**1. Introduction**

34 Technical Problems in Patients on Hemodialysis

Waltz P, Ladowski JS, Hines A. (2007) Distal Revascularization and interval ligation (DRIL)

Wedgewood KR, Wiggins PA, Guillou PJ. (1984) A prospective study of end-to-side verses

Wali MA, Eid RA, Dewan M, Al-Homrany MA. (2006) Pre-existing histopathological

US Renal Data System, USRDS (2009) Annual Data Report: Atlas of chronic kidney disease

17419003

1984) pp. 640-642, PMID 6743990

Maryland, http://www.usrds.org

pp.341-348, PMID 17095976

procedure for the treatment of ischemic steal syndrome after arm arteriovenous fistula. *Annals of Vasc Surgery* Vol. 21, No.4, (July, 2007), pp. 468-473, PMID

side-to side arteriovenous fistulas for hemodialysis *Br J Surg* Vol.71, No.8, (August,

Changes in the cephalic vein of renal failure patients before arterio-venous fistula (AVF) construction *AnnThorac Cardiovasc Surg* 2006, Vol.12, No.5, (October, 2006),

and end-stage renal disease in the United States. National Institute of Health, National Institute of Diabetes and Digestive and Kidney Disease: Bethesda

The autogenous arteriovenous fistula (AVF) is the preferred access for chronic hemodialysis in patients with end-stage kidney disease. Careful examination of the upper extremity is essential for the creation of a successful fistula. The quality of the arterial and venous circulation should be well established prior to surgery. However, there are cases when the superficial venous system of the upper extremity is unsuitable for the creation of an autogenous AVF. This problem has two solutions: the use of a prosthetic graft or the creation of a brachio-brachial AVF. Prosthetic grafts have a 1-year patency rate of 65- 75%(Haimov, 1978), mostly due to the frequent and varying complications that they may sustain, especially ischemia, thrombosis, infection, and aneurysms. The brachio-brachial AVF, a relatively new type of angioaccess, is shown to have similar patency rates to the prosthetic grafts, but without their number of complications and is a very good alternative for patients with an unsatisfactory superficial venous system (Dorobanţu et al., 2006, 2010).

### **2. Anatomy of the brachial artery and the venous system of the upper arm**

The brachial artery is the continuation of the axillary artery beyond the inferior margin of the teres major muscle. It continues down the anterior aspect of the arm to the cubital fossa, being accompanied by two venae comitantes and the brachial nerve. Proximally, the nerve is lateral to the artery but it crosses the medial side of the artery distally, lying anterior to the elbow joint. The brachial artery divides into its terminal branches, the radial and the ulnar, 2 cm below the elbow bend (Gabella, 1995).

The venous system of the upper extremity comprises the superficial and the deep veins. Both groups have valves. The superficial veins (figure 1) are the the cephalic, the basilic and the median vein of the forearm; they are subcutaneous in the superficial fascia. The cephalic vein forms over the "anatomical snuffbox" and ascends along the forearm's radial side and then in front of the elbow, in a groove between the brachioradialis and the biceps. It then crosses anteriorly the lateral cutaneous nerve and continues along the lateral border of the biceps, up to the delto-pectoral groove. It pierces the clavipectoral fascia and joins the axillary vein below the clavicular level.

The basilic vein begins medially in the hand's dorsal venous network and continues on the medial side of the forearm and then anterior to the elbow. Just distally to the elbow, it is joined by the median vein of the forearm. It ascends superficially between the biceps and the pronator teres, between filaments of the medial cutaneous nerve. It perforates the deep

The Brachio-Brachial Arteriovenous Fistula 37

The brachial veins (figure 2) share their path with the brachial artery. They begin at the junction between the radial and the ulnar veins and end at the inferior margin of the teres major muscle, where they are joined by the basilic vein, forming the axillary vein. There are many collaterals between the two veins and small tributaries that drain the muscles of the

The arteriovenous fistula is an abnormal connection between a donor artery and a receiving vein. The permeability of the fistula depends on several factors. One of them is the resistance of the outflow vascular bed, which in this case is venous, and thus has a low pressure and a low resistance. As the vein's diameter increases through the maturation process, the venous resistance decreases. This process occurs during the first 4-8 weeks after the creation of the AVF and comprises a thickening of the venous wall, an increase in diameter for the vein, its distal branches, and for the arterial segment proximal to the anastomosis. As the vein is connected to a high-pressure, high-velocity artery, the blood flow through the vein induces an increased wall shear stress. Experiments have shown that acute increases in wall shear stress results in endothelial release of nitric oxide, which in turn increases the lumen radius. This is available for both acute and chronic wall shear alterations (Zarins et al., 2004). Experimentally produced arteriovenous fistulas produce an immediate 10-fold increase in blood flow and a three-fold increase in wall shear stress. Within 24 hours, vessel enlargement begins, and at the end of 4 weeks lumen radius enlarges twofold and wall shear stress returns to normal (Masuda & Bassiouny, 1989). The flow through the AVF is insignificant as long as the vein's diameter doesn't exceed that of the artery by at least 20%; however, a palpable thrill means that the AVF is functional. When the diameter of the vein exceeds that of the artery by 75%, the venous resistance is virtually null, and the flow through the fistula is limited only by the arterial flow. Between 20 and 75%, the flow through the AVF increases on an exponential basis and it depends

