LIVER DISEASES IN

PREGNANCY

Diseases only related to liver

AFLD,obstrectic cholestasis….etc

Muliti system diseases with hepatic

manefestations

hyperemesis gravidarum,HELLP

Some diseases are unique to pregnancy

HELLP Xd

AFLP

Some diseases are not unique but more severe

Hepatitis E

HSV

Some diseases are precipitated by pregnancy

Gall stone disease

Budd chiari

USE OF GESTATIONAL AGE

It is the best guide to differential diagnosis of liver

disease

T1-hyperemesis g.

T2,T3-cholestasis

T3 – HELLP,AFLP

Any trimester- viral hepatitis,drug induced,

gall stone disease,malignancy

FINDINGS IN NORMAL PREGNANCY WHICH

MAKE DIFFICULTY IN DIFFERENTIATION

Physical ex: spider navae

palmer erythema

late pregnancy-palpation of liver is difficult

USS- NL billiary tract

fasting gall bladder volume & residual

volume after contraction may be increased

S. proteins & lipids

bcoz of haemodilution,s.alb decreases in all

trimesters

T.cholesterol & TGA increased

LIVER FUNCTION TESTS DURING PREGNANCY

Affected during pregnancy Not affected

during

pregnancy

increased decreased

ALP increased in

T2,T3

S.fibrinogen increases

in late pregnancy

Alb & T. proteins

decreased from T1

Billirubin-slightly reduced

from T1

Gamma GT-slightly

reduced in late pregnancy

ALT,AST

PT

Total bile acid

Concentration

LDH

Making the correct diagnosis is of paramount

importance,

As failure to do so can result in morbidity and

mortality,

for not only the mother

but also for her fetus

HISTORY

features of O.J.

-jaundice

pale stools

dark urine

pruritus(ask for

rash)

complications

of O.J.

-steatorrhoea

coagulopathy

infections

Nausea,

vomiting-

hyperemesis

Hypoglycaemic

features-

sweating,dizziness,p

alpitations

Polyuria,polydypsi

a

•Booking visit blood

preasure

•In which POA high BP is

detected

•Abnormalities in urine

tests

•Epigastric or right upper

quadrant pain

•Headache

•Visual disturbances

Symptoms-duration

progression

Past obstetric history:

past Hx of ob cholestasis

past hx of PIH,eclampsia

Past medical Hx:

hepatitis

gall stone disease

CLCD

blood transfution

Drug Hx;

methyl dopa,MTX

Family Hx:

ob.cholestasis

PIH

Social Hx:

exposure to viral hepatitis

travel Hx

PHYSICAL EX

Temperature

Pallor

Icterus

Scratch marks

Polished nails

Odeama in non dependent parts

Features of dehydration-dry mucus membrane,sunken eyes

BP

ophthalmoscopy

Reflexes,clonus

Abdominal Ex:RHC tenderness

Liver examination

Ix;

Blood tests

FBC-high WBC

lymphocytosis

low Hb-haemolysis

low PLT

LFT

S.Cr,RFT

S.electrolytes-hyponatraemia

RBS-hypoglycaemia

S.urates

PT/INR

Clotting profile

Serology for hepatitis,CMV

Urinalysis-proteinuria

USS-gall stones,focal lesions,extra hepatic obstruction

Role of liver biopsy

LIVER DISEASES

Viral hepatitis-commonest cause

Obstetric cholestasis-2nd commonest

Acute fatty liver of pregnancy

HELLP syndrome

Pre-existing liver disease

Gall bladder disease

Hyperemesis gravidarum

OBSTETRIC CHOLESTASIS

Generally manifest in T3(mean 30wks)-due to high

oestrogen peak

Increased risk in multiple gestation,due to high

oestrogen level

Complete recovery is usually rapid following

delivery.(when placental hormones return to NL)

In some women,abnormal liver function tests may

return to normal only slowly.taking 4-6 wks after

delivery.

