GC004 The Pain Is Intolerable - Pain Control
Pain control is the systematic assessment and management of acute or chronic pain using pharmacological, interventional, and non-pharmacological strategies to reduce suffering and restore function.
The Pain Is Intolerable — Pain Control
This lecture by Professor Cheung Chi Wai is a foundational anaesthesiology/pain-medicine session. It follows pain from definition → classification → nociceptive pathways and sensitisation → effects of acute pain → assessment → acute multimodal analgesia → chronic pain and specialist interventions.
Lecture-era material versus current practice
The deck was created in 2022 but includes teaching figures and prescribing tables inherited from much older sources. The "pain as the fifth vital sign" campaign, 1990 WHO ladder, opioid/NSAID dose tables, and local-anaesthetic concentration table are historical lecture material, not current prescribing instructions. Current care uses patient-centred assessment (pain, function and treatment safety), an indication-specific multimodal plan, and the current local formulary/protocol. [10][13][14]
Why it matters clinically and for exams:
- Pain questions appear in surgery, anaesthesia, orthopaedics, oncology, palliative care, and emergency medicine MCQs/SAQs.
- The WHO analgesic ladder, opioid side effects, NSAID contraindications, PCA principles, and the concepts of allodynia/hyperalgesia/wind-up are perennial exam favourites.
- Past papers (2017–2025) frequently ask about pain control in crush syndrome, spinal cord compression, abdominal emergencies, and bone metastases. [1][2][3]
At the end of this lecture, you should be able to:
- Define pain and recognise its features
- Classify pain and describe its characteristics
- Understand pain mechanisms
- Understand the physiologic consequences of acute pain
- Describe the assessment of pain and pain relief
- Know the treatment options for acute pain
- Know briefly chronic pain and its psychological effects
- Appreciate the treatment options for chronic pain [1]
1. Pain: Definition and Features
"An unpleasant sensory AND emotional experience associated with, or resembling that associated with, actual or potential tissue damage." — IASP 2020 (slide says 2018 revision) [1]
Why both "sensory" and "emotional"? Pain is never purely a nociceptive input. The emotional component (suffering, fear, distress) is inseparable from the sensory component. This is why psychological interventions are legitimate pain treatments, and why patients with no tissue injury (e.g. fibromyalgia, chronic pain syndromes) still have "real" pain.
Exam Trap
A common MCQ distractor says pain requires "actual tissue damage." That is wrong — the IASP definition explicitly includes "potential" tissue damage and even pain "resembling" tissue damage. Pain can exist without identifiable pathology.
Pain is essential for survival:
- Serves as a warning to avoid or prevent further body injury
- Enforces rest of injured or diseased parts of the body for healing [1]
Congenital insensitivity to pain can lead to repeated unnoticed injury, burns and neuropathic arthropathy, illustrating the protective value of nociception and pain.
The slide reflects the 1995 American Pain Society campaign and later routine 0–10 screening initiatives. Its valuable legacy is that pain should be asked about and reassessed. A pain score is not a physiological vital sign, however, and a rigid numerical target can drive unsafe treatment. Current assessment pairs the patient's report with function, goals, sedation/respiration, adverse effects and response to treatment. The Joint Commission's current standard emphasises defined assessment/reassessment criteria, evidence-based plans made with the patient, safe opioid prescribing and extra monitoring for high-risk patients. [13][14]
Patients have the right to appropriate assessment and management of pain. Patients are involved in all aspects of their care, including pain management. [1]
The 2020 IASP notes sharpen the clinical meaning: pain is personal and influenced by biological, psychological and social factors; pain is not the same as nociception; a person's report should be respected; and inability to communicate does not exclude pain. [10]
The lecture mixes time course, mechanism and clinical context. Keep these as separate axes:
| Axis | Categories | Practical point |
|---|---|---|
| Time course | Acute; subacute; chronic (> 3 months) | Acute pain may be severe or diffuse; chronic pain can have acute flares. |
| Mechanism | Nociceptive (somatic/visceral/inflammatory); neuropathic; nociplastic; mixed | Mechanism guides treatment; a patient may have more than one mechanism. |
| Context | Postoperative/traumatic, cancer-related, palliative, chronic primary, chronic secondary | Cancer pain is often mixed and may be acute or chronic; it is not a separate mechanism. |
| Mechanism | Core definition / clues |
|---|---|
| Nociceptive | Activation of nociceptors by actual or threatened non-neural tissue injury; somatic pain is often localised, whereas visceral pain may be diffuse or referred. |
| Neuropathic | Pain caused by a lesion or disease of the somatosensory nervous system; neuroanatomically plausible distribution plus sensory signs supports the diagnosis. Burning, tingling, numbness, allodynia or hyperalgesia are clues, not proof by themselves. |
| Nociplastic | Pain arising from altered nociception without clear evidence that nociceptor activation or a somatosensory lesion fully explains it. [11] |
Neuropathic pain is defined as "pain caused by a lesion or disease of the somatosensory nervous system" (IASP). [1]
Why this classification matters: Treatment is mechanism- and condition-specific. Nociceptive pain may respond to paracetamol, an NSAID (if safe), regional techniques or an opioid when indicated. Neuropathic pain often needs a neuropathic-pain agent. Chronic pain needs a biopsychosocial plan focused on participation and quality of life, not merely a lower numerical score.
