Acute Pain & Procedural Sedation — Part 1: Pain Assessment & Non-Opioid Analgesics
Pain assessment scales (NRS, VAS, FACES, FLACC, PAINAD), oligoanalgesia prevention, and first-line non-opioid analgesics including acetaminophen, NSAIDs, subdissociative ketamine, IV lidocaine, trigger point injections, and nitrous oxide.
1. Pain Assessment in the Emergency Department
Pain is the most common reason patients present to the emergency department, with estimates ranging from 60% to 78% of all ED visits involving a pain complaint. Accurate, timely, and repeated pain assessment is the foundation upon which all analgesic decision-making rests. Failure to assess pain consistently leads to oligoanalgesia — one of the most well-documented quality gaps in emergency medicine.1 2 3
1.1 Principles of ED Pain Assessment
Pain is a subjective experience, and the patient’s self-report is the most reliable indicator of pain intensity. Assessment should occur:
- At triage (initial assessment)
- Within 30 minutes of arrival or sooner for severe pain
- After each analgesic intervention (30 minutes post-IV, 60 minutes post-PO)
- At reassessment intervals (typically every 1–2 hours for admitted patients)
- At discharge (to establish a baseline for outpatient management)
Clinicians should assess four dimensions of pain: location, quality (sharp, dull, burning, cramping), intensity (using validated scales), and temporal pattern (constant, intermittent, worsening, improving).
1.2 Pain Assessment Scales
The choice of pain assessment tool depends on the patient’s age, cognitive status, developmental level, and ability to communicate. The following table summarizes the validated scales recommended for ED use:1 3 4
| Scale | Population | Range | Method | Key Points |
|---|---|---|---|---|
| Numeric Rating Scale (NRS) | Adults and children ≥8 years | 0–10 | Patient selects a number: 0 = no pain, 10 = worst pain imaginable | Most widely used in the ED; validated across many pain conditions; clinically significant change is ≥1.3 points (some studies suggest ≥2.0) |
| Visual Analog Scale (VAS) | Adults and children ≥8 years | 0–100 mm | Patient marks a point on a 100-mm line anchored by “no pain” and “worst pain imaginable” | More sensitive to small changes than NRS; requires a printed or digital tool; minimum clinically significant difference is 13 mm |
| Wong-Baker FACES Pain Rating Scale | Children 3–8 years; adults with limited numeracy or language barriers | 0–10 (6 faces) | Patient selects the face that best represents their pain | Each face corresponds to 0, 2, 4, 6, 8, or 10; validated in pediatric and cross-cultural populations; can be used in adults with cognitive impairment |
| FLACC Scale | Infants and children <3 years; nonverbal patients | 0–10 | Observer rates 5 categories: Face, Legs, Activity, Cry, Consolability (each 0–2) | Behavioral observation scale; does not require patient self-report; validated in preverbal children and cognitively impaired adults |
| PAINAD Scale | Patients with dementia or severe cognitive impairment | 0–10 | Observer rates 5 categories: Breathing, Negative Vocalization, Facial Expression, Body Language, Consolability (each 0–2) | Specifically validated for patients who cannot self-report due to dementia; correlates with other validated scales |
| CRIES Scale | Neonates (0–6 months) | 0–10 | Observer rates: Crying, Requires O2, Increased vital signs, Expression, Sleeplessness (each 0–2) | Designed for neonatal postoperative pain; useful in neonatal ED patients |
1.2.1 FLACC Scale Detailed Scoring
| Category | 0 | 1 | 2 |
|---|---|---|---|
| Face | No particular expression or smile | Occasional grimace or frown; withdrawn, disinterested | Frequent to constant frown, clenched jaw, quivering chin |
| Legs | Normal position or relaxed | Uneasy, restless, tense | Kicking or legs drawn up |
| Activity | Lying quietly, normal position, moves easily | Squirming, shifting back and forth, tense | Arched, rigid, or jerking |
| Cry | No cry (awake or asleep) | Moans or whimpers; occasional complaint | Crying steadily, screams or sobs; frequent complaints |
| Consolability | Content, relaxed | Reassured by occasional touching, hugging, or being talked to; distractible | Difficult to console or comfort |
1.2.2 PAINAD Scale Detailed Scoring
| Category | 0 | 1 | 2 |
|---|---|---|---|
| Breathing (independent of vocalization) | Normal | Occasional labored breathing; short period of hyperventilation | Noisy labored breathing; long period of hyperventilation; Cheyne-Stokes respirations |
