Cirrhosis - MRCEM Success

3/24/23, 3:32 PM Cirrhosis - MRCEM Success
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Cirrhosis
Gastroenterology &
Hepatology
MRCEM Success
USEFUL LINKS
 NICE CKS
CURRICULUM CODE
GP3 Ascites
GC1 Alcohol Related Liver Disease
GC2 Decompensated Cirrhosis
GP1 Abdominal and Loin Pain
GP2 Abdominal Swelling and Mass
KEYWORDS
https://intermediate.mrcemsuccess.com/explanation/cirrhosis/?_sft_qc=gastroenterology-hepatology 1/9
Ascites Decompensated Cirrhosis

Hepatic Encephalopathy
Hepatorenal Syndrome
Oesophageal Varices Portal Hypertension
Spontaneous Bacterial Peritonitis
RELATED TOPICS
Gastroenterology & Hepatology
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Cirrhosis LAST UPDATED: 10TH

MAY 2022
GASTROENTEROLOGY & HEPATOLOGY
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Cirrhosis develops progressively as a result of damage to the liver (which can be due to a
number of causes), usually over a number of years. The normal smooth liver structure
becomes distorted, with nodules surrounded by fibrosis. This affects the liver's synthetic,
metabolic and excretory actions.
Cirrhosis can be described as:
Compensated — when the liver can still function effectively and there are no, or few,
noticeable clinical symptoms.
Decompensated — when the liver is damaged to the point that it cannot function
adequately and overt clinical complications (such as jaundice, ascites, variceal
haemorrhage, and hepatic encephalopathy).
Risk factors
The most common risk factors for cirrhosis in the UK and Europe include:
Alcohol misuse
Hepatitis B and C infection
Obesity (body mass index of 30 kg/m2 or more) or type 2 diabetes — people in
these groups are at risk of cirrhosis if they have non-alcoholic fatty liver
disease (NAFLD)
Less common causes of cirrhosis include:

Autoimmune liver disease (for example, autoimmune hepatitis, primary biliary
cholangitis, primary sclerosing cholangitis)
Genetic conditions (for example, haemochromatosis, Wilson's disease, alpha-1
antitrypsin deficiency, cystic fibrosis)
Medication use, usually over a long period of time (for example, methotrexate)
Budd-Chiari syndrome (hepatic vein outflow obstruction)
Sarcoidosis and glycogen storage disease
Complications
Portal hypertension (a pathological increase in portal venous pressure) is one of the earliest
sequelae of cirrhosis, and many complications of cirrhosis arise as a result of this rather
than hepatocyte failure.
The major complications of cirrhosis are:
Ascites
Ascites is a pathological fluid accumulation in the peritoneal cavity as a
result of splanchnic vasodilation and sodium and water retention. It
causes abdominal swelling, bloating, and pain, and is the most common
complication of cirrhosis often necessitating hospital admission. Newly
diagnosed ascites always requires urgent evaluation with imaging,
usually starting with an abdominal ultrasound scan to confirm or refute
the diagnosis and detect evidence of cirrhosis or malignancy. Doppler
ultrasound and diagnostic paracentesis are also required. People with
cirrhosis and ascites are at high risk of further complications such as
spontaneous bacterial peritonitis, hyponatraemia, and hepatorenal
syndrome.
N.B. Other causes of portal hypertension that may be associated with
ascites include congestive heart failure, constrictive pericarditis,
alcoholic liver disease, fulminant hepatitis, subacute hepatitis, massive
liver metastasis, and Budd-Chiari syndrome. Conditions causing
hypoalbuminaemia such as nephrotic syndrome and protein-losing
enteropathy may result in ascites. Peritoneal diseases including
infectious peritonitis and malignancies can also cause ascites.
Hepatic encephalopathy
Hepatic encephalopathy is a dysfunction of the brain as a result of liver
insufficiency and/or portosystemic shunting and is related to the effect of
nitrogenous waste products (such as ammonia and glutamine) on the
brain. It presents with a variety of symptoms, including cognitive and
behavioural changes (for example irritability, disinhibition, disorientation),

