Objective: To report the original observation of a patient with legionella’s pneumopathy complicated with acute respiratory distress syndrome (ARDS) and a concomittant cerebral oedema occurred in the setting of positive end-expiratory pressure, reversible with the weaning of mechanical ventilation. Design and Setting: Case report, Intensive Care Unit, General Hospital.

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A 48 year-old Hispanic gentleman presented to the emergency department (ED) with 2-hour history of acute dyspnea. The patient had the history of motor vehicle accident 15 years prior to presentation. A chest x-ray done in the ED revealed pneumothorax and hydrothorax in the left chest. The patient had emergency closed tube thoracotomy with resolution of the pneumothorax. The chest tube began to drain fecal contents.

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Several molecules, chemicals and cells are involved in tissue damage during any hypoxic event, such as a cardiac arrest, a respiratory arrest or a cerebrovascular accident. Among them: calcium, protein kinase enzymes, calcium binding proteins, S-100â protein and adhesion molecules such as intracellular adhesion molecule-1 (ICAM-1) are frequently cited in the literature. Controversy exists as to whether these “hypoxic aggressors” can be modified favorably by the use of therapeutic hypothermia.

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Life-threatening hyponatremia can occur when sodium concentration falls to 125 mmol/L or less. Symptoms usually do not depend on the absolute sodium concentration but on the rate of fall. Estimates of mortality in acute hyponatremia are as high as 50%. Marathon runners are at particular risk of developing a syndrome which consists of severe hyponatremia, pulmonary edema and cerebral edema as originally described by Varon and Ayus. This syndrome, if not managed appropriately has a very high morbidity and mortality.

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