There is always a better option

We have many meds to choose from for emergency intubations. Sometimes we use propofol works well (status epilepticus, severe hypertension), sometimes versed/fentanyl (severe pain, head injured), methohexital (if you have a time machine and are intubating in 1999), thiopental (your toxicologist needs consults) and of course ketamine is basically always the best choice (if their BP is already too high just add propofol).

Etomidate is an ok drug, decent for intubation and sometimes helpful for sedation for imaging or even for a procedure (watch out for myoclonus). But I usually point out that there is always a better option than etomidate.

This meta-analysis of only 11 studies looked at etomidate vs other agents for intubations in critically ill patients. The summary seems to support the “always a better option than etomidate statement.” See results below, how about that number needed to harm?!

Results

We included 11 randomized trials comprising 2704 patients. We found that etomidate increased mortality (319/1359 [23%] vs. 267/1345 [20%]; risk ratio (RR) = 1.16; 95% confidence interval (CI), 1.01–1.33; P = 0.03; I2 = 0%; number needed to harm = 31). The probabilities of any increase and a 1% increase (NNH ≤100) in mortality were 98.1% and 92.1%, respectively.

Conclusions

This meta-analysis found a high probability that etomidate increases mortality when used as an induction agent in critically ill patients with a number needed to harm of 31.

Reanimating the Dead

It’s trauma season once again. As room 9 after room 9 roll in the door the rising 2nd and 3rd years will soon be dealing with traumatic arrest patients (if they haven’t already). While the ED resident works to control the airway, the trauma team is placing bilateral chest tubes and a cordis. All of this while the nurses and techs continuously perform compressions and give 1mg of epi every 3-5 minutes, while inadvertently interrupting everything else going on. At the end of the day are all those compressions and all the epi going to change outcomes? We know in medical cardiac arrest it will but is traumatic cardiac arrest different?

Reanimating Patients After Traumatic Cardiac Arrest A Practical Approach Informed by Best Evidence discusses 5 key principles to guide management. The emphasize this is only for isolated traumatic cardiac arrests and that if there is any indication that a medical cardiac arrest occurred prior to a trauma following guidelines such as ACLS should be given priority.

 

The 5 Key Principles:

  1. Start or Stop
  2. Deprioritrize Chest Compressions
  3. Fix Ventilation
  4. Stop the Bleeding
  5. Fix the Physiology

 

 

Start or Stop:

When do you start or stop a traumatic resuscitation? What Factors do you consider? Well there is some food for thought:

Favorable Prognostics Factors:

  1. Penetrating injury, particularly to the Thorax
  2. Vitals Signs at any time
  3. Signs of Life at any time
  4. Short Duration (<10min)
  5. Cardiac Contractility on POC USN

Without 1 of these signs, survival is <1%. Important to keep in mind when EMS is giving a report and you are try to determine how long to attempt a resuscitation.

Spectrum of Output States:

They note for their practice the category of “dead” does NOT receive any further resuscitation. The note this is in part to save the vital limited resource of blood prodcuts. I also found it interesting that they separate PEA from pseudo-PEA from severe hypovolemia. Thats why having the cardiac probe in hand on arrival can save be useful in determining how far you are going to push the resuscitation.

 

 

Deprioritize Chest Compressions

Chest compressions may work for medical arrest but the pathology behind traumatic arrest is so vastly different all they do is get in the way of more vital procedures: intubation, chest tubes, central access, cardiac USN. Until all this has been established it would probably be better just to hold compression. Be warned however this will likely be an uncomfortable experience for the nurses/techs.

 

Fix Ventilation:

Referring back to Table 3 we can clearly see that establishing an airway and decompressing both sides of the chest should be top priority in a traumatic arrest.

Remember that traumatic arrests are a low flow state and while most patients while not require a induction agent or paralytic if you do use a paralytic use TWICE the dose.

 

Stop the Bleeding:

Simple and straight forward if it’s bleeding make it stop. Direct Pressure, tourniquets, topical hemostatic agents (which as far as I’m aware we don’t have) and pelvic binders are all easily performed in room 9. Thoracotomy is also something to consider discussing with Trauma early on in these resuscitations. Both the Eastern Association for  the Surgery of Trauma and the Western Trauma Association recommend thoracotomy and though their conditions vary penetrating trauma to the torso and arrest for less than 15 minutes seems to be a good rule of thumb.

