Liver cirrhosis is the Chronic injury of the hepatic parenchyma and include extensive fibrosis in association with the formation of regenerative nodules.
These features result from hepatocyte necrosis, collapsing of the supporting reticulin
network with subsequent connective tissue deposition, distortion of the vascular beds, and
nodular regeneration of the remaining liver parenchyma.
Livercirrhosis


Causes of Liver Cirrhosis
Cirrhosis can be caused by several conditions, including long-standing
inflammation, poisons, infections, and heart disease, as well as chronic alcoholism and
chronic hepatitis.
For 30-50 percent of cirrhosis cases, however, no cause can be found.
Chronic Alcoholism
Alcohol can poison all living cells, causing liver cells to become inflamed and die.
The death of liver cells leads to the formation of scar tissue around veins of the liver.
Healing liver cells form nodules, which also press on the liver veins.
This scarring process occurs in 10-20 percent of alcoholics.
The severity of the process depends on how much you drink and how long you have been
abusing alcohol.
The amount of alcohol needed to injure the liver varies widely from individual to
individual. Some families are more susceptible to cirrhosis than others.
Hepatitis: Means inflammation of the liver from any cause, but it usually refers to a viral
infection of the liver.
Over many years the inflammation damages liver cells and leads to scarring.
Hepatitis B, hepatitis C, and hepatitis D all can cause cirrhosis but worldwide, hepatitis B
is the most common cause of cirrhosis.
Biliary Cirrhosis
Bile is a substance produced by the liver to help the body digest fats.
Bile is carried from the liver to the gallbladder and eventually into the intestines by small
tubes called bile ducts.
If these ducts become blocked, the bile backs up, and can damage the liver.
The liver becomes inflamed, starting the long process of cell damage that leads to
cirrhosis.
In adults, gallstones are a common cause of bile duct blockage.
Surgery to remove the gallbladder also blocks the bile ducts.
Children maybe born with a condition that blocks the bile ducts called biliary atresia.
Autoimmune Cirrhosis
The body's immune system defends against "invaders" such as bacteria, viruses, or
allergens.
Autoimmune diseases occur when the immune system instead begins to fight healthy
body tissues and organs.
In autoimmune hepatitis, the body's immune system attacks the liver, causing cell damage
that leads to cirrhosis.
Non-alcoholic Fatty Liver
This is a condition in which fat builds up in the liver, eventually causing scar tissue to
form.
This kind of cirrhosis is linked to diabetes, obesity, coronary artery disease, protein
malnutrition, and treatment with corticosteroids such as prednisone.
It is sometimes called ‘steatohepatitis.’
Inherited Diseases
A variety of genetic diseases can damage the liver.
These are diseases that interfere with the metabolism of different substances by the liver.
They include Wilson disease, cystic fibrosis, alpha-1 antitrypsin deficiency,
hemochromatosis, galactosemia, and glycogen storage disease.
Most of these diseases are not common but they can be devastating.
Drugs, Toxins, and Infections
Various substances and germs can cause damage to the liver.
Certain medications (for example, acetaminophen [Tylenol]), poisons, and environmental
toxins can lead to cirrhosis.
Reactions to certain drugs can damage the liver, this is rare.
Long-term infections with various bacteria or parasites can damage the liver and cause
cirrhosis.
Cardiac Induced Cirrhosis
When the heart doesn't pump well, blood "backs up" into the liver
This congestion causes damage to the liver
It may become swollen and painful
Later it becomes hard and less painful
Clinical Features of Liver Cirrhosis
Many people with cirrhosis have no symptoms in the early stages of the disease.
However, as scar tissue replaces healthy cells, liver function starts to fail and a patient
may experience the following symptoms
Exhaustion
Fatigue
Loss of appetite
 Nausea
 Weakness
 Weight loss
 Abdominal pain
 Spider-like blood vessels (spider angiomas) that develop on the skin as the disease
progresses
 Edema and ascites
Jaundice
Itching
Complication, Investigations, Differential Diagnosis, and Treatment of
Liver Cirrhosis
Complications
Loss of liver function affects the body in many ways.
Following are the common problems, or complications caused by cirrhosis.
Gastrointestinal Bleeding
Portal hypertension causes backing up of blood flow in the veins of the stomach and
esophagus.
This causes the veins to enlarge, forming ‘varies (varicose veins).
These varices can tear and bleed, and this bleeding can be life-threatening.
This usually shows up as vomiting blood.
When the liver slows or stops the production of the proteins needed for blood clotting, a
the person will bruise or bleed easily.
The palms of the hands may be reddish and blotchy with palmar erythema.
Infection
Patients with liver cirrhosis are at risk for many infections because the liver cannot form
proteins needed to fight off infection.
Hepatic Encephalopathy
• In this condition, toxins build up in the bloodstream because the scarred liver is unable to
clear them from the body.
The toxins can cause someone to behave bizarrely, become confused, and lose the ability
to take care of themselves or others.
Some people become very sleepy and cannot wake up easily.
The common toxins are nitrogenous compounds.
