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Medical Conditions in the Athlete, Third Edition With Web Study Guide, equips health care providers with the information they need to develop a framework for decision making when working with injured and recovering athletes and active populations. The updated and streamlined third edition provides comprehensive medical information that assists health care providers and athletic trainers in recognizing and identifying underlying and potentially serious medical conditions that may affect their chosen course of treatment.
The highly esteemed authors, Katie Walsh Flanagan and Micki Cuppett, have combined their professional skills and educational expertise to revitalize the content of Medical Conditions in the Athlete, Third Edition, with current, research-driven assessment and treatment information for medical conditions that affect the physically active population. The updated content aligns with Board of Certification (BOC) and Commission on Accreditation of Athletic Training Education (CAATE) standards. The book addresses medical conditions by body system, their mechanism of acquisition, signs, symptoms, differential diagnoses, referral, treatment, and return-to-participation criteria.
The 18 comprehensive chapters are organized into three sections: Introduction to Medical Conditions, Pharmacology and Interventions, and Medical Conditions by System. Throughout the text, more than 380 updated, full-color illustrations and photographs visually enhance readers’ comprehension of anatomy, physiology, and pathophysiology. Pharmacological tables organize drugs by categories that include generic and trade names, therapeutic uses, adult dosage information, and possible adverse effects. Important terminology is highlighted throughout the chapters, and a glossary appears at the end of the text.
At the beginning of the text, a Condition Finder serves as a quick reference so health care providers can easily flip to the information they need on specific conditions. Throughout the book, learning aids draw attention to important facts and figures, presented in three practical categories:
• Red Flags are warning signs that health care providers should look for when working with clients.
• Clinical Tips discuss information that is critically important to professionals.
• Condition Highlights cover specific medical conditions common to athletes that require special attention or medical care.
New to this edition is an accompanying web study guide that houses case studies corresponding to specific chapters. Each case study is followed by questions to help students apply the strategies covered in the text. Instructors who adopt the text will have access to a comprehensive collection of ancillary materials: chapter quizzes, a presentation package of slides, and an image bank that can be used to enhance presentation slides or student handouts.
Medical Conditions in the Athlete, Third Edition With Web Study Guide, provides readers with research-driven assessment and treatment information for medical conditions that affect all types of athletes. It is a comprehensive textbook and an important reference for health care providers such as athletic trainers and physical therapists who work with active populations.
Part I. Introduction to Medical Conditions
Chapter 1. Introduction to Medical Conditions
Role of the Athletic Trainer in Evaluation of Medical Conditions
Communication in the Medical Field
Prevention of Disease Transmission
Legal Considerations, Medical Care, and Disposition
Summary
Chapter 2. Medical Examination
Examination of the Patient With a Medical Condition
Physical Examination
Summary
Chapter 3. Diagnostic Imaging and Testing
Radiography: X-Rays
Radionuclide Bone Scan
Fluoroscopy
Computed Tomography Scan
Positron Emission Tomography Scan
Magnetic Resonance Imaging
Diagnostic Ultrasound (Sonography)
Electromyography and Nerve Conduction Studies
Electrocardiography
Holter Monitor
Cardiac Stress Test
Laparoscopy
Colonoscopy
Urinalysis
Complete Blood Count
Lumbar Puncture
Pulse Oximeter
Reporting Cancer Diagnoses
Summary
Part II. Pharmacology and Interventions
Chapter 4. Basic Principles of Pharmacology
Regulation
Pharmacology
Summary
Chapter 5. Therapeutic Drug Categories
Anti-Inflammatory Agents
Pain Management
Infectious Disease
Oral Anticoagulants
Summary
Chapter 6. Common Procedures and Interventions in the Athletic Training Clinic
Informed Consent
Preventing Infection
Asepsis
Closing Lacerations
Summary
Part III. Medical Conditions by System
Chapter 7. Respiratory System
Overview of Anatomy and Physiology
Evaluation of the Respiratory System
Asthma
Exercise-Induced Bronchospasm
Bronchitis
Chronic Obstructive Pulmonary Disease
Pneumonia
Pleurisy
Influenza
Upper Respiratory Infections
Tuberculosis
Lung Cancer
Spontaneous Pneumothorax and Hemothorax
Summary
Chapter 8. Cardiovascular System
Overview of Anatomy and Physiology
Cardiovascular Adaptations to Exercise
Preparticipation Examination
General Evaluation of the Cardiovascular System
Sudden Cardiac Death
Hypertrophic Cardiomyopathy
Coronary Artery Abnormalities
Marfan Syndrome
Myocarditis
Congenital Aortic Stenosis
Mitral Valve Prolapse
Arrhythmias
Syncope
Hypertension
Deep Vein Thrombosis
Pulmonary Embolus
Peripheral Arterial Disease
Anemia
Hemolysis
Sickle Cell Trait or Anemia
Summary
Chapter 9. Gastrointestinal System
Overview of Anatomy and Physiology
Evaluation of Abdominal Pain
Evaluation of the Athlete With Acute, Traumatic Abdominal Pain
Nausea, Vomiting, and Diarrhea
Viral Gastroenteritis
Food Poisoning or Bacterial Diarrhea
Parasitic Infection
Stress-Induced Gastrointestinal Symptoms
Constipation
Heartburn and Gastroesophageal Reflux Disease
Gastritis and Peptic Ulcer Disease
Irritable Bowel Syndrome
Celiac Disease
Inflammatory Bowel Diseases
Appendicitis
Cholecystitis and Cholelithiasis
Colorectal Cancer
Summary
Chapter 10. Genitourinary and Gynecological Systems
Overview of Anatomy and Physiology
Evaluation of the Genitourinary and Gynecological Systems
Kidney Stones
Sports Hematuria
Urinary Tract Infection
Urethritis
Human Immunodeficiency Virus and Acquired Immunodeficiency Syndrome
Genital Warts
Syphilis
Gonorrhea
Chlamydia
Testicular Torsion
Hydrocele
Varicocele
Testicular Cancer
Prostate Cancer
Vaginitis
Pelvic Inflammatory Disease
Dysmenorrhea
Amenorrhea
Mittelschmerz
Ovarian and Cervical Cancer
Breast Cancer
Pregnancy
Ectopic Pregnancy
Summary
Chapter 11. Neurological System
Overview of Anatomy and Physiology
Evaluation of the Neurological System
Pathological Conditions
Sport-Related Concussion
Stroke
Guillain-Barré Syndrome
Headaches
Seizure Disorder and Epilepsy
Vertigo
Multiple Sclerosis
Amyotrophic Lateral Sclerosis
Bell's Palsy
Rabies
Complex Regional Pain Syndrome
Summary
Chapter 12. The Eye
Overview of Anatomy and Physiology
Evaluation of the Eye
Refractive Error
Conjunctivitis
Hyphema
Subconjunctival Hemorrhage
Corneal Abrasions
Corneal or Scleral Lacerations
Corneal and Conjunctival Foreign Bodies
Orbital Fracture
Retinal Tear and Detachment
Dislocated Contact Lens
Chemical Burns
Periorbital Contusion
Traumatic Iritis
Proptosis
Eyelid Lacerations
Protective Eyewear
Summary
Chapter 13. Ear, Nose, Throat, and Mouth
Overview of Anatomy and Physiology
Evaluation of the Ear, Nose, Mouth, and Throat
Hearing Loss
Otitis Externa
Otitis Media
Ruptured Tympanic Membrane
Allergic Rhinitis
Nonallergic Rhinitis
Sinusitis
Deviated Septum
Epistaxis
Pharyngitis and Tonsillitis
Laryngitis
Oral Mucosal Lesions
Oral Candidiasis
Oral Cancers
Dental Disease
Dental Caries
Summary
Chapter 14. Systemic Disorders
Anatomy and Physiology of the Lymphatic System
Non-Hodgkin's Lymphoma
Hodgkin's Lymphoma
Leukemia
Lyme Disease
Raynaud's Disease
Systemic Lupus Erythematosus
Fibromyalgia
Chronic Fatigue Syndrome
Pancreatitis
Diabetes Mellitus
Hyperthyroidism
Hypothyroidism
Summary
Chapter 15. Infectious Diseases
Transmission
Prevention
Influenza
Infectious Mononucleosis
Mumps
Rubeola
Rubella
Chickenpox and Shingles
Hepatitis A to D
Streptococcal Infections
Staphylococcal Infections
Sexually Transmitted Diseases and Infections
Encephalitis
Zika Virus
Viral Meningitis
Acute Bacterial Meningitis
Summary
Chapter 16. Dermatological Conditions
Overview of Anatomy and Physiology
Evaluation of the Skin
Urticaria
Dermatographism
Solar Urticaria
Epidermoid Cysts
Eczema and Atropic dermatitis
Psoriasis
Skin Cancer
Frostbite
Impetigo
Folliculitis
Abscesses, Furuncles, and Carbuncles
Acne
Paronychia or Onychia
Herpes Simplex
Varicella-Zoster
Molluscum Contagiosum
Human Papillomavirus
Tinea Corporis
Tinea Cruris
Tinea Unguium
Tinea Pedis
Tinea Capitis
Tinea Versicolor
Head Lice
Body Lice
Pubic Lice
Scabies
Insect Bites
Summary
Chapter 17. Psychological and Substance Use Disorders
Layne A. Prest
Understanding the Role of Mental Health Professionals
Overview of Mental Health Issues in the Athlete
Role of Stress in Psychological and Substance Use Disorders
Anxiety Disorders
Mood Disorders
Eating Disorders
Substance Use and Dependence
Attention Deficit Hyperactivity Disorder
Stages of Readiness
What to Do in a Crisis
Summary
Chapter 18. Working With Special Populations
Monique Mokha
Preparticipation Examination for Athletes with Disabilities
Overview of Anatomy and Physiology
Traumatic Tetraplegia and Paraplegia
Autonomic Dysreflexia
Boosting
Thermoregulation Concerns
Skin Breakdown and Pressure Sores
Spasms
Bladder Dysfunction
Spina Bifida
Poliomyelitis
Cerebral Palsy
Amputations
Sensory Disabilities
Intellectual Disabilities
Summary
Katie Walsh Flanagan, EdD, ATC, is a professor and director of the sports medicine and athletic training program in the department of health education and promotion at East Carolina University, where she has worked for more than 20 years. A Board of Certification (BOC) certified athletic trainer, Walsh Flanagan previously worked as a lecturer and assistant athletic trainer at California State University, Fresno, and as the head athletic trainer for the Chicago Power, a men’s professional soccer team. She has also assisted as an athletic trainer for various sports in international competitions, including the 1996 Summer Olympic Games and 1987 Pan American Games.
In 2012, Walsh Flanagan was elected to the North Carolina Athletic Trainers’ Association Hall of Fame. The organization named her the North Carolina Athletic Trainer of the Year–College/University in 2000 and 2006. She received the Most Distinguished Athletic Trainer award from the National Athletic Trainers’ Association in 2010 and their Athletic Trainer Service award in 2006.
Micki Cuppett, EdD, ATC, is the executive director of the Commission on Accreditation of Athletic Training Education (CAATE) after having served as its president and as a board member. She previously worked for 16 years as a professor of athletic training in the department of orthopedics and sports medicine at the University of South Florida, where she was the athletic training program director. She has also been a professor and director of athletic training education at the University of Nebraska at Omaha.
In addition to her work in academe, Cuppett has been an athletic trainer for three decades, having worked in high school, collegiate, military, and hospital settings. Cuppett is known internationally for her work with human patient simulators and interprofessional education, and she has often been an invited speaker at national and international conferences. She received the Athletic Trainer Service award from the National Athletic Trainers’ Association in 2007 and their Most Distinguished Athletic Trainer award in 2012.
Addressing mental health issues in the athlete
Everyone has symptoms of some type of mental health issue at some time in life when one or several stressors overwhelm the person’s ability to self-regulate or repair. The symptoms are usually, and arbitrarily, labeled either physical or mental.
Everyone has symptoms of some type of mental health issue at some time in life when one or several stressors overwhelm the person's ability to self-regulate or repair. The symptoms are usually, and arbitrarily, labeled either physical or mental. This artificial dichotomy usually does not align with the affected person's reality. Rarely is an athlete with a strained hamstring not also worried about the injury or distressed by the pain. Similarly, the most common initial warning signs of depression are the physical symptoms of tension, restlessness, and disturbed sleep, energy, and appetite. This is because we have overlapping systems of mind, body, spirit, and relationships, each integrally connected to the others. When the homeostasis of one or more systems is disrupted, people instinctively try to correct the problem regardless of its origin. In the mental health domain, signs of distress are emotional, mental, behavioral, and physical.
Framework for Understanding Mental Health
In almost all situations, a variety of overlapping factors contribute to symptom development. The biopsychosocial - spiritual model (BPSS) is a framework for understanding the person's responses in a given situation and the development of symptoms. Symptom etiology may be conceptualized as a pie. Figure 17.1 shows how these various factors overlap and contribute to well-being. In a given person, the various pieces of the BPSS pie may be larger or smaller at any one time. The relative sizes of the pieces greatly influence the person's symptoms and ability to adapt.
The biopsychosocial - spiritual model is a framework for understanding a person's responses in a given situation and the development of symptoms.
For example, two runners may have identical injuries, but the impact of the injury and the course of rehabilitation in these two athletes will usually differ. The amount of pain they have, as well as the length of time until they are ready to compete again, will be influenced not only by the difference in respective levels of physical conditioning and injury history but also by other physical and emotional conditions such as pain tolerance, attitude, perception of the problem, and its implications for life. The situation may also be affected by personality and temperament issues, variable resources for coping, and so on. Another example involves two wrestlers who seem to be equally competitive, but wrestler A, in a struggle to make or maintain weight, develops more obviously disordered eating patterns than wrestler B. Perhaps wrestler A has a family history of obesity and is genetically predisposed toward weight gain more than the other; temperamentally, wrestler A may tend to think more negatively about life challenges, become somewhat self-defeating in the face of adversity, and find emotional comfort in food and the process of eating. Often a variety of factors will help to explain the development of clinically significant problems.
This interplay of variables is the same for athletes as it is for others who are physically active, regardless of whether the symptoms of an injury or condition are physical or emotional. Whereas one athlete may become depressed, another's symptoms may include anxiety or outbursts of anger and physical aggression. Sometimes one piece of the BPSS pie is so big that it seems to account for virtually the whole reason that someone is symptomatic (e.g., the chemical disequilibrium that comes with bipolar disorder). For this reason, it is a good practice to regularly consider the possibility that an organic cause may be the culprit and refer the person for a medical evaluation.
The treatments that have proven effective for the problems discussed in this chapter are based on the same BPSS approach as the assessment and diagnosis. Different strategies can be useful, depending on the biopsychosocial - spiritual components that are implicated in the assessment process. Practitioners often recommend treatment plans based on their assessment and experience, and then these are negotiated with the patient or family members according to personal preferences. The treatment may be offered on either an inpatient or, more commonly, an outpatient basis.
Treatment may also involve the collaboration of a variety of treatment professionals. For example, eating disorder treatment often involves a physician, a registered dietitian, and a psychotherapist. This will be determined based on the severity of symptoms, the difficulty the athlete has in making changes, the amount of support the athlete has, and other resources that affect care, including financial concerns or insurance benefits. The important first step in treatment is accurate assessment followed by clear and well-timed communication and education with the athlete and family. The athletic trainer can play a valuable role here because people are much more likely to engage in treatment or some type of change process if they become convinced that there is a problem, they know what it is, and they know that something can be done about it. This is because most people will want to know what is going on with themselves, how they "got it," and what they can do to "get rid of it" or at least cope more effectively. Additional treatment recommendations specific to various clinical problems are listed in subsequent sections.
Implications for Participation in Athletics
Early identification and treatment are very helpful in preventing problems from worsening, but sometimes the stigma still associated with mental health conditions prevents people from recognizing these problems in themselves or others. In those cases, functioning in one or more areas of life can be affected, sometimes severely. Restricting participation in a sport, if necessary, will depend on the assessment of the athlete's level of functioning by the athlete, the coach, and the athletic trainer. Initially, while the medication dosage is being adjusted, the athlete could experience adverse effects that could affect participation or performance, such as nausea, headache, sedation, disturbed balance, or overstimulation. The National Collegiate Athletic Association (NCAA) has no restrictions on the medications typically used to treat these conditions except for pemoline, a medication prescribed to treat ADHD (National Collegiate Athletic Association 2015).
The last general point to be made is that some people experiencing psychological or substance use disorders may consider suicide or become homicidal. Most health care professionals or other professionals are required by law or by a professional code of ethics to report to the authorities if a patient is a danger to self or others. Athletic trainers, too, may encounter an athlete with depression, panic disorder, or substance abuse who is considering suicide or harming someone else. The athletic trainer must seek immediate consultation if in doubt about the need to report. An assessment of whether one is suicidal or homicidal includes determining whether the person has a specific plan, the means to carry it out, the intention to carry it out, and how lethal the plan is. Those with a personal or family history of this type of ideation or action or whose judgment is impaired, perhaps through the use of substances, are more at risk to follow through.
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Identifying Exercise-Induced Bronchospasm
The terms EIA and EIB are often used interchangeably, but EIB specifically denotes the reduction in lung function that occurs after a standardized exercise test (Carver 2009). More recently, the term exercise-induced bronchoconstriction has been introduced as actual spasm of the airways does not always occur.
The terms exercise-induced asthma (EIA) and exercise-induced bronchoconstriction (EIB) are often used interchangeably, but EIB specifically denotes the reduction in lung function that occurs after a standardized exercise test (Carver 2009). More recently, the term exercise-induced bronchoconstriction has been introduced as actual spasm of the airways does not always occur. Some clinicians use EIA to describe individuals with known asthma who have bronchoconstriction during exercise. However, some use EIA to describe patients who have bronchoconstriction only during exercise, and they use EIB to describe patients with asthma who have bronchoconstriction with exercise. Generally, EIB is used to indicate bronchospasm with decreased pulmonary function testing following exercise, and EIA is used to indicate those patients with asthma difficulties associated with exercise.
Symptoms of EIB usually occur 10 to 15 min after the onset of strenuous exercise and are defined by a fall in FEV1 of 15% or more during exercise spirometry. EIB is more common in winter sport athletes who compete in cold ambient temperatures (Carey, Aase, and Pliego 2010).
Signs and Symptoms
EIB should be suspected in any athlete who complains of shortness of breath, dyspnea, cough, chest congestion, or tightness with exertion. These symptoms usually occur during strenuous exercise and peak about 5 to 10 min after exercise (Hull 2012; Krafczyk and Asplund 2011; Simpson, Romer, and Kippelen 2015). Other subtle clues might be a dry cough that develops after practice or exercise (i.e., locker-room cough) or simply unusual fatigue compared with similarly trained athletes. Athletes will often complain that they feel out of shape despite regular training. Self-reported symptoms have been shown to be poor predictors of EIB because other conditions can cause similar symptoms. Symptoms alone should not be used to diagnose EIB.
In athletes suspected of having EIB, other etiologies, such as acute sinusitis, otitis media (middle ear infection), bronchitis, or even pneumonia, need to be excluded, particularly in the context of other constitutional symptoms, such as fever, chills, or night sweats. If fatigue is the only presenting symptom, deconditioning may also be a cause. In addition, environmental allergies can account for many of the nonspecific symptoms that mimic EIB (Backer 2010; Hull et al. 2012; Stack and Hakemi 2011). More serious cardiac causes, such as arrhythmias and pericarditis, might also need to be excluded. Another important differential is exercise-induced laryngeal obstruction (EILO), where the wheezing and dyspnea are caused by transient obstruction of the upper airways during exercise (Nielsen 2013; Backer 2010).
Referral and Diagnostic Tests
The physical examination is usually normal. Some athletes with EIB may experience symptoms that develop several hours after exercise. This late-phase response is due to the activity of inflammatory mediators. Most commonly, a bronchial provocation challenge is used to determine the diagnosis of EIB (Parsons et al. 2011; Hayden et al. 2011; Morris 2010). Figure 7.9 shows a decision tree commonly used for the diagnosis of EIB. Alternatively, many physicians choose to just evaluate the patient's response to an empirical trial of a ß-agonist medication before exercise.
Decision tree for the diagnosis of exercise-induced bronchoconstriction (EIB).
Treatment and Return to Participation
The treatment of choice in EIB is an inhaled ß2-agonist from a metered-dose inhaler (e.g., albuterol) taken 15 to 30 min before the onset of exercise. An athlete who has asthma symptoms outside the exercise setting or who is using a ß2-agonist more than three times per week should be treated with a regular inhaled corticosteroid. Here is how to properly use an inhaler:
- Remove dust cap and shake the inhaler system before each use.
- Inspect mouthpiece for contamination or foreign objects.
- Breathe out through the mouth, exhaling as completely as possible.
- Hold the inhaler system upright with mouthpiece in mouth and lips closed tightly around mouthpiece.
- Breathe in slowly while pressing down on the metal cartridge.
- Hold breath as long as possible.
- Release pressure while still holding breath.
- Remove mouthpiece.
- Wait for the container to repressurize, shake, and then repeat steps 3 through 8 when more than one inhalation is prescribed.
- Rinse mouth with water after prescribed number of inhalations.
- Clean the inhaler system every few days by removing metal cartridge and rinsing the plastic inhaler and cap with running warm water. Replace cartridge and cap.
Emerging studies show promise using long-acting ß2-agonists such as salmeterol and leukotriene inhibitors such as montelukast (Singulair) (Parsons 2010). Other nonpharmacological strategies include pre - warm-up bursts of physical activity at 80% to 90% of the individual's maximal workload to induce a refractory period that lasts up to 3 h after the initial attack of EIB (Hull et al. 2012; Millward et al. 2009; Boulet, Hancox, and Fitch 2010). Strategies to humidify inspired air and dietary interventions may also prove to be beneficial (Carey, Aase, and Pliego 2010; Bussotti, Di Marco, and Marchese 2014).
For an athlete experiencing a severe asthma attack or when an inhaler is ineffective, a nebulizer may be used. A nebulizer, also known as an atomizer, is a machine that vaporizes liquid medication into a fine mist to be inhaled into the lungs via a mouthpiece or mask. Although studies have shown that both inhalers and nebulizers tend to be equally effective in delivering medications, nebulizers are preferred for use in more serious rescue situations when the patient is experiencing a severe asthma attack. Nebulizers can administer a higher dose of medication, but inhalers are easier to use, preferred for their portability and low cost, and good for everyday use. Medications typically administered with a nebulizer include albuterol and ipratropium (Atrovent).
Athletes with controlled EIB need not be excluded or discouraged from participating in sports. Effective strategies, both pharmacological and nonpharmacological, exist that can allow an athlete to compete even at an elite level.
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Causes of Sudden Cardiac Death in Athletes
Death by sudden cardiac arrest (SCA) is a rare event in the young athlete. In the United States, elite athletes are viewed as near invincible because of their incredible physical feats.
Death by sudden cardiac arrest (SCA) is a rare event in the young athlete. In the United States, elite athletes are viewed as near invincible because of their incredible physical feats. Nevertheless, it is reported that the rate of collegiate athlete death due to SCA is higher than that of high school athletes, with a suspected 110 SCA deaths annually in the United States among young athletes (Casa et al. 2012). Any time a tragedy of this proportion occurs, the public reacts with disbelief, and medical knowledge is called into question. Studies that have tracked these deaths during sports used the National Federation of State High School Associations (NFHS), the National Collegiate Athletic Association (NCAA) governing organizations, and state and federally funded research groups for data collection, such as the National Center for Catastrophic Sport Injury Research (NCCSIR), based in Chapel Hill, North Carolina. Approximately 90% of the data collected involved male athletes, with an equal distribution between Caucasians and African-Americans (Borjesson and Pelliccia 2009). According to the NCCSIR, there were 10 indirect (due to exertion) fatalities in middle school through college football athletes in 2014, and six were attributed to a cardiac event (Kucera et al. 2015). An additional five football athletes died of suspected cardiac conditions due to nonexertional factors in the same year (Kucera et al. 2015). Sudden death cases in young women are rare, and the most common cause of sudden cardiac death was congenital cardiac disease.
The prevalence of sudden cardiac death in young athletes (those less than 35-year-old) is estimated to be between 1 and 3 in 100,000 (Borjesson and Pelliccia 2009). This is much higher than statistics reported in a more general population of active individuals (Harmon, Klossner, and Drezner 2011). These data indicate that active people are not immune to cardiovascular events that may result in death.
Causes
The most common cause of sudden cardiac death in the young athlete is hypertrophic cardiomyopathy, which accounts for up to 50% of the cases. Other significant causes of sudden cardiac death in a young athlete are coronary artery anomalies, increased cardiac mass, aortic rupture, myocarditis, and aortic stenosis(Borjesson and Pelliccia 2009).Rare causes include dilated cardiomyopathy, atherosclerotic coronary artery disease, mitral valve prolapse, isolated arrhythmias such as long QT syndrome and Wolff-Parkinson-White syndrome, and arrhythmogenic right ventricular dysplasia (ARVD) (Harmon, Klossner, and Drezner 2011). In the Veneto region of Italy, researchers have found ARVD to be the most common cause of sudden cardiac death in the athlete (Thiene et al. 1988). This research suggests that a specific population may have different genetic subtraits.
In the older athlete, coronary artery disease is by far the most common cause of sudden death. Rarely is sudden death in the older athlete caused by hypertrophic cardiomyopathy, mitral valve prolapse, or acquired valvular conditions (Maron et al. 2014; Nagashima et al. 2003; Semsarian, Sweeting, and Ackerman 2015; Marijon et al. 2015).
Traumatic sudden cardiac death has not captured as much attention because its epidemiology is more difficult to track. However, it is a growing problem that strikes without warning. Between 1996 and 2007, a reported 180 cases of blunt-force death in the United States were attributed to commotio cordis (Maron et al. 2006). Most cases involved children with a mean age of 13, with 95% of the deaths occurring in males (Maron et al. 2013).
Commotio cordis refers to trauma to the chest wall that interrupts the electrical impulse in the heart. If the cardiac rhythm is not promptly normalized, the individual dies. Typically the ribs or sternum is not broken, although some contusions may be found. Research has found that a chest blow occurring during the vulnerable phase of repolarization, just prior to the T-wave peak in the cardiac cycle, can induce ventricular fibrillation (Maron and Estes 2005).
Although children and teenagers with thin chest walls are most vulnerable to commotio cordis (figure 8.6), deaths have been reported in adults. Sports such as baseball, ice hockey, lacrosse, and softball, which have hard projectiles that can strike the chest, have been associated with the greatest number of deaths. Commotio cordis also has occurred in sports such as soccer, football, rugby, and karate, in which the blow came from a soft projectile or a collision. It appears that the timing of the incident, rather than the degree of impact of the object, is the causative factor (Maron and Estes 2005). Commotio cordis is the only significant cause of traumatic sudden cardiac death in athletes.
The type of injury associated with commotio cordis is a blow to the chest wall that interrupts the usual cardiac rhythm.
Red Flags for Traumatic Sudden Cardiac Death
Sports with projectiles that can hit the chest at an inopportune time in the cardiac rhythm cycle have been known to cause commotio cordis in young athletes. These sports include the following: baseball, softball, hockey, lacrosse, soccer, football, karate.
Prevention
Because death can be the outcome, prevention has become the focus of attention for commotio cordis. Changes in practice have ranged from protective padding to softer balls that are used in Little League and softball. Because this may not completely resolve the problem, another solution is defibrillation in conjunction with cardiopulmonary resuscitation (CPR). Defibrillation interrupts the heart rhythm so the heart can "reboot" into a normal rhythm.
The American Heart Association estimates that communities with comprehensive CPR and automated external defibrillator (AED) training achieve 40% survival rates for cardiac arrest victims. If defibrillation is performed within 3 min, the likelihood of survival is high. For every minute of delay the chance of survival drops by as much as 10% (American Heart Association 2013).
The advent of the AED has provided greater public access to life-saving technology. These devices can be operated by trained laypeople and are increasingly affordable in all sectors. The AED is portable, rechargeable, simple to operate, and easy to maintain. The American Red Cross, American Heart Association, and National Safety Council offer AED certification courses in addition to CPR courses for the lay public. The NCAA Sports Medicine Guidelines require planned access to an AED and mandating CPR and first aid certifications for all who work with athlete practices, competition, and skill sessions. Athletic trainers are required to maintain certification in emergency cardiac care, including AED use. They need to have ready access to an AED in order to provide rapid cardiac assessment and care to those in fibrillation. Athletes who suffer a sudden collapse and have agonal or gasping breathing should be treated because they are suffering from a cardiac event (Casa et al. 2012; Solberg et al. 2015). An AED should be applied as soon as possible for heart rhythm analysis and possible defibrillation.
Clinical Tips
Potential Causes of Sudden Death
Sudden collapse in athletes could be caused by heatstroke, a cardiac event, sickle cell collapse, or injury. Understanding the presentation of each will facilitate rapid response and the appropriate disposition.
Emergency Planning
Every athletic site should have planned access to an AED, an emergency medical service (EMS), and an established emergency action plan (EAP), as well as medical personnel trained to respond to sudden collapse.
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How to identify celiac disease
Celiac disease is an autoimmune disorder that affects the gastrointestinal tract and is thought to be triggered by dietary gluten in affected individuals. The disease is characterized by chronic inflammation of the small intestinal mucosa, which leads to atrophy of the small intestinal villi and subsequent malabsorption (Pelkowski and Viera 2014).
Celiac disease is an autoimmune disorder that affects the gastrointestinal tract and is thought to be triggered by dietary gluten in affected individuals. The disease is characterized by chronic inflammation of the small intestinal mucosa, which leads to atrophy of the small intestinal villi and subsequent malabsorption (Pelkowski and Viera 2014). Celiac disease affects approximately 1% of the U.S. population and typically occurs in persons of European ancestry as well as persons of Middle Eastern, Indian, South American, and North African descent. It is two to three times more common in women. Celiac disease is not a food allergy.
Signs and Symptoms
Typical presentation includes chronic diarrhea with cramping and gas pains. Patients often have weight loss, or in the adolescent, delayed onset of growth or puberty. A history of nervousness and/or depression is often present, as is a family history of autoimmune disease. Other complaints may include bone or joint pain, migraines, weakness, fatigue, and anemia (Volta et al. 2015; Vivas et al. 2015; Byrne and Feighery 2015; Mancini, Trojian, and Mancini 2011). Physical examination is often normal, but the patient may present with abdominal distension or dermatitis herpetiformis.
Referral and Diagnostic Tests
Lab tests are performed for differentiating celiac disease and to rule out more common diseases. These include a basic metabolic panel, CBC (iron deficiency), TSH (thyroid disease), vitamin D level, and allergy testing. If celiac disease is suspected from history and physical exam, the initial serologic test is a tissue transglutaminase (tTG) antibody level. This antibody is found in every tissue in the body and acts to join proteins together. In people with celiac disease, tTG activates specific immune cells and triggers the inflammatory response that leads to atrophy of the villi in the small intestine (Mancini, Trojian, and Mancini 2011). The diagnosis is often confirmed with repeat blood tests after 4 wk on a gluten-free diet. Endoscopy with biopsies of the duodenal mucosa may be necessary to confirm the diagnosis. Celiac disease should be differentiated from GERD, pancreatic insufficiency, Crohn's disease, or other inflammatory bowel diseases.