| Negative vocalization | None | Occasional moan or groan; low-level speech with negative or disapproving quality | Repeated troubled calling out; loud moaning or groaning; crying |
| Facial expression | Smiling or inexpressive | Sad; frightened; frown | Facial grimacing |
| Body language | Relaxed | Tense; distressed pacing; fidgeting | Rigid; fists clenched; knees pulled up; pulling or pushing away; striking out |
| Consolability | No need to console | Distracted or reassured by voice or touch | Unable to console, distract, or reassure |
1.3 Pain Severity Classification
| Severity | NRS Score | Clinical Implication |
|---|---|---|
| Mild | 1–3 | Non-opioid analgesics typically adequate; consider non-pharmacologic interventions |
| Moderate | 4–6 | Multimodal approach recommended; non-opioids ± low-dose opioids or adjuvants |
| Severe | 7–10 | Aggressive multimodal analgesia; parenteral analgesics often required; reassess frequently |
1.4 Oligoanalgesia: Recognition and Prevention
Oligoanalgesia (the undertreatment of pain) is a systemic problem in emergency departments worldwide. Key findings from the literature:1 2 5
- Prevalence: 40–60% of ED patients with moderate-to-severe pain do not receive adequate analgesia
- Time to analgesia: Median time from ED arrival to first analgesic administration ranges from 58 to 90 minutes in many systems
- Disparities: Oligoanalgesia disproportionately affects elderly patients, pediatric patients, non-English-speaking patients, patients of minority racial and ethnic groups, and patients with cognitive impairment
- Contributing factors: Overcrowding, provider knowledge gaps, opiophobia (excessive fear of opioid use for acute pain), lack of reassessment, inadequate pain assessment documentation
Strategies to reduce oligoanalgesia:
| Strategy | Implementation |
|---|---|
| Triage-initiated analgesia protocols | Nurse-initiated protocols allowing administration of acetaminophen, ibuprofen, or topical anesthetics at triage before physician evaluation |
| Standing analgesic orders | Pre-approved order sets for common pain presentations (e.g., fractures, renal colic) |
| Pain reassessment mandates | Institutional policy requiring documented reassessment within 30–60 minutes of analgesic administration |
| Multimodal default approach | Defaulting to non-opioid first-line therapies reduces barriers to initiating analgesia |
| Education and feedback | Regular provider education on pain management; real-time feedback on time-to-analgesia metrics |
| Regional anesthesia programs | ED-based nerve block programs reduce reliance on systemic analgesics and improve pain control |
1.5 Assessment Documentation Requirements
Accreditation standards mandate comprehensive pain assessment documentation. The required elements include:3
- Pain screening using a validated tool appropriate to the patient population
- Pain intensity score recorded at each assessment
- Pain location and quality documented in the medical record
- Functional assessment: how pain affects the patient’s ability to function (move, breathe deeply, sleep)
- Reassessment after intervention with documented response to treatment
- Patient education about pain management plan, expectations, and safe medication use
- Individualized pain management plan that considers the patient’s goals, values, and preferences
- Documentation of any barriers to pain assessment (language, cognition, developmental level)
2. Non-Opioid Analgesics: The First-Line Approach
The contemporary approach to ED pain management prioritizes non-opioid, multimodal analgesia as the first-line strategy for most acute pain presentations. Multimodal analgesia targets multiple pain pathways simultaneously — peripheral nociception, central sensitization, inflammation, and descending modulation — producing additive or synergistic analgesic effects while minimizing the adverse effects of any single agent. Evidence consistently demonstrates that multimodal approaches reduce opioid requirements, improve pain scores, decrease adverse events, and shorten ED length of stay.6 7 8
2.1 Acetaminophen (Paracetamol)
Acetaminophen is one of the most widely used analgesics worldwide and remains a cornerstone of multimodal ED analgesia. Its mechanism involves central COX inhibition, serotonergic pathway modulation, and possible cannabinoid receptor activity. It provides effective analgesia for mild-to-moderate pain and has an opioid-sparing effect when used as part of a multimodal regimen.6 9
2.1.1 Acetaminophen Dosing Table
