SECTION 3
Respiratory 18.
Practical Approach to Breathlessness Alladi Mohan, D Arun kumar
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19.
Spirometry: As Routine as Measuring Blood Pressure Geoff Chadwick
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20.
Approach to a Patient with Intractable Cough T Geetha
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Practical Approach to Breathlessness
ABSTRACT
Breathlessness is one of the most common presenting symptoms encountered by clinicians. The causes of breathlessness can range from cardiac, pulmonary, anaemia, hysterical/psychogenic, infectious, traumatic, neuromuscular, haematological conditions among others. Dyspnoea has to be measured to assess it adequately. Instruments pertaining to dyspnoea measurement are classified as pertaining to domains of sensory–perceptual experience, affective distress, or symptom/disease impact or burden. Patients presenting with acute dyspnoea should be immediately evaluated and triaging should be done for signs of clinical instability. While evaluating a patient with dyspnoea, the following should be meticulously recorded: onset, duration, pattern, progression, severity, diurnal variation, relation to exercise, exertion, aggravating and relieving factors. A detailed history, thorough clinical examination, judicious use of laboratory investigations including imaging is essential for rational, scientific evaluation and management of patients presenting with dyspnoea.
INTRODUCTION
Dyspnoea is one of the most common presenting symptoms encountered by clinicians.1,2 The causes of dyspnoea can be several and range from cardiac, pulmonary, anemia, obesity, hysterical/psychogenic, physical deconditioning, among others. As these causes are varied, it is essential to differentiate life-threatening causes causes from benign, self-limiting conditions.
EPIDEMIOLOGY
Dyspnoea has been reported in 50% of patients admitted to acute, tertiary care hospitals3 and in 25% of patients in ambulatory settings.4,5 Data from population-based studies have shown that the prevalence of mild to moderate dyspnoea ranged from 9%-13% in adults.6-8 This figure ranged from 15%-18% in adults aged 40 years or older; and 25%-27% in persons aged 70 years or more.7,9,10
PATHOPHYSIOLOGICAL CORRELATES
A given disease/condition may result in dyspnoea by one or more mechanisms. The respiratory motor system is unique in having both automatic (brainstem) and voluntary (cortical) sources of motor command. Respiratory sensations are thought to be the consequence of interactions between the efferent motor output from the brain to the muscles of ventilation (feed-forward) and the afferent sensory input from chemoreceptors, mechanoreceptors and metaboreceptors (feedback) as
Alladi Mohan, D Arun kumar
well as the integrative processing of this information that is postulated to be occurring in the brain. This incongruity may be the consequence of increased metabolic demand, increased dead-space volume, decreased compliance or from other disorders.11,12 In addition to the traditionally defined sensory afferents like chest wall receptors, pulmonary vagal receptors, chemoreceptors, among others, information on the state of respiration available from respiratory motor areas of the brain which send an ascending copy of their descending motor activity to perceptual areas (corollary discharge). The corollary discharge from these different sources is thought to give rise to different sensations.
DEFINITION
Several definitions for describing dyspnea have been postulated including “uncomfortable sensation of breathing”,13 “difficult, laboured, uncomfortable breathing”,14 “sensation of feeling breathless or experiencing air hunger”.15 The American Thoracic society (ATS) defined dyspnoea11,12 as “subjective experience of breathing discomfort that consists of qualitatively distinct sensations that vary in intensity. The experience derives from interactions among multiple physiological, psychological, social, and environmental factors and may induce secondary physiological and behavioral responses.” The ATS statement11,12 also reiterates that dyspnoea per se can only be perceived by the person experiencing it. Therefore, adequate assessment of dyspnoea depends on self-report . Further, it is important to distinguish dyspnoea from the signs of increased work of breathing.
MEASUREMENT OF DYSPNOEA
Dyspnoea has to be measured to assess it adequately. Instruments pertaining to dyspnoea measurement are classified as pertaining to domains of sensory–perceptual experience (e.g., visual analogue scale, Borg scale), affective distress (single- / multi-item ratings), or symptom/disease impact or burden [unidimensional rating of disability or activity limitation like Medical Research Council (MRC) scale, multidimensional scales of quality of life/health status].11,12
DIAGNOSTIC APPROACH
Dyspnoea is a usual symptom related to disturbances in cardiovascular and respiratory systems; other potential causes that can cause dyspnoea include metabolic, infectious, traumatic, neuromuscular, haematological and other conditions (Table 1). Patients describe dyspnoea in
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Table 1: Some of the common causes of acute onset dyspnoea in adults
Table 2: Causes of paroxysmal nocturnal dyspnoea
Cardiac
Nocturnal episodes of asthma
Heart failure with reduced ejection fraction Coronary artery disease, acute coronary syndromes
Nocturnal episodes of recurrent minute pulmonary emboli
Arrhythmias
Postnasal discharge with attendant severe cough
Pericarditis
Sleep apnea with arousal
Valvular heart disease
Nocturnal angina with dyspnoea (angina equivalent)
Respiratory
RESPIRATORY
Left heart failure
Chronic obstructive pulmonary disease Bronchial asthma
Nocturnal aspiration in gastro-oesophageal reflux disease
History
Pulmonary oedema
While evaluating a patient with dyspnoea, the following should be meticulously recorded: onset, duration, pattern, progression, severity, diurnal variation, relation to exercise, exertion, aggravating and relieving factors. The terminology used by the patient can sometimes give a clue to the cause of dyspnoea: chest tightness or constricted breathing (bronchial asthma); smothering or suffocating sensation (heart failure, acute coronary syndromes); need to sigh (heart failure).
