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SEMINAR PRESENTATION

Clinical approach to a case of
Blistering disorder

MODERATOR: Dr. Amit Malhotra
Introduction
• A blister is a fluid filled cavity formed within or beneath the
epidermis.
• Can be categorized as vesicles or bullae.
• Vesicle- < 0.5 cm in diameter
• Bulla- > 0.5 cm in diameter
• Blisters are an obvious sign of disease that always draw
attention of patient and physician.
Common causes of blistering
• Infection
–
–
–
–
–

Herpes simplex
Herpes zoster
Varicella
Bullous impetigo
SSSS

• Genetic
– Epidermolysis bullosa
– Hailey-Hailey disease
– Incontinentia pigmenti
• Immunobullous
–
–
–
–
–
–
–

Pemphigus group of diseases
Paraneoplastic pemphigus
Bullous pemphigoid
Mucous membrane pemphigoid
Linear IgA disease
Dermatitis herpetiformis
Epidermolysis bullosa acquisita

• Mechanical
– Friction blister
• Dermatitis
– Allergic contact dermatitis
– Irritant dermatitis

• Drugs
– Bullous FDE
– Erythema multiforme
– SJS/ TEN

• Metabolic
– Diabetic bullae
– Porphyria
• Disorders, in which blistering is the primary event are
traditionally termed as blistering disorders or vesiculobullous
disorders.
• This group includes hereditary blistering disorders and
immunobullous diseases.
Approach
• History
• Clinical examination
Age of onset
Pemphigus vulgaris

Middle age (40-60 yrs)

Pemphigus foliaceus

Middle age

Paraneoplastic pemphigus

Adult, children

Bullous pemphigoid

Elderly (60-75 yrs)

Mucous membrane pemphigoid

Old age (60-80 yrs)

Pemphigoid gestationis

Pregnant women

Dermatitis herpetiformis

Adult

Linear IgA disease

Before 5 & after 60 yrs

EBA

Adults & children

Hailey- hailey disease

Adults

Epidermolysis bullosa

At birth or during infancy
Initial site
Pemphigus vulgaris

Oral mucosa

Pemphigus foliaceus

Scalp, chest

Bullous pemphigoid

extremities

Mucous membrane pemphigoid

Oral or other mucosa

Pemphigoid gestationis

Periumblical, extremities

Dermatitis herpetiformis

Trunk, scalp

Linear IgA disease

Genital in children; no
predilection in adults

EBA

Mucosa, extremities

Hailey- hailey disease

Friction sites
Mucosal involvement
Pemphigus vulgaris

Almost all

Pemphigus foliaceus

None

Intercelluar IgA dermatosis

Uncommon

Paraneoplastic pemphigus

Severe mucositis

Bullous pemphigoid

10 – 40%, transient, mild

Mucous membrane pemphigoid

Almost all

Pemphigoid gestationis

Rare

Dermatitis herpetiformis

Rare

Linear IgA disease

80%

EBA

50%

Hailey- hailey disease

Uncommon
Distribution of lesions
Pemphigus vulgaris

Scalp, face, flexures, trunk

Pemphigus foliaceus

Seborrhoeic distribution

Intercelluar IgA dermatosis

Axillae, groins, face, scalp,
proximal limbs

Paraneoplastic pemphigus

Upper body, palmoplantar

Bullous pemphigoid

Trunk, limbs, flexures

Mucous membrane pemphigoid

Infrequent; head, neck, upper
trunk
Pemphigoid gestationis

Abdomen, extremities

Dermatitis herpetiformis

Symmetrical over extensors of
trunk including buttocks, elbows,
knees.

Linear IgA disease

Perineum, face, trunk, limbs

EBA

Generalized, variable

Epidermolysis bullosa

Sites of trauma

Hailey- Hailey disease

Sides of neck, axillae, groins,
perineum
Morphology of lesions
Characteristics of bullae based on level of split
Lesions characteristics
Pemphigus vulgaris

Flaccid blisters, erosions,
flexural vegetations

Pemphigus vegetans

Vesicles, pustules, erosions,
vegetating Plaques

Pemphigus foliaceus

Scaly papules, crusted erosions,
Erythroderma

Intercelluar IgA dermatosis

Flaccid pustules annular or
circinate configuration

Paraneoplastic pemphigus

Polymorphous, bullae, erosions,
‘target lesions’

Bullous pemphigoid

Urticated plaques, tense
blisters, (milia)

