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MSK Red Flags — quick reference manual
Who this is for: clinicians working in MSK/physio outpatient settings. Use to screen, triage and safety-net. Not personal medical advice. Follow local pathways and policies.
Author: CP Last updated: 2025-08-10

Section 1 – Universal MSK Red Flag Framework

1.1 🔴 What are Red Flags?

Red flags are clinical indicators suggesting the presence of a serious underlying pathology requiring urgent or emergency medical attention.

In MSK practice, these include but are not limited to:

  • Serious spinal pathology (e.g., cauda equina, myelopathy, fracture, infection, malignancy)
  • Systemic inflammatory disease (e.g., AxSpA, RA)
  • Vascular compromise (e.g., DVT, PE, cervical artery dysfunction, acute limb ischaemia)
  • Infection (e.g., septic arthritis, osteomyelitis, discitis)
  • Metastatic disease
  • Other medical emergencies

1.2 Why do we ask about them?

  • Early identification prevents life-threatening consequences (e.g., sepsis, paralysis, amputation, death)
  • Protects the patient by ensuring urgent escalation rather than inappropriate physio management
  • Protects the clinician legally — demonstrates due diligence and adherence to best-practice screening
  • Guides decision-making:
    • Proceed with physiotherapy
    • Delay treatment pending investigations
    • Urgent same-day referral
    • Immediate emergency referral

1.3 How do we ask them? (framing principles + example questions)

General principles:

  • Use neutral, non-leading language — avoids under-reporting or over-reporting
  • Contextualise questions so patients understand relevance without becoming alarmed
  • Ask one at a time and allow silence for recall
  • Use time frames (“in the past few weeks”)
  • Clarify severity, onset, progression

Example Phrasing Across Key Domains

DomainWhy We AskExample QuestionsConcerning Answers
Trauma/FractureRule out unstable fracture or occult injury“Have you had any fall, accident, or sudden injury?”Recent high-energy trauma, osteoporosis + minor trauma, inability to weight bear, severe pain at rest
CancerScreen for metastasis or primary malignancy“Have you ever been diagnosed with cancer?” / “Any unexplained lumps or swelling?”History of cancer (esp. breast, prostate, lung, kidney, thyroid), unexplained weight loss, night sweats
InfectionDetect septic arthritis, discitis, osteomyelitis“Have you had any fevers, chills, or sweats?”Fever + acute joint pain, IV drug use, recent surgery, immunosuppression
InflammatoryIdentify autoimmune or systemic inflammatory conditions“Do you get prolonged morning stiffness or pain that’s worse at night?”Stiffness > 45 min, night waking, improvement with movement
VascularDetect DVT, PE, arterial occlusion“Any swelling, colour changes, or sudden coldness in your arms/legs?”Unilateral swelling, erythema, pulselessness, sudden severe limb pain
NeurologicalIdentify cauda equina, myelopathy, progressive deficits, MS, stroke.“Any changes in bladder/bowel control?” / “Any numbness between your legs?”Saddle anaesthesia, new urinary retention/incontinence, progressive limb weakness, UMN signs

1.4 What answers matter most?

  • Any “first-ever” or “worst-ever” symptom (e.g., headache, neurological deficit)
  • Rapid progression — from onset to functional loss in hours/days
  • Combination of symptoms — e.g., night pain + weight loss + past cancer
  • Symptoms unexplained by mechanical pattern — pain at rest, constant, severe, not eased by position
  • Systemic features — fever, night sweats, unintentional weight loss, fatigue

1.5 How do we manage them? (Emergency vs urgent vs safe-to-proceed)

🚨 Immediate Emergency Referral (A&E / 999)

  • Acute neurological deficit + bladder/bowel symptoms (suspected cauda equina)
  • Acute limb ischaemia (cold, pale, pulseless limb)
  • Suspected septic arthritis with systemic symptoms
  • Stroke/TIA symptoms (5D/3N, facial droop, speech disturbance)

⚡ Urgent Same-Day Medical Referral (GP / Specialist)

  • Suspicion of new cancer or metastasis
  • Suspected vertebral/carotid artery dissection without stroke signs
  • Signs of infection without systemic instability
  • Inflammatory arthritis with rapid joint deterioration

✅ Proceed with Caution (Physio + Safety Net)

  • No red flags identified
  • Mechanical pattern clearly established
  • Provide explicit safety-net advice (document exact wording)

Section 2 – Vascular Red Flags

Scope: clinician-facing reference for recognising and acting on vascular red flags in patients with neck pain and/or headache (and wider MSK presentations).

2.1 Cervical Artery Dysfunction (CAD)

What it is & why it matters. Cervical Artery Dysfunction (CAD) includes vertebral and carotid artery pathology that may lead to cervico-cranial ischaemia, TIA, or stroke. Early phases often mimic benign MSK neck pain/headache, so recognition relies on pattern-based risk screening rather than a single provocative test.

  • Key risk in MSK practice: missing subtle pre-ischaemic patterns.
  • Serious event during physiotherapy is very rare, but screening decisions should be driven by risk recognition, not rarity.

Clinical mantra: Intercept risk before classic neuro signs (the “5 D’s / 3 N’s”) appear.

🩺 Anatomical overview

CirculationApprox. shareVesselsSuppliesTypical presentations
Posterior~20%Vertebral → VertebrobasilarBrainstem, cerebellum, occipital lobesPosterior neck pain, occipital headache, vertigo, ataxia, drop attacks
Anterior~80%Carotid (ICA/ECA)Cerebrum, eyes (via ICA branches)Frontal/temporal headache, amaurosis fugax, facial/visual symptoms

🧬 Pathophysiology (umbrella)

  • Dissection (spontaneous or micro/traumatic)
  • Atherosclerosis / plaque narrowing
  • Thrombosis / in-situ clot; Embolism (remote source)
  • External compromise (major trauma)
  • Less common: fibromuscular dysplasia, connective-tissue disorders, vasculitis

These can first present as neck pain or headache.

