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ICSC04 – Emergency Procedures
Section 1 – Instructor Doctor Ira Shapiro
Video Lesson: 1:00:03

ENGLISH VERSION DOWNLOAD:ICSC04_Section 1_TRANSCRIPT

This is module 1 of 3 on Emergency Procedures for the Sports Chiropractor. I have been practicing sports chiropractic for approximately 40 years and I have extensive background in dealing with on-site events. I am a two-time member of United States Olympic team medical staff and I have worked with FICS at the World Games in Cali, Colombia and the Pan Am Games in Guadalajara, Mexico. I have also taught this course for FICS internationally, both in Japan and in Mexico.

A sports chiropractic doctor/physician should be able to identify and perform the tasks that are required to act as a team physician on field and/or a sports physician in office. We should be able to identify triage and manage sports-related injuries on an emergent on-field basis as well as a non-emergent office setting. I have been in many situations doing things internationally, sometimes as a full contingent of medical staff. Other times at the venues, we have 6 doctors working to be a very sparse medical staff. There have been times where, on the field, I was present when an athlete fractured their cervical spine. I was also present in the Olympic Village when a coach for one of the teams had a heart attack. Understanding and knowing and being familiar with how to treat and handle emergency procedures on an emergent on-field basis is important for you to be a full member of an integrated medical staff.

The objectives of this course are: Knowing how to spot it, what it is and what to do for it. These are all action steps that we will cover in this presentation. In this first module, we will discuss personal protective equipment, uncertain situations, scene safety, the mechanism of injury, the golden hour. We will spend a large period of time on doing the initial assessment, getting a general impression, assessing mental status, airway, breathing, the use of oxygen, and circulation.

Minor symptoms may be the early warning signs of a more serious injury. That means, when in doubt, we always err on the side of caution. An ounce of prevention is better than a pound of cure. We should turn around and be prepared to handle any kind of situation that may develop. Protecting ourselves out there, is the first thing I want you to remember. Because if we are the care provider and something happens to us and we get injured, then the medical teams that are only two people, or two athletes get injured, there is nobody there to help with the injured athletes.

Be aware of your personal protective equipment. We must assume that all body fluids present a possible risk for infection. Therefore, we must protect ourselves against them. We should have gloves, usually, non-latex because there are several people unable to handle latex against the skin and they will get a reaction to it. We want to use Nitrile gloves, and in a lot of instances, especially nowadays with what is going on with the pandemic worldwide, we should have some form of eye protection. Either a face shield or goggles.

Just as there is a proper way of putting on the protective equipment, there is a proper way of removing the protective equipment. As we see in this slide, when the doctor is taking off the gloves, he is rolling down the gloves on one side, then using his gloved hand to roll down the glove on the other side, pulling the glove inside out, then using the inside of the glove to pull the other glove off. This way, at no time are your sterile hand touching the non-sterile glove or any other part of the body that is not sterile.

When we are out in the field,  make sure of the safety for yourselves and other members of the medical staff. Have a proper mindset and make sure that we know what is going on around you. If you are at a rodeo and a cowboy gets thrown from the bull and gets stepped on, you see him lying there, not moving in the arena, are we going to jump right in and run over to the cowboy? Usually, medical staff, in a rodeo setting has red shirts. When you have a matador in a bullfight and he has a cape, what color is the cape? The cape is red. If I am going to have a red shirt and I am going to run into an arena where there is an athlete down and there is a bull in the arena and I am wearing a red shirt, who do you think the bull is going to start to charge after? Me because I have the red on.

If you were looking after motocross, or some form of BMX bike racing, and an athlete goes down, are you going to run onto the course or are you going to make sure that 30 other motorcycles or bicycles are not coming around the bend and going to run you over while you are on the field assessing the injured athlete? It is important for us to make sure we are aware of the scene safety.

Let us discuss the mechanism of injury. We are not there to enjoy ourselves on the sidelines, we are there to work and to pay attention. Being alert to what is happening on the field is important. If I am at a soccer match and the athlete plants his foot and turns to run up field and goes down, that is a completely different mindset than if you have two athletes go up to head the ball and collide, and they go down. When they collide like that, my mindset changes and I have to right away think the possibility of there being some form of cervical spine injury. By paying attention on the sidelines, you can determine what the mechanism of injury is.

Then we are going to talk about the golden hour. That is the time from when an athlete gets injured, if it is life-threatening, for them to be in the hospital on the operating table that gives them the best chance to survive. If you notice, the first 20 minutes of this golden hour is activating the Emergency Medical Services and having them get to the scene, and then starts the golden 10 minutes. That is the most important time. This is when we are going to do our initial assessment and our initial interventions. By being on-site, being able to handle emergency procedures, we are starting this golden 10 minutes right away, giving the athlete a better chance for survival, if there is some form of a life-threatening injury.

If we get on the scene and we see no signs of life with the athlete, lying there motionless, what are the signs of life? Is he moving? Are we seeing his chest or stomach rise or fall as he breathes? If we are finding no pulse, those are all indications of no signs of life. Then right away, we are going to start CPR. Most of you, if not all of you, should already have your CPR certification. That is one of the requirements for getting your certification and for being on-site and doing any sporting events with FICS.

We have done our protective equipment (PPE), our scene safety and mechanism of the injury. Now, our next step is being on the field and what do we do? The first thing you want to do is you want to develop a general impression. Scene safety, mechanism injury and looking to see what is going on, so now the next step is to assess mental status, airway, breathing, circulation, and then we are going to identify the priority of injury to the patient.

You are on the field of play. When assessing mental status, use the AVPU scale. A stand for alert and V stands for verbal stimulus, meaning the athlete is lying supine or prone, and you are talking to them and they are giving you a response. If they are lying down and you talk to them but get no response, you either give them a sternal rub or you tug on their hair, or you pinch them. You get a response and that is a painful response. Is the patient or the athlete unresponsive? The AVPU scale is.

• A is for alert.
• V is responsive to verbal stimulus.
• P is response to pain.
• U is unresponsive. It is not as important in these situations about the Glasgow Coma Scale because we just want to do action steps on the field.

If possible, and if there is time, we always want to take a SAMPLE history.

• Signs & symptoms
• Allergies
• Medications
• Past Medical History
• Last oral intake
• Events leading up to the present injury

If it is not written down, it was not done, therefore if there is time, we want to be able to find out what the signs and symptoms are. Does the athlete have any allergies? Is the athlete on any medication? Is there any pertinent past medical history? When was the last time they had something to eat? What were the events that were leading up to the actual event, the actual injury? If there is time, these are some of the questions we want answered so we can provide this information to the next level higher of medical care that is going to take the athlete and you are going to turn the athlete over to.

Here is the Glasgow Coma Scale, but again, we do not want to sit there and must add up all the numbers. I got 3 for voice, and I got a 4 if he is confused when he gives a verbal response. They get a 2 if there are other kinds of things from a motor response. We do not have the time. It is not the need to do that. We are more interested in being able to use the AVPU scale in these kinds of situations.

Let us look at airway which is always assessed first. Advanced techniques are going to be used after basic airway management, but the first step is going to be opening the airway, and once the airway is open, we can make a decision if we need to use any adjuncts to keep the airway open. How do we assess the airway? What are some of the things we are looking for? It is the athlete speaking in two or three-word sentences. Are they using the accessory muscles to breathe? Is there nasal flaring or rib retraction in young children? Remember, we are going to work with a vastly different age population in dealing with sporting events. Certain things have to be done for different age population, which is why in children, we are looking for nasal flaring and rib retraction. We are also making sure in assessing whether there is any labored breathing.

The airway may be obstructed by the tongue and in this case, we will use the head tilt-chin lift technique to open the airway, or if we suspect there being some cervical spine injury, we are going to use the jaw-lift maneuver. As we can see from the picture, here is an instance of the athlete lying supine and the relaxation of the tongue is occluding the airway. Take the proper steps to open the airway and opening the airway using the head-tilt chin-lift maneuver. Put one hand on the head, the other fingers underneath the chin, and tilt the head and lift the chin. Notice in this picture that the doctor has gloves on. There is his PPE. Otherwise, we want to use the jaw thrust maneuver when we suspect a cervical spine injury. In this picture, we see that we are maintaining in-line alignment of the cervical spine and we are using our index finger and long fingers to jut the jaw forward to open the airway. This is used anytime we are suspecting there to be a cervical spine injury.

There are different sizes of airways for different age of the population of the athletes we are dealing with. Younger people have a larger tongue relative to the mouth. They have less well-developed rings of cartilage in the trachea and the head-tilt chin-lift maneuver may occlude the airway. That is why we open the airway in children with not as much head tilt and chin-lift because we do not want to occlude the airway.

Once the airway is open, make the determination if we would need any airway adjuncts. There are two different kinds. There is an oropharyngeal airway. This keeps the tongue from blocking the upper airway. This allows for easier suctioning of the airway if it is needed and this is used in conjunction with a BVM device, a bag valve mask of which we will discuss later. This is used on an unconscious athlete without a gag reflex. As you notice from the picture, these airways come in different sizes.

How do we insert the oral airway? The first thing we need to do is we need to select the proper size. We want to measure from the corner of the mouth to the ear lobe. That determines what size airway we are going to use. Then we are going to open the mouth, either with the head tilt chin lift or the jaw thrust maneuver. We want to hold the airway upside down, so it looks like a U. We want to insert it into the mouth. Once it gets to the end of the hard palate, we want to rotate it 180 degrees until the flange rests against the athlete’s lips.

The other airway is a nasopharyngeal airway. This is used on a conscious patient who cannot maintain an airway. This can also be used on a patient who has a gag reflex. This airway should not be used on a patient with a possible skull fracture. Insert this into the nose and if there is some form of skull fracture, we do not want to be pushing the bones further back into the brain, adding possible injury to that.

Measure for a nasal airway from the side of the nose to the earlobe. Select the proper size and lubricate the airway with a non-petroleum-based lubricant. We do not want them to inhale any of the petroleum bases into the lungs. Believe it or not, most people’s right nostril is larger than their left nostril, so you want to gently push open the nostril with the bevel turned towards the septum we want to insert the airway. It goes very easily. The first time I did this, I was surprised how easy it was, so being familiar with how to use the device is half the battle.

What happens if there is some form of mechanical obstruction of the airway? Be prepared to act quickly. These obstructions may be from the positioning of the head, the tongue, some form of aspiration of vomitus into the throat or some foreign body. We are talking about a foreign body. Most of the time, these athletes have a mouth guard in. They may have taken a hit, and bite hard on the mouth guard, a piece of the mouth guard comes off, and gets lodged in the throat. If they get hit and they lose a tooth, and the tooth becomes lodged in the throat, opening up the airway with the head-tilt chin-lift maneuver may resolve this problem of mechanical airway obstruction.

What about there being a partial airway obstruction? The patient is going to be breathing noisily. They are going to be able to cough and speak. Encourage them to cough and speak. That is the body’s way of trying to force out the obstructed airway. That novel concept, the body knows how to take care of itself, just give them the chance. The one thing we do not want to do is back blows to a conscious child or adult who is choking. If they are taking a breath in and we are giving that back blow, we could force the object further on down the airway, causing more of an obstruction. We want to give the athlete 100% oxygen using a non-rebreather mask of which we will discuss that later when we are also discussing about the BVMs we spoke about in the prior slides. As in all instances, when there is an airway obstruction, we want to provide prompt transport to the patient to a hospital facility.

What are some signs then? We talked about a partial airway obstruction, and we talked about an obstruction in the conscious patient. What happens if we have an obstruction in an unconscious athlete? It could be due to obvious trauma or blood or other obstructions in the area. There will be some noisy breathing sounds such as bubbling, gurgling, crowing or any other kind of abnormal sound. We will see that the patient has extremely shallow or absent breathing, the rise and fall of the chest. We will not feel any of the breath coming out of their mouth and nose.

What are some of the causes of these foreign body obstructions? We discussed relaxation of the tongue, vomit, blood clots, bone fragments, tissue damage, any kind of thing that will happen to the esophagus, the trachea, and anything in the neck region. Swelling due to an anaphylactic reaction, allergic reaction to something, will cause some form of obstruction of the airway along with the possibility of foreign objects, teeth, biting off a piece of the mouth guard that they are wearing.

How do we recognize an obstruction? Is it partial or is it complete? Is the patient able to speak and breathe or cough? If the patient is unconscious, then we are going to attempt to deliver artificial ventilation of which we will discuss later. How do we remove the obstruction? We are going to perform an abdominal thrust maneuver. If the attempts to clear the airway and the obstruction are unsuccessful, then we might have to begin CPR. In these instances where there is either a mechanical, a partial or a complete obstruction, we must transport the athlete to the appropriate facility.

To do the abdominal thrust maneuver, we must recognize and assess choking. The international sign for choking is crossing your hands across your neck and your chest. Position our self behind the athlete, spread their legs and put our leg between their legs. This way, our head will be to the side in case the athlete falls backwards, ensuring the athlete does not hit his head. Additionally, while having the legs spread, you could rest the athlete on your knee, in case they are going to fall either forwards or backwards, you can position yourself to keep them supported.

Wrap our arms around the athlete, making a fist right above the belly button. When we make the fist, we want to keep the thumb outside. A lot of times, if you tuck the thumb inside, when you give the thrust, you will break your thumb. Keep the thumb outside and give a posterior superior thrust. The sign of a J. Remember, when we started out in chiropractic school, our big problem was we were thrusting. We were pushing when we tried to move the segments. It is the same thing with doing this maneuver. It is not a push; it is a thrust that needs to be performed. If the patient becomes weak or unconscious due to air not getting into the body and the patient passes out, we want to gently assist them to the floor and attempt to ventilate them. That is artificial ventilation. If this fails, we want to try to reposition the head with the head-tilt chin-lift maneuver and try again. If this is unsuccessful and the airway is still obstructed, begin CPR.

When we are dealing with the younger population, we want to kneel on one knee behind the child. We want to give them abdominal thrusts and keep on doing it until the object comes out. If the child becomes unconscious, bring them gently to the ground, open up the airway, and look to see if we can see any foreign object. We only try to remove an object if we see it. The blind sweep is no longer performed. We only want to remove the object if we can see it. Then, attempt the rescue breath if the airway remains obstructed, begin CPR.

We discussed all those things about airway, assessing the airway, head-tilt chin-lift maneuver, jaw thrust maneuver, oral airway, nasal airway, mechanical obstructions, being a partial obstruction or a complete obstruction, the unconscious athlete’s airway, and we talked about removing the obstruction using the abdominal thrust maneuver.

Now, we are going to move on into breathing. How do we assess breathing? Is the athlete’s respiration shallow or is it deep? Does a patient appear to be choking? Is the patient cyanotic or blue around the lips indicating that oxygenated blood is not getting throughout the body? Is the patient moving air in and out of their lungs as their chest rises and falls? These are all different ways we use to assess breathing.

The active part of breathing is inhaling. This is when the diaphragm and the intercostal muscles contract allowing your lungs to expand. This decreased pressure allows the lungs to be filled with air and the air travels and are exchanged through the lower parts of the lung. Exhaling does not usually require any kind of muscular effort. The diaphragm and intercostal muscles are going to relax. The thorax decreases in size, and the ribs of the muscles assume their normal position. This increase in pressure forces out the air from the lungs.

We are talking about respirations. The rate is the number of breaths in 30 seconds times 2 or the number of breaths in 15 seconds times 4. What is the quality? Are they hyperventilating, breathing heavy and fast? Is their breathing rhythm regular or is it irregular? Is there a normal effort or a labored effort in breathing, is the breathing noisy, wheezing, snoring, gurgling, all different kinds of sounds coming out that indicate to us the possibility of some form of airway obstruction affecting breathing? Is the athlete’s breath shallow or is it deep? All things that we are going to use to determine if there is any difficulty in breathing.

The normal breathing rates. Numbers are important as they are the way we are going to determine in an emergency on-field situation if there were any problems developing in the athlete. In an adult, it is normally 12 to 20 breaths per minute when breathing. In children, it is 15 to 30 breaths per minute and in an infant, it is 25 to 50 breaths per minute. As you notice, the younger the patient, the more breaths per minute is in the normal range.

Normal breathing characteristics. Is there a normal rate and depth, regular rhythm, good breath sounds in both lungs? We should, on the sidelines, have the appropriate equipment we need to determine the extent of the injury to the athlete. We will discuss that in another module when we talk about what our sideline kit bag should contain. We are also looking for the regular rise and fall movements of the chest. Is their breathing easy or is it labored? Is there adequate depth to the chest when the athlete is taking the breath in?

Abnormal characteristics. Slower than 8 breaths a minute or faster than 24 breaths a minute are indications of abnormal breathing. Remember, we said in the adult, it is 12 to 20 breaths per minute. We are going 4 less breaths at 8 or 4 more breaths at 24. Those are the indications of there being abnormal breathing. Is their rhythm irregular? Is it labored? Is there muscle retraction? Remember, we spoke about that before, especially young children. Is there pursing of the lips? The skin is an organ. You will get a lot of information from an organ in terms of blood flow. That is why checking the skin to see if it is pale or blue, cool or clammy are going to give us indications if there is some problem with insufficiency in breathing, insufficiency of oxygenated blood getting throughout the system. We can pick up a lot of that from the skin. Let us look at nasal flaring in young athletes. Are the respirations shallow or are they irregular? All indications there is some form of abnormal breathing developing.

What about hyperventilation? It is over breathing resulting in a decrease in the levels of carbon dioxide. Remember, when we breathe in, the air contains 21% oxygen. We are breathing in 21% oxygen. When we exhale, we are exhaling 15% oxygen. We are only using about 5% of the oxygen that we inhale when we take a breath. When an individual is breathing too quickly, hyperventilating, we are going to find them to be a lot of anxiety. Numbness will be in the extremities. There will be a sense of difficulty breathing despite rapid breathing. There might be some dizziness, and one of the classic signs is tingling in the hands and in the feet, which usually indicate hyperventilation.

How do we treat when there is respiratory insufficiency? Secure and support the airway. Remember Airway is always assessed first. After the airway is cleared of any obstructions, we might have to help ventilate the athlete, thinking about the BVM device and the amount of breaths used for ventilation. We will cover this later on when we look at providing oxygen and when there is a problem with an obstructed airway and difficulty breathing, the athlete must be transported to the appropriate facility.

What we are trying to do is prevent dyspnoea. Dyspnoea is defined as a shortness of breath or difficulty breathing. The athlete might not be alert enough to complain about shortness of breath. That is why we must be familiar what the signs and the symptoms are that indicate difficulty breathing. Difficulty breathing, a lot of anxiety, a lot of restlessness. We are looking for decreased respiration. Remember, less than 8 breaths per minute, greater than 24 breaths per minute. Is there cyanosis, blue around the lips, indicating that oxygenated blood is not getting throughout the body? Do they have abnormal breath sounds when you are listening with the stethoscope? That is why we should be using this in our clinics all the time. When we are giving initial exams or we are giving comparative exam to our patients in an office setting, listen to the breath sounds. You might not be able to know exactly what the abnormality is but by listening on a regular basis, you are going to be able to pick up if something is abnormal. That is what we want to do as we pick up any type of abnormal breathing on the field. Does the athlete have difficulty speaking? Are they using their accessory muscles of breathing to help them breathe? These are all the different signs and symptoms that there is dyspnoea or difficulty breathing.

How about the altered mental status? That is where that AVPU scale comes in. In the beginning, the patient was alert and orientated. Now, their eyes are closed, and they are only responding when we talk to them. We are seeing their mental status is altering. Is the athlete coughing, trying to expel something that might be obstructing the airway? Is there an irregular breathing rhythm? The athlete might breathe better sitting in a tripod position. Are we finding increased pulse or increased respiration? Again, signs that there is some form of difficulty breathing, maybe some form of obstruction of the airway. Usually, we are going to see people with a barrel chest. We see those who have COPD or emphysema breathing that way. You are saying, “I am not going to see that. I am an athlete,” but you might see it on somebody in the stands because if something happens to a spectator and you are part of the medical staff at the event, they may turn to you to look to help evaluate the individual who is in the stands. You just need to be aware of some of the things to look at.

What is the treatment for dyspnoea? We are going to perform that initial assessment and check the airway, check the breathing and give the patient oxygen. When we cover oxygen later in the module, we will talk about using the non-rebreather mask, the bag valve mask (BVM), and how we will give ventilations because if the patient is in respiratory distress, we need to ventilate them or help them breathe. Of course, we want to check the pulse. Remember, airway breathing circulation. If the airway is not open, they are not breathing, they do not have a pulse, we want to start CPR.

Artificial ventilations. This is only used when a patient cannot breathe adequately on their own. We are going to use a barrier device, like we see in the picture here. First, what you want to do is you want to open the airway. Place the barrier device over the patient’s mouth and nose with the pointy part of the mask over the nose. Take a regular normal breath and give a slow rescue breath at the rate of 10 to 12 breaths per minute for an adult. Remember, as we said, numbers are important. In an adult, we want to give 1 breath every 5 seconds. In a child, we want to give 1 breath every 4 seconds. In an infant, give 1 breath every 3 seconds.

Use the mouth to mask technique and kneel at the patient’s head or on the side, as we see in this picture here. Place the mask on the patient’s face, take a regular normal breath and breathe into the patient for one and a half to two seconds. Remove our mouth from the device and watch the patient’s chest rise and fall. Here is an example of the caregiver standing at the head. We notice they have their gloves on, the proper PPE. We are showing that they are having a C-shape with their hands around the breathing device, or the mask, to help get a secure fit. If the fit of the mask is not secure, when you give the breath, the breath is going to go out the side of the mask instead of inside the injured athlete.

