Medical Related Issues in Sports Medicine: Difference between revisions

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Typically a SCA is diagnosed after the fact by a cardiologist or a specialist known as a cardiac electrophysiologist. A barrier of tests are done to elicit the underlying cause for the arrest in those lucky enough to survive it. Tests and measures analyzed by these specialists include but are not limited to electrocardiograms, echocardiography, multiple gated acquisition testing, cardiac catheterization, electrophysiology study, and blood tests to ascertain levels of potassium, magnesium and other chemicals important in electrical signaling<ref name="NIH" />. <br>  
Typically a SCA is diagnosed after the fact by a cardiologist or a specialist known as a cardiac electrophysiologist. A barrier of tests are done to elicit the underlying cause for the arrest in those lucky enough to survive it. Tests and measures analyzed by these specialists include but are not limited to electrocardiograms, echocardiography, multiple gated acquisition testing, cardiac catheterization, electrophysiology study, and blood tests to ascertain levels of potassium, magnesium and other chemicals important in electrical signaling<ref name="NIH" />. <br>  


 
<br>


The American Heart Association has compiled a preparticipation screening known as the 12-Element Preparticipation Cardiovascular Screening for Competitive Athletes. It details important history questions to ask the athlete in their personal and family history as well as important physical examination techniques <ref name="National" />.  
The American Heart Association has compiled a preparticipation screening known as the 12-Element Preparticipation Cardiovascular Screening for Competitive Athletes. It details important history questions to ask the athlete in their personal and family history as well as important physical examination techniques <ref name="National" />.  
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<br>'''Treatment for the Arrested Athlete:'''<br>  
<br>'''Treatment for the Arrested Athlete:'''<br>  


 
<br>


Any athlete who is unresponsive after a collapse should be treated immediately and SCA is suspected. CPR protocols should be initiated if breathing and pulse are absent. Initiate EMS. CPR should not be stopped until the AED has been retrieved and an analysis of the rhythm is initiated. Continue CPR and defibrillation as indicated until the appropriate emergency responders arrive<ref name="Emergency">Emergency Care Committee, Subcommittees and Task Forces of the American Heart Association. 2005 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care, part 3: overview of CPR. Circulation. 2005;112(suppl 24):IV12–fckLRIV18.</ref>. <br>  
Any athlete who is unresponsive after a collapse should be treated immediately and SCA is suspected. CPR protocols should be initiated if breathing and pulse are absent. Initiate EMS. CPR should not be stopped until the AED has been retrieved and an analysis of the rhythm is initiated. Continue CPR and defibrillation as indicated until the appropriate emergency responders arrive<ref name="Emergency">Emergency Care Committee, Subcommittees and Task Forces of the American Heart Association. 2005 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care, part 3: overview of CPR. Circulation. 2005;112(suppl 24):IV12–fckLRIV18.</ref>. <br>  
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Although the exact number of people in the United States living with SCD is not known, it is estimated that the disease affects 90,000 to 100,000 Americans. The disease most commonly occurs in people of African American heritage. About 1 in every 500 African American children born has SCD. Hispanic Americans are the second most likely to have a child born with SCD at 1 in every 36,000 births <ref name="NIH What">National Institutes of Health, National Heart, Lung, and Blood Institute. What causes sickle cell disease?. http://www.nhlbi.nih.gov/health/health-topics/topics/sca/causes (accessed 7 Nov 2015).</ref>.  
Although the exact number of people in the United States living with SCD is not known, it is estimated that the disease affects 90,000 to 100,000 Americans. The disease most commonly occurs in people of African American heritage. About 1 in every 500 African American children born has SCD. Hispanic Americans are the second most likely to have a child born with SCD at 1 in every 36,000 births <ref name="NIH What">National Institutes of Health, National Heart, Lung, and Blood Institute. What causes sickle cell disease?. http://www.nhlbi.nih.gov/health/health-topics/topics/sca/causes (accessed 7 Nov 2015).</ref>.  


In the athletic world, sickle cell disease has been most prominently discussed in relation to football. Since the year 2000 more than 16 deaths have taken athletes lives in division one football. These deaths are attributed to four causes: cardiac, asthma, exertional heat stress, and exertional sickling <ref name="Van Camp 95">Van Camp SP, Bloor CM, Mueller FO, Cantu RC, Olson HG. Nontraumatic sports death in high school and college athletes. Med Sci Sports
In the athletic world, sickle cell disease has been most prominently discussed in relation to football. Since the year 2000 more than 16 deaths have taken athletes lives in division one football. These deaths are attributed to four causes: cardiac, asthma, exertional heat stress, and exertional sickling <ref name="Van Camp 95">Van Camp SP, Bloor CM, Mueller FO, Cantu RC, Olson HG. Nontraumatic sports death in high school and college athletes. Med Sci SportsfckLRExerc 1995;27:641-647.</ref>, <ref name="Eichner 2010">Eichner ER. Sickle cell trait in sports. Curr Sports Med Rep. 2010;9 (6):347–351.</ref><br>  
Exerc 1995;27:641-647.</ref>, <ref name="Eichner 2010">Eichner ER. Sickle cell trait in sports. Curr Sports Med Rep. 2010;9 (6):347–351.</ref><br>  