AETIOLOGY

multifactorial

Hormonal factors

hyperoestrogenaemia (T3 peak)

abnormal progesterone metabolism

Genetic factors

higher prevalence in family members

defect in multi drug resistance type 3

gene(MDR-3)

PATHOGENESIS:

Not clearly understood

MDR 3

-encodes for the canalicular phospholipid pump

protein

Changes induced by genetic mutation leads to

increased sensitivity to oestrogens

Increased oestrogens and progesterons causes

cholestatic effect

-progesterone:

Due to impairment of sulphation of

bile acids due to sulphated progesterone

metabolites

-oestrogens

act on hepatocytes,causing decreased

hepatocyte membrane fluidity which results in

reduced bile acid uptake by the liver

Slowing of normal bile flow in maternal liver

Increase of bile acid in blood

Damage of liver cell membrane

Consequential rise in liver enzymes in maternal blood

Increase in transfer of bile acids from the mother to

her fetus

CLINICAL FEATURES-

severe pruritus affecting limbs and trunk particularly

palms and soles

Insomnia, Malaise

Excoriation but no rash.

Dark urine.

Anorexia.

Malabsorption of fat with steatorrhoea.

Jaundice(10-25%)

Diagnosis

Is a diagnosis of exclusion

Therefore,diagnosis is made in 3 steps.

1 - typical Hx of pruritus without rash

2 - Abnormal LFT

3- Exclusion of other causes of itching and abnormal

LFT

PATTERN OF ABNORMAL LFT Moderate elevation of transaminase (< 3 fold)

Raised ALP (beyond normal pregnancy values)

Raised gamma GT (About 20% cases)

Mild elevation of bilirubin (less common)

Increased serum total bile acid concentration.

10-100 folds rise in primary bile acids(cholic and

chenodeoxycholic acid)

Some times increased bile acid may be the only

biochemical abnormality

Pruritus may proceed abnormal LFT- serial

measurements are advised in persistent itching

IX TO EXCLUDE OTHER CAUSES Uss liver (presence of gallstone without evidence of

extra-hepatic obstruction-Not exclude OC)

Viral serology(for Hep A,B,C,E, EBV, & CMV)

Liver autoantibodies

pre-existing liver disease,

anti smooth muscle antibody-Chronic active hepatitis

anti mitochondrial antibodies-primary biliary cirrhosis

COMPLICATIONS

Maternal risk-

Vit K deficiency

Increases risk of PPH

Fetal risk-

Amniotic fluid meconium(25-45%)

Spontaneous pre term delivery(12-44%)

Intrapartum fetal distress(12-22%)

IUD

Fetal ICH

Risk of still birth increases towards term. But doesn’t

correlate with maternal symptoms/ transaminase levels,

may be related to concentration of maternal bile

acids.

High concentration of bile acids have been found in

amniotic fluid and fetal circulation.

Maternal to fetal transfer of bile acids across

placenta becomes increased

Potentially toxic levels in fetus

Vasoconstriction increased myometrial

of chorionic veins contractility

Abrupt reduction of

blood flow to fetus preterm delivery

Fetal distress

PREDICTION OF FETAL COMPROMISE

No use of doppler blood flow analysis.

Risk is high if having past Hx.

Repeated amniocentesis to detect meconium is the

best predictor.

MANAGEMENT

Councelling

LFT, PT, Bile acids should be check weekly.

Monitoring fetal well-being. (CTG, USS, Doppler)

Early delivery at 37-38 wk or when fetal lung

maturity is evident.

DRUG THERPY

Vit k

10mg oraly daily(reduced risk of bleeding)

Preferable to use water soluble formulation(due to co-

exsistant fat malabsorption)

Anti histamines (pruritus)

Chlorpheniramine 4mg tds

Promethazine 25mg nocte

Ursodeoxycholic acid(UDCA)-

Endogenous hydrophilic bile acid.

Alter bile acid pool by reducing hydrophobic bile acid.

Insert transport proteins or bile salt export pumps into

canalicular membranes

Increases expression of placental bile acid transporters

which may allow for improved bile acid transfer

Dose 1000-1500mg daily in divided doses.

Improves pruritus

Reduce total bile acid.

Reduce liver enzymes.

Cholestyramine

Bile acid chelating agent.

4g bd/ tds.

Dexamethasone

Supresses feto-placental oestrogen production.

Dose 12 mg oral daily.

Consider S/E of high doses.

Other drugs

S-Adenosylmethionine

Epomediol

INTRAPARTUM MX

Induction of labour at 37-38 wk.

Close monitoring is required throughout induction

and labour.

To neonate- IM Vit K

ICP is not a C/I for breast feeding

RECURRENCE RISK/ PRE PREGNANCY

COUNCELLING

Recurrence risk 90%

Avoid oestrogen containing OCP.

Progesteron has less risk of cholestasis but should

monitor LFT.

