Medical/Pharmacological Related Issues in Sports Medicine

 

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Sudden Cardiac Death in Sports

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.


In 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 first until ruled out. CPR protocols should be initiated if breathing and pulse are absent. Initiate EMS protocols. 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 he or she must be moved before defibrillation is safe. Likewise, move athletes who are on a metal surface to a nonmetal surface before defibrillation[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 Disease in Sports

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 arm, 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 the sickle cell trait (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 [10].

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 [14]. An athletic trainer at Oklahoma University, Scott Anderson, screened the football team at the university and found 20 athletes with SCT. Only three knew they had the disease[15]. Revelations such as these suggest that physicians should administer a new test for SCT as a part of the preparticipation physical examination screening [15].


Lab Values Used in Identifying SCD [16]:


SCD.png


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 no 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 severe 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 [16].


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 testing 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 cause 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

Description/definition:
Diabetes’ prevalence in the United States continues to rise exponentially largely owing to the obesity epidemic.[18]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.[19]


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.[18]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.[19], [18]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.[19]The increased prevalence of DM in the American population is largely due to the national obesity epidemic.[18]

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.[20] 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.[19]


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.[18] 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.[21]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.[21]The test does not require fasting and can be performed at any time.


Fasting Plasma Glucose (FPG) testing detects both diabetes and prediabetes.[21]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.[21]


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.[19]Typical treatment of DM includes a combination of diet, exercise, and medication alterations.[19] Pharmaceutical treatment includes the use of insulin, biguanides, sulfonylureas, thiazolidinediones, alpha-glucosidase inhibitors, dipeptidyl peptidase-4 inhibitors, meglitinides, and amylin mimetics.[18]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.[18]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.[18]


     PT management:

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.[22]Exercise has been associated with improved quality of life and metabolic control in the DM population.[19]With the appropriate adjustment of insulin dosage, glucose self-monitoring, dietary management, and properly timed exercise, children with DM should be able to participate.[22]When considering athletics for individuals with DM, glycemic control is crucial and should be addressed through diet, exercise, and medication.[19]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.[23]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.[23]


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.[18]


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.[19], [24]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.[19], [24]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.[19]


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.[23]This can occur directly after exercise and up to 7-11 hours later.[24]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.[24]This type of intermittent exercise can be seen in recreational team or field sports like soccer, basketball, or football.[23]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.[24]


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.[19], [18]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.[18]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.[23]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.[19], [18]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.[19]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.[20]


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).[19]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.[24]


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.[19]Coaches and athletic trainers also play a very large role in the management of this athletic population.[23], [20]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.[20]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.[19]


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.[18]However, mild to moderate exercise has been shown to have the best effects on athletes with DM while producing the least risk.[19]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.[19], [18]

Hypertension in Sports

Definition/Description

Hypertension is the chronic elevation of the blood pressure in the arteries. It is also known as high blood pressure and arterial hypertension. Blood pressure is indicated by a ratio of systolic blood pressure over diastolic blood pressure. Systolic blood pressure tyically runs between 100-140 mmHg, and diastolic blood pressure typically ranges from 60-90 mmHg. In adults, hypertension is present if blood pressure is frequently above 140/90 mmHg[25]. In pediatrics, hypertension is determined based on the child's height, weight, and sex. Tables demonstrating hypertensive numbers among a pediatric population can be found here.

Prevalence

In the United States, 29% of adults have high blood pressure, and only 52% of those have their blood pressure under control. For people under the age of 45, men are more likely to be hypertensive; for those over the age of 65, women are more likely to be hypertensive than men. African Americans are more likely to be hypertensive at all ages, followed by Whites and then Hispanics. Hypertension was listed as either the primary cause or a contributing factor to more than 36,000 deaths in the United States in 2013[26].

Causes

There are two types of hypertension: primary and secondary. Primary hypertension is high blood pressure with no underlying cause and accounts for 90-95% of cases. Secondary hypertension is due to an identifiable cause such as arteriosclerosis, chronic kidney disease, and endocrine disorders[25].

A list of contributing factors of primary and secondary hypertension are:

  • genetics
  • high salt intake
  • lack of physical activity
  • obesity
  • stress
  • depression
  • vitamin D deficiency
  • insulin resistance
  • low birth weight
  • maternal smoking
  • lack of breast feeding
  • Cushing's syndrome
  • hyper/hypo-thyroidism
  • acromegaly
  • sleep apnea
  • pregnancy
  • arsenic exposure (from drinking water)
  • many more...

