SBEM is a frequent complication in cirrhotic patients with hydrothorax. E. coli is the most frequent organism responsible for SBEM. The modified method of pleural fluid culture is more sensitive than the conventional method for diagnosis of SBEM.
BACKGROUND:Noninvasive diagnosis of pleural tuberculosis (TB) remains a challenge due to the paucibacillary nature of the disease. As Mycobacterium tuberculosis (MTB)-specific T cells are recruited into pleural space in TB effusion; their indirect detection may provide useful clinical information.OBJECTIVES:Evaluation of pleural fluid interferon (INF)-γ levels vs Quantiferon–TB Gold In tube assay (QFT- IT) in blood and its adapted variants, using pleural fluid or isolated pleural fluid cells in the diagnosis of pleural TB.METHODS:Thirty-eight patients with pleural effusion of unknown etiology presented at Assiut University Hospital, Egypt, were recruited. Blood and pleural fluid were collected at presentation for INF-γ assays. Ex vivo pleural fluid INF-γ levels, QFT-IT in blood and its adapted variants were compared with final diagnosis as confirmed by other tools including blind and/or thoracoscopic pleural biopsy.RESULTS:The final clinical diagnosis was TB in 20 (53%), malignancy in 10 (26%), and effusion due to other causes in eight patients (21%). Ex vivo pleural fluid INF-γ levels accurately identified TB in all patients and were superior to the QFT-IT assays using blood or pleural fluid (70 and 78% sensitivity, with 60 and 83% specificity, respectively). QFT-IT assay applied to isolated pleural fluid cells had 100% sensitivity and 72% specificity. The optimal cut-off obtained with ROC analysis was 0.73 for TB Gold assay in blood assay, 0.82 IU/ml for the cultured pleural fluid assay, and 0.94 for isolated pleural cells assay.CONCLUSION:The ex vivo pleural fluid INF-γ level is an accurate marker for the diagnosis of pleural TB. QFT- IT assay in peripheral blood or its adapted versions of the assay using pleural fluid and/or washed pleural fluid cells had no diagnostic advantage over pleural fluid INF-γ in the diagnosis of pleural TB.
The pathogenesis of inflammatory complication after chest trauma and pulmonary injury is incompletely understood. Injury can trigger a systemic inflammatory response, which leads to pre-activation of neutrophils in blood. The aim of this study was to determine the specific expression profiles of neutrophil receptors in relation to the systemic inflammatory response after chest trauma. Blood samples from fifty patients with isolated thoracic injury were analysed for changes in the neutrophil phenotype within 3, 6 and 24 hours after injury. Study patients was assessed for any inflammatory complications during the first 24 hours. L-Selectin expression remained decreased until 24 hrs while CXCR1, CXCR2 and C5aR levels gradually increased. Expression of FcγRII and expression of the active form were lower in trauma patients, no patients developed ARDS. Thoracic trauma leads to activation of the circulating neutrophils which is transient accompanied by mobilization of young neutrophils into the circulation which leads to systemic inflammatory reactions which need a second stimulus to cause inflammatory complications like ARDS.
Hemostatic system abnormalities have been previously associated with congestive heart failure (CHF). Here, we report a rare case of disseminated intravascular coagulopathy (DIC) in the setting of non-ischemic cardiomyopathy with right atrial and biventricular thrombus. We present a 55-year-old female with a past medical history of bronchial asthma who presented with a six-day history of bilateral leg swelling and dry cough. Her physical examination on admission was significant for signs of biventricular heart failure. Initial workup was significant for elevated pro-brain natriuretic peptide (ProBNP), elevated transaminases, marked thrombocytopenia (19,000/mcL), and coagulopathy with international normalized ratio (INR) of 2.5 and Ddimer of 15,585 ng/mL. Transthoracic echocardiogram (TTE) showed a large mobile right atrial thrombus protruding into the right ventricle and a more adherent left ventricular (LV) thrombus with severely reduced biventricular contractility. Pan CT was done and was significant for multifocal multilobar pulmonary emboli. A lower limb venous duplex was done and revealed extensive bilateral lower limb deep venous thrombosis (DVT). This rare case demonstrates an unusual association between DIC with non-ischemic cardiomyopathy, biventricular thrombus, extensive deep vein thrombosis, and pulmonary embolism (PE). In comparison, there are multiple prior reports for DIC with CHF and LV thrombus. However, our case differs from prior reports in terms of the presence of right atrial and biventricular thrombus. The patient received antibiotics, diuretics, and cryoprecipitate in the setting of persistent low fibrinogen levels. The patient underwent Interventional radiology-guided thrombectomy for extensive pulmonary emboli followed by inferior vena cava (IVC) filter insertion, resulting in the resolution of the right atrial thrombus and extensive decrease of the pulmonary emboli burden. The patient was then given apixaban after normalization of the platelet count and fibrinogen level. Hypercoagulability workup was inconclusive. The patient was then discharged after improvement of symptoms. Early recognition of DIC and cardiac thrombi in patients with new-onset heart failure is crucial for the implementation of the correct management by thrombectomy, optimizing heart failure medications, and anticoagulation to achieve better outcomes.
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