Gastro-oesophageal reflux disease with aspiration
Onset
Pneumonia, other respiratory infections (e.g., SARS) Acute respiratory distress syndrome Pneumothorax Pulmonary embolism Pleural effusion Lung cancer, metastatic lung disease
Restrictive lung disease Interstitial lung disease (e.g., acute interstitial pneumonitis) Upper airway obstruction Epiglottitis Foreign body Croup
In adult patients presenting with sudden onset dyspnoea (Table 1), acute pulmonary thromboembolism, acute coronary syndrome or spontaneous pneumothorax, acute respiratory distress syndrome (ARDS), foreign body aspiration, psychogenic causes should be high in the list of differential diagnosis.
Duration
Anaphylactic reaction
Common causes of dyspnoea that is slowly progressing over hours or days include bronchial asthma, chronic obstructive pulmonary disease (COPD), pleural effusion, pneumonia, congestive heart failure, small pulmonary emboli, interstitial lung disease or malignancy; psychogenic acuses; and cardiac diseases like coronary artery disease, congestive heart failure.16
Laryngeal spasm, laryngeal tumours
Pattern
Central Neuromuscular disease Pain Others
Anaemia Metabolic acidosis Drugs (e.g., aspirin overdosage) SARS = severe acute respiratory sndrome
their own phrases and a focussed diagnostic approach is necessary for a clinician for ascertaining diagnosis and providing treatment.
Immediate evaluatoin
Patients presenting with acute dyspnoea should be immediately evaluated and triaging should be done for signs of clinical instability, such as: (i) suspected upper airway obstruction (e.g., stridor); (ii) tachypnoea (> 24 breaths/minute) or apnoea; (iii) gasping or breathing effort without movement of air; (iv) chest retractions or use of accessory muscles of respiration; (v) presence of hypotension; (vi) presence of hypoxaemia; (vii) unilateral or absent breath sounds; and (viii) altered consciousness.
Prolonged bed rest prior to acute onset dyspnoea may indicate acute pulmonary embolism. Orthopnoea (dysnoea in supine position, relieved on assuming upright position) is classically seen in left heart failure but can also occur in COPD, bilateral diaphragmatic palsy, asthma triggered by gastric reflux, among others. Paroxysmal nocturnal dyspnea (PND) is not always diagnostic of left heart failure as nocturnal episodes of dyspnoea occur in variety of conditions (Table 2). Dyspnoea and deoxygenation upon assuming upright position is termed platypnoea-orthodeoxia and is seen in right-to-left shunting of blood (e.g., large patent foramen of ovale, hepatopulmonary syndrome). Dyspnoea in upright position, relieved in supine position is called platypnoea and it seen in left atrial myxoma or hepatopulmonary syndrome. Trepopnoea is dyspnoea in lateral decubitus position and is seen in unilateral pleural effusion.
Table 3: Differential diagnosis for some common presenting symptoms
Table 4: Some of the common causes of chronic dyspnoea
Symptom
Differential Diagnosis
Wheeze
COPD/emphysema, asthma, allergic reaction, CHF (cardiac wheeze)
Bronchial asthma
Respiratory Chronic obstructive pulmonary disease Interstitial lung disease
Pleuritic chest pain
Pneumonia, pulmonary embolism, pneumothorax, COPD, asthma
Chronic pulmonary thromboembolism
Fever
Pneumonia, bronchitis, TB, malignancy
Cardiovascular
Cough
Pneumonia, asthma, COPD/ emphysema
Haemoptysis
Pneumonia, TB, pulmonary embolism, malignancy
Valvular heart disease
Oedema
Acute heart failure, pulmonary embolism (unilateral)
Anaemia
Tachypnoea
Pulmonary embolism, acidosis (including aspirin toxicity), anxiety
COPD= chronic obstructive pulmonary disease; CHF= congestive heart failure; TB = tuberculosis; ARDS = acute respiratory distress syndrome.
Pulmonary hypertension Occupational lung disease Coronary artery disease
CHAPTER 18
Pulmonary oedema Acute and chronic heart failure, end-stage renal and liver diseases, ARDS
Congestive heart failure Haematological Others Psychogenic conditions Gastro-oesophageal reflux disease Neuromuscular Thyroid disease some of the commonly encountered physical examination clues are described below.
