JAUNDICE IN

PREGNANCY
 Occurs in 1to 4/1000 deliveries .
 Serum bilirubin > 2 mg % leads to
visible yellow satining of tissues .
Physiological changes in LFT
in pregnancy
 ALP – almost doubles .
 AST
 ALT slightly lower
 GGT
 S.BILIRUBIN
 S. albumin -decreases though total
albumin increases .
CAUSES OF JAUNDICE

A) Causes peculiar to pregnancy

1) Hyperemesis gravidarum .
2) Cholestasis of pregnancy .
3) Acute fatty liver of pregnancy .
4) Severe pre eclampsia , HELLP
syndrome
5) Endotoxic shock
1) Hyperemesis
gravidarum
 Mild to moderate nausea , vomiting –
common upto 16 weeks .
 Severe unrelenting nausea & vomiting is
HYPEREMESIS GRAVIDARUM defined as
sufficiently severe to cause
 weight loss
 dehydration
 ketoacidosis
 alkalosis ( due to loss of acid)
 hypokalemia
 Transient hepatic dysfunction
develops , biliary sludge
accumulates in some cases.
 ETIOPATHOGENESIS – multifactorial
i. High or rapidly rising pregnancy
hormones .
ii. Biological factors
iii. Environmental factors
iv. Psychological factors
v. H.pylori infection .
 COMPLICATIONS
i. Depression
ii. Boerhaave syndrome
iii. Diaphragmatic rupture
iv. Mallory weiss tear
v. Rhabdomyolysis
vi. Wernicke encephalopathy
vii. AKI
viii.Hypoprothrombinemia .
 Obstetric complications
i. Preterm labor
ii. Placental abruption
iii. Pre eclampsia
 MANAGEMENT
1. Mild – dietary management , ginger
extract,
doxylamine + pyridoxine .
2. Moderate – promethazine ,
prochlorperazine, chlorpromazine ,
ondanstron , metoclopramidem .
3. Severe – IV hydration
thiamine – 100 mg in 1
L crystalloid
parentral –
ondanasertron metoclopramide ,
promethazine .
4. Intractable –
enteral nutrition – nasojejunal
feeding , percutaneus endoscopic
gastrostomy .
2) INTRAHEPATIC
CHOLESTASIS OF PREGNANCY
 Also known as
recurrent jaundice of pregnancy
Cholestatic hepatosis
Obstetric hepatosis
Icterus gravidarum .
 2nd most common cause of jaundice in
pregnancy .
 O.2 – 2 % of pregnancies .
 Presents after 28 weeks .
 Recurrence rate is 50 to 60 % .
 PATHOGENESIS
i. Sex steroid level variation ( excess
estrogen)
ii. Mutation in genes that control
hepatocellular transport system .
iii. Drugs that decrease canalicular
transport of bile acids aggravate
the disorder .
 So , finally incomplete clearance of
bile acids leads to their
accumulation in plasma .
 Retention of conjugated pigment
leads to hyperbilirubinemia .
 CLINICAL FEATURES –
i. Pruritus – may preceed lab findings
by several weeks .
ii. Approx 10% have jaundice .
 INVESTIGATIONS –
i. Total bilirubin rarely exceed 4 –
5mg/dL .
ii. ALP – elevated
iii. Transaminase – normal to
moderately elevated but seldom
exceed 250u/L .
iv. LIVER biopsy – mild cholestasis with
bile plugs in hepatocytes &
canaliculi of centrilobular region but
 TREATMENT –
i. Antihistamines
ii. Topical emolients
iii. Cholestyramine – bile acid
sequestrant .
iv. Ursodeoxycholic acid –
 relieves pruritus
 Lowers bile acid
 Lowers serum enzyme levels
 Lowers neonatal complications.
 COMPLICATIONS –
 Cholestasis canbe associated with
preeclampsia , GDM .
 Labor induction , preterm births ,
cesarean section rate are increased.
 Neonatal complications –
 Respiratory distress syndrome
associated
 Foetal distress
with
 Meconium aspiration
bile acid>40

