LIVER CIRRHOSIS

DEF

Cirrhosis is a chronic disease characterized by replacement of normal liver tissue with diffuse fibrosis
that disrupts the structure and function of the liver. Typically, the disease develops slowly over months
or years

Fibrous tissue – composed of parallel bundle of collagen fibers

CAUSES

Cirrhosis is most commonly caused by

alcohol, hepatitis B, hepatitis C,

non-alcoholic fatty liver disease.

Non-alcoholic fatty liver disease has a number of causes, including being overweight, diabetes, high
blood fats, and high blood pressure.

Typically, more than two or three alcoholic drinks per day over a number of years is required for
alcoholic cirrhosis to occur

autoimmune hepatitis, primary cholangitis,( INFLAMMATION OF BILE DUCT)

hemochromatosis, ( more iron buildup in body)

certain medications, ( amiodarone, chlorpromazine , oral contracetive )

gallstones.

Diagnosis is based on blood testing, medical imaging, and liver biopsy

TYPES

• Alcoholic cirrhosis, in which the scar tissue characteristically surrounds the portal areas. This is
most frequently due to chronic alcoholism and is the most common type of cirrhosis.
 • • Postnecrotic cirrhosis, in which there are broad bands of scar tissue as a late result previous of
acute viral hepatitis.

• • Biliary cirrhosis, in which scarring occurs in the liver around the bile ducts. This type usually is
the result of chronic biliary obstruction and infection (cholangitis); it is much less common than
the other two types.

• Cardiac cirrhosis; long standing severe right sided heart failure in patients with cor pulmonale,
constructive pericarditis, and tricuspid insufficiency.

PATHOPHYSIOLOGY

The liver plays a vital role in synthesis of proteins (for example, albumin, clotting factors
and complement), detoxification, and storage (for example, vitamin A). In addition, it participates in the
metabolism of lipids and carbohydrates

several factors have been implicated in the etiology of cirrhosis, alcohol consumption . Although
nutritional deficiency with reduced protein intake contributes to liver destruction in cirrhosis, excessive
alcohol intake is the major causative factor in fatty liver and its consequences.

• Cirrhosis is often preceded by hepatitis and fatty liver (steatosis), independent of the cause.

• The pathological hallmark of cirrhosis is the development of scar tissue ( accumulation of excess
fibrous 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

• Damage to the hepatic parenchyma (due to inflammation) leads to activation of stellate cells,
which increases fibrosis through production of myofibroblasts ( responsible for collagen
production)) and obstructs hepatic blood flow. In addition, stellate cells secrete TGF-β1, which
leads to a fibrotic response and proliferation of connective tissue.

• As this processes continues, fibrous tissue bands (septa) separate hepatocyte nodules, which
eventually replace the entire liver architecture, leading to decreased blood flow throughout.
The spleen becomes congested, which leads to hypersplenism and the spleen's retention
of platelets, which are needed for normal blood clotting. Portal hypertension is responsible for
the most severe complication of cirrhosis

• Clinical Manifestations of Cirrhosis

Compensated

• Intermittent mild fever

• Vascular spiders
• Palmar erythema (reddened palms)
• Unexplained epistaxis
• Ankle edema
• Vague morning indigestion
• Flatulent dyspepsia
• Abdominal pain
• Firm, enlarged liver
• Splenomegaly
 Decompensated

• Ascites
• Jaundice
• Weakness
• Muscle wasting
• Weight loss
• Continuous mild fever
• Clubbing of fingers
• Purpura (due to decreased platelet count)
• Spontaneous bruising
• Epistaxis
• Hypotension
• Sparse body hair
• White nails
• Gonadal atrophy

• LIVER ENLARGEMENT

• Early in the course of cirrhosis, the liver tends to be large and its cells loaded with fat. The
liver is firm and has a sharp edge noticeable on palpation. Abdominal pain may be present
because of recent, rapid enlargement of the liver, producing tension on the fibrous covering of
the liver (Glisson’s capsule). Later in the disease, the liver decreases in size as scar tissue
contracts the liver tissue.,The liver edge, if palpable, is nodular.

• PORTAL OBSTRUCTION AND ASCITES

• These late manifestations are due partly to chronic failure of liver function and partly to
obstruction of the portal circulation. Practically all the blood from the digestive organs is
collected in the portal veins and carried to the liver. Because a cirrhotic liver does not allow
the blood free passage, it backs up into the spleen and the GI tract and these organs become
the seat of chronic passive congestion; that is, . Indigestion and altered bowel function result.

