Thermal Burns

Injury of varying intensity may be caused by the action of excessive heat on the skin ( Fig. 3.1 ). If this heat is extreme, the skin and underlying tissue may be destroyed. The changes in the skin resulting from dry heat or scalding are classified in four degrees, as follows:

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  First-degree burns of the skin result merely in an active congestion of the superficial blood vessels, causing erythema that may be followed by epidermal desquamation (peeling). Ordinary sunburn is the most common example of a first-degree burn. The pain and increased surface heat may be severe, and some constitutional reaction can occur if the involved area is large.

  
  
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  Second-degree burns are subdivided into superficial and deep forms.

  
  
  
  
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    In the superficial second-degree burn, there is a transudation of serum from the capillaries, which causes edema of the superficial tissues. Vesicles and bullae are formed by the serum gathering beneath the outer layers of the epidermis. Complete recovery without scarring is usual in patients with superficial burns.

    
    
  • •
    

    The deep second-degree burn is pale and anesthetic. Injury to the reticular dermis compromises blood flow and destroys appendages, so healing takes more than 1 month and results in scarring.

  
  
  
  
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  Third-degree burns involve loss of the full thickness of the dermis and often some of the subcutaneous tissues. Because the skin appendages are destroyed, there is no epithelium available for regeneration of the skin. An ulcerating wound is produced, which on healing leaves a scar.

  
  
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  Fourth-degree burns involve the destruction of the entire skin, including the subcutaneous fat, and any underlying tendons.

Hot water burn.

(Courtesy Steven Binnick, MD.)

Both third-degree and fourth-degree burns require grafting for closure. All third- and fourth-degree burns are followed by constitutional symptoms of varying severity, depending on the size of the involved surface, the depth of the burn, and particularly the location of the burned surface. The more vascular the involved area, the more severe are the symptoms.

The prognosis is poor for any patient in whom a large area of skin surface is involved, particularly if more than two thirds of the body surface has been burned. Women, infants, and toddlers all have a greater risk of death from burns than men. Excessive scarring, with either keloid-like scars or flat scars with contractures, may produce deformities and dysfunction of the joints, as well as chronic ulcerations from impairment of local circulation. Delayed postburn blistering may occur in partial-thickness wounds and skin graft donor sites. It is most common on the lower extremities and is self-limited. Although burn scars may be the site of development of carcinoma, evidence supports only the possibility of a modest excess of squamous cell carcinomas in burn scars. With modern reconstructive surgery, this unfortunate end result can be minimized.

Electrical Burns

Electrical burns may occur from contact or as a flash exposure. A contact burn is small but deep, causing some necrosis of the underlying tissues. Low-voltage injuries usually occur in the home, are treated conservatively, and generally heal well. Oral commissure burns may require reconstructive procedures ( Fig. 3.2 ). High-voltage burns are often occupational; internal damage may be masked by minimal surface skin change and may be complicated by subtle and slowly developing sequelae. Early surgical intervention to improve circulation and repair vital tissues is helpful in limiting loss of the extremity.

Electrical burn from biting electrical cord.

(Courtesy Paul Hong, MD.)

Flash burns usually cover a large area and, being similar to any surface burn, are treated as such. Lightning may cause burns after a direct strike, where an entrance and an exit wound are visible. This is the most lethal type of strike, and cardiac arrest or other internal injuries may occur. Other types of lightning strike are indirect and result in the following burns:

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  Linear burns in areas on which sweat was present

  
  
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  Burns in a feathery or arborescent pattern, which is believed to be pathognomonic

  
  
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  Punctate burns with multiple, deep, circular lesions

  
  
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  Thermal burns from ignited clothing or heated metal, which may occur if the patient was speaking on a cell phone or listening to an iPod or similar device when struck

Hot Tar Burns

Polyoxyethylene sorbitan in bacitracin zinc–neomycin–polymyxin B (e.g., Neosporin) ointment, vitamin E ointment, and sunflower oil are excellent dispersing agents that facilitate the removal of hot tar from burns.

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  Alemayehu H, et al: Management of electrical and chemical burns in children. J Surg Res 2014; 190: 210.

  
  
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  Carta T, et al: Use of mineral oil Fleet enema for the removal of a large tar burn. Burns 2015; 41: e11.

