History Taking for Back Pain

A focused but comprehensive history is key to identifying red flags and guiding diagnosis.

Pain Assessment (SOCRATES):

• Site: Localized, diffuse? Lumbar, thoracic, cervical?
• Onset: Sudden (trauma, disc prolapse) or gradual (degenerative, inflammatory, tumour)?
• Character: Sharp, dull, aching, burning, shooting?
• Radiation:
  • Sciatica: Radiating down back of leg, often below knee, in a dermatomal pattern (suggests L4, L5, S1 nerve root).
  • Groin/anterior thigh pain: May suggest upper lumbar roots (L1-L3) or hip pathology.
  • Non-radicular referred pain: Dull ache into buttock/thigh, not dermatomal.
• Associated Symptoms: Numbness, paraesthesia, weakness in legs? Sphincter disturbance?
• Timing: Constant or intermittent? Worse at night (malignancy, infection, AS)? Worse in morning with prolonged stiffness (inflammatory)?
• Exacerbating/Relieving Factors: Worse with movement/activity (mechanical)? Better with exercise, worse with rest (inflammatory)? Worse with coughing/straining (disc)? Worse with walking, relieved by leaning forward/sitting (spinal stenosis – neurogenic claudication)?
• Severity: Pain score (0-10). Impact on daily life.

Red Flag Questions (Systematic Enquiry):

Cauda Equina Syndrome (CES):

• Bilateral leg pain/sciatica?
• Saddle anaesthesia or paraesthesia (numbness/tingling around genitals/buttocks)?
• Bladder dysfunction: Difficulty initiating micturition, urinary retention, overflow incontinence, loss of sensation of bladder fullness?
• Bowel dysfunction: Faecal incontinence, loss of anal tone/sensation?
• Sexual dysfunction (new onset)?
• Progressive or severe bilateral lower limb weakness or sensory loss?

Malignancy/Infection:

• Age >50 years?
• History of cancer (prostate, breast, lung, kidney, thyroid are common bone mets)?
• Unexplained weight loss?
• Pain worse at night or at rest? Non-mechanical pain?
• Fever, chills, sweats? Recent infection?
• IV drug use? Immunosuppression (steroids, HIV)? Recent spinal procedure?
• Thoracic pain (higher suspicion for sinister pathology)?

Fracture:

• Significant trauma (fall from height, RTA)?
• Minor trauma or even just strain in elderly or osteoporotic patients?
• History of osteoporosis? Long-term steroid use?
• Sudden onset severe pain, point tenderness?

Inflammatory Features (suggesting Spondyloarthropathy, e.g., Ankylosing Spondylitis):

• Insidious onset, often age <40 years.
• Morning stiffness >30 minutes.
• Improves with exercise/activity, NOT with rest.
• Pain at night (may wake patient in second half of night).
• Alternating buttock pain.
• Associated features: Peripheral arthritis, enthesitis (e.g., Achilles tendonitis, plantar fasciitis), uveitis, psoriasis, IBD, family history.

Yellow Flags (Psychosocial factors predicting chronicity/disability):

• Beliefs: Expectation of persistent pain, catastrophizing.
• Behaviour: Fear avoidance, reduced activity levels.
• Mood: Depression, anxiety.
• Work: Dissatisfaction, absence from work.
• Social: Lack of support, compensation issues.

Past Medical History, Drug History, Social History:

• Previous episodes of back pain, treatments tried.
• Other medical conditions, medications (especially anticoagulants, steroids).
• Occupation (manual labour, sedentary), hobbies, functional impact.

Examination of the Spine (OSCE Steps – focusing on Lumbar Spine)

Always explain what you are doing and ask for consent. Expose back adequately (patient in underwear or gown open at back).

1. General Inspection: Patient standing. Observe posture, gait (antalgic?), ability to undress, general comfort.
2. LOOK (from back, side, front if needed):
   • Spinal Alignment: Scoliosis (lateral curvature), kyphosis (excessive thoracic curve), lordosis (excessive lumbar curve – may be lost in spasm/AS). Pelvic tilt.
   • Scars: Previous surgery.
   • Skin Changes: Rashes (herpes zoster), naevi, hair patches (spina bifida occulta), café-au-lait spots (NF1).
   • Muscle Wasting: Gluteal, paraspinal.
   • Swelling (rare).
3. FEEL (Patient standing or prone):
   • Palpate Spinous Processes: For tenderness (fracture, infection, mets), step deformity (spondylolisthesis).
   • Palpate Paraspinal Muscles: For tenderness, spasm.
   • Palpate Sacroiliac Joints (SIJs): For tenderness.
   • Temperature (if infection suspected).
4. MOVE (Patient standing): Assess active range of motion of lumbar spine. Ask patient to:
   • Flexion: “Try to touch your toes, keeping knees straight.” Note range, pain. (Schober’s test can quantify flexion).
   • Extension: “Lean backwards as far as you can.” Note range, pain.
   • Lateral Flexion (Side Bending): “Slide your hand down the side of your leg.” Both sides.
   • Rotation (Thoracolumbar): “Turn your shoulders to the right/left, keeping hips still.” (Stabilize pelvis).
5. NEUROLOGICAL EXAMINATION (Lower Limbs – Patient ideally supine/sitting): Essential to detect radiculopathy or myelopathy/CES. Compare sides.
   • Tone: Assess at knee and ankle.
   • Power (MRC Scale 0-5): Test major myotomes:
     • Hip Flexion (L1, L2, L3 – Iliopsoas)
     • Knee Extension (L3, L4 – Quadriceps)
     • Knee Flexion (L5, S1 – Hamstrings)
     • Ankle Dorsiflexion (L4, L5 – Tibialis Anterior)
     • Ankle Plantarflexion (S1, S2 – Gastrocnemius, Soleus)
     • Great Toe Extension (L5 – Extensor Hallucis Longus)
   • Reflexes:
     • Knee Jerk (L3, L4)
     • Ankle Jerk (S1)
     • Plantar Response (Babinski sign – UMN lesion if upgoing)
   • Sensation (Light touch, pinprick): Test key dermatomes:
     • L1: Groin
     • L2: Anterior mid-thigh
     • L3: Medial knee / distal thigh
     • L4: Medial malleolus / medial aspect of lower leg
     • L5: Dorsum of foot / great toe / lateral aspect of lower leg
     • S1: Lateral malleolus / lateral border of foot / sole
     • Saddle Area (S2-S5): Crucial if CES suspected. Ask about altered sensation when wiping.
6. SPECIAL TESTS:
   • Straight Leg Raise (SLR) / Lasègue’s Test (Patient supine): For L4, L5, S1 nerve root irritation. Passively lift extended leg. Positive if reproduces radicular pain down leg (not just back/hamstring tightness) between 30-70 degrees. Note angle. Dorsiflexion of foot may exacerbate pain (Bragard’s sign). Crossed SLR (pain in affected leg when contralateral leg raised) is more specific for disc prolapse.
   • Femoral Nerve Stretch Test (Patient prone): For L2, L3, L4 nerve root irritation. Flex knee and extend hip. Positive if pain in anterior thigh.
   • Schober’s Test (Patient standing): For lumbar flexion. Mark 5cm below and 10cm above dimples of Venus (or PSIS level). Measure distance. Ask patient to flex fully. Increase <5cm is abnormal (suggests restricted flexion, e.g., in AS).
7. GAIT: Observe walking, heel walking (L5), toe walking (S1). Antalgic gait? Foot drop? Broad-based?
8. PERIPHERAL VASCULAR EXAM: Check peripheral pulses if vascular claudication is a differential for leg pain.
9. ABDOMINAL EXAM: If referred pain suspected (e.g., AAA, pancreatitis, renal colic).
10. RECTAL EXAM (if CES suspected): Assess anal tone, perianal sensation, voluntary squeeze. (Usually state you would do this with a chaperone rather than perform in OSCE without specific instruction).
11. Summarise Findings.

Investigations for Back Pain

Most acute non-specific low back pain does NOT require imaging. Investigations are primarily indicated if red flags are present, or if pain persists despite conservative management and a specific diagnosis is sought.

• Blood Tests (if red flags for infection, malignancy, or inflammatory cause):
  • FBC (WCC, Hb)
  • ESR, CRP (inflammatory markers)
  • Serum Calcium, Alkaline Phosphatase, PSA (for bony mets, myeloma screen)
  • Protein Electrophoresis / Urine Bence Jones Protein (myeloma screen)
  • HLA-B27 (if inflammatory spondyloarthropathy suspected)
  • Blood cultures (if infection suspected)
• Imaging:
  • X-rays (Lumbar Spine – AP, Lateral, +/- Obliques):
    • Limited utility in acute non-specific LBP.
    • Indications: Trauma, suspected fracture (especially in elderly/osteoporotic), suspected spondylolisthesis, monitoring known deformity, initial screen if malignancy/infection suspected (but MRI much better).
    • Can show: Fractures, spondylolisthesis, degenerative changes (disc space narrowing, osteophytes), lytic/sclerotic lesions, sacroiliitis (less sensitive than MRI).
  • MRI Scan (Lumbar Spine):
    • Investigation of choice for suspected serious pathology: CES, spinal cord/nerve root compression, tumour, infection, significant neurological deficit, inflammatory spondyloarthropathy (sacroiliitis, vertebral inflammation).
    • Provides detailed images of soft tissues (discs, nerves, ligaments, cord) and bone marrow.
    • Often shows degenerative changes in asymptomatic individuals, so findings must be correlated clinically.
  • CT Scan (Lumbar Spine):
    • Better for bony detail than MRI (e.g., complex fractures, bony stenosis, post-op assessment of fusion).
    • CT Myelogram (CT after contrast into a dural sac) if MRI contraindicated or inconclusive.
  • Bone Scan (Radionuclide Scintigraphy): Sensitive for detecting areas of increased bone turnover (mets, infection, fracture, Paget’s). Non-specific. Often followed by MRI/CT for characterisation.
• Nerve Conduction Studies / Electromyography (NCS/EMG):
  • To assess nerve function and differentiate radiculopathy from peripheral neuropathy or myopathy.
  • Not usually first-line for back pain.

OSCE Tips for Back Pain Station

• Safety Netting is Key: If no red flags, explain natural history of non-specific LBP, advise on self-management (stay active, analgesia), and crucially, provide clear “red flag” advice (what symptoms warrant urgent re-assessment – especially CES symptoms).
• Red Flag Focus: Systematically ask about red flags. If any are positive, state your concern clearly and your plan for urgent investigation/referral. “Given the new onset bladder dysfunction and saddle anaesthesia, I am concerned about Cauda Equina Syndrome, which is a surgical emergency. I would urgently refer this patient to the on-call orthopaedic/neurosurgical team for an MRI and assessment.”
• Neurological Examination: Perform a competent and structured lower limb neuro exam if indicated. Verbalize what you are testing (myotomes, dermatomes, reflexes).
• Straight Leg Raise: Explain what constitutes a positive test (reproduction of radicular leg pain, not just hamstring tightness).
• Be Empathetic: Back pain can be very distressing and disabling.
• Psychosocial Factors: Briefly acknowledge or ask about “yellow flags” if appropriate, as they influence prognosis and management.
• Management for Non-Specific LBP: Reassurance, encourage activity, simple analgesia (paracetamol, NSAIDs if appropriate), consider physiotherapy referral. Avoid prolonged bed rest.
• Key Phrases:
  • “I need to ask you some important questions to ensure there’s nothing serious causing your back pain.” (Then go through red flags).
  • “Are you having any problems with your waterworks, like difficulty passing urine or any numbness when you wipe yourself?”
  • “I’m now going to test the power in your legs. Can you try to… against my resistance?”
  • “This is called the straight leg raise test. Please tell me if you feel your usual leg pain as I lift your leg.”
  • “Based on my assessment, your back pain appears to be mechanical in nature, and I don’t see any red flag signs at present. However, if you develop [list key CES symptoms], you must seek urgent medical attention.”
• Common Pitfalls:
  • Missing or not adequately exploring red flags.
  • Performing an incomplete or disorganized neurological examination.
  • Not providing adequate safety netting advice.
  • Over-investigating non-specific low back pain.
  • Failing to consider psychosocial factors in chronic pain.

Flashcards: Back Pain Assessment

Click on each card to reveal the answer.

Relevant Anatomy & Classification of Hip Fractures

Understanding the anatomy of the proximal femur and fracture classification is key to determining management.

Proximal Femur Anatomy:

• Femoral Head: Articulates with the acetabulum of the pelvis.
• Femoral Neck: Connects the head to the shaft. Vulnerable to fracture.
• Trochanters:
  • Greater Trochanter: Lateral prominence, attachment site for abductor muscles.
  • Lesser Trochanter: Medial prominence, attachment site for iliopsoas muscle.
• Intertrochanteric Line/Crest: Connects the trochanters.
• Subtrochanteric Region: Area below the lesser trochanter.

Blood Supply to Femoral Head:

• Mainly via retinacular arteries (branches of medial and lateral circumflex femoral arteries) which run along the femoral neck.
• Small contribution from artery of ligamentum teres (more important in children).
• Significance: Intracapsular fractures (especially displaced femoral neck fractures) can disrupt this blood supply, leading to avascular necrosis (AVN) of the femoral head.

Classification of Hip Fractures:

Broadly classified based on anatomical location relative to the hip joint capsule:

• 1. Intracapsular Fractures (Femoral Neck Fractures):
  • Occur within the hip joint capsule.
  • Risk of AVN and non-union is higher.
  • Garden Classification (for displacement):
    • Type I: Incomplete, undisplaced, impacted (valgus).
    • Type II: Complete, undisplaced.
    • Type III: Complete, partially displaced (varus tilt, but some contact remains).
    • Type IV: Complete, fully displaced (no contact between fracture fragments).
    (Simplified: Undisplaced = Garden I & II; Displaced = Garden III & IV)
• 2. Extracapsular Fractures:
  • Occur outside the hip joint capsule. Better blood supply, lower risk of AVN/non-union, but can be unstable and associated with more blood loss.
  • Intertrochanteric Fractures: Occur between the greater and lesser trochanters. Classified by stability (number of fragments, comminution).
  • Subtrochanteric Fractures: Occur below the lesser trochanter, extending down the femoral shaft. Often require different fixation methods. Can be associated with pathological fractures or bisphosphonate use (atypical femoral fractures).

Visual Classification Aid (Simplified)

Image depicting common hip fracture types: Subcapital (intracapsular), Transcervical (intracapsular), Basicervical (intracapsular/extracapsular border), Intertrochanteric (extracapsular), Subtrochanteric (extracapsular). Source: Orthobullets.com (Illustrative)

Clinical Assessment & Diagnosis

Prompt recognition and diagnosis are vital.

History:

• Mechanism of Injury: Usually a fall in older adults. Enquire about circumstances (trip, slip, collapse, “found on floor”). Consider syncope/pre-syncope.
• Symptoms: Hip/groin/thigh/knee pain, inability to weight-bear.
• Past Medical History: Osteoporosis, previous fractures, comorbidities (cardiac, respiratory, renal, diabetes, cognitive impairment), medications (anticoagulants, steroids).
• Social History: Baseline mobility and function (ADLs, IADLs), living situation, social support, smoking/alcohol. This informs rehabilitation potential and discharge planning.
• Pre-fall functional status is crucial.

Examination (ABCDE approach initially if trauma/unwell):

• General: Pain, distress. Signs of shock if significant blood loss (more common with extracapsular).
• Look: Affected leg often shortened and externally rotated (classic sign, especially with displaced fractures). Swelling, bruising (may be delayed).
• Feel: Tenderness over hip region (femoral neck, greater trochanter).
• Move: Pain on any attempted movement of the hip (active or passive). Log-rolling the leg is painful. Inability to straight leg raise. Avoid excessive movement if fracture strongly suspected to prevent further displacement or pain.
• Neurovascular Assessment: Check distal pulses, capillary refill, sensation, and motor function in the affected leg. (Sciatic nerve or femoral nerve injury is rare but possible).
• Assess for other injuries from the fall (e.g., head injury, wrist fracture, rib fractures).

Investigations:

• Imaging:
  • X-ray: AP pelvis and lateral hip views of the affected side are standard.
    • Look for fracture line, displacement, angulation. Shenton’s line disruption.
    • If X-ray is negative but high clinical suspicion (e.g., patient unable to weight-bear, significant pain): Further imaging is indicated.
  • MRI: Gold standard for occult hip fractures (not visible on X-ray). Should be performed within 24 hours if X-ray negative and suspicion remains.
  • CT Scan: Alternative if MRI contraindicated or unavailable quickly. Less sensitive than MRI for occult fractures but good for characterising complex fractures or pre-operative planning.
  • Bone Scan: Rarely used acutely for diagnosis now due to delay; MRI/CT preferred.
• Blood Tests (Pre-operative Workup):
  • FBC (anaemia, platelets), U&Es (renal function, electrolytes), LFTs.
  • Coagulation screen (PT/INR, APTT) – especially if on anticoagulants.
  • Group & Save (Crossmatch if high risk of bleeding or surgery imminent).
  • Glucose, Calcium, Vitamin D, TFTs (may be part of orthogeriatric assessment).
• ECG: Pre-operative assessment, check for arrhythmias that may have caused fall.
• Chest X-ray: If respiratory symptoms or for pre-operative assessment.

Initial Management (Pre-operative Care)

Focus on pain relief, medical stabilisation, and preparation for surgery. NICE NG124 provides detailed guidance.

Key Principles (often in A&E and Orthopaedic Ward):

• Analgesia:
  • Offer regular paracetamol and opioids (e.g., morphine) as needed. Titrate to effect.
  • Consider regional anaesthesia (fascia iliaca compartment block or femoral nerve block) if available and expertise exists – provides excellent analgesia and reduces opioid requirements. Should be performed by trained personnel.
  • Avoid NSAIDs in older adults due to renal, GI, and cardiac risks.
• IV Fluids: If dehydrated or hypotensive. Monitor fluid balance.
• Oxygen: If hypoxic.
• Nil By Mouth (NBM): In anticipation of surgery. Check local NBM guidelines.
• VTE Prophylaxis: Pharmacological prophylaxis (e.g., LMWH) should be started as soon as possible unless contraindicated or surgery imminent (within hours). Mechanical prophylaxis (anti-embolism stockings) may also be used, but ensure correct fitting and no contraindications (e.g., PVD).
• Pressure Area Care: Assess risk, use pressure-relieving mattress. Regular repositioning (as pain allows).
• Medical Optimisation:
  • Identify and manage acute medical problems (e.g., infection, electrolyte imbalance, cardiac issues).
  • Review and manage anticoagulation/antiplatelet therapy in discussion with orthopaedics/anaesthetics/haematology. Bridging may be needed.
  • Optimise chronic conditions (e.g., diabetes, heart failure).
• Orthogeriatric Liaison: Early involvement of geriatricians is crucial for comprehensive medical assessment and co-management, especially for frail older patients. This improves outcomes.
• Fasting & Theatre Planning: Aim for surgery on the day of, or day after, admission (ideally within 36 hours of presentation if medically fit). Delays increase complications.
• Catheterisation: Consider if urinary retention or for accurate fluid balance monitoring, but avoid routine catheterisation.
• Cognitive Assessment: Screen for delirium and dementia (e.g., AMTS, 4AT).

Surgical Management Options

The aim of surgery is to achieve stable fracture fixation or replacement, allowing early mobilisation and pain relief. Choice of surgery depends on fracture type, displacement, patient age, pre-fracture mobility, cognitive status, and comorbidities.

1. Intracapsular (Femoral Neck) Fractures:

• Undisplaced (Garden I & II):
  • Internal Fixation: Usually with cannulated screws or dynamic hip screw (DHS) with anti-rotation screw. Aims to preserve the native femoral head.
• Displaced (Garden III & IV):
  • Younger, fit patients (<60-65 years, physiologically young): Internal fixation may be attempted if fracture pattern suitable, but high risk of AVN/non-union. Requires informed discussion.
  • Older patients (typically >65-70 years, or less mobile/cognitively impaired younger patients):
    • Hemiarthroplasty: Replacement of the femoral head with a prosthesis. Articulates with native acetabulum. (e.g., Austin Moore (monopolar, older design), Thompson (monopolar), or more commonly now, Unipolar/Bipolar cemented or uncemented stems). Quicker surgery, less dislocation risk than THR.
    • Total Hip Replacement (THR): Replacement of both femoral head and acetabulum. Considered for patients who were independently mobile outdoors, cognitively intact, medically fit for longer surgery, and not needing walking aids before fracture. Better long-term functional outcomes and less pain/re-operation than hemiarthroplasty if criteria met. Higher dislocation risk.

2. Extracapsular Fractures:

• Intertrochanteric Fractures:
  • Dynamic Hip Screw (DHS) / Sliding Hip Screw (SHS): Plate and screw construct allowing controlled collapse/impaction at fracture site. Common for stable patterns.
  • Cephalomedullary Nail (Intramedullary Nail): Rod inserted into femoral canal with screws into head/neck. Preferred for unstable patterns, reverse oblique fractures, or subtrochanteric extension. Allows earlier weight-bearing.
• Subtrochanteric Fractures:
  • Usually require Intramedullary Nailing (long nail). Plate fixation is an alternative in some cases.

Anaesthesia:

• Choice between general anaesthesia (GA) and regional anaesthesia (e.g., spinal, epidural) depends on patient factors, anaesthetist/surgeon preference. Regional often preferred in frail elderly if suitable.

Post-operative Care & Rehabilitation

Multidisciplinary team (MDT) approach is essential for recovery.

Immediate Post-operative Care:

• Pain Management: Continue regular analgesia, adjust based on need. Consider patient-controlled analgesia (PCA) initially if appropriate. Transition to oral.
• Fluid Balance & Nutrition: Monitor intake/output. Encourage oral intake as tolerated. Nutritional supplements if at risk of malnutrition.
• VTE Prophylaxis: Continue pharmacological and/or mechanical prophylaxis as per local protocol (usually for ~28-35 days post-op).
• Wound Care: Monitor for signs of infection, haematoma.
• Prevention of Complications: E.g., pressure sores, chest infection (encourage deep breathing, mobilisation).
• Delirium Prevention & Management: Maintain orientation, hydration, avoid problematic medications.

Mobilisation & Rehabilitation:

• Early Mobilisation: Aim for mobilisation (sit out of bed, stand, walk with aid) on the day after surgery, guided by physiotherapists. Weight-bearing status depends on fracture type and fixation (often full weight-bearing as tolerated for arthroplasty and most internal fixations).
• Physiotherapy: Crucial for restoring mobility, strength, balance, and confidence. Individualised exercise programme. Gait re-education with appropriate walking aids.
• Occupational Therapy: Assess ADL function, provide equipment, plan for safe discharge (e.g., home assessment, adaptations).
• Orthogeriatric Review: Continued medical co-management, addressing comorbidities, optimising bone health, falls prevention.

Discharge Planning:

• Starts early. MDT discussion involving patient and family/carers.
• Aim for discharge to usual place of residence if possible.
• May require intermediate care, community rehabilitation, or package of care at home.
• Clear information on follow-up, exercises, wound care, pain relief, and when to seek help.

Complications of Hip Fracture (Medical & Surgical)

Hip fractures are associated with a high rate of complications.

Medical Complications (Common in frail elderly):

• Delirium (Post-operative Confusion): Very common.
• Infections: Chest infection (pneumonia), Urinary Tract Infection (UTI), wound infection.
• Venous Thromboembolism (VTE): Deep Vein Thrombosis (DVT), Pulmonary Embolism (PE).
• Pressure Sores.
• Cardiovascular: Myocardial Infarction (MI), heart failure, arrhythmias.
• Anaemia: Due to blood loss from fracture/surgery, or pre-existing. May require transfusion.
• Electrolyte Imbalance, Renal Impairment.
• Malnutrition, Dehydration.
• Constipation (opioid-related, immobility).
• Functional Decline, Loss of Independence.
• Depression.

Surgical Complications (Specific to fracture type/procedure):

• General Surgical Risks: Infection (superficial or deep prosthetic joint infection), bleeding/haematoma, nerve/vessel damage, anaesthetic risks.
• Complications of Internal Fixation (e.g., for femoral neck or intertrochanteric fractures):
  • Non-union: Fracture fails to heal.
  • Malunion: Fracture heals in an abnormal position.
  • Avascular Necrosis (AVN) of Femoral Head: Especially with displaced intracapsular fractures.
  • Fixation Failure / Cut-out of screws: Implant loosens or cuts through bone.
  • Implant-related pain.
• Complications of Arthroplasty (Hemiarthroplasty or THR):
  • Dislocation: Higher risk with THR than hemiarthroplasty. Specific precautions taught.
  • Prosthetic Joint Infection (PJI): Serious, may require revision surgery.
  • Periprosthetic Fracture: Fracture around the implant.
  • Loosening of Prosthesis (aseptic or septic).
  • Leg length discrepancy.
  • Heterotopic ossification.
• Mortality: Significant risk, especially in the first year post-fracture.

Secondary Prevention of Future Fractures

A hip fracture is often a sentinel event indicating underlying osteoporosis and high risk of future fractures. All patients with a hip fracture should be assessed and managed for osteoporosis and falls risk.

Osteoporosis Assessment & Management:

• All patients with a fragility hip fracture should be considered to have osteoporosis and usually offered treatment without necessarily needing a DEXA scan first (though DEXA may be done for baseline or if uncertainty).
• Lifestyle Advice:
  • Adequate dietary calcium intake.
  • Sufficient Vitamin D (sun exposure, diet, consider supplements for all).
  • Regular weight-bearing exercise (as able post-rehab).
  • Smoking cessation, sensible alcohol intake.
• Pharmacological Treatment for Osteoporosis (usually initiated in hospital or by GP post-discharge):
  • Calcium and Vitamin D Supplementation: Often co-prescribed with bone-sparing agents, especially if dietary intake is insufficient or for housebound individuals. (e.g., Adcal-D3®, Calcichew D3 Forte®).
  • Bisphosphonates (First-line):
    • Oral: Alendronate (weekly), Risedronate (weekly/monthly). Counsel on administration: take on empty stomach with plenty of water, remain upright for 30-60 mins. Side effects: Oesophagitis, GI upset. Contraindications: oesophageal abnormalities, hypocalcaemia, severe renal impairment (eGFR <30-35).
    • IV: Zoledronic acid (annual infusion). Option if oral bisphosphonates contraindicated/not tolerated, or for adherence. Requires adequate renal function. Acute phase reaction common (flu-like symptoms).
    • Rare risks: Osteonecrosis of the jaw (ONJ), atypical femoral fractures (AFFs) with long-term use. Review treatment duration (e.g., after 3-5 years).
  • Denosumab: Monoclonal antibody (subcutaneous injection every 6 months). Alternative if bisphosphonates not suitable. Risk of ONJ/AFFs. Rapid bone loss on cessation if not followed by another agent.
  • Other options (specialist use): Teriparatide (PTH analogue), Raloxifene (SERM), Romosozumab.

Falls Prevention:

• All hip fracture patients should have a multifactorial falls risk assessment and interventions implemented (as discussed in Falls section).
• This is a crucial part of secondary fracture prevention.

Flashcards: Hip Fracture Management

Click on each card to reveal the answer.

History Taking for Knee Pain

A detailed history is crucial for narrowing down the differential diagnosis.

