Maximally Aggressive Care, Everywhere
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Jamie Lan

Discussion  - 
Hi all,

Are people giving TXA in trauma with bleeding patients only within 3 hours of injury, since figure3 in the article suggests that after 3 hours from injury, there's no difference in RR reduction in mortality. OR are people still giving it within 8 hours of injury as per the study design?

EMCrit's profile photoJamie Lan's profile photo
Thanks for the prompt responses

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Yogesh Apte

Discussion  - 
Can anyone of the EMCrit-izens share a link of penicillin dosage conversion from million units to grams per day?
don zweig's profile photo
400,000 U = 250mg
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Stephen Herbe

Discussion  - 
Hi Scott/EMCrit Community,

I'm an RN in the CTICU and absolutely love the podcasts/articles. The topics I find myself gravitating towards the most are vasopressors, necessity of fluids in sepsis/shock and the usefulness/uselessness of measuring a patients CVP. My questions are:

When we get people out of the OR and they're hypotensive one of the first things we do is bolus them via rapid infusion with LR. Generally the surgeons like to see a CVP of 10-12. If measuring the CVP is not a true marker of fluid status/responsiveness do you feel that we may be drowning some of these patients? Sometimes they will come out on a little bit of Epinephrine and as soon as a blood gas is drawn and they see a lactate going up or is elevated they'll stop the Epi and switch over to Dobutamine....Do you think its worth keeping them on the Epi if we know thats the cause of the elevated lactate?

I am trying to best tailor my practice to serve my/our patients and if there is any insight you guys have into these things as they pertain to CT Surgery I would be super interested in learning.
Stephen Herbe's profile photoTrip699's profile photo

what you will find among ICU folks is that the training is varied a little bit depending on specialty. A cardio thoracic ICU may run a bit differently than a medical ICU for example. What I find is that medicine is a little bit of lore with some art and some facts in literature than can change after a few more new studies. I some cardiac ICU's the heart failure specialist will trend lactates and ask me to swan those patients that require dobutamine. In others they trend lactates. In others they just follow map. It depends on the literature that you subscribe to and your rationale for your choices.
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Sting Jor

Discussion  - 
So, interesting question hopefully to get pointed in the right direction or answer regarding norepinephrine(levophed). I know the necrotic aftermath of this particular drug for extravasation through peripheral lines. At what point downstream from the insertion site does this drug lose the potency to necrose tissue? Is it localized the venous side, decrease in the arterial side? Here's why I ask. Say we have a hypothetical case:
We have an active Superior Mesenteric Artery bleeding into the abdomen with retroperitoneal hematoma without previous injury mid 70s male. Pt is hypotensive of 70/40-50/30 routinely, acute abdominal pain distention, 4liters of fluid (over approx 2 hours) and 2 units PRBC infused rapidly through warmer/pressure. I won't get into why the pt did not scream to the OR but I'm the RN managing care in ED. Diaphoretic, clammy and cool and pale, awake alert but mentation is wavering. With the active bleed in the abdomen, levophed came to mind however the necrotic component came to mind and nobody could answer how far in the circulatory system does levophed decrease in necrotic ability if any? Therefore they didn't pursue it. I had the patient about 3 hours in ED before receiving an ICU bed. Consults for surgery wanted to 'watch the patient' and hope the clot formed would stop the bleeding and then lyse itself and the blood would be absorbed into system.

*At what point downstream from the insertion site does this drug lose the potency to necrose tissue? How far in the circulatory system as well?* My concern was having this leak into his abdomen and necrose the area of the active bleed? Should this be a concern? I know the pressor would need very close management to not pop whatever clot had formed but also knowing it was only a bandaid approach to definitive care. I know it may be a heavy pharmokinetics question but seems mildly valid given the scenario.
Also, I considered recommending Tranexamic acid for this case. Thoughts?

