Acute Pain Management

Short Note - 20 Marks

Introduction

Pathophysiology

• Nociceptive pain - from tissue damage; responds well to NSAIDs and opioids
• Neuropathic pain - from nerve injury; poorly responsive to opioids; managed with tricyclics, anticonvulsants, or SNRIs
• Visceral pain - poorly localized, often with associated autonomic symptoms

Pain Assessment

• Pain should be assessed at triage and reassessed after each intervention
• No single scale is universally superior; the choice should suit the patient

Pain Scales (Table 35-2)

Special Populations (Pain Scale Performance)

• Children: Behavioral or observational scales (e.g., FLACC, FACES scale) are used for preverbal patients
• Elderly: Cognitive impairment may limit verbal reporting; behavioral cues and caregiver input become important
• Cognitively impaired: Observer-based scales required

Pharmacologic Acute Pain Treatment

Approach to Initial Analgesic Selection

• Mild pain: Acetaminophen or NSAIDs
• Moderate pain: NSAIDs ± weak opioids; consider combinations
• Severe pain: Systemic opioids; regional/local anesthesia as adjunct

1. Non-Opioid Analgesics

Acetaminophen (Paracetamol)

• Mechanism: Inhibits central prostaglandin synthesis; may modulate the endocannabinoid system
• Effective for mild-moderate pain; useful as part of multimodal regimens
• IV formulation (1 g) provides faster onset and is useful when oral route unavailable
• Safe in renal impairment; maximum dose 4 g/day (reduced in liver disease, alcoholism, malnutrition)

NSAIDs (Non-Steroidal Anti-Inflammatory Drugs)

• Mechanism: Inhibit COX-1 and COX-2 enzymes → reduce prostaglandin synthesis → peripheral and central anti-inflammatory and analgesic effects
• Particularly effective for:
  • Musculoskeletal pain
  • Renal colic and biliary colic (smooth muscle spasm)
  • Dysmenorrhea
  • Dental and soft tissue inflammation
• IV ketorolac (15-30 mg) is widely used in the ED for moderate-severe pain; comparable to opioids for renal colic
• Caution: renal impairment, GI bleeding risk, cardiovascular events, platelet inhibition
• COX-2 selective agents (celecoxib) spare GI effects but carry cardiovascular risk

Nitrous Oxide (N₂O)

• 50% N₂O in O₂ (Entonox) provides rapid-onset, short-duration analgesia and anxiolysis
• Useful for procedural pain and dressing changes
• Onset: ~2-3 minutes; wears off rapidly on discontinuation
• Avoid in: pneumothorax, bowel obstruction, middle ear problems

2. Opioid Analgesics

Common Opioids in the ED

Opioid Dosing Principles

• IV titration is safest - small incremental doses with reassessment
• Weight-based dosing for children
• Reassess at expected time to peak effect (morphine IV: 15-20 min)
• Avoid IM route when IV access available - variable absorption
• Caution in elderly: reduce starting dose by 25-50%

Opioid Side Effects

• Nausea/vomiting: give antiemetic concurrently
• Respiratory depression: rare with proper titration; treat with naloxone 0.4-2 mg IV
• Constipation, urinary retention, pruritus
• Hypotension (especially in hypovolemic patients)

Patient-Controlled Analgesia (PCA)

• Allows patient to self-administer small incremental IV opioid doses within preset limits
• Reduces oligoanalgesia; improves satisfaction and reduces nurse-administered variability

3. Adjuvant and Non-Traditional Analgesics

Ketamine (Sub-dissociative)

• Dose: 0.1-0.5 mg/kg IV (sub-dissociative)
• NMDA receptor antagonist; effective for opioid-refractory pain, neuropathic pain, and procedural analgesia
• Can reduce total opioid consumption ("opioid-sparing")
• Side effects: dysphoria, hallucinations (less common at low doses); give midazolam 1-2 mg to reduce emergence reactions if needed

Nitrous Oxide

Alpha-2 Agonists (e.g., dexmedetomidine, clonidine)

• Analgesic and sedative properties
• Used as opioid adjuncts; useful in procedural sedation

Anticonvulsants (Gabapentin, Pregabalin)

• For neuropathic pain components; reduce central sensitization
• Increasingly used in multimodal perioperative analgesia

Antidepressants (TCAs, SNRIs)

