↑↓ 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?
hepatomegaly → ↓ blood flow to liver
↑ edema of bile channels → pressure & obstruction (jaundice is a late sign) as well as Pruritus and dark-colored urine and clay colored stool
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 |
| 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
Nonabsorbable antibiotics: intestinal antiseptic that Destroy normal flora/ ↓ protein breakdown/production
Rifaximin: given with lactulose