PEDIATRIC DERMATOLOGY

Dr. Angeles, October 5, 2017 2.04

I. LAYERS OF THE SKIN Epidermis
II. PHYSICAL EXAMINATION OF THE SKIN Dermis – where collagen, elastic fibers, adnexal structures (i.e.
A. Primary Skin Lesions hair follicles, sebaceous glands, eccrine glands, apocrine glands,
B. Secondary Skin Lesions blood vessels) are found
III. THE NEONATE
A. Cutis Marmorata II. PHYSICAL EXAMINATION OF THE SKIN
B. Harlequin Color Change
C. Salmon Patch When examining a patient presenting with skin lesions, the order
D. Dermal Melanocytosis of examination is backwards in comparison with an internal
IV. VASCULAR ANOMALIES medicine patient. With IM patients, you try to get the history
A. Capillary Malformation first. In dermatology, you look at the skin lesions or do the PE
B. Infantile Hemangioma first or in conjunction with the history taking because depending
V. CUTANEOUS NEVI on the primary lesion, we can ask more directed, intelligent, and
A. Acquired Melanocytic Nevus relevant questions.
B. Congenital Melanocytic Nevus
C. Nevus of Ota II-A. PRIMARY SKIN LESIONS
D. Nevus of Ito
E. Epidermal Nevus Table 1. Primary skin lesions.
VI. CUTANEOUS MANIFESTATIONS OF SYSTEMIC DISEASE Lesion Description Example
A. Autoimmune Macule Flat
B. Vasculitides
< 1 cm
VII. ECZEMATOUS DISORDERS
Skin color change
A. Eczema Dermatitis
B. Atopic Dermatitis
C. Dyshidrotic Eczema Patch Flat
D. Nummular Eczema > 1 cm
E. Seborrheic Dermatitis Skin color change
F. Allergic Contact Dermatitis
G. Irritant Contact Dermatitis
VIII. BACTERIAL INFECTIONS Papule Elevated
A. Impetigo < 1 cm
B. Cellulitis Varying colors
C. Infections of the hair follicle
IX. CUTANEOUS FUNGAL INFECTIONS
Plaque Elevated
A. Tinea Versicolor
> 1 cm
B. Dermatophytoses
C. Tinea Infections Varying colors
D. Candidal Diaper Dermatitis
X. CUTANEOUS VIRAL INFECTIONS Nodule > 1 cm
A. Verruca Elevated
B. Molluscum Contagiosum Rounded surface
XI. ARTHROPOD BITES
XII. INFESTATIONS
A. Scabies Tumor Larger than a nodule
B. Pediculosis Rounded surface
NOTE: Header marked with * was discussed but not included in the Primary lesion of
lecturer’s powerpoint. It was taken from the recording or 2018 trans. cancers like squamous
cell carcinoma
I. LAYERS OF THE SKIN Wheal Evanescent (comes and
goes within 24 hours)
edematous plaque

Vesicle < 1 cm
raised
Clear-fluid filled

Bullae > 1 cm
Figure 1. Layers of the skin. Raised
Functions of the skin: Clear-fluid filled
o Protection
Pustule Elevated
o Vitamin D synthesis
Yellowish fluid filled
o Sensory perception
o Fluid balance
o Thermoregulation

1 of 16|Pediatric Dermatology (Ilagan, Imperial, Jacinto, Juliano, Laganse) | Edited by: Dorosan
2.04 Pediatric Dermatology [Dr. Angeles]

.00 II-B. SECONDARY SKIN LESIONS III. THE NEONATE

Result from patient’s manipulation of primary skin lesion  Evanescent lesions of newborn infants may cause undue
anxiety and concern
Table 2. Secondary skin lesions.  These are transient, benign conditions that do not require
Lesion Description Photo intervention
Scale Desquamating
stratum corneum III-A. CUTIS MARMORATA

Crust Dried serous

exudates and debris

Figures 2. Cutis marmorata of the face, leg.

Excoriation Removal of  Evanescent, lacy, reticular red and/or blue cutaneous vascular
epidermis due to pattern appears over most of the body surface
scratching  Exposure to low environmental temperatures
 An accentuated physiologic vasomotor response to cold
 Disappears with increasing age, but sometimes discernible in
Fissure Linear break in the older children
skin (epidermis + o Usually transient and is outgrown by the baby
dermis)
III-B. HARLEQUIN COLOR CHANGE

Erosion Focal loss of

epidermis, (-)
scarring

Ulcer Loss of entire

epidermis
Figure 3. Harlequin color change.
 Infant placed on one side  body is bisected longitudinally into
a pale upper half and a deep red dependent half (erythema on
Petechiae, Small reddish flat one side of the body)
can also be lesion due to bleeding  Color change lasts for a few minutes, usually outgrown by
ecchymosis into the skin patient
Usually because blood  Repeated episodes may occur
has seeped into dermis  Temporary imbalance in the autonomic vascular regulatory
Purpura Red-purple color, mechanism
bleeding into the
III-C. SALMON PATCH
skin
Usually elevated

Atrophy Reduction in skin

thickness

Lichenification Accentuation of skin Figure 4. Salmon patch (nevus simplex).

markings and lines  Nevus simplex
Caused by  Ill-defined, erythematous macule or patch
chronic/constant  Becomes more visible and accentuated during crying or
rubbing or scratching changes in the environmental temperature
of the skin  Usually symmetric, on both sides of the midline
o Usually midline if found in the forehead
 Glabella, eyelids, upper lip, nuchal area
 Facial lesions eventually fade and completely disappear
 Lesions on the nape, nuchal, and occipital areas usually persist
2 of 16| Pediatric Dermatology (Ilagan, Imperial, Jacinto, Juliano, Laganse) | Edited by: Dorosan
2.04 Pediatric Dermatology [Dr. Angeles]

.00 III-D. DERMAL MELANOCYTOSIS IV-B. INFANTILE HEMANGIOMA

Figures 8.A: superficial type, B: mixed type, C: deep type.

