Why this topic matters in emergency medical care
Musculoskeletal medicines span acute pain relief, inflammation control, fracture care, gout flares, osteoporosis and autoimmune disease. EMTs must relieve suffering without worsening bleeding, kidney injury, respiratory depression or occult fracture. A hot swollen joint may be gout, septic arthritis or haemarthrosis; a “simple” back pain may be spinal cord compression. Safe medicine use begins with examination, mechanism and red-flag recognition.
This lesson supports EMT and nursing learning. Use current Uganda Ministry of Health guidance, local protocols, prescriber orders and patient-specific contraindication checks in practice.
Learning outcomes
- Classify non-opioid/opioid analgesics, NSAIDs, corticosteroids, DMARDs, gout medicines, muscle relaxants and bone medicines.
- Explain mechanisms, onset, routes, adverse effects, interactions and monitoring for each major class.
- Recognise fracture, compartment syndrome, septic arthritis, spinal cord compression, cauda equina syndrome and neurovascular compromise.
- Apply safe pain assessment, immobilisation, renal/GI/bleeding precautions and reassessment after analgesia.
- Understand long-term medicines for rheumatoid arthritis, osteoarthritis, gout, osteoporosis and inflammatory disease.
1. Musculoskeletal physiology and medicine targets
| Target | Effect | Medicine examples | Emergency relevance |
|---|---|---|---|
| Cyclo-oxygenase/prostaglandins | Pain, inflammation, fever, gastric and renal protection | NSAIDs, aspirin | Analgesia and anti-inflammatory effect balanced against ulcer, bleeding and AKI. |
| Opioid receptors | Central/peripheral analgesia and respiratory drive | Morphine, fentanyl, tramadol, naloxone | Severe pain relief but monitor ventilation and mental state. |
| Glucocorticoid receptors | Suppress inflammatory gene transcription | Prednisolone, dexamethasone, intra-articular steroids | Rapid anti-inflammatory effect; infection, hyperglycaemia and adrenal suppression risks. |
| Urate crystal/inflammation pathways | Neutrophil activation in gout | Colchicine, NSAID, corticosteroid, allopurinol | Acute flare treatment differs from long-term urate lowering. |
| Bone resorption/remodelling | Osteoclast and osteoblast balance | Bisphosphonates, denosumab, teriparatide, calcium/vitamin D | Fragility fracture prevention; hypocalcaemia and jaw/renal precautions. |
2. Practical classification of musculoskeletal medicines
| Group | Examples | Main role | Major concern |
|---|---|---|---|
| Paracetamol | Paracetamol/acetaminophen | Mild–moderate pain and fever | Liver toxicity in overdose or malnutrition/alcohol disease |
| NSAIDs | Ibuprofen, diclofenac, naproxen, ketorolac | Inflammatory pain, renal colic, gout | GI bleed, AKI, hypertension, heart failure and bronchospasm |
| Opioids | Morphine, fentanyl, codeine, tramadol | Moderate–severe acute pain | Respiratory depression, sedation, dependence and constipation |
| DMARDs | Methotrexate, hydroxychloroquine, sulfasalazine, leflunomide | Rheumatoid/inflammatory arthritis disease control | Immunosuppression, liver/blood toxicity and pregnancy warnings |
| Gout medicines | Colchicine, allopurinol, febuxostat | Acute flare and long-term urate lowering | Colchicine toxicity and incorrect initiation during acute illness |
| Bone medicines | Alendronate, zoledronic acid, denosumab, calcium/vitamin D | Osteoporosis and fracture prevention | Hypocalcaemia, renal impairment, oesophagitis and rare jaw problems |
3. Paracetamol and multimodal analgesia
Paracetamol is useful for many acute pain presentations and can be combined with an NSAID or opioid. It has a ceiling effect, so repeating extra doses does not provide unlimited relief. Ask about combination cold/flu products, alcohol, malnutrition, liver disease and the total dose in the previous 24 hours.
- Record weight and cumulative dose before giving another dose.
