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We have a family history of allergic rhinitis and I treat everyone in my family for united airway disease because I have found the reaction can move up and down between the upper and lower airways. I can usually hear how reactive the airways are by the sounds coming from my children after years of watching and monitoring I have it down to a well-oiled machine but it takes vigilence to be on it and sometimes I miss it and then I quickly start to treat both airways so it doesn’t progress. I have worked really hard to prevent lower airway remodelling. The report below states “After direct allergen challenge in one part of the airway, an inflammatory response can be shown in both the target area and the reciprocal part of the airway within 24–48 hours of the challenge.” “‘Atopic asthma’ and ‘non-atopic asthma’, are not well separated disease entities.” The report also states “The presence of lower AHR without symptoms of clinical asthma has been well documented in population studies” which is what has caused me sooooo much grief because my youngest child does not wheeze except when he has an infection and then he needs antibiotics and most doctors look for a wheeze. We have spent hours in ER waiting to be assessed by the doctor because my son doesn’t wheeze whereas another individual will arrive at ER and the nurse hears a wheeze and they are treated with asthma medication and discharged long before we have seen the doctor. It’s exhausting so I try to avoid ER because in my local hospital they aren’t familiar individuals can have clinical asthma without symptoms. Click here to learn more or read an excerpt below.
• United airway disease is characterised by inflammation of the respiratory tract, in which asthma and rhinitis are the upper and lower respiratory tract manifestations, respectively, of the same disease process.
• Irrespective of cause, the upper and lower respiratory tract manifestations are characterised by a systemic inflammatory response.
• Patients with rhinitis or asthma should always be assessed for coexistent disease in the reciprocal area.
• Treatment of upper airway disease can modify the severity of lower airway disease and vice versa.
• The potential for early treatment of allergic rhinitis to prevent progression to asthma merits further study
MJA 2006; 185: 565–571
Hence it is much easier to demonstrate airway hyper-responsiveness (AHR) in the bronchi than in the nose. The different anatomy also explains the differential effects of drugs such as antihistamines and β2-agonists on the upper and lower airways.1,2
Both the upper and lower airways act as a transport system moving air in and out of the lungs. Both provide defence against inhaled foreign substances, with most particles of 5–10 μm diameter filtered out by the nose, and irritant and soluble gases being extensively removed by dissolution in nasal secretions. The lower airway functions similarly, with smaller inhaled particles that reach the lower airway being trapped and cleared by the mucociliary escalator.
Allergic rhinitis and asthma are common manifestations of the allergic response. It is important to note that non-IgE-mediated disease (eg, hypersensitivity pneumonitis) can also occur in response to inhaled allergens and that non-allergic airway disease (eg, intrinsic asthma and some forms of occupational asthma) is often difficult to distinguish clinically from allergic airway disease.
The UAD hypothesis The UAD hypothesis proposes that any disease process that affects the upper airway is likely to affect the lower airway, and vice versa, by both direct and indirect means. It is postulated that rhinitis and asthma represent the manifestations of one syndrome in two parts of the respiratory tract, the upper and lower airways, respectively. At the low end of the severity spectrum, rhinitis may occur alone; in the middle range of the spectrum, rhinitis and AHR may be present; and, at the high end, rhinitis and asthma may both be present, with the severity of each condition tracking in parallel.6 Disease manifestations in the upper and lower airways may be linked via a systemic inflammatory response. The hypothesis may hold for not only allergic but also non-allergic presentations.
• Mild: normal sleep and no impairment of daily activities, sport, leisure, work or school; no troublesome symptoms.
• Moderate to severe: one or more of (a) abnormal sleep; (b) impairment of daily activities, sport or leisure; (c) problems caused at work or school; and (d) troublesome symptoms.
The allergic inflammatory response
Acute and chronic changes in the upper and lower airways in response to an allergic stimulus are summarised in Box 2. Although the nose is usually the first site of exposure to allergens or other noxious substances, the presence of nasal epithelial damage is minimal, whereas, in the bronchi, marked epithelial disruption may be present. Thus, it is postulated that the nasal mucosa has developed protective mechanisms that minimise remodelling and enhance epithelial regeneration.7 In support of this hypothesis, animal models of airway inflammation show that, although the majority of allergen is deposited in the nose, more inflammation occurs in the lower airway.2 Basement membrane thickening, a consistent hallmark of lower airway remodelling in asthma, is present even in children with asthma, and also in atopic patients without asthma and patients with allergic rhinitis; however, it has not been reproducibly demonstrated to occur in the nose.
