For Jen:

Click here to view the embedded video.

Go to Vimeo to see in Full HD Glory

You just read the post: How to Use RSS Feeds to Follow Medical Blogs on your IPAD from EMCrit Blog - Emergency Department Critical Care.

An anonymous EM Intensivist writes:

Scott,

I am writing to comment on a trend that I’m noticing among my residents, and I wonder if others are noticing a similar trend.  I am an emergency physician and an intensivist at the University of XXXXXXX, and I have a number of EM residents who avidly listen to your podcasts.

 

Over the course of the last year, most of our residents have made the transition to using rocuronium for RSI (mostly based on recommendations from your podcast, I think).  I use rocuronium preferentially as well, for many of the same reasons that you cite.

 

What has not accompanied the use of rocuronium, though, is an accompanying willingness to provide adequate sedation and pain control.  I find that this is especially true with trauma intubations.  I would say that the usual course of events goes something like this: etomidate and rocuronium for RSI, tube goes in, patient is hypotensive (trauma patient), so patient gets crystalloid or blood during emergent evaluation.  After 5-10 minutes, blood pressure and HR start to trend back up, and most everyone in the trauma bay is patting themselves on the back because they have resuscitated a hypotensive trauma patient.  They are going to CT.

 

In the old world order (the etomidate and sux days) — which I do NOT think was better — the clinical course would be the same … except.  After 10-15 minutes, that hypotensive trauma patient would start coughing (with better vitals), then would sit up and give someone the finger while he was preparing to pull his endotracheal tube out.  The janitor would peer into the trauma bay and would recognize a trauma patient who needs sedation, and sedation would be provided.

 

Now, everyone is hesitant to give long-acting sedative medications to our patients immediately post-intubation, because pts are “sedated” and we’re worried about hypotension.

 

I think that this is an unintended consequence to the transition of moving to rocuronium as a paralytic agent for RSI.  I think it’s a great drug, but I think that when the tube goes through the cords, the intubator needs to announce to everyone in the room “I’ve given a paralytic drug that lasts for an hour, the sedative agent that I gave does not, so we are going to give ___ right now so that this guy does not wake up paralyzed.”  Propofol infusion +/- fentanyl, bolus of midazolam and dilaudid — I don’t really care what people use, but I think that the way that people are starting to practice is to unintentionally use pain and awareness as a pressor, and I hate to see this happen.  I also think that people need to think to watch the vitals and respond with sedation as necessary.  I had one case of a SAH that started with intubation and ended with a resident using labetalol IVP for HTN that started about 20 minutes after intubation.  In many of these patients, propofol can be a very effective antihypertensive.

 

I have not done in depth analyses to see what our patients remember (perhaps we should), but I’m a little worried that someone out there is aware of their resuscitation while they are paralyzed because we are not rigorously applying the pharmacokinetics we know about the agents we are using.  I think that in some cases, their physiology would suggest that they might.

 

Thanks for all the good work you do for our community,

N.

This wee is my audio response. But to sum it up:

• If you are going to use roc, you better be starting sedation the second you are done securing the tube
• There is no patient so unstable that they do not deserve analgesia and sedation.

You just read the post: Pain and Terror as Effective Pressors from EMCrit Blog - Emergency Department Critical Care.

Recently, Minh had some questions for James DuCanto on fiberoptics and airway management in general. Here were the questions:

1. Some anaesthetists I talk to argue that if you are going to get an optical or video assisted airway device then having it in the same design or functional shape as your traditional devices like the Macintosh laryngoscope, makes more sense than having devices that are of different designs. The Levitan FPS stylet is clearly no Macintosh shape design. What are your thoughts on video laryngoscopes more akin to the traditional Macintosh device like the CMAC versus the Levitan FPS?
2. We describe a technique of insertion of an intubating LMA then fibreoptic guided stylet assisted intubation. In what situations have you found this helpful, in your experience?
3. In an earlier post you mention having performed a needle cricothyrotomy and rescue jet oxygenation using a dedicated jetting device. It was successful?
4. What about ketamine assisted awake intubation?
5. How do you intubate through a laryngeal tube airway?

and boy did Jim have answers.

Jim DuCanto is an incredibly prolific anesthesiologist from Wisconsin.

Links Mentioned in the Show

• Jim DuCanto’s Intubating Videos
• Jim’s Guide to the Cookgas
• Reference for Mouth, Screen, Mouth, Screen (Anesth Anal 2007;104:1611)
• My skills of laryngoscopy video
• Seth Manoach Cric-ing a Sheep
• My Awake Intubation Video

Minh Le Cong has a new podcast–check it out to hear a 1-hour Q&A with Jim DuCanto: prehospitalmed.com

If you are listening to the show, why not get CME as well?

need an audio-only version of the video podcast below? Right Click Here and Choose Save-as

Now on to the podcast…

You just read the post: Podcast 73 – Airway Tips and Tricks with Jim DuCanto, MD from EMCrit Blog - Emergency Department Critical Care.

Minh has taken Laryngoscope as a Murder Weapon^TM to a new level with his presentation: Doctors with Guns. See his slideset…

Minh’s doctors with guns

and even better, Minh dug up this lecture which deserves highlighting:

Click here to view the embedded video.

You just read the post: Minh’s Airway Slides from EMCrit Blog - Emergency Department Critical Care.

I get a ton of clinical cases and questions by email or the contact form on the blog. I love this–it exposes me to some great cases I would never hear about otherwise. Problem is, up until this point, it has been a 1 on 1 conversation. This is sort of a waste because nobody else benefits except you and me. So in the future, when you have a  case or question like this, I would love it if you posted to the Google Plus EMCrit page. This allows a few things:

1. it allows my answer to be seen by a much larger group of people
2. it allows folks smarter than me to chime in as well
3. it keeps a record of these case interactions so I can refer people to them in the future

So how do you do it? Easiest way to learn is to watch this video:

Click here to view the embedded video.

Here are the Steps Outlined

1. Go to the Google Plus EMCrit page

2. Click on the follow link

3. You may be asked to log-in or create a google account

4. Go to the share button in the upper right of the screen

5. Type “+emcrit” and choose the emcrit logo that appears

6. Type in your case

7. Make sure to leave the public sharing alone

8. Click Share

9. Check back on the EMCrit Google Plus Page to see the responses

You just read the post: How to Post a Case or Question to EMCrit Google Plus from EMCrit Blog - Emergency Department Critical Care.

James DuCanto just emailed me with a guide to intubating through LMAs. My first question, of course, is can I share it with the listeners, so…

Here is the guide

You just read the post: A Guide to Intubating through the Intubating Laryngeal Airway by James DuCanto from EMCrit Blog - Emergency Department Critical Care.

Hemodynamically unstable pelvic fractures are a talk-and-die situation. These folks require aggressive, rapid treatment if they are going to survive the injury. Inspired by my mentor, Thomas Scalea, I discuss the management of the unstable pelvic trauma patient.

Read these Incredible Posts by Chris Nickson

Part I

Part II

Young-Burgess Shock Trauma Pelvic Fracture Classification

(J Trauma 30(7): 848-856)

from the handbook of fractures

Open Iliac Artery Clamping

Dubose and Inaba (J Trauma. 2010;69: 1507?1514)

How to Kill when Intubating

Forgot to mention on the podcast–The combination of an open-book pelvis that you have not bound yet and paralytics is a great way to cause massive bleeding. Bind the open pelvis before tubing!!!

New East Pelvic Trauma Guidelines

(J Trauma 2011;71(6):1850)

• external fixation doesn’t limit blood loss, but reduces fracture displacement (III)
• unstable patients should get angio (I)
• pts with blush may require angio even if stable (I)
• ongoing bleeding after angio should get repeat angio (II)
• >60 y/o with major fx should get angio even if stable (II)
• anterior fxs assoc with ant vessel injury and posterior = posterior (III)
• Bilateral non-selective is safe, gluteal ischemia is more likely from injury not angio (III)
• And doesn’t affect male potency (III)
• FAST is insensitive in pelvic trauma (I)–don’t agree with this one
• Adequate Specificity (I)
• DPA is test of choice (II)
• Use CT if stable (II)
• Fracture pattern doesn’t predict need for angio (II)
• Nor hematoma location (II)
• Absence of ICE doesn’t exclude active hemorrhage (II)
• Volume > 500 cm3 predicts need for angio (III)
• Isolated acetabular fx may still need angio (III)
• Perform cystogram after ct (III)
• Binders reduce fx as well as definitive stabilization and decrease pelvic volume (III)
• And they limit hemorrhage (III)
• They work as well or better than external fixation in controlling hemorrhage (III)
• RetroP Packing can be used to salvage after failed angio (III)
• Can be used as primary in an integrated protocol (III)

You just read the post: Severe Pelvic Trauma from EMCrit Blog - Emergency Department Critical Care.

Tim Ellender, EM Intensivist and all around cool guy just dropped his picks for the top EMCCM articles all trainees and attendings must read:

1. Hébert PC, et al. A multicenter, randomized, controlled clinical trial of transfusion requirements in critical care. Transfusion Requirements in Critical Care Investigators, Canadian Critical Care Trials Group. N Engl J Med. 1999 Feb 11;340(6):409-17. Erratum in: N Engl J Med 1999 Apr 1;340(13):1056.
2. The Acute Respiratory Distress Syndrome Network. Ventilation with Lower Tidal Volumes as Compared with Traditional Tidal Volumes for Acute Lung Injury and the Acute Respiratory Distress Syndrome. N Engl J Med 2000; 342:1301-1308.
3. Michard F, et al. Relation between respiratory changes in arterial pulse pressure and fluid responsiveness in septic patients with acute circulatory failure. Am J Respir Crit Care Med 2000; 162:134-138.
4. Rivers M, et al. Early Goal-Directed Therapy in the Treatment of Severe Sepsis and Septic Shock. N Engl J Med 2001; 345(19): 1368-77.
5. Bernard SA, et al. Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. N Engl J Med. Feb 21 2002; 346(8):557-63.
6. Hypothermia after Cardiac Arrest Study Group. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med. Feb 21 2002; 346(8):549-56.
7. Annane D, et al. Effect of treatment with low doses of hydrocortisone and fludrocortisone on mortality in patients with septic shock. JAMA 2002; 288:862-871.
8. The SAFE Study Investigators. A Comparison of Albumin and Saline for Fluid Resuscitation in the Intensive Care Unit. N Engl J Med 2004; 350:2247-2256.
9. Nguyen HB, et al. Early lactate clearance is associated with improved outcome in severe sepsis and septic shock. Crit Care Med 2004; 32:1637-42.
10. Jones AE, et al. Randomized, controlled trial of immediate versus delayed goal-directed ultrasound to identify the cause of nontraumatic hypotension in emergency department patients. Crit Care Med 2004; 32:1703-8.
11. Cremer OL, et al. Effect of intracranial pressure monitoring and targeted intensive care on functional outcome after severe head injury. Crit Care Med 2005; 33:2207–13.
12. Kumar A, et al. Duration of hypotension before initiation of effective antimicrobial therapy is the critical determinant of survival in human septic shock. Crit Care Med 2006; 34: 1589-1596.
13. Marik PE, et al. Does central venous pressure predict fluid responsiveness? A systematic review of the literature and the tale of seven mares. Chest 2008; 134:172–178.
14. Sprung CL, et al. Hydrocortisone therapy for patients with septic shock. N Engl J Med 2008; 358:111-124.
15. Russell JA, et al. for the VASST Investigators. Vasopressin versus Norepinephrine Infusion in Patients with Septic Shock. N Engl J Med 2008; 358:877-887.
16. De Backer D, et al. Comparison of dopamine and norepinephrine in the treatment of shock. N Engl J Med 2010; 362:779-789.
17. CRASH-2 trial collaborators. Effects of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage (CRASH-2): a randomised, placebo-controlled trial. Lancet 2010; 376(9734):23-32.
18. Kilgannon JH, et al. Association Between Arterial Hyperoxia Following Resuscitation From Cardiac Arrest and In-Hospital Mortality. JAMA 2010; 303:2165-2171.
19. Jones AE, et al. Lactate Clearance vs Central Venous Oxygen Saturation as Goals of Early Sepsis Therapy: A Randomized Clinical Trial. JAMA. 2010;303(8):739-746.
20. Perera P, et al. The RUSH exam: Rapid Ultrasound in SHock in the evaluation of the critically lll. Emerg Med Clin North Am. 2010; 28(1):29-56.
21. Vandromme MJ, et al. Identifying risk for massive transfusion in the relatively normotensive patient: utility of the prehospital shock index. J Trauma. 2011; 70(2):384-8.

You just read the post: Top EMCCM Articles from Tim Ellender from EMCrit Blog - Emergency Department Critical Care.

You’ve got to love the twitter! Seth Trueger (@mdaware) tweeted that his EM Attending brother-in-law, Charles Maddow, has started using bougies to guide in thoracostomy tubes on morbidly obese patients with thick soft tissue around the entry site. I worried whether the bougie is long enough to allow a sig. portion to be placed in the chest cavity but still allow seldinger maneuver.

My amazing friends from (@HQMedEd) sent this photo:

Click to Enlarge

Then Graham Walker (@grahamwalker) pulled this shot from his sim lab:

Click to Enlarge

Minh (@rfdsdoc) mentioned this article where they used a similar technique with ET tubes instead of chest tubes, originally posted on Cliff’s (@cliffreid) blog.

You just read the post: Bougie-Guided Chest Tube from EMCrit Blog - Emergency Department Critical Care.

A few years ago, John McGill, of the Hennepin Crew posted an amazing video on bougie placement

Click here to view the embedded video.

Now we have a sequel to take you to next level of bougie use

Click here to view the embedded video.

You just read the post: How to Place a Bougie from John McGill from EMCrit Blog - Emergency Department Critical Care.

Can we monitor ETCO2 with extraglottic airways? The answer is definitive–I don’t know.

You just read the post: EMCrit Wee – ETCO2 with EGA? from EMCrit Blog - Emergency Department Critical Care.

Today, I got to interview Kenji Inaba; an incredibly prolific trauma surgeon from USC/LA County, California. He is the SICU director and surgical critical care fellowship director. If you flip through any issue of the Journal of Trauma, odds are good that Kenji will have an article there.

Here are the questions I got to ask:

From the military studies, 1:1 (PRBCs to FFP) has emerged as the goal during hemostatic resuscitation. The civilian data is less robust, but there are cohort studies out there. Some of them suffer from survival bias and confounding by indication, but enough is out there for most of US trauma centers to attempt to meet the 1:1 goal? What are you folks doing at USC?

This excellent editorial (Resuscitation 82 (2011) 627–628) discusses the problems with 1:1 civilian studies and why we should shoot for this ratio anyway.

What is your transfusion goal with your 1:1. We are giving a mix of PRBC and FFP whenever the patient’s MAP drops below 65 and we don’t even bothering looking at the labs to determine which of these two products the patient needs. We are using them just like some saline in the dehydrated patient. If their MAP drops below our goal, they get the PRBC and FFP 1:1 until we get the MAP back up. How about you folks?

For more on this see Rich Dutton’s Interview

Where do platelets fit into the mix? At many hospitals they are not available in large amounts and most places are using old platelets and non-type-specific platelets. Some of your own work is on this very subject, should we be matching 1:1 with platelets as well? How about if we only have old, non-type-specific products?

See Kenji’s Paper on the topic of old platelets.

Now most of our European and Canadian Colleagues have moved to concentrates instead of FFP and platelets. They use PCCs and fibrinogen concentrates in the initial stages of the hemostatic resuscitation. Is this the future?

Are you using TEG or ROTEM, if so how does this fit into the picture? Should it be available in the ED, the OR?

Let’s talk TXA. I interviewed Tim Coats, one of the lead authors of Crash 2, last week—he advocates using it with any trauma patient who will need any amount of PRBCs, and to give it as early as possible. I think I agree with him. When are you USC guys giving TXA?

MATTERs trial shows that intermittent boluses may be effective rather than starting the infusion. We are giving the 10-minute bolus in the trauma room and then deferring infusion to the STICU if the patient still has active bleeding. Starting an infusion in the trauma bay can be frustrating when we are trying to pour blood products in. How about you?

Are you using Rh specific in males? If you give O+ to an Rh – male are you giving rhogam?

This is the AAST Plenary Paper (J Trauma 2012;72(1):48) we mentioned

I am a member of the Kenji fan club; I think you folks will be as well after hearing his sincerity and brilliance.

You just read the post: Podcast 71 – Critical Questions on Massive Transfusion Protocols with Kenji Inaba from EMCrit Blog - Emergency Department Critical Care.

Two studies were mentioned:

Hagihara A, et al. Prehospital Epinephrine Use and Survival Among Patients With Out-of-Hospital Cardiac Arrest. JAMA. 2012;307(11):1161-1168

See Ryan’s blog for some great commentary.

&

The PACA Trial: Jacobs et al. Effect of adrenaline on survival in out-of-hospital cardiac arrest: A randomised double-blind placebo-controlled trial. Resuscitation. 2011 Sep;82(9):1138-43.

You just read the post: EMCrit Wee – Abandon Epinephrine? from EMCrit Blog - Emergency Department Critical Care.

The best lecture on Airway Management–Ever?

Rich Levitan is one of the best teachers on the skills of laryngoscopy–or as he would probably put it, epiglottoscopy. Here is an hour long lecture he delivered last month at Mount Sinai School of Medicine. It is surely one of the best airway lectures I have ever heard.

