Dermatoses Resulting from Physical Factors

Dermatoses Resulting from Physical Factors
Chapter 3 Andrew’s Diseases of the Skin JoAnne M. LaRow, D.O.

Heat Injuries Thermal Burns Electrical Burns Hot Tar Burns Miliaria
Miliaria Crystalline (Sudamina) Miliaria Rubra (Prickly Heat, Heat Rash) Miliaria Pustulosa Miliaria Profunda Postmiliarial Hypohidrosis Tropical Anhidrotic Asthenia Occlusion Miliaria

Thermal Burns First-degree burn- active congestion of superficial blood vessels This causes erythema sometimes followed by epidermal desquamation Sunburn Constitutional reactions occur if area is large Pain and increased surface heat may be severe

Second-degree burns Two types-superficial and deep
Superficial-transudation of serum from capillaries, causing edema of superficial tissues Vesicles and blebs form from serum gathering beneath the outer layers of the dermis Complete recovery without scar or blemish is usual Deep –is pale and anesthetic Injury to reticular dermis compromises blood flow and destroys appendages Healing takes > 1 month Scarring occurs

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-and-droplet pattern of an accidental scald from hot cup of tea

Second-Degree Burn Curling iron burn

Third-degree burns Full-thickness tissue loss
Often loss of subcutaneous tissue occurs Since skin appendages are destroyed there is no epithelium for regeneration An ulcerating wound occurs Healing leaves a scar Followed by constitutional symptoms

Fourth-degree burns Destruction of entire skin and subcutaneous fat with any underlying tendons Requires grafting for closure Constitutional symptoms occurs Constitutional symptoms depend on size of area involved, depth, and especially location The more vascular the involved area, the more severe the symptoms

Thermal Burns Prognosis is poor when large surfaces are involved
Particularly when > two thirds of body surface is burned Infection of the wound Cellulitis, sepsis, with seeding of internal organs (ie meninges, lungs, kidneys) Irregularities in electrolytes and fluid balance, loss or serum proteins Symptoms of shock may appear within 24-hrs Next, symptoms of toxemia from the absorption of destroyed tissue on wound surface Symptoms of wound infection may then occur as a result of contamination with pyogenic organisms Symptoms of all three may merge making differentiation difficult

Complications of thermal burns
Excessive scarring with keloidlike scars or flat scars with contractures of joints Chronic ulcerations because of local impaired circulation Burn scars may be the site of carcinoma or sarcoma

Treatment For minor thermal burns-prompt cold applications until pain has resolved Do not open vesicles or blebs, they provide a natural barrier If tense and painful evacuate fluid under strict aseptic conditions via puncture of the wallto allow blister to collapse Apply topical antibiotic Severe deep wounds silver sulfadiazine ointment is indicated Antibiotics, fluid, and electrolyte support, supplemental vitamins Collagen-synthetic bilaminate membranes may be used In many centers, cultured epidermal grafts, both autologous and allogeneic, are being utilized Morbidtiy and mortality following severe burns is often due to bacterial and fungal infection Definitive tx consists of antishock measures, debridement of loose skin and dirt, and application of silver sulfadiazine ointment

Treatment Expedient primary excision of deep dermal and full-thickness burn wounds with subsequent grafting is standard of care Severe second- and third degree burns require specialized teams of physicians working together to provide most effective tx

Electrical Burns Two varieties: Contact and flash
Contact- small but deep, causing some necrosis of underlying tissues Flash-burns usually cover a large area and are similar to a surface burn and should be tx as such Lightening may cause burns after direct strike, where an exist and an entrance wound are visible Lightening is the most lethal type of strike, cardiac arrest or other internal injuries may occur Electrical Burns

Electrical Burns Other types of strikes are indirect and result in linear 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

Hot Tar Burns Demling has reported that the polyoxyethylene sorbitan in Neosporin ointment is an excellent dispersing agent that facilitates the removal of hot tar from burns

Miliaria Retention of sweat as a result of occlusion of eccrine sweat ducts and pores Produces an eruption that is common in hot, humid climates such as the tropics and during the hot summer months in temperate climates Occlusion of eccrine sweat gland obstructs delivery of sweat to the skin surface Eventually backed-up pressure causes rupture of sweat gland or duct at different levels Escape of sweat into adjacent tissue produces miliaria Different forms of miliaria occur depending on the level of injury to the sweat gland

Miliaria Crystalline Characterized by small, clear, superficial vesicles without inflammation Appears in bedridden pts in whom fever produces increased perspiration or when clothing prevents dissipation of heat and moisture, as in bundled children Lesions are asymptomatic and rupture at the slightest trauma Self-limited; no tx is required

Miliaria Crystallina Minute, descrete vesicles resulting from profuse sweating secondary to a high fever

Miliaria Crystallina

Miliaria Rubra Lesions are descrete, extremely pruritic, erythematous papulovesicles with sensation of prickling, burning, or tingling Tingling may become confluent on a bed of erythema Most frequently affected sites: antecubital and popliteal fossae, trunk, inframammary areas, abdomen Site of injury is prickle cell layer where spongiosis is produced

Miliaria Rubra

Always preceded by some other dermatitis that has produced injury, destruction, or blocking of sweat duct Pustules are distinct, superficial, and independent of hair follicle Pruritic pustules occur most frequently on intertriginous areas, flexure surfaces of extrmities, sctrotum, and back of bedridden pts Usually pustules contain sterile material, but may contain nonpathogenic cocci Miliaria Pustulosa

Miliaria Profunda Nonpruritic, flesh-colored, deep-seated, whitish papules Asymptomatic, usually lasting only 1 hr after overheating has ended Concentrated on the trunk and extremities Except for face, axillae, hands, and feet(where there may be a compensatory hyperhydrosis), all sweat glands are nonfunctional Occlusion is in upper dermis Only seen in tropics usually following a severe bout of miliaria rubra