  
  
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  Compton CC: The delayed postburn blister. Arch Dermatol 1992; 128: 24.

  
  
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  El-Zawahry BM, et al: Ablative CO2 fractional resurfacing in treatment of thermal burn scars. J Cosmet Dermatol 2015; 14: 324.

  
  
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  Esteban-Vives R, et al: Second-degree burns with six etiologies treated with autologous noncultured cell-spray grafting. Burns 2016; 42: e99.

  
  
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  Heffernan EJ, et al: Thunderstorms and iPods. N Engl J Med 2007; 357: 198.

  
  
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  Kalantar Motamedi MH, et al: Prevalence and pattern of facial burns. J Oral Maxillofac Surg 2015; 73: 676.

  
  
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  Russell KW, et al: Lightning burns. J Burn Care Res 2014; 35: e436.

  
  
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  Saracoglu A, et al: Prognostic factors in electrical burns. Burns 2014; 40: 702.

  
  
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  Sheridan RL, Greenhalgh D: Special problems in burns. Surg Clin North Am 2014; 94: 781.

  
  
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  Sokhal AK, et al: Clinical spectrum of electrical burns. Burns 2017; 43: 182.

  
  
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  Wallingford SC, et al: Skin cancer arising in scars: a systematic review. Dermatol Surg 2011; 37: 1239.

  
  
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  Wang KA, et al: Epidemiology and outcome analysis of hand burns. Burns 2015; 41: 1550.

Miliaria

Miliaria, the retention of sweat as a result of occlusion of eccrine sweat ducts, produces an eruption that is common in hot, humid climates, such as in the tropics and during the hot summer months in temperate climates. Staphylococcus epidermidis, which produces an extracellular polysaccharide substance, induces miliaria in an experimental setting. This polysaccharide substance may obstruct the delivery of sweat to the skin surface. The occlusion prevents normal secretion from the sweat glands, and eventually pressure causes rupture of the sweat gland or duct at different levels. The escape of sweat into the adjacent tissue produces miliaria. Depending on the level of the injury to the sweat gland or duct, several different forms are recognized.

Miliaria Crystallina

Miliaria crystallina is characterized by small, clear, superficial vesicles with no inflammatory reaction ( Fig. 3.3 ). It appears in bedridden patients whose fever produces increased perspiration or when clothing prevents dissipation of heat and moisture, as in bundled children. Hypernatremia without fever may induce it. The lesions are generally asymptomatic, and their duration is short-lived because they tend to rupture at the slightest trauma. Drugs such as isotretinoin, adrenergic/cholinergic drugs, and doxorubicin may induce it. The lesions are self-limited; no treatment is required.

Miliaria crystallina.

Miliaria Rubra (Prickly Heat)

The lesions of miliaria rubra appear as discrete, extremely pruritic, erythematous papulovesicles ( Fig. 3.4 ) accompanied by a sensation of prickling, burning, or tingling. They later may become confluent on a bed of erythema. The sites most frequently affected are the antecubital and popliteal fossae, trunk, inframammary areas (especially under pendulous breasts), abdomen (especially at the waistline), and inguinal regions; these sites frequently become macerated because evaporation of moisture has been impeded. Exercise-induced itching or that of atopic dermatitis may also be caused by miliaria rubra. The site of injury and sweat escape is in the prickle cell layer, where spongiosis is produced.

Miliaria rubra.

Postmiliarial Hypohidrosis

Postmiliarial hypohidrosis results from occlusion of sweat ducts and pores, and it may be severe enough to impair an individual’s ability to perform sustained work in a hot environment. Affected persons may show decreasing efficiency, irritability, anorexia, drowsiness, vertigo, and headache; they may wander in a daze.

It has been shown that hypohidrosis invariably follows miliaria, and that the duration and severity of the hypohidrosis are related to the severity of the miliaria. Sweating may be depressed to half the normal amount for as long as 3 weeks.

Tropical Anhidrotic Asthenia

Tropical anhidrotic asthenia is a rare form of miliaria with long-lasting poral occlusion, which produces anhidrosis and heat retention.

Erythema Ab Igne

Erythema ab igne is a persistent erythema—or the coarsely reticulated residual pigmentation resulting from it—that is usually produced by long exposure to excessive heat without the production of a burn ( Fig. 3.5 ). It begins as a mottling caused by local hemostasis and becomes a reticulated erythema, leaving pigmentation. Multiple colors are simultaneously present in an active patch, varying from pale pink to old rose or dark purplish brown. After the cause is removed, the affection tends to disappear gradually, but sometimes the pigmentation is permanent.

