Dear Readers
The British Thoracic Society made certain recommendations for patients with chest problems wishing to travel by air. I am a
chest physician working in the UK and I hope this information will be helpful to the patients and health-care professionals
in the North East. The article is very medical and lay person will find it difficult to understand. I, therefore, suggest that
readers should consult a physician to understand the recommendation.
RESPIRATORY DISORDERS WITH POTENTIAL COMPLICATIONS FOR AIR TRAVELLERS
Asthma
Guidelines were identified relating to professional aircrew and
potential recruits with asthma, but none were found relating
to passengers. The flight environment experienced by commercial
passengers should not pose a problem for most patients with asthma.
In a review of all consecutive in-flight medical incidents reported
for QANTAS airlines in 1993 there were 454 significant medical
incidents, 9% of which were reported as respiratory tract infection
or asthma.[38] A review of incidents on US commercial aircraft
where an enhanced medical kit was used found that 10% of 362
episodes were due to asthma, lung disease or breathlessness.[39]
All airlines permit use of dry cell battery operated nebulisers,
but there is usually a restriction during take off and landing
because of the risk of electrical interference.[40] However,
a Cochrane review has shown that spacers are as effective as
nebulisers in treating acute asthma.[41] Co-morbidity may present
a problem if the patient has severe airflow obstruction and hypoxia
or if there is complicating cardiac disease. Low cabin humidity
may present a theoretical risk of bronchospasm as a result of
water loss from bronchial mucosa. A doctor's letter describing
the patient's condition and listing medications is recommended.[42]
Cardiac disease
Cardiac disease is considered here briefly because it often co-exists
with lung disease and may give rise to symptoms attributable
to respiratory disease.
Co-morbidity may present more of a risk
to the passenger than the respiratory disease alone, although
no data exist to support or refute this view. One study measured
SpO2 at simulated altitudes and on commercial flights in 12 patients
with cyanotic congenital heart disease (CCHD) and acquired pulmonary
hypertension and in 27 control subjects.[43] At the simulated
altitude (equivalent to FiO2 15%) mean SpO2 fell from 86% (range
69–98%) to 78% (range 56–90%) in the patients and from 98% to
90% in the controls. During air travel the mean in-flight SpO2
was higher at 83% (range 78–94%). There were no changes in lactic
acid concentrations, pH, or PaCO2 , and no clinical problems.
The tolerance of patients with cardiorespiratory disease in a
stable clinical condition to a moderate increase in hypoxaemia
is unremarkable since they are effectively “acclimatised” to
hypoxia. From the point of view of oxygen delivery to the tissues,
a fall in SpO2 of 10% is easily overcome by a similar percentage
increase in cardiac output. Hypoxaemia is a cardiac stimulant,
and even patients in severe but stable heart failure can increase
their cardiac output by 50% on mild exercise.
COPD
Data on patients with COPD are limited, and existing guidelines
contain largely empirical advice based on relatively small studies.
In addition to the risk of hypoxaemia, patients with severe COPD
may be put at risk from high levels of carboxyhaemoglobin resulting
from smoking. They may experience expansion of non-functioning
emphysematous bullae and abdominal gases which could further
compromise lung function.
Gong et al[27] studied 22 patients (13 men) with stable mild
COPD (FEV1 < 80% predicted), 17 of whom reported variable discomfort
(chest tightness or exertional dyspnoea) on previous flights.
They inhaled sequential gas mixtures of 20.9% (sea level baseline),
17.1% (simulating 1524 m), 15.1% (simulating 2438 m), 13.9% (simulating
3048 m), and 20.9% oxygen (sea level recovery). With 15.1% inspired
oxygen there was a mean fall in SpO2 of 11% from 94% to 83%.
The lowest recordings were 87% on 21% inspired oxygen and 74%
on 15.1% inspired oxygen. Progressive hypoxia induced mild
hyperventilation resulting in small but significant falls in PaCO2 .
