Best Saves Thread

[alpinism]

Great case recently that qualifies as one of the best saves I’ve had over the past 10 years.

Healthy 20s female who’s family called EMS for an episode of syncope. Complained of severe mid upper back pain and shortness of breath. Rapidly decompensated in route and arrived periarrest looking near death and gasping for breaths. Initial vitals were BP 60/40s Sats 40s despite max NRB. Textbook symptom presentation so threw an US probe on the chest for a quick exam. Massively dilated RV actively pushing into the LV causing outflow obstruction with little overall cardiac motion. Immediately cancelled the Intubation and fluids. Put her on high flow oxygen and hung a dirty epi drip both at max rates. Managed to stabilize a little with repeat BP 120/80s Sats 80s with improved work of breathing. Straight to CTA with massive bilateral PEs confirmed with radiology attending on call. Wheeled back right away then slammed in a RIJ central line. Placed the catheter tip deep into the heart to maximize the effect for a sort of bedside performed catheter directed thrombolytics. Gave full dose of TPA over the next 2 hours. Responded beautifully with rapid improvement in her vitals and CCM even asked if she needed an ICU bed after her infusion.

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[Mount Asclepius]

Also felt like a save recently. 30s year old with obesity presented primarily with anxiety also endorsing shortness of breath. Quickly coded with PEA arrest prior to CTA imaging. Treated empirically with bolus Alteplase 50 mg due to concern for possible PE. Shortly thereafter with ROSC. CTA with bilateral PE with severe clot burden and right heart strain.

Some evidence shows half dose TPA equally efficacious (50 mg vs. 100 mg). Weight based maybe preferable. In hindsight maybe should have done 100 mg given obesity although unclear.

Rarely give TPA in cardiopulmonary arrest. How do the rest of you administer? 50 mg or 100 mg? Bolus or slow push? Or in case of non-arrested, but toxic appearing massive PE? Infusion?

 

[valianteffort]

Chronic shoulder pain. 50s or so years old. Has been dealing with it for a decade. Recommended Ibuprofen. Pt saved from years of future pain, was in tears with how effective my treatment was. He vows to never come back to ER after years of missed diagnoses and no answers.

 

[oldtown]

Also felt like a save recently. 30s year old with obesity presented primarily with anxiety also endorsing shortness of breath. Quickly coded with PEA arrest prior to CTA imaging. Treated empirically with bolus Alteplase 50 mg due to concern for possible PE. Shortly thereafter with ROSC. CTA with bilateral PE with severe clot burden and right heart strain.

Some evidence shows half dose TPA equally efficacious (50 mg vs. 100 mg). Weight based maybe preferable. In hindsight maybe should have done 100 mg given obesity although unclear.

Rarely give TPA in cardiopulmonary arrest. How do the rest of you administer? 50 mg or 100 mg? Bolus or slow push? Or in case of non-arrested, but toxic appearing massive PE? Infusion?

I had one like this in her 50’s a few years back. Walk in patient, extremely dyspneic, sats in 70’s. Lung sounds clear as could be, coded shortly after being roomed. Pushed tPA immediately based on high suspicion for PE (without even having a CXR or labs yet). Coded her for about 20 minutes before ROSC, pressures gradually came up. Cooled her and sent her to ICU, and she walked out of the hospital 5 days later on eliquis.

 

[thegenius]

Great case recently that qualifies as one of the best saves I’ve had over the past 10 years.

Healthy 20s female who’s family called EMS for an episode of syncope. Complained of severe mid upper back pain and shortness of breath. Rapidly decompensated in route and arrived periarrest looking near death and gasping for breaths. Initial vitals were BP 60/40s Sats 40s despite max NRB. Textbook symptom presentation so threw an US probe on the chest for a quick exam. Massively dilated RV actively pushing into the LV causing outflow obstruction with little overall cardiac motion. Immediately cancelled the Intubation and fluids. Put her on high flow oxygen and hung a dirty epi drip both at max rates. Managed to stabilize a little with repeat BP 120/80s Sats 80s with improved work of breathing. Straight to CTA with massive bilateral PEs confirmed with radiology attending on call. Wheeled back right away then slammed in a RIJ central line. Placed the catheter tip deep into the heart to maximize the effect for a sort of bedside performed catheter directed thrombolytics. Gave full dose of TPA over the next 2 hours. Responded beautifully with rapid improvement in her vitals and CCM even asked if she needed an ICU bed after her infusion.