Any idea to my question? Thanks in advance from an ER nurse. Go easy if I missed something, only a nurse two years. The patient did finally go to surgery and is stable but somewhat critical. I've learned so much from the emcrit podcasts and interventions and can't say how much I enjoy the education. I started from podcast zero in the beginning of the year and just about through 2015.
Brian Pongracz's profile photoSting Jor's profile photo
Brian- Thanks for the input. Your approach is how I went but you put into words better than I tried. I totally agree with the permissive hypotension and that's the route I personally went as the RN. My question really was generated in the moment of knowing if the extravasation of norepinephrine into the belly would be detrimental as in a local IV site. I do see the logic in the dilution factor you present and maybe didn't think of it to the extent you present. Thanks for the comments and it gives clarity for future cases. I do wonder if there is a study performed to answer the question directly about "data available about how dilute norepinephrine needs to be to be safe extravasated." 
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Robert Mabe

Discussion  - 
Dr. Weingart,

Was happily cruising down the highway enjoying another fine EMCrit podcast this week when a statement caught me off guard. In episode 172c (VAPOX) you noted that your preferred ventilator setting is Assist/Control - Volume. I have been preaching for years now that in my setting, rotor-wing transport, and in the setting of smaller referral ERs that SIMV - Volume is the way to go for emergent patients. Less potential for barotrauma, hypercapnea secondary to breath stacking, pressure support for spontaneous breaths, less stressful for the patient should sedation or paralysis be allowed to wane temporarily... you know, all the usual arguments in support of SIMV (which are my usual arguments against A/C).

Could you elaborate for us why A/C is your preferred mode over SIMV in the post emergent intubation patient population?

Many thanks! Enjoy the show!
EMCrit's profile photoTrip699's profile photo
I would like to chime in

A patient breathing say 20 time a minutes on ACVC is just as likely to have issues as a patient breathing 20 times a minute on SIMV (as long as they are set to same tidal volumes). The issues begin when the patient breaths over the set rate. If this patient is breathing say 10 over the set rate on the ACVC mode, you will have much less minute volume variation and work of breathing than if that same patient was breathing Pressure supported breaths over the set rate.

ACVC TV of 450 rate of 20 with 5 of peep and a flow rate of 60L/min
is about the same as
SIMV TV of 450 rate of 20 with 5 of peep and a flow rate of 60L/min

but if the patient on AC starts breathing over, then the vent does the work.
If the patient is breathing over on the SIMV with pressure support, then depeniding on the patients effort and degree of obstructive lung disease, the minute ventilation changes.

The purpose for intubation in a patient with sick lungs is partly to limit work or breathing and gaurantee a minute ventilation while the patient has time to recover. SIMV with PS may not provide this.

Some will argue that the pressure support is much more comfortable and this may well be the case but the goal is control over the physiology to ensure adequate minute ventilation and then treat pain and anxiety after the primary goal is achieved.

People write books on the modes of ventilation, but from my decade of critical care work, I would argue that SIMV has its place but I do not usually consider it with my sick ICU patients. I have settings where it is useful but rarely in the acute stage of injury.

Craig Rosebrock

Pulm/CC medicine
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ken t

Discussion  - 
theoretical case here at our own Jannus general

68 yr old F presents w ch pain
CTA--massive PE -bilat prox pe [heparin iv started pre scan]

Good hemodynamics on arrival- but had near syncope at home. She crashes just after CTA chest done and she comes back to ER, quickly develops PEA arrest
Gets ROSC w ACLS, tubed as part of resuscitation
still hypotensive on pressors
TPA given-- "bolus" over 15 minutes
comes to icu w persistent hypotension needing pressors -

Labs 2 hrs post lytic tx--drop of Hb 12 down to 6 [no overt bleeding, no trauma pre arrival or known bleeding disorders], PT, PTT way high [and stay that way-they were normal on arrival], fibrinogen very low, PLTS stay near 100 K

I am interested in recommendations re: timing of restarting heparin and what folks say about using cryo or other products for what looked like DIC caused by her massive PE associated with cardiac arrest
ken t's profile photoTrip699's profile photo
hard case and likely no right way to go about it.

agree with scott.
This person is likely bleeding.

regarding when to start back AC
I would do lower ext dopplers and just see if there is a big clot burden in legs. If so it will likely push one to place a greenfield -- if one suspects that shock may get worse.

