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PRURITIS IN PREGNANCY
PREPARED BY-
Ankit mandal
INTERN
MODERATOR
Dr. Indra yadav
Department of obstetrics and gynaecology
KU-BMCTH
PRURITIS RELATED TO PREGNANCY
• Intrahepatic cholestasis of pregnancy /obstetric
cholestasis (ICP)
• Pruritic urticarial papules and plaques of
pregnancy(PUPPP)
• Atopic eruption of pregnancy
• Pemphigoid gestations
Unrelated to pregnancy
• Scabies
• Urticaria
• Drug eruptions
• Allergy
• Psoriasis
• Insect bites
INTRAHEPATIC CHOLESTASIS OF
PREGNANCY/OBSTETRIC CHOLESTASIS
• Incidence ranges from o.1% to 15.6% in South
Asia.
• No primary skin lesion
• characterized by pruritus, icterus in the absence
of a skin rash
• Resolve after child birth
ETIOPATHOGENESIS
• Exact Cause is unknown
• Estrogen impairs the synthesis, metabolism, transport of bile
acids, causing downsteam dysfunction of bile acids
homeostasis.
• Progesteron causes inhibition of cholecystokinin mediated
action on Gallbladder
• Decreased contractility of gallbladder leads to bile stasis.
• Bile pigments binds in subcutaneous layer, irritates the nerve
ending
• Genetic mutation of hepatocellular transport system eg-
mutation of ABCB4 gene assosciated with progressive
familial intrahepatic cholestasis
• Bile acids are cleared incompletely and accumulate in
plasma .
• Increase myometrial contractilily and enhanced sensitivity
to oxytocin- Preterm labour
• Marked Vasoconstriction in the
placental chorionic veins resulting
foetal death.
• Particularly taurocholic acid, toxic to
cardiomyocytic cell leads to cardiac
arrhythmias- Death
CLINICAL PRESENTATION
• Pruritis develops in late pregnancy, sudden in onset
• Starts on palms and soles later generalised
• Sleep disturbances, pruritis worse at night
• Skin changes- excoriation from scratching
• Jaundice is rare
• LFT may dearrange after several weeks of development of pruritis.
• Hyperbilirubinemia results from retention of conjugated
pigment , but total plasma concentration rarely exceeds 4 to 5
mg/dl.
• Mild : bile acids > 14mmol/L
• Moderate : bile acids > 40mmol/L
• Severe : bile acids > 100mmol/L
• Increasing fetal risks are directly associated with increasing
maternal serum bile acids (Glantz et al, 2004).
• Alkaline phosphatase - elevated more than in normal
pregnancy.
Investigations
DISORDER ONSET AST(IU/L) BILIRUBIN
(MG/DL)
PT
CHOLESTASIS LATE NL-200 1-5 NL
FATTY LIVER LATE 200-800 4-10 ↑
PREECLAMPSIA MID-LATE NL-300 1-4 NL
HEPATITIS VARIABLE 2000+ 5-20 ↑↑
• Serum Aminotransferase are normal to moderately elevated but
seldom exceeds 4 to 5 mg/dl.
• Sonography done to exclude cholelithiasis and billiary
obstruction.
• No altered blood pressure or proteinurea rule out preeclamptic
liver disease .
• Low serum aminotransferase levels with cholestasis rule out
acute viral hepatitis.
MANAGEMENT
• Counseling - Risk to the foetus
• Surveillance -liver function test
-Prothrombin time
• Foetal wellbeing - Cardiaotocography
- USG - growth , liquor volume,
umbilical artery doppler blood flow
PHARMACOLOGICAL TREATMENT
a) Topical emollients –
calamine lotion .
b) Antihistamines - Chlorpheniramine 4mg TDS)
Promathazine (phanergan) 25mg at night
• Cholestyramine is effective but it causes decreased
absorption of fat soluble vitamins.
• Ursodeoxycholic acid is effective for both pruritis and
feotal outcome -ACOG
• Ursodeoxycholic Acid (UDCA) can reduce serum bile
acids and helps relieve pruritus.
• Starting dose: Ursodeoxycholic Acid 300mg TDS
Maximum dose: Ursodeoxycholic Acid 600mg QDS
Orally
• Increase UDCA weekly following blood tests (LFTs, bile
acids) if bile acids not responding OR >40mmol/L.