| Route | Population | Dose | Frequency | Maximum Daily Dose | Notes |
|---|---|---|---|---|---|
| PO | Adults (≥50 kg) | 650–1000 mg | Every 4–6 hours | 3000 mg (healthy); 2000 mg (hepatic impairment, chronic alcohol use) | Onset 30–60 min; peak 1–2 hours |
| PO | Pediatric (≥2 years) | 10–15 mg/kg | Every 4–6 hours | 75 mg/kg/day (max 4000 mg) | Liquid formulations available (160 mg/5 mL) |
| PR | Adults | 650–1000 mg | Every 4–6 hours | 3000 mg | Erratic absorption; reserve for patients who cannot take PO or IV |
| PR | Pediatric | 10–20 mg/kg | Every 4–6 hours | 75 mg/kg/day | Higher initial dose (20 mg/kg) may be given as loading dose |
| IV | Adults (≥50 kg) | 1000 mg | Every 6 hours | 4000 mg (3000 mg if hepatic impairment) | Infuse over 15 minutes; onset 5–10 min; peak ~1 hour; faster onset than PO but similar efficacy at 1 hour |
| IV | Adults (<50 kg) | 15 mg/kg | Every 6 hours | 75 mg/kg/day (max 3750 mg) | Weight-based dosing for patients <50 kg |
| IV | Pediatric (≥2 years, ≥33 kg) | 15 mg/kg (max 750 mg) | Every 6 hours | 75 mg/kg/day (max 3750 mg) | Infuse over 15 minutes |
| IV | Pediatric (≥2 years, <33 kg) | 12.5 mg/kg | Every 4–6 hours | 75 mg/kg/day | Use caution with dosing calculations |
| IV | Neonates/Infants (<2 years) | 7.5–12.5 mg/kg | Every 6 hours | 37.5–50 mg/kg/day | Reduced clearance in neonates; dose conservatively |
2.1.2 Hepatic Considerations and Contraindications
| Consideration | Detail |
|---|---|
| Hepatic impairment | Reduce maximum daily dose to 2000 mg PO or 2000 mg IV; avoid in severe hepatic failure (Child-Pugh C) |
| Chronic alcohol use | Maximum 2000 mg/day; risk of hepatotoxicity increases with CYP2E1 induction |
| Acute overdose | N-acetylcysteine (NAC) protocol for serum levels above Rumack-Matthew nomogram line; dose-dependent hepatotoxicity above 150 mg/kg single ingestion |
| Malnutrition/fasting | Depleted glutathione stores increase susceptibility to hepatotoxicity at therapeutic doses |
| Drug interactions | Warfarin: INR may increase with regular use >2 g/day; monitor closely |
| G6PD deficiency | Generally safe at standard doses; high doses may theoretically increase oxidative stress |
2.2 Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)
NSAIDs inhibit cyclooxygenase (COX-1 and COX-2) enzymes, reducing prostaglandin synthesis and thereby decreasing inflammation, pain, and fever. They are among the most effective analgesics for musculoskeletal pain, renal colic, headache, and dental pain. In the ED, NSAIDs are a critical component of multimodal analgesia and in many conditions are equivalent or superior to opioids for pain control.6 7 10
2.2.1 NSAID Dosing Table
| Drug | Route | Adult Dose | Pediatric Dose | Frequency | Max Daily Dose (Adult) | Onset | Duration |
|---|---|---|---|---|---|---|---|
| Ibuprofen | PO | 200–800 mg | 5–10 mg/kg | Every 6–8 hours | 3200 mg (2400 mg for chronic use) | 30–60 min | 4–6 hours |
| Ketorolac | IV/IM | 15–30 mg IV; 30–60 mg IM | 0.5 mg/kg IV/IM (max 15 mg) | Every 6 hours | 120 mg (day 1); ≤5 days total | 10–30 min (IV); 30–60 min (IM) | 4–6 hours |
| Ketorolac | PO | 10 mg | Not routinely recommended PO in pediatrics | Every 4–6 hours | 40 mg; ≤5 days total (combined routes) | 30–60 min | 4–6 hours |
| Ketorolac | IN (nasal spray) | 15.75 mg per nostril (31.5 mg total) | Not approved | Every 6–8 hours | 126 mg; ≤5 days total | 20–30 min | 4–6 hours |
| Naproxen | PO | 250–500 mg | 5–7 mg/kg | Every 8–12 hours | 1250 mg (day 1); 1000 mg (thereafter) | 30–60 min | 8–12 hours |
| Diclofenac | PO | 50 mg | Not routinely used | Every 8 hours | 150 mg | 30–60 min | 6–8 hours |
| Diclofenac | IV | 37.5 mg in 100 mL NS | Not recommended | Every 6 hours | 150 mg; ≤2 days IV | 15–30 min | 6–8 hours |
| Diclofenac | Topical (gel 1%) | Apply 4 g to affected area | Age ≥6 years per area | Every 6–8 hours | 32 g per joint per day | Variable | 4–6 hours |
| Meloxicam | PO | 7.5–15 mg | 0.125 mg/kg (limited data) | Once daily | 15 mg | 1–2 hours | 24 hours |
| Celecoxib | PO | 200–400 mg initial, then 200 mg | Limited pediatric use | Every 12–24 hours | 400 mg | 1–3 hours | 12–24 hours |
2.2.2 Ketorolac Evidence and Practical Considerations
Ketorolac deserves special emphasis as the most commonly used parenteral NSAID in the ED:7 10
- Low-dose equivalence: 10 mg IV ketorolac has been shown in multiple randomized trials to provide equivalent analgesia to 15 mg and 30 mg IV doses, with significantly fewer adverse effects. Low-dose (10–15 mg IV) ketorolac is now recommended as the default in many ED protocols.
