Talking Tall Rounds®: Complicated Wounds

Podcast Transcript

Announcer:

Welcome to the Talking Tall Rounds series, brought to you by the Sydell and Arnold Miller Family Heart, Vascular and Thoracic Institute at Cleveland Clinic.

Michael Maier, DPM:

Good morning everyone. It's a pleasure to be with you here. For those in the room and those joining us virtually, my name is Mike Maier. I'm a longtime member of the section of vascular medicine with specialty interest in lower extremity wounds, and it's my distinct pleasure to serve as a moderator today for the Heart, Vascular and Thoracic Institute Tall Rounds entitled Comprehensive Cutting-Edge Care for Complicated Wounds.

So in today's Tall Rounds, we're fortunate to have a wide range of specialty expertise to cover this broad topic of complicated wound management. And to get us started, Dr. Scott Cameron to the podium to present a complicated wound case. Dr. Cameron serves as the Section Head of Vascular Medicine. He has numerous academic and clinical awards. He's a prolific scientific author and researcher whose specialty interests include a variety of vascular disorders, thrombosis and platelet dysfunction. Dr. Cameron.

Scott Cameron, MD, PhD:

Thanks so much, Dr. Maier. I thought I would start by introducing a case just to sort of make the point that patients with cardiac and coronary disease, and reliably, one third of them actually, will have peripheral artery disease. And so this case sort of highlights a teaching case when I used to be the cardiac ICU individual.

So we've got a 56-year-old female. Had a known history of Raynaud's phenomenon, presented with acute chest discomfort. And you can see she has a clear inferoposterior transmural infarction pattern on her 12-lead electrocardiogram. She obviously went for angiography right away where it's pretty clear you can see here the culprit lesions, probably the left circumflex, which ultimately was stented. I was alerted at that time that the patient has an allergy to aspirin, which should have been a tip-off for what was about to come. So she was started on a glycoprotein IIb-IIIa receptor antagonist. In this case it was Integrilin. Underwent aspirin desensitization therapy, which was the standard of care at the facility I was serving at that time, and then transitioned over to dual antiplatelet therapy.

I was forever telling the residents, make sure you do a comprehensive vascular exam for every patient you admit and present. And so one very astute medical intern on rounds pointed out that the patient had bruit over various vascular compartments. And as you can see here, if you just look at the aorta, there's some calcific atherosclerotic disease, increased velocities in the celiac and IMA artery. The internal carotid artery, again, has got calcific disease, and if you just pan down through the CT angiogram, you can see it sort of throughout. So this is a patient that clearly has non-coronary vascular disease, but just didn't know it, and just sort of emphasizes we should obviously be looking for extra things in our patients to serve them.

The patient did quite well, was given anti-platelet-therapy, a statin, an ACE inhibitor and was discharged and did well with cardiac rehabilitation phase II. So when I saw her in clinic, to my absolute surprise, no cardiac issues, was thriving, but endorsed this new ulcer on the finger, as you can see, and asked me what I thought it might be. So we ended up doing a extensive workup, finding out there was some inflammation in the bone, which is, of course, concerning for an infection which has gone further down.

And you can see if you look at the noninvasive vascular study, the thing that jumped out to me, if you look at the blood pressure in the upper arm limb on the right side compared to just below the elbow, there's a drop of about 20 mmHg, which is consistent with a hemodynamic compromise, probably in the axillary artery, maybe in the brachial, but certainly some disease there, which did turn out to be atherosclerosis.

When we did PVRs on the fingers, not unexpectedly, there were dampened waveforms in several of the fingers, which we quite often see in Raynaud's phenomenon or secondary Raynaud's. So the clot thickened, so to speak. A hand angiogram was conducted... and we'll see if we can play it here... had very, very diminutive vessels. Sometimes we see this pattern in patients with Buerger's disease, so quite a broad differential at this point for this wound. So what do I do? Here's my diagnostic workup.

