EMCrit Wee – A Case to Threaten Current ECMO Evidence from Sam G

Over at EDECMO we talk about the huge benefits of ECPR demonstrated by the fact that there are neurologically intact survivors when ECMO is initiated at the point of cessation of standard ACLS. But what if standard ACLS had not stopped… What if you just kept going?

Mirroring Cliff Reid’s amazing talk: When Should We Stop Resuscitation?, I present Sam’s case.

 

From Sam G:

I just experienced probably the most amazing case I’ve ever been a part of this past Monday.     This case has become the talk of the place, as it was very controversial within the world emergency medicine, critical care and cardiology here @ Janus General.  It was discussed in M&M and there is gonna be a joint multidisciplinary thing, etc.  But otherwise there is no one else’s opinion I would be more interested to hear than yours, so I wanna share it with you:

I was working shift in Major Treatment Area here at Janus General, and we hear we’re getting a med resusc… rolls in a guy looks to be in about his 60’s (turns out he was 59).  Story was :

Witnessed Arrest with bystander CPR… shockable for EMS, but shocked 6-7 times… meds given were for some reason only bicarb and Lidocaine (not sure why?)

I will share with you my documentation, only b/c it will save me tons of typing and I trust sending it to you..

This patient was seen in the resuscitation bay along side Dr. XXXXX concurrently.  This patient presents status-post witnessed cardiac arrest after return of spontaneous circulation.  His rhythm was always shockable per EMS.  He arrived with a King airway in place.  There was a large air leak noted.  CPR was in progress shortly after arrival as he was noted to not have pulses.  Chest compressions were resumed immediately and multiple rounds of CPR with multiple rounds of epinephrine, and medications including amiodarone, bicarbonate, calcium, magnesium were administered.  Please see nursing medications charting.

Multiple echocardiographic images were obtained by myself.  Please see computer for images.  The patient was noted to be in and out of ventricular fib.  CPR was continued in line with ACLS protocol.  The King Airway was removed and endotracheal intubation was performed by myself using a MAC 4 blade and an 8.0 endotracheal tube without difficulty.  There was good condensation on the tube, good chest rise, and end tidal CO2 was detected immediately with excellent wave-form.  Intra-code bedside echo was performed and revealed no evidence of right ventricular enlargement or strain on echo, or any other signs of massive pulmonary embolism.  There was also no pericardial effusion.  Echo did show akinesis/hypokinesis inferiorly and somewhat laterally as well.  The inferior wall was essentially akinetic.   Anterior wall motion was clearly preserved.  This was best seen on the parasternal long and short axes.

There was very high suspicion for acute coronary event.  Furthermore there was no evidence of hypoglycemia, hyperglycemia, hypokalemia, hyperkalemia.  The patient’s pH was noted to be significantly acidotic, and 2 additional ampules of sodium bicarbonate were administered at that time.  There was good sliding bilaterally on ultrasound.  There was no evidence of massive pulmonary embolism on echo, and there was no evidence of pneumothorax.  Intravenous fluids were pressure bagged in.  There was no significant hypothermia.   End tidal was difficult to interpret due to multiple ampules of sodium bicarbonate.  After nearly 45 minutes of aggressive CPR the decision was made to use thrombolytics because we felt strongly that this was an acute myocardial event, it was also strongly felt that without thrombolytics stabilization and termination of electrical storm could otherwise not be accomplished, in order to get this patient to the cath lab.

The decision was made to was give teneceteplase intravenously, as again, stabilization and return of spontaneous circulation continued to only be transient.  It was felt that the patient could not be stabilized for cath lab intervention, and this was our last resort. Following the administration of TNK, the patient did not have any further episodes of v-tac/fib/pulselessness.  EKG finally obtained after termination of storm revealed injury pattern in inferior leads II, III, and aVF.  There was evidence of left bundle branch block, however there was severely excessive DISCORDANCE in leads 3 and aVF.  Elevation was 7 or 8 mm,greater than 5mm being concerning for STEMI, and also of note far greater than 25% of the S Wave.    Lead II showed excessive CONCORDANT ST Elevation of multiple mms, far surpassing the 1mm requirement of Sgarbossa’s Criteria. These findings of inferior coronary artery distribution involvement correlated excellently with the wall motion abnormalities noted on echo . Code STEMI was called, and code cool was initiated as well.  The patient was placed on norepinephrine drip.  The patient was also placed on amiodarone drip. This case was discussed at length with critical care and cardiology attendings at the bedside.

