NSG210 Hinkle Ch. 43: Assessment and Management of Patients with Hepatic Disorders

Source: Hinkle & Cheever, Brunner & Suddarth’s Medical-Surgical Nursing 15e, Chapter 43, pp. 1364-1413 (textbooks/HINKLE_MS_CH43.pdf, also in textbooks/exam04/). Week 12 reading (hepatic disorders: hepatitis, cirrhosis, liver cancer); Exam 4 content. Numbering note: the syllabus lists “Ch. 44” (16th edition); hepatic disorders is Ch. 43 in the 15th edition (see nsg210-textbook-chapter-crosswalk). Gallbladder and pancreas are in nsg210-hinkle-ch44-biliary-pancreatic.

Learning Outcomes

1. Identify the metabolic functions of the liver, the alterations and manifestations of hepatic disorders, and the significance of liver function tests.
2. Perform a health history and physical assessment for liver disorders and discriminate normal from abnormal findings.
3. Relate jaundice, portal hypertension, ascites, varices, nutritional deficiencies, and hepatic encephalopathy to liver pathophysiology.
4. Describe medical, surgical, and nursing management of esophageal varices.
5. Compare types of hepatitis: causes, prevention, manifestations, management, prognosis, home care.
6. Use the nursing process for the patient with cirrhosis.
7. Specify management and nursing care for liver cancer and liver transplantation.

Key Terms

• Acute hepatic failure: sudden severe liver failure within 8 weeks after first jaundice (formerly fulminant hepatic failure)
• Ascites: albumin-rich fluid in the peritoneal cavity
• Asterixis: involuntary flapping of the hands (“liver flap”)
• Cirrhosis: chronic disease with fibrosis, dense connective tissue, degeneration, and loss of functioning cells
• Constructional apraxia: inability to draw figures in two or three dimensions
• Endoscopic variceal ligation (EVL, banding): rubber band placed on a varix via endoscope
• Fetor hepaticus: sweet, slightly fecal breath odor
• Hepatic encephalopathy: CNS dysfunction associated with elevated ammonia; mental status changes, altered LOC, coma
• Jaundice: yellow or greenish-yellow sclera and skin from high bilirubin
• Orthotopic liver transplantation (OLT): donor liver placed in normal location after removal of diseased liver
• Portal hypertension: elevated portal pressure from obstruction of flow into and through the liver
• Sclerotherapy: injection of agents into or around varices to harden them and stop bleeding

I. Anatomy and Physiology

• Largest gland; RUQ behind ribs; 1200 to 1500 g; four lobes divided into lobules.
• Blood supply: about 80 percent from portal vein (nutrient rich, oxygen poor), rest from hepatic artery (oxygen rich); mix in sinusoids; drain via central veins to hepatic vein to inferior vena cava.
• Kupffer cells: phagocytes that remove bacteria from portal blood.
• Bile ducts: canaliculi to hepatic duct; hepatic duct plus cystic duct form common bile duct; sphincter of Oddi controls flow into duodenum.
• Functions:
  • Glucose: glycogen storage; glycogenolysis; gluconeogenesis (in hypoglycemia).
  • Ammonia conversion: ammonia (from protein breakdown and gut bacteria) converted to urea for urinary excretion.
  • Protein: makes almost all plasma proteins (albumin, clotting factors, transport proteins, lipoproteins); vitamin K needed for prothrombin.
  • Fat: breaks fatty acids into ketone bodies (starvation, uncontrolled diabetes); makes cholesterol, lipoproteins.
  • Storage: vitamins A, B, D, B complex; iron, copper.
  • Bile: water, electrolytes, lecithin, fatty acids, cholesterol, bilirubin, bile salts; bile salts emulsify fats; enterohepatic circulation reabsorbs bile salts in distal ileum.
  • Bilirubin: from hemoglobin breakdown; conjugated with glucuronic acid by hepatocytes; excreted in bile; converted to urobilinogen in intestine.
  • Drug metabolism: barbiturates, opioids, sedatives, anesthetics, amphetamines; first-pass effect lowers oral bioavailability.
• Older adults (Chart 43-1): smaller liver, less blood flow, decreased drug metabolism and clearance, slower repair, more gallstones, faster hepatitis C progression; LFTs do not normally change with age, so abnormal results mean disease; reduced drug doses may be needed.