- Suspected overdose, staggered ingestion or intentional self-harm requires urgent assessment even when the patient feels well.
- Analgesia should accompany immobilisation, elevation, ice when appropriate and treatment of the underlying injury.
4. Non-steroidal anti-inflammatory drugs
| Benefit | Mechanism | Important harm | Use caution/avoid |
|---|---|---|---|
| Reduce inflammatory pain | COX inhibition reduces prostaglandins | Dyspepsia, ulcer and GI bleeding | Previous ulcer, anticoagulation, steroid use or active bleeding |
| Relieve renal colic/gout | Suppresses inflammation and ureteric prostaglandins | AKI and sodium/fluid retention | Dehydration, CKD, shock, heart failure or pregnancy restrictions |
| Reduce fever/swelling | Peripheral anti-inflammatory action | Bronchospasm in aspirin-sensitive asthma | Previous NSAID reaction or uncontrolled asthma |
| Topical NSAID | Local exposure with lower systemic levels | Skin reactions and some systemic absorption | Broken skin, allergy and extensive use |
Use the lowest effective dose for the shortest duration and consider gastroprotection when risk is high. NICE recommends NSAIDs as one first-line option for acute gout and as first-line analgesia for suspected renal colic when not contraindicated; patient-specific renal, GI and cardiovascular risk remains decisive.
5. Opioid analgesics and emergency monitoring
| Medicine | Useful feature | Major risk | Monitoring |
|---|---|---|---|
| Morphine | Strong titratable analgesia | Hypoventilation, hypotension, nausea and histamine release | Respiratory rate, SpO2, ventilation, BP, GCS and pain score |
| Fentanyl | Rapid potent analgesia with less histamine | Apnoea, chest-wall rigidity, bradycardia | Continuous observation; prepare ventilation and naloxone. |
| Codeine | Oral mild–moderate pain option | Variable metabolism, sedation and constipation | Check respiratory disease, age and other sedatives. |
| Tramadol | Opioid plus serotonin/noradrenaline action | Seizure and serotonin syndrome risk | Ask about antidepressants, epilepsy and renal function. |
5.1 Opioid safety checklist
- Assess pain, airway, breathing, circulation, mental state and cause of pain before dosing.
- Check allergies, opioid tolerance, alcohol/benzodiazepines, sleep apnoea, renal/hepatic disease and pregnancy.
- Use the lowest authorised dose and titrate; do not repeat without a timed reassessment.
- Monitor ventilation—not only oxygen saturation—because supplemental oxygen can conceal hypoventilation.
- Have suction, bag-mask ventilation and naloxone access when giving parenteral opioid.
6. Muscle relaxants and spasm medicines
Muscle relaxants may reduce spasm but can cause sedation, hypotension, anticholinergic effects and falls. They should not delay examination for fracture, compartment syndrome, meningitis or spinal cord compression. Avoid combining sedating muscle relaxants with opioids or alcohol without close monitoring.
7. Osteoarthritis medicines
Osteoarthritis affects the whole joint and is managed with exercise, strengthening, weight support, education and selected medicines. NICE does not recommend routine paracetamol or weak opioids when alternatives are appropriate; topical NSAIDs may be useful for knee/hand disease, while oral NSAIDs require risk assessment.
| Option | Role | Safety point |
|---|---|---|
| Topical NSAID | Local pain/inflammation relief | Check skin integrity and allergy; systemic absorption still occurs. |
| Oral NSAID | Short-term pain/inflammation when appropriate | Consider GI protection and renal/cardiovascular contraindications. |
| Intra-articular corticosteroid | Short-term relief for selected joints | Exclude infection first; monitor glucose and post-injection infection. |
| Opioid | Only selected severe pain when other measures unsuitable | Falls, dependence, constipation and respiratory depression. |
8. Rheumatoid arthritis and DMARDs
Rheumatoid arthritis is systemic autoimmune inflammation. Disease-modifying antirheumatic drugs (DMARDs) prevent joint damage; analgesics reduce symptoms but do not control disease progression. Methotrexate, sulfasalazine, hydroxychloroquine, leflunomide, biologics and targeted synthetic medicines require specialist monitoring.
