Possible myocarditis and anesthesia

[Planktonmd]

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45 Y/O M, admitted to hospital 7 days ago for night sweats, general weakness, low grade fever and epigastric discomfort.
He is a businessman who was on a trip to Africa when his symptoms started.
He is otherwise healthy and does not take any medications although he mentions that his BP was elevated everytime he checked it in the past 2-3 years but his primary physician did not think he needed anti-hypertensives!
On admission they wanted to R/O cardiac ischemia so they checked Troponin level and it was 17.6.
The EKG showed SR, RBB, and first degree AV block.
He had a transthoracic Echo that showed no wall motion abnormalities and normal EF, it also showed severe LV hypertrophy and small Pericardial effusion.
Cardiac catheter showed: Normal coronaries, and confirmed normal EF.
They ended doing an ultrasound of the RUQ that showed edema and stones in the gall bladder.
They also did a HIDA scan that was highly suggestive of acute cholecystitis.
Cardiologist thinks that patient has viral myocarditis causing the troponin elevation and he also thinks that it's OK to proceed with cholecystectomy at this point.
Patient is in the holding area, Vitals are:
BP= 160/110, HR 55 regular, Sat= 99% on RA, Afebrile.
He is in no distress.
What's your next step?

 

[smgilles]

45 Y/O M, admitted to hospital 7 days ago for night sweats, general weakness, low grade fever and epigastric discomfort.
He is a businessman who was on a trip to Africa when his symptoms started.
He is otherwise healthy and does not take any medications although he mentions that his BP was elevated everytime he checked it in the past 2-3 years but his primary physician did not think he needed anti-hypertensives!
On admission they wanted to R/O cardiac ischemia so they checked Troponin level and it was 17.6.
The EKG showed SR, RBB, and first degree AV block.
He had a transthoracic Echo that showed no wall motion abnormalities and normal EF, it also showed severe LV hypertrophy and small Pericardial effusion.
Cardiac catheter showed: Normal coronaries, and confirmed normal EF.
They ended doing an ultrasound of the RUQ that showed edema and stones in the gall bladder.
They also did a HIDA scan that was highly suggestive of acute cholecystitis.
Cardiologist thinks that patient has viral myocarditis causing the troponin elevation and he also thinks that it's OK to proceed with cholecystectomy at this point.
Patient is in the holding area, Vitals are:
BP= 160/110, HR 55 regular, Sat= 99% on RA, Afebrile.
He is in no distress.
What's your next step?

He has had a complete cardiac work-up. Echo looks "normal", he has preserved systolic function without diastolic dysfunction. Due to the LV hypertrophy I assume he has had high BP a lot longer than 2-3 years, but you know he is not in heart failure - overtly or clinically.

The first degree AV block and RBBB may be from the myocarditis. His blood pressure is not the prettiest and a slow/smooth induction may help precipitate a large drop in blood pressure, but he is also 45 and healthy.

Long of the short. Propofol/vercuronium/lidocaine/fentanyl - tube. Recommend better BP control. He may need to be started on a heart failure regimen (including diuretics, β-blockers, angiotensin-converting enzyme-inhibitors or angiotensin II receptor blockers) but he is being followed by cardiology.

Just my CA-1 little brain's thoughts.

 

[dhb]

Pent/sux/tube. 😀

The EKG showed SR, RBB, and first degree AV block.

Cardiac catheter showed: Normal coronaries, and confirmed normal EF.

Patient is in the holding area, Vitals are:
BP= 160/110, HR 55 regular, Sat= 99% on RA, Afebrile.
He is in no distress.
What's your next step?

Seriously there's not much more you can do his heart looks good, i'd go with the cardiologist this time.
I wouldn't r/o tuberculosis here if he had repeat trips to 3rd world countries.

 

[huktonfonix]

If he is symptomatically improving and troponin is trending down, its likely the myocarditis is resolving and it should be ok to proceed if this is an emergent/urgent surgery. If its elective and amenable to more conservative therapy in the meantime, then I would wait.

 

[Planktonmd]

He has had a complete cardiac work-up. Echo looks "normal", he has preserved systolic function without diastolic dysfunction. Due to the LV hypertrophy I assume he has had high BP a lot longer than 2-3 years, but you know he is not in heart failure - overtly or clinically.

