The Elderly Patient With a Thoracolumbar Fracture and Osteoporosis
A 72-year-old woman on long-term prednisolone for polymyalgia rheumatica presents with 6 weeks of worsening mid-back pain after a minor fall. Radiographs show a T12 compression fracture with 40% height loss and no neurological deficit. MRI shows bone marrow oedema at T12 without retropulsion. DEXA T-score is −3.2 at the lumbar spine. She is on calcium and vitamin D but no specific osteoporosis treatment. She asks whether she needs surgery or 'just a brace.'
1. How do you decide between non-operative management and vertebral augmentation, and what are the evidence-based indications?
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Non-operative management is first-line for a stable osteoporotic compression fracture without neurological deficit:
- Analgesia, early mobilization, physiotherapy, and a custom moulded thoracolumbar orthosis for comfort (not proven to change union).
- Most patients improve over 6–12 weeks.
Vertebral augmentation (vertebroplasty/kyphoplasty) is considered when:
- Severe, disabling pain persists despite conservative therapy (usually >4–6 weeks), with MRI-confirmed oedema at the fractured level (as here).
- The fracture is acute/subacute (oedema on MRI is the key predictor of response).
- There is progressive collapse or a vertebral body cleft (Kümmell disease).
- Contraindications: burst fracture with retropulsion, cord compression, active infection, coagulopathy, severe cardiopulmonary disease.
Evidence caveat: sham-controlled trials show modest benefit; patient selection by MRI oedema is critical. Do not offer augmentation for chronic fractures without oedema.
Exam point: the decision is driven by pain duration, MRI oedema, and absence of neurological compromise, not by the degree of height loss alone.
2. What is the underlying metabolic diagnosis and how do you treat it? Address the glucocorticoid contribution.
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Diagnosis: glucocorticoid-induced osteoporosis (GIOP) with a fragility fracture.
- T-score −3.2 plus a low-energy fracture = severe osteoporosis.
- Glucocorticoids cause rapid bone loss (especially trabecular bone) in the first 3–6 months, increase fracture risk at any T-score, and impair bone quality.
Treatment:
- Review glucocorticoid dose with rheumatology - use the lowest effective dose; consider steroid-sparing agents.
- Calcium and vitamin D (ensure adequate intake; check 25-OH vitamin D and PTH).
- Bone-forming agent preferred in severe GIOP: teriparatide (or abaloparatide) is favoured for severe osteoporosis/glucocorticoid-induced disease with fractures, followed by an antiresorptive to maintain gains. Romosozumab is an alternative but has cardiovascular contraindications.
- Antiresorptives (bisphosphonates, denosumab) are used if bone-forming agents are not available; denosumab requires careful renal monitoring and cannot be stopped abruptly (rebound fractures).
- Fracture liaison service referral, falls assessment, and home safety review.
Exam point: in GIOP with a fragility fracture, do not just give calcium and vitamin D - anabolic therapy is often indicated, and the glucocorticoid dose must be addressed.
3. She returns 3 months later with new leg weakness and urinary hesitancy. What is your immediate management?
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Red flag: possible cord/cauda equina compression or progressive collapse.
- Urgent MRI of the whole spine (within hours) to assess for retropulsion, epidural haematoma, cord compression, or a new fracture level. Do not wait for outpatient imaging.
- Examine: full neurological assessment including perianal sensation, anal tone, and lower limb power. Document.
- If cord compression or cauda equina syndrome is confirmed: emergency surgical decompression (within 24 hours, ideally sooner for CES). In an osteoporotic spine, this may require posterior decompression and stabilization with cement-augmented pedicle screws or vertebroplasty-augmented fixation.
- If no compression but progressive collapse: consider vertebral augmentation or bracing, and optimize medical therapy.
- Catheterize for urinary retention and involve urology if needed.
Exam point: new neurological symptoms in a patient with a known vertebral fracture mandate emergency MRI and surgical review - do not attribute weakness to 'deconditioning' or the steroid myopathy.