🧭 Clinical course & symptom phases

Pre-ischaemic phase (often mimics MSK)
  • New, unusual neck pain or headache (occipital → vertebral; frontal/temporal → carotid)
  • Poorly mechanical / constant pain; may follow minor trauma or new activity
  • Subtle imbalance, visual disturbance, “brain-fog”
  • Possible Horner’s syndrome (ptosis, miosis) → think carotid dissection
Ischaemic phase (late, urgent/emergent)
  • 5 D’s: Dizziness, Diplopia, Dysarthria, Dysphagia, Drop attacks
  • 3 N’s: Nystagmus, Numbness, Nausea; +A: Ataxia
  • Focal neurological deficit, facial droop, unilateral weakness, visual loss (e.g., amaurosis fugax)

🩺 Risk factor stack

CategoryExamplesWhy it matters
Vascular disease historyPrior TIA, stroke, carotid stenosisIndicates arterial fragility/narrowing
Cardiovascular riskHypertension, hyperlipidaemia, diabetes, smokingPromotes atherosclerosis & thrombosis
HaematologicalClotting disorders, anticoagulants↑ risk of dissection/haemorrhage
Connective tissueEhlers–Danlos, MarfanVessel wall weakness
Recent traumaRTA/whiplash, contact sportsMechanical vessel injury
Hormonal/metabolicPregnancy/postpartum, migraineVascular instability
InflammatoryGCA, vasculitisLumen narrowing / ischaemia

Key pattern: new neck/head pain + vascular risks ± subtle neuro features.

🧩 Focused subjective (C-spine vascular screen)

  • “Is this pain mechanical (linked to movement/posture) or constant/non-mechanical?”
  • “Any vision changes, double vision, speech or swallowing difficulty?”
  • “Any imbalance, clumsy hands, or loss of coordination?”
  • “Any new severe or unusual headache?”
  • “Any history of stroke/heart disease/clotting problems or recent neck injury?”

Clarify: time course (sudden vs gradual), first-ever/worst-ever headache, precipitants (minor trauma/sport/illness), duration (TIA <1 hr; stroke >24 hrs), and progression.

🧪 Objective exam (MSK + neuro + vitals)

Avoid relying on vertebral artery positional/provocation tests (low diagnostic accuracy).

  • Vitals: BP (consider both arms if suspicious), HR, SpO₂, temperature
  • Cranial nerves (pupils/eye movements, facial symmetry, palate, tongue)
  • Cerebellar/coordination: finger–nose, heel–shin, Romberg, tandem gait
  • UMN signs where appropriate (Hoffmann’s, clonus, Babinski)
  • Motor/sensory/reflexes for focal deficit; gait observation
  • MSK screen to exclude a clear mechanical cause (avoid end-range cervical rotation)

🧪🧪 Differential diagnosis — pattern contrasts

PatternVascular CAD more likely when…MSK/Other more likely when…
Pain behaviourNew, unusual, non-mechanical; nocturnal; not posture-dependentClear mechanical pattern; reproduced by movement/load
HeadacheFirst-ever/worst-ever; occipital (vertebral) or frontal/temporal (carotid); visual symptomsTypical cervicogenic; reproduced by cervical palpation/movement
Neuro features5D/3N/ataxia, Horner’s, cranial nerve signsAbsent; or peripheral pattern consistent with MSK
Onset/contextRecent neck trauma/infection; pregnancy/postpartum; stacked vascular risksOveruse/strain; posture-related; prior similar benign episodes
VitalsBP disparity; context-specific tachy/brady; fever if vasculitis/infectionNormal

🧭 Decision pathway

RED — Emergency (999 / A&E now)
  • New focal neuro deficit, drop attacks, acute visual/speech/swallow deficit
  • Escalating neuro signs; severe sudden headache + neuro deficit
AMBER — Urgent medical (same-day GP/TIA clinic)
  • Strong vascular risk profile + atypical neck/head pain or subtle neuro features
  • Suspected carotid/vertebral dissection without current stroke signs
GREEN — Proceed with caution (physio + safety net)
  • Convincing mechanical pattern, no vascular risks, no neuro features
  • Give clear safety-net advice and review if symptoms change

Manual therapy precautions: If AMBER/RED risk, avoid end-range rotation and thrust techniques; prioritise education, relative rest, and urgent medical referral.

🗣️ Safety netting — exact phrases

  • “If you notice new dizziness, double vision, trouble speaking or swallowing, sudden weakness, or loss of coordination, call 999 or go to A&E immediately.”
  • “If this headache becomes the worst you’ve had, or your symptoms change suddenly, seek urgent medical care.”
  • “If any visual loss (like a curtain coming down) occurs, go straight to A&E.”

📝 Documentation checklist (clinician)

  • Vascular risk factors reviewed (positives & negatives)
  • 5D/3N/Ataxia asked (document wording + response)
  • Onset/context incl. recent trauma/infection/pregnancy
  • Vitals and relevant neuro findings
  • Reasoning: AMBER/RED/GREEN rationale
  • Advice given (safety-net) recorded verbatim
  • Referral details (pathway, urgency) or plan + review date

2.2 Avascular Necrosis (AVN) / Osteonecrosis

🔍 What is it & why it matters

Avascular Necrosis (AVN) is death of bone tissue from interrupted blood supply. Without timely intervention it can progress to subchondral collapse, secondary osteoarthritis, and long-term disability. Early symptoms often mimic benign joint pain, so recognition before collapse is critical.

