This document discusses various causes of jaundice that can occur during pregnancy. It begins with definitions of jaundice and normal liver physiology during pregnancy. It then discusses changes in liver function tests during pregnancy and the effects of maternal hyperbilirubinemia on the fetus. The main causes of jaundice unique to pregnancy are identified as intrahepatic cholestasis of pregnancy, acute fatty liver of pregnancy, HELLP syndrome, and severe hyperemesis gravidarum. Viral hepatitis, gallstones, autoimmune disorders and drugs are identified as causes that can coincide with pregnancy. Details are provided on diagnosis and management of specific conditions like obstetric cholestasis, acute fatty liver of pregnancy, HEL

1. Dr . Sunita Mishra
Associate Professor
Dept of OBG
Kamineni Institute Of Medical Sciences
Narketpally
Dist:Nalgonda
Andhra Pradesh

2. DEFINITION
Jaundice is the clinical manifestation of raised bilirubin
levels in blood
Detected clinically at bilirubin concentration of 2 mg % or
more ( normal being 0.2 – 0.8 mg % )

3. NORMAL LIVER PHYSIOLOGY IN
PREGNANCY
 Outside pregnancy , liver receives upto 25-35 % of
cardiac output which does not change significantly
during pregnancy
 Size of the liver does not increase
 Postero-superior displacement by the enlarging uterus
PALPABLY ENLARGED LIVER IS ABNORMAL IN
PREGNANCY
Metabolic ,synthetic & excretory functions of liver
affected by increased levels of estrogen & progesterone
in pregnancy

4. LIVER FUNCTION TESTS IN PREGNANCY
bilirubin Unchanged or slightly
decreased
Aspartate transaminase(AST) Unchanged initially but 25%
decrease by 3rd trimester
Alanine transaminase (ALT) Unchanged initially but 25%
decrease by 3rd trimester
Gamma glutamate
transaminase (GGT )
Unchanged or slightly
decreased
Alkaline phosphatase 2-4 fold increase in 3rd
trimester
cholesterol Two fold increase
Triglycerides 2-3 fold increase
Globulin Increase in alpha & beta
globulins

5. MATERNAL HYPERBILIRUBINEMIA
& THE FOETUS
Elevated levels of maternal unconjugated bilirubin do
not have deleterious effect on neurodevelopmental
status of offspring

6. MAIN CAUSES OF JAUNDICE IN
PREGNANCY
 UNIQUE TO PREGNANCY
-Intrahepatic cholestasis of pregnancy
-Acute fatty liver of pregnancy
-HELLP syndrome
-Severe hyperemesis gravidarum

7. MAIN CAUSES OF JAUNDICE IN
PREGNANCY
 COINCIDENTAL TO PREGNANCY
-Viral hepatitis
-Gallstone disease(cholelithiasis)
-Congenital disorders of bilirubin metabolism
-Autoimmune hepatitis
-Drug induced – isoniazide , phenothiazine
-Hemolytic jaundice- mismatched blood transfusion ,
malaria , clostridium welchii infection
-Cirrhosis
-Neoplasia

8. INTRAHEPATIC CHOLESTASIS OF
PREGNANCY
OBSTETRIC CHOLESTASIS
Incidence being 1.24 % of all pregnancies in Indian
population
CLINICAL FEATURES
 Severe itching/pruritus in 3rd trimester
 Malaise & insomnia
 Dark urine, anorexia, steatorrhoea

9. OBSTETRIC CHOLESTASIS
LABORATORY FINDINGS
 Raised bile acids
 Moderate elevation in ALT
 Raised alkaline phosphatase
 Raised bilirubin
 Raised GGT

10. OBSTETRIC CHOLESTASIS
 Maternal risks:
vitamin K deficiency
increased risk of PPH
 Fetal risks:
Intrauterine fetal death
Spontaneous preterm delivery
Intra partum fetal distress
Meconium stained liquor
The risk of still birth greatest after 37 weeks