Well done dude. Love the "SLAMMED IN AN RIJ"

 

[thegenius]

Also felt like a save recently. 30s year old with obesity presented primarily with anxiety also endorsing shortness of breath. Quickly coded with PEA arrest prior to CTA imaging. Treated empirically with bolus Alteplase 50 mg due to concern for possible PE. Shortly thereafter with ROSC. CTA with bilateral PE with severe clot burden and right heart strain.

Some evidence shows half dose TPA equally efficacious (50 mg vs. 100 mg). Weight based maybe preferable. In hindsight maybe should have done 100 mg given obesity although unclear.

Rarely give TPA in cardiopulmonary arrest. How do the rest of you administer? 50 mg or 100 mg? Bolus or slow push? Or in case of non-arrested, but toxic appearing massive PE? Infusion?

I almost never give TPA in undifferentiated cardiac arrest. Data suggests don't do it. The only time I do is if the person is really young. I've done it a few times and it never worked.

I have given it a few times in massive PE on pressors, worked well. CC got mad at me for some reason too

 

[Dred Pirate]

Rarely give TPA in cardiopulmonary arrest. How do the rest of you administer? 50 mg or 100 mg? Bolus or slow push? Or in case of non-arrested, but toxic appearing massive PE? Infusion?

I have seen it done probably 30-40 times. Nearly all die.
Of those that survived the initial arrest.
3 died before discharge.
1 spent 30 days in the ICU and received 50+ blood products over that time, physically recovered, but has massive short term memory loss - ironically this was the first patient where I saw this.
1 received a new diagnosis of metastatic liver CA - not sure whatever happened to her.
2 had a full recovery neurologically intact.

We push 50mg x 1 - repeat in 10-15min - no evidence that the second push helps, but if they are young we are more likely to do it - I would say half the patients get the second bolus.

 

[BoardingDoc]

Also felt like a save recently. 30s year old with obesity presented primarily with anxiety also endorsing shortness of breath. Quickly coded with PEA arrest prior to CTA imaging. Treated empirically with bolus Alteplase 50 mg due to concern for possible PE. Shortly thereafter with ROSC. CTA with bilateral PE with severe clot burden and right heart strain.

Some evidence shows half dose TPA equally efficacious (50 mg vs. 100 mg). Weight based maybe preferable. In hindsight maybe should have done 100 mg given obesity although unclear.

Rarely give TPA in cardiopulmonary arrest. How do the rest of you administer? 50 mg or 100 mg? Bolus or slow push? Or in case of non-arrested, but toxic appearing massive PE? Infusion?

Have given tPA in a code that got Rosc once. 50mg push.

Also, gave a 30 yr old, mottled periarrest guy 20mg ivp followed by 80mg over a couple hours. Discharged 5 days later with no adverse event.

 

[CoolDoc1729]

We push 50mg x 1 - repeat in 10-15min - no evidence that the second push helps, but if they are young we are more likely to do it - I would say half the patients get the second bolus.

This is the dosing I’ve done as well , about a half dozen times. It worked once but the patient died a few days later. It sucked. I’d seen and hospitalized him a few weeks earlier for relatively minor thing that required surgery, his only risk factor was recent hospitalization, otherwise totally healthy 70ish yo man. He came back short of breath, soft BP, off to CT and coded on the way back .. I ran up to my computer confirmed PEs everywhere and gave tpa - we had ROSC by the time telerad called the PEs. But he died a few days later. He never regained consciousness.

All the other times they just remained dead.

Glad for you guys, we sure need a win once and a while.

 

[Mount Asclepius]

We push 50mg x 1 - repeat in 10-15min - no evidence that the second push helps, but if they are young we are more likely to do it - I would say half the patients get the second bolus.

Does this dosing come from somewhere?

I learned something similar to this in my training. I never understood the split first and second dose. If they are dead, just give them the dose, what do you have to lose. Your odds of a great neurologically intact outcome aren’t great if you are doing another 10-15 minutes of CPR anyways. I didn’t know what to do once ROSC achieved and still on pressors hemodynanically unstable, but improving. Intensivist hem and hawed too about whether to give the second dose of 50 mg.

 

[Rockinacoustic]

Does this dosing come from somewhere?

I learned something similar to this in my training. I never understood the split first and second dose. If they are dead, just give them the dose, what do you have to lose. Your odds of a great neurologically intact outcome aren’t great if you are doing another 10-15 minutes of CPR anyways. I didn’t know what to do once ROSC achieved and still on pressors hemodynanically unstable, but improving. Intensivist hem and hawed too about whether to give the second dose of 50 mg.

It's all case reports using anything from weight based dosing up to 100mg boluses of alteplase. Even the AHA doesn't recommend a specific dosing strategy, though i too was taught 50mg and repeat dose in 15 minutes if no ROSC.

