alcohol withdrawal A condition that occurs after stopping heavy and prolonged alcohol intake; results in tremors, acute confusion, psychotic behaviors (such as delusions and hallucinations), and autonomic symptoms including tachycardia, elevated blood pressure, and diaphoresis.
ascites The collection of free fluid in the peritoneal cavity caused by increased hydrostatic pressure from portal hypertension.
asterixis A coarse tremor characterized by rapid, nonrhythmic extensions and flexions in the wrists and fingers (hand flapping).
cirrhosis A disease characterized by widespread fibrotic (scarred) bands of connective tissue that change the liver’s anatomy and physiology.
ecchymoses Large purple, blue, or yellow bruises.
esophageal varices A complication of cirrhosis in which fragile, thin-walled esophageal veins become distended and tortuous from increased pressure (portal hypertension).
fetor hepaticus The distinctive breath odor of chronic liver disease and hepatic encephalopathy that is characterized by a fruity or musty odor.
hepatic encephalopathy (also called portal-systemic encephalopathy [PSE]) A complex cognitive syndrome that is caused by liver failure and cirrhosis.
hepatitis Widespread inflammation and infection of liver cells.
hepatomegaly Liver enlargement that commonly occurs in patients with early cirrhosis.
hepatopulmonary syndrome A complication of cirrhosis caused by excessive ascitic volume and manifested by dyspnea as a result of intraabdominal pressure, which limits thoracic expansion and diaphragmatic excursion.
hepatorenal syndrome A late complication of cirrhosis affecting the kidneys and manifested by oliguria, elevated blood urea nitrogen (BUN) and creatinine levels, and increased urine osmolarity.
icterus Yellow coloration of the eye sclerae.
jaundice Yellowish coloration of the skin caused by increased serum bilirubin.
nonalcoholic fatty liver disease (NAFLD) A liver disease associated with obesity, diabetes mellitus type 2, and metabolic syndrome that occurs when the liver stores excessive amounts of fat from the body unrelated to alcohol consumption.
nonalcoholic steatohepatitis (NASH) An advanced form of nonalcoholic fatty liver disease.
paracentesis An invasive procedure performed to remove abdominal fluid in patients who have massive ascites.
petechiae Round, pinpoint, red-purple hemorrhagic lesions.
portal hypertension A major complication of cirrhosis resulting in persistent increase in pressure within the portal vein from 3 mm Hg to at least 10 mm Hg.
splenomegaly Spleen enlargement.
spontaneous bacterial peritonitis (SBP) An infection that results from bacteria collected in ascitic fluid.
transjugular intrahepatic portal-systemic shunt (TIPS) An interventional radiologic procedure performed in patients who have not responded to other modalities to manage hemorrhage or long-term ascites.
ultrasound transient elastography A noninvasive imaging test that measures liver stiffness, which helps the primary health care provider determine the amount of liver disease present.
http://evolve.elsevier.com/Iggy/
PRIORITY AND INTERRELATED CONCEPTS
The priority concepts for this chapter are:
• Cellular Regulation
• Infection
The Cellular Regulation concept exemplar for this chapter is Cirrhosis.
The Infection concept exemplar for this chapter is Hepatitis.
The interrelated concepts for this chapter are:
• Inflammation
• Nutrition
As the largest and one of the most vital internal organs, the liver performs more than 400 functions and affects all body systems. Common problems of the liver have an impact on cellular regulation and nutrition. Liver conditions range in severity from mild hepatic inflammation and infection to chronic end-stage cirrhosis. Chapter 3 briefly reviews these concepts.
CELLULAR REGULATION CONCEPT EXEMPLAR: CIRRHOSIS
Cirrhosis is extensive, irreversible scarring of the liver, usually caused by a chronic reaction to hepatic inflammation and necrosis. This scarring process directly impairs cellular regulation. Cirrhosis typically develops slowly and has a progressive, prolonged, destructive course resulting in end-stage liver disease.
Pathophysiology Review
Cirrhosis is characterized by widespread fibrotic (scarred) bands of connective tissue that change the liver’s anatomy and physiology. Inflammation caused by toxins or disease results in extensive degeneration and destruction of hepatocytes (liver cells). As cirrhosis develops, the tissue becomes nodular. These nodules can block bile ducts and normal blood flow throughout the liver. Impairments in blood and lymph flow occur due to compression caused by excessive fibrous tissue. During early cirrhosis, the liver is usually enlarged and firm. As the pathologic process continues, the liver shrinks in size and becomes harder, resulting in decreased liver function over weeks to years. Some patients with cirrhosis have no symptoms until serious complications occur. Impaired liver function results in elevated serum liver enzymes.
Cirrhosis of the liver can be divided into several common types, depending on the cause of the disease (Rogers, 2023):
• Postnecrotic cirrhosis (caused by viral hepatitis [especially hepatitis C] and certain drugs or other toxins)
• Alcoholic (Laennec’s) cirrhosis (caused by chronic alcoholism)
• Biliary cirrhosis (also called cholestatic; caused by chronic biliary obstruction or autoimmune disease)
Complications of Cirrhosis
Complications associated with hepatic cirrhosis depend on the amount of damage sustained by the liver. In compensated cirrhosis, the liver is scarred and cellular regulation is impaired, but the organ can still perform essential functions without causing major symptoms. In decompensated cirrhosis, liver function is impaired with obvious signs and symptoms of liver failure.
The loss of hepatic function contributes to development of metabolic abnormalities. Hepatic cell damage may lead to these common complications:
• Portal hypertension
• Ascites and esophageal varices
• Biliary obstruction
• Hepatic encephalopathy
Portal Hypertension
Portal hypertension is a persistent increase in pressure within the portal vein from 3 mm Hg to at least 10 mm Hg. This phenomenon is a major complication of cirrhosis. It results from increased resistance to or obstruction (blockage) of the flow of blood through the portal vein and its branches. The blood meets resistance to flow and seeks collateral (alternative) venous channels around the high-pressure area.
Blood flow backs into the spleen, causing splenomegaly (spleen enlargement). Veins in the esophagus, stomach, intestines, abdomen, and rectum become dilated. Portal hypertension can result in ascites (excessive abdominal [peritoneal] fluid), esophageal varices (distended veins), prominent abdominal veins (caput medusae), and hemorrhoids.
Ascites and Gastroesophageal Varices
Ascites is the collection of free fluid within the peritoneal cavity caused by increased hydrostatic pressure from portal hypertension. The collection of plasma proteins in the peritoneal fluid reduces the amount of circulating plasma proteins in the blood. When this decrease is combined with the inability of the liver to produce albumin because of impaired liver cell functioning, the serum colloid osmotic pressure is decreased in the circulatory system. The result is a fluid shift from the vascular system into the abdomen, a form of “third spacing.” As a result, the patient may have hypovolemia and edema at the same time (Rogers, 2023).
Massive ascites may cause renal vasoconstriction, triggering the renin-angiotensin system. This results in sodium and water retention, which increases hydrostatic pressure and the vascular volume and leads to more ascites.
As a result of portal hypertension, the blood backs up from the liver and enters the esophageal and gastric veins. Esophageal varices occur when fragile, thin-walled esophageal veins become distended and tortuous from increased pressure. The potential for varices to bleed depends on size, which can be determined through direct endoscopic observation. Varices occur most often in the distal esophagus but can be present also in the stomach and rectum.
Decreased prothrombin production occurs with cirrhosis and puts the patient at risk for bleeding. Bleeding esophageal varices are a life-threatening medical emergency. Severe blood loss may occur, resulting in shock from hypovolemia. Bleeding may present as either hematemesis (vomiting blood) or melena (black, tarry stools). Loss of consciousness may occur before any observed bleeding. Variceal bleeding can occur spontaneously with no precipitating factors. However, any activity that increases abdominal pressure may increase the likelihood of variceal bleeding, including heavy lifting or vigorous physical exercise. In addition, chest trauma or dry, hard food in the esophagus can cause bleeding.
Patients with portal hypertension may have portal hypertensive gastropathy. This complication can occur with or without esophageal varices. Slow gastric mucosal bleeding occurs, which may result in chronic slow blood loss, occult-positive stools, and anemia.
Splenomegaly results from the backup of blood into the spleen. The enlarged spleen destroys platelets, causing thrombocytopenia (low serum platelet count) and increased risk for bleeding. Thrombocytopenia is often the first clinical sign of liver dysfunction.
Biliary Obstruction
Cirrhosis causes liver bile production to decrease. This prevents the absorption of fat-soluble vitamins (e.g., vitamin K). Without vitamin K, clotting factors II, VII, IX, and X are not produced in sufficient quantities, and the patient is susceptible to bleeding and easy bruising. These abnormalities are confirmed by coagulation studies. Some patients have a genetic predisposition to obstruction of the bile duct that leads to biliary cirrhosis—typically from gallbladder disease or an autoimmune disease called primary biliary cirrhosis (PBC).
Jaundice (yellowish coloration of the skin) in cirrhosis is caused by one of two mechanisms: hepatocellular disease or intrahepatic obstruction (Fig. 50.1). Hepatocellular jaundice develops because the liver cells cannot effectively excrete bilirubin. This decreased excretion results in excessive circulating bilirubin levels. Intrahepatic obstructive jaundice results from edema, fibrosis, or scarring of the hepatic bile channels and bile ducts, which interferes with normal bile and bilirubin excretion. Patients with both types of jaundice often report pruritus (itching).
Hepatic Encephalopathy
Hepatic encephalopathy (also called portal-systemic encephalopathy [PSE]) is a complex cognitive syndrome caused by liver failure and cirrhosis. Early symptoms of this complication include sleep disturbance, mood disturbance, mental status changes, and speech problems. Hepatic encephalopathy may be reversible with early intervention. Later neurologic symptoms include an altered level of consciousness, impaired thinking processes, and neuromuscular problems.
FIG. 50.1 (A and B) Jaundice as a result of liver dysfunction such as cirrhosis and hepatitis. A from Leonard, P. C. [2020]. Quick and easy medical terminology [9th ed.]. St. Louis: Elsevier. B from Michelettie, R. G., James, W. D., Elston, D. M., & McMahon, P. J. [2023]. Andrew’s diseases of the skin clinical atlas [2nd ed.]. St. Louis: Elsevier.
Hepatic encephalopathy may develop slowly in patients with chronic liver disease and go undetected until the later stages. Symptoms develop rapidly in acute liver dysfunction. Four stages of development have been identified (Box 50.1). The patient’s symptoms may gradually progress to coma or fluctuate among the four stages.
Exact mechanisms of hepatic encephalopathy are not clearly understood, but likely are the result of shunting of portal venous blood into the central circulation, so the liver is bypassed. As a result, substances absorbed by the intestine are not broken down or detoxified and may lead to metabolic abnormalities, such as elevated serum ammonia and gamma-aminobutyric acid (GABA). Elevated serum ammonia results from the inability of the liver to detoxify protein by-products and is common in patients with hepatic encephalopathy. However, it is not a clear indicator of the presence of encephalopathy. Some patients may have major impairment without high elevations of serum ammonia, and elevations of ammonia can occur without evidence of encephalopathy.