11. OBSTETRIC CHOLESTASIS
MANAGEMENT
 Counseling
 Fetal surveillance
DFKC , BPP
 Maternal monitoring
LFTs
bile acids
coagulation screening.
 Maternal vitamin K supplementation with an oral dose of
10mg daily.
 Pruritus is symptomatically treated
 Ursodeoxy cholic acid

12. OBSTETRIC CHOLESTASIS
POST NATAL MANAGEMENT
 Monitoring of biochemical resolution is essential
 If diagnosis is suspect or condition appears to be
progressive , invasive investigation in form of liver
biopsy.
 The recurrence in future pregnancies is 50%
 Woman counseled to avoid combined OC pills

13. ACUTE FATTY LIVER OF
PREGNANCY
 Rare complication occuring in pregnancy
 Incidence: 1 in 10000 pregnancies
 Association with
maternal obesity
male fetus (3 times more common )
multiple pregnancy.
 considerable overlap with HELLP syndrome
 AFLP may be a variant of preeclampsia.

14. Clinical features
 Nausea, anorexia and malaise
after 30 weeks to term.
 Severe vomiting and abdominal pain
 Jaundice within 2 weeks of onset of symptoms.
 Ascites
 signs and symptoms of liver failure
 hepatic encephalopathy,
 DIC and renal failure.
 Hypertension and proteinuria in 50% cases
 Extreme polydipsia or pseudo diabetes .

15. Laboratory findings
 Raised transaminases and alkaline phosphatase.
 hypoglycemia
 hyperuricemia
 Blood film leukemoid
 Gold standard for diagnosis is liver biopsy
 USG, CT or MRI. May show evidence of fat infiltration

16. Maternal risks
 Fulminant hepatic failure
 Hepatic encephalopathy
 Coagulopathy
 Death

17. Fetal risks
 Intrauterine fetal death with a perinatal mortality rate
of 15-65%
 Neonatal risks include transient derangement in LFT ‘s
and hypoglycemia.

18. Management
 Maternal resuscitation and stabilization
 fetal monitoring
 Urgent delivery
 Admit to intensive care unit
 Vaginal delivery probably better
 Parenteral glucose
 Neomycin and lactulose
 Multivitamin supplementation.
 In fulminant hepatic failure ,liver transplantation.

19. Post natal management
 If abnormal LFT’s persist beyond 6 weeks consider
alternative pathologies.
 Recurrence is 20% in subsequent pregnancies
 Close surveillance of LFT’s with use of OC pills

20. HYPEREMESIS GRAVIDARUM
 Onset in first trimester of severe or protracted
vomiting causing fluid and electrolyte imbalance.
 Weight loss of approximately 3 kg
 Necessitating hospital admission
 Occurs in 0.5-1% of pregnancies.

21. INVESTIGATIONS
 raised haematocrit & white cell count
 Hyponatraemia, hypokalaemia, hypochloraemic
metabolic alkalosis
 Serum urea is low
 elevated urea to creatinine ratio : indication of
dehydration
 LFTs serve as marker of severity
 biochemical thyrotoxicosis
 Urine analysis reveals ketonuria
 Pelvic scan to confirm a viable singleton pregnancy

22. MATERNAL RISKS
 anemia & peripheral neuropathy
 Wernickes encephalopathy
 Mallory –Weiss tear
 Catabolic state
 Hyponatremia

23. FETAL RISKS
 No increase in congenital anomalies
 Low birth weight & birth weight percentiles
 If maternal WE supervenes, risk of fetal death (40%)

24. MANAGEMENT
 Rehydration : normal saline or Hartmann’s solution
 Regular urine analysis to monitor ketonuria
 Antiemetics
Ondansetron in intractable cases
Intravenous hydrocortisone in severest &
prolonged forms
 Vitamin supplements

