INTENSIVE CARE
Decompensated liver
cirrhosis
Tom G Bird
Prakash Ramachandran
Euan Thomson
Abstract
The incidence of liver disease continues to increase and is now one of the
leading causes of death in the United Kingdom. The increasing prevalence
of viral hepatitis combined with a surge in the incidence of both alcohol
and obesity related liver disease mean that critical care units are increas-
ingly being called upon to assist in managing those with life-threatening
complications of end-stage liver disease. Decompensated cirrhosis is not
a single organ illness but a complex multisystem disorder typified by
impaired immunity, malnutrition and multiorgan failure and presents a
significant challenge to the critical care physician. In this article we
describe the epidemiology, aetiology, and pathophysiology of decompen-
sated liver disease and describe the management strategies of a range of
resulting clinical complications.
Keywords Decompensated liver disease; encephalopathy; liver cirrhosis;
liver transplant
Royal College of Anaesthetists CPD matrix: 1AO1, 1A02, 2C04, 3A03,
3C00
Incidence, aetiology and pathophysiology
In the UK 10e20% of the population are potentially at risk of
liver disease and over half a million adults have cirrhosis. Ad-
missions to intensive care of cirrhotic patients continue to in-
crease and are associated with mortality rates approaching 50%.
Cirrhosis occurs as the end stage of a chronic fibrotic process
within the liver. Fibrosis occurs following protracted exposure of
hepatocytes to a wide variety of insults (Table 1). Cirrhosis re-
sults in the gradual decline of the normal metabolic and synthetic
function of the liver. Additionally, the development of fibrosis
progressively destroys normal hepatic histological and vascular
architecture resulting in a progressive increase in hepatic blood
flow resistance and portal hypertension. Decompensated liver
cirrhosis is defined by the development of clinically evident
complications of portal hypertension (ascites, variceal haemor-
rhage) or liver insufficiency (jaundice, hepatic encephalopathy).
Pathophysiological mechanisms are outlined in Figure 1.
Tom G Bird BMBCh MA MRCP PhD is a Clinical Lecturer in Hepatology at the
Royal Infirmary of Edinburgh, UK. Conflicts of interest: none declared.
Prakash Ramachandran BSc (Hons) MBChB (Hons) MRCP PhD is a Specialist
Registrar in Hepatology at the Royal Infirmary of Edinburgh, UK.
Conflicts of interest: none declared.
Euan Thomson MRCP FRCA is a Consultant in Liver Transplant
Anaesthesia at the Scottish Liver Transplant Unit, Royal Infirmary of
Edinburgh, UK. Conflicts of interest: none declared.
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Learning objectives
After reading this article, you should be able to:
C appreciate the frequency of critical illness relating to liver
disease
C recognize and investigate the causes of chronic liver disease
C understand the pathophysiology of complications of decom-
pensated cirrhosis
C formulate a management plan for patients with decompensated
cirrhosis
C understand specific considerations for anaesthesia in patients
with decompensated cirrhosis
Patients with decompensated cirrhosis must be distinguished
from patients with acute liver failure. A short history of liver
function abnormality (<24 weeks) and an absence of clinical
signs and imaging features of chronic liver disease support the
diagnosis of an acute disease process. In selected cases histo-
logical confirmation of cirrhosis may be necessary via biopsy.
Liver biopsy is performed by a transjugular approach in the
presence of ascites or coagulopathy.
Patients with suspected cirrhosis should be investigated with
a screening panel of tests to identify aetiology and allow treat-
ment of reversible causes. Additionally, staging tests are used to
identify patients with cirrhosis at risk of varices and hepatocel-
lular carcinoma and to provide prognostic information (Table 2).
A variety of scoring systems exist (MELD e model for end-stage
liver disease, UKELD e United Kingdom model for end-stage
liver disease, ChildePugh score) that can provide prognostic
information in chronic liver disease, but in the setting of critical
care the sequential organ failure assessment (SOFA) score is a
more useful prognostic tool (Table 3).
It is important to remember that cirrhosis is not necessarily an
inexorably progressive process. Successful treatment of the un-
derlying cause can potentially partially reverse the disease
course. Even patients critically ill with decompensated disease
can potentially re-compensate and hence a trial of full critical
care support is often appropriate.
Common aetiologies of chronic liver disease
Drug induced Alcohol
Infectious Hepatitis B and C
Obesity Non-alcoholic fatty liver disease
Genetic Hereditary haemochromatosis
Wilson’s disease
a1 anti-trypsin deficiency
Autoimmune Autoimmune hepatitis
Primary biliary cirrhosis
Primary sclerosing cholangitis
Vascular BuddeChiari syndrome
Biliary Secondary biliary cirrhosis
Table 1
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 INTENSIVE CARE

