Ascites is the collection of free fluid within the peritoneal cavity caused by increased hydrostatic pressure from portal hypertension (McCance et al., 2010). The collection of plasma protein in the peritoneal fluid reduces the amount of circulating plasma protein 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.

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 their size; size is determined by direct endoscopic observation. Varices occur most often in the distal esophagus but can also be present in the stomach and rectum.

Bleeding esophageal varices is a life-threatening medical emergency. Severe blood loss may occur, resulting in shock from hypovolemia. The bleeding may be 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 a variceal bleed, 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 also 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 (enlarged spleen) 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 that a patient has liver dysfunction.

Biliary Obstruction

In patients with cirrhosis, the production of bile in the liver is decreased. 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.

Jaundice (yellowish coloration of the skin) in patients with cirrhosis is caused by one of two mechanisms: hepatocellular disease or intrahepatic obstruction (Table 61-1). 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 jaundice often report pruritus (itching).

TABLE 61-1 LABORATORY DIAGNOSTIC DIFFERENTIATION OF JAUNDICE

Hepatic Encephalopathy

Hepatic encephalopathy (also called portal-systemic encephalopathy [PSE]) is a complex cognitive syndrome that results from liver failure and cirrhosis. Patients report sleep disturbance, mood disturbance, mental status changes, and speech problems early as this complication begins. Hepatic encephalopathy may be reversible with early intervention. Later neurologic symptoms include an altered level of consciousness, impaired thinking processes, and neuromuscular problems.

Hepatic encephalopathy may develop slowly in patients with chronic liver disease and go undetected until the late stages. Symptoms develop rapidly in acute liver dysfunction. Four stages of development have been identified: prodromal, impending, stuporous, and comatose (Table 61-2). The patient’s symptoms may gradually progress to coma or fluctuate among the four stages.

TABLE 61-2 STAGES OF PORTAL-SYSTEMIC ENCEPHALOPATHY

Stage I Prodromal	Stage III Stuporous
• 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	• Progressive deterioration • Marked mental confusion • Stuporous, drowsy but arousable • Abnormal electroencephalogram tracing • Muscle twitching • Hyperreflexia • Asterixis
	Stage IV Comatose
	• Unresponsiveness, leading to death in most patients progressing to this stage • Unarousable, obtunded • Usually no response to painful stimulus • No asterixis • Positive Babinski’s sign • Muscle rigidity • Fetor hepaticus (characteristic liver breath—musty, sweet odor) • Seizures
Stage II Impending
• Continuing mental changes • Mental confusion • Disorientation to time, place, or person • Asterixis (hand flapping)

The exact mechanisms causing hepatic encephalopathy are not clearly understood but probably are the result of the shunting of portal venous blood into the central circulation so that 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) (Kelso, 2008). 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.

Factors that may lead to hepatic encephalopathy in patients with cirrhosis include:

• High-protein diet

• Infections

• 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, the precipitating factors, and the degree of liver dysfunction.

Patient-Centered Collaborative Care

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), 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 needle stick 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. People with hepatitis can develop cirrhosis (American Liver Foundation, 2011).

Inquire about whether there is a family history of alcoholism and/or liver disease. Ask the patient to describe his or her alcohol intake, including the amount consumed during a given period. Is there a history of illicit drug use, including oral, IV, and intranasal forms? Is there a history of tattoos? 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? This information is sensitive and often difficult for the patient to answer. 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 are regretful and often embarrassed.

Ask the patient about previous medical conditions, such as an episode of jaundice or acute viral hepatitis, biliary tract disorders (such as cholecystitis), viral infections, surgery, blood transfusions, autoimmune disorders, obesity, altered lipid profile, heart failure, respiratory disorders, or liver injury.

Physical Assessment/Clinical Manifestations

Because cirrhosis has a slow onset, many of the early manifestations are vague and nonspecific. Assess for:

• Fatigue

• Significant change in weight

• GI symptoms, such as anorexia and vomiting

• Abdominal pain 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, requiring 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 the patient with liver dysfunction or failure because it affects every body system (Fig. 61-1). The clinical picture and course vary from patient to patient depending on the severity of the disease. Assess for:

FIG. 61-1 The clinical picture of a patient with liver dysfunction. Manifestations vary according to the progression of the disease.