personality changes, sleep disturbance, motor problems, and altered level
of consciousness. Symptoms vary in severity, with mild hepatic
encephalopathy only detectable using psychometric or
neurophysiological testing and severe cases experiencing acute
confusion, agitation, and coma. Hepatic encephalopathy is usually
associated with a predisposing event, for example, constipation,
dehydration, infection, gastrointestinal bleeding, or drugs (for example
opiates, benzodiazepines, diuretics). Serum ammonia levels are usually
elevated, but there is poor correlation between ammonia level and the
degree of encephalopathy.
Haemorrhage from oesophageal varices
The increase in portal pressure causes varices as a result of dilation of
veins in the oesophagus and stomach. Rupture of varices and associated
bleeding, which can present as haematemesis or melaena, has a high
mortality rate. Risk factors for rupture include size of varices, severity of
liver disease, sepsis, and hepatocellular carcinoma.
Infection
People with cirrhosis are at increased risk of bacterial infection and
sepsis because of immune dysfunction resulting from cirrhosis. The most
commonly occurring infections in this group are spontaneous bacterial
peritonitis (when the body's natural bacteria cause infection of ascitic
fluid), urinary tract infection, pneumonia, cellulitis, and bacteraemia.
Bacterial infections have a significant role in progression of liver failure,
development of complications, and mortality in people with cirrhosis. The
body's response to infection increases the risk of serious complications
such as shock and renal failure because of the haemodynamic
dysfunction that is already present in cirrhosis. Risk factors for infection
in people with cirrhosis include reduced liver function, low protein
ascites, and variceal bleeding.
Other complications include:
Hepatorenal syndrome — results from changes to the circulation due to the
effects of cirrhosis, plus sodium and water retention and renal vasoconstriction.
The resulting decrease in renal blood flow leads to a reduced glomerular
filtration rate and hepatorenal syndrome.
Hepatopulmonary syndrome - results from portal hypertension and symptoms
include dyspnoea and platypnoea.
Hepatocellular carcinoma.
Portal hypertensive gastropathy.
Portal vein thrombosis.

Cardiovascular complications including circulatory changes (such as decreased
blood pressure), and cirrhotic cardiomyopathy.
Clinical features
Suspect cirrhosis:
In high risk groups (e.g. alcohol misuse, intravenous drug use, high risk sexual activity,
obesity), especially if there are non-specific symptoms such as malaise, fatigue,
anorexia, nausea, weight loss, muscle wasting, or abdominal pain.
If examination identifies:
Palpable left lobe of the liver, hepatomegaly, splenomegaly.
The presence of stigmata of chronic liver disease
Spider naevi
Palmar erythema
Leuconychia
Muscle wasting
Finger clubbing
Dupuytren's contracture
Xanthelasma
Gynaecomastia
Caput medusae
Hepatosplenomegaly
Features of severe liver impairment and signs of decompensated liver disease,
such as:
Jaundice (examine the sclera under natural light)
Abnormal bruising
Peripheral oedema
Ascites - abdominal distension, shifting dullness
Sepsis
Variceal bleeding
Encephalopathy (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.)
If a person is known to have chronic liver disease and has a low platelet count,
elevated aspartate aminotransferase (AST): alanine transaminase (ALT) ratio, high
bilirubin, low albumin, or increased prothrombin time or international normalised ratio
(INR).
Investigations
All patients should receive a liver screen on presentation in order to identify the
underlying cause and severity of the cirrhosis:
LFTs
Aminotransferases (aspartate aminotransferase [AST], alanine
aminotransferase [ALT]) levels increase with hepatocellular damage and
are usually elevated to some degree. An AST/ALT ratio of ≥1 is thought to
be a predictor of cirrhosis.
Increases in GGT represents enzyme activation, which can be induced by
alcohol and certain drugs. GGT is not significantly present in bone, such
that concomitant elevated GGT and alkaline phosphatase (ALP) indicates
the liver as the source of the ALP. Cholestasis causes an increase in
alkaline phosphatase and gamma-glutamyl transferase (GGT) with
minimal derangement of AST and ALT.
Total bilirubin may be normal in patients with compensated cirrhosis, but
as the cirrhosis progresses, serum levels generally rise.
A decrease in the serum albumin is a marker of hepatic synthetic
dysfunction.
FBC – infection, anaemia, thrombocytopenia
U&Es – renal impairment, hyponatraemia
Clotting – prolonged prothrombin time
Viral serology - hepatitis A, B and C
Autoantibody profile - ANA and SMA for autoimmune hepatitis, AMA for PBC
Ferritin and transferrin saturation – hereditary haemochromatosis
Alpha1-antitrypsin - alpha1-antitrypsin deficiency
Alpha-fetoprotein – hepatocellular carcinoma
Caeruloplasmin – Wilson’s disease
Signs of advanced cirrhosis may be detected using ultrasound, computed
tomography (CT) scan, and magnetic resonance imaging (MRI). Transient elastography
is an ultrasound-based technique for detecting hepatic fibrosis and cirrhosis without
the need for liver biopsy. As with non-invasive blood tests for fibrosis evaluation,
transient elastography has best diagnostic performance in excluding liver cirrhosis.
Liver biopsy remains the most specific and sensitive test for the diagnosis of cirrhosis.
However, it is not necessary in patients with advanced liver disease and typical
clinical, laboratory, and/or radiological findings of cirrhosis, unless there is a need to
determine the degree of inflammation.
Patients with cirrhosis should be offered upper gastrointestinal endoscopy for
screening of gastro-oesophageal varices at the time of diagnosis, and at 1-3-year
intervals thereafter.
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 cytology. The serum-ascites albumin
gradient (SAAG) should be calculated: a SAAG of ≥1.1 g/dL with low ascitic fluid total
protein is consistent with portal hypertension secondary to cirrhosis.
Patients with cirrhosis, especially those with viral hepatitis (type B and C), alcohol-
related liver disease, and haemochromatosis, are at high risk of developing
hepatocellular carcinoma and should therefore undergo surveillance with ultrasound,
with or without alpha-fetoprotein, every 6 months.
Management
Ascites
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.
First-line choice of diuretic should be spironolactone due to its effects on
aldosterone. 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.
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) and albumin replacement for symptom control.
Patients not suitable for liver transplantation should be considered for
transjugular intrahepatic portosystemic shunt (TIPSS) placement. Although
TIPSS has been shown to be more effective than LVP and albumin, it is
associated with a higher incidence of hepatic encephalopathy and shows no
survival benefit.
The prognosis of patients with refractory ascites is poor. If
TIPSS/transplantation are not viable options, then long-term drain placement
for intermittent small-volume paracentesis may be considered as a palliative
measure.
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.
Spontaneous bacterial peritonitis
Spontaneous bacterial peritonitis is an infection of previously sterile ascitic fluid

