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Volume 54, Issue 26
July 14, 2006

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SUMMER HAZARDS

From “Rural, Remote, and Wilderness Medicine,” sponsored by the University of California, Davis, School of Medicine

OUTDOOR DERMATITIS —Mikla Noponen, MD, Staff Pediatrician, Tuolumne Rural Indian Health Clinic, Sonoma, CA
Hazards of outdoor exposure to sunlight: being in sunlight results in exposure to UV radiation; UVB—causes sunburn; present in high-noon sun (from 10 am to 2 pm); all sunscreens intended to block UVB radiation; UVA— present in sunlight all day long; passes through glass; penetrates skin layers and causes photoaging (wrinkles); together, UVA and UVB contribute to skin cancer; best sunscreens contain UVB and UVA blockers
Xeroderma pigmentosum: eg, 4-yr-old boy who developed second-degree sunburn, photophobia, and conjunctivitis after brief exposure to high-noon sun; genetic disorder; relatively rare (incidence 1 per 250,000 in US population); usually diagnosed early in life; leads to skin cancer (mean patient age for skin cancer 8 yr vs 60 yr in healthy population); survival poor (<40% of patients survive beyond 20 yr of age); mortality from malignant melanoma and squamous cell carcinoma; management—no definite treatment; mainstay avoidance of sunlight (sunscreens; protective clothing; not going outdoors during daylight hours); if suspected, refer immediately to dermatologist (requires definite diagnosis and regular follow-up); all cases require ophthalmology consultation (80% of patients have ocular damage from sunlight exposure); 20% of patients have neurologic problems; genetic testing available; www.xps.org excellent website for support and information
Phytophotodermatitis: eg, 2.5-yr-old girl presented with 4-day-old rash; rash result of phototoxic reaction caused by interaction of sunlight (UVA radiation) and photosensitizing compounds (furocoumarins) of certain plants on skin; sources of furocoumarins include limes, bergamot oil, and weeds (eg, sagebrush, goldenrod, ragweed, hogwood); rash typically painless and asymptomatic, occasionally pruritic; appears relatively soon after sunlight exposure; can take months for rash to fade
Cercarial dermatitis: eg, 6-yr-old and 11-yr-old boys developed papular itchy rash after swimming in lake; also known as “swimmer’s itch”; allergic reaction occurs when schistosomes penetrate skin of swimmer; no systemic infection; extremely common worldwide; exposed parts of body mostly affected; rash self-limiting (peaks in 48 hr, then subsides over 1-2 wk); treatment—oral antihistamines and topical steroids; prevention—avoid lakes known to be contaminated; towel dry vigorously after swimming; experimental longer-acting formulation of N, N-diethyl-m-toluamide (DEET) combined with liposome [LipoDEET] may be effective in preventing schistosomiasis
Seabather’s eruption: eg, after swimming in ocean, 11-yr-old girl presented with papular rash on areas of skin covered by swimsuit; occurs when larvae of jellyfish get caught between skin and swimsuit; rubbing of swimsuit against skin causes larvae to release toxin-filled barb into skin; results in extremely uncomfortable rash; can occur minutes after swimming; rash lasts 2 days to 2 wk; patients can have low-grade systemic symptoms; management—take off swimsuit and rinse in sea water; dry gingerly with towel (do not rub vigorously); avoid immediate fresh-water shower; swimsuit must be thoroughly washed and dried; treatment—oral antihistamines and topical steroids
Cutaneous larvae migrans: eg, young woman presented with itchy rash on foot; occurs when larvae of dog or cat hookworm invade skin; results from contact with soil contaminated with animal feces (usually sandy, warm, and shady areas); once under skin, larvae migrate (from mm to 1-2 cm per day); creates intensely pruritic serpiginous track (when treating, remember that larvae 1-2 cm ahead of track edge); most common in tropical and subtropical areas; management—most larvae die under skin, but this generally takes from 2 wk to 2 mo; oral thiabendazole effective but produces side effects (eg, anorexia, nausea, dizziness); good alternative topical thiabendazole (10% solution or cream) applied 3 to 4 times daily (kills larvae within 2 days); albendazole safe in children (adjusted dosing over 3 days); for adults, single 12-mg dose of ivermectin effectively kills larvae