3. Pain Mechanisms (Pathophysiology)
Three components of the nociceptive process: [1]
- The Periphery (nociceptors)
- The Nerve (first-order neurones)
- The Spinal Cord & Brain (dorsal horn, ascending tracts, thalamus, somatosensory cortex)
The visual pathway in slides 15 and 22 is:
Noxious stimulus → nociceptor → Aδ/C primary afferent (cell body in dorsal-root ganglion) → dorsal horn → second-order projection neurone → decussating anterolateral/spinothalamic pathways → brainstem/thalamus → cortical and limbic networks.
The dorsal horn also contains local interneurones, but a second-order projection neurone is not simply an interneurone. Lateral cortical processing supports localisation/intensity; medial-limbic-autonomic networks contribute salience, affect and defensive responses. Nociception is neural encoding of noxious stimuli; pain is the conscious personal experience. [10]
A descending modulatory system runs through cortex/limbic structures → periaqueductal grey (PAG) → rostroventral medulla/other brainstem nuclei → dorsal horn. It can inhibit or facilitate transmission, helping explain effects of attention, expectation, fear and endogenous opioids.
Pain sensation can therefore be modified by ascending or descending pathways at many levels (Rexed laminae concept). [1]
Types: [1]
- High-threshold mechanoreceptors
- Thermo-mechanoreceptors
- Polymodal nociceptors (respond to mechanical, thermal, and chemical stimuli)
- Super-high threshold receptors Can be "sensitised."
The nerve diagram and fibre table add an important speed distinction:
| Fibre | Structure | Typical pain signal |
|---|---|---|
| Aδ | Small, thinly myelinated; faster conduction | Early, sharp/pricking, better-localised "first pain" |
| C | Small, unmyelinated; slow conduction | Later, burning/aching, poorly localised "second pain" |
| Aβ | Large, myelinated, normally low-threshold touch/pressure | Normally non-nociceptive; altered central processing can contribute to mechanical allodynia. |
Cell damage + inflammation + sympathetic terminals → release of pain and inflammatory mediators (bradykinin, H⁺, prostaglandins) → nociceptor threshold lowered from high to low → less stimulus required for nociceptor activation [1]
Slides 17–18 depict the "inflammatory soup" around injured tissue: K⁺/H⁺, bradykinin, prostaglandins, histamine and serotonin activate or sensitise terminals; neuropeptides can contribute to neurogenic inflammation. Prostaglandins mainly sensitise nociceptors, which explains why COX inhibition is analgesic. Clinically, peripheral sensitisation produces tenderness and primary hyperalgesia; allodynia also requires altered processing and should not be reduced to a simple threshold diagram.
Prolonged stimulation of C fibres → release of Substance P + Glutamate in the Dorsal Horn → cascade of events altering neuro-cellular function → development of a POSITIVE FEEDBACK LOOP → sequential increase in spinal cord activity = "WIND-UP" of neuronal excitability → SECONDARY HYPERALGESIA [1]
Central sensitisation involves: [1]
- ↑ C-fibre output
- Hyperalgesia (primary and secondary)
- Allodynia
- Activation of NMDA receptors
Important distinction: Wind-up is a frequency-dependent, progressively increasing dorsal-horn response during repeated C-fibre input. Central sensitisation is the broader state of increased CNS nociceptive responsiveness, which can include expanded receptive fields, allodynia and secondary hyperalgesia. NMDA signalling contributes, but the terms are not interchangeable. Ketamine is a specialist adjunct in selected perioperative patients, not a routine stand-alone treatment for "wind-up." [12]
| Concept | Definition | Mechanism |
|---|---|---|
| Primary Hyperalgesia | Sensitisation of primary neurones → ↓ threshold to noxious stimuli WITHIN the site of injury; ↑ pain from suprathreshold stimuli; spontaneous pain | Peripheral sensitisation |
| Secondary Hyperalgesia | Increased pain in surrounding uninjured tissue | Predominantly central sensitisation; the slide's statement that primary neurones in the uninjured area are sensitised is misleading. |
| Allodynia | Pain due to a stimulus that does not normally provoke pain | Clinical phenomenon that does not itself specify a mechanism; central sensitisation is one mechanism. [11] |
High Yield — Hyperalgesia vs Allodynia
Hyperalgesia = an EXAGGERATED pain response to a stimulus that is already painful (suprathreshold). Allodynia = pain from a stimulus that is NORMALLY NOT painful (e.g. light touch on sunburnt skin). Both are consequences of sensitisation. The lecture graph (slide 28) shows the pain-response curve shifting left after injury. [1]
Cell damage releases: [1]
- K⁺, Bradykinin (BK), Arachidonic acid (AA), Prostaglandins (PG)