Supplemental oxygen was given during inhalation of 15.1% oxygen in five subjects
and 13.9% oxygen in 16. PaO2 increased significantly with supplemental
oxygen and PaCO2 returned to baseline or, in eight subjects,
rose modestly above baseline. Heart rate rose and asymptomatic
cardiac dysrhythmias occurred in 10 subjects; blood pressure
was unchanged. Eleven subjects had no symptoms and 11 reported
mild symptoms which did not correlate with hypoxia or hypoxaemia.
Variable sleepiness noted by the investigators was partly reversed
by supplemental oxygen.
Dillard et al [44] examined 100 patients (retired military personnel
and dependents) with severe COPD over a period of 28 months.
Forty four travelled on commercial flights, of whom eight reported
transient symptoms during air travel but reached their destination
apparently without complications. Those who did not travel by
air had a lower mean FEV1 and greater use of domiciliary oxygen,
suggesting that many patients with COPD choose not to fly.
Christensen et al [45] studied 15 patients with COPD with FEV1
<50% predicted and sea level SpO2 >94%, PaO2 >9.3 kPa. Arterial
blood gas tensions were measured at sea level, at 2438 m (8000
ft) and 3048 m (10 000 ft) in an altitude chamber at rest and
during light exercise (20–30 watts). At 2438 m (8000 ft) PaO2
fell below 6.7 kPa in three patients at rest and in 13 during
exercise. None developed symptoms, probably because of existing
acclimatisation. Resting PaO2 >9.3 kPa or SpO2 >94% do not therefore
exclude significant hypoxaemia at altitude in patients with severe
COPD. Light exercise, equivalent to slow walking along the aisle
of an aeroplane, may worsen hypoxaemia.
The risk of recurrent pneumothorax is discussed separately, but
it should be noted here that COPD patients with large bullae
are theoretically at increased risk of pneumothorax as a result
of volume expansion at reduced cabin pressures. The volume of
gas in a non-communicating bulla will increase by 30% on ascent
from sea level to 2438 m (8000 ft). There is one case report
of fatal air embolism in a patient with a giant intrapulmonary
bronchogenic cyst.[46] However, there are no data to state with
any confidence what the maximum volume of a bulla should be before
it reaches an unacceptable level of risk of rupture leading to
tension pneumothorax, pneumomediastinum, or air embolism.
Recent UK guidelines on oxygen prescribing[47] quote evidence
from two studies[24] [48] which suggest that the best predictor
of PaO2 at altitude is pre-flight PaO2 on the ground. In one
study the authors measured PaO2 and PaCO2 in 13 patients with
COPD at 1650 m and 2250 m. No symptoms attributable to hypoxia
were recorded although PaO2 fell from 9.1 kPa (68.2 mm Hg) at
sea level to 6.6 kPa (51 mm Hg) at 1650 m and 6.0 kPa (44.7 mm
Hg) at 2250 m. PaO2 on air at sea level measured some weeks before
did not correlate with that measured at altitude, but PaO2 measured
within 2 hours of flight time did. In the second study 18 retired
servicemen with severe COPD were exposed to an altitude of 2438
m (8000 ft) in a hypobaric chamber.
Mean PaO2 fell from 9.6 kPa
to 6.3 kPa after 45 minutes at steady state. The authors describe
a predictive equation and recommend using the patient's pre-flight
FEV1 to limit variation in the PaO2 result at altitude.
In a review of acute responses of cardiopulmonary patients to
altitude, Gong et al[49] recommend in-flight oxygen if the pre-flight
PaO2 breathing 15% oxygen at sea level is <6.6 kPa. They conclude
that equations do not accurately predict altitude PaO2 and favour
the hypoxia altitude test.
