Sprinkle on a little ketamine

A middle aged patient with a longstanding history of asthma (multiple intubations and ICU stays) presents with 3 days of worsening dyspnea, refractory to home bronchodilators, speaking in 2 word sentences and in tripod position. As oxygen saturations hover in the low 90s, the patient is transferred to critical care area for BiPAP.  As the patient rolls by you plan on BiPAP, solumedrol, epinephrine, and magnesium, and you and your attending think “why don’t we try some ketamine?” 

Severe Respiratory distress (Source imgkid)

Clinical Question: Can ketamine be used as a bronchodilator improve outcomes in patients with severe asthma?

Literature Review: In the review article from 2013 by Goyat et al, 20 articles were examined looking at ketamine for bronchospasm (case series, RCTs, observational, retrospective studies) 3 of which were in the ED.  Ketamine was used as a rescue agent in all studies; general doses were 0.1-0.2mg/kg IVP followed by infusion at 0.15-0.25mg/kg/hr.  Eighteen articles showed a “favorable response”, and 2 studies showed insufficient response.  No major adverse events were reported.  

To review, ketamine has 2 enantiomers: the S is more potent and faster acting, and the R enantiomer may be associated with more emergence reactions.  Most preparations are 1:1 S:R. Peak onset is at 60 seconds with a duration of 10-15 minutes. The distribution half-life is approximately 7-11 minutes and is cleared via the hepatic route with half life of 2-3 hours.  Several mechanisms have been proposed for its effect on bronchospasm: improved airway mechanics, anti-inflammatory properties, airway relaxation, reduction of nitric oxide, inhibition of reuptake of catecholamines at the synapse, and anticholinergic effects.

The first case report of ketamine use for reactive airway disease was in 1972 of a child who had anaphylaxis during skin testing that improved after ketamine, followed by a non-controlled trial in children intubated for asthma that showed a significant difference in PaO2/FiO2 and dynamic compliance after initiation of ketamine infusion.  The first controlled double blind trial in 1994 showed an improvement in “stethoscopic exam” and in Po2 and PCO2.  While it is worth noting the significant change in these objective data points, they are not exactly patient centered outcomes.

One observational study looked at pediatric ED patients. It enrolled 10 patients who were unresponsive to traditional therapy; no change in peak expiratory flow (PEF) was noted at 1 hour, but a significant change in the patients’Asthma Scores and respiratory rates (RR) was noted. 

The next prospective, double blind RCT (Howton, 1996) showed no benefit with ketamine.  Fifty-three consecutive patients with peak flows less than 40% after 3 does of albuterol were enrolled, all were given continuous albuterol, methylpredisolone and oxygen and then either a 0.2mg/kg ketamine bolus followed by 0.5mg/kg/hr x 3 hours, or an equivalent saline dose.  While there was a significant improvement in PEF, RR, FEV-1 in both groups over time, there was no difference between the groups. 

Similarly, a follow up RCT in kids (Allen, 2005), looked at 62 consecutive patients randomized to saline or the same ketamine doses as above, without improvement in pulmonary scores.

 Take-Home Points:

The conclusions of the above review are that ketamine is cheap, has a physiologic rationale, has few adverse effects and has been shown to improve asthma in case series and observational trials, though this has not been born out in the two small RCTs undertaken.  Their suggestion is that it should remain in the ED physicians armamentarium for refractory status asthmaticus and, as always, “further well-designed studies are warranted”.  It is probably not unreasonable for ketamine to be the induction agent of choice for asthmatics, and should be considered whenever NPPV is considered for status asthmaticus. 

References: 

Allen JY, Macias CG. The efficacy of ketamine in pediatric emergency department patients who present with acute severe asthma. Annals of Emergency Medicine 2005, 46 (1): 43-50

Howton JC, Rose J, Duffy S, Zoltanski T, Levitt MA. Randomized, double-blind, placebo-controlled trial of intravenous ketamine in acute asthma. Annals of Emergency Medicine 1996, 27 (2): 170-5

Shweta Goyal, Amit Agrawal.  Ketamine in status asthmaticus: A review.  Indian Journal of Critical Care Medicine 2013, 17 (3): 154-61

Submitted by Wes Watkins, PGY-4 

Edited by Louis Jamtgaard, PGY-3 @Lgaard

Faculty Review by Joan Noelker

Expert Commentary: Troubleshooting Hypoxia on the Vent

In emergency medicine education, we tend to focus on establishing the airway but spend less time discussing the aftercare and managing the ventilator.  While we have spent more time on this recently, thanks to Brian Fuller and his research on the importance of low tidal volume ventilation in the ER (see EM Journal club summary and podcast from February 2014),  most of us are still more comfortable putting the ET tube in than managing the vent.

