Institute of Nursing Education, Mumbai

Seminar on-

Liver Cirrhosis
(Medical-surgical Nursing)

Presented by –
Vireshwar Sunil Mahajani, M.Sc (CVTN) Nursing,
Institute of Nursing Education, Mumbai.
 Anatomy and Physiology of Liver
Liver
The liver is the largest gland of the body which secrets bile and takes part the in the metabolism of food. It is
situated in the right upper quadrant of the body; it is placed on the inferior surface of the diaphragm and is covered
by ribs and costal cartilage on the top. The weight of a healthy liver is about 1.5-2 kg. The liver also is called
“hepar” and so the adjective hepatic is used while referring to the liver.

External features of liver

• Externally liver is covered with a layer of connective tissue called as Glisson’s capsule. It covers the liver
and all the structures coming out and going in of the liver like the hepatic artery, portal vein, and bile duct
within the liver.
• Liver is divided into two major and two minor lobes. The right lobe and left lobe are the two major lobes
of the liver and can be seen anteriorly, while the caudate and quadrate lobe is the two minor lobes that
can be seen on the inferior part of the liver.
• Right lobe is the largest of all four lobes of the liver and forms 5/6th part of the liver. It is connected to
the left lobe with the help of connective tissue septum called the falciform ligament.
• Left lobe of liver is much smaller than right lobe and forms only 1/6th part of the liver.
• The caudate and quadrate lobe is situated to posterior and inferior surface of liver.
• The posterior surface of right lobe of liver shows a deep transverse fissure, about 5 cm long, called as
portal fissure or porta hepatis. This site act as a gate way for entry and exit of several structures like
portal veins, hepatic arteries, hepatic nerve plexus along with right and left hepatic duct and some
lymphatics.
Blood supply
Liver receives 20% of the blood from hepatic artery and 80% of blood from portal veins. Before entering into
the liver, both the hepatic artery and portal vein gets divided into left and right branches. While after entering into
liver they get redivided into segmental and interlobular vessels. Blood from lobes of the liver is collected by
interlobular veins. These veins joins to form sub lobular veins, sub lobular veins join to form hepatic veins.
Hepatic veins drains blood directly into inferior vena cava.

Nerve supply
Liver receives blood supply from hepatic plexus, which contain both sympathetic and Para- sympathetic nerves.

Histology
Liver is made up of many lobes called as hepatic lobes. These lobes shows smaller lobe like structures called
hepatic lobules. These hepatic lobules are the functional and structural unit of liver. Each hepatic lobule is
surrounded by three portal vessels- a branch hepatic artery, a branch of portal vein and tributary of bile
duct. These three ducts are together called as portal triad. Each lobule are honey comb like structures made up
of liver cells called hepatocytes. Hepatocytes are arranged in column like structures called as hepatic plates. In
between two hepatic columns there is bile canaliculus. Bile secreted by hepatic cells is emptied into bile
canaliculus. In between each plate in blood space called sinusoid. A branch of portal vein and hepatic artery
opens into sinusoid. Sinusoid opens into central vein and central vein into hepatic vein.
Extra hepatic biliary apparatus
It is a system of ducts from liver to duodenum, which serves as a pathway for bile and other secretions. It collects
bile from liver, stores it in gall bladder and transmits it to 2nd part of duodenum. The apparatus consists of –right
and left hepatic duct, common hepatic duct, gall bladder, cystic duct and bile duct.
Right and left hepatic ducts
The smaller hepatic ducts from both right and left lobes converge and empty into right and left hepatic ducts.
Right and left hepatic ducts emerge from porta hepatis of liver.
Common hepatic duct
Right and left hepatic ducts unite to form a single common hepatic duct. It runs downwards for about 3cm. At
this point common hepatic duct is joined by cystic duct on right side.
 Cirrhosis of Liver
Cirrhosis is the end-stage of liver disease. Cirrhosis is characterized by extensive degeneration and destruction of
the liver cells. This results in the replacement of liver tissue by fibrosis (scar tissue) and regenerative nodules that
occur from the liver’s attempt to repair itself. The development of cirrhosis usually happens after decades of
chronic liver disease. It is twice as common in men as compared to women.

Figure 1- Normal Liver Figure 2- Cirrhotic liver

Aetiology and Pathophysiology.

Any chronic liver disease, including disease from excessive alcohol intake and NAFLD, can cause cirrhosis. The
most common causes of cirrhosis in the world are chronic hepatitis C infection and alcohol-induced liver disease.
In patients with alcohol-induced liver disease, some controversy exists as to whether the cause is the alcohol or
the malnutrition that often coexists with alcoholism. Some cases of nutrition-related cirrhosis have resulted from
extreme dieting, malabsorption, and obesity. Environmental factors and genetic predisposition may also lead to
the development of cirrhosis, regardless of dietary or alcohol intake.

Approximately 20% of patients with chronic hepatitis C and 10%-20% of those with chronic hepatitis B develop
cirrhosis. Chronic inflammation and cell necrosis from viral hepatitis can result in progressive fibrosis and
cirrhosis. Chronic hepatitis combined with alcohol ingestion has a synergistic effect in accelerating liver damage.
Biliary causes of cirrhosis include primary biliary cholangitis (PBC) and primary sclerosing cholangitis (PSC).
Both are described earlier in this chapter.

