Download presentation
Presentation is loading. Please wait.
1
كيس I تاريخ مراجعه بهمن ماه 1381
بيمار خانم 25 ساله كه اولين حاملگي وي مي باشد يك هفته قبل از بستري در بيمارستان در سن حاملگي 34 هفته دچار درد در قسمت فوقاني شكم، تهوع، استفراغ، بي اشتهائي و تب خفيف مي گردد سپس از سه روز قبل از بستري دچار تغيير رنگ ادرار بصورت پررنگ شدن ادرار و در روز مراجعه دچار اختلال هوشياري مي گردد. در Past.H سابقه تزريق خون، كار دندانپزشكي، و مسافرت ندارد. علائم حياتي: 140 T= RR= PR= ـــــ BP= 90 در معاينه بيمار كنفوريون دارد – ردور گردن ندارد، اسكراايكتريك است سمع قلب تاكيكاردي و سمع ريه نرمال است در معاينه شكم آسيت مختصر دارد، طحال لمس نشد، لمس هيپوكندر است تندرنس دارد، كاپوت مدوزا، اريتم پالمر ندارد در معاينه ادم 1+ در اندامها تحتاني دارد بابنسكي دو طرفه منفي است.
2
هپاتيت در حاملگی دکتر داوود يادگاری
3
1- تشخيص افتراقي بيماري عبارتند از:
2- چه آزمايشي هائي را براي بيمار درخواست مي نمائيد. 3- اگر جواب آزمايش اوليه بيمار به شرح ذيل باشد چه تشخيص هائي براي بيمار فوق بيشتر مطرح ميشود. WBC=20/ Hb= Pt= FBS=40 35= بيليروبين T= Hct= %=پلي 20= مستقيم = LDH %= لنف 180< فيبرينوژن SGPt= SGot= = پلاكت نرمال = chst--Ray نرمال = كامل ادرار 4- آيا براي بيمار فوق ختم سريع حاملگي را توسط سزارين توصيه مي كنيد. 5- آيا براي تشخيص قطعي تر آزمايش ديگري را پيشنهاد مي نمائيد. 6- اگر در آزمايش بيمار HBSAg مثبت گزارش شود اقدام بعدي چيست. 7- براي نوزاد وي چه اقدامي را توصيه مي كنيد. 8- اگر بجاي HBSAg، AntiHcv بيمار مثبت باشد اقدام مناسب چيست. 9- براي نوزاد مادر مبتلا به Hcv چه اقدامي را توصيه مي كنيد. 10- اگر HBSAg مادر منفي و AntiHcv منفي گزارش شود چه اقدامي را براي بيمار توصيه مي نمائيد.
4
Approach to HBs Ag+ Dr. D. Yadeghari (Shahid Beheshti University) &
In the Name of God Approach to HBs Ag+ Dr. D. Yadeghari (Shahid Beheshti University) & Dr. Sh. Sali (Karaj District Social Security) Infectious Diseases Specialists January 2004
5
Hepatitis B Virus is a common cause of CLD in Iran.
Chronic liver disease (CLD) represents a major public health problem in the world, as well as in Iran. Hepatitis B Virus is a common cause of CLD in Iran.
6
Number of HBsAg +Patients
Prevalence % Number of HBsAg +Patients World 5 350,000,000 Iran 3 2,000,000 USA 1,250,000
7
Family/ Household Sexual Conduct
Prevalence of HBV Serologic Markers in Population Groups Who Should be Screened for HBV Infection Population Prevalence of HBV Serologic Markers(%) HBsAg All Markers Born in Endemic Areas 13 70-85 Homosexuals 6 35-80 IV Drug Users 7 60-80 Dialysis 3-10 20-80 HIV Infection 8-11 89-90 Pregnant Women - Family/ Household Sexual Conduct 3-6 30-60
8
Epidemiology Endemic Regions of HBV: Asia South Pacific
Sub Saharan Africa Alaska – Green land , north Canada Australia Newsealand South America Mid East
9
3Paterns of HBV Transmission
Perinatal Transmission Person to Person in Childhood Sexual Transmission in Adulthood (in developed countries)
10
Hepatitis B HBsAg- is the first evidence of HBV infection
persistence of HbsAg after the acute illness is evidence of chronic hepatitis Anti HBs- specific antibody to HBs Ag appears after clearance of HBsAg and after successful vaccination disappearance of HBsAg and appearance of anti HBs signals recovery and non infectivity
11
Labs markers Anti HBc- appears shortly after HBs Ag is detected.
