CMDT 2013
Disorders Related to Environmental Factors Jacqueline A. Nemer, MD, FACEP
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COLD & Heat
The human body maintains a steady temperature through the balance of internal heat production and environmental heat loss. Heat exchange between the body and environment occurs via four common processes: radiation, evaporation, conduction, and convection. In extreme temperatures, the body’s thermoregulation may fail. This results in the body’s internal temperature moving toward the temperature of the external environment. Temperature-related conditions may arise in any individual, regardless of sex, race, age, or underlying health status. Cold and heat exposure may cause a wide spectrum of conditions; the severity varies considerably among individuals. The likelihood and severity of extreme temperature-related conditions depends on physiologic and environmental factors. Physiologic risk factors include underlying medical conditions (cardiopulmonary, vascular, neurologic, psychiatric, musculoskeletal, immunologic, hematologic, endocrine [hypothyroidism, adrenal insufficiency, hypopituitarism], renal, hepatic, and infectious diseases); extremes of age; cognitive impairment; poor physical conditioning/sedentary lifestyle; poor acclimatization; concurrent injury; inadequate thermoregulation; prior temperature-related injury; and pharmacologic effects (ie, medications, recreational drugs, tobacco, and alcohol). Environmental risk factors include inadequate clothing, inadequate housing, occupational or recreational exposure.
ACCIDENTAL SYSTEMIC HYPOTHERMIA
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Essentials of diagnosis
Hypothermia is a reduction of core body temperature below 35°C. `` To accurately measure hypothermia, an intravascular, esophageal, rectal, or bladder probe that measures temperatures as low as 25°C is required; oral, axillary, and otic temperatures are inaccurate and unreliable. ``
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Rewarming is the initial, imperative treatment. Refreezing must be avoided to reduce further damage. `` The core temperature must be over 32°C before terminating resuscitation efforts. ``
``General Considerations Systemic hypothermia is defined as core body temperature < 35°C. This may be primary (from exposure to prolonged ambient extremely low temperature) or secondary (due to thermoregulatory dysfunction). Primary and secondary hypothermia may also be present at the same time. Hypothermia risk factors include prior cold weather injury as well as those factors listed in the Cold & Heat section. Heat loss occurs more rapidly with high wind velocity (“windchill factor”), water exposure (including wet clothing), or direct contact with a cold surface. The human body generates internal heat through muscle activity (ie, shivering or increased physical exertion) and preserves heat loss via peripheral vasoconstriction. In prolonged or repetitive cold exposure, these thermoregulatory responses can become impaired; hypothermia ensues. Hypothermia diagnosis can be easily overlooked and delayed in a critically ill or injured patient. Hypothermia should be considered in any patient with prolonged exposure to ambient or cold environment, trauma, inadequate clothing, or altered mental status. Systemic hypothermia depresses physiologic function, resulting in decreased respiratory drive, oxygen consumption, central and peripheral nerve conduction, gastrointestinal motility, myocardial repolarization, and coagulation cascade. Accidental hypothermia may occur iatrogenically in the hospital setting. This section does not cover induced hypothermia post-resuscitation by critical care specialists.
``Clinical Findings Symptoms and signs of hypothermia are typically nonspecific and markedly variable based on the patient’s
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s Figure 37–1. Electrocardiogram shows leads II and V5 in a patient whose body temperature is 24°C. Note the bradycardia and Osborn waves. These findings become more prominent as the body temperature lowers, and gradually resolve with rewarming. Osborn waves have an extra positive deflection in the terminal portion of the QRS complex and are best seen in the inferior and lateral precordial leads (most notably in leads II, V5, and V6).
underlying health and circumstances of hypothermia. At body core temperature between 32°C and 35°C, symptoms include tachypnea, tachycardia, hypertension, shivering, impaired coordination, poor judgment, and apathy. At body core temperature between 32°C and 28°C, the body slows down. Shivering stops; bradycardia, dilated pupils, slowed reflexes, cold diuresis, and confusion and lethargy ensue. The electrocardiogram (ECG) may reveal a J wave or Osborn wave (positive deflection in the terminal portion of the QRS complex, most notable in leads II, V5, and V6) (Figure 37–1). In extreme hypothermia (body core temperature below 28°C), the skin may appear blue or puffy; coma, apnea, loss of reflexes, asystole, or ventricular fibrillation may lead the clinician to assume that patient is dead. Prolonged hypothermia may lead to dysrhythmias and conduction abnormalities, acidemia, hyperkalemia, rhabdomyolysis, pulmonary edema, kidney disease, pneumonia, pancreatitis, hypoglycemia or hyperglycemia, and coagulopathy. Death from systemic hypothermia is usually due to ventricular fibrillation, asystole, or kidney disease.
``Treatment Resuscitation begins with rapid assessment and support of airway, breathing and circulation, initiation of rewarming, and prevention of further heat loss. Rewarming is the initial, imperative treatment. All cold, wet clothing must be removed and replaced with warm, dry clothing. To accurately measure hypothermia, an intravascular, esophageal, rectal or bladder probe that measures temperatures as low as 25°C is required; oral, axillary, and otic temperatures are inaccurate and unreliable. The patient should be evaluated for associated conditions of hypoglycemia, trauma, overdose and peripheral cold injury. Rewarming methods are
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determined by the degree of hypothermia and the resources available. During rewarming, continuous monitoring of temperature and other vital signs, cardiac rhythm, and blood sugar must be done. Common complications of rewarming occur as colder peripheral blood returns to central circulation. This may result in core temperature afterdrop, rewarming acidosis from shunting lactate into the circulation, rewarming shock from peripheral vasodilation and hypovolemia, ventricular fibrillation and other cardiac arrhythmias. Extreme caution must be taken when handling the hypothermic patient to avoid triggering arrhythmias. During the rewarming process, essential testing includes ECG, chest radiograph, arterial blood gases, and bedside glucose. Laboratory evaluation should assess for potential complications of lactic acidosis; rhabdomyolysis; electrolyte abnormalities; infection; and dysfunction of the pancreas, liver, kidneys, and coagulation. False laboratory values will occur if the blood sample is warmed to 37°C for the testing. Antibiotics are not routinely given. Comatose patients have a high risk of aspiration pneumonia.
A. Passive and Active External Rewarming Methods Patients with mild hypothermia (rectal temperature > 33°C) who have been otherwise healthy usually respond well to passive and active external warming. Passive external rewarming involves removal of cold wet clothing, then drying and covering the patient with blankets to prevent further heat loss. The patient will rewarm due to the body’s internal heat production through shivering and increased metabolism. Active external rewarming is highly effective and safe for mild hypothermia. This is a noninvasive method of applying external heat to the patient’s skin. Examples include warm bedding, heated blankets, heat packs, and immersion into a 40°C bath. Afterdrop can be lessened by active external rewarming of the trunk but not the extremities and by avoiding any muscle movement by the patient.
B. Active Internal (Core) Rewarming Methods Active internal core rewarming methods are required for patients with core temperatures of < 33°C. Patients with milder degrees of hypothermia may also benefit from these methods. Warm humidified oxygen (43–46°C) is an easy, safe, and highly effective method. Warmed intravenous saline infusions (43°C) should be used instead of lactated Ringer solution. Volume resuscitation is needed to prevent shock as vasodilation occurs during rewarming. Other rewarming methods are based on the availability of equipment and skilled personnel (ie, warm solution lavage; esophageal rewarming tubes; endovascular warming devices; and hemodialysis). For patients with core temperature < 30°C, initial treatment includes active rewarming, cardiopulmonary resuscitation (CPR), one shock attempt for dysrhythmia, and withholding of intravenous medications. Once the core temperature reaches 30°C, cardiac medications can be given but at intervals longer than standard intervals because metabolism is slowed and there is a risk of toxic
Disorders Related to Environmental Factors accumulation as circulation is restored. Defibrillation may be performed as needed. Resuscitative efforts should be continued until the patient’s core temperature increases to at least 32°C.
``Prognosis Prognosis is directly related to the patient’s underlying health and comorbidities, circumstances surrounding the hypothermia (duration, extent, and the severity of associated conditions), and degree of metabolic acidosis. Prognosis is poor with low pH (≤ 6.6), elevated potassium (≥ 4.0 mEq/L or ≥ 4.0 mmol/L), serious underlying condition, or treatment delay. If treated early, most otherwise healthy patients may survive moderate or severe hypothermia.
``When to Admit • Hypothermia patients must undergo close monitoring for potential complications. This is typically done during an inpatient admission or prolonged emergency department observation depending on the comor bidities and home care situation. • Monitoring includes vital signs, temperature, cardiac rhythm, oximetry, serial examinations (including extremity cold-induced injuries), and serial laboratory studies (electrolyte abnormalities, renal or hepatic dysfunction, cardiac ischemia, and infection).
HYPOTHERMIA OF THE EXTREMITIES
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EssentialS of diagnosis
Extremities suffering cold-induced injuries should not be exercised, rubbed, or massaged during rewarming. `` Rewarming of extremities affected by cold-induced injuries must be performed as soon as possible after there is no risk of refreezing. ``
``Clinical Findings Cold-induced injuries to the extremities (ie, frostnip, chilblain, trench foot, and frostbite) range from mild to severe. Cold exposure of the extremities produces immediate localized vasoconstriction followed by generalized vasoconstriction. When the skin temperature falls to 25°C, tissue demand for oxygen is greater than what is supplied by the slowed circulation: the area becomes cyanotic. At 15°C, tissue damage occurs due to marked reduction in tissue metabolism and oxyhemoglobin dissociation. This gives a deceptive pink, well-oxygenated appearance to the skin. Tissue damage may result from ischemia and intravascular thromboses, endothelial damage, or by actual freezing. Freezing (frostbite) may occur when the skin temperature drops below −4 to −10°C or at higher
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temperatures in the presence of wind, water, immobility, malnutrition, or vascular disease.
``Prevention “Keep warm, keep dry, and keep moving.” Individuals should wear warm, dry clothing, preferably several layers, with a windproof outer garment. Arms, legs, fingers, and toes should be exercised to maintain circulation. Wet clothing, socks, and shoes should be replaced with dry ones. Extra socks, mittens, and insoles should always be carried in a pack during travel in cold or icy areas. Caution must be taken to avoid cramped positions; constrictive clothing; prolonged dependency of the feet; use of tobacco, alcohol, and sedative medications; and exposure to wet muddy ground and windy conditions.