• Neuropathic pain management; not for acute severe pain

4. Regional and Local Anesthesia

• Local infiltration: Lidocaine, bupivacaine for wound repair, minor procedures
• Peripheral nerve blocks: Femoral, fascia iliaca, ulnar, radial, digital blocks - especially effective with ultrasound guidance
• Topical anesthesia: EMLA cream, LET (lidocaine-epinephrine-tetracaine) gel for wound/venipuncture in children

Special Pain Situations

Abdominal Pain

• Withholding analgesia to preserve diagnostic findings is no longer supported by evidence - adequate analgesia does not impair abdominal exam accuracy
• NSAIDs and opioids are both appropriate depending on severity and etiology
• Renal colic: IV ketorolac is first-line; IV opioid if inadequate

Headache/Migraine

• Mechanistic approach preferred: IV prochlorperazine 10 mg, metoclopramide 10 mg, or sumatriptan
• IV dexamethasone 8-10 mg reduces recurrence
• Opioids are not first-line for migraine - they worsen medication overuse headache and are less effective

Sickle Cell Pain Crisis

• Often undertreated; patients have high opioid tolerance from chronic exposure
• Aggressive IV opioid titration required; consider PCA
• NSAIDs and IV fluids are useful adjuncts

Elderly Patients

• Start with lower doses and titrate slowly
• Beware renal impairment affecting NSAID and morphine-6-glucuronide clearance
• NSAIDs: use with caution; consider acetaminophen first
• Risk of falls, delirium with opioids and sedatives

Pediatric Patients

• Weight-based dosing essential
• Intranasal fentanyl (2 mcg/kg) is a well-tolerated alternative to IV
• Oral sucrose and non-pharmacologic methods for neonates
• Avoid codeine in children (CYP2D6 variability risk)

Multimodal Analgesia

• Reduces individual drug doses and side effects
• Provides additive or synergistic analgesia
• Example: Acetaminophen + NSAID + low-dose opioid + regional block

Non-Pharmacologic Methods

• Verbal reassurance and information reduces anxiety and can reduce analgesic requirements
• Immobilization and splinting for fractures
• Ice/heat application
• Positioning and elevation
• Distraction and relaxation techniques (especially in children)
• Anxiolytics (e.g., midazolam) when anxiety amplifies pain and verbal reassurance is insufficient

Discharge Analgesia and Opioid Stewardship

• The minimum effective dose of the least potent opioid should be prescribed at discharge
• Short courses (3-7 days) with clear instructions
• Non-opioid regimens should be maximized before opioids are added
• Patient education: storage, disposal, no sharing
• Screening tools (AUDIT, DAST) can identify at-risk patients before prescribing

Summary

1. Accurate, repeated assessment using appropriate scales
2. Matching analgesic potency to pain severity from the outset (not tiered escalation)
3. Multimodal analgesia - combining non-opioids, opioids when needed, and regional techniques
4. Special attention to vulnerable populations (elderly, pediatric, cognitively impaired)
5. Mechanistic approaches for specific pain syndromes (migraine, renal colic)
6. Responsible opioid use with stewardship at discharge
7. Non-pharmacologic adjuncts as part of holistic care

Pain Pathways

Overview: The Four Key Processes

1. Transduction - noxious stimulus converted to electrical signal at the nociceptor
2. Transmission - signal conducted along peripheral nerves to the spinal cord and brain
3. Modulation - signal amplified or suppressed at dorsal horn and supraspinal levels
4. Perception - conscious experience of pain at cortical level

1. PERIPHERAL MECHANISMS - Transduction

Primary Afferent Nociceptors

Harrison's Fig. 14-1: Components of a cutaneous nerve showing Aβ, Aδ, and C fibers

What Activates Nociceptors?

• Intense heat or cold
• Intense mechanical distortion (pinch, crush)
• Acidic pH (H+ ions)
• Chemical irritants: ATP, serotonin, bradykinin (BK), histamine
• The TRPV1 receptor (vanilloid receptor) mediates heat and acid pain, and is the target of capsaicin

Peripheral Sensitization

Nociceptor-Induced Neurogenic Inflammation

• Cause vasodilation
• Trigger mast cell degranulation (histamine release)
• Attract leukocytes
• Increase inflammatory mediator production

Silent Nociceptors

2. CENTRAL MECHANISMS - Transmission

Dorsal Horn Entry

• Glutamate - rapid excitation of second-order dorsal horn neurons (AMPA receptors)
• Substance P and CGRP - slower, longer-lasting excitation (NK-1 receptors)

Spinothalamic Tract (STT) - The Main Ascending Pain Pathway

• Interruption of the STT produces permanent deficits in pain and temperature discrimination
• This is the anatomical basis of contralateral pain/temperature loss in Brown-Séquard syndrome and anterolateral cordotomy

Harrison's Fig. 14-4: A. Spinothalamic pain transmission pathway. B. Descending pain modulation pathway.

