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Digestive / GI

Viral Hepatitis

Verified · Sep 2026

Viral hepatitis is inflammation of the liver caused by one of the hepatotropic viruses A, B, C, D, or E — acute when it resolves within 6 months, chronic when the virus persists beyond it — in which the immune attack on infected liver cells produces the jaundice, transaminase surge, and (rarely) liver failure that define the illness.

The disorder behind the A–E comparison table, the HBsAg / anti-HBc / anti-HBs serology puzzle, dark urine and clay-colored stools, the INR that decides whether a jaundiced patient goes to a transplant center, and the needlestick protocol every nurse will one day need for themselves.

What’s going wrong in the body

The normal physiology, where it fails, and why the body’s compensation backfires.

01 Five viruses, one organ — the A-to-E comparison that organizes everything

Hepatitis is inflammation of the liver, and the five hepatotropic viruses cause it in two families of behavior. Hepatitis A (HAV) and hepatitis E (HEV) are fecal-oral viruses: HAV spreads through close personal contact, sexual contact, and food or water contaminated by an infected person who did not wash their hands — raw shellfish, ice, unpeeled produce, untreated water — while HEV genotypes 1–2 travel in contaminated water in developing regions and genotypes 3–4 are zoonotic, arriving in undercooked pork, deer and wild game, and shellfish in developed countries. Hepatitis B (HBV), hepatitis C (HCV), and hepatitis D (HDV) are blood-borne: HBV moves through infected blood and body fluids — childbirth, sex, and shared needles or injection equipment first, then needlesticks, shared razors and toothbrushes, and open sores; HCV is acquired mainly through injection drug use (transfusion transmission became rare once blood screening began in July 1992); and HDV is a defective RNA virus that can infect only a person who already has HBV, because it borrows HBsAg as its envelope. HBV is the group’s only DNA virus, and it is durable — it stays viable on environmental surfaces for at least 7 days.

The second axis is chronicity, and it is age- and virus-specific. HAV never becomes chronic. HEV is acute-only in immunocompetent people (chronic infection — HEV RNA persisting ≥ 6 months — occurs in transplant recipients and people with HIV). HBV chronicity depends on age at infection: about 90% of infants infected perinatally, 25–50% of children aged 1–5, but only about 5% of adults (2–6%) — roughly 95% of infected adults clear the virus completely. HCV becomes chronic in more than half of infected people (historically quoted as 55–85%; newer CDC data suggest spontaneous clearance may reach 46%). HDV depends on how it arrives: coinfection (HBV and HDV acquired together) leaves about 5% chronic, whereas superinfection (HDV landing on established chronic HBV) leaves about 90% chronic and accelerates cirrhosis. Chronic HBV is defined as HBsAg persisting longer than 6 months. The scale is large: CDC estimates 880,000 people in the US were living with chronic HBV during 2013–2018, two thirds of whom may not know it, and StatPearls counts about 2.4 million with chronic HCV.

Incubation is the third column of the table, and CDC gives real ranges: HAV averages 28 days (15–50); HBV averages 60 days (40–90) to abnormal enzymes and 90 days (60–150) to symptoms; HCV runs 2–12 weeks (range 2–26), with HCV RNA detectable 1–2 weeks after exposure; HEV about 15–60 days; HDV roughly 13 weeks. The last column is prevention: vaccines exist for HAV and HBV only — and because HDV cannot exist without HBV, the HBV vaccine prevents HDV too. There is no vaccine for HCV and no HEV vaccine licensed in the US.

The A–E fork: fecal-oral viruses (A, E) burn out; blood-borne viruses (B, C, D) can persist — with chronicity set by the virus and, for HBV, by age at infection.

02 Immune-mediated injury → necrosis → cholestasis: why urine darkens before the skin yellows

The virus is not what destroys the liver — the immune system is. In HBV the injury is mainly immune-mediated: cytotoxic T cells attack infected hepatocytes, and most HBV DNA is actually cleared before maximal T-cell infiltration arrives; only a minor direct cytopathic effect exists. HAV follows the same script — a T-cell-mediated response drives both viral clearance and hepatocellular injury, with CD4 helper cells crucial for resolution. The consequences unfold in a chain: infected hepatocytes are killed → hepatocyte necrosis with inflammation swells the organ and stretches its capsule (right-upper-quadrant pain, tender hepatomegaly) → the dying cells leak ALT and AST into the blood — ALT can rise 10- to 100-fold in acute HAV → injured hepatocytes can no longer move bile out, producing intrahepatic cholestasis.

Cholestasis is where the icteric-phase findings come from, and each has a bilirubin mechanism. Normal physiology: heme breakdown yields unconjugated bilirubin, the liver conjugates it (glucuronidation) into a water-soluble form, conjugated bilirubin flows out in bile, and gut bacteria convert it to urobilinogen and stercobilin — the pigment that colors stool. In hepatitis the injured cells cannot excrete conjugated bilirubin, so it backs up into the blood. Because it is water-soluble, it filters through the glomerulus and appears in urine — dark, tea-colored urine, often the first thing the patient notices, before visible jaundice. Once serum bilirubin exceeds about 2–3 mg/dL the pigment shows in the sclera first, then skin and mucous membranes. With little bile reaching the intestine, stercobilin is not made and stools turn pale, clay-colored (acholic). Cholestasis also traps bile salts in the skin, driving the pruritus that can dominate cholestatic HAV.

Two lab-interpretation rules fall out of this chain. First, the hepatocellular pattern (ALT/AST-predominant) is the signature of viral hepatitis; a cholestatic pattern with marked alkaline phosphatase elevation points instead to biliary obstruction or the cholestatic HAV variant. Second — and it is the exam’s favorite trap — the height of the transaminases does not measure severity. What measures severity is synthetic function: prothrombin time/INR and mental status. Bilirubin rises after the transaminases and keeps climbing in a bad course; a bilirubin above 10 mg/dL is one of the triggers for antiviral therapy in severe acute HBV.

The acute-phase chain: immune attack kills hepatocytes, enzymes leak, cholestasis backs conjugated bilirubin into blood — and the urine, sclera, stool, and skin each tell part of the story.

