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Department of Radiology
Seth G.S. Medical College and K.E.M. Hospital, Mumbai , India
Interventional Case Record
Interventional Case Record
No case was published in July
Contributed by Amogh Jagtap
Contributed by Amogh Jagtap
Endovascular treatment of central venous obstruction secondary to long-term hemodialysis
Endovascular treatment of central venous obstruction secondary to long-term hemodialysis
Introduction :
Introduction :
Central venous stenosis and obstruction is a major concern in patients undergoing prolonged hemodialysis (HD) causing significant morbidity with access site dysfunction. Central venous disease (CVD) has been defined as 50% or greater stenosis involving the internal jugular, subclavian, or axillary veins. The incidence of central venous stenosis and obstruction is 25-40%. The main causes of central venous stenosis in hemodialysis patients are prolonged central venous catheterization and high-flow status in arteriovenous fistula (AVF) or graft, subsequently causing venous intimal hyperplasia and stenosis. Clinically, central venous obstruction manifests as ipsilateral arm or neck swelling, elevated venous pressure during hemodialysis, and failure of hemodialysis access. The aim of the treatment is to provide symptomatic relief to (HD)patients while preserving the function of AVF. Because of the steady growth of the HD population and the persistently high percentage of late referrals requiring emergency renal replacement therapy (RRT), increasing numbers of HD catheters are being implanted and arteriovenous fistulas created. As a consequence, the treatment of CVO constitutes a growing challenge to access surgeons and interventional radiologists.[1]
Central venous stenosis and obstruction is a major concern in patients undergoing prolonged hemodialysis (HD) causing significant morbidity with access site dysfunction. Central venous disease (CVD) has been defined as 50% or greater stenosis involving the internal jugular, subclavian, or axillary veins. The incidence of central venous stenosis and obstruction is 25-40%. The main causes of central venous stenosis in hemodialysis patients are prolonged central venous catheterization and high-flow status in arteriovenous fistula (AVF) or graft, subsequently causing venous intimal hyperplasia and stenosis. Clinically, central venous obstruction manifests as ipsilateral arm or neck swelling, elevated venous pressure during hemodialysis, and failure of hemodialysis access. The aim of the treatment is to provide symptomatic relief to (HD)patients while preserving the function of AVF. Because of the steady growth of the HD population and the persistently high percentage of late referrals requiring emergency renal replacement therapy (RRT), increasing numbers of HD catheters are being implanted and arteriovenous fistulas created. As a consequence, the treatment of CVO constitutes a growing challenge to access surgeons and interventional radiologists.[1]
Surgical and endovascular treatments are available for the management of central venous stenosis. However, the optimal treatment is yet to be determined. Though high primary patency rates (80-90% at 1 year) have been reported with open surgical repair of the central veins, it carries a high rate of postoperative morbidity and mortality. Endovascular management has been widely accepted as the modality of choice for treatment of central venous stenosis. Endovascular treatment options include percutaneous transluminal angioplasty (PTA), bare metal stent or covered stent placement. The optimal endovascular treatment, however, remains unclear, with no clear advantage of primary stent placement in comparison to angioplasty. The National Kidney Foundation Disease Outcomes Quality Initiative guidelines have recommended angioplasty as the preferred treatment for CVO, with or without stent placement.[2]
Surgical and endovascular treatments are available for the management of central venous stenosis. However, the optimal treatment is yet to be determined. Though high primary patency rates (80-90% at 1 year) have been reported with open surgical repair of the central veins, it carries a high rate of postoperative morbidity and mortality. Endovascular management has been widely accepted as the modality of choice for treatment of central venous stenosis. Endovascular treatment options include percutaneous transluminal angioplasty (PTA), bare metal stent or covered stent placement. The optimal endovascular treatment, however, remains unclear, with no clear advantage of primary stent placement in comparison to angioplasty. The National Kidney Foundation Disease Outcomes Quality Initiative guidelines have recommended angioplasty as the preferred treatment for CVO, with or without stent placement.[2]
Case Record:
Case Record:
A 76 year old woman with chronic kidney disease on multi-access hemodialysis for 11 years presented with swelling of the right upper limb (Fig.1), two years after the creation of brachio-basilic fistula on the right arm. She was a known diabetic since 20 years and hypertensive since 15 years, on regular medications. She had a haemoglobin of 13.8gm%, The total leucocyte count was 7100/cu.mm, platelet count of 1,50,000/cu.mm and serum creatinine of 3.1mg/dl. The prothrombin time was 13 sec and INR was 0.8.
