Dermatoses Resulting from

Physical Factors
Chapter 3
Andrews’ Diseases of the Skin 12th Ed
Heat Injuries: Thermal burns
• Extreme heat destroys skin and underlying tissue
• Four degrees
• First degree burn
• Active congestion of superficial blood vessels
• Erythema, epidermal desquamation (peeling)
• Pain, increased surface heat
• Ex. Sunburn
• Mgt: prompt cold application (ice water, cold tap water) – until pain resolves
• Dressing: greasy gauze
Heat Injuries: Thermal burns
• Second degree burns
• Superficial – transudation of serum from capillaries = edema of superficial tissues
• Vesicles and blebs are formed by serum accumulation beneath epidermis
• Complete recovery without scarring
• Mgt: vesicles or blebs should not be opened , should be protected from injury (form natural
barrier agains contamination)
• Fluid may be evacuated (aseptic conditions via sterile needle puncture) once
vesicles/blebs become tense and painful
• Dressing: silver-containing dressing (antibiotic properties)
• Deep – injury to reticular dermis compromises blood flow and destroys appendages
• Pale, anesthetic
• Healing takes >1month, results in scarring
Heat Injuries: Thermal burns
• Third-degree burn – loss of full thickness of dermis and some of
subcutaneous tissues
• No epithelium available for regeneration =Produces ulcerating wound
• Healing leaves scar
• Manifests constitutional symptoms
• Mgt: Excision (reduces wound infections, shortens hospital stay, improves survival)
• Require grafting for closure
• Fourth degree burn - destruction of entire skin including panniculus and
underlying tendons
• Require grafting for closure
• Manifests constitutional symptoms
• Mgt: Same with 3rd deg burn
Heat Injuries: Thermal burns
• Poor prognosis if large area of skin is involved (>2/3 body surface area)
• Greatest risk: women, infants, toddlers
• Excessive scarring (contractures, keloids) may produce deformities and
dysfunction of joints
• Most common: lower extremities
• SCC: possible to arise in burn scars
Heat Injuries: Electrical burns
• From contact or flash exposure
• Contact: small but deep – causing necrosis of underlying tissues
• Low-voltage injuries – usually occur at home
• Treated conservatively
• Heal well
• Oral commussure burns –equire reconstrictive procedures
• High-voltage burns – often occupatonal
• Internal damage may be masked my minimal surface skin change and may be complicated by subtle and slowly developing
sequelae
• Mgt: early surgical intervention (improve circulation and repair vital tissues)
• Flash burns – cover large area
• Similar in tx with any surface burn
• Lightning – direct strike = entrance and exit wound (most lethal)
• May result to cardiac arrest or other internal injuries
• Lightning. - Indirect strike - result to the ff:
• Linear burns where sweat was present
• Burns in feathery or arborescent pattern (pathognomonic)
• Punctate burns with multiple, deep, circular lesions
• Thermal burns from ignited clothing or heated metal (gadgets)
Heat Injuries: Hot tar burns
• Polyoxyethylene sorbitan in bacitracin zinc-neomycin-polymixin B
ointment, vit
Heat Injuries: Treatment
• Fluid resuscitation
• Treatment of inhalation injury and hypercatabolism
• Early intervention of sepsis
• Pain control
• Environmental control
• Nutritional support
• Admission to a burn center or intensive care mgt
• Partial thickness wounds >10% BSA
• involvement of face, hands, feet, genitalia, perineum, joints
• if secondary to electrical, chemical, inhalation
• px with special needs
• Full thickness burns
• Hot tar burns – excellent dispersing agents that facilitate removal of hot tar burns:
• Polyoxythylene sorbitan in bacitracin zinc-neomycin-polymyxin B (Neosporin) ointment
• Vitamin E ointment
• Sunflower oil
Heat Injuries: Miliaria
• Retention of sweat due to occlusion of eccrine sweat ducts
• Common in hot, humid climates
• Staph. Epidermidis – induces miliaria
• Produces extracellular polysaccharide that obstruct delivery of sweat to skin
surface
• Occlusion prevents normal secretion of sweat glands = eventual pressure
causes rupture of sweat gland or duct = escape into adjacent tissue =
MILIARIA
Heat Injuries: Miliaria
• Miliaria crystallina (sudamina)
• Small, clear, superficial vesicles with no inflammatory reaction
• Appears on bedridden patients whose fever produces increased sweating or when
clothes prevent dissipation of heat and moisture (bundled children)
• Asymptomatic, short-lived (tend to rupture at slightest trauma)
• Induced by: isotretinoin, bethanechol, doxorubicin)
• No tx required
• Milaria rubra (prickly heat)
• Discrete, extremely pruritic, erythematous papulovesicles
• Sensation of prickling, burning, or tingling
• May become confluent on a bed of erythema
• Most frequent sites: antecubital & popliteal fossa, trunk, inframmamary areas,
abdomen, inguinal area (impeded evaporation of moisture)
• Site of injury: prickle cell layer – produces spongiosis
Heat Injuries: Miliaria
• Miliaria pustulosa
• Preceded by another dermatitis that produced injury, destruction, or blocking
of sweat duct (contact dermatitis, lichen simplex chronicus, intertrigo)
• Distinct, superficial, independent of hair follicle
• Most frequently: intertriginous areas, flexure surfaces of extremities,
scrotum, back of bedridden px
• Miliaria profunda
• Nonpruritic, flesh-colored, deep-seated, whitish papules
• Asymptomatic, lasts only for 1h after overheating has ended
• Concentrated on trunk and extremities
• Only in tropics
Heat Injuries: Miliaria
• Postmiliarial hypohidrosis
• Occlusion of sweat ducts and pores
• Affected patients: decreasing efficiency, irritability, anorexia, drowsiness,
vertigo, headache
• Sweating may be depressed to half the normal amount for as long as 3 weeks
• Duration and severity related to severity of mliaria preceding it
• Tropical anhidrotic asthenia
• Rare
• Long-lasting poral occlusion
• Anhidrosis
• Heat retention
Heat Injuries: Miliaria
• Treatment
• Place patient in cool environment
• Airconditioned room
• Circulating air fans
• Anhydrous lanolin: resolves occlusion
• Hydrophilic ointment: dissolve keratinous plugs
• Cooling baths with colloidal oatmeal or cornstarch
• Dusting powders (cornstarch, baby talcum powder)
Heat Injuries: Erythema ab igne
• Persistent erythema produced by long exposure to excessive heat, without
