All right. Thank you. Thank you for the opportunity to speak today. Thanks for the organizers and Jim, thanks for that introduction. Yes, you have to have a little bit of craziness I think. So all right. We're going to talk about sports emergencies, specifically heat stroke, the most serious of our heat illnesses. I have no financial disclosures as Dr. Kendra Nick just mentioned. I am a nephrologist. So I'm not Doug Casa. I think he's going to be speaking at noon in another location. Obviously, Dr. Casa has made an illustrious career informing us about the dangers of heat illness. He experienced heat stroke himself. I haven't experienced a heat stroke, but I've had my knee in the ground assessing whether this is a heat stroke with an athlete. I've also been at the bedside initiating hemodialysis on a patient that had end organ damage because of heat stroke. So that gives me that perspective. And I did have a rectal thermistor once in medical school doing physiology research. So I guess that gives me my expertise. And I did stay at Hilton last night. So here we go. So we're going to talk about some definitions, the scope. And also, most importantly, the identification, the assessment, treatment, and prevention. So football is a popular sport. We wouldn't all be here if that wasn't the case. Thankfully, fatality is rare, but still tragic. There's about 1.1 million high school players in the last estimates, maybe 100,000 participants at the NFL level, college, junior college, arena football, and semi-pro levels. There's an estimated 3 million youth that are involved in community football leagues. So about 4.2 million football at all levels. There are fatalities, thankfully, rare. When we look at those fatalities, most estimates may be 12 deaths per year. And typically, those deaths are indirect, systemic compromise, so exertional or medical etiologies rather than being direct or traumatic related. These are estimates from the National Center for Catastrophic Sports Injury Research. The 2021 data has been reviewed and published, 2022 still in the works. But if you look at this, I have a pointer here, but if you look at the totals for exertional and medical deaths, there were 13, two of which unknown, three of which were exertional heat stroke, eight of which were sudden cardiac arrest, and then exertional sickling or complications of sickle cell trait. So cardiac arrest, exertional heat stroke, exertional sickling, these are the causes of exertional or medical causes of death in football. And Bowdoin et al. reviewed 20 years of this data looking at fatalities in football, and we saw in the last 10 years of their survey still this incidence of medical causes of death. So it points out the need to emphasize identification, treatment, and prevention. So exertional heat stroke, as I mentioned, it's the most serious of all exertional heat illness. Mortality rates are estimated in the literature at 5 to 10 percent. Football, more common than all other sports, right? The time of our season start, 60 percent of the body is covered by equipment or clothing. The size of our athletes predisposing to the potential risk for heat illness. Practice more than during a game. And by definition, really it's an imbalance of heat gain, the inability to dissipate that heat during exercise. It's dissimilar to classic heat stroke. This is an imbalance. There is not a failure of thermogenesis, the thermoregulation, but it's this imbalance of this heat gain, inability to dissipate the heat due to a variety of factors. So it's exercise-induced, it's uncompensated hyperthermia. And the hallmarks of the diagnosis is the syndrome of CNS dysfunction and a core body temperature greater than 104 degrees. So it requires prompt recognition, aggressive whole body cooling to limit that dose of heat, that time in that death zone, that danger zone. So rapid recognition, rapid assessment and then rapid cooling. Because if it's unrecognized, if it's untreated or treatment is delayed or mismanaged, then we get the end organ morbidity or mortality and time is tissue. So that tissue destruction and even tissue death. So this is my infographic, if you can remember one slide and look at the features of this, it's our big men, our offensive linemen, 6'4", 300 pounds. That body mass to surface area ratio, the thermogenesis from muscle mass and fat mass, this is the individual that gets into trouble and their aerobic capacities are different than our skill set player. Our season starts in August. They've just spent four weeks off, going to Disney World, on vacation and then camp starts on the calendar. So the time of the year, that latency period perhaps, the conditioning level as they come into the camp. We've talked about prevention. We've talked about modifications in the ramp up. We've talked about modifications with our coaching staff. What about the conditioning staff? What about the decision to say an offensive lineman 110 yards, 10 reps under a certain amount of time? So sometimes it's the activities that we do, what our