Respiratory Medicine CME
Volume 2, Issue 2 , Pages 86-91, 2009

Mounier-Kuhn syndrome and tracheopathia osteoplastica in the same patient with respiratory insufficiency

  • Ines Zendah

      Affiliations

    • Department of Pneumology I, Abderrahmene Mami Hospital of Pneumology, 2080 Tunis, Tunisia
    • Corresponding Author InformationCorresponding author. Tel.: +216 9 860 2362; fax: +216 71 821 184.
    • ,
  • Imen Aissa

      Affiliations

    • Department of Pneumology I, Abderrahmene Mami Hospital of Pneumology, 2080 Tunis, Tunisia
    • ,
  • Soumaya Darouas

      Affiliations

    • Department of Pneumology I, Abderrahmene Mami Hospital of Pneumology, 2080 Tunis, Tunisia
    • ,
  • Amel Khattab

      Affiliations

    • Department of Pneumology I, Abderrahmene Mami Hospital of Pneumology, 2080 Tunis, Tunisia
    • ,
  • Majed Beji

      Affiliations

    • Department of Pneumology, La Rabta Hospital, 1007 Tunis, Tunisia
    • ,
  • Habib Ghedira

      Affiliations

    • Department of Pneumology I, Abderrahmene Mami Hospital of Pneumology, 2080 Tunis, Tunisia

Received 16 August 2008; accepted 15 October 2008.

Article Outline

Summary 

Mounier-Kuhn syndrome (MKS) or tracheobronchomegaly, and tracheopathia osteoplastica (TO) are rare diseases. MKS is a clinical entity characterized by abnormal dilatation of the trachea and main bronchi. TO is a clinical and pathologic condition characterized by multiple submucosal cartilaginous and osseous nodules lining the upper respiratory tract. Some people with MKS manifest recurrent pneumonia or chronic cough with sputum production, hemoptysis or dyspnea. Occasionally, it is found in asymptomatic individuals. CT scan imaging is the key tool for the diagnosis when showing a dilatation of the trachea and main bronchi. TO is usually benign and asymptomatic, frequently diagnosed incidentally during intubation. Flexible fiberoptic bronchoscopy and laryngoscopy are the key diagnostic tools which typically demonstrate irregular spicules of submucosal bone and cartilage projecting into the tracheobronchial lumen and causing various degrees of airway obstruction. When this aspect is found bronchial biopsy is not mandatory. We report the case of a 26-year-old man with features of both MKS and TO who presented a previous history of productive cough, recurrent pneumonia and dyspnea; admitted for pulmonary infection resulting in a respiratory insufficiency. MKS was diagnosed by CT scan and TO by fiberoptic bronchoscopy. To our knowledge, this is the first time these pathologies are reported in the same patient, and our patient is the second one having MKS who presented with respiratory insufficiency.

Keywords: Mounier-Kuhn syndrome, Tracheobronchomegaly, Tracheopathia osteoplastica, Respiratory insufficiency

 

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1. Introduction 

Mounier-Kuhn syndrome (MKS) or tracheobronchomegaly is a clinical entity characterized by abnormal dilatation of the trachea and main bronchi. Tracheopathia osteoplastica (TO) is a clinical and pathologic, usually benign condition characterized by multiple submucosal cartilaginous and osseous nodules of various sizes lining the upper respiratory tract.1, 2 Both of the two pathologies are rare.

Tracheobronchomegaly is an unusual cause of recurrent chest infections often with persistent, productive cough. TO is usually an incidental finding on chest imaging studies, especially computed tomography (CT) scanning.

We report a case of an association of both pathologies in a patient with a previous history of recurrent pneumonia, productive cough and exertional dyspnea, who presented with a respiratory insufficiency due to a respiratory infection.

The association of these diseases has not been reported as yet to our knowledge and only one patient with MKS presenting with respiratory insufficiency has been reported in the literature.

In some patients recurrent bronchial or parenchymal infections, dyspnea or other recurrent symptoms that do not respond to treatment should alert the physician to some anatomical factors among which are MKS and TO, as they can result in difficulty in eradicating the cause of the recurrent respiratory disorders.

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2. Case report 

A 26-year-old man, non-smoker, presenting a 2-year -history of productive cough, recurrent pneumonia and exertional dyspnea, was admitted to our department because he presented 10days prior a worsening dyspnea and cough associated with fever.

The patient had parental consanguinity. He had a past history of meningitis resulting in mental retardation and bilateral hypoacousia.

His physical examination revealed a fever at 38.5°C, a heart rate at 110 beats/min, a respiratory rate at 26 cycles/min, intercostal retraction and bilateral crackles.