Figures 5. Dermal melanocytosis (Mongolian spots).
 “Mongolian spots”  Most common tumor of infancy
 Blue-slate gray macules or patches  Proliferative, benign vascular tumor
 Most commonly in pre-sacral area  At birth, but more commonly become apparent in the first 2
 Usually fade during the first few years of life months of life
o In some patients, presence may persist but become lighter in  Types:
color over time o Superficial: very bright red/pinkish
 More common in Asians and Hispanics vs. Caucasians o Mixed
o Deep: violaceous discoloration
IV. VASCULAR ANOMALIES  Most are of the mixed type
 Course:
Two types:
o Unpredictable, but spontaneous resolution is seen in:
o Malformation
 60% at 5 years old (according to Nelson’s)
o Tumor of the blood vessels
 90-95% at 9 years old
IV-A. CAPILLARY MALFORMATION  According to Dra., they usually just say: 50% by 5 years
old, 60% by 6 years old, until 90% by 9 years old –
easier to remember
 Complications:
o Ulceration
o Bleeding
o Disfigurement
o May obstruct vital organs such as the eyes, urethra,
subglottis, nostrils, lips and mouth
Figures 6. Capillary malformation (Port-wine stains).
 “Port-wine stain”
 Pinkish-purplish macules-patches
 Mature dilated dermal capillaries
 Head and neck region as common sites
 Present at birth
 Most are unilateral (unlike salmon patch which are usually found
midline or bilateral) Figures 9. Complications of IH. Left: ulceration, right:
 Becomes darker as child matures; persist with age disfigurement, obstruction of eye.
 Management: pulse dye laser
o One spectrum of the UV radiation that specifically targets Table 3. Management.
hemoglobin; usually entails several treatment sessions Observation, Uncomplicated IH without obstruction of any
before there is a decrease in the size of the PWS or complete reassurance vital organs;
resolution if at all it will be attained Reassure parents with rates of resolution
 May be associated with: previously mentioned
o Sturge-Weber syndrome – glaucoma, leptomeningeal Monitor growth
venous angioma, seizures, hemiparesis contralateral to Topical timolol Small, superficial, non-ulcerating IH
the PWS solution
o Klipper-Trenaunay syndrome – PWS + varicosities + Intralesional Localized IH but w/ risks of ulceration, atrophy
hypertrophy of bone and soft tissue + ophthalmic corticosteroids
abnormalities Oral propranolol First line of treatment for disfiguring, life or
o Beckwith-Wiedemann syndrome vision-threatening or ulcerated lesions.
Adverse events: hypotension, hypoglycemia,
bradycardia
Systemic For patients unable to tolerate and/or non-
corticosteroids responsive to propranolol

Figure 7. Sturge-Weber syndrome. Port-wine stains and glaucoma.

3 of 16| Pediatric Dermatology (Ilagan, Imperial, Jacinto, Juliano, Laganse) | Edited by: Dorosan
2.04 Pediatric Dermatology [Dr. Angeles]

.00

Figure 14. Dermal Nevus all the pigment is in the dermis so it is

usually skin color to pinkish

Figure 10. Top: before and after treatment with oral V-B. CONGENITAL MELANOCYTIC NEVUS*
corticosteroids, bottom: before and after treatment with  Present in 1% of newborns
propranolol.
 Rare condition but cases have been seen in UERM
 Seen in the reticular dermis
 Classification
o Small
  1.5 cm
 Usually not associated with any systemic involvement
 Usually not associated with malignant melanoma
o Intermediate
o Giant
Figure 11. Segmental hemangioma on the face, occluding the right
 Associated with melanoma; thus, patient must be
eye. Management: propranolol (2 mg/kg/day); when giving
observed
propranolol, monitor patient for cardiovascular side effects
V-C. NEVUS OF OTA*
V. CUTANEOUS NEVI
 More commonly found in females and in Asians
V-A. ACQUIRED MELANOCYTIC NEVUS  Usually manifests as bluish patch on the face
 Does not disappear with age, and may even enlarge or darken
 Nests of melanocytes in epidermis, dermis, or both epidermis
 Management
and dermis
o Concealer is your best friend
The location of the nevus cells will dictate as to what kind of
o Laser therapy
mole you have
 At wavelengths that specifically target melanin
 Benign, very small percentage of malignant transformation
 The number of nevi increases gradually during childhood and
more slowly in adulthood, with a plateau during in the 3rd to
4th decade
 The number of nevi the greater the risk for melanoma
 Types
o Junctional nevus
 Flat and usually brownish in color
o Compound nevus Figure 15. Nevus of ota.
 Elevated and hyperpigmented nodule or plaque
o Dermal nevus V-D. NEVUS OF ITO*
 Pigment is in the dermis
 No hyperpigmented discoloration  Bluish discoloration found on the supraclavicular, scapular, and
 Usually skin colored, yellowish, pinkish nodule deltoid
 More diffuse, less speckled or mottled
 Management
o Laser therapy
 But since it can be hidden, usually they don’t have it
treated

Figure 12. Junctional Nevus is generally flat and brown in color

Figure 16. Nevus of ito.

Figure 13. Compound Nevus raised and hyperpigmented plaque

4 of 16| Pediatric Dermatology (Ilagan, Imperial, Jacinto, Juliano, Laganse) | Edited by: Dorosan
2.04 Pediatric Dermatology [Dr. Angeles]

.00 V-E. EPIDERMAL NEVUS

 Verrucous or hyperkeratotic plaques usually with linear
configuration
 May be associated with abnormalities especially if it is
widespread such as congenital dysplasia syndromes or proteus
syndrome Figure 18. (from left to right) A. Malar rash B. discoid lupus lesions
o Hemihypertrophy of the area where the nevi are C.oral uclers
 Can be excised or topical medication
VI-A-2. DERMATOMYOSITIS
 Multifactorial: genetics +environmental factors
 Most common inflammatory myositis In children
 Proximal muscle weakness +rash (has a hard time standing from
sitting or combing their hair)
Figure 17. Epidermal nevus.
 Rash develops as the first symptom or sign in 50% of the cases
VI. CUTANEOUS MANIFESTATIONS OF SYSTEMIC DISEASE  Signs and symptoms of Juvenile dermatomyositis
o Heliotrope rash – erythematous, violaceous periocular
Table 12.Only SLE, dermatomyositis, and Henoch Schonlein Purpura discoloration or patch (peri orbital area)
were dicussed o Gottron papules – erythematous papules on the knuckles
Autoimmune disorders Vasculitides o Shawl sign – poikilodermatous (dyspigmentation and
Lupus erythematosus Henoch Schonlein purpura telangiectasia) eruption on the back and shoulders
Dermatomyositis Kawasaki disease  photodistributed patches
Systemic sclerosis Behcet’s disease o V sign – poikilodermatous lesions on the chest

