Here comes the sun Pt.2

copy-of-steven-j-srommer.JPGAs promised by Dr. Dave Mozley a more in depth approach to treatment of over exposure to the sun.

Background: Paracelsus (1493-1541) observed that the difference between a poison and a good medicine was simply a matter of dose. In his recent blog, “Here Comes the Sun”, Steven J. Strommer made the same observation about sunlight. While Mr. Strommer, Benjamin Franklin, and many others are right to claim that an ounce of prevention is worth a pound of cure, “things happen”.Â

Specific aim: To review the pathophysiology and treatments of sunburn. The scope is limited to post-hoc interventions after exposures to acute, toxic doses of sunlight that are high enough to cause otherwise healthy travelers meaningful disability. The hope is that learning about how to treat solar mediated catastrophes will empower readers to effectively cope with sun-induced injuries of lesser biological significance.Â


(1) Sunburns. A first-degree sunburn is defined as radiation-induced tissue damage that affects the outer most layers of the skin (epidermis) only, causing redness (erythema) and pain but without blistering. A second-degree, or “partial thickness” burn is defined as radiation-induced tissue damage that kills cells in the underlying dermis, ultimately causing blistering as a consequence of intense inflammation. (See

(2) Radiation dose. Radiation has become a big scientific word but is actually a derivative of the common Latin term for ordinary sunlight. Physicians may loosely define light as a particular type of electromagnetic wave that stimulates photoreceptors in mammalian eyes. The dose, or amount, of any radiation energy transferred to living tissues is, in part, a function of the intensity of emissions from the source and the duration of the exposure to the source. In other words, the dose is proportional to (1) how bright the light is, and (2) how long you’re exposed to it. The higher the dose is, the more energy is deposited in tissues, and as a consequence, the greater the potential injury. Because (1) the aggressiveness of post-hoc treatments should be proportional to the severity of the impending injury, (2) it can take several days for the injury to fully develop, and (3) treatment should be instituted prior to obvious manifestations of the injury, it thus seems propitious to review a few rules about how to assess the dose of sunlight a creature has been exposed to.Â

As many others have observed, the power of radiated light reaching the surface of our Earth increases as follows:

(1) Â The directness of the angle of incoming radiation, that is,
A. Â As time of day approaches either side of high noon; or
B. Â The closer you travel to the Equator, that is, the lower the latitude;
(2)  The higher the altitude, i.e., as you lose protection from the atmosphere. UV radiation intensity increases by approximately 5% for every 1000 feet (300 meters) in altitude ( That means that if you’re in Katmandu or Denver, biologically meaningful amounts of radiant energy can begin to be deposited in your tissues after as little as 45 minutes of exposure to bright sunlight.Â
(3)  As the amount of reflective surface area increases. The primary reflective surfaces that travelers encounter are sea, snow, and cloud cover. Cloud cover can be particularly dangerous because water vapor is effective at absorbing visible light and cooling the surfaces on which you stand, but clouds are not as effective at blocking the lower wavelength, higher energy ultra-violet (UV) light that can damage your eyes or burn your skin. The sea is particularly deceptive because it can cool your skin and mislead your subjective assessment of how much exposure has occurred. Reflections off the water or snow can damage your eyes even if you keep your skin covered. Snow can be loosely thought of as almost doubling exposure per unit of time, as it reflects back about 85% of UV light, while water reflects back a little less than a third (see Auerbach PS. Medicine for the Outdoors. New York: Lyons Press, 1999).Â

Key Point: All this suggests that if you get caught in a brightly lit environment for any meaningful length of time, you should plan on taking measures to limit the extent of your injuries before they become conspicuous.

Pathophysiology: Take a flashlight (a.k.a. battery powered torch) into the dark and cover the lens with your palm. You will see a little light shining all the way through your hand. The point is that a fraction of the light hitting the surface of your body will penetrate well below the superficial layers of your skin. This trivial experiment begins to explain how some of the living cells underneath the epidermis get “nuked” by sunlight. It also partly explains why even some hairy mammals, such as cows, are also susceptible to sunburn, and why no person is well advised to think of themselves as invincible. It also starts to explain why sun exposure can require a metabolically-intensive biological response even if your skin does not actually burn.Â