 

Fix the Physiology: 

Pretty straightforward recommendations that we do everyday:

  1. Keep the Patient warm to prevent exacerbating coagulopathies
  2. Establish AccessL Large bore (14-18 gauge) IV access above the diaphragm, IO access of the proximal humerus, 8 or 9-Fr CVC preferably subclavian while avoiding multiple lumen CVCs
  3. Minimize fluids and transfuse blood products 1:1:1 and allow for permissive hypotension

They go into some post-resuscitation recommendations as well when it comes to “fix the physiology” but those are less important to use.  I would recommend that everyone should briefly review this article as it has a lot more information and reasoning behind their recommendations.

 

 

Wound prophylaxis – Should lip lacs get antibiotics (and few others)?

During my review for 72 hour returns we had a through and through lip laceration come in that returned with a wound infection a few days later.  This prompted me to look up current recommendations as I’m pretty sure that I haven’t been giving antibiotic prophylaxis for this.

Searching literature, Tintinalli and UpToDate…… Most superficial wounds do not require prophylaxis, however, through and through lip lacerations were an area of uncertainty and debate….

Tintinalli  – “matter of provider preference.”

UptoDate – no clear clinical evidence to say that these wounds should receive antibiotic prophylaxis , however, due to the pathogens of the oral cavity, they recommend prophylaxis.

Current literature – Review article in 2008, Annals of Emergency Medicine, Mark DG et al – review of studies do not show a statistically significant benefit; however, the only double-blinded randomized control trial showed a trend toward benefit in patient’s that were compliant with therapy.

Some other stats – Rate of infection in wound treated in the ED (Tintinalli)

Head and neck 1-2%

Upper extremity 4%

Lower extremity 7%

Oral wounds – 9-27%

If giving prophylaxis then Pen VK or Clindamycin is recommended for 3-5 days.

For other oral wounds, <1cm, no need to close. Close if large gap susceptible to food getting trapped, and counsel on good oral hygiene.  Dental and OMFS usually recommend d/c with chlorhexidine gluconate oral rinse (0.12%) (Peridex) and will have patients swish and spit after meals to keep the wound from contamination with food particles.

My take away from this is strongly consider antibiotic prophylaxis with through and through oral wounds as they are higher risk for infection with oral flora; however, not an absolute must based on the current evidence.  Be sure to emphasize good oral hygiene, and as always, close follow up with good return precautions.

Other wounds to strongly consider prophylaxis due to increased risk for infection are mammalian and human bite wounds, crush injury, puncture wounds, and wounds with either fresh or salt water contamination, or patients who are immunocompromised, asplenic, advanced liver disease, associated edema (according to the IDSA).

Open fractures and wounds with joint capsule violation should receive antibiotic prophylaxis.

Reminder: Update Tetanus and simple lacerations do not need antibiotic prophylaxis.

Primum Non Nocere

First, do no harm.  Sounds easy enough, but have you ever ordered a “screening CT?”  Have you ever been “better safe than sorry?”  We’re all aware of the nebulous risk of radiation from the imaging we order, we know that getting stuck for blood hurts, and sometimes medications have side effects, but what happens when the results of tests themselves are the things harming patients?

This article does a great job exploring this question.  I’ve also found patients much more receptive to my explanations as to why I’m not ordering the thing they think they need since reading this and spending some time thinking about it.  There are definitely times when my honest indication for ordering that Head CT is “patient wants it…” but in general this article has pushed me a little closer to the minimalists’ corner.

Overkill – Atul Gawande

Push Dose Pressors

Are you all tired of hearing about sepsis yet?  How about the fact that we apparently suck at sepsis?  However, I think we can all recognize when someone comes in with severe septic shock.  You know, the sick, hypotensive, altered patient with a source of infection.  With a low blood pressure, we just need to keep pushing more fluids right?  Just keep pushing them until they are in pulmonary edema.