practice looks like. Recognizing they're exhausted, recognizing they're gassed, recognizing that they're struggling. And then it's the external factors, right? It's the heat, the humidity, and it's not just the temperature, it's also the humidity and we look at our wet bulb globe temperature because it's the direction of the sun. Is there a cloud cover? Is there wind blowing? What's the humidity level? All things that predispose to the risk for heat illness. And then I'll mention why there's a dog on my slide, but it's the presence of dogs, the absence of fleas. And then remember, it's the CNS dysfunction and that may not be unconsciousness. That may be the irritability. That may be a behavior change. That may be recognition that they're struggling. They're unstable on their feet, but some level of CNS dysfunction. So presence of dogs, these are the things that are risk factors, the primary intrinsic risk factors for our players when we look at primary prevention. Dehydration, at that 2% threshold of volume loss, there's less, you start to begin to see less perfusion to the skin, so that's going to be less evaporative heat loss. At that 2% loss, their coordination, their efficiency, their performance may suffer. So again, if you're inefficient on the field as you practice, increasing that risk of that thermogenesis, that uncompensated hyperthermia. Obesity, again a problem of the big guys. And again that muscle-fat ratio, that body surface area to mass ratio. The garments, 60% of the body may be covered by a uniform. They have a helmet on. I don't know about you, but my players, they want to look right. They feel right. They look right. So they've got hoodies on underneath their uniforms. They're wearing leggings. They're dark colored. So I spend half the time getting our players to modify their practice wear. The S, stimulants, substance, sick. Has the player been ill, gastrointestinal illness, a febrile illness, something that predisposes them to again developing a heat illness? Are they on stimulants for their ADHD? Are they taking ephedra? Are they on antihistamines? Are they on other substances as performance enhancers, but again that may be guilty of causing a decreased ability to dissipate heat? Then I put as the last S is sickle cell trait. Not that necessarily someone with sickle cell trait has a higher risk of heat stroke, but there are overlaps of symptoms and signs that you may see with one of the exertional sickling complications. So you have to recognize that and identify your players that may be at risk. So the presence of dogs, the absence of fleas. So if their fitness is low, so again just starting out at the beginning of the year during that ramp-up conditioning period, their fitness is low, low energy. Is this at the tail end of the practice? Is this after a series of practices without a break, without a day off? As Lee demonstrated, there's a designated day off after day six of that initial ramp-up period. Have they had the opportunity to acclimatize to the location, to the environment, to the workload? So that's very important because we see the physiologic changes that will enhance that individual's ability to dissipate heat. Then finally sleep, adequate regenerative sleep. So studies have shown that people that are in sleep deficit, they're at higher risk for heat stroke. So when we look at primary and secondary prevention, we mentioned smart clothing, medications to stop and adjust, activity adjustment based on that wet bulb globe temperature, assessing the wet bulb globe temperature, documenting that, and then modifying the practice time, the practice content based on those things. We talked about hydration, that pre-hydration and hydration to maintain euvelemia. If you wait until someone's thirsty to hydrate, you're already at that 2% loss. By the time you get to 6% to 10% loss for that individual, level of dehydration, that person, your cardiac output decreases, your plasma volume decreases, your perfusion to your skin decreases, your ability to dissipate that heat. So compounding the issue, especially in our large athletes. So you hydrate before, during, and after, getting ready for that next practice. Intra-event cooling I think has a role again for that primary prevention. And then you have to look at their fitness level. The time and the intensity of the practice design. Position-specific modification, not the 110-yard sprints times 10 under 20 seconds. So the too hard, the too long, the too much uniform and too soon, those are all a recipe for heat illness and the dreaded heat stroke. And then probably the most important thing for our primary prevention is that acclimatization. You acclimatize to the heat and the humidity 10 to 14 days before that first competition because that first five to six days, four to six days, is really critical. It's critical for that individual to adapt their sweat composition, to increase their plasma volume, increase their cardiac efficiency, enhance their heat temperature, and truly lower their core body temperature. So