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Noninvasive ventilation (either continuous positive airway pressure or noninvasive intermittent positive-pressure ventilation) had no effect on 7-day or 30-day mortality in patients with cardiogenic pulmonary edema, as compared with standard oxygen therapy. Noninvasive ventilation should be used only to relieve symptoms and correct metabolic disturbances. Noninvasive ventilation (either continuous positive airway pressure or noninvasive intermittent positive-pressure ventilation) had no effect on 7-day or 30-day mortality in patients with cardiogenic pulmonary edema, as compared with standard oxygen therapy. Acute cardiogenic pulmonary edema is a common medical emergency that accounts for up to 1 million hospital admissions for acute conditions per year in the United States. 1 It is a leading cause of hospitalization, accounting for 6.5 million hospital days each year. 2 In-hospital mortality from acute cardiogenic pulmonary edema is high (10 to 20%), 3 especially when it is associated with acute myocardial infarction. 4 Patients who do not have a response to initial therapy often require tracheal intubation and ventilation, with the associated potential for complications. 5 Noninvasive methods of ventilation can avert tracheal intubation by improving oxygenation, reducing the work of . . .

Introduction Noninvasive pressure support ventilation (NIPSV) and continuous positive airway pressure (CPAP) are both advocated in the treatment of cardiogenic pulmonary edema (CPE); however, the superiority of one technique over the other has not been clearly demonstrated. With regard to its physiological effects, we hypothesized that NIPSV would be better than CPAP in terms of clinical benefit. Methods In a prospective, randomized, controlled study performed in four emergency departments, 200 patients were assigned to CPAP ( n  = 101) or NIPSV ( n  = 99). Primary outcome was combined events of hospital death and tracheal intubation. Secondary outcomes included resolution time, myocardial infarction rate, and length of hospital stay. Separate analysis was performed in patients with hypercapnia and those with high B-type natriuretic peptide (>500 pg/ml). Results Hospital death occurred in 5 (5.0%) patients receiving NIPSV and 3 (2.9%) patients receiving CPAP ( p  = 0.56). The need for intubation was observed in 6 (6%) patients in the NIPSV group and 4 (3.9%) patients in the CPAP group ( p  = 0.46). Combined events were similar in both groups. NIPSV was associated to a shorter resolution time compared to CPAP (159 ± 54 vs. 210 ± 73 min; p  < 0.01), whereas the incidence of new myocardial infarction was not different between both groups. Similar results were found in hypercapnic patients and those with high B-type natriuretic peptide. Conclusions During CPE, NIPSV accelerates the improvement of respiratory failure compared to CPAP but does not affect primary clinical outcome either in overall population or in subgroups of patients with hypercapnia or those with high B-type natriuretic peptide.

BackgroundThere is no accurate, non-invasive measurement to estimate the degree of pulmonary oedema in acute respiratory distress syndrome (ARDS). We developed the Radiographic Assessment of Lung Oedema (RALE) score to evaluate the extent and density of alveolar opacities on chest radiographs. After first comparing the RALE score to gravimetric assessment of pulmonary oedema in organ donors, we then evaluated the RALE score in patients with ARDS for its relationship to oxygenation and clinical outcomes.MethodsWe compared radiographs with excised lung weights from 72 organ donors (derivation cohort) and radiographs with clinical data from 174 patients with ARDS in the ARDSNet Fluid and Catheter Treatment Trial (validation cohort). To calculate RALE, each radiographic quadrant was scored for extent of consolidation (0–4) and density of opacification (1–3). The product of the consolidation and density scores for each of the four quadrants was summed (maximum score=48).ResultsAgreement between two independent reviewers for RALE score was excellent (intraclass correlation coefficient=0.93, 95% CI 0.91 to 0.95). In donors, pre-procurement RALE score correlated with height-adjusted total lung weight (ρ=0.59, p<0.001). In patients with ARDS, higher RALE scores were independently associated with lower PaO2/fractional inspired oxygen and worse survival. Conservative fluid management significantly decreased RALE score over 3 days compared with liberal fluid management.ConclusionsThe RALE score can be used to assess both the extent of pulmonary oedema and the severity of ARDS, by utilising information that is already obtained routinely, safely and inexpensively in every patient with ARDS. This novel non-invasive measure should be useful for assessing ARDS severity and monitoring response to therapy.

