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So you have a patient with intracranial bleeding or you have a high pre-ct suspicion of intracranial bleeding and they are taking coumadin, aspirin, or clopidogrel. Should you reverse them? If so, how?

What if the CT is negative? Can you just discharge these patients as soon as they have a negative CT?

In this episode of the EMCrit Podcast, I discuss reversal of anti-coagulant drugs & anti-platelet medications, with particular emphasis on the prothrombin complex concentrates (PCC). I also touch on how to disposition these patients if their initial CT scan is negative.

Reversal Meds

Here are sample guidelines for drug reversal:

Warfarin

Any patient with a history of recent warfarin use, with an INR > 1.5 should immediately receive:

1. Vitamin K 10 mg IVPB over 10 minutes (monitor for hypotension / anaphylaxis) &

2. 50 units/kg of Prothrombin Complex Concentrate (Bebulin or Profilnine) Administer over 20 minutes.

• If PCC unavailable, give 15 cc/kg of FFP

Repeat INR 10 minutes after completion of infusion

Liver failure with known coagulopathy or elevated PT or INR •1.5

1. Vitamin K 10 mg IV over 10 minutes (monitor for hypotension / anaphylaxis) &

2. 50 units/kg of Prothrombin Complex Concentrate (Bebulin or Profilnine) &

3. 2 units of FFP

• If PCC unavailable, give 15 cc/kg of FFP total

Reversal of Platelet Dysfunction: For any patient with antiplatelet (Aspirin, Aggrenox or Clopidogrel) used in last 24 hours administer:

1. dDAVP 0.3 mcg/kg x 1 (20 mcg in 50 cc NS over 15-30 minutes) &

2. 1 donor pack platelets (~6 units)

Review Article of Vitamin K antagonist reversal (Critical Care 2009, 13:209)

Review Article on PCCs (European Journal of Anaesthesiology 2008; 25: 784–789)

Recent Study on DDAVP for Aspirin (Journal of Trauma 2020;88(1);80-86

CT Negative after Head Trauma while on Anti-coagulants or Anti-plt Meds

One man's jury-rigged approach:

Minor head trauma (the definition of this in the anticoagulant literature seems to be different than most other head trauma lit, they actually define minor as NO LOC and NO AMNESIA, just a bop to the head)

* Most folks would still say scan these patients once and then observe for 6 hours. A few would say just observe, a very few would say admit for 24 hours. I watch them for 6 hours and then get the CT scan.

Head trauma with LOC, but GCS 15

* definitely scan, definitely observe at least 6 hours, most would say either rescan or admit for 24 hours

Head trauma with LOC, but GCS < 15

* scan, almost certainly admit for 24 hours, probably rescan prior to d/c

Not great literature support for any of this, here are some studies to get you started:

Delayed Posttraumatic Acute Subdural Hematoma in Elderly Patients on Anticoagulation (Neurosurgery 58:851-856, 2006)

Low Dose ASA led to secondary bleeding not seen on initial CT in patients with normal neuro exams (J Trauma 2009 67(3):521)

Update:

From EM:RAP Aug 2013

Nishijima DK et al. Immediate and delayed traumatic intracranial hemorrhage in patients with head trauma and preinjury

warfarin or clopidogrel use. Ann Emerg Med. 2012 Jun;59(6):460-8.

o A prospective, observational study at 2 trauma centers and 4 community hospitals. Most of these patients were community

Hi folks,

Sorry about the voice--got a cold off those damn ED keyboards

Thanks to my friend Reuben, this week we'll talk about the asthmatic patient that codes while on the vent

The DOPE mnemonic gives you a path to figure out why a patient is desaturating

(If anyone knows who created the DOPE mnemonic, please add a comment or send me an email. An EMCrit listener solved the mystery)

If the pt is asthmatic, add an "S" to make DOPES

The "S" stands for Stacked Breaths--and it's the first thing to address.