Dyspnoea presenting with other associated symptoms may help in localizing the system involved and understanding the nature of disease. Dyspnoea associated with central chest pain, points to aortic dissection, pulmonary embolism or acute coronary syndrome. If the pain is sharp and aggrevated by cough or deep breathing it could be due to pleural irritation. Fever indicates an infectious cause. If anxiety precedes dyspnoea it could be a panic attack or pychogenic dyspnea. When dyspnoea is associated with cough, haemoptysis, pedal oedema, or wheeze most probable aetiological causes are shown in Table 3. Some of the common causes of chronic dyspnoea are shown in Table 4.1,11,12
Whether the patient is able to complete full sentences while talking is carefully observed. In acute severe asthma, patients cannot complete full sentences while talking. Use of accessory muscles of respirations, paradoxical breathing or sitting in tripod position, signs of pallor, cyanosis, clubbing and pedal oedema are looked for. Haemodynamic stability of the patient is checked by assessing the vital signs. Further, whether the patient is able to maintain saturation on room air is assessed using pulse oximetry. On measuring blood pressure pulsus paradoxus should be watched for as its presence points to pericardial disease, restrictive heart disease. On respiratory system examination, the symmetry of chest wall movements with respiration is observed. Percussion (e.g., dull note in pleural effusion, hyperresonant in tension pneumothorax) and auscultation (wheeze, crepitations, decreased or hyperreasonant sounds, bronchial breath sounds) give valuable clue to the aetiological diagnosis. On cardiovascular system examination signs of heart failure should be looked for. Elevated jugular venous pressure (JVP), peripheral oedema, S3 gallop rhythm, presence of murmurs are valuable clues to the aetiological cause. indicate that patient is in fluid over load secondary to heart failure. Paradoxical inward movement of abdominal muscles indicate weakness of diaphragm.
Physical examination
Laboratory testing
Variations
Intermittent episodes of dyspnoea may be seen with bronchial asthma, heart failure, pleural effusion, recurrent pulmonary embolism, gastro-oesophageal reflux disease; aspiration. In addition to ardivascular diseases, exerciseinduced dyspnoea is seen in exercise-induced asthma as well. Seasonal or diurnal dyspnoea is seen in bronchial asthma. Aggravation of dyspnoea during winter months may occur with COPD.
Other associated symptoms
A thorough physical examination helps the clinician to assess the severity, diagnose the cause and in prompt management of the patient. While a detailed account of physical examination findings and their clues to the origin of dyspnoea is beyond the scope of this chapter,
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Electrocardiogram should be obtained immediately if history and physical examination are in favour of heart failure, acute coronary syndrome, cardiac arrhythmias, pulmonary embolism or pulmonary hypertension. Chest
imaging
consisting
of
chest
radiograph,
RESPIRATORY
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Fig. 1: Algorithm for evaluating an adult patient presenting with acute dyspnoea. CXR = chest X-ray; NT-proBNP = N-terminal pro-brain natriuretic peptide; ACS = acute coronary syndrome; ECG = electrocardiogram; ABG = arterial blood gas; A-a = alveolararterial; CT = computed tomography; PE = pulmonary embolism; RR = respiratory rate; V/Q = ventilation-perfusion ratio; ACE = angiotensin-converting enzyme; BiPAP = biphasic positive airway pressure; CPAP = continuous positive airway pressure. Adapted from reference 19 computed tomography of the chest, and bedside thoracic ultrasonography are helpful in diagnosing pleural effusions, pulmonary oedema, pneumothorax or consolidation. Thoracic ultrasonography is emerging as a point-of-care diagnostic test recently. It has been reported that lung ultrasonography improves diagnostic accuracy of acute dyspnoea when performed within 1 hour of admittance to emergency room (ER).17 Further, it has also been observed that combination of lung ultrasonography with or without testing for N-terminal pro-brain natriuretic peptide (NT-proBNP) has high diagnostic accuracy for differentiating acute dyspnoea due to heart failure from COPD/bronchial asthma-related acute dyspnoea in prehospital/ER setting.18
tests that are useful include cardiac biomarkers like troponin, D-dimer, N-terminal pro-brain natriuretic peptide (NT-proBNP), exercise testing, pulmonary function testing including spirometry, reversibility testing, diffusion capacity of lung for carbon monoxide, among others are useful in appropriate situations. The diagnostic approach to an adult patient presenting with acute dyspnoea is shown in Figure 1.19
Complete haemogram (anaemia) renal functions and serum electrolytes help in identifying kidney disease. Arterial blood gas (ABG) analysis will help in knowing the type of respiratory failure and also gives information about the acid-base state of the patient. Other laboratory
A detailed history, thorough clinical examination, appropriate “triage�, judicious use of laboratory investigations including imaging is essential for rational, scientific evaluation and management of patients presenting with dysponea.
TREATMENT
Depending the initial aetiological clues, further diagnostic work-up is planned and the patient is administered appropriate specific treatment accordingly.
CONCLUSIONS
REFERENCES
11.
