Comments
Abstract
Patients with chronic lung disease may have mild hypoxemia at sea level. Some of these cases may go unrecognized, and even among those who are known to be hypoxemic, some do not use supplemental oxygen. During air travel in a hypobaric hypoxic environment, compensatory pulmonary mechanisms may be inadequate in patients with lung disease despite normal sea-level oxygen requirements. In addition, compensatory cardiovascular mechanisms may be less effective in some patients who are unable to increase cardiac output. Air travel also presents an increased risk of venous thromboembolism. Patients with cystic lung disease may also be at increased risk of pneumothorax. Although overall this risk appears to be relatively low, should a pneumothorax occur, it could present a significant challenge to the patient with chronic lung disease, particularly if hypoxemia is already present. As such, a thorough assessment of patients with chronic lung disease and cardiac disease who are contemplating air travel should be performed. The duration of the planned flight, the anticipated levels of activity, comorbid illnesses, and the presence of risk factors for venous thromboembolism are important considerations. Hypobaric hypoxic challenge testing reproduces an environment most similar to that encountered during actual air travel; however, it is not widely available. Assessment for hypoxia is otherwise best performed using a normobaric hypoxic challenge test. Patients in need of supplemental oxygen need to contact the airline and request this accommodation during flight. They should also be advised on arranging portable oxygen concentrators before air travel, and a discussion of the potential risks of travel should take place.
Each year worldwide, more than 2.75 billion passengers travel by air, 736 million in the United States alone (1). One study reports that over an approximately 3-year period, there were 11,920 in-flight medical emergency calls made by airlines to a medical communications center; this was estimated to represent almost 1 medical emergency for every 600 flights (2). Respiratory symptoms accounted for 12% of these in-air emergencies. The development of respiratory symptoms during flight was associated with an increased risk of hospitalization after air travel (odds ratio [OR], 2.13), second only to possible stroke (OR, 3.36). A previous study reported an average of 72 in-flight deaths per year (3), from a population representing approximately 50–60% of the total estimated number of worldwide passengers for that period. Of those deaths, 69% occurred in passengers with no known previous medical illness (3).
Cruising altitudes of commercial aircraft typically range from approximately 30,000 to 40,000 feet, but at times may reach altitudes of 60,000 feet (4). However, the cabin altitude pressure equivalent is maintained at approximately 5,000–8,000 feet with cabin pressurization of approximately 520–570 mm Hg (5). Federal Aviation Administration (FAA) regulations require an aircraft to be capable of maintaining a minimal cabin pressure equivalent to an altitude of 8,000 feet under normal operating conditions (6). Pressurization of the aircraft cabin is achieved using exterior air that is compressed and mixed with filtered and recirculated cabin air. Up to 50% of the cabin air is not recirculated and is expelled, to be replaced with exterior air, with 20–30 complete air exchanges occurring per hour (7). As the aircraft ascends, the decreasing cabin air pressure results in gas expansion, which can cause a “popping” sensation in the ears of passengers due to air escaping from the middle ear and the sinuses.
At 8,000 feet, the reduced barometric pressure and decreased partial pressure of oxygen is equivalent to breathing air that contains approximately 15.1% of oxygen while at sea level. This calculation forms the basis of the normobaric hypoxic challenge test, and results in a partial pressure of inspired oxygen of 100–105 mm Hg and partial pressure of arterial oxygen (PaO2) of approximately 60–70 mm Hg in healthy individuals (4). Figure 1 illustrates the estimated alveolar oxygen tension (PaO2) with typical cabin altitudes experienced during commercial air travel, assuming a normal PaCO2 and a respiratory quotient of 0.8. In most healthy individuals, such a decrease in PaO2 as is seen at 8,000 feet is of little physiological consequence, as the compensatory mechanisms that occur with hypobaric hypoxia lead to increased minute ventilation, as well as increased heart rate and cardiac output (8, 9).
Figure 1. Relationship between cabin altitude and calculated alveolar oxygen tension (PaO2) in a person with normal PaO2 at sea level, an individual “at risk,” with decreased PaO2 that is within normal limits, and an individual with a PaO2 at sea level that would be associated with significant hypoxemia. Also indicated are altitude thresholds whereby pilot, air crew, and healthy passengers are required to use supplemental oxygen as per Federal Aviation Administration regulations. Data adapted by permission from Reference 20.