Sunburns are caused by the transfer of electromagnetic energy from the sun, predominantly in the form of ultraviolet (UV) light, into heat and photochemical energy inside living cells. Of course, most of this light energy is absorbed by intra-cellular water with no harm done—the water molecules get slammed by the light, they speed up, that is, become hotter, and the absorbed light energy in the form of heat is dissipated by the body via ordinary homeostatic mechanisms for temperature control. But, some fraction of the light energy can shatter water molecules, i.e., cause water to undergo a photochemical reaction and be converted into ionized particles, such as peroxides. Similar photochemical reactions with molecular oxygen form “super-oxides”. These “free radicals” are like miniature bombs that can damage many other types of vital molecules. Most biological molecules that get splattered indirectly by free radicals or directly by incoming radiation are quickly repaired or replaced, again with no harm done. But, when the insult becomes overwhelming, that is, the dose of incoming sunlight becomes too intense, a variety of pathological changes follow, including cell death and its manifestation as a burn. Burns, defined by cell injury and death, lead to inflammation and its consequences.Â

Incidentally, promotion of super-oxide formation is the mechanism by which certain drugs cause increased super sensitivity to sunlight. An overly active inflammatory system explains why people with autoimmune diseases such as lupus erythematosis are unusually sensitive to sunlight.Â

Key Point: These pathological processes leading to cell death, inflammation, and as a result, more cell death, and as a consequence, further inflammation, might take time to become apparent. Solar radiation-induced inflammatory diseases can escalate, that is, can get worse and worse, for 24-to-72 hours after exposure, depending on their severity. If you get over-exposed, then you can do several things to minimize the injury after exposure but before some of the damage is done.Â

Sun-induced inflammatory disorders can be somewhat arbitrarily modeled as causing dysfunction in three separate, albeit highly inter-related organ systems:Â (1) the skin (a.k.a. the integument that keeps bodily water inside an organism and is one of our primary barriers against infectious agents); (2) the hemodynamic system, that is, the tissues and organs that participate in regulating the movement of blood through the body; and ; (3) the central nervous system (CNS, or brain, and its direct appendages, such as the eyes).Â

I. Skin: Treatments of Solar Insults to the Integument

A. Home remedies: There are a variety of folk salves, poltices, compresses and balms that are purportedly palliative, such as smearing yogurt or potato paste on the skin, and taking a bath in cool water mixed with oatmeal (see, e.g., or ). Most seem designed to promote trans-cutaneous (“through the skin”) heat loss and “re-moisturize” the epidermis. Marigold flower (Calendula officinalis) preparations purportedly reduce inflammation. A recipe for making a preparation for treating sunburn can be found at Most travelers should probably plan on using commercially available products.

B. Topicals:Â
(i) Over the Counter (OTC) creams. These include common cosmetics designed to be used daily regardless of sunburn. Most contain a variety of fats and oils, such as aloe. Although they are described as “moisturizing”, what they actually mean is that they increase the fat content between the keratinized cells making up the outer most layer of the skin. Even if the true biological benefit of these creams is not clear, there’s no question that they make most all people feel better. Most creams and lotions have added ingredients to aid marketing, including:

A. Prophylactics: Sunscreens containing para-aminobenzoic acid (PABA), benzophenone, and other UV light absorbing chemicals are designed to prevent an insult from ever happening. After sustaining a sunburn, the water might be over the proverbial dam, but applying these preparations to burnt skin still represent a good idea. As post hoc treatments, most sunscreens contain moisturizing ingredients that help people feel better even if its too late for prevention. And since sunburned skin will become more vulnerable to new solar radiation injuries for about 2 weeks after an insult, preventing re-injury represents an important advantage to consider when applying sunscreens after it might seem too late.Â
B. Anti-inflammatory agents: A variety of commercial preparations containing low doses of steroids are available, particularly as 1% hydrocortisone creams. Their labels suggest that they are usually indicated for treating itches. Hemorrhoidal creams are essentially identical in composition, and probably cool your burn as well as any other cortisone cream, even if they’re less “cool” to pull out of your bag in public. Topical steroids will help abort the local inflammatory process and limit the amount of damage that develops. They are indicated except where there is a break or cut in the skin that might be susceptible to infection.
C. “Pain relief” creams containing capsaicins or aspirin-like salicylates are relatively contra-indicated. They might help some people with mechanical sports injuries feel better, but they will add insult to sun injury.Â

(ii) Prescription Creams. Some more effective, but potentially more risky, topicals are available by prescription only: Mineral corticoid creams are extremely effective, but their distribution is limited for good reasons related to their potential for absorption into the systemic circulation, where they can cause all kinds of mischief, including renal failure. If you carry a tube anyway, then limit your use of it to relatively small areas of your skin, and don’t use it for much more than 48 hours. Don’t apply it to skin referred to as intertriginous, such as your armpits or groin, or you might get “jungle rot”, that is, an overgrowth of bacteria, yeast, or fungi. If you see any swelling in your feet or ankles, stop using it immediately.

C. Systemic Medications:Â

(i) OTC’s Taken By Mouth.

