Spinal Fractures and Luxations

Spinal fractures and luxations refer to traumatic disruptions of the vertebral column, including fractures of the vertebral body, lamina, articular processes, pedicles, or spinous processes, and/or luxations (dislocations) of the intervertebral joints, often resulting in instability of the spinal column and potential injury to the spinal cord and nerve roots. These injuries are classified based on the affected vertebral segment (cervical, thoracolumbar, lumbosacral), the type of fracture (compression, burst, wedge, comminuted), and the degree of instability and neurological deficit. Surgical management aims to decompress neural structures, stabilize the vertebral column, and restore alignment to preserve or improve neurological function.

The primary cause of spinal fractures and luxations in small animals is high-energy trauma, most commonly vehicular accidents, falls from heights, and direct blows. Less common causes include bite wounds, gunshot injuries, and pathological fractures due to underlying bone disease such as neoplasia (e.g., multiple myeloma, osteosarcoma), infection (e.g., discospondylitis), or metabolic bone disease (e.g., hyperparathyroidism). Iatrogenic causes can occur during improper handling or surgical manipulation. Anatomical vulnerability is highest at the junctional regions: the atlantoaxial junction, cervicothoracic junction (C6-T2), thoracolumbar junction (T11-L2), and lumbosacral junction, due to biomechanical stress concentration and transition from rigid to flexible segments.

Spinal fractures and luxations account for approximately 10-15% of all fractures in dogs and cats. They are most commonly seen in young to middle-aged animals (mean age 3-5 years) with no sex predilection. Small breed dogs (e.g., Dachshunds, Poodles) may be overrepresented due to their chondrodystrophic conformation, which predisposes to intervertebral disc disease and may also influence fracture patterns. Large breed dogs (e.g., German Shepherds, Labrador Retrievers) are frequently affected due to high-energy trauma. Cats are commonly affected by high-rise syndrome (falls from heights). Working and hunting dogs have an increased risk due to exposure to trauma. The thoracolumbar junction is the most frequently affected region (approximately 50% of cases), followed by the cervical and lumbosacral regions.

The pathophysiology of spinal fractures and luxations involves direct mechanical disruption of the vertebral column and indirect injury to the spinal cord. The initial trauma causes displacement of bone fragments or vertebral segments, leading to spinal cord compression, contusion, and/or laceration. The spinal cord injury can be primary (immediate mechanical damage) or secondary (delayed biochemical and vascular cascades). Secondary injury mechanisms include hemorrhage, edema, inflammation, excitotoxicity, free radical production, and apoptosis, which exacerbate the initial damage. Instability of the vertebral column leads to continued movement and further neurological compromise. In complete luxations, the spinal cord may be completely transected, resulting in irreversible paraplegia or tetraplegia. The severity of neurological deficits correlates with the degree of spinal cord injury and the presence of concurrent injuries (e.g., head trauma, thoracic trauma).

Intrinsic predisposing factors include breed-specific conformational traits (e.g., chondrodystrophic breeds with shortened vertebral bodies), age (young animals with less mature bone), and underlying bone pathology (e.g., neoplasia, infection, osteoporosis). Extrinsic factors include high-energy trauma (vehicular accidents, falls), environmental hazards (e.g., high-rise buildings for cats), and management factors (e.g., off-leash activity in traffic). Prior spinal surgery or vertebral instability may predispose to adjacent segment fractures. Excessive physical activity or improper handling of animals with spinal disease can also precipitate fractures.

Clinical signs vary depending on the location and severity of the injury. Common signs include acute onset of pain (cervical or thoracolumbar), kyphosis or lordosis, spinal deformity, and neurological deficits ranging from mild proprioceptive ataxia to complete paralysis. Cervical fractures may present with tetraplegia, respiratory compromise (if phrenic nerve involvement), and Horner's syndrome (if sympathetic trunk injury). Thoracolumbar fractures often cause paraparesis or paraplegia, with upper motor neuron signs (spasticity, hyperreflexia) if the lesion is cranial to the L4 spinal cord segment, and lower motor neuron signs (flaccidity, hyporeflexia) if caudal to L4. Lumbosacral fractures may cause pelvic limb weakness, urinary and fecal incontinence, and perineal hypalgesia. On palpation, there may be crepitus, swelling, and severe pain over the fracture site. Neurological examination reveals spinal reflex abnormalities, proprioceptive deficits, and loss of deep pain perception in severe cases.