BOX 50.1 Key FeaturesStages of Hepatic Encephalopathy
Stage I: Subtle manifestations that may not be recognized immediately
• Personality changes
• Behavior changes (agitation, belligerence)
• Emotional lability (euphoria, depression)
• Impaired thinking
• Inability to concentrate
• Fatigue, drowsiness
• Slurred or slowed speech
• Sleep pattern disturbances
Stage II: Continuing mental changes
• Mental confusion
• Disorientation to person, place, time, or situation
• Asterixis (hand flapping)
Stage III: Progressive deterioration
• Marked mental confusion
• Stuporous, drowsy but arousable
• Abnormal electroencephalogram tracing
• Muscle twitching
• Hyperreflexia
• Asterixis (hand flapping)
Stage IV: Unresponsiveness, preceding death in patients who progress to this stage
• Unarousable, obtunded
• No response to painful stimulus
• No asterixis
• Positive Babinski sign
• Muscle rigidity
• Fetor hepaticus (characteristic liver breath—musty, sweet odor)
• Seizures
Factors that may contribute to or worsen hepatic encephalopathy in patients with cirrhosis include:
• High-protein diet
• Infection
• Hypovolemia (decreased fluid volume)
• Hypokalemia (decreased serum potassium)
• Constipation
• GI bleeding (causes a large protein load in the intestines)
• Drugs (e.g., hypnotics, opioids, sedatives, analgesics, diuretics, illicit drugs)
The prognosis depends on the severity of the underlying cause, precipitating factors, and degree of liver dysfunction (Rogers, 2023).
Other Complications
Development of hepatorenal syndrome indicates a poor prognosis for the patient with liver failure. This is often the cause of death in these patients. This syndrome is manifested by:
• A sudden decrease in urinary flow (<500 mL/24 hr) (oliguria)
• Elevated blood urea nitrogen (BUN) and creatinine levels with abnormally decreased urine sodium excretion
• Increased urine osmolarity
Hepatorenal syndrome often occurs after clinical deterioration from GI bleeding or the onset of hepatic encephalopathy. This may also complicate other liver diseases, including acute hepatitis and fulminant liver failure.
Patients with cirrhosis and ascites may develop acute spontaneous bacterial peritonitis (SBP). Those with very advanced liver disease are more susceptible to SBP. Bacteria responsible for SBP are typically from the bowel and reach the ascitic fluid after migrating through the bowel wall and the lymphatic system. Symptoms vary but may include malaise, fever, chills, pain (especially in the abdomen), and tenderness. However, symptoms can also be minimal with only mild indicators in the absence of fever. Worsening encephalopathy and increased jaundice may also be present without abdominal symptoms (Tholey, 2021).
Confirmation of SBP is typically made with paracentesis. During this procedure a sample of ascitic fluid is obtained by placing a needle into the peritoneal cavity. Following the procedure, the fluid is sent for diagnostic testing (cell count and culture). An ascitic fluid leukocyte count of more than 250 polymorphonuclear (PMN) leukocytes may indicate the need for treatment (Pagana et al., 2022).
Another major complication of cirrhosis is hepatopulmonary syndrome caused by excessive ascitic volume. The patient experiences dyspnea due to increased intraabdominal pressure, which limits thoracic expansion and diaphragmatic excursion.
Etiology and Genetic Risk
The most common causes of cirrhosis in the United States are chronic alcohol use, chronic viral hepatitis, and bile duct disease. Nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) can also lead to cirrhosis.
Hepatitis C is a bloodborne illness that usually causes chronic disease and compromises the body’s immunity. This infection is the leading cause of cirrhosis and liver cancer in the United States (American Liver Foundation, 2023a). Inflammation caused by infection over time leads to progressive scarring of the liver. It usually takes decades for cirrhosis to develop, although alcohol use in combination with hepatitis C may speed the process.
PATIENT-CENTERED CARE: VETERAN HEALTH
Veterans and Hepatitis C
Veterans are at a high risk for hepatitis C viral infection, especially individuals who served during the Vietnam and post-Vietnam era due to exposures when assisting wounded comrades, sharing toothbrushes and razors, and using unsanitary tattoo equipment. In addition, the device used for military mandatory vaccinations in the late 1990s was a needleless “jet gun” that could have contributed to transmitting hepatitis C (Elliott et al., 2021). When caring for veterans, assess whether they have been tested for hepatitis C. If they have not been tested, provide information on how they can be tested or consult with the primary health care provider to arrange for testing in the health care setting.
Hepatitis B and hepatitis D are the most common causes of cirrhosis worldwide. Hepatitis B also causes inflammation and low-grade damage over decades that can ultimately lead to cirrhosis. Hepatitis D virus (HDV) can infect the liver but only in people who already have hepatitis B (see discussion in Infection Concept Exemplar: Hepatitis).
Cirrhosis may also occur due to nonalcoholic fatty liver disease (NAFLD). NAFLD is most closely tied to obesity, diabetes mellitus type 2, and metabolic syndrome and is covered later in this chapter.
Another common cause of cirrhosis is excessive and prolonged alcohol use. Alcohol has a direct toxic effect on the hepatocytes and causes liver inflammation (alcoholic hepatitis). The liver becomes enlarged, with cellular degeneration and infiltration by fat, leukocytes, and lymphocytes. Over time, the inflammatory process decreases and the destructive phase increases. Early scar formation is caused by fibroblast infiltration and collagen formation. Damage to the liver tissue progresses as malnutrition and repeated exposure to the alcohol continue. If alcohol is withheld, the fatty infiltration and inflammation are reversible. If alcohol use continues, widespread scar tissue formation and fibrosis infiltrate the liver due to cellular necrosis. The long-term use of illicit drugs, such as cocaine, has similar effects on the liver.
PATIENT-CENTERED CARE: GENDER HEALTH
Effect of Alcohol Related to Gender
The amount of alcohol necessary to cause cirrhosis varies widely from individual to individual, but notably there are gender differences. Two or three drinks per day over a minimum of 10 years may be all it takes for women to develop cirrhosis. For men, six drinks per day over the same time frame may cause the same level of liver damage. However, a smaller amount of alcohol over a long period of time can increase memory loss from alcohol toxicity of the cerebral cortex. Binge drinking can increase risk for hepatitis and fatty liver (Rogers, 2023).
Incidence and Prevalence
Chronic liver disease and cirrhosis combined account for a large number of deaths in the United States. About 2.7 million people in the United States have hepatitis C (American Liver Foundation, 2023c) and as many as 2.2 million American have hepatitis B (American Liver Foundation, 2023b). In Canada the estimated prevalence of hepatitis B is between 250,000 and 450,000 (Public Health Agency of Canada, 2021). It is more challenging to quantify the exact number of Canadians with liver disease, but it is thought that as many as 1 in 4 Canadians are affected by liver disease (Canadian Liver Foundation, 2021).
Health Promotion/Disease Prevention
Two of the most common causes of cirrhosis are chronic hepatitis C infection and chronic alcohol use. These problems are discussed later in this chapter. Objectives to improve the incidence and management of liver diseases are included as part of the Healthy People 2030 initiative (Box 50.2).
BOX 50.2 Meeting Healthy People 2030 ObjectivesLiver Diseases
Two objectives for individuals with liver diseases are included in the Healthy People 2030 initiative:
• Reduce cirrhosis deaths.
• Increase the proportion of people who have cleared hepatitis C infection.
Therefore it is essential that nurses teach individuals the importance of avoiding risk factors that contribute to or cause cirrhosis and hepatitis C (discussed later in this chapter).
Interprofessional Collaborative Care
Care for the patient with cirrhosis can take place in various settings by many members of the interprofessional health care team. These patients may, at different times, self-manage at home, be hospitalized for acute complications, need rehabilitative care, or be cared for in the community setting, including possible hospice care.
PATIENT-CENTERED CARE: HEALTH EQUITY
Health Equity Issues Related to Cirrhosis
When compared with White patients with cirrhosis, Black patients with cirrhosis have a higher rate of hospital admission, longer length of stay during each hospitalization, and a higher 90-day hospital readmission rate, even though the quality of care is the same for both groups. Factors contributing to these differences include a lower median outcome for Blacks, a lack of transportation or access to health care, and a higher incidence of coronary artery disease and diabetes mellitus, which contribute to the incidence of cirrhosis complications (Spiewak et al., 2020). Nurses need to be aware of these social determinants of health as part of the patient’s plan of care. Provide information on community resources for transportation and health care access. Teach patients how to help ensure prevention or self-care management of comorbid chronic diseases.
Recognize Cues: Assessment
History
Obtain data from patients with suspected cirrhosis, including age, gender, and employment history, especially history of exposure to alcohol, drugs (prescribed and illicit), use of herbal preparations, and chemical toxins. Keep in mind that all exposures are important, regardless of how long ago they occurred. Determine whether there has ever been a needlestick injury. Sexual history and orientation may be important in determining an infectious cause for liver disease, because men having sex with men (MSM) are at high risk for hepatitis A, hepatitis B, and hepatitis C (Rogers, 2023).
Inquire about whether there is a family history of alcoholism and/or liver disease. Ask patients to describe their alcohol intake, including the amount consumed during a given period. Is there a history of illicit drug use, including oral, IV, and intranasal forms? Does the patient have tattoos? If so, ask about when and where they were obtained. Has the patient been in the military or in prison? Is the patient a health care worker, firefighter, or police officer? For patients previously or currently in an alcohol or drug recovery program, how long have they been sober? These questions can be difficult to answer and bring up sensitive topics. Be sure to establish why you are asking these questions and accept answers in a nonjudgmental manner. Provide privacy during the interview. For many people, the behaviors causing the liver disease occurred years before the onset of their current illness, and they may be regretful or embarrassed.
Ask the patient about previous medical conditions, such as an episode of jaundice or acute viral hepatitis, biliary tract disorders (such as cholecystitis [gallbladder inflammation]), viral infection, surgery, blood transfusions, autoimmune disorders, obesity, altered lipid profile, heart failure, respiratory disorders, or liver injury.
Physical Assessment/Signs and Symptoms
Because cirrhosis has a slow onset, many of the early signs and symptoms are vague and nonspecific. Assess for:
• Fatigue
• Significant change in weight
• GI symptoms, such as anorexia and vomiting
• Pain in the abdominal area and liver tenderness (both of which may be ignored by the patient)
Liver function problems are often found during a routine physical examination or when laboratory tests are completed for an unrelated illness or problem. The patient with compensated cirrhosis may be completely unaware that there is a liver problem. The first sign may present before the onset of symptoms when routine laboratory tests, presurgical evaluations, or life and health insurance assessments show abnormalities. These tests could indicate abnormal liver function or thrombocytopenia (decreased serum platelet count), necessitating a more thorough diagnostic workup.
The development of late signs of advanced cirrhosis (also called end-stage liver failure) usually causes the patient to seek medical treatment. GI bleeding, jaundice, ascites, and spontaneous bruising indicate poor liver function and complications of cirrhosis.
Thoroughly assess all body systems of the patient with liver dysfunction or failure because it affects the entire body. The clinical picture and course vary from patient to patient, depending on the severity of the disease. Assess for the common late disease signs and symptoms outlined in Box 50.3.
Abdominal Assessment
Massive ascites can be detected as a distended abdomen with bulging flanks (Fig. 50.2). The umbilicus may protrude and dilated abdominal veins (caput medusae) may radiate from the umbilicus. Ascites can cause physical problems including orthopnea, and dyspnea from increased abdominal distention can interfere with lung expansion. The patient may have difficulty maintaining an erect body posture, and problems with balance may affect walking. Inspect and palpate for the presence of inguinal or umbilical hernias, which may develop because of increased intraabdominal pressure. Minimal ascites is often more difficult to detect, especially in the obese patient.
When performing an assessment of the abdomen, keep in mind that hepatomegaly (liver enlargement) occurs in many cases of early cirrhosis. Splenomegaly is common in nonalcoholic causes of cirrhosis. As the liver deteriorates, it usually becomes hard and smaller with nodules.
FIG. 50.2 Patient with abdominal ascites in late-stage cirrhosis. From Leonard, P. C. [2020]. Quick and easy medical terminology [9th ed.]. St. Louis: Elsevier.