03 The four phases — and why most infections are never noticed

Acute viral hepatitis moves through four phases. (1) Incubation: no symptoms, but the lab markers are already turning positive — HBsAg is the first HBV marker detected, and HCV RNA appears 1–2 weeks after exposure. (2) Prodromal (preicteric): a systemic, immune-driven illness before hepatocellular injury peaks — anorexia, nausea, vomiting, malaise, fatigue, low-grade fever, arthralgias, urticaria, and RUQ pain; HBV can add a serum-sickness-like syndrome of fever, rash, arthralgia, and arthritis. (3) Icteric: dark urine, pale stools, jaundice, tender hepatomegaly, elevated transaminases — in HAV the icteric phase follows the prodrome by about a week, and among symptomatic adults dark urine (68–94%) is even more common than jaundice (40–80%). (4) Convalescent: symptoms fade and enzymes normalize.

How long that takes depends on the virus. HAV symptoms usually last less than 2 months; most people recover on their own within 6 months — but 10–15% have a prolonged or relapsing course up to 6 months, and HAV has two named variants: cholestatic hepatitis (< 5%: prolonged jaundice, pruritus, acholic stools, self-limiting) and relapsing hepatitis (up to 10%: recurrence within 6 months that does not mean treatment failure). Acute HBV symptoms usually last several weeks and occasionally up to 6 months. HEV’s biochemical abnormalities resolve within 1–6 weeks.

Most infections never produce this picture at all. Most people with hepatitis C have no symptoms — acute HCV brings jaundice in only 20–30% — and chronic HBV and HCV can stay silent for years or decades until the findings of cirrhosis appear. Children under 6 with HAV are asymptomatic 70% of the time and typically not jaundiced, while more than 70% of older children and adults with HAV are; symptomatic illness occurs in 30–50% of older children, adolescents, and adults with acute HBV. That silence is the reason screening is universal rather than risk-based, and the reason a first presentation can be end-stage disease.

04 Two bad roads: fulminant failure now, or fibrosis → cirrhosis → cancer later

The acute road can end in acute liver failure (fulminant hepatitis): massive hepatocyte injury activates Kupffer cells and pours out proinflammatory mediators that drive secondary necrosis. Synthetic function collapses — the liver stops making clotting factors (INR climbs) and stops sustaining glucose (hypoglycemia) — while ammonia accumulates, the blood–brain barrier is disrupted, astrocytes swell, and cerebral edema produces encephalopathy. ALF is defined by hepatic encephalopathy plus an INR ≥ 1.5 in a patient without preexisting liver disease, within 26 weeks; the hyperacute form (< 7 days) brings more cerebral edema but a better transplant-free prognosis, and the subacute form (> 4 weeks) fares worst without transplant. It is rare but lethal: under 1% of adults with HAV (about 30% of those need a transplant), roughly 0.5–1% of HBV with about 80% mortality when it occurs — but about 20% with HBV plus HDV, and a catastrophic rate in pregnant women with HEV, whose third-trimester mortality is commonly cited at 15–25% and ≥ 30% in some outbreaks, with stillbirth or neonatal death in over half of exposed fetuses. About 30% of all ALF patients need a transplant, which is why the rule is transfer to a liver transplant center early.

The chronic road is slower. Persistent infection keeps the immune attack running → ongoing inflammation → fibrosis → cirrhosis → portal hypertension and decompensation (variceal bleeding, ascites, spontaneous bacterial peritonitis, encephalopathy) → hepatocellular carcinoma (HCC). About 5–25% of people with chronic HCV develop cirrhosis over 10–20 years (CDC); 15–25% of those with chronic HBV develop chronic liver disease including cirrhosis, liver failure, or liver cancer; and about two thirds of chronic HDV patients reach cirrhosis, faster than with HBV alone. Together chronic HBV and HCV account for more than 70% of HCC worldwide. Cirrhosis from HCV carries a 1–4% annual HCC risk, and HBV has a peculiarity worth memorizing: because it is a DNA virus, it can cause HCC without cirrhosis — though more than 80% of HBV-related HCC still has cirrhosis underneath. That is why AASLD recommends ultrasound plus serum alpha-fetoprotein about every 6 months for everyone with cirrhosis and for high-risk noncirrhotic chronic-HBV groups — men over 40 and women over 50 from HBV-endemic regions, people from Africa at younger ages, and those with a family history of HCC (AASLD 2023) — and AASLD 2018 adds people with HDV coinfection.

One more chronic-road hazard: reactivation. Resolved or chronic HBV can flare back to life under chemotherapy, immunosuppressive therapy, HIV, transplantation — and during HCV direct-acting antiviral (DAA) therapy in coinfected patients. AASLD 2018 therefore has HBsAg-positive, anti-HBc-positive patients start anti-HBV prophylaxis before immunosuppressive or cytotoxic therapy, and it is why a "resolved infection" serology is counseled on reactivation risk rather than simply reassured.

The chronic road: persistent infection feeds inflammation, fibrosis, and cirrhosis, which branches into decompensation and cancer — with HBV able to jump straight to HCC.

Causes & risk factors

Modifiable factors are teaching targets — the patient can act on them.

Injection or noninjection drug use with shared needles, syringes, or equipment (the predominant HCV route; a primary HBV route) modifiable Unprotected sex, multiple partners, history of STIs, men who have sex with men (HBV; HAV; HCV — less common than parenteral, higher with HIV) modifiable Sharing razors, toothbrushes, or nail clippers with an infected person modifiable Unregulated tattoos, piercings, or acupuncture with unsterile equipment modifiable Contaminated food or water — raw shellfish, ice, unpeeled produce, food handled by an infected person; travel to Asia, South/Central America, Africa, the Middle East (HAV) modifiable Undercooked pork, deer, or wild game (HEV genotypes 3–4 — typical US patient is a man over 60) modifiable Perinatal exposure — infant born to an HBsAg-positive mother (~90% chronic without prophylaxis); infant of an HCV-positive mother (~5.8%) Birth in an HBV-endemic region; household or sexual contact of an HBsAg-positive person Health care work with needlestick and sharps exposure; hemodialysis; blood transfusion or organ transplant before July 1992 (HCV) Incarceration, homelessness, and shelter or daycare settings (HAV, HBV) Existing chronic HBV — the only way to acquire HDV, which needs HBsAg to replicate HIV, diabetes, or existing HCV (higher HBV risk); immunosuppression and transplantation (chronic HEV, HBV reactivation) Alcohol use and hepatotoxic drugs or supplements — worsen the injury of any hepatitis modifiable Age over 50, preexisting liver disease, and pregnancy — raise the risk of a fulminant course (HAV; HEV)

Signs & symptoms

Each finding tied to the mechanism that produces it — and the triage it calls for.