Erythema ab igne.

Histologically, an increased amount of elastic tissue in the dermis is noted. The changes in erythema ab igne are similar to those of actinic elastosis. Interface dermatitis and epithelial atypia may be noted.

Erythema ab igne on the legs results from habitually warming them in front of open fireplaces, space heaters, or car heaters. Similar changes may be produced on the lower back or at other sites of an electric heating pad application, on the upper thighs with laptop computers, or on the posterior thighs from heated car seats. The reason for chronically exposing the skin to heat may be pain from an underlying cancer, or from a condition which predisposes to a feeling of cold, such as anorexia nervosa. The condition occurs also in cooks, silversmiths, and others exposed over long periods to direct moderate heat.

Epithelial atypia, which may lead to Bowen disease and squamous cell carcinoma, has rarely been reported to occur overlying erythema ab igne. In remote areas of Kashmir, Kangri fire pots can induce erythema ab igne and cancer within the affected area. Treatment with 5-fluorouracil (5-FU), imiquimod, or photodynamic therapy may be effective in reversing this epidermal alteration.

The use of emollients containing α-hydroxy acids or a cream containing fluocinolone acetonide 0.01%, hydroquinone 4%, and tretinoin 0.05% may help reduce the unsightly pigmentation, as may treatment with the Q-switched neodymium-doped yttrium-aluminum-garnet (Nd:YAG) laser.

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  Brodell D, et al: Automobile seat heater-induced erythema ab igne. Arch Dermatol 2012; 148: 264.

  
  
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  Dessinoti C, et al: Erythema ab igne in three girls with anorexia nervosa. Pediatr Dermatol 2016; 333: e149.

  
  
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  Kim HW, et al: Erythema ab igne successfully treated with low fluenced 1,064-nm Q-switched neodymium-doped yttrium aluminum garnet laser. J Cosmet Laser Ther 2014; 16: 147.

  
  
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  Riahi RR, et al: Practical solutions to prevent laptop-induced erythema ab igne. Int J Dermatol 2014; 53: e395.

  
  
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  Wani I: Kangri cancer. Surgery 2010; 147: 586.

  
  
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  Wharton JB, et al: Squamous cell carcinoma in situ arising in the setting of erythema ab igne. J Drugs Dermatol 2008; 7: 488.

Acrocyanosis

Acrocyanosis is a persistent blue discoloration of the entire hand or foot worsened by cold exposure. The hands and feet may be hyperhidrotic ( Fig. 3.6 ). It occurs chiefly in young women. Cyanosis increases as the temperature decreases and changes to erythema with elevation of the dependent part. The cause is unknown. Smoking should be avoided. Acrocyanosis is distinguished from Raynaud syndrome by its persistent (rather than episodic) nature and lack of tissue damage (ulceration, distal fingertip resorption).

Acrocyanosis.

Acrocyanosis with swelling of the nose, ears, and dorsal hands may occur after inhalation of butyl nitrite. Interferon alpha-2a and beta may induce it. Repeated injection of the dorsal hand with narcotic drugs may produce lymphedema and an appearance similar to the edematous phase of scleroderma. This so-called puffy hand syndrome may include erythema or a bluish discoloration of the digits. Patients with anorexia nervosa frequently manifest acrocyanosis as well as perniosis, livedo reticularis, and acral coldness. It may improve with weight gain. Approximately one third of patients with skin findings of POEMS syndrome (polyneuropathy, organomegaly, endocrinopathy, M component, skin changes) have acrocyanosis. Also, in patients with a homozygous mutation in SAMDH1 and cerebrovascular occlusive disease, acrocyanosis was frequent.

Acral vascular syndromes, such as gangrene, Raynaud phenomenon, and acrocyanosis, may be a sign of malignancy. In 47% of 68 reported cases, the diagnosis of cancer coincided with the onset of the acral disease. If such changes appear or worsen in an elderly patient, especially a man, without exposure to vasoconstrictive drugs or prior autoimmune or vascular disorders, a paraneoplastic origin should be suspected.