[More] [Minimize]Figure 1 further illustrates how, in contrast to a healthy individual, other individuals may be at increased risk of significant hypoxemia, even at altitudes within the normal operating range of the aircraft. Compensatory mechanisms in patients with pulmonary or cardiac disease may also be less effective, placing these patients at further risk of significant hypoxemia (10–15).
The interactions between those factors predisposing to hypoxemia, the presence of comorbid illness, and the compensatory mechanisms in response to hypoxemia are illustrated in Figure 2. In expiratory flow–limited patients, for example, an increase in minute ventilation may result in hyperinflation (16), and further exacerbate respiratory discomfort (17). In patients with restrictive lung disease (e.g., interstitial lung disease, kyphoscoliosis, and obesity), although an increase in minute ventilation may occur, this may also be limited as preexisting impairment of gas exchange may attenuate other compensatory mechanisms (12).
Figure 2. Factors contributing to hypoxemia at altitude, compensatory mechanisms, the potential influence of comorbid illness, and possible end-organ complications of hypoxemia. HR = heart rate; Ve (e) = minute ventilation.
[More] [Minimize]Other conditions contributing to high-altitude hypoxemia and in-flight complications include obstructive sleep apnea, pulmonary hypertension, pneumothorax, and cystic fibrosis (8, 10, 11, 14, 18). In many of these conditions, even at rest, hypoxemia can result in respiratory symptoms, and critical end-organ dysfunction such as arrhythmia or syncope can occur (Figure 2) (19). Furthermore, patients with cardiovascular disease may be unable to adequately increase cardiac output, which could further worsen hypoxemia and exacerbate end-organ hypoxia (Figure 2).
Even healthy individuals may experience symptoms of hypoxemia at altitudes encountered in a commercial aircraft. FAA regulations stipulate cabin altitude thresholds for supplemental oxygen for pilots, cabin crew, and passengers (20), and are outlined in Figure 1 and Table 1. Symptoms of hypoxemia include at the milder end of the spectrum, an effect on night vision, most relevant to pilots (20). It is therefore recommended that pilots use supplemental oxygen at altitudes above 5,000 feet when flying at night (20). At altitudes in excess of 12,000 feet, headache, impairment of judgment or memory, and euphoria may ensue. In excess of 15,000 feet, peripheral visual field defects, further cognitive dysfunction, and unconsciousness may result (20–22).
| Cabin Altitude | PiO2: mm Hg (% of Sea-Level Values) | Symptoms | FAA Recommendations on Use of Oxygen at Altitude |
|---|---|---|---|
| Sea level | 150 (100) | • None | • Supplemental oxygen not required |
| 5,000 ft | 124 (83) | • Night vision may become affected | • Pilots to use supplemental oxygen at night |
| 8,000 ft | 110 (74) | • Night vision affected | • Pilots to use supplemental oxygen during day at cabin altitudes above 10,000 ft |
| 12,000–15,000 ft | 83–94 (56–63) | • Impairment of judgment | • Cabin crew to be provided with supplemental oxygen within 30 min of exposure to altitudes of 12,500–14,000 ft, and immediately above 14,000 ft |
| • Memory impairment | |||
| • Decreased alertness | |||
| • Headache, dizziness | |||
| • Euphoria | |||
| Above 15,000 ft | <83 (<56) | • Peripheral visual field defects occur | • All occupants of aircraft require supplemental oxygen |
| • Unconsciousness can occur |
It follows that in individuals either with preexisting hypoxemia or in those predisposed to hypoxemia, symptoms such as cognitive dysfunction could become apparent even at normal cabin altitudes. However, this does not appear to be the case for patients with mild to moderate chronic obstructive pulmonary disease (COPD) (23). The reasons for this are unclear, and may reflect an underpowered study, as acknowledged by the authors (23).
How hypoxemia may be manifested in other organ systems may be reflected by the types of illnesses reported in-flight. Although respiratory illnesses comprise approximately 12% of all in-flight emergencies, other emergencies include syncope (37.4%), cardiac symptoms (7.7%), stroke (2%), and cardiac arrest (0.3%) (2).
