1. Common and Uncommon Causes of Chronic Cough
Douglas B. Hornick, MD
Professor
Division of Pulmonary, Critical Care, and Occupational Medicine
University of Iowa

2. Objectives Differentiate acute from chronic cough
Review the most common causes as well as uncommon causes of chronic cough
Discuss treatment strategies

3. Great Reference
Irwin RS, et al: Diagnosis & Management of Cough: ACCP Evidence-based Clinical Practice Guidelines.
Chest 2006; 129:1S-292S.

4. How do you define chronic cough?

5. Definitions & Epidemiology
Cough persisting > 3 weeks
Acute = up to 3 weeks
Subacute = 3-8 weeks
Chronic = >8 weeks
2008: Most common symptom among outpatients (>26 million office visits US)
~40% of outpatient pulmonary practice
Cost > $1 billion/yr. (excludes diag. tests & meds)
Cough complications
Intrathoracic pressures 300 mmHg; exp velocity 500 mph
Exhaustion, insomnia, headache, musculoskel pain, dizziness, urinary incontinence, xs persperation
--ACCP: Consensus Statement on Cough. Chest 2006

6. Spectrum of Reasons Patients Seek Medical Care for Cough
Reassurance nothing serious (77%)
Concern that something serious is wrong (72%)
Frequent retching (56%)
Exhaustion (54%)
Others think something wrong (53%)
Embarrassment/self-consciousness (47%)
Difficulty speaking on the phone (39%)
Hoarseness (39%)
--ACCP: Consensus Statement on Cough. Chest 2006

7. Cough Reflex
Each cough occurs through the stimulation of a complex reflex arc. This is initiated by the irritation of cough receptors that exist not only in the epithelium of the upper and lower respiratory tracts, but also in the pericardium, esophagus, diaphragm, and stomach. Chemical receptors sensitive to acid, heat, and capsaicin-like compounds trigger the cough reflex via activation of the type 1 vanilloid (capsaicin) receptor [3-5]. In addition, mechanical cough receptors can be stimulated by triggers such as touch or displacement. Laryngeal and tracheobronchial receptors respond to both mechanical and chemical stimuli.
Impulses from stimulated cough receptors traverse afferent nerves (vagus, glossopharyngeal, trigeminal, or phrenic) to a "cough center" in the medulla, which itself may be under some control by higher cortical centers. Sex-related differences in cough reflex sensitivity explain the observation that women are more likely than men to develop chronic cough [1,6-8]. The cough center generates an efferent signal that travels down the vagus, phrenic, and spinal motor nerves to expiratory musculature to produce the cough.
3. Morice, AH, Geppetti, P. Cough. 5: The type 1 vanilloid receptor: a sensory receptor for cough. Thorax 2004; 59:257.
4. Trevisani, M, Milan, A, Gatti, R, et al. Antitussive activity of iodo-resiniferatoxin in guinea pigs. Thorax 2004; 59:769.
5. Groneberg, DA, Niimi, A, Dinh, QT, et al. Increased expression of transient receptor potential vanilloid-1 in airway nerves of chronic cough. Am J Respir Crit Care Med 2004; 170:1276.
6. Morice, A, Kastelik, JA, Thompson, RH. Gender differences in airway behaviour. Thorax 2000; 55:629.
7. Kastelik, JA, Thompson, RH, Aziz, I, et al. Sex-related differences in cough reflex sensitivity in patients with chronic cough. Am J Respir Crit Care Med 2002; 166:961.
8. Morice, AH, Kastelik, JA. Cough * 1: Chronic cough in adults. Thorax 2003; 58:901.
*Chemical Receptors (type 1 vanilloid): acid, heat, capsaicin-like compounds
Mechanical Receptors: Touch/displacement
Note: sex-related difference in sensitivity…women more likely to develop chronic cough
UTD 2009