Treatment and Return to Participation
The general treatment is to remove gluten from the diet. The patient can substitute rice, corn, and soybean flour for products that contain gluten. Periodic blood tests are performed to measure the levels of the antibodies. The levels will normalize with gluten abstinence. Abstinence will be required for life because the immune response to gluten will recur if gluten is consumed again. Usually no medications are prescribed for celiac disease, but athletes may benefit from iron, vitamin, and calcium supplements. The most difficult aspect for the athlete with celiac disease is the dietary restrictions while traveling with the team or with set team meals. The athletic trainer may need to check on the gluten-free status of many of the standard gluten-containing products provided by the athletic department, such as energy drinks or meal replacement bars (Mancini, Trojian, and Mancini 2011).
Condition Highlight
Gluten Sensitivity and Intolerance
Over the past 10 yr, the number of people choosing a gluten-free diet (GFD) is much higher than the projected number of celiac disease patients (Lis et al. 2015). This has fueled a global market of gluten-free products and highlights several conditions related to the ingestion of gluten. There are three main forms of gluten reactions: allergic, autoimmune (celiac disease), and immune-mediated conditions (gluten sensitivity) (Sapone et al. 2012). Wheat allergy is an adverse reaction to wheat proteins with onset in minutes to hours after gluten ingestion. It may affect the skin, GI tract, or respiratory tract. Celiac disease or other autoimmune gluten disorders generally present months to years after gluten exposure. There is a third condition where some people experience distress from eating gluten-containing products and show improvement with a GFD. It is distinct from celiac disease and wheat allergies (Vivas et al. 2015). Gluten sensitivity cannot be distinguished clinically; serology tests need to be conducted. Patients with GI discomfort or distress following gluten ingestion should be referred for a follow-up blood test and immune-allergy tests.
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Addressing mental health issues in the athlete
Everyone has symptoms of some type of mental health issue at some time in life when one or several stressors overwhelm the person’s ability to self-regulate or repair. The symptoms are usually, and arbitrarily, labeled either physical or mental.
Everyone has symptoms of some type of mental health issue at some time in life when one or several stressors overwhelm the person's ability to self-regulate or repair. The symptoms are usually, and arbitrarily, labeled either physical or mental. This artificial dichotomy usually does not align with the affected person's reality. Rarely is an athlete with a strained hamstring not also worried about the injury or distressed by the pain. Similarly, the most common initial warning signs of depression are the physical symptoms of tension, restlessness, and disturbed sleep, energy, and appetite. This is because we have overlapping systems of mind, body, spirit, and relationships, each integrally connected to the others. When the homeostasis of one or more systems is disrupted, people instinctively try to correct the problem regardless of its origin. In the mental health domain, signs of distress are emotional, mental, behavioral, and physical.
Framework for Understanding Mental Health
In almost all situations, a variety of overlapping factors contribute to symptom development. The biopsychosocial - spiritual model (BPSS) is a framework for understanding the person's responses in a given situation and the development of symptoms. Symptom etiology may be conceptualized as a pie. Figure 17.1 shows how these various factors overlap and contribute to well-being. In a given person, the various pieces of the BPSS pie may be larger or smaller at any one time. The relative sizes of the pieces greatly influence the person's symptoms and ability to adapt.
The biopsychosocial - spiritual model is a framework for understanding a person's responses in a given situation and the development of symptoms.
For example, two runners may have identical injuries, but the impact of the injury and the course of rehabilitation in these two athletes will usually differ. The amount of pain they have, as well as the length of time until they are ready to compete again, will be influenced not only by the difference in respective levels of physical conditioning and injury history but also by other physical and emotional conditions such as pain tolerance, attitude, perception of the problem, and its implications for life. The situation may also be affected by personality and temperament issues, variable resources for coping, and so on. Another example involves two wrestlers who seem to be equally competitive, but wrestler A, in a struggle to make or maintain weight, develops more obviously disordered eating patterns than wrestler B. Perhaps wrestler A has a family history of obesity and is genetically predisposed toward weight gain more than the other; temperamentally, wrestler A may tend to think more negatively about life challenges, become somewhat self-defeating in the face of adversity, and find emotional comfort in food and the process of eating. Often a variety of factors will help to explain the development of clinically significant problems.
This interplay of variables is the same for athletes as it is for others who are physically active, regardless of whether the symptoms of an injury or condition are physical or emotional. Whereas one athlete may become depressed, another's symptoms may include anxiety or outbursts of anger and physical aggression. Sometimes one piece of the BPSS pie is so big that it seems to account for virtually the whole reason that someone is symptomatic (e.g., the chemical disequilibrium that comes with bipolar disorder). For this reason, it is a good practice to regularly consider the possibility that an organic cause may be the culprit and refer the person for a medical evaluation.
The treatments that have proven effective for the problems discussed in this chapter are based on the same BPSS approach as the assessment and diagnosis. Different strategies can be useful, depending on the biopsychosocial - spiritual components that are implicated in the assessment process. Practitioners often recommend treatment plans based on their assessment and experience, and then these are negotiated with the patient or family members according to personal preferences. The treatment may be offered on either an inpatient or, more commonly, an outpatient basis.
Treatment may also involve the collaboration of a variety of treatment professionals. For example, eating disorder treatment often involves a physician, a registered dietitian, and a psychotherapist. This will be determined based on the severity of symptoms, the difficulty the athlete has in making changes, the amount of support the athlete has, and other resources that affect care, including financial concerns or insurance benefits. The important first step in treatment is accurate assessment followed by clear and well-timed communication and education with the athlete and family. The athletic trainer can play a valuable role here because people are much more likely to engage in treatment or some type of change process if they become convinced that there is a problem, they know what it is, and they know that something can be done about it. This is because most people will want to know what is going on with themselves, how they "got it," and what they can do to "get rid of it" or at least cope more effectively. Additional treatment recommendations specific to various clinical problems are listed in subsequent sections.
Implications for Participation in Athletics
Early identification and treatment are very helpful in preventing problems from worsening, but sometimes the stigma still associated with mental health conditions prevents people from recognizing these problems in themselves or others. In those cases, functioning in one or more areas of life can be affected, sometimes severely. Restricting participation in a sport, if necessary, will depend on the assessment of the athlete's level of functioning by the athlete, the coach, and the athletic trainer. Initially, while the medication dosage is being adjusted, the athlete could experience adverse effects that could affect participation or performance, such as nausea, headache, sedation, disturbed balance, or overstimulation. The National Collegiate Athletic Association (NCAA) has no restrictions on the medications typically used to treat these conditions except for pemoline, a medication prescribed to treat ADHD (National Collegiate Athletic Association 2015).
The last general point to be made is that some people experiencing psychological or substance use disorders may consider suicide or become homicidal. Most health care professionals or other professionals are required by law or by a professional code of ethics to report to the authorities if a patient is a danger to self or others. Athletic trainers, too, may encounter an athlete with depression, panic disorder, or substance abuse who is considering suicide or harming someone else. The athletic trainer must seek immediate consultation if in doubt about the need to report. An assessment of whether one is suicidal or homicidal includes determining whether the person has a specific plan, the means to carry it out, the intention to carry it out, and how lethal the plan is. Those with a personal or family history of this type of ideation or action or whose judgment is impaired, perhaps through the use of substances, are more at risk to follow through.
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Identifying Exercise-Induced Bronchospasm
The terms EIA and EIB are often used interchangeably, but EIB specifically denotes the reduction in lung function that occurs after a standardized exercise test (Carver 2009). More recently, the term exercise-induced bronchoconstriction has been introduced as actual spasm of the airways does not always occur.
The terms exercise-induced asthma (EIA) and exercise-induced bronchoconstriction (EIB) are often used interchangeably, but EIB specifically denotes the reduction in lung function that occurs after a standardized exercise test (Carver 2009). More recently, the term exercise-induced bronchoconstriction has been introduced as actual spasm of the airways does not always occur. Some clinicians use EIA to describe individuals with known asthma who have bronchoconstriction during exercise. However, some use EIA to describe patients who have bronchoconstriction only during exercise, and they use EIB to describe patients with asthma who have bronchoconstriction with exercise. Generally, EIB is used to indicate bronchospasm with decreased pulmonary function testing following exercise, and EIA is used to indicate those patients with asthma difficulties associated with exercise.
Symptoms of EIB usually occur 10 to 15 min after the onset of strenuous exercise and are defined by a fall in FEV1 of 15% or more during exercise spirometry. EIB is more common in winter sport athletes who compete in cold ambient temperatures (Carey, Aase, and Pliego 2010).
Signs and Symptoms
EIB should be suspected in any athlete who complains of shortness of breath, dyspnea, cough, chest congestion, or tightness with exertion. These symptoms usually occur during strenuous exercise and peak about 5 to 10 min after exercise (Hull 2012; Krafczyk and Asplund 2011; Simpson, Romer, and Kippelen 2015). Other subtle clues might be a dry cough that develops after practice or exercise (i.e., locker-room cough) or simply unusual fatigue compared with similarly trained athletes. Athletes will often complain that they feel out of shape despite regular training. Self-reported symptoms have been shown to be poor predictors of EIB because other conditions can cause similar symptoms. Symptoms alone should not be used to diagnose EIB.
In athletes suspected of having EIB, other etiologies, such as acute sinusitis, otitis media (middle ear infection), bronchitis, or even pneumonia, need to be excluded, particularly in the context of other constitutional symptoms, such as fever, chills, or night sweats. If fatigue is the only presenting symptom, deconditioning may also be a cause. In addition, environmental allergies can account for many of the nonspecific symptoms that mimic EIB (Backer 2010; Hull et al. 2012; Stack and Hakemi 2011). More serious cardiac causes, such as arrhythmias and pericarditis, might also need to be excluded. Another important differential is exercise-induced laryngeal obstruction (EILO), where the wheezing and dyspnea are caused by transient obstruction of the upper airways during exercise (Nielsen 2013; Backer 2010).
Referral and Diagnostic Tests
The physical examination is usually normal. Some athletes with EIB may experience symptoms that develop several hours after exercise. This late-phase response is due to the activity of inflammatory mediators. Most commonly, a bronchial provocation challenge is used to determine the diagnosis of EIB (Parsons et al. 2011; Hayden et al. 2011; Morris 2010). Figure 7.9 shows a decision tree commonly used for the diagnosis of EIB. Alternatively, many physicians choose to just evaluate the patient's response to an empirical trial of a ß-agonist medication before exercise.
Decision tree for the diagnosis of exercise-induced bronchoconstriction (EIB).
Treatment and Return to Participation
The treatment of choice in EIB is an inhaled ß2-agonist from a metered-dose inhaler (e.g., albuterol) taken 15 to 30 min before the onset of exercise. An athlete who has asthma symptoms outside the exercise setting or who is using a ß2-agonist more than three times per week should be treated with a regular inhaled corticosteroid. Here is how to properly use an inhaler:
- Remove dust cap and shake the inhaler system before each use.
- Inspect mouthpiece for contamination or foreign objects.
- Breathe out through the mouth, exhaling as completely as possible.
- Hold the inhaler system upright with mouthpiece in mouth and lips closed tightly around mouthpiece.
- Breathe in slowly while pressing down on the metal cartridge.
- Hold breath as long as possible.
- Release pressure while still holding breath.
- Remove mouthpiece.
- Wait for the container to repressurize, shake, and then repeat steps 3 through 8 when more than one inhalation is prescribed.
- Rinse mouth with water after prescribed number of inhalations.
- Clean the inhaler system every few days by removing metal cartridge and rinsing the plastic inhaler and cap with running warm water. Replace cartridge and cap.
Emerging studies show promise using long-acting ß2-agonists such as salmeterol and leukotriene inhibitors such as montelukast (Singulair) (Parsons 2010). Other nonpharmacological strategies include pre - warm-up bursts of physical activity at 80% to 90% of the individual's maximal workload to induce a refractory period that lasts up to 3 h after the initial attack of EIB (Hull et al. 2012; Millward et al. 2009; Boulet, Hancox, and Fitch 2010). Strategies to humidify inspired air and dietary interventions may also prove to be beneficial (Carey, Aase, and Pliego 2010; Bussotti, Di Marco, and Marchese 2014).
For an athlete experiencing a severe asthma attack or when an inhaler is ineffective, a nebulizer may be used. A nebulizer, also known as an atomizer, is a machine that vaporizes liquid medication into a fine mist to be inhaled into the lungs via a mouthpiece or mask. Although studies have shown that both inhalers and nebulizers tend to be equally effective in delivering medications, nebulizers are preferred for use in more serious rescue situations when the patient is experiencing a severe asthma attack. Nebulizers can administer a higher dose of medication, but inhalers are easier to use, preferred for their portability and low cost, and good for everyday use. Medications typically administered with a nebulizer include albuterol and ipratropium (Atrovent).
Athletes with controlled EIB need not be excluded or discouraged from participating in sports. Effective strategies, both pharmacological and nonpharmacological, exist that can allow an athlete to compete even at an elite level.
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Causes of Sudden Cardiac Death in Athletes
Death by sudden cardiac arrest (SCA) is a rare event in the young athlete. In the United States, elite athletes are viewed as near invincible because of their incredible physical feats.
Death by sudden cardiac arrest (SCA) is a rare event in the young athlete. In the United States, elite athletes are viewed as near invincible because of their incredible physical feats. Nevertheless, it is reported that the rate of collegiate athlete death due to SCA is higher than that of high school athletes, with a suspected 110 SCA deaths annually in the United States among young athletes (Casa et al. 2012). Any time a tragedy of this proportion occurs, the public reacts with disbelief, and medical knowledge is called into question. Studies that have tracked these deaths during sports used the National Federation of State High School Associations (NFHS), the National Collegiate Athletic Association (NCAA) governing organizations, and state and federally funded research groups for data collection, such as the National Center for Catastrophic Sport Injury Research (NCCSIR), based in Chapel Hill, North Carolina. Approximately 90% of the data collected involved male athletes, with an equal distribution between Caucasians and African-Americans (Borjesson and Pelliccia 2009). According to the NCCSIR, there were 10 indirect (due to exertion) fatalities in middle school through college football athletes in 2014, and six were attributed to a cardiac event (Kucera et al. 2015). An additional five football athletes died of suspected cardiac conditions due to nonexertional factors in the same year (Kucera et al. 2015). Sudden death cases in young women are rare, and the most common cause of sudden cardiac death was congenital cardiac disease.
The prevalence of sudden cardiac death in young athletes (those less than 35-year-old) is estimated to be between 1 and 3 in 100,000 (Borjesson and Pelliccia 2009). This is much higher than statistics reported in a more general population of active individuals (Harmon, Klossner, and Drezner 2011). These data indicate that active people are not immune to cardiovascular events that may result in death.
Causes
The most common cause of sudden cardiac death in the young athlete is hypertrophic cardiomyopathy, which accounts for up to 50% of the cases. Other significant causes of sudden cardiac death in a young athlete are coronary artery anomalies, increased cardiac mass, aortic rupture, myocarditis, and aortic stenosis(Borjesson and Pelliccia 2009).Rare causes include dilated cardiomyopathy, atherosclerotic coronary artery disease, mitral valve prolapse, isolated arrhythmias such as long QT syndrome and Wolff-Parkinson-White syndrome, and arrhythmogenic right ventricular dysplasia (ARVD) (Harmon, Klossner, and Drezner 2011). In the Veneto region of Italy, researchers have found ARVD to be the most common cause of sudden cardiac death in the athlete (Thiene et al. 1988). This research suggests that a specific population may have different genetic subtraits.
In the older athlete, coronary artery disease is by far the most common cause of sudden death. Rarely is sudden death in the older athlete caused by hypertrophic cardiomyopathy, mitral valve prolapse, or acquired valvular conditions (Maron et al. 2014; Nagashima et al. 2003; Semsarian, Sweeting, and Ackerman 2015; Marijon et al. 2015).
Traumatic sudden cardiac death has not captured as much attention because its epidemiology is more difficult to track. However, it is a growing problem that strikes without warning. Between 1996 and 2007, a reported 180 cases of blunt-force death in the United States were attributed to commotio cordis (Maron et al. 2006). Most cases involved children with a mean age of 13, with 95% of the deaths occurring in males (Maron et al. 2013).
Commotio cordis refers to trauma to the chest wall that interrupts the electrical impulse in the heart. If the cardiac rhythm is not promptly normalized, the individual dies. Typically the ribs or sternum is not broken, although some contusions may be found. Research has found that a chest blow occurring during the vulnerable phase of repolarization, just prior to the T-wave peak in the cardiac cycle, can induce ventricular fibrillation (Maron and Estes 2005).
Although children and teenagers with thin chest walls are most vulnerable to commotio cordis (figure 8.6), deaths have been reported in adults. Sports such as baseball, ice hockey, lacrosse, and softball, which have hard projectiles that can strike the chest, have been associated with the greatest number of deaths. Commotio cordis also has occurred in sports such as soccer, football, rugby, and karate, in which the blow came from a soft projectile or a collision. It appears that the timing of the incident, rather than the degree of impact of the object, is the causative factor (Maron and Estes 2005). Commotio cordis is the only significant cause of traumatic sudden cardiac death in athletes.
The type of injury associated with commotio cordis is a blow to the chest wall that interrupts the usual cardiac rhythm.
Red Flags for Traumatic Sudden Cardiac Death
Sports with projectiles that can hit the chest at an inopportune time in the cardiac rhythm cycle have been known to cause commotio cordis in young athletes. These sports include the following: baseball, softball, hockey, lacrosse, soccer, football, karate.
Prevention
Because death can be the outcome, prevention has become the focus of attention for commotio cordis. Changes in practice have ranged from protective padding to softer balls that are used in Little League and softball. Because this may not completely resolve the problem, another solution is defibrillation in conjunction with cardiopulmonary resuscitation (CPR). Defibrillation interrupts the heart rhythm so the heart can "reboot" into a normal rhythm.
The American Heart Association estimates that communities with comprehensive CPR and automated external defibrillator (AED) training achieve 40% survival rates for cardiac arrest victims. If defibrillation is performed within 3 min, the likelihood of survival is high. For every minute of delay the chance of survival drops by as much as 10% (American Heart Association 2013).
The advent of the AED has provided greater public access to life-saving technology. These devices can be operated by trained laypeople and are increasingly affordable in all sectors. The AED is portable, rechargeable, simple to operate, and easy to maintain. The American Red Cross, American Heart Association, and National Safety Council offer AED certification courses in addition to CPR courses for the lay public. The NCAA Sports Medicine Guidelines require planned access to an AED and mandating CPR and first aid certifications for all who work with athlete practices, competition, and skill sessions. Athletic trainers are required to maintain certification in emergency cardiac care, including AED use. They need to have ready access to an AED in order to provide rapid cardiac assessment and care to those in fibrillation. Athletes who suffer a sudden collapse and have agonal or gasping breathing should be treated because they are suffering from a cardiac event (Casa et al. 2012; Solberg et al. 2015). An AED should be applied as soon as possible for heart rhythm analysis and possible defibrillation.
Clinical Tips
Potential Causes of Sudden Death
Sudden collapse in athletes could be caused by heatstroke, a cardiac event, sickle cell collapse, or injury. Understanding the presentation of each will facilitate rapid response and the appropriate disposition.
Emergency Planning
Every athletic site should have planned access to an AED, an emergency medical service (EMS), and an established emergency action plan (EAP), as well as medical personnel trained to respond to sudden collapse.
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How to identify celiac disease
Celiac disease is an autoimmune disorder that affects the gastrointestinal tract and is thought to be triggered by dietary gluten in affected individuals. The disease is characterized by chronic inflammation of the small intestinal mucosa, which leads to atrophy of the small intestinal villi and subsequent malabsorption (Pelkowski and Viera 2014).
Celiac disease is an autoimmune disorder that affects the gastrointestinal tract and is thought to be triggered by dietary gluten in affected individuals. The disease is characterized by chronic inflammation of the small intestinal mucosa, which leads to atrophy of the small intestinal villi and subsequent malabsorption (Pelkowski and Viera 2014). Celiac disease affects approximately 1% of the U.S. population and typically occurs in persons of European ancestry as well as persons of Middle Eastern, Indian, South American, and North African descent. It is two to three times more common in women. Celiac disease is not a food allergy.
Signs and Symptoms
Typical presentation includes chronic diarrhea with cramping and gas pains. Patients often have weight loss, or in the adolescent, delayed onset of growth or puberty. A history of nervousness and/or depression is often present, as is a family history of autoimmune disease. Other complaints may include bone or joint pain, migraines, weakness, fatigue, and anemia (Volta et al. 2015; Vivas et al. 2015; Byrne and Feighery 2015; Mancini, Trojian, and Mancini 2011). Physical examination is often normal, but the patient may present with abdominal distension or dermatitis herpetiformis.
Referral and Diagnostic Tests
Lab tests are performed for differentiating celiac disease and to rule out more common diseases. These include a basic metabolic panel, CBC (iron deficiency), TSH (thyroid disease), vitamin D level, and allergy testing. If celiac disease is suspected from history and physical exam, the initial serologic test is a tissue transglutaminase (tTG) antibody level. This antibody is found in every tissue in the body and acts to join proteins together. In people with celiac disease, tTG activates specific immune cells and triggers the inflammatory response that leads to atrophy of the villi in the small intestine (Mancini, Trojian, and Mancini 2011). The diagnosis is often confirmed with repeat blood tests after 4 wk on a gluten-free diet. Endoscopy with biopsies of the duodenal mucosa may be necessary to confirm the diagnosis. Celiac disease should be differentiated from GERD, pancreatic insufficiency, Crohn's disease, or other inflammatory bowel diseases.
Treatment and Return to Participation
The general treatment is to remove gluten from the diet. The patient can substitute rice, corn, and soybean flour for products that contain gluten. Periodic blood tests are performed to measure the levels of the antibodies. The levels will normalize with gluten abstinence. Abstinence will be required for life because the immune response to gluten will recur if gluten is consumed again. Usually no medications are prescribed for celiac disease, but athletes may benefit from iron, vitamin, and calcium supplements. The most difficult aspect for the athlete with celiac disease is the dietary restrictions while traveling with the team or with set team meals. The athletic trainer may need to check on the gluten-free status of many of the standard gluten-containing products provided by the athletic department, such as energy drinks or meal replacement bars (Mancini, Trojian, and Mancini 2011).
Condition Highlight
Gluten Sensitivity and Intolerance
Over the past 10 yr, the number of people choosing a gluten-free diet (GFD) is much higher than the projected number of celiac disease patients (Lis et al. 2015). This has fueled a global market of gluten-free products and highlights several conditions related to the ingestion of gluten. There are three main forms of gluten reactions: allergic, autoimmune (celiac disease), and immune-mediated conditions (gluten sensitivity) (Sapone et al. 2012). Wheat allergy is an adverse reaction to wheat proteins with onset in minutes to hours after gluten ingestion. It may affect the skin, GI tract, or respiratory tract. Celiac disease or other autoimmune gluten disorders generally present months to years after gluten exposure. There is a third condition where some people experience distress from eating gluten-containing products and show improvement with a GFD. It is distinct from celiac disease and wheat allergies (Vivas et al. 2015). Gluten sensitivity cannot be distinguished clinically; serology tests need to be conducted. Patients with GI discomfort or distress following gluten ingestion should be referred for a follow-up blood test and immune-allergy tests.
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Addressing mental health issues in the athlete
Everyone has symptoms of some type of mental health issue at some time in life when one or several stressors overwhelm the person’s ability to self-regulate or repair. The symptoms are usually, and arbitrarily, labeled either physical or mental.
Everyone has symptoms of some type of mental health issue at some time in life when one or several stressors overwhelm the person's ability to self-regulate or repair. The symptoms are usually, and arbitrarily, labeled either physical or mental. This artificial dichotomy usually does not align with the affected person's reality. Rarely is an athlete with a strained hamstring not also worried about the injury or distressed by the pain. Similarly, the most common initial warning signs of depression are the physical symptoms of tension, restlessness, and disturbed sleep, energy, and appetite. This is because we have overlapping systems of mind, body, spirit, and relationships, each integrally connected to the others. When the homeostasis of one or more systems is disrupted, people instinctively try to correct the problem regardless of its origin. In the mental health domain, signs of distress are emotional, mental, behavioral, and physical.
Framework for Understanding Mental Health
In almost all situations, a variety of overlapping factors contribute to symptom development. The biopsychosocial - spiritual model (BPSS) is a framework for understanding the person's responses in a given situation and the development of symptoms. Symptom etiology may be conceptualized as a pie. Figure 17.1 shows how these various factors overlap and contribute to well-being. In a given person, the various pieces of the BPSS pie may be larger or smaller at any one time. The relative sizes of the pieces greatly influence the person's symptoms and ability to adapt.
The biopsychosocial - spiritual model is a framework for understanding a person's responses in a given situation and the development of symptoms.
For example, two runners may have identical injuries, but the impact of the injury and the course of rehabilitation in these two athletes will usually differ. The amount of pain they have, as well as the length of time until they are ready to compete again, will be influenced not only by the difference in respective levels of physical conditioning and injury history but also by other physical and emotional conditions such as pain tolerance, attitude, perception of the problem, and its implications for life. The situation may also be affected by personality and temperament issues, variable resources for coping, and so on. Another example involves two wrestlers who seem to be equally competitive, but wrestler A, in a struggle to make or maintain weight, develops more obviously disordered eating patterns than wrestler B. Perhaps wrestler A has a family history of obesity and is genetically predisposed toward weight gain more than the other; temperamentally, wrestler A may tend to think more negatively about life challenges, become somewhat self-defeating in the face of adversity, and find emotional comfort in food and the process of eating. Often a variety of factors will help to explain the development of clinically significant problems.
This interplay of variables is the same for athletes as it is for others who are physically active, regardless of whether the symptoms of an injury or condition are physical or emotional. Whereas one athlete may become depressed, another's symptoms may include anxiety or outbursts of anger and physical aggression. Sometimes one piece of the BPSS pie is so big that it seems to account for virtually the whole reason that someone is symptomatic (e.g., the chemical disequilibrium that comes with bipolar disorder). For this reason, it is a good practice to regularly consider the possibility that an organic cause may be the culprit and refer the person for a medical evaluation.
The treatments that have proven effective for the problems discussed in this chapter are based on the same BPSS approach as the assessment and diagnosis. Different strategies can be useful, depending on the biopsychosocial - spiritual components that are implicated in the assessment process. Practitioners often recommend treatment plans based on their assessment and experience, and then these are negotiated with the patient or family members according to personal preferences. The treatment may be offered on either an inpatient or, more commonly, an outpatient basis.
Treatment may also involve the collaboration of a variety of treatment professionals. For example, eating disorder treatment often involves a physician, a registered dietitian, and a psychotherapist. This will be determined based on the severity of symptoms, the difficulty the athlete has in making changes, the amount of support the athlete has, and other resources that affect care, including financial concerns or insurance benefits. The important first step in treatment is accurate assessment followed by clear and well-timed communication and education with the athlete and family. The athletic trainer can play a valuable role here because people are much more likely to engage in treatment or some type of change process if they become convinced that there is a problem, they know what it is, and they know that something can be done about it. This is because most people will want to know what is going on with themselves, how they "got it," and what they can do to "get rid of it" or at least cope more effectively. Additional treatment recommendations specific to various clinical problems are listed in subsequent sections.
Implications for Participation in Athletics
Early identification and treatment are very helpful in preventing problems from worsening, but sometimes the stigma still associated with mental health conditions prevents people from recognizing these problems in themselves or others. In those cases, functioning in one or more areas of life can be affected, sometimes severely. Restricting participation in a sport, if necessary, will depend on the assessment of the athlete's level of functioning by the athlete, the coach, and the athletic trainer. Initially, while the medication dosage is being adjusted, the athlete could experience adverse effects that could affect participation or performance, such as nausea, headache, sedation, disturbed balance, or overstimulation. The National Collegiate Athletic Association (NCAA) has no restrictions on the medications typically used to treat these conditions except for pemoline, a medication prescribed to treat ADHD (National Collegiate Athletic Association 2015).
The last general point to be made is that some people experiencing psychological or substance use disorders may consider suicide or become homicidal. Most health care professionals or other professionals are required by law or by a professional code of ethics to report to the authorities if a patient is a danger to self or others. Athletic trainers, too, may encounter an athlete with depression, panic disorder, or substance abuse who is considering suicide or harming someone else. The athletic trainer must seek immediate consultation if in doubt about the need to report. An assessment of whether one is suicidal or homicidal includes determining whether the person has a specific plan, the means to carry it out, the intention to carry it out, and how lethal the plan is. Those with a personal or family history of this type of ideation or action or whose judgment is impaired, perhaps through the use of substances, are more at risk to follow through.
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Identifying Exercise-Induced Bronchospasm
The terms EIA and EIB are often used interchangeably, but EIB specifically denotes the reduction in lung function that occurs after a standardized exercise test (Carver 2009). More recently, the term exercise-induced bronchoconstriction has been introduced as actual spasm of the airways does not always occur.
The terms exercise-induced asthma (EIA) and exercise-induced bronchoconstriction (EIB) are often used interchangeably, but EIB specifically denotes the reduction in lung function that occurs after a standardized exercise test (Carver 2009). More recently, the term exercise-induced bronchoconstriction has been introduced as actual spasm of the airways does not always occur. Some clinicians use EIA to describe individuals with known asthma who have bronchoconstriction during exercise. However, some use EIA to describe patients who have bronchoconstriction only during exercise, and they use EIB to describe patients with asthma who have bronchoconstriction with exercise. Generally, EIB is used to indicate bronchospasm with decreased pulmonary function testing following exercise, and EIA is used to indicate those patients with asthma difficulties associated with exercise.
Symptoms of EIB usually occur 10 to 15 min after the onset of strenuous exercise and are defined by a fall in FEV1 of 15% or more during exercise spirometry. EIB is more common in winter sport athletes who compete in cold ambient temperatures (Carey, Aase, and Pliego 2010).
Signs and Symptoms
EIB should be suspected in any athlete who complains of shortness of breath, dyspnea, cough, chest congestion, or tightness with exertion. These symptoms usually occur during strenuous exercise and peak about 5 to 10 min after exercise (Hull 2012; Krafczyk and Asplund 2011; Simpson, Romer, and Kippelen 2015). Other subtle clues might be a dry cough that develops after practice or exercise (i.e., locker-room cough) or simply unusual fatigue compared with similarly trained athletes. Athletes will often complain that they feel out of shape despite regular training. Self-reported symptoms have been shown to be poor predictors of EIB because other conditions can cause similar symptoms. Symptoms alone should not be used to diagnose EIB.
