Tuesday, April 2, 2013

Differential Diagnosis Of Hereditary, Congenital And Chronic Diseases Of Bronchopulmonary System In Children

Study of hereditary and congenital chronic broncho- pulmonary diseases in children is significant due to:
1. The overall incidence of recurrent and chronic diseases of this system in     children ranges from 0,85 to 1,45%  and the proportion of malformations and     hereditary diseases in the structure of this pathology is quite high (from 4.6 to 20% according to different authors).
2.  In 1-3% of deceased infants and 1/5-1/3 with chronic bronchopulmonary       pathology congenital  anomalies of the lungs is diagnosed. Moreover, with improved methods of diagnostics frequency of congenital and hereditary pathology has a tendency to increase.
 3. This group of diseases has usually unfavorable forecast, because that leads to         disability, reduced life expectancy, and often to death in early age.
 4.  A large number of pathological forms, lack of their study, low separate         experience for each pediatrician, rarity of a disease make it difficult to establish diagnosis at time and prescribe treatment.
  5. There are no effective preventive measures.
                 Physicians of different professions should be aware clinic of these diseases in order to suspect congenital or hereditary pathology, to diagnose them in children and to send a child to a specialist, as well as prevent these diseases.
                        Common clinical symptoms of congenital lung diseases:
·       debut of the disease at an early age
·       prolonged, recurrent, chronic inflammation in the lungs
·       obstructive syndrome
·       persistent prolonged wheezing in the lungs, weakened breathing
·       "drumsticks", pallor, cyanosis
·       physical retardation
·       "cor pulmonale"
·       breathlessness
·       bulging chest
·       asphyxia
·       loss of consciousness, convulsions
·       prolonged cough
·       pleural friction rub
·       combination with other symptoms

Classification of hereditary and congenital bronchopulmonary diseases   
·       Defects of the respiratory system:
·       abnormalities of the trachea and bronchi
·       anomalies of the lungs
·       Hereditary lung diseases.
·       Polyorganic hereditary disease with primary lesion of the lungs.

                         General diagnostic criteria

§        Early emergence of diseases of the respiratory system (the neonatal period, I year of life)
§        Physical retardation
§        Persistent obstructive syndrome
§        Recurrent nature of the respiratory system diseases
§        Increasing of sings of respiratory failure despite treatment
§        Inefficiency therapy

ü      Anomalies of branching tracheobronchial tree.
ü      Congenital lobar emphysema (lobar, obstructive, hypertrophic, gigant) is a malformation characterized by a sharp increase in the proportion of one lung due emphyzematous change and blowing

ü      Traheobronhomegalia / Mounier-Kuhn syndrome – 1932, France/ – congenital anomaly of the system of the trachea and bronchi, with their expansion due to underdevelopment of elastic cartilage and muscle structures of the tracheobronchial tree.
ü      Syndrome Williams-Campbell (I960) – congenital defect of the system due to generalized hypoplasia of cartilage and segmental subsegmental bronchi from 3rd to 8 th caliber, followed by the formation of secondary bronchiectasis, predominantly symmetric in the lower lobes.
ü      Tracheo(bronchi) - esophageal fistula – a severe malformation, which might result in a fatal outcome already in the early periods after birth


ü     Lung agenesia – absence of lung together with the main bronchus.
ü     Lung aplasia   – absence of lung with the presence of rudimentary main bronchus.
ü     Pulmonary Hypoplasia – underdevelopment simultaneous bronchi and lung parenchyma.
ü     Cystic hypoplasia of the lungs /polycystitis/ – congenital malformation, which except reduction is accompanied by respiratory areas of cystic like formation of cavities and bronchiectasis.
ü     Pulmonary sequestration – a section of lung placed inside or outside the pulmonary lobe and does not participate in gas exchange. Blood supply to the site is provided by the anomalous vessel from the thoracic or abdominal aorta or intercostal arteries.

                                    Malformations of lung

             Malformations of lung frequently underlie the second place amount inflammatory processes in the bronchopulmonary system and are evident more frequently in childhood and adolescence. They include, first of all, various options of cystic hypoplasia of the lung, congenital solitary cyst, pulmonary sequestration and rare abnormalities of the trachea and bronchi.
                     Agenesia, aplasia and hypoplasia of lungs
 Agenesia is the absence of lung together with the main bronchus.
              In lung agenesis, the entire lung and bronchial tree may be absent on one side. The bronchial tree may form without development of the alveoli. Pulmonary hypertension complicates lung agenesis because of a combination of factors: normal blood volume passing through reduced lung tissue, hypoxemia leading to pulmonary vasoconstriction, and any associated left-to-right shunting cardiac lesion.

