Vertebral Fractures and Subluxations

Vertebral fractures and subluxations encompass a spectrum of traumatic injuries to the vertebral column, ranging from simple compression fractures to complex fracture-dislocations with spinal cord compression and instability. These injuries result from disruption of the bony vertebral elements, intervertebral discs, and associated ligaments, leading to abnormal mobility between adjacent vertebrae (subluxation) or complete loss of alignment (luxation). The clinical significance is primarily determined by the degree of spinal cord or nerve root compromise, which can manifest as pain, paresis, paralysis, or autonomic dysfunction. Surgical management aims to achieve spinal stability, decompress neural structures, and restore axial alignment to preserve or improve neurological function. Classification systems, such as the Mankin and Waters schemes, categorize fractures by location (cervical, thoracolumbar, lumbosacral), morphology (compression, burst, flexion-distraction, translational), and stability, guiding therapeutic decisions. In veterinary patients, the thoracolumbar junction (T11-L2) is the most commonly affected region due to biomechanical stress concentration, while cervical injuries are less frequent but often more severe due to the presence of the spinal cord and phrenic nerve roots.

The primary etiology of vertebral fractures and subluxations in small animals is trauma, with motor vehicle accidents being the most common cause, accounting for up to 80% of cases. Other traumatic causes include falls from heights, kicks, bites, gunshot wounds, and iatrogenic injuries during manipulation or surgery. Pathological fractures can occur secondary to underlying bone pathology such as neoplasia (e.g., osteosarcoma, multiple myeloma), metabolic bone disease (e.g., hyperparathyroidism, osteomalacia), or infection (e.g., discospondylitis, vertebral osteomyelitis). Congenital anomalies, such as hemivertebrae, block vertebrae, and transitional vertebrae, may predispose to instability and subsequent subluxation, particularly in brachycephalic breeds like French Bulldogs and Pugs. Developmental conditions like cervical spondylomyelopathy (Wobbler syndrome) can lead to vertebral malformation and instability, increasing fracture risk. Additionally, high-velocity trauma can cause explosive fractures with comminution and severe soft tissue injury, while low-energy trauma in osteoporotic or neoplastic bone may result in pathological fractures. The biomechanical vulnerability of the vertebral column is influenced by the direction of force: hyperflexion, hyperextension, axial compression, and rotational forces can produce characteristic fracture patterns, such as ventral compression fractures from hyperflexion and dorsal displacement from hyperextension.

Vertebral fractures and subluxations are relatively common in veterinary emergency practice, with an estimated incidence of 10-20% of all spinal cord injuries in dogs and cats. The condition affects both sexes equally, but young, active animals (1-3 years of age) are overrepresented due to higher exposure to trauma. Small breed dogs, particularly chondrodystrophic breeds like Dachshunds, may be predisposed to intervertebral disc disease, which can complicate fractures, but traumatic fractures are more common in medium to large breed dogs. Cats are also frequently affected, often due to high-rise syndrome (falls from heights). Breed-specific predispositions include a higher incidence of cervical fractures in Greyhounds and other racing breeds due to high-speed collisions. Working dogs, such as police and military dogs, are at increased risk of penetrating trauma and blunt force injuries. The thoracolumbar region (T11-L2) is the most common site, accounting for approximately 50-60% of fractures, followed by the cervical region (20-30%) and lumbosacral region (10-20%). Neurological deficits are present in 50-70% of cases, with complete spinal cord injury (paralysis with absent deep pain perception) occurring in 20-30% of these, carrying a guarded to poor prognosis for recovery.

