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Fewer than 10% of patients with polytrauma have associated vascular injuries, but these injuries can cause significant morbidity and mortality. In most European countries, the majority of vascular trauma is caused by blunt (traffic accidents) and iatrogenic injuries. In South Africa, injuries are mostly penetrating and have also changed from predominantly stab wounds to injuries caused by firearms.
A clear understanding of the pathophysiology of vascular trauma and a logical approach to the management of those injuries are essential for a favourable outcome.
Vascular injuries are classified according to the mechanism of the injury.
Direct trauma to the artery accounts for the majority of blunt vascular injuries. Indirect trauma is usually the result of shearing and distraction forces following dislocation of major joints, displaced long-bone fractures and acceleration/deceleration injuries as seen with high-speed motor vehicle accidents and falls from a height. Blunt trauma causes contusion of the arterial wall with disruption of the intima. This intimal tear may cause immediate obstruction because of an intimal flap or may predispose to thrombosis and delayed occlusion ( Fig. 9.1a –d). As the vessel is stretched further, progressive layers of the media are disrupted until the continuity of the vessel is maintained only by the elastic adventitia or there is complete disruption.
Penetrating trauma may result in partial or complete transection of a vessel. Bleeding is often brisk and distal flow may be interrupted. Stab and low-velocity missile injuries cause localised damage confined to the injury tract. High-velocity missiles cause total tissue destruction around the missile tract, surrounded by an area of doubtful tissue viability, causing extensive associated soft-tissue trauma. The shock wave of a high-velocity missile can also cause intimal injury. The vessel may be macroscopically intact with minimal bruising, but on opening the vessel, there is an intimal tear with superimposed thrombosis. Shotgun injuries cause extensive local tissue destruction with often multiple sites of perforation ( Fig. 9.2 ). Bomb blasts cause complex injuries because of the combination of extensive local tissue trauma, high-velocity fragments and thermal injury.
Iatrogenic injuries are becoming increasingly important and account for more than 40% of vascular trauma in many European countries.
Vascular injuries have significant sequelae ( Box 9.1 , Figs. 9.3 and 9.4 ). A contused artery may be patent initially but thrombose later. Subsequent propagation of thrombus may cause progressive ischaemia by obstructing essential collaterals. Acute ischaemia leads to degeneration and necrosis of muscle cells and Wallerian degeneration in nerves. Findings from large-animal studies indicate that early restoration of flow within 3 hours is associated with near-complete recovery, whereas delayed revascularisation at 6 hours was associated with significant muscle necrosis and nerve degeneration.
Concomitant fractures, dislocations, injuries to accompanying veins and nerves, soft-tissue trauma and contamination of the wound with foreign material serve to compound vascular injury. Other determinants of the final outcome are the level of vascular injury, the quality of the collateral circulation and pre-existing occlusive arterial disease.
Information regarding the mechanism of the trauma, blood loss before hospital admission and underlying vascular disease should be obtained.
Initial assessment should be carried out according to advanced trauma life support (ATLS) principles and life-threatening conditions managed. Vascular injury may present with any of the sequelae listed in Box 9.1 . Clinical signs of vascular injuries can be divided into hard and soft signs.
Hard signs of vascular injury:
Active pulsatile bleeding.
Shock with ongoing bleeding.
Absent distal pulses.
Symptoms and signs of acute ischaemia.
Expanding or pulsating haematoma.
Bruits or thrill over the area of injury.
Soft signs of vascular injury:
History of severe bleeding.
Diminished distal pulse.
Injury of anatomically related structures.
Small non-expanding haematoma.
Multiple fractures and extensive soft-tissue injury.
Injury in anatomical area of major blood vessel.
Distal pulses may be difficult to evaluate in patients with extensive soft-tissue trauma, swelling and multiple wounds. A diminished or absent pulse is caused by arterial occlusion until proven otherwise and should not be attributed to vascular spasm, external compression or any other ill-defined factor.
Signs of acute arterial insufficiency (ischaemia) include pulse deficit (absent/diminished pulse), pain, pallor, paraesthesia and paralysis. Neurological deficit must be evaluated carefully to distinguish between ischaemic neuropathy and direct injury to the nerve.
