📋 Key Information Summary
- Acute pain in people with substance-use disorders (SUDs) requires structured, non-judgemental care that balances adequate analgesia with relapse prevention; liaison with addiction medicine specialists should be initiated early.
- Undertreated acute pain is a recognised relapse trigger — withholding opioids from all patients with a history of opioid use disorder (OUD) is inappropriate and may drive illicit use.
- Opioid use disorder (OUD) affects approximately 1.4 % of Australians; prevalence is disproportionately higher among Aboriginal and Torres Strait Islander peoples and in regional/remote communities.
- Patients on opioid agonist therapy (OAT — methadone, buprenorphine) should continue their maintenance dose throughout acute admissions; abrupt cessation risks withdrawal and destabilises recovery.
- Multimodal analgesia (paracetamol, NSAIDs, nerve blocks, ketamine infusions, gabapentinoids) should form the backbone of pain management in all patients with SUDs to minimise opioid requirements.
- Patients maintained on buprenorphine–naloxone (Suboxone®) can receive additional short-acting opioids for severe acute pain, but higher doses and closer monitoring are required due to high receptor occupancy.
- Naltrexone (oral or extended-release IM) blocks mu-opioid receptors for 24–72 h (oral) or ≥28 days (IM depot); patients on naltrexone will not respond to standard opioid analgesia — use non-opioid strategies and discuss with addiction medicine/pain team urgently.
- Non-opioid substance use (alcohol, methamphetamine, benzodiazepines, cannabis) alters pain perception, analgesic metabolism and complication risk; screen with AUDIT-C, ASSIST and urine drug testing.
- Alcohol withdrawal must be anticipated and managed with the CIWA-Ar protocol; thiamine (parenteral) should be given before glucose-containing fluids.
- Recovery-oriented practice includes shared decision-making, relapse-prevention planning at discharge, and referral to community-based support (SMART Recovery, NA/AA, NADA programmes).
- Methamphetamine-associated pain syndromes (dental, musculoskeletal, chest pain) require ECG, troponin and careful sympatholytic management before opioids.
- Aboriginal and Torres Strait Islander peoples experience OUD and methamphetamine-use disorder at higher rates; culturally safe care, ACCHO involvement, and strengths-based communication are essential.
Introduction & Australian Epidemiology
Acute pain is one of the most common reasons for emergency department (ED) presentation and hospital admission in Australia. When it occurs in a person living with a substance-use disorder (SUD), the clinical encounter carries unique challenges: the need for effective analgesia must be balanced against relapse risk, drug–drug interactions, altered pain pharmacology, and the potential for stigmatising care. Evidence consistently shows that undertreated pain is an independent predictor of relapse to illicit substance use.
This article provides an Australian-focused, evidence-based framework for the assessment and management of acute pain in adults with concurrent SUDs — including opioid use disorder, alcohol-use disorder, and stimulant-use disorder. It addresses pharmacological and non-pharmacological strategies, the continuation of opioid agonist therapy (OAT) during acute illness, the use of naltrexone and its implications for analgesia, and recovery-oriented discharge planning.
Australian Burden
| Metric | Data | Source |
|---|---|---|
| People on OAT (methadone + buprenorphine) | ~ 57 000 nationally (2022–23) | AIHW NODRP |
| Opioid-related hospitalisations | ~ 8 500 per year (principal diagnosis) | AIHW 2023 |
| Opioid-induced deaths | ~ 1 240 per year (2021) | Penington Institute |
| Methamphetamine use (past 12 months, ≥ 14 yr) | ~ 2.7 % of population | NDSHS 2022–23 |
| ATSI opioid hospitalisation rate ratio | 2.2× non-Indigenous rate | AIHW 2023 |
| Alcohol-related hospitalisations (acute) | ~ 78 000 per year | AIHW 2023 |
Opioid Use Disorder (OUD)
Opioid use disorder is characterised by compulsive opioid-seeking, tolerance, withdrawal, and functional impairment. In Australia, it is managed primarily through opioid agonist therapy (OAT) — methadone and buprenorphine — delivered through state-regulated programmes. Patients on OAT who present with acute pain (trauma, surgery, renal colic, acute abdomen) require nuanced management.
Key Principles for Acute Pain in OUD
- Continue OAT maintenance doses. Do not cease methadone or buprenorphine during an acute admission — abrupt cessation precipitates withdrawal and destabilises recovery.
- OAT does NOT provide adequate analgesia for acute pain. Maintenance doses produce tolerance; additional analgesic strategies are required.
- Avoid stigmatising language. Use "person with opioid use disorder" not "addict" or "drug-seeker". Document pain scores routinely as for any patient.