2. Brenner S, GĂźder G. The patient with dyspnea. Rational diagnostic evaluation. Herz 2014; 39:8-14.
12. Parshall MB, Schwartzstein RM, Adams L, Banzett RB, Manning HL, Bourbeau J, et al; American Thoracic Society Committee on Dyspnea. An official American Thoracic Society statement: update on the mechanisms, assessment, and management of dyspnea. Am J Respir Crit Care Med 2012; 185:435-52.
1. Wahls SA. Causes and evaluation of chronic dyspnea. Am Fam Physician 2012; 86:173-82.
3. Desbiens NA, Mueller-Rizner N, Connors AF, Wenger NS. The relationship of nausea and dyspnea to pain in seriously ill patients. Pain 1997; 71:149-56. 4. Hammond EC. Some preliminary findings on physical complaints from a prospective study of 1,064,004 men and women. Am J Public Health Nations Health 1964; 54:11-23.
6. Frostad A, Soyseth V, Andersen A, Gulsvik A. Respiratory symptoms as predictors of all-cause mortality in an urban community: a 30-year follow-up. J Intern Med 2006; 259:5209. 7. Bowden J, To T, Abernethy A, Currow D. Predictors of chronic breathlessness: a large population study. BMC Public Health 2011; 11:33. 8. Currow DC, Plummer JL, Crockett A, Abernethy AP. A community population survey of prevalence and severity of dyspnea in adults. J Pain Symptom Manage 2009; 38:53345. 9. Hawthorne VM, Watt GC, Hart CL, Hole DJ, Smith GD, Gillis CR. Cardiorespiratory disease in men and women in urban Scotland: baseline characteristics of the Renfrew/ Paisley (midspan) study population. Scott Med J 1995; 40:102-7. 10. Shin C, Lee S, Abbott R, Kim J, Lee S, In K, et al. Relationships between respiratory symptoms and FEV1 in men and women with normal lung function: The Korean Health and Genome Study. Lung 2005; 183:301-9.
13. Mahler DA, Harver A, Lentine T, Scott JA, Beck K, Schwartzstein RM. Descriptors of breathlessness in cardiorespiratory diseases. Am J Respir Crit Care Med 1996; 154:1357-63. 14. Wright GW, Branscomb BV. The origin of the sensations of dyspnea. Trans Am Clin Climatol Assoc 1954; 66:116-25. 15. Simon PM, Schwartzstein RM, Weiss JW, Lahive K, Fencl V, Teghtsoonian M, et al. Distinguishable sensations of breathlessness induced in normal volunteers. Am Rev Respir Dis 1989; 140:1021-7. 16. Ailani RK, Ravakhah K, DiGiovine B, Jacobsen G, Tun T, Epstein D, West BC. Dyspnea differentiation index: A new method for the rapid separation of cardiac vs pulmonary dyspnea. Chest 1999; 116:1100-4. 17. Cibinel GA, Casoli G, Elia F, Padoan M, Pivetta E, Lupia E, et al. Diagnostic accuracy and reproducibility of pleural and lung ultrasound in discriminating cardiogenic causes of acute dyspnea in the emergency department. Intern Emerg Med 2012; 7:65-70. 18. Pirozzi C, Numis FG, Pagano A, Melillo P, Copetti R, Schiraldi F. Immediate versus delayed integrated pointof-care-ultrasonography to manage acute dyspnea in the emergency department. Crit Ultrasound J 2014; 6:5. 19. Braithwaite SA, Perina D. Dyspnea. In: Marx JA, editor-inchief. Rosen’s emergency medicine concepts and clinical practice. Eighth edition. Philadelphia: Elsevier Saunders; 2014.p.206-13, 213.e1.
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5. Kroenke K, Arrington ME, Mangelsdorff AD. The prevalence of symptoms in medical outpatients and the adequacy of therapy. Arch Intern Med 1990; 150:1685-9.
American Thoracic Society. Dyspnea. Mechanisms, assessment, and management: a consensus statement. Am J Respir Crit Care Med 1999; 159:321-40.
C H A P T E R
19
Spirometry: As Routine as Measuring Blood Pressure
Literally, spirometry means ‘measuring breathing’. At its most basic it is a simple bedside or officebased test which takes less time to perform than measuring blood pressure. However, whereas sphygmomanometry is one of the most familiar clinical measurements, spirometry remains, for many, an obscure manoeuvre related to the black art of respiratory physiology. It is true that patients referred for full pulmonary function tests (PFTs) in a specialist hospital laboratory will return with a complex set of figures that may be challenging to interpret. For evaluation of those conditions that account for more than 90% of respiratory disease – asthma and COPD – simple spirometry is more than adequate. The devices now available are as robust and less expensive than a standard sphygmomanometer.
EARLY IDENTIFICATION OF COPD
On October 14, 2010, World Spirometry Day was held to promote the use of spirometry as a standard screening test to identify undiagnosed COPD and prompt early intervention with smoking cessation, flu vaccination and bronchodilator therapy. This initiative aims to demystify spirometry and incorporate it as a routine preventive health measure. Modern spirometers are compact devices (Figure 1) that measure airflow at the mouth and then calculate various measurements of lung function. In practice only two parameters are needed to evaluate airflow obstruction – the forced expiratory volume in one second (FEV1) and the forced vital capacity (FVC). However, it is worth going into a bit more detail on spirometry to place these in context.
