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ORIGINAL ARTICLE
Year : 2006  |  Volume : 23  |  Issue : 2  |  Page : 75-77 Table of Contents   

Post infectious obliterative bronchiolitis


Department of Respiratory Medicine, B.Y. L. Nair Ch Hospital, Mumbai-8., India

Correspondence Address:
J M Joshi
Department of Respiratory Medicine, B.Y. L. Nair Ch Hospital & TN Medical College, Mumbai-8.
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0970-2113.44413

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How to cite this article:
Joshi J M, Gothi D. Post infectious obliterative bronchiolitis. Lung India 2006;23:75-7

How to cite this URL:
Joshi J M, Gothi D. Post infectious obliterative bronchiolitis. Lung India [serial online] 2006 [cited 2020 Oct 25];23:75-7. Available from: https://www.lungindia.com/text.asp?2006/23/2/75/44413


   Introduction Top


Obliterative bronchiolitis (OB) also called constrictive bronchiolitis (CB) is a disorder caused by partial or complete obstruction of bronchi and bronchioles by fibrous tissue following an insult to the lower respiratory tract. [1] In paediatric population OB is frequently preceded by respiratory tract infections caused by adenovirus, influenza or measles, whereas in adults mycoplasma infection may be important. [2] Other causes include collagen vascular disorder [3] inhaled toxins, drug therapy like penicillamine or gold [4],[5] therapy, graft-versus-host reaction or idiopathic OB. The reported sequelae are obstructive lung disease, bronchiectasis, persistent atelectasis and hyperlucent lung syndrome (Macleod's Syndrome).' OB should be suspected in case of [6]

  1. Rapid progression of symptoms i.e. dry cough and dyspnoea.
  2. Severe airflow obstruction not attributable to other causes or to COPD.
  3. Lack of physiologic improvement following treatment with bronchodilators.
  4. Greater than 25% neutrophils in bronchoalveolar lavage (BAL) fluid analysis.


While radiographic features are nonspecific, high resolution computed tomography (HRCT) findings can be diagnostic in the correct clinical context. [7] The characteristic pattern is heterogeneity of lung density with lobules of increase and decrease in lung density that creates a striking "mosaic" pattern. This abnormality is exaggerated on expiratory HRCT scan. The reduced density is likely to be due overperfusion of the normal areas. Mosaic pattern is also seen, in interstitial lung diseases and vascular diseases.

Expiratory HRCT showing air trapping helps to differentiate OB from the other two conditions. Lung biopsy is not essential for diagnosis.

We present an analysis of clinical spectrum of 12 cases diagnosed as OB, all misdiagnosed as asthma, chronic obstructive pulmonary diseases (COPD) or bronchiectasis initially.


   Materials and Methods Top


Patients with dry cough, progressive dyspnoea following a childhood viral infection or pneumonia, showing a characteristic HRCT pattern, i.e. "mosaic" pattern with exaggeration on expiration, were included in this study. The patients were referred to us with an initial diagnosis of asthma COPD or bronchiectasis. The patients were further evaluated by spirometry, arterial blood gas analysis (ABG) electrocardiography and two-dimensional echocardiography (2D ECHO) where necessary. Ventilation perfusion scan (V/Qscan) and bronchography in one patient each were done before referral to our center. All patients were treated with a course of inhaled or oral beta agonist drugs oral theophylline and oral prednisolone in a dose of 1 mg/kg body weight for a period of 4 weeks, after which they were reassessed for clinical and spirometric improvement.


   Results Top


The results of the study are as shown in [Table 1] and [Table 2]. 12 patients, 6 males and 6 females were confirmed to have OB on clinical and HRCT criteria. The age range was 6 to 55 years. 6/12 patients presented with dry cough and dyspnoea whereas 4/12 patients had productive cough and dyspnoea. All the patients had an initial diagnosis of asthma, COPD or bronchiectasis and one case (case 5) had been subjected to left pneumonectomy, the details of which were not available to us. All 12 patients gave history of a serious respiratory infection or pneumonia in childhood. All except 3 patients had abnormal chest radiograph. The abnormality ranged from hyperinflated lungs, lung collapse to bilateral cystic changes. Spirometry reveals mild to severe obstructive abnormality i.e. forced expiratory volume in 1' second (FEV) less than 60 of predicted with poor bronchodilator reversibility in all except one case (case 2). HRCT showed "mosaic" pattern with exaggeration on expiratory HRCT in all, with cylindrical bronchiectasis in 10/12 cases and collapse in one case, was also noted. Response to treatment with steroids and bronchodilators was uniformly poor in all cases. ABG was normal in all patients except one PO 58mm Hg, PCO 52 mm Hg, pH 7.38 and HCO 2 23 mmol/lit).This patient also showed evidence of pulmonary hypertension and was prescribed home oxygen therapy.