No symptoms at all — most HCV, 70% of HAV in children under 6, most chronic HBV/HCV for years early
Why: Immune-mediated injury can be mild or gradual enough to produce no illness; the virus is found by screening or by an incidental transaminase rise. Silence is the argument for universal one-time testing, not a sign of safety.
Prodromal flu-like cluster — anorexia, nausea, malaise, fatigue, low-grade fever, arthralgias, urticaria, RUQ discomfort early Expected
Why: A systemic immune response to viremia before hepatocellular injury peaks — the preicteric phase. HBV may add a serum-sickness-like syndrome (fever, rash, arthralgia, arthritis) from immune complexes. Expected, and easily mistaken for a viral syndrome.
Dark, tea-colored urine — often before the skin changes Expected
Why: Cholestasis backs conjugated (water-soluble) bilirubin into the blood; it filters through the glomerulus and colors the urine. In symptomatic HAV adults it is reported in 68–94% — more often than jaundice itself.
Jaundice — sclera first, then skin and mucous membranes Expected
Why: Injured hepatocytes cannot excrete conjugated bilirubin into bile; it becomes visible once serum bilirubin exceeds about 2–3 mg/dL. Expected in the icteric phase — but jaundice that keeps deepening, especially with confusion or bleeding, is the fulminant signal.
Pale, clay-colored (acholic) stools Expected
Why: Bile is not reaching the intestine, so bilirubin is never converted to stercobilin, the pigment that colors stool. Expected during the cholestatic phase.
Pruritus — sometimes the dominant complaint Expected
Why: Cholestasis traps bile salts in the skin, triggering itch (mechanism incompletely understood). Prominent in the cholestatic HAV variant, where jaundice and itching can persist for months.
RUQ pain with tender hepatomegaly Expected
Why: The inflamed, swollen liver stretches its capsule; the exam finds an enlarged, tender edge. Expected — a marked alkaline phosphatase elevation with the same pain should raise biliary obstruction instead.
Vomiting that prevents oral intake or hydration Hold & notify
Why: Prodromal nausea and vomiting are expected, but a patient who cannot maintain hydration meets the admission criterion for acute hepatitis — hold and notify rather than reassure.
New confusion, drowsiness, or any subtle mental-status change late Report immediately
Why: Hepatic encephalopathy — ammonia accumulation, blood–brain-barrier disruption, astrocyte swelling, cerebral edema. With an INR ≥ 1.5 this defines acute liver failure: early transfer to a liver transplant center, and no sedatives that would mask the trend.
Bleeding, bruising, or a rising INR (≥ 1.5) late Report immediately
Why: Loss of synthetic function — the failing liver stops making clotting factors. INR, not transaminase height, is the severity marker; hematemesis or bloody stools are reasons to seek emergency care.
Hypoglycemia late Report immediately
Why: The failing liver cannot sustain glucose output — part of the ALF picture, and a treatable contributor to altered mental status that must be checked before the confusion is blamed on ammonia alone.
Late chronic findings — ascites, splenomegaly, spider nevi, palmar erythema, gynecomastia, caput medusae late Hold & notify
Why: When chronic HBV or HCV finally declares itself it does so as cirrhosis with portal hypertension; these are the findings of the end of the chronic road, not of hepatitis itself.
Extrahepatic immune-complex disease — glomerulonephritis, vasculitis, cryoglobulinemia late
Why: Circulating immune complexes lodge in vessels and glomeruli: HBV with polyarteritis nodosa and membranous or membranoproliferative glomerulonephritis; HCV with essential mixed cryoglobulinemia, glomerulonephritis, porphyria cutanea tarda, lichen planus, and B-cell lymphoma; HEV with neurologic complications in about 8%.

Diagnostics

Test In this disorder Normal
ALT / AST Magnitude ≠ severity — a huge ALT with a normal INR and clear mind is expected; a falling ALT with a rising INR is failure, not recovery. ALT more than 2× the upper limit of normal (AASLD 2018 uses 35 U/L men / 25 U/L women) plus a high HBV DNA is the chronic-HBV treatment trigger Markedly elevated in acute infection — up to a 10- to 100-fold rise in HAV, where ALT runs higher than in other viral hepatitis (hepatocellular pattern) StatPearls; AASLD 2018 (treatment threshold) —
Bilirubin (total / conjugated) Track the trend, not the single value — worsening jaundice with rising bilirubin is one of the heralding cues of acute liver failure Rises after the transaminases; conjugated fraction elevated in the icteric phase; jaundice visible above ~2–3 mg/dL; > 10 mg/dL is a severity trigger for antiviral therapy in acute HBV StatPearls —
PT / INR (+ albumin, glucose, ammonia) The severity marker of the whole page. In ALF, correct coagulopathy only for active bleeding or before invasive procedures — the INR is the prognostic signal you do not want to erase. ALF adds hypoglycemia, elevated ammonia, lactate/metabolic acidosis, and a rising creatinine; albumin and PT track synthetic function in chronic disease Normal unless severe — INR ≥ 1.5 with encephalopathy defines acute liver failure; acute-HBV antiviral thresholds quote INR > 1.5–1.6 StatPearls (Acute Liver Failure) —
HAV serology (IgM / IgG anti-HAV) IgM turns positive before IgG; the antibody type separates current infection from past infection or vaccination IgM anti-HAV = acute infection (positive 4–6 months); IgG anti-HAV = past infection or vaccination = lifelong immunity —
HBV serology (triple panel ± HBeAg, HBV DNA) HBsAg = current infection (first marker detected); anti-HBs = immunity; total anti-HBc = past or present infection; IgM anti-HBc = acute; HBeAg = high infectivity/viral load; HBV DNA = replication. Vaccination makes anti-HBs only — an anti-HBc tells you the person met the real virus. Protective anti-HBs = ≥ 10 mIU/mL Acute: HBsAg +, IgM anti-HBc +, anti-HBs −. Chronic: HBsAg + > 6 months, total anti-HBc +, IgM anti-HBc −. Resolved: HBsAg −, anti-HBs +, anti-HBc +. Immune from vaccine: anti-HBs + alone. Susceptible: all negative. Window period: HBsAg gone, anti-HBs not yet present — IgM anti-HBc may be the only positive marker CDC 2023 / ACIP 2018 —
HCV antibody → reflex HCV RNA Antibody appears 4–10 weeks after exposure, RNA at 1–2 weeks. Antibody stays positive for life — including after cure — so post-treatment monitoring and re-testing after reinfection use RNA. Cure (SVR) = no detectable RNA 12 weeks after finishing therapy. Staging follows: viral load, genotype, and fibrosis by APRI/FIB-4 or transient elastography (FibroScan), preferred over biopsy Anti-HCV reactive → HCV RNA (NAT) confirms current infection; anti-HCV + with RNA − = resolved infection or false positive, not current disease CDC 2020 —
HDV and HEV testing Order HDV testing on any chronic-HBV patient with a sudden severe hepatitis — superinfection is the classic cause of an unexplained flare HDV: HBsAg must be positive (no HBsAg = no HDV) + anti-HDV; HDV RNA by RT-PCR is the most sensitive test; IgM anti-HBc present = coinfection, absent = superinfection. HEV: IgM anti-HEV for acute infection; HEV RNA in serum or stool is definitive and the cornerstone in the immunocompromised —
Anti-HBs after vaccination (post-vaccination serology) Drawn 1–2 months after the final dose for health care personnel and dialysis patients; for infants of HBsAg-positive mothers at 9–12 months, not earlier, to avoid detecting passive anti-HBs from HBIG ≥ 10 mIU/mL = immune (documented responder); < 10 → revaccinate and retest ACIP 2018 —