Cardiac cirrhosis includes a spectrum of hepatic derange ments that result from long-standing, severe, right-sided
heart failure. It causes hepatic venous congestion, parenchymal dam- age, necrosis of liver cells, and fibrosis over
time. The treatment is aimed at managing the patient’s underlying heart failure.

In cirrhosis, the liver cells attempt to regenerate, but the re- generative process is disorganized, resulting in
abnormal blood vessel and bile duct architecture. The overgrowth of new and fibrous connective tissue distorts
the liver’s normal lobular structure, resulting in lobules of irregular size and shape with impeded blood flow.
Eventually, irregular and disorganized liver regeneration, poor cellular nutrition, and hypoxia (from inadequate
blood flow and scar tissue) result in decreased liver function.
Clinical Manifestations

• Early Manifestations. Patients may be unaware of their liver condition because there are relatively few
symptoms in early-stage disease. If an individual does have symptoms, it may include fatigue or an enlarged
liver. Blood tests may show nor- mal liver function (compensated cirrhosis). The diagnosis of cirrhosis is
often made later when a patient manifests symptoms of more advanced liver disease.
• Late Manifestations. Late manifestations result from liver failure and portal hypertension. Jaundice,
peripheral edema, and ascites develop gradually. Other late manifestations include skin lesions, hematologic
disorders, endocrine distur- bances, and peripheral neuropathies. In the advanced stages, the liver becomes
small and nodular. Liver function is dramatically diminished.
➢ Jaundice. Jaundice results from decreased ability to conju- gate and excrete bilirubin into the small
intestines. There is an overgrowth of connective tissue in the liver, which compresses the bile ducts and
leads to an obstruction. This re- sults in an increase in the bilirubin in the vascular system, and jaundice
occurs. jaundice may be minimal or severe, depending on the degree of liver damage..
➢ Skin Lesions. Various skin manifestations are commonly seen in cirrhosis. Spider angiomas
(telangiectasia or spider nevi) are small, dilated blood vessels with a bright red center point and spiderlike
branches. They occur on the nose, cheeks, upper trunk, neck, and shoulders. Palmar erythema (a red area
that blanches with pressure) is located on the palms of the hands. Both of these lesions are due to an
increase in circulating estrogen as a result of the damaged liver’s inability to metabolize steroid hormones.
➢ Hematologic Problems. Hematologic problems include thrombocytopenia, leukopenia, anemia, and
coagulation disorders. Thrombocytopenia, leukopenia, and anemia are thought to be caused by the
splenomegaly that results from backup of blood from the portal vein into the spleen (portal hypertension).
Overactivity of the enlarged spleen results in increased removal of blood cells from circulation. Anemia
can result from inadequate red blood cell (RBC) production and survival, poor diet, poor absorption of
folic acid, and bleeding from varices.

➢ The coagulation problems result from the liver's Inability to produce prothrombin and other factors
essential for blood clotting. Manifestations of coagulation problems (bleeding ten- dencies) include
epistaxis, purpura, petechiae, easy bruising, gingival bleeding, and heavy menstrual bleeding.
➢ Endocrine Problems. The liver plays an important role in the metabolism of hormones, such as estrogen
and testosterone. In men with cirrhosis, gynecomastia (benign growth of the glandular tissue of the male
breast), loss of axillary and pubic hair, testicular atrophy, and impotence with loss of libido may occur
because of increased estrogen levels. Younger women with cirrhosis may develop amenorrhea, and older
women may have vaginal bleeding. Aldosterone, an important hormone as- sociated with fluid balance,
 can also be altered. If the liver fails to metabolize aldosterone adequately, it can lead to hyperaldo-
steronism with subsequent sodium and water retention and po- tassium loss.
➢ Peripheral Neuropathy. Peripheral neuropathy is a com- mon finding in alcoholic cirrhosis and is
probably due to a dietary deficiency of thiamine, folic acid, and cobalamin. The neuropathy usually results
in sensory and motor symptoms, but sensory symptoms may predominate.
Complications.
Major complications of cirrhosis are portal hy pertension, esophageal and gastric varices, peripheral edema,
abdominal ascites, hepatic encephalopathy (mental status changes, including coma), and hepatorenal syndrome.
Patients who are cirrhotic but who have no obvious complications are considered to have compensated cirrhosis.
Those who have one or more complications of their liver disease have decompensated cirrhosis.

• Portal Hypertension and Esophageal and Gastric Varices. In patients with cirrhosis, the liver undergoes
structural changes. These changes lead to obstruction of blood flow in and out of the liver. Ultimately this
results in increased pressure within the liver’s circulatory system (portal hypertension). Portal hyper- tension
is characterized by increased venous pressure in the portal circulation, splenomegaly, large collateral veins,
ascites and gastric and esophageal varices.

As a way of reducing pressure, the body develops alternate circulatory pathways, referred to as collateral
circulation. The collateral channels commonly form in the lower esophagus, anterior abdominal wall, parietal
peritoneum, and rectum. Varicosities (distended veins) develop in areas where the collat eral and systemic
circulations communicate, resulting in esoph ageal and gastric varices, caput medusae (ring of varices around
the umbilicus), and hemorrhoids.

