Spine: fracture / luxation

• 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.

• More common in male cats due to increased wandering and risk of involvement in RTA/HBC.

• May require expensive investigation eg MRI Magnetic resonance imaging: spine, CT Computed tomography (CT) or myelography Radiography: myelography and surgery with prolonged intensive care.
• Simple plain radiography is relatively inexpensive.

• Due to traumatic nature of injury often associated with other injuries which may be life-threatening.
  Full evaluation of patient is essential before investigation or treatment of spinal injury.
• Movement of patient may cause further injury if fracture is unstable.
  Take particular care in anesthetized patient as muscle boarding in conscious patient can help stabilize fracture site.

General

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

Specific

• Vertebral neoplasia Spinal neoplasia as a cause of pathological fracture.

• 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.

• Signs develop acutely following injury.

• May be history of trauma - cat often discovered at site of accident as unable to ambulate afterwards.

• Caution in moving the patient to limit additional injury.
• Initial assessment of life-threatening injuries (basic emergency procedures: eg airway, breathing, circulation).
• Thorough physical examination to detect non-neural injuries (pulmonary or pleural lesion, diaphragmatic rupture    , damaged urinary tract, long bone or pelvic fracture, head and soft tissue injury).

Neurological examination - aims

• Neurolocalization Neurological examination.
• Evaluation of lesion severity.
• Neurolocalization: localized lesion(s) to one of the four following spinal cord regions [C1 - C5], [C6 - T2], [T3 - L3], or [L4 - S3] - consist in evaluating:
  • Mental status: normal in case of spinal cord injury - abnormal in case of head injury.
  • Posture.
  • Motor function: decreased voluntary movement (-paresis), absence of voluntary movement (-plegia) - divided in hemi- (forelimb and hindlimb involvement only on one side), tetra- (all four limb involvement), para- (hind limbs involvement), or mono- (only one limb involved).
  • Muscle tone and spinal reflexes: normal to increased in case of upper motor neuron lesion (UMN) - decreased to absent in case of lower motor neuron lesion (LMN).
  • Sacrocaudal fracture/luxation and tail avulsion     : frequent in cats following road traffic accident - cause tail paresis/paralysis, urinary and fecal incontinence by nerve avulsion of caudal and coccygeal nerve roots - prognosis guarded to poor if no return of voluntary urination after 1-2 months. Intact tail base sensation predicts control of urination and is therefore a useful screening test.

• Evaluation of lesion severity: correlation between severity of the injury and presence or absence of deep pain sensation (nociception) - evaluated by observing brain-mediated response (turning of the head, attempt to bite, increased respiration) to pinching the toes or tail with hemostatic forceps - prognosis for return of neurological function is very poor if loss of nociception.

• Clinical examination can determine the site and severity of the lesion.

Radiography 

• Approximately 20% of cats with thoracolumbar fractures have a second spinal column fracture/luxation Radiography: spine.
• The entire vertebral column must be radiographed    - precise lesion localization, help to discover unsuspected lesions and assess the need for surgery and the procedure to be used  .
  • Conscious examination provides physiological paraspinal muscle tone protection but difficulty in obtaining proper positioning.
  • Anesthesia abolishes physiological protective muscle tone but assists in getting proper positioning and performing myelogram.
• Myelography Radiography: myelography or other advanced imaging techniques (computed tomography or magnetic resonance imaging) can be used to establish the presence of spinal compression    .
• Because cats with spinal fractures and luxations frequently have vertebral instability, the potential for causing additional injury during positioning to obtain orthogonal views in myelography is of real concern. Advanced imaging such as CT or MRI are therefore preferred.
• CT is very helpful in determining abnormalities of bone that may not be apparent with survery radiography.
• MR imaging has the distinct advantage of showing information regarding intramedullary spinal disease or soft tissue compresssion of the spinal cord caused by hematoma or ruptured intervertebral disk.

• Vertebral fracture may be obvious.

