Transcript Dermatoses Resulting from Physical Factors

Dermatoses Resulting from
Physical Factors
Chapter 3
Andrew’s Diseases of the Skin
Adam Wray, D.O.
November 15, 2005
Heat Injuries
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Thermal Burns
Electrical Burns
Miliaria
Miliaria Crystalline (Sudamina)
Miliaria Rubra (Prickly Heat, Heat Rash)
Miliaria Pustulosa
Miliaria Profunda
Occlusion Miliaria
Thermal Burns
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First-degree burn- active congestion of
superficial blood vessels
This causes erythema sometimes followed by
epidermal desquamation
Constitutional reactions occur if area is large
Pain and increased surface heat may be severe
Second-degree burns
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Superficial
Transudation of serum
causing edema of
superficial tissues
Vesicles and blebs
Complete recovery
without scar or
blemish is usual
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Deep
Pale and anesthetic
Injury to reticular
dermis compromises
blood flow and
destroys appendages
Healing takes > 1
month
Scarring occurs
Second-degree burns
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Thermal burn: This superficial second degree
burn is characterized by bullae that contain
serous fluid
Second-Degree Burns
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Inflicted scalds:
severe second
degree burns after
dipping
B: two days after
incident-to lower
extremities and
perineum
C: foot and lower
leg
Second-Degree Burn
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Accidental scald
Splash-anddroplet pattern
of an accidental
scald from hot
cup of tea
Second-Degree Burn
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Curling iron burn
Third-degree burns
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Full-thickness tissue
loss
Skin appendages are
destroyed
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There is no epithelium
for regeneration
Healing leaves a scar
Fourth-degree burns
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Destruction of entire skin
and subcutaneous fat
with any underlying
tendons
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Rule of nines:
In adults, an
estimate of burn
extent based upon
this surface area
distribution chart.
Infants & children
have a relatively
increased head;
trunk surface area
ratio
Electrical Burns
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Contact- small but
deep, causing some
necrosis of underlying
tissues
Flash-burns usually
cover a large area and
are similar to a surface
burn and should be tx
as such
Lightening is the most
lethal type of strike,
cardiac arrest or other
internal injuries may
occur
Electrical Burns
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Indirect- burns that are
either linear in areas at
which sweat was present;
are feathery or
aborescent pattern, which
is believed to be
pathognomonic
Electrical Burn
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It is characterized by
erythema, edema,
bulla formation and
sloughing of the
necrotic epidermis
Electrical Burn-pathology
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Blistering and
elongated
keratinocytes
Miliaria
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Retention of sweat as a result of occlusion
Common in hot, humid climates
Occlusion of eccrine sweat gland obstructs
delivery of sweat to the skin surface
Eventually backed-up pressure causes rupture
of sweat gland or duct at different levels
Escape of sweat into adjacent tissue produces
miliaria
Different forms of miliaria occur depending on
the level of injury to the sweat gland
Miliaria Crystalline
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Small, clear, superficial
vesicles without
inflammation
Appears in bedridden
pts and bundled
children
Lesions are
asymptomatic and
rupture at the slightest
trauma
Self-limited; no tx is
required
Miliaria Crystallina
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Minute, discrete
vesicles resulting
from profuse
sweating secondary
to a high fever
Miliaria Crystallina
Miliaria Rubra
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Discrete, extremely
pruritic, erythematous
papulovesicles with
sensation of prickling,
burning, or tingling
Site of injury is prickle
cell layer where
spongiosis is produced
Miliaria Rubra
Miliaria Pustulosa
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Always preceded by
some injury,
destruction, or blocking
of sweat duct
Pustules independent of
hair follicle
