Liver Cirrhosis

Lecturer: c.m.s. Karataeva G.T.

 Plan of lecture
• 1. Definition of Liver cirrhosis
• 2. Epidemiology of Liver cirrhosis
• 3. Etiology and pathogenesis of Liver cirrhosis
• 3. Classification of Liver cirrhosis
• 4. Clinical manifestations of Liver cirrhosis
• 5. Additional examinations of Liver cirrhosis
• 6. Complications of Liver cirrhosis – portal hypertension,
ascites, hepatic encephalopathy, bleeding
• 7. Treatment of Liver cirrhosis
• 8. Prognosis of Liver cirrhosis
 Definition
• Liver cirrhosis is:
- a chronic polyethiological progressive disease of the liver
- diffuse process characterized by liver necrosis and fibrosis,
where hepatocytes) are replaced by scar tissue
Due to of damage, the liver is unable to perform its vital
functions of metabolism, detoxification disorders, production of
proteins, including blood clotting factors, and etc.
Liver cirrhosis
 Epidemiology
• Cirrhosis affected about 2.8 million people and resulted
in 1.3 million deaths in 2015year.
• Of these deaths, alcohol caused 348,000, hepatitis C
caused 326,000, and hepatitis B caused 371,000.
• Each year, approximately one million deaths are due to
complications of cirrhosis, making cirrhosis the 11th
most common cause of death globally.
 Epidemiology
• The cause of cirrhosis can vary:
• Alcohol and non-alcoholic fatty liver disease are
main causes in western and industrialized countries,
• whereas Viral hepatitis is the predominant cause in
low and middle income countries.
• Cirrhosis is more common in men than in women.
 Etiology
• Hepatitis B
• Hepatitis C
• Hepatitis D
• Abuse of alcohol
• Non-alcoholic fatty liver disease
• Autoimmune hepatitis
• Primary biliary cholangitis
• Cryptogenic - unknown etiology
 Pathogenesis
• The pathological hallmark of cirrhosis is the development of
scar tissue that replaces normal parenchyma.

• This scar tissue blocks the portal flow of blood through the
organ, raising the blood pressure and disturbing normal
function of the liver.

• Damage to the hepatic parenchyma (due to inflammation)

leads to fibrosis and proliferation of connective tissue.
Macronodular liver cirrhosis
 Clinical manifestations of liver cirrhosis
Complaints:
- fatigue, irritability
- feeling of bitterness and dryness in the mouth
- nausea, sometimes vomiting
- loss of appetite
- weight loss
- itching of the skin (cholestasis)
- flatulence, irregular stool (diarrhea alternating with constipation)
- impotence in men, menstrual disorders in women
 Clinical manifestations (inspection)

• Ascites - accumulation of fluid in the peritoneal

cavity, edema;
• Caput medusa - are dilated periumbilical
collateral veins due to portal hypertension;
• Palmar erythema is a reddening of palms as a
result of increased estrogen due to liver failure;
 Clinical manifestations (inspection)
• Telangiectasia (swollen blood vessels) - a central red spot
and reddish extensions which radiate outwards like a spider's
web;
• Jaundice - is yellow discoloration of the skin and mucous
membranes, due to increased bilirubin (at least 2–3 mg/dl or
30 µmol/l). The urine may also appear dark;
• Gynecomastia- increase in breast gland size in men is
caused by increased estradiol (due to liver failure) and can
occur in up to 2/3 of patients.
Ascites, “ heard of medusa”, navel hernia
Gynecomastia in men
Palmar erythema
Telangiectasia
 Additional examinations
(laboratory)
• Leukopenia, anemia, thrombocytopenia – due to
splenomegaly (Hypersplenism is an overactive spleen. This
condition causes quick and premature destruction of blood cells.
(hemoglobin – 130-180 g/l, white cells – 4-11x10/9 L, platelets
– 150-400x10/9 L);

