Intraoperative use of IV digoxin

[Burned_Out]

Anyone have any experience using perioperative IV digoxin to treat suspected hypotension from heart failure?

Here is a clinical scenario I encountered recently. 78 y.o. male with upper GI bleed. He had a STEMI 10 days ago and was stented. Due to the anti-platelet medication he was put on, he bled. He is brought to the OR for an EGD. His BP is in the 70's systolic, HR is sinus tachycardia, Hct. is 29%. Mental status is confused and he ripped out his PICC line in the ER. No central access is available. On physical exam, I hear crackles all across both lung fields. He had received a unit of blood and 2L of NS in the ER, but it did not help his BP.

I did my "Ketofol" technique using only ketamine and dexemetomidine. He survives and the GI team loves me. He is still hovering with systolic BP in the 70's post-op and we send him to the ICU for more intensive mgmt.

Since I didn't have central access, I didn't start a vasopressor on him. I would have considered milrinone in this guy. I kept his BP respectable by phenylephrine boluses but this had a waning effect throughout the case.

Given I suspected he was in heart failure, I wonder if digoxin IV bolus in 50-100 mCg doses would have made a positive difference in this guy.

My only experience with IV digoxin was years ago when the CT surgeon asked me to give it to a CABG patient trying to come off bypass.

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[vector2]

I think first things first is making sure cardiogenic shock is the cause of hypotension. Simple things are simple. In a bleeding patient, hypovolemia from blood loss is diagnosis one, two, and three. I know he received 1u in the ED, but if he is profoundly anemic still then crystalloid will not increase his MAP. It redistributes (to places like wet lungs), and even if it didn't, it doesn't help to add viscosity (and thus resistance) to thin blood.

Wrt the diagnosis of decompensated CHF, what was the patient's echo at discharge for his STEMI? Did he have any echo or POCUS on admission for his GI bleed? What was the BNP and troponin? The rest of the labs? Beyond your physical exam, how did the CXR look? Maybe he needs blood and lasix, not more volume?

But let's say it was decompensated systolic heart failure. I would not go first line to dig. People used that first line way back when the same way people used curare and sux first line way back when- because there was no better alternative. For cardiogenic shock, the data is weak for norepinephrine (which is first line and 99.9% of people who frequently treat cardiogenic shock would be going to it in this situation), and weak for using inotropes or pressors in general for improving mortality, but the alternative is letting the patient be hypotensive which no one likes. I have no problem running norepi in a good peripheral, but if you were uncomfortable you could've safely run epi or dobutamine + phenylephrine peripherally.

 

[vector2]

Also want to add that your case is a great example of why robust POCUS should be part of core anesthesiology training. Any anesthesiologist should be able to slap on a surface probe when a tough patient presents and be able to answer the following:

1. Are any chambers of the heart severely dilated or hypertrophied?

2. Does the LV fill adequately in diastole and totally eject its volume in systole (low SVR state), or is the LV small in both diastole and systole (hypovolemia)? What does the IVC look like?

2. Is there qualitatively moderate to severe LV, RV, or biventricular dysfunction?

3. Is there a severe valvular abnormality?

4. Is there a pericardial effusion?

5. Are there diffuse B-lines on lung ultrasound consistent with pulmonary edema?

 

[Radetzky]

Dig is a pretty ineffective inotrope.

I have generally found Milrinone usually makes things worse when the patient is hypotensive. I only use it when I’ve stabilized the BP and still have poor flow. In fact in animal studies when you keep afterload constant it doesn’t actually appear to have any direct inotropic action at all

 

[Burned_Out]

Hi Vector2,

Thanks for the detailed response. This guy did have an echo post-stent which showed an EF of 35%, diastolic impairment of LV fx, and no valve issues. In the ER, no echo was performed but his troponin drawn was normal ( they only got 1 set ) and I didn't see a BNP. Bun/Cr was slightly elevated (Bun 26, Cr 1.2) and the CXR showed pleural effusions. I don't have access to POCUS but I could have used a Sonosite we use for blocks and lines to take a lung ultrasound. I will remember that the next time.

 

[nimbus]

IV digoxin “load” was commonly used for rate control in rapid afib 20+ years ago. It did not work. It was not much of an inotrope either.

