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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A previously completely fit and well 62-year-old man presented with a 4-week history of lethargy and increasing shortness of breath. This had been preceded by a flu-like illness that had been treated in the community with ciprofloxacin to no effect. There was no history of smoking, tuberculosis exposure or significant exposure to birds. Clinically the patient appeared well and was comfortable and conversant with no peripheral oedema. Chest auscultation revealed normal breath sounds and a loud pansystolic murmur over the cardiac apex. A chest radiograph and a subsequent CT scan showed widespread fibrotic and bronchiectatic changes, predominantly in the right upper lobe, with bilateral pleural effusions. Echocardiography revealed a posterior mitral valve prolapse. He was treated with loop diuretics and a mitral valve repair that resolved his symptoms and radiographic findings. This is the first English language case report of pulmonary oedema causing bronchiectatic lung appearances.
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PMID:Pulmonary oedema mimicking bronchiectasis. 2409 58

We report the case of a 75-year old woman who presented with shortness of breath and haemoptysis. She had been treated for presumed essential hypertension for many years. On admission she was found to be severely hypertensive. Chest X-ray showed pulmonary oedema. However, an echocardiogram reported good systolic ventricular function. Her hypertension and pulmonary oedema did not respond to medical treatment necessitating intubation. A CT angiogram identified the cause--undiagnosed bilateral severe. We discuss this increasingly common condition that is difficult to manage and easily missed.
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PMID:Acute pulmonary oedema with normal left ventricular function in a patient with resistant hypertension--what is the likely diagnosis? 2461

A 61 year-old man presented with progressive shortness of breath. Computed tomography scan of the chest showed diffuse ground glass infiltrates and dilated pulmonary vessels in the right lung in addition to bilateral pulmonary masses with obstruction of the left main pulmonary bronchus. The patient underwent bronchoscopy with destruction of the tumor obstructing the left main pulmonary bronchus, resulting in clinical improvement and resolution of the right pulmonary infiltrates. We hypothesize that the patient developed right pulmonary edema secondary to hypoxic vasoconstriction of the left lung. This case suggests a rare mechanism of unilateral pulmonary edema and supports inclusion of pulmonary edema in the differential diagnosis of unilateral pulmonary infiltrates in the setting of contralateral bronchial obstruction.
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PMID:An unusual case of unilateral pulmonary edema with contralateral bronchial obstruction. 2497 46

Immersion pulmonary oedema (IPE) is being increasingly recognized in swimmers, snorkellers and scuba divers presenting with acute symptoms of respiratory distress following immersion, but fatal case reports are uncommon. We report two fatal cases of probable IPE in middle-aged women, one whilst snorkelling and the other associated with a scuba dive. In the snorkeller's case, an episode of exercise-related chest tightness and shortness of breath that occurred 10 months previously was investigated but this proved negative, and she was on no medications. However, at autopsy, moderate left ventricular hypertrophy was noted. The scuba diver had suffered several previous episodes of severe shortness of breath following dives, one being so severe it led to cyanosis and impaired consciousness. At inquest, the pathologist's diagnosis was given as drowning and IPE was not mentioned. Expert input from doctors trained in diving medicine should be compulsory in the investigation of diving deaths, and forensic pathologists should be properly trained in and have guidelines for the conduct of post-immersion and post-diving autopsies.
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PMID:Two fatal cases of immersion pulmonary oedema - using dive accident investigation to assist the forensic pathologist. 2531 31

Transfusion-related acute lung injury (TRALI) is primarily caused by transfusion of fresh frozen plasma or platelet concentrates and occurs by definition within 6 hours after transfusion with acute shortness of breath, hypoxemia and radiographically detectable bilateral infiltrates of the lung. Mostly leucocyte antibodies in the plasma of the blood donor (immunogenic TRALI) are responsible. Apart from antibodies, other substances such as biologically active lipids, mainly arising from the storage of platelet and red blood cell concentrates, can activate neutrophilic granulocytes and trigger a non-immunogenic TRALI. Pathophysiologically, granulocytes in the capillaries of the lung vessels release oxygen radicals and enzymes which damage the endothelial cells and cause pulmonary edema. Therapeutically, nasal oxygen administration may be sufficient. In severe cases, mechanical ventilation, invasive hemodynamic monitoring and fluid intake are required. Diuretics should be avoided. The administration of glucocorticoids is controversial. Antibody-related TRALI reactions occurred mainly after transfusion of fresh frozen plasma, which had been obtained from womenimmunized during pregnancy against leukocyte antigens. Therefore, in Germany, since 2009 only plasma from female donors without a history of prior or current pregnancy or negative testing for antibodies against HLA I, II or HNA has been used with the result that since then no TRALI-related death has been registered.
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PMID:[Transfusion-related acute lung injury (TRALI)]. 2504 84

Transfusion-related acute lung injury (TRALI) is a serious clinical syndrome associated with the transfusion of plasmacontaining blood components. Recently, TRALI has come to be recognized as the leading cause of transfusion-related mortality. This complication typically presents as shortness of breath, hypoxemia, hypotension, fever, and non cardiogenic pulmonary edema, occurring within 6 h after transfusion. Although the mechanism of TRALI has not been exactly known, it has been associated with human leukocyte antigen antibodies and with biologically active mediators in stored cellular blood components. We, hereby, present a case of a patient with dengue fever who developed acute lung injury (ALI), presumably TRALI, after transfusion of platelet concentrates. He was treated with supportive measures and mechanical ventilation. Greater knowledge and increased awareness especially amongst the clinicians regarding TRALI is needed for prevention and treatment of this potentially severe complication of blood/component transfusion.
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PMID:Acute lung injury after platelet transfusion in a patient with dengue fever. 2516 56

