Acute Skin Reactions and Bacterial Infections

Etiology

Sunburn is chiefly caused by UVB radiation (290-320 nm), while photoaging and sun-related skin cancers is attributed to UVA radiation (320-400 nm). UVA also penetrates most glass, such as untreated windows of vehicles. Individual tolerance to sun exposure is a function of skin pigmentation, genetic ability to synthesize melanin in response to UV light, and metabolic and pharmacologic factors.

Prevention

Avoidance of the sun is the ultimate protection against UV-induced conditions. The highest intensity of light occurs between 10 a.m. and 4 p.m., so limiting UV exposure during this period is helpful. Brimmed hats, long-sleeved shirts, and long pants can cover the largest areas of exposed skin. Lightweight, UV-protectant clothing designed for hot weather is available at most sporting goods stores. Sunglasses with UV-protectant lenses will limit sun-related effects on the eyes, which can sometimes go unnoticed. Sunglasses without UV protection, meanwhile, can contribute to increased sun damage to the eyes.

When shading exposed areas is not possible, sunscreen can be used to protect the skin. Choose a product with a sun protection factor (SPF) of 30 and look for sunscreens labeled as “broad spectrum.” This indicates they provide protection against both UVA and UVB wavelengths. Products may be labeled “water resistant” for either 40 or 80 minutes but then lose effectiveness. Optimal protection requires application 15-20 minutes before sun exposure. The product should be applied liberally; 1 ounce is recommended for a full-body application. The average person uses less than half of the recommended amount to achieve the advertised protection. Reapplication during the day is necessary to maintain protection, particularly after swimming or perspiring heavily. Lip protection against UV light can be provided with specially formulated lip sunscreens.

Broad-spectrum coverage can be achieved by including complementary chemicals that absorb UVA and UVB light and/or by physical agents such as zinc oxide or titanium dioxide, which scatter UVA and UVB light. UVA protection is provided by avobenzone and oxybenzone, among other chemicals. UVB protection is provided by aminobenzoic acid, homosalate, octisalate, and octinoxate. Sun blocks often combine these chemicals and/or include titanium dioxide and zinc oxide to provide broad-spectrum coverage. Newer broad-spectrum agents are now available, such as Mexoryl. Some caution should be used with spray sunscreen. Dispersion by wind and failure to rub in sprayed product may lead to less photoprotection than is provided by traditional lotions ( Fig. 36.1 ). Accidental inhalation of sprayed products presents another risk.

Self-tanning products (spray or creams) do not impact melanin synthesis and provide no sun protection. Pre-travel tanning is not recommended. It provides only minimal protection and can actually increase overall UV exposure.

Treatment

Sunburn treatment options are directed at symptom control and are minimally effective. The most important first step after a burn is to limit further UV exposure through implementing above-mentioned prevention methods of sun avoidance and sun protection.

Mild sunburn is treated with nonsteroidal anti-inflammatory drugs and cool compresses, topical calamine, or aloe-based gels. Topical steroids have not demonstrated effectiveness in trials even though they are sometimes recommended.

Severe sunburn often does not respond to the aforementioned measures. Though not commercially available in the United States, topical indomethacin or diclofenac has been reported to be effective in reducing erythema and tenderness when applied soon after exposure. While prednisone seems to be ineffective at lessening the cutaneous sequelae of sunburn, it may improve the systemic symptoms of fever and headache that can occur with severe sunburn. Brief treatment with 40-60 mg/day for 3-4 days may be used.

Etiology

Irritant contact dermatitis is caused by soaps, solvents, detergents, cleansers, cutting oils, and acid or alkaline solutions. Excessive hand washing is an example of chronic irritant contact dermatitis caused by soaps and frequent wetting of the skin. Individual susceptibility to any irritant varies greatly.

