TY - JOUR
AU - Jadoul,, Michel
AB - ABSTRACT Background Although superior vena cava (SVC) stenosis may be a life-threatening complication of haemodialysis (HD) catheters, its prevalence and risk factors in HD patients are unknown. Our aim was to assess the prevalence and risk factors for SVC stenosis in HD patients with a tunnelled cuffed catheter (TCC) and to describe its clinical presentation. Methods In this single-centre, retrospective cohort study, all in-centre chronic HD patients carrying a TCC (1 January 2008–31 December 2012) were included (n = 117 patients, 214 TCC, 80 911 catheter-days). SVC stenosis was defined as a diameter reduction >50% on phlebography or computed tomography. Imaging was triggered by clinical SVC stenosis syndrome or vascular access (VA)-related concerns. We recorded demographics, conditions potentially influencing catheter permeability (medications, carriage of thoracic devices), number of TCCs, total duration of TCC carriage, previous arteriovenous VA and last (in use at time of stenosis detection) TCC details (location, diameter and length). VAs created while a TCC was still used were also recorded. Results An SVC stenosis was found in 11 patients (9.4%, 0.14/1000 catheter-days), which represents almost one-quarter of patients undergoing imaging, whatever the cause (11/45). Only two presented with clinically obvious SVC stenosis. The number of TCCs per patient was 2.64 ± 1.8 in the SVC stenosis group versus 1.75 ± 0.94 in the negative group (P = 0.13). On multivariate analysis (Poisson), diabetes {incidence rate ratio [IRR] 4.63 [confidence interval (CI) 1.2–17.8]; P = 0.02} and total duration of TCC carriage [IRR 1.47 (CI 1.2–1.8) per year; P = 0.001] were associated with SVC stenosis, whereas age had a slightly protective effect [IRR 0.96 (CI 0.91–1.01); P = 0.01]. Limitations are the retrospective design, detection and survivor bias. Conclusion SVC stenosis is not a rare condition, is mostly asymptomatic in the absence of a peripheral VA, is strongly associated with diabetes and is promoted by long TCC carriage. Age is slightly protective. catheters, central vein stenosis, haemodialysis, superior vena cava stenosis INTRODUCTION Central vein stenosis (CVS) [i.e. subclavian/innominate veins, superior vena cava (SVC)] is a significant cause of vascular access (VA) failure and causes significant morbidity in haemodialysis (HD) patients. Although the association of CVS with previous central venous devices has been known for decades [1, 2], its actual prevalence remains unknown and is likely to be underestimated since published data report on symptomatic patients [3]. The pathogenesis of CVS remains unclear. A plausible mechanism is the trauma to the venous endothelium caused by the catheter. This intimal injury may induce an early (<14 days) inflammatory response within the vessel wall and the onset of a non-organizing thrombus [4]. Many other factors, such as postural and respiratory movements and high turbulent flow associated with HD, may contribute to increased shear stress, stimulating platelet aggregation, thrombus organization and intimal hyperplasia with subsequent thickening of the venous wall, leading eventually to intravascular thrombosis with venous occlusion [3]. Several risk factors for CVS have been postulated, i.e. the number of total central venous catheters and the duration of catheter carriage [1, 5, 6], subclavian [1, 2, 7] and/or left-sided location [8], history of catheter-related infections [9], larger catheter diameter and the presence of wires of intracardiac devices [10]. However, CVS has been reported even in HD patients without any history of previous central vein catheterization [5, 11], suggesting that the high blood flow of a functional arteriovenous fistula (AVF) or arteriovenous graft (AVG) may play a causative role [11]. The SVC syndrome results from stenosis or occlusion of the SVC or both innominate veins. The classical clinical presentation includes swelling of the upper extremities, face and neck. Without treatment, SVC syndrome may lead to life-threatening complications, such as airway compression due to oedema, downhill oesophageal varices, increased intracranial pressure and pleural effusion. However, the actual prevalence and risk factors of SVC stenosis are unknown. The purpose of this study is thus to assess the prevalence of SVC stenosis, to depict its clinical presentation and to define risk factors for SVC stenosis in a population of prevalent and incident chronic HD patients with a history of carriage of a permanent HD catheter between 2008 and 2012. MATERIALS AND METHODS Patients In this observational retrospective study we included all in-centre chronic HD patients, both prevalent and incident, carrying a tunnelled cuffed catheter (TCC), either internal jugular or subclavian, between 1 January 2008 and 31 December 2012, in a tertiary care hospital (Cliniques universitaires Saint-Luc, Brussels, Belgium). For each patient, demographic and medical history data, as well as medications potentially influencing catheter permeability such as anticoagulants and/or antiplatelet agents (coumarin and heparin derivatives, aspirin, clopidogrel), were extracted from the electronic medical records. We also recorded the