Recent published reports —a state of the science review in the Journal of the American College of Cardiology, correspondence in The New England Journal of Medicine, as well as reports in the Washington Post and CNN.com— suggested that infection with SARS-CoV-2 increases the risk of venous thromboembolism, as well as myocardial infarction and ischemic stroke.
In a virtual interview arranged by the American Heart Association, Peggy Peck, BreakingMED Editor-in-Chief, queried AHA spokespersons Comilla Sasson, MD, PhD, and Michael Kurz, MD, about these Covid-19 concerns. Sasson, who works as an emergency physician in Denver and is AHA VP of Emergency Cardiovascular Care Science and Innovation, has been working since mid-April at a field hospital in New York City. Kurz is associate professor of the departments of emergency medicine and surgery at the University of Alabama at Birmingham.
Peck: I want to ask about something that has just come up in the last few days—coagulopathy and Covid-19.
Sasson: Based on what we’re doing here in New York City — I’m actually working in one of the field hospitals out here — we’re using the same protocols that are being used throughout the public health care system here. And so, for us, we’re actually using a D-dimer cutoff, where we will say everyone is on prophylactic anticoagulation and then if they go above a certain number—2000 µg/l—we’re putting on therapeutic dosing for anticoagulation, primarily using Lovenox [enoxaparin].
That’s just been the protocol that has been really kind of handed down to us from the healthcare system.
I will say personally, just having seen a lot of Covid-19 patients out here, we have quite a lot of coagulopathic patients with micro emboli and then some who are having splenic infarcts. I’ve seen pulmonary embolisms as well. I’ve not seen personally a stroke patient, but I’ve heard of many stroke patients that have been coming through.
So, I think we don’t necessarily understand the coagulation pathway that’s occurring… Right now, maybe something to do with the cytokine storm theory that everything kind of goes into derangement, but there are also some additional data that the coagulopathies that we’re seeing may even be earlier, so it may not be when they actually go into that big cytokine storm. It could be that they could be having these blood clots even earlier, but we’re not seeing physically until later.
So, [there is] a lot of information that is still to be determined, but I do know here, at least from a protocol perspective, we are anticoagulating patients right away, primarily with either heparin or Lovenox, and then, once the hospitals run out of those drugs, they actually use some of the new novel anticoagulants as well.
More STEMI, More PE, More Cardiac Arrest
Kurz: Anecdotally, we have also seen a high correlation between thrombotic events and Covid infection.
We’ve seen a number of increases in our STEMI volume and increases in PE volume, an our cardiac arrest volume from thrombotic complications from the virus that would suggest the need for anticoagulant or antiplatelet therapy like Dr. Sasson has implemented in a systematic fashion there in New York. We in Alabama have not implemented it systematically, but we are all quite aware of these complications at both the micro-thrombotic level and at the macro level. So, you know, it’s splenic infarcts, smaller vessels, and larger vessels you think of with heart attacks and such.
Sasson: We’ve also seen really interesting derangements in the lab work. We’re seeing thrombocytosis, we’re seeing super high levels of platelet counts. And, we’re also on the other side of things — very low levels of hemoglobin and anemia — there’s no one clear clinical picture. Very high levels of ferretin. Very sky high D-dimer counts, like in the 20,000s and 30,000s… You know, I think again it’s really interesting to think about what is the pathophysiology that’s causing these derangements in lab values, and how does that translate out to clinical correlation?
Kurz: D-dimer! Dr. Sasson, you bring up a good point… I studied that as part of coagulation on cardiac arrest—the D-dimer levels that we are seeing in Covid-19 patients are similar to the ones that we see following cardiac arrest. And, we know those folks who come out of cardiac arrest are hypercoagulable for a significantly extended period of time. So, now that we can see the kind of “tip of the iceberg” in the physiology, we’re just kind of diving in just trying to figure out what the actual derangement along the coagulation cascade is.
Sasson: Exactly! This is my new favorite phrase: We’re in an opinion rich data freeze-out. Everyone has an opinion and we’re all looking for some data.
Peck: Is there any correlation between these coagulopathies you are describing and age? Are you seeing this in younger patients? Older patients?