Esophageal varices are a complex of tortuous, enlarged veins at the lower end of the esophagus. Gastric
varices are located in the upper portion of the stomach. These varices are fragle and do not tolerate high
pressure, thus they can bleed eas Large varices are more likely to bleed. varices an responsible for
approximately 80% of variceal hemorrhages."

The remaining 20% of variceal hemorrhages are due to gastric varices. The patient may present with melena
or hematemesis. Ruptured esophageal varices are the most life-threatening com- plication of cirrhosis and
considered a medical emergency.

• Peripheral Edema and Ascites. Peripheral edema occurs in the lower extremities and presacral area.
Peripheral edema can occur before, concurrently with, or after ascites development. Edema results from
decreased colloidal oncotic pressure from impaired liver synthesis of albumin and increased portacaval
pressure from portal hypertension.

Ascites is the accumulation of serous fluid in the peritoneal or abdominal cavity. It is a common manifestation
of cirrhosis. Several mechanisms lead to ascites. One mechanism of ascites occurs with portal hypertension,
which causes proteins to shift from the blood vessels into the lymph space. When the lymphatic system is
unable to carry off the excess proteins and water, they leak into the peritoneal cavity. The osmotic pressure
of the proteins pulls additional fluid into the peritoneal Cavity. A second mechanism of ascites formation is
 hypoalbumin- emia resulting from the liver’s decreased ability to synthesize albumin. The hypoalbuminemia
results in decreased colloidal oncotic pressure.

A third mechanism of ascites is hyperaldosteronism, which occurs when the hormone aldosterone is
metabolized by dam- aged hepatocytes. The increased level of aldosterone causes increased sodium by the
renal tubules. This re- tention of sodium, combined with an increase in antidiuretic hormone in blood, leads
to additional water retention. Because of edema formation, there is decreased intravascular volume and,
subsequently, decreased renal blood flow and glomerular filtration.

Ascites is manifested by abdominal distention with weight gain. If the ascites is severe, the increase in
abdominal pressure from the fluid accumulation may cause eversion of the umbilicus. Abdominal striae with
distended abdominal wall veins may be present. Patients may show signs of dehydration (e.g., dry tongue
and skin, sunken eyeballs, muscle weakness) and a decrease in urine output. Hypokalemia is common and is
due to an excessive loss of potassium caused by hyperaldosteronism. Low potassium levels can also result
from diuretic therapy used to treat the ascites.

Because of alterations in immune function associated with cirrhosis, patients with ascites are at risk for
spontaneous bacterial peritonitis (SBP). SBP is a bacterial infection of the ascitic fluid. In SBP, bacteria
normally found in the intestines are trans- located into the peritoneal space. The bacteria most frequently
responsible for the infection are a Gram-negative enteric patho- gen such as Escherichia coli. Worsening
vasodilation contributes to the development of SBP 12

• Hepatic Encephalopathy. Hepatic encephalopathy is a neuropsychiatric manifestation of liver disease. The

pathogenesis is multifactorial and includes the neurotoxic effects of ammonia, abnormal neurotransmission,
astrocyte swelling, and inflammatory cytokines. A major source of ammonia is the bacterial and enzymatic
deamination of amino acids in the intestines. The ammonia that results from this deamination process nor-
mally goes to the liver via the portal circulation and is converted to urea, which is then excreted by the
kidneys. When blood is shunted past the liver via the collateral vessels or the liver is so damaged that it is
unable to convert ammonia to urea, the levels of ammonia in the systemic circulation increase. The ammonia
crosses the blood-brain barrier and produces neurologic toxic manifestations.

Factors that increase ammonia in the circulation may precipitate hepatic encephalopathy. Hepatic
encephalopathy can occur after placement of transjugular intrahepatic portosystemic shunt (TIPS), which is
used to reduce portal hy- pertension by diverting blood flow around the liver.

Clinical manifestations of encephalopathy are changes in neurologic and mental responsiveness; impaired
consciousness; and inappropriate behavior, ranging from sleep disturbances to trouble concentrating to deep
coma. Changes may occur (1) suddenly because of an increase in ammonia in response to bleeding varices
 or infection or (2) gradually as blood ammonia levels slowly increase. A grading system is often used to
classify the stages of hepatic encephalopathy.

A characteristic manifestation of hepatic encephalopathy is asterixis (flapping tremors). This may take
several forms, with the most common involving the arms and hands. When asked to hold the arms and hands
stretched out, the patient is unable to hold this position and performs a series of rapid flexion and extension
movements of the hands.

Impairments in writing involve difficulty in moving the pen or pencil from left to right and apraxia (inability
to construct simple figures). Other signs include hyperventilation, hypothermia, tongue fasciculations, and
grimacing and grasping re- flexes. Fetor hepaticus (musty, sweet odor of the patient’s breath) occurs in some
patients with encephalopathy. This odor is from the accumulation of digestive by-products that the liver is
un- able to degrade.