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  Del Giudice P, et al: Hand edema and acrocyanosis. Arch Dermatol 2006; 142: 1084.

  
  
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  Dessinoti C, et al: Erythema ab igne in three girls with anorexia nervosa. Pediatr Dermatol 2016; 333: e149.

  
  
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  Kurklinsky AK, et al: Acrocyanosis. Vasc Med 2011; 16: 288.

  
  
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  Masuda H, et al: Bilateral foot acrocyanosis in an interferon-β-treated MS patient. Intern Med 2016; 55: 319.

  
  
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  Miest RY, et al: Cutaneous manifestations in patients with POEMS syndrome. Int J Dermatol 2013; 52: 1349.

  
  
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  Poszepczynska-Guigné E, et al: Paraneoplastic acral vascular syndrome. J Am Acad Dermatol 2002; 47: 47.

  
  
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  Xin B, et al: Homozygous mutation in SAMHD1 gene causes cerebral vasculopathy and early onset stroke. Proc Natl Acad Sci USA 2011; 108: 5372.

Pernio (Chilblains, Perniosis)

Pernio constitutes a localized erythema and swelling caused by exposure to cold. Blistering and ulcerations may develop in severe cases. In people predisposed by poor peripheral circulation, even moderate exposure to cold may produce chilblains. Cryoglobulins, cryofibrinogens, antiphospholipid antibodies, or cold agglutinins may be present and pathogenic. Chilblain-like lesions may occur in discoid and systemic lupus erythematosus (SLE; chilblain lupus), particularly the TREX1-associated familial type, as a presenting sign of leukemia cutis, or if occurring in infancy may herald the Nakajo-Nishimura syndrome or the Aicardi-Goutières and Singleton-Merten syndrome. The chronic use of crack cocaine and its attendant peripheral vasoconstriction will lead to perniosis with cold, numb hands and atrophy of the digital fat pads, especially of the thumbs and index fingers, as well as nail curvature.

Pernio occur chiefly on the feet, hands, ears, and face, chiefly in women; onset is enhanced by dampness ( Fig. 3.7 ). In surgery technicians, the hands are affected if an orthopedic cold therapy system is used; the skin under the device develops the lesions. The lateral thighs are involved in women equestrians who ride on cold, damp days and the hips in those wearing tight-fitting jeans with a low waistband. Wading across cold streams may produce similar lesions. Nondigital lesions of cold injury can be nodular.

Chilblains (pernio) in adult (A) and child (B).

Patients with chilblains are often unaware of the cold injury when it is occurring, but later burning, itching, and redness call it to their attention. The affected areas are bluish red, with the color partially or totally disappearing on pressure, and are cool to the touch. Sometimes the extremities are clammy because of excessive sweating. As long as the dampness and cold exposure continues, new lesions will continue to appear. Investigation into an underlying cause should be undertaken in patients with pernio that is recurrent, chronic, extending into warm seasons, or poorly responsive to treatment.

Pernio histologically demonstrates a lymphocytic vasculitis. There is dermal edema, and a superficial and deep perivascular, tightly cuffed, lymphocytic infiltrate. The infiltrate involves the vessel walls and is accompanied by characteristic “fluffy” edema of the vessel walls.

Frostbite

When soft tissue is frozen and locally deprived of blood supply, the damage is called frostbite. The ears, nose, cheeks, fingers, and toes are most often affected. The frozen part painlessly becomes pale and waxy. Various degrees of tissue destruction similar to that caused by burns are encountered. These are erythema and edema, vesicles and bullae, superficial gangrene, deep gangrene, and injury to muscles, tendons, periosteum, and nerves ( Fig. 3.8 ). The degree of injury is directly related to the temperature and duration of freezing. African Americans are at increased risk of frostbite. Arthritis of the small joints of the hands and feet may appear months to years later.

Frostbite.

Immersion Foot Syndromes

Warm Water Immersion Foot

Exposure of the feet to warm, wet conditions for 48 hours or more may produce a syndrome characterized by maceration, blanching, and wrinkling of the soles and sides of the feet ( Fig. 3.9 ). 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.

Tropical immersion foot.

(Courtesy Steven Binnick, MD.)

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.

Tropical immersion foot.

(Courtesy James WD [ed]: Textbook of Military Medicine, Office of the Surgeon General, United States Army, 1994.)

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.

