It is not asthma
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This document discusses several conditions that can mimic or be misdiagnosed as bronchial asthma, including vocal cord dysfunction, cardiac asthma, gastroesophageal reflux disease, postnasal drip syndrome, and reactive airways dysfunction syndrome. It provides details on the clinical presentation and diagnostic criteria for each condition. The key points are that these "asthma mimics" are commonly treated as asthma, leading to overuse of medications and poor outcomes for patients, and a high index of suspicion for alternative diagnoses should be considered for patients who do not respond to typical asthma treatment. Diagnosis of the mimics often requires specialized testing like laryngoscopy.
It is not asthma
- 1. By Dr Ahmed mahmoud fayed MSC, RICUD, ESCTM, ERSM, STSM, SCE (UK). Pulmonologist, KING AABDUL AZIZ SPECIALIZED HOSPITAL, TAIF, KSA. ICRMP 2018 KAASH oct 2018
- 2. العظيم هللا صدق أية طه ةرسو(25و26)
- 3. A heterogeneous syndrome, is a chronic inflammatory disease of the airways characterized by airway hyper- responsivenes to a variety of stimuli, resulting in reversible airflow limitation. Being a heterogeneous disease together with many endotypes and phenotypes, bronchial asthma include many varieties as cough variant asthma, exercise induced asthma, aspirin induced asthma... etc. BRONCHIAL ASTHMA Global Initiative for Asthma (GINA). Global Strategy for Asthma Management and Prevention. www.ginasthma.org (Accessed on January 08, 2018).
- 4. Although it is mainly a clinical diagnosis based on recurrent attacks of dyspnoea, wheezing, chest tightness and/or cough, the presence of these symptoms is not specific for bronchial asthma because similar symptoms can be present with other respiratory or even cardiac diseases, or may be triggered by different stimuli in non asthmatics (asthma mimics) These asthma mimics commonly treated as bronchial asthma resulting in resources exhaustion, over estimation of bronchial asthma, over estimation of resistant bronchial asthma and many side effects of improperly used asthma medications with social and financial problems for these patients. BRONCHIAL ASTHMA Christopher S King and Lisa K Moores. clinical asthma syndromes and important asthma mimics. Respiratory Care. May 2i008 53:5.
- 5. • A high index of suspicion for alternative diagnoses should be considered after evaluating a patient for bronchial asthma who presents with atypical symptoms or fails to respond to bronchial asthma therapy. BRONCHIAL ASTHMA Christopher S King and Lisa K Moores. clinical asthma syndromes and important asthma mimics. Respiratory Care. May 2i008 53:5.
- 6. • Known also as upper airway cough syndrome, was mentioned for the 1st time by Frank in 1794. • The most accepted definition is a sense of fullness deeply seated in the back of the nose, with constant stinging and tickling sensation about the uvula, soft palate and posterior part of the hard palate that is aggravated after sleep. • Patient may suffered from a cough occurring at intervals especially night and morning due to direct irritation or inflammation of the cough receptors in the upper airway and a persistent catarrh state with change in mucociliary clearance and accumulation of mucus in the postnasal space. POSTNASAL DRIP SYNDROME • Dobell H. On winter cough, catarrh, bronchitis. (Appendix. Post Nasal Catarrh). 1st ed. London 1866, pgs 172-174. • O’Hara J, Jones NS. “Post-nasal drip syndrome”: most patients with purulent nasal secretions do not complain of chronic cough. Rhinology. 2006 44: 270-273.
- 7. • Can be diagnosed strangely as a condition that responds to combination therapy of first generation antihistamine and oral decongestant. • Diagnosis largely based on direct laryngoscope. • Chest examination may be normal but wheeze is also common. • The treatments of PNDS include nasal washing with mild alkaline solutions containing borate , first generation antihistamine and oral decongestant. POSTNASAL DRIP SYNDROME • Pratter MR, Bartter T, Akers S, DuBois J. An algorithmic approach to chronic cough. Ann Intern Med. 1993; 119: 977-983. • Prat ter MR. Chronic upper airway cough syndrome secondary to rhinosinus diseases (previously referred to as postnasal drip syndrome): ACCP evidence-based clinical practice guidelines. Chest 2006; 129: 63S-71S. • Anandan P.T. Upper Airway Cough Syndrome. Pulmon, Vol. 14, Issue 3, Sept-Dec 2012.