II. Assessment

A. Health History

• Exposure to hepatotoxins (occupation, recreation, travel), alcohol and drug use (IV), hepatotoxic medications (acetaminophen, ketoconazole, valproic acid), OTC, herbs, supplements.
• Risk behaviors: IV drug use, sexual practices, foreign travel.
• Alcohol: men 60 to 80 g/day (about four drinks) and women 40 to 60 g/day are at high risk for cirrhosis.
• Symptoms: jaundice, malaise, weakness, fatigue, pruritus, abdominal pain, fever, anorexia, weight gain, edema, increasing girth, hematemesis, melena, hematochezia, easy bruising, mental changes, sleep disturbance, decreased libido (men), secondary amenorrhea (women).
• Genetic disorders (Chart 43-2): hemochromatosis, Wilson disease, alpha-1 antitrypsin deficiency, Gilbert syndrome, others.

B. Physical Assessment

• Pallor, jaundice (skin, mucosa, sclera), muscle atrophy, edema, scratch excoriation, petechiae, ecchymoses, spider angiomas, palmar erythema, gynecomastia and testicular atrophy in men; cognition; tremor, asterixis, slurred speech.
• NAFLD and NASH: fatty liver strongly linked to obesity, insulin resistance, type 2 diabetes; NASH can progress to fibrosis and cirrhosis. Obesity plus heavy drinking greatly increases risk.
• Palpate liver (firm sharp ridge); percuss borders; record distance below right costal margin. Late cirrhosis: small hard liver. Acute hepatitis: soft liver. Tenderness = recent acute enlargement (viral hepatitis tender; alcoholic hepatitis not). Fluid wave for ascites.

C. Liver Function Tests (Table 43-1)

• Over 70 percent of parenchyma may be damaged before LFTs become abnormal.

D. Other Diagnostics

• Liver biopsy (needle aspiration): most common complication is peritonitis from blood or bile; check and correct coagulation first; transvenous (jugular) route if ascites or coagulopathy.
• Ultrasound, CT, MRI, radioisotope scan, elastography (liver stiffness), laparoscopy.

III. Manifestations of Hepatic Dysfunction

• Chronic liver disease: 12th leading cause of death in young and middle-aged US adults; at least 40 percent alcohol related; men twice women. About 80 percent of compensated cirrhosis remains asymptomatic for 10 years.
• Most common cause of parenchymal damage: malnutrition, especially with alcoholism. Sarcopenia raises morbidity in end-stage liver disease (ESLD) even in obese patients.

A. Jaundice

• Visible when serum bilirubin over 2.0 mg/dL.
• Hemolytic: excess RBC destruction (transfusion reaction); unconjugated bilirubin; increased urine and fecal urobilinogen; no bilirubin in urine. Free bilirubin over 20-25 mg/dL risks CNS effects; prolonged jaundice predisposes to pigment stones.
• Hepatocellular: damaged cells cannot clear bilirubin (hepatitis, toxins, alcohol, cirrhosis); anorexia, nausea, malaise, fatigue, weight loss; elevated AST and ALT; may be reversible.
• Obstructive: bile duct blocked (stone, inflammation, tumor, enlarged organ) or intrahepatic stasis from cholestatic drugs (phenothiazines, antithyroid drugs, sulfonylureas, tricyclics, nitrofurantoin, androgens, estrogens). Deep orange foamy urine, clay-colored stools, intense pruritus, fat intolerance; bilirubin and alkaline phosphatase high, AST/ALT/GGT only moderately up.
• Hereditary: Gilbert syndrome (3 to 8 percent, mostly males; unconjugated bilirubin up, normal LFTs and histology); Dubin-Johnson, Rotor, benign cholestatic jaundice of pregnancy.

B. Portal Hypertension

• Increased portal pressure from obstructed flow through the damaged liver (usually cirrhosis). Splenomegaly common; two major consequences are ascites and varices.

