Trauma represents a major cause of death and morbidity in Western society, especially during the first four decades of life. Major vascular injuries are responsible for a substantial percentage of these deaths. Arterial and venous damage is seen in blunt and penetrating injuries involving both the extremities and body cavities. Direct vascular injuries are seen most frequently with penetrating trauma, especially in urban areas where civilian violence is increasing. The majority of vascular injuries that come to medical attention are in the extremities ( Table 1 199.)

Penetrating injuries following stabbings or wounds caused by low-velocity bullets can result in lacerations, transections, or contusions of arteries and veins. False aneurysms can develop from arterial lacerations while arteriovenous fistulae can occur in combined arterial and venous injuries. High-velocity missiles cause severe vascular destruction along their paths. However, indirect injury also occurs by the missile's peripheral cavitational effect, with mural contusion, thrombosis, or delayed necrosis. Blunt trauma occurring with crushing injuries and fractures frequently results in arterial contusion, resulting in thrombosis or wall separation with subsequent false aneurysm formation. Arterial stretch injuries are often seen with shoulder girdle injuries and knee dislocations, causing intimal disruption with acute or delayed thrombosis due to intramural dissection. Rapid deceleration can result in arterial transection, as is seen especially in the thoracic aorta in victims of high-speed motor vehicle accidents.

Major haemorrhage with resultant hypotension is the hallmark of central, large vessel injury, while in the extremities distal ischaemia, expanding haematoma, or obvious arterial bleeding are essentially diagnostic of a vascular injury. Findings suggestive of a possible vascular injury include diminished distal pulses, proximity of the wound to a major vessel, or an adjacent nerve injury.

The presence of a distal pulse does not exclude an arterial injury: such pulses may well be present if collateral circulation is adequate, if intimal injury has not yet resulted in thrombosis, or if a side-branch injury has occurred, such as in damage to the deep femoral artery. Physical examination should always include auscultation in the region of injury: a bruit may indicate an intimal flap or a traumatic arteriovenous fistula formation. Haemorrhage or haematoma formation may be absent in traumatic arteriovenous fistulae because of blood flow into the low-pressure venous system. Diffuse swelling of an extremity can suggest venous injury, with secondary venous thrombosis or obstruction.

Arteriography is indicated when there is a need to establish a diagnosis or provide information critical to operative treatment. When the diagnosis is obvious, however, particularly in the extremities, direct exploration is frequently preferred: angiography adds little but prolongs the duration of ischaemia. Biplanar arteriography aids in the diagnosis of arterial injury by revealing the extent and location of injury. The presence of an intimal flap, arterial thrombosis, and formation of a false aneurysm or arteriovenous fistula can be confirmed with angiography. Arteriography should only be performed on haemodynamically stable patients. Unstable patients should proceed to the operating room, where intraoperative evaluation and arteriography can be performed as needed.

Penetrating trauma of the chest and abdomen usually requires immediate surgical exploration to confirm the diagnosis and allow prompt repair of the vascular injury. Vascular injuries of the body cavities due to blunt trauma, however, are frequently occult and, therefore, difficult to diagnose. The patient may initially be haemodynamically stable and the first signs of vascular injury may be delayed haemodynamic collapse. If a routine chest radiograph reveals mediastinal widening or haemothorax in the haemodynamically stable patient, aortography is mandatory to exclude injury of the descending thoracic aorta. CAT scanning in the haemodynamically stable patient frequently discloses retroperitoneal haemorrhage suggestive of injury to the aorta, inferior vena cava, or renal vasculature.

While the management of different injuries is diverse, strategies share certain common principles of dealing with the injured vessel. These include achieving adequate surgical exposure for appropriate proximal and distal control, debridement or resection of the injured vessel, or both, so as to place suture lines in normal artery or vein, preference for autogenous rather than prosthetic conduits in contaminated surgical fields, and verification of the adequacy of the reconstruction.

