Common Paediatric Skin Problems

COMMON PAEDIATRIC SKIN
INFECTIONS
DR MRS ODOCHI EWURUM
MBBS, FWACP, FMCPaed.
INTRODUCTION
• The skin and its accessory organs (hair, nails
and glands) are known as integumentary
system of the body. Integument means
covering and the skin is the outer covering of
the body.
• It is however, more than a simple body
covering. The skin, is a complex system of
specialized tissues, containing glands that
secrete several types of fluids, nerves that
INTRODUCTION
carry impulses, and blood vessels that aid in the
regulation of the body temperature.
• The skin is often referred to as the largest
body organ and serves as the main protective
barrier against damage to internal tissues
from trauma, ultraviolet light, temperature,
toxins and bacteria.
FUNCTIONS OF THE SKIN
The skin has many important functions among
which include;
(i.) The skin as a protective membrane over the
entire body, guards the deeper tissues of the
body against excessive loss of water, salts, and
heat and against invasion of pathogens and
their toxins.
(ii) The skin contains two types of glands that
produce important secretions. The sebaceous
glands produce an oily secretion called sebum
which helps to lubricate the surface of the skin
and the sweat glands produce a watery
secretion called sweat that helps to cool the
body as it evaporates from the skin surface.
(iii) Nerve fibers located under the skin act as
receptors for sensations such as pain,
temperature, pressure and touch.
(iv) Several different tissues in the skin aid in
maintaining the body temperature
(thermoregulation).
ANATOMY/STRUCTURE OF THE SKIN
• There are three layers in the skin. These layers

from the outer surface to inward surface are:
• 1. Epidermis - a thin cellular membrane layer.
• 2. Corium or dermis - dense, fibrous
connective tissue layer.
• 3. Subcutaneous tissue or hypodermis - thick,
fat-containing tissue.
Cells move from the base of the epidermis up to

the surface, changing shape and structure as
they go.
• The Epidermis is divided into five layers from
upper to lower viz;
i. Stratum corneum; This is made up of stratified
squamous epithelium or hardened cells which
play a role in the skin’s protective function.
ii. Granular layer; This is the transitional layer

where keratinocyte skin cells develop into
their final form and die. It contains
keratohyalin and lamellar granules.
iii. Spinous layer; These are keratin producing
epidermal cells that provide a continuos net-
like layer of protection for underlying tissue.
iv. Basal layer; The basal layer of the epidermis
contains special cells called melanocytes.
Melanocytes form and contain a black pigment
called melanin. The number of melanocytes in all
races is the same but the amount of melanin
accounts for the color differences among the races.
v. Basement membrane: It connects and functionally
separates the epidermis and the dermis.
• The epidermis contains no blood vessels,

lymphatic vessels and connective tissue
(elastic fibers, cartilage, fat) and is therefore
dependent on the deeper dermis layer and its
rich network of capillaries for nourishment.
Dermis: It is composed of blood and lymph vessels
and nerve fibers as well as the accessory organs of
the skin, which are the hair follicles, sweat glands,
and sebaceous glands.
• The main function of the dermis is to provide
physical support and nutrients to the epidermis.
• The two layers identified within the dermis are
the papillary layer and the reticular layer.
-The papillary dermis contains;

• smaller blood vessels which supply oxygen,
elastic fibres and nutrients to the lower
epidermis.
-The thicker reticular dermis contains ;
• dense connective tissue, larger blood vessels,
elastic fibres and bundles of collagen arranged
in layers.
• Also within the reticular layer are the

following key cell types:
i. fibroblasts − a key cell involved in repairing
tissue damage.
ii. mast cells − which are involved in fighting
infection.
iii. lymphatic vessels – the lymphatic system is a
key part of the body’s defense against
infection.
iv. epidermal appendages or rete pegs – this

links the epidermis and dermis together to
prevent skin damage.
v. ground substance − a gel-like substance that
helps to support the cells within the dermis
and provides structure to the area.
• Subcutaneous layer/ hypodermis: It is

composed of adipose tissue or fat tissue. This
layer of the skin is important in protection of
the deeper tissues of the body and as a heat
insulator.
MORPHOLOGY OF SKIN LESSIONS
• A skin lesion refers to any skin area that has
different characteristics from the surrounding
skin, including color, shape, size, and texture.
• Skin lesions are very common and often appear
as a result of a localized damage to the skin, like
sunburns or contact dermatitis.
• Others, however, can be manifestations of
underlying disorders, such as diabetes,
infections etc.
• This is classified into two;
i. Primary lession
ii. Secondary lession
• Primary skin lesions originate on previously
healthy skin and are directly associated with
a specific cause. Examples include bullae,
burrow, macule, nodule, papule, plaque,
pustule, tumour, vessicle and wheal.
• Secondary skin lesions develop from the
evolution of a primary skin lesion, either due
to traumatic manipulation, such as scratching
or rubbing, or due to its treatment or
progression. Examples of secondary skin
lesions include crusts, sores, ulcers, scars, etc.
PRIMARY SKIN LESSIONS
VESICLE: A raised lesion filled with clear

fluid that is <1cm in diameter.
BULLA: A raised lesion filled with clear

fluid >1cm in diameter
PAPULE: a circumscribed palpable elevation

with distinct borders < 0.5cm in diameter.
PLAQUE: Is an elevated area of skin, with

distinct borders and an epidermal change >
than 1cm in diameter.
MACULE: a circumscribed alteration in the

colour of the skin that is flat to the surface of the
skin and not palpable. <1cm in size.
PATCH: A large macule >1cm in size .

