Problems Related to the The Diving Locale
Skin Problems Related to the Sun
Dermatoses, Photosensitivity, Sunburn and Diving
Problems Related to Marine Environment
Sea Bather’s Eruption
Dermatoses, Photosensitivity, Sunburn and Diving
Articles by Bruce Miller, MD
Bruce Miller, MD
Dr. Miller, a Dermatologist, is a Consultant for Diving Medicine Online. This is a lecture presented to Medical Seminars, 2000DOWNLOAD THIS ARTICLE ZIP.file
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Travel to the tropical climes can often aggravate preexisting skin problems as well as expose us to new hazards. Here is a review some of the more common ones and suggestions for some treatment approaches.
Tropical Acne and Hidradenitis Suppurativa:
Heat and humidity, along with the chafing of the dive gear and wet suit, can aggravate a preexisting cystic acne condition. Severe acne flares on the shoulders and back can be quite painful and lead to scarring. Large cysts in the groin and/or axillae can also occur. If a diver has a history of cystic, conglobate acne, and/or hidradenitis, it would be wise to be sure that these conditions are in a state of long-term remission. Otherwise, treatment with a course of Accutane should be considered well before the trip.
If a flare occurs while on the trip, incision and drainage under local anesthesia, intralesional steroid injections, a short course of prednisone 40 mgm/day, and coverage with cephalexin should all be considered
Atopic Dermatitis, Neurodermatitis, and Xerotic Eczema:
All these eczemas are characterized by dry, itchy skin. Paradoxically, repeated immersion in water, while temporarily hydrating the skin, in the long run dries it out because of loss of oils from the stratum
corneum. In addition the climate may superimpose a prickly heat problem on top of the dryness, causing more pruritus.
Treatment consists of mild soap, don’t over bathe, lubricate after your shower, and a good fluorinated topical steroid once or twice a day. Severe flares can be managed with prednisone or 40 mgm of Kenalog and 1 cc of Hexadrol IM.
Allergic Contact Dermatitis:
There are numerous opportunities for exposure to various allergens on dive trips. The prototypical eruption is the weeping, severely pruritic, edematous reaction from exposure to poison oak or ivy. However, there are other members of this family lurking in the background. Mango rinds, Japanese lacquer and cashew nut trees, and the marking nut trees of India contain the catechol antigen (urushiol) and cause the same reaction.
Neomycin, benzocaine and its relatives, rubber accelerators in the neoprene rubber of your wet suit, and delayed hypersensitivity reactions to hydroid stings can all cause contact dermatitis.Milder cases may respond to a high-potency topical steroid (e.g., Ultravate, Temovate, or Diprolene). More severe reactions need to be treated with prednisone. It’s important not to chase the disease with the dose. A typical regimen would be 60 mgm QDX4, then 40 mgm QDX6 to start.
Fungal Infections (Tinea cruris, corporis, and pedis):
If you have preexisting “athlete’s feet” (T. pedis) or “jock itch” (T. cruris), I can almost guarantee that these conditions will flare under the humid, soggy, wet conditions associated with diving. Carefully drying the affected body parts after your shower by using a hair dryer, followed by some talcum powder, and applying a good topical antifungal, such as Mentax, may well prevent a flare.If the problem won’t respond to topical therapy alone, add in an oral antifungal, such as Sporanox or Diflucan. For persistent nail involvement (onychomycosis), use Lamisil QD for 90 days.
A harmless superficial fungus know as m. furfur, it is mainly of cosmetic significance. Areas of involvement appear lighter than the surrounding skin in the summer due to blockage of the tanning rays. During the winter, the situation is reversed and the involved spots are reddish-brown and darker than the surrounding skin.Occasionally, people complain of itching, but usually this is an asymptomatic problem. Typically, heat and humidity aggravate the condition.Treatment consists either of a topical application of Selsun shampoo for 5 minutes QD for 7-10 days or 2 weeks QD of one of the oral antifungals.How do you tell the difference? KOH prep shows “ spaghetti and meatballs”=hyphae and spores.
Candidiasis (monilia, yeast) :
Usually seen in infants with diaper dermatitis, it can appear in adults. Diabetics and persons on broad-spectrum antibiotics are susceptible to this opportunistic organism, which is usually peacefully coexisting with the bacteria in our GI tract. Thrush, diarrhea, candidal vaginitis, and intertrigo can result from its overgrowth. The best treatment is an oral antifungal/yeast drug that will work within a few days,
(eg., Nizoral, Sporanox or Diflucan).How do you tell the difference between these similar appearing intertrigos? Do a KOH and culture..Actually, don’t do it yourself. send the patient to a Derm.!
Erythrasma (a corynebacterium):
Usually seen only in diabetics. The KOH and culture are negative. Diagnosis is made by the process of elimination and characteristic fluorescence under Wood’s light. Treatment is oral erythromycin in any of its various forms.
Trichomycosis Axillaris ( a gram positive organism):
Responds well to topical antibiotics, e.g., cleocin-T.
Hot Tub Folliculitis:
Pseudomonas infection of the hair follicles, usually found only in poorly-maintained hot tubs in private settings. It can be quite extensive and uncomfortable, so I routinely treat it with Cipro. 500 mgm BIDX1 week.