🧬 Pathophysiology

  • Arterial inflow disruption → bone ischaemia → osteocyte death
  • Venous outflow obstruction → marrow congestion
  • Fat emboli / marrow fat hypertrophy → intravascular occlusion
  • Steroid-related lipid changes → microvascular compromise
  • Structural collapse when the subchondral plate loses support

📍 Common sites & vascular vulnerability

SiteBlood supply notesClinical implication
Femoral head (most common)Lateral epiphyseal branches of the medial circumflex femoral artery run along the neck & enter near the epiphysis; intracapsular fractures can disrupt.Early AVN may have normal X-ray; high index of suspicion with pain on WB in steroid/alcohol/trauma history.
Humeral headAnterior & posterior humeral circumflex; arcuate artery vulnerable in fracture/dislocation.Post-dislocation/post-fracture shoulder pain; ROM loss as disease progresses.
ScaphoidRetrograde flow: distal → proximal; proximal pole poorly supplied.High AVN risk after fractures; watch for pain that initially improves then worsens.
LunateEnd-arterial/variable supply.Kienböck’s disease risk; dorsal wrist pain, decreased grip.
TalusSupply enters mainly via neck & sinus tarsi; body/dome tenuous (esp. after neck fractures).Post-traumatic ankle pain with limited ROM; monitor for collapse.
Knee (distal femur / proximal tibia)Rich metaphyseal supply; AVN associated with trauma, steroids, alcohol, systemic disease.Medial knee pain; may mimic meniscal pathology early.

🧾 Risk factors

  • Trauma (fracture, dislocation)
  • Prolonged/high-dose corticosteroids
  • Alcohol misuse
  • Smoking
  • Sickle cell disease
  • Connective-tissue disorders (e.g., SLE)
  • Gaucher disease
  • Decompression sickness
  • Radiotherapy / chemotherapy
  • Post-transplant status

📋 Typical presentation

Early
  • Gradual joint pain (hip, knee, ankle, shoulder, wrist)
  • Pain on weight-bearing; eases with rest
  • Minimal ROM loss initially
Progressive
  • Pain at rest; reduced ROM; antalgic gait
  • Crepitus/mechanical symptoms if collapse begins
Late
  • Severe pain, marked ROM restriction
  • Secondary osteoarthritis signs

🧪 Imaging

  • Plain radiographs: may be normal early; later show crescent sign, sclerosis, subchondral collapse.
  • MRI: most sensitive for early disease; picks up marrow change before collapse.
  • Bone scan: increased uptake; less specific than MRI.

📊 Staging – Ficat (Hip AVN)

StageKey features
INormal X-ray; MRI/bone scan positive
IISclerosis/cysts; no collapse
IIISubchondral collapse (crescent sign); joint space preserved
IVAdvanced collapse with secondary OA

🧩 Differential diagnosis

ConditionKey differences
Stress fractureFocal tenderness; overuse history; bone scan/MRI with distinct fracture pattern
Bone bruiseAcute trauma; MRI signal resolves over time
Arthritis flareSynovitis on imaging; inflammatory markers may be raised
Bone tumourAggressive imaging features; possible systemic symptoms

🧑‍⚕️ MSK management considerations

  • Avoid high-impact/aggressive loading when suspected.
  • Modify rehab to low-impact mobility & pain management pending imaging.
  • Avoid end-range loading of the affected joint.
  • Early orthopaedic input: core decompression in early stages can prevent collapse.

🧭 Referral pathway

  • 🚨 Suspected AVN → Urgent GP/orthopaedic referral.
  • Request MRI when early AVN is suspected with normal X-ray.
  • Provide risk factors, symptom timeline, and functional limitations in referral.

📝 Documentation checklist

  • Risk factors (steroids, alcohol, trauma, systemic conditions)
  • Onset & progression
  • Functional impact (e.g., walking distance, ADLs)
  • Joint findings (ROM, tenderness, gait)
  • Imaging results (if available)
  • Advice given (activity modification, safety netting)
  • Referral details (who, when, urgency)

🗣️ Safety-netting — exact phrases

  • “If your pain worsens, becomes constant, or you lose movement in the joint, contact your GP or attend A&E immediately.”
  • “Avoid high-impact activities until we have clear imaging and diagnosis.”

2.3 Deep Vein Thrombosis (DVT) & Pulmonary Embolism (PE)

Virchow’s triad

Wells score

urgent escalation

What it is & why it matters

DVT is thrombus formation within a deep vein (most often lower limb). The primary danger is embolisation to the lungs → Pulmonary Embolism (PE), which is life-threatening.
• Annual incidence ~1/1,000 adults (population).
• Physio relevance: DVT can mimic calf strain/post-op swelling; PE can present after immobilisation or surgery.
• Key role: early recognition and urgent medical referral to prevent death or permanent disability.

Pathophysiology — Virchow’s Triad

  • Stasis: immobility, post-op recovery, long-haul travel, paralysis.
  • Endothelial injury: trauma, surgery, central lines, vascular disease.
  • Hypercoagulability: cancer, pregnancy, oestrogen therapy, thrombophilia, inflammatory disease (RA/SLE).

Risk factors — screen every patient

  • Past history: previous DVT/PE, active cancer (≤6m), heart failure, varicose veins, IBD, nephrotic syndrome, genetic thrombophilia.
  • Recent triggers: major surgery (abdo/pelvic/orth), bed-rest >3 days, travel >4h, lower-limb fracture/trauma, acute infection, dehydration.
  • Drugs/hormonal: combined OCP, HRT, chemotherapy agents.
  • Other: pregnancy/postpartum, obesity, smoking.

Subjective features (DVT)

  • Calf/thigh pain (dull ache, tightness, heaviness), unilateral & evolving over hours–days.
  • Often preceded by immobility/surgery or a risk-factor trigger.

Objective signs (DVT)

  • Unilateral swelling: measure 10 cm below tibial tuberosity; >3 cm difference is concerning.
  • Warmth/erythema, pitting oedema, tenderness along deep veins, distended superficial veins.
  • Homan’s sign is unreliable and should not be used as a sole diagnostic.

