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Subglottic Stenosis, Other Considerations.
- Ali S Mallick, S. Chaudhry, S. Phillips and B. Al-Shaikh (26 March 2008)
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Ali S Mallick Worthing Hospital, S. Chaudhry, S. Phillips and B. Al-Shaikh
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Editor- We read the case report by Scholz A (1) on subglottic stenosis (SGS) in pregnancy with great interest. The report states that SGS is often misdiagnosed as asthma or recurrent bronchitis. We have recently reported a case of a patient with SGS who presented with a year long history of progressive dyspnoea (2). A month after initial onset she presented to her GP and underwent cardio-respiratory investigations which were unremarkable. In view of the absence of any ‘organic’ cause for her dyspnoea, the patient tried to ignore her symptoms and continue with her daily activities. Towards the end of the year her symptoms worsened such that excessive talking would leave her gasping for breath. Additionally she developed hoarseness, prompting the GP to refer her to an ENT specialist. The patient was medically well otherwise, with no history of tracheal intubation or trauma to the neck and no relevant ENT history. CT scan confirmed the presence of a short segmental focal stenosis in the sub- glottic region, for which she underwent endoscopic resection. Histology of the lesion was non-specific and in the absence of any clear aetiological factor, a diagnosis of idiopathic SGS was made. It is clear from both our cases and other reports in the literature (3) that in patients presenting with progressive dyspnoea without any clear cardio-respiratory cause, one must consider the diagnosis of SGS. The report mentions that the patient had unremarkable cANCA levels, which suggested that her Wegeners Granulomatosis (WG) had not worsened. Although elevated cANCA levels are highly specific for WG, 10% of patients may have positive pANCA levels and 20% of patients lack ANCA altogether (4). Thus, knowing the patient’s pANCA levels and ESR may have given further clues on the aetiology of SGS. Furthermore, knowledge of the patient’s ANCA levels at the time of her initial diagnosis would have also helped in the diagnostic process. The authors felt that the cause of the patient’s SGS was probably due to her initial presentation of WG and subsequent intubation 10 years prior to this presentation. Whilst there are a few reports of isolated involvement of the subglottis in WG in the literature (5), it is a rare phenomenon. In one particular case series examining patients with SGS due to WG, none of them had the disease confined to the subglottic region (3). In the absence of any significant evidence of WG, it is likely that the cause of this patient’s SGS was solely due to the period of prolonged tracheal intubation she experienced 10 years ago. The aetiology of SGS can be particularly difficult to deal with. Although tracheal intubation is the most common cause, there are no reports in the literature looking at the correlation between the duration of tracheal intubation and the development of subglottic stenosis. Comparison between studies is also difficult, with varying definitions of ‘prolonged tracheal intubation’. In conclusion, SGS can cause difficulties to the clinician through its ‘misleading’ presentation and the subsequent study to unravel its aetiology. References 1. Scholz A, Srinivas K, Stacey MRW, Clyburn. Subglottic stenosis in pregnancy. Br J Anaesth 2008; 100 (3): 385-8. 2. Mallick AS, Chaudhry S, Philips S, Al-Shaikh B. Aetiological factors of subglottic stenosis. The Otorhinolaryngologist (in press). 3. Alaani A, Drake Lee AB. Wegener’s granulomatosis and subglottic stenosis: management of the airway. Journal of Laryngology and Otology 2004; 118:786-790 4. Seo P, Stone JH. The antineutrophil cytoplasmic antibody- associated vasculitides. Am J Med 2004; 117:39–50 5. D Hellmann, T Laing, M Petri, D Jacobs, R Crumley, and M Stulbarg. Wegener's granulomatosis: isolated involvement of the trachea and larynx. Ann Rheum Dis. 1987 August; 46(8): 628–631. Conflict of Interest:None declared |
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