Principles of cancer and non-cancer pain assessment

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

Pain assessment begins with the person's account and ends with a testable formulation. Ask which pain is worst, what it feels like, what brings it on and what the person cannot do because of it. A score of eight may be acceptable during brief movement if recovery is rapid, while a score of four that prevents sleep or transfers may be intolerable. Agree one functional target, such as turning in bed, walking to the bathroom or completing radiotherapy positioning.

Mechanism directs treatment. Localised aching and movement tenderness suggest somatic nociception; deep diffuse pressure or colic suggests a visceral source; burning, electric shocks, allodynia and sensory change suggest neuropathic injury. Mixed pain is common in cancer, for example vertebral metastasis causing both bony pain and nerve-root compression. Mechanism can change after surgery, fracture, treatment response or prolonged opioid exposure.

Breakthrough pain needs precise description. Spontaneous episodes occur without a clear trigger; incident pain accompanies movement, care or swallowing; end-of-dose failure recurs predictably before the next regular dose and suggests inadequate background duration. Record onset speed, peak intensity, duration and how quickly rescue treatment works. A slowly absorbed medicine cannot reliably treat an episode that peaks within minutes.

Context alters both suffering and safety. Explore understanding of illness, fears about addiction or dying, sleep, mood, previous trauma, substance use, finances, housing and caregiver ability. Ask who stores and gives controlled medicines and whether the patient can read labels, open packaging and calculate doses. These questions support safer access and should not be used to stigmatise people with current or previous dependence.

People unable to use conventional scales need supported assessment. Optimise hearing, language and communication aids and ask carers about the person's usual pain behaviours. Observational tools can structure attention to facial expression, movement, vocalisation and consolability, but agitation is not specific. Examine for retention, impaction, infection, pressure damage, delirium and medication toxicity before concluding that escalating analgesia is the only response.

Key points

Pain is whatever the patient reports, but assessment must also identify mechanism, cause, emergency features, functional effect and safe treatment options.
First-line history uses site, onset, quality, radiation, severity, timing, triggers, associated features, previous response and impact on sleep, movement and roles.
Classify each pain as somatic, visceral, neuropathic or mixed; one person may need a separate formulation for several concurrent pains.
Ask about continuous background pain, spontaneous breakthrough, incident pain and end-of-dose failure because each pattern changes the plan.
Use a patient-selected numeric, verbal or visual scale consistently, but anchor improvement to an activity or goal the person values.
First-line examination is directed by location and red flags and includes neurological, musculoskeletal, vascular, abdominal and skin assessment where relevant.
The gold standard is repeated patient-centred formulation with examination and response review; no scan, biomarker or pain score independently proves the experience or mechanism.
Review prescription and non-prescription analgesics, total opioid exposure, rescue use, adherence, alcohol or sedatives, organ function and who administers medicines.
Cancer pain and pain in advanced illness can coexist with chronic primary pain; opioid escalation is not automatically appropriate for every mechanism.

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

Tumour and treatment injury

Primary or metastatic tumour can infiltrate bone, viscera, nerves and soft tissue, while surgery, radiotherapy and systemic treatment may cause inflammatory, fibrotic or neuropathic injury.

Non-malignant advanced disease

Ischaemia, arthritis, pressure damage, spasticity, oedema, organ distension and musculoskeletal deconditioning contribute pain in severe cardiac, respiratory, neurological, renal and liver illness.

Unrelated acute pathology

People receiving palliative care still develop infection, fracture, renal colic, gout, migraine, dental disease and other common conditions that require their usual diagnostic consideration.

Psychosocial amplification

Fear, insomnia, depression, isolation, financial strain and loss of role can heighten attention and reduce coping without making the nociceptive experience imaginary.

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

1
Somatic nociception
Activation of nociceptors in skin, muscle, connective tissue or bone produces relatively localised aching, sharp or movement-related pain with reproducible tenderness.
2
Visceral nociception
Distension, inflammation, ischaemia or capsular stretch in organs produces diffuse deep pain, colic or referral through shared spinal segments.
3
Neuropathic signalling
Lesion or disease affecting somatosensory pathways produces ectopic activity and central sensitisation, experienced as burning, electric shocks, allodynia or painful numbness.
4
Central sensitisation
Persistent input can increase spinal and cortical responsiveness so that pain extends beyond tissue injury and becomes less proportional to peripheral findings.
5
Total pain interaction
Biological signals, threat appraisal, mood, sleep, relationships and meaning alter one another, changing distress, behaviour and the treatment needed for acceptable function.

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

Somatic pain

The patient can often point to a localised aching or sharp site, with movement provocation, focal tenderness and guarding.

