Mwandishi:
Mhariri:
Imeboreshwa:
ULY CLINIC
ULY CLINIC
28 Julai 2026, 07:50:53
Osteoporotic vertebral compression fractures (VCFs)
28 Julai 2026, 07:50:53
Osteoporotic vertebral compression fractures (VCFs) are among the most common fragility fractures in older adults, particularly postmenopausal women and elderly men with osteoporosis. They occur when weakened vertebral bodies collapse under normal physiological loads or after minimal trauma. Although osteoporosis is the leading cause, vertebral compression fractures may also result from metastatic malignancy, multiple myeloma, infection, or prolonged corticosteroid therapy.
Most fractures involve the thoracolumbar junction (T11–L2). Untreated VCFs may result in chronic pain, progressive kyphosis, reduced pulmonary function, impaired mobility, recurrent falls, and increased mortality.
Epidemiology
Most common osteoporotic fracture after distal radius fractures
Incidence increases significantly after 50 years of age
More common in postmenopausal women
Risk increases with advancing age
Previous vertebral fracture markedly increases the risk of subsequent fractures
Etiology
Primary causes
Osteoporosis (most common)
Osteopenia with low-energy trauma
Secondary causes
Long-term corticosteroid therapy
Primary vertebral tumors
Metastatic spinal tumors
Multiple myeloma
Hyperparathyroidism
Osteomalacia
Severe vitamin D deficiency
Pathophysiology
In osteoporosis, reduced bone mineral density and deterioration of trabecular bone architecture progressively weaken the vertebral bodies. Minor trauma, bending, lifting, coughing, or even normal daily activities may generate sufficient compressive force to cause vertebral collapse. Most fractures involve the anterior vertebral body, producing wedge deformities and progressive thoracic kyphosis.
Multiple compression fractures shift the body's centre of gravity anteriorly, increasing mechanical stress on adjacent vertebrae and predisposing patients to further fractures. Vertebral collapse may also narrow the spinal canal or neural foramina, resulting in nerve root or spinal cord compression with neurological symptoms. Chronic deformity contributes to reduced pulmonary function, impaired mobility, persistent pain, and loss of independence.
Risk factors
Advanced age
Female sex
Postmenopausal state
Previous fragility fracture
Low bone mineral density
Chronic glucocorticoid therapy
Vitamin D deficiency
Calcium deficiency
Smoking
Excessive alcohol intake
Low body mass index
Physical inactivity
Family history of osteoporosis
Clinical presentation
Symptoms
Sudden severe back pain
Pain worsened by standing or walking
Pain relieved by lying down
Difficulty walking
Reduced mobility
Height loss
Progressive spinal deformity
Muscle spasms
Neurological symptoms
These occur when there is spinal canal compromise.
Extremity weakness
Numbness
Paresthesia
Radicular pain
Bladder or bowel dysfunction (rare but urgent)
Physical examination
Localized spinal tenderness
Thoracic kyphosis ("dowager's hump")
Loss of height
Reduced spinal range of motion
Pain on percussion over affected vertebra
Neurological deficits in complicated fractures
Diagnostic criteria
Diagnosis is based on clinical presentation together with imaging evidence of vertebral collapse.
Diagnosis is established by:
Acute or subacute back pain in a patient with osteoporosis or risk factors
Vertebral height loss of at least 20% or at least 4 mm on spinal imaging
Imaging consistent with acute or chronic compression fracture
Exclusion of alternative causes such as malignancy or infection when clinically suspected
Investigations
Laboratory investigations
Complete blood count (CBC)
Erythrocyte sedimentation rate (ESR)
C-reactive protein (CRP)
Serum calcium
Serum phosphate
Serum alkaline phosphatase
Serum creatinine
Serum 25-hydroxyvitamin D
Thyroid-stimulating hormone when indicated
Serum protein electrophoresis if multiple myeloma is suspected
Imaging
Plain spinal radiographs
Usually demonstrate:
Loss of vertebral body height
Wedge fracture
Biconcave deformity
Crush fracture
Kyphosis
CT scan
Useful for:
Complex fracture morphology
Posterior wall involvement
Surgical planning
MRI (preferred if neurological deficit or malignancy suspected)
Identifies:
Acute fracture oedema
Neural compression
Ligament injury
Occult fractures
Infection or malignancy
Radionuclide bone scan
Useful when:
MRI is unavailable
Multiple fractures are suspected
Occult fractures require localization
Bone mineral density assessment
Dual-energy X-ray absorptiometry (DEXA) is recommended to confirm osteoporosis and assess fracture risk.
Differential diagnosis
Metastatic vertebral disease
Multiple myeloma
Pyogenic spondylodiscitis
Tuberculous spondylodiscitis
Degenerative spine disease
Traumatic vertebral fracture
Treatment
Management aims to relieve pain, restore mobility, prevent further fractures, and preserve spinal stability.