• Albumin – levels fall as the synthetic function of the liver

declines; albumin is exclusively synthesized in the liver (35-
50 g/L);
 Laboratory examinations
• Aminotransferases – AST and ALT can be moderately
elevated, with AST > ALT. However, normal
aminotransferase levels do not preclude cirrhosis (ALT – 5-
35 IU/L, AST – 5-35 IU/L);
Prothrombin time – increases (normal values include the
following : The reference range for prothrombin time is 11.0-
12.5 seconds; 85%-100%)
• International normalized ratio(INR) - increases (the
reference range for the INR is 0.8-1.1)
 Laboratory examinations
• Bilirubin – may elevate as cirrhosis progresses (normal
level 3-17 mmol/L);
• Alkaline phosphatase – slightly elevated but less than 2–3
times the upper limit of normal (30-130 IU/L);
• Coagulation defects - the liver produces most coagulation
factors and, therefore, coagulopathy progresses with the
development of hepatic cell failure.
• Serology for hepatitis viruses, autoantibodies (ANA,
anti-smooth muscle, anti-mitochondria).
 Laboratory examinations
• Alanine transaminase (ALT) test: This test measures the
level of alanine aminotransferase (an enzyme found
predominantly in the liver) that is released into the
bloodstream after acute liver cell damage.
• Aspartate transaminase (AST) test: This test measures the
level of aspartate transaminase (an enzyme that is found in
the liver, kidneys, pancreas, heart, skeletal muscle, and red
blood cells) that is released into the bloodstream after
liver or heart problems.
 Laboratory examinations
• Gamma-glutamyl transpeptidase test: This test measures
the level of gamma-glutamyl transpeptidase (an enzyme that is
produced in the liver, pancreas, and biliary tract). This test is
often performed to assess liver function, to provide
information about liver diseases, and to detect alcohol
ingestion.

• Lactic dehydrogenase test: This test can detect tissue damage

and aides in the diagnosis of liver disease.
 Laboratory examinations

• Alpha-fetoprotein test: Alpha-fetoprotein (a

specific blood protein) is produced by fetal tissue
and by tumors.
• This test may be performed to monitor the
effectiveness of therapy in certain cancers.
 Instrumental examinations
• The gold standard for diagnosis of Cirrhosis is a
Liver biopsy.
• A biopsy is not necessary if the clinical, laboratory,
and radiologic data suggests cirrhosis.

• There is a small but significant risk of

complications from liver biopsy (bleeding).
 Instrumental examinations
• Ultrasound is commonly used in assessing liver cirrhosis:
• - The size of the liver, nodal changes in the liver
• - Splenomegaly - an enlarged spleen (the size of spleen less
than 11-12 cm in adults), may indicate portal hypertension
• - Hepatocellular carcinoma
• - Portal hypertension
• - Budd-Chiari syndrome
• - Ascites
 Instrumental examinations
• A variety of elastography techniques - for definition
degree of compaction of the liver parenchyma.
• Abdominal CT and liver/bile duct
• MRI
• Upper endoscopy (endoscopic examination of the
esophagus, stomach, and duodenum) is performed for to
exclude the possibility of esophageal varices.
 Complications of liver cirrhosis
• Ascites
• Esophageal variceal bleeding
• Hepatic encephalopathy, hepatic coma
• Hepatorenal syndrome, hepatopulmonary syndrome
• Spontaneous bacterial peritonitis
• Portal hypertensive gastropathy - erosive and ulcerative
lesions of the stomach and duodenum
Hepatocellular carcinoma
 Portal hypertension
• Portal hypertension - increased the pressure in the portal vein.
Liver cirrhosis increases resistance to blood flow and leads to
higher pressure in the portal venous system, resulting in portal
hypertension.
• Normal pressure in the portal vein is about 5-10 millimeters of
mercury.
• With portal hypertension - the pressure in the portal vein is
greater than 12 mm Hg.
Clinical manifestations of portal hypertension
• Esophageal varices result from collateral blood flow
in the portal vein through the vessels of the stomach
and esophagus (a process called portacaval
anastomosis).
• When these blood vessels enlarge, they are called
varicose veins and are more likely to rupture.
• Ruptured varicose veins often lead to severe bleeding,
which can be fatal.
Clinical manifestations of portal hypertension

