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Ugeskrift For Laeger Oct 2020Acute heart failure is a common and severe condition in Danish emergency hospitals. Hypertensive pulmonary oedema, cardiogenic shock and congestive heart failure are the... (Review)
Review
Acute heart failure is a common and severe condition in Danish emergency hospitals. Hypertensive pulmonary oedema, cardiogenic shock and congestive heart failure are the most common phenotypes. The aim of this review is to summarise the most recent international guidelines for acute triage and treatment of acute heart failure. Afterload is reduced with nitrates, congestion is treated with intravenous loop-diuretics, and in selected patients, cardiac output could be increased by inotropic drugs or mechanical support devices.
Topics: Acute Disease; Heart Failure; Humans; Hypertension; Pulmonary Edema; Shock, Cardiogenic; Vasodilator Agents
PubMed: 33046187
DOI: No ID Found -
Journal of the American Heart... Oct 2023ABSTRACTRecurring and rapidly developing (flash) pulmonary edema is the hallmark of Pickering syndrome, affecting patients with hypertension and atherosclerotic renal... (Review)
Review
ABSTRACTRecurring and rapidly developing (flash) pulmonary edema is the hallmark of Pickering syndrome, affecting patients with hypertension and atherosclerotic renal artery stenosis (either bilateral or unilateral) in a solitary functioning kidney, and impaired renal function. We herein report on a series of consecutive patients with recurrent hospital admissions for pulmonary edema, impaired renal function (chronic kidney disease class 4-5), and atherosclerotic bilateral renal artery stenosis, in whom Pickering syndrome had been long neglected. We also describe a streamlined diagnostic strategy entailing little or no need for contrast medium, thus carrying no risks of further worsening of renal function. This allowed us to make the correct diagnosis and opened the way to revascularization by percutaneous transluminal renal angioplasty with stent, which provided swift recovery of kidney function with resolution of pulmonary congestion and long-term pulmonary edema- and dialysis-free survival in all cases. In summary, these findings support the following key messages: (1) considering the diagnosis of Pickering syndrome, followed by searching atherosclerotic renal artery stenosis, is an essential step toward a life-saving revascularization that avoids dialysis and an otherwise poor outcome; and (2) a simplified strategy entailing little or no need for contrast medium, carrying no associated risks of deteriorating renal function, permits the diagnosis of Pickering syndrome.
Topics: Humans; Renal Artery Obstruction; Pulmonary Edema; Angioplasty; Renal Artery; Atherosclerosis; Syndrome; Heart Failure; Stents
PubMed: 37750563
DOI: 10.1161/JAHA.123.030474 -
Ugeskrift For Laeger Jun 2021Swimming-induced pulmonary oedema (SIPE) is a rare condition, where hemodynamic changes associated with immersion in water and swimming induces pulmonary oedema. Here,...
Swimming-induced pulmonary oedema (SIPE) is a rare condition, where hemodynamic changes associated with immersion in water and swimming induces pulmonary oedema. Here, we report a case with a 57-year old very fit female triathlete experiencing critical lung edema during low intensity open water swimming. We speculate, that SIPE in this particular patient was caused by a combination of factors: 1) Stress-induced diastolic dysfunction, 2) tendency to vasoconstriction upon stress and 3) possibly paroxysmal atrial fibrillation induced by increased atrial pressure during the event.
Topics: Female; Hemodynamics; Humans; Middle Aged; Pulmonary Edema; Swimming; Water
PubMed: 34219637
DOI: No ID Found -
Biomedicine & Pharmacotherapy =... Oct 2020Neurogenic pulmonary edema (NPE) following acute stroke is an acute respiratory distress syndrome (ARDS) with clinical characteristics that include acute onset, apparent... (Review)
Review
Neurogenic pulmonary edema (NPE) following acute stroke is an acute respiratory distress syndrome (ARDS) with clinical characteristics that include acute onset, apparent pulmonary interstitial fluid infiltration and rapid resolution. The pathological process of NPE centers on sympathetic stimulation and fulminant release of catecholamines, which cause contraction of resistance vessels. Elevated systemic resistance forces fluid into pulmonary circulation, while pulmonary circulation overload induces pulmonary capillary pressure that elevates, and in turn damages the alveolar capillary barrier. Damage to the alveolar capillary barrier leads to pulmonary ventilation disorder, blood perfusion disorder and oxygenation disorder. Eventually, NPE will cause post-stroke patients' prognosis to further deteriorate. At present, we lack specific biological diagnostic indicators and a meticulously unified diagnostic criterion, and this results in a situation in which many patients are not recognized quickly and/or diagnosed accurately. There are no drugs that are effective against NPE. Therefore, understanding how to diagnose NPE early by identifying the risk factors and how to apply appropriate treatment to avoid a deteriorating prognosis are important scientific goals. We will elaborate the progress of NPE after acute stroke in terms of its pathophysiological mechanisms, etiology, epidemiology, clinical diagnosis and early prediction, comprehensive treatment strategies, and novel drug development. We also propose our own thinking and prospects regarding NPE.
