CRACKCast E194 – Pain Management

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This episode of CRACKCast covers Chapter 3 in Rosen’s Emergency Medicine (9th Ed.) – Pain Management. This is an essential skill to master and applies to any field of medicine. This podcast will give you a solid approach to the basics pain management to use on your next shift!

Shownotes – PDF HERE


Rosen’s in Perspective

Pain is something we deal with on a daily basis in the ED. This is something that we need to be really damn good at managing. As we mentioned above, acute pain is an emergent condition for the patient that requires rapid assessment and management. Tylenol, NSAIDS, and opioids for the basis for ED management of acute pain. Additionally, we have access to a whole armamentarium of local and topical anesthetics, and we need to be well-versed in their use. 


Core Questions:


[1] Define the following terms:

See table 3.2 in Rosen’s 9th Edition Chapter in Pain Management

  • Allodynia – pain from a stimulus that does not normally provoke pain
  • Amnesia/amnestic – an agent that suppresses the formation of memories
  • Local anesthesia – creates an area of insensibility to pain by injection of a local anesthetic agent
  • Analgesia – relief from pain
  • Hypnotic – agent that promotes the onset of sleep
  • Narcotic – term with legal implications describing opioid agents together with various central nervous system depressants drugs of abuse
  • Nociceptor – receptor that is sensitive and responsible for transmitting joint stimuli
  • Noxious stimulus – stimulus that is damaging or potentially damaging and results in sensation of pain
  • Opiate – naturally occurring derivative of opium alkaloid that binds opiate receptors and produces effects similar to those of endogenous endorphins
  • Opioid – naturally occurring or semisynthetic derivative of opium alkaloid (includes all opiates) that binds opiate receptors and produces effects similar to those of endogenous endorphins
  • Pain – unpleasant sensory and emotion experience arising from actual or potential tissue damage or described in terms of such damage
  • Procedural Sedation – pharmacologic induction of a state of sedation or dissociation with amnesia for pain control during a painful procedure
  • Sedative – agent that decreases a patient’s level of awareness

[2] Describe a practical approach to stepwise management of acute pain in the ED.

This is pretty straightforward for most patients.

  • For Mild/Moderate Pain:
    • Tylenol and NSAIDS (providing there are no contraindications) are reasonable first steps. If this is not sufficient, consider addition of PO opiates.
  • For Severe Pain – parenteral opioids are the mainstay of treatment.
    • There are specific situations where adjuncts or regional anesthesia may be appropriate for you patient (e.g. – ?fascia iliac block in hip fracture)

For discharging patients with acutely painful conditions (e.g. burn or fracture), consider scheduled Tylenol and Advil q6h with a short supply (3-5 days) of opioids for breakthrough pain.

This obviously does not apply across the board:

  • NSAIDS – caution or avoid in elderly or hx gastritis, renal insufficiency, GI bleeds, etc.
  • Acute on chronic pain – be aware that some patients may become opioid tolerant and may be on multiple additional agents.
  • Methadone – be aware of non-linear morphine equivalence with higher doses
  • Suboxone – stronger affinity for mu opioid receptors means that conventional opioids will likely have little to no effect (this is why it’s useful for treating opioid abuse, but poses interesting issues if a suboxone patient comes in to the ED with an acutely painful condition)

[3] Describe the adult parenteral and oral doses for:

    • Morphine.
      1. Rosen’s – IV 0.1mg/kg PO 0.5 mg/kg
      2. I go a bit lower and titrate. IV 2.5 -5 mg. PO 5 -10 mg. Q4h typically.
      3. Duration 3-4h.
      4. Issues – histamine release and preload, accumulation of metabolites in renal insufficiency
    • Hydromorphone
      1. Rosen’s – 0.015 mg/kg IV and 0.075mg/kg PO.
      2. Again, a bit lower than this and titrate up. IV – 0.5-1mg (0.25mg if elderly or at risk). 2-4mg PO.
      3. Morphine equivalence: 5:1
      4. Duration 2-4h.
    • Fentanyl
      1. Rosens: 1.5µg/kg IV and 3 µg/kg PO
      2. Practically – I just use IV 50-100 mcg and titrate
      3. Synthetic opioid, highly lipophilic, Shorter acting – duration 30 – 60 minutes.
    • Aside – See box 3.5 in Rosen’s 9th Edition Chapter in Pain Management
      1. Disadvantage of Intramuscular Opioid Administration
        1. Pain on injection
        2. Delayed onset of action
        3. Inability to predict therapeutic effect
        4. Inability to titrate dosage
        5. Diurnal variation in level achieved
        6. Disease state may affect level achieved
        7. Level dependent on intramuscular injection site

If you prescribe an opiate in the ED, leave an antiemetic order + stool softener as needed (inpatients or outpatient Rx).

