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The Knife & Gun Club said:
I would seriously question if the liver lac was a result of the CPR by either a broken rib or some other blunt mechanism, maybe in the setting of a blood thinner?

In any case I’m sorry that happened to you, that’s a huge bummer
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That's kind of what we thought. But she was dead when she came in and stayed dead. It was more of a head scratcher. Mostly just a "nope, the ME is signing this one."
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Good case from last week:

Patient found down obtunded with vomit in their mouth

Vitals - BP 60s and HR 160s with kussmaul breaths

Has diabetes and without insulin for a month

Glucose - Elevated over 600s

Your next move?
 
alpinism said:
Good case from last week:

Patient found down obtunded with vomit in their mouth

Vitals - BP 60s and HR 160s with kussmaul breaths

Has diabetes and without insulin for a month

Glucose - Elevated over 600s

Your next move?
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Suction puke. Nursing or RT needs to be Johnny on the spot to roll+suction if puking again.
Multiple large bore IV access sites
Quick physical exam for obvious trauma/anything concerning
Pour in LR
Stat labs w/ blood gas
Insulin gtt
K containing fluids PRN
NCHCT as soon as stable enough to get to scanner
Do more things based on how the situation/labs/imaging evolves.

If their breathing slows down and blood gas still crap or they otherwise try to die:
Bolus bicarb before intubating
Push dose neo before intubating to get a BP that isn't periarrest. More ready as a gtt.
Intubate
TV = normal/high
RR = 30+
More blood gasses
 
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The Knife & Gun Club said:
I’m trying to imagine how logistically this would work in terms of getting all that equipment available to bedside quickly with CPR in progress.

Admittedly in Miami it’s pretty rare that we see that degree of hypothermia so maybe my hospital is just not set up for it but how the hell did you get a blood warmer to bedside in the span of minutes? Just announce it and someone brings one? Did it come from the OR?

In any case that’s a boss move, strong work.
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The one similar case I had, I used a level one infuser (which warms, and can throw blood OR IVF in really quick). We have one in ER/OR, people know to grab it.

Clearly it can output to a luerlock tube (normal IVF tubing).

At the time as a sole provider I had worries about (1) placing two chesttubes myself with ongoing CPR in a timely manner without poking myself and the CPR giver (2) hooking up chest tubes to the warm water source I had (the level one). I considered putting an anterior pigtail, running hot fluid through it, and putting a low lateral open tube to drain for a moment.

Instead, I basically did an open DPL and put a dialysis catheter into the peritoneum, and we would put 3-4L of max temp saline via Level one in (takes a couple minutes), let it slosh a while, then opened one port and let it drain out... rinse repeat a few times and we got impressive core temp improvement with this technique.

The patient was truly cold (mid-low 80sF) and truly had signs of life when found but lost pulses on EMS arrival, and was baseline on the younger/healthier side, so a reasonable case to try hard on.

We don't have ecmo / bypass of course.
 
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BoardingDoc said:
Suction puke. Nursing or RT needs to be Johnny on the spot to roll+suction if puking again.
Multiple large bore IV access sites
Quick physical exam for obvious trauma/anything concerning
Pour in LR
Stat labs w/ blood gas
Insulin gtt
K containing fluids PRN
NCHCT as soon as stable enough to get to scanner
Do more things based on how the situation/labs/imaging evolves.

If their breathing slows down and blood gas still crap or they otherwise try to die:
Bolus bicarb before intubating
Push dose neo before intubating to get a BP that isn't periarrest. More ready as a gtt.
Intubate
TV = normal/high
RR = 30+
More blood gasses
Click to expand...
Exactly my thinking too.

If you’ve gotta tube them, bolus of bicarb, maybe calcium too depending on the K for a little extra inotropy, neo if you’ve got it, otherwise norepi or at worst push-dose crash cart epi.

Putting in 10u of humalog subcu as soon as you have a K back can be helpful too while waiting for the insulin drip from pharmacy.
 
