بسم اهلل الرمحن الرحيم

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1 بسم اهلل الرمحن الرحيم

2 Jaundice in pregnancy By: Abdul Karim Majid 6 th stage

3 Jaundice as we know is the yellowish discolouration of skin & sclera as a clinical manifestation of hyperbilirubinaemia. Classically normal bilirubin level is <20 micromol/l and clinical jaundice has a presumed level of >40 micromol/l

4 What is bilirubin? The breakdown product of Hgb from injured RBCs and other heme containing proteins. Produced by reticuloendothelial system Released to plasma bound to albumin Hepatocytes conjugate it and extrete through bile channels into small intest.

5 Unconjugated vs. Conjugated Unconjugated production exceeds ability of liver to conjugate Ex. Hemolytic anemias, hemoglobinopathies, in-born errors of metab., transfusion rxn. Conjugated Can produce but not excrete Metabolic defect Intra- or extrahepatic obstruction

6 Causes: Pre-hepatic / hemolytic jaundice Post-hepatic causes of jaundice Intrahepatic causes such as Pregnancy related AFL of pregnancy HELLP syndrome IHC of pregnancy Hyper emesis gravidarum

7

8 Clinical Feature Skin and Eye Changes Change in Urine Change in Feces Severe Itching Advanced Symptoms

9

10

11 Laboratory Tests Of Jaundice Serum bilirubin level (total and direct) Liver aminotransferase levels Alk. Phos U/A for bilirubin and urobilinogen CBC PT Other labs pertinent to history Hgb electrophoresis Viral hepatitis panel U/S Gallbladder

12 Hyperemesis Gravidarum Morning sickness can occur in 50-90% of pregnancies % continue to 3rdTM and 5% till delivery. Hyperemesis is coined for those having 5% weight loss with ketonuria, refers to rejection of all food and drink by the pregnant. involve upto 2% of pregnancies. The cause not clear but thought to be hormonal changes and also seen in twin pregnancy and H.mole.

13 Laboratory Test Lab. abnormalities usually involve :- Electrolyte imbalance Hematocrit increase Abnormal LFT in 50%. Usually ALT > AST. But never exceeding 1000 IU/L. Bilirubin is mildly elevated up to 70micromol/L DDx:- is limited due to presentation in the 1 st TM as acute fatty liver of pregnancy as well as HELLP syndrome presents much later.

14 Treatment Treatment centres around rehydration and also using antiemetics, avoidance of trigger factors as well as dietary changes Morbidity rather than mortality is the usual accompanyment of this disease. Rarely due to excessive vomiting, UGIB due to oesophageal tears can occur.

15 Pre-eclamptic liver disease and HELLP Syndrome Hepatic dysfunction with preeclampsia has long been recognised but more recently it has been strongly associated with HELLP syndrome (Haemolysis Elevated Liver Enzyme Low Platelate) which complicates 5% pre-eclamptic pregnancy. HELLP present in 20% of ecclamptics. Overall pregnancies fortunately only 0.1%

16 Diagnosis was established by the presence of preeclampsia and all of the following criteria: Microangiopathic hemolytic anemia Platelet count 100,000 cells/ml Serum LDH 600 IU/L Total bilirubin 1.2 mg/dl Serum AST 70 IU/L Women who did not meet all of the above were considered to have partial HELLP syndrome.

17 *Investigators had classified HELLP Syndrome: Class 1 (platelet count <50,000 cells/ml, AST or ALT >70 IU/L, LDH >600 IU/L) Class 2 (platelet count ,000 cells/ml, AST or ALT >70 IU/L, LDH >600 IU/L) Class 3 (platelet count ,000 cells/ml, AST or ALT >40 IU/L, LDH >600 IU/L)

18 Incidence predominate in the 3 rd TM (70%), usually th week, even though 30% can occur post partum (usually within 48 hr but upto 7 days). Lab. abnormalities are seen, such as Hyperbilirubinaemia Thrombocytopenia Abnormal liver enzymes Hemolysis Coagulopathies are rare. BP even though frequently elevated is not necessary to diagnose HELLP Lab abnormalities peak 1-2 days postpartum and then return to normal within 3-11 days.

