Dermatoses Resulting from Physical Factors

1. Dermatoses Resulting from Physical Factors

2. -Heat Injuries. -Cold injuries. -Solar injuries. -Radiodermatitis. -Presureindused diseases.

3. Heat Injuries • Thermal Burns • Electrical Burns • Miliaria • ErythemaAbIgne

4. Thermal burns: *First-degree burn: There is active congestion of superficial blood vessels. This causes erythema, sometimes followed by epidermal desquamation. Constitutional reactions occur if large area involved. Pain and increased surface heat may be severe.

6. Deep Pale and anesthetic Injury to reticular dermis compromises blood flow and destroys appendages Healing takes > 1 month Scarring occurs Superficial Transudation of serum causing edema of superficial tissues Vesicles and blebs Complete recovery without scar or blemish is usual *Second-degree burn:

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

9. *Third degree burn: Full-thickness tissue loss. Skin appendages are destroyed. There is no epithelium for regeneration. Healing leaves a scar.

11. *Fourth degree burn: Destruction of entire skin and subcutaneous fat with any underlying tendons

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

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

14. Miliaria • Occlusion of eccrine sweat gland leads to retention of sweat with failure of 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. • Common in hot, humid climates. • Different forms of miliaria occur depending on the level of injury to the sweat gland.

15. Miliariacrystalina: • -Small, clear, superficial vesicles without inflammation. • -Appears in bedridden pts and bundled children. • -Lesions are asymptomatic and rupture at the slightest trauma. • -Self-limited; no treatment is required.

16. 2. Miliaria rubra: -Discrete, extremely pruritic, erythematous papulovesicles with sensation of prickling, burning, or tingling. -Site of injury is prickle cell layer.

17. 3. Miliaria pustulosa: -Always preceded by some injury, destruction, or blocking of sweat duct. -Pustules are independent of hair follicle and sterile. -Seen in intertriginous areas, flexure surfaces of extremities, scrotum, and back of bedridden pts.

18. 4. Miliaria profunda: -Nonpruritic, flesh-colored, deep-seated, whitish papules -Asymptomatic, usually lasting only 1 hr after overheating has ended. -Concentrated on the trunk and extremities. -Occlusion is in the upper dermis. -Only seen in tropics usually following a severe bout of miliaria rubra.

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

20. Erythema (pigmentatio) Ab Igne “toasted skin” syndrome: -Persistent erythema or coarsely reticulated residual pigmentation. -Produced by long-continued exposure to excessive heat without production of burn. -It begins as a mottling caused by local hemostasis and becomes a reticulated erythema, leaving pigmentation. -No effective treatment; they may benefit from: *Bland emollients. *Kligman’s combination of 5% hydroquinone in hydrophilic ointment containing 0.1% retinoic acid and 0.1% dexamethasone may reduce unsightly pigmentation.

22. Cold Injuries • Chilblains • Frostbite • Immersion injury

23. Chilblains: -Acute chilblains is the mildest form of cold injury, characterized by inflamed purple-pink swellings on the fingers, toes, and ears. -There is pain, itching, or burning on rewarming, caused by arteriolar and venular constriction. -Patients are usually unaware of injury until they develop burning, itching, and redness. Treatment; *Nifedipine 20mg TID, vasodilators (nicotinamide 100 mg TID or dipyridamole 25 mg TID),pentoxifylline may be useful *Smoking strongly discouraged

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

27. Immersion Foot Syndromes • Trench Foot • Warm Water Immersion Foot

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

29. Dermatosis resulting from sun exposure

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

31. Skin Types

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

33. Clinical signs and symptoms: -Sunburn is normal cutaneous reaction to sunlight in excess of an erythema dose (the amount that will induce reddening). -UVB erythema peaks at 12 to 24 hrs after exposure. -Desquamation is common about a week after sunburn even in non-blistering areas. Treatment: -Cool compresses -Topical steroids -Topical remedy: Indomethacin 100 mg Absolute ethanol 57 ml Propylene glycol 57 ml spread widely over burned area with palms and let dry

35. Prophylaxis: -Avoid sun exposure between 10 am and 2 pm. -Barrier protection with hats and clothing. -Sunscreen agents include UV-absorbing chemicals (chemical sunscreens:, and UV-scattering or blocking agents (physical sunscreens). Sunscreens: 1. Chemical sunscreens: para-aminobenzoic acid (PABA), PABA esters, cinnamates, salicylates, anthranilates, benzophenoes). 2. Physical agents: titanium/zinc dioxide. 3. Combinations of both. *Water resistant: maintaining their SPF after 40 minutes of water immersion. *Water proof: maintaining their SPF after 80 mins of water immersion. *UVA protection: sunscreens containing benzophenones or dibenzoylmethanes *Apply sunscreen at least 20mins before sun exposure

36. B. Photoaging (Dermatohelioisis): -Characteristic changes induced by chronic sun exposure -Risk of developing these changes correlated with baseline pigmentation (constitutive pigmentation) and ability to resist burning and tan following sun exposure (facultative pigmentation).

37. 1. Poikiloderma of Civatte: -Refers to reticulate hyperpigmentation with telangiectasia, and slight atrophy of sides of the neck, lower anterior 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.

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

39. Favre-Racouchot syndrome : -Thickened yellow plaques studded with comedomes and cystic lesions. -Treatment is removal , retinoic acid cream, surgical removal of cysts and redundant skin.

40. Photosensitizers may induce an abnormal reaction in skin exposed to sunlight or its equivalent. Substances may be delivered externally or internally. Increased sunburn response without prior allergic sensitization is called phototoxicity. Phototoxicity may occur from both externally applied (phytophotodermatitis and berloque dermatitis) or internally administered chemicals (phototoxic drug reaction). C. Photosensitivity:

41. Phytophotosensitivity • Plant-induced photosensitivity-linear hyperpigmentation on the face following exposure to limes and sunlight.

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

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

44. Amiodarone

45. Phototoxic reaction to a nonsteroidal antiinflammatory drug

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

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

48. Photoallergic dermatitis • Papulovesicular lesions of photoallergic dermatitis due to hexachlorophene.

49. 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

50. Drug induced photosensitivity • The backs of the hands are the classic sites to be involved in light induced eruption