Transcript Dermatoses Resulting from Physical Factors

Dermatoses Resulting from
Physical Factors
Chapter 3
Andrew’s Diseases of the Skin
Ben Adams, D.O.
July 25th 2006
Heat Injuries








Thermal Burns
Electrical Burns
Miliaria
Miliaria Crystalline (Sudamina)
Miliaria Rubra (Prickly Heat, Heat Rash)
Miliaria Pustulosa
Miliaria Profunda
Occlusion Miliaria
Thermal Burns




First-degree burn: active
congestion of superficial blood
vessels
This causes erythema, sometimes
followed by epidermal
desquamation
Constitutional reactions occur if
large area involved
Pain and increased surface heat
may be severe
Second-degree burns




Superficial

Deep
Transudation of serum
causing edema of
superficial tissues

Pale and anesthetic

Vesicles and blebs
Complete recovery without
scar or blemish is usual
Injury to reticular dermis
compromises blood flow
and destroys appendages

Healing takes > 1 month

Scarring occurs
Second-degree burn

Thermal burn: This superficial
second degree burn is
characterized by bullae that
contain serous fluid
Second-Degree Burns



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


Accidental scald
Splash-anddroplet pattern
of an accidental
scald from hot
cup of tea
Third-degree burns


Full-thickness tissue
loss
Skin appendages are
destroyed


There is no epithelium
for regeneration
Healing leaves a scar
Fourth-degree burns

Destruction of entire skin
and subcutaneous fat
with any underlying
tendons



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



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
Lightning is the most lethal
type of strike, cardiac arrest
or other internal injuries
may occur
Electrical Burns

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

It is characterized by
erythema, edema,
bulla formation and
sloughing of the
necrotic epidermis
Electrical Burn-pathology

Blistering and elongated
keratinocytes
Miliaria

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 Crystallina




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

Minute, discrete
vesicles resulting from
profuse sweating
secondary to a high
fever
Miliaria Rubra


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




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 pts
Sterile pustules
Miliaria Profunda

Nonpruritic, flesh-colored, deepseated, 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



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



Mild cases may respond to
dusting powders, such as
cornstarch or 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 Igne




Aka “toasted skin” syndrome
Persistent erythema or coarsely
reticulated residual pigmentation
resulting from it
Produced by long-continued
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

Reticulated
hyperpigmentation
with some epidermal
atrophy and scaling
secondary to use of
a heating pad
Erythema Ab Igne



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



There is a mild superficial perivascular
inflammatory infiltrate composed
predominantly of lymphocytes and
prominent pigment incontinence.
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

Chilblains

Frostbite

Immersion injury
Chilblains


Acute chilblains is the
mildest form of cold
injury
Pts are usually unaware
of injury until they
develop burning, itching,
and redness
Treatment



Nifedipine 20mg TID
Vasodilators (nicotinamide 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

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: full-thickness
dermal loss with hemorrhagic
bullae formation or waxy, dry,
mummified skin
IV- full-thickness loss of entire
part
First-Degree Frostbite
Immersion Foot Syndromes

Trench Foot

Warm Water Immersion Foot
Trench Foot



Term derived from trench
warfare in World War I, when
soldiers stood, sometimes for
hours, in trenches with a few
inches of cold water in them
Results from prolonged
exposure to cold, wet
conditions without immersion
or actual freezing
Tx-removal from environment
Tropical
Immersion Foot

AKA “paddy foot” in Vietnam

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

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

Erythrocyanosis Crurum

Acrocyanosis

Cold Panniculitis
Erythrocyanosis Crurum

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

Small tender nodules
may be found on
palpation


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






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




After exposure to severe cold, welldemarcated 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


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



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

Exception: Australia,
welders
Sunburn and Solar Erythema




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


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



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
Skin Types
Second-degree sunburn
Prophylaxis



Avoid sun exposure
between 10 am and 2 pm
Barrier protection with
hats and clothing
Sunscreen agents include
UV-absorbing chemicals,
and UV-scattering or
blocking agents (physical
sunscreens)
Sunscreens



Chemical sunscreens: paraaminobenzoic acid(PABA),
PABA esters, cinnamates,
salicylates, anthranilates,
benzophenoes)


Physical agents: titanium/zinc
dioxide
Combinations of both


Water resistant: maintaining
their SPF after 40 minutes of
water immersion
Water proof: maintaining their
SPF after 80 mins of water
immersion
UVA protection: sunscreens
containing benzophenones or
dibenzoylmethanes
Apply sunscreen at least
20mins before sun exposure
Photoaging (Dermatohelioisis)


