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Dermatoses Resulting from Physical Factors

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Title: Dermatoses Resulting from Physical Factors


1
Dermatoses Resulting from Physical Factors
  • Chapter 3
  • Andrews Diseases of the Skin
  • JoAnne M. LaRow, D.O.

2
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

3
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

4
Second-degree burns
  • Deep is pale and anesthetic
  • Injury to reticular dermis compromises blood flow
    and destroys appendages
  • Healing takes gt 1 month
  • Scarring occurs
  • 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

5
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

6
Second-Degree Burn
  • Accidental scald
  • Splash-and-droplet pattern of an accidental scald
    from hot cup of tea

7
Second-Degree Burn
  • Curling iron burn

8
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

9
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

10
Thermal Burns
  • Prognosis is poor when large surfaces are
    involved
  • Particularly when gt 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

11
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

12
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

13
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

14
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

15
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

16
Electrical Burn
  • It is characterized by erythema, edema, bulla
    formation and sloughing of the necrotic epidermis

17
Electrical Burn-pathology
  • Blistering and elongated keratinocytes

18
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

19
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

20
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

21
Miliaria Crystallina
  • Minute, descrete vesicles resulting from profuse
    sweating secondary to a high fever

22
Miliaria Crystallina
23
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

24
Miliaria Rubra
25
Miliaria Pustulosa
  • 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

26
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

27
Postmiliarial Hypohidrosis
  • Results from occlusion of sweat ducts and pores
    and may be severe enough to impair ones 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

28
Tropical Anhidrotic Asthenia
  • Rare form of miliaria with long-lasting pore
    occlusion, producing anhidrosis and heat retention

29
Occlusion Miliaria
  • May be produced with accompanying anhidrosis and
    increased heat stress susceptibility after
    application of extensive polyethylene film
    occlusion for gt 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

30
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

31
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

32
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 Bowens 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

33
Erythema Ab Igne
  • Reticulated hyperpigmentation with some epidermal
    atrophy and scaling secondary to use of a heating
    pad

34
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

35
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

36
Treatment
  • Use of bland emollients is helpful
  • No effective treatment
  • Kligmans 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

37
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

38
Chilblains
  • 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
  • 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

39
Chilblains (pernio)
40
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

41
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

42
Frostbite
43
First-Degree Frostbite
44
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

45
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

46
Immersion Foot Syndromes
  • Trench Foot
  • Warm Water Immersion Foot

47
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

48
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

49
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

50
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

51
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

52
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

53
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

54
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

55
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)

56
  • 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 adults
    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

57
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 earths surface,
    because it is absorbed by the ozone layer

58
  • 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 individuals 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

59
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

60
  • Delayed tanning is induced by UVB and UVC
    wavelengths and begin 2 to 3 days after exposure
    and last 10-14 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 individuals 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

61
  • 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

62
Skin Types
63
Second-degree sunburn
64
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

65
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

66
Ephelis (Freckle)
  • Small (lt0.5cm) 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

67
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

68
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

69
  • 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 (Milians 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

70
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

71
Dermatoheliosis
  • On the face or chest a macroscopic, translucent
    papule with a pearly color resembling a basal
    cell carcinoma may occur
  • This is Dubreuilhs elastoma, actinic elastic
    plaque
  • Similar plaques may occur on the helix or
    antihelix of ear

72
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

73
Dermatoelastosis
  • Cutis rhomboidalis nuchae (sailors neck or
    farmers 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

74
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

75
  • 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

76
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

77
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

78
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 lt 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

79
  • 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 lt 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

80
  • 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

81
Photosensitivity
  • Drug-induced photosensivity-photoallergic
    dermatitis on sun-exposed areas of an infant
    following topical use of hexachlorophene

82
Photoallergic dermatits
  • Papulovesicular lesions of photoallergic
    dermatitis due to hexachlorophene

83
Phytophotosensitivity
  • Plant-induced photosensitivity-linear
    hyperpigmentation on the face of a child
    following exposure to limes and sunlight

84
Phytophotosensitivity
  • Hyperpigmentation on the dorsal aspect of the
    hands following the use of limes and sunlight
    exposure

85
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 48-96 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

86
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

87
  • 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-tim
    e
  • Phytophotodermatits from squeezing limes

88
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)