Seen in intertriginous
areas, flexure surfaces
of extrmities, sctrotum,
and back of bedridden
pts
Sterile pustules
Miliaria Profunda
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Nonpruritic, 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
Occlusion Miliaria
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May be produced with accompanying
anhidrosis and increased heat stress
susceptibility after application of extensive
polyethylene film occlusion for > 48 hrs
Tx-place pt in a cool environment
Even a night in an air-conditioned room helps
alleviate the discomfort
Occlusion Miliaria
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Mild cases may respond to dusting powders,
such as cornstarch or baby talcum powder
A lotion containing 1% menthol and glycerin and
4% salicylic acid in 95% alcohol is effective
An oily “shake” lotion such as calamine lotion,
with 1% or 2% phenol may be effective
Erythema (pigmentatio) Ab
Aka “toasted skin”
Igne
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syndrome
Persistent erythema or
coarsely reticulated
residual pigmentation
resulting from it
Produced by longcontinued exposure to
excessive heat without
production of a burn
It begins as a mottling
caused by local
hemostasis and
becomes a reticulated
erythema, leaving
pigmentation
Erythema Ab Igne
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Reticulated
hyperpigmentation
with some epidermal
atrophy and scaling
secondary to use of
a heating pad
Erythema ag igne
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Use of bland emollients is
helpful
No effective treatment
Kligman’s combination of
5% hydroquinone in
hydrophilic ointment
containing 0.1% retinoic
acid and 0.1%
dexamethasone may
reduce unsightly
pigmentation
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Histologically, an
increased amount of
elastic tissue in the
dermis is seen
Changes are similar to
actinic elastosis, and
has been suggested
to call these changes
thermal elastosis
Cold Injuries
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Chilblain
Frostbite
Immersion injury
Chilblains
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Acute chilblains is the mildest form of cold injury
Pts are usually unaware of injury until they
develop burning, itching, and redness
Chilblains (pernio)
Treatment
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Nifedipine 20mg TID
Vasodilators (nicotina
amide 100 mg TID or dipyridamole 25 mg
TID)
Systemic corticoid tx is helpful in chilblain
lupus erythematosus
Pentoxifylline may be useful
Smoking strongly discouraged
Frostbite
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When soft tissue is frozen
and locally deprived of blood
supply
Frozen part is painless and
becomes pale and waxy
Four stages:
I- Frost-nip erythema,
edema,cutaneous anesthesia
& transient pain
II- second degree:
hyperemia, edema &
blistering, with clear fluid in
bullae
III- third-degree: fullthickness dermal loss with
hemorrhagic bullae
formation or waxy, dry,
mummified skin
IV- full-thickness loss of
entire part
First-Degree Frostbite
Immersion Foot Syndromes
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Trench Foot
Warm Water Immersion Foot
Trench Foot
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Results from prolonged
exposure to cold, wet
conditions without
immersion or actual
freezing
Term derived from trench
warfare in World War 1,
when soldiers stood,
sometimes for hours, in
trenches with a few
inches of cold water in
them
Tx-removal from causal
environment
Tropical
immersion Foot
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Seen after continuous immersion of the feet in
water or mud of temperatures above 71.6
degrees F (22 degrees C) for 2-10 days
AKA “paddy foot” in Vietnam
Erythema, edema, and pain of the dorsal feet
Also fever and adenopathy
Resolution occurs 3 to 7 days after the feet have
been dried
Dermatoses with Cold
Hypersensitivity
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Erythrocyanosis Crurum
Acrocyanosis
Cold Panniculitis
Erythrocyanosis Crurum
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Slight swelling and a
bluish pink tint of the
skin of the legs and
thighs of young girls
and women
May be unilateral
May have cramps in the
legs at night
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Small tender nodules
may be found on
palpation
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Nodules may break down
and form small, multiple
ulcers
Seen in northern
countries and probably
due to an abnormal