• Hepatorenal Syndrome. Hepatorenal syndrome is a type of renal failure with azotemia, oliguria, and
intractable ascites. In this syndrome, the kidneys have no structural abnormality. The etiology is complex,
but the final common pathway is likely to be portal hypertension along with liver decompensation, resulting
in splanchnic and systemic vasodilation and decreased ar- terial blood volume. As a result, renal
vasoconstriction occurs, and renal failure follows. This renal failure can be reversed by liver transplantation.
In the patient with cirrhosis, hepatorenal syndrome frequently follows diuretic therapy, GI hemorrhage, or
paracentesis. Diagnostic Studies. Patients with cirrhosis have abnormalities in most of the liver function
tests. Enzyme levels, including al- kaline phosphatase, AST, ALT, and y-glutamyl transpeptidase (GGT), are
initially elevated because of their release from in- flamed liver cells. However, in end-stage liver disease,
AST and ALT levels may be normal due to the death and loss of hepatocytes. Patients with cirrhosis will also
have decreased serum total protein and albumin, increased serum bilirubin and globulin levels, and prolonged
prothrombin time. Alterations in fat metabolism are reflected by decreased cholesterol levels.

Although a liver ultrasound may be able to detect the pres- ence of cirrhosis, it is not a reliable diagnostic
test for cirrhosis.Ultrasound elastography (FibroScan) is a noninvasive test that is used to quantify the degree
of liver fibrosis. A liver biopsy, which may be done to identify liver cell changes, is the gold standard for a
definitive diagnosis of cirrhosis.
Management of Patient with liver cirrhosis

The goal of treatment is to slow the progression of cirrhosis and to prevent and treat any complications.

• Ascites. Management of ascites focuses on sodium restriction, diuretics, and fluid removal. Patients may be
encouraged to limit sodium intake to 2 g/day. Patients with severe ascites may need to restrict their sodium
intake to 250-500 mg/day. Very low sodium intake can result in reduced nutritional intake and subsequent
problems associated with malnutrition. The patient is usually not on restricted fluids unless severe ascites
develops. When caring for patients with ascites, accurately assess and monitor fluid and electrolyte balance.
Albumin infusion may be used to help maintain intravascular volume and adequate urine output by increasing
plasma colloid oncotic pressure.

Diuretic therapy is an important part of management. Often a combination of drugs that work at multiple
sites of the nephron is more effective than a single agent. Spironolactone is an effective diuretic, even in
patients with severe ascites. Spironolactone is also an antagonist of aldosterone and is potassium sparing.
Other potassium-sparing diuretics include amiloride and triamterene. A high-potency loop diuretic, such as
furosemide, is frequently used in combination with a potassium-sparing drug.

Tolvaptan, a vasopressin-receptor antagonist, is used to correct hyponatremia, which is often seen in patients
with cir- rhosis. It causes an increase in water excretion, resulting in an increase in serum sodium
concentration.

A paracentesis is a sterile procedure in which a catheter is used to withdraw fluid from the abdominal cavity.
This pro- cedure can be used to diagnose a medical condition or relieve pain, pressure, or difficulty breathing.
In the patient with cir- rhosis, this procedure is reserved for the person with impaired respiration or abdominal
discomfort caused by severe ascites who does not respond to diuretic therapy. It is only a temporary measure
of palliation because the fluid tends to reaccumulate rapidly.

TIPS is used to alleviate asci- tes that does not respond to diuretics. Peritoneovenous shunt is a surgical
procedure that provides continuous reinfusion of as- citic fluid into the venous system. Its use has almost
been elimi- nated because of the high rate of complications.

• Esophageal and Gastric Varices. The main therapeutic goal for esophageal and gastric varices is to prevent
bleeding and variceal rupture by reducing portal pressure. The patient who has esophageal and/or gastric
varices should avoid ingest ing alcohol, aspirin, and nonsteroidal antiinflammatory drugs All patients with
cirrhosis should have an upper endoscopy (esophagogastroduodenoscopy (EGD) to screen for varices.
Patients with varices at risk of bleeding are generally started on a nonselective p-blocker (nadolol or
propranolol) to reduce the incidence of hemorrhage. B-Blockers decrease high pres sure, which decreases
the risk for rupture. When variceal bleeding occurs, the first step is to stabilize the patient and manage the
 airway. IV therapy is initiated and may include administration of blood products. Management that involves
a combination of drug therapy and endoscopic therapy is more successful than either approach alone. Drug
therapy for bleeding varices may include the somatostatin analog octreotide (Sandostatin) or vasopressin.
The main goal of drug therapy is first to stop the bleeding and identify the source and apply interventions to
prevent fur- ther bleeding. IV administration of octreotide or vasopressin produces vasoconstriction of the
splanchnic arterial bed, de- creases portal blood flow, and decreases portal hypertension. Currently, octreotide
is more widely used in this setting because of its limited side effect profile when compared with vasopressin.
At the time of endoscopy, band ligation or sclerotherapy of varices may be used to prevent rebleeding.
Endoscopic variceal ligation (EVL, or "banding") is performed by placing a small rubber band (elastic O-
ring) around the base of the varix (en- larged vein). Sclerotherapy involves injection of a sclerosing solution
into the swollen veins through an injection needle that is placed through the endoscope. Balloon tamponade
may be used when acute esophageal or gastric variceal hemorrhage cannot be controlled on ini- tial
endoscopy. Balloon tamponade controls the hemorrhage by mechanical compression of the varices. Different
types of tubes are available. The Sengstaken-Blakemore tube has balloons, gastric and esophageal, with three
lumens: one the gastric balloon, one for the esophageal balloon, and one for gastric aspiration. Two other
types of balloons are the Minnesota tube (a modified Sengstaken-Blakemore tube with an esophageal suction
port above the esophageal balloon) and the Linton-Nachlas tube.

