Jacqueline A. Nemer, MD, FACEP
ACCIDENTAL SYSTEMIC HYPOTHERMIA
ESSENTIALS OF DIAGNOSIS
Reduction of core body temperature (CBT) below 35°C.
Accurate CBT measurement must be obtained by an intravascular, esophageal, rectal, or bladder probe that measures as low as 25°C; oral, axillary, and otic temperatures are inaccurate.
The CBT must be over 32°C before terminating resuscitation efforts.
Refreezing must be avoided to reduce further damage.
Systemic hypothermia is defined as CBT < 35°C. This may be primary (from exposure to prolonged ambient extremely low temperature) or secondary (due to thermoregulatory dysfunction); both may be present at the same time. 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, hypothermia ensues if these thermoregulatory responses become impaired. Hypothermia should be considered in any patient with prolonged exposure to ambient or cold environment, trauma, inadequate clothing, or altered mental status.
Iatrogenic accidental hypothermia may occur in the hospital setting due to rapid infusion of intravenous fluids, prolonged exposure during resuscitation or surgical procedures, or administration of large amounts of refrigerated stored blood products (without rewarming).
Symptoms and signs of hypothermia are typically nonspecific and markedly variable based on the patient’s underlying health and circumstances of hypothermia. When CBT is 32–35°C, symptoms include tachypnea, tachycardia, hypertension, shivering, impaired coordination, poor judgment, and apathy. When CBT is 28–32°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 (ie, CBT < 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.
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).
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 (ie, hypoglycemia, trauma, infection, overdose and peripheral cold injury). Rewarming methods are determined by the degree of hypothermia and the resources available.
During rewarming, continuous monitoring of temperature, other vital signs, cardiac rhythm, and blood glucose must be done. Complications of rewarming occur as colder peripheral blood returns to central circulation. This may result in core temperature afterdrop, rewarming lactic acidosis, 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. Assessment includes acid-base status (lactate and blood gases); volume status (cold diuresis); electrolyte abnormalities (particularly potassium and glucose); metabolic acidosis; coagulopathy; rhabdomyolysis; and dysfunction of the pancreas, liver, kidneys. An ECG and a chest radiograph should be obtained. False laboratory values will occur if the blood sample is warmed to 37°C for the testing. Patient should be assessed for infection; however, antibiotics are not routinely given unless a source is identified.
Passive external rewarming involves removing 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, which is the continued falling of body temperature during rewarming, can be lessened by active external rewarming of the trunk but not the extremities and by avoiding any muscle movement by the patient. Patients with mild hypothermia (CBT > 33°C) and previous good health usually respond well to passive and active external warming.
Active internal core rewarming methods are required for patients with CBT < 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).
When CBT is < 30°C, initial treatment includes active rewarming, cardiopulmonary resuscitation (CPR), one shock attempt for dysrhythmia, and withholding of intravenous medications. Once the CBT 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 accumulation as circulation is restored. Defibrillation may be performed as needed. Resuscitative efforts should be continued until the CBT increases to at least 32°C.
Prognosis is directly related to the patient’s underlying health and comorbidities, circumstances surrounding the hypothermia, 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 comorbidities and home care situation.
HYPOTHERMIA OF THE EXTREMITIES
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.
Cold-induced injuries to the extremities 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 results in a deceptive pink, well-oxygenated appearance to the skin. Freezing (frostbite) may occur when the skin temperature drops below –4°C to –10°C or at higher temperatures in the presence of wind, water, immobility, malnutrition, or vascular disease.
“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.
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 or cold water or mud, usually < 10°C. Prehyperemic stage is marked by early symptoms of cold and anesthesia of the affected area.Hyperemic stage follows with hot sensation, intense burning, and shooting pains. Posthyperemic stage occurs with ongoing cold exposure; the affected part becomes pale or cyanotic with diminished pulsations due to vasospasm. 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 before or during the hyperemic stage. Treatment consists of air drying, protecting the extremities from trauma and secondary infection, and 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 cold injury and water immersion. Affected parts are elevated to aid in removal of edema fluid. Pressure sites (ie, heels) are protected with cushions. Bed rest is required until all ulcers have healed. Prevention involves properly fitting footwear, improved foot hygiene, and sock changes to keep feet clean and dry.
