Volume 32, Issue 4 , Pages 439-444, October 2006
Central Vein Obstruction in Vascular Access
Article Outline
- Abstract
- Introduction
- Epidemiology and Etiology
- Clinical Findings
- Diagnostic Evaluation
- Treatment
- Summary
- References
- Copyright
Central venous obstruction has become a major problem because of the frequent need for central venous catheters in haemodialysis patients. This article discusses the epidemiology and clinical features of central venous obstruction and the different surgical and interventional alternatives for its treatment.
Keywords: Central vein obstruction, Haemodialysis, Review, Interventional therapy, Veno-venous bypass
Introduction
Central vein catheters are known to be the main risk factor for the development of central vein obstruction (CVO) in haemodialysis (HD) patients. If a functioning arteriovenous (AV) access is created distal to such an obstruction, massive venous hypertension may occur producing incapacitating arm edema, ulceration and tissue loss.
Because of the steady growth of the HD population and the persistently high percentage of late referrals requiring emergency renal replacement therapy (RRT), increasing numbers of HD catheters are being implanted. In Europe between 15% (Germany) and 50% (UK) and in the US even 60% of end-stage renal disease (ESRD) patients start their HD career with a catheter.1 Among prevalent ESRD patients in Europe and the US the percentage of catheter carriers have almost doubled during the last eight years.2 As a consequence, the treatment of CVO constitutes a growing challenge to access surgeons and interventional radiologists.
Surgical treatment of CVO is often difficult and sometimes hazardous, but not always successful. Interventional therapy is less invasive, but it needs a dedicated and experienced radiologist to achieve satisfying results. This article discusses the relative efficacy of the different interventional and surgical options, with particular respect to their long-term results.
Epidemiology and Etiology
The frequency of symptomatic CVO in the HD population has not extensively been investigated. From November 1999 through September 2005, the author performed 611 primary and secondary surgical and interventional procedures on HD access in 401 patients. Twelve interventions (2.0%) were performed for CVO in nine patients (2.2%, [unpublished data]). Among 640 incident HD patients, Chemla et al.3 identified 10 (1.6%) with CVO. In prevalent US and Canadian patients much higher frequencies of CVO (23%–29%,4, 5) have been reported.
Some of these stenoses and occlusions may be attributed to thoracic inlet syndrome,6 previous clavicular fracture, extrinsic compression7, 8 or pacemaker wires.9, 10 The great majority of patients presenting with CVO, however, have a history of central vein catheterization for HD.7
CVO is believed to be caused by chronic endothelial trauma resulting from minimal movements of the catheter against the vein wall, possibly enhanced by thrombophlebitic reactions due to catheter-adherent fibrin sheaths and biofilms. Temporary HD catheters implanted in the right internal jugular vein, which has a more or less straight course to the right atrium, are associated with a lower risk of CVO than left internal jugular vein and subclavian vein catheters,11, 12, 13, 14, 15, 16, 17, 18, 19, 20 (Table 1). Femoral vein cannulation carries a 29% risk of iliofemoral vein stenosis when the catheter remains in place for longer than two weeks.21 Catheter-related infection, and repeated or prolonged catheterization enhance the frequency of CVO.13, 19, 21, 22 Thus “permanent” tunneled catheters are associated with a high incidence of CVO, even when inserted through the right internal jugular vein.23
Table 1. Frequency of central vein stenoses and occlusions following temporary catherterization of the subclavian and the internal jugular vein for hemodialysis
| Author, year [reference] | Subcl. Vein | Int. Jug. Vein | ||
|---|---|---|---|---|
| # | Obstruction | # | Obstruction | |
| Vanherweghem, 198611 | 42 | 33% | ||
| Spinowitz, 198712 | 13 | 46% | ||
| Barrett, 198813 | 36 | 50% | ||
| Schwab, 198814 | 47 | 26% | ||
| Wanscher, 198815 | 53 | 25% | ||
| Cimochowski, 199016 | 32 | 50% | 20 | 0% |
| Schillinger, 199117 | 50 | 42% | 50 | 10% |
| Surratt, 199118 | 40 | 43% | ||
| Hernández, 199319 | 54 | 53% | ||
| Salgado, 200420 (right int. jug. vein) | 127 | 0% | ||
| Salgado, 200420 (left int. jug. vein) | 44 | 9% | ||
Clinical Findings
In otherwise healthy persons, chronic central arm vein obstruction can be compensated by numerous collaterals along the chest wall, in the neck and in the mediastinum. In the majority of these patients signs and symptoms of CVO are mild or completely absent. However, when an AV access is created peripheral to a central venous stenosis or occlusion, the blood flow through the extremity may rise at least four to tenfold above the resting level. In this situation the collateral capacity may be insufficient so that venous hypertension will develop.