production of burn
• Begins as mottling caused by local hemosasis -> reticulated erythema
(leaves pigmentation)
• When cause is removed, it disappears gradually. Some become permanent
• Increased amount of elastic tissue
• May lead to: Bowen’s disease, SCC
• Tx: 5-FU, imiquimod, photodynamic therapy
• AHA, fluocinolone acetonide 0.01% hydroquinone 4%, tretinoin 0.05% (reduce
unsightly pigmentation)
• Q-switched neodymiumdioed yttrium-alimunum garnet (Nd: YAG) laser
Cold Injuries
• 3 mechanism of damage:
• Direct damage to tissue (frostbite, cold immersion foot)
• Vasospasm of vessels -> decreased perfusion + vascular injury -> tissue injury
• Adipose tissue predisposed to damage
• Tx:
• Protection against further exposure to cold or dampness
• Feet: woolen socks during cold months
• Appropriate dress / attire
• Keep whole body warm
• Heating pad
• No smoking
• Nifedipine 20mg TID
• Vasodilators – nicotinamide 500mg TID, dipyridamole 25mg TID, PDE sildenafil 50mg BID (improve circulation)
• Pentoxyfylline, hydroxychloroqine – may be effective
• Systemic corticosteroids – for chilblain lupus
• Spontaneous resolution occurs without treatment in 1-3 weeks
Cold injury: Acrocyanosis
• Persistent blue discoloration of entire hand or foot, worsened by cold exposure
• Cyanosis increases as temperature decreases
• Cause: unknown
• Smoking should be avoided
• Persistent nature and lack tissue damage (vs Reynaud syndrome – episodic)
• Seen in:
• Butyl nitriate inhalation may cause acrocyanosis (+ swelling og nose, ears, dorsal hands)
• Tx: alpha-2a
• Puffy hand syndrome: lymphedema due to frequent injection of dorsal hand with narcotic drugs
• Anorexia nervosa – acrocyanosis _ perniosis, livedo reticularis, acral coldness
• Tx: weight gain
• POEMS (polyneuropathy, organomegaly, endocrinopathy. M component, skin changes)
• Homozygous mutation in SAMDH1
• Cerebrovascular occlusive disease
• Acral vascular syndromes (gangrene, Reynaud phenomenon, acrocyanosis) – may be a sign of malignancy
Cold injury: Chilblains (pernio, perniosis)
• Localized erythema and swelling caused by exposure to cold
• Blistering, ulceration
• Cryoglobulins, cryofibrinogens, antiphospholipid antibodies, cold agglutinins
• Present in:
• Discoid and systemic lupus erythematosis (chilblain lupus)
• Leukemia cutis (presenting sign)
• Nakajo Nishimura syndrome (if presenting in infancy)
• Aicardi-Goutieres syndrome (diagnostic sign)
• Chronic use of crack cocaine
• Occur chiefly on hands, feet, ears, and face
• Enhanced by dampness
• Patients are usually unaware that it is occurring -> then later manifests with burning, itching, redness
• Manifestation: bluish red, blanching on pressure, cool to touch
• New lesions will continue to appear as long as there is exposure to cold or dampness
• Histology shows:
• lymphocytic vasculitis
• dermal edema,
• superficial and deep perivascular, tightly cuffed, lymphocytic infiltrate
Cold injury: Frostbite
• When soft tissue is frozen and locally deprived of blood supply
• Often seen in: ears, nose, cheeks, fingers, toes
• Frozen part painlessly becomes pale and waxy
• Degree of injury directly related to temperature and duration of freezing
• Erythema, edema
• Vesicles and bullae
• Superficial gangrene
• Deep gangrene
• Injury to muscles, tendons, periosteum, nerves
• Tx
• Cover part with clothing or warm hand
• Rapid rewarming in water bath between 37 and 43 degC
• Should be delayed until px has been moved to an area with no risk of refreezing
• Slow thawing = more extensive tissue damage
• Analgesics (for pain due to rapid thawing)
• Tissue plasminogen activator – lyse thrombi (decrease need for amputation if given within 24h)
• Bed rest, high-protein/high-calorie diet, wound care, avoidance of trauma
• Avoid rubbing affected area (only gentle massage of proximal portions that are not numb)
• Anticoagulants = pentoxyfilline, ibuprofen, aspirin
• Antibiotics – prophylaxis
• Tetanus immunization
• Recovery may take months
• Major RF for recurrence: prior cold injury
• Late common complication: arthritis
Cold injury: Immersion foot syndromes
• Trench foot
• Results from prolonged exposure to cold, wet conditions, without immersion or
actual freezing
• Common in fishermen, sailors, shipwreck survivors
• Seen in overuse of ice, cold water and fans
• Gangrene may occur in severe cases
• Lack of circulation
• Edema, paresthesia, blood vessel damage
• Tx:
• Removal from causal environment
• Bed rest
• Restoration of circulation
• Same as frostbite
Cold injury: Immersion foot syndromes
• Warm water immersion foot
• Exposure of feet to warm, wet conditions for 48h or more
• Maceration, blanching, wrinkling of soles and sides of feet
• Itching, burning with swelling – persists for a few days after removal of cause
• Seen in military service, in persons wearing insulated boots
• Prevention:
• allow feet to dry for a few hours in every 24
• Greasing soles with silicone grease once a day
• Recovery is rapid if feet are thoroughly dry for a few hours
• Tropical immersion foot
• Seen after continuous immersion of feet in water or mud at T>22degC for 2-10 days
• Erythema, edema, pain, pain in dorsal feet, fever, adenopathy
• Resolution: 3-7 day after the feet have been dried
Actinic Injury: Sunburn, solar erythema
• Solar spectrum in photomedicine
• UV (<400nm)
• UVA (320-400 nm)
• UVA I (340-400 nm)
• UVA II (320-340 nm)
• UVB (280-320 nm)
• UVC (200-280 nm)
• None reaches the Earth’s surface (absorbed by ozone layer)
• Visible light (400-760nm)
• Limited biologic activity, except for stimulating retina
• Infrared radiation (>760nm)
• Radiant heat
Actinic Injury: Sunburn, solar erythema
• Skin type
• Individual’s inherent baseline
pigmentation, ability to tan,
susceptibility to burns
• Used to determine starting doses of
phototherapy and sunscreen
recommendations
• Reflects the risk of development of
skin cancer and photoaging
Actinic Injury: Sunburn, solar erythema
• Minimal erythema dose (MED)
• Minimal amount of particular wavelength of light capable of inducing erythema on skin
• Amount of UVA is greater than UVB
• UVA –patients with drug-induced photosensitivity
• UVB is more erythemogenic than UVA
• All solar erythema is caused by UVB
• Most biologically effective wavelength of radiation from sun for sunburn is 308nm (UVB)

