The presence of an abnormal channel between an artery and a vein is called an arteriovenous fistula. As the normal orifice of blood from the artery flows into the accompanying vein, it can cause local vasculopathy of the fistula and hemodynamic changes in the local, peripheral circulation and systemic systems of the fistula. It can be congenitally present or acquired as a result of trauma. Arteriovenous fistulas cause a direct inflow of arterial blood into the veins instead of through the capillaries that should perfuse the tissues, and this blood is not exchanged in the tissues and becomes an ineffective circulation, resulting in ischemic necrosis of the tissues; total peripheral resistance decreases, blood pressure decreases, and the heartbeat compensates by increasing the return blood volume above the cardiac load, resulting in heart failure. Patients with arteriovenous fistula present with peripheral varicose veins, slightly elevated local skin temperature, hyperpigmentation, and ulcer formation; there may be a vascular murmur or tremor at the fistula opening. In advanced stages, there is cardiac enlargement and heart failure. Single or acquired patients should be actively treated by surgical repair or excision or intervention; congenital multiple patients are mostly treated conservatively. Etiology 1, penetrating injuries The vast majority of acquired arteriovenous fistulas are caused by penetrating injuries. Such as various puncture wounds, especially high velocity bullets, sodium iron and glass fragments flying injuries. At the time of injury, arteries and veins within the same sheath are injured together. Closed fractures are caused by sharp fracture ends or fragments of bone piercing the adjacent vessels. Percutaneous puncture arteriography and trauma during surgery are the most common etiologies. Fourth, the five lumbar discs are close to the iliac vessels, which can easily cause iliac arteriovenous fistula due to injury to the iliac vessels during laminectomy. The external opening of the general penetrating injury is very small, and because the adjacent muscles and soft tissues prevent a large amount of bleeding, a hematoma is formed within the local soft tissues, and the hematoma forms the capsule wall of the arteriovenous fistula after mechanization. 2.Crush injury Parallel arteries and veins can be crushed at the same time to form an arteriovenous fistula. Injuries of medical origin, such as splenectomy and nephrectomy, ligation of the splenic and renal tissues, ligation of the femoral artery during amputation, and ligation of the superior pole artery during thyroidectomy, can lead to arteriovenous fistulas. External violence acting on soft tissues and squeezing soft tissues on bones, such as shoulder and hip contusions can cause local arteriovenous fistula, and skull fracture can cause arteriovenous fistula of meningeal vessels. 3.Other causes Arteriovenous fistula can occur when the arteriovenous aneurysm gradually produces adhesion and corrosion and finally penetrates the accompanying vein, or even when the tumor ulcer breaks into the large vessel wall. Pathological changes The traffic between arteries and veins can be divided into two types: direct and indirect. When adjacent arteries and veins are injured at the same time, the wound edges are directly aligned with each other and within a few days they can be directly communicated, which is called direct arteriovenous fistula. If the arterial and venous wounds are not directly aligned, but a hematoma exists between them, the hematoma later becomes mechanized and forms a sac or tube between the artery and vein, called an indirect fistula. The proximal artery of the fistula is progressively dilated and elongated; the arterial wall is initially somewhat thickened and later undergoes degenerative changes with atrophy of smooth muscle fibers, reduction of elastic fibers, thinning of the wall, and atheromatous plaque formation. If the fistula hole is large, the adjacent fistula main artery may expand and form an aneurysm. The distal artery shrinks due to decreased blood flow. The vein gradually dilates, reaching the last valve distally and the vena cava proximally. If the fistula is large, a sudden increase in intravenous pressure can be seen a few weeks after trauma as a local pulsating mass due to venous distension, much like a pseudoaneurysm. When the fistula is small, the vein at the fistula gradually expands, the vein lining thickens and the fibrous tissue proliferates, forming an “action-like wall” due to the gradual thickening of the vein wall. Therefore, about six months after the trauma, it is difficult to distinguish the artery from the vein in terms of appearance. The vein wall is also degenerated and the internal elastic layer splits and disappears. Distal veins dilate and elongate, and subsequently, venous insufficiency is exacerbated by venous valve closure insufficiency. Arteriovenous fistulas promote the formation of a large number of collateral circuits, even more so than arteriovenous collateral circuits, with extensive varicose veins in the superficial surface. Most traumatic aneurysms may be arterial, venous, or between arterioles. Clinical manifestations Acute arteriovenous fistulas may appear immediately after injury or after the clot has dissolved outside the arteriovenous communication, with a hematoma localized to the injury and, in most cases, with tremors and murmurs. In most patients, arterial pulsation is still palpable in the limb distal to the arteriovenous fistula, but is weaker than on the healthy side. In cases of superficial femoral artery with deep femoral artery injury in the lower extremity, the dorsalis pedis artery is not palpable and there are symptoms of limb