3 - DERMATOSES RESULTING FROM PHYSICAL FACTORS Flashcards

Question

Treatmen of frostbite

Answer 1

Early treatment of frostbite before swelling develops should consist of covering the part with clothing or with a warm hand or other body surface to maintain a slightly warm temperature so that adequate blood circulation can be maintained. Rapid rewarming in a water bath between 37°C and 43°C (100°F and 110°F) is the treatment of choice for all forms of frostbite. Rewarming should be delayed until the patient has been removed to an area where there is no risk of refreezing. Slow thawing results in more extensive tissue damage Analgesics should be administered because of the considerable pain experienced with rapid thawing When the skin flushes and is pliable, thawing is complete The use of tissue plasminogen activator to lyse thrombi decreases the need for amputation if given within 24 hours of injury. Infusion of the vasodilator iloprost may be used if available. Supportive measures such as bed rest, a high-protein/high-calorie diet, wound care, and avoidance of trauma are imperative. Any rubbing of the affected part should be avoided, but gentle massage of proximal portions of the extremity that are not numb may be helpful. The use of anticoagulants to prevent thrombosis and gangrene during the recovery period has been advocated. Pentoxifylline, ibuprofen, and aspirin may be useful adjuncts. Antibiotics should be given as a prophylactic measure against infection, and tetanus immunization should be updated. Recovery may take many months. Injuries that affect the proximal phalanx or the carpal or tarsal area, especially when accompanied by a lack of radiotracer uptake on bone scan, have a high likelihood of requiring amputation. Whereas prior cold injury is a major risk factor for recurrent disease, sympathectomy may be preventive against repeated episodes. Arthritis may be a late complication.

Answer 2

**Trench foot** The term is 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. Fishermen, sailors, and shipwreck survivors may be seen with this condition. The lack of circulation produces edema, paresthesias, and damage to the blood vessels. Similar findings may complicate the overuse of ice, cold water, and fans by patients trying to relieve the pain associated with erythromelalgia. Gangrene may occur in severe cases. Treatment consists of removal from the causal environment, bed rest, and restoration of the circulation. Other measures, such as those used in the treatment of frostbite, should be employed.

Answer 3

maceration, blanching, and wrinkling of the soles and sides of the feet Itching and burning with swelling may persist for a few days after removal of the cause, but disability is temporary. This condition was often seen in military service members in Vietnam but has also been seen in persons wearing insulated boots. Warm water immersion foot can be prevented by allowing the feet to dry for a few hours in every 24 or by greasing the soles with a silicone grease once a day. Recovery is usually rapid if the feet are thoroughly dry for a few hours. \*I think the picture pertains to warm water immersion foot

Answer 4

Warm water immersion foot should be differentiated from tropical immersion foot, seen after continuous immersion of the feet in water or mud at temperatures above 22°C (71.6°F) for 2–10 days. This was known as “paddy foot” in Vietnam. It involves erythema, edema, and pain of the dorsal feet, as well as fever and adenopathy (Fig. 3 10). Resolution occurs 3–7 days after the feet have been dried

Answer 5

The parts of the solar spectrum important in p medicine include UV radiation (below 400 nm), visible light (400–760 nm), and infrared radiation (beyond 760 nm).

Answer 6

* UVA, 320 400 nm; * UVA is divided into two subcategories: * UVA I (340–400 nm) and * UVA II (320–340 nm) * UVB, 280–320 nm; and * UVC, 200–280 nm. * Virtually no UVC reaches the Earth’s surface because it is absorbed by the ozone layer above the Earth.

Answer 7

Minimal Erythema Dose (MED) Although he amount of UVA radiation is 100 times greater than UVB radiation during midday hours, UVB is up to 1000 times more erythemogenic than UVA, and so essentially all solar erythema is caused by UVB.

Answer 8

**308 nm** Although it does not play a significant role in solar erythema, UVA is of major importance in patients with druginduced photosensitivity and also play a role in photoaging and cutaneous immunosuppression. The amount of UV exposure increases at higher altitudes, is substantially larger in temperate climates in the summer months, and is greater in tropical regions. UVA may be reflected somewhat more than UVB from sand, snow, and ice. Whereas sand and snow reflect as much as 85% of the UVB, water allows 80% of the UV o penetrate up to 3 feet. Cloud cover, although blocking substantial amounts of visible light, is a poor UV absorber. During the middle 4–6 hours of the day, the intensity of UVB is 2–4 times greater than in the early morning and late afternoon

Answer 9

**At around 6 hours after exposure and peaks at 12–24 hours, but the onset is sooner and the severity greater with increased exposure.** The erythema is followed by tenderness and in severe cases, blistering, which may become confluent (Fig. 3.11). Discomfort may be severe; edema typically occurs in the extremities and face; chills, fever, nausea, tachycardia, and hypotension may be present. In severe cases, such symptoms may last for as long as a week. Desquamation is common about 1 week after sunburn, even in areas that have not blistered. **F g. 3.11 Acute sunburn**

Answer 10

**immediate pigment darkening (IPD, Meirowsky phenomenon) and delayed melanogenesis** IPD is maximal within hours after sun exposure and results from metabolic changes and redistribution of the melanin already in the skin. It occurs after exposure to long-wave UVB, UVA, and visible light. With large doses of UVA, the initial darkening is prolonged and may blend into the delayed melanogenesis. IPD is not photoprotective. Delayed tanning is induced by the same wavelengths of UVB that induce erythema, begins 2–3 days after exposure, and lasts 10–14 days. Delayed melanogenesis by UVB is mediated through the production of DNA damage and the formation of cyclobutane pyrimidine dimers (CPD). Therefore, although UVB-induced delayed tanning does provide some protection from further solar injury, it is at the expense of damage to the epidermis and dermis. Tanning is not recommended for sun protection. Commercial tanning bed–induced tanning, while increasing skin pigment, does not increase UVB MED and is therefore not protective for UVB damage. Such tanning devices have been shown to cause melanoma, and their use for tanning purposes should be banned. An individual’s inherent baseline pigmentation, ability to tan, and susceptibility to burns are described as the person’s “skin type.” Skin type is used to determine starting doses of phototherapy and sunscreen recommendations and reflects the risk of development of skin cancer and photoaging (Table 3 1).

Answer 11

**epidermis, especially the stratum corneum** This increased epidermal thickness leads to increased tolerance to further solar radiation. Patients with vitiligo may increase their UV exposure without burning by this mechanism.

Answer 12

Once redness and other symptoms are present, treatment of sunburn has limited efficacy. The damage is done, and the inflammatory cascades are triggered. Prostaglandins, especially of the E series, are important mediators. Aspirin (acetylsalicylic acid [ASA]) and nonsteroidal antiinflammatory drugs (NSAIDs), including indomethacin, have been studied, as well as opical and systemic steroids. Medium-potency (class II) topical steroids applied 6 hours after the exposure (when erythema first appears) provide a small reduction in signs and symptoms. Oral NSAIDs and systemic steroids have been tested primarily before or immediately after sun exposure, so there is insufficient evidence to recommend their routine use, except immediately after solar overexposure. Therefore treatment of sunburn should be supportive, with pain management (using acetaminophen, ASA, or NSAIDs), plus soothing topical emollients or corticosteroid lotions. In general, a sunburn victim experiences at least 1 or 2 days of discomfort and even pain before much relief occurs.

Answer 13

Use of the UV index facilitates taking adequate precautions to prevent solar injury. Numerous educational programs have been developed to make the public aware of the hazards of sun exposure. Despite this, sunburn and excessive sun exposure continue to occur in the United States and Western Europe, especially in white persons under age 30, more than 50% of whom report at least one sunburn per year. Sun protection programs have the following four main messages: ## Footnote **• Avoid midday sun.** **• Seek shade.** **• Wear sun-protective clothing.** **• Apply a sunscreen.**

Answer 14

**between 9 AM and 3–4 PM**, accounts for the vast majority of potentially hazardous UV exposure. This is the time when the angle of the sun is less than 45 degrees, or when a person’s shadow is shorter than his or her height. In temperate latitudes, it is almost impossible to burn if these hours of sun exposure are avoided. Trees and artificial shade provide substantial protection from UVB. Foliage in trees provides the equivalent of sun protection factor (SPF) 4–50, depending on the density of the greenery. Clothing can be rated by its ability to block UVB radiation. The scale of measure is the UV protection factor (UPF), analogous to SPF in sunscreens. Although it is an in vitro measurement, UPF correlates well with the actual protection the product provides in vivo. In general, denser weaves, washed older clothing, and loose-fitting clothes screen UVB more effectively. Wetting a fabric may substantially reduce its UPF. Laundering a fabric in a Tinosorb-containing material (SunGuard) will add substantially to the UPF of the fabric. Hats with at least a 4-inch brim all around are recommended.

