Chapter 27: Traumatic Vascular Injuries

In the ED, many things need to be coordinated at once. Primary survey of airway, breathing, and circulation according to advanced trauma life support (ATLS) algorithms should be the immediate priority.¹ Establishment of adequate intravenous access, the collection of laboratory studies, and recognition of life-threatening injuries are paramount.

The pendulum has shifted from surgical correction of all injuries fully to "damage control" of those immediate life-threatening injuries.^2-4 The rapid control of hemorrhage and prevention of coagulopathy, hypothermia, and acidosis are the perioperative goals. This is achieved via limiting the operative time as much possible with rapid transport to the intensive care unit (ICU) for further optimization. Damage-control surgery is the mainstay of acute surgical trauma care.^5,6 Polytrauma patients will often require multiple operations to deal with problems stemming from the initial traumatic insult.

Traumatic injury represents the leading cause of death nationally in those under 45 years of age and the fifth most common cause of death overall.⁷ In the multiple trauma patients, the leading cause of death is catastrophic brain injury. Hemorrhage is the second most common cause of mortality.⁸ Major vascular and severe neurologic injuries often occur together in the polytrauma victim.

The vascular tree and viscera can be affected by direct or indirect insult from blunt or penetrating trauma. Vessels can be injured by transection, rupture, or contusion. These injuries must be recognized rapidly and managed aggressively. Other vascular injuries such as dissection, true and pseudo-aneurysm formation, and embolism may develop immediately or in a delayed fashion.

Blunt Trauma

The mechanism of damage to the thoracic aorta following blunt trauma often reveals a consistent pattern of injury that is discrete from that of penetrating injury owing to physical forces and inherent points of aortic weakness. The thoracic aorta is relatively fixed at three points: the aortic valve, the ligamentum arteriosum, and the diaphragm. The descending aorta is tethered, in contrast, to the relatively mobile ascending aorta and aortic arch.⁹ In classic blunt acceleration-deceleration injury, stretch, shear, torsion forces, and extrinsic vascular compression against neighboring structures as well as the water-hammer effect of high-pressure reflection of noncompressible blood in the face of acute aortic obstruction all may contribute to injury ranging from subintimal hemorrhage to total aortic disruption.⁹

The mechanism of blunt injury to intra-abdominal structures can be classified into compression forces and deceleration forces. Compression or concussive forces may result from direct blows or external compression against a fixed object; for example, a seat belt or the spinal column. The most common sequelae are tears or subcapsular hematomas to the solid viscera. These forces may also deform hollow organs, such as the small bowel, and transiently increase intraluminal pressure, resulting in rupture.

Deceleration forces cause stretching and linear shearing between relatively fixed and free objects. These longitudinal shearing forces tend to rupture supporting structures at the junction between free and fixed segments. Classic deceleration injuries include hepatic lacerations along the ligamentum teres and renal arterial intimal injuries. Additionally, as bowel loops travel from their mesenteric attachments, thrombosis and mesenteric tears to the splanchnic vessel may result.

Penetrating Trauma

The damage caused by penetrating trauma is directly related to the amount of kinetic energy that is supplied by the projectile or penetrating object. Lower-velocity injuries, such as stab wounds, usually lead to damage to the directly contacted structures and tissues. In contrast, higher-velocity ballistic injuries have an additional pressure wave component, which creates further tissue damage.¹⁰ The full extent of injury, therefore, may not be initially apparent by recognition of entry and exit wounds. Of note, there is considerable literature supporting the delay of aggressive fluid resuscitation in hypotensive penetrating injury until operative intervention.¹¹

Splenic Injury

In cases of blunt abdominal trauma, the spleen is the most often affected organ, representing 40% of injuries to solid viscera. As with all cases of suspected abdominal trauma, initial management is guided by hemodynamic stability of the patient. ATLS protocol–driven care and timely clinical and/or imaging studies (ultrasound/FAST and/or helical computed tomographic [CT] scan) will guide patient triage to the OR, ICU, or less acute setting. Splenic injury, even rupture, may present along a spectrum from asymptomatic to diffuse abdominal tenderness, with or without hemodynamic instability. The decision to operate for splenic trauma depends largely on the hemodynamic stability of the patient. The grading of splenic injury ranges from I to V, depending on the presence and size of subcapsular hematoma, intraparenchymal laceration, laceration of segmental or hilar vessels, or complete avulsion.¹² The critical care issues in these patients are largely ongoing hemorrhage, if managed nonoperatively, so close hemodynamic monitoring with frequent laboratory assessment for bleeding is a must. Splenic artery aneurysms may also form after trauma and represent a potential source of brisk hemorrhage.

