PATHOPHYSIOLOGY,
ASSESSMENT,
TREATMENT MODALITIES
AND NURSING
INTERVENTION IN CHILD
WITH SKIN DISORDERS

INTRODUCTION
Skin is the largest and most superficial organ of
the body.
Nearly one third (1/3rd) of the pediatric
outpatient visits involve dermatology
complaints.
Skin disorders are associated manifestations of
many systemic and hereditary diseases.
2

REVIEW OF
STRUCTURE AND
FUNCTION OF THE
SKIN

DEFINITION
4
The skin is an organ of the integumentary
system made up of multiple layers of
ectodermal tissue, and guards the
underlying muscles, bones, ligaments and
internal organs.

5
STRUCTURE

Epidermis
6

7
Dermis

8
FUNCTIONS OF
SKIN

9

10
TYPES
OF SKIN
LESION
PRIMAR
SECONDARY

Primary-Macule
Well defined but flat lesions
with a change in colour. A
macule may be
hyperpigmented (e.g. cafe au
lait macule), hypopigmented
(e.g. leprosy), depigmented
(e.g. vitiligo) or erythematous
(e.g. drug rash).
11

Primary-Patch
A macule that is larger than
1cm in size.
12

Primary-Papule
A raised and palpable solid
lesion, smaller than 5mm.
13

Primary-Nodule
A large papule, usually 5 – 10
mm in diameter.
14

Primary-Plaque
A raised flat-topped lesion on
skin or mucous membrane,
usually over 1cm in size.
15

Primary-Blister
A small bubble on the skin
filled with serum and caused
by friction, burning or other
damage.
16

Primary-Vesicles
Raised fluid-filled lesion.
17

Primary-Pustule
Pus-containing well-
circumscribed lesion.
18

Primary-Abscess
A thick-walled pus-filled cavity
developed from necrosis of
tissue.
19

Primary-Wheal
A whitish, firm and elevated
lesions surrounded by red flare
as a result of dermal edema.
20

Primary-Petechiae
A circumscribed deposit of
extravasated blood, less than 5mm
in diameter.
21
Primary-Purpura
Primary-Ecchymosis
A circumscribed deposit of
extravasated blood, more than
5mm in diameter.
A blend of several petechiae and
purpuric spots, occupying a large
area of skin.

Primary-Telangiectasia
A visible dilatation of
superficial blood vessels.
22

Primary-Poikiloderma
A triad of atrophy of skin,
reticular pigmentation and
telangiectasia.
23

Primary-Cyst
A circumscribed lesion having
a wall and a lumen containing
fluid or solid matter.
24

Primary-Comedone
An inspitated plug of
sebaceous and keratinous
material lodged in dilated
orifice; closed white and open
black types are known.
25

Primary-Milia
A small subepidermal keratin
cyst that is normal finding in
neonates.
26

Primary-Burrow
A thread-like elevated
tortuous channel in the skin
typically seen in scabies
27

Secondary lesions
Scale
A visible flake comprising
shed stratum corneum
(horny layer) of he skin.
Crust
A collection of dried
serum and cellular debris.
28

Secondary lesions
Erosion
A focal breech in the
continuity of epidermis
with preservation of
dermis, leaving no
scarring after healing.
Ulcer
A focal breech in
the continuity of
epidermis as well
as upper dermis.
29
Fissure
A linear slit-like
breech in the
epidermis as well
as dermis (full layer,
not just the upper
dermis).

30
Fissure, erosion, ulcer - difference
Fissure
Erosion
Ulcer

Secondary lesions
Excoriation
A linear erosion or
ulcer caused by
scratching.
Atrophy
A formation of
connective tissue that
replaces the original
skin. Normal skin
markings are absent
in scar. 31
Scar
A thinning of
epidermis, dermis
or subcutaneous
tissue.

Secondary lesions
Sclerosis
A circumscribed or diffuse
area of induration and
binding down of skin.
Lichenification
An area of skin that is
thickened along with
hyperpigmentation and
enhanced skin markings due
to repeated scratching. 32

ARRANGEMENT OF LESIONS
33
Linear
Eg: Verrucous
epidermal nevus
Grouped
Eg: Herpes
Simplex
Dermatomal
Eg: Herpes Zoster
Arcuate
Eg: Granuloma
Annulare

34
SITES OF
PREDILECTION OF
LESIONS
The sites of predilection of
lesions indicates the sites of
preference of occurrence of
lesions.

35
COMMON DIAGNOSTIC TESTING FOR SKIN
DISEASES
Diagnostic Test Material to
obtain
Indications Findings
Potassium
hydroxide
preparation and
microscopic
examination
Skin scraping
from scale or
pustules
Presence of
scales or
pustules
Hyphae or
pseudo hyphae
indicating
dermatophyte
or yeast
infection
1

36
COMMON DIAGNOSTIC TESTING FOR SKIN
DISEASES
Diagnostic Test Material to
obtain
Indications Findings
Gram stain and
microscopic
examination
Skin scraping
from pustules
or bullae
Presence of
pustules or
bullae
Gram-positive or
Gram negative
bacteria.
2

37
COMMON DIAGNOSTIC TESTING FOR SKIN
DISEASES
Diagnostic Test Material to
obtain
Indications Findings
Tzank stain and
microscopic
examination
Skin scraping
from the base
of a vesicle
Presence of
vesicles
Rounded,
multinucleated
keratinocytes
indicating a
herpes virus
infection.
3

38
COMMON DIAGNOSTIC TESTING FOR SKIN
DISEASES
Diagnostic Test Material to
obtain
Indications Findings
Oil mount and
microscopic
examination
Skin scraping
from the base of
a burrow or non-
excoriated
papule
Presence of
burrows or
pruritic
papules
Mites or eggs
indicating
scabies
infection
4

39
COMMON DIAGNOSTIC TESTING FOR SKIN
DISEASES
Diagnostic
Test
Material to
obtain
Indications Findings
Punch biopsy Core of
anaesthetized
skin using a
punch biopsy
instrument.
Lesions suspected to
be malignant (such as
basal cell carcinoma
or squamous cell
carcinoma) or an
undiagnosed
inflammatory skin
lesion.
Microscopic
alterations in
the epidermis,
dermis and
subcutaneous
tissue.
5

