Breathing Problems NATA

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					Respiratory Disorders in Athletes

        Kevin E. Burroughs, MD
   Assistant Professor of Family Medicine
Director, Cabarrus Sports Medicine Fellowship
    Exercise and Immune Function
 The primary question is does strenuous
  exercise suppresses immune function?
 Does this increase the risk for common
  URIs and gastrointestinal infections?
 Theoretical Basis for Immune System
  Suppresion in Exercise
    – The same chemical pathways mediate
      inflammatory changes of soft tissue.
         Effects of Exercise
 Changes circulating concentration of
  immune cells and humeral factors.
 Changes the functional activity of immune
  system components
      Changes in Immunoglobulins
 Decreases in IGA and IGG in serum and saliva
 These decreases occur after either intense
  exercise or a prolonged season of training
    – Levels after strenuous bout can return to normal
      after 24 hrs of rest
   ?Significance, does this mean can’t fight viral
    – Not proven
             Exercise and URI
 Response to exercise follows a J Curve
 Sedentary individuals are at high risk
 Moderate exercisers are at low risk
 Excessive training or stressful events -
  marathons, championship games, etc. increase
    – Nieman, MSSE 1994
      Background Information
 CDC estimates the average incidence of
  Upper Respiratory Infections (URI) is 429
  million episodes
 This leads to >$2.5 billion in healthcare cost
 Most athletes suffer through a URI at some
  point in their careers
 URIs reported as the most treated condition
  by medical staff at the summer and winter
                Sevier TL. Med Clin North Am
                        78:389, 1994.
 More time is lost from sport due to upper
  respiratory tract infections than any other
  medical illness
 Viral infections cause most bronchitis and
  pneumonia, with some bacterial cases
 Bronchitis for athletes is same as non-
 Pneumonias for athletes are usually less
  serious than for non-athletes
              The Common Cold
   The common cold is most often caused by one of a
    number of viruses
    – Rhinovirus (yr round), cornavirus (winter), or the RSV
    – Others such as influenza, parainfluenza, adenovirus,
      coxsackievirus may also produce URI symptoms
   Colds occur in a seasonal pattern mid-Sept to April-May
   Symptoms begin 1-2 days after exposure and last 1-2
    weeks, with viral shedding 2-3 more weeks
   Symptoms vary as widely as causes
    – Malaise, stuffy nose, rhinorhea, nonproductive cough, mild
      sore throat, and low grade fever
   Sometimes confused with allergies
   Symptomatic care
   32 million cases annually in
   0.5-0.2% of colds are
    complicated by sinusitis
   Most acute sinusitis occurs
    from viral and bacterial co-

   Nasal Anatomy/Polyp
         Sinusitis in Athletes
 Accounts for 4.6% of visits to MD by
  young adults
 Athletes in water sports are at higher risk
 Allergic rhinitis increases risk
 Nasal obstruction increases risk
 Viral in 30% of cases
     Pathophysiology of Sinusitis
   Obstruction of ostial openings - the osteomeatal
    – decreased oxygen tension
    – decreased clearance of foreign material
    – secondary bacterial overgrowth
   Mucociliary transport
   Secretory Immune System
   Systemic Immune System
    – Anything that impairs these functions increases risk
   Major symptoms
    –   Facial Pain*
    –   Nasal Obstruction
                                Minor Symptoms
    –   Nasal Discharge
                                 –   Headache
    –   Postnasal Drainage
                                 –   Halitosis
    –   Hyposmia
                                 –   Fatigue
    –   Fever
                                 –   Oral Pain
                                 –   Cough
                                 –   Ear pain, pressure,
    *Location = diagnosis            fullness
    P.E.findings in
   Nasal mucosal swelling
    and erythema
   Unilateral purulent nasal
   Maxillary molar tooth
    pain (unilateral)*
   Malodorous breath
   Variably - percussion
    tenderness, periorbital
    swelling, otitis media