These are far and away the commonest types of skin infections I see on dive trips, not only in divers, but also in the indigenous population.
a) Impetigo, the most superficial of these infections, is usually caused by a gram +, pencillin-resistant staph. aureus, rather than beta-hemolytic strep., though occasionally there is a mixed infection. So here in the USA , I usually treat with cephalexin or dicloxacillin. In some of the less developed countries, where antibiotics are few and far between, almost any drug active against gram+ organisms seems to work well. In Yap recently, I incised an axillary abscess in one of the dive guides and gave him some Keflex with
instructions to get more at the hospital pharmacy. He ended up with Tegopen (cloxacillin) 500 mgm Q6H, the poorly absorbed predecessor to diclox.
b) Furuncles, usually due to staph., resemble small abscesses involving hair follicles, usually on the face or neck. If large enough, they should be incised and drained, as well as treated with antibiotics
c) Ecthyma is a deeper infection extending down into the subcutis and having draining sinuses. Certainly a more severe infection and again usually due to staph. aureus. This needs to be treated aggressively to prevent a rapidly-developing cellulitis and possible bacteremia.
d) Cellulitis/erysipelas is usually due to beta-hemolytic strep. and therefore can be treated with penicillin, but obtaining a culture is difficult. It often starts from a small break or fissure in the skin. “Skip cellulitis”, of the lower leg is due to fissures between the toes from tinea pedis, serving as a portal of entry for the strep.
e) Abscess formation is also usually due to staph. This problem should be treated with surgical drainage as well as cephalexin or dicloxacillin.
f) Pseudomonas otitis externa. This is a real mess that could have been prevented by prophylactic use of Domeboro Otic after each dive. Be sure that the diver hasn’t been using Cortisporin Otic, which contains neomycin. I’ve seen allergic contact dermatitis to Neomycin with secondary infection look this bad. Treatment is Domeboro soaks and Cipro.
g) Some miscellaneous skin infections due to organisms peculiar to the ocean or aquatic environment: aeromonas hydrophilica, vibrio vulnificans, protothecosis, and mycobacterium marinum (swimming pool/fish tank granuloma).
Vibrio Vulnificus is typically present in warm salt water. It can infect shellfish and, when ingested, can cause gastroenteritis or bacteremia in people with hepatic cirrhosis. It’s also an opportunistic infection that, after trauma to the skin, can result in a severe form of cellulitis.
Aeromonas hydrophilica is present in fresh or brackish waters. It’s a gas producing organism and can cause cellultis with crepitus.
Both can cause cellulitis with bullae, necrotic ulcers, and deeper soft tissue involvement, which can lead to gram-negative sepsis.
Treatment consists of Cipro.
M. Marinum is an acid-fast bacillus that can be identified by an AFB stain on biopsy. A good history and exam doesn’t hurt either. Treatment consists of minocycline 100mgm BIDX30 Days or more.
Herpes Simplex Virus (HSV) I and II: are frequently activated by sun exposure, colds, stress, and who knows what else? These outbreaks can certainly make your trip miserable for a few days. If you’re susceptible to them, use chap stick with a sun screen, although lipstick and zinc oxide work better because they stay on the skin. It’s also wise to carry a supply of Valtrex, Famvir, or Zovirax along with you on all trips. Start taking the drug at the first sign that you are developing an HSV outbreak
Insect bites: Fleas, mosquitoes, chiggers, bedbugs, no-see-ums, ticks, pediculosis, scabies, biting flies, etc., are found all over the world and remain as a constant reminder that humanity does not always control Mother Nature. Aside from the rather dramatic bullous and hemorrhagic variants seen
particularly in children, they serve as the vector for many unpleasant diseases.
Insect repellents, long sleeves, no perfumes, etc., all help but there is no way that you can completely escape. Most bites cause some itching, which is self-limited. A good topical steroid can help for the day or two it takes to resolve. Extensive bites can be treated with prednisone.
Creeping Eruption: This is caused by the larvae of the dog/cat hookworm (ancyclostoma sp.) that can’t complete its life cycle in humans.It’s endemic in certain parts of Florida. The message here is to wear sandals at all times and don’t step in the shit.
Treatment consists of topical or oral thiabendazol, a broad-spectrum
Miliaria (prickly heat): This is due to eccrine sweat gland occlusion. It used to be a common problem in the tropics before the advent of widespread air conditioning. Rupture of the sweat gland at different levels creates the different clinical presentations: superficial leads to miliaria crystallina, deeper leads to more inflammatory lesions, miliaria rubra.
Treatment consists of moving the person into a cool environment and possibly topical steroids.This condition is mainly seen nowadays in infants whose parents overdress them for bed.
a) Phillipines box jellyfish-cubozoan envenomation. During his tour of duty there, Dr. Reed reports that two children died from contact with this jellyfish while wading. Its related to the Australian box jellyfish, Chironex fleckeri, but usually not as lethal. No anti venom is available.
b) Sea bathers eruption: caused by the larvae of the thimble jellyfish (linuche unguiculata). This patient of mine had been snorkeling off the Cozumel coast. Note the typical distribution under her bathing suit. It
consists of severely pruritic, urticarial papules. It’s also endemic off the coast of Florida.
