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1/110. Fulminant lethal tuberculous pneumonia (sepsis tuberculosis gravissima) with ARDS in a non-immunocompromised western European middle-aged man.

    We report the case of a 42 years old, non-immunocompromised native Austrian living in Vienna. He presented at home with severe dyspnea and had to be intubated immediately. Shortly after hospital admission, he developed severe adult respiratory distress syndrome (ARDS) and septic shock with massive, bilobar patchy to confluent infiltrations and a need for norepinephrine. A CT-scan revealed severe loss of functional lung tissue with areas of consolidation and multiple communicating cystic spaces. air leaking into the mediastinum through fistulas produced pneumomediastinum, pneumoperitoneum, and a massive soft tissue emphysema. bronchoalveolar lavage performed within the first 24 hours of admission revealed of acid-fast bacilli. Even though appropriate tuberculostatic medication was started immediately, the patient succumbed the next day to ARDS due to massive tuberculous pneumonia and miliary disease (sepsis tuberculosis gravissima).
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2/110. ARDS in a patient with homozygous beta-thalassemia due to yersiniosis.

    We report a case of yersinia enterocolitica sepsis syndrome and the acute respiratory distress syndrome in a chronically transfused adolescent with beta-thalassemia. This manifestation of serious Y. enterocolitica infection has not previously been reported. dyspnea, hypoxia, and fever were the principal features of the clinical presentation. The acute onset of respiratory symptoms occurred after appendectomy. Chest radiographs revealed frontal bilateral infiltrates and alveolar consolidation to three quadrants. Y. enterocolitica was identified from blood and intraoperative appendix cultures. Although there was no need for mechanical ventilation, a remarkable persistence of clinical and X-ray findings was noted. Therapy with high levels of oxygen, and intravenous amikacin and piperacillin/tazobactam led to a favorable outcome.
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3/110. Acute respiratory distress syndrome in a welder exposed to metal fumes.

    A 43-year-old man began having malaise, chills, and fever 12 hours after cutting a galvanized steel grating with an acetylene torch at work. Over the next 72 hours, his symptoms persisted and became worse with progressive shortness of breath. He was admitted to the hospital and begun on antibiotics and steroids. The next day his condition had deteriorated to the point that he had to be intubated. Chest x-ray film and computed tomography showed patchy and interstitial infiltration bilaterally, consistent with acute respiratory distress syndrome. Open lung biopsy showed focal mild interstitial pneumonia. Multiple laboratory studies were negative for an infectious or an immune process. The patient remained on mechanical ventilation for 10 days and was discharged from the hospital 2 days after extubation. He continued to improve, with minimal symptoms and a return to normal activity levels several months after the incident with no continued treatment. Re-creation of his exposure was done under controlled circumstances, with air sampling revealing elevated air levels for cadmium and zinc and borderline levels of arsenic, manganese, lead, and iron.
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4/110. The pathology of transfusion-related acute lung injury.

    Transfusion-related acute lung injury is an uncommon condition characterized by the rapid onset of respiratory distress soon after transfusion. Our understanding of its pathophysiology is based on animal models of complement (C5a) and antibody-induced lung injury and a limited number of autopsies. These models suggest that transfusion-related acute lung injury is induced by granulocytes that aggregate in the pulmonary microvasculature after activation by transfusion-derived antibodies or biologically active lipids. The published autopsy reports provide little support for this model, as they are invariably confounded by underlying pulmonary infection, preexisting disease, and resuscitation injury. We report the case of a previously well 58-year-old man who died of transfusion-related acute lung injury within 2 hours of the onset of pulmonary distress; autopsy showed evidence of massive pulmonary edema with granulocyte aggregation within the pulmonary microvasculature and extravasation into alveoli. Electron microscopy revealed capillary endothelial damage with activated granulocytes in contact with the alveolar basement membranes. These findings provide direct support for the proposed model of transfusion-related acute lung injury pathogenesis.
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5/110. Surfactant treatment in a pediatric burn patient with respiratory failure.

    This report describes surfactant treatment in a burned infant with severe respiratory failure. In this patient the instillation of surfactant rapidly improved compliance, oxygen index (OI), and alveolar-capillary oxygen gradient (AaDO2), while the need for oxygen supplementation and peak positive pressure drastically decreased. The treatment was repeated after 12 hours. Although the baby had severe clinical course complications as a Gram-negative sepsis and a subglottic stenosis, she was weaned from oxygen therapy and mechanical ventilation in few weeks. Surfactant dysfunctions seem to play a central role in the respiratory insufficiency of burned patients, and its exogenous replacements could improve their outcome.
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6/110. Rapidly evolving adult respiratory distress syndrome with eosinophilia of unknown cause in previously healthy active duty soldiers at an Army training center: report of two cases.