8. What are the most common causes of chronic cough?
…after excluding smoker’s cough & ACE inhibiter

9. Common Causes of Chronic Cough
Upper Airway Cough Syndrome (38-87%) (formerly post nasal drip syndrome)
Asthma (14-43%)
GERD (10-40%)
Chronic Bronchitis (0-12%)
More than one cause (24-72%)
--Irwin et al: Chest 1998;114:133S; Irwin et al: ARRD 1990; 141:640;
Irwin et al: ARRD 1981; 123:413; Pratter et al: Ann Int Med 1993; 119:977

10. Upper Airway Cough Syndrome (UACS) Formerly Post Nasal Drip
3/4 studies: UACS most common cause chronic cough
DDx: Allergic, perennial (non)allergic, vasomotor rhinitis, nasopharyngitis, sinusitis, rhinitis medicamentosa, pregnancy, abnl nasal/sinus anatomy
Symptoms: nasal discharge, post nasal drip, frequent throat clearing
May not be apparent to the patient
Exam: cobblestone/secretions in nasopharynx
Response to Rx usually secures diagnosis
Try empiric Rx for UACS before extensive w/up for cause of cough

11. Asthma History includes episodic wheezing and dyspnea
“Cough variant asthma”…no wheezing/dyspnea, only cough, normal spirometry
Other clues from history: atopy, family history of asthma, seasonal, follows URI, worsens with exposure to cold/dry air, fragrances or fumes, exacerbated by -blocker Rx
Bronhoprovocation tests: Good negative predictive value; + test c/w but not diagnostic (false + ~ 33%)
Diagnosis: improvement post therapeutic trial (e.g., -agonist x 1 week)

12. Eosinophilic Bronchitis or Non-Asthmatic EB
Distinct from asthma; no bronchospasm
Recognized 2002; frequency uncertain (European studies 10-15%), probably under diagnosed
Clinical characteristics
Unexplained nonproductive cough
Atopic; normal spirometry & bronchoprovocation tests
(Induced) Sputum eosinophilia & airway inflammation
Bronchial biopsy is diagnostic: Eosinophilic inflammation, but no Mast cells (or BAL w/ lots of Eosinophils)
Treatment: Inhaled steroid
Natural history not certain (N=367; 1 yr f/u):
55% persistent symptoms; 33% asymptomatic
12% develop asthma…
Gibson et al: Thorax 2002
Rytila et al: Eur Respir J 2000

13. Gastroesophageal Reflux (GERD)
Second most common cause of cough in elderly
Up to 40% cases (Mello et al: Arch Int Med 1996; 156:997)
Experimental data: Acid in distal esoph. can mimic cough, blunted by lidocaine or inhaled ipatropium, does not elicit cough in normals
Laryngeal-Pharyngeal Reflux (LPR): consider Oto eval (Clues: throat clearing, hoarseness, globus sensation, VCD)
Empiric 2 week trial with proton pump inhibitor =/more reliable than pH monitor (Ours et al: Am J. Gastroent 1999)
NB: May take >8 wks of PPI Rx Acid suppression may not Rx reflux GERD can contribute to asthma exacerbation

14. Chronic Bronchitis “Smoker’s Cough”
Definition
Most are smokers, but most smokers don’t seek attention for “smoker’s cough”
Sputum clear/white
Change in character
purulent sputum: infection (viral, bacterial)
? Neoplasm

15. Common Causes of Chronic Cough
Upper Airway Cough Syndrome (38-87%)
Asthma (14-43%)
GERD (10-40%)
Chronic Bronchitis (0-12%)
More than one cause (24-72%)
Hickam’s Dictum vs. Occum’s Razor
A patient may have as many diagnoses as he darn well pleases!
--Irwin et al: Chest 1998;114:133S; Irwin et al: ARRD 1990; 141:640;
Irwin et al: ARRD 1981; 123:413; Pratter et al: Ann Int Med 1993; 119:977

