Summer Hazards: Part 1

From 22nd Annual National Conference on Wilderness Medicine, sponsored by The American College of Emergency Physicians (ACEP), the ACEP State Chapter of California, Inc, and Wilderness and Travel Medicine

Educational Objectives

The goals of this program are to improve the management and prevention of skin cancer, and to improve the diagnosis and treatment of spider bites. After hearing and assimilating this program, the clinician will be better able to:

1.   Describe which types of solar radiation are responsible for photodamage to skin and promotion of skin can­cers.

2.   Identify clinical warning signs of melanoma.

3.   Discuss specific sun protection methods.

4.   Recognize symptomatology of common venomous spider bites.

5.   Choose appropriate treatment for black widow and brown recluse spider bites.

Faculty Disclosure

In adherence to ACCME Standards for Commercial Support, Audio-Digest requires all faculty and members of the planning committee to disclose relevant financial relationships within the past 12 months that might create any personal conflicts of in­terest. Any identified conflicts were resolved to ensure that this educational activity promotes quality in health care and not a proprietary business or commercial interest. For this program, Drs. Swetter and Erickson and the planning committee reported nothing to disclose.

Acknowledgements

Drs. Swetter and Erickson spoke on August 6, 2008, in Big Sky, MT, at 22nd Annual National Conference on Wilderness Med­icine, presented and jointly sponsored by the American College of Emergency Physicians (ACEP), the ACEP State Chapter of California, Inc, and Wilderness and Travel Medicine. The Audio-Digest Foundation thanks the speakers and the sponsors for their cooperation in the production of this program.

Sun Protection and Solar Radiation

Susan M. Swetter, MD, Associate Professor of Derma-tology, Director, Pigmented Lesion and Cutaneous Mel­anoma Program, Co-Director, Stanford Multidisciplinary Melanoma Clinic, Stanford University Medical Cen­ter/Veterans Affairs Palo Alto Health Care System, Palo Alto, CA

UV light: most radiation from sun visible and infrared light; UV light 6% of sun’s radiation reaching earth; lower wavelengths effectively blocked by ozone; UV reaching earth’s surface »95% UV-A and »5% UV-B; at skin, UV light partially reflected and partially absorbed, then transmitted to deeper layers

Consequences of excessive sun exposure: stratum corneum fissures, reducing barrier function and increasing dry­ness; keratinocytes lose normal alignment and become flattened, so epidermis thins; atypical keratinocytes found in actinic keratoses (AK; precancerous); melanocytes enlarge and migrate higher; dermis thins from loss of colla­gen and elastin; more prominence of blood vessels causes easy bruising and purpura

UV-B: wavelength most responsible for sunburn and skin cancer; shorter wavelength than UV-A; penetrates epider­mis and upper dermis; seasonal and daily variations; strongest from 10 am to 4 pm; 400 times more intense in summer than in winter; absorbed by ozone layer and blocked by window glass

UV-A: causes sun damage without sunburn; longer wavelength that penetrates deeper into mid-dermis; only par­tially blocked by window glass (important for photosensitive individuals); year round and all day long; more photosensitizing than UV-B; photodamage causes wrinkling and sagging of skin, increased loss of collagen and elastin in dermis, and eventually photoimmunosuppression with reduction of T cells; contributes to skin cancer (not as much as UV-B) and cataract formation

Skin cancer incidence: »90% of skin cancers worldwide related to excessive sun exposure, particularly in fair-skinned individuals; increased near equator, where UV-B more intense; UV-B inhibits immune functions of skin (eg, antigen-presenting cells) and induces immunosuppressive cytokines; UV-B causes specific mutations in P53 tumor suppressor gene in skin, related to nonmelanoma skin cancer

Skin cancer statistics: most common cancer worldwide; in United States, basal cell carcinoma (BCC) most common skin cancer (>1 million per year); squamous cell carcinoma (SCC) second most common (»300,000 per year); mel­anoma most deadly, »4% of all skin cancers; 1 in 5 Americans develop skin cancer

Nonmelanoma cancers: less fatal but locally aggressive and invasive; occur in sites of cumulative long-term sun ex­posure (eg, head, neck, ears, face); low metastatic rate but morbidity and health care costs high