Topics: Animals; Humans; Pulmonary Circulation; Pulmonary Edema; Respiratory Distress Syndrome; Stroke
PubMed: 32739737
DOI: 10.1016/j.biopha.2020.110478 -
Ugeskrift For Laeger Mar 2024Swimming-induced pulmonary oedema (SIPE) is a rare but potentially life-threatening condition which occurs in otherwise healthy swimmers. This is a case report of a...
Swimming-induced pulmonary oedema (SIPE) is a rare but potentially life-threatening condition which occurs in otherwise healthy swimmers. This is a case report of a 62-year-old female developing severe dyspnoea, haemoptysis and hypoxia during open-water swimming. The report provides the current perspectives of SIPE regarding clinical presentation and treatment and presents theories on the pathophysiology of the condition.
Topics: Female; Humans; Middle Aged; Pulmonary Edema; Swimming; Deafness; Health Status; Hemoptysis
PubMed: 38445342
DOI: 10.61409/V10230642 -
Critical Care (London, England) Jun 2023A hallmark of acute respiratory distress syndrome (ARDS) is hypoxaemic respiratory failure due to pulmonary vascular hyperpermeability. The tyrosine kinase inhibitor... (Randomized Controlled Trial)
Randomized Controlled Trial
PURPOSE
A hallmark of acute respiratory distress syndrome (ARDS) is hypoxaemic respiratory failure due to pulmonary vascular hyperpermeability. The tyrosine kinase inhibitor imatinib reversed pulmonary capillary leak in preclinical studies and improved clinical outcomes in hospitalized COVID-19 patients. We investigated the effect of intravenous (IV) imatinib on pulmonary edema in COVID-19 ARDS.
METHODS
This was a multicenter, randomized, double-blind, placebo-controlled trial. Invasively ventilated patients with moderate-to-severe COVID-19 ARDS were randomized to 200 mg IV imatinib or placebo twice daily for a maximum of seven days. The primary outcome was the change in extravascular lung water index (∆EVLWi) between days 1 and 4. Secondary outcomes included safety, duration of invasive ventilation, ventilator-free days (VFD) and 28-day mortality. Posthoc analyses were performed in previously identified biological subphenotypes.
RESULTS
66 patients were randomized to imatinib (n = 33) or placebo (n = 33). There was no difference in ∆EVLWi between the groups (0.19 ml/kg, 95% CI - 3.16 to 2.77, p = 0.89). Imatinib treatment did not affect duration of invasive ventilation (p = 0.29), VFD (p = 0.29) or 28-day mortality (p = 0.79). IV imatinib was well-tolerated and appeared safe. In a subgroup of patients characterized by high IL-6, TNFR1 and SP-D levels (n = 20), imatinib significantly decreased EVLWi per treatment day (- 1.17 ml/kg, 95% CI - 1.87 to - 0.44).
CONCLUSIONS
IV imatinib did not reduce pulmonary edema or improve clinical outcomes in invasively ventilated COVID-19 patients. While this trial does not support the use of imatinib in the general COVID-19 ARDS population, imatinib reduced pulmonary edema in a subgroup of patients, underscoring the potential value of predictive enrichment in ARDS trials. Trial registration NCT04794088 , registered 11 March 2021. European Clinical Trials Database (EudraCT number: 2020-005447-23).
Topics: Humans; COVID-19; Imatinib Mesylate; Pulmonary Edema; Lung; Respiratory Distress Syndrome; Double-Blind Method
PubMed: 37291677
DOI: 10.1186/s13054-023-04516-4 -
The American Journal of Forensic... Mar 2021The 2019 novel coronavirus disease (COVID-19) has spread worldwide, infiltrating, infecting, and devastating communities in all locations of varying demographics. An...
