Low Back Pain (Approach & Red Flags)

Meet the patient

A 35-year-old bricklayer bent and twisted on site an hour ago, felt something go in his lower back, and now walks into the department tilted forward and to the left, unable to stand straight. Pain is in the lumbosacral area and right buttock, worse on sitting and coughing. No leg numbness, normal bladder and bowels, no fever, no weight loss, no cancer history, no significant trauma. He is asking for an MRI.[1]

Here is the central exam question, and the recurring trainee error lives inside it: what do you NOT do for this man? You do not scan him. Over 90 percent of acute low back pain is mechanical and self-limiting, and an MRI at this hour finds an incidental disc bulge in roughly a third of pain-free 35-year-olds — then starts a cascade of fear, opioids, injections and surgery that causes the very disability you meant to prevent.[4]

The mantra for this topic, repeat it on every ward round: reassure, mobilise, NSAIDs first; do not scan the 90 percent; cauda equina is the only emergency.[1]

One spine, three buckets — the triage that runs the whole topic

Low back pain is defined as pain, tension or stiffness between the lower costal margin and the inferior gluteal folds, with or without referred leg pain (sciatica). Almost everyone will have a disabling episode in their lifetime — the lifetime prevalence is about 80 to 84 percent — and it is now the leading cause of years-lived-with-disability worldwide, ahead of ischaemic heart disease, headache and depression, and rising as populations age.[2]

You do not diagnose back pain; you triage it. Every back-pain encounter, primary care or the emergency department, ends with the patient dropped into one of three buckets, and the bucket decides whether you image, refer, reassure or operate:[5]

The red-flag screen — the most examinable skill in this topic

The whole topic collapses to one habit: a deliberate, repeated search for red flags at every back-pain assessment. You are fishing a dangerous minority out of a sea of self-limiting mechanical pain, and the only rod that works is a structured screen asked the same way every time — recent trauma, age over 50 with new pain, cancer history, fever or weight loss or night sweats, immunosuppression or IV drug use, corticosteroids, night pain unrelieved by rest, and any neurological deficit.[5]

The RED FLAG mnemonic turns that list into a scene — picture the patient as you say each letter:[5]

Everyone forgets: a single element of the cauda equina triad — saddle numbness, or new urinary symptoms, or bilateral leg signs — is enough to trigger the workup. You do not need the whole triad, and you must never attribute urinary symptoms to mechanical pain. Bladder-scan for retention at the bedside.[1]

How big, who, and why the scanner is winning

Low back pain is the leading cause of years-lived-with-disability worldwide on every Global Burden of Disease count, with a lifetime prevalence of 80 to 84 percent and a point prevalence of 12 to 33 percent. Peak onset is between 30 and 50 — the working years — and it is the single biggest cause of work absence and activity limitation in adults of that age. Prevalence climbs again in the elderly, where stenosis, osteoporotic fracture and malignancy take a larger share.[2]

Risk factors split in two domains, and the second is the one that decides who gets chronic. Mechanical and physical drivers — heavy or repeated manual lifting, whole-body vibration from tractors, trucks or helicopters, twisting and bending at work, smoking, obesity, low cardiovascular and muscular fitness — load the spine. Psychosocial drivers — depression, anxiety, fear-avoidance beliefs, catastrophising, low job satisfaction, job strain, compensation-seeking, widespread pain, prior prolonged episodes — are the yellow flags, and they predict the transition to chronic disabling pain more powerfully than any disc bulge on any scan.[1]

Pathophysiology — three mechanisms, one trap

Understanding why the 90 percent recover and why the minority do not is what makes you triage correctly. Each bucket has its own mechanism.[1]