Phototypes: individual’s sun sensitivity, based on type and amount of pigment (melanin) produced; 6 phototypes ac­cording to tendency to burn or tan; type 1  —  always burns, never tans; type 2  —  burns easily and tans minimally; type 3  —  burns and tans moderately; type 4  —  does not usually burn, but almost always tans; type 5  —  rarely burns, tans easily; type 6  —  (very dark black) burns only with severe exposure; less sun-sensitive types (4, 5, and 6)  —  less prone to skin cancer but still at risk; rates of melanoma increasing, particularly in Asian and Latino populations; melanoma in darker individuals tends to occur in less sun-exposed sites

Non-UV-related risk factors: less common; individuals who had Grenz ray facial treatments for acne in 1940s and 1950s present with numerous nonmelanoma skin cancers years later; chronic wounds (eg, stasis ulcers, lupus or burn scars); arsenic-induced SCC (related to well water); family history of skin cancer related to skin type; immu­nosuppressed patients have increased rates equivalent to duration of suppression (especially SCC), and higher rates of metastatic lesions

Basal cell carcinoma: translucent pearly pink nodule in sun-exposed area with telangiectasias; most on head, neck, and shoulders (especially in men); metastatic rates low but BCC locally destructive; friable; suspect any nonhealing sore in sun-exposed area, especially in older persons

Squamous cell carcinoma: less friable, more indurated than BCC; adherent keratotic scale; frequently erodes or ul­cerates; second most common cause of skin cancer death after melanoma in United States (1500 deaths per year); AK treatable precursor lesion with low rate of malignant transformation; SCC more common on lip than BCC; ker­atoacanthoma type grows rapidly, is painful, and can involute

Treatment of nonmelanoma skin cancer: treat superficial BCC or SCC in situ (Bowen disease) with topical agents (eg, 5% 5-fluorouracil, 5% imiquimod); electric desiccation and curettage useful in individuals with superficial tu­mors on back; surgery mainstay of therapy; Mohs micrographic surgery allows intraoperative microscopic assess­ment of peripheral and deep tissue margins; use for large tumors, especially on face or lip, to spare tissue and optimize cosmesis; highest cure rate but more costly than standard surgery

Melanoma: cure rate related to early detection; one death every hour from melanoma in United States; responsible for >80% of skin cancer deaths; invasive tumor cells infiltrate below epidermis into dermal lymphatic and blood vessels and metastasize; in situ cases (do not extend below basal layer) curable; incidence  —  sixth most common cancer in men and seventh in women; >8000 deaths per year

Risk factors: changing nevus; most melanomas do not originate from true nevi (moles), but arise de novo; older age, male sex, large number of moles, atypical moles, sun sensitivity, and strong family history should prompt careful examination of skin

Warning signs: ABCDs of melanoma detection developed in mid 1980s; asymmetry (one half of lesion does not match other); border irregularity (notching or blurring of edges); color variegation; diameter (greater than size of pencil eraser [>6 mm]); ABCDs effective for signs of superficial spreading melanoma (most common type); nod­ular melanoma does not follow guidelines, so E added for evolving or changing over time; “ugly duckling” sign (something that does not match or fit mole pattern) promoted in Europe

Primary prevention of skin cancer: reducing harmful exposure to sun should start in early childhood; majority of lifetime sun exposure received before age 20 yr; childhood sun exposure increases moles in adulthood, and high number of moles independent risk factor for melanoma; »65% of melanomas worldwide attributed to sun exposure; in Australia “slip, slap, slop” (slip on shirt, slap on hat, slop on sunscreen) marketed to school-aged children, par­ents, and teachers; implemented in 1970s; lowered rates of sunburn and now leveling incidence of melanoma in younger persons; melanoma typically develops in midlife, so full effect of campaign will not be known for few more decades

Prevention of sun damage: sun-safe strategies; sunscreen, sun avoidance between 10 am and 4 pm, covering with clothing, hats, and protective eyewear; avoiding intentional tanning (does not confer sun protection; still need sun­screen)

Tanning beds: emit more UV-A than UV-B at levels 15 times stronger than natural sunlight; 30 min in tanning booth equivalent to full day of sun exposure; largely unregulated; only 25 states in United States regulate use by minors; frequent early use of tanning beds doubles risk for nonmelanoma skin cancers as well as for melanoma; worldwide data show 15% higher risk for melanoma in those with ³ 1 use of tanning beds, and 75% increased lifetime risk if first used before age 35 yr