• Higher amount of UV exposure

• Higher altitudes
• Temperate climates and summer
• Tropical regions
• UVA reflected more than UVB in sand, snow, ice (reflects 85% of UVB)
• Water allows 80& of UV to penetrate up to 3 feet
• Cloud cover is a poor UV absorber
• Midday = intensity of UVB is 2-4x greater than in early morning and late afternoon
• UV exposure – increases thickness of epidermis (Esp s. corneum)
• Increased tolerance to further solar radiation
Actinic Injury: Sunburn, solar erythema
• Clinical signs and symptoms: Sunburn
• UVB erythema– normal reaction to sunlight in excess of erythema dose
• Evident 6h after exposure, peaks 12-24h
• Increased exposure = sooner onset, greater severity
• Tenderness
• Blistering
• Edema – face, extremities
• Chills, fever, nausea, tachycardia, hypotension – severe cases
• Desquamation – 1 week after sunburn
• After UV exposure: 2 changes:
• Immediate pigment darkening (Meirowsky phenomenon)
• Redistribution of melanin already in skin
• Hours after exposure
• Delayed melanogenesis
• UVB tanning: 2-3 days after exposure, lasts 10-14 days
• DNA damage, formation of cyclobutane pyrimidine dimers – may damage epidermis and dermis
• Commerical tanning is not protective (does not increase UVB MED) – only increases skin pigment
• Causes melanoma
Actinic Injury: Sunburn, solar erythema
• Tx
• Once redness and other symptoms are present, treatment of sunburn has
limited efficacy (damage is done, inflammatory cascades are triggered)
• Prostaglandins (esp E series) - mediators
• Aspirin – small reduction in SSx
• NSAIDs – insufficient evidence
• Topical and systemic steroids – insufficient evidence
• Supportive
• pain management
• Soothing topical emolients
• Corticosteroid lotions
• Recovery
• Relief of pain and discomfort after 1 or 2 days
Actinic Injury: Sunburn, solar erythema
• Prophylaxis
• Avoid midday sun
• Seek shade
• trees (SPF 4-50), artificial shade (provide substantial protection again
• Wear sun-protective clothing
• denser weaves, washed older clothing, loose-fitting clothes screen UVB more effectively
• Wetting fabric reduces UPF (UV protection factor)
• Hats with at least 4-inch brim all around
• Apply sunscreen
• Highest UVB intensity: 9am, 3-4pm
• Angle of sun is less than 45deg (shadow shorter than height)
Actinic Injury: Sunburn, solar erythema
• SPF
• Sunscreen’s. efficacy in blocking UVB
• Ratio of the number of MEDs of radiation required to induce erythema
through a film of sunscreen compared with unprotected skin
• If applied thinly, applied SPF is about half that on the label
• Sunscreen agents
• UV-absorbing chemicals (chemical sunscreens)
• P-aminobenzoic acid [PABA], PABA esters, cinnamates, salicylates, anthranilates,
benzophenones, benzylidene camphors (ecamsule), dibenzoylmethanes, and Tinosorb
• UV-scattering or blocking agents (physical sunscreens)
• Zinc oxide, titanium dioxide
Actinic Injury: Sunburn, solar erythema
• Skin Types I-III
• Daily application of a broad-spectrum sunscreen with SPF 30
in facial moisturizer, foundation, or aftershave
• Outdoor exposure
• SPF 30 or higher – regular use
• Severe photosensitivity or high sun exposure
• High-intensity sunscreens of SPF 30+ with inorganic blocking
agents
• Apply sunscreen at least 20 mins before and 30mins after
sun exposure
• Reduce the amount of skin exposure by 2-fold to 3-fold over a
single application
• Should be reapplied after swimming or vigorous activing or
toweling
• May be applied to babies on limited areas
• Vit D supplementation is recommended
• 600 IU daily (70 or younger)
• 800 IU (older)
• Photoaging and cutaneous immunosuppresion – UVA and
UVB
• Need broad-spectrum sunscreens (contains both UVA and UVB
protecting agents)
Ephelis (freckle) and lentigo
• Freckles
• Small (<0.5cm) brown macules that occur in profusion on sun-exposed skin (Face, neck, shoulders, back of hands)
• Prominent in summer when exposed to sunlight, and subside during winter
• May be genetically determined
• Appear at around 5 years old
• Histo: increased production of melanin by normal number of melanocytes
• Lentigo
• Benign, discrete, hyperpigmented macule appearing at any age and on any part of the body, including mucosa
• Intensity of color is not dependent on sun exposure
• Solar lentigo – later age (due to long-term sun exposure)
• Favored sites: back of hands, face
• Histo: elongated rete ridges that appear to be club-shaped
• Prevention
• Adequate sun protection
• Tx
• Cryotherapy
• Topical retinoids
• Hydroquinone
• Intense pulse light
• Undecylenoyl phenylalanine
• lasers
Photoaging (Dermatoheliosis)
• Characteristic changes induced by chronic sun exposure
• Risk depends on skin type
• Most susceptible: Skin type I - blue-eyed, fair-complexioned
• Chronic sun exposure and chronologic aging are additive
• Smoking induces wrinkles, making it difficult to determine whether skin aging is solar-induced or smoking-induced
