Pruritus in Pregnancy - Family Medicine Resident Presentations

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Transcript Pruritus in Pregnancy - Family Medicine Resident Presentations

Pruritus in Pregnancy
Carol Mendez, MD
Albert Einstein College of Medicine
Montefiore Medical Center
Department of Family and Social Medicine
April 29, 2010
Pruritus in Pregnancy
• Normal skin changes: linea nigra, melasma, striae
distensae.
• Unrelated to pregnancy: flare of preexisting dermatosis
• Without rash
– Intrahepatic cholestasis of pregnancy
• With rash
– Related to pregnancy
• Early onset, trunk & limbs involved: atopic eruption
• Late onset, predominant abdominal involvement
– Polymorphic eruption of pregnancy
– Pemphigoid gestationis
Intrahepatic Cholestasis of Pregnancy
• Occurs in 3rd TM
• Incidence 1 in 100 to 150 pregnancies, #2 cause
of jaundice in pregnancy
• Pruritus without primary lesions
• Only secondary excoriations/prurigo nodularis
• Elevated total serum bile acid levels
• Prematurity, fetal distress, stillbirths
• Spontaneous resolution after delivery
• Synonym: pruritus gravidarum
Causes and Pathogenesis
• Unclear
• Probably increased hepatic sensitivity to
estrogen
• Risk factors: hepatitis C virus associated with
ICP
Clinical Picture-ICP
• Symptoms are worst at night
• Trunk, Palms and Soles
• Jaundice, clay colored stools, dark urine
– 20%-50% of patients
• Steatorrhea can lead to vit. K malabsorption and
prolongation of PT  risk of hemorrhage.
• LAB: mild-moderate elevation of transaminases,
marked elevation in alkaline phosphatase
• Bile acid levels 10-100x normal
Fetal risks with ICP
• Distress, still birth and preterm delivery
• Neonatal respiratory distress syndrome
• Placental anoxia from vasoconstriction of
placental chorionic veins from toxic bile acids
and meconium.
• Can be reduced by tx and delivery b/t 36-38
weeks with favorable lung maturity and cervix.
Treatment of ICP
• Mild: symptom relief with emollients and topical
antipruritics.
– Systemic antihistamines are not useful
– Ursodeoxycholic acid (UDCA)-naturally occuring
hydrophilic bile acid that enhances excretion of
hydrophobic bile acids, other hepatotoxic compounds,
and sulfated progesterone metabolites.
• Controls pruritus and serologic abnormalities
• Works faster than cholestyramine, safe for mother and fetus
• May result in decreased fetal mortality associated with ICP
– Plasmapheresis
– Cholestyramine may be effective up to 50%
• May precipitate vit K  worsening coagulopathy
Prognosis
• Recurrence in subsequent pregnancies:
60% to 70%
• Use of oral contraceptives
• Resolves within the first month after delivery
Early onset-trunk and limbs involved
Atopic Eruption of Pregnancy
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Very common, incidence 1 in 300 to 450
20% exacerbated atopic dermatitis
80% firm manifestation
Lab: elevated IgE levels
No maternal or fetal risk
Cause of AEP
• Unknown
• Reported cases of increased IgE
• Cholestasis
Clinical Course-AEP
• Onset during 2nd and 3rd TM
• Discrete, excoriated papules, predominnately
on extensor surfaces and occasionally on
abdomen.
• May last for weeks to months after delivery
with variable recurrence in subsequent
pregnancies.