Postmiliarial Hypohidrosis
Results from occlusion of sweat ducts and pores and may be severe enough to impair one’s ability to perform sustained work in a hot environment Affected pts may show decreasing efficiency, irritability, anorexia, drowsiness, vertigo, and headache; they may wander in a daze Hypohidrosis invariably follows miliaria The duration and severity of hypohidrosis are related to severity and duration of miliaria Sweating may be depressed to half the normal amount for as long as 3 weeks

Tropical Anhidrotic Asthenia
Rare form of miliaria with long-lasting pore occlusion, producing anhidrosis and heat retention

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 Anhydrous lanolin resolves occlusion of pores and may help restore normal sweat secretions Hydrophilic ointment helps dissolve keratinous plugs facilitating sweat flow Soothing, cooling baths containing Aveeno colloidal oatmeal or cornstarch in moderation

Occlusion Miliaria Mild cases may respond to dusting powders, such as cornstarch or baby talcum powder A lotion containing 1% menthol and glycerin and 4% salicylic acid in 955 alcohol is effective This should be dabbed on affected areas several times daily until desquamation sets in 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 Most common on the legs of women as a result of warming in open fireplaces, radiators, or heaters Similar changes may be produced with a hot water bag or electric heating pad Also occurs in cooks, stokers, invalids, and others exposed to long periods of moderate heat Epithelial atypia and Bowen’s disease has been reported All the various phases usually are present simultaneously in a patch, the color varying from pale pink to old rose or dark purplish brown After cause is removed the color tends to disappear gradually, but sometimes pigment is permanent

Erythema Ab Igne Reticulated hyperpigmentation with some epidermal atrophy and scaling secondary to use of a heating pad

Heat sources causing EAI
Steam radiators Car heaters Heated reclining chairs Heating blankets Hot bricks Infrared lamps Heating pads Hot water bottles Electric stove/heater Open fires Coal stoves Peat fires Wood stoves

Key Features Localized areas of reticulated erythema and hyperpigmentation Due to chronic exposure to a nonburning heat source Common locations: lumbosacral region and shins Key pathologic finding is squamous atypia There is a risk of cutaneous malignancy, in particular squamous cell carcinoma Also Merkel cell carcinoma risk Latent period of 30 years or more with carcinoma

Treatment Use of bland emollients is helpful No effective treatment Kligman’s combination of 5% hydroquinone in hydrophilic ointmant containing 0.1% retinoic acid and 0.1% dexamethasone may reduce unsightly pigmentation 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 Local cold injuries are divided into chilblain, frostbite, and immersion injury Immersion foot is encountered almost entirely in the armed forces Intense vasoconstriction resulting from local action of cold and reflex vasoconstrictor stimulation is reinforced by the passage of cold blood through the vasomotor center Vasoconstriction evokes tissue anoxia Decreased muscular activity further diminishes blood supply Ice crystal formation in blood vessels usually does not occur, but when it does necrosis occurs

Occurs chiefly on hands, feet,ears, and face, especially in children
Onset is enhanced by dampness Pts are usually unaware of injury until they develop burning, tiching, and redness Areas are bluish red, the color partial or totally blanches with pressure, and are cool to touch Chronic chilblains occurs repeatedly during cold weather and disappears during warm weather Chilblains Recurrent, localized erythema and swelling caused by exposure to cold Blistering and ulcerations may develop in severe cases In pts predisposed by poor circulation even moderate exposure to cold may produce chilblains Acute chilblains is the mildest form of cold injury

Chilblains (pernio)

Treatment Affected areas should be cleansed with water and massaged gently with warm oil each day and should be protected against further injury and exposure to cold or dampness If feet are affected, woolen socks should be worn at night during cold months Careful use of electric pads may be used Smoking strongly discouraged Nifedipine 20mg TID Vasodilators (nicotinaamide 100 mg TID or dipyridamole 25 mg TID) Systemic corticoid tx is helpful in chilblain lupus erythematosus Pentoxifylline may be useful

Frostbite (Congelation)
When soft tissue is frozen and locally deprived of blood supply Ears, nose, cheeks,fingers,and toes most common sites Frozen part is painless and becomes pale and waxy Various degrees of tissue destruction similar to those of burns are seen Erythema and edema, vesicles and bullae, superficial gangrene, deep gangrene Injury to muscles, tendons, periosteum, and nerves Arolla index-formula linking duration of exposure (defined by temperature and wind chill index) with frostbite

Frostbite

First-Degree Frostbite

Treatment When the skin flushes and is pliable, thawing is complete
Supportive measures: bed rest, high protein/high calorie diet, wound care, avoidance of trauma, avoid rubbing of affected parts After swelling and hyperemia have developed, bed rest with limb slightly flexed, elevated and at rest Room temperature relieves pain and helps prevent tissue damage Early- (before swelling develops) covering body with clothing or a warm hand or other body surface to maintain a warm temperature to maintain adequate blood circulation Rapid rewarming in bath water between 100 degrees and 110 F Analgesics(because rewarming is painful) Slow thawing results in more extensive tissue damage

Treatment Protection by a heat cradle may be helpful
Anticoagulants to prevent thrombosis and gangrene Papaverine and nicotinic acid may reduce vasospasm Antibiotics for prophylactic measures and an updated tetanus immunization is recommended Recovery may take months

Immersion Foot Syndromes
Trench Foot Warm Water Immersion Foot

Trench Foot Results from prolonged exposure to cold, wet conditions without immersion or actual freezing Term derived from trench warfare in World War 1, when soldiers stood, sometimes for hours, in trenches with a few inches of cold water in them Lack of circulation produces edema, paresthesias, and damage to blood vessels Gangrene may occur in severe cases Tx-removal from causal environment, bed rest, and circulatory restoration Measures underlined on tx for frostbite should be performed

Warm Water Immersion Foot
Exposure of feet to warm, wet conditions for 48 hrs or more may produce a syndrome of maceration, blanching, and skin wrinkling of soles and sides of feet Itching and burning with swelling may persist a few days after removal of the cause, but disability is temporary Commonly seen in military service members in Vietnam Also seen in persons wearing insulated boots, the so-called moon-boot syndrome Tx-by allowing feet to dry for a few hrs out of 24 hrs Or by greasing soles with a silicone grease once/day Recovery is usually rapid and complete if dried thoroughly for a few hrs