Vitamin D: obtained from UV-B, diet, and supplements; UV-B responsible for photoconversion to active pre-metab­olite of vitamin D; beneficial for bone health; potential benefits include decreased incidence of and mortality from certain cancers (eg, colorectal, non-Hodgkin lymphoma, prostate, breast, and melanoma); exact amount of UV-B needed daily for adequate serum vitamin D levels unknown; fair-skinned persons (types 1 and 2) efficient at photo­conversion and production of vitamin D₃ in skin; type 2 needs 5 to 15 min of incident light exposure before maxi­mizing skin production of serum vitamin D; darker-skinned individuals and elderly less efficient at photoconversion; darker-skinned phototypes require 7 times more UV-B for same skin production of vitamin D₃

Sun protection factor (SPF): sunscreens absorb or reflect UV radiation, thus preventing sunburn; SPF related to per­son’s minimal erythema dose (MED; amount of time for sunlight to cause redness of skin within 24 hr of exposure with sunscreen compared to without); darker skin types have higher MEDs; depends on geographic location, time of day, and season of year; SPF is ratio of amount of time before burning with sunscreen, compared to without (eg, SPF of 15 affords 15 times longer sun exposure); once MED reached, more sunscreen will not delay sunburn; higher SPFs provide some greater protection, but SPF >50 questionable

Sunburn: mild to severe; general erythema; severe reactions analogous to thermal burns (pain, fever, chills, nausea, blisters, scarring); symptomatic relief with, eg, cool compresses, colloidal oatmeal baths, soothing lotions; nonste­roidial anti-inflammatory drugs reduce pain and inflammation through prostaglandin inhibition; topical steroids shown to reduce erythema, edema, burning, and itching, if applied at first sign of sunburn; systemic steroids not ef­fective

Sunscreen efficacy: applied correctly, »93% of UV blocked by SPF 15, »96% by SPF 30, and 98% by SPF 50 or 60; consumers underapply sunscreen, so not getting advertised SPF; now looking at efficacy of sunscreens for UV-A; many UV-A filters degrade after »30 min of use; broad-spectrum sunscreens prevent sunburn and reduce AKs and SCC; not preventive against melanoma development; sunscreen adjunct to “sun protection package” that includes protective clothing, hat, and eyewear; need minimum SPF of 15 for prevention of photoaging and skin cancer

Types of sunscreens: chemical sunscreens absorb UV light and dissipate its energy; physical sunscreens reflect and scatter UV light; UV-B absorbers include para-aminobenzoic (PABA) derivatives, salicylates (useful but weak), benzophenones (oxybenzone) and cinnamates, anthranilates, and triazenes; UV-A absorbers include benzophe­nones and dibenzoylmethanes; avobenzone (Parsol 1789) effective UV-A filter but photolabile, ie, breaks down af­ter 30 min of sun exposure; photostabilizers —approved in United States for SPF 15 (ecamsule [Mexoryl]) combined with arobenzone and octocrylene [Anthelios] or combination of avobenzone with oxybenzone [Helio­plex]; physical sunblocks  —  include micronized titanium dioxide and micronized zinc oxide; to maximize UV-A absorption, titanium dioxide coated with manganese

Water-resistance: no sunscreen waterproof; “water resistant” indicates SPF maintained after sunscreen applied and person immersed in still water for 40 min; Australia requires 240 min in moving water

Ideal sunscreen use: SPF >30; use copiously; apply to dry skin 15 to 20 min before exposure; efficacy wanes, so re­apply every 2 hr; SPF renamed sunburn protection factor; adjunct to shade, long sleeves, hats, and avoidance of midday sun; altitude  —  at >8000 ft, UV intensity increased by 60% to 80%; more frequent application of sunscreen required, as well as hat and sunglasses

Future directions: when added to sunscreens, antioxidants (eg, vitamin C and E, b-carotene, a-lipoic acid) improve photoprotection and skin repair

Arthropod Bites and Stings: Part 1

Timothy B. Erickson, MD, Professor and Assistant Head, Department of Emergency Medicine, and Director, Clinical Toxicology, University of Illinois College of Medicine, Chicago

Case presentation: 41-yr-old man presents to emergency department (ED) with severe abdominal pain and cramping of 6 hr duration; also diaphoresis, low grade fever, and anorexia; recent deer hunting trip; symptoms began  1 hr af­ter suffering scrotal bite from insect while using cabin outhouse; normal past history, no previous abdominal sur­gery or kidney stones; patient rocking side-to-side in fetal position and has tachycardia; abdominal examination consistent with peritonitis; genitourinary examination shows scrotal erythema, otherwise normal; no focal deficits on neurologic examination; laboratory results show leukocytosis and normal electrolytes, creatinine, glucose, liver function tests, amylase, and lipase; check for free air on x-ray negative, so viscus perforation unlikely; consider re­nal stone even without hematuria, as 15% to 20% of patients with renal colic have normal urine; patient unrespon­sive to calcium and morphine; friends brought in remains of black widow spider found in outhouse; patient given antivenin and recovered rapidly