I have placed lines with plts of 10,000 and INR's out the wazoo so I dont really worry too much about placements of things unless its arterial.

When Hg drops that fast there is usually some active site and belly is usually where i look first. If they too unstable US of abdomen ext may be helpful.

Also I cant recall where i read this but I seem to recall some literature on bolus from IV contrast causing issues with failing RV's

very hard case man
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Rasmus Aagesen

Discussion  - 
I was called out to a fire in a big apartment building last night, due to sucspision that several people where trapped in side. I'm a Swedish resident in anaesthesiology, critical care and prehospital retrieval. We had no seriously injured and the team preformed great. Ran the scenario through my head and prepared the usual stuff - tube, trach kit, escaotomy and so one - but on my way home I got unnerved by the fact that most of these things I learned in medschool and started wondering what is new in the early stage of burn victim care in prehospital or ER situation. We had a 5 min drive by ambulance to level 2 trauma center and 45min to dedicated burn unit. We prepared Ketamine and roc on the ride out. Standard fluids and a pac of cyanokit. We had an average of 3-5 ambulances on scen at any given point with emt that we reguralarly work with
Andrew Haynes's profile photo
Not sure I've seen much new material on pre-hospital burns management since I qualified in 2006! The most important things are good basic supportive management of airway, oxygenation, volume status and analgesia.

Burn specific interventions seem to be very infrequent other than RSI for inhalation burns. Even this can very often be delayed until arrival in hospital since the swelling doesn't come on that quickly.

The thing that appears to be done the worst in the pre-hospital phase is good analgesia, and that make the job of the receiving trauma team much more difficult. Most burns patients don't need to go immediately to a burns centre if the bypass time is long, since the burns surgeons aren't going to get involved for 24 hours or so. 
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Scott Weingart

Discussion  - 
Folks--this page will be shut down in the next month or so. Please start moving over to REDDIT. It will provide us a markedly better experience.
Come to and hit the subscribe button
Rhett Rhemann's profile photo
I hope it's better because your page is literally the only reason I signed up for Reddit. Thanks for the great discussions and info though!
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Ben Seymour

Discussion  - 
Hi Dr. Weingart & Dr. Farkas, 

I recently came across the PulmCrit article on Rapid Sequence Termination of Status Epilepticus (linked below) and became quite interested in the idea of using propofol +/- ketamine as an aggressive management option; the protocol makes sense to me and seems like a reasonable option with relatively few risks.

I've had a fairly thorough look at the available literature and it seems while early propofol is considered somewhat standard amongst the neurocrit. world that early ketamine is almost unheard of. 

Of the available papers and case series I have found two retrospective observational studies: Gaspard et. al. (2013) which describe ketamine use in ~60 patients with initial administration times from 6hours - 30 days; and Synowiec et al (2013) includes only 13 patients who all had SE for >24 hours. 

Barring one case study where administration occured "within hours of SE onset" because of haemodynamic complications the remaining case series available that discuss ketamine use only in refractory SE and usually when SE has been ongoing for a very long time (20+ days).

What are your thoughts on this? Has your treatment protocol changed since the publication of that PulmCrit article/have you had recent success with early propofol + ketamine?

Quick discussions with my ICU consultant made it clear that their preferred route/the hospitals protocol here is managing with a barbituate coma if 3rd/4th line anti-epileptics fail.

I'd love to hear your thoughts on this.