Differential diagnoses include intervertebral disc disease (IVDD), spinal neoplasia (e.g., osteosarcoma, multiple myeloma), discospondylitis, vertebral osteomyelitis, spinal trauma without fracture (e.g., spinal cord concussion), fibrocartilaginous embolic myelopathy, and congenital vertebral anomalies (e.g., hemivertebrae). IVDD typically presents with acute or progressive neurological signs without a history of major trauma; imaging shows disc degeneration and extrusion. Spinal neoplasia often has a slower onset, with lytic or proliferative bone changes on radiographs. Discospondylitis presents with fever, spinal pain, and radiographic evidence of endplate lysis. Spinal trauma without fracture may show no radiographic abnormalities but similar neurological signs. Fibrocartilaginous embolic myelopathy is peracute and non-painful. Congenital anomalies are usually incidental findings but can predispose to instability.

The diagnostic algorithm begins with a thorough history and physical examination, including assessment of cardiovascular and respiratory stability. Neurological examination is performed to localize the lesion and assess severity. If spinal fracture or luxation is suspected, immediate immobilization of the patient is crucial (e.g., placement on a rigid board). Survey radiographs of the entire spine are obtained (lateral and ventrodorsal views) to identify fractures, luxations, and alignment. If radiographs are inconclusive or if spinal cord compression is suspected, advanced imaging such as computed tomography (CT) or magnetic resonance imaging (MRI) is recommended. CT provides excellent bone detail and is ideal for characterizing fractures and planning surgical fixation. MRI is superior for evaluating soft tissue structures, including the spinal cord, intervertebral discs, and ligaments. In cases with neurological deficits, a myelogram may be performed if advanced imaging is unavailable. Surgical exploration is indicated when there is evidence of spinal cord compression, instability, or progressive neurological deterioration.

Laboratory findings are generally non-specific but are important for preoperative assessment and to rule out concurrent disease. Complete blood count may reveal leukocytosis due to stress or inflammation. Serum biochemistry may show elevated muscle enzymes (creatine kinase) due to trauma. Coagulation profile (PT, aPTT, platelet count) is essential to assess bleeding risk. Blood gas analysis and lactate measurement are useful in trauma patients to evaluate perfusion and acid-base status. Inflammatory biomarkers such as C-reactive protein (CRP) and serum amyloid A (SAA) may be elevated. If infection is suspected, blood cultures and serology for infectious agents (e.g., Brucella canis) are indicated. Cerebrospinal fluid analysis may be performed if inflammatory or neoplastic disease is suspected, but is often contraindicated in unstable spinal fractures.

Radiography: Lateral and ventrodorsal radiographs of the entire spine are the initial imaging modality. Findings include vertebral body fractures (compression, wedge, comminuted), luxations (subluxation or complete dislocation), misalignment, and changes in the intervertebral disc spaces. Stress views (flexion and extension) may be performed under sedation to assess instability, but must be done with extreme caution to avoid further spinal cord injury. Radiographic measurements such as the vertebral body height and width can help assess severity. Ultrasonography: Not typically used for spinal fractures, but may be useful for evaluating soft tissue injuries (e.g., abdominal ultrasound for concurrent trauma). CT: Provides detailed 3D bone anatomy, allowing precise characterization of fracture fragments, comminution, and canal compromise. CT is essential for surgical planning and can be used to create patient-specific implants. MRI: Superior for evaluating spinal cord compression, edema, hemorrhage, and ligamentous injuries. MRI is particularly useful in cases with neurological deficits but no obvious fracture on radiographs. Arthroscopy: Not applicable to spinal fractures. Angiography/Fluoroscopy: May be used intraoperatively to guide implant placement, but is not routine.

Cytology and histopathology are not typically performed for spinal fractures unless there is suspicion of an underlying pathological process. If a mass or abnormal tissue is identified during surgery, fine-needle aspiration or biopsy may be obtained. Cytology of bone lesions may reveal neoplastic cells (e.g., osteosarcoma, multiple myeloma) or inflammatory cells (e.g., in osteomyelitis). Histopathology of bone biopsies can confirm the diagnosis and guide further treatment. In cases of suspected discospondylitis, culture and sensitivity of the affected disc or vertebral body may be performed.

Treatment of spinal fractures and luxations can be conservative or surgical. Conservative management is reserved for stable fractures (e.g., spinous process fractures) or non-displaced fractures with minimal neurological deficits. It involves strict cage rest, analgesia, and supportive care for 6-8 weeks. Surgical treatment is indicated for unstable fractures, fractures with spinal cord compression, progressive neurological deterioration, or loss of deep pain perception. The goals of surgery are to decompress the spinal cord and stabilize the vertebral column. Surgical techniques include: 1) Dorsal laminectomy for decompression, 2) Vertebral body plating or screw fixation, 3) Spinal stapling, 4) External skeletal fixation, 5) Vertebral body pin and polymethylmethacrylate (PMMA) fixation, and 6) Intervertebral body fusion. The choice of technique depends on the location and type of fracture. For cervical fractures, ventral stabilization with plates or screws is common. For thoracolumbar fractures, dorsal stabilization with pins and PMMA or vertebral body plating is often used. Lumbosacral fractures may require sacral fixation. Postoperative management includes pain control, antibiotics, and strict confinement. Physical rehabilitation is initiated after 4-6 weeks.

