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JAUNDICE IN PREGNANCY
DR. S.N. BERA & MITALI DASH
M K C G MEDICAL COLLEGE
 Yellow discoloration
of skin, conjunctiva,
sclera and mucosa
associated with rise
in serum bilirubin
above 2mg/dl
( normal 0.2-01mg/dl)
Latent jaundice:1-2mg/dl
Mechanisms:
 ↑ production of bilirubin
 ↓ hepatocyte transport or conjugation
 Impaired excretion of bilirubin
 Impaired delivery of bilirubin into intestine
--“surgically relevant jaundice” or obstructive
jaundice
“Cholestasis” refers to the latter two, impaired
excretion and obstructive jaundice.
Physiological changes in liver
during pregnancy
 Liver is not palpable during pregnancy.
 Sr. protein decrease by 20%. Bilirubin also decrease
 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 is significantly raised but GGT
slightly decrease.
 Increase sr. triglyceride and VLDL. Cholesterol
increases up to 2 times the normal.
 10-15% normal pregnant may have bilirubin level
of over 1mg% d/t delayed excretion of bilirubin
that may leads to increase incidence of purities in
pregnancy.
 Incidence: 1 to 4/1000 deliveries.
 Maternal mortality 12% in our country
Grade of jaundice:
Mild: bilirubin <6mg%
Moderate 6-15mg%
Severe >16mg%
Cause of jaundice during
pregnancy
Liver disease unique to
pregnancy
Coincidental
occurrence of liver
disease in pregnancy
 Acute fatty liver of
pregnancy.
 Intrahepatic cholestasis of
pregnancy.
 Pre-eclampsia, eclampsia,
HELLP syndrome.
 Hyperemesis gravidarum
 Acute viral hepatitis.
 Hemolytic jaundice.
 Cholelithiasis.
 Drug induced
 Obstructive jaundice
Jaundice develop during pregnancy
on chronic liver disease:
A. Cirrhosis of liver.
B. Chronic hepatitis
Liver disease probably related to
pregnancy:
 Portal HTN.
 Cholecystitis.
 Pancreatitis.
 Wilsons ds.
 Gilbirts syndrome.
 Budd chiari syndrome.
Acute fatty liver of pregnancy
 Acute hepatic failure in absence of viral hepatitis, IHC,
etc.
 Manifest usually in 3rd trimester sometimes present
after delivery.
 Incidence: 1 in 7000-15000 pregnancies.
 More common in primipara and associated with pre-
eclampsia, multiple 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.
 Table 4 . 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
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.
 Puritus and ascites 50% cases.
 Hepatic encephalopathy seen in latter.
 Clinical improvement occurs 1-4 weeks after
delivery..
 Conjugated hyperbilirubinimia up to 5-15 mg/dl.
 ↑ALT but <1000iu/ml.
 ↑ALP 3-4times. 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.
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.
Management
 Supportive and directed towards management of
liver insufficiency and complication.
 Optimal management is prompt delivery.. Transfer
to high dependency unit.
 FFP, platelets, blood transfusion to correct
coagulopathy.
 iv glucose to maintain normoglycemia.
 monitor LFT with PT.
 In fulminant hepatic failure liver transplantation
is only treatment.
Intrahepatic cholestasis of
pregnancy
 Typically occurs in late pregnancy. Affecting 1.5-2% of
pregnancies.
 Disappears spontaneously, recurs in subsequent
pregnancy.
 ETIOLOGY:
i. Hereditary hepatic ↑ sensitivity of pregnancy
hormone → affects gallbladder function →slow or
stop the bile flow →build up of bile acid in liver.
ii. Genetic mutation in the hepatocellular phospholipid
transporter MDR3 in 15% case.
iii. Familial.
iv. Selenium deficiency in diet.
v. Previous liver damage.
Intrahepatic cholestasis of
pregnancy
 Typically manifest in 3rd trimester but can occure as
early as 10 weeks.
 Puritus in 2nd half of pregnancy which is otherwise
unexplained is most charecteristic manifestation 70%
cases.
 Puritus on palm and sole, intensity more in night.
 Severe puritus leads to insomnia, fatigue, depression
,mental disturbance.
 Dark colour urine.
 Jaundice seen in 10% cases usually mild ,develop 1-4
wks after puritus.
 Jaundice usually disappears with in weeks following
delivery.
 Puritus begins to decline a few hours after delivery and
disappears with in few days. Purities 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.
 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.
management
a. Ursodeoxycholic acid(UDCA):10-20mg/kg/day, even in high
dose(1.5-2gm/d) It relieves purities by decreasing the
concentration of bile acid.
- -improve hepato-cellular secretion by stimulation of
canilicular 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 puritus.
c. S-adenosyl methionine: it improve puritus by decreasing
the negative effects of estrogen on bile acid secretion.
d. Cholestyramine: relives puritus.
- binds to bile acids in gut.
- It increases the risk of vit-k deficiency, thus ↑ risk of
PPH.
-therefore monitoring of PT .
e. Vit-k: 10 mg daily.
Prognosis
 Fetal risk:
-- morbidity increase if bile acid more than 40micmol/l,. Perinatal
mortality 35-70/1000 live birth
-preterm delivery 15-60%
-intrapartum fetal distress. - meconium aspiration.
-fetal respiratory distress. -IUFD 0.4-4.1%.
 Maternal risk:
-↑caesarean section rate 25-36%.
-PPH 20-22%.
-developing gallstones subsequent to pregnancy.
- recurrence in next pregnancy.
