Excerpt from The Prepper's Medical Handbook. Page reference numbers point to more in-depth treatment and self-reliant care available within the book.
High environmental temperatures are frequently aggravated by strenuous work; humidity; reflection of heat from rock, sand, or other structures (even snow!); and the lack of air movement. It takes a human approximately 10 days to become heat acclimated. Once heat stress adaptation takes place, there will be a decrease in the loss of salt in the sweat produced to conserve electrolytes. Another major change is the rapid production of sweat and the formation of larger quantities of sweat. Thus, the body is able to start its efficient cooling mechanism—sweating—more fully and with less electrolyte disturbance to the body.
Risk factors for heat-stress injuries include:
Very young or very old
Unaccustomed to heat
Illness with fever or taking drugs such as antihistamines
Clothing or equipment that interferes with heat loss (certain helmets, too much or restrictive clothing)
Dehydration (drinking to prevent thirst will keep dehydration above 2%)
Salt lost in sweat during work can normally be replaced at mealtimes. An unacclimated man working an 8-hour shift would sweat 4 to 6 liters. The salt content is high, 3 to 5 grams per liter of sweat. With acclimatization, salt concentration drops (1 to 2 grams per liter). An acclimatized man might lose 6 to 16 grams of salt during an 8-hour shift in 6 to 8 liters of sweat.The unacclimated man could lose 18 to 30 grams of salt in 4 to 6 liters of sweat. The average American diet contains 10 to 15 grams per day of salt. This means that an unacclimated worker could suffer from a salt deficit of 3 to 20 grams per day. In the 10 days that it would take his body to become conditioned to heat stress, the total salt deficit could become substantial.
A concern in heat-illness prevention is that a heat-stressed individual must obtain adequate fluid replacement. If we focus on salt replacement to the exclusion of adequate water intake, the individual may become salt loaded and accelerate his dehydration. Generally, an excess of salt or water over actual needs is readily controlled by kidney excretion.
Depletion of body salt can lead to progressive dehydration because the body will attempt to maintain a balance between electrolyte concentrations in tissue fluids with that in the cells. Deficient salt intake, with continued intake of water, tends to dilute tissue fluid. This suppresses the antidiuretic hormone (ADH; vasopressin) of the pituitary gland, preventing the kidney from reabsorbing water. The kidney will then excrete a large volume of very dilute urine. The salt concentration of body fluids will be maintained, but at the cost of increasing the depletion of body water, with a rapid onset of dehydration. Under heat stress, this can result in symptoms of heat exhaustion similar to those resulting from water restriction, but with more severe signs of circulatory insufficiency and notably little thirst. Absence of chloride in the urine (less than 3 grams per liter) is diagnostic of salt deficiency, a test not performable in the field.
An opposite defect in the regulation of ADH can lead to severe loss of sodium by the body, resulting in hyponatremia. A deficiency of ADH causes water retention by the kidney and hyponatremia with rather low amounts of water ingestion. Another cause of hyponatremia would be overhydrating, basically causing water intoxication. The discovery of hyponatremia as a reason for the collapse of hikers in the Grand Canyon has been blamed on overhydration. But it is hard to imagine carrying that much water. Their condition may have resulted from ADH deficiency. Military personnel during training have also suffered from hyponatremia collapse, but in the case of an individual being allowed multiple breaks for water whenever he felt like it (unrestricted access to limitless water), overhydration as the cause for hyponatremia makes sense.
The ideal replacement fluid for the unacclimated worker in heat would be lightly salted water (0.1%, or 1 teaspoon per gallon or 1 gram per liter) to prevent water or salt depletion. He needs 13 to 20 ounces (400 to 600 milliliters) of water before activity, and 3 to 6 ounces (90 to 180 milliliters) of water every 10 to 15 minutes during an active period. Do not go longer than 30 minutes between drinks of water. Replacement fluids should not contain sugar concentrations greater than 6 grams per 100 milliliters, as higher concentrations slow gastric emptying. Acclimatized subjects need only water as a replacement fluid, but need 32 ounces (1 liter) per hour in activity during hot weather. Thirst develops when a person is about 2% dehydrated, so “drinking to thirst”—that is, drinking to satisfy thirst—is a safe way to prevent dehydration and avoid overhydration.