BOX 50.3 Key FeaturesLate-Stage Cirrhosis
• Jaundice and icterus (yellow coloration of the eye sclera)
• Dry skin
• Pruritus (itchy skin)
• Rashes
• Purpuric lesions, such as petechiae (round, pinpoint, red-purple hemorrhagic lesions) or ecchymoses (large purple, blue, or yellow bruises)
• Warm and bright red/hyperpigmented palms of the hands (palmar erythema)
• Vascular lesions with a red center and radiating branches, known as spider angiomas (also called telangiectasias, spider nevi, or vascular spiders), on the nose, cheeks, upper thorax, and shoulders
• Abdominal ascites
• Peripheral dependent edema of the extremities and sacrum
• Vitamin deficiency (especially fat-soluble vitamins A, D, E, and K)
Measure the patient’s abdominal girth to evaluate the progression of ascites (see Fig. 50.2). For measurement of abdominal girth, the patient lies flat while the examiner pulls a tape measure around the largest diameter (usually over the umbilicus) of the abdomen. The girth is measured at the end of exhalation. The abdominal skin and flanks should be marked to ensure the same tape measure placement on subsequent readings. However, a rapid increase in body weight is the most reliable indicator of fluid retention.
Other Physical Assessments
Observe any vomitus and stool for blood. This may be indicated by frank blood in the excrement or by a positive fecal occult blood test (FOBT). Gastritis, stomach ulceration, or oozing esophageal varices may be responsible for the blood in the stool. Note the presence of fetor hepaticus, which is the distinctive breath odor associated with chronic liver disease and hepatic encephalopathy and is characterized by a fruity or musty odor. Amenorrhea (no menstrual period) may occur in women. Men may exhibit testicular atrophy, gynecomastia (enlarged breasts), and impotence related to inactive hormones.
Continually assess the patient’s neurologic function; it may also be helpful to include family members in conversations about the patient’s baseline mental status if the patient is unable to effectively communicate. Subtle changes in mental status and personality often progress to coma—a late complication of hepatic encephalopathy. Monitor for asterixis—a coarse tremor characterized by rapid, nonrhythmic extensions and flexions in the wrists and fingers (hand flapping).
Psychosocial Assessment
Patients with hepatic cirrhosis may undergo subtle or obvious personality, cognitive, and behavior changes. They may experience sleep pattern disturbances or exhibit signs of emotional lability (fluctuations in emotions), euphoria (a very elevated mood), or depression. A psychosocial assessment identifies needs and helps guide care.
Repeated hospitalizations are common for patients with cirrhosis. It is a life-altering chronic disease that affects not only the patient but also the immediate and extended family members and significant others. There are significant emotional, physical, and financial changes. Substance use may continue even as health worsens. Use available community resources whenever possible. Collaborate with social workers, substance use counselors, and mental health/behavioral health care professionals as needed for patient assessment and management.
Part of the psychosocial assessment is to determine if the patient is alcohol dependent. If this is the case, the health care team should observe and prepare for alcohol withdrawal. Alcohol withdrawal occurs after stopping alcohol intake after heavy and prolonged use. Monitor for tremors, sometimes called the “jitters,” which can begin as early as 6 to 8 hours after alcohol cessation. Cognitive and neurologic changes associated with delirium tremens (DTs) may include acute confusion, anxiety, and psychotic behaviors, such as delusions and hallucinations. Autonomic changes may include tachycardia, elevated blood pressure, and diaphoresis (Elliott, 2019). Care of the patient experiencing withdrawal can be a medical emergency. Consult professional resources for more information about caring for the alcohol-dependent patient.
Laboratory Assessment
Laboratory study abnormalities are common in patients with liver disease (Table 50.1). Serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactate dehydrogenase (LDH) typically are elevated because these enzymes are released into the blood during hepatic inflammation. However, as the liver deteriorates, the hepatocytes may be unable to create an inflammatory response, and the AST and ALT levels may be normal. ALT levels are more specific to the liver, whereas AST can be found in muscle, kidney, brain, and heart. An AST/ALT ratio greater than 1.0 is usually found in alcoholic liver disease (Pagana et al., 2022).
TABLE 50.1
Significance of Abnormal Laboratory Findings in Liver Disease
Abnormal Finding Significance
Serum Enzymes
Elevated serum aspartate aminotransferase (AST) Hepatic cell destruction, hepatitis
Elevated serum alanine aminotransferase (ALT) Hepatic cell destruction, hepatitis (most specific indicator)
Elevated lactate dehydrogenase (LDH) Hepatic cell destruction
Elevated serum alkaline phosphatase Obstructive jaundice, hepatic metastasis
Elevated gamma-glutamyl transpeptidase (GGT) Biliary obstruction, cirrhosis
Bilirubin
Elevated serum total bilirubin Hepatic cell disease
Elevated serum direct conjugated bilirubin Hepatitis, liver metastasis
Elevated serum indirect unconjugated bilirubin Cirrhosis
Elevated urine bilirubin Hepatocellular obstruction, viral or toxic liver disease
Elevated urine urobilinogen Hepatic dysfunction
Serum Proteins
Increased serum total protein Acute liver disease
Decreased serum total protein Chronic liver disease
Decreased serum albumin Severe liver disease
Elevated serum globulin Immune response to liver disease
Other Tests
Increased serum creatinine Indication of kidney damage related to hepatorenal syndrome
Elevated serum ammonia Advanced liver disease or hepatic encephalopathy
Prolonged prothrombin time (PT) or international normalized ratio (INR) Hepatic cell damage and decreased synthesis of prothrombin
Increased alkaline phosphatase and gamma-glutamyl transpeptidase (GGT) levels are caused by biliary obstruction and therefore may increase in patients with cirrhosis. Alkaline phosphatase is a nonspecific bone, intestinal, and liver enzyme. Total serum bilirubin levels also rise. Indirect bilirubin levels increase in patients with cirrhosis because of the inability of the failing liver to excrete bilirubin. Because of this, bilirubin is present in the urine (urobilinogen) in increased amounts. Fecal urobilinogen concentration is decreased in patients with biliary tract obstruction. These patients have light- or clay-colored stools.
Total serum albumin levels are decreased in patients with severe or chronic liver disease as a result of decreased synthesis by the liver. Loss of osmotic “pull” proteins such as albumin promotes the movement of intravascular fluid into the interstitial tissues (e.g., ascites). Prothrombin time/international normalized ratio (PT/INR) is prolonged because the liver decreases the production of prothrombin. The platelet count is low, resulting in a characteristic thrombocytopenia of cirrhosis. Anemia may be reflected by decreased red blood cell (RBC), hemoglobin, and hematocrit values. The white blood cell (WBC) count may also be decreased. Ammonia levels are usually elevated in patients with advanced liver disease. Serum creatinine may be elevated in patients with deteriorating kidney function. Dilutional hyponatremia (low serum sodium) may occur in patients with ascites.
NCLEX Examination Challenge 50.1
Physiological Integrity
The nurse is assessing a client diagnosed with advanced liver cirrhosis. Which abnormal serum laboratory finding would the nurse anticipate for this client?
A. Elevated ammonia
B. Increased albumin
C. Decreased alkaline phosphatase
D. Decreased alanine aminotransferase
Imaging Assessment
Plain x-rays of the abdomen may show hepatomegaly, splenomegaly, or massive ascites. A CT scan may be requested. MRI is another test used to diagnose the patient with liver disease. This test can reveal mass lesions, giving additional specific information. MRI results are helpful in determining whether the condition is malignant or benign.
Other Diagnostic Assessments
Ultrasonography (US) of the liver is often the first assessment for an adult with suspected liver disease to detect ascites, hepatomegaly, and splenomegaly. It can also determine the presence of biliary stones or biliary duct obstruction. Liver US with Doppler is useful in detecting portal vein thrombosis and evaluating whether the direction of portal blood flow is normal.
Ultrasound transient elastography is a noninvasive test that measures liver stiffness, which helps the primary health care provider determine the amount of liver disease present. The normal amount of stiffness is 5.0 kilopascals (kPa). Higher degrees of stiffness indicate liver fibrosis. More than 13 kPa indicates that the patient has cirrhosis. The imaging study may not be as reliable in patients who have excessive ascites or obesity (Barr et al., 2020).
A liver biopsy may be necessary to determine the exact pathology and the extent of disease progression. This procedure can be problematic because patients with liver disease are at risk for bleeding. Even a percutaneous (through the skin) biopsy can pose a significant risk to the patient. To minimize this risk, an interventional radiologist can perform a liver biopsy by using a long sheath through a jugular vein, which then is threaded into the hepatic vein and liver. A tissue sample is obtained for microscopic evaluation. If a biopsy procedure is not possible, a radioisotope liver scan may be used to identify cirrhosis or other diffuse disease.
The primary health care provider may request arteriography if US is not conclusive in finding portal vein thrombosis. To evaluate the portal vein and its branches, a portal venogram may be performed instead by passing a catheter into the liver and portal vein.
The primary health care provider may perform an esophagogastroduodenoscopy (EGD) to directly visualize the upper GI tract to detect complications of liver failure. These complications may include bleeding or oozing esophageal varices, stomach irritation and ulceration, or duodenal ulceration and bleeding. EGD is performed by introducing a flexible fiberoptic endoscope into the mouth, esophagus, and stomach while the patient is under moderate sedation. The scope has a camera attached that permits direct visualization of the mucosal lining of the upper GI tract. In endoscopic retrograde cholangiopancreatography (ERCP), an endoscope is used to inject contrast material via the sphincter of Oddi to view the biliary tract and allow for stone removals, sphincterotomies, biopsies, and stent placements if required. These procedures are described in more detail in Chapter 45.
Analyze Cues and Prioritize Hypotheses: Analysis
The priority collaborative problems for patients with cirrhosis include:
1. Fluid overload due to third spacing of abdominal and peripheral fluid (ascites)
2. Potential for hemorrhage due to portal hypertension and subsequent GI varices
3. Acute confusion and other cognitive changes due to increased serum ammonia levels and/or alcohol withdrawal
4. Pruritus due to increased serum bilirubin and jaundice
Generate Solutions and Take Actions: Planning and Implementation
Managing Fluid Volume
Planning: Expected Outcomes
The patient with cirrhosis is expected to have less excess fluid volume as evidenced by decreased ascites and peripheral edema while maintaining an adequate circulatory volume.
Interventions
Fluid accumulations are minimal during the early stages of cirrhosis. During this stage nursing and interprofessional interventions are aimed at preventing the accumulation of additional fluid and decreasing any existing fluid collection. Nonsurgical treatment measures are used to treat ascites in most cases.
Supportive measures to control abdominal ascites include nutrition therapy, drug therapy, paracentesis, and respiratory support. The patient’s fluid and electrolyte balance is carefully monitored during the treatment period.
Nutrition Therapy
The primary health care provider usually places the patient with early abdominal ascites on a low-sodium diet as an initial means of controlling fluid accumulation. The amount of daily sodium (Na+) intake restriction varies, but a 1- to 2-g (2000 mg) Na+ restriction may be tried first. Collaborate with a registered dietitian nutritionist to explain the purpose of the restriction and advise the patient and family to read the sodium content labels on all food and beverages. Table salt should be completely excluded. Low-sodium diets may be difficult to tolerate, so suggest alternative flavoring additives such as lemon, vinegar, parsley, oregano, and pepper. Remind patients that seasoned and salty food is an acquired taste; in time, they will become used to the decrease in dietary sodium.