Rocky Mountain spotted fever: eg, 6-yr-old girl presented with rash on palms and ankles; rash typically starts on wrists and ankles, moves to soles and palms, then starts moving centripetally to trunk and head (macular rash, blanching or partially blanching; becomes petechial at 5 days; if left untreated, can progress from petechial to purpuric); disease caused by Rickettsia rickettsii; most common fatal tick-borne disease in United States; >54% of cases in Southeastern United States (Oklahoma, Arkansas, Tennessee, North Carolina, and South Carolina); mostly occurs April to September; incubation period between tick bite and symptoms 1 wk; transmitted by Rocky Mountain wood tick, American dog tick, and brown dog tick; diagnosis clinical; tick bite history in 50% of cases; classic triad of symptoms fever, headache, and rash (rash present in 75%-95% of documented cases; headache typically unremitting); laboratory diagnosis—serum antibody titer (either single high titer or 4-fold increase in titer 2-3 wk apart; other laboratory tests not helpful); treatment— doxycycline for adults and children; dose 100 mg bid intravenously (IV) or po; in patients <100 lb, dose 4 mg/kg per day; continue until patient afebrile for at least 2 to 3 days
Lyme disease: eg, young man living in Connecticut presented with 5-day-old rash on leg that was getting bigger and had symptoms of low-grade fever, malaise, and myalgia; rash characteristic of Lyme disease stage 1, erythema migrans (EM); typically flat, red, round rash that gradually expands; can exceed 1 ft in diameter (takes 2-3 wk); disease caused by spirochete (Borrelia burgdorferi); >10,000 cases/yr reported to Centers for Disease Control and Prevention (CDC); incubation period from tick bite to rash 1 to 2 wk; patients develop flu-like symptoms; transmitted by deer tick and Western deer tick; high-risk areas for Lyme disease include New England and some parts of Great Lakes region (most of West Coast low risk); laboratory diagnosis—2-step process; enzyme-linked immunosorbent assay (ELISA) to screen for serum antibodies; if ELISA positive, follow with Western immunoblot; if immunoblot also positive, patient has Lyme disease; if immunoblot negative, ELISA considered false-positive and patient does not have Lyme disease
Clinical manifestations: stage 1—EM; stage 2—multiple, smaller EM; arthritis in 60% of patients; constitutional symptoms; transient heart block in 5% of patients; stage 3—chronic arthritis; tertiary neuroborreliosis (rare); all stages effectively treated with antibiotics
Treatment: adults and children 8 yr of age—doxycycline po bid for 2 to 3 wk; children <8 yr of age—amoxicillin 25 to 50 mg/kg per day po bid for 2 to 3 wk; cefuroxime recommended for patients with allergies and pregnant women; if stage 2 or 3 disease, consult with infectious disease specialist on treatment (IV ceftriaxone recommended for documented central nervous system [CNS] infection); 2001 study in New England Journal of Medicine reported that single 200-mg dose of doxycycline given within 72 hr of tick bite can prevent infection
Poison oak: appearance of rash depends on how patient exposed; also called rhus dermatitis; includes poison ivy, poison oak, and poison sumac; allergen (urushiol) in sap of plant; allergic reaction typically occurs 48 hr after exposure; causes intense pruritus; rash can continue to erupt for 2 wk (if it continues to erupt beyond that period, patient being reexposed); severity (duration and extent) of rash depends on amount of exposure and patient’s level of sensitization
Treatment: wash oil off skin, clothing, pets, tools; severe reaction within 6 hr of exposure requires IV steroids; for reaction within 24 hr, can give steroids intramuscularly (IM); most patients present 48 hr after exposure; assess severity of rash; make sure patient has washed self well; give topical corticosteroids; if swelling present, give oral prednisone; speaker gives 5-day course of medication (tapered); learn to recognize plant and avoid exposure; use barrier lotions; protective clothing; off-label products used for washing poison oak oil off skin include Zanfel (safe for children; extremely expensive) and Fels-Naptha (laundry soap; comes with warning to avoid prolonged contact with skin)
Questions and answers: percentage of patients with Lyme disease that have EM rash (50%-75%); does rash always begin at site of bite? (yes); has speaker given prophylactic antibiotics in children with tick bite? (yes); why is doxycycline recommended for treatment of Rocky Mountain spotted fever in children but contraindicated for Lyme disease in children <8 yr of age? (Rocky Mountain spotted fever progresses rapidly and is fatal in 40% of children; with Lyme disease, have more time; also, with Rocky Mountain spotted fever, doxycycline works best)
