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Physiological Research 2008Neurogenic pulmonary edema is a life-threatening complication, known for almost 100 years, but its etiopathogenesis is still not completely understood. This review... (Review)
Review
Neurogenic pulmonary edema is a life-threatening complication, known for almost 100 years, but its etiopathogenesis is still not completely understood. This review summarizes current knowledge about the etiology and pathophysiology of neurogenic pulmonary edema. The roles of systemic sympathetic discharge, central nervous system trigger zones, intracranial pressure, inflammation and anesthesia in the etiopathogenesis of neurogenic pulmonary edema are considered in detail. The management of the patient and experimental models of neurogenic pulmonary edema are also discussed.
Topics: Anesthesia; Humans; Intracranial Pressure; Nervous System; Pulmonary Edema; Sympathetic Nervous System
PubMed: 18052674
DOI: 10.33549/physiolres.931432 -
Journal of Biomedical Science 2003Acute respiratory distress syndrome (ARDS) can be associated with various disorders. Among these, coronavirus infection may cause life-threatening severe acute... (Review)
Review
Acute respiratory distress syndrome (ARDS) can be associated with various disorders. Among these, coronavirus infection may cause life-threatening severe acute respiratory syndrome (SARS). In this review, we present animal models and techniques for the study of ARDS, and discuss the roles and possible mechanisms of various chemical factors, including nitric oxide (NO). Our early work revealed that cerebral compression elicits severe hemorrhagic pulmonary edema (PE), leading to central sympathetic activation that results in systemic vasoconstriction. The consequence of systemic vasoconstriction is volume and pressure loading in the pulmonary circulation. Vasodilators, but not oxidant radical scavengers, are effective in the prevention of centrogenic PE. In isolated perfused lung, exogenous and endogenous NO enhances lung injury following air embolism and ischemia/reperfusion. In contrast, NO synthase (NOS) inhibitors reverse such lung injury. Although NO is important in maintaining vasodilator tone, hypoxia-induced pulmonary vasoconstriction is accompanied by an increase instead of a decrease in NO release. In animal and isolated lung studies, endotoxin produces acute lung injury that is associated with increases in cytokines and inducible NOS mRNA expression, suggesting that NO is toxic to the lung in endotoxin shock. Recently, we reported several rare cases that indicate that ARDS in patients with Japanese B encephalitis, lymphangitis with breast cancer and fat embolism is caused by different mechanisms. Our early and recent studies on ARDS and PE may provide information for clinical practice and the understanding of the pathogenesis of SARS.
Topics: Animals; Disease Models, Animal; Humans; Nitric Oxide; Nitric Oxide Synthase; Pulmonary Edema; Respiratory Distress Syndrome
PubMed: 14576460
DOI: 10.1159/000073523 -
Medicine Apr 2019Negative pressure pulmonary edema (NPPE) is a dangerous clinical complication and potentially life-threatening emergency without prompt diagnosis and intervention during... (Review)
Review
RATIONALE
Negative pressure pulmonary edema (NPPE) is a dangerous clinical complication and potentially life-threatening emergency without prompt diagnosis and intervention during recovery period after anesthetic extubation.
PATIENT CONCERNS
A 25-year-old woman has undergone endoscopic thyroidectomy. After extubation, the patient developed acute respiratory distress with high airway resistance accompanied with wheezing, oxyhemoglobin saturation (SpO2) decreased to 70%. With positive pressure mask ventilation, her condition was stable, SpO2 99%. However, the patient developed pink frothy sputum with diffuse bilateral rales 30 min later after transported to surgical intensive care unit (SICU).
DIAGNOSES
Negative pressure pulmonary edema.
INTERVENTIONS
The patient was undergone assisted ventilation with continuous positive airway pressure (CPAP) and furosemide 20 mg was given intravenously.
OUTCOMES
Postoperative day (POD) 2 her condition became stable, computed tomography (CT) scan indicated the pulmonary edema disappeared. The patient was discharged 6 days later. No abnormalities were observed during following 4 weeks.
LESSONS
Although usually the onset of NPPE is rapid, with individual differences NPPE is still challenging. Increased vigilance in monitoring, diagnosis, and treatment are essential to prevent aggravation and further complication.