My current shop has tenecteplase and we use STEMI dosing for cardiac arrest due to suspected/known PE.

 

[AlmostAnMD]

Convinced a med student not to do em and now he's applying for ENT

My Man.

@Tenk messed that up bad with his scribe, telling him not to do em for years and guy goes and does em

 

[cyanide12345678]

I just saved a 19 yo viral URI from going to work. Epic save.

I swear I’m going to build a website doctorsworknote.com some day. I already own the domain -_-

 

[Tenk]

Convinced a med student not to do em and now he's applying for ENT

My Man.

@Tenk messed that up bad with his scribe, telling him not to do em for years and guy goes and does em

Technically I messed that up for you as well. 🤷‍♂️

 

[bearstanley]

pre-hospital arrest, prolonged arrest time and intubated in the ED, ROSC, ARDS probably from aspiration, aggressive vent tinkering for refractory hypoxemia, diagnosed prox LAD / LMCA occlusive MI based on EKG and echo, cards recommends "not a STEMI, let him cool off in ICU," decide not to do that, transfer to a real hospital, stented / balloon pump / CCU / stepdown / walks out of the hospital. saw a video of him with his kids a few months later. give me one of those a year and maybe i can keep doing this job.

 

[RustedFox]

pre-hospital arrest, prolonged arrest time and intubated in the ED, ROSC, ARDS probably from aspiration, aggressive vent tinkering for refractory hypoxemia, diagnosed prox LAD / LMCA occlusive MI based on EKG and echo, cards recommends "not a STEMI, let him cool off in ICU," decide not to do that, transfer to a real hospital, stented / balloon pump / CCU / stepdown / walks out of the hospital. saw a video of him with his kids a few months later. give me one of those a year and maybe i can keep doing this job.

I had one of these about 2-3 years back. Guy recognized me at a pub... somehow.

 

[CoolDoc1729]

pre-hospital arrest, prolonged arrest time and intubated in the ED, ROSC, ARDS probably from aspiration, aggressive vent tinkering for refractory hypoxemia, diagnosed prox LAD / LMCA occlusive MI based on EKG and echo, cards recommends "not a STEMI, let him cool off in ICU," decide not to do that, transfer to a real hospital, stented / balloon pump / CCU / stepdown / walks out of the hospital. saw a video of him with his kids a few months later. give me one of those a year and maybe i can keep doing this job.

Good for you as that takes some cojones to go around your home hospital consultants.

1) Was this recently? There’s not a chance I could get anywhere near me to accept this patient for transfer currently.

2) in the spirit of the Emtala thread, does this risk a violation ? Obviously it was the right thing to do, just wondering since your place could do the needed procedure whether the accepting hospital could report that.

 

[Dred Pirate]

Does this dosing come from somewhere?

I learned something similar to this in my training. I never understood the split first and second dose. If they are dead, just give them the dose, what do you have to lose. Your odds of a great neurologically intact outcome aren’t great if you are doing another 10-15 minutes of CPR anyways. I didn’t know what to do once ROSC achieved and still on pressors hemodynanically unstable, but improving. Intensivist hem and hawed too about whether to give the second dose of 50 mg.

Iike @Rockinacoustic said, mainly from case reports, I will pull up out actual policy to see if there is any "real" reference.

I think the second dose comes down to "do nothing or let them die" and well, sometime doing nothing is the right call. Usually it is in those younger patients who we are hoping for a miracle in.

As far as if you get ROSC back, one of the cases that walked out fully recovered was actually sort of that situation. She was recovering from a femur fracture, and about to go to PT. Presented with SOB, we never actually confirmed a PE because she arrested before we got to the scanner. We decided to give TPA 50mg. One of those on again off again ROSC's finally got her to the scanner, confirmed PE. Short arrest again, but ROSC back quickly, so I suggested give the remainder over an hour. The question is, if she never re-arrested, what should have we done? Honestly it is a miracle she lived, she wasn't young (maybe in her 60's).

 

[RoyBasch]

pre-hospital arrest, prolonged arrest time and intubated in the ED, ROSC, ARDS probably from aspiration, aggressive vent tinkering for refractory hypoxemia, diagnosed prox LAD / LMCA occlusive MI based on EKG and echo, cards recommends "not a STEMI, let him cool off in ICU," decide not to do that, transfer to a real hospital, stented / balloon pump / CCU / stepdown / walks out of the hospital. saw a video of him with his kids a few months later. give me one of those a year and maybe i can keep doing this job.

