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JAUNDICE IN PREGNANCY

DR. S.N. BERA & MITALI DASH M K C G MEDICAL COLLEGE

Yellow discoloration of skin, conjunctiva, sclera and mucosa associated with rise in serum bilirubin above 2mg/dl( normal 0.2-01mg/dl)Latent jaundice:1-2mg/dl

Mechanisms: production of bilirubin hepatocyte transport or conjugationImpaired excretion of bilirubinImpaired delivery of bilirubin into intestine--surgically relevant jaundice or obstructive jaundiceCholestasis refers to the latter two, impaired excretion and obstructive jaundice.

Physiological changes in liver during pregnancy

Liver is not palpable during pregnancy.Sr. protein decrease by 20%. Bilirubin also decreaseIn 3rd trimester ALP level increase up to 2-4 times the normal. It returns to normal in 2-3 month of post delivery.ALT and AST level normal, but increase during labour and normalize in 1-2 days postpartum.

5 nucleotides is significantly raised but GGT slightly decrease.Increase sr. triglyceride and VLDL. Cholesterol increases up to 2 times the normal. 10-15% normal pregnant may have bilirubin level of over 1mg% d/t delayed excretion of bilirubin that may leads to increase incidence of purities in pregnancy.

Incidence: 1 to 4/1000 deliveries.Maternal mortality 12% in our country

Grade of jaundice:Mild: bilirubin 16mg%

Cause of jaundice during pregnancyLiver disease unique to pregnancyCoincidental occurrence of liver disease in pregnancy

Acute fatty liver of pregnancy.Intrahepatic cholestasis of pregnancy.Pre-eclampsia, eclampsia, HELLP syndrome.Hyperemesis gravidarum

Acute viral hepatitis.Hemolytic jaundice.Cholelithiasis.Drug inducedObstructive jaundice

Jaundice develop during pregnancy on chronic liver disease:

Cirrhosis of liver.Chronic hepatitis

Liver disease probably related to pregnancy:

Portal HTN.Cholecystitis.Pancreatitis.Wilsons ds.Gilbirts syndrome. Budd chiari syndrome.

Acute fatty liver of pregnancy

Acute hepatic failure in absence of viral hepatitis, IHC, etc.Manifest usually in 3rd trimester sometimes present after delivery.Incidence: 1 in 7000-15000 pregnancies.More common in primipara and associated with pre-eclampsia, multiple pregnancy, having male fetus.

Etiology: may be mitochondrial dysfunction.--- >LCHAD def.--->defect in oxidation pathway of fatty acid.

estrogen in 3rd trimester leads to mitochondrial oxidation.

Table 4 . Swansea criteria for diagnosis of acute fatty liver ofpregnancySix or more criteria required in the absence of another causeVomitingAbdominal painPolydipsia/polyuriaEncephalopathyElevated bilirubin >14 mol/lHypoglycaemia 340 mol/lLeucocytosis >1110 6 cells/lAscites or bright liver on ultrasound scanElevated transaminases (AST or ALT) >42 IU/lElevated ammonia >47 mol/lRenal impairment; creatinine >150 mol/lCoagulopathy; prothrombin time >14 s or APPT>34 sMicrovesicular steatosis on liver biopsy

Clinical features and diagnosisClinical features: Anorexia, nausea, vomiting, headache, fatigue, altered mental status, polydypsia with or with out polyuria.Jaundice 90%, Right upper quadrant pain.Puritus and ascites 50% cases.Hepatic encephalopathy seen in latter. Clinical improvement occurs 1-4 weeks after delivery..

Conjugated hyperbilirubinimia up to 5-15 mg/dl.ALT but 10 6 log copies/ml and higher) should beoff ered antiviral medication with tenofovir or telbivudine inthe third trimester to reduce perinatal transmission of HBV(strong recommendation, low level of evidence).24. C-section should not be performed electively in HBV-positivemothers to prevent fetal infection (strong recommendation,very low level of evidence).25. Women chronically infected with HBV should be allowed tobreastfeed as recommended for infant health (strong recommendation,very low level of evidence).

Hepatitis C

Prevalance in pregnancy 2.3-17%.Transmitted by parenteral route, IP 30-60daysVertical transmission 3-6%.Diagnosed by HC antibody and RNA-PCR.NO vaccination is available. Routine screening not mandatory.All infants born of HCV positive mother should be follow up.

