INTRODUCTION — The central and peripheral venous systems are critical to dialysis vascular access planning, creation, and management. A common problem in the management of patients undergoing hemodialysis is the development of venous obstruction (ie, stenosis, occlusion) involving the thoracic central veins that return blood from the extremity to the heart. An important goal for all clinicians who care for patients with severe renal dysfunction should be to preserve and protect these central veins, a task that is not easily accomplished. Central vein obstruction in a dialysis patient is a serious issue, and it has a greater impact compared with obstruction of a peripheral vein. If central stenosis is allowed to progress, the hemodialysis vascular access may eventually be lost. In addition, the development of central vein obstruction obviates the possibility of creating a new vascular access on the affected side. An unfortunate consequence of the loss of central vein patency for the patient is diminished life expectancy.
The veins of the thoracic central venous system include the intrathoracic segments of the internal jugular vein, subclavian veins, brachiocephalic veins, and the superior vena cava (figure 1). Anatomy, nomenclature, and classification of the thoracic central veins and vein obstruction are described separately and shown in the figure (figure 2). (See "Overview of thoracic central venous obstruction", section on 'Classification'.)
Central vein obstruction associated specifically with upper extremity hemodialysis access is reviewed. General issues related to thoracic central vein obstruction (TCVO) or other non-hemodialysis catheters are reviewed separately. Thrombosis observed in patients with hemodialysis arteriovenous fistulas and grafts is also reviewed separately. (See "Overview of thoracic central venous obstruction" and "Malignancy-related superior vena cava syndrome" and "Catheter-related upper extremity venous thrombosis in adults" and "Hemodialysis arteriovenous graft dysfunction and failure".)
INCIDENCE — The true incidence of TCVO in the dialysis population is not known. The lesion is detected either as an incidental finding when a venogram is performed or because the patient has typical signs or symptoms. If neither of these occurs, the lesion generally goes undetected. Another issue affecting reported incidence rates is the denominator that is used to calculate the percentage of occurrence (eg, is it based upon total dialysis patients examined or upon the number of patients having had prior catheters?). Several factors exert a major influence on the incidence of this pathology, including the frequency with which the population in question is exposed to central venous catheters or to transvenous leads of a cardiac implantable electronic device (CIED) and the specific vein into which these devices have been inserted. It is not surprising that the reported incidence represents a broad range of 3 to 60 percent [1-7].
●In one study, 47 patients with a dysfunctional arteriovenous (AV) fistula were evaluated with an upper extremity venogram. Of these cases, 24 had a history of a central venous catheter [7]. TCVO was observed in 12 cases. Only six of these were symptomatic with swelling of their access arm. All 12 patients had a history of an ipsilateral catheter in the central veins. The 50 percent incidence observed would have been reduced to 12.8 percent had the evaluation been based on the presence of symptoms.
●In another study, 133 patients in a dialysis cohort of 235 cases had venography to evaluate AV hemodialysis access dysfunction [1]. Of this group, 100 patients had peripheral vein stenosis, and 55 (41 percent) had TCVO. Both lesions were present in 42 cases. Only 11 of these patients had symptoms of arm edema that would have suggested the presence of TCVO.
●A study of 69 consecutive patients undergoing placement of right internal jugular vein tunneled catheters, 30 percent (14 of 46 cases) of whom had not had previous catheters, showed evidence of stenosis and/or angulation of the central veins that was sufficiently severe to alter or abandon the catheter insertion procedure [8]. This same approximate incidence in asymptomatic patients was also confirmed in a later study [9].
MECHANISMS OF OBSTRUCTION — TCVO that presents clinically can have multiple etiologies; however, there are three predominant mechanisms of venous obstruction: vein wall thickening, endoluminal obstruction, and extrinsic compression [10]. While the mechanisms involved in these differ, there is some overlap. The etiologies most commonly encountered in patients with hemodialysis vascular access are reviewed below. Other mechanisms are reviewed separately. (See "Overview of thoracic central venous obstruction", section on 'Etiologies'.)
Vein wall thickening — Vein wall thickening is the most common mechanism resulting in TCVO. Vein wall thickening may be caused by de novo smooth muscle hyperplasia, organized mural thrombus, or fibrosis and be secondary to an indwelling foreign object. Because of the constant movement of the thoracic central veins due to respiratory and cardiac activity, the central veins are constantly irritated by an indwelling foreign object. A postmortem histologic study included two groups: those with a catheter <14 days and those with a catheter for >90 days [11]. Evidence of venous injury was seen in both groups with two patterns observed. With the short-term catheters, there were foci of endothelial denudation with adherent thrombi. With the longer-term catheters, venous injury progressed to vein wall thickening due to smooth muscle cell proliferation. In addition, there were focal sites of catheter attachment to the vein wall composed of thrombi in varying stages of organization. (See "Overview of thoracic central venous obstruction", section on 'Intravascular device related'.)
In addition, there is evidence to suggest that high-volume access blood flow can either result in or aggravate these mechanisms [1,12]. While the exact mechanism for this is unknown, it has been postulated that high blood-flow rates related to hemodialysis access predispose to endothelial damage and subsequent stenosis [1].
●In a small cohort of cases with TCVO, flow rates ranged from 1440 to 2900 mL/minute [12].