Treatment is the same for all hydroid stings: spraying the affected area(s) with alcohol or vinegar and avoidance of fresh water or trauma to the areas till the nematocysts have been inactivated.
Dr. Auerbach has obliquely referred to this in several articles, but I want to emphasize that a delayed hypersensitivity, contact dermatitis, poison oak/ivy type of allergic reaction COMMONLY develops after exposure. If it’s the first time, it may take several days. If it’s a subsequent exposure, after you’ve been sensitized, this eczematous, severely pruritic reaction may appear within hours. At this point, treatment usually requires systemic steroids in the dose previously recommended.
Bruce Miller, MD
Dr. Miller, a Dermatologist, is a Consultant for Diving Medicine Online. This is a lecture presented to Medical Seminars, 2000
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A brief review of the physics and photobiology of ultraviolet radiation (UVR):
Transformation of H to He in sun’s interior liberates vast amounts of energy which reaches the earth’s surface in the form of electromagnetic radiation (EMR) : x-rays, cosmic rays, electric waves, radio waves, infrared, visible light, and ultraviolet radiation (UVR).
EMR travels in the form of waves containing packets of energy called photons. In the case of x-rays and cosmic rays, the wavelengths are very short, measuring only a few nanometers(nm):1 nanometer = 1 billionth of a meter. On the other hand radio waves are very long, measuring several kilometers (km):
1 km=1000 meters. The amount of energy contained in EMR is inversely proportional to its wavelength. The ozonosphere blocks all EMR shorter than 297 nm (thank goodness!).
UVA vs. UVB-what’s the difference and why it’s important:
UVR includes wavelengths of EMR between 297-400 nm. Convention divides this spectrum into UVB = 297-320 and UVA = 320-400. UVA may be further divided into UVA II = 320-340 and UVA I = 340-400. UVB is also known as the “sunburn spectrum” and is the prime factor in photo aging and photocarcinogenesis. UVA also contributes to photo trauma but is the spectrum primarily responsible
for photosensitivity reactions because of its deeper penetration into the skin.
UVB only penetrates into the epidermis and the papillary (uppermost) dermis and is blocked by window glass. UVA penetrates into the reticular (deep) dermis and passes through window glass unchanged. Unlike UVB these rays don’t vary in intensity with the time of day or the season. Compared to UVB, 100 times as many reach the surface of the earth.
Ozone depletion due to fluorocarbons found in aerosols, auto air conditioners, refrigerators, etc., pose a significant threat to us all in the form of an increased incidence of melanomas and other skin cancers, depressed immunity, accelerated aging, etc., due to high energy particles and increased UVR reaching the earth’s surface.
Under photosensitivity diseases, we will cover phototoxic and photoallergic systemic photoeruptions (mainly drugs), phototoxic and photoallergic contact dermatoses (mainly plants and perfumes), nature’s phototoxic diseases (the porphyrias), and a common photo eruption of unknown etiology, polymorphous
light eruption (PMLE).
Photoxic vs. Photoallergic:
Fundamental to both is the absorption of photons of light by a chromophore. However, once this event occurs, the mechanisms leading to cellular damage diverge.
In phototoxic reactions the photosensitivity is mediated by non-immunologic mechanisms. Absorption of photons of a specific wavelength (UVA in nearly all cases) by the photosensitizing chromophore results in electrons changing their orbits and creating unstable singlet or triplet states, which release
energy when the molecule returns to a stable ground state. This energy causes cellular damage and the release of products of inflammation, as well as free radicals, causing cellular damage and resultant erythema, edema, and occasionally vesiculation, i.e., an exaggerated sunburn reaction, which is restricted to sun-exposed areas. This reaction can occur upon first exposure to the drug.These chromophores are typically polycyclic ring structures withalternating single and double bonds, and fluorination at critical sites onthe molecule. The fluoroquinolones are typical examples, as are the porphyrins. Apart from sunburn, phototoxic drug eruptions are the commonest photosensitivity reactions.
In photoallergic reactions, following absorption of the specific photons, a new compound is formed, which acts as a haptene. This molecule then combines with a protein to form a complete antigen, which possesses immunologic properties. The mechanism of the host response is then similar to other forms
of delayed hypersensitivity and is mediated by T-lymphocytes. Morphologically, this response presents as an eczematous eruption, and while it may start in sun exposed areas, it may spread to non-sun exposed parts of the body. These reactions are relatively unusual and require at least one prior exposure to the drug
Diseases such as discoid and systemic lupus, PMLE, solar urticaria, and dermatomyositis may also fall into this category, although their morphologies vary widely.
List of drugs that may cause photosensitivity reactions
Sparfloxacin (Zagam) photox. as a prototype.
tetracycline photox. eruption, photo -onycholysis, vesicles
Lomotil (erythema multiforme)
Porphyria Cutanea Tarda (PCT) and Erythropoetic Protoporphyria (EPP):
These photoxic diseases are caused by an increased concentration of porphyrins in the blood. Porphyrins are pyrimidines arranged in a ring-shaped structure with alternating double bonds and are derived from the metabolic breakdown of old RBC’s. Due to enzymatic defects,which are probably hereditary in both types, porphyrins build up in the bloodstream and act as chromophores, absorbing UVA and causing cellular damage by energy transfer. Which type of porphyria develops depends on the specific defect. PCT causes elevated porphyrin levels in the serum. EPP causes elevated levels within the
Usually caused by plants containing furocoumarins (psoralens) and called “phytophotodermatoses”. Also seen with perfumes and colognes containing oil of bergamot -”berlock dermatitis”. Shalimar perfume was a prime example. These phototoxic reactions are typically blistering and leave a brownish hyperpigmentation in their wake
Plants which can cause this are parsnips, fennel, dill, parsley, masterwort, celery, coriander, common rue, gas plant, bergamot, lime and other citrus, buttercup, mustard, blindweed, agrimony, yarrow, meadow grass, S. John’s wort, buckwheat, and ragweed. They all contain furocoumarins. We’ve
frequently seen this in celery pickers here in Oregon.