- 8. • Known also as paradoxical vocal fold motion (PVFM) It is first described clinically in 1842 in hysterical women and was first visualized during laryngoscope in 1869 by Mackenzie. • Abnormal adduction of the vocal cords during inspiration (less commonly during expiration) that produces airflow obstruction at the level of the larynx commonly among women and usually misdiagnosed as bronchial asthma not only due to similar presentation but also due to similar triggers of symptoms. • The exact cause of this condition is not clearly defined and may be multi- factorial VOCAL CORD DYSFUNCTION • Hoyte FC. Vocal cord dysfunction. Immunol Allergy Clin N Am. 2013; 33(1): 1–22.. • Prat ter MR. Chronic upper airway cough syndrome secondary to rhinosinus diseases (previously referredDunglison RD. The practice of medicine Lea and Blanchard. 1842. • Portman G, Stevenson R. Ear, nose and throat treatment in general practice. London: William Heinemann, 1924, 124-126.
- 9. • The clinical presentation is widely variable and similar to BA. • Sudden onset and offset poor response to bronchial asthma treatment absent of hypoxemia during attack hoarseness of voice or a phonia absent of nocturnal awakening due to breathlessness can help to differentiate it from bronchial asthma. VOCAL CORD DYSFUNCTION • Hicks M, Brugman SM, Katial R. Vocal cord dysfunction/paradoxical vocal fold motion. Prim Care2008;35(1):81–103. • Vlahakis NE, Patel AM, Maragos NE, Beck KC. Diagnosis of vocal cord22- dysfunction: the utility of spirometry and plethysmography. Chest 2002;122(6): 2246–9. • Christo pher KL, Morris MJ. Vocal cord dysfunction, paradoxic vocal fold motion, or laryngomalacia? Our understanding requires an interdisciplinary approach. OtolaryngolClin N Am. 2010;43(1):43–66.
- 10. • Diagnosis largely based on direct laryngoscope , flow-volume loop obtained through spirometry (insp. Flattening) or pulmonary function testing • Management often requires a multidisciplinary approach with the mainstays of treatment is vocal cord relaxation techniques and breathing exercises with psychological support in difficult cases. VOCAL CORD DYSFUNCTION Sandage MJ, Zelazny SK. Paradoxical vocal fold motion in children and adolescents. Lang Speech Hear Serv Sch. 2004; 35 (4): 353–62.
- 11. • Cardiac asthma is the presentation of congestive heart failure (CHF) with wheezing that more prevalent in the elderly. • It is 1st published in 1833 by James Hope. • In CHF, inability of heart to pump blood out of the left ventricle results in accumulation of fluid in the pulmonary circulation with pulmonary congestion and asthma like symptoms so misdiagnosed as BA. • About 10% of cases of dyspnea referred to a pulmonary specialist may have a cardiac cause rather than pulmonary cause. CARDIAC ASTHMA • Pratter MR, Curley FJ, Dubois J, Irwin RS. Cause and evaluation of chronic dyspnea in a pulmonary disease clinic. Arch Intern Med 1989; 149: 2277-82. • Ceridon M, Wanner A, Johnson BD. Does the bronchial circulation contribute to congestion in heart failure? Med Hypotheses. 2009; 73: 414-419.
- 12. • Circulation time prolonged in heart failure patients and can be estimated by radionuclide angiocardiography CT and MRI. • Serum Brain Natriuretic peptide (BNP) increased in heart failure. • Chest x-ray is useful tool for confirming the presence of pulmonary congestion as well as for identifying cardiomegaly. • The lung auscultation may reveal rales. • Bronchial hyper-reactivity, the hallmark of BA, can be present in some degree in some patients with LVF and persist inspite of treatment suggesting that LVF can cause chronic changes to the airways. CARDIAC ASTHMA • Hamilton JG. Cardiac asthma. Br Med J. 1955; 1:39-41. • Perl man F. Asthma and cardiac dyspnea; a differential diagnosis. Calif Med. 1951; 75: 199201. • Pison C, Malo JL, Rouleau JL, Chalaoui J, Ghezzo H, Malo J. Bronchial hyperresponsiveness to inhaled methacholine in subjects with chronic left heart failure at a time of exacerbation and after increasing diuretic therapy. Chest. 1989; 96 (2) 230–235. • Chua TP, Lalloo UG, Worsdell MY, Kharitonov S, Chung KF, Coats AJ. Airway and cough responsiveness and exhaled nitric oxide in non-smoking patients with stable chronic heart failure. Heart. 1996; 76 (2) 44–149.