The first degree AV block and RBBB may be from the myocarditis. His blood pressure is not the prettiest and a slow/smooth induction may help precipitate a large drop in blood pressure, but he is also 45 and healthy.

Long of the short. Propofol/vercuronium/lidocaine/fentanyl - tube. Recommend better BP control. He may need to be started on a heart failure regimen (including diuretics, β-blockers, angiotensin-converting enzyme-inhibitors or angiotensin II receptor blockers) but he is being followed by cardiology.

Just my CA-1 little brain's thoughts.

Very good.
Any concern about the risk of surgery in a patient with acute myocarditis?
Is this patient at any increased risk for mortality and morbidity post-op?
Would you suggest any invasive monitoring intra-op?
Do you agree with the cardiologist diagnosis of viral myocarditis?
How do you confirm such diagnosis?
Is it possible to develop ischemia with normal coronaries?
Does LV hypertrophy make it more likely to develop ischemia with normal coronaries?
If you have the choice to wait and treat conservatively with antibiotics would you rather wait?

 

[dhb]

Very good.
Any concern about the risk of surgery in a patient with acute myocarditis?
Is this patient at any increased risk for mortality and morbidity post-op?
Would you suggest any invasive monitoring intra-op?
Do you agree with the cardiologist diagnosis of viral myocarditis?
How do you confirm such diagnosis?
Is it possible to develop ischemia with normal coronaries?
Does LV hypertrophy make it more likely to develop ischemia with normal coronaries?
If you have the choice to wait and treat conservatively with antibiotics would you rather wait?

His function is normal so his myocarditis isn't too bad at the moment probably higher risk but i'd have to look at the literature which is probably more case reports than randomized studies.
Confirmation is by biopsy which they could have done during the cath.
Ischemia with normal coronaries: yes: Prinzmetal angina, intramyocardic arteries, AS...
Medical management is an option but what happens if the patient becomes septic the combination with the myocarditis might not be the best for his heart.

 

[dragonfly99]

The LV hypertrophy does make it more likely to develop ischemia with normal coronaries.

Does he really need the gallbladder out right now, or could it wait a few days?
I think you can probably safely operate, but he just has a lot going on lately....a 17 troponin is pretty high.

He definitely needs an ACE-I later....this dude needs a PCP who will treat his HTN. Damn. Of course, patients always say their primary doctor told them this or that didn't need to be treated...it isn't true half the time.

 

[dfk]

aside from what's already been suggested, why not wait and get control of BP? don't the AHA guidelines recommend a DBP less than 110?

 

[Jeff05]

ACC/AHA 2007 Guidelines on Perioperative Cardiovascular
Evaluation and Care foExecutive Summary
Circulation. 2007;116:1971-1996.

B. Hypertension
For stage 3 hypertension (systolic blood pressure
greater than or equal to 180 mm Hg and diastolic blood
pressure greater than or equal to 110 mm Hg), the
potential benefits of delaying surgery to optimize the
effects of antihypertensive medications should be
weighed against the risk of delaying the surgical
procedure. With rapidly acting intravenous agents,
blood pressure can usually be controlled within a
matter of several hours. One randomized trial was
unable to demonstrate a benefit to delaying surgery in
chronically treated hypertensive patients who pre-
sented for noncardiac surgery with diastolic blood
pressure between 110 and 130 mm Hg and who had
no previous MI, unstable or severe angina pectoris,
renal failure, pregnancy-induced hypertension, LV
hypertrophy, previous coronary revascularization,
aortic stenosis, preoperative dysrhythmias, conduc-
tion defects, or stroke.23
Several authors have suggested withholding
angiotensin-converting enzyme inhibitors and angio-
tensin receptor antagonists the morning of sur-
gery.24 –26 Consideration should be given to restarting
angiotensin-converting enzyme inhibitors in the post-
operative period only after the patient is euvolemic, to
decrease the risk of perioperative renal dysfunction.

this is clearly a case of cardiac mets from squamous cell GB carcinoma.
maybe not.

the QUESTION: should cholecystectomy be postponed until cardiac status returns to baseline - no more troponin leak.

