11.3 Osteoporosis, Common Fractures & Orthopaedic Emergencies

Osteoporosis, Common Fractures & Orthopaedic Emergencies

Metabolic bone disorders and acute orthopaedic emergencies form a vital pillar of clinical practice. Osteoporosis represents a silent, progressive disease that remains asymptomatic until a debilitating fragility fracture occurs. Conversely, acute compartment syndrome, cauda equina syndrome, and open fractures are time-critical emergencies where rapid clinical diagnosis and immediate operative intervention dictate whether limb function, neurological integrity, and patient survival are preserved.

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Osteoporosis & Metabolic Bone Disease

Osteoporosis is a systemic skeletal disease characterized by reduced bone mineral density (BMD) and microarchitectural deterioration of bone tissue, leading to bone fragility and a marked susceptibility to fragility fractures (fractures sustained from low-energy mechanical force equivalent to a fall from standing height or less).

Clinical Spectrum of Fragility Fractures

1. Vertebral Compression (Crush) Fractures (#1 most common): Often clinically silent or presenting with acute episodic back pain. Manifests chronologically with progressive height loss, dorsal hyperkyphosis ("dowager's hump"), and reduced vital capacity.
2. Neck of Femur (Hip) Fractures: Associated with severe morbidity and 20–30% one-year excess mortality in elderly patients.
3. Distal Radius Fractures (Colles' Fracture): Classical "dinner-fork" deformity resulting from a fall onto an outstretched hand (FOOSH).

Major Risk Factors & Screening Indications

• Non-Modifiable: Advanced age (≥ 65 years in women, ≥ 75 years in men), female sex, postmenopausal status (abrupt decline in circulating oestrogen accelerates osteoclast-mediated bone resorption), Caucasian or Asian ethnicity, low body weight / body mass index (BMI < 19 kg/m²), and parental history of hip fracture.
• Modifiable Lifestyle Factors: Cigarette smoking, excessive alcohol consumption (≥ 3 units daily), sedentary physical inactivity, and inadequate dietary calcium or vitamin D intake.
• Secondary Causes & High-Risk Medications:
  • Systemic Corticosteroids: Oral prednisolone ≥ 7.5 mg daily for ≥ 3 months. Glucocorticoids directly suppress osteoblast activity, accelerate osteoclast survival, and inhibit intestinal calcium absorption.
  • Endocrine: Untreated hyperthyroidism, primary hyperparathyroidism, Cushing's syndrome, premature ovarian insufficiency (< 40 years), hypogonadism in men.
  • Gastrointestinal / Malabsorptive: Coeliac disease, Crohn's disease, post-gastrectomy syndrome.
  • Rheumatological: Active rheumatoid arthritis, ankylosing spondylitis.
  • Pharmacological: Aromatase inhibitors (anastrozole, letrozole), androgen deprivation therapy (GnRH agonists), proton pump inhibitors (long-term), anticonvulsants.
• Fracture Risk Assessment Tools: FRAX (Fracture Risk Assessment Tool) and QFracture compute the 10-year probability of sustaining a major osteoporotic fracture (hip, clinical spine, forearm, or proximal humerus). Calculated risk stratifies patients into low, intermediate (mandating DEXA scan), or high risk (indicating immediate pharmacological intervention).

Dual-Energy X-Ray Absorptiometry (DEXA) & T-Score Interpretation

DEXA scanning measures areal bone mineral density (in g/cm²) at two standardized anatomical reference sites: the lumbar spine (L1–L4) and the femoral neck / total hip.

• T-Score Definition: The number of standard deviations (SD) by which the patient's BMD differs from the mean peak BMD of a healthy young adult reference population of the same sex.
• Z-Score Definition: The number of standard deviations by which the patient's BMD differs from an age-, sex-, and ethnicity-matched reference control. A Z-score ≤ -2.0 SD suggests an underlying secondary cause of osteoporosis (e.g., hyperparathyroidism, hypogonadism, myeloma).

Pharmacological Management (NICE Guidelines)