Geoff Chadwick
they do not depend on how quickly or how forcefully the patient performs the manoeuvre. The tidal volume (TV) is the amount of air that is moved by each breath during normal resting breathing – typically around 400ml. If a patient is asked to take in a full breath then the difference between a normal tidal inspiration and a maximal inspiration is the inspiratory reserve volume (IRV). If a patient is asked to breathe out to the maximum possible then the difference between a normal tidal expiration and a maximal expiration is the expiratory reserve volume (ERV). The difference between a maximal inspiration and a maximal expiration is the vital capacity (VC). Figure 2 also shows three other measurements which are important to know about but which cannot be measured with a spirometer. The residual volume (RV) is the amount of air remaining in the lungs at the end of a maximal expiration. No matter how much air is forced out of the lungs there is always some left behind. The functional residual capacity (FRC) is the amount of air in the lungs at the end of a normal tidal breath and is the sum of RV and ERV. The total lung capacity (TLC) is the total amount of air in the lungs at the end of maximal inspiration and is the sum of RV and VC. Most medical students are taught that reduction in VC
Figure 2 shows the static lung volumes, so called because
Fig.1: Simple desktop spirometer
Fig. 2: Static lung volumes
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Table 1: Examples of restrictive lung disease Diseases of the lung parenchyma • Fibrosing alveolitis • Pneumoconiosis • Allergic alveolitis • Drug induced pneumonitis Diseases of the chest wall • Kyphoscoliosis Diseases of the respiratory muscles • Muscular dystrophy • Myasthenia
Fig. 3: Dynamic lung volumes
Lung resection
in Figure 3, obstructive diseases like COPD will also reduce FVC as a result of air trapping and increased RV. So, is it possible to differentiate restrictive and obstructive diseases without being able to measure RV? In practice the ratio of FEV1 to FVC (FEV1/FVC) is helpful.
is caused by restrictive lung disease and that obstructive diseases affect only the dynamic measurements and rates of airflow (see below). Looking at Figure 2, we can see that there are two ways in which VC can be reduced – from the ‘top down’ by a reduction in TLC or from the ‘bottom up’ by an increase in RV. In restrictive diseases (Table 1) VC is reduced by a reduction in TLC – ie. from the ‘top down’. In obstructive diseases – asthma and COPD – TLC is normal or may even be increased, particularly when emphysema is present. However, VC is reduced because airway obstruction prevents maximal expiration due to ‘air trapping’ and RV is increased – ‘bottom up’. Figure 3 shows the dynamic lung volumes that are measured from a single forced expiration that is the basis for the most commonly performed spirometric manoeuvre. The graphs in Figures 2 and 3 have the same axes – volume in litres on the vertical axis with inspiration upwards and time on the horizontal axis. In Figure 3 the graph starts with a maximal inspiration. The patient is asked to “take a deep breath in and hold it, and then blow out as long and as hard as you can”. The entire test is repeated two or three times and the best set of measurements recorded. Two measurements are made from the forced expiratory manoeuvre. The FVC is exactly the same as the VC except it is measured with a ‘dynamic’ or ‘forced’ technique. The FEV1 is the amount of air that is blown out in the first second of the manoeuvre. Change in volume with time is, by definition, flow and the FEV1 is a measurement of airflow during the first second of a forced expiration. Understandably, diseases that affect airflow such as asthma and COPD will have their predominant impact on FEV1. As explained above, however, and as illustrated
AIRFLOW AND FEV1/FVC
Although obstructive lung diseases will reduce FVC, their predominant effect is on airflow and the reduction in FEV1 will be proportionately greater than the reduction in FVC. As a result, FEV1/FVC is always reduced (< 80%) in obstructive disease. Indeed in a pure restrictive disease such as fibrosing alveolitis (idiopathic pulmonary fibrosis) the patient may have such a reduction in TLC that they can blow virtually the whole breath out in the first second and the ratio is abnormally high (> 90%).
USE OF SPIROMETRY TO DIAGNOSE AND EVALUATE AIRWAYS OBSTRUCTION
As a simple rule of thumb, the FEV1/FVC ratio tells us about the presence of airways obstruction and FEV1 alone about the severity. Thus a patient with an exacerbation of asthma may have FEV1 of 1.0L, FVC of 2.0L, ratio 50%. Next day the FEV1 may rise to 1.3L, FVC to 3.0L, ratio 43%. On both days the FEV1/FVC ratio is reduced, more so on day two. However, the FEV1 rises on day two by 30% indicating improvement in severity.
SUMMARY
Finally, does spirometry tell us everything we need to know? Not quite. Certainly patients with severe COPD have very little variation in spirometry – hence the term ‘irreversible airways obstruction’, but they have obvious clinical variations in disease severity and exacerbations. In these cases subjective symptom scores (eg. Borg score) and other measures such as the six-minute walking distance may be useful.
