Case report 1
A five-year-old male was being treated for asthma with inhaled steroids. Symptoms were recurring coughs, night coughs and daytime fatigue. No response to this therapy was observed and repeated courses of antibiotics also made no impression. Parents advised he was a “difficult asthmatic”. Reviewed elsewhere: Child had upper airways obstruction and sleep apnoea. An x-ray of the post-nasal space showed enlarged adenoids obstructing his airway.Adenoidectomy produced a dramatic turn around in the boy’s health and all inhalers were abandoned. He no longer has coughs, night-time or otherwise. He is bright and alert and in good health. His ‘asthma’ was cured surgically. Conclusion: His upper airway obstruction was producing lower airway symptoms.
Case report 2
A seven-year-old boy presents with troublesome asthma, not controlled with adequate doses of inhaled steroids. Breakdown in control is preceded by ‘head cold’. History of atopy in family but no attention paid to parents’ request for allergy testing (‘waste of time, could be anything, try lifting the carpets’). They were advised the boy had difficult asthma that was viral-driven. However, evaluation revealed a child with clinical rhinosinusitis (swollen, pale and boggy nasal mucosa. Oedematous changes in upper poles both nostrils). Scattered wheeze observed in both lungs despite adequate anti-asthma therapy. Allergy testing revealed strong positives to dust mites and cat hair (cat, family pet, often slept on boy’s bed). Management included an aggressive anti-allergy regimen, restoring his nasal mucosa to normal and stabilising with inhaled nasal steroid. Because of the combination of upper and lower allergic airways, he was started on a leukotriene antagonist. The boy showed dramatic improvement and chest symptoms abated. He was able to reduce inhaled (lung) steroids by 80 per cent. He now has excellent symptom control and his inhaled steroid load has been reduced. Conclusion: Upper airways were impacting on his lower airways. Selected drug therapy gave symptom control without concerns of steroid side-effects.Introduction
“I feel, without disrespecting the scientific community too much, that there should be some conclusions from this. We are over-thinking science in too many ways.” The words of Simon Meehan, 15-year-old winner of this year’s BT Young Scientist of the Year award. He was awarded the prize after presenting his discovery of a natural antibiotic in a blackberry bramble plant in his back garden. “People,” he continued, “are going deep into the Amazon rainforest looking for new antibiotics. But I’m a 15-year-old boy who found this down his own back garden.” Sometimes — like Simon’s discovery — what is staring you in the face can enlighten your understanding of certain medical conditions. How frustratingly true this is in the management of asthma. Maybe we are over-thinking treatments. Maybe the reliance on inhaled drugs is wrong. Maybe (damned sure) it is time to re-think strategies. Current asthma guidelines seem straightforward: Inhaled beta2-agonists for occasional or exercise-induced asthma. Inhaled steroids for moderate asthma, or combination long-acting beta2-agonists with steroids. Warnings are issued on the dangers and ineffectiveness of high doses of inhaled steroids in troublesome asthma. In essence, if you go past a certain point, there is little benefit and a risk of systemic absorption. Nowhere in the many words of wisdom is there mention of a link between upper airway pathology and lower airway symptoms. Nowhere are there practical and useful guidelines on the correct management of coexisting rhinosinusitis and asthma. Nowhere is there mention of the (now accepted) connection between untreated upper respiratory pathology and poor asthma control. In simple English, the answer to asthma is as plain as the nose on your face. It starts there and continues unabated if the nasal-sinus component is not treated properly. Let’s start with facts: A clinical relationship between allergic rhinitis and asthma has been defined for some time and patients commonly present with both disorders (Figure 1). There is an increasing body of evidence confirming the existence of a clear link between upper and lower airways. Allergic rhinitis and asthma are connected epidemiologically, anatomically, physiologically, immuno-pathologically and therapeutically (see photographs A and B).Allergic rhinitis
Many children with bronchial asthma also have allergic rhinitis. When allergic rhinitis is very active, airway hyper-responsiveness increases, often aggravating the symptoms of asthma. Furthermore, the onset of allergic rhinitis sometimes precedes bronchial asthma and the onset of asthma may be prevented by successful treatment of allergic rhinitis (Figure 1).Allergic rhinitis involves the sinuses as well as the nose.
Allergic rhinitis may cause nose and sinus symptoms only.
Allergic rhinitis may provoke lower airways hyper-reactivity.
Allergic rhinitis (untreated, poorly treated, etc) may eventually trigger asthma.
Allergic rhinitis may coexist with asthma.
Allergic rhinitis (untreated) may allow nasal polyps to develop.
Coexistent allergic rhinitis in asthmatic children causes more asthma-related hospital admissions and greater total days spent in hospital. What are the implications of this in daily practice? Set aside guidelines (they are not writ in stone) and consider the whole respiratory tract in any child or adult with suspected or established asthma. Evaluate the nose and sinuses in the same way you listen for wheeze and do peak flow readings. Do separate symptom scores for upper and lower airways (Tables 1 and 2). Before prescribing, remember that the upper airways (nose and sinuses and post-nasal space) influence the lower airways (lungs). Pathology in the upper airways can produce symptoms in the lower respiratory tract. Treat the upper respiratory pathology and you can alleviate or even cure the lower respiratory trouble.
Guidelines
If you suspect asthma, look for any trigger factors (allergy, passive smoking, rhinosinusitis or upper airway obstruction). Allergy test to evaluate the situation more clearly and hopefully identify significant inhaled allergens involved in the problem. You have a better chance of parental co-operation in ongoing management if they feel you are being thorough and not ‘prescription-happy’. (Many doctors say they don’t believe in allergy tests when they really mean they don’t know how to do them, don’t know how to interpret them, couldn’t be bothered as workload is hard enough, etc, etc. It is no big deal, very interesting and will further your understanding of your asthma patients significantly.) Do symptom scores for upper and lower airways. Management protocols begin by dealing with any upper airway pathology. This will produce a significant improvement in all symptoms. For improved but persisting asthma, do not start inhaled steroids but consider adding a leukotriene receptor antagonist (montelukast). This ‘disease modifier’ may protect the patient from further steroid load, or at least minimise the dose. Other than producing a symptom-free patient, you will have relieved the not-insignificant discomfort of untreated rhinosinusitis. Now re-check the upper and lower airway symptom scores; there should be a significant improvement in both. In the 1980s, the catch-cry in paediatrics was the ‘under-diagnosis and under-treatment of asthma’. I believe that term could now be applied to allergic rhinitis. Challenge anyone who uses the phrase ‘viral-driven’ in respiratory problems. It usually reflects a lack of understanding of nasal symptoms. Look up more noses. Suggested reading: Riccio et al, Clin Exp Allergy 2002; 32:422-6, where the authors explore the link between upper and lower airways in great detail and offer the concept of united airways disease.References available on request
