Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Systolic anterior motion (SAM) of mitral valve is the prolapse of a mitral leaflet into the left ventricle outflow tract (LVOT) during systole, causing LVOT obstruction and mitral valve regurgitation. We report the case of a patient who developed SAM-induced hemodynamic instability during bleeding with a clinical picture resembling pulmonary edema. A 77-year-old woman was admitted to our emergency room for abdominal bleeding in polycystic renal disease. Upon arrival, she was normotensive, despite being anuric and acidotic. After infusion of fluids and packed red blood cells (total 3 680 mL in 6 hours) she developed atrial fibrillation and clinical and radiological signs of pulmonary edema. Sedation and non-invasive ventilation brought to immediate severe hypotension. A transesophageal echocardiogram showed an "empty" hypertrophic hypercontractile left ventricle, SAM with LVOT obstruction (intraventricular gradient 154 mmHg) and moderate-to-severe mitral regurgitation. With further fluid infusion hemodynamic stability and sinus rhythm were recovered. SAM, LVOT obstruction and mitral regurgitation disappeared. SAM is a rare but dangerous cause of hemodynamic instability. It has been described in patients with and without left ventricular hypertrophy, in presence of hypovolemia and sympathetic stimulation. In our case it presented with a misleading clinical picture of pulmonary edema simulating fluid overload in an actually hypovolemic patient. In fact, SAM-associated mitral regurgitation together with diastolic dysfunction and tachycardia induced a pulmonary edema whose treatment worsened hypovolemia and precipitated LVOT obstruction and hypotension. Further fluid infusion was resolutive. Echocardiography was fundamental for diagnosis and treatment.
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PMID:Systolic anterior motion causing hemodynamic instability and pulmonary edema during bleeding. 2066 Dec 9

Ventilator-associated pneumonia (VAP) is one of the most commonly encountered hospital-acquired infections in intensive care units and is associated with significant morbidity and high costs of care. The pathophysiology, epidemiology, treatment and prevention of VAP have been extensively studied for decades, but a clear prevention strategy has not yet emerged. In this article we will review recent literature pertaining to evidence-based VAP-prevention strategies that have resulted in clinically relevant outcomes. A multidisciplinary strategy for prevention of VAP is recommended. Those interventions that have been shown to have a clinical impact include the following: (i) Non-invasive positive pressure ventilation for able patients, especially in immunocompromised patients, with acute exacerbation of chronic obstructive pulmonary disease or pulmonary oedema, (ii) Sedation and weaning protocols for those patients who do require mechanical ventilation, (iii) Mechanical ventilation protocols including head of bed elevation above 30 degrees and oral care, and (iv) Removal of subglottic secretions. Other interventions, such as selective digestive tract decontamination, selective oropharyngeal decontamination and antimicrobial-coated endotracheal tubes, have been tested in different studies. However, the evidence for the efficacy of these measures to reduce VAP rates is not strong enough to recommend their use in clinical practice. In numerous studies, the implementation of VAP prevention bundles to clinical practice was associated with a significant reduction in VAP rates. Future research that considers clinical outcomes as primary endpoints will hopefully result in more detailed prevention strategies.
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PMID:Prevention of ventilator-associated pneumonia in the intensive care unit: a review of the clinically relevant recent advancements. 2626 Nov 74