Burst Fracture Explained: Treatments and Recovery

A burst fracture is a serious spinal injury that occurs when a vertebra breaks apart due to high-energy trauma. Unlike other fractures, this type of break can send bone fragments into the spinal canal, potentially leading to nerve damage or paralysis. These injuries often result from car accidents, falls from height, or sports-related impacts and require careful medical evaluation to determine the best course of treatment.

Prompt diagnosis and appropriate intervention are crucial for minimizing complications and optimizing recovery. Treatment options vary depending on severity and neurological involvement, ranging from conservative management to surgical stabilization.

Vertebral Column Structure

The vertebral column serves as the central support structure of the human body, providing stability and flexibility while protecting the spinal cord. Composed of 33 vertebrae, it is divided into five regions: cervical, thoracic, lumbar, sacral, and coccygeal. Each section has unique biomechanical properties that influence how forces are distributed along the spine, which is particularly relevant in high-energy trauma leading to burst fractures.

The cervical spine allows for extensive range of motion but is more vulnerable to hyperflexion injuries. The thoracic and lumbar regions bear greater axial loads, making them more prone to compression fractures. Structurally, each vertebra consists of a vertebral body, pedicles, laminae, and various processes. The vertebral body, the largest and most load-bearing component, absorbs compressive forces and is the primary site affected in burst fractures. The posterior elements—including the spinous and transverse processes—provide attachment points for muscles and ligaments that help maintain spinal alignment.

Intervertebral discs, composed of a tough outer annulus fibrosus and a gel-like nucleus pulposus, sit between adjacent vertebral bodies to cushion impact and facilitate movement. Their ability to absorb shock diminishes with age-related degeneration, which can worsen spinal fractures. Ligaments such as the anterior and posterior longitudinal ligaments further reinforce spinal stability, limiting excessive motion that could contribute to vertebral collapse.

How Burst Fractures Occur

A burst fracture develops when an extreme compressive force is applied to a vertebra, causing it to shatter into multiple fragments. This typically results from high-energy trauma, such as a motor vehicle collision or a fall from height, where the spine is subjected to sudden axial loading. Unlike wedge fractures, which involve a partial collapse of the vertebral body, a burst fracture disperses bone fragments more uniformly, often encroaching upon the spinal canal.

The thoracolumbar junction (T10–L2) is particularly vulnerable because it serves as a transition zone between the rigid thoracic spine and the more flexible lumbar spine. In falls, landing on the feet or buttocks transmits force upward through the spine, while car accidents generate immense compression forces, especially when the upper body is thrust forward while restrained by a seatbelt.

The severity of a burst fracture depends on the extent of bony displacement and involvement of adjacent structures. Stable fractures maintain some load-bearing capacity if the posterior ligamentous complex remains intact. However, when fragments displace into the spinal canal, they can compromise the neural elements, increasing the risk of spinal cord injury. Fractures with more than 50% canal compromise are significantly associated with neurological impairment, highlighting the importance of assessing fragment displacement.

Diagnostic Methods

Accurately diagnosing a burst fracture requires clinical evaluation and imaging to assess vertebral damage and potential spinal canal involvement. Patients typically present with acute back pain following trauma, often with restricted mobility or neurological symptoms such as numbness or weakness. A physical examination helps identify localized tenderness, muscle spasms, and signs of spinal instability. Given the high-energy mechanisms involved, clinicians must also evaluate for concurrent injuries, particularly in polytrauma cases.

Radiographic imaging is the first step in assessing vertebral integrity. Standard X-rays provide an overview of spinal alignment, vertebral height loss, and potential retropulsion of bone fragments. However, plain radiographs may not fully capture the complexity of a burst fracture. Computed tomography (CT) scans offer high-resolution images that delineate fracture patterns, fragment displacement, and spinal canal compromise. CT reconstructions in sagittal and coronal planes aid in surgical planning.

Magnetic resonance imaging (MRI) is critical for evaluating soft tissue involvement, including spinal cord compression, ligamentous injuries, and epidural hematomas. Unlike CT, which focuses on bony structures, MRI provides insights into neural integrity and spinal cord edema, which can influence treatment decisions. Increased signal intensity in the spinal cord on T2-weighted sequences correlates with a higher likelihood of neurological deficits, making MRI essential when neurological impairment is suspected.

Neurological Involvement

Neurological impairment in a burst fracture depends on the degree of spinal canal encroachment and spinal cord or nerve root compression. Bone fragments displacing into the canal can exert pressure on the spinal cord, leading to anything from mild paresthesia and localized weakness to complete paralysis. The thoracolumbar junction, often affected in burst fractures, is particularly unpredictable in its neurological outcomes due to the transition from the spinal cord to the conus medullaris.

Spinal cord involvement is classified using the American Spinal Injury Association (ASIA) Impairment Scale, which grades deficits from complete (Grade A) to incomplete (Grades B through E). A complete injury results in total loss of movement and sensation below the fracture, while an incomplete injury may preserve some function. Early neurological assessment is predictive of long-term recovery, with incomplete injuries carrying a better prognosis. Secondary damage from post-traumatic inflammation and vascular compromise can worsen neurological deficits, emphasizing the need for timely intervention.

Conservative Approaches

For stable burst fractures without significant neurological deficits, non-surgical management can be effective. Stability is determined by the integrity of the posterior ligamentous complex, which, if intact, allows the vertebra to maintain structural support. Immobilization with a rigid brace, such as a thoracolumbosacral orthosis (TLSO) or a Jewett brace, limits spinal motion and promotes healing. These devices are typically worn for 8 to 12 weeks, with follow-up imaging to monitor progress. Patients must avoid activities that place excessive strain on the spine, such as heavy lifting or prolonged sitting.

Pain management includes nonsteroidal anti-inflammatory drugs (NSAIDs) and muscle relaxants to reduce discomfort and inflammation. Physical therapy is introduced gradually, beginning with isometric core exercises to maintain spinal support. As healing progresses, supervised weight-bearing activities restore mobility and prevent deconditioning. Long-term outcomes for stable burst fractures treated conservatively are generally favorable, but close monitoring is necessary to detect delayed instability or progressive kyphotic deformity, which may require surgery.

Surgical Pathways

Surgical intervention is necessary for burst fractures with significant instability, neurological impairment, or severe vertebral collapse. The choice of procedure depends on factors such as canal compromise, ligamentous injury, and overall patient health. Advances in spinal surgery have led to various stabilization techniques that optimize recovery while minimizing complications.

Decompression and fusion procedures are common when bone fragments encroach upon the spinal canal. Laminectomy, which removes the posterior vertebral arch, relieves spinal cord pressure but is often combined with spinal fusion to maintain stability. Fusion involves bone grafts and instrumentation, such as pedicle screws and rods, to immobilize the affected segment. Minimally invasive techniques, including percutaneous screw fixation, have shown promising outcomes in reducing blood loss and recovery time. Early surgical intervention in patients with incomplete neurological deficits can improve functional outcomes by preventing secondary spinal cord injury from ongoing compression.

Recovery Highlights

Rehabilitation after a burst fracture is individualized based on injury severity and treatment approach. Patients treated conservatively transition from bracing to structured physical therapy, focusing on core strengthening and postural training. Those undergoing surgery often require a longer period of restricted activity, with movement reintroduced gradually under medical supervision.

Recovery timelines vary, but most individuals regain functional independence within three to six months. Full bone healing can take up to a year.