Want to hear more from Dr. Levitan? Visit his airway site at airwaycam.com.

or, read his incredible book:

Get a big discount on the Emergency Medicine Critical Care Journal

Just go to ebmedicine.net/emcrit

Want the handout?

Here are Rich Levitan’s Slides

Audio-Only Version

Right-Click on this Link and Choose Save-as

This episode is eligible for CME

Now, on to the Vodcast…

You just read the post: Podcast 70 – Airway Management with Rich Levitan from EMCrit Blog - Emergency Department Critical Care.

Long time friend of the show, Ram Reddy, has started compiling an excellent set of videos on youtube. One of them brings an ENT surgeon and Ram himself to a cadaver lab to explore all of the permutations of surgical cricothyrotomy.

Click here to view the embedded video.

For more videos from Ram, go to the EM London Ontario Youtube Site.

You just read the post: Even More on Surgical Cricothyrotomies from EMCrit Blog - Emergency Department Critical Care.

Ketamine sedation is effective and safe in agitated patients with a psychiatric illness in the aeromedical setting and does not lead to worsening agitation in the subsequent 72-h period. (Emerg Med J 2012;29:335)

You just read the post: Minh’s Ketamine Article from EMCrit Blog - Emergency Department Critical Care.

I am not arrogant enough to believe that I can understand any man’s or woman’s motivations, so I only argue their words & actions, but I don’t force this viewpoint upon any of you. I do ask that you name yourself on any comments, accurately and in a verifiable manner. If you do that I will publish anything you write only editing out curse words for the delicate eyes of my listeners.

This wee was prompted by comments on episode 69.

This post is closed for comments, please go to the link above to make comments regarding this post.

You just read the post: EMCrit Wee – On Editing Comments and Ad Hominem Attacks from EMCrit Blog - Emergency Department Critical Care.

The Future of CPR

I got to interview two cutting edge researchers on what CPR will look like in the next decade; their answers were fascinating.

Flow-Enhanced CPR

They discuss the use of the impedance threshold device and the active-compression/decompression device to augment flow during CPR. See the results of the ResQ trial listed below to see what this does in cardiac arrest patients.

Note: Dr. Lurie is the founder, chief medical officer, and a major shareholder of the company that manufactures these two devices. Dr. Yannopoulos has no conflicts of interest.

Reperfusion Injury Protection

Stutter CPR is giving 3 cycles of 20 seconds of compressions/ventilations, 20 seconds of pause. In pigs, this has markedly reduced the reperfusion injury when resuscitating a patient with prolonged arrest.

New Medications

Sodium nitroprusside (in addition to small doses of epi and flow-enhanced CPR) increases flow to the heart and the brain. May also blunt reperfusion injury to heart and brain. In addition adenosine and cyclosporine A may have a role as well.

Note: None of this is ready for clinical use–this may be the future, it is not the present

Want More?

• A presentation on the topic by Dr. Yannopoulos
• Read the ResQ Trial (Lancet  2011;377(9762):301–311)

Supplemental Audio

More on the ROC-Primed Trial and the ResQ Trial (MP3 File–Right Click and choose Save As)

More on Dosing and Intra-Arrest Hypothermia and Cath (MP3 File–Right Click and choose Save As)

This podcast is eligible for EMCrit CME

And Now to the Podcast…

You just read the post: EMCrit Podcast 69 – The Future of CPR with Keith Lurie and Demetris Yannopoulos from EMCrit Blog - Emergency Department Critical Care.

From Minh’s Interview, I stole this five minute piece for an EMCrit Wee.

Cliff Reid discusses some tips for occasional intubators.

You just read the post: EMCrit Wee – Cliff Reid’s Tips for Occasional Intubators from EMCrit Blog - Emergency Department Critical Care.

This is a recording of the first EMCrit Live episode. Hope you enjoy.

Please check out the new EMCrit CME Site!

You just read the post: EMCrit Live Show # 1 from EMCrit Blog - Emergency Department Critical Care.

Crash 2 and Tranexamic Acid

One of the most exciting and underutilized therapies for trauma is tranexamic acid (txa). TXA inhibits the breakdown of clot–it is an anti-fibrinolytic. Is there evidence for using this in trauma patients?

First came the Crash 2 Trial (Effects of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage (CRASH-2): a randomised, placebo-controlled trial. Lancet 2010; 376: 23–32),

then the subgroup reanalysis (Lancet. 2011 Mar 26;377(9771):1096) showing the benefit of treatment as early as possible.

Recently, the MATTERS trial (Arch Surg. 2012; 147:113-119) was published demonstrating the benefits of TXA in military situations, particularly massive transfusion.

How about an incredible review from the J Trauma (2011; 71(1) Supplement S9)

Then there is this paper describing current military protocol rationale.

To discuss TXA in Trauma, I got to interview Dr. Tim Coats, one of the primary authors of Crash 2.

Here is a List of Resources from the Crash 2 Investigators

This is the official resource page from Crash 2

We also discussed the concept of the pragmatic trial…

Future Research in Emergency Medicine: Explanation or Pragmatism

(Emerg Med J 2011;28(12):1004)

Listen to the podcast excerpt on pragmatic trials (mp3–right click the link and choose save-as if you want to download)

In an amazing demonstration of synchronicity, Jeff Guy of the ICU Rounds Podcast put out a tranexamic acid episode on the same day.

Minh Le Cong provided this prehospital protocol for TXA use.

An incredible review article can be found at this citation (Journal of TRAUMA 2011;71(1) July Supplement)

Now, on to the podcast…

You just read the post: Podcast 67 – Tranexamic Acid (TXA), Crash 2, & Pragmatism with Tim Coats from EMCrit Blog - Emergency Department Critical Care.

If you want to understand this post you probably need to listen to the episode on c-spine imaging approach and the follow-up regarding the evidence behind it.

Mike Wells from Scotland Writes:

Hi Scott,

Your two excellent podcasts on C spine imaging really got me thinking.
I work in the UK where resource constraints within our public
healthcare system mean that even if I wanted to, I would not be able
to obtain CTs as the first imaging port of call for all my neck trauma
patients. I can however argue individual cases with the radiology
department and therefore effectively need to try to choose high risk
patients.

I pulled the Canadian C spine and NEXUS studies and looked back
through their methodology and results. In both studies ordering a neck
CT was at the discretion of the treating physicians – but most
patients only got plain C spine films (in CCspine 436 patients got CTs
= 7% of total patients who were imaged; for NEXUS I could find data to
allow me to make this calculation). I also went through the further
NEXUS study looking at missed fractures – another way of looking at
their data is that in the 581 patients with technically adequate C
spine films, only 3 unstable fractures were missed – giving a
sensitivity of 99.4% for the unstable injuries which I am most scared
of missing.

I absolutely agree with you though that very often plain films are
technically inadequate and that their sensitivity is therefore much
lower.

However I would argue that the real sensitivity we are interested in
is not that of C spine films alone, but rather than the sensitivity of
the combination of plain C spine films and clinical examination and
acumen. CTs in the NEXUS and Canadian studies were after all ordered
at clinician discretion. It’s possible that fractures were missed in
the patients who weren’t scanned but both studies did seem to attempt
follow up (NEXUS in particular checked local ‘event logs’ although I’m
not clear on what these are).

So I think over here in the NHS I would argue that in ‘minor’ trauma
patients failing the CCspine rule I am still obliged to use plain C
spine films as my first imaging step. On the basis of what you have
said I’ll will set the bar higher in terms of making sure films are
technically adequate (over here we still use Swimmer’s views, which I
detest). However for patients with adequate films and the roughly 3%
prevalence of fractures in the group failing Canadian C spine, I would
hope that my clinical exam would then identify those patients with
normal films but underlying injuries.

Utimately I think from my view what this is about is not the
sensitivity of plain films on their own – which I agree is
unacceptably low – but about the sensitivity of plain films + clinical
skills.

Please feel free to put this in your comments section if you wish!

Thanks again for your fantastic podcast and blog.

Best wishes

Mike Wells

Here is my response to Mike and the others who voiced similar questions about what to do when CT is not easily obtained…

You just read the post: EMCrit Wee – More on C-Spine Imaging from EMCrit Blog - Emergency Department Critical Care.

Minh Le Cong is a frequent guest and commenter on EMCrit. I have asked him, whenever inspiration strikes, to write guest posts on the blog. Minh is an airway guru and can share the unique perspective of a doc doing prehospital retrieval and care. Here’s Minh:

Needle Cricothyrotomy

Oxygenation with a needle cricothyrotomy based technique:

I want to provide a host of reference articles for you to decide for yourself the science and the practicality in the cannot intubate/cannot oxygenate  scenario. The astute reader will note the crucial difference between total upper airway obstruction model of research and the partially obstructed or unobstructed airway model. High pressure, high flow via a needle catheter carries a low safety index with the margin between safe oxygenation and lethal barotraumas being narrow. Short inspiratory times and long expiratory times ( ratio of more than 1:4 and ideally 1: 9) appear to be safest. In the more common situation of a partially obstructed or unobstructed airway but a failed intubation, failed BVM oxygenation and critical hypoxia, high flow oxygenation via a 14 G needle cannula is practical and much safer as pressure is released via the upper airway.

In his article, Patel describes successful repeat intubation in more than half of the rescue oxygenated patients using the needle cricothyroidotomy technique, avoiding the open surgical technique completely. Low flow transtracheal insufflations of oxygen at 2 l/min as demonstrated by the research Black, Janus and Grothwohl is even safer yet capable in their animal model of rescue oxygenating successfully for at least 1 hr. There are multiple case reports in the literature of human patients being successfully rescued using the needle catheter technique with a variety of improvised as well as dedicated transtracheal oxygenation setups. The reader must decide for themselves but it needs to be pointed out that the needle catheter technique is the only one that is most applicable across all age groups, with open surgical technique in children being even less practiced than in adults!

References compiled by Dr. Minh Le Cong, Jan 2012-01-02:

Patel RG. Percutaneous transtracheal jet ventilation: a safe, quick, and temporary way to provide oxygenation and ventilation when conventional methods are unsuccessful. Chest. 1999 Dec; vol. 116(6) pp. 1689-94. PMID: 10593796

Based on the subsequent insertion of an endotracheal tube into the trachea, there were two important benefits in the patients who underwent PTJV successfully. First, PTJV provided effective oxygenation, while allowing adequate time for upper airway visualization and possible suctioning of oropharyngeal secretions. Second, tracheal intubation was subsequently easier, possibly because the high tracheal pressure from the gas insufflation opened the collapsed glottis, making visualization of the glottic aperture better. PTJV is safe and quick in providing immediate oxygenation, and therefore should be considered as an alternative to insistent, multiple intubation attempts, when neither bag-mask-valve ventilation nor endotracheal intubation is feasible in providing adequate gas exchange.

Black IH, Janus SA, Grathwohl KW. Low-flow transtracheal rescue insufflation of oxygen after profound desaturation. PMID: 16294073

Low-flow TRIO rescued animals from profound hypoxia and maintained oxygenation for at least 1 hour. Low-flow TRIO did not prevent hypercarbia with its subsequent sympathetic activation.

Ayoub IM, Brown DJ, Gazmuri RJ. Transtracheal oxygenation : an alternative to endotracheal intubation during cardiac arrest. Chest. 2001 Nov; vol. 120(5) pp. 1663-70  PMID: 11713151

TTO was as effective as conventional positive-pressure ventilation with 100% O(2) for securing oxygenation, resuscitation, and short-term survival and more effective than O(2) delivered through a mask.

Jawan B, Cheung HK, Chong ZK, Poon YY, Cheng YF, Chen HS, Huang CJ, Lee JH. Aspiration in transtracheal oxygen insufflation with different insufflation flow rates during cardiopulmonary resuscitation in dogs. Anesth. Analg. 2000 Dec; vol. 91(6) pp. 1431-5

PMID: 11093994

We investigated whether transtracheal insufflation of oxygen with different insufflation flow rates protects against aspiration of gastric contents during cardiopulmonary resuscitation (CPR). Its ventilation and oxygenation effects were also evaluated. Cardiac arrest was induced in anesthetized and paralyzed 18 mongrel dogs. Chest compression using an automatic thumper was performed while the dogs randomly received no mechanical ventilation (Group I, n = 6) or were transtracheally insufflated with 4 L/min oxygen (Group II, n = 6) or 10 L/min oxygen (Group III, n = 6). Blood samples were drawn every 5 min for 20 min for blood gas analysis. the mouths of the dogs were then filled with 70 mL mixed barium, and 10 min after chest compression, chest radiographs were taken to evaluate the incidence of pulmonary aspiration. Results showed that pulmonary aspiration occurred in all dogs of Group I and three of the six dogs in Group II, whereas dogs in Group III were free from pulmonary aspiration. Both transtracheal oxygen insufflation groups maintained oxygen saturation significantly better than Group I, but mild hypercapnia was observed in all groups after 20 min of CPR. We conclude that transtracheal oxygen insufflation, but not chest compression alone, was able to maintain oxygenation for 20 min during CPR in dogs with cardiac arrest. Mild hypercapnia was noted in all groups. Chest compression alone caused pulmonary aspiration, whereas insufflation of 10 L O(2)/min provided better protection against pulmonary aspiration than that of 4 L O(2)/min.

Stothert JC, Stout MJ, Lewis LM, Keltner RM. High pressure percutaneous transtracheal ventilation: the use of large gauge intravenous-type catheters in the totally obstructed airway.Am J Emerg Med. 1990 May; vol. 8(3) pp. 184-9. PMID: 2331256

Percutaneous transtracheal ventilation using a large gauge intravenous-type catheter can be used successfully in the setting of complete upper airway obstruction in animals. In this study, using a large animal model, satisfactory oxygenation and ventilation was achieved by inversely varying the catheter size and the inspiration to expiration ratio (I:E). Specifically, 30 to 63 kg ruminants with an obstructed upper airway were resuscitated for 30 minutes from a hypoxic, hypercarbic, and acidotic state using 12- and 14-gauge catheters connected to a 50 psi oxygen source via a two-way valve with an I:E of 1:4 and 1:9 seconds, respectively. Shorter expiratory time or increased inspiratory time with these intravenous catheters resulted in significant hemodynamic compromise, barotrauma, inadequate carbon dioxide elimination, acidemia, and frequent death.

Now, Watch the Video…

Click here to view the embedded video.

You just read the post: Guest Post: More from Minh Le Cong on Needle Cricothyrotomy from EMCrit Blog - Emergency Department Critical Care.

The Lewis Lead (S5)

How to place the electrodes for the Lewis Lead (S5)

from Christopher Watford’s blog My Variables Only Have 6 Letters…

S5 Lead: You can produce this using many variations of the electrodes, however, for simplicity’s sake we will stick with Kelly’s description:

1. Place the Right Arm electrode on the patient’s manubrium.
2. Place the Left Arm electrode on the 5th intercostal space, right sternal border.
3. Place the Left Leg electrode on the right lower costal margin.
4. Monitor Lead I.

Image from Paramedic Watford

Lewis Lead Enhances Atrial Activity Detection in Wide QRS Tachycardia

The Lewis Lead – Making Recognition of P Waves Easy During Wide QRS Complex Tachycardia

Christopher’s ideal path to learning ECGs if he had to do it all again

1. Structured Learning: Garcia and Holtz “12-Lead ECG: The Art of Interpretation”

2. Depth of Knowledge: skip Dubin, get Chou’s/Goldman’s/Marriott’s (something with meat)

3. Deliberate Practice: read 1000′s of ECGs. Brady & Mattu “ECGs for the Emergency Physician“, Marriott’s “Challenging ECGs“, Harvard’s WaveMaven

4. Participate!

• Dr. Smith’s ECG Blog
• The EKG Club
• EMS 12-Lead Blog

Structured Learning/Depth of Knowledge links:

http://library.med.utah.edu/kw/ecg/ (Alan E. Lindsay’s ECG Learning Center)

http://lifeinthefastlane.com/ecg-library/

 CCTMC Conference

The Air Medical Physician Association is co-sponsoring an upcoming conference called CCTMC: Critical Care Transport Medicine Conference—info and brochure available here.

It’s 4.2.12 through 4.4.12 in Nashville.

This year’s opening talk at the conference, is “Upstairs Care Outside: Top Ten Tricks of the Trade for Bringing ICU-Level Care to the Transport Environment.”

And now on to the wee…

You just read the post: EMCrit Wee: The Lewis Lead and a course in ECGs with Christopher Watford from EMCrit Blog - Emergency Department Critical Care.

Severe Accidental Hypothermia

It is winter and that means cardiac arrests coming in with extremely low body temperatures after environmental exposure. How do you treat these patients? How do you rewarm if you don’t have bypass?