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 thrombosis 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.
Evaluate and treat the patient for associated systemic hypothermia, concurrent conditions, and injury. Avoid secondary exposure to cold. Early use of systemic analgesics is recommended for nonfrozen injuries. Fluids and electrolytes should be monitored.
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.
Patient education must include ongoing care of the cold injury and prevention of future hypothermia and cold injury. Gentle, progressive physical therapy to promote circulation should be instituted as tolerated.
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
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]
Lantry J et al. Pathophysiology, management and complications of hypothermia. Br J Hosp Med (Lond). 2012 Jan;73(1):31–7. [PMID: 22241407]
McIntosh SE et al. Wilderness Medical Society practice guidelines for the prevention and treatment of frostbite. Wilderness Environ Med. 2011 Jun;22(2):156–66. [PMID: 21664561]
McMahon JA et al. Cold weather issues in sideline and event management. Curr Sports Med Rep. 2012 May;11(3):135–41. [PMID: 22580491]
DISORDERS DUE TO HEAT
ESSENTIALS OF DIAGNOSIS
Spectrum of preventable heat-related illnesses: heat cramps, heat exhaustion, heat syncope, and heat stroke.
Heat stroke: hyperthermia with cerebral dysfunction in a patient with heat exposure.
Best outcome: early recognition, initiation of rapid cooling, and avoidance of shivering during cooling.
Best choice of cooling method: whichever can be instituted the fastest with the least compromise the patient. Delays in cooling result in higher morbidity and mortality in heat stroke victims.
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. 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, sunbathing or sauna).
Heat cramping results from dilutional hyponatremia as sweat losses are replaced with water alone. 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.
Heat syncope or sudden collapse may result in unconsciousness from volume depletion and cutaneous vasodilation with consequent systemic and cerebral hypotension. Exercise-associated postural hypotension is usually the cause of this: it may occur during or immediately following exercise. Heat stroke, the hallmark of which is cerebral dysfunction with CBT over 40°C, 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 cramps are slow, painful skeletal muscle contractions (“cramps”) and severe muscle spasms lasting 1–3 minutes, usually of the muscles most heavily used. The examination findings typically include stable vital signs; normal or slightly increased CBT; moist and cool skin; and tender, hard, lumpy muscles that may be twitching. The patient is alert, with stable vital signs, and may be agitated and complaining of focal pain. There is almost always a history of vigorous activity just preceding the onset of symptoms. Laboratory evaluation may reveal no abnormalities or show low serum sodium, hemoconcentration, and elevated urea and creatinine.
The diagnosis of heat exhaustion is based on symptoms and clinical findings of a CBT 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. Hyperventilation secondary to heat exhaustion can cause respiratory alkalosis; lactic acidosis may also occur due to poor tissue perfusion. Heat exhaustion may progress to heat stroke if sweating ceases and mental status declines.
With heat syncope, there is usually a history of prolonged vigorous physical activity or prolonged standing in a hot humid environment. The skin is cool and moist, the pulse is weak, and the systolic blood pressure is low.
Heat stroke is a life-threatening emergency, the hallmarks of which are cerebral dysfunction with CBT over 40°C. Presenting symptoms include all findings seen in heat exhaustion with additional symptoms of dizziness, weakness, emotional lability, confusion, delirium, blurred vision, convulsions, collapse, and unconsciousness. Physical examination findings include 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 (with subsequent respiratory alkalosis). Exertional heat stroke may present with sudden collapse and loss of consciousness followed by irrational behavior. Sweating may not be present. Increased mortality rates are associated with a high Simplified Acute Physiology Score II (http://clincalc.com/IcuMortality/SAPSII.aspx), 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. 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; 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.
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.
Treatment consists of moving patient to a shaded, cool environment, providing adequate fluid and electrolyte replacement, 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.