• Fluid rich in protein may accumulate in the peritoneal cavity, producing ascites. This can be
demonstrated through percussion for shifting dullness

• EDEMA

• Another late symptom of cirrhosis is edema, which is attributed to chronic liver failure. A
reduced plasma albumin concentration predisposes the patient to the formation of edema.

• Edema is generalized but often affects lower extremities, upper extremities, and the presacral
area.

• VITAMIN DEFICIENCY AND ANEMIA

• Because of inadequate formation, use, and storage of certain vitamins (notably vitamins A, C,
and K), signs of their deficiency are common, particularly hemorrhagic phenomena associated
with vitamin K deficiency.
 • Chronic gastritis and impaired GI function, together with inadequate dietary intake and
impaired liver function, account for the anemia often associated with cirrhosis.

• MENTAL DETERIORATION

Additional clinical manifestations include deterioration of mental function with impending hepatic
encephalopathy and hepaticcoma

• DIAGNOSTIC EVALUATION

• Abdominal computed tomography (CT) scan This procedure combines special x-ray equipment
with sophisticated computers to produce multiple, digital images or pictures of the liver. It can
help determine the severity of cirrhosis as well as other liver diseases.

• Abdominal ultrasound: Ultrasound is a type of imaging exam that uses sound waves to create
pictures of the inside of the abdomen and/or pelvis, including images of the liver. Doppler
ultrasound allows for evaluation of blood flow to and from the liver.

• Elastography: This exam assesses the stiffness of your liver and can help diagnose how severe
the scarring is in your liver (known as liver fibrosis). Left untreated, liver fibrosis can
eventually lead to cirrhosis of the liver which is not reversible. Elastography can detect
stiffness of the liver caused by liver fibrosis earlier than other imaging tests. The test can be
performed by ultrasound or MRI.

• Biopsy: Part of the liver tissue is sampled and examined by a pathology doctor to analyze the
extent of liver damage. The biopsy is often done by a radiologist using ultrasound guidance
and is minimally invasive.

• Liver function test: This test involves analyzing the blood for particular enzymes that signal
that liver damage is present.

Blood test

LFT ( SGOT (AST) , SGPT (ALT)

TOTAL PROTEIN ( ALBUMIN GLOBULIN)

S BILURUBIN

GAMA GLOBULIN ( antibodies) produced by B lymphocyte , it is increase

Prothrombin time

• Medical Management

• antacids are prescribed to decrease gastric distress and minimize the possibility of GI bleeding.

• Vitamins and nutritional supplements promote healing of damaged liver cells and improve the
general nutritional status.

• Potassium-sparing diuretics (spironolactone [Aldactone], triamterene

• [Dyrenium]) may be indicated to decrease ascites,

• Albumin
 • Somatostatin analogu – octreotide

• Beta adregenic blocker, nitroglycerine

• Paracentesis

• B complex vitamin, vitamin k

• Iv therapy

• High carbohydrate, high protein, low fat, low sodium diet

• Lifestyle changes including, diet changes such as a low-sodium or plant-based diet, and
discontinuing the use of alcohol.

• Medications, such as antibiotics, may be prescribed in order to avoid infections as well as

vaccinations for viral hepatitis, pneumonia and influenza to help you avoid possible illnesses
that can cause infection

• Transjugular intrahepatic portosystemic shunt (TIPS), a procedure to treat the portal

hypertension caused by cirrhosis. An interventional radiologist places a small tube (stent) into
the liver to help bypass blood flow into the liver by directing it back towards the heart.

• Sengstaken-Blakemore or Minnesota tube. The Sengstaken-Blakemore or Minnesota tube

may also help control hemorrhage by applying pressure on the bleeding site.

• Surgery—

• In severe cases, a liver transplant may be needed. A liver transplant replaces the damaged
liver with a healthy one from a donor.

Nursing management

• Nursing assessment focuses on the onset of symptoms and the history of precipitating factors,
particularly long-term alcohol abuse, as well as dietary intake and changes in the patient’s
physical and mental status.. The nurse documents

• The nurse assesses the patient’s mental status through the interview and other interactions
with the patient; orientation to person, place, and time is noted.

• . Abdominal distention and bloating, GI bleeding, bruising, and weight changes are noted.

• The nurse assesses nutritional status, which is of major importance in cirrhosis, by daily
weights and monitoring of plasma proteins, transferrin, and creatinine levels.