reaction of blood
vessels to prolonged
cold
Acrocyanosis
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A persistent cyanosis with coldness and
hyperhidrosis of hands and feet
Chiefly occurs in young women
At times, on cold exposure, a digit becomes
stark white and insensitive (acroasphyxia)
Cyanosis increases as the temperature
decreases and changes to erythema with
elevation of dependent part
Cause is unknown
Smoking, coffee, and tea should be avoided
Acrocyanosis
Cold Panniculitis
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After exposure to severe cold, well-demarcated
erythematous warm plaques may develop,
particularly on the cheeks of young children
Lesions usually develop within a few days after
exposure, and resolve spontaneously in 2
weeks(approx)
No tx is indicated
Popsicle dermatitis is a temporary redness and
induration of the cheek in children resulting from
sucking Popsicles
Sunburn and Solar Erythema
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Parts of solar spectrum
important to
photomedicine:
Visible light 400 to 760
nm
Infrared radiation
beyond 760 nm
Visible light has little
biologic activity, except
for stimulating the
retina
Infrared radiation is
experienced as radiant
heat
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Below 400 nm is the
ultraviolet spectrum,
divided into three
bands:
UVA, 320 to 400 nm
UVB, 290 to 320 nm
UVC, 200 to 290 nm
Virtually no UVC
reaches the earth’s
surface, because it is
absorbed by the ozone
layer
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Exception: Australia,
welders
Sunburn and Solar Erythema
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UVB is 1000 times more
erythemogenic than
UVA
UVA is 100 times
greater than UVB
radiation during the
midday hours
Most solar erythema is
cause by UVB
Sunlight early and late
in the day contains
more UVA
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UVA is reflected from
sand, snow, or ice to a
greater degree than
UVB
Amount of ultraviolet
exposure increases at
higher altitudes, is
greater in tropical
regions, and temperate
climates in summer
Clinical signs and symptoms
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Sunburn is normal cutaneous reaction to
sunlight in excess of an erythema dose
(the amount that will induce reddening)
UVB erythema peaks at 12 to 24 hrs after
exposure
Desquamation is common about a week
after sunburn even in non-blistering areas
Sunburn treatment
Cool compresses
 Topical steroids
 Topical remedy:
Indomethacin 100 mg
Absolute ethanol 57 ml
Propylene glycol 57 ml
spread widely over burned area with palms and
let dry
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Skin Types
Second-degree sunburn
Prophylaxis
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Avoid sun exposure between 10 am and 2 pm
Barrier protection with hats and clothing
Suncreen agents include UV-absorbing chemicals
and UV-scattering or –blocking agents(physical
sunscreens)
Sunscreens
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Chemical suncreens-paraaminobenzoic acid(PABA),
PABA esters,
cinnamates,salicylates,
anthranilates,
benzophenoes)
Physical agents-titanium
dioxide
Combinations of the two
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Water resistantmaintaining their SPF
after 40 minutes of water
immersion
Water proof-maintaining
their SPF after 80 mins of
water immersion
UVA protectionsunscreens containing
benzophenones or
dibenzoylmethanes
Apply sunscreen at least
20mins before sun
exposure
Photoaging(Dermatohelioisis)
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Characteristic changes induced by chronic sun
exposure
Risk of developing these changes correlated with
baseline pigmentation(constitutive pigmentation)
and abilitiy to resist burning and tan following
sun exposure(facultative pigmentation)
Dermatoheliosis
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Poikiloderma of Civatterefers to reticulate
hyperpigmentation with
telangiectasia, and slight
atrophy of sides of the
neck, lower anterior neck
and V of neck, and V of
chest
Submental area is spared
frequently presents in
fair-skinned men and
women in their middle to
late thirties or early
forties
Dermatoelastosis
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Cutis rhomboidalis
nuchae (sailor’s neck or
farmer’s neck) is
characteristic of longterm, chronic sun
exposure
Skin on back of neck
becomes thickened,
tough, and leathery and
normal skin marking
become exaggerated
Dermatoheliosis
