Anatomy, Physiology, and Investigations of Liver Disease PDF

Anatomy, physiology symptomatology of liver& investigations of liver disease Anatomy ▪ The liver is the largest gland in the body, weighing approximately 1500 gm, ▪ it is situated in the right hypochondrium. ▪. Anatomy ▪ The functional unit of the liver is the acinus ▪ This consists of the...

Anatomy, physiology symptomatology of liver& investigations of liver disease Anatomy ▪ The liver is the largest gland in the body, weighing approximately 1500 gm, ▪ it is situated in the right hypochondrium. ▪. Anatomy ▪ The functional unit of the liver is the acinus ▪ This consists of the fusiform area lying between two hepatic veins and draining into them Anatomy ▪ The liver has two main lobes: right and left. if there's disease in one segment we can eaasily remove it and the other will not be effected ▪ The right lobe is further divided into anterior and posterior segments; the right segmental fissure, which cannot be seen externally, separates the segments. ▪ The externally visible falciform ligament divides the left lobe into medial and lateral segments. Liver segments Liver segments Blood supply ▪ Portal vein carries 70% of blood to liver ▪ Hepatic artery carries 30% ▪ Approximately 1500 mL of blood per minute circulates through the liver and exits via the right and left hepatic veins into the inferior vena cava. BILE ▪ Bile, which is formed in the liver cells, exits the liver through a series of bile ducts that increase in size as they approach the common bile duct. ▪ Bile is a thick, viscous fluid secreted from the liver, stored in the gallbladder, and released into the duodenum when fatty foods enter the duodenum. ▪ It emulsifies fats in the intestine and forms compounds with fatty acids to facilitate their absorption. formed from liver cells --> collected in bile canuclai --> then in common hepatic duct --> right + left hepatic form the common hepatic duct --> then common hepatic combine with cystic duct (from gallbladder) to form the common bile duct --> open in the 2nd part of duodenum Functions of the liver ▪ The main functions of the liver include: ▪ (1) Metabolism of carbohydrate, protein, and fat ▪ (2) Storage and activation of vitamins and minerals ▪ (3) Formation and excretion of bile ▪ (4) Conversion of ammonia to urea ▪ (5) Metabolism of steroids ▪ (6) Detoxification of substances such as drugs, alcohol, and organic compounds ▪ (7) Function as a filter and flood chamber. Protein metabolism ▪ The liver is the principal site of synthesis of all circulating proteins apart from gamma globulins, which are produced in the reticuloendothelial system. ▪ The liver receives amino acids from the intestine and muscles and, by controlling the rate of gluconeogenesis and transamination, regulates plasma protein levels. glucose from the amino acid llike copper + iron ▪ It synthesizes transport or carrier proteins such as transferrin and ceruloplasmin, acute-phase and other proteins (e.g., 0,-antitrypsin and a-fetoprotein) ▪ It synthesizes all factors involved in coagulation (apart from factor VIII) as well as components of the complement system. ▪ Amino acids are degraded by transamination and oxidative deamination to produce ammonia, which is then converted to urea by the liver and excreted by the kidneys Carbohydrate metabolism ▪ During and after meals, the absorbed glucose reaches the liver via portal blood flow and the excess is stored as liver glycogen. ▪ In the fasting state, blood glucose is maintained either by glucose released from the breakdown of glycogen (glycogenolysis) or by newly synthesized glucose (gluconeogenesis). ▪ In prolonged starvation, ketone bodies and fatty acids are used as alternative sources of fuel and the body tissues adapt to a lower glucose requirement. Lipid metabolism ▪ Fats are insoluble in water and are transported in the plasma as