Dilantin (Phenytoin) Loading: IV vs. 4 hour oral load, or is there another way? by Dr. Carly Darr

Dilantin (Phenytoin) Loading: IV vs. 4 hour oral load, or is there another way?

You have a breakthrough seizure patient on Dilantin whose level came back undetectable (or really low), and you plan to load them and then discharge them.  Reference guidelines for oral phenytoin loading recommend about 1g in 3 divided doses spaced by 2hrs each.  This is usually done with 400mg, waiting 2hrs, 300mg, waiting 2hrs, then a final 300mg, resulting in a total of 1g after 4 hours.  Alternatively, some people will load phenytoin IV while the patient is on a cardiac monitor for 20 minutes (a GIGANTIC waste if the patient can tolerate PO meds).  So, why can’t we give patients 1g orally all at once?  The short answer is that we CAN give 1g oral load all at once.  ALIEM has a nice summary of the research behind this and the link is included below.   The long answer is that the side effects of nausea and vomiting were believed to be less and the absorption higher with the divided dosing, but research shows these effects are minimal.  Several small studies in which patients were given about 1g oral load and then serum levels tested at varying time points after the load have shown that therapeutic range (10 mcg/mL) is reached within 3-5 hours.  Furthermore, there have been only a handful with vomiting or severe nausea. So, go ahead and give them 1g orally, maybe consider a dose of antiemetic, and remember that they won’t be therapeutic for the first few hours with any type of oral loading.  Or, if that makes you nervous, try 2 doses of 500mg and/or more rapid spacing between doses.  Please note that these are small studies, and our DMC reference recommends the 4 hour load, so discuss with your attending.

ALIEM article on single oral load: https://www.aliem.com/2013/04/trick-of-trade-rapid-oral-phenytoin-loading/

Teaching in the Emergency Department by Zeid K.

The challenges of effective teaching in Emergency Medicine are well documented. The ED is not a comfortable learning environment. Time is limited and this creates a significant barrier to education. There are books, blogposts, tweets, research papers and podcasts that all attempt to answer one question: How do I become a more effective teacher in the Emergency Department? My recently concluded teaching elective was an attempt to experience these challenges first-hand. My month was cut short by a vacation as well as being scheduled for 5 shifts in the department by everyone’s least favorite chief resident, Christopher Sponaugle. This blog post will discuss some of the more important aspects of bedside teaching and the tools that we have at our disposal.

Whatever your motivation might be, accepting your role as a clinician-educator is extremely important. This role is not limited to those of us pursuing academic interests post-graduation. Regardless of what environment you will be practicing in, you will have some degree of teaching responsibilities; as an educator, you have a professional and ethical obligation to your learners.

Successful teaching in emergency medicine (EM) begins with enthusiasm and a desire to positively influence the learner. Learner-centered teaching has been repeatedly shown to be the most effective method of teaching in EM. Taking a few minutes at the beginning of your shift to get to know your learner is key. This helps to establish your relationship, determine their goals and set expectations. One of the most powerful questions that you as a teacher possess is, “What are you hoping to get out of this shift today?”

One of the more useful tricks to being an effective teacher comes from Amal ‘put the mess in Messman’ Mattu. Something he likes to do, which I see a lot of attendings do as well, is play the “what if” game. Playing this game can make routine patient encounters become a productive conversation that allows you to explore differential diagnosis, pathophysiology and treatment options for a variety of diagnoses. Every case can provide a teaching point. Train yourself to ask questions that promote critical thinking in a non-threatening fashion. Make an effort to deliver a clear, concise and focused message. Avoid “over-teaching” or providing an excessive amount of information that obscures the original teaching point.

There are several, widely adopted frameworks that educators use in emergency medicine. One- Minute Preceptor is a 5-step model of clinical teaching that acknowledges the hectic nature of Emergency Medicine. The acronyms SPIT and SNAPPS are other teaching methods that have been adopted quite widely. These were featured during our MedEd Grand Rounds and discussing them in further detail would be beyond the scope of this blog post. A quick Google search and review of the references at the end of this post will provide everything you need to know about these and other teaching techniques.

Providing feedback is just as vital to the educational process as effective teaching. Feedback should be provided consistently, objectively and in real-time. We have all received the proverbial “shit sandwich” during the course of residency and while this is a well-known method to provide feedback, there are other important aspects of providing effective feedback. Allowing self-evaluation at the initiation of the feedback process can provide valuable information to the educator regarding the effectiveness of their teaching methods. Similar to over-teaching, avoid giving too much feedback as this can diminish the effectiveness of your message. Always finish the conversation with a positive or encouraging summary.

“I desire no other epitaph… than the statement that I taught medical students in the wards, as I regard this as by far the most useful and important work I have been called upon to do.” While asking you to uphold yourselves to the lofty standards set by the great Sir William Osler in the above quote is impossible, I only ask you all to take a more methodical and refined approach to teaching your learners. This will serve you well for not only the rest of residency, but for the entirety of your careers.