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&nbsp;  
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The most common locations for pain exacerbation include the low back region, left, arms, abdomen, and chest. Temperature changes, stress, illness, dehydration, and high altitudes often bring on these crises <ref name="National" />. <br>  
The most common locations for pain exacerbation include the low back region, left, arms, abdomen, and chest. Temperature changes, stress, illness, dehydration, and high altitudes often bring on these crises <ref name="National" />. <br>  


 
<br>


'''Medical Exam/screening/testing: '''<br>  
'''Medical Exam/screening/testing: '''<br>  
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Every newborn in the United States is required to have screening tests performed for SCT. This is done via a blood test in which the newborn’s heel is pricked and blood is taken and tested for abnormalities in the child’s hemoglobin. If the test is positive, the child’s parents are notified and further blood testing is done to affirm the screening test. Prenatal testing is another alternative in which doctor’s extract amniotic fluid and analyze it for abnormalities in the HBB gene mentioned earlier <ref name="NHR GIH" />. <br>  
Every newborn in the United States is required to have screening tests performed for SCT. This is done via a blood test in which the newborn’s heel is pricked and blood is taken and tested for abnormalities in the child’s hemoglobin. If the test is positive, the child’s parents are notified and further blood testing is done to affirm the screening test. Prenatal testing is another alternative in which doctor’s extract amniotic fluid and analyze it for abnormalities in the HBB gene mentioned earlier <ref name="NHR GIH" />. <br>  


Although this screening is mandated, it is important to note that a survey performed by Kavanaugh, Wang, Therrell, and Sprinz found that only 37% of parents were informed of a positive SCT test <ref name="Kav">Kavanaugh PL, Wang CJ, Therrell BL, Sprinz PG. Communication of positive newborn screening results for sickle cell disease and sickle cell trait: variations across states. AJM Genet C Semin Med Genet 2008; 148C:15-22.</ref>. An athletic trainer at Oklahoma University, Scott Anderson, screened the football team at the university and found 20 athlets with SCT and only three knew they had the disease<ref name="Anderson">Anderson S, Doperak J. Recommendations for routine sickle cell trait screening for ncaa division 1 athletes. PM &amp; R 2011;3:168-174.</ref>. Revelations such as these suggest that physicians should administer a new test for SCT as a part of the preparticipation physical examination screening <ref name="Anderson" />. <br>
Although this screening is mandated, it is important to note that a survey performed by Kavanaugh, Wang, Therrell, and Sprinz found that only 37% of parents were informed of a positive SCT test <ref name="Kav">Kavanaugh PL, Wang CJ, Therrell BL, Sprinz PG. Communication of positive newborn screening results for sickle cell disease and sickle cell trait: variations across states. AJM Genet C Semin Med Genet 2008; 148C:15-22.</ref>. An athletic trainer at Oklahoma University, Scott Anderson, screened the football team at the university and found 20 athlets with SCT and only three knew they had the disease<ref name="Anderson">Anderson S, Doperak J. Recommendations for routine sickle cell trait screening for ncaa division 1 athletes. PM &amp;amp; R 2011;3:168-174.</ref>. Revelations such as these suggest that physicians should administer a new test for SCT as a part of the preparticipation physical examination screening <ref name="Anderson" />. <br>  


 
<br> '''Identifying an Athlete in Crisis:'''<br>  
'''Identifying an Athlete in Crisis:'''<br>  


Identifying an athlete in crisis from the sideline is essential for sports medicine practioners. The following are features of an exertional sickle cell collapse <ref name="Eichner 2011">Eichner ER. Sickle cell consideration in athletes. Clin Sports Med. 2011;30:537–549.</ref>:  
Identifying an athlete in crisis from the sideline is essential for sports medicine practioners. The following are features of an exertional sickle cell collapse <ref name="Eichner 2011">Eichner ER. Sickle cell consideration in athletes. Clin Sports Med. 2011;30:537–549.</ref>:  


<br>1) Athletes will slump to the ground which differentiates the presentation from cardiac pathology (sudden fall) and heat cramps (hobbling). <br>2) Muscle strength will be abnormally weak comparative to the level of pain experienced by the athlete. The opposite presentation will occur in athletes with heat cramps.<br>3) Athletes will initially be able to communicate to the practioner as opposed to an athlete who experiences a cardiac arrhythmia. Typically a cardiac arrhythmia leads to unconsciousness. <br>4) Muscles will look and feel normal upon palpation unlike someone undergoing heat cramps.<br>5) Rapid tachypnea will be present despite optimal air flow due to lactic acidosis<br>6) Temperatures usually are under 103 degrees Farenheit as opposed to over 106 degrees found in heat stroke. <br><br>
<br>1) Athletes will slump to the ground which differentiates the presentation from cardiac pathology (sudden fall) and heat cramps (hobbling). <br>2) Muscle strength will be abnormally weak comparative to the level of pain experienced by the athlete. The opposite presentation will occur in athletes with heat cramps.<br>3) Athletes will initially be able to communicate to the practioner as opposed to an athlete who experiences a cardiac arrhythmia. Typically a cardiac arrhythmia leads to unconsciousness. <br>4) Muscles will look and feel normal upon palpation unlike someone undergoing heat cramps.<br>5) Rapid tachypnea will be present despite optimal air flow due to lactic acidosis<br>6) Temperatures usually are under 103 degrees Farenheit as opposed to over 106 degrees found in heat stroke. <br><br>  