- Substance P from nociceptor terminals
- Histamine from mast cells
- Serotonin from platelets
Arachidonic acid → COX (cyclooxygenase activity) → PGG₂ → (peroxidase activity) → PGH₂ → PGF₂α, PGD₂, PGE₂, PGI₂ (prostacyclin), TXA₂ (thromboxane) [1]
| Prostanoid | Key Activities |
|---|---|
| PGE₂ | Context-dependent effects including nociceptor sensitisation, fever, vasodilation and gastric/renal homeostasis |
| TXA₂ | ↑ platelet activation/aggregation, smooth muscle contraction (arteries + bronchi) |
| PGI₂ (Prostacyclin) | ↓ platelet aggregation, vasodilation, ↑ renin release |
| COX-1 (Constitutive) | COX-2 (Inducible) | |
|---|---|---|
| Function | Often constitutive; contributes to gastric mucosal protection, platelet TXA₂ and renal homeostasis | Often inducible by inflammation and contributes to pain/fever, but is also constitutively expressed in sites such as kidney and brain |
| Where | Gastric mucosa, kidney, platelets, vascular endothelium | Induced at sites of inflammation by cytokines; constitutive in brain and kidney |
| Inhibition effect | Gastrotoxicity, ↓ platelet aggregation, renal toxicity | Anti-inflammatory, analgesic, antipyretic |
Conventional NSAIDs inhibit BOTH COX-1 and COX-2 → analgesic + anti-inflammatory BUT gastrotoxicity and impaired platelet function [1]
COX-2 Selective Inhibitors (Coxibs)
COX-2 selective agents spare platelet COX-1 at usual doses and may reduce some GI toxicity, but they do not remove renal, cardiovascular or GI risk. Choice is patient-specific; use the lowest effective dose for the shortest appropriate duration. [15]
This section explains why pain control is both humane and functional. The diagrams show associations within the wider injury–surgery–stress–immobility–drug response; they should not be read as proof that pain alone causes every complication listed.
4.1 Systemic Effects
| System | Consequences of Acute Pain | Why It Matters |
|---|---|---|
| Endocrine/Metabolic | ↑ ACTH, cortisol and catecholamines; insulin resistance, hyperglycaemia and catabolism | Part of the surgical/injury stress response; pain can amplify it. |
| Water/Electrolyte | H₂O and Na⁺ retention | Fluid overload risk |
| Respiratory | Guarding/splinting → shallow breathing, impaired cough, reduced mobilisation → atelectasis and V/Q mismatch | Most relevant after thoracic/upper-abdominal surgery and rib fractures; analgesia enables deep breathing, coughing and mobilisation. |
| Cardiovascular | Sympathetic activation can increase HR, BP and myocardial oxygen demand | Important in patients with limited cardiovascular reserve; avoid claiming that analgesia alone prevents MI. |
| GI | Reduced motility/ileus | Surgery, inflammation, immobility and opioids are also major contributors. |
| Coagulation/Immune | Hypercoagulability and altered immune function occur in the perioperative stress response | Do not attribute DVT or infection to pain alone; use standard prophylaxis and recovery measures. |
| Pain-signalling | Persistent nociceptive input can promote peripheral/central sensitisation | Severe acute pain is one risk marker for persistent postsurgical pain, but chronification is multifactorial rather than inevitable. |
| Psychological | Anxiety, depression, sleep deprivation | Worsens pain perception (vicious cycle) |
High Yield Summary — Consequences
5. Assessment of Pain and Pain Relief
Pain is a personal experience influenced by biological, psychological and social factors, including age, prior experience, expectations, context, communication and culture. [1][10]
Use an interpreter or communication aid where needed and avoid stereotyping pain expression by sex, age or culture. Self-report is preferred when possible; behaviour and physiological signs can support assessment but neither prove nor disprove pain.
From the lecture: [1]
- Where (location, radiation)
- Time course (onset, duration, pattern)
- Intensity (use validated tools)
- Factors relieving or exacerbating pain
- Pain on function and life (functional impact)
- Investigations for pain
- Treatments received (what worked, what didn't)
- Medical condition and prognosis
- Psychological profile
- Social background
Add quality/character, radiation, examination, red flags and a working cause/mechanism. Record pain at rest and on relevant movement, plus the patient's functional goal (for example, deep breath/cough, transfer, sleep). Review comorbidities, renal/hepatic function, current medicines, previous analgesic response, allergy, pregnancy where relevant, opioid exposure, substance-use risk and mood/suicide risk when indicated. Reassessment must cover benefit and harm: pain/function, sedation, respiratory rate/ventilation, nausea, bowel/bladder effects and other adverse events.