These reactions are now rare since halogenated salicylanilides were removed as antibacterial agents from soaps, and people learned to stop handling phenothiazine drugs.
Review of the ideal characteristics of a sunscreen reveals that while there are many excellent products on the market, they are primarily effective against UVB. Protection against UVA from 350-400nm has yet to be achieved, despite claims to the contrary.
“The physical agents we tested provided only weak UVA protection in both the shorter (320-340) and the longer (340-400) UVA ranges. Dibenzoylmethane derivatives (eg., parsol 1789) are much more efficient in the shorter but not in the longer UVA ranges. The best UVA protection over the entire UVA range is, without doubt, provided by the combination of real UVA filters (eg., benzophenones, parsol 1789, eusolex 6300 and 8020, lawsone with dihydroxy acetone, diphenylacrylate, methyl anthranilate, and octocrylene) and physical agents (eg., titanium dioxide, red petrolatum, talc, kaolin, and zinc oxide). The protection afforded by this combination also appears to be cumulative.”
Roelandts R. Which components in broad-spectrum sunscreens are most necessary for adequate UVA protection? J Am Acad Dermatol 1991;25:999-1004.
In a broad-spectrum sunscreen, the UVA filters are combined in varying combinations with UVB absorbing chemicals: PABA and its esters, methoxycinnamates, homosalate, salicylate, sulfonic acid, digalloyl trioleate, diphenyl acrylate, and lawson with dihydroxyacetone.
Sun Protection Factor (SPF). If your burn time (MED=minimal erythema dose, defined as the minimum amount of energy required to produce a uniform, clearly demarcated erythema response at 24 hours) without a sunscreen is 10 minutes, then a SPF of 15 will extend your MED to 150 minutes. This does NOT mean you can stay out in the sun all day. A SPF of 15 should be the absolute minimum level of protection, and we recommend higher numbers. The SPF only measures protection against UVB. There is no analogous number available for UVA protection. However, you should always use a “broad-spectrum” , UVA-UVB sunscreen that is labeled as WATERPROOF, not water resistant.
There are two new UVA filters : Parsol 1789, aka “Avobenzone”, a dibenzoylmethane derivative, and octocrylene.
We are currently doing a study for Galderma/L’Oreal in PMLE using a combination sunscreen with two UVB and two UVA filters. Mexoryl is the investigational UVA filter.
Photoprotective clothing is the only sure way to block the longer wavelengths.
For a catalog, write to:
2815 Wetmore Ave.
Everett, WA 98210
1. Gonzalez E, Gonzalez S. Drug photosensitivity, idiopathic photodermatoses,
and sunscreens.. J Am Acad Dermatol 1996;35:871-885.
2. Gould J, Mercurio M, Elmets C. Cutaneous photosensitivity diseases induced
by exogenous agents. J Am Acad Dermatol 1995;33:551-571.
3. Miller, B Sunning-and still having fun. Alert Diver 1996;Nov-Dec:37-39.
1. Electomagnetic radiation below 297 nm does not reach the earth’s surface
c) the Van Allen belt
d) the ozonosphere
e) rap music
2. The following drugs have been associated with photoeruptions:
3. Phototoxic drug reactions most resemble:
a) eczematous dermatitis
c) an exaggerated sunburn
e) none of the above
2. c, d, e
|SUNLIGHT, SKIN CANCER AND AGING
PHOTODAMAGE, PHOTOPROTECTION AND SUNSCREENS
Bruce H. Miller, M.D.
* Lecture presented Bruce Miller, MD, Medical Seminars, Palau, 1996Download this Article in zip format
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Humanity evolved on earth, bathed in solar radiation from our star, the sun. The nuclear reactions in its interior transform hydrogen atoms into helium, liberating vast amounts of energy in the process. This energy reaches the earth in the form of electromagnetic radiation (EMR) and includes x-rays, cosmic rays, electric waves, radio waves, infrared, visible light and ultraviolet radiation (UVR). Without the effects of EMR on the earth’s surface, life itself could not have begun, and our planet may have been covered by oceans of liquid nitrogen and enveloped in an atmosphere of methane. Sunlight also plays a crucial role in a wide range of photobiological processes, touching all forms of life on earth. However, under certain circumstances, the same sunlight that has given us life can also cause significant morbidity in the form of sunburns, drug reactions, exacerbation of photosensitive diseases and photoaging. In addition, recurrent episodes of phototrauma over a lifetime can lead to the development of skin cancers.