Thalamic Projections and Cortical Processing

Referred Pain

• Cardiac ischemia → left arm/jaw pain (T1-T4 convergence)
• Diaphragmatic irritation → shoulder tip pain (C3-C4 dermatome)
• Appendicitis → periumbilical pain (T10) before right iliac fossa localization

3. PAIN MODULATION

Gate Control Theory (Dorsal Horn Level)

• Large Aβ fibers (activated by touch/rubbing) collateralize into the dorsal horn and activate inhibitory interneurons
• These interneurons suppress the relay of nociceptive input from Aδ and C fibers - effectively "closing the gate"

Opioid Modulation at the Dorsal Horn

Ganong's Fig. 9-10: Opioid mechanisms at the dorsal horn

• Presynaptic inhibition: opioid receptors on nociceptor terminals → decrease Ca²⁺ influx → less glutamate/substance P release
• Postsynaptic inhibition: opioid receptors on dorsal horn neurons → increase K⁺ conductance → hyperpolarization → reduced excitability

Descending Inhibitory System

1. Periaqueductal gray (PAG) in the midbrain - the central node; rich in opioid receptors
2. Projects to rostroventromedial medulla (RVM) and locus coeruleus (LC)
3. Descending axons reach the dorsal horn of the spinal cord
4. Release serotonin (from RVM) and norepinephrine (from LC) to inhibit pain transmission

• Stress-induced analgesia (soldiers in battle unaware of injuries)
• Placebo analgesia (endogenous opioid release)
• How morphine, at supraspinal sites, activates this system to produce analgesia

Central Sensitization

1. Wind-up: repetitive C-fiber stimulation causes progressive increase in action potential generation in wide dynamic range (WDR) neurons via NMDA receptor activation
2. Receptor field expansion: dorsal horn neurons begin responding to inputs from previously subthreshold somatic areas
3. Hyperexcitability of flexion reflexes

• Allodynia - pain from normally non-painful stimuli (e.g., light touch on sunburned skin)
• Hyperalgesia - exaggerated pain from mildly painful stimuli
• Chronic pain states - where the central nervous system becomes the primary pain generator

4. PERCEPTION - Cortical Processing

• Sensory-discriminative dimension (somatosensory cortex): "where, how intense, what quality"
• Affective-motivational dimension (anterior cingulate cortex, insula): "how unpleasant, how distressing"
• Cognitive-evaluative dimension (prefrontal cortex): prior experience, expectations, context

• Fear and anxiety → amplify pain (via limbic connections)
• Focused distraction, stress, morphine → suppress pain (via PAG activation)
• Cultural beliefs, past pain history, emotional state → alter threshold and tolerance

Clinical Correlations

Summary Diagram (Conceptual)

NOXIOUS STIMULUS
      ↓
[NOCICEPTOR - Transduction]
  TRPV1, ion channels, BK/PG sensitization
      ↓
[PRIMARY AFFERENT - Transmission]
  Aδ (fast, sharp) / C fibers (slow, burning)
  Cell bodies in Dorsal Root Ganglion
      ↓
[DORSAL HORN - 1st Synapse]
  Glutamate + Substance P / CGRP
  Modulation: Gate control, Opioids, Enkephalin
      ↓
[SPINOTHALAMIC TRACT - Contralateral]
  Crosses at cord level → Anterolateral column
  Ascends: Medulla → Pons → Midbrain → Thalamus
      ↓
[THALAMUS - Relay]
  Lateral → Somatosensory cortex (S1/S2)
  Medial → Anterior cingulate + Insular cortex
      ↓
[CORTEX - Perception]
  Discriminative + Affective dimensions
  
DESCENDING INHIBITION (top-down):
  Cortex/Hypothalamus → PAG → RVM/LC → Dorsal Horn
  (Serotonin + Norepinephrine suppression)

