The term reactive airway disease was first coined in 1986. It is also commonly referred to as reactive airway dysfunction syndrome. This condition has a great similarity with asthma and as a result, it is often mistaken to be asthma. Reactive airway disease is caused by exposure of the airway to irritants. Such irritants include chlorine and isocyanates among others. Respiratory syncytial virus has also been associated with causing this condition in children. There is not specific way of diagnosing this condition other than finding out the causes by specifically going through its historical development. The pathological explanation for this disorder has not been well understood. However, the condition has been associated with inflammation of the airway. The mechanism which has been speculated for this condition proposes that the inflammatory cells are responsible for triggering bronchoconstriction in the airway. The Pharmacotherapeutic intervention is through the use of drugs which enhance bronchodilation and those that fight inflammation. Beta adrenergics are used in bronchodilation. They accomplish this by relaxing the airway smooth muscle. A specific sample of a bronchodilator is Salbutamol. Steroids are used in controlling inflammation. Controlling of inflammation is important for complete recovery of a patient suffering from this condition. Management is carried out in a similar manner as that of asthma. The patient needs to be informed on how to use the medication prescribed. He or she also needs to be aware of what environmental conditions to avoid and completely avoid re-exposure to the causative agents especially at high levels provocative thresholds. Reactive airway disease is still being studied and there is a lot that need to be ascertained in regard to this condition.
Reactive Airway Disease
Reactive Airway Disease is a condition that is closely associated with asthma but is not asthma. More often than not the two conditions are erroneously assumed to be the same. Reactive airway disease is a condition that is triggered by the inhalation of corrosive substance which causes inflammation to the airway and results to asthma like symptoms. Since the symptoms are the same as those of asthma, treatment and management is very similar in both cases.
Reactive Airways Disease
The term Reactive Airways Diseases was first termed ‘Reactive Airways Dysfunction Syndrome’ – this was in 1985 (Fallon, Awosika-Olumo, & Trangle, 2002; Patel, Patel, & Patel, 2012). This condition is characterized with “development of a persistent asthma-like condition with hyper-responsiveness developing in a previously healthy asymptomatic individual within 24 hours of a single exposure to concentrated respiratory irritants” (Patel et al., 2012, p. 10). This condition is often confused with asthma and many literature materials use the term Reactive Airway Disease as a synonym for asthma. The symptoms of the two conditions are quite similar hence the confusion. However, it is worth noting that the asthma symptoms are ongoing while those of Reactive Airway Disease come and go (Patel et al., 2012). This condition is irreversible (Fallon et al., 2002).
Signs and Symptoms
The signs of Reactive Airway Disease are similar to those of asthma and include:
- Fine crackles in the lungs
- Dry continuous cough
- Wheezing when breathing (this is a high pitched sound which is produced as a result of the contraction of the airway)
- Short breaths (this is manifested in the form of tightness in the chest )
- There is no manifestation of fever
According to Fallon et al. (2002), the irritants which bring about this condition are “chlorine, sulfur dioxide, nitrogen dioxide, ammonia, isocyanates such as MDI and TDI, and ethylene oxide” (p. 10). Evidence as shown that infection from Respiratory Syncytial Virus (RSC), in early life, may induce reactive air disease later. This has been shown to happen as virus induces inflammation on the respiratory tract (Renzi, n.d).
The confusion of this condition with asthma comes in because of the way it manifests itself. Once irritants get in touch with the airway, bronchial hyper-responsiveness is induced. This condition makes a person vulnerable to bronchospastic responses from a range of environmental triggers such as “cigarette smoke, cold air, traffic fumes and common household chemicals such as hair sprays, perfumes, and bleaches” (Fallon et al., 2002, p. 10).
According to Patel et al. (2012), no ‘gold standard’ procedure has been developed for diagnosis of Reactive Airway Disease. Accurate diagnosis of this condition is dependent on “history compatibility and demonstration of persistent nonspecific bronchial hyper-responsiveness” (Patel et al., 2012, p. 10). Patel et al. (2012) proposed the criteria proposed by Brooks et al. as a diagnostic tool. This is shown in that table below.
|Step 1||A documented absence of preceding respiratory complaints|
|Step 2||The onset of symptoms occurred after a single exposure incident or accident|
|Step 3||The exposure was a gas, smoke, fume or vapor which was present in very high concentration and had irritant quantities to its nature|
|Step 4||The onset of symptoms occurred within 24 hours after the exposure and persisted for at least three months|
|Step 5||Symptoms simulated asthma with cough wheezing and dyspnea predominating|
|Step 6||Pulmonary function tests may show airflow obstruction|
|Step 7||Other types of pulmonary disease were ruled out|
|Step 8||Methacholine challenge testing was positive|
|Step 9||Requires immediate medical attention|
|Step 10||No atopic predisposition|
|Step 11||Bronchial biopsy specimen with mucosal damage and inflammation without eosinophilia|
Patel et al. (2012) noted that reported cases of histological findings of this condition are few. Some of the few reported cases pointed to inflammation of the airway. Histopathological features were “acute desquamation of the epithelium, subepithelial hemorrhage and swelling inflammatory infiltrate, and regeneration of the epithelium” (Patel et al., 2012, p. 12). It was further noted that there were no signs of “eosinophilia, mucus gland hypertrophy, basement membrane thickening, smooth muscle hyperplasia, thickening of basal lamina, alteration of tight junctions or of cilia” (Patel et al., 2012, p. 12). However, some discrepancy has been noted in some studies and there is no possible explanation for that therefore it is speculated that it is due to the extent of exposure incurred, how treatment is carried out, and the time taken after exposure before diagnosis is carried out (Patel et al., 2012). Patel et al. (2012) noted that more studies need to be carried out on the histopathologic state of reactive airway disease.