89
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

90
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, demthylchlortetracyc
    line 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

91
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

92
Drug-induced photosensitivity
  • Not only the nose was but also the V of the
    neck which was highly suggestive of phototoxicity
  • Same pt

93
Drug-induced photosensitivity
  • There is erythema and edema on the exposed sites,
    the V of the neck .
  • This distribution would suggest the diagnosis

94
Drug induced photosensitivity
  • The backs of the hands are the classic sites to
    be involved in light induced eruption
  • Same pt

95
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

96
  • Phototoxic reaction to a nonsteroidal
    antiinflammatory drug

97
  • Photoallergic dermatitis on sun-exposed areas

98
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

99
Treatment
  • Both acute and chronic photosensitivity are
    treated similarly to any other inflammatory
    dermatitis, with topical corticosteroids

100
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

101
PLE
  • 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 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

102
PML
  • Exposed areas such as the backs of the hands and
    forearms are affected. Ultraviolet A is mainly
    responsible and may penetrate window glass

103
PML
  • The patchiness of the edematous papules and
    plaques is characteristic

104
PML
  • The eruption is less red and confluent than a
    sunburn

105
PML
  • The lesions are typically papular and clustered

106
PML-pathology
  • Characteristic perivascular mononuclear cell
    infiltration

107
PML
  • Very itchy, red,edematous papules, which may
    coalesce into plaques, occur 1 or 2 days after
    exposure to light

108
PML
  • This young women developed a widespread pruritic,
    papular eruption after using a sunbed, which
    emitted ultraviolet A

109
Juvenile springeruption
  • 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
  • Therapeuticallysunscreen, avoiding sun, topical
    steroids for itch and clearing eruption,
    antihistamines, systemic steroids,
    hydroxtchloroquine sulfate, chloroquine, PUVA,
    thalidomide, Azathioprine
  • 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

110
PML
  • Polymorphous light eruption erythematous
    papulovesicular and plaque-like lesions with
    characteristic distribution on the sun-exposed
    areas of the cheek

111
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

112
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

113
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)

114
AP
115
Actinic prurigo
  • Actinic prurigo in Native American brothers

116
Actinic prurigo
  • Actinic prurigo in Native American boy

117
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)

118
Solar Urticaria
  • Wavelengths of sensitivity may vary with anatomic
    location and over time with same pt
  • Leenutaphong et al divided SU into two typesType
    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

119
Solar Urticaria
  • Sunlight-induced whealing with surrounding
    erythema of the abdomen

120
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

121
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

122
HV
  • Hydroa vacciniforme-the face was also involved

123
Hydroa Vacciniforme
  • There is an early, PML-like eruption, but with
    vesicles around the mouth and umbilicated lesions
    on the nose

124
Hydroa Vacciniforme
  • A later, more severe example shows vesiculation
    with umbilication, but also marked hemorrhagic
    crusting

125
Hydroa Vacciniforme
  • A severe example of the typical vacciniform
    facial scarring that may develop following
    repeated acute attacks

126
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

127
Chronic Actinic Dermatitis
  • A disease concept in evolution
  • Previously known as persitent light reactivity,
    actinic reticuloid, photosensitive eczema and
    chronic photosensitivity dermatitis
  • Basic components area 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

128
Chronic Actinic Dermatitis
129
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

130
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(albi
    nism, vitiligo)
  • Heritable disorders with increased sensitivity to
    ultraviolet cellular or DNA damage such as
    xeroderma pigmentosum, Bloom syndrome, and
    Cockaynes disease
  • Disease where ultraviolet light seems to act by a
    Koebners phenomenon- Dariers, and perhaps
    pemphigus foliacus

131
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
  • 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

132
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

133
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

134
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

135
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

136
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

137
Radiation Cancer
  • SCC developing in a chronic radiation ulcer on
    the chest

138
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 glycol1 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

139
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 typeshard and soft
  • Hardoccur on dorsa of toes or on soles
  • Softoccur between toes, softened by macerating
    action of sweat

140
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

141
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

142
Hard Corn
143
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

144
Corns-tx
  • 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
  • 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

145
Surfers Nodules
  • Nodules 1 to 3 cm (rarely as much as 5 or 6 cm)
  • Sometimes eroded or ulcerated
  • Develop on top
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