With no water available, how long could a person expect to survive? The answer is generally dependent upon the temperature and the amount of activity. At a temperature of 120°F (49°C) with no water available, the victim would expect to survive about 2 days (regardless of activity). This temperature is so high that survival would not be increased beyond 2 days by even 4 quarts (3.7 liters) of water. Ten quarts (9.5 liters) might provide an extra day. At 90°F (32°C) with no water, the person could survive about 5 days if she walked during the day, 7 days if travel was only at night or if no travel was undertaken at all. With 4 quarts of water, survival would extend to 6.5 days with day travel and to 10 days with only night travel. With 10 quarts, days of survival would increase to 8 and 15 respectively. If the highest temperature was 60°F (15.5°C) with no water, the active person could expect to survive 8 days, the inactive person 10 days.
Recommendations for preventing heat illness include:
Water to prevent thirst.
Wearing baggy clothing that promotes evaporation of sweat.
Covering the head and shading the face.
Keeping physically fit and allowing time for heat acclimatization.
Avoiding exercise during the hottest time of the day.
This is a condition in which the blood sodium level falls too low to maintain normal body function, and is typically caused by drinking too much water and not consuming adequate salt-containing food. Drinking only to treat thirst can prevent overhydration.
Symptoms include headache, weakness, fatigue, lightheadedness, muscle cramps, nausea with or without vomiting, sweaty skin, normal core temperature, normal or slightly elevated pulse and respirations, and a rising level of anxiety. These patients appear to have heat exhaustion or heat stroke since the signs and symptoms overlap. Treating it like heat exhaustion by just adding water will harm the hyponatremia patient, making it worse. Increased severity of hyponatremia includes disorientation, irritability, and combativeness, which gives the problem a more common name: water intoxication. Untreated, the ultimate result will be seizures, coma, and death.
Note that heat-exhausted patients have a typically low output of yellowish to brown urine (urinating every 6 to 8 hours) combined with thirst. Hyponatremia patients urinate a clear stream frequently. Hyponatremia patients deny thirst and will admit to drinking lots of water.
Patients with mild to moderate symptoms and a normal mental status may be treated in the field: The treatment for this condition is rest in shade with no fluid intake (even sports electrolyte drinks) and a gradual intake of salty foods while the kidneys reestablish a sodium balance. The ideal treatment fluid would be an approximately 9% salt solution, which would be the equivalent of 3 to 4 bouillon cubes in 1/2 cup (100 ml) of water. Once a patient develops hunger and thirst combined with normal urine output, the problem is solved. Restriction of fluids for someone who is well hydrated, fortunately, is harmless. Patients with an altered mental status require rapid evacuation to a medical facility.
Salt depletion can result in nausea, twitching of muscle groups, and at times severe cramping of abdominal muscles, legs, or elsewhere. Treatment of heat cramps consists of stretching the muscles involved (avoid aggressive massage), resting in a cool environment, and replacing salt losses. Generally, 10 to 15 grams of salt (a pinch per quart) and drinking to satisfy thirst should be adequate treatment.
Heat exhaustion is a classic example of compensatory shock (see page 13) and is encountered while working in a hot environment. The body has dilated the blood vessels in the skin to divert heat from the core to the surface for cooling. However, this dilation is so pronounced, coupled with profuse sweating and loss of fluid (also a part of the cooling process), that the blood pressure to the entire system falls too low to adequately supply the brain and the visceral organs. The patient will have a rapid heart rate and other findings associated with the compensatory stage of shock: pale color, nausea, dizziness, headache, and a lightheaded feeling. Generally, the patient is sweating profusely, but this may not always be the case. The temperature may be elevated but often is not at all.
Treat as for shock. Have the patient lie down immediately, elevate the feet to increase the blood supply to the head, and restrict direct sunlight and the hot environment. Provide copious amounts of water, a minimum of 1 to 2 quarts (0.9 to 1.8 liters); lightly salted water would be best. Obviously, fluids can be administered only if conscious. If the patient is unconscious, elevate the feet 3 feet (1 meter) above head level and protect from aspiration of vomit. Give water when the patient awakens.
Heat stroke (sun stroke) represents the complete breakdown of the heat control process (thermal regulation) in the human body. With the loss of the ability to sweat, core temperatures rise over 105°F (40°C) rapidly and soon exceed 107.6°F (42°C), resulting in death if not treated aggressively. This is a true emergency. It is a progressive stage of shock. The patient will be confused, very belligerent, and uncooperative, and will rapidly become unconscious. Immediately move into shade or erect a hasty barrier for shade. Spray with water or other suitable fluid and fan vigorously to lower the core temperature through evaporative cooling. Lacking other available fluid, this is the one time in medicine when it may be justifiable to urinate on your patient. Massage the limbs to allow the cooler blood of the extremities to return to core circulation more readily, and fan to increase evaporative heat loss. Carefully monitor the core temperature and cease cooling when it lowers to 102°F (39°C). The temperature may continue to fall or suddenly rise again.