ischemia. Patients with chronic arteriovenous fistula have swelling, numbness, pain, and weakness in the affected limb. There is a humming sound localized to the pulsatile mass. Heart failure may have chest tightness, palpitations, and shortness of breath. Common signs include: 1. murmurs and tremors in the fistula area, regardless of the size of the arteriovenous fistula, a typical, rough and continuous rumbling sound called “machine-like” murmur can be heard at the arteriovenous fistula site. The murmur increases during cardiac systole and travels proximally and distally along the main vessels. This murmur is distinguished from the weak diastolic murmur caused by a pseudoaneurysm and the systolic murmur caused by arterial stenosis.2. Increased pulse rate: This is the result of the Braibridge reflex caused by an increase in venous blood return or an increase in cardiac workload due to a decrease in mean arterial pressure (Marey’s law).3. Heart enlargement and heart failure: The venous pressure increases due to the rapid flow of blood through the fistula. veins, venous pressure increases and the amount of blood returning to the heart increases, causing heart enlargement. Progressive enlargement of the heart can lead to heart failure. The degree of heart enlargement and heart failure is closely related to the size and location of the fistula and the length of time it has been present. The closer the fistula is to the heart, the earlier and more severe the heart failure occurs, such as venous fistulas formed by direct branches of the aortic arch (carotid artery, arteries without each, subclavian artery) and accompanying veins.4. Elevated local temperature: The surface skin temperature of the affected limb is elevated at the site of the arteriovenous fistula, while the skin temperature may be normal or below normal at the more distant site of the high arteriovenous fistula.5. Venous insufficiency: The direct traffic between the arteries and veins increases the venous . In most patients, the superficial veins near or distal to the arteriovenous fistula are dilated and curved. Skin pigmentation is accompanied by cellulitis of the lower legs, and ulcers often occur in the toes or fingers, showing symptoms similar to those following deep phlebitis. Diagnosis The diagnosis of arteriovenous fistula is generally not difficult. In the history of penetrating trauma, the patient may find a pulsating mass on his own and there is a localized buzzing sound. The diagnosis of an arteriovenous fistula should be considered when there is swelling of one limb, varicose veins and venous valve insufficiency, higher local skin temperature than the contralateral limb, and scarring, murmurs, and tremors at the site of injury. Patients with acute arteriovenous fistula often have severe multiple trauma or penetrating injuries to the limb. The diagnosis and management of arteriovenous fistulas is often delayed because of the focus of attention on the severely injured bones and soft tissues during the examination of the patient. Arteriography can clarify the location and size of the fistula as well as the enlargement of nearby vessels and collateral circulation. When the fistula is small, the artery is visualized and so are the veins near the fistula, but the veins distal to the fistula are rarely visualized. When the fistula is large, a rapid radiograph is needed to see the artery, but the dilated veins near the fistula are clearly visible, and the most clearly dilated part often suggests the site of the fistula, and the veins distal to the fistula may be shown in increased numbers and with varicosities. 2. Measurement of fistula by acupressure (Brankam’s sign) The fistula is blocked by acupressure, and the heart rate and blood pressure before and after blocking the shunt are measured and compared. The heart rate is significantly slower after the shunt is blocked. This is because the fistula closes, forcing the blood to flow through the normal capillary network, thus increasing the peripheral resistance. At the same time, after the fistula is suddenly blocked, the blood volume that used to be shunted through the fistula is infiltrated into the peripheral arterial system. The increase in peripheral resistance and the sudden increase in additional blood volume in the arterial system increase the blood pressure, which correspondingly stimulates the aortic decompression nerve and the nerve endings in the carotid sinus, causing the vasodilatory center to act as an inhibitor, resulting in a slower pulse rate. When the fistula is large and there is little collateral circulation, the decrease in mean arterial pressure is particularly pronounced; when the fistula is small and there is abundant collateral circulation, the mean arterial pressure at the distal end of the fistula does not change much. In general, arterial pressure is measured by direct puncture of the artery, but arterial pressure distal to the fistula can also be measured by Doppler ultrasonography and volumetric tracing of the limb. 4. Measurement of cardiac output Echocardiography and the indicated dilution method can be used to determine cardiac output and to understand cardiac function. 5.Venous blood oxygen measurement When blood is drawn from a vein at the arteriovenous fistula or from a vein proximal to the fistula and compared with venous blood from the same part of the opposite limb, the venous pressure of the affected limb is redder than the venous blood of the normal limb, and the partial pressure of oxygen is significantly higher. 6, venous pressure measurement The venous pressure of the affected limb was increased. The increase in venous pressure near the fistula was more pronounced.
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