So the next talk that I get to give is going to be on chemical and frostbite injuries. Not the sexiest of topics, but it comes up every year on the exam, typically multiple questions every year on the self-assessment exam. A quick word on about terbutaline for pressure infiltration. There have been a number of threads in the last year or two on the list about dwindling supplies of fentolamine. This is just to have in your handout about use of terbutaline for pressure infiltration. Don't forget also about 2% nitroglycerin paste. Again, lots of questions. Some might even argue disproportional on frostbite and chemical injuries in the last many years in self-assessment examinations and on the certification exam. Why? Skin's important. It's the body's largest organ. It's a vapor and moisture barrier, thermoregulation, homeostasis. It has immunologic functions, mechanical functions, and a strong aesthetic component. This is what everybody can see. How severe the injury is depends on how concentrated the agent is, how long it was in contact, how deep did it get, how much of it was it, and how did it get there. Was it a splash? Was it an immersion? Was there a wound there to begin with that the chemical then got to? Moving on to more specifics, alkali or base injuries. These unfortunately can get deeper because of what they do to the tissue. They saponify the fat under the skin, which unfortunately lets the alkali penetrate deeper as it goes. Agents include lime, bleach, sodium hydroxide, potassium hydroxide, cement. What are we doing for these? Water, water, lots of it. Hopefully that's already happened before the patient has come to us. A little bit in contrast, acid injuries. These damage by hydrolysis of proteins. The one thing that is primarily different is as they do this they generate heat which can actually cauterize the wound bed and to some extent prevent deeper penetration. So if you had to pick one I suppose you would pick an acid. Hydrofluoric acid, sulfuric acid, hydrochloric and phosphoric are common ones that we see. A quick word about hydrofluoric acid. It injures both as an acid but it also injures as a leacher of calcium and magnesium. It literally can pull them out of the blood. It can even pull them out of the bone if given enough time and these really, really hurt. If a dilute chemical exposure occurs also your patient may have had hours of contact time before it starts hurting and they come to see you. What are we gonna do for them? Topical calcium gluconate. You can also inject calcium gluconate under the wound bed or into the arterial circulation heading out toward the limb that was affected. Slightly in contrast, phosphoric acid will also pull calcium out of the body and we treat it with topical copper sulfate. Do not inject copper sulfate. Don't worry, your pharmacy won't send it to you if somehow you ask for it. Copper sulfate intravenously will kill your patient. This is the first of a number of fairly busy tables. Don't worry, they are all in your handout. I put them here so that when you're looking back at this afterwards you have all these categories of type of agents, what are they doing to the tissue and then what are our first line treatments. There'll be a number of these and they'll come up again where I highlight different areas. Lot of questions on the self-assessment exam. So the first one you've got or occur in a chemical plant with a hydrofluoric acid spill. Presents to the ED with a burn to the dorsum of the hand. Still hurts despite copious water dilution. What are we gonna do? Again, calcium gluconate is your agent of choice, both topical and injected. Moving on to chemotherapy, infiltration and extravasation injuries. Two major groups, they're the irritants that are not inherently toxic to human cells but do cause inflammation. And then there are the vesicants that directly kill human cells. Not surprising, that's what in theory we want the chemotherapy to do but only to the cancer cells. These are gonna cause blistering. They come in two flavors, DNA binding and DNA non-binding. There are gonna be a number of tables in here. Again, don't worry about frantically writing them down. They're in your handout with several iterations including the source in case your handout didn't print clearly enough to make sure you can see them. Recent retrospective review of a Japanese study, 44,000 chemotherapy infusion center. This is probably more useful practice information than test information. Fortunately, these are rarer than they used to be. We're using more PICC lines, more ports, fewer peripheral IVs. Not surprisingly, the longer the infusion, the more likely the infiltration is to occur. And when did it occur? When the patient got up or sat back down to go to the bathroom was one of the most common times. Grading of injury, again, this table's in your handout. But basically, more blanching, more pain, more immediate visibility of disruption of the skin with blistering as the injury gets more severe. Again, just more injury factors associated. And here are the agents. Unfortunately, it's a long list. This is less likely to be tested. This is just in your handout for completeness sake. Here's the important part. What do we do? Hopefully, several of these steps have happened before you get called. First and foremost, stop infusing. With the catheter that is in, aspirate