PRIMARY SKIN LESSION
NODULE
WHEAL
A circumscribed raised solid lesion ≤ 1cm.
A transient area of dermal or dermal and
hypodermal oedema, compressible and
usually evanescent.
Pustule Burrow
A circumscribed elevation A small linear tunnel in the skin
of Pus-filled skin lesion that houses a parasite such as
<1cm. scabies.
SECONDARY SKIN LESSIONS
• Crust: A hard, friable irregular layer of dried blood,
serum, pus, tissue debris or any combination of these,
adherent to the surface of injured or inflamed skin.
• Ulcer: An open sore or erosion of the skin or mucous
membrane.
• Scaling: Whitish plates or flakes of stratum corneum
present on the skin surface.
• Scar: Fibrous tissue replacing normal tissue
destroyed by injury or disease.
• Erosion and oozing: Moist, circumscribed,
slightly depressed areas representing a blister
base with the roof of the blister removed.
• Desquamation: Refers to the peeling of sheets
of scale after an acute injury to skin (burns,
toxic drug reaction)
• Excoriation: Oval to linear depressions in the
skin with a complete removal of the
epidermis, exposing a broad section of the red
dermis (atopic dermatitis)
• Fissure: Linear, wedge-shaped cracks in the
epidermis extending down to the dermis and
narrowing at the base (warts)
• Lichenification; A thickening of the epidermis
(and to some extent also of the dermis) in
response to prolonged rubbing.
• Gangrene; A death of tissue, usually due to
loss of blood supply.
Classification of skin disorders of infancy and childhood
• Transient skin disease/neonatal dermatosis