(i) Aspirin-like compounds: Early ingestion of anti-inflammatory drugs such as aspirin or ibuprofen not only relieves the symptoms of pain but also interrupts the underlying pathophysiological processes causing the pain. The earlier these drugs are taken, the better. For otherwise healthy people who can tolerate them and don’t have another medical condition that prohibits their use, a general rule of thumb is to take twice the recommended dose on the OTC label twice as often as recommended for the first 24-to-48 hours. Remember, as always, taking them with food helps prevent their harmful effects on the stomach lining.Â
(i) Antihistamines: For severe sunburns, these anti-inflammatory drugs can be more effective than aspirin-like medications. Use drugs like diphenhydramine (Benadryl, others) before bedtime if the side effect of sedation is desired, as sunburn can disrupt sleep through a variety of mechanisms besides simple pain. Use drugs like loratadine (Claritin) that do not enter the brain during the day or if you’re taking other drugs that cause drowsiness.Â
(i) Alcohol: The active ingredient in whiskey and wine is a peripheral vasodilator that increases blood flow to your skin. But, there are no hard data in the literature to indicate whether this is a good thing, a bad thing, or both depending on the phase of the illness. Common sense and loose scientific logic indicate that the goal is to break the disease process that causes vasodilatation in the skin, not promote it, so all other things being equal, it might be wise to avoid alcohol. Regardless of its effects on the vasculature in the skin, alcohol will place additional stress on most brains, and that might be something to avoid during the acute phases of the illness.
(i) Tobacco: The hazards of nicotine addiction are well established, but bias-free, science based, medical practice cannot claim that nicotine is contra-indicated in cases of sunburn. Nicotine is a vasoconstrictor. If you smoke, of course you should stop, but probably not until after you recover from a major sunburn.Â

(ii) Controlled Substances. Potentially dangerous, but more effective, medications are available by prescription only: Steroids like prednisone and related drugs can suppress almost any inflammatory disorder, including sunburn. Almost any form, when taken in the proper dosage, seems effective and reasonably safe when used appropriately for a very few days. But caveat emptor: Steroids can cause major side effects. In some people, the side effects can be worse than the disease they are used to treat. In general medical practice, steroids are reserved for the treatment of second degree sunburns, i.e., those that cause obvious blistering. Most physicians will prescribe 40-to-80 mg equivalents of prednisone per day for 2-to-3 days. I prefer a single, 4 mg dose of dexamethasone, but that bias is based on my familiarity with it as a relatively safe and convenient form of transient immunosuppression, not hard data.

II. Â Treatment of Secondary Problems

A. Treatment of Blisters (a.k.a. “bullae” or “bullous erythema”). The inflammatory response can cause intra-vascular water to extravasate into the extra-vascular spaces in the dermis, forming pockets of fluid, or blisters. Blisters can burst, and as a consequence, lead to breaks in the skin that can in turn lead to overt fluid loss and secondary infections. For these reasons, blisters from second degree sunburns are usually treated like blisters from any other second degree burns. Second degree burns deserve professional care. Admission to a hospital based burn unit can be required in rare cases. If you’re caught in the field with second degree burns, try to protect breaks in the skin with dry bandages and antibiotic creams until you can get professional help.Â

B. Treatments of Secondary Dehydration. Neuronal sensors in the skin detect the increases in heat and trigger general mechanisms for heat loss. Vastly more important, cellular injury and death lead to inflammation. Chemicals are released from damaged tissues that provoke the release of chemicals from local immune cells in the dermis and with its vascular spaces. A very large number of chemicals are released by these immune cells, but loosely speaking, they can be thought of as two types: one promotes the inflammation, i.e., fans the fire, and the others ultimately recruit more immune cells to come help. All or their consequences lead to increased demands for metabolic energy and relative dehydration from the perspective of your skeletal muscles and internal organ systems. A variety of inflammation-mediated processes are involved in the response to solar energy deposition, with or without sunburn, each of which should be recognized, honored, and treated logically.Â