Tropical immersion Foot
Seen after continuous immersion of the feet in water or mud of temperatures above 71.6 degrees F (22 degrees C) for 2-10 days AKA “paddy foot” in Vietnam Erythema, edema, and pain of the dorsal feet Also fever and adenopathy Resolution occurs 3 to 7 days after the feet have been dried

Warm Water Immersion Foot
This was known as “paddy foot” in Vietnam It involves erythema, edema, and pain of the dorsal feet, and fever and adenopathy Resolution occurs 3-7 days after the feet have been dried Can be prevented by allowing the feet to dry for a few hrs out of every 24 or by greasing the soles with a silicone grease once daily Recovery is usually rapid if feet are thoroughly dried for a few hrs

Dermatoses with Cold Hypersensitivity
Erythrocyanosis Crurum Acrocyanosis Cold Panniculitis Exposure to cold produces abnormal reactions in several disease states These reactions are mediated through globulins ie cryoglobulin and cryofibrinogen Also histamine, serotonin, leukotrienes, protaglandins, kinins, and cold hemolysins may be involved

Erythrocyanosis Crurum
Small tender nodules may be found on palpation Nodules may break down and form small, multiple ulcers Affected limbs are cold to touch Seen in northern countries and probably due to an abnormal reaction of blood vessels to prolonged cold Characterized by slight swelling and a bluish pink tint of the skin of the legs and thighs of young girls and women May be unilateral Atypical varieties are common, some presenting cinnabar red spots, bullae, indurations, and lichenoid papules May be a history of cramps in the legs at night

Acrocyanosis A persistent cyanosis with coldness and hyperhidrosis of fingers and hands May also be present on toes and feet Chiefly occurs in young women, but not rare in young men 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 Remitting necrotizing acrocyanosis is a term applied to functional vascular spasm or organic occlusion that produces pain in hands and feet, with ateas of coldness, cyanosis, andnecrosis of the tops of fingers and toes This has been reported to occur without prodromal or constitutional symptoms

Cold Panniculitis After exposure to severe cold, well-demarcated erythematous warm plaques may develop, particularly on the cheeks of young children Lesions usually develop within a few days after exposure, and resolve spontaneously in 2 weeks(approx)

Lesions are readily reproducible by placing an ice cube on the volar aspect of the forearm for 2 minutes This type of panniculitis is seen mostly in young children whose fat contains more high saturated fatty acids, which have a higher melting point and a lower solidification point than an adult’s less saturated fat Pts outgrow this susceptibility 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: Ultraviolet radiation , 400nm 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 UVA is divided into two subcategories: UVA I(340 to 400 nm) and UVA II(320 to 340 nm) Virtually no UVC reaches the earth’s surface, because it is absorbed by the ozone layer

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 A large portion of UVA and UVB may be reflected from sand, snow, ice, and water Cloud cover is a poor UV absorber Mercury-vapor lamp or sunlamp bulb produces mostly UVB( stronger inducer of erythema) Minimal erythema dose (MED) is the minimal amount of a particular wavelengh of light capable of inducing erythema on an individual’s skin 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

Clinical signs and symptoms
Sunburn is normal cutaneous reaction to sunlight in excess of an erythema dose ( the amount that will induce redding) UVB erythema peaks at 12 to 24 hrs after exposure, but onset is sooner and severity greater with increased exposure Erythema is followed by tenderness, blistering, which may become confluent Edema commonly occurs in extremities and face; chills, fever, nausea, tachycardia, and hypotension may be present Sever cases symptoms may last as long as a week Dequamation is common about a week after sunburn even in non-blistering areas

Delayed tanning is induced by UVB and UVC wavelengths and begin 2 to 3 days after exposure and last days Delayed tanning does produce some protection from further solar injury , it is at the expense of damage to the dermis and epidermis Tanning is not recommended for sun protection An individual’s inherent ability to tan and the ease with which they burn are described as their “skin type” After UV exposure, skin pigment undergoes two changes: immediate pigment darkening (IPD, Meirowsky phenomenon) and delayed melanogenesis IPD is maximal immediately after sun exposure(it results from changes in melanin already in the skin) IPD occurs after exposure to long-wave UVB, UVA, and visible light Large doses of UVA produce initial prolonged darkening

TX- Prostaglandins are important mediators of sunburn (ASA or Indomethacin) Cool compresses Sunburn victim experiences at least 1-2 days of discomfort and even pain before much relief occurs Topical remedy: Indomethacin 100 mg Absolute ethanol 57 ml Proplene glycol Sig: spread widely over burned area with palms and let dry “Skin type” is useful to determine the starting dose of phototherapy, suncreen recommendations, and reflects the risk of skin cancer Exposure to UVB and UVA causes an increase in epidermal thickness, especially of the stratum corneum, leading to increased tolerance to further solar radiation

Skin Types

Second-degree sunburn

Prophylaxis Avoid sun exposure between 10 am and 2 pm
Barrier protection with hats and clothing Avoidance plus physical barriers can virtually always prevent sunburn Suncreen agents include UV-absorbing chemicals and UV-scattering or –blocking agents(physical sunscreens) Use of the UV index, published daily by the National Weather Service for many US cities Sun protection factor-the ratio of the number of MEDs of radiation required to induce erythema through a thin film of sunscreen, compared with unprotected skin

Sunscreens Chemical suncreens-para-aminobenzoic acid(PABA), PABA esters, cinnamates,salicylates, anthranilates, benzophenoes) Physical agents-titanium dioxide Combinations of the two Water resistant-maintaining their SPF after 40 minutes of water immersion Water proof-maintating their SPF after 80 mins of water immersion UVA protection- sunscreens containing benzophenones or dibenzoylmethanes Apply sunscreen at least 20mins before sun exposure

