Reexpansion pulmonary edema (RPE) is a rare, but frequently lethal, clinical entity. The precise pathophysiologic abnormalities associated with this disorder are still unknown: decreased surfactant levels and a pro-inflammatory status are putative mechanisms. Early diagnosis is crucial, since prognosis depends on early recognition and prompt treatment. Considering the high mortality rates related to RPE, preventive measures are still the best available strategy for patient handling. This review provides a brief overview of the pathophysiology, diagnosis, treatment, and prevention of RPE, with practical recommendations for adequate intervention.

Although pneumonectomy is a technically simple procedure, it has been associated with a high (60%) incidence of complications. Respiratory complications account for approximately 15% of such complications. Worldwide, the mortality rate among patients subjected to pneumonectomy is 8.6%. However, the rate among patients developing respiratory complications is 30%. Although postpneumonectomy pulmonary edema is rare (occurring in 3% to 5% of cases), it is a serious complication and is almost always fatal. It was first described twenty years ago and, despite these alarming statistics, little is known regarding the physiopathology of postpneumonectomy pulmonary edema. Once it has become entrenched, the condition is difficult to treat, and there is no proven efficient treatment. Various risk factors have been correlated with postpneumonectomy pulmonary edema onset. Fluid overload was the first to be identified as a factor to avoid. However, many studies have shown that there is no direct correlation between fluid overload and the development of edema. Prevention is the best way to avoid postpneumonectomy pulmonary edema and must be performed in a multidisciplinary fashion, involving the entire medical staff - from the initiation of anesthesia through the surgical procedure and extending into the critical care management phase. Equally important is early identification and testing of patients at risk for postpneumonectomy pulmonary edema when there is clinical suspicion of this serious complication.

Keywords: Key Words: Pulmonary edema/complications. Pneumonectomy/adverse effects. Risk factors. Pulmonary edema/prevention & control.

Objective: This study aimed to use high-resolution computed tomography scans of the chest to characterize the principal alterations occurring in cases of hydrostatic pulmonary edema. Methods: A retrospective analysis was made of the tomography scans of 15 patients presenting clinical profiles of hydrostatic pulmonary edema. The cases were divided into five groups by etiology: congestive heart failure (n = 7); acute mitral valve disease (n = 2); acute myocardial infarction (n = 2); myocarditis (n = 2); and fibrosing mediastinitis (n = 2). Results: The principal findings in the cases of hydrostatic pulmonary edema were ground-glass opacities (in 100%), interlobular septal thickening (in 100%), pleural effusion (in 87%) and peribronchovascular interstitial thickening (in 80%). Other, less common, findings were increased blood vessel diameter, consolidations and air-space nodules. Conclusion: The predominant pattern found in the patients studied was that of ground-glass opacities accompanied by interlobular septal thickening (mosaic attenuation pattern) and bilateral (predominantly right-sided) pleural effusion.

Keywords: Pulmonary edema; Tomography, X-ray computed; Lung diseases

Negative-pressure pulmonary edema accompanied by hemorrhage as a manifestation of upper airway obstruction is an uncommon problem that is potentially life-threatening. The principal pathophysiological mechanism involved is the generation of markedly negative intrathoracic pressure, which leads to an increase in pulmonary vascular volume and pulmonary capillary transmural pressure, creating a risk of disruption of the alveolar-capillary membrane. We report the case of an adult male with diffuse alveolar hemorrhage following acute upper airway obstruction caused by the formation of a cervical and mediastinal abscess resulting from the insertion of a metallic tracheal stent. The patient was treated through drainage of the abscess, antibiotic therapy, and positive pressure mechanical ventilation. This article emphasizes the importance of including this entity in the differential diagnosis of acute lung injury after procedures involving upper airway instrumentation.

Keywords: Hemorrhage; Pulmonary edema; Airway obstruction; Abscess; Prostheses and implants.