Topics: Adult; Anesthesia, General; Diagnosis, Differential; Endoscopy; Female; Humans; Postoperative Complications; Pulmonary Edema; Thyroidectomy
PubMed: 31027133
DOI: 10.1097/MD.0000000000015389 -
BMJ Case Reports May 2019
Topics: Acute Coronary Syndrome; Administration, Intravenous; Aged; Angioplasty; Diuretics; Dyspnea; Furosemide; Humans; Male; Mitral Valve Insufficiency; Platelet Aggregation Inhibitors; Pulmonary Edema; Treatment Outcome
PubMed: 31122960
DOI: 10.1136/bcr-2019-230596 -
Cleveland Clinic Journal of Medicine 1990Hydrochlorothiazide-induced acute pulmonary edema has been reported rarely. Despite the frequency of hydrochlorothiazide use and the potential for this life-threatening... (Review)
Review
Hydrochlorothiazide-induced acute pulmonary edema has been reported rarely. Despite the frequency of hydrochlorothiazide use and the potential for this life-threatening side effect, it has received little organized attention in the literature. Treatment of the syndrome involves supportive therapy. The authors present a case report and review the 16 previously described cases.
Topics: Acute Disease; Diagnosis, Differential; Female; Humans; Hydrochlorothiazide; Male; Middle Aged; Pulmonary Edema; Radiography; Sex Factors
PubMed: 2182219
DOI: 10.3949/ccjm.57.2.181 -
BMJ Case Reports Mar 2018
Topics: Adult; Aneurysm, Ruptured; Carotid Artery Diseases; Female; Humans; Pulmonary Edema; Subarachnoid Hemorrhage; Tomography, X-Ray Computed
PubMed: 29540352
DOI: 10.1136/bcr-2017-224011 -
European Journal of Vascular and... Feb 1999Non-cardiogenic pulmonary oedema, an early manifestation of the adult respiratory disease syndrome, is a serious complication following major vascular surgery.... (Review)
Review
Non-cardiogenic pulmonary oedema, an early manifestation of the adult respiratory disease syndrome, is a serious complication following major vascular surgery. Hypovolaemia, ischaemia-reperfusion injury, massive blood transfusion, transient sepsis and transient endotoxaemia are insults responsible for initiating the process in vascular surgical patients. Free radicals, cytokines and humoral factors released secondary to the above insults activate neutrophils and facilitate their interaction with the endothelium. Activated neutrophils marginate through the endothelium where they are responsible for tissue injury by the release of free-radicals and proteases. The lungs are a large reservoir of neutrophils and bear a significant part of the injury. Conventional therapy includes treating the underlying condition and providing respiratory support. A better understanding of the pathophysiology of this process has led to new experimental treatment options. Novel therapeutic interventions have included the use of compounds to scavenge free radicals, anti-cytokine antibodies, extracorporeal lung support, nitric oxide and artificial surfactant therapy. The multifactorial nature of this process makes it unlikely that a single "magic bullet" will solve this problem. It is more likely that a combination of preventative, prophylactic and therapeutic modalities may reduce the mortality of this condition.
Topics: Humans; Pulmonary Edema; Respiratory Distress Syndrome; Vascular Surgical Procedures
PubMed: 10063402
DOI: 10.1053/ejvs.1998.0750 -
Canadian Medical Association Journal Feb 1979Pulmonary edema is common cause of acute respiratory failure and can be seen in not only cardiac but also noncardiac diseases. The pathophysiologic mechanism for the... (Review)
Review
Pulmonary edema is common cause of acute respiratory failure and can be seen in not only cardiac but also noncardiac diseases. The pathophysiologic mechanism for the development of acute pulmonary edema in any clinical situation can usually be explained alterations in the forces governing the transvascular flux of fluid in the pulmonary microvasculature, according to the Starling equation. "Cardiac" pulmonary edema is primarily due to an increase in the capillary hydrostatic pressure of sufficient magnitude to overcome the forces maintaining fluid within the vessel and the ability of the lymphatics to drain the transudated fluid. On the other hand, pulmonary edema occurring in association with noncardiac disease (e.g., sepsis, aspiration or shock) is secondary to an increase in the permeability of the pulmonary microvasculature and is referred to as noncardiogenic pulmonary edema or the adult respiratory distress syndrome. This article examines the mechanisms for the development of pulmonary edema and discusses the differences between the cardiac and noncardiac types.
