Dermatoses Resulting from Physical Factors

Transcript Dermatoses Resulting from Physical Factors

Dermatoses Resulting from Physical Factors

Chapter 3 Andrew’s Diseases of the Skin Adam Wray, D.O.

November 15, 2005

Heat Injuries

        Thermal Burns Electrical Burns Miliaria Miliaria Crystalline (Sudamina) Miliaria Rubra (Prickly Heat, Heat Rash) Miliaria Pustulosa Miliaria Profunda Occlusion Miliaria

Thermal Burns

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

Second-degree burns

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Superficial

Transudation of serum causing edema of superficial tissues Vesicles and blebs Complete recovery without scar or blemish is usual     

Deep

Pale and anesthetic Injury to reticular dermis compromises blood flow and destroys appendages Healing takes > 1 month Scarring occurs

Second-degree burns

 Thermal burn: This superficial second degree burn is characterized by bullae that contain serous fluid

Second-Degree Burns

   Inflicted scalds: severe second degree burns after dipping B: two days after incident-to lower extremities and perineum C: foot and lower leg

Second-Degree Burn

  Accidental scald Splash-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 Skin appendages are destroyed  There is no epithelium for regeneration Healing leaves a scar

Fourth-degree burns

 Destruction of entire skin and subcutaneous fat with any underlying tendons

  Rule of nines: In adults, an estimate of burn extent based upon this surface area distribution chart. Infants & children have a relatively increased head; trunk surface area ratio

Electrical Burns

   Contact- small but deep, causing some necrosis of underlying tissues Flash-burns usually cover a large area and are similar to a surface burn and should be tx as such Lightening is the most lethal type of strike, cardiac arrest or other internal injuries may occur

Electrical Burns

 Indirect- burns that are either linear in areas at which sweat was present; are feathery or aborescent pattern, which is believed to be pathognomonic

Electrical Burn

 It is characterized by erythema, edema, bulla formation and sloughing of the necrotic epidermis

Electrical Burn-pathology

 Blistering and elongated keratinocytes

Miliaria

      Retention of sweat as a result of occlusion Common in hot, humid climates Occlusion of eccrine sweat gland obstructs delivery of sweat to the skin surface Eventually backed-up pressure causes rupture of sweat gland or duct at different levels Escape of sweat into adjacent tissue produces miliaria Different forms of miliaria occur depending on the level of injury to the sweat gland

Miliaria Crystalline

    Small, clear, superficial vesicles without inflammation Appears in bedridden pts and bundled children Lesions are asymptomatic and rupture at the slightest trauma Self-limited; no tx is required

Miliaria Crystallina

 Minute, discrete vesicles resulting from profuse sweating secondary to a high fever

Miliaria Crystallina

Miliaria Rubra

  Discrete, extremely pruritic, erythematous papulovesicles with sensation of prickling, burning, or tingling Site of injury is prickle cell layer where spongiosis is produced

Miliaria Rubra

Miliaria Pustulosa

    Always preceded by some injury, destruction, or blocking of sweat duct Pustules independent of hair follicle Seen in intertriginous areas, flexure surfaces of extrmities, sctrotum, and back of bedridden pts Sterile pustules

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 Occlusion is in upper dermis Only seen in tropics usually following a severe bout of miliaria rubra

Occlusion Miliaria

   May be produced with accompanying anhidrosis and increased heat stress susceptibility after application of extensive polyethylene film occlusion for > 48 hrs Tx-place pt in a cool environment Even a night in an air-conditioned room helps alleviate the discomfort

Occlusion Miliaria

   Mild cases may respond to dusting powders, such as cornstarch or baby talcum powder A lotion containing 1% menthol and glycerin and 4% salicylic acid in 95% alcohol is effective An oily “shake” lotion such as calamine lotion, with 1% or 2% phenol may be effective

Erythema (pigmentatio) Ab Igne

 Aka “toasted skin” syndrome  Persistent erythema or coarsely reticulated residual pigmentation resulting from it   Produced by long continued exposure to excessive heat without production of a burn It begins as a mottling caused by local hemostasis and becomes a reticulated erythema, leaving pigmentation

Erythema Ab Igne

 Reticulated hyperpigmentation with some epidermal atrophy and scaling secondary to use of a heating pad

Erythema ag igne

   Use of bland emollients is helpful No effective treatment Kligman’s combination of 5% hydroquinone in hydrophilic ointment containing 0.1% retinoic acid and 0.1% dexamethasone may reduce unsightly pigmentation   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

   Chilblain Frostbite Immersion injury

Chilblains

  Acute chilblains is the mildest form of cold injury Pts are usually unaware of injury until they develop burning, itching, and redness

Chilblains (pernio)

Treatment

      Nifedipine 20mg TID Vasodilators (nicotina amide 100 mg TID or dipyridamole 25 mg TID) Systemic corticoid tx is helpful in chilblain lupus erythematosus Pentoxifylline may be useful Smoking strongly discouraged

