Liver disease in pregnancy can have severe maternal and fetal effects. Unique conditions include hyperemesis gravidarum, intrahepatic cholestasis of pregnancy, HELLP syndrome, and acute fatty liver of pregnancy. Physiological changes occur in hepatic parameters during pregnancy. Conditions like viral hepatitis and cirrhosis may impact an existing pregnancy. Accurate diagnosis and management of liver conditions is important to optimize outcomes.

1. Liver Disease and Pregnancy
Dr.Harsh Saxena
J.R 1 medicine

2. Challenging disease to manage
• Because of physiology of pregnancy certain
disorders take more ominous course in
pregnancy than in non pregnant state and some
are unique to pregnancy
• May have severe maternal & fetal effects
Therefore it is important to have accurate
diagnosis

3. Physiological changes in hepatic
parameters
NO CHANGE WITH CHANGE
• Hepatic blood flow • Albumin - ↓ 20%-50%
• Hepatic & splenic size • Globulin -↑
• Liver histopathology • Fibrinogen - ↑50%↑
• Bilirubin- direct or • ALP - ↑2-4 fold
indirect, AST, ALT, • LDH - ↑slight
• PT,APTT • Cholesterol & TGL - ↑2fold
↑ AST, ALT,S Bb, during
pregnancy indicate liver disease

4. Classification
Unique to pregnancy
• Hyperemesis Gravidarum
• Intrahepatic cholestasis of pregnancy
• HELLP
• Acute fatty liver of pregnancy
concurrent with pregnancy
• Viral hepatitis A,B,C,E
Pregnancy on Preexisting ch liver disease
• Cirrhosis & Portal HT

5. Hypermesis Gravidarum
• Hyperemesis Gravidarum occurs in 1 in 20 pts
per 1,000,in the first trimester usually between 4
to 10 weeks of gestation.
• Hormones levels seem to play a role ,having
peak of human chorionic gonadotrophin and
oestradiol levels high.
• Risk factors are :hyperthyroidism,molar
pregnancy ,pre existing diabetes,multiple
gestataion,multiparity.

6. • Symptoms: severe nausea and vomiting,patient
may often present dehydrated and shows
evidence of malnutrition and poor weight gain.
• Upto half patients have abnormal liver
enzymes,aminotransferase levels may rise up to
200IU/L,alkaline phosphatase may rise to twice
the normal values.both direct and indirect
bilirubin values may rise to 4mg/dl.

7. • Serum amylase and lipase may rise to 5 times
normal.
• Non pharmacological interventions are avoiding
nausea triggers odours from
perfumes,smoke,cooking,foods.low fat,small
frequent diets.

8. • Vitamin B6 in a dose of 10 to 25 mg QID is the
initial treatmet of choice,in conjuncton with
doxylamine12.5 mg qid
• Promethazine 12.5 mg orally or rectally every 4
hrs.
• Diphenhydramine 50 to 100 mg orally or rectally
every 4 to 6 hours can be used in unresponsive
patients.

9. • In absence of dehydration, metoclopramide 5 to
10 mg im orally thrice a day or promethazine
12.5 or 25 mg IM/ orally/ rectally every 4 hours
can be added.
• If all these agents fails then methylprednisolone
16 mg thrice a day per orally or iv for 3 days
followed by 2 weeks taper.

10. • Minor complication acid base,electrolyte
disturbances,serious complication are
oesophageal rupture,retinal haemorrhage,renal
damage.

11. Intra hepatic cholestasis
• Intra-hepatic cholestais of pregnancy is common
disorder in the third trimester , and resolve after
delivery.
• Having multifactorial aetiology genetic,
hormonal , exogenous factor.
• Intra hepatic cholestasis of pregnancy is due to
abnormal bililary transport resulting in
saturation of hepatic transport system

12. It is associated with intrauterine growth
retardation and premature birth.
Recurrent familial intra hepatic cholestasis of
pregnancy as heritable defect in the multidrug
resistance MDR3 gene,encoded for canalicular
phospholipid translocator involved in bile duct
secretion of phospholipids.