Address it by disconnecting the vent circuit. Don't think about it, don't dither, just disconnect the vent.

"E" is for equipment. Attach a BVM hooked up to O2 and you'll eliminate ventilator equipment failures.

"D" is for tube displacement. Verify the tube with ETCO2, either qualitative or quantitative.

"O" reminds you to check for obstruction of the tube. See if you can put a suction cath all the way down.

If all of these don't fix the problem, then consider "P" for pneumothorax.

Lung sounds are not always definitive. Throw on the UTS if you have the time.

Otherwise perform bilateral finger thoracostomies. What the hell is that, you say?

Listen to the podcast.

Then you can read more about it in this article

C.D. Deakin, G. Davies and A. Wilson, Simple thoracostomy avoids chest drain insertion in prehospital trauma, J Trauma 39 (2) (1995), pp. 373–374.

Update:

Is the tube mainstem, is there a ball-valve obstruction?

Consider reintubation

Consider Bronchoscopy

Finger Thoracostomy BET

Emerg Med J 2017;34:417-418.

Don't intubate the severe asthmatic,

try NIV first

continue the nebs on the NIV

obviously they need steroids and throw in Mag Update: (3 MG RCT tells us to skip the Magnesium even in severe asthma)

does ketamine work? maybe...

If you intubate, Ron Walls says add lidocaine to your sedative and paralytic

if you put them on the vent make sure your plateau pressure stays below 30 cm H20

or make sure the flow graph shows flow has stopped before the next breath

Here is the vent lecture:

"Not the Greatest Vent Lecture Ever"

Please Listen to this Addendum

In response to a comment below

Now on to the Podcast...

Chris Nickson is an Aussie, oops Kiwi, who is a lead author of a great blog: lifeinthefastlane.com and tweets under the moniker @precordialthump; check him out, he's doing really good stuff. He wrote a comment about the last podcast--

Hey Scott, Great to hear your views and approach to EGDT. I agree with the need for aggressive resuscitation of the septic patient – with fluid, antibiotics, vasopressors (we’re a ‘norad/ norepi shop’ too) and adequate oxygen delivery being the mainstays – and, if nothing else, the Rivers paper deserves credit for bringing this into the spotlight. However, the Rivers study itself is still a cause of concern for me – a single center study that has never been repeated as an RCT, with a very high mortality in the control arm (mid-40s%), and more recently the WSJ allegations about about methodological ‘dodginess’ behind the scenes and concerns about conflicting financial interests (of which I’m not sure what to make). Most ICUs in Australia don’t use CV02 monitoring, yet our mortality rates are substantially better than the Rivers study (ICU sepsis mortality around 20% these days, down from 34% in 1997) – different populations or something else? I’m also uneasy about the blood transfusion phase of the Rivers protocol. Hopefully trials like ARISE and ProCESS will help clear up what actually works. In the mean time, I heed your call to resuscitate! Cheers,

Chris Nickson

ED/ICU Registrar, Perth

So in this brief aside, I respond to Chris' comments and tell you a bit about the EMCrit Podcast EBM philosophy.

Here are the links mentioned:

* Henry Ford Hospital Reply to WSJ - 10.27.2008

* New MSSM ED Crit Care Sepsis Protocol

* MR of Early Quantitative Therapies for Sepsis

Hi all--Sorry for the delayed posting, but I just moved to a new apt.

In this episode I rant and rave about why for the most part Emergency Medicine has disappointed me by not doing something about our sick septic patients.

If you are offering aggressive therapy in the ED, then good on you.

Of course everything in this talk stems from River's seminal work: EGDT Study

...but there is more. Don't forget to check out a brief aside (PodCast 14.5), in which I respond to Chris Nickson's experience of EGDT in Australia and tell you a bit about the EMCrit Podcast EBM philosophy

On this podcast,

I recap from last show, especially the concept of bare minimum normotension (called erroneously permissive hypotension by just about everyone else) and why we should keep the MAP higher if there is suspected elevations in intracranial pressure

I then talk about massive transfusion. This is probably the best strategy for a patient that will require greater than 8-10 units of PRBCs.

