So, our next speaker is Dr. Best. Dr. Best is going to finish the series of medical issues in sports medicine. Dr. Best has joined us from Miami. Yeah, thanks, Bruce. All right, well, good morning, everybody. Thanks Bruce, and thanks to Chris as well for inviting me back. Hopefully, this is going to be, Bruce did a great job. I still don't know the difference between a parametric and a non-parametric test. So, it's simple, he said, right? Just don't pick Wilk and Cox and rank tests. So, what I want to do in the next 50 minutes or so is take you through, kind of finish up what Dr. Borcher started this morning on the medical side of things, and provide some test questions as well. So, as you can see, I've got a fairly ambitious number of topics to cover here. And this, to be honest, has evolved over the years. I remember presenting this one year at the AOS with Mark Miller, and they gave me 45 minutes to do the entire side of the medical aspects for your exam. So, we've evolved over the years. I want to start with the pre-participation evaluation. This is something that comes up rather frequently, and maybe distills some of the misconceptions here. So, what is its real purpose? Well, to detect medical conditions that may interfere with sport participation. Determine contraindications to participation. Discover predisposition to injury, including previous injuries that may require rehabilitation. Fulfill legal and insurance requirements. The fourth addition, of course, as many of you may know, emphasize the importance of functional testing. And the fifth one is about to come off our desks here soon. But what it really comes down to, and we've learned this, and we'll get this in particular when we talk about the cardiovascular section. And that is that the history is the key, right? So, when we talk about the pulmonary section, we talk about athletes who've ever had shortness of breath, asthma, and seasonal allergies. Dr. Borchers mentioned earlier the whole concept of paired organs, and we'll talk a little bit about that as well. Visual problems. Immunizations is one they like to test, and the reason is the mingococcemia vaccine, right? Let's not forget that, particularly in the college athletes who are living in the dormitories. We'll talk a little bit about heat illness, sickle cell, some of the nutritional issues we'll finish up with, and relate that to the menstrual history as well. Just to drive home this concept that it's really the history, this is something you need to know. And we'll talk more about that in terms of what's recommended now for screening for sudden cardiac death. But to make a long story short, in 2014, here are the guidelines that are still in place from the American Heart Association, and you can take a look at these at your leisure. But this is an important slide to know. This is another important slide, although I'm gonna point out some evolving concepts in this domain as well, and that's the Bethesda guidelines. Why is that important? Well, the Bethesda guidelines are really what drive us towards our decision making when we're looking at athletes who've got some sort of cardiovascular problem. And again, we'll talk more about this in a couple of minutes time. For purposes of this slide, what you need to think about is the so-called static and dynamic components of exercise, and I'll show you a typical question on that as well. There's an important concept, though, that's coming out in the literature. And I'll be very honest, I don't think this is gonna be testable at this point, but you really need to understand this. And that's this whole idea about shared decision making, right? If you think about that last slide, the Bethesda conference, it was a binary yes or no eligibility. When I started 25 years ago, it was very simple. If somebody had manifestations and findings of hypertrophic obstructive cardiomyopathy, they were disqualified from sport. That is no longer gonna be the case, and that's, we'll spend a couple minutes on that later. So really then, we're evolving from this, what I call paternalistic decision making, right? Where it's the doctors, the schools, and the athletic organizations that we're really making the decisions for these athletes. Well, if you go back and look in the literature, the Institute of Medicine in 2001, this is a pretty classical paper when they talked about crossing the quality chasm. And really, this is where we're at right now. And this is something, again, I don't know that's gonna necessarily be testable, because it's only come out in the last couple of years. So let's go back and look at this binary decision making. And so what we used to say is if you had things like marfans, you were disqualified. Well, that's probably no longer the case. So what's out there now, at least in the cardiovascular literature, is three different classes. Class one is it's recommended you can participate. Class 2A and 2B, the eligibility is reasonable or may be considered. And finally, age, or class three, which is not recommended. Again, I don't know that this is necessarily testable, because it's just coming down, but it is starting to drive our decision making. And a great example here is long QT syndrome. It used to be, if you had long QT syndrome, you received an implantable defibrillator, and you were disqualified from competitive sport. That is no longer the case. It's now what's referred to as a class two risk. Dr. Borchers mentioned this earlier as well, this whole idea about the single solitary organ, right? And what you need to remember here is that you can no longer, and this has been around for a while, so it's very testable, right? That the American Disabilities Act in 1990 moved us forward in this field to say, and it really parallels this whole idea of shared decision making, if you think about it. Because at the end of the day, the risk is really with the athlete and his or her family. I mentioned earlier heat intolerance, and this is something that's certainly come to the forefront here in the last little while. And so what do you need to know about this? Well, this is really a tough area. Why? Well, first of all, the predictive value of a first episode and its risk for subsequent problems is not well known. In other words, if you have an athlete that has had a problem, let's say even heat stroke, for example, that doesn't necessarily mean that they are predisposed to further problems. So it's a little bit tricky. There's some suggestion in the literature back in 2013 that genetics may play a role. Sickle cell is probably the one condition we deal with in this country, of course, that you need to always keep in mind, and we'll spend a couple minutes on that later. And finally, as I mentioned earlier, return to play guidelines are not well established whatsoever. So this is probably not testable, but you obviously need to know about heat intolerance, and we'll talk about that later as well. The so-called physically challenged athletes, a couple things seem to pop up every now and then. The first one is the so-called spinal cord injured patient. As we