A study of eight patients with mild to moderate COPD (FEV1 25–78%
predicted) at sea level and after ascent to 1920 m (6298 ft)
revealed no significant complications at altitude and
2,3-diphosphoglycerate levels remained unchanged.[50]
This was despite levels of hypoxaemia similar to those observed in healthy mountaineers at altitudes
of 4000–5000 m (13 000–16 000 ft).
The authors suggest that pre-existing hypoxaemia resulting from disease may facilitate adaptation of
patients to hypoxia and prevent symptoms of acute mountain sickness.
One study has examined the vasopressor responses to hypoxia in
18 men with severe COPD (mean (SD) FEV1 0.97 (0.32) l) at sea
level, at 2438 m in a hypobaric chamber, and after oxygen
supplementation at 2438 m.[51] Mean arterial pressure, systolic and diastolic
blood pressure, and pulsus paradoxicus were unchanged at simulated
altitude; oxygen reduced systolic blood pressure, pulsus paradoxicus,
and pulse pressure. In one subject who developed increased cardiac
ectopy, it was reduced by supplemental oxygen. The authors conclude
that vasopressor responses to hypoxia do not increase the risk
of flying in this group, but that in-flight oxygen may be beneficial.
In summary, the clinical significance of temporary altitude induced
hypoxaemia in patients with COPD is unclear.
The available controlled studies involve relatively small numbers of patients with stable
disease and no co-existing medical problems. Simulated altitude
exposure did not generally exceed 1 hour. These studies also
largely excluded additional stressors such as exercise, dehydration,
sleep, and active smoking. The only report to study exercise
suggested that FEV1 <50% predicted is a risk factor for desaturation.
We therefore recommend that patients with severe COPD are assessed
before flying. Although there are no data to support this view,
we also recommend that patients who require in-flight oxygen
should receive oxygen when visiting high altitude destinations.
Major high altitude destinations are listed in Appendix 4.
Cystic fibrosis
There are few data on the risks of air travel to patients with
cystic fibrosis. In 1994 a study of 22 children with cystic fibrosis
aged 11–16 years examined the value of hypoxic challenge testing.[52]
The children were assessed in the laboratory, in the Alps, and
on commercial aircraft and all desaturated at altitude. Hypoxic
challenge was found to be the best predictor of hypoxia. However,
a more recent study[37] of 87 children with cystic fibrosis aged
7–19 years who travelled on flights lasting 8–13 hours suggested
that spirometric tests were a better predictor of desaturation.
Low cabin humidity may increase the risk of acute bronchospasm
and retention of secretions with possible lobar or segmental
collapse, but there are no data to quantify this risk.
Diffuse parenchymal lung disease
There are no published data; clearly this is an area needing
future research.
Infections
There is concern about the potential for transmission of infectious
disease to other passengers on board commercial aircraft. There
is also concern about the effect of travel after recent respiratory
tract infections. The most important consideration is that of
transmission of pulmonary tuberculosis, especially that of multiple
drug resistant (MDR) tuberculosis.
Seven cases of possible transmission of Mycobacterium tuberculosis
on aircraft have been reported to the Center for Disease Control
and Prevention (CDC), Atlanta, Georgia, USA. The first concerned
a flight attendant with documented tuberculin skin test (TST)
conversion who did not receive prophylaxis and who developed
pulmonary tuberculosis 3 years later.[53] The CDC concluded that
the index case transmitted M tuberculosis to other flight crew
members, but evidence of transmission to passengers was inconclusive.
The second case concerned a passenger with pulmonary tuberculosis
on a transatlantic flight.[54] Following a TST in 79 crew and
passengers, eight had a positive TST. All had received Bacille
Calmette-Guërin (BCG) vaccine or had a history of past exposure
to M tuberculosis. The CDC found no evidence of in-flight transmission
of tuberculosis. The third report concerned a passenger with
pulmonary tuberculosis who travelled from Mexico to San Francisco.[55]
Ninety two passengers were on the flight. The TST was positive
in 10 of the 22 who completed screening, nine of whom were born
outside the US and the tenth was a 75 year old passenger who
had lived overseas and was thought likely to have been exposed
to tuberculosis previously. The San Francisco Department of Health
found no conclusive evidence of M tuberculosis transmission during
the flight.