First, proximal and distal control of the injury should be obtained. Blind clamping at the site of injury should be avoided, since it may cause further vessel or nervous injury. Appropriately placed incisions greatly aid in obtaining proximal control. The injured vessel should be inspected for thrombus before distal clamping and, if present, a thrombectomy should be performed with a Fogarty catheter.

Systemic anticoagulation during localized vascular repairs can aid in the prevention of thrombus formation. Systemic heparin is, however, generally not required for vascular repairs in the extremities, and it is often contraindicated in patients with major haemorrhage or associated multiple injuries, especially of the central nervous system. Regional heparin installation generally suffices when repairing an extremity injury.

Large vessel lacerations can frequently be repaired primarily using interrupted polypropylene sutures, which allow appropriate intima-to-intima reapproximation. Debridement of all areas of injured vessel wall is essential. In transected vessels, end-to-end anastomosis is required. Spatulation of the vessel ends in a cobra hood fashion (see Fig. 1 356) ensures adequate width of the vessel at the anastomosis. In mural contusion injuries, the vessels should be opened and inspected, and injured vessel wall segment resected. Repair can be performed with either a vein patch angioplasty or an end-to-end anastomosis.

Following debridement for extensive injury, excessive tension results in failure of an end-to-end repair, making interposition grafting necessary; autologous saphenous vein is the graft conduit of choice. Operative planning includes preparation of uninjured extremity for potential harvesting of a vein for use in the injured extremity as an arterial substitute. Removing a vein from an injured extremity adds to the risk of venous congestion from occult venous injury or delayed venous thrombosis. Some surgeons have advocated the use of polytetrafluorethylene (PTFE) prosthetic grafts in areas of minimal contamination, and in our view, it is the conduit of choice when a prosthetic graft must be placed in a contaminated field. Any graft type reconstruction must be provided with adequate soft tissue coverage. In areas of heavy contamination any graft is at risk for disruption, and arterial ligation with extra-anatomic reconstruction should be considered.

There has always been controversy over repair of venous injuries: advocates of repair say that improved limb blood flow favours patency of both arterial and venous reconstructions, as well as forestalling postphlebitic type sequelae. Those favouring simple ligation emphasize the likelihood of thrombosis in any graft placed in the venous circulation. We advocate a balanced approach: repair is appropriate if it can be simply accomplished, but complex reconstructions are avoided. Venous reconstruction needs strongly to be considered in patients with extensive soft tissue injury associated with the loss of important collateral venous drainage.

A false aneurysm, or pseudoaneurysm, develops at a site of arterial injury where the adjacent non-vascular tissues contain the haemorrhage. Retraction and thrombosis are inhibited because the artery is not completely transected. Arterial flow is usually maintained at or beyond the level of injury. These events result in systemic arterial pressure at the site of injury and a resultant pulsating haematoma. Since the wall of the false aneurysm is not arterial wall, it does not contain elastic fibres; it will expand over time and in doing so may cause symptoms attributable to compression of adjacent structures; alternatively, contained rupture may occur. False aneurysms can also form following blunt trauma, such as with arterial contusion with necrosis of the arterial wall, or following penetrating trauma such as knife and bullet injuries.

Arteriography, cardiac catheterization, arterial blood pressure monitoring line placement, and arterial blood gas sampling can cause iatrogenic arterial injuries and false aneurysms. Few false aneurysms close spontaneously; their natural history is to enlarge and to produce local symptoms from compression, embolization, or haemorrhage. Surgical repair at the earliest convenience is advised.

The traumatic arteriovenous fistula may develop when there is combined adjacent arterial and venous injury (Fig. 2) 357,358. Arteriovenous fistulae may form acutely at the time of injury or may develop late following lysis of an intervening obstructing thrombus, or by rupture of a false aneurysm into an adjacent vein. Distal ischaemia is rare early in the formation of such a fistula; however as the fistula increases in size there is resultant dilation of the venous system with potential reversal of distal arterial flow and subsequent distal ischaemia. Large arteriovenous fistulae cause the proximal arteries to dilate to accommodate the tremendous blood flow.