Mucous membrane pemphigoid

Erosions, blisters, gingivitis,
milia, Scarring
Pemphigoid gestationis

Urticated plaques, tense blisters

Dermatitis herpetiformis

Papulovesicles

Linear IgA disease

Urticated plaques, annular lesions,
tense blisters

EBA

Urticated plaques, tense blisters,
milia ,Scarring

Hailey- Hailey disease

Flaccid vesicopustules, crusted
erosions or expanding circinate
plaques appear in areas exposed to
friction
Pemphigus vulgaris
A: flaccid blisters on normal skin.
B: superficial blisters and erosions which take long to heal.
Pemphigus vegetans: heaped up vegetating
plaques in flexures

Pemphigus foliaceus: extensive areas of scaling and crusting
and no blisters. removal of scale-crust reveals a minimally
moist area.
Bullous pemphigoid:

urticarial lesions.

large hemorrhagic blisters some on
normal skin
Pemphigoid gestationis
Early pruritic erythematous stage

Bullae arising on urticated erythematous skin on
the thigh.
Chronic bullous disease of childhood: string of
pearl appearance is typical

Dermatitis herpetiformis: grouped vesicles
develop either on normal or erythematous
skin. Since the lesions are extremely itchy,
they are rapidly excoriated
Differentiating features of Epidermolysis bullosa
Type

Time of inhe Clinical features
present riatn
ation
ce

MM/Nail Associated
/Teeth
features

WeberCockyne
EBS

Childho AD
od

Localised to palms, Normal
soles, waist or
neck, no scarring,
more in summers

Hyperhydrosis good
of palms,
soles

Koebner
EBS

At birth AD
or
infancy

On occiput, back
or legs in infancy,
Hands or feet in
childhood, no
scarring

Aggravated by
warm
weather,
Hyperhydrosis
of palms,
soles

Normal

Progno
sis

May
improv
e after
puberty
Epidermolysis bullosa
Type

Time of inhe Clinical features
present ritan
ation
ce

MM/Nail/Te Associated
eth
features

Progno
sis
Severe
in
infancy,
better
with
age

DowlingAt birth AD
meara EBS or
infancy

Herpitiform
blisters on trunk,
limbs, neck,
No scarring

MM, nails
involved

Milia,
hyperpigme
ntation
seen

EBS with
muscular
dystrophy

Blisters on hands
and feet then
generalized

Nail
deformities,
MM
involvement
, alopecia

Muscle
Poor
weakness
early or late
onset,
milia

At birth AD
or early
infancy
Epidermolysis bullosa
Type

Time
inhe Clinical features
of
ritan
presen ce
tation

MM/Nail/
Teeth

Associated
features

Progno
sis

Autosomal
recessive
lethal EBS

At
birth

AR

Generalised more
on distal limbs

Normal,
oral
mucosa
mildly
affected

No scarring
or milia
seen

Poor

EBS with
mottled
pigmentati
on

At
AD
birth
or
infancy

Reticulate pattern
of macular
pigmentation over
trunk, limbs

Nails
involved,
MM, teeth
normal

Punctate
Improv
keratoses on es with
palms and
age
soles
Epidermolysis bullosa
Type

Time of inhe Clinical features
present ritan
ation
ce

MM/Nail Associated
/Teeth
features

Prognosi
s
Poor,
child
may die
in early
infancy
due to
infection

Herlitz JEB At birth AR
or soon
after
birth

Severe generalised
blistering, skin
fragility, difficult to
handle child,
erosions slow to
heal

Mm,
nails
teeth
involved,
larynx
may be
involved

Sepsis or
multiorgan
failure may
occur

NonAt birth AR
Herlitz JEB

Generalised
blistetrs, scalp
involvement
causes alopecia

Involved

Pigmentation Improve
and nevi
s with
seen
age
Epidermolysis bullosa
Type

Time inhe Clinical features
of
ritan
prese ce
ntatio
n

MM/Nail/ Associated
Teeth
features

Progno
sis

JEB with
pyloric
atresia

At
birth

AR

Generalised skin
and mucosal
blisters

Nail, teeth Non- bilious
involved
vomiting in
newborn

Very
poor

Progressive
JEB

5-8
years

AR

Hands, feet, knees, Nail, teeth Finger
elbows (sites of
involved
contractures,
friction)
deafness