HRT need not to be avoided as this provides only

physiological level of oestrogen.

VIRAL HEPATITIS

Commonest cause of hepatic dysfunction in

pregnancy.

Acute hepatitis in T1-associated with higher rate of

spontaneous miscarriage.

Causative organisms-

Hepatitis viruses- A, B, C ,D, E

CMV

EBV

HSV

HEPATITIS A

Faeco oral route

Acute self limiting illness

Not result in chronic infection.

Clinical features in pregnant women do not differ

from those in non pregnant women.

Vertical transmission rare

Transmit at or around the time of delivery.

In such case neonate should be given

immunoglobulin at birth.

Vaccination-safe in pregnancy

HEPATITIS B

Transmission to baby- at the time of delivery 95%

vertical/ transplacental 5%

Mothers may be asymptomatic

who have both HBs Ag and Hbe Ag positive – greatest risk of

vertical transmission 95%

Who are HBs Ag positive but Hbe Ag negative have 2-15%

risk of vertical transmission

Outcome of neonate

Infected neonates have > 90% chance of becoming

chronic carrier

Increase risk of cirrhosis and hepato cellular carcinoma

All neonates born to women with acute or chronic HBV

should be given

-hep B immunoglobulin

-HBV vaccine within 24 hours

Immunisation is 85-95% effective at preventing both HBV

infection and chronic carrier state.

Provided babies are immunised HBs Ag positive mothers

can breast feed.

HEPATITIS C

Transmission via blood

Vertical transmission uncommon- maximum risk to

fetus at T3

Commonly seen in IV drug uses.

Significant risk of chronic infection.

Treatment- Interferon alpha combined with ribavirin

but not recommended in pregnancy.

S/E of interferon- Fever, fatigue, depression.

Pregnancy doesn’t induse deterioration in liver diseases.

But have high risk of obstetric cholestasis and that may

present earlier than usual.( mean 29 wks in Ab positive,

mean 34wks in Ab negative)

No vaccine to prevent HCV infection.

Immunoglobulin not recommended for infants of HCV

positive mother.

Transmission by breast milk uncommon.

HDV

Only found in HBs Ag positive people.

Prevention of HBV infection will also prevent HDV

infection.

HEV

Transmission- Faeco-oral route.

Mild self limiting disease in non pregnant women.

Increase mortality in pregnant women. Specialy if it

is acquired in T3.

Increased incidence of hepatic encephalapathy and

fulminant hepatic failure.( Risk 15-20% )

HSV

May cause fulminant hepatitis in pregnant women.

Most cases are due to primary HSV type2 infection.

Although oral or vulval vesicles may only appear after

presentation with liver failure.

Clinical features- Fever , Abdominal pain

Ix- marked elevation of transaminases.

prolong PT time

Disseminated infection causes pneumonitis ,

encephalitis.

Diagnosis by liver biopsy.

Treatment- anti viral therapy

acyclovir therapy for infant.

HELLP SYNDROME [HAEMOLYSIS,ELEVATED LIVER

ENZYMES,LOW PLATELETS] May develop as a variant of severe pre eclampsia

Incidence in pre eclamptic patients is about 5-20%

Increased maternal (1%) and perinatal (10-60%) mortality

PATHOGENESIS

The pathophysiology of HELLP syndrome is ill-

defined.some theorize that because it is a variant of pre

eclampsia, the pathophysiology stems from a common

source.

In pre eclampsia, defective placental vascular

remodelling during wks of 16-22 of pregnancy with the

second wave of trophoblastic invasion into the decidua

results in inadequate placental perfusion.

The hypoxic placenta then releases various placental

factors , causing endothelial cell and placental

dysfunction.

This results in hypertension,proteinuria and increase

platelet activation and aggregation.

Furthermore,activation of the coagulation cascade

causes consumption of platelet due to adhesions

on to a damaged and activated endothelium in

addition to microangiopathic haemolysis caused by

shearing of erythrocyte as they traverse through

capillaries laden with platelet-fibrin deposits.

Multiorgan microvascular injury and hepatic

necrosis causing liver dysfunction contribute to the

development of HELLP syndrome.

