Vertebral Compression Fractures

Genant's semiquantitative grading is the standard classification for osteoporotic VCFs. It records two things from the lateral radiograph: the morphology (wedge, biconcave or crush) and the grade, judged by the reduction in anterior, middle or posterior height. It is how an osteoporotic fracture is recorded and its progression tracked.

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Grade is not acuity. Compare with prior imaging and date the fracture on MRI: a chronic fracture may be stable and asymptomatic despite severe height loss.

AO Spine Type A - compression injuries. Five subtypes:

Pure compression fractures are A1 or A2, with the middle column intact. Once the posterior vertebral body wall is involved (A3, A4) the injury is a burst fracture and its management is different.

TLICS (Thoracolumbar Injury Classification and Severity Score)

TLICS scores three components and the total guides operative versus non-operative management:

A total of 3 or less is managed non-operatively, 4 is surgeon's discretion and 5 or more is operative. A simple compression fracture (morphology 1, intact neurology 0, intact PLC 0) scores 1.

Assessing the PLC is the pivotal variable. On radiograph or CT look for interspinous widening, facet diastasis or perched facets, or a spinous-process avulsion. On MRI the PLC (supraspinous and interspinous ligaments and ligamentum flavum) shows disruption or oedema, high signal on STIR or fat-saturated sequences, with loss of the normal low-signal "black stripe". A disrupted PLC converts an apparent compression fracture into an unstable flexion-distraction injury.

Wedge. Anterior height loss greater than posterior, from axial load with flexion. The most common pattern, about 60%, and the one that creates focal kyphosis.

Biconcave. Central height loss at both endplates, the fish vertebra. Common in osteoporosis, where the endplates are weak, and it produces less kyphosis than a wedge.

Crush. Uniform loss of anterior, middle and posterior height. Less common, and it may be difficult to distinguish from a burst on plain films; CT confirms the posterior wall.

Kummell Disease (Delayed Post-Traumatic Vertebral Collapse)

Kummell disease is a delayed osteonecrotic collapse of a vertebral body presenting weeks to months after an often minor injury, after an initial pain-free or improving interval. It represents a nonunion or avascular necrosis of the fractured body, and its radiographic hallmark is the intravertebral vacuum cleft: a gas-filled cleft on radiograph or CT, or a fluid-filled cleft bright on T2 on MRI, within the collapsed vertebra. Recognising it matters because it is a pseudarthrosis, mobile and often dynamic on flexion-extension views, that is a recognised indication for cement augmentation (the cleft accepts cement well), and it must be distinguished from malignant collapse.

Acute phase (0-2 weeks). Adequate analgesia (paracetamol, NSAIDs, short-term opioids), gentle mobilisation as tolerated and a physiotherapy assessment. Prolonged bed rest is avoided: it accelerates bone loss at 1-2% per week, and the goal of early mobilisation is to maintain bone density and prevent deconditioning.

Subacute phase (2-6 weeks). A TLSO or Jewett brace for comfort if needed, a progressive mobilisation programme, physiotherapy for core strengthening and a falls-prevention assessment. Bracing is for comfort; it is not essential for healing a stable fracture.

Chronic phase (6-12 weeks). Gradual return to normal activities, ongoing physiotherapy and a weight-bearing exercise programme, and initiation of osteoporosis treatment.

Treat the bone. Treating the fracture without treating the osteoporosis is incomplete care. Start a bisphosphonate or denosumab, ensure calcium and vitamin D supplementation, and coordinate with endocrinology or a geriatrician.

Vertebroplasty. Direct injection of PMMA cement into the fractured vertebra with no attempt at height restoration. Technically simpler and less expensive.

Kyphoplasty. A balloon is inflated inside the vertebral body to create a cavity and restore height, and PMMA is injected into the cavity. It theoretically restores sagittal alignment, and it costs more than vertebroplasty.

Indications. Every one of them is contested:

• Refractory pain despite 6 weeks of conservative treatment
• Acute fracture on MRI (marrow oedema present)
• Single or few levels involved
• No neurological deficit
• No infection or coagulopathy

What the trials say. The unblinded trials look convincing and the blinded ones do not. INVEST (2009) found vertebroplasty no better than a sham procedure for pain relief, and Buchbinder's sham-controlled trial, published alongside it, found the same. VERTOS II, open-label, found a benefit at 1 month that attenuated but was still significant at 12 months. VAPOUR, the one positive blinded trial, found an effect only in fractures under 6 weeks old with severe pain and an adequate cement fill. Use is therefore highly selective, not routine.

Why deformity matters. Progressive kyphosis leads to sagittal imbalance, pain and functional decline, and multiple adjacent VCFs create severe deformity. A kyphotic deformity of more than 30 degrees may warrant surgical correction.

Indications. Surgical stabilisation is for:

• Progressive neurological deficit
• Disrupted PLC (no longer a simple compression)
• Progressive kyphosis despite bracing (over 30 degrees)
• Associated burst component with canal compromise
• Failure of conservative treatment with functional limitation

Options. The construct depends on the deformity:

• Posterior instrumented fusion (pedicle screws)
• Anterior corpectomy and reconstruction, if the collapse is severe
• Combined anterior-posterior in severe deformity

Surgery is rare. True compression fractures rarely need it, because the PLC is intact and they are stable. If surgery is being considered, reassess the diagnosis: this may be a burst fracture, a flexion-distraction injury or a pathological fracture, each needing a different approach.

Set-up. Prone on a radiolucent table with bolsters under the chest and pelvis for lordosis, arms forward and the face in a padded rest. Biplanar fluoroscopy is required. Local anaesthesia with sedation, or general anaesthesia.

Approach. Transpedicular or parapedicular, with an 11- or 13-gauge trocar, typically bilateral.

The procedure, in order:

1. AP view: align the pedicle at the lateral edge of the vertebral body
2. Lateral view: confirm the trocar tip in the anterior third of the body
3. Kyphoplasty only: inflate the balloon and restore height
4. Mix the PMMA and allow partial polymerisation to a toothpaste consistency
5. Inject under live fluoroscopy, watching for extravasation; stop at once if cement approaches the posterior wall or enters a vein or the disc
6. Inject 2-4 ml per side

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Positioning. Prone on a Wilson frame or Jackson table, in lordosis to help reduce the kyphosis, with every bony prominence padded.

Approach. A midline incision and subperiosteal dissection out to the transverse processes, then identify the pedicle entry points.

Construct. Pedicle screws one level above and one below at minimum; cement-augmented screws may be needed in osteoporotic bone. Contour the rods to restore sagittal alignment, and consider index-level screws for cantilever correction.

Fusion. Prepare the posterolateral fusion bed and use local autograft from the morselised spinous process. Bone morphogenetic protein (BMP) is worth considering in osteoporotic bone for improved fusion rates.