Berger, Todd J., et al. “The impact of the demand for clinical productivity on student teaching in

academic emergency departments.” Academic emergency medicine 11.12 (2004): 1364-1367


Practical teaching in emergency medicine / chief editor, Robert L. Rogers; associate editors,

Amal Mattu … [et al.].–2nd ed


https://www.aliem.com/2016/09/idea-series- asynchronous-curriculum- for-resident- as-




Zeid Kalarikkal, Chief Resident Extraordinaire

Picture this; you have a previously healthy 14-week-old boy who is brought by his very concerned first-time parents. The mother notes that the infant had an episode where he went blue and was not breathing. She quickly picked him up, tapped on his back and maybe 30 seconds later the baby was noted to be awake and breathing comfortably.

You note that the child was born at-term with an uncomplicated birth history. He has been doing well since and they follow up regularly with their pediatrician. Parents deny any history of fever, URI symptoms, cough, vomiting or diarrhea. Vital signs and physical are normal and the baby is noted to feeding from the bottle during your evaluation.

You complete your evaluation and conclude that this child had an Acute Life Threatening Event or ALTE.

ALTE was previously defined as “an episode that is frightening to the observer and that is characterized by some combination of apnea, color change, marked change in muscle tone, choking, or gagging”

You return to the room to explain this to the parents. While your gestalt tells you that the child is and probably will be fine, you start explaining your diagnosis. At the mere mention of the word ‘Life-Threatening’, the father collapses to the ground and the mother starts sobbing. You curse yourself for picking up the chart and start consoling the parents.

In most cases, this case had an obvious disposition – Transfer to a Pediatric hospital.  Previously, there was no data to identify a subset of ALTE patients that could be safely discharged home. While some do get discharged home, it depended heavily on provider gestalt, comfort and degree of risk aversion.

Enter BRUE

Brief Resolved Unexplained Event or BRUE has replaced ALTE in the most recent guidelines from the American Academy of Pediatrics.

BRUE brings some clarity to the definition of ALTE by specifying that:

  • The term only applies to infants less than 1 year old
  • Episode must be less than 1 minute and have resolved
  • Patient must have a reassuring history, physical exam and vitals during evaluation
  • Episode must be unexplained

First thing to do with a child meeting the definition of BRUE is to classify them as low or high risk.

Features that have been defined as low risk are age greater than 60 days, a lack of prematurity (gestational age > 32 weeks and post-conceptual age > 45 weeks), a first and isolated event, duration of less than one minute, no need for CPR provided by a trained medical provider and no concerning historical features or physical exam findings. 

If your patient does not meet all of these criteria, they are now high risk and the guidelines offer no further recommendation.

For low-risk patients, the guidelines offer further recommendations.

  • Parent/caregiver education regarding these events and use shared-decision making for further testing, discharge and follow-up.
  • You may consider pertussis testing, EKG and cardiorespiratory monitoring.
  • You do not need obtain viral panels, CBC, CSF/blood cultures, electrolytes, CXR, EEG or other advanced testing.
  • You DO NOT need to admit these patients for the event alone and they can be discharged home with close outpatient follow-up within 24 hours.

Remember, BRUE is only used when no other condition can be found as the etiology of the event. It only represents a constellation of symptoms and you should use your history and physical examination skills to determine a more precise diagnosis before labeling it a BRUE. The biggest strength of these updated guidelines is that you now have some support for discharging a low risk patient.



Tieder JS, Bonkowsky JL, Etzel RA, Franklin WH, Gremse DA, Herman B, Katz ES, Krilov LR, Merritt JL 2nd, Norlin C, Percelay J, Sapién RE, Shiffman RN, Smith MB; SUBCOMMITTEE ON APPARENT LIFE THREATENING EVENTS. Brief Resolved Unexplained Events (Formerly Apparent Life-Threatening Events) and Evaluation of Lower-Risk Infants. Pediatrics. 2016 May;137(5). PMID: 27244835.




Ryan Ernst’s trauma lecture summary

Trauma, VS, and Shock

Here is a brief summary of my 30-minute presentation:

No single vital sign is reliable to determine severity of injury or degree of traumatic shock. There have been papers that indicate correlation of mortality/injury severity with increased HR, RR > 25, BP <90, and GCS < 14.[i]

Location of palpable pulse does not correlate accurately with estimated BP, is no longer taught in ATLS, and should not be used as a surrogate to estimate blood pressure. It can be useful to assess improvement or decline in a single patient over time.[ii],[iii]

When automated BP measurements have been studied, they significantly overestimate BP in hypotensive trauma patients. Consider using a manual cuff if there is any question of the accuracy of the BP. Definitely cycle the initial BP two or three times to verify.[iv]

ATLS guidelines for degree of shock are not based on firm literature, and will tend to underestimate the degree of shock based on HR and BP. Do not rely on this to assess stability of your trauma patient – take the entire picture into account.[v],[vi],[vii],[viii],[ix]