protein-lipid complexes (lipoproteins). ▪ The liver synthesizes very-low-density lipoproteins (VLDLs) and high-density lipoproteins (HDLs). ▪ Triglycerides are mainly of dietary origin but are also formed in the liver from circulating free fatty acids (FFAs) and glycerol. ▪ Cholesterol may be of dietary origin, but most is synthesized from acetyl-CoA mainly in the liver, intestine, adrenal cortex, and skin. In severe liver disease, increasing the ratio of free cholesterol alters membrane structures. One result of this is the red cell abnormalities (e.g., target cells) seen in chronic liver disease. ° Phospholipids (e.g., lecithin) are synthesized in the liver. bile secreted in duodenum ( do it's own function --> break down of fats ) then reabsorbed again from the terminal ileum then portal veins and go back to the liver ad the liver use it again is synthase of bile and repeat the lope --> this called entero-hepatic secration of bile acids Bile secretion terminal ileum --> absorption of vit. B12 + bile acid ▪ Bile consists of water, electrolytes, bile acids, cholesterol, phospholipids, and conjugated bilirubin. ▪ The average total bile flow is approximately 600 mL per day. ▪ In the fasting state half of the bile flows directly into the duodenum and half diverted into the gall bladder ▪ The mucosa of the gall bladder absorbs 80-90% of the water and electrolytes. ▪ Following a meal, cholecystokinin is secreted by the duodenal mucosa and stimulates contraction of the gall bladder and relaxation of the sphincter of Oddi, so that concentrated bile enters the duodenum. ▪ An adequate bile flow is dependent on bile salts being returned to the liver by the enterohepatic circulation. Hormone and drug inactivation: ▪ The liver catabolizes hormones such as insulin, glucagon, estrogen, growth hormone, glucocorticoids, and parathyroid hormone. ▪ It is also the prime target organ for many hormones (e.g., insulin). ▪ It is the major site for the metabolism of drugs and alcohol. ▪ Hepatocytes detoxify ammonia by converting it to urea, 75% of which is excreted by the kidneys. ▪ The remaining urea finds its way back to the gastrointestinal tract (GIT). Immunological function ▪ The liver acts as a 'sieve' for the bacteria and other antigens carried to it via the portal tract from the gastrointestinal tract. ▪ These antigens are phagocytosed and degraded by Kupffer cells, which are macrophages attached to the endothelium. Major manifestations of liver disease Symptoms ▪ Acute disease: HVP/HVC/HVA HVA --> most common from the food ▪ Acute liver diseases are mostly viral in origin; ▪ fever, malaise, fatigue is a common presentation of acute hepatic disorder. ▪ Acute hepatic disease may originally be anicteric. ▪ Jaundice appears as the disease progresses. ▪ Change in the color of urine and/or stools.  Major manifestations of liver disease ▪ Chronic disease: ▪ A chronic hepatic patient may be completely asymptomatic; ▪ a patient with liver cirrhosis may be completely asymptomatic for several years. ▪ Common symptoms may be: ▪ Chronic fatigue , Right hypochondrial pain due to hepatomegaly, Distention due to ascites flappy tremmors + aciyts + spleenomegaly ▪ Bleeding (hematemesis, melena) ▪ Bilateral lower limb edema due to fluid retention itching edema a. Liver 'function' tests: biggest volum in the blood ▪ 1. Serum albumin 3.5-5 gm/.. lower ▪ il. Prothrombin time increase / prolonged easily bleeding ▪ iii. Serum bilirubin increase ▪ b. Liver biochemistry: normal 30-40 ▪ i. Necro inflammatory markers: serum aspartate and alanine aminotransferases - reflecting hepatocellular damage very high in acute HVA 2000-3000 chronic hepatitis + cherosis --> 200-300 when the liver is all destoroyied --> enzymes are normal ▪ ii. | Cholestasis markers: serum alkaline phosphatase, y-glutamyl transpeptidase obestructive junidus --> both above is increase guma ggt Investigations