Hepatic Injury

Hepatic injury may occur in isolation or alongside other injuries. Nonoperative management is widely used in the hemodynamically stable patient, but is also increasingly being employed in more hemodynamically unstable patients as well.¹³ The grading of hepatic injuries follows a similar pattern to that of the spleen, with grades I through VI ranging from small subcapsular hematoma to hepatic vascular avulsion. Renal, pancreatic, and small- and large-bowel injuries may also be seen.

Endovascular homeostatic techniques involving embolization or stenting without the associated surgical stress intuitively confer benefit. The key question of what clinical scenarios of hemodynamic control offer better outcomes with minimally invasive management over open-surgery approaches remains controversial with a lack of robust supporting evidence at this time. There is some evidence pointing toward equal outcomes with interventional management of hepatic and splenic injuries.^13,14 Direct examination of pelvic and retroperitoneal injuries is difficult during laparotomy, and surgical exploration and control of hemorrhage in these anatomic areas are technically challenging.¹⁵ Therefore, currently, although interventional radiologic management of pelvic bleeding in the hemodynamically unstable patient is gaining acceptance, the standard approach to other organ injuries remains surgery.^1,16

The concern here would be carotid artery dissection. Traumatic blunt vascular injuries to head and neck vessels occur in motor vehicle accidents because of rapid deceleration resulting in stretching of the internal carotid artery over the lateral masses of the cervical vertebrae or hyperflexion of the neck causing compression of the artery between the mandible and cervical spine. Vertebral dissections can occur as a result of excessive rotation, distraction, or flexion-extension injuries and are often associated with fractures extending into the transverse foramen or facet joint dislocations.

Presenting symptoms define the laterality of the cerebrovascular injury and isolate it to the respective extracranial arterial supply. Carotid injuries typically present with a contralateral sensory or motor deficit, and vertebral injuries present with ataxia, vertigo, emesis, and possible visual field deficits. Intra-arterial angiography was traditionally the mainstay of diagnostic imaging but has given way to other modalities such as ultrasound, CT angiography (CTA), and magnetic resonance imaging/magnetic resonance angiography (MRI/MRA) for both initial diagnosis and follow-up.^17,18 Pathopneumonic angiographic findings of dissection or aneurysm formation include a flame-shaped or tapered narrowing, "string sign." An MRI and MRA can demonstrate the luminal abnormalities seen with intra-arterial studies.

Multisection CTA provides high-resolution images of the arterial wall and vessel lumen and, in the setting of trauma, can also demonstrate the relationship of arterial injuries to bone structures of the cervical spine and skull base.

The natural history of blunt trauma causing vascular injuries in the neck is often initially occult, and even after this "silent period," devastating neurologic symptoms may be delayed for hours or even days. It has only recently become clear that these injuries are more common than previously appreciated and that disability secondary to cerebrovascular ischemia can be prevented by early intervention. Indeed, the overall incidence of blunt carotid and vertebral injury has been universally reported as less than 1% of all trauma admissions for blunt trauma, but this relatively small population of patients has a stroke rate ranging from 25% to 58% and mortality rates of 31% to 59%.^19,20 The index of suspicion for this type of injury should be high, and a low threshold for designated imaging may lead to earlier diagnosis. Aggressive screening protocols exist in trauma centers. Patients with cervical spine injury, diffuse axonal injury, basal skull fracture, Le Forte facial fracture, significant thoracic injury, or any neurologic deficit not explained by admission CT scanning should undergo additional imaging.

Intervention consists of anticoagulant and/or antiplatelet therapy, open repair or stenting, and hemodynamic management. A grading system exists with prognostic and therapeutic implications for blunt carotid injuries based on the angiographic appearance of the lesion. Grade I injuries are defined as irregularity of the vessel wall or dissection with less than 25% stenosis. Grade II injuries include those with intraluminal thrombus or a raised intimal flap, or dissections with intramural hematoma causing greater than 25% stenosis. Dissecting aneurysms are classified as grade III and complete occlusions as grade IV injuries. Grade V injuries are those associated with complete vessel transection and evidence of free contrast extravasation.

