Cirrhosis

Overview 
Theory 
Diagnosis 
Management 
Follow up 
Resources 

The mainstay of therapy for liver cirrhosis remains the treatment of the underlying chronic liver disease, when possible, and prevention of superimposed hepatic insult, which could result in acute-on-chronic liver failure (ACLF). Early detection, control, and treatment of complications is essential; patients who develop complications should be referred for liver transplant evaluation.

Patients should be advised of the necessity for adequate nutrition, regular exercise, and the avoidance of hepatotoxins.[92]

Treatment of underlying chronic liver disease and prevention of superimposed hepatic insult

As cirrhosis is the pathological end-stage of any chronic liver disease, it is essential to treat the underlying causative condition in order to slow or halt the progression of cirrhosis. Oral direct-acting antivirals are considered a first-line treatment for chronic hepatitis C virus infection. One systematic review and meta-analysis found that early treatment with direct-acting antivirals reduced the recurrence of hepatocellular carcinoma, liver decompensation, and all-cause mortality, and prevented hepatocellular carcinoma in patients with compensated cirrhosis and without cirrhosis but did not prevent liver transplantation.[93] Regimens depend on the genotype and presence or absence of cirrhosis.[94] Local guidance should be consulted. See Hepatitis C.

Antivirals may be indicated for patients with chronic hepatitis B.[84][95] See Hepatitis B.

Superimposed hepatic insult may be prevented through the avoidance of alcohol and other hepatotoxic drugs (e.g., non-steroidal anti-inflammatory drugs [NSAIDs] and high doses of paracetamol [>2-3 g/day]), immunisation against hepatitis A and B for susceptible patients, management of metabolic risk factors, maintenance of adequate nutrition, and regular exercise.

Monitoring for complications

Cirrhosis is associated with serious complications including portal hypertension causing ascites (further complicated by spontaneous bacterial peritonitis and hepatic hydrothorax), gastro-oesophageal varices and portosystemic encephalopathy, acute kidney injury and hepatopulmonary syndromes, portopulmonary hypertension, ACLF, and hepatocellular carcinoma.

Prompt detection and treatment of these complications is essential in order to minimise related morbidity and mortality. Imaging tests include:

Abdominal ultrasound for the detection of ascites and surveillance for hepatocellular carcinoma
Upper gastrointestinal endoscopy for the detection of gastro-oesophageal varices
Abdominal ultrasound, computed tomography (CT), or magnetic resonance imaging (MRI) for the detection of hepatocellular carcinoma.

Other specialised tests may be required depending on individual symptoms.

Ascites

The most common complication of cirrhosis.

Every patient with new-onset ascites should undergo a diagnostic paracentesis: cell count with differential, albumin, and total protein should be measured in the ascitic fluid. Ascitic fluid should also be sent for culture and cytology.

Abdominal paracentesis animated demonstration

Demonstrates how to perform diagnostic and therapeutic abdominal paracentesis.

The serum-ascites albumin gradient (SAAG) should be calculated: a SAAG of ≥11 g/L with low ascitic fluid total protein is consistent with portal hypertension secondary to cirrhosis.

Ascites develops in part due to activation of the renin-angiotensin-aldosterone system, resulting in sodium retention. Evidence suggests that severe dietary sodium restriction may be more harmful than beneficial, and many clinicians advise a no-added-salt diet rather than a low-salt diet.[101] This means excluding additional table salt being added to foods and avoidance of foods with high salt content, such as crisps and some processed meals. This results in a moderate sodium restriction with daily intake of not more than 5 to 6.5 g.

First-line choice of diuretic should be spironolactone due to its effects on aldosterone and maintaining normal serum potassium.[101] Furosemide may be added in patients who do not respond. Renal function and electrolytes should be monitored carefully when initiating diuretics and after dose escalation.