Figure 1

Complications of chronic liver disease treatment (e.g. terlipressin 2 mg IV) should be commenced as
soon as variceal bleeding is suspected and continued (e.g. terli-
Variceal haemorrhage
pressin 1e2 mg q.d.s. IV) for up to 5 days following endoscopic
As portal blood pressure increases, blood is forced through
therapy.3 Terlipressin should be avoided in patients with signif-
anatomical venous anastomoses between portal and systemic
icant cardiovascular disease. Empirical broad-spectrum antibiotic
circulations. These dilated varices are thin walled and prone to
therapy (e.g. ceftriaxone 2 g o.d. IV) has been shown to reduce
spontaneous bleeding. The majority of varices occur within the
bacterial infection, rebleeding and mortality and should be
lower oesophagus (90%) but can also occur in the stomach or
commenced at time of presentation and continued for 5e10 days.
elsewhere in the GI tract. Despite the improvements in man-
Upper GI endoscopy should be performed as soon as possible
agement, the mortality from variceal haemorrhage remains high.
after adequate resuscitation. These patients are at risk of aspi-
In those with advanced cirrhosis and active variceal bleeding the
ration, especially those with massive haemorrhage or hepatic
mortality is 30%. For many patients variceal haemorrhage may
encephalopathy, and endotracheal intubation and mechanical
be the initial presentation of their chronic liver disease.
ventilation should always be considered. These patients are best
Initial management of variceal bleeding is with volume resus-
managed in the critical care or theatre environment. Endoscopic
citation, aiming for a target mean arterial pressure (MAP)
management of bleeding oesophageal varices is with band liga-
>65 mmHg. The administration of fresh frozen plasma and plate-
tion, whereas gastric or ectopic varices are treated with injection
lets to correct coagulopathy is widely undertaken, but it should be
therapy using cyanoacrylate (glue) or thrombin.
borne in mind that a prolonged prothrombin time/INR in cirrhotic
Balloon tamponade using a Sengstaken-Blakemore tube can
patients does not necessarily reflect bleeding risk. Blood product
be used for up to 24 hours in uncontrolled haemorrhage as a
administration should be undertaken judiciously1 and, if possible,
‘bridge’ to more definitive therapy. Patients requiring this should
be guided by thromboelastometry. Vitamin K 10 mg IV is often
always be intubated for airway protection.
appropriate. Current evidence indicates that a restrictive blood
Transjugular intrahepatic portosystemic shunt (TIPSS) inser-
transfusion policy may reduce rebleeding risk and improve sur-
tion is usually considered in patients with uncontrolled or
vival.2 A transfusion threshold of 7e8 g/dl has been suggested.3
recurrent variceal bleeding. Recent data suggests early TIPSS
Vasoactive drugs (terlipressin or somatostatin/somatostatin
(within 72 hours) may improve mortality in patients with a high
analogues), which selectively reduce portal blood pressure, have
risk of rebleeding.4
been shown to reduce rebleeding risk and mortality. Appropriate