Shock Index is also not completely reliable, but may be more sensitive than HR or BP alone to assess severity of injury and degree of shock. SI is calculated as HR/SBP. Results > 0.9 suggest increased level of injury and shock.[x],[xi],[xii],[xiii]

SBP < 110mmHg may be a more sensitive indicator of severity of injury, level of hemorrhagic shock, and impending mortality than the traditional 90mmHg. This previous cutoff is not based in any specific literature, and is used by arbitrary convention, likely based on estimated needs for cerebral and renal perfusion.[xiv],[xv],[xvi],[xvii]

If you’re in the mood for some easy listening on the topic of trauma resuscitation, I suggest the following:





Disclaimer: My lecture and EMSGH blog post are a summary of my personal opinions, based on extensive literature review, well-vetted online podcast and blogs, training I have received both within and outside of SGH/DMC, and personal experience. Any implementation into your personal practice should be thoroughly discussed with your attending, and if any question persists, with ED and hospital administration.

[i] Pacagnella RC, Souza JP, Durocher J, Perel P, Blum J, Winikoff B, Gülmezoglu AM. A systematic review of the relationship between blood loss and clinical signs. PLoS One. 2013;8(3):e57594. doi: 10.1371/journal.pone.0057594. Epub 2013 Mar 6. Review. Erratum in: PLoS One. 2013;8(6). PMID: 23483915

[ii] Deakin CD, Low JL. Accuracy of the advanced trauma life support guidelines for predicting systolic blood pressure using carotid, femoral, and radial pulses: observational study. BMJ. 2000 Sep 16;321(7262):673-4. PMID: 10987771

[iii] Poulton TJ. ATLS paradigm fails. Ann Emerg Med. 1988 Jan;17(1):107. PubMed PMID: 3337405

[iv] Davis JW, Davis IC, Bennink LD, Bilello JF, Kaups KL, Parks SN. Are automated  blood pressure measurements accurate in trauma patients? J Trauma. 2003 Nov;55(5):860-3. PubMed PMID: 14608157

[v] Guly HR, Bouamra O, Little R, Dark P, Coats T, Driscoll P, Lecky FE. Testing the validity of the ATLS classification of hypovolaemic shock. Resuscitation. 2010 Sep;81(9):1142-7. PMID: 20619954

[vi] Guly HR, Bouamra O, Spiers M, Dark P, Coats T, Lecky FE; Trauma Audit and Research Network. Vital signs and estimated blood loss in patients with major trauma: testing the validity of the ATLS classification of hypovolaemic shock. Resuscitation. 2011 May;82(5):556-9. PMID: 21349628

[vii] Mutschler M, Nienaber U, Brockamp T, Wafaisade A, Wyen H, Peiniger S, Paffrath T, Bouillon B, Maegele M; TraumaRegister DGU. A critical reappraisal of the ATLS  classification of hypovolaemic shock: does it really reflect clinical reality? Resuscitation. 2013 Mar;84(3):309-13. PMID: 22835498

[viii] Mutschler M, Paffrath T, Wölfl C, Probst C, Nienaber U, Schipper IB, Bouillon  B, Maegele M. The ATLS(®) classification of hypovolaemic shock: a well established teaching tool on the edge? Injury. 2014 Oct;45 Suppl 3:S35-8. PMID: 25284231

[ix] Mutschler M, Hoffmann M, Wölfl C, Münzberg M, Schipper I, Paffrath T, Bouillon B, Maegele M. Is the ATLS classification of hypovolaemic shock appreciated in daily trauma care? An online-survey among 383 ATLS course directors and instructors. Emerg Med J. 2015 Feb;32(2):134-7. doi: PMID: 24071947

[x] Bruijns SR, Guly HR, Bouamra O, Lecky F, Lee WA. The value of traditional vital signs, shock index, and age-based markers in predicting trauma mortality. J Trauma Acute Care Surg. 2013 Jun;74(6):1432-7. PMID: 23694869

[xi] Schafer K, Van Sickle C, Hinojosa-Laborde C, Convertino VA. Physiologic mechanisms underlying the failure of the “shock index” as a tool for accurate assessment of patient status during progressive simulated hemorrhage. J Trauma Acute Care Surg. 2013 Aug;75(2 Suppl 2):S197-202. PMID: 23883908

[xii] McNab A, Burns B, Bhullar I, Chesire D, Kerwin A. An analysis of shock index as a correlate for outcomes in trauma by age group. Surgery. 2013 Aug;154(2):384-7. PMID: 23889965

[xiii] Mutschler M, Nienaber U, Münzberg M, Wölfl C, Schoechl H, Paffrath T, Bouillon B, Maegele M; TraumaRegister DGU. The Shock Index revisited – a fast guide to transfusion requirement? A retrospective analysis on 21,853 patients derived from the TraumaRegister DGU. Crit Care. 2013 Aug 12;17(4):R172. PMID: 23938104