●In a study involving 525 patients undergoing vascular mapping (27 percent before initiation of hemodialysis), the prevalence of TCVO was 10 percent for the total group and 13 percent among patients with tunneled central venous dialysis catheters [13]. Factors independently associated with TCVO included current use of a tunneled hemodialysis catheter, presence of cardiac rhythm devices, previous fistula or graft, and previous kidney transplant.
De novo venous changes — While TCVO is generally the result of an identifiable instance in which an indwelling foreign object was introduced into the central venous system, it can develop de novo without an identifiable antecedent [1,5,12,14].
●In a study of 57 hemodialysis patients, six patients (10 percent) had de novo TCVO [12]. Each had massive swelling of their access arm, which was located at the elbow in five and at the wrist in one. Three had stenosis of the left subclavian vein and three had stenosis of the left brachiocephalic vein. Among four patients in whom access blood flow volume was available, the average was 2347 mL/min.
●In another review of 69 hemodialysis patients, 14 of 46 patients (30 percent) had TCVO but no antecedent history of central venous intervention [5].
●In a study involving 103 patients with TCVO, 63 percent had no history of prior central venous catheterization [14].
It should be noted that a lack of prior central venous intervention simply means that there was no record. The age and comorbidity burden of patients with chronic kidney disease (CKD) and the nature of the disease makes it unlikely that a patient would arrive at the point of starting dialysis without having had at least a temporary catheter placed, even if documentation of the event is lacking.
Secondary to indwelling venous device — In the dialysis population, the introduction of an indwelling foreign object into the central venous system occurs frequently, with the central venous hemodialysis catheter as the most common device. In general, the frequency of TCVO is directly proportional to the frequency of hemodialysis catheter usage. Peripherally inserted central venous catheters [15,16] and transvenous leads associated with cardiac rhythm devices [17-24] are also problematic. (See "Overview of thoracic central venous obstruction", section on 'Intravascular device related'.)
Central venous catheters — The incidence of central vein stenosis associated with a hemodialysis catheter varies considerably with the vessel used, the population studied, and the type of catheter [1]. An increased incidence of subclavian vein stenosis is also observed with an increased number of inserted catheters, length of time in place, number of dialysis sessions, and incidence of catheter-related infections [6,25,26]. In one study involving 106 hemodialysis patients [27], the prevalence of TCVO among cases with a history of 0 to 1, 2 to 3, and ≥4 central venous catheters was 3.4, 29.4, and 53.8 percent, respectively. TCVO was more common in patients with a history of a subclavian vein catheter than with either an internal jugular or femoral catheter, 48 percent versus 28 and 35 percent, respectively. (See "Overview of thoracic central venous obstruction", section on 'Intravascular device related' and "Catheter-related upper extremity venous thrombosis in adults".)
●Jugular – The right internal jugular vein is the preferred site for the insertion of a hemodialysis access catheter. Although associated with the lowest incidence, TCVO occurs in the range of 10 percent [25,28-30]. This lower incidence has been attributed to the relatively straight pathway the catheter follows from the internal jugular vein into the right brachiocephalic vein and superior vena cava. A catheter inserted through the left internal jugular vein is associated with appreciably more complications than are observed with the right internal jugular vein. Despite its problems, the left internal jugular is the usual site selected as a second choice when cannulation of the right side is not an option.
●Subclavian – For catheters placed into the subclavian vein (not limited to hemodialysis catheters), the incidence of subsequent TCVO is approximately 30 to 50 percent [6,25,27,31]. The primary cause for this high incidence is thought to be the mechanical effects of the intravascular device in relationship to the anatomic configuration of the vein. A study was designed to evaluate the long-term effects of subclavian vein dialysis catheters in 42 patients using serial angiographic evaluation [6]. At the time of catheter removal, 45 percent of patients had stenoses and 7 percent had total thrombosis of the subclavian vein. Follow-up studies revealed that 45 percent of these patients had at least some resolution of these abnormalities during the three-month period following catheter removal. In a retrospective review of 279 central venous infusion catheters in 238 patients [26], catheter-related venous thrombosis occurred in 13 percent of patients with subclavian vein catheters compared with 3 percent of patients with internal jugular vein catheters. The mean time to thrombosis was 36 days for subclavian catheters and 142 days for internal jugular vein catheters.
●Short-term versus long-term catheters – To minimize the risk of developing central vein stenosis, a short-term temporary hemodialysis catheter is frequently advocated; however, these can also be associated with TCVO. In a prospective study, 57 patients with temporary hemodialysis catheters were studied using venography at the time of catheter removal [32]. Although the mean dwell time for the catheters was only 21 days, eight patients (14 percent) had central vein stenosis; in two cases it was greater than 50 percent. There were no differences with respect to rates of stenosis between those with right internal jugular vein and right subclavian vein catheters. However, in an earlier study involving 52 patients with temporary catheters (32 subclavian, 20 internal jugular), 50 percent of the subclavian sites had mild to severe stenosis of the subclavian vein compared with none for the internal jugular cases [33].
●Peripherally inserted central catheters – The peripherally inserted central catheter (PICC) has become widely used. However, PICCs are associated with a high incidence of venous stenosis, particularly in the peripheral veins, but also in the central veins [16,34]. In a review of angiographic studies performed before and after PICC insertion in 150 patients, 7.5 percent of patients with previously normal central venograms developed subsequent angiographic abnormalities after PICC placement, 4.8 percent developed central vein stenosis, and 2.7 percent had central venous occlusion [15]. It has been recommended that PICC lines not be used in patients either at risk for or with known CKD (algorithm 1) [34,35]. (See "Peripherally inserted central catheter (PICC)-related venous thrombosis in adults" and "Approach to the adult patient needing vascular access for chronic hemodialysis", section on 'Strategy for lifelong hemodialysis access'.)