40
COMMON DIAGNOSTIC TESTING FOR SKIN
DISEASES
Diagnostic
Test
Material to
obtain
Indications Findings
Shave or snip
biopsy
All parts of an
anaesthetized
skin lesion that
protrudes from
the surface of
the skin.
Raised lesions
suspected to be
malignant (such as
basal cell carcinoma or
squamous cell
carcinoma) or
bothersome raised
lesions.
Microscopic
alterations in
the
epidermis
and upper
dermis.
6

41
COMMON DIAGNOSTIC TESTING FOR SKIN
DISEASES
Diagnostic
Test
Material to
obtain
Indications Findings
Excisional
biopsy
An entire
anaesthetized
skin lesion
Lesions
suspected to be
malignant (such
as melanoma) or
bothersome flat
skin lesion.
Microscopic
alterations in the
epidermis, dermis
and subcutaneous
tissue with the entire
architecture of the
lesion in the
specimen.
7

42
TYPES/CLASSIFICATION OF SKIN DISORDERS IN
CHILDHOOD
Infections Infestations
(Parasitic skin
infections)
Bacterial
Viral
Fungal
Scabies
Pediculosis
Disorders of skin
appendages
Acne Vulgaris
Miliaria/Prickly
heat

43
TYPES/CLASSIFICATION OF SKIN DISORDERS IN
CHILDHOOD
Papulosquamous
disorders
Others
Lichen
Planus (LP)
Psoriasis
Eczematous
dermatitis

INFECTIONS
44
A. BACTERIAL
B. VIRAL
C. FUNGAL
The invasion and multiplication of
microorganisms such as bacteria, viruses, and
parasites that are not normally present within
the body. An infection may cause no symptoms
and be subclinical, or it may cause symptoms
and be clinically apparent. Infection may be
local or generalized and spread throughout the
body.

BACTERIAL INFECTIONS
45
A. IMPETIGO
B. ECTHYMA
(ULCERATIVE
IMPETIGO)
C. CELLULITIS
D. FOLLICULITIS,
BOILS AND
CARBUNCLES

46
Classification
Based on
predisposing
factors
Based on
morphology
Primary
Secondary
Non-
follicular
Follicular
Localized
Spreading
Folliculitis
Boils
Carbuncles
Cellulitis
Ecthyma
Impetigo

IMPETIGO
DEFINITION:
Impetigo is a highly-contagious bacterial infection of
the surface layers of the skin, usually exhibited as
painful and itchy blisters and sores around the
mouth and nose (in very young children it can also
occur in the nappy area). It is not serious, but it is
sore and itchy in nature
47

TYPES:
48
(1)
Bullous impetigo:
It causes large,
painless, fluid-filled
blisters that stay
longer.
(2)
Impetigo Contagiosa (Non-
bullous impetigo): It is
more contagious and
causes sores that quickly
burst to leave a yellow-
brown crust.

Etiology
49
 Staphylococcus aureus
 Streptococcus pyogenes
Common bacteria, some of which are found normally on the skin, causes
impetigo. When the bacterium enters an open area in the skin, infection can
occur.

Incidence
∆Common in children below 10
years of age with poor
personal hygiene.
∆Toddlers and preschool
children are the most
commonly affected, often
when recovering from upper
respiratory tract infection
50
Risk Factors
∆Local skin trauma such as
insect bites, wounds
∆Skin lesions from other
disorders such as eczema,
scabies, pediculosis
∆Age: more common in
toddlers and pre-schoolers (2-
5yrs)
∆Crowded living condition
∆Poor hygiene
∆Warm, moist climate

51
PATHOPHYSIOLOGY

CLINICAL FEATURES AND SITES OF PREDILECTION: BULLOUS IMPETIGO
Clinical features
► Thin-walled blisters on erythematous
base (Crusted blisters, that pop and
leave wet patches of red skin, initially
with vesicles or pustules on reddened
skin)
► The vesicles or pustules eventually
rupture to leave the characteristic
honey-colored (yellow-brown) crust.
► Lesions spread without central clearing.
► Lymphadenopathy frequent
52
Face, especially around the mouth and
nose
Sites of Predilection
Bullous impetigo

53
Clinical features
► Thick-walled, persistent blisters on
bland skin.
► Rupture only after a few days to
leave thin golden yellow crusts.
► Lesions heal in center to form
annular plaques.
► Lymphadenopathy rare
Occurs on the face and extremities
Sites of Predilection
Non - Bullous
impetigo
CLINICAL FEATURES AND SITES OF PREDILECTION: BULLOUS IMPETIGO

54
DIAGNOSTIC
EVALUATION
COMPLICATIONS TREATMENT
 Complete medical history
and physical examination
of the child.
 The lesions of impetigo
are unique and usually
allow for a diagnosis
which is based simply on
physical examination.
 A culture and sensitivity
of lesions may be done to
confirm the diagnosis and
the type of bacteria that is
present.
Impetigo contagiosa
 Post streptococcal
glomerulonephritis
(PSGN)
 Eczematization
Bullous impetigo
 Staphylococcal
scalded skin
syndrome
∆ The affected area must be cleaned
several times per day with either
water or an antibacterial wash
∆ Warm saline compresses to be
applied qid for 15 minutes to soften
and soak away the crusts
∆ Topical antibiotics should be applied
after every soakage
─ Mupirocin ointment
─ Fusidic acid ointment or cream
∆ Oral antibiotics in case of systemic
symptoms
─ Cephalexin
─ Cloxacillin

ECTHYMA (ULCERATIVE IMPETIGO)
55
Ecthyma is a pyogenic
infection of the skin
characterized by the
formation of adherent
crusts beneath which
ulceration occurs
ETIOLOGY
Streptococcus
pyogenes
Staphylococcus
aureus
DEFINITION

56
Predisposing
Factors

57
Vesicle or veiscopustule on
erythematous base
Enlarge and becomes indurated,
tender plaque and thickly crusted
Removal of crust
Saucer-shaped ulcer with raw
irregular base and elevated edges
Healing and scar formation
(rarely: gangrene)
Ecthyma is similarly to superficial
impetigo. The difference is that in
impetigo the erosion is at the
stratum corneum and in ecthyma
the ulcer is full thickness (includes
both epidermis and dermis) and
thus heals with scarring