Pathophysiology

There are many theories to the actual pathophysiology of hypertension, but their is no one model that describes all cases because pathogenesis is multifactorial and very complex. Many factors regulate blood pressure, including cardiac output, vessel elasticity, blood mediators, circulating blood volume, blood viscosity, vascular reactivity, and more[27].

Classical progression of essential (primary) hypertension is as follows[27]:

  • Pre-hypertension -- ages 10-30, characterized by increased cardiac output
  • Early hypertension -- ages 20-40, characterized by prominent increased peripheral resistance
  • Established hypertension -- ages 30-50
  • Complicated hypertension -- ages 40-60

Clinical Manifestation

High blood pressure can often be asymptomatic, so it is important to monitor blood pressure regularly. However, some signs and symptoms that manifest due to hypertension are[28]:

  • severe headache
  • confusion
  • fatigue
  • chest pain
  • vision problems
  • difficulty breathing
  • blood in urine
  • pounding in chest, neck, or ears
  • chest pain
Hypertensive Crisis

If systolic blood pressure is greater than 180 OR diastolic blood pressure is higher than 110, the individual is considered to by in a hypertensive crisis and requires immediate emergency medical attention. Symptoms that can indicate hypertensive crisis are nose bleeds, severe anxiety, shortness of breath, and severe headaches[29].

Diagnosis

Hypertension is typically diagnosed on the basis of persistently high blood pressure. The American Heart Association recommends at least three phygmomanomitor readings on at least two seperate healthcare visits. However, monitoring ambulatory blood pressure over a 12-24 hour period is the most accurate method of diagnosis[30]. Other possible tests used for diagnosis are listed below[30]:

  • microscopic urinalysis
  • protein in urine
  • BUN levels
  • creatinine levels
  • serum sodium, potassium, calcium, and TSH
  • hematocrit
  • ECG
  • chest radiograph
  • fasting blood glucose
  • LDL and HDL
  • total choelsterol
  • triglycerides

Complications

Hypertension is a precursor to many more serious conditions, including, but not limited to[30]:

  • hypertensive heart disease
  • coronary heart disease
  • stroke
  • aortic aneurysm
  • peripheral artery disease
  • chronic kidney disease

Treatment 

Lifestyle Changes[31]
  • frequent exercise
  • less sodium intake
  • cessation of smoking
  • limited alcohol consumption
  • maintaining a healthy weight
Medications[31]
  • thiazide diuretics
  • beta blockers
  • angiotensin-converting enzyme (ACE) inhibitors
  • angiotensin II receptor blockers (ARBs)
  • calcium channel blockers
  • renin inhibitors
  • alpha blockers
  • alpha-beta blockers
  • central-acting agents
  • vasodilators
  • aldosterone antagonist

Hypertension and Sports

Athletes and physically active individuals are often (and inaccurately) thought to be free of hypertension and cardiovascular disease. Although athletic individuals are 52% less likely to develop hypertension than the general population, it can occur. African americans, the elderly, people who are obese, and individuals with a history of renal disease, diabetes, or familial hypertension are at a greater risk of developing hypertension themselves. Additionally, wheelcheer athletes who sustained a spinal cord injury are more likely to have hypertension due to abnormal autonomic control[32].

Athletes that are known to have hypertension should monitor their blood pressure prior to physical activity, and should not resume or initiate sports participation until their blood pressure is controlled. Dynamic and isometric exercise have an especially significant effect on blood pressure. The following recommendations have been made for exercise restrictions of hypertensive athletes:[32]

High-normal blood pressure No restrictions
Controlled mild to moderate hypertension (<140/90 mm Hg) No restrictions on dynamic exercise; possible limit on isometric training or sports in some patients
Uncontrolled hypertension (>140/90 mm Hg) Limited to low-intensity dynamic exercise; avoid isometric sports
Controlled hypertension with end-organ damage Limited to low-intensity dynamic exercise; avoid isometric sports
Severe hypertension with no end-organ involvement Limited to low-intensity dynamic exercise, with participation only if blood pressure is under adequate control
Secondary hypertension of renal origin Limited to low-intensity dynamic exercise; avoid “collision” sports that could lead to kidney damage

 Below is a chart that describes sports in terms of their dynamic and static properties:[33]

Capture.JPG

ALL potential athletes should go be screened and evaluated for cardiovascular disease, and is discussed in further detail in the following section.