    DeAlleaume L. J Fam Prac 52(7):2003
   Transillumination
    – Maxillary Sinus-
       » infraorbital rim towards
    – Frontal Sinus -
       » superomedial aspect of
         orbit towards floor of
         frontal sinus
Medications Achieving the Goals
  of Treatment for Sinusitis
   Decongestants oral or topical
    – open the sinus ostia
   Mucolytics such as guaifenesin
    – restore mucociliary clearance
   Antihistamines, Inhaled steroids or
    – treat underlying disorder
    Medication concerns in athletes
 Topical decongestants - allowed by NCAA
  & USOC
 Oral decongestants - banned by USOC &
  allowed by NCAA
 Mucolytics - allowed by NCAA & USOC
 Sedative antihistamines - not allowed by
  USOC for shooters
             Antibiotics - Sinusitis
   Acute bacterial sinusitis that is mild-moderate does not
    require antibiotic treatment
   In those with severe or persistent symptoms
   First Line
    – Amoxicillin
    – Trimethoprim-sulfamethoxazole
    – Doxycycline
   Second Line
    – Amoxicillin-Clavulanate
    – Cephalosporins (Omnicef, Vantin, Suprax)
    – Macrolides
                      CDC Guidelines on Appropriate
                      Antibiotic Use for Rhinosinusitis
    Cautions for the athlete with
 Good clearance of sinus congestion before
  any diving sport (barosinusitis)
 Myalgias indicate reduced muscle function
  and suggest limiting activity
 Fever reduces oxygen consumption by 13%
  per degree > 37º C (98.6 º F)
 Medications may adversely affect
       Oropharynx – Anatomy
   Normal
        Tonsillitis

   Strep                    Mono
   Posterior Pharynx Cobblestoning
    – Post-nasal drip or viral
    – Foreign material on R
   Peri-tonsilar abscess

All that wheezes is
not asthma, and all
that’s asthma does
  not wheeze….
            Begin with the PPE
   Do you have recurrent episodes of coughing or
    wheezing, especially at night or early in the
   Do you cough or wheeze after exercise?
   Do you get tightness in your chest during or
    immediately after exercise?
   Do you have frequent chest colds that last more
    than 10 days?
   Do you have a history of asthma, and if so what
    medications do you take and how often?
         Differential Diagnosis of Airway
          Obstruction – Peds/Adolescent
   Oral Cavity
    – Trauma, Angioedema
   Pharynx
    – Trauma, Peritonsilar abscess, Tonsilar
   Larynx
    – VCD, Epiglotitis, Vocal cord paralysis
   Trachea
    – Web (congenital-early), Foreign body,
      Thyroid enlargement
   Endobronchial
    – Asthma, tracheobronchitis
         Inspiratory Stridor (IS)
 Symptom of vocal cord dysfunction (VCD)
 Mistaken for EIA b/c of “wheezing”
 IS predominates during inhalation,
  originating in the neck region
    – EIA primarily during exhalation, more chest
      than neck dominate
    Laryngeal Hyperresponsiveness
   Analagous to nasal hyperres in asthma/allergic
   Inhalation of histamine laryngeal narrowing in
    both normal and asthmatics
    – Conversely, laryngeal widening in both with exercise
      and panting
    – Panting overrides the glottic narrowing
   VCD ? Caused by insult ? Inflammatory then
    autonomic imbalance (short/persistent)
    – Altered protective reflex of the larynx in lung
                      Ayres JG, Gabbott PLA. Thorax
   Symptoms of airway obstruction such as:
    – Stridor, cough wheezing and shorthess of breath.
   Rarely, during attack, neck pain, hoarseness,
    dysphonia, tightness in throat/chest, +/- difficulty
   Cough can by only symptom
   PE unremarkable if asymptomatic, with episode high
    pitch wheeze, over larynx/large airways
   Flexed neck posture during attack
   No true hypoxemia, or drop in O2 sat and a-a gradient
    (<20mm Hg)
           Demographics of VCD
   2-3% of the general and athlete pop affected
   Overall prevalence is unknown, but 1994 study
    showed 10% PVCM alone, 30% PVCM and asthma
   Other studies have shown up to 50% in those with
   Hard to fully discuss as 14-56% have EIB as comorbid
   Seems to be female predominate
   Psych risk factors
   Reflux/GERD
     The History and Names of VCD
   First described in 1842 by Dunglison
    – Disorder of the laryngeal muscles brought on by “hysteria”
    – Initially only described in the psych literature
   Paradoxical vocal cord motion (PVCM)
   Laryngeal dyskinesia
   Vocal cord malfunction
    – All have the basic tenant of adduction of the vocal cords
      during inspiration
   Several synonyms
    – False croup, Munchausen stridor, psychogenic stridor,
      hysterical stridor, factitious asthma, episodic laryngeal
      dyskinesia, paradoxical vocal cord motion (PVCM)
                         Bahrainwala AH, Simon MR. Curr
                           Opin Pulm Med 2001;7:8-13.
       VCD- How does it happen?
   By itself or with asthma
   If together, increase refractory nature of asthma
   Most likely syndrome with full spectrum of
    psych  non-psych etiology
   Initially ? Conversion reaction
   With psychogenic cause, important that this is
    subconscious – can’t get reproduced voluntarily
   Nonpsychogenic triggers reported to be those similar to
    – Ammonia, cleaning chemicals, organic solvents, and smoke
    – One report of direct relationship to chlorine
 Normally signal from brain to stimulate
  muscles to contract abducting the cords
 Varies according to CO2 and O2 levels
 One set of muscles abducts, the other
  adducts (not just relaxation)
    – VCD dec in abduction tone
                  VCD Symptoms
   Symptoms of airway obstruction such as:
    – Stridor, cough wheezing and shorthess of breath.
   Rarely, during attack, neck pain, hoarseness,
    dysphonia, tightness in throat/chest, +/- difficulty
   Cough can by only symptom
   PE unremarkable if asymptomatic, with episode high
    pitch wheeze, over larynx/large airways
   Flexed neck posture during attack
   No true hypoxemia, or drop in O2 sat and a-a gradient
    (<20mm Hg)
           Criteria for Diagnosis