BoardingDoc said:
Suction puke. Nursing or RT needs to be Johnny on the spot to roll+suction if puking again.
Multiple large bore IV access sites
Quick physical exam for obvious trauma/anything concerning
Pour in LR
Stat labs w/ blood gas
Insulin gtt
K containing fluids PRN
NCHCT as soon as stable enough to get to scanner
Do more things based on how the situation/labs/imaging evolves.

If their breathing slows down and blood gas still crap or they otherwise try to die:
Bolus bicarb before intubating
Push dose neo before intubating to get a BP that isn't periarrest. More ready as a gtt.
Intubate
TV = normal/high
RR = 30+
More blood gasses
Click to expand...

It's all good...an EKG would be helpful before a lot of this stuff. Rate is 160. Is it something shockable or is the rhythm fugly as all hell?
 
Would have a very low threshold to empirically push bicarbonate and calcium. Patient is suspected severe DKA so likely very acidotic, renal failure, and hyperkalemia contributing to the hemodynamic instability. Dumping in fluids to of course.

If patient cannot turn around quickly and requires intubation would go hemodynamicly cautious RSI with levophed primed and ready as would anticipate big crash in pressure. Once tubed fast RR on vent (30) especially if got roc to keep up with respiratory compensation.

If pH below 7.0 would start bicarbonate gtt.

Definitely a case where you need to resuscitate the hemodynamics before intubate unless patient loses respiratory drive (which usually causes cardiac arrest)
 
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thegenius said:
It's all good...an EKG would be helpful before a lot of this stuff. Rate is 160. Is it something shockable or is the rhythm fugly as all hell?
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Yup. Seems like most of the peri-arrest DKAers I've seen are hyperkalemic (although 160s is pretty fast for this). Will usually give a bolus of IV insulin in these cases as well.
 
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RoyBasch said:
Would have a very low threshold to empirically push bicarbonate and calcium. Patient is suspected severe DKA so likely very acidotic, renal failure, and hyperkalemia contributing to the hemodynamic instability. Dumping in fluids to of course.

If patient cannot turn around quickly and requires intubation would go hemodynamicly cautious RSI with levophed primed and ready as would anticipate big crash in pressure. Once tubed fast RR on vent (30) especially if got roc to keep up with respiratory compensation.

If pH below 7.0 would start bicarbonate gtt.

Definitely a case where you need to resuscitate the hemodynamics before intubate unless patient loses respiratory drive (which usually causes cardiac arrest)
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Yea I would only tube if there is vomit in his trachea, or continues to have vomit in the trachea. i wouldn't do it for AMS. as long as air can get into the lungs and there isn't significant shunt, I would just stay in the room for the next 30-60 mins (or be very close by) trying to resuscitate (with NS not LR [EDIT: I'm wrong on this]) and get the lay of the land with labs.
 
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BoardingDoc said:
???? This seems like the opposite of what you should be doing.
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Well...completely undifferentiated like this guy without knowing anything except BP. I would be concerned that adding K+ from LR, even though it's a small amount, would be counter productive. I'm aware that NS is hyperchloremic and can cause slight metabolic acidosis, but how to balance if K is 7.3? What I'm talking about is what's the first 1L to give, if that is even going to make a difference. As opposed to to the first 3-4 L this guy will get over the next several hours. and maybe I'm wrong about this. Maybe unequivocally LR would be better no matter what in just about every situation.

EDIT:
I'm looking at this now at Fluid selection & pH-guided fluid resuscitation Looks like I'm wrong
 
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thegenius said:
Well...completely undifferentiated like this guy without knowing anything except BP. I would be concerned that adding K+ from LR, even though it's a small amount, would be counter productive. I'm aware that NS is hyperchloremic and can cause slight metabolic acidosis, but how to balance if K is 7.3? What I'm talking about is what's the first 1L to give, if that is even going to make a difference. As opposed to to the first 3-4 L this guy will get over the next several hours. and maybe I'm wrong about this. Maybe unequivocally LR would be better no matter what in just about every situation.