Liver Cancer
Hepatocellular carcinoma, a type of liver cancer commonly caused by cirrhosis.
Summary of complications of Cirrhosis
Portal Hypertension - Gastroesophageal varices, Portohypertensive gastropathy,
Splenomegaly and hypersplenism, Ascites, Spontaneous bacterial endocarditis.
Hepatorenal Syndrome
Hepatic Encephalopathy
Hepatopulmonary Syndrome
Portopulmonary Hypertension
Malnutrition
Coagulopathy: Factor deficiency, Fibrinolysis, Thrombocytopenia
Bone disease-Osteopenia, Osteoporosis, Osteomalacia
Haematological abnormalities-Anaemia, Haemolysis, Thrombocytopenia, Neutropenia
Investigations
Full Blood Picture
Anemia: Normocromic normocytic
Low white blood count
Reduced platelets due to hypersplenism
Raised ESR
Liver Function Test
Raised AST, ALT
Reduced albumin,
Prolonged prothrombin time
A liver biopsy will confirm the diagnosis
Others include:
Liver ultrasound
CT scan-abdomen
Note: Investigations for liver cirrhosis is not available in the primary health care facilities
(health centers and dispensaries) therefore referral of the patients is important.
Differential Diagnosis
Hepatitis
Hepatocellular carcinoma
Congestive cardiac failure
Treatment
Mainly directed towards specific complications and cause, though there are some
general measures.
General Principles
Include abstinence from alcohol use, high protein diet (except in encephalopathy) with
vitamin supplements and adequate rest.
Management of Complications
Most of these complications require referral after initial resuscitation.
Portal Hypertension
B-Adrenergic blockade with propranolol or nadolol reduces portal pressure through
vasodilator effects on both the splanchnic arterial bed and the portal venous system in
combination with reduced cardiac output.
Variceal Bleeding
Resuscitation
Make sure the airway is patent and the patient is breathing.
Assess the general condition of the patient; pulse and blood pressure.
Insert an IV line and obtain blood for grouping and cross-matching and hemoglobin
estimation.
Restore blood volume with plasma expanders, if possible blood transfusion.
Refer the patient immediately after this initial resuscitation for further management
including endoscopic procedures to confirm the diagnosis.
Specific intervention to stop the bleeding e.g. use of vasoconstrictors
(somatostatin/octreotide or vasopressin), balloon tamponade, and endoscopic banding
of varices or endoscopic sclerosis of varices (sclerotherapy) is done at higher
centers.
Replacement of clotting factors with fresh-frozen plasma is important in patients with
coagulopathy.
Splenomegaly
Usually requires no specific treatment, if severe splenectomy may be required.
Ascites
Salt and water restriction
Use of Diuretics
Start with spironolactone orally dose ranging from 100mg to 400mg daily.
In resistant cases low doses of frusemide can be given while monitoring pulse and
blood pressure to avoid hypotension and circulatory collapse.
Paracentesis
Spontaneous Bacterial Peritonitis (SBP)
Empirical therapy with ceftriaxone or ampicillin and an aminoglycoside, until a causative
the organism is identified then specific therapy is undertaken.
Hepatorenal Syndrome
Treatment is usually unsuccessful.
In appropriate candidates, the treatment of choice for the hepatorenal syndrome is liver
transplantation.
Hepatic Encephalopathy
Early recognition and prompt treatment of hepatic encephalopathy are essential.
Patients with acute, severe hepatic encephalopathy (stage IV) require the usual supportive
measures for the comatose patient.
Specific treatment of hepatic encephalopathy is aimed at
Elimination or treatment of precipitating factors and
Lowering of blood ammonia (and another toxin) levels by decreasing the absorption of
protein and nitrogenous products from the intestine.
In the setting of acute gastrointestinal bleeding, blood in the bowel should be promptly
evacuated with laxatives (and enemas if necessary) to reduce the nitrogen load.
Protein should be excluded from the diet, and constipation should be avoided.
Ammonia absorption can be decreased by the administration of lactulose.
Acutely, lactulose syrup can be administered in a dose of 30 to 60 ml every hour until
diarrhea occurs; thereafter the dose is adjusted (usually 15 to 30 mL three times daily) so
that the patient has two to four soft stools daily.
Intestinal ammonia production by bacteria can also be decreased by oral administration of
a "non-absorbable" antibiotic such as neomycin (0.5 to 1.0 g every 6 h).
Equal benefits may be achieved with broad-spectrum antibiotics such as metronidazole
400mg 8 hourly.
Prognosis
Overall The prognosis of liver cirrhosis is poor.
Overall only 25%of patients survive 5 years of diagnosis, but if liver function tests are
good, 50% survive for five years and 25% for up to 10 years.
Alcohol cirrhosis, hemochromatosis, and Wilson’s disease cirrhosis have a good
prognosis if the etiology is removed.
Deteriorating liver functions, evidenced by jaundice, ascites, encephalopathy, decreased
plasma proteins, marked hyponatremia and prolonged prothrombin time indicates a poor
prognosis.                                                                                                        
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