Cardiology felt that since thrombolytics were given, Cath Lab was not indicated at this time.   Of note, it was contemplated to cease efforts, however since this was a witnessed arrest with immediate CPR, and the rhythms were always shockable, the decision was made to continue efforts.  As the patient was in dire straits, it was felt that benefits outweighed the risks of bleeding, and it my sincerest hope that the thrombolytics  benefit the patient for his  highly suspected STEMI.    The patient was admitted to the intensive care unit in very critical condition.

So…

We weren’t able to get an EKG until well near the end of the code, bc he would revert right back to v-fib after transient ROSC… he did this the entire code..  I might have stopped if it wasn’t for the resident, Dr. Karina Reyner, insisting that she was not comfortable calling it as the patient was still shockable…we discussed the increasing likelihood as the code went on of bringing back the heart but not the brain … well, she asked “why not just push lytics?” …. My philosophy is I will not run a half-ass code… if the code is running it’s all or nothing, I figured this was 1. witness with immediate CPR 2. He was consistently in a shockable rhythm… and  3. knew the CPR he got for the past 45 minutes was excellent.. the tech’s were doing amazing compressions.. (in fact we broke his sternum) ..so –we pushed lytics…   After lytics were pushed the storm relented and the patient had no further episodes of V fib/tac…

It’s crazy that he got lytics at a cath center w/one of the best door balloon times in the nation… weird and interesting concept… I know he would have not made it without lytics though… cards doesn’t take CPR in progress patients, and when they came down, I was shocked at the overwhelming resistance, even before they knew we pushed lytics…  there was not only resistance to taking the patient to cath, but even questioning the diagnosis.   I was amazed at the response… this is despite clinical picture, hx, EKG, and Echo all pointing to a diagnosis of nothing other than STEMI.

Overall, we got a lot of shit from both Cards and Crit Care for pushing lytics at a cath center… but here’s the most amazing part of the story, and what makes it such a big deal:

Patient was following commands a few hrs later in the ICU… (ICU doc called down to tell us)… he did have a GI bleed, but that did resolve without surgical intervention.  He was extubated w/in 24 hrs.. A-line removed.. His GCS is 15.  I went and saw him yesterday and he was very tearful and appreciative… kept saying “so humbling…”  “I guess it wasn’t my time…”  He has picts on the wall in the ICU of his granddaughter an was saying how he gets to see her again…

This case is amazing for so many different reasons, but.. the obvious is lytics given for suspected STEMI @ cath center…

Should lytics be pushed intra-code with refractory and electrical storm even if at a cath center?

Also interesting that we didn’t give him 9 to 15 doses of Epi as ACLS would call for…  I have a feeling this would’ve crushed his chances as well…

Anyway I have attached the EKG’s… 1st one was the only one done in the ED.  The remainder were when he was upstairs… Cards Echo’s showed exactly what mine did.  Trop next day was >100… but he made it and is doing stellar.

I will send the Echo clips as well… amazing that you can see the wall motion abnormalities even when he is in Vtac/Fib…

This is by far the longest CPR to make it neuro intact that I’ve ever experienced… Dying to know what you think about all the pertinent issues!  Let me know if you have any other questions about the case…Thanks so much..

