GUIDELINES [ back to index ]
23. Management of central venous obstruction (1)
*1 Physical examination
• Chronic swelling of the access arm is the most important clinical sign of central venous stenosis 1 2. The superficial veins may become prominent (collaterals), and pain and paraesthesia may occur.
• Central venous lesions have to be treated only in cases of clinically significant impairing arm swelling, troublesome pain or if they lead to inadequate haemodialysis. Limited oedema or high venous pressure without consequences on the quality of dialysis are acceptable.
*2 Imaging: Angiography of access and complete venous outflow tract
• Only the lateral part of the subclavian vein can be examined ultrasonographically. To completely visualise all mediastinal veins, venography (using DSA technique) is needed. 3 4 This can be achieved as arterio-venography via a transfemoral (see algorithm “Management of Ischaemia (1), *9”) or a transbrachial approach, if the arterial access anastomosis is at or distal to the elbow region and arm swelling does not preclude arterial puncture, or, preferably, after direct puncture of the access 5 6 7.
*3 Assess for other causes
• In patients without a history of central venous catheterisation, extrinsic compression of mediastinal veins (lymphoma, goitre, thoracic aortic aneurysm, mediastinal fibrosis) should be considered. Plain X-rays and/or computed tomography may be helpful for differential diagnosis. If treatment of the underlying disease is not possible or fails to resolve arm swelling, PTA with stent insertion is indicated 8.
• Chronic uni- or bilateral arm swelling can occur secondarily to extensive axillary or mediastinal lymphatic destruction (post-surgery or post-radiation, primary or metastatic lymphoma, primary mediastinal fibrosis). In some cases, such as lymphoma, treatment of the underlying disease will improve arm swelling.
• If venous stenosis or occlusion is excluded, then access ligation may not have any effect on oedema and hence the fistula may be kept unless, as stated above, it cannot be needled or is causing other symptoms.
*4 Thoracic outlet syndrome
• Axillary-subclavian vein thrombosis may be caused by costoclavicular compression, the so called thoracic outlet syndrome. In order to prevent rethrombosis, transaxillary resection of the first rib should be performed 10. A relatively infrequent complication is the thrombosis of the subclavian vein of uncertain aetiology. Thrombolysis with urokinase infusion is successful in most cases, otherwise thrombectomy may be performed 9 10.
*5 Hypercoagulopathy
• Such a condition can be due to reduced levels of protein C and S and factor X or hyperfibrinogenaemia.
*6 PTA (stent implantation)
• Since the late 1980’s, several studies of patients treated with PTA alone have been published. Patency rates of 7 % to 12 % 11 12 at one year were disappointing. Stent implantation has clearly been shown to improve primary one year patency rates to 56 – 76 % 2 8 11 13 14. These figures do not differ significantly from those of surgical intervention, where primary one year patency rates between 80 % and 86 % 1 2 11 14 have been reported.
• Due to the relative invasiveness of surgery for central venous obstructions (see Algorithm “Management of Central Venous Obstruction (2)”), the less invasive interventional therapy , PTA with or without stent implantation,- is recommended as first-line treatment 14 15.
• Stent placement should avoid overlapping the ostium of a patent internal jugular vein to achieve a safe and sufficient result, if possible, since this latter vein is essential for future placement of central catheters. Similarly, a stent placed in the brachio-cephalic trunk must not overlap the ostium of the contralateral trunk, otherwise contralateral stenosis may be produced and preclude future use of the contralateral limb for fistula creation 16.
*7 Local thrombolysis or thrombaspiration
• Little data is available on the use of thrombolytic agents in central vein thrombosis in dialysis patients although successful thrombolysis has been described in cancer patients treated with thrombolytic agents and PTA . 17 18 19