’No Rhyme or Reason’
Sasson: In New York City, in the patient population that I’ve seen, it has not been one specific age range. Very, very variable, actually. I think I thought that when I was coming here, 65 and older was going to be where primarily most of our patients would be. We’re actually seeing quite a few that are in that 40-to-59-year old range as well. And, again, I’m not sure why. It’s consistent with what the NSW piece had shown. There is a sort of defined modal curve right between sort of the older patient populations that we all think about, and the sort of 30-to-50-year old range as well, and I would say clinically that’s what I’m seeing.
Peck: So, no age correlation for the coagulopathies?
Sasson: Exactly. I think, you know, there’s no rhyme or reason.
That’s the most challenging part, even when we’re looking at the lab values, because we’re trending them out seeking a peak and… sometimes we actually see sort of a peak, then they’ll start to trend downwards and then, you know, it’s back up.
These patients are in the hospital for such a long time… I think, you know, as ER doctors the last thing we are is patient. Patience is a virtue here because it’s 3-4 weeks to get these patients weaned down, and then, all of a sudden, they’ll have an acute hypoxic event and then their D-dimer skyrockets again. So, is it a micro-emboli that’s causing the hypoxia? I don’t know that we really know.
Peck: When we first heard about Covid-19, the sense was that this was a pulmonary disease and the big worry was ARDS. But recent reports show that Covid-19 is a disease of many organs: the heart, the kidneys, the liver, and so on. Also, questions are arising about the virus affecting the circulation, reducing the ability of the blood to carry oxygen—hypoxic patients with no breathing issues. How different is this experience for you?
Kurz: Dr. Sasson earlier said, “there doesn’t seem to be any rhyme or reason.” And so, we see multi-organ system failure with these patients, and it is not isolated to an issue with just ARDS… So, this virus, unlike other viruses, is a truly multi-organ system, disease, and so we are seeing, in fact, all of those organ system complications that you described. It not just your lungs are failing from ARDS.
We see kidney failure; we see liver failure; we see cardiovascular failure; we see a myocarditis-like picture in a small minority, which suggests that there is clearly a mechanism to this virus — and what it does — that we don’t yet understand.
And so, unlike being prepared for a single organ failure, and it being handled by a single specialty in medicine, this is truly an all-hands-on-deck, multi-disciplinary effort in order to save lives from this epidemic.
Not So Happy Hypoxics
Sasson: I can’t agree more with you on that, Dr. Kurz, because I will say that it’s been really fascinating to see how different the emergency department presentations are. So, you have a spectrum of Covid patient that has no symptoms whatsoever. Then you have the spectrum of what we’re calling “the happy hypoxics” that we’re now actually realizing maybe they’re not that happy.
And then, we have this whole subset of patients who actually come in looking okay but then crash very quickly.
And so, all of a sudden, they go from a five-liter requirement to a non-rebreather to bypass high-flow nasal canula.
And I think the mantra at least out here has been: Do not intubate. Do whatever you can do, but do not intubate them, because the mortality is so high once they get on the vent, and so suddenly.
You know, I think in ARDS we say that ventilation is the ultimate strategy to get their lungs a break and to give them the opportunity to heal.
And, in this sort of disease process, I think the shift has been really apparent that… doing everything you could possibly do to get them to not be on the ventilator is a really, really important step.
And, I think the last thing that I wasn’t really familiar with until I came up to New York City is just how much they’re using high-flow nasal canula and bypass.
And, then there’s a whole, you know, very controversial topic of aerosol generating procedures: How do you keep your patients safe? How do you keep your providers safe?
It’s been really fascinating to see how they’ve kind of worked around it so that they can still keep people on those sort of temporizing measures and see if maybe they can ride that until, hopefully, the patient starts to improve.
A Risk Like No Other
Kurz: I think that the tension that Dr. Sasson describes between trying to protect providers from aerosolized procedures and doing what’s best for the patient is a tension that’s been overlooked in media. So, we have many temporizing procedures to prevent you from having to go on the vent. However, each one of those is incrementally more aerosolizing, meaning it puts incrementally more healthcare providers at risk of contracting the disease. Even though it probably — you know what, at least our experience it sounds like can relate with bearing out in New York — is actually best for the patient. And so, this is a tension that is inherent to the way we take care of these folks that I think is probably unique specifically to this disease.