Frostnip & CHILBLAIN (Erythema Pernio) Frostnip is a mild temporary form of cold-induced injury. The involved area has local paresthesias that completely resolve with passive external rewarming. Rewarming can be done by placing cold fingers in the armpits and, in the case of the toes or heels, by removing footwear, drying feet, rewarming, and covering with adequate dry socks or other protective footwear. Chilblains or erythema pernio are inflammatory skin changes caused by exposure to cold without actual freezing of the tissues. These skin lesions may be red or purple papular lesions, which are painful or pruritic, with burning or paresthesias. They may be associated with edema or blistering and aggravated by warmth. With continued exposure, ulcerative or hemorrhagic lesions may appear and progress to scarring, fibrosis, and atrophy. This may resemble vasculitis or peripheral thromboemboli. A detailed history of cold exposure will differentiate chilblains from these other conditions, thereby avoiding unnecessary diagnostic testing. Treatment consists of elevating and passively externally rewarming the affected part. Caution must be taken to avoid rubbing or massaging injured tissues and to avoid applying ice or heat. The area must be protected from trauma, secondary infection, and further cold exposure.
Immersion Foot or Trench Foot Immersion foot (or hand) is caused by prolonged immersion in cool or cold water or mud, usually < 10°C. Prehyperemic stage is marked by early symptoms, which include cold and anesthesia of the affected area. Hyperemic stage follows with hot sensation, intense burning, and shooting pains. With ongoing cold exposure, the affected part becomes pale or cyanotic with diminished pulsations due to vasospasm (posthyperemic stage). This may result in blistering, swelling, redness, ecchymoses, hemorrhage, necrosis, peripheral nerve injury, or gangrene and secondary complications such as lymphangitis, cellulitis, and thrombophlebitis. Treatment is best instituted during the hyperemic stage. Treatment consists of air drying, protecting the extremities from trauma and secondary infection, and
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gradual rewarming by exposure to air at room temperature (not ice or heat). Caution must be taken to avoid massaging or moistening the skin and to avoid further water immersion. Bed rest is required until all ulcers have healed. Affected parts are elevated to aid in removal of edema fluid. Pressure sites (ie, heels) are protected with pillows. Prevention involves properly fitting footwear, improved foot hygiene, and sock changes to keep feet clean and dry.
FROSTBITE Frostbite is injury from tissue freezing and formation of ice crystals in the tissue. Most tissue destruction follows the reperfusion of the frozen tissues, with damaged endothelial cells and progressive microvascular throm bosis resulting in further tissue damage. In mild cases, only the skin and subcutaneous tissues are involved; the symptoms are numbness, prickling, itching, and pallor. With increasing severity, deep frostbite involves deeper structures. The skin appears white or yellow, loses its elasticity, and becomes immobile. Edema, hemorrhagic blisters, necrosis, and gangrene may appear. This may cause paresthesias and stiffness.
``Treatment
from physical contact. Wounds should be kept open and allowed to dry before applying dressings. Nonadherent sterile gauze and fluffy dressing should be loosely applied to wounds and cushions used for all areas of pressure. Antibiotics should not be administered empirically. Systemic antibiotics are reserved for deep infections not responding to local wound care.
B. Medical and Surgical Treatment Options With the availability of telemedicine, specialists are able to provide advice on early field treatment of cold-injured patients in remote areas, thereby improving outcome. Eschar formation without evidence of infection may be conservatively treated. The underlying skin may heal spontaneously with the eschar acting as a biologic dressing. Intra-arterial thrombolytic administration within 24 hours of exposure has resulted in improved tissue perfusion and has reduced amputation.
C. Follow-Up Care Gentle, progressive physical therapy to promote circulation should be instituted as tolerated. Debridement and amputation should be considered only after it is established that the tissues are necrotic.
A. Immediate Treatment Evaluate and treat the patient for associated systemic hypothermia and injury. Avoid secondary exposure to cold. Early use of systemic analgesics is recommended for nonfrozen injuries. Fluids and electrolytes should be monitored. 1. Rewarming—Rapid rewarming at temperatures slightly above body heat may significantly decrease tissue necrosis and reverse the tissue crystallization. If there is any possibility of refreezing, the frostbitten part should not be thawed, even if this might mean prolonged walking on frozen feet. Refreezing results in increased tissue necrosis. Rewarming is best accomplished by warm bath immersion. The frozen extremity is immersed for several minutes in a moving water bath heated to 40–42°C until the distal tip of the part being thawed flushes. Dry heat (ie, stove or open fire) is more difficult to regulate, increases likelihood of accidental burns and is not recommended. Thawing may cause tenderness and burning pain. Once the frozen part has thawed and returned to normal temperature (usually in about 30 minutes), discontinue external heat. In the early stage, rewarming by exercise, rubbing, or friction is contraindicated. The patient must be kept at bed rest with the affected parts elevated and uncovered at room temperature. Casts, occlusive dressings, or bandages are not applied. Blisters should be left intact unless signs of infection supervene. 2. Anti-infective measures and wound care—Frostbite increases susceptibility to tetanus and infection. Tetanus prophylaxis must be considered. Infection risk may be reduced by aseptic wound care and protection of skin blebs
``Prognosis Recovery from frostbite depends on the underlying comorbidities, the extent of initial tissue damage, the rewarming reperfusion injury, and the late sequelae. The involved extremity may be at increased susceptibility for discomfort and injury upon reexposure to cold. Neuropathic sequelae such as pain, numbness, tingling, hyperhidrosis, and cold sensitivity of the extremities, and nerve conduction abnormalities may persist for many years after the cold injury.
``When to Admit • Patients with local cold-induced injury may require admission for management of tissue damage, comorbidities, associated injuries, or an inadequate living situation, which could compromise patient safety or recovery.
Grieve AW et al. A clinical review of the management of frostbite. J R Army Med Corps. 2011 Mar;157(1):73–8. [PMID: 21465915] Imray C et al. Cold damage to the extremities: frostbite and non-freezing cold injuries. Postgrad Med J. 2009 Sep; 85(1007): 481–8. [PMID: 19734516] Mohr WJ et al. Cold injury. Hand Clin. 2009 Nov;25(4):481–96. [PMID: 19801122] Prakash S et al. Idiopathic chilblains. Am J Med. 2009 Dec; 122(12):1152–5. [PMID: 19958897]
Disorders Related to Environmental Factors
DISORDERS DUE TO HEAT
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EssentialS of diagnosis
There is a spectrum of preventable heat-related illnesses: heat cramps, heat exhaustion, heat syncope, and heat stroke. `` Pre-event planning and adequate preparation are the best preventive measures. Salt tablets are not recommended without medical supervision. `` The hallmarks of heat stroke are hyperthermia with cerebral dysfunction in a patient with heat exposure. `` The best outcome is related to early recognition, initiation of rapid cooling, and avoidance of shivering during cooling. `` The best choice of cooling method depends on which can be instituted the fastest with the least compromise to the overall care of the patient. Delays in cooling result in higher morbidity and mortality in heat stroke victims. ``
``General Considerations Hyperthermia results from the body’s inability to maintain normal internal temperature through heat loss. The body’s heat source is a result of internal metabolic function and environmental conditions (temperature, humidity). Heat loss occurs through sweating and peripheral vasodilation. There is a spectrum of preventable heat-related illnesses related to environmental exposure, ranging from mild forms, such as heat cramps and heat exhaustion, to severe forms, such as heat syncope and heat stroke. The common comorbidities and risk factors leading to heat-related conditions are listed in the chapter’s introduction “Cold & Heat” section. Additional risk factors include duration of exertion, hot environment, physical inactivity, and insufficient acclimatization, skin disorders or other medical conditions that inhibit sweat production or evaporation, obesity, dehydration, prolonged seizures, hypotension, reduced cutaneous blood flow, reduced cardiac output, the use of drugs that increase metabolism or muscle activity or impair sweating, and withdrawal syndromes. Nonexertional heat-related illness can also occur in a hot relaxing environment (ie, hot bath, steam room, or sauna).
``Prevention Public education is necessary to improve prevention and early recognition of heat-related disorders. Individuals should take steps to reduce personal risk factors and to acclimatize to the hot environment. Acclimatization is achieved by scheduled regulated exposure to hot environments and by gradually increasing the duration of exposure and the workload until the body adjusts. Proper acclimatization must be achieved before heavy physical exertion is performed in hot environments. Heat-related
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illnesses are the leading cause of morbidity and mortality in high school sports in the United States. All children’s athletic programs must set heat-acclimatization guidelines. Parents, coaches, athletic trainers and athletes must be educated about heat-related illness, specifically about prevention, risks, signs and symptoms, and treatment. Medical evaluation and monitoring should be used to identify the individuals and the weather conditions that increase risk of heat-related disorders. Athletic events should be organized with attention to thermoregulation. Guidance regarding heat hazard is found in the National Weather Service’s Heat Index, which rates weather conditions based on humidity and temperature measurements (http://www.nws.noaa.gov/os/heat/index.shtml). Those who are physically active in a hot environment should increase fluid consumption before, during, and after physical activities. Fluid consumption should include balanced electrolyte fluids and water. Water consumption alone may lead to electrolyte imbalance, particularly hyponatremia. It is not recommended to have salt tablets available for use without medical supervision. Close monitoring of fluid and electrolyte intake and early intervention are recommended in situations necessitating exertion or activity in hot environments. Exertional heat-related disorders are common in unconditioned participants in strenuous activities in hot humid conditions. Classic (nonexertional) heat-related disorders occur when extreme environmental conditions (heat, humidity) affect patients who are not physically active, in the extremes of ages, or with chronic medical or psychiatric illnesses.
SPECIFIC SYNDROMES DUE TO HEAT EXPOSURE 1. Heat Syncope or Collapse Heat syncope or sudden collapse may result in unconsciousness from volume depletion and cutaneous vaso dilation with consequent systemic and cerebral hypotension. Exercise-associated postural hypotension is usually the cause of this: it may occur during or immediately following exercise. There is usually a history of prolonged vigorous physical activity or prolonged standing in a hot humid environment. Typically, the skin is cool and moist, the pulse is weak, and the systolic blood pressure is low. Treatment consists of rest and recumbency in a cool place and fluid and electrolyte rehydration by mouth (or intravenously if necessary).
2. Heat Cramps Fluid and electrolyte depletion may result in slow, painful skeletal muscle contractions (“cramps”) and severe muscle spasms lasting 1–3 minutes, usually of the muscles most heavily used. The skin is moist and cool. The muscles are tender, hard and lumpy, and muscle twitching may be present. The patient is alert, with stable vital signs, and may be agitated and complaining of focal pain. The body temperature may be normal or slightly increased. There is almost always a history of vigorous activity just preceding the onset of symptoms.
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The patient should be moved to a cool environment and given oral saline solution (4 tsp of salt per gallon of water) to replace both salt and water. Oral salt tablets are not recommended. The patient may have to rest for 1–3 days with continued dietary supplementation before returning to work or resuming strenuous activity in the heat.