conditions that might be considered as risk factors for an SVC stenosis, such as carriage of a venous port, pacemaker or defibrillator, and all episodes of catheter-related bacteraemia. Time spent on chronic HD, the number of previous AVFs or AVGs (VA), the total number of TCCs and characteristics of the last TCC carried during 2012—or the one in use when SVC stenosis was diagnosed [location (right or left, internal jugular or subclavian), brand, diameter, length and duration of carriage]—were also recorded. We further recorded the presence of a VA created while a TCC was still in use. We calculated the number of days the TCC(s) stayed in place in every patient until the diagnosis of SVC stenosis, death, kidney transplantation, transfer to another HD centre, TCC removal after use of a mature AVF or until 31 December 2012, whichever came first. Femoral TCCs and non-tunnelled, temporary catheters were excluded. All patients were dialysed three times a week (4 h in > 90% of cases) using hollow-fibre high-flux or superflux polysulphone dialysers (Fresenius, Bad Homburg, Germany). The study protocol was performed in accordance with the Helsinki Declaration and was approved by the Ethics Committee of the Université catholique de Louvain. Endpoint and definitions The endpoint of this study was SVC stenosis or thrombosis. This diagnosis was made in two situations: Clinically evident SVC stenosis: swelling of the face, neck and/or upper part of the chest, extending in some cases to the proximal part of the upper limbs. The SVC stenosis then had to be confirmed by a venography showing significant stenosis of the SVC (see below). SVC stenosis diagnosed radiologically, without the typical clinical signs described above, in the context of any clinical situation (i.e. VA-related concerns; isolated arm, breast or face oedema) leading to the prescription of a venography or a standard chest computed tomography (CT) with contrast. Catheter malfunction was defined as a persistent inability to achieve a blood flow >250 mL/min (despite postural changes of the patient, additional flushing and use of urokinase as a catheter lock for three consecutive HD sessions). In patients carrying a recently created AVF while still using a TCC, indications of a venography included arm oedema, impaired AVF maturation, hand ischaemia or decreased thrill. Criteria defining a significant stenosis of the SVC were set according to those proposed by Lumsden et al. [12] in 1997, currently widely used in the field of veno-occlusive diseases; that is, a stenosis is significant when the diameter reduction is >50% with or without upstream collaterals. Stenoses of superior central veins other than the SVC were not recorded as SVC stenosis, even in case of clinical SVC syndrome (i.e. bilateral subclavian or innominate veins occlusion). Diagnostic venography was performed over both lumens of the TCC (in case of TCC dysfunction) or by direct VA puncture in patients with VA-related concerns. When appropriate, percutaneous balloon angioplasty of the SVC was performed after TCC removal over a guidewire and local administration of 3000 U of heparin. The balloon size was determined according to the angiographic findings (12–18 mm); after the insertion of the guide wire, balloons were inflated at 8–12 atm for 60 s. A technical success was defined by a residual stenosis <30%. A bare self-expanding nitinol stent (Sinus-XL stent; Optimed, Ettlingen, Germany) was placed in case of elastic vein recoil leading to a significant residual stenosis after angioplasty, or for relapsing stenosis. Restenosis was defined as a previously treated segment with an angiographic >50% stenosis. All venographies were performed by the same interventional radiologist (F.H.), except in Patient 4 (whose images were reviewed by F.H.). All venographies and chest CTs performed in included patients during follow-up, whatever the indication, were reviewed retrospectively. To retrieve possibly missed cases of SVC stenosis, we screened the medical imaging database, looking after the billing codes associated with venous angioplasty and stenting procedures. Statistical analysis For each patient, the total time on HD was retrieved from the charts. The incidence rate of SVC stenosis was calculated as a person-time rate with the numerator equal to the number of observed episodes of SVC stenosis over the period of interest and was standardized to 1000 catheter-days per patient. The incidence rate per categorical explanatory variable was corrected for the risk period (catheter-days per patient). Univariate analysis was performed using chi-square for categorical variables and t-test for continuous variables. Incidence rate ratios (IRRs) were calculated using Poisson regression, adjusting for variables showing a significant association with endpoint in univariate analysis. Statistical significance level was set at P < 0.05. Given that the duration of the last TCC was associated with SVC stenosis in the group with two or more TCCs (t-test 2.26; P = 0.043), but not in the group with only one TCC, we created a binary variable (0/1) to flag patients who had more than one TCC. RESULTS A total of 117 patients (59 males), 214 TCC and 80 911 catheter-days, were included (i.e. 100% of the candidate