Low Back Pain

Low back pain is pain, muscle tension, or stiffness localized below the costal margin and above the inferior gluteal folds, with or without pain referred into the leg (sciatica). The overwhelming majority of cases are nonspecific (mechanical) low back pain -- no single structural finding on imaging reliably explains the pain, and imaging findings correlate poorly with symptoms even in people without any back pain at all.^[1] Management is staged by duration: acute (roughly the first 4 weeks, sometimes defined as 0-30 days), subacute (4 to 12 weeks), and chronic or persistent (over 12 weeks) low back pain, with sciatica -- pain referred below the knee, with or without a demonstrable radiculopathy -- treated as a distinct but overlapping presentation. The single highest-yield task at every visit, regardless of duration, is a brief screen for the small minority of patients with a serious underlying cause -- cauda equina syndrome, malignancy, infection, or fracture -- since missing one of these has far greater consequence than a delay in treating routine mechanical pain.

Nonspecific (mechanical) low back pain

Axial low back pain that worsens with movement or prolonged static posture and improves with rest or position change, without radiation below the knee and without a demonstrable neurologic deficit. This is the presentation in the large majority of patients and does not require imaging or a specific structural diagnosis before starting treatment.

Sciatica

Pain referred from the back into the leg, below the level of the knee. There are two distinct patterns: sciatica with radiculopathy, where a specific nerve root lesion is demonstrable on neurologic exam, electromyography, CT, or MRI (most often from a herniated disc compressing a nerve root); and sciatica without radiculopathy, a referred-pain mechanism without a demonstrable focal nerve root lesion. The distinction matters because radiculopathy points toward a specific anatomic cause and a specific dermatomal exam pattern (see Assessment & Diagnosis), while nonradicular referred sciatica is managed the same as nonspecific low back pain.

Risk factors for developing low back pain

• Heavy manual labour, repetitive lifting, bending, or twisting.
• Prolonged sitting or a sedentary lifestyle.
• Obesity.
• Smoking.
• Poor physical conditioning and reduced core/trunk strength.
• Prior episode of low back pain -- the strongest predictor of a future episode.
• Pregnancy (see Special Populations).

Risk factors for chronicity ("yellow flags") -- screen for these explicitly by 4-6 weeks if symptoms or work absence persist

• Duration of work absence to date, and a history of prolonged sick-listing after previous injuries or prior absenteeism.
• High self-reported functional disability, or self-reported extreme and constant pain across multiple body areas.
• Delays or obstacles in the work re-entry process, an adversarial attitude toward the employer, or a belief that one will never return to work.
• A long-standing history of psychiatric distress or maladjustment.
• Compensation or litigation in progress, particularly where compensation levels are high or the patient is in active conflict with the employer or insurer.
• Mental-status indicators of significant anxiety or depression: insomnia or nightmares, irritability, social withdrawal, panic episodes, persistent tearfulness, poor concentration, anhedonia (inability to enjoy activities), and poor appetite or libido.
• Any expression that life is not worth living needs the same urgent same-day mental health assessment it would in any other clinical context -- do not let it pass unaddressed as just a pain symptom.

Differentiating serious spinal pathology from mechanical low back pain

Because several of these serious causes can present with pain alone at their earliest stage, use this table alongside the red-flag list above rather than waiting for a fully developed presentation.

History

• Onset, duration, character, and location of pain; whether pain radiates below the knee (sciatica); aggravating and relieving factors.
• Explicit screen for every red flag above at the first visit, and again at any reassessment.
• Explicit screen for yellow flags (see Risk Factors) by 4-6 weeks if symptoms or work absence have not resolved.
• Prior episodes, prior treatment response, and current medication use including any recent antibiotic, corticosteroid, or anticoagulant use.