1. First-Line Antiresorptive Therapy — Oral Bisphosphonates:
   • Alendronic acid 70 mg ONCE WEEKLY OR Risedronate 35 mg ONCE WEEKLY.
   • Mechanism of Action: Synthetic pyrophosphate analogues that bind avidly to hydroxyapatite crystals on bone resorption surfaces. When internalized by osteoclasts during bone resorption, they inhibit farnesyl pyrophosphate (FPP) synthase, inducing osteoclast apoptosis and suppressing bone breakdown.
   • CRITICAL PATIENT COUNSELING INSTRUCTIONS (To Prevent Chemical Oesophagitis):
     • Take the tablet first thing in the morning on an entirely empty stomach.
     • Swallow the tablet whole with a full glass of plain tap water (at least 200 mL; do NOT use mineral water, milk, coffee, or juice).
     • Remain fully upright (sitting or standing, NOT lying down) for at least 30 minutes following ingestion.
     • Do NOT eat food, drink other fluids, or ingest any other oral medications/supplements for at least 30 minutes after taking the tablet (calcium, iron, and food eliminate the < 1% oral bioavailability).
2. Calcium & Vitamin D Optimization:
   • Ensure adequate daily calcium (1000 mg) and vitamin D (800–1000 IU / 20–25 mcg cholecalciferol) intake. If dietary intake is deficient, co-prescribe combined calcium/vitamin D supplements (e.g., Adcal-D3). Treat vitamin D deficiency before bisphosphonate initiation to avoid severe hypocalcaemia.
3. Second-Line / Intolerant Regimens:
   • Intravenous Zoledronic Acid (5 mg once yearly IV infusion): Ideal for patients with upper gastrointestinal disease or poor adherence. Contraindicated if eGFR < 35 mL/min.
   • Subcutaneous Denosumab (60 mg every 6 months SC injection): Fully human monoclonal antibody against Receptor Activator of Nuclear Factor Kappa-B Ligand (RANKL), preventing osteoclast maturation. Safe in renal impairment; do not discontinue abruptly without transitioning to bisphosphonates (rebound accelerated bone loss).
   • Teriparatide (Recombinant human PTH 1–34 SC daily): Recombinant parathyroid hormone that stimulates osteoblast bone formation; reserved for severe refractory osteoporosis.
4. Rare Long-Term Bisphosphonate Complications:
   • Osteonecrosis of the Jaw (ONJ): Painful, exposed non-healing bone in the oral cavity, often precipitated by invasive dental extractions. Recommend a dental examination and completion of dental work prior to starting bisphosphonates.
   • Atypical Femoral Fractures (AFF): Subtrochanteric or diaphyseal femoral stress fractures presenting with prodromal thigh or groin pain. Re-evaluate ongoing bisphosphonate indication after 3 to 5 years ("bisphosphonate holiday").

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Orthopaedic Emergencies

1. Acute Compartment Syndrome (ACS)

Acute compartment syndrome is a surgical emergency characterized by increased interstitial tissue pressure within a closed, non-compliant osteofascial compartment. As intracompartmental pressure rises above capillary perfusion pressure (typically within 30 mmHg of diastolic blood pressure, $\Delta P = P_{\text{diastolic}} - P_{\text{compartment}} \le 30\text{ mmHg}$), capillary microcirculation collapses, triggering cellular hypoxia, muscle ischaemia, and nerve infarction. Irreversible muscle necrosis and nerve death occur within 4 to 6 hours.

• Aetiology:
  • Fractures: Tibial shaft fractures (#1 cause in adults), supracondylar humeral fractures in children, distal radius fractures.
  • High-energy blunt crush trauma, severe contusions, reperfusion following acute arterial revascularization.
  • Iatrogenic: Overly tight circular plaster casts, tight dressings, pneumatic anti-shock garments.
• Clinical Presentation (The 6 Ps):
  1. Pain out of proportion to the original injury: The earliest and most consistent symptom. Unresponsive to escalating parenteral opioids.
  2. Pain on passive stretch of compartment muscles: The earliest, most reliable, and most sensitive physical sign (e.g., passive extension of toes stretches the deep posterior compartment of the leg; passive flexion of fingers stretches the volar forearm compartment).
  3. Paresthesia / altered sensation: Follows early nerve ischaemia (e.g., deep peroneal nerve deficit in the anterior leg compartment manifests as sensory loss in the 1st dorsal web space of the foot).
  4. Pallor: Pale, cool, tense extremity.
  5. Paralysis / motor weakness: A late finding reflecting extensive neuromuscular infarction.
  6. Pulselessness: A VERY LATE sign indicating terminal arterial obliteration and irreversible tissue necrosis.
  • CRITICAL CLINICAL PEARL: The presence of palpable distal pulses and normal capillary refill NEVER rules out acute compartment syndrome! Arterial systolic pressure (120 mmHg) far exceeds tissue compartment pressures (40–50 mmHg), so pulses persist until tissue necrosis is already complete.
• Immediate Emergency Management:
  1. Bivalve and split all circular plaster casts down to the bare skin immediately (cutting all layers of underlying cotton wool padding). This decompression alone reduces compartment pressure by up to 50–70%.
  2. Maintain the limb at heart level. DO NOT ELEVATE the limb above heart level (elevation reduces mean arterial inflow pressure, exacerbating ischaemia). DO NOT lower the limb into a dependent position (worsens venous congestion).
  3. Administer high-flow supplemental oxygen and intravenous fluid boluses to maintain systemic normotension.
  4. Emergency Operative Intervention: Emergency surgical decompressive fasciotomy of all compartments (e.g., all 4 compartments of the lower leg: anterior, lateral, superficial posterior, deep posterior) performed in theatre within 6 hours of symptom onset. Fasciotomy wounds are left open with delayed secondary closure.