Mechanical (non-specific). Decades of axial loading, bending and twisting desiccate the nucleus pulposus, tear the annulus fibrosus, and collapse disc height. The overload falls on the facet joints, which develop osteoarthritis, and on the paraspinal muscles, ligaments and thoracolumbar fascia, which strain. These structures are richly innervated by the sinuvertebral nerve, the medial branch of the dorsal ramus, and segmental sensory nerves; their nociceptors fire on mechanical distortion and local inflammation, producing the familiar mechanical pattern — worse with activity and sitting, better with rest.[1]

Why a 'slipped disc' is the wrong word — and the two engines of sciatica

Radicular (sciatica). The disc does not slip — it herniates, classically posterolaterally where the annulus is thinnest and the posterior longitudinal ligament tapers, compressing and inflaming a lumbar root. The L4-L5 and L5-S1 segments carry the greatest axial load and move the most, so L5 and S1 are the roots you will meet. The pain has two engines running at once: mechanical compression of the dorsal root ganglion (worse on sitting, coughing, sneezing, straight leg raise — all increase nerve tension) and inflammatory cytokines (TNF-alpha, IL-1, IL-6) leaking from the herniated nucleus, which sensitise the root to otherwise painless stimuli. The dual mechanism is why anti-inflammatories help and why bed rest does not.[1]

Cauda equina. The spinal cord ends at the L1-L2 conus medullaris; below it the lumbar and sacral roots travel as a bundle — the cauda equina, Latin for horse's tail, because that is exactly what they look like. A large central or paracentral disc, or any mass effect from tumour, abscess, haematoma or retropulsed bone, crushes the S2 to S4 sacral roots that carry pelvic visceral afferents and efferents — producing saddle anaesthesia, bladder and bowel dysfunction, sexual dysfunction, and bilateral leg motor and sensory loss. Internal sphincter tone falls and the bulbocavernosus reflex drops out.[1]

Chronic pain. In the minority, acute pain fails to resolve and central sensitisation takes over — dorsal horn and brain nociceptive pathways amplify and perpetuate the signal long after the tissue has healed. Fear-avoidance, catastrophising, low mood, deconditioning, sleep loss and work or compensation stress are the chief drivers, and they are the primary targets of multidisciplinary rehabilitation.[1]

Read the history for the bucket — the patterns that decide

Tempo and pattern beat every scan in the first six weeks. Take a deliberate structured history — site, onset, character, radiation, associated features, timing, exacerbators, course — and bolt on an explicit red-flag and cauda equina screen every time.[1]

Mechanical (non-specific). Worse with activity and prolonged sitting, better with rest and lying flat, acute or subacute onset after a recognisable trigger such as lifting, twisting or a fall, and unaccompanied by red flags or objective neurological deficit. It may radiate to the buttock or thigh as sclerotomal pain but not below the knee. The patient is systemically well.[1]

Inflammatory (axial spondyloarthritis). Suspect it when the ASAS inflammatory back pain pattern is present — onset under 40, insidious, better with exercise and not with rest, morning stiffness over 30 minutes, and alternating buttock pain. Ask about the extra-articular clues — uveitis with a red, painful, photophobic eye, psoriasis, inflammatory bowel disease, dactylitis, enthesitis at the Achilles or plantar fascia — and a family history of spondyloarthritis or psoriasis.[5]

Radicular (sciatica). Leg pain radiating below the knee in a dermatomal pattern, often worse than the back pain itself, aggravated by sitting, coughing, sneezing and straight leg raise. L5 weakens great-toe and ankle dorsiflexion (foot drop when severe) with no reliable reflex; S1 weakens ankle plantarflexion and loses the ankle jerk; L4 weakens knee extension and loses the knee jerk.[5]

Cauda equina syndrome. This is the must-not-miss. Classical features: saddle anaesthesia in the perianal, genital and inner thigh S2 to S4 dermatomes; urinary dysfunction with a painless distended bladder as a late and ominous sign; faecal incontinence or loss of anal tone; bilateral sciatica or neurological deficit — the bilaterality is the discriminator from an ordinary unilateral disc; progressive leg weakness; reduced anal tone and bulbocavernosus reflex; and sexual dysfunction. The patient may simply say they have lost control down below or report numbness when wiping after the toilet — those phrases are the trigger, not a throwaway.[1]