Predisposing factors

hypoglycemia, malnutrition, ETOH, Addison’s, infection, and Myxedema (especially if failure to rewarm)

In urban environments, in patients > 32° C, failure to passively rewarm at least 1 C per hour should make you suspect one of the above factors. (Acad Emerg Med 2006;13(9):913)

Do not need to worry much until temp hits ~32° C

Bradycardia (refractory to atropine), but should not be treated anyway as it is appropriate to body temperature as long as it is sinus brady; but if you needed to, you can pace hypothermia internally (Ann Emerg Med 2007;49(5):)

Labs

FS, CBC, Lytes, TFTs, Cortisol, and blood cultures if you can’t figure out why a patient got hypothermic or is not warming appropriately

Get Temperature Probe in early for sick patients

Place rectal probe in 15 cm or much better IMNHO is an esophageal probe

See this post for how to place the esophageal temperature probe

Active Rewarming

Active rewarming if pt temp <32° C, CNS sx, or age extremes

Rewarming Methods

Shivering 1.5° C/hr

Warming Blanket 2° C/hr

Warm O2 1 C/hr with mask; 1.5° C/hr ET tube

IV Fluids do not add, but do not take away either

Peritoneal Lavage 3° C/hr

Thoracic Lavage with Chest Tubes 3-6° C/hr

Cardiac Bypass 9-18° C/hr

When to Stop Rewarming

If K>10, pt is not coming back, even if cold and dead

Must be greater than 30-32° C degrees to be considered dead

Rewarming with Chest Tubes

32-36 F Chest tubes one anterior and one posterior lateral

Use Level 1 Device or similar to pump warm fluids into the anterior chest tube

attach auto-transfuser or pleur-evac to posterior-lat chest tube to allow cont. emptying

Review article with two case reports (Resuscitation 2005;66:99-104)

Click to see image

Click to see image

Extra-corporeal rewarming

Easiest method is to place an HD catheter and then get a dialysis machine to do CVVH or standard HD

CAVR Level I Rewarming

Here is an actual protocol from a Trauma Nursing Journal

J Trauma 1991;31:1151 and 1992;32:316 both by Gentilello

Bypass Rewarming

Crit Care Med 2011;39:1064

—

Maryland Life-saving Procedures Course

Click Here for the Brochure

Now on to the Podcast…

You just read the post: Podcast 66 – …Until they are warm and dead: Severe Accidental Hypothermia from EMCrit Blog - Emergency Department Critical Care.

BVM Ventilation

Today I want to talk about proper ventilation with a Bag-Valve-Mask, aka the BVM. I am joined by my friend Reuben Strayer, MD of EM Updates. You’ll see Reub’s talk from this year’s EMCrit ED Critical Care Conference and hear some of my thoughts as well.

After Reuben’s lecture, I made a few points of my own:

• Anesthesiologists can’t do one hand BVM as well as they think, at least according to this article: (Anesthesiology 2010; 113:873-9)
• How about the best article on how to manipulate the jaw for optimal BVMing
• Here is a link to an article where I discuss Vent as a Bag and here is the video as well.

need an audio-only version, (right click here and choose save-as), otherwise

And now to the Vodcast…

You just read the post: Podcast 65 – A Primer on BVM Ventilation with Reuben Strayer from EMCrit Blog - Emergency Department Critical Care.

Today I had the pleasure to interview Dr. Paul Marik, Professor and Division Chief of Pulmonary Critical Care at Eastern Virginia Medical Center. We got to speak on the topic of fluid responsiveness–one of the toughest questions in critical care.

Fluid Responsiveness

The definition we are using for fluid responsiveness is an increase of stroke volume of 10-15% after the patient receives 500 ml of crystalloid over 10-15 minutes

Dr. Marik’s Path through the Morass

this is a modification of the algorithm from Dr. Marik’s upcoming paper

* if using passive leg raise, give a 500 ml bolus if the response is positive

What is Passive Leg Raising?

For a brief period of time, a bolus of fluid is sent to the heart, allowing you to test fluid responsiveness without doing anything permanent to the patient’s fluid status.

What is the Monitor that Dr. Marik mentioned?

The NICOM Monitor by Cheetah Med uses bio-reactance to yield cardiac output/stroke volume non-invasively. I have been trialing the monitor and have been very impressed so far. It is inexpensive and correlates with my echocardiograms.

Articles of Interest

• This systematic review basically was the end of using CVP in the ICU for fluid responsiveness: Does central venous pressure predict fluid responsiveness? A systematic review of the literature and the tale of seven mares
• Marik’s review of hemodynamic parameters to guide fluid therapy
• An even better review by Dr. Marik will be published in the journal Resuscitation, as soon as it is published, I’ll put it up on the site
• If using Pulse Pressure Variation, probably only helpful if <9 or >13: Assessing the diagnostic accuracy of pulse pressure variations for the prediction of fluid responsiveness: a “gray zone” approach. by Maxime Cannesson (Anesthesiology. 2011 Aug;115(2):231-41.)

Neither Dr. Marik nor I have any Conflicts of Interest!

and Now to the Podcast…

You just read the post: Podcast 64 – Fluid Responsiveness with Dr. Paul Marik from EMCrit Blog - Emergency Department Critical Care.

Podcast 63 set off some expected controversy given my take that plain films are a dead imaging modality for c-spine injuries. I wanted to briefly outline my impression of the existing evidence:

Worst Case Scenario for Sensitivity

Mathen R, Inaba K, et al. (J Trauma 2007;62:1427)

Showed a sensitivity of 45% for plain films.

Prospective study of trauma patients who could not be cleared by NEXUS. Got 3-view plain films and CT. Gold standard was evidence of injury during entire hospitalization.

Post NEXUS Prevalence was ~10%, so probably a mix of moderate and high risk patients.

Best Case Scenario for Sensitivity

Mower WR, Hoffman JR, et al. Use of Plain Radiography to Screen for Cervical Spine Injuries (Ann Emerg Med 2001;38(1):1)

It is a reanalysis of the NEXUS Data (NEJM 2000;343(2):94)

818 Patients with 1496 c-spine injuries

Missed 320 and found 498 of the c-spine injuries in those 818 patients

Of the 320 misses, 237 were deemed inadequate plain films

So 498 out of 581 patients with adequate plain films

So sensitivity of the exam is 85%; We’ll assume a specificity of 100%

If you evaluate the performance by fracture instead of patient, the numbers become worse

I will say in the Mower paper, they tried to exclude SCIWORA patients, but from what I can glean from this paper (J Trauma 2002;53:1-4), these patients had their MRI without CT scans preceding it. CT may have picked up most of these injuries.

Now how can we get away with such a crappy sensitivity

The reason quoted is the NPV is excellent, they state 99.6% NPV. But NPV is a really crappy number, why…

Because as you change the prevalence, the NPV changes.

So now we need to go to a second enormous study…

Let’s look at the Canadian C-Spine Studies (JAMA 2001;286(15):1841 & NEJM 2003;349(26):2510), why? Because their entry criteria are exactly the patients we want to discuss–namely, acute trauma with alert mental status, an injury within the past 48 hours, and in stable condition. The prevalence of c-spine injuries in these patients was ~2% and in the NEXUS trial it was 2.4% So now we have some numbers for a low risk cohort. However, after you get a group of patients who could not be excluded by CCR, the prevalence of the group increases to ~4%. I would argue these patients are now moderate risk. If you pursue plain film strategy in this group, from the best numbers I can gather, you will miss 1 in 100 c-spine injuries and half of these will be clinically significant injuries.

75% of your plain films will be inadequate and require a CT scan

Plain films read as normal but which have loss of lordosis or soft tissue swelling were interpreted as abnormal by NEXUS folks and demand CT scan, this will account for patients going on to CT as well

Finally, patients with persistent midline pain probably deserve a CT prior to d/c in a collar as well

Let’s Put it all Together

The authors of this paper from the journal Medical Physics (Med Physics 2009;36(10):4461) attempted to take all the variables: radiation risk, cancer, missed injuries, etc. and evaluate whether plain films or CT is a better strategy. The results…in all risk levels, CT was the smarter move. This was with factoring in the putative cancer risks.

What about MRI for patients with persistent Midline Tenderness

BF asked about this in the comments

(Ann Emerg Med 2011;58:521)

44% of patients with persistent pain had an MRI abnormality

and (American Surgeon 2010;76(2):157)

3/20 patients who were alert, oriented but with persistent neck pain after negative CT had MRI findings

Of relevance to Oli Flower’s comments from the previous podcast, a whopping 24% of clinically unevaluable patients had injuries found on MRI.

Now, on to the podcast…

You just read the post: More on a Diagnostic Strategy for C-Spine Injuries from EMCrit Blog - Emergency Department Critical Care.

Cervical Spine Injuries in the ED

In this episode, I discuss the diagnosis of c-spine injuries. I argue that we should not send patients to imaging unless we have used the NEXUS rule and then added the Canadian C-spine Rule to the sequence. If we are imaging, it should be with a 3-view reconstructed CT scan. And even after that is done, you still need a clearance exam before removing the collar.

 The Fine Print of the NEXUS rule

You Need to Read Your Footnotes

The folks from Virginia think (J Trauma. 2011 Apr;70(4):829-31. & J Trauma2011;70(4):829-831) Nexus can’t be used, but I think if you follow my advice in the podcast, you are probably going to come as close to 100% as a rule can provide. The Canadians also showed less than 100% Sens when using NEXUS (N Engl J Med. 2003 Dec 25;349(26):2510-8), but I would make the same argument–did they really do it the same as the NEXUS study advocates? Do you do it the same? If not, you may be missing injuries.

Then add the Canadian C-Spine Rule if there is Midline Tenderness, but no other NEXUS Criteria

Click on the Image for the Whole Algorithm

Plain Films Suck!

Want the evidence, cehck out the Spinal Cord Injury chapter at CrashingPatient

Injuries Missed on CT scan

You just read the post: Podcast 63 – A Pain in the Neck – Part I from EMCrit Blog - Emergency Department Critical Care.

EMCrit’s favorites from 2011

An Ultrasound Podcast

The Emergency Ultrasound Podcast is some of the best emergency medicine podcasting out there. Matt and Mike have a fabulous teaching style and I can’t get enough of their ultrasound education.

A New Blog on EM Evidence

EM Literature of Note provides concise and incisive commentary from Ryan Radecki

EM Posts with Care Pathways and some Ketamine

My friend Reuben Strayer doesn’t post often, but when he does, it is pure gold: Emergency Medicine Updates

A Flying Doctor who seems to love Airway

Minh Le Cong is brilliant and I hope he posts on the EMCrit blog as much as he likes.

An Intensive Care Blog with Lectures

The Intensive Care Network is a fantastic blog with lectures, videos, and board preparation resources.

A Surgeon who can communicate–Who would have thunk it?

The Trauma Professionals Blog is the fantastic perspective of a trauma surgeon, Dr. Michael McGonigal.

For more of my favorite things, check out the dirty dozen from 2010

You just read the post: EMCrit Podcast – Hard Six – My Picks from 2011 from EMCrit Blog - Emergency Department Critical Care.

One of the best new podcasts of the year is certainly the Emergency Ultrasound Podcast with Matt Dawson and Mike Mallon. If you haven’t checked it out yet, I am replaying their wall motion abnormality talk here on the podcast, because it is so damn good.

If you like it please subscribe to these guys at their website: http://ultrasoundpodcast.com

Here is the handout from the lecture.

Audio only would not be helpful for this lecture.

You just read the post: Replay of the Emergency Ultrasound Podcast – Wall Motion Abnormality Lecture from EMCrit Blog - Emergency Department Critical Care.

Needle vs. Knife Part II

In this podcast, I explain why I don’t think needle compression is such a clever idea. Main points are: most people can’t find anterior target, most angiocaths won’t reach, and if used diagnostically you may not be in the pleura leading to an unidentified pneumo or hemothorax. Also, when used diagnostically, if the chest was negative you just caused a pneumothorax.

If you haven’t already, you should listen to Needle vs. Knife Part I with Minh. Also, may of the issues discussed here are also mentioned in the finger thoracostomy episode and the traumatic arrest episode.

Why the standard approach to needle decompression sucks

Normal IV catheters do not reach in up to 65% of the cases

Can J Surg. 2010 Jun;53(3):184-8.

Prehosp Emerg Care. 2009 Jan-Mar;13(1):14-7

J Trauma. 2008 Jan;64(1):111-4

J Trauma 2008 Oct;65(4)”:964

Accid Emerg Med 1996;6:426–7

Injury 1996;5:321–2.

Anterior Approach is not Where You Think it is

Emerg Med J 2003;20:383-384

ED Docs got it wrong a lot! (Emerg Med J 2005;22:788)

Use the Lateral Approach if you are going to do Needle Thoracostomy

ANZ J Surg. 2004 Jun;74(6):420-3

Study says Anterior is closer, but (smooth concept here) the patients had their arms in the air

(Acad Emerg Med 2011;18:1022)

Even if you get it right, Cannula may kink, occlude, or compress

Emerg Med J 2002;19:176-177

Traumatic Arrest is not Dismal until Tension Pneumo is Ruled Out

Emerg Med J. 2009 Oct;26(10):738-4

This device makes much more sense to me

Evaluation of ThoraQuik: a new device for the treatment of pneumothorax and pleural effusion (Emerg Med J 2011;28:750-753)

You just read the post: Podcast 62 – Needle vs. Knife II: Needle Thoracostomy? from EMCrit Blog - Emergency Department Critical Care.

I recently spoke at a symposium at the Greater NY Hospital Assoc’s with the title: Controversies in Critical Care. I debated Paul Mayo, MD on the topic of whether paralytics should be used for ICU emergent intubations. Of course, I took the pro side of the debate. Dr. Mayo based his con side on an amazing study that came out of his ICU at LIJ hospital in NY.

Here is the abstract of that study:

Seth Koenig, MD; Viera Lakticova, MD^*; Abhijeth Hegde, MD; Pierre Kory, MD; Mangala Narasimhan, DO; Peter Doelken, MD and Paul Mayo, MD
The Safety of Emergency Endotracheal Intubation Without the Use of a Paralytic Agent

Here is some literature you may want to cast a more informed vote:

Mort on Complications of Repeated Laryngoscopic Attempts

Here is the article I wrote with Rich Levitan on Preoxygenation for Intubation:

Weingart, S. Levitan, R. Preoxygenation and Prevention of Desaturation During Emergency Airway Management (In Press, For Review Only)

Cast your Vote:

[poll id="2"]

Need an audio only version:

Mp3 of the Paralytic Debate (right click and choose save as)

Now on to the Podcast…

You just read the post: Podcast 061 – Debate: Paralytics for ICU Intubations? from EMCrit Blog - Emergency Department Critical Care.

Click here to view the embedded video.

If you’ve been reading the comments on some of the posts, you may have seen a new face: Jim DuCanto, MD. Jim is an anesthesiologist at the Medical College of Wisconsin. He has recorded 100′s of intubations in the OR. The above video shows two of them.

• First case: the patient was intubated after 8 ml of topical anesthesia applied to vocal cords through the Air-Q mask itself.  Patient was anesthetized with inhalational anesthesia first, mask inserted, and Jim went from there.
• Second case, he was simply practicing with the Levitan scope alongside DL (not a difficult airway).

You’ll be hearing more from Jim on the podcast soon.

You just read the post: Two OR Intubation Videos from EMCrit Blog - Emergency Department Critical Care.

In this episode, I discuss the takedown and restraint of the violent, agitated delirium patient. This is a team sport and requires a coordinated approach for the safety of the patient and staff.

Essentials of EM

See my experience at Essentials of EM 2011.

How to apply restraints in the ED

This video by Gary Thedo is the best instructional source for the proper way to restrain a patient in the ED

Click here to view the embedded video.

If you have ideas of your own and how to accomplish safe takedown of these patients, please put your comments below.

Some Evidence

Haldol vs. Droperidol

• J Clin Psychiatry. 1984 Jul;45(7):298-9. Droperidol vs. haloperidol in the initial management of acutely agitated patients.
• Ann Emerg Med. 1992 Apr;21(4):407-13. Droperidol versus haloperidol for chemical restraint of agitated and combative patients.

Droperidol vs. Midazolam

10 mg IM droperidol was not associated with greater QTc prolongation than the midazolam group. The DORM Study. Ann Emerg Med 2010;56:392-401.

Droperidol Safety

Article froms Peds literature looked at safety of high doses in patients aged 15-21 (Peds Emerg Care 2010;26(4):248)

The DORM Study

Randomized Controlled Trial of Intramuscular Droperidol Versus Midazolam for Violence and Acute Behavioral Disturbance: The DORM Study(Annals of Emergency Medicine Volume 56, Issue 4 , Pages 392-401.e1, October 2010)

This study showed that 10mg of IM droperidol was safe and more effective than midazolam or a combination of the two at half does of each.

Now on to the podcast…

You just read the post: Podcast 060 – On Human Bondage and the Art of the Chemical Takedown from EMCrit Blog - Emergency Department Critical Care.

I just got back from Essentials of Emergency Medicine 2011. In my opinion, this is the première Emergency Medicine Conference in the world! Mel Herbert continues to be the master of EM education.

There were three people I very much wanted to hang out with…

Michael Cadogan

The visionary behind the life in the fast lane blog–Mike did not disappoint. The words that come to mind are iconoclastic genius. The first night I met Mike, he saved my butt. My presentations this year were mostly video, and since I’m a PC guy and essentials is an all Mac event, not a single one of the videos worked. The AV folks were busy getting set up and did not respond to my pleading eyes and frank begging. I was not a happy camper, especially after not having slept for 38 hours at this point. I finally could not handle keeping my eyes open for a moment longer and figured I would just deal with it the next day. Mike stayed up for I don’t know how many hours and actually fixed the computer of the AV company to get my videos to work. Mike–I owe you mate, you are a gracious and kind man!

Mike did a series of three incredible lectures on social media that will soon be posted on life in the fast lane.

ZdoggMD

I got to meet da dog for the first time at essentials prior to him performing 10 minutes of stand-up gold at the conference. He is exactly how I imagined he would be–funny, smart, and cynical with a heart of gold (gold as in golden shower-playa). If you have not watched his videos, what the hell is wrong with you. Got to zdoggmd.com IMMEDIATELY!