In athletes suspected of having EIB, other etiologies, such as acute sinusitis, otitis media (middle ear infection), bronchitis, or even pneumonia, need to be excluded, particularly in the context of other constitutional symptoms, such as fever, chills, or night sweats. If fatigue is the only presenting symptom, deconditioning may also be a cause. In addition, environmental allergies can account for many of the nonspecific symptoms that mimic EIB (Backer 2010; Hull et al. 2012; Stack and Hakemi 2011). More serious cardiac causes, such as arrhythmias and pericarditis, might also need to be excluded. Another important differential is exercise-induced laryngeal obstruction (EILO), where the wheezing and dyspnea are caused by transient obstruction of the upper airways during exercise (Nielsen 2013; Backer 2010).
Referral and Diagnostic Tests
The physical examination is usually normal. Some athletes with EIB may experience symptoms that develop several hours after exercise. This late-phase response is due to the activity of inflammatory mediators. Most commonly, a bronchial provocation challenge is used to determine the diagnosis of EIB (Parsons et al. 2011; Hayden et al. 2011; Morris 2010). Figure 7.9 shows a decision tree commonly used for the diagnosis of EIB. Alternatively, many physicians choose to just evaluate the patient's response to an empirical trial of a ß-agonist medication before exercise.
Decision tree for the diagnosis of exercise-induced bronchoconstriction (EIB).
Treatment and Return to Participation
The treatment of choice in EIB is an inhaled ß2-agonist from a metered-dose inhaler (e.g., albuterol) taken 15 to 30 min before the onset of exercise. An athlete who has asthma symptoms outside the exercise setting or who is using a ß2-agonist more than three times per week should be treated with a regular inhaled corticosteroid. Here is how to properly use an inhaler:
- Remove dust cap and shake the inhaler system before each use.
- Inspect mouthpiece for contamination or foreign objects.
- Breathe out through the mouth, exhaling as completely as possible.
- Hold the inhaler system upright with mouthpiece in mouth and lips closed tightly around mouthpiece.
- Breathe in slowly while pressing down on the metal cartridge.
- Hold breath as long as possible.
- Release pressure while still holding breath.
- Remove mouthpiece.
- Wait for the container to repressurize, shake, and then repeat steps 3 through 8 when more than one inhalation is prescribed.
- Rinse mouth with water after prescribed number of inhalations.
- Clean the inhaler system every few days by removing metal cartridge and rinsing the plastic inhaler and cap with running warm water. Replace cartridge and cap.
Emerging studies show promise using long-acting ß2-agonists such as salmeterol and leukotriene inhibitors such as montelukast (Singulair) (Parsons 2010). Other nonpharmacological strategies include pre - warm-up bursts of physical activity at 80% to 90% of the individual's maximal workload to induce a refractory period that lasts up to 3 h after the initial attack of EIB (Hull et al. 2012; Millward et al. 2009; Boulet, Hancox, and Fitch 2010). Strategies to humidify inspired air and dietary interventions may also prove to be beneficial (Carey, Aase, and Pliego 2010; Bussotti, Di Marco, and Marchese 2014).
For an athlete experiencing a severe asthma attack or when an inhaler is ineffective, a nebulizer may be used. A nebulizer, also known as an atomizer, is a machine that vaporizes liquid medication into a fine mist to be inhaled into the lungs via a mouthpiece or mask. Although studies have shown that both inhalers and nebulizers tend to be equally effective in delivering medications, nebulizers are preferred for use in more serious rescue situations when the patient is experiencing a severe asthma attack. Nebulizers can administer a higher dose of medication, but inhalers are easier to use, preferred for their portability and low cost, and good for everyday use. Medications typically administered with a nebulizer include albuterol and ipratropium (Atrovent).
Athletes with controlled EIB need not be excluded or discouraged from participating in sports. Effective strategies, both pharmacological and nonpharmacological, exist that can allow an athlete to compete even at an elite level.
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Causes of Sudden Cardiac Death in Athletes
Death by sudden cardiac arrest (SCA) is a rare event in the young athlete. In the United States, elite athletes are viewed as near invincible because of their incredible physical feats.
Death by sudden cardiac arrest (SCA) is a rare event in the young athlete. In the United States, elite athletes are viewed as near invincible because of their incredible physical feats. Nevertheless, it is reported that the rate of collegiate athlete death due to SCA is higher than that of high school athletes, with a suspected 110 SCA deaths annually in the United States among young athletes (Casa et al. 2012). Any time a tragedy of this proportion occurs, the public reacts with disbelief, and medical knowledge is called into question. Studies that have tracked these deaths during sports used the National Federation of State High School Associations (NFHS), the National Collegiate Athletic Association (NCAA) governing organizations, and state and federally funded research groups for data collection, such as the National Center for Catastrophic Sport Injury Research (NCCSIR), based in Chapel Hill, North Carolina. Approximately 90% of the data collected involved male athletes, with an equal distribution between Caucasians and African-Americans (Borjesson and Pelliccia 2009). According to the NCCSIR, there were 10 indirect (due to exertion) fatalities in middle school through college football athletes in 2014, and six were attributed to a cardiac event (Kucera et al. 2015). An additional five football athletes died of suspected cardiac conditions due to nonexertional factors in the same year (Kucera et al. 2015). Sudden death cases in young women are rare, and the most common cause of sudden cardiac death was congenital cardiac disease.
The prevalence of sudden cardiac death in young athletes (those less than 35-year-old) is estimated to be between 1 and 3 in 100,000 (Borjesson and Pelliccia 2009). This is much higher than statistics reported in a more general population of active individuals (Harmon, Klossner, and Drezner 2011). These data indicate that active people are not immune to cardiovascular events that may result in death.
Causes
The most common cause of sudden cardiac death in the young athlete is hypertrophic cardiomyopathy, which accounts for up to 50% of the cases. Other significant causes of sudden cardiac death in a young athlete are coronary artery anomalies, increased cardiac mass, aortic rupture, myocarditis, and aortic stenosis(Borjesson and Pelliccia 2009).Rare causes include dilated cardiomyopathy, atherosclerotic coronary artery disease, mitral valve prolapse, isolated arrhythmias such as long QT syndrome and Wolff-Parkinson-White syndrome, and arrhythmogenic right ventricular dysplasia (ARVD) (Harmon, Klossner, and Drezner 2011). In the Veneto region of Italy, researchers have found ARVD to be the most common cause of sudden cardiac death in the athlete (Thiene et al. 1988). This research suggests that a specific population may have different genetic subtraits.
In the older athlete, coronary artery disease is by far the most common cause of sudden death. Rarely is sudden death in the older athlete caused by hypertrophic cardiomyopathy, mitral valve prolapse, or acquired valvular conditions (Maron et al. 2014; Nagashima et al. 2003; Semsarian, Sweeting, and Ackerman 2015; Marijon et al. 2015).
Traumatic sudden cardiac death has not captured as much attention because its epidemiology is more difficult to track. However, it is a growing problem that strikes without warning. Between 1996 and 2007, a reported 180 cases of blunt-force death in the United States were attributed to commotio cordis (Maron et al. 2006). Most cases involved children with a mean age of 13, with 95% of the deaths occurring in males (Maron et al. 2013).
Commotio cordis refers to trauma to the chest wall that interrupts the electrical impulse in the heart. If the cardiac rhythm is not promptly normalized, the individual dies. Typically the ribs or sternum is not broken, although some contusions may be found. Research has found that a chest blow occurring during the vulnerable phase of repolarization, just prior to the T-wave peak in the cardiac cycle, can induce ventricular fibrillation (Maron and Estes 2005).
Although children and teenagers with thin chest walls are most vulnerable to commotio cordis (figure 8.6), deaths have been reported in adults. Sports such as baseball, ice hockey, lacrosse, and softball, which have hard projectiles that can strike the chest, have been associated with the greatest number of deaths. Commotio cordis also has occurred in sports such as soccer, football, rugby, and karate, in which the blow came from a soft projectile or a collision. It appears that the timing of the incident, rather than the degree of impact of the object, is the causative factor (Maron and Estes 2005). Commotio cordis is the only significant cause of traumatic sudden cardiac death in athletes.
The type of injury associated with commotio cordis is a blow to the chest wall that interrupts the usual cardiac rhythm.
Red Flags for Traumatic Sudden Cardiac Death
Sports with projectiles that can hit the chest at an inopportune time in the cardiac rhythm cycle have been known to cause commotio cordis in young athletes. These sports include the following: baseball, softball, hockey, lacrosse, soccer, football, karate.
Prevention
Because death can be the outcome, prevention has become the focus of attention for commotio cordis. Changes in practice have ranged from protective padding to softer balls that are used in Little League and softball. Because this may not completely resolve the problem, another solution is defibrillation in conjunction with cardiopulmonary resuscitation (CPR). Defibrillation interrupts the heart rhythm so the heart can "reboot" into a normal rhythm.
The American Heart Association estimates that communities with comprehensive CPR and automated external defibrillator (AED) training achieve 40% survival rates for cardiac arrest victims. If defibrillation is performed within 3 min, the likelihood of survival is high. For every minute of delay the chance of survival drops by as much as 10% (American Heart Association 2013).
The advent of the AED has provided greater public access to life-saving technology. These devices can be operated by trained laypeople and are increasingly affordable in all sectors. The AED is portable, rechargeable, simple to operate, and easy to maintain. The American Red Cross, American Heart Association, and National Safety Council offer AED certification courses in addition to CPR courses for the lay public. The NCAA Sports Medicine Guidelines require planned access to an AED and mandating CPR and first aid certifications for all who work with athlete practices, competition, and skill sessions. Athletic trainers are required to maintain certification in emergency cardiac care, including AED use. They need to have ready access to an AED in order to provide rapid cardiac assessment and care to those in fibrillation. Athletes who suffer a sudden collapse and have agonal or gasping breathing should be treated because they are suffering from a cardiac event (Casa et al. 2012; Solberg et al. 2015). An AED should be applied as soon as possible for heart rhythm analysis and possible defibrillation.
Clinical Tips
Potential Causes of Sudden Death
Sudden collapse in athletes could be caused by heatstroke, a cardiac event, sickle cell collapse, or injury. Understanding the presentation of each will facilitate rapid response and the appropriate disposition.
Emergency Planning
Every athletic site should have planned access to an AED, an emergency medical service (EMS), and an established emergency action plan (EAP), as well as medical personnel trained to respond to sudden collapse.
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How to identify celiac disease
Celiac disease is an autoimmune disorder that affects the gastrointestinal tract and is thought to be triggered by dietary gluten in affected individuals. The disease is characterized by chronic inflammation of the small intestinal mucosa, which leads to atrophy of the small intestinal villi and subsequent malabsorption (Pelkowski and Viera 2014).
Celiac disease is an autoimmune disorder that affects the gastrointestinal tract and is thought to be triggered by dietary gluten in affected individuals. The disease is characterized by chronic inflammation of the small intestinal mucosa, which leads to atrophy of the small intestinal villi and subsequent malabsorption (Pelkowski and Viera 2014). Celiac disease affects approximately 1% of the U.S. population and typically occurs in persons of European ancestry as well as persons of Middle Eastern, Indian, South American, and North African descent. It is two to three times more common in women. Celiac disease is not a food allergy.
Signs and Symptoms
Typical presentation includes chronic diarrhea with cramping and gas pains. Patients often have weight loss, or in the adolescent, delayed onset of growth or puberty. A history of nervousness and/or depression is often present, as is a family history of autoimmune disease. Other complaints may include bone or joint pain, migraines, weakness, fatigue, and anemia (Volta et al. 2015; Vivas et al. 2015; Byrne and Feighery 2015; Mancini, Trojian, and Mancini 2011). Physical examination is often normal, but the patient may present with abdominal distension or dermatitis herpetiformis.
Referral and Diagnostic Tests
Lab tests are performed for differentiating celiac disease and to rule out more common diseases. These include a basic metabolic panel, CBC (iron deficiency), TSH (thyroid disease), vitamin D level, and allergy testing. If celiac disease is suspected from history and physical exam, the initial serologic test is a tissue transglutaminase (tTG) antibody level. This antibody is found in every tissue in the body and acts to join proteins together. In people with celiac disease, tTG activates specific immune cells and triggers the inflammatory response that leads to atrophy of the villi in the small intestine (Mancini, Trojian, and Mancini 2011). The diagnosis is often confirmed with repeat blood tests after 4 wk on a gluten-free diet. Endoscopy with biopsies of the duodenal mucosa may be necessary to confirm the diagnosis. Celiac disease should be differentiated from GERD, pancreatic insufficiency, Crohn's disease, or other inflammatory bowel diseases.
Treatment and Return to Participation
The general treatment is to remove gluten from the diet. The patient can substitute rice, corn, and soybean flour for products that contain gluten. Periodic blood tests are performed to measure the levels of the antibodies. The levels will normalize with gluten abstinence. Abstinence will be required for life because the immune response to gluten will recur if gluten is consumed again. Usually no medications are prescribed for celiac disease, but athletes may benefit from iron, vitamin, and calcium supplements. The most difficult aspect for the athlete with celiac disease is the dietary restrictions while traveling with the team or with set team meals. The athletic trainer may need to check on the gluten-free status of many of the standard gluten-containing products provided by the athletic department, such as energy drinks or meal replacement bars (Mancini, Trojian, and Mancini 2011).
Condition Highlight
Gluten Sensitivity and Intolerance
Over the past 10 yr, the number of people choosing a gluten-free diet (GFD) is much higher than the projected number of celiac disease patients (Lis et al. 2015). This has fueled a global market of gluten-free products and highlights several conditions related to the ingestion of gluten. There are three main forms of gluten reactions: allergic, autoimmune (celiac disease), and immune-mediated conditions (gluten sensitivity) (Sapone et al. 2012). Wheat allergy is an adverse reaction to wheat proteins with onset in minutes to hours after gluten ingestion. It may affect the skin, GI tract, or respiratory tract. Celiac disease or other autoimmune gluten disorders generally present months to years after gluten exposure. There is a third condition where some people experience distress from eating gluten-containing products and show improvement with a GFD. It is distinct from celiac disease and wheat allergies (Vivas et al. 2015). Gluten sensitivity cannot be distinguished clinically; serology tests need to be conducted. Patients with GI discomfort or distress following gluten ingestion should be referred for a follow-up blood test and immune-allergy tests.
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Addressing mental health issues in the athlete
Everyone has symptoms of some type of mental health issue at some time in life when one or several stressors overwhelm the person’s ability to self-regulate or repair. The symptoms are usually, and arbitrarily, labeled either physical or mental.
Everyone has symptoms of some type of mental health issue at some time in life when one or several stressors overwhelm the person's ability to self-regulate or repair. The symptoms are usually, and arbitrarily, labeled either physical or mental. This artificial dichotomy usually does not align with the affected person's reality. Rarely is an athlete with a strained hamstring not also worried about the injury or distressed by the pain. Similarly, the most common initial warning signs of depression are the physical symptoms of tension, restlessness, and disturbed sleep, energy, and appetite. This is because we have overlapping systems of mind, body, spirit, and relationships, each integrally connected to the others. When the homeostasis of one or more systems is disrupted, people instinctively try to correct the problem regardless of its origin. In the mental health domain, signs of distress are emotional, mental, behavioral, and physical.
Framework for Understanding Mental Health
In almost all situations, a variety of overlapping factors contribute to symptom development. The biopsychosocial - spiritual model (BPSS) is a framework for understanding the person's responses in a given situation and the development of symptoms. Symptom etiology may be conceptualized as a pie. Figure 17.1 shows how these various factors overlap and contribute to well-being. In a given person, the various pieces of the BPSS pie may be larger or smaller at any one time. The relative sizes of the pieces greatly influence the person's symptoms and ability to adapt.
The biopsychosocial - spiritual model is a framework for understanding a person's responses in a given situation and the development of symptoms.
For example, two runners may have identical injuries, but the impact of the injury and the course of rehabilitation in these two athletes will usually differ. The amount of pain they have, as well as the length of time until they are ready to compete again, will be influenced not only by the difference in respective levels of physical conditioning and injury history but also by other physical and emotional conditions such as pain tolerance, attitude, perception of the problem, and its implications for life. The situation may also be affected by personality and temperament issues, variable resources for coping, and so on. Another example involves two wrestlers who seem to be equally competitive, but wrestler A, in a struggle to make or maintain weight, develops more obviously disordered eating patterns than wrestler B. Perhaps wrestler A has a family history of obesity and is genetically predisposed toward weight gain more than the other; temperamentally, wrestler A may tend to think more negatively about life challenges, become somewhat self-defeating in the face of adversity, and find emotional comfort in food and the process of eating. Often a variety of factors will help to explain the development of clinically significant problems.
This interplay of variables is the same for athletes as it is for others who are physically active, regardless of whether the symptoms of an injury or condition are physical or emotional. Whereas one athlete may become depressed, another's symptoms may include anxiety or outbursts of anger and physical aggression. Sometimes one piece of the BPSS pie is so big that it seems to account for virtually the whole reason that someone is symptomatic (e.g., the chemical disequilibrium that comes with bipolar disorder). For this reason, it is a good practice to regularly consider the possibility that an organic cause may be the culprit and refer the person for a medical evaluation.
The treatments that have proven effective for the problems discussed in this chapter are based on the same BPSS approach as the assessment and diagnosis. Different strategies can be useful, depending on the biopsychosocial - spiritual components that are implicated in the assessment process. Practitioners often recommend treatment plans based on their assessment and experience, and then these are negotiated with the patient or family members according to personal preferences. The treatment may be offered on either an inpatient or, more commonly, an outpatient basis.
Treatment may also involve the collaboration of a variety of treatment professionals. For example, eating disorder treatment often involves a physician, a registered dietitian, and a psychotherapist. This will be determined based on the severity of symptoms, the difficulty the athlete has in making changes, the amount of support the athlete has, and other resources that affect care, including financial concerns or insurance benefits. The important first step in treatment is accurate assessment followed by clear and well-timed communication and education with the athlete and family. The athletic trainer can play a valuable role here because people are much more likely to engage in treatment or some type of change process if they become convinced that there is a problem, they know what it is, and they know that something can be done about it. This is because most people will want to know what is going on with themselves, how they "got it," and what they can do to "get rid of it" or at least cope more effectively. Additional treatment recommendations specific to various clinical problems are listed in subsequent sections.
Implications for Participation in Athletics
Early identification and treatment are very helpful in preventing problems from worsening, but sometimes the stigma still associated with mental health conditions prevents people from recognizing these problems in themselves or others. In those cases, functioning in one or more areas of life can be affected, sometimes severely. Restricting participation in a sport, if necessary, will depend on the assessment of the athlete's level of functioning by the athlete, the coach, and the athletic trainer. Initially, while the medication dosage is being adjusted, the athlete could experience adverse effects that could affect participation or performance, such as nausea, headache, sedation, disturbed balance, or overstimulation. The National Collegiate Athletic Association (NCAA) has no restrictions on the medications typically used to treat these conditions except for pemoline, a medication prescribed to treat ADHD (National Collegiate Athletic Association 2015).
The last general point to be made is that some people experiencing psychological or substance use disorders may consider suicide or become homicidal. Most health care professionals or other professionals are required by law or by a professional code of ethics to report to the authorities if a patient is a danger to self or others. Athletic trainers, too, may encounter an athlete with depression, panic disorder, or substance abuse who is considering suicide or harming someone else. The athletic trainer must seek immediate consultation if in doubt about the need to report. An assessment of whether one is suicidal or homicidal includes determining whether the person has a specific plan, the means to carry it out, the intention to carry it out, and how lethal the plan is. Those with a personal or family history of this type of ideation or action or whose judgment is impaired, perhaps through the use of substances, are more at risk to follow through.
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Identifying Exercise-Induced Bronchospasm
The terms EIA and EIB are often used interchangeably, but EIB specifically denotes the reduction in lung function that occurs after a standardized exercise test (Carver 2009). More recently, the term exercise-induced bronchoconstriction has been introduced as actual spasm of the airways does not always occur.
The terms exercise-induced asthma (EIA) and exercise-induced bronchoconstriction (EIB) are often used interchangeably, but EIB specifically denotes the reduction in lung function that occurs after a standardized exercise test (Carver 2009). More recently, the term exercise-induced bronchoconstriction has been introduced as actual spasm of the airways does not always occur. Some clinicians use EIA to describe individuals with known asthma who have bronchoconstriction during exercise. However, some use EIA to describe patients who have bronchoconstriction only during exercise, and they use EIB to describe patients with asthma who have bronchoconstriction with exercise. Generally, EIB is used to indicate bronchospasm with decreased pulmonary function testing following exercise, and EIA is used to indicate those patients with asthma difficulties associated with exercise.
Symptoms of EIB usually occur 10 to 15 min after the onset of strenuous exercise and are defined by a fall in FEV1 of 15% or more during exercise spirometry. EIB is more common in winter sport athletes who compete in cold ambient temperatures (Carey, Aase, and Pliego 2010).
Signs and Symptoms
EIB should be suspected in any athlete who complains of shortness of breath, dyspnea, cough, chest congestion, or tightness with exertion. These symptoms usually occur during strenuous exercise and peak about 5 to 10 min after exercise (Hull 2012; Krafczyk and Asplund 2011; Simpson, Romer, and Kippelen 2015). Other subtle clues might be a dry cough that develops after practice or exercise (i.e., locker-room cough) or simply unusual fatigue compared with similarly trained athletes. Athletes will often complain that they feel out of shape despite regular training. Self-reported symptoms have been shown to be poor predictors of EIB because other conditions can cause similar symptoms. Symptoms alone should not be used to diagnose EIB.
In athletes suspected of having EIB, other etiologies, such as acute sinusitis, otitis media (middle ear infection), bronchitis, or even pneumonia, need to be excluded, particularly in the context of other constitutional symptoms, such as fever, chills, or night sweats. If fatigue is the only presenting symptom, deconditioning may also be a cause. In addition, environmental allergies can account for many of the nonspecific symptoms that mimic EIB (Backer 2010; Hull et al. 2012; Stack and Hakemi 2011). More serious cardiac causes, such as arrhythmias and pericarditis, might also need to be excluded. Another important differential is exercise-induced laryngeal obstruction (EILO), where the wheezing and dyspnea are caused by transient obstruction of the upper airways during exercise (Nielsen 2013; Backer 2010).
Referral and Diagnostic Tests
The physical examination is usually normal. Some athletes with EIB may experience symptoms that develop several hours after exercise. This late-phase response is due to the activity of inflammatory mediators. Most commonly, a bronchial provocation challenge is used to determine the diagnosis of EIB (Parsons et al. 2011; Hayden et al. 2011; Morris 2010). Figure 7.9 shows a decision tree commonly used for the diagnosis of EIB. Alternatively, many physicians choose to just evaluate the patient's response to an empirical trial of a ß-agonist medication before exercise.
Decision tree for the diagnosis of exercise-induced bronchoconstriction (EIB).
Treatment and Return to Participation
The treatment of choice in EIB is an inhaled ß2-agonist from a metered-dose inhaler (e.g., albuterol) taken 15 to 30 min before the onset of exercise. An athlete who has asthma symptoms outside the exercise setting or who is using a ß2-agonist more than three times per week should be treated with a regular inhaled corticosteroid. Here is how to properly use an inhaler:
- Remove dust cap and shake the inhaler system before each use.
- Inspect mouthpiece for contamination or foreign objects.
- Breathe out through the mouth, exhaling as completely as possible.
- Hold the inhaler system upright with mouthpiece in mouth and lips closed tightly around mouthpiece.
- Breathe in slowly while pressing down on the metal cartridge.
- Hold breath as long as possible.
- Release pressure while still holding breath.
- Remove mouthpiece.
- Wait for the container to repressurize, shake, and then repeat steps 3 through 8 when more than one inhalation is prescribed.
- Rinse mouth with water after prescribed number of inhalations.
- Clean the inhaler system every few days by removing metal cartridge and rinsing the plastic inhaler and cap with running warm water. Replace cartridge and cap.
Emerging studies show promise using long-acting ß2-agonists such as salmeterol and leukotriene inhibitors such as montelukast (Singulair) (Parsons 2010). Other nonpharmacological strategies include pre - warm-up bursts of physical activity at 80% to 90% of the individual's maximal workload to induce a refractory period that lasts up to 3 h after the initial attack of EIB (Hull et al. 2012; Millward et al. 2009; Boulet, Hancox, and Fitch 2010). Strategies to humidify inspired air and dietary interventions may also prove to be beneficial (Carey, Aase, and Pliego 2010; Bussotti, Di Marco, and Marchese 2014).
For an athlete experiencing a severe asthma attack or when an inhaler is ineffective, a nebulizer may be used. A nebulizer, also known as an atomizer, is a machine that vaporizes liquid medication into a fine mist to be inhaled into the lungs via a mouthpiece or mask. Although studies have shown that both inhalers and nebulizers tend to be equally effective in delivering medications, nebulizers are preferred for use in more serious rescue situations when the patient is experiencing a severe asthma attack. Nebulizers can administer a higher dose of medication, but inhalers are easier to use, preferred for their portability and low cost, and good for everyday use. Medications typically administered with a nebulizer include albuterol and ipratropium (Atrovent).
Athletes with controlled EIB need not be excluded or discouraged from participating in sports. Effective strategies, both pharmacological and nonpharmacological, exist that can allow an athlete to compete even at an elite level.
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Causes of Sudden Cardiac Death in Athletes
Death by sudden cardiac arrest (SCA) is a rare event in the young athlete. In the United States, elite athletes are viewed as near invincible because of their incredible physical feats.
Death by sudden cardiac arrest (SCA) is a rare event in the young athlete. In the United States, elite athletes are viewed as near invincible because of their incredible physical feats. Nevertheless, it is reported that the rate of collegiate athlete death due to SCA is higher than that of high school athletes, with a suspected 110 SCA deaths annually in the United States among young athletes (Casa et al. 2012). Any time a tragedy of this proportion occurs, the public reacts with disbelief, and medical knowledge is called into question. Studies that have tracked these deaths during sports used the National Federation of State High School Associations (NFHS), the National Collegiate Athletic Association (NCAA) governing organizations, and state and federally funded research groups for data collection, such as the National Center for Catastrophic Sport Injury Research (NCCSIR), based in Chapel Hill, North Carolina. Approximately 90% of the data collected involved male athletes, with an equal distribution between Caucasians and African-Americans (Borjesson and Pelliccia 2009). According to the NCCSIR, there were 10 indirect (due to exertion) fatalities in middle school through college football athletes in 2014, and six were attributed to a cardiac event (Kucera et al. 2015). An additional five football athletes died of suspected cardiac conditions due to nonexertional factors in the same year (Kucera et al. 2015). Sudden death cases in young women are rare, and the most common cause of sudden cardiac death was congenital cardiac disease.
The prevalence of sudden cardiac death in young athletes (those less than 35-year-old) is estimated to be between 1 and 3 in 100,000 (Borjesson and Pelliccia 2009). This is much higher than statistics reported in a more general population of active individuals (Harmon, Klossner, and Drezner 2011). These data indicate that active people are not immune to cardiovascular events that may result in death.
Causes
The most common cause of sudden cardiac death in the young athlete is hypertrophic cardiomyopathy, which accounts for up to 50% of the cases. Other significant causes of sudden cardiac death in a young athlete are coronary artery anomalies, increased cardiac mass, aortic rupture, myocarditis, and aortic stenosis(Borjesson and Pelliccia 2009).Rare causes include dilated cardiomyopathy, atherosclerotic coronary artery disease, mitral valve prolapse, isolated arrhythmias such as long QT syndrome and Wolff-Parkinson-White syndrome, and arrhythmogenic right ventricular dysplasia (ARVD) (Harmon, Klossner, and Drezner 2011). In the Veneto region of Italy, researchers have found ARVD to be the most common cause of sudden cardiac death in the athlete (Thiene et al. 1988). This research suggests that a specific population may have different genetic subtraits.
In the older athlete, coronary artery disease is by far the most common cause of sudden death. Rarely is sudden death in the older athlete caused by hypertrophic cardiomyopathy, mitral valve prolapse, or acquired valvular conditions (Maron et al. 2014; Nagashima et al. 2003; Semsarian, Sweeting, and Ackerman 2015; Marijon et al. 2015).
Traumatic sudden cardiac death has not captured as much attention because its epidemiology is more difficult to track. However, it is a growing problem that strikes without warning. Between 1996 and 2007, a reported 180 cases of blunt-force death in the United States were attributed to commotio cordis (Maron et al. 2006). Most cases involved children with a mean age of 13, with 95% of the deaths occurring in males (Maron et al. 2013).
Commotio cordis refers to trauma to the chest wall that interrupts the electrical impulse in the heart. If the cardiac rhythm is not promptly normalized, the individual dies. Typically the ribs or sternum is not broken, although some contusions may be found. Research has found that a chest blow occurring during the vulnerable phase of repolarization, just prior to the T-wave peak in the cardiac cycle, can induce ventricular fibrillation (Maron and Estes 2005).
Although children and teenagers with thin chest walls are most vulnerable to commotio cordis (figure 8.6), deaths have been reported in adults. Sports such as baseball, ice hockey, lacrosse, and softball, which have hard projectiles that can strike the chest, have been associated with the greatest number of deaths. Commotio cordis also has occurred in sports such as soccer, football, rugby, and karate, in which the blow came from a soft projectile or a collision. It appears that the timing of the incident, rather than the degree of impact of the object, is the causative factor (Maron and Estes 2005). Commotio cordis is the only significant cause of traumatic sudden cardiac death in athletes.
The type of injury associated with commotio cordis is a blow to the chest wall that interrupts the usual cardiac rhythm.
Red Flags for Traumatic Sudden Cardiac Death
Sports with projectiles that can hit the chest at an inopportune time in the cardiac rhythm cycle have been known to cause commotio cordis in young athletes. These sports include the following: baseball, softball, hockey, lacrosse, soccer, football, karate.
Prevention
Because death can be the outcome, prevention has become the focus of attention for commotio cordis. Changes in practice have ranged from protective padding to softer balls that are used in Little League and softball. Because this may not completely resolve the problem, another solution is defibrillation in conjunction with cardiopulmonary resuscitation (CPR). Defibrillation interrupts the heart rhythm so the heart can "reboot" into a normal rhythm.
The American Heart Association estimates that communities with comprehensive CPR and automated external defibrillator (AED) training achieve 40% survival rates for cardiac arrest victims. If defibrillation is performed within 3 min, the likelihood of survival is high. For every minute of delay the chance of survival drops by as much as 10% (American Heart Association 2013).
The advent of the AED has provided greater public access to life-saving technology. These devices can be operated by trained laypeople and are increasingly affordable in all sectors. The AED is portable, rechargeable, simple to operate, and easy to maintain. The American Red Cross, American Heart Association, and National Safety Council offer AED certification courses in addition to CPR courses for the lay public. The NCAA Sports Medicine Guidelines require planned access to an AED and mandating CPR and first aid certifications for all who work with athlete practices, competition, and skill sessions. Athletic trainers are required to maintain certification in emergency cardiac care, including AED use. They need to have ready access to an AED in order to provide rapid cardiac assessment and care to those in fibrillation. Athletes who suffer a sudden collapse and have agonal or gasping breathing should be treated because they are suffering from a cardiac event (Casa et al. 2012; Solberg et al. 2015). An AED should be applied as soon as possible for heart rhythm analysis and possible defibrillation.
