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Year : 2019  |  Volume : 8  |  Issue : 2  |  Page : 127-129

Postintubation tracheal stenosis: Report of two cases and literature review

Department of Pulmonary Medicine, SS Institute of Medical Sciences and Research Centre, Davanagere, Karnataka, India

Date of Submission03-Dec-2018
Date of Decision24-Dec-2018
Date of Acceptance18-Jan-2019
Date of Web Publication1-Jul-2019

Correspondence Address:
Dr. Eti Ajit
Department of Pulmonary Medicine, SS Institute of Medical Sciences and Research Centre, Davanagere, Karnataka
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijrc.ijrc_51_18

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Tracheal stenosis(TS) is a well-recognized yet underdiagnosed complication of prolonged intubation. Mechanisms include tracheal injury during intubation and ischemia of tracheal mucosa at the site of the endotracheal tube cuff and resultant fibrotic stenosis. TS usually develops 3–6weeks following extubation and is often misdiagnosed as bronchial asthma. We report two such cases who developed TS following prolonged intubation.

Keywords: Endotracheal tube cuff pressure, postintubation tracheal stenosis, prevention

How to cite this article:
Ajit E, Banur A, Bondade K, Raykar P. Postintubation tracheal stenosis: Report of two cases and literature review. Indian J Respir Care 2019;8:127-9

How to cite this URL:
Ajit E, Banur A, Bondade K, Raykar P. Postintubation tracheal stenosis: Report of two cases and literature review. Indian J Respir Care [serial online] 2019 [cited 2022 Aug 18];8:127-9. Available from: http://www.ijrc.in/text.asp?2019/8/2/127/261906

  Introduction Top

Tracheal stenosis(TS) is a serious complication of common procedures performed in intensive care such as endotracheal intubation and tracheostomy. The incidence of TS following intubation and tracheostomy ranges from 10% to 22%.[1],[2],[3] The advent of endotracheal tubes(ETT) with high volume and low-pressure cuff has dramatically reduced its incidence. However, the incidence of iatrogenic TS still remains as high as 11% in critically ill patients on prolonged intubation.[3]

TS is typically a long-term complication of intubation. It manifests clinically 3–6weeks following the injury in the form of progressive dyspnea and wheeze/stridor. The presentation can mimic obstructive airway disease such as bronchial asthma or chronic obstructive pulmonary disease(COPD). We present two such cases of postintubation TS who were initially misdiagnosed as asthma/COPD.

  Case Reports Top

Case 1

A 62-year-old female, known case of ischemic heart disease and hypertension, presented to us with chronic cough, dyspnea on exertion, and wheezing of 3weeks duration. Symptoms were insidious in onset and gradually progressive. She denied a history of fever, chest pain, expectoration, hemoptysis, loss of weight, or appetite. Her chest radiograph and blood investigations were normal. General examination was normal. Bilateral wheeze was heard on her chest auscultation. She could not perform spirometry and her nasopharyngolaryngo scopy was normal. She was initially diagnosed to have COPD clinically and was treated for the same. Since her symptoms persisted, her past history was probed in detail. Two months before the onset of symptoms, she had been mechanically ventilated for 7days for cardiogenic shock secondary to myocardial infarction. With this background, TS was suspected. Computed tomography(CT) of the neck and the upper thorax revealed a stenotic area 4cm above the carina. Diagnostic bronchoscopy showed multiple-web-like stenosis in the upper trachea occluding 70%–80% of the lumen[Figure1]. It was diagnosed with Grade 3 TS according to the Myer-Cotton system for grading of stenosis.[4] She underwent balloon dilatation at a higher center and her stridor got relieved in the immediate postprocedure period.
Figure1: Bronchoscopy image of tracheal stenosis(Case 1)

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Case 2

A 24-year-old young male nonsmoker was referred to our department as uncontrolled bronchial asthma not responding to bronchodilators. He had 2weeks of unproductive cough and wheeze. His general physical examination was normal. On auscultation, he had bilateral expiratory wheeze. Chest radiograph was normal. Pulmonary function tests showed reduction in the expiratory flow rate. Since the patient gave a history of organophosphorus poisoning and was on mechanical ventilation for about 10days–1month before the onset of symptoms, TS was suspected. Diagnostic bronchoscopy was done and it showed significant mid-tracheal stenotic segment occluding 70%–80% of the tracheal lumen(Myer-Cotton Grade3 stenosis)[Figure2]. The patient underwent balloon dilatation successfully at a higher center and is presently doing well without any symptoms.
Figure2: Bronchoscopy image of tracheal stenosis(Case 2)

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  Discussion Top

Postintubation TS was first recognized by MacEwen in 1880[5] but it remains an important cause of acquired tracheal obstruction. Tracheal or subglottic stenosis is seen in 10%–22% of the patients on prolonged intubation.[1],[2],[3] Incidence in the general population is roughly 4.9cases per million per year.[6]