SNAKEBITES —Robert W. Derlet, MD, Professor and Chief, Department of Emergency Medicine, University of California, Davis, School of Medicine
Introductory remarks: most snakes not poisonous; only place that has more poisonous than nonpoisonous snakes Australia; relative toxicity of snake venoms (Pacific rattlesnake, 1.0; cottonmouth, 0.1; Eastern diamondback, 2.0; Mojave rattlesnake, 10.0; coral snake, 2.0; Australian elapids, 10-50); in addition to toxicity of snake venom, probability of envenomation also important (if bitten by viper, 70%-75% chance of being envenomated; if bitten by elapid, only 50% chance; if bitten by sea snake, small chance of envenomation, but venom fairly toxic); if abroad and bitten by snake, will probably be given antivenin approved for all poisonous snakes in that area
Management of rattlesnake bites: do not cut and do not apply tourniquet to snakebites (take patient to hospital); 25 species of rattlesnakes (potentially, 25 different effects); symptoms often progress slowly; surgery only if antivenin fails
Grades of envenomation in rattlesnake bites: minimal—local signs and symptoms; no systemic effects; no laboratory abnormalities; moderate—extensive local effect or mild local effect with systemic effects; severe—severe systemic symptoms and signs; abnormal laboratory findings; grade of envenomation important as amount of antivenin given for treatment based on severity of bite
Envenomation grade of snakebites that occur in field: most moderate (56%); mild 25%; remainder severe
Clinical effects: local—pain; swelling; ecchymosis; systemic—vomiting; coagulation abnormalities, bleeding; altered mental status; rhabdomyolysis (more severe in some types of snakes, eg, canebrake rattlesnake in Florida); cardiac and blood pressure (BP) issues, and ultimately, circulatory failure (in severe snakebites); respiratory failure
Thrombocytopenia and rattlesnake bite: study looked at 19 cases of bites from timber rattlesnakes; found severe thrombocytopenia in 50% of patients; treating with platelets ineffective; thrombocytopenia effectively managed (reversed) with antivenin
Comments: when bitten, patient may initially go to clinic or emergency department (ED), do well, and be discharged, only to later come down with clinical symptoms; case example—32-yr-old patient bitten on left ring finger; had mild swelling and erythema that resolved; left ED because feeling better; returned 5 hr later with marked swelling and coagulation abnormalities that required 20 U of antivenin; key point—patients who present at ED with snakebite need to be observed to determine whether they have “dry bite” or clinical effects delayed
First aid in rattlesnake bites: keep wound clean; immobilize; transport victim to nearest hospital; do not—“cut and suck” bite; apply tourniquet; put ice on snakebite; use snakebite kits (study looking at efficacy of “extractor” marketed for removing venom from snakebite in field found device removed insufficient amounts of venom [only 0.4% on average, maximum of 1%]; in other studies looking at “cut and suck” method, no more than 8% of venom removed)
Reasons for treating rattlesnake bites: to prevent death in small number of patients (rattlesnake bites generally not lethal, unlike cobra and black mamba bites); to prevent necrosis and amputation; to reduce chronic pain and disability
Treatment for rattlesnake bites: 2 types of antivenin; antivenin (Crotalidae) polyvalent (equine origin; Wyeth)—developed in 1920s from hyperimmune horse serum; improved and purified in 1950s; efficacy proven in animal models in 1960s; problem is that patients developed delayed hypersensitivity reactions to this form of antivenin; Crotalidae polyvalent immune Fab (ovine origin; CroFab)—underwent clinical trials in 1990s; approved by Food and Drug Administration (FDA) in 2001
Procedure for use of antivenin (Crotalidae) polyvalent (equine origin): estimate amount needed; mix vials of antivenin; apply skin test to patient; place antivenin in IV solution; administer cautiously; skin test has high false-positive rate, relatively low false-negative rate; allergic reactions to antivenin include urticaria, itching, and cardiovascular collapse (extremely rare); doses (mild bite, 5-8 vials; moderate, 8-12 vials; severe, 13 vials); if after giving first dose of antivenin, patient continues to worsen, give more (“it doesn’t hurt to give a lot”); downside of traditional antivenin is that serum sickness usually not seen until 4 to 7 days after bite; nearly every patient who receives >10 vials of standardized older antivenin will develop serum sickness and need to receive steroids