Luckily for us, here at WashU we have some EM-Critical Care wise guys who can teach us a thing or two, and today we share with you Brian Fuller's method for trouble-shooting hypoxia on the vent, forwarded to us by PGY-3 Brendan Fitzpatrick:

>>From: Fitzpatrick, Brendan
>>To: Fuller, Brian
>>Subject: vent desats

Dr. Fuller,

Good working with you last night. I was trying to recall how you broke down desats on the vent last night, but somewhere between little sleep and my kids' halloween parade, I've lost the finer points.

In all your free time, would you mind jotting down what you told me so I can review it?

thanks,

Brendan

 
>From: "Fuller, Brian"
>To: "Fitzpatrick, Brendan"
>Subject: RE: vent desats

For the purposes of acute deterioration (in the form of hypoxia) on the ventilator, we are gonna talk about two airway pressures: peak pressure and plateau pressure. As an aside, mean airway pressure is the average pressure over one cycle of inspiration and expiration. It is largely governed by PEEP and I:E ratio. It really governs oxygenation- higher it is, more you open up stiff alveoli in sick vented patients.

Peak pressure is the summation of pressure generated from: 1) tidal volume and compliance; 2) resistance and peak inspiratory flow; and 3) PEEP
 
Plateau pressure is a reflection of compliance. Think "how stiff the lungs are"; or "how much transalveolar stretch is occurring".
Compliance is ∆ volume/∆pressure. Specifically, tidal volume/(plateau pressure - PEEP)




So the first thing I do when somebody becomes acutely hypoxic on the ventilator is to look at their peak airway pressure:

1. If decreased: you have an air leak or the patient is hyperventilating/tugging hard and therefore pulling the airway pressures down. Air leak would be something like: bronchopleural fistula, the chest tube you just put in has a leak in the system, your ETT has migrated or cuff has a leak and air is escaping.

2. If increased: see above- this could either be primarily a compliance or resistance problem. So your next step is to look at the plateau pressure to figure out where the problem lies.

If no change in plateau, you therefore have a bigger difference between the peak pressure and the plateau pressure than existed before the hypoxic event. See above for what governs these pressures, so you can tell that this is therefore a resistance problem. Think: airway obstruction from bronchospasm, clogging of the ETT with secretions, kinking of the ETT.

If plateau pressure is also increased, you now have a situation where the peak and plateau pressures both increased. See above for what governs these pressures, so you can tell that this is therefore a compliance problem. Think: pulmonary edema, abdominal distention, pneumothorax, atelectasis, etc.

3. If no change: think "Something made my patient hypoxic but didn't change my airway pressures." Not a lot of stuff does that. Think: pulmonary embolism, PFO.

Sometimes it is difficult to figure out "Is the ventilator and my ventilator settings the problem, or is this a patient problem?" If you remove the patient from the ventilator, and therefore take that out of the equation, bag them and they get better, it is probably a ventilator problem. If you bag them and they stay bad, it is probably a patient problem.

Hope this helps. Hit me back with questions PRN.

Feel free to share with others.
Be good man.
B


For those of you who like pictures, here is a visual representation of the algorithm:

Want to do a little more reading or watching about this? Life in the Fast Lane had a nice review of Pulmonary Mechanics.  I recommend the second Eric Strong video on pulmonary pressures as a supplement to understanding the above material (and hell, it only takes 9 minutes to watch).

Expert Commentary by Brian Fuller
Visual aids by Maia Dorsett (@maiadorsett), PGY-3 
Expert inquiry, sharing skills and parenting by Brendan Fitzpatrick, PGY-3.

Steroids for Acute Chest Syndrome?