patients and catheter-days). Overall, patients were 65.9 ± 15 years of age and 43.5% were diabetic. TCCs were carried for 697 (range 44–4246) days. The median number of TCCs per patient was 1.8 (range 1–7). All TCCs were routinely locked with heparin 5000 IU/mL. Table 1 shows the main demographic characteristics of the included patients as well as those of the SVC stenosis group compared with the SVC stenosis negative group, without adjustments. The use of antiplatelet agents, oral anticoagulants and thoracic venous devices was not significantly different between groups (data not shown). Table 1 Patients demographics and catheter-related factors in the SVC stenosis group compared with the SVC stenosis–negative group Total SVC stenosisgroup SVC stenosis–negative group P-value (n = 117) (n = 11) Venography (n = 34) No venography (n = 72) All (n = 106) Age (years), mean (SD) 66 (11.9) 57.9 (11) 68.4 (6.8) 66.2 (12.3) 66.8 (11.8) 0.02 Diabetes, n (%) 51 (43.6) 9 (81.8) 11 (30.5) 36 (51.4) 42 (39.6) 0.007 BMI (kg/m2), mean (SD) 24.9 (4.4) 26.5 (4.7) 27.1 (5.1) 24.2 (3.9) 24.7 (4.3) 0.2 HD vintage (days)  Mean (SD) 1202 (953) 1503 (1303) 1250 (693) 1131 (937) 1176 (1279) 0.3  Median (range) 720 (60–6126) 1640 (115–4246) 1037 (270–3780) 641 (60–6126) 709 (60–6126) Number of AVF per patient 0.2  Mean (SD) 0.85 (0.67) 1.1 (0.9) 1.2 (0.5) 0.8 (0.7) 0.8 (0.65)  Median (range) 1 (0–3) 1 (1–3) 1 (0–3) 1 (0–3) 1 (0–3) Total number of TCCs per patient 0.1  Mean (SD) 1.84 (1.02) 2.64 (1.8) 2.8 (1.7) 1.6 (0.7) 1.75 (0.94)  Median (range) 1 (1–7) 2 (1–7) 2 (1–6) (1–5) 1 (1–6) Catheter-days per patient 0.08  Mean (SD) 677 (548) 1302 (1218) 1044 (813) 525 (391) 634 (691)  Median (range) 375 (44–4246) 1350 (44–4246) 543 (218–3780) 343 (50–2338) 371 (50–3780) Characteristics of last TCC  Duration (days) 0.2  Mean (SD) 391 (297) 250 (192) 592 (455) 360 (260) 400 (299)  Median (range) 240 (11–3780) 240 (21–1035) 309 (30–3780) 225 (11–2180) 241 (11–3780) Side, n (%)  Right 96 (82.1) 8 (72.7) 33 (91.7) 55 (78.5) 88 (83) 0.5  Left 21 (17.9) 3 (27.3) 3 (8.3) 15 (21.4) 18 (17) Vein, n (%)  Jugular 110 (94) 11 (100) 32 (88.9) 67 (95.7) 99 (93.4) 0.4  Subclavian 7 (6) 0 4 (11.1) 3 (4.3) 7 (6.6) Brand, n (%)  Hemosplit 85 (72.6) 7 (63.6) 25 (70) 53 (75.7) 78 (73.6) 0.8  DuraFlow 11 (9.4) 1 (9.1) 2 (5) 7 (10) 9 (8.5)  Arrow 2 (2.6) 1 (9.1) 0 0 2 (1.9)  Other 8 (6.8) 1 (9.1) 5 (15) 2 (2.9) 7 (6.6)  Unknown 10 (8.5) 1 (9.1) 4 (11) 15 (21.4) 19 (17.9) Length (cm), n (%) 0.8  19 27 (23.1) 3 (36.4) 5 (15) 18 (25.7) 23 (21.7)  23 43 (36.8) 1 (27.3) 14 (40) 28 (40) 42 (39.6)  24 6 (5.1) 0 0 6 (8.6) 6 (5.7)  26 2 (1.7) 0 2 (5) 0 2 (1.9)  27 13 (11.1) 2 (18.2) 2 (5) 9 (12.9) 11 (10.4)  28 10 (1.7) 0 0 2 (2.9) 2 (1.9)  Unknown 21 (17.5) 2 (18.2) 7 (20) 12 (17.1) 19 (17.9) Diameter (F), n (%) 0.4  13 1 (0.85) 1 (9.1) 0 0 0  13.5 1 (0.85) 0 0 1 (1.4) 1 (0.94)  14 1 (0.85) 0 0 1 (1.4) 1 (0.94)  14.5 30 (25.6) 5 (45.5) 6 (17) 19 (27.1) 25 (23.6)  15 1 (0.85) 0 0 1 (1.4) 1 (0.94)  15.5 5 (4.3) 1 (9.1) 2 (5.5) 2 (2.9) 4 (3.8)  16 2 (1.7) 0 0 2 (2.9) 2 (1.9)  Unknown 76 (65) 4 (36.4) 22 (61) 50 (71.4) 72 (67.9) Total SVC stenosisgroup SVC stenosis–negative group P-value (n = 117) (n = 11) Venography (n = 34) No venography (n = 72) All (n = 106) Age (years), mean (SD) 66 (11.9) 57.9 (11) 68.4 (6.8) 66.2 (12.3) 66.8 (11.8) 0.02 Diabetes, n (%) 51 (43.6) 9 (81.8) 11 (30.5) 36 (51.4) 42 (39.6) 0.007 BMI (kg/m2), mean (SD) 24.9 (4.4) 26.5 (4.7) 27.1 (5.1) 24.2 (3.9) 24.7 (4.3) 0.2 HD vintage (days)  Mean (SD) 1202 (953) 1503 (1303) 1250 (693) 1131 (937) 1176 (1279) 0.3  Median (range) 720 (60–6126) 1640 (115–4246) 1037 (270–3780) 641 (60–6126) 709 (60–6126) Number of AVF per patient 0.2  Mean (SD) 0.85 (0.67) 1.1 (0.9) 1.2 (0.5) 0.8 (0.7) 0.8 (0.65)  Median (range) 1 (0–3) 1 (1–3) 1 (0–3) 1 (0–3) 1 (0–3) Total number of TCCs per patient 0.1  Mean (SD) 1.84 (1.02) 2.64 (1.8) 2.8 (1.7) 1.6 (0.7) 1.75 (0.94)  Median (range) 1 (1–7) 2 (1–7) 2 (1–6) (1–5) 1 (1–6) Catheter-days per patient 0.08  Mean (SD) 677 (548) 1302 (1218) 1044 (813) 525 (391) 634 (691)  Median (range) 375 (44–4246) 1350 (44–4246) 543 (218–3780) 343 (50–2338) 371 (50–3780) Characteristics of last TCC  Duration (days) 0.2  Mean (SD) 391 (297) 250 (192) 592 (455) 360 (260) 400 (299)  Median (range) 240 (11–3780) 240 (21–1035) 309 (30–3780) 225 (11–2180) 241 (11–3780) Side, n (%)  Right 96 (82.1) 8 (72.7) 33 (91.7) 55 (78.5) 88 (83) 0.5  Left 21 (17.9) 3 (27.3) 3 (8.3) 15 (21.4) 18 (17) Vein, n (%)  Jugular 110 (94) 11 (100) 32 (88.9) 67 (95.7) 99 (93.4) 0.4  Subclavian 7 (6) 0 4 (11.1) 3 (4.3) 7 (6.6) Brand, n (%)  Hemosplit 85 (72.6) 7 (63.6) 25 (70) 53 (75.7) 78 (73.6) 0.8  DuraFlow 11 (9.4) 1 (9.1) 2 (5) 7 (10) 9 (8.5)  Arrow 2 (2.6) 1 (9.1) 0 0 2 (1.9)  Other 8 (6.8) 1 (9.1) 5 (15) 2 (2.9) 7 (6.6)  Unknown 10 (8.5) 1 (9.1) 4 (11) 15 (21.4) 19 (17.9) Length (cm), n (%) 0.8  19 27 (23.1) 3 (36.4) 5 (15) 18 (25.7) 23 (21.7)  23 43 (36.8) 1 (27.3) 14 (40) 28 (40) 42 (39.6)  24 6 (5.1) 0 0 6 (8.6) 6 (5.7)  26 2 (1.7) 0 2 (5) 0 2 (1.9)  27 13 (11.1) 2 (18.2) 2 (5) 9 (12.9) 11 (10.4)  28 10 (1.7) 0 0 2 (2.9) 2 (1.9)  Unknown 21 (17.5) 2 (18.2) 7 (20) 12 (17.1) 19 (17.9) Diameter (F), n (%) 0.4  13 1 (0.85) 1 (9.1) 0 0 0  13.5 1 (0.85) 0 0 1 (1.4) 1 (0.94)  14 1 (0.85) 0 0 1 (1.4) 1 (0.94)  14.5 30 (25.6) 5 (45.5) 6 (17) 19 (27.1) 25 (23.6)  15 1 (0.85) 0 0 1 (1.4) 1 (0.94)  15.5 5 (4.3) 1 (9.1) 2 (5.5) 2 (2.9) 4 (3.8)  16 2 (1.7) 0 0 2 (2.9) 2 (1.9)  Unknown 76 (65) 4 (36.4) 22 (61) 50 (71.4) 72 (67.9) BMI, body mass index. Hemosplit: Bard Access Systems, C.R. Bard, Murray Hill, NJ, USA; DuraFlow: AngioDynamics, Latham, NY, USA; Arrow: Teleflex, Athlone, Westmeath, Ireland. Table 1 Patients demographics and catheter-related factors in the SVC stenosis group compared with the SVC stenosis–negative group Total SVC stenosisgroup SVC stenosis–negative group P-value (n = 117) (n = 11) Venography (n = 34) No venography (n = 72) All (n = 106) Age (years), mean (SD) 66 (11.9) 57.9 (11) 68.4 (6.8) 66.2 (12.3) 66.8 (11.8) 0.02 Diabetes, n (%) 51 (43.6) 9 (81.8) 11 (30.5) 36 (51.4) 42 (39.6) 0.007 BMI (kg/m2), mean (SD) 24.9 (4.4) 26.5 (4.7) 27.1 (5.1) 24.2 (3.9) 24.7 (4.3) 0.2 HD vintage (days)  Mean (SD) 1202 (953) 1503 (1303) 1250 (693) 1131 (937) 1176 (1279) 0.3  Median (range) 720 (60–6126) 1640 (115–4246) 1037 (270–3780) 641 (60–6126) 709 (60–6126) Number of AVF per patient 0.2  Mean (SD) 0.85 (0.67) 1.1 (0.9) 1.2 (0.5) 0.8 (0.7) 0.8 (0.65)  Median (range) 1 (0–3) 1 (1–3) 1 (0–3) 1 (0–3) 1 (0–3) Total number of TCCs per patient 0.1  Mean (SD) 1.84 (1.02) 2.64 (1.8) 2.8 (1.7) 1.6 (0.7) 1.75 (0.94)  Median (range) 1 (1–7) 2 (1–7) 2 (1–6) (1–5) 1 (1–6) Catheter-days per patient 0.08  Mean (SD) 677 (548) 1302 (1218) 1044 (813) 525 (391) 634 (691)  Median (range) 375 (44–4246) 1350 (44–4246) 543 (218–3780) 343 (50–2338) 371 (50–3780) Characteristics of last TCC  Duration (days) 0.2  Mean (SD) 391 (297) 250 (192) 592 (455) 360 (260) 400 (299)  Median (range) 240 (11–3780) 240 (21–1035) 309 (30–3780) 225 (11–2180) 241 (11–3780) Side, n (%)  Right 96 (82.1) 8 (72.7) 33 (91.7) 55 (78.5) 88 (83) 0.5  Left 21 (17.9) 3 (27.3) 3 (8.3) 15 (21.4) 18 (17) Vein, n (%)  Jugular 110 (94) 11 (100) 32 (88.9) 67 (95.7) 99 (93.4) 0.4  Subclavian 7 (6) 0 4 (11.1) 3 (4.3) 7 (6.6) Brand, n (%)  Hemosplit 85 (72.6) 7 (63.6) 25 (70) 53 (75.7) 78 (73.6) 0.8  DuraFlow 11 (9.4) 1 (9.1) 2 (5) 7 (10) 9 (8.5)  Arrow 2 (2.6) 1 (9.1) 0 0 2 (1.9)  Other 8 (6.8) 1 (9.1) 5 (15) 2 (2.9) 7 (6.6)  Unknown 10 (8.5) 1 (9.1) 4 (11) 15 (21.4) 19 (17.9) Length (cm), n (%) 0.8  19 27 (23.1) 3 (36.4) 5 (15) 18 (25.7) 23 (21.7)  23 43 (36.8) 1 (27.3) 14 (40) 28 (40) 42 (39.6)  24 6 (5.1) 0 0 6 (8.6) 6 (5.7)  26 2 (1.7) 0 2 (5) 0 2 (1.9)  27 13 (11.1) 2 (18.2) 2 (5) 9 (12.9) 11 (10.4)  28 10 (1.7) 0 0 2 (2.9) 2 (1.9)  Unknown 21 (17.5) 2 (18.2) 7 (20) 12 (17.1) 19 (17.9) Diameter (F), n (%) 0.4  13 1 (0.85) 1 (9.1) 0 0 0  13.5 1 (0.85) 0 0 1 (1.4) 1 (0.94)  14 1 (0.85) 0 0 1 (1.4) 1 (0.94)  14.5 30 (25.6) 5 (45.5) 6 (17) 19 (27.1) 25 (23.6)  15 1 (0.85) 0 0 1 (1.4) 1 (0.94)  15.5 5 (4.3) 1 (9.1) 2 (5.5) 2 (2.9) 4 (3.8)  16 2 (1.7) 0 0 2 (2.9) 2 (1.9)  Unknown 76 (65) 4 (36.4) 22 (61) 50 (71.4) 72 (67.9) Total SVC stenosisgroup SVC stenosis–negative group P-value (n = 117) (n = 11) Venography (n = 34) No venography (n = 72) All (n = 106) Age (years), mean (SD) 66 (11.9) 57.9 (11) 68.4 (6.8) 66.2 (12.3) 66.8 (11.8) 0.02 Diabetes, n (%) 51 (43.6) 9 (81.8) 11 (30.5) 36 (51.4) 42 (39.6) 0.007 BMI (kg/m2), mean (SD) 24.9 (4.4) 26.5 (4.7) 27.1 (5.1) 24.2 (3.9) 24.7 (4.3) 0.2 HD vintage (days)  Mean (SD) 1202 (953) 1503 (1303) 1250 (693) 1131 (937) 1176 (1279) 0.3  Median (range) 720 (60–6126) 1640 (115–4246) 1037 (270–3780) 641 (60–6126) 709 (60–6126) Number of AVF per patient 0.2  Mean (SD) 0.85 (0.67) 1.1 (0.9) 1.2 (0.5) 0.8 (0.7) 0.8 (0.65)  Median (range) 1 (0–3) 1 (1–3) 1 (0–3) 1 (0–3) 1 (0–3) Total number of TCCs per patient 0.1  Mean (SD) 1.84 (1.02) 2.64 (1.8) 2.8 (1.7) 1.6 (0.7) 1.75 (0.94)  Median (range) 1 (1–7) 2 (1–7) 2 (1–6) (1–5) 1 (1–6) Catheter-days per patient 0.08  Mean (SD) 677 (548) 1302 (1218) 1044 (813) 525 (391) 634 (691)  Median (range) 375 (44–4246) 1350 (44–4246) 543 (218–3780) 343 (50–2338) 371 (50–3780) Characteristics of last TCC  Duration (days) 0.2  Mean (SD) 391 (297) 250 (192) 592 (455) 360 (260) 400 (299)  Median (range) 240 (11–3780) 240 (21–1035) 309 (30–3780) 225 (11–2180) 241 (11–3780) Side, n (%)  Right 96 (82.1) 8 (72.7) 33 (91.7) 55 (78.5) 88 (83) 0.5  Left 21 (17.9) 3 (27.3) 3 (8.3) 15 (21.4) 18 (17) Vein, n (%)  Jugular 110 (94) 11 (100) 32 (88.9) 67 (95.7) 99 (93.4) 0.4  Subclavian 7 (6) 0 4 (11.1) 3 (4.3) 7 (6.6) Brand, n (%)  Hemosplit 85 (72.6) 7 (63.6) 25 (70) 53 (75.7) 78 (73.6) 0.8  DuraFlow 11 (9.4) 1 (9.1) 2 (5) 7 (10) 9 (8.5)  Arrow 2 (2.6) 1 (9.1) 0 0 2 (1.9)  Other 8 (6.8) 1 (9.1) 5 (15) 2 (2.9) 7 (6.6)  Unknown 10 (8.5) 1 (9.1) 4 (11) 15 (21.4) 19 (17.9) Length (cm), n (%) 0.8  19 27 (23.1) 3 (36.4) 5 (15) 18 (25.7) 23 (21.7)  23 43 (36.8) 1 (27.3) 14 (40) 28 (40) 42 (39.6)  24 6 (5.1) 0 0 6 (8.6) 6 (5.7)  26 2 (1.7) 0 2 (5) 0 2 (1.9)  27 13 (11.1) 2 (18.2) 2 (5) 9 (12.9) 11 (10.4)  28 10 (1.7) 0 0 2 (2.9) 2 (1.9)  Unknown 21 (17.5) 2 (18.2) 7 (20) 12 (17.1) 19 (17.9) Diameter (F), n (%) 0.4  13 1 (0.85) 1 (9.1) 0 0 0  13.5 1 (0.85) 0 0 1 (1.4) 1 (0.94)  14 1 (0.85) 0 0 1 (1.4) 1 (0.94)  14.5 30 (25.6) 5 (45.5) 6 (17) 19 (27.1) 25 (23.6)  15 1 (0.85) 0 0 1 (1.4) 1 (0.94)  15.5 5 (4.3) 1 (9.1) 2 (5.5) 2 (2.9) 4 (3.8)  16 2 (1.7) 0 0 2 (2.9) 2 (1.9)  Unknown 76 (65) 4 (36.4) 22 (61) 50 (71.4) 72 (67.9) BMI, body mass index. Hemosplit: Bard Access Systems, C.R. Bard, Murray Hill, NJ, USA; DuraFlow: AngioDynamics, Latham, NY, USA; Arrow: Teleflex, Athlone, Westmeath, Ireland. During the study period, 75 patients started chronic HD. Thirty peripheral VAs (29 AVFs and 1 AVG) were created while a TCC was still used for HD (11 AVFs were ipsilateral to the TCC), and conversely six patients had a maturating AVF (three ipsilateral to the TCC) when a TCC was placed. Eight venographies were performed because of AVF- or AVG-related concerns, including arm oedema (n = 1), increased venous pressures (n = 4), impaired access maturation (n = 2) and prolonged haemostasis (n = 1). Only two showed CVS (one at the subclavian vein level in the patient with arm oedema and one at the innominate vein level in an AVF with increased venous pressures); the others documented a peripheral vein stenosis. Two patients, one of whom was carrying a left AVF ipsilateral to the TCC, had AVF failure due to thrombosis. SVC stenosis During follow-up, 45/117 patients underwent venography in the setting of one of the clinical situations detailed in the ‘Materials and methods’ section. Eleven patients had an SVC stenosis (9.4%, 0.14 case/1000 catheter-days). Only two of them (Patients 3 and 4) presented with clinically evident SVC syndrome (Table 2). None of them had concomitant bilateral occlusion of innominate veins. Interestingly, both patients had been diagnosed with a ‘food allergy’ in the emergency room 2 days before. Table 2 Characteristics of the 11 patients carrying a TCC and diagnosed with an SVC stenosis Patient Age (years) BMI (kg/m2) Diabetes Thoracic venous devices HD vintage (days) TCC (n) Clinical presentation Maturating AVF Relapse during follow-up Treatment Catheter removal 1 80 35.6 Yes No 248 1 Asymptomatic No No No No 2 50 27.8 Yes No 2040 1 TCC malfunction No No PTA Yes 3 34 22.3 Yes No 252 1 SVC syndrome No Yes Local lysis/PTA Yes 4 37 19.3 Yes No 1648 4 SVC syndrome No No Systemic lysis / PTA Yes 5 55 18.4 No No 2871 2 Arm oedema No No No Yes 6 53 33.4 Yes No 2010 3 TCC malfunction No No PTA Yes 7 69 20.3 No No 4246 7 TCC malfunction No No PTA/stent Yes 8 69 30.1 Yes PM 1640 6 TCC malfunction No No PTA Yes 9 60 26.4 Yes PAC 118 1 Asymptomatic No NA No No 10 65 30.8 Yes No 115 1 TCC malfunction Yes No No Yes 11 65 26.9 Yes No 1350 2 TCC malfunction No Yes PTA/stent Yes Patient Age (years) BMI (kg/m2) Diabetes Thoracic venous devices HD vintage (days) TCC (n) Clinical presentation Maturating AVF Relapse during follow-up Treatment Catheter removal 1 80 35.6 Yes No 248 1 Asymptomatic No No No No 2 50 27.8 Yes No 2040 1 TCC malfunction No No PTA Yes 3 34 22.3 Yes No 252 1 SVC syndrome No Yes Local lysis/PTA Yes 4 37 19.3 Yes No 1648 4 SVC syndrome No No Systemic lysis / PTA Yes 5 55 18.4 No No 2871 2 Arm oedema No No No Yes 6 53 33.4 Yes No 2010 3 TCC malfunction No No PTA Yes 7 69 20.3 No No 4246 7 TCC malfunction No No PTA/stent Yes 8 69 30.1 Yes PM 1640 6 TCC malfunction No No PTA Yes 9 60 26.4 Yes PAC 118 1 Asymptomatic No NA No No 10 65 30.8 Yes No 115 1 TCC malfunction Yes No No Yes 11 65 26.9 Yes No 1350 2 TCC malfunction No Yes PTA/stent Yes BMI, body mass index; NA, not applicable; PAC, venous port; PM, pacemaker; PTA, percutaneous angioplasty. Table 2 Characteristics of the 11 patients carrying a TCC and diagnosed with an SVC stenosis Patient Age (years) BMI (kg/m2) Diabetes Thoracic venous devices HD vintage (days) TCC (n) Clinical presentation Maturating AVF Relapse during follow-up Treatment Catheter removal 1 80 35.6 Yes No 248 1 Asymptomatic No No No No 2 50 27.8 Yes No 2040 1 TCC malfunction No No PTA Yes 3 34 22.3 Yes No 252 1 SVC syndrome No Yes Local lysis/PTA Yes 4 37 19.3 Yes No 1648 4 SVC syndrome No No Systemic lysis / PTA Yes 5 55 18.4 No No 2871 2 Arm oedema No No No Yes 6 53 33.4 Yes No 2010 3 TCC malfunction No No PTA Yes 7 69 20.3 No No 4246 7 TCC malfunction No No PTA/stent Yes 8 69 30.1 Yes PM 1640 6 TCC malfunction No No PTA Yes 9 60 26.4 Yes PAC 118 1 Asymptomatic No NA No No 10 65 30.8 Yes No 115 1 TCC malfunction Yes No No Yes 11 65 26.9 Yes No 1350 2 TCC malfunction No Yes PTA/stent Yes Patient Age (years) BMI (kg/m2) Diabetes Thoracic venous devices HD vintage (days) TCC (n) Clinical presentation Maturating AVF Relapse during follow-up Treatment Catheter removal 1 80 35.6 Yes No 248 1 Asymptomatic No No No No 2 50 27.8 Yes No 2040 1 TCC malfunction No No PTA Yes 3 34 22.3 Yes No 252 1 SVC syndrome No Yes Local lysis/PTA Yes 4 37 19.3 Yes No 1648 4 SVC syndrome No No Systemic lysis / PTA Yes 5 55 18.4 No No 2871 2 Arm oedema No No No Yes 6 53 33.4 Yes No 2010 3 TCC malfunction No No PTA Yes 7 69 20.3 No No 4246 7 TCC malfunction No No PTA/stent Yes 8 69 30.1 Yes PM 1640 6 TCC malfunction No No PTA Yes 9 60 26.4 Yes PAC 118 1 Asymptomatic No NA No No 10 65 30.8 Yes No 115 1 TCC malfunction Yes No No Yes 11 65 26.9 Yes No 1350 2 TCC malfunction No Yes PTA/stent Yes BMI, body mass index; NA, not applicable; PAC, venous port; PM, pacemaker; PTA, percutaneous angioplasty. One patient (Patient 5) suffered from right arm oedema ipsilateral to the TCC, in the absence of a maturating AVF. In six patients the venography was performed because