- 13. • While BA medications like bronchodilators and corticosteroid usually are ineffective in treating cardiac asthma, ipratropium bromide, an inhaled anticholinergic bronchodilator, may improve pulmonary function in patients with CHF and steroids may be clearly helpful for patient with pulmonary edema and significant wheezing that fails to resolve with the initial therapy. • Traditional medications used in the acute treatment of cardiac asthma include furosemide, morphine and nitrates. • Supplemental oxygen, noninvasive ventilation (NIV) and proper positioning of the patient. • After resolving of the acute attack, heart failure therapy should be initiated or optimized CARDIAC ASTHMA • Snashall PD, Chung KF. Airway obstruction and bronchial hyperresponsiveness in left ventricular failure and mitral stenosis. Am Rev Respir Dis.1991; 144: 945-956. • Tsuyoshi Tanabe, Henry J Rozycki, Soichiro Kanoh & Bruce K Rubin. Cardiac asthma: new insights into an old disease, Expert Rev. Respir. Med. 2012; 6 (6) 705-714. • Jorge S, Becquemin MH, Delerme S, et al. Cardiac asthma in elderly patients: incidence, clinical presentation and outcome. BMC Cardiovasc Disord. 2007;7:16.
- 14. GASTRO ESOPHAGEAL REFLUX DISEASE • Gastro esophageal reflux disease is the most common disease encountered by the gastroenterologist and defined as symptoms or complications resulting from the reflux of gastric contents into the esophagus, oral cavity and /or the lung . • Symptoms include dyspepsia, epigastric pain, nausea, bloating, early satiety and belching Chronic cough but asthma symptoms and chronic laryngitis may be also the presenting symptoms. • GERD have a complex relationship with bronchial asthma. both conditions can coexist together and either one of them can induce the other or exacerbate it. • P hilip O. Katz ,Lauren B. Gerson and Marcelo F. Vela. Diagnosis and Management of Gastroesophageal Refux Disease. Am J Gastroenterol. 2013; 108: 308 – 328. • Stein, M.R. (1999) Advances in the approach to gastroesophageal reflux (GER) and asthma. J Asthma 36: 309-314.
- 15. GASTRO ESOPHAGEAL REFLUX DISEASE • BA a much greater prevalence of GERD symptoms than the general population. Hyperinflation and descent of the diaphragm in bronchial asthma with increased work of breathing increases the pressure gradient between the abdomen and chest causing herniaion of the lower esophageal sphincter into the chest allowing more reflux of gastric contents. Also asthma medications as beta2-agonists and theophylline may decrease lower esophageal sphincter tone which cause a repeated cycle of GERD-induced asthma symptoms resulting in increased use of bronchodilators, which in turn promotes more GERD. • GERD may induce asthma symptoms either by direct effects on airway hyper-responsiveness or via increases in airway inflammation. Microaspiration of acid is a very potent direct stimulus for bronchospasm and may trigger bronchospasm indirectly by the inflammatory changes which is either chronic localized inflammation with subsequently increased airway reactivity or from released cytokines as a result of injury of the epithelial lining of the upper airway. • Treatment of GERD has variable effect on asthmatic patients while some patients with BA get benefits from GERD treatment with more symptoms control, some report no any benefits . For this some recommend with an empiric trial of GERD therapy in poorly controlled asthmatics even if they do not have GERD symptoms and others recommend against and this again show the complex relation between GERD and asthma. • Gibson, P.G., Henry, R.L. and Coughlan, J.L. (2000) Gastro-oesophageal reflux treatment for asthma in adults and children. • Cochrane Database Syst Rev 2: CD001496. Busse, W.W. and Lemanske Jr, R.F. (2007) Expert Panel Report 3: Moving forward to improve asthma care. J Allergy ClinImmunol. 120: 1012-1014.
