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September, 2002 >>

Deep Vein Thrombosis at High Altitude

Acute mountain sickness high altitude pulmonary oedema (HAPE) and high altitude cerebral oedema (HACE) are common at high altitude but just a few cases of coronary and cerebral thrombosis and phlebitis of limbs have been reported1.
A young man who was performing his duties at 17000 ft in northern areas of Pakistan developed progressive painless swelling of his right leg. He was a chronic smoker and did not have any trauma, fever and chest pain. Examination revealed signs of deep vein thrombosis in his right leg. Rest of systemic examination was unremarkable.
He was descended within next forty-eight hours of incident to Rawalpindi at 2000 ft. above sea level. The investigations revealed following:
Haemoglobin- 14.8g/dl, platelets - 190x 109 per liter while total leukocytes count, ECG, X-rays chest, bleeding time, clotting time, PT, PTTK were with in normal limits. Lung scan was also normal. Doppler duplex ultrasound and radioisotope scanning of right leg revealed a large thrombus in popleteal artery extending up to femoral artery. Blood lupus anticoagulant was positive while anticardiolipin antibody, factor V Leiden and protein C levels were within normal limits. Inj. heparin 1000 unit per hour was given by continuous infusion for 4 days. Concurrently oral warfarin 10 mg per day was started before stopping heparin. Within one week swelling of the leg resolved and he became hilly mobile. He was advised to continue warfarin for next four months.
The patient was healthy but developed deep vein thrombosis when he went to high altitude. Various factors attribute to the hypercoagulability at high altitude, In this case smoking, decreased physical activity, coagulation disparities and probably dehydration are important. Decreased physical activity and dehydration lead to stasis of blood and hence cause tendency to coagulate. Coagulation enhancement may also result from abnormal platelets with increased adhesiveness2, red cell anisocytosis3 and polythermia4 leading to microthrombi which initiate progressive coagulation cascade. Thromboembolism manifests itself in various ways like crebrovascular accident5 pulmonary embolism6 and deep vein thrombosis. The role of microthrombi in acute mountain sickness has also been theoretically suggested. The successful medical treatment results from the fact that all disorders of coagulation return to normal on decent to lower heights i.e. less than 10000 ft (ideally sea levels) and early anticoagulant therapy with adequate mobilization.
This is to highlight the role of high altitude as a factor leading to tendency towards hypercoagulability. Management of cases of thrombosis occurring at high altitude depends on rapid evacuation to lower heights and early anticoagulant therapy.

1. Hussain, A. Niaz
Department of Medicine, Medical Unit II, Military Hospital, Rawalpindi.


1.Funimaki T, Matsutani M, Asai A, et al. Cerebral venous thrombosis due to high altitude polycythemia. Case report. J. Neurosurg., I 986;64: 148-50.
2.Sharma SC. Platelet count and adhesiveness on induction to high altitude by air and road. lnt.J. Biometeorol, 1982;26:219-24.
3.Rowel PM, William ES. Abnormal red cell morphology in venous blood of men climbing at high altitude. Br. Med. J., 1983;286:1396-97.
4.Whittaker S, Winton FR. The apparent viscosity of blood flowing in the isolated hind limb of the dog and its variation with corpuscular concatenation. J. Physical, 1983;78:339-69.
5.Asajin T, Sakoral E, Tanizaki V. et al. Report of medical aspects of Mt. Lhotse and Everest expedition in 1983: with special reference to a case of cerebral venous thrombosis in the altitude. Jpn. J. Mount. Med., 1984;4:98.
6.Winslow RM, Monge CC. Hypoxia, polycythemia and chronic mountain sickness. John Hopkins University Press, Baltimore, 1987, p. 37.


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