| Tool | Description | Best Use |
|---|---|---|
| VAS (Visual Analogue Scale) | Patient marks a position on an unnumbered line, commonly 100 mm | Patients able to understand and physically mark it; research |
| NRS (Numerical Rating Scale) | Discrete 0–10 verbal or written number | Communicating adults; common clinically. The slide labels one line as both VAS and NRS, but they are distinct tools. |
| Faces scale | Validated faces representing increasing pain (not simply distress) | Selected children or adults who understand the scale; do not assume cognitive impairment automatically makes it valid. |
| McGill Pain Questionnaire | Multidimensional; good but complex | Research, chronic pain clinics |
| Behavioural scores | CHEOPS/FLACC in appropriate paediatric populations; CPOT in selected critically ill adults | Use a tool validated for the population. Inability to communicate does not exclude pain. [10] |
Pain intensity is one outcome, not the sole treatment target. A fall from 8/10 to 4/10 may be clinically useful if the patient can now cough and mobilise safely; driving a score to zero with escalating opioid despite sedation is unsafe.
Pain should be assessed: [1]
- Preoperatively
- Routinely at regular intervals postoperatively
- With each new report of pain
- At suitable intervals after each analgesic intervention
Also reassess after a change in condition, transfer of care or adverse effect. The interval depends on route/onset and patient risk; document the intervention, response, function and safety observations.
6. Treatment Options for Acute Pain
Step 1: Non-opioid ± Adjuvant (e.g. paracetamol, NSAIDs) Step 2: Opioid for mild-to-moderate pain ± Non-opioid ± Adjuvant (e.g. codeine, tramadol) Step 3: Opioid for moderate-to-severe pain ± Non-opioid ± Adjuvant (e.g. morphine, fentanyl) Step up if pain persists or increases. [1]
Scope correction
The three-step ladder was developed for cancer pain, not as a mandatory algorithm for acute postoperative pain or all chronic pain. Current care starts with the patient's diagnosis, severity, mechanism, comorbidities and goals. Severe acute pain can require a titrated immediate-release opioid and/or regional technique from the outset; recovery then requires reassessment and step-down. Modern WHO cancer-pain guidance is individualised and includes rescue medication, route, opioid rotation and cessation rather than requiring every patient to pass through a "weak opioid" step. [17]
From the lecture: [1]
- Opioid analgesics
- Non-opioid analgesics: Paracetamol, anti-inflammatory agents, others
- Combination analgesic products
- Local anaesthetics, nerve, neuraxial blocks
Correction: tramadol is an opioid (with additional monoamine-reuptake effects), not a non-opioid. Current postoperative care uses a multimodal plan: treat the cause; use non-drug measures, paracetamol and/or an NSAID when appropriate; add regional/local techniques when useful; reserve an immediate-release opioid for pain severe enough to justify it; and reassess function and adverse effects. [12][16]
6.3 Opioid Analgesics
Binding at µ, δ, κ receptors. Highly efficacious. May be combined with anti-inflammatory agents. Effects may be reversed (naloxone). Side effects common. Pain recurrence possible. Tolerance develops. [1]
Respiratory depression, ↓ GI motility / nausea / vomiting, CNS depression / sedation / cognitive effects (elderly), pruritus (especially spinal opioids), urinary retention [1]
| Risk | Bedside implication |
|---|---|
| Sedation / ventilatory impairment | Increasing sedation may precede respiratory arrest. Monitor consciousness, respiratory pattern/rate and oxygenation according to route, dose and risk; oxygen saturation can remain deceptively normal with supplemental oxygen. Escalate immediately and follow the local opioid-emergency/naloxone protocol. |
| Nausea/vomiting, pruritus, urinary retention | Anticipate, ask and treat according to cause and local protocol; neuraxial opioids have particular monitoring requirements. |
| Constipation / ileus | Tolerance to constipation is limited; prescribe a bowel plan when ongoing opioid therapy is expected unless contraindicated. |
| Delirium, cognitive impairment, falls | Higher risk in frailty, sleep-disordered breathing, renal/hepatic impairment and with other sedatives. Reduce exposure and review interacting drugs. |
| Tolerance, physical dependence, opioid use disorder | These are distinct. Avoid abrupt cessation after sustained use; plan duration and taper/stop strategy, and offer treatment if opioid use disorder is identified. [16] |
Suspected opioid toxicity
Call for help, stop opioid administration, support airway/ventilation and use titrated naloxone according to the local emergency protocol. Continue observation because recurrent toxicity can occur when the opioid outlasts naloxone. Do not rely on pinpoint pupils or a single respiratory-rate threshold to exclude toxicity.