good
Epidermolysis bullosa
Type

Time of inhe Clinical features
present ritan
ation
ce

MM/Nail/T Associated
eeth
features

Progno
sis

Dominant At birth AD
dystrophic or early
EB
infancy

Hands, feet, knees, Nail
elbows (sites of
dystrophy,
friction)
MM, teeth
normal

White
Good
papules on
trunk, pasini
variant

Hallopeau
- siemens
EB

At birth AR
or early
infancy

Large, flaccid
bullae at sites
friction, healing
slow, scarring

Dystrophic
nails,
scarring
alopecia,
carious
teeth

Flexural
contractures
, esophagial
strictures,
inability to
protude
tongue

Poordeath
by 3-4
decade

Non
Hallopeau
- siemens
EB

At birth AR

Skin and mucosae
are fragile

Changes
are
localised

Few
complicatio
ns

good
Configuration
• Grouping of blisters: dermatitis herpetiformis.
• String of pearls sign- annular, polycyclic lesions often with
blistering around the edge in CBDC
NIKOLSKIY SIGN
• A positive Nikolskiy sign indicates intraepidermal cleavage and
differentiates intraepidermal blisters from subepidermal
blisters.
• It is pathognomonic of pemphigus and staphylococcal scalded
skin syndrome
• The sign is best elicited by applying lateral pressure with the
thumb or fingerpad on skin over a bony prominence.
• This results in a shearing force that dislodges the upper layers
of epidermis from the lower epidermis producing an erosion.
• Specifically, elicitation of the sign can help distinguish
pemphigus vulgaris, which is strongly associated with the sign,
from bullous pemphigoid, in which the sign is usually absent.
• other diseases associated with a positive Nikolsky’s sign
-toxic epidermal necrolysis, bullous impetigo, and
epidermolysis bullosa
(a) Eliciting Nikolsky's sign on perilesional skin. Note the tangential
pressure, (b) Eliciting Nikolsky's sign, peeling of skin revealing moist
erosion
BULLA SPREAD SIGN
• In the traditional "bulla spread" sign or Lutz sign, the margin
of an intact bulla is first marked by a pen.
• Slow, careful and unidirectional pressure applied by a finger to
the bulla causes peripheral extension of the bulla beyond the
marked margin.
• The bulla thus extended has an irregular angulated border in
pemphigus vulgaris, while a regular rounded border is
observed in bullous pemphigoid or other subepidermal
blistering disorders.
• This sign is positive in all varieties of pemphigus and many
cases of subepidermal blisters, including bullous pemphigoid,
DH , EBA, cicatricial pemphigoid, dystrophic epidermolysis
bullosa, SJS, TEN.
• Due to fragility of the roof of the blister it is usually negative
in Hailey-Hailey disease and staphylococcal scalded skin
syndrome.
Tzanck Smear
• Is a quick bedside test.
• A fresh blister is ruptured, the roof detached and the floor
scraped using a scalpel blade.
• If blister not present, then taken from erosion, after removing
the crust.
• The material so obtained is spread on a glass slide and stained
with Giemsa stain.
Tzanck smear findings in bullous disorders
PEMPHIGUS VULGARIS
• It reveals multiple acantholytic
cells (Tzanck cells).
• A typical Tzanck cell
–
–
–
–

Large round keratinocyte
Hypertrophic nucleus,
Hazy or absent nucleoli, and
Abundant basophilic cytoplasm.

• The basophilic staining is deeper
peripherally on the cell leading to
a perinuclear halo.
Other differentials
Differential

History

Examination

Herpes simplex

primary or recurrent outbreak of
herpes simplex virus (HSV) vesicles
associated with tenderness, burning,
or tingling; HSV-1 is spread primarily
through direct contact with infected
saliva or other infected secretions,
HSV-2 is spread primarily through
sexual contact, symptoms typically
start within 1 week after exposure

grouped vesicles on an
erythematous base, may
evolve to pustules or
erosions, lesions resolve
within 2 to 6 weeks

Herpes zoster
(shingles)

prior history of varicella infection,
presents with prodrome of pain,
itching, hyperesthesia followed by
vesicular eruption

painful, grouped vesicles
on an erythematous base
in a sensory dermatomal
distribution, rarely crosses
midline
Differential

History

Examination

Varicella,
initial viremia between days 4
acute(chickenpox) and 6; appearance of
characteristic vesicular eruption
on erythematous base, often
referred to as "dewdrops on rose
petals," low-grade fever, malaise,
and headache

successive crops of lesions
appear over several days on
trunk, face, and oral mucosa;
typically lesions are in
different stages of evolution
from vesicles to crust and do
not scar

Impetigo

bullae are ≥2 cm in diameter
and initially clear,
subsequently becoming
turbid; buccal mucosa may be
involved, classic facial
yellowish to golden crusting,
streptococcal form tends to
have thicker and darker crusts

typically occurs in children, very
contagious, risk factors include
increased humidity, poor
hygiene, malnutrition and
overcrowding, concomitant skin
disease
Differential

History

Examination

Staphylococcal typically child or adult with
scalded skin
renal insufficiency
syndrome

prodromal fever, tender skin
evolve to generalized erythema
with flexural accentuation and
then flaccid bullae formation;
Nikolsky sign present,
desquamation follows starting in
flexural areas; in contrast to toxic
epidermal necrolysis, does not
affect oral mucosa and may be a
helpful clue to diagnosis