- Renal colic: Ketorolac is first-line for renal colic, with efficacy equivalent to or exceeding parenteral opioids, and with fewer adverse effects (less nausea, no respiratory depression, no sedation)
- Duration limit: Maximum 5 days of use across all routes combined due to increased risk of GI bleeding, renal injury, and cardiovascular events with prolonged use
- IM vs. IV: IV administration provides faster onset and more predictable pharmacokinetics; IM injection is painful and offers no efficacy advantage
2.2.3 NSAID Contraindications and Cautions
| Contraindication/Caution | Detail |
|---|---|
| Active GI bleeding or peptic ulcer disease | Absolute contraindication; COX-1 inhibition reduces mucosal prostaglandin protection |
| Chronic kidney disease (eGFR <30) | Contraindicated; NSAIDs reduce renal prostaglandin-mediated afferent arteriolar vasodilation, precipitating acute-on-chronic kidney injury |
| Acute kidney injury | Avoid; may worsen renal perfusion |
| Dehydration/hypovolemia | Increased risk of AKI; ensure adequate hydration before NSAID administration |
| Heart failure (NYHA III–IV) | Contraindicated; sodium and water retention, increased afterload |
| Third trimester pregnancy | Contraindicated; risk of premature closure of ductus arteriosus |
| Aspirin-exacerbated respiratory disease | Contraindicated; cross-reactivity with all non-selective NSAIDs |
| Coagulopathy or concurrent anticoagulation | Use with caution; platelet inhibition increases bleeding risk (ketorolac particularly; celecoxib has less platelet effect) |
| Post-CABG | Contraindicated per FDA black box warning |
| Elderly (≥65 years) | Use lower doses (ketorolac 15 mg IV max); increased GI, renal, and cardiovascular risk |
| Neonates and infants | Generally avoided; limited safety data |
2.3 Subdissociative-Dose Ketamine (SDK)
Ketamine is a phencyclidine derivative that acts primarily as a non-competitive NMDA receptor antagonist. At subdissociative doses (approximately one-tenth of dissociative doses), ketamine provides significant analgesia by blocking central sensitization and wind-up phenomena without producing dissociation, significant hemodynamic changes, or respiratory depression. SDK has emerged as a powerful non-opioid analgesic option in the ED, supported by a growing body of randomized controlled trials and systematic reviews.7 8 11 12
2.3.1 Subdissociative Ketamine Dosing
| Route | Dose | Administration | Onset | Duration | Key Considerations |
|---|---|---|---|---|---|
| IV push | 0.1–0.3 mg/kg | Administer over 10–15 minutes (short infusion preferred to reduce dysphoria) | 1–2 min | 15–30 min | Rapid IV push increases risk of dysphoria, nystagmus, dizziness; always administer slowly or as short infusion |
| IV infusion | 0.1–0.3 mg/kg in 100 mL NS | Infuse over 15–30 minutes | 5–10 min | 30–60 min | Preferred method; lower incidence of emergence phenomena and dysphoria compared with IV push |
| Intranasal (IN) | 0.5–1 mg/kg | Via mucosal atomization device (MAD); divide dose between nares; max 1 mL per nostril | 5–10 min | 30–60 min | Bioavailability ~45%; use concentrated preparation (100 mg/mL); painless administration; excellent for pediatric patients |
| IM | 0.5–1 mg/kg | Standard IM injection | 5–15 min | 30–60 min | Reserve for patients without IV access; higher incidence of dysphoria |
| Nebulized | 0.75–1 mg/kg in 3 mL NS | Via standard nebulizer | 5–15 min | 20–40 min | Emerging route; limited data but promising for needle-averse patients |
2.3.2 SDK Evidence Summary
| Study/Review | Key Finding |
|---|---|
| Motov et al. (2015) RCT | SDK 0.3 mg/kg IV equivalent to morphine 0.1 mg/kg IV for acute pain in the ED; fewer serious adverse events in the ketamine group |
| Beaudoin et al. (2014) RCT | SDK 0.15–0.3 mg/kg IV produced significant pain reduction at 5 and 30 minutes; dose-response relationship identified |