C. Ascites

• Mechanisms: portal hypertension, splanchnic vasodilation, failure to metabolize aldosterone (sodium and water retention), low albumin (low oncotic pressure), increased lymph flow; self-perpetuating. May reach 20 L or more.
• Signs: increased girth, rapid weight gain, dyspnea, striae, distended abdominal veins, umbilical hernia, fluid and electrolyte imbalance.
• Assessment: bulging flanks supine, shifting dullness, fluid wave (only with large volume); daily girth and weight.
• Nutrition: negative sodium balance; 2 g sodium diet (avoid table salt, salty foods, salted butter, canned and frozen foods not low sodium); taste adjusts in 2 to 3 months; lemon, oregano, thyme; salt substitutes only if approved (ammonia-containing ones can precipitate encephalopathy; potassium ones dangerous with renal impairment); 500 mg sodium if needed but rarely accepted. About 10 percent respond to diet alone.
• Diuretics: with sodium restriction effective in 90 percent. Spironolactone (aldosterone antagonist) first line; prevents potassium loss. Furosemide may be added cautiously (hyponatremia). Ammonium chloride and acetazolamide contraindicated (encephalopathy).
• Weight loss limit: no more than 1 kg/day with ascites and peripheral edema; 0.5 to 0.75 kg/day without edema. Fluid restriction only if sodium very low.
• Diuretic complications: hypovolemia, hypokalemia, hyponatremia, hypochloremic alkalosis, encephalopathy (low potassium raises ammonia).
• Bed rest: upright posture activates RAAS and sympathetic system; bed rest helps refractory cases.
• Paracentesis: now mainly diagnostic or for massive refractory ascites; large volume (5 to 6 L) is safe and is treatment of choice for large-volume ascites, given with IV salt-poor albumin to prevent postparacentesis circulatory dysfunction. Ultrasound guidance if coagulopathy or adhesions. Have patient void before (bladder injury). Ascites recurs.
• TIPS (transjugular intrahepatic portosystemic shunt): stent between portal and hepatic veins lowers portal pressure; effective for refractory ascites but higher encephalopathy risk and cost, so second line. Ascites in cirrhosis carries 50 percent mortality.
• Peritoneovenous shunt (rare); palliative peritoneal catheters in ESLD.
• Nursing: I&O, girth, daily weight, respiratory status (ascites limits lung expansion), ammonia, creatinine, electrolytes.
• Teaching (Chart 43-3): no alcohol; low-sodium diet; avoid NSAIDs, alcohol-containing medicines (cough syrups), sodium-containing antacids; daily weights; report decreasing urine output; signs of encephalopathy, SBP, dehydration.

D. Esophageal Varices

• Present in 30 percent of compensated and 60 percent of decompensated cirrhosis at diagnosis.
• Dilated tortuous submucosal veins in lower esophagus (or stomach) from portal hypertension diverting blood through fragile collaterals.
• First bleed mortality 10 to 30 percent; overall acute variceal bleed mortality 10 to 40 percent; survivors have about 70 percent rebleed risk and 30 to 50 percent death.
• Bleeding raises ammonia (nitrogen load in gut) and causes hemorrhagic shock.
• Triggers: lifting, straining at stool, sneezing, coughing, vomiting, esophagitis, poorly chewed food, irritating fluids, reflux (especially alcohol), salicylates.
• Signs: hematemesis, melena, mental status decline, shock (cool clammy skin, hypotension, tachycardia).
• Screening endoscopy for all with cirrhosis; repeat in 2 to 3 years if none, 1 to 2 years if small varices.
• Immediate endoscopy for bleeding (about 40 percent actually bleed from another source such as gastritis or ulcer); NPO until gag reflex returns.
• Hepatic venous pressure gradient over 10 mm Hg = clinically significant portal hypertension.

Medical management:

• ICU; IV fluids, electrolytes, volume expanders, blood; avoid overhydration (raises portal pressure); indwelling catheter.
• Octreotide (somatostatin analog): preferred for immediate control; splanchnic vasoconstriction; give before endoscopy; mild hypoglycemia, cramping.
• Vasopressin: constricts splanchnic bed; only if urgent or octreotide unavailable; contraindicated in coronary artery disease (coronary vasoconstriction, MI); given with nitroglycerin; monitor I&O and sodium (antidiuretic effect, hyponatremia).
• Beta-blockers (propranolol, nadolol, carvedilol): prevent first bleed and rebleeding; NOT used in acute hemorrhage. Nitrates (isosorbide) with beta-blockers for prevention.
• Balloon tamponade (esophageal and gastric balloons; Sengstaken-Blakemore tube): temporary, 12 hours or less; test balloons before insertion; intubate first to protect airway; risk of airway obstruction if balloon migrates or ruptures; ICU with continuous observation; frequent mouth and nasal care; stops bleeding in 90 percent but 60 to 70 percent rebleed.
• Endoscopic sclerotherapy: injects sclerosing agent; complications: bleeding, perforation, aspiration pneumonia, stricture; antacids, H2 blockers, or PPIs afterward.
• Endoscopic variceal ligation (banding): treatment of choice; fewer rebleeds and complications than sclerotherapy; complications: superficial ulceration, dysphagia, chest discomfort, rare stricture. Used with drugs, and for those who bleed on or cannot tolerate beta-blockers.
• TIPS for bleeding refractory to drugs and endoscopy (10 to 20 percent); complications: bleeding, sepsis, heart failure, perforation, shunt thrombosis, liver failure, encephalopathy.
• Other: tissue adhesives, stents, BRTO.
• Surgical shunts (distal splenorenal and mesocaval are selective; portacaval nonselective), devascularization and transection: rescue therapy; high encephalopathy rate; consider only if MELD under 15, not transplant candidate, or limited TIPS access.
• Nursing: VS, nutrition, neuro status; parenteral nutrition if esophagus must rest; gastric suction; oral hygiene and moist sponges for thirst; vitamin K and transfusions; quiet environment; watch for alcohol withdrawal delirium; support family (Table 43-2).

E. Hepatic Encephalopathy and Coma

• Neuropsychiatric manifestation of liver failure with portal hypertension and portosystemic shunting; reversible; may start subclinical.
• Ammonia is the major cause (stimulates GABA, depressing CNS).
• Raise ammonia: GI bleeding, high-protein intake, infection, uremia, ammonium salts, alkalosis, hypokalemia.
• Other triggers: excessive diuresis, dehydration, infection, surgery, fever, sedatives, tranquilizers, analgesics, potassium-wasting diuretics; manganese, false neurotransmitters (mercaptans).
• Manifestations: early mental status and motor changes; confused, unkempt; mood and sleep changes (day-night reversal); disorientation; coma, seizures. Asterixis (stage 2); constructional apraxia (daily handwriting or star drawing); hyperactive reflexes early, then flaccid; fetor hepaticus.
• Table 43-3 stages:
  1. Normal LOC with lethargy, euphoria, reversed sleep; impaired writing; normal EEG.
  2. Drowsy, disoriented, inappropriate, mood swings, agitation; asterixis, fetor hepaticus; EEG slowing.
  3. Stuporous, hard to rouse, marked confusion, incoherent; asterixis, increased reflexes, rigidity.
  4. Coma; asterixis absent, reflexes absent, flaccid.
• EEG: slowing, triphasic waves. Survival after first overt episode about 40 percent at 1 year; refer for transplant.
• Treatment: find and remove precipitant (bleeding, electrolytes, sedation, azotemia).
• Lactulose: traps ammonia and expels it in stool; goal 2 to 3 soft stools a day; watery diarrhea = overdose; monitor ammonia, potassium, dehydration; may dilute in juice; no other laxatives; can give by NG tube or enema.
• IV glucose to limit protein breakdown; vitamins; correct electrolytes (potassium); antibiotics (neomycin, metronidazole, rifaximin) reduce ammonia-forming bacteria.
• Monitoring: frequent neuro checks, daily handwriting and arithmetic, daily I&O and weight, VS every 4 hours, infection sites, daily ammonia.
• Protein should NOT be restricted: 1.2 to 1.5 g/kg/day; calories 35 to 40 kcal/kg/day; small frequent meals plus late-night snack; branched-chain amino acids if protein intolerant (Chart 43-4).
• Stop sedatives, tranquilizers, analgesics; flumazenil may help short term.
• Nursing: safety, deep breathing, turning (respiratory compromise), family support; teach subtle signs of recurrence; constipation can precipitate encephalopathy (continue lactulose); no driving or machinery with even subtle deficits; avoid sedating medications.

F. Other Manifestations

• Edema (low albumin); bleeding (low clotting factors, thrombocytopenia from hypersplenism, alcohol marrow suppression, folate deficiency).
• Vitamin deficiencies: A (night blindness), thiamine (beriberi, Wernicke-Korsakoff), riboflavin and pyridoxine (skin and mucous lesions), C (scurvy), K (bleeding), folic acid (macrocytic anemia). Supplement A, B complex, C, K, folic acid.
• Glucose: hyperglycemia after meals, hypoglycemia when fasting. Medications in reduced doses.
• Estrogen not inactivated: gynecomastia, amenorrhea, testicular atrophy, loss of pubic hair.
• Pruritus (bile salts), spider angiomas, palmar erythema.