Clinical Tips
Potential Causes of Sudden Death
Sudden collapse in athletes could be caused by heatstroke, a cardiac event, sickle cell collapse, or injury. Understanding the presentation of each will facilitate rapid response and the appropriate disposition.
Emergency Planning
Every athletic site should have planned access to an AED, an emergency medical service (EMS), and an established emergency action plan (EAP), as well as medical personnel trained to respond to sudden collapse.
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How to identify celiac disease
Celiac disease is an autoimmune disorder that affects the gastrointestinal tract and is thought to be triggered by dietary gluten in affected individuals. The disease is characterized by chronic inflammation of the small intestinal mucosa, which leads to atrophy of the small intestinal villi and subsequent malabsorption (Pelkowski and Viera 2014).
Celiac disease is an autoimmune disorder that affects the gastrointestinal tract and is thought to be triggered by dietary gluten in affected individuals. The disease is characterized by chronic inflammation of the small intestinal mucosa, which leads to atrophy of the small intestinal villi and subsequent malabsorption (Pelkowski and Viera 2014). Celiac disease affects approximately 1% of the U.S. population and typically occurs in persons of European ancestry as well as persons of Middle Eastern, Indian, South American, and North African descent. It is two to three times more common in women. Celiac disease is not a food allergy.
Signs and Symptoms
Typical presentation includes chronic diarrhea with cramping and gas pains. Patients often have weight loss, or in the adolescent, delayed onset of growth or puberty. A history of nervousness and/or depression is often present, as is a family history of autoimmune disease. Other complaints may include bone or joint pain, migraines, weakness, fatigue, and anemia (Volta et al. 2015; Vivas et al. 2015; Byrne and Feighery 2015; Mancini, Trojian, and Mancini 2011). Physical examination is often normal, but the patient may present with abdominal distension or dermatitis herpetiformis.
Referral and Diagnostic Tests
Lab tests are performed for differentiating celiac disease and to rule out more common diseases. These include a basic metabolic panel, CBC (iron deficiency), TSH (thyroid disease), vitamin D level, and allergy testing. If celiac disease is suspected from history and physical exam, the initial serologic test is a tissue transglutaminase (tTG) antibody level. This antibody is found in every tissue in the body and acts to join proteins together. In people with celiac disease, tTG activates specific immune cells and triggers the inflammatory response that leads to atrophy of the villi in the small intestine (Mancini, Trojian, and Mancini 2011). The diagnosis is often confirmed with repeat blood tests after 4 wk on a gluten-free diet. Endoscopy with biopsies of the duodenal mucosa may be necessary to confirm the diagnosis. Celiac disease should be differentiated from GERD, pancreatic insufficiency, Crohn's disease, or other inflammatory bowel diseases.
Treatment and Return to Participation
The general treatment is to remove gluten from the diet. The patient can substitute rice, corn, and soybean flour for products that contain gluten. Periodic blood tests are performed to measure the levels of the antibodies. The levels will normalize with gluten abstinence. Abstinence will be required for life because the immune response to gluten will recur if gluten is consumed again. Usually no medications are prescribed for celiac disease, but athletes may benefit from iron, vitamin, and calcium supplements. The most difficult aspect for the athlete with celiac disease is the dietary restrictions while traveling with the team or with set team meals. The athletic trainer may need to check on the gluten-free status of many of the standard gluten-containing products provided by the athletic department, such as energy drinks or meal replacement bars (Mancini, Trojian, and Mancini 2011).
Condition Highlight
Gluten Sensitivity and Intolerance
Over the past 10 yr, the number of people choosing a gluten-free diet (GFD) is much higher than the projected number of celiac disease patients (Lis et al. 2015). This has fueled a global market of gluten-free products and highlights several conditions related to the ingestion of gluten. There are three main forms of gluten reactions: allergic, autoimmune (celiac disease), and immune-mediated conditions (gluten sensitivity) (Sapone et al. 2012). Wheat allergy is an adverse reaction to wheat proteins with onset in minutes to hours after gluten ingestion. It may affect the skin, GI tract, or respiratory tract. Celiac disease or other autoimmune gluten disorders generally present months to years after gluten exposure. There is a third condition where some people experience distress from eating gluten-containing products and show improvement with a GFD. It is distinct from celiac disease and wheat allergies (Vivas et al. 2015). Gluten sensitivity cannot be distinguished clinically; serology tests need to be conducted. Patients with GI discomfort or distress following gluten ingestion should be referred for a follow-up blood test and immune-allergy tests.
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Addressing mental health issues in the athlete
Everyone has symptoms of some type of mental health issue at some time in life when one or several stressors overwhelm the person’s ability to self-regulate or repair. The symptoms are usually, and arbitrarily, labeled either physical or mental.
Everyone has symptoms of some type of mental health issue at some time in life when one or several stressors overwhelm the person's ability to self-regulate or repair. The symptoms are usually, and arbitrarily, labeled either physical or mental. This artificial dichotomy usually does not align with the affected person's reality. Rarely is an athlete with a strained hamstring not also worried about the injury or distressed by the pain. Similarly, the most common initial warning signs of depression are the physical symptoms of tension, restlessness, and disturbed sleep, energy, and appetite. This is because we have overlapping systems of mind, body, spirit, and relationships, each integrally connected to the others. When the homeostasis of one or more systems is disrupted, people instinctively try to correct the problem regardless of its origin. In the mental health domain, signs of distress are emotional, mental, behavioral, and physical.
Framework for Understanding Mental Health
In almost all situations, a variety of overlapping factors contribute to symptom development. The biopsychosocial - spiritual model (BPSS) is a framework for understanding the person's responses in a given situation and the development of symptoms. Symptom etiology may be conceptualized as a pie. Figure 17.1 shows how these various factors overlap and contribute to well-being. In a given person, the various pieces of the BPSS pie may be larger or smaller at any one time. The relative sizes of the pieces greatly influence the person's symptoms and ability to adapt.
The biopsychosocial - spiritual model is a framework for understanding a person's responses in a given situation and the development of symptoms.
For example, two runners may have identical injuries, but the impact of the injury and the course of rehabilitation in these two athletes will usually differ. The amount of pain they have, as well as the length of time until they are ready to compete again, will be influenced not only by the difference in respective levels of physical conditioning and injury history but also by other physical and emotional conditions such as pain tolerance, attitude, perception of the problem, and its implications for life. The situation may also be affected by personality and temperament issues, variable resources for coping, and so on. Another example involves two wrestlers who seem to be equally competitive, but wrestler A, in a struggle to make or maintain weight, develops more obviously disordered eating patterns than wrestler B. Perhaps wrestler A has a family history of obesity and is genetically predisposed toward weight gain more than the other; temperamentally, wrestler A may tend to think more negatively about life challenges, become somewhat self-defeating in the face of adversity, and find emotional comfort in food and the process of eating. Often a variety of factors will help to explain the development of clinically significant problems.
This interplay of variables is the same for athletes as it is for others who are physically active, regardless of whether the symptoms of an injury or condition are physical or emotional. Whereas one athlete may become depressed, another's symptoms may include anxiety or outbursts of anger and physical aggression. Sometimes one piece of the BPSS pie is so big that it seems to account for virtually the whole reason that someone is symptomatic (e.g., the chemical disequilibrium that comes with bipolar disorder). For this reason, it is a good practice to regularly consider the possibility that an organic cause may be the culprit and refer the person for a medical evaluation.
The treatments that have proven effective for the problems discussed in this chapter are based on the same BPSS approach as the assessment and diagnosis. Different strategies can be useful, depending on the biopsychosocial - spiritual components that are implicated in the assessment process. Practitioners often recommend treatment plans based on their assessment and experience, and then these are negotiated with the patient or family members according to personal preferences. The treatment may be offered on either an inpatient or, more commonly, an outpatient basis.
Treatment may also involve the collaboration of a variety of treatment professionals. For example, eating disorder treatment often involves a physician, a registered dietitian, and a psychotherapist. This will be determined based on the severity of symptoms, the difficulty the athlete has in making changes, the amount of support the athlete has, and other resources that affect care, including financial concerns or insurance benefits. The important first step in treatment is accurate assessment followed by clear and well-timed communication and education with the athlete and family. The athletic trainer can play a valuable role here because people are much more likely to engage in treatment or some type of change process if they become convinced that there is a problem, they know what it is, and they know that something can be done about it. This is because most people will want to know what is going on with themselves, how they "got it," and what they can do to "get rid of it" or at least cope more effectively. Additional treatment recommendations specific to various clinical problems are listed in subsequent sections.
Implications for Participation in Athletics
Early identification and treatment are very helpful in preventing problems from worsening, but sometimes the stigma still associated with mental health conditions prevents people from recognizing these problems in themselves or others. In those cases, functioning in one or more areas of life can be affected, sometimes severely. Restricting participation in a sport, if necessary, will depend on the assessment of the athlete's level of functioning by the athlete, the coach, and the athletic trainer. Initially, while the medication dosage is being adjusted, the athlete could experience adverse effects that could affect participation or performance, such as nausea, headache, sedation, disturbed balance, or overstimulation. The National Collegiate Athletic Association (NCAA) has no restrictions on the medications typically used to treat these conditions except for pemoline, a medication prescribed to treat ADHD (National Collegiate Athletic Association 2015).
The last general point to be made is that some people experiencing psychological or substance use disorders may consider suicide or become homicidal. Most health care professionals or other professionals are required by law or by a professional code of ethics to report to the authorities if a patient is a danger to self or others. Athletic trainers, too, may encounter an athlete with depression, panic disorder, or substance abuse who is considering suicide or harming someone else. The athletic trainer must seek immediate consultation if in doubt about the need to report. An assessment of whether one is suicidal or homicidal includes determining whether the person has a specific plan, the means to carry it out, the intention to carry it out, and how lethal the plan is. Those with a personal or family history of this type of ideation or action or whose judgment is impaired, perhaps through the use of substances, are more at risk to follow through.
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Identifying Exercise-Induced Bronchospasm
The terms EIA and EIB are often used interchangeably, but EIB specifically denotes the reduction in lung function that occurs after a standardized exercise test (Carver 2009). More recently, the term exercise-induced bronchoconstriction has been introduced as actual spasm of the airways does not always occur.
The terms exercise-induced asthma (EIA) and exercise-induced bronchoconstriction (EIB) are often used interchangeably, but EIB specifically denotes the reduction in lung function that occurs after a standardized exercise test (Carver 2009). More recently, the term exercise-induced bronchoconstriction has been introduced as actual spasm of the airways does not always occur. Some clinicians use EIA to describe individuals with known asthma who have bronchoconstriction during exercise. However, some use EIA to describe patients who have bronchoconstriction only during exercise, and they use EIB to describe patients with asthma who have bronchoconstriction with exercise. Generally, EIB is used to indicate bronchospasm with decreased pulmonary function testing following exercise, and EIA is used to indicate those patients with asthma difficulties associated with exercise.
Symptoms of EIB usually occur 10 to 15 min after the onset of strenuous exercise and are defined by a fall in FEV1 of 15% or more during exercise spirometry. EIB is more common in winter sport athletes who compete in cold ambient temperatures (Carey, Aase, and Pliego 2010).
Signs and Symptoms
EIB should be suspected in any athlete who complains of shortness of breath, dyspnea, cough, chest congestion, or tightness with exertion. These symptoms usually occur during strenuous exercise and peak about 5 to 10 min after exercise (Hull 2012; Krafczyk and Asplund 2011; Simpson, Romer, and Kippelen 2015). Other subtle clues might be a dry cough that develops after practice or exercise (i.e., locker-room cough) or simply unusual fatigue compared with similarly trained athletes. Athletes will often complain that they feel out of shape despite regular training. Self-reported symptoms have been shown to be poor predictors of EIB because other conditions can cause similar symptoms. Symptoms alone should not be used to diagnose EIB.
In athletes suspected of having EIB, other etiologies, such as acute sinusitis, otitis media (middle ear infection), bronchitis, or even pneumonia, need to be excluded, particularly in the context of other constitutional symptoms, such as fever, chills, or night sweats. If fatigue is the only presenting symptom, deconditioning may also be a cause. In addition, environmental allergies can account for many of the nonspecific symptoms that mimic EIB (Backer 2010; Hull et al. 2012; Stack and Hakemi 2011). More serious cardiac causes, such as arrhythmias and pericarditis, might also need to be excluded. Another important differential is exercise-induced laryngeal obstruction (EILO), where the wheezing and dyspnea are caused by transient obstruction of the upper airways during exercise (Nielsen 2013; Backer 2010).
Referral and Diagnostic Tests
The physical examination is usually normal. Some athletes with EIB may experience symptoms that develop several hours after exercise. This late-phase response is due to the activity of inflammatory mediators. Most commonly, a bronchial provocation challenge is used to determine the diagnosis of EIB (Parsons et al. 2011; Hayden et al. 2011; Morris 2010). Figure 7.9 shows a decision tree commonly used for the diagnosis of EIB. Alternatively, many physicians choose to just evaluate the patient's response to an empirical trial of a ß-agonist medication before exercise.
Decision tree for the diagnosis of exercise-induced bronchoconstriction (EIB).
Treatment and Return to Participation
The treatment of choice in EIB is an inhaled ß2-agonist from a metered-dose inhaler (e.g., albuterol) taken 15 to 30 min before the onset of exercise. An athlete who has asthma symptoms outside the exercise setting or who is using a ß2-agonist more than three times per week should be treated with a regular inhaled corticosteroid. Here is how to properly use an inhaler:
- Remove dust cap and shake the inhaler system before each use.
- Inspect mouthpiece for contamination or foreign objects.
- Breathe out through the mouth, exhaling as completely as possible.
- Hold the inhaler system upright with mouthpiece in mouth and lips closed tightly around mouthpiece.
- Breathe in slowly while pressing down on the metal cartridge.
- Hold breath as long as possible.
- Release pressure while still holding breath.
- Remove mouthpiece.
- Wait for the container to repressurize, shake, and then repeat steps 3 through 8 when more than one inhalation is prescribed.
- Rinse mouth with water after prescribed number of inhalations.
- Clean the inhaler system every few days by removing metal cartridge and rinsing the plastic inhaler and cap with running warm water. Replace cartridge and cap.
Emerging studies show promise using long-acting ß2-agonists such as salmeterol and leukotriene inhibitors such as montelukast (Singulair) (Parsons 2010). Other nonpharmacological strategies include pre - warm-up bursts of physical activity at 80% to 90% of the individual's maximal workload to induce a refractory period that lasts up to 3 h after the initial attack of EIB (Hull et al. 2012; Millward et al. 2009; Boulet, Hancox, and Fitch 2010). Strategies to humidify inspired air and dietary interventions may also prove to be beneficial (Carey, Aase, and Pliego 2010; Bussotti, Di Marco, and Marchese 2014).
For an athlete experiencing a severe asthma attack or when an inhaler is ineffective, a nebulizer may be used. A nebulizer, also known as an atomizer, is a machine that vaporizes liquid medication into a fine mist to be inhaled into the lungs via a mouthpiece or mask. Although studies have shown that both inhalers and nebulizers tend to be equally effective in delivering medications, nebulizers are preferred for use in more serious rescue situations when the patient is experiencing a severe asthma attack. Nebulizers can administer a higher dose of medication, but inhalers are easier to use, preferred for their portability and low cost, and good for everyday use. Medications typically administered with a nebulizer include albuterol and ipratropium (Atrovent).
Athletes with controlled EIB need not be excluded or discouraged from participating in sports. Effective strategies, both pharmacological and nonpharmacological, exist that can allow an athlete to compete even at an elite level.
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Causes of Sudden Cardiac Death in Athletes
Death by sudden cardiac arrest (SCA) is a rare event in the young athlete. In the United States, elite athletes are viewed as near invincible because of their incredible physical feats.
Death by sudden cardiac arrest (SCA) is a rare event in the young athlete. In the United States, elite athletes are viewed as near invincible because of their incredible physical feats. Nevertheless, it is reported that the rate of collegiate athlete death due to SCA is higher than that of high school athletes, with a suspected 110 SCA deaths annually in the United States among young athletes (Casa et al. 2012). Any time a tragedy of this proportion occurs, the public reacts with disbelief, and medical knowledge is called into question. Studies that have tracked these deaths during sports used the National Federation of State High School Associations (NFHS), the National Collegiate Athletic Association (NCAA) governing organizations, and state and federally funded research groups for data collection, such as the National Center for Catastrophic Sport Injury Research (NCCSIR), based in Chapel Hill, North Carolina. Approximately 90% of the data collected involved male athletes, with an equal distribution between Caucasians and African-Americans (Borjesson and Pelliccia 2009). According to the NCCSIR, there were 10 indirect (due to exertion) fatalities in middle school through college football athletes in 2014, and six were attributed to a cardiac event (Kucera et al. 2015). An additional five football athletes died of suspected cardiac conditions due to nonexertional factors in the same year (Kucera et al. 2015). Sudden death cases in young women are rare, and the most common cause of sudden cardiac death was congenital cardiac disease.
The prevalence of sudden cardiac death in young athletes (those less than 35-year-old) is estimated to be between 1 and 3 in 100,000 (Borjesson and Pelliccia 2009). This is much higher than statistics reported in a more general population of active individuals (Harmon, Klossner, and Drezner 2011). These data indicate that active people are not immune to cardiovascular events that may result in death.
Causes
The most common cause of sudden cardiac death in the young athlete is hypertrophic cardiomyopathy, which accounts for up to 50% of the cases. Other significant causes of sudden cardiac death in a young athlete are coronary artery anomalies, increased cardiac mass, aortic rupture, myocarditis, and aortic stenosis(Borjesson and Pelliccia 2009).Rare causes include dilated cardiomyopathy, atherosclerotic coronary artery disease, mitral valve prolapse, isolated arrhythmias such as long QT syndrome and Wolff-Parkinson-White syndrome, and arrhythmogenic right ventricular dysplasia (ARVD) (Harmon, Klossner, and Drezner 2011). In the Veneto region of Italy, researchers have found ARVD to be the most common cause of sudden cardiac death in the athlete (Thiene et al. 1988). This research suggests that a specific population may have different genetic subtraits.
In the older athlete, coronary artery disease is by far the most common cause of sudden death. Rarely is sudden death in the older athlete caused by hypertrophic cardiomyopathy, mitral valve prolapse, or acquired valvular conditions (Maron et al. 2014; Nagashima et al. 2003; Semsarian, Sweeting, and Ackerman 2015; Marijon et al. 2015).
Traumatic sudden cardiac death has not captured as much attention because its epidemiology is more difficult to track. However, it is a growing problem that strikes without warning. Between 1996 and 2007, a reported 180 cases of blunt-force death in the United States were attributed to commotio cordis (Maron et al. 2006). Most cases involved children with a mean age of 13, with 95% of the deaths occurring in males (Maron et al. 2013).
Commotio cordis refers to trauma to the chest wall that interrupts the electrical impulse in the heart. If the cardiac rhythm is not promptly normalized, the individual dies. Typically the ribs or sternum is not broken, although some contusions may be found. Research has found that a chest blow occurring during the vulnerable phase of repolarization, just prior to the T-wave peak in the cardiac cycle, can induce ventricular fibrillation (Maron and Estes 2005).
Although children and teenagers with thin chest walls are most vulnerable to commotio cordis (figure 8.6), deaths have been reported in adults. Sports such as baseball, ice hockey, lacrosse, and softball, which have hard projectiles that can strike the chest, have been associated with the greatest number of deaths. Commotio cordis also has occurred in sports such as soccer, football, rugby, and karate, in which the blow came from a soft projectile or a collision. It appears that the timing of the incident, rather than the degree of impact of the object, is the causative factor (Maron and Estes 2005). Commotio cordis is the only significant cause of traumatic sudden cardiac death in athletes.
The type of injury associated with commotio cordis is a blow to the chest wall that interrupts the usual cardiac rhythm.
Red Flags for Traumatic Sudden Cardiac Death
Sports with projectiles that can hit the chest at an inopportune time in the cardiac rhythm cycle have been known to cause commotio cordis in young athletes. These sports include the following: baseball, softball, hockey, lacrosse, soccer, football, karate.
Prevention
Because death can be the outcome, prevention has become the focus of attention for commotio cordis. Changes in practice have ranged from protective padding to softer balls that are used in Little League and softball. Because this may not completely resolve the problem, another solution is defibrillation in conjunction with cardiopulmonary resuscitation (CPR). Defibrillation interrupts the heart rhythm so the heart can "reboot" into a normal rhythm.
The American Heart Association estimates that communities with comprehensive CPR and automated external defibrillator (AED) training achieve 40% survival rates for cardiac arrest victims. If defibrillation is performed within 3 min, the likelihood of survival is high. For every minute of delay the chance of survival drops by as much as 10% (American Heart Association 2013).
The advent of the AED has provided greater public access to life-saving technology. These devices can be operated by trained laypeople and are increasingly affordable in all sectors. The AED is portable, rechargeable, simple to operate, and easy to maintain. The American Red Cross, American Heart Association, and National Safety Council offer AED certification courses in addition to CPR courses for the lay public. The NCAA Sports Medicine Guidelines require planned access to an AED and mandating CPR and first aid certifications for all who work with athlete practices, competition, and skill sessions. Athletic trainers are required to maintain certification in emergency cardiac care, including AED use. They need to have ready access to an AED in order to provide rapid cardiac assessment and care to those in fibrillation. Athletes who suffer a sudden collapse and have agonal or gasping breathing should be treated because they are suffering from a cardiac event (Casa et al. 2012; Solberg et al. 2015). An AED should be applied as soon as possible for heart rhythm analysis and possible defibrillation.
Clinical Tips
Potential Causes of Sudden Death
Sudden collapse in athletes could be caused by heatstroke, a cardiac event, sickle cell collapse, or injury. Understanding the presentation of each will facilitate rapid response and the appropriate disposition.
Emergency Planning
Every athletic site should have planned access to an AED, an emergency medical service (EMS), and an established emergency action plan (EAP), as well as medical personnel trained to respond to sudden collapse.
Learn more about Medical Conditions in the Athlete, Third Edition.
How to identify celiac disease
Celiac disease is an autoimmune disorder that affects the gastrointestinal tract and is thought to be triggered by dietary gluten in affected individuals. The disease is characterized by chronic inflammation of the small intestinal mucosa, which leads to atrophy of the small intestinal villi and subsequent malabsorption (Pelkowski and Viera 2014).
Celiac disease is an autoimmune disorder that affects the gastrointestinal tract and is thought to be triggered by dietary gluten in affected individuals. The disease is characterized by chronic inflammation of the small intestinal mucosa, which leads to atrophy of the small intestinal villi and subsequent malabsorption (Pelkowski and Viera 2014). Celiac disease affects approximately 1% of the U.S. population and typically occurs in persons of European ancestry as well as persons of Middle Eastern, Indian, South American, and North African descent. It is two to three times more common in women. Celiac disease is not a food allergy.
Signs and Symptoms
Typical presentation includes chronic diarrhea with cramping and gas pains. Patients often have weight loss, or in the adolescent, delayed onset of growth or puberty. A history of nervousness and/or depression is often present, as is a family history of autoimmune disease. Other complaints may include bone or joint pain, migraines, weakness, fatigue, and anemia (Volta et al. 2015; Vivas et al. 2015; Byrne and Feighery 2015; Mancini, Trojian, and Mancini 2011). Physical examination is often normal, but the patient may present with abdominal distension or dermatitis herpetiformis.
Referral and Diagnostic Tests
Lab tests are performed for differentiating celiac disease and to rule out more common diseases. These include a basic metabolic panel, CBC (iron deficiency), TSH (thyroid disease), vitamin D level, and allergy testing. If celiac disease is suspected from history and physical exam, the initial serologic test is a tissue transglutaminase (tTG) antibody level. This antibody is found in every tissue in the body and acts to join proteins together. In people with celiac disease, tTG activates specific immune cells and triggers the inflammatory response that leads to atrophy of the villi in the small intestine (Mancini, Trojian, and Mancini 2011). The diagnosis is often confirmed with repeat blood tests after 4 wk on a gluten-free diet. Endoscopy with biopsies of the duodenal mucosa may be necessary to confirm the diagnosis. Celiac disease should be differentiated from GERD, pancreatic insufficiency, Crohn's disease, or other inflammatory bowel diseases.
Treatment and Return to Participation
The general treatment is to remove gluten from the diet. The patient can substitute rice, corn, and soybean flour for products that contain gluten. Periodic blood tests are performed to measure the levels of the antibodies. The levels will normalize with gluten abstinence. Abstinence will be required for life because the immune response to gluten will recur if gluten is consumed again. Usually no medications are prescribed for celiac disease, but athletes may benefit from iron, vitamin, and calcium supplements. The most difficult aspect for the athlete with celiac disease is the dietary restrictions while traveling with the team or with set team meals. The athletic trainer may need to check on the gluten-free status of many of the standard gluten-containing products provided by the athletic department, such as energy drinks or meal replacement bars (Mancini, Trojian, and Mancini 2011).
Condition Highlight
Gluten Sensitivity and Intolerance
Over the past 10 yr, the number of people choosing a gluten-free diet (GFD) is much higher than the projected number of celiac disease patients (Lis et al. 2015). This has fueled a global market of gluten-free products and highlights several conditions related to the ingestion of gluten. There are three main forms of gluten reactions: allergic, autoimmune (celiac disease), and immune-mediated conditions (gluten sensitivity) (Sapone et al. 2012). Wheat allergy is an adverse reaction to wheat proteins with onset in minutes to hours after gluten ingestion. It may affect the skin, GI tract, or respiratory tract. Celiac disease or other autoimmune gluten disorders generally present months to years after gluten exposure. There is a third condition where some people experience distress from eating gluten-containing products and show improvement with a GFD. It is distinct from celiac disease and wheat allergies (Vivas et al. 2015). Gluten sensitivity cannot be distinguished clinically; serology tests need to be conducted. Patients with GI discomfort or distress following gluten ingestion should be referred for a follow-up blood test and immune-allergy tests.
Learn more about Medical Conditions in the Athlete, Third Edition.
Addressing mental health issues in the athlete
Everyone has symptoms of some type of mental health issue at some time in life when one or several stressors overwhelm the person’s ability to self-regulate or repair. The symptoms are usually, and arbitrarily, labeled either physical or mental.
Everyone has symptoms of some type of mental health issue at some time in life when one or several stressors overwhelm the person's ability to self-regulate or repair. The symptoms are usually, and arbitrarily, labeled either physical or mental. This artificial dichotomy usually does not align with the affected person's reality. Rarely is an athlete with a strained hamstring not also worried about the injury or distressed by the pain. Similarly, the most common initial warning signs of depression are the physical symptoms of tension, restlessness, and disturbed sleep, energy, and appetite. This is because we have overlapping systems of mind, body, spirit, and relationships, each integrally connected to the others. When the homeostasis of one or more systems is disrupted, people instinctively try to correct the problem regardless of its origin. In the mental health domain, signs of distress are emotional, mental, behavioral, and physical.
Framework for Understanding Mental Health
In almost all situations, a variety of overlapping factors contribute to symptom development. The biopsychosocial - spiritual model (BPSS) is a framework for understanding the person's responses in a given situation and the development of symptoms. Symptom etiology may be conceptualized as a pie. Figure 17.1 shows how these various factors overlap and contribute to well-being. In a given person, the various pieces of the BPSS pie may be larger or smaller at any one time. The relative sizes of the pieces greatly influence the person's symptoms and ability to adapt.
The biopsychosocial - spiritual model is a framework for understanding a person's responses in a given situation and the development of symptoms.
For example, two runners may have identical injuries, but the impact of the injury and the course of rehabilitation in these two athletes will usually differ. The amount of pain they have, as well as the length of time until they are ready to compete again, will be influenced not only by the difference in respective levels of physical conditioning and injury history but also by other physical and emotional conditions such as pain tolerance, attitude, perception of the problem, and its implications for life. The situation may also be affected by personality and temperament issues, variable resources for coping, and so on. Another example involves two wrestlers who seem to be equally competitive, but wrestler A, in a struggle to make or maintain weight, develops more obviously disordered eating patterns than wrestler B. Perhaps wrestler A has a family history of obesity and is genetically predisposed toward weight gain more than the other; temperamentally, wrestler A may tend to think more negatively about life challenges, become somewhat self-defeating in the face of adversity, and find emotional comfort in food and the process of eating. Often a variety of factors will help to explain the development of clinically significant problems.
This interplay of variables is the same for athletes as it is for others who are physically active, regardless of whether the symptoms of an injury or condition are physical or emotional. Whereas one athlete may become depressed, another's symptoms may include anxiety or outbursts of anger and physical aggression. Sometimes one piece of the BPSS pie is so big that it seems to account for virtually the whole reason that someone is symptomatic (e.g., the chemical disequilibrium that comes with bipolar disorder). For this reason, it is a good practice to regularly consider the possibility that an organic cause may be the culprit and refer the person for a medical evaluation.
The treatments that have proven effective for the problems discussed in this chapter are based on the same BPSS approach as the assessment and diagnosis. Different strategies can be useful, depending on the biopsychosocial - spiritual components that are implicated in the assessment process. Practitioners often recommend treatment plans based on their assessment and experience, and then these are negotiated with the patient or family members according to personal preferences. The treatment may be offered on either an inpatient or, more commonly, an outpatient basis.
Treatment may also involve the collaboration of a variety of treatment professionals. For example, eating disorder treatment often involves a physician, a registered dietitian, and a psychotherapist. This will be determined based on the severity of symptoms, the difficulty the athlete has in making changes, the amount of support the athlete has, and other resources that affect care, including financial concerns or insurance benefits. The important first step in treatment is accurate assessment followed by clear and well-timed communication and education with the athlete and family. The athletic trainer can play a valuable role here because people are much more likely to engage in treatment or some type of change process if they become convinced that there is a problem, they know what it is, and they know that something can be done about it. This is because most people will want to know what is going on with themselves, how they "got it," and what they can do to "get rid of it" or at least cope more effectively. Additional treatment recommendations specific to various clinical problems are listed in subsequent sections.
Implications for Participation in Athletics
Early identification and treatment are very helpful in preventing problems from worsening, but sometimes the stigma still associated with mental health conditions prevents people from recognizing these problems in themselves or others. In those cases, functioning in one or more areas of life can be affected, sometimes severely. Restricting participation in a sport, if necessary, will depend on the assessment of the athlete's level of functioning by the athlete, the coach, and the athletic trainer. Initially, while the medication dosage is being adjusted, the athlete could experience adverse effects that could affect participation or performance, such as nausea, headache, sedation, disturbed balance, or overstimulation. The National Collegiate Athletic Association (NCAA) has no restrictions on the medications typically used to treat these conditions except for pemoline, a medication prescribed to treat ADHD (National Collegiate Athletic Association 2015).