Local Anesthetic Agents

Short Note - 20 Marks

Introduction

Classification

Mechanism of Action

• The drug enters the axon in its unionized form and binds the inner face of the Na⁺ channel in its ionized form
• Blockade is use-dependent - rapidly firing nerves are blocked preferentially
• Nerve fibers are blocked in a specific sequence based on fiber size:
  1. Pain and temperature (small Aδ and C fibers) - blocked first
  2. Touch and deep pressure (larger fibers) - blocked second
  3. Motor function (largest Aα fibers) - blocked last

Pharmacology: Key Determinants

1. Onset of Action - Determined by pKa

• The pKa is the pH at which 50% of the drug is ionized and 50% is unionized
• The unionized (free base) form crosses lipid membranes to enter the nerve
• Lower pKa = more drug in unionized form at physiologic pH = faster onset
• Agents with lower pKa: mepivacaine, lidocaine, prilocaine (faster onset)
• Agents with higher pKa: bupivacaine (slower onset)
• The pH of LA solutions is acidic (3.3-6.8), which shifts drug toward ionized form - this explains the initial pain on injection and reduced efficacy in infected/acidic tissues

2. Duration of Action - Determined by Protein Binding

• Higher protein binding = longer receptor affinity = longer duration
• Bupivacaine, tetracaine, ropivacaine: high protein binding → long duration (2-8 hours)
• Lidocaine, prilocaine: medium binding → intermediate duration (1-2 hours)
• Procaine: low binding → short duration (15-45 minutes)

3. Potency - Determined by Lipid Solubility

• More lipophilic agents penetrate nerve membranes more easily → higher potency
• Bupivacaine: high lipid solubility → highly potent
• Procaine: low lipid solubility → low potency

Individual Agents (Table 36-2)

Vasoconstrictors (Epinephrine)

• Causes local vasoconstriction → reduces systemic absorption → prolongs duration and increases maximum safe dose
• Provides a marker of intravascular injection (sudden tachycardia if injected IV)
• Achieves hemostasis at the injection site
• Standard concentration: 1:100,000 to 1:200,000 (5-10 micrograms/mL)

• End-arterial territories: digital blocks (fingers, toes), penis, nose, ear pinna
• Patients on MAO inhibitors or non-selective beta-blockers
• Known coronary artery disease or peripheral vascular disease (relative)

Topical Anesthetic Agents (Table 36-1)

Intact Skin

Open Wounds

Mucous Membranes

General Principles of Safe Use

1. Always calculate total dose before injection - especially in small patients or large wounds
2. Aspirate before injection to avoid intravascular deposition
3. Inject slowly - reduces pain and allows detection of inadvertent IV injection
4. Use smallest effective volume at the lowest effective concentration
5. Alkalinization (adding NaHCO₃): raises pH of solution → more drug in unionized form → faster onset and less injection pain (1 mEq NaHCO₃ per 10 mL lidocaine)
6. Warming the LA to body temperature reduces injection pain

Techniques to Reduce Pain of Injection

• Apply topical anesthetic before needle puncture
• Use small-bore needle (27-30 gauge)
• Slow injection rate
• Warm the solution
• Stretch or vibrate skin at puncture site
• Distract the patient during injection
• Insert needle through pores or hair follicles
• Use bevel-up needle orientation

Local Anesthetic Systemic Toxicity (LAST)

Risk Factors

• Excessive dose
• Inadvertent intravascular injection
• Highly vascular injection site (intercostal > paracervical > epidural > brachial plexus > sciatic/femoral)
• Patients with reduced hepatic function, cardiac disease, or extremes of age

Clinical Progression (CNS then Cardiovascular)

• Circumoral/tongue numbness and tingling
• Metallic taste
• Light-headedness, tinnitus, visual disturbances
• Agitation, confusion, tremors
• Seizures (hallmark of significant CNS toxicity)
• CNS depression, respiratory arrest

• Hypotension
• Conduction block (PR prolongation, QRS widening)
• Ventricular arrhythmias (especially with bupivacaine - due to its high lipid solubility and tight Na⁺ channel binding)
• Cardiovascular collapse / refractory cardiac arrest

Management of LAST

• Bolus: 1.5 mL/kg IV over 1 minute
• Infusion: 0.25 mL/kg/min, continued for 10 minutes after hemodynamic stability
• Repeat bolus if hemodynamic instability persists
• Maximum dose: ~10 mL/kg over the first 30 minutes