Well, what could we possibly do to improve outcomes?  The longer they are hypotensive, the more end organ damage they are going to sustain, and the worse the outcomes.  I know that most of you all listen to EMCrit.  If you don’t, you should.  So while waiting for that central line to be placed by our intern (and we know that can take a while, j/k interns, I love you) and waiting for the levophed gtt to be started, we can be like Weingart and give some push dose pressors.  Not only could they be used for that septic patient needing a boost in BP, but can also be used for the peri- or post-intubation or sedation patient that becomes hypotensive.

Epi-It’s not ideal to give code dose epi to someone with a pulse.  Instead take a 10 mL syringe and fill it with 9 mL of NS.  Then draw up 1 mL of epi from the cardiac amp.  This gives you 10 mcg/mL of epi.  Now, give 0.5-2mL (5-20mcg) q1-5 min until improved BP.

Phenylephrine- Draw up 1 mL of phenyl from a vial that is 10 mg/mL and put in a 100 mL bag of NS.  This gives you 100mL of phenylephrine at the concentration of 100mcg/mL   Now you draw up 10mL into a syringe at push 0.5-2 mL (50-200mcg) q1-5 min.

And for your convenience, here is a link to a PDF from EmCrit with the instructions on how to mix these.  Take a pic, keep it on your phone.  While doing this, don’t forget patient safety.  Make sure you’re labeling your syringes when you mix up push dose pressors.  Avoiding medication errors is always plus.

Also, until you are comfortable doing this, make sure you are collaborating with your attending and the pharmacist if they are there at the time.

Finally, read this article on safety considerations in push dose pressors.

And for added fun, read all room9ER posts in Danny DeVito’s voice.  It makes everything better.

 

Neonatal Airway

I’m currently on peds anesthesia and behind on reading Annals, which worked out in my favor.  I was looking through the February 2017 issue and there’s an EM:RAP commentary about the neonatal airway.  So I figured I would give you all the highlights from that article.

  • At birth, an oxygen level of 60% is normal.  There’s a nice chart showing the oxygen saturation and how it increases after birth.
    • 1 minute- 60-65%
    • 2 minutes- 65-70%
    • 3 minutes 70-75%
    • 4 minutes 75-80%
    • 5 minutes 80-85%
    • 10 minutes 85-95%
  • Remember when doing BVM on a neonate, not to press too hard on their face.  Their nose is not stiff and they are obligate nose breathers.  So don’t close off their airway by pressing too hard.
  • Don’t worry about using a paralytic in the neonate.  You can either time passing the tube through the cords or just push it through.
  • Tube size/Blade size
    • Normally in peds we use the formula (age in yrs/4) + 4
    • For neonates, they suggest the 0-1-2-3 rule: Use a 0 straight blade in a 1-2 kg newborn with a 3.0 mm uncuffed tube
    • They also recommend resting your pinky on the cric to provide your own cric pressure since neonatal airways can be very anterior
  • How far to pass the tube
    • 1 kg neonate- 7 cm
    • 2 kg neonate- 8 cm
    • 3 kg neonate- 9 cm

Poor Lonely Repeat Troponin – posted by Bertolotti and Huecker

We have noticed more and more this culture in our ED of obtaining an initial ECG, an initial troponin, and then waiting 2 or 3 or 6 hours to obtain a second troponin only and then discharge if negative.


I dove into the literature and wrote this post to address the SECOND ECG AT TIME OF SECOND TROPONIN as part of a rule out strategy for low risk ED patients.


I will not even address the fact that people are not obtaining a 2nd ECG at time 20-30 minutes from the first. This is on UpToDate, in ACC guidelines, in ACEP guidelines. It is simply standard of care to obtain an early, repeat ECG on anyone you remotely suspect of having ACS. I harp on this in lectures and have posted on it before. I also will not be talking about hs-Troponin (high sensitivity troponin). Many articles and FOAMed commentaries have covered hs-Trop, and we do not have this test at UL. So please do not think you can rule out all comers with 1 troponin, because you need the hs-trop to even consider this.


This post relates to the issue of a repeat ECG at time 2hr or 3hr (I am not a 6 hour guy, I like the 2 or 3 hr depending on symptom time frame). Don and I discussed the 2nd ECG phenomenon and he said it is just our culture at UofL, hence inspring our Room9ER post. Well we need to change the culture.


Now I didn’t want Geralds to cherry-pick an article to try to rebut me on this, so I went down a rabbit hole of ACS rule out, nSTEMI, HEARTS, TIMI and cardiac markers.