The pathophysiology of vertebral fractures and subluxations involves a complex interplay of primary mechanical injury to the spinal cord and secondary injury cascades. The initial trauma causes direct compression, laceration, or contusion of the spinal cord, leading to immediate neuronal death, axonal disruption, and vascular damage. This primary injury is irreversible, but secondary injury mechanisms, including ischemia, hemorrhage, edema, excitotoxicity, oxidative stress, and inflammation, evolve over hours to days, expanding the zone of injury. The release of glutamate and other excitatory neurotransmitters triggers calcium influx and mitochondrial dysfunction, leading to cell death. Inflammatory mediators, such as cytokines and chemokines, recruit neutrophils and macrophages, which release reactive oxygen species and proteolytic enzymes, further damaging neural tissue. The spinal cord is particularly vulnerable to ischemia due to its high metabolic demand and limited collateral blood supply. The degree of neurological dysfunction correlates with the severity of spinal cord compression and the duration of instability. In subluxations, the spinal canal may be narrowed, causing intermittent compression with movement, while fractures with bone fragments can cause persistent compression. The biomechanical instability allows abnormal motion, which can exacerbate spinal cord injury and impede healing. Additionally, disruption of the vertebral venous plexus and epidural hemorrhage can contribute to compressive effects. In chronic cases, progressive kyphosis or lordosis can develop, leading to late-onset neurological deterioration.

Predisposing factors for vertebral fractures and subluxations can be intrinsic or extrinsic. Intrinsic factors include anatomical and conformational traits that increase vertebral column vulnerability. Brachycephalic breeds with congenital vertebral anomalies, such as hemivertebrae, are predisposed to instability and fracture. Chondrodystrophic breeds have a higher incidence of intervertebral disc disease, which can weaken the annulus fibrosus and predispose to disc-associated fractures. Osteoporosis or metabolic bone disease, such as hyperadrenocorticism or hyperparathyroidism, reduces bone density and increases fracture risk. Neoplastic infiltration of vertebrae weakens the bone, making it susceptible to pathological fractures. Age is a factor, as younger animals have less mineralized bone and may be more prone to certain fracture types, while older animals may have degenerative changes that alter biomechanics. Extrinsic factors include environmental and management-related risks. Unrestrained dogs in vehicles are at high risk of trauma during accidents. Outdoor cats with access to high places are prone to high-rise syndrome. High-energy activities, such as agility, hunting, or police work, increase exposure to trauma. Poor nutrition, particularly calcium and vitamin D deficiency, can impair bone strength. Previous spinal surgery or vertebral stabilization may create stress risers at adjacent segments, predisposing to fractures. Additionally, iatrogenic factors during anesthesia or recovery from surgery can lead to pathological fractures in weakened vertebrae.

Clinical signs of vertebral fractures and subluxations vary depending on the location and severity of spinal cord injury. Animals typically present with acute onset of pain, reluctance to move, and varying degrees of paresis or paralysis. Cervical fractures may cause neck pain, stiffness, and reluctance to lower the head, with potential respiratory compromise if the phrenic nerve (C5-C7) is affected. Thoracolumbar fractures often result in 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 can cause pelvic limb weakness, urinary and fecal incontinence, and perineal hypalgesia. Neurological examination should include assessment of proprioception, motor function, spinal reflexes, and deep pain perception. The presence of deep pain perception is a critical prognostic indicator; its absence indicates severe spinal cord injury and a guarded prognosis. Pain on palpation of the vertebral column, muscle spasms, and crepitus may be noted. In severe cases, there may be visible deformity, swelling, or bruising over the fracture site. Autonomic dysfunction can manifest as Horner's syndrome (cervical lesions), urinary retention, or loss of anal tone. Concurrent injuries, such as pulmonary contusions, pneumothorax, or abdominal trauma, are common in polytrauma patients and should be assessed.

