A case of miliary tuberculosis associated with ARDS, DIC and bilateral pneumothorax

We reported a case of 64 a year-old male patient of miliary tuberculosis associated with ARDS, DIC and pneumothorax, who had a history of gastric ulcer and pulmonary tuberculosis. On admission his chief complaints were fever, fatigue, palpitation, appetite loss and weight loss, and most noticeable abnormalities were bleeding from the gastric ulcer and miliary shadow on the chest x-ray film with hypoxemia. On the day after admission to the hospital he was diagnosed as ARDS as he showed severe hypoxemia due to extensive tuberculous infiltration in bilateral lung fields, and treatment with antituberculous drugs and steroids were started. On the third hospital day DIC appeared on laboratory data, Gabexate mesilate (FOY) for DIC and respirator for ARDS were introduced. Two weeks later pulmonary infiltration, PaO2 and general condition were somewhat improved. On the 15th day after admission pneumothorax occurred on the right side, and on the 20th day on the left. Tube drainage of both pleural cavities, and instillation of OK-432 and Fibrinogen HT into the right pleural cavity were done, but it showed no effect. Two months after admission pouring Fibrinogen HT and thrombin into the left B1+2 and right B1 with cannula washing pipe through the instrument channel of bronchoscope was carried out. A few days later air leakage stopped and collapsed lungs were completely expanded. This method is effective in the case of incurable pneumothorax with pulmonary hypofunction.     

A case of spontaneous pneumothorax due to metastasis of urinary bladder carcinoma to the lung

We reported a case of spontaneous pneumothorax associated with pulmonary metastasis of urinary bladder carcinoma. A 73-year-old male patient complaining of chest pain and dyspnea was admitted, who had undergone transurethral resection of the urinary bladder carcinoma and diagnosis of inactive pulmonary tuberculosis based on the chest X-ray film finding one year previously. On admission, chest X-ray film showed right pneumothorax, and the re-expanded chest X-ray film revealed a cystic lesion in the right upper lung field adjacent to the anterior chest wall, corresponding to the previous pulmonary lesion. Three months later, right thoracotomy was performed because of relapse accompanying by profuse air-leakage. There was a pleural fistula on the surface of the cystic lesion and necrotic tissue in it. Drainage bronchi were involved by surrounding tumorous tissue. Histological examination of the specimen from the cyst wall disclosed metastasis of transitional cell carcinoma of the bladder. The probable mechanism of the spontaneous pneumothorax probable consisted of stenosis of the right B3 bronchus caused by the metastatic tumor produced a check valve mechanism leading to cystic lesion, the rupture of which caused the spontaneous pneumothorax.     

A case of invasive thymoma with pulmonary tuberculosis

A 68-year old male was referred to our hospital for the treatment of pulmonary tuberculosis. Chest X-ray film revealed left diffuse pleural thickening. Treatment of pulmonary tuberculosis was started with streptomycin, isoniazid and rifampicin. Three months later, although smear and culture of the patient's sputum became negative for M. tuberculosis, he started to complain of dyspnea on exercise and left chest pain. Biopsies of a pleural tumor and a left subclavicular lymph node were done and a diagnosis of invasive thymoma with pleural dissemination and bone and lymph node metastasis was established. After three cycles of combination chemotherapy consisting of cyclophosphamide, adriamycin and vincristine, left chest pain disappeared and pleural thickening showed shrinkage.     

A case of pulmonary sarcoidosis with pneumothorax and pleural effusion after improvement of pulmonary impairment]

A 23-year-old man was admitted to our hospital for a complete medical evaluation of abnormal pulmonary shadows found on a chest radiograph during his annual check-up. Chest radiography and chest CT showed a diffuse spread of micronodules in both lung fields and mediastinal lymphadenopathy. A transbronchial lung biopsy demonstrated evidence of noncaseating epithelioid cell granuloma with multinucleated giant cells, and a diagnosis of sarcoidosis was made. The pulmonary shadows improved without therapy. Twenty months later, the patient was readmitted to the hospital because of chest pain and dyspnea. Pneumothorax appeared on the right in a chest radiograph, but subsided after drainage therapy, and two weeks later, a right side pleural effusion was seen. We determined that the pleura was involved in the sarcoidosis, and the patient was treated with oral prednisolone 20 mg daily. The pleural effusion gradually subsided. This is the first reported case in Japan of pulmonary sarcoidosis with pneumothorax and pleural effusion after improvement of pulmonary impairment.     