Rob Orman

I met Rob once before, but I couldn’t wait to see him again. I feel like Rob’s precocious younger brother. We talk by skype all the time and I feel like I know him well despite this only being the second time we have met. Rob’s ERCAST is some of the best general EM podcasting out there.

Rob gave 3 lectures that established him as a presentation pro.

ZdoggMD, Me, Rob Orman, and Mike Cadogan

I also got to have the best dinner ever with my incredible blogging buddies: Leon Gussow, Graham Walker, and Michelle Lin.

See the all of the Tweets from EM Essentials 2011

Essentials of EM Conference in Tweets

You just read the post: Essentials of EM 2011 from EMCrit Blog - Emergency Department Critical Care.

Richard Levitan and I just got our preoxygenation article accepted to Annals of EM. This video describes one of the concepts in the paper.

Email me if you need further explanation.

Here’s the Video:

You just read the post: How to generate constant CPAP with a BVM for Preoxygenation and Reoxygenation from EMCrit Blog - Emergency Department Critical Care.

Today I am joined by toxicology master, Leon Gussow to discuss a new quasi-legal class of drugs: Bath Salts. I saw my first OD of this a month ago; despite the drug’s name, this patient was neither clean nor pleasantly refreshed. He was violent, agitated, and overheated.

This class of drugs are chemically altered hallucinogenic stimulants. Depending on which chemical is used in the salts, the patient can look like they took meth or ecstasy. They will present with a sympathomimetic toxidrome including hyperadrenergic vitals and profound hyperthermia.

How many folks out there have ever used the Bellevue-style metal tub to immerse these patients in ice baths? Let me know in the comments.

Here is a link to Leon’s bath salt article in EM News.

You just read the post: Podcast 059 – Bath Salts with Leon Gussow from EMCrit Blog - Emergency Department Critical Care.

Gabe writes:

REMCS notification of an obese female in her 50s being brought in on CPAP for resp distress, history of CHF, tachypneic and tachycardic.
Immediate page for respiratory to bring down NIV.
When she came through the ambulance bay, I categorized her immediately (thanks to your podacst): SCAPE. Tachycardic, hypertensive, tachypneic, diaphoretic, and severely agitated saturating upper 80s with crackles to her apices. With intubation gear ready, I placed her on a PEEP of 8 and dropped at SL NTG 0.4mg under her tongue (couldn’t get the IV nitro in time) and gave 50mcg fentanyl.
2 minutes later: RR 24 (from 40s), sat 100%, HR 80s, dry skin, and talking to us behind the CPAP. My attending was so proud and, quite frankly, relieved at not having to intubate an impossible airway.
My question is: once the patient has stabilized on the NIV, do we wean it down? Switch to NRB? Leave it to the CCU?
Thanks!

Gabe, Great question!

Here is how I wean the CPAP on these folks:

• The patient must look good–I mean really good before I’ll even think of turning the dial. No diaphoresis, no labored breathing, can talk to you easily under the mask.
• The blood pressure must have dropped to the patient’s norm or what you think is the patient’s norm.
• The nitro drip must have done its precipitous drop thing, by which I mean, at some point these SCAPE patients turn off their sympathetic surge. Their nitro drip necessity will go from a level such as 180 mcg/min to 30 mcg/min. Once that happens, you know you are over the hump.
• When all of the above have occurred, I drop the fiO2 to 40% and then I start weaning down the PEEP setting about 2 cmH20 every 5-10 minutes.
• Check the patient for the above before each subsequent PEEP drop.
• When they are at 5 cmH20, give them a trial of nasal cannula.
• Keep the entire CPAP set-up ready at the bedside
• If the patient’s BP spikes or they get sweaty and are having trouble breathing, put them back on CPAP and go back up on your nitro.
• Now is the time to assess whether you think they are volume overloaded and if you think it is clever, give them a diuretic. For me I’d rather they get their kidneys going with the nitro instead of the diuretic.

Hope that helps

You just read the post: When to wean the CPAP in SCAPE from EMCrit Blog - Emergency Department Critical Care.

A novel set-up to allow suctioning during direct endotracheal and fiberoptic intubation

To the Editor:

Fig. 2.

Swivel adapter attached to a meconium aspirator and suction.

Fig. 3.

Swivel adapter and meconium aspirator set-up, allowing for suctioning through a styletted endotracheal tube.

Fig. 4.

Swivel adapter and meconium aspirator set-up, allowing for suctioning during fiberscope intubation.

You just read the post: A novel set-up to allow suctioning during direct endotracheal and fiberoptic intubation from EMCrit Blog - Emergency Department Critical Care.

You might remember Minh Le Cong from the needle vs. the knife – part I podcast. He is a retrieval (EMS) physician from down under and he has a particular interest in prehospital airway management. He was kind enough to review the king vision video laryngoscope for the blog. Neither Minh nor myself have any conflicts of interest with this company. This is the device that Cliff Reid has been keen on as well. If you are an ED doc in a shop that doesn’t have difficult airway equipment, this would seem the ideal device to buy for yourself as well. Now on to Minh’s review…

Brief Review of the King Vision Video Laryngoscope

by Dr Minh Le Cong

Introduction

The King Vision video laryngoscope is the latest in a long series of devices that claim to provide the “perfect view” for intubation via use of video and digital technology. I chose to purchase one to test it, having personally reviewed a number of the major players earlier this year at an airway conference in Australia.  I am a rural generalist medical practitioner working in Cairns , Queensland, Australia for the Royal Flying Doctor Service, the longest continuously running aeromedical service in the world. My primary medical specialist training was in rural and remote medicine with subspecialty training in emergency medicine and internal medicine. My clinical work is a mix of aeromedical retrieval and remote medicine. I was not sponsored by anyone to write this review and purchased the device for personal use.

The design

The King Vision Video laryngoscope is a two piece design. It has a reuseable monitor that attaches to disposable blades. In some respects this is a similar approach to the Pentax Airway Scope which has a reuseable monitor and disposable blades. Where the King Vision differs is that the LED light and CMOS camera are mounted on the disposable blades. This makes the design simpler to use as you essentially just have to connect the two pieces together by simply sliding them into each other.

The blades are all Macintosh #3 size and compared to a normal Macintosh #3 bladed laryngoscope, the King Vision blades appear wider and shorter. There are blades with a guiding channel and standard blades without. Both only come in #3 size though .The guide channel blade is very similar to the Pentax and Airtraq blade designs.  . When you use the device you quickly come to the conclusion that all you will need is a #3 size blade.

The display is an OLED design of surprisingly good clarity and resolution when you consider the pricing of the device ( see Cost section below). It is turned on with a single power button on the back of the display and turned off by depressing it for 3 seconds. It is certainly a no frills design which makes it simple to understand and use. There is no brightness adjustment nor in built video recording function. There is a mini USB port for a video out function to either a display or digital recorder. The LED light on the blade tip is very good with nice intensity and a pale white illumination. The device is powered by standard AAA size batteries x 3 and is rated to last at least 90 minutes or greater.

Performance

My colleagues and I tested the device using a Trucorps Air Sim intubation mannikin, using  size 6 and 7.5 cuffed endotracheal tubes as well as a Frova bougie. We compared it to direct laryngoscopy with a Macintosh #3 blade. We tested using standard intubating conditions and simulated difficult intubation by inflating the mannikin tongue to simulate swelling and upper airway obstruction. We conducted the testing indoors with normal fluorescent tube lighting and then outdoors in midday sunlight. As expected in the simulated difficult intubation the King Vision performed significantly better than direct laryngoscopy, both in terms of laryngeal visualization but also speed and success of intubation. There were some initial learning issues with passing the tracheal tube via the guide channel but these were quickly mastered within 3 practice intubations.

[click images to see full size]

The finding that most impressed me about the King Vision was using a bougie with it. You can use the bougie with or without the aid of the guide channel and getting the tip pass the cords is much easier using the video laryngoscope. Then passing the ETT over the bougie under video guidance is a major advantage as you can see how the tip of the ETT catches on the right arytenoids.

[click images to see full size]

Okay those images were of course of the indoors testing. Here are the results of the outdoor testing. Remember this is relevant for the prehospital work we do in RFDS as sometimes you are outdoors doing RSI  at a cattle station for someone who has fallen off a horse and sustained a severe head injury!

Here is my colleague Dr Shaun Parish, performing the testing outdoors. Note the bright sun light. Direct larynogoscopy interestingly performed fairly well in this testing which is probably because we did not have the mannikin directly on the ground. When trying to intubate a person flat on the ground with bright sunlight we have usually found this quite difficult due to the glare of the sun into the field of view particularly if directly coming from behind. The King Vision performed well even in this brightly sunlit setting with little difference to performance indoors. It was difficult to get a good picture of the LED screen view  during intubation so the best I could do was take out the King Vision and point it at an object and take this photo in direct sunlight from behind. You can see the image although degraded and washed out of colour is still an effective resolution with clearly discernible structures.

[click images to see full size]

Now there has been one published study finding the Pentax AWS screen does not perform well in bright outdoor conditions and I was aware of this so it surprised me that the King Vision was more capable in this setting.

Pricing and Overall package

The King Vision is sold by Critical Assist in Australia for the delivered price of $1100 approximately. This is what you get for that money.

A kit with the monitor display and 4 disposable blades ( 3 channeled and 1 standard). The monitor has a 1 year guarantee and the disposable blades can only be bought in boxes of 10 at $30each.

Bottom line for me

This is the best overall package for getting started in video laryngoscopy due to low pricing, quality imaging and simplicity of use. It is excellent I think for prehospital airway management having a display that performs well in outdoor testing. Its closest rival would be the AV laryngoscope distributed by LMA Pacmed in Australia but that costs approx $7000 each. Another close rival would be the Airtraq by Prodol which is cheaper and disposable but has the disadvantage of using a shielded eyepiece as the viewing display. With the King Vision you can maintain an overall view of the patient without having to lean down and peer into a black hole. Therefore you can maintain situational awareness and keep an eye on oxygen saturation monitor and cardiac rhythm as well as anterior neck and chest whilst getting that “perfect view”! I think the expense of previous video laryngoscopes has made most airway providers resist the jump into learning the skill of this new technique but now with the King Vision there is little barrier to make that leap of faith! It costs less than most airway courses!

You just read the post: Brief Review of the King Vision Video Laryngoscope from EMCrit Blog - Emergency Department Critical Care.

This Part II of an interview with Cliff Reid of the amazing blog, resus.me. Cliff is truly a doc after my own heart as you will hear from the cast.

If you haven’t already, please listen to Part I of Cliff’s interview as well.

He is currently an EMS physician and Director of Training at the New South Wales Ambulance Service.

Cliff’s blog, resus.me is an incredible collection of timely articles on emergency medicine, ems, critical care and resuscitation.

Here are some details on what Cliff carries on a mission.

Prehospital Amputation

One of the topics we discuss is prehospital amputation. For more information on this topic, check out the deep-dive page on prehospital amputation.

Come visit me at ACEP and AOCEP Scientific Assemblies.

Now to the Podcast…

You just read the post: Podcast 058 – Interview with Cliff Reid – Part II from EMCrit Blog - Emergency Department Critical Care.

Resuscitative Extra-Corporeal Life Support for Cardiac Arrest (ECMO)

Joe Bellezzo, MD along with his partner-in-crime, Zack Shinar, MD have started an ED ECMO service at Sharp Memorial Hospital in San Diego. I am so jealous! In this episode of the podcast, I get to talk to Joe about how it works.

What is ECMO?

ECMO is actually a misnomer. Extra-corporeal life support (ECLS) is probably a better term. If a catheter is placed in a major artery and a major vein (VA ECMO), the patient can be provided with full hemodynamic and respiratory support, aka cardiopulmonary bypass. If catheters are placed in two major veins (VV ECMO), the patient’s respiratory status can be maintained, but without the hemodynamic augmentation. Dr. Bellezzo’s shop is using VA ECMO to treat refractory cardiac arrest patients.

This is not the first attempt to use ECMO in this patient group, (see the articles in the EMCrit Hypothermia/Post-Arrest Section) but I think this is the first ED physician initiated service.

Which patients are they crashing on to ECMO?

What are the stages to placing a patient on ECMO?

Stage I-get catheters into a femoral artery and femoral vein

Stage II-exchange these catheters for the enormous ECMO catheters vias guidewire and serial dilations

Stage III-attach them to the ECMO machine, which is run by specially trained ICU nurses for the first 45-60 minutes and then by a perfusionist.

Don’t you have a video?

Dr. Bellezzo was kind enough to let me post this video

Click here to view the embedded video.

If you have any questions, place them in the comments and anything I can’t answer, I’ll forward to Dr. Bellezzo

Now, on to the Podcast:

You just read the post: Podcast 057 – Resuscitative Extra-Corporeal Life Support (ECMO) from EMCrit Blog - Emergency Department Critical Care.

Part III of Dr. Rivers’ talk on Severe Sepsis

Dr. Emanuel Rivers brought the concept of aggressive therapies for sepsis down to the Emergency Department with his seminal article on EGDT published in the NEJM in 2001. We were lucky enough to get an hour of his time to do a conference call with the NYC STOP Sepsis collaborative.

I broke the ~1 hour lecture into 3 parts.

If you haven’t already, check out Part I and Part II.

In Part III, Dr. Rivers discusses:

•  Protein C?
• Can you do EGDT in small community EDs?
• How do you handle the tachycardic patient with severe sepsis?
• Steroids in the ED?
• Procalcitonin?

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The Video Podcast

You just read the post: Podcast 056 – Dr. Rivers on Severe Sepsis – Part III from EMCrit Blog - Emergency Department Critical Care.

Part II of Dr. Rivers’ talk on Severe Sepsis

Dr. Emanuel Rivers brought the concept of aggressive therapies for sepsis down to the Emergency Department with his seminal article on EGDT published in the NEJM in 2001. We were lucky enough to get an hour of his time to do a conference call with the NYC STOP Sepsis collaborative.

I broke the ~1 hour lecture into 3 parts.

If you haven’t already, check out Part I.

In Part II, Dr. Rivers discusses:

• CVP and Fluid Responsiveness
• Should End-Stage Renal Failure patients get lots of fluids?
• Should we be using albumin?
• Should vasopressin be a first line pressor?
• Steroids/Etomidate (See a paper by Dr. Marik on steroids in sepsis)

Here is a pdf of Dr. Rivers’ Slides

Remember–Get a Free Trial of EM Critical Care Journal

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How do I get the videos to work on my IPOD

View here in Full Screen

and now the Podcast…

Right Click Here for an Audio-Only Version

Video

You just read the post: Podcast 055 – Dr. Rivers on Severe Sepsis – Part II from EMCrit Blog - Emergency Department Critical Care.

A listener, Dave Glaser, points out that one portion of the EGDT protocol doesn’t get spoken about very often: the use of vasodilators for MAP optimization.

In the original trial, patients in the EGDT arm of the study got a vasodilator if their MAPs were >90. The original trial publication makes no mention of which vasodilator and how many patients received it. If you want that information, you need to go to the Otero et. al publication (Chest 2006;130;1579-1595), which expanded on the original trial with additional information. Here is the relevant excerpt:

Vasodilator Therapy

After adequate volume and hemoglobin targets were met, we surprisingly found that 9% of EGDT patients met the protocol criteria for afterload reduction for a mean arterial pressure (MAP) of > 90 mm Hg by utilizing nitroglycerin therapy. Nitroglycerin was chosen because of its effects on preload, afterload, and coronary vasodilation. All of these patients had a history of hypertension and congestive heart failure. The median baseline Scvo2 was 46% in this subset of patients. Although the use of nitroglycerin was unexpected on study initiation, therapy with afterload reduction is not without precedent in treating sepsis patients.

Cerra et al (J Surg Res 1978;25:180–183) provided vasodilator therapy to sepsis patients with low cardiac output and observed physiologic improvement.

Spronk et al (Lancet. 2002 Nov 2;360(9343):1395-6) found that nitroglycerin may improve microcirculatory flow in normotensive or even hypotensive patients with septic shock.

It is becoming increasingly evident that disordered microcirculatory flow is associated with systemic inflammation, acute organ dysfunction, and increased mortality. Using new technologies to directly image microcirculatory blood flow may help to define the role of microcirculatory dysfunction in oxygen transport and circulatory support.

I can’t remember the last time I saw a patient who would be eligible for this therapy b/c of high MAP. We have given nitroglycerin occasionally for a patient that is not clearing their lactate with a high ScvO2.

For anyone who really wants to dive deep on this issue, there is a free supplement in Critical Care.

You just read the post: Vasodilators for Severe Sepsis from EMCrit Blog - Emergency Department Critical Care.

Part I of Dr. Rivers’ talk on Severe Sepsis

Dr. Emanuel Rivers brought the concept of aggressive therapies for sepsis down to the Emergency Department with his seminal article on EGDT published in the NEJM in 2001. We were lucky enough to get an hour of his time to do a conference call with the NYC STOP Sepsis collaborative.

I broke the ~1 hour lecture into 3 parts. In Part I, Dr. Rivers discusses:

• Prehospital Antibiotics
• Comparison between the original EGDT Study and the Jones study (showing the non-inferiority of the non-invasive approach).
• Alactemic Septic Shock

Here is a pdf of Dr. Rivers’ Slides

Get a Free Trial of EM Critical Care Journal

Click Here for a 6 Month Free Trial of the New EMCC Journal

and now the Podcast…

Right Click Here for an Audio-Only Version

Video

You just read the post: Podcast 054 – Dr. Rivers on Severe Sepsis – Part I from EMCrit Blog - Emergency Department Critical Care.