• Areas primarily affected are the ones frequently exposed to the sun
• V area of neck and chest, back, sides of neck, face, back of hands, extensor arms, skin between knees and ankles
• Characteristics:
• Skin atrophies, scales, wrinkles, lose elasticity, become leathery with a yellow hue (milian citrine skin)
• Uneven pigmentation
• Solar (actinic) elastosis - Sun damaged skin: alternation in upper dermal elastic tissue and collagen
• Sebcaeous hyperplasia (small yellowish papules along sides of neck, ear helix/antihelox)
• Poikiloderma of Civatte (reticulate hyperpigmentation with telangiectasia)
• Cutis rhomboidalis nuchae – nape skin becomes leathery, thick, tough, long term sun exposure
• Favre Racouchot syndrome – nodular elastoidosis with cysts and comedones on inferior periorbital and malar skin on forearms or ear helix
• Telangiectasias – cheeks, ears, neck sides
• Dermatoporosis – prominent skin fragility, skin tearing from trivial injuries
Photoaging: Pathogenesis
• UVA and UVB induce reactive oxygen species and hydrogen peroxide
• Through activator protein 1 (AP-1)
• Transcription of matrix-degrading enzymes is upregulated
• Matrix metalloproteinases
• MMP-1; collagenase
• MMP-3 (stromelysin 1)
• MMP-9 (gelatinase)
• Solar elastosis
• Seen in chronically sun-exposed skin
• Faint blue color of connective tissue of the upper reticular dermis
• From elastic fibers
• Increased deposition of fibulin 2 and its breakdown products
• Decreased collagen types I and III
Colloid millium
• 2 forms: adult, juvenile
• Primary skin lesion: translucent, flesh-colored or slightly yellow, 1-5mm papule
• Histo: intradermal, amorphous fissured eosinophilic material
• Adult: appear on sun-exposed areas of hands, face, neck, forearms, ears (middle-age
and older adults, usually men)
• Lesions often coalesce into plaques, rarely verrucous
• Associated with petrochemical exposures, hydroquinone (pigmented forms of colloid milium)
• Induced by tanning bed exposure
• May be unilateral (commercial drivers)
• Juvenile: rarer, develops before puberty, usually with family history
• Lesions similar to adult, appear initially on face then extending to neck and hands
• Sun exposure is a factor
• Keratinocyte apoptosis in overlying epidermis
Colloid millium: Prevention, Tx
• Prevention
• Sun protection – broad spectrum sunscreen (reduction of UV exposure)
• Emolients – reduce scaling, improve fragility of skin
• Moisturizing cream – reduce scaling, improve fragility of skin
• AHA – may improve skin texture
• Tx for photoaging
• Topical tretinoin, adapalene, tazarotene
• Chemical peels
• Resurfacing techniques
• Laser
• Botulinum toxins
• Soft tissue augmentation
Photosensitivity: Chemically-induced
• Photosensitizers – induces abnormal reaction in skin exposed to sunlight
• Externally applied/contact
• Internally administered
• Phototoxicity
• occurs on initial exposure
• onset less than 48h
• Exposure to phototoxic substance and sunlight
• Histo pattern similar to sunburn
• Non-immunologic
• Sunburn type – erythema (within 2-6hrs, worsens 48-96 hrs), tenderness, blistering
• Required greater amt of photosensitizing substance to elicit sensitivity reaction than in photoallergy
• Photoallergy
• Occurs in sensitized persons
• May have delayed onset (up to 14 days)
• Histo features similar to allergic contact dermatitis
Photosensitivity: Action spectrum
• Photosensitizers: resonating compounds with molecular wt of <500daltons
• Absorption of radiant energy (sunlight) produces an excited state
• Returning to lower-energy state gives off energy through fluorescence,
phosphorescence, charge transfer, hear, or formation of free radicals
• Photosensitizers absorbs only specific wavelengths of light (absorption spectrum)
• Action spectrum – one that produces phototoxicity
• included in absorption spectrum
• Mostly in UVA region, may extend to visible light region
• Only occur when:
• there is sufficient concentration of photosensitizer in skin
• Skin is exposed to a sufficient intensity and duration
• Intensity of photosensitivity reaction is dose-dependent
Phototoxic tar dermatitis
• Photosensitizer: volatile hydrocarbons (+ sunlight exposure)
• coal tar, creosote, crude tar, pitch
• May be airborne
• Found in cosmetics, drugs, dyes, insecticides, disinfectants
• SSx
• Severe burning sensation
• Erythema
• Hyperpigmentation after the acute reaction
Phytophotodermatitis
• Photosensitizer: furocoumarins in plants (+UVA)
• Oil of bergamot (bergapten), St. John’s wort, mustard, parsley, lime, fig, rot fungus, wild rose
• 5-mothexypsoralen
• SSx
• Severe burning erythema several hours after exposure
• Followed by edema
• Vesicles, bullae Dermatitis bullosa striata pratensis (rose)
• Intense rediual hyperpigmentation that may persist for weeks or months
• Tx
• Topical steroids
• Strict sun avoidance
• Cool compress
• Mild analgeics
• Topical emollients
Idiopathic photosensitivity disorders:
Polymorphous light eruption (PLE)
• No known cause