In-stent stenosis — In-stent stenosis appears to be more pronounced with the use of bare-metal stents, which were the device initially used to treat TCVO, compared with a stent-graft [36]. The development of neointimal hyperplasia within a bare-metal stent was a common occurrence and at times aggressive, leading to complete obstruction. In a study involving 46 cases in which a bare-metal stent was placed in a central vein with a mean follow-up of 24 months, 27 cases (59 percent) required 80 reinterventions for obstruction recurrence within the stent [37]. Lesions were treated with angioplasty; however, in 22 cases, an additional stent was required. There is evidence to suggest that refractory lesions requiring a second stent represent a lesion category that has a more aggressive tendency for restenosis compared with native untreated stenosis [38]. For stent-graft, the graft material covering the device limits the development of in-stent stenosis [39], but stenosis can occur at the ends of the stent (ie candy-wrapper stenosis), which is more likely to occur with a stent-graft having bare-metal struts at either end of the device. In one report of 25 cases of TCVO treated with a stent-graft, three cases (12 percent) required treatment for stenosis developing at the end of the device [40].
Cardiac implantable electronic device — Placement of a cardiac implantable electronic device (CIED; eg, cardiac pacemaker, implantable cardioverter defibrillator, cardiac resynchronization) is frequently needed in the dialysis patient. The prevalence of CIED usage in end-stage kidney disease is unknown for certain. In a single-center report involving 1235 hemodialysis patients, the incidence was 10.5 percent (4.4 percent in those with a cardiac pacemaker, and 6.1 percent in those with an implantable cardioverter defibrillator) [41]. Although specific studies in patients with end-stage kidney disease have not been reported, it has become apparent that when placed using a transvenous approach in the general population, these devices are associated with a relatively high frequency (25 to 64 percent) of central vein stenosis [20,22,33]. (See "Overview of thoracic central venous obstruction", section on 'Intravascular device related'.)
Endoluminal occlusion — In the hemodialysis patient, TCVO secondary to endoluminal occlusion may be caused by thrombus or by an indwelling venous device. Central venous catheters and CIEDs can also cause complete occlusion, especially as the lumen is narrowed by neointimal hyperplasia. Vein wall thickening is discussed above for these devices. (See 'Vein wall thickening' above.)
●Central venous thrombosis – The frequency with which any catheter within the central veins precipitates thrombosis of the vein is unclear. However, it is apparent that this complication is more frequently seen with an acute, nontunneled hemodialysis catheter compared with a chronic hemodialysis catheter. Since most of these thrombi are asymptomatic, the frequency with which central venous thrombosis is discovered is related to the aggressiveness for which it is sought in asymptomatic patients. (See "Malfunction of chronic hemodialysis catheters", section on 'Catheter-related central venous thrombosis'.)
The development of a mural thrombus at the point of contact between the hemodialysis catheter tip and the atrium or vessel wall is not uncommon. In addition, with thrombosis of a hemodialysis arteriovenous access, the thrombus is generally limited to the peripheral access; however, in some cases in which there is a central venous lesion, thrombosis within a central venous structure can also occur. Thrombus within the central venous system associated with the access can generally be cleared if addressed early. However, over time, thrombus in contact with the vein wall can become attached and become organized, creating a permanent obstruction. (See "Malfunction of chronic hemodialysis catheters", section on 'Catheter-related atrial thrombus' and "Malfunction of chronic hemodialysis catheters", section on 'Intrinsic thrombus'.)
●Stents and stent-grafts – In addition to stimulating the development of neointimal hyperplasia, if a stent-graft is inadvertently deployed at the confluence of two veins so that it bridges across one of the lumens ("jails" the vessel), it creates an endoluminal obstruction.
Two anatomic sites prone to this complication include the confluence of the internal jugular and subclavian veins and the confluence of the right and left brachiocephalic veins. Unfortunately, jailing of a confluent vessel is not uncommon. In a review of 52 cases in which a central venous stent-graft was placed for TCVO, the confluence of the internal jugular vein was covered in 40 patients (77 percent), and the contralateral brachiocephalic vein was covered in three cases (5.7 percent) [42]. Jailing the internal jugular vein generally does not result in a major problem. In this report, none of the patients experienced neck or facial edema. With a bare-metal stent, the open construction of the device allows for the free flow of blood. It is even possible to use a jailed internal jugular vein for dialysis catheter insertion. This is not the case when the confluence of a brachiocephalic vein is covered with a stent-graft. In this instance, the problem can render the ipsilateral extremity unusable for placement of an AV access.
A diameter of stent that is too large or too small can also create problems. If a stent-graft is oversized, compression of the fabric covering of the stent can buckle and form pleats, which can obstruct the lumen of the device, resulting in TCVO. Undersizing a bare-metal stent/stent-graft can lead to problems. In addition to the risk of migration, if the stent is smaller than the adjacent normal vessel's diameter, it will create a mechanical obstruction. In addition, enlargement of the vein over time after the stent has been placed can also result in or worsen a mechanical obstruction since the size of the stented zone remains static and does not dilate. This creates a permanent endoluminal stenosis, which is not amenable to dilation.