| Medicine | Role | Key monitoring/risk |
|---|---|---|
| Methotrexate | Anchor DMARD for inflammatory arthritis | Weekly vs daily dosing error can be fatal; monitor CBC, liver/renal function; infection, pneumonitis and pregnancy risk. |
| Hydroxychloroquine | DMARD for mild RA/lupus | Retinal toxicity; baseline and ongoing eye screening. |
| Sulfasalazine | DMARD for peripheral inflammatory arthritis | Rash, blood dyscrasia, liver injury; monitor CBC and liver function. |
| Leflunomide | Immunomodulatory DMARD | Hepatotoxicity, hypertension, cytopenias and long persistence. |
| Biologic/targeted medicines | Block cytokines or immune pathways | Serious infection, TB/hepatitis reactivation and vaccination considerations. |
| Glucocorticoid bridge | Rapid inflammatory suppression while DMARD acts | Hyperglycaemia, infection, osteoporosis and adrenal suppression. |
9. Gout: acute flare versus long-term prevention
Gout is caused by monosodium urate crystals. An acute flare is treated with an anti-inflammatory medicine; urate-lowering therapy prevents future flares and joint damage. A hot swollen joint with fever may be septic arthritis, so do not label it gout without appropriate assessment.
| Medicine | Acute/long-term role | Safety concerns |
|---|---|---|
| NSAID | First-line acute flare if safe | GI bleed, AKI, heart failure, hypertension and anticoagulant interaction. |
| Colchicine | Acute flare and prophylaxis when starting urate lowering | GI toxicity, marrow suppression, neuromyopathy; dangerous accumulation in renal/hepatic disease and with CYP3A4/P-gp inhibitors. |
| Oral/intra-articular corticosteroid | Acute flare when NSAID/colchicine unsuitable | Hyperglycaemia, infection risk and joint infection must be excluded before injection. |
| Allopurinol | Long-term xanthine oxidase inhibition | Rash/SCAR, renal dose adjustment; do not stop/start casually during illness without advice. |
| Febuxostat | Alternative urate-lowering medicine | Cardiovascular and liver considerations; specialist selection. |
10. Osteoporosis and fracture-prevention medicines
| Medicine/class | Mechanism/role | Precautions |
|---|---|---|
| Calcium/vitamin D | Provide substrate and support mineralisation | Check renal stones, hypercalcaemia and total dietary intake; supplements do not replace antiresorptive therapy when indicated. |
| Bisphosphonates | Reduce osteoclast bone resorption | Oesophageal irritation, renal impairment, hypocalcaemia and rare jaw/atypical femur problems; take oral dose correctly. |
| Zoledronic acid | IV bisphosphonate for selected osteoporosis or malignancy | Renal function, hydration, acute-phase reaction and calcium monitoring. |
| Denosumab | RANKL inhibition reduces osteoclast formation | Hypocalcaemia and rebound vertebral fracture if stopped without follow-on plan. |
| Teriparatide/abaloparatide | Intermittent PTH-receptor stimulation promotes bone formation | Specialist use; monitor calcium and contraindications. |
11. Musculoskeletal red flags and medication limits
- Compartment syndrome: escalating pain out of proportion, pain on passive stretch, tense swelling, paraesthesia or weakness. Analgesia must not delay surgical review.
- Septic arthritis: hot swollen joint, fever and severe pain with movement. Steroid injection is unsafe until infection is excluded.
- Spinal cord/cauda equina compression: new weakness, saddle anaesthesia, urinary retention/incontinence or severe back pain. Urgent imaging and specialist transfer.
- Fracture/neurovascular compromise: deformity, absent pulse, cool limb, sensory loss or severe swelling. Immobilise, reassess circulation and transfer.
- Rhabdomyolysis: muscle pain/weakness and dark urine after crush injury, seizure or extreme exercise. Renal-protective fluid and electrolyte monitoring are urgent.