Treatment consists of rest and recumbency in a cool place, and fluid and electrolyte replacement by mouth (or intravenously if necessary).
Treatment is aimed at rapidly reducing the CBT (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). Monitoring includes vital signs, temperature, and cardiac rhythm. The patient should also be observed for the following: potential complications of metabolic abnormalities, cardiac arrhythmias, coagulopathy, acute respiratory distress syndrome (ARDS), hypoglycemia, seizures, organ dysfunction, and infection. 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. Hypovolemic and cardiogenic shock must be carefully distinguished and managed. 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. Hypokalemia frequently accompanies heat stroke but may not appear until rehydration. Maintenance of extracellular hydration and electrolyte balance should reduce the risk of acute kidney injury due to rhabdomyolysis.
Cooling methods are evaporative and conductive-based. 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. Cold water immersion includes cool baths, localized ice or ice slush application (groin, axillas, neck), and cool gastric and bladder lavage, and infusion of cool intravenous fluids. Intravascular heat exchange catheter systems as well as hemodialysis using cold dialysate (30–35°C) have been successful in reducing CBT. Research suggests that brain cooling may lessen cerebrovascular injury from heat stroke.
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 CBT drops to 39°C.
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, ARDS, and inflammation may continue after temperature is normalized. Following heat stroke, immediate reexposure should be avoided.
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. 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: the wet bulb globe temperature (WBGT) index should be monitored. Competition is not recommended when the WBGT exceeds 26–28 °C. 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 because of the risk of hypertonic hypernatremia. 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.
When to Admit
All patients with suspected heat stroke must be admitted to the hospital for close monitoring.
Becker JA et al. Heat-related illness. Am Fam Physician. 2011 Jun 1;83(11):1325–30. [PMID: 21661715]
Calvello EJ et al. Management of the hyperthermic patient. Br J Hosp Med (Lond). 2011 Oct;72(10):571–5. [PMID: 22041727]
Casa DJ et al. Exertional heat stroke: new concepts regarding cause and care. Curr Sports Med Rep. 2012 May;11(3):115–23. [PMID: 22580488]
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]
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.
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.
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.
Figure 37–2. Estimation of body surface area in burns.
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.
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).
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. Severe burns from any source may cause gastrointestinal complications including pancreatitis and stress ulcers.
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.
Telemedicine evaluation of acute burns offers accurate, cost-effective access to a burn specialist during the crucial 48 hours after the burn injury.
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.
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.
Wound infection is the top cause of skin graft rejection and failure.
Burn patients require extensive supportive care, both physiologically and psychologically. It is important to maintain normal CBT 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, multiorgan failure, and venous thromboembolism are common. Burn patients are at risk for developing ARDS or respiratory failure unresponsive to maximal ventilatory support.
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 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. If the patient does not tolerate low-residue tube feedings, total parenteral nutrition should be started without delay through a central venous catheter. Contrary to conventional teachings, data indicate that most patients can be fed adequately with energy equal to 100% to 120% of estimated basal energy expenditure (BEE). A useful guide is to provide 25 kcal/kg body weight plus 40 kcal per percent of burn surface area. Early aggressive nutrition (by parenteral or enteral routes) reduces infections, recovery time, noninfectious complications, length of hospital stay, long-term sequelae, and mortality. Occasionally, ARDS or respiratory failure unresponsive to maximal ventilatory support may develop in burn patients. Anticatabolic treatments such as beta-blockade, growth hormone, insulin, oxandrolone, and synthetic testosterone have been advocated. Melatonin, which appears to possess multifaceted antioxidant properties, may reduce proinflammatory cytokines and have beneficial chronobiotic effects in severely burned patients.
Prevention of long-term scars remains a formidable problem in seriously burned patients. The usual regimen consists of corticosteroid injections, silicone gel or patches, compression, and scar revision. Long-term sequelae can be reduced by the following strategies: (1) burn specialist consultation either directly or via telemedicine, (2) prevention of infection, (3) early nutrition, (4) early aggressive rehabilitation, (5) compressive garments, and (6) early and continual psychological support.