Needle or the Knife for the Cricothyrotomy

In this episode, I debate Minh Le Cong, a retrieval physician from Australia. The question is what technique should we use in the can’t intubate/can’t oxygenate (CICO) situation.

Throughout the podcast, you will hear reference to Dr. Andrew Heard, who has written some fantastic papers on the subject. Perhaps most pertinent is his description of the formation of a CICO protocol based on his experience with a wet sheep airway instruction lab.

Heard AM, Green RJ, Eakins P. The formulation and introduction of a ‘can’t intubate, can’t ventilate’ algorithm into clinical practice. Anaesthesia. 2009 Jun;64(6):601-8.

Here is the algorithm from the paper (Click for full size)

Here is his video on the cannula cricothyrotomy technique

Click here to view the embedded video.

Here is his video on the scalpel-finger-cannula technique

Click here to view the embedded video.

Here is a video describing why Dr. Heard prefers the 14G Insyte Catheter for Needle Cric

Click here to view the embedded video.

Here is his preferred method for oxygenation through the cannula

The paper on the use of ultrasound to find the cricothyroid membrane is quite interesting.

See my prior posts on how to perform the bougie-aided cricothyrotomy and the cric show.

One of the best things Minh expressed is the need to say OUT LOUD: “This is a can’t intubate/can’t oxygenate situation.” Saying it out loud lets everyone in the room know, there will be no more screwing around with attempts at direct laryngoscopy.

Go to the Broome Docs Blog for more Minh Le Cong.

He is an incredible guy, expect to hear more from Minh on the podcast.

I also gave a shout-out to a new podcast, the Emergency Ultrasound Podcast.

and now the EMCrit Podcast 53…

You just read the post: Podcast 053 – Needle vs. Knife: Part I from EMCrit Blog - Emergency Department Critical Care.

Organ Donation in the Emergency Department

Though it may not seem as important as some of the things we do in ED Critical Care, managing the potential organ donor can lead to many lives saved. In this episode I interview Isaac Tawil, an Emergency Intensivist of University of New Mexico Health Sciences and associate medical director of New Mexico Organ Donor Services.

Here are the current standards for determining brain death

Wijdicks et al. Evidence-based guideline update: Determining Brain Death in Adults

Here is a video of Dr. Tawil demonstrating the brain death exam

Click here to view the embedded video.

You just read the post: Podcast 052 – Organ Donation in the ED from EMCrit Blog - Emergency Department Critical Care.

Jeff Kline is the master of all things pulmonary embolism in emergency medicine. This is a lecture he gave on fibrinolysis for pulmonary embolism. He discusses both massive and sub-massive PE.

Here is a pdf of the slides.

If you haven’t already, you should also check out the AHA PE guidelines. I have a summary and the diagrams in another post.

Fibrinolysis in Pulmonary Embolism with Dr. Jeff Kline

The lecture starts with a few non-fibrinolytic points:

• Use PERC with clinical gestalt
• You can use a high-senstivity d-dimer in ALL risk groups
• Use a d-dimer with elevated cut-offs based on trimester in pregnant patients
• A high-sensitivity CTPA is the best thing we have and a negative is negative for all risk groups

Feel free to discuss any of those in the comments

Massive PE

In the guidelines, the definition is PE with SBP < 90 for > 15 minutes

Dr. Kline basically says that if you have an SBP < 90 at any point, the patient MUST be given fibrinolysis or you better have a good reason why on your chart.

Sub-Massive PE

Here are the points Dr. Kline can state definitively:
After lytics,

• The patient will feel better
• The clot will resolve more quickly
• There will be no increase in serious bleeding (Note in the original study, 2 patients with pre-lytic ICH were coded as complications)

What he can’t say yet (but he has the largest RCT going on now) is mortality reduction

So who does he think should get lytics in sub-massive PE?

• BNP >90 or Pro-BNP >900 elevation (he states BNP is his go to marker). SENSITIVE
• Troponin positive SPECIFIC
• Echo with RV dysfunction, hypokinesis, dilation

He also states a low room air pulse ox is an indicator of needing lytics.

Choice of Drugs

Alteplase-he continues heparin during the infusion. He also feels you can just give the 100 mg as a bolus if you need to.

Tenecteplase-this is what he would want to receive if he had a PE. He gives it simultaneously with LMWH.

Mentions that lytics don’t destroy all of the clot they just chew away at the big ones a bit.

For more PE stuff see the diagnosis protocol post and the PE debate insanity.

You just read the post: Podcast # 51: Fibrinolysis in Pulmonary Embolism from EMCrit Blog - Emergency Department Critical Care.

Recently, the AHA published guidelines on the management of pulmonary embolism. I extracted only the stuff relevant to ED w/u and management:

Source: Circulation 2011;123:1788

Anticoagulation

Anticoagulate with LMWH, IV/Sub-Q UFH, or fondaparinux (IA)

While working up PE, if pretest is moderate or high, and there are no contra-indications, start anticoagulation during the work-up (IC)

Fibrinolytics

Definition of Massive PE-Acute PE with sustained hypotension (systolic blood pressure <90 mm Hg for at least 15 minutes or requiring inotropic support, not due to a cause other than PE, such as arrhythmia, hypovolemia, sepsis, or left ventricular [LV] dysfunction), pulselessness, or persistent profound bradycardia (heart rate <40 bpm with signs or symptoms of shock).

Definition of Submassive PE-Acute PE without systemic hypotension (systolic blood pressure >90 mm Hg) but with either RV dysfunction or myocardial necrosis.

• RV dysfunction means the presence of at least 1 of the following:

  • —RV dilation (apical 4-chamber RV diameter divided by LV diameter >0.9) or RV systolic dysfunction on echocardiography

  • —RV dilation (4-chamber RV diameter divided by LV diameter >0.9) on CT

  • —Elevation of BNP (>90 pg/mL)

  • —Elevation of N-terminal pro-BNP (>500 pg/mL); or

  • —Electrocardiographic changes (new complete or incomplete right bundle-branch block, anteroseptal ST elevation or depression, or anteroseptal T-wave inversion)

• Myocardial necrosis is defined as either of the following:

  • —Elevation of troponin I (>0.4 ng/mL) or

  • —Elevation of troponin T (>0.1 ng/mL)

Fibrinolysis is reasonable for pts with massive PE and acceptable risk of bleeding complications (IIa/B)

Fibrinolysis may be considered for pts with submassive PE judged to have clinical evidence of adverse prognosis (hemodynamic instability, worsening resp. insufficiency, severe RV dysfunction, or major myocardial necrosis) and low risk of bleeding complications (IIb/C)

Fibrinolysis is not recommended for patients with submassive PE with only mild dysfunction, i.e. low risk PEs (III/B)

Fibrinolysis is not recommended for undifferentiated cardiac arrest (III/B)

Interventional and Surgical Options

Either catheter embolectomy or surgical embolectomy can be considered depending on institutional and operator preference (IIa/C)

Either of these are reasonable if the pt is still unstable in massive PE after fibrinolysis (IIa/C)

Also reasonable in massive PE, if the pt has a contra-indication to lysis (IIa/C)

May be considered in lieu of fibrinolysis in patients with submassive PE and evidence of adverse prognosis (IIb/C)

Not recommended for pts with PE at low risk (III/C)

PE Fibrinolytic Treatment Algorithm

You just read the post: AHA PE Guidelines from EMCrit Blog - Emergency Department Critical Care.

Based on Master Nickson’s comments on the PE debate, you could argue this would be an acceptable paradigm. Using Wells as your entry forces gestalt into the equation. Since Wells’ low risk arguably gets you somewhere between 1-6% in ED populations, PERC should be acceptable.

You just read the post: Imaging in PE Diagram from EMCrit Blog - Emergency Department Critical Care.

This is Part 4 of the Acid Base saga. In this episode, I discuss the acid base effects of fluids and when and how to use sodium bicarbonate.

If you haven’t checked out the previous episodes, you should definitely do that first:

• Part I lays out the background of the quantitative approach
• Part II puts it in mathematical terms to allow calculation of acid base status
• Part III takes you through some real world examples

The Acid Base of Fluids

Crystalloids will have acid-base effects by their SID and the dilution of extracellular Atot

“Balanced Fluids” are fluids with a SID just low enough to balance the dilution of the weak acid, albumin (SID of 24-28)

For the effects on a patient with altered pH, any fluid with a SID the same as the pt’s bicarb will keep the patient at the same pH. If the SID is greater than the pt’s bicarb, then the fluid will be alkalotic and if less than the pt’s bicarb–acidotic (Intens Care Med 2011;37:461).

Hypertonic fluids are even more acidifying b/c they draw pure water into the extracellular space

Chart with a bunch more fluids is on crashingpatient.com

Sodium Bicarbonate

If not stored in glass, bicarb containing solutions leech CO2 and become not so much bicarbonate.

If given at all, should be given slowly by push over 5-10 minutes or by drip; never by rapid push

In hyperkalemia, NaBicarb isotonic is essentially a potassium-free, non-acidic fluid that dilutes down the potassium.

NaBicarb can be used as a substitute for hypertonic saline in increased ICP (Neurocrit Care 2010;13:24). They used 85 ml of 8.4% sodium bicarb infused over 30 minutes.

Articles

Best Review of the Stewart/Quant Approach to Fluids

Best Review of Sodium Bicarb Use Ever

Balanced solutions (p-lyte) led to lower Cl and higher bicarb (Am J Emerg Med. 2011 Jul;29(6):670-4)

Also of interest may be the previous episode on intubating the patient with the severe metabolic acidosis

You just read the post: EMCrit Podcast 50 – Choose the Solution Based on the Problem from EMCrit Blog - Emergency Department Critical Care.

Richard Dutton is a trauma anesthesiologist who was one of the primary formulators of the concept of 1:1:1 resuscitation. Here he is speaking on hemostatic resuscitation.

This lecture was recorded at the EMCrit Conference 2011.

You just read the post: Hemostatic Resuscitation by Richard Dutton, MD from EMCrit Blog - Emergency Department Critical Care.

amateurs discuss strategy; experts discuss logistics
–Napoleon?

This Part I of the Mind of a Resus Doc Series, in which we delve into the philosophies that make a good resuscitationist.

You just read the post: EMCrit Podcast 49 – The Mind of a Resus Doc: Logistics over Strategy from EMCrit Blog - Emergency Department Critical Care.

 Reversal of Dabigatran

The incredible folks from hqmeded have put up a video on how to deal with bleeding patients on the new oral anticoagulant, dabigatran…

Click here to view the embedded video.

Here is the Hennepin County Reversal Protocol from the Video

Hennepin County Dabigatran Reversal

What I took from this excellent resource:

• Thrombin Time is probably the best available way to monitor this drug, but due to lack of lab standardization, we cannot establish non-institutional ranges
• If aPTT is totally normal (<1.5x), unlikely that sig. drug effect is present
• Can be dialyzed and ~60% will be removed at 2-3 hour mark
• Despite the rec that FFP or PCC may be helpful, I am not sure why this would be the case. Factor VIIa or FEIBA seems the best choices, albeit not great or proven ones. I could totally be talking out of my arse, though.
• Activated charcoal will adsorb this drug if the patient took it <2 hours ago.

Here is a great review article on dabi.

The blog Clot Connect MD put up these references:

References

1. van Ryn J. Dabigatran etexilate – a novel, reversible, oral direct thrombin inhibitor: Interpretation of coagulation assays and reversal of anticoagulant activity. Thromb Haemost 2010; 103: 1116–1127.
2. Crowther MA. Managing bleeding in anticoagulated patients with a focus on novel therapeutic agents. J Thromb Haemost 2009; 7 (Suppl 1):107–110.
3. Eerenberg ES et al. Prothrombin Complex Concentrate reverses the anticoagulant effect of Rivaroxaban in healthy volunteers (abstract 1094; ASH annual meeting Dec 4-7, 2010, Orlando, FL).
4. Morishima Y et al. Anti-Inhibitor Coagulant Complex, Prothrombin Complex Concentrate, and recombinant factor VIIa reverse prothrombin time prolonged by Edoxaban in human plasma (abstract 3319; ASH annual meeting Dec 4-7, 2010, Orlando, FL)

and linked to another reversal protocol from UNC

great post from EM Lit of Note, pointing to a study that PCCs will reverse Rivaroxaban, but Not Dabigatran (these were non-activated PCCs AFAIK)

“Reversal of Rivaroxaban and Dabigatran by Prothrombin Complex Concentrate.” www.ncbi.nlm.nih.gov/pubmed/21900088

Leon Gussow of the Poison Review has another excellent post on the top 10 questions on Dabigatran

Just published study indicates that Dabi may not cause enlarged hematomas in head bleeds (Circulation 2011;124:1654-1662)

For a better understanding (if you are smarter than me) of how Dabigatran Etexilate affects lab assays, see this article Thromb Haemostasis 2012;107(5) Douxfils et al.)

You just read the post: Bleeding Patients on Dabigatran aka Pradaxa from EMCrit Blog - Emergency Department Critical Care.

Left Bundle Branch Block (LBBB) doesn’t = STEMI!

A few months ago, we had Dr. Stephen Smith on the podcast to discuss a variety of EKG issues. Dr. Smith has an EKG blog that is required reading for every ED and ICU doc. This is Part II and I think it discusses an incredibly important issue: right now major medical societies including the AHA and ACEP are asking us to fibrinolyse or PCI patients with new or presumed new LBBB. However, your interventionalists will tell you that this strategy is a ridiculous waste given how few acute occlusions will actually be found. Why this discrepancy?

Dr. Smith actually created a post specifically for this podcast; here is the full text:

A 45 year old male with no history of cardiac disease presented with new onset pulmonary edema.  He was intubated prehospital.  BP before and after intubation was 110 systolic, with HR of 120.

In a study of 19 patients with LAD occlusion, vs. 129 controls with ischemic symptoms and LBBB, at least one complex in V1-V4 with at least 2mm of STE and an ST/S ratio > 0.20 was highly specific for LAD occlusion (1).   Here is the reference for the abstract on proportionally excessively discordant ST depression (2).

Cases with excessive discordance of at least 5mm [Sgarbossa criteria 3] that did not have proportional discordance, did not have LAD occlusion.  The mean highest ST/S ratio for those without occlusion was 0.10 (95% CI: 0.09-0.11); the mean highest ST/S ratio for those with occlusion was 0.44 (95% CI: 0.19-1.05)

Because of this study, I believe the following rule is as good for diagnosis of STEMI in the setting of LBBB as standard interpretation of STEMI in the absence of BBB (and that it is more sensitive and specific than the Sgarbossa rule):

Smith modified Sgarbossa rule:

1) at least one lead with concordant STE (Sgarbossa criterion 1) or
2) at least one lead of V1-V3 with concordant ST depression (Sgarbossa criterion 2) or
3) proportionally excessively discordant ST elevation in V1-V4, as defined by an ST/S ratio of equal to or more than 0.20 and at least 2 mm of STE. (this replaces Sgarbossa criterion 3 which uses an absolute of 5mm)

It is important to remember that this is not sensitive for “MI” which is diagnosed by biomarkers. The lack of sensitivity of the Sgarbossa rule in previous studies is because the ECG is always (even without BBB) insensitive for MI.  It is, however, much more sensitive for occlusion.

Followup:
Because of proportionally excessive discordance in lead V4, (and, of course, clinical instability), the patient was taken for immediate angiography, which confirmed a 100% mid-LAD occlusion.

For a case with more than 5 mm of ST elevation in V1-V4, but without excessive proportional discordance, see this post:
http://hqmeded-ecg.blogspot.com/2011/02/new-lbbb-and-massive-st-elevation-do.html

Tom Bouthillet has done a great job of describing my ratio rule here:
http://ems12lead.com/2010/12/29/excessive-discordance-as-a-marker-of-acute-stemi-in-lbbb/

To learn more about the meaning of New LBBB, look here:
http://hqmeded-ecg.blogspot.com/2010/03/new-left-bundle-branch-block-is-poor.html

Caution: these data have not been published in a peer review journal, and the ACC/AHA still (though I believe wrongly, and this recommendation is rarely followed) recommends reperfusion for patients with ischemic symptoms and new LBBB, even without any specific findings of STEMI.

1. Dodd KW. Aramburo L. Broberg E. Smith SW. For Diagnosis of Acute Anterior Myocardial Infarction Due to Left Anterior Descending Artery Occlusion in Left Bundle Branch Block, High ST/S Ratio Is More Accurate than Convex ST Segment Morphology (Abstract 583). Academic Emergency Medicine 17(s1):S196; May 2010.

2. Dodd KW. Aramburo L. Henry TD. Smith SW. Ratio of Discordant ST Segment Elevation or Depression to QRS Complex Amplitude is an Accurate Diagnostic Criterion of Acute Myocardial Infarction in the Presence of Left Bundle Branch Block (Abstract 551). Circulation October 2008;118 (18 Supplement):S578.

Additional References

(1) Jain S, et al. Utility of left bundle branch block as a diagnostic criterion for acute myocardial infarction Am J Cardiol 2011;107(8):1111-6.
(2) Poon K, et al. Abstract 4317: Does a New or Presumed New Left Bundle Branch Block Have Equivalent Mortality to an Acute ST-Elevation Myocardial Infarction? Circulation 120: S935.
(3) Kontos MC, et al. Outcomes in patients with chronicity of left bundle-branch block with possible acute myocardial infarction Am Heart J 2011;161(4): 698-704.
(4) Chang AM, et al. Lack of association between left bundle-branch block and acute myocardial infarction in symptomatic ED patients Am J Emerg Med 2009;27(8):916-21.