If your attention span is reaching its limit here is the bottom line:


All rapid rule out tools and their validation studies involve at least a SECOND ECG with the repeat troponin. HEARTS, ACC/AHS guidelines, TIMI-based rule outs, etc.


I was early to drop the CK and CK-MB on initial and repeat marker testing in favor of solely the troponin, but dropping the ECG is irresponsible. And is not evidence-based.


Below are many quotes and a figure, then a letter to the editor, from various sources. It was actually somewhat difficult to find in the methods exactly when or even if a repeat ECG was done. Much of the time, the ECG done at time of 2nd trop was not even the 2nd ECG, as mentioned above. “Serial ECGs” is the rule. It seemed as though the repeat ECG(s) were implied in the study, and that the research question was simply timing a troponin.


 Dr Huecker composed most of this post because Dr Bertolotti is so excited about and diligently preparing for Research Day. 


Enjoy, and please post comments! 

  


— Patients with probable or possible ACS but whose initial 12-lead ECG and cardiac biomarker levels are normal should be observed in a facility with cardiac monitoring (e.g., chest pain unit or hospital telemetry ward), and repeat ECG (or continuous 12-lead ECG monitoring) and repeat cardiac biomarker measurement(s) should be obtained at predetermined, specified time intervals (see Section 2.2.8). (Level of Evidence: B)


— The c-statistic of troponin only was 0.70. With addition of the ECG the c-statistic improved significantly to a value 0.78, with a likelihood ration test p-value of <0.001


— Anderson et al. JACC Vol. 50, No. 7, 2007 ACC/AHA UA/NSTEMI Guideline Revision August 14, 2007:e1–157                                                                                                    If the initial ECG is not diagnostic but the patient remains symptomatic and there is high clinical suspicion for ACS, serial ECGs, initially at 15- to 30-min intervals, should be performed to detect the potential for development of ST-segment elevation or depression. (Level of Evidence: B)


— ACEP (What will be used for or against you in court, as the case may be)

Acute Coronary Syndromes (Non–ST-Segment Elevation – Adult)

Critical Issues in the Evaluation and Management of Adult Patients with Non–ST-Segment Elevation Acute Coronary Syndromes (September 2006)

Complete Clinical Policy on Non–ST-Segment Elevation Acute Coronary Syndromes (PDF)

Scope of Application. This guideline is intended for physicians working in hospital-based emergency departments (EDs) or chest pain evaluation units.

Inclusion Criteria. This guideline is intended for adult patients presenting to the ED with suspected non–ST-segment elevation acute coronary syndromes.

Exclusion Criteria. This guideline is not intended for pediatric patients, patients in cardiogenic shock, or patients with injury on the initial 12-lead electrocardiogram (ECG).

Critical Questions

  1.  Are serial ECGs useful during the ED evaluation of patients with suspected acute coronary syndromes?
  • Level A recommendations. None specified.
  • Level B recommendations.Perform repeat ECG or automated serial ECGs during the ED evaluation of patients in whom the initial ECG is nondiagnostic for injury and who have symptoms consistent with ongoing or recurrent ischemia. No recommendations can be made in regards to the exact timing of repeat ECGs. Studies suggest that 30 to 60 minutes after baseline may be a reasonable time interval for repeat ECG. 
  • Level C recommendations. None specified.

— Letter: Re: “Troponin-negative chest pain”—a diagnostic evasion?

This brief article is well written and I agree the diagnostic label of ‘troponin negative chest pain’ is unhelpful. However the article repeats some common misconceptions which require correction.

Firstly, the article implies that the majority of patients attending hospital with chest pain have an acute coronary syndrome. This is absolutely not the case – in fact most patients with suspected acute coronary syndrome do not have it. (1) Often patients receive a label of acute coronary syndrome and this is later corrected by the cardiology registrar or consultant on call – although by then it may be too late to change the patient’s perception that they have ‘had a heart attack’.