of liver diseases good +ve --> if high --> tumor but not good -ve --> if low --> doesn't mean absence of tumor ▪ C. Alpha-Fetoprotein. [n 0-11 ng/dl] This is normally produced by the fetal liver. o Its reappearance in increasing and high concentrations [above 400 ng/dl] in the adult indicates hepatocellular carcinoma. + focal lesion by the ultrasonic ▪ Viral markers ▪ D. Immunological tests ▪ E. Urine tests: for bilirubin and urobilinogen. ▪ F. Imaging techniques: to define anatomical and gross pathological abnormalities. ▪ G. Liver biopsy: for histopathology. used if there's disturb in the liver function and the cause is unkown ultrasound guided --> core biopsy Investigations of liver diseases ▪ Serum autoantibodies: ▪ Immunological Tests ▪ Antimitochondrial antibody (AMA) is found in the serum in over 95% of patients with primary biliary cirrhosis. ▪ Nucleic, smooth muscle (actin), liver/kidney microsomal antibodies can be found in the serum in high titer in patients with autoimmune hepatitis. ▪ These antibodies can be found in the serum in other autoimmune conditions and other liver diseases. ▪ Antinuclear cytoplasmic antibodies (ANCA) are present in primary sclerosing cholangitis. It is also present in different vasculitis syndromes. segmental constriction in the bile ducts ANCA + ASCA --> inflammatory bowel disease Investigations of liver diseases ▪ Hematologic Tests ▪ thrombocytopenia from hypersplenism, which can be a surrogate marker of portal hypertension. ▪ Anemia may reflect low-grade hemolysis or marrow depression. ▪ Bone marrow suppression may be caused by ethanol or drugs, and aplastic anemia has an uncommon but recognized association with acute viral hepatitis. ▪ Chronic liver disease, especially if cholestatic, may be accompanied by target cells in the peripheral blood smear. Investigations of liver diseases ▪ Imaging techniques ▪ Ultrasound examination ▪ A non-invasive safe and relatively cheap technique. ▪ Abdominal ultrasound is useful in: ▪ 1. A jaundiced patient to differentiate medical from surgical jaundice; the latter is diagnosed by the presence of dilated intrahepatic biliary radicals. ▪ 2. Hepatomegaly/splenomegaly ▪ The detection of gallstones ▪ Focal liver disease — detects lesions >1 cm ▪ Diffuse parenchymal liver disease &Lymph node enlargement. Ultrasound Gall stones Liver cirrhosis normal --> smooth outline liver cirrhosis --> irregular + shrinken Investigations of liver diseases ▪ Color Doppler ultrasound will demonstrate the vascularity of a lesion and the direction of blood flow in the portal and hepatic veins. ▪ Fibro scan: for staging hepatic fibrosis and liver fat content “steatosis”.. Investigations of liver diseases ▪ Computed tomography (CT) examination ▪ It provides excellent visualization of the liver, pancreas, spleen, lymph nodes and lesions in the porta hepatis. ▪ CT allows assessment of the size, shape and density of the liver and can characterize focal lesions in terms of their vascularity ▪ High resolution spiral CT allows more precise detection of anatomy ▪ triphasic CT for diagnosis od hepatocellular carcinoma Triphasic CT Investigations of liver diseases ▪ Magnetic resonance cholangiopancreatography (MRCP): ▪ This technique produces high-quality images of ductal anatomy. ▪ This non-invasive technique is replacing diagnostic (but not therapeutic) ERCP ▪ Magnetic resonance angiography (MRA): ▪ This technique had largely replaced the traditional angiography. ▪ It allows better detection of any abnormal anatomy and its vascularity. portal or hepatic veins thrombosis Investigations of liver diseases ▪ Endoscopy: ▪ Upper GI endoscopy: This is used for the diagnosis and treatment of varices, for the detection of portal hypertensive gastropathy, and for associated lesions such as peptic ulcers. ▪ Endoscopic ultrasound (EUS): e In this technique, a small high-frequency ultrasound