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
Cancio LC et al. Evolving changes in the management of burns and environmental injuries. Surg Clin North Am. 2012 Aug;92(4):959–86. [PMID: 22850157]
Wasiak J et al. Dressings for superficial and partial thickness burns. Cochrane Database Syst Rev. 2013 Mar 28;3:CD002106. [PMID: 23543513]
Zanni GR. Thermal burns and scalds: clinical complications in the elderly. Consult Pharm. 2012 Jan;27(1):16–22. [PMID: 22231994]
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.
Electricity-induced injuries are common and most are preventable. These injuries 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 comorbidities. 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.
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 yellow-brown areas (Joule burn) with inflammatory reaction.
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 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.
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.
The initial assessment involves airway, breathing, and circulation followed by a full trauma protocol. Fluid resuscitation is important to maintain adequate urinary output (0.5 mL/kg/h if no myoglobinuria is present, 1.0 mL/kg/h if myoglobinuria is present). 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 (eg, ophthalmic, otologic, muscular, compartment syndromes), organ injury (myocardium, liver, kidney, pancreas), blunt trauma, dehydration, skin burns, hypertension, posttraumatic stress, acid-base disturbances, and neurologic damage.
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.
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 depends on the degree and location of electrical injury, initial tissue damage, associated injuries, comorbidities, and complications. Complications may occur in almost any part of the body but most commonly include sepsis; gangrene requiring limb amputation; or neurologic, cardiac, cognitive, or psychiatric dysfunction. Psychiatric support may be necessary following electrical injury.
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.
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]
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.
All patients should keep records of their medical imaging radiation exposures, and copies of the medical images and interpretations.
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.
Radiation exposure results in acute and delayed effects. Acute effects involve damage of the rapidly dividing cells (ie, the mucosa, skin, and bone marrow). This may be manifested as mucositis, nausea, vomiting, gastrointestinal edema and ulcers, skin burns, and bone marrow suppression over hours to days after exposure. Delayed effects include malignancy, reproduction abnormalities, liver, kidney, and central nervous system and immune system dysfunction.
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 radiation syndrome (http://emergency.cdc.gov/radiation/arsphysicianfactsheet.asp).
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.
Therapeutic Radiation Exposure
Radiation therapy has been a successful component to treating many malignancies. This growing population of 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 & 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 is focused on decontamination, symptomatic relief, supportive care, and psychosocial support. Specific treatments focus on the dose, route, and effects of exposure.
Prognosis is determined by the radiation dose, duration, and frequency as well as by the underlying condition of the victim. Death is usually due to hematopoietic failure, 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. 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.
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]
Dainiak N et al. First global consensus for evidence-based management of the hematopoietic syndrome resulting from exposure to ionizing radiation. Disaster Med Public Health Prep. 2011 Oct;5(3):202–12. [PMID: 21987000]
Dainiak N et al. Literature review and global consensus on management of acute radiation syndrome affecting nonhematopoietic organ systems. Disaster Med Public Health Prep. 2011 Oct;5(3):183–201. [PMID: 21986999]
Pearce MS et al. Radiation exposure from CT scans in childhood and subsequent risk of leukaemia and brain tumours: a retrospective cohort study. Lancet. 2012 Aug 4;380(9840):499–505. [PMID: 22681860]
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.
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.
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.
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. Metabolic acidosis is common.
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.
Preventive 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.
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. Nasogastric suctioning can decompress the stomach. Antibiotics are reserved for clinical evidence of infection and should not be given prophylactically.
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 following near drowning. This includes continuous monitoring of cardiorespiratory, neurologic, renal and metabolic function. Pulmonary edema may not appear for 24 hours.
Centers for Disease Control and Prevention (CDC). Drowning—United States, 2005–2009. MMWR Morb Mortal Wkly Rep. 2012 May 18;61(19):344–7. [PMID: 22592273]
ENVIRONMENTAL DISORDERS RELATED TO ALTITUDE
DYSBARISM & DECOMPRESSION SICKNESS
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.
