CHAPTER
RESULTING
FACTORS
sepsis, pain control, environmental control and
nutritional support and key components of critical
care of burns
3:
DERMATOSES
FROM
PHYSICAL
HEAT INJURIES
1. THERMAL BURNS- from excessive heat on the skin
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If heat is extreme, underlying tissue may be destroyed
Changes -> dry heat /scalding
A. First-degree burn – active congestion of superficial
BV  erythema  epidermal desquamation (peeling)
Ex. Sunburn
May have pain and increased surface heat that may
be severe
B. Second-degree burn – superficial and deep
Superficial 2nd degree burn- w/ transudation of serum
from capillaries  edema of superficial tissues 
vesicles and bullae
 Complete recovery without scarring in usual
patients
Deep 2nd degree burn – pale and anesthetic
 Reticula r dermis injury compromises blood flow
and destroys appendages
 Healing takes >1 month  scarring
C. Third- Degree burn – loss of full thickness of der is and
often subcutaneous tissues , no epithelium for
regeneration of skin
 With ulcerating wound  scar
D. Fourth- degree burn – destruction of entire skin + SC
fat + underlying tendons
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3rd and 4th degree burns- require grafting for closure
 With constitutional symptoms of varying severity
 The more vascular area involved, the more
severe symptoms
 >2/3 of BSA burned, poor prognosis.
 Women, infant and toddlers- greater risk for
death than men
 Excessive scarring  keloid-like scars, flat scars
with contractures  deformities and dysfunction
of joints
 Chronic ulcerations may lead to impairment of
circulation
TREATMENT – immediate first aid : cold applications
 Vesicles and bullae should not be opened from
injury because they form a natural barrier against
contamination from microorganisms.
 If they become painful and tense, fluid may be
evacuated under strictly aseptic conditions by
puncturing it with a sterile needle
 Excision of full-thickness and deep dermal
wounds that will not reepithelialized within 3
weeks reduced wound infections, shortens
hospital stay, and improves survival.
 Skin grafting, allograft/xenograft skin, cultured
epidermal autografts or skin substitute also assist
in healing
 Early ablative laser- area of active investigation
 Superficial wounds- gauze, silver- containing
dressings
 Fluid resuscitation , tx of inhalaton injury and
hypercatabolism monitoring, early intervention of
COLD INJURIES – exposure to cold damages by the skin at least
3 mechanisms:
1. Reduced temperature directly damages the tissue
(E.g. frost bite, cold immersion foot)
2. Vasospasm of vessels- perfusing the skin prevents
adequate perfusion of the tissue and causes vascular
injury and tissue injury (eg. Pernio, acrocyanosis and
frostbite)
3. In unusual circumstances, adipose tissue is
predisposed to damage by cold temperature because
of fat composition or location
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ACROCYANOSIS- persistent blue discoloration of the
entire hand and foot worsened by cold exposure.
- hands and feet may be HYPERHIDROTIC
- Occurs chiefly on young women
- smoking should be avoided
- distinguished to Raynaud syndrome by persistent
nature and lack of tissue damage
- swelling of nose, ears and dorsal hands may occur
after inhalation of butyl nitrite
- may be a sign of malignancy
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- may be seen in patients with anorexia nervosa
PERNIO ( Chilblain, perniosis)
- localized erythema and swelling caused by
exposure to cold
- blisterings and ulcerations may develop in severe
cases
- chilblain- like lesions- occur in discoid and SLE
- TREX-1 associated familial type – presenting sign
of leukemia cutis
- if occurring in infancy may herald NakajoNishimura syndrome or Aicardi- Goutieres and
Singleton- Merten syndrome
- may occur in chronic use of crack cocaine ->
peripheral vasoconstriction -> perniosis with cold,
numb hands and atrophy of digital fat pads
- occur chiefly on feet, hands, ears and face, chiefly
on women
- onset enhanced by dampness
- in lateral thighs of women equestrians who ride,
on cold, damp days and the hips in those wearng
tight-fitting jeans w/ a low waistband
- non digital lesions can be nodular
- histologically demonstrated lymphocytic vasculitis
- dermal edema and superficial and deep
perivascular tightly cuffed, lymphocytic infiltrate
- fluffy edema of the vessel walls
- TREATMENT – heating pads, Nifedipine 20mg TID
has been effective , other vasodilators
- spontaneous resolution w/o tx in 1-3 weeks
- chilblain lupus- systemic corticosteroid
FROSTBITE – when soft tissue is frozen and locally
deprived of blood supply
- ears, nose, cheeks, fingers and toes most often
affected.
