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LetterCorrespondence

Mechanical Ventilation for the Treatment of Severe Excessive Dynamic Airway Collapse

Helder Novais Bastos, Nélson Teixeira, Margarida Redondo, Miguel Gonçalves and Maria Sucena
Respiratory Care April 2015, 60 (4) e90-e91; DOI: https://doi.org/10.4187/respcare.03972
Helder Novais Bastos
Department of Pneumology Centro Hospitalar de São João Porto, Portugal and Life and Health Sciences Research Institute (ICVS) School of Health Sciences University of Minho Braga, Portugal and ICVS/3B's-PT Government Associate Laboratory Braga/Guimarães, Portugal
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Nélson Teixeira
Department of Pneumology Centro Hospitalar de São João Porto, Portugal
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Margarida Redondo
Department of Pneumology Centro Hospitalar de São João Porto, Portugal
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Miguel Gonçalves
Department of Pneumology Centro Hospitalar de São João Porto, Portugal and Faculty of Medicine University of Porto Porto, Portugal
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Maria Sucena
Department of Pneumology Centro Hospitalar de São João Porto, Portugal
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To the Editor:

We read with interest the case report by Ismael et al1 describing a patient with Sjögren's syndrome and cystic lung disease who could not be weaned from a ventilator due to severe central excessive dynamic airway collapse (EDAC) of the lower part of the trachea and proximal bronchi. EDAC corresponds to the expiratory bulging of the tracheobronchial wall without known airway structural abnormalities, leading to a decrease of at least 50% in internal diameter.2 It is a rare and underdiagnosed entity, commonly confused with other respiratory diseases such as asthma and COPD. Although noninvasive procedures such as cervicothoracic computed tomography scan on inspiration and expiration may suggest the disorder, the accepted standard method for diagnosis is bronchoscopy.3–7

There is no consensus on the best treatment. The authors stated that stenting could resolve the collapsibility in that case.1 In our practice, endotracheal or endobronchial stenting is effective when the collapse affects only a small area of the trachea or main bronchi. In some patients with diffuse airway involvement, stenting is frequently useless. Murgu and Colt2 proposed an algorithm for the management of EDAC. Preceding invasive measures, the authors recommend the appropriate pharmacologic treatment of comorbidities, including COPD, asthma, and gastroesophageal reflux disease, because they may be predisposing factors for airway collapse. When treatment is not sufficient or the exacerbations become more frequent, noninvasive ventilation (NIV) may be tried. There are reports of significant improvement with CPAP > 6 cm H2O.8

We want to report our case of a female patient with scleroderma and a longstanding history of poorly controlled asthma who presented with severe and diffuse EDAC. Bronchoscopy (Fig. 1) showed a striking expiratory bulging (75–100%) of the larynx, posterior wall of the trachea, and bronchial tree bilaterally (main, lobar, and segmental bronchi), with some parts of the airway walls making contact. Pulmonary involvement with connectivitis was excluded, and histological examination of bronchial and hypopharynx biopsies was inconclusive (chronic nonspecific inflammation). Following consecutive hospitalizations requiring invasive mechanical ventilation support, the patient started nocturnal CPAP with 10 cm H2O (see Fig. 1).

Fig. 1.
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Fig. 1.

Bronchoscopic images of the trachea. A: The beginning of the bulging of the posterior wall over its lumen in expiration. B: Intermediate bronchus in inspiration. C: Intermediate bronchus in expiration with complete luminal collapse. D: The diameter of the intermediate bronchus is shown in expiration with the application of CPAP.

