Acute Spinal Cord Injury (SCI)

1. Pathophysiology: Primary vs. Secondary Injury

Primary Injury: This is the immediate mechanical damage to neural tissue. It can be concussive (rapid transfer of kinetic energy, as in ANNPE), compressive (sustained mechanical pressure, as in IVDE), or lacerating. The primary injury is instantaneous and irreversible.

Secondary Injury: This is the complex biochemical cascade triggered by the primary insult. It includes ischemia, ATP depletion, excitotoxicity (massive glutamate release), intracellular calcium influx, lipid peroxidation, and free radical generation. This cascade leads to delayed neuronal apoptosis and progressive tissue destruction. All acute medical management is aimed at blunting this secondary cascade.

2. Primary Assessment & Immobilization

Stabilize the patient (airway, breathing, circulation) as for any other emergency. Early consideration must be given to systemic blood pressure and oxygenation. Hypotension will result in a further decrease in the already compromised perfusion of the injured spinal cord, while hypoxemia exacerbates local energy failure. Oxygen supplementation is particularly important for animals with cervical SCI, where hypoventilation is common.

Feline Considerations: FIV and FeLV testing should be performed in feline patients, as a positive result markedly increases the likelihood of lymphoma as the cause of neurological deficits.

Immobilization: Immediate cage confinement is the minimum requirement for suspected Hansen Type I disc extrusions. If vertebral fracture or subluxation is suspected, strapping the patient to a rigid board is strictly recommended to prevent catastrophic secondary injury during handling.

3. Neurological Grading & Conscious Nociception

A rigorous, standardized neurological examination is paramount. The presence or absence of deep pain remains the single most powerful prognostic indicator in veterinary neurology. It is vital to evaluate deep pain before administering potent mu-agonist opioids, as a patient with weak sensation may appear to have completely lost perception under their influence.

• Grade 1: Spinal hyperesthesia (pain) only. Normal gait and proprioception.
• Grade 2: Ambulatory paraparesis/tetraparesis. Proprioceptive deficits are present, but the patient can bear weight and take purposeful steps.
• Grade 3: Non-ambulatory paraparesis/tetraparesis. Voluntary motor function is present but insufficient to bear weight.
• Grade 4: Paraplegia/tetraplegia with intact deep pain. No voluntary motor function.
• Grade 5: Paraplegia/tetraplegia with absent deep pain. The worst prognostic category.

4. Diagnostic Imaging & The Radiography Trap

While plain radiographs are useful for identifying gross fractures, luxations, or discospondylitis, they cannot reliably diagnose spinal cord compression or parenchymal damage. High-field MRI is the gold standard. It differentiates between surgical/compressive lesions and non-surgical/concussive lesions, while also evaluating for intramedullary T2W hyperintensity, an indicator of potential myelomalacia. CT-myelography or X-ray myelography remain alternatives to visualize the site of compression.

Should you undertake pre-referral radiography? Generally, no. Plain radiographs rarely yield sufficient information for surgical planning. More importantly, taking radiographs poses a massive physical risk. Spinal trauma causes paraspinal muscles to spasm, creating a "splinting" effect that stabilizes the column. Sedation or anesthesia results in the loss of this muscle splinting. Unstable vertebral segments are more likely to displace, often leading to severe neurological deterioration immediately following sedation for X-rays.

Clinical Warning: Suspected atlantoaxial (AA) subluxation radiographs taken with a ventroflexed cervical spine are highly dangerous. This position exacerbates compression and risks acute respiratory failure or cardiac arrest. A neutral position is sufficient.

5. Analgesia and the Glucocorticoid Consensus

Analgesia should be instigated immediately following the exam. NSAIDs are useful (if the patient is normotensive and hydrated), and pure mu-agonist opioids are appropriate for severe pain.

The Glucocorticoid Stance: Glucocorticoids prejudice the survival of injured neurons by interfering with glucose metabolism.

• Dexamethasone: Associated with a poorer prognosis and significantly increased risk of severe GI ulceration. Its use in spinal trauma is considered unwise and potentially negligent.
• Methylprednisolone Sodium Succinate (MPSS): There are NO veterinary studies demonstrating benefits. Endoscopic studies have revealed severe, subclinical gastrointestinal hemorrhage in 90% of dogs following MPSS treatment. Routine glucocorticoid therapy in spinal patients is strongly discouraged.

6. Evidence-Based Protocols and Prognosis

Medical Management: Indicated for Grades 1 and 2, or strictly non-compressive concussive injuries (FCE/ANNPE). The cornerstone is strict cage confinement for 4-6 weeks to allow the annulus fibrosus to scar. Analgesia should be multimodal (NSAIDs/Gabapentin + Opioids).

Surgical Decompression: Indicated for compressive lesions in Grade 3, 4, or 5 patients, or those failing medical management. For Grade 5 dogs, decompression ideally should occur within 12–24 hours of deep pain loss to maximize recovery chances.