It is noteworthy that the portion of the artery distal to the AVF does not suffer any modifications, thereby maintaining its high resistance relative to the outflow of the fistula. This can lead to a reversal of flow in this segment, the so-called "steal syndrome", which can

The body's adaptation to the presence of an AVF includes global decreased vascular resistance and an increase in cardiac output, which can lead to a hyperdynamic syndrome or even to congestive heart failure. This is easily explained when the flow through a fistula ranges from 650 ml/min (for a radio-cephalic fistula) to 1000-1100 ml/min (for a brachiocephalic, brachio-brachial or prosthetic fistula) (Schanzer, 2004; Ştiru, 2006). Any

A great number of studies have proven higher patency rates and lower complication rates for autogenous AVF when compared to synthetic bridge AVF (Palder et al., 1985; Enzler et al., 1996; Matsuura et al., 1998; Kherlakian et al., 2006; Kappos et al., 2007). Taking this into account, the National Kidney Foundation Dialysis Outcomes Quality Initiative (NKF-DOQI) guidelines for vascular access emphasize the use of the former over the latter (NKF-DOQI,

result in ischemic complications. This is especially true in proximal fistulas.

cardiovascular comorbidity can alter these patients' long-term prognosis.

**4. Advantages of an autogenous arteriovenous fistula** 

upper arm (Lupu et al., 2010).

**3. Hemodynamics of an arteriovenous fistula** 

mainly on the venous resistance (Hobson et al., 1973).

fascia midway in the arm, continuing medial to the brachial artery to the lower border of the teres major, where it becomes the axillary vein.

Fig. 1. The superficial veins of the upper limb

Fig. 2. The deep veins of the upper limb

fascia midway in the arm, continuing medial to the brachial artery to the lower border of the

teres major, where it becomes the axillary vein.

Fig. 1. The superficial veins of the upper limb

Fig. 2. The deep veins of the upper limb

The brachial veins (figure 2) share their path with the brachial artery. They begin at the junction between the radial and the ulnar veins and end at the inferior margin of the teres major muscle, where they are joined by the basilic vein, forming the axillary vein. There are many collaterals between the two veins and small tributaries that drain the muscles of the upper arm (Lupu et al., 2010).

#### **3. Hemodynamics of an arteriovenous fistula**

The arteriovenous fistula is an abnormal connection between a donor artery and a receiving vein. The permeability of the fistula depends on several factors. One of them is the resistance of the outflow vascular bed, which in this case is venous, and thus has a low pressure and a low resistance. As the vein's diameter increases through the maturation process, the venous resistance decreases. This process occurs during the first 4-8 weeks after the creation of the AVF and comprises a thickening of the venous wall, an increase in diameter for the vein, its distal branches, and for the arterial segment proximal to the anastomosis. As the vein is connected to a high-pressure, high-velocity artery, the blood flow through the vein induces an increased wall shear stress. Experiments have shown that acute increases in wall shear stress results in endothelial release of nitric oxide, which in turn increases the lumen radius. This is available for both acute and chronic wall shear alterations (Zarins et al., 2004). Experimentally produced arteriovenous fistulas produce an immediate 10-fold increase in blood flow and a three-fold increase in wall shear stress. Within 24 hours, vessel enlargement begins, and at the end of 4 weeks lumen radius enlarges twofold and wall shear stress returns to normal (Masuda & Bassiouny, 1989).

The flow through the AVF is insignificant as long as the vein's diameter doesn't exceed that of the artery by at least 20%; however, a palpable thrill means that the AVF is functional. When the diameter of the vein exceeds that of the artery by 75%, the venous resistance is virtually null, and the flow through the fistula is limited only by the arterial flow. Between 20 and 75%, the flow through the AVF increases on an exponential basis and it depends mainly on the venous resistance (Hobson et al., 1973).

It is noteworthy that the portion of the artery distal to the AVF does not suffer any modifications, thereby maintaining its high resistance relative to the outflow of the fistula. This can lead to a reversal of flow in this segment, the so-called "steal syndrome", which can result in ischemic complications. This is especially true in proximal fistulas.