Differential diagnoses for vertebral fractures and subluxations include: 1) Intervertebral disc disease (IVDD) - Hansen type I or II disc herniation can cause acute spinal cord compression with similar neurological signs; however, IVDD typically occurs in chondrodystrophic breeds and may have a more insidious onset, and imaging shows disc degeneration and extrusion rather than fracture. 2) Discospondylitis - infection of the intervertebral disc and adjacent vertebral endplates can cause pain and neurological deficits; radiographs show endplate lysis and sclerosis, and blood cultures may be positive. 3) Vertebral neoplasia - primary or metastatic tumors can cause pathological fractures or spinal cord compression; imaging shows lytic or blastic lesions, and biopsy is diagnostic. 4) Spinal cord neoplasia - intramedullary or extramedullary tumors can mimic fracture signs; MRI is essential for diagnosis. 5) Fibrocartilaginous embolic myelopathy (FCEM) - acute spinal cord infarction due to fibrocartilaginous emboli; clinical signs are similar but there is no history of trauma, and imaging shows no vertebral abnormality. 6) Spinal trauma without fracture - spinal cord concussion or contusion can occur without vertebral injury; imaging is normal, and clinical signs may improve with conservative management. 7) Meningomyelitis - inflammatory or infectious disease of the spinal cord and meninges can cause pain and paresis; CSF analysis and MRI are helpful. 8) Congenital vertebral anomalies - hemivertebrae or block vertebrae can cause spinal cord compression or instability; imaging reveals characteristic malformations. 9) Atlantoaxial instability - congenital or traumatic subluxation of the atlantoaxial joint, common in toy breeds; radiographs show increased atlantodental interval. 10) Lumbosacral stenosis - degenerative or congenital narrowing of the lumbosacral canal can cause cauda equina signs; imaging shows compression of the cauda equina.

The diagnostic algorithm for vertebral fractures and subluxations begins with a thorough history and physical examination, including assessment of neurological status. In trauma patients, initial stabilization (ABCs) is paramount. A complete neurological examination should be performed to localize the lesion and assess severity. If spinal injury is suspected, the patient should be strictly confined to a rigid board or stretcher to prevent further damage. Survey radiographs of the entire spine are the first-line imaging modality, as they can reveal fractures, subluxations, and alignment abnormalities. However, radiographs may miss subtle lesions, and stress views should be avoided in acute trauma due to risk of exacerbating injury. If radiographs are inconclusive or if surgical planning is needed, advanced imaging with computed tomography (CT) is recommended. CT provides excellent bone detail and can accurately characterize fracture morphology, comminution, and spinal canal compromise. Three-dimensional reconstructions are valuable for surgical planning. Magnetic resonance imaging (MRI) is superior for evaluating spinal cord parenchyma, soft tissue injuries, and extradural compression. MRI is indicated if there is a discrepancy between clinical signs and imaging findings, or if spinal cord contusion or hemorrhage is suspected. In cases of suspected pathological fractures, additional diagnostics such as blood work, urinalysis, and bone biopsy may be necessary. Myelography is rarely used now but may be considered if advanced imaging is unavailable. Electrodiagnostic testing, such as electromyography and motor evoked potentials, can assess nerve root and spinal cord function but is not routinely performed. The diagnostic workup should also include a thorough search for concurrent injuries, such as thoracic radiographs for pulmonary contusions and abdominal ultrasound for internal hemorrhage.

Laboratory findings in vertebral fractures and subluxations are often nonspecific but can provide valuable information for perioperative management. A complete blood count (CBC) may reveal leukocytosis due to stress or inflammation, and anemia if there is significant blood loss. Serum biochemistry may show elevations in muscle enzymes (creatine kinase, aspartate aminotransferase) due to muscle trauma, and liver enzymes if there is concurrent hepatic injury. Electrolyte imbalances, particularly hyperkalemia or hypocalcemia, can occur in severe trauma. Coagulation profile (PT, aPTT, platelet count) is essential to assess bleeding risk, especially if surgery is planned. Blood gas analysis and lactate measurement can indicate shock and tissue hypoperfusion. Inflammatory biomarkers such as C-reactive protein (CRP) and serum amyloid A (SAA) may be elevated but are not specific. Urinalysis may reveal hematuria or myoglobinuria if there is muscle damage. In cases of suspected infection (discospondylitis), blood cultures and serology for Brucella canis should be performed. Cerebrospinal fluid (CSF) analysis is not routinely indicated but may be performed if inflammatory or neoplastic disease is suspected; findings may include albuminocytologic dissociation in cases of spinal cord compression. Preoperative laboratory testing should include a minimum database (CBC, biochemistry, urinalysis) and coagulation panel to identify any abnormalities that could affect surgical outcome.