Blood gas analysis whilst breathing air showed the following results: pH 7.4, PaO2 52.2mmHg, PaCO2 24.7mmHg, HCO3− 15.6mmol/l and SaO2 85%.

Chest X ray film showed thoracic distension, significant increase in the diameter of the trachea and of the main bronchi, elevated diaphragmatic cupala, diffuse and bilateral bronchial shadows and multiple bilateral nodules (Figure 1).

White blood cell count was elevated at 20.700×109/l, CRP elevated at 144mg/ml and sedimentation rate elevated at 98/110mm.

Acid fast bacilli were absent from the sputum. Pseudomonas aeruginosa and Haemophilus influenzae were isolated in the sputum culture. They were sensitive to all the tested antibiotics.

The diagnosis of hypoxemic pulmonary infection with probable bronchiectasis was made and the patient started being treated with intravenous ceftazidime 3g per day for 15days in combination with gentamycin 160mg for 5days. The patient also underwent bronchial drainage and nasal oxygen was administered for the hypoxemia.

Flexible bronchoscopy revealed an abnormal trachea flattened anteroposteriorly with multiple whitish osteocartilaginous nodules protruding into the tracheal lumen involving the anterolateral wall. Posterior tracheal membrane was spared. The entire trachea and the right main bronchi were involved. They were of hard consistency when grasped with biopsy forceps. They extended from the proximal portion of the trachea to the proximal part of the right main bronchus, leading to a narrowing of the first third part of the trachea by almost 40%. These formations spared the posterior face of the trachea (Figure 2). The bronchial biopsy done twice was superficial. Histopathological examination showed a superficial respiratory epithelium. The diagnosis of TO was therefore made.

  • View full-size image.
  • Figure 2 

    Flexible bronchoscopy. Trachea flattened anteroposteriorly, multiple whitish osteocartilaginous nodules protruding into the tracheal lumen involving the anterolateral wall and sparing the posterior face of the trachea.

Chest CT scan revealed an enlarged trachea in its lower cervical and thoracic portions with a sagittal tracheal diameter reaching 30cm. The anterior wall was thin with multiple calcified densities protruding into the anterior and lateral walls, resulting in an irregular shape of the tracheal contour. The posterior wall was thin with multiple diverticula but without the nodules. This enlargement continued to the main, lobar and segmental bronchi which had thin walls. The nodules were located evenly in the main bronchi. The carina was elevated. There was a right apical consolidation with paraseptal emphysema. Both lower lobes had mosaic perfusion. There was ground-glass haziness in the lingula. A small left pneumothorax was noted (Figure 3). The CT aspect made the diagnosis of MKS and confirmed its association to TO. Respiratory functional tests revealed a restrictive syndrome. No similar cases have been seen in the family.

Over the first three days, fever disappeared. After a few days biological findings and blood gas analysis values reverted to within the normal limits. The patient was discharged and advised to return regularly to the clinic for follow-up. Symptomatic measures will be prescribed whenever necessary.

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3. Discussion 

Our patient has the features of two unusual conditions: MKS and TO. Although first recognized at post-mortem examination by Czyhlarz in 18973 and latterly described by Mounier-Kuhn in 19324 the term tracheobronchomegaly derives from the review of Katz et al in 1962.5 The disease remains rare. Himalstein and Gallagher,6 however, found a 1% prevalence in a series including 500 bronchograms. Most cases of tracheobronchomegaly probably are underdiagnosed. This disease is defined as a transverse and sagittal tracheal diameter exceeding 25 and 27mm respectively.7 Men are more often affected than women.

TO is a disorder detected in approximately 1 in 2000 patients who undergo bronchoscopy and usually manifests in the sixth to seventh decades of life with no sexual predominance.8

MKS is due to atrophy or absence of the longitudinal elastic fibers and the smooth muscles that form its walls.9, 10 The longitudinal elastic fibers of the trachea and the main bronchi are severely atrophied and the muscularis mucosa is thick. These abnormalities result in dilatation of the membranous and cartilaginous portions of the trachea and main bronchi. The most important respiratory impairment in patients with MKS is the total collapse of the airways during expiration.7, 9 In our patient, however, there was no obstructive syndrome but a restrictive one. This is probably explained by the fact that the collapse of the airways is not important enough to cause an obstructive syndrome and the restrictive syndrome is probably due to the bronchiectasis. This increased compliance of the chest wall results in protrusions of the musculomembranous tissue between the cartilaginous rings. In our patient the protrusions were too hard and macroscopically typical of a TO.