• Most common form

• Onset: 1st 4 decades of life, F>/m (2:1 or 3:1)

• Pathogenesis: unknown

• Family history elicited in 10-50% of px

• May have +ANAs
• FH of lupus erythematosus

• Associated with SLE

• Ssx:
• Morphology: Papular / erythematopapular – most common
• Others: papulovesicular, eczematous, erythematous, plaquelike (elderly)
• Hyperpigmentation (PIH: postinflamm hyper-/hypopigmentation) in dark races
• Pruritus
• Juvenile spring eruption of ears: grouped small papules or papulovesicles on helices (with vesicles, crusting)

• Histo
• Perivascular, predominantly Tcell infiltrate in upper and middle dermis
• Edema, endothelial swelling, with occasional neutrophils
• Epidermal spongiosis and exocytosis
• Some: absence of findings (pauci0inflammatory photodermatitis)

• Pathogenesis
• UVA mostly responsible, UVB
• Women are more sensitive than men to UVA, men more sensitive to visible light

• Tx:
• Avoid sun
• Use barrier protection, high SPF, broad-spectrum sunscreens (woith absorbers or blockers)
• Tint films on windows
• Topical tacrolimus
• Antihistamines (hydroxyzine, diphen, dozepin) for pruritus
• Systemic corticosteroids – short course
• Systemic hydrochloroquine sulfate )200-400mg/day) / chloroquine, quinacrine (inferior to phototherapy)
• Severe: azathioprine, cyclosporine, thalidomide, mycophenolate mofetil
Actinic prurigo
• Variant of PLE
• Native americans
• 75% of patients have positive family history (hereditary PLE of Native Americans)
• Childhood: small papules or papulovesicles that crust and become impetiginized
• Intensely pruritic, excoriated
• Cheeks, distal nose, ears, lower ip
• Cheilitis
• Prurigo nodule-like configuration
• Adults: chronic, dry papules and plaques with cheilitis and cristing
• Lesions persist throughout the year
• Worse with sun exposure
• Hardening does not occur
• Tx identical to that for PLE
• Thalidomide
• Refractory: cyclospon A 2%
Brachioradial pruritus
• PLE on brachioradial area
• Severe, refractory, intractable pruritus
• Secondary severe lichenification
• Represent a form of neuropathic pruritus sometimes related to cervical
spin disease
• Sunlight – eliciting factor
• Cervical spin disease – predisposing factor
• To differentiate: high-SPF sunscreen applied to one arm for several weeks
• Improvement in patients with PLE
• Minimal improvement in patients with primarily neuropathic disease
Solar urticaria
• Most common in women age 20-40
• Urticarial lesions appear within seconds to minutes after light exposure
• Resolve in 1-2h, rarely last more than 24h
• Rare delayed rxns
• Reduced sensitivity in chronically exposed areas
• Severe attacks: syncope, bronchospasm, anaphylaxis
• Sensitivity to wavelengths over a broad spectrum
• UVA sensitivity : most common
• Virtually always idiopathic
• Prevention / tx
• Broad-spectrum sunscreen
• Antihistamines (increase MUD – minimal urticarial dose)
• Sun avoidance
• Cyclosporin A, IVIg
• Plasmapheresis (difficult cases) to remove circulating photoallergen
Hydroa vacciniforme
• Rare, chronic photodermatosis with onset in childhood
• Bimodal onset (age 1-7, 12-16)
• Spontaneous remission before age 20
• Ssx
• Within 6h exposure: stinging sensation
• Within 24h: erythema, edema, 2-4mm vesicles
• Within few days: rupture of vesicles, central necrosis, heal with smallpox-like scar
• Lesions appear in crops with disease-free intervals
• Affected: ears, nose, cheeks, extensor arms and hands
• May also occur: subungual hemorrhage, ocular involvement, oral ulcerations
• Histo: intraepidermal vesiculation, dermal edema, evolve into a subepidermal bloster
• Nectrotic lesions: reticular degeneration of keratinocytes, epidermal necrosis flanked by spongiosis with dense perivascular infiltrate of
neutrophils and lymphocytes
• Thrombosed dermal vessels
• Tx:
• Avoid sunlight exposure
• Broad-spectrum sunscreens
• Prophylactic NB UVB phototherapy
Chronic actinic dermatitis
• Represents the end stage of progressive photosensitivity
• Basic components
• Persistent, chronic, eczematous eruption in the absence of exposure to known photosensitizers
• Usually, broad-spectrum photosensitivity with decreased MED to UVA and/or UVB and at times visible light
• Histology consistent with a chronic dermatitis, with or without features of lymphoma