Ephelis (Freckle) Small (<0.5cm) brown macules occuring on sun-exposed skin of face, neck,shoulders,backs of hands Become prominent during summer when exposed to sunlight and subside in winter Blondes and redheads, with blue eyes, of Celtic origin (skin types I or II) are especially susceptible May be genetically determined May occur in successive generations in similar locations and patterns Usually appear around age five Must be differentiated from lentigo simplex LS- a benign discrete hyperpigmented macule appearing at any age and on any part of the body, including mucosa Intensity of color is independent of sun exposure

Ephelis Solar lentigo (frequently misnamed “liver spot”) appears at at a later age, mostly in persons with long-term sun exposure Favored sites are backs of hands and face Histologically, the ephelis shows increased production of melanin pigment by a normal number of melanocytes Otherwise epidermis is normal Lentigo has elongated rete ridges that appear club shaped

Photoaging(Dermatohelioisis)
Characteristic changes induced by chronic sun exposure AKA photoaging or dermatoheliosis Risk of developing these changes correlated with baseline pigmentation(constitutive pigmentation) and abilitiy to resist burning and tan following sun exposure(facultative pigmentation) Individuals can be divided into six skin types(or phototypes) Risk for melanoma and nonmelanoma is also related to these skin types

Most susceptible to effects of sunlight are those of skin type I-blue-eyed, fair-complexioned persons who do not tan These pts require more frequent and careful skin exams Many of the changes of chronic sun exposure were formerly ascribed to chronic aging Primary sites involved are: V area of neck and chest, back, and sides of neck,face, backs of hands and extensor arms Skin becomes atrophic, scaly, wrinled, inelastic. Or leathery with a yellow hue (Milian’s citrine skin) In some pts of Celtic ancestry, dermatoheliosiis produces profound atrophy without wrinkling, resulting in an almost translucent appearance of skin through which hyperplastic sebaceous glands and prominent telangiectasias are seen These people are at high risk for nonmelanoma cancer

Dermatoheliosis Solar elastosis(actinic)
Caused by alterations in upper dermal elastic tissue and collagen Imparts a yellow color to skin A textural and tinctorial change in sun-damaged skin Striated beaded lines- are small yellowish papules and plaques developing along the sides of the neck These are a result of sebaceous hyperplasia Fibroelastolytic papulosis – of the neck(psuedoxanthoma elasticum-like papillary dermal elastolysis

Dermatoheliosis On the face or chest a macroscopic, translucent papule with a pearly color resembling a basal cell carcinoma may occur This is Dubreuilh’s elastoma, actinic elastic plaque Similar plaques may occur on the helix or antihelix of ear

Dermatoheliosis Poikiloderma of Civatte-refers to reticulate hyperpigmentation with telangiectasia, and slight atrophy of sides of the neck, lower anterior neck and V of neck, and V of chest Submental area is spared frequently presents in fair-skinned men and women in their middle to late thirties or early forties

Dermatoelastosis Cutis rhomboidalis nuchae (sailor’s neck or farmer’s neck) is characteristic of long-term, chronic sun exposure Skin on back of neck becomes thickened, tough, and leathery and normal skin marking become exaggerated

Dermatoheliosis Nodular elastoidosis with cysts and comedomes occurs on the inferior periorbital and malar skin-Favre-Racouchot syndrome or on the forearms (actinic comedonal plaque) Both consist of thickened yellow plaques studded with comedomes and cystic lesions Tx-removal , retinoic acid cream, surgical removal of cysts and redundant skin

Telangistasias over cheeks, ears, and sides of neck may develop
Due to damage to connective tissue of dermis, skin fragility is prominent, and pts note skin tearing with minimal trauma Especially to extensor surface of arms leading to an ecchymosis, called actinic purpura As ecchymoses resolve, dusky brown macules remain for months, increasing mottled appearance of skin White stellate pseudoscars on forearms are a frequent complication of this enhanced skin fragility Some pts develop soft, flesh-colored to yellow papules and nodules that coalesce on the forearms to form cordlike bands extending from the dorsal to the flexural surfaces- solar elastotic bands

Solar Elastosis Histologically, chronically sun-exposed skin demonstrates homogenization and a faint blue color of connective tissue of the upper reticular dermis, so-called solar elastosis The elastotic material is derived from elastic fibers mainly Characteristically there is a zone of normal connective tissue below the epidermis

Adult –Onset Colloid Milium
Translucent, flesh-colored, or slightly yellow 1- to 2-mm papules on sun exposed areas of hands, face, neck, ears in middle-aged adults Refinery workers and persons using high-concentration hydroquinone creams may also develop colloid degeneration Histologically, homogenous, fissured masses occupy the upper dermis, resembling amyloid

Photosensitivity 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) 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 Chemically induced – many substances known as photosensitizers may induce an abnormal reaction in skin exposed to sunlight or its equivalent Substances may be delivered externally (by contact) or internally by enteral or parenteral administration Resulting in a markedly increased sunburn response without prior allergic sensitization called phototoxicity

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 Chemicals known to cause photosensitivity (photosensitizers) are usually resonating compounds with a molecular weight of < 500 Absorption of radiant energy (sunlight) by the photosensitizer produces an excited state When returning from returning from an excited state to a lower energy state gives off energy through fluorescence, phosphorescence, charge transfer, heat, or formation of free radicals Each photosensitizing substance absorbs only a specific wavelengths of light called its absorption spectrum Action spectrum-specific wavelength of light that evokes a photosensitive reaction

Action potential for photoallergy is mostly in the long ultraviolet (UVA) region and may extend into the visible light region (320 to 425 nm) Photosensitivity reactions occur only when there is sufficient concentrations of the photosensitizer in skin, and the skin is exposed to a sufficient intensity and duration of light in the action spectrum of that photosensitizer The intensity of the photosensitivity reaction is dose dependent and is worse with a greater dose of photosensitizer and greater light exposure

Photosensitivity Drug-induced photosensivity-photoallergic dermatitis on sun-exposed areas of an infant following topical use of hexachlorophene