Atypical presentations. The elderly may have lumbar spinal stenosis with neurogenic claudication — bilateral leg pain, heaviness or cramping on walking, relieved within minutes by sitting and forward flexion, because cycling flexes the spine and opens the canal. The pregnant patient has mechanical and postural pain from the shifted centre of gravity and relaxin-mediated ligamentous laxity, with limited imaging options. The immunocompromised patient or IV drug user may harbour spinal infection with an indolent, fluctuating, febrile course. Osteoporotic compression fracture presents as sudden severe back pain after minimal or no trauma.[1]

Etymology for viva gold: sciatica runs through the Latin ischiadicus from the Greek ischion, meaning hip — the pain that travels the hip and leg. Cauda equina is straightforward Latin, horse's tail, for the bundle of lumbar and sacral roots below the conus. Both words earned their metaphors the day anatomy was named, and neither has improved on them.[5]

The deadly mimics — palpate the belly, feel the pulses

Before you call it mechanical, examine the abdomen and feel the pulses. The most dangerous mimic of low back pain in the elderly is a ruptured abdominal aortic aneurysm — tearing back or abdominal pain, hypotension, a pulsatile abdominal mass — and missing it is a fatal miss. Referred non-spinal causes head the list whenever the pain is vague, unrelieved by posture, or accompanied by systemic or abdominal features.[1]

The differential, organised by the triage buckets:[1]

• Mechanical (over 90 percent of presentations): muscle or ligament strain, degenerative disc disease, facet arthropathy, spondylolysis (a pars defect, in athletes), spondylolisthesis (anterior slip of one vertebra on another), sacroiliac joint dysfunction, myofascial pain.
• Radicular: lumbar disc herniation (L4-L5, L5-S1 commonest), lumbar spinal stenosis, foraminal or lateral recess stenosis, piriformis syndrome.
• Inflammatory: axial spondyloarthritis — ankylosing spondylitis, psoriatic, reactive, enteropathic, undifferentiated.
• Infective: vertebral osteomyelitis, epidural abscess, discitis — Staphylococcus aureus commonest, Gram-negatives from a urinary or gastrointestinal source, Mycobacterium tuberculosis as Pott disease in endemic areas, Brucella in herd-animal regions, fungi when immunocompromised.
• Malignancy: spinal metastasis (the spine is the commonest site of bony metastasis — breast, lung, prostate, kidney, thyroid, the classic BLT-with-Kosher-Pickle), multiple myeloma, lymphoma, primary bone tumours such as chordoma, Ewing sarcoma in children, osteosarcoma.
• Fracture: osteoporotic compression, traumatic, pathological through tumour or infection.
• Referred (non-spinal): abdominal aortic aneurysm, pancreatitis, peptic ulcer disease, renal colic, pyelonephritis, pelvic inflammatory disease, endometriosis, retrocaecal appendicitis, prostatitis, hip pathology.[1]

The deadly mimic in one line: the elderly back-pain patient who is hypotensive may be exsanguinating from a ruptured AAA — palpate the abdomen for a pulsatile mass and feel the femoral and pedal pulses before you reach for the back.[1]

The bedside round — map the root, find the emergency

Examination rarely makes the diagnosis; it finds the neurological deficit, the cauda equina, and the mimics. Run it in this order.[1]