The last general point to be made is that some people experiencing psychological or substance use disorders may consider suicide or become homicidal. Most health care professionals or other professionals are required by law or by a professional code of ethics to report to the authorities if a patient is a danger to self or others. Athletic trainers, too, may encounter an athlete with depression, panic disorder, or substance abuse who is considering suicide or harming someone else. The athletic trainer must seek immediate consultation if in doubt about the need to report. An assessment of whether one is suicidal or homicidal includes determining whether the person has a specific plan, the means to carry it out, the intention to carry it out, and how lethal the plan is. Those with a personal or family history of this type of ideation or action or whose judgment is impaired, perhaps through the use of substances, are more at risk to follow through.
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Identifying Exercise-Induced Bronchospasm
The terms EIA and EIB are often used interchangeably, but EIB specifically denotes the reduction in lung function that occurs after a standardized exercise test (Carver 2009). More recently, the term exercise-induced bronchoconstriction has been introduced as actual spasm of the airways does not always occur.
The terms exercise-induced asthma (EIA) and exercise-induced bronchoconstriction (EIB) are often used interchangeably, but EIB specifically denotes the reduction in lung function that occurs after a standardized exercise test (Carver 2009). More recently, the term exercise-induced bronchoconstriction has been introduced as actual spasm of the airways does not always occur. Some clinicians use EIA to describe individuals with known asthma who have bronchoconstriction during exercise. However, some use EIA to describe patients who have bronchoconstriction only during exercise, and they use EIB to describe patients with asthma who have bronchoconstriction with exercise. Generally, EIB is used to indicate bronchospasm with decreased pulmonary function testing following exercise, and EIA is used to indicate those patients with asthma difficulties associated with exercise.
Symptoms of EIB usually occur 10 to 15 min after the onset of strenuous exercise and are defined by a fall in FEV1 of 15% or more during exercise spirometry. EIB is more common in winter sport athletes who compete in cold ambient temperatures (Carey, Aase, and Pliego 2010).
Signs and Symptoms
EIB should be suspected in any athlete who complains of shortness of breath, dyspnea, cough, chest congestion, or tightness with exertion. These symptoms usually occur during strenuous exercise and peak about 5 to 10 min after exercise (Hull 2012; Krafczyk and Asplund 2011; Simpson, Romer, and Kippelen 2015). Other subtle clues might be a dry cough that develops after practice or exercise (i.e., locker-room cough) or simply unusual fatigue compared with similarly trained athletes. Athletes will often complain that they feel out of shape despite regular training. Self-reported symptoms have been shown to be poor predictors of EIB because other conditions can cause similar symptoms. Symptoms alone should not be used to diagnose EIB.
In athletes suspected of having EIB, other etiologies, such as acute sinusitis, otitis media (middle ear infection), bronchitis, or even pneumonia, need to be excluded, particularly in the context of other constitutional symptoms, such as fever, chills, or night sweats. If fatigue is the only presenting symptom, deconditioning may also be a cause. In addition, environmental allergies can account for many of the nonspecific symptoms that mimic EIB (Backer 2010; Hull et al. 2012; Stack and Hakemi 2011). More serious cardiac causes, such as arrhythmias and pericarditis, might also need to be excluded. Another important differential is exercise-induced laryngeal obstruction (EILO), where the wheezing and dyspnea are caused by transient obstruction of the upper airways during exercise (Nielsen 2013; Backer 2010).
Referral and Diagnostic Tests
The physical examination is usually normal. Some athletes with EIB may experience symptoms that develop several hours after exercise. This late-phase response is due to the activity of inflammatory mediators. Most commonly, a bronchial provocation challenge is used to determine the diagnosis of EIB (Parsons et al. 2011; Hayden et al. 2011; Morris 2010). Figure 7.9 shows a decision tree commonly used for the diagnosis of EIB. Alternatively, many physicians choose to just evaluate the patient's response to an empirical trial of a ß-agonist medication before exercise.
Decision tree for the diagnosis of exercise-induced bronchoconstriction (EIB).
Treatment and Return to Participation
The treatment of choice in EIB is an inhaled ß2-agonist from a metered-dose inhaler (e.g., albuterol) taken 15 to 30 min before the onset of exercise. An athlete who has asthma symptoms outside the exercise setting or who is using a ß2-agonist more than three times per week should be treated with a regular inhaled corticosteroid. Here is how to properly use an inhaler:
- Remove dust cap and shake the inhaler system before each use.
- Inspect mouthpiece for contamination or foreign objects.
- Breathe out through the mouth, exhaling as completely as possible.
- Hold the inhaler system upright with mouthpiece in mouth and lips closed tightly around mouthpiece.
- Breathe in slowly while pressing down on the metal cartridge.
- Hold breath as long as possible.
- Release pressure while still holding breath.
- Remove mouthpiece.
- Wait for the container to repressurize, shake, and then repeat steps 3 through 8 when more than one inhalation is prescribed.
- Rinse mouth with water after prescribed number of inhalations.
- Clean the inhaler system every few days by removing metal cartridge and rinsing the plastic inhaler and cap with running warm water. Replace cartridge and cap.
Emerging studies show promise using long-acting ß2-agonists such as salmeterol and leukotriene inhibitors such as montelukast (Singulair) (Parsons 2010). Other nonpharmacological strategies include pre - warm-up bursts of physical activity at 80% to 90% of the individual's maximal workload to induce a refractory period that lasts up to 3 h after the initial attack of EIB (Hull et al. 2012; Millward et al. 2009; Boulet, Hancox, and Fitch 2010). Strategies to humidify inspired air and dietary interventions may also prove to be beneficial (Carey, Aase, and Pliego 2010; Bussotti, Di Marco, and Marchese 2014).
For an athlete experiencing a severe asthma attack or when an inhaler is ineffective, a nebulizer may be used. A nebulizer, also known as an atomizer, is a machine that vaporizes liquid medication into a fine mist to be inhaled into the lungs via a mouthpiece or mask. Although studies have shown that both inhalers and nebulizers tend to be equally effective in delivering medications, nebulizers are preferred for use in more serious rescue situations when the patient is experiencing a severe asthma attack. Nebulizers can administer a higher dose of medication, but inhalers are easier to use, preferred for their portability and low cost, and good for everyday use. Medications typically administered with a nebulizer include albuterol and ipratropium (Atrovent).
Athletes with controlled EIB need not be excluded or discouraged from participating in sports. Effective strategies, both pharmacological and nonpharmacological, exist that can allow an athlete to compete even at an elite level.
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Causes of Sudden Cardiac Death in Athletes
Death by sudden cardiac arrest (SCA) is a rare event in the young athlete. In the United States, elite athletes are viewed as near invincible because of their incredible physical feats.
Death by sudden cardiac arrest (SCA) is a rare event in the young athlete. In the United States, elite athletes are viewed as near invincible because of their incredible physical feats. Nevertheless, it is reported that the rate of collegiate athlete death due to SCA is higher than that of high school athletes, with a suspected 110 SCA deaths annually in the United States among young athletes (Casa et al. 2012). Any time a tragedy of this proportion occurs, the public reacts with disbelief, and medical knowledge is called into question. Studies that have tracked these deaths during sports used the National Federation of State High School Associations (NFHS), the National Collegiate Athletic Association (NCAA) governing organizations, and state and federally funded research groups for data collection, such as the National Center for Catastrophic Sport Injury Research (NCCSIR), based in Chapel Hill, North Carolina. Approximately 90% of the data collected involved male athletes, with an equal distribution between Caucasians and African-Americans (Borjesson and Pelliccia 2009). According to the NCCSIR, there were 10 indirect (due to exertion) fatalities in middle school through college football athletes in 2014, and six were attributed to a cardiac event (Kucera et al. 2015). An additional five football athletes died of suspected cardiac conditions due to nonexertional factors in the same year (Kucera et al. 2015). Sudden death cases in young women are rare, and the most common cause of sudden cardiac death was congenital cardiac disease.
The prevalence of sudden cardiac death in young athletes (those less than 35-year-old) is estimated to be between 1 and 3 in 100,000 (Borjesson and Pelliccia 2009). This is much higher than statistics reported in a more general population of active individuals (Harmon, Klossner, and Drezner 2011). These data indicate that active people are not immune to cardiovascular events that may result in death.
Causes
The most common cause of sudden cardiac death in the young athlete is hypertrophic cardiomyopathy, which accounts for up to 50% of the cases. Other significant causes of sudden cardiac death in a young athlete are coronary artery anomalies, increased cardiac mass, aortic rupture, myocarditis, and aortic stenosis(Borjesson and Pelliccia 2009).Rare causes include dilated cardiomyopathy, atherosclerotic coronary artery disease, mitral valve prolapse, isolated arrhythmias such as long QT syndrome and Wolff-Parkinson-White syndrome, and arrhythmogenic right ventricular dysplasia (ARVD) (Harmon, Klossner, and Drezner 2011). In the Veneto region of Italy, researchers have found ARVD to be the most common cause of sudden cardiac death in the athlete (Thiene et al. 1988). This research suggests that a specific population may have different genetic subtraits.
In the older athlete, coronary artery disease is by far the most common cause of sudden death. Rarely is sudden death in the older athlete caused by hypertrophic cardiomyopathy, mitral valve prolapse, or acquired valvular conditions (Maron et al. 2014; Nagashima et al. 2003; Semsarian, Sweeting, and Ackerman 2015; Marijon et al. 2015).
Traumatic sudden cardiac death has not captured as much attention because its epidemiology is more difficult to track. However, it is a growing problem that strikes without warning. Between 1996 and 2007, a reported 180 cases of blunt-force death in the United States were attributed to commotio cordis (Maron et al. 2006). Most cases involved children with a mean age of 13, with 95% of the deaths occurring in males (Maron et al. 2013).
Commotio cordis refers to trauma to the chest wall that interrupts the electrical impulse in the heart. If the cardiac rhythm is not promptly normalized, the individual dies. Typically the ribs or sternum is not broken, although some contusions may be found. Research has found that a chest blow occurring during the vulnerable phase of repolarization, just prior to the T-wave peak in the cardiac cycle, can induce ventricular fibrillation (Maron and Estes 2005).
Although children and teenagers with thin chest walls are most vulnerable to commotio cordis (figure 8.6), deaths have been reported in adults. Sports such as baseball, ice hockey, lacrosse, and softball, which have hard projectiles that can strike the chest, have been associated with the greatest number of deaths. Commotio cordis also has occurred in sports such as soccer, football, rugby, and karate, in which the blow came from a soft projectile or a collision. It appears that the timing of the incident, rather than the degree of impact of the object, is the causative factor (Maron and Estes 2005). Commotio cordis is the only significant cause of traumatic sudden cardiac death in athletes.
The type of injury associated with commotio cordis is a blow to the chest wall that interrupts the usual cardiac rhythm.
Red Flags for Traumatic Sudden Cardiac Death
Sports with projectiles that can hit the chest at an inopportune time in the cardiac rhythm cycle have been known to cause commotio cordis in young athletes. These sports include the following: baseball, softball, hockey, lacrosse, soccer, football, karate.
Prevention
Because death can be the outcome, prevention has become the focus of attention for commotio cordis. Changes in practice have ranged from protective padding to softer balls that are used in Little League and softball. Because this may not completely resolve the problem, another solution is defibrillation in conjunction with cardiopulmonary resuscitation (CPR). Defibrillation interrupts the heart rhythm so the heart can "reboot" into a normal rhythm.
The American Heart Association estimates that communities with comprehensive CPR and automated external defibrillator (AED) training achieve 40% survival rates for cardiac arrest victims. If defibrillation is performed within 3 min, the likelihood of survival is high. For every minute of delay the chance of survival drops by as much as 10% (American Heart Association 2013).
The advent of the AED has provided greater public access to life-saving technology. These devices can be operated by trained laypeople and are increasingly affordable in all sectors. The AED is portable, rechargeable, simple to operate, and easy to maintain. The American Red Cross, American Heart Association, and National Safety Council offer AED certification courses in addition to CPR courses for the lay public. The NCAA Sports Medicine Guidelines require planned access to an AED and mandating CPR and first aid certifications for all who work with athlete practices, competition, and skill sessions. Athletic trainers are required to maintain certification in emergency cardiac care, including AED use. They need to have ready access to an AED in order to provide rapid cardiac assessment and care to those in fibrillation. Athletes who suffer a sudden collapse and have agonal or gasping breathing should be treated because they are suffering from a cardiac event (Casa et al. 2012; Solberg et al. 2015). An AED should be applied as soon as possible for heart rhythm analysis and possible defibrillation.
Clinical Tips
Potential Causes of Sudden Death
Sudden collapse in athletes could be caused by heatstroke, a cardiac event, sickle cell collapse, or injury. Understanding the presentation of each will facilitate rapid response and the appropriate disposition.
Emergency Planning
Every athletic site should have planned access to an AED, an emergency medical service (EMS), and an established emergency action plan (EAP), as well as medical personnel trained to respond to sudden collapse.
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How to identify celiac disease
Celiac disease is an autoimmune disorder that affects the gastrointestinal tract and is thought to be triggered by dietary gluten in affected individuals. The disease is characterized by chronic inflammation of the small intestinal mucosa, which leads to atrophy of the small intestinal villi and subsequent malabsorption (Pelkowski and Viera 2014).
Celiac disease is an autoimmune disorder that affects the gastrointestinal tract and is thought to be triggered by dietary gluten in affected individuals. The disease is characterized by chronic inflammation of the small intestinal mucosa, which leads to atrophy of the small intestinal villi and subsequent malabsorption (Pelkowski and Viera 2014). Celiac disease affects approximately 1% of the U.S. population and typically occurs in persons of European ancestry as well as persons of Middle Eastern, Indian, South American, and North African descent. It is two to three times more common in women. Celiac disease is not a food allergy.
Signs and Symptoms
Typical presentation includes chronic diarrhea with cramping and gas pains. Patients often have weight loss, or in the adolescent, delayed onset of growth or puberty. A history of nervousness and/or depression is often present, as is a family history of autoimmune disease. Other complaints may include bone or joint pain, migraines, weakness, fatigue, and anemia (Volta et al. 2015; Vivas et al. 2015; Byrne and Feighery 2015; Mancini, Trojian, and Mancini 2011). Physical examination is often normal, but the patient may present with abdominal distension or dermatitis herpetiformis.
Referral and Diagnostic Tests
Lab tests are performed for differentiating celiac disease and to rule out more common diseases. These include a basic metabolic panel, CBC (iron deficiency), TSH (thyroid disease), vitamin D level, and allergy testing. If celiac disease is suspected from history and physical exam, the initial serologic test is a tissue transglutaminase (tTG) antibody level. This antibody is found in every tissue in the body and acts to join proteins together. In people with celiac disease, tTG activates specific immune cells and triggers the inflammatory response that leads to atrophy of the villi in the small intestine (Mancini, Trojian, and Mancini 2011). The diagnosis is often confirmed with repeat blood tests after 4 wk on a gluten-free diet. Endoscopy with biopsies of the duodenal mucosa may be necessary to confirm the diagnosis. Celiac disease should be differentiated from GERD, pancreatic insufficiency, Crohn's disease, or other inflammatory bowel diseases.
Treatment and Return to Participation
The general treatment is to remove gluten from the diet. The patient can substitute rice, corn, and soybean flour for products that contain gluten. Periodic blood tests are performed to measure the levels of the antibodies. The levels will normalize with gluten abstinence. Abstinence will be required for life because the immune response to gluten will recur if gluten is consumed again. Usually no medications are prescribed for celiac disease, but athletes may benefit from iron, vitamin, and calcium supplements. The most difficult aspect for the athlete with celiac disease is the dietary restrictions while traveling with the team or with set team meals. The athletic trainer may need to check on the gluten-free status of many of the standard gluten-containing products provided by the athletic department, such as energy drinks or meal replacement bars (Mancini, Trojian, and Mancini 2011).
Condition Highlight
Gluten Sensitivity and Intolerance
Over the past 10 yr, the number of people choosing a gluten-free diet (GFD) is much higher than the projected number of celiac disease patients (Lis et al. 2015). This has fueled a global market of gluten-free products and highlights several conditions related to the ingestion of gluten. There are three main forms of gluten reactions: allergic, autoimmune (celiac disease), and immune-mediated conditions (gluten sensitivity) (Sapone et al. 2012). Wheat allergy is an adverse reaction to wheat proteins with onset in minutes to hours after gluten ingestion. It may affect the skin, GI tract, or respiratory tract. Celiac disease or other autoimmune gluten disorders generally present months to years after gluten exposure. There is a third condition where some people experience distress from eating gluten-containing products and show improvement with a GFD. It is distinct from celiac disease and wheat allergies (Vivas et al. 2015). Gluten sensitivity cannot be distinguished clinically; serology tests need to be conducted. Patients with GI discomfort or distress following gluten ingestion should be referred for a follow-up blood test and immune-allergy tests.
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Addressing mental health issues in the athlete
Everyone has symptoms of some type of mental health issue at some time in life when one or several stressors overwhelm the person’s ability to self-regulate or repair. The symptoms are usually, and arbitrarily, labeled either physical or mental.
Everyone has symptoms of some type of mental health issue at some time in life when one or several stressors overwhelm the person's ability to self-regulate or repair. The symptoms are usually, and arbitrarily, labeled either physical or mental. This artificial dichotomy usually does not align with the affected person's reality. Rarely is an athlete with a strained hamstring not also worried about the injury or distressed by the pain. Similarly, the most common initial warning signs of depression are the physical symptoms of tension, restlessness, and disturbed sleep, energy, and appetite. This is because we have overlapping systems of mind, body, spirit, and relationships, each integrally connected to the others. When the homeostasis of one or more systems is disrupted, people instinctively try to correct the problem regardless of its origin. In the mental health domain, signs of distress are emotional, mental, behavioral, and physical.
Framework for Understanding Mental Health
In almost all situations, a variety of overlapping factors contribute to symptom development. The biopsychosocial - spiritual model (BPSS) is a framework for understanding the person's responses in a given situation and the development of symptoms. Symptom etiology may be conceptualized as a pie. Figure 17.1 shows how these various factors overlap and contribute to well-being. In a given person, the various pieces of the BPSS pie may be larger or smaller at any one time. The relative sizes of the pieces greatly influence the person's symptoms and ability to adapt.
The biopsychosocial - spiritual model is a framework for understanding a person's responses in a given situation and the development of symptoms.
For example, two runners may have identical injuries, but the impact of the injury and the course of rehabilitation in these two athletes will usually differ. The amount of pain they have, as well as the length of time until they are ready to compete again, will be influenced not only by the difference in respective levels of physical conditioning and injury history but also by other physical and emotional conditions such as pain tolerance, attitude, perception of the problem, and its implications for life. The situation may also be affected by personality and temperament issues, variable resources for coping, and so on. Another example involves two wrestlers who seem to be equally competitive, but wrestler A, in a struggle to make or maintain weight, develops more obviously disordered eating patterns than wrestler B. Perhaps wrestler A has a family history of obesity and is genetically predisposed toward weight gain more than the other; temperamentally, wrestler A may tend to think more negatively about life challenges, become somewhat self-defeating in the face of adversity, and find emotional comfort in food and the process of eating. Often a variety of factors will help to explain the development of clinically significant problems.
This interplay of variables is the same for athletes as it is for others who are physically active, regardless of whether the symptoms of an injury or condition are physical or emotional. Whereas one athlete may become depressed, another's symptoms may include anxiety or outbursts of anger and physical aggression. Sometimes one piece of the BPSS pie is so big that it seems to account for virtually the whole reason that someone is symptomatic (e.g., the chemical disequilibrium that comes with bipolar disorder). For this reason, it is a good practice to regularly consider the possibility that an organic cause may be the culprit and refer the person for a medical evaluation.
The treatments that have proven effective for the problems discussed in this chapter are based on the same BPSS approach as the assessment and diagnosis. Different strategies can be useful, depending on the biopsychosocial - spiritual components that are implicated in the assessment process. Practitioners often recommend treatment plans based on their assessment and experience, and then these are negotiated with the patient or family members according to personal preferences. The treatment may be offered on either an inpatient or, more commonly, an outpatient basis.
Treatment may also involve the collaboration of a variety of treatment professionals. For example, eating disorder treatment often involves a physician, a registered dietitian, and a psychotherapist. This will be determined based on the severity of symptoms, the difficulty the athlete has in making changes, the amount of support the athlete has, and other resources that affect care, including financial concerns or insurance benefits. The important first step in treatment is accurate assessment followed by clear and well-timed communication and education with the athlete and family. The athletic trainer can play a valuable role here because people are much more likely to engage in treatment or some type of change process if they become convinced that there is a problem, they know what it is, and they know that something can be done about it. This is because most people will want to know what is going on with themselves, how they "got it," and what they can do to "get rid of it" or at least cope more effectively. Additional treatment recommendations specific to various clinical problems are listed in subsequent sections.
Implications for Participation in Athletics
Early identification and treatment are very helpful in preventing problems from worsening, but sometimes the stigma still associated with mental health conditions prevents people from recognizing these problems in themselves or others. In those cases, functioning in one or more areas of life can be affected, sometimes severely. Restricting participation in a sport, if necessary, will depend on the assessment of the athlete's level of functioning by the athlete, the coach, and the athletic trainer. Initially, while the medication dosage is being adjusted, the athlete could experience adverse effects that could affect participation or performance, such as nausea, headache, sedation, disturbed balance, or overstimulation. The National Collegiate Athletic Association (NCAA) has no restrictions on the medications typically used to treat these conditions except for pemoline, a medication prescribed to treat ADHD (National Collegiate Athletic Association 2015).
The last general point to be made is that some people experiencing psychological or substance use disorders may consider suicide or become homicidal. Most health care professionals or other professionals are required by law or by a professional code of ethics to report to the authorities if a patient is a danger to self or others. Athletic trainers, too, may encounter an athlete with depression, panic disorder, or substance abuse who is considering suicide or harming someone else. The athletic trainer must seek immediate consultation if in doubt about the need to report. An assessment of whether one is suicidal or homicidal includes determining whether the person has a specific plan, the means to carry it out, the intention to carry it out, and how lethal the plan is. Those with a personal or family history of this type of ideation or action or whose judgment is impaired, perhaps through the use of substances, are more at risk to follow through.
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Identifying Exercise-Induced Bronchospasm
The terms EIA and EIB are often used interchangeably, but EIB specifically denotes the reduction in lung function that occurs after a standardized exercise test (Carver 2009). More recently, the term exercise-induced bronchoconstriction has been introduced as actual spasm of the airways does not always occur.
The terms exercise-induced asthma (EIA) and exercise-induced bronchoconstriction (EIB) are often used interchangeably, but EIB specifically denotes the reduction in lung function that occurs after a standardized exercise test (Carver 2009). More recently, the term exercise-induced bronchoconstriction has been introduced as actual spasm of the airways does not always occur. Some clinicians use EIA to describe individuals with known asthma who have bronchoconstriction during exercise. However, some use EIA to describe patients who have bronchoconstriction only during exercise, and they use EIB to describe patients with asthma who have bronchoconstriction with exercise. Generally, EIB is used to indicate bronchospasm with decreased pulmonary function testing following exercise, and EIA is used to indicate those patients with asthma difficulties associated with exercise.
Symptoms of EIB usually occur 10 to 15 min after the onset of strenuous exercise and are defined by a fall in FEV1 of 15% or more during exercise spirometry. EIB is more common in winter sport athletes who compete in cold ambient temperatures (Carey, Aase, and Pliego 2010).
Signs and Symptoms
EIB should be suspected in any athlete who complains of shortness of breath, dyspnea, cough, chest congestion, or tightness with exertion. These symptoms usually occur during strenuous exercise and peak about 5 to 10 min after exercise (Hull 2012; Krafczyk and Asplund 2011; Simpson, Romer, and Kippelen 2015). Other subtle clues might be a dry cough that develops after practice or exercise (i.e., locker-room cough) or simply unusual fatigue compared with similarly trained athletes. Athletes will often complain that they feel out of shape despite regular training. Self-reported symptoms have been shown to be poor predictors of EIB because other conditions can cause similar symptoms. Symptoms alone should not be used to diagnose EIB.
In athletes suspected of having EIB, other etiologies, such as acute sinusitis, otitis media (middle ear infection), bronchitis, or even pneumonia, need to be excluded, particularly in the context of other constitutional symptoms, such as fever, chills, or night sweats. If fatigue is the only presenting symptom, deconditioning may also be a cause. In addition, environmental allergies can account for many of the nonspecific symptoms that mimic EIB (Backer 2010; Hull et al. 2012; Stack and Hakemi 2011). More serious cardiac causes, such as arrhythmias and pericarditis, might also need to be excluded. Another important differential is exercise-induced laryngeal obstruction (EILO), where the wheezing and dyspnea are caused by transient obstruction of the upper airways during exercise (Nielsen 2013; Backer 2010).
Referral and Diagnostic Tests
The physical examination is usually normal. Some athletes with EIB may experience symptoms that develop several hours after exercise. This late-phase response is due to the activity of inflammatory mediators. Most commonly, a bronchial provocation challenge is used to determine the diagnosis of EIB (Parsons et al. 2011; Hayden et al. 2011; Morris 2010). Figure 7.9 shows a decision tree commonly used for the diagnosis of EIB. Alternatively, many physicians choose to just evaluate the patient's response to an empirical trial of a ß-agonist medication before exercise.
Decision tree for the diagnosis of exercise-induced bronchoconstriction (EIB).
Treatment and Return to Participation
The treatment of choice in EIB is an inhaled ß2-agonist from a metered-dose inhaler (e.g., albuterol) taken 15 to 30 min before the onset of exercise. An athlete who has asthma symptoms outside the exercise setting or who is using a ß2-agonist more than three times per week should be treated with a regular inhaled corticosteroid. Here is how to properly use an inhaler:
- Remove dust cap and shake the inhaler system before each use.
- Inspect mouthpiece for contamination or foreign objects.
- Breathe out through the mouth, exhaling as completely as possible.
- Hold the inhaler system upright with mouthpiece in mouth and lips closed tightly around mouthpiece.
- Breathe in slowly while pressing down on the metal cartridge.
- Hold breath as long as possible.
- Release pressure while still holding breath.
- Remove mouthpiece.
- Wait for the container to repressurize, shake, and then repeat steps 3 through 8 when more than one inhalation is prescribed.
- Rinse mouth with water after prescribed number of inhalations.
- Clean the inhaler system every few days by removing metal cartridge and rinsing the plastic inhaler and cap with running warm water. Replace cartridge and cap.
Emerging studies show promise using long-acting ß2-agonists such as salmeterol and leukotriene inhibitors such as montelukast (Singulair) (Parsons 2010). Other nonpharmacological strategies include pre - warm-up bursts of physical activity at 80% to 90% of the individual's maximal workload to induce a refractory period that lasts up to 3 h after the initial attack of EIB (Hull et al. 2012; Millward et al. 2009; Boulet, Hancox, and Fitch 2010). Strategies to humidify inspired air and dietary interventions may also prove to be beneficial (Carey, Aase, and Pliego 2010; Bussotti, Di Marco, and Marchese 2014).
For an athlete experiencing a severe asthma attack or when an inhaler is ineffective, a nebulizer may be used. A nebulizer, also known as an atomizer, is a machine that vaporizes liquid medication into a fine mist to be inhaled into the lungs via a mouthpiece or mask. Although studies have shown that both inhalers and nebulizers tend to be equally effective in delivering medications, nebulizers are preferred for use in more serious rescue situations when the patient is experiencing a severe asthma attack. Nebulizers can administer a higher dose of medication, but inhalers are easier to use, preferred for their portability and low cost, and good for everyday use. Medications typically administered with a nebulizer include albuterol and ipratropium (Atrovent).
Athletes with controlled EIB need not be excluded or discouraged from participating in sports. Effective strategies, both pharmacological and nonpharmacological, exist that can allow an athlete to compete even at an elite level.
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Causes of Sudden Cardiac Death in Athletes
Death by sudden cardiac arrest (SCA) is a rare event in the young athlete. In the United States, elite athletes are viewed as near invincible because of their incredible physical feats.
Death by sudden cardiac arrest (SCA) is a rare event in the young athlete. In the United States, elite athletes are viewed as near invincible because of their incredible physical feats. Nevertheless, it is reported that the rate of collegiate athlete death due to SCA is higher than that of high school athletes, with a suspected 110 SCA deaths annually in the United States among young athletes (Casa et al. 2012). Any time a tragedy of this proportion occurs, the public reacts with disbelief, and medical knowledge is called into question. Studies that have tracked these deaths during sports used the National Federation of State High School Associations (NFHS), the National Collegiate Athletic Association (NCAA) governing organizations, and state and federally funded research groups for data collection, such as the National Center for Catastrophic Sport Injury Research (NCCSIR), based in Chapel Hill, North Carolina. Approximately 90% of the data collected involved male athletes, with an equal distribution between Caucasians and African-Americans (Borjesson and Pelliccia 2009). According to the NCCSIR, there were 10 indirect (due to exertion) fatalities in middle school through college football athletes in 2014, and six were attributed to a cardiac event (Kucera et al. 2015). An additional five football athletes died of suspected cardiac conditions due to nonexertional factors in the same year (Kucera et al. 2015). Sudden death cases in young women are rare, and the most common cause of sudden cardiac death was congenital cardiac disease.
The prevalence of sudden cardiac death in young athletes (those less than 35-year-old) is estimated to be between 1 and 3 in 100,000 (Borjesson and Pelliccia 2009). This is much higher than statistics reported in a more general population of active individuals (Harmon, Klossner, and Drezner 2011). These data indicate that active people are not immune to cardiovascular events that may result in death.
Causes
The most common cause of sudden cardiac death in the young athlete is hypertrophic cardiomyopathy, which accounts for up to 50% of the cases. Other significant causes of sudden cardiac death in a young athlete are coronary artery anomalies, increased cardiac mass, aortic rupture, myocarditis, and aortic stenosis(Borjesson and Pelliccia 2009).Rare causes include dilated cardiomyopathy, atherosclerotic coronary artery disease, mitral valve prolapse, isolated arrhythmias such as long QT syndrome and Wolff-Parkinson-White syndrome, and arrhythmogenic right ventricular dysplasia (ARVD) (Harmon, Klossner, and Drezner 2011). In the Veneto region of Italy, researchers have found ARVD to be the most common cause of sudden cardiac death in the athlete (Thiene et al. 1988). This research suggests that a specific population may have different genetic subtraits.
In the older athlete, coronary artery disease is by far the most common cause of sudden death. Rarely is sudden death in the older athlete caused by hypertrophic cardiomyopathy, mitral valve prolapse, or acquired valvular conditions (Maron et al. 2014; Nagashima et al. 2003; Semsarian, Sweeting, and Ackerman 2015; Marijon et al. 2015).
Traumatic sudden cardiac death has not captured as much attention because its epidemiology is more difficult to track. However, it is a growing problem that strikes without warning. Between 1996 and 2007, a reported 180 cases of blunt-force death in the United States were attributed to commotio cordis (Maron et al. 2006). Most cases involved children with a mean age of 13, with 95% of the deaths occurring in males (Maron et al. 2013).