   Presence of symptoms including wheezing, cough,
    dyspnea, stridor, hoarseness
   Laryngoscopic confirmed adduction of vocal
    cords during inspiration, early expiration, or both
    inspiration and expiration
   Absence of gagging or coughing during
   Presence of a posterior glottic chink
   Exclusion of alternative vocal cord disease
   PFTs can be used
    – Better for deciding on asthma as a cofounder or
    – May show limitation on inspiratory loop
    – CXR usually doesn’t show much
       » i.e. no hyperinflation
   Acute
    –   Heliox (Helium and Oxygen)
    –   CPAP
    –   Panting
    –   Anxiolytics
    –   Botox injection
   Long-term
    – Speech Therapy
    – Psychotherapy
    – Patient education
              EIA vs IS (VCD)
          EIA                        IS (VCD)
   Chest tightness             Throat tightness
   Especially susceptible      No circadian rhythm
    to night sxs                Usually soon after
   Takes 5-10 min of            exercise starts
    exercise to incite          Resolves within 5 min
   Symptoms peak 5-20           of cessation of activity
    min after stop              Not provoked by
   Reproducible on              surrogate challenges
          Definition of Asthma
    – “a chronic inflammatory disorder of the
      airways in which many cells and cellular
      elements play a role… In susceptible
      individuals, this inflammation causes recurrent
      episodes of wheezing, breathlessness, chest
      tightness, and coughing particularly at night.”
 Approximately 10 million in US, with inc
  prevalence over the last 10 yrs
 More than 90% can also have exercise-
  induced bronchospasm if provoked
                              Asthma Cascade


                                 Mast Cell
   Allergen                                              Cellular infiltration and airway edema


                                    Interleukins         Blood vessels become permeable


           Smooth Muscle Contracts in response
        Testing for Asthma and EIB
   Pulmonary Function Testing
    – Permits objective measure of the severity
    – Objective evidence of the responses to meds
   Characteristic changes in obstruction
    – FEV1 decrease
    – FVC somewhat decreased (dec in FEV1/FVC)
    – Decreased Peak Expiratory Flow (PEF)
   Diagnosis
    – >15% decrease in PEF (lg and small airways)
    – >15% (10% for EIB) decrease in FEV1 (lg airway)
    – >35% decrease in FEF 25-75% (small airways)
       Classification of Asthma Severity:
       Clinical Features Before Treatment
                 Days With            Nights With          PEF or        PEF
                 Symptoms             Symptoms                FEV1
Step 4           Continuous            Frequent           60%           30%
Step 3             Daily                5/month        60%-<80%        30%
Step 2           3-6/week             3-4/month             80%         20-30%
Step 1              2/week             2/month          80%           20%
Footnote: The patient’s step is determined by the most severe feature.
    Asthma at the Summer Olympics

