Chapter 10 – Hepatobiliary Disease




Chapter 10 Hepatobiliary Disease


Anish Gupta and Charl Jooste



Key Points





  • Liver disease is increasingly prevalent in the developed world. Many patients may present with only mildly deranged bloods, but could be at risk of decompensation in the perioperative period.



  • Perioperative risk is significantly heightened in patients with severe liver disease. The Child-Turcotte-Pugh scoring system can help to risk stratify patients into high- and low-risk groups.



  • Patients undergoing non-elective surgery, the elderly, patients with moderate-to-severe cardiac or respiratory co-morbidities and malnourished patients are at increased risk.



  • A careful history and systems examination is crucial to identify the multi-systemic features of liver disease that may be optimised prior to surgery, and hepatic syndromes that predispose to perioperative complications.



  • Strict asepsis and prudent antibiotic selection will reduce the risk of infection in this relatively immuno-incompetent subgroup.



  • Patients with severe chronic liver disease live on a precarious physiological balance. Stress testing prior to surgery may identify those who are sufficiently physiologically robust, though ultimately this group of patients is best managed in a specialist liver centre.


The incidence of liver disease is rising and is now recognised as the fifth largest cause of mortality in England (10,948 deaths in 2012). Worldwide, the major causes of liver disease remain hepatitis B and C, whereas in developed nations, non-alcoholic fatty liver disease (NAFLD) and alcohol are the principal culprits.


Patients requiring elective surgery may present with stable chronic disease, cholestasis, or may be post-transplant. Chronic liver disease includes chronic hepatitis (inflammation persisting beyond 24 weeks) and cirrhosis. Causes include hepatitis B and C, alcohol, non-alcoholic fatty liver disease, drug-induced, autoimmune and metabolic. Any cause of chronic active hepatitis may progress to cirrhosis, characterised by fibrosis and nodular regeneration. Patients with cirrhosis may lack symptoms, but will eventually develop features of portal hypertension or hepatic insufficiency (decompensated cirrhosis).


Patients with jaundice may have hepatocellular damage or cholestasis. Long-standing biliary obstruction may progress to secondary biliary cirrhosis. Failure of bile salts to reach the intestine results in fat malabsorption, steatorrhea and deficiency of fat-soluble vitamins – A, D, E and K – leading to factors II, VII, IX and X deficiency.


The risk profiles of these patients correspond with disease severity, therefore a comprehensive assessment of underlying liver function, co-morbidities and physical exercise tolerance is imperative. Anaesthesia and surgery may exacerbate liver dysfunction, and in some cases predispose to fulminant hepatic failure. Patients with fulminant liver disease are extremely high risk, and should be transferred to a specialist unit.



Risk Stratification


Morbidity and mortality are greatly increased in the context of liver disease; Pronovost (1999) found an odds ratio of 4:6 in patients with mild liver disease in aortic surgery. Discussion with specialist hepatobiliary centres should take place at an early opportunity if any doubt exists as to the suitability of performing the surgical intervention outside of a transplant centre.


Pugh (1973) modified Child and Turcotte’s original risk classification, and although partly subjective, this classification is useful in staging the progress of hepatic dysfunction (Table 10.1). It has since been validated for use in general surgical procedures, where 90-day mortality is as high as 2 per cent in Child-Pugh A (score 5–6), 22 per cent in B (score 7–9) and 55 per cent in C (score 10–15).




Table 10.1 Pugh Scoring System for Chronic Liver Disease.










































Points attributed
Parameter 1 2 3
Encephalopathy Grade Absent Mild (1 or 2) Advanced (3 or 4)
Ascites Absent Mild Moderate
Serum Bilirubin µmol/l <34 34–51 >51
Serum Albumin g/l >35 28–35 <28
INR <1.7 1.7–2.3 >2.3


(Pugh, 1973)

Legend: µmol/l = micromole per litre, g/I = gram per litre, INR = International Normalised Ratio


The Model for End-Stage Liver Disease (MELD) was initially developed for predicting survival following trans-jugular intrahepatic portosystemic shunt (TIPS) (Kamath, 2001). It has been shown to be equally useful in predicting survival in those awaiting liver transplantation as well as outcome in non-transplant surgery. Adding plasma sodium level (MELD-Na) increases its discriminatory ability. MELD scores of 20–4 and ≥25 carry 90-day mortality of 21 per cent and 50 per cent, respectively.



MELD = [3.78 × loge (plasma bilirubin)] + [11.2 × loge (INR)] + [9.57 × loge (plasma creatinine)] + 6.43
MELD=[3.78×loge(plasmabilirubin)]+[11.2×loge(INR)]+[9.57×loge(plasmacreatinine)]+6.43

Additional predictors of poor outcome include those undergoing emergency surgery, the elderly, cardiac and respiratory co-morbidities and malnutrition. In practical terms, surgery can be performed safely in Child-Pugh group A with careful perioperative consideration; however, groups B and C are at high risk of perioperative complications, and therefore should be considered for transfer to a transplant unit if surgery is necessary.