Physical examination

• Observe gait, including heel walking (tests L4-L5) and toe walking (tests S1), and watch for a Trendelenburg gait pattern (suggests L5 weakness).
• Standing: modified Schöber test (lumbar flexion range), trunk lateral bending, and spine extension.
• Sitting: patellar reflex and quadriceps power (L3-L4); ankle dorsiflexion power (L4-L5) and ankle plantarflexion power (S1); great toe extension (L5) and flexion (S1); straight leg raise (SLR) test with a Slump test to check consistency; FABER (Patrick’s) test to screen for hip/sacroiliac pathology as a mimicker of radicular pain.
• Lying prone: femoral nerve stretch test (assesses L3-L4 root tension) and saddle sensation testing (S2-S4, screens specifically for cauda equina).
• Sensation: dermatomal light touch and pinprick testing from L3 to S2; generalized diffuse tenderness across trunk and all four limbs raises suspicion for a centralized or nonorganic pain pattern rather than a focal lesion.

Diagnostic imaging

Reserve MRI (or CT with contrast where MRI is unavailable) for a patient with a red flag, or one of these specific risk factors: low-velocity trauma, osteoporosis, older age, chronic corticosteroid use, suspected cancer, suspected infection, or immunosuppression. Imaging is also reasonable for a surgical candidate with persistent or progressive symptoms after 6 weeks of conservative management, new or progressive neurologic findings, a history of prior lumbar surgery, or suspected cauda equina syndrome or a rapidly progressive neurologic deficit (the last two need emergency, not routine, imaging).^[5]

• Acute low back pain: promote rapid functional recovery, encourage continued or early return to activity and work, and reduce pain-related distress and fear-avoidance behaviour.
• Subacute or recurrent low back pain: prevent progression to chronic pain and disability through timely reassessment, and prevent or minimize prolonged work absence.
• Chronic low back pain: restore function, fitness, and role participation (including work) by addressing both the physical and psychological contributors to persistent pain, rather than pursuing complete pain resolution as the primary endpoint.
• At every stage: identify and act on red flags promptly, avoid unnecessary imaging and over-medicalization, and minimize long-term opioid exposure.

• Patient education and reassurance about the self-limiting nature of most low back pain -- this alone reduces distress and improves outcomes, and should be delivered explicitly, not assumed to happen by default.
• Encourage staying active and continuing or resuming work and normal activity as soon as tolerated; avoid unnecessary bed rest, and avoid premature physical therapy referral for straightforward acute pain that has not yet been given a chance to improve on its own.
• Superficial heat for acute low back pain.
• Spinal manipulative therapy has a modest effect on pain and disability in acute low back pain, and is most effective when combined with another modality (e.g., exercise, a psychological intervention) rather than used alone.^[9]
• Structured exercise therapy is beneficial at every stage. Core/motor-control exercise programs and supervised walking programs (building toward 30 minutes of brisk walking 5 days a week, with a pedometer and walking diary) are both reasonable, evidence-supported options, particularly for chronic low back pain.
• For subacute or chronic low back pain with work absence: a coordinated, workplace-integrated return-to-work program with a defined treatment timeline -- the workplace intervention itself, not the specific clinic treatment modality chosen, is what most reliably drives successful return to work.
• For chronic low back pain: combine 2 or more nonpharmacologic modalities -- multidisciplinary rehabilitation, cognitive behavioural therapy, relaxation therapy, and mindfulness-based stress reduction all have supporting evidence, especially in combination and when integrated with workplace re-entry planning.
• Evidence is weak, contradictory, or insufficient for several other commonly used modalities: acupuncture, yoga, therapeutic ultrasound, transcutaneous electrical nerve stimulation (TENS), lumbar supports, insoles, and prolotherapy. These are not routinely recommended, though an individual trial alongside evidence-based care is reasonable if a patient wants to pursue one.
• Interventional/procedural options exist for refractory chronic low back pain but require specialist referral and have inconsistent evidence: trigger point injections, epidural steroid injections, and facet joint injections have not shown consistent benefit for pain or work disability, though some patients report improvement with only minor side effects; image-guided radiofrequency facet rhizotomy can be considered for intractable facet-mediated pain.

