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Acute versus chronic vertebral compression fracture in a patient on long-term steroids

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Acute versus chronic vertebral compression fracture in a patient on long-term steroids

A 74-year-old woman on long-term prednisolone 10 mg daily for polymyalgia rheumatica presents with 10 days of severe mid-thoracic back pain that began when she bent to pick up a bag. There is no history of trauma, fever, weight loss or known malignancy. Examination shows focal tenderness at T8 with no neurological deficit and no sphincter disturbance. Radiographs show a wedge compression fracture of T8 with approximately 40% loss of anterior height, no posterior wall retropulsion, and normal height of the remaining vertebrae. DXA gives a T-score of -3.1 at the lumbar spine. Blood tests show a normal white cell count, normal ESR and CRP, normal calcium and alkaline phosphatase; serum protein electrophoresis is pending. She asks whether 'the cement injection' will fix her pain. The MRI slot is tomorrow morning.

1. What MRI sequences would you request and what are you trying to establish?

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Sequences:

  • Sagittal T1 and T2 of the whole thoracic spine (not just the symptomatic level) - marrow signal, posterior wall, cord.
  • Sagittal and axial STIR or fat-suppressed T2 - oedema, which indicates acuity.
  • Axial T1 and T2 at T8 - posterior element and canal assessment.
  • Post-gadolinium T1 fat-suppressed images if there is any suspicion of infection or tumour.

What I need to establish:

  1. Acuity - high STIR signal and low T1 signal indicate an acute or subacute fracture. A STIR-negative, T1-low vertebra suggests a chronic fracture, and vertebral augmentation is very unlikely to help.
  2. Benign versus malignant - a band-like or linear pattern of oedema confined to the vertebral body, sparing the pedicles and with preserved posterior cortex, favours osteoporotic fracture. Pedicle involvement, a convex posterior border, an epidural or paravertebral soft-tissue mass, or low T1 signal throughout the body including the pedicles all raise concern for metastasis or myeloma.
  3. Mechanical features - posterior wall integrity, retropulsion, canal compromise, and whether there is a fluid sign or intravertebral vacuum cleft.
  4. Other levels - additional occult fractures, which change the rehabilitation plan.

The MRI will therefore determine whether cement augmentation is appropriate at all, and whether a biopsy is needed first.

2. Under what circumstances would you advise against vertebral augmentation?

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Advise against, or defer, when:

  • The fracture is not the pain generator - symptoms longer than about 8–12 weeks, no focal tenderness at the level, or a STIR-negative chronic fracture. Sham-controlled trials (VERTOS II versus later blinded trials and the VAPOUR and INVEST trials) showed limited benefit over sham in many patients, so patient selection is critical.
  • The posterior wall is disrupted with retropulsion or canal compromise, particularly with any neurological deficit - risk of cement leak into the canal.
  • Malignancy or infection is suspected on MRI - cementing a metastasis without tissue diagnosis is poor practice; a burst metastasis with posterior element involvement needs biopsy and oncology input, not cement.
  • Coagulopathy or active infection at the puncture site.
  • Severe cardiopulmonary comorbidity or an inability to lie prone, since the procedure is performed prone and cement can embolise.
  • A stable, minimally painful fracture that is responding to analgesia, bracing and osteoporosis treatment.

Also important: augmentation is an analgesic procedure, not a treatment for osteoporosis. She must be started on bone-protective therapy (bisphosphonate or denosumab), have vitamin D and calcium checked, and be reviewed for reducing her steroid dose - otherwise she will re-fracture.

3. The MRI shows T1 low signal and STIR high signal throughout T8 with involvement of the posterior elements and a paravertebral soft-tissue component. What is your interpretation and next step?

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This is not a simple osteoporotic fracture. The combination of a low T1 signal extending into the pedicles, STIR hyperintensity throughout the vertebra, and a paravertebral soft-tissue mass is highly suspicious for a pathological fracture - metastasis, myeloma, or, less likely in this context, infection.

Next steps:

  1. Do not perform vertebral augmentation at this stage. Cementing an undiagnosed malignancy can compromise later surgery and radiotherapy planning, and cementing infection can disseminate it.
  2. Obtain tissue: a CT-guided core biopsy of the vertebral body or the paravertebral component, with a sample sent for histology and microbiology (including mycobacterial and fungal culture). Check coagulation first.
  3. Staging and laboratory workup: whole-body imaging - FDG PET/CT or a myeloma screen (serum and urine electrophoresis, free light chains, skeletal survey or low-dose whole-body CT). Review the pending serum electrophoresis now.
  4. Urgent MRI of the whole spine with contrast to look for other levels and for epidural disease, and assess the cord.
  5. Refer to oncology/haematology and, if there is cord compression or instability, to the spinal surgical team. Start analgesia and consider dexamethasone only if there is epidural cord compromise.

This is the key teaching point: a compression fracture in a patient with a known malignancy history or atypical features is a tumour until proven otherwise, and MRI is what separates the two.