Abdominal Assessment

Massive ascites can be detected as a distended abdomen with bulging flanks. The umbilicus may protrude, and dilated abdominal veins (caput medusae) may radiate from the umbilicus. Ascites can cause physical problems. For example, 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 are likely to develop because of increased intra-abdominal pressure.

Minimal ascites is often more difficult to detect, especially in the obese patient. Advanced assessment techniques, such as the percussion test for shifting dullness and the presence of a fluid wave, may be performed by the health care provider.

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 may become hard and small. The advanced practice nurse or other health care provider palpates the right upper quadrant for hepatomegaly below the costal (rib cage) border. It may also be assessed by percussing for dullness over the enlarged liver.

Measure the patient’s abdominal girth to evaluate the progression of ascites (Fig. 61-2). To measure abdominal girth, the patient lies flat while the nurse or other 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. Mark the abdominal skin and flanks to ensure the same tape measure placement on subsequent readings. Taking daily weights, however, is the most reliable indicator of fluid retention.

FIG. 61-2 How to measure abdominal girth. With the patient supine, bring the tape measure around the patient and take a measurement at the level of the umbilicus. Before removing the tape, mark the abdomen along the sides of the tape on the patient’s flanks (sides) and midline to ensure that later measurements are taken in the same place.

Other Physical Assessment

Observe vomitus and stool for blood. This may be indicated by frank blood in the excrement or by a positive fecal occult blood test (FOBT) (Hema-Check, Hematest). 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 of chronic liver disease and hepatic encephalopathy and is characterized by a fruity or musty odor. Fetor hepaticus results from the inability of the damaged liver to metabolize and detoxify mercaptan, which is produced by bacterial breakdown of methionine, a sulfurous amino acid.

Amenorrhea (no menstrual period) may occur in women and men may exhibit testicular atrophy, gynecomastia (enlarged breasts), and impotence as a result of inactive hormones. Patients with problems of the hematologic system caused by hepatic failure may have bruising and petechiae (small, purplish hemorrhagic spots on the skin).

Continually assess the patient’s neurologic function. Subtle changes in mental status and personality often progress to coma, a late complication of encephalopathy. Monitor for asterixis, a coarse tremor characterized by rapid, nonrhythmic extensions and flexions in the wrists and fingers.

Psychosocial Assessment

The patient with hepatic cirrhosis may undergo subtle or obvious personality, cognitive, and behavior changes, such as agitation. He or she may experience sleep pattern disturbances or may 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, impacting not only the patient but also the immediate and extended family members and significant others. There are significant emotional, physical, and financial changes. Substance abuse may continue even as health worsens. It is important, whenever possible, to use resources available to these patients and their families. Collaborate with social workers, substance abuse counselors, and mental health/behavioral health care professionals as needed for patient assessment and management.

Laboratory Assessment

Laboratory study abnormalities are common in patients with liver disease (Table 61-4). Serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactate dehydrogenase (LDH) may be 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 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 2 is usually found in alcoholic liver disease.

TABLE 61-4 ASSESSMENT OF ABNORMAL LABORATORY FINDINGS IN LIVER DISEASE

ABNORMAL FINDING	SIGNIFICANCE
Serum Enzymes
Elevated serum aspartate aminotransferase (AST)	Hepatic cell destruction, hepatitis (most specific indicator)
Elevated serum alanine aminotransferase (ALT)	Hepatic cell destruction, hepatitis
Elevated lactate dehydrogenase (LDH)	Hepatic cell destruction
Elevated serum alkaline phosphatase	Obstructive jaundice, hepatic metastasis
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
Decreased fecal urobilinogen	Obstructive liver disease
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
Elevated serum ammonia	Advanced liver disease or portal-systemic encephalopathy (PSE)
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 (Kelso, 2008). However, alkaline phosphatase also increases when bone disease, such as osteoporosis, is present. 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. Therefore 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 protein and albumin levels are decreased in patients with severe or chronic liver disease as a result of decreased synthesis by the liver (Pagana & Pagana, 2010). Loss of osmotic “pull” proteins like 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.

Patients with primary biliary cirrhosis, an autoimmune disease, usually have high disease-specific AMA and anti-nuclear antibody (ANA) titers and elevated levels of immunoglobulin M (IgM) (Lindor et al., 2009).