[xiv] Eastridge BJ, Salinas J, McManus JG, Blackburn L, Bugler EM, Cooke WH, Convertino VA, Wade CE, Holcomb JB. Hypotension begins at 110 mm Hg: redefining “hypotension” with data. J Trauma. 2007 Aug;63(2):291-7; discussion 297-9. PMID: 17693826

[xv] Edelman DA, White MT, Tyburski JG, Wilson RF. Post-traumatic hypotension: should systolic blood pressure of 90-109 mmHg be included? Shock. 2007 Feb;27(2):134-8. PMID: 17224786

[xvi] Hasler RM, Nuesch E, Jüni P, Bouamra O, Exadaktylos AK, Lecky F. Systolic blood pressure below 110 mm Hg is associated with increased mortality in blunt major trauma patients: multicentre cohort study. Resuscitation. 2011 Sep;82(9):1202-7. PMID: 21632168

[xvii] Hasler RM, Nüesch E, Jüni P, Bouamra O, Exadaktylos AK, Lecky F. Systolic blood pressure below 110 mmHg is associated with increased mortality in penetrating major trauma patients: Multicentre cohort study. Resuscitation. 2012  Apr;83(4):476-81. PMID: 22056618

Analeptics – Quinn’s Toxicology Post

Analeptics: The Modern Coma Cocktail


I had never actually heard this term analeptic before and it seems somewhat old fashioned.

It means something that is restorative and invigorating, in this context, used to wake up someone with a decreased level of consciousness.

First, a quick practice case:

A middle-aged man presents to your hospital obtunded with poor respiratory effort. Which of the below treatments/Medications do you administer?

  1. Place patient in Ice bath
  2. Strychnine
  3. Camphor.
  4. Picrotoxin
  5. Caffeine

Of course all of these answers seem ridiculous, if not downright dangerous. However, depending on the where and when of your medical practice, any one of these may have been the standard of care.

At one time or another, these have been treatments of choice for decreased levels of consciousness. And some of them even work… In a fashion.  Strychnine for example might even wake you up so hard that you are totally conscious for the painful muscle convulsions that may eventually cause you do die of anoxia. Ew. But at least you woke up, so that’s good.

Granted, these are from a time where mechanical ventilation was not really a thing, so you would go to great lengths to avoid deep coma. No matter the cost.

The risk benefit here is a little different than most things we deal with nowadays and was basically “probably dead vs possibly dead”

Such is the dubious history of Analeptics and the “coma cocktail,” which is still evolving and is argued about to this day.

The coma cocktail:

In the modern era, say for the past 20 years or so, this contains dextrose, thiamine, naloxone, and flumazenil.

The concept for this when it was first devised is that it was something you could just reflexively give to people with decreased levels of responsiveness, to rapidly address reversible causes of depressed consciousness while reducing permanent neurological injury.

You are probably quite familiar with the medications listed above, although you may not use all of them, and may not use any of them in the reflexive manner that this concept was designed for.

The prevailing practice attitudes now have shifted against indiscriminate administration of this cluster of potentially harmful medicines, so it is probably most appropriate to break it down and look at each component individually.


Dextrose is a sugar, used to treat hypoglycemia.

Hypoglycemia is a common endpoint that may result from a drug or toxin exposure, nutritional deprivation, or numerous nontoxic events.

Hypoglycemia is common. The rate of hypoglycemia in patients with altered mental status of any cause is approximately 8.5%. This means that about 1 in 12 of your altered mental status patients have a hypoglycemic component. This is extremely significant because prolonged hypoglycemia can result in permanent brain damage, and mortality in hypoglycemic patients ranges from 11-27%.

This alone might be enough to persuade you administrate this in your altered patients. You would use D50 in adults, and D25 or D10 for pediatric patients.

In the end, the dosage that is required is “enough” because every patient is different, and have their own thresholds at which they become symptomatic. Dosing for pediatric patients is as follows. D10W: 2.5ml/kg,    D25 4ml/kg. In adults, starting with 1-2 ampules of D50 is appropriate, each ampule contains 25g of dextrose.

What if they get too much?

Concerns for making the blood sugar too high are generally not demonstrated clinically.  Renal losses alone keep it from going way too high, which is something we routinely take advantage of in patients with DKA and HHS. And anyway, one ampule of D50 only generally raises blood glucose by 60mg/dL.

What if it wasn’t hypoglycemia at all?

If their altered mentation is from something nontoxic, like an ICH, there has been no demonstrated long term change in survival or functional ability.

The solution to these concerns is to be able to reliably detect hypoglycemia right?

Well, if we accept that treatment should be administered as fast as possible to reduce hypoglycemia, then bedside testing might be completely impractical.

On the flip side, and in defense of standard bedside testing, a potentially very high number of patients (up to 25!) are misdiagnosed based on purely clinical findings, as many appear agitated instead of somnolent, and for this reason their blood glucose may not be tested, so maybe we should just test everyone.