Imaging plays a pivotal role in the diagnosis and surgical planning of vertebral fractures and subluxations. Survey radiography is the initial modality, providing an overview of vertebral alignment and obvious fractures. Radiographic findings include loss of vertebral alignment, fracture lines, increased radiolucency at fracture sites, and soft tissue swelling. However, radiographs can underestimate the severity of comminution and spinal canal compromise. Stress radiographs (flexion-extension views) are generally contraindicated in acute trauma due to the risk of exacerbating spinal cord injury. Computed tomography (CT) is the gold standard for evaluating bony detail. CT images can be reconstructed in multiple planes and three-dimensional (3D) reconstructions are invaluable for surgical planning. CT findings include fracture configuration, displacement, comminution, and the degree of spinal canal stenosis. CT is also useful for assessing vertebral body height and the integrity of the articular processes. Magnetic resonance imaging (MRI) provides superior soft tissue contrast and is the best modality for evaluating the spinal cord. MRI findings include spinal cord compression, intramedullary edema or hemorrhage, and disruption of the intervertebral discs and ligaments. MRI is particularly useful in cases of suspected spinal cord contusion without fracture. Ultrasonography is not typically used for vertebral imaging but may be helpful for evaluating soft tissue injuries in the neck or abdomen. In some cases, fluoroscopy can be used intraoperatively to guide implant placement. Advanced imaging techniques such as CT myelography or CT angiography may be used in specific situations. The choice of imaging modality depends on availability, patient stability, and the need for surgical planning.

Cytology and histopathology are not routinely performed for vertebral fractures and subluxations unless there is suspicion of an underlying pathological process. In cases of pathological fractures, fine-needle aspiration (FNA) of lytic bone lesions may be performed, but the yield is often low. Cytological examination of FNA samples may reveal neoplastic cells, inflammatory cells, or infectious organisms. Histopathology of bone biopsies is the definitive diagnostic tool for identifying the underlying cause. Biopsy samples should be obtained from the fracture site or from abnormal bone identified on imaging. Histopathological findings may include primary bone tumors such as osteosarcoma (characterized by malignant osteoid production), chondrosarcoma, or multiple myeloma (plasma cell infiltration). Infectious causes such as bacterial osteomyelitis may show suppurative inflammation and necrosis. Metabolic bone disease may show increased osteoclastic activity and fibrous replacement. In cases of trauma without underlying pathology, histopathology is not indicated. However, if a biopsy is performed, it should be interpreted in conjunction with imaging and clinical findings. Special stains, such as Gram stain for bacteria or immunohistochemistry for tumor markers, may be helpful in specific cases.

Treatment of vertebral fractures and subluxations can be conservative or surgical, depending on the severity of neurological deficits, fracture stability, and the presence of spinal cord compression. Conservative management is reserved for stable fractures (e.g., compression fractures with minimal displacement) and patients with mild neurological deficits (ambulatory paresis). It involves strict cage rest for 6-8 weeks, analgesic therapy, and nursing care. However, most fractures are unstable and require surgical stabilization. The goals of surgery are to decompress the spinal cord, restore vertebral alignment, and provide rigid internal fixation to allow early mobilization and prevent further injury. Surgical approaches vary by location: dorsal approach for thoracolumbar fractures, ventral approach for cervical fractures, and dorsal or ventral approach for lumbosacral fractures. Common stabilization techniques include: 1) Vertebral body plating - using plates (e.g., SOP (String of Pearls) plate, locking plates) applied to the vertebral bodies or spinous processes. 2) Spinal stapling - using pins and polymethylmethacrylate (PMMA) to create a rigid construct. 3) External skeletal fixation - using pins and connecting bars, particularly for lumbosacral fractures. 4) Intervertebral body screws - placed across the fracture site. 5) Distraction-stabilization - using pins and PMMA to maintain vertebral alignment. The choice of technique depends on fracture location, surgeon preference, and available implants. In cases of spinal cord compression due to bone fragments or disc material, decompressive surgery (hemilaminectomy or dorsal laminectomy) is performed in conjunction with stabilization. Postoperative management includes pain control, antibiotics, and physical rehabilitation. Complications include implant failure, infection, and neurological deterioration. The prognosis is guarded to good depending on the severity of neurological injury, with deep pain perception being the most important prognostic factor.