• Common congenital malformations of skin
• Birthmarks
• Infections in infancy and childhood (viral,
bacterial, fungal)
• Infestations
• Genodermatosis
Classification of skin disorders of infancy and
childhood contd.
• Neurocutaneous disorders
• Metabolic and nutritional dermatoses
• Cutaneous manifestations of systemic diseases
• Miscallaneous conditions
CLASSIFICATION OF SOME COMMON SKIN
DISORDERS
• VIRAL • BACTERIAL
- Measles - Furunculosis
- Chicken pox - Carbuncles
- Rubella - Impetigo
- Herpes simplex - Staphylococcal scalded
- Roseola infantum skin syndrome
- Erythema infectiosum
- Hand, foot and mouth
disease
DISORDERS CONTD.
• FUNGAL • INFESTATIONS
- Oral candidiasis (Thrush) - Scabies
- Tinea Capitis • ATOPIC
- Tinea Corporis -Atopic dermatitis
- Tinea Pedis - Seborrheic dermatitis
- Pityriasis Versicolor
- Pityriasis Rosea
DISORDERS CONTD.
• BIRTH MARKS • MISCELLANEOUS
- Mongolian Spots/Slate- - Erythema Toxicum
grey naevus of childhood - Transient neonatal
- Portwine Stain/ Naevus pustular melanosis
flammeus
- Milia
- Salmon patch/Angel
- Miliaria/Heat rash
kiss /Stork bite
- Haemangioma of - Diaper rash
infancy /Strawberry naevi - Neonatal acne
MEASLES
• Caused by measles virus which is a single
stranded RNA virus in the family paramyxoviridae
and genus morbillivirus.
• It is characterized by high fever, an enanthem
(kopliks spot),cough, catarrh, conjunctivitis and a
prominent exanthem (rash).
• Incubation period is 8-12 days.
• Kopliks spot is pathognomonic of measles
appearing 1-4 days before onset of the rash.
MEASLES
MEASLES
• Kopliks spot appear as ‘tiny white spots’ like grains of
sand on mucous membrane of the cheek opposite
the lower molars
• Erythematous, maculopapular rash begins on the
forehead(around the hairline), behind the ears,
upper neck and spreads over the face, trunk and
limb.
• The rash fades over about 7 days in the same
progression as it evolved often leaving a fine
desquamation.
MEASLES
DIAGNOSIS
• Almost always clinical and based on
epidemiology especially in measles outbreak.
• Serological confirmation is by serum IgM
antibody identification or four fold rise in IgG
antibodies in serum collected after 2-4 weeks.
• Viral RNA detection by PCR
MEASLES
TREATMENT
• Usually supportive
• Maintenance of hydration, antipyretics
• Vitamin A supplementation
PROPHYLAXIS
• Measles or MMR vaccine
• For post exposure prophylaxis, give measles vaccine
within 72 hours of exposure, immunoglobulin
within 6 days of exposure
VARICELLA (CHICKEN POX)
• Cause by Varicella Zoster virus (VZV) (DNA α-
herpes virus group).
• Illness may begins 14-16 days after exposure
although incubation period is 10-21 days.
• Fever, malaise, headache, anorexia and
abdominal Pain may occur 24 – 48 hours before
the rash.
• Eruption is characterized by the appearance of
“tear drop” vesicles on an erythematous base.
• The rash(exanthem) consists of intensely pruritic
macules that evolve through papules which
become vesicules, pustules and later encrusted.
• The presence of lesions of different stage at the
same time is typical of chicken pox.
• The distribution of the rash is mostly central or
centripetal.
• Mucous membranes of the mouth and throat are
often involved
TREATMENT
• Antiviral treatment modifies the course of both
varicella and herpes zoster.
• Acyclovir 20mg/kg/dose 6hourly for 5 days PO
within 24hrs of onset of rash.
• Intravenous Acyclovir 500mg/m2 8 hrly for 7-10
days is given for severe illness.
• Supportive care: Fluid, antipyretics, antipruritics.
RUBELLA (GERMAN MEASLES)
• Also called 3-day measles.
• Caused by RNA virus of the family Togaviridae and
genus rubivirus.
• Incubation perod is 14-21 days.
• Prodromal symptoms such as low grade fever,
sore throat, red eyes, headache, malaise, anorexia
and lymphadenopathy occur.
• A notable feature is involvement of suboccipital,
post auricular and cervical lymph nodes.
• The rash begins on the face and neck and
spreads centrifugally to reach the extremities.
• The rash appears as irregular pink macules on
the face & neck but coalesce to form discrete
macules at the extremities.
• The rash fades from the face as it extends to
the rest of the body so that the whole body
may not be involved at any point in time.
• Rose coloured lessions (Forchheimer spots) or
petechial hemorrhages may be seen on the
soft palate about the time of onset of the
rash.
• The pink lesions differ from the more vivid-red
lesions of measles
• Treatment: Supportive, no specific treatment
is available.
HERPES SIMPLEX
• Herpes simplex is a DNA virus.
• HSV type 1 (HSV-1) and HSV type 2 (HSV-2), cause
a variety of illnesses.
• HSV-1 causes more recurrent oral infections, while
HSV-2 cause more recurrent genital infections.
• The hallmarks of common HSV infections are skin
vesicles and shallow ulcers.
• Classically on the skin, herpes lessions appears as
grouped 2-4 mm vesicles on erythematous base.
HERPES SIMPLEX
HERPES SIMPLEX
HERPES SIMPLEX
• On mucous membrane as blister-base erosion,
seen due to easy shedding of blister roof.
• Sites of infection:60% of primary infections in oral
cavity, lips, nose, cheeks, fingers, eyes and scalp
• Some common clinical presentations include:
- Herpes gingivostomatitis occurs in the gums and
oral cavity and most often affects children 6 mo to
5 yr of age
- Herpes Labialis; Fever blisters, or cold sores
HERPES SIMPLEX
- Herpes whitlow is a term generally applied to HSV
infection of fingers or toes
- Neonatal Herpes
- Genital HSV infection is common in sexually experienced
adolescents and young adults.
TREATMENT
• Gingivostomatitis: Oral Acyclovir
• Herpes Labialis: Oral Valacyclovir
• Eczema herpeticum: Oral Acyclovir
• Keratitis: Eye drops 1% trifluridine, 3% Vidarabin
ROSEOLA INFANTUM (EXANTHEM SUBITUM)
ROSEOLA INFANTUM (EXANTHEM SUBITUM)
• Also called sixth disease

• Caused by human herpes virus – 6 (HHV6).
• Predominantly occurs <2 years of age
• Prodomal symptoms such as mild URTI, catarrh ,
pharyngeal inflammation and conjunctival redness may
be present.
• Clinical illness starts with high temperature, usually
ranging from 37.9 to 40°C lasting 3-5 days.
• A rash appears within 12–24 hr of fever resolution and
fades after 1-3 days.
ROSEOLA INFANTUM (EXANTHEM SUBITUM
• The roseola rash begins as discrete, small (2–5 mm),

slightly raised pink lesions on the trunk and usually
spreads to the neck, face, and proximal extremities.
• The rash is not usually pruritic, and no vesicles or
pustules develop. Lesions typically remain discrete
but occasionally may become almost confluent.
• Mild periorbital edema and lymphadenopathy are
occasionally seen
• Treatment: Supportive, antipyretics
ERYTHEMA INFECTIOSUM( FIFTH DISEASE)
• Caused by human parvovirus B19 virus, a DNA