Severe head injuries are evenly distributed across the injury grades. However, the incidence of delayed stroke increased with injury grade from 3% with grade I injuries to 44% for grade IV, and therefore choice of intervention is often stratified according to grade.²¹ Anticoagulant and/or antiplatelet medications (to which there are often contraindications in the severely injured trauma patient) represent the mainstay of medical treatment with excellent results in terms of stroke rate reduction. However, complications associated with anticoagulation range from 25% to 54% in the trauma population.²⁰ Most concerning is intracranial hemorrhage; however, more common are gastrointestinal bleeds, retroperitoneal hemorrhage, blunt solid organ injury with hemorrhage, or rebleeding from surgical wounds. In those patients with contraindications to anticoagulation or with evidence of hemodynamic insufficiency due to severe stenosis or occlusion, augmentation of cerebral blood flow is required on an urgent basis. Medical management with induced hypertension and hypervolemia can be employed. If symptoms persist despite maximal medical management, an intervention aimed at restoration of normal vessel diameter to improve cerebral perfusion should be considered.

Reconstruction with an in situ vein graft or extracranial to intracranial bypass may be technically feasible, although formal open repair has largely given way to the application of endovascular stents and covered stent grafts. Stent placement is associated with a risk of early or late thromboembolic complications or occlusion and requires periprocedural anticoagulation and continuation of single or combination antiplatelet therapy for several weeks subsequently.

These changes represent a probable acute compartment syndrome (ACS) of the extremity. The pathophysiology involves insult to compartment homeostasis, leading to increased tissue pressure, reduced capillary blood flow, local tissue hypoxia, and later necrosis. Older age confers a decreased risk presumptively due to weaker, less strong fascia. The vast majority of causes of traumatic ACS of the extremity are soft tissue injuries, ischemia, or fractures (open or closed), or a combination of these insults. Diagnosis is notoriously difficult, especially in the sedated, intubated patient, since the earliest clinical symptom is pain. Palpable tenseness, paresthesia, paresis, pallor, and pulselessness may also be associated with compartment syndrome. To confirm the clinical diagnosis, especially in difficult clinical situations, measurement of intracompartmental pressure may be useful. Normal resting intracompartmental pressure is 0 to 8 mm Hg. When intracompartmental pressure rises above capillary blood pressure, intracompartmental blood circulation ceases. The first clinical symptoms of ischemia appear at approximately an intracompartmental pressure of 20 to 30 mm Hg. Expert consensus opinion advocates for fasciotomy for absolute compartment pressures of 30 to 45 mm Hg.²² Once the diagnosis of ACS has been established, urgent surgical decompression of the affected osseofascial compartments should be undertaken with the objective to relieve increased pressure. This can be done formally in the operating room or at the bedside.

Aneurysms can be categorized as true or false (pseudoaneurysm). True aneurysmal disease can occur anywhere within the vascular tree, but the vast majority develop within the arterial circulation. True aneurysms, resulting from a developing defect of the muscular layers of a contiguous arterial wall, can develop over time as a result of weakening of the wall caused by aging, smoking, hypertension, and atherosclerosis as well as occasionally infections, vasculitides, genetic conditions, and blunt trauma. The majority of true aneurysms are found in the aorta, of which 95% are infrarenal, and also in the cerebral circulation. Pseudoaneurysm, or false aneurysm, formation is a common complication of arterial injury. A pseudoaneurysm is a disruption of one or more layers of the arterial wall, resulting in leaking and external hematoma formation in communication with the arterial lumen. Approximately 0.6% of percutaneous femoral artery catheterization results in pseudoaneurysm formation.²³ When the wall stress from circulation exceeds the tensile strength of the vessel wall, rupture occurs. Wall stress is directly proportional to vessel diameter and blood pressure according to Laplace law, and therefore with increasing aneurysm size, risk of rupture or dissection increases. For example, the annual rupture rates for abdominal aortic aneurysms of less than 3 cm is 0.3%, whereas for abdominal aortic aneurysms greater than 7 cm the rupture rate is 31%.²⁴ The scenarios in which this would be seen include trauma patients with concomitant true aneurysm formation, where hemodynamic control would be the mainstay of treatment. Recognition of pseudoaneurysm formation after injury is paramount and should be followed with serial CTA or another imaging modality. Intervention should be considered on the basis of absolute size, increasing size, or worsening symptomatology.

