Author Archives: Brian Ferguson

Building Resilience

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So with the topic of resiliency at the forefront of Emergency Medicine’s fight against burnout, experts are now recommending programs focus on resilience rather than wellness. This is taken from the American Psychological Association.  If you have thoughts about incorporating resiliency into our program or conference, please email me.

10 ways to build resilience:

  1. Make connections. Good relationships with close family members, friends or others are important. Accepting help and support from those who care about you and will listen to you strengthens resilience. Some people find that being active in civic groups, faith-based organizations, or other local groups provides social support and can help with reclaiming hope. Assisting others in their time of need also can benefit the helper.
  2. Avoid seeing crises as insurmountable problems. You can’t change the fact that highly stressful events happen, but you can change how you interpret and respond to these events. Try looking beyond the present to how future circumstances may be a little better. Note any subtle ways in which you might already feel somewhat better as you deal with difficult situations.
  3. Accept that change is a part of living. Certain goals may no longer be attainable as a result of adverse situations. Accepting circumstances that cannot be changed can help you focus on circumstances that you can alter.
  4. Move toward your goals. Develop some realistic goals. Do something regularly — even if it seems like a small accomplishment — that enables you to move toward your goals. Instead of focusing on tasks that seem unachievable, ask yourself, “What’s one thing I know I can accomplish today that helps me move in the direction I want to go?”
  5. Take decisive actions. Act on adverse situations as much as you can. Take decisive actions, rather than detaching completely from problems and stresses and wishing they would just go away.
  6. Look for opportunities for self-discovery. People often learn something about themselves and may find that they have grown in some respect as a result of their struggle with loss. Many people who have experienced tragedies and hardship have reported better relationships, greater sense of strength even while feeling vulnerable, increased sense of self-worth, a more developed spirituality and heightened appreciation for life.
  7. Nurture a positive view of yourself. Developing confidence in your ability to solve problems and trusting your instincts helps build resilience.
  8. Keep things in perspective. Even when facing very painful events, try to consider the stressful situation in a broader context and keep a long-term perspective. Avoid blowing the event out of proportion.
  9. Maintain a hopeful outlook. An optimistic outlook enables you to expect that good things will happen in your life. Try visualizing what you want, rather than worrying about what you fear.
  10. Take care of yourself. Pay attention to your own needs and feelings. Engage in activities that you enjoy and find relaxing. Exercise regularly. Taking care of yourself helps to keep your mind and body primed to deal with situations that require resilience.

 

QTc

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Yesterday I had a 21 yo female come in by BLS crew, tachycardic with a GCS of 3, spontaneously breathing with equal and reactive pupils bilaterally at ~ 6mm, with vomitus around her airway.  She was found down at home after her significant other called EMS due to concern that she was going to attempt suicide.  Report received that she was found with multiple empty pill bottles nearby.  No response to Narcan either in the field or in Room 9.

Here is her ECG: Calculated QTc (automated) is 401 ms, rate is 143.   The accepted normal value for QTc is: below 450ms for men and below 460ms for women.  The 99th percentile of normal: 470ms (men) and 480 ms (women).

ecg_case_micu

Just how does the computer calculate this?

By using the Bazett formula: QTc = QT / sqrt( R-R interval in seconds)

This means of course that if our rate is 60 BPM, then our R-R interval would be 1000ms, (or 1 second), and thus our QTc = QT/sqrt(1); and therefore in this situation QTc equals QT.

In our particular case: the R to R interval is 10.5 boxes (thus 420 ms, or in seconds: 0.420).  The QT was autocalculated at 260 ms, and when using the Bazett equation, this gives us a QTc of 401 ms.

What if you cannot rely on the computer calculated QT (which certainly can be inaccurate)? Then calculate the QT yourself by finding the tangential intersection of the T wave downslope with the ECG baseline, and measuring the intersection distance from the start of the QRS.  See the diagram below:

qt_picture

Using this measurement principal, and (in our case) using the lead V2 where the p wave and T wave are 180 degrees out of phase, we obtain a QT ranging from 8-9 boxes (320-360 ms).  When using the Bazett, this gives us a calculated QTc of 493-555. Of course qualitatively we can tell the QTc seems long as it exceeds half the R-R interval, quantitatively this is an increased QTc of 38% from the auto calculated, and is certainly in the significantly prolonged QTc range.

Follow-up: TCAs and benzos positive on her drug screen.  She was started on a bicarb drip in the ED (placed 3 amps of bicarb in a bag of D5); pH 7.34, lactic acid 1.2.  She is supposedly on Flexeril (similar in structure to TCA and will light up as TCAs on the drug screen), treated the same, however appears to be less cardiogenic in toxicity:J Emerg Med 1995;13(6):781-5.  Pt is intubated and stable currently.