of catheter malfunction. In the remaining two patients, SVC stenosis was found on chest CT scans performed for a reason unrelated to the VA (thoracic pain and suspected pneumonia in Patients 1 and 9, respectively) and subsequently confirmed by venography in both patients. Only one patient (Patient 9) suffered from active neoplasia. Four patients also had a stenosis at the right innominate vein (Patients 5 and 6) or at the junction of both innominate veins (Patients 4 and 8) concomitant to a severe SVC stenosis. In Patients 4 and 7, the SVC was completely occluded. A thrombus within the SVC stenosis was documented in Patients 1, 4, 5 and 9. In only one patient (Patient 10), an AVF was created while a TCC was still in use (both the AVF and TCC were right-sided). In this patient, the AVF matured without problems and the venography was performed because of catheter malfunction. The TCC was eventually removed in all but one case (Patient 9, suffering from advanced neoplasia). In both patients with an SVC syndrome, a thrombolytic treatment by local (Patient 4) or systemic (Patient 3) urokinase was unsuccessful; the TCC was removed over guidewire and replaced after SVC angioplasty. In Patients 7 and 11, a stent (18 × 60 mm and 22 × 60 mm, respectively) was placed after SVC angioplasty: during the study, SVC stenosis recurred in two patients, Patients 3 and 11, 2 and 4 months after SVC angioplasty, respectively. The clinical presentation was catheter malfunction in Patient 11. Patient 3 was asymptomatic when SVC stenosis relapsed. One month after relapse she received kidney transplantation. Patient 11 died 2 months after SVC stenosis relapse. Patients in the SVC stenosis group were younger and more likely to be diabetic (Table 1), whereas the number of previous AVFs and characteristics of the last TCC did not differ between groups. Of note, only 3 of 11 TCCs in the SVC stenosis group were placed on the left side (Patients 5, 7 and 8) and 11/11 were internal jugular TCCs. Also of note, 5 of 11 patients in the SVC stenosis group carried only one TCC. The number of TCCs and catheter-days per patient were higher in the SVC stenosis group compared with the negative group, but this did not reach statistical significance (2.64 ± 1.8 versus 1.75 ± 0.94, P = 0.13 and 1302 ± 122 versus 634 ± 691, P = 0.08, respectively). The duration of total TCC carriage in the SVC stenosis group was strongly driven by Patient 7 (>4000 catheter-days). Univariate analysis Only diabetes {IRR 5.7 [confidence interval (CI) 1.2–26.2], P = 0.03}, age [IRR 0.96 (CI 0.91–1.01), P = 0.01] and duration of last catheter carriage [IRR 0.996 (CI 0.993–0.999), P = 0.03] were significantly associated with SVC stenosis in univariate analysis. Body mass index, HD vintage, number of previous AVFs/AVGs, number of TCCs and characteristics of the last TCC [diameter, length, location (either side or vein)] were not significantly associated with IRR. Multivariate analysis In the multivariate Poisson regression, diabetes [IRR 4.9 (CI 1.03–23.6), P = 0.04] and the duration of last catheter carriage [IRR 0.99 (CI 0.994–1.0002), P = 0.07] were independent predictors of SVC stenosis (Table 3). After adjustment for the number of previous catheters, the impact of duration of the last catheter carriage was non-significant. After excluding the duration of last catheter carriage, diabetes and the total duration of TCC carriage remained significantly associated with SVC stenosis [IRR 4.63 (CI 1.2–17.8), P = 0.02 and 1.47 (CI 1.22–1.76), P = 0.001, respectively]. Age was slightly protective [IRR 0.96 (CI 0.91–1.01), P = 0.01]. Using a Fisher test, the age category (considered as 20-year increments) remained borderline significant (P = 0.06). Table 3 Multivariate analysis (Poisson regression) IRR CI P-value Diabetes 4.63 1.2–17.8 0.02 Total catheter-days 1.47 1.22–1.76 0.001 Age 0.96 0.91–1.01 0.01 Total number of TCCs 1.09 0.76–1.57 0.6 IRR CI P-value Diabetes 4.63 1.2–17.8 0.02 Total catheter-days 1.47 1.22–1.76 0.001 Age 0.96 0.91–1.01 0.01 Total number of TCCs 1.09 0.76–1.57 0.6 Table 3 Multivariate analysis (Poisson regression) IRR CI P-value Diabetes 4.63 1.2–17.8 0.02 Total catheter-days 1.47 1.22–1.76 0.001 Age 0.96 0.91–1.01 0.01 Total number of TCCs 1.09 0.76–1.57 0.6 IRR CI P-value Diabetes 4.63 1.2–17.8 0.02 Total catheter-days 1.47 1.22–1.76 0.001 Age 0.96 0.91–1.01 0.01 Total number of TCCs 1.09 0.76–1.57 0.6 DISCUSSION Although SVC stenosis may be a life-threatening condition in HD patients with a TCC, its current prevalence and risk factors are unknown. To our knowledge, this is the first long-term (5 years) report documenting a prevalence of SVC stenosis in in-centre HD patients carrying a tunnelled central venous catheter. Additionally, this study provides a description of the clinical presentation and management of SVC stenosis in HD patients. The presumed prevalence of SVC stenosis was 0.14 case/1000 catheter-days. This corresponds to 1.8 episodes of SVC stenosis per year in a centre with 100 HD patients, one-third of whom carry a TCC, thus it is not very rare. Moreover, the prevalence might be even higher since only symptomatic patients (45/117) underwent imaging. Furthermore, an SVC stenosis was found in almost one-quarter of the