Photoallergic dermatits
Papulovesicular lesions of photoallergic dermatitis due to hexachlorophene

Phytophotosensitivity
Plant-induced photosensitivity-linear hyperpigmentation on the face of a child following exposure to limes and sunlight

Phytophotosensitivity
Hyperpigmentation on the dorsal aspect of the hands following the use of limes and sunlight exposure

Phototoxic Reactions A nonimmunologic reaction developing after exposure to a specific wavelength and intensity of light in the presence of a photosensitizing substance A sunburn-type reaction(erythema, tenderness, and blistering) Can occur in pts without prior history of exposure to that particular substance Erythema begins (like sunburn) after 2-6 hrs and worsens for hrs before beginning to subside Exposure of the nail bed may lead to onycholysis, called photo-onycholysis Phototoxic ractions may cause hyperpigmentation, even without preceding erythema The action spectrum for most phototoxic reactions is in the UVA range

Phototoxic Tar Dermatitis
Persons with type V and VI skin are protected from this Up to 70% of whites exposed to such combinations will develop this Hyperpigmentation occurs, and may persist for years Coal tar or its derivatives may be found in cosmetics, drugs, dyes, insecticides, and disinfectants Coal tar, creosote, crude coal tar, or pitch, in conjunction with sunlight exposure, may induce a sunburn reaction associated with a severe burning sensation Direct contact may not be needed, since these hydrocarbons are airborn Burning and erythema may continue for 1 –3 days

Phytophotodermatits from squeezing limes
When furocoumarins in many plants may cause a phototoxic reaction when these plants come in contact with moist skin exposed to UVA light Several hrs after exposure, a burning erythema occurs, followed by edema and development of vesicles or bullae Intense hyperpigmenation occurs that may persist for weeks or months Tx-similar to tx of sunburn; hyperpigmentation-time Phytophotodermatits from squeezing limes

Berloque Dermatitis Characterized by lavaliere(hanging drop)-shaped pigmented patches Word for pendant in French is berloque, and in German is berlocke Seen most frequently on sides of neck, and retroauricular area in women In men usually beard area caused by aftershave lotion Chief cause-oil of bergamount, containing a furocoumarin (bergapten)

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 If occurs, either the tattooed person must avoid sunlight exposure

Phototoxic Drug Reactions
Most occur from tetracyclines, nonsteroidal antiinflammatory drugs, amiodarone, and phenothiazines Action spectrum for all is in the UVA range Among the NSAIDs, piroxicam is the most potent photosensitizer Among the tetracycline group, demthylchlortetracycline and doxycycline are most phototoxic In the case of amiodarone and chlorpromazine, while typical phototoxic reactions (resembling sunburn) may occur, hyperpigmentation is a well-recognized pattern of phototoxicity It causes slate blue(amiodarone) or slate gray (chlorpromazine) coloration, resulting from drug deposition in the tissues

Drug induced photosensitivity
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
There is erythema and edema on the exposed sites, the “V” of the neck . This distribution would suggest the diagnosis

Drug induced photosensitivity
The backs of the hands are the classic sites to be involved in light induced eruption Same pt

Photoallergy Over time lichenification develops, leading to thick plaques Face, hands, neck, forearms are most frequently involved Over time the dermatitis develops to sunprotected skin Removal of offending agent may not lead to complete resolution of the photoallergic reaction-referred to as a persistent light reaction Clinical and path findings are similar to those of allergic contact dermatitis Photoallergic dermatitis is caused by a photosensitizing substance plus sunlight exposure in a sensitized person If photosensitizer is delivered internally, it is called a photoallergic drug reaction If it comes to the skin externally, is is called a photoallergic contact dermatitis Clinically the pt develops a pruritic eruption, initially on sun-exposed areas

Phototoxic reaction to a nonsteroidal antiinflammatory drug

Photoallergic dermatitis on sun-exposed areas

Photoallergy Testing Practical office procedure is that each of the suspected photosensitizers is applied in duplicate to two symmetrical sites on the back that have not been exposed to sunlight Usual concentration used for the patch test is 1& petrolatum After 48 hrs, one set is removed and examined for reactions as a contactant without exposure to light Then the site is exposed to UVA After another 48 hrs, the irradiated site is compared with the other patch test site (unexposed site) When both sides are positive, there is a contact sensitivity or photoallergy When the irradiated site alone is positive ther is only photoallergy When the irradiated site is more positive than the unirradiated site, ther is both allergic contact and phototcontact dermatitis

Treatment Both acute and chronic photosensitivity are treated similarly to any other inflammatory dermatitis, with topical corticosteroids

Polymorphous Light Eruption
The papular (or erythmatopapular) variant is the most common, but papulovesicular, eczematous, erythematous and plaquelike lesions also occur Lesions occur 1-4 days after exposure to sunlight Pts report itching and erythema within the first 24 hrs A change in the amount of radiation is important Most common form of sensitivity All races and skin types affected Typically in first three decades Females outnumber males Unknown pathogenesis Positive family history in 10-50% of pts Different morphologies seen, although in the individual the morphology is constant

Pts living in the tropics are free of eruption but may develop disease when they move to temperate zones Most commonly involved areas are chest, face, neck, and arms Typically areas protected during the winter, as the extensor surface of the forearms, are particularly affected, whereas areas exposed all year (face and dorsa of hands) may be relatively spared Eruption appears in springtime commonly PLE PLE is induced by UV light, but the wavelengths responsible varies Visible light does not induce PLE Standard phototesting usually does not induce an abnormal response in pts If an abnormal response occurs it is only erythema Provocation testing with repeated exposures may be required Two unusual variants of PLE are juvenile spring eruption of the ears and solar purpura

PML Exposed areas such as the backs of the hands and forearms are affected. Ultraviolet A is mainly responsible and may penetrate window glass