Pregnancy

Breastfeeding

Acetaminophen at therapeutic doses is appropriate. Ibuprofen has been used safely during breastfeeding, and short-term use of most other NSAIDs is generally considered compatible -- prefer a shorter-half-life agent where possible. Opioid transfer into breast milk is generally small, but given the seriousness of opioid toxicity, limit use to 2-3 days and counsel on toxicity signs in both mother (oversedation, constipation) and infant (drowsiness, poor feeding, breathing difficulty); stop breastfeeding if either develops signs of toxicity. Avoid codeine during breastfeeding given the (debated but still standing) concern for rare, serious neonatal toxicity in ultra-rapid CYP2D6 metabolizers. Tramadol has a long half-life in newborns and limited infant outcome data -- use cautiously if at all. Diazepam accumulates in the breastfed infant and should be avoided; gabapentin produces low infant serum levels with no reported adverse effects at typical maternal doses.

Pediatrics

This chapter addresses adult mechanical low back pain. Low back pain in a child or adolescent is much less common than in an adult and is more likely to have an identifiable structural or systemic cause -- it should prompt a lower threshold for further assessment and referral rather than being managed with the same adult mechanical-low-back-pain algorithm, and pediatric-specific dosing for the drugs in this chapter is not established here.

Older adults

Diazepam and the other muscle relaxants in this chapter (cyclobenzaprine, methocarbamol, orphenadrine, tizanidine, baclofen) are not recommended in patients over 65 given increased sedation, fall risk, and (for diazepam) accumulation risk. NSAIDs carry a higher GI, renal, and cardiovascular risk in this population -- prefer a topical NSAID or acetaminophen trial first, and use the lowest effective oral NSAID dose for the shortest duration if one is needed. Start any opioid at a lower dose with closer monitoring.

Renal and hepatic impairment

Avoid NSAIDs, including a topical NSAID used over a large area or for a prolonged period, in significant renal impairment. Duloxetine is contraindicated at ClCr under 30 mL/min. Baclofen and gabapentin both require renal dose adjustment. Acetaminophen requires a lower total daily dose and closer monitoring in significant hepatic impairment; baclofen has a rare hepatotoxicity risk requiring caution in hepatic disease.

• Acute low back pain: reassess within 1-4 weeks if symptoms are not clearly improving, or sooner if a new red flag develops. Track return to function and activity/work, not pain score alone, as the primary marker of progress.
• Subacute low back pain: reassess at 4-6 weeks if pain or work absence has not resolved -- this is the trigger point to screen (or re-screen) for yellow flags and escalate to active, coordinated management.
• Chronic low back pain: scheduled follow-up with explicit functional goals (not only pain intensity) tracked at each visit.
• Whenever an opioid is prescribed: confirm an agreed tapering strategy was documented before starting, reassess the ongoing need and morphine-equivalent dose at every refill, and do not exceed 90 mg morphine-equivalent/day.^[8]
• Chronic high-dose acetaminophen or duloxetine use: periodic liver function monitoring.
• Long-term NSAID use: periodic renal function and blood pressure monitoring, and GI risk reassessment.

1. Reassess for a red flag that may have been missed or has since developed -- do not assume the working diagnosis of nonspecific low back pain is still correct just because it was correct initially.
2. Confirm adherence to, and adequate dose/duration of, the first-line therapy already tried before adding or switching a medication.
3. Add or intensify a nonpharmacologic modality -- structured exercise or physiotherapy if not yet trialled, or combining modalities (e.g., manipulation plus exercise) if a single modality alone has been inadequate.
4. Explicitly reassess psychosocial (yellow-flag) risk and screen for depression or anxiety if not already done; consider a workplace-based intervention for a patient with ongoing work absence.
5. Consider imaging if symptoms are persistent or progressive after 6 weeks of conservative management, or if the patient is a genuine surgical candidate.
6. Refer to a multidisciplinary chronic pain management program for marked functional disability persisting despite the above.
7. For radicular pain (sciatica with radiculopathy) not improving with conservative management, refer for specialist assessment of injection therapy or surgical evaluation.
8. If an opioid trial is being considered or is already underway and not achieving its goal, reassess appropriateness against the criteria in Choose Initial Treatment and begin the pre-agreed taper rather than continuing to escalate the dose.
9. After a failed multidisciplinary program, identify specific barriers before considering a second attempt: an undertreated psychiatric disorder (especially major depression, anxiety, or dysthymia), an attitudinal barrier to change, a substance or medication misuse problem, a previously undetected medical or surgical issue, or an unresolved workplace obstacle.