EDIT:
I'm looking at this now at Fluid selection & pH-guided fluid resuscitation Looks like I'm wrong
Click to expand...
Yeah I dunno the way I think about it is that DKA patients are actually potassium deficient, they just need it to shift back into the cells. By increasing pH you shift it back into the intercellular fluid. So LR is quite a nice solution because it lowers potassium in the blood by dilution with a lower potassium concentration, it is alkaline so it helps move potassium into cells, it provides volume to help counteract dehydration that is increasing catecholamine release, and it comes with some potassium (albeit very little) that the patient will need to replete total body potassium stores. I think Weingart will also do isotonic bicarbonate +/- potassium, harder to have on hand at most places.
 
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lucid_leprechaun said:
Yeah I dunno the way I think about it is that DKA patients are actually potassium deficient, they just need it to shift back into the cells. By increasing pH you shift it back into the intercellular fluid. So LR is quite a nice solution because it lowers potassium in the blood by dilution with a lower potassium concentration, it is alkaline so it helps move potassium into cells, it provides volume to help counteract dehydration that is increasing catecholamine release, and it comes with some potassium (albeit very little) that the patient will need to replete total body potassium stores. I think Weingart will also do isotonic bicarbonate +/- potassium, harder to have on hand at most places.
Click to expand...

Yup agree with all.

The bold part is key right there and it's not obvious (to me). Intravascular K+ is high. Therefore diluting that space in any way possible is good. Just basic chemistry there.

The potassium concentration in LR isn't that high, but it's there. So we are hoping the vascular potassium moves in the cells rather quickly. Like immediately.

Let's say that same patient above is having a malignant arrhythmia from (presumed) hyperK. Would you still give LR? here's my thinking. Even though LR K concentration is very low, if the hyperK is irritating the myocardium causing a life-threatening conduction disturbance, elevating the serum potassium level transiently even 0.1% higher just for a few minutes can be bad and cause PEA or asystole. (just assume for a moment that you haven't given calcium. let's just keep that treatment out of this equation).

I guess it all depends on how fast the extracellular potassium moves intravascular. I know it's fast but do you get what i'm trying to say

I can see an expert witness situation LOL. Pt with known diabetes p/w peri-arrest with an awful looking EKG suggestive of hyperK. They will presumably arrest in the next 5 minutes. You can do
a) calcium, bicarb, insulin and LR
b) calcium, bicarb, insulin, and NS
I know insulin won't do chit immediately but that's what we would all order immediately. Expert witness be like "LR has potassium!!!"

What about giving a fictitious crystalloid LR-sans-K? This would be LR that has no K+.

The way to study this would be to do animal models and measure the concentration of K+ every minute for the first 30 minutes when giving LR vs NS.
 
thegenius said:
Yup agree with all.

The bold part is key right there and it's not obvious (to me). Intravascular K+ is high. Therefore diluting that space in any way possible is good. Just basic chemistry there.

The potassium concentration in LR isn't that high, but it's there. So we are hoping the vascular potassium moves in the cells rather quickly. Like immediately.

Let's say that same patient above is having a malignant arrhythmia from (presumed) hyperK. Would you still give LR? here's my thinking. Even though LR K concentration is very low, if the hyperK is irritating the myocardium causing a life-threatening conduction disturbance, elevating the serum potassium level transiently even 0.1% higher just for a few minutes can be bad and cause PEA or asystole. (just assume for a moment that you haven't given calcium. let's just keep that treatment out of this equation).

I guess it all depends on how fast the extracellular potassium moves intravascular. I know it's fast but do you get what i'm trying to say

I can see an expert witness situation LOL. Pt with known diabetes p/w peri-arrest with an awful looking EKG suggestive of hyperK. They will presumably arrest in the next 5 minutes. You can do
a) calcium, bicarb, insulin and LR
b) calcium, bicarb, insulin, and NS
I know insulin won't do chit immediately but that's what we would all order immediately. Expert witness be like "LR has potassium!!!"

