Perioperative management is targeted to the optimization of the patient prior to surgery and prevention of liver-related complications. The optimal approach to the management of the coagulopathy associated with liver disease is complex, but can be summarized by saying “less is more” [35]. Routinely used tests of coagulation such as the platelet count, international normalized ratio (INR) and activated partial thromboplastin time (aPTT) do not reflect true hemostatic function in liver disease or risk of bleeding complications [36, 37]. More sophisticated tests of blood coagulation, such as the modified thrombin generation test and whole blood thromboelastography, demonstrate that coagulation function is largely preserved, referred to as hemostatic rebalancing. Unfortunately, these tests are not widely available and have not yet been clinically validated. The preoperative use of blood products to correct platelet count, INR, and aPTT has not been shown to be clinically beneficial and aggressive volume expansion may increase the risk of portal hypertensive bleeding, often the most significant cause of bleeding in this population. Hence, a restrictive approach to the use of red blood cells, platelets, and plasma products is preferred. Furthermore, the use of the thrombopoietin agonist eltrombopag, has been shown to be associated with an increased risk of thrombotic complications [38]. The best approach is therefore to avoid platelet and plasma transfusion prior to procedures and to intervene only where there is clinical evidence of hemostatic failure, often indicated by bleeding from multiple sites. Low fibrinogen levels (< 1 g/L) can be replaced with cryoprecipitate or fibrinogen concentrates to minimize volume expansion. The use of antifibrinolytics and prothrombin complex concentrates is currently being studied in clinical trials. It has been proposed that volume contraction and maintenance of a low intraoperative central venous pressure help reduce the need for blood transfusion during liver transplantation (LT) and liver resection [39–41]. This must be balanced against the risk of reduced perfusion of the kidneys and liver [35, 42]. Prevention of kidney injury, acidosis, hypothermia and hypocalcemia, as well as the early identification and treatment of infection, including the prophylactic use of antibiotics, will all help to improve surgical outcomes and reduce the risk of hemostatic failure.

Cirrhotic patients are also at increased risk of thrombosis, including portal and deep vein thrombosis. The use of anticoagulants in cirrhotic patients is a complex issue and the decision to use anticoagulants should be made on a case-by-case basis. Low molecular weight heparin appears to be safe in patients with Child class A and B disease undergoing surgery and is probably the treatment or choice in this setting [43].

Ascites is managed with salt restriction and diuretics . When paracentesis is required, ascitic fluid should be sent for culture and cell count. Postoperatively, care should be taken to minimize the accumulation of fluid through oral and intravenous salt restriction and judicious use of diuretics. Colloids and blood products can be used for intravascular volume replacement where needed. A key focus in postoperative management is the prevention of renal injury, through adequate volume replacement and avoidance of nephrotoxic agents including antibiotics , nonsteroidal anti-inflammatory drugs (NSAIDs) and intravenous contrast. Nutritional support should be commenced as soon as possible after surgery, preferably via the enteral route [44].

Pain management in patients with cirrhosis or end-stage liver disease is a clinically challenging issue with many misconceptions that generate much apprehension amongst health-care providers. Adverse events from analgesics are frequently observed and may lead to various complications ranging from the mild to life threatening. These include fluid and sodium retention, HE, hepatorenal syndrome (HRS) , and gastrointestinal bleeding.

The metabolism and excretion of most analgesic drugs are dependent on liver and/or kidney function and is summarized in Table 28.3. The ability of the liver to clear drugs is dependent on portal blood flow, hepatic enzyme activity, and plasma protein binding capacity, all of which can be significantly impaired in cirrhosis. Changes in any of these factors may substantially alter the bioavailability of the parent compound or its metabolites, increasing the risk of drug toxicity or adverse events. Increased plasma levels of drugs with a high first pass metabolism are observed in patients with cirrhosis. Highly protein bound drugs are also affected by cirrhosis. Hypoalbuminemia leads to increased levels of free drug, which may cause toxicity. Drugs that are primarily excreted by the kidneys are less often affected by liver disease, but these drugs may still be dependent on hepatic metabolism prior to renal excretion. However, renal dysfunction associated with advanced liver disease can lead to decreased renal metabolism and excretion. In these cases, it is recommended that the dose be adjusted according to the estimated glomerular filtration rate (eGFR) using the Cockcroft-Gault or modification of diet in renal disease (MDRD) equations [45]. These equations often overestimate the GFR in cirrhotic patients, so close monitoring for evidence of toxicity is still recommended, even after the “appropriate” dose modification. It should also be noted that end-organ sensitivity may be increased or decreased in the setting of cirrhosis. For example, cirrhotic patients are often more sensitive to agents with sedative effects and to drugs with adverse effects on the kidney.