• Middle age or elderly men

• Skin lesions: edematous, scaling , thickened patches and plaques that tend to be confluent
• With marked depigmentation resembling vitiligo

• Occur most severely on exposed skin, spare upper eyelids, behind the ears, bottom of wrinkles
• Diagnosis: histologic evaluation and phototesting
• Phototesting reproduces lesions (sensitivity to UVA, UVB, visible light)

• Tx
• Identifying possible topical photosensitizers by photopatch testing and avoiding them
• Maximum sun avoidance
• Broad spectrum sunscreens
• Topical tacrolimus
• Topical and systemic steroids
• Azathioprine – most reproduciblt effective tx
• Low dose PUVA or NB UVB – adjunct to steroids
• Hydroxyurea 500mg BID, cyclosporin A, thalidomide, mycophenolate mofetil
• Immunosuppresive agents – allow px to tolerate PUVA
HIV photosensitivity
• Seen in about 5% of px with HIV
• Seem when CD3 count is <200 (AIDS), often <50
• May be initial manifestation of HIV
• May be associated with ingestion of photosensitizing medication (NSAIDs, efavirenz), or TMP-SMX
• Skin eruption does not improve even when medication is discontinued
• Histo:
• Subacute or chronic dermatitis
• Dense dermal infiltrate with many eosinophils
• May have features identical to PLE, lichen planus, lichen nitidus
• CD4 <50: may have features of actinic prurigo
• Widespread vitiliginous lesions may develop
• Tx: difficult
• Thalidomide may be beneficial
Radiodermatitis
• Radiation damage: DNA
• effect depends on the amount of radiation, intensity, characteristics of the individual cell
• Increased radiosensitivity: rapidly dividing cells, anaplastic cells
• When radiation therapy is delivered, it is frequently ”fractionated” (divided into small
doses), which allows normal cells to recover between doses
• Large dose = cell death
• Small amounts = effect is insidious and cumulative
• Mitosis is arrested temporarily = retardation of growth
• Greater chromosome breaks
• More rapid delivery
• Higher exposure rate
• Presence of oxygen
Acute radiodermatitis
• Exposure of skin to a large amount of ionizing radiation
• Usually happens during treatment of malignancy and in accidental overexposure
• Manifests as:
• Initial erythema – lasts 2-3 days
• Second phase of erythema at 3-6 days
• Vesiculation, edema, erosion, or ulceration may occur
• Pain
• Dark skin color mistaken for hyperpigmentation but desquamates
• Cutaneous necrosis (yttrium-90 synovectomy)
• Skin that receives large amount of radiation can never return to normal
• Dry, atrophic, smooth, hypopigmented or depigmented
• Tx: topical corticosteroid ointment + emollient cream BID
Eosinophilic, polymorphic, and pruritic
eruption associated with radiotherapy
• polymorphic, pruritic eruption arising several days to several months after radiotherapy for
cancer tends to favor the extremities
• SSx
• Acral excoriations
• Erythematous papules
• Vesicles
• Bullae
• Not limited to areas of radiation treatment
• Histo
• Superficial and deep perivascular lymphohistocytic infiltrate eith eosinophils
• Tx
• Topical steroids
• Antihistamins
• UVB
• Spontaneous resolution
Chronic radiodermatitis
• Chronic exposure to “suberythema” doses of ionizing radia- tion over a prolonged period
• varying degrees of damage to the skin and its underlying parts after a variable latent period
• Manifestation:
• Telangiectasia
• Atrophy
• Hypopigmentation
• Residual focal increased pigment (freckling)
• Skin dry, thin, smooth, shiny
• Nails: brittle, striated, fragmented
• Ulceration (reduced capacity to repair injury)
• Hair: brittle, sparse
• Radiation keratosis, carcinoma
• Subcutaneous fibrosis, thickening, binding of surface layers to deep tissues -> tender, erythematous plaques months after radiation therapy
• Tx:
• Requires little to no attention
• Protection from sunlight and extreme heat or cold
• Careful cleansing with mild soap and water
• Emollients
• Hydrocortisone ointment
Radiation cancer
• After a latent period averaging 20–40 years, various malignan- cies may develop
• Most frequent: BCC
• On head, neck, lumbosacral area
• Second most frequent: SCC
• Arise in sites of radiation therapy (Metastasize more frequently than purely sun-induced SCC)
• More common in arms, hands
• RF:
• Prior radiation
• Sun damange
• Other radiation-induced CA
• Angiosarcoma
• Kaposi sarcoma
• Malignant fibrous histiocytoma
• Sarcoma
• Thyroid carcinoma
• Prevention
• Early removal of precancerous keratosis and ulcerations
• Radiation keratosis: cryosurgery, 5-FU, imiquimod cream, ingenol, topical 5-aminolevulinic acid
• Diagnosis
• Radiation ulcers: biopsy (excision or incision)
Mechanical Injuries: Callus
• nonpenetrating, circumscribed hyperkeratosis produced by pressure
• occurs on parts of the body subject to intermittent pressure
• Palms, soles, bony prominences of joints
• Surfer’s nodules, boxer’s knuckle pads, jogger’s toe, rower’s rump, milker’s
callus, tennis toe, jogger’s nipple, prayer callus, the yoga sign, neck
callosities of violinists, pillar knocker’s knuckles, bowler’s hand, and
Russell’s sign
• Tc
• Padding to relieve pressure
• Paring of thickened callus
• Keratolytics (40% salicylic acid)
• 12% ammonium lactate lotion
• Urea-containing cream
Mechanical Injuries: Clavus
• circumscribed, horny, conical thickenings with the base on the surface and the apex pointing
inward and pressing on subjacent structures
• Arise at sites of friction of pressure (lesions disappear when cause is removed)
• Hard corns
• Dorsa of toes, soles
• Surface is shiny and polished
• Core: densest (produces pain by pressing underlying nerves)
• Soft corns
• between toes, softened by macerating action of sweat
• Tx
• Relief of pressure or friction by corrective footwear
• Application of a ring of soft felt wadding around the region of corn
• Soaking the feet in hot water and paring the surface by means of a scalpel blade or pumice stone leads to
symptomatic improvement
• 40% salicylic acid plaster is applied. Soaking the foot for h before reapplying the medication enhances the effect. After 48 h,
12