virus belonging to the genus Erythrovirus in the
family Parvoviridae.
• Transmission is by respiratory droplets, blood
and blood products.
• Incubation 4–28 days (average 16–17 days).
• The prodromal phase is mild and consists of low-
grade fever, headache, and symptoms of mild
upper respiratory tract infection.
• Erythematous, macular rash often begins on the face, giving
the so called characteristic slapped cheek appearance.
• Rash on extremities and trunk also present, with central
fading of the eruption giving a lacy reticulated appearance.
• Rash usually fades within a week but may reappear often
several times, especially after bathing or exposure to sun up
to 4 months.
• Diagnosis confirmed by increased serum IgM level within 30
days.
• Treatment – No specific antiviral treatment.
HAND FOOT AND MOUTH DISEASE
• Most frequently caused by coxsackievirus A16
and can also be caused by enterovirus 71;
coxsackie A viruses 5, 7, 9, and 10; and
coxsackie B viruses 2 and 5.
• Scattered vesicles may occur on the tongue,
buccal mucosa, posterior pharynx, palate,
gingiva, and/or lips
HAND-FOOT AND MOUTH DISEASE
• Maculopapular, vesicular, and/or pustular lesions
may also occur on the hands and fingers, feet,
and buttocks and groin.
• Hands are more commonly involved than the feet
• The illness is usually mild, with or without low-
grade fever.
• Clears spontaneously in about 7 days.
• No specific treatment is required.
FURUNCULES (BOILS)
FURUNCLES (BOILS)
• The causative agent is usually S. aureus, which
penetrates abraded perifollicular skin.
• The lesions may originate from a preceding
folliculitis or may arise initially as a deep-seated,
tender, erythematous, perifollicular nodule.
• The progression is indurated lession → central
necrosis → suppuration → leading to rupture
and discharge of a central core of necrotic tissue
and destruction of the follicle
FURUNCLES (BOILS)
• Healing occurs with scar formation.
• Sites of predilection are the hair-bearing areas on
the scalp, face, back of neck, axillae, buttocks,
and groin.
• Predisposing factors to furuncle formation
include obesity, hyperhidrosis, maceration,
friction, and pre-existing dermatitis
• Treatment: Antibiotics, personal hygiene, hot
moist compress, incision and drainage.
CARBUNCLES
CARBUNCLES
• Caused by Staphylococcus aureus.
• Carbuncle is an infection of a group of
contiguous follicles, with multiple drainage
points, accompanied by inflammatory changes in
surrounding connective tissue.
• The lessions are painful, tender, firm to hard,
indurated lump.
• It may be accompanied by fever, leukocytosis,
and bacteremia.
CARBUNCLES
• Sites of predilection include the back of neck,
shoulder, hip and thigh.
• TREATMENT
-Oral or parenteral antibiotics such as cloxacillin,
cephalexin
- Cephalosporin, clindamycin, or erythromycin for
penicillin allergic patients
- In MRSA: Rifampicin, cotrimoxazole
- Attention to personal hygiene
IMPETIGO
• This is a contagious bacterial infection of
epidermis.
• It is transmitted by direct contact with infected
persons or fomites.
• Can affect any skin region, but most common on
face around nose, mouth and hand.
• Commonly affects children aged 4-7 years.
• Primary impetigo: more common in children,
infection via minor breaks in skin.
IMPETIGO
IMPETIGO
• Secondary impetigo: occurs at any age on
secondary infection of trauma/wounds.
• Superficial blisters rupture easily, releasing yellow
exudates that dries and forms a honey-colored
crust
• Diagnosis is clinical but can be confirmed by gram
stain or culture of crust or fluid from bullae.
• Has two classic types; Bullous and Non- bullous
impetigo.
IMPETIGO
BULLOUS IMPETIGO
• Always caused by S. aureus phage group 2.
• Developes on intact skin.
• Vesicles and flaccid transparent bullae (large
vesicles) contain clear yellow or slightly turbid
fluid +/- surrounding erythema.
• Occurs more on face, buttocks, trunk,
perineum, and extremities.
IMPETIGO
• Common in neonates and children <5 years
• Systemic symptoms are common.
NON- BULLOUS IMPETIGO
• More common than bullous
• Usually due to S. aureus or S. pyogenes or mixed
infection
• Typically affects trauma sites.
IMPETIGO
• Presents as scattered discrete 1-3cm lesions with
honey-coloured crust and surrounding erythema.
• Most common around mouth/nose.
• Patients may have lymphadenopathy.
• Presisposing lessions include insect bites, abrasions,
lacerations, chickenpox, scabies ,pediculosis, and
burns.
• The infection may be spread to other parts of the
body by the fingers, clothing, and towels.
IMPETIGO
• Local infections are treated with topical saline or
aluminium acetate, then 2% mupirocin ointment.
– Normal saline or potassium permanganate soaks
will help remove the crusts
– Mupirocin ointment or fusidic acid as a topical
antibiotic
• If systemic symptoms present, use cloxacillin or a
beta-lactamase resistant antiobiotic eg. Cephalexin.
• If impetigo is due to MRSA use Clindamycin.
STAPHYLOCOCCAL SCALDED SKIN SYNDROME
(SSSS)/RITTER’S DISEASE
