Signs and symptoms of VTE may include paresthesias, swelling, chest pain, discoloration or pain in the dependent extremity, dyspnea, and cardiac arrhythmias. The clinical presentation is dependent upon the simple development of thrombosis or the addition of embolic activity. Although the lower extremity is involved in the preponderance of cases, upper extremity involvement has also been described.
The annual incidence of venous thromboembolic (VTE) disease has been reported to be 1 in 1000. Kesteven (2) refined the median estimate to from 1.6 to 1.8 per 1000. However, age adjusted data demonstrate a wide range from 1 per 10,000 in young adults to 3-5 per 1000 in persons greater than 60 years of age.
Although there are numerous studies in the literature examining VTE disease, variability of population demographics resists combined analysis. There are no published prospective clinical studies in asymptomatic travelers identifying VTE or activation of the thrombotic system (2). Close examination of the literature clearly demonstrates that VTE is multi-causal in nature, resulting from differing etiologic and predisposing factors across different age groups. A dynamic model dependent upon age and co-morbid factors is necessary to understand the relative risk for each set of clinical criteria (3).
Risk factors for VTE include prior personal or family history of VTE, pregnancy, postpartum period, obesity, malignancy, hormone replacement therapy, recent trauma (surgical or injury), dehydration, alcohol consumption, lower limb paralysis, low cardiac output syndromes, chronic disease, autoimmune disease, genetic factors such as coagulopathies (blood clotting disorders) and other blood disorders, and finally, immobilization.
Genetic predisposition to excessive clotting is reported to affect 3 to 5% of the general population. When the acquired forms of coagulopathies are considered, the prevalence is even higher. Most prominent amongst this category of disorders are anti-thrombin III deficiency, Protein S and Protein C deficiencies, Factor V Leiden mutation, lupus anti-coagulant (anti-phospholipids), high Factor VIII concentration, hyperhomocysteinaemia, and prothrombin 20210A (3).
Although venous thromboembolic disease during air travel is the focus of recent attention, lack of activity such as a long car, bus, train ride, sitting in the theatre or long hours at a desk are all causes of prolonged immobilization. However, review of the literature indicates that most cases of VTE seem to be associated with an underlying disorder. Clinicians and the public at large should focus on existing medical conditions in addition to immobilization and be aware of measures to reduce the risk of VTE.
Berndt and associates (4) reported that none of the comprehensive studies report crew members suffering from thromboembolism. Although the activity of the cabin crew minimizes the immobilization effect, the same cannot be said for the cockpit crew. Eklof and associates (5) studied cases of VTE originating from Honolulu International Airport for the 6-year period from 1988 to 1993. It was estimated that 6 million passengers annually traveled through the airport. Forty-four cases of VTE were identified. All but 7 cases had one or more risk factor in addition to immobilization.
There is one report suggesting an association between increased activity of coagulation system and the hypobaric hypoxic (low pressure and low oxygen) environment experienced in flight. This study lacked a control group and screening for predisposing genetic factors. There was no association between increased activity of the coagulation system and VTE. Although the study is not conclusive, it is certainly suggests that further study is justified (6).
The wisdom of John Homas, written in 1954 (1), is still true today. He wrote, "As is so often true of venous thrombosis, this group of cases reveals a tendency rather than a proved relation of cause and effect." He continued, saying "Such matters are important enough to suggest the advisability of making movements of the toes, feet and lower legs when one is sitting for long periods and of getting up and exercising when opportunity offers." Some have suggested a 5-minute period of activity every hour. This may be problematic in modern aircraft and additionally may pose a separate safety risk, as well as increased opportunity for injury if the aircraft encounters turbulence.
The House of Lords' Committee on Science and Technology has published recommendations, which can be found here. Alternatively, try this location.
The Aerospace Medical Association likewise has published recommendations to reduce the risk of deep vein thrombosis (7).
Avoidance of alcohol and sedating medications, hydration before and during flight, use of compression stockings, and having adequate legroom and leg exercises are all measures that will lower the risk of VTE. Use of aspirin and or low molecular weight heparin clearly needs consultation with a physician to assess the risk and benefits of such pharmacologic intervention.
- Homans, John. Thrombosis of the deep leg veins due to prolonged sitting. NEJM;1954;V.250:148-9.
- Kesteven, PLJ. Traveller's thrombosis. Thorax; Aug 2000;55:532-6.
- Rosendaal, FR. Venous thrombosis: A multicausal disease. Lancet; April 3, 1999; 353:1167-73.
- Berndt, A. et al. Risk Factors for venous thromboembolism following prolonged air travel. Hematology/Oncology Clinics of North America; 14/2; April 2000: 391-7.
- Eklof B et al. Venous thromboembolism in association with prolonged air travel. Dermatol Surg; Jul 1996;22:637-41.
- Bendz, B et al. Association between acute hypobaric hypoxic and activation of coagulation in human beings. Lancet; Nov 11, 2000; 356:1657-58.
- Aerospace Medical Association, Medical Guidelines for Airline Travel, 1997
This article originally appeared in the Federal Air Surgeon's Medical Bulletin, Spring 2001.