Patients with late-stage cirrhosis are usually malnourished and have multiple dietary deficiencies. IV vitamin supplements such as thiamine, folate, and multivitamin preparations are typically given because the liver cannot store vitamins. For patients with biliary cirrhosis, bile may not be available for fat-soluble vitamin transport and absorption. A study by Chaney et al. (2020) found that malnutrition associated with end-stage cirrhosis caused patients to require multiple hospitalizations (see the Evidence-Based Practice box).
EVIDENCE-BASED PRACTICE
What Is the Effect of Malnutrition in Patients With Cirrhosis?
The purpose of this study was to determine the incidence and outcomes of malnutrition in patients with end-stage liver cirrhosis. A retrospective medical record review of 134 patients waiting for liver transplant was conducted using the Subjective Global Assessment score at the time of transplant evaluation, at follow-up nutritional visits, and at the time of transplant. Findings showed that malnutrition was present in 51.9% of patients at end-stage cirrhosis on their initial nutritional visit but increased to 61% by the time of transplant. Most patients had to wait over 180 days to obtain a transplant. During that wait time, increasing malnutrition led to more than 53% of patients being hospitalized.
Level of Evidence: 4
This was a descriptive study using a convenience sample.
Commentary: Implications for Practice and Research
This study demonstrated that malnutrition in patients who have end-stage cirrhosis leads to or contributes to hospitalizations, which increases health care costs and decreases quality of life. Nurses can help identify patients who have or are at risk for developing malnutrition and refer them to a registered dietitian nutritionist who can create an individualized plan of care to manage their nutritional status. More research is needed on the role of nurses in performing nutritional screening and the best evidence-based nutritional interventions that lead to more positive outcomes.
Chaney, A., Rawal, B., Harnois, D., et al. (2020). Nutritional assessment and malnutrition in patients with cirrhosis. Gastroenterology Nursing, 43(4), 284–291.
Drug Therapy
A diuretic is usually prescribed by the primary health care provider to reduce fluid accumulation and prevent cardiac and respiratory problems. Monitor the effect of diuretic therapy by weighing the patient daily, measuring daily intake and output, measuring abdominal girth, documenting peripheral edema, and assessing electrolyte levels. Serious fluid and electrolyte imbalances, such as dehydration, hypokalemia (decreased potassium), and hyponatremia (decreased sodium), may occur with loop diuretic therapy. Depending on the diuretic selected, the provider may prescribe an oral or IV potassium supplement. Some clinicians prescribe furosemide and spironolactone as a combination diuretic therapy for the treatment of ascites. Because these drugs work differently, they are used for preservation of sodium and potassium balance.
All patients with ascites have the potential to develop spontaneous bacterial peritonitis (SBP) from bacteria in the collected ascitic fluid. Mild symptoms such as low-grade fever and loss of appetite occur may occur in some patients. In others, there may be abdominal pain, fever, and change in mental status. When performing an abdominal assessment, listen for bowel sounds and assess for abdominal wall rigidity. Treatment involves IV antibiotics including cephalosporins or fluroquinolones.
Paracentesis
Abdominal paracentesis may be needed if ascites affects a patient’s respiratory effort. Paracentesis is an invasive procedure performed to remove abdominal fluid. The procedure is performed at the bedside, in an interventional radiology department, or in an ambulatory care setting. During this procedure the primary health care provider inserts a trocar catheter or drain into the abdomen to remove the ascitic fluid from the peritoneal cavity. This procedure is done using ultrasound for added safety. A short-term ascites drain catheter may be placed while the patient is awaiting surgical intervention, or tunneled ascites drains can allow a patient or family caregiver to drain ascitic fluid at home. Nursing implications associated with this procedure are described in Box 50.4.
If SBP is suspected, a sample of fluid is withdrawn and sent for cell count and culture. For the patient with symptoms of infection, the primary health care provider may prescribe antibiotics while awaiting the culture results.
Respiratory Support
Excessive ascitic fluid volume may cause patients to have respiratory problems. They may develop hepatopulmonary syndrome. Dyspnea develops due to increased intraabdominal pressure, which limits thoracic expansion and diaphragmatic excursion. Auscultate lungs every 4 to 8 hours for crackles or other adventitious breath sounds that could indicate pulmonary complications.
BOX 50.4 Best Practice for Patient Safety and Quality CareThe Patient Having a Paracentesis
• Explain the procedure and answer patient questions.
• Obtain vital signs, including weight, before the procedure.
• Ask the patient to void before the procedure to prevent injury to the bladder.
• Position the patient in bed with the head of the bed elevated.
• Monitor vital signs per protocol or primary health care provider request during the procedure.
• Measure the drainage and record precisely.
• Document the characteristics of the collected fluid.
• Label and send the fluid for laboratory analysis; document in the patient health record that specimens were sent.
• After the catheter has been removed, apply a dressing to the site; assess for leakage.
• Maintain bed rest per protocol.
• Take vital signs and weigh the patient after the paracentesis; document in the patient record the weight both before and after paracentesis. (The patient should experience a weight loss due to fluid removal.)
NURSING SAFETY PRIORITY
Action Alert
For patients with hepatopulmonary syndrome, monitor their oxygen saturation with pulse oximetry. If needed, notify the primary care provider and obtain an order for oxygen therapy to ease breathing. Elevate the head of the bed to at least 30 degrees or as high as the patient wants in order to improve breathing. This position with feet elevated to decrease dependent ankle edema often relieves dyspnea. Remind assistive personnel to weigh the patient daily every morning before breakfast using the same scale.
Fluid and electrolyte balance problems are common as a result of the disease or treatment. Laboratory tests, such as blood urea nitrogen (BUN), serum protein, hematocrit, and electrolytes, help determine fluid and electrolyte status. Elevated BUN, decreased serum proteins, and increased hematocrit may indicate hypovolemia.
When medical management fails to control ascites, the primary health care provider may choose to divert ascites into the venous system by creating a shunt. Patients with ascites are poor surgical risks. The transjugular intrahepatic portal-systemic shunt (TIPS) is a nonsurgical procedure that is used to control long-term ascites and reduce variceal bleeding. This procedure is described in the discussion of Interventions in the Preventing or Managing Hemorrhage section that follows.
Preventing or Managing Hemorrhage
Planning: Expected Outcomes
The patient is expected to be free of bleeding episodes. However, a hemorrhage is present, it is expected to be controlled by prompt, evidence-based interventions. Esophageal variceal bleeds are the most common cause of upper GI bleeding (also see Chapter 47 on management of upper GI bleeding).
Interventions
All patients with cirrhosis should be screened for esophageal varices by endoscopy to detect them early before they bleed. When patients have varices, they are placed on preventive therapy. If acute bleeding occurs, early interventions are used to manage it. Because massive esophageal bleeding can cause rapid blood loss, emergency interventions are needed.
The role of early drug therapy is to prevent bleeding and infection in patients who have varices. A nonselective beta-blocking agent such as propranolol is usually prescribed to prevent bleeding. Decreasing the heart rate and the hepatic venous pressure gradient may reduce the chance of bleeding. Monitor the patient’s vital signs for bradycardia and hypotension.
Up to 20% of patients with cirrhosis who are admitted to the hospital as a result of upper GI bleeding have bacterial infection, and even more patients develop health care–associated infection. Infection is one of the most common indicators that patients will have an acute variceal bleed (AVB). Therefore patients with cirrhosis with GI bleeding should receive antibiotics when admitted to the hospital.
When bleeding occurs, the health care team intervenes quickly to control it by combining vasoactive drugs with endoscopic therapies. Vasoactive drugs, such as octreotide acetate and vasopressin, reduce blood flow through vasoconstriction to decrease portal pressure. Octreotide also suppresses secretion of gastrin, serotonin, and intestinal peptides, which decreases GI blood flow to help with pressure reduction within the varices. Vasopressin is rarely used because it is a very potent drug and has several adverse effects (Sole et al., 2021).
Endoscopic therapies include ligation of the bleeding veins or sclerotherapy. Both procedures are very effective in controlling bleeding and improving patient survival rates. Esophageal varices may be managed with endoscopic variceal ligation (EVL) (banding). This procedure involves the application of small “O” bands around the base of the varices to decrease their blood supply. The patient is unaware of the bands, and they cause no discomfort.
Endoscopic sclerotherapy (EST), also called injection sclerotherapy, is a method used to control bleeding. The varices are injected with a sclerosing agent via a catheter. Complications of this procedure include mucosal ulceration, which could result in further bleeding.
Rescue therapies may be warranted if bleeding recurs. These therapies include a second endoscopic procedure, balloon tamponade and esophageal stents, and shunting procedures. Short-term esophagogastric balloon tamponade with esophageal stents is a very effective way to control bleeding. However, the procedure can cause potentially life-threatening complications, such as aspiration, asphyxia, and esophageal perforation. Similar to a nasogastric tube (NGT), the tube is placed through the nose and into the stomach. An attached balloon is inflated to apply pressure to the bleeding variceal area. Before this tamponade, the patient is usually intubated and placed on a mechanical ventilator to protect the patient’s airway. This therapy is used if the patient is not able to have a second endoscopy or TIPS procedure.
The transjugular intrahepatic portal-systemic shunt (TIPS) is a nonsurgical procedure performed by an interventional radiologist. This procedure is used for patients who have not responded to other modalities for hemorrhage or long-term ascites. When the procedure is preformed nonemergently, patients have an ultrasound exam to assess jugular vein anatomy and patency. IV sedation or general anesthesia is used for this procedure. During the procedure the radiologist places a large sheath through the jugular vein. A needle is guided through the sheath and pushed through the liver into the portal vein, a balloon enlarges this tract, and a stent is placed to keep it open. Most patients also have an ultrasound study of the liver after the TIPS procedure to verify blood flow through the shunt. Patients undergoing the TIPS procedure who have esophageal/gastric varices and hemorrhage problems may also require esophageal/gastric vein embolization as a part of the procedure. Patients with severe liver cirrhosis usually have little flow through the liver parenchyma. These patients develop large portal-esophageal (or portal-gastric) veins diverting blood away from the diseased liver. Even after a successful TIPS, the diverting veins may persist and must be embolized (intentionally blocked) so they will not rebleed.
Serious complications of the TIPS procedure are not common. Patients are usually discharged in 1 or 2 days and are followed up with ultrasound studies for the first year after the shunt is placed, to ensure continued patency. Patients must also be monitored for hepatic encephalopathy, which can be caused by a TIPS. After creation of the TIPS, blood now bypasses most of the liver’s filtration processes, allowing toxins to circulate throughout the body. In some patients this can cause disturbances in consciousness and behavior. Lactulose or other medications are given to counteract this effect, and dietary modification may also be helpful. For severe cases a TIPS may have the flow reduced or closed completely to reverse the encephalopathy. This is done by deploying a smaller stent or occluding device inside the original TIPS. The decision can be a difficult one for the health care provider to make because reduction of flow through the shunt will likely cause the initial esophageal hemorrhaging to recur.
Patients receiving TIPS may have a significant elevation of their pulmonary artery pressure. This is a result of the sudden increase of blood flow to the right side of the heart. Diuretics help to treat this problem. For this reason, patients must be evaluated for right-sided heart failure before TIPS placement.
Depending on the procedure done to control esophageal bleeding, patients usually have a nasogastric tube (NGT) inserted to detect any new bleeding episodes. They often receive packed red blood cells, fresh frozen plasma, dextran, albumin, and platelets through large-bore IV catheters. Monitor vital signs every hour and check coagulation studies, including prothrombin time (PT), partial thromboplastin time (PTT), platelet count, and international normalized ratio (INR).