              Aplasia is the absence of lung tissue in the presence of rudimentary bronchus.

           Hypoplasia is a state when the main and lobar bronchi terminate functionally insolvent rudiment, lung tissue is underdeveloped. Intrathoracic or extrathoracic lesions can cause pulmonary hypoplasia. Therefore, prolonged rupture of membranes, renal dysplasia, neuromuscular diseases, and congenital diaphragmatic hernia can lead to lung hypoplasia. Reduced urine volume during fetal life may retard lung growth. Pulmonary aplasia leads to respiratory distress, which may vary according to the degree of alveolar involvement. Pulmonary hypoplasia may be primary when the entire lung or when one lobe is reduced in size.

               Both pulmonary agenesis and hypoplasia may be accompanied by renal anomalies, which are usually apparent soon after birth and associated with respiratory distress. Cardiac defects occur in 50% of patients.
              Pulmonary agenesis is differentiated from lung aplasia by the absence of the carina in the latter. Lung agenesis is less common than aplasia, about 75% of cases affect the left side, and it is lethal in half of all patients. It may be associated with other manifestations of the syndrome of abnormalities of the vertebrae, anus, cardiovascular system, trachea, esophagus, renal system, and limb buds (VACTERL syndrome). The survival rate is better with left-sided lung agenesis than with right-sided agenesis because the right lung is the larger of the two.

                 Asymptomatic clinic is rare. Children have physical retardation.  Respiratory failure is observed: dyspnea, cyanosis of varying severity. Cough and the allocation of purulent phlegm are associated with the accession of the inflammatory process. Sometimes there is a pain in the chest. On the lesion side thorax is flattened, and the healthy half is convex. At the site of the lesion there are observed shortening of percussion sounds, absent or weakened respiratory noises. The heart is shifted toward the lesion, which may erroneously be interpreted as dextracardia. When expressed hypoxia is observed for a long time the nail phalanx become thickened as "drumsticks."
            Clinic of hypoplasia is less pronounced. The process proceeds by the type of chronic lung disease, vital lung capacity, GLC are decreased.
X-rays reveal the decrease of lung volume on the side of lesion, intense darkness, highstanding of diaphragm. The heart and mediastinum organs are removed so that the spine looks bare. However, there may be a "pneumocele" when healthy lung is prolaboring through the anterior mediastinum in the other direction.
           The final diagnosis is based on bronchography.

                In pulmonary hypoplasia, development of the distal lung tissue is incomplete. At earlier the delivery of a child the incidence of lung hypoplasia is higher. In babies delivered before 28 weeks' gestation, the incidence approaches 20%. Pulmonary hypoplasia occur as a result of conditions that restrict lung growth, such as oligohydramnios, Potter syndrome (with bilateral renal agenesis or dysplasia), abnormalities of the thoracic cage, Scimitar syndrome (right-sided pulmonary hypoplasia), and diaphragmatic hernia (usually left-sided hypoplasia). More than 50% of patients have associated cardiac, gut, or skeletal malformations. They may have a small thoracic cage, decreased breath sounds on the affected side, and a mediastinal shift to the side of the lesion. Therefore, aplasia of the right lung can be confused with dextrocardia. Patients may present with lung infections, dyspnea upon exertion, and/or scoliosis.
 Radiography of the newborn the first day of life with suspected hypoplasia of the left lung (right lung volume more)

Hypovascularity of the entire left lung in a 16-year-old patient with mild exercise intolerance. This patient had hypoplasia of the left lung

Bronchogram in simple hypoplastic left lung: the left lung is reduced
 in volume.

Displacement of mediastinum and heart to the left. Loculated translucencies in right middle and lower lung fields with flattened right diaphragm. (reprinted by permission from W. B. Saunders Company Ltd. Manual of Neonatal Emergency X-Ray Interpretation, 1994.)