 Spontaneous preterm birth bile

acid > 100
 Obstetric management –
 Induce labor at 38/39 weeks
 If bile acid > 40 umol /L , increased
AST , ALT are present – deliver at 37
weeks .
 Monitor PT
 Follow up 6 weeks postpartum with
LFT including bile acids .
 Avoid combined oral contraceptives .
 Recurrence rate – 50 to 60 % .
3) ACUTE FATTY LIVER OF
PREGNANCY
 Also known as
acute fatty metamorphosis
acute yellow atrophy
 1 in 1000 pregnancies .
 MOST FREQUENT CAUSE OF ACUTE
LIVER FAILURE DURING
PREGNANCY .
 Characterized by accumulation of
microvesicular fat that leads to
abnormal hepatocyte function .
 Grossly liver – small , soft , yellow ,
greasy .
 ETIOPATHOGENESIS –
 Associated with abnormal fatty acid
oxidation .
 MC mutation – LCHAD mutation –
long chain 3hydroxy co A
dehydrogenase .
 Hemolysis
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 AKI
 Ascites
 Pulmonary edema
 Clotting dysfunctiondue to
decreased hepatic procoagulant
synthesis , increased consumption in
DIC .
 CLINICALFEATURES –
 Manifest late in pregnancy
 Persistent nausea , vomiting – major
complaints
 Malaise , anorexia , epigastric pain ,
progressive jaundice .
 Hypertension , proteinuria , edema in
50 % cases .
 INVESTIGATIONS –
 USG – poor sensitivity
classic sonographic findings –
maternal ascites , echogenic
hepatic appearance .
 Serum bilirubin – elevated upto
10mg/dL.
 Serum transaminase < 1000IU/L.
 Leukocytosis , nucleated red cells ,
mild to moderate thrombocytopenia
 HCt – NORMAL inspite of hemolysis
due to hemoconcentration .
 Fibrinogen < 100 mg /dL , elevated d
dimer or fibrin split poducts indicate
consumption .
 HYPOGLYCEMIA – COMMON .
 MANAGEMENT
 Intensive supportive care & good
obstetric care is needed .
 Sometimes IUD occurs before
diagnosis – route of delivery is less
problematic .
 Living foetus – tolerate labor poorly .
 Delay in delivery – increases
maternal & foetal risk
 Trial of labor with close FHR
monitoring is preferred .
 Cesarean section to hasten hepatic
healing is associated with increased
maternal risk when coagulopathy is
severe .
 Whole blood , packed red blood
cells , FFP , platelets , cryoprecipitate
– transfuse if surgery is performed or
if obstetric laceration complicate
 Hepatic dysfuction resolves
postpartum .
 Becomes normal within a week .
 associated conditions in this time
period are
1. DIABETES INSIPIDUS – due to
decreased hepatic production of
vasopressinase inactivating
enzymes .
2. ACUTE PANCREATITIS .
 COMPLICATIONS
 Maternal death due to sepsis ,
hemorrhage , aspiration , renal
failure , pancreatitis , GI bleed .
 Maternal mortality rate – 4%
 Perinatal mortality rate – 12 % .
4) HELLP SYNDROME