Supportive measures during an acute variceal bleed include administration of fresh frozen plasma and packed
RBCs, vitamin K, and proton pump inhibitors (e.g., pantoprazole). Lactulose and rifaximin may be
administered to prevent hepatic encephalopathy from breakdown of blood and the release of ammonia in the
intestine. Antibiotics are given to prevent bacterial infection.

Because of the high incidence of recurrent bleeding with each bleeding episode, continued therapy is
necessary. Long-term management of patients who have had an episode of bleeding includes nonselective B-
blockers, repeated band ligation of the varices, and portosystemic shunts in patients who develop re- current
bleeding.

• Shunting Procedures. Nonsurgical and surgical methods of shunting blood away from the varices are
available. Shunting procedures tend to be used more after a second major bleeding episode than during an
initial bleeding episode. Transjugular in- trahepatic portosystemic shunt (TIPS) is a nonsurgical procedure in
which a tract (shunt) between the systemic and portal venous systems is created to redirect portal blood flow.
A catheter is placed in the jugular vein and then threaded through the su- perior and inferior vena cava to the
hepatic vein. The wall of the hepatic vein is punctured, and the catheter is directed to the portal vein. Stents
are positioned along the passageway, overlap- ping in the liver tissue and extending into both veins.
 This procedure reduces portal venous pressure and decom- presses the varices, thus controlling bleeding.
TIPS does not interfere with a future liver transplantation. Limitations of the procedure include the increased
risk of hepatic encephalopathy (toxin-containing blood bypasses the liver) and stenosis of the stent. TIPS is
contraindicated in patients with severe hepatic encephalopathy, hepatocellular carcinoma, severe hepatorenal
syndrome, and portal vein thrombosis.

Various surgical shunting procedures may be used to de- crease portal hypertension by diverting some of the
portal blood flow while allowing adequate liver perfusion. Currently, the surgical shunts most commonly
used are the portacaval shunt and the distal splenorenal shunt.

• Hepatic Encephalopathy. The goal of management of he- patic encephalopathy is the reduction of ammonia
formation. Ammonia formation in the intestines is reduced with lactulose, a drug that traps ammonia in the
gut. It can be given orally, as an enema, or through a nasogastric (NG) tube. The laxative ef- fect of the drug
expels the ammonia from the colon. Antibiotics such as rifaximin may also be given, particularly in patients
who do not respond to lactulose. Constipation should be prevented, and regular and frequent bowel
movements are necessary to minimize the ammonia buildup.

Control of hepatic encephalopathy also involves treatment of precipitating causes. This includes lowering
one’s dietary protein intake, preventing and controlling GI bleeds, and in the event of a bleed, removing the
blood promptly from the GI tract to decrease the protein accumulation in the gut.

Drug Therapy. There is no specific drug therapy for cirrhosis.However, a number of drugs are used to treat
symptoms and Complications of advanced liver disease.
Nutritional Therapy. The diet for the patient who has cir- rhosis without complications is high in calories
(3000 cal/day) with high carbohydrate content and moderate to low levels of fat. Protein restriction may be
appropriate in some patients im- mediately after a severe flare of symptoms (ie., episodic hepatic
encephalopathy). However, protein restriction is rarely justified in patients with cirrhosis and persistent
hepatic encephalopa- thy. For many patients, malnutrition is a more serious clinical problem than hepatic
encephalopathy.

A patient with alcoholic cirrhosis frequently has protein- calorie malnutrition. Oral nutritional supplements
containing protein from branched-chain amino acids that are metabolized by the muscles may be
recommended. These supplements provide protein that is more easily metabolized by the liver. Parenteral
nutrition or enteral nutrition therapy may be required, although rarely used, and only reserved for severe cases
of malnutrition.

The patient with ascites and edema is put on a low-sodium diet. The degree of sodium restriction depends on
the patient’s condition. Instruct the patient and caregiver about the degree of restriction. Table salt is a well-
known source of sodium, but sodium is also present in baking soda and baking powder. Foods that are high
in sodium content include canned soups and vegetables, many frozen foods, salted snacks (e.g.. potato chips),
nuts, smoked meats and fish, crackers, bread, olives, pickles, ketchup, and beer. Advise the patient to read
labels for sodium content. Provide suggestions to the patient and caregiver about how to make the diet more
palatable. Seasonings such as garlic, parsley, onion, lemon juice, and spices may make food more appetizing.
Collaborate with a dietitian regarding dietary strategies.
Nursing Management:
Nursing Assessment.