If I see a patient with a wound that consider, is it a patient who has increased sympathetic tone? For example, if they have Raynaud's phenomenon, do they have increased tone in the smooth muscle? Do they have endothelial dysfunction? Do they have platelet activation, or is there a vasculitis that we need to consider? And so if you're looking at wounds, either in the fingers or in the feet, they appear sort of looking like this, various flavors, but they all have the same principle, that endothelial-derived dilating agents like prostacyclin and nitric oxide are not as operational as they should be or the smooth muscle tone is enhanced or they just don't have the ability to deliver blood to the distal regions because there may be inflammation in the tunica intima.

So again, the diagnostic framework is as follows. So if I'm considering this may be an ischemic wound, is it an atheroembolic phenomenon from a proximal upstream source, which I'll submit to you is probably about 50% of the time, either plaque rupture or cardioembolic source. Is it a thrombotic event because the patient has an atrial arrhythmia? Is there a coagulopathy that we need to consider, which as, most folks know, this is a very big part of our service from our section. Do they have a primary vasospastic disorder, such as Raynaud's phenomenon, secondary Raynaud's from an underlying autoimmune condition? Is it a medication that's causing it? In my practice, I see Vyvanse causing that, so bad sometimes it can cause ulcers on the extremities, or is there an environmental trigger?

One that's quite rare is a Martorell's ulcer. In patients that have very uncontrolled hypertension, you can actually get wounds on the extremities from this. So this is a good one just to keep in your back pocket when you're seeing your outpatients in cardiology. And then finally, as I mentioned, rheumatologic disorders such as Buerger's, scleroderma, CREST and cryoglobulinemia, which we'll hear a bit about today. Finally, it could be multifactorial. So overall, this patient, we did obviously say stop smoking because tobacco abuse is a strong driver of Buerger's disease or TAO as it's now known as. Ischemia, certainly medial calcific disease was on our differential. But in terms of the autoimmune phenomena, it turns out this patient actually tested positive for an anti-centromere B antibody, which would be consistent with limited scleroderma, even though the patient also had atherosclerosis. So you can see how it's easy just to dismiss a wound as having one etiology when it may actually have a mixed etiology that needs attention.

So what did we do for this patient? Well, we gave oral vasodilator therapy, in our practice there's various things you can use. A nitric oxide donor like sildenafil is reasonable. I made the decision at this point to stop aspirin because it does inhibit endothelial-derived prostaglandins from basically relaxing smooth muscle. We put the patient, at this point, on monotherapy of P2Y12 receptor antagonists. This was more than six months after her primary MI, and to minimize vasospasm, we also decreased her metoprolol. Actually, one of you just sent a patient to me last week for this very reason, and the symptoms went away of peripheral vasospasm with just decreasing the beta blocker dose. So just keep in mind that that may be something that precipitates vasospasm. And of course we gave nicotine replacement therapy.

So the ulcer healed, but recurred two months later. And so we changed some of the medications slightly. We did add a phosphodiesterase 3 inhibitor, pentoxifylline, in part because it's got known anti-inflammatory properties. And so that would serve our patient quite well. So the ulcer healed, but then recurred one month later. So now it's getting a bit more difficult. And so what we had decided to do was admit the patient for treprostinil, which is basically a prostaglandin analog, which can be done. And we have admitted patients here for that reason, to basically promote vasodilation and allow the wound to heal. The ulcer healed, but then came back two months later. So at this point, a decision was made to give the patient botulinum toxin to close down some of the sympathetic innervation to that particular blood vessel. And we found that the ulcer healed again, but then once again, it came back. So this was obviously a complicated wound.

So what was done this time? Well, now I'm really starting to worry. So I phoned a friend. I called up a medical school classmate who's a hand surgeon, and ultimately the patient underwent a digital sympathectomy and did quite well. So just showing before and after sympathectomy. Obviously didn't give perfect tracings, but you can see some improvement in some of the blood flow to the acral areas.

So in summary, digital ulcers, the etiology and understanding it is critical. That's where a section can be most helpful to serve you. Local wound care is critical. Medications, we maximize vasodilation through about six or seven different means. Minimize vasoconstrictors. Those are the usual suspects if your patients are on them. And then antiplatelet therapies, I prefer those that don't promote vasoconstriction and might even promote vasodilation. I have used dipyridamole a couple of times, minimize environmental triggers for spasm. And then lastly, just know that interfering with sympathetic tone is something that we can do. Thank you so much.

Announcer:

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