Chronic Cough. Abhishek Kumar, MD, MPH Pulmonary and Critical Care Mercy Medical Center, Cedar Rapids, IA

Transcription

1 Chronic Cough Abhishek Kumar, MD, MPH Pulmonary and Critical Care Mercy Medical Center, Cedar Rapids, IA

2 What we shall discuss? Cough anatomy and pathophysiology Common etiologies Work-up Role of spirometry/pulmonary function test Treatment options When to refer

3 Definition Cough is an protective mechanism that ensures the removal of mucus, noxious substances, and infectious organisms from the larynx, trachea, and large bronchi. Cough is an explosive expiration that provides a normal protective mechanism for clearing the tracheobronchial tree of secretions and foreign material.

4 Why talk about cough? Most common reason to consult providers Antitussive drug sales in USA: >$4billion/year Chronic cough (>8wk): 12% population 10-38% of outpatients referrals

5 IMPACT OF COUGH Does your cough disturb or worry your partner, family or friends? Does your cough affect your quality of life? Not at all, 5% Never, 8% Severely, 22% Yes, 61% Sometimes, 32% A little, 40% Moderately, 34%

6 Anatomy C-fiber nociceptors: terminals in and around the mucosa surface of the airways; sensitive to a wide variety of inhaled or locally produced chemical mediators, which may either activate or sensitize nociceptor nerve endings. Mechanically sensitive cough receptors : positioned beneath the epithelium in the large airways; relatively insensitive to most chemical mediators (with the exception of low ph) but are exquisitely sensitive to punctate stimuli delivered to the mucosal surface (for example, inhaled particulate matter).

7 Anatomy Peripheral Mechanism of Cough

8 Description A dual-sensory neuron model subserving cough. Extensive studies in animals and humans support the concept that at least two subtypes of primary sensory neurons can induce coughing when stimulated. C-fiber nociceptors, which have their terminals in and around the mucosa surface of the airways, are sensitive to a wide variety of inhaled or locally produced chemical mediators, which may either activate or sensitize nociceptor nerve endings. Mechanically sensitive cough receptors are positioned beneath the epithelium in the large airways and are relatively insensitive to most chemical mediators (with the exception of low ph) but are exquisitely sensitive to punctate stimuli delivered to the mucosal surface (for example, inhaled particulate matter). A number of peripherally acting compounds that block nociceptor and or mechanoreceptor activation to reduce coughing are listed in the gray box. TRPA1 = transient receptor potential A1; TRPV1 = transient receptor potential vanilloid 1.

9 Airway Afferent Nerves C-fibers (<2 m/s) Unmyelinated, hence slower Widdicombe cough receptors (5 m/s) Myelinated, hence faster Pulmonary stretch receptors ( 15 m/s) Both rapidly adapting receptors (RARs) and slowly adapting receptors (SARs) are activated by sustained lung inflation RARs are active primarily during the dynamic phase of lung inflation SARs continue firing throughout the distension

10 Extrapulmonary Modulation of Cough Cough Evoked From the Ear (Arnold Reflex) Nasal Afferent Nerve Regulation of the Cough Reflex Cough Initiated From the Pharynx Cough Initiated From the Esophagus

11 Central Mechanisms Regulating Cough

12 Description Airway sensory neurons project to the brainstem, where they terminate predominately in the nts. Projections from the nts can reflexively induce coughing by modifying activity of the respiratory CPG, a collection of neurons that generates respiratory rhythm in the VRG of the brainstem. Output from the CPG via MNs provides the drive to respiratory muscles needed to elicit the cough motor pattern. Superimposed on this reflex pathway is a complex higher brain network that also receives inputs from the nts in the brainstem. Higher brain processing gives rise to respiratory sensations and emotions associated with airway irritation as well as enabling a higher level of motor control over the basic reflexive cough pathways. Centrally acting antitussive agents likely affect both brainstem and higher brain processes to modify coughing. CPG = central pattern generator; GABA = gammaaminobutyric acid; MN = motor neuron; NMDA = N-methyl-D-aspartate; nts = nucleus tractus solitarius; VRG = ventral respiratory group.

13 Classification Acute cough (<3 weeks) Is most often due to upper respiratory infection (common cold, acute bacterial sinusitis, and pertussis), serious disorders, such as pneumonia, pulmonary embolus, and congestive heart failure, can also present in this fashion. Sub acute cough (between 3 and 8 weeks) Is commonly post-infectious, resulting from persistent airway inflammation and/or postnasal drip following viral infection, pertussis, or infection with Mycoplasma or Chlamydia. Chronic cough (>8 weeks) In a smoker raises the possibilities of asthma, COPD or bronchogenic carcinoma, Eosinophilic Bronchitis, Esophageal Disease, Post Nasal Drip, ACEI, Smoking.

14 Etiology An exogenous source (smoke, dust, fumes, foreign bodies) An endogenous origin (upper airway secretions, gastric contents). Any disorder resulting in inflammation, constriction, infiltration, or compression of airways can be associated with cough. Asthma is a common cause of cough. In a nonsmoker the most common causes of chronic cough are postnasal drip, asthma, and gastroesophageal reflux.

15 Common Causes of Cough Postnasal drip (38-87%) Asthma (14-43%) GERD (10-40%) Chronic Bronchitis (0-12%) More than one cause (24-72%)

16 Chronic cough (> 8 weeks) Chronic Cough of Post-Nasal Drip PNDS is a symptom complex without objective findings. The diagnosis is by a history of the sensation of something dripping into the throat, frequent throat clearing, nasal congestion/discharge. There is wide cultural diversity in reporting such symptoms by patients with colds. In the USA, 50% with colds reported these symptoms, in the UK less than 25%, and in Latin America and India almost none. Cough may be the only manifestation of PNDS. There may be no symptoms of the drip. PNDS is often seen due to Allergic Rhinitis, Non-Allergic Rhinitis, Vasomotor Rhinitis and Chronic Bacterial Sinusitis.