 

[GassYous]

Guy is bleeding = needs blood

This ain't rocket surgery

 

[Katheudontas parateroumen]

I haven’t used digoxin much in the OR as you’ve said. But I use it sometimes in the ICU. It’s mainstay so far is afib control in a a patient with low EF. Having said that, ionotropic affects are small. Not enough to do anything appreciable. Also onset might be slowish, Iv may even take up to half an hour to start working. Also a respectable loading dose would be around 0.5mg to start and then 0.25 and another 0.25 subsequent 6 hours. So it is definitely a process.

 

[lymphocyte]

Digoxin definitely increases cardiac inotropy. Takes forever to work. Not a huge fan, but it has its place. It's not unreasonable in septic rAF for example. I load at least 500microg. 100microg is farting in the wind.

I think you have a patient with undifferentiated shock and clinical signs of congestion, which are stunningly unreliable (ARDS is a key differential in this case, for example). I wouldn't consider fourth or fifth line treatment modalities and instead focus on establishing a working hypothesis for the shock and treating that, especially 10 days after a STEMI. POCUS is perfect for this. Or, if you don't have time, you can play the numbers game and pretend it's the most likely thing, like haemorrhage.

I also think it's dogma to not give vasoactive agents through a peripheral line and do it routinely for short periods of time.

To answer your very specific question, I don't think digoxin would have been appropriate in this situation, especially at that dose, and especially on the time scale you were working with, if at all.

Stroke volume change after digoxin loading in septic shock patients with transient left ventricular systolic dysfunction.

Transient left ventricular (LV) systolic dysfunction is a challenging complication of septic shock. Although Levosimendan, a calcium sensitizer has been reported to have a therapeutic role, digoxin, which increases intra-myocardial calcium level and cardiac contractility has no available data...

erj.ersjournals.com

Safety of peripheral administration of vasopressor medications: A systematic review - PubMed

Reports of the administration of vasopressors via PiVCs, when given for a limited duration, under close observation, suggest that extravasation is uncommon and is unlikely to lead to major complications.

pubmed.ncbi.nlm.nih.gov

 

[anaesthetic]

Agreed with above. I don’t know where your GI lab is, but I would never get digoxin down there in a timely manner. As mentioned before, put your own PIV in, temporize MAPs with pressors as blood’s going in, drop off to ICU. Inotropy comes secondary (if not last) to all of his other issues (i.e., hypotensive, tachycardic, anemic, ongoing UGI bleed = hypovolemia). Hematocrit can often lag behind.

 

[Beeftenderloin]

If this guy is hypotensive with rhales up to the clavicles and you’ve determined the cause is cardiac in origin, we have a name for this in medicine and it’s not heart failure, it’s cardiogenic shock. This guy doesn’t need dig. He needs blood and proper inotropic support so his ventricle can tolerate it.

I would have started some epi peripherally, hanged some blood, intubated him for the procedure, then mid/central line either pre or post procedure depending on urgency and quality of other access.

I’ve run epi peripherally many times as I’m putting low EF patients to sleep until I have more reliable access. I’ve also found that in patients who are tachycardic, but need inotropy, epi tends not to worsen the tachycardia like people think it will, especially at low doses (0.03-0.05 mcg/kg/min), but you still see a nice inotropic effect. Milrinone will tank his pressure. Dobutamine will make him more tachycardic and is an inferior inotropic agent to the other 2 IMO.

Norepi would be a reasonable first line agent to start, and probably what many, maybe even most people would hang first. It’s possible that if you fix his coronary perfusion pressure, his ventricle will kick into gear and start tolerating the volume better, maybe. My $0.02: sick patients with sick hearts need epi (Unless they have AS, MS and HOCM).

If he goes into an arrhythmia, shock him.

 

[vector2]

Hi Vector2,

Thanks for the detailed response. This guy did have an echo post-stent which showed an EF of 35%, diastolic impairment of LV fx, and no valve issues. In the ER, no echo was performed but his troponin drawn was normal ( they only got 1 set ) and I didn't see a BNP. Bun/Cr was slightly elevated (Bun 26, Cr 1.2) and the CXR showed pleural effusions. I don't have access to POCUS but I could have used a Sonosite we use for blocks and lines to take a lung ultrasound. I will remember that the next time.