Using “SOCRATES” Framework:

• Site:
  • Anterior: Patellofemoral pain, patellar tendinopathy, Osgood-Schlatter, prepatellar bursitis.
  • Medial: Medial meniscus tear, MCL sprain, medial compartment OA, anserine bursitis.
  • Lateral: Lateral meniscus tear, LCL sprain, lateral compartment OA, ITB syndrome.
  • Posterior: Baker’s cyst, hamstring tendinopathy, PCL injury, referred pain.
  • Diffuse/generalized: OA, inflammatory arthritis, septic arthritis.
• Onset:
  • Acute/Traumatic: Mechanism of injury is vital (e.g., twisting, direct blow, valgus/varus force, hyperextension). Did they hear a “pop” or “snap” (suggests ACL tear, fracture)? Immediate swelling (haemarthrosis) vs. delayed swelling (effusion)? Ability to weight-bear immediately?
  • Gradual/Insidious: Overuse injury, degenerative condition (OA), inflammatory process.
• Character: Sharp, dull, aching, burning, stabbing.
• Radiation: Any radiation to thigh or shin? (May suggest referred pain from hip/back, or nerve involvement).
• Associated Symptoms:
  • Swelling: Timing (immediate suggests haemarthrosis – ACL tear, fracture; delayed suggests synovial effusion – meniscal tear, OA flare), location.
  • Stiffness: Morning stiffness (prolonged in inflammatory arthritis, brief in OA), stiffness after inactivity.
  • Mechanical Symptoms:
    • Locking: True locking (inability to fully extend/flex) suggests meniscal tear, loose body. Pseudo-locking due to pain/effusion.
    • Giving Way / Instability: Sensation of knee “buckling” – suggests ligamentous laxity (ACL, PCL, collaterals) or quadriceps weakness/inhibition.
    • Clicking/Popping/Grinding (Crepitus): Common, can be meniscal tear, OA, patellofemoral issues.
  • Weakness, numbness, paraesthesia in leg/foot.
  • Fever, malaise, warmth, erythema (suggests infection, gout).
• Timing / Pattern: Worse with specific activities (stairs, squatting, running, walking), worse at night (inflammatory, tumour, severe OA), better/worse with rest.
• Exacerbating / Relieving Factors: Activity, rest, analgesia, ice/heat.
• Severity: Pain score (0-10), impact on function (walking distance, ADLs, work, sport).

Other Important History:

• Past Medical History: Previous knee injuries/surgery, OA, gout, pseudogout, inflammatory arthritis (RA, PsA, SpA), IBD, psoriasis, bleeding disorders, DVT/PE risk factors (for Baker’s cyst complications).
• Drug History: Analgesics used, steroids, anticoagulants, fluoroquinolones.
• Family History: OA, inflammatory arthritis.
• Social History: Occupation, sports/hobbies, impact on life.
• Red Flags & Yellow Flags (see dedicated sections).

Knee Examination (“Look, Feel, Move, Special Tests”)

A systematic examination comparing both knees is essential.

General:

• Observe patient walking (gait assessment – antalgic, Trendelenburg, varus/valgus thrust).
• Patient standing: Alignment (varus/valgus), muscle bulk, fixed flexion deformity.

LOOK (Patient supine, knee exposed from mid-thigh to ankle):

• Skin: Scars, erythema, bruising, rashes (e.g., psoriasis), swelling (localised, diffuse).
• Swelling:
  • Effusion: Diffuse swelling, loss of normal hollows around patella. Test for effusion (patellar tap, bulge/sweep test).
  • Localised swelling: Prepatellar bursitis (anterior to patella), Baker’s cyst (popliteal fossa).
• Muscle Wasting: Quadriceps (especially VMO – vastus medialis obliquus).
• Deformity: Varus (bow-legged), valgus (knock-kneed), fixed flexion deformity. Patellar position.

FEEL (Palpation):

• Temperature: Compare knees. Warmth suggests inflammation/infection.
• Tenderness: Systematically palpate:
  • Joint lines (medial and lateral – for meniscal tears, OA).
  • Patellar facets, tibial tuberosity, quadriceps/patellar tendons.
  • Collateral ligaments (MCL, LCL insertions).
  • Popliteal fossa (Baker’s cyst).
  • Around bursae (prepatellar, anserine).
• Effusion Tests:
  • Patellar Tap (Ballottement): For moderate/large effusion. Push fluid from suprapatellar pouch downwards, then sharply tap patella. Positive if patella “bounces” or clicks on femur.
  • Bulge Test / Sweep Test / Wipe Test: For small effusion. Stroke medial side of knee upwards to “milk” fluid into suprapatellar pouch, then stroke lateral side downwards. Positive if fluid bulge seen on medial side.
• Crepitus: Palpable grinding with movement (common in OA, patellofemoral issues).

MOVE (Range of Motion – Active and Passive):

• Flexion: Normal ~0-135/140 degrees. (Heel to buttock).
• Extension: Normal 0 degrees (straight). Hyperextension up to 5-10 degrees can be normal. Note any fixed flexion deformity (inability to fully extend).
• Assess for pain, crepitus, or restriction during movement. Compare sides.

SPECIAL TESTS (Perform selectively based on history. A few key tests for GP):

Note: Sensitivity/specificity of these tests vary. Often used in combination.

• Meniscal Tear Tests:
  • McMurray’s Test: Flex knee, externally/internally rotate tibia, then extend knee while applying varus/valgus stress and palpating joint line. Pain or click suggests meniscal tear. (Often difficult to perform reliably in primary care).
  • Thessaly Test (Standing): Patient stands on affected leg with knee flexed at 5° and 20°, then rotates body internally/externally. Pain/locking/catching suggests meniscal tear. (Requires good balance).
  • Joint Line Tenderness: Good sensitivity but lower specificity.
• Ligament Stability Tests:
  • Anterior Cruciate Ligament (ACL):
    • Anterior Drawer Test: Knee flexed 90°, sit on foot, pull tibia anteriorly. Increased anterior translation suggests ACL tear.
    • Lachman’s Test: Knee flexed 20-30°, stabilise femur, pull tibia anteriorly. More sensitive than anterior drawer. Look for laxity and quality of end-feel (soft/mushy in ACL tear).
  • Posterior Cruciate Ligament (PCL):
    • Posterior Drawer Test: Knee flexed 90°, push tibia posteriorly. Increased posterior translation suggests PCL tear. Sag sign (tibia drops back) may be visible.
  • Collateral Ligaments (MCL & LCL):
    • Valgus Stress Test (for MCL): Knee slightly flexed (20-30°), apply valgus force to knee while stabilising ankle. Pain or increased medial joint line opening suggests MCL injury. Repeat in full extension (if lax in extension, suggests more severe injury involving ACL/PCL/capsule).
    • Varus Stress Test (for LCL): Knee slightly flexed, apply varus force. Pain or increased lateral joint line opening suggests LCL injury.
• Patellofemoral Joint Tests:
  • Patellar Grind Test / Clarke’s Sign: Press patella distally, ask patient to contract quadriceps. Pain suggests patellofemoral chondromalacia/pain syndrome. (Low sensitivity/specificity).
  • Patellar Apprehension Test: Gently push patella laterally. Apprehension or pain suggests patellar instability.

Also examine hip and lumbar spine if referred pain is suspected.

Red Flags in Knee Pain

These indicate potentially serious underlying pathology requiring urgent investigation or referral.

• Suspected Septic Arthritis: (MEDICAL EMERGENCY – A&E)
  • Hot, swollen, erythematous joint.
  • Severe pain, especially on minimal movement.
  • Restricted range of motion (active and passive).
  • Systemic signs: Fever, rigors, malaise, tachycardia.
  • Recent infection, joint surgery/injection, immunosuppression, IV drug use are risk factors.
• Suspected Fracture: (A&E or Ortho)
  • Significant trauma.
  • Inability to weight-bear immediately after injury or for 4 steps (Ottawa Knee Rules apply here).
  • Obvious deformity.
  • Bony tenderness (patella, fibular head).
  • Consider fragility fracture in elderly/osteoporotic with less trauma.
• Acute Ligament Rupture with Significant Instability / Haemarthrosis: (Urgent Ortho/A&E)
  • Audible “pop” at time of injury (e.g., ACL tear).
  • Rapid onset large effusion (haemarthrosis) within hours.
  • Gross instability or giving way.
  • Inability to continue activity.
• Locked Knee (True Mechanical Lock): (Urgent Ortho)
  • Inability to fully extend or flex the knee, often due to displaced meniscal tear or loose body.
• Neurovascular Compromise: (EMERGENCY – A&E)
  • Signs after trauma/dislocation: Pale/cold foot, absent pulses, paraesthesia, weakness (foot drop). Suspect popliteal artery injury or peroneal nerve injury.
• Suspected Malignancy (Bone Tumour): (Urgent Ortho/Oncology via 2WW)
  • Persistent, progressive bone pain, especially night pain unrelated to movement.
  • Unexplained swelling or mass.
  • History of cancer.
  • Unexplained weight loss, fatigue.
  • Pathological fracture.
• Deep Vein Thrombosis (DVT) / Complicated Baker’s Cyst: (Urgent Assessment/USS)
  • Calf swelling, tenderness, warmth, erythema (can mimic cellulitis or Baker’s cyst rupture). Consider DVT risk factors (Wells’ score). Baker’s cyst can dissect or rupture causing calf pain/swelling.
• Compartment Syndrome (Acute): (EMERGENCY – A&E/Ortho)
  • Severe pain out of proportion to injury, tense swollen compartment, pain on passive stretch of muscles in compartment, paraesthesia, pulselessness (late sign). Often after significant trauma/fracture.

Always consider the patient’s age, mechanism of injury, and overall clinical picture when assessing for red flags.

Common Causes of Anterior Knee Pain

Pain felt at the front of the knee.

• Patellofemoral Pain Syndrome (PFPS) / “Runner’s Knee”:
  • Common in young, active individuals, often females.
  • Diffuse ache around or behind patella, worse with stairs (especially going down), squatting, prolonged sitting (“cinema sign”), running, jumping.
  • May have crepitus, mild swelling. Often related to maltracking, muscle imbalance (weak VMO/glutes, tight ITB/hamstrings).
  • Management: Physio (VMO strengthening, gluteal activation, stretching), activity modification, taping, orthotics if foot mechanics contribute.
• Patellar Tendinopathy / “Jumper’s Knee”:
  • Pain localised to inferior pole of patella or along patellar tendon.
  • Overuse injury, common in jumping sports. Pain worse with activity, tender on palpation.
  • Management: Activity modification, eccentric exercises, physio, analgesia.
• Osgood-Schlatter Disease: (Adolescents)
  • Pain, tenderness, and swelling over tibial tuberosity.
  • Apophysitis (inflammation of growth plate) due to repetitive traction from patellar tendon during growth spurts. Common in sporty adolescents.
  • Management: Activity modification, ice, analgesia, stretching. Usually self-limiting once growth ceases.
• Sinding-Larsen-Johansson Syndrome: (Adolescents)
  • Similar to Osgood-Schlatter but pain is at inferior pole of patella. Apophysitis at patellar origin.
• Prepatellar Bursitis / “Housemaid’s Knee”:
  • Swelling, tenderness, +/- warmth directly over anterior patella. Pain with kneeling or direct pressure.
  • Caused by repetitive friction/pressure or direct trauma. Consider infection if very red/hot/systemic symptoms.
  • Management: Avoid aggravating activities, ice, NSAIDs. Aspiration +/- steroid injection if persistent (ensure no infection). Antibiotics if septic.
• Infrapatellar Bursitis / “Clergyman’s Knee”:
  • Swelling and tenderness over infrapatellar region, either side of patellar tendon.
• Chondromalacia Patellae:
  • Softening/degeneration of articular cartilage on undersurface of patella. Often part of PFPS spectrum. Retropatellar pain, crepitus.
• Patellar Instability / Subluxation / Dislocation:
  • Often traumatic. Sensation of patella “slipping out,” acute pain, swelling. Apprehension test positive. Refer if recurrent or significant first episode.

Common Causes of Medial & Lateral Knee Pain

Medial Knee Pain (Pain on inner side):

• Medial Meniscus Tear:
  • Often twisting injury on a flexed, weight-bearing knee. Can be degenerative in older adults with minimal trauma.
  • Medial joint line tenderness, effusion (may be delayed), pain with twisting/squatting. May have locking or catching.
  • McMurray’s/Thessaly test may be positive.
  • Management: RICE, physio. Refer if mechanical symptoms or persistent pain despite conservative care.
• Medial Collateral Ligament (MCL) Sprain:
  • Valgus stress injury (force to outer knee pushing it inwards).
  • Medial knee pain, tenderness over MCL, +/- instability, local swelling/bruising. Pain on valgus stress test.
  • Management: RICE, analgesia, hinged knee brace (for Grade II/III), physio. Most heal non-operatively.
• Medial Compartment Osteoarthritis (OA):
  • Gradual onset pain, stiffness <30 mins, worse with activity. Medial joint line tenderness, crepitus, possible varus deformity.
  • See Osteoarthritis section for management.
• Pes Anserine Bursitis/Tendinopathy:
  • Pain and tenderness over medial aspect of proximal tibia, inferior to medial joint line (insertion of sartorius, gracilis, semitendinosus).
  • Common in runners, OA patients.
  • Management: Activity modification, ice, NSAIDs, physio, steroid injection.

Lateral Knee Pain (Pain on outer side):

• Lateral Meniscus Tear:
  • Similar mechanism and symptoms to medial tear but pain/tenderness on lateral joint line.
  • Management similar to medial meniscal tears.
• Lateral Collateral Ligament (LCL) Sprain:
  • Varus stress injury (force to inner knee pushing it outwards). Less common than MCL sprain.
  • Lateral knee pain, tenderness over LCL, +/- instability. Pain on varus stress test.
  • Management: Similar to MCL sprains. LCL injuries can be associated with other posterolateral corner injuries requiring specialist input.
• Lateral Compartment Osteoarthritis (OA):
  • Gradual onset pain, stiffness, worse with activity. Lateral joint line tenderness, crepitus, possible valgus deformity.
• Iliotibial Band (ITB) Syndrome / “Runner’s Knee”:
  • Common overuse injury in runners/cyclists.
  • Pain over lateral femoral epicondyle or lateral tibial condyle, worse with repetitive knee flexion/extension (e.g., running downhill). Tender over ITB insertion. Noble’s compression test positive.
  • Management: Activity modification, physio (stretching ITB, gluteal strengthening), foam rolling, NSAIDs.

Common Causes of Posterior Knee Pain & Swelling

Pain or swelling at the back of theknee.

• Baker’s Cyst (Popliteal Cyst):
  • Swelling in popliteal fossa, often causing tightness or ache. Usually a communication with knee joint, fluid accumulates due to underlying intra-articular pathology (e.g., OA, meniscal tear, inflammatory arthritis).
  • Can rupture or dissect into calf, causing acute pain, swelling, erythema (mimicking DVT – “pseudothrombophlebitis”).
  • Management: Treat underlying knee pathology. Aspiration +/- steroid injection (of cyst or joint) may provide temporary relief. Reassure if asymptomatic/mild. USS can confirm and rule out DVT if ruptured.
• Hamstring Tendinopathy/Injury:
  • Pain at insertion of hamstring tendons (semimembranosus, semitendinosus, biceps femoris) on posterior aspect of knee/proximal calf.
  • Often overuse or acute strain. Pain with resisted knee flexion or stretching hamstrings.
  • Management: RICE, physio, eccentric exercises.
• Posterior Cruciate Ligament (PCL) Injury:
  • Less common than ACL. “Dashboard injury” (direct blow to anterior tibia with knee flexed) or fall onto flexed knee.
  • Posterior knee pain, instability (especially downhill/stairs), positive posterior drawer/sag sign.
  • Management: Often conservative (physio) for isolated Grade I/II. Refer for Grade III or combined injuries.
• Gastrocnemius Strain / “Tennis Leg”:
  • Acute pain in medial head of gastrocnemius (upper calf), often during forceful push-off. May feel a “pop”. Bruising, tenderness.
• Referred Pain:
  • From lumbar spine (e.g., S1/S2 radiculopathy) or hip.
• Deep Vein Thrombosis (DVT):
  • Although typically calf pain, DVT in popliteal vein can cause posterior knee pain/swelling. Consider risk factors, Wells’ score. Urgent USS if suspected.
• Popliteal Artery Aneurysm (Rare):
  • Pulsatile mass in popliteal fossa. Can cause claudication or distal embolisation. Refer to vascular surgery.

Common Causes of Knee Pain in Children & Adolescents

Knee pain in this age group has some specific considerations.

• Osgood-Schlatter Disease: (See Anterior Knee Pain) – Apophysitis of tibial tuberosity. Common in sporty adolescents during growth spurts.
• Sinding-Larsen-Johansson Syndrome: (See Anterior Knee Pain) – Apophysitis of inferior pole of patella.
• Patellofemoral Pain Syndrome (PFPS): Common, especially in adolescent girls. (See Anterior Knee Pain).
• Patellar Tendinopathy.
• Juvenile Idiopathic Arthritis (JIA):
  • Persistent joint swelling, pain, stiffness >6 weeks, onset <16 years. Knee is commonly affected.
  • Morning stiffness, limp, systemic features (fever, rash in systemic JIA).
  • Refer to paediatric rheumatology if suspected.
• Traumatic Injuries (Sprains, Strains, Meniscal/Ligament Tears):
  • Increasingly common with sports participation. Mechanism of injury important. Physeal (growth plate) fractures can occur.
  • ACL tears are seen in adolescents.
• Osteochondritis Dissecans (OCD):
  • Localized area of bone and overlying cartilage separates from articular surface, often on medial femoral condyle.
  • Vague, activity-related pain, swelling, catching, locking if fragment loose.
  • More common in adolescent males. Refer to orthopaedics.
• Slipped Capital Femoral Epiphysis (SCFE): (EMERGENCY/URGENT ORTHO REFERRAL)
  • Displacement of femoral head epiphysis. Typically occurs in overweight adolescent males during growth spurt (age 10-16).
  • Presents with hip, groin, thigh, OR referred knee pain. Limp, externally rotated leg.
  • Always examine the hip in a child presenting with knee pain. X-ray hips (AP and frog-leg lateral).
• Perthes Disease (Legg-Calvé-Perthes):
  • Avascular necrosis of femoral head. Typically younger children (age 4-8). Presents with hip/groin/thigh or referred knee pain, limp. Hip examination crucial.
• Transient Synovitis of the Hip (“Irritable Hip”):
  • Common cause of acute hip pain/limp in children (age 3-10), often post-viral. Can present with referred knee pain. Diagnosis of exclusion. Hip examination.
• Growing Pains:
  • Diagnosis of exclusion. Bilateral, intermittent, non-articular pain (shins, calves, thighs), often at night, resolves by morning. Child well between episodes, normal examination.
• Septic Arthritis / Osteomyelitis: (EMERGENCY – A&E/Ortho)
  • As in adults, but child may present with pseudoparalysis (refusal to move limb), fever, irritability. Knee is a common site.
• Benign or Malignant Bone Tumours (Rare):
  • Persistent, progressive pain, night pain, swelling, pathological fracture. E.g., Osteosarcoma, Ewing’s sarcoma often around knee. Red flag.

Investigations for Knee Pain in Primary Care

Many knee conditions are diagnosed clinically. Investigations are used selectively.

Blood Tests:

• Generally NOT required for most acute traumatic or mechanical knee pain.
• Consider if:
  • Suspected Septic Arthritis: FBC, CRP, ESR, Blood Cultures (before antibiotics if possible). Joint aspiration for MC&S and crystals by specialist is diagnostic.
  • Suspected Inflammatory Arthritis (e.g., RA, JIA, PsA, Gout, Pseudogout): FBC, ESR, CRP, U&Es, LFTs.
    • If RA suspected: Rheumatoid Factor (RF), Anti-CCP antibodies.
    • If Gout suspected: Serum Urate (can be normal during acute attack, better checked 4-6 weeks later).
    • If other connective tissue disease features: ANA.
  • Suspected Malignancy: FBC, ESR, CRP, Calcium, Alk Phos.
  • If considering NSAIDs long-term: Baseline U&Es, LFTs.

Imaging:

• X-rays (Weight-bearing AP, lateral, skyline/patellar views often requested):
  • Indicated if:
    • Suspected fracture (Ottawa Knee Rules can guide necessity after acute injury).
    • Suspected Osteoarthritis (to confirm diagnosis if atypical, assess severity, or pre-referral). Look for joint space narrowing, osteophytes, subchondral sclerosis/cysts.
    • Suspected bone tumour or other bony lesion.
    • Persistent pain unresponsive to conservative treatment.
    • In children: Osgood-Schlatter (may show fragmentation of tibial tuberosity but often clinical diagnosis), SCFE/Perthes (hip X-rays crucial).
  • Often normal in soft tissue injuries (ligament, meniscus, tendinopathy).
• Ultrasound (USS):
  • Useful for:
    • Detecting effusions, synovitis.
    • Assessing tendons (tendinopathy, tears – e.g. patellar, quadriceps).
    • Assessing bursae (bursitis).
    • Diagnosing Baker’s cyst and assessing for rupture/DVT.
    • Guiding aspirations or injections.
    • Assessing some superficial ligament injuries.
  • Not good for intra-articular structures like menisci or cruciate ligaments.
• Magnetic Resonance Imaging (MRI):
  • Gold standard for soft tissue pathology (menisci, ligaments, cartilage, tendons, bone marrow oedema).
  • Not routinely available/indicated from primary care for most knee pain. Usually requested by specialists or MSK interface services.
  • Consider requesting (or referring for consideration of MRI) if:
    • Red flags for serious pathology (e.g., tumour, infection, osteonecrosis) not clear on X-ray.
    • Persistent mechanical symptoms (locking, instability) suggestive of significant meniscal tear or ligament rupture, where surgical intervention is being considered.
    • Diagnostic uncertainty despite clinical assessment and other imaging.
    • Failure of conservative management for significant symptoms.

Ottawa Knee Rules (To decide if X-ray needed after acute knee injury):

An X-ray of the knee is required if ANY of the following are present:

1. Age ≥55 years.
2. Isolated tenderness of the patella (no bone tenderness of knee other than patella).
3. Tenderness at the head of the fibula.
4. Inability to flex knee to 90 degrees.
5. Inability to weight-bear both immediately after injury AND in the emergency department/clinic (for 4 steps – unable to transfer weight twice onto each leg regardless of limping).

These rules have high sensitivity for detecting clinically significant fractures.

Initial Management Principles & Referral Criteria for Knee Pain

General Initial Management (Non-Red Flag, Mechanical Pain):

Based on the “PEACE & LOVE” principle for soft tissue injuries, or general MSK advice.

• Protection: Avoid aggravating activities for first few days.
• Elevation: Raise the knee above heart level to reduce swelling.
• Avoid Anti-inflammatories (initially): Some debate, but avoiding NSAIDs in first few days may allow natural healing. Consider paracetamol.
• Compression: Elastic bandage can help control swelling and provide support.
• Education: About the condition, expected recovery, self-management.

---

• Load: Gradual introduction of mechanical stress once symptoms allow, to promote healing and strength.
• Optimism: Encourage positive outlook, address yellow flags.
• Vascularisation: Pain-free cardiovascular activity to improve blood flow.
• Exercise: Restore mobility, strength, and proprioception.

Specific Initial Advice:

• Analgesia:
  • Paracetamol (regularly).
  • Topical NSAIDs (e.g., for OA, localised soft tissue pain).
  • Oral NSAIDs (short course, if appropriate, consider PPI cover) for inflammatory component or more severe pain.
  • Weak opioids for short-term use in severe acute pain if other options insufficient/contraindicated.
• Relative Rest / Activity Modification: Avoid activities that clearly worsen pain.
• Ice/Heat: Ice for acute swelling/pain (15-20 mins, wrapped). Heat for muscle stiffness.
• Simple Exercises: Gentle range of motion, isometric quadriceps exercises.
• Weight Management advice if overweight/obese (especially for OA, PFPS).
• Support/Bracing: Simple neoprene sleeve or hinged brace may provide comfort/support for some conditions but avoid over-reliance.

Referral Criteria (General – specific conditions may have own pathways):

• Emergency (A&E / Same-day Ortho):
  • Suspected septic arthritis.
  • Acute fracture or dislocation.
  • Neurovascular compromise.
  • Acute compartment syndrome.
  • Irreducible locked knee.
  • SCFE in children (urgent ortho).
• Urgent Referral (e.g., within days to 2 weeks, depending on local pathways):
  • Suspected malignancy (2WW pathway).
  • Significant acute ligamentous injury (e.g., ACL tear with haemarthrosis/instability) in active individual.
  • Persistent true locking.
  • Inflammatory arthritis with acute flare or diagnostic uncertainty requiring rapid specialist input.
• Routine Referral (to Orthopaedics, Rheumatology, Physiotherapy, MSK Interface Clinic, Pain Clinic):
  • Orthopaedics:
    • Severe OA unresponsive to conservative measures, for consideration of joint replacement.
    • Persistent mechanical symptoms (locking, giving way) from meniscal tear or ligament instability not improving with physio.
    • Specific conditions requiring surgical opinion (e.g., recurrent patellar dislocation, OCD).
  • Rheumatology:
    • Suspected inflammatory arthritis (RA, PsA, SpA, crystal arthropathy).
    • Diagnostic uncertainty for widespread MSK pain (e.g., ?fibromyalgia vs other).
  • Physiotherapy / MSK Interface Clinic:
    • Most non-red flag MSK knee pain not resolving with initial self-management/GP advice (e.g., PFPS, tendinopathies, mild/moderate OA, stable meniscal/ligament injuries).
    • For rehabilitation, exercise prescription, manual therapy, advice.
  • Pain Management Clinic:
    • Chronic knee pain (>3-6 months) with significant functional impact, especially if complex psychosocial factors or failure of other treatments.

Always provide safety netting advice: what to do if symptoms worsen, new red flags develop, or no improvement within expected timeframe.

Flashcards: Knee Pain Assessment

Click on each card to reveal the answer.

History & Examination of Ankle & Foot Injuries

History:

• Mechanism of Injury (Crucial):
  • How did it happen? (e.g., twisting, direct blow, fall from height).
  • Inversion injury (foot turns inwards): Suggests lateral ligament sprain, lateral malleolus fracture, 5th metatarsal base fracture.
  • Eversion injury (foot turns outwards): Suggests deltoid ligament sprain, medial malleolus fracture, fibula fracture (Maisonneuve).
  • Forced dorsiflexion/external rotation: Suggests syndesmotic injury (“high ankle sprain”).
  • Axial load (fall from height): Consider calcaneal, talar, tibial pilon, or spinal fractures.
• Sound at time of injury: “Pop” or “snap” may suggest ligament rupture or fracture.
• Immediate ability to weight-bear: Key component of Ottawa Ankle Rules.
• Pain: Onset (immediate/delayed), location (point tenderness?), character, severity (VAS score).
• Swelling & Bruising: Onset, location, extent.
• Previous injuries to ankle/foot.
• Past Medical History: Diabetes (neuropathy, healing), peripheral vascular disease, osteoporosis, anticoagulants.
• Occupation/Activities: Impact on management and rehabilitation.
• Tetanus status (if open wound).

