↑↓ Hepatitis

Virus(infection); Hepatotoxins (industrial toxins, ETOH, drugs); secondary to infections ( Epstein-Barr, herpes, varicella, CMV) [even though they target other parts of the body it can still lead to hep] → widespread inflammation & infection of liver cells

  • report to local health department/CDC


What hepatitis causes?

  1. hepatomegaly → ↓ blood flow to liver

  2. ↑ edema of bile channels → pressure & obstruction (jaundice is a late sign) as well as Pruritus and dark-colored urine and clay colored stool

  3. necrosis if widespread - fulminant (fatal form)

  •     severe acute mainly seen w/ B and D before jaundice can even occur

    • trx. EMERGENCY TRANSPLANT


overall s/s:

  • Dark colored urine

  • clay colored stool (obstruction of bile ducts)

  • Pruritus, Fatigue (chronic form), anorexia

  • Gallstones

  • abd pain/liver tenderness, fever

  • Jaundice (LATE SIGN) also icterus —excessive accumulation of bile pigments (bilirubin) deposited in skin, excreted in urine → Hyperbilirubinemia (acute obstruction)


labs: liver enzymes ( AST/ALT)

dx.

C: Anti-HCV antibodies → indicates exposure (detectable ~ 4 weeks after infection) using the HCA RNA test (measures viral load (OraQuick – Rapid Antibody Test))

D; delta antigen or rise in HDV-Ab titer

E: no detection: dentified by finding HEV-Ab/IgM in clients blood

Liver Biopsy to confirm; stage/grade of damage or cancer; distinguish cause

  • RISK FOR BLEEDING


  • Viral hepatitis (acute or chronic) most common

    • HIV positive is more likely to get A,B,D



HAV

HBV

HCV

HDV (need B)

HEV

common

worldwide & US

US; baby boomers; HW;

US, BB, HW, prisoner, HIV+ ; BLOODBORNE


other countries

transmission

fecal-oral

blood & bodily fluids

blood & bodily fluids


Fecal-oral Waterborne

risk factors

poor sanitation; contaminated water; shellfish

unprotected sex w/ infected person; needle sharing/ accidental sticks; blood transfusions before 1992;

needle sharing (highest); unprotected sex w/ multiple partners, M-M; accidental sticks; blood transfusions before 1992

Sexual contact; IV drug user


s/s

acute onset, mild GI or Flu like; possible asy

usually asy

hepatomegaly → RUQ abd pain

Systemic "Flu-like" Symptoms; GI distress; arthralgia (joint pain) or myalgia (muscle pain)

asy

Acute onset


prevention

destroyed by bleach; Sanitation; VACCINE (kids/infants) and before traveling

VACCINE (kids/infants; HW) ; use condoms; don’t share needles

no vaccine; not from normal household contact but should not share razors, tooth brushes, pierced earrings; ALL BB be screened; all adult be screened for B; use condoms; don’t share needles


AVD ice/fruits washed in tap in other countries

meds


  1. Nucleoside analogs (1st) for chronic too-inhibits viral DNA synthesis

  2. Interferon alfa

Direct-acting antivirals (DAAs)-Target HCV replication

1st determine genotype

Chronic Hep C - 2nd gen protease inhibitors (PIs) (glecaprevir)

NS5A Inhibitors Drug Combos: Ledipasvir-only geneotype 1

NS5A-NS5B polymerase inhibitor: Sofosbuvir-all types



trx

resolve on own; HIV PEP: Post-Exposure Prophylaxis (IgM)—w/in 14 days of expose to hep A if not vaccinated

once cleared → immunity ; if in 6 mon not clear → chronic form → ↑ risk cirrhosis & liver CA; PEP: Post-Exposure Prophylaxis (IbM)) + vaccine

cure

no trx → chronic hep → needs liver transplant

good prognosis = acute; not good = chronic

self limiting; no chronic form

NSG considerations

fam needs to be vaccinated; Prep- pre prophylactic for fam after

prevent hep D;

Nucleoside analogs- monitor kidney function

1st determine genotype before giving med; can suppress the immune system (AVD crowds and sick contact);

PI: Monitor CBC & chem panel; Kidney & liver fx; impaired ‘lytes imbalances



leads to


chronic hep inflammation lasting > 6 months → cirrhosis & liver CA

chronic hep inflammation lasting > 6 months → cirrhosis & liver CA

Extrahepatic complications (outside the liver): polyarthritis, renal insufficiency, cardio problems: Vasculitis &Heart disease

most common in D than acute: chronic hep inflammation lasting > 6 months → cirrhosis & liver CA



Nursing considerations:

  • acute: Supportive care, individualized

    • Goals - Promote liver regeneration, prevent complications

  • Promote nutrition & manage fatigue

    • Educate: Rest ↓ liver’s metabolic demands; activity as tolerated

      • vaccinated

    • ↑ cals/carb diet, mod fat/protein, small frequent meals

    • NO ALCOHOL or acetaminophen

    • Vitamins, anti-emetic PRN N&V; limit most meds

    • Antiviral drugs (HBV & HCV)

  • evaluation of outcomes:

    • maintain adequate nutrition

    • report inc energy levels

    • achieve appropriate management of infection and inflammation


Nonalcoholic Fatty Liver Disease (NAFLD) - liver stores excessive amounts of fat from the body not r/t EtOH → Hepatomegaly, firmness & ↓ function

