The association between immobility with prolonged sitting and venous thromboembolism has been recognised forw60 yrs, most recently with long distance air travel. The case of a 32-yr-old male, in whom immobility associated with sitting for long periods at a computer represented the major provoking risk factor for his lifethreatening venous thromboembolism, is presented. The authors propose the term "eThrombosis" to describe this 21st Century variant of venous thromboembolism associated with immobility from prolonged sitting. In view of the widespread use of computers in relation to work, recreation and personal communication, the potential burden of eThrombosis may be considerable. The link between prolonged sitting and venous thromboembolism (VTE) was first recognised during the London blitz in World War II when SIMPSON [1] reported fatal pulmonary embolism occurring in persons who had sat for prolonged periods in deck chairs while taking refuge in air-raid shelters. In 1954 HOMANS [2] reported that VTE may occur after prolonged sitting in a number of other situations, such as in aeroplane flights, car trips and even attendance at the theatre. More recently interest has focused on VTE associated with prolonged air travel, due in part to the reported frequency of VTE in up to 10% of high-risk travellers and the trend of increasing air travel with w1 billion passengers flying every year [3,4]. Another sedentary life-style pattern that has developed over recent decades is the extensive use of computers in relation to work, recreation and personal communication. In this report the authors present a case in which immobility associated with sitting for long periods at a computer represented the major provoking risk factor for a life-threatening VTE.
Case reportThe authors report the case of a 32-yr-old male who gave a history of a swollen painful calf 6 weeks previously, which resolved after 10 days. During the 4 weeks prior to presentation he noticed increasing breathlessness on exertion, to the extent that he was breathless during minimal activity. On the day of the presentation he experienced a syncopal episode in which he lost consciousness. He denied haemoptysis or pleuritic pain; there was no family history of VTE. On examination he was afebrile, heart rate 120 beats?min -1 , blood pressure 130 over 95, respiratory rate 20 breaths?min -1 , jugular venous pressure not raised, chest clear on auscultation and prominent facial contusions were noted.The electrocardiogram showed sinus tachycardia and severe right heart strain ( fig. 1); arterial blood gases on room air showed pH 7.45, carbon dioxide arterial tension 3.86 kPa (29 mmHg), arterial oxygen tension 7.45 kPa (56 mmHg), bicarbonate 19 mmol?L -1 , oxygen saturation 93% and the chest radiograph showed prominence of the hila and airspace consolidation of the superior segment of the left lower lobe. A provisional diagnosis of pulmonary embolism was made and this was confirmed by pulmonary angiography with helical computer tomography angiogram, which sho...