NSAIDs, ACE inhibitors, and other nephrotoxins should be avoided in patients with ascites.[90]

Large volume refractory ascites

Some patients may develop large volume ascites refractory to medical treatment because of lack of efficacy, or unacceptable adverse effects or complications. These patients may require recurrent large-volume paracentesis (LVP) with albumin replacement for symptom control.[102]

Patients not suitable for liver transplantation should be considered for transjugular intrahepatic portosystemic shunt (TIPS) placement.[103] Meta-analyses indicate that TIPS is more effective than paracentesis for control of refractory ascites, but is associated with a higher incidence of hepatic encephalopathy.[103][104][105][106][107][108][109] Overall mortality does not appear to differ between the two interventions, but TIPS may confer a modest benefit with respect to transplant-free survival.[103][104][105][106][107][108][109] TIPS placement can improve the nutritional status of patients with cirrhosis, indicated by an increase in ascites-free weight, body mass index, and muscle mass.[110] One individual patient data meta-analysis found that TIPS treatment decreased the overall risk of a further decompensation and improved survival compared with standard of care.[111] One Cochrane systematic review and network meta-analysis reported that the overall certainty (quality) of evidence was very low, primarily because of unclear or high risk of bias in trials assessing interventions for the treatment of refractory ascites in patients with cirrhosis.[103] [ ] Disease severity at the time of TIPS placement is an important predictive factor for outcomes.[112]

The prognosis of patients with refractory ascites is poor. If TIPS/transplantation are not viable options, then long-term drain placement for intermittent small-volume paracentesis may be considered as a palliative measure.[113] Prospective randomised controlled trials are warranted.

The use of vaptans (vasopressin V2-receptor antagonists) may have a slight beneficial effect on ascites and hyponatraemia, but they do not reduce mortality, liver complications, or renal failure.[114][115]

Gastro-oesophageal varices

Varices are present in 50% of patients with cirrhosis. Variceal bleeding is a life-threatening complication of cirrhosis with an associated mortality of 20% at 6 weeks.[116] Patients with cirrhosis have historically been offered upper gastrointestinal endoscopy for screening of gastro-oesophageal varices at the time of diagnosis, and at 1- to 3-year intervals thereafter.[56] However, guideline recommendations vary regarding screening intervals.

The Baveno VII criteria suggest that screening endoscopy could be reserved for a subgroup of patients, based on liver stiffness measurement (LSM) and platelet count assessment.[54] In particular, patients with compensated cirrhosis, who have a liver stiffness <20 kPa (as measured by transient elastography) and platelet count >150 × 10⁹ cells/L, have a very low risk of having varices requiring treatment and can avoid screening endoscopy.[54] In practice, however, many centres still offer baseline endoscopy to all patients with liver cirrhosis.

In compensated patients with no or small varices at screening endoscopy, expanded Baveno VI criteria recommend screening for gastro-oesophageal varices at 1- to 3-year intervals thereafter.[87]

Baveno VII consensus guidelines conclude that patients who avoid screening endoscopy can be followed up by yearly repetition of transient elastography and platelet count. If LSM increases (≥20 kPa) or platelet count declines (≤150 × 10⁹/L), these patients should undergo screening endoscopy.[54]

[Figure caption and citation for the preceding image starts]: Oesophageal varices in a patient with portal hypertensionFrom the collection of Douglas G. Adler, MD [Citation ends]. com.bmj.content.model.Caption@48a6c504

Primary prophylaxis of bleeding

Prophylaxis with either non-selective beta-blockers (propranolol, nadolol, or carvedilol) or endoscopic variceal ligation (EVL), which requires several sessions to obliterate varices, should be implemented if high-risk oesophageal varices are present, due to the increased risk of variceal bleeding.[57] [ ] High-risk varices include small varices with red signs, medium or large varices irrespective of Child-Pugh classification, or small varices in Child-Pugh C patients.[88]

Non-selective beta-blockers

Advantages of non-selective beta-blockers include low cost and ease of administration. Once a patient is on a non-selective beta-blocker, there is no need for repeat oesophagogastroduodenoscopy (OGD), and haemodynamic responders to non-selective beta-blockers have a lower incidence of decompensation and death. Disadvantages are that approximately 15% of patients may have absolute or relative contraindications to therapy, and another 15% require dose reduction or discontinuation attributed to common adverse effects (e.g., fatigue, weakness, and shortness of breath) that resolve upon discontinuation, but that may discourage patients and their physicians from using these drugs.