3. Heat Exhaustion Heat exhaustion results from prolonged strenuous activity with inadequate water or salt intake in a hot environment. It is characterized by dehydration, sodium depletion, or isotonic fluid loss with accompanying cardiovascular changes. The diagnosis is based on symptoms and clinical findings of a rectal temperature over 37.8°C, increased pulse, and moist skin. Symptoms are similar to those associated with heat syncope and heat cramps. Additional symptoms include nausea, vomiting, malaise, myalgias, hyperventilation, thirst, and weakness. Central nervous system symptoms include headache, dizziness, fatigue, anxiety, paresthesias, hysteria, impaired judgment, and occasionally psychosis. Heat exhaustion may progress to heat stroke if sweating ceases and mental status declines. Treatment consists of moving patient to a shaded, cool environment, providing adequate hydration (1–2 L over 2–4 hours), oral salt replenishment, and active cooling (ie, fans, cool packs) if necessary. Physiologic saline or isotonic glucose solution should be administered intravenously when oral administration is not appropriate. At least 24 hours of rest and rehydration are recommended.
4. Heat Stroke Heat stroke is a life-threatening medical emergency. The hallmarks of heat stroke are cerebral dysfunction with core temperature over 40°C. It presents in one of two forms: classic and exertional. Classic heat stroke occurs in patients with impaired thermoregulatory mechanisms; exertional heat stroke occurs in healthy persons undergoing strenuous exertion in a hot or humid environment. Persons at greatest risk are those who are at the extremes of age, chronically debilitated, and taking medications that interfere with heat-dissipating mechanisms (ie, anticholinergics, antihistamines, phenothiazines). Heat stroke is associated with high morbidity and mortality from cerebral, cardiovascular, liver, or kidney damage. Increased mortality rates are associated with a high Simplified Acute Physiology Score II, high body temperature, prolonged prothrombin time, use of vasoactive drugs within the first day in the intensive care unit (ICU), and an ICU without air conditioning.
``Clinical Findings A. Symptoms and Signs Heat stroke must be considered in any patient with hyperthermia and cerebral dysfunction. Presenting symptoms include all those seen in heat exhaustion with additional symptoms of dizziness, weakness, emotional lability, confusion, delirium, blurred vision, convulsions, collapse, and
unconsciousness. Physical examination findings include core temperature usually over 40°C, hot skin, initially covered with perspiration, then later it dries; strong pulse initially; widened pulse pressure; blood pressure is slightly elevated at first, but hypotension develops later; tachycardia; and hyperventilation. Exertional heat stroke may present with sudden collapse and loss of consciousness followed by irrational behavior. Sweating may not be present. Multiorgan dysfunction or failure is a common and serious complication.
B. Laboratory Findings Laboratory evaluation may reveal dehydration; leukocytosis; elevated blood urea nitrogen (BUN); hyperuricemia; hemoconcentration; acid-base abnormalities (lactic acidosis, respiratory alkalosis); decreased serum glucose, sodium, calcium, and phosphorus; thrombocytopenia, fibrinolysis, and coagulopathy; elevated creatine kinase (CK); elevated aminotransferase levels and liver dysfunction; and elevated cardiac markers. Urine is concentrated, with proteinuria, hematuria, tubular casts, and myoglobinuria. Potassium may be high or low. ECG findings may include ST–T changes consistent with myocardial ischemia. Pco2 may be < 20 mm Hg.
``Treatment Treatment is aimed at rapidly reducing the core temperature (within 1 hour) while supporting circulatory and organ system function to prevent irreversible tissue damage and death. Clinicians must assess for possibility of concurrent conditions (infection, trauma, and drug effects, including adverse side effects, withdrawal, or overdose). Circulatory failure in heat-related illness is mostly due to shock from relative or absolute hypovolemia. Intravascular volume status should be assessed and managed early to reduce the risk of hypovolemic shock. Central venous monitoring is useful to guide volume status. Oral or intravenous fluid administration must be provided to ensure adequate urinary output. Fluid output should be monitored through the use of an indwelling urinary catheter. Cooling methods are evaporative and conductivebased. Systemic review of the research found that there are comparable effects of these cooling methods whether used singly or in combination. No single cooling method is found to be superior. Choice of cooling method depends on which can be instituted the fastest with the least compromise to the overall care of the patient. Evaporative cooling is a noninvasive, effective, quick and easy way to reduce temperature. Large fans circulate the room air while the entire undressed body is sprayed with lukewarm water (20°C). Inhalation of cool air or oxygen is also effective. Conductive-based cooling involves cool fluid infusion, lavage, ice packs, and immersion into ice water or cool water. Intravascular heat exchange catheter systems as well as hemodialysis using cold dialysate (30–35°C) have been successful in reducing core temperature. Research suggests that brain cooling may lessen cerebrovascular injury from heat stroke.
Disorders Related to Environmental Factors Shivering must be avoided because it inhibits the effectiveness of cooling by increasing internal heat production. Medications that can be used to suppress shivering include magnesium, quick-acting opioid analgesics, benzodiazepines, and quick-acting anesthetic agents. Skin massage is recommended to prevent cutaneous vasoconstriction. Antipyretics (aspirin, acetaminophen) have no effect on environmentally induced hyperthermia and are contraindicated. Treatment should be continued until the rectal temperature drops to 39°C.
``Prognosis Multiorgan dysfunction is the usual cause of heat stroke– related death, and it can be predicted by elevated creatine kinase, metabolic acidosis, coagulopathy and elevated liver enzymes. Multiorgan dysfunction, rhabdomyolysis, acute respiratory distress syndrome (ARDS), and inflammation may continue after temperature is normalized. Following heat stroke, immediate reexposure should be avoided. Sensitivity to high environmental temperature may persist for prolonged periods.
``When to Admit • A ll patients with suspected heat stroke must be admitted to the hospital for close monitoring. • Monitoring includes vital signs, temperature, and cardiac rhythm, and observation for potential complications of metabolic abnormalities, cardiac arrhythmias, coagulopathy, ARDS, hypoglycemia, seizures, organ dysfunction, and infection. Becker JA et al. Heat-related illness. Am Fam Physician. 2011 Jun 1;83(11):1325–30. [PMID: 21661715] Centers for Disease Control and Prevention (CDC). Heat illness among high school athletes–United States, 2005–2009. MMWR Morb Mortal Wkly Rep. 2010 Aug 20;59(32):1009–13. [PMID: 20724966] Marom T et al. Acute care for exercise-induced hyperthermia to avoid adverse outcome from exertional heat stroke. J Sport Rehabil. 2011 May;20(2):219–27. [PMID: 21576713] O’Connor FG et al. American College of Sports Medicine Roundtable on exertional heat stroke—return to duty/return to play: conference proceedings. Curr Sports Med Rep. 2010 Sep–Oct;9(5):314–21. [PMID: 20827100] Zeller L et al. Exertional heatstroke: clinical characteristics, diagnostic and therapeutic considerations. Eur J Intern Med. 2011 Jun;22(3):296–9. [PMID: 21570651]
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THERMAL BURNS
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Epidemiologic data on thermal burn injury show that the incidence and severity have been declining over recent years. Scald, direct thermal, and flame burns account for the majority of such injuries. Over three-fourths of burns involve < 10% of total body surface area. Related injuries include smoke inhalation, fractures, and blast injuries. Subsequent problems include bacterial superinfection, sepsis, respiratory damage, and multiorgan failure. Telemedicine evaluation of acute burns offers accurate, cost-effective access to a burn specialist during the crucial 48 hours after the burn injury. The first 48 hours after the burn injury offer the greatest opportunity to impact the survival of the patient. Early surgical intervention, wound care, enteral feeding, glucose control and metabolic management, infection control, and prevention of hypothermia and compartment syndrome have contributed to significantly lower mortality rates and shorter hospitalizations.
``General Considerations A. Classification Burns are classified by extent, depth, patient age, and associated illness or injury. Accurate estimation of burn size and depth is important since this figure will quantify the parameters of resuscitation. 1. Extent—In adults, the “rule of nines” (Figure 37–2) is useful for rapidly assessing the extent of a burn. It is important to view the entire patient to make an accurate assessment of skin findings on initially and on subsequent examinations. One rule of thumb is that the palm of an open hand constitutes 1% total body surface area in adults. Only second- and third-degree burns are included Adult Rule of Nines
9%
Entire head and neck = 9% Posterior surface of upper trunk = 9%
9% Entire arm = 9%
9%
9%
9% 1%
Posterior surface of each leg = 9%
Posterior surface of lower trunk = 9%
9% 9%
EssentialS of diagnosis
Estimates of the burn location, size and depth greatly determine treatment plan. `` The first 48 hours of burn care offers the greatest impact on morbidity and mortality of a burn victim. ``
s Figure 37–2. Estimation of body surface area in burns.
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in calculating the total burn surface area, since first-degree burns usually do not represent significant injury in terms of prognosis or fluid and electrolyte management. However, first- or second-degree burns may convert to deeper burns, especially if treatment is delayed or bacterial colonization or superinfection occurs. 2. Depth—Judgment of depth of injury is difficult. The first-degree burn may be red or gray but will demonstrate excellent capillary refill. First-degree burns are not blistered initially. If the wound is blistered, this represents a partial-thickness injury to the dermis, which is referred to as a second-degree burn. As the degree of burn is progressively deeper, there is a progressive loss of adnexal structures, referred to as a third-degree burn. Hairs can be easily extracted or are absent, sweat glands become less visible, and the skin appears smoother. Deep second- and third-degree burns are treated in a similar fashion. Neither will heal appropriately without early debridement and grafting; the resultant skin is thin and scarred.
B. Survival after Burn Injury The Prognostic Burn Index is the sum of the patient’s age and percentage of full thickness or deep partial thickness burn. An additional 20% mortality is added if inhalation injury is present. The Prognostic Burn Index is most useful at the extremes of age. Transfer to a burn unit is indicated for large burn size, circumferential burn, or burn involving a joint or high-risk body part, and patients with comorbidities. Mortality rates have been significantly reduced due to treatment advances including improvements in wound care, treatment of infection, early burn excision, skin substitute usage, and early nutritional support through parenteral or enteral feeding. Telemedicine consultation with a burn center is an alternative, cost-effective way to access burn specialists when there are barriers that prevent transfer (distance, bed unavailability, travel risks, etc).
