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Volume 59, Issue 13 April 7, 2011
THE IMPAIRED AIRWAY: GUIDELINES ON MANAGEMENT
From the Interstate Postgraduate Medical Association of North America’s 2010 Primary Care Update
Mark S. Regan, MD, Associate Professor of Medicine, University of Wisconsin School of Medicine and Public Health, Madison
Asthma control: after initiating therapy, follow patients ev- Management of patient on controller medication: reassess
ery 2 to 6 wk; once stable, follow every 3 mo (consider at each appointment; determine whether asthma well con-
stepping down therapy); domains — 1) reducing impair- trolled, not well controlled, or poorly controlled (assessed
ment; prevent daily symptoms; reduce use of short-acting via domains or validated questionnaires); patient can have
-agonist; maintain lung function, normal activity levels, well-controlled asthma and 0 to 1 exacerbations per year (if
and patient satisfaction with care; 2) reducing risk for loss >1/yr, classify as persistent asthma on initial evaluation, or
of lung function and recurrence of exacerbations; minimize asthma not well controlled or poorly controlled on follow-
incidence of adverse effects; day-to-day function of patient up); annual or biannual assessment for progressive loss of
does not correlate well with risk for exacerbation lung function and treatment-related adverse effects recom-
Principles of management: anti-inflammatory controller mended; frequent reassessment important for patients with
medication best for inflammatory asthma; patient-clinician asthma not well controlled or poorly controlled
partnership essential; avoidance of allergens important in Management of moderate persistent asthma: educate pa-
atopic asthma; all patients must avoid irritants; control co- tient about self-management of asthma; use action plan;
morbid conditions (eg, obesity, obstructive sleep apnea, add medium-dose IC for daily use, or low-dose IC with
gastroesophageal reflux disease [GERD]); written action LABA or leukotriene receptor antagonist; follow up in 4
plan can be based on symptoms or peak flow; consider re- wk; if nocturnal symptoms resolve, use of rescue inhaler
ferral to asthma specialist therapy decreases, and spirometry normal, continue current
2007 National Asthma Education and Prevention Pro- therapy and reassess in 3 mo
gram guidelines: updates — separate recommendations in Chronic Obstructive Pulmonary Disease (COPD)
place for patients 12 yr of age; recommendations about
Initial clinical assessment: based on forced expiratory vol-
initiating therapy separate from recommendations about
ume in 1 sec (FEV1; does not correlate particularly well
adjusting therapy; impairment based on quality of life
with health-related QOL and functional capacity); tobacco
(QOL) and functional capacity; response to medication smokers with chronic productive cough require further
may differ between domains of asthma control; in patients evaluation; determine whether mild, moderate, severe, or
not controlled with low-dose inhaled corticosteroid (IC), very severe based on FEV1; severe asthma with CO2 reten-
consider increasing dose or adding adjunctive treatment tion classified as very severe
(eg, long-acting -agonist [LABA]); omalizumab (anti-IgE Patient education: stages I and II — educate about nature of
antibody) available; management of special situations in- COPD (eg, loss of lung function over time), use of inhalers,
cludes response to therapy based on ethnicity recognizing acute exacerbations, and strategies for mini-
Initial assessment of patient not on controller therapy: deter- mizing dyspnea; cessation of tobacco smoking shown to af-
mine whether asthma intermittent (symptoms include night- fect loss of lung function; stages III and IV — inform about
time awakenings, use of -agonist, interference with normal potential complications (eg, chronic respiratory failure, os-
activity) or persistent (mild, moderate, or severe); patient who teoporosis); discuss O2 therapy (check baseline arterial
has nighttime awakenings 3 to 4 times per month but all other blood gases [ABG] and assess for hypoxemia and CO2 re-
symptoms within intermittent level of severity classified as tention); for patients >65 yr of age, begin discussing ad-
having mild persistent asthma; short-acting -agonist (as vance directives and end-of-life decisions
needed) preferred therapy for intermittent asthma; patients Management of stable disease: use of continuous bronchodila-
with persistent asthma require daily controller medication; IC tion for airflow obstruction reasonable; LABAs or anticholin-