Monitoring haemodynamic response while treating a patient with beta-blockers is associated with a lower risk of variceal bleeding, but large cohort randomised controlled trials are required to confirm these findings.[117] There is ongoing debate regarding the safety of non-selective beta-blockers in patients with cirrhosis and refractory ascites. The expanded Baveno VI criteria proposed that in patients with refractory ascites and (i) systolic blood pressure <90 mmHg, or (ii) serum creatinine >133 micromoles/L (>1.5 mg/dL), or (iii) hyponatraemia <130 millimoles/L, the beta-blocker should be reduced in dose or even temporarily discontinued.[87] However, there is evidence to suggest that the risk of harm may not be significant.[118][119][120][121]

Endoscopic variceal ligation (EVL)

EVL is a local therapy that involves placing elastic bands around oesophageal varices until they are obliterated. EVL can theoretically be performed in the same session as screening endoscopy with hardly any contraindications. Disadvantages of EVL include the risks associated with sedation, plus the risk of causing dysphagia, oesophageal ulceration, strictures, and bleeding. Adverse effects associated with EVL may be severe, with reports of deaths resulting from EVL-induced bleeding ulcers. EVL is unable to prevent complications other than variceal haemorrhage. Surveillance endoscopies are necessary after variceal eradication, at least annually, to detect variceal recurrence.[122] Child-Pugh class C, ascites, or low prothrombin index are all indicators for high risk of early bleeding following EVL.[123]

The choice of whether to use non-selective beta-blockers or EVL should be based on local resources and expertise, patient preference and characteristics, contraindications, and adverse events.[87] One meta-analysis that included 1023 patients compared prophylactic EVL with beta-blockers and found that there was no difference between the treatments with regard to gastrointestinal haemorrhage, all-cause mortality, or haemorrhage-related mortality. While there was a decrease in variceal haemorrhage with EVL compared with beta-blockers (relative risk [RR] 0.72, 95% CI 0.4 to 0.96), variceal haemorrhage was not significantly different between the two groups when only high-quality trials were considered (RR 0.84, 95% CI 0.60 to 1.17).[124] Subjective factors influence the physician's choice in selecting non-selective beta-blockers versus EVL, as illustrated in an interview-based study in which gastroenterologists who spent at least half their time performing endoscopy were more likely to choose EVL, whereas physicians who had a less procedural-based practice were more likely to choose non-selective beta-blockers.[125]

Transjugular intrahepatic portosystemic shunts (TIPS)

TIPS may be used as a secondary treatment option for oesophageal varices in cirrhosis but is not recommended for primary prophylaxis of variceal haemorrhage.[2][126] Evidence obtained from trials of prophylactic surgical shunt therapy show a significantly higher rate of encephalopathy and a tendency for a higher mortality in patients randomised to shunt surgery.[127] [128]

Due to very low‐certainty evidence, conclusions cannot be drawn about the benefits and harms of portosystemic shunts compared with endoscopic interventions for people with cirrhosis and previous hypertensive portal bleeding (i.e., secondary prophylaxis). [ ]

Gastric varices

Gastric varices are present in about 20% of patients with cirrhosis and can present either as isolated gastric varices or as gastro-oesophageal varices.[129] In the latter, the oesophageal varices extend below the cardia into the lesser curvature of the stomach (type 1 gastro-oesophageal varices [GOV 1]) or into the fundus (type 2 gastro-oesophageal varices [GOV 2]).[129] They have different physiology and clinical characteristics compared with oesophageal varices. Gastric varices bleed less frequently but more significantly than oesophageal varices. Bleeding is less directly related to the degree of portal hypertension and more related to the size of the varix and wall tension.[129] There is little literature regarding the management of gastric varices compared with oesophageal varices. Hence, most recommendations are based on expert opinion.[129] Currently, non-selective beta-blockers are suggested for primary prevention of variceal bleeding from GOV 2 or isolated gastric varices. Treatment for GOV 1 should follow the above guidance for oesophageal varices.

Acute variceal haemorrhage

An episode of acute variceal haemorrhage should be managed as a medical emergency with intravascular volume support, blood transfusion (with the aim of keeping the haemoglobin around 70-80 g/L [7-8 g/dL]), and a combination of endoscopic and pharmacological therapy.[130][131]

Terlipressin (a vasopressin analogue), or somatostatin (or its analogue octreotide) should be initiated as soon as a variceal bleed is suspected and continued for 2-5 days if it is confirmed.[132]

Upper gastrointestinal endoscopy should be performed within 24 hours to confirm the diagnosis and allow treatment with EVL or sclerotherapy.[133]

Short-term (up to 7 days) antibiotic prophylaxis should be instituted in all patients following a gastrointestinal haemorrhage (regardless of the presence of ascites) as this has been shown to decrease the rate of bacterial infections and increase survival.[134] [ ] Ceftriaxone is the first choice in patients with decompensated cirrhosis, in those already on fluoroquinolone prophylaxis, and in hospital settings with high prevalence of fluoroquinolone-resistant bacterial infections. Oral fluoroquinolones should be used in the remaining patients.[135][136]