CLINICAL FEATURES

Epigastic or right upper quadrant pain (65%)

Nausea and vomiting (35%)

Tenderness in the right upper quadrant

Hypertension with or without proteinuria

Other features of eclampsia (persistent

headache,visual disturbance,muscle twitching,facial

oedema,hypereflexia)

Acute renal failure (7%)

Placental abruption (16%)

Metabolic acidosis

DDS

Acute fatty liver of pregnancy

Haemolytic uraemic syndrome

TTP

Haemolytic anaemia

Placental abruption

Hyperemesis gravidarum

DIAGNOSIS

Low grade haemolysis evident on peripheral blood smear

Low (usually < 100x109/l) or falling platelets

Elevated transaminases

Elevated lactate dehydrogenase (LDH) (indicative of

haemolysis )

Raised bilirubin (unconjucated,reflecting the extent of

haemolysis)

USS

Differential diagnosis from TTP and HUS is

important since delivery rather than plasmapheresis

is the optimal management for HELLP syndrome.

TTP and HUS are both rare compared to HELLP

syndrome.

Abnormal liver function and coagulopathy suggest

HELLP rather than TTP.

Co existence of renal failure is well recognised in

HELLP symdrome.

Profound thrombocytopaenia (< 10x109/l) is

unusual in HELLP syndrome.

EFFECT OF HELLP SYNDROME ON

PREGNANCY

Abruption

Subcapsular liver haematoma

Acute renal failure

Massive hepatic necrosis

Liver rupture

MANAGEMENT

Prompt delivery , especially if there is severe right

upper quadrant pain and tenderness

Ensure adequate control of blood pressure prior to

delivery

Platelet trasfusion should be reserved for active

bleeding or prior to surgery if the platelet count is

below 50x109/l

Fresh frozen plasma should be given to correct any

coagulopathy

POST PARTUM COURSE

Since delivery is usually expedited in diagnosed

cases , a woman may deteriorate before she

improves after delivery ,developing a very low

platelet count ,severe hypertension and proteinuria.

Upto 30% of cases arise postpartum in women

thought to have no or uncomplicated pre eclampsia

Recovery from HELLP syndrome is usually rapid

and complete with no hepatic sequale.

Corticosteroids should be considered to hasten

recovery

RECURRENCE

Women who have had HELLP syndrome are at a

substantially increased risk of developing pre

eclampsia,preterm delivery and intra uterine growth

restriction in future pregnancies.

The risk of recurrent HELLP syndrome is low(3-5%)

For women with essential hypertension that

predates the pregnancy complicated by HELLP

syndrome , the risk of pre eclampsia in subsequent

pregnancies may be as high as 75%

ACUTE FATTY LIVER OF

PREGNANCY.

AFLP

Is rare.( 1 in 7000 to 1 in 15000 )

Potentially lethal for both mother and the fetus

especially in delayed diagnosis.

Associated with abnormalities in mitochondrial

β oxidation and LCHAD deficiency.

Is more common in ; primigravidae

multiple pregnancy

obesity

male fetus(M:F = 3:1 )

DIFFERENTIAL DIAGNOSIS.

HELLP syndrome.

CLINICAL FEATURES

Usually presents after 30 weeks of gestation and often

near term.

Gradual onset ;

1. Anorexia ,Nausea ,and Vomiting.

2. Abdominal pain.

3. Jaundice – usually appears within 2 weeks of the onset

of symptoms.

4. Headache.

5. Fever.

6. Confusion.

7. Coma.

8. Polyuria and polydipsia (features of diabetes insipidus).Cont…

9. Co-existing features of mild pre-eclampsia. ( but

hypertension and protienuria are usually mild.)

10. Liver function test ; elevated transaminase levels and

elevated alkaline phosphatase

11. Marked hypoglycaemia.

12. Cagulopathy ( may present post-partum with severe

haemorrhage )

13. Renal impairment.

14. May develop fulminant liver failure with hepatic

encephalopathy.

COMPLICATIONS.

High maternal (2-18%) and fetal (7-58%) mortality.

DIC.

Renal failure.

Pancreatitis.

(transient) Diabetes insipidus.

Hepatic encephalopathy.

Fulminant liver failure.

MATERNAL COMPLICATIONS.

DIAGNOSIS

Six or more of the following features in the absence of another explanation.

