skin changes during pregnancy

1. Skin Changes and Disease in
Pregnancy
 By—
Dr. Usha Chandra
Department of Dermatology And Venereology
Institute of Medical science , B.H.U

2. •Cutaneous changes results from the altered
endocrine, metabolic and immunological milieus
that characterize pregnancy
•Cause physiological and pathological changes
both

3. Pigmentery changes(most common)
most marked in darker skin type
 due to oetrogen,progesterone ,MSH and other uncertain
factors.
1.Generalized or increase in pigment at specific areas such
as genital axillae, areolae, recent scars ,linea nigra.

4.  3.Melasma(chlosma ,
mask of pregnancy)-(70%)
• Irregular,blotchy,symmetrical
facial hyper pigmentation
due to epidermal melanin
deposition.
• Due to combination of light
exposure and elevated
hormone( estrogen,
progesterone and
melanocyte stimulating
hormone)
• May regress postpartum.

5. 4.Darkening of ephelids and melanocytic nevi-
 Can be confused with malignant melanoma(age
presentation).
 Can caused increase in dermoscopic Stole ABCD scoring
system(Asymmetry, Border change ,Color, Diameter) &
vascularity.
 Chan et al identified characteristic histological feature
unique to nevi including increase in mitotic index.

6. Hair changes
• During pregnancy, hair growth is more pronounced.
• In second half of pregnancy, changes are due to
androgen
 Hypertrichosis
 Hirsutism accompanied by acne(rarely virilization)
• In postpartum, compensatory decrease in hair growth
associate with shedding known as, telogen effluvium,
which recover within 6 to 12 months.
 Mild frontoparietal recession may occur.
 Postpartum androgenic alopecia

7. Hair changes
Androgenic alopecia Telogen effluvium

8. Nail changes –
Subungual hyperkeratosis.
Distil onycholysis.
Transverse grooving.
Brittleness of nail.
Accelerated growth of nail.
Longitudinal melanonychia

9. Vascular changes
 Occurs due to sustain high level of
oestrogen.
 Changes are similar to those seen
in hyperthyroidism or cirrhosis.
1. Spider angioma (spider nevi
aranei)- These have central
“ body” and small vessel (legs)
extending out from it. Occurs on
chest,leg,face.
Disappear postpartum.

10. Vascular changes
2. Palmer erythema.
3. Non pitting edema(50%) of hands,ankles,face,feets
more pronounced in early morning.
4. Varicosities of haemorrhoids ,leg(rare but serious
complication of deep vein thombosis,occasionaly death
occur d/t pulmonary embolism)
5. Cutis marmorata.
6. Hemangioendotheliomas, Unilateral neviods
telangiectasia (unilateral dermatomal superficial
telangiectasia)

11. Vascular changes
7. Vasomotor instability.
8. Dermatographism/ pruritis.
9. Pyogenic granuloma or granuloma gravidarum,
pregnancy epulis. (5%)
10. Purpura
11. Gingival hyperemia or hyperplasia(2%)

12. Vascular changes
Pyogenic granuloma Varicosities

13. Glandular function changes
1. Increased eccrine function (except palm) – It includes
miliaria ,dyshydrotic eczema, hyperhydrosis
2. Increase sebaceous function- Growth in Montgomery’s
tubercles, Acne (variant- pruritic folliculitis of pregnancy)
It return normal after delivery.
3. Decreased apocrine function( improved Fox Fordyce
disease).
4. Elevated thyroid activity with resultant relative iodine
deficiency.