                   Patients with pulmonary agenesis and pulmonary hypoplasia seem to have one of 3 presentations. The first group consists of patients with insufficient lung tissue who may have received mechanical ventilation for some time. However, ventilator-induced lung injury results in slow decompensation and death. The second group of patients is identified serendipitously when chest radiography is obtained to assess a minor complaint. These patients require no intervention. The third group does not have respiratory distress requiring mechanical ventilation, but they have respiratory limitations to activity or kinking of the airway with shift of the lung to the contralateral side of the chest. In addition to the aplasia or hypoplasia, congenital narrowing of the upper airway also affects many patients.

                             Cystic adenomatoid malformation                            
           Cystic adenomatoid malformation is a defect in the development of the terminal bronchioles. A hamartomatous proliferation of cysts occurs and resembles bronchioles (airways without cartilage).
           Congenital Cystic Adenomatoid Malformation was first identified in 1949 by Ch'in and Tang. Cystic adenomatoid malformation accounts for 25% of all congenital lung malformations. Respiratory distress occurs in the neonatal period, when collateral pores of Kohn ventilate the alveolar tissue present. This process is responsible for the cystic appearance on radiographs. Patients may have mediastinal shift and a pneumothorax. The affected area is dull on percussion, and air entry is decreased. The radiographic depiction of a solid or cystic mass on one side of the thorax suggests the diagnosis. Cystic changes underdeveloped lungs or it lobe are a good ground for the development of chronic suppuration, as the drainage function of bronchi is severely disturbed.
                Three histologic categories of cystic adenomatoid malformation are described: (1) macrocystic (13%), which has the best prognosis and in which one or more large (>5 mm on prenatal ultrasound) cysts are lined with normal pseudostratified ciliated epithelium; (2) microcystic (73%), which has small cysts lined with ciliated columnar or cuboidal epithelium; and (3) solid cystic adenomatoid malformation (13%), which has the worst prognosis and is an airless tissue mass composed of cuboidal epithelium-lined bronchioles. The difference in prognosis may be because the solid and microcystic lesions involve a relatively large amount of lung tissue. Macrocystic lesions are comprised of large, air filled, nonfunctioning spaces involving smaller areas of lungs.
                 One lobe, multiple lobes, or multiple segments on both sides may be affected. The upper lobes are usually involved. The bronchiolar proliferation is terminal without much alveolar development. The abnormal hamartomatous proliferation usually retains its communication with the normal bronchiolar tree. However, no cartilage or bronchiolar tubular glands are present in the malformation itself. Columnar mucinous epithelium is present.

            Polyhydramnios may be present if the cystic adenomatoid malformation presses on the esophagus. Pressure on the heart and large vessels may lead to hydrops fetalis.
           Cystic adenomatoid malformation results when the terminal bronchiolar component of the advancing endodermal lung bud proliferates haphazardly because of disruption of humoral factors from the surrounding mesenchyme. Apoptosis in the advancing lung bud is decreased. Glial cell–derived neurotrophic factor is a growth factor that is abnormally expressed in the epithelial cells of the cystic adenomatoid malformation. Cystic adenomatoid malformations usually appear before 7 weeks' gestation but can occur in the mid stage of lung development. The growth is thought to plateau at 28 weeks' gestation. Communication with the normal airways can lead to overinflation and compression of the surrounding lung tissue. At the larger the sonographic volume of cystic adenomatoid malformation in relation to head circumference the chance for developing hydrops because of more severe central venous compression is the greater.

                    In approximately 60% of patients, cystic adenomatoid malformation manifests soon after the neonatal period. It results in recurrent infections because the mucociliary clearance is poor. Malignancy can occur in the cystic adenomatoid malformation (pulmonary blastoma, rhabdomyosarcoma, and bronchoalveolar carcinoma).
                     The disease may occur immediately after birth or later, sometimes even in  teens agers, depending on the join of infection. Patients complain of a cough with purulent sputum, frequent colds, dyspnea during physical exertion, fatigue. Early the developing phalanges and nail changes in the form of drum sticks and watch glasses
occur. As result of the decline in lung maturation asymmetry of the chest is observed. Children suffer from malnutrition and have physical retardation. On auscultation over the affected areas of lung there are constantly listened dry and moist rales of various sizes.
X-ray picture depends on the level and extent of damage of bronchial tree. In hypoplasia of the lung there is marked shift of the mediastinum in the affected side, the high standing of the diaphragm. Affected lung is reduced in volume, sealed, sometimes with annular illumination. In hypoplastic lobe pattern develops equity fibroatelectasia with a decrease and compaction percentage, usually pressed against the mediastinum and therefore not always immediately visible. Adjacent healthy areas of the lung appear to be more transparent in comparison with the opposite lung due to hyperinflation.