probe is mounted on the tip of an endoscope and placed by direct vision into the duodenum. ▪ The proximity of the probe to the pancreas and biliary tree permits high- resolution ultrasound imaging. ▪ It allows accurate staging of small, potentially operable, pancreatic tumors and offers a less-invasive method for bile duct imaging. Endoscopic ultrasound Investigations of liver diseases ▪ Endoscopic retrograde cholangiopancreatography (ERCP): ▪ 1. This technique is used to outline the biliary and pancreatic ducts. ▪ 2. It involves the passage of a side viewing endoscope into the second part of the duodenum and cannulation of the ampulla.of vadar --> is collected of pancreatic duct + common bile duct ▪ Contrast is injected into both systems and the patient is screened radiologically. 3. In addition, other diagnostic and therapeutic procedures can be carried out ▪ Common bile duct stones can be removed ▪ The biliary system can be drained by passing a tube (stent) through an obstruction ERCP Investigations of liver diseases ▪ Percutaneous transhepatic cholangiography (PTC): - ▪ Under a local anesthetic, a fine flexible needle is passed into the liver. ▪ Contrast is injected slowly until a biliary radicle is identified and then further contrast is injected to outline the whole of the biliary tree. ▪ In patients with dilated ducts the success rate is near 100%. ▪ ERCP is the preferred first investigation because therapy (e.g. stone removal) can be undertaken at the same time. Investigations of liver diseases ▪ Liver biopsy: ▪ - Histological examination of the liver is valuable in the differential diagnosis of diffuse or localized parenchymal disease. – ▪ Indications of liver biopsy: ▪ - Unexplained hepatomegaly ▪ - Chronic hepatitis ▪ - Diagnosis of infiltrative diseases ▪ - Fever of unknown origin ▪ - Tumors not any more ▪ - Diagnosis of early cirrhosis Investigations of liver diseases ▪ Contraindications of liver biopsy: ▪ - Bleeding diathesis ▪ - Thrombocytopenia (platelet count less 80x10/L) ▪ low prothrombin concentration (less than 50%) ▪ - Ascites JAUNDICE ▪ Definition: ▪ Jaundice (icterus) is yellow discoloration of the skin and mucous membrane due to rise of bilirubin in blood above normal levels. ▪ Total serum bilirubin is normally 0.2–1.2 mg/dL ▪ Jaundice is detectable clinically if serum bilirubin is around 2-3mg/dl. ▪ Jaundice (icterus) results from the accumulation of bilirubin—a product of heme metabolism—in body tissues. Hyperbilirubinemia may be due to abnormalities in the formation, transport, metabolism, or excretion of bilirubin. Bilirubin metabolism ▪ Bilirubin is derived from two main sources. RBC --> 120 days ▪ Roughly, 80% of bilirubin is made from the breakdown of hemoglobin in senescent red blood cells, and prematurely destroyed erythroid cells in the bone marrow. ▪ The remainder originates from the turnover of various heme-containing proteins found in other tissues, primarily the liver and muscles. ▪ These proteins include myoglobin, cytochromes, catalase, peroxidase, and tryptophan pyrrolase. breaking of hemoglobin --> hem --> iron + biliverden ( --> break into unconjugated bilirubin --> go to hepatic cell --> there's a protient will carry it to enter the cell ( if this protein is not present --> cogenital hyperbilirubinia called gelbiret sydrom ) to conjugation by enzym called UDP glucuronyl transferase --> this conjugated bilirubin very small amount of it will go to circulation and the rest will go to bile and to duodenum ) globin --> amino acid --> go to amino acid pool ??  Hyperbilirubinemia ▪ Jaundice may be caused by predominantly unconjugated or conjugated bilirubin in the serum. indirect ▪ Unconjugated hyperbilirubinemia may result from overproduction of bilirubin because of hemolitic anemia ▪ hemolysis; ▪ impaired hepatic uptake of bilirubin due to certain drugs; ▪ or impaired conjugation of bilirubin by glucuronide, as in Gilbert syndrome due to mild decreases in uridine diphosphate (UDP) glucuronyl transferase, or Crigler-Najjar syndrome caused by moderate decreases (type II) or absence (type I) of UDP glucuronyl transferase.  