Many physicians struggle with death-telling in sudden death. Families can be negatively impacted by suboptimal death-telling. Appropriate preparation and education can make death notification less stressful for the physician and may help decrease the development of pathologic grief in the surviving family members that can occur when death is unexpected. Although still controversial, there is a growing body of evidence that family witnessed resuscitation may be beneficial to the grieving process and desired by the public. A previously healthy 21-year-old male comes toyour community emergency department (ED) for a cough that started 4 days ago. He denies fever, shortness of breath, and chest pain. He does admit to a remote history of drug abuse. He states he is feeling "OK" and is only here because his family insisted he come because they were worried he might have pneumonia. His vital signs are normal and he appears well; therefore, he is triaged to the waiting room. About 30 minutes lates the patient complains of shortness of breath and he is brought back to an exam room. The patient is now hypotensive, tachycardic, and pulse oximetry is noted to be 87% on room air. A chest x-ray reveals severe pulmonary edema and an EKG shows ST segment elevation in multiple leads. The patient is taken to the cardiac catheterization lab by the interventional cardiologist, who makes the diagnosis of a ruptured aortic valve due to damage from endocarditis. The patient is returned to the ED to await emergent transfer to a tertiary facility; however, the patient rapidly decompensates and a Code Blue is called. Despite the absence of return of spontaneous circulation, resuscitation efforts are prolonged while the ED social worker attempts to contact the patient's family to come to the ED. Finally, the resuscitation is terminated and the patient is pronounced dead. Several hours later the patient's elderly mother arrives and asks you: "What's going on with Mikey?"
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PMID:Breaking bad (news) death-telling in the emergency department. 2581 64

A 73-year-old woman presented with acute shortness of breath and exacerbation of chronic back pain. She was diagnosed with pulmonary oedema and a non-ST-elevation myocardial infarction following chest X-ray, ECG and high sensitivity troponin levels. She subsequently underwent coronary angioplasty with deployment of drug-eluting stents to her circumflex and left anterior descending arteries and was started on aspirin and clopidogrel for her dual antiplatelet therapy. Unfortunately, following the procedure, she gradually lost power and sensation in both lower limbs. MRI of her spine confirmed an extradural haematoma causing thoracic cord compression. She was managed conservatively following discussions with neurosurgeons and developed further complications secondary to her immobility.
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PMID:Acute spinal cord compression: a rare complication of dual antiplatelet therapy. 2620 14

Background. We study the clinical significance and management of pulmonary venous obstruction in cancer patients. Methods. We conducted a prospective cohort study to characterize the syndrome that we term "pulmonary vein obstruction syndrome" (PVOS) between January 2005 and March 2014. The criteria for inclusion were (1) episodes of shortness of breath; (2) chest X-ray showing abnormal pulmonary hilum shadow with or without presence of pulmonary edema and/or pleural effusion; (3) CT scan demonstrating pulmonary vein thrombosis/tumor with or without tumor around the vein. Results. Two hundred and twenty-two patients developed PVOS. Shortness of breath was the main symptom, which was aggravated by chemotherapy in 28 (13%), and medical/surgical procedures in 21 (9%) and showed diurnal change in intensity in 32 (14%). Chest X-rays all revealed abnormal pulmonary hilum shadows and presence of pulmonary edema in 194 (87%) and pleural effusion in 192 (86%). CT scans all showed pulmonary vein thrombosis/tumor (100%) and surrounding the pulmonary veins by tumor lesions in 140 patients (63%). PVOS was treated with low molecular weight heparin in combination with dexamethasone, and 66% of patients got clinical/image improvement. Conclusion. Physicians should be alert to PVOS when shortness of breath occurs and chest X-ray reveals abnormal pulmonary hilum shadows.
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PMID:Pulmonary Venous Obstruction in Cancer Patients. 2642 21

We are living in an environment full of gases, and any change in the concentration of a component of the air or contaminants (usually toxic) in the air may significantly threaten human health. Thus, to investigate the influence of gases in animal models it is helpful to elucidate the pathogenesis of gas-related injury. Although there are devices used for gas exposure in animals, there are still limitations in the establishment of these animal models, such as the change in gas concentration during the refreshing of water, food and litter, and the contamination of toxic gases released by animals. Herein, we freshly prepared a chamber for normobaric gas exposure. During the exposure in this chamber, the refreshing of water, food and litter does not require opening of the chamber. The chamber gases are continuously circulated and filtered, and the gas concentration remains very stable. To validate the feasibility of this chamber, rats were exposed to pure oxygen as an example. Results showed that rats with hyperoxia-induced lung injury simulated by pure oxygen exposure displayed the representative characteristics as observed in humans: shortness of breath, lung edema, alveolar septal rupture, infiltration of inflammatory cells, oxidative and inflammatory injury. This suggests that it is feasible to establish animal models using this chamber for the investigation of gas toxicity.
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PMID:A normobaric gas exposure animal chamber and its validation in hyperoxia exposure. 2659 77


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