Depending on the location of the obstruction and the collateral capacity there is a wide variety of possible clinical findings. When the subclavian vein is affected, venous collaterals will become visible around the shoulder and the upper chest. Moderate to severe and sometimes painful and incapacitating arm swelling (Fig. 1) is the most frequent finding.24 Extreme venous hypertension can lead to skin ulceration and tissue loss.25, 26 Acral skin changes, hyperpigmentation, pincer nail deformity and pseudo-Kaposi's sarcoma, have also been described.27 In more central (brachiocephalic or superior caval) vein obstruction unilateral face and breast swelling (Fig. 3a) may additionally occur.24 Pelvic vein obstruction following femoral vein catherisation frequently cause leg swelling without a thigh access being fashioned, which, of course, would markedly deteriorate with creation of a functioning access.21, 28

Fig. 1.
Massive left arm edema in a 79 year old woman on HD for diabetic nephropathy due to filiform subclavian vein stenosis six months after creation of a brachiocephalic fistula. Note the subcutaneous venous collaterals around the left shoulder.
Swelling may cause difficulties in needling the access with the risk of bleeding and haematoma. Skin ulceration will further enhance the risk of infection and access loss. Therefore, once swelling becomes painful and incapacitating or causes needling or skin problems, CVO should be treated.
Diagnostic Evaluation
Before treatment, exact delineation of the venous pathology is essential. Colour-coded duplex-ultrasound is of limited value for this, because it fails to adequately visualize either the innominate vein or the proximal third of the subclavian vein.29 Although phlebography is still the gold standard for diagnosis of upper extremity venous stenoses and occlusions,30 MR phlebography should be considered, especially in patients with residual renal function.31
Treatment
In HD access-associated CVO, a variety of surgical and interventional, palliative and therapeutic, options have to be discussed.
Access abandonment
The easiest surgical solution for access-associated CVO is ligation of the access, which results in immediate relief of symptoms.20, 22, 27, 32 At the same time ligation is the most frustrating option as the vascular pathology causing the patient's problem is not corrected and the respective extremity is rendered unsuitable for further access procedures. Access abandonment makes creation of a new permanent vascular access necessary, in the other arm or in the leg, and should therefore be performed only when interventional or surgical therapy of CVO is impossible or has failed.
Because CVO frequently occurs bilaterally,16 phlebography should be performed before the creation of a new access in another extremity. It is also advisable to create the new access and allow its maturation before ligating the old one to avoid the further use of a temporary catheter.
Interventional options
Most patients present with long standing symptoms of CVO so that thromboaspiration or thrombolysis alone is unlikely to restore adequate venous patency. However, in selected cases with evidence of fresh thrombus causing total obstruction of a preexisting tight venous stricture, thrombolysis may help to re-establish the stenosed lumen and allow an additional percutaneous transluminal angioplasty (PTA).33, 34
PTA of CVO in HD patients has been reported since the early 1980s.35, 36, 37 Because of frequent restenoses, however, primary one-year patency of PTA alone was less than 40% in most of the studies,5, 38, 39, 40, 41, 42 (Table 2). To reduce the number of re-interventions, several groups have routinely performed stent placement with each PTA procedure (Fig. 2a–c), and most reported improved primary patency rates when compared to PTA alone,24, 34, 40, 41, 43, 44, 45, 46, 47(Table 2). A more moderate use of stents (only for significant rest-stenoses or elastic recoil after PTA, and for early or frequent re-stenoses) has been practiced by other investigators48, 49 with satisfying results. The use of covered stents or endovascular brachytherapy following stent placement does not enhance patency rates.50, 51
