Someone please post an academic topic.

[thegenius]

yea yea

Wait even then I have my units wrong.

I mean 100 mcg / min is the max I've ever done...and I usually start around 50 mcg / min.

I've seen too much hypotension with nitro

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[WilcoWorld]

There was a study recently on high dose nitro in CHF

High-Dose Nitroglycerin Bolus for Sympathetic Crashing Acute Pulmonary Edema: A Prospective Observational Pilot Study - PubMed

Use of our specific SCAPE treatment algorithm, which included high-dose NTG and NIV, was safe and provided rapid resolution of symptoms.

pubmed.ncbi.nlm.nih.gov

But in my opinion is kind of silly. Put them on PPV with typical high dose nitro dosing and appropriate after load reduction (in my mind 200-400 mcg/min infusion. Super high dose nitro is a treatment for a problem we don’t actually have. These patients typically improve very quickly with SOC.

And in that study "The mean bolus dose of NTG given was 872 μg"

20mg must be a typo.

 

[Dred Pirate]

Wait even then I have my units wrong.

I mean 100 mcg / min is the max I've ever done...and I usually start around 50 mcg / min.

I've seen too much hypotension with nitro

a couple of times I have seen 200-300 mcg/min x 2 minutes - then drop down to 50 or lower. But I always stand by the pump and time it, and make the adjustment myself, I have seen a rn not understand the issue that can come up if they don't decrease the rate promptly.

 

[alpinism]

20mg of nitro?!?! Is that a typo?

I love high dose NTG for sick heart failure patients, but 20,000mcg makes even me do a double take.

Yep I've given 20,000 mcg multiple times for patients with extremely high SBPs in SCAPE.

Now to be clear its not in one dose but I'll stand at bedside and push 2,000 mcg every 2 mins.

I trained at DRH with hundreds of these patients and it was standard practice among the attendings.

Funny enough they actually just put out a case report where they gave 60,000 mcg to a patient.

Link:(PDF) Ultra-high dose intravenous nitroglycerin in an ESRD patient with acutely decompensated heart failure

 

[aafisahar]

Yep I've given 20,000 mcg multiple times for patients with extremely high SBPs in SCAPE.

Now to be clear its not in one dose but I'll stand at bedside and push 2,000 mcg every 2 mins.

I trained at DRH with hundreds of these patients and it was standard practice among the attendings.

Funny enough they actually just put out a case report where they gave 60,000 mcg to a patient.

Link:(PDF) Ultra-high dose intravenous nitroglycerin in an ESRD patient with acutely decompensated heart failure

this is key in bad CHF, not just SCAPE, but even with preserved and reduced EF. Gotta stop flooding the engine before someone feels better, either intake or outtake (eg preload or afterload). I love nitroprusside for this reason (potent afterload), but it takes 45 minutes before pharmacy will mix it up and bring it and it's like 1k/bottle.

 

[bravotwozero]

Ok I'll bite.

This has been the bane of my existence the past few shifts: Isolated or "reactive leukocytosis"

How high can a reactive leukocytosis be?

See this all the time in cocaine/meth users, psychotic patients, post seizure/pseudo seizure patients.

But sometimes it's like 23k.

I hate chasing isolated white counts. If vitals, lactic, ua, CXR are all normal, would you guys be comfortable calling a 20k white count 'reactive' in the above scenarios?

 

[WilcoWorld]

Ok I'll bite.

This has been the bane of my existence the past few shifts: Isolated or "reactive leukocytosis"

How high can a reactive leukocytosis be?

See this all the time in cocaine/meth users, psychotic patients, post seizure/pseudo seizure patients.

But sometimes it's like 23k.

I hate chasing isolated white counts. If vitals, lactic, ua, CXR are all normal, would you guys be comfortable calling a 20k white count 'reactive' in the above scenarios?

Based on zero literature, my cut off is in the neighborhood of 20k, adjusted to the clinical context.

 

[aafisahar]

Ok I'll bite.

This has been the bane of my existence the past few shifts: Isolated or "reactive leukocytosis"

How high can a reactive leukocytosis be?

See this all the time in cocaine/meth users, psychotic patients, post seizure/pseudo seizure patients.