Cystic adenomatoid malformation of right lung

                         Polycystiс malformation of left lung

Polycystiс malformation of the upper lobe of right lung
 Most demonstrably picture is given at bronchography, and computed tomography (CT). They reveal multiple cystic cavities, which are the ends of lobe, segmental or smaller bronchi. At angiopulmonography may be found signs of malformation of the pulmonary blood vessels - their thinness, lack of contrasting small branches, the expansion of branching angles.
Cystic hypoplasia of right lung (bronchography in lateral projection)

                          Air cysts of right lung
Changes in cystic hypoplasia that develops in the later stages of embryogenesis are very similar to those of acquired atelectasis bronchiectasia. In the absence of typical radiological signs to determine the innate pathology is possible only by the morphological study of resected preparates and even then not always.
             In cystic adenomatoid malformation, resection of even asymptomatic masses is recommended because of the risk for infection, hemorrhage, acute respiratory compromise (which may occur anytime), and neoplastic transformation. This disease is usually segmental; however, as noted for sequestration, lobectomy may reduce morbidity.
            During surgery, lung cysts are often found to be cystic adenomatoid malformations, though simple cysts do occur. Some lesions can be shelled out or unroofed. If they are not congenital but related to barotrauma, they may communicate directly with small bronchi. In this case, unroofing leads to major air leaks. These lesions can sometimes be controlled with figure-8 sutures, but wedge resection, segmentectomy, or even lobectomy may be required to avoid a bronchopleural fistula.

                  Congenital (real) solitary cysts
                   Bronchogenic cysts are also known as foregut duplication. They arise from an abnormal budding of the ventral foregut. Approximately 85% are mediastinal, and 15% are intrapulmonary. The peripheral cysts are multiple and appear late in gestation. They may be filled with air or fluid, or they may have air-fluid levels. The cysts can be central or peripheral. Many are asymptomatic, but incidental findings may be observed on chest radiography. Infection, hemorrhage, and, in rare cases, malignancy can occur. Respiratory distress may result in a stridor or wheeze. Airtrapping may lead to emphysema, atelectasis, or both. Dysphagia, chest pain, and epigastric discomfort can occur.
                Lung cysts are rare lesions that may arise from any of the parenchymal tissues of the lung. They can cause symptoms if they enlarge and occupy substantial space. Resection is performed to diagnose lung cyst and to stop the progression of symptoms.
                Bronchogenic cysts represent outpouchings of the ventral foregut in the early part of gestation. These outpouchings generally arise close to the bronchial tree. A cyst may become infected, or it may compress adjacent structures to produce signs and symptoms. Chronic infection and inflammation may predispose the patient to malignancy. Peripheral cysts appear late in gestation and are multiple.
     Bronchogenic cysts are most commonly mediastinal in a pericarinal, paratracheal, or retrocardiac location. The cysts are thin walled and lined with columnar epithelium. The common central cysts represent outpouchings of the ventral foregut in the early part of gestation.
                     Many cysts are asymptomatic, but incidental findings may be observed on chest radiography. Infection, hemorrhage, and, in rare cases, malignancy can occur. Respiratory distress may result in a stridor or wheeze. Airtrapping may lead to emphysema, atelectasis, or both. Dysphagia, chest pain, and epigastric discomfort can occur.
                      Unlike cystic hypoplasia solitary cysts usually do not have widespread reports of bronchi and therefore become infected less often and later than cystic. True cysts of the lung at birth are filled with mucus, often having a dark brown color (so-called chocolate cysts). Communicating with the small bronchi of the cyst may be complicated by valve mechanism (tense cysts), a breakthrough in the pleural cavity or infection.
       At infected cysts on the first place there are the symptoms of purulent intoxication: high fever, sweating, increasing weakness, lethargy, loss of appetite. For large scale cysts symptoms of respiratory failure may appear: shortness of breath, cyanosis of lips and limbs, which are more common in young children. Characteristic is   the appearance of dry or wet cough. At percussion over the cavity of the cyst when it is of sufficient size may be noted dullness of sound and auscultation with the weakening of breath and wheezing of various sizes.
       On plain radiograms and tomograms lung festering cysts are seen as round or oval hollows formations with, as a rule, the level of liquid and air over it. Unlike lung abscesses inner and outer contours of the cyst are clear and smooth, perifocal reaction is expressed slightly. Often cysts are a multi, and the upper edge of the liquid in individual cells may be at different levels.  Bronchi and vessels, clearly visible in contrasting and tomograms uniformly bend around the contours of the cyst, which is not at the case with lung abscess.

