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Hepatitis C

5 min read

Hepatitis C

Key Points

  • Hepatitis C (HCV) is a blood-borne virus transmitted primarily via contaminated needles; sexual and perinatal transmission is possible but less common.
  • No vaccine exists for HCV — prevention relies on harm reduction and screening.
  • The majority of HCV infections become chronic — 55–85% of acutely infected individuals develop chronic HCV.
  • Modern direct-acting antivirals (DAAs) achieve >95% cure rates within 8–12 weeks of treatment.
  • Chronic HCV is a leading cause of cirrhosis, liver failure, and liver transplantation.

Pathophysiology

HCV is an RNA virus that infects hepatocytes. Unlike HBV, HCV does not integrate into host DNA, but the immune response to persistent infection causes ongoing hepatic inflammation and fibrosis. Over decades, fibrosis progresses to cirrhosis — the irreversible structural scarring of the liver.

Cirrhosis complications include:

  • Portal hypertension → varices, ascites, splenomegaly
  • Hepatic encephalopathy — ammonia accumulation due to impaired detoxification
  • Coagulopathy — decreased clotting factor synthesis
  • Hepatocellular carcinoma (HCC) — significantly elevated risk in cirrhotic patients

Transmission Routes

RouteRisk Level
IV drug use (needle sharing)Highest risk — most common route
Blood transfusions/organ transplants (before 1992)High historical risk; current blood screening markedly reduces risk
Needlestick injuries (health care workers)Moderate risk (~1.8% per percutaneous exposure)
Sexual contactLow but possible (higher with multiple partners, HIV coinfection)
Perinatal (mother to infant)5–6% transmission rate

Clinical Manifestations

  • Acute infection: Often asymptomatic — 70–80% of patients have no symptoms during acute infection, delaying diagnosis
  • Chronic infection: Fatigue (most common), RUQ discomfort, nausea, arthralgia
  • Cirrhosis: Jaundice, ascites, peripheral edema, variceal bleeding, hepatic encephalopathy (confusion, asterixis)

Nursing Assessment

NCLEX Focus

HCV is often called the “silent epidemic” because most patients are asymptomatic for years. High-risk groups (IVDU, born 1945–1965, prior blood transfusion) should be screened with anti-HCV antibody testing even without symptoms.

  • Assess for fatigue and RUQ pain.
  • Assess for signs of cirrhosis: jaundice, ascites (abdominal girth), peripheral edema, splenomegaly.
  • Assess for bleeding: hematuria, melena, ecchymosis, esophageal varices history.
  • Monitor laboratory values:
    • ALT/AST: Elevated (may be only mildly elevated in early chronic HCV)
    • Bilirubin: Elevated in liver dysfunction
    • PT/INR: Elevated in cirrhosis (impaired clotting factor synthesis)
    • Albumin: Decreased in chronic liver disease
    • Ammonia: Elevated in hepatic encephalopathy
    • HCV RNA: Viral load (confirms active viremia and monitors treatment response)
    • HCV genotype: Determines treatment regimen selection

Nursing Interventions

  • Transmission prevention education: Reinforce needle safety (never share needles, syringes, or drug equipment); harm reduction programs (needle exchange); safe sex practices; no sharing of razors, toothbrushes, or nail clippers.
  • Activity and fatigue management: Plan rest periods; energy-conserving strategies; avoid strenuous activity during acute phase.
  • Nutrition: Balanced diet with adequate protein (unless hepatic encephalopathy requires restriction); avoid alcohol completely — accelerates fibrosis; avoid hepatotoxic drugs (acetaminophen in high doses, herbal supplements).
  • Bleeding precautions: Soft-bristle toothbrush; electric shaver; fall precautions (esophageal varices rupture is life-threatening); monitor for hematochezia or hematemesis.
  • Medication adherence: Educate on DAA regimen — strict daily adherence achieves high cure rates; missed doses risk treatment failure.
  • Referral: Substance use disorder treatment for IVDU; social work for support services; hepatologist referral for advanced disease.

No Vaccine Available for HCV

Unlike hepatitis A and B, there is no vaccine for hepatitis C. Primary prevention depends entirely on avoiding blood-to-blood contact. Health care workers must follow standard precautions with all patients. Post-exposure prophylaxis (PEP) is NOT available for HCV — close follow-up with serial HCV RNA testing after exposure is recommended.

Pharmacology

Drug RegimenTypeDurationNotes
Sofosbuvir/ledipasvir (Harvoni)DAA8–12 weeksHCV genotype 1, 4
Sofosbuvir/velpatasvir (Epclusa)DAA (pan-genotypic)12 weeksAll HCV genotypes
Glecaprevir/pibrentasvir (Mavyret)DAA (pan-genotypic)8 weeksAll genotypes; no cirrhosis

DAAs have replaced older interferon-based regimens due to higher efficacy (>95% sustained virologic response), fewer side effects, and shorter duration.

Clinical Judgment Application

Clinical Scenario

A 58-year-old patient with a history of IV drug use in the 1980s presents for a routine physical. He has no current complaints. Labs show elevated ALT (72 U/L) and a positive anti-HCV antibody test.

  • Recognize Cues: Positive HCV antibody, elevated ALT, risk history (IVDU), asymptomatic presentation.
  • Analyze Cues: Chronic HCV with subclinical liver inflammation is likely; elevated ALT confirms hepatocyte damage.
  • Prioritize Hypotheses: Undiagnosed chronic HCV with potential liver fibrosis requires confirmation and treatment planning.
  • Generate Solutions: Order confirmatory HCV RNA test and genotype; refer to hepatologist; assess for cirrhosis with liver biopsy or FIB-4 score.
  • Take Action: Educate patient on HCV diagnosis and transmission prevention; prepare for specialist referral; reinforce alcohol abstinence.
  • Evaluate Outcomes: HCV RNA undetectable at 12 weeks post-treatment (sustained virologic response = cure).

Self-Check

  1. Why is HCV often diagnosed years after initial infection?
  2. What test confirms active HCV viremia after a positive anti-HCV antibody screen?
  3. What patient education is most important for preventing HCV transmission to close contacts?

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