But sometimes it's like 23k.

I hate chasing isolated white counts. If vitals, lactic, ua, CXR are all normal, would you guys be comfortable calling a 20k white count 'reactive' in the above scenarios?

I just had a case of a patient having a white count of 50k that got a bm biopsy and it was all reactive leukocytosis. She presented with only renal failure with nsaid abuse, no infectious source identified despite pan scan and LP.

 

[Zebra Hunter]

I know this is blasphemous for an EM doc to say, but I’m actually pretty skeptical of high dose nitro having much of an effect for acute, cardiogenic pulmonary edema. I, too, have not intubated a SCAPE or decompensated heart failure patient in years, but I think it has very little to do with nitro and everything to do with NIPPV. I’ve lost count of the number of times I asked the nurse to bolus the patient 500mcg of nitro and start them at a rate of 100mcg/min and titrate down afterward, only to find the nurse never bolused the patient and started them at 5mcg/min (because that’s what the instructions on the bottle say) only to find the patient already looks significantly better just on BPAP and BP has already improved dramatically likely due to the patient feeling like they can breath again leading to a reduction in their sympathetic surge.

I have no evidence to back up my skepticism, but there is also no high quality data to back up the use of high dose nitro either. I still give it, but it’s just never as important to me as getting the patient on NIPPV. Honestly, I think it would be an interesting study to randomize SCAPE patients to standard cardene dosing vs high dose nitro therapy. I think the only problem with this study would be that you couldn’t blind the physicians to the therapies.

 

[thegenius]

Ok I'll bite.

This has been the bane of my existence the past few shifts: Isolated or "reactive leukocytosis"

How high can a reactive leukocytosis be?

See this all the time in cocaine/meth users, psychotic patients, post seizure/pseudo seizure patients.

But sometimes it's like 23k.

I hate chasing isolated white counts. If vitals, lactic, ua, CXR are all normal, would you guys be comfortable calling a 20k white count 'reactive' in the above scenarios?

It can be quite high, reactive leukocytosis. WBCs demarginate all the time for non sepsis/infectious reasons

 

[thegenius]

Ok I'll bite.

This has been the bane of my existence the past few shifts: Isolated or "reactive leukocytosis"

How high can a reactive leukocytosis be?

See this all the time in cocaine/meth users, psychotic patients, post seizure/pseudo seizure patients.

But sometimes it's like 23k.

I hate chasing isolated white counts. If vitals, lactic, ua, CXR are all normal, would you guys be comfortable calling a 20k white count 'reactive' in the above scenarios?

Most leukocytosis we see are reactive, as opposed to a leukemia for instance.

 

[lymphocyte]

I know this is blasphemous for an EM doc to say, but I’m actually pretty skeptical of high dose nitro having much of an effect for acute, cardiogenic pulmonary edema. I, too, have not intubated a SCAPE or decompensated heart failure patient in years, but I think it has very little to do with nitro and everything to do with NIPPV. I’ve lost count of the number of times I asked the nurse to bolus the patient 500mcg of nitro and start them at a rate of 100mcg/min and titrate down afterward, only to find the nurse never bolused the patient and started them at 5mcg/min (because that’s what the instructions on the bottle say) only to find the patient already looks significantly better just on BPAP and BP has already improved dramatically likely due to the patient feeling like they can breath again leading to a reduction in their sympathetic surge.

I have no evidence to back up my skepticism, but there is also no high quality data to back up the use of high dose nitro either. I still give it, but it’s just never as important to me as getting the patient on NIPPV. Honestly, I think it would be an interesting study to randomize SCAPE patients to standard cardene dosing vs high dose nitro therapy. I think the only problem with this study would be that you couldn’t blind the physicians to the therapies.

Very interesting topic! I've just done a deep dive on this.

There are multiple lines of evidence to support vasodilator therapy in acute decompensated heart failure, going back thirty years before NIV was commonly used or available. In fact, there was one prospective trial that compared NIV with vasodilator therapy directly and purported a benefit in favour of vasodilator therapy. Vasodilators even work wonders in frank cardiogenic shock. It's always fun to watch the nurses eyes when the MAP goes UP after starting sodium nitroprusside.