12. Clinical scenarios
Scenario 1: Renal/GI risk and fracture pain
An older patient with CKD and previous ulcer has a painful hip fracture. Avoid uncritical NSAID use, support the limb, give protocol-based multimodal analgesia with careful opioid titration and monitor ventilation and BP.
Scenario 2: Septic arthritis versus gout
A hot swollen knee is accompanied by fever and confusion. Do not assume gout or inject steroid. Treat as possible sepsis, obtain urgent aspiration/antibiotic pathway and transfer.
Scenario 3: Compartment syndrome
After a leg fracture, pain is increasing despite opioids and the calf is tense. Reassess pulses, sensation and passive stretch, avoid tight casts/dressings and call for urgent surgical review.
Scenario 4: Colchicine toxicity
A patient with CKD takes extra colchicine and develops vomiting, diarrhoea and weakness. Stop further doses, arrange urgent toxicology/renal assessment and monitor ECG, blood count and organ function.
Scenario 5: Methotrexate dosing error
A patient has taken methotrexate daily instead of weekly and now has mouth ulcers and fever. Treat as a high-risk toxicity, isolate if infection is suspected, avoid further doses and transfer urgently.
Scenario 6: Rhabdomyolysis
After a crush injury, the patient has severe muscle pain and cola-coloured urine. Establish access, monitor ECG/potassium, begin authorised renal-protective fluid and transfer for laboratory and dialysis-capable care.
13. Administration, monitoring and handover
Document pain score and functional impact, injury mechanism, neurovascular status, renal/GI/cardiovascular history, pregnancy possibility, allergies, last analgesic/DMARD dose, medicine concentration, route, exact time, response and adverse effects. Handover red flags, immobilisation, serial circulation checks and need for orthopaedic/rheumatology/renal review.
14. Revision questions
- Compare paracetamol, NSAIDs and opioids for acute musculoskeletal pain.
- Why can NSAIDs cause AKI and GI bleeding?
- What respiratory monitoring is needed after opioid analgesia?
- List red flags for compartment syndrome.
- Differentiate osteoarthritis and rheumatoid arthritis medicine goals.
- Why is methotrexate dosing error dangerous?
- What eye monitoring is required with hydroxychloroquine?
- Compare acute gout flare treatment with long-term urate lowering.
- Why can colchicine become toxic in renal disease?
- What are the signs of septic arthritis?
- Explain bisphosphonate and denosumab precautions.
- What is the risk of abrupt denosumab discontinuation?
- List symptoms of spinal cord or cauda equina compression.
- How should a fracture with neurovascular compromise be managed?
- What are the initial priorities in rhabdomyolysis?
- Why should analgesia not be withheld while awaiting diagnosis?
- Which patient factors alter NSAID choice?
- How should a DMARD toxicity be documented and escalated?
15. Key takeaways
- Analgesia is essential, but pain relief must be paired with examination, immobilisation, serial neurovascular checks and red-flag screening.
- NSAIDs are effective but can cause GI bleeding, AKI, fluid retention and cardiovascular harm.
- Opioids require ventilation monitoring, titration and naloxone/airway preparedness.
- A hot swollen joint may be septic arthritis; a severe pain crisis may be compartment syndrome or spinal compression.
- DMARDs and bone medicines require long-term laboratory, eye, renal, pregnancy and infection monitoring.
- Gout flare therapy and urate-lowering prevention are different clinical decisions.
16. Recommended references for further study
- Pharmacology of the Musculoskeletal System – SlideShare teaching resource
- NICE: Osteoarthritis diagnosis and management
- NICE: Rheumatoid arthritis management
- NICE: Gout diagnosis and management
- WHO: Osteoarthritis
- WHO: Fragility fractures and osteoporosis
Clinical note: This page supports EMT learning and revision. It does not replace an authorised prescription, local protocol, specialist supervision or patient-specific advice. In a deteriorating patient, stabilise ABCDE, call for advanced help and transfer urgently.
