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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
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