In other words, the evidence definitely supports the view that GTN works, even in the absence of NIV.

(Sorry for the copious references but I believe they are all the studies related to this question in particular. And it's meant in the academic spirit of the thread.)

Mullens Wilfried, Abrahams Zuheir, Francis Gary S., et al. Sodium nitroprusside for advanced low-output heart failure. Journal of the American College of Cardiology. 2008;52(3):200-207.

Nashed AH, Allegra JR. Intravenous nitroglycerin boluses in treating patients with cardiogenic pulmonary edema. Am J Emerg Med 1995;13(5):612–3 Sep.

Nashed A, Allegra JR, Eskin B, Garg S, Roche LM. Prospective trial of the treatment of acute cardiogenic pulmonary edema with intravenous nitroglycerine boluses. Ann Emerg Med 1997 Sep;30(3):382.

Cotter G, Metzkor E, Kaluski E, Faigenberg Z, Miller R, Simovitz A, et al. Randomised trial of high-dose isosorbide dinitrate plus low-dose furosemide versus high-dose furosemide plus low-dose isosorbide dinitrate in severe pulmonary oedema. Lancet 1998;351(9100):389–93 Feb 7.

Sharon A, Shpirer I, Kaluski E, Moshkovitz Y, Milovanov O, Polak R, et al. High-dose intravenous isosorbide-dinitrate is safer and better than Bi-PAP ventilation combined with conventional treatment for severe pulmonary edema. J Am Coll Cardiol 2000;36(3):832–7 Sep.

 

[Zebra Hunter]

Very interesting topic! I've just done a deep dive on this.

There are multiple lines of evidence to support vasodilator therapy in acute decompensated heart failure, going back thirty years before NIV was commonly used or available. In fact, there was one prospective trial that compared NIV with vasodilator therapy directly and purported a benefit in favour of vasodilator therapy. Vasodilators even work wonders in frank cardiogenic shock. It's always fun to watch the nurses eyes when the MAP goes UP after starting sodium nitroprusside.

In other words, the evidence definitely supports the view that GTN works, even in absence of NIV.

(Sorry for the copious references but I believe they are all the studies related to this question in particular. And it's meant in the academic spirit of the thread.)

Mullens Wilfried, Abrahams Zuheir, Francis Gary S., et al. Sodium nitroprusside for advanced low-output heart failure. Journal of the American College of Cardiology. 2008;52(3):200-207.

Nashed AH, Allegra JR. Intravenous nitroglycerin boluses in treating patients with cardiogenic pulmonary edema. Am J Emerg Med 1995;13(5):612–3 Sep.

Nashed A, Allegra JR, Eskin B, Garg S, Roche LM. Prospective trial of the treatment of
acute cardiogenic pulmonary edema with intravenous nitroglycerine boluses. Ann
Emerg Med 1997 Sep;30(3):382.

Cotter G, Metzkor E, Kaluski E, Faigenberg Z, Miller R, Simovitz A, et al. Randomised
trial of high-dose isosorbide dinitrate plus low-dose furosemide versus high-dose
furosemide plus low-dose isosorbide dinitrate in severe pulmonary oedema. Lancet
1998;351(9100):389–93 Feb 7.

Sharon A, Shpirer I, Kaluski E, Moshkovitz Y, Milovanov O, Polak R, et al. High-dose
intravenous isosorbide-dinitrate is safer and better than Bi-PAP ventilation com-
bined with conventional treatment for severe pulmonary edema. J Am Coll Cardiol
2000;36(3):832–7 Sep.

Yeah, I’ve read BiPap vs ISDN study before, but found it questionable that 80% of the BPAP group required mechanical ventilation which is just not consistent with anything I have seen in practice.

Appreciate the other references, but nothing I would consider high quality data. Literature review during COVID has taught me that small unblinded RCTs are difficult to take seriously.

Ultimately the physiology makes sense why nitro should work, and I certainly will keep giving it, but the annoying little voice in my head that questions everything we do in medicine without great evidence (which is most of medicine) always speaks up as I’m hitting another SCAPEr with 500mcg of NTG while they are already looking more comfortable simply on NIPPV.