 

Scott- I think a wee about this would be awesome.  There just are so many critical issues to discuss, like:

  1. Should we maybe be lysing more cardiac arrest STEMI’s (whether you have a pre-hospital confirmatory EKG, or strong evidence to suspect), despite being at a cath center?
  2. If you do lyse and the patient attains and maintains ROSC, shouldn’t these people get cath still?
  3. Does TNK vs other lytics play a big rule?  We have TNK here b/c of Kline, and I have pushed it one other time earlier in the year on a crashing pt with high clinical suspicion, and u/s showing everything (Huge Rv, Huge Ra, flattening, paradoxical motion, McConnel’s) and this guy stabilized after a few hrs, got a repeat cardiology echo that was read as  normal, got a follow up ct that showed b/l PE’s… and was d/c’d after a short stay of only 4-5 days.  It just makes me wonder how much of a difference other lytics would/wouldn’t make.
  4. When do you stop CPR?  Our patient had end tidals that were like 30’s or 40’s or so I believe, but he also got prehospital bicarb, and then 3 additional total amps by us… but even in the absence of bicarb admin, I don’t know of any evidence showing that a higher end-tidal means don’t stop…  (versus saying less than 10 with 20 mins of CPR  you can basically stop)
  5. I am also convinced that if we slammed him with epi every 3-5 minutes, that he wouldn’t have made it neurologically intact… possibly another point of discussion.
  6. This wasn’t as much of a problem for us b/c the patient would convert with electricity, (end-tidal spike) as well as after the 2 mins of continuing right back on the chest after the shock, he would be in a perfusing rhythm (junctional, etc)… and then quickly revert back… Buuuut- Amal shared with me an extremely interesting idea that I had not heard of, and he says they are doing this at Maryland, and the medics are doing it in the field as well (no great evidence), but putting 2 defibrillators attached to the patient (4 pads), and shocking at 720J!. (double-sequential defibrillation)

Anyway- I’m sure there are more issues as well, but obviously the biggest in our case is lysis, intracode, cath center, cath after lysis, etc

If you have any more questions or want any other info about our case let me know.  Looking forward to this!

 

This is just one of many echo clips from this case. The Ultrasound Podcast guys will be doing an episode with Sam on intra-arrest echo to discuss these clips further.

Initial ECG

Initial ECG

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SMACC-Back – On the Beliefs of Early Adopters and Straw Men

scarecrow

This is the first SMACC-Back for SMACCgold. The creator of the lecture that led to this was Simon Carley. Simon is a brilliant emergency physician and lecturer who practices at St. Emlyn’s. I can only imagine he was expecting this SMACC-Back as he all but threw his metal glove on the ground in front of me (all in good fun). Unfortunately, I was in another session during this lecture, but I’ve been eagerly awaiting it as many of the EMCritters came up to me afterwards to tell me about it.

My response will make no sense if you don’t listen to Simon’s talk first, so here it is. I advise watching the video, because I love watching the emotions flash across his face whenever he is lecturing–truly a captivating speaker.

Audio Only Version [right-click and choose save-as to download]

Also, please read the original post on St. Emlyn’s.

Technology Adoption Curves

Diffusion of Innovations was a book I read in college. It explains how technology and ideas get taken up by a population. Here is an entry from wikipedia:

Diffusion of innovations is a theory that seeks to explain how, why, and at what rate new ideas and technology spread through cultures. Everett Rogers, a professor of communication studies, popularized the theory in his book Diffusion of Innovations; the book was first published in 1962, and is now in its fifth edition (2003).[1] The book says that diffusion is the process by which an innovation is communicated through certain channels over time among the members of a social system. The origins of the diffusion of innovations theory are varied and span multiple disciplines. The book espouses the theory that there are four main elements that influence the spread of a new idea: the innovation, communication channels, time, and a social system. This process relies heavily on human capital. The innovation must be widely adopted in order to self-sustain. Within the rate of adoption, there is a point at which an innovation reaches critical mass. The categories of adopters are: innovators, early adopters, early majority, late majority, and laggards (Rogers 1962, p. 150). Diffusion of Innovations manifests itself in different ways in various cultures and fields and is highly subject to the type of adopters and innovation-decision process.

The book posits that uptake is a bellshaped curve that looks like this:

Technology-Adoption-Lifecycle

Bayesian Approach to New Ideas

Anyone who looks at new evidence with tabula rasa is missing the point and is likely to get things wrong. Not only do we filter new evidences through out beliefs, we must do so. It is not irrational, it is essential-the process should be a willful and deliberate filtration of new information through your existing schema.