What about giving a fictitious crystalloid LR-sans-K? This would be LR that has no K+.

The way to study this would be to do animal models and measure the concentration of K+ every minute for the first 30 minutes when giving LR vs NS.
Click to expand...
Evidence from anesthesia literature suggests the acidosis from NS outweighs the effect of the K in the LR.
 
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thegenius said:
Yup agree with all.

The bold part is key right there and it's not obvious (to me). Intravascular K+ is high. Therefore diluting that space in any way possible is good. Just basic chemistry there.

The potassium concentration in LR isn't that high, but it's there. So we are hoping the vascular potassium moves in the cells rather quickly. Like immediately.

Let's say that same patient above is having a malignant arrhythmia from (presumed) hyperK. Would you still give LR? here's my thinking. Even though LR K concentration is very low, if the hyperK is irritating the myocardium causing a life-threatening conduction disturbance, elevating the serum potassium level transiently even 0.1% higher just for a few minutes can be bad and cause PEA or asystole. (just assume for a moment that you haven't given calcium. let's just keep that treatment out of this equation).

I guess it all depends on how fast the extracellular potassium moves intravascular. I know it's fast but do you get what i'm trying to say

I can see an expert witness situation LOL. Pt with known diabetes p/w peri-arrest with an awful looking EKG suggestive of hyperK. They will presumably arrest in the next 5 minutes. You can do
a) calcium, bicarb, insulin and LR
b) calcium, bicarb, insulin, and NS
I know insulin won't do chit immediately but that's what we would all order immediately. Expert witness be like "LR has potassium!!!"

What about giving a fictitious crystalloid LR-sans-K? This would be LR that has no K+.

The way to study this would be to do animal models and measure the concentration of K+ every minute for the first 30 minutes when giving LR vs NS.
Click to expand...
That expert witness would need a physiology/chemistry lesson.

LR has a K concentration of 4meq/L. It has nothing to do with how fast potassium moves in and out of cells. The potassium could stop moving completely. By giving a solution which has a lower concentration of K than the body currently has, you will definitionally LOWER the body's concentration of potassium. The more LR you give the patient, the more the patient's K will approach 4meq/L. Giving LR to a patient with a K of 8 won't push them to 8.0001. It will bring them towards 4.

This is a very common misunderstanding of chemistry that seems to show up specifically when it comes to potassium, and yet I've never seen this apply to discussions about sodium. Imagine a poor neglected nursing home patient who shows up with a Na of 160. OMG you gave them NS! Are you trying to kill them? That's full of Na! Yeah, but at a concentration of 154meq/L, so their [Na] will definitionally fall.

If you want to change the discussion about the perceived danger of giving a K containing solution and instead make the argument that using NS which contains no K will cause the K to fall faster than LR... then you can get into the nuance about this and see how the hyperchloremic acidosis from NS outweighs the gains of using it vs LR in DKA, as the increased acidosis --> extracellular shifting of K in exchange for H+ --> worsening hyperkalemia.
 
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BoardingDoc said:
That expert witness would need a physiology/chemistry lesson.

LR has a K concentration of 4meq/L. It has nothing to do with how fast potassium moves in and out of cells. The potassium could stop moving completely. By giving a solution which has a lower concentration of K than the body currently has, you will definitionally LOWER the body's concentration of potassium. The more LR you give the patient, the more the patient's K will approach 4meq/L. Giving LR to a patient with a K of 8 won't push them to 8.0001. It will bring them towards 4.

This is a very common misunderstanding of chemistry that seems to show up specifically when it comes to potassium, and yet I've never seen this apply to discussions about sodium. Imagine a poor neglected nursing home patient who shows up with a Na of 160. OMG you gave them NS! Are you trying to kill them? That's full of Na! Yeah, but at a concentration of 154meq/L, so their [Na] will definitionally fall.