13. symptoms
Generalised pruritis that begins in the
periphery,often worse on the palms and soles
that moves to the trunks.
Pruritis progress as pregnancy continues and
resolves within 48 hours of delivery
Some patients have diarehoea and steatorrhoea.

14. • Diagnosis:serum bilirubin usually <6mg/dl and
transaminses are elevated from a minimal rise to
20 times normal.bile acids levels are > 10
umol/L and may be 100 folds normal all these
resolves within 2 to 8 weeks of delivery.

15. treatment
• Patients should be treated at centres capable of
treating premature infants.
• Medical treatment of choice is ursodeoxycholic
acid UDCA, dose of 1 g per day.
• Cholestyramine also reduces pruritus in total
divided doses of 10 to 12 g per day.
• Maternal outcome is good with symptom
resolution after delivery.

16. Acute Fatty Liver of Pregnancy
• Prevalence is 1 per 10,000 to 15,000 pregnancies
and mostly in the 2 half of pregnancy.
• AFLP is in the family of microvesicular fat
diseases.
• Risk factors: older maternal
age,primiparity,multiplegestations,pre-
eclampsia,male foetus.

17. • Genetic mutation that affects their
mitochondrial fatty acid oxidation pathway
• A foetus with long chain 3 hydroxyacl-coenzyme
A dehydrogenase LCHAD deficiency.

18. Symptoms
• Patient will have
nausea,anorexia,lethargy,abdominal
pain,ascitis,and progressive jaundice.
• Acute renal failure occurs in 50% ,HE in 60%
and 50% have hypertension,proteinuria and
oedema, suggestive of pre-eclampsia.

19. Diagnosis
• Serum aminotransferase levels are moderately
elevated around 300-500 U/L,bilirubin < 5
mg/dl other abnormalities includes
hypoglycemia, elevated ammonia
levels,thrombocytopaenia,renal dysfunction.
• Liver biopsy shows microvesicular steatosis.

20. Treatment
• Continuous foetal monitoring should be
initiated.
• Supportive measures are required in the form of
glucose infusion,adequate hydration and blood
products .
• Primary treatment is prompt delivery of the
foetus, recovery before delivery is not seen.
•

21. • Liver functions normalises within a week.
• Maternal complication include post partum
haemorrhage, renal
failure,hypogycaemia,DIC,pancreatitis and
pulmonary oedema.

22. HELLP syndrome
• Its presents as complication of pre-
eclampsia.HELLP syndrome affects 1 to 6 per
1000 pregnancies.
• Pre-eclampsia is characterised by hypertension,
proteinuria, oedema with onset in the second or
third trimester and affects 5 -7 % of pregnancies.

23. • Risk factors:mutliparous.
• Initial source of the insult is unknown but all
patients have evidence of endothelial injury with
fibrin deposit that causes a microangiopathic
haemolytic anaemia and platelet activation and
consumption, leading to thrombocytopaenia .
fibrin deposits cause obstruction in the hepatic
sinusoids which leads to areas of haemorrhage
and eventual necrosis I the liver.

24. symptoms
• Right upper quadrant or epigastric pain,
nausea,vomiting,malaise, and non specific flu like
symptoms.
• Physical examination includes right upper quadrant
or epigastrium tenderness and generalised
oedema.hypertension and proteinuria are common.
• Lab findings includes platelet count of less than
then 100,000,serum aspartate aminotransferase
greater than 70U/L,serum lactic dehydrogenase
greater than 600U/L

25. • Peripheral blood smear may shows
schistocytes,burr cells and echinocytes.

26. Treatment
• HELLP syndrome is progressive, can sometimes
have sudden, severe advancement
compromising maternal and foetal outcome.
• A good blood pressure control should be
maintained IV hydralazine or labetalol may be
used to maintain SBP pressure less than 160 mm
Hg and DBP less than 105 mm Hg.