know, they're at increased risk for heat-related illness. That's if the lesion's at T6 and above. And of course, that's getting at the concept of autonomic dysreflexia. These individuals have decreased cardiac output. So as a result, they have decreased stroke volume with minimal compensatory increase in heart rate. So what do they do? Well, they use this technique called boosting, and this is something you need to be aware of, right? And so this is where they try to increase their blood pressure due to the unopposed sympathetic discharge. And then finally, of course, is the Downs athlete and their risk for C1, C2 pathology. And at minimum, you need AP and lateral films, although I would say you need flexion extension views as well. So just to kind of wrap up then, this pre-participation evaluation, we do all these physical exams and so on, and where are we really at with this? Well, first of all, very few athletes are denied clearance, as we know. Some studies suggest up to 10% need further evaluation, and you can see the conditions here, particularly elevated blood pressure, some of the cardiac symptoms, and then some of the musculoskeletal issues that you know better than I. A couple of questions here. First, the PPE is designed to A, substitute for a routine health exam. B, protect the institution from medical legal issues. C, identify athletes with coronary artery disease. D, detect any medical or musculoskeletal conditions that may predispose the athlete to injury or illness during competition. And finally, exclude participation of athletes from pre-existing conditions. Well, we know that one of the primary purposes, right, is to detect any condition that will predispose athletes to injury or illness. But as we're learning from current literature, we're not very good at this, are we, in terms of our abilities to actually predict. In fact, probably the major risk factor, and this is testable, for subsequent injury is having had an injury. So we do a lot of musculoskeletal examination. Functional testing is now advocated. But the major risk factor for subsequent injury is a previous injury. Second question. A football PPE reveals that an athlete has a normal functioning solitary kidney. After appropriate consultation and discussion, here we are again with shared decision making. What should the team physician recommend? A, participation after explaining the risks. B, participation in non-contact sports only. C, participation avoiding NSAIDs and seeking nutritional counseling. D, participation with the addition of special padding to protect the athlete's kidney. And E, participation after modifying weightlifting program, emphasizing core strength. And the answer is A, right? That this is, gets at this concept of shared decision making. When evaluating the cardiovascular risks of a certain sport, this takes us back to the Bethesda guidelines. The physician must consider both the static and dynamic aspects of the sport. What is an example of a sport with both high static and high dynamic demands? Rowing, long distance running, sprinting, baseball, or American football? The answer is A. Exercise, as I mentioned earlier, you've got static or isometric and dynamic isotonic components. Static exercise involves development of large intermuscular force with little or no change in muscle length or joint movement. Dynamic exercise induces changes in muscle length and joint movement with relatively small intramuscular force. So rowing is the answer. Okay, I mentioned earlier cardiovascular screening, and this is really where I think the money is, at least in terms of test taking. You're gonna get a couple of questions on this particular area. So again, what is really the goal with screening? Well, Dr. Borchers mentioned a few things earlier, and Dr. Miller in his stats as well talked about screening. So what is it with the heart? Well, it's to prevent sudden cardiac death. And we know that the American Heart Association and the European Society of Cardiology both recommend screening. What's interesting is there are differences. So high school and collegiate athletes are probably our top priority in this country at least, although the age to best screen and the frequency of screening is still unknown. And that's really important concept, right? And we'll talk about that in a couple of minutes with the so called hypertrophic obstructive cardiomyopathy. The test question, I think the point you wanna drive home here is that it's the AHA 14 element screening, which is the seven personal and three family history plus four items targeting the physical examination, okay? So that's really what they're gonna test you on. And finally, as we know, less than age 35, right? This is where we'll go with this whole idea about screening with ECHOs and EKGs. So less than 35, the answer is hypertrophic obstructive cardiomyopathy. Over age 35 is coronary artery disease. A little bit about the pros and cons of screening. So why screen? Well, obviously, highly visible events, loss of numerous years of life, association between exercise and sudden death has been established, and there may be interventions to prevent death, i.e., implantable defibrillator. What's against it? Well, it's really uncommon. If you go back to Dr. Miller's statistical lecture, I think this drives us home, right? There are very few cases of sudden cardiac death, fortunately. These are rare disorders with diverse pathologies, and elaborate screening programs have never been shown to be cost effective. It's been estimated in this country by Bill Roberts and others that if we just did EKGs alone with our high school and collegiate athletes, we would spend up to $2 billion. So what are the current best practices? Well, we heard from Dr. Borchers on some other concepts, so here's where we're at with cardiac screening. So we know that the US, the UK, and the Canadian models, it's the physical examination, it's the pre-participation examination, the 14-point American Heart Association. The Italian model, though, they include, along with the PPE, an EKG and an echo, and we'll talk about this as to why. So again, just to drive that point home, right, it's the American Heart Association 14-element screening. We know that 80% of athletes who die from sudden cardiac death are asymptomatic with a normal physical examination. That's a really important point. The EKG adds some value, but at least still up until today, it has a high false positive rate. And these are some data from a couple of papers showing that it's up to 2.5% to 3%. The EKG changes in the athlete heart versus a true abnormality, and we'll go over this in a second. This is definitely something you need to be aware of for the exam. So speaking of which, what are the exercise EKG changes? This slide you have to know, okay? So what are the normal changes? Well, really what you wanna think about is with exercise, there's increased vagal tone. So what will that lead to over time? It'll lead to sinus bradycardia, first degree AV block, incomplete right bundle bench block, early repolarization changes, and isolated QRS voltage