Well, it's 4.30, so in deference to those of you who have come to this course on a beautiful Friday afternoon, we'll get started on time. My name is Andy Komen, and I'll be moderating. Other panelists are David Roosh from Durham and Chris Peterson from San Antonio. You can actually send your questions on your iPads, or you can come up and talk on the microphones, whichever is easiest, if I could have, I guess, that's good, so I don't have anything to disclose. I'll talk a little bit about the evaluation of upper extremity occlusive and vasospastic disease. Then, Dave Roosh will go into some detail on managing vasospastic disease and Chris about occlusive disease with some newer options. Now, upper extremity vascular disease is actually a significant societal issue and is increasing in frequency. Occlusive disease in one study showed 14% of workers who used their hands as a hammer actually get occlusive disease with not necessarily very symptomatic, but some symptoms and ulnar artery thrombosis. Peripheral vascular disease is increasing, and vasospastic diseases can be a significant problem. Now, thermoregulatory dysfunction affects millions, and cold sensitivity affects 10% of the population and 20% of women, and abnormal control of the microvasculature does impair health-related quality of life. A little bit about Raynaud's phenomenon, disease, syndrome, and vasomotor changes in vasospastic conditions, and Dr. Roosh will go into these in some detail as we go along. But occlusive disease includes thrombosis, aneurysm, and embolism. For all of you who now have these fancy new electronic medical records, you can see there are a lot of codes, and just wait until you get to ICD-10. Like is Raynaud's and vasospasm, and those are the things that we'll talk about. And here's just an example of occlusive disease with an ulnar artery occlusion here, and multiple emboli and occlusions distally. Now, what do all of these have in common? They produce pain, they impair quality of life, they cause functional limitations, they can result in ulcers and infection and gangrene, and all of these patients have cold sensitivity, and as you'll see, treating them doesn't often help this, they'll still have problems with that. When we look at it, we need to determine which they have, and we can start with obviously history, examination, testing, going a little bit about the natural history, because that helps you to determine how you want to treat them, and what are the classifications. So history we start off with, and unfortunately the history is often very nondescript. It's one of vascular insufficiency or peripheral nerve irritation, often from a mass effect. Occasionally you have problems with obviously color changes, which they'll talk about. The symptoms are similarly often nondescript, with pain, cold intolerance, neural changes, and occasionally a mass. You want to know if there's a history of trauma, and this is very important. Do they have a coagulopathy of some kind? And it's often helpful to ask if they ever had DVTs, if they ever had a pulmonary embolus, but a question that frequently is not asked, is anyone in the family, your mother, sisters, had a history of stillbirth? Because that is actually fairly common in some coagulopathies, especially factor V Leiden. Obviously in women, is there a collagen vascular disease, but occasionally men, trouble swallowing may be the first sign of scleroderma, and not color changes, but color changes in the finger. And do they use their hand as a hammer? I had to take my car, I went to a friend's house to go to play golf, and the first thing he did was back into my car. So I took it to the body shop, and the first thing the guy comes out and bangs the car with the palm of his hand. I said, please don't do that, I have to fix it. And he said, my hand's okay, but can you look at my shoulder? So you never know when knowing this stuff will be helpful. And we looked at a study in baseball catchers, and they actually have problems with their index finger and with their ulnar artery. Now Raynaud's disease, go over this very quickly, it's in your handout, and this is something we often don't see. These patients don't get ulcers, they get better when they're older, they don't have systemic diseases, generally women. So hand surgeons don't see these patients. What we see are the patients with secondary Raynaud's or Raynaud's phenomenon. And if you look at that, like Raynaud's disease, they have triphasic color changes. Many of these patients will be sent to you with the diagnosis of Raynaud's disease, and they don't have that, they actually have Raynaud's phenomenon. They tend to be a little bit older, women are more frequently involved in both. And the key thing here is, is that in phenomenon, you have abnormal lab tests, you have asymmetric findings, not infrequently, and you have trophic changes. That's really the key. And so the key to this is if you have vasospastic disease, and Dr. Rusch will go into this, and secondary thrombosis, that's when you get digit necrosis. You really don't get structural changes without occlusive disease superimposed on vasospastic. Now how can we look at the upper extremity vasculature? So it's helpful to assess vasomotor tone, to look at their response to stress. You can do this just by asking them questions. You can get often just seeing you is enough stress, and you'll start to see the problems in the patient's hand. You can look at nutritional versus non-nutritional blood flow, and I'll show you a little bit of that. But that really isn't as important as looking at what their pressures are, and seeing if they have structural damage. Clinical exam, obviously a patient with a non-healing ulcer. And we see changes in skin, temperature, texture, ulceration or gangrene, and trophic changes. Their pulp just may be atrophic. They can have little splinter hemorrhages and other findings. They can have a mass. Here's a