<br> '''Steps to take on the sideline when a Crisis is identified <ref name="Eichner 2011" />, <ref name="National" />:'''
<br> '''Steps to take on the sideline when a Crisis is identified <ref name="Eichner 2011" />, <ref name="National" />:'''
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'''Medical Management/ Treatment:'''<br>  
'''Medical Management/ Treatment:'''<br>  


Pain related to an episode or crisis can be managed with OTC medications such as ibuprofen or aspirin. In the most sever crises, the patient will be admitted to the hospital and administered opioids such as morphine and other pain relieving medications. In severe crises where anemia, splenic sequestration, or acute chest syndrome occur, medicinal intervention includes blood transfusion, a spleenectomy, antibiotics to prevent infection, medicine to open airways, or administration of oxygen may be warranted. Interventions are considered on a case-by-case basis . <br><br>  
Pain related to an episode or crisis can be managed with OTC medications such as ibuprofen or aspirin. In the most sever crises, the patient will be admitted to the hospital and administered opioids such as morphine and other pain relieving medications. In severe crises where anemia, splenic sequestration, or acute chest syndrome occur, medicinal intervention includes blood transfusion, a spleenectomy, antibiotics to prevent infection, medicine to open airways, or administration of oxygen may be warranted. Interventions are considered on a case-by-case basis <ref name="EVB Sickle">National Heart, Lung and Blood Institute. Evidence-based management of sickle cell disease: expert panel report, 2014. http://www.nhlbi.nih.gov/health-pro/guidelines/sickle-cell-disease-guidelines/(accessed 8 Nov 2015).</ref>. <br><br>  


'''PT Management:'''<br>  
'''PT Management:'''<br>  
''


'''''Prevention and Appropriate Exercise Parameters:'''''<br>  
'''''Prevention and Appropriate Exercise Parameters:'''''<br>  
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As mentioned previously, many parents of athletes are unaware of positive tests for SCT in their offspring. The problem of sickle cell crisis is compounded in the high school athlete where requirements for SCT are not mandated. Therefore, sports medicine personnel must engage in proper preventative techniques.  
As mentioned previously, many parents of athletes are unaware of positive tests for SCT in their offspring. The problem of sickle cell crisis is compounded in the high school athlete where requirements for SCT are not mandated. Therefore, sports medicine personnel must engage in proper preventative techniques.  


<br>
The following are tips for preventing a sickling crisis.<br>1) The athlete should be allowed to set his/her own pace in conditioning exercises. They should be allowed to build training sessions slowly and have longer rest periods between bouts and repetitions. <br>2) Preseason strength and conditioning programs are encouraged to maintain the athlete’s preparedness for physical activity and should be sports specific. <br>3) When athlete’s with SCT set their own workout pace, they typically do not have exacerbations into crisis.<br>4) Immediately stop activity with the onset of muscle cramps, inability to “catch breath,” pain, and swelling.<br>5) Remember that repetitive high level training leads to lactic acidosis and could perpetrate a crisis. Therefore, training that leads to high levels of lactic acidosis must allow for extended recovery periods between repetitions in order to prevent a crisis.<br>6) Educate athletes on the importance of communication regarding the occurrence of sickle cell symptoms.<br>7) Finally, heat stress, dehydration, asthma, infection, and altitude can all predispose an athlete to a sickle cell crisis. Therefore, the athlete must hydrate, manage asthma effectively, modulate work load to fit the environmental stressors, not workout if ill, and modify workout load if new to a region with altitude<ref name="Eichner 2011" />, <ref name="National" />. <br><br>  
 
The following are tips for preventing a sickling crisis.<br>1) The athlete should be allowed to set his/her own pace in conditioning exercises. They should be allowed to build training sessions slowly and have longer rest periods between bouts and repetitions. <br>2) Preseason strength and conditioning programs are encouraged to maintain the athlete’s preparedness for physical activity and should be sports specific. <br>3) When athlete’s with SCT set their own workout pace, they typically do not have exacerbations into crisis.<br>4) Immediately stop activity with the onset of muscle cramps, inability to “catch breath,” pain, and swelling.<br>5) Remember that repetitive high level training leads to lactic acidosis and could perpetrate a crisis. Therefore, training that leads to high levels of lactic acidosis must allow for extended recovery periods between repetitions in order to prevent a crisis.<br>6) Educate athletes on the importance of communication regarding the occurrence of sickle cell symptoms.<br>7) Finally, heat stress, dehydration, asthma, infection, and altitude can all predispose an athlete to a sickle cell crisis. Therefore, the athlete must hydrate, manage asthma effectively, modulate work load to fit the environmental stressors, not workout if ill, and modify workout load if new to a region with altitude. <br>http://www.sicklecelldisease.org/index.cfm?page=sickle-cell-trait-athletic<br>  