Clinical Scenario:

A 41 year-old male with a history of well-controlled sickle cell disease and a remote history of CVA and Acute Chest Syndrome (ACS) presents to the ED with three days of left sided chest, shoulder, and flank pain. The pain was subacute in onset, was not pleuritic, was worse with movement, and was not improved with NSAIDs. He also complained of a dry cough but reported no fevers. He had an oxygen saturation of 88% on room air, but his vital signs were otherwise normal. His physical exam demonstrated clear lungs and pain with palpation of his left shoulder and left anterior chest wall. His EKG showed stable borderline LVH. Labs were notable for a negative troponin and Hgb of 5.8, and a left basilar airspace opacity on lateral chest X-ray. He was given IV fluids, morphine, and IV ceftriaxone & azithromycin to cover for Community-Acquired PNA (CAP) triggering Acute Chest Syndrome.

Clinical Question:

Do steroids have a role in treatment of Acute Chest Syndrome?

Plain CXR showing patchy infiltrates of acute chest syndrome. Image credit from AccessMedicine.

FOAMed Digest #6 Update: The Paper Trail

Today, we'd like to introduce a new section to the Everyday EBM FOAMed Digest, which will be published as a standalone post. It may seem a bit counterintuitive, but each week we're going to draw your attention to some of the latest-and-greatest papers from the primary EM literature. Most of these will not be open-access, but we hope you can still access them via the medical library at your institution. A lot of the discussion in the FOAMed world centers around recently-published papers from EM journals. The EM trainee should view FOAMed as a tool to assist with understanding and analysis of this literature, as a forum for discussion and further discovery -- not as a replacement for reading the papers for his/her self. We'll provide you a very short summary here and link you to relevant FOAMed resources if applicable.

Antihistamines for asthmatics?

You walk into the exam room, and find an older female patient complaining of an asthma exacerbation. She reports three days of symptoms consistent with her prior asthma exacerbations, including dry cough, wheezing, increased work of breathing, and exertional dyspnea. She had tried her home MDI and continued her maintenance medications, but her symptoms had gradually worsened to the point that she did not feel she could manage at home.

Her exam is significant for wheezing bilateral full fields, somewhat prolonged expiratory phase but good air exchange. She is speaking in full sentences, and maintaining adequate SpO2 on room air. She is afebrile, and the rest of her VS are stable. The patient's only other complaint is that her "allergies had been acting up lately." The patient appears to have a life-long history of seasonal and recurrent allergic rhinitis, but is not prescribed a daily antihistamine or other anti-allergy therapy.


Clinical Question:

Is there any evidence that antihistamine treatment has a clinically significant effect on asthma symptoms?


The Literature:

A systematic review of the efficacy of 2nd-generation antihistamines in patients with allergic rhinitis (AR) and comorbid asthma was published in the Journal of Asthma in 2011. Epidemiological and histopathological evidence confirms the strong association of AR and asthma. The two conditions share histaminergic mediators released by mast cells & basophils, and the cumulative weight of clinical & laboratory evidence suggests a strong pathophysiologic role.

The study authors performed a comprehensive literature search for double-blind randomized controlled trials in which patients with both asthma & AR were treated with 2nd-gen antihistamines -- cetirizine, loratadine, & fexofenadine being the most common. The authors first summarized the findings of several older trials which did not meet their inclusion criteria (i.e., were not double-blind RCTs). Overall, 1st-gen antihistamines (e.g., diphenhydramine, doxylamine, hydroxyzine, meclizine) have not been shown to have an effect on asthma symptoms except at doses high enough to cause anti-cholinergic and CNS-related ADRs. Some in vitro studies have suggested a steroid-sparing effect or diminished airway hyperreactivity with 2nd-gen antihistamines, but these results are inconsistent in the literature. There is fairly strong evidence in the form of large retrospective studies that effective treatment of AR reduces health-care utilization and improves quality-of-life scores in patients with concomitant asthma, but these cohorts included patients utilizing other AR therapies such as intranasal steroids as well as antihistamines.

A multicenter RCT with N=274 comparing cetirizine-D (cetirizine + pseudoephredine) to placebo found improvement in AR & PM asthma symptoms, but no significant effect on AM symptoms or pulmonary function scores. Another RCT of cetirizine alone had similar results. Several double-blind RCTs comparing the drug desloratadine to placebo, with total N >1100, showed significant reductions in both AM/PM & total asthma sx scores (including specific scores for wheezing & cough) and rescue inhaler use.