All pregnant women with risk factors for HCV shouldbe screened with anti-HCV antibody. Screening shouldnot be performed in women without risk factors forHCV acquisition (strong recommendation, low level ofevidence).27. Invasive procedures (e.g., amniocentesis, invasive fetal monitoring)should be minimized in infected mothers and theirfetus to prevent vertical transmission of hepatitis C (strongrecommendation, very low level of evidence).28. C-section should not be performed electively in HCV-positivemothers to prevent fetal infection (strong recommendation,very low level of evidence).29. Women chronically infected with HCV should be allowed tobreastfeed as indicated for infant health (strong recommendation,very low level of evidence).30. Hepatitis C therapy should not be off ered to pregnantwomen to either treat HCV or decrease the risk for verticaltransmission (strong recommendation, very low level of

Autoimmune hepatitis31. Pregnant women with autoimmune hepatitis (AIH) shouldbe continued on their treatment with corticosteroids and/orazathioprine (AZA) (strong recommendation, very low levelof evidence).32. Pregnant women with primary biliary cirrhosis (PBC) shouldbe continued on their treatment with UDCA (strong recommendation,very low level of evidence).33. Pregnant women with Wilsons disease (WD) should becontinued, with dose reduction if possible, on their treatmentwith penicillamine, trientine, or zinc (strong recommendation,very low level of evidence).34. Pregnant women with suspected portal hypertension shouldundergo screening with upper endoscopy for esophagealvarices in the second trimester (strong recommendation, lowlevel of evidence).35. Pregnant women who are found to have large esophagealvarices should be treated with beta-blockers and/or bandligation (conditional recommendation, very low level ofevidence).36. Pregnant women with a history of liver transplantationshould continue their immunosuppression except formycophenolic acid (strong recommendation, moderate level

Hepatitis D

Delta virus; defective RNA virus. Must co-infect with HBV.Transmission similar to HBV.Chronic co-infection with HBV and HDV is more severe. Neonatal transmission is unusual.

Hepatitis E

Transmitted by feco-oral route.Fulminant varity is most common among all types.HEV specific IgM and IgG can be detected.Chance of vertical transmission.Chronic infection is uncommon but may occurs.Hepatitis E vaccine(Hecolin) .Maternal mortality 15-20%.

Clinical features of viral hepatitisProdromal phase: nausea, vomiting, pyrexia, loss of appetite, upper abdominal pain, myalgia, artthralgia, dark urine, clay colour stool. Palpable liver.Icteric phase: appears 1-2 weeks after symptom.Recovery phase: jaundice recedes, liver enlargement regress, it takes 6-12 weeks for complete recovery.Investigation: ---LFT ---liver biopsy.

Effects on pregnancy and fetus.

incidence of abortion, pre term labour, still birth,

incidence of primary pulmonary hypertention , hemorrhagic manifestation, hepatic coma,

ManagementPreventive: --disposable syringe & needle are used --blood transfusion with due care. --sanitation and clean water supply, --health personnel should be provided with the guidelines while dealing with pregnant women and during delivery. --active and passive immunization.

Therapeutic: - bed rest until jaundice disappears. - isolation as far as possible. -diet rich in carbohydrate. -vit B-complex .

Acute HepatitisICPHELLPAFLPTrimesterAny TrimesterThirdThirdThirdPresenting symptomsFever, JaundicePruritusHTN, Nausea, Vomiting,PainNausea, Vomiting,PainALT & ASTMarkedly highNormal to Mild riseModerately highModerately highAlkaline PhospataseNormal to mild riseHighNormalNormalPlateletsNormalNormalLowNormalFetal ComplicationsInfection with HBV & HCVPrematurity, IUGR, FDIUGR, PrematurityPrematurityMaternal ComplicationsAcute liver failure(HEV)NoneThrombocytopenia, septicemia, DICAcute liver failure

Hemolytic jaundiceHereditary ----thalassemia, sickle cell anemia. ----spherocytosis.Acquired ---- malaria. ---- mismatched blood transfusion. ---- leptospira, ----cl. Wiilchi All causes unconjugated hyperbilirubinemia,

Sickle cell anaemia with pregnancy : Pregnancy is high risk in sickle cell disease (mostly SS Haemolytic crisis causes rapidly developing anemia with jaundice. Vaso-occlusive crisis causes osteonecrosis, infarction of kidney, lung. Hepato-splenomegaly, heart failure are common.Increased incidence of maternal pre-eclampsia, PPH, infection. Increased morbidity and mortality due to CVA, pulm infarction, CHF, embolism etc. Increased risk of abortion, prematurity, IUGR, fetal loss, perinatal mortality.

Management includes : Pre-conceptional councellingDuring pregnancy: Regular ANC, Prophylactic folic acid 1 mg daily, Iron supplementation etc. Infection or appearance of unusual symptoms needs hospitalizationDuring labour: Oxygen inhalation, Adequate hydration, Antibiotics . Epidural anesthesia preferred. Caesarian section should be performed for obstetric indication only. Contraception: Sterilization even with low parity. OC pills, IUCD contraindicated. Barrier method is ideal.

MalariaMalaria is imp. cause of jaundice in our country. Effects on mother: Anemia, Hypoglycemia, Metabolic acidosis, Hepatic dysfunction with jaundice, Renal failure, Pulmonary edema, Convulsions, coma etc.Effects on the fetus: Abortion, Preterm labour, Pre-maturity, IUGR, IUFD etc. Congenital malaria is rare (