Commotio cordis refers to trauma to the chest wall that interrupts the electrical impulse in the heart. If the cardiac rhythm is not promptly normalized, the individual dies. Typically the ribs or sternum is not broken, although some contusions may be found. Research has found that a chest blow occurring during the vulnerable phase of repolarization, just prior to the T-wave peak in the cardiac cycle, can induce ventricular fibrillation (Maron and Estes 2005).
Although children and teenagers with thin chest walls are most vulnerable to commotio cordis (figure 8.6), deaths have been reported in adults. Sports such as baseball, ice hockey, lacrosse, and softball, which have hard projectiles that can strike the chest, have been associated with the greatest number of deaths. Commotio cordis also has occurred in sports such as soccer, football, rugby, and karate, in which the blow came from a soft projectile or a collision. It appears that the timing of the incident, rather than the degree of impact of the object, is the causative factor (Maron and Estes 2005). Commotio cordis is the only significant cause of traumatic sudden cardiac death in athletes.
The type of injury associated with commotio cordis is a blow to the chest wall that interrupts the usual cardiac rhythm.
Red Flags for Traumatic Sudden Cardiac Death
Sports with projectiles that can hit the chest at an inopportune time in the cardiac rhythm cycle have been known to cause commotio cordis in young athletes. These sports include the following: baseball, softball, hockey, lacrosse, soccer, football, karate.
Prevention
Because death can be the outcome, prevention has become the focus of attention for commotio cordis. Changes in practice have ranged from protective padding to softer balls that are used in Little League and softball. Because this may not completely resolve the problem, another solution is defibrillation in conjunction with cardiopulmonary resuscitation (CPR). Defibrillation interrupts the heart rhythm so the heart can "reboot" into a normal rhythm.
The American Heart Association estimates that communities with comprehensive CPR and automated external defibrillator (AED) training achieve 40% survival rates for cardiac arrest victims. If defibrillation is performed within 3 min, the likelihood of survival is high. For every minute of delay the chance of survival drops by as much as 10% (American Heart Association 2013).
The advent of the AED has provided greater public access to life-saving technology. These devices can be operated by trained laypeople and are increasingly affordable in all sectors. The AED is portable, rechargeable, simple to operate, and easy to maintain. The American Red Cross, American Heart Association, and National Safety Council offer AED certification courses in addition to CPR courses for the lay public. The NCAA Sports Medicine Guidelines require planned access to an AED and mandating CPR and first aid certifications for all who work with athlete practices, competition, and skill sessions. Athletic trainers are required to maintain certification in emergency cardiac care, including AED use. They need to have ready access to an AED in order to provide rapid cardiac assessment and care to those in fibrillation. Athletes who suffer a sudden collapse and have agonal or gasping breathing should be treated because they are suffering from a cardiac event (Casa et al. 2012; Solberg et al. 2015). An AED should be applied as soon as possible for heart rhythm analysis and possible defibrillation.
Clinical Tips
Potential Causes of Sudden Death
Sudden collapse in athletes could be caused by heatstroke, a cardiac event, sickle cell collapse, or injury. Understanding the presentation of each will facilitate rapid response and the appropriate disposition.
Emergency Planning
Every athletic site should have planned access to an AED, an emergency medical service (EMS), and an established emergency action plan (EAP), as well as medical personnel trained to respond to sudden collapse.
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How to identify celiac disease
Celiac disease is an autoimmune disorder that affects the gastrointestinal tract and is thought to be triggered by dietary gluten in affected individuals. The disease is characterized by chronic inflammation of the small intestinal mucosa, which leads to atrophy of the small intestinal villi and subsequent malabsorption (Pelkowski and Viera 2014).
Celiac disease is an autoimmune disorder that affects the gastrointestinal tract and is thought to be triggered by dietary gluten in affected individuals. The disease is characterized by chronic inflammation of the small intestinal mucosa, which leads to atrophy of the small intestinal villi and subsequent malabsorption (Pelkowski and Viera 2014). Celiac disease affects approximately 1% of the U.S. population and typically occurs in persons of European ancestry as well as persons of Middle Eastern, Indian, South American, and North African descent. It is two to three times more common in women. Celiac disease is not a food allergy.
Signs and Symptoms
Typical presentation includes chronic diarrhea with cramping and gas pains. Patients often have weight loss, or in the adolescent, delayed onset of growth or puberty. A history of nervousness and/or depression is often present, as is a family history of autoimmune disease. Other complaints may include bone or joint pain, migraines, weakness, fatigue, and anemia (Volta et al. 2015; Vivas et al. 2015; Byrne and Feighery 2015; Mancini, Trojian, and Mancini 2011). Physical examination is often normal, but the patient may present with abdominal distension or dermatitis herpetiformis.
Referral and Diagnostic Tests
Lab tests are performed for differentiating celiac disease and to rule out more common diseases. These include a basic metabolic panel, CBC (iron deficiency), TSH (thyroid disease), vitamin D level, and allergy testing. If celiac disease is suspected from history and physical exam, the initial serologic test is a tissue transglutaminase (tTG) antibody level. This antibody is found in every tissue in the body and acts to join proteins together. In people with celiac disease, tTG activates specific immune cells and triggers the inflammatory response that leads to atrophy of the villi in the small intestine (Mancini, Trojian, and Mancini 2011). The diagnosis is often confirmed with repeat blood tests after 4 wk on a gluten-free diet. Endoscopy with biopsies of the duodenal mucosa may be necessary to confirm the diagnosis. Celiac disease should be differentiated from GERD, pancreatic insufficiency, Crohn's disease, or other inflammatory bowel diseases.
Treatment and Return to Participation
The general treatment is to remove gluten from the diet. The patient can substitute rice, corn, and soybean flour for products that contain gluten. Periodic blood tests are performed to measure the levels of the antibodies. The levels will normalize with gluten abstinence. Abstinence will be required for life because the immune response to gluten will recur if gluten is consumed again. Usually no medications are prescribed for celiac disease, but athletes may benefit from iron, vitamin, and calcium supplements. The most difficult aspect for the athlete with celiac disease is the dietary restrictions while traveling with the team or with set team meals. The athletic trainer may need to check on the gluten-free status of many of the standard gluten-containing products provided by the athletic department, such as energy drinks or meal replacement bars (Mancini, Trojian, and Mancini 2011).
Condition Highlight
Gluten Sensitivity and Intolerance
Over the past 10 yr, the number of people choosing a gluten-free diet (GFD) is much higher than the projected number of celiac disease patients (Lis et al. 2015). This has fueled a global market of gluten-free products and highlights several conditions related to the ingestion of gluten. There are three main forms of gluten reactions: allergic, autoimmune (celiac disease), and immune-mediated conditions (gluten sensitivity) (Sapone et al. 2012). Wheat allergy is an adverse reaction to wheat proteins with onset in minutes to hours after gluten ingestion. It may affect the skin, GI tract, or respiratory tract. Celiac disease or other autoimmune gluten disorders generally present months to years after gluten exposure. There is a third condition where some people experience distress from eating gluten-containing products and show improvement with a GFD. It is distinct from celiac disease and wheat allergies (Vivas et al. 2015). Gluten sensitivity cannot be distinguished clinically; serology tests need to be conducted. Patients with GI discomfort or distress following gluten ingestion should be referred for a follow-up blood test and immune-allergy tests.
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Addressing mental health issues in the athlete
Everyone has symptoms of some type of mental health issue at some time in life when one or several stressors overwhelm the person’s ability to self-regulate or repair. The symptoms are usually, and arbitrarily, labeled either physical or mental.
Everyone has symptoms of some type of mental health issue at some time in life when one or several stressors overwhelm the person's ability to self-regulate or repair. The symptoms are usually, and arbitrarily, labeled either physical or mental. This artificial dichotomy usually does not align with the affected person's reality. Rarely is an athlete with a strained hamstring not also worried about the injury or distressed by the pain. Similarly, the most common initial warning signs of depression are the physical symptoms of tension, restlessness, and disturbed sleep, energy, and appetite. This is because we have overlapping systems of mind, body, spirit, and relationships, each integrally connected to the others. When the homeostasis of one or more systems is disrupted, people instinctively try to correct the problem regardless of its origin. In the mental health domain, signs of distress are emotional, mental, behavioral, and physical.
Framework for Understanding Mental Health
In almost all situations, a variety of overlapping factors contribute to symptom development. The biopsychosocial - spiritual model (BPSS) is a framework for understanding the person's responses in a given situation and the development of symptoms. Symptom etiology may be conceptualized as a pie. Figure 17.1 shows how these various factors overlap and contribute to well-being. In a given person, the various pieces of the BPSS pie may be larger or smaller at any one time. The relative sizes of the pieces greatly influence the person's symptoms and ability to adapt.
The biopsychosocial - spiritual model is a framework for understanding a person's responses in a given situation and the development of symptoms.
For example, two runners may have identical injuries, but the impact of the injury and the course of rehabilitation in these two athletes will usually differ. The amount of pain they have, as well as the length of time until they are ready to compete again, will be influenced not only by the difference in respective levels of physical conditioning and injury history but also by other physical and emotional conditions such as pain tolerance, attitude, perception of the problem, and its implications for life. The situation may also be affected by personality and temperament issues, variable resources for coping, and so on. Another example involves two wrestlers who seem to be equally competitive, but wrestler A, in a struggle to make or maintain weight, develops more obviously disordered eating patterns than wrestler B. Perhaps wrestler A has a family history of obesity and is genetically predisposed toward weight gain more than the other; temperamentally, wrestler A may tend to think more negatively about life challenges, become somewhat self-defeating in the face of adversity, and find emotional comfort in food and the process of eating. Often a variety of factors will help to explain the development of clinically significant problems.
This interplay of variables is the same for athletes as it is for others who are physically active, regardless of whether the symptoms of an injury or condition are physical or emotional. Whereas one athlete may become depressed, another's symptoms may include anxiety or outbursts of anger and physical aggression. Sometimes one piece of the BPSS pie is so big that it seems to account for virtually the whole reason that someone is symptomatic (e.g., the chemical disequilibrium that comes with bipolar disorder). For this reason, it is a good practice to regularly consider the possibility that an organic cause may be the culprit and refer the person for a medical evaluation.
The treatments that have proven effective for the problems discussed in this chapter are based on the same BPSS approach as the assessment and diagnosis. Different strategies can be useful, depending on the biopsychosocial - spiritual components that are implicated in the assessment process. Practitioners often recommend treatment plans based on their assessment and experience, and then these are negotiated with the patient or family members according to personal preferences. The treatment may be offered on either an inpatient or, more commonly, an outpatient basis.
Treatment may also involve the collaboration of a variety of treatment professionals. For example, eating disorder treatment often involves a physician, a registered dietitian, and a psychotherapist. This will be determined based on the severity of symptoms, the difficulty the athlete has in making changes, the amount of support the athlete has, and other resources that affect care, including financial concerns or insurance benefits. The important first step in treatment is accurate assessment followed by clear and well-timed communication and education with the athlete and family. The athletic trainer can play a valuable role here because people are much more likely to engage in treatment or some type of change process if they become convinced that there is a problem, they know what it is, and they know that something can be done about it. This is because most people will want to know what is going on with themselves, how they "got it," and what they can do to "get rid of it" or at least cope more effectively. Additional treatment recommendations specific to various clinical problems are listed in subsequent sections.
Implications for Participation in Athletics
Early identification and treatment are very helpful in preventing problems from worsening, but sometimes the stigma still associated with mental health conditions prevents people from recognizing these problems in themselves or others. In those cases, functioning in one or more areas of life can be affected, sometimes severely. Restricting participation in a sport, if necessary, will depend on the assessment of the athlete's level of functioning by the athlete, the coach, and the athletic trainer. Initially, while the medication dosage is being adjusted, the athlete could experience adverse effects that could affect participation or performance, such as nausea, headache, sedation, disturbed balance, or overstimulation. The National Collegiate Athletic Association (NCAA) has no restrictions on the medications typically used to treat these conditions except for pemoline, a medication prescribed to treat ADHD (National Collegiate Athletic Association 2015).
The last general point to be made is that some people experiencing psychological or substance use disorders may consider suicide or become homicidal. Most health care professionals or other professionals are required by law or by a professional code of ethics to report to the authorities if a patient is a danger to self or others. Athletic trainers, too, may encounter an athlete with depression, panic disorder, or substance abuse who is considering suicide or harming someone else. The athletic trainer must seek immediate consultation if in doubt about the need to report. An assessment of whether one is suicidal or homicidal includes determining whether the person has a specific plan, the means to carry it out, the intention to carry it out, and how lethal the plan is. Those with a personal or family history of this type of ideation or action or whose judgment is impaired, perhaps through the use of substances, are more at risk to follow through.
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Identifying Exercise-Induced Bronchospasm
The terms EIA and EIB are often used interchangeably, but EIB specifically denotes the reduction in lung function that occurs after a standardized exercise test (Carver 2009). More recently, the term exercise-induced bronchoconstriction has been introduced as actual spasm of the airways does not always occur.
The terms exercise-induced asthma (EIA) and exercise-induced bronchoconstriction (EIB) are often used interchangeably, but EIB specifically denotes the reduction in lung function that occurs after a standardized exercise test (Carver 2009). More recently, the term exercise-induced bronchoconstriction has been introduced as actual spasm of the airways does not always occur. Some clinicians use EIA to describe individuals with known asthma who have bronchoconstriction during exercise. However, some use EIA to describe patients who have bronchoconstriction only during exercise, and they use EIB to describe patients with asthma who have bronchoconstriction with exercise. Generally, EIB is used to indicate bronchospasm with decreased pulmonary function testing following exercise, and EIA is used to indicate those patients with asthma difficulties associated with exercise.
Symptoms of EIB usually occur 10 to 15 min after the onset of strenuous exercise and are defined by a fall in FEV1 of 15% or more during exercise spirometry. EIB is more common in winter sport athletes who compete in cold ambient temperatures (Carey, Aase, and Pliego 2010).
Signs and Symptoms
EIB should be suspected in any athlete who complains of shortness of breath, dyspnea, cough, chest congestion, or tightness with exertion. These symptoms usually occur during strenuous exercise and peak about 5 to 10 min after exercise (Hull 2012; Krafczyk and Asplund 2011; Simpson, Romer, and Kippelen 2015). Other subtle clues might be a dry cough that develops after practice or exercise (i.e., locker-room cough) or simply unusual fatigue compared with similarly trained athletes. Athletes will often complain that they feel out of shape despite regular training. Self-reported symptoms have been shown to be poor predictors of EIB because other conditions can cause similar symptoms. Symptoms alone should not be used to diagnose EIB.
In athletes suspected of having EIB, other etiologies, such as acute sinusitis, otitis media (middle ear infection), bronchitis, or even pneumonia, need to be excluded, particularly in the context of other constitutional symptoms, such as fever, chills, or night sweats. If fatigue is the only presenting symptom, deconditioning may also be a cause. In addition, environmental allergies can account for many of the nonspecific symptoms that mimic EIB (Backer 2010; Hull et al. 2012; Stack and Hakemi 2011). More serious cardiac causes, such as arrhythmias and pericarditis, might also need to be excluded. Another important differential is exercise-induced laryngeal obstruction (EILO), where the wheezing and dyspnea are caused by transient obstruction of the upper airways during exercise (Nielsen 2013; Backer 2010).
Referral and Diagnostic Tests
The physical examination is usually normal. Some athletes with EIB may experience symptoms that develop several hours after exercise. This late-phase response is due to the activity of inflammatory mediators. Most commonly, a bronchial provocation challenge is used to determine the diagnosis of EIB (Parsons et al. 2011; Hayden et al. 2011; Morris 2010). Figure 7.9 shows a decision tree commonly used for the diagnosis of EIB. Alternatively, many physicians choose to just evaluate the patient's response to an empirical trial of a ß-agonist medication before exercise.
Decision tree for the diagnosis of exercise-induced bronchoconstriction (EIB).
Treatment and Return to Participation
The treatment of choice in EIB is an inhaled ß2-agonist from a metered-dose inhaler (e.g., albuterol) taken 15 to 30 min before the onset of exercise. An athlete who has asthma symptoms outside the exercise setting or who is using a ß2-agonist more than three times per week should be treated with a regular inhaled corticosteroid. Here is how to properly use an inhaler:
- Remove dust cap and shake the inhaler system before each use.
- Inspect mouthpiece for contamination or foreign objects.
- Breathe out through the mouth, exhaling as completely as possible.
- Hold the inhaler system upright with mouthpiece in mouth and lips closed tightly around mouthpiece.
- Breathe in slowly while pressing down on the metal cartridge.
- Hold breath as long as possible.
- Release pressure while still holding breath.
- Remove mouthpiece.
- Wait for the container to repressurize, shake, and then repeat steps 3 through 8 when more than one inhalation is prescribed.
- Rinse mouth with water after prescribed number of inhalations.
- Clean the inhaler system every few days by removing metal cartridge and rinsing the plastic inhaler and cap with running warm water. Replace cartridge and cap.
Emerging studies show promise using long-acting ß2-agonists such as salmeterol and leukotriene inhibitors such as montelukast (Singulair) (Parsons 2010). Other nonpharmacological strategies include pre - warm-up bursts of physical activity at 80% to 90% of the individual's maximal workload to induce a refractory period that lasts up to 3 h after the initial attack of EIB (Hull et al. 2012; Millward et al. 2009; Boulet, Hancox, and Fitch 2010). Strategies to humidify inspired air and dietary interventions may also prove to be beneficial (Carey, Aase, and Pliego 2010; Bussotti, Di Marco, and Marchese 2014).
For an athlete experiencing a severe asthma attack or when an inhaler is ineffective, a nebulizer may be used. A nebulizer, also known as an atomizer, is a machine that vaporizes liquid medication into a fine mist to be inhaled into the lungs via a mouthpiece or mask. Although studies have shown that both inhalers and nebulizers tend to be equally effective in delivering medications, nebulizers are preferred for use in more serious rescue situations when the patient is experiencing a severe asthma attack. Nebulizers can administer a higher dose of medication, but inhalers are easier to use, preferred for their portability and low cost, and good for everyday use. Medications typically administered with a nebulizer include albuterol and ipratropium (Atrovent).
Athletes with controlled EIB need not be excluded or discouraged from participating in sports. Effective strategies, both pharmacological and nonpharmacological, exist that can allow an athlete to compete even at an elite level.
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Causes of Sudden Cardiac Death in Athletes
Death by sudden cardiac arrest (SCA) is a rare event in the young athlete. In the United States, elite athletes are viewed as near invincible because of their incredible physical feats.
Death by sudden cardiac arrest (SCA) is a rare event in the young athlete. In the United States, elite athletes are viewed as near invincible because of their incredible physical feats. Nevertheless, it is reported that the rate of collegiate athlete death due to SCA is higher than that of high school athletes, with a suspected 110 SCA deaths annually in the United States among young athletes (Casa et al. 2012). Any time a tragedy of this proportion occurs, the public reacts with disbelief, and medical knowledge is called into question. Studies that have tracked these deaths during sports used the National Federation of State High School Associations (NFHS), the National Collegiate Athletic Association (NCAA) governing organizations, and state and federally funded research groups for data collection, such as the National Center for Catastrophic Sport Injury Research (NCCSIR), based in Chapel Hill, North Carolina. Approximately 90% of the data collected involved male athletes, with an equal distribution between Caucasians and African-Americans (Borjesson and Pelliccia 2009). According to the NCCSIR, there were 10 indirect (due to exertion) fatalities in middle school through college football athletes in 2014, and six were attributed to a cardiac event (Kucera et al. 2015). An additional five football athletes died of suspected cardiac conditions due to nonexertional factors in the same year (Kucera et al. 2015). Sudden death cases in young women are rare, and the most common cause of sudden cardiac death was congenital cardiac disease.
The prevalence of sudden cardiac death in young athletes (those less than 35-year-old) is estimated to be between 1 and 3 in 100,000 (Borjesson and Pelliccia 2009). This is much higher than statistics reported in a more general population of active individuals (Harmon, Klossner, and Drezner 2011). These data indicate that active people are not immune to cardiovascular events that may result in death.
Causes
The most common cause of sudden cardiac death in the young athlete is hypertrophic cardiomyopathy, which accounts for up to 50% of the cases. Other significant causes of sudden cardiac death in a young athlete are coronary artery anomalies, increased cardiac mass, aortic rupture, myocarditis, and aortic stenosis(Borjesson and Pelliccia 2009).Rare causes include dilated cardiomyopathy, atherosclerotic coronary artery disease, mitral valve prolapse, isolated arrhythmias such as long QT syndrome and Wolff-Parkinson-White syndrome, and arrhythmogenic right ventricular dysplasia (ARVD) (Harmon, Klossner, and Drezner 2011). In the Veneto region of Italy, researchers have found ARVD to be the most common cause of sudden cardiac death in the athlete (Thiene et al. 1988). This research suggests that a specific population may have different genetic subtraits.
In the older athlete, coronary artery disease is by far the most common cause of sudden death. Rarely is sudden death in the older athlete caused by hypertrophic cardiomyopathy, mitral valve prolapse, or acquired valvular conditions (Maron et al. 2014; Nagashima et al. 2003; Semsarian, Sweeting, and Ackerman 2015; Marijon et al. 2015).
Traumatic sudden cardiac death has not captured as much attention because its epidemiology is more difficult to track. However, it is a growing problem that strikes without warning. Between 1996 and 2007, a reported 180 cases of blunt-force death in the United States were attributed to commotio cordis (Maron et al. 2006). Most cases involved children with a mean age of 13, with 95% of the deaths occurring in males (Maron et al. 2013).
Commotio cordis refers to trauma to the chest wall that interrupts the electrical impulse in the heart. If the cardiac rhythm is not promptly normalized, the individual dies. Typically the ribs or sternum is not broken, although some contusions may be found. Research has found that a chest blow occurring during the vulnerable phase of repolarization, just prior to the T-wave peak in the cardiac cycle, can induce ventricular fibrillation (Maron and Estes 2005).
Although children and teenagers with thin chest walls are most vulnerable to commotio cordis (figure 8.6), deaths have been reported in adults. Sports such as baseball, ice hockey, lacrosse, and softball, which have hard projectiles that can strike the chest, have been associated with the greatest number of deaths. Commotio cordis also has occurred in sports such as soccer, football, rugby, and karate, in which the blow came from a soft projectile or a collision. It appears that the timing of the incident, rather than the degree of impact of the object, is the causative factor (Maron and Estes 2005). Commotio cordis is the only significant cause of traumatic sudden cardiac death in athletes.
The type of injury associated with commotio cordis is a blow to the chest wall that interrupts the usual cardiac rhythm.
Red Flags for Traumatic Sudden Cardiac Death
Sports with projectiles that can hit the chest at an inopportune time in the cardiac rhythm cycle have been known to cause commotio cordis in young athletes. These sports include the following: baseball, softball, hockey, lacrosse, soccer, football, karate.
Prevention
Because death can be the outcome, prevention has become the focus of attention for commotio cordis. Changes in practice have ranged from protective padding to softer balls that are used in Little League and softball. Because this may not completely resolve the problem, another solution is defibrillation in conjunction with cardiopulmonary resuscitation (CPR). Defibrillation interrupts the heart rhythm so the heart can "reboot" into a normal rhythm.
The American Heart Association estimates that communities with comprehensive CPR and automated external defibrillator (AED) training achieve 40% survival rates for cardiac arrest victims. If defibrillation is performed within 3 min, the likelihood of survival is high. For every minute of delay the chance of survival drops by as much as 10% (American Heart Association 2013).
The advent of the AED has provided greater public access to life-saving technology. These devices can be operated by trained laypeople and are increasingly affordable in all sectors. The AED is portable, rechargeable, simple to operate, and easy to maintain. The American Red Cross, American Heart Association, and National Safety Council offer AED certification courses in addition to CPR courses for the lay public. The NCAA Sports Medicine Guidelines require planned access to an AED and mandating CPR and first aid certifications for all who work with athlete practices, competition, and skill sessions. Athletic trainers are required to maintain certification in emergency cardiac care, including AED use. They need to have ready access to an AED in order to provide rapid cardiac assessment and care to those in fibrillation. Athletes who suffer a sudden collapse and have agonal or gasping breathing should be treated because they are suffering from a cardiac event (Casa et al. 2012; Solberg et al. 2015). An AED should be applied as soon as possible for heart rhythm analysis and possible defibrillation.
Clinical Tips
Potential Causes of Sudden Death
Sudden collapse in athletes could be caused by heatstroke, a cardiac event, sickle cell collapse, or injury. Understanding the presentation of each will facilitate rapid response and the appropriate disposition.
Emergency Planning
Every athletic site should have planned access to an AED, an emergency medical service (EMS), and an established emergency action plan (EAP), as well as medical personnel trained to respond to sudden collapse.
Learn more about Medical Conditions in the Athlete, Third Edition.
How to identify celiac disease
Celiac disease is an autoimmune disorder that affects the gastrointestinal tract and is thought to be triggered by dietary gluten in affected individuals. The disease is characterized by chronic inflammation of the small intestinal mucosa, which leads to atrophy of the small intestinal villi and subsequent malabsorption (Pelkowski and Viera 2014).
Celiac disease is an autoimmune disorder that affects the gastrointestinal tract and is thought to be triggered by dietary gluten in affected individuals. The disease is characterized by chronic inflammation of the small intestinal mucosa, which leads to atrophy of the small intestinal villi and subsequent malabsorption (Pelkowski and Viera 2014). Celiac disease affects approximately 1% of the U.S. population and typically occurs in persons of European ancestry as well as persons of Middle Eastern, Indian, South American, and North African descent. It is two to three times more common in women. Celiac disease is not a food allergy.
Signs and Symptoms
Typical presentation includes chronic diarrhea with cramping and gas pains. Patients often have weight loss, or in the adolescent, delayed onset of growth or puberty. A history of nervousness and/or depression is often present, as is a family history of autoimmune disease. Other complaints may include bone or joint pain, migraines, weakness, fatigue, and anemia (Volta et al. 2015; Vivas et al. 2015; Byrne and Feighery 2015; Mancini, Trojian, and Mancini 2011). Physical examination is often normal, but the patient may present with abdominal distension or dermatitis herpetiformis.
Referral and Diagnostic Tests
Lab tests are performed for differentiating celiac disease and to rule out more common diseases. These include a basic metabolic panel, CBC (iron deficiency), TSH (thyroid disease), vitamin D level, and allergy testing. If celiac disease is suspected from history and physical exam, the initial serologic test is a tissue transglutaminase (tTG) antibody level. This antibody is found in every tissue in the body and acts to join proteins together. In people with celiac disease, tTG activates specific immune cells and triggers the inflammatory response that leads to atrophy of the villi in the small intestine (Mancini, Trojian, and Mancini 2011). The diagnosis is often confirmed with repeat blood tests after 4 wk on a gluten-free diet. Endoscopy with biopsies of the duodenal mucosa may be necessary to confirm the diagnosis. Celiac disease should be differentiated from GERD, pancreatic insufficiency, Crohn's disease, or other inflammatory bowel diseases.
Treatment and Return to Participation
The general treatment is to remove gluten from the diet. The patient can substitute rice, corn, and soybean flour for products that contain gluten. Periodic blood tests are performed to measure the levels of the antibodies. The levels will normalize with gluten abstinence. Abstinence will be required for life because the immune response to gluten will recur if gluten is consumed again. Usually no medications are prescribed for celiac disease, but athletes may benefit from iron, vitamin, and calcium supplements. The most difficult aspect for the athlete with celiac disease is the dietary restrictions while traveling with the team or with set team meals. The athletic trainer may need to check on the gluten-free status of many of the standard gluten-containing products provided by the athletic department, such as energy drinks or meal replacement bars (Mancini, Trojian, and Mancini 2011).
Condition Highlight
Gluten Sensitivity and Intolerance
Over the past 10 yr, the number of people choosing a gluten-free diet (GFD) is much higher than the projected number of celiac disease patients (Lis et al. 2015). This has fueled a global market of gluten-free products and highlights several conditions related to the ingestion of gluten. There are three main forms of gluten reactions: allergic, autoimmune (celiac disease), and immune-mediated conditions (gluten sensitivity) (Sapone et al. 2012). Wheat allergy is an adverse reaction to wheat proteins with onset in minutes to hours after gluten ingestion. It may affect the skin, GI tract, or respiratory tract. Celiac disease or other autoimmune gluten disorders generally present months to years after gluten exposure. There is a third condition where some people experience distress from eating gluten-containing products and show improvement with a GFD. It is distinct from celiac disease and wheat allergies (Vivas et al. 2015). Gluten sensitivity cannot be distinguished clinically; serology tests need to be conducted. Patients with GI discomfort or distress following gluten ingestion should be referred for a follow-up blood test and immune-allergy tests.
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Addressing mental health issues in the athlete
Everyone has symptoms of some type of mental health issue at some time in life when one or several stressors overwhelm the person’s ability to self-regulate or repair. The symptoms are usually, and arbitrarily, labeled either physical or mental.
Everyone has symptoms of some type of mental health issue at some time in life when one or several stressors overwhelm the person's ability to self-regulate or repair. The symptoms are usually, and arbitrarily, labeled either physical or mental. This artificial dichotomy usually does not align with the affected person's reality. Rarely is an athlete with a strained hamstring not also worried about the injury or distressed by the pain. Similarly, the most common initial warning signs of depression are the physical symptoms of tension, restlessness, and disturbed sleep, energy, and appetite. This is because we have overlapping systems of mind, body, spirit, and relationships, each integrally connected to the others. When the homeostasis of one or more systems is disrupted, people instinctively try to correct the problem regardless of its origin. In the mental health domain, signs of distress are emotional, mental, behavioral, and physical.
Framework for Understanding Mental Health
In almost all situations, a variety of overlapping factors contribute to symptom development. The biopsychosocial - spiritual model (BPSS) is a framework for understanding the person's responses in a given situation and the development of symptoms. Symptom etiology may be conceptualized as a pie. Figure 17.1 shows how these various factors overlap and contribute to well-being. In a given person, the various pieces of the BPSS pie may be larger or smaller at any one time. The relative sizes of the pieces greatly influence the person's symptoms and ability to adapt.
The biopsychosocial - spiritual model is a framework for understanding a person's responses in a given situation and the development of symptoms.
For example, two runners may have identical injuries, but the impact of the injury and the course of rehabilitation in these two athletes will usually differ. The amount of pain they have, as well as the length of time until they are ready to compete again, will be influenced not only by the difference in respective levels of physical conditioning and injury history but also by other physical and emotional conditions such as pain tolerance, attitude, perception of the problem, and its implications for life. The situation may also be affected by personality and temperament issues, variable resources for coping, and so on. Another example involves two wrestlers who seem to be equally competitive, but wrestler A, in a struggle to make or maintain weight, develops more obviously disordered eating patterns than wrestler B. Perhaps wrestler A has a family history of obesity and is genetically predisposed toward weight gain more than the other; temperamentally, wrestler A may tend to think more negatively about life challenges, become somewhat self-defeating in the face of adversity, and find emotional comfort in food and the process of eating. Often a variety of factors will help to explain the development of clinically significant problems.