changes. Contrast that with abnormal findings, T wave inversion, ST segment depression, pathological Q waves, LA or LV enlargement, right ventricular hypertrophy, longer short QT, and the so-called brugada pattern. So this is a slide you need to know. In fact, I would argue if you know this slide, you can probably do okay on the exam along with the 14 element screening test. So let's talk a little bit about this. This may be philosophical, but just to really think about screening and when we should be screening. So here's the so-called HOCUM, right? This is hypertrophic obstructive cardiomyopathy. For test-taking purposes, it's the most common cause of sudden cardiac death in exercising less than age 35, okay? However, look at this. The incidence is probably one in 500. The male to female ratio is one to one. It's autosomal dominant. Problem is the expression of the gene is unknown. So the physical examination, canon is often normal. I've seen two in my career, one had a murmur, one did not. You may hear that systolic murmur. Testable here is it increases with a Valsalva maneuver. So don't be surprised if you hear something like, you know, there's a pre-participation evaluation. As a physician, you hear a murmur. What should you do next? You should have them squat or try to increase Valsalva, increase intra-abdominal pressure to see if that murmur increases. And of course, most deaths are due to ventricular tachycardia leading to ventricular fibrillation. EKG findings are variable. You can see Q waves, you can see voltage changes in T wave inversion. ECHO can be diagnostic, although today I think most of us are in favor of looking for MRI and of course, genetic studies. What is the treatment? The treatment is beta blockers and or an implantable defibrillator. Here's the change, right? ICD, implantable defibrillator should not be placed just to allow sport participation. However, what used to be an automatic disqualification is probably no longer. And I think we're gonna start to see this emerge in the literature and in our own practices as well. That this whole concept of shared decision making may, in fact, change how we're doing things. Here's another condition I'd like to ask you about, comedial cortis. Remember, that's a result of blunt, non-penetrating chest blow. Ventricular fibrillation from a blow delivered during the vulnerable part of the cardiac cycle. Just prior to the onset of ventricular contraction, I've seen this come up before, mean age is 13, and you can see it's in contact sports. And Dave Jand and others at the University of Michigan published a study back in 2009 showing that proper equipment does reduce the incidence. Myocarditis in athletes. Dr. Borchers mentioned this briefly, so I'll touch on it a little bit. They do like to ask about this. I probably have only seen it a couple times in my career, so maybe it has seen me and I didn't see it. But the point is, it's often due to an infectious ideology. Keep in mind though, and this may be something you'll see, right? Drugs, cocaine, and some of the synthetic agents can also lead to myocarditis. These individuals present with shortness of breath, chest pain, fever, and it's often preceded by a flu-like illness. The EKG is really the finding here. You see nonspecific ST and T wave changes across the precordium. So that's probably what they're going to test. And for test taking purposes, they like to say you're restricted for up to six months time from sport. This is one you may see. And the reason is, for some reason, we're starting to see this more in America. This used to be why the Italians, this is what drove them towards saying, not only is it a physical examination, but it's an EKG and an echocardiogram. Because they had a high incidence of arrhythmogenic right ventricular cardiomyopathy. So it's fibro fatty infiltration of the myocardium. 4 to 6% of sudden cardiac deaths in the US, and it's up to 22% in Italy. So again, that's what drives their decision making towards including an EKG and an echo. An EKG, as you can see down on the bottom here, the so-called epsilon wave. It's also an autosomal dominant condition. Generally, we restrict from all but the 1A sports. Note the word generally. So again, it's no longer to say they're automatically disqualified. Long QT, I mentioned earlier, I think the most important point here is the last one in the Mayo Clinic study, and this is really what's driving us now towards saying that maybe all of these athletes don't necessarily need to be restricted. The other thing I'd highlight here on this slide is what are the medications that can lead to long QT syndrome? For some reason, they like to ask you that, and it's Celdane and Zithromax. We use a lot of Zithromax, so be aware of long QT in the setting of that, as well as H2 blockers. Marfan syndrome, I've actually never seen this in person. There are some high-level athletes, in this country at least, that have experienced sudden cardiac death as a result of this. As you know, it's a connective tissue disorder involving the proximal aorta. Again, it's an autosomal dominant with variable expression genetics. Some of the skeletal findings that you're well aware of. Some of the cardiac findings, as you can see, they present with mitral valve prolapse. So, as I always tell my fellows in residence, if we've got somebody with an echo showing mitral valve prolapse, we need to look at their musculoskeletal examination to see if they fit at all with the condition. They'll ask you about the ocular findings, including ectopic lentis, myopia, and retinal detachment. As you can see, the EKG is often normal. They may present with left atrial enlargement. The treatment here, again, is yearly echoes and beta blockers to decrease their wall stress. Generally, again, as I said, no contact sports. We used to just say no contact sports. I think it's important, though, we now say generally. Okay, couple of questions here. 19-year-old female basketball player born in Indiana presents for her college sports pre-participation exam. She has all negative findings on her American Heart Association 14-point cardiovascular H&P. Which of the following is true regarding further evaluation in the United States? EKG should be done on all collegiate athletes, echo should be done on all collegiate athletes, EKG and echo should be done, or no further testing is necessary? Remember, we talked about this earlier. Low risk, it's that 14-point American Heart Association, so the answer is going to be D, right? Now, again, as I said, keep in mind, in Italy, because of the differences in terms of what's causing sudden cardiac death, they mandate echoes and EKGs. Another 12-year-old baseball player heard of another young boy dying after being struck by a baseball in the chest. What is true about this condition? Produces fatal inflammation, including pericarditis, damages the heart valves, leading to heart failure, occurs when the chest is impacted at a vulnerable period in the cardiac cycle, leading to a fatal arrhythmia, can be prevented with avoidable chest protectors if worn correctly, is usually