Jose L. Mendez

Acute lung injury after blood transfusion in mechanically ventilated patients.

BACKGROUND:  Liberal transfusion strategy increases the risk of acute lung injury (ALI), but specific transfusion‐related factors have not been characterized. We tested the hypotheses that storage age and specific type of blood products are associated with increased risk of ALI in mechanically ventilated patients.

New insights into the pathology of acute respiratory failure.

Purpose of review The purpose of this review is to provide a historical perspective and to analyze the recent advances in the understanding of the cellular and tissue pathology of acute respiratory failure, specifically of the acute respiratory distress syndrome. The scope of mechanisms involved in acute lung injury and acute respiratory distress syndrome is far too great to do it justice in a single review. Therefore, this review will focus only on recent advances in the understanding of the morphologic changes that occur in acute lung injury, acute respiratory distress syndrome, and ventilator-induced lung injury. Recent findings The use of fluorescent labels brought a novel method to identify and quantify cell wounding in the whole organ animal model of ventilator-induced lung injury. Real-time in vivo microscopy demonstrated the injurious effects of alveolar instability in the pathogenesis of ventilator-induced lung injury. Lipid tether mechanics, using laser tweezers, have advanced the understanding of the mechanical properties of the plasma membrane in response to mechanical stress. New animal injury models have brought forward new insights into the pathogenesis and structural abnormalities seen in acute respiratory distress syndrome. Apoptosis and epithelial wounding and repair have been examined in novel methods, and new mechanisms in lung edema formation have been proposed. Summary New mechanisms in the pathology of acute respiratory failure have shifted the focus to lung mechanics, tissue damage, remodeling, and the systemic effects derived from the mechanical stress imposed by the ventilator in patients with adult respiratory distress syndrome.

Chronic Nitrofurantoin-Induced Lung Disease

OBJECTIVE To reassess the clinical and radiological features of chronic nitrofurantoin-induced lung disease and eventual clinical outcome. PATIENTS AND METHODS We retrospectively reviewed the medical records of 18 patients with chronic nitrofurantoin-induced lung disease who were seen at the Mayo Clinic in Rochester, Minn, from January 1, 1997, to December 31, 2002. RESULTS The median age of the 18 patients was 72 years (range, 47-90 years) at the time of diagnosis; 17 (94%) were women. Onset of symptoms occurred after a median interval of 23 months (range, 10-144 months) following the initiation of nitrofurantoin therapy for the prevention of recurrent urinary tract infections. All patients presented with persistent dyspnea and cough associated with lung infiltrates detected on chest radiography. Ten computed tomograms were available for review and revealed bilateral areas of ground-glass opacities in all cases and showed subpleural Irregular linear opacities and patchy consolidation in some cases. Nitrofurantoin therapy was discontinued in all patients, and most improved subsequently; 9 patients received corticosteroid therapy. CONCLUSIONS Chronic nitrofurantoin-induced lung disease is seen predominantly in older women who present with respiratory symptoms after a year or more of nitrofurantoin therapy. Associated radiological features are relatively nonspecific but usually include bilateral areas of ground-glass opacities on computed tomography of the chest. Cessation of nitrofurantoin therapy leads to improvement and suffices in the management of some patients, although corticosteroid therapy may be helpful in those more severely affected.

Plasma Membrane Stress Failure in Ventilator-Injured Lungs A Hypothesis about Osmoregulation and the Pharmacologic Protection of the Lungs against Deformation Injury

Cell injury and repair are invariable consequences of mechanical ventilation with large tidal volumes. Rate and amplitude of deforming stress affect numerous cell metabolic functions including host defense and wound repair. Recently, we have focused on the role of plasma membrane stress failure as a trigger for a pro-inflammatory response in mechanically ventilated lungs. We have developed both cell- and organ-based models to study this problem. Alveolar epithelial cells that are exposed to deforming stresses seek to maintain sublytic plasma membrane tension and may activate mechanisms of cell surface area regulation to control membrane tension. Interventions which either increase the amount of excess plasma membrane or enhance lipid trafficking should be cytoprotective against deformation induced injury. Osmotic manipulation may be one such intervention. Preconditioning the lungs with anisosmotic solutions may allow the cells to recruit excess plasma membrane and thus be more resistant to ventilator-induced lung injury.