basis of therapy; systemic corticosteroid not added until severe ergics preferred over shorter-acting agents due to more
persistent asthma or poor control on follow-up; use short burst favorable side effect profile, more consistent bronchodilation
of oral corticosteroid and consider omalizumab in atopic over 24 hr, improved health status, and fewer exacerbations
asthma; exacerbations — if 2/yr, classify as persistent asthma Medications: LABAs — meta-analysis found patients treated
(therapy based on symptoms and lung function) with salmeterol less likely to suffer moderate to severe exacer-
Educational Objectives Faculty Disclosure
The goal of this program is to improve management of airway In adherence to ACCME Standards for Commercial Support,
disorders and chronic cough. After hearing and assimilating Audio-Digest requires all faculty and members of the planning
this program, the clinician will be better able to: committee to disclose relevant financial relationships within
1. Initiate therapy for asthma based on severity. the past 12 months that might create any personal conflicts of
2. Monitor and adjust asthma therapy based on control of interest. Any identified conflicts were resolved to ensure that
symptoms and/or peak flow variation. this educational activity promotes quality in health care and
3. Select appropriate agents for the treatment of chronic not a proprietary business or commercial interest. For this pro-
obstructive pulmonary disease. gram, Dr. Regan and the planning committee reported nothing
to disclose.
4. Use directed testing and empiric therapy to identify
causes of chronic cough.
5. Optimize therapy before ruling out possible contribu-
tors to chronic cough.
AUDIO-DIGEST FAMILY PRACTICE 59:13
bations, compared to patients treated with placebo (absolute chronic productive cough usually associated with tobacco
difference, 5%); ICs — not well established for use in stage I smoking; determine whether patient meets criteria for
or stage II COPD; not shown to alter decline in FEV1 or natu- chronic bronchitis (eg, productive cough lasting 3 mo for 2
ral history of disease; effective in reducing rate of exacerba- consecutive years); assess for COPD; cough usually re-
tions in patients with more severe disease; appear to be solves in 4 wk after smoking cessation; in travelers, con-
associated with fewer hospitalizations and lower mortality; sider parenchymal disease due to tuberculosis (TB) or
larger trials suggest risk for pneumonia, but that patients with endobronchial TB (rare); systemic symptoms uncommon
very severe disease and frequent (2/yr) exacerbations may be Initial management: chest x-ray; patient history and physical
candidates for use; tiotropium — causes prolonged blockade examination typically unremarkable; 40% of patients have
of M3 muscarinic receptors; half-life 3 days; clinical trials multiple causes; combination of directed testing and empiric
consistently show improvements in clinically relevant patient- approach to treatment most efficient and cost-effective; if pa-
centered outcomes, relative to placebo; “fares well” against tient has no symptoms other than cough, begin empiric ther-
salmeterol, but differences in clinically relevant outcomes un- apy for upper airway cough syndrome (UACS; eg, chronic
clear; theophylline — may be helpful to patients who do not nasopharyngitis, chronic sinusitis, chronic postnasal drip); if
respond to LABAs and ICs (ie, patients with severe disease); no response to treatment of UACS in 2 to 4 wk, evaluate for
target level low (<10 mg/dL); interacts with corticosteroids at cough variant asthma with baseline spirometry (usually nor-
gene transcription level; in subset of patients, small changes mal), bronchodilator reversibility (if evidence of obstruction),
seen in dyspnea rating, exercise capacity, lung mechanics, and and/or bronchial provocation challenge testing; if options not
respiratory muscle strength; concern for potential drug interac- readily available, empiric treatment with bronchodilator and
tions with, eg, macrolide antibiotics IC reasonable; consider nonasthmatic eosinophilic bronchitis
Current guidelines: mild symptomatic COPD — acceptable (NAEB; eosinophil infiltration; not manifested by symptoms
to use short-acting -agonist as needed; moderate or severe other than cough; bronchial challenge testing negative); diag-
COPD — add long-acting bronchodilator (based on symp- nose specifically rather than by empiric treatment (look for
toms); use IC in patients with severe or very severe disease sputum eosinophils); GERD requires longest duration (8 wk)
