Download the Free Unbound MEDLINE PubMed App to your smartphone or tablet.
Available for iPhone, iPad, iPod touch, and Android.
Pulmonary Edema [keywords]
- Effects of oxygen in lungs of rats. [JOURNAL ARTICLE]
- Acta Cir Bras 2014 Dec; 29(12):771-775.
To analyze microscopically the effects of different concentrations of oxygen in the lungs of rats.There were 20 rats distributed in three experimental groups (concentration of oxygen to 40%, 70% and 100%) and a control group. The animals were exposed to the oxygen in a chamber of acrylic during three days and after exposition, the animals were submitted to median thoracotomia to remove the lungs. The lung tissue of all of the animals was analyzed as regards presence of acute and chronic inflammation, capillary congestion, alveolar walls thick, interstitial and alveolar edema, alveolar hemorrhage, denudation capillary and alveolar endothelium areas and atelectasis.The analysis histopathologic revealed significant statistics difference for acute and chronic inflammation, capillary congestion, alveolar walls thick, interstitial and alveolar edema, alveolar hemorrhage, denudation capillary and alveolar epithelium areas.Exposition to the oxygen during 72 hours in the concentration of 40% does not produce significant histopathologic alterations in the lung tissue; in the concentration of 70%, can promotes the alveolar walls thick and capillary congestion and in the concentration of 100% can cause death and originate diffuse pulmonary lesion.
- Mitragynine 'Kratom' Related Fatality: A Case Report with Postmortem Concentrations. [JOURNAL ARTICLE]
- J Anal Toxicol 2014 Dec 16.
A 24-year-old man whose medical history was significant for alcohol abuse and depression was found unresponsive in bed. He had several prior suicide attempts with 'pills' and had also been hospitalized for an accidental overdose on a previous occasion. Autopsy findings were unremarkable apart from pulmonary edema and congestion, and urinary retention. Postmortem peripheral blood initially screened positive for mitragynine 'Kratom' (by routine alkaline drug screen by gas chromatography-mass spectrometry, GC-MS), which was subsequently confirmed by a specific GC-MS selective ion mode analysis following solid-phase extraction. Concentrations were determined in the peripheral blood (0.23 mg/L), central blood (0.19 mg/L), liver (0.43 mg/kg), vitreous (<0.05 mg/L), urine (0.37 mg/L) and was not detected in the gastric. Therapeutic concentrations of venlafaxine, diphenhydramine and mirtazapine were also detected together with a negligible ethanol of 0.02% (w/v). The results are discussed in relation to previous cases of toxicity, and the lack of potential for mitragynine postmortem redistribution.
- Sunitinib-induced severe toxicities in a Japanese patient with the ABCG2 421 AA genotype. [JOURNAL ARTICLE]
- BMC Cancer 2014 Dec 16; 14(1):964.
Sunitinib is a multi-targeted receptor tyrosine kinase inhibitor that acts against receptors for vascular endothelial growth factor and platelet-derived growth factor. Common toxicities of sunitinib treatment include hypertension, hand-foot syndrome, vomiting, and diarrhea, and the proportion of grade 3 or 4 adverse events relating to sunitinib treatment range from 1 to 13% for all categories. It is reported that increased exposure to sunitinib is associated with improved clinical outcomes but also carries an increased risk of adverse effects.A 73-year-old Japanese woman with metastatic renal cell carcinoma who received sunitinib at a dose of 50 mg once daily suffered a high-grade fever on day 11 of treatment. Sunitinib treatment was discontinued on day 12; however, severe thrombocytopenia and transaminase elevation occurred and persisted more than a week. Additionally, severe hypoxia due to pleural effusion and pulmonary edema developed despite immediate discontinuation of sunitinib. On day 14, three days after the discontinuation of sunitinib, the plasma concentrations of sunitinib and its major active metabolite N-desethyl sunitinib (SU12662) were extremely high (131.9 ng/mL and 28.4 ng/mL, respectively). By day 25, all toxicities had resolved, and a CT scan revealed marked tumor shrinkage. Genotyping of seven single-nucleotide polymorphisms that are potentially relevant to the pharmacokinetics of sunitinib was performed. The patient's genotype of ABCG2 (ATP-binding cassette, sub-family G (WHITE), member 2) 421C > A was homozygous for the variant allele (AA), which was reported to be associated with high exposure to sunitinib. Therefore, we speculated that the extremely high plasma concentrations of sunitinib and SU12662 caused by the ABCG2 421 AA genotype might have resulted in severe toxicities to the patient.The minor allele frequencies of ABCG2 421C > A are approximately three-fold higher in Asians than in Caucasians. Our report suggests that pharmacogenetic factors should be considered when severe and rapid-onset adverse drug reactions occur in Asian patients, including Japanese treated with sunitinib.
