Welcome back! This week, we are going to talk about acute lower extremity ischemia. This is our last week of our six-week modules with the, hopefully, most common things that you see when you're working in the hospital, and I trust this has been valuable. I'm going to appreciate your time and engagement with it. So, we'll get started. So, acute lower extremities ischemia, the incidence is, to me, more than what I would have thought. 1.5 cases per 10,000 persons per year, and again, this is patients that are showing up in your EDs with significant ischemic limbs, and I'm going to show you a picture here in a minute. Presentation greater than two weeks after event changes the diagnosis to chronic lower extremity ischemia, and we typically have two etiologies, so either an embolism that's traveled from somewhere or a severely diseased arterial area in a limb where thrombosis has occurred related to plaque rupture and that kind of thing. Now, that is excluding trauma. All right, so, etiology, as you see, we're giving you a visual of what this looks like. Just looking at that leg, it feels, looks cold and numb and painful, numb and painful, but that's how these patients present. So, typically, it's acute lower extremity ischemia due to arterial occlusion, high morbidity, mortality, and limb loss rates. These are a big deal and, typically, an emergency and things that need to be managed fairly quickly at least to come up with a treatment plan. So, what do we see and what do we listen or what do we hear from these patients? So, sudden cessation of blood supply and nutrients to the tissues and the distribution of the vessel including skin, muscle, and nerves. So, that's important because when we look at the symptoms, it's going to include all of those. The symptoms can be variable with onsets from hours to days, with new or worsening claudication, so pain with activity or pain with walking, to sudden paralysis of the affected leg. So, we've seen them kind of a slow onset and worsening or just quick, acute, fast, and now suddenly we have a severely ischemic limb. The symptoms are the six P's. So, number one, pain, two, pallor, so color's changed, three, poikilothermia, so cold, cold leg, four, pulselessness, five, paresthesia, and six, paralysis. So, what do we see on exam? The skin is going to be cool. It's going to be, you know, the poor color such as I showed you in that picture. Your neurologic exam, you're going to want to check strength and sensation, and likely both of those are impaired. Pulses, you're going to compare to the contralateral extremity. So, that's one thing that's nice about having two, but you want to check all the way down. So, femoral, popliteal, dorsalis pedis, and posterior tibialis, and oftentimes with these, they may not have a pulse. You need to get your Doppler out, and even then, you may not find a pulse. That's the whole reason they're here. So, as we think about how severe this might be, and if there are pulses that even are Doppler-able, doing an ankle brachial index can be extremely helpful. So, this is where we're comparing the blood pressures and the upper extremities to the blood pressures and the lower extremities, and we're doing a little bit of math. So, the ankle systolic pressure divided by the brachial systolic pressure, and anything less than 0.41 would be indicative of severe peripheral arterial disease, and therefore requires pretty emergent high acuity type treatment. So, we'll talk about that. So, diagnosis generally, these are made by history and physical exam. It's pretty hard not to see that cold leg or extremity. Timing is based on category of ischemia modalities available, so I'm going to show you and kind of walk you through a classification structure. Options for further diagnosis are catheter-based arteriography, so if we're actually going to go in and shoot dye into that leg or limb and look for the blockage. CT angiography will give you a similar, and then MRA is another important modality. So, again, depending on your organization and the modalities available, and then some cases the concern or it's such an emergent, we're concerned about loss of limb, that urgent revascularization with no imaging prior, they go straight to the lab, and we're looking to fix whatever we find, similar to what we would do with a STEMI. So, differential diagnosis includes chronic limb ischemia. So, if this has been longer than two weeks, is it a new acute issue? Not that they don't need assistance with chronic, but how acute is it? Acute compartment syndrome. So, tissue pressures exceed perfusion pressure. I'm going to talk a little bit more about that in a bit, but there are several things that can cause that, and that, again, is a very painful scenario, and then something called phlegmasia, which is an extensive deep vein thrombosis with accompanying superficial vein thrombosis, so loss of venous clot that creates a backup of the arterial flow that can make it look almost like an arterial occlusion, where really it's a vein issue. Not that it still isn't an emergency, but the cause is a little bit different. So, when it comes to arterial occlusion, there's really four different areas. There's the native arterial thrombosis, so it's a clot that happens because of atherosclerosis, an aneurysm, a dissection, arterial entrapment, ophelia, or a low flow state, so that's actually native to that artery where it's at. There's arterial thrombosis post-intervention, so we had a vein bypass graft, maybe there was a prosthetic graft, an angioplasty site, or a previously stented site. Those are going to be higher risk, and you get clot back into that area that you fixed. Then there's arterial embolism, so it may come from another source and land there, so there's the cardiac source, so aphids, something along that line, other arterial source where there may have been a clot, and then a paradoxical embolism, where it comes from the venous side, but crosses over maybe through a hole, like an ASD or VSD, that somehow that venous gets into the arterial system. And then finally, there's arterial injury, that one may be iatrogenic, thromboembolism, from something that we've done, related to a previous procedure, or a closure device, or device embolization, and then there's traumatic. Again, either way, you