PML The patchiness of the edematous papules and plaques is characteristic

PML The eruption is less red and confluent than a sunburn

PML The lesions are typically papular and clustered

PML-pathology Characteristic perivascular mononuclear cell infiltration

PML Very itchy, red,edematous papules, which may coalesce into plaques, occur 1 or 2 days after exposure to light

PML This young women developed a widespread pruritic, papular eruption after using a sunbed, which emitted ultraviolet A

Juvenile spring eruption
Solar purpura-rare variant of PLE, presenting as macular or palpable purpura on the legs It is also UVA induced, but its distribution suggests other factors asuch as high hydrostatic pressure are required Therapeutically:sunscreen, avoiding sun, topical steroids for itch and clearing eruption, antihistamines, systemic steroids, hydroxtchloroquine sulfate, chloroquine, PUVA, thalidomide, Azathioprine Juvenile spring eruption Most common in boys ages 5-12 yrs Presents in spring with grouped s,all papules or papulovesicles on the helices It is self-limited and does not scar UVA is the inducing spectrum and some pts have PLE lesions elsewhere

PML Polymorphous light eruption: erythematous papulovesicular and plaque-like lesions with characteristic distribution on the sun-exposed areas of the cheek

Actinic Prurigo In children the cheeks, distal nose, ears, and lower lip are involved Cheilitis may be the initial and only feature for years Conjunctivitis is seen in 10-20% of pts Lesions of arms and legs are also common but usually exhibit a prurigo nodule configuration May extend and involve sun-protected areas, especiall buttocks In adults dry papules and plaques are typical, cheilitis and crusting occur less frequently Variant of PLE Most common in Native Americans of North and Central America and Colombia More common in females Begins before age 10 in 45% of cases and before age 20 in 72% of Native Americans Up to 75% have a family history In childhood begins as small papules or papulovesicles that crust and become impetiginized Intensely pruritic

Actinic Prurigo In temperate and high-latitude regions, lesions occur from March through the summer and remit in winter In tropics lesions tend to last all yr Hardening as seen with PLE does not occur Up to 60% of pts with actinic prurigo that present before age 20 have resolution within 5 yrs Adults, however continue with disease all through life IgE levels may be elevated Pts are more commonly positive for HLA-A24 and Cw4 and neg for A3 than are control pts Tx same as PLE Thalidomide has been used extensively with excellent results

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)

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)

Solar Urticaria Wavelengths of sensitivity may vary with anatomic location and over time with same pt Leenutaphong et al divided SU into two types:Type I the photoallergen precursor is an abnormal endogenous substance; in type II it is a normal skin component Type I SU has an action spectrum in visible range; type II has a variable action spectrum Ddx-SLE Most common in females aged 20-40 Within seconds to mins after light exposure, typical urticarial lesions appear and resolve in 1-2 hrs Delayed reactions may rarely occur In severe attacks syncope, bronchospasm, and anaphylaxis may occur Pts with SU are sensitive to wavwlenghs of light from UVB-visible light

Solar Urticaria Sunlight-induced whealing with surrounding erythema of the abdomen

SU Phototesting is useful in SU to determine the wavelengths of sensitivity Lasers and natural sunlight may be used to elicit positive reactions Many pts have a sensitivity in the UVA or even visible range, standard sunscreens are of limited benefit Antihistamines and sun avoidance are first line tx Doxepin may be added if these are not effective Antimalarials can help in some pts PUVA or increasing UVA exposures are effective in more difficult cases Plasmapheresis may be used to remove the circulating photoallergen, allowing PUVA to be given leading to remission

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 At 24 hrs or sooner erythema and edema appear, followed by vesicles Over a few days the lesions rupture, becoming centrally necrotic, and heal with a smallpoxlike scar Lesions may bebome confluent, forming bullae, and recurrent disease may lead to contractures of digits Conjunctivitis with photophobia may occur and corneal ulcers and opacities may result Natural history is improvement by second decade often complete resolution

HV Hydroa vacciniforme-the face was also involved

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

HV Ddx-PLE, actinic prurigo, and erythropoietic protoporphyria (EPP) Porphyrin levels are normal in hydroa vacciniforme In EPP the burning typically begins within mins of sun exposure, and healing is diffuse, thickened, wax-like scarring, rather than the smallpox-like scars of hydroa vacciniforme Histology is helpful in differentiating between the two Tx-avoid sunlight exposure, use broad-spectrum or barrier sunscreens that block UVA range Hydroxychloroquine and prophylactic PUVA may be partially effective

Chronic Actinic Dermatitis
A disease concept in evolution Previously known as persitent light reactivity, actinic reticuloid, photosensitive eczema and chronic photosensitivity dermatitis Basic components are:a persistent, chronic, eczematous eruption in absence of exposure to known photosensitizers; decreased MED to UVA, and/or UVB, and visible light Disease affects middle-aged or elderly men In US skin types V and VI more affected Skin lesions are edematous, scaling, thickened patches and plaques that become confluent Lesions occur on most sun-exposed skin

Chronic Actinic Dermatitis

Therapy Danazol 600mg daily was effective in one pt
Hydroxychloroquine may be added to systemic steroids or azathioprine Low-dose PUVA is bebficial but may not be tolerated Cyclosporine is tx of last resort but is effective in severe cases (it is associated with acute and chronic toxicity and relapse occurs rapidly after discontinuation Difficult-possible topical photosensitizers should be identified via photopatch testing Maximum sun avoidance and broad-spectrum sunscreens Topical and systemic steroids are effective in some cases Azathioprine, 50 to 200 mg/day(most reproducibly effective tx), may be required annually during periods of increased sun exposure

Dermatoses with Photoexacerbation or Photosensitivity
Pts with lupus erythematosus and dermatomyositis, among other connective tissue diseases, often exhibit photosensitivity Moa may be UV alteration of cellular cytoplasmic or nuclear antigen expression, allowing antigens to interact with circulating autoantibodies Pts with diseases characterized by a deficiency of protective pigmentation are photosensitive(albinism, vitiligo) Heritable disorders with increased sensitivity to ultraviolet cellular or DNA damage such as xeroderma pigmentosum, Bloom syndrome, and Cockayne’s disease Disease where ultraviolet light seems to act by a Koebner’s phenomenon- Darier’s, and perhaps pemphigus foliacus

