hepatitis ppt includes hepatitis in children- pathophysiology, signs & symptoms, diagnostic tests, treatment options and nursing care. it also includes prevention

it is about hepatitis in children and treatment options

1. SEMINAR ON HEPATITIS “ HEPATITIS” POONAM

2. CONTENT OUTLINE

3. Introduction Hepatitis, a general term referring to inflammation of the liver, may result from various causes, both infectious and non-infectious and metabolic diseases.

4. Liver LIVER- Is located in the upper right quadrant of the abdomen

5. Functions of liver Storage of vitamins A, B, D; iron; and copper. Synthesis of plasma proteins, including albumin and globulins. Synthesis of the clotting factors vitamin K and prothrombin. Storage of glycogen and synthesis of glucose from other nutrients (gluconeogenesis). Breakdown of fatty acids for energy. Production of bile. Detoxification and excretion of waste products.

6. Definition of hepatitis Viral hepatitis is a systemic, viral infection in which necrosis and inflammation of liver cells produce a characteristic cluster of clinical, biochemical, and cellular changes.

7. Definition of hepatitis

8. Types of viral hepatitis

9. Hepatitis causes

10. Viral Hepatitis causes

11. Viral Hepatitis causes

12. Pathophysiology of hepatitis Due to causes (viral, toxin) Damage to the hepatocytes by body’s immune response Altered cellular function Changes in the endoplasmic reticulum* Alteration in the liver function Kupffer cells increase in size & no. *SER detoxifies products of natural metabolism

13. Contd ……. Liver inflammation Pain Fever Anorexia Increased WBCs Nausea, vomiting Fatigue Alteration in blood and lymph flow Decreased vit K absorption Bleeding tendency Decreased bilirubin metabolism or obstruction hyperbillirubinemia Decreased bile in G.I tract & increased urobilinogen jaundice Dark urine Clay colored stool

14. CLINICAL MANIFESTATIONS Malais e Muscle and join t ache Fever Nausea or vomiting Loss of apetite Abdominal pain Dark urine Jaundice Malaise, tiredness, weakness

15. Type A Hepatitis

16. Type A Hepatitis

17. Type A Hepatitis

18. INCIDENCE Occurs sporadically and  epidemically  worldwide, with a tendency to cyclic recurrences. 1.4 million cases annually. High endemic areas include most of Africa, Asia and Central and South America. Contributory conditions include household crowding, poor levels of sanitation and inadequate water supplies.

19. MODE OF TRANSMISSION

20. Patient are an-icteric and symptomless Mild, flu like upper respiratory tract infection Fever Anorexia Clinical manifestation

21. DIAGNOSIS

22. DIAGNOSIS: Hepatitis A: The diagnosis of viral hepatitis is confirmed by characteristic serologic testing. The presence of IgM-specific antibody to HAV with low or absent IgG antibody to HAV is presumptive evidence of HAV. There is no chronic carrier state of HAV.

23. Prevention of hepatitis Proper community and home sanitation Personal hygiene Safe practices for preparing and dispensing food Effective health supervision of schools, dormitories, extended care facilities, barracks, and camps Community health education programs Mandatory reporting of viral hepatitis to local health departments Vaccination for travelers to developing countries, illegal drug users (injection and non-injection drug users), men who have sex with men, and persons with chronic liver disease Vaccination to interrupt community-wide outbreaks.

24. Hepatitis A Prevention - Immune Globulin Pre-exposure: Travelers to intermediate and high HAV-endemic regions Post-exposure: within 14 days 2 doses 2 nd dose is given 6 months after 1 st dose.

25. VACCINE: Two types of HAV vaccines are currently available internationally: Killed vaccines: 0.5ml IM 2 doses, 6 months apart, 1-12 years ( Hebrix ) Live attenuated vaccines (based on H2 or LA-1 HAV strains): 0.5 ml SC, single dose at 1-12 years (BIOVAC)

26. TREATMENT No specific treatment. Supportive Rx; 1. IV hydration 2. Anti-pruritic agents 3. Fat soluble vitamins

27. Hepatitis B

28. Hepatitis B 1. Infants & children not infected during the perinatal period remain high risk acquiring person-to-person transmission from their mother, with 30% incidence of transmission during the first years of life. 2. The incubation period ranges from 45 to 180 days with an average of 120 day. 3. Can cause a carrier state and lead to chronic hepatitis with eventual cirrhosis or hepatocellula carcinoma in adulthood.