Complete Analgesic Pharmacology Tables
Clinical principle: Assess the cause, intensity, site, quality, duration and functional effect of pain before treatment. Combine non-drug measures with the safest effective medicine, review response, and never allow analgesia to delay urgent diagnosis of shock, acute abdomen, compartment syndrome, meningitis or myocardial infarction. Doses below are common teaching examples; follow the prescriber, Uganda Clinical Guidelines and local protocol.
Analgesic selection and the WHO approach
Use regular non-opioid analgesia for mild pain where appropriate, add an opioid for moderate-to-severe acute or cancer pain, and add an adjuvant when neuropathic, inflammatory or bone pain is present. The modern approach is individualized rather than a rigid ladder: choose the least harmful effective route, schedule background analgesia when pain is continuous, prescribe rescue doses for breakthrough pain, and reassess sedation, respiratory rate, function and adverse effects.
| Medicine/class | Pharmacodynamics | Pharmacokinetics | Indications and example adult dose | Contraindications/precautions | Interactions | Common side effects | Serious adverse effects/toxicity | Nursing monitoring and teaching |
|---|---|---|---|---|---|---|---|---|
| Paracetamol | Predominantly central analgesic and antipyretic action; little peripheral anti-inflammatory activity. | Rapid oral absorption; hepatic conjugation; a small CYP-mediated fraction forms NAPQI, normally detoxified by glutathione; renal excretion. | Mild–moderate pain/fever. Common adult dose 0.5–1 g orally every 4–6 hours; do not exceed the local maximum, commonly 4 g/day in healthy adults and less in low body weight, malnutrition, liver disease or regular alcohol use. | Severe active liver disease; caution with fasting, malnutrition, alcohol use and duplicate combination products. | Regular prolonged use may increase warfarin effect; enzyme inducers and chronic alcohol exposure may increase toxicity risk. | Nausea, rash; usually well tolerated at therapeutic dose. | Dose-dependent hepatic necrosis, hypoglycaemia, metabolic acidosis and acute kidney injury in severe poisoning. | Count every paracetamol-containing product; record dose/time; monitor liver tests when indicated. Suspected overdose needs urgent level-based assessment and N-acetylcysteine per protocol—do not wait for symptoms. |
| Ibuprofen / diclofenac (NSAIDs) | Reversible COX inhibition reduces prostaglandin synthesis, producing analgesic, antipyretic and anti-inflammatory effects. | Well absorbed orally, highly protein bound, hepatically metabolized and renally eliminated; effects may outlast plasma half-life. | Inflammatory musculoskeletal pain, dysmenorrhoea, dental/postoperative pain. Ibuprofen commonly 200–400 mg orally every 6–8 hours with food; use the lowest dose for the shortest time. Diclofenac dosing is product/protocol specific. | Active peptic ulcer/GI bleeding, severe renal failure, NSAID hypersensitivity, uncontrolled heart failure; avoid in late pregnancy. Caution in asthma, dehydration, hypertension and older adults. | Anticoagulants/antiplatelets and SSRIs increase bleeding; ACE inhibitor/ARB plus diuretic increases AKI risk; lithium and methotrexate concentrations may rise; avoid combining NSAIDs. | Dyspepsia, nausea, oedema, headache, raised BP. | GI ulcer/haemorrhage, acute kidney injury, bronchospasm/anaphylaxis, myocardial infarction/stroke risk, severe skin reactions. | Check hydration, renal history, BP, ulcer/bleeding risk and pregnancy. Watch urine output, melaena, haematemesis, wheeze and oedema. Give with food if prescribed, but food does not prevent ulceration. |