PT Management

Measurement of vital signs is an important aspect of a thorough systems review, which physical therapists should be conducting with every single patient. Physical therapists that work with athletic and physically active populations should known how to accurately measure blood pressure and monitor response to exercise. In order to fully understand how an athlete responds to various levels of exercise, the physical therapist should use blood pressure measurements to gain information on the athletes baseline cardiovascular status,their response to exercise and physical activity, and how those measurements impact clinical decision making.[34]

Physical therapists should also be able to serve as a fitness and wellness coach to individuals with hypertension and guide them to making the best diet and exercise decisions. 

Rhabdomyolysis

Definition/Description

The rapid destruction of skeletal muscle due to injury, overuse, or other health conditions, leading to the rapid release of myoglobin into the blood. The myoglobin then has to be filtered out of the blood by the kidneys, which can lead to renal failure in extreme cases.

Causes

There are three main categories of rhabdomyolysis[35]:

  1. traumatic or muscle compression (crush syndrome, immobilization)
  2. non-traumatic, exertional (extreme exertion, hyperthermia, metabolic myopathies)
  3. non-traumatic, non-exertional (drugs or toxins, infections, electrolyte disorders)

Among athletes, a non-traumaticexertional etiology is most common. Risk factors, signs and symptoms, diagnosis, and treatment of athletes with rhabdomyolysis is discussed in later sections. For more information on the other two categories of rhabdomyolysis, please refer to this website.

Prevalence 

Approximately 26,000 cases of rhabdomyolysis occur in the United States[36], more commonly in men than in women[37].The majority of rhabdomyolysis cases (26%) are caused by trauma and crush injuries where the individual(s) are trapped under rubble for extended periods of time[35]. Approximately 85% of victims with traumatic injury develop rhabdomyolysis. Non-traumatic, exertional rhabdomyolysis in becoming increasingly more common, and is often seen in athletes who participate in crossfit, marathon running, weightlifting, and sprinting[38]. Out of those patients who develop rhabdomyolysis, 10-50% of them develop acute renal failure (ARF). Patients with severe rhabdomyolyisis-induced renal failure have a mortality of 20%[39]

Clinical Presentation

Signs and symptoms of athletes who have developed rhabdomyolysis[40]:

  • Dark red to brown urine
  • Decrease urine production and output
  • Weakness and fatigue
  • Local edema
  • Cramps
  • Muscle aching, stiffness, tenderness, and/or weakness
  • Joint pain
  • Seizure
  • Unintentional weight gain

Note: This is not an inclusive list of all possible symptoms, and absence of one or more of these symptoms does not indicate the absence of rhabdomyolysis.

Diagnosis, Screening, and Testing  

Patient Interview and History

The patient interview is one of the most important factors in determining if rhabdomyolysis has occured. It is critical to ask the athlete about their recent physical activity level, drug medication,and alcohol use, and any trauma or accidents that recently may have occurred.

Lab Testing - Blood and Urine Analysis

Diagnosis of rhabdomyolysis is primarily determined by blood and urine testing. The chart below demonstrates the normal values and how those values are effected by rhabdomyolysis[37].

 Rhabdomyolysis lab values.jpg


Medical Management of Complications of Rhabdomyolysis

Renal Failure

The most common complication from rhabdomyolysis is acute renal failure (ARF). During ARF, the kidneys are unable to efficiently remove waste and balance fluid and electrolyte levels in the body. Signs that an athlete is experiecing renal failure are: bloody stools, flank pain, bad mouth odor, decreased appetite, high blood pressure, nose bleeds, seizures, shortness of breath, decreased sensation in hands and feet, nausea or vommitting, swelling, and urination changes[41]. Mild cases of renal failure can be treated with intravenous fluids and electrolytes, but more severe cases may require dialysis.

Hypocalcemia

Hypocalcemia, low levels of calcium, occur in the early stages of ARF. The signs and symptoms of hypocalcemia are: muscle cramps, dysphagia, irritability, changes in mental capacity, fatigue, and seizures. Magnesium and calcium are frequently used to treat hypocalcemia[42].