29. Hepatitis B Occurs in children and adolescents in specific high risk groups, which are

30. Diagnosis HBsAg - 1-6 months after exposure HBeAg - 1-3 months after acute anti-HBc - past infection A nti-HBs - implies vaccination HBsAg - positive for at least 6 months - hepatitis B carriers (may have chronic hepatitis B )

31. HBsAg : signifies acute or chronic infection with HBV. HBeAg : acute HBV. Anti- Hbe : predicts a low degree of infectivity during the carrier state. HBsAg and HBeAg in the absence of antibody to e antigen (anti- HBe ) indicates high risk of transmissibility that is associated with ongoing viral replication. Diagnosis

32. Antibody to surface antigen (anti-HBs): indicating recovery and immunity from hepatitis B virus infection. successfully vaccination. Antibody to core antigen (anti-HBc) : indicates recent Previous or ongoing infection with in an undefined time frame. IgM anti-HBc : indicates recent infection with hepatitis B virus (<6 mos ) acute infection. Diagnosis

33. Prevention

34. Prevention Schedule of hepatitis B vaccine: At birth- o dose At 6, 10 & 14 weeks: 1 st , 2 nd and 3 rd doses alongwith DPT and Hib

35. HBSAG-POSITIVE MOTHERS: Infants born to HBsAg-positive women should receive vaccine at birth, 1-2 months, and 6 months of age. The first dose should be accompanied by administration of 0.5 mL of HBIG as soon after delivery as possible (within 12 hr ). Post-vaccination testing for HBsAg and anti-HBs should be done at 9- 18 months. If the result is positive for anti-HBs, the child is immune to HBV.

36. HBSAG-POSITIVE MOTHERS:

37. Treatment PEG-INTERFERON Finite duration Rapid disappearance of HBs Ag Better tolerability Inconvenient SC injection Frequent side effects ALT flares NUCLEOSIDE/ NUCLEOTIDE ANALOG Negligible side effects Convenient Potent inhibition of replication Reduced drug resistance Risk of nephropathy Long and indefinite use Expensive

38. GOALS OF Rx

39. Hepatitis c Identified in 1989 Blood test became available in 1992 HCV is transmitted parenterally through exposure to blood and blood products from HCV-infected persons- most common mode of transmission of children No vaccine available to prevent hepatitis C Can cause lifelong infection, fibrosis (mild to moderate liver scarring), cirrhosis (serious liver scarring), liver cancer, liver failure, and death. 

40. Hepatitis c

41. Incidence The incidence of HCV on a global scale is not well known, because acute infection is generally asymptomatic. As many as 2 to 4 million persons may be chronically infected in the United States, 5 to 10 million in Europe, and about 12 million in India, and most do not know they are infected . About 150 000 new cases occur annually in the US and in Western Europe, and about 350 000 in Japan.

42. LABORATORY STUDIES: Hepatitis C: Sero -conversion after HCV infection may occur 6 months after infection. A positive result of HCV ELISA should be confirmed. Detection of HCV RNA by PCR is a sensitive marker for active infection, and results of this test may be positive 3 days after inoculation.

43. Diagnostic evaluation

44. Hepatitis D (Delta) Rare in children and occur in individuals already infected with HBV. The incubation period is 2-8 weeks, but with coinfection of HBV, the infection. Transmission through blood and sexual contact and commonly occurs among drug abusers, individuals with hemophilia, and persons immigrating from endemic areas. It can only contract hepatitis D if patient is already infected with hepatitis B.

45. Incidence Areas of high prevalence include the Mediterranean Basin, the Middle East, Central Asia, West Africa, the Amazon Basin of South America and certain South Pacific islands. Severe, often fatal, acute and chronic type D hepatitis occurs among indigenous people of Venezuela, Colombia, Brazil, and Peru, all regions with high chronic HDV infection rates. Hepatitis D is less common in Eastern Asia, but is present in Taiwan, China and India.

46. Mode of transmission Mode of transmission same as HBV exposure to infected blood and serous body fluids. contaminated needles, syringes or blood and plasma product transfusions. Sexual transmission may also occur but is less common than with hepatitis B. Perinatal infection is rare. Infection may occur at the same time as a new HBV infection (co-infection) or after someone has been infected with HBV and become a chronic HBV carrier (super-infection)

47. Diagnosis Detection of total antibody to HDV (anti-HDV) A positive HDV IgM result indicates ongoing replication Detection of HDV-specific RNA by polymerase chain reaction (PCR) testing. PCR is the most sensitive assay for assessing HDV viraemia.

48. Preventive measure Prevention of hepatitis B infection with hepatitis B vaccine prevents infection with HDV. For persons with chronic hepatitis B infections, the only preventive measure is avoidance of exposure to potential sources of HDV. This means always using a new needle and syringe when injecting drugs and practising safe sex .

49. Hepatitis E

50. Incidence

51. Mode of transmission Transmission mainly through the faecal -oral route foodborne transmission transfusion of infected blood products vertical transmission from a pregnant woman to her fetus .

