The NYC prehospital approaches to smoke inhalation and cyanide exposure are nearly identical, so it’s worth knocking them both out at once. Both protocols start with ABCs and burn management, and both then focus on the administration of cyanide toxicity kits for post-exposure patients who are symptomatic. You can refer to the PDFs directly for advice on dosing and administration considerations (remember: hydroxocobalaminBEFORE sodium thiosulfate to avoid medication inactivation!). Otherwise, note that prior to administering the cyanide toxicity kit is the ONLY instance in these protocols where paramedics are trained and ordered to draw blood (for pre-medication cyanide levels).
The key difference in the protocol for cyanide exposure is the early recognition of a possible MCI scenario, which would require a Class Order for widespread medication orders that would then be dispatched through our OLMC line. We touched on this months ago with the WMD protocol and the use of nerve agent antidotes.
Scary stuff, but always better to be aware ahead of time! Want to get even MORE ahead? Check out www.nycremsco.org or the protocol binder to stay on top of it all!
Dave
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POTD: Digoxin toxicity
Many of our patients are on digoxin, a potentially scary drug. Today we’re going to discuss what digoxin toxicity looks like, how to approach acute v. chronic toxicity, and digiFab/digiBind.
How does digoxin work?
Inhibits cardiac Na/K antiporter → increased intracellular Na, decreased intracellular K
Decreased intracellular K → HYPERKALEMIA in dig overdose
Increased intracellular Na → increased intracellular Ca
Increased Ca → INOTROPY
Increased inotropy → reflex INCREASED VAGAL TONE
In afib, this decreases conduction rate through AV node → slowed ventricular rate
Some pharmacology
Oral bioavailability = 40-90%
Onset of action 2-6 hours after ingestion
CANNOT be removed via hemodialysis
Renally excreted
Things that INCREASE digoxin levels:
Amiodarone, carvedilol, ranolazine, ticagrelor
Verapamil, tacrolimus, cyclosporine
Macrolides (Azithromycin)
Azoles
Things that DECREASE digoxin levels:
Carbamazepine, fosphytoin, phenobarbital
Rifampin
Digoxin toxicity: Acute or Chronic
ACUTE - usually starts with GI sxs, and then later neuro sxs
CHRONIC - insidious onset neuro sxs
Precipitating factors:
Any AKI causes accumulation since digoxin is renally excreted
Drug interactions that INCREASE digoxin levels (above)
Tissue sensitivity to digoxin increased by: Hypo-K, hypo-Mg, hyper-Ca, MI, hypoxemia
Symptoms:
Arrhythmias:
Sinus bradycardia, high degree AV block
SVTs with AV block are CLASSIC
Afib with slow ventricular rate
Afib with junctional rhythm
Focal atrial tach with AV block
Junctional tachycardia
Ventricular arrhythmias usually in CHRONIC toxicity
Bidirectional v-tach strongly suggests digoxin
GI sxs: nausea, vomiting, abd pain, diarrhea
Neuro sxs: delirium, fatigue, visual changes (change in color perception, blurry vision, photophobia, blindness)
Rarely seizures
Some EKGs attached.
“Salvador dali mustache” = scooped ST segment with ST depression, flat/inverted T wave +/- prominent U wave, short QT
Checking digoxin levels:
PO digoxin requires 6+ hours to distribute into tissues
ONLY POST-DISTRIBUTION levels actually reflect severity of intoxication
Used to calculate antiserum dose
ACUTE intox: check baseline digoxin then repeat another in 6 hours
CHRONIC intox: one digoxin level is fine assuming it was >6 hours after last dose
How much is too much?
Normal/therapeutic is 0.5-2 ng/ml
Scary levels:
ACUTE: > 10 ng/ml
CHRONIC: >4 ng/ml
However - serum digoxin doesn’t actually correlate that much with tissue levels or cynical toxicity
After getting antidote, levels don’t mean anything
The antidote: digoxin specific antibody fragments (DSFab)
Indications:
Significant arrhythmias or HD instability
K > 5-5.5 if it’s caused by digoxin
Softer indications:
Acute ingestion > 10 mg
Moderate-severe GI sxs
Serum digoxin > 10-12
Renal failure
AMS
Should consult toxicologist or poison control if not sure
Poison control: 1-800-222-1222
Digibind or digifab available (2 diff brands)
Comes in vials of 40 mg antibody fragments, which neutralize 0.5 mg of digoxin
Dosage:
Chronic poisoning: (dig level x wt in kg) / 100, can start lower initially
Acute ingestion of known dose: (mg digoxin ingested) x 1.6
Acute toxicity unknown levels: 5 vials (HD stable) or 10 vials (unstable)
Chronic toxicity unknown levels: 3-6 vials and reeval
Or you can use MDCalc
The most important thing about digoxin toxicity is to recognize it!! Hopefully this helps!
POTD: Cordis placement
Here is another addition to our video series. Today we go through how to place a cordis. For those who are unfamiliar with it, this is basically a fat central line that is primarily used for rapid infusion of fluids or blood. It only has a single lumen.
The trialysis lumen is actually larger than the cordis lumen, but the cordis is way faster and easier to place since there are less steps and less separate parts, so this makes to place for crashing patients who just need large bore access and not multiple ports. (Of note - oftentimes 2 large bore peripheral IVs in the AC is FINE for resuscitation. But you might need a crash cordis if it's taking too long to place the peripherals.)
To compare:
Standard triple lumen central line = 7 french
Trialysis catheter = 13 french
Cordis = 6 french or 9 french
We have 2 size cordis kits, 6 french and 9 french. The 6 french is actually the size you use for TVP. Clinically it makes more sense to place a 9 french if you need large bore access, but just know that we have both sizes in resus.
Of note, the 9 fr kit has the cooler blue syringe that allows you to place the wire through the syringe, reducing another step in the procedure. 9 fr kit also has the wire holder, which makes threading the wire easier.
So in summary, if you have a patient bleeding out on to the floor, please reach for the 9 fr cordis kit since it is A) larger, and B) has better things inside of it, imo.
Here is the video:
Enjoy!