have arterial injury that that clot then begins to form. So I talked a little bit earlier about how do we manage? Well, we manage based on risk stratification, and one of the classic ways we have of doing this is through the Rutherford's classification. I provided the full document to you as part of the references, but you can kind of read through there, and the goal here is to figure out what's viable versus non-viable, and depending on symptoms and what you see on signs and physical exams, it'll get you a little better idea of if you have viable versus non-viable tissue, and there's a reason that's important, and I'll show you that in just a minute. So, initial management is, again, vital signs, start your ID. There's a lot of labs, so there's some things we're looking for, so certainly chemistry panel, CDC, coagulation, if we're thinking about taking them to surgery or some sort of an intervention, but lactic acid, myoglobin, creatinine kinase, so CPK, LDH, those are all going to begin to give you information related to viability and or how much ischemia has occurred, how much death of that muscle. If there's been a lot of muscle death, your myoglobin is going to be really high. Same thing with your lactic acid. You're going to have a lot of anaerobic metabolism that's really going to drive that lactic acid up, and some of these patients can become quite acidotic, so checking our tier of blood gases can be helpful, and then, again, if you're worried about a thrombotic state, then a hypercoagulable workup with a protein CNS, an anti-cardiolipin antibody, and antithrombin 3 are all very helpful, and then adding a urinalysis to that as well. Just, again, look for other systemic issues that could potentially be an issue as you look to intervene on these patients. Echocardiogram is helpful, mostly for a pre-op. If you're going to take them to surgery, it's helpful to know if they've got any cardiac issues, as well as their option for looking for potential thrombus, although, again, if you're really concerned about that, you'd have to do a TEE to really make to rule that out, and then start IV heparin unless contraindicated. There's a clot somewhere, and we need to try to minimize that or kind of slow it down until we can get in there and intervene. So here is an algorithm that looks at who gets surgery and when, or revascularization when, based on that Rutherford's classification, and as you can see, those that get a class 3, they're not in very good shape, and most of those will end up going on to amputation, and this is why, actually, I'll tell you why in just a second. First, I'll give you the options. So the revascularization options include surgical treatment, where we do a thromboembolectomy and bypass surgery. There's endovascular treatment, where we have catheter-directed thrombolysis, so they actually go and inject lytics right into that area where the clot is, percutaneous thrombus aspiration, and go and pull the clot out and or place a stent, and then some do a little bit of both. They take a hybrid approach that is both an open and a closed sort of option there, so lots of different things going on. Okay, this is why. There's a couple things that can happen related to reperfusion complications, so these patients, you don't just fix and then walk away. There's things you got to think about, so the first one is called myonephrotic metabolic syndrome, or MNMS, and when prolonged ischemia occurs, this can cause muscle cell liquefactive necrosis. That's great. They have issues with the potassium ion leaking, myoglobin obviously leaks, CK leaks, they have lactic acid buildup, and a superoxide accumulation, and then when you reperfuse, all of that goes systemic, and when that goes systemic, it's almost like the body is hit with all of these toxins, and you can cause renal failure, so patients can get renal failure from high myoglobin levels as well as heart failure from all of that lactic acid and superoxide accumulation. It can make these patients really, really sick, and so that is, you know, there's, it can be a tough call, and those patients that have a lot of ischemic zone and they've been ischemic for a long time, are we helping them out by reperfusing them or not? Is that area viable, or will we be just be flushing all those toxins into the systemic and causing some multi-system organ failure? The second one is compartment syndrome, so compartment syndrome is where our muscles kind of live in compartments, and what you get is this localized edema and increased intramuscular compartment pressure, which leads to circulatory disturbance and neuromuscular dysfunction, so in that compartment where these muscles are, we reperfuse, but as we reperfuse, they become very edematous, but they're stuck. The skin, the, there's actually fascia, let me talk about that muscle fascia, around these compartments, tightens that, and as those muscles swell, they compress down on the vasculature and the nerves that run through there, and they actually cause more ischemia and more nerve compartment, or I'm sorry, nerve compression, and so the treatment for this, they actually have to go in and open them up and do a fasciotomy and allow that muscle to kind of have a place to go so that it doesn't impinge on the blood flow and the nerve supply. This is one of those things that when you've seen it, you'll never forget it, and so, and I, I have seen it, so it's, it's, there's this thoughts and decision-making that goes into who we revascularize and who is going to have high risk for these sorts of things, so again, if you're working in a vascular service and or on a service where these patients are coming in, this, there's lots of things to think about with this patient population, and that brings us to the end, so again, there'll be several readings associated with this content with a little deeper dive into some of these guidelines with therapies and things to think about, but again, any questions that you have, please feel free to reach out, and again, we are always happy for your feedback as well, so thank you for your engagement. Thank you for sticking with us six weeks, and let us know if you have any questions. Have a great day. Thank you.

acute lower extremity ischemia

symptoms

diagnosis

management options

complications