52. Clinical manifestation Asymptomatic or causes a very mild illness without jaundice that goes undiagnosed. Typical signs and symptoms of hepatitis include : Jaundice (yellow discolouration of the skin and sclera of the eyes, dark urine and pale stools). Anorexia (loss of appetite) An enlarged, tender liver (hepatomegaly) Abdominal pain and tenderness Nausea and vomiting Fever.

53. Prevention Maintaining quality standards for public water supplies. Establishing proper disposal systems to eliminate sanitary waste . On an individual level, infection risk can be reduced by: Maintaining hygienic practices such as hand washing with safe water, particularly before handling food; Avoiding drinking water and/or ice of unknown purity; Adhering to WHO safe food practices.

54. Vaccine In 2011, the first vaccine to prevent hepatitis E infection was registered in China. Although it is not available globally, it could potentially become available in a number of other countries

55. Hepatitis G GB virus C (GBV-C), formerly known as hepatitis G virus (HGV) and also known as HPgV is a  virus  in the  Flaviviridae  family and a member of the  Pegivirus  genus is known to infect humans, but is not known to cause human disease Risk factor are similar to Hepatitis C THE INCUBATION PERIOD for post transfusion is 14 to 145 day

56. Clinical manifestation Abdominal pain (upper-right side, usually not serious) Nausea /vomiting Diarrhea Fatigue Loss of appetite Fever Muscle or joint pain Weight loss

57. Contd …. Additional symptoms of advanced non-viral hepatitis: Jaundice (yellowing of the skin, eyes) Dark-colored urine Light, pale-colored stools Liver enlargement or swelling Severe abdominal pain Changes in mental state (confusion, lethargy, dizziness) Hepatic encephalitis (swelling in the brain) Coma Death

58. Complication Fibrosis Cirrhosis Liver cancer Liver failure Brain damage

59. HEPATIS IN GENERAL

60. CLINICAL MANIFESTATIONS of Hepatitis: Considerable overlap in the characteristic clinical courses for HAV, HBV, and HCV. Jaundice and tender hepatomegaly are the most common physical findings and are characteristic of the icteric phase. Prodromal symptoms, particularly in children, may abate during the icteric phase.

61. CLINICAL MANIFESTATIONS: Asymptomatic or mild, nonspecific illness without icterus is common with HAV, HBV, and HCV, especially in young children. Hepatitic enzymes may increase 15-fold to 20-fold. Resolution of the hyperbilirubinemia and normalization of the transaminases may take 6 to 8 weeks. Anorexia, malaise, lethargy and easy fatigability are the most common symptoms. Fever may be present, especially adolescents.

62. CLINICAL MANIFESTATIONS: Some cases of acute viral hepatitis not cause symptoms can be mistaken influenza. In young children, most of the prodromal symptoms disappear with the onset of jaundice, the icteric phase. Many children with acute hepatitis, however, never develop jaundice.

63. CLINICAL MANIFESTATIONS: Children with chronic active hepatitis may be asymptomatic But more commonly have nonspecific symptoms malaise, fatigue, lethargy, weight or vague abdominal pain. Hepatomegaly be present, and the transaminases often high, with mild-to-severe hyperbilirubinemia. Fulminant hepatitis due primarily HBV or HCV.

64. CLINICAL MANIFESTATIONS: Many children with fulminant hepatitis develop liver failure, including encephalopathy, coagulation defects, ascites, deepening jaundice, an increasing WBC count. Changes in mental status or personality indicate impending liver failure. A rapid decrease in the size of the liver (indicating loss of tissue due to necrosis) is a serious sign of fulminant hepatitis including GI bleeding, sepsis, renal failure and disseminated coagulopathy.

65. LABORATORY AND IMAGING STUDIES:

66. HISTORY:

67. TREATMENT: The treatment of acute hepatitis is largely supportive and involves rest, hydration, and adequate dietary intake. Hospitalization is indicated for persons with severe vomiting and dehydration, a prolonged prothrombin time, or signs of hepatic encephalopathy. When the diagnosis of viral hepatitis is established, attention should be directed toward preventing its spread to close contacts.

68. TREATMENT: For HAV, hygienic measures include hand washing and careful disposal of excreta, contaminated diapers or clothing, needles, and other blood-contaminated items. Chronic HBV infection may be treated with interferon alfa-2b or lamivudine, and HCV may be treated with interferon alfa alone or more often in combination with oral ribavirin.

69. THERAPEUTIC MANAGEMENT : The goals of management include early detection, support and monitoring of the disease, recognition of chronic liver disease, and prevention of spread of the disease. Special high-protein, high-carbohydrate low-fat diets are generally not of value.

70. THERAPEUTIC MANAGEMENT : The use of corticosteroids alone or with immunosuppressive drugs is not advocated in the treatment of chronic viral hepatitis. However, steroids have been used to treat chronic autoimmune hepatitis. Hospitalization is required in the event of coagulopathy or fulminant hepatitis. Therapy for hepatitis depends on the severity of inflammation and the cause of the disorder.

