As otolaryngologists, we often see patients who have both sinonasal and lower airway symptoms and ask this question. The relationship between inflammatory conditions of the upper and lower airways is well recognized and has resulted in the unified airway hypothesis. When the upper airway is affected with allergic rhinitis, there is concern regarding the "atopic march". It appears that as inflammation of the respiratory tract develops, it typically begins in the upper airway and then progresses to the lower airway. When the upper airway is affected with chronic rhinosinusitis (CRS), studies have demonstrated that 25-30% of CRS patients have been diagnosed with asthma^{1, 2}. Conversely, 80-94% of asthmatics already have involvement of the upper airway with rhinitis and/or CRS with nasal polyps (CRSwNP)^1-3. This progression of disease from the upper airway to the lower airway was demonstrated by Williamson² who examined a cohort of patients with CRSwNP and found that while 39% had diagnosed asthma, an additional 30% had subclinical asthma. While they had no clinical symptoms, these patients had signs of inflammation on fractional exhaled nitric oxide (FENO) or pulmonary function tests (PFTs). Only 31% of CRS patients had no evidence of lower airway involvement. Thus there are a significant number of patients who present with upper airway symptoms and have subclinical inflammation of the lower airway, but once lower airway disease has developed, there is a high likelihood that the upper airway is already involved.

Williamson⁴ examined CRSwNP patients and found that serum eosinophilia, but not clinical staging of sinus disease with endoscopy or symptom scores correlated with objective lung function. This is not surprising given that all CRS patients had CRSwNP, thus representing the most severe spectrum of upper airway disease. A number of inflammatory markers in the nasal mucus of CRS patients, including total IgE, Staphylococcus aureus enterotoxin (SAE) IgE, and markers of eosinophilic inflammation, may be important predictors for asthma⁵ but are not currently used widely in clinical practice. Conversely, in patients already diagnosed with asthma, severity of asthma is associated with nasal polyposis and worse CT scores¹. So for now, when patients present to us for CRS evaluation, we must simply maintain a high level of suspicion in patients with lower airway symptoms and work up should include pulmonary function tests with challenge.

Will medical or surgical treatment of the upper airway improve asthma?

Prior studies have examined the impact of medical and/or surgical therapy of CRS upon asthma outcomes. Both medical and surgical treatments of CRS do improve asthma symptoms, however lack of standardized medical treatment protocols make it difficult to determine superiority of one modality over the other. Current practice is typically to reserve surgery for patients who have failed aggressive medical therapy. Surgery for the patient with CRS and asthma must take into consideration that patients will likely need postoperative topical therapies with steroids to control the underlying mucosal inflammation. Evidence supports surgery to open the sinuses widely and then use of large volume delivery so that steroid medication is able to reach the paranasal sinuses⁶. Newer delivery techniques, such as steroid eluting stents, may play a role in the future.

Endoscopic view of left sided sinuses in patient with aspirin exacerbated respiratory disease who underwent her 4th surgery. Widely patent Lothrop cavity and ethmoid sinuses for access of steroid irrigations resulting in no polyps and no systemic steroids for CRS or asthma in the last 2 years.