The most recently published British Thoracic Society (BTS) guidelines on the management of patients with respiratory disease who are planning air travel highlight many of the important issues relating to air travel in a population at increased risk of complications of hypoxemia (8). The BTS guidelines address specific pulmonary diseases, as well as patients with cardiac disease who may also be at risk of significant complications as a result of hypoxemia (8). Table 2 outlines the pulmonary disease–specific recommendations in addition to recommendations for cardiac disease.
| Disease | Considerations | Recommendation | SIGN Grading |
|---|---|---|---|
| Asthma and COPD | • Acute exacerbation during flight | • Give patient’s own bronchodilator | D |
| • Severe asthma or COPD with FEV1 < 30% predicted | • Consult specialist beforehand | D | |
| • Bring supply of prednisone | D | ||
| Bronchiectasis | • General | • Nebulized antibiotics or bronchodilators not required | D |
| Interstitial lung disease | • General | • Careful assessment of patients recommended | D |
| • Consider oxygen supplementation if high-altitude destination | D | ||
| • Bring supply of antibiotics ± prednisone | D | ||
| Cystic fibrosis | • General | • HCT recommended if FEV1 < 50% predicted | C |
| • If SpO2 < 90% during HCT, supplemental oxygen is advised | C | ||
| Obstructive sleep apnea | • General | • Avoid alcohol and sedatives | D |
| • CPAP device | • Use dry-cell batteries in-flight | D | |
| • CPAP device should be capable of operating at altitude | D | ||
| • Verify that device is operable at altitude and with power supply at destination | D | ||
| Pulmonary hypertension/heart failure | • NYHA class I–III without PH | • May fly without oxygen | D |
| • NYHA class I–II with PH | • May fly without oxygen | D | |
| • NYHA class III–IV with PH | • Should receive in-flight oxygen | D | |
| • NYHA class IV and severe PH | • Should avoid flying | D | |
| Neuromuscular disease and kyphoscoliosis | • General | • All patients should undergo hypoxic challenge testing | C |
| Cardiac disease | • Coronary artery disease | • May fly 2 d after PCI | C |
| • Low-risk patients after NSTEMI may fly after 3 d | C | ||
| • Those with NSTEMI should undergo PCI before planning air travel | C | ||
| • After coronary artery bypass grafting | • May fly 14 d after CABG once chest radiograph has excluded pneumothorax | C | |
| • Angina CCS class III symptoms | • Patients with stable CCS class III angina are not expected to develop symptoms | C | |
| • Angina CCS class IV symptoms | • Patients with CCS class IV symptoms should be discouraged from flying | C | |
| • Cyanotic congenital heart disease | • At physician’s discretion to advise HCT and/or use supplemental oxygen | D | |
| • NYHA functional class IV should not travel, or should receive in-flight oxygen at 2 L/min | D | ||
| • Unstable arrhythmia | • Should not fly | C | |
| • Valvular disease | • If hypoxemic at sea level, and coexisting lung or pulmonary vascular disease, consider HCT | D |
Cardiac arrest or sudden death accounts for 57% of the in-flight deaths reported by the International Air Transport Association (3), with pulmonary disease responsible for 8% of in-flight deaths (24). Although patients with preexisting pulmonary disease represent the largest group of patients attending preflight medical screenings, much of the remainder is composed of patients with cardiac disease (25).
Coexistent cardiac and pulmonary disease is also an important consideration given the interplay between hypoxemia, compensatory mechanisms, and comorbid illness. It is primarily for this reason that the authors of the 2011 BTS guidelines retained recommendations for patients with cardiac disease (8). Disease-specific recommendations are also summarized in Table 2.
Air travel is also associated with an increased risk of venous thromboembolism, with the incidence of pulmonary embolism being 1.5 cases per million passengers if traveling distances greater than 5,000 km, and more than three times that for distances in excess of 10,000 km (26). The risk of venous thromboembolism in travelers is 2.8 times the risk for nontravelers (27), the risk being greatest among those traveling by air rather than using other means. These data suggest that the conditions encountered during commercial air travel may also predispose individuals to thrombotic complications. Immobility and dehydration may be important contributing factors to this increased risk; window seating and obesity are also associated with increased risk of venous thromboembolism during air travel (28, 29). Other important risk factors include a history of previous venous thromboembolism, malignancy, oral contraceptive or hormone replacement therapy use, and a family history of venous thromboembolism (29, 30).