this is in the lab, but this looks at a climatization process. And you can see here in this first four to five days, you see increase in the plasma volume, increasing that sweat rate, a decrease in the skin temperature, a decrease in the core body temperature, decrease in the heart rate. Again, the athlete is in better shape, better condition, better efficiency. So those are the physiologic changes that happen. But if we start out the blocks, day one, especially in the heat and humidity of the external environment, this is a recipe for disaster. So you need that acclimatization period, not only for our soft tissue injuries, but also for this sports emergency, heat illness. So I borrowed this slide, part of it from Dr. Jonathan Drezner with some modification. But if we look at the collapsed athlete or the struggling athlete, our differential, typically four, maybe five things. Sudden cardiac arrest, that athlete's unresponsive. Sudden collapse, they might have a seizure. They may be gasping. Their eyes may be open. They're unresponsive. Sickle cell trait, that individual's in distress. They may complain of back, lower extremity, muscle cramping, chest pain, but the muscles are supple. They complain of fatigue and shortness of breath. We need to be able to distinguish that from our exertional heat illness. Head and neck, traumatic event, signs or symptoms of concussion, neuropraxia, cervical spine injury, impact seizure may be present. But then for this topic, exertional heat stroke, dizzy, headache, gassed, gait may be unstable. They may have a personality change. They're disoriented. They may be delirious. They may have loss of consciousness. Well into the heat stroke, they may have a seizure. So some of those early signs and symptoms, fatigue, they're hyperventilating, they're tachycardic, they may vomit, they may have hypotension. So this individual that's confused may precede the actual collapsed athlete. So how do we tell the difference if this is our differential? Well we need that rectal temperature. We need to have an assessment of this core temperature. It's mandatory. It's important because is it exertional heat stroke or is it something else? Kind of the five H's. Is this heat? Is it sudden cardiac arrest? Is this heart? Is it head? Is it heme? Is it a hematologic complication? Exertional sickling. And then the last would be hyponatremia, exertional hyponatremia. By having that core body temperature both for diagnosis and determination, it also minimizes the risk of poor outcomes. We know how long this athlete is in the danger zone. We identify where they are in the danger zone and then we know how long to cool. Simply by looking at their skin, feeling their skin, they're not hot and dry like a classic heat stroke. They may be wet and warm or the skin could be cool because of that evaporative loss. The skin appearance may be pale or ashen. So the skin can be paradoxical when we're trying to diagnose the exertional heat stroke. Oral, skin, axillary temperatures are inaccurate. They're confounded. If they've been hydrating, if the wind's blowing, if their skin surface is already hot because of the external temperature, it's not going to give us an accurate assessment of their core body temp. And of course it determines when we need to stop cooling because we're gonna cool first, transport second. How long do we cool before we allow them to transport our athlete? So having that rectal thermistor, knowing starting temp is important. And then ultimately if a true exertional heat stroke occurred, that has implications for that athlete in terms of returning to sport, returning to play. And what we say, hey, we're not gonna use the AED because we'd have to expose the chest. I think the emphasis here is this is part of our diagnostic therapeutic intervention. The core temperature is mandatory. This just highlights, this is actually a model of hyperthermia, the need for rapid assessment. If you look at where the red arrow is, the time of collapse or the recognition that they're struggling, the rapid recognition and evaluation, including that core body temperature, determining that the core body temperature is above 40 degrees or 104 degrees Fahrenheit. And then that onset to cooling. So where that asterisk is, that's that danger zone within that rectangle. If it takes 10 minutes to recognize that they're struggling to recognize and evaluate and to begin cooling, far different than if it takes 60 minutes. Because that's the period in the danger zone and time is tissue. That's when the tissue destruction and the potential risk of death. And then that next phase and that delta phase, that's the cooling phase starts. So again, the rapidity in which the cooling begins determines how long that athlete is within that danger zone. Because the cell toxicity and tissue damage are a function of that time degree interval and that duration of hyperthermia. There's a period of reversibility. And realize that the collapse does not coincide with that point of critical core body temperature