19 Management is prompt delivery and there is currently insufficient evidence to support the use of adjunctive steroids to reduce maternal and perinatal mortality and major morbidity. Maternal mortality associated with HELLP is about 2%. The most serious complications :- DIVC, placental abruption (16%). ARF (8%). pulmonary oedema (1%). liver haematoma/rupture (1%) Perinatal mortality rate is 20%, Prematurity in 70%

20 Cont. Risk of recurrence in future pregnancies is upto 6%. Lab abnormalities may still worsen upto 48 hours postpartum but and improve later.

21 Acute fatty liver of pregnancy Rare <1 in 10,000 pregnancies. Most patients are in the third decade of life and typically developed in 3TM Risk factors: nulliparity, pre-eclampsia and male births. Signs and symptoms include nausea, vomiting, abdominal pain, jaundice, encephalopathy, polydipsia, headache and itching.

22 Usually beginning at 35 th week of pregnancy but can occur much earlier. May also appear immediately after delivery or earlier at 26 th week but rare. Pathogenesis is postulated to one of the inherited defects in mitochondrial beta-oxidation of fatty acids,

23 The acute fatty liver of pregnancy presents with :- Hyperbilirubinaemia Transaminases <1,000 IU/l Hypoglycemia Hyperuricaemia Leucocytosis High creatinine Beginning disseminated intravascular coagulation. But NORMAL pregnancy levels of ALP in a majority of cases. Liver biopsy is diagnostic, showing the characteristic picture of microvesicular fatty infiltration of hepatocytes.

24 Acute fatty liver of pregnancy is a life-threatening condition with a 18% maternal and 23% fetal mortality rate (up to 85% if associated with pre-eclampsia).

25 Complications of acute fatty liver in pregnancy Gastrointestinal bleeding Renal failure Coagulopathy Hypertension/preeclampsia/HELLP Infections Pancreatitis Hypoglycemia

26 Treatment Sadly no specific treatment has proved successful except early delivery because after delivery(by cessarian section) the Condition resolves with complete recovery (may rarely take up to 4 weeks). Can recur with subsequent pregnancies but frequency is unknown

27 TABLE 1 -- Laboratory Differences of ACUTE FATTY LIVER OF PREGNANCY with HELLP Syndrome Hematologic AFLP HELLP Platelet count Low or normal Low Fibrinogen Low Normal to increased Prothombin time (PT) Prolonged Normal Partial thromboplastin time (PTT) Prolonged Normal Serum chemistries Glucose Low Normal Uric acid High High Creatinine High High Ammonia High Normal

28 Intrahepatic cholestasis of pregnancy Reversible form of cholestasis developing in the third trimester of pregnancy and usually resolving rapidly after delivery. Postulated to be secondary to hormones (oestrogen/ progesterone) and transport defects. Complicates % of pregnancies Increased prevalence in certain populations with likely dominant inheritance.

29 Pruritus is the commonest complaints but clinical jaundice only occurs in 10% of patients. Jaundice without pruritus is rare Incidences are usually in the 3 rd TM 1 st TM (10%), 2 nd TM (25%), 3 rd TM (65%) Serum bile salts are increased minimal or no ALT elevation. ALP & GGT can be raised but the significance is unknown

30 Medical treatment of ICP is controversial where ursodeoxycholic acid is used where pruritis is severe and provides safe and effective relief. Cholestyramine anionbinding resin AND (diphenhydramine and other antihistamine) help slightly. COMPLICATION OF ICP :- increased risk of bleeding to mother and increased risk of preterm labour(19-60%), fetal distress (22-33%) and increased perinatal mortality rate (1-3%). Hence weekly CTG is recommended. ICP recurs in 60-70% of subsequent pregnancies. Symptoms resolves 2-14 days post delivery

31 Infective viral hepatitis Commonest cause of jaundice in pregnancy are associated with viral hepatitis, with infections due to hepatitis viruses A, B, C, D and E. Incidence of hepatitis varies greatly around the world: from 0.1% in developed countries upto 20% in developing countries. About hepatitis E : pregnant women exhibit fatality rates of upto 20% (1% in non pregnant) (Mortality in the 1 st TM 1.5%, 2 nd TM 8.5%, 3 rd TM 20%). Reason of high fatality is unknown.

