A study of empyema thoracis and role of intrapleural streptokinase in its management.
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BACKGROUND: Clinical spectrum, microbiology and outcome of empyema thoracis are changing. Intrapleural instillation of fibrinolytic agents is being increasingly used for management of empyema thoracis. The present study was carried out to describe the clinical profile and outcome of patients with empyema thoracis including those with chronic empyema and to study the efficacy and safety of intrapleural streptokinase in its management. METHODS: Clinical profile, etiological agents, hospital course and outcome of 31 patients (mean age 40 +/- 16 years, M: F 25: 6) with empyema thoracis treated from 1998 to 2003 was analyzed. All patients were diagnosed on the basis of aspiration of frank pus from pleural cavity. Clinical profile, response to therapy and outcome were compared between the patients who received intrapleural streptokinase (n = 12) and those who did not (n = 19). RESULTS: Etiology was tubercular in 42% of the patients (n = 13) whereas the rest were bacterial. Amongst the patients in which organisms could be isolated (n = 13, 42%) Staphylococcus aureus was the commonest (n = 5). Intrapleural streptokinase was instilled in 12 patients. This procedure resulted in increase of drainage of pleural fluid in all patients. Mean daily pleural fluid drainage after streptokinase instillation was significantly higher for patients who received intrapleural streptokinase than those who did not (213 ml vs 57 ml, p = 0.006). Only one patient who was instilled streptokinase eventually required decortication, which had to be done in five patients (16.1%). Mean hospital stay was 30.2 +/- 17.6 days whereas two patients died. CONCLUSIONS: Tubercular empyema is common in Indian patients. Intrapleural streptokinase appears to be a useful strategy to preserve lung function and reduce need for surgery in patients with late stage of empyema thoracis. (+info)
Redistribution of pulmonary EC-SOD after exposure to asbestos.
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Inhalation of asbestos fibers leads to interstitial lung disease (asbestosis) characterized by inflammation and fibrosis. The pathogenesis of asbestosis is not fully understood, but reactive oxygen species are thought to play a central role. Extracellular superoxide dismutase (EC-SOD) is an antioxidant enzyme that protects the lung in a bleomycin-induced pulmonary fibrosis model, but its role has not been studied in asbestos-mediated disease. EC-SOD is found in high levels in the extracellular matrix of lung alveoli because of its positively charged heparin-binding domain. Proteolytic removal of this domain results in clearance of EC-SOD from the matrix of tissues. We treated wild-type C57BL/6 mice with 0.1 mg of crocidolite asbestos by intratracheal instillation and euthanized them 24 h later. Compared with saline- or titanium dioxide-treated control mice, bronchoalveolar lavage fluid (BALF) from asbestos-treated mice contained significantly higher total protein levels and increased numbers of inflammatory cells, predominantly neutrophils, indicating acute lung injury in response to asbestos. Decreased EC-SOD protein and activity were found in the lungs of asbestos-treated mice, whereas more EC-SOD was found in the BALF of these mice. The EC-SOD in the BALF was predominantly in the proteolyzed form, which lacks the heparin-binding domain. This redistribution of EC-SOD correlated with development of fibrosis 14 days after asbestos exposure. These data suggest that asbestos injury leads to enhanced proteolysis and clearance of EC-SOD from lung parenchyma into the air spaces. The depletion of EC-SOD from the extracellular matrix may increase susceptibility of the lung to oxidative stress during asbestos-mediated lung injury. (+info)
Pharmacological stabilization of mast cells abrogates late thrombotic events induced by diesel exhaust particles in hamsters.
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BACKGROUND: Particulate air pollution is associated with cardiovascular diseases and myocardial infarction (MI). METHODS AND RESULTS: We investigated the relationship between airway inflammation and thrombosis 24 hours after intratracheal (IT) instillation of diesel exhaust particles (DEP; 50 microg/hamster). Mild thrombosis was induced in the femoral vein by endothelial injury, and the consequences of airway inflammation on thrombogenicity were studied via online video microscopy. Lung inflammation and histamine analysis in bronchoalveolar lavage (BAL) and plasma were performed after pretreatment with dexamethasone (DEX) or sodium cromoglycate (SC). DEP induced airway inflammation and histamine release in BAL and in plasma, and increased thrombosis, without elevating plasma von Willebrand factor (vWF) levels. The IT instillation of 400-nm positively charged polystyrene particles (500 microg/hamster), serving as particles that do not penetrate into the circulation, equally produced airway inflammation, histamine release, and enhanced thrombosis. Histamine in plasma resulted from basophil activation. Intraperitoneal (IP) pretreatment with DEX (5 mg/kg) abolished the DEP-induced histamine increase in BAL and plasma and abrogated airway inflammation and thrombogenicity. The IT pretreatment with DEX (0.5 mg/kg) showed a partial but parallel inhibition of all of these parameters. Pretreatment with SC (40 mg/kg, IP) strongly inhibited airway inflammation, thrombogenicity, and histamine release. CONCLUSIONS: Our results are compatible with the triggering of mast cell degranulation and histamine release by DEP. Histamine plays an initial central role in airway inflammation, further release of histamine by circulating basophils, and peripheral thrombotic events. Antiinflammatory pretreatment can abrogate the peripheral thrombogenicity by preventing histamine release from mast cells. (+info)
In vivo measurement of brain extracellular space diffusion by cortical surface photobleaching.
