Venous thrombosis is a fundamental pathological entity. Our patient provides an opportunity to consider etiology in terms of Virchow’s classic triad. We also draw attention to the effort syndrome, in which recurrent, vigorous exertion of an upper extremity is thought to produce venous thrombosis by virtue of local endothelial trauma.
- Effort syndrome
- upper limb DVT
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A 44 year old man was referred by his General Practitioner to the A&E department with a 4 to 5 day history of left-sided neck swelling, symptoms of pleuritic chest pain, and weight loss of one stone.
He had just returned from holiday in Africa and had suffered from altitude sickness whilst climbing Mount Kilimanjaro. He had then suffered a prolonged bout of diarrhoea.
At a first visit, the GP had advised fluids because of dehydration. After a few days, the patient developed swelling in the left supraclavicular region with intermittent chest pain. He was, therefore, referred to A&E.
On examination he looked well. There was a non-pulsatile, diffuse swelling, in the left supraclavicular region. It extended to the base of the neck. Its margins were not palpable. The swelling was red, hot, and tender. There was no lymphadenopathy.
The chest was clear and the heart sounds were pure. Abdominal examination was unremarkable.
He was thought to have an abscess. However, chest x rays showed broadening of the left superior mediastinum with a small left basal effusion. Ultrasound of the neck demonstrated extensive thrombus in the left jugular, subclavian, and axillary veins (figure 1). A thoracic CT scan demonstrated diffuse tissue swelling in the left side of the neck and superior mediastinum. CT did not disclose any lymphadenopathy. There were bilateral pleural effusions, more so on the left (figure 2).
The patient was admitted to a medical ward and he was treated for venous thrombosis with low molecular weight heparin initially, then Warfarin. The swelling improved. His CRP, initially significantly elevated (200), returned to normal. His full blood count, renal functions and liver functions were normal
The patient was discharged after 5 days of hospital admission with advice to continue Warfarin for 6 months. He will have another CT scan after 6 weeks.
Spontaneous thrombosis of the axillary or subclavian veins was first postulated as a cause of upper extremity pain and swelling by Sir James Padget in 1875.1 Von Schroetter demonstrated thrombotic occlusion of upper limb veins, hence the Padget-Schroetter syndrome. More recently, the association between strenuous repetitive movement of the upper extremity and axillosubclavian thrombosis has been recognised and termed effort syndrome.2 Apart from iatrogenic factors such as catheter placement, venous thrombosis of the axillary, or subclavian vein may be caused by external compression by an anatomical structure such as a congenital cervical rib or by the pathological development of a local tumour.3
Virchow’s triad explains thrombosis in terms of venous stasis, vessel wall abnormality or disorders of the blood itself.4
In this patient, it is suspected that venous stasis may have been added to local tissue trauma. The patient had worn a rucksack, possibly obstructing venous flow as well as causing trauma to the vessel wall. He had suffered altitude sickness and it is of interest that hypoxia may also produce endothelial injury.5 Finally, he had suffered a period of significant dehydration likely to have been attended by hemoconcentration and increased blood viscosity. In other patients, it is important to bear in mind that the occurrence of thrombosis at an unusual anatomic location may provide the first evidence of a hypercoagulable state, especially if there is a previous personal or a positive family history of thrombosis.6 Suitable investigations would then include a haemobilia screen.
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