Advertisement - Members don't see this ad
The best we could. We were working around the Lucas device and would wait for pulse checks to do the gross motor skill parts of it
This place is getting boring, post something good.
Started by RustedFox
Get help with your application
Use all the free resources available to you from SDN: articles, guides, expert advising, forums discussions, and school research.
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)
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)
Advertisement - Members don't see this ad
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.
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.
Last edited:
???? This seems like the opposite of what you should be doing.
Yeah preferred would be LR or D5w-bicarbonate fluid for initial fluid resuscitation
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
Last edited:
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.
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.
Evidence from anesthesia literature suggests the acidosis from NS outweighs the effect of the K in the LR.
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.
1.) Agree.
2.) But as we learned from my lawsuit, anything the muggles can't understand is immediately "wrong".
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.
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.
Advertisement - Members don't see this ad
About half my ICU residents argue with me about this 🙄 i tell them to go read about lol
Yet another Kobayashi maru.
Agreed, nephrologists get this wrong all the time. Same as Zosyn causing AKI, contrast, etc.
I really, really, really want a firm guideline on contrast and AKI to shut them up.
Maybe it I say it out loud three times....
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.
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…
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"
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.
Last edited:
Oh god, don’t get me started on nephrologists and LR….
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.
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.
Correct me; but I seem to remember that you're either CC or rads.
If I'm wrong, I'm wrong. No shade. I just seem to remember your avatar in this context.
You care to share that dotphrase?
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.
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.
Advertisement - Members don't see this ad
Wook is into puns today
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
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).
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).
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.
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.
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!
WIN.
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...
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...
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.
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.
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
Good work. Airway team is very much unneeded, particularly in an ICU.
Please tell me you nonchalantly replied "I am the airway team..." or "your secret airway team" or something like that...
Advertisement - Members don't see this ad
Academically more interesting…
60yo M presents to ED as pedestrian hit by car. AO3/GCS15 on arrival but w/ BP 85/50, palpably widened pubic symphesis on survey. No other injuries. 2 units blood in the bay. BP doesn’t budge but he’s mentating fine and fast is negative. Place pelvic binder. Trauma scan with an open book pelvis and hematoma but nothing crazy.
Booked for the OR with ortho, ED/Trauma teams call me down to admit the guy to the unit post-op. He says he has a “problem with his heart and high pressure.”
Anesthesia goes to intubate the dude and he drops like a f*ing stone. Pressures in the 60/20 range. Ortho aborts the case and throws on an ex fix, he comes up to the unit with a BP of 50/— in RVR and having runs of pulseless vtach. ABG with a pH of 7.1, K 6.9, lactic 7. POCUS with RV completely blown out, LVEF looks fine. Bolus amio, then start epi—>norepi—>vaso and max then all. Push 3 amps of bicarb, calcium, mag and BP creeps up to 70/40. Dude starts hemorrhaging from his ex-fix site so call for blood, took quick clot and shoved in down holes for the ex-fix rods and pack it tight against the bone. Repeat fast negative. Optimize the vent with low tidal volumes and peep to try to unload the strain off the right heart. Maybe a PE?
Every time the vent delivers a breath his a-line flatlines.
Probably time to stop screwing around and call the adults, so call in my attending from home, and he suggests calling the CVICU in too. Luckily today the Trauma ICU attending is EM+surgical critical care and the CVICU attending is EM+medicine critical care. The cavalry arrives.
CV guy drops a TEE probe in while I float a swan with the trauma attending. PA pressures are 70/40. On TEE we can see he’s got a flail mitral valve. Hook up nitric to the vent to drop the PA pressure. Add on milrinone, dig load, 8 of bumex + 120 of lasix + drip, start to peel back the NE and the dude starts to turn pink again (from a robust shade of purple).
Lactic starts to come down and urine starts to flow in the foley. By morning the labs normalized and he’s being prepped for OR for a new mitral valve.
Personally convinced if it wasn’t for it being all EM people doing the resus the dude would have been dead as a rock.
60yo M presents to ED as pedestrian hit by car. AO3/GCS15 on arrival but w/ BP 85/50, palpably widened pubic symphesis on survey. No other injuries. 2 units blood in the bay. BP doesn’t budge but he’s mentating fine and fast is negative. Place pelvic binder. Trauma scan with an open book pelvis and hematoma but nothing crazy.
Booked for the OR with ortho, ED/Trauma teams call me down to admit the guy to the unit post-op. He says he has a “problem with his heart and high pressure.”
Anesthesia goes to intubate the dude and he drops like a f*ing stone. Pressures in the 60/20 range. Ortho aborts the case and throws on an ex fix, he comes up to the unit with a BP of 50/— in RVR and having runs of pulseless vtach. ABG with a pH of 7.1, K 6.9, lactic 7. POCUS with RV completely blown out, LVEF looks fine. Bolus amio, then start epi—>norepi—>vaso and max then all. Push 3 amps of bicarb, calcium, mag and BP creeps up to 70/40. Dude starts hemorrhaging from his ex-fix site so call for blood, took quick clot and shoved in down holes for the ex-fix rods and pack it tight against the bone. Repeat fast negative. Optimize the vent with low tidal volumes and peep to try to unload the strain off the right heart. Maybe a PE?
Every time the vent delivers a breath his a-line flatlines.
Probably time to stop screwing around and call the adults, so call in my attending from home, and he suggests calling the CVICU in too. Luckily today the Trauma ICU attending is EM+surgical critical care and the CVICU attending is EM+medicine critical care. The cavalry arrives.
CV guy drops a TEE probe in while I float a swan with the trauma attending. PA pressures are 70/40. On TEE we can see he’s got a flail mitral valve. Hook up nitric to the vent to drop the PA pressure. Add on milrinone, dig load, 8 of bumex + 120 of lasix + drip, start to peel back the NE and the dude starts to turn pink again (from a robust shade of purple).
Lactic starts to come down and urine starts to flow in the foley. By morning the labs normalized and he’s being prepped for OR for a new mitral valve.
Personally convinced if it wasn’t for it being all EM people doing the resus the dude would have been dead as a rock.
I AM THE LAW!
Jeezus. I thought I had put in some complex work. Holy hell, you rocked that one!
Very few things infuriate me more than a non-physician trying to dictate what is within a physician's scope of practice.
When pts would say, "what are they going to do?", I would say, "I am 'they'."