Complications

Warning: Acute liver failure (fulminant hepatitis) Report immediately
Encephalopathy (confusion → coma) plus INR ≥ 1.5, hypoglycemia, and jaundice that keeps deepening — in a patient who was well weeks ago.
Massive immune-mediated necrosis collapses synthetic function and swells the brain. Rare with HAV (< 1% of adults) and HBV (0.5–1%, ~80% mortality when it occurs), but about 20% with HBV + HDV and concentrated in pregnancy with HEV. About 30% of ALF patients undergo transplantation, and some patients survive only with an emergency liver transplant — so the rule is early transfer to a transplant center, serial neuro checks, glucose monitoring, no sedatives, and correcting the INR only for bleeding or procedures.
Warning: HEV in pregnancy Report immediately
Third-trimester maternal mortality commonly cited at 15–25%, ≥ 30% in some outbreaks; stillbirth or neonatal death in over half of exposed fetuses.
The mechanism is unclear (a proposed Th1→Th2 immune shift and higher viral loads); fulminant failure may present with bleeding, eclampsia, or DIC. Ribavirin, the off-label drug for chronic HEV, is contraindicated in pregnancy — management is supportive, and any pregnant traveler with jaundice is a now-emergency.
Caution: HDV superinfection of chronic HBV Hold & notify
A stable chronic-HBV patient suddenly has severe acute hepatitis or an exacerbation — HDV has arrived and borrowed the HBsAg envelope.
Superinfection leaves about 90% chronically infected with HDV, accelerates cirrhosis (about two thirds), and brings HCC within 5–10 years. Nucleos(t)ide analogs do not treat HDV; peginterferon alfa for 48 weeks is the main (off-label) option and there is no cure. Prevention is HBV vaccination — immune to HBV means protected from HDV.
Caution: Cirrhosis → decompensation → hepatocellular carcinoma Hold & notify
Chronic HCV: 5–25% reach cirrhosis over 10–20 years; chronic HBV: 15–25% develop chronic liver disease; HCV cirrhosis carries a 1–4% annual HCC risk, and HBV can cause HCC without cirrhosis.
Decompensation looks like variceal bleeding, ascites, spontaneous bacterial peritonitis, and encephalopathy — managed as cirrhosis. HCC presents late (abdominal pain, jaundice, ascites, weight loss), and about 40% of small tumors secrete no AFP, so ultrasound + AFP every 6 months (AASLD 2023) is the surveillance that finds it early. Keeping that appointment is a nursing teaching point, not a formality.
Caution: HBV reactivation under immunosuppression or HCV therapy Hold & notify
A "resolved" or quiet chronic HBV flares back during chemotherapy, immunosuppressive or anti-CD20 therapy, HIV, transplantation — or HCV DAA treatment.
AASLD 2018: HBsAg-positive, anti-HBc-positive patients start anti-HBV prophylaxis before immunosuppressive or cytotoxic therapy, and HBV serology is checked with HBV DNA/ALT monitoring before HCV DAAs in coinfected patients. This is why the triple panel is drawn before oncology treatment, and why the patient must disclose HBV status to every prescriber.

Medications for this condition

Why each class is prescribed here — every card links to its full pharmacology page.

Antivirals First-line
Immune / Anti-infective · acyclovir

The one class whose role changes with the letter. HAV and HEV: no antivirals — acute infection is supportive care only (ribavirin is used off-label for chronic HEV in the immunosuppressed and is contraindicated in pregnancy). Acute HBV: supportive unless severe — nucleos(t)ide analogs are reserved for bilirubin > 10 mg/dL, INR > 1.5–1.6, encephalopathy, or a protracted course. Chronic HBV: entecavir, tenofovir disoproxil, or tenofovir alafenamide (high barrier to resistance) suppress HBV DNA but do not cure — HBsAg loss is desired but rare — treatment is indefinite for HBeAg-negative and cirrhotic patients (AASLD 2018), and stopping can trigger a hepatitis flare, so ALT is monitored every 3 months for at least a year after any discontinuation; in pregnancy, third-trimester tenofovir for HBV DNA > 200,000 IU/mL further reduces transmission. HCV: an 8–12-week course of oral direct-acting antivirals cures more than 95% regardless of genotype (glecaprevir/pibrentasvir 8 weeks; sofosbuvir/velpatasvir 12 weeks), is recommended for nearly everyone with HCV including acute infection, and is confirmed by SVR — undetectable RNA 12 weeks after finishing; check HBV serology first because DAAs can reactivate HBV. HDV: nucleos(t)ide analogs do not work; peginterferon alfa is the off-label mainstay.
Vaccines & Immunizations
Immune / Anti-infective

The prevention arm exists for A and B only — and B covers D. HAV vaccine: inactivated, 2 doses 6–18 months apart, seroconversion approaching 100%, protection about 4 weeks after dose 1; routine at 12–23 months with catch-up to 18 years, and for travelers, MSM, people who use drugs, people experiencing homelessness, chronic liver disease (including HBV, HCV, cirrhosis), HIV, and anyone who wants immunity (ACIP 2020). It doubles as post-exposure prophylaxis within 2 weeks for healthy people aged 12 months–40 years; immune globulin (± vaccine) covers those over 40, under 12 months, immunocompromised, or with chronic liver disease. HBV vaccine: recombinant, universal at birth and for all adults 19–59 (the 2022 ACIP recommendation, as restated by CDC 2023) — the standard adult series is 3 doses at 0, 1, and 6 months (ACIP 2018); testing should never delay vaccinating (CDC 2023). Post-vaccination anti-HBs (≥ 10 mIU/mL) is checked 1–2 months after the last dose in health care personnel and dialysis patients. HBIG is passive, temporary anti-HBs (3–6 months) for post-exposure use only, always paired with vaccine in the unvaccinated. There is no HCV vaccine and no HCV post-exposure prophylaxis.