   Study by Weiler et al on the US Team health
    questionnaire for 1996 Atlanta
    – Of 699 athletes, 15.3% prev dx of asthma,
    – 13.9% used asthma med at some time in past
    – 10.4% were currently taking asthma med
    – Highest prevalence reported in Mtn Bike, cycling
    – Least in divers and weight lifters
                      J Aller & Clin Immunology
                          102(5):722-6, 1998
     Asthma at the Winter Olympics

   Study on the US Team health history for 1998
    –   21.9% had previous dx of asthma
    –   18.4% recorded use of asthma med at some time
    –   17.4% were currently taking asthma med
    –   Highest percentage in Nordic combined, X-country,
        and short track events

                       J Aller & Clin Immunology
                          106(2):267-71, 2000
Asthma at the Summer Olympics
   For 2004 had to submit medical justification
    – Pre/post, Exercise dec, Eucapnic, Hypertonic
      Saline, methacholine challenge
   2004 Athens 10,653 athletes
    – 4.2% approved for B2 agonist medications
    – 0.4% rejected
    – Approval rate down 26% from Sydney 2000

                    J Aller & Clin Immunology
                       117(4):767-73, 2006
              Managing Seasonal
              Asthma Symptoms
•   Medical history is usually sufficient to determine
    sensitivity to seasonal allergens.

•   Just before allergy season:
    • Start daily anti-inflammatory therapy

•   During allergy season:
    • Continue anti-inflammatory therapy

    • Use stepwise approach to control symptoms
                    EIA / EIB
   Two commonly used terms
    – EIA – exercise induced asthma
       » Some use as bronchial obstruction caused by
       » Symptoms worsened by exercise in those with
    – EIB - exercise induced bronchospasm
       » Found as bronchial spasm/obstruction with exercise
         in persons with normal lung function at rest
           Clinical Features
   During Exercise, bronchioles normally dilate
    allowing increased air flow. After exercise,
    pulmonary function generally decreases up to 10
    percent in normal persons.
   In EIA airway obstruction begins shortly after
    exercise, reaches its peak in 5-10 minutes, and
    then remits spontaneously with complete recovery
    usually within 30-60 minutes.
   The effect of ventilation and the heat content of
    inspired air help to determine the response.
      Managing Exercise-Induced
        Bronchospasm (EIB)
•   Anticipate EIB in all patients
•   Teachers and coaches need to be notified
•   Diagnosis
    • History of cough, shortness of breath, chest pain or
      tightness, wheezing, or endurance problems
      during exercise
    • Conduct exercise challenge OR have patient
      undertake task that provoked the symptoms
    • 15% decrease in PEF or FEV1 is compatible with EIB
          Managing Exercise-Induced
          Bronchospasm (EIB) (continued)
•   Management Strategies
    • Short-acting inhaled beta2-agonists used shortly before
      exercise last 2 to 3 hours
    • Salmeterol may prevent EIB for 10 to 12 hours
    • Cromolyn and nedcromil are also acceptable
    • A lengthy warmup period before exercise may preclude
      medications for patients who can tolerate it
    • Long-term-control therapy, if appropriate
 EIB is the bronchial obstruction (“spasm”)
  found after exercise in persons with normal
  lung function at rest.
 EIA is sometimes used to describe the
  exacerbation of a patient’s asthma when
  they exercise.
 Exercise Induced Asthma or EIA is defined
  as a transient increase in airway resistance
  following 6-8 minutes of vigorous exercise
 Increased resistance causes a 15% or greater
  decrease in forced expiratory volume in one
  second FEV1 or in peak expiratory flow rate
 The underlying inflammation in asthma
  determines the need for daily preventative
  anti-inflammatory controller medications
 If unchecked, airway remodeling may occur
  in the lungs, lead to irreversible changes
     How common is the problem?