This is an amazing save and I applaud you.

But when I hear this story all I can think of is the receiving hospital will write an EMTALA violation against you (transferring a patient who needs interventional cardiology, when you have interventional cardiology, so not a higher level of care and potentially a "dump.") Your hospital somehow makes this your "fault" because they want to shield a very valued and esteemed sub specialist who generates millions of dollars of pre-authorized elective procedure revenue a year from any complaints/liability/concern.

 

[bearstanley]

Good for you as that takes some cojones to go around your home hospital consultants.

1) Was this recently? There’s not a chance I could get anywhere near me to accept this patient for transfer currently.

2) in the spirit of the Emtala thread, does this risk a violation ? Obviously it was the right thing to do, just wondering since your place could do the needed procedure whether the accepting hospital could report that.

over a year ago. this was at a small hospital with nothing but a small ICU, called our 'affiliate' interventional cards located at a different hospital to say i think this is a type 1 event that needs angiography, and he said no STEMI = no cath, you can just admit to the ICU. IIRC we didn't even have an ICU bed (even if we did, most real ICU patients get shipped out overnight because there's no in-house intensivist), so i pitched it to the bigger academic hospital as a post-arrest ICU patient that should have a cath now. i spoke with their cards fellow prior to transfer, and when i woke up that afternoon he had texted me that it was a prox LAD.

 

[GonnaBeADoc2222]

pre-hospital arrest, prolonged arrest time and intubated in the ED, ROSC, ARDS probably from aspiration, aggressive vent tinkering for refractory hypoxemia, diagnosed prox LAD / LMCA occlusive MI based on EKG and echo, cards recommends "not a STEMI, let him cool off in ICU," decide not to do that, transfer to a real hospital, stented / balloon pump / CCU / stepdown / walks out of the hospital. saw a video of him with his kids a few months later. give me one of those a year and maybe i can keep doing this job.

I love this. You're a literal hero.

 

[bearstanley]

I love this. You're a literal hero.

nah man i'm a reasonable doctor functioning in a completely broken system, as all of us are.

 

[alpinism]

pre-hospital arrest, prolonged arrest time and intubated in the ED, ROSC, ARDS probably from aspiration, aggressive vent tinkering for refractory hypoxemia, diagnosed prox LAD / LMCA occlusive MI based on EKG and echo, cards recommends "not a STEMI, let him cool off in ICU," decide not to do that, transfer to a real hospital, stented / balloon pump / CCU / stepdown / walks out of the hospital. saw a video of him with his kids a few months later. give me one of those a year and maybe i can keep doing this job.

I wish I could do this since our cards almost never cath post arrest patients even for ACS with significant ECG changes.

The problem is that its almost impossible to get anyone transferred immediately and even if i get really lucky it often takes over twelve hrs for the next ambulance to come available. By then most of the patients have passed away and those who've been able to survive likely already have significant levels of irreversible cardiac damage. I've considered just aggressively pushing lytics to see if that can make a difference.

 

[cyanide12345678]

nah man i'm a reasonable doctor functioning in a completely broken system, as all of us are.

Yeah broken system indeed.

Called OMF surgery at outside hospital today for a transfer for a submandibular abscess that was encroaching into the muscles of mastication. Their transfer line called back and stated that the surgeon does not want to talk to me because ‘we’re too far away’. We were 1 hour away.

I literally called back to tell them that this is ridiculous since their hospital is actually the nearest facility with oral surgery coverage. Shut down by transfer line stating they can’t do anything if the surgeon said no.

Too far away??? I mean what kind of an excuse is that. It’s my problem sending the patient to them. Why do they care how far the patient is. Eventually had to send the patient even further away -_-

 

[SpacemanSpifff]

Great case recently that qualifies as one of the best saves I’ve had over the past 10 years.

Healthy 20s female who’s family called EMS for an episode of syncope. Complained of severe mid upper back pain and shortness of breath. Rapidly decompensated in route and arrived periarrest looking near death and gasping for breaths. Initial vitals were BP 60/40s Sats 40s despite max NRB. Textbook symptom presentation so threw an US probe on the chest for a quick exam. Massively dilated RV actively pushing into the LV causing outflow obstruction with little overall cardiac motion. Immediately cancelled the Intubation and fluids. Put her on high flow oxygen and hung a dirty epi drip both at max rates. Managed to stabilize a little with repeat BP 120/80s Sats 80s with improved work of breathing. Straight to CTA with massive bilateral PEs confirmed with radiology attending on call. Wheeled back right away then slammed in a RIJ central line. Placed the catheter tip deep into the heart to maximize the effect for a sort of bedside performed catheter directed thrombolytics. Gave full dose of TPA over the next 2 hours. Responded beautifully with rapid improvement in her vitals and CCM even asked if she needed an ICU bed after her infusion.