anything that you can get out. Then get the catheter out. Then elevate and splint, like we would for any hand injury. Marking the area of extravasation is important. You want to track this over time. All of our phones have cameras on them now. Photo documentation is typically very useful because you want to see how is this changing over time. Is this getting better? Is it getting worse? Back to the self-assessment exam. The soft tissue injury that occurs as a result of extravasation of IV fluid, what property of that fluid is gonna correlate with severity of injury? So this is actually osmolarity. So these are the patients who get D50 infiltration, radiocontrast infiltration, where a small amount of liquid draws in a lot more liquid to balance its hyperconcentration. These can lead not only to tissue injuries, but even in their most advanced forms, compartment syndrome. That'll get covered in a different talk today. Moving on to chemo infiltration injury specifically. Unfortunately, you will see agent-specific questions on the exam. There have been a number of them over the years, but I will go through them as we go. Specific classes, the vinca alkaloids, the anthracyclines, mitomycin, the platinum-based agents. But don't forget there are also pressor infiltrations that you may see in nutritionals, like TPN and PPN, that can all cause injury by their mechanisms, which I'll go into. Again, another very busy table. This specifically about anthracyclines, Donorubicin and Doxorubicin. And the drawing on the right is what's called the GALT technique. This was a case, had a historical control series. The idea was if you know where the agent got in, infiltrate fluid and then suck it out as best you can, you may get better results. So in GALT series, he got less tissue destruction, less need for debridement and grafting than a historical control group where he didn't do this. So this is called the GALT technique. Again, self-assessment exam, extravasation of Doxorubicin into the antecubital fossa. Early treatment measures that decrease the extensive tissue loss include, again, the GALT technique, saline washout. So what's been on recent exams? Antidote agents, unfortunately these come up commonly. This is in your handout, so you can just glance through this as you get close to your testing day. The anthracyclines, dexrazoxane or dimethyl sulfoxide and cold saline irrigation. Vincristine, that's one of the exceptions. You actually put warm on the vinca alkaloids. I'll mention this again a couple more times in the talk. Meclorethamine, sodium thiosulfate and cold. Radiocontrast elevation, pretty much all of these are gonna be elevation and splinting, radiocontrast included. Bleomycin is the exception because you don't do anything for it other than elevate and splint it. So again, this is meant to sort of include many of these things on one single slide. Elevate, get as much of it out as you can. Document where the problem is starting at. Elevate and splint like we would for any hand injury. Cold for the vesicans except the vinca alkaloids. They get heat. Dexrazoxane for the anthracyclines. Again, that's downerubicin and doxorubicin. Fortunately, these are not typically operative. In theory, with any of the hyperosmolar agents, actually, fasciotomy might be a surgery that you would need to do if you're gonna get a Holden type two compartment syndrome. Less commonly, and again, as more and more of these are given through PICC lines and ports, very uncommon for us to have to do debridement and skin grafting. Much less common than it was in the 70s, 80s and 90s. This is the next of the very busy charts. Don't worry, it is in your handout. In the PDF form, it is magnifiable. I'm gonna focus on a number of different areas of this. Also, the citation is there if you want to pull it up online in an even more magnified form. What I like about this is it has all of the agents in one place, and kind of a flowchart of what you do with them. A slightly more simple line drawing, but the same agent. What are we doing, depending on if it's a neutral agent like bleomycin, an irritant like cyclophosphamide, or a vesicant, either a vinca alkaloid, which doesn't bind DNA, or an anthracycline like doxorubicin that does bind DNA. Just to have it all in one table. Back to the self-assessment exam. Following extravasation of epirubicin, so this is like a donna or doxorubicin and anthracycline during chemotherapy. What do we do for them? Well, all of these are to some extent correct, but the one specific thing for this is destrazoxane. And actually, heat is incorrect. DMSO and sodium thiosulfate are incorrect. You would technically remove the cannula, but E is more correct for this question. Again, the same drawing. Same test, but a different question that asks essentially the same material. These show up a lot. Why? Because we can give very algorithm, there's a right answer and a wrong answer, so these show up, again, you'd argue, somewhat disproportionately. Which of the following does not, I'm sorry, cold therapy is not indicated for vincristine extravasation because, again, the vinca alkaloids, they're gonna blister with cold, they get heat. Skin ulceration is what happens if you forget and you give them cold. 44-year-old woman with breast cancer is getting doxorubicin. The outpatient center notices an extravasation into