With the impairment of the cough reflex and of the mucociliary defense mechanism, the airways are extremely widened and weakened, which causes mucus accumulation, recurrent pneumonia, bronchiectasis, emphysema and fibrosis.7, 9, 11, 12

As for TO, it is postulated that the cough results from a combination of factors, including turbulent airflow, increased airway sensitivity, and impaired ciliary clearance.13 In our patient presenting with MKS and TO many mechanisms may be associated to cause cough and therefore bronchial and parenchymal infection, which explains the presence of bronchiectasis.

The cause of the MKS is still unknown but it is thought to have an acquired origin because of the extreme rarity of the disease and its association with chronic respiratory infections and delayed onset. Moreover, it has been suggested that this disease may be caused by barotrauma in neonates who received intensive ventilatory and oxygen support.14 Cigarette smoke and air pollution may also be the physiopathologic explanation of the disease.12 However, a genetic link is also suggested because MKS was reported in siblings, in association with Ehlers–Danlos syndrome and with cutis laxa. The association with these pathologies may suggest a congenital defect in connective tissue as the basis for tracheobronchomegaly; most cases, however, presented in the third or the fourth decade or even in later decades of life and showed no evidence of other connective tissue disorders.15, 16

Tracheobronchomegaly was reported to be also associated with duplication of the distal trachea, double carina, tracheal trifurcation, and with a congenitally short abnormal right upper-lobe bronchus.17, 18, 19 One case of association to the Kenny–Caffey syndrome has been reported (dwarfism, normal intelligence, thickened bone cortices with small medullary cavities, ocular abnormalities, and transient hypocalcemia).20 Our patient presents a mental retardation which would be another associative factor to the disease but in his case it seems to be rather due to the meningitis that he had presented. An autosomal recessive pattern of inheritance has been suggested from studies in one family.21

The cause of TO is also still unknown. Some authors,22 however, present the theory of neoplastic lesions arising directly from the cartilaginous rings or local trauma of the trachea with resultant osseous, cartilaginous metaplasia, chronic infection, congenital anomalies, chronic inflammation, metabolic abnormalities, mechanical and chemical irritation and genetics.23 Recently, a familial case has been recorded involving both mother and daughter.8 We would like to emphasize that among the chronic inflammations caused by MKS in our patient, as far as we know this is the first case in which MKS and TO coexist.

In both MKS and TO, inheritance has been suggested. Our patient presents a consanguinity which increases the occurrence of hereditary diseases, making it probable that both pathologies are hereditary in this patient. However, the probability of having two hereditary diseases is poor in the same patient and no similar cases were described in our patient's family.

The symptoms of MKS are not specific and may mimic chronic bronchitis or bronchiectasis. Some people manifest recurrent pneumonia or chronic cough with sputum production, hemoptysis or dyspnea.12, 15 Occasionally, it is found in asymptomatic individuals.

TO is usually benign and asymptomatic, frequently diagnosed incidentally during intubation, bronchoscopy or CT performed for other reasons.1, 24, 25 Although many patients are asymptomatic, progressive growth of the nodules may lead to dyspnea, stridor, hoarseness, cough and dysphagia caused by the narrowing of the airway lumen. Hemoptysis may occur if the underlying mucosa ulcerates. Distal bronchial lesions may result in atelectasis and wheezing. In our patient fiberoptic bronchoscopy revealed that the nodules caused an important narrowing of the trachea, which explains the cough and dyspnea presented by him.

In fact, accurate diagnosis of TO can be challenging because of the nonspecific nature of the symptoms. TO is in general a relatively benign and a slowly progressive disease, and this partly explains the low incidence of reports.26Although some clinical signs of TO may be present at diagnosis, it is usually an incidental finding on chest imaging studies, CT being the imaging modality of choice in this entity.27 To our knowledge this is the second case of TO presenting with respiratory insufficiency.28

Diagnosis of MKS depends on the demonstration of the characteristically large trachea and proximal bronchi by plain radiography, CT or magnetic resonance imaging (MRI).13, 29 Radiologic findings of an irregular air column reflect the “corrugated” effect that is produced when redundant mucosa prolapses through the tracheal rings, and CT scan reveals these abnormalities better than chest radiographs.7 In our patient, the diagnosis was overlooked on plain radiography as it revealed an enlarged tracheal silhouette. However, its significance was not appreciated until CT scanning revealed the diameter of the trachea allowing the diagnosis of tracheobronchomegaly.