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 INTENSIVE CARE

primarily caused by increased renal sodium retention in response

Investigations for chronic liver disease to the splanchnic vasodilation which occurs in portal hyperten-
Biochemistry Liver function tests sion. Cirrhotic ascites is transudative with a low serum-ascites
Urea and electrolytes albumin gradient (<1.1 g/dl). Management of uncomplicated
Plasma electrophoresis cirrhotic ascites is based around dietary sodium restriction and
Immunoglobulins diuretic therapy with spironolactone (titrated incrementally up to
Iron studies 400 mg/day)  furosemide (titrated incrementally up to 80 mg
Caeruloplasmin  urinary copper b.d. orally) Large volume paracentesis (LVP) should be per-
a1 anti-trypsin formed if the ascites becomes tense. During LVP, IV albumin
a fetoprotein (for hepatocellular ca surveillance) should be administered at 20 g/2.5 L drained, to minimize post-
Haematology Full blood count paracentesis circulatory dysfunction and hepatorenal syndrome
Coagulation screen (HRS).5
Immunology Anti-nuclear antibody Patients with more advanced liver disease may develop re-
Anti-smooth muscle antibody fractory ascites (diuretic-resistant or diuretic-intolerant) which is
Anti-mitochondrial antibody an indicator of even poorer prognosis. TIPSS may be beneficial in
Liver kidney spleen antibody selected patients with refractory ascites and fairly well preserved
Virology Hepatitis B serology synthetic liver function, but has not convincingly been shown to
Hepatitis C serology improve survival and so liver transplantation should be consid-
HIV serology ered where appropriate.
Genetic Haemachromatosis genetic screening
Sepsis
Radiology Chest X-ray
Patients with cirrhosis are prone to a variety of bacterial and
Doppler ultrasound liver/biliary tree
other infectious complications. Most common infections include
CT/MRI liver/biliary tree (if indicated)
urinary tract and lower respiratory infection together with bac-
Fibroscan
teraemia and spontaneous bacterial peritonitis. Sepsis is esti-
Other Upper GI endoscopy
mated to cause up to a quarter of all deaths in cirrhotic patients.
Trans-jugular liver biopsy
Furthermore, patients with cirrhosis show a greater systemic
Table 2 response to infection than non-cirrhotic patients, resulting in an
increased incidence of septic shock, multiorgan failure and
Without treatment the risk of recurrent variceal bleeding ex- death. Early recognition and empirical broad-spectrum antimi-
ceeds 60%. Secondary prevention should be started after the crobial therapy is key to the successful management of this
index bleed. Regular screening endoscopy and repeat band complication.
ligation  non-selective beta-blocker therapy (e.g. carvedilol Goal-directed therapy is advocated, but specific targets in
titrated to 12.5 mg/day orally) reduce the risk of further bleeding. cirrhotic patients have not been defined. Targets for this patient
group may well differ from the general population due to dif-
Ascites
ferences in baseline physiology (e.g. cirrhotic patients often have
Ascites is the most common complication of cirrhosis and is
a lower baseline MAP, urine output and haematocrit).6
associated with a poor prognosis and quality of life. It is

Sequential organ failure score (SOFA)

Organ Score
System 0 1 2 3 4

Respiratory (PaO2/FiO2 mmHg) >400 <400 <300 <200 and ventilated <100 and ventilated
Cardiovascular (MAP mmHg) >70 <70 Dopamine <5 or Dopamine >5 or Dopamine >5 or
(doses in mg/kg/min) Any Dobutamine Noradrenaline <0.1 or Noradrenaline >0.1 or
Adrenaline <0.1 Adrenaline >0.1
Coagulation (platelets 109/l) >150 <150 <100 <50 <20
Renal (creatinine mmol/l) <110 110e170 171e299 300e440 >440
Hepatic (bilirubin mmol/l) <20 20e32 33e101 102e204 >204
Neurology (GCS) 15 13e14 12e10 6e9 <6
Score Mortality