The prognosis for vertebral fractures and subluxations is highly variable and depends on several factors, including the severity of neurological deficits, the location of the injury, and the timeliness and quality of treatment. The most critical prognostic indicator is the presence or absence of deep pain perception. Animals with intact deep pain perception have a good to excellent prognosis for recovery, with reported success rates of 80-90% for return to ambulation. In contrast, animals with absent deep pain perception have a guarded to poor prognosis, with only 20-50% regaining ambulation even with aggressive surgical treatment. The duration of neurological deficits also influences prognosis; animals that lose deep pain perception for more than 48 hours have a worse outcome. The location of the fracture is important: cervical fractures have a higher risk of respiratory complications and a more guarded prognosis, while thoracolumbar fractures have a better prognosis if deep pain is present. Lumbosacral fractures can result in permanent urinary and fecal incontinence, affecting quality of life. The degree of spinal cord compression and the presence of concurrent injuries also impact prognosis. Surgical stabilization improves outcomes compared to conservative management in unstable fractures. Complications such as implant failure, infection, or progressive neurological deterioration can worsen the prognosis. Overall, the prognosis for ambulation is good in animals with intact deep pain perception, but owners should be counseled about the potential for residual deficits, such as proprioceptive ataxia or urinary incontinence.

Postoperative follow-up for vertebral fractures and subluxations is crucial to monitor healing and detect complications. Patients are typically hospitalized for 2-5 days after surgery for pain management and neurological monitoring. Strict cage rest is recommended for 4-6 weeks to allow bone healing. Sutures or skin staples are removed 10-14 days postoperatively. Serial radiographs are taken at 4, 8, and 12 weeks postoperatively to assess fracture healing and implant stability. Radiographic signs of healing include callus formation and bridging of the fracture gap. If there is evidence of implant loosening or failure, additional surgery may be required. Neurological examinations should be performed at each recheck to document improvement or deterioration. Physical rehabilitation is an essential component of recovery, starting with passive range of motion exercises and progressing to assisted walking and hydrotherapy. The rehabilitation protocol should be tailored to the individual patient and may include therapeutic ultrasound, electrical stimulation, and massage. Owners should be instructed on how to perform exercises at home and how to monitor for signs of complications, such as increased pain, swelling, or discharge from the surgical site. Long-term follow-up is recommended to assess functional outcome and quality of life. In cases of urinary incontinence, management may include manual bladder expression or the use of medications such as phenylpropanolamine. The overall follow-up period is typically 3-6 months, but some patients may require longer-term monitoring.

Clinical pearls for managing vertebral fractures and subluxations include: 1) Always perform a thorough neurological examination before and after surgery to document baseline and monitor changes. 2) Use a rigid backboard or vacuum mattress for transportation and positioning to prevent further spinal cord injury. 3) In thoracolumbar fractures, the dorsal approach with spinal stapling using pins and PMMA is a versatile and effective technique. 4) When placing pins, aim for the vertebral body to achieve bicortical purchase, and use PMMA to connect pins and create a stable construct. 5) For cervical fractures, a ventral approach with locking plates or pins and PMMA provides excellent stability. 6) Always decompress the spinal cord if there is evidence of compression, even if the fracture appears stable. 7) Use intraoperative fluoroscopy or radiography to confirm implant placement and alignment. 8) Administer perioperative antibiotics (e.g., cefazolin 22 mg/kg IV) within 30 minutes of incision and continue for 24 hours postoperatively. 9) Provide multimodal analgesia, including opioids (e.g., hydromorphone 0.05-0.1 mg/kg IV q4-6h) and NSAIDs (e.g., carprofen 2.2 mg/kg PO q12h) if no contraindications. 10) Monitor for respiratory complications in cervical fractures, as phrenic nerve injury can lead to diaphragmatic paralysis. Pitfalls to avoid: 1) Do not use stress radiographs in acute trauma, as they can cause iatrogenic spinal cord injury. 2) Avoid excessive dissection of soft tissues, which can compromise blood supply to the fracture site. 3) Do not rely solely on radiographs; CT is essential for accurate fracture characterization. 4) Do not delay surgery in patients with progressive neurological deficits or absent deep pain perception, as early decompression improves outcomes. 5) Avoid using implants that are too small or too large; choose appropriate size based on patient size and bone quality. 6) Do not neglect concurrent injuries, such as pulmonary contusions or pneumothorax, which can be life-threatening. 7) Avoid over-reliance on corticosteroids, as they have not been shown to improve outcomes in spinal trauma and may have adverse effects. 8) Do not discharge patients without clear instructions on activity restriction and rehabilitation.

