Spinal Cord Injury

Absolute indications

Complete spinal cord injury above C5 level

Respiratory distress

Hypoxemia despite attempts at oxygenation

Severe respiratory acidosis

Relative indications

Complaint of shortness of breath

Development of quad breathing^a

Vital capacity of <10 mL/kg or decreasing vital capacity

Consideration should be given

Need to travel remote from emergency department (e.g., MRI, transfer to another facility)

^aQuad breathing refers to the stereotypical breathing pattern in patients with cervical and upper thoracic spinal cord injury in which the chest wall retracts and the abdominal wall protrudes with inspiration (Adapted from Stein et al. [11])

Patients with cervical and high thoracic injuries experiencing impending respiratory failure often describe heaviness in the chest or inability to catch their breath, or may appear breathless while speaking. Loss of chest wall and abdominal innervation produce a pattern where the chest goes in and the abdomen goes out with diaphragmatic contraction, so call “quad breathing”. Treatment of respiratory insufficiency in a patient with SCI should include urgent endotracheal intubation [12, 13]. Caution should be employed during intubation as tetraplegic patients can develop bradycardia and hypotension due to autonomic instability.

Once hemodynamic stability it achieved, the secondary survey should begin with a detailed exam to quantify neurologic disability.

15.3.1 Imaging

CT scan is the modality of choice for initial evaluation. It detects bony injury and dislocation [14].

MRI is useful in detecting injury in the obtunded patient with a suspected SCI where physical exam is less reliable. Additionally, MRI is used for diagnosis, to plan operative interventions, and for prognostication, as it is the modality which determines the degree of edema and hemorrhage in the spinal cord [15].

15.3.2 Evaluation and Classification of SCI

The American Spinal Injury Association (ASIA) developed a standard classification of SCI which is widely used [16] (Fig. 15.1). The ASIA examination tests 2 components; sensory and motor. The sensory examination tests 28 dermatomes bilaterally for two aspects of sensation, light touch and pin prick. The motor examination tests ten paired myotomes bilaterally for strength. The American Spinal Injury Association has also described the ASIA Impairment scale which is the standard for determination of completeness of an SCI. Complete injuries are losses of all sensory and motor function below the level of injury ASIA A. Incomplete injuries retain some neurologic function below the level of injury ASIA B-D. ASIA should be assessed at least daily as a decreased score is usually a result of spinal cord edema ascension, new or worsening spinal cord hemorrhage, or ischemia.

Fig. 15.1

ASIA Standard neurological classification of spinal cord injury (From International Standards for Neurological Classification of Spinal Cord Injury [16])

15.3.3 Specific Clinical Syndromes [11]

Central cord syndrome

Most common, seen in older adults
Extensive weakness noted in the upper extremities compared to the lower extremities
Existing degenerative ligament and/or osteophytic changes to spine prior to hyperextension injury of the neck causing the spinal cord to be squeezed or pinched
Usually not associated with a bony injury or evidence of spinal instability

Brown-Sequard syndrome

Typically from penetrating spinal cord injury or a lateral mass fracture of the spine
Hemiplegia with ipsilateral loss of light touch and proprioception with contralateral loss of pain and temperature sensation

Anterior cord syndrome

Motor and sensory pathways in the anterior part of the spinal cord are injured
Cause is not usually traumatic
Ischemic insult from disruption of flow in the anterior spinal artery
Poor prognosis for recovery

Posterior cord syndrome

Result of vascular compromise to the spinal cord
Rarely occurs from trauma
Posterior aspect of spinal cord affected
Loss of proprioception with preservation of motor function, pain and temperature sensation and light touch

Cauda equina syndrome

Traumatic cause is typically retropulsion of a fracture fragment in the lumbosacral region resulting in lower spinal nerve root compression
Non traumatic cause most commonly results from a massive herniated disc in the lumbar region
Other non-traumatic causes are spinal lesions/tumors, lumbar stenosis, spinal hemorrhages, spinal arteriovenous malformations, birth abnormalities, spinal anesthesia
May include one or more symptoms:
- Severe low back pain
- Motor weakness/sensory loss or pain in one or both legs
- Saddle numbness
- Recent onset of bladder dysfunction (incontinence or retention)
- Recent onset bowel dysfunction
- Abnormal sensation in the bladder or rectum
- Recent onset of sexual dysfunction
- Loss of reflexes in the lower extremities

15.3.4 Spinal Shock

Spinal shock was first described by Whytt in 1750 as the loss of sensation with motor paralysis with gradual recovery of reflexes [17]. Following spinal cord injury, the reflexes above the injury level remain intact while the reflexes below the injury level become depressed or absent. In SCI, the term ‘shock’ does not refer to the circulatory system, and should not be confused with neurogenic shock. Ditunno et al. [18] described spinal shock in a four phase model.

Phase 1: areflexia or hyporeflxia, 0–24 h post injury.
Phase 2: reflexes return, 1–3 days post injury.
Phase 3: early hyper-reflexia, day 4 to 1 month post injury.
Phase 4: spascity/hyper-reflexia, 1–12 months post injury.

15.4 Management and Interventions

The majority of treatment for patients with spinal cord injury is supportive, with focus on minimizing secondary injury, and preventing and treating complications as they occur. Patients with injury in the cervical or high thoracic spine are at high risk of organ failure and require high-level intensive care support [19]. It should be expected that over hours to days following injury the neurologic deficits will worsen, which in turn will trigger further cardiovascular and respiratory dysfunction.

15.4.1 Neurogenic Shock

Neurogenic shock can occur in patients with SCI on or above T6. It is caused by the loss of supraspinal control of the sympathetic nervous system [20, 21]. This causes hypotension and stimulation of the vagus nerve, with unopposed parasympathetic activity leading to bradycardia and the block of the atrioventricular node [21]. Neurogenic shock is a form of distributive shock with excessive vasodilatation and the characteristic finding of bradycardia. Patients are usually hypotensive with warm and dry skin. Neurogenic shock may not be present on admission but can develop over days to hours and last for 1–3 weeks. The first line therapy is fluid resuscitation to maintain euvolemia. Second line treatment is the use of pressors, inotropes or a combination of both (Table 15.2). Treating hypotension and hypoperfusion is paramount, as these are known mediators of secondary injury. Severe hemodynamic abnormalities will ultimately resolve after the first 2–6 weeks post injury, however patients with SCI can have life-long alterations in cardiovascular function.

Table 15.2

Vasoactive agents used to treat neurogenic shock

Agent	α Activity	β Activity	Considerations
Norepinephrine	+++	++	Probably the preferred agent
Phenylephrine	++	None	May worsen bradycardia
Dopamine
Low dose (3–10 mcg/kg/min)	+	++	May lead to inadvertent diuresis at low dose
High dose (10–20 mcg/kg/min)	++	+++
Epinephrine	+++	++	Rarely needed
Dobutamine	None	+++	May cause hypotension if not euvolemic