without apparent intra-abdominal source of infection. Abdominal pain and fever
are the most characteristic symptoms. Diagnostic paracentesis is the most
important test to confirm ascites and help diagnose the cause and to determine
if the fluid is infectious.
A peritoneal fluid absolute neutrophil count >250 cells/mm³ is the accepted
criterion for the diagnosis for spontaneous bacterial peritonitis. Treatment is
with intravenous cefotaxime or a fluoroquinolone and intravenous human
albumin solution.
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 ≤1 g/dL are at high
risk of developing spontaneous bacterial peritonitis, and should be considered
for primary antibiotic prophylaxis.
Gastroesophageal varices
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 gastro-oesophageal varices are
present.
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) and a combination of
endoscopic and pharmacological therapy.
Terlipressin (a vasopressin analogue) should be initiated as soon as a variceal
bleed is suspected and continued for 3-5 days if it is confirmed.
Upper gastrointestinal endoscopy should be performed within 12 hours to
confirm the diagnosis and allow treatment with EVL or sclerotherapy.
Transjugular intrahepatic portosystemic shunting (TIPSS) may be used to treat
patients at high risk of failed endoscopic variceal ligation or re-bleeding.
Short-term (up to 7 days) antibiotic prophylaxis with norfloxacin 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.
Life-threatening bleeding may be controlled with a Sengstaken-Blakemore tube
or a Danis stent until haemostasis can be achieved endoscopically, or with
TIPSS with or without embolisation.
Hepatic encephalopathy
Precipitating factors include gastrointestinal haemorrhage, constipation,
diarrhoea and vomiting, hypoglycaemia, and electrolyte imbalance; drugs
(diuretics, sedatives) and medical procedures (paracentesis, TIPSS); infection,

anaemia, hypoxia, and hypotension.
Serum electrolytes, liver tests, urea and creatinine, full blood count, serum
glucose, arterial or venous blood gas, coagulation profile, urine toxin screen,
urine culture, and blood cultures should be ordered. A chest x-ray and head
computed tomography (CT) scan may help to rule out other diagnoses. Lumbar
puncture might be considered to exclude meningitis as a cause of altered
mental status. An upper-quadrant ultrasound should be considered in all
patients with unexplained acute decompensation, as acute portal or hepatic
vein thrombosis can be the cause. In patients with ascites, a diagnostic
paracentesis should also be performed to rule out spontaneous bacterial
peritonitis, which may precipitate HE.
Treatment involves identification and correction of reversible precipitating
factors and lactulose, used alone or in combination with antibiotics such as
rifaximin. Appropriate candidates should be referred to liver transplant centres
after a first episode of encephalopathy.
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
referrals are preferable. Orthotopic liver transplantation remains the only
curative treatment option for patients with decompensated cirrhosis.

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3/24/23, 3:32 PM Cirrhosis - MRCEM Success

← Back to Search Results

Ascites Decompensated Cirrhosis

Cirrhosis LAST UPDATED: 10TH

Less common causes of cirrhosis include:

behavioural changes (for example irritability, disinhibition, disorientation),

Portal vein thrombosis.

Spontaneous bacterial peritonitis is an infection of previously sterile ascitic fluid

(diuretics, sedatives) and medical procedures (paracentesis, TIPSS); infection,

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