1 In a patient presenting with hepatitis symptoms and/or abnormal liver function tests, take a focused history to assist in establishing the etiology (e.g., new drugs, alcohol, blood or body fluid exposure, viral hepatitis).
S/Sx:
- HAV: lasting 2mo, fulminant illness <1%, 70% children asymptomatic
- Pre-icteric phase: abrupt onset of fever, jaundice, malaise, anorexic, n/v, abd/p, h/a, HSM, bradycardia, Cervical LN
- Icteric phase: ↑ conjungated Bili, pale color stool, jaundice
- HBV:
- Acute (subclinical 70% adult, 90% children, resolves 1-3mo)
- N/V, anorexia, fatigue, low grade fever,
- RUQ/epigastric pain, jaundice,
- myalgia/joint pain, urticaria
- Chronic: asymptomatic until cirrhosis – portal HTN,
- hepatocellular carcinoma
- Acute (subclinical 70% adult, 90% children, resolves 1-3mo)
- HCV:
- Acute usually asymptomatic: 20% spontaneously clear
- Chronic usually silent: fatigue, rheumatologic symptoms: myalgias, arthralgia, paresthesia
- itching, sjogren’s syndrome (WBC destroys exocrine glands – lacrimal and salivary) – dry mouth, eye, vagina, bronchitis
- Raynaud’s syndrome (reduce blood flow to fingers/toes due to cold/emotions)
- chronic mild inflammation → fibrosis
Hx
- Hepatotoxins:
- EtOH (>210g / wk in men or >140g/wk in women for >2 yr)
- medications – identify all meds, amount, durations of use (include OTC, herbal, dietary supplements, and illicit drug)
- Viral hepatitis risks –
- IVDU, blood transfusion (before 1992),
- travel to endemic areas, exposure to pt with jaundice
- Hep B/C – transmitted parenterally
- Hep A/E – transmitted via a fecal-roal route
- Autoimmune conditions –
- female, +ANA, anti-smooth muscle Ab, elevated IgG
- IBD (primary sclerosing cholangitis, gallstones),
- Occupational / recreational exposures: mushroom picking, industrial chemicals
- Vascular dz:
- Budd-chiari syndrome (abd pain, ascites, hepatomegaly)
- R-sided CHF, constrictive carditis
- Sepsis, heat stroke
- pregnancy (gallstones),
- Metabolicdz:
- hemochromatosis
- Wilson’s dz
- early onset emphysema (alpha 1 antitrypsin deficiency)
- celiac dz, thyroid dz
- DM, obesity (nonalcoholic fatty liver dz)
- muscle disorders: polymyositis, Sz, heavy exercise
- Others
- HELLP
- malignant infiltration
- partial hepatectomy
2 In a patient with abnormal liver enzyme tests interpret the results to distinguish between obstructive and hepatocellular causes for hepatitis as the subsequent investigation differs.
- Hepatocellular pattern
- AST/ALT >> ALP
- may have ↑ bilirubin & ↓ clotting factors
- Cholestatic (obstructive) pattern
- ALP >> AST / ALT
- ↑ GGT distinguish ↑ ALP from liver disorders instead of bone disorder (if normal GGT – r/o bone dz)
- may have ↑ bilirubin & ↓ clotting factors
- Isolated hyperbilirubinemia
- ↑ bilirubin
- normal AST/ALT & ALP
- Alcoholic liver dz
- AST:ALT of 2:1 or greater
- more suggestive if ↑ GGT
- Most hepatocellular injury are associated with ALT>AST
3 In a patient where an obstructive pattern has been identified,
a) Promptly arrange for imaging,
b) Refer for more definitive management in a timely manner. GI referral!
DDx
- Bile duct obstruction
- PBC (primary biliary cirrhosis)
- PSC Primary sclerosing cholangitis
- Drugs: phenytoin, androgenic steroids
- Infiltrative dz: sarcoidosis, amyloidosis, cancer
Ix in pt with ↑ ALP of hepatic origin starts with RUQ u/s to assess the hepatic parenchyma & bile ducts
1) + biliary dilatation – extrahepatic cholestasis
- ERCP to confirm dx if acute (stone or malignancy)
- If chronic or high risk for ERCP – MRCP or CT (then ERCP if evidence of stone, strictiue, malignancy)
- ddx:
- Choledocholithiasis
- Malignant obstruction (pancreas, gallbladder, ampulla, bile duct cancer)
- PSC (extrahepatic bile duct stricture)
- Chronic pancreatitis with stricturing of the distal bile duct
- AIDS cholangiopathy
2) – biliary dilatation – intrahepatic cholestasis or (extrahepatic) partial obstruction due to PSC
- Check AMA (dx of PBC) – if +, liver biopsy to confirm dx
- If – AMA
- MRCP to look for evidence of PSC
- Hep A/B/C/E / EBV / CMV testings
- Liver biopsy to look for infiltrative dz (sarcoidosis / cancer)
4 In patients positive for Hepatitis B and/or C,
a) Assess their infectiousness,
b) Determine human immunodeficiency virus status.