related to underlying congenital heart problem. So again, that's the so-called comedial cortis, as you know, and that occurs with blunt trauma. Okay, let's shift gears a little bit and talk about the respiratory pulmonary system. So we need to know about exercise-induced bronchoconstriction. What's the differential diagnosis? Well, obviously, cardiac conditions, as you can see, vocal cord dysfunction, which we'll talk about, exercise-induced anaphylaxis, GERD, and then some congenital problems. So EIB is probably more common than we think. As you can see, presents with cough, wheeze, shortness of breath, or tightness. Most commonly occurs after exercise. This is important, okay? Athletes who complain during exercise, and we'll talk about it in a minute, that tends to be more vocal cord dysfunction. Athletes who complain after exercise, you have to think about EIB, and it's reversible, right? We understand the pathophysiology of asthma. There's a drop in the FEV1 greater than 10%. In the old days, we used to empirically treat these athletes. I know when I started at the University of Wisconsin, if we had somebody with shortness of breath during exercise, we just gave them albuterol and sent them on their way. No longer is that the case, right? The standard of care today is that you need to test these individuals to confirm the problem. And why is that? Well, you can see some of the common symptoms on the left-hand side here. On the right-hand side are some of the more subtle symptoms that EIB will present with. And again, their examination's often normal unless you see them during an exacerbation. So current standard of care, if you will, best practices, is an objective confirmation of suspected EIB is essential. What is therapy for EIB? I mentioned earlier the short-acting beta agonists. So albuterol is the one we classically still use, right? Two to four plus, 15 minutes before exercise. That can last for up to four hours, although if you're in a hockey rink, for example, cold, contained area, maybe two to three hours or even between periods. The longer-acting beta agonists are effective prophylactically, but may stunt growth, as we all know. Chromelamine sodium and leukotriene modifiers have been used in selective athletes, but remember, they are permitted by WADA. If you use inhaled corticosteroids, this is important, right? You need documentation for WADA. You don't need it for NCAA, but you do need it for WADA. And then some of the preventive measures. And finally, don't forget about carbon monoxide, particularly in closed, cold areas, such as a hockey rink. I mentioned earlier vocal cord dysfunction, and there's a really simple way to distinguish between EIB and vocal cord dysfunction. So these are the athletes that come in complaining more of throat tightness. You'll see them often clutching their throat, for example. Flow volume loops, which we use for exercise-induced bronchospasm, may or may not be as useful for VCD. The diagnostic test of choice here is direct visualization of the vocal cords while exercising with these symptoms. And the treatment, they actually do quite well going off to a speech therapist, getting them to relax their vocal cords, and many of us will add an H2 blocker as well for concomitant reflux. Just a picture to drive home. This is actually a picture of an athlete that I recently saw for vocal cord dysfunction. You can see normal with inspiration on the left with vocal cords abducting, and then paradoxically on the right, they're sitting closed. So vocal cord dysfunction comes up. Couple of questions here. 20-year-old swimmer reports coughing, chest tightness, and shortness of breath after completing a 1,000-meter freestyle event. What would be the next step in the evaluation? So what are we thinking here? Well, we're thinking EIB. So as I mentioned earlier, in the old days, we used to just put them on albuterol and send them on their way, and if they got better, we assumed we had the diagnosis. Today, do we do an arterial blood gas? Do we do electrocardiogram, pulmonary function testing, and echo or bronchoscopy? And the answer, of course, is pulmonary function testing, right? So again, think about EIB in the right setting. These people tend to complain about symptoms after exercise. They really should be confirmed by pulmonary function testing, and most of them do very, very well with short-acting beta agonists. Previous athlete does not have PFTs consistent with asthma. During her next episode, you are present, and notice that she is clutching her throat and is inspiratory strider. So where are we going? This is a classical presentation for vocal cord dysfunction. When you see it, it can be actually quite alarming. I had a coach one time who called me for a hockey player and said that he was actually having a heart attack, he thought, on the ice. So I came over, and there he was, literally clutching his throat, and this young man did have VCD as well. So what is the treatment of choice here? Well, it's going to be answer C, okay? They actually do quite well with speech therapy and can go on and become very effective in terms of their sport. All right, we're gonna shift gears again. I mentioned a little bit about heat earlier, so now we're gonna talk about heat, cold, and altitude. But before we do that, this is something that you really need to know as well, and this gets at sort of a philosophical approach to what does it really mean to be a team physician, if you will, right? And there's been a lot of consensus statements over the years. I think we're all in agreement that there's certain standards you should meet, and one of them is recognizing and understanding how to run a mass participation event. And the way I look at this with my fellows is I always approach this as a planned disaster. As the medical director, this is something they'll ask you. It seems simple, but you can often get led astray. It's the health and safety advocate for participants. You're the medical decision maker, and you're the spokesman accordingly. You're not somebody there on the sidelines to treat patients up in the stands. So think about mass participation events really as sort of a mini ER, and you can see some of the basic requirements that should be available. What I would draw your attention to here, and we'll talk more about this with hyponatremia, is the importance of having 3% saline available. Always remember to have a rectal thermometer, right? One of the questions that they'll ask you, often I've seen this, is when you're trying to make the diagnosis of hyperthermia, you cannot rely on an axillary temperature. You must have a rectal temperature, okay? That is testable. Let's talk a little bit about the collapsed athlete, because this is a little bit different, okay? So what's our differential? Well, first of all, cardiac arrest, obviously, exertional heat stroke, hyponatremia, hypoglycemia, hypo or hyperthermia, again, the importance of having a rectal temp. Dr. Borchers mentioned seizures earlier, and then finally, the so-called exercise-associated collapse. This is another one they like