 

[Apollyon]

Most leukocytosis we see are reactive, as opposed to a leukemia for instance.

WBC 30-50k is a "leukemoid reaction". Greater than 50k is leukemia until proven otherwise.

 

[WilcoWorld]

Most leukocytosis we see are reactive, as opposed to a leukemia for instance.

WBC 30-50k is a "leukemoid reaction". Greater than 50k is leukemia until proven otherwise.

Fair points. I think what @bravotwozero meant to be getting at was "what's the highest WBC you're comfortable not chasing as a sign of hidden badness"?

 

[gutonc]

Fair points. I think what @bravotwozero meant to be getting at was "what's the highest WBC you're comfortable not chasing as a sign of hidden badness"?

When you guys call me about these cases in otherwise healthy and well appearing people (no cytopenias, nml renal fn, lytes, LFTs and uric acid) and you're not suspicious about an underlying or intercurrent infection, I usually ask for peripheral flow cytometry and I'll see them in 1-2 days (that test usually turns around in 24-36h where I am).

An adult with an acute leukemia and a WBC that high is not going to meet any of those other criteria, so they're getting admitted or transferred for workup and management. Most of the ones I see like that have CLL or CML and don't need to be hospitalized for workup or treatment unless there's other badness going on.

 

[thegenius]

Fair points. I think what @bravotwozero meant to be getting at was "what's the highest WBC you're comfortable not chasing as a sign of hidden badness"?

All depends. There is no straight forward answer to this.

I have sent home young people who come in with some odd complaint and their entire workup is negative except a WBC of 20K or 22K. I talk to them and say their WBC is very high and I could do $1M of tests and CT scans...or you can just get this rechecked in a few days either here in the ED or with your PCP.

Maybe i've gotten wiser (or perhaps more stupid) over time, but I really think that often times patients just need to wait a few days for something to declare itself.

Note that I'm much more hesitant to do this with 60+ year old people.

 

[WilcoWorld]

Maybe i've gotten wiser (or perhaps more stupid) over time, but I really think that often times patients just need to wait a few days for something to declare itself.

Note that I'm much more hesitant to do this with 60+ year old people.

Exactly, "it depends".

I think a sign of a mature EP is the ability to tell which patients are safe to wait for a disease to declare itself, and to communicate that in an effective way to a patient. Much more helpful (for the patient) than knowing all the literature or ordering all the tests.

 

[Apollyon]

Exactly, "it depends".

I think a sign of a mature EP is the ability to tell which patients are safe to wait for a disease to declare itself, and to communicate that in an effective way to a patient. Much more helpful (for the patient) than knowing all the literature or ordering all the tests.

I've said it innumerable times - "Good discharge instructions are better than an accurate diagnosis".

 

[Beeftenderloin]

Ok I'll bite.

This has been the bane of my existence the past few shifts: Isolated or "reactive leukocytosis"

How high can a reactive leukocytosis be?

See this all the time in cocaine/meth users, psychotic patients, post seizure/pseudo seizure patients.

But sometimes it's like 23k.

I hate chasing isolated white counts. If vitals, lactic, ua, CXR are all normal, would you guys be comfortable calling a 20k white count 'reactive' in the above scenarios?

A close family member of mine was getting progesterone injections for IVF. A couple days after initiation she started getting extreme fatigue, night sweats and fevers to 101. No injection site erythema or fluctuance. Complained of some frequency/urgency so recommended go to UC to rule out UTI. UA negative but WBC 24K Plt 600. PCP concerned/confused. I’m convinced it’s the meds at this point, reproductive endocrinologist adamantly refuses this as a possibility. Recheck in a week, WBC 29k Plt 700.

::confused PCP noises::

Turfed to heme onc. Heme onc checks again 27k, 650. Explain situation, most notably, it all started when she started the injections. Checks again, still up. He says just re-check a week after stopping the med.

So after 3 months of being on that medication and 3 months of WBC in the high 20s and Plt over 600 and the reproductive endocrinologist saying there’s no way it was the med, she stops the med and everything goes back to normal.