In the fourth case a refugee from the former Soviet Union with
pulmonary tuberculosis travelled on three separate flights from
Germany to his final destination in the USA.[56] Of 219 passengers
and flight crew, 142 completed screening. The TST was positive
in 32, including five TST conversions. Twenty nine had received
BCG vaccine or had lived in countries where tuberculosis is endemic.
The five passengers with TST conversions were seated throughout
the plane and none sat near the index case. None of the US born
passengers had TST conversions. The investigation concluded that
transmission could not be excluded but that the TST conversions
probably represented previous exposure to tuberculosis.
The fifth report was of an immunosuppressed US citizen with pulmonary
tuberculosis domiciled in Asia. He flew from Taiwan to Tokyo,
then to Seattle, and subsequently to two further US destinations.[55]
Of the 345 US residents on these flights, 25% completed screening.
Fourteen had a positive TST, of whom nine were born in Asia.
Of the remaining five, one had a positive TST before the flight,
two had lived in a country with a high prevalence of tuberculosis,
and two were aged over 75.
The investigators concluded that transmission of tuberculosis could not be excluded but that the positive TST
results may have resulted from prior M tuberculosis infection.
In the sixth report a passenger with pulmonary tuberculosis flew
from Honolulu to Chicago and then to Baltimore where she stayed
1 month.[57] She then returned to Hawaii by the same route. Of
925 passengers resident in the US, 802 completed screening. Six
passengers on the longer flight had TST conversions, four of
whom were born in the USA and sat in the same section of the
plane as the index case. The investigation considered that transmission
of M tuberculosis had probably occurred.
In the final report a passenger with pulmonary and laryngeal
tuberculosis flew from Canada to the US on three separate flights
and returned 1 month later by the same route.[58] Five passengers
had positive TST results but all had other possible explanations,
and it was concluded that the likelihood of M tuberculosis transmission
was low.
In all these reports the index patient was considered highly
infectious and sputum specimens were heavily positive for acid
fast bacilli. All were culture positive and had extensive pulmonary
disease on chest radiography. Laryngeal tuberculosis is the most
infectious form. In two instances the M tuberculosis strain isolated
was resistant to at least isoniazid and rifampicin.[54] [57]
Despite the highly infectious nature of all seven index cases,
only two reports yielded evidence of TST conversion.[53] [57]
In the first case evidence of transmission was limited to crew
members exposed to the index case for over 11 hours. In the second
report transmission was demonstrated only in a few passengers
seated in close proximity to the index case, and only on a flight
lasting more than 8 hours. Although pulmonary tuberculosis does
therefore appear to be transmissible during the course of air
travel, none of the passengers with documented TST conversion
have since developed active tuberculosis. The World Health Organisation
(WHO) concludes that air travel does not carry a greater risk
of infection with M tuberculosis than other situations in which
contact with infectious individuals may occur, such as travelling
by rail, bus, or attending conferences.[59]
There are other studies of potential transmission of airborne
infectious diseases on aircraft. An influenza outbreak occurred
in 1979 among passengers on a flight with a 3 hour ground delay
before take off.[60] Seventy two percent of the 54 passengers
developed symptoms; a similar virus was isolated from eight of
31 cultures, and 20 of 22 patients had serological evidence of
infection with the same virus. The high attack rate was attributed
to the ventilation system being switched off during the ground
delay. Measles may be transmitted during international flights.[61]
[62] In a study of patients with recent lower respiratory tract
infections, Richards reported that 23 patients travelling by
air after acute respiratory infection suffered no adverse effects.[63]
There are no other data specifically relating to patients travelling
after infection, and there is no evidence that recirculation
of air facilitates transmission of infectious agents on commercial
aircraft.