• Caused by Exfoliative toxins A and B produced by
staphylococcal aureus belonging to phage group B.
• Scarlatiniform erythema develops diffusely with a
predilection of flexural and periorificial areas.
• Development of extensive superficial sterile flaccid blisters
or bullae which become deroofed revealing large areas of
raw red moist skin similar to hot water burn occurs.
• Fever, rhinitis, conjunctivitis, irritability, malaise, poor
feeding and exquisite tenderness may occur prior to onset
of rash.
(SSSS)/RITTER’S DISEASE
(SSSS)/ RITTER’S DISEASE
• Circumoral erythema ,radial crusting and fissuring around
the eyes, mouth, and nose are characteristically
prominent. Child may appear toxic.
• Nikolsky’s sign (separation of areas of epidermis in
response to sheering pressure on skin) is positive.
TREATMENT
• Antibiotics eg Flucloxacillin, Erythromycin.
• Analgesics.
• Application of an emollient, clean with isotonic saline.
• Fluid and electrolyte balance.
ORAL CANDIDIASIS(THRUSH)
• Caused by yeast like fungi of genus candida –
most commonly by candida albicans.
• Characterized by curdy or whitish- gray, friable,
cheesy pseudomembranous patches or plaques
on markedly reddened mucosa.
• The plaques of thrush invade the mucosa
superficially and may be found on the lips,
buccal mucosa, tongue, and palate extending to
esophagus/pharynx.
ORAL CANDIDIASIS (ORAL THRUSH)
ORAL CANDIDIASIS (ORAL THRUSH)
• Removal of plaques from these surfaces may cause
mild punctate areas of bleeding, which helps to
confirm the diagnosis.
• Factors predisposing to candidiasis include DM,
Retroviral disease, prolonged antibiotic and
corticosteroid use, leukemia etc.
TREATMENT:
• Antifungal drugs such as Clotrimazole, Nystatin,
Amphotericin B, Miconazole gel
• Proper oral hygiene
TINEA CAPITIS
• Tinea capitis is a dermatophyte infection of the
scalp most often caused by Trichophyton
tonsurans, occasionally by Microsporum canis,
and, much less commonly, by other
Microsporum and Trichophyton spp.
• Lessions occur as erythematous and scaly
circular plaque (ringworm) within which the
infected hairs become brittle and broken with
different lengths.
TINEA CAPITIS
TINEA CAPITIS
• Multiple affected sites produce a moth-eaten
appearance of hair
• Scaling and inflammation of scalp are variable.
• Numerous confluent patches of alopecia develop,
and patients may complain of severe pruritus.
DIAGNOSIS: Scraping and KOH examination
TREATMENT
-Oral griseofulvin, itraconazole or terbinafine .
- Topical antifungal cream, shampoo.
TINEA CORPORIS
• Tinea corporis is fungal infection of the glabrous skin,
excluding the palms, soles, and groin.
• The most common aetiologic organisms are T. rubrum
and T. mentagrophytes. Infections with M. canis are
also frequent.
• Characteristically appears as a dry, mildly
erythematous, elevated, scaly papule or plaque that
spreads centrifugally and clears centrally to form the
characteristic annular lesion.
• Active edge shows vesicles and pustules.
TINEA CORPORIS
TINEA CORPORIS
• It is usually acquired from direct contact from
infected person, surfaces and pets(M canis)
DIAGNOSIS – skin scraping and KOH
examination. Culture for identifying the
species of dermatophytes.
TREATMENT: i. topical antifungal agents e.g.,
imidazoles, terbinafine, naftifine
ii. In severe cases, oral griseofulvin, itraconazole.
TINEA PEDIS
• Tinea pedis (athlete's foot) is a fungal infection of
the toe webs and soles of the feet.
• The usual etiologic agents are T. rubrum, T.
mentagrophytes, and E. floccosum.
• The subdigital crevice are fissured, with
maceration and peeling of the surrounding skin
• Less commonly, a chronic diffuse hyperkeratosis
of the sole of the foot occurs with only mild
erythema.
TINEA PEDIS
TINEA PEDIS
• Ocassionally, the papules progress to vesicles and
bullae that may become pustular.
• Severe tenderness, itching, and a persistent foul odor
are characteristic.
• DIAGNOSIS: Fungal mycelia seen on microscopic
examination of a KOH preparation or by culture.
• TREATMENT: i. avoidance of occlusive footwear, careful
drying between the toes after bathing.
ii. Topical zinc undecylenate powder, imidazole cream ,
oral griseofulvin.
PITYRIASIS VERSICOLOR
• This is a common chronic fungal infection of the stratum
corneum caused by the dimorphic yeast Malassezia
furfur found in areas of skin that are rich in sebum
production.
• Predisposing factors include a warm, humid
environment, excessive sweating, occlusion, high plasma
cortisol levels, immunosuppression, malnourishment,
and genetically determined susceptibility.
• The disease is most prevalent in adolescents and young
adults.
• They lesions may be either hypopigmented or
hyperpigmented macules covered with a fine
scale, that often merge to form confluent
patches.
• Occurs most commonly on the neck, upper
chest, back, and upper arms.
DIAGNOSIS: Wood lamp, KOH preparation of
scrapings, skin biopsy.
TREATMENT
i. Selenium sulfide suspension applied
overnight.