the following may help answering that question:
Dig Surg 1996;13:328-331
Although there is a high degree of consensus among surgeons on how acute cholecystitis should be managed, it is not possible to formulate one single standard. Acute cholecystitis should, in fact, be subdivided into three clinical groups, i.e. acute calculous cholecystitis in the average-risk patient, acute calculous cholecystitis in the high-risk group of patients, and acute acalculous cholecystitis in severely ill patients being nursed in intensive-care units (ICUs). The standard for acute calculous cholecystitis in average-risk patients is an early operation, which does not mean an emergency operation for most patients but rather a short period of preoperative medical therapy followed by operation within a few days. Acute calculous cholecystitis in the high-risk group requires prompt surgical intervention within 24-48 h of onset. Laparoscopic cholecystectomy was once considered contraindicated in acute cholecystitis, but the percentage of cases treated by laparoscopic cholecystectomy has been steadily increasing and it is well on its way to becoming a new standard. Acute acalculous cholecystitis in ICU patients is a facet of the multiple-organ dysfunction syndrome, and is known for its aggressive clinical course with a high rate of gangrene and perforation. Percutaneous transhepatic or open cholecystostomy may be curative treatment when applied early but the diagnosis is not an early one in many patients, for whom open cholecystectomy appears more appropriate.

this guy can probably wait for a couple of days.

however, if deemed as surgical emergency i would proceed as though this patient has a higher likelyhood of cardiac arrhythmias:

Acute viral myocarditis presenting as sudden cardiac arrest and refractory ventricular tachycardia
The American Journal of Emergency Medicine, Volume 22, Issue 7, Pages 628-629

and

SADS, or sudden arrhythmia death syndrome, is a term used to describe sudden death due to cardiac arrest brought on by an arrhythmia. The most common cause of sudden death in the US is coronary artery disease.[citation needed] Approximately 300,000 people die suddenly of this cause every year in the US.[citation needed] SADS can also occur from other causes. Also, there are many inherited conditions and heart diseases that can affect young people that can cause sudden death. Many of these victims have no symptoms before dying suddenly.[citation needed]
Causes of SADS in young people include viral myocarditis, long QT syndrome, Brugada syndrome, Catecholaminergic polymorphic ventricular tachycardia and hypertrophic cardiomyopathy and arrhythmogenic right ventricular dysplasia.

pre-induction a line. smooth cardiac induction. tight control of electrolytes. pads on patient connected to defibrillator for the procedure.

 

[periopdoc]

What was he on for malaria prophylaxis while on his trip?

- pod

 

[smgilles]

aside from what's already been suggested, why not wait and get control of BP? don't the AHA guidelines recommend a DBP less than 110?

Recycle the cuff and the diastolic will be 99

His symptoms (according to my text book) look like a typical presentation of myocarditis. Most likely viral in origin - unless he picked up a parasite in Africa 😀

I think an arterial line is a stretch in a healthy 45 y/o, but with a troponin of 17 and diastolic >100 - one could definitely make a decent argument for it. I think the biggest issue is the myocarditis leading to cardiomyopathy and heart failure, or developing intraoperative ischemia secondary to his LV hypertrophy, or new onset arrhythmia.

If he looked clinically sound and wasn't actively complaining of chest pain I would proceed with the case.

 

[Planktonmd]

So, since the literature is basically silent on how to approach a patient with acute myocarditis who requires anesthesia should we think of it as an acute myocardial injury similar to a recent MI?
Can we say that this patient has the same risk profile of a patient with an acute MI 7 days ago?
Does the presence of conduction abnormalities (RBBB and 1st degree AV block) make you hesitate more?
And since the diagnosis here is mostly based on the clinical picture and the cardiologist's opinion, should we demand that the diagnosis be confirmed by a myocardial biopsy?
Could a tropical parasite be the problem here? (something like Chagas disease or cardiac chistosomiasis...) 😀
Could it be what Jeff has suggested (metastatic biliary cancer)? 😱
Does it actually matter what the etiology is?


Disclaimer: I know this is more mental masurbation than we usually tolerate around here but there are a few important points that we could all learn from, so bare with me.

 

[OB1🤙]

I'll play along with you Plank, thanks for the effort in bringing up some clinical stuff. I'm not gonna look up anything before I answer.