Consequences of Chronic Liver Disease


Cirrhosis manifests haemodynamically as a hyperdynamic circulation, with low systemic vascular resistance (SVR), high cardiac index and a proportionately reduced central circulating volume. However, in some patients this state may compensate for degrees of cirrhotic cardiomyopathy, characterised by systolic and diastolic dysfunction, electrophysiological abnormalities and a blunted b-adrenoceptor response in the presence of an increased cardiac stress.


Portal hypertension (portal vein to inferior vena cava pressure gradient >12mmHg) results from hepatic fibrosis and consequent increased hepatic vascular resistance. This leads to the development of collateral vessels at portosystemic anastomoses, and the development of ascites, encephalopathy, splenomegaly and the risk of spontaneous bacterial peritonitis.


The incidence of coronary artery disease is comparable with the general population; symptomatic patients require cardiac screening. In the cirrhotic patient, the left ventricular workload may be reduced by the low SVR, which may unmask coronary disease at the time of surgical stress.


Hypoxaemia may result from intrapulmonary shunting, increased ventilation-perfusion mismatching, hepatic hydrothorax and pneumonia.


There are numerous causes of renal failure including relative hypovolaemia, intrinsic renal disease, toxins and hyperbilirubinemia, diuretic therapy and hepatorenal syndrome.


Synthetic dysfunction predisposes to potential coagulopathy, though due to the concomitant underproduction of anticoagulants (protein C/S and anti-thrombin III), these patients are able to maintain haemostasis on a more precarious balance.


The contribution of the liver to the immune system cannot be emphasised enough. Patients with chronic liver disease are susceptible to infection, including fungal infections.



Hepatic Syndromes


A hyperdynamic state with high cardiac output, long-standing portal hypertension with the development of collateral flows, together with an imbalance of vasoactive mediators either synthesised or metabolised by the liver, may lead to characteristic changes in both flow and pressure through the pulmonary vasculature. Two ends of the spectrum are hepatopulmonary syndrome (HPS) and portopulmonary hypertension (PPHTN) (Aldenkortt et al., 2014). The kidneys are also particularly susceptible to cirrhosis-related hypoperfusion. All three syndromes significantly elevate perioperative risk.



Hepatopulmonary Syndrome


Hepatopulmonary syndrome is present in approximately 20 per cent of cirrhotic patients. Hypoxia is characteristic, resulting from intrapulmonary vascular dilatation at the pre- and postcapillary levels, leading to decreased ventilation/perfusion ratios; uncommonly, anatomical shunt is present with arteriovenous communication. Diagnosis is confirmed by contrast-enhanced echocardiography or 99mTc macro-aggregated albumin scintigraphy. Medical treatment has been disappointing; transplantation is the only option in severe cases. Severe hypoxia (PaO2 <6.5 kPa) and high levels of vascular shunt (shunt fraction >20%) carry high mortality.



Portopulmonary Hypertension


Up to 20 per cent of pre-transplant patients have high flow-related pulmonary hypertension with normal pulmonary vascular resistance (PVR). Portopulmonary hypertension (PPHTN) is the presence of pulmonary hypertension with high PVR (>240 dynes/s/cm−5) (seen in <4%). The aetiology is complex, but it is characterised by a hyperdynamic high-flow state with excess central volume and non-embolic pulmonary vasoconstriction. The pathological changes associated with this syndrome match those associated with primary pulmonary hypertension except that cardiac output is high.


In comparison to HPS, PPHTN has some response to the agents used in primary pulmonary hypertension. Perioperatively, the higher the mean pulmonary artery pressure (MPAP), PVR and trans-pulmonary gradient (TPG), the greater the risk of death, usually due to acute right ventricular decompensation. If the MPAP is >35 mmHg or the PVR is >250 dyne/s per cm, mortality reaches 40 per cent; if MPAP is >50 mmHg, mortality approaches 100 per cent.



Hepatorenal Syndrome


Hepatorenal syndrome (HRS) is a potentially reversible cause of renal dysfunction in a small proportion of acute kidney injury (AKI) cases with cirrhosis. (Table 10.2). Two subtypes exist; type 1 results in acute renal deterioration following a precipitating event, whereas type 2 is a progressive form occurring over weeks. It represents an advanced stage of the cirrhotic haemodynamic dysfunction. The prognosis of HRS is poor with the worst survival rates out of all the causes of renal failure (Salerno, 2007).


Sep 15, 2020 | Posted by in ANESTHESIA | Comments Off on Chapter 10 – Hepatobiliary Disease
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