Answer 15

**sun protection factor (SPF)** This is the ratio of the number of MEDs of radiation required to induce erythema through a film of sunscreen (2 mg/cm2 ) compared with unprotected skin. Most persons apply sunscreens in too thin a film, so the actual “applied SPF” is about half that on the label. Sunscreen agents include UV absorbing chemicals (chemical sunscreens) and UV-sca tering or blocking agents (physical sunscreens). Available sunscreens, especially those of high SPFs (\>30), usually contain both chemical sunscreens (e.g , p-aminobenzoic acid [PABA], PABA esters, cinnamates, salicylates, anthranilates, benzophenones, benzylidene camphors such as ecamsule [Mexoryl], dibenzoylmethanes [Parsol 1789, in some products present as multicompound technology Helioplex], and Tinosorb [S/M]) and physical agents (zinc oxide or titanium dioxide). Sunscreens are available in numerous formulations, including sprays, gels, emollient creams, and wax sticks. Sunscreens may be water resistant, with some maintaining their SPF after 40 minutes of water immer sion and others maintaining their SPF after 80 minutes of water immersion.

Answer 16

**For skin types I to III (see Table 3.1), daily application of a broad-spectrum sunscreen with an SPF of 30 in a facial moisturizer, foundat on, or aftershave is recommended.** For outdoor exposure, a sunscreen of SPF 30 or higher is recommended for regular use. In persons with severe photosensitivity and at times of high sun exposure, high-intensity sunscreens of SPF 30+ with inorganic blocking agents may be required. Application of the sunscreen at least 20 minutes before and 30 minutes after sun exposure has begun is recommended. This dual-application approach will reduce the amount of skin exposure by twofold to threefold over a single application. Sunscreen should be reapplied after swimming or vigorous activity or toweling. Sunscreen failure occurs mostly in men, from failure to apply it to all the sun-exposed skin or failure to reapply sunscreen after swimming. Sunscreens may be applied to babies (under 6 months) on limited areas. Vitamin D supplementation is recommended with the most stringent sun protection practices. The dose is 600 IU daily for those 70 and younger and 800 IU for older patients.

Answer 17

**UVA as well as UVB** For this reason, sunscreens with improved UVA coverage have been developed. Those containing excellent protection for both UVB and UVA are identified on the label by the words “broad spectrum,” and these sunscreens should be sought by patients.

Answer 18

**Ephelis (Freckle)** They become prominent during the summer when exposed to sunlight and subside, sometimes completely, during the winter when there is no exposure. Blonds and redheads with blue eyes and of Celtic origin (skin types I or II) are especially susceptible. Ephelides may be genetically determined and may recur in successive generations in similar locations and patterns. They usually appear at about age 5 years.

Answer 19

**Lentigo** The intensity of the color is not dependent on sun exposure. The solar lentigo appears at a later age, mostly in persons with long-term sun exposure The backs of the hands and face (especially the forehead) are favored sites (Fig. 3.12). **Fig. 3.12 Solar lentigines.** Histologically, the ephelis shows increased production of melanin pigment by a normal number of melanocytes. Otherwise, the epidermis is normal, whereas the lentigo has elongated rete ridges that appear to be club shaped.

Answer 20

Freckles and solar lentigines are best prevented by appropriate sun protection. Cryotherapy, topical retinoids, hydroquinone, intense pulse light, undecylenoyl phenylalanine, and lasers are effective in the treatment of solar lentigines.

Answer 21

**photoaging or dermatoheliosis** An individual’s risk for developing these changes correlates with the person’s skin type (see Table 3.1). Risk for melanoma and nonmelanoma skin cancer is also related to skin type.

Answer 22

**skin type I: blue-eyed, fair-complexioned persons who do not tan** They are frequently of Irish or other Celtic or Anglo-Saxon descent. Individuals who develop photoaging have the genetic susceptibility and have had sufficient actinic damage to develop skin cancer, and they therefore require more frequent and careful cutaneous examinations. Chronic sun exposure and chronologic aging are additive. Cigarette smoking is also important in the development of wrinkles, resulting in the inability of observers to distinguish solar-induced from smoking-induced skin aging accurately. The areas primarily affected by photoaging are those regularly exposed to the sun: the V area of the neck and chest, back and sides of the neck, face, backs of the hands and extensor arms, and in women the skin between the knees and ankles. The skin becomes atrophic, scaly, wrinkled, inelastic, or leathery with a yellow hue (milian citrine skin). In some persons of Celtic ancestry, dermatoheliosis produces profound epidermal atrophy without wrinkling, resulting in an almost translucent appearance of the skin through which hyperplastic sebaceous glands and prominent telangiectasias are seen (Fig. 3.13). These persons are at high risk for nonmelanoma skin cancer. Pigmentation is uneven, with a mixture of poorly demar cated, hyperpigmented and white atrophic macules observed. The photodamaged skin appears generally darker because of these irregularities of pigmentation; in addition, dermal hemosiderosis occurs from actinic purpura. Solar lentigines occur on the face and dorsa of the hands. **Fig. 3.13 Dermatoheliosis.**

Answer 23

**solar (actinic) elastosis**, which imparts a yellow color to the skin Many clinical variants of solar elastosis have been described, and an affected individual may simultaneously have many of these changes. Small yellowish papules and plaques may develop along the sides of the neck. They have been variably named “striated beaded lines” (the result of sebaceous hyperplasia) or “fibroelastolytic papulosis” of the neck, which is caused by solar elastosis At times, usually on the face or chest, this elastosis may form a macroscopic, translucent papule with a pearly color that may closely resemble a basal cell carcinoma (actinic elastotic plaque). Similar plaques may occur on the helix or antihelix of the ear (elastotic nodules of the ear).

Answer 24

**Fig. 3.14 Poikiloderma of Civatte** Poikiloderma of Civatte frequently presents in fair-skinned men and women in their mid to late thirties or early forties.

Answer 25

**Fig. 3.15 Cutis rhomboidalis nuchae (sailor’s or farmer’s neck)** The skin on the back of the neck becomes thickened, tough, and leathery, and the normal skin markings are exaggerated.

Answer 26

**Fig. 3.16 Favre-Racouchot Syndrome** These lesions appear as thickened yellow plaques studded with comedones and keratinous cysts. The ears may exhibit one or more firm nodules on the helix, known as weathering nodules. Biopsy reveals fibrosis and cartilage metaplasia.

Answer 27

**dermatoporosis** Most frequently, patients complain that even minimal trauma to their extensor arms leads to an ecchymosis, a phenomenon called actinic purpura. As the ecchymoses resolve, dusky brown macules remain for months, increasing the mottled appearance of the skin. Deep dissecting hematomas may result as well, causing large areas of necrosis. Again, minor trauma may lead to a painful deep bruise or simply erythema, without fever. This severe complication of dermatoporosis occurs primarily on the legs of elderly women, many of whom are taking anticoagulants or systemic steroids. Slowly growing erythematous plaques called acquired elastotic hemangiomas, which show horizontal proliferation of capillary blood vessels in the upper dermis, may also appear on the sundamaged skin of the arms and neck. White stellate pseudoscars on the forearms are a frequent complication of this enhanced skin fragility. In some patients, soft, flesh-colored to yellow papules and nodules coalesce on the forearms to form a cordlike band extending from the dorsal to the flexural surfaces (solar elastotic bands).

Answer 28

**reactive oxygen species (ROS) and hydrogen peroxide** Acting through activator protein 1 (AP-1), transcription of various matrix-degrading enzymes is upregulated, specifically matrix metalloproteinase 1 (MMP-1; collagenase), MMP-3 (stromelysin 1), and MMP-9 (gelatinase). In darkly pigmented persons, UV exposure does not activate MMP-1, in part explaining the protective effect of skin pigmentation against photoaging. In chro ologically aged skin, MMP-1 levels are also increased through AP-1. Thus chronologic aging and photoaging may be mediated through an identical biochemical mechanism.

Answer 29

**solar elastosis** This “elastotic” material is derived largely from elastic fibers, stains with histochemical stains for elastic fibers, and demonstrates marked increased deposition of fibulin 2 and its breakdown products. Types I and III collagen are decreased. Characteristically there is a zone of normal connective tissue immediately below the epidermis and above the elastotic material.