the skin on the dorsum of the hand. What are we gonna do for this? Again, doxorubicin and anthracycline. We're gonna apply ice, these get cold. Destrazoxane would have been another acceptable answer, but wasn't a choice on this one. Warming is not appropriate, that's for the vinca alkaloids. Again, the University of Kansas drawing, this is just highlighting where doxorubicin is on it. Systemic antidote for the treatment of an anthracycline, we just covered this. Again, these are all different questions, I'm not repeating these, these are all individual different questions that have shown up, we ask this a lot. Destrazoxane. Again, the University of Kansas table. In the course of a CT scan, so now we're in radiocontrast hyperosmolar, but not directly tissue toxic. You've got contrast that extravasates into the antecubital fossa. This is a call I get about once a month or so from outpatient therapy. What do we do after elevating and examining the patient? If it's warm, if they're neurovascularly normal, they don't need anything else. You watch them for a period of time, and if they are normal and the skin is perfused and has capillary refill, you don't need to get fancier than that. Which of the following agents is used at the site of meclorethamine? So we haven't asked that one yet. For extravasation, meclorethamine is gonna get sodium thiosulfate, and this is just a quick table, again, with some of the things we've talked about. Again, the University of Kansas table. Proper treatment for extravasation of encristine. Again, a couple of things that would be the right answer, but only one of them is available on this one, and that's hot compressine. It's a hot compress and hyaluronidase. Again, vinca alkaloids get heat. Most of the other ones get cold. Again, the University of Kansas flow chart. So now I'm gonna move on to frostbite, which is the other thing that shows up not quite as commonly on the test. For those of you who practice in warm environments, you just need to know this, about one or two questions will be on this. For those in the cold environment, this may be fairly familiar to you. So how does this happen? Well, cold exposure relates to a number of things. Obviously, we start with the temperature, but also how windy is it, how humid is it. Moisture and metal conduct heat away faster, and of course, how long was the duration of exposure. Things that increase your patient's susceptibility. I know this has shown up on some of the plastics exam. I haven't seen this specifically on the hand exam. Intoxication, high association with psychiatric illness, peripheral vascular disease. The one that gets tested when it does very often is previous frostbite injury. So they've had a frostbite, they heal, they are now more vulnerable than an otherwise totally equal person to a second frostbite injury with another exposure. What happens when we get cold? Well, first we shiver, then we stop, then we get arrhythmias, and of course, the next step, then you die. This is not the part that we're gonna manage, but just for you to be aware of, if we're called to see a frostbite in a hypothermia injury, this is what the trauma service is gonna be doing that may delay us from doing things that we would wanna do. Again, initially vasoconstriction. Then you actually get cold-induced vasodilation, or sometimes called the hunting response. After that, you start losing sensation, and at minus two Celsius, you actually get ice in the interstitium. Again, very bad scene for the patient. This is a schematic drawing of this. The interstitial fluid, like any solution, if you get it cold enough, the ice will freeze, but it's gonna freeze just the water component. So what happens is the remaining liquid becomes hyperconcentrated, draws the liquid now out of the cells, and you see the cells get smaller and thinner, and they start to lyse as they wrap around these ice crystals. Microvascularly, so this is where frostbite that we sometimes use similar terms to burns kills in a different way, or kills tissue in a different way than burns do. Dave's gonna talk to us about burns in a little bit. You get red blood cell sludging, intimal disruption, and this actually kills tissue from the inside out. The microcirculation fails, and then if that lasts for a long enough period of time, the skin over it dies, as compared to a thermal injury which burns from the outside inward. So this is different from frostbite. We use similar terminology. Unfortunately, we're just stuck with that. Superficial being first and second degree, third and fourth degree being deep. As you get deeper, the blister walls get thicker, the fluid within them gets darker, and they're more cytokines, which are thrombogenic and pain-inducing. Again, for hypothermia, mostly this is what our trauma colleagues are gonna do, but just to be aware of it, know how cold they are, get them warm, monitor them. And equally important, once you get them warm, keep them warm. So some of the things that we're gonna wanna do for them, which I'll talk about in a moment, is testing and interventions. You have to make sure you don't make them cold as part of getting those interventions for them. Rapidly warming, only if they're still frozen. If they are already warm, you don't need to do this just because they came in with a frostbite injury. Again, prevent refreezing is