14. Structural changes during pregnancy
1. Striae distensae/gravidarum-
Develop in 90% of pregnant in second
third trimester.
Pink to purple atrophic band at right
angle of skin tension
Most common over abdomen, breast,
thigh, buttock.
2. Molluscum fibrosum gravidarum

15. Mucosal changes
1. Jacquemier – Chadwick sign – It is bluish discoloration
of vagina and cervix
2. Goodell’s sign – cervical softening.
3. Gingivitis (marginal gingivitis, papillomatous
hypertrophy of gums )

16. SKIN INFECTIONS AFFECTING
PREGNANCY
 Human papilloma virus (condyloma lata)
Herpes simplex
Varicella zooster
HIV infection
Scabies

17. HUMAN PAPILLOMA VIRUS
Also k/a Condyloma acuminata.
Exacerbated or grow rapidly in second trimester.
Contain of epidermal or dermal papule or nodule on perineum
genital or crural fold or anus, of varying size.(Occasionally
obstructing birth canal)
Physical treatment should be done(cryotherepy,electrocautery)
Prevention – bivalent vaccine (Cervarix) against 16 & 18 and
quadrivalent (Gardasil) against 6,11,16,18.

18. HUMAN PAPILLOMA VIRUS

19. HUMAN PAPILLOMA VIRUS
 Infant have high risk of
laryngeal papillomatosis
(HPV 6 and 11)
 No link has been found
between HPV
and miscarriage,
premature delivery, or
other pregnancy
complications.

20. HERPES SIMPLEX VIRUS
Primary herpetic infection occur in 2% of pregnancy
More severe than non pregnant.
HSV1 is associated with herpetic gingivostomatitis
and pharyngitis.
Reactivation involves outer one third of lower lips,
most common.
HSV-2 involve genitalia (10 to 40% by HSV-1)

21. Development of vesicles, ulcer or hard crusts starting with
erythema and papule and then followed by dry flaking and
residual swelling.
 Primary and recurrent genital infection is indication of
caesarean section and treatment (acyclovir).
Babies with low birth weight infection can be life theatening
HSV can be vertically transmitted to the infant before,
during, or after delivery, although intrapartum transmission
accounts for most cases.

22. HERPES SIMPLEX VIRUS
Herpes Labialis Genital herpes

23. Varicella zoster
 Primary VZV infections occur in upto 1:2000 pregnancy.
 Primary infection have risk of pneumonia and encephalitis
(both in mother and child) ,spontaneous abortion, fetal
demise, and varicella embryopathy (eg, limb hypoplasia,
microcephaly, muscle atrophy, cataracts, and mental
retardation).
 Reactivation of latent varicella is not associated with faetal
risk
 High risk of fetal varicella syndrome (1-2%) infection during
13 to 20 weeks of gestation.
 Treatment should be done with intravenous or oral acyclovir.

24. Varicella zooster
Multiple, discrete,
vesiculopustular, and
maculopapular
lesions on an
erythematous base
Neonatal infection
may occur in 10% to
20% of neonates
whose mothers
became acutely
infected from 5 days
before delivery to 2
days after the
delivery.

25. Scabies
 Caused by the human mite Sarcoptes scabiei var hominis
 Areas affected include the fingers webs,flexor surfaces of
the wrist, axillae, waist, feet and ankles
 Primary lesions are the first manifestation of the typically
include small papules, vesicles, and burrows(S shaped).
 Secondary lesions are the result of rubbing and
scratching,they may be the only clinical manifestation.

26. Scabies
 No faetal risk.
 First line of treatment is topical permethrin 5%,
and antihistamine to reduce ithching.
oral ivermectin is not safe

27. HIV infection
 Skin disease which are characteristic of HIV are-
Oral hairy leukoplakia ,Bacillary angiomatosis ,Kaposi
sarcoma.
• ART can be given during labor or pregnancy.
• C section is considered if viral load is high.
• Breast feeding should be avoided.
• HIV positive infant should given pneumocystic
prophylaxis with co trimoxazole.

28. Oral Hairy - Bacillary angiomatosis Kaposi sarcoma
leukoplakia

29. Auto immune disorder in pregnancy
 Systemic lupus erythematosus
 Pemphigus vulgaris and foliaceus.

30. Systemic lupus erythrematosis
 Immune system in pregnancy cause shift from
predominantly TH1 lymphocyte to TH2 profile.
 Level of IL-12 and gamma interferon are reduced and
level of IL-4 10 are increased.
 So increase in susceptibility to skin disease like SLE.
 About 60% of women with pre existing SLE have flare
during pregnancy or puerperium.