The body's adaptation to the presence of an AVF includes global decreased vascular resistance and an increase in cardiac output, which can lead to a hyperdynamic syndrome or even to congestive heart failure. This is easily explained when the flow through a fistula ranges from 650 ml/min (for a radio-cephalic fistula) to 1000-1100 ml/min (for a brachiocephalic, brachio-brachial or prosthetic fistula) (Schanzer, 2004; Ştiru, 2006). Any cardiovascular comorbidity can alter these patients' long-term prognosis.

#### **4. Advantages of an autogenous arteriovenous fistula**

A great number of studies have proven higher patency rates and lower complication rates for autogenous AVF when compared to synthetic bridge AVF (Palder et al., 1985; Enzler et al., 1996; Matsuura et al., 1998; Kherlakian et al., 2006; Kappos et al., 2007). Taking this into account, the National Kidney Foundation Dialysis Outcomes Quality Initiative (NKF-DOQI) guidelines for vascular access emphasize the use of the former over the latter (NKF-DOQI,

The Brachio-Brachial Arteriovenous Fistula 39

saline) verifies the vein's permeability. The entire length of the catheter is inserted into the vein. Now the brachial artery is cross-clamped proximally and distally to the proposed site of anastomosis and a longitudinal arteriotomy is performed. An end-to-side anastomosis is performed using a running nonabsorbable 7-0 polypropilene suture. The posterior wall is performed first and the brachial vein is divided distally before completing the anastomosis. Before tying the suture, the permeability of the fistula, as well as of the brachial artery should be evaluated. The vein should be inspected for a thrill; its absence indicates poor outflow and the surgeon must look for a potential problem and correct it (figure 3). All bleeding sources should be controlled and the skin is closed using interrupted simple

sutures, without drainage (Ştiru, 2006; Iliescu, 2007).

Fig. 3. The brachio-brachial fistula – intraoperative view

After 4 weeks, the vein is evaluated using Duplex scanning and, if its diameter is greater than 4 mm, it is transposed in a superficial plane in order to ease access for punctures. A longitudinal incision is performed on the antero-medial side of the arm, from the antecubital fossa to the axillary region. The neuro-vascular bundle is exposed, with the vein on the lateral side, the artery in the middle and the median nerve on the medial side. All of the venous collaterals are ligated, thus mobilizing the vein so that the aponeurosis can be closed underneath the vein with interrupted sutures (figure 4). A drainage tube is inserted and kept in place for 24 hours. The skin is closed with interrupted sutures, making sure that there is a 1.5 cm layer of tissue between the vein and the skin's surface to allow healing between needle punctures. The fistula can be used for hemodialysis after 3 weeks (Schanzer, 2004; Ştiru, 2006).

2001). Prosthetic and autologous AVF have similar patency rates for the first 4 postoperative weeks. After this period of time, synthetic bridge grafts require further interventions for angioplasty. Even with newer types of grafts, such as the Vectra Vascular Access grafts, the primary assisted rate of the prosthetic AVF is lower that of the autogenous AVF at 18 months of follow-up (58% vs 78%, respectively) (Kappos, 2007). The same study shows an overall access thrombosis rate of 17% for autogenous AVF and 34% for the Vectra graft. This rate is higher for other materials, such as ePTFE (Segal et al., 2003; Choi et al., 2003).

Most complications can be treated conservatively, without compromising the fistula (Matsuura et al., 1998). Severe hand ischemia, necessitating surgical treatment, occurs in 1% of patients with AVF and 2.7-4.3% of patients with graft AVF (Porter et al., 1985). Also, steal syndrome occurs in 73% of autogenous AVF and in 91% of graft AVF, as demonstrated by hemodynamic studies. Therapeutic options for hand ischemia always involve surgical interventions and include banding of the AVF (which is sometimes impractical, especially with prosthetic AVFs) and complex revascularization procedures.

Infection is a rare complication of the autogenous AVF; because there is no foreign body, it responds well to drainage and antibiotics. On the other hand, an infected prosthetic graft is a potentially lethal complication. The presence of foreign material makes this complication very difficult to treat. Prophylactic antibiotics are given before constructing the prosthetic AVF. Treatment requires removal of the whole prosthetic segment, debridement and systemic antibiotics.

Perigraft seroma is a very rare complication of the autogenous AVF (Blumenberg et al., 1985). It is more common with prosthetic grafts, because of changes in the structure of the ePTFE and of certain biological alterations in the host (Sladen & Mandl, 1985; Ahn & Machleder, 1986). Minimally invasive treatment is often unsuccesful, so more aggressive measures must be taken, leading even to replacement of the graft.

There is also a decreased risk of intimal hyperplasia because the anastomosis is much smaller compared to the one used with a prosthetic graft (Lumsden & Chen, 1997). In the rare case of fistula failure, the surgeon still has the backup possibility of creating a synthetic bridge fistula, an option that he would lose should he employ a prosthetic fistula in the first place.