Beyond medications

  • Rest, fluids, and nutrition are the treatment of acute hepatitis — no specific therapy exists for HAV, and acute HBV is usually managed without antivirals unless it is severe. Nutrition is ordinary healthy eating with plenty of fluids — talk with the provider about diet — and no alcohol, which adds liver damage. Admit for vomiting that defeats hydration or any sign of liver failure.
  • Infants of HBsAg-positive mothers: HepB vaccine + HBIG within 12 hours of birth, at different injection sites (separate limbs) — without it about 90% become chronically infected. Every infant gets a birth dose as a safety net against unknown or misdocumented maternal status; breastfeeding is safe after prophylaxis; post-vaccination serology at 9–12 months.
  • Occupational HBV exposure — act by vaccination status (ACIP 2018). Documented responder (anti-HBs ≥ 10 after a full series) → no action. Unvaccinated or incomplete series + HBsAg-positive source → 1 dose HBIG + start/complete the vaccine series, anti-HBs 1–2 months after the last dose; unknown or negative source → start the series and test. Unknown response → draw the worker’s anti-HBs and the source HBsAg together; if < 10 and the source is positive or unknown → HBIG + revaccination. Documented nonresponder (two series, still < 10) → 2 doses of HBIG, first as soon as possible, second 1 month later. HBIG goes in as soon as possible, preferably within 24 hours; its value falls after 7 days for percutaneous and 14 days for sexual exposure.
  • HCV exposure — testing, not prophylaxis (CDC 2020). No vaccine, no PEP. Test the source with HCV RNA (or antibody with reflex RNA); test the exposed worker at baseline within 48 hours, then HCV RNA at 3–6 weeks and anti-HCV with reflex RNA at 4–6 months; anyone found RNA-positive goes straight to DAA treatment. Percutaneous transmission from an HCV-positive source is about 0.2% (older data 1.8%); the ordering to remember is HBV ≫ HCV > HIV. First aid: wash with soap and water, flush mucous membranes, do not squeeze or apply bleach, report immediately.
  • Precautions (CDC Isolation Guideline, Appendix A): HBV, HCV, HDV → standard precautions only — no isolation. HAV and HEV → standard, plus contact precautions for diapered or incontinent patients: infants and children under 3 for the whole hospitalization, ages 3–14 for 2 weeks after symptom onset, over 14 for 1 week after symptom onset (HEV: for the duration of illness). HAV is most transmissible in the 2 weeks before jaundice; most people are non-infectious 1 week after jaundice appears, which is the usual return-to-work point — food handlers stay out until shedding ceases.
  • Screening is universal, not risk-based. CDC 2023: every adult ≥ 18 gets HBV screening at least once with the triple panel (HBsAg, anti-HBs, total anti-HBc), and every pregnant person each pregnancy, preferably first trimester. CDC 2020: every adult ≥ 18 gets one-time HCV screening and every pregnant woman is screened each pregnancy; people who inject drugs are retested periodically while risk continues; infants of HCV-positive mothers are tested. Testing is not a prerequisite for vaccination.
  • Surveillance and transplant. Chronic HBV/HCV follow-up tracks albumin, LFTs, PT, viral load, and elastography; cirrhosis and high-risk noncirrhotic HBV get HCC ultrasound + AFP every 6 months. Some patients with acute liver failure need an emergency liver transplant — about 30% of ALF patients undergo transplantation — and HCV was the leading transplant indication before DAAs.

Nursing considerations

The RN-specific layer — each action paired with the reason it matters.