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 absent in10-20% cases.
Pathogenesis: as in preeclampsia activation of
complement and coagulation cascade→increse
vascular tone,platlet aggregation , alteration in
TXA2 and prostacycline ratio. Leade 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,
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.
Complication:
Maternal:--eclampsia. —abruptio placentae,
--DIC -- ARF
--pulmonary oedema
--Cerebral oedema.
Fetal : ---IUGR ---PREMATURITY
--perinatal asphyxia .– still birth
Management
 Stabilizes 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.
 If CS has to be done 10 units of platlets should be
arranged if count <40000/cmm,
 Intensive monitoring for 48 hrs,
 Dexamethasone therapy to continue untill
postpartum resolution of disease occurs.
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.
Hyper emesis gravidarum
 Extreme of spectrum of morning sickness.
 c/b intractable nausea, vomiting ,dehydration, metalic
acidosis or alkalosis, electrolyte imbalance, weight
loss.
 Incidence less than 1 in 1000 pregnancy.
 Limited in 1st trimester, more in 1st pregnancy , recur 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 with out
necrosis.
 Heart: small heart , occasonal sub endocardial
hemorrhage.
 Brain: small hemorrhage in hypothalamic region
giving the manifestation of wernick’s
encephalopathy
Complication:
1. Neurological: wernick’s encephalopathy,
korsakoff’s psychosis, pontine myelinolysis,
peripheral neuritis.
2. Stress ulcer in stomach,
3. Mallory weiss syndrome,
4. Convulsion, coma.
5. jaundice
Management
 Hospitalization in severe case,
 Restriction of oral fluid, and iv fluid given to
correct dehydration.
 Anti emetics and vitamins.
 Hydrocortisone use in severe case.
 Nutritional support with vit b1, vitb6, vit b12, vitc.
Acute viral hepatitis
 MC cause of jaundice in pregnancy.
 Caused by hepatiti A,B,C,D and E VIRUS.
Hepatitis A:
 Occurs in area of crowding or poor sanitation
 Transmitted by feco oral route, with IP 28-30 days.
 c/b initial period of fever, anorexia , nausea, vomiting,
jaundice, subsides 2-4 weeks
 In acute stage IgM, and IgG promotes immunity.
 Self limited, no carrier state, no vertical transmission,
 Not teratogenic, but ↑ risk of preterm birth.
 Post exposure immunoglobin and vaccine may be
given to seronagative.
 Infant born of seropositive mother may be given active
and passive immunization.
Hepatitis B
 Prevalance in india 0.2-7.7% in pregnant women.
 Transmitted by parenteral route , IP 30-180 days.
 Routine screening in early pregnancy should be
done.
 Diagnosed by HBV DNA, HBsAg(Ab), HBcAb,
HBeAg(Ab).
 Vertical transmission 10-90%.
 5-10% may go to carrier state,
 Post exposure immunoglobin and vaccination
should be given to sero negative pregnant women.
 All infant born of sero positive mother must be
given active and passive immunization
 Hepatitis B .
 22. Active–passive immunoprophylaxis with hepatitis B immune
 globulin and the HBV vaccination series should be administered
 to all infants born to HBV-infected mothers to prevent
 perinatal transmission (strong recommendation, low level of
 evidence).
 23. Women chronically infected with HBV and high viral load
 (>200,000 U/ml or >10 6 log copies/ml and higher) should be
 off ered antiviral medication with tenofovir or telbivudine in
 the third trimester to reduce perinatal transmission of HBV
 (strong recommendation, low level of evidence).
 24. C-section should not be performed electively in HBV-positive
 mothers to prevent fetal infection (strong recommendation,
 very low level of evidence).
 25. Women chronically infected with HBV should be allowed to
 breastfeed as recommended for infant health (strong recommendation,
 very low level of evidence).
Hepatitis C
 Prevalance in pregnancy 2.3-17%.
 Transmitted by parenteral route, IP 30-60days
 Vertical transmission 3-6%.
 Diagnosed by HC antibody and RNA-PCR.
 NO vaccination is available.
 Routine screening not mandatory.
 All infants born of HCV positive mother should be
follow up.
 All pregnant women with risk factors for HCV should
 be screened with anti-HCV antibody. Screening should
 not be performed in women without risk factors for
 HCV acquisition (strong recommendation, low level of
 evidence).
 27. Invasive procedures (e.g., amniocentesis, invasive fetal monitoring)
 should be minimized in infected mothers and their
 fetus to prevent vertical transmission of hepatitis C (strong
 recommendation, very low level of evidence).
 28. C-section should not be performed electively in HCV-positive
 mothers to prevent fetal infection (strong recommendation,
 very low level of evidence).
 29. Women chronically infected with HCV should be allowed to
 breastfeed as indicated for infant health (strong recommendation,
 very low level of evidence).
 30. Hepatitis C therapy should not be off ered to pregnant
 women to either treat HCV or decrease the risk for vertical
 transmission (strong recommendation, very low level of
 Autoimmune hepatitis
 31. Pregnant women with autoimmune hepatitis (AIH) should
 be continued on their treatment with corticosteroids and/or
 azathioprine (AZA) (strong recommendation, very low level
 of evidence).
 32. Pregnant women with primary biliary cirrhosis (PBC) should
 be continued on their treatment with UDCA (strong recommendation,
 very low level of evidence).
 33. Pregnant women with Wilson’s disease (WD) should be
 continued, with dose reduction if possible, on their treatment
 with penicillamine, trientine, or zinc (strong recommendation,
 very low level of evidence).
