The skin can react to a large number ofmechanical, physical, biological and chemicalagents, acting alone or in combination.Human skin, except for palms and soles, isquite thin and of variable thickness.It has two layers: the epidermis (outer) anddermis (inner). Collagen and elasticcomponents in the dermis allow it to functionas a flexible barrier.
The skin provides a unique shield whichprotects within limits against differentphysical agents.The skin limits water loss from the body andguards against the effects of natural andartificial light, heat and cold. Intact skin andits secretions provide a fairly effectivedefence zone against these factors providingthat the degree or the severity of the injurydoes not impair this defence.
Cutaneous defence systems are effective onlywithin limits. Anything which breaches one ormore of the links endangers the entiredefence chain.A remarkable feature of cutaneous defence isthe ability of the skin to continually replacethe basal cells which provide the epidermiswith its own built-in, replication and repairsystem.
The skin’s ability to act as a heat exchanger isessential to life. Sweat glandfunction, vascular dilation and constrictionunder nervous control are vital to regulatingbody heat, as is evaporation of surface wateron skin.Constriction of the blood vessels protectsagainst cold exposures by preserving centralbody heat. Multiple nerve endings within theskin act as sensors for heat, cold and otherstimuliants.
A major skin component against injury fromultraviolet radiation, a potentially harmfulpart of sunlight and some forms of artificiallight is the pigment (melanin) manufacturedby the melanocytes located in the basal celllayer of the epidermis.Melanin granules are picked up by theepidermal cells and serve to add protectionagainst the rays of natural or artificial lightwhich penetrate the skin.
Sweat-induced reactionsMany types of work or life style involveexposure to heat and where there is toomuch heat and sweating, followed by toolittle evaporation of the sweat from the skin,prickly heat (Miliaria) can develop.When there is skin rubbing against skin, asecondary bacterial or fungal infection mayfrequently occur. This happens particularly inthe axillae, under the breast, in the groin andgluteal folds.
Pigment changeExposure to ultraviolet light may causehyperpigmentation which generally resultsfrom melanin stimulation andoverproduction.Hypopigmentation or depigmentation atselected sites can be caused by a previousburn, contact dermatitis, contact with certainhydroquinone compounds or otherantioxidant agents.
Neoplastic growthsNeoplastic lesions may be malignant or benign(cancerous or non-cancerous).Melanoma and non-melanocytic skin cancerare probable. Traumatic cysts, fibromata andkeratoacanthoma, are typical benign newgrowths. Keratoacanthomas can beassociated with excessive exposure tosunlight and it is a premalignant condition.
sunlight and ionizing radiation, among otheragents, can damage the skin cells so thatabnormal cell growth results in cancerouschange of the exposed skin.Unlike primary irritation, allergic sensitizationis the result of a specifically acquiredalteration in the capacity to react, broughtabout by T-cell activation.
Physical agentsHeat, cold, electricity, sunlight, artificial ultraviolet,laser radiation and high energy sources such as xrays, radium and other radioactive substancesare potentially injurious to skin and to the entirebody.High temperature and humidity at work or in atropical environment can impair the sweatmechanism and cause systemic effects known assweat retention syndrome. Milder exposure toheat may induce prickly heat, intertrigo (chafing),skin maceration and supervening bacterial orfungal infection, particularly in overweight anddiabetic individuals.
Thermal burns are frequently experienced in certainoccupations. Prolonged exposure to cold water orlowered temperatures causes mild to severe injuryranging from erythema to blistering, ulceration andgangrene. Frostbite affecting the nose, ears, fingersand toes of construction workers, firemen, postalworkers, military personnel and other outdoorworkers is a common form of cold injury.Electricity exposure resulting from contact with shortcircuits, bare wires or defective electrical apparatuscause burns of the skin and destruction of deepertissue.High-intensity electromagnetic energy associated withlaser beams is well able to injure human tissue,notably the eye. Skin damage is less of a risk but canoccur.