If you want a .doc or .pdf of these abstracts, email: dr.smiths.ecg.blog@gmail.com

You just read the post: EMCrit Podcast 48 – PhD in EKGs Part II: Left Bundle Branch Block from EMCrit Blog - Emergency Department Critical Care.

Cliff Reid of Resus.Me fame put out an incredible post on NAP4, the audit done on all of the airway complications in Great Britain. It was such a phenomenal post that I got in touch with Cliff and asked if he wanted to come on the podcast to speak about it. He did me one better and got an interview with one of the authors of the Emergency and Critical Care Section.

So in this podcast, we interview Dr. Jonathan Benger, professor of Emergency Medicine with a particular interest in the management of the airway.

Points that came out of the show

• Mortality is higher in the ED and ICU compared to the operating room. Our patients are sicker, so we must be more diligent in planning
• Quantitative wave-form ETCO2 should be the standard of care for EVERY ED and ICU intubation
• Needle cricothyrotomy seems to fail more often than surgical cricothyrotomy
• Awake intubation was not used when it was indicated
• Junior resident anesthesiologists were often responding to the ED and ICU
• There was a failure to plan for failure
• Obesity figured into a large percentage of the airway disasters

For more from the NAP4

Executive Summary

Full Report (Skip to the EM/ICU Chapter)

How to subscribe to Cliff Reid’s Brand New Podcast

• Go to itunes
• Choose Podcasts
• Go to the advanced menu and choose subscribe to podcast
• Paste this link: http://feeds.feedburner.com/ResusMePodcasts

Great Conferences Coming Up

• Essentials of Emergency Medicine in San Francisco – November 9-12
• Emergency Medicine in the Developing World in Capetown – November 15-17

You just read the post: EMCrit Podcast 47 – Failure to Plan for Failure: A Discussion of Airway Disasters from EMCrit Blog - Emergency Department Critical Care.

This is the 3rd part of a 4 part series on acid base.

You should listen to Acid-Base Part I first where you will learn about the underlying chemisty of acid base. Part II then delves into the underpinnings of the mathematics of acid base. In part III, we will go through two actual problems and show how the EMCrit method plays out. Part IV delves into the acid-base of solutions.
Before we get to the clinical stuff, I am giving three lectures at the 8th annual NY Symposium on Neurological Emergencies and Neurocritical Care. Should be a great conference. If you are free for some of the days between June 14-17, 2011; consider coming.

Ok back to acid base stuff.

For this podcast to be optimally effective, you need to print out my acid base sheet:

EMCrit Acid Base Method

Here is the 1st problem from last podcast:

Here is the same patient after we treated his DKA:

Mike asked if there was any literature to support the simplification I am using to make the incredible complex quantitative formula more approachable. The answer is yes and here is the pdf you want to read:

Story DA, Morimatsu H, Bellomo R. Strong ions, weak acids and base excess: a simplified Fencl-Stewart approach to clinical acid-base disorders. Br J Anaesth. 2004 Jan;92(1):54-60.

Want an incredible program that will do all of the work for you and teach you about the quantitative method at the same time? Look no further than this incredible site:

AcidBase.org’s analysis model

Need an Audio Only Version?
Acid Base Part III MP3 [Play]
[Play]
(Right Click and Choose Save as)

>

Click here to view the embedded video.

You just read the post: EMCrit Podcast 46 – Acid Base: Part III from EMCrit Blog - Emergency Department Critical Care.

You just read the post: Bonus – Passing the Esophageal Temperature Probe from EMCrit Blog - Emergency Department Critical Care.

This is the second part of a 4 part series on acid base.

You should listen to Acid-Base Part I first. In Part III, we solve the problem below and reunify everything. Part IV discusses the acid-base of administered solutions.
For this podcast to be optimally effective, you need to print out my acid base sheet:

EMCrit Acid Base Method

Here is the problem to work on for the next podcast:

I gave some shout-outs during the talk, here are the links:

• The Air Medical Memorial honors those flight medics, docs, pilots, and nurses who have fallen in the line of duty.
• Josh Mularella developed the free app call ERRES, search for it on itunes.
• Casey Parker created a site for outback EM and Crit Care called Broome Docs.
• Ivor Kovic donated three free codes to his cpr app, CPRPRO. Sign up for the mailing list if you want to enter to win one.

Click here to view the embedded video.

Need an Audio Only Version?
Acid Base Part II MP3 [Play]


(Right Click and Choose Save as)

>

You just read the post: EMCrit Podcast 45 – Acid Base: Part II from EMCrit Blog - Emergency Department Critical Care.

I have spoken about it for a while, but I’ve finally gotten it done: the acid-base podcast. The podcast is going to be in 3 or 4 parts. They are segmented from a lecture I gave to my residents recently. Part II discusses the mathematics of acid base and Part III goes through actual problems. Part IV then discusses the acid-base of administered solution.

This lecture discusses a quantitative approach to acid base management. This is also known  as the Fencl-Stewart approach, the strong-ion approach or the physicochemical approach. It provides explanations for why acid base disorders occur in human pathophysiology. The classic method used in the USA is the Henderson-Hasselbalch (misspelled on my slides) approach. I find this method to provide no comprehensive explanation for why things are as they are. Through the quantitative approach, you can also understand the H&H approach and continue to use it with new insight.

This first part deals with the preliminaries. Part II will go into clinical applications.

After listening to the podcast, I recommend reading this article:

Kaplan LJ,Frangos S. Clinical review: Acid–base abnormalities in the intensive care
unit. Critical Care 2005;9(2):198

For the next part of the series, you will need a print out of this sheet:

EMCrit Acid-Base Sheet

Need an Audio Only Version?
Acid Base Part I MP3 [Play]
(Right Click and Choose Save as)

…

You just read the post: EMCrit Podcast 44 – Acid Base: Part I from EMCrit Blog - Emergency Department Critical Care.

Since we had the Kayexalate episode, I did not want to do a full podcast, so I thought I would just air some listener questions:

• Adrian wrote asking about why A/C over SIMV when choosing a vent mode
• Cory wanted to know if NIV is any good for COPD
• Michael was worried about the level of dogma that has crept into EM/Critical Care podcasts

You just read the post: Listener Questions – Episode 1 from EMCrit Blog - Emergency Department Critical Care.

In EMCrit Podcast 32, we discussed the management of hyperkalemia. Of course, I recommended kayexalate in the treatment regimen. It is standard of care, right? So I thought, until I heard a brilliant piece by Dr. Siamak (Mak) Moayedi, MD. Dr. Moayedi reviewed the evidence and he found nothing to indicate that kayexalate is effective for the acute management of elevated potassium.

This was too good not to share with you folks, so first I got permission from Amal Mattu (EKG deity). Dr. Mattu had interviewed Dr. Moayedi for this piece and had placed it on the February episode of  his excellent EMcast podcast. I also got permission from Rick Nunez, MD who runs the incredible educational resource, EMEDhome.

For more from Dr. Moayedi, listen to his fantastic piece on how to teach procedures from Rob Roger’s, EM:RAP Educators Edition.

References Mentioned in the Piece:

1. Levine M, Nikkanen H, Palin DJ. The effects of intravenous calcium in patients with digoxin toxicity. J Emerg Med 2011;40:41-46.
2. Sterns RH, Rojas M, Bernstein P, Chennupati S. Ion-exchange resins for the treatment of hyperkalemia: Are they safe and effective? J Am Soc Nephrol 21: 733-5, 2010.
3. Scherr L, Ogden DA, Mead AW, et al. Management of hyperkalemia with a cation-exchange resin. N Engl J Med 264: 115-9, 1961.
4. Flinn RB, Merrill JP, Welzan WR. Treatment of the oliguric patient with a new sodium ion exchange resin and sorbitol: A preliminary report. N Engl J Med 264: 111-5, 1961.
5. Gruy-Kapral C, Emmett M, Santa Ana CA, et al. Effect of single dose resin-cathartic therapy on serum potassium concentration in patients with end-stage renal disease. J Am Soc Nephrol 9: 1924–30, 1998.
6. Mahoney BA, Smith WAD, Lo D, et al. Emergency interventions for hyperkalaemia (review).
   Cochcran Database of Systematic Reviews 2005, issue 3, 2009.
7. Kamel K, Wei C. Controversial issues in the treatment of hyperkalaemia. Nephrol Dial Transplant 18: 2215-8, 2003.
8. Rogers BR, LI SC. Acute colonic necrosis associated with sodium polystyrene sulfonate (kayexalate) enemas in a critically ill patient: Case report and review of the literature. J Trauma 51: 395-7, 2001.
9. Nyirenda MJ, Tang JI, Padfield PL, Seckl JR. Hyperkalaemia. BMJ 339: 1019-24, 2009.
10. Bomback A, Woosley JT, Kshirsagar AV. Colonic necrosis due to sodium polystyrene sulfate (kayexalate). Am J of EM 27: 753.e1-753.e2, 2009.
11. Welsberg LS. Management of severe hyperkalemia. Crit Care Med 36: 3246-51, 2008.
12. Sood MM, Sood AR, Richardson R. Emergency management and commonly encountered outpatient scenarios in patients with hyperkalemia. Mayo Clin Proc 82: 1553-61, 2007.

If you want to just hand the Gen Med Residents a Single Article:

Then I think this one by Sterns et al. is the one.

Here is the Audio:

You just read the post: Bonus – Is Kayexalate Useless? from EMCrit Blog - Emergency Department Critical Care.

Folks have asked for a video to go with Podcast 43 and as always I do what folks ask for.

You just read the post: Video for Podcast 43 – Inserting the Air-Q from EMCrit Blog - Emergency Department Critical Care.

My favorite supraglottic airway is the Cookgas Air-Q; it was created by an anesthesiologist, Dr. Daniel Cook. He just created a new device that allows the placement of an esophageal blocker through the laryngeal airway. I gave him a call to hear about the new product and in the course of that conversation, he gave me a ton of tips on the placement of laryngeal airways. Part II will specifically discuss the new device.

Placement of the ILA

• Put the patient in sniffing position
• Lube it really well (get the bottom, the cuff, and the horizontal ridges up front)
• Dr. Cook recommends an insertion using a tongue depressor to pull the tube forward. He inserts straight back instead of riding the hard palate. If the LMA doesn’t quite turn the corner, he inserts his left index finger just posterior to the tip and flexes his finger to get the LMA to make the curve into the lower pharynx
• He gently advances until the LMA comes to a rest—don’t push too hard
• At this point he puts 4-5 cc of air in for the 4.5 size and 3-4 cc of air for the 3.5 size (same amount of air as the size of the LMA)

Blind Intubation through the ILA

• First step is to lube the inside of the ILA. Use the ET tube itself—put a big glob of lube on the distal portion of the ETT and then advance it until it is just about to pop out of the keyhole opening of the ILA. This distance will be 20 cm in the 4.5 size and 18 cm in the 3.5 size (keep subtracting 2cm for each downsizing)
• No readvance the ETT to that same point, put your index finger on the top and use it to ever so slowly advance the ET. You can have a hand over the cricoid to feel the ETT as it passes.
• Inflate and confirm by listening over the stomach and looking for End-Tidal CO2.
• If you missed, pull back to that same point that is just before the opening of the cuff and inflate the ETT cuff with 1-2 cc of air. You can now reoxygenate the patient before your next attempt.
• The second attempt should probably be with a fiberoptic device or a bougie.

Bougie Intubation through the ILA

• First lube the ILA using the ETT, then remove the ETT
• Advance the bougie using the coude end with the coude facing towards the ceiling.

Here is the podcast:

You just read the post: EMCrit Podcast 43 – Laryngeal Airways with Daniel Cook, MD (Part I) from EMCrit Blog - Emergency Department Critical Care.

Today, I got to interview Dr. Stephen Smith. Dr. Smith is faculty at the Hennepin Program and author of one of the best books on EKGs in the ED, The ECG in Acute MI.

Dr. Smith’s EKG Blog is probably the best free EKG site out there for Emergency Physicians and Intensivists.

Here are the points we covered:

1. Ischemia Doesn’t Localize

If you see depressions in just one anatomic area, think reciprocal changes to subtle ST-elevations elsewhere

2. If you see Inferior Depressions, think High Lateral Wall STEMI

here are two good cases from Dr. Smith’s Blog:

• Case: This is a 35 yo woman who had LAD occlusion that was very subtle on ECG, but easily seen with inferior ST depression
• Case: This is one of a high lateral MI due to OM-2 occlusion that shows up mostly with inferior ST depression.

3. Lateral Wall STEMIs are often Subtle

• Case: A patient had chest pain, went to his doctor who did an EKG, said it was fine, and sent my friend home. He had a cardiac arrest at home and was resuscitated because of good CPR by his wife.  Later, I asked him to find the ECG.  I told him I’m pretty sure it was not normal.  And here it is: a very subtle high lateral MI detected by subtle ST depression in II and aVF
• Another Case

4. Absolute millimeter criteria for STEMI will often fail you, it is the Pattern that Matters.

5. Benign Early Repolarization and LAD Occlusion can look very similar–You may need to do the math.

Dr. Smith derived this formula:

(1.196 x STE60 in V3 in mm) + (0.059 x computerized QTc in milliseconds) – (0.326 x RA in V4 in mm),

where RA is R-wave amplitude and STE60 is ST elevation at 60ms after the J-point relative to the PR interval.

If the value of the formula is greater than or equal to 23.4, it is MI (Sens, spec, accuracy all around 90%); if less, then it’s early repolarization.

• Case: Here is a case that illustrates this, it shows a very subtle anterior STEMI, and how use of the complicated new rule that he developed. One need not use the complicated rule; among other  features, it was the long QTc of 455ms that made it unlikely to be normal.   The followup ECG is also very instructive.

You can also see a video of the concept

6. If you are calling it BER, there need to be R waves in the Precordial Leads

7. Q-waves can develop instantly after a STEMI

qR waves can develop instantly and are not indicative of poor response to lytics or PCI (J Am Coll Cardiol 1995;25:1084); this concept is not  applicable to a QS pattern.

8. If you see a wide (>190 ms) QRS, think Hyperkalemia

9. The treatment for VT with hyper-K is Calcium, Calcium, Calcium

• Check out this Case, it says it all

10. Check Out these Two Other Great Sites

HQMEDED: High Quality Medical Education and Ultrasound

The Prehospital 12-lead ECG Blog which despite the name, is great for all levels

You just read the post: EMCrit Podcast 42: A phD in EKG with Steve Smith from EMCrit Blog - Emergency Department Critical Care.

I was able to cajole Cliff Reid of the amazing blog, resus.me on to the EMCrit program. Cliff is truly a doc after my own heart as you will hear from the cast.

He is currently an EMS physician and Director of Training at the New South Wales Ambulance Service.

Cliff’s blog, resus.me is an incredible collection of timely articles on emergency medicine, ems, critical care and resuscitation.

Cliff mentions the HEMS service in London. This amazing service sends a physician/paramedic team to the scenes of bad traumas by helicopter and response cars. A well done video is available on youtube:

Click here to view the embedded video.

The winner of the Toxicology Handbook is Jenny Mendelson. Yeah!!!

photo by Mad Scientist

Click Here to Play the Podcast

You just read the post: EMCrit Podcast 41 – Interview with Cliff Reid of RESUS.me from EMCrit Blog - Emergency Department Critical Care.

Mike Cadogan’s book is the Toxicology Handbook; Click the link in the sidebar to win a copy

Here is the reference for the incredible guidelines on ketamine in the ED.

On to Delayed Sequence Intubation (DSI)

The Case

You have a 50 y/o male with bad bilateral pneumonia. BP 108/70, HR 96, RR 28. He is delirious, agitated, and looks sick, sick, sick! Saturation is 70% on a nasal cannula; when you try to place the patient on a non-rebreather (NRB) he just swats your hand away and rips off the mask. It is obvious to everyone in the room that this patient needs intubation, but the question is how are you going to do it?

Your first impulse may be to perform RSI, maybe with some bagging during the paralysis period. This is essentially a gamble. If you have first pass success, you (and your patient) may just luck out, allowing you to get the tube in and start ventilation before critical desaturation and the resultant hemodynamic instability. However, the odds are against you: bagging during RSI predisposes to aspiration, conventional BVM without a PEEP valve is unlikely to raise the saturation in this shunted patient, and if there is any difficulty in first-pass tube placement your patient will be in a very bad place.

A Better Way

Sometimes patients like this one, who desperately require preoxygenation will impede its provision. Hypoxia and hypercapnia can lead to delirium, causing these patients to rip off their NRB or non-invasive ventilation (NIV) masks. This delirium, combined with the low oxygen desaturation on the monitor, often leads to precipitous attempts at intubation without adequate preoxygenation.

Standard RSI consists of the simultaneous administration of a sedative and a paralytic agent and the provision of no ventilations until after endotracheal intubation (1). This sequence can be broken to allow for adequate preoxygenation without risking gastric insufflation or aspiration; we call this method “delayed sequence intubation” (DSI). DSI consists of the administration of specific sedative agents, which do not blunt spontaneous ventilations or airway reflexes; followed by a period of preoxygenation before the administration of a paralytic agent.(2)

Another way to think about DSI is as a procedural sedation, the procedure in this case being effective preoxygenation. After the completion of this procedure, the patient can be paralyzed and intubated. Just like in a procedural sedation, we want our patients to be calm, but still spontaneously breathing and protecting their airway.

