Problems in Liver EASY

Acute Liver Failure (ALF)

• ALF is a clinical syndrome characterized by a sudden and severe impairment of liver function in a previously healthy individual.
• Diagnostic criteria include neurologic dysfunction, PT/INR ≥1.5, no prior liver disease, and a disease course ≤26 weeks.
• Hyperacute liver failure occurs within hours, acute within days to weeks.
• Jaundice to encephalopathy durations: hyperacute (0-7 days), acute (8-28 days), subacute (28-72 days).
• Survival rates for ALF range from 20% to 50%, depending on the cause, with death typically resulting from hepatocellular injury and necrosis.
• Common causes include viral hepatitis, toxic medications (e.g., acetaminophen), chemicals, metabolic disturbances (e.g., Wilson disease), and structural changes (e.g., Budd–Chiari syndrome).
• Initial symptoms may include jaundice and anorexia, frequently accompanied by coagulation defects, kidney disease, electrolyte disturbances, cardiovascular abnormalities, infection, hypoglycemia, encephalopathy, and cerebral edema.
• Management involves rapid recognition, ICU support, liver transplant assessment, and antidotes (e.g., N-acetylcysteine for acetaminophen toxicity). Plasmapheresis reduces serum ammonia levels and stabilizes the patient awaiting liver transplantation, and prostaglandin therapy enhances blood flow.
• ELAD and BAL devices are experimental short-term liver support systems.
• Molecular Adsorbent Recirculating System (MARS) and therapeutic plasma exchanges (TPE) removes protein-bound toxins, useful in unstable patients.
• Stage 4 encephalopathy patients are at high risk of cerebral edema, which may be treated with intracranial pressure monitoring, fluid balance, hemodynamic assessments, a quiet environment, and mannitol.
• Pharmacologic neuromuscular blockade (NMB) and sedation prevent intracranial pressure surges.
• Liver transplantation is the treatment of choice for ALF due to the high mortality rate despite other treatments.

Hepatic Cirrhosis

• Cirrhosis is a chronic liver disease marked by the replacement of normal liver tissue with diffuse fibrosis, disrupting liver structure and function.
• Three types: alcoholic, postnecrotic, and biliary cirrhosis.
• Alcoholic cirrhosis is the most common type, with scar tissue surrounding the portal areas, typically caused by chronic alcoholism.
• Postnecrotic cirrhosis features broad bands of scar tissue and is a late result of acute viral hepatitis.
• Biliary cirrhosis involves scarring around the bile ducts, typically from chronic biliary obstruction and cholangitis.
• The disease primarily affects the portal and periportal spaces, obstructing bile ducts with thickened bile and pus.

Pathophysiology

• Nutritional deficiency and excessive alcohol intake are major contributing factors.
• Other factors include exposure to certain chemicals (e.g., carbon tetrachloride) or infectious schistosomiasis.
• Men are affected twice as often as women, but women are at greater risk for alcohol-induced liver disease.
• Alcoholic cirrhosis involves repeated necrosis of liver cells, replaced by scar tissue, resulting in a hobnail appearance.
• The Child–Pugh classification is useful for predicting outcomes and guiding management approaches.

Clinical Manifestations

• Severity of symptoms categorizes cirrhosis as compensated or decompensated.
• Compensated cirrhosis may be discovered secondarily with vague symptoms.
• Decompensated cirrhosis results from liver failure to synthesize proteins and clotting factors, as well as portal hypertension.

Assessing for Cirrhosis: Compensated

• Abdominal pain
• Ankle edema
• Firm, enlarged liver
• Flatulent dyspepsia
• Intermittent mild fever
• Palmar erythema
• Splenomegaly
• Unexplained epistaxis
• Vague morning indigestion
• Vascular spiders

Assessing for Cirrhosis: Decompensated

• Ascites
• Clubbing of fingers
• Continuous mild fever
• Epistaxis
• Gonadal atrophy
• Hypotension
• Jaundice
• Muscle wasting
• Purpura
• Sparse body hair
• Spontaneous bruising
• Weakness
• Weight loss
• White nails

Liver Enlargement

• Early cirrhosis the liver is large with fat, firm, and palpable.
• Abdominal pain may occur due to rapid enlargement of the liver.
• Later, the liver decreases in size as scar tissue contracts the liver tissue, with a nodular edge.

Portal Obstruction and Ascites

• Caused by liver dysfunction and obstruction of the portal circulation.
• Blood backs up into the spleen and GI tract, leading to chronic passive congestion, indigestion, and altered bowel function.
• Protein-rich fluid accumulates in the peritoneal cavity, producing ascites.

Infection and Peritonitis

• Spontaneous bacterial peritonitis (SBP) may occur without an intra-abdominal source of infection.
• Bacteremia from intestinal flora translocation is the likely route of infection.
• Antibiotic therapy is effective in treatment and prevention of SBP.
• SBP may precipitate hepatorenal syndrome, a form of acute kidney injury.

Gastrointestinal Varices

• Fibrotic changes cause blood to be shunted from the portal vessels, forming collateral vessels in the GI system.
• Distended abdominal blood vessels (caput medusae) and varices or hemorrhoids may form.
• These vessels may rupture and bleed due to high pressure and volume of blood.