ii. Imidazole or terbinafine cream may be used
twice daily for 2–4 wk.
iii. Oral therapy with ketoconazole or
fluconazole, or itraconazole.
SCABIES
• Caused by the female mite Sarcoptes scabiei var
hominis.
• The extent and duration of physical contact with
an affected individual is the most important
factor that determines spread of scabies.
• Various types of lesions can be seen in scabies
and include include papules(some of which are
excoriated, crusted, or scaling), wheals, vesicles,
and a superimposed eczematous dermatitis.
SCABIES
SCABIES
• History of contact and Intense pruritus
particularly at night are significant findings.
• Sites of predilection differ with age;
-Infants: The palms, soles, face, scalp and genitalia
are often affected.
-Older children, adolescents and adults: The
interdigital spaces, wrist flexors, anterior axillary
folds, ankles, buttocks, umbilicus and belt line,
groin, genitals in men, and areolas in women.
SCABIES
• Note that itching may be absent and lesions may not be
obvious in contacts who are asymptomatic carriers.
• TREATMENT
i. Application of Sulphur cream in < 2mths of age & 5%
Permethrin in > 2mths of age by all household members
ii. Antihistamines to control itching
iii. Soak all household clothings and beddings with hot
water , sun dry and put in a new or decontaminated bag
or box.
ATOPIC DERMATITIS (ECZEMA)
• Atopic dermatitis, or eczema, is a common
inflammatory condition of the skin characterized by
intense itching (pruritis)
• Hence it is commonly referred to as “the itch that
rashes.”
• Individuals with atopic dermatitis have a
predisposition toward developing hypersensitivity
reactions such eczema, asthma and allergic rhinitis.
• There is a strong familial association in atopic
dermatitis and it is very common in children.
PATHOGENESIS
• Specific cause is unknown.
• The leading theory suggests an impairment of the
skins function as a protective barrier due to
intrinsic structural or functional abnormalities of
the skin.
• The other theory is that of immune dysfunction
in which immune cells modulate an inflammatory
response to environmental factors.
CLINICAL PRESENTATION
• Pruritis is the most outstanding clinical feature.
• The lesion may present with any of the following:
– Xerosis (dry skin), Scaly skin
– Ill-defined erythema
– Small coalescing erythematous papules or vesicles.
– Crusting (if secondarily infected)
– Lichenification and/or excoriations (secondary to
excessive scratching)
STAGES
Age-related stages of atopic dermatitis
• Infantile (2 months – 2 years)
– Often pruritic, red, scaly or crusted lesions.
– Facial and extensor distribution predominates. The
cheeks and scalp are commonly affected.
– Entire body may be affected, however diaper area is
commonly spared.
• Childhood (2-12 years)
– More lichenification and excoriations are seen.
– Often has a flexural distribution involving antecubital
and popliteal fossae, wrists and ankles.
• Adult (>12 years)
– Typically lichenified and more localized (primarily to the
hands)
– Flexural areas commonly involved.
– The condition generally improves with age and may
remit by early adulthood.
DIAGNOSIS
• Atopic dermatitis is a clinical diagnosis. CRITERIA is;
• Evidence of pruritis (eg. scratching or rubbing reported by
parent)
• Plus three or more of the following:
– Involvement of skin creases (antecubital or popliteal fossae, ankles,
neck, eyes)
– Dry skin within the past year
– Visible involvement of flexural surfaces (cheeks, forehead, outer
extremities)
– Symptoms beginning in a child before two years age (this criterion not
used for children under four).
TREATMENT
• Avoidance of irritating or trigger factors
• Emollients and moisturizers to re-establish the
cutaneous permeability barrier
• Topical steriods (creams or ointments)
• Topical immunomodulators (eg. Tacrolimus)
• Antibiotics if secondary staphylococcus infection
• Oral antihistamines for sedation & control of itching
SEBORRHEIC DERMATITIS
• This is a chronic inflammatory condition.
• Specific cause is unknown however Malassezia furfur
has been implicated as a causative agent.
• Diffuse or focal scaling and crusting of the scalp, or a
greasy yellow scale on an erythematous base
sometimes called cradle cap may be the initial and at
times the only manifestation.
• A greasy, scaly, erythematous papular dermatitis,
which is usually non-pruritic, may involve the face,
neck, retroauricular areas, axillae, and diaper area.
• The lesion may be patchy and focal or may spread to
involve almost the entire body.
• Affected regions may also develop fissures, weeping &
maceration.
TREATMENT: i. Antiseborrheic shampoo such as selenium
sulfide, sulfur, salicylic acid, zinc pyrithione, tar.
ii. For inflamed lesions apply topical corticosteroid therapy.
iii. Topical antifungal agents effective against Malassezia
may be required.
MONGOLIAN SPOTS/SLATE-GREY NAEVUS OF
CHILDHOOD
Mongolian Spots/Slate-grey naevus of childhood
• These are bluish or slate-gray macular lesions with variably