Assessment & monitoring
Assess mental status every shift and with every change — orientation, subtle slowing, drowsiness, asterixis — and grade encephalopathy; check a fingerstick glucose with any new confusion.
Why: Encephalopathy plus INR ≥ 1.5 is acute liver failure, and early recognition of subtle change is what allows transfer to a transplant center before irreversible cerebral injury. Hypoglycemia from lost synthetic function is a treatable cause of the same confusion.
Track PT/INR as the severity marker, alongside bilirubin trend, glucose, and (in ALF) ammonia and creatinine; watch for bleeding gums, bruising, hematemesis, and melena.
Why: A falling ALT with a rising INR is failure, not recovery — transaminase height does not measure severity, synthetic function does. In ALF the INR is corrected only for active bleeding or before procedures because it is the prognostic signal.
Read the serology before you read the chart summary: HBsAg, IgM anti-HBc, anti-HBs, HBeAg, and HBV DNA for B; anti-HCV with reflex RNA for C; IgM anti-HAV for A.
Why: The pattern sets everything downstream — acute vs chronic, infectivity (HBeAg), whether the patient is immune from vaccine (anti-HBs alone) or from resolved infection (anti-HBs + anti-HBc, who needs reactivation counseling), and who gets isolation vs standard precautions.
Monitor intake, output, weight, and the ability to keep fluids down; report vomiting that prevents hydration.
Why: Severe nausea and vomiting with inability to maintain hydration is the admission criterion for acute hepatitis — rest, fluids, and nutrition are the treatment, and a patient who cannot take them in needs a different plan.
Document jaundice progression (sclera, skin, mucous membranes), urine and stool color, and pruritus severity daily.
Why: Dark urine precedes visible jaundice, clay stools mark cholestasis, and a bilirubin that keeps climbing — above 10 mg/dL in acute HBV — is a heralding cue of a fulminant course and a trigger for antiviral therapy.
In pregnant patients with jaundice or travel exposure, escalate immediately and confirm HEV testing.
Why: HEV in the third trimester carries maternal mortality commonly cited at 15–25% and fetal loss in over half of cases; supportive care and early recognition are the only tools, and ribavirin is contraindicated.
Interventions & safety
Use standard precautions for HBV, HCV, and HDV (gloves for blood and body fluids, no isolation); add contact precautions for diapered or incontinent HAV/HEV patients for the age-based durations (< 3 years: whole stay; 3–14: 2 weeks; > 14: 1 week after symptom onset).
Why: Blood-borne viruses do not spread by touch, coughing, or shared meals, so isolating them is stigma without benefit; fecal-oral viruses are shed in stool, most heavily in the 2 weeks before jaundice.
Protect yourself: safety-engineered devices, never recap, sharps containers at the point of use, HAV and HBV vaccination, and a documented anti-HBs ≥ 10 mIU/mL on file.
Why: HBV survives on surfaces for at least 7 days and transmits far more readily than HCV or HIV after a needlestick; a documented responder needs no post-exposure action, while an unknown status means HBIG decisions under a 24-hour clock.
After any needlestick: wash with soap and water, flush mucous membranes, do not squeeze or apply bleach, and report immediately so the source can be tested and HBIG/vaccine started within 24 hours.
Why: HBIG effectiveness falls after 7 days (percutaneous) or 14 days (sexual); HCV has no PEP, so the value of reporting is baseline testing and the 3–6-week RNA and 4–6-month follow-up that catch infection early enough for immediate DAA treatment.
Avoid sedatives and hepatotoxic medications; clear every PRN, OTC, supplement, and herbal with the prescriber, and use acetaminophen cautiously.
Why: Sedatives mask the mental-status trend that is the ALF alarm; the inflamed liver clears drugs poorly, and acetaminophen excess and some OTC or herbal products cause acute hepatitis on their own.
Manage pruritus without scratching: cool compresses, lukewarm or oatmeal baths, moisturizer, avoid irritating fabrics and heat, OTC antihistamines as ordered — and prescribed cholestyramine, rifampicin, or ondansetron for severe cholestatic itch.
Why: Bile salts trapped in the skin drive the itch; scratching breaks skin in a patient who may be coagulopathic, and heat and rough fabric intensify it.
For infants of HBsAg-positive mothers, give HepB vaccine and HBIG within 12 hours of birth in separate limbs and document both.
Why: About 90% of unprotected exposed infants acquire chronic HBV; prophylaxis is the single highest-yield intervention on the page and breastfeeding becomes safe once it is given.
Patient teaching
No alcohol — during recovery and for life with chronic HBV or HCV.
Why: Every teaching source agrees: alcohol causes additional liver damage on top of the immune injury and accelerates the road to cirrhosis.
Blood-borne prevention: never share toothbrushes, razors, nail clippers, needles, or injection equipment; cover cuts; use latex condoms; choose licensed, sterile tattoo and piercing equipment; do not donate blood or organs.
Why: HBV is most concentrated in blood and survives on surfaces for a week; HCV cure does not confer immunity, so risk reduction continues after treatment. Coughing, hugging, and sharing food do not spread B or C.
Fecal-oral prevention: handwashing ≥ 20 seconds after the toilet and before food; when traveling, bottled or boiled water, no ice, no raw shellfish, no unpeeled produce; cook pork and game thoroughly. With HAV, no food handling until shedding stops; return to work typically 1 week after jaundice appears.
Why: HAV survives months on surfaces and hours on hands but is removed by thorough washing; peak transmissibility is the 2 weeks before jaundice, when the patient does not yet know.
Report symptoms that persist or worsen, and seek emergency care for vomiting blood, black or bloody stools, or new confusion.
Why: Those three are the patient-facing cues of acute liver failure and variceal bleeding; a relapse of HAV within 6 months is expected in up to 10% and does not mean failure, but confusion never is.
Chronic HBV: never stop the antiviral on your own; keep every 6-month ultrasound if cirrhotic or high-risk; tell every prescriber your HBV status before chemotherapy, immunosuppression, or HCV treatment. Chronic HCV: finish the full 8–12-week DAA course, confirm cure with HCV RNA at 12 weeks, and expect the antibody to stay positive for life.
Why: Stopping HBV therapy can trigger a hepatitis flare (monitor 3-monthly for a year); reactivation under immunosuppression is preventable with prophylaxis; and a lifelong positive anti-HCV is not a treatment failure.
Get the household tested and vaccinated: HBV contacts need the triple panel and vaccine; HAV contacts need vaccine or immune globulin within 2 weeks; children of HCV-positive mothers need testing.
Why: Household and sexual contacts of an HBsAg-positive person are a named risk group, and vaccine-induced immunity (anti-HBs ≥ 10 mIU/mL) also blocks HDV; the 2-week HAV window is the ACIP 2020 rule, not 48 hours.

How a real nurse thinks

The clinical-judgment loop, worked for a typical presentation — reasoning, not reference.

  1. 1
    Recognize cues

    Two patients hide in this handoff. The admitted patient’s cues: icteric phase findings (dark urine, pale stools, jaundice, tender hepatomegaly, pruritus), ALT in the thousands with ALT > AST, a bilirubin that rose overnight, an INR of 1.4 that also crept up — and a serology of HBsAg +, IgM anti-HBc +, anti-HBs −, HBeAg +. The reassuring cues: alert and fully oriented, glucose normal, no bleeding, tolerating intake. The second patient is the night nurse: a hollow-bore needlestick from an HBsAg-positive, HBeAg-positive, anti-HCV-negative source, with an incomplete vaccine series and no documented titer.

  2. 2
    Analyze cues

    The serology reads as acute hepatitis B: HBsAg says current infection, IgM anti-HBc says it is acute (chronic infection would have total anti-HBc with IgM negative), anti-HBs negative says no immunity yet, and HBeAg says high infectivity — which matters for the nurse. The ALT of 2,140 is expected for acute viral hepatitis and is not the severity signal; the bilirubin trend (7.1 → 8.6, still below the 10 mg/dL antiviral trigger) and the INR (1.3 → 1.4, below 1.5) are. Right now he has severe-looking numbers with intact synthetic function and a clear mind — but both severity markers are moving in the wrong direction. The trap is to file the INR as "within a whisker of normal" instead of as a trend that is one step from the ALF definition.