VI-A. AUTOIMMUNE Table 5. Diagnostic Criteria for Juvenile Dermatomyositis

VI-A-1. SYSEMIC LUPUS ERYTHEMATOSUS

Table 4. Classification criteria for systemic lupus erythematosus

 Presence of 4 (including 1 clinical +1 immunologic criterion)

establishes the diagnosis of SLE
 Idiopathic inflammatory autoimmune response
 May be systemic or localized to the skin
The erythema usually spares the knuckles
 Cutaneous findings in SLE Figure 19. Signs and symptoms of Dermatomyositis
o Malar rash (associated with acute SLE)
 thin scaly erythematous plaques VI-B. VASCULITIDES
o Discoid lupus lesions
o Photosensitive erythematous macular or popular eruption VI-A-1. HENOCH SCHONLEIN PURPURA
o Oral or nasal ulcers
o Non-scarring alopecia (patchy or diffused)  Vasculitis means there is destruction of blood vessel walls
o Others  Most common vasculitis in children
 Livedo reticularis  Palpable purpura dependent areas
 erythematous patches on hands o Buttocks and legs
 Raynaud’s phenomenon o Usually resolves spontaneously without any medical
 Thrombocytopenic and non-thrombocytopenic intervention
purpura o Usually on the lower extremities

5 of 16| Pediatric Dermatology (Ilagan, Imperial, Jacinto, Juliano, Laganse) | Edited by: Dorosan
2.04 Pediatric Dermatology [Dr. Angeles]

.00 o If the erythema is caused by true purpura, vasculitis, or VII-A. ECZEMA DERMATITIS
extravasation of blood cells, the erythema will not go away
when a glass slide is pressed over it  Acute
 Small vessels vasculitis affecting school age children o Erythematous macules, papules
o H – hematuria o Swelling or edema
o S – spots on the buttocks, legs and feet o Vesicles, bullae
o P – purpura  Subacute (secondary due to pruritus)
o A – any IgA immune complex deposition o Excoriations
 Extraneous manifestation o Crust, scabs, and scales
o GIT – abdominal pain, vomiting, diarrhea (70-80%) o Slight thickening of the skin
 GIT is the most common o There are secondary lesions already
o Musculoskeletal – arthritis, arthralgia (50%)  Because these dermatitis are usually pruritic
o Renal – microscopic hematuria proteinuria (urinalysis)  Chronic
 Ask for urinalysis o Lichenificationand scaling are pronounced
o Neurologic – headaches, intracerebral headaches o Well defined lesion
 Management o Scale desquamation
o Usually spontaneously resolves o If left untreated or the patient still has uncontrolled eczema
o Hydration
o Analgesics
o Oral corticosteroids
o If the symptoms are not so great, opt to give analgesics
because this may be painful due to inflammation

Table 6. Classification criteria for Henoch schonlein purpura. 2 of

the following must be present

Figure 21. (top to bottom) Acute, Subacute, Chronic

VII-B. ATOPIC DERMATITIS

 Very pruritic dermatitis
 Most common chronic relapsing skin disease seen in infancy
and childhood or even adulthood
 Pathology
o There is imbalance in cell immunity favoring Th2
o Unable to maintain skin moisture
 Have defective skin barrier and are unable to maintain moisture
because of lack of a certain fatty acid in the stratum corneum of
the skin
Figure 20. (left to right) A. On glass slide test the redness will not go  Onset: infancy, 50% experience symptoms in 1st year of life
away B. Palpable purpura C. Immunoflorences: Circular flourences  Hallmark: severe dryness of the skin
IgA complexes  Acute AD
o Erythematous, intensely pruritic papules and plaques
VII. ECZEMATOUS DISORDERS  Subacute AD
o Erythematous, excoriated, scaling plaques
 Divided into two  Chronic AD
o Endogenous o Lichenification
 Comes from within
 Body’s reaction to stress
o Exogenous
 Develop as a response to something that it is exposed to

Figure 22. (left to right) Acute AD, Subacute, Chronic

6 of 16| Pediatric Dermatology (Ilagan, Imperial, Jacinto, Juliano, Laganse) | Edited by: Dorosan
2.04 Pediatric Dermatology [Dr. Angeles]

.00 VII-B-1. MAJOR FEATURE Very important even without rash

 Having a dry skin could cause itchiness so it is
Table 7. Clinical features of atopic dermatitis important to still apply moisturizer
 If the patient has dry skin, he/she may scratch
his/herself and may have rash after
 WET WRAPS
o Promotes transepidermal penetration of topical
medications
o Effective barrier against scratching
o You may use gauze (see Figure 24)

 Pruritus
 Area of predilection
o Infants and children: face (cheeks) and extensor surfaces
o Adolescents: flexural areas (popliteal fossa, antecubital
fossa)
 Chronic and relapsing
 Personal or family history of atopic disease
o e.g. allergic rhinitis, bronchial asthma
Figure 24.After putting moisturizer or corticosteroid, you may wrap
 Associated features the baby in gauze or put occlusive garments so that the penetration of
o Dry skin the moisturizer would be enhanced; also it would prevent the baby
o Hyperpigmented discoloration of the eyes (Dennie-Morgan from scratching the lesion.
sign)
o Sparing the area around the nose eyes and mouth
 TOPICAL CORTICOSTEROIDS
o Cornerstone of anti-inflammatory treatment for acute
exacerbations of AD
 Usually given to patients with atopic dermatitis
o Ointment preferred over creams (Ointment >> Creams)
 Ointments are usually given instead of creams because
the ointment is more moisturizing and creams have a
Figure 22. Dennie-Morgan fold (extra infraorbital fold) and hyper lot of additives so patients with asthma of the skin
linear palms become highly irritated
o Lotion preparation for large surface areas
 If the patient has a lot more lesion, a lotion preparation
would be more practical
o Grouped based on potency (See tables below)
Note that not all steroids have the same potency