External compression — Not all cases of TCVO are due to intraluminal pathology. There are situations in which the problem is related to external compression from adjacent anatomic structures. Arterial compression and musculoskeletal compression of the venous structures are commonly encountered in association with dialysis vascular access.
●Ectatic aortic arch – One of the most frequent occurrences of external compression resulting in TCVO occurs when the left brachiocephalic vein, enlarged from the AV access, becomes compressed between an ectatic aortic arch and its associated arteries and the sternum. This creates a characteristic compression type of deformity of the left brachiocephalic vein. The fact that this is a true obstruction is attested to by the appearance of collateral vessels (but not always) peripheral to the defect. In one review, some degree of extrinsic compression was observed in 21 of 48 patients (44 percent) [43]. Twelve (25 percent) had mild, six (13 percent) had moderate, and three had (6 percent) severe compression. Collateral veins were seen in 11 (52 percent). All three patients with severe extrinsic compression were symptomatic and were treated with stent placement.
●Costoclavicular junction compression – TCVO due to costoclavicular compression is not a rare occurrence in the hemodialysis population [44-46]; however, the exact incidence is not known. Frequently, the problem goes unrecognized. The exact mechanism for this lesion is not known, but it appears that as the subclavian vein enlarges from increased arteriovenous hemodialysis access blood flow, the vein becomes increasingly vulnerable to compression at the thoracic outlet (figure 3). It has also been postulated that turbulent blood flow occurs at this unique area, promoting the development of neointimal hyperplasia [45]. The general principles established in the treatment of this problem in the nondialysis population are also applicable to the condition occurring in association with dialysis AV access. Angioplasty generally has poor results, and stenting may actually be detrimental [45,46]. Surgical treatment is required, and the bony compression must be treated to assure long-term success [44-46]. (See "Primary (spontaneous) upper extremity deep vein thrombosis", section on 'Thoracic outlet decompression'.)
CLINICAL FEATURES AND DIAGNOSIS — Although many TCVO lesions in the hemodialysis patient are asymptomatic, the clinical picture of the symptomatic lesion is quite typical and diagnostic if the lesion is ipsilateral to an arteriovenous (AV) hemodialysis access.
TCVO causing malfunction of hemodialysis catheters is reviewed separately. (See "Malfunction of chronic hemodialysis catheters".)
Symptoms and signs of TCVO — The symptomatic patient characteristically develops ipsilateral arm edema, which is often progressive and can become severe. Severe extremity edema can cause considerable patient discomfort and increase the patient's risk for serious complications, such as skin ulceration and infection. Frequently, swelling of the ipsilateral shoulder, breast, neck, and face develops as the arm edema progresses [18,21,33,47]. However, superior vena cava (SVC) syndrome is an uncommon complication of either SVC stenosis or obstruction or bilateral brachiocephalic vein narrowing or occlusion in these patients [48,49]. (See "Clinical features, diagnosis, and classification of thoracic central venous obstruction", section on 'Edema and pain'.)
As with any TCVO, collateral veins over the arm and chest are frequently evident. Depending somewhat upon the site of the lesion, these may connect to the veins of the chest wall and through the intercostal veins to the azygos system, or they may drain through the jugular veins or the middle thyroid vein to bypass the blockage. (See "Clinical features, diagnosis, and classification of thoracic central venous obstruction", section on 'Collateral venous patterning'.)
It is unusual for arm edema to occur with even a total obstruction of a peripheral vein (defined as a vein outside of the bony thorax). This is because these lesions do not result in a total obstruction to venous outflow from the extremity, and collateral veins develop into which flow can be diverted, avoiding the development of venous hypertension. It is not until the dialysis outflow reaches the central veins that it is channeled into a single common pathway. When the central veins are obstructed, the increased resistance to flow affects all of the venous structures in the extremity. This global increase in venous pressure causes the exudation of fluid into the tissue. Occasionally, in a patient with both a central and peripheral lesion, the peripheral stenosis appears to prevent the markedly increased central venous pressure that would otherwise result from the central location. In this setting, symptoms may appear only after the peripheral lesion has been treated.
With the development of collaterals, it is possible for the obstruction to be decompressed. In this instance, the symptoms abate, and if flow is adequate, the AV access can continue to function.
Cannulation difficulties — The AV dialysis access can be markedly affected in the patient with significant TCVO. Dialysis treatment becomes increasingly difficult due to problems with cannulating the AV access because of venous hypertension. Fluid accumulation in the subcutaneous tissue makes it more difficult to palpate the access and increases the skin-to-access distance, which in some cases can exceed the length of the dialysis needle. With increasing degrees of edema of the extremity, cannulation of the access becomes increasingly difficult. With increasing resistance as the severity of the lesion progresses, intra-access pressure rises, resulting in dilatation of the vein.
Unlike stenosis in a peripheral vein, which causes significant hyperpulsatility in the access, TCVO generally causes only minimal or no increase in intensity of the pulse. The greater distance, along with the elastic and compliant nature of the veins, serves to dampen the pulse.
Megafistula — In the patient with an AV fistula, the increase in size can reach aneurysmal proportions, resulting in what has been referred to as a megafistula (picture 1A-B). Access blood flow decreases with increasing downstream resistance. This affects the efficiency of dialysis, and, as it progresses, it can eventually lead to access thrombosis. In most instances, a thrombosed AV access does not contain a large volume of clot, and the thrombus is limited to the access [50]. However, markedly dilated veins associated with TCVO can result in a very large clot volume that can extend up to the site of the lesion. Thrombectomy is difficult in these cases, and there are anecdotal reports of fatal pulmonary embolism associated with thrombectomy attempts. (See "Overview of thoracic central venous obstruction".)