The pathophysiology of arterial dissection involves a tear in the intimal vessel lining, with blood entering the media at this point of discontinuity. The force of systolic blood pressure will extend the intimal flap antegrade and/or retrograde and create a false lumen. With trauma, the inciting injury is often a wall hematoma rather than a weakness of collagen or elastin. Medical management would include pharmacotherapy to avoid extension of dissection by controlling the patient's heart rate and blood pressure as well as support of end-organ perfusion while awaiting definitive interventional or surgical management. The rate of acceleration of pulsatile flow (ΔP/Δt) and the depth of intimal tear are the determinants of intimal flap extension; therefore, management must include rapid and strict heart rate and blood pressure control. The large inflammatory response accompanying dissection often leads to profound hypertension requiring multiple antihypertensive agents. Age, hypertension, connective tissue disorders, and trauma remain the leading risk factors for generation of arterial dissection.²⁵ Acute aortic dissection remains a morbid disease.

In contrast, chronic aortic dissections are complex lesions with a fairly predictable natural history depending on factors such as the baseline aortic diameter, the degree of false lumen thrombosis, the presence of a persistent communication, an underlying connective tissue disorder, and the control of hypertension. Medical management with antihypertensive therapy including β blockers is the treatment of choice for all stable chronic aortic dissections. Repair is indicated in the case of complications: aortic rupture, malperfusion syndromes, symptomatic dissections, asymptomatic dissections that become significantly aneurysmal or demonstrate a rapid growth rate. In this regard, serial imaging of the aorta is crucial to detect unstable lesions requiring surgery or an endovascular intervention.

In general, the management of vascular injury can be categorized into surgical or medical. Surgery can be approached via an open or endovascular modality. The mainstays of medical management are supportive care, anticoagulation, and hemodynamic control.

Preoperatively, transesophageal echocardiography may be performed to assess the extent and type of injury and anti-impulse therapy with short-acting β blockade and potentially vasodilatory drugs should be started. Anti-impulse therapy has been shown to reduce in-hospital aortic rupture rates without adversely affecting the outcome of other injuries.

Open Repair

Conventional open repair of contained aortic rupture, elective aneurysm treatment, or traumatic aortic disruption with interposition grafting is the standard with which all other management strategies should be compared. Traditionally, simple aortic cross-clamping has been used, but more contemporary practice using extracorporeal lower body perfusion techniques lower the rate of paraplegia, which is as high as 30% with simple "clamp and sew" techniques with cross-clamp times longer than 30 minutes. Paradoxically, it is possible that young trauma victims have not developed significant vascular collateral flow and, therefore, are thought to be at higher risk of organ dysfunction distal to the aortic clamp site.

The spinal cord blood supply is through the anterior and posterior spinal arteries. The anterior two-thirds of the spinal cord is supplied by the anterior spinal artery arising from radicular and medullary branches of the posterior intercostal arteries off the aorta. The anterior spinal artery is well developed in the upper thorax and receives collateral flow from the left vertebral artery and the internal mammary artery through the intercostals, whereas in the lower thorax and abdomen, it is more dependent on collateral flow that it receives from the intercostals and lumbar arteries at these levels. The artery of Adamkiewicz comes off the aorta at approximately the level of the first lumbar vertebra (with much variation around T8 to L4) and is essential for the blood supply to the spinal cord in at least 25% of patients. Risk factors for postoperative paraplegia include increased cross-clamp time, the length of the aorta excluded, low distal perfusion pressure, systemic hypotension, the number of intercostal arteries ligated, increased body temperature, and increased cerebrospinal fluid pressure.

In addition to lower-body perfusion, several adjunctive measures can be used to reduce the risk of spinal cord ischemia during the management of thoracic aortic surgery, such as motor or somatosensory evoked potentials, lumbar cerebrospinal fluid drainage, and hypothermia. These modalities should certainly be considered in the perioperative care of these patients. Aside from the spinal cord, organ beds distal to the cross-clamp are also affected, most notably the mesentery, the kidneys, and the lower extremities. Monitoring of renal function, acid-base, liver enzymes, creatine kinase, arterial lactate, and serial examinations of the abdomen and lower extremities along with a low index of suspicion for abdominal compartment syndrome should be considered in the postoperative care plan.