Background Flash pulmonary edema is a medical emergency in which immediate recognition can be life-saving, especially when patients do not have typical clinical manifestations. Case presentation Herein, we report the case of a 56-year-old man who was admitted to the hospital due to paroxysmal palpitations for one week. His pro-B-type natriuretic peptide (BNP) level and left ventricular ejection fraction (LVEF) were normal, and he had no obvious symptoms of dyspnea. However, a CT scan of the chest indicated flash pulmonary edema. Through anti-heart failure treatment, the lung lesions improved. Results The patient was diagnosed with HFpEF caused by paroxysmal supraventricular tachycardia. The abnormal imaging manifestations in the lung were due to flash pulmonary edema, which was caused by acute heart failure. Conclusion Flash pulmonary edema is a medical emergency in which immediate recognition can be life-saving, especially when patients do not have typical clinical manifestations.

Millions of people visit high-altitude regions annually and more than 80 million live permanently above 2,500 m. Acute high-altitude exposure can trigger high-altitude illnesses (HAIs), including acute mountain sickness (AMS), high-altitude cerebral oedema (HACE) and high-altitude pulmonary oedema (HAPE). Chronic mountain sickness (CMS) can affect high-altitude resident populations worldwide. The prevalence of acute HAIs varies according to acclimatization status, rate of ascent and individual susceptibility. AMS, characterized by headache, nausea, dizziness and fatigue, is usually benign and self-limiting, and has been linked to hypoxia-induced cerebral blood volume increases, inflammation and related trigeminovascular system activation. Disruption of the blood–brain barrier leads to HACE, characterized by altered mental status and ataxia, and increased pulmonary capillary pressure, and related stress failure induces HAPE, characterized by dyspnoea, cough and exercise intolerance. Both conditions are progressive and life-threatening, requiring immediate medical intervention. Treatment includes supplemental oxygen and descent with appropriate pharmacological therapy. Preventive measures include slow ascent, pre-acclimatization and, in some instances, medications. CMS is characterized by excessive erythrocytosis and related clinical symptoms. In severe CMS, temporary or permanent relocation to low altitude is recommended. Future research should focus on more objective diagnostic tools to enable prompt treatment, improved identification of individual susceptibilities and effective acclimatization and prevention options. Acute or chronic exposure to elevations above 2,500 m can lead to altitude illnesses, including acute mountain sickness, high-altitude cerebral or pulmonary oedema, and chronic mountain sickness. In this Primer, Gatterer et al. summarize the epidemiology and pathophysiology of these disorders, discuss diagnosis, prevention and treatment, and highlight areas for future research.

Patients hospitalized with decompensated cirrhosis and a serum albumin level of less than 30 g per liter were randomly assigned to daily albumin infusions to raise the albumin level to 30 g per liter or higher or to standard care. Albumin infusions did not reduce the incidences of infection, kidney dysfunction, and death. More serious adverse events occurred in the albumin group.

Patients with heart failure exacerbation can present in a variety of ways, including sympathetic crashing acute pulmonary edema (SCAPE). Emergency physicians play a key role in the diagnosis and management of this condition. This narrative review evaluates key evidence-based updates concerning the diagnosis and management of SCAPE for the emergency clinician. SCAPE is a subset of acute heart failure, defined as a patient with sudden, severe pulmonary edema and hypertension, resulting respiratory distress, and hypoxemia. This is associated with significantly elevated afterload with fluid maldistribution into the pulmonary system. Evaluation and resuscitation should occur concurrently. Laboratory assessment, electrocardiogram, and imaging should be obtained. Point-of-care ultrasound is a rapid and reliable means of confirming pulmonary edema. Management focuses on respiratory support and vasodilator administration. Noninvasive positive pressure ventilation (NIPPV) with oxygen support is associated with reduced need for intubation, improved survival, and improved respiratory indices. If the patient does not improve or decompensates on NIPPV, endotracheal intubation is recommended. Rapid reduction in afterload is necessary, with the first-line medication including nitroglycerin. High-dose bolus nitroglycerin is safe and effective, followed by an infusion. If hypertension is refractory to NIPPV and high-dose nitroglycerin, other agents may be administered including clevidipine or nicardipine. Angiotensin-converting enzyme inhibitors such as enalaprilat are an option in those with normal renal function and resistant hypertension. Diuretics may be administered in those with evidence of systemic volume overload (e.g., cardiomegaly, peripheral edema, weight gain), but should not be routinely administered in patients with SCAPE in the absence of fluid overload. Caution is recommended in utilizing opioids and beta blockers in those with SCAPE. An understanding of the current literature concerning SCAPE can assist emergency clinicians and improve the care of these patients.