  • R/T obesity, ↑ cholesterol, T2DM, metabolic syndrome

TX – lifestyle, diet, weight loss, glucose control

NAFLD → NASH (Nonalcoholic steatohepatitis) is the more

severe form - inflammation→ cirrhosis/failure, liver cancer, death


Cirrhosis

acute hepatic inflammation → fibrosis/irreversible scarring (nodular) retrograde ↑ pressure/circulation, ↑ metabolic wastes → impairs cellular regulation (structural changes & loss of fx at 75% damage) → necrosis


Types of Cirrhosis:

Post-necrotic

  • Viral hepatitis (esp. Hep C)

  • Certain drugs or toxins — Alcohol; tylenol; acetaminophen


Biliary

  • Chronic biliary obstruction (gallstones)

  • Autoimmune disease - primary biliary cirrhosis (PBI)


Alcoholic (Laennec’s) cirrhosis*

  • has genetic predisposition (hypersensitivity)

  • > 2 drinks/day or 7/wk in women

  • > 3 drinks/day or 14/wk in men


Complications:

  • Compensated cirrhosis: Liver scarred, still performs essential fx

  • Decompensated cirrhosis ~ impaired fx, S/S (at 75%)

  • Portal hypertension → Portal vein is blocked by fibrosis → ↑ BP → Ascites & esophageal varices (thin walls = BLEEDING RISK)

    • ascites → blood flows back to spleen (splenomegaly) → Platelet destruction (thrombocytopenia)/BLEEDING RISK

      • Hypoalbuminemia (third spacing-fluid leave the cells into interstitial space)

      • s/s Caput medusae—visible, dilated vessels around umbilicus

    • esophageal varices (life-threatening)→ rupture ( can be Spontaneous OR with lifting, exercise, eating dry/hard food)→ shock

      • Upper GI bleeding = hematemesis

      • Lower GI bleeding = melena; frank blood (bright)

      • longer coag times bc liver damage ↓ production of clotting factors (ANEMIA)

      • Spleen involvement: platelet loss/thrombocytopenia

  • Biliary obstruction → serum bilirubin levels→ Jaundice

    • ↓ production of bile → ↓ digestion of fats → Prevents absorption of fat-soluble vitamins (K) (BLEEDING RISK (PT/INR)

    • caused by either Intrahepatic obstruction (acute) by gallstone or Hepatocellular (chronic disease) from edema, scarring/fibrosis

  • Hepatic encephalopathy (late stages): Ammonia build up in blood that reaches the brain → CNS depressant/neuro S/S (Asterixis (hand-flapping) or “liver flap”) -stage III; Seizures, unarousable, coma (Stage IV)


other complications:

  • Hepatorenal Syndrome (HRS): Poor prognosis; Sudden ↓ in urinary flow

  • Spontaneous Bacterial Peritonitis (SBP): Very advanced liver disease → low protein levels → Bacteria from bowel reach ascitic fluid → Fever, chills, abdominal pain

    • DX ~ ascitic fluid analysis via paracentesis

Hepatopulmonary Syndrome: Ascites → breathing/dypsnea


s/s: hepatomegaly (firm & hard) → atrophy

early sys:

  • fatigue

  • GI ~ anorexia, vomiting (PRIORITY) → catch hepatomegaly early

    • abd girth

  • Significant changes in wgt

  • Abdominal pain, liver tenderness (often ignored)


Late signs:

  • Jaundice (skin), icterus (sclerae)

  • bruising; Vascular lesions: spider angiomas

  • caput medusae: Dilated abdominal veins

  • Vitamin deficiency (ADEK)


Report: GI bleeding, jaundice, ascites, easy bruising, neuro S/S


dx. liver enzymes (everthing thing is elevated) except:

  • ↓ serum albumin (hypoalbuminemia)

  • ↓ total protein

  • US 1ST

  • Liver biopsy — caution risk for bleeding


Main concerns:

  • Fluid overload: 3rd spacing/ascites & peripheral edema

    • monitor abd girth, daily wgts, i/o, lytes

    • monitor for spontaneous, bacterial peritonitis

  • Potential for hemorrhage: Portal HTN, bleeding esophageal varices → infection → shock (ME)

    • trx. for rupture: IV vasoactive drugs, BALLOON TAMPONADE

      • complication: aspiration, asphyxia, perforation

        • Shunting procedure ~ TIPS: addresses portal HTN

          • screening: endoscopy

          • prevention med: propranolol

  • Acute confusion/cognitive changes: ↑ serum ammonia +/or ETOH withdrawal

    • Neuro checks (q 2-4 hrs) ~ Glasgow Coma Scale (GCS)

    • Assess ~ liver flap (asterixis), breath (fetor hepaticus)

    • Monitor ammonia levels (normal 10-80 mcg/dL)

    • Seizure precautions

    • Prevent GI bleeding

    • mod-protein


trx.

  • Nutrition therapy Na+ restriction

    • take vitamins like thymine/folate

  • Drug therapy diuretics like spironolactone or furosemide

    • monitor K

    • DON’T GIVE TYLENOL (edu)

  • Fluid volume: PARACENTESIS: IF SBP suspected send to lab

    • Nursing Care/Monitoring: bleeding, infection, perforation

    • Semi-Fowlers, vs & weight before/after

    • Resp support: Hepatopulmonary syndrome

      • monitor: Dyspnea: O2, monitor pulse ox, ↑ HOB


drug therapy:

1st. Lactulose ~ ↑ excretion in stool/ ↓ absorption

  • laxative effect

    • Observe for cramping, hypokalemia, dehydration

  1. Nonabsorbable antibiotics: intestinal antiseptic that Destroy normal flora/ ↓ protein breakdown/production

  • Rifaximin: given with lactulose