Hyperkalemia

Hyperkalemia is defined as elevated amounts of potassium in the blood, and is a common complication of rhabdomyolysis. Because the cardiac system requires delicates amount of potassium to function properly, hyperkalemia can lead to life threatening cardiac arrhythmias. Symptoms of hyperkalemia include a slow heart rate, abnormal heart rhythms, and weakness. Hyperkalemia can be diagnoses with laboratory tests or an EKG. Severe hyperkalemia can result in death, so immediate medical intervention should be provided to an athlete with hyperkalemia[43].

Compartment Syndrome

Following trauma or tissue injury, bleeding and swelling in the involved limbs can lead to increase intracompartmental pressures. If left untreated, compartment syndrome can lead to ischemia, muscle cell lysis, and irreversible nerve damage. If pressures within a compartment exceed 40 mmHg, a fasciotomy should be performed[44] .

Acidosis

When muscles undergo ischemia, lactic acid is produced resulting in metabolic acidosis[45]. Signs of metabolic acidosis are: tachycardia, rapid respiration, headaches, confusion, weakness and fatigue, decreased appetite, and nausea or vomitting[46]. Acidosis is treated by eliminating the causative factor. 

Death

A number of these factors combined, especially acute renal failure, hyperkalemia, and hypocalcium, can lead to death if untreated. 

Prognosis

Prognosis of rhabdomyolysis is primarily dependent on the presence of and severity of acute renal failure. Mild cases of rhabdomyolysis rarely result in long term effects. If severe kidney damage occurs, the athlete may require dialysis. If complications go untreated or their is a delay in treatment, their is a risk of death.

Physical Therapy Management

Physical therapists may play an essential role in preventing rhabdomyolysis, identifying athletes who demonstrate signs and symptoms of rhabdomyolysis, and making return to sport decisions following rhabdomyolysis. 

Prevention[47]
  • Acclimatization - gradually increase physical activity, intensity, duration, and frequency
  • Monitor environmental factors - high heat and humidity are risk factors to developing rhabdomyolysis
  • Hydrate - make sure athletes are drinking plenty of water before, during, and after physical activity
  • Replenish electrolytes
  • Maintain good sodium and potassium intake
  • Wear light clothing that easily allows for heat dissipation
Treatment[47]
  • Provide medical treatment for any complications (renal failure, hyperkalemia, hypocalcemia)
  • Hydrate
  • Increase carbohydrates to replenish glycogen stores
  • Avoid drugs and alcohol, as well as any medications that can lead to rhabdomyolysis
  • Allow proper time for the body to heal before returning to physical activity
Return to Sport

Currently, there is no evidence based guidelines for determining return to sport post-rhabdomyolysis. In mild cases, athletes are usually able to return within 2-4 weeks. The best way to determine return to sport is to monitor CK levels, but that is rarely possible because baseline measures are not often available. The first step in making return to sport decisions is to classify the athlete as either high or low risk for reoccurance.

High Risk for Reoccurrance:[47]

  • When activities have been restricted, it still takes more than one week for the athlete to recover from activity.
  • Persistent elevation of blood CK levels(greater than five times the upper limit of the normal range), even when they have had strict rest from physical activity for longer than two weeks.
  • Their rhabdomyolysis experience was complicated by a kidney injury of any sort.
  • They have a personal history or a family history of rhabdomyolysis
  • Personal or family history of recurrent muscle cramps or severe muscle pain that interferes with activities of daily living or sports performance.
  • Personal or family history of malignant hyperthermia or family history of unexplained complications or death following general anesthesia.
  • Personal or family history of sickle cell disease.
  • Muscle injuries after low to moderate physical activity.
  • Personal injury of significant heat stroke.
  • Their original CK blood value was over 100,000.

Low Risk for Reoccurrance[48]

To be considered low risk, the athlete must not have any of the high risk conditions and must display at least one of the following:

  • Rapid clinical recovery and CK normalization after exercise restrictions
  • Sufficiently fit or well trained athlete with a history of very intense training/exercise bout
  • No personal or family history of rhabdomyolysis orprevious reporting of debilitating exercise-induced muscle
    pain, cramps, or heat injury
  • No existence of other group or team-related cases of exertional rhabdomyolysis during the same exercise sessions
  • Not suspected or documented concomitant viral illness or infectious disease
  • Not taking a drug or dietary supplement that could contribute to the development of ER

Return to sport decisions should be individualized, and should take into account whether or not the athlete is at a low or high risk for reoccurrance. Although there is no evidence-based protocol for RTS, the military came up with their own guidelines for return to activity following an episode of rhabdomyolysis, and is pictured below.