- 16. • Known also as upper air way reactive syndrome (UAWRS) • A sudden onset of asthma-like symptoms after a single exposure to a high concentration of irritant agent. • It is 1st described in 1981 by Brooks and Lockers as a non- immunological asthma resulting from exposure to an irritant gas. • Patient may develop burning sensation in the throat and nose in addition to cough, dyspnea, wheeze and chest pain with symptoms of nasal mucosal irritation such as nasal congestion, sneezing, nasal pruritis and or increased nasal secretions. • Symptoms usually manifest within 24 hours of exposure although a few patients report symptoms after up to seven days of the exposure. REACTIVE AIRWAYS DYSFUNCTION SYNDROME • White CW, Martin JG. Chlorine gas inhalation: human clinical evidence of toxicity and experience in animal models. Proc Am ThoracSoc 2010; 7:257. • Gautrin, D, Bernstein, et al. Reactive airways dysfunction syndrome or irritant-induced asthma. In: Asthma in the workplace, Bernstein, IL, Chan- Yeung, M, Malo, J L, Bernstein, DI (Eds), Marcel Dekker Inc, New York 1999. p.565.
- 17. REACTIVE AIRWAYS DYSFUNCTION SYNDROME Shakeri MS, Dick FD, Ayres JG. Which agents cause reactive airways dysfunction syndrome (RADS)? A systematic review. Occup Med. 2008; 58: 205–211. • chlorine, toluene diisocyanate and oxides of nitrogen .
- 18. • The pathology shows nonspecific inflammation with cellular infiltration primarily lymphocytic and epithelial desquamation . This inflammatory state with the toxic mediators causes epithelial injury. • The criteria for the diagnosis of RADS include documented absence of preceding respiratory complaint, exposure to very high concentration of irritant properties onset of symptoms within 24 hours after single exposure (but may delayed up to seven days), persistence for at least 3 months of asthma like symptoms, presence of airflow obstruction on pulmonary function ± nonspecific bronchial hyper-responsiveness and all other pulmonary disease were excluded . • A chest radiograph may be obtained and HRCT chest usually is not required. • For patients with chronic symptoms either allergy skin testing or immunoassay to a panel of common aeroallergens may be done to exclude allergic asthma. • Spirometry usually obstructive with some reversibility but restrictive pattern documented in literature. REACTIVE AIRWAYS DYSFUNCTION SYNDROME • Shakeri MS, Dick FD, Ayres JG. Which agents cause reactive airways dysfunction syndrome (RADS)? A systematic review. Occup Med. 2008; 58: 205–211. • Mendelson DS, Roggeveen M, Levin SM, et al. Air trapping detected on endexpiratory high-resolution computed tomography in symptomatic World Trade Center rescue and recovery workers. J. Occup Environ Med. 2007; 49: 840. • Vandenplas O, Fievez P, Delwiche JP, et al. Persistent asthma following accidental exposure to formaldehyde. Allergy 2004; 59: 115.
- 19. • While patient with RADS less responsive to Beta2 agonist than asthmatic patient, the treatment is the same as that of BA. • Systemic glucocorticoids is used in acute reactive airways dysfunction typically oral prednisone 40-60 mg for 10 to 15 days, which is longer than that used for typical exacerbations of bronchial asthma. • Nebulized sodium bicarbonate. • lung transplantation. • Unlike immunologic occupational asthma, patient with RADS can return to their working environment with proper asthma treatment as long as their asthma is well-controlled and safety measures are taken to avoid high-level exposures. REACTIVE AIRWAYS DYSFUNCTION SYNDROME • Banauch GI, Dhala A, Alleyne D, et al. Bronchial hyperreactivity and other inhalational lung injuries in rescue/recovery workers after the World Trade Center collapse. Crit Care Med. 2005; 33. • Vandenplas O, Wiszniewska M, Raulf M, et al. EAACI position paper: irritantinduced asthma. Allergy 2014; 69: 1141.