Update:

Simon responded to this SMACC-Back with a SMACC-Back-Back. Here it is:

Now on to the SMACC-Back:

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MOTR: Cliff Reid on When Should Stop Resuscitation

when-should-we-stop-resus

Cliff Reid gave this inspiring lecture at SMACCgold. He was tasked to talk on when we should stop a resuscitation, but instead he speaks about when we shouldn’t stop.

EMCrit Wee – Four More Minutes with Rob Mac Sweeney

So yesterday, I spoke with Rob Mac Sweeney about Intra-Arrest Meds. On that cast, I told you today we would have a bit of discussion on Rob’s FOAM. Well here it is…

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Critical Care Reviews

It’s amazing, it’s hugely helpful, and it is free. Subscribe ASAP at criticalcarereviews.com.

 

CCH Banner

Critical Care Horizons

Here is Rob describing this new journal:

Announcing a new development in critical care publishing.

It is with great delight we announce the launch of a new open access critical care journal. Critical Care Horizons is a fresh, original voice in the critical care literature, offering thought-provoking, cutting-edge commentary and opinion papers, plus state-of-the-art review articles. As a Journal, we see discussion, commentary, and the sharing of insight, experience and ideas, as central to progress in our speciality. We are free to publish with, free to read, opening authorship opportunity to all working with the critically ill. We are driven by a desire to improve the care we offer our patients, and operate without financial aim or incentive.

We strive to be different, combining the rapidity, broad exposure, and dynamic discussion characteristic of social media with the academic standards of an indexed, peer-reviewed journal. Covering the full spectrum of clinical care, we welcome submissions from all disciplines involved in the care of the critically ill and injured, from pre-hospital resuscitation to Emergency Department care to ICU-based management to post-discharge follow-up, and anywhere else.

The Journal publishes dynamically, releasing material to the website as the final PDF as soon as it has cleared peer-review and editorial processes. Issues will be published quarterly, with additional special editions and articles as required. The Journal is run on a not-for-profit basis, with editorial staff operating on a voluntary basis without monetary reimbursement.

Critical Care Horizons is aligned with the altruistic ethos of the FOAMed movement, and affiliated with several of the leading critical care and emergency medicine blogs. We have an energetic editorial board, consisting of a deliberate mix of clinicians active in social media and world renowned academics. This is a journal for the critical care community, by the critical care community, without access impediment or financial bias. This is your journal. We hope you will enjoy the content, get involved in the discussions available with each article, and, by publishing with us, share your thoughts and opinions with the world.

With this, we issue a call for both papers and peer reviewers. Neither finance nor profile will be an impedement to publication. The only barrier is you – your willingness to commit time to write and your ability to produce an engaging, skillfully written manuscript. If you have something interesting to say, but feel locked outside the traditional publishing environment, this is your opportunity. If you are an inexperienced author, please enlist the help of an experienced colleague, as formal scientific writing is a skill to be mastered. If you have an idea for a themed issue, and would like to act as a guest editor, please contact the editor-in-chief. Further affilitations from similar altruistic bodies and websites are welcome. The first articles will be published on January 1st 2015.

Join us on an amazing journey.

 

Rob Mac Sweeney – Editor-in-Chief

Andrew Ferguson – Senior Deputy Editor

www.criticalcarehorizons.com

@CCHjournal

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EMCrit Wee – Rob Mac Sweeney on Intra-Arrest Meds

argument

Rob Mac Sweeney is an anaesthetist-intensive care doc. His gig is evidence: analysis, assimilation, and dissemination. Tomorrow, you’ll hear a ton more about the great stuff he does on sites such as Critical Care Reviews. For today, we discuss the topics raised in my recent posting of my SMACC Intra-Arrest Talk.