Educational Objectives

The goal of this activity is to review some of the medical problems associated with outdoor activities, specifically dermatologic problems and snakebite. After hearing and assimilating this program, the clinician will be better able to:
1. Recognize the signs of the genetic disorder xeroderma pigmentosum, participate in establishing a definitive diagnosis, and advise the patient’s family on protection from sunlight.
2. Identify the characteristics and causes of forms of outdoor dermatitis such as phytophotodermatitis, cercarial dermatitis, seabather’s eruption, cutaneous larvae migrans, and rhus dermatitis, and offer effective treatment and/or prevention strategies.
3. Cite the epidemiology and clinical effects of Rocky Mountain spotted fever and Lyme’s disease, recognize the dermatologic manifestations of these diseases, and employ the recommended steps for diagnosis and treatment.
4. Understand and explain the risk for envenomation when bitten by a snake, as well as the clinical effects of mild, moderate, and severe snakebites.
5. Describe the recommended (and contraindicated) steps in the management of rattlesnake bite, and explain the procedure for using antivenin (Crotalidae) polyvalent (equine origin).

Discussed on This Program

Acetaminophen (N -acetyl-P -aminophenol; APAP) [several trade names and formulations]
Albendazole [Albenza]
Amoxicillin [Amoxil, Amoxil Pediatric Drops, Trimox, Trimox Pediatric Drops]
Antivenin (Crotalidae) polyvalent (equine origin)
Ceftriaxone sodium [Rocephin]
Cefuroxime [Ceftin, Kefurox, Zinacef]
Crotalidae polyvalent immune Fab (ovine origin) [CroFab]
Diphenhydramine HCl [Benadryl, others]
Doxycycline [Adoxa, Atridox Injection, Bio-Tab, Doryx, Doxy 100, Doxy 200, Periostat, Vibramycin, Vibra-Tabs]
Ibuprofen (several trade names and formulations)
Ivermectin [Stromectol]
N, N-diethyl-m-toluamide (DEET)
Prednisone [Deltasone, Liquid Pred, Meticorten, Orasone, Panasol-S, Prednicen-M, Prednisone Intensol Concentrate, Strerapred DS]
Thiabendazole [Mintezol]