Wells Clinical Prediction Rule (suspected DVT)

CriterionPoints
Active cancer (treatment ≤6 months or palliative)+1
Paralysis/paresis or recent plaster immobilisation of lower limb+1
Bedridden >3 days or major surgery within past 12 weeks+1
Localised tenderness along the deep venous system+1
Entire leg swollen+1
Calf swelling >3 cm compared with other leg+1
Pitting oedema confined to the symptomatic leg+1
Collateral superficial veins (non-varicose)+1
Previous DVT+1
Alternative diagnosis at least as likely as DVT−2

Risk stratification: ≥2 → DVT likely → urgent D-dimer & Doppler; <2 → unlikely → consider D-dimer/monitor.

Pulmonary Embolism (PE) — recognise immediately

  • Sudden breathlessness, pleuritic chest pain, cough ± haemoptysis.
  • Tachycardia/tachypnoea, dizziness, collapse/syncope, anxiety/“impending doom”.

Context: often days–weeks after DVT onset or triggering event.

Management pathway

  • Suspected DVT: urgent same-day referral to GP/UCC/ED. Advise mobility as tolerated and hydration; avoid compression until diagnosis confirmed.
  • Suspected PE: immediate ED (999 if unstable); oxygen if hypoxic; monitor vitals.
  • Physio: document findings, risks, Wells score, and escalation route.

Safety netting — exact phrases

  • “If you develop sudden breathlessness, chest pain, cough up blood, or collapse, call 999 immediately.”
  • “If leg pain/swelling worsens or redness/heat develops, seek urgent medical care.”

Documentation checklist (clinician)

  • Risk factors present/absent (full list).
  • Wells score with criteria breakdown.
  • Leg measurements (if taken).
  • Vitals if PE suspected.
  • Escalation pathway & who contacted.
  • Safety-net wording recorded verbatim.

2.4 Acute Limb Ischaemia (ALI) / Arterial Occlusion

🔍 What it is & why it matters
ALI is a sudden decrease in limb perfusion that threatens viability — a vascular emergency.

  • Time-critical: irreversible tissue damage within 6 hours.
  • Causes: embolism, in-situ thrombosis (often on background of PAD), trauma, dissection.

🧠 Classic presentation — “The 6 Ps”

  1. Pain – sudden, severe, distal to occlusion
  2. Pallor – pale skin, may progress to mottling
  3. Pulselessness – absent distal pulses
  4. Paraesthesia – numbness, pins & needles
  5. Paralysis – late, ominous sign of muscle necrosis
  6. Poikilothermia – limb feels cold compared to other side

👥 Risk factors

  • Atrial fibrillation (cardioembolic source)
  • Previous MI or cardiac thrombus
  • Peripheral arterial disease (PAD)
  • Recent vascular surgery or angioplasty
  • Hypercoagulable states (as per DVT risks)
  • Trauma to limb or artery

🗣 Subjective clues

  • Sudden onset compared to gradual claudication of chronic PAD
  • “My leg went cold and dead”
  • May have history of intermittent claudication suddenly worsening

🧑‍⚕️ Objective findings

  • Cool, pale limb with well-defined demarcation from healthy tissue
  • Absent pulses distal to occlusion
  • Capillary refill > 2s
  • Possible muscle tenderness if late presentation

🧭 Management pathway

Emergency — call 999
Position: keep limb at level of heart (not elevated)
Do not apply heat
Monitor neurovascular status while awaiting ambulance
Record onset time (surgeons need this to plan intervention)

🗣 Safety netting phrase (post-event or for at-risk patients)

“If you suddenly notice your leg or arm becomes cold, pale, numb, or weak, call 999 immediately — do not wait for it to improve.”

📝 Documentation checklist (clinician)

  • Onset time and trigger
  • 6 Ps status (positive/negative for each)
  • Pulses palpated (document site and findings)
  • Sensory/motor exam results
  • Escalation route (ambulance, ED)
  • Advice given

Section 3 – Neurological Red Flags

This section covers multi-level neurology patterns, Cauda Equina Syndrome (CES), and Cervical Myelopathy (CM). See 3.1, 3.2, and 3.3 below.

3.1 Multi-level Neurology

Neurological changes affecting multiple spinal levels (sensory, motor, reflex) strongly suggest cord-level pathology (e.g. tumour, stenosis, transverse myelitis) rather than a single nerve root issue.

Lesion LevelKey SignsExample Conditions
Central (Brain/Brainstem)Hoffmann’s, Babinski, clonus, ataxic gait, widespread sensory changes, coordination deficitsBrain tumour, MS, stroke
Spinal CordBilateral limb symptoms, multi-level deficits, long tract signs, dermatomal changes, hyperreflexiaSpinal cord compression, MSCC
Peripheral NerveLocalised motor loss, wasting, sensory loss in single nerve distribution, reduced reflexesRadiculopathy, peripheral neuropathy, entrapment syndromes

3.2 Cauda Equina Syndrome (CES)

🔍 What it is & why it matters

Cauda Equina Syndrome is compression of the nerve roots at the base of the spinal cord, affecting:

  • Bowel
  • Bladder
  • Saddle sensation
  • Sexual function
  • Lower limb motor and sensory function

Main causes:

  1. Central lumbar disc herniation (most common)
  2. Tumour / Metastatic Spinal Cord Compression (MSCC) – see Oncology section
  3. Infection (e.g., epidural abscess, discitis) – see Infections section
  4. Spinal stenosis (bony overgrowth/osteophytes)
  5. Haemorrhage (spontaneous or post-procedure)

Missed or delayed diagnosis can cause permanent disability. Progressive symptom worsening over hours to days is common and must be recognised early.

📈 Typical Symptom Evolution

“My back hurts” → “Now my leg hurts” → “My leg(s) feel weak” → “It’s harder to wee” → “I can’t feel when I wipe”

🗣️ Framing CES questions

Clinical introduction:
“I know these questions may sound strange, but they’re very important, and we ask every patient with back pain these questions.”

  • “It was like asking what colour you paint your toe nails when you are in labour.”
  • “Can’t even think about sex, why are you asking me that?”
  • “What’s that got to do with the price of fish?”

