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Nose and paranasal sinuses

respiratory tract infection (URI) and tested their cough sensitivity to capsaicin, a known inducer of cough reflex [14]. They found a decreased threshold to coughing during the infection. Thresholds returned to baseline when retested 4–8 weeks after their URI [13]. Patients with chronic cough may have an increased baseline sensitivity to environmental irri tants termed sensory hyperactivity. A cross sectional study of patients with chronic cough showed that a high proportion of patients noted increased sensi tivity to chemical irritants on standard question naires [15]. Following that study, Ternesten-Hasseus et al. performed capsaicin inhalation testing on the subset of these patients they deemed chemical-sen sitive patients and showed an increase in sensitivity to capsaicin-induced cough. Moreover, the testing with capsaicin generated symptoms of rhinitis during provocation suggesting that patients with airway hypersensitivity may mimic symptoms of allergic rhinitis [16]. Further research needs to be performed to better understand the role of sensory hypersensitivity in the chronic cough paradigm. EVALUATION AND MANAGEMENT UACS/PND remains a clinical diagnosis [5]. Nasoen doscopy performed by an otolaryngologist may identify rhinitis or mucopurulent discharge but these findings are suggestive and not diagnostic [17]. As one reviewer put it, ‘the differential diag nosis of PND-induced cough includes all other causes of rhinitis, including, allergic rhinitis, peren nial nonallergic rhinitis, bacterial sinusitis, allergic, fungal sinusitis, rhinitis because of anatomic sino nasal abnormalities, rhinitis because of physical or chemical irritants, occupational rhinitis, rhinitis medicamentosa, and rhinitis of pregnancy’ [17]. Initial evaluation should include a detailed history and physical examination outlining the details and nature of the chronic cough symptom. As noted earlier, smoking history and smoking related pulmonary diseases or use of ACE inhibitor should be evaluated as possible sources of cough. Chest radiographs should be performed to rule out pulmonary cause. If negative, then the cough may likely be attributed to one or a combination of CVA, GERD, or PND [3]. See Fig. 1 for a checklist for work up and management of PND. CVA is associated with approximately 25% of patients with chronic cough [2,18]. It is a challeng ing diagnosis as patients with asthma and cough as their primary symptom may have a normal spiro metry. Diagnosis is confirmed after improvement of symptoms with use of antiasthmatic therapies such as inhaled bronchodilators or steroids [19]. Empiric

Several studies support this century old argu ment that increases in nasal secretions coursing posteriorly into the larynx and pharynx is the cause of irritation and chronic cough. Irwin et al. [7] reviewed nine patients with evidence of PND and found extrathoracic obstruction that they proposed was secondary to stimulation of cough receptors in the hypopharynx and larynx by secretions leading to edema. Bucca et al. [8] evaluated patients with PND and sinusitis and identified airway hyperres ponsiveness, with reflexes originating in pharynx made hypersensitive by local seeding of the inflam matory process from secretions. During this same time period, other studies have called into question the cause of postnasal drip. Pratter et al. reported upwards of 20% of patients with diagnosis of PND will not have evidence of nasal secretions, coining the term ‘Silent PND’. O’Hara and Jones [9] examined 89 patients with sinusitis and purulent drainage to the back of the throat described as PND and found that only nine patients (8%) who had nasal secretions on physical examination had cough. Such studies call into ques tion the direct relationship between secretions and mucosal irritation in PND. Because of the controversy behind the patho physiology of PND, in 2006 the American College of Chest Physicians (ACCP) coined the term upper airway cough syndrome (UACS) to replace Dobell’s 150-year-old term citing that it is ‘unclear whether the mechanism of cough is PND, direct irritation, or inflammation of the cough receptors in the upper airway’ [5,10]. New evidence suggests that a subset of patients diagnosed with UACS may have less to do with chronic laryngeal and pharyngeal irritation from nasal secretions and more related to a baseline cough hypersensitivity [11,12]. Increased sensitivity of upper airway for coughing from irritants is an established phenomenon. Dicpinigaitis et al. [13] looked at 24 patients suffering from an acute upper KEY POINTS UACS/PND lacks objective diagnostics and has variable symptoms making clinical diagnosis difficult. Evaluation of UACS/PND should include rule out of smoking, ACE inhibitor use, GERD, and CVA. Treatment should be directed at source of UACS/PND. Use of first generation antihistamine and consideration of workup for sinonasal disease in patients with UACS/ PND without evidence of underlying source.

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Volume 24 Number 1 February 2016

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