• Vomiting

• Polydipsia/polyuria

• Abdominal pain

• Encephalopathy

• Elevated bilirubin (>14 mmol/L)

• Hypoglycaemia (<4 mmol/L)

• Elevated urate (>340 mmol/L)

• Leucocytosis (>11×109/L)

• Ascites or bright liver on ultrasound scan

• Microvesicular steatosis on liver biopsy

• Elevated ammonia (>47 mmol/L)

• Elevated transaminases (aspartate aminotransferase or alanine aminotransferase >42 IU/L)

• Renal impairment (creatinine >150 mmol/L)

• Coagulopathy (prothrombin time >14 s or activated partial

thromboplastin time >34 s)

SWANSEA CRITERIA FOR DIAGNOSIS OF AFLP

DIFFERENTIAL DIAGNOSIS OF HELLP SYNDROME AND AFLP.

symptom HELLP AFLP

Epigastric pain ++ +

Vomiting +/- ++

Hypertension ++ +

Protienuria ++ +

Elevated liver enzymes + ++

Hypoglycaemia +/- ++

Hyperuicaemia + ++

DIC + ++

Thrombocytopaenia(without DIC) ++ +/-

Elevated white blood count + ++

Ultrasound / CT NL/hepatic

haematoma

NL/Hepatic

steatosis

Multiple pregnancy +

primiparous ++ +

Male fetus 50% 70%(M:F=3:1)

Distinctive features of Acute Fatty Liver of Pregnancy that

may help in its distinction from HELLP syndrome are ;

Profound hypoglycaemia.

Marked hyperuricaemia.

(out of proportion to the other features of pre-eclampcia).

Coagulopathy in the absence of thrombocytopaenia.

Fatty infiltration on imaging the liver.

INVESTIGATIONS

serological Investigations.

Full Blood Count.

Fasting Blood Sugar.

Serum Urate.

Liver Function Test.

Clotting Profile.

Blood gases.

Radiological Assessment.

MRI scan of the abdomen

CT scan of the abdomen hepatic steatosis

Ultrasound scan of the abdomen

Histopathology.

Liver Biopsy with special stains for fatty changes or electron

microscopy – Gold standard for diagnosis.

Microvascular fatty infiltration of hepatocytes

Most prominent in the central zone

Periportal spairing

Little or no inflammation or hepatocellular necrosis.

Liver Biopsy is not always necessary or practical in the

presence of coagulopathy.

MANAGEMENT.

This should be in a high dependency or intensive care setting

with a multidisciplinary team.

Antenatal period.- maternal management.

Management aims are ;

Treatment of hypoglycaemia – large amount of 50% glucose.

Correction of coagulopathy - IV vitamin K and Fresh Froze

Plasma .

Strict control of blood presssure and fluid balance.

Delivery should follow stabilization.

Plasmapheresis has been used in some cases.

N-acetylcystein (NAC) ;

-an antioxidant and glutathione pricursor.

-promotes selective inactivation of free radicals.

-a logical treatment in hepatic failure.

-often given by liver units in AFLP.

Multiple system failure may necessitate ventilation and dialysis.

Patients with fulminant hepatic failure and enephalopathyshould be referred urgently to a specialist liver unit.

Liver transplantation is Indicated in :

• fulminant hepatic failure.

• irreversible liver failure despite delivery of the fetus and aggressive supportive care.

Post-partum period-maternal management.

Post delivery most women recover quickly.

Management is conservative and supportive.

Liver functions may take up to 4 weeks to recover.

Neonatal management.

Baby should be screened for LCHAD deficiency.

RECURRENCE.

Recurrence rate is about 25%

Recurrence is particularly likely in women who are

heterozygous for disorders for β-fatty acid

oxidation.

Screening for LCHAD deficiency may be indicated.

HYPEREMESIS GRAVIDARUM

Is the persistent vomiting with onset in the first

trimester with the inability to maintain adequate

hydration, fluid and electrolyte balance, and

nutritional status

Excessive vomiting results in >5% BW

reduction & associated ketosis

Risk factors

Past Hx

Molar pregnancy

Multiple gestations

Hyperthyroidism

Psychiatric illness

Pre-existing DM

Increased body mass index

High daily intake of saturated fat before pregnancy

CLINICAL FEATURES

Nausea and vomiting

Weight loss

Ketosis

Muscle wasting

Postural hypotention

Sign of dehydration

DIAGNOSIS

Is by exclusion

Vomiting refectory to treatment and new symptom

appear after 12 week of gestation should not be

attributed to hyperemesis gravidarum

D/D-UTI

,peptic ulceration,

pancreatitis

hyperthyroidism,

hypercalcaemia

addison disease

INVESTIGATION

FBC- raised haematocrit

Urea and electrolytes-are used to test for

hyponatraemia,hypokalaemia

Liver function test- abnormal in <50% of

cases,moderate rise in transaminases(>50mmol

but <200mmol)

