Non-specific low back pain and inflammatory back-pain red flags

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Low back pain is a classification task before treatment. Establish onset, trauma, distribution, leg symptoms, weakness, numbness, fever, cancer, infection exposure, steroid use, weight loss, night pattern, abdominal or urinary symptoms and vascular risk. Ask directly about urinary flow sensation, retention, saddle sensation, sexual function and bowel control. Examine gait, spine, hip and abdomen; test myotomes, dermatomes and reflexes; check pulses and observations. A reassuring appearance or chronic pain history never replaces a new neurological examination.

Non-specific pain commonly fluctuates with position and load but can be severe without dangerous pathology. The label means no single anatomical lesion can be reliably assigned, not imaginary or trivial pain. Routine radiographs or MRI reveal disc bulges, degeneration and facet change in many asymptomatic adults. Imaging can therefore increase fear and intervention unless a specific question—fracture, infection, cancer, compression or procedural planning—makes it actionable.

Inflammatory back pain needs a parallel route. Axial spondyloarthritis commonly begins before 45 and improves with movement rather than rest, with nocturnal waking, buttock pain and extra-articular disease. NICE combines duration, age and additional features and does not require HLA-B27 positivity or radiographic sacroiliitis. In specialist care, sacroiliac radiographs are followed by inflammatory-back-pain MRI if films are non-diagnostic. Mechanical and inflammatory mechanisms may coexist, so persistent pain after inflammation control does not automatically justify immunosuppression escalation.

Key points

Screen every new or changed episode for cauda equina, progressive motor loss, infection, cancer, fracture and vascular or visceral causes before calling it non-specific.
Do not routinely image non-specific low back pain in non-specialist care; incidental degeneration is common and imaging is useful only when it changes management.
Advise continued ordinary activity, self-management and return to work where feasible; prolonged bed rest weakens muscle and reinforces fear.
Offer exercise appropriate to needs; manual therapy should be used only in a package including exercise, with psychological treatment for persistent obstacles or high poor-outcome risk.
If medicine is needed, consider a brief oral NSAID after gastrointestinal, renal, cardiovascular and pregnancy review; paracetamol alone, gabapentinoids, antidepressants and chronic opioids are not recommended.
Inflammatory clues include onset before 45, over three months of pain, second-half night waking, buttock pain, improvement with movement, rapid NSAID response, psoriasis, uveitis, IBD, enthesitis or family history.
Use the NICE axial-spondyloarthritis referral combination; normal CRP, normal ESR, negative HLA-B27 or a normal radiograph does not exclude disease.
Immediate MRI is required for suspected cauda equina or compressive neurological emergency; cancer or infection may require broader spinal coverage than routine lumbar imaging.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Non-specific mechanical pain

Most episodes cannot be assigned to one precise structure; disc, facet, ligament, muscle and altered movement may contribute while serious pathology is absent.

Nerve-root irritation

Disc protrusion, foraminal narrowing or local inflammation produces leg-dominant radicular pain, sensory change, weakness or reflex loss rather than isolated axial pain.

Inflammatory axial disease

Axial spondyloarthritis causes sacroiliac and spinal inflammation, often linked to HLA-B27, psoriasis, uveitis, bowel disease, enthesitis or family history.

Specific dangerous causes

Malignant epidural disease, infection, osteoporotic fracture, aneurysm, abdominal pathology and major neural compression are uncommon but time-sensitive explanations.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Mechanical nociception
Loaded spinal and paraspinal tissues generate nociceptive input after strain or degeneration, but imaging abnormalities correlate imperfectly and often occur without pain.
2
Protective sensitisation
Pain, guarding and fear alter movement; persistent threat expectation, poor sleep and inactivity can amplify sensitivity after initiating tissue irritation settles.
3
Radicular mechanisms
Root compression and local inflammation produce dermatomal pain or paraesthesia; clinically important motor loss reflects axonal dysfunction and changes urgency.
4
Enthesis-driven inflammation
In axial spondyloarthritis immune inflammation at sacroiliac and spinal entheses causes marrow oedema, erosion and later new bone, stiffness and ankylosis.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Non-specific pattern

Axial pain varies with movement and activity without consistent neurological loss, systemic illness or a specific destructive cause on assessment.

Radicular pattern

Leg pain with dermatomal paraesthesia, tension signs, reflex change or myotomal weakness suggests nerve-root involvement.

Cauda-equina pattern

New bladder-flow sensory change, retention, saddle numbness, bilateral symptoms or progressive weakness requires emergency assessment; no single feature is sufficiently sensitive alone.

Inflammatory pattern

Young onset, chronicity, nocturnal waking, alternating buttock pain and improvement with exercise rather than rest cluster with axial spondyloarthritis.

Extra-articular linkage

Psoriasis, anterior uveitis, inflammatory bowel disease, peripheral arthritis, dactylitis, enthesitis or first-degree family history raises inflammatory probability.

Infection or cancer pattern

Constant progressive pain, fever, immune risk, previous malignancy, weight loss or multi-level neurological signs requires urgent specific-pathology investigation.