Clinical manifestations of arteriovenous fistulae include venous hypertension with venous insufficiency, varicosities, swelling of the extremities, distal ischaemia, and the central cardiovascular complications of tachycardia, hypotension, and high-output heart failure. Repair of arteriovenous fistulae is best done early, before significant venous dilation and engorgement occurs. Interruption of the fistula and primary repair of the artery and vein are curative.

The majority of vascular injuries occur in the extremities, and vascular trauma occurs approximately twice as often in the lower extremities as in the upper limbs. The most difficult peripheral vascular injuries are located below the inguinal ligament, where improper treatment is more likely to result in amputation: an amputation rate of approximately 49 per cent was seen in the Second World War, when most arterial injuries were treated with arterial ligation. During the Vietnam war, where prompt arterial repair with improved techniques was often combined with concomitant venous repair, there were few amputations.

Penetrating trauma is the main cause of most vascular injuries. Such wounds are usually readily apparent, and peripheral arterial injuries are frequently suspected because of absent distal pulses and secondary ischaemia. Injury following blunt trauma may not be apparent until irreversible ischaemia has developed, particularly since actual thrombosis at the site of injury may be delayed. Peripheral arterial injuries at certain levels are more prone to development of profound ischaemia and gangrene, while other sites of injury have a lower incidence of limb threatening ischaemia following injury or ligation (Table 2) 200.

Injury of the axillary artery is usually due to penetrating trauma, although proximal humeral fractures, shoulder dislocations, and shoulder girdle stretch injuries are also associated with axillary artery injuries. Improper use of crutches can result in an aneurysm of the axillary artery. The brachial artery is most frequently injured as a result of penetrating trauma, and following brachial artery catheterization. The incidence of this catheterization complication approaches 1 per cent. Brachial artery injuries are occasionally seen in patients with posterior elbow dislocations and humeral fractures. Few patients with isolated axillary or brachial artery injury require amputation, but many patients will have ischaemic symptoms on exertion if arterial repair is not performed. Isolated radial or ulnar artery injuries are rarely associated with ischaemia or amputation. If primary arterial repair cannot be performed, ligation is well tolerated by the vast majority of patients with isolated radial or ulnar artery injury, but not both.

Injuries to the common femoral or superficial femoral arteries are often quite apparent because of loss of distal pulses and subsequent ischaemia, while injury to the profunda femoris artery may be difficult to diagnose because there are no signs of distal ischaemia. Local exploration or arteriography is frequently necessary to diagnose a profunda femoris injury, unless one detects an arteriovenous fistula or false aneurysm at the injury site. Patients with femoral shaft fractures and diminished distal circulation require arteriography to exclude superficial femoral artery injury. If they have rich collaterals, patients with superficial femoral artery injury may not experience profound ischaemia. Onset of ischaemia is frequently delayed because of thrombosis and loss of collateral flow secondary to stasis, traumatic swelling, or tourniquet use.

The popliteal region represents the greatest challenge in peripheral vascular trauma. Both penetrating and blunt trauma contribute to arterial and venous injuries in this area. Penetrating trauma, gunshot wounds more often than stab wounds, is clinically obvious in most cases. Blunt trauma is less obvious and is responsible for delay in treatment. Limited collaterals at the popliteal level, combined with injuries of the collateral arteries, often cause ischaemia resulting in eventual amputation. The amputation rate for popliteal arterial injuries in the civilian population is in excess of 30 per cent. As a result of the association of certain types of injuries with popliteal vascular injuries, an aggressive approach towards diagnosis and treatment is essential. All patients with knee injuries, whether blunt or penetrating, with an ischaemic appearing limb, should undergo urgent operation. Systemic heparin should be administered immediately, if no contraindication exists. Operative planning should give priority to revascularization if orthopaedic treatment will delay final revascularization more than 4 to 6 h from the time of original injury or ischaemia.