9e12 25%
13e16 50%
17e20 75%
>20 100%

Table 3

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 INTENSIVE CARE
Spontaneous bacterial peritonitis
Approximately 10% of in-patients with ascites will develop
spontaneous bacterial peritonitis (SBP). Early recognition and
treatment can reduce mortality from >90% to approximately
20%. Ascitic fluid neutrophil count >250/mm3 is diagnostic.
Culture of ascitic fluid may be negative. Empirical antibiotics
(e.g. piperacillin/tazobactam 4.5 g t.d.s IV) should be started
immediately following diagnosis. Albumin infusion 1.5 g/kg at
diagnosis and 1 g/kg on day 3 reduces the risk of developing
renal impairment and improves survival.5
Patients with ascites should be considered for long-term
antibiotic prophylaxis (norfloxacin 400 mg o.d. or cotrimox-
azole 960 mg o.d) if they have a history of previous SBP or severe
liver disease with a low ascites total protein (<15 g/l).
Renal dysfunction
Renal impairment is frequently seen in cirrhotic patients and is a
poor prognostic sign. Up to 60% of those admitted to ICU with
cirrhosis will have renal dysfunction. Acute renal dysfunction
may be due to sepsis, hypovolaemia, acute tubular necrosis,
drug-induced renal failure, parenchymal renal disease or hep-
atorenal syndrome (HRS). Treatable causes for renal dysfunction
should be sought and treated.
In hepatorenal syndrome portal hypertension induces
splanchnic vasodilation leading to a reduction in effective arterial
blood volume, subsequent activation of the sympathetic nervous
system and renin-angiotensin-aldosterone system and conse-
quently profound renal vasoconstriction. Two forms of HRS are
described: type 1 HRS in which renal dysfunction is acute and
rapidly progressive, and has extremely high mortality without
liver transplantation; type 2 is more indolent.
The diagnostic criteria for HRS are: cirrhosis with ascites; a
serum creatinine of over 133 mmol/l, which fails to improve
following the cessation of diuretics and administration of IV al-
bumin (1 g/kg/day) for 2 days; no other apparent cause for renal
dysfunction.
HRS is often triggered by bacterial infection, particularly SBP,
so full cultures (including ascites) should be performed and
infection treated promptly if identified. Patients with type 1 HRS
should be closely monitored, ideally with central venous pressure
measurements to aid fluid management. Specific management
using the combination of terlipressin 1 g q.d.s. IV (increasing to 2
g q.d.s. on day 3 if creatinine not reduced by >25%) and IV al-
bumin (1 g/kg body weight on day 1 followed by 40 g/day
thereafter) can be effective in reversing type 1 HRS in up to 50%
of patients and may improve short-term survival.5 Monitoring for
ischaemic complications secondary to terlipressin is essential,
although these are usually reversible on cessation of the drug.
In patients where the underlying liver disease is treatable,
those with reasonable potential for hepatic recovery or those
who are potential candidates for liver transplantation, renal
replacement therapy should be considered if required.
Hepatic encephalopathy
Hepatic encephalopathy (HE) is a frequent and debilitating
complication of cirrhosis. Overt HE occurs in 30e40% of patients
with cirrhosis and has a high rate of recurrence. It is a potentially
reversible syndrome which produces a wide spectrum of
neuropsychiatric manifestations. The pathophysiology is
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complex and incompletely understood but relates to elevated
plasma and CNS ammonia levels resulting in neuronal oedema. It
is graded according to the West Haven criteria (Table 4).7 Diag-
nosis is usually clinical but a raised serum ammonia or slow-
wave activity on electroencephalography (EEG) may support the
diagnosis of HE. Consideration should also be given to other
causes of altered mental status, particularly in the presence of a
focal neurological deficit or atypical features.
Management of HE is based on identifying and controlling
precipitating factors. These can be numerous and sometimes
difficult to define. Common precipitants of HE include infection,
GI bleeding, dehydration, constipation, electrolyte disturbance
and drugs (e.g. benzodiazepines, opiates). Certain patients, e.g.
those following TIPSS procedure, are at increased risk of devel-
oping HE.
Treatment/removal of the precipitant, if identified, may
improve the clinical situation. Patients with severe HE (grades III
and IV) may require supportive management and airway pro-
tection. Specific additional treatment for HE includes the non-
absorbable disaccharide lactulose (start at 10 ml t.d.s and
titrate to achieve 2 soft stools per day) and non-absorbable an-
timicrobials (eg rifaximin 550 mg b.d.) which, when used in
combination, can reduce recurrent HE and may be beneficial in
refractory acute HE.7
Recurrent HE, refractory to standard medical therapy, is an
indication for liver transplantation even in the patient with well
preserved synthetic liver function. Problematic HE, in the
absence of progressive liver disease, should raise the suspicion of
porto-systemic shunting and abdominal cross-sectional imaging
should be considered with a view to potential radiological
embolization.
Hepatopulmonary syndrome (HPS)
Hepatopulmonary syndrome (HPS) is a complication of liver
disease in which there is marked dilation of the pulmonary
West Haven criteria for classification of severity hepatic
encephalopathy7
Grade Description
I Trivial lack of awareness
Euphoria or anxiety
Shortened attention span
Altered sleep pattern
II Lethargy/apathy
Disorientation in time
Personality change
Inappropriate behaviour
Dyspraxia
Asterixis
III Somnolence
Gross disorientation
Confused
Bizarre behaviour
IV Coma
Table 4
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 INTENSIVE CARE
vascular beds leading to abnormalities of perfusion/ventilation
matching and profound hypoxaemia. The pathophysiology is
incompletely understood but thought due to the increase in
circulating vasodilator substances. The clinical signs of pla-
typnoea (breathlessness on standing) and orthodeoxia (arterial
desaturation on standing) are typical of HPS. The diagnosis of
HPS requires the triad of arterial hypoxaemia (PaO2 <8 kPa on