the plaster is removed, the white macerated skin is rubbed off, and a new plaster is reapplied. This is continued until the corn is
gone.
Mechanical injury: Pseudoverrucous papules
and nodules
• striking 2–8 mm, shiny, smooth, red, moist, flat-topped round lesions
in the perianal area of children
• a result of encopresis or urinary incontinence
• Tx
• Protect skin
Mechanical injury: coral cuts
• from the cuts of coral skeletons
• painful, and local therapy may provide little or no relief.
• Healing – months
• Prevent secondary infection
• Mycobacterium marinum
Mechanical injury: pressure ulcers (decubitus)
• pressure ulcer produced anywhere on the body by prolonged
pressure
• Four-stage system
• Stage I: changes in skin temp, tissue consistency,
• caused by ischemia of the underlying structures of the skin, fat, sensasion; area of persistent redness
and muscles as a result of sustained and constant pressure
• Stage II: superficial ulcer involving epidermis and/or
• bony prominences of the body are the most frequently affected dermis
sites
• Stage III: ulcers damage the subcutaneous fat
• 95% lower body • Stage IV: muscle, bone, tendon, joint capsule
• 65% pelvic area
• 30% legs • Prevention
• Manifestation • redistributing pressure at a minimum interval of 2 h.
•
•
Begins as erythema a pressure point
Punches out ulcer
• Tx
• Necrosis with grayish pseudomembrane • Relief of pressure (frequent change in position,
meticulous nursing care, foam, flotation devices, air-
• Complications filled products
• Sepsis • Ulcer care, mgt of bacterial colonization and
• Local infection infection, surgical repair
• Osteomyelitis
• Adequate nutrition
• Fistulas
• SCC • Mgt of pain
• Debridement (sharp, mechanical, enzymatic, and
• RF autolytic measures) at least once weekly
• FM, PVD, CVD, sepsis, hypotension
• Wound hygiene
Mechanical injury: Friction blisters
• occur at sites of com- bined pressure and friction
• may be enhanced by heat and moisture.
• formation of vesicles or bullae
• Tx
• Drainage of blister (if skin is tense and uncomfy) but roof should not be
completely removed because it may act as its own dressing
• Prevention
• Acrylic fiber socks with drying action
• Pretreatment with 20% aluminum chloride hexahydrate x 3 days
Mechanical injury: Fracture blisters
• overlie sites of closed fractures, especially the ankle and lower leg.
• blisters appear a few days to 3 weeks after the injury
• caused by vascular compromise
• Complications
• Infection
• Scarring
• Heal spontaneously in 5-14 days
• May cause delay of surgical reduction of fracture
Mechanical injury: Sclerosing lymphangitis
• cordlike structure encircling the coronal sulcus of the penis or running
the length of the shaft
• attributed to trauma during vigorous sexual play
• result from a superficial thrombophlebitis
• Mondor’s disease of the penis
• Tx: not necessary (benign, self-limiting course)
Mechanical injury: Black heel
• sudden shower of minute, black, punctate macules
• most often on the posterior edge of the plantar surface of one or
both heels
• Seen in athletes: basketball, volleyball, tennis, lacrosse
• bleeding is caused by shearing stress of sports activities.
• Paring with a No. 15 blade and performing a guaiac test will confirm
the diagnosis.
• Treatment is unnecessary.
Mechanical injury: Subcutaneous emphysema
• Free air occurring in the subcutaneous tissues
• presence of cutaneous crepitations
• Source:
• Gas-producing organisms: Clostridia
• Leakage of free air from lungs or GI tract
• Causes
• Injuries (penetrating and nonpenetrating)
• Iatrogenic causes during hospital procedures
• Spontaneous pneumomediastinum (violent cough, childbirth, asthma, Boerhaave syndrome)
• Inflammatory bowel disease
• Cancer
• Perirectal abscess
• Pancreatitis or cystitis
• Dental procedures
Traumatic asphyxia
• Ssx
• Cervicofacial cyanosis and edema
• Multiple petechiae of the face, neck, and upper chest
• Bilateral subconjunctival hemorrhage
• May occur after prolonged crushing injuries of thorax or upper
abdomen
• Trauma reverses blood flow in SVC and tributaries
Mechanical injury: painful fat herniation /
painful piezogenic pedal papules
• fat herniations through thin fascial layers of the weight-bearing parts of the
heel
• become apparent when weight is placed on the heel and disappear as soon
as the pressure is removed
• extrusion of the fat tissue together with its blood vessels and nerves may
initiate pain on prolonged standing
• Tx
• Avoidance of prolonged standing
• taping of the foot
• use of compression stockings
• use of plastic heel cups or padded orthotic devices to restrict the herniations.
Mechanical injury: Narcotic dermopathy
• results in thrombosed, cordlike, thickened veins at the sites of
injection of heroin (diacetylmorphine)
• Prep: dissolving the heroin powder in boiling water and then injecting it.
• favored route of administration is intravenous.
• subcutaneous injection (“skin popping”) can result in multiple,