   Discussion Top


Lange described obliterative bronchiolitis for the first time in 1901. OB has been a documented pattern of tissue response to various types of tissue injury, infections being a common cause. The reported sequelae include hyperlucent lung syndrome or Macleod's syndrome in which lung damage is predominantly unilateral. [10] Symptoms of OB vary from mild asthma like symptoms to rapidly progressive symptoms of dyspnoea and cough and a high index of suspicion is necessary to make the correct diagnosis. The CT pattern of heterogeneity of lung density (mosaic pattern) with exaggeration on expiration is diagnostic in the appropriate clinical context.

In the pontinfectious OB the classical CT pattern is associated with bronchiectasis. This was noted in 10/12 of our case. Spirometry showed airflow limitation with a poor response to inhaled bronchodilators in all except one case (case 2). In a study by Hansell et al, it was found that such changes of mosaic attenuation due to OB are common in bronchiectasis, and suggested that in these cases, OB might have been an early event in the pathogenesis. In most cases childhood respiratory infections cause either bronchiectasis or OB, however in some individuals both bronchiectasis and OB may result. In these cases small airway obstruction causes early and irreversible airflow limitation, pulmonary HT and cor pulmonale. [10]

Another characteristic feature of OB is preservation of gas transfer [11] adjusted for alveolar ventilation. We had not performed gas transfer studies this could not be confirmed. Pulmonary hypertension was present in one (case 2). Inhaled bronchodilators and oral theophylline may be used but corticosteroids have been reported to be important. The rationale for their use is to arrest airway inflammation and progression of fibrosis. Kindt and colleagues have used oral prednisolone in 1 mg/kg daily dose for 12 to 16 weeks followed by maintenance low dose up to 2 years, with significant improvement in 73% cases. However, others have reported a variable efficacy of corticosteroids in therapy of adult OB patients. Long-term results of oral steroids with bronchodilators were poor in all our cases. Presence of pulmonary hypertension required home oxygen therapy in one case. Immuno suppressants have been tried in patients who failed to respond to steroids or if persistent inflammation in indicated by bronchial lavage fluid analysis.

To summarize, several cases diagnosed as asthma, COPD or bronchiectasis in children and adults may actually be cases of OB. A high index of suspicion and use of HRCT may prove that the disease is a frequent cause of chronic airflow limitation.

 
   References Top

1.HardyKA SchilovD V Zaerin Obliterative bronchiolitis in children. Chest 1988,93:460-466.  Back to cited text no. 1    
2.Skokes D, SiglerA, Khavri NF, Telamo R C. Unilateral hyperlucent Lung (Swyer -James Syndrome) after severe Mycoplasma pneumoniae infection. Am RevRespir Dis 1976;117:145 - 152.  Back to cited text no. 2    
3.HakaloM, Paakko P, SutinerS, Hohti E, Koivisto U, Tarkka M. Association of bronchiolitis with connective tissue diseases. Ann Rheum Dis 1986;45:656-662.  Back to cited text no. 3    
4.Lahdensuo A, Mattila J, Vilppula A. Bronchiolitis in,rheumatoid arthritis. Chest 1984;185:705-706.  Back to cited text no. 4    
5.Epler G R, Colby T V. The spectrum of bronchoilitis obliterans. Chest 1983;83;161-162.  Back to cited text no. 5    
6.Kindt CG, Wailand JE, Davis WS, Godeh JE Dorinsky P M. Bronchiolitis in adults Am Rev Respir Dis 19891140:483-492.  Back to cited text no. 6    
7.Myers T L., Colby T V. Pathologic manifestations of bronchiolitis, constrictive bronchiolitis, cryptogeric organizing pneumonia and diffuse panbronchialitis. Clin Chest Med - 1993114:611-622.  Back to cited text no. 7    
8.WorthySA, MullerNL, Hartman TE, Swenson SJ, Padley S P G, Hansell D M. Mosaic attenuation pattern on thin section CT scan of the lung s differentiation among infilterative lung, airway and vascular disease as a cause. Radialogy 1997,;205:465-470.  Back to cited text no. 8    
9.Lange W. Bronchitis ofbronchiolitis obliterans. Arch Clin Med 1901;70:347.  Back to cited text no. 9    
10.Hansell DM, Wells AW, Rubens MB, Cole PJ. Bronchiectasis functional significance of areas of decreased attenuation on expiratory CT. Radiology 1994, 173: 369-374.  Back to cited text no. 10    
11.Lynch DA. Imaging of small airways. Clin Chest Med 1993;14:623-634.  Back to cited text no. 11  [PUBMED]  



 
 
    Tables

  [Table 1], [Table 2]



 

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    Introduction
    Materials and Me...
    Results
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    References
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