who have 2 exacerbations per year; consider long-term O2 of empiric therapy before identification as cause of cough
therapy in all patients with severe or very severe disease Initial treatments: UACS — diagnostic trial of first-genera-
(based on ABG); consider lung volume reduction surgery tion antihistamine with or without decongestant (older pa-
or lung transplantation in patients with very severe disease tients may have difficulty tolerating due to somnolence);
Acute exacerbations: symptoms — increased shortness of consider using intranasal steroid preceded by saline rinse
breath; increased sputum volume and purulence; acute con- and first-generation antihistamine; cough variant asthma —
fusion; diagnosis — chest x-ray in patients who present to IC or bronchodilator (short- or long-acting); leukotriene re-
emergency department or hospital (20% have abnormali- ceptor antagonist (eg, montelukast [Singulair] or zafirlukast
ties that alter management); spirometry not recommended; [Accolate]) can be added if response slow or partial; when
ABG assessment; sputum samples have limited value; em- response partial, consider giving short burst of systemic
piric therapy effective; purulent sputum suggests need for steroid; NAEB — ICs; consider giving short burst of sys-
antibiotic therapy (obtain samples from patients requiring temic steroids when specific diagnostic tests unavailable;
hospitalization); check brain natriuretic peptide (patients GERD — moderate dosing of proton pump inhibitor (PPI;
often have cardiac comorbidities) eg, 40 mg of omeprazole once daily) combined with diet
Outpatient steroid use: data about use of systemic steroids lim- and lifestyle changes (eg, elevation of head of bed by 30º);
ited, but more rapid improvement in lung function and hypox- nonacidic reflux can perpetuate cough
emia and decrease in relapse and treatment failure suggested; Further work-up: current guidelines suggest empiric approach
patients with dyspnea (particularly those with severe or very se- based on sensitivity and specificity of 24-hr esophageal pH
vere disease) candidates for prednisone (burst and taper); 30 to monitoring; consider swallow evaluation (particularly in older
40 mg/day for 7 to 10 days adequate; consider risks of frequent population); assess for esophageal dysmotility with barium
short courses (eg, osteoporosis); role of ICs not well defined in esophagraphy or esophageal manometry; multichannel intralu-
acute exacerbations; use same dosing and duration of therapy minal impedance testing helps tease out nonacidic GERD; in
for hospitalized patients (14 days); all hospitalized patients patients with partial response to treatment of UACS, consider
need prednisone (burst and taper) imaging of sinuses (unclear whether computed tomography
Antibiotics: 80% of exacerbations due to infections (50% due [CT)] better than plain imaging); additional investigations—
to bacterial infection); important in patients with severe exacer- high-resolution CT to look for interstitial lung disease or airway
bations who have more severe underlying disease; treatment disease not apparent on plain chest imaging; bronchoscopy to
based on development of purulent sputum; color of sputum sen- evaluate for endobronchial lesion that may not be apparent on
sitive indicator of bacterial infection, but relatively nonspecific chest imaging or high-resolution CT; echocardiography (rarely,
pericardial disease can cause cough); complete otolaryngologic
Chronic Cough
examination to rule out otic disease; assess environmental expo-
Classification: acute — duration <3 wk; subacute — 3 to 8 sure to allergens
wk; chronic — >8 wk; often multiple causes; characteristics General considerations: optimize therapy for each diagnosis
(eg, productive, nonproductive) and medical history often before ruling out as contributing etiology; check compliance
not helpful in identifying etiology with therapy; due to possibility of multiple etiologies, main-
Patient history: 15% of patients with history of angioten- tain all partially effective therapies
sin-converting enzyme (ACE) inhibitor use have problems Management: UACS — intranasal antihistamines or anticholin-
with chronic nonproductive cough; onset of cough usually ergics; expect improvement in cough within short time
early but can be delayed; ACE inhibitor should be stopped (marked improvement or resolution may take longer); cough
or patient should be switched to other agent (eg, angioten- variant asthma — spirometry typically normal with no acute
sin-receptor blocker); median duration of cough, 26 days; bronchodilator response; negative predictive value of bron-