- Extravascular Lung Water and Pulmonary Vascular Permeability Index as Markers Predictive of Postoperative Acute Respiratory Distress Syndrome: A Prospective Cohort Investigation. [JOURNAL ARTICLE]
- Crit Care Med 2014 Dec 15.
Robust markers of subclinical perioperative lung injury are lacking. Extravascular lung water indexed to predicted body weight and pulmonary vascular permeability index are two promising early markers of lung edema. We aimed to evaluate whether extravascular lung water indexed to predicted body weight and pulmonary vascular permeability index would identify patients at risk for clinically significant postoperative pulmonary edema, particularly resulting from the acute respiratory distress syndrome.Prospective cohort study.Tertiary care academic medical center.Adults undergoing high-risk cardiac or aortic vascular surgery (or both) with risk of acute respiratory distress syndrome.None.Extravascular lung water indexed to predicted body weight and pulmonary vascular permeability index measurements were obtained intraoperatively and in the early postoperative period. We assessed the accuracy of peak extravascular lung water indexed to predicted body weight and pulmonary vascular permeability index as predictive markers of clinically significant pulmonary edema (defined as acute respiratory distress syndrome or cardiogenic pulmonary edema) using area under the receiver-operating characteristic curves. Associations between extravascular lung water indexed to predicted body weight and pulmonary vascular permeability patient-important with important outcomes were assessed. Of 150 eligible patients, 132 patients (88%) had extravascular lung water indexed to predicted body weight and pulmonary vascular permeability index measurements. Of these, 13 patients (9.8%) had postoperative acute respiratory distress syndrome and 15 patients (11.4%) had cardiogenic pulmonary edema. Extravascular lung water indexed to predicted body weight effectively predicted development of clinically significant pulmonary edema (area under the receiver-operating characteristic curve, 0.79; 95% CI, 0.70-0.89). Pulmonary vascular permeability index discriminated acute respiratory distress syndrome from cardiogenic pulmonary edema alone or no edema (area under the receiver-operating characteristic curve, 0.77; 95% CI, 0.62-0.93). Extravascular lung water indexed to predicted body weight was associated with the worst postoperative PaO2/FIO2, duration of mechanical ventilation, ICU stay, and hospital stay. Peak values for extravascular lung water indexed to predicted body weight and pulmonary vascular permeability index were obtained within 2 hours of the primary intraoperative insult for the majority of patients (> 80%).Perioperative extravascular lung water indexed to predicted body weight is an early marker that predicts risk of clinically significant postoperative pulmonary edema in at-risk surgical patients. Pulmonary vascular permeability index effectively discriminated postoperative acute respiratory distress syndrome from cardiogenic pulmonary edema. These measures will aid in the early detection of subclinical lung injury in at-risk surgical populations.
- [Study of quercetin on pulmonary fibrosis by silica particles]. [English Abstract, Journal Article]
- Wei Sheng Yan Jiu 2014 Sep; 43(5):814-8.