                           Incidence of EIA
   In recent years
                      Cross-country skiers    50%
    there’s been a
    significant       Ice Hockey              35%

    increase in       Speed Skaters           43%
    EIA in both       Figure Skaters          35%
                      Olympic Athletes        17%
    and elite
    athletes          School children         12%
          Two main theories
 #1 Water-loss theory:
 Loss of water from the bronchial mucosa
  into the exhaled air during exercise
 Leads to hyperosmolar condition on the
  bronchial lining and in cells
 Leads to release of pro-inflammatory
  mediators (histamine, leukotrienes, etc.)
  resulting in local events that cause
          Two main theories
 #2 Thermal expenditure theory:
 Hyperventilation of exercise leads to
  cooling of the surface cells
 After exercise, or with excessive cooling,
  there is a re-warming heat transfer from the
  pulmonary vascular bed
 Leads to hyperemia, swelling and fluid
  exudate into the submucosa triggering
  inflammatory mediators
       Factors to help diagnosis
   Can improve likelihood of diagnosis
    – Increased sxs with cold air exposure
    – Family history of asthma
    – Personal history of asthma, OR recurrent
      allergic rhinitis or sinusitis.
              Clinical Clues
                           SUBTLE
- Wheezing              - Cough
- Dyspnea on exertion   - Chest pain
- Chest tightness       - Cramps, especially stomach
                        - Shortness of breath
                        - More symptoms with cold
                        - Problems change in
                           different environments
   Challenge testing
    – Most specific to test on the field of their sport
    – IOC recommends Eucapnic voluntary
      hyperventilation (EVH) challenge with dry air
       » Or, EVH using mixture of 5% CO2, 21% O2, N2,
       » Expensive equipment, complex test
    – Methacholine challenge, not as good
   In patients with classic history, appropriate to start therapeutic
    trial of pre-exercise medication both to confirm the diagnosis
    and to treat the patient.
   Formal exercise PFTs can also establish diagnosis and monitor
    treatment efficacy.
   Although formal testing can be used, office testing may be
   In the office Peak Flow (which corresponds to FEV1) is
    measured pre and immediately post exercise, then every 5
    minutes for 20-30 minutes.
   A decrease of 15% or greater of FEV1 is considered positive
    Summary of USOC Asthma
       Summit Conference
                        Patient with suspected EIA by history

                       Pulmonary function tests (PFTs) at rest

 PFT less than 90% predicted normal           Normal PFT at rest but positive history

Patient probably has chronic persistent      Pretreatment before exercise empirically
   asthma and needs treatment with             with albuterol MDI or albuterol plus
  daily inhaled corticosteroids plus                       nedocromil
         albuterol preexercise

 Follow up with repeat PFTs at rest                       Follow-up visit
 and possibly pre- and post exercise

                                       Improved                                  Not improved

                                  Continue Therapy                     Order pre and post exercise PFTs
                                                                            with flow-volume loops;
                                                                  consider: higher dose pre-exercise albuterol
                                                                  consider: daily steroids, salmeterol, atrovent
          Therapy - Education
   First, advise the athlete regarding the types of
    exercise less likely to exacerbate the condition.
Factors most likely to cause     Factors least likely to cause
    Continuous hard exercise -      Intermittent exercise or team
    running                         games
    Exercise in cold                Swimming
    Exercise in polluted air        Exercise in warm, humid air
    indoor/outdoor                  Outside of pollen season
    Pollen season in allergic       Non-polluted air
    With a URI
     The “Run Through” Therapy
   Special warm-up routine can reduce the
    severity of EIA
    – Warm-up 80-90% of maximum workload before
      formal exercise
    Beta Agonist Medications
   First line: short acting beta agonist such as
    albuterol (Proventil, Ventolin),
    metaproterenol sulfate (Alupent), or
    pirbuterol (MaxAir).
    Administered via MDI about 15-30 minutes before
   An alternative is salmeterol, which is longer
    acting and can be given 30-60 minutes
    before exercise and may control EIA up to
    12 hours.
          Therapy - The next step
   If this is not sufficient, can ADD:
   Cromolyn sodium or neocromil sodium (2 puffs) can
    also be given before exercise either alone or in
    combination with a beta-agonist.
   Some may require a higher dose of either to block
    EIA; the dose of either of these can be increased to 4
    puffs immediately before exercise
   If no response, daily inhaled corticosteroids should be
    considered and re-evaluate to see if athlete is suffering
    from chronic persistent asthma.
       Side Effects of the Beta’s
 Short and long-acting have problems
 Most common, tremor or tachycardia
    – Leads to false starts, impair fine motor skills
   Chronic use can lead to tachyphylaxis or
    – Typically only in those on daily doses, may
      need to revert to cromolyn in these.
            Oral Montelukast