scattered ulcerations, which heal with discrete atrophic scars
• Cocaine-associated vasculitis – may ulcerate
Foreign body reactions: Tattoo
• Tattoo: introduction of insoluble pigments into the skin
• may be traumatic, cosmetic, or medicinal in nature
• Pigment is applied to the skin, and then needles pierce the skin to force the material into the dermis
• “Invisible tattoos” – seen only under UV light
• Polymethylmethacrylate and melamine (may cause geanulomatous reaction)
• Dermopathies may be reactive (allergic, lichenoid, granulomatous, or photosensitive) or infective
(inoculation of syphilis, infectious hepatitis, tubercu- losis, HIV, warts, molluscum, Hansen’s disease)
• Severe allergic reactions to temporary tattoos: p-phenylenediamine
• Red tattoo - most common cause of delayed reactions
• Histo: lichenoid process
• Tx:
• topical or intralesional steroids
• Excision – if lesions are small enough
• Q-switched lasers +/- ablative fractional resurfacing
• Allergy: antihistamines or oral steroids
Foreign body reactions: Paraffinoma
(Sclerosing lipogranuloma)
• Injection of oils into the skin
• smoothing of wrinkles and augmentation of breasts
• Paraffin, camphorated oil, cottonseed or sesame oil, mineral oil, and
beeswax
• may produce plaque- like indurations with ulcerations within months and up
to 40 years
• Tx:
• Surgical removal – wide and complete
Foreign body reactions: Silicone Granulomas
• Silicone granuloma
• Liquid silicones (long chains of dimethyl siloxy groups - biologically inert)
• Used for correcting wrinkles, reducing scars, and building up atrophic depressed areas of the
skin
• Acupuncture needles are coated with silicone
• Medical-grade silicone injected in small volume should be the rule, and it should
not be injected into the penis or the glandular tissue of the breast.
• For breast augmentation, silicone may be used as Silastic implants
• Bioplastique (polymerized silicone particles dispersed in a gel carrier)
• When used for lip augmentation, nodules may develop.
• Histologically, these are foreign body granulomas.
• Tx
• Surgical removal – may lead to fistulas, abscesses, and marked deformity.
• minocycline, 100 mg twice daily for several months, and imiquimod cream have been
anecdotally useful.
Foreign body reactions: Mercury Granulomas
• Mercury may cause foreign body giant cell or sarcoidal-type granulomas,
pseudolymphoma, or membranous fat necrosis.
• egg shaped, extracellular, dark-gray to black, irregular globules.
• Diagnosis
• Gold lysis test is positive in tissues
• Energy-dispersive radiographic spectroscopy may be done and will identify mercury
by the characteristic emission spike.
• Complication
• Systemic toxicity
• Embolus
• Tx
• Excision under xray guidance
Foreign body reactions: Beryllium granuloma
• seen as a chronic, persistent, granulo- matous inflammation of the
skin with ulceration
• may follow accidental laceration
Foreign body reactions: Zirconium granuloma
• papular eruption involving the axillae
• allergic reaction in those shaving their armpits and using a deodorant
containing zirconium
• poison ivy lotions
• Lesions
• Brownish, red, dome-shaped, shiny papules
• Acquired, delayed-type, allergic reaction resulting in a granuloma of
the sarcoidal type
• After many months, the lesions involute spontaneously.
Foreign body reactions: Silica granuloma
• Automobile crashes and other types of trauma may produce tattooing of
dirt (silicon dioxide) into the skin = induces silica granulomas
• black or blue papules or macules arranged in a linear fashion
• The granulomas may be caused by amorphous or crystalline silicon dioxide
(quartz), magnesium silicate (talcum), or complex polysilicates (asbestos).
• Talc granulomas of the skin and peritoneum may develop after surgery
from the talcum powder used on surgical gloves
• Tx
• immediate and complete removal (excision)
• Systemic steroids
• Dermabrasion - for the removal of dirt accidentally embed- ded into the skin of the
face or scalp.
Foreign body reactions: Carbon stain
• Discoloration of the skin from embedded carbon
• occurs in children from improper use of firearms or fireworks or from
a puncture wound by a pencil
• Narcotic addicts who attempt to clean needles by flaming them
• Tx
• Carbon particles may be removed immediately after their deposition using a
toothbrush and forceps (best possible cosmetic result)
• If the particles are left in place long enough, they are best removed using the
Q-switched Nd:YAG laser at 1064 nm.
• microexplosions producing poxlike scars have occurred with each laser pulse.
• Dermabrasion
Foreign body reactions: Injected filler
substances
• Injected or implanted filler substances used for facial rejuvenation
may produce foreign body or sarcoidal granulomas
• Palpable thickening and nodules, occasionally painful
• Tx
• topical, intralesional, or systemic steroids,
• sometimes augmented by tacrolimus
• minocycline or doxycycline