Preventing or Managing Confusion
Planning: Expected Outcomes
The patient is expected to be free of acute or chronic confusion. If it occurs, early intervention by the interprofessional health care team is the goal to maintain patient safety and prevent further health problems or death from encephalopathy.
Interventions
Collaborative interventions are planned around the management of slowing or stopping the accumulation of ammonia in the body to improve mental status and orientation. Assess the patient’s neurologic status, and monitor during treatment.
Because ammonia is formed in the GI tract by the action of bacteria on protein, nonsurgical treatment measures to decrease ammonia production include dietary modifications and drug therapy to reduce bacterial breakdown. Patients with cirrhosis have increased nutritional requirements—high-carbohydrate, moderate-fat, and high-protein foods. However, the diet may be changed for those who have elevated serum ammonia levels with signs of encephalopathy. Patients should have a moderate amount of protein and fat foods and simple carbohydrates. Strict protein restrictions are not required because patients require protein for healing. In collaboration with the registered dietitian nutritionist, be sure to include family members or significant others in nutrition counseling. The patient is often weak and unable to remember complicated guidelines. Brief, simple directions regarding dietary modifications are recommended. Keep in mind any financial, cultural, or personal implications and the patient’s food allergies when discussing food choices to provide optimal patient-centered care.
Drugs are used sparingly because they are difficult for a failing liver to metabolize. In particular, opioid analgesics, sedatives, and barbiturates should be limited, especially in the patient with a history of encephalopathy.
However, several types of drugs may eliminate or reduce ammonia levels in the body. These include lactulose or lactitol and nonabsorbable antibiotics. The primary health care provider may prescribe lactulose (or lactitol) to promote the excretion of ammonia in the stool. This drug is a viscous, sticky, sweet-tasting liquid that is given either orally or by NGT. This drug has a laxative effect. It works by increasing osmotic pressure to draw fluid into the colon and prevents absorption of ammonia in the colon. The drug may be prescribed to the patient who has manifested signs of encephalopathy, regardless of the stage (Burchum & Rosenthal, 2022). The desired effect of the drug is production of two or three soft stools per day and a decrease in patient confusion caused by increased ammonia.
Observe for response to lactulose and side effects including intestinal bloating and cramping. Serum ammonia levels are monitored but do not always correlate with symptoms. Hypokalemia and dehydration may result from excessive stools. Remind assistive personnel to support the patient’s personal and skin care to prevent breakdown caused by excessive stools.
Several nonabsorbable antibiotics may be given if lactulose does not help the patient meet the desired outcome or if the patient is unable tolerate the drug. These drugs should not be given together. Older adults can become weak and dehydrated from multiple stools. Neomycin sulfate or rifaximin, both broad-spectrum antibiotics, may be given to act as intestinal antiseptics. These drugs destroy the normal flora in the bowel, diminishing protein breakdown and decreasing the rate of ammonia production. Maintenance doses of neomycin are given orally but may also be administered as a retention enema. Long-term use has the potential for kidney toxicity, and therefore this agent is not commonly used for an extended period. It is not used in patients with existing kidney disease (Sole et al., 2021).
Frequently assess for changes in level of consciousness and orientation. Check for asterixis and fetor hepaticus. These signs suggest worsening encephalopathy. Thiamine supplements and benzodiazepines may be needed if the patient is at risk for alcohol withdrawal.
NCLEX Examination Challenge 50.2
Physiological Integrity
The nurse is caring for a client who experiences upper GI bleeding due to esophageal varices caused by cirrhosis. Which of the following interventions would the nurse anticipate as appropriate to manage the client’s bleeding? Select all that apply.
A. Administration of octreotide
B. Liver transplantation
C. Endoscopic sclerotherapy
D. Administration of lactulose
E. Administration of a beta-blocking agent
Managing Pruritus
Planning: Expected Outcomes
The patient is expected to experience decreased pruritus as a result of comfort measures and possibly drug therapy.
Interventions
Patients frequently report pruritus and dry skin due to jaundice from increased levels of serum bilirubin as cirrhosis progresses. Pruritus tends to increase in warmer conditions and in the early evening and at night. Comfort measures include avoiding being too warm, moisturizing the skin, and avoiding irritants to the skin. Some patients find that cool compresses and/or corticosteroid creams provide temporary relief. If these measures are not effective, drug therapy, including selective serotonin reuptake inhibitors such as sertraline, may be helpful.
Care Coordination and Transition Management
If patients with late-stage cirrhosis survive life-threatening complications, they are usually discharged to home or to a long-term care facility after treatment measures have managed acute medical problems. A home care referral may be needed if the patient is discharged to home. Chronically ill patients are often readmitted multiple times. Community-based care is aimed at optimizing comfort, promoting independence, supporting caregivers, and preventing rehospitalization.
INTERPROFESSIONAL COLLABORATION
Care of Patients With Cirrhosis
For patients with moderate to late-stage liver disease, collaborate with the case manager (CM) or other discharge planner to coordinate interprofessional continuing care. According to the Interprofessional Education Collaborative (IPEC) Expert Panel’s Competency of Roles and Responsibilities, using the unique and complementary abilities of other team members optimizes health and patient care (IPEC Expert Panel, 2016). Collaborate with health care team members to help the patient to be as independent as possible, including physical and occupational therapists. Patients with end-stage disease may benefit from hospice care.
Assess physical adaptations needed to prepare the patient’s home for recovery. The sleeping area needs to be close to a bathroom because diuretic and/or lactulose therapy increases the frequency of urination and stools. If the patient has difficulty reaching the toilet, additional equipment (e.g., bedside commode) is necessary. Special adult-size incontinence pads or briefs may be helpful if the patient has an altered mental status and incontinence. For the patient with shortness of breath from massive ascites, elevating the head of the bed and maintaining a semi-Fowler’s to high-Fowler’s position may help alleviate respiratory distress. Alternatively, a reclining chair with an elevated footrest may be used.
The patient who has a tunneled ascites drain is taught how to access the drain and remove excess fluid. Review the home care instructions that are provided with the drainage system with both the patient and family/caregiver. Remind them not to remove more than 2000 mL from the abdomen at one time to prevent hypovolemic shock.
The patient with encephalopathy often finds that small, frequent meals are best tolerated. If the nutritional intake or albumin/prealbumin is decreased after discharge, multivitamin and oral nutritional supplements are usually needed. Teach patients to avoid excessive vitamins and minerals that can be toxic to the liver, such as fat-soluble vitamins, excessive iron supplements, and niacin. Remind patients to check with their primary health care provider before taking any vitamin supplement.
Patients with bleeding from gastric ulcers may receive an H2-receptor antagonist agent or proton pump inhibitor to reduce acid reflux (see Chapter 47). Those with episodes of spontaneous bacterial peritonitis (SBP) may be on a daily low-dose maintenance antibiotic.
Teach family members how to recognize signs of encephalopathy and to contact the primary health care provider if these signs develop. Reinforce that constipation, bleeding, and infection can increase the risk for encephalopathy.
One of the most important aspects of ongoing care for the patient with cirrhosis is health teaching about the need for the client to avoid alcohol, smoking, and illicit drugs. Advise the patient to avoid all over-the-counter drugs, especially acetaminophen, NSAIDs, and liver-toxic herbs, vitamins, and minerals. Reinforce the need to keep appointments for follow-up medical care. Remind the patient and family to notify the primary health care provider immediately if any GI bleeding (overt bleeding or melena) is noted so that reevaluation can begin quickly.
The patient is discharged to the home setting with an individualized teaching plan that includes nutrition therapy, drug therapy, and alcohol abstinence The encephalopathic patient may need to be monitored for adherence to drug therapy and alcohol abstinence, if appropriate. Individual and group therapy sessions may be arranged to help patients deal with alcohol abstinence if they are too ill to attend a formal treatment program. Because some patients may have alienated relatives over the years because of substance use, it may be necessary to help them identify a friend, neighbor, or sponsor in their recovery group for support. Refer the patient and family to self-help groups, such as Alcoholics Anonymous and Al-Anon. In Canada, SMART Recovery offers similar support, as well as additional services to manage addictions.
The patient with cirrhosis may also desire spiritual or other psychosocial support. Finances are frequently a problem for the chronically ill patient and family; social support and community services need to be identified. The American Liver Foundation (www.liverfoundation.org) and American Gastroenterological Association (www.gastro.org) are excellent sources for more information about liver disease.
Some patients may receive a liver transplant, which is discussed later in this chapter. For patients who are not candidates for liver transplantation, address end-of-life issues. Discuss options such as hospice care with patients and their families (see Chapter 8). Be aware and prepared that the patient and family may go through a grieving process.
Evaluate Outcomes: Evaluation
Evaluate the care of the patient with cirrhosis based on the identified priority patient problems. The expected outcomes include that the patient will:
• Have a decrease in or have no ascites
• Achieve fluid and electrolyte balance
• Not have hemorrhage or will be managed immediately if bleeding occurs
• Not develop encephalopathy or will be managed immediately if it occurs
• Successfully abstain from alcohol or drugs (if disease is caused by one or more of these substances) and have adequate nutrition
NONALCOHOLIC FATTY LIVER DISEASE
Pathophysiology Review
Nonalcoholic fatty liver disease (NAFLD) occurs when the liver stores excessive amounts of fat from the body unrelated to alcohol consumption. NAFLD is primarily related to obesity, increased levels of cholesterol and triglycerides, diabetes mellitus type 2, and metabolic syndrome. Therefore, preventing obesity and practicing a healthy lifestyle, if possible, can decrease the risk of NAFLD.
Individuals carrying the patatin-like phospholipase domain-containing 3 gene (PNPLA3) have an increased risk of developing NAFLD. People of Latino decent have this gene more often and are therefore at the highest risk for NAFLD (Salari et al., 2021). Over the past decade the prevalence of NAFLD has increase dramatically. Currently it is estimated that 100 million Americans have NAFLD (Vacca, 2020).
Nonalcoholic steatohepatitis (NASH) is a more severe form of NAFLD. NASH is defined by increased liver inflammation, hepatocyte injury, and liver fibrosis (Rogers, 2023). Nearly 20% of those diagnosed with NAFLD will develop NASH (American Liver Foundation, 2023d). As NAFLD and NASH progress they contribute to liver cancer, cirrhosis, or failure, causing premature death.
Interprofessional Collaborative Care
Recognize Cues: Assessment
When examining the patient’s history, it is important to focus on risk factors for NAFLD. These include age, obesity, metabolic syndrome, and diabetes mellitus. Although risk factors may be present, many patients with NAFLD and NASH remain asymptomatic for years before they are diagnosed.
Physical Assessment
Initially these patients describe general symptoms including fatigue and malaise. Inquire about specific symptoms including right upper quadrant pain and pruritus (itching). Perform a comprehensive pain assessment if pain is present. Jaundice may also be present as the disease progresses.
Diagnostic Assessment
Laboratory findings for NAFLD and NASH include elevated ALT and AST, similar to those seen in other types of liver disease (see Table 50.1). Although important when establishing the presence of liver damage, increased liver enzymes cannot alone confirm the presence of NAFLD. The studies used to detect NAFLD are similar to those used for cirrhosis. Ultrasound transient elastography and liver biopsy are often used to gauge liver damage and level of liver fibrosis. These studies help to confirm the diagnosis of NAFLD and NASH (see Other Diagnostic Assessments in the Cirrhosis section of this chapter for in-depth discussion regarding these diagnostic procedures).
Take Actions: Interventions
Currently there are no approved drugs to treat NAFLD. Patient management relies primarily on lifestyle modifications aimed at weight and fat loss including nutrition, exercise, and behavioral changes (Vacca, 2020). These adjustments can be challenging and have an impact on the physical and psychosocial aspects of the patient’s life. With this in mind, it is important to use the interprofessional team approach including a registered dietitian nutritionist and qualified mental health practitioner.