Hyperbilirubinemia direct ▪ Conjugated hyperbilirubinemia may result from impaired excretion of bilirubin from the liver due to hepatocellular disease, drugs, sepsis, or hereditary hepatocanalicular transport defects (such as Dubin-Johnson syndrome, progressive familial intrahepatic cholestasis syndromes, and intrahepatic cholestasis of pregnancy) ▪ or from extrahepatic biliary obstruction. Clinical findings ▪ A. Unconjugated Hyperbilirubinemia ▪ Stool and urine color are normal, ▪ there is mild jaundice and indirect (unconjugated) hyperbilirubinemia with no bilirubin in the urine. ▪ Splenomegaly occurs in all hemolytic disorders except in sickle cell disease Clinical findings dark urine + clay colored stool + pruritus --> obustractive jaundice ▪ B. Conjugated Hyperbilirubinemia clay colored ▪ Conjugated hyperbilirubinemia is often accompanied by pruritus, light-colored stools, and jaundice. ▪ Malaise, anorexia, low-grade fever, and right upper quadrant discomfort are frequent with hepatocellular disease. ▪ Dark urine, jaundice, and, in women, amenorrhea occur. ▪ An enlarged tender liver, spider telangiectasias, palmar erythema, ascites, gynecomastia, sparse body hair, fetor hepaticus, and asterixis may be present, depending on the cause, severity, and chronicity of liver dysfunction. Clinical findings ▪ C. Biliary Obstruction ▪ pruritus, dark urine, and light-colored stools. ▪ May be right upper quadrant pain, weight loss (suggesting carcinoma), jaundice, ▪ Symptoms and signs may be intermittent if caused by a stone, carcinoma of the ampulla, or cholangiocarcinoma. ▪ Pain may be absent early in pancreatic cancer. ▪ A palpable gallbladder (Courvoisier sign) is characteristic, but neither specific nor sensitive, of a pancreatic head tumor. Fever and chills are more common in benign obstruction with associated cholangitis.  liver disease ( jaundice ) --> biphasic --> both the direct and indirect is high --> ( if hemoglobin is 3) 1.5 d + 1.5 ind hemolysis --> 0.2 direct and rest indirect obstruction --> 0.2 indirect and rest direct jaundice normal --> 1.2 --> 0.2 indirect and the rest is direct Normal bile duct Obstructive jaundice normal common bile duct is almost same size as portal vein common bile duct 6mm double parile sign ?? portal 11-13 mm Acute hepatitis A ▪ Hepatitis can be caused by viruses, including the five hepatotropic viruses—A, B, C, D, and E—and many drugs and toxic agents; ▪ clinical manifestations may be similar regardless of cause. ▪ Hepatitis A virus (HAV) is a 27-nm RNA hepatovirus (in the picornavirus family) that causes epidemics or sporadic cases of hepatitis. HAV infection is hyperendemic in developing countries. ▪ The virus is transmitted by the fecal-oral route by either person to-person contact or ingestion of contaminated food or water, and its spread is favored by crowding and poor sanitation Symptoms and signs ▪ The incubation period averages 30 days. HAV is excreted in feces for up to 2 weeks before clinical illness ▪ There is no chronic carrier state unlike the HVB ▪ The onset may be abrupt or insidious, with malaise, myalgia, arthralgia, easy fatigability, upper respiratory symptoms, and anorexia. ▪ Nausea and vomiting are frequent, and diarrhea or constipation may occur. Fever is generally present but is low-grade except in occasional cases in which systemic toxicity may occur. Symptoms and signs ▪ Abdominal pain is usually mild and constant in the right upper quadrant or epigastrium, often aggravated by exertion, and rarely may be severe enough to simulate cholecystitis. ▪ Jaundice occurs after 5–10 days but may appear at the same time as the initial symptoms. ▪ In many patients, jaundice never develops. ▪ With the onset of jaundice, prodromal symptoms often worsen, followed b  Symptoms and signs ▪ Liver tenderness is usually present. mild ▪ Splenomegaly is reported in 15% of patients, and soft, enlarged lymph nodes— especially in the cervical or epitrochlear areas—may be noted. ▪ The acute illness usually subsides over 2–3 weeks with complete clinical and laboratory recovery by 9 weeks. ▪ In some cases, clinical, biochemical, and serologic recovery may be followed by one or two relapses, but recovery is the rule. Acute cholecystitis occasionally complicates the course of acute hepatitis A Laboratory findings ▪ Strikingly elevated ALT or AST levels occur early, followed by elevations of bilirubin and alkaline phosphatase; jaundace --> will be biphasic ▪ Cholestasis is occasionally marked. ▪ Antibody to hepatitis A (anti-HAV) appears early in the course of the illness. ▪ Both IgM and IgG anti-HAV are detectable in serum soon after the onset. ▪ Peak titers of IgM anti-HAV occur during the first week of clinical disease and usually disappear within 3–6 months. ▪ Detection of IgM anti-HAV is an excellent test for diagnosing acute hepatitis A. ▪ Titers of IgG anti-HAV rise after 1 month of the disease and may persist for years. Treatment ▪ Bed rest is recommended only if symptoms are marked. ▪ If nausea and vomiting are pronounced or if oral intake is substantially decreased, intravenous 10% glucose is indicated. ▪ Dietary management consists of palatable meals as tolerated, without overfeeding; breakfast is usually tolerated best. ▪ Strenuous physical exertion, alcohol, and hepatotoxic agents should be avoided Acute hepatitis B ▪ Hepatitis B virus (HBV) is a 42-nm hepadnavirus with a partially double- stranded DNA genome, inner core protein (hepatitis B core antigen, HBcAg), and outer surface coat (hepatitis B surface antigen, HBsAg). ▪ There are 10 different genotypes (A–J). ▪ HBV is usually transmitted by inoculation of infected blood or blood products or by sexual contact, and it is present in saliva, semen, and vaginal secretions. HBsAg-positive mothers may transmit HBV at delivery Acute hepatitis B ▪ The incubation period of hepatitis B is 6 weeks to 6 months (average 12–14 weeks). not reach HAV ▪ The onset of hepatitis B is more insidious, and the aminotransferase levels are higher on average, than in HAV infection. ▪ Acute liver failure occurs in less than 1%, with a mortality rate of up to 60%. ▪ Following acute hepatitis B, HBV infection persists in 1–2% of immunocompetent adults, but in a higher percentage of children and immunocompromised adults. Acute hepatitis B ▪ Persons with chronic hepatitis B, particularly when HBV infection is acquired early in life and viral replication persists, are at substantial risk for cirrhosis and hepatocellular carcinoma (up to 25–40%); men are at greater risk than women. child can take it from his mother by transplacental infection when born --> have to take immunoglubin + vaccien and the mother during 3rd trimester start to take medication Symptoms and signs ▪ The clinical picture of viral hepatitis is extremely variable, ranging from asymptomatic infection without jaundice to acute liver failure and death in a few days to weeks. ▪ The onset may be abrupt or insidious, and the clinical features are similar to those for acute hepatitis A. ▪ The clinical picture of viral hepatitis is extremely variable, ranging from asymptomatic infection without jaundice to acute liver failure and death in a few days to weeks. Figure 16–2 shows the typical course of acute HBV infection. The onset may be abrupt or insidious, and the clinical features are similar to those for acute hepatitis A. Laboratory findings ▪ The laboratory features are similar to those for acute hepatitis A, ▪ There are several antigens and antibodies as well as HBV DNA that relate to