CHAPTER 19
• Thoracoplasty
C H A P T E R
20
Approach to a Patient with Intractable Cough
INTRODUCTION
T Geetha
CAUSES OF CHRONIC INTRACTABLE COUGH
Cough is a protective reflex, to clear the respiratory passages. It is among the commonest symptoms presenting to the out patient department.
Causes can be categorised as respiratory and non respiratory and systemic.
Cough lasting less than 3 weeks is called acute cough. If the duration is 3 to 8 weeks, it is subacute.
Post nasal drip
Intractable cough is chronic cough, which is arbitrarily defined as any cough lasting for more than 8 weeks. This can be the presenting complaint in 20% - 40% of new patients. This definition is based on the criteria that post infectious cough is unlikely to last for 8 weeks.1
The most common respiratory causes of chronic cough include Post infectious Asthma
Environmental causes
Smoking, both active and passive – this is the commonest environmental factor Particulate matter of 10micro meter or less
Cough is a natural defence mechanism of the airways and lungs. It helps clear secretions, noxious substances and foreign materials from the airways. So suppressing cough can result in infections, and excess cough can result in both physical and psychological complications.
Occupational exposure to irritants
The aetiology can arise anywhere along the tracheobronchial tree or from the systems, so a multidisciplinary approach is often needed.
NSAIDs
Regardless of cause, chronic cough often worsens initially on lying down at night, while talking or with the hyperpnoea of exercise2. It improves with sleep. In general, this cough is non productive. Recently the term, ‘Chronic cough hypersensitivity syndrome’ is being used to label chronic cough, because it is being recognised as due to an abnormally sensitive cough reflex3, since, even after an extensive work up, the cause of the chronic cough may remain undiagnosed in as many as 46% of patients.4
Pathophysiology of cough
Cough receptors are present from the hypopharynx and larynx, upto the segmental bronchi. There are many types of sensory receptors which respond to mechanical, inflammatory, thermal and chemical stimuli. These are connected to the vagal afferent nerves. The cough centre located in the medulla and receives signals from these cough receptors. The efferent fibres reach the various muscles that produce the forced expiratory effort. Since the higher cortical centres have an influence over the cough centre, it is possible to produce or suppress cough, voluntarily.
Drugs
ACE inhibitors Beta blockers Drugs causing pulmonary fibrosis : Bleomycin, Busulphan, Methotrexate, Carmustine, Amiodarone, Cyclophosphamide, Hydralazine
Other respiratory causes include Bronchiectasis Bronchitis COPD Cystic fibrosis Interstitial Lung Disease (ILD) Primary or secondary lung tumours Sarcoidosis Tuberculosis
OTHER UPPER AIRWAY CONDITIONS TO BE RULED OUT
Chronic tonsillar enlargement
Obstructive Sleep Apnoea- wherein the apnoea may induce an increase in trans diaphragmatic pressure leading to decrease in lower oesophageal pressure, GERD and cough5. Chronic snoring Irritation of external auditory meatus Laryngeal problems
Foreign bodies in the large airways Non respiratory Causes Common causes GERD Recurrent aspiration Other systemic causes Left Ventricular Failure Mitral Stenosis Psychogenic cough is a diagnosis of exclusion. The cough does not cause nocturnal awakening and is absent during positive distractions5. Very rare conditions Cardiac arrhythmias Aortic aneurysm Cough only when supine (due to collapse of large airways)6 Following complex involuntary tics (Touretteâ&#x20AC;&#x2122;s syndrome), where patient may have paroxysms of cough7 Vit.B12 deficiency (probably due to sensory neuropathy)8 Of all these conditions: Cough Variant Asthma, GERD and UACS (Upper Airway Cough Syndrome) are called the Pathogenic Triad, and they constitute 90% cases. Apart from the pathogenic triad, a fourth aetiology that deserves mention is, Non asthmatic Eosinophilic Bronchitis (NAEB). This condition is7relatively common, easily amenable to early diagnosis and treatment.
POSTNASAL DRIP SYNDROME
It is not a disease per se, it is a syndrome. This condition arises commonly from rhinitis or rhinosinusitis. Rhinitis may be allergic or non allergic and sinusitis may be infectious or non infectious. This is among the commonest causes of chronic cough. It has been renamed as Upper Airway Cough Syndrome, (UACS) by the guidelines committee of American College of Chest Physicians. Symptoms of postnasal drip include: Throat clearing sensation, sneezing, rhinorrhoea, nasal congestion, cough triggered by deep breath, laughing or prolonged talking, nasal quality of voice due to concomitant nasal blockade and hoarseness of voice. Many may not experience cough at all. Speculum examination of the nose reveals inflamed, oedematous nasal mucosa with or without polyps and cobble stoned appearance of mucosa along the posterior pharyngeal wall. Improvement of cough with antihistaminic therapy, confirms the diagnosis.