Hep B – DNA virus
- Immunization: + Anti-HBs only (negative Anti-HBc – requires actual infection)
- Resolved infection: – HBsAg & IgG for anti-HBc ± Anti-HBs / Anti-HBe
- Acute infection: + HBsAg (infectious) & HBeAg, IgM for anti-HBc
- Chronic infection: + HBsAg & IgG for anti-HBc, if + HBeAg (high HBV DNA)
Hep C – RNA virus
- dx by HCV-RNA in serum
5 In patients who are Hepatitis C antibody positive determine those patients who are chronically infected with Hepatitis C, because they are at greater risk for cirrhosis and hepatocellular cancer.
- HCV RNA – + within 2 wks, marker of active infection
- Resolved hepatitis: – HCV RNA ± anti-HCV ( + in 6 weeks, doesn’t = recovery / immunity)
- Chronic hepatitis: + HCV RNA, + anti-HCV
6 In patients who are chronically infected with Hepatitis C, refer for further assessment and possible treatment.
Tx of Hep C – always refer
- blood-borne precautions; HepB/A vaccines if serology negative, avoid EtOH
- Clinically significant liver dz:
- persistently elevated transaminases,
- liver biopsy shows fibrosis / cirrhosis,
- moderately necrosis / inflammation
- Tx with interferon-a & ribavirin (50-80% success rate)
- Length of Tx based on time required for HCV-RNA to fall
- measure HCV-RNA at 1 & 3 mo after Tx
- Adverse effects:
- depression / fatigue,
- hemolysis, bone marrow suppression,
- fever / myalgia, skin rashes
- Poor response:
- cirrhosis,
- genotype 1, high HCV-RNA,
- co-infection with HIV,
- African-American race
7 In patients who are at risk for Hepatitis B and/or Hepatitis C exposure,
a) Counsel about harm reduction strategies, risk of other blood borne diseases,
b) Vaccinate accordingly.
- HAV / HEV – fecal-oral through close contact andfood-borne & rarely through blood products
- Risk Factors
- Travelers
- MSM
- Drug abusers
- Recipients of clotting factor replacement
- Risk Factors
- HBV – parenteral (incubation for days) / sexual: body fluids – semen, saliva (incubation 4-8 weeks)
- Anal > vaginal > oral
- Horizontal: household contacts
- Vertical: Mother to neonate
- Parenteral: IVDU
- Risk factors:
- STI Hx, MSM, >1 sexual partner in past 6months
- Household contact, infant born to HBV infected mother
- Healthcare worker
- Hemodialysis; IVDU
- HCV – parenteral (transfusion, IVDU) > sexual; 40% with unknown risk factors
- Risk factors
- Blood transfusion before 1992
- Incarceration / imprisonment
- Unhygienic tattoos or body piercing
- Sharing sharp personal items
- High risk sexual activity
- Pregnancy is not C/I & not transmit through coughing, kissing, shaking hands, sharing utensils / food/water
- Risk factors
Prevention:
- vaccinate high-risk pt for HepB (3 doses, 0, 1, 6 months)
- Vaccine all chronic HCV pt against HBV & HAV if not immune
- Hep A – vaccinate children & pts with chronic HBV, HCV or other liver dz
8 Offer post-exposure prophylaxis to patients who are exposed or possibly exposed to Hepatitis A or B.
Post-exposure – Hep B
- risk infxn ~ 30%
- Tx: HBIG & vaccine (if unvac or known nonresponder)
Post-Exposure – Hep A
- Vaccine age <1 or > 40yo or immunosupp
Post-exposure – Hep C (needle stick injury)
- If HCV RNA +, consider Rx within 3 months
9 Periodically look for complications (e.g., cirrhosis, hepatocellular cancer) in patients with chronic viral hepatitis, especially hepatitis C infection.
Prognosis of Hep C
- 80% acute Hep C become chronic and 20% evolve to cirrhosis
- ↑ hepatocellular carcinoma risk if cirrhotic
- ↑ risk of B-cell non-Hodgkin lymphoma
- Can cause cryoglobulinemia: ↑ membranoproliferative glomerulonephritis, lymphoma
HBV & HCV are oncogenic – hepatocellular carcinoma secondary to cirrhosis
EBV – associated with Burkitt’s lymphoma & nasopharyngeal carcinoma
References:
- TN2014
- UpToDate 2015
- Pocket Medicine 4th edition
Preparing for the CCFP Exam 2015 
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