The value and accuracy of a thorough clinical examination in predicting significant vascular injury has been reported in various series.
Arterial Doppler pressure measurement is a useful supplement to the clinical examination. An arterial pressure index (API) above 0.9 reliably excludes significant occult arterial injury.
Special investigations should only be performed in patients who have been adequately resuscitated and who are haemodynamically stable. Haemodynamic instability, active bleeding and an expanding haematoma are indications for immediate surgery.
ATLS guidelines are followed, keeping in mind that the resuscitation of the unstable patient in urgent need of surgery may be best conducted in the operating room.
The amount, type and timing of fluid resuscitation is important. In uncontrolled haemorrhagic shock where bleeding has been temporarily stopped because of hypotension, vasoconstriction and thrombus formation, aggressive fluid resuscitation may lead to increased intravascular pressure, decreased blood viscosity and loss of the haemostatic plug, with resultant increased bleeding and mortality. Hypotensive resuscitation (permissive hypotension) aims for a systolic blood pressure of between 70 and 90 mmHg to maintain cerebral and renal perfusion until operative control of bleeding has been achieved. Haemostatic resuscitation is indicated in patients with massive bleeding/blood loss. Immediate administration of plasma, platelets and red blood cells as part of the resuscitation protocol has resulted in improved survival.
Temporary occlusion of the aorta with a percutaneously placed balloon has been used as an adjunct to resuscitation and haemorrhage control in abdominal and pelvic trauma (see section on abdominal trauma).
Active bleeding is an indication for urgent exploration, but can usually be temporarily controlled by direct pressure. Blind clamping of vessels in the depth of a wound is discouraged, because of the danger of injuring adjacent nerves and vessels. Tourniquets should be used in cases of massive bleeding that cannot be controlled with direct pressure.
Fractures must be stabilised during the period of resuscitation and diagnostic investigation to protect blood vessels and other soft tissue from further trauma. Preliminary reduction of a displaced fracture or dislocation may improve distal circulation.
Plain radiographs are usually taken for associated skeletal injuries. A high index of suspicion for vascular trauma should exist with dislocations and displaced fractures ( Fig. 9.5 ). Chest radiography is valuable in patients with chest trauma.
Computed tomographic angiography (CTA) is valuable in diagnosing blunt and penetrating vascular injuries in the neck, thorax, abdomen and extremities and should be the first-line investigation for all patients with suspected vascular trauma who do not require immediate surgical intervention.
Digital subtraction angiography (DSA) may still be indicated for selected conditions in haemodynamically stable patients, and where endovascular management of the injury is considered. The use of magnetic resonance angiography (MRA) in trauma is limited because of time constraints and inaccessibility to the patient during the examination.
Surgical intervention should not be delayed for special investigations where vascular injury is evident, and the patient is unstable or the limb is at ischaemic risk. On-table arteriography can be performed in the operating room for vascular injuries where surgery cannot be delayed, and the additional information is considered valuable.
Duplex Doppler examination is mostly used as a screening test in the absence of hard signs, in zone 2 neck injuries, in extremity vascular trauma and for follow-up evaluation in patients managed expectantly.
Procedures are performed under general anaesthesia in a suitably equipped theatre. Blood products should be available and arrangements for intra-operative autotransfusion should be made where further bleeding is expected. The value of prophylactic antibiotics in vascular surgery is established.
Adequate exposure is vital for obtaining proximal and distal control of injured vessels. This often requires inclusion of adjacent anatomical areas in the operative field, for example, preparing the neck in thoracic injuries (and vice versa) and the abdomen in groin injuries. An uninjured leg is prepared for possible vein harvesting should bypass be required. Vascular control must be achieved proximally and distally before directly approaching the area of injury. Bleeding may be temporarily arrested by digital compression or by endovascular means until clamps have been applied.
In blunt and high-velocity trauma, there is often extensive intimal damage, and careful debridement of the vessel is necessary until normal-appearing intima is found ( Fig. 9.6 ). Antegrade and retrograde flow should be evaluated. Arteries are cleared of thrombus by careful passage of embolectomy catheters followed by irrigation with heparin-saline solution.