AUDIO-DIGEST FAMILY PRACTICE 59:13
chial provocation challenge testing 100% (positive predic- of long-term therapy (dose- and duration-dependent) include
tive value 60%-85%); patient can have persistent bronchial increased risk for community-acquired pneumonia, calcium
hyperreactivity with subacute cough and post-viral upper re- malabsorption and risk for hip fracture, vitamin B12 malab-
spiratory infection or lower respiratory infection; if test posi- sorption, community-acquired Clostridium difficile infection,
tive, begin trial of IC and long-acting bronchodilator; consider and atrophic gastritis
adding leukotriene receptor antagonist if response slow or in- Unexplained cough: after high-resolution CT and no response
complete; short course of prednisone to rule out diagnosis of to treatment, consider bronchoscopy; possible causes include
cough variant asthma or NEAB reasonable (rarely required); nonacid reflux disease, swallowing disorder (particularly in
NAEB — can be ruled out by absence of sputum eosinophils; older patients), congestive heart failure, otic disease, or
response to IC expected within 4 wk; natural history vari- “habit” or psychogenic cough (rare); etiology identified in
able; 33% of patients asymptomatic at 1 yr; 10% to 15% de- 92% of patients
velop other symptoms that characterize asthma within 1 yr; Questions and answers: normal pre- and postbronchodilator
other subset remains stable with only cough; GERD — if no spirometry — does not rule out asthma; additional testing (ie,
improvement after 2 mo of empirical treatment with moderate bronchial challenge testing) to evaluate for asthma, or empiric
doses of PPI and lifestyle modifications, consider 24-hr therapeutic trial required; man 40 yr of age with cough for 1
esophageal pH monitoring; with partial response, consider yr and globus sensation with intermittent hoarse voice —
adding prokinetic agent (risk for side effects high, particularly associated symptoms suggest UACS or GERD; treat patient
in older population); if no response to addition of prokinetic empirically for UACS, then work up as needed
agent, proceed to esophageal pH monitoring; adverse effects
Acknowledgments
Dr. Regan spoke in Tampa, FL, at 2010 Primary Care Update: Improving Patient Care, presented October 24-26, 2010, by Interstate Post-
graduate Medical Association. For information about next year’s meeting, visit http://www.ipmameded.org/. The Audio-Digest Founda-
tion thanks Dr. Regan and the Interstate Postgraduate Medical Association for their cooperation in the production of this program.
Suggested Reading intranasal antihistamines in the treatment of allergic rhinitis. Ann
Allergy Asthma Immunol. 2011 Feb;106(2 Suppl):S6-S11; Na-
Birring SS: Controversies in the evaluation and management of
tional Asthma Education and Prevention Program: Expert
chronic cough. Am J Respir Crit Care Med. 2010 Dec 10. [Epub
Panel Report 3 (EPR-3): Guidelines for the Diagnosis and Man-
ahead of print]; Bousquet J et al: Persistency of response to agement of Asthma–Summary Report 2007. J Allergy Clin Im-
omalizumab therapy in severe allergic (IgE-mediated) asthma. munol. 2007 Nov;120(5 Suppl):S94-138; Pratter MR et al: An
Allergy. 2011 Jan 21. [Epub ahead of print]; Brightling CE: empiric integrative approach to the management of cough:
Chronic cough due to nonasthmatic eosinophilic bronchitis: ACCP evidence-based clinical practice guidelines. Chest. 2006
ACCP evidence-based clinical practice guidelines. Chest. 2006 Jan;129(1 Suppl):222S-231S; Pratter MR: Unexplained (idio-
Jan;129(1 Suppl):116S-121S; Brown KK: Chronic cough due to pathic) cough: ACCP evidence-based clinical practice guide-
chronic interstitial pulmonary diseases: ACCP evidence-based lines. Chest. 2006 Jan;129(1 Suppl):220S-221S; Pratter MR:
clinical practice guidelines. Chest. 2006 Jan;129(1 Suppl):180S- Overview of common causes of chronic cough: ACCP evidence-
185S; D'Urzo A, Jugovic P: Chronic cough. Three most com- based clinical practice guidelines. Chest. 2006 Jan;129(1
mon causes. Can Fam Physician. 2002 Aug;48:1311-6; Dono- Suppl):59S-62S; Sethi S, Cote C: Bronchodilator Combination
hue JF, Jones PW: Changing patterns in long-acting Therapy for COPD. Curr Clin Pharmacol. 2011 Jan 11. [Epub
bronchodilator trials in chronic obstructive pulmonary disease. ahead of print]; Wechsler ME: Managing asthma in primary
Int J Chron Obstruct Pulmon Dis. 2011 Jan 7;6:35-45; Irwin care: putting new guideline recommendations into context. Mayo
RS: Chronic cough due to gastroesophageal reflux disease: Clin Proc. 2009 Aug;84(8):707-17.
