Liver diseases (3)

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Liver diseases


Diseases only related to liver AFLD,obstrectic cholestasis.etc

Muliti system diseases with hepatic manefestations hyperemesis gravidarum,HELLPSome diseases are unique to pregnancyHELLP XdAFLP

Some diseases are not unique but more severe Hepatitis EHSV

Some diseases are precipitated by pregnancyGall stone diseaseBudd chiari

Use of gestational ageIt is the best guide to differential diagnosis of liver disease

T1-hyperemesis g. T2,T3-cholestasis T3 HELLP,AFLP Any trimester- viral hepatitis,drug induced, gall stone disease,malignancy Findings in normal pregnancy which make difficulty in differentiationPhysical ex: spider navae palmer erythema late pregnancy-palpation of liver is difficultUSS- NL billiary tract fasting gall bladder volume & residual volume after contraction may be increasedS. proteins & lipids bcoz of haemodilution,s.alb decreases in all trimesters T.cholesterol & TGA increasedLiver function tests during pregnancyAffected during pregnancyNot affected during pregnancyincreaseddecreasedALP increased in T2,T3

S.fibrinogen increases in late pregnancy

Alb & T. proteins decreased from T1

Billirubin-slightly reduced from T1

Gamma GT-slightly reduced in late pregnancy



Total bile acid Concentration


Making the correct diagnosis is of paramount importance,

As failure to do so can result in morbidity and mortality,

for not only the mother

but also for her fetus

Historyfeatures of O.J.-jaundice pale stools dark urine pruritus(ask for rash) complications of O.J. -steatorrhoeacoagulopathyinfectionsNausea,vomiting-hyperemesisHypoglycaemic features-sweating,dizziness,palpitationsPolyuria,polydypsiaBooking visit blood preasureIn which POA high BP is detectedAbnormalities in urine testsEpigastric or right upper quadrant painHeadacheVisual disturbancesSymptoms-duration progressionPast obstetric history: past Hx of ob cholestasis past hx of PIH,eclampsiaPast medical Hx: hepatitis gall stone disease CLCD blood transfutionDrug Hx; methyl dopa,MTXFamily Hx: ob.cholestasis PIHSocial Hx: exposure to viral hepatitis travel Hx Physical exTemperaturePallorIcterusScratch marksPolished nailsOdeama in non dependent partsFeatures of dehydration-dry mucus membrane,sunken eyesBPophthalmoscopyReflexes,clonusAbdominal Ex:RHC tenderness Liver examinationIx;Blood testsFBC-high WBC lymphocytosis low Hb-haemolysis low PLTLFTS.Cr,RFTS.electrolytes-hyponatraemiaRBS-hypoglycaemiaS.uratesPT/INRClotting profileSerology for hepatitis,CMV

Urinalysis-proteinuriaUSS-gall stones,focal lesions,extra hepatic obstructionRole of liver biopsyLiver diseasesViral hepatitis-commonest causeObstetric cholestasis-2nd commonestAcute fatty liver of pregnancyHELLP syndromePre-existing liver diseaseGall bladder diseaseHyperemesis gravidarum

Obstetric cholestasisGenerally manifest in T3(mean 30wks)-due to high oestrogen peakIncreased risk in multiple gestation,due to high oestrogen levelComplete recovery is usually rapid following delivery.(when placental hormones return to NL)In some women,abnormal liver function tests may return to normal only slowly.taking 4-6 wks after delivery.

aetiologymultifactorialHormonal factors hyperoestrogenaemia (T3 peak) abnormal progesterone metabolismGenetic factors higher prevalence in family members defect in multi drug resistance type 3 gene(MDR-3)Pathogenesis:

Not clearly understood MDR 3 -encodes for the canalicular phospholipid pump proteinChanges induced by genetic mutation leads to increased sensitivity to oestrogens

Increased oestrogens and progesterons causes cholestatic effect

-progesterone: Due to impairment of sulphation of bile acids due to sulphated progesterone metabolites

-oestrogens act on hepatocytes,causing decreased hepatocyte membrane fluidity which results in reduced bile acid uptake by the liver

Slowing of normal bile flow in maternal liver

Increase of bile acid in blood

Damage of liver cell membraneConsequential rise in liver enzymes in maternal blood

Increase in transfer of bile acids from the mother to her fetus

Clinical features-

severe pruritus affecting limbs and trunk particularly palms and soles Insomnia, MalaiseExcoriation but no rash.Dark urine.Anorexia.Malabsorption of fat with steatorrhoea.Jaundice(10-25%)

DiagnosisIs a diagnosis of exclusion

Therefore,diagnosis is made in 3 steps.

