Topics in this EM Quick Hits podcast

Anand Swaminathan on update on the appropriate selection of induction agents (1:10)

Hans Rosenberg on when to use gabapentinoids for pain control in the ED (8:47)

Katie Lin on clinical pearls for neuroprotective intubation (14:35)

Nour Khatib and Hamza Jalal on a simple approach to paresthesias in the ED (23:15)

Eric Wortmann on preventing burnout in emergency medicine (40:10)

Podcast production, editing and sound design by Anton Helman

Written summary & blog post by Shaila Gunn, edited by Anton Helman

Cite this podcast as: Helman, A. Swaminathan, A. Rosenberg, H. Lin, K. Khatib, N. Jalal, H. Wortmann, E.  EM Quick Hits 55 – Induction Agents, Gabapentinoids for Pain Control, Neuroprotective Intubation, Approach to Paresthesias. Emergency Medicine Cases. February, 2024. Accessed July 21, 2024.

An update on induction agents for RSI

The primary medication choices for RSI induction are etomidate, ketamine, and propofol.

Etomidate: traditionally, the “workhorse”

  • Hemodynamics: No vasodilatory properties therefore hemodynamically stable
  • Pharmacokinetics: Fast onset (1 minute) and short duration (3-5 minutes)
  • Other benefits: There are few contraindications
  • Risks:
    • Adrenal suppression (though this is transient and has not been shown to change patient outcomes)
    • Emerging evidence suggests that etomidate may increase mortality [1]

Ketamine: a good replacement for etomidate

  • Hemodynamics: Increases the release of endogenous catecholamines. This may increase blood pressure. It may not increase blood pressure in those who are catecholamine deplete (i.e. severe septic shock) and should not be relied upon to increase blood pressure. It can also lower blood pressure by depleting catecholamines. This is not thought to be dose dependent so a reduced dose is unlikely to protect hemodynamics.
  • Pharmacokinetics: Fast onset (30-50 s) and longer duration (30-45 minutes)
  • Other benefits:
    • Has analgesic properties
    • Can be used in head trauma and hypertension and may even be neuroprotective
    • Longer duration of action makes it a good choice in patients who are receiving a longer acting paralytic
  • Best use: for the shocky patient


  • Hemodynamics: Causes vasodilation and cardiac depression which intrinsically drops blood pressure in a dose dependent fashion
  • Pharmacokinetics: Fast onset (15-30 s) and short duration (5-10 minutes)
  • Other benefits:
    • Decreases blood pressure making it useful in hypertensive emergencies
    • Has anti-epileptic properties making it useful for post-stroke, ICH, status epilepticus, or alcohol withdrawal patients
  • Risks: Because it drops blood pressure, it is important to reduce the dose in critically ill and hypotensive patients; either slowly administer until you reach the desires dissociative effect or use 10-20% of usual dose (~10-15 mg total)
  • Best uses: In patients at risk for seizure, hypertensive patients, and for post-intubation sedation

=> Key points:

  • Emerging evidence that etomidate may increase mortality
  • Dose reductions for etomidate and ketamine are unlikely to reduce the risk of hypotension post-RSI but, reduced dose may increase awareness of paralysis
  • Propofol dose should be reduced in shocky patients or avoided completely; good in choice in hypertensive stroke, ICH, status epilepticus, alcohol withdrawal patients

emcases-updateUpdate 2024: A Bayesian meta-analysis including 7 randomized trials and one propensity matched study totalling 2978 patients found an 83.2% probability that ketamine lowers mortality compared to etomidate in critically ill adults requiring tracheal intubation. Abstract

  1. Kotani Y et al. Etomidate as an induction agent for endotracheal intubation in critically ill patients: a meta-analysis of randomized trials. J Crit Care 2023; 77.
  2. Driver BE et al. Sedative dose for rapid sequence intubation and post intubation hypotension. Is there an association? Ann Emerg Med 2023.

When to use gabapentinoids for pain control in the ED

Back in Episode 126 Drugs that Work and Drugs That Don’t – Part 1: Analgesics the bottom line for use of gabapentinoids in the ED:

  • They are not recommended for routine use in patients with low back pain
  • They should be reserved for patients with post-herpetic neuralgic and diabetic nephropathy; they should be used at the lowest dose and stopped on day 3 if there is no effect.
  • There is an associated risk of suicidal behaviour, unintentional injuries, traumatic injuries, and road traffic incidents and offences (pregabalin > gabapentin.)

Mechanism of action: not directly on GABA. Instead, they inhibit calcium influx into glutaminergic neurons in the CNS modulating pain.