25. MANAGEMENT
 Antigastroesophageal refux measures :
elevation of head of bed
small frequent bland meals
alginates
H2 receptor antagonists
 Psychological support & reassurance
 Termination of pregnancy in intractable cases

26. HELLP SYNDROME
H – HEMOLYSIS
EL- ELEVATED LIVER ENZYMES
LP – LOW PLATELET COUNT
Incidence : 0.5 – 0.9 % of all pregnancies
10-20 % of cases with severe pre-eclampsia
C/F : 90% present with generalized malaise
epigastric pain
nausea & vomitting
headache

27. DIAGNOSTIC CRITERIA
Hemolysis
 abnormal peripheral smear
 Increased total bilirubin (indirect mostly) > 1.5 mg / dl
 Fall in hemoglobin unrelated to blood loss
Elevated liver enzymes
 Increased transaminases AST & ALT > 70 IU / L
 LDH > 600 IU / L
Thrombocytopenia

28. MANAGEMENT
 Assessment & stabilization of woman’s condition
especially coagulation dysfunction
 Fluid management
 Control of hypertension
 Prevention of seizures
 Platelet transfusion
 Evaluation of fetal well being
 Decision about delivery

29. Complications
 Abruptio placentae
 DIC
 Retinal detachment
 Acute renal failure
 Pulmonary edema
If not treated in a timely manner, a mother can become
critically ill or die due to liver rupture/ hemorrhage

30. VIRAL HEPATITIS
Viral hepatitis is the commonest cause of hepatic
dysfunction in pregnancy
Incidence being 8.8 % in 1st , 19.4 % in 2nd & 18.6% in 3rd
trimester
HEPATITIS A
 Management and prognosis similar to non-pregnant women.
 Post-exposure immunoprophylxis may not prevent viral
shedding.
 Potentially infected individuals isolated.
 Asymptomatic women in the 3rd trimester in contact with an
index case given immunoglobulin.

31. HEPATITIS B
Vertical transmission is the predominant route of
transmission
Prognosis:
 Complete resolution in 90% of cases within 6 months.
 Remaining 10% become chronic carriers.
 Diagnosis:
 Through detection of viral specific antigens and
antibodies.
 HbsAg indicates infectivity.

32. MANAGEMENT
 Symptomatic and supportive
 Monitor
hydration
uterine activity
LFTs
 Counselling, testing and vaccination of family
members and sexual contacts.
 No congenital syndrome or risk of teratogenesis.

33. OBSTETRIC SIGNIFICANCE
 Vertical transmision carries
90% risk of chronic active or chronic persistant
hepatitis
 Majority of infants infected at time of birth
 Antenatal detection of HbsAg mandates
preventive programme of active and passive
immunization at birth.

34. HEPATITIS C
 Higher risk of vertical transmission
if mother +ve for both HCV RNA & anti-HCV Ab
 No vaccines to prevent HCV infections

35. HEPATITIS E
 Obstetric significance: Prediliction for pregnant
women for reasons unknown
 Fulminant hepatic failure in 61%
 Infection in pregnancy in 3rd timester associated with
increased maternal mortality.
 No immunoprophylaxis available.

36. KEY POINTS
 obstetric cholestasis can cause fetal death after 37 wks,
as such delivery suggested at 36 wks
 non immunized pregnant women exposed to HBV
should receive active & passive immunization
HBV has high rate of vertical transmission causing
fetal & neonatal hepatitis
Hepatitis A ,C, E rarely transmitted transplacentally
Viral hepatitis is the commonest cause of jaundice in
pregnancy

37. KEY POINTS
Pregnancy does not alter management of hepatitis
Hepatitis is not associated with increased congenital
anomaly
All pregnant women should be screened for HBS Ag
 acute fatty liver of pregnancy needs induction of
labour
Definitive trt of pre-eclampsia & HELLP syndrome is
immediate delivery
The most serious & life threatening maternal risk is
that of hemorrhage

38. THANK YOU