 34. Pregnant women with suspected portal hypertension should
 undergo screening with upper endoscopy for esophageal
 varices in the second trimester (strong recommendation, low
 level of evidence).
 35. Pregnant women who are found to have large esophageal
 varices should be treated with beta-blockers and/or band
 ligation (conditional recommendation, very low level of
 evidence).
 36. Pregnant women with a history of liver transplantation
 should continue their immunosuppression except for
 mycophenolic acid (strong recommendation, moderate level
Hepatitis D
 Delta virus; defective RNA virus.
 Must co-infect with HBV.
 Transmission similar to HBV.
 Chronic co-infection with HBV and HDV is more
severe.
 Neonatal transmission is unusual.
Hepatitis E
 Transmitted by feco-oral route.
 Fulminant varity is most common among all types.
 HEV specific IgM and IgG can be detected.
 Chance of vertical transmission.
 Chronic infection is uncommon but may occurs.
 Hepatitis E vaccine(Hecolin) .
 Maternal mortality 15-20%.
Clinical features of viral hepatitis
 Prodromal phase: nausea, vomiting, pyrexia, loss of
appetite, upper abdominal pain, myalgia, artthralgia,
dark urine, clay colour stool. Palpable liver.
 Icteric phase: appears 1-2 weeks after symptom.
 Recovery phase: jaundice recedes, liver enlargement
regress, it takes 6-12 weeks for complete recovery.
 Investigation:
---LFT
---liver biopsy.
•Effects on pregnancy and fetus.
• ↑incidence of abortion, pre term labour, still birth,
• ↑incidence of primary pulmonary hypertention ,
hemorrhagic manifestation, hepatic coma,
Management
Preventive:
--disposable syringe & needle are used
--blood transfusion with due care.
--sanitation and clean water supply,
--health personnel should be provided with the
guidelines while dealing with pregnant women and
during delivery.
--active and passive immunization.
Therapeutic:
- bed rest until jaundice disappears.
- isolation as far as possible.
-diet rich in carbohydrate.
-vit B-complex .
Acute
Hepatitis
ICP HELLP AFLP
Trimester Any Trimester Third Third Third
Presenting
symptoms
Fever, Jaundice Pruritus HTN, Nausea,
Vomiting,Pain
Nausea,
Vomiting,Pain
ALT & AST Markedly high Normal to Mild
rise
Moderately
high
Moderately
high
Alkaline
Phospatase
Normal to mild
rise
High Normal Normal
Platelets Normal Normal Low Normal
Fetal
Complications
Infection with
HBV & HCV
Prematurity,
IUGR, FD
IUGR,
Prematurity
Prematurity
Maternal
Complications
Acute liver
failure(HEV)
None Thrombocytope
nia, septicemia,
DIC
Acute liver
failure
Hemolytic jaundice
 Hereditary
----thalassemia, sickle cell anemia.
----spherocytosis.
 Acquired
---- malaria.
---- mismatched blood transfusion.
---- leptospira,
----cl. Wiilchi
All causes unconjugated hyperbilirubinemia,
Sickle cell anaemia with pregnancy :
 Pregnancy is high risk in sickle cell disease (mostly SS
 Haemolytic crisis causes rapidly developing anemia with
jaundice.
 Vaso-occlusive crisis causes osteonecrosis, infarction of
kidney, lung. Hepato-splenomegaly, heart failure are
common.
 Increased incidence of maternal pre-eclampsia, PPH,
infection. Increased morbidity and mortality due to CVA,
pulm infarction, CHF, embolism etc.
 Increased risk of abortion, prematurity, IUGR, fetal loss,
perinatal mortality.
Management includes :
• Pre-conceptional councelling
• During pregnancy: Regular ANC, Prophylactic folic
acid 1 mg daily, Iron supplementation etc. Infection or
appearance of unusual symptoms needs
hospitalization
• During labour: Oxygen inhalation, Adequate
hydration, Antibiotics . Epidural anesthesia preferred.
Caesarian section should be performed for obstetric
indication only.
• Contraception: Sterilization even with low parity. OC
pills, IUCD contraindicated. Barrier method is ideal.
Malaria
 Malaria is imp. cause of jaundice in our country.
 Effects on mother: Anemia, Hypoglycemia, Metabolic
acidosis, Hepatic dysfunction with jaundice, Renal
failure, Pulmonary edema, Convulsions, coma etc.
 Effects on the fetus: Abortion, Preterm labour, Pre-
maturity, IUGR, IUFD etc.
 Congenital malaria is rare (<5%) unless placenta is
damaged (with Plasmodium falciparum in 2nd half of
pregnancy ).
 Effects of pregnancy on malaria: Risk and severity of
infection increases, Complications are high.
Management:
Management:
• Prevention from mosquito bite.
• Chemoprophylaxis: Cloroquine ( 300mg base weekly, 2
weeks before travel, covering the period of exposure and 4
weeks after leaving the endemic zone). Mefloquine
250mg/week in cloroquine resistant cases.
• Treatment:
i. Cloroquine- 10mg base/kg followed by 10mg/kg base at
24 hr and 5mg/kg at 48 hr.
ii. Cloroquine resistant cases: Quinine- 10mg salt/kg p.o
,every 8 hr for 7 days.
iii. Complicated malaria: Artesunate IV 2.4mg/kg at 0, 12, 24
hr, then daily for 5 days. Oral therapy ( 2mg/kg) when
the pt is stable.