Another thing then to consider is that he was almost certainly started on goal directed therapy for HFrEF, diastolic dysfunction, and CAD before he was discharged, which means he was likely taking a few potent antihypertensives/vasodilators in the face of ongoing bleeding. Mixed shock picture here (distributive + cardiogenic + hypovolemic) certainly likely upon his initial presentation to the ED, and I would empirically be treating all three while trying to narrow the diagnosis with labs (how does the ED not order a BNP given history???) + imaging + echo.

 

[woopedazz]

Bleeding**, hypotensive, sinus tachy, not perfusing his brain, APO, recent MI, known diastolic dysfunction, known HFrEF, resus with 2L crystalloid... Lots going on, but basically just a dude in cardiogenic shock.

First thing: The bleeding. This guy is actively dying from cardiogenic shock, not hypovolaemia. Hct is fine considering the IVT he's been slugged with and lack of pRBC. He's NOT anticoagulated, just antiplatelets. He just doesn't sound like a guy who is hosing... Surely he'd already be dead/would be fluid responsive/other things. Not just wallowing there slowly filling up his lungs.

Leads me to my second point: Why is this guy in theatre? Why not ICU? Or have I missed something here? Normally I'd go to ICU: BiPAP, POCUS TTE, fill him, line him up, norad, tube, milrinone, IABP/other, then go look at the trickle of blood that caused him to infarct in the first place. If he's not for ICU, fair enough. He'd probably just be palliated in ED where I currently work.

Thirdly: What's with the dexmedetomidine induction? You're bolussing phenylephrine and think he's in failure. What's the thought process here? Not sure I follow.

Presume he went to ICU tubed at the end right?

 

[Beeftenderloin]

Bleeding**, hypotensive, sinus tachy, not perfusing his brain, APO, recent MI, known diastolic dysfunction, known HFrEF, resus with 2L crystalloid... Lots going on, but basically just a dude in cardiogenic shock.

First thing: The bleeding. This guy is actively dying from cardiogenic shock, not hypovolaemia. Hct is fine considering the IVT he's been slugged with and lack of pRBC. He's NOT anticoagulated, just antiplatelets. He just doesn't sound like a guy who is hosing... Surely he'd already be dead/would be fluid responsive/other things. Not just wallowing there slowly filling up his lungs.

Leads me to my second point: Why is this guy in theatre? Why not ICU? Or have I missed something here? Normally I'd go to ICU: BiPAP, POCUS TTE, fill him, line him up, norad, tube, milrinone, IABP/other, then go look at the trickle of blood that caused him to infarct in the first place. If he's not for ICU, fair enough. He'd probably just be palliated in ED where I currently work.

Thirdly: What's with the dexmedetomidine induction? You're bolussing phenylephrine and think he's in failure. What's the thought process here? Not sure I follow.

Presume he went to ICU tubed at the end right?

Respectfully disagree. Sick, bleeding patients belong in the OR/theater. I can do everything they can do in the unit in the OR (POCUS, lines, resuscitation), faster than they can, with the added benefit of prompt hemorrhage control.

 

[woopedazz]

I just don't think he's bleeding all that much. 78 year old cardiac cripples tend to wear their vitals on their sleeves when it comes to fluid challenges in my experience

Unless they're dying from something else.

EDIT: but I've been wrong before!

 

[teacher2md]

I’ll just add that many times people are afraid to adequately resuscitate someone with reduced EF.

Even with an EF of 15%, they can still be too far left on the Starling curve. I’ll use POCUS or a TEE if there’s a real question.

I have no problem running NE and Epi through a large (US-guided) peripheral if needed for a few hours.

 

[MirrorTodd]

I’ll just add that many times people are afraid to adequately resuscitate someone with reduced EF.

Even with an EF of 15%, they can still be too far left on the Starling curve. I’ll use POCUS or a TEE if there’s a real question.

I have no problem running NE and Epi through a large (US-guided) peripheral if needed for a few hours.