Answer 30

**adult and juvenile** ## Footnote In both the adult and the juvenile form of colloid milium, the primary skin lesion is a translucent, flesh colored or slightly yellow, 1–5 mm papule. Minimal trauma may lead to purpura from vascular fragility. Histologically, the colloid consists of intradermal, amorphous fissured eosinophilic material. In adult colloid milium, lesions appear in the sun exposed areas of the hands, face, neck, forearms, and ears in middle-age and older adults, usually men. Lesions often coalesce into plaques and may rarely be verrucous. Petrochemical exposures have been associated with adult colloid milium. Pigmented forms of colloid milium are associated with hydroquinone use. Lesions have been induced by tanning bed exposure, and they can be unilateral, usually in commercial drivers. Adult colloid milium may be considered a papular variant of solar elastosis. The colloid material is derived from elastic fibers, and solar elastosis is found adjacent to the areas of colloid degeneration histologically. Juvenile colloid milium is much rarer. It develops before puberty, and there may be a family history. The lesions are similar to the adult form but appear initially on the face, later extending to the neck and hands. Sun exposure also appears to be important in inducing lesions of juvenile colloid milium. Juvenile colloid milium, ligneous conjunctivitis, and ligneous periodontitis may appear in the same patient and are probably of similar pathogenesis. Histologically, juvenile colloid milium can be distinguished from ad lt colloid milium by the finding of keratinocyte apoptosis in the overlying epidermis. The colloid material in juvenile colloid milium is derived from the apoptotic keratinocytes and stains for cytokeratin. Treatment with fractional photothermolysis or MALphotodynamic therapy may be effective for colloid milium.

Answer 31

Because both UVB and UVA are capable of inducing the tissuedestructive biochemical pathways implicated in photoaging, sun protection against both portions of the UV spectrum is the primary prevention required against photoaging. Because photoaging, as with other forms of radiation damage, appears to be cumulative, reducing the total lifetime UV exposure is the goal. The guidelines previously outlined for sunburn prophylaxis should be followed. The regular use of emollients or moisturizing creams on the areas of sun damage will reduce scaling and may improve fragility by making the skin more pliable. α-Hydroxy acids may improve skin texture when used in lower, nonirritating concentrations. Topical tretinoin, adapalene, and tazaro ene can improve the changes of photoaging. Changes are slow and irritation may occur. Chemical peels, resurfacing techniques, laser and other light technologies (for vascular alterations, pigmented lesions, and dermal alterations), botulinum toxins, and soft tissue augmentation are all used to treat the consequences of photoaging. The surgical and laser treatments of photoaging are discussed in Chapter 38.

Answer 32

**photosensitizers**

Answer 33

**phototoxicity** ## Footnote Phototoxicity may occur from both externally applied (phytophotodermatitis and berloque dermatitis) and internally administered chemicals (phototoxic drug reaction). In contrast, photoallergic reactions are true allergic sensitizations triggered by sunlight, produced either by internal administration (photoallergic drug reaction) or by external contact (photoallergic contact dermatitis) Chemicals capable of inducing phototoxic reactions may also produce photoallergic reactions. In the case of external contactants, the distinction between phototoxicity and photoallergy is usually straightforward. Phototoxicity occurs on initial exposure, has an onset of less than 48 hours, occurs in the vast majority of persons exposed o the phototoxic substance and sunlight, and shows a histologic pattern similar to sunburn. By contrast, photoallergy occurs only in sensitized persons, may have a delayed onset (up to 14 days, the period of initial sensitization), and shows histologic features of allergic contact dermatitis.

Answer 34

**Action Spectrum** ## Footnote The action spectrum is included in the absorption spectrum of the photosensitizing chemical. The action spectrum that produces phototoxicity is mostly in the long ultraviolet (UVA) region and may extend into the visible light region (320–425 nm). Photosensitivity reactions occur only when there is sufficient concentration of the photosensitizer in the skin, and when 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 generally dose dependent and is worse with a greater dose of photosensitizer and greater light exposure.

Answer 35

**phototoxic reaction** It is a sunburn-type reaction, with erythema, tenderness, and even blistering occurring only on the sun-exposed parts. This type of reaction can be elicited in many persons who have no previous history of exposure or sensitivity to that particular substance, but individual susceptibility varies widely. In general, to elicit a phototoxic reaction, a considerably greater amount of the photosensitizing substance is necessary than that needed to induce a photoallergic reaction. The erythema begins, as with any sunburn, within 2–6 hours but worsens for 48–96 hours before beginning to subside. Exposure of the nail bed may lead to onycholysis, called photo-onycholysis (Fig. 3.17). Phototoxic reactions, especially from topically applied photosensitizers, may cause marked hyperpigmentation, even without significant preceding erythema. **Fig. 3.17 Photo-onycholysis from minocycline.**

Answer 36

Coal tar, creosote, crude coal tar, or pitch, in conjunction with sunlight exposure, may induce a sunburn reaction associated with a severe burning sensation. These volatile hydrocarbons may be airborne, so the patient may give no history of touching tar products. The burning and erythema may continue for 1–3 days. Although up to 70% of white persons exposed to such a combination develop this reaction, persons with type V or VI skin are protected by their constitutive skin pigmentation. After the acute reaction, hyperpigmentation occurs, which may persist for years. Coal tar or its derivatives may be found in cosmetics, drugs, dyes, insecticides, and disinfectants.

Answer 37

**phytophotodermatitis** Several hours after exposure, a burning erythema occurs, followed by edema and the development of vesicles or bullae. An intense residual hyperpigmentation results that may persist for weeks or months. The intensity of the initial phototoxic reaction may be mild and may not be recalled by the patient despite significant hyperpigmentation. Fragrance products containing bergapten, a component of oil of bergamot, will produce this reaction. If a fragrance containing this 5-methoxypsoralen or other furocoumarin is applied to the skin before exposure to the sun or tanning lights, berloque dermatitis may result. This hyperpigmentation, which may be preceded by redness and edema, occurs primarily on the neck and face. Artificial bergapten-free bergamot oil and laws limiting the use of furocoumarins in Europe and the United States have made this a rare condition. However, “Florida Water” and “Kananga Water” colognes, formerly popular in the Hispanic, African American, and Caribbean communities, contain this potent photosensitizer and can still be ordered online, as can other aromatherapy products containing furocoumarins.

Answer 38

Most phototoxic plants are in the Umbelliferae, Rutaceae (rue), Compositae, and Moraceae families. Incriminated plants include agrimony, angelica, atrillal, bavachi, buttercup, common rice, cowslip, dill, fennel, fig, garden and wild carrot, garden and wild parsnip, gas plant, goose foot, zabon, lime and Persian lime (Fig. 3.18), lime bergamot, masterwort, mustard, parsley, St. John’s wort, and yarrow. In Hawaii, the anise-scented mokihana berry (Pelea anisata) was known to natives for its phototoxic properties (mokihana burn). It is a member of the rue family. Exposure through limes used to flavor gin and tonics and Mexican beer may result in phototoxic reactions in outdoor bartenders and their customers. Home tanning solutions containing fig leaves can produce phytophotoderma itis. These conditions may be widespread and severe enough to require burn unit management (Fig. 3.19). **Fig. 3.18 Two friends who made limeade in the sun to sell in the summer.** Occupa ional disability from exposure to the pink rot fungus (Sclerotinia sclerotiorum), present on celery roots, occurs in celery farmers. In addition, disease-resistant celery contains furocoumarins and may produce phytophotodermatitis in grocery workers. Usually, insufficient sensitizing furocoumarin is absorbed from dietary exposure; however, ingested herbal remedies may cause systemic phototoxicity.

Answer 39

**Dermatitis bullosa striata pratensis (grass or meadow dermatitis)** ## Footnote The eruption consists of streaks and bizarre configurations with vesicles and bullae that heal with residual hyperpigmentation. The usual cause is sunbathing in fields containing the phototoxic plants. Similarly, tourists in the tropics may rinse their hair with lime juice outdoors, and streaky hyperpigmentation of the arms and back will result where the lime juice runs down (Fig. 3.20). Blistering phytophotodermatitis must be differentiated from rhus dermatitis. The vesicles and bullae of rhus are not necessarily limited to the sun-exposed areas, and itching is the most prominent symptom. Lesions continue to occur in rhus dermatitis for a week or more. In phytophotodermatitis, the reaction is limited to sunexposed sites, a burning pain appears within 48 hours, and marked hyperpigmentation results. The asymmetry, atypical shapes, and streaking of the lesions are helpful in establishing the diagnosis. These features may lead to a misdiagnosis of child abuse. Treatment of a severe, acute reaction is similar to the management of a sunburn, with cool compresses, mild analgesics if required, and topical emollients. Use of topical steroids and strict sun avoidance immediately after the injury may protect against the hyperpigmentation. The hyperpigmentation is best managed by “tincture of time.”

Answer 40

**Idiopathic Photosensitivity Disorders** These disorders are not associated with external photosensitizers (except for some cases of chronic actinic dermatitis) or inborn errors of metabolism

Answer 41

**Polymorphous light eruption (PLE, PMLE)** In various studies of Northern European white persons, a history of PLE can be elicited in between 5% and 20% of the adult population. It represents about one quarter of all photosensitive patients in referral centers. All races and skin types can be affected. The onset is typically in the first four decades of life, and females outnumber males by 2 : 1 or 3 : 1. The pathogenesis is unknown, but a family history may be elicited in 10%–50% of patients. Some investigators report that 10%– 20% of patients with PLE may have positive antinuclear antigens (ANAs) and a family history of lupus erythematosus. Photosensitive SLE patients may give a history of PLE-like eruptions for years before the diagnosis of SLE is made. PLE patients should be followed for the development of symptoms of SLE.