[4] Differentiate between opioid side effects and opioid toxicity.

Opioid Toxidrome – we all know this. Respiratory Depression, Depressed LOC, Miosis; below are additional findings from UpToDate.

  • Vital Signs:
    • Heart rate decreased or increased
    • Blood pressure decrease or unchanged
    • Respiratory rate decreased
    • Temperature decreased or unchanged
  • Gastrointestinal:
    • Decreased bowel sounds
  • Neurological:
    • Sedation or coma
    • Seizure (Meperidine, propoxyphene, tramadol, or as a result of hypoxia)

Vs. Side effects (multiple)

New: risk factor for invasive pneumococcal disease and other infections

  • Opioid Analgesic Use and Risk for Invasive Pneumococcal Disease: A Nested Case-Control Study – Wiese et al.
    • Constipation (reduced peristalsis and longer transit times)
    • Sedation (typically with dose escalation or initiation)
    • Nausea and vomiting
    • Myoclonus (often associated with opiate mediated neurotoxicity and sedation)
    • Neuroendocrine effects – adrenal suppression and hypogonadism
    • Sleep disordered breathing
    • Pruritis
    • Rare – true opioid allergy
    • Urinary retention due to peripheral effect on nerves that innervate bladder and regulate tone
    • Weight gain
    • Hyperalgesia

[5] How do you manage opioid toxicity?

  • Prevention is key – know your safe doses (and then cut them in half if you’ve got an at risk patient – elderly or frail especially)!
  • Recognition (we’ve talked about this) – triad of respiratory depression, coma, miosis
  • ABC’s plus naloxone!
  • IV, IM, SubQ: Initial: 0.4 to 2 mg; may need to repeat doses every 2 to 3 minutes. A lower initial dose (0.1 to 0.2 mg) should be considered for patients with opioid dependence to avoid acute withdrawal or if there are concerns regarding concurrent stimulant overdose (Mokhlesi 2003). After reversal, may need to re-administer dose(s) at a later interval (ie, 20 to 60 minutes) depending on type/duration of opioid. If no response is observed after 10 mg total, consider other causes of respiratory depression. Note: May be given endotracheally (off-label route) as 2 to 2.5 times the initial IV dose (ie, 0.8 to 5 mg) (AHA [Neumar 2010]).

[6] Describe relative safety profiles, interactions, and at risk populations for NSAIDS.

See box 3.6 in Rosen’s 9th Edition Chapter in Pain Management

NSAIDRelative Risk of Serious GI Toxicity
COX2 Inhibitor0.6
Proton Pump Inhibitor0.09
  • Patients at Risk for Adverse Events During Nonsteroidal Anti-Inflammatory Drug (NSAID) Therapy
    • Patients with dehydration, hypovolemia or who have impaired renal function are at increased risk for decreasing renal function or renal failure
    • Patients with liver disease or CHF – in particular, those who already taking ACEi, ARBs, or diuretics – in who liver or heart conditions may worsen
    • Older patients are at enhanced risk for GI and renal events
    • Patients with asthma and known aspirin hypersensitivity are increased risk of bronchospasm
    • Women in the third trimester of pregnancy – NSAIDs may prolong gestation or prematurely close the ductus arteriosus
    • Patients who use tobacco or ethanol with a history of gastritis or peptic ulcer disease are at increased risk for peptic ulcer or GI bleed


  • OAC’s – add to anticoagulant properties of warfarin, displace protein bound warfarin.
  • ACEI – may impair renal function and impair antihypertensive effects of ACEI’s
  • Diuretics – increased risk of renal failure as NSAIDS decrease renal blood flow
  • Glucocorticoids – increased risk of peptic ulcer disease
  • Lithium – NSAIDS enhance lithium reabsorption and reduce excretion, leading to increased lithium levels.

No NSAID is more effective as an analgesic than ibuprofen, 400 mg, including ibuprofen, 600 and 800 mg.

[7] List the classes of local anesthetics. How do they work?

  • Esters and Amides – Local anesthetics work by reversibly blocking sodium channels in the nerve cell membrane which prevents the generation of action potentials
    • Amides – Lidocaine, bupivicaine, and co. Hepatic metabolism
    • Esters – Cocaine, procaine, tetracaine and others. metabolized by plasma cholinesterase

[8] List the toxic doses for each local anesthetic

  • Lidocaine – 3-5mg/kg
  • Lidocaine with Epi – 5-7mg/kg
  • Bupivicaine – 1.5 mg/kg
  • Bupivicaine with Epi – 3mg/kg

These are approximate guides – some patients could become toxic below the threshold and some may receive doses in excess of the thresholds and be fine.