Neuromuscular disease and kyphoscoliosis
The data in this area are sparse, but there is one case report
of cor pulmonale developing in a patient with congenital kyphoscoliosis
after intercontinental air travel.[64] The patient was a 59 year
old man with apparently stable cardiorespiratory function who
developed a first episode of pulmonary hypertension and right
heart failure after a long haul flight. The authors conclude
that this resulted from prolonged exposure to the low FiO2 in
the cabin. There are also anecdotal reports of oxygen dependent
patients with scoliosis whose PaO2 has fallen precipitously during
hypoxic challenge, despite a baseline oxygen saturation above
94% (A K Simmonds, personal communication).
Obstructive sleep apnoea
Few data exist regarding the effects of air travel on patients
with obstructive sleep apnoea. Toff[65] reported a morbidly obese
woman who developed respiratory and cardiac failure at the end
of a 2 week tour involving two flights and a stay at altitude.
It has been recognised since the 19th century that climbers to
high altitude experience periodic breathing during sleep.[66]
[67] [68] Apnoeic periods arise with reductions in arterial oxygen
saturation and are nearly universal above 2800 m. Although generally
thought harmless, periodic breathing can cause insomnia. It has
also been speculated that the desaturations may contribute to
altitude sickness. Three studies have examined this phenomenon
in greater detail[69] [70] [71] but all the subjects were healthy
volunteers. The apnoeas are thought to be central in origin.
However, in the light of these observations it would seem prudent
to recommend that patients using CPAP should take their CPAP
machine with them when visiting high altitude destinations above
2438 m (8000 ft). Major high altitude destinations are listed
in Appendix 4.
Previous pneumothorax
Thirty seven papers were reviewed. Airlines currently advise
a 6 week interval between having a pneumothorax and travelling
by air. The rationale for this recommendation is not explicit,
but it is assumed that it reflects the time period during which
a recurrence of a pneumothorax is most likely. In fact, the risk
for a patient with a pneumothorax, if one were present, relates
to ascent and descent, and a “new” pneumothorax occurring at
altitude may be hazardous because of absence of medical care,
but there should be no particular risk associated with pressure
change. The “6 week rule” appears to have been arbitrarily applied
with no account being taken of the type, if any, of underlying
disease, or of any therapeutic intervention that has been undertaken,
or of demographic factors.
The literature was reviewed to examine whether better evidence
could be found for the timing of maximum risk of a recurrence
of pneumothorax and to determine whether different advice should
be offered to different subgroups of patients. Two papers were
found relating to therapeutic interventions which included evidence
about recurrence rates, and the following conclusions regarding
timing of the recurrence or differences between subgroups were
drawn.
If the pneumothorax was treated by a thoracotomy and surgical
pleurodesis or by insufflation of talc (at thoracotomy), the
recurrence rate should be so low that no subsequent restriction
on travel is necessary.[72] Talc pleurodesis performed via a
thoracoscopy may not be as successful in preventing recurrence
of a pneumothorax—a 93% success rate was reported in one study[73]
and a 92% success rate in another.[74] Similarly, other interventions
via a thoracoscopy, even when using the same techniques as performed
by a more major thoracotomy, may not always carry the same certainty
of success,[72] although some good reports with no recurrence
of pneumothorax have been published.[75] Further studies are
required.
Non-talc chemical pleurodeses (for example, with tetracycline)
are associated with a more significant and continued risk of
recurrence—16% in one study with 50% of the recurrences arising
in 30 days[76] and 13% in another.[74] The best figure found
was a 9% rate of recurrence after chemical pleurodesis.[77] These
recurrence rates suggest that, even after such an intervention,
the patient should still be subject to travel advice applied
to others after a spontaneous pneumothorax.
For patients who have not had a definitive surgical pleurodesis
via a thoracotomy, a risk of recurrence should therefore be expected.