32 Summary of hepatitis: Hepatitis A: Disease usually lasts 2-3 weeks with death in <1% of patients and NO chronic form. Pregnant women exposed to the virus can be given immune globulin within 2 weeks of exposure together with vaccine. Not clear if virus transmitted from mother to baby and if IgM is present in mother during third trimester, prophylactic treatment of the neonate is probably unnecessary.

33 Hepatitis B: The presence of HBeAg is associated with a very high risk of neonatal infection. Infants of HBsAg ve women should receive hepatitis B immuno globulin immunoprophylaxis at birth AND hepatitis B vaccine at one week, one month and six months old. This regime reduces the incidence of hepatitis B vertical transmission to <3%. The prevalence of neonatal infection depends on the time during gestation that maternal infection takes place: rare in first trimester, 10% in second trimester and 70-85% of those in the third trimester.

34 Hepatitis C: No therapy has been shown to influence the neonatal transmission of hepatitis C virus Interferon should not be used during pregnancy because of possible adverse effects on the fetus Transmission is increased in mothers with higher viral load (upto 33% in those with viral load >10 19 copies per ml

35 Hepatitis D: When present it increases the incidence of acute hepatic failure. Hepatitis E: Rare in the developed world but in developing worlds where it is more common, responsible for high level of fulminant hepatic failure and mortality in pregnant women (20%). It is a waterborne virus spreading through faecal-oral transmission. Outbreaks occur after flooding.

36 Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) concentrations increase to levels of from 500 to 5,000 mu/ml, becoming abnormal approximately 1 week before and usually peaking approximately 1 week after symptoms develop While bilirubin >40 will result in clinically apparent jaundice.

37 TABLE 1 -- CLASSIFICATION AND BIOLOGIC PROPERTIES OF THE HEPATOTROPIC VIRUSES Species HAV HBV HCV HDV HEV Family Picornaviridae Hepadnaviridae Flaviviridae Deltaviridae Uncertain Genus Hepatovirus Orthohepadnavirus Hepacivirus Deltavirus Unnamed Genotypes 7 5 >6 3 3 Serotypes 1 1?? 1 Main transmission Fecal-oral Parenteral/sexual Parenteral Parenteral Fecal-oral Vertical transmission No Yes Rare Rare Yes Incubation period d d d d d Clinical illness Pediatric, 5% Adult, 80% 30% 5% 10% 80% Chronicity No 5% 85% Yes No Fulminant course <1% <1% Rare or no <5% Pregnancy Antigen test Fecal Serum None Serum Fecal Antibody test Serum Serum Serum Serum Serum Nucleic acid test Feces/serum Serum Serum Serum Feces Vaccine Yes Yes No Yes (HBV) No IG Yes Yes No No No

38 Cholelithiasis Pregnancy alters bile composition and gall bladder emptying slows in the second trimester increasing the risk of gall stones. Risk factors are multiparity and previous gallbladder disease. Choledocholithiasis accounts for approximately 7% of patients with jaundice in pregnancy but jaundice occurs in only 5% of cholelithiasis. Treatment involves laparoscopic cholecystectomy. Uncomplicated cholecystectomy is safer in first and second trimesters with fetal loss about 5% But with common bile duct exploration and if with pancreatitis then 15 % maternal and 60% fetal mortality

39

40 In summary: Causes of Jaundice in Pregnancy % Incidence Viral Hepatitis 42% ICP 21% AFLP / HELLP Syndrome 6% Bile Duct Obstruction 6% Hyperemesis Gravidarum 6% Hemolytic Jaundice 4% Others 15%

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