Diagnosis — Although not all central vein lesions are hemodynamically significant, significant lesions can usually be diagnosed by physical examination. Central venous obstruction should be suspected in any hemodialysis patient who presents with any of the symptoms and/or signs discussed above. (See 'Symptoms and signs of TCVO' above.).
The presence of massive arm edema in the AV access arm is virtually pathognomonic of TCVO. However, venography is required for diagnosis and localization of the lesion, which may be observed in the subclavian veins, brachiocephalic veins, and even the superior vena cava. At the first sign of extremity edema ipsilateral to an AV access, the patient should be referred for angiographic evaluation. Delay can result in the lesion progressing to the point that it becomes untreatable, resulting in the loss of the access and rendering the extremity unusable for future access placement.
For patients without ipsilateral AV access, duplex ultrasound is the initial study to evaluate venous anatomy. Depending on the clinical scenario, computed tomographic or magnetic resonance venography may be indicated.
An anatomic classification for thoracic central venous obstruction has been described as type 1 through type 4, reflecting increasingly severe venous outflow obstruction (figure 2) [10]. (See "Clinical features, diagnosis, and classification of thoracic central venous obstruction", section on 'Anatomic classification'.)
TREATMENT — The goal of TCVO treatment is twofold: controlling the symptoms of venous obstruction and preserving vascular access that is capable of providing adequate dialysis.
Indications for intervention — The key indication for treatment of TCVO in hemodialysis patients is the presence of pathophysiology, not abnormal anatomy. To qualify for endovascular intervention, a venous stenosis with a >50 percent decrease in the luminal diameter must be associated with clinical/physiological abnormalities [34]. Prophylactic treatment of a stenosis (>50 percent diameter reduction) but not associated with a hemodynamic, functional, or clinical abnormality is not warranted and should not be performed [51-54]. This is especially important for central venous lesions. Asymptomatic TCVO is better managed by simple observation [38].
The success of a conservative approach to asymptomatic lesions was demonstrated in a retrospective study of 86 lesions in 35 patients in which the natural history of high-grade (>50 percent) asymptomatic central venous stenosis in hemodialysis patients and the outcome of treatment with PTA were documented. Differences in the rate of lesion progression between treated, and untreated patients were tabulated. Twenty-eight percent of lesions (24 of 86) were not treated, while the remainder (62 of 86) were treated with angioplasty. No untreated lesion progressed to symptoms, stent placement, or additional stenosis. Eight percent (six cases) of treated cases were followed by stenosis or symptom escalation; one patient developed arm swelling, four required stents, and four developed additional stenosis.
When indicated, several treatment options are available depending on the location and nature of the lesion. However, there are no trials comparing various techniques, and wide variability has been reported for outcomes of endovascular intervention. A critical review of these reports reveals that this is most likely the result of inconsistent inclusion criteria, such as location, length, and severity of the venous obstruction. In addition, very little attention has been paid to differences in the morphology or etiology of the lesions treated. Nevertheless, percutaneous transluminal angioplasty (PTA) with stent placement for angioplasty failure has been adopted as the standard for the treatment of TCVO. This approach is preferred because of its minimally invasive nature compared with surgery for these lesions. (See 'Endovascular outcomes' below and 'Surgical outcomes' below.)
Endovascular outcomes — TCVO associated with hemodialysis arteriovenous (AV) access can be treated using a variety of techniques.
Whether endovascular outcomes differ for AV fistulas compared with AV grafts was reviewed in a retrospective study that included 38 patients (22 with fistulas and 16 with grafts) [55]. Eighty-nine interventions were performed; 83 were angioplasties, and 6 were stent placements. Intervention-free survival for TCVO was longer in patients with AV fistulas compared with AV grafts and in patients who did not previously undergo hemodialysis catheter insertion. Previous catheter placement on the side of the TCVO occurred in 29 of the 38 patients (76 percent). With multivariate analysis, intervention patency remained significantly longer for AV fistulas and in patients who did not have a previous catheter. The primary patency rates (±standard error) at three, six, and nine months in the AV fistula group were 88.5±4.8 percent, 59.4±7.6 percent, and 46±7.9 percent, respectively. In the graft group, the rates were 78.1±7.3 percent, 40.7±9 percent, and 16±7.3 percent, respectively.
Angioplasty — Studies evaluating PTA for the treatment of TCVO are small and retrospective, with reported technical success rates ranging from 70 to 90 percent [3,56-63]. The primary and cumulative patency rates for PTA treatment of TCVO vary widely. Reported six-month primary patency rates are 23 to 63 percent, and six–month cumulative patency rates range between 29 and 100 percent. The reported 12-month primary patency rates range from 12 to 50 percent, with cumulative patency rates between 13 and 100 percent [3,56-63].
A major problem with lesions in the central veins is that many are elastic. It has been postulated that there are actually two types of lesions based upon their response to angioplasty, elastic and inelastic [59]. In one series, 21/28 (70 percent) showed ≥50 percent improvement in the luminal diameter and 7/21 (23 percent) showed no improvement due to the elasticity of the lesion [59]. Subsequently, 81 percent of the successful PTAs restenosed at an average of 7.6 months, while 100 percent of elastic lesions occluded in an average of 2.9 months. The authors proposed stenting for the elastic lesions. (See 'Rescue stenting' below.)