Its presence indicates a diagnosis of acute hepatitis B HBeAg- is a soluble protein found only in HBs Ag-Positive area indicates viral replication and infectivity HBV DNA- is more sensitive and precise marker of viral replication and infectivity
12
2. Diagnostic Criteria: Chronic Hepatitis B: Resolved Hepatitis B:
1- HBsAg+ > 6 m 2- HBV DNA > 10 5 3- Persistent or Intermittent ALT/AST 4- Liver Biopsy Score ≥ 4 Resolved Hepatitis B: 1- Previous known history of hepatitis or anti-HBC ± anti HBs 2- HBsAg - 3- Undetectable HBV DNA 4- Normal ALT
13
In-active Carrier State:
- HBeAb+ - Normal ALT - Minimal or No Necroinflammation - Outcome is Benign - Serial tests should be performed before determined - 20% can have exacerbations: - ALT > 5 – 10 times - HBeAg± - Repeat can lead to progressive Fibrosis
14
Outcome of In-active Carriers
- 0.5% will Clear HBsAg Yearly (Low level DNA in 50% of these Persons) - 0.5 per 1,000 years incidence of de-compensated Cirrhosis
15
-Personal History -Medical History
History of Icter Hospitalisation surgery(major or minor-time ) Delivery or abortion Tooth Cleaning Dental surgery ( time-kind ) Experimental dentist Endoscopy Dialysis Hejamat HBV vaccination Blood donation Transfusion
16
Organ transplant CRF Hemophillia Major thallasemia
Special Disorders: Organ transplant CRF Hemophillia Major thallasemia
17
Needle Sticks Accidents War Injuries Electerolysis,Tatooing
Blood Contact Needle Sticks Accidents War Injuries Electerolysis,Tatooing
18
Occupational Exposure
Physicians Nurses Hospital staffs Laboratory Personnel
19
History of high risk behavior:
Addiction: IV or non IV Imprison Sexual contact -Heterosexual -Homosexual -Bisexual
20
History of Hepatitis History of HCC or Cirrhosis
Family History History of Hepatitis History of HCC or Cirrhosis
21
Traveling History: Traveling Abroad
22
Symptoms : Weight loss Malaise Fatigue Concentration i Mood i Nausea
Vomiting Diarrhea Constipation Pale stool Dark urine Pruritis Jaundice Hemorrhage Edema Irregularity of Mensturation Impotence
23
Physical Examination :
Pale Conjectiva Icteric Sclera Palmar Erythema Skin Pigmentation Clubbing Fetor Hepaticus Caput Medusa Gynecomastia Muscle wasting Ascitis Small liver Splenomegaly Umblical hernia Excoriation
24
Laboratory Tests -a1 -a2 -b -g Globulin CBC,Plt Liver function tests :
FBS-chol-TG HBsAg,HBsAb,HBeAg,HBeAb,HBcAb CBC,Plt Liver function tests : Ast Alt,Alkp,GGt Bili(T,D)PT,PTT Total protein Albumin
25
In High Risk Patients HIV Ab HCV Ab HDV Ab
26
HBsAg-HBeAg-HBeAb - HBcAb- HBsAb i Confirmation of HBsAg(+) Filing
1-Hepatits B panel HBsAg-HBeAg-HBeAb - HBcAb- HBsAb i Confirmation of HBsAg(+) Filing
27
Abdominal Sonography Liver-Spleen-Diameter of Portal vein Liver Biopsy Grading Staging
28
Evaluation of patients with chronic HBV infection
Initial evaluation History and physical examination Laboratory tests to assess liver disease -complete blood counts with platelets, hepatic panel, and prothrombin time Tests for HBV replication-HBeAg/anti-HBe, HBV DNA Tests to rule out other causes of liver disease -anti-HCV,anti -HDV Tests to screen for HCC-AFP and, in high risk patients, ultrasound Liver biopsy to grade and stage liver disease-for patients who meet criteria for chronic hepatitis
29
Follow-up for Patients Not Considered for Treatment
1- HBeAg+, HBV DNA>105, Normal ALT - ALT Every 3-6 months - If ALT > 1-2 uln, Every 1-3 m. - If ALT>2, for 3-6 m., Consider Liver Biopsy and Treatment - Screening for HCC
30
2- In-Active HBsAg Carrier State
- ALT Every 6-12 months - If ALT > 1-2 x U.L.N, Check HBV DNA and Exclude Other Causes of Liver Disease - Screening for HCC
31
Outcome of Inactive HBsAg Carriers:
-Generally Benign Exacerbation of hepatitis to 20% (as evidenced by Alt ) Seroconversion of HBsAg to Anti HBs (0.5-1%per year) Progression to cirrhosis or HCC
32
- De-Compensated – 14% at 10y
Outcome of Cirrhosis - HBeAg+ 72% - Compensated – 84% at 5y - HBeAg- 97% - 68% at 10 y - De-Compensated – 14% at 10y Risk Factors for De-compensation: - HBeAg+ - Failure to Respond to Interferon
33
Counseling and Prevention of Hepatitis B