to ask you about. So you have a male or female high school 800-meter runner. They're coming to the finish line, and as they stop at the finish line, they go down. So the question is, is that sudden cardiac arrest? Well, probably not in a 14-year-old, but what they're getting at here is, how do we treat this? Well, we tell people to keep walking around, right? Why is that? Venous pooling, okay? So the take-home message here is, collapse that occurs during the event is typically much more significant than collapse that occurs at the end of the event, okay? Those are typically benign. You get these athletes up, they walk around, you increase their venous return, and they do okay. So that's a testable point. All right, so let's talk about the heat now. 10 to 14 days, just remember this number, okay? It takes about 10 to 14 days to acclimatize to heat, and obviously that's important as we entered high school and collegiate football here in the last week or so. Adaptations that occur, you need to know, all right? They're all sort of based on physiology. So decreased heart rate, increased plasma volume. You sweat earlier, that's a good thing, right? Increased sweat volume and skin distribution, i.e. to control temperature, and decreased sweat sodium losses. Again, these are very testable points. What are our mechanisms of thermal regulation? Well, the biggest one, right? What is what generates heat during exercise? It's the skeletal muscle system. So obviously, the bigger the athlete, the more they should sweat, which means the more we have to replace, right? So the point here is skeletal muscle, exercising contracting skeletal muscle produces heat. At the same time, blood is shunted to the periphery. Why do we do that? To control temperature. So evaporation is about 85% of heat loss with exercise. So as I always tell my fellows, if you drag somebody off the course during a marathon and they're not sweating, you should be concerned, right? Because they're not sweating, that means they're not dissipating heat. So the first thing I need to know is what's their rectal temperature. This is a number you need to know. A 70-kilogram athlete sweats on average one to two liters an hour. They'll ask you about that. Here's another testable point. Children are at greater risk for heat illness because they have a smaller surface area to body mass ratio and they have a lower sweat rate. Please remember that. Risks for heat illness. I think the take-home message here, and we see this every year, right? It's the first one or two days of practice, right? So for example, on a practical note, your sicklers, these are the ones that you may wanna start off a little bit simpler during the first couple of days of practice. It's tough to do, it's tough to tell the coaches that, but we don't want problems with heat. Another point here is the wet bulb globe temperature. All right, this is something that you need to know a little bit about as well. That really drives our decision-making for whether or not we will hold, for example, a marathon. Okay, so it's the wet bulb globe temperature. In other words, it's not just the temperature, it's also the relative humidity as well as the wind speed. And there are actually some downloadable apps. I didn't know this, but our head athletic trainer, Vinny Scavo, showed me at football practice a couple days ago. There's a downloadable app now and you can just calculate it in real time, so it makes life a little bit easier. Exertional heat stroke. I don't want to spend too much time here, but this is something you want to know about, okay? If they're gonna ask you anything about heat, it's probably gonna be a bad situation here, okay? So again, remember by definition, hyperthermia, okay, the importance of rectal temperature. Early on can be very nonspecific, okay? Really important point here, seizure is not common in exertional heat stroke. So if you see somebody with a seizure, heat stroke should not be the first thing to think about. All right, another practical point I like to drive home to my fellows. Cardiac arrest, right? Short duration seizure. Hyponatremia is a longer duration seizure, okay? That's the sweaty athlete, if you will. Exertional hyponatremia. I mentioned this earlier, please remember this. First point, thirst is not an overall good indicator of hydration status. As you can see here, there's sort of gradients of hyponatremia. I think there's a lot of people, I'm the chief medical officer at Acona, Ironman once every five years, and we probably see a lot of sodiums in that 130 to 132 range, and those people do well with just simple hydration, right? They like IVs, but we try to get them just to take fluids, and actually in the last couple years started using chicken noodle soup, and they seem to like that because it's got a lot of sodium. But here's what you need to know about hyponatremia. Who's at risk? This is a really important point. So these are the slow runners, okay? And often you'll see a body weight increase. So for example, one of the things we do out in Kona is we make sure athletes must sign informed consent if they will not consent to a body weight before the race as well as immediately afterwards. If they don't do that, we will not provide them with fluid resuscitation. And why is that? Because these are the people who are out on the course for a long period of time, okay? Not the winners coming in at eight and a half to nine hours. These are the people that are out there 14 or 15 hours, and when you weigh them, they've actually increased their body weight. So imagine being in Kona where it's 85 degrees, you're running across hot concrete for four or five hours, and you're increasing your body weight. That tells you something bad is going on, and that, of course, is hyponatremia. And the treatment, as I mentioned earlier, is 100 mils of 3% saline. They talk about central pontine myelitis. To my knowledge, it's never been reported. So exercise hyponatremia. Mentioned sickle cell earlier, right? So sickle cell trait is probably, fortunately, what we see more than sickle cell disease. It's autosomal recessive. 