'''Multidisciplinary Teams: '''<br>  
'''Multidisciplinary Teams: '''<br>  


When working with an athlete who has SCD, it is critical to coordinate the athlete’s training, medical care, and engagement in team activities. To effectively accomplish this, the primary care physician, athlete and parental units, sports medicine personnel, coaching staff, and other support personnel must work to maintain optimal sports participation. Sports are not contraindicated for those with SCD, but the aforementioned persons must work to establish appropriate workout regimens, provide adequate access to emergency response intervention, and have open lines of communication.<br>  
When working with an athlete who has SCD, it is critical to coordinate the athlete’s training, medical care, and engagement in team activities. To effectively accomplish this, the primary care physician, athlete and parental units, sports medicine personnel, coaching staff, and other support personnel must work to maintain optimal sports participation. Sports are not contraindicated for those with SCD, but the aforementioned persons must work to establish appropriate workout regimens, provide adequate access to emergency response intervention, and have open lines of communication.<br>  


'''Resources: '''<br>  
'''Resources: '''<br>  
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Please refer to the National Institute of Health, the National Athletic Training Association, and local physicians for more information on the proper management and monitoring for athletes with SCD.<br>  
Please refer to the National Institute of Health, the National Athletic Training Association, and local physicians for more information on the proper management and monitoring for athletes with SCD.<br>  


'''Clinical Bottom Line: '''<br>Physical activity and participation in sport are not prohibited for those with SCD. However the athlete should not be subjected to exercise conditioning tests, must be given elongated time to reach appropriate conditioning levels, must be cognizant of current health status, and be educated on the disease. <br><br>  
 
'''Clinical Bottom Line: '''<br>
 
Physical activity and participation in sport are not prohibited for those with SCD. However the athlete should not be subjected to exercise conditioning tests, must be given elongated time to reach appropriate conditioning levels, must be cognizant of current health status, and be educated on the disease. <br><br>  


== Diabetes in Sports  ==
== Diabetes in Sports  ==

Revision as of 21:25, 15 November 2015

 

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Sudden Cardiac Death in Sports[edit | edit source]

Definition/Epidemiology/Etiology/Prevalence/Incidence:

Sudden cardiac death (SCD) is defined by the NIH as a condition in which the heart unexpectedly ceases beating [1]. SCD is thought to be the leading cause of death among young athletes [2]. Most commonly, a structural abnormality is the cause of SCD. Coronary artery disease (CAD), commoto cordis, and hypertrophic cardiomyopathy are the most common abnormalities related to SCD. [3]Other abnormalities include Marfan Syndrome, atherosclerotic CAD, dilated cardiomyopathy, myocarditis, and arrythmogenic right ventricular dysplasia.


Incidences where an abnormality cannot be identified post mortem, the cause for SCD has been hypothesized to be related to inherited arrhythmic disorders, ion channel disorders, or familial catecholamenergic polymorphic ventricular tachycardia.
Incidence of SCD in the high school athletic population is estimated at 1 out of every 100,000 to 200,000. In collegiate athletics, the estimate is higher[4]. Incidence in collegiate athletes is 1 out of every 65,000 to 69,000 [5]. There seems to be a higher incidence in the African American population (1 out of every 1,700.)


Clinical Presentation/Characteristics:

Sports Medicine personnel should suspect sudden cardiac arrest (SCA) and impending death when an athlete collapses and is unresponsive. Immediately asses the patient’s airway, breathing, circulation, and rhythm if an AED is available. Look for seizure like activity or myoclonic jerking as both can be present following a SCA[6]. Some athlete may make complaints of dizziness, lightheadedness, or a racing pulse before collapsing. An hour before the incident, athletes may complain of chest pain, shortness of breath, nauseas and or vomiting [1]


Medical Exam/screening/testing:

Typically a SCA is diagnosed after the fact by a cardiologist or a specialist known as a cardiac electrophysiologist. A barrier of tests are done to elicit the underlying cause for the arrest in those lucky enough to survive it. Tests and measures analyzed by these specialists include but are not limited to electrocardiograms, echocardiography, multiple gated acquisition testing, cardiac catheterization, electrophysiology study, and blood tests to ascertain levels of potassium, magnesium and other chemicals important in electrical signaling[1].


The American Heart Association has compiled a preparticipation screening known as the 12-Element Preparticipation Cardiovascular Screening for Competitive Athletes. It details important history questions to ask the athlete in their personal and family history as well as important physical examination techniques [6].


Treatment for the Arrested Athlete:


Any athlete who is unresponsive after a collapse should be treated immediately and SCA is suspected. CPR protocols should be initiated if breathing and pulse are absent. Initiate EMS. CPR should not be stopped until the AED has been retrieved and an analysis of the rhythm is initiated. Continue CPR and defibrillation as indicated until the appropriate emergency responders arrive[7].


The greatest factor that causes a SCA to advance to a SCD is the time from arrest to defibrillation [8]. Rates of survival are estimated to be 41% to 74% of a bystander performs CPR appropriately and defibrillation occurs within 3 to 5 minutes of the arrest. Remember that AEDs are safe to use in weather conditions such as rain or ice. However, if the athlete is lying in a puddle or on a wet surface must be moved before defibrillation is safe. Likewise, move athletes who are on a metal surface to a nonmetal surface before defrillation[6].


Resources:

Please refer to the National Institute of Health, the National Athletic Training Association, the American Heart Association, and local physicians for more information on the proper management and monitoring for athletes with SCD.