| Route | Key Points from Lecture |
|---|---|
| IM | Painful, slow onset, variable plasma levels |
| IV | Less painful, faster onset, more reliable levels; risk of overdose with continuous infusion |
| PCA | Patient-activated preset bolus + lockout; can match demand and avoid IM peaks/troughs. Only the patient should press the button unless a formal nurse-controlled protocol applies. Confirm cognitive/manual ability and continue sedation/respiratory monitoring; a lockout is not a substitute for monitoring. |
| Epidural/Spinal | Opioid receptors in spinal cord → profound segmental analgesia with reduced systemic side effects; may combine with LA; prolonged effects; danger of late-onset respiratory depression |
| Other | Use oral immediate-release opioid when feasible. SC can be useful in selected settings. Transdermal fentanyl and other long-acting preparations are not for routine acute pain in opioid-naive patients. [12][16] |
PCA provides more stable plasma concentrations compared to IM dosing (slide 59 shows PCA maintains drug level within therapeutic window vs wide swings with IM). [1]
Unsafe/outdated lecture table
The slide's fixed weight-based doses and intervals are not reproduced as a prescribing guide. Several are unsuitable for an opioid-naive adult, and the table includes pethidine, methadone, codeine and an IV tramadol "loading dose" without the patient factors and monitoring needed to use them safely. Use the current local formulary/order set, check opioid exposure, age/frailty, respiratory risk, renal/hepatic function and interactions, and titrate an immediate-release opioid to pain-related function and adverse effects. Use the lowest effective dose for no longer than the expected duration of severe pain. Methadone requires an experienced prescriber because of accumulation, interactions and QT risk. [16]
- Pethidine (meperidine): norpethidine can accumulate and cause neurotoxicity, especially in renal dysfunction; it is generally a poor routine choice.
- Codeine: CYP2D6 variability makes response and toxicity unpredictable. FDA restrictions include no codeine or tramadol in children under 12 and additional restrictions in some adolescents; avoid both during breastfeeding under FDA advice. [18]
- Tramadol: is an opioid and serotonin/noradrenaline reuptake inhibitor; risks include respiratory depression, dependence, seizures and serotonin toxicity.
| Drug | Mechanism | Adverse Effects |
|---|---|---|
| Paracetamol | Central analgesic mechanisms remain incompletely defined; it has little peripheral anti-inflammatory activity | Hepatotoxic in overdose or excessive cumulative dosing; check all combination products and use the local age/weight/liver-risk maximum. |
| Tramadol (opioid, not a non-opioid) | Parent drug inhibits serotonin and noradrenaline reuptake; parent/active metabolite have µ-opioid activity | Opioid adverse effects, dependence, nausea/dizziness, seizures and serotonin toxicity; CYP2D6 and interaction variability. |
Inhibit COX, key enzyme in prostaglandin synthesis. Conventional NSAIDs inhibit both COX-1 and COX-2. COX-1 inhibition → gastrotoxicity, ↓ platelet aggregation. Some newer agents target COX-2 but do not inhibit COX-1 at full therapeutic doses. [1]
Slide 63 Dose Table — Historical, Not a Current Drug Chart
Do not use the slide 63 doses
The table mixes adults and children, places paracetamol under an NSAID heading, and can exceed safe local daily limits if followed literally (particularly its paracetamol and diclofenac intervals). Its aspirin entry is unsafe as a generic paediatric analgesic instruction. Verify every drug, route, interval, maximum daily dose and duration in the current local formulary.
Before an NSAID, check: prior hypersensitivity/NSAID-exacerbated respiratory disease, active or high-risk GI ulcer/bleeding, renal function and volume status, heart failure/cardiovascular risk, anticoagulants/antiplatelets and procedural bleeding risk, pregnancy, age/frailty and interacting nephrotoxins. Use the lowest effective dose for the shortest appropriate duration; avoid multiple NSAIDs. NSAID use from around 20 weeks of pregnancy requires specific risk assessment, and later pregnancy carries additional fetal risk. [15]
NSAIDs and the Kidney
NSAIDs inhibit prostaglandin-mediated renal afferent arteriolar vasodilation → impaired renal blood flow → AKI, especially in patients with pre-existing CKD, heart failure, or hypovolaemia. This is a very common exam trap. [6]
NMDA signalling contributes to dorsal-horn plasticity. Ketamine is a non-competitive NMDA-receptor antagonist with analgesic and opioid-sparing effects. [1]
In current perioperative guidance, IV ketamine is a monitored anaesthetic/acute-pain adjunct for selected cases (for example inadequate relief from IV opioid or abnormal opioid sensitivity), not a routine ward prescription. Account for dissociation, nausea, cardiovascular stimulation and other contraindications; follow the anaesthesia/acute-pain protocol. [12]
Two or more agents with different yet complementary mechanisms of action. Severity of dose-related side effects may be reduced (lower doses of each agent). Range of side effects increased (each drug has its own profile). [1]
Example: Morphine + NSAIDs/Paracetamol + Nerve blocks → reduced doses of each → improved antinociception via synergistic/additive effects → may reduce severity of side effects of each drug [1]
This is the modern principle, but not a fixed recipe. Match components to the procedure, mechanism and patient. Paracetamol and an NSAID can be opioid-sparing when safe; a regional technique may improve function; an immediate-release opioid can be rescue or primary therapy for severe pain. Combining drugs also combines harms—especially multiple sedatives—and duplicate paracetamol in combination products is a common preventable error. [12][16]
Mechanism: Na⁺ channel blockade; possible interaction at pre- and postsynaptic junctions. Tachyphylaxis can develop. Dose-related CNS and cardiovascular toxicity. [1]
| LA Drug | Concentration |
|---|---|
| Lignocaine | 1%–2% |
| Bupivacaine | 0.25%–0.5% |
| Prilocaine | 0.5%–1% |
| Ropivacaine | 0.2%–1% |
| Routes | Advantages | Disadvantages |
|---|---|---|
| Local infiltration, regional nerve block, spinal block, epidural block, caudal block | Excellent analgesia; opioid-sparing effect; decreased blood loss | Motor blockade; hypotension; LA toxicity; variable duration; require skill; malplaced block; high spinal block |
Ten-fold concentration typo on slide 68
The slide prints bupivacaine 2.5%–5%; the intended common concentrations are 0.25%–0.5%. Never infer dose from this teaching slide. Safe concentration, volume and maximum dose vary by agent, site, patient and use of adrenaline and must come from the current regional-anaesthesia protocol.