The most significant finding in heat stroke is the altered mental status of the victim. While heat exhaustion victims can be confused, this should resolve rapidly when they are in the shock treatment position (head down, feet up). The confusion and very often belligerent behavior of heat stroke victims make them very hard to handle. While their skin is normally dry and hot, this is not always the case. Suspect heat stroke in anyone who becomes confused and erratic in behavior, or unconscious, during exercise in a hot environment.
This person should be evacuated as soon as possible, since his thermal regulation mechanism is quite unstable and will remain so for an undeterminable length of time. He should be placed under a physician’s care as soon as possible. Return to the grid if possible. Otherwise, treat as above.
Prickly heat is a heat rash caused by the entrapment of sweat in glands in the skin. This can result in skin irritation and frequently severe itching. Treatment includes cooling and drying the involved area and avoiding conditions that may induce sweating for a while. Providing several hours in a cool, dry environment daily is the only reliable treatment for prickly heat, but you may treat for itch as indicated on page 149.
Other than being totally toasted, cardiopulmonary arrest is the most significant lightning injury. People who can scream from fright or pain after an electrical bolt has struck are already out of immediate danger. Their wounds may be dressed later. Those who appear dead must have immediate attention, as they may be saved. Normally, when dealing with mass casualties, the wounded are cared for preferentially while the dead are left alone. Not in this instance! The victim is highly unlikely to die unless cardiopulmonary arrest occurs. If cardiopulmonary arrest does happen, 75% will die unless CPR is performed. As the heart tends to restart itself due to its inherent ability (automaticity), the heartbeat may return spontaneously in a short time. However, the respiratory system may be shut down for 5 to 6 hours before being able to resume its normal rhythm. Lack of oxygen will cause a person whose heart has restarted spontaneously to die.
When administrating CPR, take precautions with the cervical spine, as the explosion may have caused fractures of the neck or other portions of the body. While CPR is being performed, check for the pulse periodically. When the heart restarts, maintain ventilations for the patient until respirations also resume. Attempt to continue this as long as possible; a victim may be revived even after many hours with no neurological defects—but only if CPR or respiration ventilation has been properly performed. Remember, after a lightning strike the victim’s eyes may be fixed and dilated, respirations ceased, heart stopped, blood pressure 0/0—all signs of clinical death. Pay no attention to these findings and administer CPR as long as physically possible.
Lightning strike frequently causes vascular spasms in its victim. This can result in faint, or even nonpalpable, pulses. When the vasospasm clears, which it generally does within a few hours, the pulses return.
Neurological defects are the second major consequence of lightning hits. Approximately 72% of victims suffer loss of consciousness, and three-quarters of these people will have a cardiopulmonary arrest. Direct damage to the brain can result, but frequently the neurological defects, including seizure activity and abnormal brainwave studies, eventually revert to normal. Two-thirds of victims will have neurological defects in the lower half of their bodies; one-third will suffer from paralysis of the upper half. Amnesia and confusion of events after the accident are common but are usually transient.
Most will have amnesia, confusion, and short-term memory loss that may last from 2 to 5 days. These effects are similar to those experienced by electroconvulsive shock therapy patients. The person may be able to talk intelligently but shortly thereafter not remember the conversation had taken place.
Burns from lightning itself are generally not severe. Very high voltage is carried over the surface of conductors; the high voltage of lightning is similarly carried over the surface of the body with minimal internal burn damage, the so-called flashover effect.
Direct electrical burn damage can occur, however, and when it does it usually consists of one of several types. Linear burns start at the head, progress down the chest, and split to continue down both legs. These burns are usually 1/2 to 11/2 inches (1.3 cm to 3.8 cm) in width, and are first and second degree. They follow areas of heavy sweat concentration. Punctate burns look like a buckshot wound. These are full thickness, third-degree burns that are discrete, round wounds, measuring from a few millimeters to a centimeter (1/4 inch to 1/2 inch) in width. These seldom require grafting as the area is so small. Feathering or ferning burns are diagnostic of lightning injury. They fade within a few hours to days and require no treatment. This phenomenon is not a true burn but the effect of electron showers on the skin. They have a characteristic reddish fern appearance that covers the skin surface—especially the trunk. Thermal burns also result from vaporization of surface moisture, combustion of clothing, heated metal buckles, and so on. Thermal burns are the most common type of lightning-associated burn, and they can be first, second, or third degree.