C. Associated Injuries or Illnesses Smoke inhalation, associated trauma, and electrical injuries are commonly associated with burns. Smoke inhalation (see Chapter 9) must be suspected when a burn victim is found in an enclosed space, or in close proximity to the fire. Electrical injury (see following section of this chapter) may cause deep tissue burns without significant superficial skin findings and may also produce cardiac arrhythmias that require immediate attention. Severe burns from any source may cause gastrointestinal complications including pancreatitis and stress ulcers.
D. Systemic Reactions to Burn Injury The actual burn injury is only the incipient event leading to cascade of deleterious local tissue and systemic inflammatory reactions causing multisystem organ failure in the severely burned patient. When burns greater than approximately 20% of total body surface area are present, systemic metabolic alterations occur and require intensive support. The inflammatory cascade can result in shock.
``Treatment A. Initial Resuscitation 1. Primary survey—The clinician must proceed with a full trauma assessment, starting with “ABCDE” (airway, breathing, circulation, disability, exposure). Airway assessment and management is the first priority. A patient with an inhalation injury needs to be intubated early to maintain airway patency even though he or she may appear to be breathing normally. To assess and support breathing and circulation, the clinician should administer supplemental oxygen and obtain vascular access for fluid resuscitation simultaneously with initial resuscitation. Disability assessment is next followed by complete patient exposure and thorough examination to assess the extent of burn and associated injuries. Serial assessments of airway and breathing are necessary since endotracheal intubation or tracheotomy may be needed for major burn victims, particularly those with possible inhalation injury. Generalized edema develops during fluid resuscitation, including edema of the soft tissues of the upper airway and perhaps the lungs as well. Chest radiographs are typically normal initially but may develop an ARDS picture in 24–48 hours with severe inhalation injury. The use of corticosteroids or routine use of antibiotic therapy is not indicated. A. Airway control—Early intubation is recommended before airway edema occurs in cases of smoke inhalation or direct thermal injury to the upper airway (look for singed eyebrows or facial hair, carbonaceous sputum). B. Vascular access—Large bore peripheral venous catheter access should be established. Femoral lines provide good temporary access during resuscitation if central venous access is needed. Intraosseous access can be obtained if venous access is unsuccessful or contraindicated. Venous access catheters placed in the emergency department should be changed within 24 hours because of the high risk of nonsterile placement. An arterial line is useful for monitoring mean arterial pressure and for drawing serial blood gases and other laboratory tests in critically ill patients. C. Fluid resuscitation—Generalized capillary leak results from burn injury over more than 20% of total body surface area. This often necessitates replacement with large volumes of crystalloid. There are many guidelines for fluid resuscitation. The Parkland formula relies on the use of lactated Ringer injection. The fluid requirement in the first 24 hours is estimated as 4 mL/kg body weight per percent of body surface area burned. Half the calculated fluid is given in the first 8-hour period. The remaining fluid, divided into two equal parts, is delivered over the next 16 hours. An extremely large volume of fluid may be required. For example, an injury over 40% of the total body surface area in a 70-kg victim may require 11.2 L in the first 24 hours [4 mL × 40(%) × 70 (kg) = 11,200 mL]. The first 8-hour period is measured from the hour of injury. These guidelines may be inadequate, since crystalloid solutions alone may be insufficient to restore cardiac preload during the period of burn shock. Deep electrical burns and inhalation injury increase the fluid requirement.
Disorders Related to Environmental Factors Adequacy of resuscitation is determined by clinical parameters, including urinary output and specific gravity, blood pressure, pulse, temperature, and central venous pressure. Overly aggressive crystalloid administration must be avoided in patients with pulmonary injury or cardiac dysfunction, since significant pulmonary edema can develop in patients with normal pulmonary capillary wedge and central venous pressures. A Foley catheter is essential for monitoring urinary output. Diuretics have no role in this phase of patient management unless fluid overload has occurred. The need for fluid replacement of more than 150% of calculated values indicates possible unrecognized injury, possible comorbidities, and a worse prognosis.
B. Management 1. Chemoprophylaxis— A. Tetanus immunization—For all burns deeper than superficial thickness, tetanus immunization must be updated. Tetanus toxoid-containing vaccine should be given intramuscularly to all patients with wounds regardless of how recently the patient received tetanus immunization. In addition, if a patient has not completed the recommended three doses of primary immunization or this is unknown, then tetanus immunoglobulin should also be administered intramuscularly in a different site than the tetanus toxoid. (See Chapter 33) B. Antibiotics—All nonsuperficial depth wounds should be covered with topical antibiotics. Prophylaxis with systemic antibiotics is not indicated. 2. Surgical management— A. Abdominal compartment syndrome—Abdominal compartment syndrome is emerging as a potentially lethal condition in severely burned patients, even if abdominal decompression is performed. Markedly increased intraabdominal pressures can cause pulmonary damage and multisystem organ failure. Only 40% of patients with this complication survive. Bladder pressures over 30 mm Hg establish the diagnosis in at-risk patients. Surgical abdo minal decompression may be indicated to improve ventilation and oxygen delivery, but even after this surgery, survival remains low. B. Escharotomy—As edema fluid accumulates, ischemia may develop under any constricting eschar of an extremity, neck, chest, or trunk if the full-thickness burn is circumferential. Escharotomy incisions through the anesthetic eschar can save life and limb and can be performed in the emergency department or operating room. C. Fasciotomy—Similar to escharotomy, fasciotomy is indicated to prevent further soft tissue, vascular, and nerve damage when soft tissue edema produces high pressures in the deep tissue compartments in the arms and legs since these compartments are divided by unyielding fascia. D. Debridement, dressings, and topical and systemic antibiotic therapy—Minor burn wounds should be debrided at the bedside to determine the depth of the
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burn and then thoroughly cleansed. Thereafter, the wound should be debrided daily and dressed with a topical anti biotic and a wound dressing. Patient compliance and adequate pain treatment is essential for successful outpatient treatment. The wound should be reevaluated by the treating clinician within 24–72 hours to evaluate for signs of infection. The goal of burn wound management is to protect the wound from desiccation and avoid further injury or infection. Regular and thorough cleansing of burned areas is a critically important intervention in burn units. Minor burn wounds (first- and superficial second-degree types, partial thickness) will spontaneously reepithelialize in 7–10 days. Topical wound agents should be applied. Topical antibiotic wound agents are painless, easy to apply, and effective against most skin pathogens. For severely burned patients, early excision and grafting of burned areas may be performed as soon as 24 hours after burn injury or when the patient can hemodynamically tolerate the excision and grafting procedure. Meticulous prevention of infections, seromas, hypergranulation tissue formation, and malnutrition all decrease the time to complete wound healing in skin-grafted patients. Skin autograft is the most definitive treatment. Prevention of autograft infection is paramount since autograft loss is most commonly due to autograft infection. Systemic infection remains a leading cause of morbidity among patients with major burn injuries, with nearly all severely burned patients having one or more septicemic episodes during the hospital course. Healthcare-associated infections are increasingly common. Routine use of blood culture in the severely burned population is indicated to elucidate systemic blood infections that do not manifest these clinical predictors of sepsis. E. Wound closure—The goal of therapy after fluid resuscitation is rapid and stable closure of the wound. Wounds that will not heal spontaneously in 7–10 days (ie, deep second-degree or third-degree burns) are best treated by excision and autograft. With severe burns, skin substitution with cultured grafts can be lifesaving. However, although the replaced dermis does have nearly normal histologic dermal elements, there are no adnexal structures present and very few, if any, elastic fibers. Wound infection is the top cause of skin graft rejection and failure.
C. Patient Support Burn patients require extensive supportive care, both physiologically and psychologically. It is important to maintain normal core body temperature and avoid hypothermia (by maintaining environmental temperature at or above 30°C) in patients with burns over more than 20% of total body surface area. Respiratory injury, sepsis, and multiorgan failure are common. Burn patients require careful assessment and provision of optimal nutritional needs since their metabolism is higher and they require more energy, nutrients, and antioxidants for wound healing. Enteral feedings may be started once the ileus of the resuscitation period has resolved, usually the day after the
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injury. There is often a markedly increased metabolic rate after burn injury, due in large part to whole body synthesis and increased fatty acid substrate cycles. Early aggressive nutrition (by parenteral or enteral routes) reduces infections, recovery time, noninfectious complications, length of hospital stay, long-term sequelae, and mortality. Careful control of the postinjury blood glucose has been associated with improved hepatic function and better survival after severe burns. Occasionally, ARDS or respiratory failure unresponsive to maximal ventilatory support may develop in burn patients. In addition, the incidence of venous thromboembolism is high among burn patients. Prevention of long-term scars remains a formidable problem in seriously burned patients. Long-term sequelae can be reduced by burn specialist consultation either directly or via telemedicine, prevention of infection, early nutrition, early aggressive rehabilitation, compressive garments, and early and continual psychological support.
``Prognosis Prognosis depends on the extent and location of the burn tissue damage, associated injuries, comorbidities, and complications. Hyperglycemia from poor glucose control is a predictor of worse outcomes. Psychiatric support may be necessary following burn injury.
``When to Admit • All burn patients require extensive supportive care, both physiologically and psychologically. • Patients with significant burns (based on location and extent), comorbidities, and suboptimal home situations must be admitted to the hospital for close monitoring. Burn center consultation can advise which patients require transfer and which can be managed via telemedicine/telephone consultation. • Monitoring includes vital signs, wound care, and observation for potential complications of electrolyte abnormalities, acute kidney injury, hepatic failure, cardiopulmonary compromise, hypoglycemia, and infection.
