Cardiopulmonary Thromboembolism as an Unusual Cause of Death During Orthotopic Liver Transplantation

R. Renard Sessions, MD, J. A. Cohen, MD
Dept of Anesthesiology, University of Florida

Introduction: Orthotopic liver transplantation (OLT) has developed into a procedure that is as frequent as other major abdominal operations at experienced institutions. However, the risk of perioperative mortality is still relatively high (approximately 5%) for these patients. We present an unusual cause of intraoperative mortality in a patient undergoing OLT.
Case Presentation: A 39 year old man presented for OLT. His previous history included significant hepatitis C, cirrhosis, encephalopathy, motor vehicle accident with 67% TBSA burns 16 yr previously, chronic low back pain, upper GI bleed 10 months previously, and gastroparesis. During the patient’s admission 1 mo previously, he was treated for encephalopathy and pneumonia. On the night prior to OLT, he denied any chest pain or dyspnea and related an exercise tolerance of approximately 4 METs. On examination: he weighed 92 kg, was normotensive and slightly tachycardic at 105 bpm. His chest was clear to auscultation and no cardiac murmurs were detected. Laboratory examination showed a normal BUN/Cr ratio, Hct of 27%, alkaline phosphatase was 320, AST was 142, ALT was 70, albumin was 2.6, total protein was 8.2 and PT/PTT was normal.
After general anesthesia was induced and immediately after incision, the surgical team noted a dense fibrous capsule surrounding the liver and adjacent bowel that increased the technical difficulty of the procedure. During the final stages of removal of the native liver the patient suffered a period of hemodynamic collapse as evidenced by a BP of 54/32, increased PA pressure of 40/20, and decreased end-tidal CO2 of 12. A transesophageal echocardiogram (TEE) demonstrated air entrained in both the right and left heart. The surgeons found and occluded an open hepatic vein containing air in the posterior portion of the fibrous capsule that lead to resolution of pulmonary hypertension and hemodynamic stability. During the remainder of the procedure the patient was relatively stable despite ongoing diffuse oozing at the time of closure. The patient received 16 L of crystalloid, 800 cc of 5% albumin, 16 U of PRBC, 10 U of FFP, 10 U of platelets and 8 U of cryoprecipitate. Estimated blood loss was 11 liters.
During the patient’s 5 hr stay in the ICU, he continued to ooze. Coagulation studies did not improve despite multiple attempts to correct with FFP and platelets. Amicar (2 g administered in divided doses) was given after multiple thromboelastograms demonstrated massive fibrinolysis. Emergent reexploration was performed in the operating room after his drains abruptly filled with large quantities of blood. On arrival in the OR, his PA pressures (65/52) were greater than systemic (48/38). He stabilized somewhat with the addition of more blood products and epinephrine at 0.06 µg/kg/min. Amicar, 2 g, was again given to help correct persistent fibrinolysis as evidenced by TEG. TEE was performed to evaluated cardiac function and during placement of the probe BP, PAP, EtCO2, and HR decreased rapidly to asystole. Chest compressions were begun. Massive clot was observed in the right atrium, ventricle, and pulmonary arteries by TEE. The patient was pronounced dead shortly thereafter. At autopsy, new clot was demonstrated in the above locations with a small-organized clot in the pulmonary artery. The patient was also found to have diffuse Histoplasmosis pneumonia with abscess formation and severe three-vessel coronary artery disease.
Discussion: This patient had multiple comorbid conditions that compromised his chances of surviving an OLT. However, the ultimate cause of death is most directly related to his coagulopathy. He died from a clot that either formed in or embolized to his right heart and pulmonary artery. Of concern is the potential that the use of an antifibrinolytic agent (Amicar) may accelerate occult thrombosis and, thereby, causing or exacerbating embolic events, while still not controlling fibrinolysis. Caution in the use of this product is therefore indicated, although an exact protocol for its use during OLT is not defined.


 

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2000 - Cole, Deckinga, Denson, Fuchs, Maples, Naik, Robicsek, R. Zhang

2001 - Denney, Fuchs, Liem, Palacios, Rajasekaran, Rice, Sessions

2002
- Fuchs, Li #1, Li #2, Mayo, Ozcan, Tagalakis,

2003 - Barotti, Barry, Ozcan, Patel, Robinson, Swinney, Tran, van der Heusen , Walters

2004 - Abbasian, Bird, Cahill, Chang, Dahleen, Durret, Horowitz, Perschau, Robinson, Muehlschlegel, Santiago, Velez, Wendling

2005 case reports - Bauernfeind, Cummens, Dagen, Dobija, Yavas

2006 - Book, Chen, Covington, Eisenman, Ficarotta, Hyde, Jordan, Le, Lesko, Moorjani, Muehlschlegel, Seghal, Stine, Tilman