Secondly, there appears to be a misunderstanding of the value of troponin testing. Troponin assays are positive when there has been myocardial necrosis. They do not give any information about the mechanism of myocardial necrosis – a positive troponin can indicate acute coronary syndrome, but may also occur in heart failure, prolonged arrhythmia, sepsis, pulmonary embolism and many other situations. (2)

Similarly, a negative troponin does not absolutely exclude a cardiac cause for symptoms – nor does it mean the patient is necessarily in a low risk group. (3) Patients with unstable angina, dynamic ECG changes, but negative troponin should be considered as having a similar risk of mortality and morbidity to those with a normal ECG but a positive troponin.

Troponin assays should generally be considered a prognostic, not a diagnostic test, and should be used in conjunction with the patients history and ECG – never alone.

 


Reub Strayer – Droperidol and the Dangerous Patient

Every resident must listen to this podcast (or watch this video) at once. I finally listened to it and was pleased to find it a concise, evidence-based and accurate talk. I avoided watching because I thought he would talk about how much he loves his droperidol and that we should all use it, which would fill me with unbearable envy, since we have not had it in Louisville for years. I have been aware that no US company manufactures it but many EM / FOAMed docs still talk about it. Well Dr Strayer now has no access to the drug and shares his disappointment.

Take home points:

  1. Droperidol is a magical, wonderful drug and we need it back.
  2. The end

No but seriously many great points related to managing the combative patient. From the mildly disorganized schizophrenic, all the way to the truly medico legally dangerous excited delirium, Strayer gives inarguable advice. I love the “shove an O2 mask on the patient who is being restrained by 6 security guards.” He notes that this will often calm the patient, it will protect from spitting, and it will oxygenate the patient. Many other practical pearls here that you WILL USE pretty much every shift at UofL.

Post your favorite tips in the comments.

ED Thoracotomy

Link

Resuscitative Thoracotomy

OVERVIEW

  • resuscitative thoracotomy is a thoracotomy performed prehospital, in the emergency department or elsewhere that is an integral part of the initial resuscitation of a patient
  • an alternate term is emergency thoractomy
  • survival 4-33%
  • determinants of survival include mechanism of injury, the location of injury and the presence or absence of vital signs
  • best outcomes in:

-> penetrating chest
-> those exsaunginating from chest tube
-> isolated chest trauma
-> cardiac injuries
-> abdominal trauma that benefits from aortic clamping
-> time since loss of vitals

REQUIREMENTS

  • ETT
  • shock or arrest with a suspected correctable intrathoracic lesion
  • specific diagnosis (cardiac tamponade, penetrating cardiac lesion or aortic injury)
  • evidence of ongoing thoracic haemorrhage

INDICATIONS

Accepted

  • penetrating injury + arrest + previous signs of life
  • blunt injury + arrest + previous signs of life

Relative

  • penetrating injury + no signs of life and CPR < 15min – blunt injury + signs of life in field or during transport -> arrest 15 min
  • blunt injury + no signs of life
  • multiple blunt trauma
  • severe head injury

RESUSCITATION IN TRAUMATIC ARREST

  • 1. Intubate (reverses hypoxia)
  • 2. Insert bilateral chest drains (or thoracostomies)
  • 3. Resuscitative Thoracotomy
  • 4. Limit fluid as this worsens outcome in penetrating thoracic trauma unless haemorrhage controlled
  • 5. Limit inotropes and pressors until circulation restored (will need once defect repaired)

TECHNIQUE

Goals

  • relieve cardiac tamponade
  • perform open cardiac massage
  • occlude aorta to increase blood flow to heart and brain
  • control life threatening thoracic bleeding
  • control bronchovenous air embolism

1. Full aseptic technique*** –> This was recently an issue where the Trauma attending cited both his team and ours in Rm9 for lack of full prep –> masks, surgical gloves, gowns, etc. should be worn when performing this procedure.
2. Scalpel through skin and intercostal muscles to mid axillary line.
3. Insert heavy duty scissors into thoracostomy incisions.
4. Cut through sternum.
5. Lift up (clam shell)

-> relieve tamponade (longitudinal incision through pericardium)
-> repair cardiac wounds (non-absorbable sutures, 3.0)
-> stop massive lung or hilar bleeding with finger (partial or intermittent occlusion may be performed to avoid right heart failure)
-> identify aortic injuries (repair with 3.0 non-absorbable sutures or use finger)
-> consider aortic cross clamping at level of diaphragm (limits spinal cord ischemia)

Abandon the BVM?

