four cases of intraoperative PE and/or ICT were identified; PE alone in 32 patients (43%) and a combination of PE and ICT in 42 patients (57%). Most frequent clinical symptoms included systemic hypotension and concomitant rising pulmonary artery pressure, often leading to complete circulatory collapse. PE and ICT occurred in every stage of the operation and were reported equally in patients with or without the use of venovenous bypass or antifibrinolytics. A large variety of putative risk factors have been suggested in the literature, including the use of pulmonary artery catheters or certain blood products. Nineteen patients underwent urgent thrombectomy or thrombolysis. Overall mortality was 68% (50/74) and 41 patients (82%) died intraoperatively. Conclusion: Mortality was significantly higher in patients with an isolated PE, compared to patients with a combination of PE and ICT (91% and 50%, respectively; P < 0.001). Intraoperative PE and ICT during OLT appear to have multiple etiologies and may occur unexpectedly at any time during the procedure.

Background— The predictive value of the preoperative hemoglobin value after coronary artery bypass grafting (CABG) has not been well established. We studied how the preoperative hemoglobin level affects the survival of patients after CABG. Late mortality was compared with that of a general population. Methods and Results— Early and late mortality of all consecutive patients undergoing isolated CABG between January 1998 and December 2007 were determined. Patients were classified into 4 groups stratified by preoperative hemoglobin level. The cutoff point for anemia was 13 g/dL for men and 12 g/dL for women. Expected survival of a matched general Dutch population cohort was obtained from the database of the Dutch Central Bureau for Statistics. After the exclusion of 122 patients who were lost to follow-up and 481 patients with missing preoperative hemoglobin levels, complete data were obtained in 10 025 patients. Multivariate logistic regression analyses revealed anemia to be an independent risk factor for higher early mortality. Cox regression analyses revealed low hemoglobin level, both as a continuous variable and as a dichotomous variable (anemia), to be a predictor of higher late mortality. Compared with expected survival, patients with the lowest preoperative hemoglobin levels had a worse outcome, whereas patients with the highest hemoglobin levels had a better outcome. Conclusions— A lower preoperative hemoglobin level is an independent predictor of late mortality in patients undergoing CABG, whereas anemia is a risk factor for early and late mortality. Compared with the general population, anemic patients had worse survival than expected, whereas nonanemic patients had better survival than expected.

The pharmacokinetics of dexmedetomidine in volunteers with severe renal impairment differed little from those in volunteers with normal renal function. In addition, there were no clinically significant differences in the hemodynamic responses to dexmedetomidine. However, dexmedetomidine resulted in more prolonged sedation in subjects with renal disease.

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