Clinical Bottom Line:

AED implementation is crucial to the survivability of the athlete. Your goal as a sports medicine provider should be to provide the first shock before the 3-5 minute mark. Access to resources and proper planning before any incident takes place is a necessity. Additionally, a preparticipation physical examination is essential to uncover episodes of exertional syncope, presyncope, chest pain, personal and/or family history of SCA, a family history of SCD, and exercise intolerance[6].

Sickle Cell Trait in Sports[edit | edit source]

Definition/Epidemiology/Etiology/Prevalence/Incidence:

Sickle Cell Disease (SCD) involves a distortion of red blood cells from their typical form. In an individual with sickle cell disease the red blood cells are sticky, hard, and take on the sickle like appearance characteristic to the disease. Because the red blood cells have changed in morphology, they are more likely to clog blood flow leading to infection, stroke and acute chest syndrome [9]. Distortion of blood cells occurs due to an inherited autosomnal recessive genetic mutation. This means that the child must inherit mutated copies from both parents to develop the disease. The mutations in occur in a gene known as the Hemoglobin, beta gene (HBB). This gene codes for the production of beta globin a subunit of hemoglobin. Mutations in this gene can lead to sickle cell anemia, a form of SCD [10].

Although the exact number of people in the United States living with SCD is not known, it is estimated that the disease affects 90,000 to 100,000 Americans. The disease most commonly occurs in people of African American heritage. About 1 in every 500 African American children born has SCD. Hispanic Americans are the second most likely to have a child born with SCD at 1 in every 36,000 births [11].

In the athletic world, sickle cell disease has been most prominently discussed in relation to football. Since the year 2000 more than 16 deaths have taken athletes lives in division one football. These deaths are attributed to four causes: cardiac, asthma, exertional heat stress, and exertional sickling [12], [13]

 

Clinical Presentation/Characteristics:

Signs and symptoms will be different from person to person and are mostly related to disease complications. A sickle cell crisis can occur without warning with pain more severe than childbirth or postsurgical pain. The pain is often described as sharp, stabbing, knifelike, or throbbing [10].

The most common locations for pain exacerbation include the low back region, left, arms, abdomen, and chest. Temperature changes, stress, illness, dehydration, and high altitudes often bring on these crises [6].


Medical Exam/screening/testing:

Every newborn in the United States is required to have screening tests performed for SCT. This is done via a blood test in which the newborn’s heel is pricked and blood is taken and tested for abnormalities in the child’s hemoglobin. If the test is positive, the child’s parents are notified and further blood testing is done to affirm the screening test. Prenatal testing is another alternative in which doctor’s extract amniotic fluid and analyze it for abnormalities in the HBB gene mentioned earlier [14].

Although this screening is mandated, it is important to note that a survey performed by Kavanaugh, Wang, Therrell, and Sprinz found that only 37% of parents were informed of a positive SCT test [15]. An athletic trainer at Oklahoma University, Scott Anderson, screened the football team at the university and found 20 athlets with SCT and only three knew they had the disease[16]. Revelations such as these suggest that physicians should administer a new test for SCT as a part of the preparticipation physical examination screening [16].


Identifying an Athlete in Crisis:

Identifying an athlete in crisis from the sideline is essential for sports medicine practioners. The following are features of an exertional sickle cell collapse [17]:


1) Athletes will slump to the ground which differentiates the presentation from cardiac pathology (sudden fall) and heat cramps (hobbling).
2) Muscle strength will be abnormally weak comparative to the level of pain experienced by the athlete. The opposite presentation will occur in athletes with heat cramps.
3) Athletes will initially be able to communicate to the practioner as opposed to an athlete who experiences a cardiac arrhythmia. Typically a cardiac arrhythmia leads to unconsciousness.
4) Muscles will look and feel normal upon palpation unlike someone undergoing heat cramps.
5) Rapid tachypnea will be present despite optimal air flow due to lactic acidosis
6) Temperatures usually are under 103 degrees Farenheit as opposed to over 106 degrees found in heat stroke.


Steps to take on the sideline when a Crisis is identified [17], [6]:
1) Treat as a medical emergency
2) Monitor Vital Signs
3) Give supplemental oxygen if available
4) Cool Athlete as needed
5) If know immediate improvement is made activate emergency response and prepare for cardiopulmonary resuscitation.
6) Tell physicians to expect explosive rhabdomyolysis


Medical Management/ Treatment:

Pain related to an episode or crisis can be managed with OTC medications such as ibuprofen or aspirin. In the most sever crises, the patient will be admitted to the hospital and administered opioids such as morphine and other pain relieving medications. In severe crises where anemia, splenic sequestration, or acute chest syndrome occur, medicinal intervention includes blood transfusion, a spleenectomy, antibiotics to prevent infection, medicine to open airways, or administration of oxygen may be warranted. Interventions are considered on a case-by-case basis [18].

PT Management:

Prevention and Appropriate Exercise Parameters:

As mentioned previously, many parents of athletes are unaware of positive tests for SCT in their offspring. The problem of sickle cell crisis is compounded in the high school athlete where requirements for SCT are not mandated. Therefore, sports medicine personnel must engage in proper preventative techniques.