Current scientific thinking holds that EMR travels in the form of waves that contain packets of energy called photons. These wavelengths can be very short, measuring only a few manometers (a manometer, NM = I billionth of a meter) in the case of cosmic and x-rays or very long, measuring several kilometers (kilometer = 1000 meters), in the case of radio waves. The shorter the wave length, the more energy the EMR contains.
The wave lengths that concern us lie in the ultraviolet range, specifically ultraviolet B (UVB) from 290 – 320 NM, and ultraviolet A (UVA) from 320 – 400 NM. Fortunately for us, the ozone layer in our atmosphere, the ozonosphere, blocks all EMR below 290 NM so these high energy particles can’t reach the earth’s surface. For many years photobiologists and sunscreen manufacturers have concentrated on UVB, also known as the “sunburn spectrum”. Recently, increasing attention has focused on UVA, also known as “long wave UV”, and its additive role in photodamage when combined with UVB. UVA also seems to be primarily responsible for causing photodrug eruptions and exacerbating photosensitivity in diseases. In recognition of this increasing awareness, many sunscreens now contain UVA blockers.
The ability of a sunscreen to protect the user from UVB is defined as its Sun Protection Factor (SPF). The SPF is the ratio between the time it usually takes your skin to sunburn and how long it takes if you’ve applied that sunscreen. For example, an SPF of 15 will provide 15 times the amount of protection you’d get without using anything. Thus, if 10 minutes in the sun is enough to turn you red, your sunscreen would allow you to stay out for 150 minutes before burning. An SPF of 15 filters approximately 92% of the sunburning rays. For UVA the degree of protection is defined as the Phototoxic Protective Factor (PPF). These values are much lower, ranging from 1.5 – 4.8, because the energy contained in UVA is so much less. PPF’s have yet to make it out of the laboratory.
How should you select your sunscreen? Divers should use sunscreens that are water proof, broad spectrum (UVA/UVB) screens, and that have an SPF of at least 15. Next, you should determine your skin type (Table 1). Then you need to take into account such environmental factors as time of year, geographical location, altitude, reflecting surfaces, time of day, air pollution, water immersion, proximity to the equator, clothing (or lack thereof), and exposure time.
Now you need to think about protection from UVA as well. Are you taking or contacting any of the medications or substances in Table 2? Do you have any of the diseases listed in Table 3 that are aggravated by sun exposure, If so, you need an effective UVA sunscreen as well!
Why should you use a sunscreen? Isn’t a tan “healthy”? Prolonged and repetitive sun exposure causes phototrauma (sunburn and cellular damage) which, over a period of time, causes photodamage: coarse wrinkling, mottled hyperpigmentation (“age” or “liver” spots), roughness, sagging, yellowing, broken blood vessels, and skin fragility. In addition, prolonged sun exposure causes skin cancers: basal cell carcinomas, squamous cell carcinomas and melanomas (malignant moles). In 1990, over 600,000 new cases of skin cancer were diagnosed, afflicting more people than all other cancers combined. Of this group, there were 8,800 deaths, 6,300 from melanoma and 2,500 from squamous cell carcinomas. The incidence- of melanoma is doubling every decade! By the year 2000, it is estimated that one in every 90 people will develop a melanoma, if our UVR exposure patterns remain unchanged. What can you do to prevent these undesirable side effects from sun exposure? Follow these guidelines:
1. Avoid sun exposure from 10:00 a.m. to 3:00 p.m.
2. Beware of cloudy days and reflecting surfaces: snow,, water, sand and concrete. YOU CAN STILL BURN.
3. Wear tightly knit, dry clothing and a hat. Wearing sun-protective clothing is a good idea.(‘Solumbra’).
4. Ban chlorofluorocarbons! These compounds are destroying the ozonosphere and permitting more UVB to reach the earth’s surface.
5. Stay away from tanning beds.
6. Stop all elective photosensitizing medications while on vacation (e.g. Tetracycline and Retin-A for acne). If you’re unable to stop your medications, use the most effective UVA blocker available currently “Parsol 1789″ (Butylmethoxydibenzoyl methane). People with photosensitivity diseases should follow the previous recommendations and avoid UVR exposure, if at all possible. They should use a screen of the highest SPF that also contains Titanium dioxide, a physical screen.
8. Regularly apply a sunscreen that you find cosmetically acceptable and will prevent you from sunburning whatever your skin type and wherever you are. Preferably this sunscreen will resist washing off and will contain a UVB blocker with an SPF of at least 15 and a UVA blocker with a PPF of at least 1.5 (benzophenones) to 4.8 (Parsol 1789). You can tan through your sunscreen, and stay young and beautiful.
||Sensitivity to the Sun
||Risk of Skin Type
||Always burns easily
||Always burns easily
|| Burns moderately
||tans gradually and uniformly (light brown)
|| tans well (moderate)
||tans profusely (dark brown)
||deeply pigmented (black)
2. Thiazide Diuretics:
Hygroton, Dyazide, etc.
3. Hypoglycemic agents (Antidiabetics)
Stelazine, Compazine, etc.
