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1/56. 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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2/56. A case for steroids in acute lung injury associated with the retinoic acid syndrome.

    A 62-year-old woman with acute promyelocytic leukaemia was treated with all-trans retinoic acid. On day 2 she suffered with dyspnoea and general fatigue. Marked hypoxia suggested the occurrence of retinoic acid syndrome. She underwent endotracheal intubation and mechanical ventilation with the administration of dexamethasone. Her symptoms promptly abated. She was subsequently treated with conventional chemotherapy and achieved complete remission.
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3/56. fludrocortisone for the treatment of heparin-induced hyperkalemia.

    OBJECTIVE: To report the use of fludrocortisone for heparin-induced hyperkalemia and to briefly review the available literature relating to heparin-induced hyperkalemia. CASE SUMMARY: A 34-year-old African-American man was admitted to the hospital for pneumococcal pneumonia and sepsis. His hospital course was complicated by the development of acute respiratory distress syndrome, severe sepsis, acute renal failure, placement of a tracheostomy, and recurrent nasopharyngeal bleeding. The patient also developed a subclavian vein thrombosis with extension to the cephalic and basilic veins secondary to placement of a pulmonary artery catheter; anticoagulation with heparin was required. On day 9 of heparin therapy, the patient developed symptomatic hyperkalemia refractory to conventional therapies. Oral fludrocortisone 0.1 mg/d was initiated with resolution of the hyperkalemia within 24 hours despite the continued administration of heparin. DATA SOURCES: A medline (1966-October 1999) search was performed to identify case reports and clinical trials discussing heparin-induced hyperkalemia or the use of fludrocortisone for hyperkalemia. DISCUSSION: heparin has the potential to induce hyperkalemia by several mechanisms, including decreased aldosterone synthesis, reduction in number and affinity of aldosterone II receptors, and atrophy of the renal zona glomerulosa. fludrocortisone promotes potassium excretion by its direct actions on the renal distal tubules. In this patient, fludrocortisone resulted in a significant and rapid decrease in serum potassium even with continued heparin administration and acute renal failure. CONCLUSIONS: This case suggests that fludrocortisone is a reasonable alternative therapy for patients with hyperkalemia secondary to heparin therapy when the continued administration of heparin is necessary.
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4/56. Respiratory distress secondary to both amphotericin b deoxycholate and lipid complex formulation.

    A 73-y-old female with a history of adenocarcinoma of colon and refractory anemia developed febrile neutropenia following chemotherapy. Therapy with iv infusion of amphotericin b deoxycholate (AmBd) was initiated on day 8 of hospital admission. Premedications included acetaminophen, diphenhydramine and meperidine. Patient developed rigor, chill and elevated temperature approximately 100 min into the infusion. The infusion was temporarily discontinued and rigors subsided following administration of 25 mg meperidine im. Infusion was continued after cessation of the rigors with no further sequelae. During each infusion of AmBd over the next 3 d, the patient developed rigor, chill and elevated temperature which was managed with meperidine. However, on day 4 she developed respiratory distress, bronchospasm and visible cyanosis with oxygen saturation of 88% while on 2 L oxygen. The infusion was stopped and the symptoms subsided with administration of albuterol via nebulizer. Amphotericin lipid formulation infusion was reinstituted after 3 d because of the patient's worsening clinical status. However, the patient developed severe respiratory distress approximately 130 min into the infusion. The infusion was discontinued and she was treated with albuterol via nebulizer. itraconazole therapy was instituted without any adverse sequelae. Clinicians should be aware of this potential adverse event since it can occur with all formulation of amphotericin.
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5/56. Acute respiratory distress syndrome following intrathecal methotrexate administration: a case report and review of literature.

    Acute Respiratory distress syndrome (ARDS) is a rare complication following intrathecal (IT) injection of methotrexate (MTX) in adult acute lymphoblastic leukemia (ALL) patients. A 19-year-old man with ALL developed strikingly acute respiratory failure during central nervous system (CNS) prophylaxis with IT MTX administration and cranial irradiation. Histopathologic study of the lungs revealed a pattern of diffuse alveolar damage with interstitial cellular infiltration. His symptoms were relieved soon following treatment with corticosteroids and the pulmonary infiltrates resolved gradually. Pulmonary symptoms did not recur as he was continuously treated with oral corticosteroids.
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6/56. Bronchoscopic instillation of surfactant in acute respiratory distress syndrome.

