Problems in Liver MEDIUM

Acute Liver Failure (ALF)

• ALF is a syndrome characterized by a sudden and severe impairment of liver function in a previously healthy individual.
• Key diagnostic criteria include neurologic dysfunction, PT/INR ≥1.5, absence of prior liver disease, and a disease course ≤26 weeks.
• Hyperacute liver failure involves a very rapid injury (hours), acute or subacute failure involves a slower, immune-based injury (days to weeks).
• Jaundice to encephalopathy duration: hyperacute (0-7 days), acute (8-28 days), subacute (28-72 days).
• Survival rates for acute liver failure range from 20% to 50%, varies depending on the cause.
• Common causes of ALF include viral hepatitis, toxic medications (acetaminophen), chemicals (carbon tetrachloride), metabolic disturbances (Wilson disease), and structural changes (Budd-Chiari syndrome).
• Initial symptoms may include jaundice and severe anorexia.
• ALF is often accompanied by coagulation defects, kidney disease, electrolyte imbalances, cardiovascular abnormalities, infection, hypoglycemia, encephalopathy, and cerebral edema.
• Rapid recognition and intensive intervention are crucial for optimized treatment.
• Management includes ICU support and assessment for liver transplantation feasibility.
• Antidotes like N-acetylcysteine for acetaminophen toxicity and penicillin for mushroom poisoning may be indicated.
• Treatment modalities like plasmapheresis and prostaglandin therapy do not have evidence indicating any clinical improvement with their use.
• ELADs and BALs are experimental short-term devices that aim to bridge patients to liver transplantation.
• Molecular Adsorbent Recirculating System (MARS) and Therapeutic Plasma Exchanges (TPE) may remove protein-bound toxins and stabilize unstable patients with ALF.
• Stage 4 encephalopathy in ALF carries a high risk of life-threatening cerebral edema.
• Intracranial pressure monitoring is necessary for patients with cerebral edema risk.
• Promote cerebral perfusion via fluid balance, hemodynamic assessments, quiet environment, and osmotic diuretics (mannitol).
• Neuromuscular blockade and sedation prevent intracranial pressure surges.
• Monitor and treat hypoglycemia, coagulopathies, and infection.
• Liver transplantation is the definitive treatment.

Hepatic Cirrhosis

• Cirrhosis is a chronic disease where normal liver tissue is replaced by diffuse fibrosis, disrupting liver structure and function.
• Alcoholic cirrhosis involves scar tissue around portal areas, frequently from chronic alcoholism.
• Postnecrotic cirrhosis features broad bands of scar tissue, often a late result of acute viral hepatitis.
• Biliary cirrhosis involves scarring around bile ducts, usually from chronic biliary obstruction and cholangitis, less common.
• Cirrhosis primarily affects the portal and periportal spaces, causing inflammation and bile duct occlusion.
• The liver attempts to form new bile channels, leading to overgrowth of tissue and scar tissue.
• Nutritional deficiency (reduced protein intake) and excessive alcohol intake are key factors.
• Cirrhosis can occur in non-alcoholics, although some individuals are more susceptible.
• Exposure to chemicals (carbon tetrachloride, arsenic, phosphorus) or schistosomiasis may play a role.
• Men are more affected, but women are at greater risk for alcohol-induced liver disease.
• Most patients are 40-60 years old.
• Alcohol-associated cirrhosis accounts for up to 50% of cirrhosis cases.
• Cirrhosis deaths in the US increased by 65% from 1999-2016, reaching approximately 35,000 annually.
• Alcoholic cirrhosis involves repeated liver cell necrosis and replacement by scar tissue.
• The cirrhotic liver exhibits a hobnail appearance due to scar tissue constriction and residual/regenerating tissue islands.
• Child-Pugh classification can predict the outcome of liver disease.

Clinical Manifestations of Cirrhosis

• Signs and symptoms increase in severity as the disease progresses.
• Severity classifies cirrhosis as compensated or decompensated.
• Compensated cirrhosis may be found during routine physicals; less severe vague symptoms.
• Decompensated cirrhosis results from liver failure to synthesize proteins/clotting factors and from portal hypertension.

Assessing for Cirrhosis

• Compensated: abdominal pain, ankle edema, firm, enlarged liver, flatulent dyspepsia, mild fever, palmar erythema, splenomegaly, unexplained epistaxis, vague morning indigestion, vascular spiders.
• 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
• Early cirrhosis presents with a large liver loaded with fat, noticeable on palpation.
• Abdominal pain may occur due to rapid liver enlargement stretching Glisson capsule.
• Later, the liver shrinks as scar tissue contracts; the edge is nodular if palpable.

Portal Obstruction and Ascites

• Caused by chronic liver failure and portal circulation obstruction.
• Blood backs up into spleen/GI tract, causing chronic passive congestion and impaired function.
• Indigestion and altered bowel function result.
• Fluid rich in protein accumulates in the peritoneal cavity, causing ascites, detectable via percussion.

Infection and Peritonitis

• Spontaneous bacterial peritonitis (SBP) can develop without an intra-abdominal infection source often caused by intestinal flora translocation.
• Clinical signs may be absent, necessating paracentesis for diagnosis.
• SBP is treated with antibiotics and can trigger hepatorenal syndrome (acute kidney injury unresponsive to fluids or diuretics).
• Hepatorenal syndrome features no kidney pathology.

Gastrointestinal Varices

• Fibrotic changes obstructing blood flow lead to collateral vessel formation and blood shunting
• Patients exhibit caput medusae (prominent abdominal blood vessels) and distended GI blood vessels.
• Esophagus, stomach, and lower rectum are common sites for varices/hemorrhoids.
• Risk of rupture and bleeding due to high pressure and volume.