The ideal agent for this use is ketamine. This medication will not blunt patient respirations or airway reflexes and provides a dissociative state, allowing the application of preoxygenation. A dose of 1–2 mg/kg by slow intravenous push will produce a calmed patient within ~ 30 seconds. Preoxygenation can then proceed in a safe controlled fashion. This can be accomplished with a NRB, or preferably in a patient exhibiting shunt, by use of a non-invasive mask hooked up to ventilator with a CPAP setting of 5-15 cm H₂0 (or some of the new masks that don’t require a machine, but more on that soon). After a saturation of > 95% is achieved, the patient is allowed to breathe the high fiO₂ oxygen for an additional 2–3 min to achieve adequate denitrogenation. A paralytic is then administered and after the 45–60 second apneic period, the patient can be intubated.

In patients with high blood pressure or tachycardia, the sympathomimetic effects of ketamine may be undesirable. While, these effects can be blunted with small doses of benzodiazepine and perhaps, labetalol (3), a preferable sedation agent is available for these hypertensive or tachycardic patients. Dexmedetomidine is an alpha-2 agonist, which provides sedation with no blunting of respiratory drive or airway reflexes (4-5). A dose of 1 mcg/kg administered over 10 minutes will lead to a sedated patient who will accept preoxygenation after 3-5 minutes in most cases.

Another advantage of DSI is that frequently, after the sedative agent is administered and the patient is placed on non-invasive ventilation, the respiratory parameters improve so dramatically that intubation can be avoided. In these cases, we then allow the sedative to wear off and reassess the patient’s mental status and work of breathing. If we deem that intubation is still necessary at this point, we can proceed with standard RSI by administering a conventional sedation agent (e.g. etomidate or additional ketamine) in combination with a paralytic, as the patient has already been appropriately preoxygenated.

A video demonstrating the above concepts is at: http://emcrit.org/misc/preox/

A version of this article originally appeared in ACEP News.

1. Walls RM, Murphy MF. Manual of emergency airway management, 3rd edn. Philadelphia, PA: Lippincott Williams & Wilkins; 2008.

2. Weingart SD. Preoxygenation, reoxygenation, and delayed sequence intubation in the emergency department. J Emerg Med2010 Apr 7. [Epub ahead of print]

3. Aroni F, Iacovidou N, Dontas I, Pourzitaki C, Xanthos T. Pharmacological aspects and potential new clinical applications of ketamine: reevaluation of an old drug. J Clin Pharmacol 2009;49:957–64.

4. Carollo DS, Nossaman BD, Ramadhyani U. Dexmedetomidine: a review of clinical applications. Curr Opin Anaesthesiol 2008;21:457–61.

5. Abdelmalak B, Makary L, Hoban J, Doyle DJ. Dexmedetomidine as sole sedative for awake intubation in management of the critical airway. J Clin Anesth 2007;19:370–3.

You just read the post: EMCrit Podcast 40 – Delayed Sequence Intubation (DSI) from EMCrit Blog - Emergency Department Critical Care.

Hi there Dr.Scott.

I’m Ahad (pronounced as “AA” like when the doc wants to examine your throat then followed by ”had”) an emergency medicine resident and junior educator for King Saud University at King Khalid University Hospital from Saudi Arabia.

I wanted to tell you the whole story about the mnemonic “DOPE”. It was initially used by plumbers and oil workers in the 1950s. They used a substance which was a chemical sealant called “pipe dope” to seal pipes. They used to check the integrity of the pipes by saying “Don’t forget DOPE” and also to remind them to apply it in the first place.

How they used the mnemonic is very similar to how doctors use it…

D=displacement of the pipes that are joined

O=obstruction within the pipes tested due to the substance clogging the inside of the pipe

P=pneumatic pump to test for air leaks

E=equipment failure in testing e.g hydraulics…etc

One day there was a plumbing problem and a leak was found in one of the ORs the plumbers were there and one shouted “Don’t forget DOPE” while explaining what to do to the other plumber… This incident occurred right in front of Dr.John Joseph Bonica (Wrestling Champ 1941and Anesthesiologist) and a couple of his residents/medical students (not sure) while he was explaining checking anesthesia equipments… he laughed and said “Don’t forget DOPE”.

At that time it wasn’t linked with endotrachial intubation! One of his student/residents linked it later on. That doctor was Prof.Thomas Michals who mentioned this story to the professor who told me this story Prof.Edward Luther Strivani ….

Hope that helped… By the way it was officially mentioned in the ATLS book in the 7th ed only…

Regards,

Ahad

You just read the post: Origins of the Dope Mnemonic from EMCrit Blog - Emergency Department Critical Care.

Hmm… he’s tasty, but he just needs a little salt

In this podcast, I discuss the management of hyponatremia in the ED. After reading countless articles from the nephrology literature…I can still attest that I have not a friggin’ clue about renal physiology. But I think I have found a simpler path to the work-up and treatment of low sodium in the ED.

When they are <130 is when I get a little worried

Step I-Send Lots of Labs

Here is what you need:

Serum-electrolytes, osmolality, uric acid, and you might as well send a TSH and cortisol as well

Urine-UA, urine lytes, urine urea, urine uric acid, urine osm, urine creatinine

Step II-Treat CNS dysfunction

If the patient is altered, comatose, seizing, or has neurologic findings, then raise the sodium by a little bit

Give 3% saline, 100 ml over 10-60 minutes

10 minutes later, may repeat X 1

may be given peripherally through any reasonable IV

each 100 ml will raise sodium by ~2 mmol/l

Step III-Hang tight

Do not feel the need to do anything else, just fluid restrict the patient

Place a foley

Do not feel tempted to give NS

Do not be clever, just fluid restrict and admit.

Patients are at a fall risk with hyponatremia

Get a CT scan if they are still a little wacky

Remember the rules of 6’s (from the Stern article below)

Be incredibly careful when correcting hypokalemia, potassium repletion will raise the Na

Step IV-What to do when you couldn’t follow step III

dDAVP 1-2 mcg IV or SubQ x 1

Consult renal

Consider D5W 6ml/kg over 1 hour in consultation with renal if you have really screwed up

Articles

Read this excellent case report from Stern

Excellent Review by Schrier (Curr Opin Crit Care 2008;14:627)

Review of Drug-Induced Hyponatremia (Am J Kidney Dis 2008;52:144)

Understanding Lab Testing for Hyponatremia (Clin J Am Soc Nephrol 2008;3:1175)

The hyponatremia formulas do not work so well (Clin J Am Soc Nephrol 2007;2:1110 and Nephrol Dial Transplant 2006;21:1564)

You just read the post: EMCrit Podcast 39 – Hyponatremia from EMCrit Blog - Emergency Department Critical Care.

Here are my 12 favorite ED Critical Care things for 2010…the EMCrit Dirty Dozen:

12. SmartEM by David Newman and Ashley Shreves

11. The Poison Review by Leon Gussow

10. Academic Life in Emergency Medicine by Michelle Lin

9. Zdoggmd–the funniest internist I have ever come across

8. Emergency Medicine Cases Podcast by Anton Helman

7. One Night in the ED, an incredible radiology blog for EM folks by a radiologist, Daniel Cornfeld

6. Steve Smith’s EKG Blog-even the cardiologists are not giving the same amount of detail as you will find here

5. Resus.me by Cliff Reid

4. EM:RAP by med ed hero, Mel Herbert

3. Ercast by my friend, Rob Orman

2. the Life in the Fast Lane Blog headed up by the amazing Mike Cadogan and Chris Nickson

1. Well for #1, you are just going to have to listen

You just read the post: EMCrit Podcast 38 – The ED Critical Care Dirty Dozen for 2010 from EMCrit Blog - Emergency Department Critical Care.

For the past few months, I have been co-chairing a NYC-wide sepsis collaborative under the auspices of a hospital organization. 56 hospitals have joined the collaborative with the goal of breaking down the barriers to aggressive sepsis care in the ED.

The protocols and educational materials for the project will always be cross-posted here:

http://emcrit.org/sepsis/

Many of the questions we have been getting relate to the use of lactate as a screen and an indicator of adequate treatment. Last week, I discussed these issues during a webinar. This podcast is the recording of that cast.

Here is the Lactate Reference Sheet

Other important info:

The emcrit webtext is now at crashingpatient.com and the blog has moved to http://emcrit.org

Scott Gallagher sent in the comment regarding commotio cordis as a cause of v-fib/v-tach in trauma patients. He is quite right to point out that ACLS works for these folks. Shock and use anti-dysrhythmics.

Here is a reference from the New England Journal:

NEJM 2010;362:917

You just read the post: EMCrit Podcast 37 – Lactate in Sepsis from EMCrit Blog - Emergency Department Critical Care.

Thanks to a suggestion from Melanie, this week I am discussing the management of traumatic arrest. Many things to do in these patients, but two things you definitely should not be doing are closed-chest CPR or giving ACLS medications. We discuss who gets a thoracotomy, what to do if a thoracotomy is not indicated, and when to stop.

Here is a great review article:

Hunt PA, Greaves I, Owens WA.  Emergency thoracotomy in thoracic trauma-a review. Injury. 2006 Jan;37(1):1-19.

This is one of the figures from the text. I think it is a great algorithm to determine who gets a thoracotomy:

From Hunt et al. Injury 2006;37:1

Place comments or questions here or on the facebook page at facebook.com/emcrit.

.

You just read the post: EMCrit Podcast 36 – Traumatic Arrest from EMCrit Blog - Emergency Department Critical Care.

In this podcast, I discuss extubating patients in the ED. Specifically, I deal with patients who have only been intubated for a few hours in distinction to extubation of the patient who has been lingering in your ED for 2-3 days. The best patients for this short-term extubation are those intox folks with a low GCS and signs of trauma, overdoses, or endoscopy cases.

My approach is outlined in this article; click on the link for the full text:

Weingart SD, Menaker J, et al. Trauma Patients Can Safely Be Extubated in the Emergency Department. J Emerg Med. 2009 Aug 22. [Epub ahead of print]

Here are the steps from the article:

Photo by EddieB55

You just read the post: EMCrit Podcast 35 – Extubation in the ED from EMCrit Blog - Emergency Department Critical Care.

Yes, there is an app for that

You just read the post: The Iphone for Head Impulse Testing from EMCrit Blog - Emergency Department Critical Care.

The brand new ACLS & BCLS guidelines were published last week. Not huge changes, but some good stuff! The free full text is available at the Circulation website. It takes hours to make your way through all of it. I boiled it down to just the facts and posted a summary on the Crashing Patient Site.

ACLS 2010 Guidelines Summary

In this EMCrit Podcast I discuss some of the highlights that I think are particularly important.

There have also been many questions about the head impulse testing discussed in episode 33. I have an easier method; check out this post.

You just read the post: EMCrit Podcast 34 – 2010 ACLS Guidelines from EMCrit Blog - Emergency Department Critical Care.

This is the video for cerebellar stroke diagnosis. Listen to the podcast first.

Video clips are from Dr. David Newman-Toker’s site

and from the article:

Kattah JC, Talkad AV, Wang DZ, Hsieh YH, Newman-Toker DE. HINTS to diagnose stroke in the acute vestibular syndrome: three-step bedside oculomotor examination more sensitive than early MRI diffusion-weighted imaging. Stroke. 2009 Nov;40(11):3504-10.

You just read the post: Video for Diagnosing Posterior Stroke from EMCrit Blog - Emergency Department Critical Care.

What if I told you that I think that patient you just sent home with vertigo may have been a missed cerebellar stroke? Would you be dialing risk management or could you tell me all of the reasons why I’m wrong? Isolated vertigo without other neurological findings can’t be a stroke, right? That is true, if you are doing the right exam, but if you are just doing your standard ED neuro screening exam then you might be missing serious pathology. In this episode of the EMCrit podcast, I discuss how to perform the tests that will differentiate a peripheral cause of continuous vertigo from a cerebellar stroke.

Drs. David Newman-Toker & Jorge Kattah, neurologists at John Hopkins, have done a ton of work on this topic. They have created an mnemonic for the exam you should be doing on all of your patients with continuous vertigo (as opposed to positional, intermittent vertigo, i.e. BPPV). Benign positional paroxysmal vertigo is not ED critical care. Continuous vertigo, also known as acute vestibular syndrome, may be. The mnemonic is HiNTS.

Hi for head impulse testing, or head thrust testing.
N for nystagmus to remind you to look for direction-changing or vertical nystagmus
TS for test of skew.

I will discuss what all of these terms mean and how to perform the exams in the podcast.

Here is the HiNTS article.

Here is a link to another study by the same authors on head impulse testing.

Here is a fantastic review article by James A. Nelson on the topic.

Here is a video demonstrating the exam with positives and negative examples.

Update

Insanely good systematic review on Dizzy Stroke Patients (CMAJ 2011;183(9):E571)

You just read the post: EMCrit Podcast 33 – Diagnosis of Posterior Stroke from EMCrit Blog - Emergency Department Critical Care.

If you have just attended one of my two lectures at ACEP 2010, here are the promised additional resources:

Neurocritical Care in the ED

Hemostasis: Stop that Bleed

You just read the post: Additional Resources for ACEP 2010 Lectures from EMCrit Blog - Emergency Department Critical Care.

>>> Update: For a new take on kayexalate, see Mak Moayedi’s Lecture

Hey folks. As I get ready for ACEP, I just wanted to get a quick podcast put up. One of the listeners requested an episode on the treatment of hyperkalemia in the ED.

There was a fantastic article published in Critical Care Medicine on the topic by a Dr. Weisberg. I go through my management and discuss some of the pearls from the article.

Weisberg LS. Management of severe hyperkalemia. Crit Care Med. 2008 Dec;36(12):3246-51.

Additional References added Feb 2012

ECG is insensitive and non-specific for severe hyperkalemia issues; essentially is crap (Clin J Am Soc Nephrol 3: 324-330, 2008). ECG peaked T waves, that resolved after K normalized were noted in only 1 of the 14 hyperkalemic patients who went on to have arrhythmia or cardiac arrest. Only half of them had any T-wave changes.

and now to the podcast…

You just read the post: EMCrit Podcast 32 – Treatment of Severe Hyperkalemia from EMCrit Blog - Emergency Department Critical Care.

This week we talk about managing the intra-arrest period of cardiac arrest. My paradigm has changed dramatically over the past few years. In the past, I viewed the arrest as a period to teach my residents how to place a subclavian central line, how to intubate when the patient is moving, and how to cram as many drugs as possible into a patient in a short period of time.

Looking at how I manage an arrest today, so much has changed.

I use the ACLS ABCDABCD mnemonic, though I’ve changed some of the intent:

A
Place an Oropharyngeal Airway

B
Place the patient on the ventilator with a BVM mask.
Set the vent to VT 500, Flow 30 lpm, Rate 10, FiO2 100%. Increase the pressure limit to 80-100 cm H20.

C
Compressions, Compressions, Compressions

The most important thing these days are continuous, rhythmic, chest compressions. If you want to get perfusion to the coronaries and get a chance at shocking (the only other effective therapy for arrest), you need perfect compressions.

I use a metronome and switch out providers every 1-2 minutes. Got the idea from this article.

Here is the metronome I use.

ETCO2 can be used as a marker of how well compressions are being performed.

D

Defib. Shock early and shock often.

You can shock without having the compressor stop compressions if they are wearing gloves and you have a biphasic defib with pads. (Circulation 2008;117:2510-2514.)

A

Advanced airway = LMA, not an ET Tube
Here is my LMA video

B
Advanced Breathing

Put the patient back on the vent. If you know how, switch them to pressure control at 20 cm H20, with an insp time of 1-2 seconds

C
Advanced circulation

pop in an IO

listen to the podcast for my feelings on meds

D
Differential

I recommend the RUSH exam created by my colleagues and me.

Last, we talk about when to stop: for me ETCO2 < 10 and no heart motion = stop, if I have been trying for 10-20 minutes.

You just read the post: EMCrit Podcast 31 – Intra-Arrest Management from EMCrit Blog - Emergency Department Critical Care.

After the meningitis episode, one of the listeners, David Thomas, recommended I check out a new opthalmoscope from a UK company.

I checked out the web site and had them send me a sample for evaluation.

The optyse opthalmoscope is lens free, you focus on the fundi by moving closer to the patient. It is really a well made, compact, dead simple little product.

My experience was that it was far superior to the wall fundoscopes. The light was brighter and the visualization better. Unfortunately, it doesn’t hold a candle to the far more expensive panoptic. When I dilated the eyes, I had a perfect view with the optyse. In undilated, ED eyes, only the panoptic gave me a great view of the fundi.

Check out the optyse at Opthalmos’ website

Disclaimer: Opthalmos sent me an evaluation model at my request. After the evaluation I sent the product back to the company; I did not keep it. I was not paid or compensated for reviewing their product.

You just read the post: Product Review: Optyse Ophthalmoscope from EMCrit Blog - Emergency Department Critical Care.

Hey folks,

I’m lecturing at ACEP in Las Vegas this year. This is one of two lectures I’m giving there. If you are going to the conference and plan on coming to my lecture, don’t listen to this lecture; I’d rather you hear the real one in person.

But if you can’t make it this year, and you have 50 minutes, take a listen and let me know what you think.

Here is the Handout

Here are the Slides

You just read the post: ACEP Preview – Hemostasis: Stopping the bleeding in a crashing trauma patient from EMCrit Blog - Emergency Department Critical Care.