Hell yeah! Love this idea for a thread - helps to remember that what we do matters.

A couple years back had a 45yo guy brought in by bus after seizing in jail. Prehospital ECG was transmitted and had a wide complex tachycardia with a terminal r wave, suspicious for TCA toxicity. Arrested on arrival to the ED. Coded intermittently for 30 minutes, we emptied the code carts of bicarb, got a dirty double, hypertonic saline, cranked up the epi and threw some intralipid at him. Sent up to the ICU on rocket fuel - walked out neuro intact on hospital day 5. Turns out he had swallowed a bag of cocaine and suffered sodium channel blockade as a result. Despite his presentation, he turned out to be a pretty normal guy - has been following up regularly with his PCP for diabetes care since.

 

[RustedFox]

Hell yeah! Love this idea for a thread - helps to remember that what we do matters.

A couple years back had a 45yo guy brought in by bus after seizing in jail. Prehospital ECG was transmitted and had a wide complex tachycardia with a terminal r wave, suspicious for TCA toxicity. Arrested on arrival to the ED. Coded intermittently for 30 minutes, we emptied the code carts of bicarb, got a dirty double, hypertonic saline, cranked up the epi and threw some intralipid at him. Sent up to the ICU on rocket fuel - walked out neuro intact on hospital day 5. Turns out he had swallowed a bag of cocaine and suffered sodium channel blockade as a result. Despite his presentation, he turned out to be a pretty normal guy - has been following up regularly with his PCP for diabetes care since.

There's so much "TOP GUN" talk in this post that I have to ask what a "dirty double" and "rocket fuel" are.

Not that it's not awesome. I love it... I just want to understand it so I can love it more.

 

[bearstanley]

Yeah broken system indeed.

Called OMF surgery at outside hospital today for a transfer for a submandibular abscess that was encroaching into the muscles of mastication. Their transfer line called back and stated that the surgeon does not want to talk to me because ‘we’re too far away’. We were 1 hour away.

I literally called back to tell them that this is ridiculous since their hospital is actually the nearest facility with oral surgery coverage. Shut down by transfer line stating they can’t do anything if the surgeon said no.

Too far away??? I mean what kind of an excuse is that. It’s my problem sending the patient to them. Why do they care how far the patient is. Eventually had to send the patient even further away -_-

isn't this -literally- an emtala violation? "so you're saying you have the means and capability to care for this patient, and you're declining transfer?"

 

[Jabbed]

There's so much "TOP GUN" talk in this post that I have to ask what a "dirty double" and "rocket fuel" are.

Not that it's not awesome. I love it... I just want to understand it so I can love it more.

Dirty double: non-sterile femoral arterial lines and central lines, typically placed in peri-arrest or arrest conditions

Rocket fuel: epinephrine gtt; bonus points if you have someone make it at the bedside by adding 4 mg of epinephrine to 250 cc bag of NS

 

[cyanide12345678]

isn't this -literally- an emtala violation? "so you're saying you have the means and capability to care for this patient, and you're declining transfer?"

I don’t think emtala applies if you decline a transfer. Doesn’t it only apply if you send someone despite having ability to care for them?

I’ve just never heard someone say that we are declining the transfer and the surgeon doesn’t even want to talk to you because you are too far away -_-

 

[BoardingDoc]

I don’t think emtala applies if you decline a transfer. Doesn’t it only apply if you send someone despite having ability to care for them?

I’ve just never heard someone say that we are declining the transfer and the surgeon doesn’t even want to talk to you because you are too far away -_-

It is an EMTALA violation if the receiving facility declines a transfer for a reason other than a lack of capability to care for the patient.

Saying "the surgeon is refusing the transfer/refusing to talk to you" is absolutely an EMTALA violation.

Honestly, it's even crazier than that in that it's likely an EMTALA violation even if the hospital refuses because they're at capacity and boarding patients in the halls.

The statute and the regulations provide that any participating hospital which has "specialized capabilities or facilities" such as burn units, shock-trauma units, or neonatal intensive care units, or which is a "regional referral center" in a rural area, may not refuse to accept a patient in transfer, if it has the capacity to treat the individual. [42 USC 1395dd(g); 42 CFR 489.24(f)] The receiving hospital will be obligated to accept the transfer in most cases, so long as it has the ability to treat the patient and its capabilities exceed those of the referring hospital, even if only because of overcrowding or temporary unavailability of personnel.

