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 effects of environmental pressure on gases in the body during underwater descent and ascent. These are most likely to occur when scuba diving is followed closely by travel to high altitudes (ie, air travel, hiking), or when the scuba diver is not adherent to the conservative dive guidelines for dive duration, course, depth, and surface times.
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. These gases are in compressible (eg, lungs, gastrointestinal) and noncompressible (eg, sinuses, joints) areas of the body. At low depths the greatly increased pressure (eg, at 30 meters [100 feet] the pressure is four times greater than at the surface) compresses the respiratory gases into the blood and other tissues. During the ascent, gases in the body expand. This depends on the difference between the atmospheric pressure and the partial pressure of the gas dissolved in the tissues.
Dysbarism results from barotrauma when gas compression or expansion occurs in parts of the body that are noncompressible or have limited compliance. Pulmonary overinflation syndrome is one of the most serious and potentially fatal results of barotrauma. Pulmonary overinflation syndrome is due to an inappropriately rapid ascent causing alveoli rupture and air bubble extravasation into tissue planes or even the cerebral circulation. Barotrauma can also result in pneumomediastinum, pneumothorax, and rupture of the pulmonary vein causing arterial gas embolism. Overpressurization of the bowels (especially if underlying bowel pathology is present) 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, and tooth squeeze.
Decompression sickness occurs when the ascent is too rapid and gas bubbles form and cause damage depending on their location (ie, coronary, pulmonary, spinal or cerebral blood vessels, joints, soft tissue). These gas bubbles cause damage due to mechanical disruption of tissue, local inflammatory response, occlusion of blood flow, platelet activation, endothelial dysfunction, and capillary leakage. 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 (ie, patent foramen ovale), diver’s overall health, dehydration, alcohol and medication effects, and panic attacks. Decompression sickness may also occur in those who take hot showers after cold dives.
Preventive measures include diver education; pre-dive medical screening and dive planning; strict adherence to dive course, timing, and depths; and a slow and controlled ascent plus proper control of buoyancy. Conservative recommendation is to avoid high altitudes (air travel or ground ascent) for at least 24 hours after surfacing from the dive, especially following multiple dives.
A pre-dive medical screening assessment by a clinician knowledgeable in dive medicine is strongly recommended for anyone with any underlying medical conditions. Contraindications to scuba diving include: active asthma, reduced pulmonary function, lung cysts, or recent thoracic trauma or pneumothorax, cardiovascular disease, history of bowel obstruction, recent brain or eye surgery, seizure disorder, diabetes and hypoglycemic episodes, history of syncope or dysrhythmia.
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); cardiac symptoms (acute coronary syndrome, conduction abnormalities); spinal cord or cerebral symptoms (focal neurologic dysfunction or “dissociation” symptoms that do not follow typical distribution neuroanatomy 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; coma and death.
The onset of acute decompression symptoms occurs within 30 minutes in half of cases and almost invariably within 6 hours. Symptoms, which are highly variable, include pain (largely in the joints), headache, fatigue, numbness, confusion, pruritic rash, visual disturbances, nausea, vomiting, loss of hearing, weakness, paralysis, dizziness, vertigo, dyspnea, paresthesias, aphasia, and coma. Decompression sickness involving the brain and spinal cord may occur by different mechanisms due to air bubbles causing arterial occlusion, venous obstruction, or in situ toxicity. MRI is the most accurate neuroimaging to detect these brain and spinal cord lesions.
The clinician must assess for associated conditions of hypothermia, hypoglycemia, hypovolemia, 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. Continuous administration of 100% oxygen is indicated and beneficial for all patients. Hyperbaric oxygen treatment is commonly recommended for decompression sickness symptoms. Immediate consultation with a diving medicine or hyperbaric oxygen specialist is indicated even if mild decompression sickness symptoms resolve, since relapses with worse outcomes have occurred. ECMO therapy has been reported as effective when hyperbaric oxygen treatment was not an option. Nonsteroidal anti-inflammatory drugs, acetaminophen or aspirin may be given for pain control if there are no contraindications. Opioids should be used very cautiously, since these may obscure the response to recompression.
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. It has been recommended that decompression symptoms be treated whenever they are seen—even up to 2 weeks postinjury—since it is still possible to reduce morbidity. The clinician should be familiar with the nearest hyperbaric facility. 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.
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ESSENTIALS OF DIAGNOSIS
The severity of the high-altitude illness is affected by the rate and height of ascent, and the individual’s susceptibility.
Prompt recognition and medical treatment of early symptoms of high-altitude illness may prevent progression.
Clinicians should assess other conditions which may coexist or mimic symptoms of high altitude illness (severe dehydration, hyponatremia, or hypoglycemia, trauma, or infection).