🧠 CES nerve root functions

  • ✅ Skin sensation around the saddle region
  • ✅ Motor & sensory control for bowel & bladder
  • ✅ Motor & sensory input for sexual function

Questions must target these domains directly.

📋 Structured screening questions

  1. Lower limb neuro symptoms
    • Progressive unilateral or bilateral leg pain/paraesthesia (dermatomal/myotomal pattern)
    • Reflex or myotome changes
    • ⚠️ May be early sign before CES fully develops.
  2. Saddle anaesthesia
    • “Can you feel when wiping yourself?”
    • “Have you found you had urinated and didn’t realise?”
  3. Bowel dysfunction
    • “Are you going to the toilet as normal?”
    • “When you feel the need to go, can you actually go?” (Retention if not)
    • “Have you had any bowel accidents?”
  4. Bladder dysfunction
    • “Are you able to urinate as normal?”
    • “Do you feel the urge to go but can’t pass anything?” (Retention)
    • “Are you going more often than usual?” (Early sign)
    • “Are you incontinent of urine?”
  5. Sexual dysfunction
    • “Does it feel normal?”
    • Males: inability to get/maintain erection
    • Females: lack of sensation during sex, pain during intercourse (dyspareunia)

📊 CES progression stages

StageLabelKey Features
CESSSuspectedBilateral leg pain/paraesthesia, progressing unilateral symptoms
CESIIncompleteReduced urinary sensation, poor stream, loss of desire to void
CESRRetentionPainless urinary retention, overflow incontinence
CESCCompleteAbsent perineal sensation, loss of anal tone, paralysed bowel/bladder

🧩 Subjective Clues Suggesting CES

  • Pain is non-mechanical or worsening despite rest
  • Symptoms progressing over hours/days
  • Back pain with new bladder/bowel/sexual function change
  • Bilateral or rapidly progressing neuro symptoms

🧑‍⚕️ Management & referral pathway

  1. Step 1: Speak to a senior immediately (Senior Physio/ESP)
  2. Step 2: Triage
    • Yes/Could be CES: 📤 Urgent A&E referral
    • No/Not yet: ⚠️ Monitor + safety net; arrange MRI if worsening
  3. Step 3: Referral
    • Use CES Warning Card (if available)
    • Follow GIRFT CES Pathway (2023):
      • Suspected → A&E
      • Confirmed → Surgical decompression
      • Post-op → rehab pathway

📝 Clinician documentation checklist

  • All CES screening questions asked and responses documented verbatim
  • Presence or absence of saddle anaesthesia recorded
  • Bowel, bladder, sexual function status clearly noted
  • Any lower limb neuro deficits described (myotome, dermatome, reflex changes)
  • CES stage classification (CESS/CESI/CESR/CESC) recorded if applicable
  • Timeline of symptom onset and progression
  • Details of escalation: who was contacted, when, and outcome
  • Safety netting advice given (include exact wording)
  • Copies of CES warning cards or written information provided to patient

🗣️ Safety netting phrases

“If you develop any new numbness in your groin or buttocks, problems passing urine, loss of control of bowel or bladder, or changes in sexual function, go to A&E immediately.”

3.3 Cervical Myelopathy (CM)

🔍 What it is & why it matters

Cervical Myelopathy is spinal cord compression within the cervical spine, most often due to degenerative changes, but also trauma, tumours, or inflammatory disease. It is a progressive neurological condition that can cause irreversible spinal cord damage if untreated. Early detection and referral for surgical decompression are critical.

🧬 Causes

  • Degenerative cervical spondylosis (most common)
  • Disc herniation
  • Ossification of the posterior longitudinal ligament (OPLL)
  • Tumours (primary or metastatic)
  • Congenital spinal canal stenosis
  • Rheumatoid arthritis with atlantoaxial instability
  • Post-traumatic changes

🧠 Pathophysiology

Narrowing of the cervical spinal canal compresses the spinal cord, disrupting both ascending sensory and descending motor pathways. Chronic compression may cause demyelination and neuronal loss, leading to spasticity, weakness, and coordination deficits.

📋 Typical clinical presentation

Early symptoms (often subtle)

  • Hand clumsiness (difficulty with buttons, handwriting changes)
  • Mild balance issues or unsteadiness
  • Changes in gait pattern (wide-based, slow)
  • Upper limb paraesthesia without clear dermatomal pattern

Progressive / advanced symptoms

  • Weakness in hands or legs
  • Stiffness and spasticity in lower limbs
  • Numbness or altered sensation in arms, hands, or legs
  • Bladder or bowel urgency

Red flag signs

  • Upper Motor Neuron (UMN) signs:
    • Hoffmann’s sign
    • Babinski reflex
    • Clonus (>3 beats)
    • Hyperreflexia (especially brisk patellar reflexes)
  • Sensory changes:
    • Altered joint position sense
    • Loss of vibration sense in feet
  • Lhermitte’s sign: electric shock sensation with neck flexion

🗣️ Screening questions

  • “Have you noticed clumsiness in your hands or difficulty with buttons?”
  • “Do you feel unsteady or off balance when walking?”
  • “Have you had any changes in handwriting or fine motor skills?”
  • “Any new urgency or changes in bladder or bowel habits?”
  • “Do your symptoms worsen when you move your neck?”