- Involve addiction medicine early. Contact the treating OAT prescriber (often GP or community pharmacist) and hospital addiction medicine or consultation-liaison psychiatry within 24 hours of admission.
- Use multimodal analgesia first-line to reduce opioid requirements (see Pharmacological Management below).
- Use scheduled (not PRN-only) dosing for the first 24–48 h to prevent pain spirals and reduce breakthrough requests.
- Document an analgesic plan at the time of admission, agreed with the patient and communicated to nursing staff.
Managing Opioid Analgesia by OAT Type
| OAT Regimen | Acute Pain Strategy | Key Notes |
|---|---|---|
| Methadone maintenance (typical 60–120 mg/day) | Continue daily methadone; add short-acting opioids (oxycodone, morphine, fentanyl) at standard doses. Full mu-receptor availability — standard opioid dosing usually effective. | Monitor for QTc prolongation if high-dose methadone + other QTc-prolonging agents. ECG if dose > 100 mg/day. |
| Buprenorphine SL (Subutex® / Suboxone®) (typical 8–24 mg/day) | Option A: Continue buprenorphine + add multimodal non-opioid analgesia ± short-acting opioids at higher doses (30–50 % dose increase) due to partial agonist blockade. Option B: Split buprenorphine into TDS dosing (e.g. 8 mg SL TDS) for more consistent analgesic coverage. Option C: For major surgery, temporarily convert to methadone or low-dose buprenorphine patch (Butrans®) with addiction medicine input. |
Buprenorphine has high receptor affinity; competing opioids need higher doses. Do NOT simply increase buprenorphine SL for acute pain — ceiling effect limits analgesia. |
| Buprenorphine depot IM (Sublocade®) | Continue depot injection on schedule. Add multimodal non-opioid analgesia. Short-acting opioids may be needed at increased doses. Contact addiction medicine. | Cannot be "adjusted" acutely; depot provides stable background. Consider ketamine, regional blocks as adjuncts. |
Recovery
Recovery from substance-use disorder is a dynamic, person-centred process defined by the Substance Abuse and Mental Health Services Administration (SAMHSA) as "a process of change through which individuals improve their health and wellness, live a self-directed life, and strive to reach their full potential." In the acute pain setting, recovery-oriented practice means that every clinical decision — from prescribing to discharge planning — should support the patient's ongoing recovery journey.
Recovery-Oriented Principles in Acute Pain Management
- Shared decision-making: Involve the patient in analgesic planning; acknowledge their expertise in their own pain and substance-use history.
- Strengths-based communication: Focus on what the patient is doing well (e.g. "You've been stable on your methadone for 18 months — let's make sure we protect that") rather than deficit-focused language.
- Trauma-informed care: Recognise that many patients with SUDs have experienced trauma; avoid restraints where possible, provide clear explanations, and offer choices.
- Relapse prevention planning: Before discharge, ensure the patient has a structured plan including OAT continuity, pain management script with limited supply, follow-up appointments, and community support referrals.
- No "cold turkey" discharge: Never discharge a patient on OAT without confirming their next OAT dose (community pharmacy, prescriber appointment within 24–48 h).
Discharge Checklist — Acute Pain + SUD
Australian Recovery Support Resources
| Resource | Description | Access |
|---|---|---|
| SMART Recovery Australia | Evidence-based mutual support groups (CBT-based) | smartrecoveryaustralia.com.au |
| Narcotics Anonymous (NA) Australia | 12-step peer support | na.org.au |
| Alcoholics Anonymous (AA) Australia | 12-step peer support for alcohol use | aa.org.au |
| National Alcohol and Other Drug Hotline | 24/7 telephone counselling and referral | 1800 250 015 |
| Counselling Online | Free online/phone counselling | counsellingonline.org.au |
| NADA (Network of Alcohol and other Drugs Agencies, NSW) | Sector support and service directory (NSW) | nada.org.au |
Naltrexone
Naltrexone is a competitive mu-opioid receptor antagonist used in the management of alcohol-use disorder (AUD) and opioid-use disorder (OUD). Unlike methadone and buprenorphine, it is not an agonist — it provides no opioid effect and instead blocks exogenous opioids. This has critical implications for acute pain management.