Figure 23. Facial erythema with oral (periorificial) sparing Table 8. Selected Topical Corticosteroid Preparations

VII-B-2. NONMEDICAL MANAGEMENT

 Avoid triggers: remove identified triggers for eczema
o Clothing: wool, too warm clothing
o Cool temperature
o Food allergens
o Aeroallergens
o Food
 Food allergy in 40% of infants and young children
with moderate to severe atopic dermatitis (AD)
 Soy, egg, milk, peanut, & wheat
 A holistic approach

VII-B-3. MEDICAL MANAGEMENT

 MOISTURIZERS
o First line therapy
o Bathe for 15-20 mins then apply an occlusive emollient to
retain moisture
limit the bathing time of the child to prevent
drying/dehydration of the skin *Note: Group 1 - Superpotent; Group 7 - Least Potent steroids

7 of 16| Pediatric Dermatology (Ilagan, Imperial, Jacinto, Juliano, Laganse) | Edited by: Dorosan
2.04 Pediatric Dermatology [Dr. Angeles]

.00
Table 9. Group of steroids based on potency o Short-term or intermittent long-term treatment for
Group Indications chronic dermatitis of > 2 y/o
Superpotent 1 Not on face o Not usually used
Steroids Use for short periods only  PHOTOTHERAPY
For adults For severe and generalized, non-responsive atopic
For children: applied on thick dermatitis to steroids
skin palms & soles o We have it here in UERM; more often used for patients with
Avoid in infants because it’s very psoriasis than AD
potent! o Emits narrow band UVB so it has therapeutic effects by
Midpotent 2 to 6 For chronic AD down regulating immune cells in the skin
Steroids For the trunk
May be used longer periods VII-B-4. COURSE AND PROGNOSIS
There should be a rest phase
 More severe & persistent in young children
Least potent 7 Face, flexural areas
 Periods of remission occur more frequently as one ages
steroids For thin skin
 AD resolves in 20% of infants with AD & becomes less severe in
Genital area, also the axilla (areas
65%
with occlusion)
Chronic & relapsing
Adults: poorer prognosis; lasts longer
Infants/Children: higher chance to outgrow AD
Predictive Factors for Poor Prognosis:
1. Widespread AD in childhood
2. Fillagrin gene null mutation
3. Concomitant allergic rhinitis & asthma
4. Family history of AD in parents, sibling
5. Early age at onset of AD
6. Being an only child
7. High serum IgE levels

VII-C. NUMMULAR ECZEMA*

 Coin-shaped; Erythematous on the lower legs
Figure 25. Adverse Effects of Corticosteroids: For topical
 Flares precipitated by cirrhosis
corticosteroids, we do not let them use it for more than 2 weeks on the
 Not so common in infants
same area because patients may develop striae or steroid-induced
 Manage with topical corticosteroids
acne.

 SYSTEMIC CORTICOSTEROIDS
o Rarely indicated
o Associated with severe rebound flare of AD after
discontinuation
 ANTIHISTAMINES
o Reduces histamine-induced pruritus; to address itchiness
o Sedating antihistamines at bedtime
Figure 26. Nummular Eczema in an infant (image from the internet)
 1st generation is given at night because they are
sedating VII-D. DYSHIDROTIC ECZEMA
 They can take the 2nd generation in the morning if one
antihistamine would not suffice but others would still  Pruritic vesicles on the lateral aspects of the digits of the
experience sedation hands & feet, palms & soles
Table 10. 1st and 2nd generations of antihistamines (PPT) First appears on the lateral aspect of your fingers/toe then later
1st generation 2nd generation Intranasal 2nd on your palms & soles
antihistamines antihistamines generation Very itchy
antihistamines Precipitated by stress
Brompheniramine Cetirizine Azelastine
Chlorpheniramine Loratadine* Olopatadine
Clemastine Fexofenadine*
Diphenhydramine Desloratadine*
Hydroxyzine Levocetirizine
*non-sedating antihistamines

 TOPICAL CALCINEURIN INHIBITORS Figure 27. Dyshidrotic eczema: Fingers/toes  palms/soles

An option aside from corticosteroids; steroid-sparer
o Pimecrolimus
o Tacrolimus ointment
8 of 16| Pediatric Dermatology (Ilagan, Imperial, Jacinto, Juliano, Laganse) | Edited by: Dorosan
2.04 Pediatric Dermatology [Dr. Angeles]

.00 VII-D-1. MANAGEMENT

 Aluminum salts (tawas)
 Saline soaks
 Topical corticosteroids with or without occlusion
Usually the potent corticosteroids are given since they are found
on the hands or on the palms where skin is very thick Figure 29. (Left to right): Rhus dermatitis due to poison ivy/oak;
Allergic Contact Dermatitis to rubber or leather shoes; Nickel
VII-E. SEBORRHEIC DERMATITIS dermatitis
 Unknown cause VII-G. IRRITANT CONTACT DERMATITIS
 Malasseiza furfur has been implicated
 Greasy, scaly plaques on the scalp, face (nasolabial fold,  Also an exogenous dermatitis
glabellar area), chest  Results from prolonged or repetitive contact with physical,
 If it involves the face usually at the glabellar area, or around the chemical, or mechanical irritants
eyebrows, and in nasolabial folds or near the nose o Saliva, urine, feces, detergents, dyes, henna, plants
 Can also be found on the cheeks, inguinal area of babies Does not only present with pruritus but patient may have
In adults, it is not greasy; your seborrheic dermatitis comes in the painful sensation as well
form of dandruff Due to a base or acid

Figure 30. Left: Irritant diaper dermatitis: usually spares the crural
folds; due to elevsted pH, urinary & fecal enzymes, friction &
occlusion. Change diaper frequently. Right: Lip-licking dermatitis:
happens when the child licks their lips because saliva is acidic

Figure 28. Seborrheic dermatitis seen on the scalp, face, inguinal

area, and cheeks.