16. Can you name some of the uncommon causes of chronic cough?

17. Less Common Causes of Chronic Cough
Bronchiectasis (0-5%)
ACE inhibitor Rx
Post-infectious
Occult aspiration
Lung Cancer
Obstructive Sleep Apnea
Occult CHF
Interstitial Pulmonary Fibrosis
Occult infection (eg, TB, NTM, suppurative bronchitis)
Foreign body
Broncholith
Eosinophilic Bronchitis
Industrial bronchitis
Nasal polyps
Problems with:
Auditory canal
Larynx
Diaphragm
Pleura
Pericardium
Esophagus
Psychogenic
--Irwin et al: Chest 1998;114:133S; Irwin et al: ARRD 1990; 141:640;
Irwin et al: ARRD 1981; 123:413; Pratter et al: Ann Int Med 1993; 119:977

18. Cough & Sleep
Cough suppression during REM & non-REM sleep occurs naturally
“Cough Variant Obstructive Sleep Apnea”…
44% chronic cough pts have OSA
Hx not suggestive of OSA, cough only manifestation
Risk Factors: Female, nocturnal heartburn, rhinitis
Not associated: BMI, Epworth Sleepiness Scale, Dyspnea, snoring
CPAP treatment relieves cough
Chan KK et al. Eur Resp J 2010;35:368-72
Sundar KM et al. Cough 2010;6:2-8

19. Bronchiectasis Repeated/persistent airway inflammation & damage
poor mucous clearance; secretion pooling
dilated bronchi; thickened bronchial wall
chronic infection
Cough with mucopurulent sputum
Chest x-ray insensitive, but may show crowded lung markings, thickened bronchial walls, fluid-filled cystic bronchi, “tram-tracks”, “signet ring”
High resolution chest CT more specific

20. Engagement (Signet) ring:
Thin Section CT (1.5-3 mm)
Normal:
Engagement (Signet) ring:
Other Characteristics
Lack of tapering of bronchi
Clusters = Grape-like appearance
Enlarged bronchi can appear cystic vs. Bullae of emphysema (thinner walls)
Distribution of bronchiectasis suggests Dx
CentralABPA; Upper lobe  CF; Lobar  Post-infectious; obstructive (eg, LN, FB)
Bronchus
Vessel
Bronchus
Vessel

21. Bronchiectasis Differential Diagnosis
Post-infectious (e.g. Pertussis, severe pneumonia, Mycobacterium tuberculosis or avium complex)
Airway obstruction or recurrent aspiration
Cystic Fibrosis (Case report: Dx made at 65)
Immunodeficiency (Agammaglobulinemia)
Esoterica…
Alpha-1-Antitrypsin Deficiency
Inflammatory Disease (eg, Sjogren’s)
Allergic Bronchopulmonary Aspergillosis
Dyskinetic Cilia Syndrome
Diffuse Pan Bronchiolitis
Young’s Syndrome

22. Mnemonic: IA-SPICE Idiopathic Airway Obstruction
Sjogren’s & other inflammatory (RA, IBD)
Post-Infectious (Pertussis, Pneumonia, MAC, Mtb)
Immunodeficiency (Agammaglobulinemia
Cystic Fibrosis
Esoterica
Alpha-1-Antitrypsin Deficiency
Dyskinetic Cilia Syndrome
Allergic Bronchopulmonary Aspergillosis
Diffuse Pan Bronchiolitis
Young’s Syndrome

23. Pulmonary Fascinoma with an Infectious Attitude
77 yo WF, persistent non-productive cough x 4.5 yrs
Nonsmoker, denies S/S of PND, GERD, Asthma
H/O ovarian cancer resection 4.5 years ago
Right middle lobe infiltrate on CXR
Bronchoscopy by local surgeon: Mycobacterium avium complex
Advice: nonpathogen, no treatment
Cough worsening severity over the last 1 year
Intermittent night sweats, temp 99
More fatigue, increased dyspnea, no weight loss
CXR & CT

24. WF. 77 y.o. F

25. What is your working diagnosis? What would you do now?
Case Summary (cont’d)
CXR varies little, going back 4.5 years
1 year ago (another university MD) bronchoscopy:
Biopsy: non-caseating granulomas; AFB
Lavage: Mycobacterium avium complex (MAC)
Advice: nonpathogen, no specific treatment
Failed therapeutic trials: bronchodilators, steroids (oral/inhaled), & H2 blockers
What is your working diagnosis? What would you do now?