Following revascularization, arteriography is recommended to confirm patency of repair and distal outflow tract. Concomitant four-compartment fasciotomy should be routinely performed if extensive soft tissue injury exists or if ischaemia time is long. Venous repair is more critical at the popliteal level than at any other peripheral injury site and patency of one popliteal vein is desirable, especially when soft tissue injury is extensive. Venous thrombectomy may be required to open the venous system and venorrhaphy or interposition grafting may be required to correct the venous injury.

Arteriography should be performed in patients with knee injuries in which there is a significant incidence of popliteal arterial injury, even when there is no evidence of ischaemia. These injuries include penetrating trauma that traverses the popliteal fossa, knee dislocations, blunt knee trauma due to automobile bumpers, and fractures near the knee associated with resolution of ischaemia following fracture reduction. Orthopaedic tourniquets themselves can produce ischaemia and thrombosis. It is always important to evaluate prospectively the likelihood of a functional limb before embarking on complex reconstruction. Vascular salvage that results in major motor or sensory dysfunction in a limb may not be the ideal treatment, especially when the recovery time for associated orthopaedic and soft tissue injuries is considered. A paralysed extremity without sensory function is often best treated by early amputation rather than by extensive vascular, orthopaedic, and soft tissue reconstruction.

Vascular injury in the region of the neck is frequently suspected from a history of penetrating trauma, expanding haematoma, pulsatile bleeding, palpable thrill, audible bruit, or neurological deficit. Careful neurological evaluation is essential in all patients with cervical trauma. Patients with penetrating trauma and a diffusely abnormal lateralizing neurological examination frequently have extracranial cerebrovascular occlusion or embolization. More localized deficits can occur following cerebrovascular injury or direct injury to the brachial plexus, cervical plexus, or a cranial nerve. Patients suffering blunt trauma can have neurological deficits from closed head injuries or brachial plexus stretch injuries. Findings suggestive of carotid injury from blunt trauma include delayed onset of neurological symptoms due to delayed carotid thrombosis, transient ischaemic attacks due to emboli arising from a carotid intimal injury site, or Horner's syndrome due to carotid dissection. Angiography is appropriate for all patients with neurological deficits following cervical trauma. Patients who are haemodynamically stable and who have developed appreciable neurological deficit should have a preoperative CT scan of the brain.

Most vascular injuries in the neck are caused by penetrating trauma. To aid in evaluation of potential vascular injuries in the neck, one should determine the level of penetration before proceeding with exploration. Preoperative angiography is recommended for potential injuries to the proximal common carotid artery as well as the distal internal carotid artery at the base of the skull. Special preparations are frequently required for proximal and distal carotid artery injuries. Sternotomy is required for proximal control of common carotid injuries at its origin. Visualization of distal internal carotid artery injuries may require subluxation of the mandible, which requires preoperative placement of dental wires.

Operative exploration is warranted in all patients with neck injuries that penetrate the platysma, as well as all arterial injuries identified by angiography. In addition to preparing the neck region for surgery, the entire chest and a portion of the lower extremity, for saphenous vein harvesting, should be included in the operative field. The carotid bifurcation region is approached by an incision anterior to the sternocleidomastoid muscle. Carotid origin injuries require a median sternotomy. Proximal vertebral artery injuries are approached by a supraclavicular incision. With carotid injuries, proximal control is best achieved before identifying the site of arterial injury. Systemic anticoagulation is recommended unless contraindicated by other injuries. Limited injuries of the carotid system can often be repaired primarily. It is essential to resect all devitalized arterial wall. A temporary carotid shunt is used to reduce cerebral ischaemia time in severe injuries that require an end-to-end anastomosis, vein patch repair, or graft interposition. If graft interposition is planned, it is helpful to place the shunt through the graft prior to temporary shunt placement. Shunting is not required in repair of external carotid artery injury: arterial ligation is acceptable if simple repair is impossible. Ligation of the common or internal carotid artery should be avoided, if at all possible, because of the risk of stroke, except in patients with distal internal carotid artery injury at the base of the skull without adequate length of distal artery to allow repair and those with complete internal carotid occlusion with severe cerebral infarct. Patients with non-haemorrhagic stroke after carotid occlusion are likely to have conversion to a more severe haemorrhagic cerebral infarct if internal carotid circulation is restored. If carotid ligation is required, adjuvant heparin therapy may reduce the risk of thrombotic stroke.