Special Considerations

Allergy

• True allergy to amide LAs is extremely rare
• Ester LAs produce PABA (para-aminobenzoic acid) as a metabolite - a known allergen; cross-reactivity exists among esters
• No cross-reactivity between ester and amide classes
• Patients with suspected allergy to both classes: diphenhydramine 1% or benzyl alcohol with epinephrine can be used as alternative infiltration agents

Methemoglobinemia

• Prilocaine and benzocaine can oxidize ferrous (Fe²⁺) hemoglobin to ferric (Fe³⁺) methemoglobin
• Cyanosis occurs when methemoglobin concentration exceeds 1.5 g/dL
• Treatment: IV methylene blue 1-2 mg/kg
• Risk: excessive doses, neonates (reduced methemoglobin reductase activity)

Pregnancy

• Most LAs are category B/C
• Avoid large doses; placental transfer occurs (fetal bradycardia risk with bupivacaine)
• Prilocaine avoided (methemoglobin risk to fetus)

Regional Anesthesia (Nerve Blocks)

• Eliminates wound distortion from large-volume local injection
• Superior pain control on extremities
• Less total drug required
• Reduces procedure-related anxiety

Ultrasound-Guided Nerve Blocks

Fig. 36-2A: A nerve in cross-section on ultrasound appears as a white, hyperechoic "honeycomb" structure (arrow)

• Nerves appear as white, hyperechoic, honeycomb-patterned structures in cross-section
• The needle appears as a bright white hyperechoic line on US
• Allows real-time visualization of needle tip and LA spread
• Increases success rate, reduces volume of LA required, reduces complications

Agent Selection for Regional Blocks

• Lidocaine: fastest onset (~10-20 min to optimal block); intermediate duration
• Bupivacaine / ropivacaine / levobupivacaine: longer onset (15-30 min) but duration of 4-8 hours; preferred when prolonged post-procedure analgesia is desired
• Levobupivacaine and ropivacaine are preferred for blocks where large volumes are needed due to significantly lower cardiotoxicity than bupivacaine

Common ED Nerve Blocks

Summary

1. Understanding ester vs amide classification and metabolism
2. Matching agent to clinical need: onset (pKa), duration (protein binding), potency (lipid solubility)
3. Respecting maximum doses and using aspiration technique
4. Recognizing and managing LAST - CNS symptoms precede cardiovascular collapse; treat with benzodiazepines for seizures and 20% IV lipid emulsion for cardiovascular toxicity
5. Using topical agents to reduce needle pain and vasoconstrictors to extend duration
6. Employing ultrasound-guided regional blocks as a powerful, opioid-sparing analgesic strategy in the ED

Regional Blocks

Short Note - 20 Marks

Introduction

• Eliminates wound distortion from large-volume local injection
• Requires smaller total drug volume
• Provides superior pain control on extremities
• Reduces patient anxiety and improves procedural outcomes
• With careful technique, serious complications are uncommon

Pre-Block Assessment (Mandatory)

• Vascular: skin color, temperature, capillary refill time, pulses
• Neurologic: cutaneous sensation (pain, touch), motor function (active movement, strength)
• Digital injuries: test two-point discrimination on the volar pad before injection
  • Normal: <6 mm at fingertips (often <2 mm)
  • Compare with contralateral digit

Nerve Localization Techniques

1. Landmark Technique

• Most common in ED practice
• Relies on anatomical surface landmarks to guide needle placement
• Disadvantage: anatomic variation; requires larger LA volumes to compensate for imprecision

2. Peripheral Nerve Stimulator

• Uses electrically insulated needles
• Stimulates motor response at 0.5-1.0 mA when needle is near the target nerve (motor twitch)
• Reduces reliance on paresthesia and improves success rate

3. Ultrasound (US) Guidance

• Now the preferred technique in well-equipped EDs
• Nerves appear as white, hyperechoic, honeycomb-patterned structures in cross-section
• Needle visualized as a bright white hyperechoic line
• Allows real-time confirmation of needle tip position and LA spread around the nerve

Fig. 36-2B: US visualization of the hyperechoic needle approaching the target nerve, with the adjacent vessel