Congenital
syphilis

primarily acrally located vesicles
and bullae, may be hemorrhagic

40% of infected newborns have
skin findings, neonate develops
lesions within first 2 weeks of
life through transplacental
transmission, mother with
history of secondary or tertiary
syphilis
Differential

History

Examination

Eczematous
dermatitis
(contact,
nummular, and
pompholytic)

personal or family history of atopy,
recent exposure to chemicals,
personal hygiene products, fabrics,
or plant allergens (e.g., poison ivy,
poison oak)

predominantly localized
distribution of vesicles and
papules with surrounding
erythematous base, later
lesions may be covered by
scale or crusting

Friction blister

recent activity involving affected
area (new shoes, gloves, or
products)

tense bullae in area of
pressure or friction

Miliaria

exposure to hot or humid climates, pruritic or asymptomatic
febrile illness in bedridden patient, papules or vesicles
layered clothing preventing
dissipation of heat or moisture
Differential

History

Examination

Coma bullae

coma from trauma, illness, or an
overdose of a narcotic drug

erythema with vesicles or
bullae at sites subjected to
pressure (hands, wrists,
scapulae, sacrum, knees,
heels)

Bullous arthropod recent arthropod exposure in a
bite reaction
sensitized patient, typically present
as grouped pruritic or
asymptomatic blisters in patients
who are otherwise well

grouped pruritic or
asymptomatic blisters,
distribution and location of
the lesions usually localized
to a specific area of body
(depending on causative
arthropod)
Differential

History

Examination

Nutritional
deficiencies (zinc,
biotin, niacin,
essential fatty
acids)

inherited or acquired deficiency,
breastfed newborns, history of
parenteral nutrition, characteristic
cutaneous finding is a
photosensitive eruption
(preferentially involving the face,
neck, upper chest, dorsal hands,
and extensor forearms), which
worsens in spring and summer

dermatitis is bullous or
pustular, periorificial and
acral locations, associated
erythematous eroded,
crusted patches; with
repeated sun exposure, the
involved areas become
thickened, scaly, and
hyperpigmented

Diabetic bullae
(bullosis
diabeticorum)

longstanding history of diabetes,
spontaneously healing blisters
within 4 to 5 weeks of onset

painless noninflammatory
blisters typically on acral
locations, including
amputation sites
Differential

History

Porphyria cutanea photosensitivity, fragility of suntarda
exposed skin that results in
blistering and erosions of the
dorsal hands, forearms, ears, feet,
and face; ingestion of alcohol,
estrogens, and polychlorinated
cyclic hydrocarbons exacerbates
condition

Pseudoporphyria
cutanea tarda

Examination
tense blisters on sunexposed skin, heal with
scarring, dyspigmentation,
and milia; hypertrichosis,
sclerodermatous
thickenings, and scarring
alopecia

hemodialysis, drug exposures
bullae on sun-exposed body
(NSAIDs, furosemide, nalidixic acid, areas (face, ears, dorsal
tetracycline), skin fragility,
hands, forearms)
photosensitivity, absence of
hypertrichosis, and skin sclerosis
Differential

History

Examination

Incontinentia
pigmenti

X-linked dominant, female infant 4
to 6 weeks old with vesicles in a
patterned distribution (Blaschko
lines), cutaneous features evolve
through 4 stages from infancy to
adolescence

noninflammatory vesicles in
a patterned distribution
(Blaschko lines),
abnormalities of teeth, eyes,
hair

Bullous
ichthyosiform
erythroderma
(epidermolytic
hyperkeratosis)

presents at birth, or shortly after,
with erythema, blistering, or
peeling; may be confused with
staphylococcal scalded skin
syndrome or epidermolysis bullosa

widespread erythema,
blistering and peeling infant
with or without palmarplantar involvement
Differential

History

Examination

Mastocytosis

acquired solitary or widespread
cutaneous eruption, lesion
periodically urticates and blisters
then returns to original form

5 mm to 15 mm papules,
yellow-brown to yellow-red
in color; edema, urtication,
and vesicle and bullae
formation, urticaria
surrounding erythematous
flare when rubbed (Darier
sign)

Bullous lupus
erythematosus

occurs in patients with a diagnosis
of systemic lupus, sun-exposed
skin is preferentially involved

lesions are not pruritic or
symmetric, do not have a
predilection for extensor
surfaces of arms, elbows,
knees, or scalp; vesicles and
bullae typically photodistributed or widespread,
asymptomatic
Differential