Shoot, as long as I placed the IV and I am confident in it, I'll run anything through it.

 

[GassYous]

Bleeding**, hypotensive, sinus tachy, not perfusing his brain, APO, recent MI, known diastolic dysfunction, known HFrEF, resus with 2L crystalloid... Lots going on, but basically just a dude in cardiogenic shock.

First thing: The bleeding. This guy is actively dying from cardiogenic shock, not hypovolaemia. Hct is fine considering the IVT he's been slugged with and lack of pRBC. He's NOT anticoagulated, just antiplatelets. He just doesn't sound like a guy who is hosing... Surely he'd already be dead/would be fluid responsive/other things. Not just wallowing there slowly filling up his lungs.

Leads me to my second point: Why is this guy in theatre? Why not ICU? Or have I missed something here? Normally I'd go to ICU: BiPAP, POCUS TTE, fill him, line him up, norad, tube, milrinone, IABP/other, then go look at the trickle of blood that caused him to infarct in the first place. If he's not for ICU, fair enough. He'd probably just be palliated in ED where I currently work.

Thirdly: What's with the dexmedetomidine induction? You're bolussing phenylephrine and think he's in failure. What's the thought process here? Not sure I follow.

Presume he went to ICU tubed at the end right?

Yeah I'd probably just spray his throat with some benzocaine and call it a day

 

[deleted875186]

I used dig as an intern in IM, mostly rate control for AF. Not sure how much ionotropy you get from it, but it’s long acting and takes time to work, I personally would never use it acutely.

Not a cardiac person, but why don’t run a low dose epi infusion so long as there no tachycardia or AF? It’s an easily titratible and effect ionotrope, fast off as well in case there’s an issue.

 

[anaesthetic]

I used dig as an intern in IM, mostly rate control for AF. Not sure how much ionotropy you get from it, but it’s long acting and takes time to work, I personally would never use it acutely.

Not a cardiac person, but why don’t run a low dose epi infusion so long as there no tachycardia or AF? It’s an easily titratible and effect ionotrope, fast off as well in case there’s an issue.

There's good evidence for the safety of temporary, peripherally administered vasoactive medications. Epi at lower doses typically doesn't cause significant tachycardia, especially when compared to dobutamine.

 

[IlDestriero]

I always start with epi when someone is tanking and I didn’t have time to order infusions, place central lines, etc., primarily because I can make it myself in the OR in about 10 seconds and run it in an IV.
The big brains in the ICU can decide if they want a picc line or a triple lumen IJ, or Levophed, milrinone or whatever else. The cardiac cripples love blood with a Lasix chaser too.

 

[aafisahar]

don't rate control sinus tachycardia

 

[Angus Avagadro]

The GI lab is a bad place for an emergency as it usually has the oldest equipment and spotty restocking of meds. I believe the patient is hyovolemic. Only 1 U PRBC given? UGI bleeds can be hard to gauge due to unwitnessed hemetemesis and blood in the stomach. HCT takes some time to equilibrate and can be misleading early in the hemorrhage. I would give more PRBC and evaluate cardiac function by some modality, either PA cath or echo. He is asleep for the scope, so maybe a TEE machine and a probe can be brought to the GI lab.I also have no problem giving epi via peripheral iv in a pinch. The GI lab is a crappy place for an emergency, pun intended.

 

[abolt18]

Only time I've ever used Digoxin was to treat AFib w RVR in a patient whose blood pressure was too soft to tolerate BB or CCB. It worked very well, but again, was not instantaneous.

 

[deleted875186]

Only time I've ever used Digoxin was to treat AFib w RVR in a patient whose blood pressure was too soft to tolerate BB or CCB. It worked very well, but again, was not instantaneous.

Yes, this is a chronic med, not sure why it’s often stocked in ORs. Have to load, give daily dose, check level in a week, it’s an internal medicine drug.

 

[fakin' the funk]

Anyone have any experience using perioperative IV digoxin to treat suspected hypotension from heart failure?