The prognosis for spinal fractures and luxations depends on the severity of neurological deficits, the presence of deep pain perception, and the success of surgical stabilization. Animals with intact deep pain perception have a good to excellent prognosis (80-90% recovery) with appropriate surgical treatment. If deep pain perception is absent, the prognosis is guarded to poor, with a recovery rate of less than 50%. Other negative prognostic indicators include complete luxation, severe comminution, and concurrent spinal cord injury. Complications include implant failure, infection, nonunion, and progressive neurological deterioration. With successful stabilization, most animals regain ambulation within 4-8 weeks, although some may have residual deficits.

Postoperative follow-up includes serial neurological examinations and radiographs. Radiographs are typically taken immediately postoperatively, then at 4, 8, and 12 weeks to assess implant position and bone healing. Restricted activity is enforced for 8-12 weeks, with gradual increase in exercise. Physical therapy (e.g., passive range of motion, swimming, walking) is initiated after 4-6 weeks. Suture removal is typically 10-14 days postoperatively. Long-term monitoring includes assessment of neurological function and detection of late complications such as implant loosening or infection. In cases of spinal fusion, radiographic evidence of fusion may take 3-6 months.

Pearls: 1) Always stabilize the patient before imaging to prevent further spinal cord injury. 2) Use advanced imaging (CT) for precise surgical planning. 3) In thoracolumbar fractures, consider dorsal stabilization with pins and PMMA for immediate rigidity. 4) Preserve the spinous processes when possible for attachment of implants. 5) Monitor for concurrent injuries (e.g., pneumothorax, abdominal trauma) in trauma patients. Pitfalls: 1) Failure to recognize instability, leading to conservative management of an unstable fracture. 2) Inadequate decompression, leaving bone fragments in the spinal canal. 3) Improper implant placement, causing iatrogenic spinal cord injury. 4) Overlooking postoperative infection, which can lead to implant failure. 5) Allowing excessive activity too early, leading to implant failure or nonunion.

Perioperative antimicrobial prophylaxis: Cefazolin 22 mg/kg IV at induction and every 90 minutes during surgery. Postoperative antibiotics (e.g., cephalexin 22 mg/kg PO q8h) are continued for 24 hours or longer if infection is suspected. Analgesia: Opioids (e.g., hydromorphone 0.05-0.1 mg/kg IV q4-6h, or fentanyl CRI 2-5 mcg/kg/hr) are used for severe pain. NSAIDs (e.g., carprofen 2.2 mg/kg PO q12h, or meloxicam 0.1 mg/kg PO q24h) are used for mild to moderate pain, but should be used cautiously in patients with renal or gastrointestinal disease. Local anesthetic blocks (e.g., epidural morphine 0.1 mg/kg) can provide additional analgesia. Muscle relaxants (e.g., methocarbamol 15-20 mg/kg PO q8h) may be used to reduce muscle spasms. Corticosteroids (e.g., dexamethasone 0.1-0.2 mg/kg IV) are controversial but may be used in acute spinal cord injury, though their use is not universally recommended. Chondroprotectants (e.g., polysulfated glycosaminoglycan 4.4 mg/kg IM q7d) may be used for long-term joint health. Gastroprotectants (e.g., omeprazole 1 mg/kg PO q12h) are recommended if NSAIDs are used.

Landmark studies include: 1) A retrospective study by McKee et al. (1998) on 100 dogs with spinal fractures, reporting a 70% recovery rate in dogs with deep pain perception. 2) A study by Bruce et al. (2008) comparing surgical versus conservative treatment, showing superior outcomes with surgery for unstable fractures. 3) A consensus statement from the American College of Veterinary Surgeons (ACVS) on the management of spinal trauma, emphasizing the importance of early decompression and stabilization. 4) A meta-analysis by Jeffery et al. (2016) on the use of corticosteroids in acute spinal cord injury, concluding that high-dose methylprednisolone is not recommended due to lack of benefit and potential adverse effects. 5) AO Vet guidelines recommend the use of locking plates for vertebral stabilization to improve biomechanical stability. 6) A study by Forterre et al. (2011) on the use of vertebral body plating in cervical fractures, reporting excellent outcomes. These studies support the current recommendation for surgical stabilization in most cases of spinal fractures and luxations.