Red flags requiring action

New bladder dysfunction, saddle sensory change, bilateral neurological symptoms or progressive motor deficit requires immediate cauda-equina or spinal compression assessment.
Fever, bacteraemia, immunosuppression, injecting drug use, spinal procedure or constant severe pain raises vertebral osteomyelitis or epidural abscess and needs urgent cultures and MRI.
Cancer history, weight loss, progressive night pain or multi-level neurological findings requires an urgent malignant spinal pathway and appropriately timed whole-spine imaging.
Significant trauma, older age with fragility risk, prolonged glucocorticoids or focal percussion tenderness suggests vertebral fracture even after low energy.
Sudden tearing back or abdominal pain, syncope, pulse deficit, hypotension or a pulsatile abdominal mass suggests vascular catastrophe and needs emergency transfer.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
First-line clinical triageFirst stepFirst line
Why
Classify non-specific, radicular, inflammatory and dangerous patterns and choose emergency care or active conservative management.
Interpretation and limitations
Absence of red flags supports non-imaging care, but evolving bladder, motor, systemic or traumatic features change classification and require reassessment.
02
Emergency MRI for cauda equina
Why
Confirm or exclude compression rapidly enough to preserve bladder, bowel, sexual and lower-limb neurological function.
Interpretation and limitations
Use the local emergency pathway; bladder scan or rectal findings may inform assessment but must not be used alone to rule out compression.
03
Urgent MRI and bloods
Why
Detect epidural, vertebral, marrow or multi-level infection or malignant disease and obtain microbiological or oncological evidence.
Interpretation and limitations
Request FBC, CRP or ESR, renal profile and blood cultures for infection; choose whole-spine coverage for metastatic cord risk according to NICE.
04
Fracture radiography or CT
Why
Define vertebral body injury, alignment and posterior-element involvement after trauma or fragility-risk focal pain.
Interpretation and limitations
Plain films may miss occult injury; CT or MRI is required when probability remains high or neurological and malignancy questions coexist.
05
Axial SpA laboratory assessment
Why
Support referral and evaluate inflammation without treating a negative biomarker as exclusion.
Interpretation and limitations
CRP or ESR can be normal; HLA-B27 increases probability in the correct phenotype but is neither necessary nor sufficient.
06
Sacroiliac film then inflammatory MRI
Why
Identify radiographic sacroiliitis or active and structural inflammation within specialist assessment.
Interpretation and limitations
If X-ray does not meet modified New York criteria, use an unenhanced inflammatory-back-pain MRI protocol; a negative scan does not end review when suspicion remains high.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Cauda equina compression

Bladder, saddle or bilateral neurological features identify central neural compromise; thoracic signs or upper-motor-neurone findings point above the cauda equina.

Spinal infection or malignancy

Constant focal pain, systemic risk, fever, immunosuppression or cancer history requires urgent MRI and specific tests; normal early radiographs are not reassuring.

Vertebral fracture

Abrupt focal pain after low energy, steroid exposure or osteoporosis may be compression fracture, while high-energy trauma requires formal trauma assessment.

Visceral and vascular referral

Aortic, renal, pancreatic, pelvic and gastrointestinal disease can refer to the back; abdominal, urinary, vascular or constitutional findings redirect evaluation.

Hip and regional pain

Hip osteoarthritis, trochanteric pain and myofascial disorders alter gait and mimic lumbar symptoms; joint movement and neurological examination localise them.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01First-line non-specific careKeep recovery activeFirst stepFirst lineAssessment finds no serious cause, progressive neurological loss or compelling inflammatory referral pattern.

1Explain favourable natural history, advise normal activity and early work participation within tolerance, and provide return advice for bladder, saddle, weakness, fever, trauma or deterioration.
2Use risk stratification at first contact to match simple self-management to low-risk episodes and intensive physical or psychological support to likely poor recovery.
3Offer group or individual exercise chosen around capability and preference; consider manual therapy only within a package including exercise.
4For persistent pain or psychosocial obstacles, combine exercise with CBT-informed treatment and address sleep, mood, work and dependence-prone medicines.

02Stepwise medicine careUse brief analgesia to support movementPain obstructs sleep, ordinary activity or participation in active recovery.

1Consider an oral NSAID at the lowest effective dose briefly after gastrointestinal, kidney, liver, cardiovascular, interaction and pregnancy assessment, with gastroprotection.
2For acute low back pain only, consider a brief weak opioid with or without paracetamol when an NSAID is contraindicated, not tolerated or ineffective.
3Do not use paracetamol alone, gabapentinoids, antiepileptics or antidepressants for non-specific low back pain, and never offer opioids for chronic low back pain.
4EscalationReview according to severity, stop ineffective medicine and reassess if analgesic needs escalate or neurological and systemic features emerge.

03Inflammatory referralApply the NICE feature combinationPain began before 45, has lasted over three months and has inflammatory or spondyloarthritis associations.