31. Systemic lupus erythrematosis
 Cutaneous flare are most
common.
Fetal risk includes– spontaneous abortion, faetal loss,
preterm delivery, intra uterine growth restriction.
Corticosteroids are drug of choice but not reduce flares.
It can be associated with APLA syndrome with increased
risk of thromboembolism.

32. PEMPHIGUS
 Pemphigus vulgaris and foliaceus can both develop and
worsening during pregnancy.
 The primary lesion of pemphigus vulgaris is a flaccid
blister filled with clear fluid that arises on healthy skin or
on an erythematous base.
 Clinical symptom is similar to pemphigoid gestationalis.
 Featal prognosis is variable.
 Fetal skin shares same desmoglein3 profile as in oral adult
mucosa.

33. PEMPHIGUS
Flaccid bulla of pemphigus DIF of skin biopsy

34. PEMPHIGUS
 Treatment ladder-
First line- prednisolone
Second – azathioprine
Third- plasma exchange,plasmapheresis

35. INFLAMMATORY SKIN DISEASE
 Pustular psoriasis of pregnancy( impetigo
herpetiformis)
 Acne vulgaris and rosacea
 Pityriasis rosea
 Urticaria

36. Pustural psoriasis of pregnancy or
Impetigo herpetiformis
 Psoriasis typically improve during pregnancy, but in 10 to
20 % it can worsen.
 It is variant of Pustural psoriasis due to hormonal
alteration during pregnancy
 Classically during last trimester but occur as early as first
trimester resolve after delivery.
 Typically on flexures, spreads centrifugally sometimes
generalized. Mucosa rarely involves. Sparing face palm
and soles.

37. Pustural psoriasis of pregnancy
 Characterized by acute
eruption of
erythematous patches
whose margin are
studded with sub
corneal pustules with
constitutional
symptoms(eg. Fever,
tetany,hypocalcemia)

38.  Laboratory investigation shows anemia, leucocytosis
neutrophilia, increase in ESR, hypoalbuminia.
 Histopathology shows typical changes of pustular
psoriasis with parakeratosis and abscesses of
neutrophils (Kogoj's spongiform pustules).
 Recurrence with subsequent pregnancy are common
and characteristically more severe with onset earlier in
gestation.
 Featal risk –
Placental insufficiency, stillbirth or neonatal death.
Pustural psoriasis of pregnancy

39. Pustural psoriasis of pregnancy
 Treatment ladder—
 First line- emollients, topical steroids(low to mild )
Second line- narrow band UV-B or Braod Band UV-B
Third line-Ciclosporin ,systemic corticosteriod in
impetigo herpetiformis(second and third
trimester),tumor necrosis factors(adalimumab,
etanercept, infliximmab)

40. Acne vulgaris
 Occurs due to blockage and/or inflammation of
pilosebaceous units .
 Affecting face (mostly ),back and chest.
 Occurs due to increase in androgen level.
 It improve early but worsen in third trimester.
 Acne conglobata( severe) may require systemic
corticosteroids with or without oral antobiotic.
 Acne neonatoram may occur due to passive transfer of
materal androgen across placenta.

41. Acne vulgaris
acne vulgaris acne conglobata

42. Acne Rosacea
 Due to increase level of oestrogen.
 Affects the central region of the face presenting itself as
a flushing of the face, and then redness develops with
small red bumps and cysts similar to acne vulgaris
 Rosacea fulminans is rare
variant that may flare in
pregnancy.

43. Acne vulgaris and acne rosacea
 Treatment ladder –
First line- topical (azelic acid 10 -15%), benzoyl peroxide
gel (2.5 – 10%), oral erythromycin (avoid in first
trimester), oral azithroymycin.
Second line- narrow band UV-B
Third line- prednisolone( can be combine by oral
antobiotic)
Retinoid(oral / systemic) are avoided

44. Pityriasis Rosea
 Caused by HHV-6.
 Oval scaly plaque on trunk preceded
by “herald patch”.
 Can be asscociated with fetal demise
(in first trimester) premature delivary.
 Treatment is conservative as rash
fades.