IV. Viral Hepatitis (Table 43-4)

• Phases: viral replication (asymptomatic, labs positive), preicteric/prodromal (anorexia, nausea, vomiting, fatigue, pruritus), icteric (jaundice, dark urine, abdominal pain), convalescent.

A. Hepatitis A

• RNA enterovirus; 20 to 25 percent of clinical hepatitis; contaminated food or water, shellfish, poor hygiene, daycare, oral-anal sex. Not transmitted by transfusion. Virus in stool before symptoms; noninfectious by the time jaundice appears. Illness 4 to 8 weeks.
• Many anicteric; flulike symptoms, low-grade fever, severe anorexia, aversion to cigarette smoke and strong odors; symptoms clear as jaundice peaks (about 10 days).
• HAV antigen in stool 7 to 10 days before illness and 2 to 3 weeks after; antibodies in serum after symptoms.
• Vaccine (95 to 100 percent effective): adults 2 doses, second at 6 to 12 months; all children at 1 year; travelers, MSM, drug users, daycare staff, health care workers, chronic liver disease. Combined HAV/HBV vaccine for adults, 3 doses.
• Immune globulin within 2 weeks of exposure: 6 to 8 weeks passive immunity; for household and sexual contacts, institutional contacts; not casual contacts; epinephrine available.
• Management: bed rest in acute stage, small frequent nutritious meals; gradual ambulation; avoid alcohol; hand hygiene after toileting and before eating.

B. Hepatitis B

• DNA virus; blood, saliva, semen, vaginal secretions; mother to infant at birth. Risk factors (Chart 43-7): carrier contact, health care workers, hemodialysis, IV drugs, MSM, multiple partners, transfusions, STIs, tattooing, travel.
• Over 90 percent recover in 6 months; 1 percent mortality acute; about 10 percent become carriers or chronic (cirrhosis, HCC). Older adults: more severe.
• Clinical: like HAV but longer incubation; arthralgias, rash; jaundice may be absent; liver tender, 12 to 14 cm.
• Markers:
  • HBsAg: surface antigen, active infection; appears 1 to 10 weeks after exposure; persists 6 months or more = carrier.
  • HBeAg: appears within a week of HBsAg; high infectivity.
  • anti-HBc: persists in acute phase; may mean ongoing HBV.
  • anti-HBs: recovery and immunity.
  • anti-HBe: reduced infectivity.
• Prevention: screen blood; disposable needles, needleless systems; gloves; no eating in labs.
• Vaccine: high-risk groups, all infants, catch-up to age 19, STI evaluation, MSM, HCV and chronic liver disease. HEPLISAV-B 2 doses 1 month apart (adults); older recombinant series over 90 percent protective. Deltoid injection. Boosters only if immunocompromised. Does not protect if already exposed.
• HBIG (passive immunity): for unvaccinated exposure (needlestick, mucosal splash, sexual contact); infants of HBV mothers within 12 hours of birth; give with vaccine at separate sites and syringes.
• Treatment: pegylated interferon, entecavir, or tenofovir preferred for chronic HBV; interferon side effects (flulike, marrow suppression, thyroid dysfunction, alopecia). Bed rest until symptoms subside; no protein restriction (1.2 to 1.5 g/kg/day); avoid medications if vomiting; test for other bloodborne diseases (HIV).
• Nursing: convalescence 3 to 4 months or more; avoid sexual contact or use condoms; minimize isolation; vaccine or HBIG for intimate contacts; no alcohol.

C. Hepatitis C

• Most common chronic bloodborne infection in US (about 2.4-2.5 million); IV drug use, needlesticks, multiple partners, transfusion before 1992; highest in ages 40 to 59.
• Mild or absent symptoms; chronic carrier state common; cirrhosis, HCC (about one third of HCC), common reason for transplant.
• Even small regular alcohol amounts speed progression; avoid alcohol and hepatotoxic drugs. Rest, diet, vitamins give no benefit.
• Direct-acting antivirals (DAAs): over 90 percent cure in 8 to 12 weeks of oral therapy; sustained virologic response (no virus 12 weeks after treatment) = cure. Examples: ledipasvir-sofosbuvir, glecaprevir/pibrentasvir, sofosbuvir/velpatasvir. Avoid St. John’s wort with HCV protease inhibitors.