Thoracic Endovascular Aortic Repair (TEVAR)

There are currently many reports of the efficacy of TEVAR for acute traumatic aortic disruption. Experience gleaned from the selective use of TEVAR in the repair of thoracic aortic aneurysms in high-risk patients has transformed the management of traumatic thoracic aortic injuries. Endovascular repair is the preferred management modality in many institutions. Although the long-term durability of these grafts in this younger subset of trauma patients is unknown, the accepted risk of chronic complications is offset by the benefits afforded by a less-invasive, less time-consuming technique where the added potential morbidity of an open repair is avoided.²⁶

Complications occurring after TEVAR include endoleak, stent-graft collapse, stroke, embolization, bronchial obstruction, migration, paralysis, dissection, or rupture. Endoleaks are categorized as type I (leak around the proximal or distal end of the graft); type II (leak from an artery excluded by the graft that perfuses the vessel in a retrograde fashion between the wall of the aorta and the graft); type III (leak between modular components); and type IV (failure of graft integrity).

The main concern would be mesenteric ischemia from either a discrete thromboembolic event or a more prolonged and persistent low-flow state. Clinical examination, flow-based imaging, and serial laboratory studies focusing particularly on acid-base and lactate levels may show a trend. There should be a constant assessment of the need for bowel resection. Large-bore intravenous cannulas should be placed immediately in case of a massive upper or lower gastrointestinal bleed. Blood for transfusion should be made available in case of hemorrhagic shock. Invasive monitors should be considered and transfer to an ICU location should be arranged if the patient is in a poorly monitored location.

Securing the airway, fluid and vasopressor therapy, and rapid assessment and treatment of what must be assumed to be profound hemorrhagic hypovolemic shock from cardiac and/or great vessel trauma in the hope of survival are the goals of care.

Penetrating and Blunt Cardiac Trauma

The goals of penetrating cardiac trauma are immediate surgical intervention. Of those patients with penetrating stab wounds to the heart who reach the hospital, one-third have right ventricular injuries and one-quarter have left ventricular injuries. Coronary artery lacerations are also common.²⁷ Management involves fluid resuscitation and immediate transfer to the operating room or ED for thoracotomy. The majority of blunt cardiac trauma is seen with motor vehicle accidents. The compression and deceleration forces that are at play in blunt aortic injuries are similar to those resulting in cardiac trauma. An abrupt change in pressures within and surrounding the heart can cause disruption to the fairly static and fixed components of the heart; namely, the cardiac free wall, the septum, the coronary arteries, and the valvular apparatus. More often, and less morbidly, myocardial contusion to the anterior right ventricle may also occur.

Chest radiography, serum troponin levels, and electrocardiographic (ECG) monitoring can be used to screen trauma patients for cardiac contusion. If these tests are reassuring, they essentially rule out significant cardiac injury in young patients. If concern persists, echocardiography (either trans-thoracic or transesophageal) may be used to assess regional myocardial functionality. Cardiac injuries are graded according to the presence of structural injury and hemodynamic compromise. The management of such injuries spans a spectrum from conservative medical management to support the contractile state of the myocardium to percutaneous intervention to operative intervention.

Non–Aortic Great Vessel Injury

Blunt trauma to the great venous structures and the pulmonary arteries is rare, presumably because of their distensibility and low pressure, with the majority of injuries to these vessels being from penetrating injuries. Even with penetrating trauma the incidence of great vessel injury is in the order of 5%. Most commonly, exsanguination from pulmonary vessel hemorrhage into the thorax or pericardial tamponade is seen and requires appropriate management. As with other penetrating injuries, permissive hypotension has been shown to improve outcome until definitive surgical control has been achieved.

Penetrating (PAI) and Blunt Aortic Injury (BAI)

Penetrating aortic injury is unsurprisingly almost always fatal.

There is a spectrum of diseases related to BAI. Intervention must now be tempered in the context of other associated injuries. Minimal injuries have been successfully managed and may heal with appropriate medical management. Additionally, the increased use of and familiarity with endovascular aortic stenting techniques has simplified the repair of BAI and reduced the burden of organ dysfunction previously seen with open repair, at least in the relatively short term. Long-term data on the trauma population are sparse as to endovascular versus open techniques, but extrapolation from the elective aneurysm group may show an equalization of morbidity and mortality rates longitudinally.²⁸

Broadly speaking, 75% of BAI victims die at the scene, with a further 5% presenting with instability, in whom the mortality rate is still 100%. The final 20% of patients with BAI, who often present later, have little or no hemodynamic perturbation. The mortality rate in this group is a more acceptable 25%.²⁷ It is in this group that timing and method of intervention warrant a balance of other injuries and there may be a role for delayed intervention, although optimal timing is still unclear.