Examination (“Look, Feel, Move” + Special Tests):

• General: Assess gait (if able), use of aids.
• Look:
  • Swelling: Localised or diffuse.
  • Bruising (Ecchymosis): Pattern can indicate site of injury.
  • Deformity: Obvious angulation, malalignment. Compare to other side.
  • Skin: Open wounds, abrasions, blisters, signs of compartment syndrome (tense, shiny skin).
• Feel:
  • Temperature: Warmth (inflammation) vs. coolness (vascular compromise).
  • Pulses: Dorsalis pedis and posterior tibial arteries. Capillary refill.
  • Sensation: Assess dermatomes for nerve injury.
  • Palpation for Tenderness (Systematic Approach):
    • Bony tenderness: Medial malleolus (posterior edge/tip), lateral malleolus (posterior edge/tip), navicular bone, base of 5th metatarsal (key points for Ottawa Rules). Also palpate along tibia, fibula, talus, calcaneus, other metatarsals/phalanges.
    • Ligamentous tenderness: ATFL, CFL, deltoid ligament, syndesmosis.
    • Tendon tenderness: Achilles tendon, peroneal tendons, tibialis posterior tendon.
• Move (Active and Passive, if pain allows):
  • Ankle: Dorsiflexion, plantarflexion, inversion, eversion.
  • Subtalar joint: Inversion, eversion (stabilise ankle).
  • Midfoot & Forefoot joints.
  • Compare range of motion to unaffected side. Assess for pain or crepitus on movement.
• Special Tests (Perform cautiously if fracture suspected):
  • Anterior Drawer Test (for ATFL integrity): Stabilise tibia, pull heel anteriorly. Increased laxity/soft end-feel suggests ATFL rupture.
  • Talar Tilt Test (for CFL integrity): Stabilise tibia, invert calcaneus. Increased laxity suggests CFL rupture.
  • Squeeze Test / External Rotation Stress Test (for Syndesmosis injury): Squeeze tibia and fibula together at mid-calf (squeeze test) or externally rotate foot with ankle in dorsiflexion (stress test). Pain over syndesmosis suggests injury.
  • Thompson’s Test (for Achilles tendon rupture): Patient prone with feet off edge of couch. Squeeze calf muscle. Absence of plantarflexion is a positive test.
• Neurovascular Assessment: Essential, especially with significant swelling or suspected fracture/dislocation. Check pulses, capillary refill, sensation, motor function distally.

Ottawa Ankle & Foot Rules

The Ottawa Ankle Rules (OAR) and Ottawa Foot Rules are validated clinical decision tools designed to help clinicians decide whether an X-ray is necessary for acute ankle or midfoot injuries. Their use reduces unnecessary radiographs, costs, and radiation exposure.

Ankle X-ray series is required ONLY IF there is any pain in the malleolar zone AND any of these findings:

1. Bone tenderness along the distal 6 cm of the posterior edge of the tibia or tip of the medial malleolus.
   (Point A on diagram)
2. Bone tenderness along the distal 6 cm of the posterior edge of the fibula or tip of the lateral malleolus.
   (Point B on diagram)
3. An inability to bear weight both immediately after injury AND for 4 steps in the emergency department or clinic (unable to transfer weight twice onto each leg).

Foot X-ray series is required ONLY IF there is any pain in the midfoot zone AND any of these findings:

1. Bone tenderness at the base of the fifth metatarsal (lateral side).
   (Point C on diagram)
2. Bone tenderness at the navicular bone (medial side).
   (Point D on diagram)
3. An inability to bear weight both immediately after injury AND for 4 steps in the emergency department or clinic.

Important Considerations for Ottawa Rules:

• Apply to patients >18 years (some evidence supports use in older children, but caution). Not validated for children <5 years typically.
• Apply for acute injuries (within 10 days).
• High sensitivity (approaching 100%) for clinically significant fractures, meaning if rules are negative, fracture is very unlikely.
• Moderate specificity, meaning some patients who are positive by the rules will not have a fracture.
• Do not apply if: patient intoxicated, distracting painful injury elsewhere, diminished sensation in legs, gross swelling preventing palpation.
• Not for assessing chronic pain or re-injury.

Ankle Sprains (Ligament Injuries)

Ankle sprains are one of the most common musculoskeletal injuries. They involve stretching or tearing of ligaments.

Mechanism:

• Lateral Ankle Sprains (Most Common – ~85%):
  • Caused by an inversion injury (foot rolls inwards) with plantarflexion.
  • Typically affects the lateral ligament complex:
    • Anterior Talofibular Ligament (ATFL) is the most frequently injured.
    • Calcaneofibular Ligament (CFL) may be involved in more severe sprains.
    • Posterior Talofibular Ligament (PTFL) injured only in severe sprains, often with dislocation.
• Medial Ankle Sprains (Deltoid Ligament):
  • Caused by an eversion injury (foot rolls outwards).
  • Less common due to strength of deltoid ligament. Often associated with fractures (e.g., fibula) due to the force required.
• Syndesmotic Sprain (“High Ankle Sprain”):
  • Injury to the ligaments connecting distal tibia and fibula (syndesmosis).
  • Caused by forced external rotation of the foot or excessive dorsiflexion.
  • Takes longer to heal than typical lateral sprains.

Grading of Ligament Sprains (General):

• Grade I (Mild): Stretching or microscopic tearing of ligament fibres. Mild pain, swelling, minimal loss of function, able to bear weight. No instability.
• Grade II (Moderate): Partial tearing of ligament fibres. Moderate pain, swelling, bruising. Some loss of function, pain with weight-bearing. Mild to moderate instability.
• Grade III (Severe): Complete rupture of ligament fibres. Severe pain, swelling, bruising. Significant loss of function, unable to bear weight. Gross instability.

Clinical Features:

• Pain, swelling, bruising, tenderness over affected ligaments.
• Limited range of motion.
• Instability or “giving way” sensation (especially with Grade II/III).
• Positive special tests (Anterior Drawer, Talar Tilt, Squeeze test for syndesmosis) if performed, but may be difficult in acute phase due to pain/swelling.

Management (See also “General Management Principles”):

• Confirm no fracture (Ottawa Ankle Rules).
• Initial (PRICE/POLICE): Protection, Optimal Loading, Ice, Compression, Elevation.
• Analgesia: Paracetamol, NSAIDs (oral or topical).
• Support/Immobilisation:
  • Grade I: Minimal support, early mobilisation.
  • Grade II: Functional support (e.g., ankle brace, strapping) for 2-6 weeks.
  • Grade III: May require short period of immobilisation (e.g., walker boot, cast) followed by functional support.
• Early Mobilisation & Rehabilitation: Crucial to prevent chronic instability and re-injury.
  • Range of motion exercises.
  • Strengthening exercises (especially peroneal muscles for lateral sprains).
  • Proprioception and balance training (e.g., wobble board).
  • Gradual return to activity.
• Physiotherapy referral is often beneficial, especially for Grade II/III sprains or persistent symptoms.
• Surgery: Rarely indicated for acute lateral ankle sprains. Considered for chronic instability despite adequate conservative management, or for some severe syndesmotic injuries.

Most ankle sprains heal well with appropriate conservative management, but recurrent sprains and chronic instability can occur if not rehabilitated properly.

Ankle Fractures

Ankle fractures involve a break in one or more of the malleoli (medial, lateral, posterior – which is part of the distal tibia).

Classification (Simplified – based on malleoli involved):

• Unimalleolar Fracture:
  • Isolated lateral malleolus fracture (most common).
  • Isolated medial malleolus fracture.
• Bimalleolar Fracture: Involves both medial and lateral malleoli. Often indicates an unstable ankle joint.
• Trimalleolar Fracture: Involves medial malleolus, lateral malleolus, AND posterior malleolus (fracture of posterior aspect of distal tibia). Highly unstable.

More complex classifications (e.g., Weber, Lauge-Hansen) are used by orthopaedic specialists to guide treatment based on fracture pattern and mechanism, predicting ligamentous injury and stability.

Mechanism:

• Similar to ankle sprains (inversion, eversion, rotation), but with greater force.
• Direct blows.

Clinical Features:

• Severe pain, often immediate inability to weight-bear.
• Significant swelling and bruising.
• Deformity may be present, especially with displaced fractures or dislocations.
• Point tenderness over the fractured malleolus/malleoli.
• Crepitus may be felt.

Investigations:

• X-rays: Standard ankle series (Anterior-Posterior, Lateral, Mortise views).
  • Mortise view is crucial for assessing congruity of the ankle joint and syndesmotic integrity (widening suggests instability).
  • Look for fracture lines, displacement, angulation, talar shift.
• CT scan may be used for complex fractures, pre-operative planning, or if posterior malleolus fracture extent is unclear.

Management:

Goal: Achieve a stable, congruent joint to allow healing and restore function.

• Undisplaced, Stable Fractures (e.g., some isolated lateral malleolus fractures – Weber A):
  • Conservative management: Immobilisation in a below-knee cast or walker boot for 4-6 weeks.
  • Non-weight bearing or partial weight-bearing initially, progressing as tolerated.
  • Follow-up X-rays to ensure no displacement.
  • Rehabilitation with physiotherapy after immobilisation.
• Displaced or Unstable Fractures (e.g., most bimalleolar, trimalleolar, displaced unimalleolar, Weber B/C with talar shift or syndesmotic injury):
  • Require Orthopaedic Referral URGENTLY.
  • Initial Management in ED/Urgent Care:
    • Analgesia.
    • Neurovascular assessment.
    • Attempt closed reduction if significantly displaced or dislocated (often under sedation). Check post-reduction X-ray and neurovascular status.
    • Immobilise in a well-padded backslab or cast.
    • Elevate limb.
  • Surgical Management (Open Reduction and Internal Fixation – ORIF): Most common treatment for unstable fractures. Involves plates and screws to restore anatomical alignment.
• Open Fractures: Surgical emergency. IV antibiotics, tetanus prophylaxis, urgent debridement and fixation.

Specific Types to Note:

• Maisonneuve Fracture: Spiral fracture of the proximal fibula associated with a tear of the deltoid ligament and/or syndesmosis, and often a medial malleolus fracture. Caused by eversion/external rotation. Ankle X-ray may seem “normal” or show only medial injury; requires palpation of entire fibula and potentially full-length tib/fib X-rays if high index of suspicion. Unstable, usually requires surgery.

Common Foot Fractures

Fractures can occur in any of the 26 bones of the foot. Some common or significant ones include:

Metatarsal Fractures:

• Stress Fractures: Common in 2nd and 3rd metatarsals (march fracture) due to repetitive stress (e.g., runners, military recruits). Insidious onset of pain, worse with activity. X-rays may be normal initially; bone scan or MRI more sensitive. Management: rest, activity modification, supportive footwear, sometimes boot.
• Acute Fractures (e.g., shaft, neck): Usually due to direct trauma or twisting. Management depends on displacement and location. Most can be treated conservatively with boot/stiff-soled shoe and protected weight-bearing. Displaced fractures may need ORIF.
• Fifth Metatarsal Fractures:
  • Tuberosity Avulsion Fracture (Pseudo-Jones / Dancer’s fracture): Avulsion at base by peroneus brevis tendon due to inversion injury. Usually heals well with symptomatic treatment (boot/stiff shoe).
  • Jones Fracture: Transverse fracture at the metaphyseal-diaphyseal junction (Zone 2). Higher risk of non-union due to tenuous blood supply. Often requires non-weight bearing cast for 6-8 weeks; surgery (screw fixation) considered for athletes or displaced fractures.
  • Diaphyseal Stress Fracture (Zone 3): Also prone to delayed union/non-union.

Phalangeal Fractures (Toes):

• Very common, usually due to direct trauma (stubbing toe).
• Most are undisplaced or minimally displaced.
• Management: Buddy strapping to adjacent toe, stiff-soled shoe, analgesia.
• Displaced fractures of great toe or intra-articular fractures may need reduction or surgical referral.

Calcaneal Fractures:

• Usually due to high-energy trauma (fall from height, MVA). Often severe and debilitating.
• Associated with lumbar spine fractures (check spine!).
• Pain, swelling, inability to weight-bear, heel bruising/widening.
• X-rays (lateral, axial views). CT scan essential for characterising fracture pattern and intra-articular involvement (subtalar joint).
• Many require ORIF, but outcomes can be variable. High risk of post-traumatic arthritis.
• URGENT ORTHOPAEDIC REFERRAL.

Talar Fractures:

• Relatively uncommon, often due to high-energy trauma (forced dorsiflexion).
• Risk of avascular necrosis (AVN) of talar body, especially with displaced neck fractures, due to tenuous blood supply.
• Pain, swelling, inability to weight-bear.
• URGENT ORTHOPAEDIC REFERRAL. Many require surgical fixation.

Navicular Fractures:

• Can be acute (often body fractures) or stress fractures (common in athletes).
• Tenderness over dorsal navicular (“N-spot”).
• Stress fractures may have vague midfoot pain. Risk of AVN/non-union.
• Displaced fractures or some stress fractures may require surgery.

Lisfranc Injury (Tarsometatarsal Fracture-Dislocation):

• Injury to the Lisfranc joint complex (articulation between midfoot and forefoot). Can be purely ligamentous or involve fractures.
• Often subtle on X-ray, easily missed. Look for widening between 1st and 2nd metatarsal bases, or dorsal displacement.
• Mechanism: Axial load on plantarflexed foot, or severe twisting.
• Pain, swelling in midfoot, inability to bear weight, bruising on sole of foot (plantar ecchymosis) is a key sign.
• High index of suspicion needed. Weight-bearing X-rays or CT/MRI may be required.
• URGENT ORTHOPAEDIC REFERRAL. Most require surgical stabilisation to prevent long-term pain and arthritis.

Achilles Tendon Injuries

The Achilles tendon is the largest and strongest tendon in the body, connecting calf muscles (gastrocnemius, soleus) to the calcaneus. Injuries include tendinopathy and rupture.

Achilles Tendinopathy:

• Overuse injury causing pain, swelling, and stiffness of the Achilles tendon.
• Types:
  • Non-insertional: Affects mid-portion of tendon (2-6 cm proximal to insertion).
  • Insertional: Affects tendon at its insertion onto calcaneus. Often associated with bony spurs (Haglund’s deformity).
• Risk Factors: Sudden increase in activity, improper footwear, tight calf muscles, foot malalignment (e.g., overpronation).
• Clinical Features: Gradual onset pain, worse with activity (especially at start), morning stiffness. Palpable thickening or nodule in tendon.
• Management:
  • Activity modification, relative rest.
  • Ice, NSAIDs for pain.
  • Eccentric strengthening exercises (e.g., heel drops) are the cornerstone of treatment.
  • Stretching of calf muscles.
  • Heel lifts/orthotics may provide temporary relief.
  • Avoid corticosteroid injections directly into tendon (risk of rupture).
  • Refer to physiotherapy. Surgery rarely needed.

Achilles Tendon Rupture:

• Complete tear of the Achilles tendon.
• Mechanism: Sudden, forceful plantarflexion or dorsiflexion (e.g., pushing off to sprint, landing from jump, sudden stumble). Often in “weekend warriors” (middle-aged recreational athletes). Risk increased by fluoroquinolone antibiotics and corticosteroids.
• Clinical Features:
  • Sudden, sharp pain in back of ankle/lower calf, often described as being “kicked” or “shot”.
  • Audible “pop” or “snap” may be reported.
  • Difficulty weight-bearing, weak plantarflexion.
  • Palpable gap in the tendon (may be obscured by swelling later).
  • Positive Thompson’s Test (Simmonds’ Triad): Squeeze calf muscle while patient is prone with feet off couch edge. Absence of passive plantarflexion indicates rupture. Highly sensitive and specific.
  • Increased passive dorsiflexion compared to other side.
• Diagnosis: Usually clinical. Ultrasound or MRI can confirm diagnosis if uncertain or to assess extent of tear/gap. X-rays usually normal.
• Management: URGENT ORTHOPAEDIC REFERRAL (same/next day).
  • Non-operative: Functional bracing or casting with foot in equinus (plantarflexion), gradually brought to neutral over several weeks. Requires strict adherence. Similar functional outcomes to surgery for many, but potentially higher re-rupture rate.
  • Operative (Surgical Repair): Open or percutaneous repair of the tendon. May allow earlier mobilisation and potentially lower re-rupture rate, but carries surgical risks (infection, wound problems, nerve injury).
  • Choice of treatment depends on patient factors (age, activity level, comorbidities), surgeon preference, and patient preference after discussion.
  • Both require prolonged rehabilitation.

Red Flags & Urgent Orthopaedic Referrals (Ankle & Foot)

Recognizing conditions that require immediate or urgent specialist orthopaedic input is vital to prevent long-term disability or limb-threatening complications.

IMMEDIATE / EMERGENCY ORTHOPAEDIC REFERRAL (Often via ED):

• Open Fractures or Dislocations: Bone exposed, high risk of infection. Requires IV antibiotics, tetanus, urgent surgical debridement and stabilisation.
• Irreducible Dislocation: Ankle or foot joint remains dislocated after attempts at closed reduction.
• Neurovascular Compromise: Absent pulses, cold/pale foot, paraesthesia, paralysis distal to injury. Suggests arterial injury or compartment syndrome. Requires immediate attempts to restore circulation (e.g., reducing dislocation/fracture).
• Compartment Syndrome: Increased pressure within a fascial compartment, compromising circulation and function.
  • Symptoms (6 P’s): Pain out of proportion (early & key), Pallor, Pulselessness (late), Paraesthesia, Paralysis (late), Poikilothermia (coolness). Pain on passive stretch of muscles in compartment is a key sign.
  • Clinical diagnosis, compartment pressures can be measured. Requires URGENT fasciotomy.
• Suspected Septic Arthritis or Osteomyelitis: Hot, swollen, erythematous joint/bone with severe pain on movement, fever, systemic upset. Requires joint aspiration/blood cultures, IV antibiotics, possible surgical washout.
• Significant, Unstable Fractures requiring immediate reduction/stabilisation: e.g., grossly displaced ankle fracture-dislocation.
• Suspected Calcaneal or Talar neck fractures (displaced): High risk of complications.
• Suspected Lisfranc Fracture-Dislocation: Easily missed, high morbidity if untreated.

URGENT ORTHOPAEDIC REFERRAL (e.g., within 24-72 hours, via fracture clinic pathway):

• Achilles Tendon Rupture: For discussion of operative vs. non-operative management.
• Most displaced or unstable ankle fractures that have been temporarily stabilised.
• Significant foot fractures requiring specialist assessment/management (e.g., Jones fracture, displaced metatarsal fractures, some navicular fractures).
• Syndesmotic injuries (“High ankle sprains”) that are unstable or not improving.
• Persistent severe pain or inability to weight-bear despite negative X-rays, where significant ligamentous injury or occult fracture is suspected.
• Children with suspected physeal (growth plate) fractures.

Considerations for Routine Orthopaedic Referral (Non-urgent):

• Chronic ankle instability despite physiotherapy.
• Persistent pain from conditions like Achilles tendinopathy or plantar fasciitis unresponsive to conservative measures.
• Degenerative conditions (e.g., ankle/foot arthritis) significantly impacting quality of life.
• Foot deformities causing problems (e.g., severe bunions, hammer toes).

Always document neurovascular status thoroughly. If in doubt about urgency, discuss with orthopaedic registrar on call or local fracture clinic.

General Management Principles for Acute Ankle & Foot Injuries

Many acute soft tissue injuries and some minor fractures can be managed with similar initial principles.

PRICE / POLICE Acronyms:

These guide initial self-care and professional advice for acute soft tissue injuries (e.g., sprains, strains).

• P – Protection: Protect the injured area from further damage. This might involve crutches, splints, braces, or avoiding certain activities.
• R – Rest (Relative Rest): Avoid activities that cause pain. Complete rest is often not ideal; “Optimal Loading” is now preferred for many injuries.
  OR
  OL – Optimal Loading: Gradually reintroduce movement and stress to the injured tissue as tolerated, to promote healing and prevent deconditioning. Pain should guide progression. Avoid complete immobilisation unless necessary.
• I – Ice: Apply ice packs (wrapped in a damp cloth) for 15-20 minutes every 2-3 hours during the first 24-48 hours to reduce pain and swelling. Avoid direct contact with skin.
• C – Compression: Apply a compression bandage (e.g., elasticated bandage, tubigrip) to help reduce swelling. Ensure it’s not too tight to impede circulation.
• E – Elevation: Elevate the injured limb above the level of the heart as much as possible, especially in the first 24-48 hours, to reduce swelling.

Analgesia:

• Paracetamol: Regular dosing for pain relief.
• Non-Steroidal Anti-Inflammatory Drugs (NSAIDs):
  • e.g., Ibuprofen, Naproxen (oral or topical).
  • Can help reduce pain and inflammation.
  • Consider starting 48 hours after injury for soft tissue injuries to avoid potentially interfering with early healing phases (though evidence is debated).
  • Use with caution in patients with asthma, renal impairment, GI issues, cardiovascular disease.
• Opioid analgesia (e.g., codeine) may be needed for short periods for severe pain (e.g., fractures) but use sparingly due to side effects.

Immobilisation & Support:

• Splints/Casts: For fractures requiring immobilisation or severe ligament injuries. Backslabs are often used initially to allow for swelling.
• Walker Boots: Provide support and allow for some controlled weight-bearing or non-weight bearing. Useful for stable fractures and severe sprains.
• Ankle Braces/Supports: For moderate sprains or as a step-down from more rigid immobilisation. Provide stability during rehabilitation.
• Crutches: To allow non-weight bearing or partial weight-bearing. Ensure correct fitting and patient education on use.

Rehabilitation:

• Crucial for restoring function, strength, range of motion, and proprioception.
• Should be started as soon as appropriate, guided by pain and type of injury.
• Involves:
  • Range of motion exercises.
  • Strengthening exercises.
  • Balance and proprioception exercises.
  • Gradual return to functional activities and sports.
• Physiotherapy referral is often very beneficial.

Patient Education & Safety Netting:

• Explain the likely diagnosis and expected recovery timeframe.
• Clear instructions on weight-bearing status, use of supports, exercises.
• Advice on when to seek further medical attention (e.g., worsening pain, swelling, numbness/tingling, signs of infection, DVT symptoms).
• Arrange appropriate follow-up (e.g., fracture clinic, GP review, physiotherapy).

Flashcards: Ankle & Foot Injuries

Click on each card to reveal the answer.

Causes & Risk Factors for Acute Compartment Syndrome

Any condition that increases the volume within a compartment or decreases the size of the compartment can cause ACS.

Increased Compartment Volume:

• Fractures (Most Common Cause): Especially tibial shaft fractures (up to 10% risk), forearm fractures (both bones), supracondylar humerus fractures (children). Bleeding and oedema from the fracture site.
• Soft Tissue Injury / Contusion: Severe crush injuries, muscle trauma, vigorous exercise (especially in unconditioned individuals).
• Bleeding / Haemorrhage:
  • Coagulopathy (e.g., haemophilia, anticoagulation therapy).
  • Vascular injury (arterial or venous).
  • Post-operative haematoma.
• Reperfusion Injury: After prolonged ischaemia (e.g., revascularisation of an ischaemic limb), leading to oedema.
• Burns: Oedema formation. Circumferential burns can also decrease compartment size.
• Intravenous or Intra-arterial Infiltration/Extravasation: Large volumes of fluid or irritant substances.
• Snake Bites / Envenomation.
• Nephrotic Syndrome (rarely, due to severe oedema).

Decreased Compartment Size:

• Tight Casts or Dressings: Especially circumferential casts applied too early after injury before swelling peaks.
• Circumferential Burns: Constricting eschar.
• External Compression / Lying on Limb: Prolonged immobilisation or unconsciousness with limb compression (e.g., drug overdose, prolonged surgery in lithotomy).
• Surgical Closure under Tension.

Patient-Related Risk Factors:

• Young age (especially young males, due to larger muscle mass and tighter fascia).
• High-energy trauma.
• Altered mental status (e.g., head injury, intoxication) making clinical assessment difficult.
• Patients on anticoagulation.

Common Anatomical Locations for Compartment Syndrome

ACS can occur in any closed fascial compartment, but some locations are more common.

Lower Limb:

• Anterior Compartment of the Leg (Most Common Site Overall):
  • Contents: Tibialis anterior, extensor hallucis longus (EHL), extensor digitorum longus (EDL), peroneus tertius muscles; deep peroneal nerve; anterior tibial artery & vein.
  • Clinical Signs of Dysfunction: Weakness of ankle/toe dorsiflexion (foot drop), paraesthesia/numbness in 1st web space (deep peroneal nerve).
• Lateral Compartment of the Leg:
  • Contents: Peroneus longus, peroneus brevis muscles; superficial peroneal nerve.
  • Clinical Signs of Dysfunction: Weakness of foot eversion, paraesthesia/numbness on dorsum of foot (superficial peroneal nerve).
• Deep Posterior Compartment of the Leg:
  • Contents: Tibialis posterior, flexor hallucis longus (FHL), flexor digitorum longus (FDL) muscles; tibial nerve; posterior tibial artery & vein, peroneal artery & vein.
  • Clinical Signs of Dysfunction: Weakness of ankle/toe plantarflexion, paraesthesia/numbness on sole of foot (tibial nerve). Pain on passive dorsiflexion of toes/ankle.
• Superficial Posterior Compartment of the Leg:
  • Contents: Gastrocnemius, soleus, plantaris muscles; sural nerve.
  • Clinical Signs of Dysfunction: Weakness of ankle plantarflexion (less pronounced than deep posterior). Pain on passive dorsiflexion of ankle. Sural nerve sensation may be affected.
• Thigh Compartments (Anterior, Posterior, Medial): Less common than leg, usually after high-energy trauma or femoral fracture. Can be life-threatening due to large muscle volume and potential for massive fluid shifts/rhabdomyolysis.
• Foot Compartments: Rare, often after severe crush injuries. Multiple small compartments.

Upper Limb:

• Volar (Anterior) Compartment of the Forearm (Second Most Common Site):
  • Contents: Flexor muscles of wrist/fingers; median nerve, ulnar nerve; radial artery, ulnar artery.
  • Clinical Signs of Dysfunction: Pain on passive extension of fingers/wrist, weakness of finger/wrist flexion, paraesthesia/numbness in median/ulnar nerve distributions. Late: Volkmann’s ischaemic contracture.
• Dorsal (Posterior) Compartment of the Forearm:
  • Contents: Extensor muscles of wrist/fingers; posterior interosseous nerve (branch of radial).
  • Clinical Signs of Dysfunction: Pain on passive flexion of fingers/wrist, weakness of finger/wrist extension.
• Hand Compartments (Interossei, Thenar, Hypothenar, Adductor Pollicis): Often after crush injuries or high-pressure injection.
• Arm Compartments (Anterior, Posterior): Rare, usually with humeral fractures or severe trauma.

Understanding the contents of each compartment is key to recognizing specific neurological and motor deficits associated with ACS in that location.

Clinical Features of Acute Compartment Syndrome

The “classic” signs are often taught as the “6 P’s”, but some are late and unreliable findings. Pain out of proportion is the most important early symptom.

Key Symptoms & Signs (In approximate order of appearance/reliability):

1. Pain out of Proportion to Injury (Earliest & Most Sensitive Symptom):
   • Severe, deep, throbbing, burning pain that is poorly localized within the affected compartment.
   • Often described as “bursting” or “tense.”
   • Pain is typically not relieved by immobilization, elevation, or standard analgesia (including opioids).
   • Pain on Passive Stretch of the muscles within the affected compartment is a very important early sign (e.g., passive toe dorsiflexion for deep posterior leg compartment, passive finger extension for volar forearm compartment).
2. Palpably Tense (Firm, “Woody”) Compartment:
   • Affected compartment feels very firm, tense, and tender to palpation compared to the contralateral limb or unaffected compartments.
3. Paraesthesia and/or Numbness (Altered Sensation):
   • Indicates nerve ischaemia. Often follows specific nerve distributions within the affected compartment (e.g., deep peroneal nerve in anterior leg compartment – 1st web space numbness).
   • May start as tingling or burning.
4. Paresis / Muscle Weakness (Motor Deficit):
   • Weakness of muscles within the affected compartment. A later sign than sensory changes.
   • E.g., foot drop with anterior leg compartment syndrome.
5. Pallor:
   • Uncommon and a very late sign, indicating severe arterial insufficiency. Not reliable for diagnosis.
6. Pulselessness:
   • A very late and ominous sign, indicating that intracompartmental pressure exceeds arterial pressure. Irreversible damage is likely by this stage. Peripheral pulses are often INTACT in early compartment syndrome. Absence of a pulse is NOT required for diagnosis.