Source: FAQ on EMTALA Item number 16.

 

[SpacemanSpifff]

There's so much "TOP GUN" talk in this post that I have to ask what a "dirty double" and "rocket fuel" are.

Not that it's not awesome. I love it... I just want to understand it so I can love it more.

See @bearstanley above. Rocket fuel, colloquially, is any combination of high dose vasoactives - a pressor cocktail so stiff it could get you to the moon.

 

[gamerEMdoc]

One of my best saves:

Chronic HA patient, on home narcs. Hospital worker. Sent to the ED for suspicion of being intoxicated, by policy had to obtain UDS/ETOH. She said she was just super run down and tired, wasn't sleeping much with her HAs, that's why she was falling asleep at work but she was clearly somnolent and altered. I did labs too, and she had a mild transaminitis (like AST/ALT 100). Did a depakote level (she was on this for chronic migraines) which was therapeutic. On a hunch with the transaminitis, I added an ammonia and it was ridiculously high. Started her on L-carnitine for depakote induced hyperammonemic encephalopathy and 2 days later she was completely normal and discharged. She told me when back at work a few days later she didn't even remember seeing me in the ED.

 

[BoardingDoc]

One of my best saves:

Chronic HA patient, on home narcs. Hospital worker. Sent to the ED for suspicion of being intoxicated, by policy had to obtain UDS/ETOH. She said she was just super run down and tired, wasn't sleeping much with her HAs, that's why she was falling asleep at work but she was clearly somnolent and altered. I did labs too, and she had a mild transaminitis (like AST/ALT 100). Did a depakote level (she was on this for chronic migraines) which was therapeutic. On a hunch with the transaminitis, I added an ammonia and it was ridiculously high. Started her on L-carnitine for depakote induced hyperammonemic encephalopathy and 2 days later she was completely normal and discharged. She told me when back at work a few days later she didn't even remember seeing me in the ED.

This is fantastic. I'd literally never heard of this. I'm now slightly less dumb. Thanks for that.

 

[gamerEMdoc]

This is fantastic. I'd literally never heard of this. I'm now slightly less dumb. Thanks for that.

I knew it happened with depakote toxicity, but it can happen with a normal depakote level too; the crazy part was the only reason I knew that was it was on EMRAP like a month or two before I saw this case. It causes cerebral edema I think and is often fatal if unrecognized.

 

[thegenius]

One of my best saves:

Chronic HA patient, on home narcs. Hospital worker. Sent to the ED for suspicion of being intoxicated, by policy had to obtain UDS/ETOH. She said she was just super run down and tired, wasn't sleeping much with her HAs, that's why she was falling asleep at work but she was clearly somnolent and altered. I did labs too, and she had a mild transaminitis (like AST/ALT 100). Did a depakote level (she was on this for chronic migraines) which was therapeutic. On a hunch with the transaminitis, I added an ammonia and it was ridiculously high. Started her on L-carnitine for depakote induced hyperammonemic encephalopathy and 2 days later she was completely normal and discharged. She told me when back at work a few days later she didn't even remember seeing me in the ED.

That is f’ing dope I never would have thought of that ever. Well done

 

[Mount Asclepius]

I was once taught that seizures and Depakote can both falsely elevate ammonia levels with the severity of the level not correlating to hepatic dysfunction or encephalopathy. Is that not the case? Might need to take my own deep dive into.

 

[chillaxbro]

Great case recently that qualifies as one of the best saves I’ve had over the past 10 years.

Healthy 20s female who’s family called EMS for an episode of syncope. Complained of severe mid upper back pain and shortness of breath. Rapidly decompensated in route and arrived periarrest looking near death and gasping for breaths. Initial vitals were BP 60/40s Sats 40s despite max NRB. Textbook symptom presentation so threw an US probe on the chest for a quick exam. Massively dilated RV actively pushing into the LV causing outflow obstruction with little overall cardiac motion. Immediately cancelled the Intubation and fluids. Put her on high flow oxygen and hung a dirty epi drip both at max rates. Managed to stabilize a little with repeat BP 120/80s Sats 80s with improved work of breathing. Straight to CTA with massive bilateral PEs confirmed with radiology attending on call. Wheeled back right away then slammed in a RIJ central line. Placed the catheter tip deep into the heart to maximize the effect for a sort of bedside performed catheter directed thrombolytics. Gave full dose of TPA over the next 2 hours. Responded beautifully with rapid improvement in her vitals and CCM even asked if she needed an ICU bed after her infusion.