As is the case for 1st-gen antihistamines, in vitro data suggests higher doses may be needed to treat asthma as compared with AR. A small RCT (N=28) compared cetirizine 20mg daily to placebo (usual dosing 5-10mg daily), and found significant improvement in reported asthma & AR symptoms without a significant rate of adverse effects compared to placebo. Unfortunately, this dosing regimen has not been compared to standard dosing.


Take home:

- Overall, these studies suggest that antihistamine treatment may improve overall asthma symptom severity in patients with concomitant allergic rhinitis.
- Unfortunately, no study to date has evaluated effects, if any, of antihistamines during acute asthma exacerbation, or if addition of antihistamine prevents ED visits or hospitalizations.
- It seems reasonable to offer these patients antihistamine prescription if they are not already taking them.


Reference:
1) J Asthma, 48(2011):965–973.

Contributed by Sam Smith, PGY-3.

#FOAMed Digest No. 4: Butter My Biscuit, Baby

Welcome back, to the brand new edition of the WUEMR FOAMed Digest. Get out your Tintinalli’s and strap in, because we’re going back to basics today. It’s all about the bread and butter. The things any PGY-2 setting off to an overnight Saturday shift in the Deuce should have down cold…yet us seniors still screw up on the daily.

FOAMed…ENGAGE!

Three Stars:

1. If my last shift at Children’s is any indication, the season is upon us – pharyngitis in every exam room. Casey Parker over at Broome Docs (a blog authored by EPs & GPs practicing in rural Australia), presents a magnificent summary of the data surrounding rapid strep swabs, antibiotic use for symptom relief, and antibiotic use for preventing secondary complications of strep. As always, be sure to check out the original literature for yourself. And don’t miss Minh Le Cong’s excellent counterpoint in the comments, which is also well-referenced.

2. What’s your record for most C-collars cleared in one shift? (When you hit double-digits, then we can talk.) The best tools in our arsenal for clearing C-spine in low-risk patients remain the Canadian C-spine and NEXUS instruments. But which one should you use? Do you even remember which criteria belong in each rule, or do you find yourself trying to apply the “Canadi-EXUS” criteria, like I do? Luckily for us, Alayna Hawling at BoringEM authored an excellent rundown and comparison – with a pretty flowchart!

3. As much as you want to start the fist-pumping and beer-chugging as soon as you drop that tube past the cords, your work with the intubated patient is not done, my friend! We’ve already touched on our persistently poor rates of achieving adequate analgesia & sedation in the intubated patient. Another part of quality post-intubation care is knowing what to do if your ventilated patient acutely decompensates. Check out Chris Cresswell’s summary of the DOTTS mnemonic over at EM Tutorials.

(EXTRA CREDIT: He also included a link to Scott Weingart’s notes regarding care of the crashing ventilated patient, which are well worth a look.)

Oldie But Goodie:

There’s been some e-mail discussion lately among our attendings regarding the best way to clean lacs prior to closure. Back in February, Ken Milne at the Skeptic’s Guide (along with Eve Purdy, a rockstar med student and creator of the excellent Manu et Corde blog) published a piece dedicated to breaking down the dogma of management of simple lacerations. Tap water vs sterile water, sterile gloves vs clean gloves, to sew or not to sew…it’s all covered here. Plus there’s links to other excellent FOAMed resources regarding wound care dogma.

F(FN)OAMed:

The good folks over at EB Medicine recently published a stem-to-stern guide to UTI diagnosis and management in the ED, all based on best available evidence. A bit lengthier than your average blog post, but incredibly high-yield and well worth your time. It’s a bit difficult for me to place a direct link here, but you can find it simply by logging into your account at EBMedicine, following the link to browse issues of Emergency Medicine Practice, and opening the July 2014 issue on UTI.
(As always, contact your friendly neighborhood Social Media Committee member if you need help obtaining access to EB Medicine resources.)

The Gunner Files:

1. Hard to get through a Deuce shift without breaking out the prochlorperazine at least once. We’ve all seen patients get jittery, agitated, or downright whacky following its use. Does Benadryl help? A PharmD expert at ALiEM has a good lit review of the topic.

2. Short and sweet: some diabetic medications are more likely to cause harmful hypoglycemia after overdose than others. Quick table-based rundown over at ALiEM.