6. Nalidixic Acid
7. Quinidine and Quinine
|1. Oil of Bergamot – perfumes, cologne
2. Deodorant soaps
3. Plants – figs, lines, celery, parsnips
|1. Herpes Simplex
Porphyria Cutanea Tarda
3. Discoid and Systemic
4. Polymorphous Light Eruption
5. Xeroderma Pigrnentosa
6. Solar Urticaria
7. Dermatomyositis 8. Actinic Reticuloid
Polymorphous light eruption is an acquired disease, and is the most common of the idiopathic photodermatoses. It is characterized by recurrent, abnormal delayed reactions to sunlight, ranging from erythematous papules, papulovesicles, and plaques, to erythema multiforme like lesions on sunlight exposed surfaces. Within any one patient, only one clinical form is consistently manifested.
Photos, description, differential diagnosis
Article devoted to PMLE in “Emergency Medicine”
PMLE at UC Davis
PMLE at University of Pittsburgh
Insect Bites & Illnesses Caused By Insects
Divers often are faced with significant problems with biting insects, particularly in parts of Africa, Central America, South America and Mexico. Most of the time these insects are just a nuisance, but there are definite dangers involved with the mosquito. The sand gnat (no see um, flying teeth, punkie) does not transmit disease but can make life miserable to the diver. Using scissor-like mouth parts, the female injects anticoagulant and sucks blood resulting in a painful, itching dermatitis.
Mosquitoes can transmit malaria, yellow fever and dengue fever and precautions should be taken if diving trips are to be made into areas endemic with these diseases.
Malaria chemoprophylaxis should be taken regardless of how short the visit and the CDC should be contacted for the areas at risk. The vector for malaria is the female Anopheles mosquito and in addition to Chloroquine, other preventive measures should be used. One should sleep in screened areas, wear long clothing in the evenings and use some kind of repellent containing N,N diethyl-meta toluamide (deet). Fansidar (pyrimethamine sulfadoxine) is used against chloroquine resistant Plasmodium falciparum malaria.
Malaria Drugs (CDC)
Drugs Used in Chloroquine-Resistant areas:
Trade name “Lariam“
Dosage=200mg/week. One tablet. It should be taken 1 week before leaving, weekly while in the malarious area, and weekly for 4 weeks after leaving the area. It should not be used by travellers with a history of epilepsy or psychiatric disorders. The drug company, Roche, has placed a ’suicide’ warning in the drug insert. There is also considerable discussion about whether or not divers should take this drug because of the neuropsychiatric side effects.
Malarone is a new antimalarial drug in the United States. Malarone is a combination of two drugs (atovaquone and proguanil) and is an effective alternative for travelers who cannot or choose not to take mefloquine or doxycycline.
For those who cannot take Mefloquine.
Dosage= 100mg daily beginning the day before entering the malarious area,, while there and for 4 weeks after leaving. This drug photosensitizes the skin.
Chloroquine & Proguanil–
Trade Name for Chloroquine is Aralen. For those who cannot take Mefloquine or Doxycycline.
Dosage for Chloroquine is 500 mg weekly as above. Proguanil should be added if traveling to sub-Saharan Africa. Dosage of Proguanil is 200 mg daily (not found in US, can be bought in canada, Europe and many African countries).
Drugs used for self-treatment of malaria
Fansidar (pyrimethamine sulfadoxine)
For usage in Chloroquine-resistant areas.
Dosage= three 75 mg tablets as a single dose for any fever while traveling. People allergic to sulfa should not take this medication.
Bradley, D.J. “Malaria prophylaxis: guidelines for travelers from Britain.” BMJ. (1995) 310: 709.
Centers for Disease control and Prevention. World Wide Web site, posted on Aug. 18, 1995.
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F. Hoffmann-La Roche & Co. Lariam (lariam hydrochloride). Basle, Switzerland.
Hennequine, C. “Severe psychiatric side effects observed during prophylaxis and treatment with mefloquine.” Archives of Internal Medicine. (1994) October, 24.
Jenkins, Artie. 401-453-6000
Kondrachine, A.V. “Malaria: hope for the future.” World Health. (1995) March.
Luzzi, G.A. and Tim E.A. Peto. “Adverse effects of antimalarials – an update.” Drug Safety. (1993) 8: 295.
Nevill, C.G. “Daily Chloroproguanil is an effective alternative to daily proguanil in the prevention of Plasmodium falciparum malaria in Kenya.” Transactions of the Royal Society of Tropical Medicine and Hygiene. (1994) 88: 319.
Peterson, Faye. “Mefloquine approved for malaria.” FDA Talkpaper. 1989.
Sanchez, J.L. and R.F.DeFraites “Mefloquine or doxycycline prophylaxis in US troops in Somalia.” The Lancet .(1993) 341: 1021.
Schlagenhauf, P. “Behavioral aspects of travelers in their use of malaria presumptive treatment.” World Health Organization Bulletin. (1995) March.
Wetsteyn, J.C. “Comparison of three regimes for malaria prophylaxis in travelers to east, central and southern Africa.” JAMA. (1994) 307:1041.
White, N.J. “Mefloquine: in the prophylaxis and treatment of falciparum malaria.” BMJ. (1994). January, 29.
Zeneca Limited. “Patient information leaflet.” Paludrine (proguanil hydrochloride). Cheshire, UK.
This fever remains endemic throughout the caribbean, the South Pacific, Asia, Mexico, Central and South America. The vector is the Aedes Aegypti mosquito. Prevention is important since the risk is small; when outdoors, use mosquito repellants, netting and protective clothing and spray your hotel room.