INFECTION CONCEPT EXEMPLAR: HEPATITIS
Hepatitis is the widespread inflammation and infection of liver cells. Viral hepatitis, which can be acute or chronic, is the most common type. Less common types of hepatitis are caused by chemicals, drugs, and some herbs. This section discusses hepatitis caused by a virus. Viral hepatitis results from an infection caused by one of five categories of viruses:
• Hepatitis A virus (HAV)
• Hepatitis B virus (HBV)
• Hepatitis C virus (HCV)
• Hepatitis D virus (HDV)
• Hepatitis E virus (HEV)
Some cases of viral hepatitis are not caused by any of these viruses. These patients have non–A-E hepatitis. This section focuses on the most common viral types.
Pathophysiology Review
Liver injury with inflammation can develop after exposure to drugs and chemicals by inhalation, ingestion, or parenteral (IV) administration. Toxic and drug-induced hepatitis can result from exposure to hepatotoxins (e.g., industrial toxins, alcohol, and drugs). Hepatitis may also occur as a secondary infection during the course of infections with other viruses, such as Epstein-Barr, herpes simplex, varicella-zoster, and cytomegalovirus.
After the liver has been exposed to any causative agent (e.g., a virus), it becomes enlarged and congested with inflammatory cells, lymphocytes, and fluid, resulting in right upper quadrant pain and discomfort. As the disease progresses, the liver’s normal lobular pattern becomes distorted as cellular regulation is compromised due to widespread inflammation, necrosis, and hepatocellular regeneration. This distortion increases pressure within the portal circulation, interfering with the blood flow into the hepatic lobules. Edema of the liver’s bile channels results in obstructive jaundice.
Failure of the liver cells to regenerate, with progression of the necrotic process, results in a severe acute and often fatal form of hepatitis known as fulminant hepatitis. Hepatitis is considered chronic when liver inflammation lasts longer than 6 months. Chronic hepatitis usually occurs due to hepatitis B or hepatitis C. Superimposed infection with hepatitis D virus (HDV) in patients with chronic hepatitis B may also result in chronic hepatitis. Chronic hepatitis can lead to cirrhosis and liver cancer. Many patients have multiple infections, especially a combination of HBV with HCV, HDV, or human immunodeficiency virus (HIV) infections (Rogers, 2023).
Etiology and Genetic Risk
The five major types of acute viral hepatitis vary by etiology, mode of transmission, manner of onset, and incubation periods. Hepatitis cases must be reported to the local public health department, which then notifies the Centers for Disease Control and Prevention (CDC). Genetic factors do not play a major role in the cause of viral hepatitis.
Hepatitis A
The causative agent of hepatitis A, hepatitis A virus (HAV), is a ribonucleic acid (RNA) virus of the Enterovirus genus. It is a hardy virus and survives on human hands. The virus is resistant to detergents and acids but is destroyed by chlorine (bleach) and extremely high temperatures.
Hepatitis A usually has a mild course similar to a typical flulike infection and often goes unrecognized. It is spread most often by the fecal-oral route by fecal contamination either from person-to-person contact (e.g., oral-anal sexual activity) or by consuming contaminated food or water. Common sources of infection include shellfish caught in contaminated water and food contaminated by food handlers infected with HAV. The incubation period of hepatitis A is usually 15 to 50 days, with a peak of 25 to 30 days. The disease is usually not life-threatening, but it may be more severe in adults older than 40 years and those with preexisting liver disease such as hepatitis C (Rogers, 2023).
In a small percentage of hepatitis A cases, severe illness with extrahepatic signs and symptoms can occur. Advanced age and conditions such as chronic liver disease may cause widespread damage that requires a liver transplant. When the patient’s immunity is decreased, death may occur. Incidence of hepatitis A is particularly high in countries where sanitation is poor; however, cases are diagnosed internationally across the globe. Some adults have hepatitis A and do not know it. The course is similar to that of a GI illness, and the disease and recovery are usually uneventful.
Hepatitis B
The hepatitis B virus (HBV) is not transmitted like HAV. It is a double-shelled particle containing DNA composed of a core antigen (HBcAg), a surface antigen (HBsAg), and another antigen found within the core (HBeAg) that circulates in the blood. HBV may be spread through these common modes of transmission (Rogers, 2023):
• Unprotected sexual intercourse with an infected partner
• Sharing needles, syringes, or other drug-injection equipment
• Sharing razors or toothbrushes with an infected individual
• Accidental needlesticks or injuries from sharp instruments, primarily in health care workers (low incidence)
• Blood transfusions (that have not been screened for the virus, before 1992)
• Hemodialysis
• Direct contact with the blood or open sores of an infected individual
• Birth (spread from an infected mother to baby during birth)
In addition, patients with compromised immunity from either disease or drug therapy are more likely to develop hepatitis B. The clinical course of hepatitis B may be varied. Symptoms usually occur within 25 to 180 days of exposure.
Blood tests confirm the disease, although many individuals with hepatitis B have no symptoms. Most adults who get hepatitis B recover and clear the virus from their body and develop immunity. However, a small percentage of people do not develop immunity and become carriers. Hepatitis carriers can infect others even though they are not sick and have no obvious signs of hepatitis B. Chronic carriers are at high risk for cirrhosis and liver cancer. Because of the high number of newcomers from endemic areas, the incidence of hepatitis B has increased in the United States.
Hepatitis C
The hepatitis C virus is an enveloped, single-stranded RNA virus that is genetically unstable and has at least six known major genotypes. Transmission is via blood to blood. The rate of sexual transmission is very low in a single-couple relationship but increases with multiple sex partners or in men who have unprotected sex with men. HCV is contracted by (Chaney, 2019):
• Illicit IV drug needle sharing (highest incidence)
• Blood, blood products, or organ transplants received before 1992
• Baby boomers (adults born between 1945 and 1965)
• Needlestick injury with HCV-contaminated blood (health care workers at high risk)
• Hemodialysis
• Health care workers
• People who are incarcerated (prisoners)
• Sharing of drug paraphernalia
The disease is not transmitted by casual contact or intimate household contact. However, those infected are advised to not share razors, toothbrushes, or pierced earrings because microscopic blood may be on these items.
The incubation period ranges from 2 weeks to 6 months. Acute infection and illness are not common. Most people are completely unaware that they have been infected. They may be asymptomatic and not diagnosed until many months or years after the initial exposure when an abnormality is detected during a routine laboratory evaluation or when liver complications occur. Unlike with hepatitis B, most people infected with hepatitis C do not clear the virus, and a chronic infection develops.
HCV does damage to the body’s immunity over decades by causing a chronic inflammation in the liver that eventually causes the liver cells to scar. Scarring from chronic infection with either HBV or HCV frequently leads to cirrhosis, which is a risk factor for developing primary liver cancer (Rogers, 2023). Patients who develop liver cancer may have interventional radiologic procedures (such as transarterial chemoembolization [TACE]), cryotherapy, ablation, traditional chemotherapy, or selective internal radiation therapy (SIRT) (see Chapter 18 for more information on cancer management modalities and associated nursing care). Liver cancer can also occur as a metastatic disease process and is not associated with hepatitis or cirrhosis.
Hepatitis D
Hepatitis D (delta hepatitis) is caused by a defective RNA virus that needs the helper function of HBV. Therefore, it occurs only with HBV to cause viral replication. This usually develops into chronic disease. The incubation period is about 14 to 56 days. As with hepatitis B, the disease is transmitted primarily by parenteral routes, especially in patients who are IV drug users. Having sexual contact with someone with HDV is also a high-risk factor (Rogers, 2023).
Hepatitis E
The hepatitis E virus (HEV) causes a waterborne infection associated with epidemics in the Indian subcontinent, Asia, Africa, the Middle East, Mexico, and Central and South America. Many large outbreaks have occurred after heavy rains and flooding. Like hepatitis A, hepatitis E is caused by fecal contamination of food and water.
HEV is not commonly acquired in the United States. Most cases occur in those who have traveled to a country where HEV is endemic. Similar to hepatitis A, it is transmitted via the fecal-oral route with a similar clinical course. HEV has an incubation period of 15 to 64 days. There is no evidence at this time of a chronic form of the disease. The disease tends to be self-limiting and resolves on its own (CDC, 2020).
Incidence and Prevalence
The incidence of hepatitis A and hepatitis B is declining as a result of CDC recommendations for vaccination. However, hepatitis B and hepatitis C are a concern because of their association with cirrhosis and liver cancer. It is estimated that over 58 million people worldwide have chronic hepatitis C, with 1.5 million new cases occurring every year (World Health Organization [WHO], 2021).
Currently there is no vaccine for HCV. Patients may be treated with antiviral drug therapies. The desired outcome of treatment of HCV-infected patients is to reduce mortality and liver-related health adverse consequences, including end-stage liver disease and liver cancer. It is expected that the cases of HCV may rise over the next several decades due to increasing illicit drug use.
Health Promotion/Disease Prevention
Hepatitis vaccines for infants, children, and adolescents have helped to decrease the incidence of hepatitis A and hepatitis B. These vaccines are safe and not associated with major complications. Some adults are also advised to receive these immunizations.
Measures to prevent hepatitis A include:
• Proper handwashing, especially after handling shellfish
• Avoiding contaminated food or water (including tap water in countries with high incidence)
• Receiving immunoglobulin within 14 days if exposed to the virus
• Receiving the HAV vaccine before traveling to areas where the disease is common (e.g., Mexico, Caribbean)
• Receiving the vaccine if living or working in enclosed areas with others, such as college dormitories, correctional institutions, day-care centers, and long-term care facilities
Although there are also vaccines available to protect against hepatitis B virus (HBV) infection, objectives to improve the incidence and management of HBV and hepatitis C virus are included as part of the Healthy People 2030 initiative (Box 50.5).
A combination HAV and HBV vaccine is also available for adults. Immunization against HBV is recommended for the following groups:
BOX 50.5 Meeting Healthy People 2030 ObjectivesHepatitis A, B, and C
Several objectives to improve health related to liver infection include:
• Reduce the rate of hepatitis A.
• Reduce the rate of acute hepatitis B.
• Reduce the rate of acute hepatitis C.
• Increase the proportion of people who know they have chronic hepatitis B.
• Reduce the rate of deaths with hepatitis B as a cause.
• Increase the proportion of people who have cleared hepatitis C infection.
Teach individuals how to prevent these liver infections, including obtaining vaccines as available.
BOX 50.6 Best Practice for Patient Safety and Quality CarePrevention of Viral Hepatitis in Health Care Workers
• Use Standard Precautions to prevent the transmission of disease between patients or between patients and health care staff (see Chapter 19).
• Eliminate needles and other sharp instruments by substituting needleless systems (needlesticks are the major source of hepatitis B transmission in health care workers).
• Receive the hepatitis B vaccine, which is given in a series of three injections. This vaccine also prevents hepatitis D by preventing hepatitis B.
• For postexposure prevention of hepatitis A, seek medical attention immediately for immunoglobulin (Ig) administration.
• Report all cases of hepatitis to the local health department.
• People who have sexual intercourse with more than one partner
• People with sexually transmitted infection (STI) or a history of sexually transmitted infection (STI)
• Men having unprotected sex with men (MSM)
• People with any chronic liver disease (such as hepatitis C or cirrhosis)
• Patients with HIV infection
• People who are exposed to blood or body fluids in the workplace, including health care workers, firefighters, and police
• People in correctional facilities (prisoners)
• Patients needing immunosuppressant drugs
• Family members, household members, and sexual contacts of people with HBV infection
Multiple hepatitis C virus (HCV) genotypes have made it difficult to develop an effective vaccine against hepatitis C. Teach baby boomer adults to have a one-time screening test for HCV due to the high risk of this infection in this population (Chaney, 2019).