Subjective Data
• Important Health Information Past health history: Previous viral, toxic, or idiopathic hepatitis.
Alcohol intake, metabolic syndrome, chronic biliary obstruction and infection,Severe right-sided heart
failure
• Medications: Adverse reaction to any medication. Use of anticoagulants NSAIDs, acetaminophen
• Functional Health Patterns Health perception-health management: Chronic alcohol abuse Weakness,
fatigue Nutritional-metabolic: Anorexia, weight loss, dyspepsia, nausea and Vomiting, gingival bleeding
• Elimination: Dark urine, decreased urine output, light-colored or black stools, flatulence, change in bowel
habits. Dry, yellow skin,Bruising
• Cognitive-perceptual: Dull, right upper quadrant or epigastric pain.Numbness, tingling of extremities.
Pruritus •
• Sexuality-reproductive: Impotence, amenorrhea

Objective Data
• General Fever, cachexia, wasting of extremities
• Integumentary - Icteric sclera, jaundice, petechiae, ecchymoses, spider angiomas, palmar erythema,
alopecia, loss of axillary and pubic hair, peripheral, Edema
• Respiratory- Shallow, rapid respirations. Epistaxis
• Gastrointestinal - Abdominal distention, ascites, distended abdominal wall veins. Palpable liver and
spleen, foul breath. Hematemesis. Black, tarry stools. Hemorrhoids
• Neurologic - Altered mentation, asterixis
• Reproductive - Gynecomastia, testicular atrophy, and impotence (men); loss of libido in men and women;
amenorrhea or heavy menstrual bleeding (women)

Nursing Diagnoses
Nursing diagnoses for the patient with cirrhosis include:

• Impaired nutritional status

• Ineffective tissue perfusion
• Activity intolerance

Planning
The overall goals are that the patient with cirrhosis will (1) have relief of discomfort, (2) have minimal to no
complications (ascites, esophageal varices, hepatic encephalopathy), and (3) return to as normal a lifestyle as
possible.

Nursing Implementation
Health Promotion. Common risk factors for cirrhosis include alcoholism, malnutrition, viral hepatitis, biliary
obstruction, obesity, and right-sided heart failure. Prevention and early treatment of cirrhosis focus on reducing
or eliminating these risk factors. Urge patients to abstain from alcohol, and encourage

Those with a chronic alcohol use history to enroll in Alcoholics Anonymous or other support groups. Adequate
nutrition, especially for the person who abuses alcohol and other individuals at risk for cirrhosis, is essential to
promote normal liver regeneration. Identify and treat acute hepatitis early so that it does not progress to chronic
hepatitis and cirrhosis. Bariatric surgery for morbidly obese individuals reduces the incidence of NAFLD.

Acute Care, Nursing care for the patient with cirrhosis focuses on conserving the patient’s strength while
maintaining muscle strength and tone. When the patient requires complete bed rest, implement measures to
prevent pneumonia, thrombo- embolic problems, and pressure ulcers. Modify the activity and rest schedule
according to signs of clinical improvement (e.g.. decreasing jaundice, improvement in liver function studies).

Anorexia, nausea and vomiting, pressure from ascites, and poor eating habits all interfere with adequate intake of
nutrients. Oral hygiene before meals may improve the patient’s taste sensation. Make between-meal snacks
available so that the patient can eat them at times when food is best tolerated. Provide food preferences whenever
possible. Explain the reason for any dietary restrictions to the patient and caregiver.

Nursing assessment and care should include the patient’s physical status. Is jaundice present? Where is it
observed-sclera, skin, hard palate? What is the progression of jaundice? If the jaundice is accompanied by
pruritus, carry out measures to relieve itching. Cholestyramine or hydroxyzine may be ordered to help relieve the
pruritus. Other measures to alleviate pruritus include baking soda or moisturizing bath oils, lotions containing
calamine, anti-histamines, soft or old linens, and control of the temperature (not too hot and not too cold). Keep
the patient's nails short and clean. Teach patients to rub with their knuckles rather than a scratch with their nails
when they cannot resist scratching. Note the color of urine and stools and assess for improvement or
normalization of color. When jaundice is present, the urine is often dark brown and the stool is gray or tan.

Edema and ascites are frequent manifestations of cirrhosis and require nursing assessments and interventions.
Accurate calculation and recording of intake and output, daily weights, and measurements of extremities and
abdominal girth help in the ongoing assessment of the location and extent of the edema. Mark the abdomen with
a permanent marker so that the girth is measured at the same location each time.
Immediately before a paracentesis have the patient void to prevent puncturing of the bladder during the procedure.
Other nursing care associated with a paracentesis is outlined in Table 40.16.

Dyspnea is a frequent problem for the patient with severe ascites and can lead to pleural effusions. A semi-
Fowler’s or Fowler’s position allows for maximal respiratory efficiency. Use pillows to support the arms and
chest to increase the patient’s comfort and ability to breathe.

Meticulous skin care is essential because the edematous tissues are prone to breakdown. Use an alternating-air
pressure mattress or other special mattress. A turning schedule (minimum of every 2h) must be adhered to rigidly.
Support the abdomen with pil- lows. If the abdomen is taut, cleanse it gently. The patient will tend to avoid
moving because of abdominal discomfort and dyspnea. Range-of-motion exercises are helpful. Implement
measures such as coughing and deep breathing to prevent respiratory problems. The lower extremities may be
elevated. If scrotal edema is pres- ent, a scrotal support provides some comfort.