In summary, technical failures will occur in 10 to 30 percent of patients treated with PTA for TCVO. There are patients with TCVO who have elastic lesions that will be unresponsive to PTA. It is also apparent that multiple repeated interventions with close surveillance are required with PTA to maintain patency and prevent occlusion over the long term.
Stenting — Stents have evolved through three generations (stainless-steel stents, nitinol stents, and stent-grafts), and although the reported data for each have shown considerable overlap in patency rates, there is a general impression on the part of many interventionalists that results have progressively improved with each new generation. However, reports in which stainless steel and nitinol stents have been compared [37,64-66] have failed to detect a difference.
Bare-metal stents have come to be referred to as simply stents. There are two types: stainless-steel and nitinol. No differences have been reported between these in the same series. Most of the series that have been reported involve data collected using a stainless-steel stent.
Rescue stenting — The outcomes for stenting for the treatment of TCVO in hemodialysis patients have also been quite variable. It should be noted that in most instances, these stenting procedures should be classified as salvage procedures, assuming that the cases were done for the recommended indications. That being the case, a comparison with PTA results is not appropriate. The comparison would have to be with similar PTA failure cases that were not stented. No such comparisons have been reported. Primary stenting is discussed below. (See 'Primary stenting' below.)
Stenting for TCVO is appropriate in the following situations, provided there are associated hemodynamic or clinical abnormalities [67]:
●Acute elastic recoil (>50 percent) following PTA
●Recurrent stenosis within a three-month period of PTA
For various case series, the primary and cumulative patency rates, respectively, at varying time intervals are below [37,59,60,66,68-75]. All of these series used a stainless-steel stent.
●3 months – 63 to 100 percent; 72 to 100 percent
●6 months – 42 to 89 percent; 55 to 100 percent
●12 months – 14 to 73 percent; 31 to 91 percent
The largest of these series used the Wallstent in 50 hemodialysis patients [72]. Primary patency rates were 92 percent at 3 months, 84 percent at 6 months, and 56 percent at 12 months. Cumulative patency rates were 97 percent at 6 and 12 months. Unfortunately, these results have not been replicated by others. More typical results for the use of stainless steel stents for treating central venous stenosis are exemplified in a study of 20 cases (also using Wallstent) in which primary patency rates at 1, 3, 6, and 12 months were 90, 67, 42, and 25 percent, respectively [73]. Assisted primary rates at 3, 6, and 12 months were 88, 62, and 47 percent, respectively, and cumulative patency rates at 3, 6, 12, and 24 months were 89, 64, 56, and 22 percent, respectively.
A later study of 14 cases using various stents, including nitinol, provided 1-, 3-, 6-, and 12-month primary patency rates of 93, 86, 50, and 14 percent, respectively, and 3-month, 6-month, 12-month, and two-year assisted primary patency rates of 100, 89, 56, and 33 percent, respectively [66]. A series of 16 cases of TCVO treated using a nitinol stent demonstrated 3-, 6-, and 12-month primary patency rates of 81, 74, and 67 percent, respectively [71].
In a larger study that included 147 lesions in 126 hemodialysis patients, stents were used for angioplasty-resistant obstructions [37]. Primary patency was significantly higher in the angioplasty group (mean 24.5 versus 13.4 percent). The average number of interventions per vein was significantly higher in the stented patients compared with angioplasty (2.7 versus 1.5 interventions). Assisted primary patency was similar between the groups. There were no significant differences in patency rates with regard to patient sex, the type of stent used, the vein or veins treated, or the type of lesions.
Primary stenting — The high rate of recurrent stenosis following PTA has led some investigators to suggest primary stent placement to improve patency [60,63,65,66,70,72,74,76-78]. Based upon observational data that stenting does not improve long-term central vein patency and likely necessitate more reinterventions, we suggest that stenting should not be used as the primary intervention; rather, it should be reserved for cases of PTA-resistant lesions and recurrence. (See 'Rescue stenting' above.)
A possible exception to this recommendation is a procedure referred to as recanalization (also sharp-needle recanalization). In this procedure, a TCVO that is a total obstruction is crossed by penetration with a sharp device. In this instance, there is no true vessel wall. A stent is placed to reconstitute the vascular lumen [79]. There are only anecdotal reports of these cases in the literature.
There is considerable overlap when comparing patency rates of primary angioplasty versus primary stent placement for treating central venous stenosis, suggesting no advantage. In addition, secondary interventions appear to be the rule even for stenting, and assisted primary patency rates are generally comparable. These results are similar regardless of whether a stent or stent-graft has been used as the primary intervention in hemodialysis patients [63,80,81].
●A study compared 26 patients who underwent angioplasty alone with 15 patients who underwent primary stent placement [81]. There were no significant differences in patency rates for PTA compared with stent placement. Primary patency rates at 12 and 36 months for PTA were 52 and 20 percent, and assisted primary patency rates were 78 and 33 percent, respectively. Primary patency rates for stent placement at 12 and 36 months were 47 and 7 percent, and assisted primary patency rates were 60 and 20 percent, respectively. Fifteen of 26 patients undergoing angioplasty (58 percent) required repeated interventions because of restenosis, and 14 of 15 patients (93 percent) undergoing stent placement required secondary interventions because of restenosis and combined migration (n = 1) and shortening (n = 6) of the first stent.