If you want to change the discussion about the perceived danger of giving a K containing solution and instead make the argument that using NS which contains no K will cause the K to fall faster than LR... then you can get into the nuance about this and see how the hyperchloremic acidosis from NS outweighs the gains of using it vs LR in DKA, as the increased acidosis --> extracellular shifting of K in exchange for H+ --> worsening hyperkalemia.
Click to expand...

1.) Agree.
2.) But as we learned from my lawsuit, anything the muggles can't understand is immediately "wrong".
 
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thegenius said:
Yup agree with all.

The bold part is key right there and it's not obvious (to me). Intravascular K+ is high. Therefore diluting that space in any way possible is good. Just basic chemistry there.

The potassium concentration in LR isn't that high, but it's there. So we are hoping the vascular potassium moves in the cells rather quickly. Like immediately.

Let's say that same patient above is having a malignant arrhythmia from (presumed) hyperK. Would you still give LR? here's my thinking. Even though LR K concentration is very low, if the hyperK is irritating the myocardium causing a life-threatening conduction disturbance, elevating the serum potassium level transiently even 0.1% higher just for a few minutes can be bad and cause PEA or asystole. (just assume for a moment that you haven't given calcium. let's just keep that treatment out of this equation).

I guess it all depends on how fast the extracellular potassium moves intravascular. I know it's fast but do you get what i'm trying to say

I can see an expert witness situation LOL. Pt with known diabetes p/w peri-arrest with an awful looking EKG suggestive of hyperK. They will presumably arrest in the next 5 minutes. You can do
a) calcium, bicarb, insulin and LR
b) calcium, bicarb, insulin, and NS
I know insulin won't do chit immediately but that's what we would all order immediately. Expert witness be like "LR has potassium!!!"

What about giving a fictitious crystalloid LR-sans-K? This would be LR that has no K+.

The way to study this would be to do animal models and measure the concentration of K+ every minute for the first 30 minutes when giving LR vs NS.
Click to expand...

How do so many people get this wrong? It doesn't even make sense!

The metabolic acidosis from NS will likely increase the K. The 4 meq of K in LR will decrease the K.
 
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RustedFox said:
1.) Agree.
2.) But as we learned from my lawsuit, anything the muggles can't understand is immediately "wrong".
Click to expand...
True, but this also seems to be a common misconception amongst physicians as above. Somehow a lot of people think "if it contains K it must make your K go up." This clearly is not the case and bears repeating.
 
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Some people also put too much into their notes. Simpler can be better. Explaining why you used LR over NS or vice versa just lays out another bad avenue for someone to try to attack your care.
 
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GassYous said:
How do so many people get this wrong? It doesn't even make sense!

The metabolic acidosis from NS will likely increase the K. The 4 meq of K in LR will decrease the K.
Click to expand...
About half my ICU residents argue with me about this 🙄 i tell them to go read about lol
 
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BoardingDoc said:
True, but this also seems to be a common misconception amongst physicians as above. Somehow a lot of people think "if it contains K it must make your K go up." This clearly is not the case and bears repeating.
Click to expand...

Yet another Kobayashi maru.
 
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SpacemanSpifff said:
Ask and you shall receive, sort of. Here's a consensus statement from the American College of Radiology and the National Kidney Foundation.

My takeaway: I have their full support all the way down to eGFR of 30, in the context of evaluating for a potential life threat.
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I’ll let you scan below 30 if you say in your note it’s clinically necessary. But I might be rare?