So, since the literature is basically silent on how to approach a patient with acute myocarditis who requires anesthesia should we think of it as an acute myocardial injury similar to a recent MI?

I don't think so. This is a diffuse injury that has not compromised the contractile function of the heart (as far as we can tell), rather than an injury that has produced a hemodynamically specific wall motion abnormality.

Can we say that this patient has the same risk profile of a patient with an acute MI 7 days ago?

We can say it, but it doesn't make it true. We don't know what the risk profile is in this patient. I'd think it would be less than a recent AMI, but I don't think there's any data to support this opinion one way or another.

Does the presence of conduction abnormalities (RBBB and 1st degree AV block) make you hesitate more?

It gives pause, but these are nonspecific abnormalities, and the cardiologist doesn't seem too concerned with them. It's not enough to change your management, I don't think, but having a copy of the 12 lead on hand is a good idea in case changes present themselves intraop.

And since the diagnosis here is mostly based on the clinical picture and the cardiologist's opinion, should we demand that the diagnosis be confirmed by a myocardial biopsy?

I don't think it changes our management to do so.

Could a tropical parasite be the problem here? (something like Chagas disease or cardiac chistosomiasis...) 😀

Our friendly colleagues in ID are a page away, and I'm sure they'd be delighted to weigh in on the answer to that question, and thank us kindly for the (actually) interesting consult. Seems unlikely, as this isn't a dilated cardiomyopathy.

Could it be what Jeff has suggested (metastatic biliary cancer)? 😱

Sure, and the rustling and rattling I heard in the shrub while hiking in the Santa Monica mountains yesterday could have been a zebra that escaped the LA zoo and swallowed a baby rattle and not a rattlesnake.

Does it actually matter what the etiology is?

This depends entirely on how urgent the surgery is. Surgeon says gotta go-> document urgency and proceed.

 

[Planktonmd]

I'll play along with you Plank, thanks for the effort in bringing up some clinical stuff. I'm not gonna look up anything before I answer.

I don't think so. This is a diffuse injury that has not compromised the contractile function of the heart (as far as we can tell), rather than an injury that has produced a hemodynamically specific wall motion abnormality.

We can say it, but it doesn't make it true. We don't know what the risk profile is in this patient. I'd think it would be less than a recent AMI, but I don't think there's any data to support this opinion one way or another.

It gives pause, but these are nonspecific abnormalities, and the cardiologist doesn't seem too concerned with them. It's not enough to change your management, I don't think, but having a copy of the 12 lead on hand is a good idea in case changes present themselves intraop.

I don't think it changes our management to do so.

Our friendly colleagues in ID are a page away, and I'm sure they'd be delighted to weigh in on the answer to that question, and thank us kindly for the (actually) interesting consult. Seems unlikely, as this isn't a dilated cardiomyopathy.

Sure, and the rustling and rattling I heard in the shrub while hiking in the Santa Monica mountains yesterday could have been a zebra that escaped the LA zoo and swallowed a baby rattle and not a rattlesnake.

This depends entirely on how urgent the surgery is. Surgeon says gotta go-> document urgency and proceed.

Very good.
So, anyone objects to how I proceeded:
I had a discussion with the cardiologist, he stated that he feels strongly that this is actually a viral myocarditis and that the Cholecystitis is a separate entity.
So we placed an A line Pre-op just to watch the BP closely and induced GA.
The surgery was uneventful and lasted 40 minutes.
Patient was extubated post-op and was doing OK in the PACU for 15 minutes then I was called by the nurses for bradycardia (30 BPM) and hypotension 70/40.
On the monitor there was wide complex QRS and 3rd degree AV block.
Patient feels drowsy but still conscious and not complaining of chest pain.
What now?
Retrospectively was it wrong to proceed with the surgery?

 

[huktonfonix]

transcutaneous or chemical (isoproterenol) pacing. sounds like third degree block with venticular escape beat. You can try atropine or ephedrine, but in a third degree block they'll likely not be very effective. check electrolytes, correct hypoxemia, hypercarbia, blah, blah, blah. call the cardiologist.

 

[dhb]

I don't see how the anesthetic/surgery would have affected his av conduction. He probably would have had the same course without the surgery.
Treat symptomatically repeat an echo.