Felis ISSN 2398-2950

Spine: fracture / luxation

Synonym(s): Spinal trauma

Contributor(s): Laurent Garosi

Introduction

  • Common cause of spinal dysfunction.
  • Feline spinal injuries are often more devastating than in dogs.
  • Approximately 20% of cats with traumatic spinal injuries also have acute intervertebral disk extrusion secondary to trauma.
  • Deep pain perception (nociception) in affected limbs is the most important prognostic indicator following spinal trauma.
  • Cause: most often secondary to road traffic accident/hit-by-car (RTA/HBC) or fall from a height.
  • Signs: often associated with other injuries (pulmonary or pleural lesion, diaphragmatic rupture, damaged urinary tract, long bone or pelvic fractures, head injury).
  • Diagnosis: radiography.
  • Treatment: conservative, surgical.
  • Prognosis: guarded for unstable fractures.

Pathogenesis

Predisposing factors

General

  • Anything increasing risk of trauma, eg entire male cats roaming.

Specific

Pathophysiology

  • Injury mediated by primary and secondary mechanisms:
    • Primary event is mechanical injury to the tissue.
    • Secondary injuries are a cascade of biochemical and vascular events that will lead to progressive destruction of spinal cord tissue.
  • Four basic mechanisms injure the spinal cord:
    • Laceration.
    • Compression.
    • Concussion.
    • Ischemia.
  • Laceration: mechanical destruction of neuroaxonal and vascular structures at the time of the injury.
  • Compression: mass effect on the spinal cord parenchyma and vascular structures by traumatic disc herniation, displace vertebral fracture or hematoma.
    • Affects preferentially superficial and large diameter fibers (proprioceptive function) before small deeply seated fibers (nociception).
    • Compromise spinal cord blood flow and therefore oxygen delivery.
    • In the long-term causes white matter degenerative changes (myelin vacuolation and demyelination, axonal loss and spheroid formation, Wallerian type degeneration in ascending dorsal funiculi and spinocerebellar tract and descending lateral and ventral funiculi).
    • Tissues changes depend on the degree and duration of compression.
  • Concussion Spinal cord: concussion: force applied to the spinal cord at the time of the injury without residual compression - injury to the spinal cord will result from:
    • Physical disruption of the parenchyma.
    • Initiation of secondary injury.
  • Ischemia: effects very similar to concussion - result in hypoxia - principally affect gray matter (six-fold greater oxygen demand than gray matter) - caused by:
    • Direct vascular damage (laceration or occlusion of spinal cord blood supply).
    • Loss of vascular autoregulation.
    • Compromised systemic arterial pressure (sympathetic paralysis and hypotension).
    • Release of vasoactive substances (catecholamines, excitatory amino acid, intracellular calcium).
  • Secondary injury phenomenon: develop over the next 48 hours after injury - results from cascade of vascular and biochemical events that is responsible for an expanding zone of necrosis. The mechanisms can be summarized as energy failure, changes in membrane permeability, excitotoxicity, oxidative damage and inflammation.
    • Vascular events: progressive spinal cord ischemia (see above) and rapid energy depletion - failure of ATP-ase ionic pump to maintain ionic gradient will cause cytotoxic edema.
    • Biochemical events:
      • Increased intracellular calcium (following direct membrane damage, activation of N-methyl D-aspartate (NMDA) glutamate-gated channel and voltage-gated calcium channel) causes activation of intracellular proteases, phospholipase A2, spasm of vascular smooth muscles.
      • Free radical production (during arachidonic acid and iron oxidation) causes lipid membrane peroxidation of neuronal and endothelial cells - free radical scavenging system overwhelmed (catalase, dismutase, glutathione peroxydase), especially during reperfusion (xanthine oxidase uses oxygen instead of NAD+).
      • Increases in excitatory amino acids such as glutamate cause increased intracellular sodium (cellular swelling) and calcium concentration (activation of proteases).
      • Release of endorphin causes local ischemia.

Biomechanics of spinal fractures

  • Four different forces can be applied to the vertebral column:
    • Bending forces (laterolateral or dorsoventral).
    • Axial forces.
    • Rotational forces.
    • Shear forces.
  • Although all segments of the spine are susceptible to trauma, the cervicothoracic, thoracolumbar, lumbosacral and sacrocaudal (coccygeal) junctions are the most common sites of fractures and luxations.
  • Vertebrae can be divided in three anatomical compartments:
    • Ventral: ventral 3/4 of the vertebral body and disk, and the ventral longitudinal ligament.
    • Middle: dorsal 1/4 of the vertebral body, the disk and the dorsal longitudinal ligament.
    • Dorsal: articular facets, lateral pedicles, dorsal laminae, interarcuate ligaments and dorsal spinous processes.
  • Assessment of instability: considered unstable if lesion of two or more compartments.
    • Fracture of articular processes: most susceptible to rotation forces.
    • Fracture of vertebral body: most susceptible to bending forces.
    • Fracture of articular processes and vertebral body: susceptible to all forces, especially rotation and bending forces.
    • Disruption of the soft tissues of the intervertebral disk, dorsal and ventral longitudinal ligaments, and synovium of the articular facets disrupts all the compartments and causes instability.

Timecourse

  • Signs develop acutely following injury.

Diagnosis

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Treatment

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Grasmueck S, Steffen F (2004) Survival rates and outcomes in cats with thoracic and lumbar spinal cord injuries due to external trauma. JSAP 45 (6), 284-288 PubMed.
  • Marioni-Henry K, Vite C H, Newton A L et al (2004) Prevalence of diseases of the spinal cord of cats. JVIM 18 (6), 851-858 PubMed.
  • Voss K, Monatavon P M (2004) Tension band stabilization of fractures and luxations of the thoracolumbar vertebrae in dogs and cats: 38 cases (1993-2002). JAVMA 225 (1), 78-83 PubMed.
  • Muñana K R, Olby N J, Sharp N J H et al (2001) Intervertebral disk disease in 10 cats. JAAHA 37 (4), 384-389 VetMedResource.
  • Bagley R S (2000) Spinal fracture or luxation. Vet Clin N Amer Small Anim Pract 30 (1), 133-153 PubMed.
  • Bagley R S, Silver G M, Connors R L et al (2000) Exogenous spinal trauma- surgical therapy and aftercare. Comp Small Anim Pract 22 (3), 218-230 VetMedResource.
  • Kathman I, Cizinauskas S, Rytz U et al (2000) Spontaneous lumbar intervertebral disc protrusion in cats: literature review and case presentations. J Feline Med Surg (4), 207-212 PubMed.
  • Olby N (1999) Current concepts in the management of acute spinal cord injury. JVIM 13 (5), 399-407 PubMed.
  • Selcer R R, Bubb W J, & Walker T L (1991) Management of vertebral column fractures in dogs and cats - 211 cases (1977-1985). JAVMA 198 (11), 1965-1968 PubMed.
  • Carberry C A, Flanders J A, Dietze A E et al (1989) Nonsurgical management of thoracic and lumbar spinal fractures and fracture/luxations in the dog and cat -A review of 17 cases. JAAHA 25 (1), 43-54 VetMedResource.
  • Smeak D D & Olmstead M L (1985) Fracture/luxations of the sacrococcygeal area in the cat - A retrospective study of 51 cases. Vet Surg 14 (4), 319-324 VetMedResource.
  • Feeney D A & Oliver J E (1980) Blunt spinal trauma in the dog and cat - insight into radiographic lesions. JAAHA 16 (6), 885-890 VetMedResource.


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