🧪 Objective examination

  • Observe gait (may be stiff, wide-based, or ataxic)
  • Test coordination (finger–nose, heel–shin)
  • Assess reflexes (biceps, triceps, patellar, Achilles)
  • Check for UMN signs (Hoffmann’s, Babinski, clonus)
  • Sensory exam: proprioception, vibration, light touch
  • Assess for Lhermitte’s sign (with caution)

📊 Differential diagnosis

FeatureCervical MyelopathyPeripheral NeuropathyMSK Neck Pain
OnsetGradual, progressiveGradual or acuteOften acute/mechanical
ReflexesHyperreflexicReduced/absentNormal
UMN signsPresentAbsentAbsent
SensoryNon-dermatomalStocking–gloveLocalised to neck/shoulder
CoordinationImpairedOften normalNormal

🧑‍⚕️ Management & referral pathway

  1. Step 1: Suspect CM in presence of UMN signs or progressive neuro symptoms.
  2. Step 2: Immediate actions
    • Avoid cervical manipulations or high-velocity techniques
    • Refer urgently to spinal/orthopaedic/neurosurgical team for assessment and imaging (MRI preferred)
  3. Step 3: Document findings clearly, including:
    • Positive/negative UMN signs
    • Functional impairments
    • Onset and progression timeline
    • Safety netting advice

📝 Clinician documentation checklist

  • All screening questions and patient responses recorded
  • Detailed neuro exam findings (motor, sensory, reflexes, coordination)
  • Positive/negative UMN signs clearly noted
  • Functional impact described (e.g., hand function, gait stability)
  • Symptom timeline and progression documented
  • Escalation steps (who contacted, when, and outcome)
  • Safety netting advice recorded verbatim

🗣️ Safety netting phrases

“If you notice worsening balance, weakness in your hands or legs, or new bladder/bowel symptoms, seek urgent medical attention.”

🔥 Section 4 – Inflammatory Pathologies

Scope: Clinician-facing reference for recognising and managing systemic inflammatory conditions that present in MSK settings. Early identification prevents irreversible joint damage, organ involvement, and limits systemic complications.

📋 Common inflammatory red flag conditions

  • Rheumatoid Arthritis (RA)
  • Psoriatic Arthritis (PsA)
  • Polymyalgia Rheumatica (PMR)
  • Axial Spondyloarthropathy (AxSpA)

🧬 4.1 Axial Spondyloarthropathy (AxSpA)

  • Onset: 20–45 years
  • Sex: Male > Female (3:1)
  • Symptoms: Morning stiffness > 45 min; night pain (2nd half of night); worse with rest, improves with movement
  • Risk factors: Family history of autoimmune disease, HLA-B27 positivity, history of IBD
  • Extra-articular: GI symptoms, uveitis, psoriasis

🤲 4.2 Rheumatoid Arthritis (RA)

  • Onset: Most common between 30–50 years; female > male (3:1)
  • Pattern: Symmetrical small joint polyarthritis (MCP, PIP, wrists)
  • Symptoms: Morning stiffness > 60 min, joint swelling, systemic fatigue, weight loss
  • Extra-articular: Rheumatoid nodules, vasculitis, lung involvement, pericarditis, scleritis
  • Risk factors: Female sex, smoking, family history, HLA-DR4/DR1 positivity
  • Complications: Joint destruction, cervical spine instability, increased CV risk

🧴 4.3 Psoriatic Arthritis (PsA)

  • Onset: 30–50 years; affects men and women equally
  • Pattern: Asymmetrical oligoarthritis, symmetrical polyarthritis, spondylitis, or predominant DIP joint involvement
  • Symptoms: Morning stiffness, joint swelling, pain, dactylitis (“sausage digits”)
  • Extra-articular: Psoriasis (skin plaques), nail changes (pitting, onycholysis), uveitis
  • Risk factors: Family history of psoriasis, HLA-B27 positivity
  • Complications: Joint deformity, enthesitis, increased metabolic syndrome risk

👵 4.4 Polymyalgia Rheumatica (PMR)

  • Onset: > 50 years; female > male (2:1)
  • Pattern: Bilateral pain and stiffness in shoulders, neck, hips
  • Symptoms: Morning stiffness > 45 min, difficulty rising from chair or lifting arms, fatigue, low-grade fever
  • Risk factors: Northern European ancestry, history of autoimmune disease
  • Complications: 20% develop temporal arteritis (GCA) — risk of vision loss; concurrent inflammatory arthritis

🔡 SCREEND-EM — Inflammatory disease screening (Kirwan, 2020)

LetterMarkerExample
SSkinPsoriasis
CCrohn’s / ColitisIBD
RRelativesFamily history of autoimmune conditions
EEyesPainful/red/blurred/photophobic
EEarly morning stiffness> 30–60 min
NNailsPitting, thickening, onycholysis
DDactylitis“Sausage fingers”
EEnthesitisTendon pain without mechanical cause
MMovement/MedicationImproves with movement, NSAID relief

🌙 Night pain in inflammatory disease

  • Wakes patient in early morning hours
  • Driven by increased parasympathetic tone at rest
  • Relieved by movement; associated with prolonged stiffness

🧪 Investigations

  • Bloods: ESR, CRP, WCC, HLA-B27 (AxSpA, PsA), Anti-CCP (RA), Rheumatoid Factor
  • Imaging:
    • X-ray: sacroiliitis, joint space narrowing, erosions (later stages)
    • MRI: early inflammatory changes (bone marrow oedema, synovitis)
    • Ultrasound: synovial thickening, effusion, Doppler activity

🧭 Management pathway

  • 🗣 Discuss with senior or rheumatology link
  • 📄 Urgent referral if SCREEND-EM markers positive or red flag features present
  • 💊 Early DMARDs/biologics initiated by rheumatology
  • ⚠️ Check infection risk before starting immunosuppression

📝 Clinician documentation checklist

  • SCREEND-EM responses
  • Stiffness duration and timing
  • Night pain presence/absence
  • Extra-articular features documented
  • Functional limitations
  • Investigations ordered/results
  • Referral details and urgency
  • Safety netting advice
🗣 Safety netting phrase: “If you notice increased night pain, loss of function, eye redness or pain, or new swelling in other joints, please contact your GP or rheumatology team immediately.”

🦠 5. Infections

Scope: Clinician-facing reference for recognising and managing MSK infections that can progress rapidly and require urgent action.

  • Why it matters: risk of irreversible cartilage/bone damage (e.g., septic arthritis) and systemic sepsis.
  • Higher-risk groups: immunosuppressed, post-operative, IVDU, diabetics, those with indwelling devices.