Allergic contact dermatitis can result from exposure to an enormous array of chemical compounds but requires specific sensitization. The most common sensitizers include nickel, fragrances, rubber, formaldehyde, paraphenylenediamine, ethylenediamine, and neomycin. It is important to remember that many products sold for use on the skin contain sensitizers such as neomycin, benzocaine, ethylenediamine, fragrances, and lanolin.

Some topical agents can act in concert with UV light to produce photocontact dermatitis. This includes fragrances and, ironically, sunscreen agents, such as PABA and oxybenzone, which can cause photosensitive reactions.

Plant dermatitis ( phytodermatitis ) is a subset of contact dermatitis of particular importance to those traveling to rural areas. Many plants in a number of different families produce sensitizing chemicals. Poison ivy, poison oak, and poison sumac are members of the family Anacardiaceae and produce a resin capable of sensitizing 70% of the population. Related plants containing cross-reacting chemicals include the Japanese lacquer tree ( Rhus verniciflua ), the India marking nut tree, raw cashew shells ( Anacardium occidentale ), mango rind ( Mangifera indica ), and the fruit of the ginkgo ( Ginkgo biloba ). Causes of plant dermatitis depend on the local flora. Mango dermatitis is the most common plant dermatitis in Hawaii. Philodendron is the most common cause in India. Primrose is a frequent sensitizer in Europe.

Phytophotodermatitis is a sun-induced plant dermatitis. Celery, limes, lemons, parsley, figs, and others contain natural psoralens that can incite a phototoxic reaction when contact with these plants is followed by sun exposure. Cases of systemic phototoxicity after ingestion of these plants followed by UV exposure have been reported.

Clinical Features

The primary lesions of dermatitis are erythematous papules and vesicles. In severe cases, bullae form and papules coalesce into plaques. Chronic lesions show scale, secondary changes of lichenification, and, sometimes, bacterial superinfection. Pruritus is a constant feature of dermatitis. Contact dermatitis is distributed in sites of contact. The thicker skin of the palm and soles is more resistant. Allergic reactions may be spread with the hands to other sites of the body, such as the face, eyelids, and genitals. Plant dermatitis classically shows linear blisters where the skin brushed against the causative plant.

Diagnosis

Dermatitis is usually diagnosed clinically. Establishing the cause of contact dermatitis requires a careful history on exposure to plants, soaps, chemicals, topical medications, and the activities associated with the dermatitis. Patch testing is invaluable in establishing the etiology of allergic contact dermatitis.

Differential diagnosis of dermatitis includes scabies, insect bites, drug eruptions, swimmer's itch (cercarial dermatitis), atopic dermatitis, and psoriasis.

Treatment

Dermatitis of any etiology is treated in a similar manner. Known offending agents are avoided and protective clothing or gloves may be helpful when the person must continue activities associated with the dermatitis. Mild cases of dermatitis are treated with mid-potency topical steroids. Weeping or exudative lesions should be compressed with tap water or Burow's solution (see Chapter 35 ) for 15-30 minutes, four times a day, followed by topical steroids. Severe contact dermatitis is treated with prednisone 40-60 mg/day (adult dose), tapering the dose over 2-3 weeks. In allergic contact dermatitis, stopping prednisone too soon often results in recurrence. If a sensitized person contacts a known allergen, the skin should be promptly washed with soap and water. If secondary bacterial infection is present, it should be treated with antibiotics effective for Staphylococcus and Streptococcus spp.

Clinical Features

Common presentations and etiologies of drug eruptions are listed in Table 36.1 .

Diagnosis

Take a careful history, inquiring about over-the-counter and herbal/complementary medicines, including the date started. Exanthematous eruptions may be initially confused with viral exanthems. Urticaria may be caused by foods, parasitic and viral infections, or physical agents and often occurs idiopathically. The differential diagnosis of drug-induced photoeruptions includes other photosensitive rashes, such as polymorphous light eruption, lupus erythematosus, and some porphyrias.

Treatment

• Discontinue non-essential drugs.