Symptoms/signs:
weakness, Dark urine, anemia,
Icterus, splenomegaly
Lab:
 UB without bilirubinuria
 fecal and urine urobilinogen
 hemolytic anemia
 hemoglobinuria (in acute intravascular hemolysis)
 Reticulocyte counts
Drug induced
 Methyldopa
 Acetaminophen
 Rifampicin
 Nitrofurantoin
 Phenytoin
 INH-1% severe hepatitis,
 OCP’s-cholestasis,
 Erythromycin
 Valproic Acid
 Methotrexate-indolent
cirrhosis
 Clinical picture:nausea, vomiting, abdominal pain,
jaundice and puritus, sign of liver failure, cerebral
oedema, encephalopathy.
 Morphological change:
 Hepatitis, cholestasis, fatty liver, granulomatous
hepatitis.
 Clinical diagnosis: regression of symptom when
treatment is interrupted and recurrence when it is
administered again.
 May be confirmed by biopsy.
o Pregnancy is relative hyper coagulable state.
o Thrombosis of one or more hepatic veins and IVC.
o Resulting injaundice, ascitis, oedema and
coagulopathy.
o Liver is enlarged and tender.
oDiagnosis by
---- doppler USG of IVC and hepatic vein.
----hepatic venous angiography.
Hepatic venous outflow
obstruction
Pregnancy and chronic liver
disease
 CLD has mainly two types of manifestation
Firstly ,those related to portal HTN such as
oesophageal and gastric varices. The varices may
be low or high grade
secondly ,features of liver failure such as
ascites, jaundice, coagulopathy, hepatorenal
syndrome, hepatic encephalopathy.
CLD with well preserved liver function
--cirrhosis is not contraindication to pregnancy.
--pregnancy may be uneventful.
--all pregnant patient should screen for varices in second
trimester.
--low grade varices should be observed, high risk varices should
receives primary prophylasix either beta blockers or
endoscopic variceal ligation.
--vasopressin is contraindicated in pregnancy as it may causes
placental ischemia, necrosis and amputation of fetal digit.
--coagulation should be corrected before induction or cs.
--vaginal delivery prefered, should be assited and second stage
shortened.
--early termination of pregnancy should be consider when
hepatic decompensation is present.
CLD with decompensation of liver function
 Most women are amenorrhoeic and unable to
conceive because of associated hypothalamic-
pituitary dysfunction.
 It is high risk pregnancy with maternal and fetal
complication 50% with increase fetal loss .
Obstructive jaundice
Intrahepatic-Liver cell Damage/Blockage of Bile
Canaliculi
 Drugs or chemical toxins
 Dubin-Johnson syndrome
 Estrogens or Pregnancy
 Infiltrative tumors
 Intrahepatic biliary hypoplasia or atresia
 Primary biliary cirrhosis
Extrahepatic-Obstructive of bile Ducts
 Compression obstruction from tumors
 Congenital choledochal cyst
 Extrahepatic biliary atresia
 Intraluminal gallstones
 Stenosis-postoperative or inflammary
Cholestasis
Clinical features:
 Pain due to gallbladder disease, malignancy,
or stretching of the liver capsule
 Fever due to ascending cholangitis
 Palpable and / or tender gallbladder
 Enlarged liver, usually smooth.
 Scratch marks: excoriation
 Finger clubbing
 Loose, pale, bulky, offensive stools
 Dark orange urine
Lab Findings
 Serum Bilirubin
 Feceal urobilinogen (incomplete obstruction)
 Feceal urobilinogen absence (complete obstruction)
 urobilinogenuria is absent in complete obstructive
jaundice
 bilirubinuria 
 ALP 
 cholesterol 
Imaging for Obstructive Jaundice
 RUQ Ultrasound
 See stones, CBD diameter
 CT scan
 Identify both type & level of obstruction
 ERCP
 Direct visualization of biliary tree/panc ducts
 Procedure of choice for choledocholithiasis
 Diagnostic –AND- therapeutic (unlike MRCP)
 PTC useful of obstruction is prox. to CBD
 Endoscopic Ultrasound or EUS
Treatment
 If Medical, then treat the etiology
 If Obstructive Jaundice:
 Should r/o ascending cholangitis,
 For cholangitis: IVF, IV Antibiotics, Decompression
 Stones (remove stones vs stent vs drainage)
 Done via ERCP or PTC or open (surgery)
 Benign stricture (stent vs drainage catheter)
 Cancer (Stent vs drainage +/- resect the CA)
 The key principle is decompression, either
externally(drainage) or internally(stenting) the duct
open to allow better drainage
Cholelithiasis
 Pregnancy alters bile composition and gall bladder
emptying slows in the second trimester increasing the risk
of gall stones.
 Risk factors are multiparity and previous gallbladder
disease.
 Choledocholithiasis accounts for approximately 7% of
patients with jaundice in pregnancy but jaundice occurs in
only 5% of cholelithiasis.
 Treatment involves laparoscopic cholecystectomy.
 Uncomplicated cholecystectomy is safer in first and second
trimesters with fetal loss about 5%
 But with common bile duct exploration and if with
pancreatitis then 15 % maternal and 60% fetal mortality
Jaundice in pregnancy should be evaluated thoroughly
with proper history, clinical examination, laboratory
investigation to identify the underlying cause.
Proper management may improve maternal and
fetal outcome.