patients undergoing a venography, whatever the trigger (11/45). A PubMed search using the keywords ‘superior vena cava stenosis and hemodialysis’ ‘superior vena cava stenosis and dialysis catheter’, and ‘superior vena cava stenosis and vascular access’ yielded 46 articles. All but one [13] were case reports and case series, reporting a total of 91 cases of SVC stenosis in HD patients. Most published cases (n = 35) describe a classical SVC syndrome, followed by catheter malfunction (n = 14) and ‘downhill’ oesophageal varices (n = 11). In seven cases, clinical presentation included other symptoms (chylothorax and chylopericardium, haemoptysis, obstructive sleep apnoea, stridor, intracranial hypertension and recurrent right-sided transudative pleural effusion) [14–16]. In our study, a classical SVC syndrome was present in only two patients. Indeed, in most cases SVC stenosis was diagnosed in the context of catheter malfunction. Similarly, in a very small prospective study focusing on SVC and including 20 patients with a permanent jugular catheter who underwent systematic transesophageal echocardiography, 5 of 6 patients with an SVC thrombosis presented with reduced catheter blood flow during HD [13]. Although small and cross-sectional, this is the only published study focusing on SVC stenosis in HD patients. Jean et al. [17] showed that only 50% of the 24 patients with a documented CVS in a systematic cavographic study (n = 51, including 7 AVFs, 2 AVGs, 2 Thomas shunts and 40 TCCs) were symptomatic, but unlike in the study by Grote et al. [13] and in our study, symptoms/signs included limb oedema, collateral circulation and hepatalgia. This difference in clinical presentation may be explained by the fact that in the study by Jean et al. [17], 9 of 12 symptomatic patients were using an AVF/AVG at the time of the cavography (versus no asymptomatic patient). Indeed, increased blood flow through the AVF can lead to venous congestion [18]. Similarly, in 55 cases of CVS among 133 prevalent HD patients undergoing a venography due to a problematic AVF, arm oedema was a frequent clinical manifestation of CVS (10 CVSs out of 13 cases of arm oedema) and 8 patients had a clinical classical SVC syndrome among 13 carrying an SVC stenosis [5]. However, Renaud et al. [11] found that among 103 patients carrying an AVF and a high-grade CVS, only 50 were symptomatic (severe arm oedema) and the AVF-related problems in the other 53 patients were all due to peripheral vein stenoses [11]. In our study, the fact that only three patients with SVC stenosis were symptomatic strongly suggests that, just like stenosis of other central veins, it does not necessarily correlate with clinical symptoms, especially in the absence of an AVF or AVG, and that a number of SVC stenoses are incidentally detected. However, it is important to emphasize that, even if clinically silent in most cases, SVC stenosis can lead to dramatic complications, such as massive bleeding by ‘downhill’ oesophageal varices [19, 20] or torrential haemoptysis [16], chylopericardial tamponade [15] and death [5]. Our study demonstrates, as already shown for CVS [2, 5, 21], that a longer duration of catheterization is associated with the development of SVC stenosis. In our study, the number of previous TCCs was higher in patients with SVC stenosis, but without reaching statistical significance. This may be explained by the small number of positive cases and also the fact that temporary catheters were not included. Unlike McRae et al. [5], we found that diabetes was strongly associated with SVC stenosis. In this study there was no difference in the prevalence of diabetes in patients carrying a CVS (49%) versus those without (43%). However, only patients with a problematic AVF were included, which could have caused an overrepresentation of diabetes in both groups [5]. Intimal hyperplasia—currently considered as one of the culprit lesions in failing AVFs [22]—is caused by the accumulation of myofibroblast-like cells in the venous intima [23] and seems to be associated with endothelial dysfunction due to turbulent flow [22]. Some [24] but not all [25] studies found a significant association of histologic intimal hyperplasia with diabetes in patients carrying an AVF. To our knowledge, no study has investigated this potential association in patients carrying catheters. Diabetes has been identified as a predictor of AVF loss [26]. Admittedly, it is unclear if this may be extrapolated to patients carrying central catheters. Nonetheless, it is tempting to speculate that the endothelial dysfunction and the pro-inflammatory status due to diabetes itself could exacerbate the biological response to the mechanical injury caused by the catheter and abnormal flow conditions, increasing the expression of pro-coagulant and pro-inflammatory mediators and predisposing to intimal hyperplasia and vessel stenosis. FIGURE 1 View largeDownload slide Venography performed in Patient 3. Injection performed through the caudal extremity of the occluded right internal jugular vein shows (A) occlusion of the subclavian–jugular confluent extending into the proximal innominate vein (B) followed by retrograde delayed filling of the azygos vein and intercostal veins (arrow) due to SVC