While many studies have included details of the percentage of
patients suffering a recurrence, very few have given much detail
of the timing of these recurrences after the first episode, and
few have characterised those most at risk. In one study a 54.2%
recurrence rate was recorded with the majority occurring within
1 year of the first pneumothorax,[78] and in another study 72%
of the recurrences occurred within 2 years of the first episode.[79]
Cumulative freedom from recurrence data have been published by
Lippert et al[79] and stratified according to smoking history
and underlying lung disease over a follow up period of up to
13 years. The shape of the curve (fig 2) does indeed imply that
the biggest risk of recurrence is in the first year. One author
has intimated that a further prospective trial he and colleagues
are currently undertaking may provide a clearer month by month
detail of recurrence rates.
At present the recommended 6 week cut off seems to be arbitrary,
with a significant fall in risk only appearing to occur after
1 year has elapsed. Furthermore, current advice does not take
into account those with a higher risk of recurrence such as smokers,
those with pre-existing lung disease, taller men, and possibly
women.[79] [80] Thoracoscopic examination of the pleura does
not permit any greater prediction of those at greatest risk of
recurrence.[79] [81]
In conclusion, a definitive surgical intervention makes the risk
of recurrence of a pneumothorax negligible. Such patients may
be able to fly 6 weeks after surgery and resolution of the pneumothorax
in the absence of other contraindications. Careful medical assessment
is required beforehand. For others the risk of a further pneumothorax
is considerable for at least a year after the first episode.
This risk is greatest for those with underlying lung disease
and for continuing smokers.
While the likelihood of recurrence during flight is low and there
is no evidence that air travel precipitates recurrence, the sequelae
of recurrence at altitude may be significant. Recurrence of a
pneumothorax while flying is likely to have more serious effects
than a first episode, and recurrence in passengers with pre-existing
lung disease is more likely to have serious consequences. Passengers
may therefore choose to avoid this risk by delaying air travel
for 1 year after a pneumothorax. This strategy should be given
special consideration by those who smoke and/or have underlying
lung disease.
Venous thromboembolic disease (VTE)
Fourteen papers were reviewed but the evidence is conflicting
with many questions unanswered. BTS guidelines on suspected pulmonary
thromboembolism list six major risk factors for VTE.[82] Air
travel is classified as one of several lesser risks. The evidence
quoted in favour of an increased risk of air travel relates to
long haul flights.[83] [84] Such reports are supported by others
dating back over 20 years,[85] [86] [87] [88] and by more recent
surveys.[89] [90] [91] It is not possible from the published
data to quantify the risk, and the underlying mechanisms have
not been elucidated. Hypotheses include immobility, seated position,
dehydration, and alcohol ingestion. Owing to delayed onset of
symptoms and rapid dispersal of patients after a flight, many
current reports are likely to underestimate the size of the problem.
In small studies evidence suggests that co-morbidity may increase
the risk of VTE associated with air travel.[89] [90] Some studies
suggest that previous VTE increases the risk of air travel associated
recurrence,[89] [90] [91] [92] [93] but the data are controversial.
Further research is needed to determine whether delay in travel
for those at risk is beneficial, and whether avoidance of alcohol
and dehydration and upgrading reduce risk. Research is also required
to examine the potential role of prophylactic low molecular weight
heparin, full formal anticoagulation, and mechanical prophylactic
methods including graded elastic compression hosiery and full
leg pneumatic compression devices. The latter may be impractical
on board an aeroplane and have not been studied in this context.
However, they have been shown to have an additive effect in other
at risk situations.[94] A recent study suggests that symptomless
deep vein thrombosis may occur in up to 10% of airline passengers,
and that wearing elastic compression stockings during long haul
flights is associated with a reduced incidence.[95]
The role of aspirin in this setting also requires investigation.