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 greater than 2000 meters or 6560 feet). High-altitude illness includes a spectrum of disorders categorized by end-organ effects (mostly cerebral and pulmonary), and exposure duration (acute and long-term). Acute high-altitude conditions are acute mountain sickness (AMS), high-altitude cerebral edema (HACE), and high-altitude pulmonary edema (HAPE). 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).
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. This is a result of fluid shifts from intravascular to extravascular spaces, especially in the brain and lungs. 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 meters (18,045 feet) 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.
Patient assessment for high-altitude illness should also include evaluation for other conditions (ie, severe dehydration, hyponatremia, hypoglycemia, infection, or trauma), which may coexist or may present in a similar manner.
1. High-Altitude–Associated Neurologic Conditions: AMS & HACE
There is a spectrum of neurologic conditions caused by high altitude, ranging from AMS to the more serious form HACE. Clinicians must rely on patient’s report of symptoms to determine the severity of AMS. In addition to the patient’s report of symptoms, HACE includes neurologic examination findings.
AMS includes symptoms such as headache (most severe and persistent symptom), lassitude, drowsiness, dizziness, chilliness, nausea and vomiting, difficulty sleeping. Later symptoms include irritability, difficulty concentrating, anorexia, insomnia, and increased headaches.
HACE includes the severe symptoms of AMS and results from cerebral vasogenic edema and cerebral cellular hypoxia. It usually occurs at elevations above 2500 meters (8250 feet) but may occur at lower elevations. It is more common in unacclimatized individuals. Hallmarks are altered mental status, ataxia, severe lassitude, and encephalopathy. The patient appears "mildly drunk." Examination findings may include confusion, ataxia, urinary retention or incontinence, focal neurologic deficits, papilledema, and seizures. Symptoms may progress to obtundation, coma, and death. High-altitude retinopathy is a separate but related effect of altitude. It can include dilated vessels, retinal hemorrhage, vitreous hemorrhage, and papilledema.
Definitive treatment is immediate descent. Descent should be at least 610 meters (2000 feet), and it should continue until symptoms improve. Descent is essential if the symptoms are persistent, severe, worsening or if HACE or HAPE are present. If immediate descent is not possible, portable hyperbaric chambers can provide symptomatic relief but they should not delay descent.
Initial treatment involves oxygen administration to keep the pulse oximetry SpO2 to greater than 90%.
Acetazolamide (250 mg twice daily) is an effective medication for treatment of mild symptoms of AMS. This is a sulfonamide drug and should be used with caution or avoided in persons with past reactions to this class of drug. Adverse reactions include peripheral paresthesias, altered taste of carbonated beverages, polyuria, nausea, drowsiness, erectile dysfunction, and myopia.
Dexamethasone is most effective for moderate to severe AMS (4 mg orally every 6 hours). Dexamethasone is the primary treatment for HACE (8 mg once then 4 mg every 6 hours). Acetazolamide can be added as an adjunct in severe HACE cases. In most individuals, symptoms clear within 24–48 hours. Dexamethasone does not facilitate acclimatization, so the patient needs to complete dexamethasone therapy and be asymptomatic before they can ascend any further.
It is imperative that the clinician also assess for other conditions that may mimic or coexist with AMS and HACE (ie, dehydration, exhaustion, hypoglycemia, hypothermia, hyponatremia, trauma, infection).
If HAPE symptoms and signs are present along with HACE, nifedipine or a selective phosphodiesterase inhibitor may be added for pulmonary vasodilation. The clinician must be cautious when using combinations of vasodilators. These medications lower the mean arterial pressure, and in combination, these may result in lowering the cerebral perfusion pressure and thereby increasing the risk of cerebral ischemia.
HAPE is the leading cause of death from high altitude illness. Although it is often seen in conjunction with AMS and HACE, the important difference is its underlying pathology of hypoxia-induced pulmonary hypertension, which requires different management and treatment approaches than AMS and HACE. The hallmark is markedly elevated pulmonary artery pressure followed by pulmonary edema. It usually occurs at altitudes above 3000 meters (9840 feet), although it may occur at lower levels. 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. Later, wheezing, orthopnea, and hemoptysis may occur as pulmonary edema worsens.
Physical findings may include tachycardia, mild fever, tachypnea, cyanosis, prolonged respiration, rales, and rhonchi. The clinician must assess for other potential medical conditions because the clinical picture may resemble other etiologies (pneumonia, viral upper respiratory tract infection, mucous plugging, bronchospasm, or acute coronary syndrome). Diagnosis is usually clinical; ancillary tests are nonspecific or unavailable on site. Prompt recognition and medical attention of early symptoms of HAPE may prevent progression.