Hypobaric hypoxia may also increase the risk of venous thromboembolism. Although simulated flight using a hypobaric chamber does not appear to alter blood coagulation in healthy individuals (31), air travel itself may affect blood clotting. Increases in levels of plasminogen activator inhibitor type 1 occur during long-haul flights, along with increases in the ratio of plasminogen activator inhibitor type 1 to tissue plasminogen activator, and also increases in factors VII and VIII (32). This suggests that a hypercoagulable state develops during air travel, with increases in clotting factors in addition to decreases in fibrinolytic mechanisms (32).
In contrast to these findings, a study of male airline pilots demonstrated a decreased risk of thromboembolism. It is possible that such a finding may reflect a selection bias as a result of age and sex, and also the regular medical screening evaluations that airline pilots undergo before obtaining a flying permit and throughout their career (33). Nonetheless, it is interesting that despite the duration and frequency of exposure to hypoxic conditions throughout their career, no increased risk was found. This would suggest that risk factors in addition to hypobaric hypoxia may be of greater significance.
Although controversial, overall there appears to be at least some evidence that flying predisposes to venous thromboembolism. Obesity and immobility are risk factors both at altitude and at sea level. Such factors are also particularly important for those with cardiac or pulmonary disease, as mobility in certain patients may become even more limited, especially in a hypoxic environment.
To date, assessment of fitness to fly in patients with pulmonary disease has largely been studied in patients with COPD, although patients with restrictive lung disease and cystic fibrosis have also been studied (10–14, 18, 34–37). The Centers for Disease Control and Prevention (CDC, Atlanta, GA) estimates that approximately 15 million people have a diagnosis of COPD in the United States alone (38), while globally, although precise data from outside Europe and North America are lacking, the prevalence of COPD within other populations may be even greater (39). Furthermore, precise data on patients either with or at risk of significant hypoxemia are not available. However, within the COPDGene cohort, for example, 7.7% of those with an FEV1 less than 80% had resting hypoxemia (oxygen saturation as determined by pulse oximetry [SpO2] < 88%) (40). Although this may be an overestimation, as many of these patients were recruited from the Denver study site (at an altitude of 5,280 ft) (40), this study highlights the frequency of hypoxemia even at a modest altitude in a significant number of patients with mild COPD.
Extrapolating these data to the CDC estimates, up to 288,750 patients with COPD in the United States may therefore be at increased risk of hypoxemia and in-flight complications. Even among those patients who are receiving supplemental oxygen, a significant number may be traveling with insufficient oxygen supplementation (25). The COPDGene study also found that 25% of patients with severe resting hypoxemia were not using supplemental oxygen (40). Data from 20 years ago also highlighted this issue, indicating that only 25% of the patients who were prescribed supplemental oxygen actually used it when traveling by air (25). However, a notable finding of this study was that despite arrangements being made with airlines before traveling, oxygen was still not available for some patients (25).
As part of a preflight screening evaluation, medical history and physical examination should be performed. Comorbid conditions such as cardiovascular disease, cerebrovascular disease, other neurological disease, and anemia should be evaluated. In one study, up to 55% of patients attending a preflight screening had flown within the preceding 2 years (25). Any previous flying history should therefore be explored, as this may yield important information as to symptoms or complications that may have occurred during or after air travel. In the absence of any contraindication, spirometry should be performed on patients with a history of acute or chronic lung disease or with symptoms suggestive of lung disease. Contraindications would include pneumothorax, massive hemoptysis, recent chest surgery, and tuberculosis. Pulse oximetry at rest should also be done, with arterial blood gas confirmation in addition to this if hypercapnia is suspected.
A number of methods of assessment for hypoxemia risk during air travel are available (8, 34, 41). These include sea-level measurement of SpO2 and PaO2, the use of equations to predict hypoxemia at altitude, and also hypoxic challenge testing, performed under either normobaric or hypobaric conditions. Table 3 summarizes the relative advantages and disadvantages of these methods.