(i) Shunting of blood from the body “core” to the periphery, i.e., to the skin, where the heat can be lost to the atmosphere and cooler surfaces in contact with your skin. This aspect of increased blood flow to the periphery is only partly well modeled as a healthy response to an unhealthy situation. Regardless, it is energy intensive, so expect to give up some of your ordinary feelings of vigor. The proper response is to drink more clear fluids, lie down if feasible, and rest your muscles so that they don’t start demanding more blood from a source that has become relatively scarce.
(ii) Panting, like dogs do. Panting creates transient changes in air pressure that promote the evaporation of fluid from within your mouth and respiratory tree. Heat is lost when liquid water undergoes a phase transition to a vapor. From the perspective of the cells lining your mucosa, water gets scarce. Thirst results. You should drink.
(iii) Sweating. Sweating works like panting. Sweat production can be promoted by eating peppers and mustards. There are drugs for people with dry mouth that promote sweating, but they are rare medications you might not find even with a prescription. A cold shower would be a lot safer, cheaper, and better. The problem with bathing is that it tends to promote the loss of water, electrolytes, and fats from the skin. If you take a bath, try to pour salts in the water (a similar idea is behind the recommendations for oatmeal baths by folk healers, but salt goes down the drain much easier).
(iv) Drinking cold fluids, such as ice water. The capacity of water to absorb heat is remarkably high, and potentially useful in the treatment of sunburn and subclinical variants of “heat stroke”. Putting ice water in your stomach for short periods of time can be beneficial in this scenario.Â
(v) Maintaining proper electrolyte balances. Sweating, panting, blistering, and inflammation can lead to the loss of electrolytes along with the fluid. A great way for travelers to replace their electrolytes is by taking a daily multi-vitamin pill. It’s not the vitamins you’re looking for in this scenario, it’s the potassium, chloride, and trace metal salts in the commercial vitamin formulations that you’re after. Travelers do well to take a small pack of once-a-day vitamins with them regardless of whether they take them at home or not.

The bottom line is that sun-induced inflammatory disorders of the skin can lead to dehydration, dehydration can lead to lassitude, and lassitude can lead to disability that most travelers would be better off without. Repairing cells damaged takes a lot of energy, leading to a loss of vitality. It follows that one of the treatments for sunburn that should not be overlooked is drinking plenty of free water and trying to replenish your bodily salts.Â

C.  Treatment of Brain Dysfunction. The medical literature on sunburn is pervaded by vague descriptions of non-specific brain dysfunction. Most symptoms can be thought of as non-specific variants of lethargy. As one of the most finely tuned instruments in the mammalian symphony, the brain is all too easily perturbed by inflammation from any cause and the intense metabolic requirements that result. It might also be that some aspects of lethargy can be thought of as part of a healthy adaptation to sunburn. Either way, its important for travelers to realize that their normal cognitive reserves and their typical abilities to think nimbly in novel situations might not be as robust after sunburns as they usually are. Plans should be made to avoid intellectual, as well as physical, challenges until after healing from sunburn is well underway. Â

D. Treatment of Sunburns to the Eyes. Acute Snow Blindness (a.k.a. ophthalmia nivialis): In this limited context, it may be defined as a radiation-induced burn of the outer layers of the eye causing pain, lacrimation (tearing) and photophobia (aversion to light).  When the conjunctiva covering the whites of your eyes burn, the eyes appear to be “bloodshot”. When the clear tissue covering the pupil called the cornea burns, visual dysfunction ensues. Corneal sunburn can occur with as little as one hour of unprotected exposure at sea level. (See

The key point about radiation-induced corneal injury is that it can take 12 hours or more after exposure to fully develop. Treatment should begin as soon as feasible, and consists of maneuvers that are conceptually similar to those for other types of local radiation-induced burns, including systemic anti-inflammatory drugs ( and topical steroids. Here, however, only ophthalmic solutions of topical steroids will do, and most of these are available by prescription only. In the USA, ofloxacin solutions are safe and effective as long as there is no trauma or other infectious eye disease complicating the snow blindness. If you cannot get an ophthalmic solution, then a few drops of mineral oil is recommended by the writers of the Merck Manual (see above). When radiation-induced eye injuries occur in metropolitan areas, physicians will often “patch” the eyes closed. That might not be practical out on the road, but retreating to your hotel and resting your eyes to the extent feasible for about 2 days is advisable, and usually all that’s required for full recovery. Permanent impairment and even blindness has been reported from exposure related injuries in which radiation played a contributing role, but as best as can be inferred from the literature, only in extreme scenarios or occupational settings that are beyond the scope of this review.

Summary: The deposition of solar energy in living tissues produces consequences that demand large amounts of metabolic energy. Sunburn results from radiation-induced cell damage and death. Sunlight can cause an inflammatory process that can take up to 2-to-3 days after exposure to peak. Early immunosuppressive therapy can limit the extent of injury. The aggressiveness of the treatment should be proportional to the extent of the injury, which in turn is proportional to the extent of exposure.Â

Afterward: It might be that everyone benefits from learning a little bit about the treatment of sun toxicity. While individual vulnerability can vary significantly as an imperfect function of age, race, and prior sun exposure, no human is immune. Perhaps even more importantly, everyone should want to possess knowledge about how t o help others who become transiently stricken.Â


P. David Mozley MD

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