-
Clinical Journal of the American... May 2022Fluid overload is a common complication in patients with CKD, particularly patients with kidney failure, a population with a very high risk for pulmonary edema. Lung... (Review)
Review
Fluid overload is a common complication in patients with CKD, particularly patients with kidney failure, a population with a very high risk for pulmonary edema. Lung ultrasound is now a well-validated technique that allows for reliable estimates of lung water in clinical practice. Several studies in patients with kidney failure documented a high prevalence of asymptomatic lung congestion of moderate to severe degree in this population, and this alteration was only weakly related with fluid excess as measured by bioimpedance spectroscopy. Furthermore, in these studies, lung congestion correlated in a dose-dependent fashion with death risk. In the Lung Water by Ultra-Sound Guided Treatment to Prevent Death and Cardiovascular Complications in High Risk Kidney Failure Patients with Cardiomyopathy (LUST) trial, a treatment strategy guided by lung ultrasound safely relieved lung congestion but failed to significantly reduce the risk for a combined end point including death, nonfatal myocardial infarction, and decompensated heart failure. However, in line with three trials in patients with heart failure, a analysis of the LUST trial showed that the use of lung ultrasound reduces the risk for repeated episodes of acute heart failure and repeated cardiovascular events. Given the high cardiovascular risk of pulmonary edema in patients with predialysis CKD, defining the epidemiology of lung congestion in this population is a public health priority. Specific trials in this population and additional trials in patients with kidney failure will establish whether targeting lung congestion at an asymptomatic phase may improve the severe cardiovascular prognosis of both patients predialysis and patients on dialysis.
Topics: Female; Heart Failure; Humans; Kidney Failure, Chronic; Lung; Male; Pulmonary Edema; Renal Insufficiency; Ultrasonography; Water-Electrolyte Imbalance
PubMed: 35140128
DOI: 10.2215/CJN.14591121 -
JAAPA : Official Journal of the... Apr 2022Acute respiratory distress syndrome (ARDS) is a severe, often fatal, lung condition frequently seen in patients in the ICU. ARDS is triggered by an inciting event such...
Acute respiratory distress syndrome (ARDS) is a severe, often fatal, lung condition frequently seen in patients in the ICU. ARDS is triggered by an inciting event such as pneumonia or sepsis, which is followed by an inappropriate host inflammatory response that results in pulmonary edema and impaired gas exchange, and may progress to fibrosis. With the increased spotlight and discussion focused on ARDS during the COVID-19 pandemic, healthcare providers must be able to identify and manage symptoms based on evidence-based research.
Topics: COVID-19; Humans; Pandemics; Pneumonia; Pulmonary Edema; Respiratory Distress Syndrome
PubMed: 35276715
DOI: 10.1097/01.JAA.0000823164.50706.27 -
The Spine Journal : Official Journal of... Apr 2016Respiratory complications are a major cause of morbidity and mortality during the first days after acute spinal cord injury (ASCI). However, the pathophysiology of...
BACKGROUND CONTEXT
Respiratory complications are a major cause of morbidity and mortality during the first days after acute spinal cord injury (ASCI). However, the pathophysiology of respiratory insufficiency resulting from spinal cord injury that involves lower levels is less well understood.
PURPOSE
The aim of the present study was to investigate pulmonary pathophysiology after ASCI.
STUDY DESIGN
This is an experimental animal study of ASCI investigating pulmonary pathophysiology after ASCI.
METHODS
Eighty-four (N=84) rats were divided into two groups: a sham surgery (n=42) and an injury group (n=42). In the injury group, ASCI was induced at the level of the tenth thoracic vertebra by a modified Allen method. Rats were sacrificed 6 hours, 12 hours, 24 hours, 3 days, 1 week, 2 weeks, and 4 weeks after surgery. Pulmonary edema was assessed by calculating the ratio of the wet-to-dry lung weight (W:D). Pulmonary edema and hemorrhage were evaluated by observing gross and microscopic morphology. The study was funded by Natural Science Foundation of China (NSFC, 81272172). The funder of the present study had no capacity to influence the scholarly conduct of the research, interpretation of results, or dissemination of study outcomes.
RESULTS
In the injury group, W:D was significantly increased 12 hours after surgery compared with the sham surgery group; W:D peaked 3 days after ASCI (p<.05). Gross morphologic observations showed hemorrhagic lesions on the lung tissue 12 hours after ASCI and pulmonary edema 24 hours after ASCI. Pulmonary edema peaked 3 days after ASCI and was obviously decreased 1 week after ASCI. Hemorrhage was apparent until 2 weeks after ASCI. Light microscopy showed congestion of pulmonary capillaries 6 hours after ASCI. The pulmonary alveoli were filled with erythrocytes and serous extravasate 12 hours after ASCI. Hemorrhage and edema were observed in the interstitium and lung alveoli 24 hours after ASCI.
CONCLUSIONS
Early pathologic changes such as pulmonary congestion, hemorrhage, and edema after injury may be the basis for early respiratory dysfunction following ASCI.