The 2019 novel coronavirus disease (COVID-19) has spread worldwide, infiltrating, infecting, and devastating communities in all locations of varying demographics. An overwhelming majority of published literature on the pathologic findings associated with COVID-19 is either from living clinical cohorts or from autopsy findings of those who died in a medical care setting, which can confound pure disease pathology. A relatively low initial infection rate paired with a high biosafety level enabled the New Mexico Office of the Medical Investigator to conduct full autopsy examinations on suspected COVID-19-related deaths. Full autopsy examination on the first 20 severe acute respiratory syndrome coronavirus 2-positive decedents revealed that some extent of diffuse alveolar damage in every death due to COVID-19 played some role. The average decedent was middle-aged, male, American Indian, and overweight with comorbidities that included diabetes, ethanolism, and atherosclerotic and/or hypertensive cardiovascular disease. Macroscopic thrombotic events were seen in 35% of cases consisting of pulmonary thromboemboli and coronary artery thrombi. In 2 cases, severe bacterial coinfections were seen in the lungs. Those determined to die with but not of severe acute respiratory syndrome coronavirus 2 infection had unremarkable lung findings.
Topics: Adult; Age Distribution; Aged; Aged, 80 and over; Autopsy; Body Mass Index; Brain Edema; COVID-19; Cardiomegaly; Comorbidity; Coronary Thrombosis; Databases, Factual; Fatty Liver; Female; Forensic Pathology; Glomerulosclerosis, Focal Segmental; Hepatomegaly; Humans; Lung; Male; Middle Aged; Nephrosclerosis; New Mexico; Overweight; Pandemics; Pleural Effusion; Pulmonary Edema; Sex Distribution; Streptococcus pneumoniae; Tomography, X-Ray Computed; Vitreous Body; Whole Body Imaging
PubMed: 33416234
DOI: 10.1097/PAF.0000000000000664 -
Microvascular Research Mar 2022Evidence suggests severe coronavirus disease-19 (COVID-19) infection is characterised by pulmonary and systemic microvasculature dysfunction, specifically, acute... (Review)
Review
Evidence suggests severe coronavirus disease-19 (COVID-19) infection is characterised by pulmonary and systemic microvasculature dysfunction, specifically, acute endothelial injury, hypercoagulation and increased capillary permeability. Diabetes, which is also characterised by vascular injury in itself, confers an increased risk of adverse COVID-19 outcomes. It has been suggested that pre-existing endothelial dysfunction and microvascular disease in diabetes will exacerbate the vascular insults associated with COVID-19 and thus lead to increased severity of COVID-19 infection. In this article, we evaluate the current evidence exploring the impact of microvascular complications, in the form of diabetic retinopathy and nephropathy, in individuals with COVID-19 and diabetes. Future insights gained from exploring the microvascular injury patterns and clinical outcomes may come to influence care delivery algorithms for either of these conditions.
Topics: Albuminuria; COVID-19; Capillary Permeability; Delivery of Health Care; Diabetic Angiopathies; Diabetic Nephropathies; Diabetic Neuropathies; Diabetic Retinopathy; Endothelium, Vascular; Humans; Microcirculation; Obesity; Pandemics; Pulmonary Circulation; Pulmonary Edema; SARS-CoV-2; Severity of Illness Index; Thrombophilia; Treatment Outcome
PubMed: 34979154
DOI: 10.1016/j.mvr.2021.104310 -
Cleveland Clinic Journal of Medicine Jun 2022
Topics: Humans; Pulmonary Edema
PubMed: 35649558
DOI: 10.3949/ccjm.89c.06002 -
Journal of Applied Physiology... May 2020Heritable pulmonary arterial hypertension (PAH) is an autosomal dominantly inherited disease caused by mutations in the () gene and/or genes of its signaling pathway in...
Heritable pulmonary arterial hypertension (PAH) is an autosomal dominantly inherited disease caused by mutations in the () gene and/or genes of its signaling pathway in ~85% of patients. A genetic predisposition to high-altitude pulmonary edema (HAPE) has long been suspected because of familial HAPE cases, but very few possibly disease-causing mutations have been identified to date. This minireview provides an overview of genetic analyses investigating common polymorphisms in HAPE-susceptible patients and the directed identification of disease-causing mutations in PAH patients. Increased pulmonary artery pressure is highlighted as an overlapping clinical feature of the two diseases. Moreover, studies showing increased pulmonary artery pressures in HAPE-susceptible patients during exercise or hypoxia as well as in healthy mutation carriers are illustrated. Finally, high-altitude pulmonary hypertension is introduced and future research perspectives outlined.
Topics: Altitude; Altitude Sickness; Humans; Hypertension, Pulmonary; Hypoxia; Pulmonary Edema
PubMed: 32324476
DOI: 10.1152/japplphysiol.00113.2020