patient with an ulnar artery aneurysm, and they can have a thrill or bruit, but this is very unusual. Lower extremity, you have thrills and bruit. You really don't very often in the upper extremity. And then you can do an Allen test, just shown here schematically. The important part of this is, and here you see no flow through the ulnar artery and then flow through the radial artery. And the key here is you have to put a fair amount of pressure, about 11 pounds of force or the blood will go through. Coagulation studies, we get these routinely, and I'll show you some of the significance of this. Factor V line, we get protein S and C, antithrombin 3, homocysteine, and then of course look for collagen vascular disorders. And this has a significant prognostic effect. George Kloros reviewed our patients with greater than two-year follow-up. 37 had systemic disease. Those patients had, after this is short-term successful reconstruction of a radial or ulnar artery, they were all patent at six months. When we looked at them at two years, if they had any systemic disease or abnormal coagulopathy they had 83% patency. And when we looked at the ones that didn't have that, just post-traumatic, we had a 93% patency. This study actually had, for six weeks, 100% patency. And then a patient had the audacity to come back and so we dropped it to 93%. But they can occur late. You can look at Doppler and you want to hear a nice triphasic sound. Stenosis is higher pitched and occlusion obviously is very blunted. And the key here, I think, is looking at the digital brachial index, which is the ratio of the digital pressure to the brachial pressure, digital blood pressure over brachial blood pressure. And if it's less than 0.7, you have symptoms and disability. And if it's greater than 0.7, you have minimal symptoms. So this is very, very helpful. If you look at it, if it's less than 0.5, you can have severe symptoms. These patients don't heal if they get a cut and they can get gangrene. Now we've looked at these in some detail to verify that this actually, those digital pressures do correlate with much more sophisticated tests looking at upper extremity vascular evaluation using temperature to look at thermal regulation and laser Doppler flux to look at vasomotion, which is a surrogate for actually nutritional blood flow, which is where all the money is actually, is in nutritional blood flow. That's what keeps your finger alive. That's what keeps you from not hurting. And we can actually look at nutritional blood flow directly using a vital capillaroscopy where we use a microscope, taking advantage of the fact that the digital capillaries are parallel, just approximate to the nail bed. And by looking at that, we can actually look at, these are papillary, capillaries, digital, and you can actually measure the flow. And this correlates with laser Doppler, does not correlate very directly with temperature, and correlates with symptoms and prognosis. So vital capillaroscopy gives you a direct measure of nutritional flow that's in these capillaries. And as we'll see in patients with vasospastic disease, they shunt proximally and they may have adequate flow, but even in the face of ischemia, they're shunning and they have decreased nutritional blood flow. Here's just an example of a patient that had sympathectomies, and you see pre-op. Here's normal and post-op, they improve, but they don't get better. You just maximize the nutritional blood flow. We can also look at laser Doppler for fusion imaging. This is a little bit different study. Here's an ulnar artery thrombosis pre-op, contralateral hand, red is good. We actually analyzed this with grayscale, but the red is good, and black and blue are bad. And here we see post-op, here's the pre-op and post-op at three and a half months, with a successful reconstruction that you can improve this. The gold standard still is arteriography. We use subtraction techniques, we warm the patient, we give them the newer contrasts, which are less vasoreactive, give them nitroglycerin, and here you see sort of your worst case scenario. Here's a patient with an ulnar artery aneurysm, classic corkscrew appearance, and a thrombosis of the radial artery at the snuff box. Now when we look at this, there are a myriad of normal anatomic findings. What they all have in common, if you go back and look at Coleman, Sherm Coleman's study with Barry Anson from Chicago, there are hundreds of variations. What they all have in common is at the metacarpophalangeal level, there are three common volar digital arteries coming from somewhere, the deep arch, the superficial arch, retained median artery. So you just have to remember that. If you don't see three common digital arteries at the metacarpophalangeal joint level, it is abnormal. Now what about the natural history, which of course leads us to why we should operate or not operate? Well, it doesn't matter what you do, there are going to be some symptoms. Ulnar artery patient, even with a good reconstruction, when we looked at these patients carefully, they still had some cold sensitivity. They got better, they returned to work, but they had problems. And what's our goal? It's really to restore nutritional blood flow. Pulsatile flow, which responds to stress, is your goal that is then delivered to nutritional capillaries. Patients with hypercoagulable states have poor prognosis and they'll thrombose off. Vein grafts, we used to think that they'd stay open if they're open at two or three years. We've now looked at patients and they thrombose over time. So in younger patients, we're using artery grafts. And the patency still can be 80 to 95%, but if you have coagulopathies or systemic disease, it drops down. And that sympathectomy improves nutritional blood flow. So what about occlusive disease? So there are three groups. The first is they have good collateral circulation, near normal sympathetic tone. Those are those 14% of