History

Examination

Erythema
multiforme

ingestion of new medications in
the days or weeks before onset,
implicated medications include
antibiotics (trimethoprimsulfamethoxazole), anticonvulsants
(lamotrigine), NSAIDs, and
allopurinol

characterized by atypical
targetoid lesions, macules,
vesicles, bullae on palms and
soles; may be generalized

Stevens-Johnson
syndrome

more fulminant form of erythema
multiforme with systemic and
mucosal involvement of <10% of
body surface area, severe
mucocutaneous reaction with
prodrome of fever, malaise, chills,
1 day to 2 weeks before onset

palms, soles, and extensor
surfaces with macules, may
evolve to papules, vesicles,
bullae, urticarial plaques, or
confluent erythema; center
of lesions purpuric, vesicular,
or necrotic imparting
targetoid appearance,
secondary infection follows
Clinicl aproch to blistering dissorder
Clinicl aproch to blistering dissorder
Clinicl aproch to blistering dissorder
THANK YOU

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Clinicl aproch to blistering dissorder

  • 1. SEMINAR PRESENTATION Clinical approach to a case of Blistering disorder MODERATOR: Dr. Amit Malhotra
  • 2. Introduction • A blister is a fluid filled cavity formed within or beneath the epidermis. • Can be categorized as vesicles or bullae. • Vesicle- < 0.5 cm in diameter • Bulla- > 0.5 cm in diameter • Blisters are an obvious sign of disease that always draw attention of patient and physician.
  • 3. Common causes of blistering • Infection – – – – – Herpes simplex Herpes zoster Varicella Bullous impetigo SSSS • Genetic – Epidermolysis bullosa – Hailey-Hailey disease – Incontinentia pigmenti
  • 4. • Immunobullous – – – – – – – Pemphigus group of diseases Paraneoplastic pemphigus Bullous pemphigoid Mucous membrane pemphigoid Linear IgA disease Dermatitis herpetiformis Epidermolysis bullosa acquisita • Mechanical – Friction blister
  • 5. • Dermatitis – Allergic contact dermatitis – Irritant dermatitis • Drugs – Bullous FDE – Erythema multiforme – SJS/ TEN • Metabolic – Diabetic bullae – Porphyria
  • 6. • Disorders, in which blistering is the primary event are traditionally termed as blistering disorders or vesiculobullous disorders. • This group includes hereditary blistering disorders and immunobullous diseases.
  • 8. Age of onset Pemphigus vulgaris Middle age (40-60 yrs) Pemphigus foliaceus Middle age Paraneoplastic pemphigus Adult, children Bullous pemphigoid Elderly (60-75 yrs) Mucous membrane pemphigoid Old age (60-80 yrs) Pemphigoid gestationis Pregnant women Dermatitis herpetiformis Adult Linear IgA disease Before 5 & after 60 yrs EBA Adults & children Hailey- hailey disease Adults Epidermolysis bullosa At birth or during infancy
  • 9. Initial site Pemphigus vulgaris Oral mucosa Pemphigus foliaceus Scalp, chest Bullous pemphigoid extremities Mucous membrane pemphigoid Oral or other mucosa Pemphigoid gestationis Periumblical, extremities Dermatitis herpetiformis Trunk, scalp Linear IgA disease Genital in children; no predilection in adults EBA Mucosa, extremities Hailey- hailey disease Friction sites
  • 10. Mucosal involvement Pemphigus vulgaris Almost all Pemphigus foliaceus None Intercelluar IgA dermatosis Uncommon Paraneoplastic pemphigus Severe mucositis Bullous pemphigoid 10 – 40%, transient, mild Mucous membrane pemphigoid Almost all Pemphigoid gestationis Rare Dermatitis herpetiformis Rare Linear IgA disease 80% EBA 50% Hailey- hailey disease Uncommon
  • 11. Distribution of lesions Pemphigus vulgaris Scalp, face, flexures, trunk Pemphigus foliaceus Seborrhoeic distribution Intercelluar IgA dermatosis Axillae, groins, face, scalp, proximal limbs Paraneoplastic pemphigus Upper body, palmoplantar Bullous pemphigoid Trunk, limbs, flexures Mucous membrane pemphigoid Infrequent; head, neck, upper trunk
  • 12. Pemphigoid gestationis Abdomen, extremities Dermatitis herpetiformis Symmetrical over extensors of trunk including buttocks, elbows, knees. Linear IgA disease Perineum, face, trunk, limbs EBA Generalized, variable Epidermolysis bullosa Sites of trauma Hailey- Hailey disease Sides of neck, axillae, groins, perineum
  • 13. Morphology of lesions Characteristics of bullae based on level of split
  • 14. Lesions characteristics Pemphigus vulgaris Flaccid blisters, erosions, flexural vegetations Pemphigus vegetans Vesicles, pustules, erosions, vegetating Plaques Pemphigus foliaceus Scaly papules, crusted erosions, Erythroderma Intercelluar IgA dermatosis Flaccid pustules annular or circinate configuration Paraneoplastic pemphigus Polymorphous, bullae, erosions, ‘target lesions’ Bullous pemphigoid Urticated plaques, tense blisters, (milia) Mucous membrane pemphigoid Erosions, blisters, gingivitis, milia, Scarring
