#ResusX19 came and went too quickly! I guess that's what happens when you're having fun while learning. All the attendees, including our St. V's EM residents, had an amazing time at the conference. The lectures were short and extremely high-yield, and they catered directly to the mind of the EM resuscitationist. The workshops allowed us to interact one-on-one with knowledgable educators to deep-dive into various topics. Here are the learning pearls from the final day of #ResusX19!
Blood Pressure in Neuro Emergencies; What's My Target? by Dr. Evie Marcolini
Lots of flavors of neuro disasters; each has its own blood pressure target
Hemorrhagic stroke - mostly caused by untreated hypertension - SBP<140; if patient has chronic HTN then SBP<180 - Our job is to prevent secondary injury by reversing AC and treating blood pressure - ATACH-2 trial - Nicardipine: goal <180 and <140; no difference. Lower is not better.
Ischemic stroke - Need to keep BP higher to allow perfusion via collateral flow - Keep SBP relatively high, but must be <185 for tPA
Traumatic Brain Injury - SBP>100 for ages 50-69; SBP>110 for everyone else (from BTF guidelines) - SBP<90 increased mortality - Every 5mmHg above SBP 90 (up to 135) decreases mortality
Subarachnoid hemorrhage - SBP<140 - Goal is to prevent re-rupture - Do it quickly: give a bolus and infusion (Nicardipine or Clevidipine) - AVOID Nitroglycerin and Nitroprusside; these are vasodilating, making the vessels take up more space in the brain
How to Intubate the Injured Head and Why Your Decision Matters by Dr. Erin Sabolick
It is critically important to prevent secondary injury (too late to prevent primary injury when patient is in front of us in the ED)
Neuro exam is extremely valuable, and we lose that when we intubate the patient
Important components of the neuro exam: eye opening, pupils, voice, motor response on both sides, upper and lower extremities - Exam can be performed while preoxygenation (flush rate NC & NRB) and premedication (fentanyl, NO lidocaine) takes place
Use video laryngoscope
Ramped intubation: gravity helps with venous drainage
Ketamine - No ICP spikes (MYTH BUSTED: Systematic Review, LITFL) - Hemodynamically neutral - Allows for spontaneous respiration
Have your post-intubation sedation ready before the intubation - Paralytics may last longer than sedative, so you will either need to redose the sedative or start your infusions - Have extra induction and paralytic ready at the bedside
Be present at the bedside when the consultant performs a repeat neuro exam
Mastering Acids & Bases by Dr. Rory Spiegel
Dr. Spiegel gave a two-part lecture on digesting acid-base problems in our patients. There is absolutely no good way to do justice to Dr. Spiegel's engaging lecture by typing out notes. Instead, I would highly recommend you watch his Acid-Base lecture from The Hospitalist and The Resuscitationist Conference.
The actual pH number doesn't matter
Study conducted on rabbit hearts: heart beat better in neutral solution vs acidic solution; inotropes worked better in neutral solution - However, in humans, results are different
"Apneic Oxygenation in Man" Frumin et al. - heart did just fine with extreme acidosis and elevated pCO2 - The acidosis doesn't really cause issues in humans
The name of the game is: Cations (Sodium) must equal Anions (Cl-, HCO3-, Anion gap) - you can only become acidotic in two ways: either chloride increases and HCO3 decreases or gap increases and HCO3 drops - alkalosis occurs by the opposite mechanism
SID (Strong Ion Difference) = Na-Cl. Normal is 36-40 - SID >40 = Alkalosis - SID <40 = Acidosis
Ex: SID>40 occurs in (Cl decreases, HCO3 increases): Vomiting: lose H+ and Cl Dehydration: "Contraction alkalosis", Aldosterone retains Na, so Na and HCO3 increase Chronic resp acidosis: Na and HCO3 increase
Ex: SID<36 occurs in (Cl increases, HCO3 decreases): Diarrhea: Losing Na and HCO3 AKI: not absorbing back Na and HCO3 RTA: peeing out Na and HCO3 Saline Infusion: significant Cl load (Normal Saline is a SID 0 fluid, will lower body SID). In LR, sodium lactate is the buffer --> lactate gets broken down and body gets free sodium; similar in Plasmalyte. NaHCO3 administration --> CO2 blown off, you get free Na
Take home: if you use SID, no need for calculating a delta delta. We are looking at the chloride and how it influences the acid/base.
