Overview This topic covers pulmonary conditions seen in the athlete and covers Asthma Exercise-Induced Bronchospasm (EIB) Exercise-Induced Laryngeal Obstruction (EILO) Exercise-Induced Anaphylaxis Pneumothorax Hemothorax Pulmonary Embolism Asthma Introduction transient lower airway obstruction due to underlying hypersenstivity reaction primarily an expiratory problem exercise can be a trigger for asthmatic episode known as exercise-induced asthma (EIA) History wheezing and shortness of breath may have cough, though less common in classic asthma chest tightness Physical examination expiratory labored breathing respiratory retractions with use of accessory respiratory muscles expiratory wheezing or rhonchi Diagnosis pulmonary function testing +/- bronchial provocation challenge with methacholine tests airway hypersensitivity low forced expiratory volume in 1 second (FEV1) and low FEV1/FVC ratio improves with administration of bronchodilators Treatment rest, controlled breathing rate, inhaled beta-2 agonist acute exacerbation rest albuterol Q15 minutes PRN epinephrine (Epipen), transport to ER severe and/or refractory episode inhaled glucocorticoids maintenance therapy for moderate to severe asthma Return to play as tolerated active wheezing is a contraindication to RTP Exercise-Induced Bronchospasm (EIB) Introduction often thought of as exercise-induced asthma (EIA), though technically they are distinct disorders EIA occurs in patients with an underlying asthma diagnosis in which exercise is a trigger EIB occurs in athletes with no underlying asthmatic disease transient lower airway obstruction resulting from exertion primarily an expiratory problem risk factors winter sports drying and and cooling of mucosa leads to edema and constriction endurance athletes sports requiring high minute ventilation History classic triad of wheezing, shortness of breath and cough associated with exercise nonspecific symtoms "poor performance", fatigue, headache onset 10-15 minutes after exertion resolves with 20 minutes of rest Physical examination often normal Differential diagnosis exercise-induced hyperventilation "pseudo-asthma syndrome" hyperventilation during exercise causes respiratory symptoms (wheezing, chest tightness) not related to bronchial constriction Diagnosis pulmonary function testing can be normal at baseline eucapnic voluntary hyperventilation (EVH) test gold standard for diagnosis of EIB patient hyperventilates dry gas with a % carbon dioxide level to mimic exercise conditions spirometry findings > 10% reduction in FEV1 is diagnostic improves with administration of bronchodilators Treatment prevention warm-up, environmental control "refractory period" purposeful induction of asthmatic response effective for ~50% of athletes inhaled beta-2 agonist albuterol 2 puffs 15-20 minutes prior to activity rest, controlled breathing rate, inhaled beta-2 agonist acute exacerbation albuterol Q15 minutes PRN Return to play as tolerated active wheezing is a contraindication to RTP Exercise-Induced Laryngeal Obstruction (EILO) Introduction transient upper airway obstruction caused by paradoxical closure of the vocal cords or narrowing of the supraglottic structures during heavy exertion inspiratory problem has prominent psychological component Types supraglottic glottic (vocal cord dysfunction) mixed supraglottic and glottic History ranges from mild shortness of breath to severe respiratory distress more rapid onset than bronchospastic disorders throat tightness and choking sensation compared to chest tightness seen in asthma, EIA, EIB "breathing through a straw" failure to respond to bronchodilator treatment often misdiagnosed as EIA/EIB and prescribed beta-2 agonist inhaler Physical examination inspiratory labored breathing inspiratory stridor (high pitched) Diagnosis pulmonary function testing can be normal at baseline may show blunted inspiratory portion of flow-volume loop continuous exercise laryngoscopy (CEL) test gold standard to diagnose EILO flexible laryngoscope to assess laryngeal movement while patient performs exercise distinguishes supraglottic from glottic and allows grading of obstruction Treatment nonoperative mainstay of treatment psychotherapy laryngeal control therapy (LCT) focuses on breathing with lower abdominal movement and controlled exhalation through mouth speech therapy SSRIs botulinum toxin injections operative rare surgical debulking of redundant tissue Exercise-Induced Anaphylaxis Introduction rare life-threatening systemic hypersensitivity response triggered by physical exertion type I hypersensitivity reaction (IgE mediated) can be preceeded by ingestion of food allergen prior to exercise known as food dependent exercise-induced anaphylaxis (FDEIA) thought to be due multifactorial increase gastrointestinal permeability alterations in tissue enzymatic activity and plasma pH redistribution of mast cells from gut with concomitant transport of recently ingested allergens to other areas of the body and subsequent intensification of prior low-grade allergic reaction History onset usually within 30 minutes of initiating exercise early fatigue, generalized