27. • In patients at less than 34 wks gestation with a
reassuring foetal and maternal status, delivery
may be delayed for a steroid course of
betamethasone 12 mg every 24 hours for 2 doses
with delivery 24 hours after the last dose.
• During labour and 24 hours post partum pts
should receive IV Mgso4 for seizures prophylaxis
with 4 g loading dose follwed by 2 g per hour,
with delivery 24 hours after the last dose.

28. • If patients is already in labour, a vaginal delivery
may proceed, as long as no evidence exists of foetal
distress or DIC .
• Platelets are generally transfused when the platelet
count is less than 20,000/mm3,delivery eventually
leads to improvement in thrombocytopenia.
• Patients should be monitored for 48 hrs at least in
post partum period for evidence of pulmonary
oedema due to fluid shifts or renal or hepatic
dysfunction.

29. Viral hepatitis
• The incidence of viral hepatitis A,B,C is the same
in pregnancy as it is for general population, but
incidence of hepatitis E is much higher.
• In hepatitis A which is fecal orally
transmitted,signs and symptoms are nonspecific
and majority of cases are anicteric and usually
mild.
• There is no evidence that hepatitis A virus is
teratogenic and transmission to the fetus
negligible.

30. • Active immunization using formalin inactivated
viral vaccine is more than 90 % effective.

31. • Hepatitis B is endemic in Asia and Africa.
• Occurs often among intravenous drug abusers ,
homosexuals, health care personnel , sexually
transmitted by saliva , vaginal secretion and
semen.
• All pregnant women should be screened for
hepatitis B in the first trimester.
• Most neonatal infection is vertically transmitted
by peripartum ingestion of infected maternal
fluids including breast milk.

32. • The risk perinatal transmission is greatest
during the third trimester , to decrease this risk
lamivudine 100 mg per day can be given from
the start of the third trimester.
• Infants born to HBsAg positive mothers should
receive both HBIG and HB vaccine IM at seprate
sites within 12 hours followed by second and
third dose of vaccine at 1 and 6 months.

33. • Hepatitis C infection does not seem to alter the
course of pregnancy and does not place the
mother at risk of pre-term labour ,
• pre-eclampsia , or gestational diabetes.
• Risk factors included intravenous drug users,
history of transfusion , multiple sex partners,
• No vaccine for hepatitis C exists and primary
prevention is necessary to avoid infection

34. • Treatmemt of hepatitis C with ribavirin and
alpha interferon is contraindicated in
pregnancy,as ribavirin is teratogenic and alpha
interferon causes severe neurotoxicity under age
of 2 years.
• Breastfeeding is not contraindicated.

35. • Hepatitis E has a higher incidence rate and
higher rate of fulminant hepatitis versus general
population.
• Incresed rates of abortion stillbirths,neonatal
deaths are reported.
• Post exposure or pre exposure anti HEV
immunoglobulins have no benefit,breast feeding
is not contraindicated.

36. Cirrhosis
• Hepatic cirrhosis is characterized by irreversible
chronic liver with extensive fibrosis and
regenerative nodules.
• Having clinical manifestation of
jaundice,edema,coagulopathy,metabolic
abnormalities and portal hypertension.

37. • Usually patients with cirrhosis are infertile
woman,and who do became pregent have poor
prognosis.
• Comman complication are transient hepatic
failure, variceal hemorrhage, preterm delivery
and fetal growth restriction.

38. Varices in pregnancy
• In pregnant women,as in young nonpregnent
women,esophageal varies are caused equally by
either cirrhosis or extrahepatic portal
hypertension.
• Bleeding during pregnancy from varices occurs
in third to half and a major cause of maternal
mortality.

39. Treatment
• Beta blocking drugs such as propranolol are
given to reduce portal pressure and to reduce
risk of bleeding.
• Endoscopic band ligation done for acute
bleeding.banding can also be done
prophylactically.
• Transjugular intrahepatic portosystemic stent
shunting TIPSS is done in emergency.