Inflammatory changes can be detected in both the upper and lower airways without accompanying clinical symptoms. In patients with rhinitis, lower airway inflammation can be demonstrated by increased levels of eNO and by eosinophils found in induced sputum, bronchoalveolar lavage fluid and bronchial biopsies. Similarly, in patients with asthma, nasal biopsies show eosinophilic inflammation, even in those who do not have symptoms of rhinitis.8 After direct allergen challenge in one part of the airway, an inflammatory response can be shown in both the target area and the reciprocal part of the airway within 24–48 hours of the challenge.9,10 These two seminal studies have underpinned further development of the UAD hypothesis.
Intrinsic asthma, such as aspirin-exacerbated respiratory disease (Samter’s triad of aspirin sensitivity, nasal polyposis and asthma), demonstrates that upper and lower airway inflammation can sometimes be found in the absence of atopy (Box 5).1 A study by Gaga et al8 assessed nasal biopsies in 19 non-atopic subjects with asthma, with or without nasal symptoms. Both study groups showed similarly high nasal eosinophil counts compared with normal patients. Given that lower airway inflammation is accepted as universal in asthma (Box 1), this finding supports the coexistence of upper and lower airway inflammation in non-atopic subjects. However, a larger number of subjects would need to be studied to establish whether this finding can be generalised.
The presence of lower AHR without symptoms of clinical asthma has been well documented in population studies. In addition, the relationship between AHR and inflammation is complex, with many studies not supporting a relationship between the two. As airway inflammation is central to the concept of UAD, it is possible that the upper airway may not be involved in isolated, nonasthmatic AHR. Eosinophilic bronchitis, a newly identified condition of the lower airway associated with persistent cough, is an example of lower airway inflammation without AHR, but, as yet, upper airway disease has not been looked for in association with this condition.15
An analysis of the same Belmont population showed that the presence of hayfever at the age of 8–10 years was predictive of the presence of troublesome asthma by the age of 23–25 years (likelihood ratio, 2.14; 95% CI, 1.59–2.89).21
It is well documented that allergic rhinitis is associated with increased AHR, even if there is no diagnosis of asthma. People subject to allergic rhinitis have demonstrable AHR both outside the pollen season (11%–73%) and during the pollen season (50%).1 Clinical studies indicate that 80%–100% of patients with asthma have rhinitis and 50% of patients with rhinitis have asthma, and that both the presence and severity of rhinitis are associated with worse asthma outcomes.1
An association between asthma and sinusitis has long been recognised. In a recent study, 100% of subjects with severe asthma (requiring steroid treatment) had abnormal sinus computed tomography scans versus 77% of subjects with mild to moderate asthma.22 However, perhaps the most direct evidence of the relationship between sinusitis and asthma is provided by studies that show significant improvement in asthma symptoms when sinusitis is appropriately treated.23
Allergen immunotherapy can also prevent the development of sensitisation to new allergens. A group of 134 children who had intermittent asthma (with or without rhinitis) and who were singly sensitised to dust mite were enrolled into active treatment and placebo groups. Specific dust mite immunotherapy was given for 3 years and subjects were followed up for a further 3 years. Only 24.6% of children in the immunotherapy group developed new sensitisation (most commonly to pollens), compared with 66.7% in the control group (P < 0.001).37
Sublingual/oral immunotherapy (SLIT), which is easier to administer to children than injection therapy and also has the advantage of carrying minimal or no risk of anaphylaxis, leads to improvement in symptoms of rhinitis. There is limited evidence that SLIT may prevent the development of allergic disease in childhood.39
The value of allergen avoidance as a therapeutic measure for rhinitis or asthma, or both, has long been controversial. Avoidance studies can be categorised according to the specific allergen avoided and the outcome measures: relief of current symptoms or the primary prevention of allergic disease. In the case of occupational asthma, allergen avoidance is highly recommended and often successful.3
My son had “an overnight O2 saturation study, which revealed significant, though not severe, desaturations; However, by discharge it was decided not to recommend home O2, and this did not seem an issue afterwards.” Apparently once you are placed on oxygen you never get off oxygen so I was glad this wasn’t pursued. My son will also sleep right through them as the article states “the person may sleep right through the episodes completely unaware of them, often a partner will notice and become alarmed.” Click here to learn more or read an excerpt below.
