Delayed Sequence Intubation

This case and pearls are provided by Dr. Samia Farooqi. Thank you so much for the excellent case! Edited by Michael Macias. 

A middle aged female with a history of cirrhosis complicated by hepato-pulmonary syndrome and severe diastolic dysfunction presented to the ED in acute respiratory distress. The patient was brought in by medics with an initial O2 saturation at a concerning level of 78%. She appeared panicked and tachypneic. She was immediately placed on a non-rebreather face mask for temporizing measure as respiratory therapy was paged for stat Bipap. However as her O2 saturation continued to remain low, she became progressively more agitated and anxious.

Once Bipap was placed, this too appeared to only be a temporizing measure as the patient continued to intermittently tear off the face mask leading to desaturations into the 70s. Amongst all the hullaballoo, a portable CXR was obtained which revealed profound pulmonary edema: 


It was clear that this patient would require intubation however there was significant concern for rapid desaturation during RSI. A decision was made to administer 1mg/kg IV ketamine while the patient remained on Bipap to assist with oxygenation. Following administration, the patient became quite compliant with her NIPPV, allowing her O2 saturation to climb back up to a safe 96-98%. After a few minutes of continued oxygenation, the patient was properly positioned (ear-sternal notch), paralyzed with succinylcholine and successfully intubated on first pass without desaturation. 

This case is a perfect example of delayed sequence intubation, which Scott Weingart refers to as “procedural sedation for pre-oxygenation.”  In the difficult-to-oxygenate patient who is anxious and/or delirious, this may be your best option to create a period of safe apnea during intubation.  In his 2011 Journal of Emergency Medicine paper titled 'Preoxygenation, Reoxygenation, and Delayed Sequence Intubation in the Emergency Department', he breaks down DSI into four steps:

1. Administer 1-1.5mg/kg IV ketamine by slow IV push.

2. Once the patient is calm/dissociated, apply NRB or NIPPV.

3. Once 100% O2 sat is achieved, allow the patient to breathe high FiO2 oxygen for an additional 2-3 minutes to allow for adequate alveolar de-nitrogenation.

4. Administer a paralytic and intubate the patient, with a nasal cannula  set @15L/min in place during the entire apneic period. 

Weingart notes that often when patients are sedated with ketamine and become compliant with oxygenation, they often have such drastic improvements in respiratory parameters that intubation can be avoided completely. 

Just remember that RSI isn't for everyone and when you can't adequately oxygenate a patient prior to intubation secondary to agitation/delirium, consider 'procedural sedation for oxygenation' and delayed sequence intubation as an alternative option. Increase your safe apnea time with pre-oxygenation and shoot for no desaturation! We know that when @^#@ hits the fan we have a decline in our cognitive abilities as well as motor skills and this is where errors will occur. So prevent this potentially deadly situation and pre-oxygenate like a champion (To understand more on our response to stress and potential for cognitive deterioration, listen to this excellent podcast regarding lessons from combat).

If you are at all interested in DSI, Weingart’s paper is an easy must-read: 

Original Article

Original Article

More information on topics related to this clinical case:


Weingart, S. (2011). Preoxygenation, Reoxygenation, and Delayed Sequence Intubation in the Emergency Department. Journal of Emergency Medicine, 40 (6): 661-667.

Ethical dilemmas in Emergency Medicine 4: The ethics of triage

St Emlyns - Meducation in Virchester #FOAMed

It’s been a while since we published our last ‘Ethical Dilemmas’ post at St. Emlyn’s. Hopefully you’ve already seen the other posts in this series but, if not, you should check out part 1, part 2 and part 3. This time let’s take a look at triage – something we do every day in the […]

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The 25 Most Followed #FOAMed Women on Twitter

TwitterEKGWe recently published a list of the 30 Most Followed #FOAMed Twitter Users (FOAM = Free Open Access Meducation). One observation, keenly pointed out by Dr. Nikita Joshi (@njoshi8), was the lack of female representation on the list. Even more recently, Dr. Esther Choo (@choo_ek) published a blog post entitled Women in Emergency Medicine Who Give Great Talks. As a follow up to our original post, here are the most ‘followed’ women on Twitter in the FOAM world.

We are particularly interested in understanding the landscape such as who is involved, geographic locations, areas of expertise, and association with blogs/podcasts. Our search strategy was simple:

  1. Twitter was searched for all users with #FOAMed, #FOAMcc, #FOAMtox, #FOAMped, #FOAMems, #FOAM4GP, and/or #FOAM in her Twitter profile. *
  2. This was cross-referenced with Dr. Mike Cadogan’s (@sandnsurfFOAMed Twitter list (920 members as of August 29, 2014).