Additional measures to prevent viral hepatitis for health care workers and others in contact with infected patients are listed in Box 50.6.
Interprofessional Collaborative Care
Care for the patient with hepatitis can take place in various settings. These patients may, at different times, self-manage at home, be hospitalized for immediate concerns, or be cared for in the community setting.
Recognize Cues: Assessment
History
Ask patients whether they have known exposure to a person with hepatitis. For the patient who presents with few or no symptoms of liver disease but has abnormal laboratory tests (e.g., elevated alanine aminotransferase [ALT] or aspartate aminotransferase [AST] level), the patient history may need to include additional questions regarding risk factors.
Physical Assessment/Signs and Symptoms
Assess whether the patient has any of the signs and symptoms associated with most types of vital hepatitis as listed in Box 50.7. Although HCV may be asymptomatic for most adults, some patients with a new HCV infection can experience some of the following signs and symptoms.
Lightly palpate the right upper abdominal quadrant to assess for liver tenderness. The patient may report right upper quadrant pain with jarring movements. Inspect the skin, sclerae, and mucous membranes for jaundice. The patient may present for medical treatment only after jaundice appears, believing that other vague symptoms are related to a flulike syndrome.
Jaundice in hepatitis results from intrahepatic obstruction and is caused by edema of the liver’s bile channels. Dark urine and clay-colored stools are often reported by the patient. If possible, obtain a urine and stool specimen for visual inspection and laboratory analysis. The patient may also have skin abrasions from scratching because of pruritus (itching).
Patients with chronic HCV infection often have extrahepatic complications. Examples include:
• Depression
• Polyarthritis
• Myalgia
• Renal insufficiency
• Cognitive impairment
• Cardiovascular problems such as vasculitis and heart disease
Psychosocial Assessment
Viral hepatitis has various presentations; for most infected people the initial course is mild with few or no symptoms. The long-term complications of fibrosis and cirrhosis cause the more serious problem. This is especially true for patients who have chronic HBV and HCV infection.
BOX 50.7 Key FeaturesViral Hepatitis
• Abdominal pain
• Yellowish sclera (icterus)
• Arthralgia (joint pain) or myalgia (muscle pain)
• Diarrhea or constipation
• Light clay-colored stools
• Dark-yellow to brownish urine
• Jaundice
• Fever
• Fatigue
• Malaise
• Anorexia
• Nausea and vomiting
• Dry skin
• Pruritus (itching)
Patients may experience emotional problems that center on their feeling sick and fatigued. General malaise, inactivity, and vague symptoms contribute to depression. Some patients often feel guilty and are remorseful about decisions made that caused the disease. These feelings are most likely to occur when the source of infection is from drug use.
Infectious diseases such as hepatitis continue to have a social stigma. The patient may feel embarrassed by the precautions that are imposed in the hospital and continue to be necessary at home. This embarrassment may cause the patient to limit social interactions. Patients may be afraid that they will spread the virus to family and friends.
Family members may be concerned about contracting the virus and may distance themselves from the patient. Allow them to verbalize these feelings and explore the reasons for these fears. Educate the patient and family members about modes of transmission and clarify information as needed.
Patients may be unable to return to work for several weeks during the acute phases of illness. The loss of wages and the cost of hospitalization for a patient without insurance coverage may produce great anxiety and financial burden. This situation may last for months or years if hepatitis becomes chronic.
Laboratory Assessment
Hepatitis A, hepatitis B, and hepatitis C are usually confirmed by acute elevations in levels of liver enzymes, indicating liver cellular damage, and by specific serologic markers.
Levels of ALT and AST may rise into the thousands in acute or fulminant cases of hepatitis. Alkaline phosphatase levels may be normal or elevated. Serum total bilirubin levels are elevated and are consistent with the clinical appearance of jaundice.
The presence of hepatitis A is established when hepatitis A virus (HAV) antibodies (HAV-Ab/IgM) are found in the blood. Ongoing inflammation of the liver by HAV is indicated by the presence of immunoglobulin M (IgM) antibodies, which persist in the blood for 3 to 6 weeks. Previous infection is identified by the presence of immunoglobulin G (IgG) antibodies. These antibodies persist in the serum and provide permanent immunity to HAV (Pagana et al., 2022).
The presence of the hepatitis B virus (HBV) is established when serologic testing confirms the presence of hepatitis B antigen-antibody systems in the blood and a detectable viral count (HBV polymerase chain reaction [PCR] DNA). Antigens located on the surface (shell) of the virus (HBsAg) and IgM antibodies to hepatitis B core antigen (HBcAg) are the most significant serologic markers. The presence of these markers establishes the diagnosis of hepatitis B. The patient is infectious as long as hepatitis B surface antigen (HBsAg) is present in the blood. Persistence of this serologic marker after 6 months or longer indicates a carrier state or chronic hepatitis. HBsAg levels normally decline and disappear after the acute hepatitis B episode. The presence of antibodies to HBsAg in the blood indicates recovery and immunity to hepatitis B. People who have been vaccinated against HBV have a positive HBsAg because they also have immunity to the disease (Pagana et al., 2022).
To detect HCV infection, blood is tested for anti-HCV antibodies to HCV recombinant core antigen, NS3 gene, NS4 antigen, and NS5 antibody. The antibodies can be detected within 4 weeks of the infection (Pagana et al., 2022). To identify the actual circulating virus, the HCV RNA test is used. This confirms active virus and can measure the viral load. A diagnostic tool called the OraQuick HCV Rapid Antibody Test has the advantage of providing a quick diagnosis of the disease as a point-of-care test.
The presence of hepatitis D virus (HDV) can be confirmed by the identification of intrahepatic delta antigen or, more often, by a rise in the hepatitis D virus antibodies (HDV-Ab) titer. This increase can be seen within a few days of infection (Pagana et al., 2022).
Hepatitis E virus (HEV) testing is usually reserved for travelers with a history of hepatitis infection. HEV virus itself cannot be detected, so infection is identified by finding hepatitis E antibodies (HEV-Ab/IgM) in the patient’s blood.
Other Diagnostic Assessment
Liver biopsy may be used to confirm the diagnosis of hepatitis and establish the stage and grade of liver damage or cancer. Characteristic changes help the pathologist distinguish among a virus, drug, toxin, fatty liver, iron, and other disease. This procedure is usually performed in an ambulatory care setting as a percutaneous procedure (through the skin) after a local anesthetic is given. If coagulation is abnormal, it may be done using either a CT-guided or transjugular route to reduce the risk for pneumothorax or hemothorax. Ultrasound also may be used.
Analyze Cues and Prioritize Hypotheses: Analysis
The priority collaborative problems for patients with hepatitis include:
1. Weight loss due to complications associated with inflammation of the liver
2. Fatigue due to infection and decreased metabolic energy production
Generate Solutions and Take Actions: Planning and Implementation
The patient with viral hepatitis can be mildly or acutely ill, depending on the severity of the inflammation and infection. Most patients are not hospitalized, although older adults and those with dehydration may be admitted for a short-term stay. The plan of care for all patients with viral hepatitis is based on measures to rest the liver, promote hepatic regeneration, strengthen immunity, and prevent complications, if possible.
Promoting Nutrition
Planning: Expected Outcomes
The patient will maintain appropriate weight and nutrition status.
Interventions
Patients with hepatitis, especially hepatitis A, may decline food because of general malaise, anorexia, abdominal discomfort, or nausea. The patient’s diet should be high in carbohydrates and calories, with moderate amounts of fat and protein added after nausea and anorexia have subsided. Small, frequent meals are often preferable to three standard meals daily. Ask the patient about appealing food preferences because favorite foods are tolerated better than randomly selected foods. High-calorie snacks may be needed. Supplemental vitamins are often prescribed.
Managing Fatigue
Planning: Expected Outcomes
The patient will progressively exhibit increasing energy as evidenced by participation in ADLs and self-reported decrease in level of fatigue.
Interventions
During the acute stage of viral hepatitis, interventions are aimed at resting the inflamed liver to promote hepatic cell regeneration. Rest is an essential intervention to reduce the liver’s metabolic demands and increase its blood supply. Collaborative care is generally supportive. The patient is usually tired and expresses feelings of general malaise. Complete bedrest is usually not required, but rest periods alternating with periods of activity are indicated and are often enough to promote hepatic healing. Individualize the patient’s plan of care and change it as needed to reflect the severity of symptoms, fatigue, and results of liver function tests and enzyme determinations. Activities such as self-care and ambulating are gradually added to the activity schedule as tolerated.
Drugs are used sparingly for patients with hepatitis to allow the liver to rest. An antiemetic to relieve nausea may be prescribed. However, because of the life-threatening nature of chronic hepatitis B and hepatitis C, several drugs are given, including antiviral and immunomodulating drugs.
Two groups of drugs are approved for management of hepatitis B—interferon alfa preparations and nucleoside analogs. Examples of interferon alfa drugs include interferon alfa-2b and peginterferon alfa-2a. These drugs are not used as often today because newer, more effective medications are available. Examples of nucleoside analogs include lamivudine and adefovir (Table 50.2).
For many years, the standard of care for hepatitis C was pegylated (PEG) interferon alfa plus ribavirin. In the past decade, new direct-acting antiviral (DAA) drugs such as second-generation protease inhibitors (PIs) that target specific steps in HCV replication are being used with much more success and fewer side or adverse effects. The current standard of practice for hepatitis C treatment is that a patient’s drug regimen is determined by HCV viral genotype (American Association for the Study of Liver Diseases [AASLD], 2020). Examples of newer drugs, including second-generation PIs, are presented in Table 50.2. All these drugs can affect the immune system and make patients susceptible to infection. Teach patients to avoid crowds and people who could be infectious.
Care Coordination and Transition Management
Home care management varies according to the type of hepatitis and whether the disease is acute or chronic. A primary focus in any case is preventing the spread of the infection. For hepatitis transmitted by the fecal-oral route, careful handwashing and sanitary disposal of feces are important. Therefore patient and family education is very important.
NURSING SAFETY PRIORITY
Action Alert
Teach the patient with viral hepatitis and the family to use measures to prevent infection transmission. In addition, instruct the patient to avoid alcohol and check with the primary health care provider before taking any medication or vitamin, supplement, or herbal preparation.
Encourage the patient to increase activity gradually to prevent fatigue. Suggest that the patient eat small, frequent meals of high-carbohydrate foods and plan frequent rest periods.
Collaborate with the certified infection control practitioner and infectious disease specialist if needed in caring for these patients. These experts can suggest appropriate resources for the patient and family.
TABLE 50.2
Common Examples of Drug Therapy
Drug Therapy Used for Chronic Hepatitis B and Hepatitis C
Drug Category Selected Nursing Implications
Chronic Hepatitis B: Nucleoside Analogs
Tenofovir
Monitor kidney function. Drug is excreted through kidneys; monitoring for renal impairment is important.
Teach risk for falls to prevent fractures. Can cause bone demineralization.
Adefovir Monitor kidney function. Drug is excreted through kidneys; monitoring for renal impairment is important.
Lamivudine
Monitor kidney function. Drug is excreted through kidneys; monitoring for renal impairment is important.
Remind patient to not discontinue drug without consulting with primary health care provider. Discontinuation of drug can cause flareup of hepatitis B.
Entecavir Monitor kidney function. Teach the patient to avoid alcohol to prevent serious interaction. Drug is excreted through kidneys; monitoring for renal impairment is important.