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Molecular diffusion in the brain extracellular space (ECS) is an important determinant of neural function. We developed a brain surface photobleaching method to measure the diffusion of fluorescently labeled macromolecules in the ECS of the cerebral cortex. The ECS in mouse brain was labeled by exposure of the intact dura to fluorescein-dextrans (M(r) 4, 70, and 500 kDa). Fluorescein-dextran diffusion, detected by fluorescence recovery after laser-induced cortical photobleaching using confocal optics, was slowed approximately threefold in the brain ECS relative to solution. Cytotoxic brain edema (produced by water intoxication) or seizure activity (produced by convulsants) slowed diffusion by >10-fold and created dead-space microdomains in which free diffusion was prevented. The hindrance to diffusion was greater for the larger fluorescein-dextrans. Interestingly, slowed ECS diffusion preceded electroencephalographic seizure activity. In contrast to the slowed diffusion produced by brain edema and seizure activity, diffusion in the ECS was faster in mice lacking aquaporin-4 (AQP4), an astroglial water channel that facilitates fluid movement between cells and the ECS. Our results establish a minimally invasive method to quantify diffusion in the brain ECS in vivo, revealing stimulus-induced changes in molecular diffusion in the ECS with unprecedented spatial and temporal resolution. The in vivo mouse data provide evidence for: (1) dead-space ECS microdomains after brain swelling; (2) slowed molecular diffusion in the ECS as an early predictor of impending seizure activity; and (3) a novel role for AQP4 as a regulator of brain ECS. (+info)
VCAM-1 upregulation via PKCdelta-p38 kinase-linked cascade mediates the TNF-alpha-induced leukocyte adhesion and emigration in the lung airway epithelium.
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Vascular cell adhesion molecule (VCAM)-1 plays a central role in the recruitment of inflammatory cells, and its expression is rapidly induced by proinflammatory cytokines such as TNF-alpha. In the present study, we show that pretreatment with rottlerin, a specific inhibitor of protein kinase C (PKC)-delta, or transient transfection with antisense PKCdelta oligonucleotides significantly inhibits TNF-alpha-induced expression of VCAM-1, but not of intercellular adhesion molecule (ICAM)-1 in human lung epithelium A549 cells. In addition, TNF-alpha was shown to induce the expression of VCAM-1 in a p38 kinase-dependent manner; also, TNF-alpha-induced p38 kinase activation was blocked by inhibition of PKCdelta, suggesting that p38 kinase is apparently situated downstream of PKCdelta in the TNF-alpha-signaling pathway to VCAM-1 expression. Notably, inhibition of the PKCdelta-p38 kinase cascade also attenuated the TNF-alpha-induced adhesion of neutrophils to lung epithelium and the trafficking of leukocytes across the epithelium into the airway lumen in vivo. Together, these findings indicate that signaling via PKCdelta-p38 kinase-linked cascade specifically induces expression of VCAM-1 in lung epithelium in response to TNF-alpha and that this effect is both functionally and clinically significant. (+info)
Intrapleural instillation of rituximab for the treatment of malignant pleural effusions in NHL.
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A patient with CD20(+) leukaemic lymphoplasmacytic Non-Hodgkin's lymphoma (NHL) presented with bilateral malignant pleural effusions. Systemic chemotherapy, repeated percutaneous drainage and bilateral continous chest tube drainage were unable to control the effusions. Rituximab was instilled in a dose-escalating manner via the chest tubes into both pleural spaces, within two weeks the effusions resolved, and the patient has stayed free of symptoms for eight months ongoing. Rituximab may be a promising novel treatment option for malignant effusions in CD20(+) NHL. (+info)
Wound instillation--the next step in negative pressure wound therapy. Lessons learned from initial experiences.
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Negative pressure wound therapy uses a reticulated sponge and subatmospheric pressure to facilitate healing of a variety of wounds. The therapy appears to assist wound healing by decreasing wound bacterial burden and edema while facilitating granulation tissue formation. The latest development in negative pressure wound therapy allows clinicians to instill a solution into the wound and is indicated for use when patients receiving negative pressure wound therapy would benefit from the controlled delivery of topical wound treatment solutions and suspensions. A retrospective analysis of five cases was conducted to describe initial experiences with instillation and negative pressure wound therapy (average treatment time on negative pressure wound therapy with instillation 15 days, range 5 to 24 days). In two of the five cases where traditional negative pressure wound therapy was tried, infected wounds improved and culture results became negative following instillation of antibiotics in a saline solution. In all cases where used, instillation of a topical anesthetic appeared to effectively minimize wound pain that is occasionally associated with negative pressure wound therapy. Negative pressure wound therapy with instillation and possibly hyperbaric oxygen therapy may be initiated from the onset of treatment to manage high-risk wounds that appear severely infected and may be limb-threatening if located on an extremity. Controlled clinical studies to ascertain the efficacy and cost-effectiveness of this treatment modality are needed. (+info)
A comparison of bupivacaine instillation and inguinal field block for control of pain after herniorrhaphy.
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In a single-blind, randomised trial, 50 consecutive adult patients for inguinal herniorrhaphy under general anaesthesia received either an inguinal field block or bupivacaine instilled into the wound to provide postoperative analgesia. Bupivacaine instillation was found to be simple, safe and effective. The method is particularly appropriate for day-case surgery. (+info)