• Report decrease in fatigue and increased ability to participate in activities.

• Maintain a positive nitrogen balance, no further loss of muscle mass, and meet nutritional
requirements.

• Decrease potential for pressure ulcer development and breaks in skin integrity.

• Reduce the risk of injury.

• Verbalize feelings consistent with improvement of body image and self-esteem.

• Increase level of comfort.

• Restore normal fluid volume.

• Improve mental status, maintain safety, and ability to cope with cognitive and behavioral
changes.

• Improve respiratory status.

• NURSING DIAGNOSES

• • Activity intolerance related to fatigue, general debility, muscle wasting, and discomfort

• • Imbalanced nutrition, less than body requirements, related to chronic gastritis, decreased GI
motility, and anorexia

• • Impaired skin integrity related to compromised immunologic status, edema, and poor
nutrition

• Risk for injury and bleeding related to altered clotting

• Disturbed body image related to changes in appearance, sexual dysfunction, and role
function.

• Chronic pain and discomfort related to enlarged liver and ascites.

• Fluid volume excess related ascites and edema formation.

• Disturbed thought processes and potential for mental deterioration related to abnormal liver
function and increased serum ammonia level.

• Ineffective breathing pattern related to ascites and restriction of thoracic excursion secondary
to ascites, abdominal distention, and fluid in the thoracic cavity

• COMPLICATIONS
• • Bleeding and hemorrhage

• • Hepatic encephalopathy

• • Fluid volume excess

----------------------------------------------------------
HEPATIC ENCEPHALOPATHY.
def

• ,it is a life-threatening complication of liver disease, occurs with profound liver failure and
may result from the accumulation of ammonia and other toxic metabolites in the blood.
Hepatic coma represents the most advanced stage of hepatic encephalopathy.
 • Causes

• Acute or chronic liver disease

• Benzodiazipine or opoids

• Infection

• Electrolyte imbalance

• Kidney failure

• pathophysiology

• liver dysfunction might lead to encephalopathy. normally, nitrogen-containing

compounds from the intestine, generated by gut bacteria from food, are transported by
the portal vein to the liver,

• 80–90% are metabolised through the urea cycle and or excreted immediately. This process
is impaired in all subtypes of hepatic encephalopathy, either because the hepatocytes (liver
cells) are incapable of metabolising the waste products

• Nitrogenous waste products accumulate in the systemic circulation The most important
waste product is ammonia (NH3). This small molecule crosses the blood–brain barrier and is
absorbed and metabolised by the astrocytes, a population of cells in the brain that constitutes
30% of the cerebral cortex.

• Astrocytes use ammonia when synthesising glutamin from glutamate. The increased levels of
glutamine lead to an increase in osmotic pressure in the astrocytes, which become swollen.

• There is increased activity of the inhibitory γ-aminobutyric acid (GABA) system, and the
energy supply to other brain cells is decreased. This can be thought of as an example of brain
edema of the "cytotoxic" type. The patient unergoes coma

DIAGNOSTIC EVALUATION

• Electroencephalogram

• CT SCAN

• MRI SCAN

• LFT

• PROTHROMBIN TIME

• LIVER BIOPSY

• CBC

• NEUROPSYCHOLOGICAL TEST

• SPINAL TAP
 Clinical Manifestations

• The earliest symptoms of hepatic encephalopathy include minor mental changes and motor
disturbances.

• slightly confused, has alterations in mood, , and

• has altered sleep patterns.

• restlessness and insomnia at night.

• Asterixis (flapping tremor of the hands) may occur

• In the early stages of hepatic encephalopathy, the deep tendon reflexes are hyperactive; with
worsening of hepatic encephalopathy, these reflexes disappear and the extremities may
become flaccid.

Medical management

intubation of the airway

Placement of a nasogastric tube permits the safe administration of nutrients and medication

Lactulose/lactitol Lactulose is given for encephalopathy.

Enema More commonly, phosphate enemas are used. This may relieve constipation, one of the
causes of encephalopathy, and increase bowel transit., it decrease ammonia level in body

• L-ornithine and L-aspartate

• L-ornithine and L-aspartate (LOLA) lowers the level of ammonia in a person's blood. LOLA
lowers ammonia levels by increasing the generation of urea through the urea cycle,
a metabolic pathway that removes ammonia by turning it into the neutral substance urea.