Bronchogenic cyst. Conventional radiographs demonstrate a subcarinal mass.
Bronchogenic cyst. Media file shows a right paratracheal mass.


Bronchogenic cyst. CT scan demonstrates a thin-walled cyst in the right upper lobe.

Review chest X-ray of the child with a congenital air cyst of the right lung in
 direct projection: annular shadow of the cyst is indicated by arrows.

Review chest X-ray of the child with a congenital air cyst of the right lung in
 lateral projection: annular shadow of the cyst is indicated by arrows.

               In the differential diagnosis of purulant cysts it is needed to remember about tuberculous cavity, the more so that their localization (mainly in the upper lobes) usually coincides. For tuberculous cavern characteristic features are rugged, "moth" inner contour and fibrose focal shadows on the periphery of the cavity. In addition, the cavity is characterized by the presence of shadows and enlarged lymph gland in the root of the lungs and shadow of draining bronchus, well visible on the tomograms.

                                           Pulmonary sequestration

               Pulmonary sequestration accounts for 6% of all congenital lung malformations and mostly occurs in the lower lobes. A sequestration is a bronchopulmonary tissue without a normal bronchial communication and with normal or anomalous vascular supply. Sequestered lung may be intralobar or extralobar.
                     A pulmonary sequestration there is a benign mass of non-functioning lung tissue that appears during early lung development. This lesion has no connection with the airway and receives its blood supply from the systemic circulation usually off the abdominal or thoracic aorta. The most common type of BPS is formed within the normal lung itself and is referred to as intralobar. The other type of BPS is known as extralobar, and is formed outside the normal lung. This type of lesion is usually found in the chest cavity although rarely it may be found in the abdomen. There is a higher incidence of associated anomalies in babies with extralobar BPS.
                       The involved lung segments can be classified on the basis of their pleural coverage into intrapulmonary or extrapulmonary types. Variants of pulmonary sequestration are described as disconnected or abnormally communicative bronchopulmonary masses with normal or anomalous vascular supply. The lesions may have some sort of communication with the gut.
                     About 50% of pulmonary sequestration cases are intrapulmonic, and 60% of intrapulmonic cases occur in the left lower lobe with equal sex distributions. Patients with intrapulmonary sequestration usually present late. They may have a chronic cough, recurrent pneumonias, or poor exercise performance. Systemic arterial flow may produce a murmur, and shunts may lead to congestive cardiac failure. Squamous cell carcinoma, adenocarcinoma, and rhabdomyosarcoma may arise in the sequestration.
                   Approximately 95% of extrapulmonary cases are left sided. Most extrapulmonary cases are detected in infancy, with boys affected 4 times more than girls. Infants usually present with a chronic cough and recurrent chest infections. Radiographs may reveal signs of consolidation. If communication with the gut is present, children may present with vomiting, failure to thrive due to poor oral intake, and abdominal pain.
         Clinical manifestations are due to inflammatory changes: cough, fever, shortness of breath, over the lesions listened small bubbling moist rales.
         There are three forms of the pathological process:
§         bronchiectasis, in which repeated inflammation leads to
              fusion of lung tissue and secondary connection with
                bronchial tree
§         pseudotumoral that is characterized by small clinical symptoms
§         local abscess formation or empyema
The main distinguishing feature of sequestration of the lung is an additional large vessel which deviates from the aorta and branching in the sequestered lung tissue. This vessel can be identified at aortography, tomography and CT. Sometimes   it is finding during the operation as an accident.
            Diagnose of pulmonary sequestration is based on angiography. Much less importance has bronchography. At radiograph may be darkening of the affected segment inflammation.
Sequestration of the lung. There is cystic changed area
                 of S10 of the lower lobe of the left lung.

