Complications Of Liver Transplantation
Careful and frequent clinical review is required post transplant to identify deterioration suggestive of complications. Post-transplant biochemical monitoring uses the same markers of liver dysfunction as were used before transplantation, namely:
1. Prothrombin time, for synthetic function;
2. Alanine transaminase (alt) and aspartate transaminase (ast), for hepatocellular damage;
3. Alkaline phosphatase (alp): reflects bile duct damage;
4. Serum lactate, should start to fall towards normal within an hour or two of reperfusion of the liver giving earliest sign of function;
5. Ultrasonography is used to detect biliary dilatation and assess blood flow to the liver, supplemented by ctyangiography.
Non-specific complications of surgery
Bleeding is common due to a combination of factors:
· The presence of abdominal varices
· A coagulopathy, particularly if the liver is slow to resume full protein synthesis
· Thrombocytopaenia due to splenomegaly
Wound infection is common due to the prolonged nature of the surgery (many hours), the poor nutritional state of the recipient and the reaccumulation of ascites post-operatively.
Wound breakdown, with superficial or complete dehiscence, may follow.
Atelectasis, pneumonia and pleural effusion are also common, as with all upper abdominal surgery, and occasionally paralysis of the right hemidiaphragm occurs as a consequence of cross-clamping the suprahepatic vena cava alongside which runs the right phrenic nerve.
The bile duct is the commonest source of problems following transplantation. In part this relates to its blood supply, which usually passes from the duodenal end of the duct towards the liver; the common hepatic duct and confluence receive a blood supply from the common or right hepatic artery. Following transplant the only blood supply to the bile duct is from the liver and so it is prone to ischaemia unless cut short; if cut too short the ensuing anastomosis is under tension, which predisposes to anastomotic disruption.
Bile leak may occur as a result of ischaemia, infection or traction on the anastomosis. It commonly affects a duct-to-duct anastomosis and requires conversion to a Roux-en-Y choledochojejunostomy. Since it may signify stenosis or thrombosis of the main or accessory right hepatic artery this should be excluded before surgery.
Anastomotic stricture may occur, usually as a result of ischaemia. Diagnosis is suggested by raised bilirubin and ALP, with dilated bile ducts on ultrasound. The stricture may be confirmed on magnetic resonance imaging followed by endoscopic retrograde cholangio-pancreatography (ERCP), balloon angioplasty and stenting. Persistent strictures may require conversion to Roux-en-Y drainage.
Hepatic artery thrombosis early post-transplant usually manifests with a sudden clinical deterioration and concomitant worsening of liver biochemistry. Thrombosis in the late post-operative period, months or years after transplant, may present more insidiously with biliary complications (intrahepatic strictures) or liver abscess formation.
Hepatic artery stenosis may also present with biliary complications in the early post-transplant period.
Venous outflow problems are usually secondary to a suprahepatic vena caval anastomotic stenosis where a classical caval replacement technique has been used for transplant. Presentation is with marked ascites and lower limb oedema. Diagnosis is by measurement of a pressure gradient across the anastomosis, and balloon angioplasty is the treatment of choice.
Portal venous inflow
Portal vein thrombosis is unusual but may occur early post-transplant, particular in patients with a prior portal or mesenteric venous thrombosis.
As with post-operative surgical complications, the medical complications of liver transplantation can be early or late. All the well-recognised general medical complications seen after major surgery, including myocardial infarction/cardiac decompensation, chest sepsis, confusion, electrolyte disturbances and renal dysfunction, can also occur post-liver transplantation.
In addition, in keeping with other transplants, acute rejection is common in the early post-transplant period but rarely causes longterm damage. Rejection is usually cell-mediated, although antibody-mediated rejection may also occur.
Hepatocellular tumours may recur following transplant, as well as other liver diseases, including:
Hepatitis C virus (HCV) invariably infects the transplanted liver and can result in aggressive disease, such that up to 10% of patients develop graft failure within a year post-transplant and around 30% develop cirrhosis in the transplanted liver within 5 years. Antiviral treatment can be used to modify the prognosis of hepatitis C post-transplant.
Hepatitis B can infect the transplanted liver, although the combination of regular infusions of hepatitis B immune globulin (HBIG) together with HBV replication inhibitors, such as lamivudine, usually controls disease.
Primary biliary cirrhosis, autoimmune hepatitis and primary sclerosing cholangitis are all recognised to recur in a minority of liver transplant recipients.
Alcoholic liver disease
Alcohol-related liver disease (ALD) and non-alcoholic fatty liver disease can also recur post transplant, although steps are taken pre-transplant to attempt to determine those ALD patients who are at high risk of harmful drinking post transplant and thereby reduce disease recurrence.
With good short-term outcomes following liver transplantation, the aim is to reduce long-term morbidity. To that end, every effort is made to minimise cardiovascular risk factors (treating hypertension, hyperlipidaemia and diabetes), to recognise disease recurrence early and to limit renal toxicity by using low doses of calcineurin inhibitor or converting to non-nephrotoxic agents such as mTOR inhibitors.
Long-term survival after liver transplantation is good, with more than 90% of recipients surviving a year and 70% more than 5 years.