Local-anaesthetic systemic toxicity (LAST): early features may include circumoral/tongue paraesthesia, metallic taste, tinnitus, agitation or seizures, progressing to hypotension, conduction disturbance, ventricular arrhythmia or cardiac arrest; presentations can be atypical. Stop injection, call for help, support airway/oxygenation and follow the ASRA/local LAST checklist, including early 20% lipid emulsion when indicated. LAST resuscitation differs from routine ACLS. [19]
The lecture advocates giving analgesia before severe pain is established. [1]
Current perioperative guidance supports planning ahead and considering analgesia for when a local block wears off. This does not mean every drug should be scheduled or that pre-incision timing reliably prevents chronic pain. Schedule suitable non-opioids when appropriate; titrate opioids to functional need, safety and recovery, with a stop/step-down plan. [12]
Goals: [1]
- Improve management of surgical pain (twice-daily ward rounds, pain consultation service, pain clinic, therapeutic interventions)
- Promote continuing education of healthcare providers
- Increase awareness of importance of effective pain management
- Serve as a clinical research centre
7. Chronic Pain
Current definition: chronic pain persists or recurs for more than 3 months. ICD-11 distinguishes:
- Chronic primary pain: pain is itself the principal health condition and cannot be better accounted for by another chronic pain condition.
- Chronic secondary pain: pain is a symptom of an underlying condition (for example cancer-related, postsurgical/post-traumatic, neuropathic, secondary headache/orofacial, visceral or musculoskeletal pain).
- Primary and secondary mechanisms can coexist. [20]
Correcting stigmatizing lecture-era language
"Lack of objective signs," "pain behaviour established" and "psychological factors prominent" must not be used to dismiss a patient. Normal imaging, vital signs or examination do not prove absence of pain. Psychological and social factors modify all pain and should be assessed to improve care, not to imply that pain is imagined. Chronic secondary pain may remain a symptom; chronic primary pain can be a disease entity. [10][20]
The slide prompts a useful whole-person review, but psychosis is not a defining or routine effect of chronic pain. Assess bidirectional effects on mood/anxiety, sleep, cognition, activity, work/study, relationships, sexuality and finances; ask what the pain means to the patient, what they fear, coping strategies, support and achievable goals. Screen for depression, substance use and suicide risk when clinically indicated. Explain explicitly that psychological therapy is a pain-management skill, not a claim that the pain is unreal.
From the lecture (slides 74–75): [1]
| Layer | Current approach |
|---|---|
| Reassess diagnosis/mechanism | Exclude red flags and reversible drivers; distinguish chronic primary, nociceptive secondary, neuropathic, nociplastic and mixed pain. Agree goals around activity, sleep and participation. |
| Active self-management / rehabilitation | Education, pacing, graded/supervised exercise and return to valued activity; avoid prolonged non-indicated rest or immobilisation. Treat sleep and relevant comorbidities. |
| Psychological treatment | Pain-focused CBT or ACT can improve coping, function and quality of life; integrate with physical rehabilitation. |
| Condition-specific medicine | Treat the underlying condition. For most non-trigeminal neuropathic pain, NICE offers a choice of amitriptyline, duloxetine, gabapentin or pregabalin, with review/titration; tramadol is short-term rescue only and long-term use is specialist. [21] |
| Chronic primary pain | NICE recommends exercise, pain-focused CBT/ACT, and consideration of a limited acupuncture course. It advises not to initiate paracetamol, NSAIDs, opioids, gabapentinoids, benzodiazepines or antipsychotics for chronic primary pain; an antidepressant may be considered after discussing benefits/harms even without depression. [22] |
| Specialist intervention | Diagnostic/therapeutic blocks, radiofrequency denervation, neuromodulation, intrathecal therapy or neurolysis only for selected indications after specialist/MDT assessment and informed consent—not a generic escalation ladder. |
The lecture lists relaxation, imagery, hypnosis, biofeedback, heat/cold, massage, exercise, immobilisation, TENS, chiropractic and acupuncture. Evidence is condition-specific. For chronic primary pain, NICE supports supervised group exercise, pain-focused CBT/ACT and a limited acupuncture/dry-needling course, but advises against TENS, ultrasound, interferential therapy and biofeedback. Immobilisation is appropriate only for specific injuries/procedures and is usually short-term; prolonged inactivity can worsen disability. [22]
- A clinician performing a fluoroscopy-guided spinal pain procedure with sterile preparation and C-arm positioning.