How do we assess if we are doing the right thing? Is it adequate ventilation? Is there equal rise and fall of the chest? Are we ventilating at the appropriate rate? In the adult, 1 breath per 5 seconds. Is the athlete’s heart rate returning to normal? These are all indications we are doing the appropriate thing. What happens if there is minimal, or no chest rise and fall? What happens if we are ventilating too fast or too slow? What happens if the heart rate does not return to normal? Those are all indications of inadequate ventilation. We are doing something wrong when we are trying to ventilate the injured athlete.

We do not want to end up in gastric distension. This is when artificial ventilations fill the stomach with air. This usually occurs if you are going to blow too hard, if you are going to give too many breaths, or if the patient’s airway is obstructed and the air bypasses the trachea and the esophagus right to the stomach. This may cause the stomach to become distended and eventually, the patient is going to vomit. We do not want that to happen. That is why we must know that we are doing things adequately and we must take our time to make sure things are being performed, these tasks are being done, the correct way.

Now, reassess athlete and make sure that the airway is supported. Be aware of any onset of shortness of breath and whether the condition worsened? When we are dealing with an unstable athlete, reassess every 5 minutes, obtain their vital signs and perform our reassessments. We want to transport the patient, as we discussed, any time there is any airway obstruction or difficulty breathing.

When we are dealing with breathing, it is important to be able to provide oxygen to the athlete. If oxygenated blood does not circulate through the body for zero to 1 minute, we are going to find some sort of cardiac irritability. Between zero and 4 minutes of un-oxygenated blood getting to the brain, you are not going to have too much of a problem, but between 4 and 6 minutes, there is the possibility of brain damage if the brain is not getting a sufficient amount of oxygenated blood. From 6 to 10 minutes, brain damage is very likely, and more than 10 minutes of there being non-oxygenated blood circulating throughout the brain, there is going to be irreversible brain damage. That is why having oxygen on the sideline is important.

How do we know it is oxygen? All oxygen containers are green and white, and all containers are marked oxygen. Even more so, to prevent you from giving the athlete something other than oxygen refer to the pin index safety system. This is the regulator, the device that delivers the oxygen, has pins in it that will only fit in the holes in an oxygen tank. This way, the oxygen delivered device cannot be put on some sort of tank that does not have oxygen in it.

What we are trying to do here is preventing hypoxia, which is the body’s cells and tissue not having enough oxygen. How do we know that? What are we going to look for? There will be nervousness, irritability, and fear in the athlete. There will be tachycardia that is speeding up in the heart. There may be a change in their mental status. There is where that AVPU scale comes into play again. They might be using the accessory muscles of breathing. There will be difficulty in breathing and the patient might complain of the possibility of chest pain.

We want to use supplemental oxygen and we know the oxygen container is white and green. It says oxygen on it. We are inspecting the cylinder for the appropriate markings. Then we are going to crack the cylinder and if the delivery device is not attached, this way, we are going to blow out any kind of dust that is in the top of the tank. This way, if we are putting it on the athlete, his or her first breath is not going to be all the dust that was accumulated in the holes in the oxygen container.

After we crack the cylinder, we will attach the flow meter and regulator. The regulator is what delivers the oxygen from the container to the injured athlete. Open the cylinder and attach the proper delivery device to the flow meter. As you can see in the picture on the bottom right, that little piece jutting out is referred to as the Christmas tree and attach that to the device we are using to put on the athlete to administer the oxygen. Adjust the flow meter to desired flow rate and apply the oxygen device to the patient. When done, discard the delivery device, which are disposable, and a one person use device. After we discarded the delivery device, turn off the flow meter and shut down the oxygen container.

What is the oxygen delivery equipment? This is what is called a non-rebreather mask. The picture of it is to the right. We want to provide up to 90% oxygen, and we use this at between 10 to 15 liters per minute. That is what you are going to set the oxygen delivery device to after it is attached to the oxygen cylinder. Another optional delivery device, which you will very rarely use, is called the nasal cannula. That provides between 24 and 44% oxygen to the athlete. If we are going to use that, the setting is between 1 and 6 liters per minute, but most often, we are going to be using the non-rebreather mask. It is important to know the numbers. We want to use this at 10 to 15 liters per minute and will use the bag valve mask (BVM).

This can be used with the help of one to two doctors administering it to the patient. This is a mouth-to-mask ventilation, and this device can also be hooked up to the oxygen container. It is an oxygen-powered ventilation device. A BVM can deliver more than 90% oxygen to the athlete. It delivers less tidal volume than mouth to mask. When we are giving mouth to mask, remember, we talked about taking a breath in and slowly giving the breath to the injured athlete. Everybody’s lung capacities are a little different. You might be blowing too hard, but by using the BVM, as you can see in the picture on the bottom, when we squeeze the bag, we are getting a lesser amount of oxygen into the lungs. Less chance we are going to get that gastric distention we spoke about before. This BVM device, like we discussed earlier, is used when we are using an oral or a nasal pharyngeal airway that helps keep the obstructed airway open.

Two people can use this device. Inserting the oral airway, one caregiver is going to maintain a good seal while the other caregiver is going to squeeze the bag. We want to place the mask on the patient’s face and squeeze the bag to deliver the ventilations. We could see here on the left; it is two people. One person is holding the mask on the patient’s face to get a good seal. The other caregiver is squeezing the bag to make sure we are delivering the appropriate amount of oxygen in a sufficient amount. The picture on the right shows one person using the device. This is a device that is needed to have practice with. The more you practice, the better you are going to be able to and have more comfort in using the device.

Remember, oxygen supports combustion. That means you want to keep all open flames away from the oxygen container. You also must remember that the oxygen container is under high pressure. If the container falls over and the top of the container breaks off, your oxygen container is going to work like a torpedo. It is going to go through the wall and the next wall after that and keep on going until it runs out of high pressure. Because remember, the tanks are under high pressure.

We just talked about breathing, excessive breathing, normal and abnormal characteristics, are we adequately or inadequately providing breathing, dyspnea, ventilating the athlete and gastric distension. We talked about the using of oxygen, and at critical times, it is needed to use the oxygen, how we are operating the oxygen delivery device, and how to use the different types of delivery systems when providing oxygen. Now, we are going to move on to circulation.

Circulations assess after the airway is open and we give 2 rescue breaths. Remember, airway breathing circulation. After we assess for the airway and gave rescue breaths, we know the airway is open, and the athlete is breathing, so now check the pulse and circulation and evaluate for all signs of circulation. We are professionals; therefore, you should be able to pick up a pulse. If it is taking you more than 10 seconds to find the pulse, there is a strong chance the patient has no pulse.

Numbers are important. The normal pulse range for an adult at rest is between 60 to 100 beats per minute. In a child, it is between 80 and 100 beats per minute. In a toddler, it is between 100 and 120 beats per minute. In the newborn, it is between 120 and 140 beats per minute. You will notice the pulse rate and normal ranges is quicker for the younger, smaller patient. We must be careful of what is going on. If an athlete intercepts a pass playing American football and runs the full length of the field and is lying down in the end zone on their back and you get there, and they are breathing more than 24 breaths per minute, you have to realize the athlete might just have ran 100 yards. You must assess the situation. Within a minute or so, if the breaths are backed or the pulse rate is back down to its normal beats, then we know that the athlete is recovering, and things are doing fine. If it stays for a longer period of higher than 100 beats per minute, then we have to start looking for some other form of condition that is developing, and we might have to do some other types of interventions for the injured athlete.

How do we deal with circulation? Check the pulse for 30-seconds x 2, or 15-seconds x 4. We either want to track at the carotid in the neck or the radio in by the wrist, or if we are dealing with a child, we could check the brachial in the arm. Is the pulse strong and bounding, weak or thready, regular or irregular? These different things will determine if there is any problem with the athlete’s circulation.

How do we assess circulation? You need the pulse, the rate, the rhythm, the strength. Assess and control any kind of external bleeding, which we will cover a little later. We spoke about how the skin is the largest organ in the body. The skin is going to give us a lot of indication of whether or not we are getting oxygenated blood or circulation of blood throughout the system by seeing, is it blue around the lips, is the skin pale or flushed? All indications of the possibility of problems with the circulation of blood throughout the system.

Evaluate the skin temperature. Is the skin moist, dry, hot or cold? In children, we want to check the capillary refill. Capillary refill evaluates the ability of the circulatory system to restore blood flow to the capillary system, commonly referred to as perfusion, and is done by depressing the patient’s fingertip, and looking for the return of blood. When you look at a patient’s fingertip, it is nice and pink. When we depress the fingertip, it will turn white. Once we let go, within two seconds, it should be nice and pink again. That indicates that we are getting blood supply throughout the system to the smallest part of the circulatory system, which is the capillary. This is very good when dealing with children, less effective when dealing with adults. One of the things you have to look out for is if the athlete has on now polish, using the capillary refill is not going to be able to see the change in color of the fingernails.

What are the circulatory differences? The heart rate is going to increase for any kind of injury. There is going to be vasoconstriction of the blood vessels to keep the vital organs nourished with blood. Constriction of blood vessels can affect the blood flow to the extremities. That is why things like capillary refill in children are very good to pick up if there are any circulatory deficiencies.

When we are dealing with perfusion, it is circulation within the tissues in adequate amounts to meet the cells’ need for oxygen, nutrients, and waste removal. Some tissues and organs need a constant supply of blood while others can survive with very little when at rest. The heart demands a constant supply of blood, otherwise, if it is not oxygenated blood getting through the heart, that is when there will be a problem of a heart attack. The brain and spinal cord can survive for only 4 to 6 minutes without there being a good supply of oxygenated blood to the brain. The kidneys can survive for up to 45 minutes without oxygen supply. Skeletal muscle can last up to 2 hours. That is why if there is ever an instance that a part of a finger or a hand or something is amputated, you can turn around, find the piece that has been amputated, wrap that in a dry cloth, put it in some water, and put it in a cool place. That can be taken to the hospital because if it has been less than 2 hours, there is a good chance that limb can be reattached.

We want to restore circulation, control bleeding, and improve oxygen delivery as soon as possible. If the athlete is unresponsive and has no pulse, begin CPR.  When you took your CPR class, you learned about why you use an AED, an automated external defibrillator, because the quicker this is used on somebody, we are performing CPR on, the better chance it is going to be for the athlete to survive, however do not use an AED on a patient who has a catastrophic traumatic injury.

[END]

ICSC04 – Emergency Procedures
Section 2
Instructor Doctor Ira Shapiro
Video Lesson: 1:06:04
ENGLISH VERSION DOWNLOAD: ICSC04_Section 2_TRANSCRIPT

This is module 2 of 3 modules for emergency procedures for the sports chiropractor. A quick review of what we did in module one, we talked about PPE, uncertain situations on the field, scene safety mechanism of injury, and the golden hour. We spend most of our time dealing with the initial assessment, developing general impression, assessing the athlete’s mental status, airway, breathing, using an oxygen container, the oxygen delivery system and assessing circulation.

In this module, what will spend time on the patient assessment, dealing with the unresponsive athlete, signs of stroke, the scene, spinal immobilisation using a backboard and using cervical collars. We are going to talk about doing focus and detailed exams, as well as a rapid trauma assessment on the injured athlete whilst on the field. We will cover transporting the athlete, and reassessing vitals. Ongoing assessments, discuss helmet removal and the equipment we should be having in our sideline kit bag.

Dealing with an unresponsive athlete. Ensure the scene is safe before approaching, turn around and establish unresponsiveness in the athlete. Tap them on both shoulders and tried to elicit a response. Are you all, right? Are you okay? If we get no response, then turn around and point to somebody and tell them to go get help, and an AED. These days with phone cameras on the sidelines, someone can be taking out a phone and you are thinking they are calling 911 or medical control but they are just filming the incident that is going on. That is why you need to point to an individual and say to them, you in the red shirt, go get help come back to me and tell me what they say.

This way after a period of time if nobody is coming back you point to somebody else and send them for help. Check for breathing and pulse, remember no shorter than 5 Seconds, no more than 10 seconds. Remember, if we cannot find a pulse within 10 seconds, they probably do not have a pulse and if you are dealing with a smaller population, children and infants, look for their stomachs to rise and fall to give us an indication if they are breathing and remember in a child or an infant, check for pulse at the brachial artery in the arm.

Unresponsive athlete who is breathing. Do a physical exam and continually monitor breathing. They are unresponsive to you but may be breathing, so you might have to assist breathing if needed. We talked about ventilations so remember one to five seconds for an adult, four seconds for a child. Once every 3 seconds for an infant, we want to be able to supply oxygen using a non-rebreather using a BVMS. Remember what we said to container at for a non-rebreather mask? It’s 10 to 15 liters per minute and the BVM, the bag valve mask is an oxygen-powered device.

In an un-responsible athlete treat any obvious injuries and transport them. If the individual is alert and responsive, start out with the ABCs (airway breathing circulation). If our athlete is unresponsive who will start CPR? Deal with compressions, airway, and breathing, why do we want to do compressions? There’s 21% oxygen in the air when we breathe in, when we exhale, we are exhaling 15% oxygen. That means we are only using 6% of the oxygen in the air because the blood in the body is saturated with oxygen and by doing the compressions early on, we are circulating that oxygenated blood throughout the system. Between four to six minutes without oxygenated blood getting to the brain, that is when we are going to get the possibility of brain damage. It’s CAB, start with compressions, airway and then breathing. An adult is someone who shows signs of puberty and older. In the male, it’s underarm hair, in the female, it is the start of breast developments. Whether it is one or two-persons giving CPR to an adult, we want to give 30 compressions because it is usually cardiac-related. If you are dealing with a child, it’s 30 compressions with one rescuer and with two rescuers, it’s 15 compressions. The same thing for an infant under the age of 10. It is only 15 compressions in the younger people, because in a child is usually respiratory-related. That is why we want to give, less compressions before we are giving a breath.

For the airway, use the head toe chin lift maneuver or if we suspect there to be a spinal cord injury, use the jaw thrust maneuver. Compressions, 30 in an adult, child or infant, however if there’s two rescuers, it’s 15 compressions for child and infant before you open the airway and deliver a breath.

Give two breaths and observe the chest rising and falling. If the breaths do not go in, re-tilt the head, chin lift maneuver and attempt a second breath. If the second breath does not go in, do not attempt a third breath, just go right back to doing the compressions. It is compressions, opening up the airway, breathing, going back to compressions if the breathing does not go in. We will continue this until the next higher level of medical personnel get there to take over for you.

How do we determine on the sideline if there is a stroke. A stroke is defined as an acute impairment of the neurological function that results from an interruption of cerebral blood flow to a specific area of the brain. The acronym for this is F.A.S.T.

• Facial drooping
• Arm weakness
• Speech difficulty
• Time to call for emergency help

We will cover the major parts of the patient assessment. On the field after we have completed the initial assessment of the airway, breathing, and the circulation the next thing is to provide spinal immobilisation. If we think there is some form of spinal injury, we deal with mechanism of injury. That is why you should keep an eye on what is happening on the field. If the soccer player plants his foot and turns and goes down, I am thinking the knee injury. But if two of the players go up to head the ball and collide, I am now thinking the possibility of the cervical spine injury and I want to make sure that I immobilise the cervical spine.

Then after that, dentify and treat all life-threatening injuries. Undertake a focused and physical exam and make the determination if transport of the athlete is required so we can do a detailed physical exam. Reassess vital signs and undertake an ongoing assessment. Those are all part of the patient assessment, which fall under the initial assessment. Determine responsiveness using the AVPU scale. An alert and orientated patient does not need CPR, but if you suspect there being a cervical spine injury, you want to protect the cervical spine.

A rapid trauma assessment is a quick once-over to pick up any major obvious injuries. Maintain spine immobilisation, keeping the airway intact, assess the head and neck. Apply a cervical or immobilisation collar if this is part of your training in your country. Once we put the collar on, we are going to obstruct part of the neck so we are not going to be able to determine if there is an airway or a tracheal deviation or whether they have any distended jugular vein. If the patient is wearing a necklace around their neck, warning of some form of medical condition they have, ensure you have assessed the head and the neck before we put on a cervical collar.

Then we want to assess their chest, their abdomen, their pelvis, and all four extremities. Roll the patient with spinal precautions and then assess baseline vital signs. Baseline vital signs are key signs used to evaluate the patient’s condition and we repeat the vital signs further later on so we can compare them to the baseline. This is going to tell us whether or not the patient is improving, whether they are getting worse or whether the interventions that we have done are helping or not helping.

Vital signs are basically respiration, pulse, and blood pressure. These are things you should be doing in your office every time on all patients come in, whether it is your initial exam or it is your comparative exams. However when you are on the sidelines if you are familiar in taking these vitual signs, they should be second nature for you in an emergency situation.

Other key factors when dealing with baselines are skin temperature in adults capillary refill in children. AVPU scale that level of consciousness or direct looking into the pupils. Remember the pupils on the eye is the direct line or the shortest line from outside the body to get into what is affecting the brain. When you are dealing with pupils, one of the things you have to remember is, does the person have an artificial eye? Because if they have an artificial eye, it is not going to respond to light or to the different other responses and this will determine if it is truly a problem or you are getting no response because there is an artificial eye. Stabilising the cervical spine hold the head firmly with both hands, and support the lower jaw. Move the eyes to the forward position and maintain this position until we secure the injured athlete to a backboard.

There is always exceptions, so don’t force the head into a neutral inline position as it may increase muscle spasm, increase pain if the athlete develops numbness, tingling, or weakness in their extremity which is a result of a compromise to the airway or breathing by moving the cervical spine inline neutral position. If any of these things arise, then stabilise the head in the position we found the athlete. Do this rapid trauma assessment, feel the head and neck for any deformity, any tenderness, any crepitation. Both individuals have gloves in this slide. We can see how the first person is securing the cervical spine, which is why being familiar with these types of pre-emergency procedures, may take more than one individual.

A lot of times there are multiple steps, so if the sports chiropractor is familiar with the procedures and, the different steps that need to be done, they become an asset out on the field. After we check for deformities, check for any bleeding. Ask the patient if there are any tenderness in pain when you are checking the head, neck, and cervical spine. Move down to the chest and as you notice, whoever is supporting the cervical spine keep that support until the athlete is on the backboard. We are now looking at rise and fall of the chest with breathing. Looking for any degrading of the bones as the patient breathes, making sure the chest is rising or falling together, not one side is rising as the other side is falling. That is referred to as paradoxical breathing. That usually indicates that there could be the possibility of a flail chest, which is defined as two or more ribs broken or the sternum broken. Listen to breath sounds, and you should be practicing this in the office when you are working on your regular patients. This way, when you get into that emergency situation on the field, you might not know what the abnormal condition is, but you do know that something is abnormal. As you move down to the abdomen, look for obvious injury, obvious bruising, and bleeding. Evaluate tenderness or any other kind of internal bleeding, the lighter the touch, the better. You do not want to palpate too hard. Look at the pelvis for any signs of obvious injury, bleeding or deformity.

We want a gently, inward, and downward pressure on the pelvic bones. That is going to give us an indication of the possibility of there being any kind of pelvic fracture, so again, inward and downward pressure on the pelvic bones. Next, look for any obvious injuries to the extremities and palpate both upper and lower extremities and then assess for pulse, motor and sensory function. This is commonly referred to as neurovascular function. We are going to do an examination of a limb to determine whether or not there is any compromise to the artery, the vein, or the nerves below the site of the injury. That’s what this neurovascular function is for. Check the pulse, the upper or lower extremity.

Check for the motor and function, the motor and sensory function. Ask the Athlete questions? Do you feel me touching your hand? Do you feel me touching your foot or your toe? Can you open and close your hand? Can you wiggle your feet? We are checking the sensory and motor function below the site of the injury. It is indicating any artery or vein or nerve function interruption which is the importance of neurovascular function. Now do a detailed physical exam, which is a more in-depth exam, which is done if time allows. Visualise palpate and record things using the DCAP-BTLs system. Remember, when you are on the field, we are in the medical realm, so use their terminology.

By understanding what the DCAP-BTLs system means, when you are providing a handover to the next higher level of medical care, if you use the medical terminology it will be a more precise handover.

• D there is a deformity
• C stands for a contusion
• A stand for abrasion
• P is the pain level
• B stands for burns
• T stands for tenderness
• L stands for laceration
• S stands for swelling

Let us now perform a detailed physical exam. Look at the face, looking at the area around the eye and the eyelids. Examine the eye, pull back the ears and look for any bruising behind the ear. That is called battle sign. That is a prime indicator of there being some sort of basal skull fracture. We are looking around the ear, at the pupil to see if there is any deformities.

We want to use a penlight and look for drainage or blood in the ears. We are looking for bruising lacerations around the head. When you see drainage or blood in the ears or the nose, look for cerebral spinal fluid which will indicate there has been some sort of skull fracture. Palpate the zygomatic, the maxillae and  the mandible looking for crepitus, deformity, or tenderness. We want to assess for any obstruction in the mouth and see whether or not there’s any cyanosis gluing around the lips, an indication that oxygenated blood is not getting to the area. Check for unusual odors. Remember if we are getting that fruity-type smell in there, that is an indication of a diabetic condition. Make sure if you are doing something at a recreational type of event, non-professional, are we smelling alcohol on the athlete’s breath?

Are they playing in a beer game while they are playing softball at some tournament, which is why we want to check. We are looking for missing teeth, any other kind of foreign body in the mouth, pulling out their mouthpiece, to see if a piece of it is missing on the side. There is a good chance they bit down on the mouthguard and broke a piece off that could get lodged in the throat. Looking at the neck for that tracheal deviation, look for distended jugular veins. Palpate in the front and the back of the neck for any type of deformity and look at the chest. Gently palpate over the ribs, and listen for breath sounds. Listen to both at the base and the apex of the breath of the lungs for these breath sounds.