    Abnormalities of surfactant action in acute respiratory distress syndrome (ARDS) result in decreased lung compliance and significant hypoxemia. Several case reports and small studies suggest that there is an improvement in patients with ARDS following the administration of surfactant. However, there is no clear-cut ideal method for surfactant administration. The bronchoscopic administration of surfactant may represent an effective method of surfactant delivery in ARDS. Bronchoscopic instillation offers the theoretical advantages that the surfactant may be distributed directly to the desired regions of the lung, a more economical use of surfactant, and the opportunity to lavage leaked serum proteins prior to instillation. Surfactant has been administered in adults with success. We present a case of initial improvement in oxygenation index, ventilation index, and mechanical ventilatory support in a pediatric patient with ARDS following the bronchoscopic administration of surfactant.
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7/56. Pulmonary toxicity with mefloquine.

    This report presents a case of acute lung injury developing within hours after administration of mefloquine for a low-level plasmodium falciparum malaria, which was persistent despite halofantrine therapy. Extensive microbiological investigation remained negative and video-assisted thoracoscopic lung biopsy demonstrated diffuse alveolar damage. The evolution was favourable without treatment. This is the second report of acute lung injury and diffuse alveolar damage caused by mefloquine. glucose-6-phosphate dehydrogenase deficiency was present in the former case and was thought to contribute to the lung injury. However, glucose-phosphate dehydrogenase was normal in the present case, suggesting that it is not a predisposing condition to the lung injury.
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8/56. Inhibition of granulocyte activation by surfactant in a 2-yr-old female with meningococcus-induced ARDS.

    Activated polymorphonuclear neutrophils (PMNs) play a crucial role in acute respiratory distress syndrome (ARDS) via extracellular release of reactive cell products such as elastase. Surfactant has proved valuable in restoring lung function in ARDS. The significance of its immunomodulatory properties with respect to this effect has not yet been clarified. The aim of the present study was to determine the anti-inflammatory effects of surfactant administration in an infant with ARDS. During the acute phase of ARDS in a 2-yr-old female, levels of PMN-derived elastase complexed with alpha1-protease inhibitor (E-alpha1PI) were measured in both arterial and central venous blood samples obtained simultaneously. The results were correlated with oxygen demand and plasma concentrations of tumour necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) after endotracheal administration of surfactant (Alveofact 60 mg x kg x body weight(-1)). In the present case, for the first time, a higher E-alpha1PI concentration was detected in arterial blood (4.51 mg x L(-1)) than in central venous blood (2.28 mg x L(-1)). After administration of surfactant, these concentrations and the arteriovenous difference decreased, indicating that during ARDS, most PMN degranulation takes place in the pulmonary vascular bed and is inhibited by surfactant administration. Simultaneously, TNF-alpha and IL-6 plasma concentrations decreased within hours and lung function was restored. This local inhibition of polymorphonuclear neutrophil activation by exogenous surfactant may play a key role in the early improvement in lung function after surfactant administration.
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9/56. Common features in the onset of ARDS after administration of granulocyte colony-stimulating factor.

    STUDY OBJECTIVE: Respiratory disturbance caused by ARDS has been reported during administration of granulocyte-colony stimulating factor. The clinical features of such respiratory distress were investigated in this study. DESIGN: Retrospective case review. SETTING: A 1,100-bed university teaching hospital. patients: Five patients who had dyspnea caused by ARDS develop after chemotherapy or bone marrow transplantation (BMT) at our hospital. INTERVENTIONS: None. MEASUREMENTS AND RESULTS: Levels of cytokines, human leukocyte antigen (HLA) typing, and the clinical course were analyzed to clarify common features. All five patients possessed HLA-B51 or HLA-B52, and all had fever and an enhanced inflammatory response at the time of the WBC nadir. The tumor necrosis factor (TNF)-alpha and interleukin (IL)-8 levels increased when respiratory distress syndrome occurred. CONCLUSIONS: If patients with HLA-B51 or HLA-B52 have infection develop at the time of WBC nadir after chemotherapy or BMT, ARDS may occur in association with elevation of TNF-alpha and IL-8 during WBC recovery.
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10/56. The effects of inhalation of a novel nitric oxide donor, DETA/NO, in a patient with severe hypoxaemia due to acute respiratory distress syndrome.

    Aerosolized NONOates have been investigated in animal models in acute pulmonary hypertension, but none have been used in humans. We report the first use of aerosolized diethylenetriamine nitric oxide adduct (DETA/NO), a NONOate, in a patient with severe acute respiratory distress syndrome. Both pulmonary vascular resistance index and mean pulmonary arterial pressure were reduced by a mean of 26% and 18% respectively after the administration of a single dose of DETA/NO (150 micromol). Intrapulmonary shunting also improved. There were no significant changes in systemic arterial pressure or arterial methaemoglobin concentration after DETA/NO inhalation. We conclude that DETA/NO aerosol produced selective pulmonary vasodilation, with an improvement in pulmonary haemodynamics and oxygenation, while having no measurable effect on the systemic circulation.
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