Frostbite

       When soft tissue is frozen and locally deprived of blood supply Frozen part is painless and becomes pale and waxy Four stages: I- Frost-nip erythema, edema,cutaneous anesthesia & transient pain II- second degree: hyperemia, edema & blistering, with clear fluid in bullae III- third-degree: full thickness dermal loss with hemorrhagic bullae formation or waxy, dry, mummified skin IV- full-thickness loss of entire part

First-Degree Frostbite

Immersion Foot Syndromes

  Trench Foot Warm Water Immersion Foot

Trench Foot

   Results from prolonged exposure to cold, wet conditions without immersion or actual freezing Term derived from trench warfare in World War 1, when soldiers stood, sometimes for hours, in trenches with a few inches of cold water in them Tx-removal from causal environment

Tropical immersion Foot

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

Dermatoses with Cold Hypersensitivity

   Erythrocyanosis Crurum Acrocyanosis Cold Panniculitis

Erythrocyanosis Crurum

   Slight swelling and a bluish pink tint of the skin of the legs and thighs of young girls and women May be unilateral May have cramps in the legs at night   Small tender nodules may be found on palpation  Nodules may break down and form small, multiple ulcers Seen in northern countries and probably due to an abnormal reaction of blood vessels to prolonged cold

Acrocyanosis

      A persistent cyanosis with coldness and hyperhidrosis of hands and feet Chiefly occurs in young women At times, on cold exposure, a digit becomes stark white and insensitive (acroasphyxia) Cyanosis increases as the temperature decreases and changes to erythema with elevation of dependent part Cause is unknown Smoking, coffee, and tea should be avoided

Acrocyanosis

Cold Panniculitis

    After exposure to severe cold, well-demarcated erythematous warm plaques may develop, particularly on the cheeks of young children Lesions usually develop within a few days after exposure, and resolve spontaneously in 2 weeks(approx) No tx is indicated Popsicle dermatitis is a temporary redness and induration of the cheek in children resulting from sucking Popsicles

Sunburn and Solar Erythema

     Parts of solar spectrum important to photomedicine: Visible light 400 to 760 nm Infrared radiation beyond 760 nm Visible light has little biologic activity, except for stimulating the retina Infrared radiation is experienced as radiant heat      Below 400 nm is the ultraviolet spectrum, divided into three bands: UVA, 320 to 400 nm UVB, 290 to 320 nm UVC, 200 to 290 nm Virtually no UVC reaches the earth’s surface, because it is absorbed by the ozone layer  Exception: Australia, welders

Sunburn and Solar Erythema

    UVB is 1000 times more erythemogenic than UVA UVA is 100 times greater than UVB radiation during the midday hours Most solar erythema is cause by UVB Sunlight early and late in the day contains more UVA   UVA is reflected from sand, snow, or ice to a greater degree than UVB Amount of ultraviolet exposure increases at higher altitudes, is greater in tropical regions, and temperate climates in summer

Clinical signs and symptoms

   Sunburn is normal cutaneous reaction to sunlight in excess of an erythema dose (the amount that will induce reddening) UVB erythema peaks at 12 to 24 hrs after exposure Desquamation is common about a week after sunburn even in non-blistering areas

Sunburn treatment

 Cool compresses  Topical steroids  Topical remedy: Indomethacin 100 mg Absolute ethanol 57 ml Propylene glycol 57 ml spread widely over burned area with palms and let dry

Skin Types

Second-degree sunburn

Prophylaxis

   Avoid sun exposure between 10 am and 2 pm Barrier protection with hats and clothing Suncreen agents include UV-absorbing chemicals and UV-scattering or –blocking agents(physical sunscreens)

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-maintaining their SPF after 80 mins of water immersion UVA protection sunscreens containing benzophenones or dibenzoylmethanes Apply sunscreen at least 20mins before sun exposure

Photoaging(Dermatohelioisis)

  Characteristic changes induced by chronic sun exposure Risk of developing these changes correlated with baseline pigmentation(constitutive pigmentation) and abilitiy to resist burning and tan following sun exposure(facultative pigmentation)

Dermatoheliosis

   Poikiloderma of Civatte refers to reticulate hyperpigmentation with telangiectasia, and slight atrophy of sides of the neck, lower anterior neck and V of 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

   Favre-Racouchot syndrome Thickened yellow plaques studded with comedomes and cystic lesions Tx-removal , retinoic acid cream, surgical removal of cysts and redundant skin

Solar Elastosis

  Homogenization and a faint blue color of connective tissue of the upper reticular dermis, so-called solar elastosis Characteristically there is a zone of normal connective tissue below the epidermis

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Photosensitivity

Photosensitizers may induce an abnormal reaction in skin exposed to sunlight or its equivalent Substances may be delivered externally or internally Increased sunburn response without prior allergic sensitization called phototoxicity   Phototoxicity may occur from both externally applied (phytophotodermatitis and berloque dermatitis) or internally administered chemicals (phototoxic drug reaction) Or by external contact (photoallergic contact dermatitis)