26. Page 3, The Rest of the Story
Page 3, The Rest of the Story... Nodular Bronchiectais (Lady Windemere’s Syndrome)
AM Sputa x 3 smear positive AFB; grew MAC
Treated for MAC
Sputa cleared; cough/fatigue/night sweats resolved by 6 mos.
Non-productive cough returned at 9 months; AM sputa remained negative for MAC
W/u revealed GERD; possibly allergic rhinitis
Resolved with proton pump inhibitor & nasal steroid

27. MAC Lung Infections
Majority of NTM respiratory isolates are MAC and are pathogenic in 50% cases
Incidence rising…~8/100,000
Worldwide, most common in temperate regions
Isolated in bedding mat’l, house dust, soil, plants, swimming pools, hospital H2O, natural bodies of H2O
Most infections: rural locations in SE, Atlantic & Pacific coastal regions of US
Reactivity with PPD-B (70%) highest in southeast

28. MAC Skin Test Reactors Distribution
Edwards et al: ARRD 1969

29. MAC Lung Infection— Nodular/Bronchiectasis Form
Persistent cough, dyspnea, malaise, weakness
Symptoms antedate MAC diagnosis (months-years)
Elderly>>young, Non-smoking female >>male w/o pre-existing lung disease
Pathogenesis uncertain
Medically uninitiated women; Lady Windermere’s syndrome implies pathogenesis linked to fastidiousness, habitual cough suppression
Body morphotype: Tall/thin plus increased a/w Pectus excavatum, Scoliosis, Mitral valve prolapse, Joint hypermobility
Undetectable defect in muco-cilliary fxn or mucosal immunity
Linked to gene for multi-drug intolerance
Chronic indolent process (symptoms can spontaneously abate)
MAC Infection is not the disease, but symptom of the disease
Patients die with, rather than from disease (Mortality estimates: 5-20%)
Oscar Wilde’s play 1892…Lady Windemere’s fan

30. Anthropometrics of women w/ N/B NTM Disease
Data from NIH study on Anthropometrics…
Left panel shows schematic depiction of the anthropometrics of the women with pulmonary nontuberculous mycobacterial (PNTM) (n = 60) compared with (right
panel) National Health and Nutrition Examination Survey age-, sex-, and race-matched control subjects. *P <
…Marfan’s question: Because Marfan syndrome is also associated with leanness, increased height, scoliosis, and mitral valve prolapse, we examined body segment ratios and other physical findings that are highly correlated with Marfan syndrome. The frequency of high-arched palate in PNTM was 79%, which is similar to the reported rate of 60–75% in Marfan syndrome (30). However, none of our 63 patients met major criteria for skeletal involvement under the revised (Ghent) diagnostic criteria for Marfan syndrome (31). The mean upper:lower body segment ratio in PNTM infection was 0.99 (vs. <0.86 in Marfan), and the mean armspan:height ratio was 1.00 (vs. >1.05 in Marfan). Only 38% had positive wrist and thumb signs, and only 24% had the benign joint hypermobility syndrome, compared with 85% of patients with Marfan syndrome (32). Therefore, this is a morphologic syndrome distinct from Marfan syndrome.
Kim et al AJRCCM 2008; 178:1066

31. MAC Lung Infection— Nodular/Bronchiectasis Form
Persistent cough, dyspnea, malaise, weakness
Symptoms antedate MAC diagnosis (months-years)
Elderly>>young, Non-smoking female >>male w/o pre-existing lung disease
Pathogenesis uncertain
Medically uninitiated women; Lady Windermere’s syndrome implies pathogenesis linked to fastidiousness, habitual cough suppression
Body morphotype: Tall/thin plus increased a/w Pectus excavatum, Scoliosis, Mitral valve prolapse, Joint hypermobility
Undetectable defect in muco-cilliary fxn or mucosal immunity
Linked to gene for multi-drug intolerance
Chronic indolent process (symptoms can spontaneously abate)
MAC Infection is not the disease, but symptom of the disease
Patients die with, rather than from disease (Mortality estimates: 5-20%)
Oscar Wilde’s play 1892…Lady Windemere’s fan