Life-threatening bleeding may be controlled with a Sengstaken-Blakemore tube or a Danis stent until haemostasis can be achieved endoscopically, or with TIPS, with or without embolisation.[137]

Malnutrition and sarcopenia

It is recommended that patients hospitalised with cirrhosis receive formal dietician assessment, and steps should be taken to minimise the fasting period prior to procedures (e.g., by giving them a pre-bedtime snack or early-morning snack if the procedure will be in the late afternoon).[138] Parenteral supplementation may be required for those who cannot meet their nutritional intake needs orally. Recommended protein intake for adults with cirrhosis is 1.2 to 1.5 g/kg (ideal body weight) per day, and 1.2 to 2 g/kg (ideal body weight) per day if critically ill.

Hepatocellular carcinoma

See Hepatocellular carcinoma (Management approach).

Spontaneous bacterial peritonitis

A peritoneal fluid absolute neutrophil count >250 cells/mm³ is the accepted criterion for the diagnosis for spontaneous bacterial peritonitis.[88]

Treatment is with intravenous antibiotics, such as cefotaxime or a fluoroquinolone, and intravenous human albumin solution. Albumin has been shown to reduce mortality in patients with cirrhosis with spontaneous bacterial peritonitis.[139][140]

All patients who have survived an episode of spontaneous bacterial peritonitis require lifelong secondary antibiotic prophylaxis.

Patients with ascites and an ascitic fluid total protein level of ≤10 g/L are at high risk of developing spontaneous bacterial peritonitis, and should be considered for primary antibiotic prophylaxis.[88][141][142] There appears to be an increased risk of spontaneous bacterial peritonitis with the use of proton-pump inhibitors.[143] High-quality evidence for this intervention is lacking and further trials are needed to establish whether antibiotic prophylaxis for people with cirrhosis is beneficial.[144]

See Spontaneous bacterial peritonitis (Management approach).

Hepatic hydrothorax

Occurs in approximately 5% to 10% of patients with cirrhosis, usually in patients with ascites.[145] Hepatic hydrothorax may cause dyspnoea. Management is similar to that of ascites. In some patients, long-term indwelling pleural catheters are required for symptomatic management.[146][147] Patients with hepatic hydrothorax should be evaluated for liver transplantation.[148]

Portosystemic hepatic encephalopathy

Approximately 11% of patients with cirrhosis have hepatic encephalopathy at the time of cirrhosis diagnosis.[149] Around 30% to 40% of patients with cirrhosis have an episode of hepatic encephalopathy during their illness, and there is a 30% to 40% chance of recurrence in the following year.[150]

Hepatic encephalopathy is characterised by changes in consciousness, behaviour, and personality with disorientation, drowsiness, forgetfulness, confusion, agitation, and eventual coma. Slurred speech, asterixis (liver flap), increased muscle tone, and extensor plantar reflexes may be present.

Precipitating factors include gastrointestinal haemorrhage, constipation, diarrhoea and vomiting, hypoglycaemia, and electrolyte imbalance; drugs (diuretics, sedatives) and medical procedures (paracentesis, TIPS); infection, anaemia, hypoxia, and hypotension. Gut-derived toxins such as ammonia and bacterial products that induce systemic inflammation cause hepatic encephalopathy.[3][18] There appears to be an increased risk of hepatic encephalopathy with the use of proton-pump inhibitors.[151][152]

Treatment involves identification and correction of reversible precipitating factors and lactulose, used alone or in combination with antibiotics such as rifaximin.[153][154][155][156][157][158] [ ] [Evidence B] Management of hepatic encephalopathy is not affected by ammonia levels.[3][18] Dietary protein restriction is not recommended.[159]

See Hepatic encephalopathy (Management approach).