something that we can do as we're starting to do our interventions for frostbite of the hands, and sometimes we're asked about feet too. Topical treatment. There's a little bit of disagreement about what do you do with the blisters, whether you just suck the fluid out or whether you debride them as well. Some overlap with what we do for burns. Silvadene is a good topical antimicrobial, but aloe vera is what's gonna neutralize the thromboxane and the prostacyclin F2-alpha, which are thrombogenic and pain-inducing. Your pharmacy may be able to compound something that has both agents in a single salve. And then just as we would do for any hand trauma, elevate splinting, hand therapy, get these patients moving as early as you safely can. So which of the following is a sign of deep frostbite injury? Getting into the questions. So for these, if your patient is still numb once you thaw them, you have a bigger problem. More questions. The single most important step in the salvage of tissue and thumb function of the frostbite injury. So now this gets into what can we actually do for these patients? What is the test that we wanna do to figure out what we do for them? Well, that you actually can't do right away. First things first, make them warm. We also, in algorithms that I'll show, we wanna use NSAIDs, and why do these help for our patients? Yes, they provide pain relief, but the main way we think they are helping them is preventing platelet aggregation. Again, we've got red blood cell sludging. We've got intimal disruption. All of these things that are gonna be promoting thrombus, NSAID, or even specifically aspirin therapy is hoping to fight against those. So what do we do for these patients surgically? Well, the old dictum was frostbite in January, amputate in July, and that's great for preserving tissue, but that's six months that your patient's had this morbidity. Conversely, if you operate early, you may take off more tissue than you ultimately needed to. So we want a way to predict what's gonna make it, and therefore make our cut level there. In the literature as it exists right now, the study with the best predictive value is nucleotide-labeled perfusion scanning, and triple-phase bone scanning. So for any of you who haven't done one of these recently, the three phases are the immediate flow phase, the one-hour-later blood pool phase, and then the 24-hour-later bone pool phase. That third phase is what correlates the best with what's gonna survive if you don't intervene. And I'm gonna get into what can you do to intervene. Again, strong correlation. Some centers use MRI, and that is getting better data, but if you look in the literature, even as recently as a couple of months ago, the last time I looked, triple-phase bone scan still has the best literature to support its use. And actually, just getting back to keeping your patients warm, this is a major place where you have to be careful about keeping your patient warm. You're gonna leave this area exposed for a long time under the gamma collector, make sure the room is warm, make sure the rest of them is covered. What modality provides the most cost-effective means of predicting demarcation zone following severe frostbite? Again, triple-phase bone scan. Well, what can we do? Can we do anything to help these patients? Well, it turns out we can, and for some of you who practice in colder areas, you may have seen a patient who was treated with this. The articles that have come out have come out of Utah, Minnesota, places with colder environments, that have studied TPA for early intervention to try to save more tissue. Again, what these studies have shown, typically you have to get to them within 24 hours, but if you do, you can save tissue that you otherwise would have predicted would have died. There's some European literature to suggest that illiprost, which is a prostacyclin analog, may help as well. That's starting to be available in the U.S. As far as I know, it's only available, though, for scleroderma patients. I'm not aware of it being available for frostbite as of yet. From the self-assessment exam, a patient's been outside an indeterminate period of time. You've rewarmed them. How are we going to improve digital salvage? Thrombolytic therapy, TPA. Sorry, I'll get through the last of these. This is if you want to read more about this. Another flowchart. This is in your handout, so don't feel the need to frantically write this down. It's all there. And a couple of questions, then I'll stop. Which of the following treatments has been shown to decrease the expected amputation rates when used for acute frostbite injuries? Again, TPA. Why? Because we can ask a question about it. It's got data to support it, and actually, for our sake, it's something we can do, or recommend that interventional radiology do. Which of the following provides early indication of eventual demarcation? Again, that's your triple-phase bone scan. A mountaineer's been outside less than 24 hours. He's been rewarmed. The triple-phase bone scan shows the fingers aren't getting flow. What are we gonna do? TPA. So, not the most exciting of information, but it shows up year after year. The tables are in there so that you can have all the information in one place. Thanks. Thank you.

chemical injuries

frostbite injuries

management

exams

skin effects

chemotherapy infiltration