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Favre-Racouchot
syndrome
Thickened yellow
plaques studded with
comedomes and cystic
lesions
Tx-removal , retinoic
acid cream, surgical
removal of cysts and
redundant skin
Solar Elastosis
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Homogenization and a
faint blue color of
connective tissue of the
upper reticular dermis,
so-called solar elastosis
Characteristically there is
a zone of normal
connective tissue below
the epidermis
Photosensitivity
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Photosensitizers may
induce an abnormal
reaction in skin exposed
to sunlight or its
equivalent
Substances may be
delivered externally or
internally
Increased sunburn
response without prior
allergic sensitization
called phototoxicity
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Phototoxicity may occur
from both externally
applied
(phytophotodermatitis
and berloque
dermatitis) or internally
administered chemicals
(phototoxic drug
reaction)
Or by external contact(photoallergic contact
dermatitis)
Phototoxicity vs photoallergy
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In the case of external contactants –
phototoxicity occurs on initial exposure, has
onset < 48 hrs, occurs in most people
exposed to the phototoxic substance and
sunlight
Photoallergy, in contrast, occurs only in
sensitized persons, may have delayed onset, up
to 14 days( a period of sensitization), and shows
histologic features of contact dermatitis
Photosensitivity
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Drug-induced
photosensivityphotoallergic
dermatitis on sunexposed areas of
an infant following
topical use of
hexachlorophene
Photoallergic dermatits
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Papulovesicular
lesions of
photoallergic
dermatitis due to
hexachlorophene
Phytophotosensitivity
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Plant-induced
photosensitivity-linear
hyperpigmentation on
the face of a child
following exposure to
limes and sunlight
Phytophotosensitivity
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Hyperpigmentation on the dorsal
aspect of the hands following the use
of limes and sunlight exposure
Photosensitivity in
Tattoos
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Yellow cadmium sulfide
may be used as a
yellow dye or may be
incorporated into red
mercuric sulfide
pigment to produce a
brighter red color for
tattooing
When exposed to 380,
400, and 450 nm
wavelengths of light,
these areas in tattoos
may swell, develop
erythema, and become
verrucose
Phototoxic Drug Reactions
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Most occur from
tetracyclines,
nonsteroidal
antiinflammatory drugs,
amiodarone, and
phenothiazines
Action spectrum for all
is in the UVA range
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In the case of
amiodarone and
chlorpromazine,
hyperpigmentation is a
well-recognized
pattern of phototoxicity
It causes slate
blue(amiodarone) or
slate gray
(chlorpromazine)
coloration, resulting
from drug deposition in
the tissues
Drug induced photosensitivity
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The erythema is less
apparent in black
skin, but the
involvement of the
nose in this patient
suggests
phototoxicity, in this
case caused by
thiazide
Drug-induced photosensitivity
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Not only the nose
was but also the
“V” of the neck
which was highly
suggestive of
phototoxicity
Same pt
Drug-induced photosensitivity
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There is erythema
and edema on the
exposed sites, the “V”
of the neck .
This distribution
would suggest the
diagnosis
Drug induced photosensitivity
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The backs of the
hands are the classic
sites to be involved in
light induced eruption
Same pt
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Phototoxic reaction to
a nonsteroidal
antiinflammatory drug
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Photoallergic
dermatitis on sunexposed areas
Polymorphous Light Eruption
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Most common form of sensitivity
All races and skin types affected
Typically in first three decades
Females outnumber males
Unknown pathogenesis
Positive family history in 10-50% of pts
Different morphologies seen, although in the
individual the morphology is constant
PMLE
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Exposed areas such
as the backs of the
hands and forearms
are affected.