| Method | Patients Studied | Advantages | Disadvantages |
|---|---|---|---|
| Sea-level SpO2 | COPD, ILD, CF | Ease of use | Underestimates oxygen requirements |
| Predictive equations | COPD, ILD, CF | Ease of use | Overestimates oxygen requirements |
| Normobaric hypoxic testing | COPD, ILD, CF | Widely available | May underestimate SpO2 on exertion; suboptimal at titrating supplemental oxygen |
| Good correlation with in-flight SpO2; technically easy to perform | |||
| Hypobaric hypoxic testing | COPD, ILD, CF | Reproduces hypobaric environment | Not widely available |
| More accurate estimation of SpO2 at altitude; superior at titration of supplemental oxygen | Technically more complex to perform |
Compared with other methods, the use of SpO2 measurements at sea level to risk-stratify patients has become recognized as a less reliable predictor of in-flight SpO2 (8). In the 2002 BTS guidelines, an SpO2 of 92–95% without risk factors or SpO2 greater than 95% was used to indicate that no further testing was warranted (41). However, despite having SpO2 greater than 96%, 23% of patients in one study had significant hypoxemia warranting in-flight oxygen supplementation when tested by hypoxic challenge testing (42).
In addition, among 100 patients with COPD who were stratified on the basis of SpO2 thresholds from the 2002 BTS algorithm and then underwent pulse oximetry and normobaric hypoxic challenge testing, the sensitivity and specificity for these SpO2 thresholds were only 59 and 72%, respectively (43). Thus, a lower-normal SpO2 even without risk factors is no longer considered a sufficiently robust test by which to screen patients, and additional hypoxic challenge testing is recommended.
Predictive equations have also been used to estimate the risk of hypoxemia at high altitude; they incorporate sea-level measurements of PaO2 and other parameters such as FEV1 or anticipated cabin altitude (44, 45). However, predictive equations do not compare favorably with hypoxic challenge testing in identifying the need for supplemental oxygen among patients with COPD, interstitial lung disease, or cystic fibrosis (34), as many of the equations consistently overestimated the need for supplemental oxygen, thus incurring unnecessary additional cost.
Normobaric hypoxic challenge testing is now the preferred method to assess risk of hypoxemia at altitude. It is becoming more widely available and correlates well with other means of assessment, and with air travel itself (42). It uses a decreased (normobaric) fraction of inspired oxygen (FiO2) to simulate the hypoxic conditions at altitude. Data from normobaric hypoxic challenge testing have been compared with actual in-flight data collated in the same individual patients with COPD (46). SpO2 decreased from 95% at sea level to 86% in-flight, which compared well with hypoxic challenge testing with a sea-level SpO2 of 96%, decreasing to 84% at simulated altitude. Hypoxic challenge testing correlated strongly with actual flight data (r = 0.84). However, the mean nadir for SpO2 during commercial flight was 78%, occurring during periods of activity, demonstrating that the hypoxic challenge test tended to underestimate the severity of in-flight hypoxemia.
Although normobaric testing compares well with both hypobaric testing and actual air travel (35–37, 46), the potential effects of decreased barometric pressure are not reproduced with a normobaric study. However, hypobaric testing is not widely available (8). It is unclear to what extent lower barometric pressure might alter the physiological changes encountered during commercial air travel. In experimental studies, a hypobaric environment is associated with a decrease in FEV1 and FVC in both normal individuals and those with COPD (47). An increase in residual volume, FRC, and TLC is also seen (48). Residual volume increases significantly in patients with COPD (47), and FRC and TLC increase in patients with cystic fibrosis (18). In a hypobaric hypoxic environment, these factors together with the demand for increased minute ventilation might further increase the risk of dynamic hyperinflation. Detection of clinically significant hyperinflation before air travel may therefore be relevant in some patients with obstructive lung disease.
The BTS guidelines (2011) outline thresholds for prescribing supplemental oxygen for air travel. After the administration of a 15% fractional concentration of inspired oxygen for 20 minutes, a PaO2 greater than 50 mm Hg or an SpO2 of at least 85% could suggest that in-flight oxygen is not required. However, pulse oximeter or arterial blood gas values less than that require oxygen supplementation via nasal cannulas (8).
After a positive hypoxic challenge test, titration of supplemental oxygen can be performed. However, this presents a number of challenges with normobaric testing. Compared with titration during hypobaric testing, there is an underestimation of supplemental oxygen requirements (35, 49), which may reflect poorer accuracy in terms of the actual FiO2 administered during a normobaric test with supplemental oxygen. In addition, during a normobaric or hypobaric hypoxic challenge test, pulsed dose oxygen may result in a lower PaO2 than continuous flow oxygen (35). Continuous flow oxygen may be delivered at rates of up to 6 L/minute depending on the portable concentrator used. Pulsed dose flow rates also vary depending on the portable oxygen concentrator used. For example, on a pulsed dose setting of 1, oxygen delivery may range from 9 to 16 ml/breath depending on the device, with rates of up to 192 ml/breath possible at higher settings on some devices. For this reason, if pulsed dosing rather than continuous flow is planned, it may be prudent to instruct the patient to bring his or her own particular portable oxygen concentrator to the hypoxic challenge test to assist in titration of oxygen using this specific setting.