defined margins.
• This is caused by the dermal location of melanin-containing
melanocytes (mid-dermal melanocytosis) that were
presumably arrested in their migration from neural crest to
epidermis.
• They occur most commonly in the presacral area but may
be found over the posterior thighs, legs, back, and
shoulder.
• They may be solitary or numerous and often involve large
areas.
MONGOLIAN SPOTS/SLATE-GREY NAEVUS OF
CHILDHOOD
• Usually congenital.
• May look like bruises.
• Common in dark skinned infants.
• Usually fade during the first few years of life
due to darkening of the overlying skin.
• Malignant degeneration does not occur.
• Requires no treatment.
Portwine Stain/ Naevus flammeus
Portwine Stain/ Naevus flammeus
• These are macular, sharply circumscribed

pink/red/purple patches of various sizes
occuring typically on face, neck, limbs due to
vascular malformations.
• These vascular malformations consist of mature
dilated dermal capillaries.
• Usually Present at birth and unilateral.
• Can be any size, grow proportionately with child.
PORTWINE STAIN/ NAEVUS FLAMMEUS
• May thicken or develop into nodules in adult.

• Social/emotional complications occur.
• Some association with glaucoma & seizures.
• Do not resolve, they are permanent.
• The most effective treatment for port-wine
stains is the pulsed dye laser (PDL).
SALMON PATCH/ANGEL KISS /STORK BITE
• These are small, pale pink, ill-defined, vascular

macules occuring due to localized vascular
ectasia (malformation).
• Occur most commonly on the glabella, eyelids,
upper lip, and nuchal area of 30–40% of
normal newborn infants.
• May become more visible during crying or
changes in environmental temperature.
• Usually symmetric with lessions on both sides

of the midline.
• Facial lesions usually fade completely over
years while occipital and neck lesions may
persist into adulthood.
• TREATMENT:
- No treatment is required
HAEMANGIOMA OF INFANCY /STRAWBERRY
NAEVI
HAEMANGIOMA OF INFANCY /STRAWBERRY
NAEVI
• Hemangiomas are proliferative hamartomas of vascular
endothelium.
• They are classified as superficial, deep, or mixed.
• Superficial hemangiomas are bright red, protuberant,
compressible, sharply demarcated lesions that may
occur on any area of the body.
• Deep haemangiomas are more diffuse, cystic, firm, or
compressible lesions with the overlying skin appearing
normal in color or having a bluish hue.
• Most hemangiomas are mixed.
HAEMANGIOMA OF INFANCY /STRAWBERRY NAEVI
• May be present at birth or, more commonly, become

apparent in the 1st 2 months of life.
• Represents clonal expansion of endothelial cells.
• Usually grow rapidly from 6 months – 1 year of age, up to 3
inches in diameter.
• Hemangiomas undergo a phase of rapid expansion, followed
by a stationary period and finally by spontaneous involution.
• Tend to fade/shrink with time, 50% by 5 years, 90% by 9
years, often disappearing completely
• Treatment with steroids/interferon/laser indicated only if
multiple, very large or interferes with function.
ERYTHEMA TOXICUM NEONATORUM
• This is a benign, self-limited, evanescent
eruption.
• The cause is unknown.
• The lesions are firm, 1–2 mm papules or
pustules with a surrounding erythematous flare
over trunk, face & extremities.
• Lesions may be sparse or numerous and
clustered in several sites or widely dispersed over
much of the body surface.
• Palms and soles are usually spared.