Non-pharmacological treatment
Conservative measures
Short period of bed rest
External spinal immobilization using spinal braces
Early mobilization as pain improves
Activity modification
Nutritional optimisation
Adequate calcium and vitamin D intake
Vertebral augmentation procedures
Consider referral for image-guided vertebral cement augmentation in patients with persistent severe pain despite optimal conservative therapy.
Procedures include:
Vertebroplasty
Kyphoplasty
Physical and occupational therapy
Back extensor muscle strengthening
Balance training
Postural correction
Walking programme
Weight-bearing exercise 3–5 sessions weekly (45–60 minutes/session)
Low-impact aerobic exercise such as walking and cycling
Occupational therapy for activities of daily living
Behavioural modification
Smoking cessation
Limit alcohol intake
Moderate caffeine consumption
Encourage regular physical activity
Fall prevention
Install handrails in bathrooms and stairways
Improve household lighting
Remove loose rugs and obstacles
Wear supportive low-heeled footwear
Use walking aids where appropriate
Pharmacological treatment
Principles of conservative treatment
External spinal immobilization
Adequate analgesia
Muscle relaxants when indicated
Osteoporosis treatment
Monitor for spinal instability and neurological deterioration
Mild pain
Ibuprofen
400 mg orally stat then 200 mg every 8 hours
OR
Diclofenac sodium
50 mg orally every 8 hours for 7–14 days
OR
Meloxicam
7.5–15 mg orally every 12–24 hours for 7–14 days
Severe pain
Diclofenac
75 mg intramuscularly every 12 hours by deep IM injection for 1–3 days
±
Tramadol
100 mg intramuscularly every 12 hours by deep IM injection for 1–3 days
THEN
Diclofenac
50 mg orally every 8 hours for 14 days
±
Tramadol
50 mg orally every 8 hours for up to 14 days
Topical analgesics
Diclofenac gel
Apply every 12 hours
OR
Ketoprofen gel
Apply every 12 hours
Gastroprotection
For patients receiving NSAIDs for two weeks or longer or those at high gastrointestinal risk:
Omeprazole
20 mg orally once daily for 2–4 weeks
OR
Pantoprazole
40 mg orally once daily for 2–4 weeks
OR
Lansoprazole
30 mg orally once daily for 2–4 weeks
OR
Esomeprazole
40 mg orally once daily for 2–4 weeks
Radicular symptoms
Pregabalin
75–150 mg orally once daily for 4 weeks (dose may be increased according to response)
AND
Vitamin B1 + Vitamin B6 + Vitamin B12
One tablet orally once daily for 4 weeks
AND
Baclofen
5 mg orally every 8 hours initially; increase by 5 mg per dose every 3 days up to 20 mg every 8 hours for up to 2 weeks
OR
Tizanidine
Initially 2 mg orally every 8 hours; increase gradually to 4 mg daily every 1–4 days according to response. If discontinuing, taper gradually by reducing 2–4 mg daily.
Calcium supplementation
Calcium 600 mg + Vitamin D 800 IU
Orally once daily for 3 months, then re-evaluate
(1 microgram vitamin D = 40 IU)
Bisphosphonate therapy
Bisphosphonate therapy should be continued for five years unless contraindicated.
Ibandronate
3 mg intravenously every 3 months administered over 15–20 minutes for treatment
Surgical management
Surgical intervention is indicated for patients with instability, neurological compromise, or failure of conservative management.
Indications
Progressive neurological deficits due to neural compression
Progressive spinal deformity with disabling pain
Mechanical instability
Failure of conservative treatment
Pathological fractures requiring stabilization
Surgical procedures
Posterior spinal decompression
Instrumented spinal stabilization
Vertebral reconstruction where indicated
Minimally invasive or open techniques depending on patient factors and surgical expertise
Complications
Chronic back pain
Progressive kyphosis
Loss of height
Recurrent vertebral fractures
Respiratory compromise
Reduced mobility
Deep vein thrombosis
Pressure ulcers
Spinal cord compression
Permanent neurological deficits
Prognosis
Most osteoporotic vertebral compression fractures improve with conservative management over several weeks to months. Early osteoporosis treatment significantly reduces the risk of subsequent fractures. Patients with multiple fractures have an increased risk of chronic pain, disability, spinal deformity, and reduced quality of life.
Prevention
Early diagnosis and treatment of osteoporosis
Adequate calcium and vitamin D intake
Regular weight-bearing and resistance exercise
Smoking cessation
Moderate alcohol consumption
Fall prevention strategies
Minimise long-term corticosteroid use where possible
Routine osteoporosis screening in high-risk individuals
Patient education
Patients should be advised to:
Adhere to osteoporosis medications as prescribed.
Take calcium and vitamin D supplements regularly.
Maintain regular physical activity within their ability.
Avoid smoking and excessive alcohol intake.
Use walking aids if balance is impaired.
Report new back pain or neurological symptoms immediately.
Attend follow-up visits for reassessment and bone density monitoring.