Other Important Considerations:

• Agitation and Anxiety: Patients are often very distressed due to severe pain.
• Symptoms may develop insidiously over hours or rapidly after acute injury.
• Clinical assessment can be difficult in:
  • Unconscious or sedated patients (e.g., head injury, ITU).
  • Patients with nerve blocks or epidural analgesia.
  • Young children who cannot articulate symptoms.
  • Polytrauma patients with distracting injuries.
  In these situations, a lower threshold for objective pressure measurement is required.

Diagnosis & Intracompartmental Pressure (ICP) Measurement

Diagnosis of ACS is primarily clinical, supported by ICP measurement in equivocal cases or when clinical assessment is unreliable.

Clinical Diagnosis:

• Based on high index of suspicion in at-risk patients, combined with characteristic symptoms and signs (especially pain out of proportion and pain on passive stretch).
• Serial examinations are vital if ACS is suspected but not definitive. Document findings meticulously.
• If clinical diagnosis is clear (e.g., conscious patient with tibial fracture, severe pain unrelieved by opioids, tense anterior compartment, pain on passive toe dorsiflexion, and 1st web space paraesthesia), proceed directly to fasciotomy without necessarily needing ICP measurement, as this can delay treatment.

Indications for Intracompartmental Pressure (ICP) Measurement:

• Equivocal clinical findings.
• Patient unable to cooperate with clinical examination (e.g., unconscious, sedated, intoxicated, distracting injuries, regional anaesthesia).
• Young children.
• To confirm diagnosis before fasciotomy if any doubt exists.
• Monitoring high-risk patients prophylactically (less common).

ICP Measurement Techniques:

• Various devices available:
  • Stryker ICP Monitor (or similar handheld devices): Commonly used. Needle connected to a pressure transducer.
  • Arterial line transducer system.
  • Slit catheter / Wick catheter (for continuous monitoring, less common for acute diagnosis).
• Procedure (General Principles):
  • Sterile technique.
  • Needle inserted perpendicular to skin into the suspected compartment(s). Ensure correct anatomical landmarking for each compartment.
  • Needle tip should be at the level of the muscle belly, avoiding proximity to fracture site (which can give falsely high readings).
  • Inject small amount of sterile saline to prime system (if required by device).
  • Measure pressure in all compartments of the affected limb if suspicion is high, as multiple compartments can be involved.
  • Compare with diastolic blood pressure (DBP) to calculate Delta P (ΔP).

Interpretation of ICP Values:

• Normal ICP: 0-10 mmHg.
• Absolute ICP concerning for ACS:
  • Often quoted as >30 mmHg.
  • Some use >40-45 mmHg as a stronger indication.
• Delta P (ΔP = DBP – ICP):
  • ΔP <30 mmHg is highly suggestive of ACS.
  • Some use ΔP <20 mmHg as a more specific threshold.
  • This relative measure is generally considered more reliable than absolute ICP, especially in hypotensive patients (where a lower absolute ICP might still compromise perfusion).
• Continuous monitoring may show rising pressures.

Management: Urgent Fasciotomy

Once ACS is diagnosed or strongly suspected, urgent surgical decompression via fasciotomy is the definitive treatment. This is a surgical emergency.

Immediate Pre-Fasciotomy Measures:

• Summon Senior Orthopaedic Help IMMEDIATELY.
• Nil By Mouth (NBM): In preparation for surgery.
• Remove All Constricting Dressings/Casts: Bivalve casts and loosen all bandages down to skin. This may reduce ICP somewhat but is rarely sufficient alone.
• Place Limb at Heart Level: Avoid elevation above heart level, as this can further reduce arterial inflow and worsen perfusion pressure. Avoid dependency if it increases swelling/pain.
• Analgesia: Opioids may be needed but often provide poor relief. Avoid NSAIDs if surgery imminent (bleeding risk).
• Oxygen: If hypoxic.
• IV Fluids: For resuscitation if hypotensive or signs of rhabdomyolysis.
• Correct Hypotension: Maintain adequate systemic blood pressure to optimize perfusion pressure (CPP = MAP – ICP).
• Consent for surgery (if patient able). Explain risks/benefits/alternatives.
• Pre-operative bloods (FBC, U&Es, Coagulation screen, Group & Save/Crossmatch).

Surgical Fasciotomy:

• Goal: To decompress all involved fascial compartments by making long incisions through skin and fascia.
• Timing: URGENT. Aim for surgery within hours of diagnosis (ideally <6 hours from onset of symptoms if possible, but still beneficial even if delayed, though prognosis worsens).
• Technique:
  • Performed under general or regional anaesthesia.
  • Leg Fasciotomies:
    • Anterolateral Incision (Single Incision Technique – less common now for full decompression): For anterior and lateral compartments. Risk to superficial peroneal nerve.
    • Dual Incision Technique (Most Common for Leg):
      • Anterolateral Incision: Decompresses anterior and lateral compartments. Made midway between tibial crest and fibula.
      • Posteromedial Incision: Decompresses superficial and deep posterior compartments. Made ~2cm posterior to posteromedial border of tibia. Care to protect saphenous nerve and vein.
    • Incisions must be long enough to decompress entire length of compartments. Fascia incised fully.
  • Forearm Fasciotomies: Volar (Henry) approach for volar compartment, often extending to release carpal tunnel. Dorsal incision for dorsal compartment.
  • Thigh/Arm: Long incisions over respective compartments.
• Muscle Viability Assessment: After decompression, muscle viability is assessed (color, consistency, contractility, bleeding). Any necrotic muscle must be debrided.
• Wound Management:
  • Fasciotomy wounds are typically left open initially due to swelling. Covered with sterile, non-adherent dressings or a vacuum-assisted closure (VAC) device.
  • Serial debridement and “second look” operations may be needed every 24-72 hours.
  • Delayed primary closure or skin grafting is performed once swelling subsides and muscle viability is confirmed (usually 5-7 days later).

Post-Operative Care:

• Analgesia, limb elevation (once stable), monitor neurovascular status.
• Monitor for rhabdomyolysis (CK, urine myoglobin, renal function, electrolytes) and manage accordingly (IV fluids, alkalinisation of urine – controversial).
• Physiotherapy for range of motion and rehabilitation.

Complications & Sequelae of Acute Compartment Syndrome

Complications depend on the severity and duration of ischaemia before decompression.

Early Complications:

• Rhabdomyolysis: Release of myoglobin from necrotic muscle, leading to myoglobinuria and potentially Acute Kidney Injury (AKI). Monitor CK, U&Es, urine. Requires aggressive IV hydration.
• Hyperkalaemia: Release of potassium from damaged cells, can cause cardiac arrhythmias.
• Metabolic Acidosis.
• Infection: Of fasciotomy wounds or underlying devitalised tissue.
• Need for Amputation: If extensive muscle necrosis or limb non-viable.

Late Sequelae (Often Permanent):

• Muscle Necrosis & Fibrosis: Leads to loss of muscle function and contractures.
• Volkmann’s Ischaemic Contracture: Classic deformity of forearm/hand due to untreated or late-treated volar forearm compartment syndrome. Characterized by flexion contracture of wrist and fingers, muscle atrophy, and paralysis.
• Nerve Damage / Neuropathy:
  • Persistent pain (neuropathic pain, complex regional pain syndrome – CRPS).
  • Sensory loss (numbness, paraesthesia).
  • Motor weakness or paralysis (e.g., foot drop from peroneal nerve damage).
• Chronic Pain.
• Joint Stiffness & Contractures.
• Cosmetic Deformity: From scarring of fasciotomy wounds, muscle loss.
• Non-union or Malunion of associated fractures.
• Psychological impact.

The goal of prompt fasciotomy is to minimize these devastating long-term complications.

Special Considerations

1. Chronic Exertional Compartment Syndrome (CECS):

• Not an acute emergency like ACS, but a cause of activity-related limb pain, often in athletes (runners, military recruits).
• Pathophysiology: Repetitive muscle expansion during exercise within a non-compliant fascial compartment leads to transiently increased ICP and ischaemic pain. Pain resolves with rest.
• Common Sites: Anterior and deep posterior compartments of the leg.
• Symptoms: Cramping, aching, or burning pain that occurs at a predictable point during exercise, forcing cessation of activity. Resolves within minutes to hours of stopping. May have associated paraesthesia or weakness during episodes. Examination between episodes is often normal.
• Diagnosis: Clinical history is key. Dynamic ICP measurement (pre- and post-exercise) can confirm (e.g., resting pressure >15 mmHg, 1-min post-exercise >30 mmHg, or 5-mins post-exercise >20 mmHg – criteria vary). MRI may show muscle oedema after exercise.
• Management:
  • Conservative: Activity modification, physio (stretching, gait analysis, orthotics).
  • Surgical: Elective fasciotomy of involved compartments if conservative measures fail and diagnosis confirmed. Good outcomes in selected patients.

2. Abdominal Compartment Syndrome (ACS):

• Life-threatening condition where increased intra-abdominal pressure (IAP) leads to organ dysfunction. Seen in critically ill patients (e.g., severe trauma, pancreatitis, major abdominal surgery, massive fluid resuscitation).
• Pathophysiology: Increased IAP impairs perfusion to abdominal organs (kidneys, gut, liver) and has systemic effects (reduced venous return, increased intrathoracic pressure, respiratory compromise, intracranial hypertension).
• Diagnosis: Clinical suspicion + measurement of intra-abdominal pressure (IAP) via bladder catheter transducer (IAP >20 mmHg with new organ dysfunction).
• Management: Medical (sedation, paralysis, diuresis, NG/rectal tube decompression, body positioning) and surgical (decompressive laparotomy) if IAP remains high and organ dysfunction progresses. Managed in ITU setting.

While distinct from limb ACS, understanding the general principle of pressure impairing perfusion is common.

Flashcards: Compartment Syndrome

Click on each card to reveal the answer.

Applied Anatomy of the Hand & Wrist

A fundamental understanding of hand and wrist anatomy is essential for diagnosing and managing injuries.

Bones:

• Distal Radius & Ulna: Form the proximal articulation of the wrist. Key landmarks: radial styloid, ulnar styloid, Lister’s tubercle.
• Carpal Bones (8): Arranged in two rows.
  • Proximal Row (Radial to Ulnar): Scaphoid, Lunate, Triquetrum, Pisiform.
  • Distal Row (Radial to Ulnar): Trapezium, Trapezoid, Capitate, Hamate.
  • Mnemonic (Proximal to Distal, Radial to Ulnar): “Some Lovers Try Positions That They Can’t Handle”
• Metacarpals (5): Numbered 1 (thumb) to 5 (little finger). Each has a base, shaft, neck, and head.
• Phalanges (14): Thumb has 2 (proximal, distal). Fingers 2-5 have 3 (proximal, middle, distal).

Joints:

• Radiocarpal Joint: Distal radius and scaphoid/lunate.
• Midcarpal Joint: Between proximal and distal carpal rows.
• Carpometacarpal (CMC) Joints: Distal carpal row and metacarpal bases. Thumb CMC is a saddle joint.
• Metacarpophalangeal (MCP) Joints: Metacarpal heads and proximal phalanges.
• Interphalangeal (IP) Joints: Proximal (PIP) and Distal (DIP) joints.

Key Ligaments:

• Scapholunate Ligament: Critical for wrist stability; injury leads to scapholunate dissociation.
• Lunotriquetral Ligament: Stabilizes ulnar side of the wrist.
• Triangular Fibrocartilage Complex (TFCC): Major stabilizer of the distal radioulnar joint (DRUJ) and ulnar carpus.
• Collateral Ligaments: Stabilize MCP and IP joints (e.g., Ulnar Collateral Ligament of thumb MCPJ).

Nerves (Major branches in hand/wrist):

• Median Nerve:
  • Course: Passes through carpal tunnel.
  • Sensory: Volar aspect of thumb, index, middle, and radial half of ring finger. Dorsal tips of these fingers.
  • Motor: Thenar muscles (LOAF: Lumbricals 1&2, Opponens pollicis, Abductor pollicis brevis, Flexor pollicis brevis – superficial head). Prone to compression in Carpal Tunnel Syndrome.
• Ulnar Nerve:
  • Course: Passes through Guyon’s canal at the wrist.
  • Sensory: Little finger and ulnar half of ring finger (volar and dorsal).
  • Motor: Hypothenar muscles, interossei, adductor pollicis, lumbricals 3&4, flexor pollicis brevis (deep head).
• Radial Nerve:
  • Course: Superficial branch provides sensation to dorsum of hand. Deep branch (Posterior Interosseous Nerve – PIN) is motor.
  • Sensory: Dorsal aspect of thumb, index, middle fingers proximal to DIPJs, and radial side of dorsum of hand (1st dorsal webspace).
  • Motor (via PIN): Wrist extensors, finger extensors, thumb extensors (supinator).

Tendons:

• Flexor Tendons: Pass through carpal tunnel (except FCR) and digital flexor sheaths. Flexor Digitorum Superficialis (FDS – flexes PIPJ), Flexor Digitorum Profundus (FDP – flexes DIPJ), Flexor Pollicis Longus (FPL – flexes thumb IPJ).
• Extensor Tendons: Organized into 6 dorsal compartments at the wrist. Responsible for wrist, finger, and thumb extension.

Vascular Supply:

• Mainly from Radial and Ulnar arteries, forming superficial and deep palmar arches.

Clinical Assessment of Hand & Wrist Injuries

A systematic approach (History and Examination) is crucial.

History:

• Patient Demographics: Age, occupation, hand dominance, hobbies.
• Mechanism of Injury (MOI): How did it happen? (e.g., FOOSH, direct blow, twisting). Force involved?
• Presenting Complaint:
  • Pain: SOCRATES (Site, Onset, Character, Radiation, Associated symptoms, Timing, Exacerbating/Relieving factors, Severity).
  • Swelling, Deformity, Bruising.
  • Loss of Function: Inability to move wrist/fingers, weakness, difficulty gripping.
  • Neurological Symptoms: Numbness, tingling (paresthesia), weakness. Which digits/area?
  • Sounds at time of injury: Pop, snap, crack.
• Past Medical History: Previous injuries to hand/wrist, arthritis, diabetes, osteoporosis, smoking, medications (e.g., steroids, anticoagulants).
• Allergies, Tetanus status.

Examination: (Always compare with the uninjured side)

“Look, Feel, Move, Special Tests, Neurovascular Assessment”

• General: If polytrauma, follow ATLS guidelines first. Expose the entire limb adequately.
• Look (Inspect):
  • Attitude of the hand/fingers at rest.
  • Swelling, bruising (ecchymosis), erythema.
  • Deformity: Angulation (e.g., “dinner fork” in Colles’), rotation, shortening.
  • Wounds: Open vs. closed fracture. Note size, contamination. Check for “fight bites” over MCPJs.
  • Skin integrity, scars, muscle wasting (e.g., thenar/hypothenar).
• Feel (Palpate):
  • Temperature (warmth may suggest inflammation/infection).
  • Tenderness: Systematically palpate bony landmarks and soft tissues.
    • Distal radius, ulnar styloid, Lister’s tubercle.
    • Anatomical snuffbox, scaphoid tubercle, hook of hamate.
    • Metacarpal shafts and heads, phalanges.
    • Ligaments (e.g., UCL of thumb), tendon sheaths.
  • Crepitus, swelling (soft, boggy, tense).
  • Assess for fluctuance (abscess/haematoma).
• Move (Assess Range of Motion – ROM):
  • Active ROM first, then passive ROM if active is limited and tolerated.
  • Wrist: Flexion, extension, radial deviation, ulnar deviation, supination, pronation.
  • Fingers: MCPJ, PIPJ, DIPJ flexion/extension. Abduction/adduction.
  • Thumb: Flexion/extension (MCPJ, IPJ), abduction/adduction, opposition.
  • Note pain, crepitus, or block to movement.
• Neurovascular Assessment (CRITICAL – perform before and after any manipulation/reduction):
  • Vascular:
    • Capillary refill time (CRT <2 seconds).
    • Radial and Ulnar pulses.
    • Skin colour and temperature.
    • Allen’s Test (if considering radial artery cannulation or harvest).
  • Neurological (Motor & Sensory for each nerve):
    • Median Nerve:
      • Sensory: Volar tip of index finger. Two-point discrimination (2PD).
      • Motor: “OK” sign (FPL and FDP to index finger), or thumb abduction against resistance (Abductor Pollicis Brevis).
    • Ulnar Nerve:
      • Sensory: Volar tip of little finger. 2PD.
      • Motor: Finger abduction/adduction (interossei – “starfish”), or Froment’s sign (tests Adductor Pollicis – patient grips paper, if weak, IPJ of thumb flexes due to FPL compensating).
    • Radial Nerve (Superficial and PIN):
      • Sensory: Dorsum of 1st web space.
      • Motor: Wrist extension, finger MCPJ extension, thumb extension (“hitchhiker’s sign”).
• Special Tests (Perform as indicated by history and initial findings):
  • Scaphoid: Snuffbox tenderness, scaphoid tubercle tenderness, axial compression of thumb.
  • Ligamentous instability: Watson’s test (scapholunate), UCL stress test (thumb MCPJ).
  • Tendon integrity: Test FDS/FDP isolation, Elson’s test (central slip), test for Mallet/Jersey finger.
  • Nerve compression: Tinel’s test, Phalen’s test (Carpal Tunnel Syndrome).
  • Tenosynovitis: Finkelstein’s test (De Quervain’s).

Imaging & Investigations for Hand & Wrist Injuries

1. X-rays (Radiographs):

• Indications: Suspected fracture, dislocation, foreign body, or bony abnormality. Follow Ottawa Ankle/Knee rules equivalent for wrist if local guidelines exist, but generally lower threshold for X-raying wrist/hand injuries.
• Standard Views:
  • Wrist: Posteroanterior (PA), Lateral, Oblique.
  • Hand: PA, Lateral, Oblique.
  • Fingers: PA, Lateral.
• Specific Views:
  • Scaphoid Series: PA with ulnar deviation, lateral, oblique (often supinated and pronated obliques), and a coned PA view of the scaphoid.
  • Clenched Fist View (PA): For suspected scapholunate instability (shows widening of scapholunate interval – “Terry Thomas sign”).
  • Carpal Tunnel View: Axial view to assess carpal tunnel space and hook of hamate.
  • Stress Views: To assess ligamentous instability (less common in acute setting).
• Systematic Interpretation (ABCDE’S or similar):
  • Alignment & Articular congruity: Check carpal arcs (Gilula’s lines), joint spaces, displacement, angulation.
  • Bones: Trace cortices for breaks/fracture lines. Note bone density, lytic/sclerotic lesions.
  • Cartilage: Inferred from joint space width.
  • Distribution: Is the injury pattern typical for a certain mechanism?
  • Soft Tissues: Swelling, effusions, foreign bodies, gas (infection).
• Describing a Fracture: Use a systematic approach (e.g., “LOST CABS” mnemonic – see Overview section).

2. Computed Tomography (CT) Scan:

• Indications:
  • Detailed assessment of complex intra-articular fractures (e.g., comminuted distal radius, Rolando’s).
  • Pre-operative planning.
  • Suspected occult fractures not clearly visible on X-ray (e.g., scaphoid, hook of hamate, carpal boss).
  • Assessment of fracture healing (non-union/malunion).

3. Magnetic Resonance Imaging (MRI):

• Indications:
  • Suspected significant soft tissue injuries: Ligaments (scapholunate, TFCC), tendons (ruptures, tendinopathy), cartilage.
  • Early detection of Avascular Necrosis (AVN) (e.g., scaphoid, lunate – Kienbock’s disease).
  • Occult fractures or bone bruising if X-ray/CT inconclusive.
  • Nerve compression or injury assessment.
  • Infection (osteomyelitis, abscess).

4. Ultrasound (USS):

• Indications:
  • Dynamic assessment of tendons (ruptures, subluxation, tenosynovitis – e.g., De Quervain’s).
  • Assessment of ligaments, ganglion cysts, foreign bodies (especially radiolucent).
  • Guiding aspirations or injections.
  • Assessment of nerve morphology (e.g., median nerve in CTS).

5. Nerve Conduction Studies (NCS) / Electromyography (EMG):

• Indications:
  • To confirm and quantify nerve entrapment syndromes (e.g., Carpal Tunnel Syndrome, Cubital Tunnel Syndrome).
  • To assess severity and prognosis of nerve injuries.
  • Differentiating radiculopathy from peripheral neuropathy.

Common Hand & Wrist Fractures

1. Distal Radius Fractures:

• Epidemiology: Most common fracture in adults, especially elderly women (osteoporosis) and young active individuals. MOI: FOOSH.
• Key Types:
  • Colles’ Fracture: Extra-articular or intra-articular, dorsal displacement and angulation, radial shortening. “Dinner fork” deformity. MOI: FOOSH with wrist dorsiflexion.
  • Smith’s Fracture (“Reverse Colles’”): Volar displacement and angulation. “Garden spade” deformity. MOI: Fall on back of hand (wrist flexed).
  • Barton’s Fracture: Intra-articular fracture with associated radiocarpal subluxation/dislocation. Can be dorsal or volar. Unstable.
  • Chauffeur’s (Hutchinson’s) Fracture: Intra-articular fracture of the radial styloid.
• Assessment: Deformity, swelling, pain. Crucially, assess median nerve function and vascular status.
• Management Principles:
  • Undisplaced/Minimally displaced stable #: Cast immobilisation (e.g., below-elbow backslab initially, then full cast).
  • Displaced #: Closed reduction (under haematoma block, Bier’s block, or sedation/GA) followed by cast. Check post-reduction X-rays and neurovascular status.
  • Surgical Indications (ORIF with volar plate common, K-wires, Ex-fix): Open #, irreducible #, unstable # (e.g., significant comminution, Barton’s), severe displacement/angulation/shortening despite reduction, intra-articular step >2mm, associated neurovascular injury requiring repair.
• Complications: Median nerve injury (acute or carpal tunnel syndrome), malunion, stiffness, CRPS, EPL tendon rupture (late).

2. Scaphoid Fractures:

• Epidemiology: Most common carpal bone fracture. MOI: FOOSH with wrist hyperextension and radial deviation.
• Clinical Features: Pain and tenderness in anatomical snuffbox, pain over scaphoid tubercle (volar), pain with axial compression of thumb. Swelling may be minimal.
• Anatomical Significance: Precarious retrograde blood supply (mainly from dorsal carpal branch of radial artery), especially to proximal pole, leading to high risk of Avascular Necrosis (AVN) and non-union.
• Investigations: Scaphoid X-ray series. If negative but high clinical suspicion: immobilise in thumb spica and repeat X-ray in 10-14 days, OR early MRI/CT.
• Management:
  • Undisplaced waist/distal pole #: Thumb spica cast for 6-12 weeks (longer for proximal pole).
  • Displaced (>1mm), proximal pole #, unstable #, or established non-union: Surgical fixation (e.g., percutaneous or open headless compression screw).
• Complications: Non-union (can lead to SNAC wrist – Scaphoid Non-union Advanced Collapse), AVN, osteoarthritis.

3. Metacarpal Fractures:

• Commonly due to direct trauma or axial loading (punching).
• Types by Location:
  • Metacarpal Neck (e.g., Boxer’s Fracture): Fracture of the 5th (or 4th) metacarpal neck, typically from punching a solid object. Apex dorsal angulation. Check for rotational deformity (“scissoring” of fingers) – this is unacceptable.
    • Management: Acceptable angulation varies (more tolerated in 4th/5th MCs, e.g., up to 30-40° for 5th MC). Ulnar gutter splint/cast. Surgical fixation (K-wires, plate) for excessive angulation, rotation, or open fracture.
  • Metacarpal Shaft: Transverse, oblique, spiral, or comminuted. Rotational alignment is key.
  • Metacarpal Base (e.g., Bennett’s, Rolando’s):
    • Bennett’s Fracture: Intra-articular fracture-dislocation at the base of the 1st metacarpal (thumb). Small ulnar fragment held by ligaments, while the larger fragment is pulled radially and dorsally by Abductor Pollicis Longus (APL). Inherently unstable. Often requires CRPP or ORIF.
    • Rolando’s Fracture: Comminuted intra-articular fracture at the base of the 1st metacarpal (T or Y-shaped). Difficult to manage, often poor prognosis. Usually requires surgical fixation.

4. Phalangeal Fractures:

• Common, result from direct blows, crush injuries, or sporting injuries.
• Types:
  • Tuft Fractures (Distal Phalanx): Crush injury (e.g., door slam). Often associated with subungual haematoma or nail bed injury. Management: Symptomatic, protective splint. Drain large/painful subungual haematoma by trephination.
  • Shaft/Neck/Base Fractures (Proximal and Middle Phalanges): Rotational and angular deformities are poorly tolerated.
    • Management: Stable, undisplaced fractures can be managed with buddy taping to adjacent finger and early mobilisation. Unstable, displaced, or intra-articular fractures often require closed reduction and splinting, or surgical fixation (K-wires, mini-screws/plates).
• Complications: Stiffness, malunion (especially rotational), non-union, tendon adhesions.

Common Soft Tissue & Nerve Injuries

Tendon Injuries:

• Mallet Finger (Baseball Finger):
  • Mechanism: Forced flexion of an actively extended distal interphalangeal joint (DIPJ), e.g., ball hitting tip of finger. Results in rupture or avulsion of the extensor tendon from its insertion on the distal phalanx (± small bony fragment).
  • Clinical: Inability to actively extend the DIPJ. The DIPJ rests in a flexed position (~30-40°). Passive extension is possible.
  • Management: Continuous extension splinting of the DIPJ (e.g., Stack splint, custom thermoplastic splint) for 6-8 weeks, followed by night splinting. Surgical intervention if large bony fragment (>30% articular surface) or joint subluxation.
• Jersey Finger:
  • Mechanism: Forced hyperextension of an actively flexed DIPJ, e.g., player grabs opponent’s jersey. Avulsion of the Flexor Digitorum Profundus (FDP) tendon from its insertion on the volar base of the distal phalanx. Ring finger is most commonly affected.
  • Clinical: Inability to actively flex the DIPJ of the affected finger. Tenderness over volar aspect. The avulsed tendon may retract into palm (Leddy and Packer classification based on retraction level).
  • Management: Surgical repair is usually required, ideally within 7-10 days to prevent tendon retraction and scarring.
• Boutonnière Deformity:
  • Mechanism: Disruption of the central slip of the extensor tendon at its insertion on the base of the middle phalanx, often from forced flexion of PIPJ or volar dislocation. Lateral bands displace volarly.
  • Clinical: PIPJ flexion and DIPJ hyperextension. Deformity may not be apparent immediately. Elson’s test can be diagnostic.
  • Management: Splinting of the PIPJ in full extension for 4-6 weeks, allowing DIPJ active flexion. Surgery for failed conservative treatment or open injuries.
• Flexor/Extensor Tendon Lacerations:
  • Mechanism: Usually penetrating trauma (e.g., knife, glass).
  • Assessment: Carefully assess individual tendon function (e.g., FDS and FDP isolation). Note zone of injury (Verdan’s zones for flexors, Doyle’s zones for extensors).
  • Management: Requires specialist hand surgical repair, followed by complex rehabilitation protocol.

