Hepatitis B (HBV)

Occupational exposure is the headline - HBV is transmitted by needlestick and by wounds from other instruments, and healthcare workers are a named high-risk group. Standard precautions on every case, no recapping during lines and blocks, and know your own anti-HBs — antibody to surface antigen is what documents that you are immune.

Read the serology, don't just read the diagnosis - HBsAg means active infection, under six months acute and over six months chronic. Anti-HBs means recovery or vaccination. Anti-HBc IgM means acute infection. HBeAg goes with a high viral load and anti-HBe with a low replicative phase. That panel is the difference between a vaccinated patient, a recovered one, and an infectious one.

Normal transaminases don't clear anyone - Liver enzymes rise late, in the latter part of the replicative phase, and can sit inside the reference range. Transaminases should not be the sole guide to diagnosing HBV, so use the serology for status and reserve the enzymes for tracking inflammation.

Synthetic function is what changes the plan - INR/PT, albumin, platelets, and bilirubin. A compensated carrier with intact synthetic function gets a standard anesthetic; the patient with a rising INR, low albumin, and thrombocytopenia does not, and neuraxial decisions follow those numbers.

Look for the stigmata - Jaundice, ascites, hepatomegaly, splenomegaly, palmar erythema, Dupuytren contracture, spider nevi, gynecomastia, caput medusae, and encephalopathy on the preop exam point to portal hypertension and cirrhosis. GI bleeding from esophageal varices and coagulopathy are the two that will find you intraoperatively — see the Cirrhosis entry for managing an established cirrhotic.

Acute HBV can be fulminant - Severe acute disease presents with jaundice, encephalopathy, ascites, variceal bleeding, and coagulopathy, and HBV causes most severe viral acute liver failure. Antivirals are the etiology-directed treatment for acute hepatitis B; everything else is ICU supportive care at a transplant-capable center.

Reactivation with immunosuppression - Reactivation with fulminant hepatitis, hepatic failure, and death can occur. Before rituximab, all patients are screened with HBsAg and anti-HBc and monitored during and after treatment. If your patient is heading for chemotherapy, transplant, or biologic immunosuppression, HBV status matters before the drugs start, not after — flag it if it hasn't been done.

Extrahepatic disease - Polyarteritis nodosa, membranous nephropathy and less often membranoproliferative glomerulonephritis, and aplastic anemia are described with HBV. A creatinine and a CBC catch the two that matter to you: impaired renal clearance and a marrow that will not replace what you lose.

Obstetric patients - Universal HBsAg screening at the first prenatal visit is recommended. The newborn of an HBsAg-positive or unknown-status mother receives hepatitis B immune globulin and vaccine within 12 to 24 hours of birth, which cuts exposure risk from 90% to 5% to 10%. Cesarean section is not recommended as the sole means of reducing vertical transmission, so HBV alone does not change the delivery plan or your anesthetic for it.

Chronic disease is a separate problem - Chronic infection is where cirrhosis and hepatocellular carcinoma come from. Work the long-term perioperative implications from the Chronic Viral Hepatitis and Cirrhosis entries rather than re-deriving them here.

Hepatitis B virus (HBV) is a partially double-stranded DNA hepadnavirus transmitted percutaneously and across mucosal surfaces: blood and blood products, injection drug use, needlesticks and instrument injuries in healthcare workers, hemodialysis, unprotected sex, and perinatal exposure. Incubation runs 30 to 180 days. It is detectable in serum, semen, vaginal secretions, saliva, and tears.

Liver injury is mostly immune-mediated. HBsAg and nucleocapsid proteins displayed on the hepatocyte membrane drive T-cell lysis of infected cells, though HBV can also injure hepatocytes directly — the fibrosing cholestatic hepatitis seen in immunosuppressed transplant recipients is the clearest example. More than 95% of immunocompetent adults clear the acute infection; the acute illness ranges from anicteric through icteric to, less often, fulminant, and HBV accounts for most severe viral acute liver failure. HBsAg persisting past six months defines chronic infection.