| Morphine | Primarily μ-opioid receptor agonism reduces nociceptive transmission and pain perception; also depresses respiratory drive and gut motility. | Variable oral bioavailability from first-pass metabolism; hepatic glucuronidation; active metabolites accumulate in renal impairment. | Severe acute, postoperative, cancer or palliative pain. Dose and route must be individualized and titrated; opioid-naïve adults often start with small immediate-release doses under close observation. | Significant respiratory depression, paralytic ileus; caution in head injury, hypotension, renal impairment, older/frail patients and sleep-disordered breathing. | Benzodiazepines, alcohol, sedating antihistamines, gabapentinoids and other CNS depressants markedly increase sedation/overdose risk; MAOI interactions require specialist advice. | Constipation, nausea, vomiting, pruritus, urinary retention, drowsiness. | Respiratory arrest, profound hypotension, aspiration, dependence and withdrawal. | Before and after dose assess pain, respiratory rate, oxygenation, sedation score, BP and pupils. Hold/escalate for concerning sedation or respiratory depression. Start bowel care when ongoing. Keep naloxone and resuscitation equipment available where required. |
| Tramadol | Weak μ-opioid agonism plus inhibition of serotonin and noradrenaline reuptake. | Hepatic CYP metabolism to an active metabolite varies genetically; renal elimination; accumulation occurs with renal/hepatic dysfunction. | Selected moderate pain when alternatives are unsuitable; common adult immediate-release dosing is 50–100 mg every 4–6 hours, maximum according to product/local protocol. | Uncontrolled epilepsy, acute intoxication with CNS depressants, severe respiratory depression; caution in older adults and renal/hepatic impairment. | SSRIs/SNRIs/TCAs/MAOIs/linezolid increase serotonin toxicity; medicines lowering seizure threshold increase convulsions; CNS depressants increase overdose risk. | Dizziness, nausea, constipation, sweating, somnolence. | Seizures, serotonin syndrome, respiratory depression, dependence, hypoglycaemia. | Check interacting medicines, seizure history and renal function. Observe mental state, clonus, fever, autonomic instability and respiratory status; teach not to mix with alcohol or unprescribed sedatives. |
| Codeine | Prodrug partly converted by CYP2D6 to morphine; analgesic effect varies greatly between patients. | Hepatic metabolism; renal elimination. Ultra-rapid metabolizers may develop toxicity while poor metabolizers obtain little benefit. | Short-term selected moderate pain, usually combined with a non-opioid; follow product and age restrictions. | Respiratory depression; breastfeeding; children below locally permitted age and after tonsil/adenoid surgery; caution in renal impairment. | CYP2D6 inhibitors may reduce effect; sedatives/alcohol increase respiratory depression. | Constipation, nausea, drowsiness. | Apnoea, especially in susceptible children or breastfed infants; dependence. | Do not assume predictable effect. Monitor breathing and sedation and avoid duplicate paracetamol in combination tablets. |
Adjuvant and specialist analgesics
| Medicine | Mechanism/kinetics | Best use and dosing principle | Major cautions/interactions | Adverse effects | Nursing responsibilities |
|---|---|---|---|---|---|
| Amitriptyline | Inhibits serotonin/noradrenaline reuptake; anticholinergic and antihistamine effects. Long half-life; hepatic metabolism. | Neuropathic pain; usually started at a low night dose and titrated slowly—not an immediate rescue analgesic. | Recent MI, arrhythmia, severe glaucoma/urinary retention; interacts with MAOIs, serotonergic drugs and CNS depressants. | Dry mouth, constipation, postural hypotension, sedation; overdose may cause seizures and fatal dysrhythmias. | Assess suicide/overdose risk, falls, ECG risk and anticholinergic burden; teach delayed benefit and safe storage. |
| Gabapentin/pregabalin | Bind α2δ calcium-channel subunit, reducing excitatory neurotransmitter release; not GABA receptor agonists. Renally eliminated unchanged. | Neuropathic pain; titrate gradually and reduce dose in renal impairment. | Respiratory disease, frailty and substance-use risk; additive sedation with opioids/alcohol; do not stop abruptly. | Dizziness, somnolence, ataxia, oedema, weight gain; serious respiratory depression can occur with opioids. | Check eGFR, falls and sedation; counsel on gradual titration/taper and avoiding driving until effects are known. |
