Figures
Overview
Burst fractures result from axial loading, often combined with flexion. The anterior and middle columns fail, and the posterior wall is retropulsed into the canal. In the AO Spine system they are type A3 (one endplate involved) or A4 (both endplates involved). Most occur at the thoracolumbar junction, with L1 the most frequently affected level. The key determinant of stability is the integrity of the posterior ligamentous complex (PLC): a burst fracture with PLC disruption is a type B injury and behaves very differently.
Clinical Presentation
Patients report severe back pain after a fall or high-energy trauma. Neurological status ranges from intact to complete conus or cauda equina syndromes. Canal compromise on imaging correlates poorly with the presence or severity of the deficit. A palpable interspinous gap suggests PLC injury. Associated calcaneal, tibial plateau and noncontiguous spinal fractures should be sought.
Imaging
CT defines comminution, retropulsion, canal compromise, local kyphosis and loss of vertebral body height (Figure 1). Widening of the interpedicular distance indicates a sagittal split of the body and posterior arch. Combined with a laminar fracture and a neurological deficit, it suggests a dural tear with entrapped nerve roots. MRI is indicated for neurological deficit and for equivocal PLC status (M1 modifier); it shows disruption of the interspinous and supraspinous ligaments, facet capsules and disc.
Canal compromise is measured on axial CT at the level of maximal retropulsion relative to the adjacent normal canal, and local kyphosis with the Cobb method from the superior endplate of the vertebra above to the inferior endplate of the vertebra below. The Load Sharing Classification grades comminution, fragment apposition and kyphosis correction. High scores (≥7) predict failure of short-segment posterior fixation and favor anterior column support or longer constructs [4].
Figure 1. Burst fracture morphology. (A) Sagittal view showing anterior wedging and comminution of the vertebral body, retropulsion of the posterior wall into the canal, local kyphosis and an intact posterior ligamentous complex (PLC). (B) Axial view showing canal compromise, a laminar fracture and widening of the interpedicular distance.
Treatment
Neurologically intact patients with an intact PLC (A3/A4, N0) can be treated nonoperatively. Early mobilization as tolerated is safe, and a randomized trial found no advantage of a thoracolumbosacral orthosis over no brace [5]. Standing radiographs are obtained at first mobilization and repeated during the first 3 months to detect progressive kyphosis.
Randomized trials comparing surgery with nonoperative care in this group are conflicting: one showed similar or better long-term pain and function after nonoperative care [1], whereas another favored short-segment posterior fixation [2]. Meta-analysis has not shown a consistent advantage of surgery [3].
When surgery is required, posterior pedicle screw fixation with indirect reduction (ligamentotaxis) is usually sufficient. Adding screws in the fractured vertebra improves kyphosis correction in short-segment constructs. Ligamentotaxis works best within the first days and requires an intact posterior longitudinal ligament. Direct decompression, posterolateral or anterior, is reserved for persistent compression with a deficit. Severe comminution, poor bone quality and late presentation favor anterior reconstruction or longer posterior fixation.
Anterior corpectomy with cage reconstruction is particularly useful when an incomplete deficit coexists with large anterior canal compromise presenting late, when indirect reduction is unlikely to succeed. Posterior-only approaches with transpedicular decompression and anterior column support are an alternative in experienced hands.