32. MAC Lung Infection-- Nodular/Bronchiectasis Form (cont’d)
Episodic co-infection by other organisms (P. aeruginosa, Nocardia, rapidly growing mycobacteria)
Chest x-ray: (non-cavitary) infiltrates in middle lobe or lingula…Inadequate to appreciate N/B pattern
High resolution chest CT:
Bronchiectasis (multi-lobe more common)
Large and small (<5 mm) nodules (centrilobular)
Peripheral “tree-in-bud” pattern

33. Location of Infiltrates
Kennedy & Weber: AJRCCM 1994

34. MAC Lung Infection-- Nodular/Bronchiectasis (cont’d)
Episodic co-infection by other organisms (P. aeruginosa, Nocardia, rapidly growing mycobacteria)
Chest x-ray: (non-cavitary) infiltrates in middle lobe or lingula…Inadequate to appreciate N/B pattern
High resolution chest CT:
bronchiectasis (multi-lobe)
Large and small (<5 mm) nodules (centrilobular)
Peripheral “tree-in-bud” pattern

35. General MAC Lung Infection Treatment
Careful patient selection
~50% nonpathogen
ATS/IDSA criteria
Expensive, long duration, intolerance & toxicity (elderly), compliance
Extended spectrum macrolides
Clarithro- > azithromycin
Improved outcomes to ~80% clinical cure (40%)
>90% susceptibility if previously untreated
Continue treatment until culture neg. x 12 months

36. MAC Lung Infection Treatment (cont’d)
Nodular/Bronchiectasis:
Clarithro- 1 gm TIW or Azithro- 500 mg TIW
Ethambutol 25 mg/kg TIW
Rifampin 600 mg TIW
Adjunctive measures: nutrition, chest physiotherapy, surgery
Susceptibility testing unreliable except Clarithro-
Severe disease: Strep or Amikacin; Rifabutin vs Rifampin

37. Nodular Bronchiectasis/MAC (Lady Windemere’s) Take Home Points
Mycobacteria avium complex is an unusual cause of cough in the general clinic
MAC as a pathogen in the “normal host” is frequently not appreciated…Recall Morphotype
CT will show nodular bronchiectasis, tree-in-bud, inflammatory nodules
Symptoms for years before diagnosis common
Specific antibiotic treatment successful in some but not all cases (medication intolerance common)
Some patients may exhibit several causes for cough that require treatment simultaneously.
…Hickam’s Dictum!

38. Post-Infectious Cough
Diagnosis of exclusion
Cough post viral or other URI can persist for 8 weeks
Mycoplasma, Chlamydia, B. pertussis
Proposed mechanisms:
Post nasal discharge
Enhanced sensitivity of airway (exposure of cough afferent nerves in epithelia due to epithelial necrosis)
Airway hyper-responsiveness

39. Return of the 100 day Cough…
No. & Incidence of Pertussis Cases Among Adults (19-64yo)
CDC: MMWR Rec&Rep Dec 15, 2006

40. Post-infectious Cough: Pertussis in Adults
B. pertussis (GNB)…very contagious
Household: % of contacts
School: 50-80% of contacts
Increased incidence (highest among yo)
Immunization effect wanes during 1st 10 yrs post vaccination
Decreasing # adults carrying natural immunity obtained during pre-vaccine era
Clinical characteristics
Incubation period: 1-3 wks
Viral-like initial phase (catarrhal): ~2 weeks (conjunctivitis, rhinorrhea, fever, cough late)
Paroxysmal phase: 3-6 months, Worsening cough (whoop uncommon…post-tussive vomiting)
Note: Protracted cough may be the only symptom, & Many infection can result in no cough (elderly)

