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1/10. 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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2/10. 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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3/10. Generalized pustular psoriasis complicated by acute respiratory distress syndrome.

    psoriasis has a chronic and relatively benign course. However, severe complications are possible. One rare complication is acute interstitial pneumonitis. This entity should be suspected when a patient presents with dyspnoea and high fever. knowledge of this pathology is crucial, for although it is essential to rule out aetiologies requiring specific management such as microbial infection or drug-related syndromes, diagnosis should not be delayed as its severe clinical course is improved by corticosteroids. We report two patients with an acute respiratory distress syndrome arising during the course of pustular psoriasis. Repeated bacteriological testing in lungs and blood remained negative. In both cases lung involvement was severe, requiring artificial ventilation. Dramatic clinical resolution was obtained by using corticosteroids. Besides infectious causes and drug hypersensitivity to methotrexate or acitretin, acute respiratory distress syndrome, sometimes due to a pulmonary capillary leak syndrome, is a rare cause of pneumonitis in the course of psoriasis, and may be fatal. Its pathogenesis is unknown. However, animal models suggest a role for T-helper (Th) 1 lymphocytes, known to be activated in psoriasis, and a role for tumour necrosis factor-alpha, a major Th1 cytokine, in alveolar damage.
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4/10. Occurrence of the adult respiratory distress syndrome in neutropenic patients.

    neutrophils are believed to play an essential role in the pathogenesis of the adult respiratory distress syndrome (ARDS). This concept is largely based on the observation that neutrophil depletion protects against altered pulmonary vascular permeability in several models of acute lung injury produced in laboratory animals. Four patients who developed ARDS during periods of profound neutropenia are presented. These patients met commonly accepted clinical and roentgenographic criteria for the syndrome, and each had the characteristic findings of diffuse alveolar damage by lung histologic examination. The failure of this degree of neutropenia to protect against ARDS in humans raises questions about whether neutrophils or neutrophil products are essential in the pathogenesis of the syndrome.
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5/10. Respiratory distress syndrome from lymphangiography contrast medium.

    adult respiratory distress syndrome (ARDS) has been reported as a rare complication of lymphangiography with ethiodized oil. We report 2 patients who developed otherwise unexplained pulmonary edema after lymphangiography, and describe an animal model of pulmonary injury after an injection of ethiodized oil. We injected 0.25 ml/kg of body weight intravenously into 45 rabbits, and followed arterial blood gases and/or killed the rabbits randomly at various intervals for morphologic lung examination by light and electron microscopy. Within 24 h after injection, there was moderate hypoxemia from oil embolization, but only minimal lung edema. However, by 2 to 4 days after injections, hypoxemia was most severe and was accompanied by extensive alveolar and interstitial inflammation, hemorrhage, and edema. After 4 days, there was gradual blood gas and morphologic recovery, with complete restoration of normal anatomy by 6 wk. Our data showed that in rabbits, ethiodized oil can reproducibly cause delayed, severe pulmonary injury, thus supporting the clinical reports that ARDS may occur several days after lymphangiography.
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6/10. Pulmonary leukostasis in fatal human pneumococcal bacteremia without pneumonia.

    An asplenic man developed fulminant pneumococcal bacteremia without pneumonia. He died of irreversible shock within 24 h. autopsy revealed extensive pulmonary vascular leukostasis. This condition has been described in laboratory animals after intravascular challenge with endotoxin, gram-negative bacilli, and gram-positive organisms including pneumococci. This case illustrates that death in pneumococcal disease can occur in the absence of pneumonia and may be attributable to cardiovascular collapse. We present a proposed mechanism based on activation of complement and release of vasoactive mediators.
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7/10. Acute respiratory failure after sodium morrhuate esophageal sclerotherapy.