Ben Seymour
Final year medical student from Australia

PulmCrit article:

Retrospective study references:

Gaspard N, Foreman B, Judd LM, Brenton JN, Nathan BR, McCoy BM, et al. Intravenous ketamine for the treatment of refractory status epilepticus: A retrospective multicenter study. Epilepsia. 2013;54(8):1498–503.

Synowiec AS, Singh DS, Yenugadhati V, Valeriano JP, Schramke CJ, Kelly KM. Ketamine use in the treatment of refractory status epilepticus. Epilepsy Research [Internet]. Elsevier B.V.; 2013;105(1-2):183–8. Available from:
don zweig's profile photoBen Seymour's profile photoDominik Daszuta's profile photo
Dosing for initial Lorazepam/Midaz is as per the RAMPART trial (link below). Specific excerpt is as follows: 

"All adults and those children with an estimated body weight of more than 40 kg received either 10 mg of intramuscular midazolam followed by intravenous placebo or intramuscular placebo followed by 4 mg of intravenous lorazepam. In children with an estimated weight of 13 to 40 kg, the active treatment was 5 mg of intramuscular midazolam or 2 mg of intravenous lorazepam."
Pg 593 

Again further discussion with Dr Bleck on the EMCRIT show makes it clear that his personal opinion is that if the first line treatment is given (regardless of loraz/midaz/phenytoin) subsequent treatments have diminishing returns/reduced effect. He has some evidence for this claim from an old Veterans Affairs trial where more data was later published but it is not available in the public domain as far as I can see.

RAMPART Trial results:
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ken t

Discussion  - 
RE: monitoring during resuscitation of Cardiac Arrest. While I know that pulse oximetry is not accurate when patient does not have "pulsatile flow", it's been my observation that during "good CPR/ Resp Support" the O2 sats improve and the pleth on monitor looks good. So the question is: what are your recommendations about looking at the pulse ox during CPR in the ICU and ER. We are finally implementing routine use of End tidal CO2 monitoring during all resuscitation [up until now it has been sporadic]. Thanks
Vince DiGiulio's profile photoJordan Schooler's profile photo
I can't see any reason why the oximetry value wouldn't be accurate. 
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About this community

The place for EMCritters to share cases and ideas on resuscitation, ED critical care, and trauma.

Robert Hutton

Discussion  - 
Can anyone help with these questions:
Does Vasopressin have any role in CPR?
Is there evidence it may improve neurological outcomes?
Appreciate any help

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Dean Burns

Discussion  - 

I'd be interested in hearing the opinions of the Emcrit universe on the difficulties with IV access in sickle cell crises.

Do any hospitals use a standard operating procedure to escalate difficulties with IV access in these patients?

Are IO/SC fluids used routinely as part of the management on your wards?

Are PICC lines placed early in the patient's admission to circumvent these difficulties?

If you're successfully overcome these problems, please get in touch.

Best wishes

EMCrit's profile photoDean Burns's profile photo
Is SC a feasible route for gentle fluid (1-1.5 x maintenance)?
Our hospital prefers PICCs to mid lines because of the difficulties with drawing blood back from a midline. The vascular access nurses are of the view that PICCs are more reliable in that regard.
What about SC PCAs?
Any better than PO meds for painful crises?
Is IO an absolute no no?
I saw your back & forth with RR on the EMLitOfNote. IO might incur an increased osteomyelitis risk. I'd have some concerns in the non Resus situation.
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Beatrice Lai

Discussion  - 
Dear Scott,

Thank you for the podcast on Sepsis-3 with Dr Singer. My question is that there seems to be confusion with the " SOFA score of >=2 " (which means a total SOFA score of 2 or more) and "ACUTE CHANGE of SOFA of >=2 " . These two phrases seem to be used interchangeably (and incorrectly I think) in the original Sepsis-3 JAMA paper or even in many other medical websites.