   Singulair
    – Cysteinyl leukotrienes (LTC4, LTD4, and LTE4)
      synthesized from AA
    – Potent bronchoconstrictors (1000x histamine)
    – Leukotriene receptor antagonist
    – Head-to-head with Salmeterol
       » Effect of Singulair maintained through 8 wks
       » Salmeterol protection dropped between 4-8 wks
    – 10mg qhs
              Future Therapies
 LMWH (Enoxaparin) partially block EIA
 Symbicort
    – combination steroid (budesonide) and long-
      acting beta (formoterol) [like Advair]
   Xolair
    – anti-Ig E antibody, injection, chronic therapy
   PDE 4 inhibitors
    – Will be similar to theophylline
           If still doesn’t respond
   ?other etiology
    –   Vocal cord dysfunction
    –   Idiopathic arterial hypoxemia of exercise
    –   Cystic fibrosis
    –   Atrial Septal Defect
    –   Interstitial pneumonia
    –   Cardiac arrhythmia
What about something other than
 Data overall supporting vitamins, herbals or
  diets very limited.
 Anti-oxidants may be beneficial
 Low salt diet may be beneficial
         Influenza Immunization
   May be beneficial for athletes in fall/winter sports
   No if allergic to eggs/currently febrile
   Antibodies can be present for up to a year
   Immunize around Sept so peak at mid season
   Myalgia, soreness at injection site not an issue
   2002 Salt Lake Olympics Influenza A/B dx’d in
    36 or 188 patients suspected.

                    Emer Infect Dis 12(1):144-6, 2006.
              Acute Bronchitis
 Respiratory infection characterized by
  inflammation of the bronchial tree leading
  to recurrent cough
 Diagnosis requires exclusion of pneumonia
  or other URT sources
 Multiple etiologies:
    – Viral or bacterial
    – asthmatic
    – chemical/irritant
     Acute Bronchitis-Symptoms
   Persistent cough sometimes producing clear
    mucus or purulent sputum
   Coughing may interrupt sleep and/or daily
    – Acute (<3wks), Chronic (>3 wks)
   If temp >38 º C (100.4 º F), tachycardia (>100
    bpm), tachypnea (>24/min) or hypoxemia have
    increased likelihood of pneumonia
   Consider influenza if season appropriate
      Acute Bronchitis – Clinical
   Fever usually absent, and low-grade if present
   Rhonchi or coarse breath sounds, though
    auscultation can be clear (rales indicate localized
    process such as pneumonia)
   No sinus tenderness or purulent nasal discharge
   WBC – minimal elevation if any
   CXR – may reveal hyperinflation, but no infiltrate
    Acute Bronchitis-Etiology
 Common respiratory viruses are primary
 Epidemics occur secondary to rhino virus,
  RSV, influenza A, corona virus
 Bacteria are less common cause of acute
 Agents responsible for pneumonia and
  sinusitis can cause bronchitis as well
    Acute Bronchitis vs.. Asthma
 Line of distinction between acute bronchitis
  and asthma is often blurred
 Ruling out bronchospasm/irritants is key to
  diagnosis of bronchitis
 Some believe bronchitis is a variant of
  asthma and is not primarily infectious
 Known allergies, history of asthma or
  primarily exercise-related symptoms
  indicate a likely asthmatic condition
    Acute Asthmatic Bronchitis
 Persistent cough and wheezing following a
  bout with bronchitis
 Cough/bronchospasm persisting up to 3
  months post-infection, with residual
  pulmonary function changes lasting several
 Patients non-asthmatic prior to illness
 May develop in 15-30% of acute bronchitis
Acute Bronchitis and Antibiotics
 NO bacterial etiology for bronchitis has
  been successfully established
 NO convincing evidence for antibiotic
  treatment has emerged
 Prospective studies have shown some
  symptomatic response to antibiotics
 Doxycycline is endorsed as empiric therapy
  for acute bronchitis
    Acute Bronchitis and Antibiotics
   New, resistant, strains of bacteria warrant caution in
    prescription of antibiotics
   Antibiotic therapy should be limited to those with
    clinically severe cases
   Many consider bronchitis an inflammatory process,
    not an infectious one
   Cough may be marker for immune reaction to
    inflammation, foreign bodies, bacteria, chemicals, or
   Trials of erythromycin vs. albuterol in treatments
    revealed albuterol was more effective in patient
    Special Considerations for
 Athletes require maximal pulmonary
  function for peak performance and thus may
  suffer greater consequences from bronchitis
  than the non-athlete
 Peak flow measurements may be used as
  objective measure of pulmonary capacity
  and aid in determining return to
       Special Considerations for
   Return to activity should be gradual and less
    intense while in recovery
   Excess stress may promote relapse or development
    of a secondary condition
   Rapid air flow is important within physical
    activity, but is essential in several known asthma
   Athletes recovering from bronchitis will be
    predisposed to irritable bronchospasm
     Treatment Considerations for
   Athletes will usually recover with symptomatic
   Antibiotic treatment is appropriate for severe
    infections or those whose symptoms have not
    abated in 7-10 days
   Erythromycin, tetracycline, amoxicillin are all first
    line agents
   If at key point in season, empiric treatment with
    antibiotics is preferable to waiting
    Treatment Considerations for