All nongap acidosis is due to increases in chloride
Gap alkalosis: gap (composed of weaker acids: lactate, albumin, ketones, alcohols) decreases and bicarb increases (eg. drop in albumin).
Elevated anion gap acidosis (Mnemonic MUDPILES) - THESE WILL KILL YOUR PATIENT > Methanol --> Formate > Uremia --> phosphates and sulfates (high BUN; it's not urate) > DKA --> Ketones > Paraldehyde (used for alc withdrawal)/Phenformin (inhibit Kori cycle) --> Lactate > INH/Iron --> Lactate (due to seizures) > Lactic acidosis --> Lactate, CO, CN, ischemia > Ethylene Glycol --> Oxalate, Glycolate > Salicylate --> Ketones, lactate
What labs do we need? - BUN - Lactate - Ketone - ASA Level If all are negative, only one left is toxic alcohol
Where are we with Acute Ischemic Stroke: I Can't Keep Up by Dr. Evie Marcolini
Thrombectomy improves outcome as shown by multiple studies
What about wake-up strokes? - DAWN trial - you can still perform thrombectomy 6-24 hours out and patients do better - DEFUSE trial - small core, big penumbra --> perform thrombectomy. Look for a high mismatch ratio (ratio of penumbra to core; unsure exactly what that number is; shared decision making between providers and patient). Risk of reperfusion bleed is higher if core is as large as penumbra.
Interhospital transfer prior to thrombectomy is associated with delayed treatment and worse outcomes. Some patients should go directly to the comprehensive stroke center from home.
How to decide who goes directly to stroke center? There are a number of clinical decision instruments for prehospital providers:
MR WITNESS and WAKE-UP studies - DWI vs FLAIR mismatch to time the stroke
Tenecteplase vs Alteplase before thrombectomy for ischemic stroke - Talk with family and patient about risks/benefits
Know the data, know your system, share the knowledge and options with the patient and family
Status Epilepticus: Where's the evidence? by Dr. Erin Sabolick
Definition: continuous seizure for 5 minutes or two seizures without interval return to baseline
RAMPART trial showed that IM midazolam terminated more seizures without rescue therapy than IV lorazepam. IV midazolam hasn't been looked at properly.
Some extra tips: - Start looking for reversible causes early > Home medications/toxicology > ETOH vs Benzo withdrawal > INH toxicity > Decreased Na/Ca/Glucose > Consider eclampsia in any pregnant or postpartum patient - Involve consultants early - Consider taking the airway early if indicated
If hypotensive, can switch propofol to midazolam
Consider adding ketamine
STAT EEG (ensure no underlying seizure after paralysis)
ESETT Trial: results coming out soon - compares fosphenytoin vs valproic acid vs levetiracetam
Traumatic Brain Injury by Dr. Evie Marcolini
New guidelines from Brain Trauma Foundation in 2016 (be on the lookout for my BTF TBI guidelines summary soon!!!)
Avoid hypotension. As from above: SBP>100 for ages 50-69; SBP>110 for everyone else.
Optimize cerebral perfusion pressure (CPP = MAP-ICP), 60-70mmHg
Don't use induction agents that will drop BP. Use etomidate for induction. Ketamine is now an option; ICP increase has been debunked.
Lidocaine: no longer used in RSI; can cause hypotension in RSI, so don't use it.
Laryngoscopy will increase blood pressure. Use fentanyl, which can help decrease pain and blood pressure and mitigate seizures.