●In another study that compared angioplasty (n = 49) versus stent placement (n = 27), primary patency rates at 3, 6, and 12 months for angioplasty were 58, 25, and 29 percent, respectively, compared with 65, 54, and 45 percent, respectively, for stents [63]. Cumulative patency rates at 3, 6, and 12 months were 76, 62, and 53 percent, respectively, with PTA, compared with 72, 55, and 46 percent, respectively, with bare-metal stents.
●In a study of 30 patients, 7 patients underwent primary stent-grafting [80]. Patients who had not undergone a previous procedure had a significantly shorter time to repeat intervention compared with those who had undergone PTA or bare-metal stent placement previously. (See 'Stent-grafting' below.)
Stent-grafting — Stent-grafts have been increasingly used to treat elastic or recurrent venous stenotic lesions; this includes placing them into the central veins. Very few studies, however, have focused on TCVO. In one study, 18 hemodialysis patients with TCVO and 12 with central vein occlusion were treated with a stent-graft [80]. The technical success rate was 100 percent. A prior PTA and/or stent placement had been performed in 23/30 patients. Primary patency rates at 3, 6, 12, and 24 months were 97, 81, 67, and 45 percent, respectively. Primary assisted patency rates at 3, 6, 12, and 24 months were 100, 100, 80, and 75 percent, respectively. Patients who had not undergone a previous procedure had a significantly shorter time to repeat intervention compared with those who had undergone PTA or stent placement previously. Patients with central venous occlusive lesions had a significantly shorter primary patency interval compared with those with stenoses. Twelve patients required further stent-grafts to maintain patency.
Balloon-assisted banding — Even though angioplasty and stenting may be successful in relieving the symptoms of central vein obstruction, the results may be short lived. The alternative of surgery may not be a good choice for one of several reasons. Banding of the access to reduce blood flow and pressure has been shown to be effective in eliminating or at least markedly reducing the patient's symptoms. Balloon-assisted banding has been used for this purpose [8].
This is a combined endovascular-surgical procedure in which a 4 mm (sizes ranging from 3 to 5 mm have been used) angioplasty balloon is used as a mandrel for sizing the lumen created by the banding, which is done through a surgical incision made adjacent to the peri-anastomotic portion of the dialysis access. The goal of the procedure is to produce a controlled decrease in blood flow and pressure. The primary risk of the procedure is thrombosis of the access due to the reduced level of blood flow produced. As one would expect, the risk is greater in cases in which the initial blood flow is in a lower range (less than 800 mL/minute).
In one study, 22 patients with uncontrollable symptoms related to TCVO were treated with this technique [8]. The mean blood flow in this group of cases was 1640 mL/minute (range 870 to 4200 mL/minute). The mean blood flow following banding was 820 mL/minute (412 to 2050 mL/minute). Symptoms resolved in 20 cases and were markedly improved in the other two. Two of the arteriovenous (AV) fistulas failed, one at eight months postprocedure and the other at 13 months.
Surgical outcomes — Surgery is not usually needed; however, in selected cases, surgery can play an important role in the treatment of TCVO associated with hemodialysis access. To justify major surgery, the patient should have severe symptoms of TCVO with access malfunction and an absence of alternative access sites.
Venous bypass — When a total occlusion cannot be crossed with a guidewire, the patient is faced with the problem of intractable venous hypertension with its attendant symptoms or loss of the access unless the access can be decompressed via a surgical bypass. This is a good option because it obviates the symptoms of venous hypertension while preserving dialysis access.
There are several types of bypasses that can be performed. If the obstruction is within the subclavian vein, the simplest approach is to create a cephalic vein or axillary vein to internal jugular vein bypass of the obstructed subclavian segment via a polytetrafluoroethylene bridge graft [82,83]. With a more central obstruction, within the brachiocephalic vein, this ipsilateral option is not available. However, in these cases, it may be possible for the surgeon to create a bypass to the contralateral jugular system. In selected cases, a bypass to the right atrial appendage has been created to successfully salvage the vascular access [84,85].
In one study [85], 11 patients with complete central vein occlusion aged 20 to 70 (mean 46) years underwent atrial appendage to maintain arteriovenous (AV) access in patients. All were cases with no other upper extremity access options. Three bypasses were performed with autogenous vein, and eight were performed with polytetrafluoroethylene. There was one early mortality due to sepsis, and early morbidity was limited to one patient with a symptomatic pericardial effusion. The mean follow-up was 16 (range 3 to 43) months. Sixty-seven and 33 percent of AV fistulas remained functional at 6 and 10 months, respectively, and one patient's fistula remained functional at 21 months. Four patients (36 percent) developed central bypass stenosis or occlusion, one requiring a redo bypass and three requiring angioplasty. Infection occurred in two patients (18 percent), with the removal of autogenous vein graft in one.
Costoclavicular decompression — Costoclavicular decompression involves resection of the first rib or supernumerary rib, or clavicular resection and thorough external venolysis to assure that the adjacent muscle and other tissues are not compressing the vein. As with vein bypass surgery, this approach to management should be reserved for those cases in which symptoms are severe, and there has been significant resistance to other forms of therapy with limited availability of access sites.