Hepatorenal syndrome-acute kidney injury (HRS-AKI)

In patients with cirrhosis, the causes of acute kidney injury can be hypovolaemia, acute tubular necrosis, or hepatorenal syndrome with either acute kidney injury or acute kidney disease. Investigations to determine the cause include a careful history, physical examination, blood biochemistry, microscopic examination and chemical analysis of urine, select urine biomarkers and renal ultrasound.[90]

HRS-AKI (formerly known as type-1 hepatorenal syndrome) can be diagnosed if patients meet the following criteria, as defined by the International Club of Ascites (ICA):[89]

Cirrhosis with ascites
Diagnosis of AKI according to ICA-AKI criteria (i.e., increase in serum creatinine ≥26.4 micromoles/L [≥0.3 mg/dL] within 48 hours; or a percentage increase in serum creatinine ≥50% from baseline which is known, or presumed, to have occurred within the previous 7 days); the American Gastroenterological Association (AGA) also include a reduction of urine output to below 0.5 mL/kg/h for >6 hours[90]
No response after 2 consecutive days of diuretic withdrawal and plasma volume expansion with albumin
Absence of shock
No current or recent use of nephrotoxic drugs (NSAIDs, aminoglycosides, or iodinated contrast media)
No macroscopic signs of structural kidney injury. Structural kidney injury is indicated by proteinuria (>500 mg/day), microhaematuria (>50 red blood cells per high-power field), and/or abnormal renal ultrasonography.

European Association for the Study of the Liver (EASL) guidelines recommend using an adapted staging system for AKI that splits AKI stage 1 into stage 1A and 1B according to a serum creatinine value of <133 micromoles/L (<1.5 mg/dL) or ≥133 micromoles/L (≥1.5 mg/dL), respectively.[88]

Measures can be taken to prevent HRS-AKI from developing in patients with cirrhosis, and include:[90]

Advising patients to avoid alcohol
Monitoring serum creatinine levels and electrolytes when diuretics are given and avoiding excessive diuretics
Avoiding large-volume paracentesis without albumin replacement
Giving prophylactic antibiotics when infection is strongly suspected (investigations should include diagnostic paracentesis to evaluate for spontaneous bacterial peritonitis)
Avoiding use of non-selective beta-blockers and nephrotoxic drugs (e.g., ACE inhibitors, angiotensin-II receptor antagonists, and NSAIDs).

Once diagnosed, treatment of the precipitating cause should be initiated and any non-selective beta-blockers, diuretics, and NSAIDs held or stopped. Fluid losses should be replaced and fluid status monitored.[90] Vasoconstrictors and albumin are recommended in all patients and should be expeditiously used. Terlipressin plus albumin should be considered as the first-line therapeutic option.[132] Noradrenaline (norepinephrine) can be an alternative to terlipressin. However, there are several limitations associated with its use. Midodrine plus octreotide can be an option when terlipressin or noradrenaline are unavailable, but its efficacy is much lower than that of terlipressin.[88][160] In one phase 3 trial to confirm the efficacy and safety of terlipressin plus albumin in adults with HRS-AKI, terlipressin was more effective than placebo in improving renal function, but was associated with serious adverse events, including respiratory failure, and cases of sepsis or septic shock.[161]

For further information, see Hepatorenal syndrome (Management approach).

Hyponatraemia

Patients with cirrhosis commonly develop hyponatraemia, especially with progression of liver disease. Hyponatraemia is usually well tolerated.

Initial management consists of discontinuation of diuretic therapy once serum sodium <130 mEq/L. Fluid restriction is usually necessary for serum sodium levels <115-120 mEq/L.

In patients with severe hyponatraemia treatment with vaptans may increase serum sodium, but their use does not reduce mortality, liver complications or renal failure.[88][114]

Hyperkalaemia

Hyperkalaemia is frequently observed in patients with cirrhosis (12% to 14% of those hospitalised with cirrhosis).[44] It may indicate a poor prognosis and can present a challenge to treat.[44][45] The standard treatment of an insulin-glucose protocol to reduce serum potassium may be ineffective in the setting of cirrhosis, and therefore adjunct treatments may be preferred.[162]

Hepatopulmonary syndrome

Results from portal hypertension and occurs in at least 5% of patients awaiting liver transplantation.[163] Symptoms include dyspnoea and platypnoea. The diagnosis includes the finding of hypoxaemia with increased alveolar-arterial gradient, orthodeoxia, and the determination of intrapulmonary vascular dilation on contrast-enhanced echocardiography.

The presence of hepatopulmonary syndrome should prompt immediate evaluation for liver transplantation. The condition usually resolves following liver transplantation.[164]

Portopulmonary hypertension

This complication is diagnosed when findings of unexplained pulmonary hypertension are present in association with portal hypertension. Unlike hepatopulmonary syndrome, this condition may not completely resolve following liver transplantation.

Patients with severe pulmonary hypertension that does not improve with the use of vasodilators such as epoprostenol, bosentan, iloprost, or sildenafil are not candidates for liver transplantation in view of the high risk of death associated with the procedure.