Advisory Committee on Immunization Practices. Recommended adult immunization schedule: United States, 2011. Ann Intern Med. 2011 Feb 1;154(3):168–73. [PMID: 21282696] Avni T et al. Prophylactic antibiotics for burns patients: systematic review and meta-analysis. BMJ. 2010 Feb 15;340:c241. [PMID: 20156911] Jeschke MG et al. Glucose control in severely thermally injured pediatric patients: what glucose range should be the target? Ann Surg. 2010 Sep;252(3):521–8. [PMID: 20739853] Latenser BA. Critical care of the burn patient: the first 48 hours. Crit Care Med. 2009 Oct;37(10):2819–26. [PMID: 19707133] Saffle JR et al. Telemedicine evaluation of acute burns is accurate and cost-effective. J Trauma. 2009 Aug;67(2):358–65. [PMID: 19667890] Williams FN et al. What, how, and how much should patients with burns be fed? Surg Clin North Am. 2011 Jun;91(3):609–29. [PMID: 21621699]
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ELECTRICAL Injury
EssentialS of diagnosis
Extent of injury is determined by the type, amount, duration, and pathway of electrical current. `` Resuscitation must be attempted before assuming the electrical injury victim is dead; clinical findings are unreliable. `` Skin findings may be misleading and are not indicative of the degree of deeper tissue injury. ``
``General Considerations Electricity-induced injuries are common and most are preventable. These inquiries occur by exposure to electrical current of low voltage, high voltage, or lightning. Electrical current type is either alternating current (AC) or direct current (DC). Electricity causes acute damage by direct tissue damage, muscle tetany, direct thermal injury and coagulation necrosis, and associated trauma. Alternating current (AC) is bidirectional electrical flow that reverses direction in a sine wave pattern. This may cause muscle tetany, which prolongs the duration and amount of current exposure. AC current can be low voltage or high voltage. Low voltage (< 1000 V) is typically household AC current that ranges in severity from minor injury to significant damage and death. High voltage (> 1000 V) is most often related to occupational exposure and is associated with deep tissue damage and higher morbidity and mortality. Direct current (DC) is unidirectional electrical flow (eg, that associated with lightning, batteries, and automotive electrical systems). It is more likely to cause a single intense muscle contraction and asystole. Lightning differs from other high-voltage electrical shock in that lightning is massive DC current of millions of volts lasting a very brief duration (a small fraction of a second). The extent of damage depends on the following factors: voltage (high or low, whether greater or lesser than 1000 volts), current type, tissue resistance, moisture, pathway; duration of exposure; associated trauma and comor bidities. Current is the most important determinant of tissue damage. Current passes through the tissues of least resistance, and this energy produces heat causing direct thermal injury. Tissue resistance varies throughout the body. Nerve cells are the most vulnerable, and bone is the most resistant to electrical current. Skin resistance depends on thickness and condition of the skin. The entrance and exit points are the most damaged. Current passing through skeletal muscle can cause muscle necrosis and contractions severe enough to result in bone fracture.
``Clinical Findings Electrical burns are of three distinct types: flash (arcing) burns, flame (clothing) burns, and the direct heating effect of tissues by the electrical current. The latter lesions are usually sharply demarcated, round or oval, painless yellowbrown areas (Joule burn) with inflammatory reaction.
Disorders Related to Environmental Factors Skin damage does not correlate with the degree of injury. Significant subcutaneous damage can be accompanied by little skin injury, particularly with larger skin surface area electrical contact. Symptoms and signs may range from tingling, superficial skin burns, and myalgias to coma, paralysis, massive tissue damage, or death. Not all electrical injuries cause skin damage; only very minor skin damage may be present with massive internal injuries. The presence of entrance and exit burns signifies an increased risk of deep tissue damage. Resuscitation must be initiated on all victims of electrical injury since clinical findings are deceptive and unreliable. A victim of electrical current injury may appear dead due to dysrhythmia, respiratory arrest, or autonomic dysfunction resulting in pupils that are fixed, dilated, or asymmetric.
``Complications Complications include dysrhythmias, altered mental status, seizures, paralysis, headache, pneumothorax, vascular injury, tissue edema and necrosis, compartment syndrome, associated traumatic injuries, rhabdomyolysis, acute kidney injury, hypovolemia from third spacing, infections, and acute or delayed cataract formation.
``Treatment A. Emergency Measures The patient must be assessed and treated as a trauma victim since associated traumatic injuries are common. The victim must be safely separated from the electrical current prior to initiation of CPR or other treatment. The rescuer must be protected. Separate the victim using nonconductive implements, such as dry clothing. Resuscitation must then be initiated since clinical findings of death are unreliable.
B. Hospital Measures The initial assessment involves airway, breathing, and circulation followed by a full trauma protocol. Fluid resuscitation is important to maintain adequate urinary output. Initial evaluation includes cardiac monitoring and ECG, complete blood count, electrolytes, renal function tests, liver biochemical tests, urinalysis, urine myoglobin, serum creatine kinase, and cardiac enzymes. ECG does not show typical patterns of ischemia since the electrical damage is epicardial. Victims must be evaluated for hidden injury. Electrical burn injury remains the most underrecognized and devastating burn injury, sometimes leading to amputations (often because of unrecognized compartment syndromes) and acute kidney injury, resulting in part from rhabdomyolysis (see Chapter 22). Superficial skin may appear deceivingly benign, leading to a delayed or completely overlooked diagnosis of deep tissue injury. When electrical injury occurs, extensive deep tissue necrosis should be suspected. Deep tissue necrosis leads to profound tissue swelling and this in turn results in the high risk of a compartment syndrome. Early debridement of devitalized tissues and tetanus prophylaxis may reduce the risks of infection. In pregnant patients exposed to electrical injury, the fetus may sustain intrauterine growth retardation, fetal distress, and fetal demise. Fetal monitoring is recommended.
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Pain management is important before, during, and after initial treatment and rehabilitation. Multimodal approach to pain is the most effective. Interventions include medications (opioids, acetaminophen, nonsteroidal anti-inflammatory drugs), heat therapy, massage, and cognitive-behavioral therapy.
``Prognosis Prognosis depends on the degree and location of electrical injury, initial tissue damage, associated injuries, comorbidities, and complications. Psychiatric support may be necessary following lightning or severe electroshock exposures.
``When to Refer Surgical specialists may be needed to perform fasciotomy for compartment syndrome or devitalized tissue debridement or microvascular reconstruction.
``When to Admit Indications for hospitalization include high voltage exposure; dysrhythmia or ECG changes; large burn; neurologic, pulmonary, or cardiac symptoms; suspicion of significant deep tissue or organ damage; transthoracic current pathway; history of cardiac disease or other significant comorbidities or injuries; and need for surgery. Li AL et al. Effectiveness of pain management following electrical injury. J Burn Care Res. 2010 Jan–Feb;31(1):73–82. [PMID: 20061840] Primavesi R. A shocking episode: care of electrical injuries. Can Fam Physician. 2009 Jul;55(7):707–9. [PMID: 19602655] Schneider JC et al. Neurologic and musculoskeletal complications of burn injuries. Phys Med Rehabil Clin N Am. 2011 May;22(2):261–75. [PMID: 21624720] Vierhapper MF et al. Electrical injury: a long-term analysis with review of regional differences. Ann Plast Surg. 2011 Jan; 66(1):43–6. [PMID: 21102303] cc
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RADIATION EXPOSURE
EssentialS of diagnosis
Damage from radiation is determined by the source, type, quantity, duration, bodily location, and susceptibility and accumulation of exposures of the person. `` Radiation exposure from medical diagnostic imaging has dramatically risen over the past few decades; medical imaging radiation dosing needs to be standardized and regulated in order to minimize necessary radiation exposure. `` Clinicians and patients should be educated regarding the risks of medical diagnostic radiation. These radiation risks must be weighed against the benefits of the medical imaging needed. `` All patients should keep records of their medical imaging radiation exposures, and copies of the medical images and interpretations. ``
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Exposure to radiation may occur from environmental, occupational, medical care, accidental, or intentional (ie, terrorism) exposure. With advancements in nuclear technology in the fields of medicine, energy, and industry, there is a growing risk of radiation exposure to patients, occupational workers, and the public. The extent of damage due to radiation exposure depends on the type, quantity, and duration of radiation exposure; the organs exposed; the degree of disruption to DNA; metabolic and cellular function; and the age, underlying condition, susceptibility, and accumulative exposures of the victim. Professionals who work with radiation or its victims must have a basic understanding of radiation physics in order to identify risk, manage exposure, and minimize preventable spread of exposure. Radiation is energy waves or particles that travel through space. These energetic waves or particles radiate (move outward in all directions) from the source. Radiation occurs from both nonionizing and ionizing radiation sources. Nonionizing radiation is low energy, resulting in injuries related to local thermal damage (ie, microwave, ultraviolet, visible light and radiowave). Ionizing radiation is high energy, causing bodily damage in several ways (ie, cellular disruption, DNA damage, and mutations). Ionizing radiation is either electromagnetic (ie, x-rays and gamma rays) or particulate (ie, alpha or beta particles, neutrons, and protons). Exposure may be external, internal, or both. In acute radiation exposure, medical care includes close monitoring of the gastrointestinal, cutaneous, hematologic, and cerebrovascular symptoms and signs from initial exposure and over time. Radiation exposure results in early and delayed effects. Early effects involve damage of the rapidly dividing cells (ie, the mucosa, skin, and bone marrow). This may be manifested as nausea, vomiting, and decreased lymphocyte count over hours to days after exposure. Delayed effects include malignancy, reproduction abnormalities, liver, kidney, and central nervous system and immune system dysfunction.
ACUTE & delayed effects of RADIATION EXPOSURE ON NORMAL TISSUES ``Clinical Findings A. Injury to Superficial Structures Acute radiation exposure to the skin and mucous membranes may cause erythema, epilation, destruction of fingernails, or epidermolysis, and burns that appear similar to thermal burns but usually have a slower onset and course. Chronic damage includes skin scarring, atrophy, telangiectasis, and xerostomia. Radiation effects on the eyes include cataracts, dry eye syndrome, and retinopathy.
B. Injury to Deep Structures Hematopoietic system radiation exposure causes injury to the bone marrow that may vary from transient decreases to complete destruction of blood elements. Lymphocytes are most sensitive, followed by polymorphonuclear leukocytes; erythrocytes are the least sensitive. Hematopoietic effects consisting of anemia, thrombocytopenia, and bone marrow suppression can occur 1â&#x20AC;&#x201C;3 weeks after radiation
exposures. Bone marrow failure is the main cause of death within the first few months following exposure. Nervous system structures are sensitive to radiation. The brain and spinal cord are much more sensitive than the peripheral nerves to the acute and delayed effects of radiation. Cardiovascular system effects of ionizing radiation result in damage to the heart and coronary arteries. Smaller vessels (the capillaries and arterioles) are more susceptible to damage than larger blood vessels. Delayed effects from radiation include obliterative endarteritis; coronary artery disease; pericarditis with effusion; or constrictive pericarditis, which may occur months or years later. Myocarditis is less common. Pulmonary system radiation with high or repeated moderate doses of radiation may cause pneumonitis or pulmonary fibrosis, which is often delayed for weeks or months. Gastrointestinal system radiation results in mucositis and mucosal edema within hours or days after exposure. Symptoms include odynophagia, anorexia, nausea, vomiting, dehydration, and weakness. High doses of radiation inhibit gastric secretion and cause inflammation and ulceration of the bowels. Delayed effects include hepatitis, liver dysfunction, and intestinal stenosis. The stomach and colon are the gastrointestinal organs most at risk for cancer induction due to internal radiation. Urogenital system radiation effects are dose-dependent, varying from transient decrease in fertility to permanent sterility, chromosomal aberrations, fetal damage, or demise. Moderate to heavy irradiation of the embryo results in injury to the fetus or in embryonic death and spontaneous abortion. Microcephaly and other congenital abnormalities may occur in children exposed in utero, especially if the fetus was exposed during early pregnancy. Nephritis and kidney dysfunction may occur as immediate or delayed effects. Endocrine system organs are relatively resistant to low or moderate doses of radiation. The thyroid gland is the endocrine gland at highest risk for cancer induction from internal radiation exposure. Delayed effects of radiation include thyroid dysfunction (hypothyroidism).
