Plastic bronchitis is generally associated with some type of pulmonary disease and improves either spontaneously or with medical therapy. We present a case of plastic bronchitis with no known cause.The patients' symptoms were not responsive to medical therapy but were relieved after right middle lobectomy. Eur Respir J., 1996, 9, 612- Plastic bronchitis, also known as fibrinous bronchitis or pseudomembranous bronchitis, denotes the presence of inspissated bronchial casts that may be coughed up or found at bronchoscopy or in surgical specimens [1][2][3]. Bronchial casts are generally associated with diffuse bronchial hypersecretory disorders, such as asthma or mucoviscidosis [4][5][6], and are also reported to be present in pneumonia [4], pericardial effusion [5], and heart failure [7]. Plastic bronchitis is usually self-limited or responsive to medical therapy, with a good prognosis [1][2][3][4][5].We report a case of plastic bronchitis not related to a specific bronchopulmonary disease. Our case was not responsive to medical therapy but improved after right middle lobe resection.
Case reportA 17 year old man was admitted to the hospital with a one month history of cough and yellow sputum, which were not relieved by antibiotics and the usual expectorants. He had been relatively healthy despite being on digoxin and diuretics following heart surgery for Tetralogy of Fallot 5 yrs prior to admission. On examination, the patient appeared acutely and chronically ill. Blood pressure was 110/70 mmHg, pulse rate 80 beats路min -1 , respiratory rate 20 breaths路min -1 , and body temperature 37藲C. A grade III systolic murmur was heard at the cardiac apex and inspiratory crackles were present over both lower lung fields. There was no pitting oedema or clubbing. White blood cell count was 6,500 cells路mm -3 , with 52% neutrophils, 42% lymphocytes, 2% monocytes and 4% eosinophils. Sputum cultures grew alpha-haemolytic streptococci but no fungi or other pathogens.Chest roentgenogram showed bilateral patchy infiltrations with cardiomegaly. The heart size was unchanged compared with that recorded 2 months before admission ( fig. 1a). High resolution computed tomography (HRCT) scan showed bilateral patchy consolidations, both centrally and peripherally. No evidence of interstitial oedema was present ( fig. 1b). Echocardiography revealed left atrial and ventricular enlargement with mitral regurgitation. These findings were unchanged compared to the findings 6 months prior to admission. Spirometry was normal, with a forced vital capacity (FVC) of 4.01 L (102% of predicted), forced expiratory volume in one second (FEV1) of 3.52 L (102% pred), and FEV1/FVC of 87%. Transfer factor of the lungs for carbon monoxide was 20.4 mL路mm -1 路mmHg -1 (74% pred). Breathing room air, arterial blood pH was 7.38, arterial carbon dioxide tension (Pa,CO 2 ) 4.8 kPa (36.2 mmHg) and arterial oxygen tension (Pa,O 2 ) 11.4 kPa (85.5 mmHg). Fibreoptic bronchoscopy disclosed widespread hyperaemic mucosa with viscid purulent secretion in the large bron...