CHAMP.png


Mononucleosis in Sports

Description & Clinical Presentation

Mononucleosis commonly known as infectious mononucleosis is normally caused by the Epstein-Barr virus (EBV). Other names used for this disease are mono, kissing disease, or glandular fever. Symptoms normally associated with mono are fever, sore throat, fatigue, and swollen cervical lymph nodes. Other common symptoms include headache, loss of appetite, palatal petechiae, splenomegaly, hepatomegaly, and jaundice. [49][50] This disease is rarely fatal, but serious complications can include splenic rupture, upper airway obstruction, and disorders of the central nervous system (Guillain-Barre’ syndrome, facial nerve palsy, transverse myelitis, etc.).[51]

Etiology/Prevalence/Incidence

About 95% of the adult population is infected with the EBV with manifestation occurring mostly during or after the second decade of life. The age group most commonly affected by infectious mononucleosis is 15 to 24 years. The transmission of EBV primarily occurs through exposure of infected saliva, often due to kissing. Onset of symptoms typically occur anywhere from 30 to 50 days from initial exposure.[51] Preadolescent children can contract infectious mononucleosis, although the process is unknown. Speculation for the transmission of EBV in children is thought to be through their parents or siblings.[50]

Relevant Anatomy

Mononucleosis can affect several systems including lymph nodes, oral cavity, pharynx, lungs, spleen, liver, and possibly central nervous system (potential future complications). Further description of the relevant anatomy can be found throughout this article.

Exam/Testing

Diagnosis of infectious mononucleosis can be confirmed in most adolescents on the basis of the clinical presentation, blood smear test for lymphocytes, and a positive heterophile antibody test. However, patients with risk factors for acute HIV infection should be screened through tests that detect HIV nucleic acids. [51]
High viral loads in the blood and oral cavity mark acute illness of mononucleosis. A heterophile antibody test is usually performed to confirm the diagnosis of infectious mononucleosis by detecting specific antibodies in response to the EBV. Although this test is useful in adults, its use in children can be ineffective due to their limited antibody production.[50]

Differential Diagnosis

  • Bacterial tonsillitis- patients typically present with swollen upper anterior cervical nodes with bacterial tonsillitis versus a common presentation of swollen posterior and anterior cervical lymph nodes in infectious mononucleosis.[51][52]
  • Common cold, influenza, or bronchitis usually all have the common symptom of a sore throat (or pharyngitis). Identifying the pathogen responsible for this particular symptom is important.[51]
  • HIV, human herpesvirus 6, cytomegalovirus, herpes simplex virus, Streptococcus pyogenes, and Toxoplasma gondii also presents with similar symptoms as mononucleosis and laboratory tests are used to confirm or refute the diagnosis of these diseases.[51][53] Although the heterophile antibody test the commonly diagnostic test, there is a high rate of false-negatives early in the course of infectious mononucleosis.[54]

Medical Management/Treatment

With the decision of treating mononucleosis, the treatment typically includes the use of systemic corticosteroid therapy (SCT). SCT can help to reduce the duration of fever and symptoms. Some studies report harmful consequences, while others demonstrate the lack of consequences. SCT is normally used when infectious mononucleosis affects the upper respiratory system.[55] Management of sore throats can be accomplished by gargling with salt water or lidocaine solution.[56] With the risk of splenic rupture, avoiding any form of exertion (including sports) is recommended during the first 3 weeks of the illness. A stool softness may be prescribed to reduce the strain with bowel movements.[56]

Diagnoses that may be related to post infectious mononucleosis include chronic fatigue syndrome, Guillian-Barre’ Syndrome, and multiple sclerosis.

