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Dermatology Spot Diagnosis
Fatima Farid
Ped Resident Year 2 
Reading Recommendations 
2
Seborrheic Dermatitis
3
Case 1
• Seborrheic dermatitis is a recurrent, waxing and waning dermatosis which occurs on areas of the
skin in which sebaceous glands are most active such as the face, scalp & diaper area
• There are 2 peaks of the disease: infancy (within the first 10 weeks of life) & adolescence
• More common in males
• Incidence is 2- 5% of the population
• Lesions are of gradual onset, typically asymptomatic or mildly pruritic
4
• Type: patches with yellowish greasy scale which can be very thick & adherent
• Distribution: diffusely located around scalp, face, chest and diaper area
• Course/ prognosis:
• Infantile seborrhea is usually asymptomatic and clears spontaneously within months
• Childhood & adolescent seborrheic dermatitis can clear spontaneously but may have a
recurrent course
5
• Treatment:
• Scalp (cradle cap):
• Removal of the thick scale with mineral oil & a fine tooth comb can provide symptomatic
& cosmetic relief
• For older children recommend shampoos containing selenium sulfide, zinc pyrithione, tar
or ketoconazole used intermittently 2- 3 times per week . It is important to let the
shampoo sit on the scalp for 5 minutes before rinsing.
• Face & diaper area:
• Creams containing ketoconazole are helpful and safe; these may be used twice daily on a
regular basis for prevention. Low potency 2.5% hydrocortisone cream can be used twice
daily sparingly for 2- 3 days over active lesions during acute flares only.
6
7
Aplasia Cutis Congenita
Case 2
• Aplasia cutis congenita is a congenital defect of the scalp characterized by localized loss of the
epidermis, dermis and sometimes subcutaneous tissue
• Present from birth with equal distribution between males & females
• Unknown etiology for most cases, some may be attributed to genetic syndromes & teratogen
effects
• It is hypothesized that aplasia cutis congenita results from incomplete neural tube closure or an
embryonic arrest of skin development
8
• Lesion type: localized ulceration that is replaced by scar tissue (no hair or appendages present),
size 1- 3 cm (or larger), round/ oval/ stellate shape, pink/ red colour healing to white/ grey
• Number: 70% are solitary lesions, 20% two lesions & so on
• Distribution is mainly on scalp vertex, 50% midline; may rarely be seen on the face, trunk or
extremities
• Aplasia cutis congenita is usually an isolated finding, but may have an association with skeletal,
cardiac, neurologic or vascular malformations
9
• Prognosis of isolated aplasia cutis is good: ulceration heals with scarring in a few weeks, the
scarred area will persist as an asymptomatic lesion for life
• Treatment is mainly localized care at time of birth:
• Gentle cleaning of the area with warm water & cotton balls
• Thin layer of topical antibiotic ointment to prevent secondary bacterial infections
• Protective covering to prevent further trauma to the area
• The area will heal with scarring and as the child grows, the scar becomes inconspicuous & covered
by surrounding hair
10
11
on
Neonatal Lupus Erythematosus
Case 3
• Neonatal lupus erythematosus is an uncommon autoimmune disease caused by transplacental
autoantibodies from mother to the fetus
• The lesions may be accompanied by cardiac conduction defects, hepatobiliary disease or
hematologic disturbances
• Skin lesions may be present at birth or appear within the first few months of life. Typically resolve
by 6 months of age (by the time maternal autoantibodies are cleared from baby’s circulation).
Equal incidence among males and females.
• Pathophysiology: passage of maternal IgG antibodies (anti- Ro/ SSA in 95% of cases) through
placenta to fetal circulation. It is felt that these autoantibodies are implicated in the development
of cutaneous and systemic findings of NLE.
