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 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 < 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 waterhammer 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 intraabdominal 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 that 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 The goal of initial resuscitation should be maintaining cerebral perfusion pressure and surgical cessation of bleeding, followed by volume repletion in the form of blood products.

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 pattern similar to that of the spleen, with grades I through VI ranging from small subcapsular hematoma to hepatic vascular avulsion. Renal, pancreatic, small-bowel 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. Intraarterial 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 intraarterial 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 < 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 < 25% stenosis. Grade II injuries include those with intraluminal thrombus or a raised intimal flap, or dissections with intramural hematoma causing > 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.