    BACKGROUND: Two previously healthy soldiers presented with rapidly evolving adult respiratory distress syndrome (ARDS) within days of their return from the National Training Center at Fort Irwin, california. There have been six similar cases reported in the National Training Center area, five with fatal outcomes. methods: Both patients were treated in an intensive care unit setting. Extensive diagnostic testing was performed, and patients were treated empirically with doxycycline, ceftriaxone, and ribavirin. RESULTS: Both patients had complete recovery. intensive care unit course was notable for circulatory collapse, respiratory distress requiring ventilatory support, approximately 10% eosinophils on bronchoalveolar lavage, and dramatic peripheral eosinophilia. All cultures, including serology cultures for hantavirus, were negative. CONCLUSION: There have been no previously described syndromes comprising "viral" prodrome, rapid progression to ARDS, and eosinophilia. Based on the geographic, temporal, and clinical similarity of these two cases, we believe that they share a common, yet undetermined, cause. Both environmental exposures and any undescribed pathogens warrant further investigation.
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7/110. Varicella pneumonia complicated by acute respiratory distress syndrome in an adult.

    Primary varicella infection is uncommon in adults, but carries a higher rate of morbidity and mortality than in children. pneumonia is the most common complication of primary varicella infection in adults. However, varicella pneumonia complicated with acute respiratory distress syndrome (ARDS) is very rare. We report a case of ARDS secondary to varicella pneumonia in a 26-year-old man with primary varicella. The patient was otherwise healthy and had no evidence of human immunodeficiency virus infection. The initial chest radiograph showed bilateral reticulonodular infiltrates, which quickly evolved to diffuse alveolar consolidations. Arterial blood gas analysis revealed a ratio of arterial partial pressure to fraction of inspired oxygen of 87. Abnormal liver function and thrombocytopenia were also noted. Treatment consisted of mechanical ventilatory support and intravenous administration of acyclovir. His pulmonary condition gradually improved and he was successfully weaned from the ventilator 1 week later. He was discharged on the 15th hospital day with a favorable outcome. His pulmonary function improved progressively, with normal spirometry and lung volumes, but persistent mild impairment of diffusing capacity, 6 months after discharge.
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8/110. vibrio vulnificus infection complicated by acute respiratory distress syndrome in a child with nephrotic syndrome.

    A 9-year-old girl with nephrotic syndrome visited a local hospital after developing fever, chills, and edematous changes and multiple hemorrhagic bullae on both legs over 2 days. Cultures of blood and an aspirate from the bullae yielded vibrio vulnificus. The patient was transferred to our hospital because of persistent fever, generalized edema, acute renal failure, and disseminated intravascular coagulopathy. We treated this patient as a V. vulnificus infection complicated with necrotizing fasciitis. With minocycline and ceftazidime combination therapy was instituted. Emergency fasciotomy and continuous peritoneal dialysis were performed. The patient developed acute respiratory distress syndrome (ARDS) during the hospitalization, requiring intubation and mechanical ventilation. She eventually died. The histopathological findings showed diffuse alveolar damage with lobular pneumonitis. Hyaline membranes, composed of proteinaceous exudate and cellular debris, covered the alveolar surfaces. Microscopic examinations of lung could not distinguish the effects of cytolysin from other insults to lungs that occur in ARDS. This report highlights the postmortem pathological findings in V. vulnificus infection in a child with nephrotic syndrome complicated by ARDS.
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9/110. Libman-Sacks endocarditis in a pregnant woman with acute respiratory distress syndrome.

    BACKGROUND: Sterile fibrinous vegetations on the mitral valve (Libman-Sacks endocarditis) might be found in one-third of patients with antiphospholipid antibodies. Usually of minor hemodynamic significance, these vegetations might complicate acute respiratory distress syndrome in pregnancy. CASE: Despite delivery and aggressive medical therapy, a 17-year-old primigravida with pyelonephritis and acute respiratory distress syndrome suffered rapid decompensation. echocardiography showed mitral valve vegetations with severe regurgitation. Blood cultures were negative, but antinuclear antibody test and lupus anticoagulant were positive. The patient died of massive cerebral infarction and brainstem herniation. autopsy found a patent foramen ovale and Libman-Sacks endocarditis. CONCLUSION: With rapid decompensation of acute respiratory distress syndrome in pregnancy, despite aggressive medical therapy, complicating processes must be considered, especially with antiphospholipid antibodies, which can be associated with sterile heart vegetations and subsequent fatal thromboembolism.
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10/110. Acute respiratory distress syndrome in a polymyositis patient with the anti-Jo-1 antibody.

    We report a case of a 66-year-old caucasian woman suffering from polymyositis with the anti-Jo-1 antibody. Shortly after admission to our hospital, despite the fact that the patient was given intravenous pulse methylprednisolone (1000 mg/day for 3 consecutive days), she developed severe, ventilatory-dependent, acute respiratory distress syndrome. Evaluation for infectious or noninfectious aetiologies of acute respiratory distress syndrome was unrevealing. bronchoalveolar lavage disclosed neutrophilic alveolitis. Histological examination of a transbronchial biopsy revealed an interstitial fibrosing process and cuboidalisation of the alveolar epithelium. In addition to high-dose methylprednisolone the patient was given intravenous pulse cyclophosphamide fortnightly for six weeks and afterwards every 4 weeks. All symptoms resolved and arterial blood gases returned to normal. Remission has been maintained with azathioprine. One year after onset, polymyositis is in complete remission. This is the first report of a patient suffering from polymyositis with the anti-Jo-1 antibody who survived such a complication. Intravenous pulse cyclophosphamide was probably a life saving therapy.
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keywords = alveolar, process
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