Patients who develop sleep disturbances often seek the aid of a physician who commonly refers them for sleep studies. Sleep studies can yield important diagnostic information about a person’s sleep cycles, oxygen levels, and the quantity and length of breathing interruptions. What is the relationship between obstructive sleep apnea and lower oxygen oxygen levels during sleep? How does sleep apnea lead to oxygen desaturations that may affect overall health?
One of the most common sleep disorders diagnosed in people with difficulty sleeping is obstructive sleep apnea, or OSA. The condition affects more than millions of Americans, and can be serious. Information gathered during a sleep study can guide a physician in making the diagnosis.
Obstructive sleep apnea occurs when there is a blockage of air flow through the throat during sleep when a person’s upper airway collapses during sleep. When this happens, breathing stops for as little as 10 seconds and even up to a minute or longer.
People with sleep apnea experience frequent, repeated episodes during a single night, sometimes hundreds. And while the person may sleep right through the episodes completely unaware of them, often a partner will notice and become alarmed.
During periods of apnea, people received less air, which results in decreased oxygen delivery to the body.
The oxygen levels of the blood may fall repeatedly. This oxygen decrease is called an oxygen desaturation. It often drops by 3 or 4 percent (and sometimes much more) in association with sleep apnea events.
Oxygen levels are considered abnormal when they drop below 88 percent. These might be deemed to be severely abnormal when the levels drop below 80 percent.
When the oxygen levels are low for more than 5 minutes during the night, this is a condition called hypoxemia.
Due to disrupted breathing in sleep, sleep apnea can cause people to feel drowsier the next day. In addition, without treatment, sleep apnea can result in any of the following signs and symptoms:
The doctors even told me my son didn’t have this when he was little. Scared the crap out of me when I learned what may cause it. The Cystic Fibrosis testing was nerve wracking enough! Click here to learn more or read an excerpt below.
Lung cancer is the most common cause of clubbing. Clubbing often occurs in heart and lung diseases that reduce the amount of oxygen in the blood. These may include:
Other causes of clubbing:
If you notice clubbing, call your health care provider.
A person with clubbing often has symptoms of another condition. Diagnosing that condition is based on:
The provider may ask questions such as:
The following tests may be done:
There is no treatment for the clubbing itself. The cause of clubbing can be treated, however.
This is what my son has. He has a combination of Post Nasal Drip and Asthma which falls under the United Airway Disease to add another level of complication. The most important and troubling aspect of this disease is this statement from the article “Often, a careful history and physical examination can suggest, but are not sufficient to diagnose, the cause of chronic cough. For example, classic findings on history and physical examination associated with PNDS, asthma, and GERD can be unreliable because there are silent forms of these diseases.11-13” Click here or on the pdf file to learn more or read an excerpt below.
CONCLUSION The most common causes of chronic cough are PNDS, asthma, GERD, or some combination of these. A systematic approach to diagnosis and treatment is effective for most cases of chronic cough.
Chronic cough can cause complications in respiratory, cardiovascular, central nervous system, gastrointestinal, genitourinary, and musculoskeletal systems. Hence, chronic cough is a multisystemic health concern for many patients seen by family physicians. This paper focuses on management of the most common causes of chronic cough in adults: postnasal drip syndrome (PNDS), asthma, and gastroesophageal reflux disease (GERD).
Quality of evidence MEDLINE was searched for articles related to diagnosis and treatment of chronic cough, using the key words chronic cough, postnasal drip syndrome, asthma, cough variant asthma, and gastroesophageal reflux disease. The search was limited to human investigations completed between 1970 and 2000, written in English and conducted on both sexes. Bibliographies from these articles were screened for additional references. A total of 33 articles were used in this review; most were cohort and case studies and review articles. Few randomized control studies were found.