58
Clinical features
◙ Adherent crusts, beneath which
purulent irregular ulcers occur.
◙ Healing occurs after few wks, with
scarring
More on distal extremities (thighs
& legs)
Sites of Predilection
Ecthyma (Ulcerative
Impetigo)
CLINICAL FEATURES AND SITES OF PREDILECTION: ECTHYMA
(ULCERATIVE IMPETIGO)

59
Treatment
Cleansing with
soap and water
Application of
Mupirocin or
Bacitracin ointment
twice a day
Oral Dicloxacillin
or first-generation
Cephalosporin
Proper hygiene
and nutrition

60
CELLULITIS
DEFINITION
Cellulitis is an acute spreading bacterial
infection below the surface of the skin
characterized by redness (erythema),
warmth, swelling, and pain. Cellulitis
occurs when an entry point through
normal skin barriers allows bacteria to
enter and release their toxins in the
subcutaneous tissues.

61
Etiology
Bacteremic spread of
infection - bacteria
arriving from a distant
source via the
bloodstream.
 Staphylococcus aureus
 streptococci pyogenes
Break in the skin
from an abrasion, a
cut, or a skin ulcer.
Local trauma,
such as an animal
bite

Pathophysiology
62
Break in the skin,
such as a fissure,
cut, laceration,
insect bite, or
puncture wound
causes entry of
bacteria into the
subcutaneous
tissue. This results
in deep
inflammation of
subcutaneous
tissue from
enzymes
produced by
bacteria.
Break in the skin
Entry of bacteria into the
subcutaneous tissue
Enzymes produced by
bacteria
Deep inflammation of
subcutaneous tissue

63
Signs
&
Symptoms
Swelling of the skin
Tenderness
Pain
Warm skin
Bruising
Blisters
Fever
Headache
Chills
Feeling weak
Red streaks from the
original site of cellulitis

64
Some cases of cellulitis are considered an emergency if any of the following
symptoms are present:
A very large
area of red,
inflamed skin
Fever
If the area is affected,
causing the child to
complain of numbness,
tingling or other changes
in a hand, arm, leg, or foot
If the skin
appears black
If the area that is
red and swollen is
around the child's
eye(s) or behind
his/her ear(s)
If the child has
diabetes or has a
weakened
immune system
and develops
cellulitis

65
Fig: Cellulitis
Fig: Cellulitis
Fig: Cellulitis

66
 History collection
 Physical examination
 Complete Blood
Count (CBC)
 Culture and
sensitivity
DIAGNOSIS COMPLICATIONS
 Blood infection
(septicaemia)
 Bone infection
(osteomyelitis)
 Inflammation of the
lymph vessels
(lymphangitis)
 Inflammation of the
heart (endocarditis)
 Meningitis
 Shock
 Tissue death
(gangrene)
 General
 Immobilize the part and
elevate the extremity above
the level of heart
 Provide moist heat to
promote wound healing
 Mild cases:
 An outpatient basis with oral
antibiotic therapy
 Dicloxacillin
 Amoxicillin
 Cephalexin
 Severe cellulitis
 The patient is hospitalized
and treated with intravenous
antibiotics for at least 7 to 14
days
MANAGEMENT

FOLLICULITIS, BOILS AND CARBUNCLES
DEFINITIONS
Folliculitis
Folliculitis is the inflammation of hair follicles due to an infection, injury or irritation. It
is characterized by tender, swollen areas that form around hair follicles, often on the neck,
breasts, buttocks and face.
67
Fig: Folliculitis

FOLLICULITIS, BOILS AND CARBUNCLES
DEFINITIONS
Boils
Boils are pus-filled lesions that are painful and usually firm. Boils are usually located in
the waist area, groins, buttocks and under the arm.
68
Fig: Boils

FOLLICULITIS, BOILS AND CARBUNCLES
DEFINITIONS
Carbuncles
Carbuncles are clusters of boils. These are usually found in the back of the neck or thigh.
69
Fig: Carbuncle

70
SIGNS
&
SYMPTOMS

71
 Diagnosis of Folliculitis,
boils, and carbuncles is
made after a thorough
medical history and
physical examination.
 After examining the
lesions, culture of the
wound is done to help to
verify the diagnosis and
select the best
treatment.
DIAGNOSIS
Specific treatment for Folliculitis, boils and
carbuncles may include:
 Topical antibiotics (for Folliculitis).
 For carbuncles and boils, a warm compress
may be used to help promote drainage of
the lesion.
 Oral or IV antibiotics (to treat the
infection).
 Possible removal of the boils and
carbuncles.
 Incision and drainage followed by
antibiotic therapy.
Carbuncles heal more slowly than a single
boil. The skin must be kept clean to help
prevent these conditions from occurring.
MANAGEMENT

VIRAL
INFECTIONS
72
VURRUCA (WARTS)
MOLLUSCUM
CONTAGIOSUM

73
Warts are benign epidermal neoplastic
growths on the skin caused by an
infection with the human papilloma virus,
or HPV.
DEFINITION
VURRUCA (WARTS)

74
Etiology
Human papilloma virus or HPV. The
incubation period is1 – 6 months.
 HPV type I, II and IV associated with
plantar warts
 Type I causes verrucae plantaris
lesions
 Type II causes mosaic warts
 Type IV causes seed corn lesions
 Type III causes genital warts
Physical factors such as infectious
location, weight-bearing pressure and
moisture help determine the clinical
appearance of the lesion
Can spread through small cuts
in skin
May disappear spontaneously,
often within 2 years of appearance
Due to immune system development,
are seen more commonly in children
and less commonly in adults

75
General Warts Characters
There are usually little black dots near the
surface of the wart, representing
thrombosed capillaries in elongated dermal
papillae.
In Immunocompromised there is a risk for
squamous cell carcinoma
There is epidermal thickening, with
particular increase in the granular cell layer

76
Fig: Warts
Fig: Warts
Fig: Warts

77
Risk Factors
Exposure to
others who
have warts
Eczema
Broken down
skin

78
Common
wart
(vurruca
vulgaris)
Plantar wart
(foot warts)
Flat wart
(plane
warts) Filiform
wart
Genital wart
(condylomata
acuminate)
Types of Warts

79
Common wart
(vurruca
vulgaris)
 Raised, cauliflower-like lesions that occur most frequently on
fingers, around the nails, and on the backs of the hands.
Grow most often on the area where skin was broken, such as
from biting fingernails or picking at hangnails.
 Can have black dots that look like seeds (often called “seed”
warts). They appear as hyperkeratotic papules with a rough,
irregular surface. They range from smaller than 1 mm to
larger than 1 cm.
 Most often feel like rough bumps.
 Common in children and early adulthood.
 They may be scattered, grouped or periungual in
distribution.
 Common warts in children usually resolve spontaneously.

