Early detection of pneumonia in febrile neutropenic patients: use of thin-section CT.

Heußel, Claus Peter; Kauczor, Hans Ulrich; Heußel, Gudula; Fischer, Berthold; Mildenberger, P.; Thelen, M.

doi:10.2214/ajr.169.5.9353456

Cited by 170 publications

(74 citation statements)

References 25 publications

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“…This result suggests that pulmonary vascular permeability was related to neutrophil activity (which differed greatly between immunocompetent and leukopenic mice) rather than to bacterial virulence factors at that time when bacterial counts did not differ between groups. This observation corroborates the limited pulmonary PMN infiltration and edema observed on radiographs of leukopenic patients at early stage of pneumonia (29). Animal models of endotoxemia suggest that PMNs are required for the development of vascular alterations (5,17,46), and it is generally believed that PMN adherence to pulmonary endothelium, with subsequent release of proteases, participate in pathological pulmonary microvascular permeability (2,19,20,27,41,52,53,55).…”

Section: Discussionsupporting

confidence: 72%

Pathogenesis of Pneumococcal Pneumonia in Cyclophosphamide-Induced Leukopenia in Mice

et al. 2002

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Streptococcus pneumoniae pneumonia frequently occurs in leukopenic hosts, and most patients subsequently develop lung injury and septicemia. However, few correlations have been made so far between microbial growth, inflammation, and histopathology of pneumonia in specific leukopenic states. In the present study, the pathogenesis of pneumococcal pneumonia was investigated in mice rendered leukopenic by the immunosuppressor antineoplastic drug cyclophosphamide. Compared to the immunocompetent state, cyclophosphamideinduced leukopenia did not hamper interleukin-1 (IL-1), IL-6, macrophage inflammatory protein-1 (MIP-1), MIP-2, and monocyte chemotactic protein-1 secretion in infected lungs. Leukopenia did not facilitate bacterial dissemination into the bloodstream despite enhanced bacterial proliferation into lung tissues. Pulmonary capillary permeability and edema as well as lung injury were enhanced in leukopenic mice despite the absence of neutrophilic and monocytic infiltration into their lungs, suggesting an important role for bacterial virulence factors and making obvious the fact that neutrophils are ultimately not required for lung injury in this model. Scanning and transmission electron microscopy revealed extensive disruption of alveolar epithelium and a defect in surfactant production, which were associated with alveolar collapse, hemorrhage, and fibrin deposits in alveoli. These results contrast with those observed in immunocompetent animals and indicate that leukopenic hosts suffering from pneumococcal pneumonia are at a higher risk of developing diffuse alveolar damage.Severe pulmonary infections and bacteremia frequently occur in leukopenic patients, since leukocytes are primary mediators of pulmonary host defense in response to invading pathogens (3, 18, 37). The high mortality rate in leukopenic patients occurs at an early stage of the infection and has been associated with signs and symptoms that resemble those in acute respiratory distress syndrome (ARDS) observed in immunocompetent persons (1,31,33,34,35,43,48). Leukopenia is also a common complication of modern aggressive anticancer chemotherapy, and Streptococcus pneumoniae is the causative agent of an increasing number of pulmonary infections in cancer patients (10). Nevertheless, the pathogenesis of pneumococcal pneumonia and lung injury in leukopenic hosts receiving cytotoxic chemotherapy remains poorly studied.The goal of the present study was to characterize lung injury in relation to host response to pneumococcal pneumonia in immunocompetent versus cyclophosphamide-induced leukopenic mice. We hypothesized that differences in the kinetics of bacterial growth and of cytokine and chemokine expression as well as of neutrophil and monocyte/macrophage emigration into lung tissue of leukopenic versus immunocompetent mice would promote different histopathologic features of lung injury in severe S. pneumoniae pneumonia. A better understanding of the pathogenesis of pneumonia in leukopenic host is not only of theoretical interest but also of therape...

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Section: Discussionsupporting

confidence: 72%

Pathogenesis of Pneumococcal Pneumonia in Cyclophosphamide-Induced Leukopenia in Mice

et al. 2002

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“…HRCT has found particular application in those patients with a normal CXR but respiratory symptoms and fever. [15][16][17][18] Here, HRCT is of particular use in patients after a BMT, having a negative predictive value of 97%. 11 Other work recommends that the use of HRCT with guided BAL is the most sensitive way to diagnose pneumonia in the immunocompromised patient.…”

Section: Discussionmentioning

confidence: 99%

Use of first line bronchoalveolar lavage in the immunosuppressed oncology patient

Murray

O’Brien

Padhani

et al. 2001

Bone Marrow Transplant

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Summary:Immunosuppressed oncology patients who develop pulmonary infiltrates during treatment have a mortality rate of the order of 55-90%. Early diagnosis and treatment is associated with increased survival. At present, diagnosis relies on invasive sampling of the respiratory tract using fibre-optic bronchoscopy. We have looked at a 30-month period, from June 1997 to December 1999, where 25 bronchoscopies were performed on patients from the Lymphoma and BMT units at The Royal Marsden Hospital for the further investigation of pulmonary infiltrates. Nine bronchoscopies (36%) yielded a positive result and seven (28%) led to a change in management. Analysis of the data showed that neither a positive result nor a change in management had any impact on overall survival. After reviewing the background literature on the investigation of pulmonary infiltrates in this group and discussion of the respective merits and limitations, we propose a management flowchart, with high-resolution computed tomography (HRCT) as the test arm in a future randomised trial of these patients. Bone Marrow Transplantation (2001) 27, 967-971. Keywords: oncology; HRCT; bronchoscopy The lung is a frequent site of infection in patients receiving treatment for malignancy. This occurs in up to 20% of cases and has a quoted mortality rate of 55-90%. 1,2 Although infection is the single most common cause of pulmonary infiltrates, a significant number are due to noninfective causes notably lung involvement with the primary malignancy, drug-related parenchymal disease, obliterative bronchiolitis, cryptogenic organising pneumonia (COP or BOOP), graft-versus-host disease and alveolar haemorrhage. The underlying pathogens are themselves dependent on the pattern of immunosuppression, as infections in patients with short bursts of neutropenia related to chemo-

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“…Experience is limited predominantly to amphotericin B. When neutropenia has resolved, the patient is clinically well, and CT of the abdomen and chest reveals no suspicious lesions, use of amphotericin B may be discontinued [134,135]. For clinically well patients with prolonged neutropenia, it is suggested that, after 2 weeks of receipt of daily doses of amphotericin B, if no discernible lesions can be found by clinical evaluation, chest radiography (or CT of the chest), and CT of abdominal organs [136,137], use of the drug can be stopped.…”

Section: Duration Of Antimicrobial Therapymentioning

confidence: 99%

2002 Guidelines for the Use of Antimicrobial Agents in Neutropenic Patients With Cancer

&NA;

2002

Infectious Diseases in Clinical Practice

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Early detection of pneumonia in febrile neutropenic patients: use of thin-section CT.

Cited by 170 publications

References 25 publications

Pathogenesis of Pneumococcal Pneumonia in Cyclophosphamide-Induced Leukopenia in Mice

Pathogenesis of Pneumococcal Pneumonia in Cyclophosphamide-Induced Leukopenia in Mice

Use of first line bronchoalveolar lavage in the immunosuppressed oncology patient

2002 Guidelines for the Use of Antimicrobial Agents in Neutropenic Patients With Cancer

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