THANK YOU

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Jaundice IN PREGNANCY

  • 1. JAUNDICE IN PREGNANCY DR. S.N. BERA & MITALI DASH M K C G MEDICAL COLLEGE
  • 2.  Yellow discoloration of skin, conjunctiva, sclera and mucosa associated with rise in serum bilirubin above 2mg/dl ( normal 0.2-01mg/dl) Latent jaundice:1-2mg/dl
  • 3.
  • 4. Mechanisms:  ↑ production of bilirubin  ↓ hepatocyte transport or conjugation  Impaired excretion of bilirubin  Impaired delivery of bilirubin into intestine --“surgically relevant jaundice” or obstructive jaundice “Cholestasis” refers to the latter two, impaired excretion and obstructive jaundice.
  • 5. Physiological changes in liver during pregnancy  Liver is not palpable during pregnancy.  Sr. protein decrease by 20%. Bilirubin also decrease  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.
  • 6.  5’ nucleotides is significantly raised but GGT slightly decrease.  Increase sr. triglyceride and VLDL. Cholesterol increases up to 2 times the normal.  10-15% normal pregnant may have bilirubin level of over 1mg% d/t delayed excretion of bilirubin that may leads to increase incidence of purities in pregnancy.
  • 7.  Incidence: 1 to 4/1000 deliveries.  Maternal mortality 12% in our country Grade of jaundice: Mild: bilirubin <6mg% Moderate 6-15mg% Severe >16mg%
  • 8. Cause of jaundice during pregnancy Liver disease unique to pregnancy Coincidental occurrence of liver disease in pregnancy  Acute fatty liver of pregnancy.  Intrahepatic cholestasis of pregnancy.  Pre-eclampsia, eclampsia, HELLP syndrome.  Hyperemesis gravidarum  Acute viral hepatitis.  Hemolytic jaundice.  Cholelithiasis.  Drug induced  Obstructive jaundice
  • 9. Jaundice develop during pregnancy on chronic liver disease: A. Cirrhosis of liver. B. Chronic hepatitis
  • 10. Liver disease probably related to pregnancy:  Portal HTN.  Cholecystitis.  Pancreatitis.  Wilsons ds.  Gilbirts syndrome.  Budd chiari syndrome.
  • 11. Acute fatty liver of pregnancy  Acute hepatic failure in absence of viral hepatitis, IHC, etc.  Manifest usually in 3rd trimester sometimes present after delivery.  Incidence: 1 in 7000-15000 pregnancies.  More common in primipara and associated with pre- eclampsia, multiple pregnancy, having male fetus.
  • 12. Etiology:  may be mitochondrial dysfunction.--- >LCHAD def. --->defect in oxidation pathway of fatty acid.  ↑estrogen in 3rd trimester leads to ↓ mitochondrial oxidation.
  • 13.  Table 4 . 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
  • 14. 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.  Puritus and ascites 50% cases.  Hepatic encephalopathy seen in latter.  Clinical improvement occurs 1-4 weeks after delivery..
  • 15.  Conjugated hyperbilirubinimia up to 5-15 mg/dl.  ↑ALT but <1000iu/ml.  ↑ALP 3-4times. 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.
  • 16. 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.
  • 17. Management  Supportive and directed towards management of liver insufficiency and complication.  Optimal management is prompt delivery.. Transfer to high dependency unit.  FFP, platelets, blood transfusion to correct coagulopathy.  iv glucose to maintain normoglycemia.  monitor LFT with PT.  In fulminant hepatic failure liver transplantation is only treatment.
  • 18. Intrahepatic cholestasis of pregnancy  Typically occurs in late pregnancy. Affecting 1.5-2% of pregnancies.  Disappears spontaneously, recurs in subsequent pregnancy.  ETIOLOGY: i. Hereditary hepatic ↑ sensitivity of pregnancy hormone → affects gallbladder function →slow or stop the bile flow →build up of bile acid in liver. ii. Genetic mutation in the hepatocellular phospholipid transporter MDR3 in 15% case. iii. Familial. iv. Selenium deficiency in diet. v. Previous liver damage.
  • 19. Intrahepatic cholestasis of pregnancy  Typically manifest in 3rd trimester but can occure as early as 10 weeks.  Puritus in 2nd half of pregnancy which is otherwise unexplained is most charecteristic manifestation 70% cases.  Puritus on palm and sole, intensity more in night.  Severe puritus leads to insomnia, fatigue, depression ,mental disturbance.  Dark colour urine.  Jaundice seen in 10% cases usually mild ,develop 1-4 wks after puritus.
  • 20.  Jaundice usually disappears with in weeks following delivery.  Puritus begins to decline a few hours after delivery and disappears with in few days. Purities 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.
  • 21.  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.
  • 22. management a. Ursodeoxycholic acid(UDCA):10-20mg/kg/day, even in high dose(1.5-2gm/d) It relieves purities by decreasing the concentration of bile acid. - -improve hepato-cellular secretion by stimulation of canilicular 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.
  • 23. b . Corticosteroids: dexamethasone 12mg/day for 1 week. ---improves biochemical abnormalities but does not improve puritus. c. S-adenosyl methionine: it improve puritus by decreasing the negative effects of estrogen on bile acid secretion. d. Cholestyramine: relives puritus. - binds to bile acids in gut. - It increases the risk of vit-k deficiency, thus ↑ risk of PPH. -therefore monitoring of PT . e. Vit-k: 10 mg daily.