80
Plantar wart (foot
warts)
* Grow most often on the soles (plantar surface) of the feet
* Can grow in clusters (mosaic warts)
* Often are flat or grow inward (walking creates pressure,
which causes the warts to grow inward)
* Painful

81
Flat wart (plane
warts)
 These are tiny, flat-topped, flesh-coloured warts which
usually occur on the dorsa of the hands and the face.
 They often occur in lines due to inoculation of the
virus into scratches and abrasions.
 Tend to grow in large numbers, 20 to 100 at a time.

82
Filiform
wart
 Long slender growths, usually seen on the face around
the lips, eyelids, or nares
 Looks like long threads or thin fingers that stick out

83
Genital wart
(condylomata
acuminate)
• Grow on the genitals, are usually sexually transmitted
• Soft and do not have a rough surface like other
common warts
• Highly infectious

84
Management
Immunotherapy,
that causes an
allergic reaction
and helps destroy
the wart. Vaccines
like BCG, MMR etc
are used.
Salicylic
(12-20%) & lactic acid
(4-20%), to soften the
infected area
Freezing with
liquid nitrogen
(cryotherapy)
Electrodessication
(using an electrical
current to destroy
the wart)
Laser
surgery

85
MOLLUSCUM
CONTAGIOSUM
Molluscum contagiosum is a viral disease of
the skin that causes small pink or skin-
colored bumps on the child’s skin.
 It is not harmful and usually does not
have any other symptoms.
 The virus is inside the bumps and is
mildly contagious.
 These bumps usually clear over an
extended period of time.
DEFINITION

86
Caused by
the poxvirus.
ETIOLOGY
&
INCIDENCE
Most common
in children and
adolescents.

Small, shiny, and
smooth in appearance
Flesh-colored,
white, or pink
87
Firm, raised and shaped
like a dome with a dent or
dimple in the middle
Filled with a
central core of
waxy material
Can become red or
inflamed
Can cause itching
sensation
Size varies between 2 to
5 mm in diameter
Lesions usually occur in
groups or clusters ,
between 2 and 20 in
children
Seen on the genitals, face,
torso, arms and lower
abdomen

88
Fig: Molluscum contagiosum
Fig: Molluscum contagiosum

• Can become red,
itchy and inflamed.
• If scratched or
touched, it can
easily spread to
other parts of the
body.
• If on eyelids, it can
develop into pink
eye (conjunctivitis).
89
COMPLICA
TIONS
DIAGNOSTIC
EV
ALUA
TION MANAGEMENT
• Medical history and
physical
examination
• The lesions are
unique and usually
diagnosed on the
basis of physical
examination.
• Additional tests are
not routinely
ordered.
Heal without treatment
over a period of 6 – 9
months. Additional
treatment include:
• Removal of the
lesions
(cryosurgery,
curettage)
• Use of topical
medications (to
speed the resolution
of the lesions).

FUNGAL
INFECTIONS
90
A. DERMATOPHYTOSIS
(RINGWORM
INFECTIONS)
B. CANDIDIASIS (YEAST
INFECTION)

DERMATOPHYTOSIS (RINGWORM
INFECTIONS)
DEFINITION
91
» Dermatophytes are aerobic fungi present in the soil. They
require keratin for growth and cause superficial skin infections.
» The dermatophytoses (ringworm) are infections caused by a
group of closely related filamentous fungi that invade
primarily the stratum corneum, hair, and nails. These are
superficial infections by organisms that live on, not in, the skin.
They are confined to the dead keratin layers and are unable to
survive in the deeper layers.

92
Trichophyton
Epidermophy
ton
Microspor
um
Etiology

93
superficial fungal
infection of the skin of
foot (between the toes
and on the soles )
Tinea pedis
(athlete’s foot)
chronic non-
inflammatory
macular patches on
the skin
Tinea Vesicolor
Fungal infection of
the scalp .
Tinea capitis
Fungal infection
of glabrous skin.
Tinea corporis
Fungal infection of
nails
Tinea unguium
(onychomycosis)
Types
ungal infection peritoneal
folds, extending upto
upper inside of the thigh.
Tine Cruris (Jock Itch)

Diagnosis
94
 Microscopy of skin and nail specimens may reveal hyphae and
spores.
 Fungal culture can identify the species but is not always reliable
and it can take 6 weeks to get results.
 Ultraviolet light (Wood’s light) is useful for tinea capitis specially.
Fluorescence is produced by the fungus. Fluorescence is not
seen with tinea corporis or tinea cruris.
 Rarely, a biopsy may be needed if the case is atypical or not
responding to treatment.

Treatment
Type Characteristics
Tinea capitis:  Oral administration of griseofulvin 15 to 20 mg/kg/day for 5 to 7 days.
 Topical application of antifungal cream
 Selenium sulfide lotion can be used twice per weeks.
 Clotrimazole, tolnaftate, etc. can be used as cream or lotions.
Tinea corporis:  Application of calamine lotion and mild fungicides.
 Griseofulvin is administered in severe generalized and resistant cases.
 Tolnaftate (Tinaderm) is used effectively for this infection.
Tinea cruris (Jock
itch):
 Griseofulvin or tolnaftate as topical applications.
Tinea pedis:  The web space between toes to be kept dry.
 Aluminium chloride and gentian violet.
 Amorolfine spray can be used daily for 3 to 6 weeks to have good result.
Tinea unguium:  It requires treatment for long period.
 Griseofulvin or other antifungal agents can be applied for 3 to 4 months for finger nails and
6 to 12 months for toe nails.
 Ciclopirox and natifine can be used for better penetration in the nails.
Tinea versicolor
(pityriasis):
 Local application of antifungal agent (Tolnaftate) and application of selenium sulfide
shampoo over affected skin 15 to 20 minutes daily for 1 to 2 weeks
 Good skin hygiene. Repeated attacks are commonly found.