Here is a clinical scenario I encountered recently. 78 y.o. male with upper GI bleed. He had a STEMI 10 days ago and was stented. Due to the anti-platelet medication he was put on, he bled. He is brought to the OR for an EGD. His BP is in the 70's systolic, HR is sinus tachycardia, Hct. is 29%. Mental status is confused and he ripped out his PICC line in the ER. No central access is available. On physical exam, I hear crackles all across both lung fields. He had received a unit of blood and 2L of NS in the ER, but it did not help his BP.

I did my "Ketofol" technique using only ketamine and dexemetomidine. He survives and the GI team loves me. He is still hovering with systolic BP in the 70's post-op and we send him to the ICU for more intensive mgmt.

Since I didn't have central access, I didn't start a vasopressor on him. I would have considered milrinone in this guy. I kept his BP respectable by phenylephrine boluses but this had a waning effect throughout the case.

Given I suspected he was in heart failure, I wonder if digoxin IV bolus in 50-100 mCg doses would have made a positive difference in this guy.

My only experience with IV digoxin was years ago when the CT surgeon asked me to give it to a CABG patient trying to come off bypass.

Personally I think it's insane that you didn't preinduction stabilize with inotrope/pressor, induce and intubate a clearly ICU-bound patient in shock, and run inotrope/pressor post procedure "because you didn't have central access", which presumably you are credentialed to place, but what do I know.

This is absolutely a **** sandwich and I have a million thoughts on this case, but the fact that this post is about digoxin kinda misses the point.

 

[cchoukal]

My experience with dig mirrors that of the others; it's not so much an inotrope as a negative chronotrope that happens to maybe not hamper inotropy as much as the others. I wouldn't use it with the hope that it would somehow improve cardiac output, but rather to lower the heart rate (which may or may not be what you want here).

As others have said, there is no good reason not to support the BP with "pressors" through a reliable PIV, and there is sufficient evidence in the literature that low MAPs increase the likelihood of Cr and Trop bumps, so leaving the guy with an SBP of 70 isn't free. I would add that "ketafol" isn't ketafol if the other drug isn't propfol, but dex. In the catecholamine-deficient heart failure patient, ketamine (and dex, for that matter) is a negative inotrope.

So what you've got here is a guy that you think is in cardiogenic shock to whom you've given two negative inotropes and hoping that digoxin will offset that. I don't think it will, but I think volume in the form of RBCs and norepi are indicated.

 

[PpfSuxTube]

Personally I think it's insane that you didn't preinduction stabilize with inotrope/pressor, induce and intubate a clearly ICU-bound patient in shock, and run inotrope/pressor post procedure "because you didn't have central access", which presumably you are credentialed to place, but what do I know.

This is absolutely a **** sandwich and I have a million thoughts on this case, but the fact that this post is about digoxin kinda misses the point.

Harsh but semi true...

When i read this, it felt a bit like a lay person post.

 

[kidthor]

Sounds like he's bleeding slowly and also in heart failure. Weird that the ED gave him 2L of NS (basically right into the lungs??) instead of another unit of blood... I personally would just run norepi peripherally and maybe slowly give another unit of blood. I wouldn't personally give digoxin as a first line treatment for hypotension or cardiogenic shock because it's so slow and there are many faster/better agents to help you here. I wouldn't have any qualms about giving a pressor through a functional large-ish bore (18g+) peripheral for a short period of time.

 

[NITRAS]

Yes, this is a chronic med, not sure why it’s often stocked in ORs. Have to load, give daily dose, check level in a week, it’s an internal medicine drug.

As an internist, digoxin isn’t something that I expect to work any time soon, and often the last drug I go for rate control in atrial fib. Occasionally on the advance CHF pt, but those are becoming more rare due to the studies suggesting it independently increases mortality.

 

[DesiredMemberName?]

POCUS is helpful in this scenario as many have mentioned already.

I agree if volume is going straight to his lungs with no HD improvement and he had recent STEMI, I’m not so sure I just assume it’s hypovolemia and keep dumping in IVF.

I’d be very worried about cardiogenic shock as the primary problem in this case. Either ischemic or maybe even acute MR/pap rupture given recent MI.

 

[nimbus]

Yes, this is a chronic med, not sure why it’s often stocked in ORs. Have to load, give daily dose, check level in a week, it’s an internal medicine drug.