Importance of chronic cough Cough, an important respiratory defense mechanism, is responsible for clearing excessive secretions, fluids, or foreign material from the airway.2,8 Despite its protective role, excessive coughing can cause multisystem problems. Common complications, such as anxiety, fatigue, insomnia, myalgia, dysphonia, perspiring, and urinary incontinence,2,9 often force patients to seek medical help. Other difficulties, including heightened self-consciousness and changes in lifestyle, are also frequent consequences of chronic cough.10 The severe effects on health and the possibility of more serious causes of cough warrant spending time to arrive at an accurate diagnosis and treatment plan.
Differential diagnosis Chronic cough can have many causes (Table 1). Almost all chronic coughs, however, can be attributed to PNDS, asthma, GERD, or some combination of these in immunocompetent, non-smoking patients who have normal results of chest radiographs and do not take angiotensin- converting enzyme (ACE) inhibitors.2 These three common clinical conditions should be considered first during diagnostic evaluation. Often, a careful history and physical examination can suggest, but are not sufficient to diagnose, the cause of chronic cough. For example, classic findings on history and physical examination associated with PNDS, asthma, and GERD can be unreliable because there are silent forms of these diseases.11-13 The features and timing of chronic cough are also of little diagnostic value.14 Additional investigations and responses to trials of empiric therapy based on the most likely etiology are essential (Figure 1).
Initial investigations should include a chest radiograph, which can detect many of the more ominous diseases mentioned in Table 1. Evidence of these diseases should prompt appropriate referral and treatment. When results of chest radiographs are normal or unchanged from those of radiographs taken for previous unrelated diseases in immunocompetent patients, PNDS, asthma, GERD, or some combination of these is highly probable.2 Additional investigations, including a methacholine challenge test, sinus radiography, and an esophageal pH probe, might be necessary.
Often, a positive response to empiric therapy for a suspected cause of chronic cough is essential for confirming its diagnosis. Optimizing therapy by adding treatments for concomitant causes of chronic cough might be required for some patients. Repeated failure of therapy or combination therapy should prompt referral to an appropriate specialist.
Postnasal drip syndrome
Postnasal drip syndrome is the most common cause of chronic cough. It most often occurs after viral upper respiratory tract infections, such as those caused by respiratory syncytial or parainfluenza viruses and sometimes by Chlamydia pneumoniae (TWAR strain), Mycoplasma pneumoniae, or Bordetella pertussis. 2,15 Other causes of PNDS include perennial rhinitis; rhinitis as a consequence of seasonal allergens, irritants, drugs, and vasomotor responses; and chronic sinusitis.2 Whatever the cause, chronic inflammation augments nasal and sinus secretions that continuously stimulate the cough reflex.
Diagnosis of PNDS is based on a combination of historic, physical, and radiologic findings, and responses to treatment. The most common complaint of those with PNDS is a sensation of tickling or a constant drip in the back of the throat.2 Throat clearing, nasal congestion, rhinorrhea, and hoarseness are other symptoms of PNDS; some of those with PNDS have no symptoms.3 Exacerbation of symptoms after exposure to allergens, irritants, or drugs suggests rhinitis as the cause of PNDS. Onset of watery rhinorrhea with changes in temperature implies vasomotor rhinitis. Radiographs of sinuses showing air-fluid levels, opacifications, or mucosal thickening (> 6 mm) are diagnostic of chronic sinusitus.2
A positive response to therapy is essential for determining that PNDS is the cause of chronic cough. Treatment for postinfectious, perennial, and vasomotor rhinitis includes a first-generation antihistamine, such as dexbrompheniramine, in combination with a pseudoephedrine decongestant.11,16,17 The cough, if caused by PNDS, usually improves within a few days to 2 weeks after therapy begins. Poor improvement suggests that an inappropriate antihistamine was used or that there are other concomitant causes of chronic cough. The efficacy of first-generation antihistamines in treating PNDS is attributed to their anticholinergic properties, which make them effective against nonhistaminemediated causes of PNDS. Insomnia, anxiety, tachycardia, palpitations, hypertension, diminished micturition, increased intraocular pressure, dr y eyes, and a dry mouth are all potential side effects. Ipratropium bromide is useful for treating perennial and vasomotor rhinitis.2,3