96
CANDIDIASIS
(YEAST INFECTION)
Candidiasis, sometimes
called moniliasis, is an
infection caused by yeast
on the skin and/or mucous
membranes.
Candida albicans, a normal
commensal, becomes
pathogenic in the presence of
predisposing factors such as
moisture, obesity, diabetes
and immunocompromised
states
DEFINITION ETIOLOGY

97
Types and
Manifestations
1. Candidal intertrigo
Area:
Skin folds or navel
Manifestations:
 Erythematous, moist,
macerated lesion with a frayed
irregular edge
 Patches, from which clear fluid
oozes
 Itching or burning

98
Types and
Manifestations
2. Candidal diaper
dermatitis
Area:
Perianal region, spreading to perineum, upper
thighs, lower abdomen and lower back.
Manifestations:
 Well defined weeping eroded lesions
with scalloped border with a collar of
overhanging scales
 White or yellow discharge from
vagina

99
Types and
Manifestations
3. Candidal paronychia
Area:
Nail beds
Manifestations:
 Nail plate is thickened and dystrophic.
 There is loss of cuticle with redness
and swelling of nail fold.
 Small beads of pus can be expressed
from under the proximal nail fold
 White or yellow nail that separates
from the nail bed

100
Types and
Manifestations
4. Oral thrush
Area:
Mouth
Manifestations:
 Seen in new born breast fed infants.
 Presents as soft, creamy white to
yellow, elevated plaques that are easily
wiped off to leave an erythematous,
eroded or ulcerated surface.
 Buccal mucosa (most frequently),
tongue, palate and gingiva.

DIAGNOSTIC
EVALUATION
 Medical history and
physical examination
 Skin scrapings are taken to
confirm the diagnosis with
a microscopic examination
or culture.
101
TREATMENT
 Predisposing factors should be
addressed and the area should be
kept dry.
 Topical therapy with imidazoles
(Clotrimazole, miconazole and
ketoconazole), amphotericin, and
nystatin is effective for thrush.
 Systemic therapy with weekly
fluconazole or pulse itraconazole is
given for onychomycosis.

102
INFESTATIONS
(PARASITIC SKIN
INFECTIONS)
A. SCABIES
A. PEDICULOSIS
(LICE
INFESTATION)

103
Scabies is an infestation of mites (tiny insects) characterized by
small red bumps and intense itching.
SCABIES
DEFINITION
 Caused by Sarcoptes scabiei
 Can spread quickly through close physical contact in a family,
child care group, school, class or nursing home
 Mites cannot survive off the human body for more than 48
hours and cannot reproduce off the body
 Scabies can affect people of all ages. Scabies occurs mostly in
children and young adults.
ETIOLOGY AND
INCIDENCE

PATHOPHYSIOLOGY
104

105
MANIFESTATIONS

106
SITES OF PREDILECTION
Lesions characteristically seen in
►Webs of hands
►On wrists
►Ulnar aspects of forearms
►Elbows
►Axillae
►Umbilical
►Area
►Genitalia
►Feet
►Buttocks
►Face is usually spared except in infants in whom
scalp, palms and soles are also involved.
►Nodular lesions are seen on genitalia

107

108
• History taking and
clinical examination.
• Microscopic
examination of
scrapings of the
lesions.
DIAGNOSTIC
EVALUATION
MANAGEMENT
 5% permethrin cream: It is safe for
children as young as 1 month old and
women who are pregnant.
 25% benzyl benzoate lotion
 10% sulphur ointment
 1% indane lotion.
 Antihistamine: To control itch and help
to sleep
 Pramoxine lotion: To control the itch
 Antibiotic: To combat an infection
 Steroid cream: To ease the redness,
swelling and itch.

109
Prevention and care:
Wash clothes,
bedding towels
Touch and
hold child less
Clean entire
home

110
DEFINITION
Pediculosis can
be explained
as infestation
of lice on the
scalp or body
ETIOLOGY
 Pediculosis humanus
(P. humanus capitis,
head louse and P.
humanus corporis,
body louse)
 Phthirus pubis (pubic
louse)
INCIDENCE
 Girls are affected
twice as often as boys.
 The peak incidence is
in preschool and
young school age
children (aged 3 to 10
years).
PEDICULOSIS (LICE INFESTATION)

111

112
Direct contact
with an infected
individual
Adolescents or
young adult pubic
lice through
sexual contact
Sharing of
clothing and
combs or brushes
Female
head
louse lays
egg
(nits),
which
glue onto
the base
of the
hair shaft
near the
scalp
1 week:
one
nymph
hatch
from the
nits
2 weeks:
nymph
develop
to adult
louse
Adult louse
feeds on
blood and
excrete
saliva
Skin
irritation
and itching
Severe
itching and
scratching
Secondary
infections

113
 Nits (covered with gelatinous
material which hardens to semi-
opaque, tiny, pearly whitish mass)
are commonly visible behind the
ears and at the nape of the neck
 Scattered lesions on the scalp
causing intense pruritus.
 Posterior cervical lymph adenopathy
associated with these lesions.
 Excessive scratching of the infested
areas can cause sores, which may
become infected.
 Tickling feeling
Fig: Head lice infestation
MANIFESTATIONS

114
DIAGNOSIS HEAD LICE/BODY LICE
• Finding a live nymph or an adult louse in the scalp or hair of someone.
• Finding nits no more than 6 mm from the scalp indicates a current
infestation and more than 6 mm indicates a previous infestation.
• Finding eggs in clothing
• Finding adults crawling in clothing (generally the seams)
• Finding adults crawling/feeding on the human body

115
MANAGEMENT
Pediculosis capitis
 Use of Pediculocides
 Permethrin, 1% lotion, single 10 minute
application to wet hair followed by rinsing.
Second application after 7 days.
 Gamma benzene hexachloride, 1% single
overnight application to dry hair followed
by rinsing. Second application used after 7
days.
 Malathion, 0.5% water based lotion,
applied on dry hair for 6 hours. Has
residual effect, so 2nd application not
needed.
Pediculosis pubis
infestation of lashes
 Petrolatum (twice daily
for 7-10 days) is used for
eyelash infestation. The
petrolatum covers the
lice and their nits,
preventing respiration.
 The dead lice are
removed mechanically
with tweezers