- 20. TRACHEOMALACIA AND TRACHEOBRONCHOMALACIA • Tracheobronchomalacia is a weakness of the tracheobronvheal wall causing narrowing of its lumen specially during expiration. • presented by barking cough, dyspnoea, stridor, wheezing, difficulty clearing secretions, recurrent bronchitis or pneumonia and syncope during coughing. • It can be classified in many ways (shape or cause). • The histopathological changes include narrowing of the lumen accompanied by atrophy of the longitudinal elastic fibers and fragmentation of the tracheal cartilage • Diagnostic tools include flexible bronchoscopy(<50% decrease in diameter), dynamic airway CT and pulmonary function testing • Sverzellati N, Rastelli A, Chetta A, et al. Airway malacia in chronic obstructive pulmonary disease: prevalence, morphology and relationship with emphysema, bronchiectasis and bronchial wall thickening. EurRadiol 2009;19:1669–78. • Co llard P, Freitag L, Reynaert MS, et al. Respiratory failure due to tracheobronchomalacia. • Thorax 1996; 51:224. Feist JH, Johnson TH, Wilson RJ. Acquired tracheomalacia: etiology and differential diagnosis. Chest 1975; 68:340.
- 21. TRACHEOMALACIA AND TRACHEOBRONCHOMALACIA Carden KA, Boiselle PM, Waltz DA, Ernst A. Tracheomalacia and tracheobronchomalacia in children and adults: an in-depth review. Chest 2005; 127: 984..
- 22. TRACHEOMALACIA AND TRACHEOBRONCHOMALACIA • Intervention is usually not necessary in children with mild-to-moderate TBM and conservative therapy is preferred. • Asymptomatic adult patients generally do not require therapy, but for symptomatic patients the initial treatment targets the underlying cause and coexisting conditions. • NIPPV maintain airway patency, facilitate secretions drainage and improve expiratory flow with reduction of the work of breathing • Airway stents can be used to restore and maintain airway patency with improvement of pulmonary function tests but more than one stent may be required. • Surgical intervention include tracheal resection reconstruction (post-intubation and focal TM) tracheal, tracheal replacement and tracheobronchoplasty (surgical splinting of the posterior wall of the trachea with polypropylene). • Sommer D, Forte V. Advances in the management of major airway collapse: the use of airway stents. OtolaryngolClin North Am 2000; 33: 163–177. • Lagisetty KH, Gangadharan SP. Tracheo bronchoplasty for the treatment of tracheobronchomalacia. J ThoracCardiovascSurg 2012; 144: S58.
- 23. CHRONIC OBSTRUCTIVE PULMONARY DISEASE • COPD, a heterogeneous disease, is a common, preventable, and treatable disease that is characterized by persistent respiratory symptoms and airflow caused by significant exposure to noxious particles or gases and include: chronic bronchitis, emphysema and chronic remodeling bronchial asthma . • Although pathological changes of COPD are mainly in the airways, lung parenchyma and pulmonary vasculature are commonly affected • Chronic inflammation in COPD is characterized by the presence of CD8+ T-lymphocytes, neutrophils, and CD68+ monocytes/macrophages in the airways ( in BA CD4 T lymphocyte, eosinophils, IL4,5). • Although cigarette smoking is clearly the single most important risk factor in the development of COPD, the prevalence is also related to outdoor, occupational and indoor pollution as biomass fuels use. • Global Strategy for the Diagnosis, Management and Prevention of COPD, Global Initiative for Chronic Obstructive Lung Disease (GOLD) 2018 Report www.goldcopd.org. • Cosio MG, Saetta M, Agusti A. Immunologic aspects of chronic obstructive pulmonary disease. N Engl J Med 2009; 360: 2445.
- 24. CHRONIC OBSTRUCTIVE PULMONARY DISEASE • Dyspnea, chronic cough, and sputum production are the cardinal symptoms of COPD together with wheezing. • The diagnosis of COPD depends on the proper history and appropriate examination with an obstructive evidence provided by spirometry specially in current or former smoker aged more than 35 years. • Chest x ray. • HRCT chest • ECHO. • Although COPD has no cure due to the permanent damage to lungs, smoking cessation is the single most effective intervention. • Management include pharmacological and non pharmacological interventions . Graeme P Currie and JoeSLegge. ABC of chronic obstructive pulmonary disease(diagnosis). BMJ 2006; 332: 1202–4.
- 25. CONCLUSION • As there is neither specific test for diagnosis nor pathognomic presentation of bronchial asthma with similarity of its symptoms to many other common clinical conditions, we should be extremely careful during evaluation of our patients with a detailed history and full proper examination with investigations • Considered always other possible diagnoses for bronchial asthma specially if there is a typical presentations or poor response to treatment taking in mind the coexisting of many conditions together.