12
• About half of NLE cases exhibit skin disease, another half exhibit congenital heart block, only 10%
have both skin disease & heart block
• Skin findings: scaly plaques with epidermal atrophy, pink or hypopigmented in colour, round/
elliptical/ annular, frequently distributed on face & scalp with concentration in peri- orbital and
malar areas, widespread involvement may occur
13
• Mortality rate of NLE is 10% - mostly secondary to intractable heart failure in the neonatal period
• Risk of NLE recurrence in future pregnancies is 25% with one previously affected child
• Management focuses on identification of high risk mothers. Screening with anti- Ro/ SSA
antibodies in mothers who have:
• Features of Sjogren syndrome or SLE
• Previous birth with congenital heart block or other features of NLE
14
• Antenatal ultrasounds should search for features of fetal heart block & hydrops fetalis
• Only 1- 2% of babies of mothers who are antibody positive actually develop NLE
• 50% of mothers who deliver a baby with NLE are asymptomatic at birth
• Treatment: skin disease is usually benign and self- limited requiring only supportive care (sun
protection & topical steroids if severe disease)
15
16
Infantile Hemangiomas
Case 4
• These are benign vascular tumours that present soon after birth (within first few weeks of life)
• More common in premature infants
• Precursor lesions are pink/ bruised macule or patch with surrounding telangiectasias
• Superficial hemangiomas (strawberry hemangioma) are situated in the superficial dermis & bright
red in colour during the proliferative phase
• Deep or cavernous hemangiomas are located deep in the dermis or subcutis, present as a blue/
purple mass with normal overlying skin +/- bruit
• Involution occurs in 50% by 5 years & 90% by 9 years of age
17
• Complications include:
• Ulceration (most common)
• Anatomic distortion with interference of normal function
• High output congestive heart failure especially with liver hemangiomas
• Regionally significant hemangiomas:
• Peri- ocular: obstruct vision & may cause ophthalmologic complications
• Beard region: clue for laryngeal hemangiomatosis with airway obstruction
• Segmental hemangiomas over lumbo- sacral area: must rule out genito- urinary, GI, spinal &
skeletal abnormalities – needs MRI spine as well
• Nasal tip hemangioma: may result in textural changes & scarring
18
19
Scabies
Case 5
• Scabies is an infestation by the mite Sarcopetes scabiei characterized by severe pruritus
• Males & females are equally affected
• The scabies mite can only survive and replicate on human skin & are transmitted by close
proximity. Once on the human host, the scabies mite lays eggs under the skin as it burrows. The
ova hatch in 5 days, reach maturity in 2 weeks and then die after 2 months. The mites & eggs can
remain alive for 1- 2 days on clothes & bedding.
20
• Skin findings: burrows, vesicles, excoriations and scales/ crust with gray/ flesh coloured skin & a
black dot (mite), distribution can be over fingers, wrist, elbows, umbilical area, genital region &
feet
• Variants:
• Nodular scabies: 10 mm red nodular lesions over the scrotum, back & feet
• Norwegian scabies: widespread mite infestation causing crusted generalized rash
21
• Diagnosis is via scabies prep: scraping will reveal mites, eggs or feces
• Treatment:
• Scabicide such as permethrin 5% applied from neck to toes, left on for 8 hours then washed
off
• All family members & close contacts should be treated simultaneously and can be repeated
after one week to ensure successful eradication
• Residual pruritic symptoms & nodules are typical and do not indicate persistent infection.
Managed with symptomatic care: emollients, antihistamines & topical steroids
• Bedding & clothing should be machines washed in hot water & machine dried on high heat
• Infected articles can be stored in an airtight garbage bag for more than 72 hours so the mites
will die off
22
Thanks for your attention! 
References
• Dermatology – Illustrated Study Guide And Comprehensive Board Review, Second Edition
• Illustrated Manual Of Pediatric Dermatology Diagnosis And Management
• Colour Atlas And Synopsis Of Pediatric Dermatology, Second Edition
24

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Pediatric Dermatology Spot Diagnosis

  • 1. Dermatology Spot Diagnosis Fatima Farid Ped Resident Year 2 
  • 4. • Seborrheic dermatitis is a recurrent, waxing and waning dermatosis which occurs on areas of the skin in which sebaceous glands are most active such as the face, scalp & diaper area • There are 2 peaks of the disease: infancy (within the first 10 weeks of life) & adolescence • More common in males • Incidence is 2- 5% of the population • Lesions are of gradual onset, typically asymptomatic or mildly pruritic 4
  • 5. • Type: patches with yellowish greasy scale which can be very thick & adherent • Distribution: diffusely located around scalp, face, chest and diaper area • Course/ prognosis: • Infantile seborrhea is usually asymptomatic and clears spontaneously within months • Childhood & adolescent seborrheic dermatitis can clear spontaneously but may have a recurrent course 5
  • 6. • Treatment: • Scalp (cradle cap): • Removal of the thick scale with mineral oil & a fine tooth comb can provide symptomatic & cosmetic relief • For older children recommend shampoos containing selenium sulfide, zinc pyrithione, tar or ketoconazole used intermittently 2- 3 times per week . It is important to let the shampoo sit on the scalp for 5 minutes before rinsing. • Face & diaper area: • Creams containing ketoconazole are helpful and safe; these may be used twice daily on a regular basis for prevention. Low potency 2.5% hydrocortisone cream can be used twice daily sparingly for 2- 3 days over active lesions during acute flares only. 6
  • 8. • Aplasia cutis congenita is a congenital defect of the scalp characterized by localized loss of the epidermis, dermis and sometimes subcutaneous tissue • Present from birth with equal distribution between males & females • Unknown etiology for most cases, some may be attributed to genetic syndromes & teratogen effects • It is hypothesized that aplasia cutis congenita results from incomplete neural tube closure or an embryonic arrest of skin development 8