Formulations Available in Australia
Analgesic Strategy for Patients on Naltrexone
| Strategy | Details |
|---|---|
| Paracetamol | 1 g PO/IV QID (max 4 g/day; 60 mg/kg/day in patients < 50 kg). IV paracetamol (Perfalgan®) available PBS Authority for inpatients. |
| NSAIDs | Ibuprofen 400 mg PO TDS, naproxen 250–500 mg PO BD, or ketorolac 10–30 mg IV stat (max 5 days). Assess renal risk and GI bleeding risk. |
| Regional anaesthesia / nerve blocks | First-line for surgical and trauma pain. Ultrasound-guided blocks (fascia iliaca, TAP, interscalene, erector spinae plane) provide excellent opioid-sparing analgesia. |
| Ketamine sub-anaesthetic infusion | 0.1–0.3 mg/kg/h IV (anaesthetic/pain team supervision). NMDA receptor antagonist — works independently of opioid receptors. PBS Authority required for inpatient use. |
| Gabapentinoids | Gabapentin 300–600 mg PO TDS or pregabalin 75–150 mg PO BD. Useful for neuropathic and musculoskeletal components. Caution: respiratory depression risk when combined with other CNS depressants. |
| Clonidine | 50–100 mcg PO/IV TDS. Alpha-2 agonist — anxiolytic and analgesic. Useful adjunct, especially if concurrent opioid withdrawal. |
| Dexmedetomidine (ICU only) | 0.2–0.7 mcg/kg/h IV infusion. For severe pain in ICU setting. Requires monitoring. |
Nonopioid Substance Use
Acute pain presentations frequently co-occur with nonopioid substance use — alcohol, methamphetamine, benzodiazepines, and cannabis are the most common in Australian EDs. Each substance has distinct effects on pain perception, analgesic pharmacology, and complication risk that must be addressed.
Alcohol-Use Disorder and Acute Pain
- Screen with AUDIT-C (≥ 4 men, ≥ 3 women = positive screen) on every acute admission.
- Anticipate alcohol withdrawal in patients with heavy daily use (> 8 standard drinks/day). Use the CIWA-Ar scale every 1–4 h. Onset typically 6–24 h after last drink; peaks at 24–72 h.
- Thiamine (vitamin B1) — give 200–300 mg IV (parenteral) before any glucose-containing fluids to prevent Wernicke's encephalopathy. Continue oral thiamine 100 mg TDS.
- First-line withdrawal management: Diazepam (Valium®) 10–20 mg PO/PR/IV QID, titrated by CIWA-Ar score. Fixed-dose or symptom-triggered regimens are both acceptable.
- Analgesic considerations: Avoid hepatotoxic doses of paracetamol in heavy drinkers (limit to 2 g/day if evidence of liver disease). NSAIDs carry increased GI bleed risk. Opioids are safe if withdrawal is managed, but monitor closely.
- Coagulopathy: Check INR; vitamin K 10 mg IV if INR > 1.5. Fresh frozen plasma for active bleeding.
Methamphetamine-Use Disorder and Acute Pain
- Methamphetamine use is rising in Australia, particularly in regional and remote communities and among young adults. Acute presentations include dental pain, musculoskeletal trauma (from agitation/psychosis), chest pain, and hypertensive emergencies.
- Sympathomimetic features — hypertension, tachycardia, hyperthermia, mydriasis — may mask or mimic pain-related vital sign changes.
- ECG and troponin are mandatory for chest pain; methamphetamine can cause acute coronary syndrome, aortic dissection, and cardiomyopathy.
- Avoid pure sympathomimetics (e.g. adrenaline in local anaesthetic — use plain solutions or add fentanyl for blocks). Avoid tramadol (seizure risk).
- Analgesia: Paracetamol + NSAIDs first-line. Short-acting opioids at standard doses are effective but monitor for agitation and respiratory depression. Benzodiazepines (diazepam 5–10 mg IV) for acute agitation and sympatholytic effect.
- Dental pain is extremely common — arrange dental review. Simple analgesia + antibiotics if dental abscess suspected (amoxicillin 500 mg PO TDS or metronidazole 400 mg PO TDS).
- Screen with ASSIST (Alcohol, Smoking and Substance Involvement Screening Test) for severity assessment.
Benzodiazepine-Use Disorder and Acute Pain
- Benzodiazepine withdrawal is a medical emergency — seizures and death can occur. Never abruptly cease benzodiazepines in a dependent patient.
- Use diazepam equivalence to calculate maintenance doses (1 mg alprazolam ≈ 10 mg diazepam ≈ 2 mg lorazepam).
- Avoid adding benzodiazepines for analgesia — they have minimal analgesic effect and increase sedation/respiratory depression risk, particularly with opioids.
- For concurrent opioid + benzodiazepine dependence: Use multimodal non-opioid analgesia preferentially; if opioids are essential, use the lowest effective dose with continuous SpO₂ monitoring.