pruritis and urticaria abdominal pain, nausea / vomiting, cramps shortness of breath and throat tightness Treatment prevention refrain from exercise 4-6 hours after eating avoid exercise in extreme temperature (very hot/humid or very cold) avoid Aspirin or NSAID use prior to exercise epinephrine (Epipen), antihistamines, corticosteroids acute episode allergist consultation Return to play only after evaluation by allergy specialist and comprehensive action plan made patient should always have Epipen and exercise with a partner Pneumothorax Introduction presence of gas within the pleural cavity between the lung and chest wall causing collapse of the lung etiology spontaneous risk factors smoking male gender family history of pneumothorax connective tissue disorders (Marfan's, Ehlers Danlos) traumatic penetrating vs. blunt trauma contact athletes (ice hockey) at highest risk iatrogenic interscalene nerve block Types closed pneumothorax no communication between outside and pleural cavity pleural cavity pressure = pulmonary pressure pleural cavity pressure < atmospheric pressure ex. spontaneous pneumothorax secondary to rupture of pulmonary bleb open pneumothorax communication between outside and pleural cavity air enters the pleural cavity during inspiration and exits during expiration pleural cavity pressure equilibrates to atmospheric pressure, no "tension" tension pneumothorax communication between outside and pleural cavity air enters the pleural cavity during inspiration but is unable to exit, resulting in further accumulation of air within the cavity and increased pleural pressure ("tension") elevated pleural pressure further compresses the lung and mediastinal structures, causing tracheal deviation and progressive cardiopulmonary compromise life-threatening emergency History sudden onset, unilateral, pleuritic chest pain sharp pain with inspiration shortness of breath syncope Physical examination anxious visible deviation of trachea and jugular venous distention in cases of tension pneumothorax tachypnea and tachycardia unilateral decreased or absent breath sounds hyperresonant to percussion Diagnosis ultrasound absent lung sliding chest XR findings pleural line formed by visible edge of collapsed lung loss of lung markings (air appears black) shift of the mediastinal structures (heart, trachea) and depression of the hemidiaphragm seen in tension pneumothorax Treatment emergent needle decompression followed by chest tube placement first line of treatment for tension pneumothorax place a needle into the 2nd or 5th intercostal space in the midaxillary line (adults) the second intercostal space, midclavicular line is still recommended for pediatric patients then transport to emergency department for chest tube placement chest tube placement, admission to hospital pneumothorax > 20% (lung edge > 2cm from chest wall) supplemental oxygen, observation, repeat CXR pneumothorax < 20% (lung edge < 2cm from chest wall) and patient clinically stable observe for 4-6 hours supplemental oxygen increases rate of pleural air absorption and can accelerate resolution repeat CXR prior to discharge from observation and at 12-48 hour post-discharge NO flying for 2-4 weeks decreased pressure on airplane can increase volume (size) of pneumthorax Return to play following radiographic resolution of pneumothorax, usually ~4 weeks pain is the primary factor limiting RTP Hemothorax Introduction most common result of major chest wall trauma can be penetrating or blunt injuries 30% patients with rib fractures have pneumohemothorax History acute onset chest pain less pleuritic compared to pneumothorax shortness of breath Physical examination anxious tachypnea and tachycardia hypotensive in large hemothorax unilateral decreased or absent breath sounds hyporesonsant (dullness) to percussion Diagnosis chest XR opacification of hemithorax Treatment chest tube placement, repeat CXR initial treatment of choice repeat CXR after 4-6 hours and again at 24 hours to assess resolution thoracoscopy (VATS) or thoracotomy indications > 1500cc initial chest tube output > 200cc/hr for 3+ hours increasing size of hemothorax incomplete resolution fo hemothorax despite 2 chest tubes placed Pulmonary Embolism Introduction athletes thought to be at increased risk due to higher rate of musculoskeletal injuries (+/- immobilization) athlete-specific repetitive motions (pitchers, tennis players) frequent long-distance travel History sudden onset, pleuritic chest pain shortness of breath lightheaded, dizziness, syncope Physical examination tachycardia and tachypnea hypotensive if large PE hypoxia Diagnosis helical chest CT scan first line imaging modality pulmonary angiography gold standard for diagnosis nuclear ventilation perfusion scan (VQ scan) Treatment systemic anticoagulation 3-6 months IV heparin drip or Lovenox injections, followed by conversion to oral anticoagulant minimum of 3 months treatment Return to play returning to sport while on systemic anticoagulation therapy is controversial contact athletes usually withheld from sport for duration of anticoagulation due to bleeding risk average time to RTP is ~ 6 months