An arteriovenous fistula is an abnormal connection or passageway between an artery and a vein. It may be congenital, surgically created for hemodialysis treatments, or acquired due to pathologic process, such as trauma or erosion of an arterial aneurysm.


The surgical creation of an AV fistula provides a long-lasting site through which blood can be removed and returned during hemodialysis. The fistula, which allows the person to be connected to a dialysis machine, must be prepared by a surgeon weeks or months before dialysis is started. When the vein and artery are joined, the vein gradually becomes larger and stronger, creating the fistula that provides vascular access years longer than other types of access and with fewer complications.

Sometimes dialysis is only needed temporarily, but some people need it for the rest of their lives or until a kidney is available for a transplant. When kidney failure is diagnosed, time is needed to prepare the patient’s body with either an AV fistula or implantable devices that will connect the person to the dialysis machine.

Arteriovenous fistula per definition describes an abnormal communication between an artery and a vein. These communications are congenital; can occur at any point in the vascular system; and vary in size, length, location, and number. Arteriovenous fistula (AVF) is a term reserved for a singular communication between an artery and a vein that usually has an acquired etiology.

The first recorded case of an arteriovenous malformation (AVM) was in the late 16th century. In 1757, William Hunter described an arteriovenous fistula (AVF) as an abnormal communication between an artery and a vein. Krause in 1862 used injection studies of an amputated specimen to characterize the abnormal vasculature. In 1875, Nicoladoni described the reflex slowing of the pulse following occlusion of an artery proximal to an arteriovenous malformation (AVM). In 1920, Halsted contended that an arteriovenous malformation (AVM) could produce cardiac enlargement and observed that a congenital arteriovenous fistula (AVF) without a nevus is rare. In 1936, Emile Holman published a text describing the pathophysiology and natural history of arteriovenous malformations (AVMs). This publication forms the basis for today’s knowledge. In 1967, Fontaine observed that puberty or pregnancy can cause enlargement of arteriovenous malformations (AVMs)

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Symptoms and Diagnosis Surgery in india

When congenital arteriovenous fistulas are near the surface of the skin, they may appear swollen and reddish blue. In conspicuous places, such as the face, they appear purplish and may be unsightly.

If a large acquired arteriovenous fistula is not treated, a large volume of blood flows under high pressure from the artery into the vein network. Vein walls are not strong enough to withstand such high pressure, so the walls stretch and the veins enlarge and bulge (sometimes resembling varicose veins). In addition, blood flows more freely into the enlarged veins than it would if it continued its normal course through the arteries. As a result, blood pressure falls. To compensate for this fall in blood pressure, the heart pumps more forcefully and more rapidly, thus greatly increasing its output of blood. Eventually, the increased effort may strain the heart, causing heart failure. The larger the fistula, the more quickly heart failure can develop.

Why does a dural arteriovenous fistula (DAVF) develop?

Unlike AVMs, which are thought to be present from birth, cranial DAVF most often develop later in life following blockage or thrombosis of a cranial dural venous sinus. Cranial dural venous sinuses are relatively large-caliber blood-containing structures that exist in-between the leaflets of the brain’s dural covering. These sinuses usually move large volumes of venous blood from the brain, back towards the base of the brain where they form the internal jugular vein on each side of the head/neck junction. When a venous sinus blocks off for whatever reason, the brain can try to compensate by moving venous blood across other parallel or collateral pathways. In this process, however, a fistula may form, representing an abnormal collateral pathway to drain blood away from the brain. Why would a venous sinus block off or thrombose? Reasons include chronic central nervous system infection, brain trauma, or a patient with some form of hypercoagulability state (tendency to experience thrombosis).

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How is a dural arteriovenous fistula (DAVF) treated?

At present, the two main ways of treating a DAVF are through open surgery or endovascular surgery. The need for treatment becomes more pressing if cortical venous drainage is seen on the cerebral angiogram or if a patient has experienced rupture or other significant neurological effects of the DAVF.

    • Open Surgery : – The goal of surgery is to physically disconnect the fistula in the dura, with particular attention to obliterating the draining vein. A craniotomy is required for surgical disconnection of a cranial DAVF and a laminectomy or laminotomy is required for surgical disconnection of a spinal DAVF. Open surgery for a DAVF typically has a very high success rate.


  • Endovascular Surgery : – This involves a catheter-based technique for “squirting” of a “glue” (or a similar particle-composite or resin) into the lumen of arteries feeding the DAVF, or directly into the vein draining the DAVF. This process is known as embolization. Sometimes, embolization is used alone to obliterate the fistula, or it may be used as a helpful additional option prior to open surgery, to help shut down as much of the fistula as possible prior to the operation.
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