C. Systemic Reaction (Acute Radiation Syndrome) Clinicians must be educated to recognize and treat acute radiation sickness also referred to as acute radiation syndrome. Acute radiation syndrome is due to an exposure to high doses of ionizing radiation over a brief time course. The symptom onset is within hours to days depending on the dose. Symptoms include anorexia, nausea, vomiting, weakness, exhaustion, lassitude and, in some cases, prostration; these symptoms may occur singly or in combination. Dehydration, anemia, and infection may follow. The Centers for Disease Control and Prevention offers web-based information for clinicians regarding acute Âradiation syndrome (http://emergency.cdc.gov/radiation/ arsphysicianfactsheet.asp).
``Therapeutic Radiation Exposure Radiation therapy has been a successful component to treating many malignancies. This growing population of
Disorders Related to Environmental Factors cancer survivors treated with radiation therapy is an important resource to review and quantify associations between radiation therapy and risk of long-term adverse health and quality of life outcomes. These radiation-treated cancer survivors have a higher risk of development of a second malignancy; obesity; and pulmonary, cardiac and thyroid dysfunction as well as an increased overall risk for chronic health conditions and mortality. Ongoing study of childhood cancer survivors is needed to establish long-term risks and to evaluate the impact of newer techniques such as conformal radiation therapy or proton-beam therapy.
``Medical Imaging Radiation Exposure Medical imaging with ionizing radiation exposure (eg, computed tomography [CT] and nuclear medicine studies) has dramatically increased over the past two decades. In addition, researchers have found that the radiation dose for the same study varies significantly among different machines and different clinicians, within and across institutions, with radiation doses varying by as much as a factor of 10. This finding highlights the urgent safety need for standardization and regulation of radiation dosing for medical diagnostics. Clinicians and patients must be aware of the dangers of radiation when deciding on an imaging test. The risks and benefits must be carefully weighed. All patients should keep records of their cumulative medical imaging radiation exposures, as well as copies of the medical images and their interpretations. The American College of Radiology website offers additional safety information (http://www.radiologyinfo.org/en/safety/).
``Occupational and Environmental Radiation Exposure Prevention of occupational radiation exposure involves adequate training of all persons handling radiation as well as creating safety policies and procedures. This will reduce occupational risk of radiation exposure and improve the emergency response to accidental exposure. Prehospital and hospital disaster plans are required for optimal management of radiation exposure. The Radiation Assistance Center (1-865-576-1005) provides 24-hour access to expert information. The Centers for Disease Control and Prevention “Radiation Emergency” website (http://emergency.cdc.gov/ radiation) is a useful resource for professionals.
``Treatment Treatment is focused on decontamination, symptomatic relief, supportive care, and psychosocial support. Specific treatments focus on the dose, route, and effects of exposure.
``Prognosis Prognosis is determined by the radiation dose, duration, and frequency as well as by the underlying condition of the victim. Approximate dose of exposure correlates with the early onset and severity of symptoms (ie, nausea, vomiting, anorexia, abdominal pain, bloody diarrhea, weight loss)
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and laboratory findings, particularly the decline in lymphocyte count on the complete blood count. Death is usually due to hematopoietic failure (ie, hemorrhage, anemia, and immunosuppression), gastrointestinal mucosal damage, central nervous system damage, widespread vascular injury, or secondary infection. Carcinogenesis is related to the total dose, duration, accumulation of exposure, and to the susceptibility of the victim. The younger the victim’s age at the time of exposure, the greater the risk of acute and long-term damage from radiation. Radiation-related cancer risks persist throughout the exposed person’s lifespan. Cancer risk is particularly increased for persons exposed to nuclear radiation (eg, those exposed at Chernobyl, Hiroshima, Nagasaki, and Marshall Island nuclear test detonations). X-rays are classified as carcinogens since exposure causes leukemia and cancers of the thyroid, breast, and lung. With the increased use of ionizing radiation for medical diagnostics and treatments, there is a growing concern for the iatrogenic increase in radiation-induced cancer risks, especially in children. There are age-related sensitivities to radiation; prenatal and younger age victims are more susceptible to carcinogenesis.
``When to Admit Most patients with significant ionizing radiation exposure require admission for close monitoring and supportive treatment. Armstrong GT et al. Long-term effects of radiation exposure among adult survivors of childhood cancer: results from the childhood cancer survivor study. Radiat Res. 2010 Dec; 174(6):840–50. [PMID: 21128808] Christodouleas JP et al. Short-term and long-term health risks of nuclear-power-plant accidents. N Engl J Med. 2011 Jun 16; 364(24):2334–41. [PMID: 21506737] Donnelly EH et al. Acute radiation syndrome: assessment and management. South Med J. 2010 Jun;103(6):541–6. [PMID: 20710137] Little MP. Cancer and non-cancer effects in Japanese atomic bomb survivors. J Radiol Prot. 2009 Jun;29(2A):A43–59. [PMID: 19454804] Nguyen PK et al. Radiation exposure from imaging tests: is there an increased cancer risk? Expert Rev Cardiovasc Ther. 2011 Feb;9(2):177–83. [PMID: 21453214] Smith-Bindman R. Is computed tomography safe? N Engl J Med. 2010 Jul 1;363(1):1–4. [PMID: 20573919] cc
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near drowning
EssentialS of diagnosis
The first requirement of rescue is immediate basic life support and CPR. `` Patient must also be assessed for hypothermia, hypoglycemia, concurrent injuries, and medical conditions. `` Clinical manifestations are hypoxemia, pulmonary edema, and hypoventilation. ``
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``General Considerations
``Treatment
Near drowning describes a submersion event leading to injury. Submersion injury may result in aspiration, laryngospasm, hypoxemia, and acidemia. Drowning describes submersion resulting in death. “Wet” drowning is due to aspiration of fluid or foreign material. “Dry” drowning is due to laryngospasm or airway obstruction. The primary effect is hypoxemia due to perfusion of poorly ventilated alveoli, intrapulmonary shunting, and decreased compliance. A patient may be deceptively asymptomatic during the initial recovery period only to deteriorate or die as a result of acute respiratory failure within the following 12–24 hours. Preventative measures should be taken to reduce morbidity and mortality from drowning. Conditions that increase risk of submersion injury include the following: (1) use of alcohol or other drugs, (2) extreme fatigue from inadequate water safety skills, (3) poor physical health, (4) hyperventilation, (5) sudden acute illness (eg, hypoglycemia, seizure, dysrhythmia, myocardial infarction, asthma flare), (6) acute trauma (particularly brain or spinal cord injury, or both), (7) venomous stings or bites, (8) decompression sickness, (9) dangerous water conditions (temperature and turbulence), and (10) carbon monoxide exposure from boat motors.
A. First Aid
``Clinical Findings A. Symptoms and Signs The patient’s appearance may vary from asymptomatic, to abnormal vital signs, anxiety, dyspnea, cough, wheezing, trismus, cyanosis, chest pain, dysrhythmia, hypotension, vomiting, diarrhea, headache, altered level of consciousness, neurologic deficit, and apnea. Hypothermia is highly likely with cold water or prolonged submersion.
B. Laboratory Findings Arterial blood gas results are helpful in determining the degree of injury since initial clinical findings may appear benign. Pao2 is usually decreased; Paco2 may be increased or decreased; pH is decreased. Bedside blood sugar must be checked rapidly. Other testing is based on clinical scenario and may include kidney function, electrolytes, urinalysis, blood count, lactate, cardiac markers, coagulation studies, and alcohol and toxicology levels. Metabolic acidosis is common.
``Prevention Prevention is multi-faceted. Physical barriers (ie, fences) should be placed around pools and other accessible bodies of water. Safety flotation devices and rescue supplies must be immediately available. Use of alcohol or sedative drugs must be avoided during swimming, boating, or other water-based activities. There must be close supervision of those who cannot swim, and personal flotation devices must be worn when boating or water skiing. Swimming lessons, water and boat safety, and basic life support (BLS) education is necessary for anyone involved in water-based activities.
The first requirement of rescue is immediate BLS treatment and CPR. At the scene, immediate measures to combat hypoxemia are critical to improve outcome. BLS care includes sustained ventilation, oxygenation, and circulatory support. Hypothermia and associated trauma, especially brain and cervical spine injury, should always be suspected. 1. Standard BLS is initiated. CPR is provided if pulse and respirations are absent. 2. Patient must be assessed for hypothermia, hypoglycemia, trauma, and concurrent medical conditions. 3. Rescuer should not attempt to drain water from the victim’s lungs. The Heimlich maneuver (subdiaphragmatic pressure) should be used only if foreign material airway obstruction is suspected. 4. Resuscitation and BLS efforts must be continued until core temperature reaches 32°C even for seemingly “hopeless” patients. Complete recovery has been reported after prolonged resuscitation of hypothermic patients.
B. Subsequent Management 1. Ensure optimal ventilation and oxygenation—The onset of hypoxemia exists even in the alert, conscious patient who appears to be breathing normally. Oxygen should be administered immediately at the highest available concentration. Oxygen saturation should be maintained at 90% or higher. Endotracheal intubation and mechanical ventilation are necessary for patients unable to maintain an open airway, adequate oxygenation, or ventilation. Continuous positive airway pressure (CPAP) is an effective noninvasive way of reversing hypoxia and hypercarbia in patients with spontaneous respirations and a patent airway. Positive end-expiratory pressure (PEEP) is also effective for treating respiratory insufficiency. Serial physical examinations and chest radiographs should be carried out to detect possible pneumonitis, atelectasis, and pulmonary edema. Bronchodilators may be used to treat wheezing and bronchospasms due to aspiration. Nasogastric suctioning can decompress the stomach, aid in removal of swallowed water, and reduce the risk of aspiration. Antibiotics are reserved for clinical evidence of infection and should not be given prophylactically. 2. Cardiovascular support—Intravascular volume status must be monitored to determine whether vascular fluid replacement and vasopressors or diuretics are needed. Standard therapy for hypotension and pulmonary edema is administered. 3. Correction of blood pH and electrolyte abnormalities—Metabolic acidosis is present in 70% of neardrowning victims, but it is usually corrected through adequate ventilation and oxygenation. Glycemic control improves outcome. 4. Cerebral and spinal cord injury—Central nervous system damage may progress despite apparently adequate treatment of hypoxia and shock. Standard treatment for brain and spinal cord injury must be followed.