- frozen part becomes pale and waxy
- various degrees of tissue destruction similar to burns
- degree of injurt directly related to the temperature
and duration of freezing
- African-Americans – increased risk
- arthritis of small joins may appear months-years later
- Tx: early – covering part with clothing or with a warm
hands
- rapid rewarming in a water bath between
37-40 degrees – TREATMENT OF CHOICE
- rewarming delayed until the px removed to
an area where there is no risk of refreezing
- slow thawing- > more extensive tissue
damage
- Analgesics
- TPa : to lyse thrombi, decreased the need
for amputation of given within 24h of injury
- vasodilator (Iloprost) infusion
- Supportive- bed rest, high CHON/calorie
diet, wound care and avoidance of trauma
- use of anticoagulants
- Antibiotics – prophylactic measure
- late complications- arthritis
IMMERSION FOOT SYNDROMES
1. Trench foot –
from prolonged
exposure to cold, wet conditions w/o
immersion or actual freezing
- derived from trench warfare in World War I
- seen on fishermen, sailors and shipwreck
survivors
- lack of circulation edema, paresthesias
and damage to the BV
- gangrene in severe cases
Treatment: removal of cause, bed rest and
restoration of circulation
2. Warm water immersion
foot – exposure of feet to warm, wet
conditions for >/= 48hrs
- characterized by maceration, blanching,
wrinkling of soles and sides of the feet
- itching and burning with swelling may persist
for few days
- seen in military service members in Vietnam
- different from “paddy foot” in Vietnam: tropical
immersion foot, immersion of feet in water or
mud at temp above 22 deg C w/c involved
erythema, edeam and pain in dorsal feet, fever
and adenopathy. Resolution 3-7 days
- Prevention: allowing feet to dry for a few hrs in
every 24 or by greasing the soles w/ silicone
grease OD
- rapid recovery
ACTINIC INJURIES
1. Sunburn and solar erythema
 Most biologically effective wavelength of
radiation from the sun for sunburn – 308nm

UVA 100 times greater than UVB during
midday hrs
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But UVB is up to 1000 times erythmogenic
than UVA – UVB is the cause of solar
erythema
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During middle 4-6hrs of the day, UVB is 24x greater than early morning and late
afternoon
Clinical signs and symptoms
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Sunburn- normal cutaneous reaction to sunlight in
excess of an erythema dose.
UVB erythema- evident at around 6hrs after exposure
and peaks at 12-24h, but onset is sooner and the
severity greater with increased exposure.
Erythema -> tenderness
In severe cases – blistering w/c may become confluent
; symptoms may last as a week
Edema- in extremities and face
Chills, fever, nausea, tachycardia and hypotension
Desquamation – common after 1 week of sunburn
2 changes after UV exposure –
1. Immediate pigment darkening (IPD, Meirowsky
phenomenon) IPD – is maximal within hours after
sun exposure and results from metabolic
changes and redistribution of the melanin already
in skin
- occurs after exposure to long-wave UVA, UVB
and visible light
- IPD is not photoprotective
Delayed melanogenesis- delayed tanning is
induced by the same wavelengths of UVB that
induce erythema, begins 2-3 days after exposure
and lasts 10-14 days
- UVB: mediated thru the production of DNA
damage and the formation of CPD, provide some
protection
Exposure to UVA and UVB causes an increase in the
thickness of the epidermis esp sratum corneum ->
leads to increased tolerance to further solar radiation
Patients w/ vitiligo – may increase their UV exposure
w/o burning by this mechanism
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2.