I thought I understand that the clinical criteria of sepsis is "suspected infection + ACUTE CHANGE ( increase ) of SOFA score of >=2". Then in the flowchart of the original paper, it confuses us by saying that patient with infection + " SOFA >=2" means sepsis. Here, it implies that a TOTAL SOFA score of >=2.

I assume this is a typo and that it should emphasize it is the CHANGE of score of >=2 and not just a SOFA of >=2 . Am I correct? Because surely many of our patients have a baseline SOFA of 2 already (e.g. A chronic renal impairment patient with baseline Creat of 200umol/L would have a baseline of 2). Just because this person comes in with infection + 2 points SOFA doesn't mean he is having sepsis. He would have to have a total of 4 or above SOFA score in order to be classified as sepsis.

However many websites, and in the paper it seems to go on about how "SOFA score of >=2 reflects mortality risks of 10%...." [Box 3] . I assume the author means TOTAL score here. and then it goes on about how CHANGE of 2 points SOFA predicts mortality, hence the consensus is to choose a cut off value of 2 when it comes to clinical criteria of sepsis. " Acute change of 2 points or more" and a mere " SOFA score of 2 points or more" are being mixed up in many comments and references over the internet. Can you please clarify ?

Thank you! 
EMCrit's profile photoBeatrice Lai's profile photo
Both??! what happens when patients baseline SOFA is already 2 before this acute infection episode?
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Eliza Anderson

Discussion  - 
Looking for some advice on getting push-dose pressors readily available in my ER. I am an RN and sent this email to my boss and others who then forwarded it to a pharmacist and below is his reply. Help!
ME: "I have been involved in several intubations in the ER in the past few weeks where either the trauma surgeon (Dr. ...) or one of the ER docs (Dr. ..., Dr. ...) have requested a push dose of phenylephrine because there was reported hypotension. We’ve requested a pharmacist to the bedside to assist because we don’t have the correct doses/concentration of either phenylephrine or epinephrine immediately available in our White Box. I think it would be beneficial to get these meds added to our White Box and have some education on the effects of these meds. Let me know what you think"

Pharm: "The practice of giving phenylephrine pushes is not new as pharmacists in quasi-codes, anesthesia and cardiology do this all the time. It does however require some math skills to admix a 100mcg/ml concentration of phenylephrine using the various stock formulary products. I have forwarded this email to Dr. ... to weigh in on placement in the white box as I do not make administrative decisions: and this would require P&T approval as I understand the process. However, the white box is intended for RSI and not for BP management. My opinion is that these types of medications do not belong in the white box. My personal opinion is that if needed emergently you need to request a pharmacist at the bedside who are familiar with medications, dosing, and compounding of emergent medications. If not emergent, then give small doses of epinephrine to buy some time and request a phenylephrine drip from pharmacy, which has a concentration of 200 mcg/ml. If Dr.(Pharmacist) okays in emergency situations for the RN to override phenylephrine from the pyxis and compound yourselves then I can educate your nurses on a ONE STEP process to make a 100 mcg/ml concentration, label, and administer at bedside via MD orders".

Shouldn't it be easier than this for an RN to get meds ready for RSI, including push-dose pressors? Or is this process physician driven and they need to mix their own (which means the RN will mix it most likely) and leave pharmacy out of it because they are not always available, especially at 3AM?
Thanks for your feedback..
EMCrit's profile photoEliza Anderson's profile photo
So no real concerns over significant tachycardia with epi?
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Alan Chang