    Two of 30 patients with esophageal varices had respiratory distress develop within 8-24 h of esophageal sclerotherapy. Evidence of aspiration and sepsis were absent in these two patients with the clinical picture of adult respiratory distress syndrome. To investigate the possible etiologic role of sodium morrhuate in this syndrome, a sheep model was established and pulmonary hemodynamics, lung lymph flow, and albumin concentration were measured before and after the intravenous injection of 2.5-15.0 cm3 of sodium morrhuate. In all 8 animals studied, mean pulmonary artery pressures increased from 11.6 /- 2.8 to 32.8 /- 4.9 mmHg (p less than 0.01) 30 s after injection. These pressures returned to baseline values over 120 min. Lymph flow increased from 0.91 /- 0.89 to 2.8 /- 1.5 ml/30 min at 90 min postinjection (p less than 0.05) and returned to baseline values in animals monitored for 6-8 h. The lymph/plasma albumin ratio decreased from 0.856 /- 0.08 to 0.74 /- 0.01 (p less than 0.05) 120 min postinjection. pulmonary edema was not evident histologically or gravimetrically (wet/dry weight ratio was 3.65 /- 0.3 and not different from normal). It was concluded that sodium morrhuate injection in sheep causes marked but transient pulmonary hypertension associated with an increased lymph flow of relatively protein-poor lymph. sodium morrhuate esophageal sclerotherapy may affect pulmonary hemodynamics and contribute to respiratory difficulties in patients.
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8/10. How far can we go with permissive hypercapnia? A case presentation and some biased comments with emphasis on maintaining normal haemoglobin level.

    The respiratory management strategy of small tidal volume with permissive hypercapnia has been adopted to avoid further aggravation of lung injury due to high airway pressure with some impressive success (1). No consensus, however, has been established in terms of the rate of increase in PaCO2 and its upper limit. Recently, our colleague in the intensive care unit experienced a severe case of ARDS successfully treated with the above strategy despite of the fact that during the course of treatment, the highest PaCO2 reached 177 mmHg and the lowest pH, 7.03 (2). The fact that PaCO2 may reach a very high level in the clinical setting and the well-known role of haemoglobin (Hb) in buffering CO2 led us to study effects of different Hb levels on pH and haemodynamic changes in response to acute CO2 loading in the blood. We will summarize the case report first with permission of authors (the case report was published in Japanese) (2) and then discuss the studies conducted in our animal laboratory.
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9/10. bordetella bronchoseptica pneumonia with shock in an immunocompetent patient.

    bordetella bronchoseptica is a rarely reported cause of human infection, but is a common respiratory tract commensal of mammals. Human infection with B. bronchoseptica is almost always associated with severe underlying disease and contact with an appropriate animal reservoir. We report a case of pneumonia with shock caused by B. bronchoseptica in an immunocompetent patient.
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10/10. Laudanosine and atracurium concentrations in a patient receiving long-term atracurium infusion.

    OBJECTIVE: atracurium is sometimes used for muscle relaxation in patients undergoing mechanical ventilation. Use of atracurium in high doses or for a long period of time has raised the possibility of the accumulation of laudanosine, a breakdown product known to cause seizure activity in animals. The objective of this report was to see if laudanosine accumulation and seizure activity had occurred in a patient who had received a long-term, relatively high-dose infusion of atracurium. DESIGN: Case report. The patient received atracurium for 38 days, at rates ranging from 0.3 to 0.96 mg/kg/hr. An electroencephalogram (EEG) was done before the discontinuation of the infusion, and plasma concentrations of atracurium and laudanosine were measured at, and after, the termination of the atracurium infusion. The laudanosine elimination half-life was calculated. SETTING: intensive care unit. PATIENT: A 23-yr-old woman admitted with sickle cell crisis, complicated by acute chest syndrome, acute respiratory distress syndrome, and hepatic and renal failure. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: As expected, laudanosine concentrations were increased but were below the level reported to cause seizure activity in animals. Laudanosine elimination half-life was prolonged to 617 mins, which was consistent with previously reported values. The patient's EEG was normal, with no ictal pattern. CONCLUSIONS: Despite long-term use of high doses of atracurium infusion and the increased elimination half-life of laudanosine, only moderate accumulation of laudanosine occurred, and the EEG was normal. Hence, it appears unlikely that toxic concentrations of laudanosine would be reached, even in a critically ill patient.
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