Definition:
It is an abnormal communication between an artery and a vein (or veins). It may be
1) a congenital malformation,
2) acquired by the trauma of a penetrating wound,
3) iatrogenic in which AVFs are created surgically in the arms or legs of patients undergoing renal dialysis. All arteriovenous communications have a structural and a physiological effect.
Structural effect:
The veins become dilated, tortuous and thick walled (arterialised).
Physiological effect:
There is high-pressure from the arterial system and an enhanced venous return/venous pressure. This results in an increase in pulse rate and cardiac output. The pulse pressure is high if there is a large and persistent shunt. Left ventricular enlargement and later cardiac failure may occur.
A congenital fistula in the young may cause overgrowth of a limb.
In the leg, indolent ulcers may result from relative ischaemia below the short circuit.
Clinical features:
Clinically, a pulsatile swelling or dilated tortuous veins may be present if the lesion is relatively superficial.
On palpation, a thrill is detected and auscultation reveals a buzzing continuous bruit.
Nicoladoni’s (1875) or Branham’s (1890) sign
Pressure on the artery proximal to the fistula causes the swelling to diminish in size, the thrill and bruit to cease and the pulse rate to fall. The pulse pressure also returns to normal.
Arteriography:
Arteriography confirms the lesion, which is noteworthy for the speed with which venous filling occurs. It is often difficult to pinpoint the actual site of the fistula.
Treatment:
Embolisation by the radiologist or excision is advocated only for severe deformity or recurrent haemorrhage. A plastic surgeon can also help for a proper ablation and reconstruction. Ligation of a ‘feeding’ artery is of no lasting value and is likely to be detrimental as it may preclude treatment by embolisation.
Clinical implications:
1) Autogenous AV fistulas have a lower risk of failure and require less revision compared to prosthetic grafts. The only problem with this is that a large number of patients lack suitable veins. This inability to make a proper vascular access is often termed as the Achilles tendon of hemodialysis.
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