- AP/oblique fluoroscopic views showing needles and small contrast patterns used to confirm target/location before injection; the unlabeled images do not justify naming every exact procedure from appearance alone.
- A radiofrequency generator, cannula/electrode placement and an illustration of lumbar medial-branch targets used for selected facet-mediated pain.
These are not generic treatments for any back pain. NICE advises against spinal injections for nonspecific low-back pain. Consider referral for lumbar medial-branch radiofrequency denervation only after non-surgical treatment has failed, pain is localised and thought to arise from medial-branch–innervated structures, and a diagnostic medial-branch block is positive. Epidural local anaesthetic/steroid may be considered for acute severe sciatica, not neurogenic claudication from central canal stenosis. [23]
9. Integration with Related Material
Opioid prescribing can lead to tolerance, physical dependence and opioid use disorder. Tolerance is reduced effect with repeated exposure; physical dependence means withdrawal can occur after abrupt reduction; opioid use disorder is a clinical syndrome of impaired control and continued use despite harm. Do not label expected tolerance/dependence alone as addiction. [1][16]
Pain history and current analgesic use are part of pre-op assessment. Patients taking long-term opioids need an individualised perioperative plan that prevents withdrawal, accounts for tolerance and avoids unsafe escalation. Whether an NSAID is withheld depends on the drug, procedure, bleeding/renal risk and local protocol. [7]
Back-pain treatment is diagnosis-specific, not a generic WHO-ladder exercise. Urgently assess suspected cauda equina syndrome, infection, fracture or malignancy. Age or night pain alone is not diagnostic; interpret all red flags in context. Nonspecific chronic low-back pain should not routinely receive opioids, gabapentinoids or spinal injections. [23]
Patient with small-cell lung Ca + bone metastases on morphine with increasing pain and confusion → DDx includes hypercalcaemia, brain metastases, opioid toxicity. [2]
Suspected metastatic spinal cord compression with neurological signs is an oncological emergency: contact the MSCC pathway/coordinator immediately, obtain urgent MRI (normally within 24 hours), and give dexamethasone according to protocol while the specialist MDT selects surgery and/or urgent radiotherapy. NICE recommends dexamethasone 16 mg as soon as possible for neurological symptoms/signs, then 16 mg daily while awaiting surgery or radiotherapy; surgery is not automatic for every patient. [8][24]
| Trap | Correct Understanding |
|---|---|
| "Pain requires tissue damage" | IASP: "actual OR POTENTIAL" tissue damage, or RESEMBLING such |
| "Chronic pain with normal imaging is not real" | Pain is personal and cannot be inferred solely from tissue findings. Classify chronic primary versus chronic secondary pain; assess biological, psychological and social contributors without invalidating the patient. |
| "NSAIDs are safe in CKD" | NSAIDs → ↓ renal prostaglandins → ↓ renal blood flow → AKI |
| "Allodynia and hyperalgesia are the same" | Allodynia = pain from innocuous stimulus; Hyperalgesia = exaggerated pain from noxious stimulus |
| "Paracetamol is an NSAID" | Paracetamol is not classified as an NSAID; its central analgesic mechanisms remain incompletely defined and it has little peripheral anti-inflammatory effect. |
| "Codeine works the same in everyone" | CYP2D6 variability can produce inadequate analgesia or excess morphine exposure/toxicity; age and breastfeeding restrictions also apply. |
| "COX-2 inhibitors have no side effects" | Selectivity may reduce some GI/platelet effects, but cardiovascular, renal and GI risks remain. |
| "Tramadol is a non-opioid" | Tramadol is an opioid with additional serotonin/noradrenaline reuptake effects and opioid/serotonergic/seizure risks. |
| "The slide dose tables are safe to copy" | They are historical and contain unsafe/ambiguous regimens. Use current local prescribing guidance and patient-specific adjustment. |
| "Bupivacaine 2.5%–5% is a routine block concentration" | Ten-fold slide typo: the intended common range is 0.25%–0.5%; always verify the exact regional-anaesthesia protocol. |
High Yield Summary
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Ask about pain and reassess it, but do not treat a number. Pair self-report with function, goals and treatment safety.