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Ephelides- may be genetically determined and may
recur in successive generations; increased production
of melanin pigment by a normal no. of melanocytes,
epidermis normal
Usually appear at age 5
Lentigo – benign discrete hyperpigmented macule
appearing at any age and on any part of the body ,
including the mucosa ; has elongated rete ridges that
appear to be club shaped
Intensity of the color not dependent on sun exposure
Solar lentigo – appear at later age , at backs of hands
and face (esp forehead)
Freckles and lentigo – best prevented by sun
protection
PHOTOAGING (DERMATOHELIOSIS) –
TREATMENT – once damage done, inflammatory cascades are
triggered
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Prostaglandins – esp E series- important mediators
Tx: Aspirin, NSAIDs, indomethacin, topical and
systemic steroids
Medium- potency (Class II) topical steroids- applied
6hrs after exposure (when erythema first appears)
provide a small reduction in s/sx
Supportive- pain management and soothing topical
emollients and corticosteroid lotions
PROPHYLAXIS – 4 MAIN MESSAGES
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Avoid midday sun
Seek shade
Wear sun-protective clothing
Apply sunscreen
Highest UVB intensity – 9am and 3-4 pm : hazardous UV
exposure
For skin Types I-III – daily applications of broad- spectrum
sunscreen w/ an SPF of 30 in a facial moisturizer, foundation or
aftershave is recommended
 For outdoor exposure – SPF 30 or higher
 Application of sunscreen- at least 20mins before
exposure and 30 mins after sun exposure – this dual
application will reduce the amount of skin exposure by
two/threefold
 Vit D – 600IU daily 70 and younger; 800IU for older px
EPHELIS (Freckle) and lentigo
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Freckles- small < 0.5 cm brown macules that occur in
profusion on the sun exposed skin of the face, neck,
shoulders and backs of the hands
Prominent during the summer
Susceptible – blondes and redheads w/ blue eyes of
Celtic origin (skin types I & II)
from chronic sun exposure
 Risk for melanoma and non melanoma skin cancer is
related
 Skin type I – most susceptible to deleterious effects of
sunlight ; blue eyed, fair-complexioned who do not tan
; frequently Irish / Celtic / anglo-saxon descent
 Individuals with genetic susceptibility
 Additive- chronic sun exposure and chronologic aging
 Smoking – is also important in devt of wrinkles
 Skin becomes atrophic, scaly, wrinkled, inelastic or
leathery w/ yellow hue (milian citrine skin)
 Celtic ancestry persons- produces profound epidermal
atrophy w/o wrinkling, resulting in an almost
translucent appearance of the skin thru w/c
hyperplastic sebaceous glands and prominent
telangiectasias are seen; high risk for melanoma
 Solar actinic elastosis- textural and tinctorial changes
in sun-damaged skin are cause by alterations in the
upper dermal elastic tissue and collagen ;imparts
yellow-color of skin
 Striated beaded lines/ fibroelastolytic papulosis- small
yellowish papules and plaques , may develop on the
sides of the neck
 Poikiloderma of Civatte – in fair skinned men and
women in their mid to late 30s or earlys 40s; refers to
reticulate hyperpigmentation w/ telangiectasia and
slight atrophy of sides of neck, lower ant neck and V of
chest; submental shaded by the chin is spared
 Cutis rhomboidalis nuchae -sailor’s or farmers neck ;
long -term sun exposure; skin of the neck becomes
thickened , tough and leathery, NORMAL SKIN
MARKINGS ARE EXAGGERATED
 Nodular elastodoisis – w/ cysts and comedone in inf
periorbital and malar skin (Favor- Racouchot
Syndrome) on the forearms (actinic comedonal
plaque) or helix of the ear; thickened yellow plaques;
ears may exhibit 1 or more firm nodules (weathering
nodules) ; biopsy – fibrosis and metaplasia
 Dermatoporosis – Skin tearing from trivial injuries ;
telangiectasias over the cheeks, ears and sides of the
neck; damage to connective tissue of the dermis , skin
fragility is prominent
 Actinic purpura – ecchymosis to extensor arms; dusty
brown macules remain for months, increasing mottled
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appearance of skin; deep dissecting hematomas 
large area of necrosis
Acquired elastotic hemangiomas- severe complication
of dermatoporosis primarily on elderly women, many
taking anticoagulants or systemic steroids; show
horizontal proliferation of capillary BV in upper dermis/
may also appear on sun-damaged skin of the arms
and neck
White stellate pseudoscars on the forearms are a
frequent complication of this enhanced skin fragility
Soft, flesh-colored to yellow papules and nodules
coalesce on the forearms to form a cordlike band
extending from the dorsal to the flexural surfaces (
solar elastotic bands)
Both UVA and UVB – induce ROS and Hydrogen
peroxide
Chronically sun-exposed skin – demonstrated
homogenization and a faint blue color of the CT of
upper reticular dermis – Solar elastosis
“elastotic” material -derived largely from elastic fibers,
with marked increased deposition of FIBULIN 2 and its
breakdown properties
Types I and III collagen decreased
PHOTOSENSITIVITY
– includes cutaneous
reactions that are chemically induced, metabolic errors such as
porphyrias, resulting in production of endogenous, idiopathic and
light exacerbated\
1.