This interplay of variables is the same for athletes as it is for others who are physically active, regardless of whether the symptoms of an injury or condition are physical or emotional. Whereas one athlete may become depressed, another's symptoms may include anxiety or outbursts of anger and physical aggression. Sometimes one piece of the BPSS pie is so big that it seems to account for virtually the whole reason that someone is symptomatic (e.g., the chemical disequilibrium that comes with bipolar disorder). For this reason, it is a good practice to regularly consider the possibility that an organic cause may be the culprit and refer the person for a medical evaluation.
The treatments that have proven effective for the problems discussed in this chapter are based on the same BPSS approach as the assessment and diagnosis. Different strategies can be useful, depending on the biopsychosocial - spiritual components that are implicated in the assessment process. Practitioners often recommend treatment plans based on their assessment and experience, and then these are negotiated with the patient or family members according to personal preferences. The treatment may be offered on either an inpatient or, more commonly, an outpatient basis.
Treatment may also involve the collaboration of a variety of treatment professionals. For example, eating disorder treatment often involves a physician, a registered dietitian, and a psychotherapist. This will be determined based on the severity of symptoms, the difficulty the athlete has in making changes, the amount of support the athlete has, and other resources that affect care, including financial concerns or insurance benefits. The important first step in treatment is accurate assessment followed by clear and well-timed communication and education with the athlete and family. The athletic trainer can play a valuable role here because people are much more likely to engage in treatment or some type of change process if they become convinced that there is a problem, they know what it is, and they know that something can be done about it. This is because most people will want to know what is going on with themselves, how they "got it," and what they can do to "get rid of it" or at least cope more effectively. Additional treatment recommendations specific to various clinical problems are listed in subsequent sections.
Implications for Participation in Athletics
Early identification and treatment are very helpful in preventing problems from worsening, but sometimes the stigma still associated with mental health conditions prevents people from recognizing these problems in themselves or others. In those cases, functioning in one or more areas of life can be affected, sometimes severely. Restricting participation in a sport, if necessary, will depend on the assessment of the athlete's level of functioning by the athlete, the coach, and the athletic trainer. Initially, while the medication dosage is being adjusted, the athlete could experience adverse effects that could affect participation or performance, such as nausea, headache, sedation, disturbed balance, or overstimulation. The National Collegiate Athletic Association (NCAA) has no restrictions on the medications typically used to treat these conditions except for pemoline, a medication prescribed to treat ADHD (National Collegiate Athletic Association 2015).
The last general point to be made is that some people experiencing psychological or substance use disorders may consider suicide or become homicidal. Most health care professionals or other professionals are required by law or by a professional code of ethics to report to the authorities if a patient is a danger to self or others. Athletic trainers, too, may encounter an athlete with depression, panic disorder, or substance abuse who is considering suicide or harming someone else. The athletic trainer must seek immediate consultation if in doubt about the need to report. An assessment of whether one is suicidal or homicidal includes determining whether the person has a specific plan, the means to carry it out, the intention to carry it out, and how lethal the plan is. Those with a personal or family history of this type of ideation or action or whose judgment is impaired, perhaps through the use of substances, are more at risk to follow through.
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Identifying Exercise-Induced Bronchospasm
The terms EIA and EIB are often used interchangeably, but EIB specifically denotes the reduction in lung function that occurs after a standardized exercise test (Carver 2009). More recently, the term exercise-induced bronchoconstriction has been introduced as actual spasm of the airways does not always occur.
The terms exercise-induced asthma (EIA) and exercise-induced bronchoconstriction (EIB) are often used interchangeably, but EIB specifically denotes the reduction in lung function that occurs after a standardized exercise test (Carver 2009). More recently, the term exercise-induced bronchoconstriction has been introduced as actual spasm of the airways does not always occur. Some clinicians use EIA to describe individuals with known asthma who have bronchoconstriction during exercise. However, some use EIA to describe patients who have bronchoconstriction only during exercise, and they use EIB to describe patients with asthma who have bronchoconstriction with exercise. Generally, EIB is used to indicate bronchospasm with decreased pulmonary function testing following exercise, and EIA is used to indicate those patients with asthma difficulties associated with exercise.
Symptoms of EIB usually occur 10 to 15 min after the onset of strenuous exercise and are defined by a fall in FEV1 of 15% or more during exercise spirometry. EIB is more common in winter sport athletes who compete in cold ambient temperatures (Carey, Aase, and Pliego 2010).
Signs and Symptoms
EIB should be suspected in any athlete who complains of shortness of breath, dyspnea, cough, chest congestion, or tightness with exertion. These symptoms usually occur during strenuous exercise and peak about 5 to 10 min after exercise (Hull 2012; Krafczyk and Asplund 2011; Simpson, Romer, and Kippelen 2015). Other subtle clues might be a dry cough that develops after practice or exercise (i.e., locker-room cough) or simply unusual fatigue compared with similarly trained athletes. Athletes will often complain that they feel out of shape despite regular training. Self-reported symptoms have been shown to be poor predictors of EIB because other conditions can cause similar symptoms. Symptoms alone should not be used to diagnose EIB.
In athletes suspected of having EIB, other etiologies, such as acute sinusitis, otitis media (middle ear infection), bronchitis, or even pneumonia, need to be excluded, particularly in the context of other constitutional symptoms, such as fever, chills, or night sweats. If fatigue is the only presenting symptom, deconditioning may also be a cause. In addition, environmental allergies can account for many of the nonspecific symptoms that mimic EIB (Backer 2010; Hull et al. 2012; Stack and Hakemi 2011). More serious cardiac causes, such as arrhythmias and pericarditis, might also need to be excluded. Another important differential is exercise-induced laryngeal obstruction (EILO), where the wheezing and dyspnea are caused by transient obstruction of the upper airways during exercise (Nielsen 2013; Backer 2010).
Referral and Diagnostic Tests
The physical examination is usually normal. Some athletes with EIB may experience symptoms that develop several hours after exercise. This late-phase response is due to the activity of inflammatory mediators. Most commonly, a bronchial provocation challenge is used to determine the diagnosis of EIB (Parsons et al. 2011; Hayden et al. 2011; Morris 2010). Figure 7.9 shows a decision tree commonly used for the diagnosis of EIB. Alternatively, many physicians choose to just evaluate the patient's response to an empirical trial of a ß-agonist medication before exercise.
Decision tree for the diagnosis of exercise-induced bronchoconstriction (EIB).
Treatment and Return to Participation
The treatment of choice in EIB is an inhaled ß2-agonist from a metered-dose inhaler (e.g., albuterol) taken 15 to 30 min before the onset of exercise. An athlete who has asthma symptoms outside the exercise setting or who is using a ß2-agonist more than three times per week should be treated with a regular inhaled corticosteroid. Here is how to properly use an inhaler:
- Remove dust cap and shake the inhaler system before each use.
- Inspect mouthpiece for contamination or foreign objects.
- Breathe out through the mouth, exhaling as completely as possible.
- Hold the inhaler system upright with mouthpiece in mouth and lips closed tightly around mouthpiece.
- Breathe in slowly while pressing down on the metal cartridge.
- Hold breath as long as possible.
- Release pressure while still holding breath.
- Remove mouthpiece.
- Wait for the container to repressurize, shake, and then repeat steps 3 through 8 when more than one inhalation is prescribed.
- Rinse mouth with water after prescribed number of inhalations.
- Clean the inhaler system every few days by removing metal cartridge and rinsing the plastic inhaler and cap with running warm water. Replace cartridge and cap.
Emerging studies show promise using long-acting ß2-agonists such as salmeterol and leukotriene inhibitors such as montelukast (Singulair) (Parsons 2010). Other nonpharmacological strategies include pre - warm-up bursts of physical activity at 80% to 90% of the individual's maximal workload to induce a refractory period that lasts up to 3 h after the initial attack of EIB (Hull et al. 2012; Millward et al. 2009; Boulet, Hancox, and Fitch 2010). Strategies to humidify inspired air and dietary interventions may also prove to be beneficial (Carey, Aase, and Pliego 2010; Bussotti, Di Marco, and Marchese 2014).
For an athlete experiencing a severe asthma attack or when an inhaler is ineffective, a nebulizer may be used. A nebulizer, also known as an atomizer, is a machine that vaporizes liquid medication into a fine mist to be inhaled into the lungs via a mouthpiece or mask. Although studies have shown that both inhalers and nebulizers tend to be equally effective in delivering medications, nebulizers are preferred for use in more serious rescue situations when the patient is experiencing a severe asthma attack. Nebulizers can administer a higher dose of medication, but inhalers are easier to use, preferred for their portability and low cost, and good for everyday use. Medications typically administered with a nebulizer include albuterol and ipratropium (Atrovent).
Athletes with controlled EIB need not be excluded or discouraged from participating in sports. Effective strategies, both pharmacological and nonpharmacological, exist that can allow an athlete to compete even at an elite level.
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Causes of Sudden Cardiac Death in Athletes
Death by sudden cardiac arrest (SCA) is a rare event in the young athlete. In the United States, elite athletes are viewed as near invincible because of their incredible physical feats.
Death by sudden cardiac arrest (SCA) is a rare event in the young athlete. In the United States, elite athletes are viewed as near invincible because of their incredible physical feats. Nevertheless, it is reported that the rate of collegiate athlete death due to SCA is higher than that of high school athletes, with a suspected 110 SCA deaths annually in the United States among young athletes (Casa et al. 2012). Any time a tragedy of this proportion occurs, the public reacts with disbelief, and medical knowledge is called into question. Studies that have tracked these deaths during sports used the National Federation of State High School Associations (NFHS), the National Collegiate Athletic Association (NCAA) governing organizations, and state and federally funded research groups for data collection, such as the National Center for Catastrophic Sport Injury Research (NCCSIR), based in Chapel Hill, North Carolina. Approximately 90% of the data collected involved male athletes, with an equal distribution between Caucasians and African-Americans (Borjesson and Pelliccia 2009). According to the NCCSIR, there were 10 indirect (due to exertion) fatalities in middle school through college football athletes in 2014, and six were attributed to a cardiac event (Kucera et al. 2015). An additional five football athletes died of suspected cardiac conditions due to nonexertional factors in the same year (Kucera et al. 2015). Sudden death cases in young women are rare, and the most common cause of sudden cardiac death was congenital cardiac disease.
The prevalence of sudden cardiac death in young athletes (those less than 35-year-old) is estimated to be between 1 and 3 in 100,000 (Borjesson and Pelliccia 2009). This is much higher than statistics reported in a more general population of active individuals (Harmon, Klossner, and Drezner 2011). These data indicate that active people are not immune to cardiovascular events that may result in death.
Causes
The most common cause of sudden cardiac death in the young athlete is hypertrophic cardiomyopathy, which accounts for up to 50% of the cases. Other significant causes of sudden cardiac death in a young athlete are coronary artery anomalies, increased cardiac mass, aortic rupture, myocarditis, and aortic stenosis(Borjesson and Pelliccia 2009).Rare causes include dilated cardiomyopathy, atherosclerotic coronary artery disease, mitral valve prolapse, isolated arrhythmias such as long QT syndrome and Wolff-Parkinson-White syndrome, and arrhythmogenic right ventricular dysplasia (ARVD) (Harmon, Klossner, and Drezner 2011). In the Veneto region of Italy, researchers have found ARVD to be the most common cause of sudden cardiac death in the athlete (Thiene et al. 1988). This research suggests that a specific population may have different genetic subtraits.
In the older athlete, coronary artery disease is by far the most common cause of sudden death. Rarely is sudden death in the older athlete caused by hypertrophic cardiomyopathy, mitral valve prolapse, or acquired valvular conditions (Maron et al. 2014; Nagashima et al. 2003; Semsarian, Sweeting, and Ackerman 2015; Marijon et al. 2015).
Traumatic sudden cardiac death has not captured as much attention because its epidemiology is more difficult to track. However, it is a growing problem that strikes without warning. Between 1996 and 2007, a reported 180 cases of blunt-force death in the United States were attributed to commotio cordis (Maron et al. 2006). Most cases involved children with a mean age of 13, with 95% of the deaths occurring in males (Maron et al. 2013).
Commotio cordis refers to trauma to the chest wall that interrupts the electrical impulse in the heart. If the cardiac rhythm is not promptly normalized, the individual dies. Typically the ribs or sternum is not broken, although some contusions may be found. Research has found that a chest blow occurring during the vulnerable phase of repolarization, just prior to the T-wave peak in the cardiac cycle, can induce ventricular fibrillation (Maron and Estes 2005).
Although children and teenagers with thin chest walls are most vulnerable to commotio cordis (figure 8.6), deaths have been reported in adults. Sports such as baseball, ice hockey, lacrosse, and softball, which have hard projectiles that can strike the chest, have been associated with the greatest number of deaths. Commotio cordis also has occurred in sports such as soccer, football, rugby, and karate, in which the blow came from a soft projectile or a collision. It appears that the timing of the incident, rather than the degree of impact of the object, is the causative factor (Maron and Estes 2005). Commotio cordis is the only significant cause of traumatic sudden cardiac death in athletes.
The type of injury associated with commotio cordis is a blow to the chest wall that interrupts the usual cardiac rhythm.
Red Flags for Traumatic Sudden Cardiac Death
Sports with projectiles that can hit the chest at an inopportune time in the cardiac rhythm cycle have been known to cause commotio cordis in young athletes. These sports include the following: baseball, softball, hockey, lacrosse, soccer, football, karate.
Prevention
Because death can be the outcome, prevention has become the focus of attention for commotio cordis. Changes in practice have ranged from protective padding to softer balls that are used in Little League and softball. Because this may not completely resolve the problem, another solution is defibrillation in conjunction with cardiopulmonary resuscitation (CPR). Defibrillation interrupts the heart rhythm so the heart can "reboot" into a normal rhythm.
The American Heart Association estimates that communities with comprehensive CPR and automated external defibrillator (AED) training achieve 40% survival rates for cardiac arrest victims. If defibrillation is performed within 3 min, the likelihood of survival is high. For every minute of delay the chance of survival drops by as much as 10% (American Heart Association 2013).
The advent of the AED has provided greater public access to life-saving technology. These devices can be operated by trained laypeople and are increasingly affordable in all sectors. The AED is portable, rechargeable, simple to operate, and easy to maintain. The American Red Cross, American Heart Association, and National Safety Council offer AED certification courses in addition to CPR courses for the lay public. The NCAA Sports Medicine Guidelines require planned access to an AED and mandating CPR and first aid certifications for all who work with athlete practices, competition, and skill sessions. Athletic trainers are required to maintain certification in emergency cardiac care, including AED use. They need to have ready access to an AED in order to provide rapid cardiac assessment and care to those in fibrillation. Athletes who suffer a sudden collapse and have agonal or gasping breathing should be treated because they are suffering from a cardiac event (Casa et al. 2012; Solberg et al. 2015). An AED should be applied as soon as possible for heart rhythm analysis and possible defibrillation.
Clinical Tips
Potential Causes of Sudden Death
Sudden collapse in athletes could be caused by heatstroke, a cardiac event, sickle cell collapse, or injury. Understanding the presentation of each will facilitate rapid response and the appropriate disposition.
Emergency Planning
Every athletic site should have planned access to an AED, an emergency medical service (EMS), and an established emergency action plan (EAP), as well as medical personnel trained to respond to sudden collapse.
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How to identify celiac disease
Celiac disease is an autoimmune disorder that affects the gastrointestinal tract and is thought to be triggered by dietary gluten in affected individuals. The disease is characterized by chronic inflammation of the small intestinal mucosa, which leads to atrophy of the small intestinal villi and subsequent malabsorption (Pelkowski and Viera 2014).
Celiac disease is an autoimmune disorder that affects the gastrointestinal tract and is thought to be triggered by dietary gluten in affected individuals. The disease is characterized by chronic inflammation of the small intestinal mucosa, which leads to atrophy of the small intestinal villi and subsequent malabsorption (Pelkowski and Viera 2014). Celiac disease affects approximately 1% of the U.S. population and typically occurs in persons of European ancestry as well as persons of Middle Eastern, Indian, South American, and North African descent. It is two to three times more common in women. Celiac disease is not a food allergy.
Signs and Symptoms
Typical presentation includes chronic diarrhea with cramping and gas pains. Patients often have weight loss, or in the adolescent, delayed onset of growth or puberty. A history of nervousness and/or depression is often present, as is a family history of autoimmune disease. Other complaints may include bone or joint pain, migraines, weakness, fatigue, and anemia (Volta et al. 2015; Vivas et al. 2015; Byrne and Feighery 2015; Mancini, Trojian, and Mancini 2011). Physical examination is often normal, but the patient may present with abdominal distension or dermatitis herpetiformis.
Referral and Diagnostic Tests
Lab tests are performed for differentiating celiac disease and to rule out more common diseases. These include a basic metabolic panel, CBC (iron deficiency), TSH (thyroid disease), vitamin D level, and allergy testing. If celiac disease is suspected from history and physical exam, the initial serologic test is a tissue transglutaminase (tTG) antibody level. This antibody is found in every tissue in the body and acts to join proteins together. In people with celiac disease, tTG activates specific immune cells and triggers the inflammatory response that leads to atrophy of the villi in the small intestine (Mancini, Trojian, and Mancini 2011). The diagnosis is often confirmed with repeat blood tests after 4 wk on a gluten-free diet. Endoscopy with biopsies of the duodenal mucosa may be necessary to confirm the diagnosis. Celiac disease should be differentiated from GERD, pancreatic insufficiency, Crohn's disease, or other inflammatory bowel diseases.
Treatment and Return to Participation
The general treatment is to remove gluten from the diet. The patient can substitute rice, corn, and soybean flour for products that contain gluten. Periodic blood tests are performed to measure the levels of the antibodies. The levels will normalize with gluten abstinence. Abstinence will be required for life because the immune response to gluten will recur if gluten is consumed again. Usually no medications are prescribed for celiac disease, but athletes may benefit from iron, vitamin, and calcium supplements. The most difficult aspect for the athlete with celiac disease is the dietary restrictions while traveling with the team or with set team meals. The athletic trainer may need to check on the gluten-free status of many of the standard gluten-containing products provided by the athletic department, such as energy drinks or meal replacement bars (Mancini, Trojian, and Mancini 2011).
Condition Highlight
Gluten Sensitivity and Intolerance
Over the past 10 yr, the number of people choosing a gluten-free diet (GFD) is much higher than the projected number of celiac disease patients (Lis et al. 2015). This has fueled a global market of gluten-free products and highlights several conditions related to the ingestion of gluten. There are three main forms of gluten reactions: allergic, autoimmune (celiac disease), and immune-mediated conditions (gluten sensitivity) (Sapone et al. 2012). Wheat allergy is an adverse reaction to wheat proteins with onset in minutes to hours after gluten ingestion. It may affect the skin, GI tract, or respiratory tract. Celiac disease or other autoimmune gluten disorders generally present months to years after gluten exposure. There is a third condition where some people experience distress from eating gluten-containing products and show improvement with a GFD. It is distinct from celiac disease and wheat allergies (Vivas et al. 2015). Gluten sensitivity cannot be distinguished clinically; serology tests need to be conducted. Patients with GI discomfort or distress following gluten ingestion should be referred for a follow-up blood test and immune-allergy tests.
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Addressing mental health issues in the athlete
Everyone has symptoms of some type of mental health issue at some time in life when one or several stressors overwhelm the person’s ability to self-regulate or repair. The symptoms are usually, and arbitrarily, labeled either physical or mental.
Everyone has symptoms of some type of mental health issue at some time in life when one or several stressors overwhelm the person's ability to self-regulate or repair. The symptoms are usually, and arbitrarily, labeled either physical or mental. This artificial dichotomy usually does not align with the affected person's reality. Rarely is an athlete with a strained hamstring not also worried about the injury or distressed by the pain. Similarly, the most common initial warning signs of depression are the physical symptoms of tension, restlessness, and disturbed sleep, energy, and appetite. This is because we have overlapping systems of mind, body, spirit, and relationships, each integrally connected to the others. When the homeostasis of one or more systems is disrupted, people instinctively try to correct the problem regardless of its origin. In the mental health domain, signs of distress are emotional, mental, behavioral, and physical.
Framework for Understanding Mental Health
In almost all situations, a variety of overlapping factors contribute to symptom development. The biopsychosocial - spiritual model (BPSS) is a framework for understanding the person's responses in a given situation and the development of symptoms. Symptom etiology may be conceptualized as a pie. Figure 17.1 shows how these various factors overlap and contribute to well-being. In a given person, the various pieces of the BPSS pie may be larger or smaller at any one time. The relative sizes of the pieces greatly influence the person's symptoms and ability to adapt.
The biopsychosocial - spiritual model is a framework for understanding a person's responses in a given situation and the development of symptoms.
For example, two runners may have identical injuries, but the impact of the injury and the course of rehabilitation in these two athletes will usually differ. The amount of pain they have, as well as the length of time until they are ready to compete again, will be influenced not only by the difference in respective levels of physical conditioning and injury history but also by other physical and emotional conditions such as pain tolerance, attitude, perception of the problem, and its implications for life. The situation may also be affected by personality and temperament issues, variable resources for coping, and so on. Another example involves two wrestlers who seem to be equally competitive, but wrestler A, in a struggle to make or maintain weight, develops more obviously disordered eating patterns than wrestler B. Perhaps wrestler A has a family history of obesity and is genetically predisposed toward weight gain more than the other; temperamentally, wrestler A may tend to think more negatively about life challenges, become somewhat self-defeating in the face of adversity, and find emotional comfort in food and the process of eating. Often a variety of factors will help to explain the development of clinically significant problems.
This interplay of variables is the same for athletes as it is for others who are physically active, regardless of whether the symptoms of an injury or condition are physical or emotional. Whereas one athlete may become depressed, another's symptoms may include anxiety or outbursts of anger and physical aggression. Sometimes one piece of the BPSS pie is so big that it seems to account for virtually the whole reason that someone is symptomatic (e.g., the chemical disequilibrium that comes with bipolar disorder). For this reason, it is a good practice to regularly consider the possibility that an organic cause may be the culprit and refer the person for a medical evaluation.
The treatments that have proven effective for the problems discussed in this chapter are based on the same BPSS approach as the assessment and diagnosis. Different strategies can be useful, depending on the biopsychosocial - spiritual components that are implicated in the assessment process. Practitioners often recommend treatment plans based on their assessment and experience, and then these are negotiated with the patient or family members according to personal preferences. The treatment may be offered on either an inpatient or, more commonly, an outpatient basis.
Treatment may also involve the collaboration of a variety of treatment professionals. For example, eating disorder treatment often involves a physician, a registered dietitian, and a psychotherapist. This will be determined based on the severity of symptoms, the difficulty the athlete has in making changes, the amount of support the athlete has, and other resources that affect care, including financial concerns or insurance benefits. The important first step in treatment is accurate assessment followed by clear and well-timed communication and education with the athlete and family. The athletic trainer can play a valuable role here because people are much more likely to engage in treatment or some type of change process if they become convinced that there is a problem, they know what it is, and they know that something can be done about it. This is because most people will want to know what is going on with themselves, how they "got it," and what they can do to "get rid of it" or at least cope more effectively. Additional treatment recommendations specific to various clinical problems are listed in subsequent sections.
Implications for Participation in Athletics
Early identification and treatment are very helpful in preventing problems from worsening, but sometimes the stigma still associated with mental health conditions prevents people from recognizing these problems in themselves or others. In those cases, functioning in one or more areas of life can be affected, sometimes severely. Restricting participation in a sport, if necessary, will depend on the assessment of the athlete's level of functioning by the athlete, the coach, and the athletic trainer. Initially, while the medication dosage is being adjusted, the athlete could experience adverse effects that could affect participation or performance, such as nausea, headache, sedation, disturbed balance, or overstimulation. The National Collegiate Athletic Association (NCAA) has no restrictions on the medications typically used to treat these conditions except for pemoline, a medication prescribed to treat ADHD (National Collegiate Athletic Association 2015).
The last general point to be made is that some people experiencing psychological or substance use disorders may consider suicide or become homicidal. Most health care professionals or other professionals are required by law or by a professional code of ethics to report to the authorities if a patient is a danger to self or others. Athletic trainers, too, may encounter an athlete with depression, panic disorder, or substance abuse who is considering suicide or harming someone else. The athletic trainer must seek immediate consultation if in doubt about the need to report. An assessment of whether one is suicidal or homicidal includes determining whether the person has a specific plan, the means to carry it out, the intention to carry it out, and how lethal the plan is. Those with a personal or family history of this type of ideation or action or whose judgment is impaired, perhaps through the use of substances, are more at risk to follow through.
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Identifying Exercise-Induced Bronchospasm
The terms EIA and EIB are often used interchangeably, but EIB specifically denotes the reduction in lung function that occurs after a standardized exercise test (Carver 2009). More recently, the term exercise-induced bronchoconstriction has been introduced as actual spasm of the airways does not always occur.
The terms exercise-induced asthma (EIA) and exercise-induced bronchoconstriction (EIB) are often used interchangeably, but EIB specifically denotes the reduction in lung function that occurs after a standardized exercise test (Carver 2009). More recently, the term exercise-induced bronchoconstriction has been introduced as actual spasm of the airways does not always occur. Some clinicians use EIA to describe individuals with known asthma who have bronchoconstriction during exercise. However, some use EIA to describe patients who have bronchoconstriction only during exercise, and they use EIB to describe patients with asthma who have bronchoconstriction with exercise. Generally, EIB is used to indicate bronchospasm with decreased pulmonary function testing following exercise, and EIA is used to indicate those patients with asthma difficulties associated with exercise.
Symptoms of EIB usually occur 10 to 15 min after the onset of strenuous exercise and are defined by a fall in FEV1 of 15% or more during exercise spirometry. EIB is more common in winter sport athletes who compete in cold ambient temperatures (Carey, Aase, and Pliego 2010).
Signs and Symptoms
EIB should be suspected in any athlete who complains of shortness of breath, dyspnea, cough, chest congestion, or tightness with exertion. These symptoms usually occur during strenuous exercise and peak about 5 to 10 min after exercise (Hull 2012; Krafczyk and Asplund 2011; Simpson, Romer, and Kippelen 2015). Other subtle clues might be a dry cough that develops after practice or exercise (i.e., locker-room cough) or simply unusual fatigue compared with similarly trained athletes. Athletes will often complain that they feel out of shape despite regular training. Self-reported symptoms have been shown to be poor predictors of EIB because other conditions can cause similar symptoms. Symptoms alone should not be used to diagnose EIB.
In athletes suspected of having EIB, other etiologies, such as acute sinusitis, otitis media (middle ear infection), bronchitis, or even pneumonia, need to be excluded, particularly in the context of other constitutional symptoms, such as fever, chills, or night sweats. If fatigue is the only presenting symptom, deconditioning may also be a cause. In addition, environmental allergies can account for many of the nonspecific symptoms that mimic EIB (Backer 2010; Hull et al. 2012; Stack and Hakemi 2011). More serious cardiac causes, such as arrhythmias and pericarditis, might also need to be excluded. Another important differential is exercise-induced laryngeal obstruction (EILO), where the wheezing and dyspnea are caused by transient obstruction of the upper airways during exercise (Nielsen 2013; Backer 2010).
Referral and Diagnostic Tests
The physical examination is usually normal. Some athletes with EIB may experience symptoms that develop several hours after exercise. This late-phase response is due to the activity of inflammatory mediators. Most commonly, a bronchial provocation challenge is used to determine the diagnosis of EIB (Parsons et al. 2011; Hayden et al. 2011; Morris 2010). Figure 7.9 shows a decision tree commonly used for the diagnosis of EIB. Alternatively, many physicians choose to just evaluate the patient's response to an empirical trial of a ß-agonist medication before exercise.
Decision tree for the diagnosis of exercise-induced bronchoconstriction (EIB).
Treatment and Return to Participation
The treatment of choice in EIB is an inhaled ß2-agonist from a metered-dose inhaler (e.g., albuterol) taken 15 to 30 min before the onset of exercise. An athlete who has asthma symptoms outside the exercise setting or who is using a ß2-agonist more than three times per week should be treated with a regular inhaled corticosteroid. Here is how to properly use an inhaler:
- Remove dust cap and shake the inhaler system before each use.
- Inspect mouthpiece for contamination or foreign objects.
- Breathe out through the mouth, exhaling as completely as possible.
- Hold the inhaler system upright with mouthpiece in mouth and lips closed tightly around mouthpiece.
- Breathe in slowly while pressing down on the metal cartridge.
- Hold breath as long as possible.
- Release pressure while still holding breath.
- Remove mouthpiece.
- Wait for the container to repressurize, shake, and then repeat steps 3 through 8 when more than one inhalation is prescribed.
- Rinse mouth with water after prescribed number of inhalations.
- Clean the inhaler system every few days by removing metal cartridge and rinsing the plastic inhaler and cap with running warm water. Replace cartridge and cap.
Emerging studies show promise using long-acting ß2-agonists such as salmeterol and leukotriene inhibitors such as montelukast (Singulair) (Parsons 2010). Other nonpharmacological strategies include pre - warm-up bursts of physical activity at 80% to 90% of the individual's maximal workload to induce a refractory period that lasts up to 3 h after the initial attack of EIB (Hull et al. 2012; Millward et al. 2009; Boulet, Hancox, and Fitch 2010). Strategies to humidify inspired air and dietary interventions may also prove to be beneficial (Carey, Aase, and Pliego 2010; Bussotti, Di Marco, and Marchese 2014).
For an athlete experiencing a severe asthma attack or when an inhaler is ineffective, a nebulizer may be used. A nebulizer, also known as an atomizer, is a machine that vaporizes liquid medication into a fine mist to be inhaled into the lungs via a mouthpiece or mask. Although studies have shown that both inhalers and nebulizers tend to be equally effective in delivering medications, nebulizers are preferred for use in more serious rescue situations when the patient is experiencing a severe asthma attack. Nebulizers can administer a higher dose of medication, but inhalers are easier to use, preferred for their portability and low cost, and good for everyday use. Medications typically administered with a nebulizer include albuterol and ipratropium (Atrovent).
Athletes with controlled EIB need not be excluded or discouraged from participating in sports. Effective strategies, both pharmacological and nonpharmacological, exist that can allow an athlete to compete even at an elite level.
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Causes of Sudden Cardiac Death in Athletes
Death by sudden cardiac arrest (SCA) is a rare event in the young athlete. In the United States, elite athletes are viewed as near invincible because of their incredible physical feats.
Death by sudden cardiac arrest (SCA) is a rare event in the young athlete. In the United States, elite athletes are viewed as near invincible because of their incredible physical feats. Nevertheless, it is reported that the rate of collegiate athlete death due to SCA is higher than that of high school athletes, with a suspected 110 SCA deaths annually in the United States among young athletes (Casa et al. 2012). Any time a tragedy of this proportion occurs, the public reacts with disbelief, and medical knowledge is called into question. Studies that have tracked these deaths during sports used the National Federation of State High School Associations (NFHS), the National Collegiate Athletic Association (NCAA) governing organizations, and state and federally funded research groups for data collection, such as the National Center for Catastrophic Sport Injury Research (NCCSIR), based in Chapel Hill, North Carolina. Approximately 90% of the data collected involved male athletes, with an equal distribution between Caucasians and African-Americans (Borjesson and Pelliccia 2009). According to the NCCSIR, there were 10 indirect (due to exertion) fatalities in middle school through college football athletes in 2014, and six were attributed to a cardiac event (Kucera et al. 2015). An additional five football athletes died of suspected cardiac conditions due to nonexertional factors in the same year (Kucera et al. 2015). Sudden death cases in young women are rare, and the most common cause of sudden cardiac death was congenital cardiac disease.