Topics: Animals; Capillary Permeability; Heart Failure; Humans; Hydrostatic Pressure; Lung; Lymphatic System; Microcirculation; Pulmonary Circulation; Pulmonary Edema; Respiratory Distress Syndrome; Respiratory Therapy
PubMed: 376080
DOI: No ID Found -
Journal of Human Hypertension Apr 2023Renal artery stenosis manifests as poorly-controlled hypertension, impaired renal function or pulmonary oedema, therefore the success of treatment is dependent on... (Review)
Review
Renal artery stenosis manifests as poorly-controlled hypertension, impaired renal function or pulmonary oedema, therefore the success of treatment is dependent on indication. This study aims to determine the outcomes of patients undergoing renal artery stenting (RASt) based on therapeutic aim compared to criteria used in the largest randomised trial. Retrospective case-note review of patients undergoing RASt between 2008-2021 (n = 74). The cohort was stratified by indication for intervention (renal dysfunction, hypertension, pulmonary oedema) and criteria employed in the CORAL trial, with outcomes and adverse consequences reported. Intervention for hypertension achieved significant reduction in systolic blood pressure and antihypertensive agents at 1 year (median 43 mmHg, 1 drug), without detrimental impact on renal function. Intervention for renal dysfunction reduced serum creatinine by a median 124 μmol/L, sustained after 6 months. Intervention for pulmonary oedema was universally successful with significant reduction in SBP and serum creatinine sustained at 1 year. Patients who would have been excluded from the CORAL trial achieved greater reduction in serum creatinine than patients meeting the inclusion criteria, with equivalent blood pressure reduction. There were 2 procedure-related mortalities and 5 procedural complications requiring further intervention. 5 patients had reduction in renal function following intervention and 7 failed to achieve the intended therapeutic benefit. Renal artery stenting is effective in treating the indication for which it has been performed. Previous trials may have underestimated the clinical benefits by analysis of a heterogenous population undergoing a procedure rather than considering the indication, and excluding patients who would maximally benefit.
Topics: Humans; Renal Artery; Retrospective Studies; Creatinine; Pulmonary Edema; Treatment Outcome; Hypertension; Renal Artery Obstruction; Blood Pressure; Antihypertensive Agents; Stents
PubMed: 36526895
DOI: 10.1038/s41371-022-00785-8 -
Chest Aug 2022Swimming-induced pulmonary edema (SIPE) occasionally occurs during swimming in cold open water. Although optimal treatment for SIPE is unknown, non-invasive positive... (Observational Study)
Observational Study
BACKGROUND
Swimming-induced pulmonary edema (SIPE) occasionally occurs during swimming in cold open water. Although optimal treatment for SIPE is unknown, non-invasive positive pressure ventilation (NPPV) is an option for prehospital treatment.
RESEARCH QUESTION
Is NPPV a feasible and safe prehospital treatment for SIPE, and which outcome measures reflect recovery after treatment?
STUDY DESIGN AND METHODS
A prospective observational study was conducted at Vansbrosimningen, Sweden's largest open water swimming event, from 2017 through 2019. Swimmers with a diagnosis of SIPE and with peripheral oxygen saturation (Spo) of ≤ 95%, persistent respiratory symptoms, or both were eligible for the study. NPPV was administered on site as CPAP by facial mask or as positive expiratory pressure (PEP) by a PEP device. Discharge criteria were Spo of > 95% and clinical recovery. Four outcome measures were evaluated: Spo, crackles on pulmonary auscultation, pulmonary edema on lung ultrasound (LUS), and patient-reported respiratory symptoms.
RESULTS
Of 119 treated individuals, 94 received CPAP, 24 received treatment with a PEP device, and one required tracheal intubation. In total, 108 individuals (91%) were discharged after NPPV for a median of 10 to 20 min and 11 individuals (9%) required hospital transfer. NPPV resulted in increased Spo from a median of 91% to 97% (P < .0001) together with improvement of six patient-reported respiratory symptoms (median numerical rating scales, 1-7 to 0-1; P < .0001). No significant decrease in auscultation of crackles (93% vs 87%; P = .508) or pulmonary edema on LUS (100% vs 97%; P = .500) was seen during NPPV treatment.
INTERPRETATION
NPPV administered as CPAP or via a PEP device proved feasible and safe as prehospital treatment for SIPE with a vast majority of patients discharged on site. Spo and patient-reported respiratory symptoms reflected recovery after treatment, whereas pulmonary auscultation or LUS findings did not.
Topics: Emergency Medical Services; Humans; Pulmonary Edema; Respiratory Sounds; Swimming; Water
PubMed: 35288117
DOI: 10.1016/j.chest.2022.02.054