Laryngotracheal stenosis is typically a late complication of endotracheal intubation which takes weeks to months to develop. The risk of developing stenosis is increased in those who are intubated for>7days and is rare if the intubation is for short periods(<3days).[7],[8] However, tracheal damage and subsequent stenosis can occur in any patient after the intubation of any duration even as short as 24h.[9]

Ischemia and subsequent fibrosis of the tracheal mucosa at the site of ETT cuff are thought to be the mechanism of stenosis. ETT cuff pressure plays a crucial role in the development of stenosis. The mean capillary pressure of tracheal mucosa approximately ranges between 20 and 30 mmHg.[10] If the cuff pressure exceeds 30 mmHg, the underlying mucosa will suffer regional blood loss leading to ischemic ulceration and destruction of cartilage. The subsequent reparative process in the form of granulation tissue formation and scarring results in lumen stricture and stenosis. Introduction of ETTs with large area of contact, i.e., high volume and low-pressure cuffs have largely cut down the incidence of cuff injury and subsequent stenosis.[3],[11],[12]

It is mandatory to monitor ETT cuff pressure in patients who are intubated at least on a daily basis. Other factors that can influence the cuff pressure, including tracheal size, ETT size, ventilatory pressures, and patient position.[13] However, as a general guideline, the cuff pressure should be maintained between 20 and 30cm H2O.[10]

Hypovolemia and circulatory collapse can be another substantial risk factor for TS as it can worsen the local ischemia of tracheal mucosa in contact with ETT cuff. Other important factors that have a predominant role in the development of TS are traumatic intubation, history of previous intubation or previous tracheostomy, size of the tube relative to the tracheal lumen, and the use of high-dose steroids. Ahistory of smoking, obesity, extremes of age, female and estrogen effect, severe gastroesophageal reflux disease, and radiation therapy for oropharyngeal and laryngeal cancer are also known risk factors for the development of TS.[14],[15],[16]

The incidence of TS can be reduced by preventing trauma during intubation. This can be achieved by the use of adequate sedation or muscle relaxant during intubation and avoidance of using large size ETT tube(>8mm in men and>7mm in women). Measures like maintaining good oral hygiene in intubated patients using oral antiseptics such as oral chlorhexidine, regular oral and ET suctioning, and anti-reflux measures should be undertaken to prevent microaspiration. Achieving swift hemodynamic stabilization is of paramount importance in patients with hypovolemic shock.

Postintubation TS can have atypical clinical presentation and is often misdiagnosed as asthma or COPD at initial presentation in as many as 44% of patients.[17] These patients present with progressive exertional dyspnea, wheezing/stridor, and unproductive cough. The clinical manifestation of TS depends on the severity of the stenosis and manifest in the later part of the disease process. In most cases, significant anatomic obstruction precedes the development of symptoms. By the time dyspnea on exertion occurs, the airway diameter at the site of obstruction is likely to be reduced to about 8mm(corresponding to 80% reduction in the tracheal lumen). Dyspnea at rest and stridor often develop when the airway diameter is about 5mm(>90% reduction).[18] Hence, these patients may remain asymptomatic for 3–6weeks until trachea is reduced to at least more than half of its original diameter.[19],[20] Further, the probability of these patients consulting primary care physician at peripheral setup is high. It requires a detailed history taking and high index of suspicion from the primary physician to suspect TS. Although one is expected to easily distinguish stridor from wheezing which originates from the lower airways, sound recordings from the neck and chest have shown that the sounds from the asthmatic wheeze and stridor have similar frequencies.[18] This often leads to misdiagnosis of these patients as asthma/COPD. Hence, awareness of postintubation TS among all primary care providers is essential for the early diagnosis.

Bronchoscopy is the definitive diagnostic modality in these cases and helps in grading the stenosis. According to the Myer-Cotton system of grading, it is classified as Grade1(<50% occlusion), Grade2(50%–70% occlusion), Grade3(71%–90% occlusion), and Grade4(100% occlusion).[4] It can also rule out differential diagnosis such as tracheomalacia, vocal cord dysfunction, and malignancy. Other modalities such as CT of the neck/thorax and virtual bronchoscopy(three dimensional imaging of airways using CT) can be helpful in establishing the diagnosis when bronchoscopy is not feasible. Spirometry of these patients shows characteristic flattening of both inspiratory and expiratory portions of flow-volume loop with “box pattern” suggestive of fixed upper airway obstruction.

Treatment options for postintubation TS include balloon dilatation, laser resection, and stent implantation. Tracheal sleeve resection and end-to-end anastomosis are the definitive surgical treatment. The choice of treatment modality depends on the severity of TS and general condition of the patient.