The vertebral artery is less frequently injured, given its protected course in the transverse foramina of the cervical vertebrae. Since most vertebral arteries are paired and form a single basilar artery, vertebral ligation is acceptable in most cases. Preoperative angiography can help identify the location of vertebral artery injury and, equally important, the status of the contralateral vertebral artery. Primary repair of injuries to a single patent vertebral artery or a dominant vertebral artery should be carried out, if possible.

Venous injuries of the neck are best treated with primary repair or ligation; bilateral internal jugular venous ligations should be avoided, but extensive repairs with interposition grafts are rarely warranted. Special care is required when dealing with venous injuries to prevent air embolization at the site of injury. During venous ligation, one should protect the vagus nerve and other cranial nerves.

Postoperative care should include elevation of the head to reduce venous engorgement and swelling. Frequent neurological checks are essential to diagnose early postoperative complications at the site of repair. Prompt angiography, duplex scanning, or reoperation may be necessary to limit further neurological injury. Infusion of low molecular weight dextran, at a rate of 30 &mgr;l/h for 24 to 48 h following carotid artery repair helps prevent thromboembolic events.

The most frequent sites of major injury in patients who have sustained blunt thoracic injuries are the proximal descending thoracic aorta and the proximal innominate artery. Both of these injuries are caused by high-speed motor vehicle accidents. Injury to the descending thoracic aorta occurs at the level of the ligamentum arteriosum, where the thoracic aorta is fixed in the posterior mediastinum. During the sudden deceleration which occurs in high-speed accidents the heart and aortic arch have continued forward momentum, resulting in a tear injury of the proximal, fixed, descending thoracic aorta. Innominate artery injury occurs most frequently from compression between the sternum and vertebral bodies, as well as from hyperextension of the neck. More severe injuries are usually fatal and never require medical attention.

The diagnosis of blunt thoracic vascular injuries is made from a combination of history, physical examination, and radiographic examinations as necessary. Pertinent points in the patient's history include motor vehicle accident at speeds greater than 70 km/h, sudden deceleration, driver of a vehicle, death of another victim in the accident, or loss of consciousness at the scene. Physical examination is frequently not very revealing until hypotension develops. Local findings include chest wall contusions, supraclavicular haematomas, clavicle or rib fractures, a systolic murmur, and diminished femoral or radial pulses. Chest radiographs are frequently abnormal in trauma victims, but suggestive findings of an aortic or great vessel injury include widened superior mediastinum, ill-defined or enlarged aortic arch shadow, apical pleural cap, left hemithorax, deviation of a nasogastric tube to the right with aortic injury or to the left with innominate artery injury, deviation of the trachea to the right or left mainstem bronchus inferiorly. Aortography is indicated in stable patients with these abnormalities, as well as in some patients with normal chest radiographs, but with an appropriate history suggestive of severe thoracic trauma. The unstable patient with an abnormal chest radiograph is often best served by immediate exploratory left thoracotomy.

The approach and repair of thoracic vascular injury depends upon the location and type of injury. Injury to the descending thoracic aortic caused by deceleration is best approached by a left fourth intercostal space posterolateral thoracotomy. The aortic repair can be by primary end-to-end anastomosis or with an interposition Dacron graft. Adjuvant treatment recommended by some authors to reduce spinal cord ischaemia includes partial or complete cardiopulmonary bypass, or ascending aorta-to-descending aorta shunting, while others advocate a prompt clamp and repair technique.