• Inspection: posture with a list to one side, gait that is antalgic or shows a foot drop pointing to L5, spinal curvature such as scoliosis, kyphosis or hyperlordosis, paraspinal spasm, a step deformity of the spinous processes suggesting spondylolisthesis, skin over the lower back with a sinus, hair tuft, lipoma or naevus suggesting spinal dysraphism, and surgical scars.
• Palpation: point tenderness (localised suggests infection or fracture; widespread non-organic tenderness is non-specific), paraspinal spasm, step deformity, sacroiliac tenderness with FABER and Gaenslen, and abdominal palpation for a pulsatile mass from an AAA and renal angle tenderness.
• Range of motion: flexion, extension, lateral flexion, rotation. Modified Schober — mark 10 cm above the S2 spinous process, ask the patient to forward-flex, and an increase under 5 cm screens for inflammatory spinal restriction, with moderate sensitivity and high specificity in established ankylosing spondylitis.[5]
• Neurology, mapped to roots:
  • L4 — quadriceps weakness on knee extension, knee jerk loss, medial leg numbness.
  • L5 — great-toe and ankle dorsiflexion weakness (foot drop when severe), lateral leg and dorsum of foot numbness, no reliable reflex.
  • S1 — ankle plantarflexion weakness (cannot tip-toe), ankle jerk loss, lateral foot numbness.
• Provocative manoeuvres:
  • Straight leg raise (Lasègue) — reproduction of leg pain below the knee at under 70 degrees of hip flexion signals L5 or S1 root irritation, with high sensitivity and moderate specificity.
  • Crossed straight leg raise — raising the asymptomatic leg reproduces the symptomatic leg pain — is more specific, and a positive crossed SLR predicts a large central disc herniation.
  • Femoral nerve stretch test (prone, knee flexed, hip extended) reproduces anterior thigh pain in an L2 to L4 lesion.
  • Slump test sensitises the nerve-root tension test.
• Cauda equina screen (mandatory whenever a red flag is present): perianal and saddle sensation, anal tone on digital rectal examination, bulbocavernosus reflex, and a bladder scan for post-void residual — a residual over 100 to 200 mL suggests retention and supports the diagnosis.[1]

Match every red flag on history to a physical sign: fever and vertebral tenderness with infection, a palpable bladder with retention, a pulsatile mass with AAA, a step deformity with spondylolisthesis, restricted spinal mobility with axial SpA. The sign confirms what the history threatened.[1]

When to image — and when to shut the scanner

Most low back pain needs no investigation at all. Imaging is reserved for red flags, progressive neurological deficit, suspected cauda equina, suspected infection or malignancy, suspected inflammatory disease, or persistent radiculopathy despite conservative care — because routine imaging of non-specific pain increases harm without improving any outcome. Incidental disc bulges drive anxiety, opioids, injections and surgery, and the patient ends up worse.[4]

The classic trap: scanning the 90 percent who will get better anyway, finding an incidental disc bulge, and starting a cascade of fear, opioids, injections and surgery that causes the very disability you meant to prevent. Incidental findings are the rule, not the exception — about 30 percent of pain-free 20-year-olds and over 80 percent of pain-free 80-year-olds carry a disc bulge on MRI. Treat the patient, not the picture.[4]

Targeted investigations by suspected diagnosis. For suspected infection such as an epidural abscess or vertebral osteomyelitis, CRP and ESR are usually markedly raised and blood cultures are drawn before antibiotics; MRI with gadolinium is the gold standard and maps the abscess. For suspected malignancy, MRI defines cord or cauda compromise and image-guided biopsy gives tissue; hunt the primary with mammogram, prostate exam and PSA, chest CT, and a myeloma screen. For suspected fracture, plain film screens; MRI defines marrow oedema as acute versus healed; DEXA confirms underlying osteoporosis. For suspected axial spondyloarthritis, HLA-B27 plus MRI of the sacroiliac joints for bone marrow oedema is diagnostic when plain films are normal.[5]

Cauda equina — the one surgical emergency

Time is nerve. Every hour of compression beyond the threshold of injury erodes the chance of neurological recovery, and a delayed or missed cauda equina produces permanent paralysis, bladder and bowel incontinence, and sexual dysfunction. This is the one resuscitation scenario in low back pain.[1]

