Overview of jaundice in pregnancy

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