116
o Avoid head-to-head contact
o Don’t share any head garments or clothes
o Don’t share combs, brushes, or towels (Disinfect them!!!)
o Wash and dry clothes bedding, and other things worn or
used by those who are infested
o Vacuum floor and furniture
o Avoid activities that are prone to spreading lice!
o Bathe regularly
o Change clothing regularly
o Machine wash and dry infested and un-infested clothing
regularly
o Seal clothes in plastic bags.
o Don’t share beds, clothes, towels, or bedding
o Dusting with chemical insecticides may be necessary to
prevent the spread of disease.
PREVENTION

117
A. ACNE
VULGARIS
B. MILIARA/PRIC
KLY HEAT
DISORDERS OF SKIN
APPENDAGES

118
ACNE VULGARIS
 Increased sebum
secretion
 Microbial
colonization
 Occlusion of
pilosebaceous
orifice
Acne, medically known as
acne vulgaris, is a skin
disease that involves the
oil glands at the base of
hair follicles. Acne is a
chronic skin condition
characterized by areas of
blackheads, whiteheads,
pimples, greasy skin, and
possibly scarring.

119
INCIDENCE
&
PREDISPOSING
FACTORS
 Usually starts during
puberty and stops around 5
years later in 7 out of 10
people.
 Occasionally, newborn
babies can get acne in the
first few weeks or months of
life.
 It affects approximately
more than 80% of
adolescents and upto 20%
of neonates.
 It is more common in boys.
It flares up at winter and
tends to improve in
summer.
 Genetic predisposition:
Found to be familial
Identical twins shows
greater concordance of
severity of acne.
 Diet: High glycemic diet.
 Cosmetics: Seen in
women using oil based
cosmetics for long time.
Follows facial massage.
 Menstrual cycle:
Premenstrual edema of
pilosebaceous duct.
 Psychological factors

PATHOPHYSIOLOGY
1.Follicular plugging
2.Increased Sebum
Production
3.Acnes Proliferation
4.Inflammation
120

CLASSIFICATION
1.MILD
2.MODERATE
3.SEVERE
121

122
MANIFESTATION
• Greasy skin and spots (whiteheads or blackheads) on face,
back and chest
• Inflamed spots (pustules, nodules and cysts) may be
painful, tender to touch and the affected skin may feel hot.
1. Comedonal acne
⁃ Open comedones
(blackheads) with a
central dark keratin
plugs.
⁃ Closed comedones
(whiteheads) with
no visible keratin
plug.
2. Papular /
Pustular acne
⁃ Patients present
with inflamed,
2- to 5-mm
papules/pustules
3. Nodular/Cystic acne
⁃ Patients present with
red, firm, or fluctuant
nodules (cyst like)
that may drain or
form sinus tracts.
⁃ These lesions may
leave permanent
scars.

TREATMENT
General measures
• Oil and oil-based skin
care products need to
be avoided.
• There is no restriction
with regard to use of
soaps and cleansers.
• No dietary restrictions
are usually needed.
123

124
DEFINITION
• Common in
tropical
environments
• Miliaria crystallina
& miliaria rubra-
occur at any age,
but common in
infants
• Miliaria profunda
is more common
in adults
INCIDENCE
Miliaria is a
disorder of the
sweat glands
where there is
blockage of the
sweat ducts,
which results in
the leakage of
eccrine sweat
into the
epidermis or
dermis
MILIARA/PRICKLY HEAT

125
ETIOLOGY
Immaturity of the eccrine ducts
Occlusion of the skin, as with
transdermal drug patches
Occlusive clothing
Lack of acclimatization
Hot, humid conditions
Drugs
Miliaria is due to obstruction and rupture of
sweat ducts resulting in spillage of sweat into
adjacent tissue.

126
01
02
03
04 Miliaria
profunda
Miliaria
rubra
Miliaria
crystallina
Miliaria
pustulosa
CLASSIFICATION

127
Classification Description Picture
Miliaria
crystallina
• Appears in bedridden
patients, bundled children
and seen during high
fever.
• Characterized by small,
clear, superficial, non-
inflamed vesicles.
• Lesions are asymptomatic
and rupture at the
slightest trauma
• Self-limited; no treatment
is required

128
Classification Description Picture
Miliaria rubra • Characterized by small
extremely pruritic,
erythematous papulo-
vesicles with sensation of
prickling, burning, or
tingling

129
Classification Description Picture
Miliaria pustulosa • Always preceded by some
injury, destruction, or
blocking of sweat duct
• Pustules independent of
hair follicle
• Seen in intertriginous
areas, flexure surfaces of
extremities, scrotum, and
back of bedridden
patients
• Sterile pustules

130
Classification Description Picture
Miliaria profunda • Characterized by large
erythematous non-pruritic,
flesh-colored, deep-seated,
whitish papules
• Asymptomatic, usually
lasting only 1 hr after
overheating has ended
• Concentrated on the trunk
and extremities
• Occlusion is in upper dermis
• Only seen in tropics usually
following a severe bout of
miliaria rubra

131
PATHOPHYSIOLOGY
Excessive Sweat and
clothing that does not
absorb sweat
Blockages in the
superficial stratum
corneum
Miliaria
crystalline
Keratin blockage or
Staphylococcus in
the sweat duct
Bubbles in the
stratum
spinosum
Inflammation
of the skin
Miliaria
rubra
Eruption
Pus
formed

132
History
Physical
examination
Education
Topical
Therapy
Systemic
Therapy
TREATMENT
DIAGNOSIS

133
COMPLICATIONS
Secondary
infection
Impetigo
Heat
Intolerance

134
A. LICHEN
PLANUS (LP)
A. PSORIASIS
PAPULOSQUAMOUS
DISORDERS

135
LICHEN PLANUS (LP)
DEFINITION
Lichen Planus is an acute or chronic
non-infectious immune mediated
disorder of skin, oral mucous
membrane or nails

