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HYPERTONIC SALINE CHALLENGE IN THE DIAGNOSIS OF VOCAL CORD DYSFUNCTION IN PATIENTS WITH ASTHMA ATTENDING A SECONDARY CARE CLINIC

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Published
  • V. K. Reay
  • I. Susnerwala
  • R. B. Gore
  • S. J. Fowler
  • Jemma Haines
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<mark>Journal publication date</mark>12/2009
<mark>Journal</mark>Thorax
Issue numberSuppl. 4
Volume64
Number of pages4
Pages (from-to)A72-A73
Publication StatusPublished
<mark>Original language</mark>English
EventWinter Meeting of the British-Thoracic-Society - London
Duration: 2/12/20094/12/2009

Conference

ConferenceWinter Meeting of the British-Thoracic-Society
CityLondon
Period2/12/094/12/09

Abstract

Introduction Symptoms of vocal cord dysfunction (VCD) are caused predominantly by vocal cord adduction during inspiration. It is commonly seen in the asthma clinic, both where asthma has been misdiagnosed and as an additional diagnosis. The current “gold standard” for diagnosis of VCD is direct visualisation of the vocal cords during laryngoscopy. A flow volume loop recorded whilst symptomatic may also demonstrate an abnormal pattern, and VCD may be induced in susceptible subjects—for example, by hypertonic saline (HS) challenge. Taramarcaz and colleagues (J Allergy Clin Immunol. 2004) have reported a decrease in forced inspiratory flow (FIF50) after HS challenge in a case series of three patients with postviral VCD.

Methods We designed a prospective, controlled study to determine whether HS challenge testing provokes VCD, as evidenced by changes in FIF50 and visual analogue scores (VAS). Baseline questionnaires (Hospital Anxiety Depression Score (HAD), adapted John Hunter Cough Questionnaire (aJHCQ) and a VCD VAS) were completed, then HS challenge performed, with a shortened VAS and spirometry recorded after each dose interval.

Results Twenty-seven subjects (mean (range) age 38 (21–62) years, 38% male) completed the study, seven subjects with VCD (6 with a previous diagnosis of asthma), six physician-confirmed asthma alone and 14 healthy controls (HCs). Subjects with VCD were older, with higher HAD, baseline VAS and aJHCQ scores than the other groups. As expected, HS induced a greater fall in forced expiratory volume in 1 s (FEV1) in the group with asthma than in the VCD or HC groups. However, change in FIF50 after the final dose of HS did not significantly differ between groups. The change in mean VAS score, and particularly items 1 and 2, discriminated between VCD and the other groups during HS challenge (table 1).

Conclusion FIF50 may not be a useful dynamic marker of VCD during HS challenge, but our modified VCD VAS did show symptom changes in subjects with VCD compared with those with asthma and healthy controls. This tool could potentially be used in the diagnosis and treatment of VCD after further evaluation and validation.