Click here for the EMCrit on TCAs (overview below):

  1. Bicarb drip:  Goals: QRS duration <100, hemodynamically stable, Na ~150, pH ~7.5.  Sodium and bicarb don’t rise significantly in severe toxicity, her repeat showed no change in either.
  2. Magnesium: may help, though risk of Torsades is low as long as the patient remains tachycardic.
  3. Lidocaine: even though lidocaine is another Na-Channel Blocker, it will antagonize the effects of the TCA-like medications.
  4. Watch the electrolytes (decreases expected in both K+ and Ca+):  Lytes and ABG Q1H; (My pt’s Ca+ dropped from 9.8->8.5 over 4 hours).
  5. Intubation: hyperventilate to ensure no hypercapnia (want alkalosis).  Sedate with versed or propofol to raise seizure threshold.
  6. ECMO: If everything else fails.

Paucis Verbis Cards “In Few Words”

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Just in case people are not familiar with the free PV review cards as posted by ALiEM (more than 150), I have linked to a particularly good one dealing with algorithms for rash management: paucis-verbis.  These were also highlighted as very useful in the ACEP Now, Nov 2016; and back in 2013 they were brought up by Buckingham on Room9ER.  I have attached photos of the rash algorithms below, might be a potentially very applicable Norton Children’s reference.

screen-shot-2016-11-23-at-7-35-59-pm screen-shot-2016-11-23-at-7-36-16-pm screen-shot-2016-11-23-at-7-36-48-pm screen-shot-2016-11-23-at-7-37-02-pm

 

 

1.4% Observed Adverse Reaction Treated With Flumazenil

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Flumazenil (Rx: Romazicon) has recently been described as coming into favor for two unique purposes: (1) hepatic encephalopathy and (2) paradoxical reactions to benzodiazepines.

Regarding the first, flumazenil’s use in hepatic encephalopathy has been well described recently in a Cochrane review of 113 RCTs with a total n = 805, wherein flumazenil had a significant beneficial effect on short term improvement of hepatic encephalopathy.1 This is thought to occur physiologically secondary to reversal of the origin of hepatic encephalopathy—i.e., an accumulation of substances that bind to a receptor-complex in the brain resulting in neural inhibition1 (principally GABA receptors which are forefront in the stimulation of sedation). Therefore GABA receptor antagonists (such as flumazenil) can be used to directly oppose this mechanism. Effect on full recovery and survival has still not been proven with flumazenil administration.1

Secondly, flumazenil can be used for paradoxical reactions to benzodiazepines2,4 and in a 10 year review of its use, published in the Journal of Emergency Medicine,3 the real safety of this drug has once again come into question, as there were relatively few adverse outcomes even in the highest of seizure provocation risk—which occurred with co administration of pro-convulsant (e.g., TCAs) at a 2.7 % incidence (8/293)—the total incidence including all subjects bore a rate of 1.4% of seizure activity (n = 904).3

I present an example of administration in the second of indications above. I took care of a 26 yo WF with PMH of asthma, a prior severe dental cavity pending root canal and an IV heroin addiction, currently sober and progressing through the the 12 Steps program at the Healing Place. She presented in sepsis, afebrile with qSOFA of 0/3 (Labs: WBC 21.2 with left shift, procal 1.33, ESR 83, CRP 201, lactic acid 0.8 s/p 2 L NS IVFs), and AKI (Cr. 1.6) with dental as well as urinary possible sources. She was eventually discharged on day 3 with Dx of urosepsis, creatinine returned to normal, and had a negative echo for routine endocarditis rule out in the setting of PMH of IVDA.

During her ER stay she was uncomfortable, diaphoretic, pale, GCS of 15, but anxious and in pain, professing severe insomnia for 3 days, stating, “I just want to sleep”. A trial of oral Ativan 2 mg was given, as she did not want any pain medication due to her prior addiction. She noted a small temporary improvement; however 2 hours later this beneficial effect was absent. By now she had received cefepime 2g and vancomycin 25 mg/kg (for potential osteomyelitis coverage), and was requesting more anxiety medications, having already received 50 mg IV Benadryl 30 minutes prior with no improvement noted. Clinically she was GCS 15, pleasant in interaction, increasingly pale, uncomfortable, wide awake at 0445, and subjectively in pain. She was then given 2 mg IV Versed.

