Liver transplant is the gold standard therapy for end-stage liver disease and many patients are on the waiting list for a transplant. In the preop assessment, patients should be evaluated for the presence of liver failure and the complications of end stage liver disease, which include the following:

Pulmonary System
Assessment of the patient’s pulmonary system should include review of a recent chest radiograph, lung function tests and ABG. Pulmonary complications associated with liver disease include:

a) Restrictive Lung Disease
b) Intrapulmonary shunts
c) Pulmonary Hypertension

Cardiovascular System
The cardiovascular system is difficult to evaluate in patients with severe liver disease. The typical high cardiac output state with low systemic vascular resistance seen in most patients with cirrhosis can masquerade as an athletic heart, disguising severe cardiomyopathy. Severe coronary artery disease is found in less than 3% of this patient population. It is thought that cirrhosis may offer some protection from coronary atherosclerosis.

CNS
Hepatic encephalopathy is a life-threatening complication of endstage liver disease. Causes include accumulation of toxins such as ammonia, GABA agonists and other neuroactivesubstances. Cerebral metabolism and the blood-brain barrier may also be abnormal in these patients.

Gastrointestinal System
Portal pressure increases because of increased hepatic vascular resistance and increased portal venous inflow. The anatomic site of the increased intrahepatic vascular resistance varies according to the etiology of the cirrhosis. Portal hypertension is sustained by the development of increased portal venous inflow from a generalized hyperdynamic circulation in both acute and chronic liver failure. Problems related to portal hypertension:

a) Oesophageal varices
b) Hypersplenism
c) Ascites
d) Spontaneous Bacterial Peritonitis (SBP)

Haematological System

a) Thrombocytopenia due to portal hypertension-induced splenic sequestration and alcohol or sepsis induced bone marrow suppression is common. DIC (consumption) also may lead to low platelet counts.
b) Anaemia normally occurs because of chronic disease, malnutrition, or bleeding.

Hepatic Synthetic Function
Plasma concentrations of albumin, plasma cholinesterase and coagulation proteins are decreased in patients with liver disease (decreased synthesis volume).

a) Haemostatic abnormalities in patients with liver disease: In patients with liver disease, impaired haemostasis reflects decreased production of clotting factors because of hepatic synthetic dysfunction and, in some cirrhotics, depletion of vitamin K stores (clotting factors II, VII, IX and X) due to malnutrition or decreased intestinal absorption. Increased fibrinolytic activity with laboratory features of mild disseminated intravascular coagulation is also frequent in patients with cirrhosis.
b) Albumin: Hypoalbuminaemia contributes to low serum oncotic pressure, which predisposes to intravascular hypovolaemia, interstitial oedema, ascites and pleural effusions. Drug protein binding is also affected.
c) Pseudocholinesterase: Plasma cholinesterase concentrations are lower due to decreased production.
d) Metabolic dysfunction: Diminished hepatic glycogen stores as well as impaired gluconeogenesis in patients with liver disease may result in severe hypoglycaemia. The blood urea nitrogen level may therefore be low in patients with endstage liver disease, whereas the ammonia concentration may be markedly elevated. Ammonia itself is neurotoxic and its accumulation in the blood is associated with hepatic encephalopathy.

Renal Function
Renal function may be impaired in patients with liver failure. This can be due to the same disease process that damaged the liver, or the result of prerenal azotemia, acute tubular necrosis, or hepatorenal syndrome. In end-stage liver disease, the renin-angiotensin system is activated with little or no sodium excretion. In addition, antidiuretic hormone activity is increased, causing water retention that exceeds sodium retention, resulting in hyponatremia. Hepatorenal syndrome is characterized by normal urinary sediment, low urinary sodium, azotemia, and oliguria. This picture is similar to prerenal azotemia; it is therefore important to exclude hypovolemia. Patients with hepatorenal syndrome usually recover renal function following OLTX. If a renal biopsy demonstrates irreversible renal disease, then a combined liver and kidney transplant should be considered.

References

1. Preoperative Evaluation of Patients with a Transplanted Organ. Stephen P. Fischer, Angela M. Bader, and BobbieJean Sweitzer. Miller: Miller’s Anesthesia, 7th ed.; Chapter 34 - Preoperative Evaluation. Copyright © 2009 Churchill Livingstone, An Imprint of Elsevier.
2. Pre operative cardio pulmonary assessment of the liver transplant candidate. Martinez-Palli G, Cardenas A. Ann Hepatol. 2011 Oct-Dec;10(4):421-33.
3. Pre-liver transplantation, cardiac assessment. Rugina M, Predescu L, Salagean M, Gheorghe L, Gheorghe C, Tulbure D, Popescu I, Bubenek-Turconi S. Chirurgia (Bucur). 2012 May-Jun;107(3):283-90.
4. Preoperative evaluation of patients with liver disease. Hanje AJ, Patel T. Nat Clin Pract Gastroenterol Hepatol. 2007 May;4(5):266-76.