Cigarette smoking is associated with an increased incidence of vascular complications after liver transplantation

Abstract

Hepatic artery thrombosis (HAT) and other vascular comIn patients with a history of cigarette smoking, incidence of vascular complications was higher than in those without history of cigarette smoking (17.8% v 8%, P ‫؍‬ .02). Having quit cigarette smoking 2 years before liver transplantation reduced the incidence of vascular complications by 58.6% (24.4% v 11.8%, P ‫؍‬ .04). The incidence of arterial complications was also higher in patients with a history of cigarette smoking compared with those without such history (13.5% v 4.8%, P ‫؍‬ .015). Cigarette smoking cessation for 2 years also reduced the risk of arterial complications by 77.6% (21.8% v 5.9%, P ‫.)500.؍‬ However, the incidence of venous complications was not associated with cigarette smoking. Furthermore, there was no significant association between development of vascular complications and all other characteristics studied. Cigarette smoking is associated with a higher risk for developing vascular complications, especially arterial complications after liver transplantation. Cigarette smoking cessation at least 2 years before liver transplantation can significantly reduce the risk for vascular complications. Cigarette smoking cessation should be an essential requirement for liver transplantation candidates to decrease the morbidity C hanges in coagulation after successful liver transplantation (LT) include a tendency toward a hypercoagulable state leading to an increased incidence of vascular complications. Such changes have been known and studied in animals and humans for more than 30 years. 1,2 In particular, hepatic artery thrombosis (HAT) and other vascular complications (hepatic artery stenosis [HAS], portal vein thrombosis [PVT] and deep vein thrombosis [DVT]) remain devastating complications after LT. 2,3 The reported incidence of HAT is estimated to be 25% in living related allografts, 4 10% to 25% in pediatric cadaver liver recipients, 5-8 2.6% to 20% in adult cadaver liver recipients, 9 and as high as 30% in children younger than 1 year old. 10 Early onset HAT usually develops within the first 2 months, 11,12 especially the first 5 days after LT. 13 Clinical presentations include acute, massive hepatic necrosis leading to fulminant hepatic failure, relapsing bacteremia with recurrent biliary sepsis from cholangitis, biliary tract ischemia leading to bile duct necrosis and leaks, and asymptomatic presentation with normal liver function tests. 7,14,15 HAT occurring early after LT is more likely to be associated with an aggressive course and higher rate of allograft loss in comparison to late onset HAT (beyond 2 months after LT). 11,14 Some evidence suggests that a prompt and accurate diagnosis by duplex ultrasonography [16][17][18][19] with confirmation by hepatic artery angiography 20 or exploratory laparotomy, followed by urgent allograft rescue modalities (e.g., interventional radiology, surgical and medical therapy) can provide temporary or permanent support, avoiding higher morbidity and mortality from retransplantation. 21,22 The repo...

Sirolimus as primary immunosuppression in liver transplantation is not associated with hepatic artery or wound complications

“…25 The incidence of HAT was increased in patients who had a history of smoking (relative risk, 3.1; P Ͻ .01).…”

Hepatic arterial reconstruction in 95 adult right lobe living donor liver transplants: Evolution of anastomotic technique

“…16,17 Though our numbers are small, we found only 2 patients with any significant smoking history, both of whom smoked up until the day of transplant.…”

Vascular complications following liver transplantation: A literature review of advances in 2015

“…However, a donor positive CMV status and a recipient negative cytomegalovirus (CMV) status have repeatedly been shown to be a possible risk factor for late HAT [27,45] . Moreover, specific factors of late HAT reported include the association of female donor and male recipient, hepatitis C virus positive recipients, episodes of rejection, tobacco consumption and retransplantation [10,17,27,45,46] . Besides, while some authors believe that HAS and hepatic artery kinking are the initiating factors, others suggest a perioperative hypercoagulable state as a possible underlying cause [5,10,17,28,29] .…”