Immediately following the administration of midazolam she became altered to GCS 12 (E4, V3, M5), eyes wide, extremities tremulous, pulled out all of her IVs, and was trying to jump off the bed. It was clear she was paradoxically agitated and hyper-aroused. Rather than reversing her (though we doubted history of benzodiazepine use), we opted to watch and see if this reaction would subside without intervention since she responded favorably to the oral Ativan; however the rarely seen but well known paradoxical reaction to Versed was suspected. She was observed 1:1 and thereafter 3:1 for 40 minutes, at which time she appeared to be steadily worsening rather than improving. The decision was made to give an IV push of 0.2 mg of flumazenil (Rx: Romazicon). Within 30 seconds after administration she once again returned to her pleasant self, she was GCS 15, appropriate, and had no recollection of the previous hour, and had no seizure activity noted throughout her stay. She maintained a healthy mental status of GCS 15 and was AAOx4 for the rest of her evaluation and admission.

In 2010, Kreshak et al. reported a similar case and treatment. This paradoxical reaction to Versed in their report is thought to occur at less than 1% incidence, however it is described as commonly as 1.4 %.4 In the reported literature this reaction is described as a patient becoming acutely agitated, restless and aggressive2. Stiffening and jerking of the extremities, and shaking of a part of the body are also noted. When observing a patient with this reaction, after ruling out other etiologies of agitated AMS, Kreshak et al. (2010) opted to administer flumazenil 0.5mg IV, and “…immediately after which the patient became conscious, oriented and calm, the paradoxical reaction was terminated”. The patient had no recollection of the events,2 similar to the patient observed in the ULED.

Per Kreshak et al. (2010), there exist “…different theories concerning the mechanism of paradoxical reactions, involving a central cholinergic effect or the serotonin imbalance”.2 Unfortunately the exact mechanism of paradoxical reactions remains unclear.

Although difficult to locate literature, if seizures develop following flumazenil administration, pharmacology guidelines recommend Valium 20-30 mg IV then immediately switching to barbiturates; some soft EM sources also suggest going straight to propofol.5

Thank you for reading my post.

References

  1. Als-Nielsen, B., Kjaergard, L., & Gluud, C. (2001). Benzodiazepine receptor antagonists for acute and chronic hepatic encephalopathy. The Cochrane Database of Systematic Reviews (Complete Reviews). doi:10.1002/14651858.cd002798
  2. Cabrera, L., Santana, A., Robaina, P., & Palacios, M. (2010). Paradoxical reaction to midazolam reversed with flumazenil. Journal of Emergencies, Trauma, and Shock J Emerg Trauma Shock, 3(3), 307. doi:10.4103/0974-2700.66551
  3. Kreshak, A. A., Cantrell, F. L., Clark, R. F., & Tomaszewski, C. A. (2012). A Poison Center’s Ten-year Experience with Flumazenil Administration to Acutely Poisoned Adults. The Journal of Emergency Medicine, 43(4), 677-682. doi:10.1016/j.jemermed.2012.01.059
  4. Tae, C. H., Kang, K. J., Min, B., Ahn, J. H., Kim, S., Lee, J. H., . . . Kim, J. J. (2014). Paradoxical reaction to midazolam in patients undergoing endoscopy under sedation: Incidence, risk factors and the effect of flumazenil. Digestive and Liver Disease, 46(8), 710-715. doi:10.1016/j.dld.2014.04.007
  5. (n.d.). Retrieved August 23, 2016, from http://www.goodfriendem.com/2013/05/flumazenil-romazicon-is-probably-safer.html

A Mysterious Death in a 21 yo Healthy White Female, and the Larson Maneuver

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My wife is at work at a hand surgery pre-op care clinic. It is her birthday. In walks a middle-aged male who is about to have tendon reconstruction after he sustained a crush trauma, and is excited about the possibility of returning to work. He is slightly abrasive and somber, despite the prospect of receiving the surgery.

My wife asks him if he is concerned about the procedure, asks if he is feeling well, asks if there is anything she can do to help. With a quiet manner he states all is well. To make discussion my wife states today is her birthday and she is excited to celebrate when she gets home. He smiles and states today is also his daughter’s birthday. She was born the same year as my wife. He states today is always a rough day for him because she passed away in an emergency room 7 years ago at 21 years of age.

We can never fully understand where those we treat are coming from, their life experiences, or what their home situations, thoughts, fears, dreams, and worries entail; and this was a reminder for me. He stated that his daughter was healthy,woke up without issue on that day, but later developed difficulty breathing and wheezing. She was diagnosed with an acute asthma attack. She had one episode in the distant past but was not on any routine medications. She was given albuterol and experienced a negative reaction to the albuterol and completely stopped breathing. She was brain dead by the time she was intubated. They withdrew care in the emergency department.