HBV infection and that are useful in diagnosis. ▪ 1. HBsAg—The appearance of HBsAg in serum is the first evidence of infection, appearing before biochemical evidence of liver disease, and persisting throughout the clinical illness. Persistence of HBsAg more than 6 months after the acute illness signifies chronic hepatitis B. carier ▪ 2. Anti-HBs—Specific antibody to HBsAg (anti-HBs) appears in most individuals after clearance of HBsAg and after successful vaccination against hepatitis B. Disappearance of HBsAg and the appearance of anti-HBs signal recovery from HBV infection, noninfectivity, and immunity ▪ 3. Anti-HBc—IgM anti-HBc appears shortly after HBsAg is detected. In the setting of acute hepatitis, IgM anti-HBc indicates a diagnosis of acute hepatitis B, and it fills the serologic gap in rare patients who have cleared HBsAg but do not yet have detectable anti-HBs. IgM anti-HBc can persist for 3–6 months. IgM anti-HBc may also reappear during flares of previously inactive chronic hepatitis B. IgG anti-HBc also appears during acute hepatitis B but persists indefinitely, whether the patient recovers (with the appearance of anti-HBs in serum) or chronic hepatitis B develops (with persistence of HBsAg).  PCR for HVB + HBeAg --> if +ve + 2000 --> have to be treated lower than 2000 --> not treared if -ve ---> more than 20000 --> have to be treatred if lower --> ot treated ▪ 4. HBeAg ▪ HBeAg indicates viral replication and infectivity. ▪ Persistence of HBeAg beyond 3 months indicates an increased likelihood of chronic hepatitis B. ▪ Its disappearance is often followed by the appearance of anti-HBe, generally signifying diminished viral replication and decreased infectivity ▪ 5. HBV DNA—The presence of HBV DNA in serum generally parallels the presence of HBeAg, although HBV DNA is a more sensitive and precise marker of viral replication and infectivity Typical course of acute hepatitis B Prevention ▪ Thorough hand washing by medical staff who may contact contaminated utensils, bedding, or clothing is essential. ▪ Medical staff should handle disposable needles carefully and not recap them. ▪ Screening of donated blood for HBsAg, anti-HBc, and anti-HCV has reduced the risk of transfusionassociated hepatitis markedly. ▪ All pregnant women should undergo testing for HBsAg. ▪ HBV-infected persons should practice safe sex. ▪ Immunoprophylaxis of the neonate reduces the risk of perinatal transmission of HBV infection; when the mother’s serum HBV DNA level is 200,000 IU/mL or higher, Prevention ▪ Antiviral treatment of the mother should also be initiated in the third trimester (see Chronic Hepatitis B & Chronic Hepatitis D). HBV-infected health care workers are not precluded from practicing medicine or dentistry if they follow CDC guidelines. ▪ Hepatitis B immune globulin (HBIG) may be protective— or may attenuate the severity of illness—if given within 7 days after exposure (adult dose is 0.06 mL/kg body weight) followed by initiation of the HBV vaccine series. Prevention ▪ This approach is recommended for unvaccinated persons exposed to HBsAg- contaminated material via mucous membranes or through breaks in the skin and for individuals who have had sexual contact with a person with HBV infection. ▪ HBIG is also indicated for newborn infants of HBsAg-positive mothers, with initiation of the vaccine series at the same time, both within 12 hours of birth (administered at different injection sites). Treatment ▪ Treatment of acute hepatitis B is the same as that for acute hepatitis A. ▪ Encephalopathy or severe coagulopathy indicates acute liver failure, and hospitalization at a liver transplant center is mandatory. ▪ Antiviral therapy ▪ unnecessary in patients with acute hepatitis B ▪ prescribed in cases of acute liver failure caused by HBV ▪ and in spontaneous reactivation of chronic hepatitis B presenting as acute-on- chronic liver failure