Cannabis-Use Disorder and Acute Pain
- Cannabis may alter pain perception (both hyper- and hypoalgesia reported). Heavy use is associated with cannabinoid hyperemesis syndrome (cyclical vomiting, hot showers relieve symptoms).
- Standard analgesic approaches are appropriate; no specific dose adjustments required. Avoid opioids for cannabinoid hyperemesis — treat with capsaicin cream (0.025–0.075 %) applied to abdomen, haloperidol 2.5–5 mg IV, or ondansetron 4–8 mg IV/ODT.
- Be aware of cannabis–drug interactions: CYP3A4 and CYP2C9 inhibition by THC/CBD may affect metabolism of some analgesics.
Substance-Specific Analgesic Cautions
| Substance | Avoid / Caution | Safe Analgesic Options |
|---|---|---|
| Alcohol (heavy use) | Hepatotoxic paracetamol doses (> 2 g/day); high-dose NSAIDs | Reduced-dose paracetamol, cautious NSAIDs, regional blocks |
| Methamphetamine | Tramadol (seizure risk); adrenaline in local anaesthetic | Paracetamol, NSAIDs, opioids (short-acting), benzodiazepines for agitation |
| Benzodiazepines | Abrupt cessation; adding benzodiazepines "for pain" | Standard analgesia; continue maintenance benzodiazepine dose |
| Cannabis | Opioids for cannabinoid hyperemesis syndrome | Capsaicin cream, haloperidol, ondansetron for CHS; standard analgesia otherwise |
| Multiple substances (polysubstance) | Cumulative CNS/respiratory depression | Multimodal non-opioid analgesia; SpO₂ monitoring; low-threshold for HDU/ICU |
Clinical Presentation & Diagnostic Criteria
Patients with SUDs presenting with acute pain may have altered pain behaviours, atypical presentations, or concurrent intoxication/withdrawal that confounds assessment. A systematic, empathetic approach is essential.
Pain Assessment in SUD
- Use a validated numeric rating scale (NRS 0–10) or visual analogue scale (VAS) as for all patients. Document pain scores at regular intervals.
- Do not assume "drug-seeking" behaviour indicates absence of pain. Patients with OUD have lower pain thresholds and higher pain sensitivity due to opioid-induced hyperalgesia (OIH).
- Assess functional impact: ability to cough, deep-breathe, mobilise, and sleep.
- Screen for opioid-induced hyperalgesia: paradoxical worsening pain despite escalating opioid doses in patients on long-term opioids.
Screening Tools
Investigations
In addition to standard acute pain investigations, patients with SUDs require targeted testing to assess substance-related organ damage, intoxication/withdrawal severity, and safe prescribing parameters.
Risk Stratification
Risk stratification guides the intensity of monitoring, analgesic strategy, and discharge planning.
Pharmacological Management
Multimodal Analgesia Ladder for SUD Patients
All patients with SUDs should receive a multimodal approach as the foundation of analgesia, reserving opioids for moderate-to-severe pain unresponsive to non-opioid strategies.
First-Line — Non-Opioid Analgesics
Second-Line — Adjuncts & Opioid-Sparing Agents
Third-Line — Opioid Analgesia (When Non-Opioid Strategies Insufficient)
Medications to AVOID in SUD Patients
| Medication | Reason |
|---|---|
| Tramadol | Seizure risk; serotonin syndrome; weak mu-agonist may trigger relapse; CYP2D6 variability. Avoid in methamphetamine users and patients on SSRIs/SNRIs. |
| Tapentadol | Mu-agonist + NRI — abuse potential; may destabilise OAT. |
| Codeine | Prodrug dependent on CYP2D6 — poor metabolisers get no effect; ultra-rapid metabolisers risk toxicity. Ineffective in patients on buprenorphine (receptor blockade). |
| Pethidine | Normeperidine metabolite causes seizures. Not recommended for acute pain in any patient. Banned from most Australian ED formularies. |
Monitoring
Inpatient Monitoring for Acute Pain + SUD
Continuous SpO₂ Monitoring — Indications
- Any patient receiving parenteral opioids AND concurrent CNS depressants (benzodiazepines, alcohol)
- Patients on PCA (patient-controlled analgesia)
- Patients with BMI > 35, OSA, or COPD receiving opioids
- Patients on naltrexone depot receiving any opioids (risk of respiratory depression if blockade wanes)
- Post-anaesthetic recovery in patients with known SUD
Special Populations
Pregnancy
Paediatrics
Elderly
Renal Impairment
Hepatic Impairment
Immunocompromised
Aboriginal and Torres Strait Islander Health
📚 References
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