45. Urticaria
 Differential diagnosis include pre bullous phase of
pemphigoid gestationis or polymorphic eruption of
eruption
Treatment –
 First line- topical emollient(aqueous cream and 1-2 %
menthol), oral histamines(loratadine and cetrizine).
 Second line- prednisolone.

46. Itching in pregnancy
Pruritus gravidarum
Occurs in one – fifth.
Intense pruritis in absence of primary cutaneous changes.
Mostly due to some underlying cause(urticaria,eczema,etc)
Mid form of reccurrent intra hepatic cholestasis of
pregnancy

47. Intra hepatic cholestasis of pregnancy
• Also known as obstetric cholestasis, cholestasis of
pregnancy, recurrent(45 to 75%) jaundice of pregnancy,
cholestatic jaundice of pregnancy, idiopathic jaundice
of pregnancy, icterus gravidarum, prurigo
gravidarum(ie.pruritis is not accompanied by jaundice).
• It is reversible(resolve within 2 to 4 weeks of after
pregnency).
• Multifactorial cause (hormonal, genetic ,
environmental and alimentary factor) which induce
biochemical changes in susceptible pregnancy.

48. Intra hepatic cholestasis of pregnancy
 Moderate to severe pruritis, begin during first (10%) and
second (25%) trimester.
 Localized to palm and soles or generalized.
 Primary cutaneous lesion are invariably absent but
intense pruritis associated with secondary excoriation.
 Progress to clinical jaundice(10%), often with
constitutional symptoms after 1 to 4 weeks of pruritis.
 Second cause of jaundice in pregnancy followed by viral
hepatitis.

49. Intra hepatic cholestasis of pregnancy
 Laboratory studies- Shows increase in serum bile
acids(single sensitive indicator) and correlates with
degree of pruritis
 Brites et al indentify following features-
1. Sr. TBA > 11 µM (normal 4.6 to 8.7 µM)
2. Cholic acid : chenodeoxycholic acid > 1.5 ( 0.7 to 1.5) or
choric acid proportion of TBA greater than 42%
3. Glycine conjugate:taurine conjugate of bile acids
<1.0(0.9 to 2.0) or glycocholic acid concentration greater
than 2.0 (0.6 to 1.5 µM)

50. Intra hepatic cholestasis of pregnancy
 Histopathology of skin not aid in diagnosis. Liver biopsy
reveals intrahepatic cholestasis with dilated , plugged bile
canaliculi and deposites of bile pigment.
 Fetal risks –
Increased rates of prematurity,intrapartal distress and
fetal death,intra/postpartum haemorrhage.
It generally correlated with acute placental anoxia and
increased of meconium stained amniotic fluid.
 Treatment is ursodeoxychilic acid , enhance efficiency
achieved by co administration with S-
adenosylmethionine.

51. Intra hepatic cholestasis of pregnancy
Treatment ladder-
 First line- topical emollient(aqueous cream and 1-2
% menthol), oral histamines(loratadine and
cetrizine), oral UDCA 15mg/kg/day.
 Second line- S-adenosyl-L-methionine,
dexamethasone, cholestyramine.
 Other- weekly CTG, maternal vitamin K
replacement,dexamethasone for fetal lung maturity.

52. SPECIFIC DERMATOSIS
 Polymorphic eruption of pregnancy.
 Pemphigoid gestationalis
 Atopic eruption of pregnancy

53. Pruritic urticarial papules and plaques of
pregnancy
(Polymorphic eruption of pregnancy)
• Also known as Bourne’s toxemic rash of pregnancy, nurse
late onset PP, toxic erythema of pregnancy
• Occurs in 1 in 160 pregnancies ,self limiting, primigravida,
in last trimester or immediate post partum (15%), may
recur in next multiple pregnancy.
• Aetiology- Abdominal distension leads to damage to
connective tissue due to overstreching.
Hormonal or imunological plays minimal role

54. Pruritic urticarial papules and plaques of
pregnancy
 Lesions are polymorphous,(most commonly, urticarial) of
1 to 2 mm surrounded by narrow pale hollow, typically
begin within striae on abdomen and thigh, papule may
coalesce to form plaque , vesicle may present (never
bulla) sparing periumblical region ,face , palm and sole.