Ligament Injuries:

• Skier’s Thumb (Gamekeeper’s Thumb):
  • Mechanism: Forced abduction and hyperextension of the thumb MCPJ, leading to injury (sprain or rupture) of the Ulnar Collateral Ligament (UCL).
  • Clinical: Pain, swelling, and tenderness on the ulnar aspect of the thumb MCPJ. Instability with valgus stress testing (compare to contralateral side).
  • Stener Lesion: If UCL is completely torn, the adductor aponeurosis can become interposed between the ruptured ends of the ligament, preventing healing. This usually requires surgical repair.
  • Management: Partial tears without instability: Thumb spica cast/splint for 4-6 weeks. Complete tears or suspected Stener lesion: Surgical repair.
• Scapholunate Ligament Injury:
  • Mechanism: FOOSH, often with wrist hyperextension and ulnar deviation. Most common carpal instability.
  • Clinical: Dorsal wrist pain (especially over SL interval), clicking, weakness, reduced grip strength. Watson’s test (scaphoid shift test) may be positive.
  • X-ray: May show scapholunate diastasis (>3mm, “Terry Thomas sign” or “David Letterman sign”), especially on clenched fist PA view. Dorsal Intercalated Segment Instability (DISI) on lateral view in chronic cases.
  • Management: Acute partial tears: Immobilisation. Complete tears or chronic instability: Arthroscopic debridement, repair, or reconstruction.

Nerve Entrapment Syndromes:

• Carpal Tunnel Syndrome (CTS):
  • Pathophysiology: Compression of the median nerve within the carpal tunnel.
  • Causes: Idiopathic (most common), pregnancy, hypothyroidism, rheumatoid arthritis, diabetes, previous wrist fracture, repetitive motions.
  • Symptoms: Pain, numbness, and tingling (paresthesia) in the median nerve distribution (thumb, index, middle, radial half of ring finger). Often worse at night, relieved by shaking hand. Weakness or atrophy of thenar muscles (Abductor Pollicis Brevis) in late stages.
  • Signs: Positive Tinel’s test (tapping over carpal tunnel), Phalen’s test (wrist flexion for 60s), Durkan’s test (carpal compression test). Thenar wasting.
  • Investigations: Nerve Conduction Studies (NCS)/EMG to confirm diagnosis and severity.
  • Management: Conservative (night splints in neutral, activity modification, NSAIDs, steroid injections). Surgical (carpal tunnel decompression/release) for persistent/severe symptoms or thenar atrophy.
• De Quervain’s Tenosynovitis:
  • Pathophysiology: Stenosing tenosynovitis of the first dorsal compartment of the wrist, affecting Abductor Pollicis Longus (APL) and Extensor Pollicis Brevis (EPB) tendons.
  • Causes: Repetitive thumb abduction and wrist ulnar deviation (e.g., new mothers lifting baby, repetitive gripping).
  • Symptoms: Pain and tenderness over the radial styloid, radiating up forearm or down to thumb. Swelling may be present.
  • Signs: Positive Finkelstein’s test (patient makes fist with thumb inside, then ulnarly deviates wrist, causing pain).
  • Management: Conservative (thumb spica splint, NSAIDs, activity modification, steroid injection into 1st dorsal compartment). Surgical release for refractory cases.

General Management Principles for Hand & Wrist Injuries

The goals of treatment are to restore anatomy, achieve stable fixation, allow early mobilisation where possible, and ultimately restore optimal function while minimising pain.

Initial Management (ED / Acute Setting):

• DRSABCD/ATLS: If part of major trauma.
• Control Haemorrhage: Direct pressure for bleeding.
• Analgesia: Provide adequate pain relief (e.g., paracetamol, NSAIDs, opioids if severe). Consider regional blocks (e.g., haematoma block for distal radius reduction).
• Neurovascular Assessment: Document pre- and post-intervention status.
• Reduction (if indicated): For displaced fractures or dislocations. Aim for anatomical alignment. Requires appropriate analgesia/anaesthesia.
• Immobilisation: Splint suspected or confirmed fractures/unstable injuries to provide pain relief, prevent further displacement, and protect soft tissues. Common splints: backslab, volar slab, U-slab, thumb spica.
• Elevation: To reduce swelling.
• Ice: Intermittent application to reduce swelling and pain.
• Wound Care: For open fractures/wounds: Clean, sterile dressing. Tetanus prophylaxis. Antibiotics (e.g., IV co-amoxiclav for open fractures).
• Referral: Refer to Orthopaedics/Hand Surgery as appropriate (e.g., open fractures, irreducible dislocations, neurovascular compromise, complex fractures needing surgery).

Non-Operative Management:

• Indications: Many stable, undisplaced or minimally displaced fractures, some ligament sprains, tendinopathies.
• Methods:
  • Casting/Splinting: For a defined period. Educate on cast care, red flag symptoms (e.g., tight cast, severe pain, numbness).
  • Buddy Taping: For stable phalangeal fractures.
  • Analgesia and Anti-inflammatories.
  • Physiotherapy/Occupational Therapy: For rehabilitation after immobilisation (ROM, strengthening, functional exercises).

Operative Management:

• General Indications:
  • Open fractures (require debridement and washout).
  • Unstable fractures (likely to displace in cast).
  • Irreducible fractures/dislocations.
  • Significantly displaced intra-articular fractures (e.g., >2mm step or gap).
  • Associated neurovascular injury requiring repair.
  • Certain fracture patterns known for poor outcomes with non-operative treatment (e.g., displaced scaphoid proximal pole, Bennett’s fracture).
  • Failed non-operative management (e.g., non-union, symptomatic malunion).
  • Tendon ruptures (e.g., FDP avulsion, some extensor tendon lacerations).
  • Significant ligamentous instability requiring repair/reconstruction.
• Common Surgical Techniques:
  • Open Reduction and Internal Fixation (ORIF): Using plates, screws, wires (e.g., volar plating for distal radius fractures, screw fixation for scaphoid).
  • Closed Reduction and Percutaneous Pinning (CRPP): Using Kirschner wires (K-wires) inserted through the skin to hold fracture fragments after closed reduction.
  • External Fixation: For severe open fractures, extensive soft tissue damage, or temporary stabilisation.
  • Tendon Repair/Reconstruction.
  • Ligament Repair/Reconstruction.
  • Nerve Repair/Decompression.
  • Arthrodesis (fusion) or Arthroplasty (joint replacement) for severe arthritis or unsalvageable joints.

Rehabilitation:

• Crucial for all significant hand/wrist injuries, whether managed operatively or non-operatively.
• Aims: Control pain and oedema, restore ROM, improve strength, restore function.
• Involves physiotherapists and occupational therapists (hand therapists).
• May include splinting, scar management, oedema control, specific exercises, and functional retraining.

Complications & Red Flags in Hand & Wrist Injuries

Red Flags (Require Urgent Senior Review / Intervention):

• Open Fracture:
  • Any fracture communicating with the external environment. High risk of infection (osteomyelitis).
  • Management: Urgent IV antibiotics (e.g., co-amoxiclav + gentamicin depending on severity/contamination), tetanus prophylaxis, surgical debridement and washout (usually within 6-24 hours). (Gustilo-Anderson classification for severity).
• Acute Neurovascular Compromise:
  • Signs: Pallor, pulselessness (late sign!), paraesthesia, paralysis, poikilothermia (coldness). Rapidly progressing neurological deficit.
  • Management: Immediate attempt at gentle realignment/reduction. If unsuccessful or deficit persists, urgent surgical exploration/decompression is required.
• Compartment Syndrome:
  • Increased pressure within a closed fascial compartment, compromising circulation and function of tissues within that space. Most common in forearm after supracondylar or distal radius fractures, or crush injuries. Can occur in hand intrinsic compartments.
  • Key Symptoms/Signs (The 6 P’s – but pain is earliest and most reliable):
    • Pain out of proportion to the injury, especially on passive stretch of muscles in the compartment (e.g., passive finger extension for forearm flexor compartment).
    • Paraesthesia (early sign of nerve ischaemia).
    • Pallor (late).
    • Pulselessness (very late and ominous sign).
    • Paralysis/Paresis (late).
    • Pressure (tense, swollen, tender compartment).
  • Diagnosis: Primarily clinical. Compartment pressure measurement can confirm if >30 mmHg or delta pressure (Diastolic BP – Compartment Pressure) <20-30 mmHg.
  • Management: Surgical emergency! Immediate removal of all constricting dressings/casts. Urgent fasciotomy to decompress all affected compartments. Delay can lead to Volkmann’s ischaemic contracture (irreversible muscle and nerve damage).
• Irreducible Dislocation / Gross Instability.
• “Fight Bite” (Human Bite over MCPJ):
  • Often appears innocuous but has very high risk of septic arthritis due to direct inoculation of oral flora (e.g., Eikenella corrodens) into joint.
  • Management: Thorough exploration (often in theatre), washout, debridement, IV antibiotics (e.g., co-amoxiclav). Do not close wound primarily.

Early Complications (Days to Weeks):

• Infection: Wound infection, pin-site infection, osteomyelitis, septic arthritis.
• Haematoma / Seroma.
• Loss of Reduction / Fixation Failure.
• Pressure Sores / Blisters: From poorly applied cast/splint.
• Thromboembolism (DVT/PE): Less common for isolated upper limb but risk increases with prolonged immobility, surgery, or polytrauma.

Late Complications (Weeks to Months/Years):

• Malunion: Fracture heals in a non-anatomical (angulated, rotated, shortened) position. Can cause pain, deformity, functional limitation, and secondary arthritis.
• Non-union: Fracture fails to heal after an adequate period (typically >6 months). Causes: poor blood supply (e.g., scaphoid proximal pole), instability, infection, smoking, systemic factors. X-ray: persistent fracture line, sclerotic bone ends.
• Avascular Necrosis (AVN): Bone death due to compromised blood supply. Common sites: scaphoid (proximal pole), lunate (Kienbock’s disease).
• Stiffness / Contractures: Very common. Due to immobilisation, oedema, adhesions, scarring. Requires intensive physiotherapy/hand therapy.
• Post-Traumatic Osteoarthritis: Degenerative joint changes following injury, especially intra-articular fractures or malunion.
• Complex Regional Pain Syndrome (CRPS):
  • Type 1 (formerly Reflex Sympathetic Dystrophy – RSD): No identifiable nerve injury.
  • Type 2 (formerly Causalgia): Identifiable nerve injury.
  • Features: Severe pain (burning, disproportionate), allodynia, hyperalgesia, swelling, stiffness, skin changes (colour, temperature, sweating abnormalities – “Sudeck’s atrophy”), trophic changes (hair, nails).
  • Management: Early recognition, multidisciplinary approach (pain team, physio/OT, psychology).
• Tendon Rupture (e.g., EPL rupture after distal radius #) or Adhesions.
• Nerve Damage Sequelae: Persistent numbness, weakness, chronic neuropathic pain.
• Implant-related Problems: Loosening, breakage, irritation, infection.

Flashcards: Hand & Wrist Injuries

Click on each card to reveal the answer.

History Taking for Shoulder Pain

A detailed history is crucial for narrowing down the differential diagnosis.

Key Areas to Cover (SOCRATES + Specifics):

• Site: Precise location of pain. Ask patient to point (“One finger test”). Is it localised or diffuse? Does it radiate?
  • e.g., Lateral deltoid area (rotator cuff, subacromial), superior (ACJ), anterior (biceps).
• Onset: Sudden (trauma, acute tear) or gradual/insidious (degenerative, overuse, inflammatory)?
• Character: Sharp, dull, aching, burning, throbbing?
• Radiation:
  • Down lateral arm (C5 dermatome – common in rotator cuff/subacromial pain, referred pain from neck).
  • To neck, scapula, or chest.
• Associated Symptoms:
  • Weakness: True weakness (tear, nerve issue) vs. pain inhibition.
  • Stiffness: Difficulty moving (e.g., frozen shoulder, OA). Morning stiffness?
  • Clicking, Clunking, Popping: Instability, labral tear, OA.
  • Locking/Catching: Loose body, labral tear.
  • Numbness/Paraesthesia: Cervical radiculopathy, brachial plexus issue, peripheral nerve entrapment.
  • Swelling, Bruising, Deformity.
  • Systemic symptoms: Fever, weight loss, malaise (red flags).
• Timing/Pattern:
  • Night Pain: Common in rotator cuff pathology, frozen shoulder, OA, malignancy. Difficulty lying on affected side?
  • Worse with specific activities (e.g., overhead, reaching behind back)?
  • Constant or intermittent?
• Exacerbating/Relieving Factors: What makes it worse/better? Rest vs. activity. Specific movements. Analgesia.
• Severity: Pain score (0-10). Impact on daily activities (ADLs), work, sleep, sport.
• Mechanism of Injury (if traumatic): Fall (FOOSH?), direct blow, forceful movement (e.g., throwing, lifting). Position of arm during injury.
• Past Medical History: Previous shoulder problems/surgery. Diabetes, thyroid disease (risk for frozen shoulder). Inflammatory conditions (RA, polymyalgia rheumatica). History of cancer.
• Drug History: Analgesics, steroids (oral/injected), anticoagulants.
• Occupation & Hobbies/Sports: Repetitive overhead activities, heavy lifting, throwing sports. Hand dominance.
• Patient’s Ideas, Concerns, and Expectations (ICE).

Physical Examination: Look, Feel, Move

A systematic examination is essential. Always compare with the contralateral (unaffected) side. Ensure adequate exposure of both shoulders (patient ideally topless or in a vest top).

1. Look (Inspection):

Inspect from anterior, lateral, and posterior aspects. Observe patient walking in and undressing.

• Symmetry: Compare both shoulders.
• Swelling: Localised (e.g., ACJ, bursa) or diffuse.
• Erythema, Rashes, Skin Changes.
• Scars: Previous surgery or trauma.
• Deformity:
  • Clavicle fracture, ACJ separation (“step deformity”).
  • Anterior shoulder dislocation (squared-off appearance, prominent acromion, anterior bulge).
  • Scapular position and symmetry.
• Muscle Wasting:
  • Supraspinatus/Infraspinatus: Wasting in fossae above/below scapular spine (suprascapular nerve palsy, chronic rotator cuff tear).
  • Deltoid: Axillary nerve injury.
• “Popeye” Sign: Bulge in lower anterior arm (rupture of long head of biceps).
• Scapular Winging: Medial (serratus anterior/long thoracic nerve) or lateral (trapezius/spinal accessory nerve). Ask patient to push against wall or do press-up.

2. Feel (Palpation):

Palpate systematically for tenderness, warmth, swelling, crepitus.

• Bony Landmarks:
  • Sternoclavicular joint (SCJ).
  • Clavicle (full length).
  • Acromioclavicular joint (ACJ) – often tender in ACJ pathology.
  • Acromion (anterolateral edge – subacromial tenderness).
  • Coracoid process.
  • Spine of scapula.
  • Greater tuberosity of humerus (attachment of supraspinatus, infraspinatus, teres minor).
  • Lesser tuberosity (attachment of subscapularis).
  • Bicipital groove (between tuberosities, for long head of biceps tendon).
• Soft Tissues:
  • Rotator cuff tendons (especially supraspinatus insertion).
  • Biceps tendon in its groove.
  • Deltoid muscle.
  • Trapezius and periscapular muscles.
  • Axilla (for lymph nodes if relevant).
• Assess temperature.

3. Move (Range of Motion – ROM):

Assess active ROM first, then passive ROM if active is restricted. Note pain, crepitus, and quality of movement. Isolate glenohumeral movement by stabilising scapula if needed.

• Active ROM:
  • Forward Flexion: (Normal ~180°) “Raise your arms forward as high as you can.”
  • Extension: (Normal ~50-60°) “Reach your arms backwards.”
  • Abduction: (Normal ~180°) “Raise your arms out to the sides.” Observe for painful arc (typically 60-120° in subacromial impingement/RC pathology). Note scapulohumeral rhythm.
  • Adduction: (Normal ~30-45°) “Bring your arm across your body.”
  • External Rotation (ER):
    • Arms by side, elbows flexed to 90°: “Turn your forearms outwards.” (Normal ~70-90°)
    • Arms abducted to 90° (if possible): “Keep your elbows high and rotate your hands backwards.” (Normal ~90°)
  • Internal Rotation (IR):
    • “Reach up your back as far as you can.” Record highest vertebral level reached (e.g., T7, L3, buttock). (Combined adduction, IR, extension). This is Apley’s Scratch Test component.
    • Can also test with arms abducted to 90° (if possible): “Rotate your hands forwards/downwards.”
• Passive ROM:
  • Gently take the patient’s arm through the same movements if active ROM is limited.
  • Assess if passive ROM is greater than active (suggests weakness or pain inhibition if full passive; suggests true stiffness/contracture if passive also limited e.g. frozen shoulder, OA).
  • Note end-feel (e.g., bony block, capsular tightness, muscle spasm).
• Resisted ROM (Isometric Muscle Testing):
  • Assess power (MRC grade 0-5) and pain for key muscle groups. Stabilise proximally.
  • Supraspinatus (Abduction): Jobe’s test position (see Special Tests).
  • Infraspinatus/Teres Minor (External Rotation): Patient’s arm by side, elbow 90° flexed, resist ER.
  • Subscapularis (Internal Rotation): Gerber’s lift-off or Belly press (see Special Tests).
  • Deltoid (Abduction): Resist abduction with arm at 90°.
  • Biceps (Flexion/Supination): Resist elbow flexion and forearm supination.
• Scapular Dyskinesis Assessment: Observe scapular movement during arm elevation/lowering. Look for abnormal winging, shrugging, or lack of smooth coordinated motion.

Special Tests: Impingement & Rotator Cuff

These provocative tests aim to reproduce the patient’s pain and help identify specific pathologies. Sensitivity and specificity vary; interpret in context of full assessment. Perform gently and warn patient about potential discomfort.

Subacromial Impingement Tests:

• Neer’s Test:
  • Procedure: Examiner passively flexes the patient’s internally rotated arm maximally (stabilise scapula).
  • Positive: Pain reproduced in anterior/lateral shoulder (impingement of supraspinatus tendon/bursa under acromion).
• Hawkins-Kennedy Test:
  • Procedure: Patient’s arm flexed to 90°, elbow flexed to 90°. Examiner passively internally rotates the arm.
  • Positive: Pain reproduced (impingement of supraspinatus tendon against coracoacromial ligament).

Rotator Cuff Integrity Tests:

• Supraspinatus Tests:
  • Jobe’s Test (Empty Can Test):
    • Procedure: Arm abducted to 90° in scapular plane (~30° anterior to coronal), thumb pointing down (full internal rotation). Examiner applies downward pressure.
    • Positive: Pain and/or weakness (supraspinatus tendinopathy/tear).
  • Drop Arm Test:
    • Procedure: Passively abduct patient’s arm to 90°. Ask them to slowly lower it.
    • Positive: Arm drops uncontrollably or patient has significant difficulty lowering it slowly (suggests large supraspinatus tear).
• Infraspinatus & Teres Minor Tests (External Rotation):
  • Resisted External Rotation:
    • Procedure: Arm by side, elbow 90° flexed. Patient attempts to externally rotate against resistance.
    • Positive: Pain and/or weakness.
  • External Rotation Lag Sign:
    • Procedure: Passively place arm in near maximal external rotation (elbow 90° flexed, by side or 90° abducted). Ask patient to hold.
    • Positive: Arm “lags” or drops into internal rotation (significant infraspinatus/teres minor tear).
• Subscapularis Tests (Internal Rotation):
  • Gerber’s Lift-Off Test:
    • Procedure: Patient places dorsum of hand on their lower back. Asks to lift hand away from back.
    • Positive: Inability to lift hand off back (subscapularis tear). If cannot get hand there, proceed to belly press.
  • Belly Press Test (Napoleon Sign):
    • Procedure: Patient places hand on their abdomen and presses inwards. Elbow should remain anterior.
    • Positive: Weakness, or if elbow drops backwards/wrist flexes to compensate (subscapularis tear).
  • Internal Rotation Lag Sign:
    • Procedure: Examiner passively lifts hand off back (as in Gerber’s) and asks patient to hold it there.
    • Positive: Hand drops back onto back (subscapularis tear).

Special Tests: ACJ, Biceps Tendon & Instability

Further tests to assess other common sources of shoulder pain and dysfunction.

Acromioclavicular Joint (ACJ) Tests:

• Direct Palpation of ACJ: Tenderness directly over the ACJ is a key sign.
• Scarf Test (Cross-Body Adduction Test):
  • Procedure: Patient’s arm flexed to 90°, elbow flexed. Examiner passively adducts the arm across the patient’s chest.
  • Positive: Pain localised to the ACJ.
• O’Brien’s Test (Active Compression Test – can also indicate SLAP lesion):
  • Part 1: Arm flexed to 90°, adducted 10-15°, fully internally rotated (thumb down). Examiner applies downward pressure.
  • Part 2: Arm in same position but fully externally rotated (thumb up). Examiner applies downward pressure.
  • Positive for ACJ: Pain localised to ACJ in Part 1, reduced/absent in Part 2. (If pain is deep/diffuse, more suggestive of labral issue).

Biceps Tendon Tests (Long Head):

• Speed’s Test:
  • Procedure: Patient’s arm flexed forward to ~60-90°, elbow extended, forearm supinated. Examiner resists further forward flexion.
  • Positive: Pain in the bicipital groove (biceps tendinopathy or SLAP lesion).
• Yergason’s Test:
  • Procedure: Patient’s elbow flexed to 90°, forearm pronated. Examiner holds patient’s wrist and resists active supination and external rotation of the shoulder.
  • Positive: Pain in bicipital groove (biceps tendinopathy, instability of biceps tendon in groove). Some find this difficult to elicit.
• Palpation of bicipital groove for tenderness.

Glenohumeral Instability Tests:

Perform with caution, especially if history of dislocation. Stop if patient is apprehensive or pain is severe.

• Anterior Apprehension Test:
  • Procedure: Patient supine or sitting. Shoulder abducted to 90°, elbow flexed 90°. Examiner gently externally rotates the arm.
  • Positive: Patient expresses apprehension (fear of dislocation) or pain. (Tests anterior instability).
• Relocation Test (Jobe’s Relocation Test):
  • Procedure: If apprehension test is positive, apply posteriorly directed pressure to the anterior humeral head while maintaining external rotation.
  • Positive: Relief of apprehension or pain (confirms anterior instability).
• Sulcus Sign:
  • Procedure: Patient sitting or standing with arm relaxed by side. Examiner applies downward traction on the arm.
  • Positive: Appearance of a sulcus (indentation) below the acromion (indicates inferior instability / multidirectional instability). Grade by size of sulcus.
• Posterior instability tests (e.g., Posterior Apprehension Test) are less commonly performed in primary care screening.

Labral Tear Tests (e.g., SLAP Lesion – Superior Labrum Anterior to Posterior):

• O’Brien’s Test (Active Compression Test) – as above:
  • Positive for SLAP lesion: Deep, diffuse pain within the shoulder in Part 1 (thumb down), reduced/absent in Part 2 (thumb up). Clicking may be present.
• Other labral tests (e.g., Crank test, Biceps Load test) are more for specialist settings.

Common Shoulder Conditions & Differential Diagnosis

Based on history and examination, a working diagnosis can often be formed.

Common Shoulder Pathologies:

Important Differential Diagnoses (Pain Referred to Shoulder):

• Cervical Spine Disease: Radiculopathy (dermatomal pain, paraesthesia, weakness, reflex changes), facet joint arthropathy, myofascial neck pain. Always consider C-spine screen.
• Myocardial Ischaemia/Infarction: Especially left shoulder/arm pain. Consider with cardiac risk factors, exertional pain, associated symptoms (chest pain, SOB, sweating).
• Diaphragmatic Irritation: (e.g., gallbladder disease, subphrenic abscess) – pain referred to shoulder tip (Kehr’s sign).
• Polymyalgia Rheumatica (PMR): Bilateral shoulder/hip girdle pain and stiffness, morning stiffness >45 mins, age >50, raised ESR/CRP. Responds dramatically to steroids.
• Malignancy: (e.g., Pancoast tumour, bony metastases) – consider with red flags.
• Peripheral nerve entrapment (e.g., suprascapular nerve).

Red Flags & Investigations in Shoulder Pain

Recognizing red flags is crucial to identify serious underlying pathology. Investigations are guided by clinical suspicion.

Red Flags in Shoulder Pain:

• History of Significant Trauma: Suspect fracture (humerus, clavicle, scapula) or acute large rotator cuff tear / dislocation. Urgent assessment/imaging.
• Unexplained Deformity or Swelling.
• Suspected Infection (Septic Arthritis/Osteomyelitis): Fever, chills, systemic illness, hot/red/swollen joint, severe pain with minimal movement. Urgent hospital admission.
• Suspected Malignancy (Primary or Metastatic):
  • History of cancer.
  • Unexplained weight loss, night sweats, persistent severe night pain not relieved by position change.
  • Age >50 with new onset, unremitting pain.
  • Palpable mass.
• Unexplained Neurological Deficit: Significant, progressive weakness or sensory loss not fitting a simple nerve root or peripheral nerve pattern, or suggesting brachial plexopathy / cord lesion.
• Vascular Compromise: Absent pulses, pallor, coldness of limb (rare, but consider in trauma or thoracic outlet syndrome).
• Systemic Inflammatory Condition: e.g., suspicion of PMR, RA with acute flare.
• Inability to Actively Move Arm (especially after trauma).
• Pain that is Unremitting, Severe, and Worsening Despite Conservative Measures.

Investigations:

Not always needed for common conditions if diagnosis clear clinically. Indicated if red flags, diagnostic uncertainty, failure to respond to conservative treatment, or pre-operative planning.

• Bloods:
  • FBC, ESR, CRP: If infection or inflammatory condition (e.g., PMR, RA) suspected.
  • U&E, LFTs, Bone profile (Calcium, ALP): If malignancy or metabolic bone disease suspected.
  • Rheumatoid Factor, Anti-CCP: If RA suspected.
• X-rays:
  • Standard views: AP (anteroposterior), axillary lateral, and/or Grashey view (true AP of glenohumeral joint). Outlet view (Y-scapular view) can show acromial morphology.
  • Indications: Trauma (fracture/dislocation), suspected OA, calcific tendinitis, instability (e.g., Hill-Sachs, Bankart lesions), assessing acromial morphology, ruling out gross bony pathology. Often first-line imaging.
• Ultrasound (USS):
  • Indications: Suspected rotator cuff tears (good for full-thickness, less for partial), tendinopathy, bursitis, biceps tendon pathology, dynamic assessment of impingement.
  • Advantages: Non-invasive, no radiation, dynamic, can guide injections.
  • Disadvantages: Operator dependent, limited view of intra-articular structures (e.g., labrum) and bone.
• Magnetic Resonance Imaging (MRI):
  • Indications: Detailed assessment of soft tissues (rotator cuff, labrum, ligaments, cartilage, capsule), bone marrow oedema, occult fractures, tumours. Used when diagnosis unclear after X-ray/USS, or for pre-operative planning.
  • MRI Arthrography (MRA): MRI with intra-articular contrast. Best for labral tears (e.g., SLAP lesions) and subtle instability.
• CT Scan: Less common for routine shoulder pain. Used for complex fractures, bony detail, pre-op planning for joint replacement if MRI contraindicated.
• Nerve Conduction Studies / EMG: If neurological cause suspected (e.g., peripheral nerve entrapment, radiculopathy, plexopathy).

OSCE Tips & Examination Summary for Shoulder Pain

General OSCE Approach (WIPER + Structured Exam):

• Wash hands, Introduce self, Patient ID & consent, Expose adequately (both shoulders, remove top), Reposition (standing/sitting as needed).
• “I’ve been asked to examine your shoulder today. This will involve me looking at your shoulder, feeling around the area, and asking you to do some movements. I’ll also do some special tests. Please let me know if you feel any pain at any point.”
• Always compare with the asymptomatic side.
• Start with observation while patient walks in and undresses if possible.
• A logical sequence: Look → Feel → Move (Active, then Passive, then Resisted) → Special Tests.
• Don’t forget to screen the neck and elbow if relevant/time permits.
• Verbalise your findings clearly.
• Summarise positive findings and offer a differential diagnosis at the end if asked.