| Ketamine | Non-competitive NMDA antagonism produces dissociative anaesthesia and analgesia while often preserving airway reflexes and sympathetic tone. | Severe acute/trauma pain or procedural sedation by trained teams using weight-based protocol and monitoring. | Severe uncontrolled hypertension, selected psychotic/cardiovascular conditions; additive effects with sedatives. | Emergence reactions, nausea, hypersalivation, hypertension/tachycardia; rare laryngospasm/apnoea. | Use only with airway-skilled staff, oxygen, suction and continuous monitoring; document dissociation, recovery and neurological observations. |
| Lidocaine topical/local | Blocks voltage-gated sodium channels, preventing nerve impulse conduction; hepatic metabolism. | Local anaesthesia or selected localized neuropathic pain; maximum dose depends on preparation, route and adrenaline content. | Severe conduction disease without pacing, significant hepatic dysfunction; additive toxicity with other local anaesthetics/antiarrhythmics. | Local numbness/irritation; toxicity causes circumoral tingling, tinnitus, seizures, hypotension and ventricular arrhythmias. | Calculate total mg from all sources and patient weight; aspirate/inject incrementally where relevant; stop immediately and activate local-anaesthetic systemic-toxicity protocol if neurological/cardiac signs appear. |
Antidotes and urgent toxicity response
| Emergency | Key findings | Immediate response | Antidote/specific treatment |
|---|---|---|---|
| Opioid toxicity | Reduced consciousness, slow/shallow breathing, pinpoint pupils may occur, hypoxia. | Call for help, open airway, ventilate with bag-mask and oxygen, monitor ECG/glucose; do not delay ventilation. | Naloxone titrated by the trained prescriber/protocol to adequate ventilation; repeated doses or infusion may be needed because naloxone can wear off before the opioid. Observe for recurrent toxicity and acute withdrawal. |
| Paracetamol overdose | Early symptoms may be mild despite evolving hepatic injury. | Establish time, formulation, dose and co-ingestants; take paracetamol level at the correct time plus liver/renal tests and INR; contact toxicology service. | N-acetylcysteine according to the treatment nomogram/protocol; start immediately when presentation is late, timing is uncertain or significant toxicity is suspected. |
| NSAID toxicity/bleeding | Vomiting, epigastric pain, GI bleeding, AKI, acidosis, seizures in severe overdose. | ABC, IV access, renal/electrolyte/acid-base assessment, manage haemorrhage and shock; activated charcoal only when specifically indicated early. | No routine antidote; supportive care, PPI for indicated GI bleeding and specialist management. |
Nursing process for a patient receiving analgesics
- Assessment: use an age-appropriate pain scale; record pain at rest and movement, likely mechanism, allergies, pregnancy status, renal/hepatic function, ulcer/bleeding risk, medicines, substance-use risk and previous response.
- Plan: agree a measurable goal such as ability to breathe deeply, mobilize or sleep—not necessarily zero pain. Match route to urgency and ability to swallow.
- Implementation: apply medicine rights, calculate weight-based doses accurately, give at prescribed intervals, combine positioning, splinting, ice/heat where appropriate, relaxation and explanation.
- Evaluation: reassess pain and function at the expected onset, and check sedation, respiratory rate, BP, nausea, bowel/bladder function and allergic reactions.
- Escalation: urgently report new neurological deficit, pain out of proportion, rigid abdomen, haemodynamic instability, rapidly increasing opioid requirement or inadequate analgesia despite treatment.
High-risk warning: pethidine/meperidine is generally a poor routine choice because its neurotoxic metabolite can accumulate, especially in renal impairment, causing agitation and seizures. Opioids must never be combined casually with benzodiazepines, alcohol or other sedatives.
Revision checkpoints
- Distinguish side effects (predictable, often dose-related) from serious adverse effects requiring urgent action.
- Know the “triple whammy”: NSAID + ACE inhibitor/ARB + diuretic increases acute kidney injury risk.
- For continuous opioid therapy anticipate constipation, nausea and sedation; respiratory depression is an emergency.
- Document the pre-dose assessment, exact drug/dose/route/time, response and adverse effects.