  • 15. Pemphigoid gestationis Urticated plaques, tense blisters Dermatitis herpetiformis Papulovesicles Linear IgA disease Urticated plaques, annular lesions, tense blisters EBA Urticated plaques, tense blisters, milia ,Scarring Hailey- Hailey disease Flaccid vesicopustules, crusted erosions or expanding circinate plaques appear in areas exposed to friction
  • 16. Pemphigus vulgaris A: flaccid blisters on normal skin. B: superficial blisters and erosions which take long to heal.
  • 17. Pemphigus vegetans: heaped up vegetating plaques in flexures Pemphigus foliaceus: extensive areas of scaling and crusting and no blisters. removal of scale-crust reveals a minimally moist area.
  • 18. Bullous pemphigoid: urticarial lesions. large hemorrhagic blisters some on normal skin
  • 19. Pemphigoid gestationis Early pruritic erythematous stage Bullae arising on urticated erythematous skin on the thigh.
  • 20. Chronic bullous disease of childhood: string of pearl appearance is typical Dermatitis herpetiformis: grouped vesicles develop either on normal or erythematous skin. Since the lesions are extremely itchy, they are rapidly excoriated
  • 21. Differentiating features of Epidermolysis bullosa Type Time of inhe Clinical features present riatn ation ce MM/Nail Associated /Teeth features WeberCockyne EBS Childho AD od Localised to palms, Normal soles, waist or neck, no scarring, more in summers Hyperhydrosis good of palms, soles Koebner EBS At birth AD or infancy On occiput, back or legs in infancy, Hands or feet in childhood, no scarring Aggravated by warm weather, Hyperhydrosis of palms, soles Normal Progno sis May improv e after puberty
  • 22. Epidermolysis bullosa Type Time of inhe Clinical features present ritan ation ce MM/Nail/Te Associated eth features Progno sis Severe in infancy, better with age DowlingAt birth AD meara EBS or infancy Herpitiform blisters on trunk, limbs, neck, No scarring MM, nails involved Milia, hyperpigme ntation seen EBS with muscular dystrophy Blisters on hands and feet then generalized Nail deformities, MM involvement , alopecia Muscle Poor weakness early or late onset, milia At birth AD or early infancy
  • 23. Epidermolysis bullosa Type Time inhe Clinical features of ritan presen ce tation MM/Nail/ Teeth Associated features Progno sis Autosomal recessive lethal EBS At birth AR Generalised more on distal limbs Normal, oral mucosa mildly affected No scarring or milia seen Poor EBS with mottled pigmentati on At AD birth or infancy Reticulate pattern of macular pigmentation over trunk, limbs Nails involved, MM, teeth normal Punctate Improv keratoses on es with palms and age soles
  • 24. Epidermolysis bullosa Type Time of inhe Clinical features present ritan ation ce MM/Nail Associated /Teeth features Prognosi s Poor, child may die in early infancy due to infection Herlitz JEB At birth AR or soon after birth Severe generalised blistering, skin fragility, difficult to handle child, erosions slow to heal Mm, nails teeth involved, larynx may be involved Sepsis or multiorgan failure may occur NonAt birth AR Herlitz JEB Generalised blistetrs, scalp involvement causes alopecia Involved Pigmentation Improve and nevi s with seen age
  • 25. Epidermolysis bullosa Type Time inhe Clinical features of ritan prese ce ntatio n MM/Nail/ Associated Teeth features Progno sis JEB with pyloric atresia At birth AR Generalised skin and mucosal blisters Nail, teeth Non- bilious involved vomiting in newborn Very poor Progressive JEB 5-8 years AR Hands, feet, knees, Nail, teeth Finger elbows (sites of involved contractures, friction) deafness good
  • 26. Epidermolysis bullosa Type Time of inhe Clinical features present ritan ation ce MM/Nail/T Associated eeth features Progno sis Dominant At birth AD dystrophic or early EB infancy Hands, feet, knees, Nail elbows (sites of dystrophy, friction) MM, teeth normal White Good papules on trunk, pasini variant Hallopeau - siemens EB At birth AR or early infancy Large, flaccid bullae at sites friction, healing slow, scarring Dystrophic nails, scarring alopecia, carious teeth Flexural contractures , esophagial strictures, inability to protude tongue Poordeath by 3-4 decade Non Hallopeau - siemens EB At birth AR Skin and mucosae are fragile Changes are localised Few complicatio ns good
  • 27. Configuration • Grouping of blisters: dermatitis herpetiformis. • String of pearls sign- annular, polycyclic lesions often with blistering around the edge in CBDC
  • 28. NIKOLSKIY SIGN • A positive Nikolskiy sign indicates intraepidermal cleavage and differentiates intraepidermal blisters from subepidermal blisters. • It is pathognomonic of pemphigus and staphylococcal scalded skin syndrome • The sign is best elicited by applying lateral pressure with the thumb or fingerpad on skin over a bony prominence. • This results in a shearing force that dislodges the upper layers of epidermis from the lower epidermis producing an erosion.