17 Asthma Chronic cough (> 8 weeks) Asthma is a chronic inflammatory disease of airways characterized by increased responsiveness of the tracheobronchial tree to many stimuli. Physiologically, there is a reversible narrowing of bronchi and clinically there are paroxysms of wheezing, cough, and dyspnea. If airway obstruction exists, reversibility is shown by > 12% and 200 ml in FEV1 after two puffs of a β2- adrenergic agonist.

18 Chronic cough (> 8 weeks) Gastro-esophageal reflux disease (GERD) Two main mechanisms of cough in GERD: Micro or macro-aspiration of esophageal contents into the tracheobronchial tree. Acid in the distal esophagus stimulating a vagally mediated esophageal-tracheobronchial cough reflex (GI symptoms may be absent).

19 Less Common Causes of Cough Bronchiectasis (0-5%) ACE inhibitor Rx Post-infectious Occult aspiration Lung Cancer Occult CHF Interstitial Pulmonary Fibrosis Occult infection (eg atypical mycobacteria) Foreign body

20 Less Common Causes of Cough Industrial bronchitis Nasal polyps Problems with: Auditory canal Larynx Diaphragm Pleura Pericardium Esophagus Psychogenic

21 Diagnosis - General Approach History Physical examination Chest radiography Pulmonary function testing Sputum gross and microscopic examination High-resolution computed tomography (HRCT) Fiberoptic bronchoscopy

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23 CHEST 2006; 129:1S 23S

24 Simple, office-based Spirometry Measures flow, volumes Volume vs. Time Can determine: Forced expiratory volume in one second (FEV 1 ) Forced vital capacity (FVC) FEV 1 /FVC Forced expiratory flow 25%-75% (FEF )

25 Who should receive spirometry? Early diagnosis relies on the recognition of the clinical features: - Persistent cough - Chronic sputum production - Breathlessness on exertion - Reduction in activity (often attributed to natural aging) About 20% of COPD patients identified in NHANES study with obstruction never smoked - Only 1/5 were explained by asthma

26 Acceptability Criteria 1. Good start of test : sharp take off 2. Meet end-of-test criteria 3. Free from artifacts: Cough or glottis closure during the first second of exhalation Variable effort, submaximal effort Leak Obstructed mouthpiece Have a satisfactory exhalation >6 s

27 Reproducibility Criteria After 3 acceptable spirograms have been obtained: Are the two largest FVC within 150ml of each other? Are the two largest FEV1 within 150ml of each other? If both of these criteria are met, the test session may be concluded. If both of these criteria are not met, continue testing until both of the criteria are met with analysis of additional acceptable spirograms; OR a total of eight tests have been performed

28 Spirometry Patterns

29 Flow-volume loops

30 Obstructive Pattern Decreased FEV 1 Decreased FVC Decreased FEV 1 /FVC <70% predicted (GOLD) FEV 1 used to follow severity in COPD

31 Obstructive Pattern Evaluation Spirometry FEV 1, FVC: FEV 1 /FVC: FV Loop Lung Volumes TLC, RV: decreased decreased (<70% predicted) scooped increased Bronchodilator responsiveness

32 Obstructive Diseases Differentials Asthma COPD chronic bronchitis emphysema Bronchiectasis Bronchiolitis Upper airway obstruction

33 Restrictive Pattern Decreased FEV 1 Decreased FVC FEV 1 /FVC normal or increased

34 Restrictive Pattern Evaluation Spirometry FVC, FEV 1 : FEV 1 /FVC: FV Loop decreased normal or increased witch s hat DLCO Lung Volumes TLC, RV: decreased decreased Muscle pressures may be important

35 Restrictive Diseases Differentials Pleural Parenchymal Chest wall Neuromuscular

36 Bronchodilator Response Degree to which FEV 1 improves with inhaled bronchodilator Documents reversible airflow obstruction Significant response if: - FEV 1 increases by 12% and >200ml Request if obstructive pattern on spirometry

37 Other Measures of Full PFT Lung volumes DLCO

38 Grading Severity of Obstruction ATS guidelines FEV1/FVC < predicted AND FEV1 > 100% of predicted normal varient FEV1/FVC < predicted AND FEV1 < 100% > 70% of predicted mild obstruction FEV1/FVC < predicted AND FEV1 < 70% > 60% of predicted moderate obstruction FEV1/FVC < predicted AND FEV1 < 60% > 50% of predicted moderately severe obstruction FEV1/FVC < predicted AND FEV1 < 50% 35% of predicted severe obstruction FEV1/FVC < predicted AND FEV1 < 35% of predicted very severe obstruction

39 Grading Severity of Obstruction GOLD Guidelines Stage I: Mild FEV 1 /FVC < 0.70 FEV 1 > 80% predicted Stage II: Moderate FEV 1 /FVC < % < FEV 1 < 80% predicted Stage III: Severe FEV 1 /FVC < % < FEV 1 < 50% predicted Stage IV: Very Severe FEV 1 /FVC < 0.70 FEV 1 < 30% predicted or FEV 1 < 50% predicted plus chronic respiratory failure

40 Grading Severity of Obstruction Asthma FEV1 80 percent predicted FEV1/FVC normal FEV1 >60 but <80 percent predicted FEV1/FVC reduced 5 percent FEV1 <60 percent predicted FEV1/FVC reduced >5 percent

41 When to refer to a pulmonologist?

42 Thank You!