Key Steps in Shoulder Examination Sequence:

1. Inspection (Anterior, Lateral, Posterior): Scars, swelling, erythema, deformity, muscle wasting (supraspinatus, infraspinatus, deltoid), symmetry, scapular position. Popeye sign.
2. Palpation:
   • Bony: SCJ, clavicle, ACJ, acromion, coracoid, greater/lesser tuberosities, bicipital groove.
   • Soft tissue: Rotator cuff insertion points, biceps tendon.
3. Active Range of Motion:
   • Forward Flexion, Extension.
   • Abduction (note painful arc), Adduction.
   • External Rotation (arm by side, and 90° abduction).
   • Internal Rotation (hand up back – Apley’s scratch test component).
4. Passive Range of Motion (if active limited):
   • Gently assess same movements, note end-feel and if greater than active.
5. Resisted Range of Motion (Isometric):
   • Supraspinatus (Jobe’s position).
   • Infraspinatus/Teres Minor (ER by side).
   • Subscapularis (Gerber’s/Belly Press).
   • Deltoid (Abduction at 90°).
   • Biceps (Elbow flexion/supination).
6. Special Tests (Select based on history and findings):
   • Impingement: Neer’s, Hawkins-Kennedy.
   • Rotator Cuff: Jobe’s, Drop Arm, Resisted ER, ER Lag, Gerber’s/Belly Press, IR Lag.
   • ACJ: Scarf test, O’Brien’s (for ACJ).
   • Biceps: Speed’s, Yergason’s.
   • Instability: Apprehension, Relocation, Sulcus sign.
   • (SLAP: O’Brien’s – deep pain)
7. Neurovascular Assessment (if indicated): Peripheral pulses, sensation (axillary nerve for deltoid patch), motor function.
8. Cervical Spine Screen (if indicated): ROM, Spurling’s test.

Summarising Findings:

“On examination of Mr./Ms. [Patient Name]’s [left/right] shoulder, key findings include [e.g., wasting of the supraspinatus fossa, tenderness over the ACJ, a painful arc on abduction, positive Jobe’s test with weakness, restricted external rotation both actively and passively…]. These findings are suggestive of [top differential, e.g., rotator cuff pathology, likely a supraspinatus tear, or adhesive capsulitis]. I would also consider [other differentials]. To complete my assessment, I would [e.g., perform a neurovascular assessment of the limb, examine the cervical spine, consider appropriate investigations like an X-ray or ultrasound].”

Flashcards: Shoulder Pain Assessment

Click on each card to reveal the answer.

Pathophysiology & Key Risks

The communication with the external environment introduces several critical challenges.

Pathophysiological Consequences:

• Bacterial Contamination: The skin barrier is breached, allowing bacteria from the environment, skin flora, or penetrating object to access the fracture site and bone. This is the primary driver of infection risk.
• Soft Tissue Damage: The energy required to cause an open fracture often results in significant damage to surrounding muscles, tendons, nerves, and blood vessels. This devitalized tissue provides a nidus for infection and impairs healing.
• Disruption of Blood Supply: Both to the bone fragments (periosteal stripping, endosteal damage) and the overlying soft tissues. This compromises healing potential and immune response.
• Inflammatory Response: Trauma and contamination trigger a significant local and systemic inflammatory response.
• Fracture Haematoma Exposure: The fracture haematoma, rich in growth factors essential for healing, is exposed and potentially lost or contaminated.

Key Risks:

• Infection:
  • Superficial wound infection.
  • Deep infection / Osteomyelitis: Infection of the bone itself. Can be very difficult to eradicate and may lead to chronic problems, non-union, and need for amputation. Risk increases with severity of soft tissue injury (Gustilo grade).
  • Gas gangrene (Clostridial myonecrosis): Rare but life-threatening, associated with severe contamination (e.g., agricultural injuries).
• Neurovascular Injury: Direct trauma to nerves and vessels, or secondary compromise from swelling/compartment syndrome. Requires careful assessment and prompt management. Gustilo IIIC fractures involve arterial injury requiring repair.
• Compartment Syndrome: Increased pressure within a fascial compartment, compromising circulation and function. High risk in tibial and forearm fractures. Clinical diagnosis (pain out of proportion, pain on passive stretch, tense compartment).
• Delayed Union / Non-Union / Malunion: Impaired healing due to infection, poor blood supply, instability, or significant bone loss.
• Soft Tissue Complications: Wound breakdown, need for complex soft tissue reconstruction (flaps).
• Systemic Complications: Sepsis, DVT/PE, fat embolism (especially with long bone fractures).
• Chronic Pain & Functional Impairment.
• Amputation: May be necessary for severe, unsalvageable injuries or intractable infection.

Initial Assessment (ATLS Principles)

Open fractures, especially from high-energy trauma, often occur in polytrauma patients. A systematic ATLS approach is paramount.

Primary Survey (ABCDE):

• A – Airway with C-spine protection: Ensure patent airway. If trauma, maintain c-spine immobilisation until cleared.
• B – Breathing and Ventilation: Assess respiratory rate, effort, oxygen saturation, chest expansion, air entry. Administer high-flow oxygen. Manage life-threatening chest injuries (e.g., tension pneumothorax).
• C – Circulation with Haemorrhage Control:
  • Assess pulse, blood pressure, capillary refill, level of consciousness. Look for signs of shock.
  • Control external haemorrhage from the open fracture: Direct pressure, elevation. Tourniquets may be needed for life-threatening bleeding (note time of application). Avoid blind clamping.
  • Establish IV access (2 large-bore cannulae). Take bloods (FBC, U&E, Coag, Group & Save/Crossmatch). Start IV fluids if shocked.
• D – Disability (Neurological Status): Glasgow Coma Scale (GCS), pupil size/reactivity, gross motor/sensory function in all limbs.
• E – Exposure and Environment: Fully expose patient to assess for other injuries, preventing hypothermia.

Secondary Survey (after primary survey and resuscitation):

Focus on the injured limb once life-threatening conditions are addressed/managed.

• History (AMPLE): Allergies, Medications, Past medical history, Last meal, Events/Environment related to injury. Mechanism of injury is crucial (high vs. low energy, type of force).
• Detailed Examination of the Injured Limb:
  • Look: Wound size, location, contamination (dirt, foreign bodies), skin viability, deformity, swelling, bruising. Take photographs if possible before dressing, for documentation and communication.
  • Feel: Palpate for tenderness, crepitus, compartment tension. Assess peripheral pulses, capillary refill, skin temperature.
  • Move: Assess active/passive movement if possible (often limited by pain/instability). Document if movement not assessed due to pain.
  • Neurovascular Assessment: CRITICAL. Document pre-reduction and post-reduction/splinting.
    • Vascular: Pulses (distal to injury), capillary refill time, skin colour, temperature. Doppler USS if pulses impalpable. Consider Ankle-Brachial Pressure Index (ABPI).
    • Neurological: Sensation (light touch, pinprick in specific nerve distributions), motor function (specific muscle groups distal to injury). Identify specific nerve at risk based on fracture location.

Emergency Management (Pre-hospital / Emergency Department)

Time-critical interventions to reduce complications and prepare for surgery.

Immediate Actions:

1. ABCDE Assessment and Resuscitation: (As per previous section). Life-saving measures take priority.
2. Control Haemorrhage:
   • Direct pressure is first-line.
   • Elevation of the limb.
   • If severe arterial bleeding unresponsive to direct pressure, a tourniquet may be applied (proximal to wound). Note time of application. Ensure it’s tight enough to stop arterial flow.
3. Remove Gross Contaminants & Cover Wound:
   • Gently remove any obvious gross debris (e.g., large pieces of dirt, grass) from the surface of the wound without deep probing.
   • Cover the wound with a sterile, saline-soaked gauze dressing, then an occlusive dressing. This helps prevent further contamination and desiccation of tissues.
4. Analgesia: Provide adequate pain relief (e.g., IV opioids like Morphine or Fentanyl). Consider regional nerve blocks if appropriate and expertise available.
5. Realign & Splint:
   • If significant deformity or evidence of neurovascular compromise, attempt gentle realignment of the limb to a more anatomical position. Document neurovascular status before and after.
   • Immobilise the injured limb using an appropriate splint (e.g., backslab, traction splint for femur, collar & cuff for upper limb) to reduce pain, prevent further soft tissue damage, and protect neurovascular structures. Ensure splint allows for neurovascular checks.
6. Photographs: Take clinical photographs of the wound (after gross decontamination, before dressing) if possible. Essential for documentation, communication with specialist teams, and medico-legal purposes.
7. IV Antibiotics: Administer broad-spectrum IV antibiotics as soon as possible (ideally within 1 hour of injury or presentation). Choice depends on local guidelines and Gustilo-Anderson grade (see specific section).
8. Tetanus Prophylaxis: Assess tetanus immunization status and administer booster and/or immunoglobulin as indicated (see specific section).
9. Imaging:
   • X-rays of the entire affected bone (AP and lateral views), including joints above and below the fracture.
   • Consider imaging of other areas if polytrauma.
   • CT scan may be needed for complex intra-articular fractures or to assess vascular injury (CT angiogram).
10. NBM (Nil By Mouth): In anticipation of urgent surgery.
11. Urgent Orthopaedic Referral: All open fractures require urgent discussion with the on-call orthopaedic team for surgical debridement and management. Plastic surgery involvement may also be needed for severe soft tissue injuries.

Gustilo-Anderson Classification of Open Fractures

This is the most widely used classification system, guiding treatment and predicting prognosis (especially infection risk). It’s based on wound size, degree of soft tissue injury, contamination, and fracture pattern.

Important Considerations:

• Classification is primarily made intra-operatively by the surgeon after debridement, as the full extent of injury may not be apparent externally.
• High-energy injuries (e.g., gunshot, farm injuries, crush) are typically at least Type IIIA, even if the skin wound appears small.
• Contamination with farm soil, sewage, or stagnant water significantly increases infection risk (consider Gram-negative and anaerobic cover).
• The higher the grade, the higher the risk of infection, non-union, and amputation.

Surgical Principles: Debridement, Irrigation, Stabilisation, & Coverage

The goals of surgery are to prevent infection, achieve bone union, and restore function. This involves several key steps, often summarised by the “6 D’s” or similar frameworks.

The “6 D’s” of Open Fracture Management (common framework):

1. Debridement (Excision):
   • This is the single most important step in preventing infection.
   • Involves meticulous surgical removal of all non-viable skin, subcutaneous tissue, muscle, and bone fragments. “Excise until it bleeds.”
   • Foreign material (dirt, clothing, debris) must be completely removed.
   • Wound edges are often excised back to healthy bleeding tissue.
   • Small, completely detached bone fragments without soft tissue attachment are usually removed as they are avascular and can act as a nidus for infection. Larger structural fragments may be retained if clean and viable.
2. Decontamination (Irrigation):
   • Copious irrigation of the wound and fracture site with large volumes of sterile fluid (typically normal saline).
   • Aims to mechanically remove bacteria, debris, and reduce contaminant load.
   • Historically, high-pressure pulsatile lavage was used, but evidence now suggests low-pressure lavage is equally effective and potentially less damaging to tissues.
   • Volume of irrigation fluid often cited: e.g., 3L for Type I, 6L for Type II, 9L+ for Type III (though evidence for specific volumes is debated; thoroughness is key).
3. Decision on Bone (Stabilisation):
   • Fracture reduction and stabilisation are essential for soft tissue healing, bone union, patient comfort, and mobilisation.
   • External Fixation: Often used for initial stabilisation in severe (Type IIIA/B/C) open fractures, especially with gross contamination or significant soft tissue injury. Allows access for wound care and further debridements. Can be converted to internal fixation later.
   • Internal Fixation:
     • Intramedullary Nailing (IMN): Preferred for many diaphyseal long bone fractures (e.g., tibia, femur) if soft tissue allows and contamination is manageable. Can be done at initial surgery or delayed.
     • Plates and Screws: Used for periarticular fractures or fractures not amenable to nailing. Risk of infection is higher if placed under compromised soft tissue.
   • The choice and timing of fixation depend on fracture type, severity, contamination, soft tissue status, and patient factors.
4. Dead Space Management:
   • Large soft tissue or bone defects (“dead space”) can fill with haematoma and become a focus for infection.
   • May require antibiotic-impregnated cement beads/spacers, bone grafting (later), or muscle flaps to obliterate dead space.
5. Definitive Soft Tissue Coverage (Closure):
   • Goal is to achieve durable soft tissue coverage over the fracture site as soon as possible after adequate debridement (usually within 5-7 days if staged).
   • Delayed Primary Closure: For less severe wounds (Type I, some Type II) if clean after initial debridement.
   • Skin Grafts (Split or Full Thickness): Require a vascularised bed.
   • Local or Free Flaps (Plastic Surgery): For larger defects or exposed bone/tendon/implants (Type IIIB). Involves transferring skin, subcutaneous tissue, fascia, and/or muscle with its blood supply.
   • Negative Pressure Wound Therapy (NPWT / VAC dressing): Can be used as a temporary measure to manage wounds, promote granulation tissue, and reduce oedema while awaiting definitive closure.
6. Delayed Reconstruction / Rehabilitation: Bone grafting for defects, management of non-union, and intensive physiotherapy are often part of the longer-term plan.

Note: Some frameworks use slightly different “D” terms (e.g., Drugs for antibiotics), but the core principles of debridement, irrigation, stabilisation, and soft tissue coverage remain central.

Antibiotics & Tetanus Prophylaxis

These are critical adjuncts to surgical management in preventing infection.

Antibiotic Therapy:

• Timing: Administer IV antibiotics ASAP after injury, ideally within 1 hour (or 3 hours at latest from injury to first dose). Pre-operative administration is crucial.
• Duration:
  • Typically continued for 24-72 hours post-operatively for uncomplicated Type I and II fractures after adequate debridement and closure.
  • For Type III fractures, or if gross contamination, delayed closure, or multiple debridements, antibiotics are often continued for longer (e.g., 5-7 days or until definitive soft tissue coverage). Duration guided by microbiology, clinical picture, and local policies.
• Choice of Antibiotics (General Guidelines – Always follow local hospital policy/microbiology advice):
  Gustilo-Anderson Type

  Recommended IV Antibiotic Cover

  Type I & II

  First-generation Cephalosporin (e.g., Cefazolin/Cefuroxime). If penicillin allergic: Clindamycin or Vancomycin.

  Type IIIA, IIIB, IIIC

  First-generation Cephalosporin PLUS an Aminoglycoside (e.g., Gentamicin) for Gram-negative cover.
  OR Broad-spectrum Beta-Lactam/Beta-Lactamase inhibitor (e.g. Piperacillin-Tazobactam, Co-amoxiclav).

  Farm/Agricultural Injuries or Gross Contamination with Soil/Sewage

  As for Type III, PLUS consider adding Penicillin G (for Clostridia) and/or Metronidazole (for anaerobes). Some guidelines recommend Piperacillin-Tazobactam + Gentamicin.

  Marine Contamination (salt water)

  Cover for Vibrio species (e.g., Doxycycline or Ciprofloxacin) in addition to standard cover.
• Intra-operative wound cultures are often taken, especially in Type III injuries, to guide later antibiotic therapy if infection develops, but initial empirical therapy should not be delayed.
• Local antibiotic delivery (e.g., antibiotic-loaded cement beads) may be used in high-risk cases.

Tetanus Prophylaxis:

• All open fractures are considered tetanus-prone wounds.
• Assess patient’s immunisation history.
• General Guidelines (UK – Green Book):
  • Fully immunised (≥3 doses of tetanus toxoid, last dose <10 years ago): No booster needed generally for clean wounds. For tetanus-prone wounds (like open fractures), give a reinforcing dose of tetanus-containing vaccine if >5 years since last dose, or if high-risk wound.
  • Fully immunised (last dose >10 years ago): Give reinforcing dose of tetanus-containing vaccine.
  • Incompletely immunised (<3 doses or unknown status): Give a dose of tetanus-containing vaccine immediately. Arrange completion of full course. Human Tetanus Immunoglobulin (HTIG) should also be given for tetanus-prone wounds if significant contamination or devitalised tissue.
  • For heavily contaminated wounds (e.g., soil, manure) in incompletely immunised individuals, HTIG is usually recommended in addition to vaccine.
• Always consult local guidelines and patient’s vaccination record.

Post-Operative & Definitive Care Considerations

Management extends well beyond the initial surgery, often involving staged procedures and long-term rehabilitation.

Early Post-Operative Period:

• Wound Monitoring: Regular checks for signs of infection (erythema, swelling, discharge, increasing pain), wound breakdown, or flap necrosis.
• Neurovascular Observations: Continue frequent checks, especially if external fixator in situ or risk of compartment syndrome.
• Pain Management: Adequate multimodal analgesia.
• Antibiotics: Continue IV antibiotics as planned, then consider switch to oral based on clinical progress and microbiology (if available).
• DVT Prophylaxis: Mechanical (e.g., anti-embolic stockings, calf pumps) and/or pharmacological (e.g., LMWH) as per local policy, especially for lower limb fractures or reduced mobility.
• Nutritional Support: Important for wound and bone healing, especially in polytrauma or malnourished patients.
• Elevation of the Limb: To reduce swelling.

Staged Management & Definitive Reconstruction:

• Second Look / Further Debridements: Often planned 24-72 hours after initial surgery, especially for severe injuries, to reassess tissue viability and perform further debridement if needed.
• Definitive Soft Tissue Coverage: If not done at initial surgery, planned within 5-7 days once wound is clean (e.g., delayed primary closure, skin graft, flap).
• Conversion of Fixation: External fixators may be converted to internal fixation (e.g., IM nail, plate) once soft tissues have settled and infection risk is reduced, if appropriate for fracture pattern.
• Bone Grafting: May be required for significant bone loss or to promote union in non-healing fractures. Can be autograft (from patient, e.g., iliac crest) or allograft (donor bone) or synthetic substitutes. Usually performed as a delayed procedure once soft tissues stable and infection controlled.

Rehabilitation:

• Early Mobilisation: As tolerated and permitted by fracture stability and soft tissue status. Crucial to prevent stiffness, muscle atrophy, and DVT.
• Physiotherapy: Essential for restoring range of motion, strength, and function. Starts early post-op.
• Occupational Therapy: To assist with activities of daily living and return to work/hobbies.
• Weight-bearing status will be determined by the orthopaedic surgeon based on fracture type, stability, and fixation.

Long-Term Follow-Up:

• Regular outpatient clinic reviews with serial X-rays to monitor fracture healing and detect complications.
• Address psychological impact (e.g., PTSD, depression, anxiety related to trauma and prolonged recovery).
• Management of chronic pain if it develops.
• Vocational rehabilitation if needed.

Complications of Open Fractures

Open fractures are prone to a range of early and late complications.

Early Complications (Days to Weeks):

• Infection:
  • Superficial Wound Infection: Cellulitis around the wound.
  • Deep Wound Infection / Abscess: May involve muscle, fascia.
  • Osteomyelitis: Bone infection. Can become chronic and very difficult to treat.
  • Gas Gangrene (Clostridial Myonecrosis): Rare but life-threatening. Rapid onset of severe pain, swelling, crepitus, systemic toxicity. Requires aggressive surgical debridement and antibiotics.
  • Sepsis: Systemic response to infection.
• Compartment Syndrome: Increased pressure within a fascial compartment impairing perfusion. Clinical diagnosis: pain out of proportion (especially on passive stretch), tense compartment, paraesthesia, weakness. Pulselessness is a LATE sign. Requires urgent fasciotomy.
• Neurovascular Injury: Damage to nerves or blood vessels from initial trauma or subsequent swelling/surgery. May require vascular repair or nerve exploration/grafting.
• Haemorrhage / Haematoma Formation.
• Fat Embolism Syndrome: Rare, typically with long bone fractures. Respiratory distress, neurological signs, petechial rash.
• DVT/PE: Due to immobility and trauma.
• Wound Breakdown / Flap Failure.
• Fixation Failure: e.g., pin site infection with external fixators, implant loosening.

Late Complications (Months to Years):

• Delayed Union: Fracture healing takes longer than expected (typically >3-6 months).
• Non-Union: Fracture fails to heal (typically >6-9 months with no progress). Can be hypertrophic (callus present but not bridging) or atrophic (no callus). Often requires further surgery (e.g., bone grafting, revision fixation). Infection is a major cause of non-union.
• Malunion: Fracture heals in an incorrect or deformed position, leading to functional impairment or cosmetic issues.
• Chronic Osteomyelitis: Persistent bone infection, often with sinus tracts, recurrent flare-ups. May require multiple debridements, long-term antibiotics, and sometimes amputation.
• Joint Stiffness / Contractures: Common after prolonged immobilisation or intra-articular injury.
• Post-Traumatic Osteoarthritis: Especially with intra-articular fractures.
• Chronic Pain Syndromes (e.g., Complex Regional Pain Syndrome – CRPS).
• Psychological Sequelae: PTSD, depression, anxiety, body image issues.
• Amputation: May be a late consequence of intractable infection, severe non-union, or chronic pain where limb salvage is not feasible or desired by patient.
• Muscle Weakness and Atrophy.

MDT Approach & Long-Term Management (GP Role)

Successful management of open fractures relies on a coordinated multidisciplinary team (MDT) approach. GPs play a key role in long-term follow-up and support.

The Multidisciplinary Team (MDT):

• Orthopaedic Surgeons: Lead surgical management (debridement, fracture stabilisation).
• Plastic Surgeons: Involved in complex soft tissue reconstruction (flaps, grafts), especially for Type IIIB/C injuries.
• Emergency Department Physicians & Nurses: Initial assessment, resuscitation, and emergency interventions.
• Anaesthetists & Critical Care Physicians: Peri-operative care, pain management, management of polytrauma.
• Radiologists: Imaging and interpretation. Interventional radiologists for angiography/embolisation if needed.
• Microbiologists & Infectious Disease Physicians: Guide antibiotic therapy, manage complex infections.
• Physiotherapists: Crucial for rehabilitation, restoring mobility and strength.
• Occupational Therapists: Assist with ADLs, functional adaptation, return to work.
• Specialist Nurses (e.g., Trauma Nurse Coordinators, Tissue Viability Nurses): Coordinate care, wound management.
• Dietitians: Nutritional support for healing.
• Social Workers & Psychologists: Address psychosocial impact, support for patient and family.
• Prosthetists/Orthotists: If amputation or specialised bracing needed.

Role of the General Practitioner (GP) in Long-Term Management:

Once discharged from hospital, the GP often becomes a key point of contact for ongoing care and support.

• Wound Care Monitoring: Liaise with community nurses. Monitor for signs of superficial infection (erythema, warmth, discharge, increasing pain) or wound breakdown after discharge.
• Recognising Signs of Deep Infection / Osteomyelitis: Persistent pain, recurrent discharge, sinus formation, fevers, general malaise. Prompt re-referral to orthopaedics if suspected.
• Pain Management: Continue and adjust analgesia as needed, stepping down opioids where possible. Consider neuropathic pain agents if indicated.
• Monitoring Fracture Healing (indirectly): Be aware of planned orthopaedic follow-up and expected healing timelines. Note persistent pain or instability.
• DVT/PE Prophylaxis & Monitoring: Ensure appropriate duration of thromboprophylaxis. Be alert for symptoms of DVT/PE.
• Psychological Support: Screen for and manage/refer for anxiety, depression, PTSD. These are common after severe trauma.
• Supporting Rehabilitation: Encourage adherence to physiotherapy. Liaise with physio/OT if concerns.
• Certification for Work / Benefits Advice: Fit notes, supporting applications for disability benefits.
• Managing Comorbidities: Optimise management of existing conditions (e.g., diabetes) that can affect healing.
• Communication Hub: Often the GP is central in coordinating communication between different services if issues arise.
• Health Promotion: e.g., smoking cessation (smoking impairs healing).

Flashcards: Open Fractures Management

Click on each card to reveal the answer.

Risk Factors & Commonly Affected Joints

Risk Factors for Osteoarthritis:

• Age: Strongest risk factor. Prevalence increases significantly after 45-50 years.
• Female Sex: More common in women, especially knee and hand OA post-menopause.
• Obesity: Major modifiable risk factor, especially for knee and hip OA (increased joint loading and metabolic factors).
• Previous Joint Injury or Trauma: E.g., meniscal tears, ACL injury, fractures involving the joint.
• Occupational Factors: Repetitive joint loading or stress (e.g., farming, construction, mining).
• Genetics/Family History: Contributes to susceptibility, especially for hand and hip OA.
• Joint Malalignment or Deformity: E.g., varus/valgus knee, hip dysplasia.
• Muscle Weakness: Particularly quadriceps weakness for knee OA.
• Certain metabolic diseases (e.g., haemochromatosis, acromegaly) and inflammatory arthritides (e.g., RA can lead to secondary OA).

Commonly Affected Joints:

• Knees: Very common, often bilateral.
• Hips: Common, can cause groin, buttock, or referred knee pain.
• Hands:
  • Distal Interphalangeal (DIP) joints – Heberden’s nodes.
  • Proximal Interphalangeal (PIP) joints – Bouchard’s nodes.
  • First Carpometacarpal (CMC) joint (base of thumb) – squaring of thumb base.
  • Metacarpophalangeal (MCP) joints are typically spared (unlike RA).
• Spine (Cervical & Lumbar): Spondylosis. Can cause neck/back pain, stiffness, radiculopathy.
• Feet: First Metatarsophalangeal (MTP) joint (big toe – can mimic gout).
• Shoulders (glenohumeral and acromioclavicular joints) and elbows are less commonly affected by primary OA unless previous injury.

Clinical Features & Diagnosis of Osteoarthritis

Diagnosis is often clinical, especially in older adults with typical symptoms and risk factors.

Key Symptoms:

• Joint Pain:
  • Typically activity-related or mechanical pain (worse on use, relieved by rest initially).
  • Can become persistent and present at rest or at night in advanced stages.
  • Often described as a deep ache.
• Joint Stiffness:
  • Morning stiffness usually lasts <30 minutes (cf. inflammatory arthritis >30-60 mins).
  • Stiffness after periods of inactivity (“gelling”).
• Functional Limitation: Difficulty with activities like walking, climbing stairs, dressing, gripping objects.
• Reduced Range of Motion.
• Joint Instability or “Giving Way” (especially knee).
• Crepitus: Grating, cracking, or popping sensation on joint movement.

Key Examination Signs:

• Bony Enlargement/Swelling: Osteophytes (e.g., Heberden’s and Bouchard’s nodes in hands).
• Joint Line Tenderness.
• Crepitus on Movement.
• Restricted Range of Motion (active and passive).
• Joint Deformity: E.g., varus/valgus knee, fixed flexion deformity.
• Muscle Wasting/Weakness around the affected joint (e.g., quadriceps wasting in knee OA).
• Joint Effusion: Usually cool, non-inflammatory (can be mildly warm if synovitis present).
• Gait Abnormalities: E.g., antalgic gait.

Clinical Diagnostic Criteria (NICE CG177 – for patients ≥45 years):

Diagnose OA clinically without investigations if a person is ≥45 years old AND has activity-related joint pain AND has either no morning joint-related stiffness or morning stiffness that lasts no longer than 30 minutes.

If atypical features or diagnostic uncertainty, consider investigations (see next section).

Investigations in Osteoarthritis

Investigations are not always needed for diagnosis if clinical picture is typical, but can be useful to exclude other conditions or assess severity, especially if considering surgery.

1. X-rays:

• Plain radiographs of affected joint(s) (weight-bearing views for knees/hips if possible).
• Characteristic Features of OA on X-ray (LOSS):
  • Loss of joint space (joint space narrowing – JSN).
  • Osteophytes (bony spurs at joint margins).
  • Subchondral sclerosis (increased bone density beneath cartilage).
  • Subchondral cysts (fluid-filled cavities in bone).
• Limitations:
  • Poor correlation between X-ray findings and symptoms (some have severe X-ray changes but few symptoms, and vice-versa).
  • Early OA may show normal X-rays.
  • Not routinely needed to make a clinical diagnosis in typical cases (NICE).
• Indications for X-ray: Atypical presentation, diagnostic uncertainty, to rule out other pathology (e.g., fracture, tumour), pre-operative planning.