  • Chronic fatigue syndrome may be associated with delayed recovery after infectious mononucleosis along with factors such as psychiatric disorders, but definitive evidence has yet to be determined.[57]
  • A history of infectious mononucleosis significantly increases the risk of developing multiple sclerosis (MS) given that the EBV is nearly a universal finding in individuals with MS.[58]

Considerations for Sports Participation

With the risk of splenic injury after contracting infectious mononucleosis, considerations must be taken when deciding to allow participation of sports. Recommendations for light, noncontact activity is participation may resume 3 weeks after initial onset of symptoms. Light, noncontact activity describes avoidance of chest or abdominal trauma and minimal exertion activities. Information provided for recommendations to return to contact activity is controversial, but literature suggests a minimal of 3 weeks and a gradual progression of participation.[56] Currently there are no set guidelines for the decision to allow players to return to their sport, and even with the 3 week time frame recommendation, each player needs individualized treatment given the course of the illness is variable.[59]

Clinical Bottom Line

  • Infectious mononucleosis is a common illness derived from the Epstein-Barr virus, affecting mostly younger populations with a combination of following symptoms: fever, sore throat, swollen cervical lymph nodes, and fatigue.[51] [49]
  • Treatment of mononucleosis can occur through the use of systemic corticosteroid therapy to combat the duration of fever and symptoms. Home remedies include gargling salt water for relief of sore throats and the use of stool softeners to prevent unnecessary exertion with bowel movements.[55][56]
  • Sports or activity participation should be limited to a minimum of 3 weeks to prevent splenic rupture with monitoring of symptoms and progression of activity.[56]

Recreational Drug Use in Sports

Description

Recreational Drug: A drug used without medicinal purposes for its psychoactive effects often in the belief that occasional use is not habit-forming or addictive.[60] The use of recreational drugs within the sports world has continually evolved which had led officials to create strict regulations with the goal of creating fair and safe opportunities for participating athletes.[61]

The World Anti-Doping Agency (WADA)[62] provides an updated list of prohibited substances or methods that are prohibited at all times, in-competition, and in particular sports. Categories for prohibited substances or methods in sports include the following:

  • Alcohol
  • Beta-blockers
  • Anabolic agents
  • Peptide hormones, growth factors, related substances and mimetics
  • Beta-2 Agonists
  • Hormone and metabolic modulators
  • Diuretics and masking agents
  • Stimulants
  • Narcotics
  • Cannabinoids
  • Glucocorticoids [62]

WADA website provides an in-depth description of each category and what each consists of. Of these, the most commonly used substances for recreational drugs in sports are alcohol, cigarettes, and cannabis for adolescents.[63]

Prevalence/Incidence

The use of recreational drugs or substances varies across the different levels and types of sports. Elite, professional, college, and high school athletes have been known to use drugs for various reasons.[64] A few reasons that have been speculated to influence adolescent athletes in particular, whether positively or negatively, with the use of recreational drugs are social activity, age segregation, adult supervision, or motivation for achievement.[65]

Some evidence demonstrates that sports participation is more associated with alcohol use, but negatively associated with cigarette or illicit drug use. Specific sports, such as baseball, football, and weightlifting, have been shown to correlate with higher alcohol assumption when compared to their colleagues. An increased risk for substance abuse was found to be associated with athletes involved in high contact sports.[66]

Screening or Testing

The National Institute on Drug Abuse website provides evidence-based screening tools for adult and adolescents for substance abuse. The following link provides not only tools for screening, but up-to-date information about known drugs: http://www.drugabuse.gov/

Medical Management/Treatment

Treatment is for each drugs varies and are normally treated according to the displayed side effects. The website provided above details short and long-term effects, medical management, health effects, available forms for drugs, and possible street names used.

Prevention

Research demonstrates implementing after school community activities, increasing parental involvement, educating parents and children about the importance of communication, and strengthening support networks can help reduce the rate of substance abuse in adolescents. [67]

Prevention measures have also included student drug testing within schools, but the evidence is controversial due to only the possibility of lowered marijuana use but with a corresponding increased use of illicit drugs in the studied middle and high schools.[68]

Resources

More information can be found through the National Institute on Drug Abuse and the WADA websites:


Performance Enhancing Drugs

Description/definition:


Performance enhancing substances (PES) are a multi-billion dollar industry that encompass all substances aimed at those looking to enhance physical performance, alter body image, or combat obesity across all sporting domains from elite athletes to recreational athletes.[69]PES grossly include anabolic-androgenic steroids (AAS), stimulants, diet pills, powders, or other liquid substances.[69]The most frequently abused PES include testosterone, nandrolone, stanozol, and methandienone.[70]Other common PES include AAS, human growth hormone, creatine, erythropoietin, blood doping, amphetamines, and stimulants.[71]PES improve sport performance through increased strength and endurance, or alter body composition to favor lean muscle mass over fat mass.[72]Improvements in athletic ability are also achieved through changes in behavior, arousal, and pain perception.[69]Anabolic steroids are synthetic derivatives of the male hormone testosterone. AAS increase skeletal muscle size and strength through the up-regulation of protein synthesis.[73], [72]