The vector again is the Aedes Aegypti mosquito. Vaccination is strongly recommended for travel to endemic areas, generally parts of Africa and South America. The same preventive measures as noted above apply.
These insects are invisible to humans until their abdomens turn red with blood. Also called sand flies, no-see-ums, punkies, and flying teeth, these insects bite with scissor-like mouth parts that introduce anti-coagulants that cause the stinging and itching.
Like mosquitoes, the females are the ones that bite. Important toknow is that they can’t bite through clothing.
Sand gnats in Central America can cause cutaneous leishmaniasis.
-Wear long-sleeved clothing and long pants. new styles of nylon that are lightweight for tropical wear and keep bugs off your skin better than cotton.
-Wear light-colored clothing
-Wear a hat to keep the sand gnats out of your hair
- Many new products contain low concentrations of deet, a chemical that has been linked to high levels of toxins in the blood stream of frequent users. Lower concentrations are safe to wear and won’t damage plastic and rubber gear. Use 10-25% deet.
-There are several new sprays and creams that don’t use deet.
-Many companies are combining sun screen and insect repellent.
-Sweet-smelling soap and shampoo attract pests. Avoid anything that has a fruity or sweet smell.
Skin So Soft and Off! These products work primarily by trapping the insect in oil; mineral oil with ‘SSS’ and aloe vera with Off! Off! also contains repellents.
These have been introduced by several companies. They act similar to a pet’s flea collar, using citronella, the liquid that is often burned to keep away insects.
A very useful insect repellent product is permethrin (one common brand name is Permanone). Usually sold as a spray, permanone was created for the U. S. Army; it is not DEET or citronella or the like. It is sprayed on clothing, insect nets and the like (NOT applied topically). Permanone is generally found in outdoor sports and fishing/hunting stores and catalogues.
The clothing or nets so sprayed repel insects quite well, and the substance persists enough it will actually survive a couple of washings! I have personally used permethrin on socks and trouser cuffs, shirt sleeves and collars, and insect nets (head nets and bed nets) in such places as the Canadian Arctic tundra (black flies and mosquitos are a terrible nuisance there!), the African veldt and other areas, to repel everything from black and tsetse flies to ticks and chiggers.
I often recommend people heading for insect-ridden areas use permanone on some of their clothing, and protect themselves with DEET 15 – 20% (higher percentages are no more effective, but they can be bad for children, plastics and synthetic materials used in clothing) on areas they will be exposed to malaria mosquitos (night-biting Anopheles) or dengue mosquitos (day biters).
(submitted by Jose’ Kirchner)
Sea Bather’s Eruption
Sea Bather’s Eruption (Sea Lice)
Photo Courtesy of David Kesler, PhD
This is a dermatitis that is thought to be caused by the larva of the thimble jellyfish. The nematocysts of these larvae accumulate in areas of bathing suit contact and cause a severe dermatitis that can be painful and/or pruritic. It usually resolves in about 1 week, but can recur if the dive suit is not rinsed carefully. Steroid creams are said to be helpful.
Dan Marelli writes that it is “also caused in Florida by larvae of a burrowing anemone (same mechanism, nematocyst stings) which is apparently more common following beach “renourishment” projects. The anemone must be an opportunist that colonizes the disturbed habitat.”
Sea Bather’s Eruption
Article in the New England Journal of Medicine
DAN section about sea lice, swimmer’s itch, coral dermatitis and scrapes.
Sea Bather’s Eruption
Sea lice survey. Boca Raton, Florida: Boca Raton Community Hospital. 1992.
Lauther OC. The lonesome road. Miami: Center Printinq, 1963:91-2.
Sams WM. Seabather’s eruption. Arch Dermatol 1949:60:227-37.
Black NA, Szmant AM. Larval thimble jellyfish (Linuche unqui culata) as a possible cause of seabather’s eruption. Presented at 1992 Symposium on Flounder Keys Regional Ecosystem. Miami, Nov 18, 1992.
Thorinqton GU, Hessinqer DA. Control of discharge: factors affecting discharge of crudes. In: Hessinqer DA. Lenhoff HM. eds. The biology of nematocysts. San Dieqo: Academic Press. 1955:232-53.
Retrospective case review/medical records of SBE cases from 4/92-7/92. Boca Raton, Florida: Boca Raton Community Hospital, 1992.
Heeger T, Moller H, Mrowietz U. Protection of human skin against jellyfish (Cyanea capillata) stings. Marine Biol 1992:113:669-78.
Another Photograph of Sea Bather’s Eruption (Sea Lice)
Another form of swimmer’s itch is associated with fresh water swimming and diving. This is swimmer’s itch (cercarial dermatitis), which is usually caused by Microbilharzia variglandis. This organism, a schistosome, is one of the blood flukes of birds. The larval form, known as a cercaria, can penetrate human skin, causing a dermatitis. Various aquatic bird species, including shore birds, ducks, and geese, are considered definitive hosts (i.e., they allow full development of the adult worm). Humans are inadvertent hosts (i.e., cercariae penetrate the skin but do not develop further). A separate entity known as “seabather’s eruption” can be distinguished from swimmer’s itch because it occurs after exposure to salt water and involves covered areas of skin. Seabather’s eruption is related to exposure to larval forms of Cnidaria, such as jellyfish and sea anemones. Cercariae are free-swimming, schistosomal larvae that develop in the tissues of certain snails and are shed mostly in certain environmental conditions.