 Return to activity requires athletes be fever-
  free and non-myalgic
 Rule: Two easy training days per every day
  missed with acute illness and temp >100.4º F
 Bronchodilator therapy may be necessary on a
  case by case basis
 Anti-inflammatory asthma meds can be used
  for bronchitis symptoms ongoing
              Pneumonia in Athletes
   Lower respiratory infection
    characterized by interstitial or
    alveolar infiltrates
   Fever, tachypnea, cough, rales,
    rhonchi or signs of
    consolidation on lung
   Chest radiographs demonstrate
    new infiltration in one or more
    areas in the lung
   Differential diagnosis is very
    difficult and diverse
 Elevated WBC
 Radiographs showing air
  bronchograms or lobar
 Productive cough, elevated
  respiration rate and
  temperature over 100 º F
 Localized rales, decreased
  breath sounds with no
  viral/asthmatic history
       ? Complicated Pneumonia

   Respiratory rate          Temp<35 º C (95 º F) or
     30/min                   >40 º C (104 º F)
   Diastolic BP 60          Confusion/dec level
    mmHG                       consciousness
   Systolic BP 90 mmHg      Multilobar involvement
   Pulse 125/min             (X-ray)
                              Presence of cavity or
                               pleural effusion (X-ray)
         Pneumonia and Athletes
   Same bacteria that cause acute bronchitis are
    responsible for pneumonia's
   Clinical presentations help to distinguish etiologic
    – Sudden onset of temperature, single episode of shaking
      chill --- streptococcus pneumoniae
    – Dry cough, insidious onset over 2-3 weeks and diarrhea
      --- mycoplasma pneumonia
   Athletes usually develop community acquired or
    atypical pneumonia's
      Pneumonia and Athletes
    Treatment/Return to Activity
 Rapid return to activity should not be focus,
  rather focus should be complete resolution
  of the infection
 Premature return risks:
    – Persistent infection
    – abscess
    – empyema
       Pneumonia and Athletes
     Treatment/Return to Activity
   Appropriate antibiotic treatment shows dramatic
    improvement in symptoms within 72 hours.
    Failure to do so warrants re-examination
   Radiographs do not return to normal as quickly,
    possibly taking 6 weeks to completely clear
   Symptoms vary with severity of infection and
    pathogenic organism
   Approx. 1-2 reduced training days for each day of
    acute infection
       Pneumonia and Athletes
     Treatment/Return to Activity
   Pneumococcal pneumonia resolves more
    gradually, requiring 4-6 weeks for resolution
   Even healthy subjects may take up to 3 months for
    full recovery of pulmonary status
   Training may resume prior to complete clearing of
    chest radiographs with near-normal pulmonary
    function tests
   HR response to exercise and perceived exertion
    measures can guide workout intensity
           Pneumonia and Athletes
            Treatment/Return to Activity
   Doxycycline
    – Increased sun sensitivity
    – GI side-effects
   Azithromycin
    – Fewer GI worries than erythromycin
    – No increased sun sensitivity
    – Prolonged half-life, extended bioavailability
   Quinolones
    – Contraindicated in young athletes with open epiphyses (may
      damage cartilage)
   Medications:
    – Levaquin, Avelox, Cipro
        Pneumonia and Athletes

   Objective testing of athletes with bronchitis
    can determine when to return to activity
    – Treated with bronchodilators, NSAIDs
   Pneumonia's usually prevent activity for a
    min. of 2 weeks
    – Treated with antibiotics
    – Athletes treated as outpatients
           Thank you…..

May your bunkers be filled with saves…..

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