Since 2009, after the U.S. Department of Transport ruling “Nondiscrimination on the Basis of Disability in Air Travel,” all airlines traveling to and from the United States are required by law to permit passengers to carry their portable oxygen concentrators (POCs), provided they have been approved for use by the Federal Aviation Administration.
The policy of individual airlines toward the specific concentrators that are permissible for use aboard the aircraft is, in turn, largely guided by the list of devices approved by the FAA. Table 4 outlines the list of portable concentrators currently approved for use by the FAA, and also those currently approved by the 10 largest airlines worldwide, based on annual passenger numbers, and information currently available from the relevant airline’s website.
| Permitted Devices | Del | Sou | Chi | Un | Am | Ry | Lu | CE | Ea | US |
|---|---|---|---|---|---|---|---|---|---|---|
| AirSep FreeStyle | + | + | + | + | + | + | + | + | + | |
| AirSep LifeStyle | + | + | + | + | + | + | + | + | ||
| AirSep Focus | + | + | + | + | + | + | + | + | ||
| AirSep Freestyle 5 | + | + | + | + | + | + | + | + | ||
| (Caire) SeQual eQuinox/Oxywell (model 4000) | + | + | + | + | ||||||
| Delphi RS-00400/Oxus RS-00400 | + | + | + | + | + | + | + | + | + | |
| DeVilbiss Healthcare iGo | + | + | + | + | + | + | + | + | ||
| Inogen One | + | + | + | + | + | + | + | + | ||
| Inogen One G2 | + | + | + | + | + | + | + | + | ||
| lnogen One G3 | + | + | + | + | + | + | + | + | ||
| lnova Labs LifeChoice Activox | + | + | + | + | + | + | + | + | ||
| International Biophysics LifeChoice/lnova Labs LifeChoice | + | + | + | + | + | + | + | + | + | |
| Invacare XPO2 | + | + | + | + | + | + | + | + | + | |
| Invacare Solo 2 | + | + | + | + | + | + | + | + | ||
| Oxylife Independence oxygen concentrator | + | + | + | + | + | + | + | + | ||
| Precision Medical EasyPulse | + | + | + | + | + | + | + | + | ||
| Respironics EverGo | + | + | + | + | + | + | + | + | + | |
| Respironics SimplyGo | + | + | + | + | + | + | + | + | ||
| SeQual Eclipse | + | + | + | + | + | + | + | + | ||
| SeQual SAROS | + | + | + | + | + | + | + | + | ||
| VBox Trooper | + | + | + | + | ||||||
| Additional considerations | ||||||||||
| Notify airline at least 48 h in advance | Y | Y | Y | Y | Y | Y | Y | Y | Y | Y |
| Physician’s statement or letter required | Y | Y | Y | Y | Y | Y | Y | Y | N | Y |
| Battery-powered use only | Y | Y | U | C | C | Y | Y | U | N | Y |
| Use of other portable concentrators allowed | N | N | N | N | N | N | N | U | Y | N |
| Rental service recommended or available through airline | Y | Y | Y | N | N | Y | N | N | N | Y |
| Cost of rental of POC unit* | 325/wk | U | 200 | — | — | U | — | — | — | 325/wk |
| Compressed medical oxygen available from airline | N | N | N | C | N | Y | C | Y | N | N |
Patients face a number of additional challenges with respect to arranging the use of portable concentrators. Table 4 also outlines some of these. Patients typically must provide at least 48 hours’ notice of intent to travel, together with a physician statement for how and when the POC is to be used during flight. Many airlines do not guarantee a power outlet for use of the POC and instead recommend ensuring the machine is fully charged and that additional charged batteries are also carried. Finally, some airlines require patients to assume all risk by signing a waiver of liability before air travel.
It is important therefore that physicians be well informed on such challenges faced by patients, to provide them with the best information available. One speculates that a physician–patient discussion akin to informed consent might be appropriate under certain circumstances given the waiver of liability that the patient is expected to sign.