Disorders Related to Environmental Factors 5. Hypothermia—Core temperature should be measured and managed as appropriate (see Systemic Hypothermia, above).
``Course & Prognosis Respiratory damage is often severe in the minutes to hours following a near drowning. With respiratory supportive treatment, improvements typically occur quickly over the first few days following the near drowning. Long-term complications of near drowning may include neurologic impairment, seizure disorder, and pulmonary or cardiac damage. There is a direct correlation between prognosis and the patient’s age, submersion time, rapid prehospital resuscitation and rapid transport to a medical facility, clinical status at time of arrival to hospital, Glasgow Coma Scale score, pupillary reactivity, and overall health assessment (APACHE II score).
``When to Admit Most patients with significant near drowning or concurrent medical or traumatic conditions require inpatient monitoring for 24 hours following near drowning. This includes continuous monitoring of cardiorespiratory, neurologic, renal and metabolic function. Pulmonary edema may not appear for 24 hours. Ballesteros MA et al. Prognostic factors and outcome after drowning in an adult population. Acta Anaesthesiol Scand. 2009 Aug;53(7):935–40. [PMID: 19496759] Gregorakos L et al. Near-drowning: clinical course of lung injury in adults. Lung. 2009 Mar–Apr;187(2):93–7. [PMID: 19132444] Nasrullah M et al. Drowning mortality in the United States, 1999–2006. J Community Health. 2011 Feb;36(1):69–75. [PMID: 20532599] Schilling UM et al. Drowning. Minerva Anestesiol. 2011 May 30. 2012 Jan; 78(1): 69-77. [PMID: 21623341] Youn CS et al. Out-of-hospital cardiac arrest due to drowning: an Utstein Style report of 10 years of experience from St. Mary’s Hospital. Resuscitation. 2009 Jul;80(7):778–83. [PMID: 19443097] cc
Environmental DISORDERS related TO Altitude DYSBARISM & DECOMPRESSION SICKNESS
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Essentials of diagnosis
Symptoms temporally related to recent altitude or pressure changes (ie, scuba diving). `` Early recognition and prompt treatment of decompression sickness are extremely important. `` Patient must also be assessed for hypothermia, hypoglycemia, concurrent injuries, and medical conditions. `` Consultation with diving medicine or hyperbaric oxygen specialist is indicated. ``
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``General Considerations Dysbarism and decompression sickness are physiologic problems that result from altitude changes and the environmental pressure effects on gases in the body during underwater descent and ascent, particularly when scuba diving is followed closely by air travel or hiking to high altitudes. Physics laws describe the mechanisms involved in dysbarism and decompression sickness. As a diver descends, the gases in the body compress; gases dissolve in blood and tissues. During the ascent, gases in the body expand. Dysbarism results from gas compression or expansion in parts of the body that are noncompressible or have limited compliance. Lung barotrauma results in pneumomediastinum, pneumothorax, and rupture of the pulmonary vein causing arterial gas embolism. Overpressurization of the bowels may occur, especially if there is underlying pathology. This can result in gastric rupture, bowel obstruction or perforation, or pneumoperitoneum. Less serious conditions can also occur such as mask squeeze, ear squeeze, sinus squeeze, headache, tooth squeeze. Decompression sickness occurs when the ascent is too rapid and gas bubbles form and cause damage depending on their location (eg, coronary, pulmonary, spinal or cerebral blood vessels, joints, soft tissue). Decompression sickness symptoms depends on the size and number and location of gas bubbles released (notably nitrogen). Risk of decompression sickness depends on the dive details (depth, duration, number of dives, and interval surface time between dives, water conditions) as well as the diver’s age, weight, physical condition, physical exertion, the rate of ascent, and the length of time between the low altitude (scuba dive) and high altitude (air travel or ground ascent). Predisposing factors for decompression sickness include obesity, injury, hypoxia, lung or cardiac disease, right to left cardiac shunt, diver’s overall health, dehydration, alcohol and medication effects, and panic attacks. Decompression sickness also occurs in those who take hot showers after cold dives. Conservative recommendation is to avoid high altitudes (air travel or ground ascent) for at least 24 hours after surfacing from the dive.
``Clinical Findings The range of clinical manifestations varies depending on the location of the gas bubble formation or the compressibility of gases in the body. Symptom onset may be immediate, within minutes or hours (in the majority), or present up to 36 hours later. Decompression sickness symptoms include pain in the joints (“the bends”); skin pruritus or burning (skin bends); rashes; spinal cord or cerebral symptoms (“dissociation” symptoms that do not follow typical distribution patterns); labyrinthine decompression sickness (“the staggers,” central vertigo); pulmonary decompression sickness (“the chokes,” inspiratory pain, cough, and respiratory distress); arterial gas embolism (cerebral, pulmonary); barotrauma of the lungs, ear and sinus; dysbaric osteonecrosis; and coma. The clinician must assess for associated conditions of hypothermia, hypoglycemia, near drowning, trauma, envenomations, or concurrent medical conditions.
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``Treatment Early recognition and prompt treatment are extremely important. Decompression sickness must be considered if symptoms are temporally related to recent diving or altitude or pressure changes within the past 48 hours. Immediate consultation with a diving medicine or hyperbaric oxygen specialist is indicated even if mild symptoms resolved, since relapses with worse outcomes have occurred. Continuous administration of 100% oxygen is indicated and beneficial for all patients. Aspirin may be given for pain. Opioids should be used very cautiously, since these may obscure the response to recompression.
``When to Admit Rapid transportation to a hyperbaric treatment facility for recompression is imperative for decompression sickness. If air transportation is chosen, the aircraft must maintain pressurization near sea level to avoid worsening decompression sickness. The Divers Alert Network is an excellent worldwide resource for emergency advice 24 hours daily for the management of diving-related conditions (www.diversalertnetwork.org). For diving emergencies, call local emergency responder first, then the Divers Alert Network. Vann RD et al. Decompression illness. Lancet. 2011 Jan 8; 377(9760):153–64. [PMID: 21215883] Webb JT et al. Fifty years of decompression sickness research at Brooks AFB, TX: 1960–2010. Aviat Space Environ Med. 2011 May;82(5 Suppl):A1–25. [PMID: 21614886]
High-ALTITUDE ILLNESS
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Essentials of diagnosis
The severity of the high-altitude illness correlates with the rate and height of ascent, and the individual’s susceptibility. `` Prompt recognition and medical attention of early symptoms of high-altitude illness should prevent progression. `` Immediate descent is the definitive treatment for high-altitude cerebral edema and high-altitude pulmonary edema. ``
`` General Considerations As altitude increases, hypobaric hypoxia results due to a decrease in both barometric pressure and oxygen partial pressure. High-altitude medical problems are due to hypobaric hypoxia at high altitudes (usually > 2000 meters or 6560 feet). Acclimatization occurs as a physiologic response to the rise in altitude and increasing hypobaric hypoxia. Physiologic changes include increases in alveolar ventilation and oxygen extraction by the tissues and increased hemoglobin level and oxygen binding.
High-altitude illness results when the hypoxic stress is greater than the individual’s ability to acclimatize. Risk factors for high-altitude illness include increased physical activity with insufficient acclimatization, inadequate education and preparation, and individual susceptibility (preexisting medical conditions and medication use), and previous high-altitude illness. The key determinants of high-altitude illness risk and severity include both individual susceptibility factors and altitudinal factors (rapid rate and height of ascent and total change in altitude). Presentations may be acute, subacute, or chronic disturbances that result from hypobaric hypoxia. Acclimatization to altitudes above 5500 m (18,045 ft) is incomplete or physiologically impossible, although individual differences in tolerance to hypoxia exist. Individual susceptibility factors include underlying conditions such as cardiac and pulmonary dysfunction, patent foramen ovale, blood disorders (ie, sickle cell disease), pregnancy, neurologic condition, recent surgery, and many other chronic medical conditions. Those with symptomatic cardiac or pulmonary disease should avoid high altitudes. High-altitude illness comprises a spectrum of conditions based on end-organ effects, mostly cerebral and pulmonary. This is a result of fluid shifts from intravascular to extravascular spaces, especially in the brain and lungs. Manifestations of altitude illness include acute and longterm disorders. Acute high-altitude disorders are high-altitude neurologic conditions (acute mountain sickness and high-altitude cerebral edema) and high-altitude pulmonary edema. Long-term exposure to high altitude over months or years with inadequate acclimatization can result in subacute mountain sickness and chronic mountain sickness (Monge disease). (While subacute mountain sickness and Monge disease are mentioned briefly below, a more detailed discussion can be found in the online version of Current Medical Diagnosis & Treatment.)
1. High-Altitude–Associated Neurologic Conditions (Acute Mountain Sickness & High-Altitude Cerebral Edema) There is a spectrum of neurologic conditions caused by high altitude, ranging from acute mountain sickness to a more serious form, high altitude cerebral edema. Acute mountain sickness includes both neurologic and pulmonary symptoms, such as headache (most severe and persistent symptom), lassitude, drowsiness, dizziness, chilliness, nausea and vomiting, facial pallor, dyspnea, and cyanosis. Later symptoms include facial flushing, irritability, difficulty concentrating, vertigo, tinnitus, visual and auditory disturbances, anorexia, insomnia, increased dyspnea and weakness on exertion, increased headaches (due to cerebral edema), palpitations, tachycardia, Cheyne-Stokes breathing, and weight loss. More severe manifestations include cerebral and pulmonary edema (high-altitude cerebral edema and high-altitude pulmonary edema; see below). High-altitude cerebral edema appears to be an extension of the central nervous system symptoms of acute mountain sickness and results from cerebral vasogenic
Disorders Related to Environmental Factors edema and cerebral cellular hypoxia. It usually occurs at elevations above 2500 meters (8250 feet) and is more common in unacclimatized individuals. Hallmarks are altered consciousness and ataxic gait. Severe headaches, confusion, truncal ataxia, urinary retention or incontinence, focal deficits, papilledema, nausea, vomiting, and seizures may also occur. Symptoms may progress to obtundation and coma.
