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Functional upper airway obstruction and
chronic irritation of the larynx
Functional upper airway obstruction and chronic irritation of the larynx. T.B. Rothe, Luzerner Hoehenklinik, Montana, Switzerland.
W. Karrer. ERS Journals Ltd 1998.
ABSTRACT: Wheezing and dyspnoea are typical symptoms of asthma but can
also be found in diseases of the extrathoracic airways. Functional upper airway
obstruction may imitate, as well as complicate asthma. Functional upper airway
obstruction was first described as a conversion disorder in young females with
inspiratory stridor. Subsequently, it was found that functional upper airway obst-
ruction was more often a secondary phenomenon in chronic asthma also involv-
ing the expiratory laryngeal airflow.

During a period of 15 months, we diagnosed six cases of functional upper air-
way obstruction. Five patients were female and one male, and four were also asth-
matics. Three cases showed chronic sinusitis with postnasal drip (PND) and/or
gastro-oesophageal reflux. Both disorders may irritate the larynx. Treatment of
sinusitis and gastro-oesophageal reflux led to a significant improvement of dysp-
noea in all three of these patients.
In asthma refractory to treatment and in the case of an asthmatic exacerbation
without obvious cause, functional upper airway obstruction should be excluded to
avoid unnecessary treatment with systemic steroids. Some of the possible causative
factors of functional upper airway obstruction, such as postnasal drip and gastro-
oesophageal reflux, are easily treatable.
Eur Respir J 1998; 11: 498–500.
First case reports on functional upper airway obstruc- Patients
tion (FUAO) [1, 2] described young female patientswith inspiratory laryngeal stridor imitating asthma. Thisentity is now called vocal cord dysfunction (VCD) [3]and may represent a distinct subform of functional dis- orders of the larynx. Recently, FUAO has been foundmore often in asthmatics, where it complicates the pri- Patient No. 1, a female aged 62 yrs, had steroid- mary disease [4]. In this situation, pathological adduc- dependent, nonallergic asthma with blood eosinophilia, tion of the vocal cords occurs during inspiration and sinusitis, nasal polyposis and aspirin-intolerance. With expiration. Within 15 months, we diagnosed six cases spheno-ethmoidectomy and aspirin-desensitization, the of FUAO amongst our in-patients. Diagnosis of FUAO daily steroid dose and number of steroid bursts could was based on: 1) a positive history (attacks of breath- be reduced. Nevertheless, she often complained of short lessness not responding to β-agonists and steroids); 2) episodes of dyspnoea, not responding to β-agonists and flattened forced inspiratory flow-volume loop; and 3) being triggered by effort or peak flow measurements.
nasolaryngoscopy (inspiratory or severe early expira- The attacks were accompanied by a conspicuous stri- Five patients were female and one was male, and four Nasolaryngoscopy showed a predominantly inspira- also suffered from asthma. Their ages ranged 42–82 yrs.
tory adduction of the vocal cords, that could be reversed In one case the adduction of the vocal cords was inspi- with administration of 2% Xylocaine with epinephrine ratory, in two cases inspiratory and expiratory, and in (fig. 1). Endoscopy revealed a heavy PND due to chro- three cases there was pure expiratory adduction. One nic sinusitis. The nasal discharge contained up to 80% patient was considered to suffer from a conversion dis- eosinophils. Twenty four hour pH measurement in the order. Three patients had significant reflux verified by oesophagus showed significant gastro-oesophageal re- pH recordings (pH <4 more than 5% of the time), or gas- flux (GER). After treatment with oral and nasal steroids troscopy, respectively. Three patients showed chronic and a combination of omeprazole and cisapride, the se- sinusitis on radiography, and two patients suffered from verity and frequency of dyspnoea attacks decreased sig- clinically defined postnasal drip (PND).
Fig. 2. – Flow-volume curve in the course of methacholine chal-lenge of a patient with vocal cord dysfunction and bronchial asthma.
a) 250 µg methacholine; b) 2,000 µg methacholine. : predicted val-ues; : measured values.
the asthma. Taking the patient's history into account, itwas assumed that a conversion disorder might have Fig. 1. – Inspiratory adduction of the vocal cords with posterior been the causal factor for the VCD. PND and GER chink aperture in an asthmatic patient with gastro-oesophageal refluxand postnasal drip on the basis of a chronic sinusitis.
Patient No. 2, a female aged 70 yrs, had a history of chronic bronchitis since 1983. Lung function showed a Patient No. 4, a female aged 82 yrs, had experienced medium obstruction (not reversible with β-agonists and chronic asthma and sinusitis since 1955, well controlled an oral steroid burst of 10 days) with check valve pheno- with topical steroids. During the last 6 weeks, attacks menon. With physical effort, a loud expiratory stridor of dyspnoea with loud inspiratory stridor had occurred.
(loudest over the larynx) could be heard. Bronchoscopy Nasolaryngoscopy showed inspiratory adduction of the revealed a collapse of the central airways. During early vocal cords and PND. Radiography revealed an obscu- expiration, an adduction of the vocal cords occurred.
red maxillary sinus. Treatment of sinusitis led to a sig- Sinus radiograph and 24 h pH measurement were neg- nificant decrease of attacks of dyspnoea and stridor.