ACCP evidence-based clinical practice guidelines. Chest. 2006
Jan;129(1 Suppl):80S-94S; Kaliner MA et al: The efficacy of
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AUDIO-DIGEST FAMILY PRACTICE 59:13
THE IMPAIRED AIRWAY: GUIDELINES ON MANAGEMENT
To test online, go to www.audiodigest.org and sign in to online services.
To submit a test form by mail or fax, complete Pretest section before listening and Posttest section after listening.
1. Which of the following is the preferred therapy for intermittent asthma?
(A) Systemic corticosteroid (C) Omalizumab
(B) Short-acting -agonist as needed (D) Long-acting bronchodilator
2. Which of the following is(are) recommended for the management of moderate persistent asthma?
(A) Educating patient about self-management
(B) Medium-dose inhaled corticosteroid (IC) for daily use
(C) Low-dose IC with long-acting -agonist (LABA)
(D) All the above
3. In early stages of chronic obstructive pulmonary disease (COPD), which of the following has been shown to affect loss
of lung function?
(A) Weight loss
(B) Increased physical activity
(C) Smoking cessation
(D) Controlling gastroesophageal reflux disease (GERD)
4. ICs are effective in:
(A) Altering decline in forced expiratory volume in 1 sec
(B) Reducing rate of exacerbations in patients with more severe COPD
(C) Reducing risk for pneumonia
(D) Stages I and II COPD only
5. Choose the correct statement about tiotropium.
(A) Causes prolonged blockade of M3 muscarinic receptors
(B) Has half-life of 7 days
(C) Side effect profile significantly better than salmeterol
(D) Contraindicated in patients on macrolide antibiotics
6. Theophylline may be most helpful in which of the following groups of COPD patients?
(A) Patients who do not respond to LABAs and ICs (C) Patients on macrolide antibiotics
(B) Patients with mild COPD (D) Older patients
7. What is the initial treatment of upper airway cough syndrome when it is the suspected etiology of chronic cough?
(A) IC
(B) Bronchodilator
(C) Leukotriene receptor antagonist
(D) First-generation antihistamine with or without decongestant
For Questions 8 to 10, match the etiology of chronic cough in Column I with its description in Column II.
Column I Column II
8. Cough variant asthma (A) Requires 8 wk of empiric therapy to be identified as
cause of chronic cough; patients should be advised
about lifestyle modifications
9. Nonasthmatic eosinophilic bronchitis (B) Not manifested by symptoms other than cough;
bronchial challenge testing negative; response to IC
expected within 4 wk
10. GERD
(C) Evaluated by baseline spirometry or bronchial
challenge testing; initially treated with IC or
bronchodilator
(D) Most often diagnosed by bronchoscopy; cause of
chronic cough in 50% of patients
Answers to Audio-Digest Family Practice Volume 59, Issue 11: 1-D, 2-D, 3-B, 4-A, 5-B, 6-C, 7-B, 8-B, 9-A, 10-C
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