  • 9. • Lesion type: localized ulceration that is replaced by scar tissue (no hair or appendages present), size 1- 3 cm (or larger), round/ oval/ stellate shape, pink/ red colour healing to white/ grey • Number: 70% are solitary lesions, 20% two lesions & so on • Distribution is mainly on scalp vertex, 50% midline; may rarely be seen on the face, trunk or extremities • Aplasia cutis congenita is usually an isolated finding, but may have an association with skeletal, cardiac, neurologic or vascular malformations 9
  • 10. • Prognosis of isolated aplasia cutis is good: ulceration heals with scarring in a few weeks, the scarred area will persist as an asymptomatic lesion for life • Treatment is mainly localized care at time of birth: • Gentle cleaning of the area with warm water & cotton balls • Thin layer of topical antibiotic ointment to prevent secondary bacterial infections • Protective covering to prevent further trauma to the area • The area will heal with scarring and as the child grows, the scar becomes inconspicuous & covered by surrounding hair 10
  • 12. • Neonatal lupus erythematosus is an uncommon autoimmune disease caused by transplacental autoantibodies from mother to the fetus • The lesions may be accompanied by cardiac conduction defects, hepatobiliary disease or hematologic disturbances • Skin lesions may be present at birth or appear within the first few months of life. Typically resolve by 6 months of age (by the time maternal autoantibodies are cleared from baby’s circulation). Equal incidence among males and females. • Pathophysiology: passage of maternal IgG antibodies (anti- Ro/ SSA in 95% of cases) through placenta to fetal circulation. It is felt that these autoantibodies are implicated in the development of cutaneous and systemic findings of NLE. 12
  • 13. • About half of NLE cases exhibit skin disease, another half exhibit congenital heart block, only 10% have both skin disease & heart block • Skin findings: scaly plaques with epidermal atrophy, pink or hypopigmented in colour, round/ elliptical/ annular, frequently distributed on face & scalp with concentration in peri- orbital and malar areas, widespread involvement may occur 13
  • 14. • Mortality rate of NLE is 10% - mostly secondary to intractable heart failure in the neonatal period • Risk of NLE recurrence in future pregnancies is 25% with one previously affected child • Management focuses on identification of high risk mothers. Screening with anti- Ro/ SSA antibodies in mothers who have: • Features of Sjogren syndrome or SLE • Previous birth with congenital heart block or other features of NLE 14
  • 15. • Antenatal ultrasounds should search for features of fetal heart block & hydrops fetalis • Only 1- 2% of babies of mothers who are antibody positive actually develop NLE • 50% of mothers who deliver a baby with NLE are asymptomatic at birth • Treatment: skin disease is usually benign and self- limited requiring only supportive care (sun protection & topical steroids if severe disease) 15
  • 17. • These are benign vascular tumours that present soon after birth (within first few weeks of life) • More common in premature infants • Precursor lesions are pink/ bruised macule or patch with surrounding telangiectasias • Superficial hemangiomas (strawberry hemangioma) are situated in the superficial dermis & bright red in colour during the proliferative phase • Deep or cavernous hemangiomas are located deep in the dermis or subcutis, present as a blue/ purple mass with normal overlying skin +/- bruit • Involution occurs in 50% by 5 years & 90% by 9 years of age 17
  • 18. • Complications include: • Ulceration (most common) • Anatomic distortion with interference of normal function • High output congestive heart failure especially with liver hemangiomas • Regionally significant hemangiomas: • Peri- ocular: obstruct vision & may cause ophthalmologic complications • Beard region: clue for laryngeal hemangiomatosis with airway obstruction • Segmental hemangiomas over lumbo- sacral area: must rule out genito- urinary, GI, spinal & skeletal abnormalities – needs MRI spine as well • Nasal tip hemangioma: may result in textural changes & scarring 18
  • 20. • Scabies is an infestation by the mite Sarcopetes scabiei characterized by severe pruritus • Males & females are equally affected • The scabies mite can only survive and replicate on human skin & are transmitted by close proximity. Once on the human host, the scabies mite lays eggs under the skin as it burrows. The ova hatch in 5 days, reach maturity in 2 weeks and then die after 2 months. The mites & eggs can remain alive for 1- 2 days on clothes & bedding. 20
  • 21. • Skin findings: burrows, vesicles, excoriations and scales/ crust with gray/ flesh coloured skin & a black dot (mite), distribution can be over fingers, wrist, elbows, umbilical area, genital region & feet • Variants: • Nodular scabies: 10 mm red nodular lesions over the scrotum, back & feet • Norwegian scabies: widespread mite infestation causing crusted generalized rash 21
  • 22. • Diagnosis is via scabies prep: scraping will reveal mites, eggs or feces • Treatment: • Scabicide such as permethrin 5% applied from neck to toes, left on for 8 hours then washed off • All family members & close contacts should be treated simultaneously and can be repeated after one week to ensure successful eradication • Residual pruritic symptoms & nodules are typical and do not indicate persistent infection. Managed with symptomatic care: emollients, antihistamines & topical steroids • Bedding & clothing should be machines washed in hot water & machine dried on high heat • Infected articles can be stored in an airtight garbage bag for more than 72 hours so the mites will die off 22
  • 23. Thanks for your attention! 
  • 24. References • Dermatology – Illustrated Study Guide And Comprehensive Board Review, Second Edition • Illustrated Manual Of Pediatric Dermatology Diagnosis And Management • Colour Atlas And Synopsis Of Pediatric Dermatology, Second Edition 24