room air), evidence of liver disease or portal hypertension and
proven intrapulmonary vasodilation (a positive bubble echo).
Although more common in severe liver disease HPS may occur in
mild or well compensated disease. The only currently available
treatment for HPS is liver transplantation.
Portopulmonary hypertension (PPH)
Portopulmonary hypertension occurs in 5e8% of patients with
cirrhosis and is characterized by intrapulmonary vasoconstric-
tion. The finding of a mean pulmonary artery pressure
>25 mmHg in a patient with cirrhosis and absence of other cause
for pulmonary hypertension is diagnostic. Pathophysiology is
currently unclear and definitive treatment is with liver trans-
plantation. Severe PPH (mPAP >50 mmHg) is a contra-indication
to transplantation. Medical vasodilator therapy (sildenafil,
ambrisentan etc.) may be useful in reducing pulmonary pressure
in those with moderate or severe disease.
Alcoholic hepatitis
Alcoholic hepatitis is clinical syndrome presenting primarily with
jaundice in patients with recent alcohol use. It can occur in
cirrhotic or non-cirrhotic patients and is often associated with
fever (with or without intercurrent infection), hepatomegaly,
anorexia and ascites. It can also precipitate other features of
decompensation in patients with cirrhosis. Severity is predicted
using scoring systems such as the Maddrey Discriminant Function
or the Glasgow Alcoholic Hepatitis Score, using variables
including bilirubin and PT. In patients with severe alcoholic
hepatitis, predicted 28 day survival can be as low as 50%. Com-
mon causes of clinical deterioration in these patients are sepsis
and renal impairment and management is based around close
monitoring, early treatment of infection, accurate fluid balance
and nutritional support. Specific treatment with either predniso-
lone 40 mg o.d. (for up to 28 days) or pentoxifylline 400 mg t.d.s.
(for up to 28 days) has been advocated.8 Liver transplantation
may be considered in highly selected cases of alcoholic hepatitis.
Anaesthesia in patients with chronic liver disease
The risks of surgery in patients with chronic liver disease are
elevated well in excess of those seen in other patient groups.
Decompensated liver disease carries an operative risk similar to
that of cardiac failure. Although judicious management may
achieve safe anaesthesia and operative intervention in those with
well-compensated or mild disease, it is recommended that sur-
gery be only considered for those with severe disease in life-
threatening situations.
When anaesthetizing the patient with liver disease particular
attention should be paid to the following:
Haemodynamic management: decompensated cirrhosis is
characterized by low peripheral vascular resistance and, usually,
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high cardiac output states. Despite peripheral fluid overload hy-
potension is often further compounded by intravascular deple-
tion. Invasive monitoring is therefore essential for these patients
to accurately guide fluid and vasopressor management. Judicious
fluid management should be paired with vasopressor infusion
(normally noradrenaline) to maintain an adequate mean arterial
pressure.
Coagulation: the coagulopathy of liver disease arises as a result
of factor deficiency, fibrinogen deficiency and reduction in
platelet number and function. Although overall there is a ten-
dency to impaired coagulation and bleeding the complex inter-
play between abnormalities of pro- and anti-coagulant pathways
mean the clinical bleeding manifestation cannot be accurately
managed with standard laboratory based measures of clotting
alone. Rotational thromboelastometry provides essential infor-
mation on clot formation, strength and persistence and should be
used where available. The coagulopathy of liver failure normally
precludes central neuraxial blockade.
Drug handing and metabolism: alterations in volume of distri-
bution, plasma protein binding, hepatic metabolism and clear-
ance make the response to anaesthetic agents, neuromuscular
blocking drugs and analgesics unpredictable. Significant renal
impairment often co-exists in these patients and further alters
drug kinetics and metabolism. Care must be taken when dosing
to ensure an appropriate response is obtained and the anaes-
thetist should remain vigilant to prolonged drug effects.
Electrolyte and blood glucose: profound abnormalities of elec-
trolytes are commonly seen in those with liver disease. Hypo-
natraemia is common and may be marked and should be correct
carefully. A serum sodium <115 mmol/l is normally considered
an absolute contra-indication to anaesthesia. Hypokalaemia/
hyperkalaemia are common as is hypomagnesemia and should
be sought and corrected. Blood glucose should be measured
frequently to avoid hypoglycaemia. In patients with significant
liver disease even an overnight fast for surgery may be sufficient
to cause marked hypoglycaemia.
Postoperative care: patients with liver disease are at increased
risk of postoperative complications including bleeding, haemo-
dynamic collapse, infection and worsening of encephalopathy
and are best managed in a critical care environment.
Transplant
Patients with decompensated cirrhosis should be considered for
liver transplantation if appropriate. Outcomes are good with
3-year survival rates of over 80%. Patients can be listed for liver
transplant if their projected 1-year mortality without a transplant
is >9%. In the UK the UKELD scoring system is used to deter-
mine the projected mortality and a score 49 is considered an
indication for transplant. The MELD scoring system is used in
other parts of the world. Under special circumstances (hepato-
cellular carcinoma, refractory encephalopathy, diuretic-resistant
ascites, intractable itch or HPS amongst others) listing may be
considered in patients with UKELD scores <49. Patients with
previous alcohol dependence will require detailed assessment by
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 INTENSIVE CARE

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Please cite this article in press as: Bird TG, et al., Decompensated liver cirrhosis, Anaesthesia and intensive care medicine (2015), http://
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