This week we discuss the resuscitation of the hemorrhagic shock patient with Dr. Richard Dutton, MD.

Rick was director of trauma anesthesia at the Shock Trauma Center when I trained there. He is an incredible teacher, clinician, and researcher.

Here are the take home points:

• Induction agent choice does not matter in these patients; what matters is DOSE! Reduce dose to 1/10 of full intubating dose.
• Blood products need to be available in the trauma bay for when these patients arrive. If you need to give crystalloid while awaiting the products, give only small amounts just to keep the patients heart beating.
• A systolic of 80 with good perfusion and normal sized vessels is very different than that same SBP in a patient who is clamped down. The former is a resuscitated state, the latter =spiral of death.
• The resuscitation fluid for trauma is equal parts PRBC and FFP.

To read more of Dr. Dutton’s thoughts, go to this article:

ITACCS Damage Control Anesthesia

photo from trauma.org

You just read the post: EMCrit Podcast 30 – Hemorrhagic Shock Resuscitation from EMCrit Blog - Emergency Department Critical Care.

It seems the government and other specialties are trying hard to make sedation as difficult as possible in the ED. We must persevere to provide the best procedural sedation to allow maximal comfort and safety for our patients. This continues the discussion started in Part I, where we discussed etomidate, ketamine, and versed/fentanyl. In this podcast, I discuss propofol, ketofol, and dexmedetomidine.

the emcrit procedural sedation chapter has tons of references for all of this

Propofol

great propofol articles:

Ann Emerg Med 2008;52:392-398
Ann Emerg Med. 2007;50:182-187

Start with fentanyl 1-1.5 mcg/kg

Then give propofol 0.5-1 mg/kg

may need additional injections of 0.5 mg/kg

When patient is where you want them, begin the procedure

May need to give additional 20-30 mgs if the patient becomes too light

Burns on injection, you can precede with 20-40 mg of lidocaine to numb the vessels

Ketofol

read more here: (Ann Emerg Med. 2007;49:23-30)

1:1 mix of ketamine and propofol

In 20 ml syringe, place 10 ml of propofol (10 mg/ml)

And 10 ml of ketamine at a concentration of 10 mg/ml

Note: your ketamine may come in a different concentration, if so dilute down to 10 ml of 10 mg/ml

Shake like a martini

Dexmedetomidine

Precede with fentanyl 1 mcg/kg

Start with 0.5-1 mcg/kg over 10 minutes for loading dose

then use an infusion 0f 0.2-1 mcg/kg/hr

Beware in the bradycardic, hypotensive or patients with heart blocks

May need to supplement with 1-2 mg of midazolam

Procedural Sedation Checklist

here it is

Stay tuned for part III coming to you some time in the future.

You just read the post: EMCrit Podcast 29 – Procedural Sedation, Part II from EMCrit Blog - Emergency Department Critical Care.

This is a piece I wrote for the excellent Emergency Medicine Practice Guidelines Update, edited by my friend, Reuben Strayer.

You just read the post: Procedural Sedation Guidelines Update from EMCrit Blog - Emergency Department Critical Care.

The audio only version of Part I of the sedation talk.

Remember to check out Part II next…

You just read the post: Procedural Sedation, Part I (Audio Only) from EMCrit Blog - Emergency Department Critical Care.

It seems the government and other specialties are trying hard to make sedation as difficult as possible in the ED. We must persevere to provide the best procedural sedation for the maximal comfort and safety for our patients. This brief lecture was originally posted on the defunct EMCrit Lecture Site on 8/7/2009.

I’m reposting it here so I can post part II sometime this week.

This episode, Part I, covers general concepts on sedation as well as ketamine and etomidate/fentanyl.

Part II will cover propofol, ketofol, and dexmedetomidine.

Part III, to be done some time in the future, will cover really difficult sedations.

In a separate post, I will place an update I did for EM Practice with my fiance on sedation guidelines.

You just read the post: Procedural Sedation – Part I from EMCrit Blog - Emergency Department Critical Care.

Severe CNS Infections are time dependent diagnoses! You must have a high index of suspicion, a good plan for your work-up, and rapid provision of treatment. After seeing a severely ill meningitis patient, I figured I would do a podcast on some tips and pearls on this topic.

When to Suspect

Here is the article I mentioned on establishing pretest prob:

http://pmid.us/15509818

What Antibiotics

Ceftriaxone 2g as empiric therapy in any suspected meningitis patient

If high risk or LP results are positive, also give

• Vancomycin 1 G
• Ampicillin 2g if age > 60
• Acyclovir 10  mg/kg if high RBC count, obtundation, seizures, or focal neurologic deficit
• Dexamethasone 10 mg
• Cefepime or Imipenem if hospitalized or neurosurgery patient

listen to the podcast for more and see the EMCrit chapter for more.

photo by Lapoland

You just read the post: EMCrit Podcast 28 – Severe CNS Infections from EMCrit Blog - Emergency Department Critical Care.

An article I wrote with one of my ED Critical Care buddies, Chad Meyers, is now free on EM Practice.

Critical Care Monitoring in the ED

You just read the post: Critical Care Monitoring in the ED from EMCrit Blog - Emergency Department Critical Care.

Chris Nickson, one of my favorite EM bloggers, wrote with some great additional resources on calcium channel blocker overdose.

I love that story about the successful use of ONE THOUSAND units of insulin in severe CCB toxicty – without any adverse effects. Indeed, the early use of high-dose insulin euglycemic therapy (HIET) for CCB overdoses is a subject close to my heart (http://lifeinthefastlane.com/2009/09/insulin-for-verapamil-overdose/).

Also, I’ve got a “case-based Q and A” that EmCrit listeners may find useful for learning/ testing their knowledge on CCB overdose and HIET here: http://lifeinthefastlane.com/2010/02/toxicology-conundrum-028/ (…where an infamous Australian pharmacist-blogger almost meets his demise).

Hope EmCrit listeners find the LitFL links useful.

Cheers,
Chris

 

 

Also, asked Leon for a review article and he recommended this one:

Calcium and Beta-Blocker OD Review

You just read the post: Life in the Fast Lane CCB OD Stuff from EMCrit Blog - Emergency Department Critical Care.

This week, I am joined by Leon Gussow, MD of the excellent blog: The Poison Review (TPR). TPR is my source for new toxicology articles; I highly recommend it as an incredible read. I got to meet Leon for a few beers a month ago; he is a great guy.

My Canadian pal, Ram, suggested calcium channel blocker OD as a podcast episode. Ram, here you go.

Calcium Channel Blocker OD

CCB Classes

Nifedipine and other dihydropyridines (amlodipine, felodipine, isradipine, nicardipine, nimodipine, nisoldipine) will cause profound hypotension without bradycardia, due to poor affinity for myocardial calcium channels.  This selectivity is not lost in overdose.  They may actually present with reflex tachycardia

How to tell CCB OD from B-Blocker

CCBs do not cause AMS

CCBs block receptor in B-Islet cells, preventing insulin release, so can see hyperglycemia as opposed to the normal-low sugar in B-Blockers

Presentation

Weak/Dizzy, mild confusion, bradycardia progressing to severe hypotension and shock

Selectivity is lost in overdose (except dihydropyridines)

Treatment

·        Activated Charcoal x 1

·        Whole bowel-Irrigation is not recommended by Leon’s group

·        Frequent glucose and k checks

·        Atropine (can try it once, but it will limit gastric motility and probably won’t work)

·        Calcium, 1 g of CaCl or 3 g of CaGluc.  Give slowly over 3 minutes for CaCl and 10 min for CaGluc.

·        Glucagon 5 mg bolus, probably won’t do much, unlike in beta blocker OD

·        IVF

·       High Dose Insulin. Start with 1 unit/kg push followed by 0.5-1 unit/kg/hr. Fingersticks q30 minutes and adequate glucose replacement if needed. Check potassium; supplement if < 2.5. (Crit Care 2006;10:212)

·        May need to use norepinephrine or dopamine (alternatively Epi). May need much higher doses of epi or norepi. Dopamine must be stopped at 20 mcg/kg/min, which is kind of a joke in this OD. Switch to one of the others if you get this high.

·        Levosimendan may have a role, but not available in the US.

·        IABP, CP Bypass

<photo by ilovespoons>

You just read the post: EMCrit Podcast 27 – Calcium Channel Blocker Overdose from EMCrit Blog - Emergency Department Critical Care.

At this stage of the game, if your hospital is not offering hypothermia to out-of-hospital cardiac arrests, you are probably lagging behind optimal care. For shockable rhythms, you essentially double your patient’s chances of leaving the hospital with good neurological outcome. However hypothermia can be tough, unless you have done a bunch. Learn from my mistakes in this lecture.

NCS 2010 Hypothermia Talk

I’d love to hear your comments and what you are doing at your hospital.

for more hypothermia resources, see my NYC Hypothermia Section

You just read the post: EMCrit Lecture – Top Ten Hypothermia Tips from EMCrit Blog - Emergency Department Critical Care.

When I was a resident, every vent lecture either put me to sleep or left me dazed and bewildered. I gave a lecture of that ilk when I started working after fellowship. I had become part of the problem. I decided there must be a way to make vent management more understandable and if not interesting, at least bearable.

This lecture was up on the soon to be defunct EMCrit Lecture site. It offers a path to managing any patient on the ventilator in the ED. I have tried to simplify as much as possible while still maintaining an evidence-based approach.

This is Part II, it deals with the obstructive strategy. Last week, we spoke about the strategy for patients with  lung injury.

Your goal with these patients is to let them have adequate time to breathe out.

There are only 4 things you need to remember for an obstructive patient

Vt (Tidal Volume) = 8 ml/kg, don’t mess with it

Flow Rate = shorter insp times, 80-100 lpm

Resp Rate = Lung protection, start at 10 work your way down if necessary

FiO2/PEEP = Oxygenation, should need much O2 (40%)m I recommend PEEP of 0, but certainly keep it less than 5

First Print out this Handout

If you need just the audio [right or cntrl click here]

Click here to view the embedded video.

You just read the post: EMCrit Lecture – Dominating the Vent: Part II from EMCrit Blog - Emergency Department Critical Care.

Dr. Gentile responded to a few listener questions below:

HOW  DIPHENHYDRAMINE ENTERED PROTOCOL

when i first started using “high”  dose opiates for the most severe patients about one third of them experienced nausea and or vomiting. Sometimes the guy in bed 2 vomits, then after /during mop up the girl in bed 3 vomits, the woman in 5 is here for asthma she is offended by  the smell and she vomits too. i was not popular with housekeeping but i was much appreciated by those who received the opiates. i asked some of the worst vomiters if the vomiting was worse than the pain. Every single one said the vomiting was no problem ,and they felt better vomiting than they did in pain. Some even vomited while they were answering the question.

The next leap was giving IV antiemetic prophylactically, with the first dose of morphine. i initially felt some trepidation giving anti-emetic when 2/3 of patients probably would not benefit from the drug. Then i remembered demerol and phenergan had been given together for ages. i felt validated by this precedent and forged ahead.  it worked great and the vomiting/mopping cycle stopped. Housekeepers stopped giving me the stink-eye.

My favorite anti-emetic was compazine. There were a few dystonic reactions and some akisthesia but overall it was a success.

Compazine was unavailable for a few years and i switched to droperidol. The droperidol gave a lot less dystonia and less akisthesia, so that too was progress. Hundreds of happy doses of droperidol and no problems. It was a useful adjunct for analgesia,

Droperidol was great for nausea and vomiting without pain. Many of the vomiting patients reaped the benefit of central dopamine antagonism as well  [Some people with abdominal pain are crazy ]. What a great drug. Droperidol got black boxed. Once again the interests of the suffering masses were sacrificed to the interests of big pharm. The instrument of destruction was our FDA, an organization that is supposed to protect people from big pharm. I started looking for other options.

A haldol overdose came in one day and i was reading about butyrophenone overdose and discovered the butyrophenones [haldol, droperidol] have antihistamine side effects. That’s when i had the insight that histamine was the real culprit causing the the vomiting.

Histamine causes an itchy feeling when the opiate goes into the vein, histamine causes hypotension, histamine causes nausea and vomiting. Do all anti-emetic drugs have anti histamine “side-effects”.  Compazine yes reglan yes droperidol yes tigan yes phenergan yes. Zofran [i'm not sure]. I would call this more than an interesting coincidence. The antihistamine side effect of anti-emetic drugs might be the mechanism of action, not really a side -effect at all.

Have you seen an orthopedic injury that hurts so bad the patient vomits? Do endogenous opiates cause histamine release?

Many ER patients have abdominal pain and vomiting; most of the time the pain protocol gets rid of both the pain and the vomiting.  Not true with small bowel  obstructions but most of the time additional “anti-emetic” is not needed.

so diphenhydramine went into the protocol; and life is very good. i got a little sad that patients receiving state of the art acute analgesia were getting admitted to the hospital and taking the elevator to 1960. i thought it might be nice if admitted pain protocol patients got a PCA pump automatically. i started reading about PCA pump protocols and most of them use diphenhydramine and morphine. The PCA literature validates what i “discovered”. The anesthesiologist/oncologists that developed PCA have known that diphenhydramine is useful for a long time.

Diphenhydramine at .5 mg/kg does not make old or young people too sleepy. Some people on the protocol go to sleep. Some of the patients are tired. If i was awake at home for three days with a broken hip, i would go to sleep the moment someone took the edge off my pain. Some of the patients are bored to sleep. If i was in the ER gurney without a book what are my options [read "patient rights and responsibilities" again, watch my heart rhythm, or sleep.] Sleep is not a little dead. Sleep is good.

i do not have references to support my statements about hypotension. Only my subjective observations that there have been a lot less of this conversation at work since we started using diphenhydramine.

aren’t you tired of this conversation.

nurse———–”the blood pressure is down in clinic 7 bed”

doctor—–”give em 500 normal saline stat”

10 minutes later

nurse——”the pressure is back up”

doctor—-”good”

was the patient in bed 7 sick? did they get better? was their life saved or even subtly improved by a transient change in a measurement they can not feel?

i agree that a blood pressure of zero is usually bad, but if my blood pressure drops 10% i am not 10% dead. The culture around blood pressure measurements and reactions/over reactions in the E.R. is irrational.

The less time spent on this futile ritual the better. i am sure there has been less of this since diphenhydramine was included. i did not count it or study it. i just noticed it like i notice the weather is usually sunny on my way to work. It’s true. if you like sun move to southern california.

You just read the post: Further Comments on Pain Protocol from EMCrit Blog - Emergency Department Critical Care.

When I was a resident, every vent lecture either put me to sleep or left me dazed and bewildered. I gave a lecture of that ilk when I started working after fellowship. I had become part of the problem. I decided there must be a way to make vent management more understandable and if not interesting, at least bearable.

This lecture was up on the soon to be defunct EMCrit Lecture site. It offers a path to managing any patient on the ventilator in the ED. I have tried to simplify as much as possible while still maintaining an evidence-based approach.

This is Part I, it deals with the lung injury strategy. Next week, we’ll talk about the strategy for patients with obstructive lung disease.

There are only 4 things you need to remember for a lung injury patient:

Vt (Tidal Volume) = Lung Protection

Flow Rate = Patient Comfort

Resp Rate = Ventilation

FiO2/PEEP = Oxygenation

First Print out this Handout

If you need just the audio [right or cntrl click here]

Click here to view the embedded video.

You just read the post: EMCrit Lecture – Dominating the Vent: Part I from EMCrit Blog - Emergency Department Critical Care.

This post is just to place the vent handout into itunes.

You just read the post: Vent Handout from EMCrit Blog - Emergency Department Critical Care.

Even when we can’t cure a patient, we can relieve suffering. On average, we kind of stink at pain control in the ED. One physician, Dr. Ed Gentile, has created a simple path to optimal acute pain control in the ED. I heard this lecture on the EM:RAP podcast and got permission from Drs. Gentile and Herbert to repost it here. This is not a critical care topic per se, but it is applicable to the critically ill, the non-critically ill–basically any patient who is in pain in the ED.

Patient Controlled Analgesia

by Ed Gentile, MD

Need for an effective and efficient process is self evident .

Acute pain protocol for moderate/severe pain

• Administer morphine 0.1 mg/kg IVP (If pt is > 55 y/o, substitute morphine 0.05 mg/kg IVP for this 1st dose)
  + diphenhydramine 0.5 mg/kg IVP
• 7 minutes later the patient is asked, “Would you like more pain medicine?”
• If the answer is yes, give a 2nd dose of morphine 0.05 mg/kg IVP
• 7 minutes later, the patient is asked again, “Would you like more pain medicine?”
• If the answer is yes, give a 3rd dose of morphine 0.05 mg/kg IVP
• This continues every 7 minutes until the patient answers “no” to the question or the patient is asleep.

According to Dr. Gentile, “We don’t want to use the minimum, but the optimum pain dose for all patients.”

The protocol uses morphine because it has the longest half-life .

Diphenhydramine prevents antihistamine effects: nausea, vomiting, hypotension.

The protocol is unbiased and controlled by the patient!

Photo by Azarius

You just read the post: EMCrit Podcast 26 – Patient Controlled Analgesia by Edward Gentile from EMCrit Blog - Emergency Department Critical Care.

Rob Orman has a fantastic podcast called the ERCast. You can also search for “ercast” on itunes. He was kind enough to have me on his latest episode. Check it out if you like.

You just read the post: ERCast Podcast from EMCrit Blog - Emergency Department Critical Care.