1 - typical Hx of pruritus without rash 2 - Abnormal LFT 3- Exclusion of other causes of itching and abnormal LFTPattern of abnormal LFTModerate elevation of transaminase (< 3 fold)Raised ALP (beyond normal pregnancy values)Raised gamma GT (About 20% cases)Mild elevation of bilirubin (less common)Increased serum total bile acid concentration.10-100 folds rise in primary bile acids(cholic and chenodeoxycholic acid)Some times increased bile acid may be the only biochemical abnormalityPruritus may proceed abnormal LFT- serial measurements are advised in persistent itching

Ix to exclude other causesUss liver (presence of gallstone without evidence of extra-hepatic obstruction-Not exclude OC)Viral serology(for Hep A,B,C,E, EBV, & CMV)Liver autoantibodies pre-existing liver disease, anti smooth muscle antibody-Chronic active hepatitis anti mitochondrial antibodies-primary biliary cirrhosiscomplicationsMaternal risk-Vit K deficiencyIncreases risk of PPH

Fetal risk-Amniotic fluid meconium(25-45%)Spontaneous pre term delivery(12-44%)Intrapartum fetal distress(12-22%)IUDFetal ICH

Risk of still birth increases towards term. But doesnt correlate with maternal symptoms/ transaminase levels, may be related to concentration of maternal bile acids.High concentration of bile acids have been found in amniotic fluid and fetal circulation.Maternal to fetal transfer of bile acids across placenta becomes increased

Potentially toxic levels in fetus

Vasoconstriction increased myometrialof chorionic veins contractility

Abrupt reduction ofblood flow to fetus preterm delivery

Fetal distress

Prediction of fetal compromiseNo use of doppler blood flow analysis.Risk is high if having past Hx.Repeated amniocentesis to detect meconium is the best predictor.

ManagementCouncellingLFT, PT, Bile acids should be check weekly.Monitoring fetal well-being. (CTG, USS, Doppler)Early delivery at 37-38 wk or when fetal lung maturity is evident.

Drug therpyVit k 10mg oraly daily(reduced risk of bleeding)Preferable to use water soluble formulation(due to co-exsistant fat malabsorption)

Anti histamines (pruritus)Chlorpheniramine 4mg tdsPromethazine 25mg nocteUrsodeoxycholic acid(UDCA)-Endogenous hydrophilic bile acid.Alter bile acid pool by reducing hydrophobic bile acid.Insert transport proteins or bile salt export pumps into canalicular membranesIncreases expression of placental bile acid transporters which may allow for improved bile acid transferDose 1000-1500mg daily in divided doses.Improves pruritusReduce total bile acid.Reduce liver enzymes.

CholestyramineBile acid chelating agent.4g bd/ tds.

DexamethasoneSupresses feto-placental oestrogen production.Dose 12 mg oral daily.Consider S/E of high doses.

Other drugsS-AdenosylmethionineEpomediol

Intrapartum MxInduction of labour at 37-38 wk.Close monitoring is required throughout induction and labour.To neonate- IM Vit K

ICP is not a C/I for breast feedingRecurrence risk/ Pre pregnancy councellingRecurrence risk 90%Avoid oestrogen containing OCP.Progesteron has less risk of cholestasis but should monitor LFT.HRT need not to be avoided as this provides only physiological level of oestrogen.Viral hepatitisCommonest cause of hepatic dysfunction in pregnancy.Acute hepatitis in T1-associated with higher rate of spontaneous miscarriage.Causative organisms- Hepatitis viruses- A, B, C ,D, E CMV EBV HSVHepatitis AFaeco oral routeAcute self limiting illnessNot result in chronic infection.Clinical features in pregnant women do not differ from those in non pregnant women.Vertical transmission rareTransmit at or around the time of delivery.In such case neonate should be given immunoglobulin at birth.Vaccination-safe in pregnancy

Hepatitis BTransmission to baby- at the time of delivery 95% vertical/ transplacental 5%Mothers may be asymptomatic who have both HBs Ag and Hbe Ag positive greatest risk of vertical transmission 95%Who are HBs Ag positive but Hbe Ag negative have 2-15% risk of vertical transmissionOutcome of neonateInfected neonates have > 90% chance of becoming chronic carrierIncrease risk of cirrhosis and hepato cellular carcinomaAll neonates born to women with acute or chronic HBV should be given -hep B immunoglobulin -HBV vaccine within 24 hoursImmunisation is 85-95% effective at preventing both HBV infection and chronic carrier state.Provided babies are immunised HBs Ag positive mothers can breast feed.Hepatitis CTransmission via bloodVertical transmission uncommon- maximum risk to fetus at T3Comm