• Recognise the triad at the bedside: saddle anaesthesia plus bladder or bowel dysfunction plus bilateral neurology or progressive weakness. Any one element mandates the workup — you do not need the whole triad.
• Urgent MRI of the lumbar spine today — whole spine if there is multifocal suspicion, prior malignancy, or a negative lumbar MRI with high clinical concern. Keep the patient nil by mouth.
• Immediate neurosurgical or orthopaedic spinal referral for decompression within 24 to 48 hours of symptom onset — laminectomy plus discectomy, plus fusion if unstable. Late decompression, over 48 hours and especially over 72 hours, gives substantially worse bladder, motor and sexual outcomes.
• Catheterise early for retention — a distended bladder worsens the voiding prognosis; protect pressure areas; give analgesia; keep nil by mouth for theatre.
• Document a careful pre-operative neurological examination — motor power by MRC grade and myotome, reflexes, sensation including the saddle area, anal tone — so recovery can be tracked.
• If infection or malignancy with cord compromise is found instead of a disc, treat the cause — long IV antibiotics, oncology referral, urgent radiotherapy — and decompress as appropriate.[2]

The must-not-miss trap, in one line: cauda equina is saddle numbness plus bladder or bowel dysfunction plus bilateral neurology — always ask, always bladder-scan for retention, never attribute urinary symptoms to mechanical pain.[1]

Management — less is more

For non-specific low back pain, the modern evidence is unequivocal: less is more. The biggest iatrogenic harms are over-imaging, opioid prescribing, spinal injections and surgery — interventions that do not improve outcomes and demonstrably cause harm. The ACP, NICE and the Lancet Low Back Pain Series all converge on the same first-line bundle: education, reassurance, stay active, return to work, simple analgesia, exercise.[1][2][3]

Acute non-specific back pain (under 6 weeks) — first line, non-pharmacological:[3]

• Education and reassurance — name it mechanical, non-serious and very likely to improve; advise the patient to stay active and return to work; avoid bed rest, which deconditions and prolongs disability.
• Simple analgesia — NSAIDs first (ibuprofen 400 mg orally three times daily, or naproxen 250 to 500 mg orally twice daily, with a PPI if there is GI risk), at the lowest effective dose for the shortest time. Paracetamol is a second choice — PACE showed regular or as-needed paracetamol at 4 g/day was no better than placebo for acute low back pain.[9]
• Heat with hot packs or hot baths, and short-term manual therapy or spinal manipulation (up to 6 to 8 sessions) for symptom relief.
• Avoid opioids (dependence, overdose, constipation, falls — no long-term benefit), avoid routine imaging, avoid injections.

Persistent or subacute pain (6 to 12 weeks):[3]

• Supervised exercise — any modality the patient will adhere to, such as Pilates, core strengthening, aerobic work, or yoga.
• CBT combined with exercise — targets fear-avoidance, catastrophising and low mood.
• Manual therapy alongside exercise (up to 12 weeks).
• Address the yellow flags — they predict chronic disabling pain more powerfully than any imaging finding.[1]

Chronic disabling pain (over 12 weeks):[3]

• Multidisciplinary biopsychosocial rehabilitation combining physical, psychological and occupational components — the only intervention with consistent evidence for improving pain, function and work outcomes in chronic disabling low back pain.
• Avoid opioids, repeat imaging and further invasive interventions unless a new red flag appears.[1]

Specific pathology: treat the cause. Spinal infection — a long IV course, typically 6 weeks of flucloxacillin 2 g IV every 6 hours with rifampicin, then oral continuation, tailored to the organism, with surgical decompression if there is cord compromise or failure of medical therapy. Osteoporotic compression fracture — vertebroplasty or kyphoplasty for unresponsive severe pain, plus antiresorptive therapy (a bisphosphonate or denosumab, calcium, vitamin D, fall prevention) for the underlying osteoporosis. Spinal metastasis — oncology referral, radiotherapy, surgery for cord compression, systemic therapy. Axial spondyloarthritis — continuous NSAIDs such as naproxen 1000 mg/day plus exercise, and biologic anti-TNF (adalimumab 40 mg subcutaneously every 2 weeks, or etanercept 50 mg weekly) for high disease activity despite NSAIDs.[5]