A study of 13 356 patients undergoing surgery for hip fracture
and 4088 patients undergoing elective arthroplasty showed that
aspirin reduces the risk of pulmonary embolism and deep vein
thrombosis by at least one third throughout a period of increased
risk.[96] The authors conclude that there is now good evidence
for considering aspirin routinely in a wide range of groups at
high risk of thromboembolism.
Thoracic surgery
There are few data available, but it is clear that the volume
of gas in air spaces will increase by 30% at a cabin altitude
of 2438 m (8000 ft). Postoperative complications such as sepsis
or volume depletion should have resolved before patients undergo
air travel. Severe headache precipitated by airline travel has
been recorded 7 days after a spinal anaesthetic, presumed to
be due to cabin pressure changes inducing a dural leak.[97] North
American guidelines[13] highlight the fact that postoperative
patients are in a state of increased oxygen consumption due to
surgical trauma, possible sepsis, and increased adrenergic drive.
Oxygen delivery may be reduced or fixed in patients who are elderly,
volume depleted, anaemic, or who have cardiopulmonary disease.
Reduced use of transfusions means that postoperative patients
are now often more anaemic than previously.
Logistics of travel with oxygen
Berg et al[98] have investigated the effects of oxygen supplementation
in a group of 18 patients with severe COPD (mean FEV1 31% predicted).
Baseline PaO2 at sea level was 9.47 kPa, which fell to 6.18 kPa
when exposed to an altitude of 2438 m in a hypobaric chamber.
The subjects were then given supplemental oxygen; 24% oxygen
by Venturi mask increased PaO2 to 8.02 kPa, 28% oxygen by Venturi
mask increased PaO2 to 8.55 kPa, and 4 l/min via nasal prongs
increased PaO2 to 10.79 kPa. This suggests that, in patients
with COPD, 24% and 28% oxygen via Venturi masks (and probably
2 l/min via nasal prongs) will improve hypoxaemia at 2438 m but
will not fully correct it to sea level values. However, oxygen
given at 4 l/min via nasal prongs will overcorrect hypoxaemia
to produce values above sea level baseline values.
In practical terms, aircraft oxygen delivery systems are usually
limited to 2 or 4 l/min. This is probably best delivered by nasal
prongs as the simple oxygen masks provided by many airlines may
allow some re-breathing and worsen carbon dioxide retention in
susceptible subjects. Using 100% oxygen at a rate of 4 l/min
via nasal prongs from a cylinder will produce a PaO2 at 2438
m (8000 ft) cabin altitude slightly higher than sea level PaO2
on air. Using 2 l/min via nasal prongs should correct the fall
in oxygenation. Patients who require LTOT are not excluded from
air travel, but no randomised controlled trials exist on which
to base recommendations on the optimal flow rate.
The method of oxygen delivery depends upon the specific aircraft,
but the supply is usually from cylinders. In some aircraft oxygen
can also be tapped from the “ring main” of oxygen.[99] Patients
are not allowed to use their own oxygen equipment on the aircraft
but can take an empty oxygen cylinder or oxygen concentrator
as baggage. Charges may be made for both services, as well as
a charge for supplemental oxygen. Regulations vary with each
airline, which can decline the patient's request to travel.[100]
A comparative study of arranging in-flight oxygen on commercial
air carriers was performed by members of the respiratory therapy
department at the Cleveland Clinic Foundation in Cleveland, Ohio;[101]
76% of the 33 carriers contacted offered in-flight oxygen. There
was significant variation in oxygen device and litre flow availability.
Flow options varied from only two flow rates (36% of carriers)
to a range of 1–15 l/min (one carrier). All carriers provided
nasal cannulae, which was the only device available on 21 carriers.
Charges varied considerably. Six carriers supplied oxygen free
of charge while 18 carriers charged a fee ranging from $64 to
$1500. Charges for an accompanying empty cylinder ranged from
none to $250. Most carriers required 48–72 hours advance notice;
one required one month's notice.
Baharul Islam is a Chest Physician working in the UK.
He can be reach at [email protected]
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