VII-E-1. MANAGEMENT
 Mild shampoo
 Baby oil to remove the scales before applying topical steroids;
emollients as needed if area is dry Figure 31. If you have lesions predominantly on dorsum of the hand
 Topical steroids: what we usually give think of irritant contact dermatitis first over dyshidrotic eczema
 Topical antifungals: can also be an option because certain fungus because the latter have vesicles on sides of fingers and palms. The
are implicated as cause dorsum has thinner skin than palm, thus irritant easily penetrates the
skin unlike the palm which is thick and is protected from irritant.
VII-F. ALLERGIC CONTACT DERMATITIS
VII-G-1. DIAGNOSTICS
 Exogenous dermatitis
 T-cell mediated delayed hypersensitivity reaction
 Sensitization to the antigen is required – no dermatitis on 1st
contact/exposure
o Not elicited during the 1st contact with an allergen;
subsequent exposures then lead to cutaneous reaction
o Example – dyeing of hair
 Cells are desensitized the first time wherein the cells
recognized the allergen but it takes time for them to
bring it to the lymphatics; the 2nd time you get hair Figure 32. Patch test done to diagnose Allergic Contact Dermatitis
dyed then you get an erythematous, swollen reaction (ACD)
on your scalp
 History & PE
VII-F-1. CLINICAL MANIFESTATIONS  Patch test
o Put allergens pasted on your back then after 3 days, the
 Erythematous plaques taking the shape of the object that
physician will interpret if you are positive for certain
has the allergen
allergens and would look for certain cutaneous signs such as
o Rashes appear on the area and configuration with the
erythema
allergen
o If it turns red  allergic to that substance

9 of 16| Pediatric Dermatology (Ilagan, Imperial, Jacinto, Juliano, Laganse) | Edited by: Dorosan
2.04 Pediatric Dermatology [Dr. Angeles]

.00 VII-G-2. MANAGEMENT

 Avoidance of contactant
 Topical corticosteroids

Figure 34. Bullous Impetigo.

Diagnosis: Contact dermatitis
Diagnosis: Dyshidrotic eczema
(may be due to laundry soap,
rubber or latex gloves)
Recall: appears on the palm &
on the lateral aspect of
fingers/toes; thick skin
Recall: on the dorsum of the
hand & on thin skin
VIII-A-3. COMPLICATIONS
 Rare
Don’t usually spread to internal organs unless they are not
properly treated or they become very severe
 Osteomyelitis
 Septic arthritis
 Pneumonia
 Acute post-streptococcal glomerulonephritis
o Streptococci has propensity to go to the kidneys

VIII. BACTERIAL INFECTIONS

VIII-A. IMPETIGO
Most common bacterial infection found in children

VIII-A-1. NON-BULLOUS
Figure 35. Complications of Impetigo.
 More common form of impetigo
o >70% of cases VIII-A-4. MANAGEMENT
 Due to Staphylococcus aureus
 Children of all ages & adults  Depends on the severity and location
Classically, you have a vesicle or pustule that rapidly develops  Topical therapy
into a honey-colored crusted plaque (usual description) o For localized disease, S. aureus
 Portal of entry  Mupirocin 2%
o Areas of traumatized skin  2-3x a day for 10-14 days
 Let’s say, you have a patient with atopic dermatitis or  Or give Fusidic Acid because of increase in
any form of eczema or any itchy lesions or lesions that Mupirocin resistance
have been traumatized or if you have a wound, then it  Retapamulin 1%
can be impetiginized or you can have impetigo  2-3x a day for 10-14 days
 Area of predilection  Systemic therapy
o Face If it’s severe, or for bullous impetigo, wherein you don’t have
 Peri-nasal open skin
The nostrils really have S. aureus, but sometimes  So the medicine can be absorbed
when the immune system is down or when we o Cephalexin 25-50 mg/kg/day
have open wounds there, there may be an  3-4x a day for 7 days
overgrowth of S. aureus  Or Cloxacillin
 Peri-oral o For Methicillin-resistant Staphylococcus aureus (MRSA)
o Areas of traumatized skin  Clindamycin
 Regional adenopathy in 90% of the cases  Doxycycline
 Sulfamethoxazole-trimethoprim

VIII-B. CELLULITIS*
 Deeper infection in the skin
Usually in the subcutaneous area
 Etiologic agents
Figure 33. Non-bullous Impetigo. o Staphylococcus
o Streptococcus
VIII-A-2. BULLOUS  Portal of entry
o Traumatized skin
Primary lesion is bullae or vesicle
 Erythematous patch
 Group A -hemolytic streptococci
When you touch it, it’s warm and painful
 Infants and young children
 Diagnosis is usually made clinically
 Flaccid bullae that turns into erosions
When in doubt, you may do cultures, but usually clinically
 Develop on intact skin
you will know if the patient has cellulitis
 No adenopathy
10 of 16| Pediatric Dermatology (Ilagan, Imperial, Jacinto, Juliano, Laganse) | Edited by: Dorosan
2.04 Pediatric Dermatology [Dr. Angeles]