The flashover effect saves most victims from burn trauma. However, as noted, burns do occur. Persons with head burns are two and a half times more likely to die than those without. Possibly more surprising, persons with leg burns are five times more likely to die than those who do not have them. This is probably related to a ground or step current phenomenon.
The four mechanisms of direct lightning injury are: (1) direct strike, (2) splash, (3) step current, and (4) blunt trauma. To minimize the chance of lightning injury, the following should be noted about these mechanisms:
Direct strikes are most likely to take place in the open, especially if you carry metal or objects above shoulder level. Shelter should be taken within the cone of safety, described as a 45-degree angle down from a tall object, such as a tree or cliff face. But that cone of safety ain’t all that safe. Being too close to the tree or cliff face can result in increased exposure to splash current or ground current; too near the outer edge and the zone of safety simply fails and you have increased exposure to direct strike.
Splash injuries are perhaps the most common mechanism of lightning hit—the current strikes a tree or other object and jumps to a person whose body has less resistance than the object the lightning initially struck. Splash injuries may occur from person to person, when several people are standing close together. It has jumped from fences after having struck the fence some distance away. It has splashed to people from plumbing fixtures inside houses that were struck. Avoid close proximity to walls, fences, plumbing, or other items that could be struck.
Step current is also called stride voltage and ground current. The lightning current spreads out in a wave along the ground from the struck object, with the current strength decreasing as the radius from the strike increases. If the victim’s feet are at different distances from the point of the strike, and the resistance in the ground is greater than through his body, he will complete a circuit. Large groups of people can be injured simultaneously in this manner. Keeping feet and legs together, while squatting down, minimizes the chances of step voltage injury.
Blunt trauma, or the sledgehammer effect, results from the force of the lightning strike, or the explosive shock wave that it produces. The victim may be forcibly knocked to the ground. Over 50% of victims will have their eardrums ruptured in one or both ears. This may result from direct thermal damage, the thunder shock wave, or even skull fractures from the blunt trauma. Barotrauma to the ears may be reduced by keeping the mouth open during times of great danger.
In the above scenario a person should squat, with legs together and mouth open in a zone of safety—but not too near the protective tree or cliff face. Spread party members out to maximize the chance that there will be survivors, and thus rescuers, if lightning strikes appear imminent. Get boats into a zone of safety near shore, against the tree line or cliff face. Other than the immediate presence of lightning, is there any warning? At times there will be the smell of ozone, hair may stand on end, metal climbing equipment may start to vibrate, or St. Elmo’s fire may be present. Good luck!
HIGH ALTITUDE ILLNESSES
You will not need to worry about high altitude illness of any kind unless you must depart suddenly from a lower attitude and head for the hills—the high hills, that is. High-altitude-related illnesses can generally be avoided by gradual exposure to higher elevation, with the sleeping ascent rate not exceeding 1,000 feet (300 meters) per day when above 9,000 feet (2,800 meters). Alternatively, avoid sleeping at greater than 2,000-foot (600-meter) increments every 2 days when suddenly traveling from near sea level to 10,000 feet (3,000 meters). A high carbohydrate diet, consisting of at least 70% carbohydrates started 1 to 2 days prior to ascent, remaining well hydrated, and exercising moderately until altitude acclimatized, all help prevent high altitude illness.
The three major clinical manifestations of this disease complex are acute mountain sickness (AMS), high altitude pulmonary edema (HAPE), and high altitude cerebral edema (HACE). As will be noted, the symptoms progress rather insidiously. They are not clearcut, separate diseases—they often occur together. The essential therapy for each of them is recognition and descent. This is lifesaving and more valuable than the administration of oxygen or drugs.To prevent high altitude illnesses, it is helpful to “climb high but camp low”— that is, spend nights at the lowest camp elevation feasible.
Acute Mountain Sickness (AMS)
Rarely encountered below 6,500 feet (2,000 meters), acute mountain sickness is common in persons going above 10,000 feet (3,000 meters) without taking the time to acclimatize for altitude. Symptoms beginning soon after ascent consist of headache (often severe), nausea, vomiting, shortness of breath, weakness, sleep disturbance, and occasionally a periodic breathing known to medical personnel as Cheyne-Stokes respiration.