Sciatica — what the two trials actually showed

Conservative management first, because the natural history is favourable — over 80 percent recover within 6 to 12 weeks. Two trials decide the surgery question, and every examiner knows them.[7]

Peul et al, NEJM 2007 — early microdiscectomy gave faster relief of leg pain in the first months, but no advantage at one and two years over prolonged conservative care. The patient who tolerates waiting can be reassured they will not be harmed by it.[7]

Weinstein et al, SPORT, JAMA 2006 — patients treated surgically for lumbar disc herniation recovered better than those treated non-operatively, though the treatment effect was attenuated by crossover between the arms.[8]

The practical synthesis: MRI if sciatica persists over 6 weeks despite conservative care or if a neurological deficit progresses; microdiscectomy for severe persistent radiculopathy (over 6 to 12 weeks with a confirmed disc on MRI) or progressive motor loss. And remember el Barzouhi's NEJM finding — for sciatica, MRI findings generally track the clinical course, so a routine early scan does not change outcomes without red flags.[6]

Neurogenic versus vascular claudication — the bicycle test

The single discriminator is the flexion requirement. Both cause leg pain on walking; only one is relieved by bending forward.[1]

One-line discriminator: if the patient says the pain goes only when they sit and bend forward — and they can ride a bicycle fine but cannot walk far — that is the canal, not the arteries. Feel the pulses to confirm.[1]

Yellow flags — stronger than any scan

The prognosis is favourable — about 90 percent of acute non-specific pain recovers within 6 weeks, and most of the rest improves by 12 weeks. But recurrence is common, at about 60 percent within a year, and a minority progress to chronic disabling pain. The predictors of that transition are not on the MRI — they are in the patient's life.[1]

The yellow flags, stronger than any imaging finding:[1]

• Depression, anxiety, somatisation.
• Fear-avoidance beliefs — the conviction that pain equals damage.
• Pain catastrophising.
• Low job satisfaction, job strain, poor social support, heavy manual work, compensation-seeking.
• Widespread pain suggesting central sensitisation, and prior prolonged episodes.
• High baseline pain intensity and disability.[1]

Consultant confession: the patient who is still off work at six weeks, frightened of movement and angry with their employer, is the one heading for chronicity — and the disc bulge on their scan is a bystander. Address the yellow flags early, with education, reassurance, CBT, graded exercise and return-to-work support, and you prevent more chronic disability than any injection or operation can fix.[1]

Special populations — where the thresholds move

Elderly: keep a lower threshold to image — lumbar spinal stenosis, osteoporotic compression fracture with sudden severe pain after minimal or no trauma, vertebral malignancy, and referred pain from an AAA all rise in prevalence. Polymyalgia rheumatica and giant cell arteritis may present with back and shoulder-girdle pain and a markedly raised ESR and CRP, and must not be missed.[5]

Pregnancy: mechanical and postural pain from the shifted centre of gravity, relaxin-mediated ligamentous laxity and weight gain. Avoid imaging unless red flags are present, and then prefer MRI without gadolinium. Simple analgesia — paracetamol, but avoid NSAIDs in the third trimester because of premature closure of the ductus arteriosus and oligohydramnios — plus exercise, posture and supportive belts.[5]

Children and adolescents: consider spondylolysis and spondylolisthesis in young athletes such as gymnasts, fast bowlers and dancers, infection (discitis — the young child who refuses to walk, with back pain or a limp), tumour (Ewing sarcoma, osteoid osteoma, aneurysmal bone cyst) and leukaemia. Persistent or night pain in a child warrants imaging — do not dismiss it as growing pains.[5]