• Rifampicin can be added when UDCA is at maximum
dose and patient is not responding (bile acids >
40mmol/L despite UDCA).
• Do not start if ALT >200IU/L.
• Works synergistically with UDCA to help reduce serum
bile acid levels – UDCA must therefore be continued
• Due to limited evidence for use, rifampicin is
considered a last line agent for the management of
refractory cases of obstetric cholestasis.
CHOLESTASIS AND PREGNANCY
OUTCOMES-
• Neonatal complication occurred in 1/3rd of pregnancies -
i.e respiratory distress, fetal distress, meconium stained
liquor.
• Abnormal amount of bile acids may cause fetal cardiac
arrest
-Gorelik and collegue
• Perinatal mortality rates were slightly increased but
infant death was limited to mother having total bile acid
level ≥40 µmol/L.
- Glantz and collegues
• Delivery by labour induction to avoid stillbirth.
• Advise active management of 3rd stage of labour due to
higher risk of postpartum haemorrhage.
• Elective early delivery was offered at 37-38 weeks of
gestation
POSTNATAL MANAGEMENT
• Intramuscular Vitamin K is recommended for neonates.
• LFTs and bile acids checked in 6 weeks at her postnatal check
up.
• Counselling patient, itching should resolve, and bile acids
and LFTs should return to normal within 6 weeks.
•
• Use of oestrogen-containing contraception pill may result in
recurrence of cholestasis.
• Recurrence risk of 45-90% in subsequent pregnancies, and the
increased incidence of 35% in family members (Geenes, 2014;
RCOG, 2011).
• Decreased prothrombin production, leading to a prolongation of
the prothrombin time.
• Increase Rate Of Cesarean section.
• Increase Risk Of PPH
THANKYOU
PRURITIC URTICARIAL PAPULES
AND PLAQUES OF PREGNANCY
(PUPPP)
PRURITIC URTICARIAL PAPULES AND
PLAQUES OF PREGNANCY (PUPPP)
• Intensly pruritic 1-2 mm erythematous Papules within the
striae
• Appears late in pregnancy
• Lesion initially form within striae but show Umbilical
sparing
• Self limiting , usually respond to oral antihistaminic, skin
emollients, topical steroids
• Good prognosis resolves after delivery without scarring.
• No recurrence
PHEMPHIGOID GESTATIONIS (PG)
PHEMPHIGOID GESTATIONIS (PG)
• Autoimmune (3%), occurs in1st pregnancy in 2nd/3rd
trimester
• Initially ,pruritic papules and urtricarial plaques followed
by vesicles and bulla
• Result of primary reaction between maternal IgG
directed against collagen xvii of basement membrane of
skin and amniotic epithelium
• Flare at time delivery and post partum
• Skin biopsy and serum Antibody assay for
confirmation
• Steroids & antihistamines
• IUGR, preterm
• 10%-cutaneous involve of newborn
• Post partum flare,
• Recurrence
ATOPIC ERUPTION OF GESTATION
ATOPIC ERUPTION OF GESTATION
• It comprises three condition;-
-Eczema in pregnancy: dry , thickened ,scaly red patches
involving flexor extremities
-Prurigo of pregnancy:5-10mm itchy,erythematous
papules found on extensor surface and trunk
-Pruritic folliculitis of pregnancy: small, erythematous
follicular papules
• All lesion resolve after delivery
• Diagnosis by exclusion
• Good prognosis,
• Low or moderate potent Corticosteroids +
antihistaminics
RCOG-
2022
TAKE HOME MESSAGE
• Good history taking is important to
rule out other causes of pruritis
• Systemic approach to include both
obstetric and non-obstetric causes
• Pruritis is common, may precede
abnormal LFT.
THANK-YOU
REFERENCES
• 25th edition Wiliams obstetrics , Mc Graw Hill
Publication.
• Zu Y, Yang J, Zhang C and Liu D (2021) The
Pathological Mechanisms of Estrogen-Induced
Cholestasis: Current Perspectives. Front. Pharmacol.