136
Unknown
RETIRE
ETIOLOGY
Lichenoid
reactions
complication
of chronic
hepatitis C

137
CLINICAL FEATURES
Violaceous, pruritic, polygonal
and flat-topped papules with
white streaks (Wickhams striae)
Lesions seen on wrists, around
ankles and may appear at sites
of trauma (Koebners
phenomenon)
Lesions on buccal
mucosa, tongue and
gingiva, annular
lesions are seen on
genitalia.
Scalp lesions:
Scarring alopecia
Nail changes:
Longitudinal grooves,
tenting of nail plates
and pterygium
formation

138
LICHEN PLANUS (LP)
ILLUSTRATIONS

139
DIAGNOSIS
& TREATMENT

140
PSORIASIS
Psoriasis is a chronic recurrent dermatisis marked by discrete
vivid red macules, papules or plaques covered with silvery
lamellated scales over scalp, knees, elbows, umbilicus and
genitalia. Removal of scales leads to multiple small bleeding
points (Auspitz sign).
DEFINITION

141
ETIOLOGY
Heredity:
Psoriasis is
polygenic trait
Immunological
factors: T cells
play a pivotal role
in pathogenesis
of psoriasis
Triggers:
a. Physical trauma,
infections (3 hemolytic
streptococci, HIV
infection)
b. Drugs (lithium, NSAIDS,
anti-malarials)
c. changes in season and
climate

142
TYPES
Type II:
onset is in
adulthood
Type I:
onset is during
childhood and
adolescents
TYPE I PSORIASIS
CHARACTERS
 Onset in second decade.
 Positive family history.
 Severe disease.
 Prominent Koebners
phenomenon.
 Prolonged course,
requiring relatively more
aggressive therapy.

143
CLASSIFICATION
Acute Chronic
Erythroderma
Psoriasis
vulgaris
Pustular
psoriasis
Acute
guttate

144
CLINICAL FEATURES
Psoriasis vulgaris
 Well demarcated, indurated,
erythematous scaly (silvery, loose)
lesions.
 Involves knees, elbows and extensors,
lower back, scalp and sites of trauma
(Koebners/isomorphic phenomenon).
Face and photo-exposed areas generally
spared.
 Auspitz sign: Removal of scales by
scraping with a glass slide reveals a
glistening white membrane (Burkleys
membrane) and on removing the
membrane, bleeding points become
visible.

145
CLINICAL FEATURES
Guttate psoriasis
◘Occurs in children and
adolescents.
◘May be precipitated by
streptococcal tonsillitis.
◘Crops as small erythematous
scaly papules.
◘Predominantly on trunk.

146
CLINICAL FEATURES
Pustular psoriasis
Two rare variants described in children:
1. Annular pustular psoriasis:
Characterized by sudden onset of fiery
red erythema rapidly covered by cluster
of very superficial creamy white pustules
which in children form circinate/annular
lesions.
2. Infantile and juvenile pustular psoriasis:
Rare; seen in infants as annular/circinate
lesions. Runs a benign course and often
confused with seborrheic and napkin
dermatitis.

147
DIAGNOSIS
History and clinical features A biopsy (which is confirmatory)

TREATMENT
Type Treatment of choice Alternative treatment
Psoriasis Vulgaris
 Localized (<30%
BSA)
Coal tar preparations Topical steroids + Salicylic
acid
 Extensive (>30%
BSA)
Narrow band Ultraviolet B
(UVB), PUVA (Psoralen +
ultraviolet light A)
Methotreaxate, Acitretin,
Cyclosporin A
 Facial lesions Topical steroids
Guttate psoriasis Antibiotics + Emollients,
PUVA (Psoralen + ultraviolet
light A)
Coal tar preparations, Mild
topical steroids
Pustular psoriasis Methotreaxate, Acitretin
148
 PUVA : Should not be used in children <6 years of age

149
0THERS
A. ECZEMATOUS
DERMATITIS
a) Atopic
Dermatitis
b) Infantile
Seborrheic
Dermatitis
c) Diaper
Dermatitis

150
ECZEMATOUS DERMATITIS
Eczema is a condition where the skin gets irritated,
red, dry, bumpy, and itchy.
Dermatitis is inflammation of the skin, typically
characterized by itchiness, redness and a rash.
DEFINITION

151
Types
01
02
03
Atopic
Dermatitis
Infantile
Seborrheic
Dermatitis
Diaper
Dermatitis

152
Atopic Dermatitis
DEFINITION
INCIDENCE
ETIOLOGY
Atopic dermatitis (AD) is a chronic, pruritic inflammatory skin disease
characterized by intense itching with episodes of exacerbation (flares
which may occur as frequently as two or three per month) and
remissions. Atopic dermatitis is also known as infantile or childhood
eczema. It is often called “the itch that rashes”.
• Affects approximately 10-20% of children worldwide
• Onset is usually before 5 years of age and may not
diminish until early adulthood.
• Genetic predisposition
• Immunological changes

153
Atopic Dermatitis: Clinical Features
Pruritus
Secondary lesions due to chronic rubbing
and scratching
Lesions appear as xerosis (dry, scaly skin), ill-defined erythema, small
coalescing edematous papules or vesicles, Lichenification and/or
excoriations (secondary to relentless scratching, crusts, etc.

154
Infantile pattern (3 months – 2 years):
» Begins after 3 months of age as
extremely itchy erythematous papulo-
vesicles
» Involves the cheeks, forehead, scalp and
extensor surfaces.
» Erythematous, ill-defined plaques on the
cheeks with overlying scale and crusting.
» Clears by 18 months of age in 40% and
in 60% changes into childhood pattern.

155
Childhood (2 – 12 years):
» Includes flexural areas of neck, elbows,
knees, wrists and ankles.
» Lichenified erythematous plaques
» Erythematous, excoriated papules with
overlying crust mainly in antecubital
fossa
» 70% clear by 10 years of age.

156
Atopic Dermatitis: Diagnosis
Diagnosis is based on Hanifin and Rajka criteria for
atopic dermatitis.
Presence of 3 or more major features and 3 or more minor
signs determine the diagnosis.

