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
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
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 .
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
Phototoxic reaction to a nonsteroidal antiinflammatory drug
Photoallergic dermatitis on sun exposed areas
Polymorphous Light Eruption
Most common form of sensitivity All races and skin types affected Typically in first three decades Females outnumber males Unknown pathogenesis Positive family history in 10-50% of pts Different morphologies seen, although in the individual the morphology is constant
PMLE
Exposed areas such as the backs of the hands and forearms are affected. Ultraviolet A is mainly responsible and may penetrate window glass
PMLE
The patchiness of the edematous papules and plaques is characteristic
PMLE
The eruption is less red and confluent than a sunburn (left) Lesions are typically papular & clustered (right)
PMLE-pathology
Characteristic perivascular mononuclear cell infiltration
PMLE
Very itchy, red,edematous papules, which may coalesce into plaques, occur 1 or 2 days after exposure to light
PMLE
This young women developed a widespread pruritic, papular eruption after using a sunbed, which emitted ultraviolet A
PMLE
Polymorphous light eruption: erythematous papulovesicular and plaque-like lesions with characteristic distribution on the sun-exposed areas of the cheek
Actinic Prurigo
The clinical features are somewhat suggestive of PML, but the lesions are persistent and the HLA type was DR4( occurs in 80-90% of AP pts)
AP
Severe actinic prurigo shows spread to buttocks (left) Arms show crusted papules that are denser distally; they are also worse in summer
Actinic prurigo
Actinic prurigo in Native American brothers
Actinic prurigo
Actinic prurigo in Native American boy
AP-pathology
Early lesions have variable acanthosis and spongiosis of the epidermis with an underlying perivascular mononuclear cell infiltrate with edema Later lesions show crusts, increasing acanthosis and variable lichenification plus a heavy infiltrate of mononuclear cells, leading to a non-specific picture(as seen here)
Hydroa Vacciniforme
Photodermatosis with onset in childhood Lesions appear in crops with disease free intervals Attacks may be preceded by fever and malaise Ears, nose, cheeks, and extensor arms and hands are affected Within 6 hrs of exposure stinging may occur
Hydroa Vacciniforme
There is an early, PML-like eruption, but with vesicles around the mouth and umbilicated lesions on the nose
Hydroa Vacciniforme
A later, more severe example shows vesiculation with umbilication, but also marked hemorrhagic crusting
Hydroa Vacciniforme
A severe example of the typical vacciniform facial scarring that may develop following repeated acute attacks
Acute Radiodermatitis
With an “erythema dose” of ionizing radiation there is a latent period of up to 24 hrs before visible erythema develops Initial erythema lasts 2-3 days but may be followed by a second phase beginning up to 1 week after the exposure and lasting up to 1 month
Acute Radiodermatitis (fluoroscopic induced)
Chronic Radiodermatitis
Chronic exposure to “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
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
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
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
Ulcer from extravascular injection of “speed” (amphetamine)
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