• Antihistamines

  • Hydroxyzine: 25 mg by mouth every 4-6 hours

  • Diphenhydramine: 25-50 mg by mouth every 4-6 hours

  • Cetirizine: 10 mg/day (a less sedating option).

• Topical steroids for symptomatic relief

• Refer urgently to dermatology if mucous membranes are involved (mouth, vagina, conjunctiva) or if skin blisters.

Etiology and Clinical Features

There are many biting spiders , but several are worth special mention. The black widow spider, Latrodectus mactans , and other Latrodectus spp. are found worldwide. L. mactans is best identified by the red hourglass shape on the ventral abdomen. The bite is often painless, but a neurotoxin, α-lactotoxin, can cause systemic symptoms including muscle spasms, headache, abdominal pain, nausea, and hypotension, which can progress to shock and death.

Loxosceles spp., including the brown recluse spider, are found in North and South America, have a violin shape on the cephalothorax and produce venom containing sphingomyelinase D, causing extensive local skin and soft tissue necrosis. Brown recluse spider bites cause a mild urticarial reaction in the majority of cases. Some bites cause severe local reactions characterized by an expanding bulla with surrounding pallor followed by cyanosis and necrosis within 48-72 hours. Systemic involvement is rare but may be fatal and includes disseminated intravascular coagulation, hemolysis, and renal failure.

The wandering spider, Phoneutria nigriventer , is a large South American spider measuring 3 cm in body length and produces a potent neurotoxin.

Hymenoptera include bees, wasps, hornets, yellow jackets, and ants and cause painful reactions from venom injected from a posterior stinger. Half of the fatal envenomations in the United States are due to Hymenoptera . Honeybees produce venom containing histamine, phospholipase A, hyaluronidase, and other constituents. Stings produce a painful wheal that subsides over a few hours. In sensitized individuals, urticaria, laryngeal edema, bronchospasm, and anaphylaxis begin immediately. Less common systemic manifestations include toxic reactions from large numbers of simultaneous stings or a serum sickness-like syndrome that follows the sting by days to weeks.

Solenopsis invicta , the imported fire ant, is common in the southern United States, Argentina, Uruguay, and Brazil. Fire ant stings may cause anaphylaxis but usually produce local reactions. Stings cause an immediate wheal, which becomes a vesicle and then a sterile pustule over 12-24 hours.

Many species of scorpions are found in arid regions of the tropics and subtropics. Fatal stings are usually seen in children in areas where species produce neurotoxic venom. Scorpion stings cause a painful local reaction, occasionally with some necrosis. Some species produce venom that can induce sympathomimetic, parasympathomimetic, and neurologic symptoms. Infants and children are at highest risk for fatal reactions. Antivenoms are available for some scorpion toxins; however, there are often little data on their benefits, and risks include anaphylactic reaction.

Other arthropods that normally cause more localized responses include the Scolopendra centipedes of Hawaii and western United States, biting flies of many varieties found worldwide, fleas (including Tunga penetrans ; see Chapter 37 ), bedbugs, and human ectoparasites ( Chapter 37 ). Bedbug bites usually occur on the face, arms, ankles, or buttocks and are often arranged in a cluster or line of two or three bites. The appearance of individual bites ranges from small hemorrhagic puncta to papular urticaria that last for several days. The bites themselves occur at night and are typically painless. Bedbugs move from crevices in furniture to the human host for only a few minutes to feed and then retreat.

In addition to bites and stings, simple contact with Lepidoptera (butterflies, moths, and their caterpillars) can cause a pruritic erythematous papular rash within hours of contact. Caterpillar and moth species worldwide have been linked to reactions including conjunctivitis, keratitis, iritis, and pharyngitis.

One particularly dangerous species, the Lonomia obliqua , or giant silkworm moth of South America, can cause a fibrinolytic reaction similar to disseminated intravascular coagulation, which can be fatal. Another dangerous species, the Premolis caterpillar, lives on rubber trees in the Amazon. Repeated contact with its bristles can cause a periarticular fibrosis with permanent disfiguration.

