Principals of acute spinal cord injury
Spinal trauma occurs from external or internal causes: external – automobile-related injury, falls, falling objects, and projectile
missile damage; internal – intervertebral disc disease, pathologic fractures, vascular. Mechanisms of primary injury include
compression, shear, laceration, bending and distraction. The thoracolumbar region is the most commonly injured are in the
dog and cat. Fractures occur between T11 and L6 in 50% to 60% of patients after blunt trauma. Fractures in the thoracic spine
may have little displacement because of the protection provided by the ribs, ligamentous support and epaxial musculature.
Fracture and luxation of the thoracolumbar spine are often associated with other systemic injuries: pneumothorax, pulmonary
contusions, orthopaedic injuries, urogenital injuries, and diaphragmatic hernia. Approximately 20% of patients with thoracolumbar
fractures have a second spinal column fracture-luxation. The amount of neural tissue injury is related to the rapidity and
severity of insult, and the amount and duration of compression.
Primary mechanical injury to the neural tissue can subsequently lead to secondary biochemical injury (secondary injury theory).
Acute spinal cord injury causes both systemic and local vascular abnormalities. Primary injury ultimately results in a progressive
decrease in perfusion and necrosis of the injured area of the spinal cord. Secondary metabolic injury results from ischemia
include abnormal release of excitatory neurotransmitters, abnormal accumulation of intracellular calcium, and activation of
membrane phospholipases and production of free radicals. Vascular mechanisms include – ischemia, impaired autoregulation,
neurogenic shock, hemorrhage, microcirculatory disruption, vasospasm, and thrombosis. Ionic derangements include – increase
intracellular calcium and sodium and increased extracellular potassium. Accumulation of neurotransmitters includes – serotonin,
catecholamines, and extracellular glutamate. The severity of the pathologic changes and the degree of recovery are related
to the duration of acute compression as demonstrated in studies of animal models. New treatments are aimed at those limiting
the secondary injury and those that promote regeneration of the injured cord (oscillating field stimulators, polyethylene
If a spinal fracture is suspected, the patient should be secured and immobilized to a back board to prevent further injury.
Additional restraint or sedation may be necessary if the animal is struggling. The animal should be evaluated in the position
that it is presented, usually in lateral or sternal recumbency. Spinal injury frequently occurs in association with multiple
organ trauma. Basic principles for management of spinal cord injury (SCI) are applied to ensure stabilization of the patient's
physical status. Upon admission, the patient is stabilized by assessing airway patency, breathing and circulatory status.
Spontaneous respiration and evidence of respiratory compromised are closely monitored in patients with cervical SCI. Blood
gas monitoring will assess severity of hypoventilation determined by measuring PaCO2 (35-45 mm Hg). Oxygen supplementation will assist to maintain PaO2 (> 90 mm Hg). Trauma may predispose to primary lung disease associated with pneumonia, atelectasis, hemorrhage or edema.
General medical management of patients with acute SCI should include restoring a normal blood pressure, enhancing intravascular
volume and avoiding hyperthermia in an effort to enhance spinal cord perfusion. Hypotension will often follow spinal cord
injury due to multiple factors: interruption to first order neurons of the sympathetics resulting in unopposed parasympathetic
influence and bradycardia; spinal shock causing loss of muscle tone and secondary hypovolemia from venous pooling; and blood
loss from other associated injuries. Integrity of the circulatory system is monitored with MABP and electrocardiogram.
Medical management specific to spinal cord injury
The pathophysiology of acute SCI has led to relevant neuroprotective approaches to attenuate the effects of secondary injury.
Neuroprotective effects of methylprednisolone sodium succinate (MPSS) include inhibition of lipid peroxidation, calcium influx,
ischemia, axonal dieback, cytoskeletal degradation, and anti-inflammatory effects. Methylprednisolone sodium succinate (MPSS)
administration protocol is 30 mg/kg IV slow bolus; two hours after the first dose administer 15 mg/kg IV; 4 hours after the
second dose administer 15 mg/kg; consider CRI 5.4 mg/kg/h for 24 hours. If more than 8 hours after injury corticosteroids
should be avoided. Therapeutic efficacy has been questioned in humans and studies report an increased rate of sepsis and pneumonia.
No scientific randomized controlled clinical trials exist with use of MPSS in animals. Complications of corticosteroid therapy
in dogs include diarrhea, melena, vomiting, hematochezia, hematemesis, and anorexia.