Problems in Liver HARD

Acute Liver Failure (ALF)

• ALF is a clinical syndrome characterized by sudden and severe liver function impairment in previously healthy individuals.
• Diagnostic criteria include neurologic dysfunction, PT/INR ≥1.5, absence of prior liver disease, and a disease course ≤26 weeks.
• Hyperacute liver failure occurs within hours, acute liver failure occurs in days to weeks.
• Jaundice to encephalopathy duration: hyperacute (0-7 days), acute (8-28 days), subacute (28-72 days).
• Survival rates range from 20% to 50%, dependent on the cause.
• Death typically results from massive hepatocellular injury and necrosis.
• Common causes of ALF are viral hepatitis, toxic medications (acetaminophen), chemicals (carbon tetrachloride), metabolic disturbances (Wilson disease), and structural changes (Budd-Chiari syndrome).
• Initial manifestations include jaundice and profound anorexia.
• Other complications: coagulation defects, kidney disease/electrolyte imbalances, cardiovascular abnormalities, infection, hypoglycemia, encephalopathy, and cerebral edema.
• Rapid recognition and intensive care are essential for optimized treatment.

Treatment Modalities for ALF

• Management hallmarks: ICU support and liver transplant assessment.
• Antidotes: N-acetylcysteine for acetaminophen toxicity, penicillin for mushroom poisoning.
• Plasmapheresis may correct coagulopathy and reduce serum ammonia levels.
• Prostaglandin therapy aims to enhance hepatic blood flow.
• Extracorporeal liver assist devices (ELAD) and bioartificial livers (BAL) are experimental short-term devices bridging to transplantation.
• BAL exposes plasma to porcine liver cells after charcoal column filtration.
• ELAD exposes whole blood to human hepatoblastoma cell cartridges.
• Molecular adsorbent recirculating system (MARS) and therapeutic plasma exchanges (TPE) remove protein-bound toxins.

Management of Cerebral Edema in ALF

• Patients with stage 4 encephalopathy are at high risk of cerebral edema.
• Potential causes of cerebral edema: disruption of the blood-brain barrier and increased intracellular osmolarity in cerebral astrocyte cells.
• Management includes intracranial pressure monitoring, fluid balance, hemodynamic assessments, quiet environment, and mannitol diuresis.
• Pharmacologic neuromuscular blockade (NMB) and sedation are used to prevent intracranial pressure surges.
• Monitor and treat hypoglycemia, coagulopathies, and infection.
• Liver transplantation is the preferred treatment.

Hepatic Cirrhosis Defined

• Cirrhosis is a chronic liver disease marked by normal liver tissue replacement with diffuse fibrosis, disrupting liver structure and function.
• Types: alcoholic, postnecrotic, and biliary.
  • Alcoholic cirrhosis: scar tissue around portal areas, caused by chronic alcoholism.
  • Postnecrotic cirrhosis: broad scar tissue bands, a late result of acute viral hepatitis.
  • Biliary cirrhosis: scarring around bile ducts, due to chronic biliary obstruction and cholangitis.
• The portal and periportal spaces are the primary sites of inflammation, leading to bile duct occlusion.

Cirrhosis Pathophysiology

• Excessive alcohol intake is a major causative factor, though nutritional deficiency contributes to liver destruction.
• Exposure to chemicals (carbon tetrachloride, chlorinated naphthalene, arsenic, or phosphorus) or infectious schistosomiasis may play a role.
• Men are more often affected but women are at greater risk of alcohol-induced liver disease.
• Most patients are between 40 and 60 years of age
• Alcoholic cirrhosis constitutes approximately 50% of cirrhosis cases in the United States and worldwide.

Disease Progression

• Alcoholic cirrhosis involves repeated liver cell necrosis and scar tissue replacement.
• The liver develops a hobnail appearance due to residual normal/regenerating tissue.
• Onset is insidious, with a course spanning 30+ years.
• The Child-Pugh classification is most useful in predicting outcomes and guiding management approaches.

Clinical Manifestation of Cirrhosis

• Severity increases as the disease progresses, categorized as compensated or decompensated.
• Compensated cirrhosis: often vague symptoms.
• Decompensated cirrhosis: protein synthesis failure, clotting factor abnormalities, and portal hypertension manifestations.

Signs and Symptoms

• Compensated: abdominal pain, ankle edema, firm/enlarged liver, flatulent dyspepsia, intermittent 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.

Physical Manifestations

• Early on, the liver is large, firm, and palpable with a sharp edge due to fat accumulation.
• Abdominal pain may result from rapid liver enlargement stretching Glisson capsule.
• Later, the liver shrinks as scar tissue contracts, with a nodular edge upon palpation.

Portal Obstruction and Ascites

• Portal obstruction and ascites result from liver function failure and portal circulation obstruction.
• Blood backs up into the spleen and GI tract, causing chronic passive congestion.
• Protein-rich fluid accumulates in the peritoneal cavity, causing ascites, detectable by percussion or fluid wave.

Infection and Peritonitis

• Spontaneous bacterial peritonitis (SBP) may occur without an intra-abdominal infection source, likely from intestinal flora translocation.
• Diagnosis requires paracentesis due to potential absence of clinical signs.
• Antibiotic therapy is effective for treatment/prevention of recurrent SBP.
• SBP can precipitate hepatorenal syndrome, a form of acute kidney injury unresponsive to fluid or diuretics.