A 76 year old woman with chronic kidney disease on multi-access hemodialysis for 11 years presented with swelling of the right upper limb (Fig.1), two years after the creation of brachio-basilic fistula on the right arm. She was a known diabetic since 20 years and hypertensive since 15 years, on regular medications. She had a haemoglobin of 13.8gm%, The total leucocyte count was 7100/cu.mm, platelet count of 1,50,000/cu.mm and serum creatinine of 3.1mg/dl. The prothrombin time was 13 sec and INR was 0.8.
Fig. 1 : :The edematous right upper limb
Fig. 1 : :The edematous right upper limb
Interventional treatment:
Interventional treatment:
DSA showed complete occlusion of the right brachiocephalic vein and multiple veno-venous collaterals and the SVC was not opacified (Fig. 2). Using a short 7F vascular access sheath, right common femoral transvenous access was obtained. With the help of H1 diagnostic catheter (Cordis) and angled tipped, single length guide wire (Terumo) the occlusion in the right brachiocephalic vein was negotiated. After advancement of the catheter over the guide wire, it was exchanged with Amplatz extra stiff guide wire and serial high pressure balloon dilatations were done with 10mm x 40mm (Mustang, Boston Scientific) and 14mm x 40mm balloons (Atlas, Bard) at the site of obstruction (Fig.3 & Fig.4). Post procedure fistulogram showed a patent right brachiocephalic vein, a normal SVC and disappearance of multiple veno-venous collaterals (Fig 5). A week later, there was significant improvement in the swelling of the right upper limb of the patient (Fig.6).
DSA showed complete occlusion of the right brachiocephalic vein and multiple veno-venous collaterals and the SVC was not opacified (Fig. 2). Using a short 7F vascular access sheath, right common femoral transvenous access was obtained. With the help of H1 diagnostic catheter (Cordis) and angled tipped, single length guide wire (Terumo) the occlusion in the right brachiocephalic vein was negotiated. After advancement of the catheter over the guide wire, it was exchanged with Amplatz extra stiff guide wire and serial high pressure balloon dilatations were done with 10mm x 40mm (Mustang, Boston Scientific) and 14mm x 40mm balloons (Atlas, Bard) at the site of obstruction (Fig.3 & Fig.4). Post procedure fistulogram showed a patent right brachiocephalic vein, a normal SVC and disappearance of multiple veno-venous collaterals (Fig 5). A week later, there was significant improvement in the swelling of the right upper limb of the patient (Fig.6).
