Neck Trauma & Spinal Cord Injury
Hard signs to the OR, the rest to the scanner — then read the cord
Penetrating neck injury
The platysma decides significance. A wound that does not breach the platysma is superficial and needs only local wound care. A wound that does may injure the carotid or vertebral arteries, jugular veins, larynx, trachea, pharynx, or esophagus. Never probe the wound or remove an impaled object in the emergency department, since either can dislodge clot and cause exsanguination or air embolism.
Airway first. Intubate early for stridor, hoarseness, air bubbling through the wound, respiratory distress, or an expanding hematoma, ideally before swelling distorts the anatomy, with a surgical airway ready if intubation fails.
Hard signs go to the operating room. These findings mandate immediate exploration without imaging, whatever the zone:
- Expanding or pulsatile hematoma, or active hemorrhage
- Bruit or thrill
- Airway compromise or air bubbling from the wound
- Shock
The no-zone approach. A stable patient whose wound breaches the platysma but shows no hard signs gets CT angiography of the neck regardless of zone. Soft signs — a stable hematoma, minor bleeding, dysphagia, hoarseness, subcutaneous emphysema, or hemoptysis — raise suspicion, and a positive or equivocal CTA leads to targeted endoscopy, esophagography, angiography, or surgery. Esophageal injuries are the easiest to miss and the most dangerous to delay, so a track near the esophagus warrants esophagoscopy combined with contrast esophagography.
| Zone | Boundaries | Key structures | Surgical access |
|---|---|---|---|
| I | Clavicles and sternal notch to cricoid | Great vessels, lung apices, trachea, esophagus, thoracic duct | May require sternotomy or thoracotomy |
| II | Cricoid to angle of mandible | Carotid and vertebral arteries, jugular veins, larynx, pharynx | Most common site; easiest to expose |
| III | Angle of mandible to skull base | Distal internal carotid, vertebral arteries, pharynx | Hardest to expose; endovascular options |
Blunt cerebrovascular injury
Mechanism and clues. Hyperextension with rotation, a seat-belt sign across the neck, cervical spine fractures, skull-base fractures through the carotid canal, severe midface fractures, and near-hanging can tear the intima of the carotid or vertebral arteries. Dissection may stay silent for hours or days before a stroke. Red flags include a neurologic deficit not explained by head CT, Horner syndrome (oculosympathetic fibers run along the internal carotid), a cervical bruit in a young patient, and an expanding neck hematoma.
Management. Screen at-risk patients with CT angiography of the neck. Treat with antithrombotic therapy (aspirin or heparin) to prevent stroke when bleeding risk allows; pseudoaneurysms and high-grade lesions may need endovascular treatment.
Spinal cord syndromes
Tract refresher. The lateral corticospinal tract (motor) and dorsal columns (proprioception, vibration, fine touch) cross in the medulla, so cord lesions affect them on the same side. Spinothalamic fibers (pain, temperature) cross within one or two segments of entering the cord, so cord lesions affect them on the opposite side.
| Syndrome | Typical mechanism | Deficits | Prognosis |
|---|---|---|---|
| Central cord | Hyperextension in an older patient with cervical spondylosis | Arms weaker than legs, hands worst; urinary retention; sacral sparing | Fair; legs recover first, hands last |
| Anterior cord | Flexion injury, burst fragment, disc herniation, anterior spinal artery occlusion | Bilateral paralysis and pain/temperature loss; dorsal columns spared | Worst of the incomplete syndromes |
| Brown-Séquard | Hemisection, classically a stab wound | Ipsilateral paralysis and proprioception loss; contralateral pain/temperature loss 1–2 levels below | Best |
| Posterior cord | Rare; hyperextension | Proprioception and vibration loss; strength preserved | Good strength, sensory ataxia |
Central cord syndrome is the most common incomplete injury and often occurs without fracture. Anterior cord syndrome reflects the territory of the anterior spinal artery, which supplies the anterior two-thirds of the cord, and can also follow aortic surgery or dissection.
Complete versus incomplete. Preserved perianal sensation, voluntary anal contraction, or great-toe flexion (sacral sparing) marks an incomplete injury with a meaningful chance of recovery. An injury is labeled complete — no motor or sensory function in S4–S5 — only after spinal shock resolves. MRI is the study of choice for any patient with a deficit, showing cord compression, edema, hematoma, disc herniation, and ligament injury.
Neurogenic and spinal shock
| Feature | Neurogenic shock | Spinal shock | Hemorrhagic shock |
|---|---|---|---|
| Cause | Loss of sympathetic outflow (injury at T6 or above) | Transient loss of cord reflex activity | Blood loss |
| Blood pressure | Low | Not a hemodynamic state | Low |
| Heart rate and skin | Bradycardia; warm, dry, flushed | No characteristic pattern | Tachycardia; cool, pale, clammy |
| Neurologic findings | Those of the cord injury | Flaccid paralysis, areflexia, absent bulbocavernosus reflex | May be normal |
| Treatment | Fluids, then norepinephrine; atropine for bradycardia | Supportive; resolves in hours to weeks | Hemorrhage control, blood products |
A hypotensive trauma patient is bleeding until proven otherwise. Attribute hypotension to neurogenic shock only after hemorrhage in the chest, abdomen, pelvis, and long bones has been excluded.
Perfusion goal. After acute spinal cord injury, keep MAP at 75 to 80 mmHg or higher (upper limit 90 to 95; 2024 AO Spine guideline) for 3 to 7 days to protect cord perfusion (older AANS/CNS guidance targets 85 to 90 mmHg), using judicious isotonic fluids and then a vasopressor with β activity such as norepinephrine. Spinal shock ends when the bulbocavernosus reflex (anal sphincter contraction on squeezing the glans or tugging the Foley) returns; spasticity and hyperreflexia then develop below the level.
Acute and ongoing care
Breathing. The phrenic nerve arises from C3–C5 ("C3, 4, 5 keeps the diaphragm alive"). High cervical injuries cause immediate ventilatory failure, and lower cervical injuries paralyze the intercostals so the diaphragm fatigues over hours to days. Trend vital capacity and intubate early with manual in-line stabilization.
Cord protection. Maintain spinal motion restriction until injuries are defined. High-dose methylprednisolone is not recommended, because it increases infection, GI bleeding, and hyperglycemia without proven neurologic benefit. Early surgical decompression, within about 24 hours, is favored when the cord is compressed.
Complications. Start VTE prophylaxis with low-molecular-weight heparin within 72 hours, catheterize for urinary retention, and prevent pressure ulcers with frequent turning and early removal from the backboard.
Autonomic dysreflexia. In chronic injuries at T6 or above, a noxious stimulus below the lesion (most often a distended bladder, then fecal impaction) triggers unchecked sympathetic discharge: severe hypertension, pounding headache, flushing and sweating above the lesion, and reflex bradycardia. Sit the patient up, loosen clothing, relieve the bladder or bowel, and give a short-acting antihypertensive if hypertension persists.