CHEMICALLY INDUCED PHOTOSENSITIVITY
 May be greatly increased sunburn response
w/o allergic sensitization called phototoxicity
 Phototoxicity – occurs on initial exposure ,
onset < 48h
 Shows histologic pattern similar to sunburn
Action Spectrum- photosensitizers usually compounds
with MW of <500 Daltons.
- each photosensitizing substance absorbs specific
wavelengths- ABSORPTION SPECTRUM
- PHOTOTOXICITY – Mostly in the long UVA region
and may extend into the visible light region (320425nm)
- intensity of photosensitivity rxn is generally dose
dependent
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COLLOID MILLIUM – 2 TYPES ADULT AND JUVENILE
In both types – primary skin lesion is a translucent ,
flesh colored or slightly yellow, 1-5 mm papule
Minimal trauma may lead to purpura from vascular
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fragility
Consists of intradermal, amorphous fissured
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eosinophilic material
Lesions appear on sun-exposed area, in middle aged,
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usually MEN
Lesions often coalesce into plaques and may rarely be
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verrucous
Assoc with petrochemical exposures
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PIGMENTED FORMS- assoc w/ hydroquinone use
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ADULT TYPE - Papular variant of solar elastosis
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JUVENILE TYPE- much rarer; develops before puberty
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and there may be family hx ; lesions same to adult
form
Juvenile colloid milium, ligneous conjunctivitis and
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ligneous periodontitis may appear in same patient and
prob same pathogenesis
Juvenile distinguished from adult by finding
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keratinocyte APOPTOSIS in the overlying epidermis
and stains CYTOKERATIN
TREATMENT
 Fractional photothermolysis or MAL- photodynamic
therapy
 Reducing lifetime UV exposure
 Use of emollients and moisturizing creams in areas of
sun damage will reduce scaling and improve fragility
 α-hydroxy acids – improve skin texture
 Topical tretinoin, adapalene and tazarotene – changes
photoaging
 Chemical peels , resurfacing techniques, laser and
other light technologies, botulinum toxins & soft tissue
augmentation
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3.
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PHOTOTOXIC REACTIONS
Nonimmunologic reaction , develops after exposure
to a specific wavelength and intensity of light in the
presence of photosensitizing substance
Sunburn type reaction w/ erythema , tenderness,
and even blistering
Can be elicited in person who have no previous hx
of exposure or sensitivity to that particular substance
Erythema- begins within 2-6 hrs but worsens for 4896h before beginning to subside
Exposure to nailbed  oncholysis
May cause market hyperpigmentation even w/o
preceding erythema
PHOTOTOXIC TAR DERMATITIS
Coal , tar, creosote, crude coal tar or pitch,in
conjunction w/ sunlight exposure
Assoc w/ severe burning sensation
Volatile hydrocarbons- may be airborne
Burning and erythema may continued for 1-3 days
70% white persons
Type V/VI skin- are protected by their skin
pigmentation
After acute rxn  hyperpigmentation
Mya be found in cosmetics, drugs, dyes, insecticides
and disinfectants
PHYTOPHOTODERMATITIS
FUROCOUMARINS- phototoxic reaction when they
come in contact w/ skin that is exposed to UVA light.
