The association between long-distance travel and pulmonary embolism has been recognized for over half a century. The mechanism for the linkage between these two events is unclear. In addition to stasis of blood caused by immobility while in the economy class compartment of the plane, investigators have speculated that the unique air travel environment makes long-distance air travel particularly risky. In a study published in Lancet earlier this year, F.R. Rosendaal and colleagues compared changes in parameters of coagulation and fibrinolysis in subjects during an eight-hour plane flight, eight hours of sitting while watching a cinema marathon, or eight hours of normal activities. In that study, thrombin-antithrombin complex levels (a measure of activated coagulation) increased significantly only in the subjects while they traveled by air. The changes in thrombin-antithrombin complexes were almost exclusively identified in the subgroup of subjects who were predisposed to thrombosis (e.g., Factor V Leiden carriers who also took oral contraceptives). This study suggested that airplane travel per se, rather than mere economy-class confinement, activated the coagulation system contributing to the thrombosis.
Since reduced oxygen tension and cabin pressures are potential environmental risk factors that could affect the coagulation system, W.D. Toff et al. analyzed subjects before and after eight seated hours in a hypobaric and slightly hypoxic chamber. These subjects did not have any known prothrombotic risk factors. Again, changes in parameters of coagulation and fibrinolysis were assayed including thrombin-antithrombin complex levels. In seeming contrast to the Lancet study, these authors did not find any effect of hypobaric hypoxia on the coagulation system. The potential discrepancy between these two studies may be explained by an environmental factor encountered during air travel that is not due to low oxygen tension or cabin pressure. Alternatively, the effect of these conditions on coagulation may be so subtle that it is only detectable in subjects who are already mildly pro-coagulable.
In Brief
In 1940, Keith Simpson, an Assistant Lecturer in Forensic Medicine in London, noted a recent six-fold increase in lethal pulmonary embolisms (see Case Record from Lancet December 14, 1940, page 744). Dr. Simpson speculated that prolonged sitting on deck chairs in public air-raid shelters contributed to this epidemic. He was further convinced that providing bunks, instead of chairs, would help alleviate this early example of “economy class syndrome.” Since that time, the association between confinement and thromboembolic disease has been recognized during car trips, air flights, and train travel. The death of David Bloom, a NBC reporter who suffered a pulmonary embolism while riding in an armored vehicle within Iraq, brought this problem to national attention. It has been estimated that the risk of a symptomatic thrombosis developing as a result of travel longer than four hours is between 1:2000 and 1:6000. However, it remains controversial whether mechanical confinement alone accounts for all of the risk.
Equally controversial is whether prophylactic anticoagulation is worthwhile to prevent thrombotic complications of long-distance travel. Some physicians advocate prophylactic therapy for their patients as well as for themselves. The use of elastic stockings certainly reduces the risk of leg edema and may provide some prophylactic benefit to prevent significant deep vein thrombosis. Aspirin has been advocated by some authorities, but failed to demonstrate efficacy in the LONFLIT III study (Angiology 2002;53:1-6). Low-molecular-weight heparin appears to reduce the incidence of thromboembolic disease, but it is also associated with a small risk of hemorrhage that is close to the risk of thrombosis during air travel. For most patients, the small benefit of prophylactic therapy does not significantly outweigh the risk. For patients with high prothrombotic risk factors (such as history of venous thrombosis, metastatic cancer, certain inherited thrombophilias, and perhaps hormonal therapy), prophylactic low-molecular-weight heparin therapy is a reasonable option for patients planning long-distance travel.
| Case RecordA woman of 60 years took a deck chair into a public air-raid shelter and sat in it continuously for 10 hours. When she got up she complained that her legs were numb and cramped and she found that her ankles were swollen. Some eight to 10 minutes after leaving the shelter to walk home she collapsed in the street, dead. At autopsy it was noted that she was of stout build, and had mild varicosities of the veins of both legs. There was no pelvic obstruction but excess of mesenteric and retroperitoneal fat and mild fatty degeneration of the myocardium likely together to promote venous stasis. Small tags of very fresh antemortem clot still lay in some parts of the tibial veins, but most of it had become separated and was found, as a series of short clots of small caliber, lodged well down in the first subdivisions of the pulmonary arteries. The caliber of the clot was much smaller than that found, for instance, in postoperative embolism, and it was also much fresher, being some hours old only, as yet hardly adherent to the small veins in which it had been formed, and consisting mainly of propagated (rather than laminated) clot. |
| Case RecordA woman of 60 years took a deck chair into a public air-raid shelter and sat in it continuously for 10 hours. When she got up she complained that her legs were numb and cramped and she found that her ankles were swollen. Some eight to 10 minutes after leaving the shelter to walk home she collapsed in the street, dead. At autopsy it was noted that she was of stout build, and had mild varicosities of the veins of both legs. There was no pelvic obstruction but excess of mesenteric and retroperitoneal fat and mild fatty degeneration of the myocardium likely together to promote venous stasis. Small tags of very fresh antemortem clot still lay in some parts of the tibial veins, but most of it had become separated and was found, as a series of short clots of small caliber, lodged well down in the first subdivisions of the pulmonary arteries. The caliber of the clot was much smaller than that found, for instance, in postoperative embolism, and it was also much fresher, being some hours old only, as yet hardly adherent to the small veins in which it had been formed, and consisting mainly of propagated (rather than laminated) clot. |
Competing Interests
Dr. Abrams indicated no relevant conflicts of interest.