1Refer when at least four additional NICE features are present: onset before 35, second-half night waking, buttock pain, movement improvement, rapid NSAID response, first-degree family history, arthritis, enthesitis or psoriasis.
2If exactly three additional features are present, test HLA-B27 and refer if positive; reassess when uveitis, IBD or another strong feature develops.
3Do not rule out axial spondyloarthritis because the person is female, HLA-B27 negative, has normal markers or lacks plain-film sacroiliitis.
4While awaiting review, support activity and safe NSAID use and give urgent eye advice for a painful red photophobic eye.

04Emergency departureAct on consequenceBladder or saddle change, progressive weakness, cancer, infection, fracture or vascular features appear.

1Stop routine care, repeat observations and neurology, document timing and arrange emergency MRI for suspected cauda equina or cord compression.
2Use urgent cultures and MRI for infection, the metastatic-spinal pathway for cancer signs, and trauma or fragility imaging for focal fracture concern.
3Call emergency vascular services for shock, pulse deficit or tearing abdominal-back pain rather than routine musculoskeletal triage.

Key medicines and prescribing safety3 treatments · regimens, roles and cautions

A reasonable oral NSAID option enabling activity after serious pathology has been excluded.

Naproxen with gastroprotection

Use 250–500 mg orally twice daily with food for the shortest acute course; when gastrointestinal risk warrants, add omeprazole 20 mg orally once daily for the duration.

Assess ulcer, anticoagulants, eGFR, blood pressure, heart failure and cardiovascular disease; avoid severe renal impairment and active ulceration, and apply pregnancy restrictions from 20 weeks.

A short weak-opioid rescue for acute, not chronic, low back pain while mobility and recovery continue.

Codeine phosphate for exceptional acute use

Use 30–60 mg orally every four hours when required for only a few days, never exceeding 240 mg in 24 hours, solely when an NSAID is unsuitable; set a stop date.

Sedation, constipation, impaired driving, falls, respiratory depression, tolerance and dependence occur; avoid alcohol or other sedatives and breastfeeding, and individualise pregnancy advice.

May accompany exceptional short weak-opioid treatment; NICE advises against paracetamol alone for non-specific low back pain.

Paracetamol in an acute combination

If used with a brief weak opioid, take 500 mg–1 g orally at intervals of at least four hours when needed, maximum 4 g daily for a suitable adult; reduce for low weight or liver risk.

Count all compound products to prevent overdose; avoid chronic automatic continuation and remember combination use retains opioid sedation, dependence and driving risks.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Persistent disability

Fear, work barriers, sleep disturbance, low mood and deconditioning can convert a self-limiting episode into chronic pain and reduced participation.

Neurological loss

Progressive root or central compression can leave foot drop, neuropathic pain, bladder, bowel and sexual dysfunction if time-critical assessment is delayed.

Inflammatory structural damage

Untreated axial spondyloarthritis may produce impaired spinal mobility, kyphosis, osteoporosis, vertebral fracture and reduced chest expansion.

Iatrogenic chronicity

Unnecessary imaging, bed rest, repeated injections, opioids and alarming structural language reinforce fear, dependence and disability without improving the episode.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Review function, sleep, return to work, exercise progression and red flags rather than ordering interval imaging because pain has not completely resolved.
Repeat neurological examination promptly when leg symptoms spread, weakness develops, gait changes or bladder, bowel, sexual or saddle symptoms emerge.
For oral NSAIDs, review benefit and stop date and monitor blood pressure, renal function, haemoglobin and gastrointestinal symptoms according to risk.
When pain persists, reassess barriers, inflammatory features, hip or visceral causes and medicine dependence before escalating procedures.
After rheumatology referral, record psoriasis, uveitis, IBD, dactylitis, enthesitis and family history because inflammatory phenotype evolves.
Provide a concrete route for urgent reassessment; an exercise plan without safety-netting is inadequate.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Imaging can cause harm

Common age-related disc findings can be misread as injury, increasing fear and invasive treatment; image only for a management-changing question.

Bladder wording matters

Ask about difficulty initiating flow, lost filling or stream sensation and retention, not only established incontinence, which may occur late.

Inflammatory tests can be normal

Neither normal CRP nor negative HLA-B27 excludes axial spondyloarthritis when age, symptom pattern and associated disease remain persuasive.

Movement response informs

Improvement with movement and worsening at rest supports inflammatory disease, while ordinary mechanical pain varies with specific load and position.

11Common pitfallsFrequent interpretation and management errors.

01
Do not use a normal bladder scan, rectal examination or absence of incontinence alone to exclude cauda equina syndrome.
02
Do not request routine lumbar MRI to reassure uncomplicated pain; incidental abnormalities may increase anxiety.
03
Do not advise prolonged bed rest or work avoidance; adapt activity while maintaining movement and confidence.
04
Do not initiate gabapentin, pregabalin, antidepressants or chronic opioids for non-specific low back pain.
05
Do not dismiss axial spondyloarthritis after normal CRP, negative HLA-B27 or normal radiography.
06
Do not retain a mechanical label when fever, weight loss, trauma, cancer, neurological loss or qualitative change creates a new problem.