3. It is asthma season, and you may find yourself in the worst-case-asthma-scenario of impending need for intubation. Check out this post from The Kings of County regarding care for the sick asthmatic, including intubation and mechanical ventilation issues.

4. FOAMed is taking the world by storm! Does the UK College of Emergency Medicine launching a dedicated FOAMed site mean it’s officially gone mainstream? Don’t worry – we were all into FOAMed before it was cool. But seriously, check out this vodcast on diagnostics in EM, and not feel quite so much increase in sphincter tone when Carpenter or Cohn pimp you on likelihood ratios or Bayesian analysis.

5. Another classic from the Skeptic’s Guide, this time addressing another oh-so-common ED complaint: renal colic. Fluids? Flomax? Any good evidence for either? In news that will surprise no one, Ken Milne is skeptical.

Never stop learning,

Sam Smith, PGY-3

#FOAMed Digest No. 2: Breathless Love

Welcome back! Fresh new FOAMy goodness for you, this time with an emphasis on airway and pulmonary care. Let’s do it!

Three Stars:

1. No way around it: “Delayed Sequence Intubation” is the new hotness. If you want to be one of the cool kids, you better get on board. I’ll let the more graphically-minded folks at EMCurious lay it all out for you with a prototypical case. Don’t miss the links – more excellent FOAMed resources on DSI.

(And Weingart’s seminal paper on the subject is required reading at this point.)

(And, oh yeah, ketamine does NOT increase ICP. Let’s use these two systematic reviews 1 & 2 to stop the foolishness already.)

2. Someday you will need to perform a cricothyrotomy. Accept it as reality, and do everything you can to prepare for it. Start here, with Weingart’s lecture on the surgical airway delivered at the SMACC Gold conference last fall. This page from the EMCrit blog has compiled all sorts of great surgical airway resources from around the FOAMed world all in one spot, including can’t-miss stuff about the scalpel-finger-bougie technique and Weingart’s pre-intubation checklist. You should probably add it to your favorites list now.

3. Wouldn’t be a FOAMed Digest without getting a little off-topic, and Rick Body’s recent contributions over at St. Elmyn’s regarding ACS & “low-risk” chest pain in the ED are too good to pass up. Great post analyzing his recent paper, which concluded ED physicians simply aren’t capable of ruling out ACS in chest pain patients with an acceptable accuracy using only the clinical exam. Dr. Body also gives you a run-down of how to properly utilize high-sensitivity troponin in his talk from SMACC Gold.

(Link to Body's paper here.)

Oldie But Goodie:

By the end of our Ultrasound rotation, we can all diagnose pneumothorax with ultrasound at the bedside. It’s time to take it next-level. A-lines, B-lines, pneumonia vs edema…the experts at the Ultrasound Podcast help you figure it all out in a two-part 1 & 2 podcast.

F(FN)OAMed:

Sanjay Arora and Mike Menchine, hosts of the PaperChase segment on EM:RAP, summarize the current literature about how terrible we are at adequately sedating patients after RSI. Roc lasts longer than Sux – the patients won’t be able to tell us they need sedation!

(Links to relevant papers in the show notes.)

The Gunner Files:

1. Brett Sweeny at EMDocs provides an exhaustive review of FOAMed resources regarding permissive hypotension in trauma. Great lectures and podcasts from some of the brightest minds in EM & trauma surgery.

2. We’re seeing it already – asthma cases are starting to pile up over on the SLCH side. Luckiliy for you, Pediatric EM rockstar Andy Sloas just published an excellent podcast on the evaluation and management of asthma in the Peds ED.

3. Next time you’re consulting Ortho or Plastics for a hand injury, sound like you know what you’re talking about. The folks over at EMin5 hit you with the quick rundown on the neuro exam of the hand.

4. Last week, St. Elmyn’s helped the rooks get up to speed when it came to dealing with the dyspneic patient in the ED (and I bet the seniors learned a thing or two as well). This time, get your mind right when faced with a syncopal patient.

5. Who doesn’t love infographics? And if they actually help us learn something about managing septic patients, that’s just a bonus! Very well done by EMCurious, with embedded links to the relevant studies!

6. New podcast from R.E.B.E.L.EM, summarizing the results of a meta-analysis just published this month in Annals which concluded prehospital application of NIPPV in patients with severe respiratory distress regardless of cause reduced need for intubation (NNT 8) and in-hospital mortality (NNT 18). 

w00t prehospital medicine!
(Original pub here.)

