An unusual cause of stridor and progressive shortness of breath.

نویسندگان

  • Carolina Q See
  • Christopher O Olopade
چکیده

A 31-year-old man was referred to the pulmonary outpatient clinic for evaluation of difficult breathing of 1 year in duration. He was well until a year prior to consultation when noisy breathing developed, which was followed 6 months later by progressive shortness of breath. At the time of his evaluation, he was unable to walk a full city block. He had occasional cough productive of clear sputum, with nocturnal awakening to catch his breath. He had been previously worked up and treated for asthma with no improvement in symptoms while receiving bronchodilators and corticosteroids. He denied fever, orthopnea, paroxysmal nocturnal dyspnea, chest pain, weight loss, preceding upper respiratory infection, or recent travel. The patient worked in an embroidery shop with exposure to lint for a few years without the use of a protective mask. Being at or away from work did not influence the symptoms of cough and dyspnea. He was a nonsmoker and had no history of childhood asthma. He underwent surgery 4 years earlier for a herniated disk under general anesthesia and was extubated postoperatively with no complications. Physical examination revealed a young, healthy appearing man with stridorous breathing but in no acute distress. There was no sinus tenderness to palpation. The lung examination revealed no wheezing, and the cardiopulmonary examination was essentially normal. The rest of the head and neck examination was normal with no palpable neck masses or lymphadenopathy. Pulmonary function test results showed the following: (1) spirometry: FVC before bronchodilator, 3.94 L (109% predicted); after bronchodilator, 4.13 L (114% predicted); FEV1 before bronchodilator, 2.89 L (94.1% predicted); after bronchodilator, 2.98 L (96.8% predicted); FEV1/ FVC before bronchodilator, 73%; after bronchodilator, 72%; forced expiratory flow, midexpiratory phase, before bronchodilator, 2.41 L/s (68.6% predicted); after bronchodilator, 2.51 L/s (71.6% predicted); forced expiratory flow at 50% of vital capacity (VC)/forced inspiratory flow at 50% of VC (FIF50) ratio before bronchodilator, 1.88; (2) lung volumes: total lung capacity, 5.25 L (103% predicted); VC, 4.10 L (114% predicted); residual volume, 1.15 L (77% predicted); functional residual capacity, 2.17 L (80% predicted); and (3) diffusion capacity: single-breath diffusion capacity of the lung for carbon monoxide, 27.3 mL/mm/mm Hg (88.8% predicted). Arterial blood gases on room air showed pH 7.4; Pco2, 41.5 mm Hg; Po2, 106 mm Hg. The flow-volume loop (Fig 1) and chest radiograph of the patient (Fig 2) are shown.

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عنوان ژورنال:
  • Chest

دوره 128 3  شماره 

صفحات  -

تاریخ انتشار 2005