patients I talked to you about out of a study in Australia that had never gone to the doctor, who had good collateral flow, didn't have significant vasospasm, and they did very well, often with nothing or if they had some problems, resection and ligation and they did quite well or a sympathectomy. In group two, they have good collateral circulation. Their DBI is greater than 0.7, but their sympathetic tone is abnormal. So these patients have symptoms because they have vasospasm. If you resect and ligate these patients or you repair their vessels, they have a good response. So this is the fun ones. Whatever you do, they're going to do pretty well unless you personally harm them. And then group three, with poor collateral circulation, abnormal sympathetic tone, abnormal laser dopplers, all of those things, but their digital brachial indices, and these are available in any hospital that has a non-invasive lower extremity vascular lab. They can do these, and they can do them quite well. In these patients, arterial reconstruction is necessary, and these patients, if they have a patent arterial reconstruction, will have a good response. So what defines poor collateral circulation? An incomplete superficial arch. So here you see, well, you can't tell what's going on because everything's clotted. Thrombosis past the common digital arteries. So it doesn't make any difference what happens if you have a clot here, if it goes past where the common digital artery comes off. And I had a doctor call me one time, and he said, I read your article, and is it okay to tie off the artery? And I said, well, of course it is if there's good collaterals. And the patient came to me three months later with hemoclips here, that's not this patient, here and here. And I had to do a reconstruction with a blind patch and endocyte and asthmosis to all three common digital arteries. So you need to have good flow. Embolism, obviously, here's a patient who has proximal occlusion and distal occlusive disease. So this type of patient would benefit from a reconstruction, even if they appear to have good refill here, because that will increase the pressure head. Diffuse lesions and injury to the parallel vessels, like the patient we saw before that had a radial artery and ulnar artery difficulties. Now in type 3 patients, that's the patient with poor collateral circulation, if you have a patent graft, they will get better. And with late thrombosis, they'll recur. Patency is obviously impacted by technique. Arterial reconstruction increases both total flow, that's temperature, and nutritional flow, laser Doppler, vital capilloscopy. And sympathectomy after occlusion improves nutritional flow. So if they're occluded, and you want to maximize the flow that gets into the end organ that provides nutritional sustenance, you need to do the sympathectomy, and you can do those simultaneously. Obviously, a reconstruction is a very good sympathectomy. So here, unfortunately, we have an experience with three patients, four patients, actually, with poor collateral circulation, and they re-thrombosed. One of them was a radial artery. I did bilateral radial arteries on this woman, and I made a horrible mistake. I sent her to our arthroscopist because her knee hurt. So this radial artery, she had this nice, big, pulsing artery on the top of her hand, and the anesthesiologist put an IV in there, never got it to come back, and her symptoms came back. So that's one of these four patients. After successful reconstruction, if they thrombosed, you get recurrence of symptoms, deterioration of function. If it's critical enough, you can get ulcers or sores, and their vascular perfusion radically changes. And if you can restore this with either arteriography and retovase or something to dissolve the clots or reconstruct them, they'll do better. So adequate collateral circulation exists in type 1 and type 2, and persistent but decreased symptoms occur, but they have good function. Inadequate circulation, they won't get better unless you reconstruct them, and that will improve their symptoms, function, and their flow. And re-thrombosis makes the problem worse. So what we're really talking about today are these types down at the bottom. We have group 3 vascular injury, occlusive embolism, but we're really talking about up here, Raynaud's disease, which we don't usually have to treat, and Raynaud's syndrome with inadequate circulation and inadequate collateral circulation. Many of these have collagen vascular diseases, and Dave Rusch is going to talk about these in some detail about the use of sympathectomy. In vasospastic disease, this time course is variable. Many of these patients have an ongoing systemic illness, and you can't fix that, and it's important to let the patients know that. Ulceration and atrophy demonstrate an occlusive component. The diseases are control of significant variables, disease control, and arterial reconstruction, if you can do it, will increase total flow and nutritional blood flow, and sympathectomy will maximize the nutritional component. So it's crucial to have a careful evaluation of these patients with appropriate testing and to base your treatment. This is not, remember that 83%, if they have a systemic disease or coagulopathy, 93, 95%, there's only one series in the literature that is not mine that has 100%, and it doesn't have sufficient patency, and it really doesn't have sufficient follow-up. When you follow these patients long enough, even with good vein graphs, you start to see problems at 10 or 12 years. So the treatment should be based on the pathophysiology as well as the natural history. And our treatment goal is, as I said before, to restore pulsatile flow that's responsive to stress, normalize vasospasm, and if you do that, then you'll maximize nutritional flow. Thank you very much.

upper extremity

occlusive diseases

vasospastic diseases

thermoregulatory dysfunction

cold sensitivity