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Passengers should reduce consumption of alcohol on flights
EDITOR Merely to move blood clotting from position 1 to position 3 in
the triad sequence gives a new explanation for thrombogenesis. This
suggests that thrombogenesis during long haul flights is attributable
to individual passengers' behaviour During deep sleep, muscle areflexia may mean that muscles stop pumping
blood towards the head and underperfuse deep venous valve pockets. The
problem starts when non-pulsatile circulation into or within venous
valves stops.5 We did not establish the time for which
valve pockets must be underperfused before their intima is suffocated
and ectopic haemostatic thrombogenesis begins: our objective was to
cause experimental thrombi, not prevent them. More than two hours'
paralysis of limb muscles harmed valve pocket intima, but less than 90 minutes' paralysis produced no thrombi.
Geroulakos points out that airlines disclaim responsibility for
thrombotic events and that no strict scientific basis exists for
the standard medical advice given to passengers. Airlines may
certainly disclaim responsibility if the lesions are caused by
passengers' self injuring behaviour.
The standard advice to sober passengers is to move their legs,
drink water, walk the aisle, be aware that there is a mild lack of
oxygen, and seek more knee room if possible.
The advice to reduce consumption of alcohol and drugs that suppress the
central nervous system is probably so pertinent that a legal limit on
consumption on long haul flights might be introduced as prophylaxis
against thrombotic disasters.
Geroulakos,1 like previous reviewers of the
relation between air travel and venous thromboembolism,2
did not mention the theoretical and experimental evidence of
thrombogenesis in venous valve pockets that colleagues and I have
published.3 Modelled on one of the six possible
permutations of Virchow's triad, our experiments produced experimental
thrombi in venous valve pockets for the first time since Virchow
described them in 1858.4 The specific triad model was (1)
interrupted circulation in venous valve pockets causing (2) hypoxaemic
metabolic endothelial injury and leading to (3) ectopic haemostatic
plug formation (blood metamorphosis) in valve pockets.
specifically, taking an excess of
drugs that suppress the central nervous system (alcohol, long acting
tranquillisers, or other sedative drugs which, alone or in combination,
may induce quasi-anaesthetic muscle paresis or paralysis).
129 Viceroy Close, Birmingham B5 7UY
pcmalone{at}Doctors.org.uk
| 1. |
Geroulakos G.
The risk of venous thromboembolism from air travel.
BMJ
2001;
322:
188 |
| 2. | House of Lords. Deep vein thrombosis, seating, and stress. London: Stationery Office, 2000: chapter 6. (Fifth report of select committee on science and technology.) |
| 3. | Hamer JD, Malone PC. Experimental deep venous thrombogenesis by a non-invasive method. Ann R Coll Surg Engl 1984; 66: 416-419[Medline]. |
| 4. | Virchow R. Cellular pathology. New York: Dover, 1859:232 (chapter 10). [Translated by J Chance.] |
| 5. | Karino T, Motomiya M. Flow through a venous valve and its implications for thrombus formation. Thromb Res 1984; 36: 245-257[Medline]. |
Pulmonary embolism after air travel may occur by chance alone
EDITOR This episode reminds me of a letter published 15 years ago in the
New England Journal of Medicine.2 Its authors
reported a pulmonary embolism in a 40 year old man the day after he
watched three consecutive football games on television on New Year's
Day. The correspondents I enjoy creative humour, but as an epidemiologist I felt compelled to
point out that many pulmonary emboli will occur by chance alone among
people viewing football games on television. In a letter (which the
journal did not publish but which is on bmj.com3) I
presented calculations estimating that pulmonary embolism would be
expected to occur by chance alone in 34 "hard-core" viewers of bowl
games during the 24 hours after the games.
One could do a similar calculation to estimate the expected occurrence
of pulmonary embolism among the millions of people who have travelled
by air during the past 24 hours. Some of those pulmonary emboli may be
caused by the conditions of air travel that favour venous
thromboembolism,1 but many are probably related to air
travel by mere coincidence.
I am not arguing against the sensible preventive measures that
Geroulakos recommends at the end of his editorial. Rather, I am
reinforcing his call for research to determine whether air travel is a
genuine risk factor for venous thromboembolism, and to identify those
at risk and the factors that correlate with risk.
In his editorial Geroulakos states that "there is only
circumstantial, but no epidemiological, evidence connecting air travel
with venous thrombosis."1 He adds that the incidence of
venous thrombosis associated with air travel is "much less than the
impression given by the recent publicity" surrounding the death of a
27 year old woman from a pulmonary embolism after she disembarked from
a flight from Australia to London.
presumably with tongue in cheek
termed this condition "bowl-game pulmonary embolism," in reference to the college football bowl games played in the United States in December and January.
Center for Health Promotion and Disease Prevention, Henry Ford
Health System, Detroit, MI 48202-3450, USA rdavis1{at}hfhs.org
1.
Geroulakos G.
The risk of venous thromboembolism from air travel.
BMJ
2001;
322:
188. (27 January.)
2.
Walsh C, Lauer MS, Huang PL, Page RL.
Bowl-game pulmonary embolism.
N Engl J Med
1986;
314:
1322-1323[Medline].
3.
Davis R. Pulmonary embolism occurs in some travelers by chance
alone. Electronic response to: The risk of venous thromboembolism from
air travel. bmj.com 2001;322. (bmj.com/cgi/eletters/322/7280/188#EL5;
accessed 1 May 2001.)
© BMJ 2001