Patient No. 5, a 78 yr old female, had experienced Patient No. 3, a 42 yr old female, formerly a teacher attacks of breathlessness for some months, with expira- in Turkey, emigrated to Switzerland with her husband in tory stridor and aphonia occurring on physical exertion 1987 and found work as a seamstress in a factory. Since and when speaking loudly. Asthma or bronchitis had 1993, she had suffered from sudden attacks of severe never been diagnosed. Lung function and methacholine dyspnoea, which never occurred during sleep. They did challenge were normal. Nasolaryngoscopy showed in- not respond to β-agonists and long-term high-dose oral flammation of the laryngeal mucosa and an expirational steroid treatment. Between acute attacks, the flow-vol- adduction of the true and the false vocal cords. A radi- ograph of the sinus was negative. Twenty four hour pH Methacholine challenge led to an overall decrease of measurement revealed massive reflux (for 40% of the expiratory flows (Tiffeneau index (forced expiratory vo- time between 10:00 and 22:00 h). Treatment with ome- lume in one second (FEV1)/forced vital capacity (FVC) prazole and cisapride led to a significant improvement in per cent) remained normal) and a flattening of the of the attacks of breathlessness and aphonia.
forced inspiratory flow-volume curve. The patient com-plained of acute dyspnoea, and a loud inspiratory stridorcould be heard over the larynx. The lungs were clear.
She refused nasolaryngoscopy. Methacholine challengewas then continued. Up to a cumulative dose of 1,500 Patient No. 6, a male aged 78 yrs, had steroid-depen- µg methacholine, the Tiffeneau index remained stable.
dent nonallergic chronic asthma. An acute deterioration At 2,000 µg, the index decreased, the expiratory flow- of the asthma caused a fall in FEV1 to 1.28 L, with occur- volume curve showed a concave shape and wheezing rence of an expiratory stridor over the larynx. Endoscopy could be heard over both lungs (fig. 2). This was inter- revealed a 40% stenosis of the trachea by intrathoracic preted as a mild asthma complicated by VCD. Reduction goitre, a functional tracheal collapse when coughing of of oral steroids to zero did not cause a deterioration of about 70%, and a pathological adduction of the vocal cords in early expiration. A sinus radiograph was positive young females, where inspiratory VCD has imitated asth- for chronic sinusitis, but no sign of PND was detected.
ma [10]. Most of the present patients suffered from ste- Gastroscopy showed an ulcer and a reflux oesophagi- roid-dependent asthma. PND and GER were identified tis. After an oral steroid burst and omeprazole therapy, as causal factors of FUAO in 50% of these patients. Se- FEV1 increased to 2.16 L and expiratory stridor sub- vere asthma complicated by PND and GER might occur more often in later life. This would explain why the meanage in the present group of patients was higher than inclassical forms of VCD.
Bearing in mind that some forms of functional upper airway disorder might be caused by chronic irritation of We have recently diagnosed six cases of FUAO. All the larynx, as by postnasal drip and gastro-oesophageal patients complained of recurrent attacks of breathless- reflux, this relationship offers a new approach to the ness not responding to β-agonists, and previous ambu- latory treatment. Four of the six patients also sufferedfrom asthma and one from chronic bronchitis. In one case,with identification of FUAO, we succeeded in stoppingoral steroids without deterioration of the asthma.
Three subforms of FUAO could be differentiated in these patients: 1) a patient with features of classical VCD, Patterson R, Schatz M, Horton M. Münchhausen's stri- where inspiratory FUAO seems to be a symptom of an dor: nonorganic laryngeal obstruction. Clin Allergy 1974; underlying conversion disorder; 2) two patients with central airway instability and severe asthmatic obstruc- Christopher KL, Wood RP, Eckert C, Blager FB, Raney tion, respectively. Adduction of the glottic chink aper- RA, Souhrada JF. Vocal cord dysfunction presenting as ture during early expiration, also called laryngeal- or asthma. N Engl J Med 1983; 308: 1566–1570.
auto-positive end-expiratory pressure (PEEP), seems to Wood RP, Milgrom H. Vocal cord dysfunction. J imitate the effect of pursed lips breathing [5, 6]; and 3) Allergy Clin Immunol 1996; 98: 481–485.
in the remaining three patients, PND and/or GER could Newman KB, Mason UG, Schmaling KB. Clinical fea- tures of vocal cord dysfunction. Am J Respir Crit Care The vocal cords are primarily designed to prevent pe- netration of fluids or foreign bodies into the lower air- Wood RP, Jafek BW, Cherniack RM. Laryngeal dys- ways by rapid closure. Reflux may reach the vocal cords.
function and pulmonary disorder. Otolaryngol Head Neck Development of posterior laryngitis [7] and acute clo- sure of the vocal cords due to massive GER (Mendel- Collet PW, Brancatisano AP, Engel LA. Upper airway son's syndrome) has been described. Therefore, it is not dimensions and movements in bronchial asthma. AmRev Respir Dis 1986; 133: 1143–1149.
surprising that by irritating the larynx GER may trigger Kamel PL, Hanson D, Kahrilas PJ. Omeprazol for the a functional adduction of the vocal cords [8].
treatment of posterior laryngitis. Am J Med 1994; 96: In an interesting study, BUCCA et al. [9] showed that PND can lead to extrathoracic airway hyperreactivity Campbell HA, Perce R. Brief upper airway dysfunction.
(EAHR), with significant reduction of the mid-inspira- Respir Med 1994; 88: 125–129.
tory flow at 50% of vital capacity during methacholine Bucca C, Rolla G, Scappaticci E, Chiampo F, Bugiani challenge. EAHR shares many features with FUAO. PND M. Extrathoracic and intrathoracic airway responsive- might, therefore, be another causal cofactor in the de- ness in sinusitis. J Allergy Clin Immunol 1995; 95: 52–59.
Mobeireek A, Alhamad A, Al-Subaei A, Alzeer A. Psy- Case reports published on FUAO in the past have chogenic vocal cord dysfunction simulating bronchial presented patients with conversion disorders, mostly asthma. Eur Respir J 1995; 8: 1978–1981.



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