• RCOG Guideline 2022
• ACOG Guideline
• Google images

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PRURITIS IN PREGNANCY aNKIT.pptx

  • 1. PRURITIS IN PREGNANCY PREPARED BY- Ankit mandal INTERN MODERATOR Dr. Indra yadav Department of obstetrics and gynaecology KU-BMCTH
  • 2. PRURITIS RELATED TO PREGNANCY • Intrahepatic cholestasis of pregnancy /obstetric cholestasis (ICP) • Pruritic urticarial papules and plaques of pregnancy(PUPPP) • Atopic eruption of pregnancy • Pemphigoid gestations
  • 3. Unrelated to pregnancy • Scabies • Urticaria • Drug eruptions • Allergy • Psoriasis • Insect bites
  • 4.
  • 5. INTRAHEPATIC CHOLESTASIS OF PREGNANCY/OBSTETRIC CHOLESTASIS • Incidence ranges from o.1% to 15.6% in South Asia. • No primary skin lesion • characterized by pruritus, icterus in the absence of a skin rash • Resolve after child birth
  • 7. • Exact Cause is unknown • Estrogen impairs the synthesis, metabolism, transport of bile acids, causing downsteam dysfunction of bile acids homeostasis. • Progesteron causes inhibition of cholecystokinin mediated action on Gallbladder • Decreased contractility of gallbladder leads to bile stasis. • Bile pigments binds in subcutaneous layer, irritates the nerve ending
  • 8. • Genetic mutation of hepatocellular transport system eg- mutation of ABCB4 gene assosciated with progressive familial intrahepatic cholestasis • Bile acids are cleared incompletely and accumulate in plasma . • Increase myometrial contractilily and enhanced sensitivity to oxytocin- Preterm labour
  • 9. • Marked Vasoconstriction in the placental chorionic veins resulting foetal death. • Particularly taurocholic acid, toxic to cardiomyocytic cell leads to cardiac arrhythmias- Death
  • 10. CLINICAL PRESENTATION • Pruritis develops in late pregnancy, sudden in onset • Starts on palms and soles later generalised • Sleep disturbances, pruritis worse at night • Skin changes- excoriation from scratching • Jaundice is rare • LFT may dearrange after several weeks of development of pruritis.
  • 11. • Hyperbilirubinemia results from retention of conjugated pigment , but total plasma concentration rarely exceeds 4 to 5 mg/dl. • Mild : bile acids > 14mmol/L • Moderate : bile acids > 40mmol/L • Severe : bile acids > 100mmol/L • Increasing fetal risks are directly associated with increasing maternal serum bile acids (Glantz et al, 2004). • Alkaline phosphatase - elevated more than in normal pregnancy. Investigations
  • 12. DISORDER ONSET AST(IU/L) BILIRUBIN (MG/DL) PT CHOLESTASIS LATE NL-200 1-5 NL FATTY LIVER LATE 200-800 4-10 ↑ PREECLAMPSIA MID-LATE NL-300 1-4 NL HEPATITIS VARIABLE 2000+ 5-20 ↑↑
  • 13. • Serum Aminotransferase are normal to moderately elevated but seldom exceeds 4 to 5 mg/dl. • Sonography done to exclude cholelithiasis and billiary obstruction. • No altered blood pressure or proteinurea rule out preeclamptic liver disease . • Low serum aminotransferase levels with cholestasis rule out acute viral hepatitis.
  • 14. MANAGEMENT • Counseling - Risk to the foetus • Surveillance -liver function test -Prothrombin time • Foetal wellbeing - Cardiaotocography - USG - growth , liquor volume, umbilical artery doppler blood flow
  • 15. PHARMACOLOGICAL TREATMENT a) Topical emollients – calamine lotion . b) Antihistamines - Chlorpheniramine 4mg TDS) Promathazine (phanergan) 25mg at night • Cholestyramine is effective but it causes decreased absorption of fat soluble vitamins.
  • 16. • Ursodeoxycholic acid is effective for both pruritis and feotal outcome -ACOG • Ursodeoxycholic Acid (UDCA) can reduce serum bile acids and helps relieve pruritus. • Starting dose: Ursodeoxycholic Acid 300mg TDS Maximum dose: Ursodeoxycholic Acid 600mg QDS Orally • Increase UDCA weekly following blood tests (LFTs, bile acids) if bile acids not responding OR >40mmol/L.