Dangers of relying on a number:

Keep in mind though that lots of people become altered at blood levels above the “definition” of hypoglycemia of a glucose below 60. If a person lives their life at a serum level of 300mg/dL, the normal lab values become less useful.

This justifiably seems like a tough balance. The clinical need to make a rapid decision in a busy or hostile environment vs a documentable objective measurement.

Hoffman and Goldfrank recommend a stratification system for your altered pts:

  1. If they have numerical hypoglycemia, treat. Problem solved.
  2. If they have nonfocal neuro exams, and have borderline glucose levels. Give dextrose.
  3. If you don’t have ability to test a patient in the above scenario, give dextrose anyway.
  4. So what do you do if they are altered and have a localizing exam: This is admittedly rare in cases caused by low sugar, 2.5%. So for these patients, if you go strictly by the numbers, you will get 90% of those rare patients. And even if you are wrong, the extra sugar won’t hurt.

So, with this method, you will admittedly over treat a large number of patients, but you probably won’t delay a single person with real hypoglycemia. Which is important, because the cost of an amp of D50 is like 5$. But the economical and physical cost of not treating it is massive.


Right off the bat, empirical use seems less complicated than with dextrose.

Thiamine (Vitamin B1) functions as a cofactor for pyruvate dehydrogenase, which links anaerobic glycolysis to the krebs cycle, as well as an enzyme in the krebs cycle itself, and the pentose phosphate pathway. It’s important.

One interesting, and possibly problematic aspect of thiamine is that the amount needed is dependent on total energy intake. More energy=more thiamine needed.

Dietary thiamine becomes decreased  in chronic liver disease, folate deficiency, malabsorption, malnutrition like with TPN/post op patients, or those juice cleanses your facebook friends from high school like to use and/or sell.

The prime example of people who take in calories without other nutrients (like thiamine!) are alcoholics. Liquor has lots of energy but not so many vitamins. The most notable result of low thiamine is everyone’s old friend Wernicke-Korsakoff.

The characteristics of Wernicke encephalopathy includes oculomotor abnormality, ataxia, and confusion. It carries a mortality rate of 10-20%, and up to 80% of survivors develop the other half of the odd couple- Korsakoff psychosis with that fun, permanent short term memory damage. Confabulation is all fun and games until you need a reliable medical history from a patient besides a lifetime of drinking.

So, this is rare. But it is very bad.

Including the 100mg IV of thiamine treats/prevents the encephalopathy. And it costs like 1$. That’s what we in the biz like to call a steal.

But what about that thing with glucose I learned about in medical school that I also had to know for step 1 and 2!?!

And of course the other benefit you may hear, is that it prevents the precipitation of the encephalopathy by the dextrose loading these people will get too, as thiamine requirement is calorie dependent.

So that part sounds right and almost makes sense from a basic physiology standpoint, but the evidence for this is very lacking. The cases that drive this are most likely people who had the encephalopathy already, or who got dextrose in large volumes for a long time (hours to days) without other nutrition.

Withholding dextrose until thiamine doesn’t do much. Thiamine uptake is way slower than glucose anyway, something like 6 hours.  So even giving them together wouldn’t even help that much if you were truly worried about Wernicke’s. Which again, you shouldn’t be.

So in that case you would basically just be withholding dextrose from a patient that may desperately need it to avoid something that is probably theoretical at best. Don’t be that person.

Now you have me all fired up to give thiamine!

You can give it oral, IM, or IV. People who need the coma cocktail probably won’t be getting it orally if they are really that altered. At least they shouldn’t. Most medications are less effective if aspirated. And if they are really malnourished, they might not have good muscle mass to take an IM injection. You can do it that way, but you will have an IV in these people anyway.

Thiamine is cheap, safe, and since you can’t measure it in a patient, this has a good place in the modern coma cocktail. At worst, it just reminds us to address nutrition, right?


Probably the best known and most talked about. It is a pure opioid antagonist used for reversal of acute intoxication. It rapidly counteracts sedation, respiratory depression, miosis, analgesia, bradycardia, and GI stasis caused by exogenous opioids through your 3 different opioid receptors.

It also fights your endogenous opioid peptides too. Which may explain why it works a certain degree on some intoxications with things that are not opioids, such as some antiepileptic medications.

Naloxone can be given IV, IM, through an ET tube, and intranasally.

There are risks like pulmonary edema and hypertension, and risk to you through precipitation of violence. However, these risks to the patient are generally considered rare. Approx 1% or less.

Except for extremely unpleasant opioid withdrawal. We know it does that. That’s the whole point. You can do that every time if you really wanted to. The effects of withdrawal are not life threatening, but it can cause other problems to arise in the setting of a polydrug intoxication. You don’t want your newly opiod-free patient vomiting from withdrawal while their benzodiazepine co-ingestion is keeping them nice and asleep.