Radiodermatitis Major target within the cell is DNA
Effects depend on the amount, its intensity(exposure rate), and characteristics of the individual cells Rapidly reproducing cells and anaplastic cells have increased photosensitivity compared to normal tissue When radiation is delivered it is fractionated-divided into small doses called fractions-allowing normal cells to recover between doses Radiodermatitis In small amounts effects are insidious and cumulative When dose is large, cell death occurs With sublethal doses many changes occur-mitosis is arrested temporarily, with subsequent growth arrest Exposure rate affects the number of chromosome breaks The more rapid the delivery the greater the number of chromosome breaks

Acute Radiodermatitis
When exposed to a large amount of ionizing radiation, an acute reaction develops, the extent of which depends on amount, quality, and duration of exposure Such reaction is used in tx of malignancy and in accidential overexposure Reaction is manifested by initial erythema, followed by a second phase of erythema at 3-6 days With an “erythema dose” of ionizing radiation there is a latent period of up to 24 hrs before visible erythema develops Initial erythema lsts 2-3 days but may be followed by a second phase beginning up to 1 week after the exposur and lasting up to 1 month

Acute Radiodermatitis
Skin develops a dark color that may be mistaken for hyperpigmention, but that desquamates This my subside in several weeks to months(depending on amount of radiation) Skin which recieves a large amount or radiation will never return to normal It will lack adnexal structure, be dry, atrophic, and smooth, and be hypopigmented or deoigmented

Chronic Radiodermatitis
Chronic exposure to “suberythema” doses of ionizing radiation over a prolonged period will produce varying amounts of damage to skin and underlying skin after a variable latent period of several months to several decades Telangiectasia, atrophy, and hypopigmentation with residual focal increased pigment (freckling) may appear

Chronic Radiodermatitis
Skin becomes dry, thin, smooth, and shiny Subcutaneous fibrosis, thickening and binding of the surface layers to deep tissues may present as tenser, erythematous plaques 6-12 months after It may resemble erysipelas or inflammatory mets Nails may become striated, brittle, and fragmented Capacity to repair is greatly reduced This results in ulceration from minor trauma Hair becomes brittle and sparse In more severe cases these chronic changes are followed by radiation keratoses and carcinoma

Radiation Cancer SCCs arising in sites of radiation therapy metastasize more frequently than purely sun-induced SCCs In some pts either type of tumor may predominate Location plays some role-SCCs are more common on the arms and hands, whereas BCCs are seen on lumbosacral area Other cancers induced by radiation :angiosarcoma, malignant fibrous histiocytoma, sarcomas, and thyroid carcinoma 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 Sun damage may be additive

Radiation Cancer SCC developing in a chronic radiation ulcer on the chest

Callus Most problems with calluses is on the soles
Ill-fitting shoes and orthopedic problems of the foot caused by aging are some of the etiologies Padding to relieve pressure, paring of thickened callus, and the use of keratolytics(40% salicylic acid plasters) Lac-Hydrin 12% Calluses may be softened by moisterizing them nightly with 2 parts propylene glycol:1 water Nonpenetrating, circumscribed hyperkeratosis produced by pressure Occurs on parts subject to intermittent pressure(palms, soles, bony prominences of the joints) Callus differs from clavus it 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) Hard corns have shiny and polished surface
When upper layers are shaved off, a core is seen in densest part of lesion The core causes the dull/boring or sharp/lancinating pain by pressing on underlying sensory nerves Corns arise on sites of friction and pressure, when these factors are removed they may resolve 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 Frequently, a bony spur or exostosis is present beneath both hard and soft corns of long duration Soft interdigital corns usually occur in the fourth interdigital space of the foot Many times there is an exostosis at the metatarsal-phalangeal joint causing pressure on the adjacent toethese are soft, soggy, and macerated so that they appear white Tx by simple excision may be effective

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

Hard Corn

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

Sometimes more feasible to use a salicylic acid-lactic acid in collodion rather than plaster
Collodion medication is painted on and allowed to dry each day until cure Soaking prior to application enhances effect-this tx especially effective for interdigital soft corns Soaking feet in hot water and paring the surface by means of a scalpel blade or pumice stone helps Corns-tx Primary-relief of pressure by corrective footwear Salicylic acid and dichloroacetic acid Careful paring in particular remove central core 40% salicylic acid application, remove after 48hrs, remove white macerated skin, and apply new plaster Continue until corn is removed

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 Surfer’s Nodules

Coal Cuts Sever type of skin injury may occur from the cuts of coral skeletons Abrasions and cuts are painful, and local therapy may sometimes provide little or no relief Healing may take months Watch for secondary infection Possibilities include-Mycobacterium marinum in persistent lesions

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 onlt a dry escar 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 colloid are often utilized Surgical debridement with reconstructive procedures may be needed Electrical stimulation of refractory stage II and stage IV ulcers may be beneficial

Friction Blisters Size of bullae depends on site of trauma
If skin is tense and uncomfortable, the blister should be drained, not removing the roof because it may act as its own dressing Studies in long distance runners and soldiers and acrylic fiber socks (Thor-lo) was found to prevent blisters The drying action and differential sock thickness of this brand were felt to be important in its success 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”)

Fracture Blisters Occur overlying sites of closed fractures, especially the ankle Appear a few days to 3 weeks after injury Caused by vascular compromise nd may create complications such as infection Generally heal spontaneously in 5 14 days, but may result in delay of surgical reduction of the fracture

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, self-limiting 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 Seeming confluence may lead to think of melanoma Bleeding is caused by shearing stress of sports activities Paring with a No. 15 blade and performing a guaiac test will confirm diagnosis Tx-none needed