25% of West Africans and 10% of African Americans are estimated to have it. What's important about sickle, what you really need to know is a testable question here is the athletes in the first couple of days of practice and the first couple of, say, two to three minutes, if they're having symptoms, that's when you need to think about the so-called sickling crisis, if you will. And this gets back to shared decision making. We talk about testing, and at the NCAA level, it's really consent screening. Shift gears a little bit and talk a little bit about hyponatremia. So this, by definition, is the core or rectal body temperature is less than 95 degrees Fahrenheit or 35 degrees Centigrade. This is the opposite in the sense that heart rate, respiratory rate, and cardiac output all decrease as a function of declining temperature. Some of the early signs and symptoms here are pretty obvious. You can see shivering. Obviously, if they're getting more into the sort of apathetic slurred speech, we have to think that this is something more significant. It's generally broken up into three definitions, if you will. Testable point here is the myocardium becomes irritable less than 90 degrees. So they may ask you, for example, if you have an athlete with a rectal temperature of 88 degrees, do you start CPR right away? And that's where you need to think about the myocardium being irritable. Okay, so what's the treatment? So we talk about mild hypothermia. So that's, by definition, the temperature still over 90 degrees Fahrenheit. And these people do generally well, right? You get them out of the cold environment, get their cold stuff off, warm them up, and they do okay. Moderate to severe is a little bit more significant, as we all know, and these are the people that probably need to be transported once they're hemodynamically stable. Now again, remember, not providing CPR unless there's definitive cardiac arrest, right? The myocardium at less than 90 degrees is quite irritable. So just rubbing their skin, for example, is not something you should really be doing if their core temperature is less than 90 degrees. Couple other points about hypothermia, if you will. The first one is frost nip, right? So we wanna distinguish between frost nip and frost bite. So what is frost nip? Well, it's superficial vasoconstriction without tissue freezing is the highlight, and the key point, without tissue freezing. It often presents with burning followed, they'll complain about burning followed by numbness, the gray or pale skin on the face or extremities, and the treatment here is direct body heat. Remember, don't rub the skin. In contrast is frost bite. This is where you have true tissue damage, and as you well know, you really can't determine that extent of that for up to perhaps six weeks or so. Once they're thawed, if you will, you'll see the blisters with the yellowish or if it's severe red and purple fluid. If there's no blisters, then that's severe. That's a bad prognostic sign, right? They probably are developing gangrene, and here the initial treatment is to really stabilize them and get them to hospital. So the point there is the difference between frost nip and frost bite. Shift gears again and talk a little bit about high altitude illness, right? So where do we see this? Well, we know that rapidly as you're ascending, for example, altitude, with increasing altitude, there's a decrease in the barometric pressure and partial pressure of oxygen. Symptoms can be very nonspecific. They can start out with just some headaches and nausea, a little bit of anorexia. Once they progress to more fatigue, you have to get a little bit more nervous. The treatment here, though, in general, as long as they're not having significant CNS findings, is it's mild and self-limited, right? The mainstay of treatment, this is what they like to ask, is get them down, okay? So you just get them down, and they do quite well. Some of the things that they'll try to trick you on once in a while is acetazolamide, dexamethasone, portable hyperbaric oxygen. They're of some value, but the main point here is get them down to sea level, and they'll do fine. Prevention, okay, is another testable point. The big thing is just going slow, right? And obviously avoiding things like alcohol and caffeine and staying hydrated. That's in contrast to severe altitude illness, if you will. And there's two conditions, right? There's a so-called HAPE, which is high-altitude pulmonary edema. This is where they have dyspnea at rest, severe hypoxemia, cyanosis, and non-cardiogenic pulmonary edema. So these patients, these individuals are sick. And the other condition is HACE, that's high-altitude cerebral edema, and as you can see here, these are markedly more progressive CNS signs and symptoms than those who are just a bit fatigued and perhaps dazed. And these folks, of course, you need to get them down right away. A couple of questions here. Which of the following is true for children? Equal risk for heat illness as adults exercising in the heat. They acclimatize to heat faster than adults. They have a higher sweating capacity than adults and can dissipate heat through sweat more efficiently. They have a smaller surface area to body mass ratio. And E, encouraged to use sports drinks rather than water for rehydration. So we talked about this earlier, right? The important point here is that children are at greater risk for heat and illness because they have a smaller surface area to body mass ratio and they have lower sweat rates than adults. You're covering a marathon in Phoenix. It's a warm, sunny day. A 38-year-old female runner collapses at the finish line. She's unconscious but breathing with a good pulse. She's warm to touch and not sweating. What should immediate management include? Well, this is not exercise-associated collapse, correct? She's unconscious. So what are we driving at here? Well, administer IV Dantrolene, measure oral temperature, give oral Tylenol or other antipyretics, encourage cool liquids, immerse in ice water bath. So what we're driving at here is a couple things, right? First of all, she's unconscious, but equally important is she's not sweating. We talked about this earlier. When they're not sweating, the first thing to think about is hyperthermia. So the correct answer here is to immerse them in ice water. She likely has exertional heat illness and possibly even heat stroke. Rectal temperature is required and is typically greater than 104 degrees Fahrenheit. Again, please, I cannot emphasize that enough, the importance of rectal temperature. This is something they'll certainly try to trick you on. When asked about the prevention of altitude sickness, what do you recommend as the best way to avoid symptoms? We talked about this a couple minutes ago. Slow ascent, premedication with scopolamine, proper nutrition, optimal physical conditioning, and appropriate clothing. And the answer is slow ascent, right? This is something they'll ask you about as well. You're covering a marathon in August. Another marathon question. Participants bringing a friend into the medical tent. It's his first marathon and he finished in four and a half hours. He's stumbling a little and somewhat confused at the finish line. So we've got some CNS changes. Encourage him to drink and he subsequently consumed four liters of water. Yep, not good, right? He becomes more unsteady and confused. The most likely diagnosis is, we talked about this earlier, right? These are the overhydrated people. Is it hypernatremia, hyperglycemia, hypokalemia, hyponatremia, or hyperkalemia? So this is the presentation for hyponatremia, right? So these are the people that are fluid overloaded, okay? So one of the first questions, and this comes up at football for us every day, what's one of the first things that you've gotta do before you put an IV in somebody when they have muscle cramping? You want a body weight, okay? Their weight in the morning before practice. So if an athlete comes off the field and they're thinking about starting an IV, the first thing I wanna know is what's their