threshold. So the athlete may have been hyperthermic for some time, it's already present. So the need to rapidly recognize and initiate cooling. So put the pads on, put the probe in. If there's one lesson to take away, we need to have that core body temperature assessment. So diagnosis, recognizing the elevated core temp combined with the CNS signs. Any exertional collapse, you have to have heat illness, heat stroke in the different and treatment, early intervention to cool that time is tissue, get them out of that death zone to restore that normal thermoregulation to prevent progression and initiate that rapid reduction in core body temperature. So this picture here from the Corey Stringer Institute looks at one sample of using a large tub for the athlete. The athlete is submerged up to the neck, has a rectal probe in place. EMS has been contacted, but we're cooling first, we're transporting second. So identifying that starting temperature, whole body cooling with ice water immersion, cool first, transport second. You're gonna cool down to a temp below 39 degrees and that is approximately about one degree for every five minute of cold water immersion, depending on the temperature of your ice water bath, your cold water immersion tub and the complications of heat stroke that we've mentioned. So this is a slide courtesy of exertional heat stroke, mortality in cooling rates and survival, looking at different outcomes. So if you took an athlete from a temperature of 108 degrees, which you're only gonna know by getting the rectal thermistor in place, if you're gonna cool them to 102 degrees down below that danger zone, that's a change about 3.36 degrees Celsius. So with ice water immersion bath at two degrees Celsius, continuing to add water, agitating, oscillating the water to increase the circulation around the body surface area, that takes about 9.6 minutes. If you have cold water immersion, 20 degrees Celsius bath, about 17 minutes. You think about the old school, I'm gonna put ice packs in their axilla and in their groin area, takes 84 minutes to make that 3.36 degrees Celsius change. So important that you're doing cool first, transport second, but the appropriate approach and you have to rehearse it, you have to plan it, you have to have the equipment, the appropriate approach to get the rate of cooling that you need before you transport the athlete. So EAP activation, but you're gonna cool on site, you're using conductive cooling, a large temperature gradient between the core body temperature and the skin, so total immersion, and then also evaporative losses, water to vapor, so having cooling fans, something to rotate the air around that site of cooling. Cool first, transport second, a rate greater than 0.8 degrees Celsius is the best and you can see the more rapid cooling, get them out of that danger zone, how critical it is. Ice water, cold water immersion, usually about 0.35 degrees Celsius per minute, that's where they calculated 9.6 minutes. So to conclude, this is a nice article, exertional heat stroke in American football, what the team physician needs to know, you'll recognize some authors there, Dr. Kasson, Dr. Fran O'Connor, and Jillian Sylvester. And this looks at again, kind of this algorithm, an athlete demonstrates CNS dysfunction during exercise, assess the temperature, their vital signs, obviously no pulse, put the pads on, put the pads on and initiate emergency cardiac care. If the athlete has a pulse, brief history assessment, getting that rectal thermistor, obviously if the temperature is greater than 40 degrees Celsius, we're beginning our emergency action plan for exertional heat stroke. Rapidly cooling with cold water immersion with that rectal temperature, down to a temperature less than 39 degrees Celsius, only then remove from cooling and transport for further evaluation. So to summarize, we've talked about some definitions of exertional heat stroke, the most serious of our heat illness, the risk factors, our sport being one of them, the primary and secondary prevention, number one is that acclimation period, increasing the plasma volume, they're less salty sweaters, they sweat more, that's gonna contribute to their ability to evaporative heat loss, recognizing that dehydration is a risk factor for compromised heat dissipation. That rapid recognition assessment and cooling, put the probe in, cool first, transport second, these are preventable emergencies, these are preventable deaths and we all need to be accountable. So I'll conclude by saying, if you fail to plan your plan, you fail from that great athlete, Benjamin Franklin. He is in the Swimming Hall of Fame, by the way, he invented the first set of swim fins, so he is in the Swimming Hall of Fame, but have an emergency action plan, have the medical knowledge, practice and drill, walk through the scenarios, be ready and everybody know their roles. And I'll conclude there. Thanks. Thank you.

sports emergencies

heat stroke

exertional heat stroke

organ damage

preventive measures

emergency action plans