| Sin et al. (2017) systematic review | SDK provides clinically significant pain reduction in the ED; adverse effects (dizziness, dysphoria, nausea) are generally mild and self-limited |
| Balzer et al. (2021) meta-analysis | SDK non-inferior to opioids for ED acute pain; opioid-sparing effect when used as adjunct |
| Shimonovich et al. (2016) RCT | IN ketamine (1 mg/kg) equivalent to IN fentanyl for pediatric extremity injuries |
2.3.3 SDK Adverse Effects and Management
| Adverse Effect | Incidence | Management |
|---|---|---|
| Dizziness/lightheadedness | 30–50% | Self-limited (5–15 min); reassurance; slow infusion rate reduces incidence |
| Nausea | 10–20% | Ondansetron 4 mg IV if needed; typically mild |
| Dysphoria/feeling of unreality | 10–30% | More common with rapid IV push; slow infusion reduces incidence; midazolam 1–2 mg IV if severe |
| Nystagmus | 10–30% | Benign; self-limited |
| Elevated blood pressure | 5–15% | Mild sympathomimetic effect; rarely clinically significant at analgesic doses |
| Emergence phenomena | <5% at SDK doses | Distinguish from dissociative doses where incidence is higher; benign at analgesic doses |
2.3.4 SDK Contraindications
| Contraindication | Rationale |
|---|---|
| Age <3 months | Limited safety data |
| Known hypersensitivity | Anaphylaxis risk |
| Conditions where elevated BP is dangerous | Uncontrolled hypertension, aortic dissection, hypertensive emergency (relative) |
| Active psychosis | May exacerbate symptoms (relative contraindication at SDK doses) |
| Globe rupture | Theoretical concern for IOP elevation (data at analgesic doses is reassuring) |
2.4 Intravenous Lidocaine
IV lidocaine is a sodium channel blocker with analgesic, anti-inflammatory, and anti-hyperalgesic properties. It has been studied in the ED primarily for renal colic and abdominal pain, with several randomized controlled trials demonstrating meaningful analgesic benefit.7 13
2.4.1 IV Lidocaine Dosing
| Indication | Dose | Administration | Onset | Duration | Notes |
|---|---|---|---|---|---|
| Renal colic | 1.5 mg/kg (lean body weight) | IV infusion over 10 minutes | 5–10 min | 30–60 min | Can repeat once at 0.5–1 mg/kg if needed; cardiac monitor required |
| Acute pain (general) | 1.5 mg/kg (lean body weight) | IV infusion over 10–15 minutes | 5–10 min | 30–60 min | Particularly useful for visceral and neuropathic pain |
| Continuous infusion (inpatient) | 1–2 mg/min (or 0.5–1.5 mg/kg/hr) | Continuous IV infusion | Ongoing | Duration of infusion | Requires cardiac monitoring; not standard ED use; more common in perioperative setting |
2.4.2 IV Lidocaine Safety Considerations
| Parameter | Detail |
|---|---|
| Cardiac monitoring | Continuous telemetry required during infusion; observe for QRS widening, PR prolongation, new arrhythmias |
| Maximum dose | 4.5 mg/kg total (without epinephrine); do not exceed 300 mg in initial bolus |
| Contraindications | Second- or third-degree heart block; severe sinoatrial block; known lidocaine allergy (amide allergy); severe hepatic impairment (reduced metabolism) |
| Toxicity signs | Perioral numbness, tinnitus, metallic taste (early); seizures, cardiovascular collapse (late); treat with lipid emulsion if severe |
| Drug interactions | Beta-blockers and cimetidine reduce hepatic clearance; amiodarone increases risk of cardiac toxicity |
2.5 Trigger Point Injections
Trigger point injections (TPIs) are effective for myofascial pain presentations in the ED, including acute muscle spasm, tension-type headache, and musculoskeletal chest wall pain.6 14
2.5.1 Technique
- Identify the trigger point: Palpate for a taut band of muscle with a hyperirritable nodule that reproduces the patient’s pain pattern
- Preparation: Clean the skin with chlorhexidine or alcohol; no draping required for superficial muscles