I still firmly believe CIN isn’t real and most of what we see as “CIN” is antibiotic toxicity to the kidney. Overshooting the vanc trough makes the gfr go down too. Ain’t nobody holding the vanc…
 
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lucid_leprechaun said:
Agreed, nephrologists get this wrong all the time. Same as Zosyn causing AKI, contrast, etc.
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Zosyn causing AKI thing is so annoying. It's like it popped out of nowhere w/ minimal evidence associating it, then became the thing. Somehow nobody pays attention to the better evidence debunking it (moa is basically competitive inhibition of creatinine secretion). Meanwhile, people don't say boo about rampant overusage of vanco (see it given routinely for UTIs and intra-abdominal infections. why not switch to linezolid for pna? etc).

Can't blame nephrologists. They need to be able say "avoid nephrotoxins" when they get consulted. Much harder to say "aki is common and most often multifactoral, as well as sometimes artifactual, in hospitalized or ill patients"
 
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turkeyjerky said:
Zosyn causing AKI thing is so annoying. It's like it popped out of nowhere w/ minimal evidence associating it, then became the thing. Somehow nobody pays attention to the better evidence debunking it (moa is basically competitive inhibition of creatinine secretion). Meanwhile, people don't say boo about rampant overusage of vanco (see it given routinely for UTIs and intra-abdominal infections. why not switch to linezolid for pna? etc).

Can't blame nephrologists. They need to be able say "avoid nephrotoxins" when they get consulted. Much harder to say "aki is common and most often multifactoral, as well as sometimes artifactual, in hospitalized or ill patients"
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I say a version of that every time the ICU consults me for "pancytopenia, eval for AML" in a 70yo morbidly obese diabetic with all the acronyms on his 3rd week of ECMO with slowly declining counts due to being sick as f*** and his marrow having finally just called it a day.
 
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Maaan.
How do I bookmark these posts so I can get to them later when I'm not busy having fun?

At giant arcade. Marvel vs. Capcom is more fun right now.
 
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So we decided to wait it out and not do the intubation.

Put in all the normal DKA vs HHS orders and told nurses to do 4 liters of fluids.

Reevaluated 10min later without any improvement and was more shallowly breathing.

Got VBG back with PH 6.65 and PCO2 35 with HCO3 below detectable limits.

Talked it over and decided we couldn't wait and do the intubation.

Patient was aggressively hyperventilated and given 2 amps of bicarbonate.

Did RSI with the HOB elevated and used the largest tube possible.

Started the vent at TV 500 and RR 30 for a MV of 15 LPM.

Goal was to achieve PCO2 15 from our winters calculations.

Labs came back severe DKA with AG of 25 but otherwise normal.

Put on fluid and bicarbonate infusions and gradually improved.

Admitted to CCM and then fortunately had a full recovery.
 
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The Knife & Gun Club said:
I’m trying to imagine how logistically this would work in terms of getting all that equipment available to bedside quickly with CPR in progress.

Admittedly in Miami it’s pretty rare that we see that degree of hypothermia so maybe my hospital is just not set up for it but how the hell did you get a blood warmer to bedside in the span of minutes? Just announce it and someone brings one? Did it come from the OR?

In any case that’s a boss move, strong work.
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was just lurking for curiosity but this reminded me that probably my most surprising case i saw as a student in Miami was a hypothermic arrest that my team was caring for in the ICU

Found unresponsive outside on the singular weekend it was legitimately "cold" my entire four years there ("cold" being like 42F), no medical cause identified other than likely alcohol playing a role based on history. Coded in ED, don't know all the details but they got ROSC after 40 minutes and when i left the rotation patient was being extubated and seemingly making a decent neuro recovery
 
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This is just a reminder to ALWAYS pull central lines with the patient at least flat if not in T-burg. Keep them flat and make sure the line site has an occlusive dressing and keep them flat for 30 minutes. Most hospitals have policies on central line pulls that reflect this.

We just had a patient decompensate and die from massive air entrainment 45 seconds after his Cordis was pulled in a semi-recumbent position and he was allowed to sit up. His RV was full of air - completely opacified. I’ve read about this but it’s the first time that I’ve seen it first hand.