Autopsy case of diffuse pleural thickening presenting respiratory impairment and benign asbestos pleurisy]

A 51-year-old man presented with back pain in 1997. He had a 30-year-history of occupational asbestos exposure. His chest CT showed bilateral pleural thickening and pleural effusion. The pleural effusion of the right thorax exhibited both elevated level of adenosine deaminase and increased numbers of lymphocytes. Antituberculous chemotherapy had no effect on the exudates. Progressive bilateral pleural thickening were found on chest CT, and pulmonary function tests showed severe restrictive ventilatory impairments since 1998. Thoracoscopic pleural biopsy was conducted in 2001 to exclude pleural malignant mesothelioma. No malignancy was found in pleural samples. After 3-year observation and excluding other causes, he was given a diagnosis of benign asbestos pleurisy. In 2005, fibrotic changes were found in both lower lung fields in chest CT. He suffered from respiratory failure with carbon dioxide retention, and died in 2006. The autopsy disclosed asbestos-related lung diseases. We suspected that diffuse pleural thickening could be a major cause of fatal respiratory impairment in this case.     

Refractory pneumothorax secondary to lung cancer in a patient with idiopathic pulmonary fibrosis

An unusual case of refractory pneumothorax secondary to lung cancer in a 69-year-old man patient with idiopathic pulmonary fibrosis (IPF) is described. High-pressure suction applied through chest tube did not resolve the large right pneumothorax. Acute exacerbation of IPF has also appeared. Respiratory state worsened acutely, and the patient died on the fifth hospital day. In the present case, the large right pneumothorax was initially thought to be associated with IPF because pneumothorax is common in patients with IPF. However, postmortem microscopic examination revealed that the refractory pneumothorax was secondary to perforation of the pleura due to a necrotic peripheral lung cancer.     

Failure of buserelin-induced medical castration to control pulmonary lymphangiomyomatosis in two patients.

Two women, aged 44 and 29 years, respectively, were admitted to the hospital in early 1987 for recurrent pneumothorax, dyspnea and a diffuse reticulonodular pattern evidenced on the chest x-ray film. Lung biopsy confirmed LAM in both patients. Both were treated sequentially with medroxyprogesterone and a LHRH agonist (buserelin) to achieve reversible medical castration. Neither subjective nor objective improvement was noted after 13 and 5 months, respectively, of buserelin therapy (900 micrograms/day, nasal spray) despite an effective suppression of the pituitary-gonadal axis. Medroxyprogesterone also was ineffective. Buserelin thus failed to control pulmonary LAM in these two patients, in spite of effective medical castration.     

A case of sub-acute onset pulmonary sarcoidosis with pulmonary dysfunction]

A 60-year-old man was admitted to our hospital because of shortness of breath and dry cough. Slight pleural thickening was observed on the chest X-ray film and chest CT on presenting. Three months later, bilateral hilar lymphadenopathy and multiple small nodular shadows were shown in both lung fields by chest CT. Serum ACE level and lysozyme levels were higher than normal upper limit. Elevation of CRP and left shift of leukocytes were not detected. Restrictive ventilatory impairment was shown in the respiratory function test. This case was diagnosed as sarcoidosis most probably with histological evidence of epithelioid cell granulomas in the lung tissue obtained by transbronchial lung biopsy. After prednisolone medication (40 mg per day) was started, symptoms, pulmonary function and chest CT findings improved. Our case was considered to be a rare case of pulmonary sarcoidosis with subacute onset of symptoms and restrictive pulmonary function abnormality which improved smoothly as a result of steroid therapy.     