Most Followed FOAM Women on Twitter **

Twitter Name
Twitter Handle
Location ***
Joined Twitter
1Michelle Lin@M_LinSan Francisco, USA7,428Apr 2009
2Michelle Johnston@EleytheriusPerth3,751Feb 2010
3Pam Nelmes@Pam007NelmesCornwall, UK3,695Sep 2010
4ER doc@ER_doc3,059Jun 2008
5Natalie May@_NMayManchester, United Kingdom2,751Jul 2012
6Heidi Allen@dreamingspiresSydney, Australia2,391Oct 2008
7Deirdre Bonnycastle@BonnycastleSaskatoon, Sask, Canada2,309Oct 2008
8Natalie Lafferty@nlaffertyDundee, UK2,247Mar 2008
9Lauren Westafer@lwestaferNew England, United States2,037Apr 2012
10K Dillon, RDMS, CPC@comalliwritesBay Area1,742Nov 2009
11Teresa Chan@TChanMDCanada (Hamilton, ON)1,653Jun 2009
12Laleh Gharahbaghian@SonoSpotSan Francisco/Stanford1,520May 2012
13Esther Choo MD MPH@choo_ek1,515Jan 2012
14Tessa Davis@TessaRDavisSydney1,491Oct 2011
15Nikita Joshi@njoshi8California1,332Dec 2012
16Annalisa Manca@AnnalisaMancaDundee, Scotland1,268Feb 2009
17Penny Wilson@nomadicgpWestern Australia1,194Mar 2012
18Petra Dolman@petradMDPrince George, BC, Canada1,011May 2013
19Eve Purdy@purdy_eve931Jul 2012
20Shannon O. McNamara@ShannonOMacNew York, NY899Jun 2009
21Melanie Clothier@drmelclothierRural South Australia835Nov 2011
22Jordana Haber@JoJoHaberBrooklyn, NY787Mar 2012
23Cathi Mon@cathimonSouth Australia710Aug 2011
24Victoria Stephen@EMcardiacJohannesburg, South Africa704Nov 2012
25Shweta Gidwani@Global_EMLondon691Feb 2009

* Those without one of the FOAM hashtags in her Twitter profile are not included on this list, even if they produce excellent, free content such as Victoria Brazil (@SocraticEM), Megan Ranney, MD MPH (@meganranney), and Ash Witt (@ash_witt).

** Information current as of August 29, 2014.

*** Locations were taken directly from Twitter profiles.


Certainly, the metric of Twitter followers does not necessarily correlate with quality, and it misses newcomers to the FOAM scene and those with a more focused area of expertise/interest.


  • There is worldwide representation from Australia, Canada, the UK, South Africa, the USA, and more.
  • A variety of healthcare professional representation including emergency physicians, nurses, and general practitioners.
  • Subspecialties within Emergency Medicine are also well represented including pediatrics, public health, medical education, simulation, and ultrasound.

It’s amazing to be part of such a great FOAM community with its breadth of expertise and diversity.

Future Direction

Others have noted the lack of gender diversity in the community and have sought solutions. Dr. Petra Dolman (@petradMD) recently launched a new twitter account (@feMedchat) and hashtag (#feMed) dedicated to discussing issues relevant to women in medicine with regular twitter chats, article discussion, and potential mentoring opportunities. This is sure to become an area to follow for future growth and opportunity.

Author information

Bryan D. Hayes, PharmD, FAACT

Bryan D. Hayes, PharmD, FAACT

ALiEM Associate Editor

Clinical Assistant Professor, University of Maryland (UM)

Clinical Pharmacy Specialist, EM and Toxicology

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Bubbles in the Wilderness

There have been many discussions and debates about the role of FOAM (free open-access meducation) in medical education, the pros, the cons and whether or not it really is useful.

It may not be for everyone, yet for some individuals – especially those who are remote or isolated – FOAM has transformed how they learn, engage and enjoy medicine. A great example of this — one the RAGE team recommends you read — is Natasha Pirie-Burley’s account, Bubbles in the Wilderness: All about FOAM, published on the Adventure Medic blog.