🔎 Quick jump

5.1 Overview & risk screen
5.2 Discitis
5.3 Septic arthritis
5.4 Osteomyelitis

🦠 5.1 Overview & why they matter

📚 Overview

  • Sites: bone, joints, intervertebral discs.
  • Routes: haematogenous spread, direct inoculation (trauma/wounds/bites), post-surgical contamination.
  • Why it matters: rapid cartilage/bone destruction (e.g. septic arthritis), risk of bacteraemia/sepsis, blunted signs in immunocompromised patients.

🧵 THREADSOCS — infection risk screen

LetterTopicWhy it matters
#FracturesOld fractures may hide chronic infection (osteomyelitis) or AVN.
TThyroidHypothyroidism slows healing; hyperthyroidism linked to osteoporosis.
HHeartEndocarditis → septic emboli risk; vascular disease affects healing.
RRheumatologyRA/PsA/AS/PMR → DMARDs/steroids → immunosuppression.
EEpilepsyFall injuries, aspiration pneumonia risk.
AAsthmaLong-term steroids reduce immunity.
DDiabetesMicrovascular disease, neuropathy, delayed healing, ↑ infection.
SSteroid useSuppressed immunity, poor tissue repair.
OOncologyCancer/chemo/radiotherapy → immune suppression.
CCatheters / DevicesDirect portal for infection.
SSurgeryPost-op wound/implant infection risk.

❗ Additional infection red flags

  • Fever, night sweats, unexplained fatigue
  • Constant, progressive pain not mechanical
  • Recent surgery, injections, wounds, dental work
  • Immunosuppression: HIV, chemo, DMARDs, steroids
  • Non-mechanical night pain
  • Rapid functional decline
  • Invasive procedures (catheterisation, endoscopy)
  • Open wounds, ulcers, cellulitis
  • IV drug use

🧪 Investigations

  • Bloods: ESR/CRP, WCC, blood cultures (before antibiotics if possible).
  • Imaging: MRI (gold standard for spine/early bone infection), US (joint effusion), X-ray (late bony change).
  • Procedures: urgent joint aspiration (cell count, Gram, culture) — do not delay if septic arthritis suspected; consider HIV/TB tests if risk.

🧭 Management pathway

  1. Escalate immediately to senior/medical team if suspected.
  2. Same-day referral: GP/consultant physio/orthopaedics/rheumatology; A&E if systemic signs or sepsis.
  3. Do not delay referral for imaging if unstable — early IV antibiotics are time-critical.
  4. Document thoroughly (see checklist).

📝 Clinician documentation checklist

  • THREADSOCS risk factors reviewed
  • Onset, progression, duration
  • Systemic signs present/absent
  • Functional impact
  • Site(s) & clinical findings
  • Investigations & results
  • Who escalated to, when, outcome
  • Safety-netting advice

🗣️ Safety-netting phrase

“If you develop fever, chills, sweats, new swelling, redness, or worsening pain, seek urgent medical attention or attend A&E immediately.”

📌 Clinical pearls

  • Immunosuppressed patients may lack fever — watch for functional decline and subtle change.
  • Septic arthritis can destroy a joint in <24h — same-day referral.
  • In diabetics, always inspect feet — ulcers may hide osteomyelitis.

🟢 5.2 Discitis

  • Definition: infection of the intervertebral disc ± adjacent vertebrae (spondylodiscitis).
  • Epidemiology: children and older adults; recent systemic infection, IVDU, or immunosuppression.
  • Presentation: severe localised back pain, fever/malaise, reduced spinal mobility; pain worse with movement.
  • Causes: Staph. aureus most common; TB in endemic/immigrant populations.
  • Complications: epidural abscess, neuro deficits from cord/root compression.

🟢 5.3 Septic Arthritis

  • Definition: infection of a joint and surrounding soft tissues (usually monoarthritis).
  • Who: children, elderly, post-op arthroplasty, immunosuppressed.
  • Presentation: hot, swollen, red, very tender joint; severely reduced ROM; fever/chills.
  • Sites: knee > hip, shoulder, ankle.
  • Causes: Staph. aureus, Strep spp., N. gonorrhoeae (sexually active adults).
  • Complications: irreversible cartilage damage in 6–12h; osteomyelitis from spread.

🟢 5.4 Osteomyelitis

  • Definition: infection of bone (acute or chronic).
  • Epidemiology: long bones in children (haematogenous); vertebrae in adults; common with diabetic foot ulcers & post-trauma.
  • Presentation: persistent localised bone pain, fever, swelling/redness; chronic: sinus tract, non-healing ulcers.
  • Routes: blood-borne, post-surgical, direct trauma.
  • Complications: chronic infection, pathological fracture, sepsis.

🔎 6.1 #THREADSOCS – Hidden Red Flag Screening Tool

LetterTopicWhy It Matters Clinically
#FracturesSuggests osteoporosis; old fractures may indicate AVN or malunion. Watch for non-union/malunion especially in diabetics, smokers, or steroid users.
TThyroidHypothyroidism: delayed healing, ↑ frozen shoulder risk. Hyperthyroidism: ↑ bone turnover → osteoporosis. Both alter MSK recovery.
HHeart / CVRCVR disease, stroke, DVT, PE, PAD. AAA risk (severe abdominal/back pain). CVR disease ↑ surgical and healing risk.
RRheumatologyRA, PsA, AS, PMR, psoriasis, Crohn’s disease. Immunosuppression → ↑ infection risk (discitis, septic arthritis, osteomyelitis).
EEpilepsyFall/fracture risk; contraindication for certain electrotherapies; seizure during assessment. Consider MSK injuries related to seizures (e.g., posterior shoulder dislocation).
AAsthma / LungHx of PE, lung cancer, TB (may spread to bone/joints). COPD. Pancoast tumour → brachial plexus involvement. Long-term steroids → AVN risk.
DDiabetesDelayed healing, neuropathy (stocking distribution), arterial ulcers, ↑ infection risk (discitis, septic arthritis, osteomyelitis), frozen shoulder, Dupuytren’s, malunion/non-union risk.
SSteroid UseWeakens bone/tendon → rupture/AVN risk. Immunosuppression ↑ infection risk (esp. post-CSI). Endogenous steroid suppression → Addison’s disease risk. Anabolic steroids → liver risk. Topical = local effect.
OOsteoporosisFragile bone, high-risk fracture sites (hip, spine, wrist), esp. post-menopause. Risk of fragility fracture, malunion, AVN.
CCancerRecurrence/metastases risk; myeloma (family history link); chemo/radiotherapy damage; neuropathy; radiotherapy fibrosis; osteomyeloma.
SSurgical HistoryAVN risk, deep infection risk, implant failure/rejection, fibrosis. New or returning pain post-op = red flag for hardware failure or infection.