Several hrs after exposure  burning erythema 
edema  vesicles / bullae
Intense residual hyperpigmentation may persist for
weeks and months
Fragrance products containing BERGAPTEN component oil of bergamot will produce this rxn
Berloque dermatitis may result
Hyperpigmentation – primarily on neck and face
Most phototoxic plant families- Umbelliferae,
Rutaceae, Compositae and Moraceae
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Pelea anisata - Anise- scented Mokihana berry in
Hawaii, known to natives for its phototoxic properties
– Moki hana burn
Home tanning solutions containing fig leaves
Pink rot fungus ( Sclerotinia sclerotium) – exposure
can lead to occupational disability ; present on
celery roots – seen in celery farmers, grocery
workers
Dermatitis bullosa stirata pratensis ( grass or
meadow dermatitis) – caused by contact w/ yellowflowered meadow parsnip or a wild, yellow-flowered
herb of the rose family ; eruption consists of streaks
and bizarre configurations w/ vesicles and bullae
that heal w/ residual hyperpigmentation
Rhus dermatitis- itching most prominent symptom;
lesions continue to occur for a week or more
Treatment: similar to management of sunburn
IDIOPATHIC PHOTOSENSITIVITY DISORDERS
No cause is known
POLYMORPHOUS LIGHT ERUPTION (PLE ,
PMLE) – most common form of photosensitivity
5-20% of the adult population
Onset typically 1st four decades of life, females
outnumber males 2:1 or 3:1 ratio
Pathogenesis unknown; family hx may be elicited in
10-50% of patients
10-20% positive ANA and family hx of SLE
Photosensitive SLE patients- may have hx of PLElike eruptions for yrs before diagnosed as SLE
PAPULAR (erythematopapular) variant – most
common
Other variants: papulovesicular, eczematous,
erythematous and plaque-like
Plaque like – more common in elderly
African -american – pinpoint popular variant
Noted marked post inflammatory hyperpigmentation
or hypopigmentation may be present
In some px , pruritus only no eruptions
Lesions appear most often 1-4 days after exposure
to sunlight
A change in the amount of sun exposure appears to
be more critical than the absolute amount of
radiation
JUVENILE SPRING ERUPTION OF EARS- unsual
variant of PLE ; boys aged 5-12 or young adult
males ; often after exposure on cold but sunny days
; grouped small papules and papulovesicles; selflimited
Treatment: avoidance of exposure ; use of topical
tacrolimus ointment at night or BID
ACTINIC PRURIGO- prob represents as variant of
PLE
Most seen in Native Americans of North and Central
America and Colombia.
Mexico incidence- 1.5 -3.5%
Reported also in Europe, Australia, Japan
F : M ratio 2:1 and 6:1
In Native Americans- begins at age 10 in 45% of
cases and before age 20 in 72%
Up to 75% have + family hx of PLE
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Europe – 80% before age 10
Canada- later and adulthood onset
Childhood-small ppaules or papulovesicles that crust
and become impetiginized ; intensely pruritic ,
frequently excoriated ; cheeks, distal nose, ears and
lower lip; cheilitis may be the initial and only feature
for years
Conjunctivitis is seen in 10-20% of px
Prurigo nodule like configuration- lesions of arms
and legs – may extend even on sun protected area
In adults- chronic dry papules and plaques
Skin lesions persist throughout the year
Initial therapy same to PLE
Thalidomide – used effectively and safely over years
Cyclosporine – in patients refractory or intolerant to
thalidomide
BRACHIORADIAL PRURITUS
PLE initially and only on BRACHIORADIAL AREA
Severe, refractory, intractable pruritus and sec
severe lichenification
Now thought to represent a neuropathic pruritus,
sometimes related to cervical spine disease
Sunlight- eliciting factor ; CSD – predisposing factor
Tx: capsaicin patch provides itch relief and physical
barrier
SOLAR URTICARIA
Most common in women age 20-40
Within secs to mins after light exposre , typical
urticarial lesions appear and resolve in 1-2hrs rarely
lasting >24hrs
In severe attacks- syncope, bronchospasm and
anaphylaxis
Patients may be sensitive to wavelengths over a
broad spectrum
UVA sensitivity most common
Suggests presence of circulating photoinducible
allergen
Phototesting – useful to determine the wavelengths
of sensitivity
Tx: Antihistamines , LTRA (Montelukast) – may
provide additive efficacy in combination
PUVA or increasing UVA exposure- effective in more
difficult cases
Cyclosporine and IVIg
HYDROA VACCINIFORME
Rare , chronic photodermatosis w/ onset of
childhood
Boys and girls equally represented
Boys present EARLIER, and on average have
longer-lasting disease
Bimodal onset – ages 1-7 ; 12-16
Usually spontaneous remission before age 20