Serum calcium-to exclude hypercalcaemia

Thyroid function test-75% cases raised free

thyroxine

Pelvic ultrasound-to confirm the gestational age, to

exclude molar pregnancy

COMPLICATION

Maternal comlication

deficiency of vitamin B1 and wernicke’s

encephalopathy-

characterized by diplopia abnormal ocular

movement,ataxia and confusion Precipitated by iv

dextrose soution

Other vitamin deficiency-vitamin B12 ,vitamin B6

Hyponatraemia-

Fetal complication

Intrautrine growth retardation

Wernicke’s encephalopathy

Intrauterine death

MANAGEMENT

1.Intravenous fluid therapy

0.9%saline or hartmann’swith KCL as needed

Avoid dextrose-increased risk of wernicke’s

Avoid hypertonic saline-due to risk of central

pontine myelinolysis

Maintain fluid balance chart

2. Give oral thiamine 25-50 mg tds

PRE-EXISTING LIVER DISEASE

AUTO IMMUNE CHRONIC ACTIVE HEPATITIS

Mild treated disease is unlikely to cause problem in

pregnancy

The issues related to immunosuppressive drug

regimes, which should be continued in pregnancy

to prevent relapse

Withdrawal of immunosuppressant-high risk of

relapse

PRIMARY BILLIARY CIRRHOSIS

Usually present with pruritis and is associate with a

raised alkaline phosphatase and gamma GT

Pruritis may worsen during pregnancy

CIRROSIS

Severe hepatic impairment associate with infertility

Liver disease may decompensate during pregnancy and pregnancy should be discouraged in women with severe impairment of hepatic function

Bleeding from esophageal varies is a risk in women with portal hypertension especially 2nd and 3rd

trimester

those with stabilised beta blocker should be advice to continue since risk to mother and fetus from variceal bleeding outweigh any risk of beta blockethreapy in pregnancy

Gall bladder

disease

Cholecystits

Cholecystitis is inflammation of the gallbladder that

occurs most commonly because of an

obstruction of the cystic duct from cholelithiasis

Commonest cause - gallstones

Incidence

6.5-8.5% - nulliparous women

18-19% - two to three pregnancy or more

Pregnancy

Oestrogen

Increase cholesterol concentration

Reduce bile acid

Bile acid super saturation

Gallstone

CHOLECYSTITISOBSTRUCTIVE

DISEASE

Progesterone

Muscle Relaxation

Reduce bile release

Increase bile stasis

Clinical features

similar as non pregnant women.

Hx -

Pain - right upper quadrant or epigastrial

-colicky

-radiate through back and tip of the scapula.

Nausea and vomiting are generally present.

fever may be noted.

Ex –

Fever, tachycardia, and tenderness in the RUQ or

epigastric region, often with guarding or rebound.

Palpable gallbladder or fullness of the RUQ (30-40% of

patients)

Jaundice (~15% of patients)

Differential diagnosis

Cholecystitis

Pancreatitis

Peptic ulcer

Acute fatty liver of pregnancy

Viral hepatitis

Obstetric cholestasis

Diagnosis

FBC –Leukocytosis in acute cholecystitis.

USS –safer & accurate method , detect gallstones.

Serum amylase -amylase may also be mildly elevated in

cholecystitis.

AST/ALT –levels may be elevated in cholecystitis or with

common bile duct (CBD) obstruction .

Bilirubin and alkaline phosphatase assays -reveal

evidence of CBD obstruction.

Management(same as non pregnant

women)

Conservative-

Withdrawal oral foods & fluids

Naso-gastric aspiration

I.V. fluids- hydration, electrolytes correction

Antibiotics

Analgesia- for pain

Surgical

Laparoscopic cholecystectomy-best in second trimester

ERCP

SUMMARY

How to differentiate abnormal findings from normal

findings

How to get proper Hx ,to do relevant

examination,investigations in pregnant mother

Detailed information about some specific diseases

REFERENCES

Philip N.B.,Louise C.K.(2011) Obstetrics by ten teachers-9th edition medical diseases

complicating pregnancy

Clare C.,Sarah G.Obstetrics Gynaecology and reproductive medicine-

Hyperemesis,gastro intestinal and liver disorders in pregnancy

Catherine N.P.-Hand book of Obstetric medicine-3rd edition liver disease