Current Medicine Research and Practice

: 2021  |  Volume : 11  |  Issue : 4  |  Page : 181--183

Pulmonary thromboembolism following seated immobility

Lydia Jesurun, Hyma Jose, Anil Thomas, Jency Maria Koshy 
 Department of Medicine, Believers Church Medical College Hospital, Thiruvalla, Kerala, India

Correspondence Address:
Dr. Lydia Jesurun
3BHK, Doctors Quarteres, Believers Church Medical College Hospital, Kuttapuzha, Thiruvalla - 689 103, Kerala


This report describes the development of deep vein thrombosis (DVT) and pulmonary embolism (PE) in a young healthy adult male who was driving an automatic car without interruption. There is mounting evidence that prolonged cramped sitting increases the risk of DVT of the legs and PE. We propose that a newer risk factor of seated immobility syndrome is the reason for this catastrophic development of DVT and PE in this patient.

How to cite this article:
Jesurun L, Jose H, Thomas A, Koshy JM. Pulmonary thromboembolism following seated immobility.Curr Med Res Pract 2021;11:181-183

How to cite this URL:
Jesurun L, Jose H, Thomas A, Koshy JM. Pulmonary thromboembolism following seated immobility. Curr Med Res Pract [serial online] 2021 [cited 2021 Dec 3 ];11:181-183
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Full Text


Venous thromboembolism (VTE) and its complication acute pulmonary embolism (PE) could be fatal if not diagnosed and treated early. There are reports of VTE following long flight journey. However, reports of VTE following automobile journey is very sparse.[1] We report a case of deep vein thrombosis (DVT) and PE in a young adult male due to journey in an automatic car.

 Case Report

A 35-year-old male who is a construction consultant in real estate, teetotaller with no known comorbidities presented to emergency room (ER) with severe left-sided chest pain for 2 days and a history of chills one day prior to his presentation. There was no history of fever, rhinitis, or sore throat. He gave a history of cough with minimal expectoration. There was no history of haemoptysis.

It was a sharp stabbing pain which was pleuritic in nature. It interfered with his sleep. There was no diaphoresis, palpitation, syncope or breathlessness.

The patient also gave a history of upper respiratory tract infection 1 month prior to admission which subsided with symptomatic treatment. In ER, the patient was tachycardic (pulse rate-105/min) and tachypnoeic (respiratory rate-24/min). His blood pressure was normal (140/80 mm of Hg). He maintained 97% saturation on room air. He had no pallor, icterus, cyanosis, clubbing, or generalised lymphadenopathy. Except for bilateral rhonchi in interscapular area, systemic examination was unremarkable.

Investigations revealed neutrophilic leucocytosis. Mild hypoxia (PO2 89.2) was noted on arterial blood gas analysis. Chest X-ray showed left lower zone non-homogeneous opacity with blunting of costophrenic angle [Figure 1]. Right bundle branch block (RBBB) was noted on electrocardiogram (ECG). Cardiac enzymes were normal.{Figure 1}

He was admitted with a probable diagnosis of community-acquired pneumonia with subpulmonic effusion was considered. He was initiated on intravenous antibiotics for the same. In the ward, it was noted that the patient was in intense pain with profuse sweating which was not relieved with tramadol injection. He was noted to have mild hypoxia. On reviewing the history, he mentioned that he had a similar episode 6 days prior to that for which he had attended another health facility where an ECG was done which revealed RBBB. His symptoms had subsided after taking injectable analgesics.

Since the patient had severe pleuritic chest pain and mild hypoxia a remote possibility of pulmonary embolism was considered and D Dimer was sent which was reported as 5099.5ng/ml. We urgently proceeded with computed tomographic pulmonary angiogram. Intraluminal filling defect involving lobar and segmental branches to left lower lobe, segmental branches to inferior lingular segment and posterobasal segment of right lower lobe along with an infarct was noted in the posterobasal segment of the left lower lobe with minimal left pleural effusion [Figure 2].{Figure 2}

We went ahead with a lower limb Doppler to evaluate for the source of thrombus which revealed a thrombus in the left popliteal vein extending to the left superficial femoral vein.

While pondering on why a young male with no comorbidities presented with DVT and PE, we went back and reviewed the history again. The patient had taken a long drive in an automatic car (103 km, 2–3 h travel) in the last week. He also experienced pain in the left leg and his wife had given vigorous massage considering a possibility of muscle pain.

It was interesting to note that DVT was in the left leg which would be immobile while driving an automatic car. The patient also told that he hardly took any breaks while on long drives.

The patient was started on injection low molecular weight heparin (Injection Enoxaparin 60 mg subcutaneous twice daily) on the same day. The patient improved remarkably. His tachycardia and hypoxia settled. After 5 days of heparin, he was switched to oral dabigatran. Rest of his hospital stay was uneventful.

Since the aetiology for VTE was evident in this case, we did not proceed with a prothrombotic workup. During follow-up in the outpatient department, the patient was comfortable. His repeat chest X-ray was normal [Figure 3]. He is currently on tablet dabigatran 150 mg bd at 3rd month.{Figure 3}


VTE encompasses PE, DVT and superficial thrombophlebitis. Interaction of three Virchow factors stasis, hypercoagulability and endothelial injury cause thrombosis.[2] Due to myriad and complex presentation, diagnosis and treatment is frequently delayed. Classic symptoms of PE is seen in only 30% of patients.[3] The classic triad of pleuritic chest pain, dyspnoea and haemoptysis is rare, and only 11% of confirmed cases of PE have clinically apparent DVT.[4]

About 70%–90% of thrombi in acute PE originates in the deep veins of the lower extremities, peritoneal cavity, pelvic cavity veins.[1] Well-known risk factors for PTE include immobility, age, venous stasis, malignancy, fracture, major trauma and procoagulant state.[5] Recently, PTE had been reported in association with different conditions, such as seated immobility thromboembolism (SIT). SIT syndrome would include prolonged sitting in relation to work or recreation including long-distance travel (air, train and road), prolonged computer use at work or in recreation, and other situations associated with seating in cramped conditions such as the theatre.[6] Risk increases with prolonged immobilisation within a confined space in a sitting posture.[7] Driving in a confined space with relative immobility of legs could be one of the many reasons for DVT in automatic car.

One case–control study showed 2.8-fold increased risk of VTE after seated for a long period Healy et al.[8] Liu et al. reported similar case of DVT and PE in a young adult male of age 27 years who was a long haul truck driver emphasising the need for looking into vocational risk factors.[9] Margiotta et al. reported a fatal case of PE after long-distance driving.[10] James Lucerna et al. reported a case of DVT and PE after prolonged tv watching for 8 h in a 57-year-old female with morbid obesity.[11]

Prevention of DVT in young population with no risk factors is possible with proper awareness and teaching about stopping the car and taking intermittent breaks with leg movements.


Acute PE in young adults is not very uncommon. A young adult presenting with acute onset of dyspnoea, PE should be kept a possibility, as most of the time PE is not considered in differential diagnosis while evaluating such patients in emergency. Apart from well-known risk factors for DVT, importance should be given to the vocation, lifestyle of young patients with no comorbidities for screening of DVT and PTE. High index of suspicion is needed to screen for DVT especially in young adult population. Need for proper history taking in the emergency department and high index of suspicion could not be overemphasised. With proper counselling and awareness, some of these catastrophic events could be prevented in younger population.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.


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