Pathophysiology of Blunt Cerebrovascular Injuries

Blunt injuries to the carotid arteries tend to be caused by the application of shear forces via one of 4 mechanisms ( Box 2 ).

In contrast, vertebral artery injuries are caused by variable directions and patterns of shear force, including hyperextension and hyperflexion. Fractures of the upper cervical spine (C1 to C3), especially to the foramen transversarium, and facet joint dislocations are particularly associated with blunt injuries to the vertebral vessels.

Most blunt cerebrovascular injuries are caused by motor vehicle collisions, but there is a diversity of causes, including sporting injuries, falls, and even trivial-appearing trauma such as chiropractic manipulation or shaving.

Once the vessel has been injured, a dissection flap forms and this acts as a nidus for platelet aggregation and thrombus formation, followed by either distal embolization or vessel occlusion. Less frequently, the vessel tears either incompletely and creates a pseudoaneurysm, or, least frequently, it ruptures altogether. If untreated, cerebral ischemia and infarction subsequently ensue.

A grading scale for injuries to the carotid and vertebral arteries (based on imaging findings) has been developed and is helpful in both understanding the pathophysiologic spectrum of injury and in guiding management ( Box 3 ).

Pathophysiology of Penetrating Injuries to the Neck Vessels

In contrast with the shear forces involved in blunt cerebrovascular injuries, penetrating injuries cause local tissue destruction as the penetrating object crushes and separates tissue planes, and, in the case of gunshot wounds, secondary to the concussive shockwave. The tight and complex anatomic confines of the deep neck spaces, coupled with localized energy dissipation associated with penetrating neck injuries (PNIs), creates a much greater potential for associated injuries to the aerodigestive, endocrine, and neurologic systems than is found with blunt neck trauma.

Diagnosis and Management of Blunt Cerebrovascular Injuries

Making the diagnosis of a blunt cerebrovascular injury (BCVI) is challenging because of the infrequency of the problem, the multitude of mechanisms of injury, and the frequently delayed development of neurologic injury. Unless there is immediate complete arterial occlusion, the development of stroke symptoms typically takes many hours to even days to develop as thrombus and/or distal embolization evolves. As a consequence, rates of severe neurologic disability with these injuries can approach 50%. Given the difficulty in establishing the diagnosis and the potential for significant morbidity and mortality, there has been great interest in the past 2 decades in developing criteria for screening patients at high risk for BCVI. Use of these screening criteria is supported by clinical practice guidelines and has been shown to be effective in preventing strokes by allowing earlier initiation of anticoagulation or antiplatelet therapies. One small, retrospective study found that the sensitivity and specificity for these screening criteria were 97% (95% confidence interval [CI], 83%–100%) and 42% (95% CI, 20%–67%), respectively.

Treatment of Blunt Cerebrovascular Injury

The treatment of BCVI remains controversial and several factors contribute to the management option undertaken, including the grade of injury, the patient’s concurrent injuries, the location of the injury, local resource availability, and clinical expertise (see Box 3 ). In general, the options are antiplatelet agents, anticoagulation, endovascular therapy, and surgery. Overall, there is a very limited evidence base to guide decision making.

Most injuries (grades I–IV) are treated with systematic anticoagulation using either unfractionated heparin (no bolus; 10 U/kg/h to target partial thromboplastin time of 40–50 s) or antiplatelet agents (aspirin or clopidogrel). The Western Trauma Association guidelines suggest unfractionated heparin for patients without contraindications because it is reversible, has proven efficacy in reducing neurologic disability, and may be more effective than antiplatelet agents. In contrast, the Eastern Association for the Surgery of Trauma (EAST) suggests that either therapy would be reasonable. For patients with contraindications to systemic anticoagulation, antiplatelet therapy is suggested. The optimal duration of treatment is unknown and guidelines suggest continuing until the injured vessel has healed on follow-up imaging, which may be as early as 7 to 10 days after injury but may be many months. In some cases, patients require lifelong antiplatelet or anticoagulation therapy.

Patients with a transection of the carotid or vertebral artery (grade V injury) have very high rates of morbidity and mortality. These patients require emergent hemorrhage control, usually via angioembolization, because the lesion is typically not surgically accessible.

Diagnosis and Management of Penetrating Vascular Injuries of the Neck

PNIs represent about 1% of trauma admissions to trauma centers in the United States and are associated with a 5% rate of mortality. Almost all deaths (∼80%) relate to cerebral infarctions, with the remainder relating to uncontrolled hemorrhage.

The initial resuscitation efforts are directed at the most likely causes of early death after a PNI: exsanguination and asphyxiation caused by airway obstruction. Additional considerations in patients with low-neck injuries or associated wounds include tension pneumothorax, massive hemothorax, and cardiac tamponade.