  • 17. • Rifampicin can be added when UDCA is at maximum dose and patient is not responding (bile acids > 40mmol/L despite UDCA). • Do not start if ALT >200IU/L. • Works synergistically with UDCA to help reduce serum bile acid levels – UDCA must therefore be continued • Due to limited evidence for use, rifampicin is considered a last line agent for the management of refractory cases of obstetric cholestasis.
  • 18. CHOLESTASIS AND PREGNANCY OUTCOMES- • Neonatal complication occurred in 1/3rd of pregnancies - i.e respiratory distress, fetal distress, meconium stained liquor. • Abnormal amount of bile acids may cause fetal cardiac arrest -Gorelik and collegue
  • 19. • Perinatal mortality rates were slightly increased but infant death was limited to mother having total bile acid level ≥40 µmol/L. - Glantz and collegues • Delivery by labour induction to avoid stillbirth. • Advise active management of 3rd stage of labour due to higher risk of postpartum haemorrhage. • Elective early delivery was offered at 37-38 weeks of gestation
  • 20. POSTNATAL MANAGEMENT • Intramuscular Vitamin K is recommended for neonates. • LFTs and bile acids checked in 6 weeks at her postnatal check up. • Counselling patient, itching should resolve, and bile acids and LFTs should return to normal within 6 weeks. • • Use of oestrogen-containing contraception pill may result in recurrence of cholestasis.
  • 21. • Recurrence risk of 45-90% in subsequent pregnancies, and the increased incidence of 35% in family members (Geenes, 2014; RCOG, 2011). • Decreased prothrombin production, leading to a prolongation of the prothrombin time. • Increase Rate Of Cesarean section. • Increase Risk Of PPH
  • 23. PRURITIC URTICARIAL PAPULES AND PLAQUES OF PREGNANCY (PUPPP)
  • 24. PRURITIC URTICARIAL PAPULES AND PLAQUES OF PREGNANCY (PUPPP) • Intensly pruritic 1-2 mm erythematous Papules within the striae • Appears late in pregnancy • Lesion initially form within striae but show Umbilical sparing • Self limiting , usually respond to oral antihistaminic, skin emollients, topical steroids • Good prognosis resolves after delivery without scarring. • No recurrence
  • 26. PHEMPHIGOID GESTATIONIS (PG) • Autoimmune (3%), occurs in1st pregnancy in 2nd/3rd trimester • Initially ,pruritic papules and urtricarial plaques followed by vesicles and bulla • Result of primary reaction between maternal IgG directed against collagen xvii of basement membrane of skin and amniotic epithelium
  • 27. • Flare at time delivery and post partum • Skin biopsy and serum Antibody assay for confirmation • Steroids & antihistamines • IUGR, preterm • 10%-cutaneous involve of newborn • Post partum flare, • Recurrence
  • 28. ATOPIC ERUPTION OF GESTATION
  • 29. ATOPIC ERUPTION OF GESTATION • It comprises three condition;- -Eczema in pregnancy: dry , thickened ,scaly red patches involving flexor extremities -Prurigo of pregnancy:5-10mm itchy,erythematous papules found on extensor surface and trunk -Pruritic folliculitis of pregnancy: small, erythematous follicular papules
  • 30. • All lesion resolve after delivery • Diagnosis by exclusion • Good prognosis, • Low or moderate potent Corticosteroids + antihistaminics
  • 32. TAKE HOME MESSAGE • Good history taking is important to rule out other causes of pruritis • Systemic approach to include both obstetric and non-obstetric causes • Pruritis is common, may precede abnormal LFT.
  • 34. REFERENCES • 25th edition Wiliams obstetrics , Mc Graw Hill Publication. • Zu Y, Yang J, Zhang C and Liu D (2021) The Pathological Mechanisms of Estrogen-Induced Cholestasis: Current Perspectives. Front. Pharmacol. • RCOG Guideline 2022 • ACOG Guideline • Google images

Editor's Notes

  1. Rifampicin stimulate 6 hydroxylation, bile acid sulfation( increases solubility, enhance fecal and urinary excretion)