41. Pertussis in Adults II Diagnosis Treatment Catarrhal Phase
NP aspirate or polymer swab of NP for culture
PCR costly supplement dx (CDC rec w/ culture)
Acute & convalescent IgG or IgA titers (PT or FHA)
Cough & linkage w/ confirmed case
Treatment Catarrhal Phase
Macrolide (erythro-, azithro-, clarithromycin)
Don’t delay Rx waiting for confirmation tests
Isolation for 5 days from start or Rx
Treatment Paroxysmal Phase:
See Post-infectious cough recommendations
Prevention after exposure
Macrolide Rx same as Treatment dose/duration
Vaccination w/ acellular pertussis vaccine (Tdap)

42. Pertussis in Adults: Vaccination Issues ACIP Recommendations
Tdap: Tetanus, Diphtheria, Acellular Pertussis
Booster Tdap in adolescents, yr
Single Tdap booster for Adults yr recommended
Improve adult coverage for pertussis, but also tetanus & diphtheria.
Single dose replacing Td at q10 year booster
<10 yr interval Td (as short as 2 years)
HCW high risk for exposure (Cost benefit for vaccination program over outbreak control cost)
Health care personnel (HCP) are at risk for being exposed to pertussis in both inpatient (acute and longterm care) and outpatient facilities. Infected personnel can then expose at-risk neonates, children and adults. Numerous nosocomial outbreaks of pertussis have been attributed to HCP exposure and infection, with considerable morbidity and mortality [46]. Investigation and control measures to prevent pertussis after unprotected exposure in such settings are labor intensive and costly.
Tdap vaccination in adult healthcare workers has been shown to be effective in controlling nosocomial outbreaks of pertussis [46,62]. A cost-benefit analysis found that the cost of vaccinating healthcare workers is considerably less than the costs associated with a hospital outbreak [63]. It is estimated that the introduction of a hospital employee vaccination program would result in a median net savings of $95,000; for every dollar spent on the vaccination program, the hospital would save $2.38 on control measures [46].
The ACIP and the Healthcare Infection Control Practices Advisory Committee (HICPAC) recommend that unvaccinated HCPs who have direct patient contact should receive a single Tdap vaccination as soon as feasible; an interval of >two years from the last Td is advised, but the vaccine may be given at shorter intervals. (See "Immunizations for healthcare workers".)
New personnel should be asked if they have recently been vaccinated with Td or Tdap, and vaccinated with Tdap, if appropriate, when they begin employment. Catch-up vaccination should be encouraged for existing personnel. One strategy is to incorporate Tdap vaccination with an annual influenza vaccine campaign, or to use tactics similar to influenza vaccination campaigns if not done together. Some health care facilities might find it necessary to vaccinate using a two-tiered strategy, initially prioritizing HCPs with contact with infants, immunocompromised patients, or other high risk patient groups. HCPs without direct patient contact should receive a single dose of Tdap to replace their next scheduled Td vaccine.
CDC: MMWR Rec&Rep Dec 15, 2006 ACIP 2009

43. ACE Inhibitor 3-20% of patients on ACE Inhibitor Rx
72% recur, if re-administered
Accumulation of bradykinin (normally degraded by ACE)
Note: Angiotensin II receptor antagonists (e.g. losartan) do not cause cough
General features:
Starts ~1 wk after start of Rx (delayed up to 6 months)
Resolves 1-4 d after stopping Rx (can take up to 4 weeks)
Recurs with same or different ACE inhib
Women > men
Incidence no greater in asthmatics
No change in spirometry
Rx = Stop ACE inhib. (Angiotensin II receptor blocker)

44. General Approach UACS, Asthma, and GERD cause 90% chronic cough
If nonsmoker, not on ACE inhibitor, normal or stable CXR, then 99% cases due to above 3 causes
Pratter et al: Antihistamine-decongestant Rx was only Rx needed in 36% & another 50% noted improvement in symptoms.
Guidelines
Recall Hickam’s Dictum!
Hx, Px, CXR, Rx aimed at clues in evaluation
If no clues, start antihistamine-decongestant or nasal steroid
If no improvement, check spirometry/bronchoprovocation; add bronchodilators
If no improvement, 24hr esoph pH monitoring