Suggested Reading

Allen PL: Leaves of three, let them be: if it were only that easy! Pediatr Nurs 30:129, 2004; Bebarta V, Dart RC: Effectiveness of delayed use of crotalidae polyvalent immune Fab (ovine) antivenom. J Toxicol Clin Toxicol 42:321, 2004; Bergeson PS, Weiss JC: Picture of the month. Phytophotodermatitis. Arch Pediatr Adolesc Med 154:201, 2000; Bond RG, Burkhart KK: Thrombocytopenia following timber rattlesnake envenomation. Ann Emerg Med 30:40, 1997; Brenner MA, Patel MB: Cutaneous larva migrans: the creeping eruption. Cutis 72:111, 2003; Bush SP: Snakebite suction devices don't remove venom: they just suck. Ann Emerg Med 43:187, 2004; Chapman AS et al: Tickborne Rickettsial Diseases Working Group; CDC. Diagnosis and management of tickborne rickettsial diseases: Rocky Mountain spotted fever, ehrlichioses, and anaplasmosis--United States: a practical guide for physicians and other health-care and public health professionals. MMWR Recomm Rep 55:1, 2006; Cleaver JE: Cancer in xeroderma pigmentosum and related disorders of DNA repair. Nat Rev Cancer 5:564, 2005; Cowles RA, Colletti LM: Presentation and treatment of venomous snakebites at a northern academic medical center. Am Surg 69:445, 2003; DePietropaolo DL et al: Diagnosis of Lyme disease. Del Med J 78:11, 2006; Dumler JS, Walker DH: Rocky Mountain spotted fever--changing ecology and persisting virulence. N Engl J Med 353:551, 2005; Gold BS, Barish RA: Venomous snakebites. Current concepts in diagnosis, treatment, and management. Emerg Med Clin North Am 10:249, 1992; Goodall J: Oral corticosteroids for poison ivy dermatitis. CMAJ 166:300, 2002; Juckett G, Hancox JG: Venomous snakebites in the United States: management review and update. Am Fam Physician 65:1367, 2002; Khachemoune A et al: What is your diagnosis? Diagnosis: Seabather's eruption. Cutis 77:148, 2006; Kumar S et al: Risk factors for seabather's eruption: a prospective cohort study. Public Health Rep 112:59, 1997; Lavonas EJ et al: Initial experience with Crotalidae polyvalent immune Fab (ovine) antivenom in the treatment of copperhead snakebite. Ann Emerg Med 43:200, 2004; LoVecchio F et al: Serum sickness following administration of Antivenin (Crotalidae) Polyvalent in 181 cases of presumed rattlesnake envenomation. Wilderness Environ Med 14:220, 2003; Magnaldo T, Sarasin A: Xeroderma pigmentosum: from symptoms and genetics to gene-based skin therapy. Cells Tissues Organs 177:189, 2004; Offerman SR, Smith TS, Derlet RW: Does the aggressive use of polyvalent antivenin for rattlesnake bites result in serious acute side effects? West J Med 175:88, 2001; Razzaq S, Schutze GE: Rocky Mountain spotted fever: a physician's challenge. Pediatr Rev 26:125, 2005; Simon MW, Simon NP: Cutaneous larva migrans. Pediatr Emerg Care 19:350, 2003; Smith RP: Current diagnosis and treatment of lyme disease. Compr Ther 31:284, 2005; Solis RR et al: Phytophotodermatitis: a sometimes difficult diagnosis. Arch Fam Med 9:1195, 2000; Tanen DA: Rattlesnake bites. Acad Emerg Med 8:688, 2001; Tanner TL: Rhus (Toxicodendron) dermatitis. Prim Care 27:493, 2000; Taylor RS, Simpson IN: Review of treatment options for lyme borreliosis. J Chemother 17 Suppl 2:3, 2005; Verbrugge LM et al: Swimmer's itch: incidence and risk factors. Am J Public Health 94:738, 2004; Weber IC et al: Phytophotodermatitis: the other "lime" disease. J Emerg Med 17:235, 1999.

Faculty Disclosure

In adherence to ACCME guidelines, the Audio-Digest Foundation requests all lecturers to disclose any significant financial relationship with the manufacturer or provider of any commercial product or service discussed. For this issue, the faculty reported nothing to disclose.


Drs. Noponen and Derlet spoke at Rural, Remote, and Wilderness Medicine: What Every Practitioner Needs to Know, held October 20-22, 2005, in San Francisco, CA, and sponsored by the University of California, Davis, School of Medicine. The Audio-Digest Foundation thanks the speakers and the UCD School of Medicine for their cooperation in the production of this program.


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