The following are tips for preventing a sickling crisis.
1) The athlete should be allowed to set his/her own pace in conditioning exercises. They should be allowed to build training sessions slowly and have longer rest periods between bouts and repetitions.
2) Preseason strength and conditioning programs are encouraged to maintain the athlete’s preparedness for physical activity and should be sports specific.
3) When athlete’s with SCT set their own workout pace, they typically do not have exacerbations into crisis.
4) Immediately stop activity with the onset of muscle cramps, inability to “catch breath,” pain, and swelling.
5) Remember that repetitive high level training leads to lactic acidosis and could perpetrate a crisis. Therefore, training that leads to high levels of lactic acidosis must allow for extended recovery periods between repetitions in order to prevent a crisis.
6) Educate athletes on the importance of communication regarding the occurrence of sickle cell symptoms.
7) Finally, heat stress, dehydration, asthma, infection, and altitude can all predispose an athlete to a sickle cell crisis. Therefore, the athlete must hydrate, manage asthma effectively, modulate work load to fit the environmental stressors, not workout if ill, and modify workout load if new to a region with altitude[17], [6].

Multidisciplinary Teams:

When working with an athlete who has SCD, it is critical to coordinate the athlete’s training, medical care, and engagement in team activities. To effectively accomplish this, the primary care physician, athlete and parental units, sports medicine personnel, coaching staff, and other support personnel must work to maintain optimal sports participation. Sports are not contraindicated for those with SCD, but the aforementioned persons must work to establish appropriate workout regimens, provide adequate access to emergency response intervention, and have open lines of communication.


Resources:

Please refer to the National Institute of Health, the National Athletic Training Association, and local physicians for more information on the proper management and monitoring for athletes with SCD.


Clinical Bottom Line:

Physical activity and participation in sport are not prohibited for those with SCD. However the athlete should not be subjected to exercise conditioning tests, must be given elongated time to reach appropriate conditioning levels, must be cognizant of current health status, and be educated on the disease.

Diabetes in Sports[edit | edit source]

Description/Definition:

Diabetes’ prevalence in the United States continues to rise exponentially largely owing to the obesity epidemic.7 Diabetes (DM) can be further categorized into one of four categories: Type 1 (DM1), Type 2 (DM2), Gestational, and DM due to other specific factors including genetic defects, medications, and various other diseases.1


DM1 is the result of an autoimmune disorder in which the body attacks its own beta cells within the pancreas leading to an insulin deficiency. This population is typically very thin and are diagnosed at an early age.7 Athletes with DM1 can actively participate in sports at both recreational and competitive levels, with the proper insulin monitoring and care.


Individuals with DM2 have varying degrees of insulin resistance or relative insulin deficiency. Risk factors include age, obesity, ethnicity, family history, and low socioeconomic status.1, 7 Lifestyle factors such as physical inactivity and poor diet also play a large role in the development of the condition. Athletics for individuals with DM2 are typically at the recreational level.


Gestational DM is characterized by relative insulin intolerance with onset during and/or after pregnancy.


Epidemiology/Etiology/Prevalence/Incidence:

DM has been reported to have higher rates among Native Americans, African Americans, Hispanic Americans, and Pacific Islanders.1 The increased prevalence of DM in the American population is largely due to the national obesity epidemic.7
Of those living with DM approximately 90% are DM2 while the remaining 10% are DM1. DM2 typically occurs in adults 40 years of age or older; however, DM2 rates in children have continued to rise due to increased incidence of childhood obesity. DM1 is more prominent in children and young adults.
DM1 less prominent than DM2, but those working in the athletic field are more likely to work with athletes with DM1.6 These athletes participate at levels from middle-school team athletics to elite-professional leagues.


Clinical Presentation/Characteristics:

Diagnostic criteria for DM have been recently revised and simplified for the basis of early recognition and diagnosis. One of three diagnostic criteria must be met for diagnosis: fasting glucose ≥ 126 mg*dL-1 , two hour plasma glucose ≥ 200 mg*dL-1 during oral glucose tolerance testing 76g of glucose, or the presence of various other symptoms including polyuria, polydipsia, and/or unexplained weight loss with a casual plasma glucose level of 200mg*dL-1.1
Micro/macrovascular complications accompany much of the population living with DM. Such complications include coronary artery disease, peripheral vascular disease, autonomic neuropathy, peripheral neuropathy, retinopathy, nephropathy, and other musculoskeletal problems.7 It is crucial to evaluate this population for any underlying complications prior to engaging in various exercise programs.


Exam/screening/testing:

DM is typically diagnosed using blood tests. Blood is drawn and sent to a designated facility for lab analysis. Over the counter blood glucose measuring tools such as finger-stick devices are not accurate enough to diagnose DM, and so lab analysis is necessary.3 Blood testing allows for early detection and treatment of DM prior to the onset of further micro and macrovascular complications. Diagnostic tests include hemoglobin A1C, fasting plasma glucose, and oral glucose tolerance tests.
The A1C is used to detect DM2 and prediabetes. The test reflects average blood glucose over a 120 day (3 month) period.3 The test does not require fasting and can be performed at any time.
Fasting Plasma Glucose (FPG) testing detects both diabetes and prediabetes.3 The test is a common practice due to its convenience and cost. In order to be tested, the individual must fast for at least eight hours prior.
The Oral Glucose Tolerance test (OGTT) is used for the diagnosis of diabetes, prediabetes, and gestational diabetes. This test is less convenient than the fasting glucose test but is more sensitive. When conducting the test the individual must fast for at least eight hours prior and another two hours after drinking a liquid containing 75 grams of glucose dissolved in water.3