Simple laceration of the vessel wall is repaired by lateral suture, provided it does not lead to stenosis, when patch graft angioplasty is indicated. Where more than 50% of the circumference of a vessel wall is damaged, this area should be excised followed by end-to-end anastomosis. This requires mobilisation of the proximal and distal arterial stumps to achieve approximation without tension. Failing this, an interposition graft is indicated. Autologous vein is the preferred conduit for reconstruction. Where there is a mismatch in diameter between the vessel that needs to be repaired and the available autologous vein, either a panelled or spiral vein graft should be used. Prosthetic material may be used in the absence of available autologous vein or as part of a damage control strategy.
Where complex arterial repair will result in delay in revascularisation, intraluminal shunts should be used to maintain antegrade flow during repair, thereby reducing ischaemic time.
Completion angiography should be performed to document a technically perfect repair and to assess the distal arterial tree. Associated injuries are addressed once vascular repair has been completed. Wound debridement should be performed with removal of all devitalised and contaminated tissue. Contaminated wounds are left open, but the vascular repair must be covered by soft tissue. Repeated wound inspections are performed, with delayed primary suture when the wound is clean.
Venous injuries found during exploration for associated arterial injury should be repaired, if the repair itself can be done simply (e.g., lateral suture repair) and only if it will not significantly delay treatment of associated injuries or destabilise the patient’s condition. Complex venous repair or bypass should only be attempted if the patient is haemodynamically stable. All veins, including the inferior vena cava (IVC), can be tied off in cases of haemodynamic instability.
The application of endovascular techniques in the injured patient has many potential advantages. General anaesthesia is not required. Surgical trauma, with further blood loss, hypothermia, etc., as well as cross-clamping of major vessels, distal ischaemia and subsequent reperfusion injury, is avoided. The main advantage is the option of approaching complex arterial lesions in anatomically challenging locations from a remote site. A difficult exploration in an injured area is avoided, with less potential damage to surrounding structures, and preventing fresh bleeding.
Endovascular techniques are increasingly applied in vascular trauma, but still have certain limitations. These techniques are usually not applicable, mainly because of time constraints, in patients with active bleeding, in unstable patients or where there is end-organ ischaemia. Endovascular techniques are contraindicated where there are compression symptoms, infected wounds or where concomitant injuries require open exploration. Technical restrictions include inability to traverse the lesion by guidewire, where intraluminal thrombus prevents the safe passage of a guidewire because of the danger of distal embolisation or where luminal discrepancy exists between the proximal and distal involved segments.
Endovascular techniques are used to manage vascular trauma in three ways:
To obtain haemostasis. Damaged vessels are embolised using a variety of substances including haemostatic agents (gel foam), coils and balloons.
Embolotherapy has become the standard treatment for managing significant bleeding following pelvic fractures and also to control bleeding caused by penetrating and blunt trauma of the liver, kidneys and spleen.
Embolotherapy is also the preferred option for treating vertebral artery lesions and lesions of non-essential, inaccessible vessels in other regions.
To obtain vascular control. Temporary balloon occlusion of a damaged vessel at the time of diagnostic angiography can prevent exsanguinating bleeding until surgical control is achieved. It is especially valuable in relatively inaccessible regions and allows limiting the extent of the exposure to obtain surgical control. This technique is valuable in injuries in zones 1 and 3 of the neck, the abdominal aorta, proximal subclavian and iliac arteries.
For vascular repair. Covered stent grafts are used for repairing vessels in anatomically challenging locations and to avoid major surgical exposures, for example, the thoracic aorta, thoracic outlet vessels, internal carotid and vertebral arteries ( Fig. 9.7 ). This will be discussed in more detail in the relevant sections. Covered stent grafts may also be used as a temporary measure to allow stabilisation of the patient until definitive open repair later.
In-stent stenosis, graft migration, stent breakage and endoleaks are well-known complications of stent graft repair. Durability is therefore of concern in the younger population, who are the main victims of trauma.
Endovascular management of vascular trauma has gained wide acceptance and it is increasingly used in most vascular beds.
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