Look at any kind of abnormality in the abdomen or in the pelvis, noticing general signs of distension of the abdomen, which indicates internal bleeding. We were at a rodeo several years ago and an athlete gets thrown from the bull and gets stepped on by the bull. After we made sure the scene was safe, we entered into the arena. We did the rapid trim assessment and noted a distended abdomen. That was a big red flag that indicates the possibility of internal bleeding. We gently palpated the abdomen, compressed the pelvis, pressed on the iliac crest which indicated the possibility of there being some form of pelvic fracture. Assess the back for any tenderness or deformities.

Then after all of that is done, undertake a focused physical exam. Now investigate the problems that were associated with the chief complaint, doing a detailed exam. The athlete may say “my knee really hurts” so we will start doing a focused exam on the major area of complaint, whilst reassessing the athletes vital signs. Then make the determination if we have to transport the injured athlete and remember you have to document your findings. If it’s not written down, it’s not done. You might remember two days after the incident, but your memory might have gaps four or five weeks down the road when someone asks you about your findings during your detailed on field evaluation.

That is why it’s important at this point as we discussed in module one about getting that sample history from the athlete documented, then the ongoing assessment that lets us know if the treatment, we provided is improving the patient’s condition. Did we do the right thing adequately or did we not? Are there any new conditions that have developed since we did our initial onset, our initial exam?

What are the steps of an ongoing assessment? Repeat our initial assessment, airway, breathing, circulation, reassess and record the vital signs and mark compare them to our baseline vitals. Repeat our focus assessment on the particular injured area the athlete talked about and check the interventions that we have done. Are they doing what they are supposed to be doing? Do we have to change them? Do we have to do additional things? It is important to reassess a stable patient every 15 minutes and reassess an unstable patient every five minutes based on vitals, checking all our interventions.

Dealing with spinal injuries is one of the reasons why other medical professions are reluctant to having chiropractors on the sidelines because they felt we didn’t know how to deal with spinal injuries. We touched more spines in a day than most other healthcare providers touch in a year, so these procedures should come natural to us. We are used to having our hands on people’s spines. What are some of the signs and symptoms of a possible spinal injury? Well of course pain or tenderness when we palpate the spine, do we feel for any deformity in the spine? Is there any tingling in the extremities? Is there loss of sensation or paralysis in the extremities? Those last two things, there is that neurovascular evaluation. Is the patient incontinent? Are there any head injuries? All indications, the possibility of there being some form of cervical spinal injury.

Hold the head firmly with both hands and support the lower jaw; move the eye to the forward position and we want to maintain this position until the patient is secured on a backboard. Do not force the head into a neutral inline position if there’s muscle spasm, pain increases, numbness, tingling or weakness develops in any extremities caused by moving the head to the neutral position as this will compromise the airway or compromises breathing. Assess mental status, using AVPU scale which will be an indication, of the possibility of a cervical spine or spinal cord injury. Assess how well the patient responds to external stimulus using the AVPU scale. Are they alert did they respond to verbal stimulus, painful stimulus, or are they unresponsive? Check their orientation, the patient’s memory to place time and event. If the athlete can recall all four, they are considered fully alert and orientated times four. What are some of the questions we want to ask a patient? If we suspect a cervical spine injury, does your neck or back hurt? What happened? Where does it hurt? Can you move your hands and your feet? Can you feel me touching your fingers and your toes? These answers will give us more of an indication of the possibility for a cervical spine injury. Do the pupils test, are they fixed with no reaction to light? Are the pupils dilated with light and constrict without light? Do the pupils react sluggishly? Are they of unequal size? Are they unequal with light or when the light is removed? Remember to find out do they have an artificial eye, if for some reason there is no reaction when you are checking the pupils. Applying a cervical collar, we checked out the head, and the neck.

Now apply a cervical collar and you should be providing continuous manual inline support of the head. We will measure the proper size for the collar, placing the chin support snugly under the chin. Wrap the collar around the neck, to ensure the collar fits correctly. If the collar doesn’t fit correctly and it is too small, we will extend the neck. If it is too large, then the a possibly for flexion of the neck, which you want to avoid. To apply the collar, start by kneeling at the patient’s head, stabilise the head and neck, maintain that stabilisation whilst you measure for the correct sizing of the cervical collar. Measure from the angle of the jaw to the top of the shoulder. Once we do that, take the cervical collar and adjust it on the side going to the black dot. Note the fingers we can fit from the black dot to the bottom of the plastic part of the collar. That’s when determined the appropriate size for the cervical collar. Make sure that chin piece will not lift the patient’s chin and hyperextend the neck. Make sure that the collar’s not too tight or too small. Put the front part of the collar underneath the chin first and then slide the other part of the collar underneath the neck to attach the velcro, setting the collar in place, making sure it is secured correctly all whilst maintaining that manual in-line stabilisation.

Spinal immobilisation as compared to spinal restriction protocols have changed depending upon where you are. Blunt trauma patients do not need full spinal mobilisation. If the following conditions are absent during the initial assessment of the patient, do they complain of neck or midline back pain? If the answer is no, they don’t need to be fully immobilised. Is there any abnormal neurological function or motor strength in the extremities? If the answer is no, they are normal. Full spine immobilisation is not required. If there is no paranesthesia, full spinal immobilisation is not required. If there is no change in the mental status, we do not have to cervical immobilise the athlete on a backboard with a collar, but if they complain of the neck pain, if there are abnormal neurological and motor, and sensory functions, if there is paranesthesia, altered mental status, then we need to fully secure the athlete on a backboard with a cervical column. Check your local protocols and note the particular area for your standard operating procedure?

We are now maintaining the inline stabilisation. This requires multiple people and we will have the other team members position the immobilisation devices. Log roll the patient, securing them to the backboard and then reassess the pulse, the motor and sensory function and each extremity. This slide you can see a four-man log roll. If there is only three people available, you can use three people, but it is important for the sideline sports chiropractor to be familiar with how to handle these situations so you can help out. The person at the head is the one who maintains the spinal immobilisation. That is now the person in charge and once you stabilise the cervical spine, you are not going to let go of the cervical spine till after the athlete is secure to the backboard.

The person at the head is going to give the rest of the commands. As we place the spinal board parallel to the patient, overlap hands at the hips and at the knees. We want to stabilise the shoulder and the ankle. We overlap at the hips and the knees, because it provides greater stability of the spine as we roll the athlete, increasing the likelihood that the upper torso is not going to be moved in synchronisation with the lower torso, thus creating a possibility of further cervical spine injury. We want to roll the patient as one, keeping the head in the inline neutral position. Once we position the patient on the board, the person who is securing a cervical spine is going to leave the hands in place. The other members are going to now secure the patient underneath the armpits, waist, and knees and slide the patient up and down the board to get them to the appropriate position so we can secure the straps and the other cervical and mobilisation devices.

Now we will apply a device with straps and tape which clips onto the spinal board. The spinal board has a piece on the top that is Velcro. Place them on either side of the cervical spine and take a piece of tape or a strap and run across the forearm and the other strap across the chin to make sure this immobilisation device is secure on the patient’s head and on the backboard. After that, use the straps to secure the injured athlete to the board. Straps go over each shoulder and attach at the waist. We are then going to attach a strap across the waist and crossing from the waist across the knee on one side and then from the waist across the knee on the other side.

This way the athlete will be fully secured to the backboard and when you pick the athlete up and move them, they will not slide off the board. Reassess the pulse, the motor and sensory function, that neurovascular function, and neuro-value vascular evaluation. Here in this slide is a picture of a board and you can see, there are holes on the board on the sides, which is where the straps will go to secure the athlete to the board and also areas for us to grab onto the board when we are ready to pick the patient up for transport. A short board is used for an individual who is in a seated position, usually from a car accident. The longboard is what we use when we want to provide full bodily immobilisation even if for some reason we are using a shortboard to extricate an athlete from a confined space.

Once they are out of the confined space, transfer them on a longboard. If you are dealing with anybody who is working with NASCAR racing, and is injured in a car accident, you will need to use the shortboard while they are in the car and then transfer them to a longboard once we get them out of the vehicle.

Next, is helmet removal. I like using this study because this is one of the first studies that used a chiropractor, Dr jay Greenstein, as part of their Executive Board when doing this study. This is a pre-hospital study on the care of the spinal injured athlete. In general, any athlete who has a helmet, will only have the helment removed on the field, under certain circumstances which include, the face mask cannot be removed to gain access to the airway, like those in a hockey goalie or a race car driver, or mongoose-type helmet where the face mask blocks the airway. Airway is the prioprity so if we can’t access the face and airway, and you can’t remove the face mask, the helmet comes off.

You will also remove the helmet if it prevents immobilisation for transport in the appropriate position, to enable you to stabilise the patient’s head.

The face mask be removed in two ways, by using a trainer’s tool or by cutting the retaining clips that are attached the face mask to the helmet. We can either unscrew the retaining clips or we can cut them. Once the face mask is removed, the helmet can be immobilised against the spinal board and the BVM. The bag valve mask will now be used to assess in ventilations and applied to the airway allowing access if we had to put the oral or nasal airway in to keep the airway open.

• Is the airway clear and is the patient breathing adequately? Yes. Leave the helmet on.
• Can the airway be maintained and the ventilation assisted with the helmet in place? Yes. Leave the helmet on.
• Does the helmet fit well? Yes. Leave the helmet on.
• Can the patient move within inside the helmet? No. Leave the helmet on. Can the spine be immobilised in a neutral position with the helmet on? Yes. Leave the helmet on.

A helmet that fits well will prevent the head from moving and should be left in place as long there is no impending or airway or breathing problem. It does not interfere with the assessment and treatment of the airway as long as the face mask is removed allowing you to properly immobilise the spine. If you are removing the helmet, we have to prevent movement of the head. Here is an example of where a helmet, even though,  weare removing the face mask, does not provide good access to the airway. Support the lower jaw and with a scissor-type movement. Then the other healthcare provider is going to grasp the helmet on the sides, pull the helmet apart and gently remove the helmet from the athlete’s head. If you are dealing with a football player, American football, or other individuals who are wearing shoulder pants, we must remove the shoulder pads before we remove the helmet because if the shoulder pads are left on and the helmet is removed, there’s a greater chance of their hyperextension of the head and neck.

If there is any cervical spine fracture, that hyperextension may actually sever part of the spinal cord. That is why we want to keep the head in a stable inline position and remove the shoulder pads before we remove the helmet. As we look at immobilising and transporting the injured athlete, care must be taken to avoid injury. Certain patient conditions call for special techniques, therefore you need to practice using the equipment. Kneel beside the unconscious athlete, so we can straighten the patient’s legs and move the nearer arm above the head. In this image the patient’s knee is bent, as there is a possibility of a broken leg. The broken leg is not the priority if the patient is unconscious and not breathing, and there is no pulse. The patient is going to die without an active airway.

Therefore our priority is to position the patient in a position that will allow us to evaluate ABC and start compression should it be needed. Straighten the patient’s legs, move the arm on the side you are turning the athlete above their head, and turn the patient by pulling the distal hip and shoulder. Control the head and neck so the torso’s movement is in one unit. When we looked at moving, using a log roll, we are now preparing to place the athlete on the spinal board, using four individuals. The more people there, the easier it is to control and stabilise the injured athlete’s body. That is why being on the sidelines and familiar with these procedures will be an asset to you and the integrated medical staff that may be there.

We will roll, put them on the backboard, and then we can assess their airway and breathing, which is all about positioning an unconscious athlete. As you look at this slide we are maintaining that inline stabilisation. Have other team members position the immobilisation devices and apply the cervical collar. Anticipate and understand every step of the process because everything you are doing, must be coordinated. The person at the head who is securing the movement of the head and gives the instruction to the other team members, overlapping the hands at the waist and at the knees, getting ready to move the patient as one unit. Instructions should be given in two parts and the team members must know what they are, “I will say, one, two, three, roll. Then on roll we will roll together”.

Sideline First Aid Equipment. Most of this initial information comes from Bart Green and Hal Rosenberg. Both these doctors have done several research papers and publications of sports-related chiropractic articles. You need to have proper knowledge of wound care, including the supplies to provide the appropriate care on the sidelines. You must be familiar and comfortable using all equipment in your sideline kit bag. If you are not trained on a piece of equipment, do not bring it. This opens up the possibility for legal action and causes negligence if you use equipment which causes further harm. If you have essential equipment in your medical bag that you do not know how to use, I would rather you not bring. Because if you are not familiar and competent in using it and then not use it the right way you could cause harm to athlete. Your sideline sports bag should be big enough for the equipment you need, depending upon the event you are going to cover. I normally have three different bags. One big bag carries everything, and one bag for my emergency equipment, like oral nasal cannulas, blood pressures, stethoscopes, cervical collars. Then I have another smaller bag, which I use for other types of injuries on the field. The bag should be big enough to carry the necessary equipment but not so large that it is difficult to carry around. The bag should have compartments and dividers. You can keep items in different areas and be familiar with where they are as opposed to them being all together in the bag. Your first aid bag should be waterproof and with you on the sidelines as long as the event goes on. If it is raining, you don’t want the content getting wet.

• Content of first aid kit:
  We should foremost have a blood pressure cuff, to check vital signs, sizes for adults and children.
• We should also have a stethoscope in there to help with blood pressure.
• To assess breath sounds we need airways, oral and nasal airways.
• We talked about cervical collars. We need to have assorted sizes. There is now something called a universal collar that you can adjust the size or different colors come in different sizes. Whatever you have, whether you have the universal collar or you have the different size collars in your bag, just be familiar with using them.
• Include a pen light so we can look in the ears and the mouth to check for fluid or objects to check the pupils.
• Qauze pads four by fours and five by nines. When you put a gauze pad on a bleeding wound, that’s called the dressing.
• When wrapped in roller gauze, that’s called the bandage, so we want to have both the four by fours, five by nines and some roller bandage.
• Pocket mask in a case for artificial ventilations and make sure that you are familiar with the proper use of the pocket mask.
• Scissors so we can expose the injured area.
• Different kinds of tape, of assorted sizes. If we have tape you should have a shark, which is used to remove the tape.
• A tooth preservation kit, especially if you are dealing with young children.
• Skin lube in case there’s abrasions or irritations. You can put the skin lube on before you apply the tape on the area.
• A digital thermometer.
• Tuning fork which is a very good instrument to use on the field to help determine if there is cracked or broken bones. Remember, the bones resonate at about 125 hertz. The tuning fork is pretty close to that. The periosteum, the outer layer of the bone is very pain sensitive, so if you put that tuning fork on it and there is a break, there is going to be a stinging sensation that the athlete is going to feel.
• A cell phone. You could be out in the middle of nowhere or far away from the medical station. You want to be able to contact the appropriate people to have additional aid brought to where you need it.
• Alcohol pads so you can clean and around an injured area.
• Band-aids (frabic strips) of assorted sizes to protect the exposed area if there is a cut.
• Ice packs to help control bleeding.
• Accident or injury reporting forms.If you didn’t write it down, it didn’t happen. Take that sample history if you can and log all the information down on a form. This way you can keep it if you have to refer to it at a later time.
• Lots of gloves. We talked about PPE, which is personal protective equipment. Protect yourself from any kind of bloodborne pathogens or from any diseases that are in any bodily fluids.
• Have a watch, preferably with a second hand, so we could check pulses and breath breathing rates. Important to have a watch with a secondhand.
• Pen and clipboard to write things down.
• Antiseptic spray.
• Antifungal spray.
• Reflex hammer.
• Steri strips to help close an open wound.
• Cotton swabs in case we have to apply creams.
• Sting swabs are used to help somebody that has a bee sting. For athletes over 18 or an adult, I will often provide allow some sort of antacids. They are under a lot of stress and anxiety and their stomach might be upset.
• Saline solution in case an athlete loses a contact lens or you need to wash a wound.
• A splint for a broken bone
• Hydrogen peroxide which is good for cleaning blood and an injured wound.
• Safety pins. You don’t know how many times we’ve been at endurance events where athletes are wearing bibs and they lost their safety pin and they can’t keep the bib on and you can’t participate without the bib.
• Nose plugs. We have looked after a lot of Taekwondo events which are prone to nose bleeds. Nose plugs will help stop nose bleeding.
• Sunblock for outside event to protect against the hot sun.
• Nail clippers. How many times do athletes get a hangnail or something and needs to be clipped.
• Tweezers or splinter remover. Sometimes athletes are getting splinters and using the tweezer can help remove the splinter.

All these little things will make a great sideline kit bag , for every situation that arise. It’s always good to have these little things there to help you out.

• I have Bio freeze China gel mineralised, icy hot, or whatever you want to use.
• I have a space blanket to keep the athlete warm if there’s any kind of life-threatening condition that’s developed and you need to keep the athlete warm.
• I also carry trauma dressings. Trauma dressing is like a big diaper that has straps on it. This way it could absorb the blood.
• We want to have triangle bandages to help for splinting and immobilisation and helps when a person is bleeding.

Make sure all your equipment is up to date and you check expiry dates. We have covered a lot in this module and I look forward to joining you to continue this conversation in the next module.

[END]

ICSC04 – Emergency Procedures
Section 3
Instructor Doctor Ira Shapiro
Video Lesson: 1:01:57
ENGLISH VERSION DOWNLOAD: ICSC04_Section 3_TRANSCRIPT

This is Module 3 of three modules for Emergency Procedures for the Sports Chiropractor. In Module 1, we spoke about PPE, Personal Protective Equipment, when dealing with uncertain situations, scene safety, mechanism of injury and the golden hour. Then we went right into initial assessment, developing a general impression, assessing mental status, assessing airway, assessing breathing, the use of oxygen and assessing circulation. In Module 2 we dealt with the unresponsive athlete and how you identify the warning signs of stroke. Then we covered scene safety, spinal mobilization, using the backboard, and using cervical collars. We looked at focused history and physical exam, a detailed exam, reassessing vitals, transporting the injured athlete, ongoing assessment, helmet removal, and what goes in a sideline kit bag.

This Module 3, we are covering bleeding, the conditions with possible serious bleeding, about dealing with internal bleeding, external bleeding, using a tourniquet and then we are going to touch on bleeding from the nose, the ears, and the mouth. We will discuss penetrating neck injuries, lacerations of the great vessels, move into dealing with shock, the types of shock, the progression of shock, perfusion, splinting and some general principles, applying a rigid splint, some of the hazards of improper splinting. Then finally we will cover environmental emergencies, dealing with heat related illnesses and cold related illnesses before finishing with discussing some soft tissue injuries.

Let us look at bleeding and shock. These are things when you will address first when undertaking your sideline assessment. What conditions are you going to think of when assessing for serious bleeding? Is there significant mechanism injury? We spoke about that in the first module, taking into account the poor general appearance of the patient and assessing to reveal signs of shock. We are going to look to see if there is significant amount of blood loss noted and if the blood loss is rapid or whether we cannot control any external bleeding? These are all conditions which lead to serious bleeding.

Internal bleeding may not be readily apparent. When I was doing a rodeo event, a cowboy got thrown from the bull and was stepped on. After we made sure that the scene was safe in the arena, we evaluated the injured athlete. The first thing we noticed was his abdomen was distended and swollen. If you do not know what the warning signs are, you are not going to know that a swollen abdomen is one of the primary things that indicates there is some possibility of internal bleeding. That is why it is important to understand the mechanism of injury and when on the sideline as a doctor, you should be watching and paying attention to what is going on the field of play at all times.

What are some signs of internal bleeding? Is there ecchymosis or bruising around the abdomen or the chest region? Is there a hematoma bleeding beneath the skin? Is the athlete vomiting blood? We are not going to be too worried about black, tarry stools because that is not something we are going to see when we are dealing with the athlete on the field. Is the athlete coughing up blood? Is there pain, tenderness, bruising, and guarding or swelling over the abdomen? That is the number one sign to look for the possibility of internal bleeding. Are there broken ribs? Is there bruising of the lower part of the chest or is that rigid distended abdomen? That is a very big sign for the indication of internal bleeding.

What about external bleeding? Hemorrhage means bleeding and the body cannot tolerate greater than a 20% loss of blood. In children, it is a 25% loss of blood. We must remember that there are five liters of blood in an adult body, so the loss of one liter can be dangerous. In children, the loss can be between 100 and 200 milliliters. That indicates that there is a possible serious problem. Children degenerate rapidly as opposed to adults. An adult is via a slow, steady decrease in their condition. A child, they are going to be fine. Then all of a sudden, they fall off the table, and out of nowhere, we have the rapid change in a the patient’s condition.

What are some of the characteristics of bleeding? We have arterial bleeding and that is blood that is bright red and spurts out. It is bright red because it is oxygenated. It spurts out because every time the heart contracts, it is pushing the blood through the arteries. That is where we are getting that blight, red blood that spurts. Venous blood is darker red and it does not spurt. It is dark red because there is not as much oxygen in it, and it does not spurt because it is going back to the heart through the venous system. The third thing is capillary bleeding, and that is when the blood just oozes out and it is controlled very easily. That is usually you see when somebody scrapes something, and it starts to bleed.

How do we get to control external bleeding? The most important thing is following the PPE, personal protective equipment, using gloves and using a face shield if necessary. Responsive athlete is ABCs, airway, breathing, and then dealing with circulation. Make sure that the patient has an open airway and the patient is breathing adequately. If necessary, we might provide oxygen. We spoke about that in one of the earlier sessions, and there are several methods to control bleeding.

Direct pressure and elevation are the most common and effective way to control bleeding. Apply pressure with a gloved hand or finger over the site, as you see in the picture here to your right on this slide. Slightly elevate a bleeding extremity which will often stop venous bleeding. Use both direct pressure and elevation whenever possible and apply addressing. We spoke about that having four by fours or five by nines, when we looked at our first aid content and having the proper equipment on the sidelines. Wrap that dressing in a bandage as we see on the bottom picture here.