PES and dietary supplements are not regulated or tested by the U.S. Food and Drug Administration (USFDA) and so little regulation can be achieved in regard to product composition, safety, and efficacy which furthers the challenge of monitoring adverse effects.[74], [69] Manufacturers may spike their supplements with actual steroids or other alternatives in an effort to enhance the effects of their products.[75], [74]These same manufacturers may also market products that contain no active ingredients. Such dietary substances are available for purchase over the counter and online by persons of any age without prescription.


Adverse effects of PES use and abuse include violent behavior, suicide attempts, hypertension, arrhythmias, myocardial infarction, stroke, seizures, and death. Adverse effects are more prominent and potentially escalated when PES are taken in conjunction with various prescription medications and caffeine.[69]


AAS have been labeled a Schedule III substance under the Anabolic Steroid Control Act of 2004 due to its potential for abuse.[69]The Ephedra Prohibition Act of 2004 banned products containing ephedra in the US; although the act was revised to permit the sale of products containing 10mg or less.[76], [69]The World Anti-Doping Code 2009 Prohibition List-International Standard lists the following substances as ‘banned’: anabolic agents and stimulants.[69] The World Anti-Doping Agency did release a Therapeutic Use Exemption (TUE) list of three criteria that would allow an athlete to use banned substances that include: the athlete would experience significant impairment to their health if the medication was withheld; the prohibited substance would not increase the athlete’s performance other than from restoring their health to normality; the athlete could not use a permitted alternative.[76]


Epidemiology/Etiology/Prevalence/Incidence:


Current data reports 14-39% of athletes are utilizing PES with a high prevalence of AAS use.[77]The use and abuse of various PES, including AAS and other stimulants, has been linked to adolescent imitation of peers, parents, and others while receiving both positive and negative reinforcement by peers and other role models via the Social Cognitive Theory.[69]Demographics such as age, gender, race, year in school, and geographical region may have a direct effect on PES use.[69]


Rates for AAS are significantly in favor of the male population while rates for dietary supplements are much higher in the female population.[75], [69]Regionally, the highest rates of illegal drug offers, sales, and use in school occurred in the Southern region of the US followed by the Northeast, Midwest, and Western regions respectively.[69]The rates for AAS use and diet supplementation both range from 6-17% among the adolescent population.[69]The highest rates for PES use in the US are in the South Atlantic region. In the female demographic race/ethnicity, and BMI are reported as significant predictors for AAS use. AAS has also been reported as more frequent in populations that describe themselves as feeling sad, hopeless, and those whom reportedly considered committing suicide within the past 12 months.[69]PES use has also been reported to have a higher instances in smokers and alcohol drinkers.[71]AAS use is correlated negatively with age, education level, and number of children.[78]Decreased likelihood of AAS use has been correlated with those men with a college education and an annual income greater than 200K. Historically, adolescents abusing AAS may progress to opioid use and abuse later in life, thus developing a drug dependence.[75], [69]


Clinical Presentation/Characteristics:


In young men, common side effects of AAS use include acne and oily skin as well as more serious problems related to testicular atrophy, infertility, gynecomastia, and liver toxicity.[76], [75], [71]Females may experience similar skin and liver related toxicity along with facial hair growth, deepening of the voice, menstrual irregularities, and enlargement of the genitalia.[76], [75]Case reports have recently found that AAS-induced liver toxicity will resolve within months after the discontinuation of AAS.[76]


Diff Dx (“red flags”):


Hypogonadism has been linked to AAS exposure with AAS use being significantly correlated with a lower education level.[78], [79]AAS induced hypogonadism is the most common etiology linked to hypogonadism.[78]Other side effects include water retention and testicular atrophy.[78], [79]Adverse effects include cardiovascular toxicity, atherosclerosis, dyslipidemia, platelet dysfunction, hypertension, cardiomyopathy, myocardial infarction, and stroke.[73], [76], [78], [80], [70], [81], [74]Other associated health risks include blood clotting, jaundice, hepatic neoplasms, carcinomas, and tendon damage.[80], [74]AAS has also been shown to change fat content decreasing gynoid fat, a known risk for cardiovascular disease.[72]