Prevention, as with all of the high altitude illnesses, is gradual ascent above 9,000 feet (2,800 meters) and light physical activity for the first several days. For persons especially prone to AMS, it may be helpful to take acetazolamide (Diamox) prophylactically, 125 mg every 12 hours starting the day of ascent and continuing the next 3 to 5 days. This medication helps prevent or treat the acid base imbalance of the blood that can occur in some people from the increased loss of carbon dioxide at high altitudes. The treatment dose of acetazolamide is 250 mg twice daily for 5 days. This prescription drug should be added to your medical kit if you expect to encounter elevations above 9,000 feet (2,800 meters) suddenly. See acetazolamide, page 265.
The best AMS treatment is descent, and relief can often be felt even if the descent is only 2,000 to 3,000 feet (600 to 900 meters). Full relief can be obtained by descending below 6,500 feet (2,000 meters). Stricken individuals should avoid heavy exercise, but sleep does not help as breathing is slower during sleep, making oxygen deprivation worse. Oxygen will help only if taken continuously for 12 to 48 hours. Aspirin may be used for headache. Percogesic or ibuprofen from the Non-Rx Oral Medication Module may be used. In addition to descent, Decadron (dexamethasone), 4 mg tablets every 6 hours until below the altitude at which symptoms appeared, has been shown to help control the symptoms of AMS. Decadron tablets or injection should be added to your medical kit if you expect to encounter elevations above 10,000 feet (3000 meters). See Decadron, pages 284 and 290.
High Altitude Pulmonary Edema (HAPE)
High altitude pulmonary edema is rare below 8,000 feet (2,500 meters) but occurs at higher altitude in those who are poorly acclimatized. It is more likely in persons between the ages of 5 and 18 (the incidence is apparently less than 0.4% in persons over 21, and as high as 6% in those younger), in those who have had this problem before, and in those who have been altitude acclimatized and who are returning to high altitude after spending approximately 2 weeks at sea level.
Prevention is altitude acclimatization as discussed in the section on AMS above. Nifedipine (Procardia), 20 mg every 8 hours to be taken during the ascent phase and for 3 additional days at altitude, has been shown to work prophylactically.
Symptoms develop slowly, within 24 to 60 hours of arrival at high altitude, with shortness of breath, irritating cough, weakness, rapid heart rate, and headache that rapidly progress to intractable cough with bloody sputum, low-grade fever, and increasing chest congestion. Symptoms may progress profoundly at night. Patients should be evaluated by listening to their chests for a fine crackling sound (called rales) and checking resting pulse rate nightly. A pulse rate of greater than 110 per minute, or respirations greater than 16 per minute after a 20-minute rest, is an early sign of HAPE. Respirations over 20 per minute and pulse over 130 per minute indicates a medical emergency, and the patient must be evacuated immediately. Without treatment, death usually occurs within 6 to 12 hours after onset of coma.
Descent to lower altitude is essential and should not be delayed. Treatment includes nifedipine, 20 mg sublingual (or chewed and swallowed), given upon diagnosis and repeated every 6 hours. A descent of as little as 2,000 to 3,000 feet (600 to 900 meters) may result in prompt improvement.
High Altitude Cerebral Edema (HACE)
High altitude cerebral edema is less common than AMS or HAPE, but it is more dangerous. Death has occurred from HACE at altitudes as low as 8,000 feet (2,500 meters); however, HACE is rare below 11,500 feet (3,500 meters). The symptoms are increasingly severe headache, mental confusion, emotional behavior, hallucinations, unstable gait, loss of vision, loss of dexterity, and facial muscle paralysis. The victim may fall into a restless sleep, followed by a deep coma and death.
Descent is essential. Oxygen should be administered starting at 6 liters/minute for the first 15 minutes, followed by a flow rate of 2 liters per minute. Decadron (dexamethasone) should be given in large doses, namely 10 mg intravenously, followed by 4 mg every 6 hours intramuscularly until the symptoms subside. Response is usually noted within 12 to 24 hours, and the dosage may be reduced after 2 to 4 days and gradually discontinued over a period of 5 to 7 days. Immediate descent and oxygen are recommended to prevent permanent neurological damage or death.
It is hard to imagine how a person planning on suddenly leaving the grid would require such a rapid ascent in altitude as to endanger themselves from an altitude-related injury. But I have included this abbreviated discussion, because that is what prepping is all about, being prepared for any circumstance.