- Needle selection: 25–27 gauge, 1.5-inch needle
- Injection: Insert the needle into the trigger point; aspirate to confirm non-vascular placement; inject 1–3 mL of:
- Bupivacaine 0.25% (longer duration, 4–8 hours) OR
- Lidocaine 1% (faster onset, 1–2 hours duration) OR
- Dry needling (needle insertion without injection; evidence supports similar efficacy)
- Post-injection: Apply pressure for 1–2 minutes; passive stretch of the affected muscle
2.5.2 Common ED Indications for Trigger Point Injections
| Presentation | Muscle(s) Targeted | Evidence Level |
|---|---|---|
| Tension-type headache | Trapezius, sternocleidomastoid, temporalis, occipitalis | Moderate; may provide rapid relief when combined with standard therapies |
| Acute low back pain | Paraspinal muscles, quadratus lumborum | Moderate; effective for muscular component of back pain |
| Chest wall pain | Pectoralis, intercostal muscles, serratus anterior | Moderate; important to exclude cardiac and pulmonary causes first |
| Neck pain/torticollis | Trapezius, levator scapulae, sternocleidomastoid | Moderate; may reduce need for systemic muscle relaxants |
2.6 Nitrous Oxide
Nitrous oxide (N₂O) is an inhaled analgesic and anxiolytic that provides rapid-onset, titratable, short-duration analgesia. It is self-administered by the patient through a demand-valve mask, providing an inherent safety mechanism (the patient must maintain a seal and inhale actively; sedation leads to the mask falling away, terminating delivery). Nitrous oxide has been used extensively in emergency departments internationally, particularly in Australasia and Europe, and its use is expanding in North American EDs.7 15
2.6.1 Nitrous Oxide Delivery and Dosing
| Parameter | Detail |
|---|---|
| Concentration | 50% N₂O / 50% O₂ (Entonox) is the standard fixed-ratio preparation; some systems use 70% N₂O / 30% O₂ (requires additional monitoring) |
| Delivery | Self-administered via demand-valve mask or mouthpiece; patient must be able to hold the delivery device |
| Onset | 30–60 seconds |
| Peak effect | 3–5 minutes |
| Recovery | 3–5 minutes after discontinuation (rapid elimination via lungs) |
| Analgesia level | Provides anxiolysis and analgesia for mild-to-moderate pain; typically reduces pain scores by 2–4 points on the NRS |
| Scavenging | Waste gas scavenging system required to minimize occupational exposure; treatment room should have adequate ventilation |
2.6.2 Nitrous Oxide Indications and Contraindications
| Indications | Contraindications |
|---|---|
| Laceration repair | Pneumothorax (N₂O expands into air-filled spaces) |
| Fracture/dislocation reduction (adjunct) | Bowel obstruction (N₂O expands into distended bowel) |
| Abscess incision and drainage | Middle ear surgery/pathology (tympanic membrane rupture risk) |
| IV cannulation in anxious patients | Decompression sickness |
| Burn wound care | Severe COPD (relative; 50:50 mix provides adequate O₂) |
| Pediatric procedures (≥1 year) | Altered mental status (cannot self-administer safely) |
| Brief painful procedures | First trimester pregnancy (theoretical teratogenicity; avoid if possible) |
| Musculoskeletal injury pain | Intracranial hypertension (relative) |
| Inability to cooperate with self-administration | |
| Vitamin B₁₂ deficiency (chronic exposure inactivates B₁₂; single use is safe) |
2.6.3 Adverse Effects
| Effect | Incidence | Management |
|---|---|---|
| Nausea/vomiting | 5–10% | Self-limited; have emesis basin available; discontinue if persistent |
| Dizziness/euphoria | 10–20% | Expected pharmacologic effect; self-limited |
| Headache | 2–5% | Mild; self-limited |
| Diffusion hypoxia | Rare | Administer supplemental oxygen for 3–5 minutes after discontinuation in prolonged use |
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