On the other side of the same coin, you could uncover dangerous and more threatening sympathomimetic symptoms from something like cocaine, like seizure and arrhythmia.

Are there any agitated people this might help with? Like dextrose does?

This differs from the case of dextrose possibly helping agitated people. People on opioids won’t be rowdy like that. You aren’t gonna help, and will probably make things worse.

What is the best metric for giving this?

This is something you want to consider giving right away to someone with decreased consciousness. In the Hoffman/Goldfrank paper, they reference prior works by Hoffman that show a respiratory rate of 12 of less predicted a naloxone responder 80% of the time. So this is where you want to focus your attention if you are thinking about opiods. Respiratory depression is what kills these people, so treat the respiratory depression. A PCO2 from a blood gas is better, but that takes a lot more time than checking out the respiratory rate.

But the PUPILS. People on opioids have miosis!

But what if they aren’t miotic? Certain opioids have a much more dramatic effect on respiration than pupils. They could die of anoxia with normal pupils. Our old friend Demerol was particular well known for that. Pupils are nice, but you can’t breathe through your pupils, to quote Dr. King.

So how much do you use?

Conventional dosing ranges from .4 to 2mg. If you reach 10mg, isolated opioid toxicity is unlikely.

The Hoffman paper suggests that you lower the dose to .2mg as a first dose. That was in 1995.

This new publication in the British Journal of Pharmacology suggest that even that may be unnecessarily high, and that a first dose of 40 micrograms is more appropriate. This way you can titrate to their breathing, which is what the lethal issue, not the sleepiness. They can be sleepy and breathe, as long as they are protecting their airway.

And what if they DO need the full 2mg to breathe? Naloxone acts so fast that you can titrate it up .04mg at a time, and it won’t keep you in the resuscitation bay for an hour. It will still be fast. They can be bagged or intubated during this of course.

Go slow. Don’t hit them with 2mg right away. If you need it, work up to it. You avoid getting punched and pooped on, and the patient doesn’t leave AMA only to have their naloxone wear off 3 blocks away.

The recommendations for naloxone drip remain the same, with an hourly infusion rate around half of what you needed to give them initially.


Last and probably least, is flumazenil. While naloxone got a WHO classification as an essential medicine, flumazenil got a black box warning.

This is no longer a standard, and essentially only exists in the coma cocktail as a historical item.

It reverses sedation from benzodiazepines, but will also precipitate withdrawl in patients dependent on them, or alcoholics.

Compared to opioids, this is less on the gross side, and more on the potentially fatal side. It can precipitate dangerous withdrawal seizures which you would then treat with benzos… which you just nullified the effectiveness of.

To be fair, it was developed for conscious sedation reversal before it was added to the coma cocktail. Which it still has a valid use for- If you have a clear history, and a low suspicion of benzo/ETOH dependence it may have a role in reversal of conscious sedation from benzos. OR… you could just intubate them and let them get better on their own.

If you are curious, Initial dosing is .2mg for adults, slowly given/titrated. In kids it is 10ug per kilogram with a max of .2mg.

You essentially want to give this the same time you perform gastric lavage. AKA basically never.

Probably best to avoid without advice from a toxicologist



  1. Hoffman, Robert S. “The Poisoned Patient With Altered Consciousness.” Jama 274.7 (1995): 562. Web
  2. Sivilotti, Marco L.a. “Flumazenil, Naloxone and the ‘coma Cocktail’.” British Journal of Clinical Pharmacology Br J Clin Pharmacol 81.3 (2015): 428-36. Web.




Zeid’s Critical Care Post – Chest Compressions in CPR

Hands off? Never!!

We have all heard that tweeter go off, “60 year old male, cardiac arrest with downtime of 20 minutes. No shocks advised and coming in a BLS unit.” As your airway and vascular access pathways run through your head, EMS comes in through Resus 4 bagging your patient while performing chest compression. They start giving you their prehospital report and while unfastening the patient from the EMS stretcher and transferring him to the hospital bed, compressions stop. Anywhere from 5-15 seconds later the patient is now on the bed and the designated team member resumes compressions.

The importance of high quality CPR is stressed during our BLS/ACLS courses. The trend continues during any high-level resuscitation lecture that you might have heard. The AHA repeats this point several times in their guidelines;

“Increased emphasis has been placed on high-quality CPR using performance targets (compressions of adequate rate and depth, allowing complete chest recoil between compressions, minimizing interruptions in compressions, and avoiding excessive ventilation).”

Of the many interventions we do, the intervention shown most to correlate with survival and positive neurological outcomes is high quality chest compressions. A lot of resuscitation research is based off animal models, for obvious reasons. Berg et all described a significant drop in coronary perfusion pressure when chest compressions are interrupted. This is depicted in the image below:

Click here for graph

An important take away point is not only the significant and sudden drop in coronary perfusion pressure when chest compressions are interrupted but also the additional time required after resumption to reach previously achieved levels of perfusion. This time period has been estimated to be anywhere from 40-45 seconds during animal studies and were shown to be associated with worsening outcomes. The red arrow in the graph above highlights this period.