Discussion  - 
Is there any literature on sepsis mortality improvement if the repeat lactic acid normalizes within 1-3 hours? Hospitalists at our hospital are always trying to block sepsis admissions on patients with intermediate lactic acid levels (2-3.9) that normalize on repeat checks (<2). Thanks!
Clark Owyang's profile photoEMCrit's profile photo
currently as per the CMS regs, these pts with an elevated initial lactate >2 should be admitted or you need to have a justification as to why not. Nothing about the subsequent clearance affects that. They need to produce the literature saying that if it clears that somehow obviates this necessity and then they need to get the regulation changed. In the minds of CMS, lactate > 2 defines severe sepsis. how can they ask you to discharge a "severe sepsis" pt.
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Scott and others,
A question came up with our ED and Hospitalists recently regarding SEP-1. We've had a few fall outs for not administering broad spectrum Abx. Situation: the patients had CMS severe sepsis criteria, c-diff positive toxin found within the first hour, and we treated with PO Vanco and IV Flagyl only. Is there evidence suggesting poorer outcomes either WITH or WITHOUT broad-spectrum coverage (as defined by CMS for mono or combo therapy such as adding meropenem or levofloxacin) in such cases when C-diff is presumed cause of the sepsis? What is your practice in these situations? Thanks for your response!
Medicine CF's profile photoChristopher Hill's profile photo
Thx for the comment. I agree, as well. I wonder if there is any evidence to support not using typical broad spectrum coverage?
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I have recently had a difficult airway that I would appreciate your opinion. 
I had a patient with a machete through the face a few times. He was GCS 15 and had mild stridor. His mandible was smashed as well as his maxilla. His teeth was inside his mouth somewhere and his tongue was lacerated. Bag-mask ventilation was not an option with the way his face looked. 

We prepared for an RSI with the crib set ready and someone with a knife in the hand. Neck infiltrated with Ligno/Adrenaline. There was also an anaesthetist observing. 

We did all the standard pre-intubation measures i.e. high flow nasal O2, checklist etc. In our institution we only intubate with the C-mac. I elected to use Ketamine 1.5mg/kg and Rocuronium 1.2mg/kg. 

Luckily everything went well and I was able to place the ET with some difficulty using a bougie. Some of his teeth was at the back of his mouth, but was not obstructing his airway.

The discussion ensued after the case and the anaesthetist thought the choice to paralise the patient was wrong (He also questioned why I used Roc and not Sux, but that is another discussion). His option would be to use Propofol and titrate until the patient is near apnoeic and then have a look with the laryngoscope. If he then felt that he could pass the tube, he would then give the Roc or even intubate with no paralytic.

My feeling is that I wanted to get the best intubating conditions with both the induction agent and the paralytic. If I failed this, the next option would be a surgical airway.

I would love your opinion on this.

EMCrit's profile photoNellis van Zyl Smit's profile photo
Thanks for the input. Really gave me food for thought.
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Chris Ackerman

Discussion  - 
Was asked by a paramedic yesterday about using Dopamine 5 mcg/kg/min during asystolic arrest as an initial measure. He stated that the EMS service in his area is doing this (i.e. arrive, verify asystole, start compressions, IO, start Dopamine and leave it at at 5 mcg. during resuscitation attempts). I have been looking and can't find any data or recommendations on this. It doesn't seem like a reasonable drug or prodedure to be doing, but perhaps there is some science showing benefit here that I can't find. Any thoughts or suggestions for finding data on this? Thanks for reading and for any feedback.
Scott Weingart's profile photoChris Ackerman's profile photo
That's what I thought, thanks.
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Stacy Turner

Discussion  - 
Hi all,
Following on from Scott's Wee on the 'vent as a bag and VAPOX,' does anyone have any experience of using the Oxylog (we have the 3000+) for this?
If so, can you share your settings?
Frank Hansen's profile photo
I have use it in NIV setting menny tims 
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Brandon Oto

Discussion  - 
Hi all,

Does anyone have experience using ketamine infusions for long-term (e.g. hours/days) sedation in the ICU setting, i.e. in an attempt to spare opioid/benzo/propofol/other sedating agents while maintaining a normal RASS and good analgesia? If so, what is your approach? Do you combine with an opiate or other agents? What patients do you consider a candidate? What dose range? Do you titrate?
Vince DiGiulio's profile photoBrandon Oto's profile photo
Mostly EM lit though, not as much in CC!
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