Immunocompromised and IV drug users: high risk of spinal infection with atypical organisms — Staphylococcus aureus commonest, but Gram-negatives, tuberculosis, fungi and Candida are all in play. Maintain a low threshold for MRI, blood cultures and inflammatory markers.[5]

Long-term corticosteroids: high risk of osteoporotic compression fracture and avascular necrosis (the latter at the hip, but it may refer pain to the back). Anticoagulated patients: any sudden severe back pain with hypotension or anaemia may be a spinal epidural haematoma — urgent MRI and neurosurgical referral.[5]

Regional differences — same evidence, different bottlenecks

The evidence base has shifted decisively toward conservative, biopsychosocial care. The Lancet Low Back Pain Series (2018) issued a global call to action against over-medicalisation, the ACP guideline (Qaseem 2017) put non-pharmacologic care first and downgraded paracetamol on the strength of PACE, and Chou's ACP high-value care advice (2011) confirmed that routine imaging does not improve outcomes and causes harm.[1][2][3][4]

Ward-round test

Carry these four stems into the viva — each defends a real contract, and the answers below are the model.[1]

Stem 1 — the bricklayer who wants a scan (answer)

A 35-year-old bricklayer bent, twisted and felt something go; he is tilted and in pain, no red flags, and is asking for an MRI. What do you do, and what do you not do? Model: This is acute non-specific mechanical low back pain — over 90 percent recover within 6 weeks. Reassure, advise stay active and return to work, prescribe an NSAID at the lowest effective dose for the shortest time, add heat and short-term manual therapy if helpful, and safety-net for red flags. Do NOT image (no red flags, under 6 weeks — routine imaging drives overdiagnosis, opioids and surgery with no benefit), do NOT prescribe opioids, do NOT recommend bed rest. Warn him recurrence is common, at about 60 percent within a year.[1][3][9]

Stem 2 — numbness when wiping (answer)

A 47-year-old with three weeks of back pain now reports numbness when wiping after the toilet and has not passed urine since morning. What is the diagnosis, the bedside test, and the next two phone calls? Model: This is cauda equina syndrome until proven otherwise — saddle anaesthesia plus urinary dysfunction. Bladder-scan for retention (a post-void residual over 100 to 200 mL supports it), perform a digital rectal exam for anal tone and a bulbocavernosus reflex, and document bilateral neurology. Order urgent MRI of the lumbar spine today, keep nil by mouth, catheterise, and call neurosurgery or the spinal orthopaedic team for decompression within 24 to 48 hours. Never attribute urinary symptoms to mechanical pain.[1]

Stem 3 — the elderly man who claudicates (answer)

A 72-year-old man gets bilateral calf heaviness after 100 metres that forces him to stop. It settles in minutes if he sits and leans forward, but also if he simply stands still. Ankle pulses are absent. Which claudication is it, and why does it matter? Model: This is vascular claudication, not neurogenic — the relief on simply standing still and the absent ankle pulses are the discriminators. Neurogenic claudication needs flexion and sitting, preserves pulses, and lets the patient cycle. Examine the arterial tree, calculate an ankle-brachial index, and refer to vascular surgery. Treating the canal with a laminectomy here would be a category error.[1]

Stem 4 — the hypotensive elderly back pain (answer)

A 78-year-old man presents with tearing lower back pain, hypotension, and a vaguely palpable abdominal mass. What must you exclude before you call it mechanical, and what is the first move? Model: This is a ruptured abdominal aortic aneurysm until proven otherwise — the deadly mimic of low back pain in the elderly. Palpate the abdomen for a pulsatile mass, feel the femoral and pedal pulses, and call surgery and anaesthetics now. This is not a back to be examined and reassured; it is a vascular emergency. Never label elderly back pain mechanical until the belly and pulses have been examined.[1]