When things get serious or there is an amputation, we will look at applying a tourniquet. Fold the triangular bandage into four inches thick and wrap the bandage, using a stick as a handle to twist and secure the stick. Write TK and the time and place it was applied to the athlete. Why do you want to do that? There are different parts of the body that can go for different periods of time without a blood supply. If a limb is amputated, we have up to two hours to be able to replace that or reattach that limb and still have the possibility of that limb to function normally. That is why it is important to write TK and the time and place that you applied the tourniquet on the athlete.

Precautions when using a tourniquet. Place the tourniquet as close to the injury as possible, but never over the joint and never use narrow material. The wider and thicker the material, the better it is. Use wide padding underneath the tourniquet and never cover a tourniquet with a bandage. Once we put the tourniquet on, we do not want to take it off or loosen it. It must be done in a controlled environment and on the sidelines, it is not a controlled environment.

Let us talk about bleeding from the nose, the ears, and the mouth and some of the causes? The athlete could have a skull fracture, some sort of face injury, or some sort of sinusitis. Usually we see this early in the morning, when somebody first wakes up and the heat has been on overnight causing a mucus membranes and the nose to dry out. you get a lot of that time some sort of sinusitis, some sort of bleeding. Athlete may be bleeding from the nose due to high blood pressure or they might have some coagulation disorders or might suffer from some sort of digital trauma.

How about controlling a nose bleed? Follow the PPE precautions and in the 60’s when I was first learning, it was always have the person tilt their head backwards, however now with advancements in our methods, we know that tilting the head backwards, the blood is going to run down and into the stomach and the patient could possibly vomit. You want to help the patient sit and lean forward and apply direct pressure by pinching the patient’s nostrils or you can put a piece of gauze underneath the patient’s upper lip and gum, which will help slow down nose bleeds. You can consider putting ice over the nose, (but monitor any ice near the head) to assist to slow down the bleeding and if you can’t stop the bleeding in a relatively short period of time (up to 10 minutes) you will now consider transporting the athlete to a medical centre for assessment.

How about bleeding from the skull fractures? Do not attempt to stop the blood flow because if there is a fracture and if you put any pressure on it, you might be pushing some of the bone fragments into the grey matter of the brain, creating more issues. Instead, loosely cover the bleeding site with a sterile gauze, being careful of any cerebral spinal fluid present. In that case, we are not only going to see. what is called a battle sign, which is swelling behind the earlobe, or we might see raccoon sign which looks like person has black eyes.

How about dealing with penetrating injuries of the neck? These injuries can cause severe bleeding, the airway, the esophagus, and the spinal cord can be damaged from penetrating neck injuries. Direct pressure should control bleeding in most situations like this. Place a dressing on the neck using a roller gauze, wrap the bandage around and under the patient’s opposite shoulder. Be careful not to wrap the bandage around the patient’s neck and start preparing for prompt transport, as this is a situation where we might see the development of shock.

The large vessels of the body, the superior vena cava, inferior vena cava, pulmonary artery and veins and aorta are all contained in the chest. Any kind of severe chest injury, whether it is blood trauma or if an open chest wound, be careful to make sure these vessels have not been lacerated because that is the possibility of there being fatal bleeding. We might have to start with CP and give some ventilatory response support. We have covered giving supplemental oxygen, types of devices to use and how to use an oxygen container in a prior module. Anytime we suspect that any of the great vessels of the body are lacerated, consider transporting the patient immediately.

What are some of the major arteries and veins? We have the aorta, pulmonary, carotid, femoral, brachial, the radial. Dealing with the upper extremity, lower extremity, chest, veins, superior vena cava, inferior vena cava and the pulmonary vein. We must be knowledgeable and understand how to find each of these along with the signs of any laceration of these large arteries or veins.

What is the emergency care? As always, follow PPE precautions. We want to maintain an airway and we want to give O2. We want to control external bleeding and care for any internal bleeding. We want to monitor and record vital signs. Remember, the first set are called baseline signs. In an unstable athlete, we want to reassess them every five minutes. If we suspect to be no possible fractures, we may elevate the legs and help maintain the body temperature by putting blankets over and under the athlete. Once again, when we suspect serious bleeding, we want to transport these athletes to the hospital immediately that goes with the golden hour that we spoke about in earlier modules. That is the time from then there is an injury to the injured athlete is in the hospital who might have a serious life-threatening condition which gives the best chance for the athlete to survive.

We are going to move into shock. Shock is when the circulatory system is unable to deliver significant amount of blood to the organs. There are many different causes and the athlete may have an increased hard rate, increased respiration or pale or blue skin. Remember, the skin is an organ, and we are dealing with circulation. Circulation has a lot to do with blood flow to the organs. That is why we might see some pale or blue skin. It is understanding when we are dealing with a different population that children do not show decreased blood flow and decreased blood pressure until shock is severe. Remember, the adult has a slow, steady decrease. The child looks fine and then like falls off the table. Degenerates very rapidly.

Shock is defined as a state of collapse and failure of the cardiovascular system that leads inadequate circulation. Without adequate circulation and blood flow, cells cannot get rid of metabolic waste and they die. Now, there are different types of shock. There is cardiogenic shock, there is neurogenic shock, there is hypervolemic shock, there is hemorrhagic shock, there is septic shock, psychogenic shock, anaphylactic shock, diabetic shock, respiratory shock, and metabolic shock. Let us talk about the each individual types, but first, we need to know the progression of shock.

The first is compensated shock. That is the body senses the decrease of perfusion. Perfusion is oxygenated blood going throughout the body and attempts to compensate for it. The body knows there is something wrong and tries to take care of it itself. How many times have you heard about that?

The next stage, which is the most important stage, is decompensated shock. This is the point when the body can no longer compensate for the lack of perfusion. This is when we see a range of conditions like the blood pressures, the pulse, the mental status changing. These are the things that we must be more aware of because if the conditions progress further, the person will go into irreversible shock. That is when the body has lost the battle to maintain perfusion to the organ system which is certain death, no matter what you do to assist the athlete, they are going to die. That is why we work fast to avoid the conditions progress to irreversible shock and important to understand the warning signs and symptoms for decompensated shock so you can act quickly.

When do we expect shock? Well, if there are multiple severe fractures. Any abdominal chest injuries, or spinal injuries, is why we are being careful and paying attention to what is happening on the field and the seeing the mechanism of injury. There are also times when shock can occur from severe infections from a major heart attack, Anaphylaxis, or a reaction to something that is happening around us, or some form of medical emergency. What are some of the signs and symptoms of compensated shock? The patient will become agitated, anxious, restless or a feeling of impending doom “as if they are going to die”. That is what they are talking about when someone is feeling of impending doom. When they feel like that the athletes mental status alters.

We spoke earlier about the Oedipus Scale and changing mental status? Is the athlete alert that he respond to verbal stimuli? Did they respond to painful stimuli or are they unresponsive? This is the changing or the altering of the mental status of the athlete and you most likely find a weak pulse because we are dealing with the circulatory system. The skin may be clammy or pale and there might be shallow or rapid breathing, shortness of breath, feeling of nauseous or vomiting, and/or delay in capillary refill. Capillary refill is by depressing the fingernail. It should go from pink blanche to a white. Once we take our finger off in less than two seconds, it should be pink again. If we are finding that it is not returning in less than two seconds, this is an indication of the possibility of shock. The athlete might complain of marked thirst, but there might be servel different reasons why the athlete may be thirsty.

What are the signs and symptoms of decompensated shock, falling blood pressure? Take those baseline vitals and if you have an unstable athlete, every five minutes recheck those basic vitals. One of the things you will notice is falling blood pressure. Is the patient having laboured or irregular breathing? Is the skin cyanotic? Remember, the skin is an organ, is there a thready or absent pulse? Do the eyes look dull, or the pupils dilated? We are probably not going to find much with poor urinary output because we are dealing with the athlete on the sidelines, because we want to make sure the athlete does not progress to irreversible shock. This is the terminal stage of shock. Even the transfusion of any type will not be enough to save the patient’s life. We are trying to prevent the patient from getting into irreversible shock.

What is some of the emergency medical care? Make sure that there is an airway, it is open and keep the patient supine. Once the patient is in the supine position, that is when we can start all our interventions. Control external bleeding and splint any broken bones or joint injuries. We always want to provide oxygen, remembering that shock is dealing with the cardiovascular system. We are not getting enough oxygenated blood throughout the system so we can provide them with high flow O2. As you see in this patient to the right has a non-rebreather mask.

We are going to set the oxygen regulator at 10 to 15 liters when we are using a non-rebreather mask, remembering how important it is to understand what the numbers are and the different settings.  Place a blanket over and under the athlete to keep them warm. If there are no broken bones, we can elevate the legs six inches to 12 inches. This will assist to regulate the blood throughout the body within the internal organs to keep them nourished. Because remember, shock is when we are not getting enough blood to the internal organs. Do not give the patients anything by mouth because if there is a serious problem and surgical intervention in the hospital is required, we want to make sure that their stomach is empty.

One of the different types of shock include, cardiogenic shock. This is when the heart lacks the power to force the blood through the circulatory system. Onset may be immediately or not apparent for a period of time, but the heart lacks the power to force the blood through the circulatory system. How do we treat cardiogenic shock? The patient may breathe better in a sitting or semi sitting position. Administer high flow oxygen and assess the patient with ventilations. Give one rescue breath every five seconds in an adult. Have the suction nearby in the case the patient vomits. If we are bringing equipment on the sideline in our kit bag, we must be able to use all the equipment that we bring. If you have a suction device and you do not know how to use it and you brought it along, that is when you can get yourself into trouble. The suction devices are usually better suited for the ambulance where they have power driven suction devices. Anytime we are going to think of any cardiogenic shock, we want to transport the patient immediately.

How about cardiovascular causes of shock? Will you also have what is called pump failure? That is inadequate function of the heart. It is not that it is not strong enough to pump, it is just inadequate function. It is not operating the right way. This causes a backup of blood into the lungs resulting in pulmonary edema, which leads to impaired ventilation where the patient is not getting enough oxygenated blood throughout the body, which will create shock. We could have poor vessel function which happens when there is damage to the cervical spine that may affect and control the size and the muscular tone of the blood vessels. What happens? The vascular system increases and the blood in the body cannot fill the enlarged space, so we get neurogenic shock. A cervical spine injury causes damage to the nerves, which causes the bodies to vascular system to increase, again, neurogenic shock. We are chiropractors. We deal with the spine all the time. This should be something very easy for us to handle. We are used to having our hands on cervical spines on a regular basis.

Next is hypovolemic shock or content failure that results from rapid blood loss. The blood loss could be external or internal. That is why we must be aware of what the signs are of internal bleeding. The number one sign is that hard, distended, bruised abdomen. Severe thermal burns can cause plasma loss. Plasma loss is the loss of fluid. It is not necessarily something we are going to see unless you are dealing with sports like motocross or NASCAR. When there is some sort of crash and there is a fire, you might be concerned about there being some sort of type of burns, fluid loss, and some form of hypovolemic shock. Remember that dehydration aggravates shock. Please make sure that the athletes are hydrated, especially in the hot humid weather.

We could also have combined vessel and content failure, multiple types of things causing shock. Some patients with severe bacterial infections or toxins or infected tissue can contract septic shock, which will not be something you would usually see on the sidelines. Toxins may also damage the blood vessel walls, causing leaking and imperative ability for them to contract, resulting in some form of shock. Shock leads to dilation of the vessels and loss of plasma, causing hypovolemic shock.

How do we treat hypovolemic shock? Start with controling the obvious bleeding, and splint any bones or joint injuries. If we see no fractures, raise the legs six to 12 inches, keeping all the blood nourishing, the vital organs. Secure the airway and maintain the airway as that is when we might have to use a nasopharyngeal or oropharyngeal airway.R emember we would want to give oxygen as soon as we suspect any form of shock, to get oxygenated blood or perfusion throughout the body as quickly as possible. Anytime we suspect shock, we want to transport the athlete quickly.

What are some instances of non-cardiovascular shock? Respiratory insufficiency. The patient may have a severe chest injury or airway obstruction and may be unable to breathe adequate amounts of oxygen. Insufficient oxygen in the body is going to produce shock. It is the failure of the cardiovascular or the inability for oxygenated blood throughout the body. We also may have anaphylactic shock. This occurs when a person reacts violently to a substance. There are normally four categories, injections, stings, ingestion, inhalation. More so than not, we will find this on the sidelines if an athlete gets stung by a bee or some type of insect, which is normally the type of anaphylactic shock you will see on a sideline.

This is part of your first aid training, however anytime an athlete has a server reaction causing anaphylactic shock, they usually carry an EpiPen with them. Help the athlete administer EpiPen, epinephrine immediately. Call emergency services immediately, to organise prompt transport and give them oxygen and be ready to assist their ventilations whilst you wait for assistance to arrive.  Remember, anytime an EpiPen is used, the athlete must be transported to the hospital.

We might have psychogenic shock that is caused by a sudden reaction of the nervous system that produces a temporary generalised vascular dilation. This is commonly referred to as fainting or syncope, and it can be brought on by several causes from fear or bad news to unpleasant sites. You have a young baseball athlete, has not really played much. A ball is hit to them in the outfield and they have a feeling of fear, “I am going to drop the ball.” They have this vasodilation and pass out, psychogenic shock. We are treating psychogenic shock. It is usually self-resolving. Once you have assessed the patient from injuries which may have been caused by passing out and falling, if the patient has difficulties after regaining consciousness, we must assess for other conditions.

We are going to hit neurogenic shock, which is damaged to the cervical spine, which causes widespread blood vessel dilation. Circulatory failure is caused by paralysis of nerves that control the size of the blood vessels. These are one of the things that they did not think sports chiropractors are capable of handling, a cervical spine injury, however we touch more spines in a day than most physicians touch probably a month or a year.

Let’s explore how do we treat neurogenic shock? Maintain the airway, assess breathing, assist ventilations which we talked about artificial ventilations. We want to maintain body temperature, keeping them warm, and getting them ready to transport promptly. In this image we see there is damage to cervical spine and the vessels are dilated, the normal vessel versus the dilated vessel at a circumference of the dilated vessel is so much larger. Same amount of blood flow just in a larger space which is a concern.

Let us move on to splinting and types of splints? There are flexible or rigid device used to protect the extremity. Unless the patient has injuries which are critical, injuries should be splinted prior to moving the patient as it helps prevent further injury. When we have the possibility of needing a splint, improvised splinting materials whenever needed. Take a branch off a tree, a piece of wood from the bench, anything you can find to make a rigid device to support a fractured limb. The principles are remove the clothing from the affected area so you can expose the injured limb. Note and record the patient’s neurovascular status. The importance of neurovascular status lets us know whether or not there is a proper blood and nerve supply below the site of the injury.

In case there is an open wound, say an example of a compound fracture, we want to cover all wounds with a dry sterile dressing. This way it is going to prevent the possibility of infection. Do not move the patient before splinting unless we think the situation is critical. Immobilise a joint above and below the injured joint and pad all rigid splints. Maintain manual immobilisation by using a constant general manual traction if needed. Find resistance to the limb alignment when you are trying to manually immobilise it, splint the limb as is in the deform position.

Immobilise all suspected spinal injuries in the inline neutral position. If the patient has signs of shock, align the limb in the normal anatomical position, and transport them. At any time we have any signs of shock, we always transport the patient and when in doubt splint.

What do we see here? They are using gloves on their hands, we see one of the medical personnel providing gentle support inline traction of the limb. The other EMT places a rigid split alongside or underneath the injured limb. The padded side goes against the body, place the padding between the limb and the splint as needed. Secure the splint to the limb with bindings. All those are cravats or strips of cloth. Never put the binding directly over the injury site. As we secure the splint, recess and assess and record the distal neurovascular function which will tell us about the blood and nerve supply below the site of the injury.

Here we see them working on an upper extremity as we see on the top picture manual inline support. A lot of times, in the upper extremity, when the forearm is fractured, it is usually both the radius and the ulna. You notice in the middle picture we are seeing that they are placing a roller bandage in the hand. That is called position of function. This way, if the hand is cupped like that, if for some reason there is a permanent damage and the patient loses use of their hand, if the hand is cupped like that, they could still use a fork or hold some sort of drinking cup in their hand. If the hand was left flat and they cannot use the hand anymore, they would not be able to use a fork or a spoon or a cup.

What are some of the hazards of improper splinting? It could be compression of the nerves and tissues and blood vessels. Correct or check for neurovascular function. Improper splinting can cause a delay in transport of a patient with a potential life-threatening condition. Improper splinting can reduce distal circulation which support the rationale for checking neurovascular function. It could also aggravate the injury, or it can cause further injury to the tissues, the nerves, the blood vessels, or the muscles.

Let us move on to environmental emergencies and this is mostly heat related illnesses. Heat illnesses is a common problem in the hot human weather. It is poor adjustment to hot weather and dehydration. All heat-related illnesses are preventable, however we need adequate time to adjust to the heat. Athletes need to have adequate liquid intake, stay hydrated, have a normal dietary intake, and  eating a normal diet. The first cause of a heat-related illness is referred to as heat cramps. This is an inadequate adjustment to the hot weather and generally not life-threatening. This is when you are going from a cold environment into a hot human environment and you are not giving the body enough time to adjust to the weather condition. We are normally going to find that muscles in the arms and the legs go into spasm. The athlete has a lot of heavy sweating. What is the treatment? In this case, it is increasing our fluids. We can massage or stretch the cramped muscles and rest the athlete in a cool environment and apply ice to the injured area.

How do we prevent heat cramps? Maintain adequate fluid intake. That means 30 minutes before the exercise, consuming at least 16 ounces of fluid, drinking four ounces of fluid every 15 minutes during exercise. After exercise, all weight is usually water weight. After we exercise, we should be drinking 16 ounces of fluid for every pound of body weight that is lost. 16 ounces of water weighs about a pound. Increased fitness will help people prevent heat-related illnesses or heat cramps. The wearing of light color or lightweight clothing. For the young athletes, avoid alcohol, caffeine, coffees, high energy drinks, and sodas. A lot of athletes are drinking energy drinks that are filled with caffeine.so be sure to keep the athletes hydrated with a balance of water.

The next stage is heat exhaustion. This is long exposure to the hot, humid weather, caused by been in the hot environment for long periods of time. Generally not life-threatening, however symptoms we are going to find here ate the skin is going to be cool, pale, and moist. The athlete might complain of headache, dizziness, or poor coordination. The athlete will be sweating profusely. What do we do for this? In this case, we are going to stop the activity and get the athlete to rest in a cool place. If the patient is conscious, give them some water and put cool compresses in the groin under the armpits and at the base of the neck.

The athlete must be referred to the medical doctor if they do not recover quickly. How do we prevent heat exhaustion? Just like anything else for heat-related illnesses, maintain adequate fluid intake, 30, 40 exercise, drink 16 ounces of fluid, four ounces of fluid every 15 minutes during the exercise or the competition, replacing lost fluids from the last time they exercise. Make sure they have appropriate fitness, allow time for rest and cool down, wear light clothing and avoid the alcohol, the caffeine, the coffees, and the soda.

Heat stroke is when the body’s temperature control system shuts down. This is a true medical emergency so you need to act quickly. What are the symptoms? Hot, dry, red skin, a rapid pulse. The major sign, no heavy sweating. You notice in the other two, heat stroke, no heat cramps. In heat exhaustion, there is heavy sweating. In heat stroke, there is no sweating at all. That is the big red flag. The athlete might be confused, or dizzy. There might be some chains in the athlete’s altered mental status. A treatment for this is immediately cooling the athlete. Put them in a tub of ice in a cool room. Ice packs underneath the armpits in the groin at the base of the neck. This is a true medical emergency. The athlete must be transported to the hospital immediately. Be alert and monitor for the athlete breathing, and be ready to assist with artificial ventilations, or other hard compromise, or CPR.

How do we prevent this? The same as we did for the other injuries. Adequate fluid intake, drinking fluids 30 minutes before the exercise, four ounces of fluid every 15 minutes during the exercise, restoring of loss fluids from the last time they exercised, making sure they have the appropriate fitness. Make sure we allow them time to rest and cool down in between sporting events, the wearing of light, color, and lightweight clothing. Remember, avoid the alcohol, the caffeins, the sodas, the coffees. Now, we dealt with heat related injuries.

Cold-related injuries and trying to prevent hypothermia. Normal body temperature is around 98.6 F (37 C). Hypothermia is when the internal body temperature falls below 95 F (35 C).

This is usually because of prolonged exposure to cold and freezing temperatures. The temperature does not need to be below zero. There are different ways of losing body heat because heat is going to travel from the warm body to the cold air.

What are some of the ways we are going to lose heat? We can lose it by conduction. That is the direct transfer of heat from the body to a cold object, like when the warm hand touches the cold metal bench or convection when heat is transferred to the circulating air. Standing outside in the windy weather in lightweight clothing. Evaporation, it is the conversion of a liquid to a gas that requires heat, like when you sweat. It is like when you come out of a swimming pool, and you have that sensation of cold as the water evaporates from you. Radiation, loss of body heat directly to a cold environment, just standing in a cold room or standing outside in the cold weather. Respiration, remember, the body loses heat as the warm air and the lungs has exhaled. Remember when we were kids, we act like we were smoking cigarettes, but blowing out the smoke when we breathe in the cold weather? That is an example of how we are going to lose heat from the body.

Some of the signs and symptoms of hypothermia are when the body internal core temperature is dropping. We are going to look for blue lips and fingernails, as the athlete is shivering because the active movement of muscle is going to create heat to help compensate for the hypothermia. The body functions begin to slow down, poor coordination might have some memory loss, loss of sensation to touch. How do we prevent hypothermia? We want to prevent further heat loss by removing the athlete from the cold environment, remove the wet clothing and wrap them in a dry blanket.

Put heat packs in the groin, the base of the neck, and the armpits.  Do not massage the arms and the legs, which is different. When we had a heat cramp, we talked about massaging the muscle that was in spasm. When there is a cold related illness, we do not want to massage the arms or the legs, but give them some food or warm drink.