 Hepatic changes in preeclampsia -

 CRITERIA FOR DIAGNOSIS
1) Hemolysis –
 Abnormal peripheral smear – burr
cells , schistocytes
 Low serum haptoglobin
 Elevated bilirubin > 1.2 g/dL
 LDH > 600 U /L
2) Elevated liver enzymes – AST , ALT
> 72 IU/L .
3) Low platelet count -< 1, 00, 000 .
 Tennessee system classifies HELLP
into
a) Complete HELLP – all 3 parameters
are abnormal .
b) incomplete – 1 or 2 abnormalities
seen .
 Mississippi classification – based on
platelet count –
i. Class 1 – severe – platetet count <
50,000.
ii. Class 2 – moderate – 50,000 to 1,
00,000.
iii. Class 3 – mil d- > 1, 00, 000 .
 Clinical features –
 Present in 3rd trimester .
 30 % cases present postpartum .
 Present wit nausea , vomiting , right
upper quadrant pqin or epigastric
pain .
 15 % - ATYPICAL – lack either HTN or
proteinuria .
 MANAGEMENT -
 Clinical course is often charcterized
by progresssive & sometimes sudden
detoriation in maternal & foetal
outcome .
SO , DELIVER REGARDLESS OF
GESTATIONAL AGE .
 Manage HELLP syndrome patient
only at tertiary centre .
 Very close monitoring till delivery &
postpartum period with lab testing at 12 hr
interval is needed
 Lowest observed platelet count occurs at
23 hrs after delivery .
 If platelet count continue to drop & liver
enzymes elevate after 4 days postpartum ,
reassess the validity of initial diagnosis of
HELLP
 AST > 2000 IU/L or LDH > 3000 IU/L is
associated with increased mortality risk .
 Vaginal delivery – only if cervix –
ripe , GA > 32 weeks , FHR – reactive
, no indication for cesarean section .
 Labor should progress rapidly
 If vaginal delivery is not foreseen in
12 hrs , better to perform LSCS .
 Platelet transfusion – if platelet <
50,000 ,patient has signs of
hemostasis .
 Plasmapheresis – lifesaving
Risk – viral hepatitis .
 MATERNAL & PERINATAL OUTCOME
 1% of maternal death .
 Morbidity is due to abruption , DIC ,
pulmonary edema , ARF , ARDS .
 prematurity , IUGR , Perinatal
mortality .
B) JAUNDICE UNRELATED TO
PREGNANCY
1) Acute viral hepatitis – hepatitis A,E,
G
2) Obstructive jaundice due to gall
stone
3) Drug induced – isoniazid
4) Hemolytic jaundice due to
mismatched blood transfusion ,
malaria , cl .welchi infection .
1) Acute viral hepatitis –
a) Hepatitis A –
 Spread by Feco oral route.
 Self limiting disease ,
 Fulminant hepatitis – rare
 Perinatal transmission is rare
 Not teratogenic .
 Diagnosis – detection of IgM
antibodies .
 Pregnant women exposed to HAV
infection – should receive
immunoglobulins 0.02 ml /kg within
2 weeks of exposure .
 She should also have hepatitis A
vaccine single dose 0.06 mL IM .
 It is safe in pregnancy .
b) Hepatitis E
 Behaves similar to hepatitis A virus .
 Chronic carrier state – present .
 May lead to fulminant hepatitis .
 ELISA – detect HEV specific IgM , IgG
antibodies .
 Perinatal transmission – rare .
 Maternal mortality – high – following
acute infection – 15 to 20 % .
c) Hepatitis G
 Related to hepatitis C virus
 More prevalent & less virulent than C
 Chronic carrier state – present .
 Perinatal transmission – documented
.
2) Obstructive jaundice –
 Due to intrahepatic / extrahepatic
causes .
 Intrahepatic causes – blockage of
bile canaliculi .
 Extrahepatic – obstruction of bile
ducts .
3) Hemolytic jaundice –
 Hereditary –
 Thalassemia
 Sickle cell anemia
 Spherocytosis .
 Acquired –
 Malaria
 Mismatched blood transfusion
 Leptospira
4) Drug induced –
 Methyl dopa
 Isoniazid
 Oc pills – cholestasis
 Valproate
C) JAUNDICE WHEN PREGNANCY IS
SUPERIMPOSED ON CHRONIC LIVER
DISEASE .
1) Chronic hepatitis
2) Cirrhosis
3) Tumors
1) Hepatitis B –
 Transmitted by parenteral route ,
sexual contact , vertical
transmission , through breast milk .
 Risk of transmission – 10% in first
trimester , 90% in 3rd trimester .
 Risk of transmission is high if
mother is positive to HBsAg , HBeAg
.
 Neonatal transmission – occurs at or
around the time of delivery .
 25 % of carrier neonates – die from
cirrhosis or hepatic carcinoma
between late childhood or early
adulthood.
 HBV IS NOT TERATOGENIC .
 Maternal infection is manifested by
 flu like illness – malaise , anorexia ,
nausea, vomiting
 Arthralgia , skin rash .
 Jaundice – rare , fever – uncommon
 Clinical course –
 90 – 95 % - full recovery .
 1% - fulminant hepatitis .
 10 – 15 % - chronic
 Diagnosis –
 Serological detectionof HBsAg ,
HBeAg , antibody to HBc
 HBV DNA titre .
 Screening –
 At first antenatal visit
 Repeat during 3rd trimester for high
risk groups .
 MANAGEMENT –
 Prevented by vaccination .
 Pregnant women seronegative –
0.06ml /kg IM soon following
exposure & a second dose after 1
month .
 Then recombinant DNA vaccine IM
should be given – IM 1ml – 3 doses –
0,1,6 months .
 Allinfants born to HBSAg positive
mothers should have HBIG 0.5ml IM
within 12 hrs of birth .
 Active immunization with HB vaccine
–o.5ml should be given at the same
time at a separate site .
 Very effective – 85 to 95 % .
 Breast feeding – not
contraindicated .
 Tenofovir & HBIG – effective to
reduce transplacental transmission
of HBV to foetus.
 Tenofovir – 300 mg /day from 34
weeks .
2) Hepatitis c
 Blood borne
 Causes chronic active hepatitis &
hepatic failure .
 Perinatal transmission is high when
viral load is high & presence of co
infection with HIV & HBV .
 Diagnosis – antibody to HCV .
 NO EFFECTIVE VACCINATION .
 Breast feeding – not
contraindicated .
3) Hepatitis D –
 Seen in patients infected with HBV
as co infection or super infection .
 Chronic carrier state – present
 Neonatal immunoprophylaxis for
HBV – effective against HDV .