Answer 42

The **papular (or erythematopapular) variant** is the most common, but papulovesicular, eczematous, erythematous, and plaquelike lesions also occur (Fig. 3.21). **Fig. 3.21 Polymorphous light eruption, papular type.** Plaquelike lesions are more common in elderly patients and may closely simulate lupus erythematosus, with indurated, erythematous, fixed lesions In African Americans, a pinpoint papular variant has been observed, closely simulating lichen nitidus but showing spongiotic dermatitis histologically (Fig. 3.22). Scarring and atrophy do not occur; in darkly pigmented races, however, marked postinflammatory hyperpigmentation or hypopigmentation may be present. In some patients, pruritus only, without an eruption, may be reported (PLE sine eruptione). Some of these patients will develop typical PLE later in life. **Fig. 3.22 Polymorphous light eruption, micropapular variant resembling lichen nitidus.** The lesions of PLE appear most often 1–4 days after exposure to sunlight, although patients may report itching and erythema during sun exposure and development of lesions within the first 24 hours. A change in the amount of sun exposure appears to be more critical than the absolute amount of radiation. Patients living in tropical climates may be free of eruption, only to develop disease when they move to temperate zones, where there is more marked seasonal variation in UV intensity. Areas of involvement include the face, the V area of the chest, neck, and arms. In general, for each individual, certain areas are predisposed. Typically, however, areas protected during the winter, such as the extensor forearms, are particularly affected, whereas areas exposed all year (face and dorsa of hands) may be relatively spared. The eruption appears most frequently in the spring. The eruption often improves with continued sun exposure (hardening), so patients may be clear of the condition in the summer or autumn.

Answer 43

An unusual variant of PLE is juvenile spring eruption of the ears (Fig. 3.23). This occurs most frequently in boys age 5–12 years but may also be found in young adult males. It presents in the spring, often after sun exposure on cold but sunny days. The ## Footnote typical lesions are grouped small papules or papulovesicles on the helices. Le ions may form visible vesicles and cru ting. Juvenile spring eruption of the ears is self-limited and does not scar. UVA is the inducing spectrum, and some patients also have lesions of PLE elsewhere. The histologic picture is identical to that of PLE. Another localized variant of PLE is spring and summer eruption of the elbows, but this occurs in adults, equally in men and women. Histologically, a perivascular, predominantly T-cell infiltrate is present in the upper and middle dermis. There is often edema and endothelial swelling, with occasional neutrophils. Epidermal changes are variable, with spongiosis and exocytosis most often observed. Occasionally, a virtual absence of findings microscopically may paradoxically be reported and has been referred to as pauci inflammatory photodermatitis. The reported action spectrum of PLE varies, possibly depending on the different ethnic backgrounds of reported populations. UVA is most often responsible; however, UVB and both wavelengths in combination are also frequently necessary. Patients often report eruptions following sun exposure through window glass. Although rare, visible light sensitivity can also occur. Typically, women are more sensitive than men to UVA only, and men are more sensitive to visible light. Men, although the minority of PLE patients, tend to have more severe PLE and broader wavelengths of sensitivity. Most patients react more in affected sites, and in some, lesions can only be induced in affected areas. Phototesting produces variable results. One protocol produced positive results in 83% of tested patients using four exposures of UVB, UVA, or a combination in previously affected sites. However, the light sources are not readily available, and reported protocols vary widely. In clinical practice, the diagnosis s usually made clinically.

Answer 44

**The differential diagnosis of PLE includes lupus erythematosus, photosensitive drug eruption, prurigo nodularis, and photoallergic contact dermatitis.** Histopathologic examination, ANA testing, and d rect immunofluorescence (DIF) are helpful in distinguishing these diseases. Serologic testing alone may not distinguish PLE from SLE because of the possibility of positive ANA tests in PLE patients. Lupus erythematosus may present initially with photosensitivity before other features of lupus occur. Sebaceous neutrophilic adenitis, is characterized by erythematous circinate plaques on the head, neck, and upper chest and has been reported in the first to second month of spring. Histologically, neutrophilic infiltration of the sebaceous glands occurs, sometimes forming microabscesses. Although it may be photoinduced, it may also be idiopathic as in the cases reported in the genital area. Acute pustular folliculitis is a recurrent eruption of the head and neck that may be photoinduced, viral associated, or idiopathic. It resolves in most cases spon aneously in several days. The presence of follicular pustules distinguishes the photoinduced cases from PLE. Therapeutically, most patients with mild PLE can be managed by avoiding the sun and using barrier protection and high-SPF, broad-spectrum sunscreens. It is critical that the sunblocks contain specific absorbers or blockers (ecamsule, avobenzone, titanium dioxide, zinc oxide) of long-wave UVA because this is the most common triggering wavelength. Sunblocks containing more than one of these agents are more effective. DermaGard film can be applied to windows at home and in the car to block the transmission of almost all UVB and UVA rays while allowing visible light to be transmitted. Degradation does occur, so the film should be replaced every 5 years. These measures of photoprotection are critical for all pa ients, because they are free of toxicity and reduce the amount and duration of other therapies required Patient education is important in the management of PLE Phototesting may be required to convince patients that they are UV sensitive and will also determine the action spectrum.

Answer 45

**The use of topical tacrolimus ointment at night or twice daily, combined with the previous measures for sun avoidance and the use of sunscreens, controls PLE in many patients.** At times, topical steroids, frequently of super or high potency and in several daily to weekly pulses, are necessary to control the pruritus and clear the eruption. Antihistamines may be used for pruritus. Systemic corticosteroids in short courses may be necessary, especially in the spring. In patients whose condition is not controlled by these measures, hardening in the spring with UVB, narrow-band (NB) UVB, or psoralen plus UVA (PUVA) can dramatically decrease the sun sensitivity of patients with PLE, and up to 80% can be controlled with phototherapy. In the most sensitive patients, systemic steroids may be needed at the inception of the phototherapy. Systemic hydroxychloroquine sulfate, 200–400 mg/day, may be used. It has a delayed onset and is best instituted in the late winter to prevent spring outbreaks. Chloroquine or quinacrine may be effective if hydroxychloroquine is not, but in general, antimalarials are inferior to phototherapy. In the most severe cases, management with azathioprine, cyclosporine, thalidomide, or mycophenolate mofetil may be considered. If these agents are used in a patient considered to have PLE, an evaluation for chronic ac inic dermatitis should be performed because patients with PLE rarely require these agents.

Answer 46

**Fig. 3.24 Actinic prurigo, prurigo nodularis–like lesions.** ## Footnote Actinic prurigo probably represents a variant of PLE; it is most often seen in Native Americans of North and Central America and Colombia. The incidence in Mexico has been reported at between 1.5% and 3.5% It has been reported in Europe, Australia, and Japan as well. The female/male ratio is between 2 : 1 and 6 : 1. Actinic prurigo in Native Americans in the United States begins before age 10 in 45% of cases and before age 20 in 72%. Up to 75% of patients have a positive family history (hereditary PLE of Native Americans). In Europe, 80% of cases occur before age 10. In the Inuit Canadian population, onset is later and frequently in adulthood. In childhood, lesions begin as small papules or papulovesicles that crust and become impetiginized. They are intensely pruritic and frequently excoriated. In children, the cheeks, distal nose, ears, and lower lip are typically involved. Cheilitis may be the initial and only feature for years. Conjunctivitis is seen in 10%–20% of patients (limbal-type vernal catarrh). Lesions of the arms and legs are also common and usually exhibit a prurigo nodule–like configuration (Fig. 3.24). The eruption may extend to involve sun-protected areas especially the buttocks, but lesions in these areas are always less severe. In adults, chronic, dry papules and plaques are most typical, and cheilitis and crusting occur less frequently. Skin lesions tend to persist throughout the year in the tropics but are clearly worse during periods of increased sun exposure. In temperate and high-latitude regions, lesions occur from March through the summer and substantially remit in the winter. Hardening, as seen with PLE, does not occur. In up to 60% of patients with actinic prurigo that present before age 20, the condition improves or resolves within 5 years, whereas adults usually have the disease throughout life. Initial therapy is identical to that for PLE. Thalidomide has been used effectively and safely over many years for this condition. In patients refractory to or intolerant of thalidomide, cyclosporine can be effective. Topical cyclosporine 2% may be effective in controlling limbal lesions of actinic prurigo–associated conjunctivitis.