Within 6hrs of exposure, stingin begins
At 24h or sonner – erythema and edema appear
2-4 mm vesicles
Next few days, lesions rupture, become centrally
necrotic and heal w/ smallpox like scar
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May have subungual hemorrhage, ocular
involvement and oral ulcerations
Early lesions- intraepidermal vesiculation and
dermal edema
Necrotic lesions- reticular degeneration of
keratinocytes w/ epidermal necrosis flanked by
spongiosis w/ dense perivascular infiltrate of
neutrophils and lymphocytes
Tx: avoidance of sun; sunscreen; prophylactic NB
UVB phototherapy ; Chloroquine and systemic
corticosteroids
CHRONIC ACTINIC DERMATITIS
End stage of progressive photosensitivity in some px
Basic components:
 Persistent chronic eczematous eruption in the
absence of exposure to known photosensitizers
 Usually broad-spectrum photosensitivity w/
decreased MED to UVA and/or UVB at at times
visible light
 Histology consistent w/ chronic dermatitis w/ or
w/o features of lymphoma
 Predominantly affects middle aged or elderly men
 Edematous scaling, thickened patches and
plaques tend to be confluent
 Lesions primarily or most severely on the
exposed skin and may spare upper eyelids,
behind ears and bottom of wrinkles
 Unexposed sites involved on most severe cases
 Marked depigmentation resembling vitiligo
 Photopatch testing – in 1/3 of px yields positive
response
 Established by histologic evaluation and
phototesting
 Tx: topical photosensitizers ; Hydroxyurea 500mg
BID , Cyclosporine, thalidomide , Mycophenolate
mofetil ; immunosuppressive agents
PHOTOSENSITIVITY & HIV INFECTION
 Resembling PLE, actinic prurigo and chronic
actinic dermatitis seen in about 5% of patients w/
HIV
 Seen when <200 CD4 count ; often <50 except in
persons with genetic predispositions (native
americans)
 May be initial manifestation of disease
 May be assoc upon ingestions of
photosensitizing meds: NSAIDs, ARV – Efavirenz
or TMP-SMX
 Lesions histologically may show subacute or
chronic dermatitis , dermal infiltrates w. many eos
 In blacks, <50 CD4 counts seen w/ features of
actinic prurigo
 Tx: Thalidomide may be beneficial
5.
RADIODERMATITIS
 Major target within the cell by w/c radiation
damage occurs is the DNA
 Effects depend on the amount of radiation
and intensity , characteristic of individual
cell
Rapidly dividing and anaplastic cells have
increased radiosensitivity
 Large dose  cell death results
 Mitosis arrested temporarily
 Chromosome breaks- high in more rapid
delivery of certain amount of radiation
ACUTE RADIODERMATITIS
Latent period of up to 24h after given erythema dose
of ionizing radiation before visible erythema
Initial erythema- last 2-3 days
May be ff w/ 2nd phase up to 1 week after exposure
and lasting up to 1 month
Radiation rxn seen in accidental overexposure in the
tx of malignancy
Initial erythema  2nd phase erythema 3-6 days 
vesiculation, edema, erosion and ulceration with
pain may occur  skin w/ dark color 
desquamates
May subside in several weeks to several months
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EOSINOPHILIC, POLYMORPHIC, AND PRURITIC
ERUPTION ASSOC WITH RADIOTHERAPY
Polymorophic, pruritic eruption arising several to
several months after RT for cancer
Acral excoriations, erythematous papules, vesicles
and bullae
Superficial and deep perivascular lymphohistiocytic
infiltrate w/ eosinophils
TX: Topical steroids, antihistamines and UVB
W/ spontaneous resolutions
CHRONIC RADIODERMATITIS
Chronic exposure to suberythema doses of ionizing
radiation
May also occur on back and flank after fluoroscopy
and roengenography
Telangiectasia, atrophy and hypopigmentation w/
residual focal increased pigment (freckling) may
appear
Nails- striated, brittle and fragmented
Hair- brittle and sparse
In most severe cases, chronic changes may be
followed by radiation keratoses and carcinoma
May resemble erysipelas or inflammatory
metastases
May 6-12 months after radiation therapy
RADIATION CANCER
After latent period ave 20-40 yrs
BCC > SCC
Sun damage – may be additive
SCC from RT metastasize more frequently
SCCs are more common on arms and hands
BCCs seen on the head and neck and lumbosacral
area
Other RT induced ca : Angiosarcoma, Kaposi
sarcoma, malignant fibrous histiocytoma, sarcomas
and thyroid ca
TX: Acute – topical corticosteroid w/ emollient cream
BID ; Chronic radiodermatitis w/o ca – protection
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from sunlight, extreme cold and heat , occ
hydrocortisone ointment
Early removal of precancerous keratoses and
ulcerations – helpful in prevention ca
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MECHANICAL INJURIES