157
Major Features
• Pruritus
• Typical morphology and distribution.
• Flexural Lichenification or linearity in
adults
• Facial and extensor involvement in infants
and children
• Chronic or chronically-relapsing
dermatitis
• Personal or family history of atopy
(asthma, allergic rhinitis, atopic dermatitis)

Minor Features
• Xerosis
• Ichthyosis, palmar hyperlinearity, or
keratosis pilaris.
• Immediate (type 1) skin-test reactivity
• Raised serum IgE
• Early age of onset
• Tendency toward cutaneous
infections (especially S aureus and
herpes simplex) or impaired cell-
mediated immunity.
• Tendency towards non-specific hand
or foot dermatitis
• Nipple eczema
• Cheilitis
Minor Features
• Recurrent conjunctivitis
• Dennie-Morgan infraorbital fold
• Keratoconus
• Anterior subscapular cataracts
• Orbital darkening
• Facial pallor or facial erythema
• Pityriasis alba
• Anterior neck folds
• Itch when sweating
• Intolerance to wool and lipid solvents
• Perifollicular accentuation
• Food intolerance
• Course influenced by environmental or
emotional factors
• White demographism or delayed blanch.
158

159
Atopic Dermatitis: Treatment
Treatment
General Symptomatic
Avoid scratching
Dietary restrictions
Vaccinations
Acute eczema
Chronic eczema

160
SEBORRHEIC DERMATITIS (CRADLE CAP)
DEFINITION
CAUSE
Seborrheic Dermatitis is a chronic, inflammatory reaction of the
skin. It is most common in the scalp but may involve the eyelids
(blepharitis), external ear canal (otitis externa), naso-labial fold
and inguinal region. It is most common in infants.
Malassezia furfur, a commensal yeast

161
CLINICAL
MANIFESTATIONS
Reddish, somewhat
swollen patches of skin
Greasy, yellow scale on
erythematous base
Itching
Burning
Self-
limiting
and usually
resolves by
12 weeks

162
Sites of predilection:

163

164
The crusts of cradle cap should be pre-
treated with warm olive oil.
Wet compress is applied over the fissured
lesion before application of ointment.
Application of 2% ketaconazole shampoo,
mild topical steroid or 1% pimecrolimus
cream hastens subsidence.
Treatment

165
DIAPER DERMATITIS
Diaper dermatitis is a prototypical
example of irritant contact dermatitis,
caused by over hydration of the skin,
maceration, prolonged contact with
urine and feces, retained diaper soaps
and topical preparations restricted to
the area covered by diapers.
DEFINITION

166
 Commonly
affects infants
 Ages 9 – 12
months
a. Irritant dermatitis in infants
caused by prolonged contact
with feces and ammonia
(produced by the action of urea
splitting organism on urine)
b. Impetigo
c. Perianal streptococcal disease
d. Allergies
INCIDENCE
CAUSES

167
Pathophysiology

168
Types and Clinical Manifestation
Candida diaper dermatitis
⁃ Rash begins in the creases or
folds of the thighs and in the
diaper area, and then spreads.
⁃ Rash is usually deep, red,
shiny rash with red and
satellite lesions.
⁃ Usually accompanied by the
yeast infection, oral thrush.

169
Types and Clinical Manifestation
Seborrheic diaper dermatitis
⁃ Affects the skin fold in the
groin area and is usually
pink.
⁃ May appear on the face,
scalp, or neck of infants at
the same time.

170
Types and Clinical Manifestation
Contact diaper dermatitis
⁃ Mainly seen on the
buttocks and may extend to
the thighs, stomach and
waist area
⁃ Does not generally involve
fold areas
⁃ Rash usually red and shiny

171
Treatment
 Diaper area has to be left open to air or covered with topical emollients.
 The first line therapy for individuals with diaper dermatitis is zinc oxide
ointment or various products containing zinc oxide
 Acetyl tocopherol
 Emollients – white petrolatum ointment (traps water beneath the
epidermis), Aquaphor ointment
 In case of candidiasis – Antifungal agents like Nystatin cream and
Econazole

172
 Health education to parents and caregivers – diaper education,
treatment
 Keep skin clean and dry
 Frequent changing of diaper
 Use of disposable diapers with sub absorbent materials
 Rinsing washed cotton diapers well (preferably in diluted lemon
juice).
 Wash genitalia with warm water and mild soap
 Apply bland protective topical agent after thorough washing
PREVENTION

173
THERAPEUTIC MANAGEMENT OF SKIN LESIONS
DRESSINGS
TOPICAL
THERAPY
SYSTEMIC
THERAPY
Wet Compresses
Soaks
Baths

174
NURSING CARE
OF THE SKIN

CARE OF SKIN
OF NEONATES
175
a)Maintain Skin
Integrity
b)Prevent Skin Injury
in the Neonate

176
CARE OF THE
DISEASED SKIN
Provide Psychological Support (f)
(e)
Ensure Maximum Patient
Comfort
(d)
Prevent Spread of Infection
(a)
(b)
(c) Recognize and Prevent
Secondary Infection
Maintain integrity of the Skin
Promote Healing of the Skin
Lesions

177
RESEARCH ABSTRACT
PREVALENCE OF CHILDHOOD SKIN DISORDERS
ATTENDING AT OUTPATIENT PEDIATRIC HOSPITAL
Thummanapally Nandini, Lawdyavath Kavitha,Guruva Charandas, Enumula, Pvk
Sastry , Anchuri Shyam
Objective: The objective of the study was to study the prevalence of
various skin diseases in pediatric population.
Methods: A prospective observational study
Results: Out of 200 pediatric skin disorders, the percentage of skin
disorders is allergic infections (26%), bacterial infections (23%), viral
infections (11%), fungal infections (7.5%), parasitic infections (6%),
autoimmune disorders (4%), and skin adnexa (2.5%).
Conclusion: The study concludes that the prevalence of allergic and
bacterial skin infections was found to be common among male
children

178
CONCLUSION
Many childhood skin problems are minor and can
be treated with OTC products. Others are more
complicated and may need prescription drug
products or other treatments. Pathological changes
may arise in epidermis, dermis and subcutaneous
tissue. The pattern of changes may allow a diagnosis
to be made or it may be non-specific. The
appearance of many skin diseases vary at different
stages of their development and may be altered by
attempted treatment and secondary changes such as
scratching or infection.

179