Fig. 2 : DSA shows occlusion of the right brachiocephalic vein, no opacification of the SVC. There are multiple collaterals
Fig. 2 : DSA shows occlusion of the right brachiocephalic vein, no opacification of the SVC. There are multiple collaterals
Fig. 3 : Initial low pressure balloon dilatation shows the with waist at the site of obstruction in the right brachiocephalic vein
Fig. 3 : Initial low pressure balloon dilatation shows the with waist at the site of obstruction in the right brachiocephalic vein
Fig. 4 : Balloon angioplasty with disappearance of waist
Fig. 4 : Balloon angioplasty with disappearance of waist
Fig. 5 : Post angioplasty image shows a patent brachiocephalic vein, a normal SVC and no collaterals
Fig. 5 : Post angioplasty image shows a patent brachiocephalic vein, a normal SVC and no collaterals
Fig. 6 : Follow up (1 week later) Significant improvement in the edema
Fig. 6 : Follow up (1 week later) Significant improvement in the edema
Discussion:
Discussion:
A knowledge of the route of the central veins and their relationship to surrounding structures is critical to why CVO occurs in typical locations. The brachial and basilic veins join at the lower border of the teres major muscle to form the axillary vein, which passes anterior to the subscapularis muscle and posterior to the pectoralis minor muscle near its insertion at the coracoid process. The axillary vein continues to the lateral border of the first rib, where it becomes the subclavian vein, which enters the thoracic inlet posterior to the clavicle and anterior to the first rib and scalenus anticus muscle (costoclavicular space) and joins the internal jugular vein after several centimeters to become the brachiocephalic vein. The right and left brachiocephalic veins, join in the mediastinum to form the superior vena cava.[3]
A knowledge of the route of the central veins and their relationship to surrounding structures is critical to why CVO occurs in typical locations. The brachial and basilic veins join at the lower border of the teres major muscle to form the axillary vein, which passes anterior to the subscapularis muscle and posterior to the pectoralis minor muscle near its insertion at the coracoid process. The axillary vein continues to the lateral border of the first rib, where it becomes the subclavian vein, which enters the thoracic inlet posterior to the clavicle and anterior to the first rib and scalenus anticus muscle (costoclavicular space) and joins the internal jugular vein after several centimeters to become the brachiocephalic vein. The right and left brachiocephalic veins, join in the mediastinum to form the superior vena cava.[3]
A suggested mechanism for the development of CVO includes central venous catheter-induced trauma to the venous endothelium and secondary inflammatory damage within the vessel wall at the time of insertion. Other proposed mechanisms include the presence of a foreign body in the vein, along with increased flow and turbulence from the creation of an AV access. Turbulent blood flow has been shown to incite an inflammatory response and stimulate intimal hyperplasia.
A suggested mechanism for the development of CVO includes central venous catheter-induced trauma to the venous endothelium and secondary inflammatory damage within the vessel wall at the time of insertion. Other proposed mechanisms include the presence of a foreign body in the vein, along with increased flow and turbulence from the creation of an AV access. Turbulent blood flow has been shown to incite an inflammatory response and stimulate intimal hyperplasia.
In otherwise healthy persons, chronic central arm vein obstruction can be compensated by numerous collaterals along the chest wall, in the neck and in the mediastinum. In the majority of these patients signs and symptoms of CVO are mild or completely absent. However, when an AV access is created peripheral to a central venous stenosis or occlusion, the blood flow through the extremity may rise at least four to tenfold above the resting level. In this situation the collateral capacity may be insufficient so that venous hypertension will develop. Depending on the location of the obstruction and the collateral capacity there is a wide variety of possible clinical findings. When the subclavian vein is affected, venous collaterals will become visible around the shoulder and the upper chest. Moderate to severe and sometimes painful and incapacitating arm swelling is the most frequent finding. Extreme venous hypertension can lead to skin ulceration and tissue loss. Acral skin changes, hyperpigmentation, pincer nail deformity and pseudo-Kaposi’s sarcoma, have also been described. In more central brachiocephalic or superior caval) vein obstruction unilateral face and breast swelling may additionally occur. Pelvic vein obstruction following femoral vein catherisation frequently cause leg swelling without a thigh access being fashioned, which, of course, would markedly deteriorate with creation of a functioning access. Swelling may cause difficulties in needling the access with the risk of bleeding and haematoma. Skin ulceration will further enhance the risk of infection and access loss. Therefore, once swelling becomes painful and incapacitating or causes needling or skin problems, CVO should be treated.
In otherwise healthy persons, chronic central arm vein obstruction can be compensated by numerous collaterals along the chest wall, in the neck and in the mediastinum. In the majority of these patients signs and symptoms of CVO are mild or completely absent. However, when an AV access is created peripheral to a central venous stenosis or occlusion, the blood flow through the extremity may rise at least four to tenfold above the resting level. In this situation the collateral capacity may be insufficient so that venous hypertension will develop. Depending on the location of the obstruction and the collateral capacity there is a wide variety of possible clinical findings. When the subclavian vein is affected, venous collaterals will become visible around the shoulder and the upper chest. Moderate to severe and sometimes painful and incapacitating arm swelling is the most frequent finding. Extreme venous hypertension can lead to skin ulceration and tissue loss. Acral skin changes, hyperpigmentation, pincer nail deformity and pseudo-Kaposi’s sarcoma, have also been described. In more central brachiocephalic or superior caval) vein obstruction unilateral face and breast swelling may additionally occur. Pelvic vein obstruction following femoral vein catherisation frequently cause leg swelling without a thigh access being fashioned, which, of course, would markedly deteriorate with creation of a functioning access. Swelling may cause difficulties in needling the access with the risk of bleeding and haematoma. Skin ulceration will further enhance the risk of infection and access loss. Therefore, once swelling becomes painful and incapacitating or causes needling or skin problems, CVO should be treated.