Erdheim-Chester disease presenting with pneumothorax

Erdheim-Chester disease (ECD) is a rare non-Langerhans cell histiocytosis most commonly characterized by symmetrical skeletal involvement and may present with pulmonary involvement leading to chronically progressive pulmonary symptoms. Characteristics on chest radiography include non-specific findings of diffuse interstitial and pleural thickening, micronodules, ground-glass opacities and parenchymal condensation as a result of infiltration by lipid-laden histiocytes. We present the case of a 50-year-old man with ECD presenting with acute pulmonary symptoms due to rupture of a large cystic lesion with resultant pneumothorax. He was brought by ambulance to our hospital, complaining of acute anterior chest pain and severe dyspnea. Chest radiography showed right-sided pneumothorax with a collapsed lung, a large, left-sided cystic lesion in the upper lung field and accentuated interstitial markings. Bullectomy and surgical biopsy were performed, demonstrating histologically histiocytic infiltrates that were strongly positive for CD68, but negative for S-100 protein and CD1a. Subsequent systemic examinations indicated widespread symmetrical skeletal involvement, leading to a definitive diagnosis of ECD.     

Miliary PCP in AIDS

The most frequent radiographic presentation of (PCP) is bilateral interstitial or alveolar infiltrates. Atypical features include lobar distribution, pleural effusions, hilar adenopathy, cyst formation and spontaneous pneumothorax. A diffuse miliary pattern has not been described previously for PCP. A 30-year-old male intravenous drug abuser, with AIDS, presented to our institution complaining of fever and productive cough. Admission chest x-ray film revealed a "classic" miliary pattern. Sputum smears were negative for acid-fast bacilli and both bronchoalveolar lavage and transbronchial biopsy revealed only PCP. Repeat bronchoscopy one month later was unrevealing and marked x-ray resolution occurred after treatment with pentamidine alone. The incidence of atypical roentgenographic features of PCP in AIDS is approximately 10 percent. Given the frequency of this infection in AIDS, knowledge of the unusual presentations is imperative. Based on this report, PCP must be included in the differential diagnosis of a miliary x-ray pattern.     

Observations of the fibrosing process in paraquat lung injury by chest X-ray and CT

A 42-year-old woman with a known history of paraquat ingestion was admitted to our hospital on the 10th day after ingestion complaining of dyspnea and general fatigue. Steroid therapy and low dose oxygen therapy were administered. She recovered and was discharged on the 190th day after paraquat ingestion. A chest X-ray film on admission disclosed a bilateral ground-glass shadow. As time passed, a reticular shadow with a loss of lung volume leaving a peripherally clear zone appeared on chest X-rays and shrank gradually toward the peri-hilar area during the course. CT of the lung clearly demonstrated progress of the pulmonary fibrosing process. In the early phase of paraquat poisoning, CT revealed diffuse high density areas dominant in the posterior part of the lungs with a subpleural intact area. The high density area was sharply demarcated from the subpleural intact area. As time passed, the high density area shrank toward the central zone, causing bullous changes in the subpleural area. The dominant fibrotic change in the intermediate and central zones seems to be one of the characteristic findings in paraquat induced pulmonary fibrosis.     

A case of malignant lymphoma showing a stratum of lymphoma cells]

A 74-year man suffered an artificial pneumothorax of the right lung because of pulmonary tuberculosis 41 years before. He was admitted, and enlargement of chronic pyothorax was noted in chest radiography in 1998. A 67Ga scintigram revealed uptake at the site of the chronic pyothorax. Cytological findings of the pleural effusion included many atypical lymphocytes. We suspected the presence of a malignant lymphoma and performed a biopsy under thoracoscopy, but could not arrive at a diagnosis. Therefore, resection of the chronic empyema was performed. Histological examination demonstrated the layer of lymphoma cells covering the wall of empyema between the layers of necrotic and connective tissue. Lymphoma cells were stained with L 26, which is known as a B cell marker. We diagnosed diffuse large cell lymphoma (B cell type). No case like this case has ever been published of malignant lymphoma bearing a layer of lymphoma cells. This case is thought to show early-phase malignant lymphoma complicated with chronic pyothorax after artificial pneumothorax. Malignant lymphoma should be suspected when chronic pyothorax undergoes enlargement, even if CT scanning or MRI does not show typical findings.     