45. Specific Treatments Upper Airway Cough Syndrome (UACS)
Anti-histamine/decongestant
1st generation sedating anti-histamines more effective
Effect takes ~1 week
Nasal steroids
May take up to 2 weeks for full effect
Add nasal ipratropium if anti-histamine or decong. failing (Vasomotor rhinitis)
Trial monteleukast if allergic rhinitis & above insufficient
Sinusitis
Document with limited sinus CT
Anti-histamine/decong. + abx (bactrim, cefurox) up to 6 wks
Short term nasal decongestant spray

46. Antihistamine and Driving Performance
Randomized, double-blinded, double dummy, N=40 (ages 25-40)
Compared fexofenadine, diphenhydramine, EtOH (0.1%), & placebo, 4 period x-over trial
Results (Driving Simulator):
Driving performance was poorest with diphenhydramine (vs. EtOH or fexofenadine)
Drowsiness self-assessment scores did not predict worse driving performance
Drivers perception of drowsiness on diphenhydramine (50 mg) not a good indicator of when they should not drive
Weiler et al: AIM 2000

47. Specific Treatments Upper Airway Cough Syndrome (UACS)
Anti-histamine/decongestant
1st generation sedating anti-histamines more effective
Effect takes ~1 week
Nasal steroids (and/or nasal antihistamine)
May take up to 2 weeks for full effect
Add nasal ipratropium if anti-histamine or decong. failing (Vasomotor rhinitis)
Trial Monteleukast if allergic rhinitis & above insufficient
Sinusitis
Document with limited sinus CT
Anti-histamine/decong. + abx (bactrim, cefurox) up to 6 wks
Short term nasal decongestant spray

48. Specific Treatments Cough Variant Asthma
Same principles as asthma
Inhaled bronchodilator trial; consider 1-2 week course of Prednisone (diagnostic & therapeutic)
Most require maintenance inhaled steroid
Limited data for leukotriene receptor antagonists
2 weeks prednisone usually sufficient
--Cheriyan et al: Ann All 1994

49. Specific Treatments GERD
Avoidance of reflux-inducing food (e.g., fatty foods, chocolate, EtOH)
Smoking cessation
Avoid snacking
No eating within 3 hrs of lying down for sleep
Elevation of head of bed
H2 antagonist or Proton pump inhibitor (preferred)
Length of time for response may be 3-6 mos.
Refractory cases:
LPR requires high dose PPI
May be d/t dyskinesis (trial metocolpromide)
Rare pt, acid suppressed still cough d/t reflux  surgery
--Irwin et al: ARRD 1990 & Irwin et al: Chest 1993

50. Non-specific Treatments
Post-infectious: nasal steroid or ipratropium MDI (steroid B/T)
Ipratropium MDI
Blocks afferent limb of cough reflex
Alters mucociliary factors  less stimulation of cough receptors
Central acting anti-tussive agents
Codeine 30 mg
Dextramethoraphan, up to 60 mg
Meta analysis (Yancy et al. Chest 2013;144: ) both > placebo; no good comparison studies, no studies examine chronic/refractory cough
Peripherally acting agents
Benzonatate: inhibits stretch receptors (Rx x50yrs)
Guaifenesin: hydrates mucous for expectoration; may suppress hypersensitive cough receptors
Studied but not generally useful when used empirically
Inhaled steroids
Inhaled lidocaine
Refractory Cough or no definable cause can be as common as 40%
Referred to as Cough Hypersensitivity Syndrome…Three possible causes (From Godsobel J All Clin Imm Sept 2012)
Post Viral neuropathy (sensory neuropathy and requires gabapentin, pregabalin, or amitriptyline)
Laryngeal dysfunction w/ chronic cough and throat clearing…oft sense dyspnea and VCD is a factor. Respond to speech Rx
Irritable larynx syndrome. Methacholine induces cough or VCD and Rx aimed at decreasing irritation

51. Summary Differentiate acute from chronic cough
Reviewed the most common causes as well as uncommon causes of chronic cough
Identified treatment strategies