Edema

• Late symptom due to chronic liver failure and reduced plasma albumin concentration.
• Generalized edema, mainly in lower/upper extremities and presacral area.
• Facial edema is not typical.
• Aldosterone overproduction causes sodium/water retention and potassium excretion.

Vitamin Deficiency and Anemia

• Inadequate vitamin formation, use, and storage (vitamins A, C, K).
• Presents with hemorrhagic phenomena due to vitamin K deficiency.
• Chronic gastritis, impaired GI function, and inadequate dietary intake contribute to anemia.
• Anemia, poor nutrition, and health lead to severe fatigue.

Mental Deterioration

• Deterioration of mental and cognitive function with progression to hepatic encephalopathy and coma demands serial neurological assessment.

Assessment and Diagnostic Findings

• Liver disease extent and treatment determined by lab findings.
• Serum albumin decreases, while globulin rises.
• Enzyme tests (alkaline phosphatase, AST, ALT, GGT) indicate liver cell damage.
• Serum cholinesterase may decrease.
• Increased bilirubin levels indicate bile excretion/retention issues.
• Prothrombin time is prolonged.
• Ultrasound, CT, MRI, radioisotope liver scans, and elastography assess liver size, blood flow, obstruction, and fibrosis.
• Diagnosis is confirmed by liver biopsy.
• Arterial blood gas analysis may show ventilation-perfusion imbalance and hypoxia.

Medical Management

• Management based on presenting symptoms.
• Antacids/H2 antagonists are prescribed to decrease gastric distress/GI bleeding risk.
• Vitamins/nutritional supplements promote liver cell healing and nutrition.
• Potassium-sparing diuretics (spironolactone, triamterene) decrease ascites while minimizing electrolyte shifts
• Adequate diet and alcohol avoidance are crucial.
• Although fibrosis is irreversible, progression may be slowed down.
• Antifibrotic medications include colchicine, angiotensin system inhibitors, statins, diuretics, immunosuppressants, and glitazones.
• Angiotensin receptor blockers (ARBs) also have antifibrogenic properties.
• Vitamin E and chemokine receptor (CCR2/CCR5) inhibitors reduce injury and inflammation.
• Peroxisome proliferator-activated receptor (PPAR) agonists cause hepatic stellate cell death.
• Farnesoid X receptor agonists prevent chronic inflammation/fibrosis.
• Milk thistle (Silybum marianum) is used for jaundice/symptoms; silymarin has anti-inflammatory and antioxidant properties.
• SAM-e (S-adenosylmethionine) may improve liver function through antioxidant effects.
• Ursodeoxycholic acid is used to treat primary biliary cirrhosis.

Nursing Management

• Promoting patient rest.
• Improving nutritional status.
• Providing skin care.
• Reducing risk of injury.
• Monitoring and managing potential complications.

Nursing Interventions

• Assess activity tolerance, fatigue, lethargy, and malaise.
• Assist with activities and hygiene when fatigued.
• Encourage rest during fatigue or abdominal discomfort.
• Assist with selecting and pacing activities/exercise.
• Provide a diet high in carbohydrates and protein (1.2-1.5 g/kg/day).
• Administer supplemental vitamins (A, B complex, C, K).
• Promote rest to reduce liver demands and increases blood supply.
• Prevent complications of immobility (atelectasis, pneumonia, venous thromboemboli, pressure injuries).
• Encourage gradual activity increase with improved nutrition and strength.

Improving Nutritional Status

• High-protein diet (if tolerated) supplemented with B complex, A, C, and K vitamins (no ascites, edema, hepatic coma).
• Small, frequent meals.
• Probiotics can manage hepatic encephalopathy.
• Steatorrhea patients should receive water-soluble forms of fat-soluble vitamins A, D, E.
• Folic acid/iron is prescribed to prevent anemia.
• Sodium restriction prevents ascites.
• Enteral or parenteral nutrition for prolonged anorexia, vomiting, or poor eating.

Providing Skin Care

• Frequent position changes prevent pressure injuries and avoid irritating soaps and adhesive tape.
• Lotions soothe irritated skin.

Reducing Risk of Injury

• Protect patients from falls and other injuries, use side rails and pads & orient patient to time and place.
• Electric razor, soft-bristled toothbrush, pressure applied to venipuncture sites.

Monitoring and Managing Potential Complications

• Bleeding and hemorrhage are risks due to decreased prothrombin production.
• Hepatic encephalopathy manifests as deteriorating mental status.
• Monitor mental status and report changes promptly.
• Monitor and correct electrolyte disturbances.
• Administer oxygen if oxygen desaturation occurs.
• Monitor for fever/abdominal pain indicative of bacterial peritonitis or other infection.
• Cardiovascular abnormalities, increased cardiac output, decreased peripheral vascular resistance, increased plasma volume promotes fluid excess.
• Assess for cardiovascular and respiratory status.
• Administer diuretics, implement fluid restrictions, and enhance patient positioning.
• Monitor I&O, weight, abdominal girth, and edema.
• Monitor for nocturia and oliguria.

Promoting Home, Community-Based and Transitional Care

• Counsel patients about dietary education and excluding alcohol from diet.
• Support groups like Alcoholics Anonymous, psychiatric care, or spiritual support.
• Avoid raw shellfish consumption.
• Focus on sodium restriction.
• Provide education about encephalopathy symptoms, bleeding, and infection susceptibility.
• Use the teach-back method for education.
• Provide support, encouragement, and positive feedback.
• Assess progress at home after discharge.

Acute Liver Failure (ALF) is a syndrome with sudden liver function impairment. Key criteria includes neurologic dysfunction, PT/INR ≥1.5, and a disease course ≤26 weeks. Common causes include viral hepatitis and toxic medications.