• Ascites
• Splenomegaly - (increase in size of the spleen) is
found in 35% to 50% of patients.
• Hypersplenism with cytopenia (decrease the levels of
RBC, leukocytes, plateletes)
• Portal hypertensive gastropathy
Clinical manifestations of portal hypertension

• The head of Medusa are enlarged paraumbilical

collateral veins due to portal hypertension.
• Blood from the portal venous system can be
bypassed into the veins of the abdominal wall,
appearing in a pattern that may resemble the
head of Medusa.
 The mechanism of development of ascites
Portal hypertension and hemodynamic disorder in
the portal system of the liver;
• Increased lymphatic formation in the liver and
lymph flow into the abdominal cavity;
• Hypoalbuminemia and decreased oncotic plasma
pressure;
• Expansion of arterioles with the formation of
arteriovenous shunts.
 Hepatic encephalopathy
• Hepatic encephalopathy is:
- a syndrome of potentially reversible of mental and neurological
manifestation;
- on the background of the liver cirrhosis;
- due to the effect on the central nervous system of nitrogenous
products of metabolism.
• 2 main mechanisms of encephalopathy development:
- hepatic-cell insufficiency;
- portosystemic shunting of blood.
 Treatment of liver cirrhosis
• General management:

- Good nutrition (avoid protein excess)

- Low salt diet (if ascites)
- Alcohol abstinence
- Avoid NSAIDs, sedatives and opioids
- Restriction of physical and mental loads
 Treatment of liver cirrhosis
• In the presence of signs of cholestasis - drugs
ursodeoxycholic acid (ursofalk, ursosan 10-15
mg/kg/day)

• In the case of cirrhosis of the viral etiology -

antiviral therapy is indicated (slows the progression
of the disease).
 Treatment of Ascites
• Restriction of salt in consumed food (0.5 g/day
at the beginning of treatment, then <2 g/day)
• Fluid intake is limited to 1000 - 1200 ml/day
 Treatment of Ascites
• Diuretic therapy:
- Spironolacton 100 mg + Furosemide 40 mg –
control of daily urinary output
- monotherapy (Torasemide)
• Control of diuretic therapy (daily weighing, control
the level of: urea, creatinine, sodium, potassium,
calcium in the blood serum)
 Treatment of ascites
• With ineffectiveness of diuretics - therapeutic
paracentesis (evacuation of liquid from
abdominal cavity through the drainage tube) with
concomitant albumin infusion.
 Treatment of ascites
• Prevention of spontaneous bacterial peritonitis:
- Ciprofloxacin 250 mg 2 times per day; duration
5-7 days.
- Levofloxacin 500mg – every 12-24 hours;
Levofloxacin 500 mg - intravenously 1-2 times a
day; duration 5-7 days.
 Treatment of Hepatic encephalopathy
• Protein restriction in food up to 1 g/kg/day
• Lactulose (Dufalac, Portolac) under the control of a stool (soft
stool up to 3 times a day)
• Ornithine (Hepa-Mertz 20-40 g/day intravenously in 2 injections,
then orally 1 packet of granulate per 200 ml of liquid 2-3 times a
day)
• Decontamination of the intestine: rifaximin, ciprofloxacin
• Ademetionine (Heptral) 400-800 mg/day intravenously,
then 800-1600 mg/day orally. Duration 1-3 months.
 Treatment of bleeding
• When bleeding from varicose dilated veins of
the esophagus, stomach and rectum –
the treatment of patients is carried out in the
intensive care unit, surgery department.
 MELD
• The MELD score (Model for End-stage Liver
Disease)is used to prioritize patients for
transplantation of the liver.
• Liver transplant programs use a model of terminal
liver disease (MELD) scoring system to assess
the relative severity of liver disease in patients.
• Transplantation necessitates the use of immune
suppressants (ciclosporin or tacrolimus).
 Liver transplantation
Liver transplantation:
- prolongs the patient's life and
- improves his(her) quality of
life.
Thank for your attention