  • 24. Prognosis  Fetal risk: -- morbidity increase if bile acid more than 40micmol/l,. Perinatal mortality 35-70/1000 live birth -preterm delivery 15-60% -intrapartum fetal distress. - meconium aspiration. -fetal respiratory distress. -IUFD 0.4-4.1%.  Maternal risk: -↑caesarean section rate 25-36%. -PPH 20-22%. -developing gallstones subsequent to pregnancy. - recurrence in next pregnancy.
  • 25. 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 absent in10-20% cases.
  • 26. Pathogenesis: as in preeclampsia activation of complement and coagulation cascade→increse vascular tone,platlet aggregation , alteration in TXA2 and prostacycline ratio. Leade 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,
  • 27. 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.
  • 28. Complication: Maternal:--eclampsia. —abruptio placentae, --DIC -- ARF --pulmonary oedema --Cerebral oedema. Fetal : ---IUGR ---PREMATURITY --perinatal asphyxia .– still birth
  • 29. Management  Stabilizes 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.  If CS has to be done 10 units of platlets should be arranged if count <40000/cmm,  Intensive monitoring for 48 hrs,  Dexamethasone therapy to continue untill postpartum resolution of disease occurs.
  • 30. 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.
  • 31. Hyper emesis gravidarum  Extreme of spectrum of morning sickness.  c/b intractable nausea, vomiting ,dehydration, metalic acidosis or alkalosis, electrolyte imbalance, weight loss.  Incidence less than 1 in 1000 pregnancy.  Limited in 1st trimester, more in 1st pregnancy , recur in next pregnancy, more in multiple pregnancy with hydatidiform mole.  Etiology: a) Hormonal: hCG, estrogen, progesterone. b) Psychological(neurosis)
  • 32. Pathology:  Liver: centri lobular hepatic infiltration with out necrosis.  Heart: small heart , occasonal sub endocardial hemorrhage.  Brain: small hemorrhage in hypothalamic region giving the manifestation of wernick’s encephalopathy
  • 33. Complication: 1. Neurological: wernick’s encephalopathy, korsakoff’s psychosis, pontine myelinolysis, peripheral neuritis. 2. Stress ulcer in stomach, 3. Mallory weiss syndrome, 4. Convulsion, coma. 5. jaundice
  • 34. Management  Hospitalization in severe case,  Restriction of oral fluid, and iv fluid given to correct dehydration.  Anti emetics and vitamins.  Hydrocortisone use in severe case.  Nutritional support with vit b1, vitb6, vit b12, vitc.
  • 35. Acute viral hepatitis  MC cause of jaundice in pregnancy.  Caused by hepatiti A,B,C,D and E VIRUS.
  • 36. Hepatitis A:  Occurs in area of crowding or poor sanitation  Transmitted by feco oral route, with IP 28-30 days.  c/b initial period of fever, anorexia , nausea, vomiting, jaundice, subsides 2-4 weeks  In acute stage IgM, and IgG promotes immunity.  Self limited, no carrier state, no vertical transmission,  Not teratogenic, but ↑ risk of preterm birth.  Post exposure immunoglobin and vaccine may be given to seronagative.  Infant born of seropositive mother may be given active and passive immunization.
  • 37.
  • 38. Hepatitis B  Prevalance in india 0.2-7.7% in pregnant women.  Transmitted by parenteral route , IP 30-180 days.  Routine screening in early pregnancy should be done.  Diagnosed by HBV DNA, HBsAg(Ab), HBcAb, HBeAg(Ab).  Vertical transmission 10-90%.  5-10% may go to carrier state,  Post exposure immunoglobin and vaccination should be given to sero negative pregnant women.  All infant born of sero positive mother must be given active and passive immunization
  • 39.  Hepatitis B .  22. Active–passive immunoprophylaxis with hepatitis B immune  globulin and the HBV vaccination series should be administered  to all infants born to HBV-infected mothers to prevent  perinatal transmission (strong recommendation, low level of  evidence).  23. Women chronically infected with HBV and high viral load  (>200,000 U/ml or >10 6 log copies/ml and higher) should be  off ered antiviral medication with tenofovir or telbivudine in  the third trimester to reduce perinatal transmission of HBV  (strong recommendation, low level of evidence).  24. C-section should not be performed electively in HBV-positive  mothers to prevent fetal infection (strong recommendation,  very low level of evidence).  25. Women chronically infected with HBV should be allowed to  breastfeed as recommended for infant health (strong recommendation,  very low level of evidence).
  • 40. Hepatitis C  Prevalance in pregnancy 2.3-17%.  Transmitted by parenteral route, IP 30-60days  Vertical transmission 3-6%.  Diagnosed by HC antibody and RNA-PCR.  NO vaccination is available.  Routine screening not mandatory.  All infants born of HCV positive mother should be follow up.