D. Hepatitis D, E, G

• D: only with HBV (needs HBsAg); IV drugs, hemodialysis, transfusions; more acute failure and cirrhosis; interferon alfa at least 1 year.
• E: fecal-oral, contaminated water; abrupt, jaundice almost always, self-limited, no chronic form; prevent with hygiene.
• G / GB virus-C: percutaneous; uncertain significance.

E. Dietary Management of Hepatitis (Chart 43-6)

• 25 to 30 kcal/kg/day; protein 1.2 to 1.5 g/kg/day; small frequent meals; enteral feeding if anorexia persists; no alcohol during illness and at least 6 months after recovery; avoid hepatotoxic substances.

V. Nonviral Hepatitis and Acute Liver Failure

• Toxic hepatitis: true hepatotoxins (carbon tetrachloride, phosphorus); anorexia, nausea, vomiting, jaundice, hepatomegaly; rapid recovery if exposure removed early; no antidotes; may progress to fever, bloody emesis, hemorrhage, delirium, coma, seizures, death without transplant.
• Drug-induced hepatitis: most common cause of acute liver failure (over 50 percent); acetaminophen is the leading cause; also isoniazid, halothane, methyldopa, antibiotics, anticonvulsants, anti-TB drugs. Abrupt chills, fever, rash, pruritus, arthralgia, then jaundice. Stop any drug causing fever, rash, or pruritus immediately.
• Acute liver failure (ALF): neurologic dysfunction, PT/INR 1.5 or more, no prior liver disease, under 26 weeks. Hyperacute (jaundice to encephalopathy 0-7 days), acute (8-28 days), subacute (28-72 days). Survival 20 to 50 percent.
• Causes: viral hepatitis, acetaminophen, carbon tetrachloride, Wilson disease, Budd-Chiari.
• Complications: coagulopathy, kidney injury, electrolyte imbalance, cardiovascular problems, infection, hypoglycemia, encephalopathy, cerebral edema (stage 4: ICP monitoring, mannitol, quiet environment, sedation and neuromuscular blockade).
• Treatment: ICU, transplant evaluation (treatment of choice); antidotes: N-acetylcysteine (acetaminophen), penicillin (mushroom poisoning); plasmapheresis; liver assist devices (BAL, ELAD, MARS) experimental.

VI. Hepatic Cirrhosis

A. Types and Pathophysiology

• Alcoholic (scar around portal areas; most common), postnecrotic (broad bands; after viral hepatitis), biliary (around bile ducts; chronic obstruction, cholangitis).
• Alcohol is the major cause; nutritional deficiency contributes; also chemicals and schistosomiasis. Men twice women (women more susceptible to alcohol damage); ages 40 to 60. Hobnail liver. May progress over 30 years.
• Child-Pugh classification (Table 43-5): ascites, bilirubin (under 2, 2-3, over 3), albumin (over 3.5, 2.8-3.5, under 2.8), PT prolongation, encephalopathy; total 5-6 grade A, 7-9 B, 10-15 C.

B. Clinical Manifestations (Chart 43-9)

• Compensated: abdominal pain, ankle edema, firm enlarged liver, flatulent dyspepsia, intermittent mild fever, palmar erythema, splenomegaly, epistaxis, morning indigestion, vascular spiders.
• Decompensated: ascites, clubbing, continuous fever, epistaxis, gonadal atrophy, hypotension, jaundice, muscle wasting, purpura, sparse body hair, spontaneous bruising, weakness, weight loss, white nails.
• Liver large and fatty early (pain from capsule stretch), small and nodular late.
• Portal obstruction and ascites: congestion of spleen and GI tract; indigestion.
• Spontaneous bacterial peritonitis (SBP): no intra-abdominal source; may lack signs; paracentesis to diagnose; antibiotics treat and prevent; can precipitate hepatorenal syndrome (acute kidney injury unresponsive to fluids or diuretics, no structural kidney damage).
• GI varices: caput medusae, esophageal, gastric, rectal (hemorrhoids); monitor for occult and frank bleeding.
• Edema: low albumin, aldosterone excess.
• Vitamin deficiency (A, C, K) and anemia; severe fatigue.
• Mental deterioration: impending encephalopathy; serial neuro assessment.

C. Diagnosis

• Low albumin, high globulin; elevated alk phos, AST, ALT, GGT; decreased cholinesterase; elevated bilirubin; prolonged PT. Ultrasound, CT, MRI, elastography; biopsy confirms. ABGs may show hypoxia.

