Hemomediastinum due to spontaneous rupture of a mediastinal bronchial artery aneurysm - A rare cause of thoracic pain.

Hemomediastinum is a rare pathological event. Multiple underlying causes and contributory factors can be identified, such as trauma, malignancy, iatrogenic, bleeding disorder or mediastinal organ hemorrhage. Also, a mediastinal bronchial artery aneurysm may be the source of a hemomediastinum. Hemoptysis is an important directive symptom, however occasionally, patients only present with thoracic pain or symptoms related to extrinsic compression of the airways or esophagus. Using contrast-enhanced computed tomography (CT) of the chest, hemomediastinum can be adequately diagnosed, and the involved vascular structures can be revealed. In case of a (ruptured) bronchial artery aneurysm, transcatheter embolization provides a minimally invasive procedure and is treatment of first choice. In this case report, a 76-year-old female is presented with spontaneous rupture of a mediastinal bronchial artery aneurysm resulting in hemomediastinum causing thoracic pain. Superselective embolization of the left bronchial artery was successfully performed.

Misidentification and diagnostic delay Caused by a false-positive amplified Mycobacterium tuberculosis direct test in an immunocompetent patient with a Mycobacterium celatum infection.

The Gen-Probe amplified Mycobacterium tuberculosis direct test can give discrepant results directly in respiratory or cultured samples from patients infected with Mycobacterium celatum, leading to inappropriate therapy for, in our case, an immunocompetent patient.

Diagnostic yield of computed tomography and densitometric measurements of the lung in thoracoscopically-defined idiopathic spontaneous pneumothorax.

In the present study, the diagnostic yield of high resolution computed tomography (HRCT) is evaluated in patients with thoracoscopically-verified idiopathic spontaneous pneumothorax (SP). Visual assessment as well as densitometry of lung parenchyma was performed. In eight of the 20 prospectively-evaluated SP patients, emphysema-like (EL) changes such as blebs and bullae could be detected. The SP patients with EL changes were significantly older and were more heavy smokers. Spirometrically-controlled CT lung densitometry showed no differences between the patient group with or without these EL changes. Comparing the densitometric measurements of the patient group with a healthy control group no significant differences in densitometry between both groups were found. In conclusion, this study confirms that HRCT is a reliable method of detecting blebs and bullae in patients with spontaneous pneumothorax. Furthermore CT lung densitometry revealed no parenchymal abnormalities or signs of air trapping in patients with spontaneous pneumothorax.

Diagnostic value of lactate dehydrogenase isoenzyme pattern in pleural effusions.

Lactate dehydrogenase isoenzymes have been used to classify the nature of pleural effusion. Nevertheless, studies have reported conflicting results. The objective of this study was to evaluate the diagnostic value of lactate dehydrogenase isoenzymes in the analysis of pleural effusions. Pleural fluid samples obtained from three respective diagnostic groups: group I transudate (n = 23), group II parapneumonic effusion (n = 29) and group III malignant effusion or pleuritis carcinomatosa (n = 41) were evaluated. Total lactate dehydrogenase activity and lactate dehydrogenase (LDH) isoenzyme pattern were significantly different between transudative (group I) and exudative (group II and III) effusions. Group II and III showed a low percentage of LDH1 (p < 0.001), whereas the percentages of LDH4 (p < 0.001) and LDH5 (p < 0.001) were higher compared to group I. Moreover, in exudative effusions the percentage of LDH1 (p < 0.005), LDH4 (p < 0.005), as well as LDH5 (p < 0.005) were significantly different between parapneumonic and malignant effusions. In contrast to relative lactate dehydrogenase isoenzyme values, the absolute values of lactate dehydrogenase isoenzymes did not differ between group II and group III. Logistic regression analysis yielded a strong discrimination between group I and II+III, simultaneously using lactate dehydrogenase, glucose and protein as explanatory variables. Logistic regression analysis yielded only a weak discrimination between group II and III, simultaneously using lactate dehydrogenase, glucose and the absolute values of LDH2 and LDH4 as explanatory variables. In conclusion, the lactate dehydrogenase isoenzyme pattern differed between pleural effusions of transudative and exudative origin. However, including lactate dehydrogenase isoenzyme activities in the biochemical work-up of pleural effusions did not reveal an additional discriminatory value in the assessment of the classification of these effusions.

Postoperative pulmonary function abnormalities after coronary artery bypass surgery.

In 18 patients, postoperative effects of coronary bypass surgery were evaluated. Pulmonary function studies were conducted preoperatively, and 1 and 6 weeks postoperatively, by means of spirometry, respiratory pressures, body plethysmography and impedance measurement of the respiratory system using the forced oscillation technique. One week postoperatively, total lung capacity (P less than 0.0001), inspiratory vital capacity (P less than 0.0001) forced expiratory volume (P less than 0.0001) and functional residual capacity (P less than 0.01) decreased significantly, while residual volume remained unchanged. This restrictive respiratory impairment was accompanied by significant decreases in inspiratory (P less than 0.0001) and expiratory (P less than 0.01) mouth pressures and significant decreases in respiratory resistance values (P less than 0.01). Six weeks postoperatively, significant differences in total lung capacity (P less than 0.0001), inspiratory vital capacity (P less than 0.0001) and forced expiratory volume (P less than 0.0001) persisted, while respiratory pressures returned to the preoperative values. It is concluded that respiratory muscle weakness contributes to the immediate postoperative restrictive lung function loss. Furthermore, structural alterations of chest wall mechanics have to be supposed for the persisting late restrictive pulmonary impairment.