71. THERAPEUTIC MANAGEMENT : HAV is treated primarily with supportive care. The US Food and Drug Administration approved several medications for treatment of children with HBV and HCV. 1. Human interferon alpha is being used successfully in the treatment of chronic hepatitis B and C in children. 2. Lamivudine is used for the treatment of HBV. It is well tolerated with no significant side effects and is approved for children older than 3 years.

72. THERAPEUTIC MANAGEMENT : Combined therapy with lamivudine and interferon alpha reduces the rate of antiviral resistance compared with lamivudine monotherapy. Adefovir is used to treat HBV in children older than 12 years. Entecavir is a recently approved treatment for HBV in adolescents aged 16 years or older.

73. THERAPEUTIC MANAGEMENT : Pegylated interferon, interferon alpha-2b, and ribavirin have been approved for use in the treatment of HCV infections in children aged 3 years or older.

74. TREATMENT COMPLICATIONS: Fulminant hepatitis with hepatic encephalopathy, gastrointestinal bleeding from oesophageal varices or coagulopathy, and profound jaundice is uncommon, but is associated with a high mortality rate .

75. PROGNOSIS: Varies and depends on the type of virus and the child's age and immunocompetency. Hepatitis A and E are usually mild, brief illnesses with no carrier state. Hepatitis B can cause a wide spectrum of acute and chrome illness Infants are more likely than older children to develop chronic hepatitis. Hepatocellular carcinoma during adulthood is a potentially fatal complication of chronic HBV infection.

76. PROGNOSIS: Hepatitis C frequently becomes chronic, and cirrhosis may develop in these children. Most cases resolve without specific therapy less than 0.1% of cases progress to fulminant hepatic necrosis. HBV, HCV, and HDV may persist as chronic infection with chronic inflammation, fibrosis, and cirrhosis and the associated risk of hepatocellular carcinoma.

77. PREVENTION OF HEPATITIS: Proper handwashing and standard precautions prevent the spread of viral hepatitis. Prophylactic use of standard immune globulin is effective in preventing hepatitis A in situations of preexposure or within 2 weeks of exposure. Hepatitis B immune globulin (HBIG) is effective in preventing HBV infection after one-time exposures and should be given to newborns whose mothers are HBsAg positive. HBIG should be given within 12-48hours of exposure.

78. VACCINE: Two types of HAV vaccines are currently available internationally: Killed vaccines: 0.5ml IM 2 doses, 6 months apart, 1-12 years ( Hebrix ) Live attenuated vaccines (based on H2 or LA-1 HAV strains): 0.5 ml SC, single dose at 1-12 years (BIOVAC)

79. NURSING CARE MANAGEMENT: Depend largely on the severity of the hepatitis, the medical treatment, and factors influencing the control and transmission of the disease. Explain any medical therapies and infection control measures. Well-balanced diet and a schedule of rest and activity adjusted to the child's condition. Standard precautions are followed when children are hospitalized. Discourage children from sharing their toys. Handwashing is the single most effective measure in prevention and control of hepatitis in any setting.

80. RESEARCH ARTICLE

81. RESEARCH ARTICLE Abstract Aim: To identify the clinical status and immunological profile of a cohort of children with chronic hepatitis B virus (HBV) infection to assess the short-term consequences of this infection. Material and methods: This prospective case-control study included 30 children in the age range 1–15 years with positive HBsAg attending the Hepatology clinic of Alexandria University Children’s Hospital. Twenty children received lamivudine (3 mg/kg, oral, once a day), and 10 children were lamivudine-resistant and received entecavir treatment (10–11 kg/0.3 mg to > 30 kg/1 mg). They were followed up every 3 months for 1 year.

82. RESEARCH ARTICLE Results: The study showed that 97% of the studied cases were discovered accidentally during routine investigations and only 3% presented by acute hepatitis. Ninety percent of them had family member infection with HBV, of which 70% were the mother. Eighty-seven percent of cases had no clinical signs, and only 13% of cases had hepatomegaly. All of the cases were HBsAg positive, 50% were HBeAg positive, 56.7% were HBeAb positive, 33.3% were HBcAb positive, and 100% were HBsAb negative. Conclusions: Most of children with HBV infection had associated family member infection and were accidentally discovered. Screening for the HBsAb level in children with family members with HBV is recommended.

83. RECAP & SUMMARY: Today we have discussed about: Definition of hepatitis. Different types of hepatitis. Causes and mode of transmission of different types of hepatitis. Pathophysiology of hepatitis Vaccination & prevention of hepatitis. Management of hepatitis.

84. Conclusion Hepatitis is an inflammation of liver. There are various risk factors of hepatitis based on the type of hepatitis. It can be prevented by: maintaining proper hygiene habits, clean environment, proper vaccination, Screening test used for blood donation or transfusion.