Ultraviolet A is mainly
responsible and may
penetrate window
glass
PMLE
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The patchiness of the
edematous papules and
plaques is characteristic
PMLE
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The eruption is less red and confluent than a
sunburn (left)
Lesions are typically papular & clustered (right)
PMLE-pathology
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Characteristic
perivascular
mononuclear cell
infiltration
PMLE
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Very itchy,
red,edematous papules,
which may coalesce into
plaques, occur 1 or 2
days after exposure to
light
PMLE
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This young women developed a widespread
pruritic, papular eruption after using a sunbed,
which emitted ultraviolet A
PMLE
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Polymorphous light
eruption:
erythematous
papulovesicular and
plaque-like lesions
with characteristic
distribution on the
sun-exposed areas
of the cheek
Actinic Prurigo
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The clinical features
are somewhat
suggestive of PML,
but the lesions are
persistent and the
HLA type was DR4(
occurs in 80-90% of
AP pts)
AP
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Severe actinic prurigo shows spread to buttocks (left)
Arms show crusted papules that are denser distally;
they are also worse in summer
Actinic prurigo
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Actinic prurigo in Native
American brothers
Actinic prurigo
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Actinic prurigo in
Native American boy
AP-pathology
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Early lesions have
variable acanthosis and
spongiosis of the
epidermis with an
underlying perivascular
mononuclear cell
infiltrate with edema
Later lesions show
crusts, increasing
acanthosis and variable
lichenification plus a
heavy infiltrate of
mononuclear cells,
leading to a non-specific
picture(as seen here)
Hydroa Vacciniforme
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Photodermatosis with onset
in childhood
Lesions appear in crops with
disease free intervals
Attacks may be preceded by
fever and malaise
Ears, nose, cheeks, and
extensor arms and hands are
affected
Within 6 hrs of exposure
stinging may occur
Hydroa Vacciniforme
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There is an early,
PML-like eruption,
but with vesicles
around the mouth
and umbilicated
lesions on the nose
Hydroa Vacciniforme
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A later, more severe
example shows
vesiculation with
umbilication, but
also marked
hemorrhagic
crusting
Hydroa Vacciniforme
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A severe example
of the typical
vacciniform facial
scarring that may
develop following
repeated acute
attacks
Acute Radiodermatitis
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With an “erythema dose” of ionizing radiation
there is a latent period of up to 24 hrs before
visible erythema develops
Initial erythema lasts 2-3 days but may be
followed by a second phase beginning up to 1
week after the exposure and lasting up to 1
month
Acute Radiodermatitis
(fluoroscopic induced)
Chronic Radiodermatitis
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Chronic exposure to
“suberythema” doses of
ionizing radiation over a
prolonged period will
produce varying
amounts of damage to
skin and underlying skin
after a variable latent
period of several
months to several
decades
Telangiectasia, atrophy,
and hypopigmentation
with residual focal
increased pigment
(freckling) may appear
Radiation Cancer
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After a latent period averaging 20 –30 yrs, various
malignancies may develop
Most frequent are basal cell carcinomas
Next frequent are squamous cell carcinomas
These may occur in sites of prior radiation even without
evidence of chronic radiation damage
SCCs arising in sites of radiation therapy metastasize
more frequently than purely sun-induced SCCs
Other cancers induced by radiation :angiosarcoma,
malignant fibrous histiocytoma, sarcomas, and thyroid
carcinoma
Radiation Cancer
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SCC developing in a
chronic radiation ulcer
on the chest
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Callus
Nonpenetrating,
circumscribed
hyperkeratosis
produced by pressure
Occurs on parts subject
to intermittent
pressure(palms, soles,
bony prominences of
the joints)
Callus differs from
clavus in that a callus
has no penetrating
central core and is a
more diffuse thickening
Calluses tend to
disappear
spontaneously when
pressure is removed
Clavus(Corns)
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Circumscribed, horny,
conical thickenings with
the base on the surface
and the apex pointing
inward and pressing on
adjacent structures
Two types:hard and soft
Hard:occur on dorsa of
toes or on soles
Soft:occur between toes,
softened by macerating
action of sweat
Hard Corn
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Plantar corns can be
differentiated from
plantar warts by paring
off the surface keratin
until either the
pathognomonic
elongated dermal
papillae of the wart with
its blood vessels, or the
clear horny core of the
corn can be visualized
Ddx: also includes
porokeratosis plantaris
discreta- a sharply