 

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Mind of the Resuscitationist – Errors of Commission and Omission

permission-to-act

I received an email from a friend and colleague on how to build mental toughness in our trainees. After hearing the case that spurred the question, I actually began to believe the problem is actually one of self-granted permission to act and the conflict between erros of commission and errors of omission.

Recommended Reading/Listening

Listen to the wee to understand what the frack I am talking about…

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EMCrit Wee – Cricolol by Dr. John Hinds

cricolol

John Hinds, Critical Care and Irish Road Racing Doc, gave my absolute favorite lecture from SMACCgold. It was the con side of a debate on Cricoid Pressure for Emergency Airway Management. Well, it was actually a rep pitch for a new drug called Cricolol. You will enjoy it!

Here is the conference write-up version in ACEP Now

Note: This is a remixed version from the one up on Intensive Care Network (love those guys!), so watch it again…

References

  1. Sellick BA. Cricoid pressure to control regurgitation of stomach contents during induction of anaesthesia. Lancet 1961;2:404-6.
  2. Koziol CA, Cuddeford JD, Moos DD. Assessing the force generated with application of cricoid pressure. AORN journal 2000;72:1018-28, 30.
  3. Smith KJ, Dobranowski J, Yip G, Dauphin A, Choi PT. Cricoid pressure displaces the esophagus: an observational study using magnetic resonance imaging. Anesthesiology 2003;99:60-4.
  4. Hartsilver EL, Vanner RG. Airway obstruction with cricoid pressure. Anaesthesia 2000;55:208-11.
  5. Allman KG. The effect of cricoid pressure application on airway patency. Journal of clinical anesthesia 1995;7:197-9.
  6. Levitan RM, Kinkle WC, Levin WJ, Everett WW. Laryngeal view during laryngoscopy: a randomized trial comparing cricoid pressure, backward-upward-rightward pressure, and bimanual laryngoscopy. Annals of emergency medicine 2006;47:548-55.
  7. Garrard A, Campbell AE, Turley A, Hall JE. The effect of mechanically-induced cricoid force on lower oesophageal sphincter pressure in anaesthetised patients. Anaesthesia 2004;59:435-9.
  8. Chassard D, Tournadre JP, Berrada KR, Bouletreau P. Cricoid pressure decreases lower oesophageal sphincter tone in anaesthetized pigs. Canadian journal of anaesthesia = Journal canadien d’anesthesie 1996;43:414-7.
  9. Heath KJ, Palmer M, Fletcher SJ. Fracture of the cricoid cartilage after Sellick’s manoeuvre. British journal of anaesthesia 1996;76:877-8.
  10. Ralph SJ, Wareham CA. Rupture of the oesophagus during cricoid pressure. Anaesthesia 1991;46:40-1.

 

EMCrit Wee – Sean Townsend of the SSC and the ProCESS Trial

debate

seantownsendRecently, I got to talk to Sean Townsend, MD; a critical care doc and a member of the Surviving Sepsis Campaign (SSC) steering committee. The spark for this conversation was the recent SSC response to the ProCESS trial (read below) as well as the elimination of CVP and ScvO2 from the National Quality Forum (NQF) sepsis bundle.

Surviving Sepsis Campaign Responds to ProCESS Trial

The Surviving Sepsis Campaign (SSC) has received many inquiries regarding the recent publication of the Protocol-Based Care for Early Septic Shock (ProCESS) trial’s effect on the continuing activities of the Campaign.

