**2. Clinical case study**

This is a 52-year-old diabetic female, who was on regular hemodialysis 3 times a week with right internal jugular vein (IJV) TCC as her vascular access for 7 months and a non-maturing left brachiocephalic vein AVF. She presented with progressively increasing orthopnea of 1-week duration and was presumed to have coronary artery disease. She was referred to our hospital cardiology department for coronary angiography (CAG), who subsequently asked nephrology services to give her a post CAG dialysis. Her CAG was normal. When on dialysis and on attempting to ultrafilter her, she had intradialytic hypotension, with persistent and increasing breathlessness. She was examined by a consultant and a clinical diagnosis of CVS was made. The patient was clinically not in fluid overload state. HD was terminated, and her blood pressure and symptoms settled. The next day, she underwent contrast-enhanced tomography of central vein, which proved stenosis at the cavo-atrial junction, at the site of the tip of the dialysis catheter. She was subjected to central vein angioplasty and her symptoms resolved (**Figure 1**) (author's personal work).

**171**

**Figure 1.**

*TCC in situ.*

**3. What are central veins?**

could constitute the lower limb central veins.

In the neck, SVC, bilateral brachiocephalic vein (BCV), IJV, external jugular vein (EJV), and SCVs would constitute the central veins for upper limb access, whereas femoral, common iliac, and external iliac veins and the infrarenal inferior vena cava

*CT scan and angiography images: (a) 3D reconstructed image showing clots around the TCC tip and also multiple collateral veins in the thoracic cage, suggestive of CTO; (b) stenosis at cavo-atrial junction at the site of TCC tip; (c) findings of (b) on CT scan are confirmed on angiography; and (d) angioplasty of the CVS with* 

*Hemodialysis Vascular Access with Central Venous Disease*

*DOI: http://dx.doi.org/10.5772/intechopen.93030*

*Cardiac Diseases - Novel Aspects of Cardiac Risk, Cardiorenal Pathology and Cardiac Interventions*

implicated in development of CVS are venous trauma resulting from cannulation of central veins and hemodynamic stress secondary to high flow due to access site AVF,

AVF is the gold standard of VA. Ideally, all patients starting HD should have AVF in place, but that is not possible. In 2015, 80% of patients were using a catheter at HD initiation, a rate that has changed only marginally since 2005, and at 90 days after the initiation of HD, 68.5% of patients were still using catheters [1, 2]. Late referral by nephrologists to surgeons has been an underappreciated cause of initiation of HD with central catheters. [3]. There are situations when a patient has multiple AVF failures, in the upper limbs. It then becomes a challenging situation to provide dialysis to these patients with a reliable access. The problem is further compounded in patients with prior central vein HD catheters, resulting in CVD. CVS is considered to be common in patients on hemodialysis, but its exact prevalence is not known. The CVS may have occurred due to insertion of central catheters, PICC, or pacemaker leads. Due to direct contact of these devices with the wall of the central veins, and the constant movement, both lateral (like a pendulum) and cephalocaudal direction associated with breathing and the cardiac cycle cause endothelial injury. Pathological examinations of central veins obtained at autopsy have shown that even short-term catheters are associated with foci of local intimal

In patients with AVF, development of CVS is partly related to turbulent blood flow and neointimal hyperplasia (NIH). Infection related to prior catheter insertion may also be responsible for CVS. Extrinsic compression, either musculoskeletal or

However, in an otherwise healthy person, the CVS hardly, if ever, causes problems. The problem comes to light when an AVF or graft is placed on the ipsilateral side where there is presence of CVS. It also gets recognized when a fresh attempt is made to insert cuffed or non-cuffed tunnel catheter in the central vein. We should realize that CVS leading to CVD is difficult to treat and often resistant to treatment. In CVD, VA for HD sometimes need to be abandoned, or in serious cases, the patient's life may be threatened. Therefore, one should strive for the ideal situation of catheter avoidance and central vein preservation and remember that prevention

This is a 52-year-old diabetic female, who was on regular hemodialysis 3 times a week with right internal jugular vein (IJV) TCC as her vascular access for 7 months and a non-maturing left brachiocephalic vein AVF. She presented with progressively increasing orthopnea of 1-week duration and was presumed to have coronary artery disease. She was referred to our hospital cardiology department for coronary angiography (CAG), who subsequently asked nephrology services to give her a post CAG dialysis. Her CAG was normal. When on dialysis and on attempting to ultrafilter her, she had intradialytic hypotension, with persistent and increasing breathlessness. She was examined by a consultant and a clinical diagnosis of CVS was made. The patient was clinically not in fluid overload state. HD was terminated, and her blood pressure and symptoms settled. The next day, she underwent contrast-enhanced tomography of central vein, which proved stenosis at the cavo-atrial junction, at the site of the tip of the dialysis catheter. She was subjected to central vein angioplasty and her symptoms resolved (**Figure 1**) (author's personal work).

injury with endothelial denudation and adherent thrombus [4].

causing central venous disease (CVD).

arterial, can be contributing to CVS.

is ideal and better than cure.

**2. Clinical case study**

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#### **Figure 1.**

*CT scan and angiography images: (a) 3D reconstructed image showing clots around the TCC tip and also multiple collateral veins in the thoracic cage, suggestive of CTO; (b) stenosis at cavo-atrial junction at the site of TCC tip; (c) findings of (b) on CT scan are confirmed on angiography; and (d) angioplasty of the CVS with TCC in situ.*