Just so I can learn…

cancelled intubation and fluids because death spiral in severe pulm htn / RV failure correct?

Would you push Tpa without the CTA, eg if she wasn’t stable enough to go to ct

 

[Jabbed]

Just so I can learn…

cancelled intubation and fluids because death spiral in severe pulm htn / RV failure correct?

Would you push Tpa without the CTA, eg if she wasn’t stable enough to go to ct

1. Yes. They are very preload dependent and do not tolerate positive pressure ventilation
2. Sensitivity of focused cardiac US increases significantly based on the acuity of the patient. A cool shocky patient with normal RV almost certainly does not have a PE. A large RV in a young person that is this ill is almost certainly a PE. A normal/large RV in a patient that is hemodynamically stable is a data point, but certainly not definitive or actionable. If you’re truly incorporating bedside US into your clinical practice you need to force yourself to act on the results— otherwise you’re just looking at stuff.

 

[The Knife & Gun Club]

Just so I can learn…

cancelled intubation and fluids because death spiral in severe pulm htn / RV failure correct?

Would you push Tpa without the CTA, eg if she wasn’t stable enough to go to ct

Yea the fluids augment preload and the oxygen decreases RV afterload because it acts as a pulmonary arterial vasodilator at high doses, so will help more blood flow through the non-clotted bits of the vasculature.

The hypotension comes from the Bowing of the septum causing a functional LV outflow tract obstruction so the epi increases systemic afterload and can help “prop open” the LV outflow tract too.

 

[Radetzky]

I hate to be a stickler but since we’re talking about it, some of the physiology posted above is not correct. The shock is not due to outflow tract obstruction, it is due to decreased diastolic filling of the LV due to the RV pushing the septum over and due to reduced RV output itself.

And the acutely dilated RV being preload dependent is a long standing myth which has been inaccurately applied from studies of RV infarction of dogs. While small boluses of fluid can help, the acutely dilated RV is actually preload intolerant and too much fluid pushes the septum over further causing even more reduced filling.

 

[SpacemanSpifff]

I hate to be a stickler but since we’re talking about it, some of the physiology posted above is not correct. The shock is not due to outflow tract obstruction, it is due to decreased diastolic filling of the LV due to the RV pushing the septum over and due to reduced RV output itself.

And the acutely dilated RV being preload dependent is a long standing myth which has been inaccurately applied from studies of RV infarction of dogs. While small boluses of fluid can help, the acutely dilated RV is actually preload intolerant and too much fluid pushes the septum over further causing even more reduced filling.

RV physiology is super interesting, and compared to LV physiology, poorly understood. Here's an excellent review for those looking to get into the weeds. In acute PE, afterload is the primary issue, and the utility of preload augmentation will depend on the patient. 500mL to a liter may give you some buydown on your pressor or get you to a place where you feel ok going to CT, but in general I agree with @Radetzky that it's not the ultimate solution. In those who have progressed to frank RV failure leading to elevated CVP and venous congestion, fluid will be harmful. The patient @alpinism describes fits this phenotype.

As the patient progresses the elevated afterload will lead to a drop in RV output, increasing the end systolic and subsequently diastolic RV volume, leading to acute RV dilation. Due to pericardial constraint this conformation change leads to interventricular septal bowing, initially in diastole, reducing LV filling. Simultaneously, right coronary flow (which occurs in both systole and diastole in the normal RV due to low ventricular pressures) is reduced as the ventricular pressure rises, propagating ischemia, and further decreasing contractility - the so called "RV death spiral".

Yea the fluids augment preload and the oxygen decreases RV afterload because it acts as a pulmonary arterial vasodilator at high doses, so will help more blood flow through the non-clotted bits of the vasculature.

The hypotension comes from the Bowing of the septum causing a functional LV outflow tract obstruction so the epi increases systemic afterload and can help “prop open” the LV outflow tract too.

I have not seen or read about LV outflow tract obstruction as a consequence of RV pathology, but I suppose it could happen. The traditional management of LVOTO is fluid loading, avoidance of inotropes/chronotropes, and addition of pure vasoconstrictors (phenylephrine, vasopressin), to reduce the intracavitary gradient and promote LV ejection. Pieces of that management can be harmful to a dying RV. If you suspected the RV was the cause of LVOTO, it makes sense to treat the RV first.

1. Yes. They are very preload dependent and do not tolerate positive pressure ventilation
2. Sensitivity of focused cardiac US increases significantly based on the acuity of the patient. A cool shocky patient with normal RV almost certainly does not have a PE. A large RV in a young person that is this ill is almost certainly a PE. A normal/large RV in a patient that is hemodynamically stable is a data point, but certainly not definitive or actionable. If you’re truly incorporating bedside US into your clinical practice you need to force yourself to act on the results— otherwise you’re just looking at stuff.