In one study [44], 10 patients were treated with costoclavicular decompression. All had severe arm symptoms of venous hypertension in the involved extremity: four had hemodialysis access dysfunction, two had severe arm pain, and one had a pseudoaneurysm. All patients had subclavian vein stenosis at the costoclavicular junction by angiography or intravascular ultrasound. The majority of patients had balloon dilation (mean 2.3 attempts) without success. Six patients underwent transaxillary first rib resection, and four had medial claviculectomy. In all, 80 percent of fistulas remained functionally patent, and all but one patient (who underwent ligation) had complete relief of upper arm edema. The median hospital length-of-stay was two days, and the mean follow-up was seven months (range 1 to 13). There was no mortality or significant morbidity. Five patients later required central venous angioplasty (four subclavian and one brachiocephalic), and three had stents placed (two subclavian, one brachiocephalic). (See "Overview of thoracic outlet syndromes", section on 'Thoracic outlet decompression'.)
TREATMENT FAILURES — For patients who have failed treatment, occlusion of the arteriovenous (AV) access becomes necessary. This will result in a rapid resolution of the symptoms of venous hypertension but creates the necessity for a new vascular access. The continued presence of the TCVO lesion renders the ipsilateral extremity unusable for this purpose.
Arteriovenous access occlusion — There are several ways to occlude the AV access, including:
●Surgical ligation – Surgical ligation requires the patient to go to surgery and have an incision made, followed by the tying of a ligature around the graft to occlude it.
●Manual occlusion – It is possible to thrombose a graft by manually occluding it for 25 to 30 minutes. Although this is not always effective, it is a simple process, and, when effective, it saves the patient from a surgical procedure. This should be done on a nondialysis day to avoid heparin effects.
●Balloon occlusion – The graft can also be occluded by inserting a balloon of appropriate diameter to occlude the fistula and inflating it. The catheter should be filled with 0.75 mL of sterile saline and equipped with a valve to prevent premature deflation. The graft will clot within 25 to 30 minutes. We generally leave the balloon inflated for one hour as a safety measure. This is also best done on a nondialysis day.
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Venous access" and "Society guideline links: Dialysis" and "Society guideline links: Hemodialysis vascular access".)
SUMMARY AND RECOMMENDATIONS
●Thoracic central venous obstruction – Thoracic central venous obstruction (TCVO) that presents clinically can have multiple etiologies; however, three mechanisms predominate and include vein wall thickening (ie, intimal hyperplasia), endoluminal obstruction (eg, thrombus, venous device), and extrinsic compression (eg, thoracic outlet syndrome). (See 'Mechanisms of obstruction' above.)
●Clinical features and diagnosis – Symptomatic patients characteristically develop ipsilateral arm swelling, which can cause considerable patient pain and discomfort. However, not all patients with TCVO are symptomatic. The development of collateral vessels may adequately decompress the venous system. When a patient on hemodialysis presents with evidence of a central venous obstruction, a venogram should be performed as early as possible to confirm the diagnosis and identify the etiology of the obstruction. (See 'Symptoms and signs of TCVO' above and 'Diagnosis' above.)
●Treatment – Treatment becomes necessary if the patient is symptomatic or has hemodynamic problems from the lesion. The approach to managing central venous obstruction is individualized in patients upper extremity hemodialysis access. Efforts should always be made to preserve access whenever possible. (See 'Treatment' above.)
•Endovenous intervention – Balloon venoplasty of the central venous lesion is the initial treatment. If the lesion persists due to elastic recoil after venoplasty to a degree that affects blood flow or it recurs rapidly (within three months or less), placement of a stent can be considered. There is no evidence to suggest that stenting under other circumstances is of any value. (See 'Endovascular outcomes' above.)
•Surgery – Although direct surgical reconstruction of the central veins is complex, patients with symptomatic lesions that are totally occlusive, unresponsive to venoplasty with stenting, or recur rapidly despite angioplasty and stenting should be referred for surgical consultation. (See 'Surgical outcomes' above.)
-For stenotic lesions within the subclavian vein, peripheral to the junction of the internal jugular vein, successful bypass to that vessel will resolve the central venous hypertension.
-For stenotic lesions proximal to the internal jugular vein (eg, within the brachiocephalic or superior vena cava), access occlusion may be necessary.
●Prevention – The use of central venous access devices, particularly centrally inserted central catheters at the subclavian site and peripherally inserted central catheters (PICCs), increase the risk for TCVO. Hemodialysis patients or those who are likely to advance to end-stage kidney disease should be managed in a way that protects the central veins. A positive history or suspicion of a prior central venous catheter should prompt upper extremity duplex ultrasound and possibly venography to evaluate the thoracic central veins prior to permanent hemodialysis arteriovenous access. (See 'Mechanisms of obstruction' above.)
•If a hemodialysis catheter is necessary, every attempt should be made to place a catheter in the right internal jugular vein, with the left internal jugular vein used as an alternative. The subclavian veins should not be used unless there is no plan for the patient to ever have an upper extremity hemodialysis access placed. (See 'Central venous catheters' above.)
•Clinicians should consider the indications for transvenous cardiac implantable electronic devices (CIEDs) carefully in this patient population given the high incidence of central vein lesions associated with them. The potential for loss of the central veins dictates the need to avoid their placement on the same side as hemodialysis vascular access. If such a CIED is already in place, the contralateral arm should be used for the placement of the dialysis access. (See 'Cardiac implantable electronic device' above.)
32 : Impact of short-term hemodialysis catheters on the central veins: a catheter venographic study.
73 : Upper extremity central venous obstruction in hemodialysis patients: treatment with Wallstents.
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