Diagnosis of pneumothorax by ultrasound immediately after ultrasonically guided aspiration biopsy.

We report two cases of pneumothorax detected by echographic examination immediately after ultrasonically guided aspiration biopsy and confirmed by chest x-ray film. The pneumothorax was characterized by the disappearance of the lung tumor. In the real-time image, the respiratory excursions of the visceral pleura also disappeared.     

A case of primary pulmonary proteinosis with bilateral pneumothorax]

A 40-year-old man was admitted to our hospital because of chronic cough and mild exertional dyspnea. Radiographs of the chest showed diffuse infiltrative shadows in both lung fields. A diagnosis of pulmonary alveolar proteinosis (PAP) was made by examination with a flexible bronchoscope and bronchoalveolar lavage, with transbronchial biopsy. After diagnosis, the patient underwent whole-lung lavage with temporary improvement. Due to the recurrence of his illness, he needed a total of four whole-lung lavages over the course of his illness. However, the exertional dyspnea became progressively worse. Bilateral pneumothorax developed suddenly and led to his death. This case indicates the possibility that deterioration of PAP despite whole-lung lavage may sometimes be followed by pneumothorax.     

A case of sarcoidosis presenting with high fever and acute respiratory failure

A 55-year-old man was admitted with complaints of remittent fever (39 degrees C) and dyspnea on exertion which began ten days previously. His family and past histories were non-contributory for diagnosis except his occupation as a stone mason for 26 years. The chest X-ray film taken on admission showed diffuse small nodular shadows associated with small amounts of pleural effusion and bilateral hilar adenopathy. Arterihl blood gas analysis showed severe hypoxemia and hypocapnea (Pao2 32.2 Torr, Paco2 31.6 Torr). The serum level of LDH was 985 IU/L and ACE was 49.0 IU/L, lysozyme was 28.8 micrograms/ml. Biopsied materials of the lung obtained by TBLB, liver and bone marrow showed non-caseating epithelioid granuloma without caseating necrosis. T-lymphocyte ratio increased in BALF. The patient was diagnosed to have sarcoidosis. The administration of prednisolone was initiated, which resulted in a marked improvement of clinical data including chest X-ray films, BGA, LDH, ACE and lysozyme.     

Tuberculous pneumothorax. Retrospective study of 23 cases in Tunisia

The tubercular pneumothorax is a rare and severe form of tuberculosis which persists in Tunisia. We reviewed retrospectively our experience at the Pneumology-Allergology Department of the Sousse Hospital with 23 cases of tubercular pneumothorax observed between 1985 and 2003. The suggestive symptom, pneumothorax, always occurred within a context poor general health and fever. The chest roentgengraph showed pneumothorax (n=8) or hydropneumothorax (n=15), and pulmonary lesions associated in 82.5% of patients. Bacteriological proof was obtained in 21 cases; in the two other patients, histological examination of the surgical specimen was highly suggestive of tuberculosis. Treatment associated antitubercular chemotherapy in compliance with the National Plan of against Tuberculosis (n=23), chest drainage (n=21) and respiratory physiotherapy (n=18). Five patients underwent surgery: pleural decortications (n=3), pulmonary resections (n=2). Two were lost to follow-up. The course was favourable in 78% of patients; there were two cases of partitioned pyopneumothorax and one post-operative death. In our experience, tubercular pneumothorax was always associated with active cavitated tuberculosis. The course was almost favorable with antitubercular chemotherapy and chest drainage.     