The white blood cell count is often slightly elevated, but the erythrocyte sedimentation rate is usually normal. Chest radiographic findings vary from irregular patchy infiltration in one lung to nodular densities bilaterally or with transient prominence of the central pulmonary arteries. Transient nonspecific ECG changes, occasionally showing right ventricular strain, may occur. Pulmonary arterial blood pressure is elevated, whereas wedge pressure is normal. Research has shown benefits from chest ultrasonography for diagnosis and monitoring of high-altitude pulmonary edema.
Immediate descent (at least 610 meters [2000 feet]) is essential although this may not be immediately possible, and may not alone improve symptoms.
Treatment must often be initiated under field conditions. The patient must rest, reclined with head elevated. Supplemental oxygen must be administered to maintain pulse oximetry reading SpO2 greater than 90%. Recompression in a portable hyperbaric bag will temporarily reduce symptoms if rapid or immediate descent is not possible, but should not delay descent.
Nifedipine (30 mg slow extended-release tablets every 12 hours) can be used as an adjunct if the other therapies (descent, oxygen, or portable hyperbarics) are not successful or available. Selective phosphodiesterase inhibitors (tadalafil, 10 mg orally every 12 hours; sildenafil, 50 mg orally every 8 hours) are used for HAPE prevention but may also provide effective symptom relief as an alternative or if nifedipine is not available. Tadalafil and sildenafil have also been shown to improve exercise capacity in adults with high-altitude pulmonary vasoconstriction. Administering nifedipine plus a phosphodiesterase inhibitor as pulmonary vasodilators is not recommended because this combination may also lower the mean arterial pressure and decrease cerebral perfusion. Treatment for ARDS (see Chapter 9) is required for some patients. If neurologic symptoms are present concurrently with HAPE and do not resolve with improved oxygenation, dexamethasone should be added according to HACE treatment guidelines.
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).
3. Subacute Mountain Sickness
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.
4. Chronic Mountain Sickness (Monge Disease)
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. The disorder is characterized by somnolence, mental depression, cyanosis, clubbing of fingers, chronic hypoxia, hemoglobin greater than 22 g/dL, polycythemia (hematocrit often greater than 75%), signs of right ventricular failure, ECG evidence of right axis deviation and right atrial and ventricular hypertrophy, and radiographic evidence of right heart enlargement and central pulmonary vessel prominence, and pulmonary hypertension in some cases. There is no radiographic evidence of structural pulmonary disease. Pulmonary function tests usually disclose alveolar hypoventilation and elevated Paco2 but fail to reveal defective oxygen transport. There is a diminished respiratory response to CO2.
Almost complete disappearance of all abnormalities eventually occurs when the patient returns to sea level. Recommended treatments include phlebotomy, oxygen supplementation, respiratory training, medroxyprogesterone (20–60 mg/day orally for 10 weeks), acetazolamide (250 mg/day orally for 3 weeks), and enalapril (5 mg orally daily).
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 and during the trip. Preventive efforts during ascent include reduced food intake; avoidance of alcohol, tobacco, and unnecessary physical activity during travel. Due to the widely variable difference in each individual's physiologic responses to high altitude and rates of acclimatization, these prevention measures may not be successful in all high altitude travelers.
Gradual ascent is the most effective way to allow acclimatization. Low-risk ascension rate is 2 or more days to arrive at 2500–3000 meters. For elevations above 3000 meters, the sleeping elevation should increase less than 500 meters every day and an extra day of rest for acclimization every 1000 meters and no ascent to higher sleeping elevation every 3–4 days. The altitude reached during waking hours is not as important as the altitude at which this hiker sleeps. If the terrain does not allow a sleeping elevation increase below 500 meters, an extra rest day should be added before or after the increased sleep elevation more than 500 meters. Mountaineering parties at altitudes of 3000 meters or higher should carry a supply of oxygen and medical equipment sufficient for several days.
Drug prophylaxis may be prescribed for AMS and HACE if no contraindications exist. Prophylactic low-dose acetazolamide (125 mg twice daily orally) has been shown to reduce the incidence and severity of AMS and HACE when started 3 days prior to ascent and continued for 48–72 hours at high altitude. Dexamethasone is an alternative prophylactic medication for AMS and HACE (2 mg every 6 hours or 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). Higher doses of dexamethasone (4 mg every 6 hours) may be considered in high-risk situations requiring immediate physical exertion (those airlifted to high altitudes for search and rescue or military).
Individuals with a past history of HAPE should use drug prophylaxis to reduce the risk of recurrence. Nifedipine, 30 mg extended-release every 12 hours started the day before ascent and continued through the fourth day at target elevation, or through the seventh day if the ascent rate was faster, is recommended. Salmeterol can be added at doses of 125 mcg by inhaler every 12 hours beginning 24 hours prior to ascent. This can be used as an adjunct to nifedipine but not as monotherapy.