  • 29. • Specifically, elicitation of the sign can help distinguish pemphigus vulgaris, which is strongly associated with the sign, from bullous pemphigoid, in which the sign is usually absent. • other diseases associated with a positive Nikolsky’s sign -toxic epidermal necrolysis, bullous impetigo, and epidermolysis bullosa
  • 30. (a) Eliciting Nikolsky's sign on perilesional skin. Note the tangential pressure, (b) Eliciting Nikolsky's sign, peeling of skin revealing moist erosion
  • 31. BULLA SPREAD SIGN • In the traditional "bulla spread" sign or Lutz sign, the margin of an intact bulla is first marked by a pen. • Slow, careful and unidirectional pressure applied by a finger to the bulla causes peripheral extension of the bulla beyond the marked margin. • The bulla thus extended has an irregular angulated border in pemphigus vulgaris, while a regular rounded border is observed in bullous pemphigoid or other subepidermal blistering disorders.
  • 32. • This sign is positive in all varieties of pemphigus and many cases of subepidermal blisters, including bullous pemphigoid, DH , EBA, cicatricial pemphigoid, dystrophic epidermolysis bullosa, SJS, TEN. • Due to fragility of the roof of the blister it is usually negative in Hailey-Hailey disease and staphylococcal scalded skin syndrome.
  • 33. Tzanck Smear • Is a quick bedside test. • A fresh blister is ruptured, the roof detached and the floor scraped using a scalpel blade. • If blister not present, then taken from erosion, after removing the crust. • The material so obtained is spread on a glass slide and stained with Giemsa stain.
  • 34. Tzanck smear findings in bullous disorders
  • 35. PEMPHIGUS VULGARIS • It reveals multiple acantholytic cells (Tzanck cells). • A typical Tzanck cell – – – – Large round keratinocyte Hypertrophic nucleus, Hazy or absent nucleoli, and Abundant basophilic cytoplasm. • The basophilic staining is deeper peripherally on the cell leading to a perinuclear halo.
  • 36. Other differentials Differential History Examination Herpes simplex primary or recurrent outbreak of herpes simplex virus (HSV) vesicles associated with tenderness, burning, or tingling; HSV-1 is spread primarily through direct contact with infected saliva or other infected secretions, HSV-2 is spread primarily through sexual contact, symptoms typically start within 1 week after exposure grouped vesicles on an erythematous base, may evolve to pustules or erosions, lesions resolve within 2 to 6 weeks Herpes zoster (shingles) prior history of varicella infection, presents with prodrome of pain, itching, hyperesthesia followed by vesicular eruption painful, grouped vesicles on an erythematous base in a sensory dermatomal distribution, rarely crosses midline
  • 37. Differential History Examination Varicella, initial viremia between days 4 acute(chickenpox) and 6; appearance of characteristic vesicular eruption on erythematous base, often referred to as "dewdrops on rose petals," low-grade fever, malaise, and headache successive crops of lesions appear over several days on trunk, face, and oral mucosa; typically lesions are in different stages of evolution from vesicles to crust and do not scar Impetigo bullae are ≥2 cm in diameter and initially clear, subsequently becoming turbid; buccal mucosa may be involved, classic facial yellowish to golden crusting, streptococcal form tends to have thicker and darker crusts typically occurs in children, very contagious, risk factors include increased humidity, poor hygiene, malnutrition and overcrowding, concomitant skin disease
  • 38. Differential History Examination Staphylococcal typically child or adult with scalded skin renal insufficiency syndrome prodromal fever, tender skin evolve to generalized erythema with flexural accentuation and then flaccid bullae formation; Nikolsky sign present, desquamation follows starting in flexural areas; in contrast to toxic epidermal necrolysis, does not affect oral mucosa and may be a helpful clue to diagnosis Congenital syphilis primarily acrally located vesicles and bullae, may be hemorrhagic 40% of infected newborns have skin findings, neonate develops lesions within first 2 weeks of life through transplacental transmission, mother with history of secondary or tertiary syphilis
