differences in investigations due to pregnancy,different types of liver disaeses which occur specifically during pregnancy

1. LIVER DISEASES IN
PREGNANCY

2.  Diseases only related to liver
AFLD,obstrectic cholestasis….etc
 Muliti system diseases with hepatic
manefestations
hyperemesis gravidarum,HELLP

3. 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

4. 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

5. 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

6. 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

7.  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

8. HISTORY

9. 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

10.  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

11. 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

12. 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

13. 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

14. 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.

15. 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)

16. PATHOGENESIS:
Not clearly understood
MDR 3
-encodes for the canalicular phospholipid pump
protein
Changes induced by genetic mutation leads to
increased sensitivity to oestrogens

17.  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

18.  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

19. 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%)

20.  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

21. 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

22. 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

23. 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

24.  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.

25.  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

26. 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.

27. 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.

28. 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

29.  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.

30.  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

31. 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

32. 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.

33. 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

34. 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

35. 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

36. 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.

37. 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.

38.  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.

39. HDV
 Only found in HBs Ag positive people.
 Prevention of HBV infection will also prevent HDV
infection.

40. 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% )

41. 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

42.  Disseminated infection causes pneumonitis ,
encephalitis.
 Diagnosis by liver biopsy.
 Treatment- anti viral therapy
acyclovir therapy for infant.

43. 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

44. 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.

45.  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.

46. 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

47. DDS
 Acute fatty liver of pregnancy
 Haemolytic uraemic syndrome
 TTP
 Haemolytic anaemia
 Placental abruption
 Hyperemesis gravidarum

48. 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

49.  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.

50. EFFECT OF HELLP SYNDROME ON
PREGNANCY
 Abruption
 Subcapsular liver haematoma
 Acute renal failure
 Massive hepatic necrosis
 Liver rupture

51. 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

52. 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

53. 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%

54. ACUTE FATTY LIVER OF
PREGNANCY.

55. 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 )

56. DIFFERENTIAL DIAGNOSIS.
 HELLP syndrome.

57. 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…

58. 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.

59. COMPLICATIONS.
 High maternal (2-18%) and fetal (7-58%) mortality.
 DIC.
 Renal failure.
 Pancreatitis.
 (transient) Diabetes insipidus.
 Hepatic encephalopathy.
 Fulminant liver failure.
MATERNAL COMPLICATIONS.

60. 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

61. 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)

62. 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.

63. 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

64. 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.

65. 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.

66.  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 enephalopathy
should 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.

67. 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.

68. 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.

69. 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

70.  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

71. CLINICAL FEATURES
 Nausea and vomiting
 Weight loss
 Ketosis
 Muscle wasting
 Postural hypotention
 Sign of dehydration

72. 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

73. 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

74. 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-

75. Fetal complication
 Intrautrine growth retardation
 Wernicke’s encephalopathy
 Intrauterine death

76. 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

77. PRE-EXISTING LIVER DISEASE

78. 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

79. PRIMARY BILLIARY CIRRHOSIS
 Usually present with pruritis and is associate with a
raised alkaline phosphatase and gamma GT
 Pruritis may worsen during pregnancy

80. 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 blocke
threapy in pregnancy

81. Gall bladder
disease

82.  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

83. Pregnancy
Oestrogen
Increase cholesterol
concentration
Reduce bile acid
Bile acid super saturation
Gallstone
CHOLECYSTITIS
OBSTRUCTIVE
DISEASE
Progesterone
Muscle Relaxation
Reduce bile release
Increase bile stasis

84.  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)

85.  Differential diagnosis
 Cholecystitis
 Pancreatitis
 Peptic ulcer
 Acute fatty liver of pregnancy
 Viral hepatitis
 Obstetric cholestasis

86.  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.

87. 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

88. 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

89. 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