Begin typing your search above and press return to search.
Volume: 18 Issue: 2 April 2020

FULL TEXT

CASE REPORT
Occlusive Hepatic Artery Thrombus in a Deceased-Donor Liver Procured From a Donor With Blunt Abdominal Trauma Following a Road Traffic Collision Accident

Here, we describe a case of occlusive hepatic artery thrombus in a liver procured from an 18-year-old deceased donor after circulatory death. The donor had died of multiple trauma following a road traffic collision. Occlusive thrombus was found at the hepatic artery bifurcation during back-table preparation. Consequently, the liver transplant did not proceed. We suggest careful assessment of hepatic arteries of all donor livers before transplant, particularly those from donors who are involved in deceleration injuries. Transplanting such livers may lead to primary nonfunction.


Key words : Donation after circulatory death, Extended criteria donors, Liver transplant

Introduction

Liver transplant remains the mainstay of treatment for end-stage liver disease. The current shortage of organ donations has led to an increase in the use of "extended criteria donors" to meet the supply and demand of organ donation.1,2 Donor livers from traumatic abdo­minal injuries are therefore occasionally used for liver transplant.3

We describe a case of occlusive hepatic artery thrombus in a liver procured from a donor with multiple trauma following a road traffic collision.

Case Report

An 18-year-old-male patient was admitted with blunt abdominal, chest, and head trauma following a road traffic collision. An abdominal computed tomography (CT) scan demonstrated multiple superficial liver lacerations. Twenty-four hours later, the full extent of the irreversible nature of the neurologic injury became apparent. The futility of further treatment was discussed with the family, and consent for organ donation was sought. Because criteria for brain stem death were not met, a donation from a donor after circulatory death was considered. The treatment was withdrawn by switching off the ventilator and extubation of endotracheal tube. Death was confirmed by the attending physician, and a "stand off" time of 5 minutes was observed before commencement of the surgical procedure of procurement.

The liver was perfused in situ with University of Wisconsin solution through the aorta and portal vein. The liver flush was satisfactory. The warm ischemia time from donor asystole to aortic perfusion was 11 minutes. On inspection of the liver, a superficial laceration was noted on the right lobe of the liver. Conventional arterial and portal venous anatomy was noted with no reported injury to hepatic artery, portal vein, hepatic veins, and inferior vena cava.

Liver perfusion continued on the back table. The procuring surgeon suspected abnormal hepatic artery appearance and alerted the implant surgeon. The liver was packed as per standard protocols and brought to the recipient's hospital where the liver was assessed by the implant surgeon. On close inspection of the hepatic artery, intramural thrombus was noted in the branches of the hepatic artery with intrahepatic extension of the thrombus (Figure 1). A decision was made not to use the liver because of increased risk of hepatic artery thrombosis and primary nonfunction after transplant.

Discussion

Liver transplant is the only viable treatment option for patients with end-stage liver disease. A shortage of donor organs for transplant is the main limiting factor for liver transplant, which has led to a 10% to 15% mortality rate for patients on wait lists.4 Expansion of donor selection criteria, including donation after circulatory death and "expanded criteria donor," and living-donor liver transplant have attempted to address this disparity. Unlike kidneys, there is no agreed definition of "expanded criteria livers." Donor livers with parenchymal injury as a result of trauma are considered expanded criteria and carry the risk of primary nonfunction, hemorrhage, intrahepatic abscesses, and pseudoaneurysm formation.5 Nevertheless, after careful assessment, some of these livers can be successfully utilized for liver transplant.

Acceptable graft and patient survival rates have been reported after transplant of traumatized livers both from donors after brain death and donors after cardiac death. Mehrabi and associates reviewed all published cases of liver transplant that utilized traumatized livers (n = 18).6 The liver injuries ranged from subcapsular hematoma, superficial laceration, to deep fractures. Most of the reported lacerations were in the right lobe. These were initially managed by any combination of pressure, suture, electrocautery, topical hemostatic agents, and packing. After transplant, there was primary nonfunction in 3 cases (17%), which required emergency retransplant. There were also poor initial function, liver abscess, biloma, and subhepatic abscess each in one case (5.5%). Six-month graft and patient survival rates were 71% and 88%, respectively. In a single-center series, Bova and associates reported similar outcomes in nontraumatized liver.7 With careful assessment and meticulous management, traumatized livers can be transplanted successfully. Because of the complexity of procurement, transplant, and subsequent care, experienced surgeons should carry out such procedures.

Blunt abdominal trauma is often associated with road traffic collisions due to deceleration and compression injuries and may result in a combination of vascular and parenchymal injuries. The liver is involved in 1% to 8% of blunt abdominal trauma cases.8 Liver parenchymal lacerations mostly involve the right lobe, can be multiple, and can be graded according to the appearance on CT scan findings.9 In our case, there were superficial liver lacerations to the right lobe and an occlusive hepatic artery thrombus at the hilum with intrahepatic extension.

Major vascular injuries involving the aorta and inferior vena cava are often fatal.10 Deceleration can lead to avulsion or intimal tear of the celiac and superior mesenteric axis at or near their retroperitoneal points of fixation. Avulsion of hepatic artery may also happen at the point of entry into the liver at the hilum. Such avulsions can go unnoticed if the adventitia is still intact. Intimal tear in contrast can lead to intramural or luminal thrombus formation. Avulsion of the peripancreatic branches of the portal vein can result in hemorrhage and hemodynamic compromise. A compression injury can cause parenchymal laceration and bleeding and may also cause intimal tears, leading to thrombosis. Intimal tears as a result of compression injury are more commonly seen in proximal renal artery but may also be seen in the branches of superior mesenteric artery and celiac axis.11

Fatal injury to hepatic veins and retrohepatic inferior vena cava may result from deceleration injuries and should be carefully assessed when considering the use of a traumatized liver for transplant.12,13 Concomitant hepatic artery and portal venous thrombosis or avulsion may result in hepatic infarction.14 A late complication can be a pseudoaneurysm of the hepatic artery and is usually associated with bile leak.8 In our case, the hepatic artery thrombus may have formed secondary to an intimal tear of the hepatic artery as a result of both deceleration and compression. It is also possible that the thrombus formed distally in the celiac axis and lodged in the hepatic artery during in situ flushing. The thrombus was clearly visible in the hepatic artery at the hilum with intrahepatic extension (Figure 1). Hepatic artery thrombus after liver trauma in the setting of deceased donations has not been previously described.