Visceral pain

Poorly localised pressure, deep ache, colic, nausea or referred surface pain suggests distension, obstruction, capsular stretch or ischaemia.

Neuropathic pain

Burning, shooting, electric pain, allodynia, hyperalgesia, numbness and a plausible neuroanatomical distribution support a somatosensory lesion.

Incident breakthrough pain

A predictable severe flare during movement, dressing, transfer or swallowing requires pre-emptive timing and treatment of the mechanical trigger.

End-of-dose failure

Pain repeatedly returning before the next maintenance dose may indicate an interval or formulation problem rather than random breakthrough.

Toxicity masquerading as painRed flag

Myoclonus, hallucinations, allodynia, diffuse pain and sedation during escalating opioid exposure should prompt toxicity review.

Red flags requiring action

Back pain with new weakness, sensory change, gait deterioration or bladder or bowel dysfunction requires emergency metastatic spinal cord compression assessment.
Sudden focal bone pain, deformity, inability to weight bear or pain on minimal movement suggests pathological fracture or impending structural failure.
Severe escalating pain with fever, haemodynamic change, peritonism, a hot joint or immunosuppression needs urgent infection or surgical evaluation.
New headache with vomiting, focal neurology, seizure or altered consciousness may indicate raised intracranial pressure or intracranial bleeding.
Pain out of proportion, a cold limb, absent pulses, new swelling or chest symptoms requires immediate vascular or thromboembolic assessment.
Marked drowsiness, hallucinations, myoclonus, pinpoint pupils or respiratory slowing during opioid therapy suggests toxicity rather than uncontrolled pain.
A patient expressing suicidal intent, unsafe opioid use or coercive medicine control requires direct risk, safeguarding and access assessment.

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 multidimensional pain historyFirst stepFirst line
Why
Define each pain's site, time course, quality, severity, triggers, associated features, response, meaning and functional impact.
Interpretation and limitations
Convert the description into separate mechanism hypotheses and identify which episode or limitation the patient wants treated first.
02
Focused clinical examination
Why
Look for neurological deficit, bony tenderness, instability, vascular compromise, visceral signs, skin injury, retention, impaction and medication toxicity.
Interpretation and limitations
New objective deficit or structural instability changes urgency; a normal examination does not invalidate pain but narrows immediate mechanisms.
03
Consistent pain and function measure
Why
Track intensity alongside sleep, movement, self-care or another patient-chosen activity before and after intervention.
Interpretation and limitations
A meaningful response is improved comfort or function with acceptable adverse effects, not necessarily zero pain or a fixed numerical reduction.
04
Complete medicine reconciliation
Why
Calculate scheduled and breakthrough analgesia, adjuvants, sedatives, missed doses, recent changes, renal dosing and non-prescribed substances.
Interpretation and limitations
Distinguish undertreatment, non-adherence, end-dose failure, interaction and accumulation before increasing a strong opioid.
05
Targeted blood tests
Why
Evaluate renal or hepatic impairment, hypercalcaemia, infection, inflammation, anaemia or another suspected reversible contributor.
Interpretation and limitations
Order only tests that influence mechanism or treatment; stable chronic pain does not require routine repeated panels without a clinical question.
06
Targeted imaging
Why
Assess fracture, metastasis, cord or nerve compression, obstruction, abscess or other structural cause when history and examination indicate.
Interpretation and limitations
Choose the modality and urgency for the suspected emergency; imaging confirms pathology but does not quantify the person's pain experience.

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

Disease progression

Increasing tumour burden, organ distension, pathological fracture or nerve compression is more likely when pain changes location, pattern or associated neurological and systemic features.

Treatment complication

Mucositis, postoperative injury, radiation fibrosis, steroid myopathy, infection and chemotherapy neuropathy can mimic or coexist with pain attributed to malignancy.

Opioid-induced hyperalgesia

Diffuse pain, allodynia and worsening sensitivity despite dose escalation may reflect opioid-related sensitisation, particularly with high exposure or neurotoxic metabolites.

Delirium or distress behaviour

Agitation, grimacing and calling out may represent pain, but retention, constipation, fear, psychosis, medication toxicity and delirium require parallel assessment.

Chronic primary pain

Pain may be driven predominantly by altered nociceptive processing without adequate structural explanation, requiring a function-centred approach distinct from progressive cancer pain.

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

01Initial assessmentFormulate before escalating analgesiaFirst stepEscalationA patient reports new, changed or inadequately controlled pain.