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Cough persisting for more than 3 weeks following an upper respiratory tract infection is considered to be post infectious cough. The patient usually has a normal chest X ray. This condition is particularly noted following outbreaks of Mycoplasma pneumoniae and Bordetella pertussis. In children, the common organisms causing chronic cough are: Respiratory Syncytial Virus and Parainfluenza viruses apart from M.Pneumoniae, B.Pertussis and Chlamydia pneumoniae. Among all the above respiratory infections, pertussis is a severe and debilitating disease, that can last for weeks or months, both in children and young adults. Careful analysis of the history, physical examination as well as serology and sputum culture are essential, since this cough can be diagnosed only by exclusion.
GERD
This condition causes an intractable cough either through reflex pathways initiated in the oesophageal mucosa or due to a laryngo pharyngeal reflux, with consequent aspiration of the gastric contents, resulting in chemical bronchitis and pneumonitis. Retrosternal burning sensation after meals or in the recumbent position, frequent eructations, hoarseness of voice, globus sensation and throat pain are indicators of GERD. Again many patients with a symptomatic reflux may not experience cough. Upto 75% of patients with GERD induced cough may not have symptoms of heart burn and hence endoscopy may be non contributory5.
COUGH VARIANT ASTHMA
Asthma can cause cough in the absence of wheezing, shortness of breath and tightness of the chest. This is seen more commonly among children than in adults. This condition is known as cough variant asthma. In these patients the history is very typical, wherein the cough starts following exposure to an asthma trigger. Spirometry will reveal the airway obstruction which gets reversed with a bronchodilator.
NONASTHMATIC EOSINOPHILIC BRONCHITIS (NAEB)
This is again another cause of chronic cough with eosinophilic inflammation of the airways, in non smokers, with a normal chest X ray, with the characteristic sputum eosinophil count that is in excess of 3%. There is no airflow obstruction or bronchial hyper responsiveness and spirometric results are essentially normal. This condition can be successfully treated with inhaled steroids2.
CHRONIC COUGH IN CHILDREN
In children, cough lasting more than 4 weeks is described as chronic. In the paediatric age group, commonest causes of chronic cough include infection and airway hyper reactivity followed by GERD9.
CHAPTER 20
Pulmonary infarction
POSTINFECTIOUS COUGH
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Pertussis is to be strongly considered in the paediatric age group, especially, if the cough is associated with long whoops, is troublesome at night and is associated with vomiting. Foreign body aspiration also needs to be considered more commonly in children.
RESPIRATORY
COMPLICATIONS OF CHRONIC COUGH
It is often the complications of cough which bring the patient to medical attention. It can cause devastating personal disturbance and social isolation. Common problems include: Sleep disturbances, musculoskeletal pain, emesis and syncope. Uncommon complications include: Pneumothorax, mediastinal emphysema, subconjunctival haemorrhage and stress incontinence.
MANAGEMENT OF CHRONIC COUGH
Cough needs to be assessed on the basis of: Intensity Severity Frequency Sensitivity Some of the strong clues in the assessment of cough : Cough worsening on supine posture: Post nasal drip, oesophageal reflux, chronic bronchitis, bronchiectasis and heart failure. Presence of clear sputum: Hypersensitivity mechanism Purulent sputum: Sinusitis, bronchiectasis (also, copious in quantity). To also rule out tuberculosis.
indicative of vasculitis, sarcoidosis and malignancies), pedal oedema, lymphadenopathy, Physical examination: Physical examination findings should include search for deviated nasal septum, turbinate hypertrophy, polyps and sinusitis. Examination of the ears for finding out inflammation of the tympanic membrane or the external canal. Examination of the respiratory system : Bilateral wheeze in COPD, bronchial asthma or even heart failure. Localised wheeze may occur in case of obstruction with a foreign body or tumor, Other systems also to be examined thoroughly. Chest X ray is mandatory in all cases. Chronic cough with normal chest X ray occurs with ACE inhibitor therapy, post nasal drip, GERD and asthma. These account for 90% of the cases. Diseases causing chronic cough but missed on chest X ray include tumors, early ILD, bronchiectasis and atypical mycobacterial pulmonary infection. Sputum examination is essential, wherever possible. Bacterial culture is needed if the sputum is purulent. Wherever feasible and in case of doubt, mycobacterial culture is also essential. Cytological examination is to identify malignant cells and to rule out eosinophilic bronchitis. Blood investigations : To rule out infections, eosinophilia
Blood tinged sputum: Malignancies, tuberculosis and bronchiectasis.
ESR and CRP may give a clue to the presence of infection, malignancy and connective tissue disorders.
Non productive cough: ACE inhibitor therapy.
Serological tests:
Improvement of cough with antihistaminic treatment confirms the diagnosis of UACS.
Cold agglutinin titre for M.Pneumoniae, in suspected cases.
The red flag symptoms of chronic cough are:
HIV Elisa
Copious sputum (Bronchiectasis)
Possible further investigations include:
Haemoptysis (Malignancy, Tuberculosis)
B.Pertussis can be detected from the nasopharyngeal secretions.
Systemic symptoms (Tuberculosis, lymphoma, lung primary or secondaries) Significant dyspnoea (CCF, COPD, fibrotic lung disease) To evaluate the symptoms, the following questions may be useful: 1.