X-ray Example: Knee Osteoarthritis

X-ray showing features of knee OA: medial joint space narrowing, osteophytes, subchondral sclerosis. Source: Wikimedia Commons (Illustrative)

2. Blood Tests:

• Generally NOT helpful for diagnosing primary OA. OA is not primarily an inflammatory systemic disease.
• Inflammatory markers (ESR, CRP): Usually normal or only mildly elevated in OA (can be raised if significant synovitis or coexisting illness). If significantly elevated, consider inflammatory arthritis or other pathology.
• Rheumatoid Factor (RF), Anti-CCP antibodies: To exclude Rheumatoid Arthritis if suspected.
• Uric Acid: If gout is suspected (especially in first MTP joint OA).
• Routine bloods (FBC, U&E, LFT) may be done as part of general workup or pre-operatively.

3. Other Imaging (Less Common for Routine Diagnosis):

• MRI: More sensitive for early cartilage changes, meniscal tears, ligament injuries, bone marrow oedema, synovitis. Not routinely needed for OA diagnosis but can be useful if internal derangement suspected or diagnostic uncertainty.
• Ultrasound: Can detect synovitis, effusions, osteophytes, and guide joint injections.
• Joint Aspiration: If significant effusion, to exclude crystal arthropathy (gout, pseudogout) or septic arthritis. Synovial fluid in OA is typically non-inflammatory (clear, viscous, low white cell count).

Conservative Management: Core Treatments (NICE CG177)

NICE recommends these core treatments should be offered to all patients with OA, irrespective of age, comorbidity, pain, or disability.

1. Information & Education:

• Provide accurate information about OA (nature of condition, prognosis, management options).
• Address misconceptions (e.g., that OA is just “wear and tear” and nothing can be done).
• Promote self-management strategies.
• Signpost to reliable resources (e.g., Versus Arthritis, NHS website).

2. Exercise & Physical Activity:

• Crucial for all patients. Should be encouraged regardless of pain severity or functional limitation.
• Types of Exercise:
  • Local muscle strengthening exercises: E.g., quadriceps strengthening for knee OA.
  • General aerobic fitness exercises: E.g., walking, cycling, swimming.
• Benefits: Reduces pain, improves muscle strength and joint stability, improves function, mood, and general health.
• Advise that some initial discomfort with exercise is normal but should settle. “Start low, go slow.”
• Referral to physiotherapy for tailored exercise programmes. Consider group exercise classes.

3. Weight Management (if overweight or obese):

• Weight loss is highly effective for reducing pain and improving function, especially in knee and hip OA.
• Even modest weight loss (5-10%) can be beneficial.
• Offer advice on diet and physical activity for weight loss.
• Referral to weight management services if appropriate.

Conservative Management: Adjunctive Non-Pharmacological Treatments

These can be considered alongside core treatments, based on individual needs and preferences.

1. Aids & Adaptations:

• Walking Aids: Canes, crutches, walkers. Can improve stability, reduce joint load, and increase confidence. Assessed by physiotherapist.
• Footwear Assessment & Advice: Appropriate, supportive, shock-absorbing footwear. Insoles or orthotics may be helpful for some (e.g., medial wedge insole for medial knee OA – evidence mixed).
• Supports & Braces: E.g., knee braces. May provide symptomatic relief and improve stability for some, but evidence is variable.
• Home Adaptations: Handrails, raised toilet seats, grab bars. Assessed by occupational therapist.

2. Thermotherapy:

• Heat: Hot packs, warm baths/showers. Can relieve pain and stiffness.
• Cold: Ice packs. Can reduce pain and swelling, especially after activity or if acute flare.

3. Transcutaneous Electrical Nerve Stimulation (TENS):

• May provide short-term pain relief for some individuals. Patient can be taught to use at home.
• NICE suggests considering it as an adjunct to core treatments.

4. Manual Therapy:

• Techniques like massage, stretching, joint mobilisation/manipulation by a physiotherapist.
• May provide short-term pain relief and improve range of motion as part of an exercise programme.

5. Acupuncture:

• NICE does NOT recommend acupuncture for OA management due to lack of strong evidence of benefit over placebo.

6. Glucosamine & Chondroitin:

• NICE does NOT recommend these supplements for OA management due to lack of evidence of clinically significant benefit.

7. Psychological Support:

• Address impact of chronic pain on mood, sleep, coping.
• Consider CBT, mindfulness, pain management programmes for those with significant psychological distress or poor coping.

Pharmacological Management (Analgesia)

Pharmacological treatments are for symptomatic relief and should be used as an adjunct to core non-pharmacological treatments, not as a replacement. Use the lowest effective dose for the shortest possible time.

Stepwise Approach (NICE CG177):

1. Paracetamol:
   • Can be tried for mild to moderate pain. Regular dosing (e.g., 1g QDS) may be more effective than PRN.
   • However, NICE notes that evidence for its benefit in OA is limited, and it should only be continued if effective.
   • Monitor for efficacy and stop if no benefit.
2. Topical NSAIDs (Non-Steroidal Anti-Inflammatory Drugs):
   • Consider for knee or hand OA, particularly if localised pain.
   • E.g., ibuprofen gel, diclofenac gel, ketoprofen gel.
   • Fewer systemic side effects than oral NSAIDs. Can be used alongside paracetamol.
3. Oral NSAIDs / COX-2 Inhibitors:
   • Consider if paracetamol and/or topical NSAIDs are insufficient.
   • Use the lowest effective dose for the shortest possible period.
   • Co-prescribe a Proton Pump Inhibitor (PPI) to reduce GI risk, especially in older adults or those with GI risk factors.
   • Assess cardiovascular, renal, and GI risk before prescribing. Caution/Contraindications: Peptic ulcer disease, GI bleed, renal impairment, heart failure, uncontrolled hypertension, asthma (can precipitate), concurrent anticoagulants/steroids.
   • COX-2 inhibitors (e.g., celecoxib, etoricoxib) have lower GI risk than non-selective NSAIDs but similar CV and renal risks.
4. Capsaicin Cream (Topical):
   • Consider for knee or hand OA if other analgesics ineffective or contraindicated.
   • Derived from chilli peppers. Depletes substance P.
   • Can cause initial burning sensation. Requires regular application for several weeks to see benefit.
5. Opioid Analgesics:
   • NICE recommends AVOIDING routine use of strong opioids (e.g., morphine, oxycodone, fentanyl) for OA due to limited evidence of long-term benefit and significant risks (dependence, tolerance, side effects like constipation, nausea, drowsiness, falls, confusion).
   • Weak opioids (e.g., codeine, tramadol – often in co-codamol, co-dydramol) may be considered for short-term use for severe pain if other options failed or contraindicated, but also have significant side effects and limited long-term efficacy.
   • If used, prescribe lowest effective dose, for shortest duration, with regular review and clear plan for stopping.
6. Intra-articular Corticosteroid Injections:
   • Consider for moderate to severe OA pain with acute flare-ups or if awaiting surgery.
   • Provide short-term pain relief (weeks to few months).
   • Can facilitate engagement with exercise.
   • Performed by trained clinician, often under ultrasound guidance for hip.
   • Risks: Post-injection flare, infection (rare), skin atrophy, tendon rupture (rare), facial flushing, temporary glucose elevation in diabetics. Limit frequency (e.g., not more than every 3-4 months per joint).
7. Intra-articular Hyaluronic Acid Injections:
   • NICE does NOT recommend these due to lack of strong evidence of clinically significant benefit.

Surgical Management & Referral Criteria

Surgery is considered for OA when conservative measures have failed to control symptoms and there is significant impact on quality of life and function.

Indications for Referral for Consideration of Joint Replacement Surgery (Arthroplasty):

(NICE CG177 – refer before severe functional limitation or established deformity)

• Persistent, significant joint pain unresponsive to adequate trial of non-surgical treatments.
• Substantial impact on quality of life (e.g., sleep disturbance, inability to perform daily activities, social isolation).
• Functional limitation (e.g., reduced mobility, difficulty with self-care).
• Radiographic evidence of OA (though severity of symptoms is more important than X-ray changes).
• Patient is medically fit enough for surgery and anaesthesia (risks/benefits discussed).
• Patient is motivated and understands the implications of surgery and rehabilitation.

There should be no arbitrary cut-offs for referral based on age, BMI, smoking status, or comorbidities, but these factors will be considered in the surgical decision-making process.

Common Surgical Procedures for OA:

• Joint Replacement (Arthroplasty): Most common surgical treatment for end-stage OA.
  • Total Hip Replacement (THR): Replacement of femoral head and acetabulum. Highly successful for relieving pain and improving function in hip OA.
  • Total Knee Replacement (TKR): Replacement of femoral, tibial, and often patellar articular surfaces. Effective for severe knee OA.
  • Unicompartmental (Partial) Knee Replacement (UKR): Option if OA is confined to one compartment of the knee (medial or lateral) and ligaments are intact. Less invasive, quicker recovery than TKR for suitable patients.
  • Shoulder, elbow, ankle, and small joint (finger) replacements are also performed but are less common.
• Arthroscopic Surgery (e.g., debridement, lavage, meniscectomy):
  • NICE recommends AGAINST arthroscopy for OA unless there is clear evidence of mechanical locking of the knee. Routine debridement or lavage has not shown significant benefit over placebo or conservative care for OA symptoms.
  • Meniscectomy may be considered if acute meniscal tear symptoms coexist with OA, but benefits specifically for OA pain are uncertain.
• Osteotomy:
  • Surgical cutting and realignment of bone to redistribute weight-bearing forces across the joint.
  • More commonly performed in younger, active patients with unicompartmental knee OA and malalignment (e.g., high tibial osteotomy for varus knee). Aims to delay need for joint replacement.
• Joint Fusion (Arthrodesis):
  • Surgical fusion of a joint to eliminate movement and pain.
  • Reserved for severe OA in certain joints where replacement is not suitable or has failed (e.g., ankle, wrist, some finger joints). Results in loss of motion but pain relief.

Flashcards: Osteoarthritis Management

Click on each card to reveal the answer.

Pathophysiology of Rheumatoid Arthritis

RA is a complex autoimmune disease involving genetic predisposition, environmental triggers, and a dysregulated immune response.

• Genetic Susceptibility:
  • Strongest association with HLA-DRB1 alleles (e.g., HLA-DR4, HLA-DR1) containing a “shared epitope.”
  • Other non-HLA genes also contribute.
• Environmental Triggers (Hypothesized):
  • Smoking: Strongest known environmental risk factor, particularly for seropositive RA. May induce citrullination of proteins.
  • Infections (e.g., Porphyromonas gingivalis in periodontal disease, Epstein-Barr virus) have been implicated but causality is not definitively proven.
• Autoimmune Process:
  1. Initiation: In genetically susceptible individuals, an environmental trigger may lead to modification of self-proteins (e.g., citrullination – conversion of arginine to citrulline). These modified proteins are recognized as foreign by the immune system.
  2. Activation of Immune Cells:
     • Antigen-presenting cells (APCs) present these autoantigens to T-cells (CD4+ helper T-cells).
     • Activated T-cells stimulate B-cells to produce autoantibodies:
       • Rheumatoid Factor (RF): Antibodies (usually IgM) against the Fc portion of IgG.
       • Anti-Cyclic Citrullinated Peptide (Anti-CCP) Antibodies (ACPA): More specific for RA than RF. Target citrullinated proteins.
     • T-cells and B-cells, along with macrophages, infiltrate the synovium.
  3. Synovial Inflammation (Synovitis):
     • Immune cells release pro-inflammatory cytokines (e.g., TNF-α, IL-1, IL-6), chemokines, and growth factors.
     • This leads to synovial cell proliferation (hyperplasia), increased vascularity (angiogenesis), and influx of more inflammatory cells into the synovium.
  4. Pannus Formation:
     • The inflamed, thickened synovium transforms into an aggressive, invasive tissue called pannus.
     • Pannus grows over the articular cartilage and invades underlying bone.
  5. Joint Destruction:
     • Pannus releases enzymes (e.g., matrix metalloproteinases – MMPs) that degrade cartilage.
     • Osteoclasts are activated (stimulated by RANKL produced by synovial cells and T-cells), leading to bone erosions.
     • This results in joint space narrowing, erosions, and eventually joint deformities and loss of function.
• Systemic Inflammation: Pro-inflammatory cytokines enter circulation, contributing to extra-articular manifestations and systemic symptoms like fatigue and malaise.

Clinical Features of Rheumatoid Arthritis

RA typically presents with insidious onset of joint pain and stiffness, but can occasionally have an acute onset.

Articular Manifestations:

• Symmetrical Polyarthritis: Affects multiple joints, usually in a symmetrical pattern (both sides of the body).
• Joints Commonly Affected (Early):
  • Hands: Metacarpophalangeal (MCP) joints, Proximal Interphalangeal (PIP) joints. Distal Interphalangeal (DIP) joints are typically spared (unlike osteoarthritis).
  • Wrists: Often involved early.
  • Feet: Metatarsophalangeal (MTP) joints (“walking on pebbles” sensation).
• Other Joints Affected (Later or Less Commonly): Knees, elbows, shoulders, ankles, cervical spine (atlantoaxial subluxation is a serious complication). Temporomandibular joint (TMJ).
• Symptoms:
  • Pain: Worse with rest, improves with activity.
  • Stiffness: Prominent morning stiffness lasting >30-60 minutes (often hours). Stiffness after periods of inactivity (“gelling”).
  • Swelling: Due to synovitis and effusion. Joints feel warm and tender (“boggy” swelling).
  • Reduced Range of Motion and Function.
• Specific Hand Deformities (Usually Late Stage):
  • Ulnar Deviation: Fingers drift towards the ulnar side at the MCP joints.
  • Swan Neck Deformity: PIP hyperextension and DIP flexion.
  • Boutonnière (Buttonhole) Deformity: PIP flexion and DIP hyperextension.
  • Z-Thumb Deformity: Hyperextension of IP joint, flexion and subluxation of MCP joint.
  • Piano Key Sign: Dorsal subluxation of ulnar styloid, which can be depressed like a piano key.
  • Volar subluxation of MCP joints.
• Other Articular Features:
  • Tenosynovitis (inflammation of tendon sheaths), carpal tunnel syndrome (median nerve compression at wrist).
  • Baker’s cyst (popliteal cyst) in the knee.

Extra-Articular Manifestations (EAMs):

Occur in ~40% of patients, more common in seropositive (RF/Anti-CCP +ve) and severe disease. Can affect almost any organ system.

• Constitutional Symptoms: Fatigue, malaise, low-grade fever, weight loss, depression.
• Rheumatoid Nodules:
  • Most common EAM (~20-30%). Firm, non-tender, subcutaneous nodules.
  • Typically found over extensor surfaces and pressure points (e.g., olecranon, fingers, Achilles tendon). Can also occur in lungs, heart, sclera.
• Pulmonary:
  • Pleural effusion (exudative, low glucose).
  • Interstitial Lung Disease (ILD) – e.g., Usual Interstitial Pneumonia (UIP), Non-Specific Interstitial Pneumonia (NSIP).
  • Rheumatoid lung nodules (can cavitate).
  • Caplan’s Syndrome: Rheumatoid nodules + pneumoconiosis in coal miners.
  • Bronchiolitis obliterans.
• Cardiac:
  • Pericarditis (most common cardiac manifestation).
  • Myocarditis, coronary artery disease (accelerated atherosclerosis), valvular disease, conduction abnormalities.
• Haematological:
  • Anaemia of Chronic Disease (most common). Iron deficiency anaemia can also occur.
  • Thrombocytosis (reactive).
  • Felty’s Syndrome (Rare Triad): RA + Splenomegaly + Neutropenia. Increased risk of infections.
  • Large Granular Lymphocyte (LGL) Leukaemia.
• Ocular:
  • Keratoconjunctivitis Sicca (Secondary Sjögren’s Syndrome): Dry eyes, dry mouth.
  • Episcleritis (usually benign, redness).
  • Scleritis (Serious): Severe deep eye pain, redness, photophobia, visual loss. Can lead to scleromalacia perforans (thinning and perforation of sclera).
• Vasculitis:
  • Rheumatoid vasculitis. Can affect small to medium-sized vessels.
  • Manifestations: Skin (digital infarcts, ulcers, purpura), peripheral neuropathy (mononeuritis multiplex), visceral involvement (rare but serious).
• Neurological:
  • Peripheral neuropathy (e.g., entrapment neuropathies like carpal tunnel syndrome, sensory neuropathy, mononeuritis multiplex due to vasculitis).
  • Cervical myelopathy (due to atlantoaxial subluxation compressing spinal cord – neck pain, upper motor neurone signs in limbs).
• Renal: Rarely directly affected by RA itself, but can be due to drugs (NSAIDs, gold, penicillamine) or secondary amyloidosis (AA type).
• Osteoporosis: Due to chronic inflammation, steroid use, and immobility.

Investigations & Diagnosis of Rheumatoid Arthritis

Diagnosis is based on a combination of clinical features, laboratory tests, and imaging. Early diagnosis is key.

Laboratory Tests:

• Inflammatory Markers:
  • Erythrocyte Sedimentation Rate (ESR): Usually elevated.
  • C-Reactive Protein (CRP): Usually elevated. More responsive to changes in inflammation than ESR.
  • Used to assess disease activity and response to treatment.
• Autoantibodies:
  • Rheumatoid Factor (RF):
    • Present in ~70-80% of RA patients (seropositive RA).
    • Not specific for RA: can be positive in other autoimmune diseases (e.g., Sjögren’s, SLE), chronic infections (e.g., hepatitis C, endocarditis), and in ~5-10% of healthy individuals (especially elderly).
    • Higher titres may correlate with more severe disease and EAMs.
  • Anti-Cyclic Citrullinated Peptide (Anti-CCP) Antibodies (ACPA):
    • Similar sensitivity to RF (~70%) but much higher specificity (>95%) for RA.
    • Can be present years before clinical onset of RA.
    • Strong predictor of erosive disease.
  • Note: Patients can be RF positive and Anti-CCP negative, RF negative and Anti-CCP positive, both positive, or both negative (seronegative RA, ~20-30%).
• Full Blood Count (FBC):
  • Normocytic, normochromic anaemia (Anaemia of Chronic Disease) is common.
  • Thrombocytosis (reactive to inflammation).
  • Neutropenia (consider Felty’s syndrome if splenomegaly present).
  • Eosinophilia (can occur).
• Liver Function Tests (LFTs) & Urea and Electrolytes (U&Es):
  • Important as baseline before starting DMARDs (many are hepatotoxic or renally cleared/toxic).
  • May show mild abnormalities due to systemic inflammation.
• Synovial Fluid Analysis (Arthrocentesis):
  • If diagnosis uncertain, or to exclude septic arthritis or crystal arthropathy (e.g., gout).
  • RA synovial fluid: Inflammatory (Type II) – cloudy, yellow, reduced viscosity, high white cell count (typically 2,000-50,000/mm³, predominantly neutrophils), negative crystals, negative culture.

Imaging:

• X-rays (Hands and Feet):
  • May be normal in early disease.
  • Early signs: Soft tissue swelling, juxta-articular osteopenia (bone thinning near joints).
  • Later signs: Joint space narrowing (due to cartilage loss), marginal erosions (bony defects at joint margins), subluxation, and deformities.
  • Used for baseline assessment and monitoring disease progression.
• Ultrasound (USS) with Power Doppler:
  • More sensitive than X-ray for detecting early synovitis, tenosynovitis, and erosions.
  • Power Doppler can show increased vascularity (active inflammation).
  • Useful for guiding joint aspirations/injections.
• Magnetic Resonance Imaging (MRI):
  • Most sensitive imaging for detecting early synovitis, bone marrow oedema (precedes erosions), and early erosions.
  • Not routinely used for diagnosis due to cost and accessibility, but can be helpful in equivocal cases or for assessing specific joints (e.g., cervical spine).

ACR/EULAR 2010 Classification Criteria for RA:

Used for classifying patients with new-onset inflammatory arthritis as having “definite RA” for research and guiding early treatment. A score of ≥6 out of 10 is needed for classification of definite RA.
(Patient must have at least 1 joint with definite clinical synovitis, with the synovitis not better explained by another disease).

1. Joint Involvement (Score 0-5):
   • 1 large joint (e.g., shoulder, elbow, hip, knee, ankle): 0 points
   • 2-10 large joints: 1 point
   • 1-3 small joints (MCPs, PIPs, MTPs, thumb IPs, wrists – large joints excluded): 2 points
   • 4-10 small joints (large joints excluded): 3 points
   • >10 joints (at least 1 small joint): 5 points
2. Serology (RF and Anti-CCP) (Score 0-3):
   • Negative RF AND Negative Anti-CCP: 0 points
   • Low-positive RF OR Low-positive Anti-CCP (<3x Upper Limit of Normal - ULN): 2 points
   • High-positive RF OR High-positive Anti-CCP (≥3x ULN): 3 points
3. Acute Phase Reactants (ESR and CRP) (Score 0-1):
   • Normal CRP AND Normal ESR: 0 points
   • Abnormal CRP OR Abnormal ESR: 1 point
4. Duration of Symptoms (Score 0-1):
   • <6 weeks: 0 points
   • ≥6 weeks: 1 point

Management of Rheumatoid Arthritis

Management is multidisciplinary (rheumatologist, specialist nurse, physiotherapist, occupational therapist, podiatrist, pharmacist, psychologist) and aims to:

• Achieve remission or low disease activity (“Treat-to-Target”).
• Control pain and inflammation.
• Prevent joint damage and deformity.
• Maintain/improve function and quality of life.
• Manage extra-articular manifestations and comorbidities.

Non-Pharmacological Management:

• Patient Education & Self-Management: Understanding RA, managing symptoms, pacing activities.
• Physiotherapy: Exercises to maintain joint mobility, muscle strength, and overall fitness. Hydrotherapy.
• Occupational Therapy (OT): Joint protection techniques, adaptive equipment, splints (e.g., resting splints for night, working splints for day), strategies for ADLs.
• Podiatry: Foot care, orthotics for MTP involvement.
• Lifestyle Modification:
  • Smoking Cessation: Crucial, as smoking worsens RA and reduces treatment efficacy.
  • Healthy diet, weight management.
• Psychological Support: Coping strategies for chronic pain, disability, depression/anxiety.

Pharmacological Management:

Follows a stepwise approach, often starting DMARDs early.

1. Symptomatic Relief (Analgesia & Anti-inflammatories):

• Paracetamol: For mild pain.
• Non-Steroidal Anti-Inflammatory Drugs (NSAIDs): E.g., Ibuprofen, Naproxen, COX-2 inhibitors (Celecoxib).
  • Provide rapid relief of pain and stiffness but do not alter disease course or prevent joint damage.
  • Use lowest effective dose for shortest possible time due to GI, renal, and cardiovascular side effects.
  • Co-prescribe a Proton Pump Inhibitor (PPI) if regular use, especially in at-risk patients.

2. Corticosteroids:

• E.g., Prednisolone (oral), Methylprednisolone (IM/IV/intra-articular).
• Potent anti-inflammatory and immunosuppressive effects.
  • Bridging therapy: Used for rapid symptom control when starting DMARDs (which take weeks/months to work). Tapered off once DMARD is effective.
  • Flares: Short courses for acute exacerbations.
  • Low-dose maintenance: Sometimes used in severe RA if other treatments fail (aim for ≤7.5mg prednisolone daily), but long-term use has significant side effects (osteoporosis, diabetes, hypertension, infections, Cushingoid features).
  • Intra-articular injections: Useful for 1-2 actively inflamed joints.
• Bone protection (e.g., bisphosphonates, calcium/Vit D) essential with long-term steroid use.

3. Disease-Modifying Anti-Rheumatic Drugs (DMARDs):

Cornerstone of RA treatment. Aim to induce/maintain remission and prevent joint damage. Start as soon as diagnosis is made.

a) Conventional Synthetic DMARDs (csDMARDs):

• Methotrexate (MTX):
  • First-line DMARD for most RA patients. Given once weekly (oral or subcutaneous).
  • Mechanism: Folate antagonist, inhibits dihydrofolate reductase, anti-inflammatory effects.
  • Co-prescribe Folic Acid (5mg once weekly, taken on a different day to MTX) to reduce side effects.
  • Side Effects: Nausea, vomiting, mouth ulcers, hepatotoxicity (LFT derangement, fibrosis/cirrhosis rarely), bone marrow suppression (leukopenia, thrombocytopenia), pneumonitis (rare but serious – cough, dyspnoea). Teratogenic.
  • Monitoring: Regular FBC, LFTs, U&Es (e.g., every 1-2 weeks initially, then 1-3 monthly). Chest X-ray baseline.
  • Contraindications: Pregnancy, breastfeeding, severe liver/renal disease, active infection, significant alcohol excess.
• Sulfasalazine (SSZ):
  • Often used in combination with MTX or as an alternative if MTX contraindicated/not tolerated.
  • Mechanism: Not fully understood, anti-inflammatory and immunomodulatory.
  • Side Effects: Nausea, rash, headache, oligospermia (reversible), bone marrow suppression, hepatotoxicity. Can cause yellow-orange discoloration of urine/skin.
  • Monitoring: FBC, LFTs.
• Leflunomide:
  • Alternative to MTX or used in combination.
  • Mechanism: Inhibits pyrimidine synthesis (dihydroorotate dehydrogenase inhibitor).
  • Side Effects: Diarrhoea, hypertension, hepatotoxicity, rash, alopecia, bone marrow suppression. Teratogenic (long half-life, requires washout procedure if pregnancy planned).
  • Monitoring: FBC, LFTs, BP.
• Hydroxychloroquine (HCQ):
  • Milder DMARD, often used for mild RA or in combination.
  • Mechanism: Not fully understood, interferes with lysosomal function and toll-like receptors.
  • Side Effects: Generally well-tolerated. Nausea, rash. Rare but serious: retinal toxicity (maculopathy – requires baseline and annual eye screening).
• Combination therapy (e.g., MTX + SSZ + HCQ) is often more effective than monotherapy.

b) Biologic DMARDs (bDMARDs):

Genetically engineered proteins that target specific components of the immune system. Used for moderate-severe RA unresponsive to or intolerant of csDMARDs (usually after trial of ≥2 csDMARDs, including MTX, unless contraindicated).

• TNF-α Inhibitors (Anti-TNF):
  • E.g., Adalimumab (SC), Etanercept (SC), Infliximab (IV – often with MTX), Golimumab (SC), Certolizumab pegol (SC).
  • Block the action of TNF-α, a key pro-inflammatory cytokine.
  • Side Effects/Risks: Increased risk of infections (especially TB – screen before starting), demyelinating disorders (rare), worsening heart failure, injection site/infusion reactions, drug-induced lupus, lymphoma (small risk).
  • Monitoring: Screen for latent TB, Hepatitis B/C before starting. Monitor for infections.
• Other Biologics (Non-TNF):
  • Rituximab (Anti-CD20): Chimeric monoclonal antibody that depletes B-cells. Given as IV infusion.
    • Side Effects: Infusion reactions, infections, Progressive Multifocal Leukoencephalopathy (PML – very rare).
  • Tocilizumab / Sarilumab (Anti-IL-6 Receptor): Monoclonal antibodies blocking IL-6 receptor.
    • Side Effects: Infections, neutropenia, thrombocytopenia, dyslipidaemia, LFT elevation, GI perforation (rare).
  • Abatacept (CTLA4-Ig): Fusion protein that inhibits T-cell co-stimulation.
    • Side Effects: Infections (especially respiratory), headache, nausea.

c) Targeted Synthetic DMARDs (tsDMARDs) – JAK Inhibitors:

• Oral small molecules that inhibit Janus Kinase enzymes, involved in cytokine signalling.
• E.g., Tofacitinib, Baricitinib, Upadacitinib, Filgotinib.
• Used for moderate-severe RA, similar indications to biologics. Can be used as monotherapy or with MTX.
• Side Effects/Risks: Infections (including herpes zoster reactivation – consider Shingrix vaccine), dyslipidaemia, LFT elevation, cytopenias, increased risk of VTE (venous thromboembolism), MACE (major adverse cardiovascular events), and malignancy (particularly in certain risk groups – debated).