“In 2007 I struggled to find my passion or heroes within my workplace. I listened to closed minds and wondered why everyone was, “just getting through it”. It was un-inspiring and at times depressing. I resigned from my job in the UK and headed to the wilderness of America, New Zealand, Nepal, and Australia. I was searching for heroes and inspiration relevant to my life. Then last year, by chance, I found that Mawson’s bravery, Shackleton’s leadership, Dean Potter’s composure and the family Robinson’s ingenuity were right here at my fingertips and living in these medical pioneers of FOAM.”
— excerpt from Bubbles in the Wilderness: All about FOAM by Natasha Pirie-Burley

Vive la FOAM!

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Treating digoxin toxicity: is less more?

Digifab3 out of 5 stars

Digoxin-specific antibody fragments in the treatment of digoxin toxicity. Chan BSH, Buckley NA. Clin Toxicol 2014 Aug 4 [Epub ahead of print]


This long detailed paper seems to be a manifesto masquerading as a review article. It is quite informative and well worth reading. But I’d keep in mind that the authors appear to have a (not so) hidden agenda: to decrease the dose of digoxin-specific antibody fragments administered in most cases of acute and chronic digoxin toxicity.

The authors state their objective up front:

To review the pharmacology, efficacy, effectiveness, indications, safety and dosage of digoxin-Fab. On the basis of the reviewed data. to propose a regimen of administering digoxin-fab to patients with digoxin poisoning based on pharmacokinetic principles.

Although they identified 140 relevant citations, they are not clear on exactly how these were selected. (Their reference list contains only 69 papers.) They note that there have been no randomized clinical trials on digoxin toxicity.

The authors say this about indications for using digoxin-specific antibody fragments:

There is general agreement that digoxin-Fab is indicated in patients with life-threatening tachy-bradyarrhythmias, hyperkalaemia (> 6 mmol/L) or haemodynamic instability with concentrations (e.g. digoxin > 2 μg/L or > 2.6 nmol/L) that support digoxin may be a contributing cause.

They point out that in acute toxicity, dose calculations based on serum digoxin levels taken before distribution is complete (approximately 6 hours) may overestimate the amount of digoxin-Fab required. They argue that 2 vials of digoxin would likely neutralize all free digoxin in the central compartment in cases of acute overdose, with clinical benefit evident within 60 minutes. The dose could be repeated if there were no clinical response.

Chronic toxicity usually involves a much lower total body load than in cases of acute ingestion, and lower doses of digoxin-Fab are generally recommended. Therefore:

. . . we recommend giving 1 vial (40 mg) at a time and observe for clinical response. If none is observed after 60 min, a second ampoule of digoxin-Fab may be administered, to neutralize digoxin re-distributing from the peripheral compartment.

The authors may very well be correct that much lower doses of digoxin-Fab than those generally used may suffice. However, I think there are a number of weaknesses in their argument and would be reluctant to adopt their suggestions at this time. With regard to acute toxicity, it would be hard to titrate the need for additional doses of digoxin-Fab, since clinical effect will not be evident for 30 minutes to an hour. When treating actual or potentially life-threatening toxicity, it seems to me risky to delay getting a reliably sufficient dose of antidote on board as soon as possible. Although the authors’ suggestions are based on pharmacokinetic modeling, there are not enough clinical data available to indicate whether their 2-vials-and-observe” protocol would be safe and effective.

I’m even more doubtful about their recommendation for treating chronic poisoning  If the indication is life-threatening toxicity, giving a single vial and then observing for an hour seems foolish. The one advantage to this is to save on the cost of digoxin-Fab. (The current price of a vial of Digibind is $728 USD.) since with chronic toxicity relatively few vials of digoxin-Fab are required in most cases, this protocol would not produce significant savings.

Of course, in treating stable patients without signs of immediate life-threatening manifestations of digoxin poisoning, the incremental start-low-and-titrate-to-response method may work just fine. Unfortunately, this paper in my opinion does not distinguishing adequately between truly life-threatening cases and those that are less dire. It is, however, dense with good information and definitely worth a look. II found it  extremely helpful to think through the authors’ recommendations and see if they made sense.






It has recently been suggested that the therapeutic blood level of digoxin be reduced from 0.8-2.0 μg/L to 0.5-0.8 μg/L in patients with congestive heart failure. (Contrary to the authors’ implication, I do not believe that this suggestion has been universally accepted.)


Pharmacologic Intervention for Prevention of Post-traumatic Stress Disorder After Trauma

In the ED we often provide first line care for patients as the result of traumatic events.  Beyond attending to clinically apparent injuries, pain, and distress, we would be in a position to apply prophylactic treatment to attempt to prevent PTSD, a debilitating sequela of trauma, if such treatment were to exist and founded in good science.

Does such pharmacologic treatment exist?