If it happens or a patient crumps after a line pull, put them on as much O2 as you can, T-burg on their left side to relieve the RV outflow obstruction. You can try aspiration if you can get a catheter in the RV (long central line, dialysis cath, or PA cath).
 
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I've had 7 days off of ER work, and I feel great. I have 5 more days off.

Last night, I had a dream where I was caring for a bunch of kids on drugs who were out partying in a farm-field somewhere, wearing Pokemon costumes. I'm trying to start an IV on Pikachu and yelling at a Charmander to "knock that off, now". Cannabinoid hyperemesis and belly pain all over.
 
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CajunMedic said:
EMS calls in with a cardiac arrest. 50ish male, found down bradycardic in the 20's, Air temp in the teens, wet clothes, and snow on the ground. Goes into V-Fib when EMS moves him, shocked to asystole. Bounces between V-Fib and asystole during transport. Has an IV, King-LT, and Lucas in place for compressions when he gets to us. EMS had been working him for at least 30 mins.

Rectal temp is less than 86 degrees. ETCO2 is 8. Keep compressions with the Lucas while actively warming the patient. 3-way-foley with warm saline and decided to put 2 chest tubes in and circulate warm saline to warm the core. Swap out the King for an ETT. After about 45 mins with 0 change in rhythm, Core is now 86 degrees. we tried amiodarone and lidocaine to no luck. I was doing my "anyone have any other ideas?" spiel when one of my interns speaks up. He's FM boarded but doing a second residency in EM. He suggested double sequential defibrillation (last month's journal club).....I'll be damned, it worked!. Sinus rhythm with J-Waves, trying to breathe over the vent, and systolic in the 120's. Labs aren't terrible. Call Big University Medical Center to transfer to ICU, and wait for ground transport (can't get a bird due to weather).

Near shift change, I get a call from the NP on the Cardiac Arrest team. EEG shows normal brain activity and a chance to recover. Clean heart cath 24 hours later. Got a message today from one of the medics that brought him in: Extubated, talking, and expected to make a full recovery

Chalk one up for the good guys!!
Click to expand...

EPILOGUE: got a text message yesterday from the intern that was running the code and suggested the double sequential defibrillation. The patient walked into the ED on his own power, fully intact, shook hands and thanked everyone involved for saving his life!
 
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CajunMedic said:
EPILOGUE: got a text message yesterday from the intern that was running the code and suggested the double sequential defibrillation. The patient walked into the ED on his own power, fully intact, shook hands and thanked everyone involved for saving his life!
Click to expand...

Booooooomm.

Wow.

Strong. Work.
 
Here's another one of CajunMedic's spinchter-clenching patients,

29 Female, seizure history, comes in by EMS in status epilepticus. Had seized 7 times prior to EMS' arrival, twice with EMS, receiving a total of 10 mg Versed PTA. Normal person, takes their meds, follows with neuro at Big University system across the state line. Promptly seizes again as soon at EMS crosses into the room. Give 4 of Ativan as that's the quickest thing we can get our hands on, then the 1 gram of Keppra we have in the Pyxis. Still seizing and now Hypoxic. Pull the trigger and RSI. Have the PA call the pharmacy for the phenobarbital dosing. Call the nursing supervisor for the EEG machine, because it's going to be a while for transfer and transport, figure we'd need it. Can't get it, only 1 in hospital and no tech on call to set it up. Gets the Phenobarb, still seizing once the roc wears off. Lactic of 11. WBC 33K, labs otherwise OK. Give the remainder of the weight-based Keppra dose. Still seizing, but not as often. Transfer center finally calls back and puts me through to the ICU doc, recommends cranking the Propofol up, giving Valproic Acid, and starting Levophed if needed for the pressure after maxing out the Propofol. Finally stops seizing, core temp 102.9. Now cooling and giving IV tylenol. Central Line, Art line, and Levo on standby. Can't get a bird due to weather and no critical care ground assets for transport. At shift change, she's stable as I can get her and I sign her out to the day doc pending transport.