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IASP Definition
- "An unpleasant sensory AND emotional experience associated with, or resembling that associated with, actual or potential tissue damage."
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Classification uses separate axes
- Time: acute/subacute/chronic (> 3 months). Mechanism: nociceptive/neuropathic/nociplastic/mixed. Context: postoperative, cancer, palliative, chronic primary/secondary.
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Mechanisms
- Injury mediators can cause peripheral sensitisation; repeated C-fibre input can produce wind-up; broader CNS plasticity can produce central sensitisation, secondary hyperalgesia and allodynia.
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Consequences of acute pain
- Guarding can impair breathing/cough and mobilisation; pain can amplify sympathetic/stress responses and sleep/anxiety cycles. Complications are multifactorial—analgesia complements, not replaces, standard recovery care.
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Assessment
- VAS/NRS, regular intervals, 10-point framework.
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Treatment — current acute principle
- Individualised multimodal analgesia; oral route when feasible; immediate-release opioid only when severity/diagnosis justifies it; lowest effective dose, shortest necessary duration; functional and safety reassessment. The WHO ladder is historical cancer-pain teaching.
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Opioid side effects (must know)
- Respiratory depression, N/V, constipation, sedation, pruritus, urinary retention. Reversal: naloxone.
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PCA
- Patient-only activation, preset bolus + lockout, appropriate patient selection and continued sedation/respiratory monitoring.
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Multimodal analgesia
- Combine agents with different MOAs → better efficacy, fewer side effects.
- Chronic pain Rx
- Diagnose primary/secondary and mechanism; prioritise active rehabilitation and meaningful function. Use pain-focused CBT/ACT and condition-specific medicines. TENS is not recommended for chronic primary pain; invasive treatment is selected, specialist care.
- Plan ahead
- Anticipate when a block wears off and prevent severe breakthrough pain, while avoiding the overclaim that pre-incision dosing reliably prevents chronic pain.
Active Recall - Pain Control
[1] Lecture slides: GC 004 - The pain is intolerable - Pain control.pdf (all slides) [2] Past papers: 2024 Fourth Summative SAQ.pdf (Question 10) [3] Past papers: 2023 Fourth Summative Minicase.pdf (Case Three, Section 1) [4] Senior notes: MBBS Final MB (Surgery) (Felix PY Lai).pdf (p93, WHO principles of pain management) [5] Senior notes: Maksim Surgery Notes.pdf (p299–300, Pain control section) [6] Senior notes: Block A – Nephrology Data Interpretation.pdf (p11, NSAIDs and renal impairment) [7] Lecture slides: GC 002 - Is he fit for surgery - Pre-operative assessment.pdf [8] Past papers: 2025 Fourth Summative MCQ.pdf (Question 61) [10] International Association for the Study of Pain (IASP): Revised definition of pain and accompanying notes (2020) [11] IASP: Pain terminology — allodynia, hyperalgesia, nociplastic pain and sensitisation [12] NICE NG180: Perioperative care in adults — managing pain (updated 2025) [13] US Department of Veterans Affairs: Pain/fifth-vital-sign history and transition to multidimensional assessment [14] The Joint Commission: National Performance Goal 6 — Pain Management [15] US FDA: NSAID safety communication — pregnancy and lowest effective dose/shortest duration [16] CDC: 2022 Clinical Practice Guideline for Prescribing Opioids for Pain (does not apply to cancer, sickle-cell, palliative or end-of-life pain) [17] WHO: Guidelines for the pharmacological and radiotherapeutic management of cancer pain in adults and adolescents [18] US FDA: Codeine information and paediatric/breastfeeding safety restrictions [19] American Society of Regional Anesthesia and Pain Medicine: Checklist for treatment of local-anaesthetic systemic toxicity [20] WHO: ICD-11 chronic-pain categories (summarised in WHO chronic-pain guidance) [21] NICE CG173: Neuropathic pain in adults — pharmacological management [22] NICE NG193: Assessment of chronic pain and management of chronic primary pain [23] NICE NG59: Low back pain and sciatica — invasive treatments and radiofrequency denervation [24] NICE NG234: Spinal metastases and metastatic spinal cord compression
GC002 Is He Fit For Surgery - Pre-operative Assessment
Pre-operative assessment is a systematic evaluation of a patient's medical history, physical status, and risk factors to determine their fitness for surgery and optimize outcomes.
GC005 The Patient Is Critically Ill - Intensive Care Medicine; Unstable Vital Organ Function
Unstable vital organ function refers to the acute failure or impending failure of one or more vital organ systems—such as cardiovascular, respiratory, neurological, or renal—requiring immediate monitoring and intervention in an intensive care setting to prevent irreversible damage or death.