  1. The ProCESS trial reflects the consensus that early diagnosis of septic shock is essential. Notably, all groups in the study received on average more than 2 liters of fluid prior to randomization and more than 75% received antibiotics prior to randomization–both elements of the 3-hour Surviving Sepsis Campaign bundle. (2) The editorial accompanying the ProCESS study highlights these points. (3)
  2. The 18% mortality rate in the “usual care” arm of ProCESS illustrates a dramatic change in the management and outcomes of patients with septic shock. (1) In comparison, septic shock mortality was 46.5% in the 2001 early goal-directed therapy trial by Rivers. (4) Given that 70% of the hospitals in ProCESS had some form of “sepsis protocol,” we believe this mortality rate demonstrates the success of the SSC in increasing awareness and attention to the challenge of early identification and management of these vulnerable patients.
  3. Given the remarkably low mortality rate in the control arm of ProCESS, the existence of sepsis protocols in the majority of participating study institutions, and the pending results of 2 large ongoing trials (the Australian Resuscitation In Sepsis Evaluation Randomised Controlled Trial [ARISE] and The Protocolised Management in Sepsis Trial [ProMISe]), the SSC has no plans to revise the bundles or National Quality Forum (NQF)-endorsed measures at this time.
  4. ProCESS does not address the protocolized management of patients with severe sepsis without septic shock, a group of patients for whom early detection and treatment remain critical. The aggressive protocolized management of these patients who do not yet have shock has likely lowered severe sepsis and septic shock mortality since the inception of the SSC. The recently formed Society of Critical Care Medicine/Society of Hospital Medicine (SCCM/SHM) Early Diagnosis and Treatment of Severe Sepsis on the Hospital Floors Collaboratives will focus in large part on this population. Further, the ProCESS results have no impact on the 3-hour bundle, which is the primary focus for the Collaboratives.
  5. Regarding the SSC 6-hour bundle:
  1. A companion paper appears to support a mean arterial pressure (MAP) target of 65 mm Hg, which is one of the indicators in this bundle. (5)
  2. The ProCESS paper does not address repeating lactate measures in patients with elevated lactate while literature supports doing so. (6,7)
  3. The majority of the patients in the usual care (56.5%) and protocol-based standard care arms (57.9%) of ProCESS had central lines inserted as part of clinical care. (1) The 6-hour bundle asks only that central venous pressure (CVP) be measured and that a venous blood gas be sent from that line to obtain the central venous oxygen saturation (ScvO2). The ProCESS manuscript does not state how the CVP line was used in the usual care arm nor in the protocol-based standard therapy arm. Similarly, the NQF-endorsed measures of SSC do not set targets for these variables so credit is given for simple collection of the results. (8)

The Surviving Sepsis Campaign looks forward to additional evidence regarding the optimal resuscitation of patients with severe sepsis and septic shock. Given the existing evidence supporting early targeted resuscitation in these patients, SSC continues to recommend all elements of the current bundles.

References:

1. Yealy DM, Kellum JA, Juang DT, et al: A randomized trial of protocol-based care for early septic shock. N Engl J Med 2014; DOI: 10.1056/NEJMoa1401602

2. Dellinger RP, Levy MM, Rhodes A, et al: Surviving Sepsis Campaign: International guidelines for management of severe sepsis and septic shock: 2012. Crit Care Med 2013; 41:580–637

3. Lilly CM. The ProCESS Trial –a new era of sepsis management. N Engl J Med 2014; DOI: 10.1056/NEJMe1402564

4. Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med 2001; 345:1368-1377

5. Asfar P, Meziani F, Hamel JF, et al. High versus low blood-pressure target in patients with septic shock. N Engl J Med 2014; DOI: 10.1056/NEJMoa1312173

6. Jones AE, Shapiro NI, Trzeciak S, et al. Lactate clearance vs central venous oxygen saturation as goals of early sepsis therapy: a randomized clinical trial. JAMA 2010: 303:739-746

7. Jansen TC, van Bommel J, Schoonderbeek FJ, et al. LACTATE study group: Early lactate-guided therapy in intensive care unit patients: A multicenter, open-label, randomized controlled trial. Am J Respir Crit Care Med 2010; 182: 752-761

8. www.Qualityforum.org

Now on to the Wee…

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EMCrit Wee – A Cric Case with Rob Bryant

baby-cric

The Case:

Rob got permission to share:

INITIAL PRESENTATION:

30 year old male with past history of SCC of the tongue at age 14 who presented with cough, and dyspnea with concerns for recurrent pneumonia. He was still on antibiotics and steroids after a recent hospitalization for pneumonia.