Edema

• Late symptom is edema, due to chronic liver failure and reduced plasma albumin concentration.
• Affects the lower and upper extremities, and presacral area.
• Facial edema is not typical.
• Overproduction of aldosterone causes sodium and water retention, and potassium excretion.

Vitamin Deficiency and Anemia

• Inadequate formation, use, and storage of vitamins (A, C, K) leads to deficiencies.
• Hemorrhagic phenomena are linked to vitamin K deficiency.
• Anemia results from chronic gastritis, impaired GI function, inadequate dietary intake, and liver function.
• Patients experiences severe fatigue, which interferes with routine activities.

Mental Deterioration

• Deterioration of mental and cognitive function with impending hepatic encephalopathy and hepatic coma.
• Serial neurologic assessment is indicated.

Assessment and Diagnostic Findings

• Liver functions are complex, and many diagnostic tests provide information.
• Serum albumin decreases, and serum globulin increases in severe liver dysfunction.
• Enzyme tests (serum alkaline phosphatase, AST, ALT, GGT) increase, and serum cholinesterase may decrease.
• Bilirubin levels increase with cirrhosis and other liver disorders.
• Prothrombin time is prolonged.
• Ultrasound, CT, MRI, radioisotope liver scans, and elastography give information about liver size, hepatic blood flow and obstruction and the presence of liver fibrosis.
• Liver biopsy confirms diagnosis.
• Arterial blood gas analysis may reveal a ventilation–perfusion imbalance and hypoxia.

Medical Management

• Management is based on presenting symptoms.
• Antacids or H2 antagonists decrease gastric distress and minimize GI bleeding.
• Vitamins and nutritional supplements promote healing and improve nutritional status.
• Potassium-sparing diuretics (spironolactone or triamterene) decrease ascites.
• Diet and avoidance of alcohol are essential.
• Medications with antifibrotic activity include colchicine, angiotensin system inhibitors, statins, diuretics, immunosuppressants, and glitazones.
• Angiotensin receptor blocker (ARB) medications have antifibrogenic properties.
• Medications that can reduce injury and inflammation and include vitamin E inhibitors.
• Peroxisome proliferator-activated receptor (PPAR) agonists have been shown to cause cell death of hepatic stellate cells that potentiate fibrosis.
• Farnesoid X receptor agonists, such as obeticholic acid, prevent chronic inflammation and liver fibrosis.

Alternative Medicines

• Milk thistle (Silybum marianum) is used to treat jaundice, HCC, and other symptoms with anti-inflammatory and antioxidant properties.
• SAM-e (S-adenosylmethionine) may improve outcomes in liver disease by improving liver function.
• Ursodeoxycholic acid treats primary biliary cirrhosis to improve liver function.

Nursing Management: Promoting Rest

• Adjust the patient’s position in bed for maximal respiratory efficiency, especially if ascites is present.
• Oxygen therapy may be required to oxygenate the damaged cells.

Nursing Management: Improving Nutritional Status

• Patients without ascites, edema, or signs of impending hepatic coma should receive a nutritious, high-protein diet and vitamin supplements.
• If ascites is present, small, frequent meals may be better tolerated.
• Probiotics for the management of hepatic encephalopathy is currently being researched.
• Patients with steatorrhea should receive water-soluble forms of fat-soluble vitamins A, D, and E.
• Folic acid and iron is prescribed to prevent anemia and sodium restriction is indicated to prevent ascites.
• Enteral or parenteral nutrition may be necessary for patients with prolonged or severe anorexia.

Nursing Management: Providing Skin Care

• Frequent changes in position are necessary to prevent pressure injuries.
• Irritating soaps and adhesive tape are avoided.
• Lotion may be soothing to irritated skin, measures taken to minimize scratching.

Nursing Management: Reducing Risk of Injury

• Protect the patient from falls and other injuries by ensuring side rails are up.
• Orient to time and place and explain all procedures to minimize agitation.
• Use an electric razor rather than a safety razor.
• Use a soft-bristled toothbrush and apply pressure to venipuncture sites to minimize bleeding.

Nursing Management: Monitoring and Managing Potential Complications

• Major role of the nurse is monitoring for complications
• Bleeding and Hemorrhage: The patient is at increased risk due to decreased production of prothrombin.
• Hepatic Encephalopathy: Closely monitor the patient’s mental status to make sure changes are reported to start treatment promptly.
• Monitor for fever or abdominal pain, which may signal the onset of peritonitis or other infection.
• Fluid Volume Excess: Close assessment of cardiovascular and respiratory status. Administer diuretic agents and implement fluid restrictions.
• Monitoring of intake and output, daily weight changes, changes in abdominal girth, and edema formation, and monitor for decrease in urination, which may indicate liver disfunction.

Promoting Home, Community-Based and Transitional Care: Educating Patients About Self-Care

• Exclude alcohol from the diet, and the patient may benefit from referral to support groups or counseling.
• Sodium restriction will continue, and support from family members is important.
• Educate the patient and family about encephalopathy, potential bleeding tendencies, and susceptibility to infection.
• Use the teach-back method when teaching patients to make sure they understand what they have been taught.

Promoting Home, Community-Based and Transitional Care: Continuing and Transitional Care

• The nurse assesses the patient’s progress at home and reinforces any previous education the patient had, and help set up ways to improve daily life with their new restrictions.