marginated, coneshaped, rubbery lesion
common beneath the
metetarsal heads
Corns
Porokeratosis Plantaris
Discreta
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Multiple lesions can
occur
Females are affected 3
times as frequently than
men
It is painful
Frequently confused
with a plantar wart or
corn
Keratosis punctata of
the palmar creases may
be seen in the creases
of the digits of the feet
where it may be
mistaken for a corn
Surfer’s
Nodules
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Nodules 1 to 3 cm
(rarely as much as 5 or
6 cm)
Sometimes eroded or
ulcerated
Develop on tops of feet
or over tibial tubercles
of surfboard riders who
paddle their boards in a
kneeling position, as is
customary in cold water
off the California coast
Nodules seldom occur in
surfers in warmer
waters like
Hawaii,because a prone
position is used
Nodules involute over
months when there is
Pressure Ulcers (Decubitus)
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The bedsore is a pressure ulcer produced
anywhere on the body by prolonged pressure
Caused by ischemia of underlying structures of
skin, fat, and muscles resulting from sustained
and constant pressure
Usually in chronically debilitated persons unable
to change position
Bony prominences of body are most frequently
involved
Care-Tx
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Ulcer care is critical
Debridement-except
stable heel ulcers(do
not need debridement if
only a dry eschar is
present)
Clean wounds initially
and at each dressing
change via
nontraumatic technique
Normal saline is best
Dressing selection
should maintain moist
environment
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Occlusive dressings like
film and hydrocolloid are
often utilized
Surgical debridement
with reconstructive
procedures may be
needed
Electrical stimulation of
refractory ulcers may be
beneficial
Friction Blisters
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Formation of vesicles or
bullae occurring at sites
of combined pressure and
friction
Enhanced by heat and
moisture
Examples: feet of military
recruits in training,palms
of oarsmen not having
developed protective
calluses, beginning
drummers (“drummer’s
digits”)
Sclerosing Lymphangiitis
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Cordlike structure
encircling the coronal
sulcus of the penis, or
running the length of
the shaft
Attributed to trauma
Produced by a
sclerosing lymphangiitis
No tx is needed
Follows a benign, selflimiting course
Black Heel
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Also called talon noir,
calcaneal petechiae, and
chromidrose plantaire
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A sudden shower of
minute macules occurs
most often on the
posterior edge of the
plantar surface of one or
both heels
Sometimes occurs distally
on one or more toes
Black heel is seen in
basketball, volleyball,
tennis, or lacrosse players
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AKA painful piezogenic
pedal papules
Rare cause of painful
feet representing fat
herniations through thin
fascial layers of weightbearing parts of the
heel
These dermatoceles
become apparent when
wt is placed on the heel
These disappear when
pressure is removed
Extrusion of fat tissue
together with its blood
vessels and nerves
initiates pain on
prolonged standing
Painful Fat
Herniation
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Avoidance of
prolonged standing is
the only way to
provide relief
Majority of people
experience no
symptoms
Painful Fat Herniation
Narcotic Dermopathy
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Heroin(diacetylmorphine)
is a narcotic prepared by
dissolving the heroin
powder in boiling water
and then injecting it
Favored route is IV
Resulting in thrombosed,
cordlike, thickened veins
Narcotic Dermopathy
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Subcutaeous injection (“skin popping”) can
result in multiple, scattered ulcerations, which
heal with discrete atrophic scars
Narcotic Dermopathy
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Ulcer from extravascular
injection of “speed”
(amphetamine)
Tatooing
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Photosensitivity can occur from pigments used
(cadmium sulfide-used for yellow color or to
brighten up cinnabar red)
Unsanitary tattooing has resulted in inoculation
of syphilis, infectious hepatitis, tuberculosis, HIV,
and leprosy
Occasionally keloid formation occurs
Accidental tattoo marks may be induced by
narcotic addicts who sterilize needles for
injection by flaming needle with a lighted match
Tattooing
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Discoid lupus has been reported to occur in
red-pigmented portions of tattoos
Sarcoid nodules and granuloma annulare-like
lesions have also been seen
Dermatitis in areas of re (mercury), green
(chromium), or blue (cobalt) have been
described in pts patch-test positive to these
metals
Tx:Q-switched laser allows removal without
scarring
One report of five pts who developed
darkening after tx due to ferrous oxide
formation
Paraffinoma
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AKA-sclerosing
lipogranuloma
Injection of paraffin into
skin for cosmetic
purposes
Smoothing of wrinkles
and breast
augmentation
Oils like paraffin,
camphorated oil,
cottonseed or sesame
oil, beeswax were used
These can produce
plaque-like indurations
with ulcerations after
time