Say we have a 70kg adult and we want to figure out the max amount of 1% lidocaine we can safely give.

Step 1 – Find max dose. 70kg x 5mg/kg = 350 mg

Step 2a – Find amount of lidocaine to use. 1% Lidocaine = 10mg/mL

Step 2b – 350mg x 1mL/10mg = 35mL of 1% Lidocaine

[9] List 5 techniques to reduce pain of injection of local anesthetic

See box 3.6 in Rosen’s 9th Edition Chapter in Pain Management

  • Techniques to Reduce the Pain of Injection
    • Buffering of local anesthetic agents
    • Counterirritation
    • Slow rate of injection
    • Use of topical anesthetics
    • Warming of solution
    • Distraction techniques

How to make a buffered solution according to Rosen’s: take a standard solution of bicarb (8.4% in 50mL) and add to a syringe containing lidocaine in a ratio of 1:10.

[10] List agents that can be used for topical anesthesia of:

  • Intact skin
    • EMLA – eutectic mixture of local anesthetics. Mixture of lidocaine and prilocaine in an alkaline oil mix which allows diffusion through intact skin.
    • Ethyl chloride and fluoromethane sprays
  • Mucous membrane
    • Potent vasoconstrictor along with anesthetic activity. Generally, avoid doses >200mg and avoid in patients with known CAD (we know all about that vasospasm)
    • Lidocaine (gel and spray formats). Applications to nasal procedures, Foley catheter placements, temporization for awake intubation, etc.
    • Tetracaine – cornea
    • Benzocaine – oral procedures. Almost insoluble in water and remains on mucous membranes in the mouth.
  • Open skin/lacerations
    • LET (lidocaine, epinephrine, tetracaine). Can apply to open wound and let it sit for 10-20 minutes to achieve superficial anesthesia. Note – tetracaine toxicity from application to mucous membranes (eye, nose) has been documented so avoid this.



[1] What agents can be used as a substitute in cases of anaphylaxis to local anesthetic?

  • Very rare. Often the offending agent is the preservative used. In this case, you could substitute an agent from a different class – the preservatives don’t typically cross- react.
  • However – if the patient has a true anaphylactic allergy to all ‘caine anesthetics – you can locally inject diphenhydramine (dilute 1 mL of a 50mg/mL ampoule with 5 or 10 mL of saline to make a 1% – 0.5% solution)

[2] Why should you avoid use of the following agents:

  • Tramadol
    • Tramadol is a dirty drug! By this I mean it acts on multiple receptors. Weak mu agonist with some effects on serotonin and norepi. Unpredictable kinetics due to individual variations in CYP2D6 which produces active metabolite ODT. Also lowers seizure threshold, can precipitate serotonin syndrome in conjunction with other serotonergic drugs, and can precipitate hypoglycemia.
  • Demerol
    • Rosen’s – “No indication for use in the ED.” metabolized by cytochrome P450 to normeperidine which can cause CNS toxicity at therapeutic doses.
    • Half-life is 12-16h, and blocks muscarinic receptors, which can result in anticholinergic effects like agitation, delirium, etc.
    • Can precipitate seizures. Can precipitate serotonin syndrome in conjunction with SSRIs, SNRIs, or MAOIs

[3] How does local anesthetic toxicity present?

Local toxicity vs. systemic toxicity.

  • Local toxicity – Theoretical risk of the reduction in blood flow to end organs (classic teaching of finger, nose, penis, toes don’t get epi). However, this has not really been borne out by the evidence. For example, it is safe to use epinephrine for ring blocks.
  • Systemic Toxicity – Has a typical progression of symptoms. Circumoral paresthesias, dysarthria, tinnitus, decreased LOC/confusion, seizures, coma, and cardiac arrest.


  • ABCs
  • Manage seizures with Benzos
  • ACLS as needed
  • The main antidote is intralipid – theoretically extracts lipid soluble molecules from cardiac tissues.

This post was uploaded and copyedited by Anson Dinh (@AnsonDinh)

Owen Scheirer

Owen is a resident in the FRCPC Emergency Medicine program at the University of Saskatchewan. When he's not running around the emergency department, he's hanging out with his wife, new baby girl, and dog. Spare time = climbing and cycling!

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Dillan Radomske

Dillan Radomske is an Emergency Medicine resident at the University of Saskatchewan. He is passionate about technology-enhanced medical education, podcast creation and production, and Indigenous advocacy. He is one of the new CRACKCast hosts, and aspires to continue to contribute to the field of FOAMed in the future.

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