Answer 47

**Fig. 3.25 Polymorphous light eruption, brachioradial distribution.** PLE may present initially and only on the brachioradial area. This type of brachioradial eruption was the initial pattern of brachioradial pruritus described and was termed solar pruritus (Fig. 3.25). The majority of cases of brachioradial pruritus, especially those characterized by severe, refractory, intractable pruritus and secondary severe lichenification, are now thought to represent a form of neuropathic pruritus, sometimes related to cervical spine disease (see Chapter 4). Sunlight may be an eliciting factor and cervical spine disease a predisposing factor in patients with brachioradial pruritus. To identify those patients in whom photosensitivity plays a prominent role, a high-SPF (UVA/UVB) sunscreen should be applied to one arm only for several weeks. In patients with PLE, this usually leads to improvement of that one arm compared with the contralateral unprotected arm. In patients with primarily neuropathic disease, sunscreen application leads to minimal improvement. The capsaicin patch provides both itch relief and a physical barrier but is expensive.

Answer 48

**Fig 3 26 Solar urticaria.** ## Footnote Solar urticaria is most common in women age 20–40. Delayed reactions rarely occur. Chronically exposed sites may have some reduced sensitivity. In severe attacks, syncope, bronchospasm, and anaphylaxis may occur. Patients with solar urticaria may be sensitive to wavelengths over a broad spectrum. The wavelengths of sensitivity and the minimal urticarial doses (MUDs) may vary with anatomical site and over time within the same patient. UVA sensitivity is the most common, but visible light sensitivity is also frequently reported. The photosensitivity can be passively transferred, and irradiation of the patient’s serum with the activating wavelength followed by reinjection will create a wheal in the patient, but not in an unaffected patient. This suggests the presence of a circulating photoinducible allergen to which the individual patient with solar urticaria is sensitive. In some patients, an inhibition spectrum may be identified that inhibits the binding of the endogenous photoallergen to mast cells. Solar urticaria is virtually always idiopathic. Rarely, medications such as tetracycline (but not minocycline), chlorpromazine, progestational agents, and repirinast have been reported to induce solar urticaria. Erythropoietic protoporphyria and more rarely porphyria cutanea tarda may present with lesions simulating solar urticaria. There are rare reports of solar urticaria in patients with lupus erythematosus. The diagnosis of solar urticaria is usually straigh forward from the history. Phototesting is useful to determine the wavelengths of sensitivity and to ascertain the MUD if UVA desensitization is being considered. Because many patients have sensitivity in the UVA or even visible range, broad-spectrum sunscreens should be instituted. Antihistamines, especially the nonsedating H1 agents loratadine, cetirizine HCl, and fexofenadine, may increase the MUD 10-fold or more. Higher doses, twice or more the standard recommendation, may be required. These drugs, plus sun avoidance and broad-spectrum sunscreens, are the first-line therapy. The leukotriene receptor antagonist motelukast may provide additive efficacy when used in combination with the above regimen. PUVA or increasing UVA exposures are effective in more difficult cases, with PUVA having greater efficacy. Rush hardening may induce UVA tolerance, allowing patients to begin PUVA therapy. PUVA is effective, even if the patient is not sensitive to UVA. Cyclosporine (4.5 mg/kg/ day) and intravenous immune globulin at various doses and time frames have been anecdotally reported as effective. For the most difficult cases, plasmapheresis may be used to remove the circulating photoallergen, allowing PUVA to be given and leading to remission. Multiple reports attest to positive responses in some patients with the use of omalizumab.

Answer 49

**Hydroa Vacciniforme** ## Footnote Boys and girls are equally represented, but boys present earlier and on average have longer-lasting disease. There is a bimodal onset, between ages 1 and 7 and between 12 and 16. The natural history of the typical disorder is spontaneous remission before age 20, but rare cases in young adults do occur. Within 6 hours of exposure, stinging begins. At 24 hours or sooner, erythema and edema appear, followed by the characteristic 2–4 mm vesicles. Over the next few days, these lesions rupture, become centrally necrotic, and heal with a smallpox like scar. Lesions tend to appear in crops with disease-free intervals. The ears, nose, cheeks, and extensor arms and hands are affected. Subungual hemorrhage, ocular involvement, or oral ulcerations may occur. Histologically, early lesions show intraepidermal vesiculation and dermal edema that evolve into a subepidermal blister. Necrotic lesions show reticular degeneration of keratinocytes, with epidermal necrosis flanked by spongiosis with a dense perivascular infiltrate of neutrophils and lymphocytes. Dermal vessels may be thrombosed, simulating vasculitis. Lesions may be reproduced by repetitive UVA, with the action spectrum in the 330–360 nm range. The differential diagnosis includes PLE, actinic prurigo, and erythropoietic protoporphyria. Porphyrin levels are normal in hydroa vacciniforme. In erythropoietic protoporphyria, the burning typically begins within minutes of sun exposure, and over time patients develop diffuse, thickened, waxlike scarring, rather than the smallpox-like scars of hydroa vacciniforme. Histologic evaluation, DIF and porphyrin studies are useful in distinguishing these two conditions. Treatment is principally to avoid sunlight exposure and to use broad-spectrum sunscreens that block in the UVA range. Prophylactic NB UVB phototherapy in the early spring may be effective. Choloroquine and systemic corticosteroids have provided relief in some cases. A subset of children and less often adults with photosensitive hydroa vacciniforme–like skin lesions manifest facial swelling, indurated nodules or progressive ulcers, fever, and liver damage. Oral, esophageal, or colonic ulcerations may occur. Hypersensitivity to mosquito bites may also be seen. These patients may develop Epstein-Barr virus (EBV)–associated natural killer (NK) cell/T-cell lymphomas and die of this or a hemophagocytic syndrome. The hydroa vacciniforme–like skin lesions may precede the diagnosis of the lymphoma by up to a decade. Initially the patient may appear to have typical hydroa vacciniforme of the self-limited type; older age is more concerning for a complex course. This is therefore a disease spectrum, with both typical and severe hydroa vacciniforme being EBV associated. Treatment of the lymphoma may lead to clearing of these lesions.

Answer 50

**Chronic Actinic Dermatitis**

Answer 51

**• Persistent, chronic, eczematous eruption in the absence of exposure to known photosensitizers** **• Usually, broad-spectrum photosensitivity with decreased MED to UVA and/or UVB and at times visible light** **• Histology consistent with a chronic dermatitis, with or without features of lymphoma** **Fig. 3.27 Chronic actinic dermatitis.** Clinically, chronic actinic dermatitis predominantly affects middle-age or elderly men. In the United States patients with skin types V and VI may be disproportionately affected (Fig. 3.27). Skin lesions consist of edematous, scaling, thickened patches and plaques that tend to be confluent. Lesions occur primarily or most severely on the exposed skin and may spare the upper eyelids, behind the ears, and the bottom of wrinkles. Involvement of unexposed sites often occurs, progressing to erythroderma in the most severe cases. Marked depigmentation resembling vitiligo may result. Patients may not realize their condition is exacerbated by exposure to light. It may persist in all seasons. The pathogenesis of this syndrome is unknown. In some patients, a preceding topical or oral photosensitizer may be implicated, but chronic actinic dermatitis fails to improve with discontinuation of the inciting agent. In about one third of patients, photopatch testing yields a positive response to previously applied agents, especially musk ambrette, sunscreen ingredients, p-phenylenediamine, and hexachlorophene. Patch testing to standard agents may have a positive result in about 30% of patients, but no particular relevance is found. However, in approximately 65% of European patients, sesquiterpene lactone contact sensitivity from Compositae has been identified. In addition, more than 75% of men over age 60 with sesquiterpene lactone sensitivity have abnormal phototesting results. CD8 (suppressor/cytotoxic) T cells are disproportionately represented in the cutaneous infiltrates in the majority of patients and less frequently in the peripheral blood. IgE levels may be elevated.

Answer 52

**histologic evaluation and phototesting** P ing often reproduces the lesions About 65% of patients are sensitive to UVA, UVB, and visible light; 22% to UVA and UVB; and 5% to UVB or UVA only. The finding of photosensitivity to UVA and UVB helps to differentiate chronic actinic dermatitis from drug-induced photosensitivity, in which patients usually exhibit only UVA photosensitivity. PLE, photoallergic contact dermatitis, airborne contact dermatitis, and mycosis fungoides or Sézary syndrome must be excluded. PLE is excluded by the broadspectrum–reduced MED in chronic actinic dermatitis, although some patients may begin with a PLE-like disease that later meets the criteria for chronic actinic dermatitis Contact dermatitis is excluded by patch and photopatch testing Mycosis fungoides may be difficult to differentiate from chronic actinic dermatitis in cases with atypical histology. Phototesting is critical in these patients. Mycosis fungoides will manifest a T-cell receptor rearrangement in lesional skin or peripheral blood and usually shows a CD4 (helper) T-cell predominance.