Traumatized livers may be considered for liver transplant with appropriate management. Active bleeding must be stopped before these livers are considered for donation, and major vascular injuries must be excluded by careful examination and review of imaging. Emergency CT scans with CT angiogram have been shown to underreport hepatic arterial injuries.15 Therefore, a thorough assessment of the hepatic vasculature by both the procurement surgeon and the implant surgeon is important. The presence of hepatic artery thrombosis in a traumatized liver is not consistent with liver transplant survival even after a successful thrombectomy and should be excluded before transplant. Donors with a history of deceleration and compression injury, such as with road traffic collision injuries, may have an occult avulsion or an intramural or occlusive thrombus. Livers from these donors should be carefully assessed and discarded if a thrombus or an avulsion is identified.


References:

  1. Cameron AM, Ghobrial RM, Yersiz H, et al. Optimal utilization of donor grafts with extended criteria: a single-center experience in over 1000 liver transplants. Ann Surg. 2006;243(6):748-755.
    CrossRef - PubMed
  2. Trotter JF. Expanding the donor pool for liver transplantation. Curr Gastroenterol Rep. 2000;2(1):46-54.
    CrossRef - PubMed
  3. Avolio AW, Agnes S, Chirico AS, Cillo U, Frongillo F, Castagneto M. Successful transplantation of an injured liver. Transplant Proc. 2000;32(1):131-133.
    CrossRef - PubMed
  4. Everhart JE, Lombardero M, Detre KM, et al. Increased waiting time for liver transplantation results in higher mortality. Transplantation. 1997;64(9):1300-1306.
    CrossRef - PubMed
  5. Cowie SE, Yoshida EM, Ryan AG, et al. Hepatic abscesses after liver transplantation secondary to traumatic intrahepatic bile duct injuries in a cadaveric allograft donor. Transpl Int. 2004;17(7):379-383.
    CrossRef - PubMed
  6. Mehrabi A, Fonouni H, Ahmadi R, et al. Transplantation of a severely lacerated liver--a case report with review of the literature. Clin Transplant. 2009;23(3):321-328.
    CrossRef - PubMed
  7. Bova R, Schumacher G, Neumann U, Pratschke J, Neuhaus P, Glanemann M. Traumatized liver grafts for organ donation? A single-center experience. Prog Transplant. 2009;19(4):349-353.
    CrossRef - PubMed
  8. Taourel P, Vernhet H, Suau A, Granier C, Lopez FM, Aufort S. Vascular emergencies in liver trauma. Eur J Radiol. 2007;64(1):73-82.
    CrossRef - PubMed
  9. MacLean AA, Durso A, Cohn SM, Cameron J, Munera F. A clinically relevant liver injury grading system by CT, preliminary report. Emerg Radiol. 2005;12(1-2):34-37.
    CrossRef - PubMed
  10. Coimbra R, Hoyt D, Winchell R, Simons R, Fortlage D, Garcia J. The ongoing challenge of retroperitoneal vascular injuries. Am J Surg. 1996;172(5):541-545.
    CrossRef - PubMed
  11. Udekwu OP, Jannetta J, Udekwu AO, Peitzman AB. Disruption of the gastroduodenal artery and right gastric artery following blunt trauma. Injury. 1993;24(4):225-226.
    CrossRef - PubMed
  12. Evans S, Jackson RJ, Smith SD. Successful repair of major retrohepatic vascular injuries without the use of shunt or sternotomy. J Pediatr Surg. 1993;28(3):317-320.
    CrossRef - PubMed
  13. Kaoutzanis C, Evangelakis E, Kokkinos C, Kaoutzanis G. Successful repair of injured hepatic veins and inferior vena cava following blunt traumatic injury, by using cardiopulmonary bypass and hypothermic circulatory arrest. Interact Cardiovasc Thorac Surg. 2011;12(1):84-86.
    CrossRef - PubMed
  14. Francque S, Condat B, Asselah T, et al. Multifactorial aetiology of hepatic infarction: a case report with literature review. Eur J Gastroenterol Hepatol. 2004;16(4):411-415.
    CrossRef - PubMed
  15. Poletti PA, Mirvis SE, Shanmuganathan K, Killeen KL, Coldwell D. CT criteria for management of blunt liver trauma: correlation with angiographic and surgical findings. Radiology. 2000;216(2):418-427.
    CrossRef - PubMed


Volume : 18
Issue : 2
Pages : 255 - 257
DOI : 10.6002/ect.2017.0183


PDF VIEW [154] KB.

From the 1Department of Transplantation, St. James's University Hospital, Leeds; and the 2Institute of Liver Studies, King's College Hospital, London, United Kingdom
Acknowledgements: No financial assistance or funding was received in the preparation
of this manuscript. The authors of this manuscript have no conflicts of interest to
disclose.
Corresponding author: Nigel Heaton, Institute of Liver Studies, King's College Hospital, Denmark Hill, London SE5 9RS, UK
Phone: +44 20 32999000
E-mail: nigel.heaton@nhs.net