- Life style Modification and Prevention of Transmission - Non-Specific Dietary Unless Use of Alcohol > 40 g/d - Precautions to Prevent Sexual Transmission - Perinatal Transmission - Blood Spill - Pregnant Women HBsAg+ should be Counseled: 1- HBIG and Vaccine can be Administrated to new born baby, immediately after delivery. 2- Follow up Testing Their Infant at 1 year of age
34
- Screening of Family Members of the patient and Vaccination, if the Screening Tests (HBsAg, HBsAb) are Negative - Available Vaccines Against HBV: - Given 3 times: At Start, 1 & 6 Months Later Age Limited? None, Can Give in Newborns HBV Prevention
35
Carriers of any age, even Asymptotic Persons with Normal ALT and Minimal or Absent Liver Disease, Can Develop HCC
36
AFPr Testing: Normal is Less than 8-12 ng/ml
- Sensitivity for Small HCC, 50-75% - Specificity is Above 90% - Negative Predictive Value > 99% - Positive Predictive Value is: 9-30%
37
Neonates >95 Age(YEARS) 2-19 ~99 20-29 ~95 30-39 ~90 40-49 ~85
Anti-HBs Seroconversion Rates after Hepatitis B Vaccination(%) Neonates >95 Age(YEARS) ~99 ~95 ~90 ~85 ~70 > ~50 Renal failure, HIV infection, Other immunosupperession Liver disease
38
Hepatitis A Incubation period- 30 days
excreted in faeces for up to 2 weeks before onset of illness early presence of antibody in course of illness (anti HAV) IgM anti HAV is test for diagnosing acute hepatitis which peaks during 1st week and disappear within 3-6 months low mortality rate
39
Continuation Hepatitis A
Chronic hepatitis A does not occur No carrier state The presence of IgG anti HAV alone indicates previous exposure
40
Hepatitis C Single stranded RNA Virus
in past HCV responsible for 90% cases of post transfusion 50%- post intravenous drug use high risk in body piercing risk of sexual and maternal-neonatal transmission is low diagnosis based on an enzyme immunoassay in Fiji still carrying out surveillance on HCV
41
Overview of Hepatitis B and C
42
Chronic Hepatitis C US Data 150,000 new cases/yr 3.5 million infected
8,000-10,000 chronic HCV patients die annually from liver related complications Canadian Data 1635 cases notified in 1993 (acute and chronic) 305 cases notified to Sentinel Health Units 28% transfusion related 71% injection drug use related 14% both risk factors 0.3% blood donors anti-HCV+
43
Chronic Hepatitis C Incubation period is 6 to 12 weeks
Chronicity rate exceeds 80% 10-20% each decade get cirrhosis <85% acute hepatitis C patients become carriers Vast majority are symptom free for at least 20 years “Healthy” carrier state does not exist
44
Chronic Hepatitis C High Risk Groups
Recipients of multiple blood transfusions Hemophiliacs Hemodialysis patients Infants of HCV+ mothers Intravenous drug users Healthcare workers
45
Chronic Hepatitis Risk Factors
Needle-stick injuries % Dialysis unit 2-3% Hematology units Newborns of Anti-HCV+ mothers 6%
46
Chronic Hepatitis C Liver Transplantation
Chronic hepatitis C is a frequent cause of end-stage liver disease Recurrence of hepatitis C after transplantation is almost universal Liver transplantation for chronic hepatitis C costs $ million (U.S.) annually
47
Chronic Hepatitis C Routes of Transmission
Blood transfusion Blood products Perinatal Intrafamilial Hemodialysis Shared needles Tattooing Needle-stick and sharps injuries Sexual Saliva
48
Chronic Hepatitis C Routes of Transmission
49
Hepatitis D Defective RNA Virus causes Hepatitis only in association with Hepatitis B specifically in presence of HBsAg it is clear only when the latter is clear Diagnosis is by detection of antibody to hepatitis D antigen best prevented by preventing Hepatitis B
50
Hepatitis E RNA Virus responsible for waterborne virus
outbreaks in India,Afghanistan and Mexico
51
Hepatitis G (HGV) been applied to a flavivirus that is percutaneously transmitted and associated with chronic viremia lasting at least 10 years been detected in blood donors, intravenous drug user, hemodialysis patients and patients with chronic hepatitis B or C but it does not appear to cause important liver disease. In Fiji, Lepstopirosis was not detected earlier and caused few death in rural areas mistaken for Viral Hepatitis Symptoms similar to viral hepatitis Hepatitis A is common in rural areas
Similar presentations
© 2024 SlidePlayer.com Inc.
All rights reserved.