The easiest surgical solution for access-associated CVO is ligation of the access, which results in immediate relief of symptoms. At the same time ligation is the most frustrating option as the vascular pathology causing the patient’s problem is not corrected and the respective extremity is rendered unsuitable for further access procedures. Access abandonment makes creation of a new permanent vascular access necessary, in the other arm or in the leg, and should therefore be performed only when interventional or surgical therapy of CVO is impossible or has failed.
The easiest surgical solution for access-associated CVO is ligation of the access, which results in immediate relief of symptoms. At the same time ligation is the most frustrating option as the vascular pathology causing the patient’s problem is not corrected and the respective extremity is rendered unsuitable for further access procedures. Access abandonment makes creation of a new permanent vascular access necessary, in the other arm or in the leg, and should therefore be performed only when interventional or surgical therapy of CVO is impossible or has failed.
Most patients present with long standing symptoms of CVO so that thromboaspiration or thrombolysis alone is unlikely to restore adequate venous patency. However, in selected cases with evidence of fresh thrombus causing total obstruction of a preexisting tight venous stricture, thrombolysis may help to reestablish the stenosed lumen and allow an additional percutaneous transluminal angioplasty (PTA). PTA of CVO in HD patients has been reported since the early 1980s.Because of frequent restenoses, however, primary one-year patency of PTA alone was less than 40% in most of the studies. To reduce the number of re-interventions, several groups have routinely performed stent placement with each PTA procedure, and most reported improved primary patency rates when compared to PTA alone. A more moderate use of stents (only for significant reststenoses or elastic recoil after PTA, and for early or frequent re-stenoses) has been practiced by other investigators with satisfying results. The use of covered stents or endovascular brachytherapy following stent placement does not enhance patency rates.
Most patients present with long standing symptoms of CVO so that thromboaspiration or thrombolysis alone is unlikely to restore adequate venous patency. However, in selected cases with evidence of fresh thrombus causing total obstruction of a preexisting tight venous stricture, thrombolysis may help to reestablish the stenosed lumen and allow an additional percutaneous transluminal angioplasty (PTA). PTA of CVO in HD patients has been reported since the early 1980s.Because of frequent restenoses, however, primary one-year patency of PTA alone was less than 40% in most of the studies. To reduce the number of re-interventions, several groups have routinely performed stent placement with each PTA procedure, and most reported improved primary patency rates when compared to PTA alone. A more moderate use of stents (only for significant reststenoses or elastic recoil after PTA, and for early or frequent re-stenoses) has been practiced by other investigators with satisfying results. The use of covered stents or endovascular brachytherapy following stent placement does not enhance patency rates.