I came back on that night to find out, she stayed stable, but could never get a helicopter. At 10 AM, They wound up sending a local ALS truck with a new medic, an ER nurse, and a hospital RT to manage the vent and went an hour by ground.

Wishing I got an RVU Bonus! Level 5 patient, with 360 mins of CC time and procedures...
 
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On ICU with all surgeons. Surgeons everywhere.

Had a normal garden variety code which is uncommon on that unit. Ran it like any other ER code while my two partner fellows, who are both PGY8/9s frantically fumbled with the getting set up for a POCUS and chest tube. Assign roles, order meds, give instructions for pads, crash cart, US machine. Anesthesia nowhere to be found, just walked to the head of bed and popped a “difficult anatomy” ETT in the seconds. Nurse screaming “YOU CANT INTUBATE WITHOUT THE AIRWAY TEAM.”

Knocked the tube in, got ROSC, none of the staff had a brain hemorrhage. By ER standards nothing in any way out of the ordinary but to the holier than thou surgeons it was my 15 minutes of them realizing EM is a speciality for a reason.
 
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CajunMedic said:
Here's another one of CajunMedic's spinchter-clenching patients,

29 Female, seizure history, comes in by EMS in status epilepticus. Had seized 7 times prior to EMS' arrival, twice with EMS, receiving a total of 10 mg Versed PTA. Normal person, takes their meds, follows with neuro at Big University system across the state line. Promptly seizes again as soon at EMS crosses into the room. Give 4 of Ativan as that's the quickest thing we can get our hands on, then the 1 gram of Keppra we have in the Pyxis. Still seizing and now Hypoxic. Pull the trigger and RSI. Have the PA call the pharmacy for the phenobarbital dosing. Call the nursing supervisor for the EEG machine, because it's going to be a while for transfer and transport, figure we'd need it. Can't get it, only 1 in hospital and no tech on call to set it up. Gets the Phenobarb, still seizing once the roc wears off. Lactic of 11. WBC 33K, labs otherwise OK. Give the remainder of the weight-based Keppra dose. Still seizing, but not as often. Transfer center finally calls back and puts me through to the ICU doc, recommends cranking the Propofol up, giving Valproic Acid, and starting Levophed if needed for the pressure after maxing out the Propofol. Finally stops seizing, core temp 102.9. Now cooling and giving IV tylenol. Central Line, Art line, and Levo on standby. Can't get a bird due to weather and no critical care ground assets for transport. At shift change, she's stable as I can get her and I sign her out to the day doc pending transport.

I came back on that night to find out, she stayed stable, but could never get a helicopter. At 10 AM, They wound up sending a local ALS truck with a new medic, an ER nurse, and a hospital RT to manage the vent and went an hour by ground.

Wishing I got an RVU Bonus! Level 5 patient, with 360 mins of CC time and procedures...
Click to expand...
I’m curious when these people board do you have a practice of “rounding” on them or anything during shift change ?

Phenomenal case btw. Phenobarb for the win
 
The Knife & Gun Club said:
On ICU with all surgeons. Surgeons everywhere.

Had a normal garden variety code which is uncommon on that unit. Ran it like any other ER code while my two partner fellows, who are both PGY8/9s frantically fumbled with the getting set up for a POCUS and chest tube. Assign roles, order meds, give instructions for pads, crash cart, US machine. Anesthesia nowhere to be found, just walked to the head of bed and popped a “difficult anatomy” ETT in the seconds. Nurse screaming “YOU CANT INTUBATE WITHOUT THE AIRWAY TEAM.”

Knocked the tube in, got ROSC, none of the staff had a brain hemorrhage. By ER standards nothing in any way out of the ordinary but to the holier than thou surgeons it was my 15 minutes of them realizing EM is a speciality for a reason.
Click to expand...
Good work. Airway team is very much unneeded, particularly in an ICU.
 
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