Exam pearls

• Over 90 percent of low back pain is non-specific and self-limiting — it recovers within 6 weeks. Over-investigation, opioids, injections and surgery cause harm.[1]
• Screen red flags at every visit: cauda equina, fracture, infection, malignancy, axial spondyloarthritis. The systematic screen is the most examinable skill here.
• Cauda equina = saddle anaesthesia plus bladder or bowel dysfunction plus bilateral neurology. Surgical emergency — urgent MRI today, decompression within 24 to 48 hours, catheterise.[2]
• Reserve MRI for red flags, progressive neurology, or persistent radiculopathy over 6 weeks — not for routine non-specific pain.[4]
• Non-specific pain: reassure, stay active, NSAIDs first (paracetamol is no better than placebo per PACE), exercise and CBT for persistent pain. Avoid opioids and routine imaging.[3][9]
• Sciatica is L5 or S1 in the vast majority, from L4-L5 or L5-S1 herniations. L5 — great-toe dorsiflexion weakness, no reflex; S1 — ankle jerk loss, plantarflexion weakness. Crossed straight leg raise is more specific.[5]
• Inflammatory back pain (ASAS) — onset under 40, insidious, better with exercise, morning stiffness over 30 minutes, alternating buttock — points to axial spondyloarthritis. Send HLA-B27 and MRI of the sacroiliac joints.[5]
• Spinal stenosis pseudoclaudication — worse walking and downhill, better with flexion and sitting (bicycle test positive). Distinguish from vascular claudication (no flexion requirement, absent pulses).
• Sciatica surgery: Peul 2007 NEJM showed early surgery gives faster leg pain relief but no advantage at one year versus prolonged conservative care; SPORT confirmed surgical superiority for disc herniation despite crossover.[7][8]
• Do not miss the AAA in the elderly back-pain patient — palpate the abdomen for a pulsatile mass.[1]

References

1. [1]Foster NE, Anema JR, Cherkin D, Chou R, Cohen SP, Gross DP, et al. Prevention and treatment of low back pain: evidence, challenges, and promising directions Lancet, 2018.PMID 29573872
2. [2]Buchbinder R, van Tulder M, Öberg B, Costa LM, Woolf A, Schoene M, Croft P, et al. Low back pain: a call for action Lancet, 2018.PMID 29573871
3. [3]Qaseem A, Wilt TJ, McLean RM, et al. Noninvasive Treatments for Acute, Subacute, and Chronic Low Back Pain: A Clinical Practice Guideline From the American College of Physicians Ann Intern Med, 2017.PMID 28192789
4. [4]Chou R, Qaseem A, Owens DK, et al. Diagnostic imaging for low back pain: advice for high-value health care from the American College of Physicians Ann Intern Med, 2011.PMID 21282698
5. [5]Chou R, Qaseem A, Snow V, Casey D, Cross JT Jr, Shekelle P, Owens DK, et al. Diagnosis and treatment of low back pain: a joint clinical practice guideline from the American College of Physicians and the American Pain Society Ann Intern Med, 2007.PMID 17909209
6. [6]el Barzouhi A, Vleggeert-Lankamp CL, Lycklama à Nijeholt GJ, et al. Magnetic resonance imaging in follow-up assessment of sciatica N Engl J Med, 2013.PMID 23484826
7. [7]Peul WC, van Houwelingen HC, van den Hout WB, et al. Surgery versus prolonged conservative treatment for sciatica N Engl J Med, 2007.PMID 17538084
8. [8]Weinstein JN, Tosteson TD, Lurie JD, Tosteson ANA, Hanscom B, Skinner JS, Abdu WA, et al. Surgical vs nonoperative treatment for lumbar disk herniation: the Spine Patient Outcomes Research Trial (SPORT): a randomized trial JAMA, 2006.PMID 17119140
9. [9]Williams CM, Maher CG, Latimer J, McLachlan AJ, Hancock MJ, Day RO, Lin CCW, et al. Efficacy of paracetamol for acute low-back pain: a double-blind, randomised controlled trial Lancet, 2014.PMID 25064594