This document discusses jaundice in pregnancy. It notes that clinical jaundice occurs in 1 in 1000 pregnancies in India. The most common cause of jaundice in pregnancy is viral hepatitis. Mortality from infectious hepatitis is 3.5 times higher in pregnancy compared to non-pregnant women. Some of the specific causes of jaundice discussed in more detail include hyperemesis gravidarum, intrahepatic cholestasis of pregnancy, HELLP syndrome, acute fatty liver of pregnancy, and various types of viral hepatitis. The document also discusses physiological changes in the liver during pregnancy and provides guidelines for diagnosis and management of different conditions that can cause jaundice.

1. JAUNDICE IN PREGNANCY
DR SOBHAN KUMAR PADHI (2ND YR PG)
GUIDE-PROF. DR. S. MOHANTY

2. Jaundice in pregnancy
● Clinical jaundice in 1:1000 pregnancy in India
● Incidence of total death due to jaundice in India 10-20%, 90% due to
AVH
● Hepatitis is the most common and serious offending cause
● Mortality from infectious hepatitis is 3.5 fold higher in pregnancy
when compared to non pregnant women
● Viral hepatitis accounts for 0.8-29.4% maternal deaths in various
parts of India Arias High risk
Pregnancy &
Delivery, 4th ed 2015

3. Physiological changes in liverduring pregnancy
 Liver is not palpable during pregnancy.
 Sr. protein decrease by 20% due to hemodilution
 In 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 & GGT unaltered.
 10-15% normal pregnant may have bilirubin level of over 1mg% due to delayed
excretion of bilirubin that may lead to increase incidence of pruritus in pregnancy.

5. Cause of jaundice during pregnancy
Pregnancy specific
 Hyperemesis gravidarum
 Intrahepatic cholestatsis of pregnancy
 Preecclampsia/eclampsia
 HELLP syndrome
 Acute fatty liver of pregnancy

6. Unrelated to pregnancy-
1.Hepatic- 3.Post hepatic
 Acute viral hepatitis CBD stone/stricture
 Drug induced biliary parasitosis
 Chronic-viral/autoimmune
 Wilsons
 Liver cirrhosis
 Budd chiari syndrome
2.Prehepatic-
 Hemolytic anemia

7. Hyperemesis gravidarum
Extreme of spectrum of morning sickness.
 c/b intractable nausea, vomiting ,dehydration, metabolic acidosis or alkalosis, electrolyte
imbalance, weight loss.
 Incidence less than 1 in 1000 pregnancy

Limited in 1st trimester, more in 1st pregnancy , recurs in next pregnancy, more in multiple
pregnancy with hydatidiform mole.
 Etiology:
a) Hormonal: hCG, estrogen, progesterone.
b) Psychological(neurosis)
Pathology:
Liver: centri lobular hepatic infiltration without necrosis.
Heart: occasonal sub endocardial hemorrhage.
Brain: small hemorrhage in hypothalamic region giving the manifestation of wernick’s
encephalopathy

15. Acute fatty liver of pregnancy/Acute fatty metamorphosis/acute yellow
atrophy(Williams 25)
 Acute hepatic failure in absence of viral hepatitis, IHC, etc.

 usually in 3rd trimester sometimes present after delivery.MMR15
20%
 More common in primipara and associated with pre-eclampsia , twin
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.

17. Clinical features and diagnosis
Clinical features:
Anorexia, nausea, vomiting, headache, fatigue, altered mental status, polydypsia
with or with out polyuria,jaundice 90%
Right upper quadrant pain. Pruritus and ascites 50% cases.
Clinical improvement occurs 1-4 weeks after delivery..
Conjugated hyperbilirubinimia up to 5-15 mg/dl.
↑ALT ,↑ALP ,Prolonged PT.↑BUN and amonia level..
↓sr. fibrinogen,hypoglycemia. Hyperurecemia,leukocytosis,
USG, CT, MRI demonstrate fatty infiltration.
liver biopsy is gold standered.
--microvesicular fatty infiltration
--portal inflamation with cholestasis.