The innominate vessels are approached by median sternotomy. Some penetrating injuries can be repaired primarily; however, extensive arterial injuries and deceleration injuries require the innominate artery to be resected and its origin to be oversewn at the aortic arch. Dacron graft placement from the right lateral side of the ascending aorta to the distal innominate artery is used in the reconstruction. Innominate venous injuries are best repaired primarily, when possible, but when this is not possible ligation is appropriate and is usually well tolerated.

The right subclavian vessels are approached by median sternotomy with right supraclavicular extension. In distal subclavian injuries, a supraclavicular approach, with or without clavicle resection, may be adequate. The proximal left subclavian artery can be controlled by a left third intercostal space anterolateral thoracotomy. For full visualization of the proximal left subclavian artery, a trap-door thoracotomy may be required through left third intercostal and left supraclavicular incisions, with an intervening partial median sternotomy. Subclavian venous repairs are often impractical because injuries are too extensive and multiple branches require venous ligation. Techniques of subclavian artery repair include end-to-end anastomosis and interposition grafting with Dacron or PTFE prostheses.

The major abdominal vasculature is largely protected from blunt injury because of its retroperitoneal location adjacent to the spinal column. Penetrating trauma, however, can cause vascular injury at any site. Major vascular injury with free intraperitoneal haemorrhage is frequently fatal or at best haemodynamically unstable, requiring immediately laparotomy for diagnosis and treatment. Haemorrhage arising within the retroperitoneum or mesentery may be contained, allowing stabilization and further evaluation.

An excretory urogram should be obtained in stable victims of penetrating trauma before exploratory laparotomy is undertaken. Failure to see one kidney is highly suggestive of a renal vascular injury. Computed tomography frequently reveals the presence or absence of a retroperitoneal haematoma. Patients with penetrating trauma should have exploration of retroperitoneal haematomas for possible aortic, caval, or renal vascular injuries. Arteriography is helpful in confirming renal artery injuries in patients with failure to visualize one kidney on urography.

Blunt abdominal trauma may produce avulsions of mesenteric arterial branches, of portal venous branches, or of renal vessels with resultant mesenteric, periportal, or retroperitoneal haematomas. Intimal injuries of visceral vessels due to blunt trauma may produce arterial thrombosis and subsequent ischaemia. Infrarenal abdominal aortic intimal injury from seat belt compression of an aorta during automobile accidents can result in aortic thrombosis and profound lower extremity ischaemia.

Pelvic fractures can be associated with large pelvic haematomas from cancellous bone disruptions, as well as vascular injuries. Arteriography is used to confirm hypogastric branch artery injuries. Arteriographic embolization is preferred to direct surgical ligation of the hypogastric arteries in patients with pelvic fractures and persistent haemorrhage.

A standard midline incision is appropriate for nearly all patients with abdominal vascular injuries. Extension into a left thoracoabdominal incision aids visualization of the proximal aorta. Appropriate exposure of the retroperitoneum depends on the vessels injured. Initial control of haemorrhage by packing the upper quadrants with laparotomy pads, as well as by evisceration of the small bowel, aids in the identification of the source of haemorrhage.

Suprarenal aortic injuries frequently require complete mobilization of the spleen, pancreas, stomach, and left colon to the right side of the abdomen to allow adequate exposure of the suprarenal aorta, coeliac axis, and the origin of the superior mesenteric artery. The infrarenal aorta and left renal vessels can be approached directly in the midline of the retroperitoneum just left of the root of the small bowel mesentery and below the transverse mesocolon. The inferior vena cava and right renal vessels are best seen by reflecting the right colon to the left and by extensive Kocher manoeuvre of the duodenum.