When the patient is taking diuretics, monitor the serum lev- els of sodium, potassium, chloride, and bicarbonate.
Monitor renal function (blood urea nitrogen [BUN], serum creatinine) routinely and with any change in the
diuretic dosage. Observe for signs of fluid and electrolyte imbalance, especially hypokale mia. May be manifested
by cardiac dysrhythmias, hypotension, tachycardia, and generalized muscle weakness. Water excess
(hyponatremia) is manifested by muscle cramping, weakness, lethargy, and confusion.

Observe for and provide nursing care for any hematologic problems. These include bleeding tendencies, anemia,
and in- creased susceptibility to infection.

Assess the patient’s response to altered body image resulting from jaundice, spider angiomas, palmar erythema,
ascites, and gynecomastia. The patient may experience anxiety and embar- rassment about these changes. Explain
these phenomena and be a supportive listener. Provide nursing care with concern and en- couragement to help the
patient maintain his or her self-esteem.

Bleeding Varices. If the patient has esophageal or gastric varices, observe for any signs of bleeding from the
varices, such as hematemesis and melena. If hematemesis occurs, assess the patient for hemorrhage, call the HCP,
and be ready to transfer the patient to the endoscopy suite and/or assist with equipment to control the bleeding.
The patient’s airway must be main- taimed. Patients with bleeding varices are usually admitted to the ICU.

Balloon tamponade may be used in patients who have bleeding that is unresponsive to band ligation or sclerother-
apy. When balloon tamponade is used, explain to the patient and caregiver the use of the tube and how it will be
inserted. Check the balloons for patency. It is usually the HCP’s respon- sibility to insert the tube by either the
nose or mouth. Then the gastric balloon is inflated with approximately 250 mL of air, and the tube is retracted
until resistance (lower esopha- geal sphincter) is felt. The tube is secured by placement of a piece of sponge or
foam rubber at the nostrils (nasal cuff). For continued bleeding, the esophageal balloon is then inflated. A
sphygmomanometer is used to measure and maintain the de- sired pressure at 20-40 mm Hg. The position of the
balloons is verified by X-ray.

Nursing care includes monitoring for complications of rup- ture or erosion of the esophagus, regurgitation and
aspiration of gastric contents, and occlusion of the airway by the balloon. If the gastric balloon breaks or is
deflated, the esophageal balloon will slip upward, obstructing the airway and causing asphyxia- tion. If this
happens, cut the tube or deflate the esophageal bal- loon. Keep scissors at the bedside. Minimize regurgitation by
oral and pharyngeal suctioning and by keeping the patient in a semi-Fowler’s position.

The patient is unable to swallow saliva because of the inflated esophageal balloon occluding the esophagus.
Encourage the patient to expectorate, and provide an emesis basin and tissues. Frequent oral and nasal care
provides relief from the taste of blood and irritation from mouth breathing.
Hepatic Encephalopathy.

Nursing care of the patient with hepatic encephalopathy focuses on maintaining a safe environment, sustaining
life, and assisting with measures to reduce the formation of ammonia. Patients with hepatic encephalopathy may
exhibit confusion and be at risk for falls or other injuries.

Assess the patient’s

(1) level of responsiveness (e.g., reflexes, pupillary reactions, orientation),

(2) sensory and motor abnormalities (eg, hyperreflexia, asterixis, Motor coordination),
(3) fluid and electrolyte imbalances,
(4) acid-base imbalances, and
(5) response to treatment measures.

Assess the neurologic status, including an exact description of the patient’s behavior at least every 2h. Plan your
care of the Patient based on the severity of the encephalopathy.

Institute measures to prevent falls or injuries. In addition, measures to minimize constipation are important to
reduce ammonia production. Give drugs, laxatives, and enemas as ordered. Encourage fluids, if not
contraindicated. Any GI bleeding may worsen encephalopathy. Assess the patient taking lactulose for diarrhea
and excessive fluid and electrolyte losses.

Control factors known to precipitate encephalopathy as much as possible, including anything that may cause
constipation (e.g., dehydration, opioid medications). In patients with altered levels of consciousness or whose
airway may become compromised, have safety measures and emergency equipment readily available.

Ambulatory Care. The patient with cirrhosis may be faced with a prolonged course and the possibility of life-
threatening problems and complications. The patient and caregiver need to understand the importance of continual
health care and medical supervision. Supportive measures include proper diet, rest, avoidance of potentially
hepatotoxic OTC drugs such as acetaminophen in high doses, and abstinence from alcohol. Abstinence from
alcohol is important and results in improvemet in most patients. However, some patients find abstinence
extremely difficult and require a lot of emotional support. Explore your own attitude toward the patient whose
cirrhosis is secondary to chronic alcohol use. Always provide care without being condescending or judgmental.
Treat patients with respect and concern for their well-being.