18. Swansea criteria for diagnosis of acute fatty liver of pregnancy
Six or more criteria required in the absence of another cause
• Vomiting
• Abdominal pain
• Polydipsia/polyuria
• Encephalopathy
• Elevated bilirubin >14 μ mol/l
• Hypoglycaemia <4 mmol/l
• Elevated urea >340 μ mol/l
• Leucocytosis >11×10 6 cells/l
• Ascites or bright liver on ultrasound scan
• Elevated transaminases (AST or ALT) >42 IU/l
• Elevated ammonia >47 μ mol/l
• Renal impairment; creatinine >150 μ mol/l
• Coagulopathy; prothrombin time >14 s or APPT>34 s
• Microvesicular steatosis on liver biopsy

19. Prognosis
Maternal mortality:10-15% d/t Hepatic encephalopathy, DIC, ARDS, Renal failure,
Acute pancreatitis, PPH.
Fetal mortality: 15-20% d/t IUD , prematurity.
 Full clinical and laboratory remission occurs over 1-4 weeks post delivery..
 Prenatal diagnosis in next can be done by CVS or amniocentesis
 Recurrence in future pregnancy 15-25% in those have LCHAD deficiency.

21. Intrahepatic cholestasis ofpregnancy
 Typically occurs in late pregnancy. Affecting 1.5-2% of pregnancies.
 Disappears spontaneously, reccurs in subsequent pregnancy.
 Typically manifest in 3rd trimester but can occur as early as 10 weeks.
 Pruritus in 2nd half of pregnancy which is otherwise unexplained is most
charecteristic manifestation 70% cases.Pruritus on palm and sole,
intensity more in night.
 Severe pruritus leads to insomnia, fatigue, depression ,mental
disturbance.
 Jaundice seen in 10% cases usually mild ,develop 1-4 wks after pruritus.
 Jaundice usually disappears with in weeks following delivery.

22.  Pruritus begins to decline a few hours after delivery and disappears with
in few days. Pruritus as a rule persist longer than jaundice.
 Biochemical abnormalities normalize in few weeks following
delivery.If persist more than three month after delivery, investigate
to rule out chronic liver disease.
ETIOLOGY:
i. Hereditary hepatic ↑ sensitivity of estrogen and progesterone→ affects
gallbladder function →slows the bile flow →build up of bile acid in liver.
i. Genetic mutation in the hepatocellular phospholipid transporter MDR3 in
15% case.
i. Familial.
ii. Selenium deficiency in diet.
i. Previous liver damage

23.  Sr.bile acid is earliest and most consistent change.
 Fasting sr. total bile acid concentration is specific test.
 10-100 fold rise in sr. cholic acid.
 ↑ALP, ↑5’ nucleotidase by 2 fold..
 AST &ALT mildly increase.
 ↑conjugated bilirubin 20% cases. But level between 2-5mg/dl.
 PT usually normal.
 Serum cholesterol increases 2-4 fold
 Sr. viral marker negative.

25. management
a. Ursodeoxycholic acid(UDCA):10-20mg/kg/day, even in high dose(1.5-2gm/d) It
relieves pruritus by decreasing the concentration of bile acid.
a
 -improve hepato-cellular secretion by stimulation of canalicular expression of
transport protein.
 restore the impaired maternal-placental bile acid transport across the trophoblast.
---liver function test should be repeated weekly until delivery and at
6weeks postpartum to ensure return to normal baseline.
b. . Corticosteroids: dexamethasone 12mg/day for 1 week.
---improves biochemical abnormalities but does not improve pruritus.
c. Cholestyramine: relives pruritus.
 binds to bile acids in gut.
 It increases the risk of vit-k deficiency, thus ↑ risk of PPH.
-therefore monitoring of PT .
d.Vit-k: 10 mg daily.