Medical Management/ Treatment:
     Pharmacology:
In treating those diagnosed with DM2, the goal is to achieve and maintain a blood glucose level at or near normal levels to prevent the onset of any macro/microvascular and/or neural complications. Although exercise has been proven to improve insulin sensitivity, it has been underutilized as a therapy treatment.1 Typical treatment of DM includes a combination of diet, exercise, and medication alterations.1 Pharmaceutical treatment includes the use of insulin, biguanides, sulfonylureas, thiazolidinediones, alpha-glucosidase inhibitors, dipeptidyl peptidase-4 inhibitors, meglitinides, and amylin mimetics.7 Out of all of the pharmaceutical options, insulin injections are the mainstay for the medical management of DM1 and DM2. Injectable insulin technology has evolved to include pump systems. These pumps provide continuous subcutaneous infusions with preprogrammed basal insulin infusion.7 Advantages for the pump system include rapid blood glucose adjustments and flexibility; however, they are susceptible to infection, pump malfunctions, and local lipodystrophy. Pumps may also be contraindicated for contact sports, water sports, and endurance events. However, pumps may be temporarily removed for contact or water sport participation and may be padded for lighter contact sports. Athletes utilizing insulin pumps should be advised to carry injectable insulin incase the pump is damaged during participation or lost while disconnected.7


PT management:
     Interventions:

The American Diabetes Association (ADA) has set guidelines that state all individuals with DM should be given the chance to experience the benefits of exercise.8 Exercise has been associated with improved quality of life and metabolic control in the DM population.1 With the appropriate adjustment of insulin dosage, glucose self-monitoring, dietary management, and properly timed exercise, children with DM should be able to participate.8 When considering athletics for individuals with DM, glycemic control is crucial and should be addressed through diet, exercise, and medication.1 Prior to initiating physical activity, glycemic index should be controlled to a reasonable level. The athlete should also consider being evaluated by their physician for coronary disease prior to the start of an exercise regime. When participating in physical activity, if glucose levels are above 250 prior to exercise and ketones are present then exercise must be postponed. If glucose are at or exceed 300, then exercise is inadvisable with or without ketones. Glucose levels at or below 200 are cleared for physical activity, but should be under close watch.4 Also be sure to watch for insulin omission by those athletes aiming to lose weight in order to compete in athletics with specific weight categories such as wrestling, boxing, and weightlifting.4


CRITICAL: When participating in various sports, diabetic athletes should be advised to wear a MedicAlert-type bracelet and/or necklace that indicates their specific diagnosis of DM1 or DM2 and the appropriate pharmaceutical information.7


     DM2:
Physical activity has been noted as a key component to acutely lower blood glucose levels in DM2. Acute effects of physical activity in DM2 are abnormal insulin secretion and peripheral insulin resistance. These effects acutely, but favorably, change abnormal glucose levels and insulin resistance. Mild to moderate physical activity has been reported to decrease blood glucose levels in this population.1, 5 The magnitude of these effects are directly correlated to exercise duration and intensity. Mild to moderate physical activity has also been shown to reduce insulin resistance by increasing peripheral and splanchnic insulin sensitivity.1, 5 The acute effects of exercise are lost within a few days and the benefits of a single exercise session are short lived; therefore, regular exercise performed at moderate intensities are required to lessen insulin resistance.1


     DM1:
Those individuals with DM1 have been encouraged to participate in regular physical activity. These athletes are often young and more competitive than their DM2 counterparts. Athletes with DM1 meeting the activity guidelines set by the ADA have triglyceride levels lower than their inactive peers; however, continuous aerobic activity frequently causes hypoglycemia.4 This can occur directly after exercise and up to 7-11 hours later.5 If exercise is performed in the late afternoon, then hypoglycemia typically occurs during late-night sleep. High intensity exercises can cause elevations in blood glucose concentrations. These elevations may be sustained long into recovery but may be corrected with appropriate insulin dosing. DM1 athletes should work closely with their personal physicians while participating in physical activity to monitor their glucose levels before, during, and after exercise. Studies have reported that periods of continuous moderate-intensity exercise interspersed with bouts of high-intensity exertions my protect from exercise-induce hypoglycemia.5 This type of intermittent exercise can be seen in recreational team or field sports like soccer, basketball, or football.4 This form of exercise has been shown to cause low recovery glucose levels due to an increase in the need for muscle glycogen restoration. Some studies have reported that an increase in glycaemia in early recovery helped to prevent post exercise hypoglycemia in DM1 athletes while others reported an increase in nocturnal hypoglycemia in the same population.5


Exercise Recommendations:

Athletes with DM should participate in aerobic exercise five or more days a week while incorporating a minimum of three days of resistance training.1, 7 There is currently not a consensus on the ideal frequency, but these values are based on expert opinion. Intensity for those beginning an exercise program should be kept at 50%-70% of their maximum oxygen consumption; at intensities where they can still carry on conversation.7 These parameters allow the athlete to participate for longer periods allowing for increase in aerobic capacity and caloric energy expenditure that will aid in weight loss/control.4 Intensity can be further increased for those who frequently participate in physical activity. When considering the type or mode of exercise, medical recommendations have focused largely on aerobic activity; however, recent studies have shown similar improvements in insulin levels with resistance type exercise.1, 7 The ADA recommends a combination of the two modes. Resistance training should target all major muscle groups consisting of six to eight separate exercises that should be progressed to include three sets of eight to ten repetitions per movement. Higher level DM athletes with well controlled blood glucose levels are able to participate in physical activity at the same level as their non-diabetic peers.