Chronic Hepatitis C
Second-generation protease inhibitors:
• Glecaprevir
• Grazoprevir
• Simeprevir
• Paritaprevir
Monitor CBC and chemistry panel.
Instruct the patient on common reactions, such as rash, itching, nausea, and headache.
Kidney and liver function may become impaired, and electrolyte imbalances may occur when taking this drug.
NS5A Inhibitor Drug Combinations
Glecaprevir/pibrentasvir Ask if the patient has had any other type of hepatitis or cirrhosis. This combination drug can reactivate hepatitis B and cause liver failure. Teach patient about monitoring liver enzymes, especially ALT. The combination drug can cause liver toxicity, including an increase in liver enzymes.
Elbasvir/grazoprevir
Ask patients if they have a history of or current hepatitis B. The combination drug can reactivate hepatitis B and cause liver failure.
Teach patients about monitoring liver enzymes, especially ALT. The combination drug can cause liver toxicity, including an increase in liver enzymes.
Ledipasvir/sofosbuvir (for hepatitis C genotype 1 only)
Ask if the patient has had any other type of hepatitis or cirrhosis. This combination drug can reactivate hepatitis B and cause liver failure.
Do not give this drug to patients receiving amiodarone. If this drug combination is taken with amiodarone, the patient may experience severe symptomatic bradycardia and other cardiac problems, including chest pain.
NS5A-NS5B Polymerase Inhibitor
Sofosbuvir/velpatasvir (for almost all main types of hepatitis C)
Ask patients if they have a history of or current hepatitis B. The combination drug can reactivate hepatitis B and cause liver failure.
Teach patients that their liver enzymes must be monitored, especially ALT elevation.
ALT, Alanine aminotransferase; CBC, complete blood count.
Evaluate Outcomes: Evaluation
Evaluate the care of the patient with hepatitis based on the identified priority patient problems. The expected outcomes include that the patient will:
• Maintain adequate nutrition for body requirements
• Report increasing energy levels as the liver rests
• Achieve appropriate management of infection and inflammation
NCLEX Examination Challenge 50.3
Physiological Integrity
The nurse is planning health teaching for a client beginning glecaprevir therapy for hepatitis C. Which question is the most important for the nurse to ask prior to administering the first dose of this drug?
A. “Do you have a history of heart problems, such as palpitations?
B. “Have you ever had any type of hepatitis, especially hepatitis B?”
C. “Has anyone ever told you that your bones are weak?”
D. “Are you planning to travel to Mexico or the Caribbean?”
LIVER TRANSPLANTATION
The first liver transplant was performed in the United States the late 1960s. Over the past five decades this surgical procedure has become a common practice worldwide (Newman, 2020). Patients with end-stage liver disease or acute liver failure who have not responded to conventional medical or surgical intervention are potential candidates for liver transplantation.
Pathophysiology Review
Many diseases can cause liver failure. Cirrhosis (scarring of the liver) is the most common reason for liver transplants. Other common reasons include chronic hepatitis B and hepatitis C, bile duct diseases, autoimmune liver disease, alcoholic liver disease, and fatty liver disease.
A patient requiring transplantation has an extensive physiologic and psychological assessment and evaluation by primary health care providers and transplant coordinators. Alternative treatment should be extensively explored before designating a patient for a liver transplant. Patients who are not considered candidates for transplantation include those with:
• Severe cardiovascular instability with advanced cardiac disease
• Severe respiratory disease
• Metastatic tumors
• Inability to follow instructions regarding drug therapy and self-management
Liver transplantation has become the most effective treatment for an increasing number of patients with acute and chronic liver diseases. Inclusion and exclusion criteria vary among transplantation centers and are continually revised as treatment options change and surgical techniques improve.
Donor livers are obtained primarily from trauma victims who have not had liver damage. They are distributed through a nationwide program known as the United Network for Organ Sharing (UNOS). This system distributes deceased donor livers based on regional considerations and patient acuity. Candidates with the highest level of acuity receive highest priority.
The donor liver is transported to the surgery center in a solution that preserves the organ for up to 8 hours. During the deceased donor liver transplant (DDLT) surgery, the diseased liver is removed through an incision made in the upper abdomen. The new liver is carefully put in its place and attached to the patient’s blood vessels and bile ducts. This procedure can take many hours to complete and requires a highly specialized team and large volumes of fluid and blood replacement.
Living donors have also been used and are usually a close family member or a spouse. Living donor liver transplant (LDLT) is done on a voluntary basis after careful psychological and physiologic preparation and testing. The donor’s liver is resected (usually removal of one lobe) and implanted into the recipient after removal of the diseased liver. In both the donor and the recipient, the liver regenerates and grows to meet the demands of the body if there are no complications (see the Legal/Ethical Considerations box).
LEGAL/ETHICAL CONSIDERATIONS
Legal/Ethical Issues Related to Liver Transplantation
A number of legal-ethical issues have surfaced as liver transplantation has become more common and the need for donors has increased. The primary issues include:
• Ensuring that living donors are provided complete information about the risks associated with transplantation surgery (informed consent)
• Increased use of hepatitis C virus–infected livers for transplantation since direct-acting antiviral (DAA) therapy has become more available
• More men than women receive liver transplants despite using the Model for End-Stage Liver Disease (MELD) score to determine the urgency of need for transplant
• Fewer liver transplants are performed for patients from Black and Hispanic populations when compared with the White population
These issues reflect the ethical principles of nonmaleficence and beneficence. Nurses need to advocate for patients who are potential living donors and assess their knowledge of the morbidity and mortality associated with LDLT to prevent patient harm. Nurses also need to advocate for all patients if they have an urgent need for liver transplantation regardless of their race, ethnicity, or gender. Nursing research is needed to explore these issues and how nurses can be the most effective advocates.
Interprofessional Collaborative Care
Care of the patient undergoing liver transplantation requires an interprofessional team approach. Receiving a transplant has a major psychosocial impact. Transplant complications cause patients to be very anxious. In collaboration with the members of the interprofessional health care team, assure them and their families that these problems can be managed and are often treated successfully.
In the immediate postoperative period, the patient is managed in the critical care unit and requires meticulous monitoring and care. Although liver transplantations are commonly performed, complications can occur. Some problems can be managed medically, whereas others require later hospitalizations or removal of the transplant. Monitor for signs and symptoms of complications of surgery and immediately report them to the surgeon (Table 50.3). The most common complications are acute graft rejection, vascular or biliary obstruction, and infection.
The success rate for transplantations has greatly improved since the introduction many years ago of cyclosporine (cyclosporin A), an immunosuppressant drug. Today, many other antirejection drugs are used. (See Chapter 16 for a discussion of rejection and preventive drug therapy for organ transplantation.)
NURSING SAFETY PRIORITY
Action Alert
For the patient who has undergone liver transplantation, monitor for clinical signs and symptoms of rejection, which may include tachycardia, fever, pain in the right upper quadrant or flank, decreased bile pigment and volume, and increasing jaundice. Laboratory findings include elevated serum bilirubin, rising ALT and AST levels, elevated alkaline phosphatase levels, and increased prothrombin time/international normalized ratio (PT/INR) (Pagana et al., 2022).
TABLE 50.3
Assessment and Prevention of Common Postoperative Complications Associated With Liver Transplantation
Assessment Prevention
Acute Graft Rejection
Occurs from 7 to 14 days postoperatively. Manifested by tachycardia, fever, right upper quadrant (RUQ) or flank pain, diminished bile drainage or change in bile color, or increased jaundice
Laboratory changes: (1) increased levels of serum bilirubin, transaminases, and alkaline phosphatase; (2) prolonged prothrombin time
Prophylaxis with immunosuppressant agents, such as prednisone, tacrolimus, or cyclosporine (CSA)
Early diagnosis to treat with more potent antirejection drugs
Infection
Can occur at any time during recovery
Manifested by fever or excessive, foul-smelling drainage (urine, wound, or bile); other indicators depend on location and type of infection
Antibiotic prophylaxis; vaccinations
Frequent cultures of tubes, lines, and drainage
Early removal of invasive lines
Good handwashing
Early diagnosis and treatment with organism-specific antiinfective agents
Hepatic Complications (Bile Leakage, Abscess Formation, Hepatic Thrombosis)
Manifested by decreased bile drainage, increased RUQ abdominal pain with distention and guarding, nausea or vomiting, increased jaundice, and clay-colored stools
Laboratory changes: increased levels of serum bilirubin and transaminases
If present, keep T-tube in dependent position and secure to patient; empty frequently, recording quality and quantity of drainage
Report signs and symptoms to surgeon immediately
May need surgical intervention
Acute Kidney Injury
Caused by hypotension, antibiotics, cyclosporine, acute liver failure, or hypothermia
Indicators of hypothermia: shivering, hyperventilation, increased cardiac output, vasoconstriction, and alkalemia
Early indicators of acute kidney injury: changes in urine output, increased blood urea nitrogen (BUN) and creatinine levels, and electrolyte imbalance
Monitor all drug levels with nephrotoxic side effects
Prevent hypotension
Observe for early signs of acute kidney injury and report them immediately to the surgeon
Transplant rejection is treated aggressively with immunosuppressive drugs. If therapy is not effective, liver function rapidly deteriorates. Multisystem organ failure, including respiratory and renal involvement, develops along with diffuse coagulopathies and portal-systemic encephalopathy (PSE). The only alternative for treatment is emergency retransplantation.
Infection is another potential threat to the transplanted graft and the patient’s survival. Immunosuppressant therapy, which must be used to prevent and treat organ rejection, significantly increases the patient’s risk for infection. Other risk factors include the presence of multiple tubes and intravascular lines, immobility, and prolonged anesthesia. Vaccinations and prophylactic antibiotics are helpful in protecting from infection.
In the early posttransplantation period, common infections include pneumonia, wound infections, and urinary tract infections. Opportunistic infections usually develop after the first postoperative month and include cytomegalovirus, mycobacterial infections, and parasitic infections. Latent infections such as tuberculosis and herpes simplex may be reactivated.
The primary health care provider prescribes broad-spectrum antibiotics for prophylaxis during and after surgery. Obtain culture specimens from all lines and tubes and collect specimens for culture at predetermined time intervals as dictated by the agency’s policy. If an infection is detected, the primary health care provider prescribes organism-specific antiinfective agents. The patient should be taught to contact the primary health care provider at any time that signs of infection are present.
The biliary anastomosis is susceptible to breakdown, obstruction, and infection. If leakage occurs or if the site becomes necrotic or obstructed, an abscess can form or peritonitis, bacteremia, and cirrhosis may develop. Observe for potential complications, which are listed in Table 50.3.
NURSING SAFETY PRIORITY
Action Alert
For the patient who has had a liver transplantation, monitor the temperature frequently per hospital protocol and report elevations, increased abdominal pain, distention, and rigidity, which are indicators of peritonitis. Nursing assessment also includes monitoring for a change in neurologic status that could indicate encephalopathy from a nonfunctioning liver. Report signs of clotting problems (e.g., bloody oozing from a catheter, petechiae, ecchymosis) to the surgeon immediately because they may indicate impaired function of the transplanted liver.
Teach patients to be aware of side effects of immunosuppressive drugs, such as hypertension, nephrotoxicity, drug-induced infection, and GI disturbances. Remind them that long-term management of care includes surveillance for malignancy, metabolic syndrome, and diabetes. Teaching the patient self-examination for skin, breast, and testicular malignancies and reminders for annual Papanicolaou (Pap) smears and other cancer screening tests are important. Posttransplant patients need to maintain lifestyle changes to increase their longevity after surgery.