  • 41.  All pregnant women with risk factors for HCV should  be screened with anti-HCV antibody. Screening should  not be performed in women without risk factors for  HCV acquisition (strong recommendation, low level of  evidence).  27. Invasive procedures (e.g., amniocentesis, invasive fetal monitoring)  should be minimized in infected mothers and their  fetus to prevent vertical transmission of hepatitis C (strong  recommendation, very low level of evidence).  28. C-section should not be performed electively in HCV-positive  mothers to prevent fetal infection (strong recommendation,  very low level of evidence).  29. Women chronically infected with HCV should be allowed to  breastfeed as indicated for infant health (strong recommendation,  very low level of evidence).  30. Hepatitis C therapy should not be off ered to pregnant  women to either treat HCV or decrease the risk for vertical  transmission (strong recommendation, very low level of
  • 42.  Autoimmune hepatitis  31. Pregnant women with autoimmune hepatitis (AIH) should  be continued on their treatment with corticosteroids and/or  azathioprine (AZA) (strong recommendation, very low level  of evidence).  32. Pregnant women with primary biliary cirrhosis (PBC) should  be continued on their treatment with UDCA (strong recommendation,  very low level of evidence).  33. Pregnant women with Wilson’s disease (WD) should be  continued, with dose reduction if possible, on their treatment  with penicillamine, trientine, or zinc (strong recommendation,  very low level of evidence).  34. Pregnant women with suspected portal hypertension should  undergo screening with upper endoscopy for esophageal  varices in the second trimester (strong recommendation, low  level of evidence).  35. Pregnant women who are found to have large esophageal  varices should be treated with beta-blockers and/or band  ligation (conditional recommendation, very low level of  evidence).  36. Pregnant women with a history of liver transplantation  should continue their immunosuppression except for  mycophenolic acid (strong recommendation, moderate level
  • 43. Hepatitis D  Delta virus; defective RNA virus.  Must co-infect with HBV.  Transmission similar to HBV.  Chronic co-infection with HBV and HDV is more severe.  Neonatal transmission is unusual.
  • 44. Hepatitis E  Transmitted by feco-oral route.  Fulminant varity is most common among all types.  HEV specific IgM and IgG can be detected.  Chance of vertical transmission.  Chronic infection is uncommon but may occurs.  Hepatitis E vaccine(Hecolin) .  Maternal mortality 15-20%.
  • 45. Clinical features of viral hepatitis  Prodromal phase: nausea, vomiting, pyrexia, loss of appetite, upper abdominal pain, myalgia, artthralgia, dark urine, clay colour stool. Palpable liver.  Icteric phase: appears 1-2 weeks after symptom.  Recovery phase: jaundice recedes, liver enlargement regress, it takes 6-12 weeks for complete recovery.  Investigation: ---LFT ---liver biopsy.
  • 46. •Effects on pregnancy and fetus. • ↑incidence of abortion, pre term labour, still birth, • ↑incidence of primary pulmonary hypertention , hemorrhagic manifestation, hepatic coma,
  • 47. Management Preventive: --disposable syringe & needle are used --blood transfusion with due care. --sanitation and clean water supply, --health personnel should be provided with the guidelines while dealing with pregnant women and during delivery. --active and passive immunization.
  • 48. Therapeutic: - bed rest until jaundice disappears. - isolation as far as possible. -diet rich in carbohydrate. -vit B-complex .
  • 49. Acute Hepatitis ICP HELLP AFLP Trimester Any Trimester Third Third Third Presenting symptoms Fever, Jaundice Pruritus HTN, Nausea, Vomiting,Pain Nausea, Vomiting,Pain ALT & AST Markedly high Normal to Mild rise Moderately high Moderately high Alkaline Phospatase Normal to mild rise High Normal Normal Platelets Normal Normal Low Normal Fetal Complications Infection with HBV & HCV Prematurity, IUGR, FD IUGR, Prematurity Prematurity Maternal Complications Acute liver failure(HEV) None Thrombocytope nia, septicemia, DIC Acute liver failure
  • 50. Hemolytic jaundice  Hereditary ----thalassemia, sickle cell anemia. ----spherocytosis.  Acquired ---- malaria. ---- mismatched blood transfusion. ---- leptospira, ----cl. Wiilchi All causes unconjugated hyperbilirubinemia,
  • 51. Sickle cell anaemia with pregnancy :  Pregnancy is high risk in sickle cell disease (mostly SS  Haemolytic crisis causes rapidly developing anemia with jaundice.  Vaso-occlusive crisis causes osteonecrosis, infarction of kidney, lung. Hepato-splenomegaly, heart failure are common.  Increased incidence of maternal pre-eclampsia, PPH, infection. Increased morbidity and mortality due to CVA, pulm infarction, CHF, embolism etc.  Increased risk of abortion, prematurity, IUGR, fetal loss, perinatal mortality.
  • 52. Management includes : • Pre-conceptional councelling • During pregnancy: Regular ANC, Prophylactic folic acid 1 mg daily, Iron supplementation etc. Infection or appearance of unusual symptoms needs hospitalization • During labour: Oxygen inhalation, Adequate hydration, Antibiotics . Epidural anesthesia preferred. Caesarian section should be performed for obstetric indication only. • Contraception: Sterilization even with low parity. OC pills, IUCD contraindicated. Barrier method is ideal.
  • 53. Malaria  Malaria is imp. cause of jaundice in our country.  Effects on mother: Anemia, Hypoglycemia, Metabolic acidosis, Hepatic dysfunction with jaundice, Renal failure, Pulmonary edema, Convulsions, coma etc.  Effects on the fetus: Abortion, Preterm labour, Pre- maturity, IUGR, IUFD etc.  Congenital malaria is rare (<5%) unless placenta is damaged (with Plasmodium falciparum in 2nd half of pregnancy ).  Effects of pregnancy on malaria: Risk and severity of infection increases, Complications are high.
  • 54. Management: Management: • Prevention from mosquito bite. • Chemoprophylaxis: Cloroquine ( 300mg base weekly, 2 weeks before travel, covering the period of exposure and 4 weeks after leaving the endemic zone). Mefloquine 250mg/week in cloroquine resistant cases. • Treatment: i. Cloroquine- 10mg base/kg followed by 10mg/kg base at 24 hr and 5mg/kg at 48 hr. ii. Cloroquine resistant cases: Quinine- 10mg salt/kg p.o ,every 8 hr for 7 days. iii. Complicated malaria: Artesunate IV 2.4mg/kg at 0, 12, 24 hr, then daily for 5 days. Oral therapy ( 2mg/kg) when the pt is stable.