Factors: pressure, friction and introduction of foreign
substances
CALLUS
–
nonpenetrating,
circumscribed
hyperkeratosis produced pressure
On parts of the body to subject to intermittent
pressure , particularly to the palms and soles, esp
bony prominence of the joints
E.g. surfer’s nodules, boxer’s knuckle pads, jogger’s
toe, rower’s rump, Playstation thumb, milker’s callus,
tennis toe, jogger’s nipple, prayer callus, yoga sign,
neck callosities of violinists , pillar knocker’s
knuckles, bowler’s hand and Russell sign
Differ from clavus as it has no penetrating central
core and more diffuse thickening
Tx: padding to relieve pressure, paring of thickened
callus, use of keratolytics such as 40% salicylic acid
plasters are effective means relieving painful
callosities ; use of 12% ammonium lactate lotion or
urea-containing cream
CLAVUS (CORNS)
Circumscribed, horny, conical thickenings w/ the
base on the surface and the apex pointing inward
and pressing on subjacent structures
Two varieties: soft and hard
Hard corns: on dorsa of toes, or subungually on the
soles; surface shiny and polished; core noted on
densest part  causes dull/boring or
sharp/lancinating pain by pressing underlying
sensory nerves
Soft corns: between the toes and softened by the
macerating action of sweat
Arise at sites of friction or pressure
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PSEUDOVERRUCOUS PAPULES AND NODULES
2-8 MM shiny, smooth, red, moist, flat-topped round
lesions in the perianal area of children, result of
encoperesis or urinary continence
Similar lesions have been described in women who
repeatedly apply an antifungal (Vagisil) in the groin
area
FRICTION BLISTERS
-Formation of vesicles or bullae at sites of combined
pressure and friction ; and may be enhanced by heat
and moisture
- feet of military recruits, palms of oarsmen, fingers of
drummers
Prevention:acrylic fiber socks; pretreatment w/ 20%
solution of Aluminum Cl hexahydrate for at least 3 days
; emollients
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muscles as a result of sustained and constant
pressure
Occurs chronically in debilitated persons
90% on lower body, 65% pelvic area and 30% on the
legs
Erythema at pressure point  “punched-out” ulcer
develops -> necrosis w/ grayish pseudomembrane
Potential complications: sepsis, local infections,
osteomyelitis, fistula and SCC
>100 risk factors: DM, PVD . CVD, sepsis and
hypotension being prominent
4 stages:
1. Stage I- changes in skin temp, tissue
consistency and sensation  persistent
redness
2. Stage II- superficial ulcer; epidermis and/or
dermis
3. Stage III- + subcutaneous fat
4. Stage IV – + muscle, bone, tendon and joint
capsules
Prevention- q2h turning
Tx: relief of pressure, frequent change of position,
use of air-filled products
Debridement
Occlusive dressings
transparent films (for stage II ulcers)
Hydrofibers – for full thickness stage III and IV
Anaerobic infections- metronidazole
FRACTURE BLISTERS
Sites of closed fractures esp in ankle and lower leg
Blisters appear few days to 3 weeks after injury
May create complications  infections and scarring
esp if blood filled or in DM patients
Generally heal spontaneously in 5-14 days
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SCLEROSING LYMPHANGITIS
Cordlike structure encircling the coronal sulcus of
the penis or running the length of the shaft and has
been attributed to trauma during vigorous sexual
play
Most cases result from a superficial thrombophlebitis
renamed to MONDOR DISEASE OF PENIS
Some early reports favor lymphatic origin; CD 31
and D240 stains will allow differentiation
Self-limiting
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CORAL CUTS
Severe type of skin injury, may occur from the cuts
of coral skeletons
Abrasions and cuts are painful, and local therapy
may provide little or no relief
If persistent, possibility of Mycobacterium marinum
infection
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PRESSURE ULCERS ( DECUBITUS)
Bedsore
Produced by prolonged pressure caused by
ischemia of underlying structures of skin, fat and
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BLACK HEEL
Include talon noir and calcaneal petechiae
Minute, black, punctate macules occurs most often
on the posterior edge of the plantar surface of one or
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both heels but sometimes distally of one or more
toes
In basketball, volleyball, tennis or lacrosse players
May lead mimicry of melanoma
Bleeding caused by shearing stress of sports
activities
SUBCUTANEOUS EMPHYSEMA
Free air occurring in the SC tissues, detected by
presence of cutaneous crepitations