The 2 most commonly used gabapentinoids are gabapentin and pregabalin

  • Gabapentin has a lower bioavailability, less predictable pharmacokinetics and requires a longer titration duration to reach an effective dose.
    • Effective dose reached in ~ 14 days.
  • Pregabalin
    • Effective dose reached in ~ 7 days.

The long titration period of these medications means they are unlikely to be effective for pain control in the ED.

When to consider prescribing gabapentinoids:

  1. Post-herpetic neuralgia
  2. Diabetic nephropathy
  3. Only in patients who have reliable follow-up for titration and/or discontinuation

Side effects and risks of gabapentinoids include dizziness, somnolence, gait disturbances, GI upset, peripheral edema, and blurred vision. The most serious side effect is respiratory depression, especially if using concurrent opioids or sedatives. They increase the risk of opioid-related death. They should be avoided in patients with CHF (increased peripheral edema and weight gain) and renal impairment (renal excretion).

Bottom line => Exercise caution when prescribing gabapentinoids in the ED. Consider only for patients with post-herpetic neuralgia and diabetic neuropathy. All patients need a good follow-up plan for titration and discontinuation.

  1. Enke O, New HA, New CH, et al. Anticonvulsants in the treatment of low back pain and lumbar radicular pain: a systematic review and meta-analysis. CMAJ. 2018;190(26):E786-E793. doi:10.1503/cmaj.171333
  2. Rowbotham M, Harden N, Stacey B, Bernstein P, Magnus-Miller L. Gabapentin for the treatment of postherpetic neuralgia: a randomized controlled trial. JAMA. 1998;280(21):1837-1842. doi:10.1001/jama.280.21.1837
  3. Wiffen PJ, McQuay HJ, Rees J, Moore RA. Gabapentin for acute and chronic pain. Cochrane Database of Systematic Reviews 2005, Issue 3. Art. No.: CD005452.
  4. Goodman CW, Brett AS. A clinical overview of off-label use of gabapentinoid drugs. JAMA Internal Medicine. Published on-line March 25, 2019.
  5. Wiffen PJ, McQuay HJ, Rees J, Moore RA. Gabapentin for acute and chronic pain. Cochrane Database of Systematic Reviews 2005, Issue 3. Art. No.: CD005452.Lundh A, Sismondo S, Lexchin J, et al. Industry sponsorship and research outcome. Cochrane Database of Systematic Reviews 2012, Issue 12. Art. No.: MR000033.

3 Pearls for neuroprotective intubation

Extra caution is required when intubating patients with neurocritical conditions.

  1. Consider airway management prior to imaging or transport.
    • These conditions can progress quickly; low threshold to intubate
    • Consider rapid airway control when: active vomiting, agitated, rapidly decreasing GCS, apneic spells
  2. Include a 10 second neuro exam pre-intubation if  possible.
    • 2 questions our stroke/neurosurgery/ICU colleagues want to know from us:
      1. Are they herniating or severely disabled?
        • Determines the urgency of intervention
      2. Is the brain still salvageable?
        • Determine if an intervention will make a difference in the outcome
    • 3 steps to the neuro exam:
      • Step 1:  GCS – What is the LOC and is it dropping?
      • Step 2:  Eyes – Are the pupils equal and reactive? Are they disconjugate or deviated? Are the corneal reflexes in tact?
      • Step 3: Lateralizing motor response: Purposeful movement equally bilaterally?  Is there asymmetry or posturing present?
  3. Keep it simple to avoid hypotension and hypoxia
    • Choose the tools and approach you are most experienced with; usually this will be an RSI
    • Here is an example approach:
      1. Preoxygenate with a non-rebreather over highflow nasal cannula
      2. Pretreat with an antiemetic if vomiting, fentanyl if hypertensive, and a vasopressor (norepinephrine or phenylephrine) if hypotensive
      3. Prepare equipment, yourself and team for A, B and C plans including a well-defined oxygenation threshold and designate someone to call this out; consider a target of 90%
      4. Position the patient with head of bed 15-30 degrees to mitigate ICP effect even if in spinal precautions
      5. Induce the patient – Ketamine 1.5 mg/kg ~100-150 mg
      6. Paralysis
        • Succinylcholine
          • Advantage: wears off quickly to resume neurologic monitoring
          • Caution: There may be a transient increase in ICP during the defasciculation phase but there is no evidence that this has any clinically significant effect of neurological outcome
        • Rocuronium advantages
          • Nondepolarizing so there is no theoretical increase in ICP
          • There are few contraindications
          • Keeps the patient imobile i.e. for imaging and transfer
      7. Post-intubation sedation
        • Propofol and fentanyl infusions if normo- or hypertensive
        • Ketamine if hypotensive
      8.  Neuroprotective ventilation targets
        • RR 16
        • TV 8 cc/kg
        • FIO2 100%
        • PEEP 5 mmHg
        • PaCO2 35-40
        • O2 sats >94%
      9. If time, some ‘nice to haves’:
        1. Fentanyl 3 mcg/kg (~200 mcg) 3 minutes prior to intubation if normo- or hypotensive.
        2. Lidocaine spray to the cords to prevent increased ICP with laryngeal stimulation.