Phototoxicity vs photoallergy

 In the case of external contactants – phototoxicity occurs on initial exposure, has onset < 48 hrs, occurs in most people exposed to the phototoxic substance and sunlight  Photoallergy, in contrast, occurs only in sensitized persons, may have delayed onset, up to 14 days( a period of sensitization), and shows histologic features of contact dermatitis

Photosensitivity

 Drug-induced 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

Photosensitivity in Tattoos

  Yellow cadmium sulfide may be used as a yellow dye or may be incorporated into red mercuric sulfide pigment to produce a brighter red color for tattooing When exposed to 380, 400, and 450 nm wavelengths of light, these areas in tattoos may swell, develop erythema, and become verrucose

Phototoxic Drug Reactions

  Most occur from tetracyclines, nonsteroidal antiinflammatory drugs, amiodarone, and phenothiazines Action spectrum for all is in the UVA range   In the case of amiodarone and chlorpromazine, hyperpigmentation is a well-recognized pattern of phototoxicity It causes slate blue(amiodarone) or slate gray (chlorpromazine) coloration, resulting from drug deposition in the tissues

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 .

  With an “erythema dose” of ionizing radiation there is a latent period of up to 24 hrs before visible erythema develops Initial erythema lasts 2-3 days but may be followed by a second phase beginning up to 1 week after the exposure and lasting up to 1 month

Acute Radiodermatitis (fluoroscopic induced)

Chronic Radiodermatitis

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

Radiation Cancer

      After a latent period averaging 20 –30 yrs, various malignancies may develop Most frequent are basal cell carcinomas Next frequent are squamous cell carcinomas These may occur in sites of prior radiation even without evidence of chronic radiation damage SCCs arising in sites of radiation therapy metastasize more frequently than purely sun-induced SCCs Other cancers induced by radiation :angiosarcoma, malignant fibrous histiocytoma, sarcomas, and thyroid carcinoma

Radiation Cancer

 SCC developing in a chronic radiation ulcer on the chest

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Callus

Nonpenetrating, circumscribed hyperkeratosis produced by pressure Occurs on parts subject to intermittent pressure(palms, soles, bony prominences of the joints) Callus differs from clavus in that a callus has no penetrating central core and is a more diffuse thickening Calluses tend to disappear spontaneously when pressure is removed

Clavus(Corns)

    Circumscribed, horny, conical thickenings with the base on the surface and the apex pointing inward and pressing on adjacent structures Two types:hard and soft Hard:occur on dorsa of toes or on soles Soft:occur between toes, softened by macerating action of sweat

Hard Corn

  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

Corns

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Porokeratosis Plantaris Discreta

Multiple lesions can occur Females are affected 3 times as frequently than men It is painful Frequently confused with a plantar wart or corn Keratosis punctata of the palmar creases may be seen in the creases of the digits of the feet where it may be mistaken for a corn

Surfer’s Nodules

     Nodules 1 to 3 cm (rarely as much as 5 or 6 cm) Sometimes eroded or ulcerated Develop on tops of feet or over tibial tubercles of surfboard riders who paddle their boards in a kneeling position, as is customary in cold water off the California coast Nodules seldom occur in surfers in warmer waters like Hawaii,because a prone position is used Nodules involute over months when there is no surfing

Pressure Ulcers (Decubitus)

    The bedsore is a pressure ulcer produced anywhere on the body by prolonged pressure Caused by ischemia of underlying structures of skin, fat, and muscles resulting from sustained and constant pressure Usually in chronically debilitated persons unable to change position Bony prominences of body are most frequently involved

Care-Tx

     Ulcer care is critical Debridement-except stable heel ulcers(do not need debridement if only a dry eschar is present) Clean wounds initially and at each dressing change via nontraumatic technique Normal saline is best Dressing selection should maintain moist environment    Occlusive dressings like film and hydrocolloid are often utilized Surgical debridement with reconstructive procedures may be needed Electrical stimulation of refractory ulcers may be beneficial

Friction Blisters

   Formation of vesicles or bullae occurring at sites of combined pressure and friction Enhanced by heat and moisture Examples: feet of military recruits in training,palms of oarsmen not having developed protective calluses, beginning drummers (“drummer’s digits”)

Sclerosing Lymphangiitis

     Cordlike structure encircling the coronal sulcus of the penis, or running the length of the shaft Attributed to trauma Produced by a sclerosing lymphangiitis No tx is needed Follows a benign, self limiting course

Black Heel

    Also called talon noir , calcaneal petechiae, chromidrose plantaire and 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

     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

Painful Fat Herniation

  Avoidance of prolonged standing is the only way to provide relief Majority of people experience no symptoms

Painful Fat Herniation