Frostnip is the long exposure to cold and in this instances, we might have some freezing of the skin. The deep tissue is unaffected, and this is usually not painful. The next involved is what they refer to as trench foot which is prolonged exposure to cold water. This can occur when the athlete sitting on the sidelines, during an event where it is raining, waiting to talk the field. Their feet are in the puddles on the sidelines underneath the bench causing prolonged exposure to the cold water. They refer to it as trench foot because during World War I, when there was a lot of trench fighting. It was so cold, and the soldiers were in the trenches for prolonged periods of time, they were getting cold-related illnesses, especially to their lower extremities. That is why it is referred to as trench foot.

Frostbite is the most serious of the cold injuries because the tissues are frozen. Emergency care for frostbite, remove the athlete from the cold environment, handle the injured part gently. Preventing further injury, we want to remove wet clothing. We rub the injured extremity or break blisters or rewarm frost biting areas. All of that must be done under a controlled environment as most cold injuries are confined. The exposed parts, the feet, ears, nose, and/or face. Most heat loss comes from the head and the neck, which is why it is important for them to wear a hat. Once they are off the field in the cold weather, make sure they keep their warmup team clothing on, to keep the body core temperature warm.

Soft tissue injuries, looking at closed injuries, soft tissue damage beneath the skin. Open injuries are breaks in the surface of the skin and burns our soft tissues receive more energy than they can absorb. All instances when we find soft tissue injuries. One of the ones is called the contusion. That results from a blunt force striking the body. Here is an example of a contusion. A hematoma, which we spoke about is a pooling of blood that collects in the body. We want to be careful to watch for compartment syndrome. The fascia is very avascular, not a lot of blood supplying in there. When there is a lot of bleeding underneath the skin, it could very well cause a lot of compression to the fascia, which can affect the muscles and the veins and the arteries inside the skin and the body. An abrasion that is caused by friction. Good example of that is road rash. Somebody falls off the bicycle, you are doing a triathlon event, or you are doing a bicycle race.

Next, a laceration. Here is an example of an athlete who was riding on a bicycle and the chain broke. We are seeing either smooth or jagged cuts to the extremity. An avulsion is a separation of various layers of the skin. Penetrating wounds results from a sharp pointed object. Just like a track and field event where an athlete gets stepped on by a cleat or in football or soccer where you will have some form of penetrating injury. Ice, compression and elevation ahead the heart will assist in slowing down the bleeding and reduce the swelling. Splinting decreases bleeding and reduces pain.  RICER, rest, ice, compression, elevation, referral. There are some concerns about whether this technique is outdated, however it is still used in emergency situation. This is sideline management, so we want to have the ice, compression, and evaluation, then splinting where required.

Impaled objects do not attempt to remove or move an impaled object. Control the bleeding and stabilise the object in place. Transfer the patient to the hospital carefully. How about amputations? Mobilise a partial amputation with a bulky dressing and a splint, being careful to wrap a complete amputation using a dry sterile dressing and place the amputation limb in a plastic bag, and send with the athlete to the hospital. Place the bag in a container filled with room-temperature water. We want to transport the severed part with the patient to the hospital. The function of bandaging and dressing and remember, to control bleeding. It protects the wound, and it prevents contamination. We want to use sterile dressings to cover the wounds and use a bandage to keep the dressing in place next.

At times we are in situations on the field when emergency procedures are needed. It is important to be familiar with how to handle these situations and be able to assist in a multi-disciplinary setting if there is more than one healthcare provider there.

[END]

ICSC04 – Emergency Procedures / Rhabdoyolysis
Section 4
Instructor Doctor James Geiselman
Video Lesson: 02:11
ENGLISH VERSION DOWNLOAD: ICSC04_Section 4 Rhabdo

Today, we are going to talk about Clinical Review of Exertional Rhabdoyolysis for the Chiropractic Sports Physician. A little bit about me, I am an assistant professor at Graceland University, in Lamoni, Iowa USA. We are just south of Des Moines, North of Kansas City. It is a small Liberal Arts institution. It is great because we get future healthcare practitioners from all fields. A lot of our students want to go chiropractic, and maybe become physician assistants and PT Athletic trainers. A lot of the content really revolves around the sports population already.

I received my Doctor of chiropractic from Logan University, where I also received my Masters of Science in Nutrition and Human Performance. I then went on and received a Diplomate from the American Clinical Board of Nutrition. I do hold additional sports medicine certifications but have my CCSP, Certified Chiropractic Sports Physician, the International Certificate in Sports Chiropractic, and on top of that, a nationally registered EMT and Paramedic in the state of Illinois.

Exertional Rhabdoyolysis (ER) is how I will refer to it throughout this presentation.

If you are not familiar, you may have heard of Rhabdoyolysis. We often think of kidney damage and when we think about it, when I go into an ER, if I have an athlete or mother and father take an athlete into the emergency department, the diagnostic testing is the same but we know that based on the level of activity that an athlete is doing versus their parents, those are very difference. One of the biggest reasons why we want to make sure that we revaluate and differentiate ER versus just regular Rhabdo is there should be a different set of criteria.

What we are going to show today is the clinical presentation. What should you be looking for sideline and what should you be looking for in an office setting? We will describe the signs and symptoms and compare them to general Rhabdo so that we try and get an understanding of what is that differentiation.

What should we be looking for? It is also important that if we were working at The World Games, the Olympic Games, or at a local high school, we need to know what athletic events may be more prone to developing ER. Know you sports?

I work with the wrestling team here at the university which is one of those top programs and if we have enough time at the end of this presentation, we will go over some of those case studies. We will identify key laboratory findings and look at what a normal diagnostic workup looks like. We will look at what that lab work looks like, what we order in the lab depending on where you are and where your location is which will depend on what sort of testing you could order. All the testing that I am referring to is based on my state license and things that work here in the state of Iowa. However how do we interpret those biomarkers and then how do we apply that knowledge to the actual treatment and management of ER?

It is great that we can recognize it but once we recognize it, then what do we do? We must have a plan and the first thing we need is to get some basic background information to help us understand exactly what we are dealing with. When we hear the word Rhabdoyolysis, it is an umbrella term. The umbrella term is simply used to describe the destruction of muscle cells. As the skeletal muscle cells get damaged through workouts, through activities, through new activity things we are not familiar with, we damage the cells. As we damage the cells, that cell begins to leak all the cellular contents in the surrounding areas into the bloodstream. Rhabdo in and of itself is a common potentially fatal condition. That is why it is important that we understand this and that we have a full understanding of what it is.

Athletic trainers, coaches, primary care physicians, and sport medicine physicians, all of these physicians and providers will probably encounter Rhabdo at some point in their career. Wrestling, is the sport that I cover predominantly here at the university. We have American football, swimming, bodybuilding, and running. If you are working a marathon race, that destruction, that constant impact, that constant stress on the body can result in the breakdown of muscle cells and muscle tissues resulting in Exertional Rhabdo.

When we look at striated muscles, the myofibrils and sarcolemma are damaged. When they are damaged, the cellular components will leak out. Those cellular components can be a lot of things. Creatine Kinase (CK/CPK) is typically the hallmark and the gold standard for what we test in the lab. We are also going to have Lactate Dehydrogenase, Aspartate Transaminase (AST/ALT), Electrolytes, Calcium, Potassium, and Myoglobin. Myoglobin is really the issue when it comes to renal tubules. If the cell explodes and breaks apart and all these contents go into the surrounding area, Myoglobin is toxic to the renal tubules. That is why you may have heard that Rhabdo is often associated with kidney damage and this is exactly why.

If we look at Exertional Rhabdoyolysis, sometimes it is called in the research as Exertional or Exercise-induced Rhabdoyolysis. It is often diagnosed simply as Rhabdo in the Emergency Department. In the emergency setting, if I am the Emergency Physician, I am going to air on the side of caution. I will go ahead and diagnose it based on the current clinical standards, which will be Rhabdo. I am not going to make that differentiation.

Working in sports though, we need to be able to make that differentiation. We need to be able to understand that it may not be a Physiological Pathological issue, it could just be physiological. They are not interchangeable. That was the position that I took in our recent paper, and I will show you that at the end of this presentation. Work with an Emergency Physician who again agreed that they are not interchangeable yet our hands are kind of tied in Sports Medicine and Emergency Medicine because we just simply don’t have enough data as of yet.

There is a debate that revolves around the diagnosis of ER because there is little consensus in the fields. If you ask somebody in the field of Emergency Medicine or Sports Medicine, they are going to tell you that the laboratory findings suggest this. If the laboratory finding suggests Rhabdo, we are going to call it Rhabdo. When in reality, an elevated CK level in a wrestler or marathon runner could just be a physiological response to a recent event, game, or run. ER is thought of as an abnormal event but in literature, if you take a deep dive into the literature, the condition is often just a normal physiological response to tissue repair and tissue adaptation by the athlete.

Think about it, if an athlete comes to you tomorrow and says, “You know what? I have sore muscles but they deserve a new workout today.” Are you, the coach or athlete automatically going to assume that it is Exertional Rhabdo? Probably not. There are some other findings that we need to consider. Typically with ER we want to consider physiological. It is often benign. It is often treated pathologically but it is often benign. ER, according to some research, could be the more advanced stage of DOMS, Delayed Onset Muscle Soreness. If you have an athlete who is pre-season or trying to work out or trying to get ready for the season, I do not know how many athletes come in with Delayed Onset Muscle Soreness, it is a very common thing.

Some of the literature is suggesting that DOMS is a milder form of Rhabdo. Again, if you have the ability to test and have research in your facility and practice, if you run a CK level and it does come back elevated, then what? The athlete could have no other symptoms and suddenly, we have an asymptomatic individual with hyper CK in the blood. Well, if that is the case, how do we treat it? Do we treat it as Rhabdo? Do we treat it as DOMS? This is a theory that is gaining some traction, but I think we just need more research on it.

Typically when we look at it, we need 3 clinical morphologies. We need 3 clinical aspects to this. One is severe muscle pain. Again, I am coming to you and saying, “I am sore after a workout”, it does not necessarily mean that I am suffering from Exertional Rhabdo. Muscle swelling is something else we want to look for. When an athlete comes to you for muscle swelling, again, this is where we might start thinking of Compartment Syndrome. We need to be understanding that we need to have a keen eye to this. Finally, Myoglobinuria, does the urine look dark? We will look at what urine color we should have versus what is typically presented. Typically, it is this triad, muscle pain, severe muscle pain, muscle swelling, and Myoglobinuria.

As you sit there, just try and think besides a heavy workout, what do you think are some of the things that can cause Exertional Rhabdo or Regular Rhabdo when thinking about the general population? We have a lot. Research has indicated a lot of potential causes, some more than others, and some we agree. Typically, these are kind of the breakdown that we have. Trauma, any sort of trauma to the muscle. That could be Crush Syndrome, some sort of abuse, some sort of electrical shock. Again, if I am electrocuted, that electricity is going to the muscle cells, damaging the muscle cells, and we have a release of the contents into the blood. This is not just an athlete experience. Vascular Obstructions, start thinking about your ischemia. If I have a clot somewhere, some type of infection, an Emboli, maybe I have seizures or if I am cramping a lot, maybe I could damage some of the muscle cells that way, releasing that content into the environment.

This is where we start to talk a lot about athletes when we look at the Environmental Related Emergencies. If you have ever been into a wrestling room or in a wrestling practice room, it is nice and warm. If you ever worked in Football, maybe Football is your sport that you work on a lot, you come back in August, at least here in the Midwest, on hot and humid days, having 2 a day practices. The athletes sweating a lot, they are getting dehydrated. They are not replenishing those fluids before their afternoon session. Football is another one, that is the Hyperthermia. We can also get it in cold weather as well. Then, we have excessive physical activity or muscle strain. Again, if we start a new workout program, maybe we are trying something new. We found the latest and greatest craze online and we want to try that out, if we are unaccustomed to the exercise, we are at a greater risk.

If you have an athlete working with a strength and conditioning coach, if you know the strength and conditioning coach, work hand in hand with them and make sure that you are educating the whole team, everyone involved. Drugs could also be a factor, toxins could be a factor, and then we could have endocrine disorders. As potential causes go, one of the biggest ones especially in the athletic populations, anything involving a heavy eccentric component. Again, if you go back to your introduction to Movement Science Course, if you go back to Weightlifting 101, anything with a big eccentric component can damage the muscle tissues. It is going to damage the muscle fibers, and the z bands. On top of that, if you add in heat and humidity, those have both been linked to an increased risk of developing ER.

Other potential causes that we want to focus on which we will probably see quite often, are some of the ones that I have tried to highlight on this slide, deconditioning. In the college population, athletes go home over the summer, do not do the workout plans like coach says, come back, all of a sudden, jump in as if they had just left from the end of the season. That is going to cause some muscle damage. They are so unaccustomed to that environment. The deconditioning is from, an office job all summer, and now, the athlete is coming back for two a days in football and has not really spent a lot of time outside. Extreme CrossFit training, not trying to pick on CrossFit but CrossFit is mentioned in several literature articles as being a culprit. Again, a lot of that will stem from unaccustomed activity. We get a lot of novice individuals who come in for CrossFit and start a plan, start a new workout regimen. On top of that, you also have the eccentric component built in.

Dehydration is one of the biggest things that we can focus on and have a direct impact with our athletes, any sport. I am going to keep picking on football and wrestling because it is usually a hot environment. Usually, a human environment, we are usually sweating a lot and we tend to become dehydrated faster. If you look at the wrestling population, it is a weight-class sport and in a weight-class sport, we worry about nutrient deficiencies because we are probably not eating appropriately. We are also probably focusing on weight cutting methods that are not ideal. That is something that we need to be always on the watch for. Electrolyte imbalances are another big key to understanding, that goes hand in hand with dehydration. That also goes hand in hand with cardiac arrhythmias. We will go over some cardiac arrhythmias today. I am sure everyone is familiar with sudden cardiac death. That is something that is pretty high in this population. At least, it is more common in this population than some of the other populations that we would have. That is typically because we have a lot of undiagnosed heart myopathies. Maybe we have electrolyte imbalances going on. We can throw the heart into a funny little rhythm.

Nutrition and diet plays a huge role, these 3 are all connected. If we can dial in an athlete’s nutrition, obviously, that is where my diplomate is. That is an area that I have an interest in. If you do not feel comfortable working with an athlete and their nutrition, by all means, there are sports RDs. There are diplomates like me more than happy to consult at any time on an athlete. Other drugs, oftentimes, the general population specially, if we are just talking about regular rhabdo, regular muscle damage, you may have read some studies on statin use. Statins have really gained a lot of following, I would say, within the last 2 decades. In statins, one of the best-known side effects is muscle damage. Nonsteroidal anti-inflammatories, your ibuprofens, and things like that. Again, College kids, at least in my experience, this population loves to take some NSAIDS before a match, before a game, or during a game.

We have recreational drug use just in the United States. Some states now, it is okay to smoke marijuana. Some states still have it illegal. It just adds another layer of things that we need to be able to address. Dietary supplements have been linked immobility, again, if I am just not moving, I could have, you might have heard the old saying, “Use it or lose it.” Immobility, if I am not working out, or not moving, I could have tissue breakdown. Then high doses of caffeine.

That takes us to our risk factors. We have covered a lot of causes. At this point, you are probably thinking about what does not cause exertional rhabdo. There are certain risk factors that we can focus on to help pinpoint what population might be at greatest risk. Risk factors and epidemiology, numerous studies have linked rhabdo and ER to various sports and professions. Maybe you are working in a population that is heavy law enforcement. It may be law enforcement training facility close by that you work with. Maybe you are at a military base and work with a Veteran. I am thinking about my days at Logan University and St. Louis, we have Scott Air Force Base close by. We have the South County Veterans. You might have a firefighter training facility close by, these are all linked in terms of profession. These have all been linked because we have heavy gear on, some unaccustomed situations or unaccustomed trainings that we are not just familiar with, and that is going to lead to the possibility that we develop some exertional rhabdom.

These are some populations that we really want to stay focused on. In terms of athletics, again, I have said wrestling and American football, but we also have swimming. Even though there is not a lot of pressure on the joints, it is a high-impact, vigorous sport. Then we have our long-distance runners. For long-distance runners, take Marathon runners and not so much the sprinters. We are causing a lot of chronic damage to those muscles to breakdown, we tend to see at least in this population right here, a higher resting CK level than we would in say, URI. Those who do vigorous exercise and high-intensity resistance training, those have been linked.

We have had cases in Physical Education (PE) classes. Again, this is one more reason why this is a topic of importance to me. As an assistant professor of Allied Health, a lot of our students, I told you, go to PT, maybe Chiro school, athletic training, go that route but we have a lot who want to go and teach. We have a lot of PE teachers coming through a lot of our courses. This is a topic that will directly affect them. There have been changes over the years. Back in my day, if you are late to PE class, you will run a couple of laps around the track, do so many push ups or so many air squats, or something like that. We will cover one of those cases in this presentation.

What are some of those risk factors? Males tend to have a higher prevalence of ER than females. That is often associated with just a greater muscle mass. We have a greater muscle mass, we have more muscles that can be damaged, males greater than females. If we take a look at ethnicity, African Americans tend to have a greater chance of developing ER than Caucasians and South Asians. That is often linked to the sickle cell trait. If I have a sickle cell trait, as an African American, and especially as a male, I am just at a higher risk, higher incidence of developing exertional rhabdo.

That takes us directly to epidemiology. While it is relatively uncommon, I am saying that you probably saw this at some point in your career simply because I have seen four cases, or four believed cases within the past three years with some of our wrestlers. If this is a population that you work with, odds are if they go to the hospital and get some labs drawn, they are at least going to get diagnosed with a high CK level or they going to get diagnosed with Rhabdo. ER itself is potentially fatal, which is what we need to understand and take it seriously. In every year, there is between 22 to 29 cases per 100,000 people. If you’re thinking that is quite a lot, other studies report about 26,000 cases per year total, which is still a fairly high number especially if we are in a sports population. Something that I have noticed in the last four years is the athletic community is a small community. As a child, I used to think how cool it was watching somebody play major league baseball, or being in NFL, and now, it still is a huge feat to get to that level but I am amazed at how many players, pro-football, Olympians, and high-level athletes I have been able to meet in just a few short years working in practice.

It is difficult to truly understand ER and define what those cases are, simply because we believed, if you remember from one of the first slides about DOMS, we are going to go on the assumption that DOMS is a mild form of Rhabdo. I personally do not know how many cases of DOMS go to the ER for lab work. I do not test a lot in the office, but if I think an athlete needs lab work for some other reason, I am not opposed to it. If you do find elevated CK levels, what is your standard of care? You cannot just automatically attribute it to them being an athlete. You must unfortunately treat it as if it is a by-product of rhabdo. I know that might be a little hard to understand and wrap your head around. Here I am saying that athletes automatically have a high-level at risk compared to the general population. Unfortunately, all our treatment standards are based on the general population conservative standards. We must meet a standard of care with our athletes. It is difficult to truly determine the frequency of ER because again, I am going out with my professional opinion that DOMS, if we are calling that mild rhabdo, as doctors we are not sending a lot of our DOMS patients or athletes to the ER. We have a lot of misdiagnosed, underreported, and underrecognized ER.

Once we do have it, there is a reoccurrence rate. That reoccurrence rate is as small as 0.08% all the way up to 11%. Typically, what we will associate this is genetic and muscular disorders. If an athlete has 2, 3, 4 cases of rhabdo at that point, the ER is going to recommend further testing. Hopefully, you as a sports physician, sideline provider, you will also recommend additional testing because there must be something going on. This simply cannot be a continuous dehydration issue.

We want to take a look at some of the complications of rhabdo which is why it is so important that we recognize rhabdo on the sideline and try to prevent it. In terms of complications, it can range from metabolic acidosis, DIC, to hypocalcaemia, low calcium in the blood, to hyperkalaemia, that is a high potassium in the blood. Both of those can trigger different arrhythmias. If we have an athlete with a sickle cell trait, we would have sickling collapse that has been documented. You can see in this slide, some of the most severe, most common ones you got here the arrhythmias, and compartment syndrome. Compartment syndrome, we have to recognize, otherwise, that could result in the loss of a limb. Then, acute renal failure is the other one. ARF is how it would be referred to in a few slides. Luckily, the ARF is associated with ER. It is often reversible, so it is not long-term.

Then, we could have end organ failure, cardiac arrest, and even death. Looking at those consequences, renal injury, so again, just injury, not necessarily failure, but renal injury has been reported in about 50% of all cases. When we do our lab work, we run a UA or Urinalysis, we are going to pick up on this. We will pick up on myoglobin and how it has been toxic to the renal tubules and be able to see what that damage looks like, and hopefully, especially if you’re in the ER setting, you can start the IV fluid replacement fairly quickly. If we do not, we were at risk of causing acute renal failure. Acute renal failure is rare but about 3 to 7% of all the cases of ER will progress eventually to ARF. That is why early recognition is key here. It is not something that we can just say, ” Oh, you know what? Let us go back to the to your room or house, and just drink plenty of fluids.” This is something that we want to address fairly quickly but usually, there are other contributing factors. If I am already dehydrated, that is putting a strain, or stress on the kidney. If there is heat stress, if there is trauma, or maybe I have, an underlying disease such as sickle cell, those typically on top of the development of ER is what is going to cause the most damage to the kidneys.

It occurs typically one to two days after the initial muscle damage. You have an athlete, it is Monday morning, we are back at school doing this nice heavy workout to start the week out, and then all of a sudden, we are in the training room or in the clinic. Wednesday afternoon, the athlete is complaining about these muscles and how bad they hurt. That is where we can start to see some of these signs. You can ask him what their urine color looks like. They will tell you, “Oh, it looked like coffee.” That is an issue right away. Dark-colored urine, that was one of our hallmarks that we will focus on here in a bit. That right there should be a red flag. We should already think, “All right, we are dehydrated, we are probably having some sort of kidney damage,” but renal tubular obstruction will occur secondary to the precipitation of the uric acid and myoglobin.