Clostridia – gas producing organisms and leakage of
free air from the lungs or GI tract are most common
causes
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9. GRANULOMAS
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TRAUMATIC ASPHYXIA
Cervicofacial cyanosis and edema
Multiple petechiae of the face, neck and upper chest
and bilateral subconjunctival hemorrhage
Trauma reverses blood flow to SVC
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- paraffin, camphorated oils, beeswax, cottonseed or
sesame oil and mineral oil may produce plaque like
indurations w/ ulcerations within months and up to 40
yrs
- penile paraffinoma- caused by self-injections
- radiofrequency device: succesfull tx
- Surgical removal- must be wide and complete
PAINFUL FAT HERNIATION
Also called painful piezogenic pedal papules
Rare cause of painful feet represent fat herniations
thru thin fascial layers of weight bearing parts of the
heel
Majority experience no symptoms
Extrusion of fat tissue togethers w/ its BV and
nerves initiate pain on prolonged standing
NARCOTIC DERMOPATHY
HEROIN (DIACETYLMORPHINE) – Used IV
Results in thrombosed, cordlike, thickened at the
sites of injections
Subcutaneous injection- “SKIN POPPING” may
result in multiple, scattered ulcerations, w/ discrete
atrophic scars
May lead to infections, complications of bacterial
abscess and cellulitis or sterile nodules
Cocaine- may cause ulcers bec of its direct
vasospastic effect ; cocaine – associated vasculitis
caused by levamisole
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7. FOREIGN BODY REACTIONS
 TATTOO
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Tattoo – associated dermopathies : may be reactive
or infective or may induce a Koebner response in px
with lichen planus or psoriasis
Discoid LE reported to occur in red-pigmented
portion of tattoos
May become keloidal
Severe allergic rxns- when allergen pphenylenediamine added to make color more
dramatic
Red tattoos – most common cause of delayed rxns ;
occasionally pseudolymphomatous rxn may occur
Tx: topical or intralesional steroids
8. Paraffinoma
-injections of oils
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SILICONE GRANULOMA
Liquid silicones : Composed of long chains of
dimethyl siloxy groups
Granulomatous reactions to silicone
Some w/ migration and reactive nodules at points
distant from the injection
Acupuncture needles- coated w/ silicone ;
granulomas may occur at entry points
w/ incidence of nodular swellings
MERCURY GRANULOMA
MERCURY mau cause a foreign body giant cell or
sarcoidal – type granulomas. Pseudolymphoma, or
membranous fat necrosis
Egg-shaped , extracellular , dark gray to black ,
irregular globules
Gold lysis test – positive
Energy dispersive radiographic spectroscopy may
be done if substance suspected to have been
implanted on px
Systemic toxicity or embolus may develop  death
Excision necessary under x-ray guidance
BERYLLIUM GRANULOMA
In chronic, persistent granulomatous inflammation of
the skin w/ ulceration that may follow accidental
laceration
ZIRCONIUM GRANULOMA
Papular eruption involving the axillae is sometimes
seen as an allergic reaction in those shaving their
armpits and using deodorant containing zirconium
In poison ivy lotions
Lesions are brownish red, dome shaped, shiny
papules
Acquired, delayed -type allergic reaction 
granuloma and sarcoidal type
After many months, involute spontaneously
SILICA GRANULOMA
Automobile crashes and other types of trauma may
produce tattooing of dirt (silicon dioxide) into the
skin, w/c includes silica granulomas
Present as black or blue papules or macules
arranged in a linear fashion
Granulomas may be caused by amorphous or
crystalline silicon , Mg silicate, or complex
polysilicates (asbestos)
Talc granulomas- skin and peritoneum may develop
after surgery if talcum powder used in surgical
gloves
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Silica may act as stimulus for granuloma formation
in px w/ latent sarcoidosis
Tx: immediate and complete removal ; dermabrasion
or simple abrasion
10. CARBON STAIN
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Discoloration of skin from embedded carbon usually
occurs in children from improper use of firearms or
fireworks or from a puncture wound by a pencil
May be mistaken as metastatic melanoma
Carbon particles may be removed immediately
11. INJECTED
SUBSTANCES
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FILLER
May produce FB or sarcoidal granulomas
Palpable thickening and nodules occasionally painful
Reaction may be delivered for years
Tx: topical, intralesional or systemic steroids,
sometimes augmented by tacrolimus and
minocycline or doxycycline