Recent studies have suggested that bone marrow-derived multipotent mesenchymal stem cells (MSCs) may have therapeutic applications in multiple clinical disorders including myocardial infarction, diabetes, sepsis, and hepatic and acute renal failure. Here, we tested the therapeutic capacity of human MSCs to restore alveolar epithelial fluid transport and lung fluid balance from acute lung injury (ALI) in an ex vivo perfused human lung preparation injured by E. coli endotoxin. Intra-bronchial instillation of endotoxin into the distal airspaces resulted in pulmonary edema with the loss of alveolar epithelial fluid transport measured as alveolar fluid clearance. Treatment with allogeneic human MSCs or its conditioned medium given 1 h following endotoxin-induced lung injury reduced extravascular lung water, improved lung endothelial barrier permeability and restored alveolar fluid clearance. Using siRNA knockdown of potential paracrine soluble factors, secretion of keratinocyte growth factor was essential for the beneficial effect of MSCs on alveolar epithelial fluid transport, in part by restoring amiloride-dependent sodium transport. In summary, treatment with allogeneic human MSCs or the conditioned medium restores normal fluid balance in an ex vivo perfused human lung injured by E. coli endotoxin.

Background In May 2018, the first patient was enrolled in the phase-IIb clinical trial “Safety and Preliminary Efficacy of Sequential Multiple Ascending Doses of Solnatide to Treat Pulmonary Permeability Edema in Patients with Moderate to Severe ARDS.” With the onset of the COVID-19 pandemic in early 2020, the continuation and successful execution of this clinical study was in danger. Therefore, before the Data Safety Monitoring Board (DSMB) allowed proceeding with the study and enrollment of further COVID-19 ARDS patients into it, additional assessment on possible study bias was considered mandatory. Methods We conducted an ad hoc interim analysis of 16 patients (5 COVID-19- ARDS patients and 11 with ARDS from different causes) from the phase-IIB clinical trial. We assessed possible differences in clinical characteristics of the ARDS patients and the impact of the pandemic on study execution. Results COVID-19 patients seemed to be less sick at baseline, which also showed in higher survival rates over the 28-day observation period. Trial specific outcomes regarding pulmonary edema and ventilation parameters did not differ between the groups, nor did more general indicators of (pulmonary) sepsis like oxygenation ratio and required noradrenaline doses. Conclusion The DSMB and the investigators did not find any evidence that patients suffering from ARDS due to SARS-CoV-2 may be at higher (or generally altered) risk when included in the trial, nor were there indications that those patients might influence the integrity of the study data altogether. For this reason, a continuation of the phase IIB clinical study activities can be justified. Researchers continuing clinical trials during the pandemic should always be aware that the exceptional circumstances may alter study results and therefore adaptations of the study design might be necessary.

In critically ill patients, fluid infusion is aimed at increasing cardiac output and tissue perfusion. However, it may contribute to fluid overload which may be harmful. Thus, volume status, risks and potential efficacy of fluid administration and/or removal should be carefully evaluated, and monitoring techniques help for this purpose. Central venous pressure is a marker of right ventricular preload. Very low values indicate hypovolemia, while extremely high values suggest fluid harmfulness. The pulmonary artery catheter enables a comprehensive assessment of the hemodynamic profile and is particularly useful for indicating the risk of pulmonary oedema through the pulmonary artery occlusion pressure. Besides cardiac output and preload, transpulmonary thermodilution measures extravascular lung water, which reflects the extent of lung flooding and assesses the risk of fluid infusion. Echocardiography estimates the volume status through intravascular volumes and pressures. Finally, lung ultrasound estimates lung edema. Guided by these variables, the decision to infuse fluid should first consider specific triggers, such as signs of tissue hypoperfusion. Second, benefits and risks of fluid infusion should be weighted. Thereafter, fluid responsiveness should be assessed. Monitoring techniques help for this purpose, especially by providing real time and precise measurements of cardiac output. When decided, fluid resuscitation should be performed through fluid challenges, the effects of which should be assessed through critical endpoints including cardiac output. This comprehensive evaluation of the risk, benefits and efficacy of fluid infusion helps to individualize fluid management, which should be preferred over a fixed restrictive or liberal strategy.