2. Cauda Equina Syndrome (CES)

Cauda equina syndrome results from acute mechanical compression of the bundle of lumbosacral nerve roots (L2 to S5) occupying the spinal canal below the termination of the conus medullaris (which ends at the L1/L2 vertebral interspace).

• Aetiology:
  • Massive central lumbar disc herniation (#1 cause, > 85% of cases): Most frequently at the L4/L5 or L5/S1 level.
  • Spinal epidural abscess or epidural haematoma (e.g., post-epidural catheterization or in coagulopathy).
  • Primary or metastatic spinal neoplasms.
  • Severe spinal burst fractures or spondylolisthesis.
• Red Flag Clinical Symptoms & Signs:
  • Bilateral sciatica: Severe shooting pain or sensory loss radiating down both lower limbs.
  • Bilateral motor weakness: Motor deficits in multiple lumbosacral myotomes (e.g., bilateral foot drop, quadriceps weakness, inability to stand).
  • Saddle Anaesthesia: Objective sensory loss (tested with pinprick and light touch) over the perineum, perianal region, buttocks, and inner thighs (S3–S5 dermatomes).
  • Bladder Dysfunction: Painless urinary retention with overflow incontinence (patient dribbles urine continuously without sensation of bladder fullness) or acute inability to void.
  • Bowel Dysfunction: Faecal incontinence or loss of bowel sensation.
  • Digital Rectal Examination (DRE): Lax / absent anal sphincter tone and absent bulbocavernosus / anal wink reflex.
  • Bladder Scan: Elevated post-void residual urine volume (> 200–300 mL indicates neurogenic urinary retention).
• Clinical Classification:
  • CES-Incomplete (CES-I): Impaired sensation, bilateral sciatica, and altered urinary stream/hesitancy, but patient retains urinary control. Immediate decompression yields excellent neurological recovery.
  • CES with Retention (CES-R): Established painless urinary retention with overflow incontinence. Less favourable prognosis for sphincter recovery.
• MANDATORY EMERGENCY PATHWAY:
  • Emergency MRI of the Lumbosacral Spine: Under the national GIRFT suspected cauda equina pathway, MRI should be performed as an emergency within 4 hours of the request, 24/7, to confirm the level of compression (some centres add a whole-spine screening sequence).
  • Emergency Surgical Decompression: Emergency lumbar discectomy or decompressive laminectomy performed as soon as possible once compression is confirmed, to limit permanent leg weakness, saddle sensory loss, chronic neuropathic pain, and urinary, bowel and sexual dysfunction.

3. Open (Compound) Fractures

An open fracture is a break in bone continuity where the fracture haematoma and underlying bone communicate directly with the external environment through a disrupted cutaneous envelope.

• Gustilo-Anderson Classification:
  • Grade I: Clean skin wound < 1 cm; minimal soft tissue injury; simple low-energy fracture pattern.
  • Grade II: Skin laceration > 1 cm without extensive soft tissue damage, flaps, or avulsions; moderate comminution.
  • Grade III: High-energy injury with extensive soft tissue damage, periosteal stripping, severe contamination, or comminution:
    • Grade IIIA: Adequate soft tissue coverage of fractured bone despite extensive lacerations.
    • Grade IIIB: Extensive soft tissue loss with periosteal stripping and exposed bone; requires plastic surgical flap reconstruction.
    • Grade IIIC: Open fracture associated with an arterial injury requiring surgical revascularization to salvage the limb.
• Emergency Management Protocol (BOA / BAPRAS Standards):
  1. Assess neurovascular status (pulses, capillary refill, motor and sensory testing) before and after any limb realignment.
  2. Obtain photographic documentation of the open wound for surgical records.
  3. Immediate Sterile Dressing: Remove gross macroscopic contamination, cover the wound immediately with sterile saline-soaked gauze, and seal with an occlusive waterproof dressing. DO NOT wash out, irrigate, probe, or manipulate the wound in the Emergency Department (this pushes surface contaminants deeper into bone tissue).
  4. Intravenous Antibiotic Prophylaxis: Administer broad-spectrum intravenous antibiotics as soon as possible, ideally within 1 hour of injury (BOAST open fracture standard) (e.g., IV co-amoxiclav 1.2 g 8-hourly, or IV cefuroxime; add IV gentamicin for Gustilo Grade III injuries).
  5. Tetanus Prophylaxis: Administer intramuscular tetanus toxoid booster and tetanus immunoglobulin if immunization is incomplete or delayed.
  6. Realign displaced limb deformities and immobilize in a rigid splint.
  7. Urgent Combined Orthoplastic Surgery: Transfer to an orthoplastic major trauma centre for formal wound excision, radical debridement, and skeletal stabilization in theatre within 12 to 24 hours (immediate if gross marine/agricultural contamination, compartment syndrome, or vascular compromise).