In one randomised controlled trial, macitentan, an endothelin-receptor antagonist, significantly reduced pulmonary vascular resistance in patients with portopulmonary hypertension compared with placebo.[165]

Acute-on-chronic liver failure

ACLF is a severe form of acutely decompensated cirrhosis with organ failure and a high risk of short-term mortality.[166] It is a heterogeneous syndrome; affected patients have features of hepatic failure (coagulopathy, elevated bilirubin) and may also have extrahepatic organ failure (kidney, lung, brain, or circulation). ACLF may be precipitated by alcohol use, viral hepatitis, drug-induced liver injury, surgery, ischaemia, or infection. It is a potentially reversible condition that may occur in people with chronic liver disease.

Treatment includes resuscitation, treatment of the precipitating factor, support of failing organs, and assessment for and early treatment of infection. Patients should be cared for in the intensive care unit. Some patients may benefit from early liver transplantation.[167]

Treatment of shock in ACLF can be challenging. Society of Critical Care Medicine guidelines recommend using albumin as a resuscitation fluid over other fluids, particularly when serum albumin is below 3 mg/dL.[168] Guidelines recommend aiming for a mean arterial pressure of 65 mmHg alongside invasive haemodynamic monitoring.[168][169] In patients with ACLF and hypotension, human albumin or crystalloids should be used for initial fluid therapy.[166] If vasopressors are required, noradrenaline is more effective than dopamine in reversing hypotension. EASL recommends against the use of dopamine in patients with ACLF.[166] Low-dose vasopressin can be added to noradrenaline in patients with ACLF who remain hypotensive despite fluid resuscitation. The American Association for the Study of Liver Diseases (AASLD) and EASL recommend noradrenaline as the first-line agent and vasopressin as the second-line agent for managing patients with hypotension.[166][169] The possible mortality benefit with the addition of vasopressin must be weighed against increased risk of digital ischaemia. As well as addressing the treatment of shock, guidelines also provide recommendations for managing endocrine, haematological, pulmonary, and renal features of ACLF in the intensive care unit setting.[168][169]

Liver transplantation

Patients who develop complications of cirrhosis such as hepatocellular carcinoma or signs of decompensation (ascites, jaundice, variceal haemorrhage, portal systemic encephalopathy, hepatopulmonary syndrome, or hepatorenal syndrome) should be referred for liver transplant evaluation without delay. Transplant assessment may be a prolonged process and early referral is preferable. Some patients with ACLF may benefit from early liver transplantation.[167]

Orthotopic liver transplantation remains the only curative treatment option for patients with decompensated cirrhosis.

Systems of liver allocation vary. In the US, liver allocation is based on the Model for End-Stage Liver Disease (MELD) score, which estimates the risk of 3-month mortality.[68] [ MELDNa scores (for liver transplantation listing purposes, not appropriate for patients under age 12 years) (SI units) Opens in new window ] A survival benefit from undergoing liver transplantation is seen when the MELD score is ≥15. In children aged <12 years, a complementary version of MELD score called Paediatric End-Stage Liver Disease (PELD) score is used.[170]

There is, however, a shortage of organ donors. In 2021, 9236 liver transplants were performed in the US, with the current waiting list standing at 11,185 candidates.[171] As a result, a significant number of patients die while waiting for an organ donor.

Presence of sarcopenia or frailty can affect liver transplantation outcomes. In one study, sarcopenia was found to be associated with adverse outcomes after liver transplantation in patients with decompensated cirrhosis.[172] One systematic review of 34 studies concluded that patients with mild to moderate frailty or sarcopenia should be prioritised for liver transplantation due to increased mortality on the waiting list, but if the frailty or sarcopenia is severe, patients may be removed from the list as the prognosis is poor.[173]

Palliative care

As cirrhosis is a life-limiting condition, palliative care should be offered alongside other curative therapies, and may be relevant for patients with compensated cirrhosis and decompensated cirrhosis.[174] The American Gastroenterological Association and the AASLD have both published guidelines on palliative care in patients with cirrhosis. These promote advanced care planning, assessment and management of symptoms (including pain, breathlessness, muscle cramps, sexual dysfunction, insomnia, daytime sleepiness, fatigue, pruritus, anxiety, and depression), screening for carer needs, and early liaison with local palliative care teams.[174][175] Particular note is given to chronic pain management in the setting of diminished liver function and novel treatments for refractory ascites.[175]

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