Black widow spider: 8 eyes, 8 legs, fangs, and spinnerets; red hourglass on female, male may have white marking; trappers, not stalkers; male usually dies after mating and/or is consumed by female

Black widow spider bites: venom releases neurotransmitters at norepinephrine, acetylcholine, and g-aminobutyric acid (GABA) receptors; rapid degeneration of motor endplates and influx of sodium; works at sodium-calcium channel exchange; bite frequently goes unnoticed; symptoms include lymph node pain, burning on soles of feet, ab­dominal rigidity, agitation, diaphoresis, salivation, slurred speech, and convulsions; treat with opioids, dantrolene, or intravenous calcium (calcium has received mixed reviews, not as effective); need antivenin if pain severe; anti­venin harvested from horses, not plentiful; save for extremes of age or severely ill patients; monitor for anaphylaxis

Case presentation: man 39 yr of age; low-grade fever, joint aches, muscle pains, and malaise; denies trauma; nor­mally healthy; working in basement woodshop, cutting wood in forest; large necrotic lesion on back of leg; labora­tory results consistent with brown recluse spider bite; patient admitted and given antibiotic; wound debrided; lesion healed with much scarring that required skin grafting

Brown recluse spider venom: hematotoxic; brown recluse spider more venomous than pit vipers but unable to inject as much venom; hematotoxic signs include international normalized ratio (INR) elevation, hematuria, and throm­bocytopenia; initial wound debridement not always appropriate

Brown recluse spider characteristics: violin-shaped marking on dorsal cephalothorax (fiddleback or violin spider); found in south, central and midwest United States, and now more north and west; not stalkers, bite in defense; brown fawn-like color, slender, and fast runners; 6 rather than 8 eyes

Venom effects: direct lytic action on red blood cells (RBCs) causes disseminated intravascular coagulation (DIC) or coagulation necrosis; bullseye necrotic lesion at bite site (central vesicular lesion, bluish hue, then blanching or red­ness); treat before necrosis occurs; severe systemic reactions in »5% of patients; send blood to laboratory (baseline for later comparison if systemic reaction occurs)

Treatment: tetanus prophylaxis, antihistamines, and antibiotics if concerned about infection; steroids not helpful; treat locally; dapsone if patient presents early, but overdosing induces methemoglobinemia; do not remove all ne­crotic tissue, as normal patient recovers that tissue; if systemic reaction occurs, treat cause; transfuse RBCs and platelets if DIC develops; dialysis if renal failure occurs; no commercially available antivenin; pesticides not effec­tive; best to inspect clothing for spiders, shake out clothing, and let spider scurry off

Suggested Reading

Brown TT et al: The epidemiology of sunburn in the US population in 2003. J Am Acad Dermatol 55:577, 2006; de Roodt AR et al: Toxicity of two North American Loxosceles (brown recluse spiders) venoms and their neutralization by antiven­oms.Clin Toxicol  45:678, 2007; Diaz JH, Leblanc KE: Common spider bites. Am Fam Physician 75:869, 2007; Furbee RB et al: Brown recluse spider envenomation.  Clin Lab Med 26:211, 2006; Greinert R: Skin cancer: new markers for bet­ter prevention. Pathobiology 76:64, 2009; Hexsel CL et al: Current sunscreen issues: 2007 Food and Drug Administration sunscreen labeling recommendations and combination sunscreen/insect repellent products. J Am Acad Dermatol 59:316, 2008; Lowe NJ: An overview of ultraviolet radiation, sunscreens, and photo-induced dermatoses.  Dermatol Clin 24:9, 2006; Murray JC et al: A topical antioxidant solution containing vitamins C and E stabilized by ferulic acid provides pro­tection for human skin against damage caused by ultraviolet irradiation.  J Am Acad Dermatol 59:418, 2008; Ridley AJ et al: Cellular and sub-cellular responses to UVA in relation to carcinogenesis.  Int J Radiat Biol  85:177, 2009; Situm M et al: The role of UV radiation in the development of basal cell carcinoma.Coll Antropol  2:167, 2008; Sotelo-Cruz N et al: Poisoning caused by Latrodectus Mactans (Black Widow) spider bite among children. Gac Med Mex 142:103, 2006; Vetter RS, Isbister GK: Medical aspects of spider bites. Annu Rev Entomol 53:409, 2008.