fluid status, right? And most of the time they've lost weight and that's fine. You can start an IV. The problem is what happens if you have somebody that's gained weight, right? These are the people that you can kill, okay, from hyponatremia. So remember the importance of body weights. Can't emphasize that enough. All right, now we're gonna talk a little bit about nutrition. So the first thing we wanna talk about here is energy storage and requirements. So we know that glucose and free fatty acids provide energy for working muscle. Muscle and liver glycogen are for carbohydrate storage. Adipose tissue is where we store free fatty acids. Caloric requirements, they seem to like to ask this. I'm not sure why, but males, as you can see, typically between 2,500 to 6,000 kcals a day. Females, about half that. Important point here is the carbohydrate needs, right? Carbohydrates are the predominant fuel beyond 65% of your VO2 max. So it's 2 thirds of your daily intake. Another thing they like to ask you is what are the protein requirements? Well, it's about 10 to 15% of total energy requirement during the day. You can see the requirements here, 1.6 to 1.8 kilograms for strength-trained athletes and 1.2 to 1.4 for endurance athletes. No benefit greater than two grams per kilogram body weight. That's something they like to ask. So let's talk a little bit about carbohydrates. So that's our primary source of fuel for exercise, right? And they do work. Well, how do they work? How do they improve performance? Well, first of all, they prevent falls in blood glucose. Secondly, they maintain muscle carbohydrate oxidation and brain glucose supply. They actually reduce the perception of fatigue and they can increase exercise time to fatigue. So this gets back to the old days of the marathons and the so-called carbohydrate loading, right? So carbohydrates are the primary fuel that we use during exercise. About 2 thirds of our caloric intake should be carbohydrates. Timing of nutrition. This is, they like to ask this. So pre-competition, okay? What do we wanna do pre-competition in that three to four hours beforehand? Well, we wanna increase our muscle glycogen stores and optimize hydration. So this is where we have high carbohydrate, moderate protein, and low fat meal three to four hours before competition. And yes, I'll talk about the ketogenic diet in a couple of minutes. Recovery nutrition, okay? Again, what do we know that's important? So this is a number they like to ask you. Roughly one to 1.5 grams per kilogram after exercise. Add some protein if there's been significant muscle damage. They'll talk to you about protein supplements. Chocolate milk works just as well and I've seen questions regarding that. Carbohydrates and proteins together do provide some advantage and don't forget fluids. So take-home message here is pre-competition, carbohydrates, right? To increase muscle glycogen stores and then post-exercise, carbohydrate plus protein. Which of the following is not true about protein intake in athletes? Protein is the last fuel source. Strength training athletes have greater protein requirements than endurance athletes. Carbohydrate and protein should be ingested together after muscle damaging workouts. Chocolate milk is as effective as a $3 protein shake. Most athletes that participate in strength sports need protein supplements. Protein should account for 15% of total energy intake. So it's a little bit trickier, right? And the answer is D, okay? So again, the importance of knowing the differences and knowing that over two grams per kilogram is just not necessary despite what all of our athletes do. Okay, I mentioned the ketogenic diet. This may be something you're gonna see because it's definitely out there. It's become particularly attractive to the endurance athletes, particularly triathletes. We're gonna publish a paper here soon based on data from Kona, from Ironman and about 30% of the athletes there have tried ketogenic diets and have experienced some success. So the question is a 33-year-old triathlete comes to your office to discuss his training for the upcoming season. He's trying to lose weight but wants to ensure optimal performance as he continues to increase his aerobic endurance. He's interested in the so-called ketogenic diet to help him meet his goals. How would you best describe the ketogenic diet? I think this is what they're gonna ask you. So a ketogenic diet, is it high in protein, low in carbohydrate? Is it low in protein, high in carbohydrate? Is it high in fat and high in carbohydrates? Or high in fat and low in carbohydrates? And the answer is D, right? So ketogenic diet is high in fat and low in carbohydrates while keeping an adequate level of protein intake. They're gaining popularity with endurance athletes as I mentioned, especially with cyclists and triathletes. Strengths of the ketogenic diet are the potential to reduce body fat without causing excessive loss of lean body tissue. Potential to reduce body fat without reducing performance and higher rates of whole body and muscle lipid utilization during submaximal aerobic exercise. Take home message here I think is you just need to know that the ketogenic diet is low carb, high fat and it's definitely on the forefront. Anemia is another topic they like to ask you about. Where do we see this? Well, we see iron deficiency anemia typically in female athletes, in endurance athletes and vegetarians. You need to know here, what else do you need to look for in an athlete who's a vegetarian? Need to watch for zinc, B12 and vitamin D deficiency. I've seen that come up before as a test question. How do we screen for iron deficiency anemia? Well, we get a serum ferritin and a hemoglobin. And for test purposes here, generally speaking we like to supplement if the ferritin is less than 30. I know that a lot of athletes who have ferritins of 40 and 50 and they will take iron as well. The other thing they'll ask you about is a dose and it's typically 100 milligrams of iron a day for at least three months. Remember to take it on an empty stomach and you can use either ferrous gluconate or sulfate. That leads us into menstrual dysfunction in athletes. You need to know the difference between primary and secondary amenorrhea. Remember primary amenorrhea is the absence of menstruation by age 16 in girls with secondary sex characteristics or females without secondary sex characteristics and pneumoniarchy at age 14. That's in contrast to secondary amenorrhea which is far more common and that's where they have an absence of at least three consecutive cycles after menarche and less from somewhere between three to six cycles a year. You need to exclude other causes and the most common one and this is what they'll ask you about, right, is the so-called energy drain hypothesis. Remember the key here is energy balance, okay? That's what you need to take away from this whole area of menstrual dysfunction. If they're gonna ask you about it, it's this concept of energy balance. We have calories in and we have calories out. And why is that important? Well, athletes expend