  Conclusion Top

Patients with a history of prolonged intubation or tracheostomy who present with dyspnea, cough, or wheezing should be evaluated for postintubation TS. Although TS is a well-recognized complication of prolonged intubation, it remains an underdiagnosed entity. Awareness among primary care physician is the immediate need. Careful and detailed history taking with a high index of suspicion leads to early diagnosis and prompt referral. Simple measures such as routine ETT cuff pressure monitoring in intubated patients can reduce its incidence.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

  References Top

PearsonFG, AndrewsMJ. Detection and management of tracheal stenosis following cuffed tube tracheostomy. Ann Thorac Surg 1971;12:359-74.  Back to cited text no. 1
GrilloHC, DonahueDM, MathisenDJ, WainJC, WrightCD. Postintubation tracheal stenosis. Treatment and results. JThorac Cardiovasc Surg 1995;109:486-92.  Back to cited text no. 2
StaufferJL, OlsonDE, PettyTL. Complications and consequences of endotracheal intubation and tracheotomy. Aprospective study of 150 critically ill adult patients. Am J Med 1981;70:65-76.  Back to cited text no. 3
Myer CM 3rd, O'ConnorDM, CottonRT. Proposed grading system for subglottic stenosis based on endotracheal tube sizes. Ann Otol Rhinol Laryngol 1994;103:319-23.  Back to cited text no. 4
MacewenW. Clinical observations on the introduction of tracheal tubes by the mouth, instead of performing tracheotomy or laryngotomy. Br Med J 1880;2:163-5.  Back to cited text no. 5
BrichetA, RamonP, MarquetteCH. Stenosis and tracheal complications after intubation. Reanimation 2002;11:1-10.  Back to cited text no. 6
Tadié JM, BehmE, LecuyerL, BenhmamedR, HansS, BrasnuD, etal. Post-intubation laryngeal injuries and extubation failure: Afiberoptic endoscopic study. Intensive Care Med 2010;36:991-8.  Back to cited text no. 7
WhitedRE. Aprospective study of laryngotracheal sequelae in long-term intubation. Laryngoscope 1984;94:367-77.  Back to cited text no. 8
YangKL. Tracheal stenosis after a brief intubation. Anesth Analg 1995;80:625-7.  Back to cited text no. 9
American Thoracic Society, Infectious Diseases Society of America. Guidelines for the management of adults with hospital-acquired, ventilator-associated, and healthcare-associated pneumonia. Am J Respir Crit Care Med 2005;171:388-416.  Back to cited text no. 10
NordinU. The trachea and cuff-induced tracheal injury. An experimental study on causative factors and prevention. Acta Otolaryngol Suppl1977;345:1-71.  Back to cited text no. 11
VerhulstJ, AdjouaRP, UrtazunH. Laryngeal and tracheal complications of prolonged intubation. Rev Laryngol Otol Rhinol(Bord) 1992;113:289-94.  Back to cited text no. 12
LizyC, SwinnenW, LabeauS, PoelaertJ, VogelaersD, VandewoudeK, etal. Cuff pressure of endotracheal tubes after changes in body position in critically ill patients treated with mechanical ventilation. Am J Crit Care 2014;23:e1-8.  Back to cited text no. 13
MathiasDB, WedleyJR. The effects of cuffed endotracheal tubes on the tracheal wall. Br J Anaesth 1974;46:849-52.  Back to cited text no. 14
KastanosN, Estopá Miró R, Marín PerezA, Xaubet MirA, Agustí-VidalA. Laryngotracheal injury due to endotracheal intubation: Incidence, evolution, and predisposing factors. Aprospective long-term study. Crit Care Med 1983;11:362-7.  Back to cited text no. 15
KoshkarevaY, GaughanJP, SolimanAM. Risk factors for adult laryngotracheal stenosis: Areview of 74cases. Ann Otol Rhinol Laryngol 2007;116:206-10.  Back to cited text no. 16
SpittleN, McCluskeyA. Lesson of the week: Tracheal stenosis after intubation. BMJ 2000;321:1000-2.  Back to cited text no. 17
WonC, MichauG, KrygerMH. Upper airway obstruction in adults. In: GrippiMA, EliasJA, FishmanJA, editors. Fishman's Pulmonary Diseases and Disorders. 5thed. USA: McGraw-Hill; 2015. p.739.  Back to cited text no. 18
Weymuller EA Jr. Laryngeal injury from prolonged endotracheal intubation. Laryngoscope 1988;98:1-5.  Back to cited text no. 19
WainJC. Postintubation tracheal stenosis. Chest Surg Clin N Am 2003;13:231-46.  Back to cited text no. 20


  [Figure1], [Figure2]


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