Subcutaeous Emphysema
Various causes of subcutaneous emphysema include: Penetrating and nonpenetrating injuries, iatrogenic causes including a spontaeous pneumomediastinum such as may occur with violent cough, childbirth, asthma, Boerhaave’s syndrome(esophageal rupture after vomiting), or the Heimlich maneuver, intraabdominal causes, inflammatory bowel disease, cancer, perirectal abscess, pancreatitis, cystitis, and factitial disease Free air occurring in subcutaneous tissues is detected by cutaneous crepitations This raises a concern of infection with gas-producing organisms, especially gas gangrene, or leakage of free air from lungs of GI tract

Traumatic Asphyxia Prolonged crushing injuries of the thorax or upper abdomen that reverses blood flow in the superior vena cava or its tributaries Characterized by cerviofacial cyanosis and edema, multiple petechiae of face, neck, and upper chest, and bilateral subconjunctival hemorrhage

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

Narcotic Dermopathy These lesions may ulcerate
Chronic persistent , firm nodules, combination of scar and foreign body reaction, may occur If cocaine is being injected it may cause ulcers because of its direct vasospastic effect Addicts will continue to inject into the chronic ulcer bed Amphetamines, cocaine, and other drugs may be injected Subcutaneous injection may result in infections, complications of bacterial abscess and cellulitis or sterile nodules(acute foreign body reactions to injected drug or adulterants mixed with it)

Narcotic Dermopathy Ulcer from extravascular injection of “speed” (amphetamine)

Narcotic Dermopathy Cutaneous manifestations of injection of heroin and other drugs also include camptodactylia, edema of eyelids, persistent nonpitting edema of hands, urticaria, abscesses, atrophic scars, and hyperpimentation IM pentazocine abuse leads to a typical tense, woody fibrosis, irregular punched-out ulcerations, and a rim of hyperpigmentation at sites of injection

Foreign body Reactions
Tattoo-introduction of insoluble pigments into the skin producing permanent inscriptions and figures Pigment is applied to skin and then needles pierce skin to force material into dermis Pigments inserted may be carmine, indigo, vermillion, India ink, chrome green, manganese, Venetian Red, aluminum, titanium or zinc oxide, lead carbonate, logwood, cobalt blue, cinnabar (mercuric sulfide), and cadmium sulfide

Tatooing 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 re (mercury), green (chromium), or blue (cobalt) have been described in pts patch-test positive to these metals Tx:Q-switched laser allows removal without scarring One report of five pts who developed darkening after tx due to ferrous oxide formation

Paraffinoma AKA-sclerosing lipogranuloma
Injection of paraffin into skin for cosmetic purposes Smoothing of wrinkles and breast augmentation Oils like paraffin, camphorated oil, cottonseed or sesame oil, beeswax were used These can produce plaque-like indurations with ulcerations after time

Paraffinoma Another eaction may be inflammatory, with mild erysipeloid attacks and tenderness Human adjuvant disease with usually presents with scleroderma-like findings may occur Present tx is unsatisfactory When these tumors are surgically excised they need to be excised widely and completely

Granulomas Silicone granuloma Mercury granuloma Beryllium granuloma
Zirconium granuloma Silica granuloma

Silicone granuloma Human adjuvant disease and sclerodermatous reactions after have been reported after such events However, large reviews have failed to establish an etiologic link to silicone and CTD’s They are no longer available in the U.S> Bioplasque consists of polymerized silicone particles dispensed in a gel carrierwhen used for lip augmentation, nodules may develop Liquid silicones, composed of long chains of dimethyl siloxy groups, are biologically inert These have been used for correction of wrinkles, reduction of scars, and for building up atrophic depressed areas of skin For breast augmentation, it was also used as silastic implants

Mercury granuloma Occur as foreign-body giant cell granulomas
Systemic toxicity may develop from cutaneous injury and may result in death

Beryllium granuloma Seen in chronic, persistent, granulomatous inflammation of skin with ulceration which may follow accidental laceration by an old-fashioned broken fluorescent lightbulb coated with zinc beryllium silicate Modern bulbs do not contain beryllium

Zirconium granuloma Papular eruption involving the axillae sometimes seen as a allergic reaction in those shaving their armpits and using a deodorant containing zirconium lactate Zirconium was eliminated from aerosol-type deodorants in 1978 It may also be seen following application of various poison ivy lotions containing zirconium compounds Lesions are brownish red, dome-shaped, shiny papules suggestive of sarcoidosis This is an acquired, delayed-type, allergic reaction resulting in a granuloma of sarcoid type; lesions spontaneously involute

Silica Granuloma They may be caused by amorphous or crystalline silicon dioxide(quartz), by magnesium silicate(talcum) or by complex polysilicates(asbestos) Talcum granulomas of skin and peritoneum may develop after surgical poerations from talcum powder used on surgical gloves Best method of cure is immediate and complete removal Automoble and other types of accidents produce tattooing of dirt(silicon dioxide) into skin, inducing silica granulomas Usually black or blue papules or macules arranged in a linear fashion At times granulomatous reactions to silica may be delayed for many years, until sensitization develops

Carbon Stain Discoloration of skin from embedded carbon usually occurs in children fron careless use of firearms or firecrackers or from a puncture wound by a pencil, which may leave a permanent black mark of embedded graphite, easily mistaken for a metatastic melanoma Carbon is deposited at various depths to produce a connective tissue reaction and even keloids Carbon particles may be removed immediately after deposition by using a tooth brush and a foreceps This provides best cosmetic outcome If left for a long time can be removed by the Q-switched neodymium-YAG laser Dermabrasion may be effective

Injectable Collagen Reactions
May occur with bovine collagen solution Major histologic differential diagnosis is granuloma annulare One report of abscess formation and local necrosis of glabellr region after Zyderm or Zyplast collagen injections Both were rare-4-9 per 10,000 pts Artecoll consists of polmethlmethacrylate micropheres suspended in bovine collagen Palpable thickening and nodules may occur when it is used for lip augmentation Pathology reveals granulomas

THE END Thank you

Dermatoses Resulting from Physical Factors

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Dermatoses Resulting from Physical Factors

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