D. Medical Management

• Treat symptoms: antacids or H2 blockers (GI bleeding risk); vitamins and supplements; potassium-sparing diuretics (spironolactone, triamterene) for ascites; adequate diet; no alcohol. Fibrosis cannot be reversed but progression can be slowed.
• Antifibrotic agents under study; milk thistle (silymarin), SAM-e; ursodeoxycholic acid for primary biliary cirrhosis.

E. Nursing Management (Chart 43-10)

• Rest: daily weight and I&O; position for respiratory efficiency (ascites); oxygen as needed; prevent immobility complications; gradual increase in activity.
• Nutrition: high-carbohydrate diet with protein 1.2 to 1.5 g/kg/day; vitamins B complex, A, C, K; small frequent meals (six a day) with ascites; HOB up at meals; oral hygiene before meals; sodium restriction; no alcohol; water-soluble forms of A, D, E if steatorrhea; folic acid and iron; enteral or parenteral if needed. Probiotic yogurt may lower ammonia (research).
• Skin: frequent position changes; avoid irritating soaps and tape; lotion; short nails; massage with emollients and turn every 2 hours; pressure-relief mattress; elevate edematous limbs.
• Injury: padded side rails; orient; avoid restraints; electric razor, soft toothbrush; pressure on venipuncture sites; small-gauge needles; evaluate any injury for internal bleeding.
• Bleeding: test stool and emesis for occult blood; watch for ecchymoses, epistaxis, petechiae, bleeding gums; VS every 1 to 4 hours; vitamin K; avoid straining, coughing, sneezing; cold liquids after bleeding stops if prescribed.
• Encephalopathy: cognitive checks, handwriting daily, ammonia; avoid opioids and barbiturates; report subtle changes; lactulose.
• Fluid volume excess: hyperdynamic circulation; monitor I&O, weight, girth, edema, nocturia then oliguria (worsening).
• Infection: temperature every 4 hours, assess abdominal pain and tenderness (peritonitis), aseptic technique.
• Paracentesis assistance: explain, have patient void, position, record amount and character, watch for cough, dyspnea, tachycardia.
• Teaching: abstain from alcohol (AA, counseling); avoid raw shellfish; long-term sodium restriction; teach-back; recovery slow with setbacks.

VII. Cancer of the Liver

• Benign hepatic adenomas: women of reproductive age on oral contraceptives; risk of hemorrhage and malignant change.
• Hepatocellular carcinoma (HCC): 75 percent of primary liver cancer; second leading cause of cancer death worldwide; rare in US. Risk factors: cirrhosis, HBV, HCV, vinyl chloride, arsenic, smoking with alcohol, aflatoxin (moldy nuts and grains).
• Metastases to liver (GI, breast, lung) are 2.5 times more common than primary tumors.
• Manifestations: dull continuous RUQ, epigastric, or back pain; weight loss, weakness, anorexia, anemia; enlarged irregular liver; jaundice if large ducts occluded; ascites.
• Labs: elevated bilirubin, alk phos, AST, GGT, LDH; leukocytosis, erythrocytosis, hypercalcemia, hypoglycemia, hypocholesterolemia. Alpha-fetoprotein elevated in 80 to 90 percent of HCC (often over 200 ng/mL); CEA. Biopsy risks tumor seeding (0.5 to 2 percent).
• Treatment: mostly palliative. Radiation via TACE (transarterial chemoembolization), DEB-TACE, interstitial; sorafenib (Child A), regorafenib; hepatic artery infusion pump; percutaneous biliary drainage (watch for sepsis, bile leak, hemorrhage, reobstruction: fever, chills, drainage around catheter, pain, pruritus, recurrent jaundice); radiofrequency ablation (tumors up to 5 cm in one session), ethanol injection, embolization, laser hyperthermia, immunotherapy.
• Surgery: resection if confined to one lobe and remaining liver adequate (lobectomy; up to 90 percent resected possible if no cirrhosis).
• Transplant: Milan criteria: single tumor under 5 cm, or up to three lesions none over 3 cm; 4-year survival about 85 percent.
• Nursing: postop like abdominal and thoracic surgery; blood and fluids; teach biliary catheter care (keep clean and dry; irrigate with sterile saline if ordered, do NOT aspirate back); hepatic artery port has one-way valve (not aspirated for blood return); report infection; hospice discussions.