Excellent 1 pager from Dr Levitan in the new ACEP now newspaper.

I have been trying to get the residents to implement the nasal cannula, and to a lesser extent the LMA, for years. Pearl: nasal cannula plus mandible traction opens the nasopharynx and allows oxygen to diffuse to the alveoli (due to gradient made by hemoglobin absorbing oxygen). This is apnea oxygenation, increased safe apnea time. See the pure gold article by Levitan/Weingart, apparently 4th most read annals of EM article.

Add the cannula and mandible thrust to a properly positioned patient, ear to sternal notch or even well above sternal notch, and you will be amazed how long it takes to desat. OOPS (Oxygen On, Pull the mandible, Sit the patient up.

Read this brief article a few times and change how you practice.

How Evidence Based Are We?

Here is a pretty comical article by Dr Ioannidis. If you do not know who this is stop now and read this.

This article was just published. It is written as a report to the father of evidence based medicine, Dr David Sackett. It takes a not terribly optimistic view of the current state of medical research. He calls out industry bias, ghost authorship, and many other flaws of our system. We are very lucky to have people like Dr Ioannidis ensuring integrity to the research process.

Can you give Vasopressors through a PIV?

I looked back and couldn’t find a post about this topic in the last year or so but forgive me if it has already been posted. I have been following R.E.B.E.L. EM for a few months now  and I would recommend it to everyone who has the time and wants quick summaries on the latest EM literature.  They have short written summaries of papers including pros/cons of the study and what they feel are the most important take away points. It was founded by Salim Rezaie with Rob Rogers, Matt Astin and Anand Swaminatham serving as editors.

Occasionally they will have a “mythbuster” post looking at common myths in the ED and the most uptodate literature available on the topic. (their latest mythbust is on “safe” glucose levels before ED discharge but I digress)

 

Back in May they reviewed the safety of vasopressors through a PIV. The topic paper was titled “A systematic review of extravasation and local tissue injury from administration of vasopressors through peripheral intravenous catheters and central venous catheters

What the review found was very interesting: of 318 events, 204 results in local tissue damage, 114 were only extravasation events and 7 events involved the use of a CVC (so clearly not completely safe). Interesting, of the 204 local tissue events 85.3% involved PIV distal to the antecubital fossa and 96.8% involved administration of >4hrs.

REBEL EM’s take away points were:

In critically ill patients, with hemodynamic instability, vasopressor infusion through a proximal PIV (antecubital fossa or external jugular vein), for <4hours of duration is unlikely to result in tissue injury and will reduce the time it takes to achieve hemodynamic stability.

What I feel like this means for us is simple: If you have a crashing, hypotensive patient who needs a pressor without a CVC but good proximal PIVs, start the pressor immediately, stabilize the patient as best you can, then take the time to properly place a CVC.

Continue to monitor the PIV until it can be switch to the CVC and stop the pressor immediately if there is any suspicion for local extravasation. I am sure this will make some people nervous but I think this is better then placing a “crash line” that is less then sterile which will expose an already ill patient to infection or other complications secondary to a hastily placed CVC.

I highly recommend read their review and how they came to this conclusion along with their other posts. I have included the link to this study at the bottom.

http://rebelem.com/mythbuster-administration-of-vasopressors-through-peripheral-intravenous-access/

Managing Migraine

As mentioned on R and R in the Fast Lane. This article by Friedman is a welcomed update to evidence-based migraine management. Some people love treating migraine patients, some hate it. But we all have our cocktails we believe in.

I am a fioricet/neurontin/IM compazine, escalating to IV compazine/benadryl/decadron/toradol OR if they want to drive home IV MAG/decadron/toradol … kind of guy.

This article starts with criteria for delineating migraine from other headache forms. Then provides a succinct algorithm for treatment, starting with reglan or compazine +/- benadryl, then another dose plus toradol, then dihydroergotamine, then occipital nerve blocks (very fun), then as a last resort, opioids. I would encourage you to attempt a few other methods before the blocks and especially before the opioids.

Many other medications can be used (keppra, depakote, propofol, etc). But this is a solid overview of the EM approach. Also of note, see the Oct 2016 EM-RAP paper chase of the reglan +/- IV fluids in migraine article which showed no real benefit to the addition of IVF.