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