The thoracic CT shows in cases of MKS greatly dilated trachea and right main bronchi with an abrupt transition to a normal caliber of the peripheral airways and protrusion of redundant musculomembranous tissue between the cartilaginous rings, resulting in an irregularly corrugated or scalloped appearance of the air columns and sometimes bronchiectasis.12, 30 Parenchymal consolidation may also be encountered.16

In TO, characteristic CT imaging findings consist of multiple calcified or uncalcified densities protruding into the anterior and lateral walls of the trachea, resulting in irregular shape of the tracheal contour and decreased frontal diameter.24, 28, 31 CT imaging may also show potential complications, including post-obstructive collapse, bronchiectasis and pneumonia.25 In our patient, CT scan showed a dilatation of the trachea and main bronchi in relation with MKS and densities of the trachea and main bronchi in relation with TO. Parenchymal complications were also seen.

MRI, with its high resolution, can help better than CT scan for the diagnosis of TO by better defining the submucosal nodules, the sparing of the tracheal posterior wall, and the extent of the tracheal thickening to the bronchi on the coronal planes.29, 32 But it is less sensitive than CT for demonstrating the punctiform calcifications in the submucosal nodules and the potential complications such as lobar collapse and post-obstructive bronchiectasis.29

In MKS, flexible fiberoptic bronchoscopy may show flattened trachea and cartilaginous nodules.16 In TO, flexible fiberoptic bronchoscopy and laryngoscopy are the key diagnostic tools which typically demonstrate irregular spicules of submucosal bone and cartilage projecting into the tracheobronchial lumen and causing various degrees of airway obstruction. The posterior pars membranacea is spared.13, 27 As the lesions arise from the cartilaginous supporting rings of the airway, endoscopic anomalies may involve the entire trachea and mainstem bronchi.23, 27 Only areas of the respiratory tree with underlying cartilage are affected. Endoscopic features of TO are typical and pathognomonic. These lesions are typically hard and their biopsy is difficult; consequently, the diagnosis is often made from the visual appearance alone such as in the case of our patient.33, 34 Histological examination of the nodules is nonspecific, but it usually reveals cartilaginous, osseous and fibrous tissue.25, 27 Occasionally, marrow is present in the new bone; however, the marrow is typically not hematopoietic.35

Expiratory studies may reveal obstructive syndrome in MKS11, 12, 36, 37 and usually show no abnormality or an obstructive pattern in TO.38, 39

MKS may be confused with Williams–Campbell syndrome, a rare form of congenital cystic bronchiectasis that results from a deficiency of cartilage in the fourth- to sixth-order bronchi. Although both diseases can result in significant bronchiectasis, patients with Williams–Campbell syndrome have normal-caliber trachea and main bronchi.37 Predominant enlargement of the central bronchi or central bronchiectasis may also be seen in allergic bronchopulmonary aspergillosis and cystic fibrosis. Allergic bronchopulmonary aspergillosis usually occurs in asthmatic patients showing a response to Aspergillus antigens and presenting large mucoid impactions, as well as fleeting peripheral air-space opacities.

TO may also be confused with many other diseases, resulting in a delay of the diagnosis,this being more due to the fact that TO is rarer than the other differential diagnoses. In TO distal bronchial lesions by generating wheezing often lead to a misdiagnosis of asthma or bronchitis.

The differential diagnosis of multiple nodules within the tracheobronchial tree includes amyloidosis, endobronchial sarcoidosis, squamous papillomatosis, relapsing polychondritis, calcified tuberculosis and neoplasia. These entities should be specially considered in cases of posterior wall involvement.24, 34

MKS requires symptomatic treatment and antibiotics when an infectious complication requires it.

Treatment modalities of TO include relief of symptoms. The tracheal diameter can be increased by means of a rigid bronchoscope, allowing the use of laser or forceps, which relieves the symptoms.27 Stent placement and even radiation therapy can be useful.2 Surgical excision of the involved trachea is reserved for severe obstruction of the lumen by the nodules.40

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4. Conclusion 

MKS and TO are rare diseases. Their symptoms are not specific. The diagnosis is made by CT scan for MKS and by fiberoptic bronchoscopy for TO. Recurrent respiratory symptoms should make physicians think of TO and MKS among the possible etiologies. However, these diseases are much more rare than the other ones, which can lead to a misdiagnosis and the resulting recurrent symptoms. The symptoms are unspecific. The diagnosis of MKS relies on CT scan and that of TO on flexible bronchoscopy. The treatment is symptomatic in the case of MKS and may sometimes be surgical or by means of a rigid bronchoscope in the case of TO.

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5. Conflict of interest statement 

None of the authors have a conflict of interest to declare in relation to this work.

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6. Ethics statement 

The work has been approved by the appropriate ethical committees related to the institution in which it was performed and the patient's parents accepted the publication of the case report (we could not have the patient's agreement as he has mental retardation).

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References 

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PII: S1755-0017(08)00094-8

doi:10.1016/j.rmedc.2008.10.013

Respiratory Medicine CME
Volume 2, Issue 2 , Pages 86-91, 2009

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