Topics: Animals; Hemorrhage; Male; Pulmonary Edema; Rats; Rats, Sprague-Dawley; Spinal Cord Injuries
PubMed: 26674444
DOI: 10.1016/j.spinee.2015.11.065 -
International Journal of Cardiology Jan 2016Morphine has for a long time, been used in patients with acute pulmonary oedema due to its anticipated anxiolytic and vasodilatory properties, however a discussion about... (Review)
Review
Morphine has for a long time, been used in patients with acute pulmonary oedema due to its anticipated anxiolytic and vasodilatory properties, however a discussion about the benefits and risks has been raised recently. A literature search in Medline and Embase using the keywords "pulmonary oedema" OR "lung oedema" OR "acute heart failure" AND "morphine" was performed. A certain vasodilation has been described after morphine administration, but the evidence for this mechanism is relatively poor and morphine-induced anxiolysis may possibly be the most important factor of morphine in pulmonary oedema and therefore some authors have suggested benzodiazepines as an alternative treatment. Respiratory depression seems to be a less relevant clinical problem according to the literature, whereas vomiting is common, which may cause aspiration. In the largest outcome study, based on the ADHERE registry, morphine given in acute decompensated heart failure was an independent predictor of increased hospital mortality, with an odds ratio of 4.8 (95% CI: 4.52-5.18, p<0.001). Other, smaller studies have shown a significant association between morphine administration and mortality, which was lost after adjusting for confounding factors. Morphine is still used for pulmonary oedema in spite of poor scientific background data. A randomised, controlled study is necessary in order to determine the effect--and especially the risk--when using morphine for pulmonary oedema. Since the positive effects are not sufficiently documented, and since the risk for increased mortality cannot be ruled out, one can advocate that the use should be avoided.
Topics: Acute Disease; Hospital Mortality; Humans; Morphine; Practice Guidelines as Topic; Pulmonary Edema; Treatment Outcome; Vasodilation
PubMed: 26476045
DOI: 10.1016/j.ijcard.2015.10.014 -
Acta Radiologica (Stockholm, Sweden :... Feb 2020
Review
Topics: Heart Diseases; Humans; Pulmonary Edema; Respiratory Distress Syndrome; Tomography, X-Ray Computed
PubMed: 31226879
DOI: 10.1177/0284185119857433 -
Archivos de Bronconeumologia Jul 2021
Topics: Humans; Pneumothorax; Pulmonary Atelectasis; Pulmonary Edema
PubMed: 35698957
DOI: 10.1016/j.arbr.2021.05.008 -
Chest Nov 2021
Topics: Humans; Incidence; Military Personnel; Pulmonary Edema; Swimming
PubMed: 34743842
DOI: 10.1016/j.chest.2021.07.023 -
Intensive Care Medicine Jun 2020
Topics: Humans; Lung; Pulmonary Edema; Radiography
PubMed: 31713061
DOI: 10.1007/s00134-019-05849-x -
The Journal of Craniofacial Surgery 2020Negative-pressure pulmonary edema is a rare but life-threatening complication of septoplasty seen in the early-postoperative period. The main cause is laryngospasm;...
Negative-pressure pulmonary edema is a rare but life-threatening complication of septoplasty seen in the early-postoperative period. The main cause is laryngospasm; often with hypoxia and hemoptysis. In our case, a 36-year-old septoplasty recipient developed symptoms of hypotension, tachycardia and low oxygen saturation 3 hours after extubation. The patient was diagnosed with negative-pressure pulmonary edema. Treatment was applied with noninvasive positive pressure ventilation and diuretics. It should be noted that negative pressure pulmonary edema may vary in terms of presentation and may not be accompanied by laryngospasm.
Topics: Adult; Airway Extubation; Humans; Hypotension; Male; Postoperative Period; Pressure; Pulmonary Edema; Rhinoplasty
PubMed: 32097382
DOI: 10.1097/SCS.0000000000006265 -
Indian Journal of Pediatrics May 2016To characterize pulmonary edema (PE) fluid induced by enterovirus 71 (EV71) infection, elucidate the relationship between angiopoietin-2 (Ang-2) and PE, and explore the...
OBJECTIVE
To characterize pulmonary edema (PE) fluid induced by enterovirus 71 (EV71) infection, elucidate the relationship between angiopoietin-2 (Ang-2) and PE, and explore the pathogenesis of PE.
METHODS
Clinical data were collected from critical infants with EV71 infection. The infants were grouped into PE, non-PE, and control groups. The control group included infants in the preoperative period of elective inguinal hernia surgery. Biochemical changes in PE fluid were evaluated, and Ang-2 levels in serum and PE fluid were measured. Human pulmonary microvascular endothelial cells (HPMECs) were incubated with serum from the control and PE groups and human recombinant Ang-2 or serum from the PE group and human recombinant Ang-1, and changes in the intercellular junctions were recorded via immunofluorescence.
RESULTS
Of the 161 infants with critical EV71 infection admitted to the hospital, 39 had PE. PE fluid was collected from 18 of these infants. The PE fluid-to-serum (P/S) ratio of total protein was 0.9 ± 0.2, and all P/S ratios of albumin were 1.0 ± 0.3. The Ang-2 level was higher in the non-PE group (333.2 ± 79.7 pg/ml) than in the control group (199.9 ± 26.7 pg/ml), although without statistical significance (P = 0.115). The Ang-2 level in the PE group (2819.2 ± 908.7 pg/ml) was higher than those in both the non-PE and the control groups (both, P < 0.001). Serum samples from the PE group had damaged cell junctions of confluent HPMEC monolayers that were reversed by Ang-1.
CONCLUSIONS
The PE fluid of infants with EV71-induced PE was protein-rich, and elevated Ang-2 expression was associated with PE. The mechanism through which PE develops may be related to Ang-2-induced cell junction damage.
Topics: Angiopoietin-1; Angiopoietin-2; Capillary Permeability; Critical Care; Critical Illness; Enterovirus A, Human; Enterovirus Infections; Fluid Shifts; Humans; Infant; Pulmonary Edema; Suction
PubMed: 26590154
DOI: 10.1007/s12098-015-1920-2