• Prescribing bed rest for uncomplicated low back pain -- it worsens, not improves, outcomes.
• Ordering imaging without a red flag or a specific therapeutic-planning indication -- imaging findings are common in people without any back pain, correlate poorly with symptoms, and are associated with a higher likelihood of unnecessary surgery.^[4]
• Reflexively combining an NSAID with a muscle relaxant, acetaminophen, and/or an opioid -- trial evidence shows this combination increases adverse effects (dizziness, drowsiness, dyspepsia, nausea) without improving pain or function over the NSAID alone.
• Assuming acetaminophen provides meaningful analgesic benefit for low back pain specifically -- current evidence does not support this; it is chosen for safety, not superior effectiveness.^[6]
• Continuing a muscle relaxant beyond a short course, or using one routinely in a patient over 65.
• Starting an opioid as first-line therapy, or continuing one beyond 3-5 days for acute pain without a documented review and tapering discussion.
• Anchoring on "just back pain" and missing a cauda equina red flag -- urinary retention, saddle numbness, or new bowel/sexual dysfunction always needs same-day emergency assessment, not a trial of conservative therapy first.
• Failing to screen for yellow flags (psychosocial risk factors for chronicity) once symptoms or work absence pass the 4-week mark.
• Managing chronic low back pain with medication alone, without a coordinated nonpharmacologic and, where indicated, workplace-integrated plan.
• Using a sustained-release opioid formulation for intermittent, activity-related pain -- these are not shown to be more effective or safer than an immediate-release formulation for this pattern of pain.
• Missing CYP2D6-related codeine treatment failure, or the (debated but still standing) breastfeeding caution around codeine, in a patient or nursing parent for whom it was prescribed.

How to use this table: doses are adult doses for mechanical low back pain and require patient-specific confirmation, including renal/hepatic adjustment. This chapter does not establish pediatric dosing -- see Special Populations. Select any drug name to open its complete Pharmasist Drug Database page.

Nonopioid analgesics

NSAIDs, oral

No NSAID or COX-2 inhibitor has been shown more effective than another for back pain specifically -- select by GI/cardiovascular risk and tolerability. Avoid in severe renal impairment.

NSAIDs, topical

Minimal systemic absorption -- a reasonable option to reduce systemic NSAID exposure, particularly with GI or renal risk factors.

Muscle relaxants

Evidence for benefit in acute low back pain is limited and contradictory; adequate evidence is lacking for chronic low back pain. Short-course use only (no more than 1-2 weeks). Not recommended in patients over 65. Avoid in pregnancy (insufficient safety data).

Benzodiazepine (short-term muscle relaxant use)

GABA derivatives (limited evidence, not a Health Canada-approved indication for low back pain)

Clinical experience only, no quality trial evidence -- may be considered for chronic low back pain with pain/tenderness across multiple sites.

Serotonin-norepinephrine reuptake inhibitor

The only antidepressant with a specific chronic low back pain indication; place in therapy not firmly established.

Opioids

Avoid as routine therapy at every stage. Reserve for severe pain unresponsive to the measures above, at the lowest effective dose, for the shortest duration, with an agreed tapering strategy in place before starting and a hard ceiling of 90 mg morphine-equivalent/day.