What circumstances surround onset of cough?
2.
What makes cough better or worse?
3.
Whether it is productive?
History of fever, weight loss, night sweats and progressive fatigue should be enquired. General examination should evaluate clubbing (maybe
Induced sputum analysis, when sputum is not easily available and it is mandatory to examine the sputum. Bronchial provocation testing with methacholine or histamine is positive in bronchial asthma2. Bronchoscopy is to be done after excluding all common causes, if foreign body inhalation is suspected. Bronchoscopy is also indicated whenever there is abnormal chest X ray, haemoptysis, obstructive lesions and infiltrates, that otherwise elude diagnosis. ECHO 24hour ambulatory oesophageal PH or oesophageal manometry for diagnosing GERD.
Radiology of the sinuses HRCT – when no other diagnosis is made out.
Role of antitussive therapy in patients with idiopathic, dry cough
Physician
Opiates may be advised for severe, distressing cough. Codeine and hydrocodeine , suppress the cough centre in the brainstem10. They may cause drowsiness, constipation and additive effect.
ENT Surgeon
Dextromethorphan may be tried, but less effective.
Pulmonologist
Benzonatate15 is another non narcotic, oral cough suppressant acting through local anaesthetic effect on the stretch receptors in the lower airways and lungs.
Specialists needed in the evaluation of chronic, intractable cough:
Medical Gastroenterologist Immunologist Neurologist Speech therapist Patients who have isolated chronic dry cough, with normal physical examination, chest Xray and spirogram are unlikely to have serious pulmonary conditions.
TREATMENT OF CHRONIC COUGH
To stop smoking, in case of smokers. Cough should improve within 8 weeks of smoking cessation. In case of ACE inhibitor therapy, to stop the therapy. Improvement occurs within 4 weeks. Persistence of cough after withdrawal of ACE inhibitors, raises the possibility of other causes of cough. Onset of asthma has been linked to its use. Advising the patient to keep away from known environmental and occupational pollutants and irritants. Treatment of UACS, depends on a presumed aetiology (infection, allergy or vasomotor rhinitis). So treatment includes first generation antihistaminics, antibiotics, nasal saline irrigation , nasal pump sprays with glucocorticoids with or without decongestants like pseudoephedrine. Beta 2 agonists with inhaled corticosteroids give relief within a week’s time in case of proven asthma. Negative response to a bronchoprovocative test, eg. Methacholine, rules out cough variant asthma. Peak Expiratory Flow Metre can be used as a cost effective method to assess therapeutic response. A course of oral steroids for 2 weeks, or inhaled steroids, gives relief in case of NAEB. Postinfectious cough can be treated with inhaled ipratropium, inhaled corticosteroids. Macrolide antibiotics with or without antitussives may be needed. GERD therapy includes prokinetic agents, H2 antagonists and proton pump inhibitors (PPIs). Appropriate dietary therapy, and proper positioning of the patient in bed are important aspects of management. PPIs should be tried for 8 to 12 weeks.
Morphine is sparingly used, in patients with distressing cough and pain due to malignant disease1. Amitryptiline, gabapentin and carbamazepine are centrally acting drugs, which may be tried in intractable cough.
CONCLUSION
Chronic cough is a debilitating problem from a personal and social point of view. It is associated with physical and psychological consequences. The causes can range from trivial to fatal. It needs a systematic, multidisciplinary approach, focussing on history and physical examination, appropriate cost effective investigations and even therapeutic trials where necessary. Wherever there are diagnostic dilemmas and therapeutic failures, appropriate referrals and management will be needed.
REFERENCES
1.
Irwin RS, Madison JM. The diagnosis and treatment of cough. N Eng J Med 2000: 343:1715-21.
2.
Harrison’s Textbook of Internal Medicine, 19th edition. Vol 1 ; 244 -245.
3.
Ryan NM, Vertigan AE, Gibson PG; Chronic cough and laryngeal dysfunction improve with specific therapy of cough. Cough 2009; 5:4
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Pavord ID, Chung KF. Management of chronic cough. Lancet 2008; 371:1375–84.
5.
SP Rai. Chronic Cough. Supplement to Journal of Association of Physicians of May 2013; 61.
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Madison JM, Irwin RS. Cough: A world wide problem; Otolaryngeal Clin of North America 2010; 43:1-13.
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Duncan KL, Faust RA. Tourette Syndrome Manifesting as Chronic cough. International J of Paediaric ORL; 2002; 65-68.
8.
Bucca CB, Culia B, Guida G, et al. Unexplained Chronic cough and Vit. B12 deficiency. Am J Clinical Nutr 2011; 93:542–8.
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Harriden A, Grant C, Harison T, Perera R, et al. Whooping cough in school age child with persistent cough: prospective cohort study in primary care. BMJ 2006; 333:174 -177.
10. Morice AH, Menon MS, Mulrennan SA, et al. Opiate Therapy in Chronic cough. Am J Respir Crit Care Med 2007; 175:312–5.
CHAPTER 20
Allergist
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