55. Pruritic urticarial papules and plaques of
pregnancy
 Laboratory investigations are normal, decreased serum
cortisol.
 Histopathology shows nonspecifically, parakeratosis,
spongiosis with dermal edema and lymphocytic,
eosinophilic, neutrophilic infiltrate.
 DIF is negative.
 Duration of symptoms averaging 6 weeks of duration with
spontaneous remmission is the rule.
 no adverse fetal outcome.

56. Pruritic urticarial papules and plaques of
pregnancy
• Treatment ladder-
 First line- topical emollient(aqueous cream and 1-2 %
menthol), oral histamines(loratadine and cetrizine), toical
steroids,
 Second line- Prednisolone
consider early induction of labour if patient is close to term

57. Pemphigoid (herpes) gestationis
• Auto immune, pruritic ,rare roughly 1 in 50,000
pregnancies.
• It presents during late pregnancy (2nd or 3rd trimster,
mean onset 21st week) or immediate post partum.
• A mismatch HLA antigens between the mother and
father, manifested by immunologic response against the
paternal class II antigens( BP-180 or bullous pemphigoid
antigen 2) at placental BMZ with cross reaction at the
skin BMZ.

58. Pemphigoid (herpes) gestationis
•Acute onset, intensely
pruritic urticarial lesions
on abdomen(typical
site) in 50% of cases
with rapid progression
to generalized
,pemphigoid like
eruption. Sparing --
face,mucous
membrane, palm and
sole

59. Pemphigoid (herpes) gestationis
• The rash wax and wanes during pregnancy ,only to flare
during labor and delivery(75%) or post partum(25%).
 Can associated with trophoblastic tumours
(choriocarcinoma, hydatid moles) and Increased risk of
other auto immune disease like Grave’s disease.
 Foetal risk–
A. Newborn affected upto 10% of the time typically mild and
self limiting.
B. Slight increase in premature and small for gestational
age birth(not affected by treatment taken i.e.
Corticosteroids)

60. •
•Lab. investigations are normal(serum complements)
•Histopathology shows sub epidermal vesicles with
perivascular infiltrate of variable no. of eosinophils(more
common) and lymphocytes.
• DIF( Gold standard) shows C3(100%) with or without IgG in
a linear band along basement membrane zone
• PG ELISA test may replace IF though not all patient react
with BP120 (NC16A site)

61. Pemphigoid (herpes) gestationis
Treatment ladder-
 First line- topical emollient(aqueous cream and 1-2 %
menthol), oral histamines(loratadine and cetrizine),
potent topical steroids,
 Second line- Prednisolone(0.5 -1 mg/kg/day)
 Third line- azathioprine, plasma exchange, i.v. Ig

62. Atopic eruption of pregnancy
It is diagnosis of exclusion.
Most common dermatosis(50%) ,75% cases occur before
third trimester. Associated with reccurrence with good
prognosis.
A. E type or eczematous type- (two third)
also known as eczema of pregnancy
in second or third trimester
consist of eczematous patches and plaques
flexural extremity,face neck chest are involved.

63. Atopic eruption of pregnancy
B. P type or papular type - (one third)
Also known as prurigo of pregnancy, Besnier’s prurigo
gestationalis, nurse’s early onset prurigo of pregnancy, papular
dermatitis of Spangler, atopic eruption of pregnancy
Excoriating or crusted erythematous papules present.
Lesion present on extremities,occasionally on trunk, shin and
arms.
Key features is severe dryness, atopic minor feature according
to Hanifin & Rajka.

64. Atopic eruption of pregnancy
Treatment ladder-
 First line- topical emollient,oral histamines(loratadine and
cetrizine), topical steroids,
 Second line- Narrow Band UV B
 Third line- Azathioprine, Prednisolone

65. THANK YOU