Treatment of AEP
• Topical corticosteroids
• Ultraviolet B light therapy
• Benzoyl Peroxide
Late onset-3rd TM
Predominant Abdominal Involvement
• Polymorphic Eruption of Pregnancy (Pruritic
Urticarial Papules and Plaques of Pregnancy)
– Abdominal striae sparing umbilicus
– No fetal risk
• Pemphigoid Gestationis
– Vesiculo-bullous eruption on urticated erythema
– Periumbilical involvement
– Small for dates babies
Polymorphic Eruption of Pregnancy
(PUPPP)
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Papular urticarial eruption
Mostly in primiparous women
Begins within abd. striae, sparing umbilicus
Resolves spontaneously & rapidly postpartum
No maternal or fetal risk
Rarely recurs
Incidence is 1 in 120 to 240 pregnancies
Causes of PEP/PUPPP
• Association with multiple gestation
• Rapid, late stretching of abdominal skin
Clinical presentation- PEP
• Late 3rd TM and immediate postpartum period
• Intensely pruritic erythematous papules, 1-3 mm,
quickly coalescing into urticarial plaques.
• Tiny vesicles, 2mm, may occur in the plaques, but
bullae are absent.
• Begin in abd. striae and spread in days to
abdomen, buttocks, thighs, upper inner arms,
and lower back.
• Spearing periumbilical area, face, breasts, palms,
and soles. No mucus membrane lesions.
PUPP Striae
Treatment of PEP/PUPPP
• Potent topical corticosteroids, tapered off
after 1 week of therapy.
• Severe cases: prednisone 10-40mg/d
• Oral antihistamines generally ineffective.
• Resolution 7-10 days after delivery
• Majority of women don’t have a recurrence.
Pemphigoid Gestationis
• Incidence is 1 in 50,000
• Intensely pruritic vesiculobullous eruptions on
urticated erythema with periumbilical involvement
• Late 3rd TM or immediate postpartum period.
• Lesions begin within or adjacent to umbilicus.
• Increased risk of small for gestational age births, risk of
prematurity and 5% of babies have urticarial, vesicular,
or bullous lesions-resolve spontaneously.
• Dx: 2 skin biopsies for histology and direct
immunofluorescence
• Synonyms:
– gestational pemphigoid
– Herpes gestationis
Pathophysiology of PG
• Production of autoantibody with potential
crossreactivity between placental tissue &
skin.
• 100% incidence of anti-human leukocyte
antigen (HLA) antibodies
• Subepidermal blisters on H&E stain
• Immunofluorescence microscopy: linear C3
depositions along dermal-epidermal junction
Clinical Course-PG
• Abrupt onset of intensely pruritic urticarial
lesions on the trunk progressing in generalized
fashion spreading along face, mucous
membranes, palms, and soles.
• A flare at delivery in 75% of cases.
• Recurs with subsequent pregnancies,
menstruation, and use of oral contraceptive.
• Complete resolution in weeks to months
postpartum.
Pemphigoid Gestationis
Treatment of PG
• Suppressing blister formation and relieving
pruritus.
• Prednisone, 20-40mg/d, higher doses may be
required, tapering to lowest effective dose.
• Refractive cases: cyclophosphamide, pyridoxine,
dapsone, cyclosprine, gold, methotrexate, and
plasmapheresis.
• No available controlled trials
• Follow up: risk for development of Grave’s dz.
Conclusion
• Pruritus in pregnancy can be due to a flare of
conditions before conception or related to
pregnancy specific dermatoses.
• Generalized pruritus without a rash should
prompt an evaluation for ICPbile acids.
• If pemphigoid gestationis is suspected, skin
biopsies are needed.
– Antepartum fetal monitoring may be indicated.
• Goal of treatment otherwise is symptom
relief.
Reference
• Olin, Stephen T. “Dermatoses of Pregnancy.”
Family Medicine Obstetrics. Ed. Stephen D.
Ratcliffe, et al. 3rd ed. Philadelphia, PA: Mosby
Elsevier, 2008. 317-321. Print.
• Woff, Klaus and Richard Allen Johnson.
Fitzpatrick’s Color Atlas & Synopsis of Clinical
Dermatology. New York: McGraw Hill, 2009.
Print.
• “Cholestasis of Pregnancy.” DynaMed. 01 Mar.
2010. Web 24 Apr. 2010
• Pictures are from UpToDate online 18.1,
“Dermatoses of Pregnancy”. Web 29 Apr. 2010