VIII. Liver Transplantation

• For ESLD with no other treatment: hepatocellular diseases (viral hepatitis, drug or alcohol injury, Wilson disease), cholestatic diseases (primary biliary cirrhosis, sclerosing cholangitis, NASH, biliary atresia), ALF, some malignancies.
• Orthotopic; deceased donor or right lobe from living donor (LDLT); split-liver.
• MELD score (bilirubin, PT/INR, creatinine, cause) predicts short-term mortality and determines organ allocation through UNOS.
• Immunosuppression: calcineurin inhibitors (cyclosporine: nephrotoxicity; tacrolimus preferred), corticosteroids, mycophenolate mofetil, sirolimus, everolimus, antithymocyte globulin, basiliximab.
• Biliary anastomosis: end-to-end with possible T-tube, or Roux-en-Y (no T-tube).
• Complications: bleeding (coagulopathy, fibrinolysis); hypertension (calcium channel blockers preferred; avoid ACE inhibitors and ARBs first year); infection (leading cause of death; pulmonary and fungal); rejection; biliary leak or obstruction; vascular thrombosis. 1-year survival about 90 percent, 5-year about 80 percent.
• LDLT donor complications: PE, portal vein thrombosis, bile duct injury, liver insufficiency; donor may have more pain than recipient; donor advocate team; exclude coercion.
• Preop nursing: support during waiting; must be reachable at all times; treat malnutrition, ascites, electrolytes; ethical issues around alcohol-related disease.
• Postop nursing: environment as free of microbes as possible; continuous hemodynamic, pulmonary, renal, neuro, metabolic monitoring; LFTs, coagulation, glucose; bile and drain output; atelectasis prevention (incentive spirometer); early ambulation; strict asepsis and hand hygiene; sepsis bundles.
• Teaching: immunosuppressants exactly as prescribed, never run out; trough levels; labs 2 to 3 times a week at first; signs of rejection and infection; T-tube care; eye exams (steroids: cataracts, glaucoma); dental care with prophylactic antibiotics; anxiety and depression; pregnancy is high risk, use birth control during waiting period.

IX. Liver Abscesses

• Amebic (Entamoeba histolytica; tropics, poor sanitation) and pyogenic (more common in developed countries; cholangitis, abdominal trauma).
• Sepsis with few localizing signs: fever, chills, diaphoresis, malaise, anorexia, nausea, vomiting, weight loss, dull RUQ pain, hepatomegaly, jaundice, anemia, pleural effusion; may progress to shock.
• Diagnosis: ultrasound, CT, MRI; blood cultures; guided aspiration.
• Treatment: IV antibiotics; percutaneous drainage (catheter); open surgery if needed.
• Nursing: drainage and skin care; VS; report increasing pain (rupture); monitor WBC; teach drain care and antibiotic adherence.

High-Yield Numbers

Priority Nursing Actions and Red Flags

• Hematemesis, melena, hypotension, tachycardia in cirrhosis: variceal hemorrhage; ICU, octreotide, prepare for endoscopy.
• Balloon tamponade: airway first (intubate before insertion); continuous ICU observation; watch for airway obstruction from balloon migration or rupture.
• Vasopressin: watch for chest pain (MI); contraindicated with coronary artery disease.
• Beta-blockers are for prevention, not acute bleeding.
• Confusion, day-night reversal, asterixis, worsening handwriting: hepatic encephalopathy; hold sedatives, give lactulose, find trigger (bleeding, infection, low potassium, dehydration, constipation).
• Watery diarrhea on lactulose: overdose; check potassium and fluid status.
• Do not restrict protein in encephalopathy.
• Ascites patient: weigh daily; no more than 1 kg loss per day; have patient void before paracentesis.
• Fever and abdominal pain with ascites: suspect spontaneous bacterial peritonitis.
• Bleeding precautions: electric razor, soft toothbrush, pressure on puncture sites.
• Fever, rash, or pruritus with any drug: stop the drug (drug-induced hepatitis).
• Post-transplant fever or confusion: infection or rejection; strict asepsis.

Medications

Related

• nsg210-hinkle-ch44-biliary-pancreatic
• nsg210-hinkle-ch45-endocrine-disorders
• nsg210-hinkle-ch48-kidney-disorders (hepatorenal syndrome context)
• INDEX