more energy than they consume. That leads to a disruption in so-called LH or luteinizing hormone, pulsatility. Amenorrhea and oligomenorrhea are both associated with low estrogen. Reversibility of bone loss. Effects of low estrogen on bone mineral density are not reversible, right? So we don't wanna miss this condition. Athletes with normal menstruation have up to 20% higher bone mineral density in the lumbar spine. There's this so-called window of bone accretion, right, which occurs from early adolescence until the mid-20s. So that's important in terms of calcium and vitamin D supplementation. And the most important point here is that the return of menses without medication is optimal for bone health. So one of the questions they'll ask you about is if you have an amenorrheic athlete, do you wanna put them on oral contraceptives? That's what we used to do 25 years ago. The first thing to do is adjust this whole so-called energy drain hypothesis. Look at their calories in and calories out, all right? So don't put them on oral contraceptives right away. That's a bad thing to do. So let's talk a little bit about some of the interventions then. I mentioned calcium earlier, right? They like you to know these numbers, at least in the prepubertal adolescent, or a child, if you will. Calcium requirements of 12 to 1,500 milligrams a day. Vitamin D is 800 international units a day. In athletes who have menstrual dysfunction and are eating disorders, remember that estrogen prevents further bone loss but has little effect on adding bone mass, okay? That's a really important point, right? Estrogen does not lead to increased bone mass. It just reduces bone loss. All contraceptives should be considered if no menses for six months and there's a history of a stress fracture. But again, think of the energy balance first. This is where they'll try to trick you, right? Nasal calcitonin is minimally effective and bisphosphonates, as we know, are contrary to Kennedy under age 18. Couple words about eating disorders, anorexia nervosa. Remember that by definition, it's a refusal to maintain a body weight at or above the minimally expected normal body weight for age and height. Weight loss leading to body weight less than 85% of expected is really the take home message here. It occurs in all sports. We're seeing this more and more and the treatment is multidisciplinary team, right? And that's the question they'll ask you about. The triad by definition, remember, is disordered eating, amenorrhea, and abnormal bone loss. The key point though is this low energy availability, right? And that's really driving our current treatment protocols which is, as I mentioned earlier, is not to put them on the pill right away or contraceptives but to address this so-called energy balance. Menstrual dysfunction, what does that lead to? It leads to a decreased release of GNRH and a decrease in LH. I've seen that question as well. Proper training and some of the things we mentioned earlier. Exercise and pregnancy, lots we could talk about in two or three slides, what's important? Well, first of all, majority of pregnant women can continue to exercise, okay? Secondly, about 80% it's estimated will experience diastasis recti. Physiological changes that occur with pregnancy is something they like to ask you about so please be aware of those as well. For some reason they like to want you to know the absolute and relative contraindications to exercise in pregnant women. So here are some of the absolute contraindications. The big ones are really down here. If you've got persistent second or third trimester bleeding, obviously placenta previa after 26 weeks gestation. So these are pretty straightforward and the relative contraindications as well. All right, so let's, a couple of questions here about exercise during pregnancy. So which of the following is true? A, should be gradually increased in intensity during the second and third trimester. Should not involve weight training because of detrimental effects on maternal fetal circulation. Increases maternal cardiac output and uterine blood flow. Maximum oxygen consumption at term is greater than in the non-pregnant female because of increased body weight and results in increased resting maternal blood volume and increased heart rate. And the answer is E, right? Exercise in setting of pregnancy seems to speed things up. So it increases maternal blood volume and heart rate. Weight training is actually safe and is effective when certain parameters are followed. Exercise results in a decrease in uterine blood flow between, particularly in the second and third trimesters. So the take home message is, they're usually pretty well through that second trimester. It's during that third trimester that we need to be a little bit more careful, if you will. 25-year-old female long distance runner presents to your office complaining of fatigue and poor performance. History and physical examination are consistent with anemia. Almost all lab work, including a peripheral smear, serum iron and TIBC are consistent with iron deficiency anemia. The one exception is that the ferritin level is normal. What is the most likely explanation for a normal ferritin in this athlete? I did not get this question, by the way, so. Answer A, sickle cell trait. B, vitamin D malabsorption. C, hepatitis. D, volume depletion. And E, malaria. And the answer is C. A low serum iron and ferritin with an elevated TIBC are typically diagnostic of iron deficiency. Because of its nature as an acute phase reactant, a normal elevated serum ferritin can be seen in patients who are deficient in iron and have co-existent conditions such as infection, chronic inflammation, malignancy or conditions causing tissue damage. So sickle cell trait, vitamin D and volume depletion would not affect ferritin levels. So malaria should not cause her peripheral, her clinical picture and peripheral smear. That's a tough question. 33-year-old female had increased her running regimen for an upcoming marathon. She's had only three periods in the last six months. Her pregnancy test is negative. That's another important point they'll sometimes trip you up on, right? What's the first thing you wanna do is get a pregnancy test? The most likely ideology of her menstrual dysfunction. So we're talking about what? This is not primary amenorrhea. This is the classical presentation for secondary amenorrhea. So what's the most likely ideology of her menstrual dysfunction? Is it increased testosterone, increased LH, decreased GnRH or increased prolactin? And the answer is C, right? We talked about this earlier. So you need to know that you get a decrease in GnRH which then leads to a decrease in LH, if you will. All right, I think at this point we're ready to wrap things up. So I appreciate the opportunity to be here and thanks for your attention. All right. I think at this point we're ready to wrap things up.

Dr. Best

medical issues

sports medicine

pre-participation evaluation

cardiovascular screening

heat illness

sickle cell disease

exercise-induced bronchoconstriction

nutrition in athletes