We don’t stock it any more. Pulled at least 10 yrs ago.

 

[Burned_Out]

I've been on vacation and only now just catching up on the responses. The response has been great and I appreciate the discussion. Is there such thing as a stupid question? Not if the information helps myself and maybe others in likely scenarios in the future. I accept any and all criticism if someone feels I did wrong. But like grand rounds in residency/fellowship, we come clean with what we've done and and through other's thoughts, we learn from it. I've been practicing for 20 years and am ABA board-certified.

Now, to answer some of the questions asked about my experience. I cannot speak of the ER and why they didn't consult with the ICU/hospitalist on getting this patient intubated, lined, resuscitated and placed on pressors. They felt it was more important to get the patient to the GI lab to stem the bleed. BTW, he had multiple bleeding ulcers which they tried to clip to no avail. In the end, they sprayed him with some $32k chalky powder throughout his upper GI tract to stop the bleed. I wanted to do this case in the OR, but they had a bring-back heart and a level 1 trauma come up there at the same time. No OR staff to handle this emergency.

I unfortunately do not have POCUS and having it would have helped me figured out his volume status. I assume all critically-ill GI patients at this hospital as hypovolemic. I didn't stop giving him crystalloid and blood was being called for when I started this case. Someone said I was wrong to give ketamine/precedex rather than just do a proper GA induction. Well, I do understand ketamine can be a negative inotrope in a volume-depleted patient. But at what level of volume-depletion does a 10mg dose become a huge problem? Also if Precedex is a negative inotrope, then why would it have been better to use Propfol? If I had chosen to intubate the guy with Etomidate, wouldn't using an inhalational agent to maintain him be a drag on his BP and inotropy as well? I chose the drugs for which I believed would have the least inotropic and vasodilative effect on his perfusion.

As a follow-up, the guy survived and ended up in the ICU after this EGD. He wasn't tubed but maintained on face mask. Lasix was given along with several units of PRBC's. No inotrope that I could see was given overnight. They ordered a TTE the next day but I've been gone on vacation so I don't know the results.

 

[Burned_Out]

I want to add that I wasn't thinking about digoxin during the time I was with this guy. I was only contemplating what other pressor, other than phenylephrine, I could give to temporize his hypotension until the blood got here.

 

[woopedazz]

Echo result would be interesting.

Bit of midazolam + ketamine + paralysis normally works pretty well for these inductions where I am; if they cannot be resuscitated first. We don't have etomidate.

If you would baulk at giving a patient clonidine for hemodynamic reasons, then Dexmedetomidine is not likely gonna be appropriate. You gave it to reduce your induction dose of ketamine, but in the context of "ketofol" it is the ketamine that is given to reduce the propofol requirements...

Seems a bit backwards to use Dexmedetomidine as a ketamine sparing agent in this context. You're probably better off going pure ketamine, or add midaz, or ketofol in preference to adding Dexmedetomidine in terms of stability

 

[nimbus]

I want to add that I wasn't thinking about digoxin during the time I was with this guy. I was only contemplating what other pressor, other than phenylephrine, I could give to temporize his hypotension until the blood got here.

With a BP in the 70s, I would have started an Aline and norepi infusion, and then proceed with ga/ETT.

Also, where I work, endo brings their own RN, tech, and cart when they bring a case to the operating room. They don’t need any OR staff or equipment, they just need the room.

 

[Gasmd98]

I do lots of complex inpatient GI cases so I will add my 2 cents. UGI bleed in a medically complex and hypotension patient equals preinduction a-line + peripheral epinephrine or norepinephrine infusion then RSI. Syringe of vasopressin at the ready. Induce with low dose whatever because recall is the last of this sick old guys problems. This guy aspirates under MAC and you will be writing out a check. If your peripheral access sucks drop a quick central line post induction. If your GI lab is poorly equipped by all means insist on doing case in main OR. When faced with a complex case that has a reasonable chance of ending up in the basement I make sure that my anesthetic will hold up to lots of Monday morning quarterbacking.

Backing things up a bit, I wonder if OP is a newer grad who did not get lots of exposure to these kinds of cases in residency? There is a strong temptation to back off from a bigger anesthetic in the setting of a proceduralist complaining that he/she will only be doing “a quick scope.”