occlusion. (C) SVC again permeable after angioplasty. FIGURE 1 View largeDownload slide Venography performed in Patient 3. Injection performed through the caudal extremity of the occluded right internal jugular vein shows (A) occlusion of the subclavian–jugular confluent extending into the proximal innominate vein (B) followed by retrograde delayed filling of the azygos vein and intercostal veins (arrow) due to SVC occlusion. (C) SVC again permeable after angioplasty. We found that age has a slightly protective effect on SVC stenosis. A plausible though purely speculative explanation may be the age-related modulation of the immune response [27]. However, we cannot exclude a detection bias, due to the fact that in elderly patients one may be less prone to perform cumbersome imaging studies and a lower blood flow may be tolerated. The main limitation of this study is its retrospective design. Second, because the study included both incident and prevalent patients, there may be a survivor bias. Third, there is a detection bias because only patients carrying a TCC during the study period were included (patients using a TCC before the study and carrying an AVF during the study were not). Furthermore, CVS has also been reported in patients carrying a functional peripheral VA who do not have a history of central vein catheterization (5–63% in two series including 51 and 103 documented CVSs, respectively [5, 11]). Additionally, unlike the study by Jean et al. [17] in which all included patients underwent a systematic cavography, imaging was performed only in symptomatic patients. Fourth, some data were missing concerning the characteristics of the last catheter, which could explain the absence of an association of SVC stenosis with some catheter characteristics previously associated with CVS, such as catheter diameter and length. Fifth, although short-term catheters have also been associated with CVS [28], temporary catheters were not included in our study. This could explain the fact that, unlike other studies investigating CVS [5], the total number of previous catheters was not associated with SVC stenosis. The monocentric design of this study has some advantages: (i) the interventional radiologist reading the imaging studies and treating SVC stenosis was the same in all except one patient; (ii) all the information is centralized in our electronic medical records; (iii) our policy of a systematic catheter imaging study in case of persistence of blood flow <250 mL/min guaranteed some detection uniformity, unlike in multicentric studies. However, the limited variability of some parameters (i.e. catheter brand and location) due to the monocentric design may have masked a potential impact of these factors. In conclusion, SVC stenosis is not a rare condition in chronic HD patients with a TCC, but classical symptoms remain infrequent in the absence of a peripheral functional VA. In patients carrying a TCC, SVC stenosis appears to be strongly associated with diabetes and promoted by a long TCC carriage. This highlights the need to decrease catheter use in HD (i.e. reduction of late referral rate, protection of veins, periodic monitoring of peripheral VA and availability of a multidisciplinary VA team) and to perform an imaging study prior to AVF creation in patients with a history of central vein catheterization, especially if prolonged, as recommended by current guidelines [29, 30]. Further large, long-term studies are warranted to confirm the current prevalence and risk factors of this potentially devastating complication in HD patients. This work was presented at the Annual Congress of the American Society of Nephrology (Chicago 2016; SA-PO1063). ACKNOWLEDGEMENTS We thank Chantal Fagot for helping with the preparation of Figure 1. AUTHORS’ CONTRIBUTIONS L.L. and M.J. were responsible for the research idea and study design. B.S., P.B. and F.H. conducted the data acquisition. R.C., L.L. and M.J. performed the data analysis/interpretation. R.C. was responsible for the statistical analysis. M.J. and L.L. were responsible for supervision or mentorship. CONFLICT OF INTEREST STATEMENT L.L. reports personal fees from Fresenius, Shire, Bellco and Janssen-Cilag outside the submitted work. M.J. reports funding from Amgen, Astellas, Fresenius, GlaxoSmithKline, MSD and Sanofi; grants from Alexion, Amgen, Baxter, Otsuka, Janssen-Cilag and Roche; personal fees from AbbVie, Menarini, MSD and Amgen outside the submitted work. B.S., R.C., P.B. and F.H. have declared no conflicts of interest. REFERENCES 1 Schwab SJ , Quarles LD , Middleton JP et al. Hemodialysis-associated subclavian vein stenosis . Kidney Int 1988 ; 33 : 1156 – 1159 Google Scholar Crossref Search ADS PubMed 2 Barrett N , Spencer S , Mclovor J et al. Subclavian stenosis: a major complication of subclavian dialysis catheters . 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TI - Superior vena cava stenosis in haemodialysis patients with a tunnelled cuffed catheter: prevalence and risk factors
JF - Nephrology Dialysis Transplantation
DO - 10.1093/ndt/gfy150
DA - 2018-12-01
UR - https://www.deepdyve.com/lp/oxford-university-press/superior-vena-cava-stenosis-in-haemodialysis-patients-with-a-tunnelled-u5JFG3OmFI
SP - 2227
VL - 33
IS - 12
DP - DeepDyve
ER -