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  Adnot J, et al: Immersion foot syndromes. In: James WD (ed): Military Dermatology. Washington, DC: Office of the Surgeon General, 1994.

  
  
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  Davis MD: Immersion foot associated with the overuse of ice, cold water, and fans. J Am Acad Dermatol 2013; 69: 169.

  
  
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  Olson Z, Kman N: Immersion foot. J Emerg Med 2015; 49: e45.

Sunburn and Solar Erythema

The solar spectrum has been divided into different regions by wavelength. The parts of the solar spectrum important in photomedicine include UV radiation (below 400 nm), visible light (400–760 nm), and infrared radiation (beyond 760 nm). Visible light has limited biologic activity, except for stimulating the retina. Infrared radiation is experienced as radiant heat. Below 400 nm is the UV spectrum, divided into three bands: UVA, 320–400 nm; UVB, 280–320 nm; and UVC, 200–280 nm. UVA is divided into two subcategories: UVA I (340–400 nm) and UVA II (320–340 nm). Virtually no UVC reaches the Earth’s surface because it is absorbed by the ozone layer above the Earth.

The minimal amount of a particular wavelength of light capable of inducing erythema on an individual’s skin is called the minimal erythema dose (MED). Although the 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. The most biologically effective wavelength of radiation from the sun for sunburn is 308 nm. Although it does not play a significant role in solar erythema, UVA is of major importance in patients with drug-induced 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 to 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.

Clinical Signs and Symptoms

Sunburn is the normal cutaneous reaction to sunlight in excess of an erythema dose. UVB erythema becomes evident 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.

Acute sunburn.

(Courtesy Dr. L. Lieblich.)

After UV exposure, skin pigment undergoes two changes: 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 ).

TABLE 3.1

Skin Types (Phototypes)

Skin Type	Baseline Skin Color	Sunburn and Tanning History
I	White	Always burns, never tans
II	White	Always burns, tans minimally
III	White	Burns moderately, tans gradually
IV	Olive	Minimal burning, tans well
V	Brown	Rarely burns, tans darkly
VI	Dark brown	Never burns, tans darkly black

 

Exposure to UVB and UVA causes an increase in the thickness of the 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.

Ephelis (Freckle) and Lentigo

Freckles are small (<0.5 cm) brown macules that occur in profusion on the sun-exposed skin of the face, neck, shoulders, and backs of the hands. 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.

Ephelis must be differentiated from lentigo simplex. The lentigo is a benign, discrete hyperpigmented macule appearing at any age and on any part of the body, including the mucosa. 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 ).

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.

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.

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  Hafner C, et al: The absence of BRAF, FGFR3, and PIK3CA mutations differentiates lentigo simplex from melanocytic nevus and solar lentigo. J Invest Dermatol 2009; 129: 2730

  
  
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  Imhof L, et al: A prospective trial comparing Q-switched ruby laser and a triple combination skin-lightening cream in the treatment of solar lentigines. Dermatol Surg 2016; 42: 853.

  
  
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  Praetorius C, et al: Sun-induced freckling. Pigment Cell Melanoma Res 2014; 27: 339.

Photoaging (Dermatoheliosis)

The characteristic changes induced by chronic sun exposure are called 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. The persons most susceptible to the deleterious effects of sunlight are those of 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 demarcated, 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.

Dermatoheliosis.

Many of the textural and tinctorial changes in sun-damaged skin are caused by alterations in the upper dermal elastic tissue and collagen. This process is called 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). Poikiloderma of Civatte refers to reticulate hyperpigmentation with telangiectasia, and slight atrophy of the sides of the neck, lower anterior neck, and V of the chest. The submental area, shaded by the chin, is spared ( Fig. 3.14 ). Poikiloderma of Civatte frequently presents in fair-skinned men and women in their mid to late thirties or early forties. Cutis rhomboidalis nuchae (sailor’s or farmer’s neck) is characteristic of long-term, chronic sun exposure ( Fig. 3.15 ). The skin on the back of the neck becomes thickened, tough, and leathery, and the normal skin markings are exaggerated. Nodular elastoidosis with cysts and comedones occurs on the inferior periorbital and malar skin (Favre-Racouchot syndrome) ( Fig. 3.16 ) on the forearms (actinic comedonal plaque) or helix of the ear. 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.

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