• Spinal concussion Spinal cord: concussion.
• Spinal compression for other reason, eg prolapsed disk Intervertebral disk disease.
• Fibrocartilagenous embolism Fibrocartilaginous embolism.
• Iliac thrombosis Thromboembolism: aorta.
• Vertebral neoplasia with secondary fracture Spinal neoplasia.

• Immediate treatment of non-neural injuries limited to those problems that are life threatening (evaluation of 'ABC' of trauma management Trauma: overview).
• Aim of spinal fracture treatment is to:
  • Prevent further mechanical damage to the spinal cord and
  • Treat/prevent secondary pathophysiologic events.
• Choice of treatment (conservative or surgical) depends on severity of the lesion, owner's finance, surgeon expertise and preference.
• Corticosteroids may be indicated for shock, but their use to treat spinal cord injury is contentious.
• Medical treatment: lipid peroxidation is an important factor in post-traumatic destruction of spinal cord tissue - numerous molecules have been advocated to limit this pathological processin vitroor following experimental spinal cord injury - unfortunately, there is limited number of clinical studies to support these.
  • Methylprednisolone sodium succinate (MPSS) Methylprednisolone: free radical scavenging properties at high doses - human clinical trials suggest the use of MPSS at 30 mg/kg intravenous bolus if it can be administered during the first eight hours and followed by infusion of 5.4 mg/kg during 24 hours (if given during the first three hours) or 48 hours (if given between three and eight hours) - could be detrimental if administered after eight hours - little information available on optimal dosage regimen in cats and clinical efficacy.
  • Other treatment protocols under trial: NMDA receptor blockers (MK801, NBQX, Thienylphencyclidine), opioid agonists (U-50488H) or antagonist (Nalmefene), thyroid releasing hormone (TRH), gangliosides (GM1), mild hypothermia.
• Non-surgical treatment: strict cage confinement for 4 to 6 weeks with or without external support bandages or casts (poorly tolerated in most cats) to immobilize the vertebral segment cranial and caudal to the damaged area.
• Surgical treatment: indicated if spinal instability (damage to two or more vertebral compartments) and/or spinal cord compression
  • Spinal fixation: use of Steinmann pins and methylmethacrylate is effective at all levels of the vertebral column, provide greatest rotational stability but poor resistance to dorsoventral bending - vertebral body plate (size often limiting factor in cats) resists dorsoventral bending forces but little resistance to rotational forces.
  • Decompression: indicated if evidence of spinal cord compression on myelogram - best achieved by hemilaminectomy in the thoracolumbar spine (least destabilizing effect compared to dorsal laminectomy).

Monitoring

• Any deterioration in neurologic status should be investigated using spinal radiography, and potentially advanced imaging if deterioration continues.
• Pain control: opiate analgesia +/- non-steroidal anti-inflammatory drugs (if corticosteroids have not already been administered).
• Prevention of complications of recumbency: turn plegic patient every four hours - use of extra padding surfaces.
• Bladder management: assessment of bladder function is crucial (transabdominal palpation) - if expression is difficult, the bladder can be drained using a sterile urinary catheter, indwelling catheter or manual expression - pharmacological agents can be used to assist bladder management (Phenoxybenzamine Phenoxybenzamine and diazepam Diazepam reduce respectively smooth and striated muscle urethral sphincter tone, bethanechol Bethanecol enhances detrusor contractibility).
• Physical therapy: use of massage and hydrotherapy is unfortunately limited in cats compared to dogs.

• Cats with absent deep pain sensation on presentation carry usually a very poor prognosis. In the presence of deep pain sensation, prognosis is guarded to fair.
• Intact tail base sensation predicts control of urination and is therefore a useful screening test in cats with sacro-caudal subluxation/luxation (tail-pull injury Tail pull injury).

• Functional recovery can take 3 to 6 weeks.

• Absence of deep pain sensation.
• For conservative management:
  • cat does not tolerate well external splint.
  • significant instability cannot be addressed.
• For surgical management:
  • implant failure.
  • implant infection.

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 2 (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.