Table 2 outlines disease-specific recommendations from the BTS 2011 guidelines, together with grading of the strength of evidence.
A detailed assessment should occur as described previously. In addition, if traveling to a high-altitude destination, supplemental oxygen should be considered. The patient should also bring a course of oral corticosteroids and antibiotics in the event of an acute exacerbation of their disease (8, 41).
All patients should undergo assessment as described previously as well as hypoxic challenge testing (Table 2).
In addition to hyperinflation within communicating airways, at an altitude of 8,000 feet, Boyle’s law predicts there will be a 38% increase in the size of closed air-filled pockets within the body (8, 50). This gas expansion may be associated with an increased risk of pneumothorax in patients with bullous or cystic lung disease (8, 14). However, from published data in patients with cystic lung disease, the incidence of pneumothorax related to air travel appears to be low (2, 25, 51). Nonetheless, in patients with chronic lung disease who are already at risk of hypoxemia, the development of a pneumothorax in-flight could be devastating. A previous history of pneumothorax may be more relevant in patients with lung disease, as rapid changes in barometric pressure may precipitate recurrence.
Patients with a closed pneumothorax generally should not fly, with rare exceptions. It is currently recommended that patients not travel after a pneumothorax unless drainage has been performed and, in the case of recurrent pneumothoraces, when definitive surgical treatment has occurred (8, 52). Otherwise, provided chest imaging has determined the pneumothorax has resolved, patients should be safe to travel provided a further 7 days has elapsed (8). However, it should be noted that patients with preexisting lung disease have a high risk of recurrence and that this risk remains increased for up to 1 year after a pneumothorax (53).
Similar to the advice pertaining to pneumothorax, in those who have undergone chest surgery, radiographic demonstration of lung reexpansion and resolution of pneumothorax after chest drain removal should be performed (8). Signs or symptoms concerning for pneumothorax or postsurgical complications should prompt further investigation before air travel (8).
In all of the previously described conditions, it would be prudent to recommend that patients not fly while symptoms of an acute exacerbation of their illness may be developing.
In contrast to this scenario, there may be some role for optimization of their pulmonary illness before flying, thus decreasing the risk of complications and potentially reducing the severity of hypoxemia. A period of more intensive chest physiotherapy may be of benefit to some patients with cystic fibrosis, for example (54). Similarly, optimized control of asthma symptoms, or symptoms of heart failure, would also seem to be appropriate recommendations, although there is no published evidence to support this.
Certain patients with pulmonary disease should be instructed not to fly. These include patients who pose risk to others such as those with active infectious diseases (e.g., tuberculosis or influenza), or those in whom air travel would pose a risk to themselves: hemoptysis, unresolved pneumothorax, and a sea-level supplemental oxygen requirement in excess of 4 L/minute.
It is important to highlight the following points in assessing patients for air travel:
| 1. | Even at 35,000 feet, different types of commercial aircraft will have widely differing cabin altitudes, ranging from an equivalent of approximately 5,400 to 8,000 feet (4). In addition, commercial aircraft may also vary their cruising altitude a number of times during the flight, which in turn can alter cabin pressure (4, 55). | ||||
| 2. | Respiratory symptoms may occur even despite having a preflight assessment. One study found 18% of patients with COPD developed respiratory symptoms despite having a preflight evaluation (56). | ||||
| 3. | Flight duration is another important factor to consider. Longer flight durations are associated with increased symptoms (42), particularly when lasting over 3 hours (57). | ||||
| 4. | The levels of activity of the patient during the flight should also be considered. Patients with COPD, restrictive lung disease, and cystic fibrosis demonstrate significant worsening of hypoxemia at simulated altitude with a workload equivalent to that of walking around the aircraft cabin (11, 12, 18). | ||||
In summary, normobaric hypoxic challenge testing should be considered for patients with chronic and acute pulmonary diseases as they are potentially at risk of significant hypoxemia and complications during air travel. In addition, patients with comorbid illness, at risk of significant complications in hypoxic environments, particularly if compensatory mechanisms might be inadequate to deal with hypoxemia, should be assessed for fitness to fly. These also include patients with significant cardiac or cerebrovascular disease. Furthermore, when prescribing supplemental oxygen, consideration should also be given to the anticipated oxygen concentrator and delivery mode and also levels of patient activity aboard the flight.
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