Answer 53

**identifying possible topical photosensitizers by photopatch testing and scrupulously avoiding them** Maximum sun avoidance and broad-spectrum sunscreens are essential. Topical tacrolimus is useful in many patients Topical and systemic steroids are effective in some patients, but chronic toxicity of systemic steroids limits chronic use. Azathioprine, 50–200 mg/day, is the most reproducibly effective treatment and may be required annually during periods of increased sun intensity. Low-dose PUVA or NB UVB can be effective when used with topical and systemic steroids, but patients may also be intolerant of this approach. Hydroxyurea, 500 mg twice daily, cyclosporine, thalidomide, and mycophenolate mofetil may also be used. Immunosuppressive agents may allow patients to tolerate PUVA therapy. With careful management, about 2 in 10 patients will lose their photosensitivity within 5 years, 1 in 4 by 10 years, and 1 in 3 of patients by 15 years. Most of the remaining will improve over this time with only one of 20 worsening in a study by Wolverton et al.

Answer 54

**200 (often \<50)** except in persons with a genetic predisposition (Native Americans). Photosensitivity may be the initial manifestation of HIV disease. African American patients are disproportionately represented among patients with HIV photosensitivity. Photosensitivity may be associated with ingestion of a photosensitizing medication, especially NSAIDs, efavirenz (an antiretroviral) or trimethoprim-sulfamethoxazole, but the skin eruption often does not improve even when the medication is discontinued. Histologically, the lesions may show subacute or chronic dermatitis, often with a dense dermal infiltrate with many eosinophils. Histology identical to PLE, lichen planus, or lichen nitidus may also occur. When the CD4 count is below 50, especially in black patients, chronic actinic dermatitis with features of actinic prurigo is typical. Widespread vitiliginous lesions may develop. Therapy is difficult, but thalidomide may be beneficial.

Answer 55

**DNA** ## Footnote The effects of ionizing radiation on the cells depend on the amount of radiation, its intensity (exposure rate), and the characteristics of the individual cell. Rapidly dividing cells and anaplastic cells in general have increased radiosensitivity compared with normal tissue. When radiation therapy is delivered, it is frequently fractionated (i.e., divided into small doses). This allows the normal cells to recover between doses. When the dose is large, cell death results. In small amounts, the effect is insidious and cumulative. Mitosis is arrested temporarily, with consequent retardation of growth. The exposure rate affects the number of chromosome breaks. The more rapid the delivery of a certain amount of radiation, the greater is the number of chromosome breaks.

Answer 56

When an “erythema dose” of ionizing radiation is given to the skin, there is a latent period of up to 24 hours before visible erythema appears. This initial erythema lasts 2–3 days but may be followed by a second phase beginning up to 1 week after the exposure and lasting up to 1 month. When the skin is exposed to a large amount of ionizing radiation, an acute reaction develops, the extent of which will depend on the amount, quality, genetic susceptibility, and duration of exposure. Such radiation reaction occurs in the treatment of malignancy and in accidental overexposure. The reaction is manifested by initial erythema, followed by a second phase of erythema at 3–6 days (Fig. 3.28). Vesiculation, edema, and erosion or ulceration may occur, accompanied by pain. The skin develops a dark color that may be mistaken for hyperpigmentation but that desquamates. This type of radiation injury may subside in several weeks to several months, again depending on the amount of radiation exposure. Skin that receives a large amount of radiation will never return to normal. It will lack adnexal structures, will be dry, atrophic, and smooth, and will be hypopigmented or depigmented. Cutaneous necrosis may complicate yttrium-90 synovectomy, a treatment given for chronic synovitis.

Answer 57

The polymorphic, pruritic eruption arising several days to several months after radiotherapy for cancer tends to favor the extremities. Acral excoriations, erythematous papules, vesicles, and bullae occur. It is not necessarily limited to the areas of radiation treatment. Histologically, a superficial and deep perivascular lymphohistiocytic infiltrate with eosinophils is present. Topical steroids, antihistamines, and UVB are all effective, and spontaneous resolution also occurs.

Answer 58

Chronic exposure to “suberythema” doses of ionizing radiation over a prolonged period will produce varying degrees of damage to the skin and its underlying parts after a variable latent period ranging from several months to several decades. Radiodermatitis may also occur on the back or flank after fluoroscopy and roentgenography for diagnostic or therapeutic purposes (Fig. 3.29). Telangiectasia, atrophy, and hypopigmentation with residual focal increased pigment (freckling) may appear (Fig. 3.30). The skin becomes dry, thin, smooth, and shiny. The nails may become striated, brittle, and fragmented. The capacity to repair injury is substantially reduced, resulting in ulceration from minor trauma. The hair becomes brittle and sparse. **Fig 3.30 Chronic radiodermatitis.**

Answer 59

The hair becomes brittle and sparse. In more severe cases, these chronic changes may be followed by radiation keratoses and carcinoma. Additionally, subcutaneous fibrosis, thickening, and binding of the surface layers to deep tissues may present as tender, erythematous plaques 6–12 months after radiation therapy (Fig. 3.31). It may resemble erysipelas or inflammatory metastases.

Answer 60

After a latent period averaging 20–40 years, various malignancies may develop, most frequently basal cell carcinoma (BCC), followed by squamous cell carcinoma (SCC). These may appear in sites of prior radiation, even if there is no evidence of chronic radiation damage. Sun damage may be additive to radiation therapy, increasing the appearance of nonmelanoma skin cancers. SCCs arising in sites of radiation therapy metastasize more frequently than purely sun-induced SCCs. In some patients, either type of tumor may predominate. Location plays some role; SCCs are more common on the arms and hands, whereas BCCs are seen on the head and neck and lumbosacral area (Fig. 3.32). Other radiationinduced cancers include angiosarcoma, Kaposi sarcoma, malignant fibrous histiocytoma, sarcomas, and thyroid carcinoma. The incidence of malignant neoplasms increases with the passage of time.

Answer 61

Acute radiodermatitis may be reduced with a topical corticosteroid ointment combined with an emollient cream applied twice a day and instituted at the onset of therapeutic radiotherapy. However the skin should be gently cleansed and dried shortly before radiation treatment. Chronic radiodermatitis without carcinoma requires little or no attention except protection from sunlight and the extremes of heat and cold. Careful cleansing with mild soap and water, the use of emollients, and occasionally hydrocortisone ointment are the only requirements for good care. The early removal of precancerous keratoses and ulcerations is helpful in preventing the development of cancers For radiation keratoses treatment with cryosurgery, 5-FU, imiquimod cream, ingenol or topical 5-aminolevulinic acid (ALA)–photodynamic therapy may be sufficient. If the keratosis feels infiltrated, a biopsy is indicated. Radiation ulcerations should be studied by excisional or incisional biopsy if they have been present for 3 months or longer. Complete removal by excision is frequently required to obtain healing and exclude focal carcinoma in the ulceration. Radiation-induced nonmelanoma skin cancers are managed by standard methods. The higher risk of metastasis from radiationinduced SCCs mandates careful follow-up and regular regional lymph node evaluation.

Answer 62

**Callus** It occurs on parts of the body subject to intermittent pressure, particularly the palms and soles, and especially the bony prominences of the joints. Those engaged in various sports, certain occupations, or other repetitive activity develop callosities of distinctive size and location as stigmata. Examples are surfer’s nodules, boxer’s knuckle pads, jogger’s toe, rower’s rump, playstation thumb, milker’s callus, tennis toe (Fig. 3.33), jogger’s nipple, prayer callus, the yoga sign, neck callosities of violinists, pillar knocker’s knuckles, bowler’s hand, and Russell sign. The latter are calluses, small lacerations, or abrasions on the dorsum of the hand overlying the metacarpophalangeal and interphalangeal joints and are seen as a clue to the diagnosis of bulimia nervosa.

Answer 63

The callus differs from the clavus in that it has no penetrating central core and is a more diffuse thickening. Callus tends to disappear spontaneously when the pressure is removed. Most problems are encountered with calluses on the soles Poorly fitting shoes, orthopedic problems of the foot caused by aging or a deformity of the foot exerting abnormal pressure, and high activity level are some of the etiologic factors to be considered in painful callosities of the feet. Padding to relieve the pressure, paring of the thickened callus, and use of keratolytics such as 40% salicylic acid plasters are effective means of relieving painful callosities. Use of 12% ammonium lactate lotion or a urea-containing cream is often helpful.

Answer 64

**Clavus (Corns)**

Answer 65

There are two varieties: the hard corns, which occur on the dorsa of the toes, or subungually on the soles, and the soft corns, which occur between the toes and are softened by the macerating action of sweat. In a hard corn, the surface is shiny and polished, and when the upper layers are shaved off, a core is noted in the densest part of the lesion. It is his core that causes a dull/boring or sharp/lancinating pain by pressing on the underlying sensory nerves. Corns arise at sites of friction or pressure, and when these causative factors are removed, they spontaneously disappear. Frequently, a bony spur or exostosis is present beneath both hard and soft corns of long duration, and unless this exostosis is removed, cure is unlikely. The soft interdigital corn usually occurs in the fourth interdigital space of the foot. Frequently, there is an exostosis at the metatarsophalangeal joint that causes pressure on the adjacent toe. These are soft, soggy, and macerated so that they appear white. Treatment by simple excision may be effective.