Cirrhosis is a chronic disease and people can live many years with symptoms and complications secondary to
cirrhosis. The patient is affected not only physically but also psychologically, socially, and economically. Major
lifestyle changes may be required, especially if chronic alcohol use is the primary cause. Provide information
regarding community support programs, such as Alcoholics Anonymous, for help with chronic alcohol use.
Teach the patient and caregiver about complications and when to seek medical attention. Include instructions
about adequate rest periods, how to detect early signs of complications, skin care, drug therapy side effects,
observation for bleeding, and protection from infection. Referral to a community or home health nurse may some-
times be necessary to ensure patient adherence to prescribed

Therapy. Home care for the patient with cirrhosis should focus on helping the patient with activities of daily living
while main- training the highest level of wellness possible.

Evaluation. The expected outcomes are that the patient with cirrhosis will

• Maintain food and fluid intake adequate to meet nutritional Needs

• Maintain skin integrity with relief of oedema and pruritus
• Have normal fluid and electrolyte balance
• Acknowledge and get treatment for a substance use problem
Recent research in the treatment of liver cirrhosis

Infusion of Anti-Fibrotic Vascular Cells to Cure Liver Cirrhosis

A new therapy that uses blood-vessel-lining cells to regenerate damaged tissue has the potential to treat liver
cirrhosis, Weill Cornell Medicine scientists demonstrate in new research.

The small-scale animal study, published in the October issue of Radiology, was a test of the basic feasibility of
the cell delivery technique and not designed to prove safety or effectiveness. Still, the researchers found that the
interventional therapy—a single, image-guided infusion of blood vessel cells called endothelial cells derived from
liver tissue—was followed by an apparent lessening of liver damage in pigs that had liver cirrhosis before the
treatment. If the scientists can replicate the findings in humans, it could offer an alternative treatment for liver
cirrhosis, which affects more than 600,000 people in the United States alone.

“There was a reduction in markers of cirrhosis and related injury to structures in the liver, and we didn’t see any
bleeding, clotting or other harm from the technique itself,” said first author Dr. Kyungmouk Steve Lee, an
assistant professor of radiology at Weill Cornell Medicine and an interventional radiologist at NewYork-
Presbyterian/Weill Cornell Medical Center.

Liver cirrhosis, which features chronic inflammation and fibrosis—an accumulation of fibrous, scar-like tissue—
is most commonly caused by chronic heavy drinking and chronic viral infection by the Hepatitis B and C viruses.
Most patients are unaware of their condition, which typically progresses to liver failure or liver cancer, and the
only truly effective treatment is a liver transplant.“The difference in the appearance of liver cells in the treated
versus untreated animals was impressive,” said senior author Dr. David Madoff, vice chair for academic affairs
in the Department of Radiology and a professor of radiology at Weill Cornell Medicine, and an interventional
radiologist at NewYork-Presbyterian/Weill Cornell Medical Center.

Scientists have been exploring the potential of stem cell and other cell therapies to regenerate fibrosis-damaged
organs including cirrhotic livers. One problem with this strategy is that inflammatory and other disease processes
within a damaged organ tend to create an inhospitable environment—or “niche”—for transplanted cells and even
for resident stem cells. Study co-author Dr. Shahin Rafii and colleagues have shown in prior work, however, that
vessel-lining endothelial cells can produce special organ-specific growth factors, known as angiocrine factors,
that restore a healthier niche and promote regeneration without provoking scarring.

“In the case of liver cirrhosis, blood vessels in the liver are damaged and fail to supply angiocrine factors that
promote regeneration. So the idea underlying this endothelial cell therapy is to rejuvenate that vascular niche,”
said Dr. Rafii, director of the Ansary Stem Cell Institute, the Arthur B. Belfer Professor of Genetic Medicine and
chief of the Division of Regenerative Medicine at Weill Cornell Medicine. Dr. Rafii is a co-founder and consultant
with equity in Angiocrine Bioscence, a cellular therapy company. “Accordingly, the remaining hepatocyte
progenitors in the liver can get the proper signals from angiocrine factors they need to suppress fibrosis and
regenerate liver tissue.”

For the study, the investigators harvested small quantities of endothelial cells from the liver vessels of eight pigs,
and multiplied the cells to large quantities in the laboratory. After inducing cirrhosis in each pig’s liver, the
researchers then treated half of the pigs in an interventional radiology suite by infusing the liver-specific
endothelial cells into a large vein that runs into the liver, using a small catheter inserted through the skin and
guided by ultrasound and live x-ray imaging.
Although the number of pigs in the study wasn’t large enough to determine the therapeutic effectiveness of the
technique, examination of the pigs’ livers three weeks after treatment revealed some striking differences between
treated and untreated animals. When the investigators examined samples of cells and tissues taken from the treated
pigs’ livers under the microscope, they found that the organ appeared much more like the livers of healthy pigs,
in contrast to the untreated livers.

“These were very encouraging results,” said Dr. Madoff, who is a member of the clinical advisory board with
equity in Angiocrine.

The Weill Cornell Medicine researchers now hope to conduct larger trials of the endothelial cell therapy in pigs
and, if they are successful, progress to clinical trials in humans. In principle, the investigators said, the cell therapy
could be used to treat not just cirrhosis but other forms of liver injury as well.

Dr. David Madoff, Dr. Kyungmouk Steve Lee, Dr. Shahin Rafii, Research, News from WCM
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