To observe the intervention effect of quercetin to silica dust cause pulmonary fibrosis.Forty-eight healthy male adult SPF SD rats were selected and they were randomly divided into six groups (control group, 7 d,14 d,21 d and 28d dust group, preventive group). Rats in the control group were administrated 1 ml saline via trachea injection. Rats in dust group and preventive group were give silica solution for 1ml at dose of 50 mg/ml, and the prevention group with quercetin of 50 mg/kg every day lavage treatment intervention. In building on days 7,14,21,28 later, the lung tissue were removaled to HE staining for determining the degree of alveolitis and pulmonary fibrosis. The content of hydroxyproline (HYP) and the activities of catalase (CAT) and glutathione peroxidase (GSH-Px) were detected by using the kits.Alveolar septal edema, inflammatory cell infiltration and fibrosis were not found in control group. In the preventive group, lots of inflammatory cells infiltration were observed on days 7. Inflammatory cells were reduced, the number of the fibroblasts and matrix in alveolar septum were obviously increased, and alveolar structure was damaged on day 14. Pulmonary fibrosis was increased, severe fibrosis was found on day 28. Silicon dust after infected lung tissue expression of HYP content increased, the activity of CAT and GSH-Px decrease gradually. After joining quercetin the expression of HYP content gradually reduce, CAT and GSH-Px activity increased, the difference was statistically significant (P<0.05).Quercetin of silica dust caused by pulmonary fibrosis have certain prevention.
- Neurogenic pulmonary edema caused by bilateral medial medullary infarction. [JOURNAL ARTICLE]
- Neurol Sci 2014 Dec 12.
- Investigating the efficacy of a new diuretic in dogs with pulmonary oedema. [Letter]
- Vet Rec 2014 Dec 13; 175(23):598.
- Wilderness Medical Society Practice Guidelines for the Prevention and Treatment of Acute Altitude Illness: 2014 Update. [JOURNAL ARTICLE]
- Wilderness Environ Med 2014 Dec; 25(4S):S4-S14.
To provide guidance to clinicians about best practices, the Wilderness Medical Society convened an expert panel to develop evidence-based guidelines for prevention and treatment of acute mountain sickness, high altitude cerebral edema, and high altitude pulmonary edema. These guidelines present the main prophylactic and therapeutic modalities for each disorder and provide recommendations about their role in disease management. Recommendations are graded based on the quality of supporting evidence and balance between the benefits and risks/burdens according to criteria put forth by the American College of Chest Physicians. The guidelines also provide suggested approaches to prevention and management of each disorder that incorporate these recommendations. This is an updated version of the original WMS Consensus Guidelines for the Prevention and Treatment of Acute Altitude Illness published in Wilderness & Environmental Medicine 2010;21(2):146-155.
- Increased incidence of transfusion-related acute lung injury during orthotopic liver transplantation: a short report. [Journal Article]
- Transplant Proc 2014 Dec; 46(10):3593-7.
Intractable severe pulmonary edema during Orthotopic Liver Transplant (OLT) can be a fatal perioperative complication. We sought to characterize the incidence, timing, and related risk factors of severe pulmonary edema during OLT. We performed a retrospective observational survey of OLT cases performed between 2007 and 2011 at Miami Transplant Institute. Of all 632 OLT patients, a total of 9 patients (1.4%) had severe pulmonary edema during OLT. All these patients received blood transfusions before and after reperfusion (Packed red blood cell 8.9 ± 2.6 units, Fresh frozen plasma 12 ± 3.7 units, Platelets 5.4 ± 8.6 units). Eight episodes occurred after reperfusion (89%) and 1 before reperfusion (11%). Median time interval from last blood transfusion to severe pulmonary edema was 79 min (25-257 min). In the 8 patients that developed severe pulmonary edema post reperfusion, median time interval from reperfusion to severe pulmonary edema was 34 min (15-85 min). Perioperative mortality among severe pulmonary edema cases was 11% (1 in 9). Incidence of severe pulmonary edema was 1.4% in our patient population, and this number is much higher than that reported for TRALI in other large series (0.075 to 0.12%). Despite a large dose of steroids given at reperfusion, 89% of pulmonary edema episodes occurred within 2.5 hours of reperfusion. Also, heart failure and pulmonary embolism were unlikely based on intraoperative transesophageal echocardiography findings. These results may suggest an association between TRALI and the post reperfusion syndrome during liver transplantation that warrants further investigation.