  • 39. Differential History Examination Eczematous dermatitis (contact, nummular, and pompholytic) personal or family history of atopy, recent exposure to chemicals, personal hygiene products, fabrics, or plant allergens (e.g., poison ivy, poison oak) predominantly localized distribution of vesicles and papules with surrounding erythematous base, later lesions may be covered by scale or crusting Friction blister recent activity involving affected area (new shoes, gloves, or products) tense bullae in area of pressure or friction Miliaria exposure to hot or humid climates, pruritic or asymptomatic febrile illness in bedridden patient, papules or vesicles layered clothing preventing dissipation of heat or moisture
  • 40. Differential History Examination Coma bullae coma from trauma, illness, or an overdose of a narcotic drug erythema with vesicles or bullae at sites subjected to pressure (hands, wrists, scapulae, sacrum, knees, heels) Bullous arthropod recent arthropod exposure in a bite reaction sensitized patient, typically present as grouped pruritic or asymptomatic blisters in patients who are otherwise well grouped pruritic or asymptomatic blisters, distribution and location of the lesions usually localized to a specific area of body (depending on causative arthropod)
  • 41. Differential History Examination Nutritional deficiencies (zinc, biotin, niacin, essential fatty acids) inherited or acquired deficiency, breastfed newborns, history of parenteral nutrition, characteristic cutaneous finding is a photosensitive eruption (preferentially involving the face, neck, upper chest, dorsal hands, and extensor forearms), which worsens in spring and summer dermatitis is bullous or pustular, periorificial and acral locations, associated erythematous eroded, crusted patches; with repeated sun exposure, the involved areas become thickened, scaly, and hyperpigmented Diabetic bullae (bullosis diabeticorum) longstanding history of diabetes, spontaneously healing blisters within 4 to 5 weeks of onset painless noninflammatory blisters typically on acral locations, including amputation sites
  • 42. Differential History Porphyria cutanea photosensitivity, fragility of suntarda exposed skin that results in blistering and erosions of the dorsal hands, forearms, ears, feet, and face; ingestion of alcohol, estrogens, and polychlorinated cyclic hydrocarbons exacerbates condition Pseudoporphyria cutanea tarda Examination tense blisters on sunexposed skin, heal with scarring, dyspigmentation, and milia; hypertrichosis, sclerodermatous thickenings, and scarring alopecia hemodialysis, drug exposures bullae on sun-exposed body (NSAIDs, furosemide, nalidixic acid, areas (face, ears, dorsal tetracycline), skin fragility, hands, forearms) photosensitivity, absence of hypertrichosis, and skin sclerosis
  • 43. Differential History Examination Incontinentia pigmenti X-linked dominant, female infant 4 to 6 weeks old with vesicles in a patterned distribution (Blaschko lines), cutaneous features evolve through 4 stages from infancy to adolescence noninflammatory vesicles in a patterned distribution (Blaschko lines), abnormalities of teeth, eyes, hair Bullous ichthyosiform erythroderma (epidermolytic hyperkeratosis) presents at birth, or shortly after, with erythema, blistering, or peeling; may be confused with staphylococcal scalded skin syndrome or epidermolysis bullosa widespread erythema, blistering and peeling infant with or without palmarplantar involvement
  • 44. Differential History Examination Mastocytosis acquired solitary or widespread cutaneous eruption, lesion periodically urticates and blisters then returns to original form 5 mm to 15 mm papules, yellow-brown to yellow-red in color; edema, urtication, and vesicle and bullae formation, urticaria surrounding erythematous flare when rubbed (Darier sign) Bullous lupus erythematosus occurs in patients with a diagnosis of systemic lupus, sun-exposed skin is preferentially involved lesions are not pruritic or symmetric, do not have a predilection for extensor surfaces of arms, elbows, knees, or scalp; vesicles and bullae typically photodistributed or widespread, asymptomatic
  • 45. Differential History Examination Erythema multiforme ingestion of new medications in the days or weeks before onset, implicated medications include antibiotics (trimethoprimsulfamethoxazole), anticonvulsants (lamotrigine), NSAIDs, and allopurinol characterized by atypical targetoid lesions, macules, vesicles, bullae on palms and soles; may be generalized Stevens-Johnson syndrome more fulminant form of erythema multiforme with systemic and mucosal involvement of <10% of body surface area, severe mucocutaneous reaction with prodrome of fever, malaise, chills, 1 day to 2 weeks before onset palms, soles, and extensor surfaces with macules, may evolve to papules, vesicles, bullae, urticarial plaques, or confluent erythema; center of lesions purpuric, vesicular, or necrotic imparting targetoid appearance, secondary infection follows