Answer 66

Plantar corns must be differentiated from plantar warts. Squeezing the lesion laterally will induce pain in a wart, while pressing perpendicularly will produce pain in a corn. 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 clearly seen is another option. Porokeratosis plantaris discreta is a sharply marginated, cone-shaped, rubbery lesion that commonly occurs beneath the metatarsal heads. Multiple lesions may occur. It has a 3 : 1 female predominance, is painful, and is frequently confused with a plantar wart or corn. Keratosis punctata of the creases may be seen in the creases of the toes, where it may be mistaken for a corn.

Answer 67

The relief of pressure or friction by corrective footwear or the application of a ring of soft felt wadding around the region of the corn will often bring a good result. Soaking the feet in hot water and paring the surface by means of a scalpel blade or pumice stone leads to symptomatic improvement. Salicylic acid is successful when carefully and diligently used. After careful paring of the corn with emphasis on removing the center core, 40% salicylic acid plaster is applied. Soaking the foot for 2 hour before reapplying he medication enhances the effect. After 48 hours, the plaster is removed, the white macerated skin is rubbed off, and a new plaster is reapplied. This is continued until the corn is gone. Punch excisions of small lesions and the Er:YAG laser ablation are other options. It should be stressed that removal of any underlying bony abnormality, if present, is often necessary to effect a cure.

Answer 68

**Pseudoverrucous Papules and Nodules** There is a s ity to lesions affecting urostomy or elderly incontinent patients. Protection of the skin will help eliminate them. Similar lesions have been described in women who repeatedly apply an antifungal (Vagisil) to the groin area.

Answer 69

A severe type of skin injury may occur from the cuts of coral skeletons (Fig. 3.34) The abrasions and cuts are painful, and local therapy may provide little or no relief. Healing may take months. As a rule, if secondary infection is guarded against, such cuts heal as well as any others. The possibility of Mycobacterium marinum infection must be considered in persistent lesions

Answer 70

Pressure Ulcers (Decubitus) / Bedsore

Answer 71

The pressure sore is caused by ischemia of the underlying structures of the skin, fat, and muscles as a result of sustained and constant pressure. Usually, it occurs in chronically debilitated persons who are unable to change position in bed. The bony prominences of the body are the most frequently affected sites. About 95% of all pressure ulcers develop on the lower body, with 65% in the pelvic area and 30% on the legs. The ulcer usually begins with erythema at the pressure point; in a short time a “punched-out” ulcer develops. Necrosis with a grayish pseudomembrane is seen, especially in the untreated ulcer. Potential complications of pressure ulcers include sepsis, local infection, osteomyelitis, fistulas, and SCC. More than 100 risk factors have been identified, with diabetes mellitus, peripheral vascular disease, cerebrovascular disease, sepsis, and hypotension being prominent. Pressure ulcers are graded according to a four-stage system, with the earliest being recognized by changes in skin temperature, tissue consistency, and sensation. The lesion first appears as an area of persistent redness. Stage II is a superficial ulcer involving the epidermis and/or dermis. The deeper stage III ulcers damage the subcutaneous fat and stage IV, the muscle, bone, tendon, or joint capsule.

Answer 72

Prevention relies on redistributing pressure at a minimum interval of 2 hours. Treatment consists of relief of the pressure on the affected parts by frequent change of position, meticulous nursing care, and use of air-filled products, liquid-filled flotation devices, or foam products. Other measures include ulcer care, management of bacterial colonization and infection, surgical repair if necessary, continual education, adequate nutrition, management of pain, and provision of psychosocial support. Ulcer care is critical. Debridement may be accomplished by sharp, mechanical, enzymatic, and autolytic measures, at least once weekly. In some patients, operative care will be required. Stable heel ulcers are an exception; debridement is unnecessary if only a dry eschar is present. Wounds should be cleaned initially and each dressing changed by a nontraumatic technique. Normal saline rather than peroxide or povidone-iodine is best. Selection of a dressing should ensure that the ulcer tissue remains moist and the surrounding skin dry. Occlusive dressings include more than 300 products, generally classified as films, alginates, foams, hydrogels, hydrofibers, and hydrocolloid dressings. Transparent films are used only for stage II ulcers because they provide light drainage, whereas hydrofibers are used only for full-thickness stage III and IV ulcers. Surgical debridement and closure with flaps and reconstructive procedures may be necessary. Adjuvant therapies such as ultrasound, laser, UV radiation, hyperbaric oxygen, electrical stimulation, radiant heat, application of growth factors, cultured keratinocyte grafts, skin substitutes, and miscellaneous topical and oral agents are being investigated to determine their place in the treatment of these ulcers. At times, anaerobic organisms colonize these ulcers and cause a putrid odor. The topical application of metronidazole eliminates this odor within 36 hours.

Answer 73

The formation of vesicles or bullae may occur at sites of combined pressure and friction and may be enhanced by heat and moisture. The feet of military recruits in training, the palms of oarsmen who have not yet developed protective calluses, and the fingers of drummers (drummer’s digits) are examples of those at risk. The size of the bulla depends on the site of the trauma. If the skin is tense and uncomfortable, the blister should be drained, but the roof should not be completely removed because it may act as its own dressing. In studies focusing on the prevention of friction blisters of the feet in long-distance runners and soldiers, acrylic fiber socks with drying action have been found to be effective. Additionally, pretreatment with a 20% solution of aluminum chloride hexahydrate for at least 3 days has been shown to reduce foot blisters significantly after prolonged hiking, but at the expense of skin irritation. Emollients decrease the irritation but reduce the overall effectiveness of the treatment.

Answer 74

Fracture blisters overlie sites of closed fractures, especially the ankle and lower leg. The blisters appear a few days to 3 weeks after the injury and are thought to be caused by vascular compromise. Fracture blisters may create complications such as infection and scarring, especially if blood filled or in diabetic patients. The blisters generally heal spontaneously in 5–14 days but may cause delay of surgical reduction of the fracture.

Answer 75

**Sclerosing Lymphangiitis** **Fig. 3.35 Sclerosing lymphangitis of penis.** Most if not all cases result from a superficial thrombophlebitis and thus has been renamed Mondor disease of the penis. Some early reports favor a lymphatic origin of some cases; CD31 and D240 stains will allow differentiation of future cases. Treatment is not necessary; sclerosing lymphangiitis follows a benign, self-limiting course.

Answer 76

**Black heel** Synonyms for black heel include talon noir and calcaneal petechiae. Black heel is often seen in basketball, volleyball, tennis, or lacrosse players. Seeming confluence may lead to mimicry of melanoma. The bleeding is caused by shearing stress of sports activities. Paring with a No. 15 blade and performing a guaiac test will confirm the diagnosis. Treatment is unnecessary.

Answer 77

**Subcutaneous Emphysema** It is detected by the presence of cutaneous crepitations. Gas-producing organisms, especially Clostridia, and leakage of free air from the lungs or gastrointestinal tract are the most common causes (Fig. 3.37). Samlaska et al. reviewed the wide variety of causes of subcutaneous emphysema, including penetrating and nonpenetrating injuries, iatrogenic causes occurring during various procedures in hospitalized patients, spontaneous pneumomediastinum such as may occur with a violent cough, childbirth, asthma, Boerhaave syndrome (esophageal rupture after vomiting or the Heimlich maneuver), intraabdominal causes such as inflammatory bowel disease, cancer, perirectal abscess, pancreatitis or cystitis, dental procedures when using air pressure instruments and high-speed drills, and factitial disease. **Fig. 3.37 Subcutaneous emphysema. (Courtesy Curt Samlaska, MD )**

Answer 78

**Traumatic Asphyxia**

Answer 79

**Painful Fat Herniation , also called painful piezogenic pedal papules** These d toceles become apparent when weight is placed on the heel and disappear as soon as the pressure is removed. These fat herniations are present in many people, but the majority experience no symptoms. However, extrusion of the fat tissue together with its blood vessels and nerves may initiate pain on prolonged standing. Avoidance of prolonged standing will relieve this pain. Other options include taping of the foot, use of compression stockings, or use of plastic heel cups or padded orthotic devices to restrict the herniations. Laing et al. found that 76% of 29 patients had pedal papules, and interestingly, by placing pressure on the wrists, found 86% to have piezogenic wrist papules **Fig. 3.38 Piezogenic papules. (Courtesy Paul Hong, MD.)**

Answer 80

**Fig. 3.39 Ulceration secondary to “skin popping.”** **Narcotic Dermopathy** Heroin (diacetylmorphine) is a narcotic prepared for injection by dissolving the heroin powder in boiling water and then injecting it. The favored route of administration is intravenous. This results in thrombosed, cordlike, thickened veins at the sites of injection. In addition, amphetamines, cocaine, and other drugs may be injected. Subcutaneous injection may result in infections, complications of bacterial abscess and cellulitis, or sterile nodules, apparently acute foreign body reactions to the injected drug or the adulterants mixed with it. These lesions may ulcerate. Chronic persistent firm nodules, a combination of scar and foreign body reaction, may result. If cocaine is being injected, it may cause ulcers because of its direct vasospastic effect. Addicts will continue to inject heroin and cocaine into the chronic ulcer bed. Cocaine-associated vasculitis caused by levamisole is discussed in Chapter 35. The cutaneous manifestations of injection of heroin and other drugs also include camptodactylia, edema of the eyelids, persistent nonpitting edema of the hands, urticaria, abscesses atrophic scars, and hyperpigmentation. Pentazocine abuse leads to a typical clinical picture of tense woody fibrosis, irregular punched-out ulcerations, and a rim of hyperpigmentation at injection sites. Extensive calcification may occur within the thickened sites.

