5.5 Spinal Trauma and Spinal Cord Syndromes
Key Takeaways
- Brown-Séquard Syndrome involves hemicord transection, resulting in ipsilateral loss of motor function/proprioception and contralateral loss of pain/temperature sensation.
- Anterior Cord Syndrome causes bilateral loss of motor function and pain/temperature sensation, while preserving proprioception, vibration, and light touch.
- Central Cord Syndrome presents with motor weakness greater in the upper extremities than the lower extremities, typically following hyperextension injuries in elderly patients.
- Neurogenic shock is a distributive shock (loss of sympathetic tone in T6 and above injuries) presenting with hypotension, bradycardia, and poikilothermia.
- Spinal shock is a temporary neurological state of flaccid paralysis and areflexia; its resolution is marked by the return of the bulbocavernosus reflex.
Spinal Trauma and Spinal Cord Syndromes
Anatomy and Secondary Injury Prevention
Spinal cord injury (SCI) is a devastating form of trauma that requires meticulous stabilization and management during critical care transport to prevent secondary injury. Primary injury occurs at the moment of mechanical impact, resulting in tissue disruption. Secondary injury occurs hours to days later, driven by systemic factors such as hypotension, hypoxia, inflammatory cascades, and intracellular calcium influx leading to lipid peroxidation and neuronal death.
Preventing secondary injury is a major goal of critical care transport, primarily achieved by maintaining spinal column alignment, ensuring adequate oxygenation (SpO2 >= 94%), and optimizing spinal cord perfusion pressure (SCPP).
Dermatomal Landmarks and Clinical Assessment
Accurate documentation of neurological level is essential. Important dermatomal landmarks include:
- C3, C4, C5: Innervate the diaphragm via the phrenic nerve ("C3, 4, 5 keep the diaphragm alive"). High cervical injuries result in immediate respiratory insufficiency or arrest.
- T4: Nipple line.
- T10: Umbilicus.
- S4-S5: Perianal sensation and voluntary anal contraction. The presence of sensation or motor function at S4-S5 is termed sacral sparing and indicates an incomplete spinal cord injury, which carries a much better prognosis for functional recovery.
Incomplete Spinal Cord Syndromes
Incomplete spinal cord injuries occur when there is partial preservation of sensory or motor function below the neurological level of injury.
1. Brown-Séquard Syndrome (Hemicord Transection)
Typically caused by penetrating trauma (e.g., stab or gunshot wound) resulting in the hemisection (half-cut) of the spinal cord.
- Ipsilateral (Same Side) Deficits: Loss of motor function (corticospinal tract) and loss of proprioception, vibration, and deep touch (dorsal columns) below the level of injury.
- Contralateral (Opposite Side) Deficits: Loss of pain and temperature sensation (spinothalamic tract) beginning 1-2 dermatomal levels below the level of injury. This occurs because the spinothalamic tract fibers cross over (decussate) at the spinal cord level near where they enter, whereas corticospinal and dorsal column fibers decussate in the brainstem.
2. Anterior Cord Syndrome
Caused by hyperflexion injuries, bone fragments compressing the anterior spinal cord, or occlusion of the anterior spinal artery (which supplies the anterior two-thirds of the cord).
- Deficits: Bilateral loss of motor function (corticospinal tract) and bilateral loss of pain and temperature sensation (spinothalamic tract) below the level of injury.
- Spared Functions: Proprioception, vibration, and light touch remain intact because the dorsal columns (located posteriorly) are supplied by the posterior spinal arteries and are spared.
3. Central Cord Syndrome
The most common incomplete spinal cord syndrome, typically occurring due to hyperextension injuries (e.g., falls in elderly patients with pre-existing cervical spondylosis or spinal stenosis).
- Deficits: Motor weakness is significantly more pronounced in the upper extremities than the lower extremities (the "man in a barrel" presentation). This occurs because the motor fibers innervating the arms are located centrally within the corticospinal tract, while the fibers for the legs are peripheral.