``Treatment Initial treatment involves oxygen administration by mask. Voluntary periodic hyperventilation will often relieve acute symptoms. Definitive treatment is immediate descent. Descent should be at least 610 meters (2000 feet) and should continue until symptoms improve. Descent is essential if the symptoms are persistent, severe, or worsening or if high-altitude pulmonary edema or high-altitude cerebral edema are present. If immediate descent is not possible, portable hyperbaric chambers can provide symptomatic relief. Acetazolamide (125–250 mg orally every 8–12 hours, conflicting data as to the optimal dose) remains the most effective medication for treatment of acute mountain sickness and for more severe forms of altitude-related conditions. Adverse reactions include peripheral paresthesias, altered taste of carbonated beverages, polyuria, nausea, drowsiness, erectile dysfunction, and myopia. This is a sulfonamide drug and should be used with caution or avoided in persons with past reactions to this class of drug. Dexamethasone (dose varies depending on the activity level of the individual, ranging from 2 to 4 mg orally every 6 hours) is effective for treatment of acute mountain sickness and acute cerebral edema; this medication should not be used for prophylaxis and should not be continued beyond 7 days. These medications can be continued for as long as symptoms persist and may be used together in severe cases. In most individuals, symptoms clear within 24–48 hours.
2. Acute High-Altitude Pulmonary Edema High-altitude pulmonary edema is a serious complication of hypoxia induced pulmonary hypertension. It is the leading cause of death from high altitude illness. The hallmark is markedly elevated pulmonary artery pressure followed by pulmonary edema. It usually occurs at levels above 3000 meters (9840 feet). High altitude increases pulmonary arterial pressure and decreases the oxygen uptake and saturation and alters oxygen kinetics. Early symptoms may appear within 6–36 hours after arrival at a high-altitude area. These include incessant dry cough, shortness of breath disproportionate to exertion, headache, decreased exercise performance, fatigue, dyspnea at rest, and chest tightness. Recognition of the early symptoms may enable the patient to descend before incapacitating pulmonary edema develops. Strenuous exertion should be avoided. An early descent of even 500 or 1000 meters may result in improvement of symptoms. Later, wheezing, orthopnea, and hemoptysis may occur as pulmonary edema worsens. Physical findings include tachycardia, mild fever, tachypnea, cyanosis, prolonged respiration, and rales and rhonchi.
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The clinical picture may resemble severe pneumonia. The patient may become confused or comatose. Diagnosis is usually clinical; ancillary tests are nonspecific or unavailable on site. Prompt recognition and medical attention of early symptoms prevent progression.
``Treatment Treatment must often be initiated under field conditions. The patient must rest in the semi-Fowler position (head raised), and 100% oxygen must be administered. Immediate descent (at least 610 meters [2000 feet]) is essential. Recompression in a portable hyperbaric bag will temporarily reduce symptoms if rapid or immediate descent is not possible. To conserve oxygen, lower flow rates (2–4 L/min) may be used until the victim recovers or is evacuated to a lower altitude and Sao2 ≥ 90%. Treatment for ARDS (see Chapter 9) may be is required for some patients. Calcium channel blockers and selective phosphodiesterase type 5 (PDE5) inhibitors are effective for symptomatic relief: nifedipine (30 mg slow-release tablets every 12 hours), tadalafil (10 mg by mouth every 12 hours), and sildenafil (50 mg by mouth every 8 hours) are alternatives.
3. Subacute Mountain Sickness This occurs most frequently in unacclimatized individuals and at high altitudes for a prolonged period of time. The hypobaric hypoxia results in pulmonary hypertension.
4. Chronic Mountain Sickness (Monge Disease) This uncommon condition is seen in residents of highaltitude communities who have lost their acclimatization to such a hypobaric hypoxic environment. It is difficult to differentiate from chronic pulmonary disease.
``Prevention of High-Altitude Disorders Pre-trip preventive measures include participant education, medical prescreening, pre-trip planning, optimal physical conditioning before travel, and adequate rest and sleep the day before travel. Preventive efforts during ascent include reduced food intake; avoidance of alcohol, tobacco, and unnecessary physical activity during travel; slow ascent to allow acclimatization (300 meters per day); and a period of rest and inactivity for 1–2 days after arrival at high altitudes. Mountaineering parties at altitudes of ≥ 3000 meters or higher should carry a supply of oxygen and medical equipment sufficient for several days. Prophylactic medications may be prescribed if no contraindications exist. Prophylactic low-dose acetazolamide (250–500 mg every 12 hours orally or 500 mg extended-release once to twice daily orally) has been shown to reduce the incidence and severity of acute mountain sickness when started 3 days prior to ascent and continued for 48–72 hours at high altitude. Dexamethasone (4 mg every 12 hours orally beginning on the day of ascent, continuing for 3 days at the higher altitude, and then tapering over 5 days) is an alternative prophylactic medication.
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``When to Admit • All patients with high-altitude pulmonary edema or high-altitude cerebral edema must be hospitalized for further observation. • Hospitalization must also be considered for any patient who remains symptomatic after treatment and descent. Pulmonary symptoms and hypoxia may be worsened by pulmonary embolism, bacterial pneumonia, or bronchitis. Butler GJ et al. Altitude mountain sickness among tourist populations: a review and pathophysiology supporting management with hyperbaric oxygen. J Med Eng Technol. 2011 Apr–May;35(3–4):197–207. [PMID: 20836748] Imray C et al. Acute mountain sickness: pathophysiology, prevention, and treatment. Prog Cardiovasc Dis. 2010 May– Jun;52(6):467–84. [PMID: 20417340] Maggiorini M. Prevention and treatment of high-altitude pulmonary edema. Prog Cardiovasc Dis. 2010 May–Jun;52(6): 500–6. [PMID: 20417343] Murdoch D. Altitude sickness. Clin Evid (Online). 2010 Mar 18;2010. pii:1209. [PMID: 21718562] Palmer BF. Physiology and pathophysiology with ascent to altitude. Am J Med Sci. 2010 Jul;340(1):69–77. [PMID: 20442648] Vann RD et al. Decompression illness. Lancet. 2011 Jan 8; 377(9760):153–64. [PMID: 21215883]
Safety OF AIR TRAVEL & SELECTION OF PATIENTS FOR AIR TRAVEL The medical safety of air travel depends on the nature and severity of the traveler’s preflight condition and factors such as travel duration, frequency and use of inflight exercise, cabin pressurization, availability of medical supplies, and presence of health care professionals on board. In-flight medical emergencies are increasing because there are an increasing number of travelers with preexisting medical conditions. Air travel passengers are susceptible to a wide range of flight-related problems: pulmonary (eg, hypoxia, gas expansion), vascular (venous thromboembolism, VTE), infectious, cardiovascular, gastrointestinal, ocular, immunologic, syncope, neuropsychiatric, metabolic, trauma, and substance-related. These air-travel risks are higher for those air travelers with preexisting medical conditions: cardiovascular disease, thromboembolic disease, asthma, chronic obstructive pulmonary disease, epilepsy, stroke, recent surgery or trauma, diabetes mellitus, infectious disease, mental illness, and substance dependence. Occupational and frequent flyers are at risk for these as well as accumulative radiation exposure, cabin air quality, circadian disturbance, and pressurization problems. Hypobaric hypoxia is the underlying etiology of most serious medical emergencies in flight. Despite commercial aircraft pressurization requirements, there is significant hypoxemia, dyspnea, gas expansion, and stress in travelers with underlying serious cardiopulmonary and other conditions. Patients with underlying respiratory or cardiac conditions are at highest risk for problems stemming from hypobaric hypoxia.
Research also demonstrates an association between VTE and air travel. Air travel has a threefold higher risk of VTE, especially severe pulmonary embolism. The VTE risk increases proportionally with the flight duration. Higher risk of VTE is seen in travelers with thrombophilia, those receiving hormonal therapy, and pregnant travelers. Air travel is not advised for anyone who is incapacitated, or who has an active pneumothorax, class III and IV pulmonary hypertension, acute worsening of an underlying lung disease, or any unstable conditions. The Air Transport Association of America defines an incapacitated passenger as “one who is suffering from a physical or mental disability and who, because of such disability or the effect of the flight on the disability, is incapable of self-care; would endanger the health or safety of such person or other passengers or airline employees; or would cause discomfort or annoyance of other passengers.” Unstable conditions include poorly controlled hypertension, dysrhythmias, angina, valvular disease, congestive heart failure, or psychiatric condition; severe anemia or sickle cell disease; recent myocardial infarction, cerebrovascular accident, or deep venous thrombosis; postsurgery, especially heart surgery (unless approved by surgeon); and any active communicable disease (influenza, tuberculosis, measles, chickenpox, or other communicable virulent infections). Risk of transmission increases when there is close contact to infected passengers.
Pregnancy and Infancy Pregnancy is a hypercoagulable state with fivefold to tenfold increase in VTE risk. Air travel increases this risk of VTE. Pregnant women may be permitted to fly during the first 8 months of pregnancy unless there is a history of pregnancy complications or premature birth. Infants younger than 1 week old should not be flown at high altitudes or for long distances. There is a higher risk of transmission of infection in-flight for pregnant women and infants due to their weaker immune response. Estimates of air travel radiation exposure are available through the Federal Aviation Administration and vary based on frequency and duration of flights.
``Prevention Air travel complications may be reduced by the following preventive measures: passenger education, passenger prescreening, and in-flight positioning and activity. Prescreening is especially important for those who have had recent surgery or an emergency condition, and those with chronic serious medical conditions. Travelers with pulmonary disease must have preflight medical assessment to determine whether supplemental oxygen is required. Travelers can reduce VTE risk by avoiding constrictive clothing, wearing support hose, changing position frequently, avoiding leg crossing, engaging in frequent in-flight leg exercises, and walking. Lowmolecular-weight heparin may be prescribed in travelers at high risk for VTE.
Disorders Related to Environmental Factors
ACOG Committee on Obstetric Practice. ACOG Committee Opinion No. 443: Air travel during pregnancy. Obstet Gynecol. 2009 Oct;114(4):954–5. [PMID: 19888065] Akerø A et al. COPD and air travel: oxygen equipment and preflight titration of supplemental oxygen. Chest. 2011 Jul; 140(1):84–90. [PMID: 21071527] Bartholomew JR et al. Air travel and venous thromboembolism: minimizing the risk. Cleve Clin J Med. 2011 Feb;78(2):111–20. [PMID: 21285343] Brenner B. Prophylaxis of travel-related thrombosis in women. Thromb Res. 2009;123(Suppl 3):S26–9. [PMID: 19203643]
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Chandra D et al. Meta-analysis: travel and risk for venous thromboembolism. Ann Intern Med. 2009 Aug 4;151(3): 180–90. [PMID: 19581633] Shrikrishna D et al; Air Travel Working Party of the British Thoracic Society Standards of Care Committee. Managing passengers with stable respiratory disease planning air travel: British Thoracic Society recommendations. Thorax. 2011 Sep; 66(9):831–3. [PMID: 21807654] Silverman D et al. Medical issues associated with commercial flights. Lancet. 2009 Jun 13;373(9680):2067–77. [PMID: 19232708]