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.
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.
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, contact local emergency responder first, then the Divers Alert Network.
Bennett MH et al. Recompression and adjunctive therapy for decompression illness. Cochrane Database Syst Rev. 2012 May 16;5:CD005277. [PMID: 22592704]
Vann RD et al. Decompression illness. Lancet. 2011 Jan 8;377(9760):153–64. [PMID: 21215883]
Weaver LK. Hyperbaric oxygen in the critically ill. Crit Care Med. 2011 Jul;39(7):1784–91. [PMID: 21460713]
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]
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.
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, 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.
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 long-term 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).
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 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.
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.
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. 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 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 commonly recommended alternatives.
There is an international effort to advance the understanding of high-altitude pulmonary edema through the International HAPE Database; susceptible individuals should register with this databank (http://www.altitude.org/hape.php).
This occurs most frequently in unacclimatized individuals and at high altitudes (above 4500 meters) for a prolonged period of time. The hypobaric hypoxia results in pulmonary hypertension. Symptoms of dyspnea and cough are probably due to hypoxic pulmonary hypertension and secondary heart failure. Dehydration, skin dryness, and pruritus also can occur. The hematocrit may be elevated, and there may be ECG and chest radiographic evidence of right ventricular hypertrophy. Treatment consists of rest, oxygen administration, diuretics, and return to lower altitudes.
This uncommon condition is seen in residents of high-altitude 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. Research also suggests potential benefit from prophylaxis with sumatriptan, nifedipine, dexamethasone, tadalafil, sildenafil, and salmeterol (125 mcg by inhaler every 12 hours beginning 24 hours prior to ascent).
When to Admit
Hall DP et al. High altitude pulmonary oedema. J R Army Med Corps. 2011 Mar;157(1):68–72. [PMID: 21465914]
Seupaul RA et al. Pharmacologic prophylaxis for acute mountain sickness: a systematic shortcut review. Ann Emerg Med. 2012 Apr;59(4):307–17. [PMID: 22153998]
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. Requirements for commercial aircraft are to maintain cabin pressurized to the equivalent of 8000 feet or less. Despite commercial aircraft pressurization requirements, there is significant hypoxemia, dyspnea, gas expansion, and stress in travelers. 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, varicose veins, hormonal therapy, obesity, and pregnancy.
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, heart failure, or acute psychiatric condition; severe anemia or symptomatic sickle cell disease; recent myocardial infarction; cerebrovascular accident; poorly controlled seizure disorder; deep venous thrombosis; postsurgery, especially heart surgery (unless approved by surgeon); and any active communicable disease (influenza, tuberculosis, measles, chickenpox, zoster, 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.
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 underlying pulmonary disease (ie, chronic obstructive pulmonary disease or pulmonary hypertension) must have preflight medical assessment to determine whether supplemental oxygen is required. Oxygen is required if the arterial oxygen tension is < 70 mm Hg or pulse oximetry < 92%. Other useful tests to determine whether oxygen is needed include the hypoxia altitude simulation test and the 6-minute walk test. 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. Low-molecular-weight heparin may be prescribed in travelers at high risk for VTE.
Bartholomew JR et al. Air travel and venous thromboembolism: minimizing the risk. Cleve Clin J Med. 2011 Feb;78(2):111–20. [PMID: 21285343]
Edvardsen A et al. Air travel and chronic obstructive pulmonary disease: a new algorithm for pre-flight evaluation. Thorax. 2012 Nov;67(11):964–9. [PMID: 22767877]
Roubinian N et al. Effects of commercial air travel on patients with pulmonary hypertension. Chest. 2012 Oct;142(4):885–92. [PMID: 22490871]
Sugerman HJ et al. JAMA patient page. Air travel-related deep vein thrombosis and pulmonary embolism. JAMA. 2012 Dec 19;308(23):2531. [PMID: 23288474]
Withers A et al. Air travel and the risks of hypoxia in children. Paediatr Respir Rev. 2011 Dec;12(4):271–6. [PMID: 22018043]