  3. 3
    Prioritize

    For the patient, the dangerous outcome is acute liver failure: encephalopathy plus INR ≥ 1.5. Priority one is therefore surveillance that would catch it — mental status every shift and with any change, INR and bilirubin trending, glucose — and removing anything that would mask it (the PRN sedating antihistamine deserves a conversation with the prescriber before the next dose). Priority two is the nurse, whose clock is already running: HBIG works best within 24 hours of exposure, so her post-exposure plan cannot wait for a titer to result. The pruritus and the room assignment (standard precautions — no isolation) are real but less urgent.

  4. 4
    Generate solutions

    Patient: continue rest, fluids, and a carbohydrate-based diet; clarify the PRN antihistamine and any acetaminophen with the prescriber; hold hepatotoxins and alcohol teaching for later in the day; set explicit re-escalation triggers — any confusion, INR ≥ 1.5, bilirubin > 10, bleeding, or hypoglycemia → notify immediately and anticipate discussion of nucleos(t)ide antiviral therapy and transfer to a liver transplant center. Nurse: under ACIP 2018 she maps to "unvaccinated/incompletely vaccinated" with an HBsAg-positive source → 1 dose of HBIG as soon as possible + complete the vaccine series, then anti-HBs 1–2 months after the final dose. The source is anti-HCV-negative, so no HCV follow-up series is needed — and there would be no HCV PEP anyway.

  5. 5
    Take action

    Confirm employee health has the source serology (HBsAg +, HBeAg +, anti-HCV −) and that the nurse’s HBIG is being given today, not after a titer. For the patient: standard precautions on the door — no contact or droplet signage; neuro check documented as a baseline others can compare against; SBAR to the provider: "34-year-old with acute hepatitis B — HBsAg, IgM anti-HBc, HBeAg positive. ALT 2,140, bilirubin up to 8.6, INR up to 1.4, mentation intact, glucose 84. Requesting parameters for repeat INR and bilirubin, clarification of the PRN diphenhydramine given the need to track mental status, and confirmation of the threshold for antiviral therapy and transplant-center referral." The trap to avoid: treating a normal-looking INR as reassurance in a patient whose INR is rising.

  6. 6
    Evaluate

    Success by end of shift: the nurse has received HBIG and a vaccine dose is scheduled; the patient remains oriented with a stable glucose, INR and bilirubin rechecked with parameters written, and teaching begun on no alcohol, no shared razors or toothbrushes, condoms, and household testing and vaccination. The re-escalation trigger is memorized in advance: new confusion, drowsiness, or slowed answers with an INR at or above 1.5 = acute liver failure — an emergency and a transplant-center call, not a note for morning rounds.

Scenario — you’re the nurse

Work each question before revealing the answer. Rationales explain the wrong options too.

Medical-surgical unit · 0700 handoff, hospital day 2

A 34-year-old man admitted with 5 days of dark urine, nausea, and yellowing eyes; history of injection drug use, never vaccinated for hepatitis B. Serology resulted overnight. On the night shift, the RN drawing his 0500 labs sustained a hollow-bore needlestick to the finger; she has had 2 of 3 hepatitis B vaccine doses and never had a titer drawn.

0700 vitals — HR 88 · BP 118/72 · RR 16 · SpO₂ 98% on room air · T 37.6 °C
Assessment — alert, oriented ×4, answers promptly · icteric sclera and skin · tender enlarged liver edge · scattered excoriations from scratching · urine tea-colored · stool pale · no bruising or bleeding
0500 labs — ALT 2,140 · AST 1,380 · total bilirubin 8.6 mg/dL (7.1 on admission) · INR 1.4 (1.3 on admission) · glucose 84 mg/dL · platelets 168
Serology — HBsAg positive · IgM anti-HBc positive · anti-HBs negative · HBeAg positive · IgM anti-HAV negative · anti-HCV negative
Chart — tolerating fluids, ate half of breakfast · PRN diphenhydramine for itching ordered · night RN’s needlestick reported to employee health; source is this patient
Q1 Multiple choice
The nurse reviews the serology: HBsAg positive, IgM anti-HBc positive, anti-HBs negative, HBeAg positive. The nurse interprets this as:
  1. A. Chronic hepatitis B infection
  2. B. Acute hepatitis B infection with high infectivity
  3. C. Resolved hepatitis B infection with lifelong immunity
  4. D. Immunity from hepatitis B vaccination
Reveal answer & rationale
Answer: B
HBsAg positive = current infection; IgM anti-HBc positive = acute; HBeAg positive = high viral load and infectivity (B). Chronic infection (A) shows HBsAg persisting beyond 6 months with total anti-HBc positive but IgM anti-HBc negative. Resolved infection (C) has HBsAg negative with anti-HBs and anti-HBc both positive. Vaccine immunity (D) produces anti-HBs alone — a positive anti-HBc of any kind means the person met the actual virus.
Q2 Select all that apply
At 1500 the patient is drowsy and slow to answer questions. Repeat labs: INR 1.7, total bilirubin 9.4 mg/dL, ALT 1,650, glucose 62 mg/dL. Which findings require immediate action? Select all that apply.
  1. A. New drowsiness and slowed responses
  2. B. INR 1.7
  3. C. ALT fallen from 2,140 to 1,650
  4. D. Glucose 62 mg/dL
  5. E. Total bilirubin 9.4 mg/dL
Reveal answer & rationale
Answer: A, B, D
New encephalopathy (A) with an INR ≥ 1.5 (B) meets the definition of acute liver failure — an emergency requiring immediate notification and early transplant-center referral. Hypoglycemia (D) reflects lost synthetic function, contributes to the altered mental status, and is treatable now. The falling ALT (C) is the trap: transaminase height does not measure severity, and a falling ALT with a rising INR reflects fewer surviving hepatocytes, not recovery — it is not itself an action item. Bilirubin 9.4 (E) is worsening and worth reporting in the same call, but it remains below the 10 mg/dL antiviral trigger and is not the emergency finding.
Q3 Multiple choice
Employee health asks the charge nurse what the night RN needs after the needlestick (2 of 3 HepB doses, no titer; source HBsAg positive, anti-HCV negative). The correct plan is:
  1. A. No action — two vaccine doses provide adequate protection
  2. B. Draw an anti-HBs titer and wait for the result before deciding on HBIG
  3. C. One dose of HBIG as soon as possible plus completion of the vaccine series, with anti-HBs testing 1–2 months after the final dose
  4. D. Two doses of HBIG one month apart and begin HCV post-exposure prophylaxis
Reveal answer & rationale
Answer: C
Under ACIP 2018 an unvaccinated or incompletely vaccinated worker exposed to an HBsAg-positive source receives 1 dose of HBIG plus start/completion of the vaccine series, with anti-HBs drawn 1–2 months after the last dose (C). Taking no action (A) ignores that only a documented responder (anti-HBs ≥ 10 mIU/mL after a complete series) needs nothing. Waiting for a titer (B) is the plan for a fully vaccinated worker with unknown response, and even then HBIG cannot wait — it works best within 24 hours and loses value after 7 days. Two HBIG doses (D) are for a documented nonresponder after two full series, and there is no HCV post-exposure prophylaxis — only baseline and follow-up testing, which this HCV-negative source does not even require.
Q4 Put in order
Put the nurse’s first four actions at 1500 in priority order:
  1. A. Notify the provider (SBAR) — anticipate transfer to a liver transplant center and antiviral orders
  2. B. Perform a focused neurologic assessment and treat the fingerstick glucose per protocol
  3. C. Institute bleeding precautions and hold any sedating PRN medication
  4. D. Document the findings and the updated plan of care
Reveal answer & rationale
Correct order: B → A → C → D
Assess and treat the reversible contributor first: a neurologic baseline plus correcting hypoglycemia (B) takes minutes and can clarify how much of the drowsiness is glucose versus ammonia. Escalation (A) follows immediately — encephalopathy with INR 1.7 is ALF, and early transplant-center transfer is the rule. Bleeding precautions and holding sedatives (C) protect the patient from the coagulopathy and keep the mental-status trend readable, but they follow the call. Documentation (D) never precedes protecting the patient. Calling first (A before B) leaves a hypoglycemic patient untreated while you are on the phone.
Q5 Multiple choice
The patient’s partner asks whether she needs to wear a gown and mask to visit and whether the family should do anything. The best response is:
  1. A. "Yes — gown, gloves, and a mask are required because hepatitis B spreads through the air."
  2. B. "Contact precautions are needed for 1 week after his jaundice started because the virus is in his stool."
  3. C. "No isolation is needed — hepatitis B spreads through blood and body fluids, not touch or breathing. Household and sexual contacts should be tested and vaccinated."
  4. D. "No special precautions, and family members do not need testing because adults rarely become chronically infected."
Reveal answer & rationale
Answer: C
HBV requires standard precautions only — it is spread through blood, sex, childbirth, and shared needles or personal items, not by coughing, hugging, or sharing meals — and household and sexual contacts of an HBsAg-positive person should be tested (triple panel) and vaccinated (C). Airborne or droplet precautions (A) have no basis. Contact precautions for 1 week after jaundice (B) is the rule for incontinent hepatitis A patients over 14, a fecal-oral virus — not B. Option D is half right and dangerously wrong: adults do clear HBV about 95% of the time, but contacts still need testing and vaccination, and vaccine immunity also blocks hepatitis D.