Paradis et all highlighted this point when they showed that ROSC is associated with higher initial and maximal coronary perfusion pressure during CPR in humans. Christenson et all also found that patients who receive longer periods of uninterrupted chest compressions are more likely to survive. These studies are in the references for further reading.

Other significant barriers to uninterrupted compressions include pulse checks and airway management. This is difficult to avoid but attempts should be made to minimize pulse check during CPR and this is reflected in the AHA guidelines as well. In the appropriate situation, EtCO2 monitoring can serve as a useful surrogate for determining ROSC. A sudden increase of >10mm Hg has shown to be an indicator of ROSC and thus allowing you to minimize interruptions for pulse checks. Obviously, this requires endotracheal intubation and represents a limitation of this method.

This brings forward the next reason for interruption in chest compressions: endotracheal intubation. In our EMS system, a majority of cardiac arrest patients come in with BVM or a supraglottic airway such as a combi-tube or King airway in place. While there is some debate regarding the timeliness of endotracheal intubation during cardiac arrest, there is no doubt that should be achieved with minimal interruptions in chest compressions. Some studies suggest that passive oxygenation (i.e. nasal cannula or non-rebreather mask) may be superior to BVM ventilation. The literature also suggests that ET intubation may be deferred till ROSC with no significant differences in outcomes. Endotracheal intubation, if attempted, should be performed by an experienced provider since the incidence of esophageal intubation is estimated to be 3-15%. This results in worsening hypoxia and hypercarbia. Additionally, Wang et all found that the median duration of all endotracheal intubation associated interruptions is about 105 seconds and represents about 23% of all interruptions in chest compressions. In summary, there is not a lot of definitive evidence regarding airway management in cardiac arrest patients but use your clinical judgment to ensure first-pass success and minimize interruptions in compressions.

In conclusion, when that cardiac arrest patient is wheeled in to your resuscitation room you should assign someone to take over compressions from EMS immediately. We already have dismal survival rates for out of hospital cardiac arrest in the metro Detroit area and it is your obligation to provide your patient with the best possible chance of survival.


  1. Berg RAR. Circulation (New York, N.Y.): Adverse hemodynamic effects of interrupting chest compressions for rescue breathing during cardiopulmonary resuscitation for ventricular fibrillation cardiac arrest. American Heart Association, etc; 11/2001;104:2465.
  2. Cardiopulmonary resuscitation for cardiac arrest: the importance of uninterrupted chest compressions in cardiac arrest resuscitation, Cunningham, Lee M. et al. The American Journal of Emergency Medicine , Volume 30 , Issue 8 , 1630 – 1638
  3. Christenson J,Andrusiek D, Everson-Stewart S, et al. Chest compression fraction determines survival in patients with out-of-hospital ventricular fibrillation. Circulation 2009;120(13):1241-7.
  4. Paradis NAN. JAMA : the journal of the American Medical Association: Coronary perfusion pressure and the return of spontaneous circulation in human cardiopulmonary resuscitation. American Medical Association; 02/1990;263:1106.
  5. Wang CC. Resuscitation: The association between timing of tracheal intubation and outcomes of adult in-hospital cardiac arrest: A retrospective cohort study. Elsevier; 08/2016;105:59.

July 28 Lectures

As promised, here are further references/reading/podcasts pertinent to this past week’s grand rounds.

From Dr. Ernst, here is further information regarding chest trauma, particularly chest tubes:

EMRAP September 2007 – Penetrating Chest Trauma (Kenji Inaba)

EMRAP April 2016 – More Penetrating Chest Trauma (Chris Hicks)

EMCrit December 2011 – Discusses Needle Decompression, Finger Thoracostomy (Weingart)

Podcast 62 – Needle vs. Knife II: Needle Thoracostomy?

Ultrasound Podcast July 2016 – Airway/Breathing in Trauma

Airway & Breathing Ultrasound in Trauma with @ultrasoundmd. #FOAMED

From Dr. Fellows, here is information regarding cardiac amyloidosis and ventilator management:

EMCrit Lecture – Dominating the Vent: Part I

EMCrit Lecture – Dominating the Vent: Part II

Here is a link that with the Echo and EKG findings of Amyloid:


Lasix Dosage in Acute Decompensated CHF

Acute decompensated CHF is something we see on almost every shift in the ED. Presuming the patient is not hypotensive, more than likely that patient will be receiving IV Lasix. When I was a resident, I was taught that if the patient is on Lasix at home, find out their home dosage and just give that IV. At SGH, it seems that many residents will find out the home dosage, double it, and give that dosage IV. So, I went on a quest to figure out if there are actually any reasonable, evidence-based recommendations on the subject.