 

[GassYous]

I do lots of complex inpatient GI cases so I will add my 2 cents. UGI bleed in a medically complex and hypotension patient equals preinduction a-line + peripheral epinephrine or norepinephrine infusion then RSI. Syringe of vasopressin at the ready. Induce with low dose whatever because recall is the last of this sick old guys problems. This guy aspirates under MAC and you will be writing out a check. If your peripheral access sucks drop a quick central line post induction. If your GI lab is poorly equipped by all means insist on doing case in main OR. When faced with a complex case that has a reasonable chance of ending up in the basement I make sure that my anesthetic will hold up to lots of Monday morning quarterbacking.

Backing things up a bit, I wonder if OP is a newer grad who did not get lots of exposure to these kinds of cases in residency? There is a strong temptation to back off from a bigger anesthetic in the setting of a proceduralist complaining that he/she will only be doing “a quick scope.”

Wheres the tee and swan

 

[Gasmd98]

Not indicated but nice try. I have never regretted putting in an a line.

 

[MirrorTodd]

I do lots of complex inpatient GI cases so I will add my 2 cents. UGI bleed in a medically complex and hypotension patient equals preinduction a-line + peripheral epinephrine or norepinephrine infusion then RSI. Syringe of vasopressin at the ready. Induce with low dose whatever because recall is the last of this sick old guys problems. This guy aspirates under MAC and you will be writing out a check. If your peripheral access sucks drop a quick central line post induction. If your GI lab is poorly equipped by all means insist on doing case in main OR. When faced with a complex case that has a reasonable chance of ending up in the basement I make sure that my anesthetic will hold up to lots of Monday morning quarterbacking.

Backing things up a bit, I wonder if OP is a newer grad who did not get lots of exposure to these kinds of cases in residency? There is a strong temptation to back off from a bigger anesthetic in the setting of a proceduralist complaining that he/she will only be doing “a quick scope.”

OP has been in practice for 20 years.

OP how remote is your GI lab? Just like Nimbus says above, our place would have this guy in one of our OR's instead of the GI lab and we also don't require any OR staff...aside from an Anesthesia provider.

 

[nimbus]

Wheres the tee and swan

For some reason our GIs don’t like TEE during EGD. Bunch of spoiled brats

 

[GassYous]

Not indicated but nice try. I have never regretted putting in an a line.

It's a 5 minute case. Spray their throat with benzocaine, give a homeopathic dose of prop and go. They will probably find an old ulcer, treat it asap and be back in icu being resuscitated before you're done intubating.

 

[Beeftenderloin]

It's a 5 minute case. Spray their throat with benzocaine, give a homeopathic dose of prop and go. They will probably find an old ulcer, treat it asap and be back in icu being resuscitated before you're done intubating.

Patient’s got systolics in the 70s in frank cardiogenic shock, confused and ripping out lines, because their brain isn’t getting perfused, and it sounds like your plan is to just cross your finger that it’s gonna be fast, then dump them in the ICU, under-resuscitated, poorly accessed, and peri-arrest?

I don’t know what kind of medicine you practice, but I’m not bringing anyone anywhere with a systolic in the 70s (except maybe back to the OR). I’d like better care than that if it was me or a loved one on the table. And if you don’t feel comfortable providing that care, that’s cool, plenty of ASCs out there to work at.

I’ve been there with the PP GI doc giving side eyes for tubing/lining a patient for “a quick 5 min upper GI” I had a bad feeling about that turned into an hour, a suction canister full of blood and a “good call tubing them” at the end.

Many of these GIs are doing mostly outpatient screenings all day and have forgotten what “sick” looks like. This guy is sick. Needs proper access, resuscitation, and an ETT.

 

[GassYous]

If you're worried about them arresting then why would you bring them down for the procedure in the first place? Have them fully prepared before they get to you.

 

[Beeftenderloin]

If you're worried about them arresting then why would you bring them down for the procedure in the first place? Have them fully prepared before they get to you.

Sounds like patient was direct to GI/OR from ED. If I walk into pre-op and this is what I see, I’m not sending them anywhere til I’ve stabilized them.