1Identify immediate red flags, give proportionate relief and describe each pain's timing, quality, triggers, functional effect and associated features.
2Examine the relevant systems, reconcile all medicines and organ function and use targeted tests only where results could change management.
3Agree a mechanism-based plan, one measurable goal, rescue and safety advice and a review interval matched to severity and titration risk.

02Breakthrough patternMatch treatment to episode kineticsSevere transient flares occur despite otherwise acceptable background comfort.

1Classify spontaneous, incident or end-dose failure and record onset, duration, frequency, predictability and prior rescue response.
2Treat the provoking cause where possible, time pre-emptive analgesia for predictable activity and select a rescue route whose onset fits the episode.
3Review repeated episodes and adverse effects; adjust background therapy only when the pattern shows persistent under-treatment rather than isolated incidents.

03Communication limitationUse supported self-report plus observationCognitive, language, sensory or motor impairment prevents a conventional pain account.

1Provide interpreter, hearing or communication support and use the person's established yes-no, symbol, gesture or device method.
2Combine caregiver knowledge of baseline behaviour with structured observation and a focused search for common painful and delirium-producing causes.
3EscalationOffer a cautious mechanism-appropriate trial, observe comfort and function repeatedly and stop escalation if sedation rises without objective benefit.

04Persistent complexityEscalate formulation, not opioid aloneEscalationPain remains unacceptable after an appropriate initial plan or adverse effects prevent titration.

1Reconsider diagnosis, emergency pathology, neuropathic component, opioid toxicity, psychosocial distress and adherence or access barriers.
2Seek specialist palliative, pain, oncology, radiotherapy, surgical, psychological or substance-use expertise with a specific clinical question.
3Combine disease treatment, rehabilitation, non-drug measures and rational analgesia and set an early multidisciplinary response review.

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

Loss of mobility

Untreated movement pain promotes immobility, deconditioning, falls, pressure injury, venous thrombosis and dependence while obscuring whether fracture or instability is present.

Sleep and mood deterioration

Persistent pain fragments sleep, narrows attention and increases anxiety, depression, demoralisation and social withdrawal, which can further amplify suffering.

Unsafe analgesic escalation

Treating every distress cue with additional opioid can cause sedation, delirium, respiratory depression and constipation while missing non-opioid mechanisms.

Caregiver and medicine risk

Complex schedules, controlled-drug access, diversion, dosing errors and caregiver fatigue can make a theoretically appropriate regimen unsafe at home.

Delayed emergency treatment

Labelling new pain as expected progression can postpone stabilisation, decompression, antibiotics, drainage or disease-directed treatment that preserves function and comfort.

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

Review pain intensity, episode frequency, sleep and the chosen functional goal after every medicine or disease-treatment change.
Monitor alertness, cognition, respiratory rate, nausea, bowel function, falls and driving or machinery risk during opioid titration.
Reassess mechanism when pain location, quality or neurological findings change rather than simply increasing the prior regimen.
Count rescue doses and response over the preceding 24 to 72 hours and check whether incident episodes are being mistaken for background failure.
Repeat renal and hepatic review when illness, hydration or medicine exposure changes enough to alter analgesic clearance.
Check storage, supply, administration and disposal arrangements for controlled drugs at every transition of care.

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

Pain score is one dimension

Function, sleep, distress and adverse effects determine whether a numerical change is meaningful to the person.

Analgesia does not mask emergencies

Prompt pain relief supports examination and humane care while definitive emergency assessment continues.

Several pains need several plans

One patient may need an opioid for visceral pain, radiotherapy for bone pain and an adjuvant for neuropathic injury.

Incident pain resists background escalation

Increasing maintenance opioid to cover a few brief movement flares may cause sedation throughout the rest of the day.

Behaviour is not mechanism

Grimacing or agitation indicates distress but cannot distinguish pain from delirium, retention, fear or drug toxicity without assessment.

Substance history improves safety

Non-judgmental discussion enables supervised supply, addiction liaison and effective analgesia instead of either unsafe access or undertreatment.

11Common pitfallsFrequent interpretation and management errors.

01
Treating a high score without identifying the pain mechanism or emergency signs.
02
Combining several distinct pains into one average severity number.
03
Escalating background opioid for brief predictable movement pain without reviewing timing.
04
Assuming all new pain in cancer is malignant progression.
05
Interpreting distress behaviour as pain while missing delirium, retention or toxicity.
06
Using a family member instead of professional interpretation for a complex pain or safety history.
07
Ignoring alcohol, sedatives, adherence, renal function and controlled-drug access.
08
Defining success as zero pain despite unacceptable sedation and lost function.
09
Delaying imaging or specialist pathways for cord compression or pathological fracture.
10
Stigmatising previous dependence and consequently leaving severe pain untreated.