If we take a look at other research, other studies have reported that elevated levels of CPK and myoglobin as a result of upper-extremity exertion did not lead to ARF versus lower-extremity damage. The correlation could be fairly weak. There is not a lot of research that have examined that but it was interesting to see that upper-extremity over exertion, damage elevated CPK levels didn’t really have an effect on the kidneys. Our big takeaway is that while renal failure is one of the most common and concerning issues that we will face with rhabdom or exertional rhabdom, specifically, ARF in the exertional rhabdom patient is almost universally a full recovery, that is a great thing. It is almost universally a full recovery because it usually is a modifiable treatable issue underlying the diagnosis. Dehydration, if I get fluids back in and replenish fluids in the ER, it is going to be IV fluids. If we were able to kind of catch this early, we want oral hydration. Oral hydration is far superior to IV hydration but I am not going to turn down the bag of fluids in the ER if I get diagnosed with this.

The other thing is compartment syndrome. This is not the same image as this case, but this is a fasciotomy. If the muscles start swelling, again, compartment syndrome, the different compartments of muscle. If they start to swell, and they have nowhere to go, it is just like in the brain right if I fall, I do not know how many people I had with brain bleeds while I was working as a paramedic. They would fall, hit their head, and suddenly, the pressure would start to build up. You get a head CT and that is the end of that story. We can talk about the recovery and the treatment for that. Same thing down in the leg, down in the arm. If a particular muscle group gets damaged, and start to swell, it is going to continue to grow, grow, grow. If it continues to grow, it is going to put pressure on now vasculature. It is going to put pressure on any sort of nerves that are running through. It is often associated with that muscle swelling. It is going to exert that pressure on those nerves. Your athlete may come to you and say, “My toes feel funny, I am tingling, my hands feel funny.” Again, as a chiropractor, we could think, “All right. Well, let’s take a look at the spine.” It is important that we have to also look at the full picture. If it is an athlete, I am going to check the leg if he is complaining of foot pain. I want to follow the leg all the way down. Does anything look abnormal? Does one side look more swollen than the other? Same thing in the arms. This is sometimes a trap for chiropractors. We think, “Numbness in the hand, that is the C5 nerve root. It must be a C5 disc.”

Numbness along the knee, going across the knee down to the big toe, we must think, “Oh, that is an L4 problem. Let’s address that. I am not saying it cannot be. I am just saying as an athlete, as an athletic population, understanding compartment syndrome, and understanding ER now, we need to be focused on that. Nerve injury is often proximal. Multiple nerves can be involved. Here was an example from research. One of the articles that was discussing about how 14 high school American football players all experienced rhabdo during a summer training session. Again, we came back from summer break. We were not accustomed to the environment, we were not accustomed to the activity, to the heat, and suddenly, we started experiencing rhabdo cases. Think about this, 14 cases, high school following push-ups and chair dips. This is compartment syndrome of the tricep muscle.

That was performed continuously, 30 seconds of rest, intervals of 30 seconds until failure. If you’ve ever tried to do, for me, it’s tricep pull down. I like tricep pull-down. I like going to failure. Personally, I obviously try not to develop ER and I do not think I ever have. The consequences though resulted in 14 players being hospitalized. First off, if you are the sideline Doctor, we need to throw up some red flags to the coaching staff, but we had 14 players get hospitalized for exertional rhabdo. We had 3 of those who just started to develop compartment syndrome who all of a sudden needed emergency fasciotomies of the tricep muscle. That would be very similar to this, only on the arm. Basically, the ER Doctor will go in, will make this big incision. Then I have often seen in the hospital setting, it is almost like a yellow yarn. It is a thick thread, they will close it back together. They will approximate it, but they won’t close it all the way. The whole idea of cutting this open is to let that pressure out and to let those muscles gradually come back down. This is something that would result in a hospital stay for sure.

As a paramedic, I can’t help but start to discuss ECG changes. I do not know how many 12 leads I have run in my life. I think, personally, all athletes should have a 12-lead EKG performed. There is some interesting research out there. Not a lot, but there is some interesting research just to have a baseline. Characteristics of hyperkalaemia, my muscle cells have broken open. I have an efflux of potassium that can cause what is just a hallmark of a peaked T wave. If you remember your PQRST, it is that peaked T wave. P waves could widen and flatten, we could have a prolonged PR interval. These could all lead to bradycardia. Bradyarrhythmia’s, if I have bradyarrhythmia, I have a slow heart rate. As that slow heart rate keeps going slower because I am just continuing to release all these electrolyte abnormalities into the blood, that’s when I could have a very slow heart rate that’s not compatible with life. It is something that if you have a high trained athlete, do not be afraid of bradyarrhythmia though. A high trained athlete who runs a lot, who has really good cardiac health could very easily have a heart rate in the 40s and be completely fine. Most heart rates are 60 to 100. Over 100, you get tachycardias. Tachycardia, we are typically going to see during activity while we are running, while we are weightlifting, while we are doing whatever activity is. Then it comes back down to resting. The resting heart rate is 60 to 100. For a high trained athlete, we could easily be in the 40s. I have seen a 38 on an athlete before who was in very fit shape. That 38, he was completely fine.

As hyperkalaemia worsens, we start to run into a few things. We could run into Ventricular Fibrillation, PEA, which is Pulseless Electrical Activity, or Asystole. All of these are not good. This is why we learn CPR. This is why we learn how to use an AED. An AED, this is what I tell my first aid and CPR class every semester, the AED is trying to stop the heart. Most people just tell me, “Oh, it’s going to shock it into a normal rhythm but how? It just changes it. It just automatically changes it to a normal signs rhythm. Well, that’s not really how it works. It is trying to stop the heart. The AED is looking for ventricular fibrillation or ventricular tachycardia. Those 2, it will recognize and say Shock Advised, if it says PEA. PEA could be literally any rhythm but there is no pulse. It is going to show up as a rhythm on the monitor. It is going to show up as a rhythm on the AED. There is no pulse associated. We treat that like Asystole or if you’ve watched any sort of medical show, it’s flatline. If you’ve ever seen flatline, that’s asystole.

When an AED shocks, AED is going to shock vfib, vtach. When it shocks vfib, vtach, it is trying to stop the heart because we want the SA node to kick back into gear. When the SA node kicks into gear, it should in theory create a normal cardiac rhythm. We will talk some more about some EKG’s here coming up. Serum potassium levels do not always correlate to ECG changes, but we do have to talk about sudden cardiac arrest is possible, and that is why this is an important topic. Let’s look at that hyperkalaemia. Hyperkalaemia, when I say peaked T waves, this is one of the early signs. Again, mild potassium, this is your peak T. See how it almost comes so your PQRST. This is a PT wave with a prolonged PR interval. As it gets worse, as it continues to get worse, we start to just see, it is flattening. We are starting to lose the QRS, 98% of the potassium is going to be found intracellularly. 60% to 70% of the total cellular mass in the human body though is going to consist of cellular muscle. Even an acute necrosis of 100 grams of muscle tissue can be life-threatening, can potentially cause the serum abnormality we take lab work. If you think about it, 100 grams of muscle mass damage is not a lot for an athlete, especially a really built athlete.

I also wanted to show you a 12 lead. Maybe it has been a while since you read EKGs. Maybe you don’t feel comfortable reading EKGs. Again, if you don’t feel comfortable, do not do this in your practice. Feel free to call, call somebody, refer out, don’t be afraid. Here we are, we are talking like some peak Ts right here. If you look at lead 2, lead 2 is kind of the common lead that we just get a good idea of what is going on. You got your peak QRS and then suddenly, a big old T wave. Now that T wave, this is definitely indicative of hyperkalaemia.

Sudden cardiac arrest, I would not be doing this justice if I did not speak of sudden cardiac arrest. This is something that hopefully no one will ever have to deal with within their career. I tell my students in CPR and first aid, you got to learn this stuff simply because you are most likely going to be using CPR on somebody that you love, a friend or family member. For us, I think of the team that I work with, I love all those guys. You become attached to the team that you work with, they become friends, they become family. Knowing CPR is absolutely crucial, which is part of our license to upkeep. That is one of the things that we must have current CPR certifications. The incidence hopefully is something you’ll never see but the incidence is about 1 per 50 to 300,000 patients. It is a wide incidence, but we typically have young athletes who are apparently healthy, who come in. They may have an undiagnosed cardiomegaly, an enlarged heart, or some other cardiomyopathy. For many, no causes ever found. When I say, “no cause”, we are talking autopsy. No causes ever found. These individuals pass their preparticipation physicals with flying colors. There is no indication that we should think suddenly in the middle of a soccer game, middle of a football game, you collapse and have a heart attack or sudden cardiac arrest.

What we do want to focus on is one of the theories surrounding some of the cases of sudden cardiac arrest in this population and that is the fact that if I have exercised induced or exertional rhabdo, if I am doing an exercise, I am already more prone to muscle damage. That muscle damage releases all the contents into the cell. I get an electrolyte imbalance which then leads to electrical abnormalities, which then leads to the sudden cardiac arrest. This is feasible, it has been documented in the research being a proposed theory for one of the causes of sudden cardiac arrest. There are multiple causes of an athlete going down. This is also one of the reasons why I think a 12-lead baseline EKG for all athletes would be very beneficial. I think the double-edged sword for some providers is if we find something, we must treat it. I also think that that’s why we do it. We try and prevent; we try and find it before it becomes a problem. I have read and heard of stories where athletes get a 12 lead, and they find out they have some sort of heart condition and they never get to play again in their life. I think that is a worry for a lot of athletes but at the same time, you have saved that athlete and I truly feel like that is way more important than you not being able to play forever. We’d rather have you around than not have you around.

Here are those most serious arrhythmias. Like I was telling you, the AED will look for this. This is basically, the ventricles are just kind of quivering back and forth. There is really nothing happening to it. There is no blood flow. Even though there is electricity down here in the ventricle, it is not enough to pump the heart. Same thing with ventricular tachycardia. We have these big waves but again, no pulse. It is going to be pulseless V tach. That is how we are going to treat it. We are going to shock this rhythm. These 2 are what the AED sees. When I get there on scene, I can take the cable from the AED and put it into my monitor. A lot of these have just become interchangeable in the workplace. I could actually start to see what I am looking at. I can see, “Okay, well, it looks like we have a rhythm, but we still have no pulse. I will diagnose it as a pulseless electrical activity.” If it is flatline, I will check this and at least 3 leads. Lead 2, 3, and 4, lead A, B1, B2, whatever, I can double-check this. Asystole and 3 leads are deceased. Unless we typically find other reasons to think otherwise.

That takes us to the clinical presentation. What is that clinical presentation of exertional rhabdo looking like? In severe cases of rhabdo, our general symptoms may include fatigue, general malaise, fevers, nausea and vomiting, electrolyte imbalances, tachycardia, so again, fast heart rate, or seizures. This is just a general list, think about the patients that may be coming to you, if you’re not in just a sport-exclusive practice, a patient comes to you with fatigue, “I don’t feel right. I had some nausea, I am vomiting,” rhabdo probably isn’t the first thing that we are jumping to, and this is where a good case history, a good medical history is going to come in. What have you been doing recently? What’s changed? What’s happening? Have you been sick? Trying to get a full picture of what’s happening. These general symptoms by them in and of themselves would not suddenly say, “Yep, that is rhabdo.” Our clinical presentation, we’re looking for muscle pain. Remember, I said severe muscle pain that is intense. It is muscle pain that the athlete has never described before. You ask the athlete, have you ever had this? It has never been this bad. This is like a 10 out of 10. I am sure you have heard it anytime an athlete or a patient goes, “My pain is 10 out of 10.” They’re just sitting there may be on their cell phone or just kind of smiling like you start to wonder. You can tell an athlete who is in severe intense pain and that’s going to usually be during active and passive ranges of motion. This is where we must actually touch our patients. We want to do a good exam on them. We want to do the active range of motion. We want to do the passive range of motion.

If they are still having this pain with passive range of motion, it is still just as intense, just as severe, our red flags should start waving. We should be focusing on muscle weakness and generalized fatigue. Again, think about it, if I come in with muscle pain and I am already that sore and it hurts that much from the active and passive range of motion, well, of course, I am going to want to focus on the weakness. Generalized weakness, unfamiliar with this exertional level, if it was a new activity, this is where the case history comes in. Then that takes us to the presence of myoglobin in the urine. You can either give them a cup, a urine sample cup, asking to go to the bathroom, fill it up, or just ask them if you don’t want to do any sort of UA in the office. If they tell you, it’s dark tea or cola-colored in nature, that is a red flag as well. Our clinical pearls, we have 3 primary symptoms. Our 3 primary symptoms, muscle pain, muscle swelling, myoglobinuria. That is slightly different than the diagnostic criteria. The diagnostic criteria are dark cola-colored urine, which typically we will start to see about 12 to 24 hours from initial muscle damage. Myalgia, that severe muscle pain, tenderness, weakness, and edema. If we are getting edema, we really need to be cautious with compartment syndrome. Then the third criteria are elevated serum muscle enzyme. We will do some lab work. This is often done possibly in an emergency setting, so in the ER simply because you can get results a lot faster than you can maybe in your office. That increase CK, it is typically going to start to be there 24 to 48 hours and then it is going to start to gradually decline over the next 7 to 10 days.

Hydration is going to play a huge role here. Hydration status, hydration is a foundational component for any athlete with ER. If we are going to factor in the athlete’s sport, their environment, is it hot humid, is it cold environment, and what are their nutritional goals, these can all help us in diagnosing and making a correct diagnosis of ER. This is one thing that I have a hard time getting some of my athletes to understand. I preach hydration levels, but this was the first time this year that I have ever had over-hydration. I partly blame myself for the cramping because again, just like I can go this way and start to cramp and have muscle issues, I can be over-hydrated. Now, overhydration is when you see and again, you might see this in your practice, I see this in class so when athletes walk in with a milk jug full of water. All they are drinking is water, water, water. I am hydrated, I am so perfect. You’re missing the electrolytes. You’re thinking hyponatremia, you’re thinking those electrolytes, you’re just really thinned out in the blood. This is where the education piece comes in. Educating that yes, it’s important to hydrate, water is great to hydrate but do not overdo it on the water. Make sure that we’re throwing in the electrolytes. That is why a lot of the wrestlers like Pedialyte. A lot of football players tend to like other sports drinks. Generally, I don’t recommend sports drinks to people just because they are going to work out for 20 minutes. The research doesn’t support it.

If it is an activity that you’re going to do for over an hour, sports drink may be exactly what you need. When we look at hydration, if an athlete says, “I am crystal clear,” I don’t want you to be crystal clear. I want you to have some yellow. Now, we start to get dehydration as that yellow starts to get higher and higher and higher. Eventually, we have extreme dehydration where we start to get dark tea color-colored urine. As a refresher, let’s talk about some of the dehydration consequences. You can look at the previous slide we had. We had some in terms of overhydration and underhydration but typically in terms of dehydration, at 1% body weight loss, we’re going to have thirst. By the time we are thirsty, we are already dehydrated. If I have an increased thirst, maybe I start to have a loss of appetite. Maybe I have discomfort. That right there is going to be a 2%. Now, eventually, we can keep going up to muscle cramps, difficulty concentrating, and this is why I really start to convince athletes that it is important. If they are in the middle of a match, middle of a game, and they cannot concentrate on the play, they cannot concentrate on what their opponent is doing, and they are 5% dehydrated, that is going to directly impact their performance level.

If we start to get to the stumbling headache, dizziness, and labored breathing, that athlete is out, at that point, we are probably getting some emergency services coming which we have had before. We have had it on the sidelines. Hot humid day, the athlete was not drinking enough. We started some electrolyte therapy on him and then suddenly, he just was not really unresponsive. He just was not really coherent. We activated emergency response because at that point, it is kind of out of our hands. Looking at dehydration, there is another way to look at it if you are an adult beverage drinker. Think of a logger as our good color of urine. Think of a pale ale as we need to hydrate, red ale, we need to hydrate more and if we’re a stout, we are coming to see one of us. We need to see a doctor, we need to get some lab testing. It should not look like this. But exercise-related renal impairment usually occurs as a result of dehydration, making sure that we are not dehydrated, making sure that we are keeping our athletes hydrated as best as possible, telling them that fluid losses of 1 to 2 liters per hour, particularly for wrestling rooms, 2 a day football, we are going to have to have an aggressive fluid replacement, especially if I am in a 2 a day. If I am in the morning, one of my colleagues, one of my good friends and colleagues worked football when he was getting his masters, he was a GA. They would make athletes weigh first thing before the morning practice, and he said, it wouldn’t be uncommon for them to lose 7, 8, 9 pounds and he would have to stay in the locker room with them or in the athletic training room with them until they rehydrated. They weren’t allowed to leave morning practice until they were rehydrated within a pound or 2, there was a percentage of leeway.

Then they could leave, go get lunch, do whatever, and then come back for their afternoon session, weigh again, they had a very good monitoring system. I have been in other places where there is no monitoring system at all. Athletes just go out. Some athletes care about their body enough that they step on the scale, they know what they need to replenish. For the most part, it is not something that is really implemented at a lot of places. We want to make sure we have an aggressive fluid replacement, but we also want to make sure that it is not just pure water because that can lead to hyponatremia. Then finally, most commonly, the ARF, the acute renal failure, it is going to be associated with hyperkalaemia maybe to follow. If we look at biomarkers, so clinical dehydration, if we’re doing lab work, if we’re able to read lab work from, maybe the athlete brings you back to the lab work from the hospital the notes or you request them. We’re looking at sodium, we’re looking at BUN, the plasma osmolarity, AST, CK, CK is our big one here, and LDH.

It has been noted that dehydrated athletes with a significance statistically will correlate of sodium and BUN which can then guide you into dehydration and skeletal muscle damage. Dehydration may prevent an athlete from clearing myoglobin. That’s our concern. If we get that precipitated, if we get that build-up of myoglobin because I do not have enough fluid to keep the kidneys filtering, keep the kidneys flowing, that is where we get to build up. That is where we get the kidney damaged. You learned a lot so far. Now, we need to start applying some of this. We need to take a look at some differential diagnoses. Without a high index of suspicion, I am willing to bet you are going to miss Rhabdo. I am just willing to go out there. Primarily due to the fact that athletes come in already with muscle pain. They already come in with swelling. They already come in with tenderness. If an athlete comes in with these, I am not just automatically going to assume exertional rhabdo but at least now, after going through this course, you can think, “Okay, you know what? That needs to be on my radar if their urine is fine, if I want to do lab work, that all checks off fine, if you want to rule it out, by all means, rule it out.” In my level of differential diagnosis, I always want to go to the most severe first and then work my way down. I want to rule out any sort of life-threatening emergency.

If ER is suspected, I need to have an immediate referral to a higher level of care. As great as it is that I can recognize it, I don’t feel comfortable necessarily starting the fluid hydration orally. If I think that somebody is at this level of ER, they are going to an ER. They are going to an emergency department, they are going to get the IVs that I, in the state of Iowa, can’t give. They are going to start getting a more definitive line of care. The other causes of that muscle pain and weakness besides ER should also be considered at, as appropriate. If I am working sideline at a football game, the athlete comes in with intense quad pain, it could be a helmet to the quad. It could be a helmet to the leg, or a helmet to the shoulder. There is a lot of reasons to explain muscle pain besides ER but knowing all of your components will help you make a better diagnosis.

If we are looking at muscle pain and weakness, that differential diagnosis may include acute myopathies, periodic paralysis, maybe we have myositis or dermatomyositis, Gan beret, muscle strain, discogenic involvement, again, chiropractors, here we go. It could be a discogenic involvement. In more serious cases, we are ruling out cardiac problems. We are ruling out heat stroke, and we are going to rule out asthma. These are the 3 most common non-traumatic causes of sudden exertional collapse in a healthy individual. Cardiac, respiratory, heat, those 3 things. How do I test, how do I tell? The signs of serious causes of exercise-related collapse may include an altered mental status. Think of your AVPU, your alert verbal pain unresponsive. Think of AVPU, think of systolic blood pressure less than a hundred. When I took my CCSP program, I feel very fortunate because I was taught by 2 fantastic individuals. One was an AT and one was an EMT. My background being an EMT, I could understand where the EMT was coming from. Keeping a blood pressure cuff in your med kit, keeping a stethoscope there because those are all things that we trained on that we learned in practice when we were going through our EMT license. Athletic trainers there and she goes, “You know what, a blood pressure cuff, I do not really use that much. That was not what I was trained on.” She had other tools in her toolkit that helped her diagnose.

There is not one right way here but I, personally, being the EMT paramedic that I am, I would recommend having a blood pressure cuff to get at least a systolic blood pressure. I also keep a pulse ox in my bag, just a little finger pulse ox so I can get a heart rate quickly. I get a heart rate, and I get an O2 saturation, and I can tell a lot by an athlete level quickly. Additional keys to that diagnosis. We want to look at dark urine. Dark urine without any other symptoms. That may not indicate ER but rather just a dehydration level and that’s fine. That is something that we can see here on the sideline. The athlete comes over on the sideline, comes up after practice, and has dark urine. Now, if we are in the office, maybe we send them for labs. Maybe they are in the ED, maybe they are going to the emergency department for muscle cramping. Automatically, they are going to order lab work. They are going to order a CK and what they are going to find is acute CK levels five times the upper limit. Five times the upper limit is usually about a thousand. If levels go up to a thousand, that is going to be a really conservative, and we will see this, we have a really conservative diagnosis for rhabdo. It is a low threshold. When I say conservative, it is a low threshold has been shown to have a high sensitivity, but it has a low specificity. That is something we need to keep in mind. Criteria, now, we are in the emergency department for sure.