4. Surgical Management:

• Considered for persistent pain, severe joint damage, instability, or functional limitation despite optimal medical therapy.
• Synovectomy: Removal of inflamed synovium.
• Tendon Repair/Release: For ruptured tendons or entrapment.
• Arthrodesis: Joint fusion (e.g., wrist, ankle, thumb IPJ) for pain relief and stability, at cost of movement.
• Arthroplasty: Joint replacement (e.g., MCPJs, PIPJs, wrist, elbow, shoulder, hip, knee) to relieve pain and improve function.

Monitoring Disease Activity & Prognosis in RA

Monitoring Disease Activity:

Regular monitoring is essential to guide treatment (“Treat-to-Target” strategy). Aim for remission or low disease activity.

• Clinical Assessment:
  • Patient-reported symptoms (pain, stiffness, fatigue, function).
  • Joint examination: Tender Joint Count (TJC), Swollen Joint Count (SJC) – typically 28 joints assessed.
• Composite Disease Activity Scores:
  • DAS28 (Disease Activity Score 28): Most commonly used.
    • Combines TJC28, SJC28, ESR or CRP, and patient global assessment of health (VAS 0-100mm).
    • Score interpretation:
      • Remission: <2.6
      • Low disease activity: 2.6 to <3.2
      • Moderate disease activity: 3.2 to ≤5.1
      • High disease activity: >5.1
  • Other scores: SDAI (Simplified Disease Activity Index), CDAI (Clinical Disease Activity Index).
• Laboratory Tests: ESR, CRP to track inflammation.
• Imaging: X-rays periodically (e.g., annually) to assess for new erosions or progression of joint damage, especially if disease activity not well controlled. Ultrasound can also be used.
• Functional Assessment: E.g., Health Assessment Questionnaire (HAQ) to measure impact on ADLs.

Monitoring for Drug Toxicity:

• Crucial for DMARDs (especially MTX, leflunomide, sulfasalazine, biologics, JAK inhibitors).
• Regular blood tests (FBC, LFTs, U&Es) as per local guidelines (e.g., for MTX: every 1-2 weeks initially, then 1-3 monthly once stable).
• Screening for infections (TB, hepatitis) before starting biologics/JAK inhibitors.
• Monitoring for specific side effects (e.g., BP for leflunomide, eye checks for hydroxychloroquine, lipid profile for JAK inhibitors/tocilizumab).

Prognosis:

Variable, but significantly improved with early diagnosis and modern treatment strategies.

• Poor Prognostic Factors:
  • High disease activity at presentation (high TJC/SJC, high ESR/CRP).
  • Early erosions on X-ray.
  • Positive RF and/or Anti-CCP (especially high titres).
  • Multiple joint involvement.
  • Extra-articular manifestations.
  • Female sex.
  • Older age at onset.
  • Smoking.
  • Lower socioeconomic status, poor functional status at baseline.
  • Certain genetic markers (e.g., HLA-DRB1 shared epitope).
• Outcomes:
  • Without effective treatment, ~50% of patients become unable to work within 10 years.
  • With early and aggressive treatment, many patients can achieve remission or low disease activity, maintain function, and prevent significant joint damage.
  • Increased risk of cardiovascular disease (MI, stroke) is a major contributor to mortality. Effective control of RA inflammation may reduce this risk.
  • Life expectancy can be reduced by 3-10 years, mainly due to CVD, infection, and malignancy.

Complications of Rheumatoid Arthritis

RA can lead to various complications, both from the disease itself and its treatment.

Articular Complications:

• Progressive joint damage, erosions, and deformities.
• Joint instability and subluxation.
• Loss of function and disability.
• Secondary osteoarthritis in damaged joints.
• Tendon ruptures (e.g., extensor tendons in hand, Achilles).
• Carpal tunnel syndrome and other entrapment neuropathies.
• Septic arthritis (increased risk due to joint damage and immunosuppression).
• Atlantoaxial subluxation (C1-C2 instability): Can lead to neck pain, occipital headache, neurological deficits (weakness, sensory changes, UMN signs), and potentially spinal cord compression (a neurosurgical emergency).

Systemic & Extra-Articular Complications:

• Cardiovascular Disease:
  • Accelerated atherosclerosis leading to increased risk of MI, stroke, peripheral vascular disease. This is a major cause of excess mortality in RA.
  • Pericarditis, myocarditis, heart failure.
• Osteoporosis: Due to chronic inflammation, steroid use, immobility. Increased fracture risk.
• Infections: Increased risk due to immune dysregulation and immunosuppressive therapies (DMARDs, biologics, steroids). Common sites: respiratory, skin, urinary tract. Opportunistic infections.
• Malignancy:
  • Slightly increased risk of lymphoma (especially diffuse large B-cell lymphoma), possibly related to chronic inflammation/immune stimulation.
  • Lung cancer (especially in smokers with RA).
  • Skin cancer (non-melanoma) with some therapies.
• Interstitial Lung Disease (ILD): Can lead to progressive respiratory failure.
• Felty’s Syndrome: RA + splenomegaly + neutropenia. High risk of severe infections.
• Amyloidosis (AA type): Rare, due to chronic inflammation. Can cause renal failure, proteinuria, cardiomyopathy.
• Vasculitis: Can affect skin, nerves, and internal organs.
• Depression and Anxiety: Common due to chronic pain, disability, and impact on quality of life.

Complications Related to Treatment:

• Side effects of NSAIDs (GI bleeding, renal impairment, cardiovascular events).
• Side effects of corticosteroids (osteoporosis, diabetes, hypertension, infections, Cushingoid features, skin thinning, cataracts).
• Toxicity of DMARDs (e.g., MTX: hepatotoxicity, bone marrow suppression, pneumonitis; HCQ: retinopathy).
• Increased infection risk with biologics and JAK inhibitors (including TB reactivation, herpes zoster).

Special Considerations in Rheumatoid Arthritis

Pregnancy and Breastfeeding:

• Disease Activity: RA may improve in ~50-75% of women during pregnancy (especially 3rd trimester), but often flares postpartum.
• Pre-conception Counselling: Essential. Aim for well-controlled disease on pregnancy-compatible medications before conception.
  • Compatible Medications:
    • Sulfasalazine, Hydroxychloroquine are generally considered safe.
    • Corticosteroids (e.g., prednisolone) at lowest effective dose if needed.
    • Some TNF inhibitors (e.g., certolizumab pegol has low placental transfer; etanercept, adalimumab may be continued until end of 2nd/early 3rd trimester after discussion).
  • Contraindicated Medications (Must be stopped pre-conception):
    • Methotrexate: Teratogenic. Stop ≥3 months before conception (men and women).
    • Leflunomide: Teratogenic (long half-life). Stop ≥2 years before conception or undergo washout procedure.
    • Most other biologics and JAK inhibitors have limited safety data or are contraindicated.
• Breastfeeding: Sulfasalazine, hydroxychloroquine, prednisolone generally considered compatible. Data limited for many biologics. MTX contraindicated.

Surgery:

• Patients with RA may require elective orthopaedic surgery (e.g., joint replacement) or other surgeries.
• Peri-operative Management of Medications:
  • NSAIDs: Usually stopped a few days before major surgery (risk of bleeding, renal impairment).
  • Corticosteroids: Continue. May need stress dose cover if on long-term steroids (e.g., hydrocortisone IV) for major surgery.
  • csDMARDs:
    • Methotrexate: Can often be continued peri-operatively if renal function stable and no active infection (some centres stop 1-2 weeks prior).
    • Sulfasalazine, Hydroxychloroquine: Usually continued.
    • Leflunomide: Often stopped 1-2 weeks prior due to long half-life and wound healing concerns.
  • Biologics & JAK Inhibitors: Usually withheld for a period before and after surgery to reduce infection risk (timing depends on drug half-life, e.g., stop anti-TNF 2-4 weeks prior, restart once wound healed and no infection). Decision by rheumatologist and surgeon.
• Cervical Spine Assessment: Pre-operative X-rays (flexion/extension views) of cervical spine may be needed before general anaesthesia if C-spine involvement suspected, to assess for atlantoaxial instability.
• Increased risk of post-operative complications (infection, poor wound healing).

Vaccinations:

• Patients with RA, especially those on immunosuppressants, are at increased risk of infections.
• Recommended Vaccinations:
  • Annual influenza vaccine.
  • Pneumococcal vaccine (PPV23 and PCV13 as per guidelines).
  • Hepatitis B vaccine (if at risk or before some biologics).
  • Shingles (Shingrix – recombinant, non-live vaccine) recommended for patients ≥50 years, especially before or on JAK inhibitors/biologics.
• Live vaccines (e.g., MMR, yellow fever, live shingles vaccine Zostavax) are generally contraindicated in patients on significant immunosuppression (biologics, JAK inhibitors, high-dose steroids, MTX >25mg/week). Should be given before starting such therapies if possible.

Flashcards: Rheumatoid Arthritis

Click on each card to reveal the answer.

Epidemiology & Risk Factors for Septic Arthritis

Epidemiology:

• Incidence: Approximately 2-10 cases per 100,000 person-years in the general population. Higher in specific risk groups.
• Can affect any age, but more common in very young, elderly, and immunocompromised.
• Most commonly affects large, weight-bearing joints:
  • Knee (most common, ~50% of cases).
  • Hip.
  • Shoulder, ankle, wrist, elbow.
  • Sternoclavicular and sacroiliac joints (especially in IV drug users).
• Usually monoarticular (80-90% of cases). Polyarticular septic arthritis is less common but seen in patients with rheumatoid arthritis, immunosuppression, or disseminated gonococcal infection.

Risk Factors:

• Pre-existing Joint Disease:
  • Rheumatoid arthritis (highest risk).
  • Osteoarthritis.
  • Gout / Pseudogout (crystal arthropathy).
  • Previous joint surgery or trauma.
• Prosthetic Joint (Periprosthetic Joint Infection – PJI): Foreign material acts as a nidus for infection. (See Special Populations).
• Increasing Age (>80 years).
• Immunocompromised State:
  • Diabetes mellitus.
  • Chronic kidney disease / dialysis.
  • Alcoholism / Liver cirrhosis.
  • Malignancy (especially haematological).
  • HIV infection.
  • Immunosuppressive therapy (e.g., corticosteroids, biologics, chemotherapy).
• Intravenous (IV) Drug Use: Often atypical joints (e.g., sternoclavicular, sacroiliac) and unusual organisms (e.g., Pseudomonas, Candida).
• Recent Joint Aspiration or Injection.
• Skin Infections / Ulcers: Allowing bacterial entry.
• Bacteraemia from other sources (e.g., endocarditis, UTI, pneumonia).
• Sickle Cell Disease (Salmonella is a notable pathogen).

Common Causative Organisms in Septic Arthritis

The most common pathogen varies by age group and risk factors.

Overall (Native Joints):

• Staphylococcus aureus (Most Common Overall): Accounts for ~40-60% of cases. Includes Methicillin-Resistant S. aureus (MRSA).
• Streptococcal species:
  • Streptococcus pyogenes (Group A Strep).
  • Streptococcus agalactiae (Group B Strep – neonates, elderly, diabetics).
  • Streptococcus pneumoniae (often polyarticular, associated with systemic infection).
  • Viridans group streptococci.
• Gram-negative bacilli: More common in elderly, immunocompromised, IV drug users, or following GU/GI procedures.
  • Escherichia coli.
  • Pseudomonas aeruginosa (IV drug users, puncture wounds through footwear).
  • Klebsiella spp., Proteus spp.
• Neisseria gonorrhoeae (Gonococcal Arthritis):
  • Common in sexually active young adults. Often presents as migratory polyarthralgia, tenosynovitis, and dermatitis, which can then localize to one or few joints (suppurative arthritis).
  • Synovial fluid cultures may be negative; culture from cervix, urethra, rectum, pharynx. NAAT testing.

Specific Age Groups / Situations:

• Neonates (<2 months): Group B Streptococcus, S. aureus, Gram-negative bacilli (e.g., E. coli).
• Infants & Young Children (<5 years): S. aureus, Streptococcus pneumoniae, Group A Streptococcus. Kingella kingae is increasingly recognized (requires specific culture media). Haemophilus influenzae type b (Hib) now rare due to vaccination.
• Older Children & Adolescents: S. aureus. Consider N. gonorrhoeae if sexually active.
• IV Drug Users: S. aureus (often MRSA), Pseudomonas aeruginosa, other Gram-negatives, Candida.
• Prosthetic Joint Infections (PJI): Coagulase-negative staphylococci (e.g., Staphylococcus epidermidis), S. aureus, Streptococci, Gram-negatives, anaerobes, Cutibacterium (Propionibacterium) acnes (shoulder PJI). Often low-virulence organisms in delayed/late PJI.
• Human or Animal Bites: Polymicrobial (aerobes and anaerobes), e.g., Pasteurella multocida (cat/dog bites), Eikenella corrodens (human bites).

Viral, fungal, and mycobacterial arthritis are much less common but can occur, especially in immunocompromised individuals.

Often, no organism is isolated (“culture-negative septic arthritis”) in up to 30-50% of cases, especially if antibiotics given prior to aspiration.

Clinical Features & Presentation of Septic Arthritis

Classic presentation is an acute monoarthritis, but this can vary.

Typical Symptoms & Signs (Often Rapid Onset):

• Severe Joint Pain: Often described as intense, constant, and deep.
• Swelling (Effusion): Joint appears visibly swollen.
• Warmth and Erythema over the affected joint.
• Markedly Restricted Range of Motion: Both active and passive movements are severely limited due to pain (“pseudoparalysis”). Patient often holds limb in position of maximal joint capacity (e.g., slight flexion).
• Pain on Minimal Movement: Exquisite tenderness even with slight attempted movement or palpation.
• Inability to Weight-Bear (if lower limb joint affected).
• Systemic Symptoms:
  • Fever and Chills/Rigors: Common but may be absent, especially in elderly or immunocompromised patients. Absence of fever does NOT exclude septic arthritis.
  • Malaise, tachycardia, general unwellness.

Kocher Criteria for Septic Arthritis of the Hip in Children:

(Primarily for hip, but principles can be considered. Presence of more criteria increases likelihood).

1. Non-weight-bearing on affected side.
2. ESR >40 mm/hr.
3. Fever >38.5°C.
4. WBC count >12 x 10⁹/L.

Probability of septic arthritis: 0 criteria = <0.2%; 1 = 3%; 2 = 40%; 3 = 93%; 4 = 99%.

Atypical Presentations:

• Elderly/Immunocompromised: May have blunted inflammatory response, less fever, less pain, or more insidious onset. High index of suspicion needed.
• Prosthetic Joint Infection (PJI): Can be acute (within weeks of surgery, similar to native joint SA) or chronic/delayed (insidious onset pain, loosening, sinus tract – often low-virulence organisms).
• Polyarticular Septic Arthritis: Affects multiple joints. More common in RA, immunosuppression, gonococcal infection.
• Deep Joints (Hip, Shoulder, SI joint): Swelling and erythema may be less obvious. Pain and restricted movement are key. Hip often held in flexion, abduction, external rotation.
• Neonates/Infants: Non-specific signs – irritability, poor feeding, pseudoparalysis (not moving limb), fever or hypothermia.

Diagnosis: Joint Aspiration & Synovial Fluid Analysis

Joint aspiration (arthrocentesis) is the cornerstone of diagnosis for suspected septic arthritis. It should be performed urgently, ideally BEFORE starting antibiotics, unless the patient is critically ill with sepsis.

Indications for Joint Aspiration:

• Any acutely swollen, painful, warm joint with restricted movement, where septic arthritis is suspected.
• To differentiate septic arthritis from other causes of acute monoarthritis (e.g., crystal arthropathy, haemarthrosis, reactive arthritis).

Procedure:

• Aseptic technique is paramount.
• Performed by trained personnel (often T&O or rheumatology). Ultrasound guidance can be helpful for deep joints (hip, shoulder) or small effusions.
• Appropriate skin preparation (e.g., chlorhexidine or iodine).
• Local anaesthesia (e.g., lignocaine) to skin and subcutaneous tissue, avoiding injection into the joint space if possible.
• Use appropriate needle size (e.g., 19-21G for knee, larger joints; smaller for smaller joints).
• Aspirate as much fluid as possible.

Synovial Fluid Analysis – Key Tests:

Other Important Investigations:

• Blood Cultures: Positive in up to 50% of cases of septic arthritis (especially S. aureus, Streptococci). Take BEFORE antibiotics.
• Full Blood Count (FBC): Often shows leucocytosis with neutrophilia.
• Inflammatory Markers: ESR and CRP usually markedly elevated. CRP rises and falls more rapidly than ESR, useful for monitoring response to treatment.
• U&Es, Creatinine: Assess renal function (for antibiotic dosing, rhabdomyolysis risk).
• Coagulation Screen: If invasive procedures planned or underlying coagulopathy.
• Urate: If gout suspected (may be normal in acute attack).
• Cultures from other suspected primary sites of infection (e.g., urine, throat, skin lesions, cervix/urethra for gonococcus).

Imaging in Suspected Septic Arthritis

Imaging is primarily adjunctive to clinical assessment and synovial fluid analysis. It should NOT delay urgent aspiration or treatment if septic arthritis is strongly suspected.

Plain X-rays (Affected Joint & Contralateral for Comparison):

• Often normal in early septic arthritis. Main initial role is to exclude other pathology (e.g., fracture, established OA, bone tumour, chronic osteomyelitis).
• Early signs (subtle): Soft tissue swelling, joint effusion (widening of joint space), periarticular osteopenia (if longstanding inflammation).
• Late signs (indicate joint destruction, usually after >1-2 weeks):
  • Joint space narrowing (cartilage loss).
  • Subchondral bone erosions.
  • Periosteal reaction.
  • Signs of osteomyelitis.
  • Joint subluxation/dislocation.

Ultrasound (USS):

• Highly sensitive for detecting joint effusion.
• Can guide joint aspiration, especially for deep or difficult-to-access joints (e.g., hip, shoulder).
• May show synovial thickening, increased vascularity on Doppler (suggests inflammation).
• Cannot definitively differentiate septic from non-septic effusions based on appearance alone.
• Can assess adjacent soft tissues for abscesses or cellulitis.

Magnetic Resonance Imaging (MRI):

• Most sensitive imaging modality for detecting early changes of septic arthritis and associated complications.
• Findings: Joint effusion, synovial enhancement (inflammation), cartilage damage, bone marrow oedema (early osteomyelitis), adjacent soft tissue inflammation/abscesses.
• Indications:
  • Suspected septic arthritis of deep joints (hip, SI joint, sternoclavicular) if diagnosis uncertain or aspiration difficult/non-diagnostic.
  • To rule out or confirm adjacent osteomyelitis.
  • When clinical suspicion is high but aspiration is negative or equivocal.
  • Pre-operative planning if complex infection.
• Not routinely required for straightforward cases where aspiration is diagnostic. Can delay treatment if used inappropriately.

Computed Tomography (CT):

• Less useful for soft tissue detail than MRI.
• May be used to assess bony destruction, sequestra (in chronic osteomyelitis), or guide aspiration/biopsy in some cases.
• CT arthrogram can show cartilage defects.

Radionuclide Bone Scan (e.g., Technetium-99m MDP) / Labelled WBC Scan:

• Historically used, less common now with availability of MRI.
• Bone scan shows increased uptake (non-specific inflammation/turnover). Labelled WBC scan more specific for infection.
• May be useful if multiple sites of infection suspected or MRI contraindicated.

Management of Septic Arthritis: Antibiotics & Surgical Drainage

Management involves two key principles: 1) Eradication of infection with appropriate antibiotics, and 2) Removal of pus and infected material from the joint via drainage.

1. Empirical Intravenous (IV) Antibiotics:

• Start URGENTLY after joint aspiration and blood cultures have been taken (unless patient critically septic, then start immediately after cultures and aspirate concurrently if possible). Do not delay if aspiration difficult/delayed and strong clinical suspicion.
• Initial choice is empirical, based on likely pathogens (age, risk factors, Gram stain result if available). Cover Staphylococcus aureus and Streptococci as a minimum.
  • Common empirical regimen (Native Joint, otherwise healthy adult): Flucloxacillin IV.
    • Alternatives if penicillin allergic: Clindamycin IV or Vancomycin IV (especially if MRSA suspected/prevalent).
  • Add Gram-negative cover (e.g., Ceftriaxone IV or Gentamicin IV) if:
    • Elderly, immunocompromised.
    • Recent GU/GI procedure or infection.
    • IV drug use (consider anti-pseudomonal like Ceftazidime or Piperacillin-Tazobactam).
    • Gram stain shows Gram-negative organisms.
  • Consider adding Rifampicin if prosthetic joint infection (PJI) or osteomyelitis suspected (aids biofilm penetration – specialist advice).
• Gonococcal Arthritis: Ceftriaxone IV (or IM). Treat for chlamydia too (azithromycin or doxycycline).
• Tailor antibiotics once culture and sensitivity results are available.
• Duration of IV therapy: Typically at least 1-2 weeks, guided by clinical response, inflammatory markers, and organism. Then switch to appropriate oral antibiotics.
• Total duration of antibiotics (IV + oral): Usually 4-6 weeks for native joint septic arthritis. Longer if osteomyelitis or PJI.

2. Joint Drainage / Debridement (Surgical Emergency):

Essential to remove pus, infected debris, and reduce intra-articular pressure to prevent cartilage damage and allow antibiotics to penetrate effectively.

• Needle Aspiration (Arthrocentesis):
  • Can be diagnostic and therapeutic initially for easily accessible joints (e.g., knee).
  • Daily or frequent aspirations may be needed if significant re-accumulation.
  • May be sufficient for some early infections or certain organisms (e.g., gonococcal) if rapid clinical improvement.
• Arthroscopic Lavage and Debridement:
  • Preferred method for most large joints (knee, shoulder, ankle, elbow).
  • Allows direct visualisation, thorough washout of the joint with large volumes of saline, removal of fibrin/pus, synovial biopsy, and debridement of infected/necrotic tissue.
  • Less invasive than open arthrotomy.
• Open Arthrotomy and Washout:
  • Indicated for:
    • Hip joint infection (especially in children, though arthroscopy is increasingly used).
    • Joints not easily accessible by arthroscopy or if arthroscopy fails.
    • Presence of extensive necrotic tissue or loculated pus.
    • Prosthetic joint infections (often requiring implant removal/exchange).
  • Allows more extensive debridement and drainage.

Other Management Principles:

• Analgesia: Adequate pain relief is crucial (opioids often required initially).
• Splinting/Immobilisation: Initially for pain relief (e.g., backslab, sling).
• Early Mobilisation & Physiotherapy: Once infection controlled and pain allows, to prevent stiffness, contractures, and muscle atrophy. Crucial for functional recovery.
• Monitor Clinical Response: Pain, swelling, range of motion, temperature, systemic signs.
• Monitor Inflammatory Markers: CRP should start to fall with effective treatment (within days). ESR falls more slowly.
• Address and manage any underlying risk factors.
• Consider DVT prophylaxis in immobilised patients.

Septic Arthritis in Special Populations

1. Prosthetic Joint Infection (PJI):

• A devastating complication of arthroplasty. Infection involving the implant and surrounding tissues.
• Classification by Onset:
  • Early (<3 months post-op): Often due to intraoperative contamination or wound healing issues. High-virulence organisms (S. aureus, Gram-negatives). Acute presentation.
  • Delayed (3-12/24 months post-op): Often low-virulence organisms (Coagulase-negative staphylococci, C. acnes). More insidious onset.
  • Late (>12/24 months post-op): Usually haematogenous spread from distant infection. Acute presentation.
• Diagnosis: Complex. Combination of clinical features (pain, swelling, sinus tract, fever), inflammatory markers (ESR, CRP), imaging (X-ray for loosening, bone scan/WBC scan), multiple synovial fluid/tissue cultures. MSIS criteria often used.
• Management: Requires specialist multidisciplinary input (ortho, micro, ID).
  • DAIR (Debridement, Antibiotics, and Implant Retention): For acute early PJI or acute late haematogenous PJI with stable implant and susceptible organism, if symptoms <3-4 weeks. Involves surgical debridement, exchange of modular components (e.g., liner), and long-term antibiotics (often with biofilm-active agents like rifampicin).
  • One-Stage Exchange Arthroplasty: Removal of infected implant, thorough debridement, and reimplantation of new prosthesis in single operation. For selected cases.
  • Two-Stage Exchange Arthroplasty (Most Common for Chronic PJI):
    • Stage 1: Removal of infected implant, radical debridement, insertion of antibiotic-loaded cement spacer. Followed by 4-8 weeks of IV/oral antibiotics.
    • Stage 2: After infection eradicated (normal inflammatory markers, negative cultures from spacer aspiration), reimplantation of new prosthesis.
  • Permanent Resection Arthroplasty (Girdlestone – hip) or Arthrodesis (fusion).
  • Amputation (rare, for limb salvage failure).
  • Long-term suppressive antibiotics may be used if surgery not feasible.

2. Septic Arthritis in Children:

• Knee and hip are common sites. Hip SA in neonates/infants is an emergency to prevent femoral head necrosis.
• Presentation: Fever, irritability, pseudoparalysis (refusal to move limb/bear weight), localized tenderness, swelling, warmth. Kocher criteria useful for hip.
• Organisms: S. aureus, Streptococci. Kingella kingae important in <4 yrs (requires specific culture). Hib rare with vaccination.
• Diagnosis: High index of suspicion. USS useful for hip effusion. Joint aspiration essential.
• Management: Urgent surgical drainage (arthrotomy for hip, arthroscopy/arthrotomy for knee) and IV antibiotics. Risk of growth plate damage (physeal arrest) if infection involves epiphysis/physis.

Complications & Prognosis of Septic Arthritis

Complications:

• Rapid Joint Destruction: Cartilage loss, erosions, leading to secondary osteoarthritis.
• Osteomyelitis: Spread of infection to adjacent bone.
• Joint Stiffness & Contractures: Due to pain, inflammation, fibrosis.
• Chronic Pain.
• Joint Instability or Subluxation/Dislocation.
• Limb Length Discrepancy or Angular Deformity (in children if growth plate affected).
• Avascular Necrosis (AVN): Especially of femoral head in paediatric hip septic arthritis.
• Sinus Tract Formation (especially in chronic or PJI).
• Systemic Sepsis & Septic Shock.
• Metastatic Infection to other sites.
• Mortality: ~5-15% for native joint septic arthritis, higher in elderly/comorbid patients.

Prognosis:

Depends on several factors:

• Time to Diagnosis and Treatment: Early intervention (within hours) is critical. Delays >24-48 hours significantly worsen outcomes.
• Organism Virulence & Susceptibility: More aggressive organisms or resistant strains lead to poorer prognosis.
• Host Factors: Age, comorbidities (diabetes, RA, immunosuppression), pre-existing joint damage.
• Joint Involved: Hip and shoulder infections may have worse functional outcomes than knee.
• Adequacy of Surgical Drainage and Antibiotic Therapy.

Even with optimal treatment, up to 25-50% of survivors may have some degree of permanent joint dysfunction or residual pain.

Flashcards: Septic Arthritis

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