.00
 Management VIII-C-4. DIAGNOSTICS
o Antibiotics
 Cloxacillin  Clinical
 Cephalosporin  Gram stain – most common causative agent is S. aureus (gram
If allergic to penicillin, do not give cloxacillin; give positive)
cephalosporin instead
IV antibiotics may be given to patients with severe cellulitis, VIII-C-5. MANAGEMENT
or to those who are immunodeficient
 Non-drug
VIII-C. INFECTION OF THE HAIR FOLLICLE* o Antibacterial soap
o Loose fitting clothes
 Superficial infection  Very tight clothing may traumatize your skin
 Small pustules  Tight clothes can cause sweat to be left there,
 Portal of entry lacerating the skin
o Impaired integrity of skin surface caused by o Moist heat, warm compresses
 Irritation o Incision and drainage
 Pressure  Especially for carbuncle
 Friction o Bed rest
 Hyperhidrosis o Immobilize involved area
 Dermatitis o Hand washing
 Dermatophytosis  Drug therapy
 Shaving o Systemic antibiotics
 Patients are usually healthy individuals, but the condition may  Especially for furuncles and carbuncles
be associated with  Cloxacillin – 30-50 mg/kg/day QID
o Obesity, blood dyscrasias, defect in neutrophil function  Cefalexin – 25-50 mg/kg/day TID
o Treatment with steroids & cytotoxic agents  PCN allergy
 Erythromycin – 30-50 mg/kg/day BID
VIII-C-1. FOLLICULITIS  Clarithromycin – 15 mg/kg/day BID
 Clindamycin
 Infection of the superficial part of the hair follicle;  In dangerous area
folliculocentric o Use maximal dosage of antibiotics
 Men can get this when they shave and don’t clean their shavers
or they’re in a hurry and the nick their skin IX. CUTANEOUS FUNGAL INFECTIONS
VIII-C-2. FURUNCLE
IX-A. TINEA VERSICOLOR*
 Infection of the deeper part of the hair follicle
 Aka “an-an”
 Involves only one hair follicle
 Caused by a yeast
 Hard, tender, folliculocentric nodule
 Hypopigmentedmacules or patches
 With pus draining from the punctum
 Has fine scaling
 In hair-bearing areas
Usually seen on the face but more often at the back
 Deep-seated inflammatory nodule
 Predisposing factors
 Develops about a hair follicle o Heat
 From a preceding folliculitis o High humidity, moist areas
 Occur more often in the absence of any local predisposing Common in athletes
factor For children, those who do not change their shirts regularly
 Recurrent furunculosis is frequently associated with carriage of after playing
S. aureus in the nares, axillae, or perineum, or close contact  Management
with someone such as a family member who is a carrier o Topical therapy
 Selenium sulfide shampoo
VIII-C-3. CARBUNCLE
 Imidazole shampoo like Ketoconazole
 Infection of >1 hair follicle  Topical antifungal creams
 Multiple pustules on surface o Oral Antifungal
 Larger, deeper base  For those with severe cases or do not want topical
 Locations  Ketoconazole
o Nape  Terbinafine
o Back
IX-A. DERMATOPHYTOSES
o Thigh
 Fever, malaise, ill-looking patient  Cause superficial skin infections
 Do not cause systemic infections
 Etiologic agents
o Filamentous fungi that thrive on keratinized areas of the
hair, skin (stratum corneum), and nails
11 of 16| Pediatric Dermatology (Ilagan, Imperial, Jacinto, Juliano, Laganse) | Edited by: Dorosan
2.04 Pediatric Dermatology [Dr. Angeles]

.00 Only stays there; does not go to other organ systems  Allylamines
 Trichophyton spp  Terbinafine
 Microsporum spp o Oral antifungals
 Epidermophyton spp
 Mode of transmission IX-B-1. TINEA CAPITIS
o Direct skin contact
 Not usually found in adults
 Usually seen in schoolchildren
 Clinical Manifestations
o May vary depending on the causative agent
o Black-dot ringworm
 Trichophyton spp
Figure 36. Dermatophytosis.  Small patches of hair loss with broken off hairs
 Fungi/dermatophytes is found within the hair follicle
IX-B. TINEA INFECTIONS  Endothrix infection
o Non-inflammatory type
 Erythematous scaly plaques with central clearing, elevated,
 Scaly patches with or without alopecic area
well-defined borders
o Inflammatory type: Kerion
There is central clearing because the dermatophytes eat the
 Elevated, boggy nodule with or without pustules
skin (stratum corneum), so when they are finished feeding,
 With or without lymphadenopathy
they move outward and move further down to find their
 Can cause scarring alopecia
food; such that if you want to do a KOH stain, you collect
scales from the lesions
Scales from the border
 Best place to get sample for a higher chance of seeing a
dermatophyte under the microscope
For tinea pedis, your differential diagnosis would be dyshidrotic
eczema; in dyshidrotic eczema, you will have vesicles that form
on the lateral aspect of the toes or fingers, but in fungal infection Figure 38. Tinea Capitis.
of the feet, lesions would appear first on the toe
websparticularlybetween the 3rd-4th, 4th-5th toe web. So first,  Diagnostics
there will be dry skin on the toe webs, and later on scales will o Potassium hydroxide (KOH) Stain
appear on your toes.  Gold standard
 Spores surrounding or within the hair strand
Table 11. Types of Tinea Infections. Name depends on the location. (according to Nelson)
Type Affected area  Hyphae (according to the lecturer)
CAPITIS Scalp  Collect scales from the periphery of the lesion
CORPORIS Glabrous skin o Wood’s lamp examination
Except palms, soles and groin  Ectothrix infections
CRURIS Crural area  Blue-green fluorescence
Medial aspects of thighs  Spores lining the cuticle of the hair
PEDIS Toes and feet  Endothrix infections
Toes: 3rd-4th, 4th-5th interdigital spaces  No fluorescence
FACIALE Face  Because the dermatophytes is inside the hair
 Diagnostics follicle
o Potassium hydroxide (KOH) smear o Fungal culture
 Segmented hyphae We do not do this since it takes about 6-8 weeks before
we can get the results

Figure 37. Segmented hyphae on KOH smear. Figure 39.Hair strands on KOH stain. Left: Endothrix infection
(invade the hair shaft). Right: Ectothrix infection (on hair surface).
 Management
o Wear loose clothing; loose cotton underwear
o Avoid tight footwear
o Keep area dry
o Topical antifungals for 2-4 weeks
 Azoles
 Ketoconazole
 Miconazole Figure 40. Ectothrix. Fluorescence on Wood’s Lamp Examination.
12 of 16| Pediatric Dermatology (Ilagan, Imperial, Jacinto, Juliano, Laganse) | Edited by: Dorosan
2.04 Pediatric Dermatology [Dr. Angeles]

.00
 Management  Mode of Transmission
We cannot give topical antifungal for tinea capitis o Skin to skin contact
o Griseofulvin – drug of choice o Autoinoculation
 20-25 mg/kg/day (microcrystalline)  One wart, let’s say on your 1 finger, can be transferred
 10-15 mg/kg/day (ultramicrosize) to another finger or on the same finger adjacent to the
 8-12 weeks lesion itself
o Terbinafine o Sexual intercourse
o Itraconazole
X-A-1. CLINICAL MANIFESTATIONS
IX-C. CANDIDAL DIAPER DERMATITIS
 Well-circumscribed rough hyperkeratotic papule, skin colored
 Etiologic agent usually
o Candida albicans (yeast)  Black dots on the surface – thrombosed capillaries
 Warm, moist occluded skin of the diaper area provides an  Lesions develop along a line of cutaneous trauma
optimal environment for the yeast’s growth
 Cutaneous manifestations
o Erythematous, scaly patch or plaque
o Well-defined borders
o Satellite papules or pustules
Required in order to know that it is a candidal infection
Usually found on the periphery of the erythematous Figure 43. Verruca Plantaris (left). Verruca Vulgaris or common wart
patch/ plaque (Right)
o Perianal skin, inguinal folds, perineum, lower abdomen