Phosphodiesterase inhibitors (eg, tadalafil 10 mg orally twice a day or sildenafil 50 mg orally every 8 hours) may be beneficial in the treatment of HAPE based on their physiologic effects of decreased pulmonary arterial pressures and pulmonary vasodilation. This drug class may be used if nifedipine is not available but should not be administered along with nifedipine since the additive vasodilation effects may increase the patient’s risk of hypotension and cerebral hypoperfusion.
All patients with HACE or HAPE 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 complications such as pulmonary embolism, secondary respiratory infection, bronchospasms, mucous plugging, or acute coronary syndrome.
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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 altitude pressure, availability of medical supplies, (including supplemental oxygen) 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 (hypoxemia, gas expansion), venous thromboembolism (VTE), infectious, cardiac, gastrointestinal, ocular, immunologic, syncope, neuropsychiatric, metabolic, trauma, and substance-related. These air-travel risks are higher for those air travelers with preexisting medical conditions: pulmonary (chronic hypoxemia, asthma, chronic obstructive pulmonary disease), thromboembolic, cardiovascular, neurologic (epilepsy, stroke), recent surgery or trauma, diabetes mellitus, infectious disease, mental illness, and substance dependence. Occupational and frequent flyers are also at risk for accumulative radiation exposure, cabin air quality, circadian disturbance, and pressurization problems.
Hypobaric hypoxia is the underlying etiology of most serious medical emergencies in flight due to cabin altitude. 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.
Any form of prolonged travel involving immobilization has been associated with increased risk of VTE (referred to as “traveler’s thrombosis”), although air travel has been the main focus of medical review. Conditions that place long-distance travelers at high risk for VTE include the following: (1) travel involving immobilization for 4 or more hours, (2) hypercoagulable disorders (ie, Factor V Leiden, deficiencies in proteins C and S or antithrombin, elevated factor VIII, hyperprothrombinemia, antiphospholipid syndrome), and (3) acquired risks (previous VTE, recent surgery, stroke or trauma, active malignancy, obesity, pregnancy or postpartum, oral contraceptives or hormone therapy, advanced age, immobilization or limited mobility,, inflammatory bowel disease, and nephrotic syndrome)
Air travel is not advised for anyone who is “incapacitated” or has 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 active pneumothorax, advanced pulmonary hypertension, acute worsening of an underlying lung disease, 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 is a hypercoagulable state with fivefold to tenfold increase in VTE risk. Long travel increases risk of VTE for the pregnant traveler. 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. The clinician’s authorization is required if travel is essential during the ninth month of pregnancy or earlier in a complicated pregnancy. Pregnant travelers are at higher risk for infection transmission and air travel radiation exposure. Radiation exposure estimates are available through the Federal Aviation Administration and vary based on aircraft type, flight frequency and duration.
Air travel complications may be reduced by the following preventive measures: passenger prescreening, passenger education, and in-flight positioning and activity. Prescreening evaluation is recommended for all high-risk patients including preexisting requirement of oxygen, continuous positive pressure or ventilator support, underlying restrictive or obstructive lung disease, comorbidities worsened by hypoxemia (pulmonary hypertension, cardiac or cerebrovascular disease), previous respiratory distress during air travel, recent pneumothorax, and being within 6 weeks of an acute respiratory illness. Clinicians and patients can obtain more airline specific information at http://www.europeanlung.org/en/lung-disease-and-information/air-travel/.
Air travel education should include risk reduction of VTE, infectious diseases, and exacerbations of underlying medical conditions. Patients and clinicians can check the World Health Organization website for the most updated information on travel health risks and infectious diseases (http://www.who.int/ith/en/). Patients requiring oxygen therapy or CPAP must be reminded to make prior arrangements for oxygen provision prior to departure and upon arrival at their destinations.
All long-distance travelers can reduce VTE risk by avoiding constrictive clothing, staying well-hydrated, changing position frequently, avoiding cramped position, avoiding leg crossing, engaging in frequent in-flight leg stretching exercises at least every hour, and walking for 5 minutes every hour. Clinicians should assess those with high risk of VTE prior to air travel to determine whether anticoagulation is indicated (see Table 14–14).
Airlines must provide steady cabin pressurization, maintenance of in-flight medical kits and automated external defibrillators, flight crew medical training, and telemedicine ground support. Passengers with motion sickness or ear pressurization problems should take medications prior to and during the flight to reduce symptoms. Small meals of easily digested food and avoidance of carbonated beverages before and during the flight may reduce the tendency to nausea and vomiting.
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