  • 55. Symptoms/signs: weakness, Dark urine, anemia, Icterus, splenomegaly Lab:  UB without bilirubinuria  fecal and urine urobilinogen  hemolytic anemia  hemoglobinuria (in acute intravascular hemolysis)  Reticulocyte counts
  • 56. Drug induced  Methyldopa  Acetaminophen  Rifampicin  Nitrofurantoin  Phenytoin  INH-1% severe hepatitis,  OCP’s-cholestasis,  Erythromycin  Valproic Acid  Methotrexate-indolent cirrhosis
  • 57.  Clinical picture:nausea, vomiting, abdominal pain, jaundice and puritus, sign of liver failure, cerebral oedema, encephalopathy.  Morphological change:  Hepatitis, cholestasis, fatty liver, granulomatous hepatitis.  Clinical diagnosis: regression of symptom when treatment is interrupted and recurrence when it is administered again.  May be confirmed by biopsy.
  • 58. o Pregnancy is relative hyper coagulable state. o Thrombosis of one or more hepatic veins and IVC. o Resulting injaundice, ascitis, oedema and coagulopathy. o Liver is enlarged and tender. oDiagnosis by ---- doppler USG of IVC and hepatic vein. ----hepatic venous angiography. Hepatic venous outflow obstruction
  • 59. Pregnancy and chronic liver disease  CLD has mainly two types of manifestation Firstly ,those related to portal HTN such as oesophageal and gastric varices. The varices may be low or high grade secondly ,features of liver failure such as ascites, jaundice, coagulopathy, hepatorenal syndrome, hepatic encephalopathy.
  • 60. CLD with well preserved liver function --cirrhosis is not contraindication to pregnancy. --pregnancy may be uneventful. --all pregnant patient should screen for varices in second trimester. --low grade varices should be observed, high risk varices should receives primary prophylasix either beta blockers or endoscopic variceal ligation. --vasopressin is contraindicated in pregnancy as it may causes placental ischemia, necrosis and amputation of fetal digit. --coagulation should be corrected before induction or cs. --vaginal delivery prefered, should be assited and second stage shortened. --early termination of pregnancy should be consider when hepatic decompensation is present.
  • 61. CLD with decompensation of liver function  Most women are amenorrhoeic and unable to conceive because of associated hypothalamic- pituitary dysfunction.  It is high risk pregnancy with maternal and fetal complication 50% with increase fetal loss .
  • 62. Obstructive jaundice Intrahepatic-Liver cell Damage/Blockage of Bile Canaliculi  Drugs or chemical toxins  Dubin-Johnson syndrome  Estrogens or Pregnancy  Infiltrative tumors  Intrahepatic biliary hypoplasia or atresia  Primary biliary cirrhosis
  • 63. Extrahepatic-Obstructive of bile Ducts  Compression obstruction from tumors  Congenital choledochal cyst  Extrahepatic biliary atresia  Intraluminal gallstones  Stenosis-postoperative or inflammary
  • 64. Cholestasis Clinical features:  Pain due to gallbladder disease, malignancy, or stretching of the liver capsule  Fever due to ascending cholangitis  Palpable and / or tender gallbladder  Enlarged liver, usually smooth.  Scratch marks: excoriation  Finger clubbing  Loose, pale, bulky, offensive stools  Dark orange urine
  • 65. Lab Findings  Serum Bilirubin  Feceal urobilinogen (incomplete obstruction)  Feceal urobilinogen absence (complete obstruction)  urobilinogenuria is absent in complete obstructive jaundice  bilirubinuria   ALP   cholesterol 
  • 66. Imaging for Obstructive Jaundice  RUQ Ultrasound  See stones, CBD diameter  CT scan  Identify both type & level of obstruction  ERCP  Direct visualization of biliary tree/panc ducts  Procedure of choice for choledocholithiasis  Diagnostic –AND- therapeutic (unlike MRCP)  PTC useful of obstruction is prox. to CBD  Endoscopic Ultrasound or EUS
  • 67. Treatment  If Medical, then treat the etiology  If Obstructive Jaundice:  Should r/o ascending cholangitis,  For cholangitis: IVF, IV Antibiotics, Decompression  Stones (remove stones vs stent vs drainage)  Done via ERCP or PTC or open (surgery)  Benign stricture (stent vs drainage catheter)  Cancer (Stent vs drainage +/- resect the CA)  The key principle is decompression, either externally(drainage) or internally(stenting) the duct open to allow better drainage
  • 68. Cholelithiasis  Pregnancy alters bile composition and gall bladder emptying slows in the second trimester increasing the risk of gall stones.  Risk factors are multiparity and previous gallbladder disease.  Choledocholithiasis accounts for approximately 7% of patients with jaundice in pregnancy but jaundice occurs in only 5% of cholelithiasis.  Treatment involves laparoscopic cholecystectomy.  Uncomplicated cholecystectomy is safer in first and second trimesters with fetal loss about 5%  But with common bile duct exploration and if with pancreatitis then 15 % maternal and 60% fetal mortality
  • 69. Jaundice in pregnancy should be evaluated thoroughly with proper history, clinical examination, laboratory investigation to identify the underlying cause. Proper management may improve maternal and fetal outcome.