My first stop was EBMedicine.net, which has a large library of evidence-based medicine articles on a variety of topics; you guys have access to all of this material. Having written an article for this publication, I can verify that these articles are well-researched and heavily peer reviewed and edited. So I found an article from 2014 called “Current Guidelines for the Evaluation and Management of Heart Failure”. Here is their recommendation regarding IV Lasix usage in acute decompensated CHF: “If patients are already receiving loop diuretic therapy, the initial IV dose should equal or exceed their chronic oral daily dose and should be given as either intermittent boluses or as a continuous infusion. Urine output and signs and symptoms of congestion should be serially assessed, and the diuretic dose should be adjusted accordingly to relieve symptoms, reduce volume excess, and avoid hypotension.”  (ACCF/AHA, Class I, Level B).

There are a couple of interesting things here. First is that the initial IV dose of Lasix should be at least as much as the patient’s DAILY dose, meaning if they are on 40mg BID, we should give 80mg IV. The other interesting thing is that they do not really specify if we should be giving more than this or not. The editor made this comment regarding dosage: “The ESC guideline does not specify dosing, noting the lack of good evidence for the use of high-dose over low-dose loop diuretics and tradeoffs that include transiently worsened renal function.”

Ok, so there’s no firm recommendation over what dosage should be used, other than it should be at least as much as the daily home dosage. So then I went to the AHA’s website and found a great article that addressed this exact question. This is what they had to say: “In a retrospective analysis, Butler et al22 identified higher loop diuretic dosage as an independent predictor of worsening renal function in ADHF even after controlling for disease severity and the degree of diuresis…however, it may be impossible to completely adjust for other confounders of disease severity that could effect both diuretics requirements and the risk of worsening renal function. Thus, it remains unknown whether higher diuretic requirement are simply a marker for higher risk or whether higher doses of loop diuretics contribute directly to the development of the cardio-renal syndrome in patients with ADHF.”

Then they give this graph, essentially stating that the more Lasix someone is given, the higher the mortality. Of course, the confounding factor here is that sicker people are probably given more Lasix, but here it is:

CHF Lasix 2

So, unfortunately, I think that all we can reliably conclude is to verify the patient’s home dosage, and give the total daily home dosage, or more, IV. I think what I will do is find out their daily home dosage, give that, then reassess the patient and give more if necessary. But it’s not wrong to find out their daily dosage and double it, so you will need to develop your own practice habits and talk to other attendings about this and get their opinions. I welcome and encourage any comments!



Burn blisters: to debride or not to debride?

Dr Duhe and I had a case last night, very straightforward. A kid burned the top of his foot with some hot water. He had some blistering over his MTP joints causing him pain. Dr Duhe wanted to send him home with pain control, I had always been taught that the blisters need to be debrided. I’m the attending, so I won and the blisters were debrided (Dr Duhe used the scissors in the suture kit and cut the dead skin overlying the blister), Silvadene was applied, the foot was bandaged and the kid was sent on his way.

This of course brought about a debate of whether burn blisters need to be debrided or not. I did a PubMed search and the first source I found that looked useful was a consensus statement from the American Burn Association, released in 2012. They stated: “Among the most direct and effective interventions for reduction of risks from cutaneous burns is removal of the burn eschar. Devitalized skin is a rich medium for microbial growth, and also is known to promote inflammation by release of cytokines and growth factors from injured or lysed skin cells. Consequently, practices for care of burn wounds have favored early and complete removal of the burn eschar.” So I thought, “cool, I win!”, except that I’m not sure that a blister is an eschar so I’m not really sure that they are advocated for popping the blister and removing the dead tissue. So the lit search continued.

To make a long story short, I ended up finding an EM Practice article that gave a class IIa recommendation to leave the blister intact. Hmm, I lose. Then, I went to Wikipedia, the ultimate source for all medical information. They state “it is not clear” what to do with intact blisters. So we both win. Then they recommend AGAINST using Silvadene! Now my world has been turned upside down. I will need to investigate this recommendation against Silvadene next.

So, at the end of the day, there is no clear answer as to what to do with intact burn blisters. Do whatever you want. Probably leaving them intact and applying a dressing is the quickest and easiest thing to do. But the real overriding message here is not everything that you are learning on-the-job is necessarily the right thing to do. I was taught that debriding a burn blister was, without question, the right thing to do. This was from a pediatric surgeon that used to run the burn unit at Children’s. Not that he’s wrong, but it’s important to know that a doctor’s opinion is not the same as fact, and new evidence is emerging all of the time, so you have to stay on top of your stuff. You have to be curious and research things on your own and form your own informed opinion. When I work with you guys, I try to make sure you are aware of certain things that you do that are “Sinai-Grace”-ish and not necessarily how things are done at other hospitals. More than a few of you have been on the receiving end of my rants against routinely ordering a BNP on patients with CHF. There are a lot of ways to practice medicine, and you need to form your own opinions based on a myriad of information thrown at you. Look things up, ask questions, and try to picture how you will handle certain patients and situations because in a few short years (or months), it’s all up to you!