• Peak incidence is on the 2nd/3rd day of life,
can appear as late as 2-3 weeks
• Distinguished from infection by lack of
tenderness, warmth, or induration.
• Self-resolving, typically by 5-7 days after
appearance, usually by 2 weeks age
• Requires no treatment
TRANSIENT NEONATAL PUSTULAR
MELANOSIS
MELANOSIS
• This is a transient, benign, self-limited
dermatosis of unknown cause.
• It is characterized by 3 types of lesions:
- i. Evanescent superficial pustules
- Ii. Ruptured pustules with a collarette of fine
scale, at times with a central hyperpigmented
macule.
- Iii. Hyperpigmented macules .
MELANOSIS
• Lesions may be found in a profuse or sparse
distribution.
• More common in dark skinned than white infants.
• Typically present at birth.
• Present as 2-5mm pustules with hyperpigmented,
non-erythematous base
• Pustular lesions resolve within 24-48 hours,
hyperpigmented macules fade over weeks/months.
• No treatment is required.
MILIA
MILIA
• Common in about 50% of infants.
• Multiple 1-3mm, firm pearly white-yellow or opalescent white
papules on nose, chin & cheeks.
• They are keratin filled epithelial superficial epidermal inclusion
cysts.
• Called Epstein pearls if seen in gingiva of neonate.
• Usually appear in 1st month of life & may persist several
months, but may occur at any age.
• Benign, self-resolving, require no treatment
• Can be excised and contents expressed with fine needle guage.
MILIARIA/HEAT RASH/PRICKLY HEAT
• Results from retention of sweat in occluded eccrine sweat
ducts as a result of a keratinous plug in the sweat duct.
• Miliaria crystallina :Asymptomatic, noninflammatory,
pinpoint clear vesicles that may suddenly erupt over large
areas of the body surface, leaving brawny desquamation
on healing.
• Miliaria rubra: A less superficial eruption characterized by
1-3mm erythematous, minute papulovesicles usually
localized to sites of occlusion or to flexural areas, such as
the neck, groin, and axillae.
• Miliaria profunda: Due to rupture of the sweat duct deeper
in the skin at the level of the dermal-epidermal junction.
• Miliaria occur secondary to heat (eg. warm climates) in skin
areas with high heat generation or covered by clothing.
• Miliaria crystallina commonly occur in infants and children
because of underdeveloped sweat glands.
• TREATMENT: Cooling the patient by regulation of
environmental temperatures and by removal of excessive
clothing/wraps.
DIAPER DERMATITIS
DIAPER DERMATITIS
• Diaper dermatitis is the most common
infection caused by Candida.
• Primary infection generally occurs in the
intertriginous areas of the perineum and
presents as a confluent papular erythema with
erythematous satellite papules.
• May occur as an adverse effect of oral
antibiotic treatment.
DIAPER DERMATITIS
• TREATMENT
- topical antifungal therapy such clotrimazole 1%
cream, miconazole 2% ointment, or amphotericin
cream or ointment.
- If significant inflammation is present, the addition of
hydrocortisone 1% may be useful for the 1st 1–2
days.
- Frequent diaper changes and short periods without
diapers are important adjunctive treatments.
NEONATAL ACNE
NEONATAL ACNE
• The cause of neonatal acne is unknown .
• It has been attributed to:
-placental transfer of maternal androgens,
-hyperactive neonatal adrenal glands
-hypersensitive neonatal end-organ response to
androgenic hormones.
• The hypertrophic sebaceous glands involute
spontaneously over a few months, as does the
acne.
NEONATAL ACNE
• Open & closed comedones (papules/pustules),
occur on face and upper trunk.
• Common in about 20% of infants.
• Often present at birth or develops in second to
third week of life
• Self-resolving, usually by three months age.
• Treatment is usually not necessary, however if
required, use topical tretinoin and/or benzoyl
peroxide.
VITILIGO
VITILIGO
VITILIGO
• This is a hypopigmented lesion.
• Postulated theories of the cause include:
i. Melanocytes are destroyed because of the
accumulation of a toxic melanin synthesis
intermediate.
ii. Neurochemical factors damage melanocytes and
cause depigmentation.
iii. Immunologic abnormalities are responsible for
the changes in vitiligo.
VITILIGO
• There are two subtypes of vitiligo:
-Generalized (type A)
-Localized (type B).
• Localized vitiligo:
i. segmental vitiligo,
ii. Halo nevus phenomenon
iii. Premature graying of scalp hair (canities).
VITILIGO
• Most children have the generalized form, but
the localized type is more common among
children than among adults.
• TREATMENT:
- Topical steroid, tacrolimus or pimecrolimus for
localized and narrow-band (UVB) for
generalized.
- Avoid sun exposure, cosmetic cover.
.
THANKS FOR LISTENING

SUGGESTED READINGS
(1) Nelsons Textbook of Paediatrics. Kleigman
MR, Berham ER, Jenson BH, Stanton FB,
editors. 18th & 19th ed. Elsevier.
(2) Dermatology notes handbook of medical
information for medical transcriptionists.
(3) Paediatric Dermatology textbook 3rd edition.
Schachner LA, Hansen RC,editors. Mosby.
.
SUGGESTED READING
(4) Cox NH, Coulson IH. Diagnosis of skin
diseaeses in Rooks texbook of dermatology.
(5)Bianchi J, Page B, Robertson S. Your
Dermatology Pocket Guide: Common skin
conditions explained.
(6) Colour atlas of paediatric dermatology. 3rd
edition. Weinberg S, Prose NS, Kristal L.editors
(7) Internet.

Common Paediatric Skin Problems

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Common Paediatric Skin Problems

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COMMON PAEDIATRIC SKIN

• There are three layers in the skin. These layers

Cells move from the base of the epidermis up to

ii. Granular layer; This is the transitional layer

• The epidermis contains no blood vessels,

-The papillary dermis contains;

• Also within the reticular layer are the

iv. epidermal appendages or rete pegs – this

• Subcutaneous layer/ hypodermis: It is

VESICLE: A raised lesion filled with clear

BULLA: A raised lesion filled with clear

PAPULE: a circumscribed palpable elevation

PLAQUE: Is an elevated area of skin, with

MACULE: a circumscribed alteration in the

PATCH: A large macule >1cm in size .

• Transient skin disease/neonatal dermatosis

• Also called sixth disease

• The roseola rash begins as discrete, small (2–5 mm),

• Caused by human parvovirus B19 virus, a DNA

• These are bluish or slate-gray macular lesions with variably

• These are macular, sharply circumscribed

• May thicken or develop into nodules in adult.

• These are small, pale pink, ill-defined, vascular

• Usually symmetric with lessions on both sides

• May be present at birth or, more commonly, become

• Palms and soles are usually spared.

THANKS FOR LISTENING

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