Aortogramme at sequestration of the lower lobe of right lung: the additional vessel (2) is going from the aorta (1) to the sequestered part of lung.

Review X-ray of the child with intrapulmonary sequestration in low medium sections of the right lung: in the zone sequestration there is shading lung tissue (indicated by arrow).

Surgical treatment: resection of the sequestered area.
                Resection is recommended, even in asymptomatic patients, to prevent infection, hemorrhage, shunting from arteriovenous anastomoses, or compression of normal lung mass leading to respiratory distress. Lobectomy can usually be performed. For patients with intralobar sequestration, segmentectomy may suffice. Segmentectomy is relatively difficult, but preserves additional functioning lung tissue.

Prognosis is  favorable.
Malformations of trachea and bronchi

  Among the rare malformation of the trachea and bronchi, facilitating the development of intrapulmonary suppuration, should first be called traheobronhomegalia usually combined with tracheomalacia (so called Moanier-Kuhn syndrome), and congenital stenosis of the bronchi, as described in the form of casuistic observations.

Traheobronchomegalia (Moanier-Kuhn syndrome)

Tracheobronchomegalia (Moanier -Kuhn syndrome (P. Moanier-Kuhn, modern French otolaryngologist), 1932) - congenital enlargement of the trachea and bronchi.

            At tracheobronchomegalia and malacia softened and lost their resilience cartilages of the trachea and major bronchi make in the airways the flaccid, extended tube, decreasing with exhalation and cough. Bronchial drainage function is disrupted, and delayed sputum, rapidly infecting, promotes suppuration in the distal lung. A similar mechanism of development of septic complications arise at bronchial stenosis, which disturb the self-cleaning of bronchi.
           Pathomorphologic changes are due to the diffuse extension of the trachea, sometimes the main bronchi. At this anomaly atrophy of the longitudinal elastic fibres and thinning of the muscle bundles occur.
           There are the following types of a defect: an isolated tracheomegalia (pathological enlargement of the trachea with a normal value of the lumen of the bronchi), isolated bronhomegalia (enlargement of one or both main bronchi with normal width of the trachea) and traheobronhomegalia (enlargement of the trachea and one or both main bronchi).
          There is a rare involving in pathological process the segmental and smaller bronchi, although in the distal bronchial tree in some cases may be secondary changes.             
                     Clinically there is the recurrent tracheobronchitis, in the course of which predominates bitonal irritating cough with prolonged sputum discharge.
                   Abnormalities of the trachea and bronchi may be suspected by the presence of the characteristic cough with metal, vibration shade, hard forced exhalation and the presence of hard discharged purulent sputum in children. On auscultation over the lungs there are listened many variegated wheezing, which do not disappear after cough. Radiographic examination often reveals signs of bronchiectasis, and in patients with acute inflammation the massive bilateral pneumonia, often with abscess formation.
          Frequent symptoms are chronic intoxication and hypoxemia, pallor, retarded physical development, the deformation of the fingers on the type of drum sticks. In the lungs, there are different changes in percussion sounds, a variety of wheezing.
          Studies of lung function and blood gas composition reveal pronounced degree of combined ventilatory insufficiency and hypoxemia.  
                   Bronchofibroscopy helps to establish the correct diagnosis. At tracheobronhomegalia there are determined a significant expansion of the lumen of the trachea and main bronchi, deformation of their walls with the curvature of the cartilaginous rings and deep, sac interchondral intervals, a thickening of the mucous membrane in the form of circular folds and the almost total collapse of the lumen by coughing and forced expiration, expiratory stenosis and the presence of inflammatory changes in the trachea and bronchi. Congenital stenosis of the major bronchi is defined as smooth wall sunken or membranous narrowing with a small round hole at the center.
Bronchoscopy - the examination of the bronchi (the main airways of the lungs) using a flexible tube (bronchoscope). Bronchoscopy helps to evaluate and diagnose lung problems, assess blockages, obtain samples of tissue and/or fluid, and/or to help remove a foreign body.
Вronchoalveolar lavage - to remove cells from lower respiratory tract to help identify inflammation and exclude certain causes.
lung biopsy - to remove tissue from the lung for examination in the pathology laboratory.

 Bronchoscopical sings at tracheobronchomegalia (Moanier-Kuhn syndrome)

                Treatment is provided as at endobronchitis.
                Prognosis for life is favourable.

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