Diff Dx (“red flags”):

Common red flags for diagnosis include increased urination, increased thirst, and unexplained weight loss.1 Other less common symptoms may include fatigue, blurred vision, increased hunger, and sores that do not heal. Typically red flags for exercise induced hyperglycemia include nausea, dehydration, reduced cognition, slowed visual reaction, fatigue, fruity odor on the breath, loss of appetite, increased thirst and polyuria.6


Relevant Anatomy:

DM is an endocrine related condition directly associated with the function and efficiency of the pancreas and the hormones produced within (i.e. insulin).1 The effects of exercise on athletes with DM1 are determined by the neuroendocrine response of epinephrine, norepinephrine, glucagon, growth hormone, cortisol, and injected/supplemental insulin.5


Multidisciplinary Teams:

The management of athletes with DM is very much a multidisciplinary team approach. The top tier includes both the athlete’s endocrinologist and primary care physician who both aid in the medical/pharmaceutical management of the condition. The next tier includes various other health professionals including nutritionists and physical/recreational therapists. These parties focus on the best nutritional regime while incorporating the most appropriate exercise schedule to ensure the best outcome while avoiding medical hazards like hypo- and hyperglycemia.1 Coaches and athletic trainers also play a very large role in the management of this athletic population.4, 6 Athletic trainers are equipped with the tools and skills needed to manage athletes with DM. These include diabetic care plans; supplies for athletic training kits; pre-participation physical examinations; the ability to recognize, treat, and prevent hypoglycemia and hyperglycemia; the skill to administer insulin; the knowledge of appropriate travel recommendations; and how to manage athletic injury in the DM population.6 The athletic trainers often get more time than anyone else with these athletes, and so their proficiency in these skills is crucial to the safety and well-being of the DM athlete.


Resources:

Please refer to the American Diabetes Association, American College of Sports Medicine, the National Athletic Training Association, and local endocrinologists/physicians for more information on the proper management of blood glucose levels for the DM athlete and their participation in regular physical activity.1


Clinical Bottom Line:

Physical activity has been shown to reduce several of the complications induced by DM. Athletes with DM are on a case-by-case basis so their participation in physical activity and insulin regime will have to be modified according to the athlete’s individual needs.7 However, mild to moderate exercise has been shown to have the best effects on athletes with DM while producing the least risk.1 Blood glucose control for these athletes may take several bouts of trial-and-error in order to develop the best practice. Hyper/hypoglycemia are the primary concerns for these athletes, but both can be controlled through insulin dosage modification and increase/decrease of carb consumption both before and after exercise.1, 7


References:

1. Albright, A., Franz, M., Hornsby, G., Kriska, A., Marrero, D., Ullrich, I., & Verity, L. (n.d.). Exercise and Type 2 Diabetes. Medicine & Science in Sports & Exercise, 1345-1360.

2. Baldi, J., Cassuto, N., Foxx-Lupo, W., Wheatley, C., & Snyder, E. (2009). Glycemic Status Affects Cardiopulmonary Exercise Response in Athletes with Type I Diabetes. Medicine & Science in Sports & Exercise, 1454-1459. doi:10.1249/MSS.0b013e3181d1fdb3

3. Diagnosis of Diabetes and Prediabetes. (2014). National Institute of Diabetes and Digestive and Kidney Disease, 1-16. Retrieved October 1, 2015, from http://www.niddk.nih.gov/health-information/health-topics/Diabetes/diagnosis-diabetes-prediabetes/Pages/index.aspx

4. Hornsby, W., & Chetlin, R. (2005). Management of Competitive Athletes With Diabetes. Diabetes Spectrum, 18(2), 102-107.

5. Iscoe, K., & Riddell, M. (2011). Continuous moderate-intensity exercise with or without intermittent high-intensity work: Effects on acute and late glycaemia in athletes with Type 1 diabetes mellitus. Diabetic Medicine, 824-832. doi:10.1111/j.1464-5491.2011.03274.x

6. Jimenez, C., Corcoran, M., Crawley, J., Hornsby, G., Peer, K., Philbin, R., & Riddell, M. (2007). National Athletic Trainers’ Association Position Statement: Management of the Athlete With Type 1 Diabetes Mellitus. Journal of Athletic Training, 42(4), 536-545.

7. Shugart, C., Jackson, J., & Fields, K. (2010). Diabetes in Sports. Sports Health, 2(1), 29-38. doi:10.1177/1941738109347974

8. Valerio, G., Spagnuolo, M., Lombardi, F., Spadaro, R., Siano, M., & Franzese, A. (2005). Physical activity and sports participation in children and adolescents with type 1 diabetes mellitus. Nutrition, Metabolism and Cardiovascular Diseases, 17, 376-382. doi:10.1016/j.numecd.2005.10.012


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