His cancer recovery was hampered by osteo-radio-necrosis of his jaw, and he was left with a scarred larynx, baseline trismus with incisor to incisor distance of <2cm, and some thickening of the anterior neck tissues. He had a G-tube for feeding.

He had normal room air sats, no stridor, productive cough and no fever. Chest Xray was normal, and he was considered safe to go home and follow up with his pulmonologist the next day. The family was nervous about going home so he was observed overnight in the ED.

A very specific discussion was has with the patient regarding the challenges emergent management of his airway would represent:

“I love to manage airways, but your airway scares me, and I would never want to be the one to intubate you”

“If you have an airway emergency on the floor, it would take longer for someone to cric you than if you had an airway emergency at home, and had to present via ems and have a surgical airway performed in the ED”

He was discharged from the ED the next morning with some racemic Epi to try at home.

 

RE-PRESENTATION:

He represented 4 days later in respiratory distress with 36 hours of ‘anxiety’ symptoms that had not been helped by escalating doses of benzodiazepines.

No fever, no cough, very hoarse voice at home.

 

HR 140, BP 160/110, RR 29. Sats 86% RA, 98% 15L NRB

ETCO2 84.

 

Altered, sweaty, moving minimal air, and non verbal with significant stridor.

Initial interventions:

Racemic epi nebs,

125mg solumedrol iv

Glycopyrollate 0.2 mg iv.

Lido 4% neb.

 

VBG: pH 7.17, pCO2 104.

 

Anesthesia was called for Awake FiberOptic Intubation (AFOI) if a trial of BiPAP failed. Due to concerns that NIV could worsen his laryngeal irritation, or that giving Ketamine to help him tolerate the BiPAP could cause laryngospasm (est 1:200 risk) BiPAP was not started until anesthesia was present and ready to perform AFOI.

 

Anesthesia presented promptly and agreed with AFOI plan after BiPAP.

Beside table was set up with 4×4’s with betadine, trach (6.0mm), pocket bougie, and #10 blade scalpel, and gloves. Lido 1% w epi was prepared.

Pt kept at 20 degrees HOB elevation, NC at 15L, then BiPAP at 15/5 was started with no decrease in his work of breathing.

 

3 AFOI attempts were made, with each attempt aborted once sats hit 90%, the patient was hard to bag due to laryngeal stenosis, but with assisted spontaneous ventilations additional attempts were considered appropriate.

The neck was palpated, and prepped prior to first AFOI, and injected w lido w epi after 2nd AFOI.

3rd AFOI was with glidescope assist. Glidescope could barely fit into the mouth, and there were no obviously recongnizable laryngeal structures.

During 3rd AFOI cricothyroid membrane was punctured with 27g needle on the Lidocaine with epi syringe and air was aspirated to confirm location.

The patient received 1mg per kg Ketamine iv prior to incision for cricothyrotomy.

With sats of 92%, a midline 3cm incision made, then horizontal incision 1.5cm through the cricothyroid membrane. There was a small spray of blood and air, and audible air movement was present in the wound.

A Bomimed Pocket bougie was placed with some digital guidance, and advanced into the trachea. No tracheal rings were obviously palpable, and I did not forcefully check for bougie holdup.

A 6.0 mm external diameter Shiley trach was railroaded over the bougie, with some hangup at the skin level, it was then advanced with firm pressure into the trachea.

Oxygen saturations were 68% at time of Shiley passage, 25-30 seconds after procedure start time. Airway confirmation was with ETCO2 detected immediately, good breath sounds and chest rise, and rising oxygen saturations.

Post intubation analgosedation was with fentanyl bolus and drip, and propofol.

 

Holy Sh-t, Right!!!

Update: See this amazing story posted on G+ Community as well

Now, on to the Wee…

 

 

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Wee – What the heck is a Mapleson B Circuit and Why You Probably Shouldn’t Care

Mapleson-b

There is a really smart anesthesiologist out there called Nicholas Chrimes. He along with his mate Peter Fritz invented the Vortex Approach to Airway Management. He also runs a blog called Clinical CrEd.