Diagnosis

Stings usually present no problem with diagnosis because of the immediate pain. Bites may be more difficult to diagnose if the injury is painless or occurs during sleep. The pruritic papules of typical bites may resemble other hypersensitivity reactions, such as urticaria or dermatitis. Patients presenting with an unwitnessed “spider bite” often have community-acquired methicillin-resistant Staphylococcus aureus (MRSA) skin infection. Bullous or necrotic reactions may mimic other rashes. Definitive diagnosis is possible only if the bite is observed. In unresolved situations a biopsy may be helpful.

Treatment

Most papular and mild bullous reactions are self-limited and can be treated with compresses and topical steroids or oral antihistamines for pruritus. As with all penetrating skin injuries, tetanus prophylaxis should be given if the patient's status is not up-to-date.

Angioedema can be treated with prednisone 30-40 mg/day for several days. More severe generalized urticarial reactions or anaphylaxis are treated promptly with epinephrine 0.3-0.5 mg subcutaneously, repeated every 15-20 minutes. Most patients respond within one or two doses. Intravenous epinephrine may be necessary if hypotension persists despite these measures.

Black widow spider reactions may require hospitalization and treatment with analgesics, muscle relaxants, intravenous calcium, and supportive care. An equine antivenom is available in several countries.

Brown recluse spider bites are usually benign and can be treated symptomatically. Ice and elevation are used for symptomatic relief. Dapsone may prove useful to treat related tissue necrosis. To prevent treatment toxicity, glucose 6-phosphate dehydrogenase status should be evaluated prior to treatment with dapsone. A surgical approach is potentially harmful and should be avoided. Systemic reactions may be life threatening and require hospitalization for supportive care. Antivenom is not available in the United States but is available for South American recluse bites where the reaction is often more severe.

Scorpion stings are treated by local wound care, ice packs, and antihistamines. The Food and Drug Administration recently approved the scorpion antivenom Anascorp, or Centruroides immune F(ab)2, for envenomations resulting in serious clinical symptoms. Antihypertensives or anticonvulsants may be needed for supportive care.

Hymenoptera stingers (from bees, yellow jackets, wasps, or fire ants) should be removed as quickly as possible. While forceps are suggested, they should be applied to the shaft of the stinger immediately proximal to the skin, to avoid squeezing more venom into the patient from the venom sack attached to the stinger. When no instruments are available, an alternative is to scrape off the stinger.

Butterfly and moth (Lepidoptera) bristles, often invisible, can be removed with cellophane tape. Clothing that has been in contact with the moth or caterpillar should be removed and washed, and exposed skin should be washed.

Prevention

People with a history of severe sting reactions at risk of further exposure can undergo venom desensitization. All people with a history of severe reactions, whether or not they have undergone desensitization, should carry kits including antihistamines and a syringe of epinephrine. Epinephrine auto-injectors are commercially available and should be prescribed pre-departure. These devices are sensitive to high temperatures and should be kept within the temperature range on the package insert (e.g., never in a car parked in the sun).

Protective clothing, insect repellant, and even repellant-treated clothing can all help prevent some stings and bites (see Chapter 6 ). However, insect repellents have no effect on spiders or bees.

Control of bedbugs involves treating crevices in walls and furniture with an insecticide, such as 0.5% lindane or 2% malathion, or spraying bed nets with a permethrin-containing insecticide.

Bacterial Skin Infections

Bacterial infections of the skin are a major problem in the tropics and a common problem among travelers. One study of travelers returning to France found that bacterial infections were the second most common presenting skin condition after cutaneous larva migrans ( Chapter 37 ).

The high prevalence of bacterial infections in tropical climates is attributed to the warm, humid environment and can be worsened by close contact and poor hygiene. Other predisposing factors include insect bites, traumatic lesions, and other dermatoses such as contact dermatitis and scabies. Infections caused by staphylococci and streptococci are far more common in the tropics than are the exotic “tropical diseases.”