First-degree burn: active congestion of superficial bloodvesselsThis causes erythema, sometimes followed byepidermal desquamationConstitutional reactions occur if large area involvedPain and increased surface heat may be severe
DeepSuperficial Pale and anestheticTransudation of serumcausing edema of Injury to reticular dermissuperficial tissues compromises blood flow and destroysVesicles and blebs appendages Healing takes > 1 monthComplete recovery withoutscar or blemish is usual Scarring occurs
Full-thickness tissue lossSkin appendages are destroyedThere is no ◦epithelium forregenerationHealing leaves a scar
Destruction of entire skin and subcutaneousfat with any underlyingtendons
Contact- small but deep, causing some necrosis ofunderlying tissuesFlash-burns usually cover a large area andare similar to a surfaceburn and should betreated as suchLightning is the most lethal type of strike,cardiac arrest or otherinternal injuries mayoccur
-Retention of sweat as a result of occlusion-Common in hot, humid climates-Occlusion of eccrine sweat gland obstructs delivery of sweat tothe skin surface-Eventually backed-up pressure causes rupture of sweat glandor duct at different levels-Escape of sweat into adjacent tissue produces miliaria-Different forms of miliaria occur depending on the level ofinjury to the sweat gland
Aka “toasted skin” syndrome Persistent erythema or coarsely reticulated residualpigmentation resulting from itProduced by long-continued exposure to excessive heatwithout production of a burnIt begins as a mottling caused by local hemostasis andbecomes a reticulatederythema, leavingpigmentation
Characteristic changes induced bychronic sun exposure.Poikiloderma of Civatte:refers to reticulatehyperpigmentation withtelangiectasia, and slight atrophyof sides of the neck, loweranterior neck and V of chestSubmental area is sparedFrequently presents in fair-skinned men and women in theirmiddle to late thirties or earlyforties
Acute chilblains is the mildest form of coldinjuryPatients are usually unaware of injury untilthey develop burning,itching, swelling andredness
When soft tissue is frozen andlocally deprived of blood supplyFrozen part is painless andbecomes pale and waxyFour stages:I- Frost-nip erythema, edema,cutaneous anesthesia & transientpainII- second degree: hyperemia,edema & blistering, with clearfluid in bullaeIII- third-degree: full-thicknessdermal loss with hemorrhagicbullae formation or waxy, dry,mummified skinIV- full-thickness loss of entire part
Nifedipine 20mg TIDVasodilators (nicotinamide100 mg TID ordipyridamole 25 mg TID)Systemic corticoid therapy ishelpful in chilblain lupuserythematosusPentoxifylline may be usefulSmoking stronglydiscouraged
Term derived from trenchwarfare in World War I,when soldiers stood,sometimes for hours, intrenches with a few inchesof cold water in themResults from prolongedexposure to cold, wetconditions withoutimmersion or actualfreezingTreatment:-removal fromenvironment
AKA “paddy foot” in VietnamSeen after continuous immersion of the feet in water or mud oftemperatures above 71.6 degrees F (22 degrees Cº) for 2-10daysErythema, edema, and pain of the dorsal feetAlso fever and lymphadenopathyResolution occurs 3 to 7 days after the feet have been dried
Parts of solar spectrum Below 400 nm is theimportant to ultravioletphotomedicine: spectrum, divided into three bands:Visible light 400 to 760 nm UVA, 320 to 400 nm UVB, 290 to 320 nmInfrared radiation beyond UVC, 200 to 290 nm760 nmVisible light has little biologic Virtually no UVC reachesactivity, except for the earth’sstimulating the retina surface, because it is absorbed by the ozoneInfrared radiation is layerexperienced as radiant heat Exception: Australia, welders
UVB is 1000 times moreerythemogenic than UVA Amount of ultravioletUVA is 100 times greaterthan UVB radiation during exposure increasesthe midday hours at higher altitudes, is greater in tropicalMost solar erythema is regions, and temperate climatescause by UVB in summerUVA is more melanogenicand reflected from sand,snow, or ice to a greaterdegree than UVB
Sunburn is normal cutaneousreaction to sunlight inexcess of MED (minimumerythema dose=the amountthat will induce reddening)UVB erythema peaks at 12 to24 hrs after exposureDesquamation is commonabout a week after sunburneven in non-blistering areas
Cool compresses Topical steroids Topical remedy: Indomethacin 100 mgCooling agents:*Absolute ethanol*Propylene glycolspread widely over burnedarea with palms and let dry
Avoid sun exposure between 10 am and 2pmBarrier protection with hats and clothingSunscreen agents include UV-absorbingchemicals, and UV-scattering or blockingagents (physicalsunscreens)
In the case of external contactants(photosensitizers) –phototoxicity occurs oninitial exposure, has onset < 48 hrs, occursin most people exposed to the phototoxicsubstance and sunlightPhotoallergy, in contrast, occurs only insensitized persons, may have delayedonset, up to 14 days (a period ofsensitization), and shows histologicfeatures of contact dermatitis