The criteria that may indicate hospitalization, and again, unless you are an emergency room physician, you are probably not making this decision. This is probably not up to you but if it is a high CK level, they may want to stay overnight for observation, and decrease creatinine clearance. Maybe they have elevated serum creatinine. Maybe I have myoglobinuria, I am worried about the kidneys. I will stay overnight. Metabolic disorders or abnormalities, or any sort of signs of compartment syndrome. All of these things are probably a good way to spend the night in the hospital to confirm diagnosis. Once I have gone through my differential, maybe I have ordered some lab test, then I am going to go through a history first. Let my questions guide what my thinking is. I am going to ask all different questions, three or four different ways to athletes depending on how many times you have done an H and P, a history and a physical, athletes and patients in my experience tend to lie. Not necessarily on purpose but they tend to lie.

If I was in the back of an ambulance and I ask a patient what kind of health conditions they had, they might say  “I don’t have any. I am fine.” Then I get to the ER and the nurse comes in and says, what kind of health conditions do you have and they give the same answer. “I don’t have anything. I am fine.” Then you might ask, “What medications do you take?” they reply with “I have a list of medications.” Some people don’t understand that they are taking medications for a reason. They think if I take the medication, I no longer have the problem. Suddenly, you start finding out patients have blood pressure problems, heart, breathing and cholesterol problems. The list is just never-ending.

I will do my exam findings as well and take the tenderness into account of the affected muscle group. I will look for possible signs of hypovolemia, take a blood pressure and if it is below a hundred systolic, that is going to be a sign that I want to focus on. Laboratory findings in the hospital. When working in the hospital most likely you will get a CBC, a complete blood count and get what we call a CMP, comprehensive metabolic panel and you will also get a CK panel. For that CK, we are typically looking for things greater than a thousand. That is five times the upper limit. Additionally, we can use a urine dipstick. A urine dipstick can test positive for myoglobin without the presence of microscopic evidence of blood. What we are doing there, this is something that we can use in practice, in our office. Have the athlete go pee in a cup, bring that back. It is just a urine dipstick. We will take a look at what that is. You dip it in, and we can gauge a lot of information based on that. Here is something interesting I found during the research that I just wanted to make sure all providers knew.

We went over, we changed to ICD 10 codes probably 5 years ago, 4 or 5 years ago, I can’t really remember. The ICD 10 codes should not be used unless absolute. An Exertional Rhabdomyolysis or a rhabdomyolysis diagnosis should not be used unless absolute, because what the authors proposes of that’s going to hinder future research. Right now, we may have a lot of misdiagnosis of rhabdo simply because, right as soon as a patient gets to a thousand, all of a sudden that’s criteria. That criteria with some muscle pain and some dark urine, and it is rhabdo.

Early detection is where we come in. We need to be monitoring urine. If we are in a weight class sport specifically, I am more concerned about urine than probably other sports. If you’re working with volleyball, you’re probably not caring too much about dehydration right here. If you work football, if you work soccer, if you work any sort of outside sport, I recommend and suggest that we focus on early detection of dehydration. What does that look like? The NATA, the National Athletic Training Association really identified 4 factors that may lead to Exertional Rhabdo. Number 1 was performing 2 to 3 minutes of all out vigorous absolute exhaustive, work till failure, maximal, activity, 2 to 3 minutes, that’s it. If I am sprinting short distances, right 800 to 1600 meters without adequate rest periods. I am constantly causing that damage, constantly causing that stress, on the quads, on the calves, on the legs, that could be a trigger. Vigorously exercising the first day of pre-season. Like I said, athletes have been off for the summer. Athletes come back, we quickly find out who did and did not do the summer workout programs, and all of a sudden, they act like they haven’t missed a beat. They’re trying to lift the same 300-pound bench that they did when they left. It may not work out because they are not acclimated. This is a big push, at least within the last couple of years. I remember, from the NATA about acclimating to the weather. You can acclimate to the weather with football.

It is not like we are going to necessarily start 2 days right away. We do a lot better monitoring the field, if we are on turf versus on grass. What’s the wet bulb? What’s the humidity? Those are all tricks that we can help our athletes and acclimate them back to activity. Then finally, sprinting at the end of practice, they are sometimes doing work out drills/exercises “gassers or suicides”, sprinting down and back while exhausted and fatigued. The athlete has gone through a 2-hour practice, and now the coach wants me to do work out drills “25 suicides”. We as the doctors need to say, “Is that really going to be the best, for the athlete?” Then we take a look, NATA, again, the National Athletic Training Association. The NATA has given some recommendations on sports programs.

Strengthening and conditioning coaches. There needs to be a transition period for vulnerable times for athletes. All strength and conditioning workouts should be exercise based, scientifically sound, and physiologically represent, representative of that sport. Does it make sense for us to be working out what we are working out? This is something that strength and conditioning coaches, especially us, as healthcare providers, we should really understand. Then conditioning program should begin with work to rest, ratios of 1 to 4 first 4 days of that transition period. We should have separate day workouts and all workouts. Then finally, all strength conditioning workouts should be documented. We should have good records of what did the athlete do. What was the volume? What was the intensity? What was the duration? All of that can be very helpful so that we can help identify, well, 2 days later athletes start coming into the training room and they all have calf problems, or they all have triceps problems.

You go back and you look and redid 13 tricep exercises for every 2 bicep exercises, that’s disproportional. Taking a look at diagnostics, we want to take a look at diagnostics. Typically, the 3 things that we are going to get, especially in the ED, it is an electrocardiogram or an EKG, ECG, we are going to get a UA. A urine analysis, we are going to use a dipstick. We can use the same dipstick in the office. We are going to have blood, we are going to get some sort of blood, we are going to get a CBC, we are going to look at renal and liver functions. We want to look at CK levels, at uric acid, and at electrolytes. Those are typically our work diagnostic workup of what we should be doing. Common ECG changes, I won’t go through all of these. These are all things that if I have exertional rhabdo, if I do have the electrolyte abnormalities, if I do have any sort of fluctuations, I could have anything from hyper to hypocalcaemia. I could have her hyper or hypokalaemia, hyper or hypomagnesemia and then hyper and hyponatremia. These are all going to be based on electrolytes, sodium, calcium, magnesium, and potassium.

Our most severe Vtach and V-fib is what we shock. PEA, asystole, we don’t shock, we just do really good high quality CPR. Here’s what a dipstick typically looks like. You have probably seen it or used them in clinic. You may not use them now; it comes in a little container. You pop it off at the top. Just pull this out, follow the instructions by placing the stick in the urine for duration listed on the instructions. Then we are testing different things like specific gravity. We want to look at PH levels, protein, glucose, Ketone levels, bilirubin, blood, nitrates, and leukocytes and if you notice, normal is negative.

I shouldn’t have any of these, however If I do have some of these, those would be abnormal. If it came back positive for blood, it is telling me that there’s myoglobin in the urine which I can see under a microscope. In terms of myoglobin, this is what I am talking about, tea colored urine. It is one of the most important consequences of significant muscle damage. This can be eyeballed, it is better if I do some testing to it, but if an athlete brings this to me right away, I am going a completely different route on my diagnosis and my plan. I am going to get them, they are going to start to drink fluids, and I am also going to get them most likely to an emergency room. It develops once there’s at least a hundred grams of skeletal muscle damage. Small amount, the myoglobin spills over into the urine and the plasma concentrations. If the plasma concentrations reach about 1.5 milligrams per deciliter. That is what causes that reddish brownish tint to it and it may be detected with a urine dip stick or on macroscopic view. Macroscopically, just looking at this, it looks reddish, brown and dark.

Serum levels will typically rise of bio level within 1 to 6 hours, peak about 8 to 12, and then start to come back down to normal within 24 hours. If the serum myoglobin will exceed 0.3 milligrams. Back here, 1.5 milligrams per deciliter spills over. Now we are talking, if we just reach 0.3 milligrams per liter it becomes detectable with a urine dipstick. That’s why having a dipstick can be sensitive. You may be on the fence of, well, does that urine look bad? Does it look normal? It looks really dark, but is there anything in it? Use a simple dipstick. The urine dipsticks are inexpensive, they are sensitive tests, ideal for the sideline and office setting but obviously if it finds something abnormal, I could send them to the ER real fast to the emergency department (ED) and have further testing followed up.

I can call the ED and say, “”I am sending an athlete to you who had positive X, Y, Z in the office. I believe X, Y, Z to be occurring.” Then the ED will start their diagnostic follow up. You would be amazed at how many facilities will appreciate that initial call. Providers appreciate having some heads up as an athlete comes in. Major drawback is that you cannot distinguish between hemoglobin, myoglobin and hemo rich red blood cells. That is where ER comes in, the ED emergency department, will do that testing and send to the lab so they can figure out what it is. Just another image showing you different colors of urine. Everything from what we call light straw. I would say over hydrated to straw, to yellow, dark yellow, amber and dark.

Same thing here, we just changed them up a little bit amber, red and dark. What I typically find on a lot of the reports that I get back I often see Amber and Dark Amber as being most often listed. We take a look at blood test, we are going to order a CBC, complete blood count, a CMP, comprehensive metabolic panel, and we will do a CK. CK, CPK, we want total serum or plasma here. It is something that I don’t really cover too much, but I just want to make sure I say it now, we are not ordering a CKMB. CKMB is looking at cardiac damage, it is a test that I could run if I am concerned that, somebody might have had a heart attack, an MI, I don’t want this one.

You need to be very aware of this one because oftentimes when you say, you want a CK, CPK level, the lab for some reason, and it is probably because they are in a hospital and they are probably running way more CKMBs than normal, they will run a CKMB. I have had it done at twice at our local hospital and we are a small hospital. I don’t fault them, it was wrong, it was incorrect and I called them up and said, I didn’t order a CKMB, I just ordered a CKCMP or a CPK and they just had to re run the test. This will not provide you with the data that you want. This is going to provide you whether or not I had some cardiac muscle damage, which is what I want. I also want you to be aware that depending on what lab and what laboratory technician is working that day, you will either get CK or you will get CPK. They are fairly interchangeable, but their reference ranges are not. They in and of itself are, one is one CK equals CPK, but they have different reference ranges. It just made it difficult when you are trying to go through a case series trying to write that up for a journal and trying to take into account different lab values. Hopefully we will see that here in a few slides. I won’t go over the CBC components or the CMP components, but again, this is where we are looking at a lot of that liver and kidney function.

Additional findings, is where we really want to focus. We focus on CK because CK is the gold standard for diagnosis of rhabdo. However, there are 4 other enzymes that could be elevated that we should know in the back of our heads, AST, ALT, lactate, and dehydrogenase. These could be elevated on the lab report, but we are looking for that CK value. If rhabdomyolysis is suspected, the serum levels of the following should be evaluated, and those things are potassium. We have seen why we want to order potassium, hyperkalaemia we want to look at uric acid, we want to look at creatine, lactate dehydrogenase. Then what we may find is that the following could be decreased on lab results, which would just further strengthen your diagnosis of rhabdo, and that’s calcium and that’s ph.

Let us take a look at creatine kinase, because this is what one of the hallmarks of this condition. Creatine kinase in and of itself, here’s a little biochemistry for you, it is part of the ATPCR energy system. Creatine kinase is the enzyme that catalyzes the reaction, transferring the phosphate from the creatine phosphate to the adenosine die phosphate, which helps us make the ATP. I know some of you right now are thinking, “my goodness, I do not care.” I can agree, as I dreaded biochemistry in grad school, yet I have opened the medical biochemistry textbook more in practice than I ever did in school. It is amazing that when you get into sports nutrition, how many of these reactions you either learned once and thought, I will never use that again or you want to reference them in a paper, in some research, or a presentation. You want to get this nice image. Don’t ever say that you will never open that textbook again, because you may in fact do it. When you are looking at creatine kinase, here is a few things that we want to know. Creatine kinase, it is the enzyme which catalyzes the conversion of creatine to phosphor creatine. There’s our PCR, we have the skeletal muscle myocardium and brain. CKMB, CKMM, CKBB those are all rich in enzymes but those are not what we want. When I order a CK level, I just want to know what the CK is, Creatine kinase.

CK is released in other tissue damage, which is why we have different forms and different specific enzymes that we can look at. If we have an MI myocarditis, rhabdo, of course, muscle trauma, severe muscle exertion surgery. If you look at lab work from a surgical patient, any sort of muscle damage, whether it is me working out with a dumbbell or a surgeon coming in with a scalpel, it is still going to cause muscle tissue damage and release of contents into the body. Tetanus, alcoholism or statins. An elevated level of CK is the most sensitive and reliable indicator of muscle injury that will constitute the diagnostic workup and diagnostic hallmark for that matter of ER. Now these are, CK levels are very specific and very affected by race, sex, and physical activity. Those are 3 things that we need to keep in mind.

Usually you will see a spike in CK levels 2 to 12 hours after muscle injury. They usually peak about 24 to 72. We have about a 1-to-3-day window of seeing when they’re going to peak, and then they gradually declined. They are going to decline over the next 5-to-10 days. Training for sports and competition, will already have a profound impact on serum CK levels and it has been documented in numerous studies that athletes already have higher CK values than non-athletes. This is the start of my premise that when an athlete goes into the ED for evaluation, they can’t be treated the same as somebody who is a couch potato who likes to play video games 23 hours a the day. Their CK levels are already going to be elevated. Treating them, treating those 2 individuals equally in terms of diagnoses is not appropriate in my professional opinion. That’s what we wrote in our presentation, in our paper.

Many cases of Exertional Rhabdo are simply subclinical. Some cases are only detected when we start to run CK levels. This is why I go back to the question I asked you early in this presentation, if I am ordering all of these lab tests on an individual and a high CK level comes back, what do I do? How do I treat the patient? Do I automatically pull them because it is a standard of care? Do they have any other symptoms? If you start asking an athlete, do you have any muscle soreness? No, I have muscle soreness. Right now you start checking off the boxes on paper I am checking off boxes for what could be ER, could be Rhabdo, but in most cases it is subclinical.

It may be really important to do for research testing. If I am trying to take a wrestling, football or a swimming population, what is the kind of baseline for this particular group of athletes, and even then, I got different weight classes to think about linemen versus the wide receivers that I have heavyweights versus the 125 pounders. All of this to try and get a reference range is where research really needs to go. CK, CPK it is one of the most used biomarkers to diagnose rhabdo. However, according to research, those levels can range from 5 times. Now 5 times, that’s where we get the diagnostic criteria to call it rhabdo. That’s why it is very conservative, but it has been proposed that to 50 times the upper limit should be used.

Think about that, we are going five times to 50 times. Typically, what we see a lot in some of the research, it is a 5 to 10 times range. I can tell you that our local hospital uses the 5 times range. In fact, the local hospital makes it difficult. This is where, if you are working with say LabCorp or Quest Diagnostics, whatever your lab is that you are working with, our facility will only read levels greater than a thousand. I don’t even know how high some of the athletes that we have had have gone because the lab sees the cut off as a thousand and that’s all they report, it is greater than that. Other labs will come back and give you numbers, 25,460, 15,230. If we take a look at all the research, in the presence of a natural history, just a normal history on a person, serum CK levels greater than 25,000 is likely to be benign in ER patients, think about that. That right there is likely to be benign. Yet we don’t even ever get to see levels up to 25,000 because as soon as they are greater than a thousand, they’re pulled from play for a week. It is not unusual to see CK levels up to a hundred thousand in some research. When we start to throw in different confounding factors, when ARF, acute renal failure is present in patients with ER, those typical CK levels, we tend to see it at about 15,000. Values have been documented as high as 3 million. That is not a typo, I promise high as 3 million. Those I will say are very rare cases, but I can also tell you that if that patient had been into my local hospital, I would’ve simply gotten greater than a thousand.

Here is the other problem. There is no standard CPK level for diagnostics for diagnosing rhabdo. That is an issue because our standard reference range is that for most labs are simply low and often lead to overdiagnosis. Because I have no definitive algorithm, because I have no consensus of what level of rhabdo or CK will have detrimental effects, most providers want to air on the side of caution. Clinically, ER is often diagnosed with CK or CPK levels at 5 times upper limits, that’s what you just need to know. Five times the upper limit is often a very conservative range. It has been reported like that in multiple sources. There is some suggestion that we should try to raise that to 10 times the upper limit. Typically, patients with 10 times the upper limit of CK, were found to be asymptomatic. No other symptoms just high CK and that’s believed to be a better diagnostic value.

As we continue on with the problem, more recently, there has been proposed suggestions of raising that limit to 50,000. No definitive pathological value for CK has been defined either. If we go back a slide, simply because there is no standard in terms of what the diagnostic criteria is, we just use the five times the upper limit as a conservative amount. There is no definitive pathological value for when it becomes dangerous, when it becomes harmful to the body. At this point, we are simply showing the elevation is occurring. The healthcare provider should be aware that some levels even 20 times the upper limit may be seen in performing repetitive strenuous exercise. If I am doing 2 a day work outs, if I am preparing for a show, if I am doing a physique competition, if I am doing body weight lifting, all of that can be just adding to this number.

It can be very scary and let me also say this, if you order this test and LabCorp comes back or Quest diagnostic comes back and says, your athlete CK level is 20,000. You could panic and rightfully, that is a high number, but only CK, CPK values over 5,000 should be concerned for renal failure. That is simply one study that found that other sources say 10,000 is the threshold.

Hopefully by now, I am either confusing you more or I am showing you the importance of what is the standard of care versus where should we be going. We should not be satisfied with a range of, well 5,000 is when we think of renal failure, but you know what? 10,000 is a normal diagnostic threshold, but you know what, 20 times the upper limit for strenuous activity, we just need better reference ranges. We need better research for our patients. At the end of the day, I often tell athletes that they are their best advocate. I sleep well at night because I know that every athlete that came into see me, I did the best I could for them. I did what I felt was in their best interest.

Let us just take a look at some crazy CK values real fast. I just want to show you some documented cases so that if you ever do see it, you don’t automatically just panic. There was an 18-year-old football place kicker, I am not getting hit necessarily all the time, I am just using my legs, 130,000 was his CK value. Another athlete was a 16-year-old male following 2 a day practices at a wrestling camp. I believe it was a five-day camp, he was at 146,000. Then, if you remember, I even told you the physical education class, here is a 12 year old male. He was late to class, his punishment, old school thinking versus new school thinking, maybe you still work with coaches who have an old school mindset of a punishment workout, but we are performing 250 squat jumps, that’s it. After performing 250 squat jumps, next couple days, the athlete went in, saw his local trainer, he was having muscle swelling, he was having pain in his legs, didn’t have a very good range of motion, was sent to the ER, his value was 244,006. That is a big number. In fact, there is evidence that suggests that CK and CPK values will range between 2 and 10,000 after doing 50 maximal eccentric contractions of the elbow flexors. I was telling you early on that I like to do tricep pull down. If I go tricep pull down to the heaviest I can do 50 of those masks maximal eccentric contractions. If I am trying to work on my arms and then I immediately go get some lab testing, maybe 12 hours after, give it some time to spike up 24 hours after I could have some high CK levels.

Knowing when an athlete is moved from the physiological state to the pathological state is often difficult, and it is often difficult to assess and manage without some sort of clinical diagnostic testing. We want to have expected elevations of CK, CBK may explain why team physicians so us or emergency room physicians often recommend intravenous hydration. At levels of 3000 and over, I am probably going to get fluids. Fluids right there in the ER. I get a couple liters of fluid lactated ringers, normal saline, depending on how my lab recheck goes. If it looks like things are trending down, clear out and mark the urine as I will probably be released. If I am over 10,000 units, I am most likely going to be staying the night in the hospital.

The question is, what is the re-evaluation process and how do I re-evaluate CK levels? This is where we as doctors come back in. The athlete has gone to the ED, been diagnosed with rhabdo, been diagnosed with Exertional Rhabdo and usually what they are told is no activity for a week. Then you going to repeat your lab work. Current laboratory ranges for CK failed to consider gender, ethnicity or any sort of activity level. As a physician, what we do is we can order those lab work and we can use that lab work to make a diagnosis or make a recommendation on whether the athlete can return to play. Usually that return to play is going to be simply based on is their values trending downward?

This leaves physicians to use the same laboratory references for athletes, even though we are not taking into account all of this as they do for a general population, often leading to the incorrect and misguided diagnoses. The athletes will have higher levels and we have said it before, and we will say it again. Athletes have higher levels of CK than non-athletes. Comparing them on a non-athlete scale is pointless, but it is the only thing we got. That is where sports specific ranges start to come in. How does that work? Do we have any of those? There is some research starting to come out showing some of the sport’s specific ranges, but it is typically like soccer is one of them, and I believe rugby has one and it is simply based in paper. It is all what I would say, still theoretical.

They have not been adopted by any sort of provider group like the emergency medicine association. They haven’t adopted those necessarily. it is just at least research is starting to come out to show yes, there are changes. Yes, we can make a difference. Asymptomatic CK elevation in the absence of symptoms or even minimal non-specific muscle symptoms. Some cramping, some spasm, some fatigue, an elevated CK is simply an incidental finding. Now, the more severe those symptoms are, we could say, okay, that is a diagnostic finding. More correct diagnosis for elevated CK levels is what we call asymptomatic hyper CK-Emia. I know say that 10 times fast. Asymptomatic hyper CK-Emia, elevated CK levels in the blood asymptomatically. That is exactly how we break that down. Our evidence exists that CK levels will rise after exercise.