Airway inflammation has been singled out as the primary cause of this condition. This inflammation triggers “hyper-responsiveness, edema, and increased mucous production” (Patel et al., 2012, p. 12). These have a net effect of making breathing hard. Little is known about the mechanism procedure and much is speculated. The little known is that inflammatory cells release mediators which in turn trigger “edema, mucous secretion, and bronchospasm” (Patel et al., 2012, p. 12). The exact procedure of this mediation is still a subject of speculation.
As mentioned above, RCV also causes Reactive Airway Disease. It is proposed that this happens through immune dysregulation and alternation of non-adrenergic and non-cholinergic pathways by the viral infection (Piedimonte, 2002).
Bronchodilators are necessary in the first place to help the patient breath normally. The treatment however has to ensure that the inflammation is stopped (Mark, Warren, & Fields, 2002). Ipratropium and corticosteroids ought to be used initially (Patel et al., 2012). Steroids are important in fighting inflammation. After administration they are likely to produce positive results within 3 to 4 hours (McMillan & Feigin, 2006). Drugs such as budesonide are administered to counter airway inflammation (Deglin, Vallerand, & Sanoski, 2009). Dexamethasone, in severe cases, can also be used to fight inflammation and allow normal immune response (Deglin et al., 2009).
β-Adrenergics are used (Chogtu, Magazine, & Bairy, 2012) as they bring about bronchodilation by acting on the airway smooth muscle (McMillan & Feigin, 2006). Salbutamol can also be used to enhance the relaxation of airway smooth muscle leading to bronchodilation (Deglin et al., 2009). Stimulation of the airway smooth muscle brings about “increased mucus clearance, vasodilation, and inhibition of mast cell degranulation” (McMillan & Feigin, 2006). It has been noted that nebulized agents may be preferred over subcutaneously administered beta agonists because of the speed of their high speed of reaction, longer time of action and minimal side effects experienced (McMillan & Feigin, 2006).
This condition is managed in a similar manner as asthma. In managing Reactive Airway Disease, there is a need to assess and monitor the signs of the condition especially during attacks. The victim also needs to be educated and made aware of the significance of collaboration in the management plan. Different drugs are used in different ways depending on the condition in question. The patient needs to be aware of the condition that worsen his or her condition and take preventive measures (NHLBI, 2007).
Patients are allowed to return to their places of work but then they have to take caution to ensure that there is no more exposure to irritants at more than provocative thresholds. Since case studies have shown that this condition may persist in a mild form for years, it is cautioned that after an initial exposure to irritants care should be taken to avoid further exposures. Some studies have reported that when symptoms persist for more than half a year, then they are likely to continue for years. Some other studies have shown that vitamins D might be used in management of the condition because of its anti-inflammatory properties (Patel et al., 2012).
Reactive Airway Disease is similar to asthma but is caused by different agents. The only way to different the conditions is by finding out their causes. Reactive Airway Disease has similar symptoms as those of asthma but is caused by inhalation of corrosive substances. The substances inhaled causes inflammation in the airway. Treatment is similar to that of asthma and is done by ensuring that the smooth airway muscle relaxes to bring about bronchodilation and fighting the inflammation from taking place.
Chogtu, B., Magazine, R., & Bairy, K. (2012). β-Blockers in reactive airway disease. Journal of Clinical and Diagnostic Research, 5(2), 414-417.
Deglin, J. H., Vallernad, A. H., & Sanoski, C. A. (2009). Davis’ drug guide for nurses. Philadelpha, PA: F.A. Davis Co.
Fallon, L. F., Awosika-Olumo, A., & Trangle, K. L. (2002). Reactive Airways Disease: A Need for caution in a medicolegal case review brief. Journal of Controversial Medical Claims, 9(2), 10-15.
Mark, B. M., Warren, L. H., & Fields, S. A. (2002). Fundamentals of Clinical Practice. New York, NY: Springer.
McMillan, J. A., & Feigin, D. R. (2006). Oski’s Pediatrics: Principles and Practice. New York, NY: Lippincott Williams & Wilkins.
NHLBI. (2007). National Asthma Education and Prevention Program Expert Panel Report. National Heart, Lung & Blood Institute. Web.
Patel, D. P., Patel, R. K., & Patel, N. J. (2012). Review on Reactive Airways Dysfunction Syndrome (RADS). Asian Journal of Pharmaceutical and Clinical Research, 5(3), 10-15.
Piedimonte, G. (2002). Origins of reactive airways disease in early life: do viral infections play a role? Acta Paediatric, 437(1), 6-11.
Renzi, P. (n.d). Viral Infections and Airway Responsiveness. Sultan Qaboos University. Web.