Completely agree that clinical context is paramount when interpreting RV findings on TTE. RV size, TAPSE, and fractional area change are all only pieces of the puzzle and should never be used in isolation. The RV can look small on a parasternal, but generous on an AP4. TAPSE is highly angle dependent. FAC has a lot of interoperator variability. The NPV and PPV for TTE in PE are not good enough for it to be used as a diagnostic tool, but it should be incorporated in patients with known to further risk stratify.

 

[WilcoWorld]

One of my best saves:

Chronic HA patient, on home narcs. Hospital worker. Sent to the ED for suspicion of being intoxicated, by policy had to obtain UDS/ETOH. She said she was just super run down and tired, wasn't sleeping much with her HAs, that's why she was falling asleep at work but she was clearly somnolent and altered. I did labs too, and she had a mild transaminitis (like AST/ALT 100). Did a depakote level (she was on this for chronic migraines) which was therapeutic. On a hunch with the transaminitis, I added an ammonia and it was ridiculously high. Started her on L-carnitine for depakote induced hyperammonemic encephalopathy and 2 days later she was completely normal and discharged. She told me when back at work a few days later she didn't even remember seeing me in the ED.

Great case - I think the big teaching point is that depakote/valproic acid toxicity diagnosis is confirmed with elevated ammonia, not the valproic acid level.

And the fact that you prevented someone from getting wrongfully terminated! Excellent.

 

[NYEMMED]

Thank you for this thread. As I walk out of the worst shift I’ve worked, it gives me hope that I made a difference for somebody

 

[thegenius]

I hate to be a stickler but since we’re talking about it, some of the physiology posted above is not correct. The shock is not due to outflow tract obstruction, it is due to decreased diastolic filling of the LV due to the RV pushing the septum over and due to reduced RV output itself.

And the acutely dilated RV being preload dependent is a long standing myth which has been inaccurately applied from studies of RV infarction of dogs. While small boluses of fluid can help, the acutely dilated RV is actually preload intolerant and too much fluid pushes the septum over further causing even more reduced filling.

both points are what I learned as well. these pt's need inotropy and maybe chronotropy, more than IV fluids. maybe 1L max but after that they need increased squeeze and BP augmentation

 

[thegenius]

Dirty double: non-sterile femoral arterial lines and central lines, typically placed in peri-arrest or arrest conditions

Rocket fuel: epinephrine gtt; bonus points if you have someone make it at the bedside by adding 4 mg of epinephrine to 250 cc bag of NS

is the quick and dirty epi drip just 1mg in 1000 ml NS 0.9%, hook it up and let it flow wide open? That's what I recall

 

[Jabbed]

is the quick and dirty epi drip just 1mg in 1000 ml NS 0.9%, hook it up and let it flow wide open? That's what I recall

Yes. If you don’t have a pump available you can do this.

 

[TooMuchResearch]

This thread excites me and makes me dread, if only slightly less, my next shift. Thanks.

I don't recall any good saves lately, other than letting a few gomers die per their wishes.

 

[alpinism]

Just so I can learn…

cancelled intubation and fluids because death spiral in severe pulm htn / RV failure correct?

Would you push Tpa without the CTA, eg if she wasn’t stable enough to go to ct

Yeah so generally speaking the goal is to minimize anything that increases pulmonary vasculature pressures to prevent the death spiral.

Believe it or not some researchers have also started to recommend the use of both nitrates and diuretics in crashing patients.

 

[alpinism]

Just so I can learn…

cancelled intubation and fluids because death spiral in severe pulm htn / RV failure correct?

Would you push Tpa without the CTA, eg if she wasn’t stable enough to go to ct

Regarding the question of when to order TPA its definitely a tough call.

I think concerning history + sonography findings = push lytics.

 

[Jabbed]

I hate to be a stickler but since we’re talking about it, some of the physiology posted above is not correct. The shock is not due to outflow tract obstruction, it is due to decreased diastolic filling of the LV due to the RV pushing the septum over and due to reduced RV output itself.

And the acutely dilated RV being preload dependent is a long standing myth which has been inaccurately applied from studies of RV infarction of dogs. While small boluses of fluid can help, the acutely dilated RV is actually preload intolerant and too much fluid pushes the septum over further causing even more reduced filling.

My mistake, you’re correct about them being preload intolerant. CVP has been shown to directly correlated with mortality in submassive PE patients.