Common questions

What causes viral hepatitis?
Common causes and risk factors include injection or noninjection drug use with shared needles, syringes, or equipment (the predominant hcv route; a primary hbv route), unprotected sex, multiple partners, history of stis, men who have sex with men (hbv; hav; hcv — less common than parenteral, higher with hiv), sharing razors, toothbrushes, or nail clippers with an infected person, unregulated tattoos, piercings, or acupuncture with unsterile equipment, contaminated food or water — raw shellfish, ice, unpeeled produce, food handled by an infected person; travel to asia, south/central america, africa, the middle east (hav), and others.
What are the early signs of viral hepatitis?
Early findings include No symptoms at all — most HCV, 70% of HAV in children under 6, most chronic HBV/HCV for years, Prodromal flu-like cluster — anorexia, nausea, malaise, fatigue, low-grade fever, arthralgias, urticaria, RUQ discomfort.
Which findings should a nurse report immediately in viral hepatitis?
Report immediately: New confusion, drowsiness, or any subtle mental-status change, Bleeding, bruising, or a rising INR (≥ 1.5), Hypoglycemia, Acute liver failure (fulminant hepatitis), HEV in pregnancy. These signal deterioration that needs rapid intervention.
How do you read a hepatitis B serology panel?
Three markers do most of the work. HBsAg means current infection. Anti-HBs means immunity. Anti-HBc means the person has met the real virus (past or present), and its IgM form means the infection is acute. So: HBsAg + with IgM anti-HBc + = acute; HBsAg + for more than 6 months with IgM − = chronic; HBsAg − with anti-HBs + and anti-HBc + = resolved (counsel on reactivation risk); anti-HBs + alone = immune from vaccine; all negative = susceptible, offer vaccine. In the window period HBsAg has vanished and anti-HBs has not appeared, so IgM anti-HBc may be the only positive test. HBeAg adds infectivity and HBV DNA adds viral load (CDC 2023).
Which types of hepatitis become chronic, and which can be cured?
Hepatitis A never becomes chronic and hepatitis E does so only in immunosuppressed people; both resolve with rest, fluids, and nutrition. Hepatitis B becomes chronic in about 90% of infected infants but only about 5% of adults; its antivirals (entecavir, tenofovir) suppress the virus but do not cure it, usually for life, and stopping them can cause a flare. Hepatitis C becomes chronic in more than half of infected people, but an 8–12-week course of oral direct-acting antivirals cures more than 95% — cure is confirmed by undetectable HCV RNA 12 weeks after treatment, and reinfection remains possible. Hepatitis D exists only with B, is chronic in about 90% after superinfection, and has no cure. Vaccines exist for A and B only; the B vaccine also prevents D.
When does acute hepatitis become an emergency?
When the liver stops doing its synthetic work. The size of the ALT does not matter — very high values are expected — a 10- to 100-fold rise in acute HAV. The alarm is new confusion or drowsiness (hepatic encephalopathy) together with an INR of 1.5 or higher, which defines acute liver failure; hypoglycemia, bleeding, and jaundice that keeps deepening (bilirubin above 10 mg/dL) are its companions. About 30% of these patients need a liver transplant, so the rule is early transfer to a transplant center, no sedatives that would mask the trend, and correcting the INR only for active bleeding or procedures. Patients are taught to seek emergency care for vomiting blood, black or bloody stools, or new confusion.

Sources

Reviewed by Hae Suk Lee, RN

Educational summary for nursing students. Scenarios are fictional teaching cases. Always verify against current guidelines and your institution's protocols before acting in practice. Not medical advice.

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