- Associated Features: Varying sensory loss and bladder dysfunction.
| Spinal Cord Syndrome | Mechanism of Injury | Motor Deficits | Sensory Deficits | Spared Functions |
|---|---|---|---|---|
| Brown-Séquard | Penetrating trauma (hemicord transection) | Ipsilateral paralysis below injury | Ipsilateral loss of proprioception/vibration; Contralateral loss of pain/temp (1-2 levels below) | Opposite motor, same-side pain/temp |
| Anterior Cord | Flexion/rotation; Anterior spinal artery occlusion | Bilateral paralysis below injury | Bilateral loss of pain and temperature | Proprioception, vibration, light touch (intact dorsal columns) |
| Central Cord | Hyperextension; Cervical stenosis | Motor weakness Upper > Lower limbs | Variable sensory loss | Variable, often lower extremity motor function is partially spared |
Neurogenic Shock vs. Spinal Shock
Flight paramedics must clearly differentiate between these two terms, as one is a hemodynamic emergency and the other is a neurological state.
Neurogenic Shock
Neurogenic shock is a hemodynamic distributive shock caused by the loss of sympathetic tone. It occurs in spinal cord injuries at or above the T6 level.
- Pathophysiology: Disruption of descending sympathetic pathways leads to massive, unchecked vasodilation (venous pooling and profound loss of systemic vascular resistance) and loss of cardiac accelerator fibers (T1–T4), leaving parasympathetic (vagal) tone unopposed.
- Classic Triad: Hypotension (due to vasodilation), Bradycardia (due to loss of sympathetic cardiac acceleration), and Poikilothermia (warm, dry, flushed skin below the level of injury due to loss of vasomotor tone and inability to sweat/regulate temperature).
- Hemodynamic Management:
- Volume Resuscitation: Administer IV crystalloids to correct relative hypovolemia, but avoid fluid overload.
- Perfusion Target: Maintain a Mean Arterial Pressure (MAP) of 85–90 mmHg for the first 5–7 days (AANS guidelines) to maintain spinal cord perfusion and prevent secondary ischemic injury.
- Vasopressors: If blood pressure is refractory to fluids, initiate vasopressors with combined alpha and beta activity. Norepinephrine is the first-line vasopressor. Dopamine can also be used. Phenylephrine (pure alpha) is avoided if severe bradycardia is present as it can trigger reflex bradycardia. Atropine (0.5–1.0 mg IV) or transcutaneous pacing should be utilized for symptomatic bradycardia.
Spinal Shock
Spinal shock is a neurological state representing the temporary physiological shutdown of the spinal cord below the level of injury.
- Pathophysiology: Loss of all spinal reflex activity, motor function, and sensation below the level of injury.
- Clinical Presentation: Flaccid paralysis, areflexia (including absence of deep tendon reflexes and the bulbocavernosus reflex), and complete sensory loss.
- Duration and Resolution: Spinal shock can last from hours to several weeks. Its resolution is marked by the return of spinal reflexes, specifically the bulbocavernosus reflex (tested by squeezing the glans penis or tugging on a Foley catheter, which causes reflex contraction of the anal sphincter). Once this reflex returns, spinal shock has resolved, and the true extent of the neurological injury can be determined.
Critical Transport and Airway Considerations
- Spinal Motion Restriction (SMR): Apply a rigid cervical collar. For long-distance transports, transition the patient off a hard backboard onto a vacuum mattress or padded stretcher as soon as possible to prevent pressure injuries, which can develop in under two hours.
- Airway Management: If intubation is required, perform inline spinal stabilization. Avoid hyperextending the neck.
- Succinylcholine Warning: Avoid Succinylcholine in patients with subacute spinal injuries older than 24 to 48 hours. Denervation leads to upregulation of nicotinic acetylcholine receptors on the muscle membrane, which can result in life-threatening hyperkalemia and cardiac arrest if Succinylcholine is administered.
A patient is involved in a high-velocity motor vehicle collision and suffers a hyperflexion injury of the cervical spine. On assessment, the patient has bilateral loss of motor function and bilateral loss of pain and temperature sensation below the C6 level, but retains the ability to perceive position (proprioception), deep touch, and vibration. Which spinal cord syndrome is this patient presenting with?
Which of the following correctly differentiates neurogenic shock from spinal shock?