Gastrointestinal Varices

• Fibrotic changes obstruct blood flow, leading to collateral vessel formation in the GI system.
• Caput medusae (distended abdominal blood vessels) and GI tract varices/hemorrhoids may develop.
• These vessels can rupture and bleed due to increased pressure/volume.

Edema and Vitamin Deficiency

• Edema, especially in extremities and the presacral area, results from chronic liver failure and reduced plasma albumin.
• Sodium and water retention/potassium excretion occurs due to aldosterone overproduction.
• Deficiencies in vitamins A, C, and K are common.
• Anemia results from chronic gastritis, impaired GI function, inadequate dietary intake, and impaired liver function.

Mental Deterioration

• Encephalopathy and hepatic coma may cause deterioration of mental and cognitive function.
• Serial neurologic assessment is indicated regularly

Diagnostics Procedures

• Liver function tests: serum albumin decreases, globulin rises, alkaline phosphatase, AST, ALT, and GGT increase, cholinesterase decreases, bilirubin increases, and prothrombin time is prolonged.
• Ultrasound, CT, MRI, radioisotope liver scans, and elastography assess liver size, blood flow, obstruction, and fibrosis.
• Liver biopsy confirms diagnosis.
• Arterial blood gas analysis detects ventilation-perfusion imbalance and hypoxia.

Medical Management

• Based on presenting symptoms.
• Antacids or H2 antagonists manage gastric distress and minimize GI bleeding risk.
• Vitamins and nutritional supplements aid liver cell healing and improve nutrition.
• Potassium-sparing diuretics (spironolactone or triamterene) reduce ascites, preferred for minimal electrolyte changes.
• Antifibrotic medications, including colchicine, angiotensin system inhibitors, statins, diuretics, immunosuppressants, and glitazones, are used.
• Angiotensin receptor blockers (ARBs) possess antifibrogenic properties.
• Drugs targeting different pathways in NASH are being evaluated, like vitamin E and chemokine receptor (CCR2/CCR5) inhibitors.
• PPAR agonists induce cell death of hepatic stellate cells.
• Farnesoid X receptor agonists (obeticholic acid) prevent chronic inflammation and liver fibrosis.

Holistic and Alternative Treatments

• Milk thistle (Silybum marianum) may treat jaundice and other symptoms due to anti-inflammatory and antioxidant properties.
• SAM-e (S-adenosylmethionine) may improve liver function through enhanced antioxidant function.
• Ursodeoxycholic acid treats primary biliary cirrhosis.

Patient Care

• Nursing interventions include rest, nutritional support, skin care, injury prevention, and monitoring for complications.
• Rest reduces liver demands and increases blood supply.
• Adjust position for maximal respiratory efficiency, especially with ascites.
• Oxygen therapy is required for liver failure.

Nursing Considerations

• Assess activity tolerance and fatigue levels during daily activities.
• Assist with activities/hygiene when fatigued.
• Encourage rest during fatigue, abdominal pain, or discomfort.
• Assist with activity selection and pacing.
• Provide high-carbohydrate diet with 1.2-1.5 g/kg/day of protein.
• Administer supplemental vitamins (A, B complex, C, and K).

Nutritional Management

• Promote positive nitrogen balance.
• Provide a nutritious, high-protein diet supplemented with vitamins B complex, A, C, and K (if tolerated).
• Small, frequent meals may be better tolerated.
• Probiotics may reduce intestinal flora imbalance; oral ingestion of 1 cup of probiotic yogurt three times a day has been shown to do so.
• Administer water-soluble forms of fat-soluble vitamins A, D, and E for steatorrhea
• Folic acid and iron are administered to prevent anemia.
• Restrict sodium intake to prevent ascites.
• Use enteral/parenteral nutrition for prolonged anorexia or poor eating.

Reducing risk of injury

• Place side rails
• Use padding
• Provide patient orientation
• Remind patient to ask for assistance getting out of bed.
• Use electric razor as opposed to safety
• Soft bristle toothbrush
• Apply pressure at venipuncture sites

Skin and Complication Management

• Frequent position changes prevent pressure injuries.
• Avoid irritating soaps and adhesive tape.
• Lotion soothes irritated skin.
• Monitor for and manage complications: bleeding/hemorrhage and hepatic encephalopathy.
• Manage electrolyte disturbances and administer oxygen for desaturation.
• Monitor for fever/abdominal pain (bacterial peritonitis or infection).

Fluid Balance

• Cardiovascular abnormalities can result from increased cardiac output and decreased peripheral vascular resistance.
• Close assessment of cardiovascular and respiratory status is key.
• Administer diuretics, restrict fluids, and optimize patient positioning to enhance pulmonary function.
• Monitor I&O, daily weight, abdominal girth, and edema.
• Monitor for nocturia/oliguria indicating increased liver dysfunction.

Home Care

• Educate patients about self-care, focusing on dietary education and alcohol exclusion.
• Consider referring to Alcoholics Anonymous, psychiatric care, counseling, or a spiritual advisor.
• Continued sodium restriction may be needed.
• Provide education and support on lifestyle changes, diet, and alcohol elimination.
• Recovery is gradual with potential setbacks; the nurses' support plays an important role
• Referral for transitional or home care may assist with the transition.