The prevalence of sudden cardiac death in young athletes (those less than 35-year-old) is estimated to be between 1 and 3 in 100,000 (Borjesson and Pelliccia 2009). This is much higher than statistics reported in a more general population of active individuals (Harmon, Klossner, and Drezner 2011). These data indicate that active people are not immune to cardiovascular events that may result in death.
Causes
The most common cause of sudden cardiac death in the young athlete is hypertrophic cardiomyopathy, which accounts for up to 50% of the cases. Other significant causes of sudden cardiac death in a young athlete are coronary artery anomalies, increased cardiac mass, aortic rupture, myocarditis, and aortic stenosis(Borjesson and Pelliccia 2009).Rare causes include dilated cardiomyopathy, atherosclerotic coronary artery disease, mitral valve prolapse, isolated arrhythmias such as long QT syndrome and Wolff-Parkinson-White syndrome, and arrhythmogenic right ventricular dysplasia (ARVD) (Harmon, Klossner, and Drezner 2011). In the Veneto region of Italy, researchers have found ARVD to be the most common cause of sudden cardiac death in the athlete (Thiene et al. 1988). This research suggests that a specific population may have different genetic subtraits.
In the older athlete, coronary artery disease is by far the most common cause of sudden death. Rarely is sudden death in the older athlete caused by hypertrophic cardiomyopathy, mitral valve prolapse, or acquired valvular conditions (Maron et al. 2014; Nagashima et al. 2003; Semsarian, Sweeting, and Ackerman 2015; Marijon et al. 2015).
Traumatic sudden cardiac death has not captured as much attention because its epidemiology is more difficult to track. However, it is a growing problem that strikes without warning. Between 1996 and 2007, a reported 180 cases of blunt-force death in the United States were attributed to commotio cordis (Maron et al. 2006). Most cases involved children with a mean age of 13, with 95% of the deaths occurring in males (Maron et al. 2013).
Commotio cordis refers to trauma to the chest wall that interrupts the electrical impulse in the heart. If the cardiac rhythm is not promptly normalized, the individual dies. Typically the ribs or sternum is not broken, although some contusions may be found. Research has found that a chest blow occurring during the vulnerable phase of repolarization, just prior to the T-wave peak in the cardiac cycle, can induce ventricular fibrillation (Maron and Estes 2005).
Although children and teenagers with thin chest walls are most vulnerable to commotio cordis (figure 8.6), deaths have been reported in adults. Sports such as baseball, ice hockey, lacrosse, and softball, which have hard projectiles that can strike the chest, have been associated with the greatest number of deaths. Commotio cordis also has occurred in sports such as soccer, football, rugby, and karate, in which the blow came from a soft projectile or a collision. It appears that the timing of the incident, rather than the degree of impact of the object, is the causative factor (Maron and Estes 2005). Commotio cordis is the only significant cause of traumatic sudden cardiac death in athletes.
The type of injury associated with commotio cordis is a blow to the chest wall that interrupts the usual cardiac rhythm.
Red Flags for Traumatic Sudden Cardiac Death
Sports with projectiles that can hit the chest at an inopportune time in the cardiac rhythm cycle have been known to cause commotio cordis in young athletes. These sports include the following: baseball, softball, hockey, lacrosse, soccer, football, karate.
Prevention
Because death can be the outcome, prevention has become the focus of attention for commotio cordis. Changes in practice have ranged from protective padding to softer balls that are used in Little League and softball. Because this may not completely resolve the problem, another solution is defibrillation in conjunction with cardiopulmonary resuscitation (CPR). Defibrillation interrupts the heart rhythm so the heart can "reboot" into a normal rhythm.
The American Heart Association estimates that communities with comprehensive CPR and automated external defibrillator (AED) training achieve 40% survival rates for cardiac arrest victims. If defibrillation is performed within 3 min, the likelihood of survival is high. For every minute of delay the chance of survival drops by as much as 10% (American Heart Association 2013).
The advent of the AED has provided greater public access to life-saving technology. These devices can be operated by trained laypeople and are increasingly affordable in all sectors. The AED is portable, rechargeable, simple to operate, and easy to maintain. The American Red Cross, American Heart Association, and National Safety Council offer AED certification courses in addition to CPR courses for the lay public. The NCAA Sports Medicine Guidelines require planned access to an AED and mandating CPR and first aid certifications for all who work with athlete practices, competition, and skill sessions. Athletic trainers are required to maintain certification in emergency cardiac care, including AED use. They need to have ready access to an AED in order to provide rapid cardiac assessment and care to those in fibrillation. Athletes who suffer a sudden collapse and have agonal or gasping breathing should be treated because they are suffering from a cardiac event (Casa et al. 2012; Solberg et al. 2015). An AED should be applied as soon as possible for heart rhythm analysis and possible defibrillation.
Clinical Tips
Potential Causes of Sudden Death
Sudden collapse in athletes could be caused by heatstroke, a cardiac event, sickle cell collapse, or injury. Understanding the presentation of each will facilitate rapid response and the appropriate disposition.
Emergency Planning
Every athletic site should have planned access to an AED, an emergency medical service (EMS), and an established emergency action plan (EAP), as well as medical personnel trained to respond to sudden collapse.
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How to identify celiac disease
Celiac disease is an autoimmune disorder that affects the gastrointestinal tract and is thought to be triggered by dietary gluten in affected individuals. The disease is characterized by chronic inflammation of the small intestinal mucosa, which leads to atrophy of the small intestinal villi and subsequent malabsorption (Pelkowski and Viera 2014).
Celiac disease is an autoimmune disorder that affects the gastrointestinal tract and is thought to be triggered by dietary gluten in affected individuals. The disease is characterized by chronic inflammation of the small intestinal mucosa, which leads to atrophy of the small intestinal villi and subsequent malabsorption (Pelkowski and Viera 2014). Celiac disease affects approximately 1% of the U.S. population and typically occurs in persons of European ancestry as well as persons of Middle Eastern, Indian, South American, and North African descent. It is two to three times more common in women. Celiac disease is not a food allergy.
Signs and Symptoms
Typical presentation includes chronic diarrhea with cramping and gas pains. Patients often have weight loss, or in the adolescent, delayed onset of growth or puberty. A history of nervousness and/or depression is often present, as is a family history of autoimmune disease. Other complaints may include bone or joint pain, migraines, weakness, fatigue, and anemia (Volta et al. 2015; Vivas et al. 2015; Byrne and Feighery 2015; Mancini, Trojian, and Mancini 2011). Physical examination is often normal, but the patient may present with abdominal distension or dermatitis herpetiformis.
Referral and Diagnostic Tests
Lab tests are performed for differentiating celiac disease and to rule out more common diseases. These include a basic metabolic panel, CBC (iron deficiency), TSH (thyroid disease), vitamin D level, and allergy testing. If celiac disease is suspected from history and physical exam, the initial serologic test is a tissue transglutaminase (tTG) antibody level. This antibody is found in every tissue in the body and acts to join proteins together. In people with celiac disease, tTG activates specific immune cells and triggers the inflammatory response that leads to atrophy of the villi in the small intestine (Mancini, Trojian, and Mancini 2011). The diagnosis is often confirmed with repeat blood tests after 4 wk on a gluten-free diet. Endoscopy with biopsies of the duodenal mucosa may be necessary to confirm the diagnosis. Celiac disease should be differentiated from GERD, pancreatic insufficiency, Crohn's disease, or other inflammatory bowel diseases.
Treatment and Return to Participation
The general treatment is to remove gluten from the diet. The patient can substitute rice, corn, and soybean flour for products that contain gluten. Periodic blood tests are performed to measure the levels of the antibodies. The levels will normalize with gluten abstinence. Abstinence will be required for life because the immune response to gluten will recur if gluten is consumed again. Usually no medications are prescribed for celiac disease, but athletes may benefit from iron, vitamin, and calcium supplements. The most difficult aspect for the athlete with celiac disease is the dietary restrictions while traveling with the team or with set team meals. The athletic trainer may need to check on the gluten-free status of many of the standard gluten-containing products provided by the athletic department, such as energy drinks or meal replacement bars (Mancini, Trojian, and Mancini 2011).
Condition Highlight
Gluten Sensitivity and Intolerance
Over the past 10 yr, the number of people choosing a gluten-free diet (GFD) is much higher than the projected number of celiac disease patients (Lis et al. 2015). This has fueled a global market of gluten-free products and highlights several conditions related to the ingestion of gluten. There are three main forms of gluten reactions: allergic, autoimmune (celiac disease), and immune-mediated conditions (gluten sensitivity) (Sapone et al. 2012). Wheat allergy is an adverse reaction to wheat proteins with onset in minutes to hours after gluten ingestion. It may affect the skin, GI tract, or respiratory tract. Celiac disease or other autoimmune gluten disorders generally present months to years after gluten exposure. There is a third condition where some people experience distress from eating gluten-containing products and show improvement with a GFD. It is distinct from celiac disease and wheat allergies (Vivas et al. 2015). Gluten sensitivity cannot be distinguished clinically; serology tests need to be conducted. Patients with GI discomfort or distress following gluten ingestion should be referred for a follow-up blood test and immune-allergy tests.
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Addressing mental health issues in the athlete
Everyone has symptoms of some type of mental health issue at some time in life when one or several stressors overwhelm the person’s ability to self-regulate or repair. The symptoms are usually, and arbitrarily, labeled either physical or mental.
Everyone has symptoms of some type of mental health issue at some time in life when one or several stressors overwhelm the person's ability to self-regulate or repair. The symptoms are usually, and arbitrarily, labeled either physical or mental. This artificial dichotomy usually does not align with the affected person's reality. Rarely is an athlete with a strained hamstring not also worried about the injury or distressed by the pain. Similarly, the most common initial warning signs of depression are the physical symptoms of tension, restlessness, and disturbed sleep, energy, and appetite. This is because we have overlapping systems of mind, body, spirit, and relationships, each integrally connected to the others. When the homeostasis of one or more systems is disrupted, people instinctively try to correct the problem regardless of its origin. In the mental health domain, signs of distress are emotional, mental, behavioral, and physical.
Framework for Understanding Mental Health
In almost all situations, a variety of overlapping factors contribute to symptom development. The biopsychosocial - spiritual model (BPSS) is a framework for understanding the person's responses in a given situation and the development of symptoms. Symptom etiology may be conceptualized as a pie. Figure 17.1 shows how these various factors overlap and contribute to well-being. In a given person, the various pieces of the BPSS pie may be larger or smaller at any one time. The relative sizes of the pieces greatly influence the person's symptoms and ability to adapt.
The biopsychosocial - spiritual model is a framework for understanding a person's responses in a given situation and the development of symptoms.
For example, two runners may have identical injuries, but the impact of the injury and the course of rehabilitation in these two athletes will usually differ. The amount of pain they have, as well as the length of time until they are ready to compete again, will be influenced not only by the difference in respective levels of physical conditioning and injury history but also by other physical and emotional conditions such as pain tolerance, attitude, perception of the problem, and its implications for life. The situation may also be affected by personality and temperament issues, variable resources for coping, and so on. Another example involves two wrestlers who seem to be equally competitive, but wrestler A, in a struggle to make or maintain weight, develops more obviously disordered eating patterns than wrestler B. Perhaps wrestler A has a family history of obesity and is genetically predisposed toward weight gain more than the other; temperamentally, wrestler A may tend to think more negatively about life challenges, become somewhat self-defeating in the face of adversity, and find emotional comfort in food and the process of eating. Often a variety of factors will help to explain the development of clinically significant problems.
This interplay of variables is the same for athletes as it is for others who are physically active, regardless of whether the symptoms of an injury or condition are physical or emotional. Whereas one athlete may become depressed, another's symptoms may include anxiety or outbursts of anger and physical aggression. Sometimes one piece of the BPSS pie is so big that it seems to account for virtually the whole reason that someone is symptomatic (e.g., the chemical disequilibrium that comes with bipolar disorder). For this reason, it is a good practice to regularly consider the possibility that an organic cause may be the culprit and refer the person for a medical evaluation.
The treatments that have proven effective for the problems discussed in this chapter are based on the same BPSS approach as the assessment and diagnosis. Different strategies can be useful, depending on the biopsychosocial - spiritual components that are implicated in the assessment process. Practitioners often recommend treatment plans based on their assessment and experience, and then these are negotiated with the patient or family members according to personal preferences. The treatment may be offered on either an inpatient or, more commonly, an outpatient basis.
Treatment may also involve the collaboration of a variety of treatment professionals. For example, eating disorder treatment often involves a physician, a registered dietitian, and a psychotherapist. This will be determined based on the severity of symptoms, the difficulty the athlete has in making changes, the amount of support the athlete has, and other resources that affect care, including financial concerns or insurance benefits. The important first step in treatment is accurate assessment followed by clear and well-timed communication and education with the athlete and family. The athletic trainer can play a valuable role here because people are much more likely to engage in treatment or some type of change process if they become convinced that there is a problem, they know what it is, and they know that something can be done about it. This is because most people will want to know what is going on with themselves, how they "got it," and what they can do to "get rid of it" or at least cope more effectively. Additional treatment recommendations specific to various clinical problems are listed in subsequent sections.
Implications for Participation in Athletics
Early identification and treatment are very helpful in preventing problems from worsening, but sometimes the stigma still associated with mental health conditions prevents people from recognizing these problems in themselves or others. In those cases, functioning in one or more areas of life can be affected, sometimes severely. Restricting participation in a sport, if necessary, will depend on the assessment of the athlete's level of functioning by the athlete, the coach, and the athletic trainer. Initially, while the medication dosage is being adjusted, the athlete could experience adverse effects that could affect participation or performance, such as nausea, headache, sedation, disturbed balance, or overstimulation. The National Collegiate Athletic Association (NCAA) has no restrictions on the medications typically used to treat these conditions except for pemoline, a medication prescribed to treat ADHD (National Collegiate Athletic Association 2015).
The last general point to be made is that some people experiencing psychological or substance use disorders may consider suicide or become homicidal. Most health care professionals or other professionals are required by law or by a professional code of ethics to report to the authorities if a patient is a danger to self or others. Athletic trainers, too, may encounter an athlete with depression, panic disorder, or substance abuse who is considering suicide or harming someone else. The athletic trainer must seek immediate consultation if in doubt about the need to report. An assessment of whether one is suicidal or homicidal includes determining whether the person has a specific plan, the means to carry it out, the intention to carry it out, and how lethal the plan is. Those with a personal or family history of this type of ideation or action or whose judgment is impaired, perhaps through the use of substances, are more at risk to follow through.
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Identifying Exercise-Induced Bronchospasm
The terms EIA and EIB are often used interchangeably, but EIB specifically denotes the reduction in lung function that occurs after a standardized exercise test (Carver 2009). More recently, the term exercise-induced bronchoconstriction has been introduced as actual spasm of the airways does not always occur.
The terms exercise-induced asthma (EIA) and exercise-induced bronchoconstriction (EIB) are often used interchangeably, but EIB specifically denotes the reduction in lung function that occurs after a standardized exercise test (Carver 2009). More recently, the term exercise-induced bronchoconstriction has been introduced as actual spasm of the airways does not always occur. Some clinicians use EIA to describe individuals with known asthma who have bronchoconstriction during exercise. However, some use EIA to describe patients who have bronchoconstriction only during exercise, and they use EIB to describe patients with asthma who have bronchoconstriction with exercise. Generally, EIB is used to indicate bronchospasm with decreased pulmonary function testing following exercise, and EIA is used to indicate those patients with asthma difficulties associated with exercise.
Symptoms of EIB usually occur 10 to 15 min after the onset of strenuous exercise and are defined by a fall in FEV1 of 15% or more during exercise spirometry. EIB is more common in winter sport athletes who compete in cold ambient temperatures (Carey, Aase, and Pliego 2010).
Signs and Symptoms
EIB should be suspected in any athlete who complains of shortness of breath, dyspnea, cough, chest congestion, or tightness with exertion. These symptoms usually occur during strenuous exercise and peak about 5 to 10 min after exercise (Hull 2012; Krafczyk and Asplund 2011; Simpson, Romer, and Kippelen 2015). Other subtle clues might be a dry cough that develops after practice or exercise (i.e., locker-room cough) or simply unusual fatigue compared with similarly trained athletes. Athletes will often complain that they feel out of shape despite regular training. Self-reported symptoms have been shown to be poor predictors of EIB because other conditions can cause similar symptoms. Symptoms alone should not be used to diagnose EIB.
In athletes suspected of having EIB, other etiologies, such as acute sinusitis, otitis media (middle ear infection), bronchitis, or even pneumonia, need to be excluded, particularly in the context of other constitutional symptoms, such as fever, chills, or night sweats. If fatigue is the only presenting symptom, deconditioning may also be a cause. In addition, environmental allergies can account for many of the nonspecific symptoms that mimic EIB (Backer 2010; Hull et al. 2012; Stack and Hakemi 2011). More serious cardiac causes, such as arrhythmias and pericarditis, might also need to be excluded. Another important differential is exercise-induced laryngeal obstruction (EILO), where the wheezing and dyspnea are caused by transient obstruction of the upper airways during exercise (Nielsen 2013; Backer 2010).
Referral and Diagnostic Tests
The physical examination is usually normal. Some athletes with EIB may experience symptoms that develop several hours after exercise. This late-phase response is due to the activity of inflammatory mediators. Most commonly, a bronchial provocation challenge is used to determine the diagnosis of EIB (Parsons et al. 2011; Hayden et al. 2011; Morris 2010). Figure 7.9 shows a decision tree commonly used for the diagnosis of EIB. Alternatively, many physicians choose to just evaluate the patient's response to an empirical trial of a ß-agonist medication before exercise.
Decision tree for the diagnosis of exercise-induced bronchoconstriction (EIB).
Treatment and Return to Participation
The treatment of choice in EIB is an inhaled ß2-agonist from a metered-dose inhaler (e.g., albuterol) taken 15 to 30 min before the onset of exercise. An athlete who has asthma symptoms outside the exercise setting or who is using a ß2-agonist more than three times per week should be treated with a regular inhaled corticosteroid. Here is how to properly use an inhaler:
- Remove dust cap and shake the inhaler system before each use.
- Inspect mouthpiece for contamination or foreign objects.
- Breathe out through the mouth, exhaling as completely as possible.
- Hold the inhaler system upright with mouthpiece in mouth and lips closed tightly around mouthpiece.
- Breathe in slowly while pressing down on the metal cartridge.
- Hold breath as long as possible.
- Release pressure while still holding breath.
- Remove mouthpiece.
- Wait for the container to repressurize, shake, and then repeat steps 3 through 8 when more than one inhalation is prescribed.
- Rinse mouth with water after prescribed number of inhalations.
- Clean the inhaler system every few days by removing metal cartridge and rinsing the plastic inhaler and cap with running warm water. Replace cartridge and cap.
Emerging studies show promise using long-acting ß2-agonists such as salmeterol and leukotriene inhibitors such as montelukast (Singulair) (Parsons 2010). Other nonpharmacological strategies include pre - warm-up bursts of physical activity at 80% to 90% of the individual's maximal workload to induce a refractory period that lasts up to 3 h after the initial attack of EIB (Hull et al. 2012; Millward et al. 2009; Boulet, Hancox, and Fitch 2010). Strategies to humidify inspired air and dietary interventions may also prove to be beneficial (Carey, Aase, and Pliego 2010; Bussotti, Di Marco, and Marchese 2014).
For an athlete experiencing a severe asthma attack or when an inhaler is ineffective, a nebulizer may be used. A nebulizer, also known as an atomizer, is a machine that vaporizes liquid medication into a fine mist to be inhaled into the lungs via a mouthpiece or mask. Although studies have shown that both inhalers and nebulizers tend to be equally effective in delivering medications, nebulizers are preferred for use in more serious rescue situations when the patient is experiencing a severe asthma attack. Nebulizers can administer a higher dose of medication, but inhalers are easier to use, preferred for their portability and low cost, and good for everyday use. Medications typically administered with a nebulizer include albuterol and ipratropium (Atrovent).
Athletes with controlled EIB need not be excluded or discouraged from participating in sports. Effective strategies, both pharmacological and nonpharmacological, exist that can allow an athlete to compete even at an elite level.
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Causes of Sudden Cardiac Death in Athletes
Death by sudden cardiac arrest (SCA) is a rare event in the young athlete. In the United States, elite athletes are viewed as near invincible because of their incredible physical feats.
Death by sudden cardiac arrest (SCA) is a rare event in the young athlete. In the United States, elite athletes are viewed as near invincible because of their incredible physical feats. Nevertheless, it is reported that the rate of collegiate athlete death due to SCA is higher than that of high school athletes, with a suspected 110 SCA deaths annually in the United States among young athletes (Casa et al. 2012). Any time a tragedy of this proportion occurs, the public reacts with disbelief, and medical knowledge is called into question. Studies that have tracked these deaths during sports used the National Federation of State High School Associations (NFHS), the National Collegiate Athletic Association (NCAA) governing organizations, and state and federally funded research groups for data collection, such as the National Center for Catastrophic Sport Injury Research (NCCSIR), based in Chapel Hill, North Carolina. Approximately 90% of the data collected involved male athletes, with an equal distribution between Caucasians and African-Americans (Borjesson and Pelliccia 2009). According to the NCCSIR, there were 10 indirect (due to exertion) fatalities in middle school through college football athletes in 2014, and six were attributed to a cardiac event (Kucera et al. 2015). An additional five football athletes died of suspected cardiac conditions due to nonexertional factors in the same year (Kucera et al. 2015). Sudden death cases in young women are rare, and the most common cause of sudden cardiac death was congenital cardiac disease.
The prevalence of sudden cardiac death in young athletes (those less than 35-year-old) is estimated to be between 1 and 3 in 100,000 (Borjesson and Pelliccia 2009). This is much higher than statistics reported in a more general population of active individuals (Harmon, Klossner, and Drezner 2011). These data indicate that active people are not immune to cardiovascular events that may result in death.
Causes
The most common cause of sudden cardiac death in the young athlete is hypertrophic cardiomyopathy, which accounts for up to 50% of the cases. Other significant causes of sudden cardiac death in a young athlete are coronary artery anomalies, increased cardiac mass, aortic rupture, myocarditis, and aortic stenosis(Borjesson and Pelliccia 2009).Rare causes include dilated cardiomyopathy, atherosclerotic coronary artery disease, mitral valve prolapse, isolated arrhythmias such as long QT syndrome and Wolff-Parkinson-White syndrome, and arrhythmogenic right ventricular dysplasia (ARVD) (Harmon, Klossner, and Drezner 2011). In the Veneto region of Italy, researchers have found ARVD to be the most common cause of sudden cardiac death in the athlete (Thiene et al. 1988). This research suggests that a specific population may have different genetic subtraits.
In the older athlete, coronary artery disease is by far the most common cause of sudden death. Rarely is sudden death in the older athlete caused by hypertrophic cardiomyopathy, mitral valve prolapse, or acquired valvular conditions (Maron et al. 2014; Nagashima et al. 2003; Semsarian, Sweeting, and Ackerman 2015; Marijon et al. 2015).
Traumatic sudden cardiac death has not captured as much attention because its epidemiology is more difficult to track. However, it is a growing problem that strikes without warning. Between 1996 and 2007, a reported 180 cases of blunt-force death in the United States were attributed to commotio cordis (Maron et al. 2006). Most cases involved children with a mean age of 13, with 95% of the deaths occurring in males (Maron et al. 2013).
Commotio cordis refers to trauma to the chest wall that interrupts the electrical impulse in the heart. If the cardiac rhythm is not promptly normalized, the individual dies. Typically the ribs or sternum is not broken, although some contusions may be found. Research has found that a chest blow occurring during the vulnerable phase of repolarization, just prior to the T-wave peak in the cardiac cycle, can induce ventricular fibrillation (Maron and Estes 2005).
Although children and teenagers with thin chest walls are most vulnerable to commotio cordis (figure 8.6), deaths have been reported in adults. Sports such as baseball, ice hockey, lacrosse, and softball, which have hard projectiles that can strike the chest, have been associated with the greatest number of deaths. Commotio cordis also has occurred in sports such as soccer, football, rugby, and karate, in which the blow came from a soft projectile or a collision. It appears that the timing of the incident, rather than the degree of impact of the object, is the causative factor (Maron and Estes 2005). Commotio cordis is the only significant cause of traumatic sudden cardiac death in athletes.
The type of injury associated with commotio cordis is a blow to the chest wall that interrupts the usual cardiac rhythm.
Red Flags for Traumatic Sudden Cardiac Death
Sports with projectiles that can hit the chest at an inopportune time in the cardiac rhythm cycle have been known to cause commotio cordis in young athletes. These sports include the following: baseball, softball, hockey, lacrosse, soccer, football, karate.
Prevention
Because death can be the outcome, prevention has become the focus of attention for commotio cordis. Changes in practice have ranged from protective padding to softer balls that are used in Little League and softball. Because this may not completely resolve the problem, another solution is defibrillation in conjunction with cardiopulmonary resuscitation (CPR). Defibrillation interrupts the heart rhythm so the heart can "reboot" into a normal rhythm.
The American Heart Association estimates that communities with comprehensive CPR and automated external defibrillator (AED) training achieve 40% survival rates for cardiac arrest victims. If defibrillation is performed within 3 min, the likelihood of survival is high. For every minute of delay the chance of survival drops by as much as 10% (American Heart Association 2013).
The advent of the AED has provided greater public access to life-saving technology. These devices can be operated by trained laypeople and are increasingly affordable in all sectors. The AED is portable, rechargeable, simple to operate, and easy to maintain. The American Red Cross, American Heart Association, and National Safety Council offer AED certification courses in addition to CPR courses for the lay public. The NCAA Sports Medicine Guidelines require planned access to an AED and mandating CPR and first aid certifications for all who work with athlete practices, competition, and skill sessions. Athletic trainers are required to maintain certification in emergency cardiac care, including AED use. They need to have ready access to an AED in order to provide rapid cardiac assessment and care to those in fibrillation. Athletes who suffer a sudden collapse and have agonal or gasping breathing should be treated because they are suffering from a cardiac event (Casa et al. 2012; Solberg et al. 2015). An AED should be applied as soon as possible for heart rhythm analysis and possible defibrillation.
Clinical Tips
Potential Causes of Sudden Death
Sudden collapse in athletes could be caused by heatstroke, a cardiac event, sickle cell collapse, or injury. Understanding the presentation of each will facilitate rapid response and the appropriate disposition.
Emergency Planning
Every athletic site should have planned access to an AED, an emergency medical service (EMS), and an established emergency action plan (EAP), as well as medical personnel trained to respond to sudden collapse.
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How to identify celiac disease
Celiac disease is an autoimmune disorder that affects the gastrointestinal tract and is thought to be triggered by dietary gluten in affected individuals. The disease is characterized by chronic inflammation of the small intestinal mucosa, which leads to atrophy of the small intestinal villi and subsequent malabsorption (Pelkowski and Viera 2014).
Celiac disease is an autoimmune disorder that affects the gastrointestinal tract and is thought to be triggered by dietary gluten in affected individuals. The disease is characterized by chronic inflammation of the small intestinal mucosa, which leads to atrophy of the small intestinal villi and subsequent malabsorption (Pelkowski and Viera 2014). Celiac disease affects approximately 1% of the U.S. population and typically occurs in persons of European ancestry as well as persons of Middle Eastern, Indian, South American, and North African descent. It is two to three times more common in women. Celiac disease is not a food allergy.
Signs and Symptoms
Typical presentation includes chronic diarrhea with cramping and gas pains. Patients often have weight loss, or in the adolescent, delayed onset of growth or puberty. A history of nervousness and/or depression is often present, as is a family history of autoimmune disease. Other complaints may include bone or joint pain, migraines, weakness, fatigue, and anemia (Volta et al. 2015; Vivas et al. 2015; Byrne and Feighery 2015; Mancini, Trojian, and Mancini 2011). Physical examination is often normal, but the patient may present with abdominal distension or dermatitis herpetiformis.
Referral and Diagnostic Tests
Lab tests are performed for differentiating celiac disease and to rule out more common diseases. These include a basic metabolic panel, CBC (iron deficiency), TSH (thyroid disease), vitamin D level, and allergy testing. If celiac disease is suspected from history and physical exam, the initial serologic test is a tissue transglutaminase (tTG) antibody level. This antibody is found in every tissue in the body and acts to join proteins together. In people with celiac disease, tTG activates specific immune cells and triggers the inflammatory response that leads to atrophy of the villi in the small intestine (Mancini, Trojian, and Mancini 2011). The diagnosis is often confirmed with repeat blood tests after 4 wk on a gluten-free diet. Endoscopy with biopsies of the duodenal mucosa may be necessary to confirm the diagnosis. Celiac disease should be differentiated from GERD, pancreatic insufficiency, Crohn's disease, or other inflammatory bowel diseases.
Treatment and Return to Participation
The general treatment is to remove gluten from the diet. The patient can substitute rice, corn, and soybean flour for products that contain gluten. Periodic blood tests are performed to measure the levels of the antibodies. The levels will normalize with gluten abstinence. Abstinence will be required for life because the immune response to gluten will recur if gluten is consumed again. Usually no medications are prescribed for celiac disease, but athletes may benefit from iron, vitamin, and calcium supplements. The most difficult aspect for the athlete with celiac disease is the dietary restrictions while traveling with the team or with set team meals. The athletic trainer may need to check on the gluten-free status of many of the standard gluten-containing products provided by the athletic department, such as energy drinks or meal replacement bars (Mancini, Trojian, and Mancini 2011).
Condition Highlight
Gluten Sensitivity and Intolerance
Over the past 10 yr, the number of people choosing a gluten-free diet (GFD) is much higher than the projected number of celiac disease patients (Lis et al. 2015). This has fueled a global market of gluten-free products and highlights several conditions related to the ingestion of gluten. There are three main forms of gluten reactions: allergic, autoimmune (celiac disease), and immune-mediated conditions (gluten sensitivity) (Sapone et al. 2012). Wheat allergy is an adverse reaction to wheat proteins with onset in minutes to hours after gluten ingestion. It may affect the skin, GI tract, or respiratory tract. Celiac disease or other autoimmune gluten disorders generally present months to years after gluten exposure. There is a third condition where some people experience distress from eating gluten-containing products and show improvement with a GFD. It is distinct from celiac disease and wheat allergies (Vivas et al. 2015). Gluten sensitivity cannot be distinguished clinically; serology tests need to be conducted. Patients with GI discomfort or distress following gluten ingestion should be referred for a follow-up blood test and immune-allergy tests.
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