The patient remained relatively stable for ∼1 y, when she was again invasively ventilated in 2 successive admissions. Due to weaning difficulties, NIV with bi-level positive airway pressure was introduced after extubation. The patient became increasingly dependent on ventilatory support and gradually began to require continuous NIV with a full-face mask (aiming to prevent skin lesions). At this stage, the patient could not tolerate more than brief periods without NIV, just enough to feed herself. Due to the high degree of dependence on the ventilator and the continued clinical worsening, a tracheotomy was proposed. Her ventilator settings were adjusted according to the presence of a fenestrated inner cannula and cuff inflation. Thus, during the day using the fenestration and a deflated cuff, the parameters were: BiPAP S/T with AVAPS (tidal volume of 500 mL guaranteed), maximum and minimum inspiratory positive airway pressures of 18 and 13 cm H2O, expiratory positive airway pressure of 8 cm H2O, breathing frequency of 12 breaths/min, and inspiratory time of 1.1 s. At night, without the fenestra and with an inflated cuff, the parameters were: BiPAP S/T, inspiratory positive airway pressure of 14 cm H2O, expiratory positive airway pressure of 8 cm H2O, breathing frequency of 12 breaths/min, and inspiratory time of 1.1 s. Because the patient was tracheostomized, she had several microbial isolates in bronchial secretions. After a few months of stability, she was again admitted with a new episode of unstoppable cough and respiratory failure. New bronchoscopic examination revealed that the patient had increased tracheal collapsibility with cuff deflation. Keeping the cuff continuously inflated and sedating the patient were the only solutions for ventilation, ending the cough, and improving gas exchange. She finally died due to septic shock with nosocomial pneumonia ∼5 y after diagnosis.

We want to emphasize the need for more research to elucidate the underlying pathogenesis and optimum management of dynamic airway collapse. As highlighted by the 2 cases, this is a condition with significant morbidity and mortality, and treatment must be adapted to the severity and extension of the disease.

Footnotes

  • The authors have disclosed no conflicts of interest.

  • Copyright © 2015 by Daedalus Enterprises

References

  1. 1.↵
    1. Ismael S,
    2. Wermert D,
    3. Dang-Tran KD,
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    5. Fagon JY,
    6. Diehl JL
    . Severe excessive dynamic airway collapse in a patient with primary Sjögren's syndrome. Respir Care 2014;59(10):e156–e159.
    OpenUrlAbstract/FREE Full Text
  2. 2.↵
    1. Murgu SD,
    2. Colt HG
    . Tracheobronchomalacia and excessive dynamic airway collapse. Respirology 2006;11(4):388–406.
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  3. 3.↵
    1. Joosten S,
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    3. Lau KK,
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    . Excessive dynamic airway collapse co-morbid with COPD diagnosed using 320-slice dynamic CT scanning technology. Thorax 2012;67(1):95–96.
    OpenUrlFREE Full Text
  4. 4.
    1. Boiselle PM,
    2. Feller-Kopman D,
    3. Ashiku S,
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    . Tracheobronchomalacia: evolving role of dynamic multislice helical CT. Radiol Clin North Am 2003;41(3):627–636.
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    1. Baroni RH,
    2. Ashiku S,
    3. Boiselle PM
    . Dynamic CT evaluation of the central airways in patients undergoing tracheoplasty for tracheobronchomalacia. AJR 2005;184(5):1444–1449.
    OpenUrlPubMed
  6. 6.
    1. Lee KS,
    2. Sun MR,
    3. Ernst A,
    4. Feller-Kopman D,
    5. Majid A,
    6. Boiselle PM
    . Comparison of dynamic expiratory CT with bronchoscopy for diagnosing airway malacia: a pilot evaluation. Chest 2007;131(3):758–764.
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  7. 7.↵
    1. Loring SH,
    2. O'Donnell CR,
    3. Feller-Kopman DJ,
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    . Central airway mechanics and flow limitation in acquired tracheobronchomalacia. Chest 2007;131(4):1118–1124.
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  8. 8.↵
    1. Macedo Neto AV,
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    . Bronchoscopic management of functional airway obstruction. Pulmão RJ 2011;20(2):8–13. Article in Portuguese.
    OpenUrl
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Respiratory Care: 60 (4)
Respiratory Care
Vol. 60, Issue 4
1 Apr 2015
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Mechanical Ventilation for the Treatment of Severe Excessive Dynamic Airway Collapse
Helder Novais Bastos, Nélson Teixeira, Margarida Redondo, Miguel Gonçalves, Maria Sucena
Respiratory Care Apr 2015, 60 (4) e90-e91; DOI: 10.4187/respcare.03972

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Mechanical Ventilation for the Treatment of Severe Excessive Dynamic Airway Collapse
Helder Novais Bastos, Nélson Teixeira, Margarida Redondo, Miguel Gonçalves, Maria Sucena
Respiratory Care Apr 2015, 60 (4) e90-e91; DOI: 10.4187/respcare.03972
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