A patient with a PNI must be considered a difficult airway and approached carefully. Patients with so-called hard signs of significant injury to vascular or aerodigestive structures require immediate airway control ( Fig. 1 ). In general, hard signs of injury should be identified during the typical primary survey component of the assessment of patients with trauma.

Approach to penetrating neck injury.

It is important to be able to distinguish hard from soft signs in PNI ( Box 6 ). The former are essentially diagnostic of a serious injury (approximately 90% rate of significant injury ) and require immediate surgical consultation, whereas the latter are nonspecific features that warrant further work-up with at least CT-A. Soft signs of injury are identified during a systemic examination after immediate life threats have been managed.

Concurrent with digital pressure to sites of hemorrhage, the patient should be passively preoxygenated with a nonrebreather oxygen mask and nasal cannula, placed on continuous cardiorespiratory monitoring devices, have large-bore intravenous access obtained, and the difficult airway equipment at the bedside.

Whenever possible, bag-mask ventilation should be avoided because there is a risk of the positive pressure displacing air into violated soft tissue spaces of the neck and further distorting the airway anatomy. Two suction catheters should be prepared to manage significant bleeding. The authors agree with EAST guidelines for the management of PNIs, which indicate that, if the patient is conscious and has no overt neurologic deficits, cervical spine immobilization is unnecessary and risks obscuring wounds, increasing patient agitation, and complicating airway management. This recommendation applies to both gunshot wounds and stab wounds, because, in these populations, neurologic deficits are established and final at the time of presentation to the emergency department. Overall, the incidence of cervical spinal cord injury among patients with penetrating trauma is less than 1%.

If bleeding persists despite direct digital pressure to the wound, an 18-F Foley catheter may be inserted with a finger into the wound and directed to the palpated or estimated location of bleeding before inflating the balloon with sterile water until the bleeding stops or moderate resistance is felt ( Fig. 2 ). A hemostat can then be applied to the distal end of the catheter to prevent it from migrating into the wound. In some cases a second catheter is required to occlude both proximal and distal ends of the vascular defect. Once inflated within the wound (not the vascular lumen), the balloon exerts extrinsic tamponade on the vessel.

Foley catheter balloon tamponade of hemorrhage from penetrating neck injury.

( From Weppner J. Improved mortality from penetrating neck and maxillofacial trauma using Foley catheter balloon tamponade in combat. J Trauma acute Care Surg 2013;75(2):221; with permission.)

Airway management in penetrating neck injuries: is the anatomy intact or distorted?

Patients with clearly distorted airway anatomy require a multidisciplinary team approach, including the emergency physician, anesthesia, respiratory therapist, and locally available surgical consultants (trauma/general surgery, otolaryngology, and so forth). In general, it should be anticipated that patients with PNI and distorted airway anatomy will require a surgical airway. Even if the anatomy initially appears intact, clinicians should be vigilant for changes in the patient’s airway status and be prepared for all possible scenarios, including the performance of a surgical airway.

If the larynx or trachea has been lacerated and is open to the skin, the preferred approach is to place the endotracheal tube directly through the wound and into the larynx or trachea ( Fig. 3 ).

Endotracheal tube passed through external neck wound and into larynx. (a) thyroid cartilage, (b) epiglottis, (c) posterior pharyngeal wall, (d) endotracheal tube.

( From Youssef N, Raymer KE. Airway management of an open penetrating neck injury. Can J Emerg Med 2015;17(1):90; with permission.)

If the airway is not accessible externally, the next best option is awake fiberoptic intubation so that any airway injury can be directly visualized and the tube clearly advanced past the lesion with the assurance that no false tract will be created.

Awake fiberoptic intubation requires a cooperative patient and is very challenging if there are significant amounts of blood in the airway. If fiberoptic intubation is not an option, then awake direct or video laryngoscopy is the next best. The limitation of these techniques is that they are blind techniques in that the operator is unable to visualize the airway distally and risks introducing the tube into a tract leading to subcutaneous tissues or converting a partial tracheal laceration into a complete laceration. There is little research on this scenario but common sense suggests that a gentle, bougie-guided intubation strategy using a smaller-than-normal endotracheal tube may be helpful in reducing the risk of creating a false passage.

Whether fiberoptic or direct techniques are used, a double setup approach is essential. In this case, the double setup includes having the skin prepped, landmarks identified, local anesthesia administered, and all equipment and personnel set up to proceed immediately to cricothyroidotomy (tracheostomy if transected larynx) if intubation is unsuccessful.

If the airway anatomy appears externally intact, then rapid sequence intubation (RSI) is generally considered to be safe and effective in the setting of PNIs. If an RSI is the initial technique chosen, clinicians should still consider the possibility of an occult airway injury and have a clear backup plan in place, including a surgical airway kit assembled and supraglottic airway devices prepared for rescue oxygenation.