Bottom line =>

  1. Consider rapid airway control prior to imaging or transport with a lower threshold if vomiting, agitation, dropping GCS, or dysregulated breathing with apneic spells
  2. Include a 10 second neuro exam if possible focusing on GCS, eyes, and lateralizing findings
  3. Keep your approach simple using tools you are familiar with; focus on avoidance of hypotension and hypoxia
  1. Kareemi H, Pratte M, English S, Hendin A. Initial Diagnosis and Management of Acutely Elevated Intracranial Pressure. J Intensive Care Med. 2023;38(7):643-650.
  2. Manley G, Knudson MM, Morabito D, Damron S, Erickson V, Pitts L. Hypotension, hypoxia, and head injury: frequency, duration, and consequences. Arch Surg. 2001;136(10):1118-1123.
  3. Kramer N, Lebowitz D, Walsh M, Ganti L. Rapid Sequence Intubation in Traumatic Brain-injured Adults. Cureus. 2018;10(4):e2530. Published 2018 Apr 25. doi:10.7759/cureus.2530
  4. Wang X. Neuroprotective effects and mechanisms of fentanyl preconditioning against brain ischemia. Crit Care. 2006;10(Suppl 1):P446. doi:10.1186/cc4793
  5. Kuzak N, Harrison DW, Zed PJ. Use of lidocaine and fentanyl premedication for neuroprotective rapid sequence intubation in the emergency department. CJEM. 2006;8(2):80-84. doi:10.1017/s1481803500013518
  6. Robba C, Poole D, McNett M, et al. Mechanical ventilation in patients with acute brain injury: recommendations of the European Society of Intensive Care Medicine consensus. Intensive Care Med. 2020;46(12):2397-2410. doi:10.1007/s00134-020-06283-0

An approach to paresthesias in the ED

Like most things in neurology, one of the goals in patients with paresthesias is to localize the lesion, which helps guide imaging choices in the ED. Here are some tips to help clarify the pattern of the paresthesias and to determine if they may have a peripheral or central nervous system source. Note: there are exceptions to the following ‘rules’.

Big 3 things to ask on history:

  1. Sensory symptoms: Positive symptoms (pins and needles/ants crawling/burning) are often the result of nerve irritation or hyperexcitation and often reflect a peripheral cause. Negative symptoms (numbness) reflect a “dead” nerve and often reflect a central cause. If multiple limbs are affected, think central if they are simultaneously affected, and peripheral if they come on at different times. 
  2. Pain: Pain usually results with peripheral etiologies; exceptions: central etiologies i.e. ALS and thalamic lesions can also be associated with pain
  3. Weakness: It is important to differentiate true weakness/no movement from incoordination

Also important to ask about timing and duration:

  • Timing: onset (abrupt vs gradual); a high yield question to ask is “when did you last feel completely normal?”
  • Duration: Is it episodic (and if so, what are the triggers/times or day)? Or continuous (and does it fluctuate)?

Physical exam

  • Weakness: To identify weakness you need to push hard.
  • Reflexes: Use a reflex hammer; if brisk/elevated, think CNS. If reduce, think PNS.
  • Sensation: best to use tissue paper to test light sensation
  • Have the patient reproduce their symptoms; ask them to assume the position that aggravates their symptoms.


  • Labs: consider TSH, electrolytes/extended electrolytes, B12, glucose and ferritin
  • Some considerations for ordering CT head in the ED for patients presenting with paresthesias:
    • More than 1 body part is involved
    • Significant lifestyle impact i.e. balance concerns
    • Constant sensory symptoms without pain
  • Consider outpatient EMG/NCS
  1. Herr K. Neuropathic pain: a guide to comprehensive assessment. Pain Manag Nurs. 2004;5(4 Suppl 1):9-18. doi:10.1016/j.pmn.2004.10.004
  2. Horlings CGC, Rath J, Finsterer J, Wanschitz JV, Löscher WN. Laboratory Tests for Neuropathies: What to do and to Avoid. J Neuromuscul Dis. 2020;7(3):279-286. doi:10.3233/JND-200488