In emergency medicine, we are very comfortable with risk. We understand that part of our job in the specialty we chose comes with some inherent risk that perhaps not all of the providers in the house of medicine step up and take every day. But the idea that perhaps the life-saving therapy in fact puts us directly at risk, that’s a tension I think that’s perhaps overlooked when we describe how to best care for these folks.
Peck: Finally, you’ve both referenced the need for a team to treat Covid-19, but I want to ask about that team. For example, several years ago, when data on transcatheter aortic valve replacement (TAVR) were first reported, there was much speculation about possible turf issues among interventional cardiologists, general cardiologists, and cardiovascular surgeons. The answer then was “heart team,” a coming together of different disciplines to determine how best to treat the patient. That team building wasn’t easy, so how easy is it to build the ’Covid Team’?
Building the Covid Team
Sasson: I think it’s continuing to evolve as we go. And, I think to your point, Peggy, I think the presentations are so different. I think that, you know, at least with a patient with an aortic valve that needs to potentially be repaired you have a finite condition, you have a disease process that people understand.
And, I think what makes Covid-19 so different is that it is a very expansive problem that we have very little understanding of, and we don’t have a cure, and we don’t have a treatment pathway. And, if you will, we don’t necessarily even know exactly what we’re treating.
And so, I think in many ways it has become multi-disciplinary, just because everybody has to weigh-in, because there is no one specialty.
Covid-19 is not infectious disease: it’s not cardiology; it’s not nephrology; it’s not pulmonology; it’s not GI. Literally, you can have all of those people on the same patient.
It just depends on what sort of rises to the top of that person’s primary complaint or primary symptomatology of Covid-19. So, that’s a long-winded answer for: it just depends.
And, each patient is very much right now case-by-case, because nobody’s an expert.
There isn’t that critical team that comes in and says, “here’s what we did for the last 900 patients.”
I can tell you what we did with less than nine patients, and I probably have more knowledge institutionally than any of my counterparts.
So, I think again we’re in this very interesting place where we have no choice but to work with each other, because I think everyone has to contribute some amount of knowledge. And, I think that’s also where you get to the point where, actually, the turf wars kind of go away, because I think we’re all kind of going into this as a team trying to figure out: Where will we land? Where are we headed?
I don’t think we have a clear direction just yet.
Kurz: To Dr. Sasson’s point, a couple of things contribute to a much more collegial environment for these patients.
One, their care is not housed in one specific specialty. Okay, so, you know, as opposed to your example — TAVR is largely housed in cardiology and cardiovascular surgery.
The care of Covid patients is not housed in a single specialty or even two specialties.
And so, a multidisciplinary approach is absolutely essential to optimize their care.
And so, the phrase that we have adopted at UAB is the same phrase that we use on our cardiac arrest service, and actually is the same model that we use, which is: “practice all of the best medicine you’ve ever known.”
We are encouraged to do the best that we can contribute and to acknowledge where we are not the expert and find someone who is. And, you know, I’m fortunate to be at… the ninth largest public Academic Center in the nation, so I have one of everything. And so, that’s an easier lift for us to be able to all come together and optimize their care.
Sasson: Out here in a field hospital with a multitude of specialties from all over the country.
It’s kind of an interesting and different problem that people have, because this is a team that’s never worked together before. And, we’re trying to figure it out. Everyone’s bringing a little bit of this and a little bit of that, and I think actually it’s been phenomenal for that reason, because we have infectious disease, we have internal medicine together, or we have pulmonary and critical care, but they’ve never actually worked together before, but it is interesting.
’The story of this disease changes every 24 hours’
Kurz: The other thing is that the time pressure also forces you to work together, right?
So, you know, we will see as we hit a critical mass of patients that have this disease, we’ll see syndromes start to coalesce. Like, we’re discussing the thrombotic complications now, right? A month ago, there was not a critical enough mass for us to see a pattern with the thrombotic complications.
The story of this disease changes every 24 hours. And, that means the composition and the current relative contribution of the team changes. Understanding that is a significantly more collaborative atmosphere than it, perhaps, usually is within the house of medicine.
Peggy Peck, Editor-in-Chief, BreakingMED™
Cat ID: 308
Topic ID: 74,308,254,930,728,791,932,730,933,308,309,358,838,914,125,190,926,142,192,927,151,590,928,925,934