He did a post advocating the Mapleson B Circuit as the Ultimate Preox Device

What is the Mapleson B? The Mapleson circuits were used for anesthetics in the good old days. At least in the US, we have move to bigger, and arguably better designs for our operative patients. Many would have thought this device would have been consigned to the trash heap, but seemingly not.

Mapleson Circuit

from anesthesia 2000

My Recommended Approaches

I recommend two approaches to preox: standard and shunt physiology strategies. I outlines these strategies in the paper Rich Levitan and I wrote.

Standard: NRB @ >=15 lpm and NC @ 10-15 lpm for 3 minutes

Shunt Physio: Choose 1

  • BVM with PEEP Valve & NC @ 10-15 lpm
  • NIPPV Ventilator with NIPPV Mask or BVM Mask & NC @ 10-15 lpm

Nick makes a number of arguments as to the superiority of the Mapleson circuit over these standard techniques. His points are excellent, but I disagree with pretty much all of them–I think it becomes a question of perspective.

Automatic Checking

Yes, using the same device for reox and preox makes sure the reox device is there and hooked up, but this for me is an inadequate argument to dispense with NRB/NC set-up.

Multiple BVM Masks

We don’t have these readily available in any ED or ICU I’ve worked in. We have neonate, peds, and adult. Our masks also are not inflatable.

PEEP

PEEP is good, Mapleson may or may not be a good way to provide this for the reasons I’ve mentioned in the wee, but a BVM with a PEEP valve or a vent are at least as good.

ApOx

Mapleson may provide this better than BVM, but not as well as a NC, which should be on during any intubation.

ETCO2

No advantage of Mapleson

Low resistance

Maybe this matters, as soon as you put on the PEEP, I can’t imagine this difference persisting

Room Air Entrainment

Release your seal for even one breath and you have blown denitrogenation. Always, always use a strapped system if possible=NRB/NC, NIV mask, or BVM mask with OR straps.

Troubleshooting Leaks

This is the real area in which Nick and I differ. Nick makes the point that a good seal in preox guarantees a good seal in reox–this may be true, but it is unimportant. What I care about is does a bad, one-handed seal in preox mean I won’t be able to reox with the BVM–this is entirely untrue. If I did to an awake patient what I will do to them when asleep and desaturating, they would, quite rightfully, punch me in the face.

Anesthesiologists should use Mapleson B/C; ED/ICU should only use BVM +/- PEEP Valve with two hands and oral airway and a rocking triple maneuver (that no pt should experience if they are conscious) otherwise they should be NIV mask with straps or (BVM mask with straps).

This is the same reason I tell my residents to just train with Macintosh blades.

Primary and secondary leaks are the main thrust of Nick’s love for the old-timey circuits. But all of us have appreciated this easily by squeezing the bag-valve-mask: Easy-squeezy or Hard Squeezy

ETCO2 with a monitor you can see

Is he holding or squeezing?

I can feel compliance with a BVM if I squeezed it, but I don’t unless the pt needs it during reox. But are they squeezing the Mapleson? If they are, they may be doing damage. This study (Anesthesiology 2014;120:326) talks about the myths of Gentle Facemask Ventilation:

>15 cmH20 may be entraining gas into the stomach via the LES (in some patients, even 10 cmH20 may be a problem)

UES will withstand at least 20 cmH20 until NMB at which point again 15 seems to be the number (The latter is why we don’t bag during apnea unless we have to)

Two hands ALWAYS on the mask

Recently, I spent 2 weeks intubating 10-15 patients per day. One hand mask skills got better and better–all for naught.

Train how you want to Fight

Hands free

BVM with a PEEP valve solves equipment issues entirely

ventilator or oxylator

Better BVMS

Lower possible Vt and restriction of Inspiratory Flow Time (Maybe a peds bag is the answer–thanks, Peter. Anaesthesia. 2011 Jul;66(7):563-7 and Resuscitation 1999;43(1):31) and Vt of 500 seems the way to go (Crit Care Med. 1998 Feb;26(2):364-8.)

or Use Ventilator or Use an Oxylator

Now on to the wee…

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