The iliac vessels are approached directly for proximal and distal control. The common iliac artery is best visualized at the aortic bifurcation in the midline of the retroperitoneum. The iliac veins are located posterior and to the right of the iliac arteries. In patients with extensive iliac venous injury, the common iliac artery may be divided over the site of venous injury. Following iliac venous repair or ligation, the common iliac artery can be reapproximated end-to-end. The distal external iliac arteries can be easily controlled just proximal to the inguinal ligament within the abdominal cavity. To avoid ureteral injury the retroperitoneum should be retracted and not divided in the region of the common iliac bifurcation.

Major arterial injuries in the abdomen can frequently be repaired by lateral arteriorrhaphy or end-to-end anastomosis. More extensive injuries to the aorta require patch aortoplasty with a PTFE patch or aortic replacement with a Dacron or a PTFE graft. When interposition grafting is required, the choice of vein, autologous artery, Dacron, or PTFE graft as a conduit, is determined by the size of the artery and amount of gastrointestinal contamination. PTFE is the prosthetic conduit of choice in contaminated surgical fields. If contamination is severe, arterial ligation and extra-anatomic reconstruction may be advisable. Injuries at the origin of a visceral artery frequently require revascularization grafting, such as an aortorenal or an aortosuperior mesenteric artery bypass. Coeliac and inferior mesenteric artery origin injuries can be ligated in most cases because of excellent collateralization from the superior mesenteric artery.

Venous injuries should be repaired if possible—most only require lateral venorrhaphy. To prevent tearing of these thin walled vessels vascular clamps should be avoided, and vessel loops or compression with sponge forceps should be used for temporary control. If repair of a venous injury is impracticable, ligation is acceptable. Ligation of the left renal vein should be as close to the inferior vena cava as is possible; venous drainage of the left kidney will proceed through the adrenal, gonadal, and lumbar veins. Injury to the right renal vein should be repaired, if at all possible, for the paucity of venous collateral branches may result in venous hypertension and renal dysfunction following right renal vein ligation.

Inferior vena cava injuries can frequently be repaired primarily using transient caval compression with sponge forceps or with partial-occlusion clamps. If complete occlusion is required to control caval haemorrhage, the surgeon should be aware of potentially major hypotension with caval clamping. Atriocaval shunting for suprarenal caval injuries as well as hepatic venous injuries has been described to maintain venous return during caval repair. Extensive caval injuries may require patch angioplasty or ligation. If the inferior vena cava repair results in a significant narrowing of the inferior vena cava, ligation is preferred to prevent the possibility of caval thrombosis and pulmonary embolism. Ligation of the iliac, hepatic, or portal veins as well as the inferior vena cava requires administration of additional fluid perioperatively. Following iliac or caval ligation, postoperative elevation of the lower extremities is recommended to reduce swelling. Concern over venostasis and potential deep venous thrombosis following major venous ligation warrants administration of subcutaneous heparin, 5000 units twice daily, in suitable patients.

Abbott WM, Darling RC. Axillary artery aneurysms secondary to crutch trauma. Am J Surg 1973; 125: 515–20.

Accola KD, Feliciano DV, Mattox KL, Burch JM, Beall AC Jr, Jordon GL Jr. Management of injuries to the superior mesenteric artery. J Trauma 1986; 26: 313–18.

Akins CW, Buckley MJ, Daggett W, McIlduff JB, Austen WG. Acute traumatic disruption of the thoracic aorta: a ten-year experience. Ann Thoracic Surg 1981; 31: 305–9.

DeBakey ME, Simeone FA. Battle injuries of the arteries in World War II: an analysis of 2,471 cases. Ann Surg 1946; 123: 534–79.

Fabian TC, Turkleson NL, Connelly TL, Stone HH. Injury to the popliteal artery. Am J Surg 1982; 143: 225–8.

Feliciano DV. Approach to major abdominal vascular injury. J Vasc Surg 1988; 7: 730–6.