Olivier L: Schistosome dermatitis, a sensitization phenomenon. Am J Hyg 49:290-302, 1949.
Anonymous: Swimmer’s itch: Schistosome cercarial dermatitis. NY State J Med 91:415-416, 1991.
Case Record 27-1985 of the Massachusetts General Hospital. N Engl J Med 313:36-42, 1985.
Centers of Disease Control: Cercarial dermatitis outbreak at a state park–Delaware. MMWR 41:225-228, 1992.
Cort WW: Studies on schistosome dermatitis. XI. Status of knowledge after more than twenty years. Am J Hyg 52:251-307, 1950.
One of the most frequently encountered skin problems is the diver who brushes up against hard coral, most often fire coral, and sustains an abrasion or a cut. In the process of the encounter, there is also the insertion of thousands of nematocytes (containing the nematocysts) and foreign particles into the wound – with the addition of the toxins, foreign body reaction and inflammatory response to the actual wound itself. It is rare that this encounter has initial appropriate cleansing and irrigation and what results is a chronically infected, wound containing foreign material and the remnants of the nematocytes. Even after some healing has taken place, these wounds can flare up into a weeping, reddened and swollen chronic inflammation that eventually results in thickening and hyperpigmentation of the skin.
A particularly frequent example of this is the diver who uses the anchor or buoy line containing coral and hydroid growth for descent and ascent without protection. This results in not only immediate injury but a delayed reaction coming on sometimes many days after the exposure to the nematocysts. Photos of such a delayed injury can be seen at this site.
Initial management of coral cuts and abrasions
Clean well with a brush, soap and water
Alcohol or vinegar flush
Scrub and debride foreign particles
Bed rest, elevation, antibiotics for severe cuts
Be aware of danger of anaerobic infection and clostridial infection
Initially, wounds should be flushed out with copious quantities of vinegar or whatever sterile fluid you have available. Fresh water will cause firing of nematocysts due to the hypotonicity of the solution. Tetanus prophylaxis should be given and the wound treated with a combination of triple antibiotic/steroid cream until healing occurs.
If the wound does not appear to be healing after 24-36 hours, it might be wise to check in with your doctor for opinion and possible debridement (removal of foreign bodies). Alternate methods that have been successful include, ‘Scotch’ tape, duct tape, shaving cream with safety razor and hair removal wax applications. These seem to work by removing very small particulate matter and unfired nematocysts
Hyperpigmentation (dark, color changes) are more difficult to manage and require the assistance of a good dermatologist.
dermatitis, seaweed dermatitis
and dermatitis from chemical contamination
of the water have been described.
Neoprene allergy is seen quite often and the obvious remedy is to discontinue it’s use and obtain any other kind of wet suit that serves the purpose of thermal protection. Interposing creams or chemicals is not effective or wise. This is a usually an allergy to one of the chemical accelerators in Neoprene and would require skin testing to find out exactly which one is the culprit. Polartec and lycra exposure suits are just two of your choices.
Bruce Miller, MD, our dermatology diving consultant feels that this is clearly a contact dermatosis to the rubber accelerator used in the suit manufacture. There are at least 5 or 6 used in the manufacture of rubber products. It is recommended that you need to see a Dermatologist and get PATCH tested (not scratch) to identify exactly what, or which one, is breaking you out. You then need to buy a suit that doesn’t contain that particular compound.
Allergy to accelerator in bootie
Fisher, AA; Atlas of Aquatic Dermatology, New York, Grune & Stratton, 1978
Miller, Bruce, MD, Dermatologist
Cutaneous Manifestations of Decompression Sickness
Carl Edmonds feels that this is a common manifestation of diving in a compression chamber, most likely due to the release of small bubbles from gas dissolved in the epidermis. In this mild form, no signs are visible, and the itching is temporary, mild, comes and goes and is more marked around the ears, wrists and hands. He does not consider this a systemic manifestation of decompression sickness.
Similar cases of itching, burning, increased heat and visible rashes occur after many dives and clear spontaneously or with 100% oxygen and aspirin and probably should not be recompressed. However, there have been recent reports of an association with skin bends with patent foramen ovale [UKSDMC] and there are now recommendations that divers with this condition be checked for PFO.
Patchy erythema (Cutis Marmorata)Patchy, reddish-purple mottled areas can occur, especially around the shoulders and trunk. These are intensely pruritic and are due to a local vascular reaction from bubbles in the tissues below the dermis. This has a more serious connotation and is thought of as a systemic manifestation of decompression sickness and is often associated with other more serious types of DCS, such as chokes. All of these divers should be treated with recompression.
Blockage of the dermal and subcuticular lymphatics with bubbles usually results in edema and a peculiar pitting of the skin called peau d’orange (French, meaning skin of the orange, or, orange-peeling). This is pigskin appearance more often seen over the trunk of the body and again is evidence of a more serious form of DCS.
Edmonds, et al: Medical Aspects of Diving, The Medical Journal Of Australia; 1972, 2:1199-1416