Managing allergic rhinitis should begin with allergen testing to identify environmental exposures and indicate exposures to be avoided. Newer nonsedating antihistamines, such as loratadine, are effective.3 Steroids, sodium cromoglycate, or intranasal antihistamines (eg, azelastine) are also successful treatments for allergic rhinitis.2
Treatment of chronic sinusitis includes a combination of antibiotic, anti-inflammatory, and decongestant therapy.2,3,11,16,17 A 3-week course of antibiotic therapy is needed to treat the most common microbes responsible for sinusitis (Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, and Staphylococcus aureus. In addition, dexbrompheniramine and pseudoephedrine should be used for 3 weeks, followed by nasal steroids, which can be used for up to 3 months. Surgery should be considered for recalcitrant chronic sinusitis.2
Chronic cough is often caused by asthma. Its usual clinical manifestations include some combination of cough, wheezing, dyspnea, and chest tightness. In up to 57% of asthma cases, however, cough is the only presenting symptom18 (cough variant asthma). Given the high prevalence of asthma in patients of all ages, asthma should always be entertained as a cause of chronic cough.
Along with the symptoms noted above, airway hyperresponsiveness19 and reversible airflow obstruction20 can establish a diagnosis of asthma. Degree of obstruction is most accurately assessed by spirometry, which measures forced expiratory volume in 1 second (FEV1). In asthma patients, at least a 12% reversibility of baseline airflow obstruction occurs spontaneously or in response to therapy.20,21 Because reversible airflow obstruction is uncommon in patients with cough variant asthma, their airway hyperresponsiveness must be measured. A methacholine challenge test has a positive predictive value up to 88% and negative predictive value of 100%.2,3,11 While negative results of a methacholine test rule out cough variant asthma, positive results only suggest it. A definitive diagnosis can be made when the cough resolves after a trial of therapy.
Conventional asthma treatment reduces both airway hyperresponsiveness and chronic cough in most patients with cough variant asthma.2,3 Canadian consensus guidelines for asthma include use of β-agonists to relieve symptoms immediately and inhaled corticosteroids (with or without oral corticosteroids, depending on severity) to control inflammation.21 β-Agonists give patients only transitory relief from chronic cough.22 Most patients’ chronic coughs are relieved completely in 6 to 8 weeks2,3 with β-agonists plus either inhaled corticosteroids23 or a combination of inhaled and oral corticosteroids.24 Steroid therapy can be discontinued once the cough stops.2,3 Sometimes cough recurs, especially with exposure to precipitating respiratory irritants or allergens.
Editor’s key points
• Chronic cough, a common condition in adults, can present a diagnostic challenge, although family physicians can readily identify the usual causes.
• The most common causes are postnasal drip syndrome, asthma, and gastroesophageal reflux disease, or a combination of these.
• Chest x-ray examination should be done first to rule out more ominous causes of cough, followed by an empirical trial of therapy directed at the most likely cause based on history and examination. Improvement in the cough confirms the diagnosis.
Conclusion Chronic cough is a common complaint with an extensive differential diagnosis, although most cases are caused by PNDS, asthma, GERD, or some combination of these. Although cough is a protective respiratory clearance reflex, for many adults it is a severe and prolonged health complaint. A systematic approach to diagnosis of chronic cough can reduce much of its morbidity for most of those who suffer from it.
11. Pratter MR, Bartter T, Akers S, Dubois J. An algorithmic approach to chronic cough. Ann Intern Med 1993;119:977-83.
12. Irwin RS, French CL, Curley FJ, Zawacki JK, Bennett FM. Chronic cough due to gastroesophageal reflux: clinical, diagnostic and pathogenetic aspects. Chest 1993;104:1511-7.
13. Irwin RS, Corrao WM, Pratter MR. Chronic persistent cough in the adult: the spectrum and frequency of causes and successful outcome of specific therapy. Am Rev Respir Dis 1981;123:413-7
I think this is a pretty good test to confirm asthma.