Note: Cognitive behavioral therapy after trauma has been shown to attenuate development of PTSD and associated symptoms.

Below lie many oversimplifications and likely misinterpretations of clinical psychology, neuroscience, and PTSD.  Proceed with caution.



Results from an exposure to traumatic event; with subsequent re-experience, avoidance and hyperarousal phenomena that cause clinical distress and impact daily functioning.

Lifetime incidence 10% in men, 5% in women.



There are many factors related to the development of PTSD, including patient characteristics, history, social support system, and type of trauma, but these are not predictive.  Multiple mechanisms are proposed to describe the development of PTSD; including cognitive attribution (how people perceive and make sense of the causes of the event, and their subsequent cognitive and behavioral responses to this interpretation), negative memory re-consolidation (patient repetitively accessing and dysfunctionally emboldening traumatic memories), and various models of neuroendocrine, neurosignalling, and other neurobiological dysfunction.


Pharmacologic Targets:

1)      Hypothalamic-pituitary-adrenal axis.

Disturbance of cortical secretion in the HPA axis studied in septic shock, and subsequent placebo controlled trials studies in septic shock survivors suggest that administration of hydrocortisone was protective against development of PTSD.  The prevailing theory is that stress doses of steroids decreases the extreme sympathetic tone of and response to shock, as well as the need for exogenous vasopressors, which decreases the overall hyperadrenergic milieu in which memories of critical illness are encoded.

2)      The amygdala, which is involved in fear, mood, and memories, contains beta adrenergic receptors that are activated by norepinephrine in stress response, and likely is involved in the initial neurobiological/psychological adaptation to a traumatic experience that subsequently becomes maladaptive.  Administration of betablocker propranolol is theorized and somewhat demonstrated to reduce development of PTSD, vividness of intrusive memory recall, and arousal symptoms.  This mechanism seems related to the above cortical dysfunction model.



A Cochrane review in 2014 was performed to investigate pharmacologic prevention of PTSD after trauma.  Generally, primary outcomes were the incidence of PTSD in at 3 months using standardized scales or interviews.  Secondary outcomes were degree of symptomatology, scales of depression, anxiety, functional impairment, and medication side effects.

The studies included participants recruited in Emergency departments, trauma centers, ICUs, surgical inpatient services, and mental health facilities.

Study protocols for hydrocortisone included single dose, such as 100mg IV bolus 1 – 5 hours after the exposure, a 3 day IV taper in post-cardiac surgery patients, bolus and continuous infusion in septic patients, or 40mg PO in a 16 day taper.

Protocols for propranolol generally used 10 to 14 days of 40mg PO QID.



9 trials randomized, placebo controlled trials

345 patients total.



4 trials studied hydrocortisone:

165 patients.

The review demonstrated a significant “moderate” effect in preventing PTSD (RR: 0.17 [95% CI 0.05 to 0.56] p=0.004).



3 trials

118 patients

RR 0.62 (95% CI 0.24-1.59) p=0.32


Cochrane conclusion:

“There is moderate quality evidence of hydrocortisone for the prevention of PTSD development in adults.  No evidence to support efficacy of propranolol, escitalopram, temazepam, and gabapentin in preventing PTSD onset. “   Further, the review authors do not believe there is sufficient evidence to recommend a medication as therapy at this point.


My conclusion:

An important, interesting, and complicated subject, with current data suggesting that hydrocortisone (after further trials) has potential as prophylactic therapy after trauma to prevent PTSD.







Amos T, Stein DJ, Ipser JC. Pharmacological interventions for preventing post-traumatic stress disorder (PTSD). Cochrane Database Syst Rev. 2014 Jul 8;7


Kar N. Cognitive behavioral therapy for the treatment of post-traumatic stress disorder: a review. Neuropsychiatr Dis Treat. 2011;7:167-81.


Kessler RC, Sonnega A, Bromet E, Hughes M, Nelson CB. Posttraumatic stress disorder in the National Comorbidity Survey. Archives of General Psychiatry 1995;52(12):1048–60


Pitman RK, Sanders KM, Zusman RM, Healy AR, Cheema F, Lasko NB, et al.Pilot study of secondary prevention of posttraumatic stress disorder with propranolol. Biological Psychiatry 2002;51:189–92.


Schelling G, Briegal J, Roozendaal B, Stoll C, Rothenhausler H-B, Kapfhammer HP. The effect of stress doses of hydrocortisone during septic shock on post traumatic stress disorder in survivors. Biological Psychiatry 2001;50:978–85.