A case of lung infection complicated by pneumothorax caused by Mycobacterium marinum

Mycobacterium marinum is a waterborne mycobacterium that commonly infects fish and amphibians worldwide, but transmission to humans can occasionally occur, typically as a granulomatous skin infection following minor hand trauma. Infection involving the lungs is very rare. We herein describe a case of M. marinum-associated pneumonia and pneumothorax. In August 2008, an 81-year-old man was admitted to a hospital for detailed examination of weight loss and an abnormal shadow on chest imaging. Based on a sputum test, nontuberculous mycobacteriosis caused by M. marinum was diagnosed. At that time, the blood chemistry revealed no respiratory symptoms or inflammatory findings, and the patient was treated on an outpatient basis with erythromycin and an expectorant. In late November 2008, sputum and coughing were observed. Furthermore, the patient developed a fever and chest pain that increased while breathing and he visited the emergency outpatient unit of our hospital on December 1. Hypoxemia, bilateral pneumonia, and right pneumothorax were observed, and a chest tube was inserted into the right thoracic cavity. Results of an acid-fast bacteria smear from the sputum and pleural effusion were positive, and M. marinum was identified on culture. The patient was diagnosed as having a lung infection complicated by pneumothorax caused by M. marinum. The lung infection was ameliorated with clarithromycin, rifampicin and ethambutol. However, no decreased in the air leaking from the chest tube was noted and inflation of the lung was incomplete. The department of respiratory surgery therefore performed thoracoplasty and lung cerclage. Subsequently, the air leak subsided, allowing removal of the chest tube and the patient was discharged.     

Pulmonary interstitial fibrosis following near-drowning and exposure to short-term high oxygen concentrations.

Following near-drowning in fresh water, a 19-year-old man experienced severe adult respiratory distress syndrome, necessitating ventilatory support with positive end-expiratory pressure and high oxygen concentrations. Post-extubation, his course was highlighted by persistent hypoxemia and interrupted by a lung abscess which responded promptly to antibiotics. Pulmonary function tests were consistent with severe restrictive disease and chest radiograph revealed persistent bilateral alveolar and interstitial infiltrates. An open lung biopsy on the 26th hospital day showed interstitial fibrosis. Over the ensuing two months, the chest radiograph and pulmonary function tests returned towards normal. We attribute the pulmonary fibrosis to incomplete resolution of the alveolar interstitial pathology secondary to the near-drowning and exposure to high oxygen mixtures.     

Persistent pulmonary interstitial emphysema in an unventilated neonate

Persistent pulmonary interstitial emphysema (PPIE) is a chronic form of pulmonary interstitial emphysema. The disease is histologically distinguished by large cysts and giant cells. Our patient was a female twin who was born at 31 weeks of gestation with a birth weight of 1,450 g. A chest X-ray at 2 hr after delivery was normal. At 12 hr, respiratory distress developed, and nasal continuous positive airway pressure (CPAP) was initiated. A chest film revealed left-sided pneumothorax. A chest tube was inserted, and the baby continued on nasal CPAP for 5 days. Her chest X-ray on postnatal day 4 showed diffuse cystic changes in the left lung. Thoracic computed tomography revealed multiple thick-walled cysts, the largest measuring 3 cm in diameter. Our case confirms that localized PIE may occur in preterm infants who have been treated with nasal CPAP only. Since this method is being used increasingly to avoid mechanical ventilation and in the postextubation period, it is very important that clinicians be aware of its complications.     

Clinical and pathologic features of rounded atelectasis in patients with empyema

Rounded atelectasis (RoA) is an uncommon pulmonary condition presenting as a peripheral round opacity on a chest roentgenogram. Six cases of empyema who underwent regional lung and pleural resection, had local atelectatic induration beneath the pleura. Their clinical and pathologic features were examined. Five cases had past histories of pulmonary tuberculosis with therapeutic pneumothorax, and one other case had tuberculous pleuritis. Five of seven atelectatic indurations displayed RoA on preoperative plain radiography ++ and/or CT and on soft X-ray films of resected lung preparations. With pathological examinations, the pleura showed one or several indentations, often with deep invaginations into the pulmonary parenchyma. In these regions, the appearance was occasionally more complex due to several small folds emanating from the larger fold. Outside the pleural folds, there was dense fibrous thickening. Fibrosis of the pleural interstitial layer itself was mild. Lung parenchyma adjacent to the folded pleura appeared collapsed with mild interstitial fibrosis. These findings lead to the hypothesis that RoA may result from pleural invaginations occuring after pleural effusion or therapeutic pneumothorax and from fibrous adhesions of the outer regions.