Figure 44. Black dots – thrombosed capillaries

Figure 41. Candidal Diaper dermatitis.  Types of Warts

Common warts (verruca vulgaris), caused most
 Diagnostics commonly by HPV types 2 and 4, occur most frequently
o KOH Smear on the fingers, dorsum of the hands paronychial areas,
 Budding yeasts and pseudohyphae face, knees, and elbows.
Flat warts(verruca plana), caused by HPV types 3 and
10, are slightly elevated, minimally hyperkeratotic papules
that usually remain <3 mm in diameter and vary in color
from pink to brown. They may occur in profusion on the
face, arms, dorsum of the hands, and knees.
 Verruca Plana (flat warts) are more commonly seen on
the face but can also be found anywhere in the body. In
Figure 42. Pseudohyphae on KOH Smear.
contrast to V. vulgaris, they are less elevated and less
rough.
 Management
 Autoinoculation to secondary sites is common
o Topical imidazoles (Ketoconazole/Miconazole) on the
Plantar warts (verruca plantaris), although similar to the
diaper area
common wart, are caused by HPV type 1 and are usually
 2x a day until 5 days after clinical cure
flush with the surface of the sole because of the constant
Tell the parents to change the diaper frequently so that
pressure from weight bearing. When plantar warts
the area is not soaked in urine or feces
become hyperkeratotic they may be painful.
o Zinc oxide cream
Genital HPV infection occurs in sexually active
Forms a protective barrier against the irritants
adolescents, most commonly as a result of infection with
HPV types 6 and 11.Condylomata acuminata (mucous
X. CUTANEOUS VIRAL INFECTIONS
membrane warts) are moist, fleshy, papillomatous lesions
that occur on the perianal mucosa, labia, vaginal introitus,
X-A. VERRUCA
and perineal raphe, and on the shaft, corona, and glans
 Develop in 5-10% of children penis.
 Etiologic Agent:  If you have anogenital warts with HPV 16 & 18, this
o Human Papillomaviruses (HPV) can predispose you to having cervical carcinoma
 Most common: HPV 2 & 4 • 65% of warts undergo spontaneous resolution
 Depending on the type of wart then you have different
types of HPV for that
 Verruca vulgaris – HPV 2 & 4

13 of 16| Pediatric Dermatology (Ilagan, Imperial, Jacinto, Juliano, Laganse) | Edited by: Dorosan
2.04 Pediatric Dermatology [Dr. Angeles]

.00 X-B-2. MANAGEMENT

 Immunotherapy – candida or trichophyton antigen
o For cases of children where extraction of the lesions is not
feasible
o Fairly New
Figure 45. Condylomata acuminata in the perianal area of a toddler.
Immunotherapy with either candida or trichophyton
X-A-2. MANAGEMENT antigen, is now the most commonly used therapy. This is
repeated every 4 wk until resolution.
Treatment is usually electro-desiccation and curettage; we burn o Injection of the candida or trichophyton antigen elicit an
the wart, but for children they may be afraid of this so they may immune response so that your immune cells will go there
opt to use topical acids to try to remove it > Salicylic acid and destroy the molluscum body
 Salicylic Acid  Cryotherapy (liquid nitrogen)
 Liquid Nitrogen (cryotherapy)  Cantharidin
 Pulsed Dye Laser
 25% podophyllin – for genital warts XI. ARTHROPOD BITES*
 5% imiquimod – for genital warts
Bites caused by insects
 Cimetidine 30-40 mg/kg/day
Characteristically an edematous papule and a central punctum or
o For multiple or generalized warts unresponsive to topical
the place where the bite occurred
treatment
Because of the hypersensitivity response of the body, you’re
X-B. MOLLUSCUM CONTAGIOSUM going to have that edematous plaque
Not everyone will have this reaction to arthropod bites
 2-6 years old (school age children) are most commonly See Appendix for complete list of Arthropod Bites and their
affected Features (from Nelson)
o They usually get this from their classmates
 Etiologic Agent: Poxvirus
 Mode of Transmission:
o Skin to skin contact
o Autoinoculation
o Sexual intercourse
Figure 48.Papular urticaria occurs principally in the 1st decade of
X-B-1. CLINICAL MANIFESTATIONS life. It may occur at any time of the year. The most common culprits
 1-5 mm skin-colored dome-shaped papule with central are species of fleas, mites, bedbugs, gnats, mosquitoes, chiggers,
umbilication and animal lice.
 Found anywhere in the body
Mosquito bites are usually in exposed areas and they itch at any
 Lesions in the genital area in children are not acquired by
time of the day, but for bed bugs, you have bites on the covered
sexual transmission
areas of the body and itch more in the morning. Bed bugs usually
o For adults, if you find it in the genital area, it is sexually
come in threes or in fours
transmitted but for children is it not.
Unlike your verruca, this is a smooth umbilicated papule XI-A. MANAGEMENT
 Potent Topical Steroids
For those with severe reactions, even if you give potent topical
steroids, they don’t go away, they’re no relieved of the itch, then
you can inject intralesional corticosteroids
 Oral Antihistamine
Figure 46. Molluscum Contagiosum. The center of the umbilication  Cooling Compresses
is where the virus is location.  Insect Repellants
 Self-limiting, some spontaneously resolve in 6-9 months or  It’s important to identify the cause of the itch, so if it’s a bed bug,
longer but since it spreads we manage the patient already you really have to clean your mattress or bed
 May spread rapidly in patients with atopic dermatitis and  See Appendix for Patient Education to Eliminate Bed Bugs
immunodeficiency
XII. INFESTATIONS