Left ventricular hypertrophy has been correlated with AAS use, leading to decreased function and diastolic impairment.[73]Alterations in body composition, lipid parameters, and resting HR are all altered with AAS use.[73], [70], [72]


Other psychosocial characteristics of AAS users include depression, mania, aggression, and psychotic episodes.[75], [81], [74]These psychotic rages have been coined ‘roid rage,’ and may be accompanied by paranoid envy, extreme irritability, and judgement errors.[79]AAS has also been linked to a dependence syndrome.[82], [79]Withdrawal symptoms include mood alterations, craving, fatigue, restlessness, loss of appetite and decreased sex drive.[79]The extremes of withdrawal may even include suicidal depression. The recognition of AAS dependence syndrome has made it increasingly important to understand the origins, mechanism, and consequences of AAS use.[72]


Relevant anatomy:


Naturally occurring testosterone is an endogenous anabolic steroid. The synthetic derivatives, AAS, trigger a molecular reaction resulting in anabolic effects including muscel and bone metabolism.[71] Creatine is a naturally occurring endogenous compound formed from arginine and glycine.[71]Creatine serves as an energy substrate for skeletal muscle that reportedly increases strength, power output, sprint performance, peak force, and peak power.[71]Human growth hormone is naturally released from the anterior pituitary gland and promotes growth through lipolysis and protein anabolism, resulting in decreased fat mass and increased lean muscle mass.[71]Amphetamines stimulate the central nervous system and other catecholamines causing the release of norepinephrine increasing the arousal rate, heart rate, blood pressure, and respiratory rate.[71]Erythropoietin (EPO) is a glycoprotein largely produced in the kidney, that when excited produces increased amounts of erythrocytes leading to a higher oxygen-carrying capacity.[71]


Exam/screening/testing:


Testing for AAS use is completed through a urine immunoassay that calculates a testosterone: epitestosterone ratio that should be less than 2:1, but have an upper allowable limit of 6:1.[71] Human growth hormone has a short half-life and is difficult to detect, but urinary tests remain the staple for testing relying on the concentrations of recombinant human growth hormone versus naturally derived isotopes.[71] Amphetamines are also detected through their presence in the athlete’s urine.[71]EPO testing is difficult and so identification relies on sophisticated algorithms based on the total amount of circulating hemoglobin.[71]


Multidisciplinary Teams:


Healthcare providers have historically been less familiar with PES abuse than with other illegal substance abuse.[69] Sport physicians play a large role in the success of athletes, but unfortunately this means that they may have the tendency to push athletes past their natural boundaries.[83]In fact, some physicians have reportedly attested to medical practices outside standard/accepted practices.[83]In order for the proper education and prevention over the use and abuse of various PES to occur, health professionals, school psychologists, nurses, and coaches must be aware of the effects of PES when taken in combination with prescribe medications, caffeine, and nicotine; they must also pass this same knowledge on to their respective athletes. [69]


Medical Management/ Treatment:


The management and treatment for those taking PES including those abusing AAS include the periodic deprivation of the substance. The dosage should be weaned down periodically to avoid aggressive withdrawal symptoms. Note that athletes who have abused AAS for long periods may have reduced natural testosterone and must supplement artificial testosterone on a regular basis.


Resources:


The American Medical Association, American Academy of Pediatrics, American College of Sports Medicine, and National Institute on Drug Abuse have all published literature on the adverse effects and health consequences related to the use and abuse of PES including AAS and various other stimulants.[69]


Additionally, health practitioners may influence PES use by encouraging the youth to educate themselves about the substances they are considering, thereby appealing to their sense of self-efficacy and empowering them to learn more.[75]


Clinical Bottom line:


PES are used by athletes of all calibers, from high school, to elite athletes, to recreational enthusiasts. Several adverse effects result for the use and abuse of these unregulated substances. Information does exist on these adverse effects, but it is up to the consumer/athlete to seek out this information and educate themselves. For this same reason, healthcare professionals, coaches, athletic trainers, and athletes alike all share the responsibility to educate themselves and each other in order to avoid the life altering/threatening results of PES abuse.


Recent Related Research (from Pubmed)

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