 

[nimbus]

If you're worried about them arresting then why would you bring them down for the procedure in the first place? Have them fully prepared before they get to you.

If patient is hemorrhaging, we need to treat (stop the bleeding) and resuscitate simultaneously.

 

[Gasmd98]

OP has been in practice for 20 years.

OP how remote is your GI lab? Just like Nimbus says above, our place would have this guy in one of our OR's instead of the GI lab and we also don't require any OR staff...aside from an Anesthesia provider.

Didn’t mean to throw any shade at OP. Sorry if it came across that way. I work at a tertiary care academic place. Our GI lab has everything I need. In a prior life I would also have insisted on main OR.

 

[vector2]

If you're worried about them arresting then why would you bring them down for the procedure in the first place? Have them fully prepared before they get to you.

When a highest level trauma is activated and the pt is hemorrhaging to death, do you stop the pt from coming to the OR so you can "prepare" them in the trauma bay?

 

[Full Metal IC]

I've been on vacation and only now just catching up on the responses. The response has been great and I appreciate the discussion. Is there such thing as a stupid question? Not if the information helps myself and maybe others in likely scenarios in the future. I accept any and all criticism if someone feels I did wrong. But like grand rounds in residency/fellowship, we come clean with what we've done and and through other's thoughts, we learn from it. I've been practicing for 20 years and am ABA board-certified.

Now, to answer some of the questions asked about my experience. I cannot speak of the ER and why they didn't consult with the ICU/hospitalist on getting this patient intubated, lined, resuscitated and placed on pressors. They felt it was more important to get the patient to the GI lab to stem the bleed. BTW, he had multiple bleeding ulcers which they tried to clip to no avail. In the end, they sprayed him with some $32k chalky powder throughout his upper GI tract to stop the bleed. I wanted to do this case in the OR, but they had a bring-back heart and a level 1 trauma come up there at the same time. No OR staff to handle this emergency.

I unfortunately do not have POCUS and having it would have helped me figured out his volume status. I assume all critically-ill GI patients at this hospital as hypovolemic. I didn't stop giving him crystalloid and blood was being called for when I started this case. Someone said I was wrong to give ketamine/precedex rather than just do a proper GA induction. Well, I do understand ketamine can be a negative inotrope in a volume-depleted patient. But at what level of volume-depletion does a 10mg dose become a huge problem? Also if Precedex is a negative inotrope, then why would it have been better to use Propfol? If I had chosen to intubate the guy with Etomidate, wouldn't using an inhalational agent to maintain him be a drag on his BP and inotropy as well? I chose the drugs for which I believed would have the least inotropic and vasodilative effect on his perfusion.

As a follow-up, the guy survived and ended up in the ICU after this EGD. He wasn't tubed but maintained on face mask. Lasix was given along with several units of PRBC's. No inotrope that I could see was given overnight. They ordered a TTE the next day but I've been gone on vacation so I don't know the results.

I hope I have this level of humility 20 years out. Not an anesthesiologist myself, but thanks for posting the case and generating discussion. We are too quick to put our colleagues on trial without knowing details.

In the cardiology world digoxin has no role in shock resuscitation. I agree with others that peripheral norepi would have been an excellent choice while the bleeding is handled, buying you time to get the patient to the ICU where we can figure out where he is on the Starling curve, whether his heart works, how he likes his eggs etc. There are a few solid studies showing that peripheral norepi is safe when given through a reliable, proximal IV when someone (nurse, anesthesiologist, whoever) is being reasonably vigilant about extravasation, even up to 48-72 hours. Here's one from the anesthesia literature PMID 32925324, and another from the ICU literature PMID 29110979. The UTD pages on norepi and epi have additional references pertaining to this topic. I don't hesitate to do it, for instance when a CS patient shows up half dead in the ER and needs a blood pressure until we can get him up to the cath lab or ICU.

 

[IMGASMD]

…how he likes his eggs etc..

What I got out of the post….. also if he can order his eggs sunny side up
1. He doesn’t belong in icu
2. Where is your hospital, that allows patient to order something other than the default yucky yellow dried chunks they call scrambled eggs?

Thanks for your other input as well….