As far as can be deduced from the few reports in the literature, the results of surgical reconstruction of mediastinal veins in HD patients are better than those of interventional radiology with primary patency rates of 80% to 90% at one year. These procedures, however, always mean major surgery. Patch angioplasty of a subclavian or innominate vein or orthotopic bypass surgery require clavicular division or sternotomy (and general anesthesia) and are associated with high rates of postoperative morbidity and mortality. Extraanatomical bypass (such as axillary-to-internal jugular vein) is less distressing to the patient but this results in the loss of another central vein for further access. When the central venous drainage of all four extremities is compromised, construction or maintenance of AV access can be difficult or impossible. In low risk patients fit for median sternotomy, a subclavian artery-to-right atrial appendix bridge graft can be constructed, or an axillary vein-to-right atrial bypass be performed. In patients unfit for major surgery, fashioning an arterio-arterial loop graft can be considered as an alternative to the insertion of a translumbar, transhepatic or transthoracic, cuffed tunneled catheter.[1-3]
As far as can be deduced from the few reports in the literature, the results of surgical reconstruction of mediastinal veins in HD patients are better than those of interventional radiology with primary patency rates of 80% to 90% at one year. These procedures, however, always mean major surgery. Patch angioplasty of a subclavian or innominate vein or orthotopic bypass surgery require clavicular division or sternotomy (and general anesthesia) and are associated with high rates of postoperative morbidity and mortality. Extraanatomical bypass (such as axillary-to-internal jugular vein) is less distressing to the patient but this results in the loss of another central vein for further access. When the central venous drainage of all four extremities is compromised, construction or maintenance of AV access can be difficult or impossible. In low risk patients fit for median sternotomy, a subclavian artery-to-right atrial appendix bridge graft can be constructed, or an axillary vein-to-right atrial bypass be performed. In patients unfit for major surgery, fashioning an arterio-arterial loop graft can be considered as an alternative to the insertion of a translumbar, transhepatic or transthoracic, cuffed tunneled catheter.[1-3]
Conclusion:
Conclusion:
The main cause of central venous obstruction in haemodialysis patients is prolonged or repeated catheterization for dialysis access. Most frequent complaints are disabling swelling and pain, sometimes combined with venous ulceration. Chronic central venous occlusion can be a debilitating condition for patients. Malignancy, such as NSCLC, is the most common etiology although indwelling intravascular devices, prior thoracic radiation therapy, and fibrosing mediastinitis can cause chronic central venous occlusions as well. Treatment goals are focused on symptomatic relief and, if the etiology is malignancy, treatment is often palliative. Percutaneous recanalization and endovascular stenting of chronic occlusions is a minimally invasive technique that can be performed in an outpatient setting, often resulting in immediate relief of symptoms.
The main cause of central venous obstruction in haemodialysis patients is prolonged or repeated catheterization for dialysis access. Most frequent complaints are disabling swelling and pain, sometimes combined with venous ulceration. Chronic central venous occlusion can be a debilitating condition for patients. Malignancy, such as NSCLC, is the most common etiology although indwelling intravascular devices, prior thoracic radiation therapy, and fibrosing mediastinitis can cause chronic central venous occlusions as well. Treatment goals are focused on symptomatic relief and, if the etiology is malignancy, treatment is often palliative. Percutaneous recanalization and endovascular stenting of chronic occlusions is a minimally invasive technique that can be performed in an outpatient setting, often resulting in immediate relief of symptoms.
References:
References:
1. Mickley V., Central vein obstruction in vascular access. Eur J Vasc Endovasc Surg. 2006;32(4):439-444. doi:10.1016/j.ejvs.2006.04.011
1. Mickley V., Central vein obstruction in vascular access. Eur J Vasc Endovasc Surg. 2006;32(4):439-444. doi:10.1016/j.ejvs.2006.04.011
2. Gipson MG, Gupta RK, Smith MT. Percutaneous management of chronic central venous occlusive disease. Semin Intervent Radiol. 2015;32(1):57-60. doi:10.1055/s-0034-1396966
2. Gipson MG, Gupta RK, Smith MT. Percutaneous management of chronic central venous occlusive disease. Semin Intervent Radiol. 2015;32(1):57-60. doi:10.1055/s-0034-1396966
3. Yadav MK, Sharma M, Lal A, Gupta V, Sharma A, Khandelwal N. Endovascular treatment of central venous obstruction as a complication of prolonged hemodialysis - Preliminary experience in a tertiary care center. Indian J Radiol Imaging. 2015;25(4):368-374. doi:10.4103/0971-3026.169463
3. Yadav MK, Sharma M, Lal A, Gupta V, Sharma A, Khandelwal N. Endovascular treatment of central venous obstruction as a complication of prolonged hemodialysis - Preliminary experience in a tertiary care center. Indian J Radiol Imaging. 2015;25(4):368-374. doi:10.4103/0971-3026.169463
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