They will rise after heavy manual labor. This is why it is not just an athlete issue. If I am working in private practice, in a small town of farmers, but also have a heavy sport population, I will see the everyday farmer who has been outside all day working in the summer heat, throwing hay, which is  heavy manual labor. They can be just as susceptible as my football player who’s is training twice a day. Increase in exercise or any heavy manual labor, which is increased and cause CK levels to go up to 30 times normal within 24 hours of that activity. Gradually, over the course of a week or so, 7 to 10 days, that value will start to slowly decline.

That is why when I order repeat labs, I am looking to see, the changes. He was 30 times normal on Monday, but by the following Monday it is only seven times. That’s a big trend downward and I now know we are going in the right direction. Our concentrations are typically going to peak, usually the 1 to 3 days, 1 to 4 days after exercise. Let us take a look at just a little bit more research as I think evidence based is where we need to be. A lot of my students I ask them, “What does the evidence say”? Prevention is key, that is what the evidence says. Future research should look at sport specific ranges and should explore contributing factors associated with developing ER. It should also evaluate a more accurate CK level for athletes versus non-athletes.

At this point I would be happy with a broader just a CK reference range athlete, CK reference range non-athlete. If I really wanted to just get greedy, I would say “I want a wrestling, football, soccer and rugby study”. Let us look at a few studies. There are 4 studies which I would like to highlight.

Study #1 Impact of Dehydration on Elite Wrestlers
This study was the impact of dehydration on elite wrestlers. It had 24 elite wrestlers who took in pre-competition weight last practices, they survey those and then there were the biomarkers.

Biomarkers were evaluated we look at the CK levels, we look at the AST, ALT, LDH and protein. We are going to be looking at something in terms of inflammation markers. Now, what researchers found was that serum CK and LDH levels were considerably increased after intense exercise. AST, ALT, CK and LDH are commonly used to evaluate muscle damage. Here is our pretest for our weight loss group and our pretest for a non-weight loss group. We can see higher levels in terms of pre and post.

Study #2 ER with D1 football. D1 NCAA division 1 athletes, research hypothesis that back squat work outs would trigger Exertional Rhabdo. What do we do? Let us do some back squat work outs. What we found was serum CK and creatinine from 96,000 to 331,000. That is a huge, huge spike. Go back to where I was saying how 50 maximal elbow flexors would cause a spike in CK levels. Here, we have back squats. The effective players went to muscle failure. They performed extra squats, you probably seen it if you ever been on the wait room with athletes. Some athletes are going to go extra, some athletes want to try and push their bodies to the extreme. They want to get better. Other athletes come up and ask, “How many of those do I have to do again?” This is the group that did extra work. They did not think that they could complete the workout because they are going so heavy. They were more likely to report symptoms of the affected players.

They did find that protein shakes may have a protective effect and decrease the risk of developing Exertional Rhabdo. One of the theories and this is my theory based on, what I know about nutrition and my background, it is going to be the fact that we have BCAs. We have the Branched-chain amino acids, the proteins. As the body is looking for energy source, hopefully we are not going to be breaking down muscle tissue. We are going to be using the BCAAs form the protein. Risk of ER, was increased based on the perfect body weight lifting, the number of sets and the time needed to complete the hundred back squats. This is only the third study to report a cluster of ER among D1 athletes.

Study #3 ER + D1 Swimming
Here is a D1, Division 1 swimming, so 7th Collegiate NCAA Division 1 swimmers. They all presented with severe pain and swelling of the tricep. Also severe pain and swelling of pectoralis major and minor. What we had was dark colored urine. We got the hallmarks, we got the pain and swelling, we also have the urine. We take a look, all swimmers denied drug use, alcohol use, supplement use. They said that they are all fully hydrated, so that’s great. The physical exam reveals that the tenderness over the palpation of the chest and arms. They had decrease fluxion, we have decrease range as a motion. That’s a red flag, we need to think Exertional Rhabdo for sure. Non-pitting edema, non-pitting localized swelling of the bilateral triceps. For these CPK level range from 14,000 all the way up to 157,000.

Depending on what lab you are using, you can see some incredible values for CK, CPK levels.

Study #4 CK Levels Post 2-A-Day
We are looking at CK levels post 2-a-days. Post exercise CK levels were typically 5 to 10 times the upper limit for men and women. The first study to examine CK levels on football players from high intensity exercise. They were in a high heat environment and in a high humidity environment doing 2-a-days. Normal clearance of CK was typically 2 to 3 days, peak levels was about 18 hours as what they found. What that study did not examine was electrolyte imbalances, lactate dehydrogenase, did not examine myoglobin, it was strictly looking at what was the CK, CPK issue. What was that response?

At this point, you are able to diagnose, identify, understand and educate. Now the question is, how do you treat? What do you do? How can you be the best provider that you can be? That is where we come in to talk about sideline management versus treatment.

My first question to you is, do you think this is the same? I am sure some of you would be saying “No” because this is not the same. If I am on the sideline working with an athlete, if I start to suspect this, what can I do to mitigate the risk? I start to ask myself is oral hydration enough? If oral hydration is enough let’s start getting hydrated. I need to consider how is the athlete? How is the environment. If it is the hot environment I need to get them out to a cool environment. What are my training variabilities? If it is a wrestler, we keep the wrestling room about 83 degrees. I am going to pull the wrestler out and we are going to get some fluid hydration, sit in the training room to cool off, and see how we are doing versus treatment. If I think they still need further treatment which is often the case, by the time an athlete comes to you, sometimes the hospital is the best place. A lot of athletes like to wait until the last minute, they don’t like to tell you that they are not feeling well. All of a sudden, they come to you and sure enough you need to go to the ED. Can they go by personal car, or can they go by ambulance? Are they stable? If they want to go by personal car, the question is, do I feel safe with them going by personal car? Do I feel comfortable with another athlete taking them? Sometimes the athlete will say “Can I have my friend take me?” Well, maybe, but if I think that you are at jeopardy, our hospitals 20 minutes away, if I feel that you can’t make that 20 minutes without having some sort of adverse effect, I don’t want to put that pressure on to another athlete. I am going to say, no, we need to call an ambulance. If I think it is that severe the ambulance the paramedics when I get there I could start IV fluid resuscitation at that point. I can start the fluids you can at least start to get the fluids and then by the time I get to the hospital I have give you 500 ml. Once you get to the hospital, the athlete is probably going to get at least another liter and a half of fluid at ED. Here is our treatment overview, mild cases may go undiagnosed and maybe manage an outpatient setting with oral hydration and rest if I catch it early enough.

I see a lot of providers around me, who have a conservative management. They will get some IV fluid replenishment in the ER but then it is just no activity for a week. Conservative management consist of rest and rehydration and that can simply be adequate. If I am in the clinic setting if I am in the hospital-based setting, I am probably going to get some intravenous rehydration, a revaluation of my labs before I go. Typically, what we find is we find lactated ringers, LR or 0.09% normal saline is being our two most common fluids of choice. With the rehydration go about 300 ml per hour. Now, the need for hospitalization is really based on the intuition of the provider and I respect that. There are certain times that my gut says something, and I just have to listen to. I must send you for an x-ray, I have to send you to the hospital. It’s just there’s certain red flags, certain things we hear in our history and our presentation that make us think this is going to be best for you. It is up to the provider in most cases. This decision is often derived from the physician’s intuition and not necessarily based on simply laboratory findings, it is again treating your patients first. You can have some crazy laboratory values and things going on but treat your patient first. With the potential of more serious consequences developing, the health care provider may just want to keep you overnight. Just keep you there for observation make sure nothing happens, repeat labs in the morning. Everything looks fine, you will get discharge. From the sideline perspective, if you work weightlifting, if you work swimming, if you work football, wrestling, or running I need you to know that you are working a sport that has a high index of suspension. Have a high index of suspension if you are involved at any of those.

The World Games 2022 are coming up, and if you are working the body building section, the weightlifting piece those are athletes that we just need to be concern about. Summer in anywhere, but summer in the south it could be hot and humid. Any sort of outdoor sport, any sort of swimming sport, these are all things that would be really beneficial just little keys as I go into that environment. I am worried about XYZ , not so much worried about hypothermia and frostbite in the middle of July in South Florida. It is just not something that I am concerned about. Here in Iowa currently, I am worried about frostbite for a lot of athletes, especially anything outdoors. Patient history will help lead to your possible diagnostics, then eventually to diagnosis. With myoglobinuria can easily be detected in the clinic or sideline setting with the dipstick analysis. That is going to be one of the simplest and easiest ways, inexpensive too so I would suggest just buy some of those. Definitive treatment again ER, got to the hospital you will get dipstick, UA and the ED usually which can be positive with  the presence of blood but microscopically is not going to show red blood cells. That’s going to tell you that the dipstick was finding the myoglobin. CK values will aid in diagnosis but one of the challenges that even an emergency  medicine physician or sport medicine physician is going to have his determining whether that is clinical, in terms of pathology or is that just physiological. Being able to differentiate physiological ER versus pathological ER is going to be big.

Hospital admission maybe required, you may end up getting 4 to 11 liters in the first 24 hours depending on what your kidney function looks like. This is the time that we want to try and prevent acute renal failure. If I am going to get 11 liters of fluid into them, that is going to be a lot of weight to cut. Then it is just your job as provider to make sure they are cutting it right, because the athlete is just going to immediately say “All right, I will just dehydrate myself again” and then we are back into the same position. Once treated the last thing an athlete really need to know is what’s my return to play protocol. What’s my return to play? A return to play is basically evaluating and assessing risk factors. This is a further complicated by the fact that there’s no standard in terms of laboratory markers, like I said I just have to evaluate all right you went in on a Saturday you were four times CK and now you are one-time CK, you are trending downwards after 7 days of no activity you have improve range of motion. You have full range of motion, you have no muscle pain, I feel comfortable you are starting back with some light activity. Laboratory Testing could rely on those biomarkers as a baseline. An athlete’s physician should be closely consulted, and the patient must be closely monitored during a return to play. Luckily for me I have a great relationship with the athletic training staff. In fact, there is an athletic trainer and myself at pretty much all practices.

If I want to release an athlete back, I just have that conversation with the trainer it is possible that if you are in the office setting most days of the week, have that conversation with the trainer who is probably at the practice. Make sure that they know that they have to watch them coming back just because you just because you have been released does not mean you’re fully released. Think of your concussion protocols, if I have a concussion, I have a gradual return to play it is not just, now go back to do everything you did right before you went to the hospital. Sports Medicine Physicians and ER, emergency medicine physician should be familiar with the high-risk patients. Those are ones with sickle cell disease familial history of rhabdo, any sort of history of hypothermia, those were recurrent episodes of ER. If this is my third or fourth time exertional rhabdo I need to be concerned about that. Patients deemed high risk, should be referred for further follow-up, an examination for further studies. Then when prop diagnosis and treatment is initiated, honestly this has a great full recovery and full return to play with usually minimal downtime of about a week to 2 weeks at most. This really is as serious as it can be, is something that we can manage quite effectively. Then finally the Champ Guidelines, which is broken down into phase 1, phase 2 and phase 3. I find that these are helpful, 72 hours of no activity and oral hydration, get good sleep, after the 72 hours you can repeat serum CK. I typically repeat after a week. That is what the ER Doctors around here wanted. If it is something in my personal practice, if I catch it, I can follow champ guidelines and still be within the standard of care. I never override an ER physician though. When ER physician sends back a discharge that says repeat labs in 7 days, I am not repeating labs in 4 days to try and get those athlete back any sooner.

Then phase 2 is your light activity no strenuous work, physical activity at their own pace. Then phase 3 is your gradual return to regular sport and physical activity. Quickly, because I just feel like with my background I would be doing an injustice if I didn’t talk about at least a little bit of nutrition. Some research has suggested that consumption of protein shakes may possibly protect against the ER. That is something that is beneficial to know and usually what the other studies have found is because of those VCAAs. Those VCAAs can also reduce serum levels of CK. You may have heard before that creatine monohydrate could cause exertional rhabdo. The most recent study that I found creatine monohydrate was extensively studied and it does not play a role into the development of exertional rhabdo. Then proper hydration is absolute key.

Here are some final key points that I want you to take away. I want you to remember some red flags for me. Patients presenting with severe muscle pain, with decreased muscle strength or myoglobin urea, we should all be worried. Common findings increased myoglobin and increased CK levels those are two things that you really want to be focusing on. Diagnosis is often made with the help of laboratory findings good clinical history. As we take some of those takeaways home, right exertional rhabdo is strong in the eccentric component some muscle lengthening. Downhill running, negatives, delayed on-set muscle soreness, which is I am sure something that we have seen several times in a given season for our athletes, has been suspected as being a mild form of a rhabdo. It maybe suspected after athlete presents muscle stiffness following eccentric exercises and is often likely due to the inflammation and sensitization of nociceptors sectors. This is where that pain comes in. Exercise related muscle injury can be considered a continuum from DOM’s to rhabdo, keep that in mind. More than half of all patients do not report muscle symptoms. Even though I said that’s one of the triad that we want to look for, half of all patients never have the muscle symptoms, they never have the stiffness, they never have the soreness. Myoglobin urea is found in only half of patients. If an athlete comes back to you and says “Yeah, it is just yellow urine” it does not mean that they do not have it. We cannot exclude the syndromes simply based on that having myoglobin urea. Then less than 10% of all patients present with all three conventional symptoms. At the end of the day, now that I probably really confuse you even more, I want you to know that this all comes down to your ability to question the patient, take a good history, get to know your athletes. This is where you are going to be able to pick up on those things to be the best clinician, the best diagnostician that you can be.

It is imperative to understand that exercise can increase CK, CPK levels in blood. Research is needed to establish specific references. At this point, I just want an athlete versus non-athlete range. Bringing awareness to healthcare providers regarding diagnosis, treatment and management. Mini athletic training and exercise physiology textbooks nowadays simply do not cover ER or just never talk about it altogether or give you a very poor clinical picture that is nowhere near this presentation. Healthcare providers working with athletes, at the end of the day we need to educate. You need to educate the athletes, needs to educate the coaches, need to educate the other health care providers around us, so that we can promote and practice mitigation techniques so, the education dissemination of appropriate information. Maybe we create a flier, something we put up in the training room. I have pull some things from the Olympic committee and put up in the training room for our athletes, just because there is a lot of good resources out there that they do not get to see.

We are going to run through just a couple of Case Studies.

Case #1
24 year old Caucasian male presented to a local clinic with vomiting, muscle cramps and low urine output. We got the cramping, vomiting so dehydration coming in and low urine output. Dehydrated. He received IV fluids 500ml at the clinic and was referred to the emergency department for re-evaluation. Once in the emergency department it was found out that he had lost 17 pounds in 2 days trying to meet his weight for an upcoming wrestling tournament. It was confirmed that he was experiencing muscle cramping, dehydration, and decreased urine output at FED and actually unable to urinate and when he did it was brown. My question is, what is next? The typical workup was this. Got a CBC, CMP, CPK and a UA. This athlete had these findings, his CPK, everything about the cramping, everything about the urine you thought instantly “he is going to have a high CK level.” His CK was 460, about 2 and a half times what their upper limit was. If you take a look, dark yellow, specific gravity hydrated and then trace-lysed amount of blood. This patient got 2 liters of normal saline, was placed on no activities for five days in a gradual return to play. Final diagnosis rhabdo. My question is, did that meet the criteria for rhabdo? Rhabdo, dehydration, muscle cramping and low urine output. Well, here he is return to play, he follows the 5 day recommendation. Six days following the ED visit, we did follow up lab work. Patient began experiencing muscle tightness at the practice. Did not tell anyone. Seven days followed the initial ED presentation, two days after a return to play, his pain has increased back. It was newly developed nausea, vomiting, muscle pain, flank pain was evaluated in the clinic. This time more labs were ordered. Again, CBC, CMP, CPK and UA those are all re-ordered.

CK were still 353, BUN does not look to terrible, color was just called darker. Sodium and Potassium were at the normal ranges. At this point, the ER doctor did this, we had 2 liters lactated ringers. He was pulled for a week now and he was told to consider metabolic myopathy. This is a repeat, just one after another. A repeat incident of Rhabdo, the athlete was told to consider metabolic pathways or metabolic myopathy. He was diagnosed with heat exhaustion, hyper uricemia, elevated CPK, acute kidney and dehydration. If you look, nowhere there was the word rhabdo or exertional rhabdo mentioned. Even though were being treated as such.

Case #2 Clinical example number 2, 21 year old African American male. Based on everything that you have learned so far, maybe a sickle cell trait but he presented to the ED by EMS after being choked out at a tournament. The shortness of breath following a wrestling tournament, he passed out, when he regains consciousness, he know that he was having trouble breathing, difficult to swallowing and his voice was different. We start to think maybe we have a crush injury at the larynx. He goes by ambulance, get’s a CT. They, of course, do labs. He admits in the ER that he had been cutting weight for several days. He has not been starving himself though, that was his quote but the last time he urinated was before today’s match. Diagnostic was CBC a BMP just a basic metabolic panel, CK and then we are looking at the heart now, CKMB. CK, 1,220, so we are definitely over that five times upper limit, we can meet criteria for the CK values now. UA was not obtained, obviously the ER felt more strongly on breathing issue, which I do not necessarily blame them.

If you take a look at the treatment that he got. He got 2 liters of normal saline, dexamethasone, Iopamidol and was discharged. A lot of this was for the upset stomach. Discharge return home with the team. Diagnose with a choking injury, mild Rhabdo based on the CK. Just like our last individual, once he was home, he woke up in the middle of the night, was feeling dizzy, felt bad, and ended up having a syncopal episode in the dorm. Roommate called 911, EMS arrived took him to the local ED, this sure look awfully familiar. This is pretty much the work up of our local hospital, got a CBC, CMP, CK/CPK and a UA. At this time this is where I am telling you and showing you that all they say is greater than a thousand. He was 1,220 at the last hospital, he is greater than a thousand at this one. I do not know if he was still going up, based on what I know and based on the research that I have had, he is continuing to go up. AST was altered, we start looking at amber urine. What are the red blood cells? His treatment was a little bit different. He had 2 liters of normal saline, some Tylenol for the pain, Zofran for the nausea. He was admitted overnight for observation because he did have a syncopal episode and they were worried about the breathing at that point. His diagnosis was recurrent Rhabdomyolysis even though he just been diagnosed 8 hours before it reoccurred, mild hypokalemia, inverted T-waves which they consult towards a cardiologist. Cardiologist came back and said that was a normal juvenile persistent pattern. Then on CT, they did find a cyst of the panela gland which was just a simple incidental finding.

Case #3 – 18 year old male presented to the ED by athletic trainer. Athletic trainer following a history of 2 syncopal episodes. First syncopal episode was earlier in the day and the second syncopal episode was inside the locker room after wrestling practice. Patient was vomiting over a toilet when he passed out for approximately 1 minute. No other neurological deficits were noticed. One’s in the ER it was found that he had bilateral flight pain that he rated 3 out of a 10. He had other muscle cramping and aching. Patient said he had a history of colitis, initially stated that he had been working out that day, was drinking some water but later admitted that he had not been drinking or eating for several days as he was trying to loose weight for a wrestling match. Local Hospital ordered the CBC, CMP, CPK and UA to which we find pretty elevated CPK levels were 848, upper end is 170, we are getting pretty high to those five times limit. Urine is amber, we are dehydrated with our specific gravity and that was all the data that we really had. This patient, 2 liters of normal saline, CBK remains elevated but has treaded downwards. This patient spent some time overnight, has trended downward. Patient should not be at any undue risk of discharge, he was then discharged with the diagnosis of elevated CK, not even Rhabdo, elevated CK and dehydration. I would argue that you could have put rhabdo here if you wanted to follow the other clinical presentations such as the cramping, urine being darker and the elevated CK he would technically be able to meet it based on current standards.

Case #4  – 18 year old male presented to the ED by athletic trainer again, after a history of 3 syncopal episodes following strenuous activity. He said that the syncopal episode had occurred in the weight room earlier that day. He felt very light headed, leaned up against the wall and felt as though he was going to pass out. Similar episodes occurred on Monday, 5 days earlier. When he went to the emergency department, patient denied any pain. He did note some muscle cramps in his hand and legs. Stated that he was trying to cut weight for an upcoming wrestling match but he had not been drinking and he did report a history of migraines. At this point, diagnostic workup looks pretty similar to everybody else because it is the same hospital. Here we go, we found CPK levels greater than a thousand again I cannot tell you what they were because I simply do not know. BUN was elevated, urine was amber, specific gravity was showing dehydration. Here is his diagnosis, elevated CK levels and dehydration. The consistency here from the same hospital, different providers is everything from elevated CK to Rhabdo to persistent Rhabdo. This is all coming down in my professional opinion just showing why we need better diagnostic criteria. I am not saying that any of these athletes were treated wrong, as they were not treated wrong and the standard of care was absolutely applied but for what is there is so inconsistent. He received 2 liters of normal saline and normal kidney functions, CK was starting to trend downwards so, he was released.

All of that is what led us to write this paper. Doctor Thomas is an ER physician, board certified and I worked on this and it was our paper for the re-evaluation of the diagnostic criteria for Exertional Rhabdo and collegiate  wrestlers. In research you want to pick a topic, my topic was topics was population of collegiate wrestlers. Though I do believe this really applies to other sports, but this was a case serious. It was a case that I just run through, that is why it went kind of fast because you have the ability to go and find this if you would like. Then, it is a review of the literature, which really covers a lot of what was presented here today. I greatly appreciate your time. I hope you learn a thing or two.

I hope you really enjoyed the presentation. I hope you found it to be of value. This is a topic that I particularly enjoy, not enjoy necessarily dealing with, but it is definitely something that I think a lot of providers will see and just may not fully understand. Having the opportunity to share that with you, share some of this knowledge, and share some of these resources is truly an honor. If you have any questions, please by all means, reach out.

To FICS to the ICSC you are more welcome to contact me, they will have a way if you have any questions, comments, or concerns about this presentation, I am more than happy to speak with you.

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