What may be the best review of the topic is by Spinella and Holcomb:

(Blood Reviews 2009;23:231-240)

I talk about

* 1:1:1 transfusion

* PCC, Factor VIIa, Cryo

* Calcium

* IV Access

coming up in the next few podcasts: Sedatives for Intubation, Trauma Airway Management, The Crashing A-fib patient

For updated thoughts

See this Mass Trans Post

Now on to the Podcast...

Thought we'd talk about some trauma stuff, specifically the resuscitation of the critically ill hemorrhagic shock patient.

There is much to discuss, so this will be a multi-episode affair.

Today, we'll concentrate on the Lethal Triad and BP Goals.

Lethal Triad

The picture says it all.

Bleeding causes acidosis, hypothermia, and coagulopathy. Then the cycle begins as they all beget each other. If this continues for too long, it is irreversible.

We can iatrogenically make things worse by keeping our patients exposed and infusing ice cold fluids and products. By diluting their existing clotting factors and platelets with too much fluid and red cells. And by not ensuring adeqaute perfusion to counter acidosis.

BP Goals

Your goal is a MAP of 65. This is not hypotensive resus, which is still not proven. It is normotensive resuscitation; beyond 65, no additional benefts will be seen, but you do risk increased bleeding and dilutional coagulopathy.

If MAP < 65 - give fluids/products

If MAP > 65 - check perfusion

there are monitors for this such as NIRS measurement of thenar eminence, but at this stage, I recommend using the presence of a nice strong pulse and warm hands.

MAP > 65 & Good Perfusion-stand tight

MAP > 65 & Bad Perfusion-give fentanyl 20-25 mcg

why fentanyl? b/c taking away pain and fear will limit endogenous catecholamines and the pt's bp will drop slightly from vasodilation. Now give fluids/products to take the MAP to > 65.

Here are the articles

resus of crit ill trauma patients

damage_control_anesthesia

Next Time: Massive Transfusion Protocols

The management of severe ETOH withdrawal and Delirium Tremens:

1. Consider alternative diagnoses

Here is my DT protocol

2. Start treatment with diazepam

3. If you reach 200 mg, switch to phenobarb or intubate and give propofol

4. Your goal is to get your patient sleepy, but arousable with a HR<120

The citation for the CCM article is (Crit Care Med 2007;35:724)

I also discuss a listener email regarding succinylcholine and whether it causes increased oxygen consumption.

Dexmedetomidine (Precedex)??

Maybe...

In short: Roc Rocks and Sux Sucks! (that one is for you Reub)

Update:

* Phenobarb for etoh withdrawal

* Phenobarb dose calculator sent by Dr. Robert Hand

* The Pharmacology of Benzos in Withdrawal

Mohamed, a listener from Sudan, emailed asking about the treatment of acute pulmonary edema in patients with low blood pressure. This is in distinction to SCAPE patients (see podcast 1).

If the patients have pulmonary edema and low BP from a cardiac cause, then they are in

Cardiogenic shock.

First, consider the etiology:

* Rate-related

* Valve Disorder

* Ischemic (Right sided infarct, STEMI, NSTEMI)

* Cardiomyopathy

* Toxicologic

At the same time, you are treating the patient with:

* Inotropes (dobutamine, milrinone, calcium)

* Pressors to achieve a MAP > 65 (allows coronary perfusion) (Meta-Analysis demonstrates norepi superior to dopamine Medicine. 96(43):e8402, OCT 2017)

* Oxygenation support, most likely with intubation

* Optimize O2 carrying capacity (Hb>10)

Here is a fantastic set of guidelines to manage these patients

Update:

* Contemporary Management of Cardiogenic Shock Circulation 2017;136:e232

* Journal Feed Summary