Answer 81

**Tattoo** They may be traumatic, cosmetic, or medicinal in nature and may be applied by a professional or an amateur. Pigment is applied to the skin, and needles pierce the skin to force the material into the dermis. Pigments used include carmine, indigo, vermilion, India ink, chrome green, magnesium (lilac color), Venetian red, aluminum, gold, titanium (white color) or zinc oxide, lead carbonate, copper, iron, logwood, azo and naptha-derived pigments, quinacridones, cobalt blue, cinnabar (mercuric sulfide), and cadmium sulfide. Cadmium, cobalt, mercury, and lead are not often used; however, occasional photosensitive reactions to cadmium, which was used for yellow color or to brighten the cinnabar red, are still seen. “Invisible tattoos,” seen only under UV light, have ingredients such as polymethylmethacrylate and melamine that may cause granulomatous reactions.

Answer 82

Tattoo-associated dermopathies may be reactive (allergic, lichenoid, granulomatous, or photosensitive) (Fig. 3.40) or infective (inoculation of syphilis, infectious hepatitis, tuberculosis, HIV, warts, molluscum, Hansen disease) or may induce a Koebner response in patients with active lichen planus or psoriasis. Discoid lupus erythematosus has been reported to occur in the redpigmen ed portion of tattoos. Tattoos over nevi may delay the diagnosis of melanoma. Occasionally, the tattoo marks may become keloidal. Severe allergic reactions to “temporary tattoos” (painting of pigments such as henna on surface of skin) occur when the allergen p-phenylenediamine is added to make the color more dramatic. Red tattoos are the most common cause of delayed reactions, with the histologic findings typically showing a lichenoid process. Occasionally, a pseudolymphomatous reaction may occur in red tattoos. Dermatitis in areas of red (mercury), green (chromium), or blue (cobalt) have been described in patients who are patch test positive to these metals. Sarcoidal, foreign body, and allergic granulomatous reactions may also occur within tattoos; aluminum may induce such reactions. Treatment of such reactions is with topical or intralesional steroids Excision is also satisfactory when the lesions are small enough and situated so that ellipsoid excisions are feasible. Reactions may also be successfully treated with Q-switched lasers, at times combined with ablative fractional resurfacing Generalized allergic reactions occasionally occur; prevention by treatment with oral steroids and antihistamines has been suggested. Tattoo darkening can occur, as well as no response to laser treatment. Caution must be used when treating flesh-colored and pink-red tattoos because they may darken after treatment, likely caused by the reduction of ferric oxide to ferrous oxide. White ink, composed mostly of titanium dioxide, is often used to brighten green, blue, yellow, and purple tattoos. Laser irradiation reduces titanium to a bluecolored pigment. Test areas are recommended when treating light-colored facial tattoos. CO 2 resurfacing lasers used conservatively are an alternative to the Q-switched lasers in such patients

Answer 83

Injection of oils into the skin for cosmetic purposes, such as the smoothing of wrinkles and the augmentation of breasts, was popular in the past. Paraffin, camphorated oil, cottonseed or sesame oil, mineral oil, and beeswax may produce plaquelike indurations with ulcerations within months and up to 40 years. Several reports document penile paraffinomas caused by self-injection. When petroleum jelly (Vaseline) gauze or a topical ointment is used to dress unsutured wounds, lipogranulomas or inflammatory mild erysipelas-like lesions with marked tenderness may occur. A radiofrequency device successfully treated a facial paraffinoma. Surgical removal must be wide and complete.

Answer 84

Liquid silicones, composed of long chains of dimethyl siloxy groups, are biologically inert. Silicones have been used for correcting wrinkles, reducing scars, and building up atrophic depressed areas of the skin. Many case reports detail granulomatous reactions to silicone, some with migration and reactive nodules at points distant from the injection site (Figs. 3.41 and 3.42). Acupuncture needles are coated with silicone, and granulomas may occur at the entry points. The incidence of the nodular swellings, which may be quite destructive and treatment resistant, remains unknown. It is clear that, if used off label, medical-grade silicone injected in small volume should be the rule, and it should not be injected into the penis or the glandular tissue of the breast. For breast augmentation, silicone may be used as Silastic implants. If trauma causes rupture of the bag, subcutaneous fibrotic nodules often develop. Bioplastique consists of polymerized silicone particles dispersed in a gel carrier. When used for lip augmentation, nodules may develop. Histologically, these are foreign body granulomas. Treatment of silicone granulomas is often not successful. Surgical removal may lead to fistulas, abscesses, and marked deformity. Both minocycline, 100 mg twice daily for several months, and imiquimod cream have been anecdotally useful. **Fig. 3.41 Silicone reaction.**

Answer 85

Mercury may cause foreign body giant cell or sarcoidal-type granulomas (Fig. 3.43), pseudolymphoma, or membranous fat necrosis. It is usually identifiable as egg-shaped, extracellular, dark-gray to black, irregular globules. The gold lysis test is positive in tissues. Energy-dispersive radiographic spectroscopy may be done and will identify mercury by the characteristic emission spike. Such testing may be helpful in identifying any foreign substance suspected to have been implanted accidentally or intentionally by the patient. Systemic toxicity or embolus may develop from mercury and may result in death. Therefore excision is necessary and can be accomplished under x-ray guidance.

Answer 86

Beryllium granuloma is seen as a chronic, persistent, granulomatous inflammation of the skin with ulceration that may follow accidental laceration, usually in an occupational setting.

Answer 87

**Zirconium Granuloma** Although zirconium was eliminated from aerosol-type deodorants in 1978, aluminumzirconium complex is present in some antiperspirants. Additionally, various poison ivy lotions contain zirconium compounds. The lesions are brownish red, dome-shaped, shiny papules. This is an acquired, delayed-type, allergic reaction resulting in a granuloma of the sarcoidal type. After many months, the lesions involute spontaneously.

Answer 88

**Silica Granuloma** Fig. 3.45 (A and B) Silica granuloma years after motorcycle crash. These typically present as black or blue papules or macules arranged in a linear fashion. At times, the granulomatous reaction to silica may be delayed for many years, with the ensuing reaction being both chronic and disfiguring. The granulomas may be caused by amorphous or crystalline silicon dioxide (quartz), magnesium silicate (talcum), or complex polysilicates (asbestos). Talc granulomas of the skin and peritoneum may develop after surgery from the talcum powder used on surgical gloves. Silica granulomas have a statistical association with systemic sarcoidosis, and silica may act as a stimulus for granuloma formation in patients wi h latent sarcoidosis. Removal of these granulomas is fraught with difficulties. The best method of care is immediate and complete removal to prevent these reactions. Excision and systemic steroids have been used, but recurrences are common. Some reactions may subside spontaneously after 1–12 months. Dermabrasion or simple abrasion with a hard-bristled toothbrush is a satisfactory method for the removal of dirt accidentally embedded into the skin of the face or scalp.

Answer 89

**Fig. 3.46 Carbon stain**, gunshot wound. ## Footnote Narcotic addicts who attempt to clean needles by flaming them with a lighted match may tattoo the carbon formed on the needle as it is inserted into the skin. Carbon particles may be removed immediately after their deposition using a toothbrush and forceps. This expeditious and meticulous early care results in the best possible cosmetic result. If the particles are left in place long enough, they are best removed using the Q-switched Nd:YAG laser at 1064 nm. In one series success was reported in 50 of 51 treated tattoos with an average of 1.7 treatments. However, microexplosions producing poxlike scars have occurred with each laser pulse. Alternatively, dermabrasion may be used.

Answer 90

**Fig. 3.47 Injected filler reaction.** The reaction may be delayed for years; at times, patients are reluctant to admit to these prior cosmetic interventions and frequently cannot name the filler used. Topical, intralesional, or systemic steroids, sometimes augmented by tacrolimus, and minocycline or doxycycline have been reported to be helpful medical interventions.

3 - DERMATOSES RESULTING FROM PHYSICAL FACTORS Flashcards

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