➕ Also ask about: A/S – Alcohol & Smoking

Why it matters: Both have multi-system effects that impair recovery, increase surgical and rehab risk, and elevate the likelihood of serious pathology behind an MSK presentation.

Risk FactorEffects
🥃 Alcohol↑ Risk of AVN (especially femoral head), neuropathies (alcoholic polyneuropathy), myopathy, liver disease (coagulopathy, ↓ protein synthesis), osteoporosis (↓ vitamin D metabolism), delayed fracture/wound healing, ↑ cancer risk (oral, throat, liver, breast), ↑ infection risk (impaired immunity), ↑ risk of falls/trauma.
🚬 Smoking↓ Tissue oxygenation (vasoconstriction & carbon monoxide), ↑ atherosclerosis, ↑ risk of DVT/PE, stroke, MI, PAD, delayed fracture/wound healing, ↑ AVN risk, ↑ infection risk (post-op & general), ↑ respiratory risk (COPD, lung cancer), peripheral neuropathy risk, ↑ osteoporosis risk.
  • Combined effect of smoking + alcohol is synergistic in worsening CVR disease, cancer risk, and impaired healing.
  • Alcohol excess → balance/gait disturbance → increased falls/fractures.
  • Smoking → ↓ surgical success rates (esp. spinal fusion, joint replacements).
  • Both reduce rehab tolerance due to fatigue, poor cardiorespiratory function, and systemic inflammation.

🧠 6.2 Other Important Pathologies — When to Think Outside MSK

⏳ First Presentation < 20 or > 55

  • Back pain is uncommon in these age groups unless there’s serious pathology.
  • High suspicion for cancer, fracture, infection in these cases.

🔁 Constant, Progressive, Non-Mechanical Pain

  • Not eased or aggravated by rest/activity.
  • Suggestive of tumour, fracture, infection, or systemic inflammation.

🟥 Thoracic Pain / Band-Like Pain

  • Rarely purely mechanical; may indicate metastases or visceral referral.
  • Always screen cancer history.
  • Particularly if constant or progressive; may indicate metastatic disease, visceral referral (lungs, abdominal organs, breast), or spinal cord pathology.

⚡ Neurological Red Flags

TypeFeatures
CentralUMN signs (Hoffmann’s, Babinski, clonus), ataxia, widespread neurology
SpinalMyotomal/dermatomal loss, reflex asymmetry, tension tests
PeripheralMotor loss, wasting, nerve-specific loss (radial, ulnar, median)

🌡️ Systemically Unwell

  • Fatigue, malaise, unintentional weight loss, night sweats, fever
  • Suggestive of systemic inflammation, infection, or cancer

🧬 Relevant PMH

  • Cancer (personal/family)
  • Drug abuse
  • HIV
  • Long-term steroids

↑ recurrence risk, immune compromise → higher infection risk (discitis, septic arthritis, osteomyelitis)

🧬 6.3 Oncology-Specific Red Flags

5 Most Common Tumours to Metastasise (Mnemonic: Pierce Brosnan – Licence to Kill)

  • Prostate – lumbar
  • Breast – thoracic
  • Lung – thoracic
  • Thyroid – cervical/thoracic
  • Kidney – lumbar

Typical cancer presentation

  • PMH of cancer
  • Progressive symptoms: “It’s getting worse”
  • Night pain
  • Unusual locations (thoracic, ribs, abdominal, band-like)
  • Systemic signs: malaise, weight loss

🌙 Night Pain (Cancer Link)

  • Pain worse at night, any position
  • “Awake pacing”, “night sweats”, “sleeping in a chair”
  • Supine position worsens symptoms (space-occupying lesion suspicion)

🧭 6.4 Management Pathway

  • 🚨 Escalate to senior
  • 📝 Urgent referral (GP, Consultant Physio, Oncology)
  • 💉 Imaging + bloods

References

  1. Braun J, Sieper J. (2007). Ankylosing spondylitis. Lancet, 369(9570), 1379–1390.
  2. Dasgupta B, et al. (2010). Polymyalgia rheumatica: Clinical update. BMJ, 340, c693.
  3. Fehlings M.G., et al. (2017). Degenerative Cervical Myelopathy: Diagnosis and Management. The Spine Journal, 17(6), 735–756.
  4. Gladman D.D., et al. (2020). Psoriatic arthritis. New England Journal of Medicine, 382(10), 957–970.
  5. IFOMPT Framework. Screening for serious pathology in the cervical spine. (Framework document).
  6. Kerry R., Taylor A.J. Cervical arterial dysfunction risk assessment (concept papers).
  7. Nouri A., et al. (2015). Degenerative Cervical Myelopathy: Epidemiology, Genetics, and Pathogenesis. Spine, 40(12), E675–E693.
  8. Rushton A., et al. Risk assessment prior to cervical spine manual therapy.
  9. Smolen J.S., et al. (2016). Rheumatoid arthritis: Strategies for improved outcomes. Lancet, 388(10055), 233–245.
  10. Tracy J.A., Bartleson J.D. (2010). Cervical spondylotic myelopathy. Neurologist, 16(3), 176–187.

Adapted for quick screening. Always apply local policies & pathways.

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