Some extra tips and tricks: - Intubate with HOB up - Hydrate your patient - Place an arterial line early if possible - Have esmolol ready (even prime tubing) to bring BP down quickly if the patient spikes - Have meds drawn up and ready with push-dose agents
Hyperventilation: do not use anymore. Keep CO2 35-40. Only use if you are headed to ventriculostomy or craniectomy. Rebound vasodilatation that takes up space in the brain can occur.
If there is a brain bleed: - Reverse anticoagulant - Seizure prophylaxis if clinically indicated - Give Osmotics: Mannitol will cause diuresis, so you need to replace the fluids; Hypertonic saline is a volume expander, you can bolus 250mL at a time to decrease swelling/ICP
Ventriculostomy is indicated for sick patients, bad CT, bad exam
Therapeutic hypothermia doesn't work, but fever is bad - treat with tylenol
Do not prognosticate within the first 24 hours
TXA in TBI: Are we there yet? by Dr. Erin Sabolick
CRASH2 and MATTERs trials show some support for TXA in trauma
Precise dosing regimen is uncertain at this time
No increase in vasoocclusive events (strokes, MI, etc)
CRASH3 results due very soon
Bottom line: TXA for TBI? Not yet.
Check out our Journal Club review of the Cal-PAT trial
Step 1: lower your standards - don't try to get all the lab numbers right
Step 2: dry them out: diurese, use pressors early, and administer less fluids
Step 3: phenotype your shunt physiology: determine if pathology is single lung vs double Lung
Double lung - ARDS - Berlin definition - Lung is not stiffer, it is just smaller. There is loss of some lung parenchyma due to fluid. - You are now dealing with "baby lungs," so use smaller tidal volumes - 4 large randomized trials that failed to show benefit of high vs low PEEP - Start with ARDSnet protocol but monitor your patient and make changes as below - Monitor your DRIVING PRESSURE = Plateau pressure - PEEP > Normal DP ~14cmH2O. > Answers the question "Is the tidal volume I am giving to this patient appropriate for their lungs?"
Start by increasing PEEP to decrease Driving pressure. If PEEP gets too high, then Plateau pressures can also rise (due to overdistension of the lungs). Solve this by lowering tidal volume. Plateau pressure will decrease and you can continue to increase PEEP and attempt to lower Driving pressure.
Single lung - PEEP increase will cause worsening hypoxia - Place patient on his/her side with good lung down (lateral decubitus) > Increases blood flow to good lung > Increases airway pressure in good lung due to weight of mediastinum and other lung, allowing more air to reach bad lung
Patients frequently just need time to re-recruit the alveoli
Posterior Stroke - What's all the Fuss? by Dr. Evie Marcolini
CAT scans don't work for posterior fossa. If you're thinking posterior stroke, get the MRI.
Vestibular syndrome - Triggered: positional, motion triggered, resolves in between motion: BPPV, orthostatic hypotension, GI bleed - Episodic: discrete episode that resolves: panic attack, arrhythmia, TIA - Acute: onset with some kind of trigger (maybe motion), can get better or worse with movement but does not resolve, symptoms persist: Vestibular neuritis, labyrinthitis, posterior stroke
Dr. Marcolini led a small group discussion about neurological emergencies and focused on the HINTS exam, giving specific recommendations about appropriate technique. - 100% sensitive and 96% specific for posterior stroke, better than MRI - However, only do the exam if the patient has active symptoms. If asymptomatic, don't do exam! - This video by Dr. Peter Johns has a great demonstration of the right exam techniques:
Sadly, the conference has come to an end. We hope that these recaps and learning pearls will come in handy for your next shifts. Review these concepts frequently to reinforce the information with some spaced repetition.
As mentioned above, be on the lookout for the Brain Trauma Foundation Traumatic Brain Injury (BTF TBI) Guidelines summary.
Shyam Murali, @smuramed
Ed Fenton, @fenton_ed