XII-A. SCABIES
 “Galis aso” or “kurikung
 Etiologic Agent:Sarcoptes scabiei (Mite)
 Mode of transmission: Skin-to-skin contact
o Rarely by fomites because the isolated mite dies within 2-
Figure 47. Molluscum Contagiosum 3 days

14 of 16| Pediatric Dermatology (Ilagan, Imperial, Jacinto, Juliano, Laganse) | Edited by: Dorosan
2.04 Pediatric Dermatology [Dr. Angeles]
.00
 Commonly affects: School-aged children
o Getting it from their classmates or playmates
Figure 49. Scabies.
XII-A-1. CLINICAL MANIFESTATIONS
 Flesh erythematous papules, vesicles, plaques
 Nocturnal pruritus (intensely pruritic)
 (+/-) Excoriations and crusting (d/t persistent scratching)
o May be secondarily infected by bacteria especially S.
aureus
 Infants: Palms soles, and scalp + generalized eczematous
dermatitis
 Older Children: Interdigital webs, axillae, flexures of the
arms/wrists, beltline, genitalia, buttocks
For infants and children, they usually don’t have lesions or bites
on the face
Figure 50. Circle of Hebra. The areas colored pink are the most
common areas where rashes may occur although they can occur
elsewhere.
Mammary area, axilla, antecubital area, wrists, fingers, genitals,
butt, toe-webs
Ask the patients if somebody else in the household is complaining
of the same symptoms
XII-A-2. MANAGEMENT
 Permethrin 5% cream (Drug of Choice) – application will be
asked on the test!
o Drug of choice for >2 months and above
o Applied twice, 1 week apart.
o Apply from the neck to the toes.
o Do not wash hands after application because the mite
also stays on your fingers
o Contact time: 8-12 hours, then rinse offotherwise you
will get an irritant contact reaction from permethrin and
systemic absorption will be increased
o Repeat after 1 week (because it does not affect the egg
of the mite, only kills the adults)
 Assume that those you did not kill on day 1 would’ve
hatched on day 7, then these larvae or small mites will
be eradicated on the 2nd application of permethrin
 Crotamiton 10% lotion – does not kill the mites, only relieves
the itching
 Lindane 1 % lotion
o neurotoxic
15 of 16| Pediatric Dermatology (Ilagan, Imperial, Jacinto, Juliano, Laganse) | Edited by: Dorosan
 Oral Ivermectin
o 200µg/kg, 2 doses, 2 wks apart
o For severe infestations
 For the pruritus: sedating antihistamines, topical
corticosteroids
Because it is very itchy, you may give antihistamines or
topical corticosteroids as long as you have already applied
the permethrin
 Bacterial Infection: Systemic antibiotics
o Two antibiotics I’ve been repeating: Cloxacillin and
Cephalexin
 Linen and towels
o Should be washed, boiled, sun dried, and ironed
o Set aside for 5 days; the mite cannot survive without a
human host for 4 days
 Spray the house with an insecticide
XII-B. PEDICULOSIS CAPITIS
 Affects 3-12 y/o school age children
 Etiologic Agent: Pediculosis humanus capitis (louse)
Suspect this in children who always scratch their head or scalp
Sometimes you can’t see it so you really have to check the hair
There are two things that can cause itchiness of the scalp. One is
your seborrheic dermatitis (dandruff) and 2nd is this pediculosis
capitis.
Figure 51. Pediculosis Capitis. The nits towards the outer part of the
hair follicle, farthest from the scalp, are the eggs of the lice that have
no larvae inside (hatched). Those very close to the scalp have not
hatched.
XII-B-1. CLINICAL MANIFESTATIONS
 Intense itchiness of the of the scalp
 Erythema and scaling of the nape, scalp
 Nits are firmly attached to the hair shaft
 Erythematous papules or macules on the neck and around the
ears
XII-B-2. MANAGEMENT
 Permethrin Shampoo
o ≥ 2 months of age
o Pedicudicidal but not ovicidal (kills only live lice)
o Leave on scalp for 10 minutes then rinse off
o Repeat after 7 days
o Very important:Mechanical removal of lice and eggs
 Malathion 0.5%: DOC but not available in the Philippines
 0.5% ivermectin lotion
 Supportive Management
o Vacuum your home
o Wash clothing and linen in close contact with infected
persons
o Place objects that could harbor lice in plastic bags for 2
weeks (combs, hats, etc.)
o Check and treat household members
o Do weekly checks to detect re-infestation
2.04 Pediatric Dermatology [Dr. Angeles]

.00 REFERENCES 3. A 7-year-old boy sought consultation because of multiple

erythematous excoriated papules on the hands, fingers, axilla,
 Dr. Angeles’ lecture recording and powerpoint abdomen, gluteal area, lower legs, toes and pruritic at night.
 Nelson’s His younger brother also developed similar lesions 5 days ago.
What is the primary impression?
REVIEW QUESTIONS A. Pediculosis
B. Tinea Versicolor
Choose the letter of the correct answer. C. Arthropod bites
1. A ten-year-old boy complain for the past months noted D. Scabies
multiple hypopigmented macules and patches as fine scales 4. Which of the following statement is true regarding the
distributed in his upper back and arms. What is your diagnosis? infection of the head, hair and scalp by the head louse?
A. Scabies A. Commonly affects 8-15 years old
B. Atopic Dermatitis B. Application of permethrin as treatment should be left for
C. Tinea Versicolor 8-12 hours
D. Impetigo C. The head louse can survive up to 2 days if taken away
2. A 3-year-old girl was brought to the OPD because of lesions on from the host.
the face, which was characteristic of honey-colored crust on D. All of the above
erythematous plaques distributed around the nose and cheeks. 5. A 17-year-old male presents with painful solitary bump on his
Which of the following is the most likely caused of this upper back measuring approximately 7 mm of 2 days duration.
condition? Pertinent physical examination positive for rubor, calor and
A. Streptococcus Pyogenes dolor on the affected area. What is your diagnosis?
B. Candida albicans A. Folliculitis
C. Staphylococcus aureus B. Furuncle
D. None of the above C. Carbuncle
D. Verruca
Answers: C, C, D, C, B

APPENDIX

16 of 16| Pediatric Dermatology (Ilagan, Imperial, Jacinto, Juliano, Laganse) | Edited by: Dorosan