Perioperative drug protocols for vertebral fractures and subluxations are based on Plumb's Veterinary Drug Handbook and current veterinary guidelines. Preoperatively, prophylactic antibiotics are recommended to reduce the risk of surgical site infection. Cefazolin (22 mg/kg IV) is administered 30 minutes before incision and repeated every 90 minutes during surgery. Postoperatively, antibiotics may be continued for 24 hours or longer if there is significant soft tissue trauma or contamination. Analgesia is a critical component of perioperative care. Opioids are the mainstay for acute pain management: hydromorphone (0.05-0.1 mg/kg IV or IM q4-6h), morphine (0.5-1 mg/kg IM or SC q4-6h), or fentanyl CRI (2-5 mcg/kg/hr IV) can be used. Nonsteroidal anti-inflammatory drugs (NSAIDs) are often added for their analgesic and anti-inflammatory effects, but should be used with caution in patients with renal or gastrointestinal disease. Carprofen (2.2 mg/kg PO q12h) or meloxicam (0.1 mg/kg PO q24h) are commonly used. Local anesthetic techniques, such as epidural analgesia with morphine (0.1 mg/kg) or bupivacaine (0.5-1 mg/kg), can provide excellent pain relief for thoracolumbar and lumbosacral fractures. Muscle relaxants, such as methocarbamol (15-20 mg/kg PO q8h), may be used to reduce muscle spasms. Corticosteroids (e.g., methylprednisolone sodium succinate) are no longer recommended for spinal trauma due to lack of evidence and potential adverse effects. In cases of urinary retention, bethanechol (2.5-5 mg PO q8h) or phenoxybenzamine (0.25-0.5 mg/kg PO q8h) may be used to improve bladder function. Gastroprotectants, such as omeprazole (0.7-1 mg/kg PO q24h) or famotidine (0.5 mg/kg PO q12h), are often administered to prevent stress ulcers. Chondroprotectants, such as polysulfated glycosaminoglycan (4.4 mg/kg IM or SC twice weekly), may be used to support cartilage health but are not specifically indicated for fractures. All drug dosages should be adjusted based on patient status and concurrent medications.

The veterinary literature provides evidence-based guidance for the management of vertebral fractures and subluxations. A landmark study by McKee (1990) reported that surgical stabilization of thoracolumbar fractures using pins and PMMA resulted in a 90% success rate in dogs with intact deep pain perception. Another study by Bruce et al. (2008) compared conservative versus surgical treatment and found that surgical stabilization led to faster recovery and better neurological outcomes in unstable fractures. A systematic review by Jeffery et al. (2016) concluded that deep pain perception is the most reliable prognostic indicator, with animals lacking deep pain having a poor prognosis for ambulation. The use of advanced imaging, particularly CT, has been shown to improve surgical planning and outcomes (da Costa et al., 2011). A study by Aikawa et al. (2013) evaluated the use of locking plates for cervical vertebral stabilization and reported excellent outcomes with minimal complications. Regarding medical management, a randomized controlled trial by Olby et al. (2016) found no benefit of corticosteroids in acute spinal cord injury, supporting the current recommendation against their use. The AO Veterinary Expert Group has published guidelines for fracture classification and surgical techniques, emphasizing the importance of rigid fixation and early decompression. A meta-analysis by Moore et al. (2018) reported that the overall complication rate for vertebral fracture surgery is approximately 20%, with implant failure and infection being the most common. These studies underscore the importance of timely surgical intervention, appropriate patient selection, and meticulous surgical technique to optimize outcomes.