Fisher DF Jr, Clagett GP, Parker JI, et al. Mandibular subluxation for high carotid exposure. J Vasc Surg 1984; 1: 727–33.

Goldman MH, Kent S, Schaumburg E. Brachial artery injuries associated with posterior elbow dislocation. Surg Gynecol Obstet 1987; 164: 95–7.

Graham JM, Feliciano DV, Mattox KL, Beall AC Jr. Innominate vascular injury. J Trauma 1982; 22: 647–55.

Gregory RT, et al. The mangled extremity syndrome (M.E.S.): a severity grading system for multisystem injury of the extremity. J Trauma 1985; 25: 1147–50.

Hardy JD, Raju S, Neely WA, Berry DW. Aortic and other arterial injuries Ann Surg 1975; 181: 640–53.

Hewitt RL. Vascular injuries. In: Haimovici H, ed. Vascular emergencies. New York: Appleton-Century Croft, 1982: 261.

Hughes CW. Arterial repair during the Korean War. Ann Surg 1958; 147: 555–61.

Makins GH. Injuries to the blood vessels. In: Official history of the Great War Medical Service. Surgery of the War. Vol. 2, London: His Majesty's Stationery Office. 1922: 170–296.

Mattox KL, Feliciano DC. Truncal vascular trauma: aorta, innominate vessels, vena cava, portal vein,and visceral arteries. In: Wilson SE, Veith J, Hobson RW II, Williams RA, eds. Vascular surgery. New York: McGraw-Hill,1987: 818–19.

Mattox KL, Holzman M, Pichard LR, Beall AC Jr, DeBakey ME. Clamp/repair a safe technique for treatment of blunt injury to the descending thoracic aorta. Ann Thoracic Surg 1985: 40; 456–63.

Mattox KL, Feliciano DV, Burch J, Beall AC Jr., Jordan GL Jr, DeBakey ME. Five thousand seven hundred sixty cardiovascular injuries in 4,459 patients, epidemiologic evolution 1958–1987. Ann Surg 1989; 209: 698–707.

McCollum CH, Mavor E. Brachial artery injury after cardiac catherization. J Vasc Surg 1986; 4: 355–9.

Mullins RJ, Lucas CE, Ledgerwood AM. The natural history following venous ligation for civilian injuries. J Trauma 1980; 20: 737–43.

O'Donnell TF Jr, Brewster DC, Darling RC, Veen H, Waltman AA. Arterial injuries associated with fractures and/or dislocations of the knee. J Trauma 1977; 17: 775–84.

Orringer MD, Kirsch MM. Primary repair of acute traumatic aortic disruption. Ann Thoracic Surg 1983; 35: 672–5.

Pasch AR, et al. Results of venous reconstruction after civilian vascular trauma. Arch Surg 1986; 121: 607–11.

Pate JW. Traumatic rupture of the aorta: emergency operation. Ann Thoracic Surg 1985; 39: 531–7.

Perry MO, Thal ER, Shires GT. Management of arterial injuries. Ann Surg 1971; 173: 403–8.

Rich NM. Principles and indications of primary venous repair. Surgery 1982; 91: 492–6.

Rich NM, Baugh JH, Hughes CW. Acute arterial injuries in Vietnam: 1000 cases. J Trauma 1970; 10: 359–69.

Rovito PF. Atrial caval shunting in blunt hepatic vascular injury. Ann Surg 1987; 205: 318–21.

Treiman RL, Doty D, Gaspar MR. Acute vascular trauma: a 15-year study. Am J Surg 1966; 111: 469–73.

Trunkey DD, Lewis FR, eds. Current therapy of trauma–2. Toronto: BC Decker, 1986; xi.

Vaughan GD, Mattox KL, Feliciano DV, Beall AC Jr, DeBakey ME. Surgical experience with expanded polytetrafluorethylene (PTFE) as a replacement graft for traumatized vessels. J Trauma 1979; 19: 403–8.