After my wife shared this with me, I searched to find any case reports of paradoxical reactions to albuterol. Below are three related cases, however bronchospasm becoming worse with beta-blockers is exceptionally rare.

Case reports of paradoxical bronchospasm to inhaled beta agonists:

What I think more probable, and possibly related to the above case reports, is acute laryngospasm. The albuterol she received may have further irritated her vocal cords potentially worsening, rather than relieving her vocal cord dysfunction. Both Resus.me and LITFL (Life In The Fast Lane) have very useful articles describing management (see below for links). Here is a brief synopsis:

Laryngospasm

What is it?: a potentially life-threatening closure of the vocal chords (can occur spontaneously). Often misdiagnosed as asthma—especially exercise-induced asthma (more common in white females).

How to diagnose (and differentiate from asthma):

  • Stridorous sounds are usually loudest over the anterior neck, beware wheezing sounds transmit throughout the lungs
  • Typically, albuterol has minimal to no beneficial effect.
  • Subjectively more difficulty on inspiration than expiration

   Clues in history: recent exercise, GERD, ENT procedures, or extubation

   Common causes & some that are not-so common:

  • Post extubation
  • Exercise
  • GERD
  • Medications (e.g., (1) ketamine sedation, incidence 1-2 %; (2) versed (very rarely), which can be reversed with flumazenil)
  • Near drowning/ aspiration
  • Inhalants (smoke, ammonia, dust, cleaning chemicals)
  • Related to anxiety
  • Strychnine (plant based poison, sometimes used as a pesticide for birds and rodents, also the poison reportedly used to kill Alexander the Great in 323 BC)

Treatment of laryngospasm:

Initially:

  1. Jaw thrust with Larson Maneuver
  2. CPAP/ NIPPV
  3. Heliox might be helpful if available, (also topical lidocaine can be applied to larynx if available)

If conservative measures fail:

  1. Low dose propofol (0.1 mg/kg) ~ give 10 mg
  2. Low dose succinylcholine (AKA: suxamethonium) 0.1-0.5 mg/kg IV
  3. All else fails: intubation with succinylcholine 1.5 mg/kg IV
    • If no IV access, then succinylcholine IM (3-4 mg/kg). Experts advocate IM injection into the tongue.
    • Perform chest thrust maneuver immediately preceding intubation to open the vocal cords and allow passage of the ET tube.
    • Monitor for negative pressure pulmonary edema—(from patient pulling hard against closed glottis in the setting of acute asphyxia).

Flow chart from Resus.me

Larygospasm_flow_high_res

What is the Larson Maneuver? (Published 1998 in Anesthesiology)

It is a manipulation jaw thrust technique targeted at the ‘Larson’s point‘, AKA: laryngospasm notch.

  • Place middle finger of each hand in the laryngospasm notch, located behind the lobule of each ear, between ascending ramus of the mandible and the mastoid process.
  • Press very firmly inward toward the base of the skull with both fingers
  • At the same time lift the mandible at a right angle to the plane of the body (perform jaw thrust).

Reportedly will convert laryngospasm within one or two breath cycles to laryngeal stridor, and in after a couple more breath cycles, to unobstructed respirations. As proposed by Larson, it is likely that the painful stimulus relaxes the vocal cords by way of either the parasympathetic or sympathetic nervous systems through the glossopharyngeal nerve.

Diagram from LITFL

Larson_man

References:

  1. Resus.Me: http://resus.me/laryngospasm-after-ketamine/
  2. LITFL (Life In The Fast Lane): http://lifeinthefastlane.com/ccc/laryngospasm/
  3. UpToDate: https://www.uptodate.com/contents/paradoxical-vocal-fold-motion?source=machineLearning&search=Laryngospasm&selectedTitle=1~150&sectionRank=1&anchor=H3#H3
  4. Larson, Philip, MD. Laryngospasm-The Best Treatment. Anesthesiology. 1998. http://anesthesiology.pubs.asahq.org/article.aspx?articleid=1947036
  5. Paradoxical bronchospasm: a potentially life threatening adverse effect of albuterol. South Med J. 2006 Mar;99(3):288-9. http://www.ncbi.nlm.nih.gov/pubmed/16553105
  6. Paradoxical response to levalbuterol. J Am Osteopath Assoc. 2008 Apr;108(4):211-3. http://www.ncbi.nlm.nih.gov/pubmed/18443029
  7. Paradoxical reaction to salbutamol in an asthma patient. Pneumologia. 2012. Jul-Sep;61(3):171-4. http://www.ncbi.nlm.nih.gov/pubmed/23173379