Etiology and Pathophysiology

The vast majority of AVFs are caused by penetrating injuries as a result of stab wounds (63%), gunshots wounds (26%), and blunt trauma (1%). Iatrogenic AVFs most commonly involve the femoral artery after coronary or peripheral arteriography. AVF of the subclavian, carotid, and innominate arteries occur less commonly and usually result from inadvertent arterial injuries during attempted central venous catheter placement.

The formation of a traumatic AVF begins with an injury to the vessel wall such as a direct puncture, laceration, or mural hematoma. Concurrent injury to the artery and vein can create an immediate vascular communication that further stabilizes with time. More commonly, the injury leads to arterial pseudoaneurysm formation or local hematoma, causing compression of the adjacent vein and thus compromising the integrity of the vessel wall. The fistulous connection is established when the ischemic wall ruptures and blood flow is established through the new opening. This process is identifiable within 1 week of injury in two thirds of patients. The remaining cases are occult and might not be evident for months or years after the inciting trauma.

Once an anomalous connection is established, blood flows preferentially into the low-pressure venous system, bypassing the higher resistance of the arterial tree and capillary beds. This arteriovenous shunt has many local and systemic consequences. As blood flow through the fistula increases, retrograde flow in the arterial segment just distal to the AVF can create a distal steal syndrome. The high pressures of the arterial system are transmitted to the venous circulation, promptly causing venous hypertension. With time, the systemic effects of a high-flow AVF may become evident. The AVF creates a dramatic drop in systemic vascular resistance, thereby necessitating an increase in cardiac output to maintain adequate blood pressures. Progression of this process activates the renin–angiotensin–aldosterone pathway, promoting ventricular enlargement and myocardial remodeling. The end result is high-output heart failure that occurs in approximately 3% of patients with chronic traumatic AVF. The changes in the venous system are no less dramatic, as chronic venous hypertension leads to valvular incompetency and distal venous engorgement.

Clinical Presentation and Diagnosis

A high index of suspicion prompts early investigation and diagnosis within 1 week of injury in 65% of AVFs. The remaining 35% are not clinically evident for months or decades. The clinical presentation for AVF is determined primarily by the length of time since the inciting injury and the flow rate through the fistula. Within the first week, many traumatic AVFs are asymptomatic, so the mechanism of injury and physical examination findings are keys to the diagnosis. The most common findings in the first week after injury are the presence of a machinery-like bruit (61%), pulsatile mass (20%), or palpable thrill (11%).

One study found that a bruit was nearly universal in AVFs after 1 week (96%), and a pulsatile mass was observed in 52% and a palpable thrill in 14%. In long-standing fistulas, arterial insufficiency can evolve to produce symptoms of claudication, ischemic rest pain, or ischemic tissue loss. Venous congestion during the chronic stage can lead to extremity edema, varicosities, stasis dermatitis, and even venous ulceration. Congestive heart failure from an AVF is exceedingly rare in the acute period, but it complicates 3% of AVFs that are diagnosed late.

Suspicion for an AVF mandates imaging for confirmation. Duplex ultrasonography (US) is the initial imaging test of choice for the diagnosis of neck or extremity AVF. Doppler flow with color images can depict a direct connection between the artery and vein. The hallmarks of AVF on duplex include turbulent flow in the venous segment adjacent to the AVF, increased diastolic flow in a dilated artery proximal to the lesion, and decreased or retrograde arterial flow distal to the suspected site of the AVF (Figure 1).

Anatomic constraints limit the accuracy of US in evaluating suspected AVF in the thoracic outlet, chest, abdomen, and pelvis. In these locations, CT angiography (CTA) is the diagnostic modality of choice in most centers. Hallmarks of an AVF on CTA include dilated veins and early venous filling (Figure 2). If the imaging during a CTA is timed appropriately, there should be opacification of arteries with contrast, but little or no venous opacification. Substantial venous opacification, especially when asymmetric, is a strong clue to the presence of an AVF (Figure 3). Engorged veins with large numbers of venous collaterals are additional CTA findings that suggest an AVF (Figure 4).

The gold standard for the diagnosis of traumatic AVF is digital subtraction arteriography (DSA). The classic findings of an AVF are early venous filling at the site of the AVF with diminished distal arterial opacification (Figure 5). Small or branch vessel AVFs may be difficult to discern at first glance, and the actual arteriovenous connection might not be visualized in all cases. However, any early venous filling on arteriography should prompt selective catheterization to confirm the presence of an AVF and identify the parent artery and vein that give rise to the AVF. Other arterial abnormalities may also be identified, including an associated pseudoaneurysm or intimal flap. The sensitivity of arteriography to diagnose arterial injuries, including AVF, approaches 100% in experienced hands.

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