That’s all, folks! Go get your learn on!

Sam Smith, PGY-3

#FOAMed Digest No. 1: Total Eclipse of the Heart

Welcome to the very first edition of the WUEMR FOAMed Digest! The Social Media Committee hopes with this segment to parse out from the overwhelming FOAMed universe a few of the most high-yield pieces of highest relevance to the general EM trainee. We hope to deliver this in an easily digestible format that you can realistically work through over a week – even if you’re stuck in an ICU.

Each post will contain several sections:

1. Three Stars: Three of the best-of-the-best from the FOAMed world published in the past week or so.

2. Oldie But Goodie: The FOAMed universe has been around long enough that there’s already a good number of very well-done and highly informative blog posts and podcasts.

3. Free (For Now) Open Access Med Ed: F(FN)OAMed for short. There are some great resources out there that are not free to the vast majority of EM practitioners but, due to your EMRA membership being graciously covered via the residency and MoCEP, you have access to them. Most notably, your EMRA membership allows you subscription to the EM:RAP podcast and the EB Medicine resources – EM Practice, EM Critical Care, etc. You should take advantage of this opportunity while you can, and this section will help you do so. (Contact your friendly local Social Media Committee member if you need help setting up your access.)

4. The Gunner Files: The Social Media Committee recognizes that, with this being Wash U and all, some of you will always be overachieving. So we’ll include a few extra selections for those of you that have a more insatiable FOAMed appetite.

Without further ado, let’s kick the tires and light the fires.

This week, “Total Eclipse of the Heart,” will focus on care of various cardiac conditions.

Three Stars:

1. Ever heard of Wellens’ Syndrome? If you have any hope of passing your boards one day, you should. Not mention that whole “you shouldn’t miss a critical EKG finding that portends certain doom” thing. Never fear, Salim Reazie, author of the excellent R.E.B.E.L.-EM blog, has you covered. 

(Don’t miss the links list at the bottom that highlights posts from other top-notch FOAMed resources!)

2. Syncope is one of those presenting complaints that really must be approached in a systematic manner. The grandmaster of EM EKG interpretation, Amal Mattu, reviews the differential while highlighting the characteristic EKG findings of a can’t-miss diagnosis.

3. Okay, so DKA isn’t exactly a “cardiac” condition – but the worst-case-scenario is still hemodynamic collapse, right? It counts. The EBM gurus over at Anand Swaminathan’s blog EMLyceum give you the latest & greatest when it comes to evidence-based care of DKA.

Oldie But Goodie:

So you’ve achieved the nigh-impossible – achieved sustained ROSC in an OHCA patient. Now what? The reigning American Idol of EM Critical Care, Scott Weingart, tells you what in an excellent two-part interview with one of the lead authors of the TTM trial, Stephen Bernard.

F(FN)OAM:

Worst-case scenario #137: Running ACLS on a patient brought in with PEA arrest. As CPR continues, the staff looks to you. “Uhhhhhh…more Epi?” Like all things resus, you need a systematic approach. The smart dudes over at EM:RAP, along with EM cardiology expert Amal Mattu, review a newly published paper that will help you do just that in the August 2014 edition.

PubMed link to the paper itself here.

(Once again, contact the Social Media Committee if you need helping subscribing to EM:RAP.)

The Gunner Files:

1. Excellent review article from the journal Emergency Medicine Australasia covering that bane of the overnight Deuce shift. No, not vaginal discharge – dental pain.

2. EMLyceum deals in pearls once again when addressing ocular emergencies.

3. Ryan Radecki over at EMLitofNote looks at a very interesting paper just published in JAMA regarding the use of pulse oximetry and dispo of bronchiolitis patients. 

(And as always, be sure to read the original paper for yourself!)

4. My FOAMed man-crush, Rory Spiegel of EMNerd, tackles the C-spine injury algorithm debate.

5. The Aussies over at St. Elmyn’s get you straightened out when dealing with the breathless patient in the ED. Incredibly high-yield for new ‘terns, but useful for docs of all ages.

Now get to FOAMing! 

As always, comments/concerns/criticisms are appreciated!

C. Sam Smith, PGY-3