27. HELLP syndrome
Coined by Dr.Louis weinstein in 1982.
0.5-0.9% of all pregnancies, and 10-20% case with preeclampsia.
characterized by haemolysis, elevated liver enzyme ,low platelet.
More common in multiparous and older pregnant women.
Develops during antepartum periods in 70% cases with frequency between 27th and
37th wks GA.
Majority with HELLP syndrome have HTN and proteinuria, but it may be absent in 10-
20% cases.
Pathogenesis: In preeclampsia activation of complement and coagulation
cascade→ increased vascular tone, platelet aggregation , alteration in TXA2 and
prostacycline ratio. Leads to
--micro angiopathic hemolytic anemia.
--elevated liver enzyme(d/t periportal hepatic necrosis)
--thrombocytopenia.
 Clincal picture: nausea, vomiting, malaise, headache,weight gain, upper
abdominal pain, HTN,

29. DIAGNOSIS
Peripheral smear: features of hemolysis i.e schizocytes, Burr Cells ,
↑reticulocytes, ↑LDH. ↑Uncojugated bilirubin
-- thrombocytopenia.
Elevated liver enzyme--↑ALT and AST.
Diagnostic criteria: Mississippi classification.
CT or USG if subcapsular hematoma is suspected.

31. Complication:
Maternal:
--eclampsia.
—abruptio placentae
,--DIC
-- ARF
--pulmonary oedema
--Cerebral oedema.
Fetal
: ---IUGR
---PREMATURITY
--perinatal asphyxia
.– still birth
Management
Stabilize maternal condition.
Control HTN.
Antiseizure prophylaxis with mgso4.
Correct coagulopathy. Assessment of fetal wellbeing.
Definitive therapy is delivery irrespective of gestation.
Mode of delivery: vaginal delivery prefered.
Platlets should be arranged if count <50000/cmm
when CS is to be done
or in case of vaginal delivery if the count is
<20,000/cmm
Intensive monitoring for 48 hrs,
Dexamethasone therapy to continue untill
postpartum resolution of disease occurs.

32. Prognosis
 Maternal mortality 2-25%.
 Perinatal mortality 33% .
 Recurrence in subsequent pregnancy 25%..
 Most patient have rapid, early resolution of HELLP syndrome after delivery, with
normalization of platlets 5-7 postpartum day.

34. Hepatitis in Pregnancy
● Specific hepatitis virus (A-E)
● Non A-E Viral hepatitis by Epstein Barr Virus, CMV, Echovirus, Yellow fever virus
● Non Viral hepatitis caused by bacterial(leptospirosis), parasitic (amoebiasis), drug toxicity and
idiosyncratic reactions
Fulminant hepatitis is more commonly seen in malnourished, immunocompromised pregnant women more
commonly in third trimester and has high morbidity and mortality..

40. FHF - Indian data
Fulminant Hepatic Failure is defined as the rapid development of
hepatocellular dysfunction, specifically coagulopathy and encephalopathy in
a patient without known hepatic disease
AVH caused by HEV in 47.4%, (HAV-5.2%, HBV-7.2%, HCV-0%, non A-E
47.4%) in a study of 97 pregnant women with Hepatitis.
● 75% of FHF caused by HEV
● Mortality 24.7%(24/97) of AVH in pregnancy and all were due to FHF
● The mortality rate was 39.1% in HEV group and 11.7% in non HEV group
● 87.5% of women died undelivered
Beniwal M, Indian J Med Microbiol Jul-Sep 2003;21(3):184-5.

41. Drug induced
• Methyldopa
• Acetaminophen
• Rifampicin
• Nitrofurantoin
• Phenytoin
 INH-1% severe hepatitis
• OCP’s-cholestasis,
• Erythromycin
• Valproic Acid
• Methotrexate-indolent
• cirrhosis