• antibiotics

NURSING MANAGEMENT

• Administer lactulose (Cephulac) to reduce serum ammonia level. Observe for watery diarrhea
stools, which indicate lactulose overdose.

• Reduce protein intake or eliminate signs of impending encephalopathy or coma occur.

• Give enema to reduce ammonia absorption from the gastrointestinal tract.

• Administer nonabsorbable antibiotics (neomycin) as an intestinal antiseptic.

• Monitor serum ammonia level daily; monitor electrolyte status and correct if abnormal.

• Discontinue medications that may precipitate encephalopathy (e.g. sedative medications,

tranquilizers, analgesic agents)

• Other treatments may include administration of intravenous glucose, vitamins and oxygen.

• Assess level of consciousness

 • Monitor for restlessness and agitation

• Monitor handwriting daily; it becomes worse with increasing ammonia levels

• Assess deep tendon reflexes

• Provide ongoing assessment.

• Evaluate serum ammonia values daily.

• Monitor for signs of impending coma. Reduce or eliminate the client’s dietary protein intake if
you detect evidence of impending coma.

• Monitor electrolyte status and intervene as indicated to correct any imbalances.

• Monitor the client closely, and administer a conservative dose of prescribed sedative or
analgesic medication, because liver damage alters drug metabolism.

PORTAL HYPERTENSION

DEF

Portal hypertension is an increase in the blood pressure within a system of veins called the portal
venous system.Veins coming from the stomach, intestine, spleen, and pancreas merge into the portal
vein, which then branches into smaller vessels and travels through the liver.

If the vessels in the liver are blocked due to liver damage, blood cannot flow properly through the
liver. As a result, high pressure in the portal system develops. This increased pressure in the portal
vein may lead to the development of large, swollen veins (varices) within the esophagus, stomach,
rectum, or umbilical area . Varices can rupture and bleed, resulting in potentially life-threatening
complications.

CAUSES

• The most common cause of portal hypertension is cirrhosis of the liver. Cirrhosis is the scar
tissue blocks the flow of blood through the liver.

• Other causes of portal hypertension include blood clots in the portal vein, blockages of the
veins that carry the blood from the liver to the heart,

• parasitic infection (schistosomiasis, )

• focal nodular hyperplasia, a disease seen in people infected with HIV.

Signs and symptoms

• Ascites (free fluid in the peritoneal cavity),

• Abdominal pain or tenderness (when bacteria infect the ascites, as in spontaneous bacterial
peritonitis).
 • Increased spleen size (splenomegaly), which may lead to lower platelet counts
(thrombocytopenia)

• Anorectal varices

• Swollen veins of the oesophagus (oesophageal varices), which may bleed and cause vomiting
of blood (haematemesis)

• Swollen veins on the anterior abdominal wall

Diagnosis

• Ultrasonography is the first-line imaging technique for the diagnosis and follow-up of portal
hypertension because it is non-invasive, low-cost and can be performed on-site.

• Doppler ultrasonography, a slow velocity of <16 cm/s in addition to dilatation in the main
portal vein are diagnostic of portal hypertension.

• The hepatic venous pressure gradient (HVPG) measurement has been accepted as the gold
standard for assessing the severity of portal hypertension. Portal hypertension is defined as
HVPG greater than or equal to 5 mm Hg and is considered to be clinically significant when
HVPG exceeds 10 to 12 mm Hg

MEDICAL MANAGEMENT

• Portosystemic shunts

• Fluoroscopic image of transjugular intrahepatic portosystemic shunt (TIPS) (transjugular

intrahepatic portosystemic shunting) is effective at reducing the rate of rebleeding. [

• Prevention of bleeding

• Both pharmacological (non-specific β-blockers, nitrate isosorbide mononitrate, vasopressin

such as terlipressin) and endoscopic (banding ligation) .

• The management of active variceal bleeding includes administering vasoactive drugs

(somatostatin, octreotide), endoscopic banding ligation, balloon tamponade and TIPS.

Ascites

• The management of ascites needs to be gradual to avoid sudden changes in systemic volume
status which can precipitate hepatic encephalopathy, renal failure and death. The
management includes salt restriction, diuretics (spironolactone), paracentesis,
and transjugular intrahepatic portosystemic shut.

• Hepatic encephalopathy

• A treatment plan may involve lactulos, enemas, and use of antibiotics such
as rifaximin, neomycin, vancomycin, and the quinolones. the maintenance of adequate
nutrition is now advocated.