Onset Times

• Lidocaine: optimal analgesia at 10-20 minutes
• Bupivacaine/ropivacaine: optimal analgesia at 15-30 minutes
• Pain and temperature are affected first, then touch, deep pressure, then motor function
• Intraneural injection causes significant pain - if excessive pain occurs on injection, withdraw the needle 2-3 mm and wait for pain to subside before resuming

HAND AND WRIST BLOCKS

Digital Nerve Block

• Hand prone (palm down)
• Insert needle on the dorsal surface of the proximal phalanx
• Advance toward the volar surface, tangential to the phalanx
• Aspirate, deposit 1 mL at the volar corner, withdraw injecting another 1 mL back to skin
• Redirect needle across the dorsum of the digit, inject 1 mL band subcutaneously
• Repeat on the opposite side of the digit

Fig. 36-3: Injection sequence for complete digital nerve block

Note: Lidocaine 1% with epinephrine provides less injection pain than bupivacaine 0.5%, though duration is approximately half as long. Metacarpal block (at metacarpal heads) is an alternative particularly useful for long and ring fingers.

Median Nerve Block at the Wrist

Ulnar Nerve Block at the Wrist

Radial Nerve Block at the Wrist

LOWER EXTREMITY BLOCKS

Femoral Nerve Block

• Patient supine; pillow under hip for obese patients
• Identify femoral artery by palpation
• Insert needle 1 cm lateral to the artery, just below the inguinal ligament
• Aspirate, inject 20-30 mL of LA with a fascial "pop" or under US guidance
• With US: deposit LA in a "donut" pattern around the nerve under direct visualization

Fascia Iliaca Block

• Draw a line from ASIS to pubic tubercle, divide into thirds
• Injection site: 1 cm below the junction of the lateral and middle thirds
• Advance needle through subcutaneous tissue and two fascial "pops" (fascia lata, then fascia iliaca)
• Inject 40 mL of LA with fan-like spread to fill the fascial compartment
• US guidance confirms the correct fascial plane (LA seen spreading beneath fascia iliaca)

FOOT AND ANKLE BLOCKS

Fig. 36-13: Five-nerve ankle block technique from three views

Posterior Tibial Nerve Block

• Most important nerve for plantar foot anesthesia
• Inject 5-7 mL just posterior to the posterior tibial artery at the level of the medial malleolus
• US guidance recommended to visualize artery and adjacent nerve

FACIAL NERVE BLOCKS

Fig. 36-14: Facial nerve distribution for targeted blocks

Supraorbital and Supratrochlear Nerve Block (V1)

• Supraorbital nerve exits the supraorbital foramen - in line with the pupil, above the superior orbital rim
• Supratrochlear nerve exits 5-10 mm medial to the supraorbital foramen

Infraorbital Nerve Block (V2)

• Apply topical anesthetic to mucosa above the maxillary canine
• Dry and retract the upper lip
• Insert needle at the gingival reflection above the canine, advance superiorly halfway to the orbital rim
• Inject 3-5 mL

Mental Nerve Block (V3)

• Apply topical anesthetic to the mucosa below the canines
• Evert the lower lip
• Insert needle at the gingival reflection, advance inferiorly approximately 1 cm
• Inject 3-5 mL

THORACIC BLOCKS

Intercostal Nerve Block

• Palpate inferior border of the rib
• Retract skin cephalad at the rib angle
• Insert needle bevel-up, angled 10-15 degrees cephalad
• Walk needle off the inferior rib edge into the subcostal groove (~3 mm advance)
• Aspirate carefully (for blood and air)
• Inject 2-5 mL per level

Agent Selection for Regional Blocks

• Long-acting agents are preferred when prolonged post-procedure analgesia is desired, or when the provider may be interrupted during a long procedure
• Adding epinephrine prolongs duration and reduces systemic absorption but is contraindicated in digital and penile blocks (end-arterial territories)

Complications of Regional Blocks

Summary

1. Always document neurovascular status before the block
2. US guidance is preferred where available - improves success and safety
3. Aspirate before every injection to avoid intravascular deposition
4. Withdraw if intraneural pain occurs - do not inject into the nerve
5. Allow adequate onset time - lidocaine ~15 min, bupivacaine ~20-30 min
6. Match agent to clinical need: lidocaine for short procedures; bupivacaine/ropivacaine for prolonged analgesia
7. Topical anesthetic before block placement reduces procedure-associated pain