Characteristic changes
induced by chronic sun
exposure
Risk of developing these
changes correlated with
baseline pigmentation
(constitutive
pigmentation) and ability
to resist burning and tan
following sun exposure
(facultative pigmentation)
Dermatoheliosis



Poikiloderma of Civatte:
refers to reticulate
hyperpigmentation with
telangiectasia, and slight
atrophy of sides of the neck,
lower anterior neck and V of
chest
Submental area is spared
Frequently presents in fairskinned men and women in
their middle to late thirties or
early forties
Dermatoelastosis

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



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


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



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 is
called phototoxicity

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


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

Drug-induced
photosensivityphotoallergic
dermatitis on sunexposed areas of
an infant following
topical use of
hexachlorophene
Photoallergic dermatitis

Papulovesicular
lesions of
photoallergic
dermatitis due to
hexachlorophene
Phytophotosensitivity

Plant-induced
photosensitivity-linear
hyperpigmentation on
the face following
exposure to limes and
sunlight
Phytophotosensitivity

Hyperpigmentation on
the dorsal aspect of
the hands following
the use of limes and
sunlight exposure
Photosensitivity in
Tattoos


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


Most occur from
tetracyclines, nonsteroidal
antiinflammatory drugs,
amiodarone, and
phenothiazines

Action spectrum for all is in
the UVA range

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
Amiodarone
Drug induced photosensitivity

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


Not only the nose
was but also the
“V” of the neck
which was highly
suggestive of
phototoxicity
Same pt
Drug induced photosensitivity

The backs of the
hands are the classic
sites to be involved in
light induced eruption

Phototoxic reaction to
a nonsteroidal
antiinflammatory drug

Photoallergic
dermatitis on sunexposed areas
Polymorphous Light Eruption







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 1050% of pts
Different morphologies seen,
although in the individual the
morphology is constant
PMLE

Exposed areas such
as the backs of the
hands and forearms
are affected.
Ultraviolet A is
mainly responsible
and may penetrate
window glass
PMLE

The patchiness of the
edematous papules and
plaques is characteristic
PMLE


The eruption is less red and confluent than a
sunburn (left)
Lesions are typically papular & clustered (right)
PMLE-pathology

Characteristic
perivascular
mononuclear cell
infiltration
PMLE

Very itchy, red, edematous papules, which
may coalesce into plaques, occur 1 or 2
days after exposure to light
PMLE

Polymorphous light
eruption:
erythematous
papulovesicular and plaquelike lesions with
characteristic distribution on
the sun-exposed areas of the
cheek
Actinic Prurigo

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


Severe actinic prurigo shows spread to buttocks (left)
Arms show crusted papules that are denser distally;
they are also worse in summer
Actinic prurigo

Actinic prurigo in Native
American brothers
Actinic prurigo

Actinic prurigo in
Native American boy
AP Pathology


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





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

There is an early,
PML-like eruption,
but with vesicles
around the mouth
and umbilicated
lesions on the nose
Hydroa Vacciniforme

A later, more severe
example shows
vesiculation with
umbilication, but
also marked
hemorrhagic
crusting
Hydroa Vacciniforme

A severe example
of the typical
vacciniform facial
scarring that may
develop following
repeated acute
attacks
Acute Radiodermatitis


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


Chronic exposure to “sub
erythema” 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






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

SCC developing in a
chronic radiation ulcer
on the chest
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)




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
Corns


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, cone-shaped,
rubbery lesion common
beneath the metetarsal
heads
Porokeratosis Plantaris Discreta





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





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 no surfing
Pressure Ulcers (Decubitus)


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





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



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



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

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

Also called talon noir, calcaneal
petechiae, and chromidrose
plantaire



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





Painful Fat
Herniation
AKA painful piezogenic pedal
papules
Rare cause of painful feet
representing fat herniations
through thin fascial layers of
weight-bearing 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


Avoidance of prolonged
standing is the only way to
provide relief
Majority of people experience
no symptoms
Painful Fat Herniation
Narcotic Dermopathy



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

Subcutaeous injection (“skin popping”) can
result in multiple, scattered ulcerations, which
heal with discrete atrophic scars
Tattooing




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





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 red (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





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 plaquelike indurations with
ulcerations after time