Table 2. Results of PTA, stent placement and surgery, for central venous obstructions in hemodialysis patients
| Author, year [reference] | # | Primary Patency | Secondary Patency | |||
|---|---|---|---|---|---|---|
| 1 year | 2 years | 1 years | 2 years | |||
| PTA | Glanz, 198738 | 30 | 35% | 10% | – | – |
| Wisselink, 199339 | 15 | 36% | 0% | 86% | 66% | |
| Quinn, 199540 | 10 | 12% | – | 100% | – | |
| Money, 199541 | 26 | 7% | – | – | – | |
| Lumsden, 19975 | 17 | 17% | – | – | – | |
| Surowiec, 200442 | 35 | 43% | 0% | 80% | 64% | |
| PTA | Shoenfeld, 199443 | 19 | 68% | – | 93% | – |
| Money, 199541 | 13 | 71% | – | – | – | |
| Quinn, 199540 | 8 | 11% | – | 78% | – | |
| Vorwerk, 199544 | 27 | 60% | 60% | – | – | |
| Mickley, 199724 | 14 | 70% | 50% | 100% | 84% | |
| Vesely, 199745 | 20 | 25% | – | 56% | 22% | |
| Haage, 199934 | 50 | 56% | 28% | – | – | |
| Chen, 200346 | 18 | 49% | – | 85% | – | |
| Aytekin, 200447 | 14 | 14% | – | 56% | 33% | |
| Surgery | Wisselink, 199339 | 13 | 86% | 66% | – | – |
| Gradman, 199452 | 9 | 88% | 88% | 100% | 100% | |
| Money, 199541 | 13 | 80% | – | – | – | |
| El-Sabrout, 199953 | 9 | 88% | 88% | 100% | 100% | |
| Haug, 199954 | 6 | 100% | 33% | 100% | 100% | |
| Mickley, 200155 | 6 | 83% | 67% | 100% | 71% | |

Fig. 2.
a. Approximately 50% narrowing of left innominate vein following subclavian vein catheterization for HD access in a 68 year old woman undergoing HD for diabetic nephropathy. Note the pacemaker wire inserted through right internal jugular vein two years earlier, which is not causing innominate or vena caval obstruction. b. Three months after creation of a radio-cephalic AV fistula on her left arm, massive arm edema developed. There is now subtotal occlusion of the left innominate vein. c. Successful PTA and stent placement (Wallstent™, 10
x
60
mm) resulted in immediate relief of symptoms.
Surgical reconstruction
As far as can be deduced from the few reports in the literature,39, 41, 52, 53, 54, 55 the results of surgical reconstruction of mediastinal veins in HD patients are better than those of interventional radiology with primary patency rates of 80% to 90% at one year. These procedures, however, always mean major surgery. Patch angioplasty of a subclavian or innominate vein or orthotopic bypass surgery52, 54, 55 require clavicular division or sternotomy (and general anesthesia) (Fig. 3a–d) and are associated with high rates of postoperative morbidity and mortality. Extra-anatomical bypass (such as axillary-to-internal jugular vein39, 41, 55) is less distressing to the patient but this results in the loss of another central vein for further access.

Fig. 3.
a. Massive left arm and breast swelling two years after creation of a left brachio-cephalic AV fistula for HD in a 59 year old woman with chronic glomerulonephritis. Note the extensive thoracic wall collaterals indicating bilateral CVO. b and c. Bilateral arm phlebography demonstrating complete occlusion of both innominate veins. The central superior vena cava is patent. The patient had had multiple central vein catheters for HD access and during intensive care treatment five years ago for peritonitis following perforated diverticulitis. d. Graft interposition between central cephalic and superior cava (ePTFE 12
mm with external ring support) through a median sternotomy.
Last resort procedures
When the central venous drainage of all four extremities is compromised, construction or maintenance of AV access can be difficult or impossible. In low risk patients fit for median sternotomy, a subclavian artery-to-right atrial appendix bridge graft56 can be constructed, or an axillary vein-to-right atrial bypass53 be performed. In patients unfit for major surgery, fashioning an arterio-arterial loop graft57, 58 can be considered as an alternative to the insertion of a translumbar, transhepatic or transthoracic, cuffed tunneled catheter.59, 60, 61
Summary
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Update on Renal Access and Transplantation — one of a series of educational articles edited by Mr Christopher Gibbons, Swansea, UK.
PII: S1078-5884(06)00213-9
doi:10.1016/j.ejvs.2006.04.011
© 2006 Published by Elsevier Inc.
Volume 32, Issue 4 , Pages 439-444, October 2006
