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Background: Since publication of the 2012 Berlin definition of acute respiratory distress syndrome (ARDS), several developments have supported the need for an expansion of the definition, including the use of high-flow nasal oxygen, the expansion of the use of pulse oximetry in place of arterial blood gases, the use of ultrasound for chest imaging, and the need for applicability in resource-limited settings. Methods: A consensus conference of 32 critical care ARDS experts was convened, had six virtual meetings (June 2021 to March 2022), and subsequently obtained input from members of several critical care societies. The goal was to develop a definition that would 1) identify patients with the currently accepted conceptual framework for ARDS, 2) facilitate rapid ARDS diagnosis for clinical care and research, 3) be applicable in resource-limited settings, 4) be useful for testing specific therapies, and 5) be practical for communication to patients and caregivers. Results: The committee made four main recommendations: 1) include high-flow nasal oxygen with a minimum flow rate of ⩾30 L/min; 2) use PaO2:FiO2 ⩽ 300 mm Hg or oxygen saturation as measured by pulse oximetry SpO2:FiO2 ⩽ 315 (if oxygen saturation as measured by pulse oximetry is ⩽97%) to identify hypoxemia; 3) retain bilateral opacities for imaging criteria but add ultrasound as an imaging modality, especially in resource-limited areas; and 4) in resource-limited settings, do not require positive end-expiratory pressure, oxygen flow rate, or specific respiratory support devices. Conclusions: We propose a new global definition of ARDS that builds on the Berlin definition. The recommendations also identify areas for future research, including the need for prospective assessments of the feasibility, reliability, and prognostic validity of the proposed global definition.

A study of structural changes in lung tissue during the formation of organ edema due to inhalation of a lipotropic poison, carbonic acid dichloride, showed the peculiarities of the formation of acute respiratory distress syndrome. The point of application of the poison is the distal bronchioles, whose epithelium is subject to dystrophic and necrotic changes followed by goblet metaplasia. The absorbed poison causes pronounced changes in blood microcirculation, steroid-resistant NO-mediated endothelial dysfunction with blood deposition in dilated capillaries, aggregation, and lysis of erythrocytes. Changes in the vascular bed in the interalveolar septa precede the formation of an acute inflammatory reaction with the accumulation of alveolar effusion and dystrophic changes in the alveolar epithelium with cell desquamation. Among the cells of the alveolar lining, type II alveolocytes are the most vulnerable. Plasma permeation of the connective tissue of the interalveolar septa interstitium is accompanied by their infiltration with polymorphonuclear leukocytes and activation of macrophages. Desquamation of epithelial cells of the distal bronchioles leads to obstruction of their lumens and, through the valve mechanism, contributes to overextension of the alveoli with the formation of emphysema and reduction of capillary blood circulation in the alveolar septa. The observed changes determined the directions for improving the treatment of poisoning by asphyxiating poisons. [ABSTRACT FROM AUTHOR]

Background Methods Results Conclusions Peripheral veno‐arterial extracorporeal membrane oxygenation (ECMO) is a powerful life‐saving tool; however, it can sometimes induce severe pulmonary edema in patients with critical heart failure. We report favorable outcomes in critically ill patients by using a central ECMO system with an innovative blood perfusion method.We analyzed 10 patients with severe heart failure and pulmonary edema who were treated with the central ECMO system at our institution between April 2022 and October 2023. The system consists of central cannulation with two inflows from the right atrium and left ventricle, and two outflows to the aorta and pulmonary artery, connected by two Y‐connectors to a single ECMO circuit (RALV‐AOPA ECMO). In this system, blood flow to the pulmonary artery is adjusted and mean pulmonary artery pressure is limited to <20 mm Hg, which reduces right ventricular afterload and prevents the worsening of pulmonary edema and hemorrhage.Six patients were diagnosed with fulminant lymphocytic myocarditis, and four were diagnosed with coronavirus disease 2019‐related myocardial injury. The ejection fraction was 6.5 ± 4.1%. The average intraoperative pulmonary vascular resistance was 4.6 ± 1.3 Wood units. After 24 h, the mean pulmonary arterial pressure was 12.8 ± 4.3 mm Hg, and pulmonary vascular resistance was 1.5 ± 0.3 Wood units. The duration of central RALV‐AOPA ECMO was 3.7 ± 2.1 days. Finally, six patients were weaned, three received HeartMate3, and one received heart transplantation. At follow‐up, all patients remained alive (428 ± 208 days), and two patients experienced cerebrovascular accidents without any lasting sequelae.The central RALV‐AOPA ECMO is an innovative system that achieves early improvement in pulmonary vascular resistance and is safe and feasible for patients with acute biventricular failure and pulmonary edema. [ABSTRACT FROM AUTHOR]

Introduction Acute respiratory distress syndrome (ARDS) is a widespread and often fatal clinical syndrome marked by the acute onset of pulmonary edema and inflammatory-mediated disruptions in alveolar-capillary permeability resulting in impaired gas exchange and tissue oxygenation with subsequent acute respiratory failure that accounts for 10.4% of all intensive care unit admissions worldwide and boasts a mortality rate of 38.5%. The current treatment for ARDS remains largely supportive. This is largely because of the many challenges of achieving a stable and sustainable animal model that recreates the pathophysiology of ARDS experimentally in a controlled setting to allow research to elucidate potential treatments of ARDS moving forward. Materials and Methods The bronchoalveolar lavage and oleic acid models are currently the 2 most frequently used experimental models in inducing ARDS in animal models. This study demonstrated that combining them into a "two-hit model" can produce sustained ARDS in swine models per the Horowitz index (PaO2/FiO2 ratio of ≤300 mmHg). Additionally, expected changes in pH, pCO2, lung compliance, cytokines, and tissue histopathology were observed and add to our confidence and reliability that the "two-hit model" produces symptomatic ARDS in a manner very similar to that observed in humans. Results and Conclusions In conclusion, we demonstrated a viable animal model of human ARDS that is maintained for a prolonged period, suitable for continuous monitoring of the progression, and evaluation of potential future treatments and procedures to reduce patient morbidity and mortality. To carry out this two-hit model, lung injury was induced through a combination of bronchoalveolar lavage and oleic acid administration and the disease process of ARDS is subsequently tracked through clinically relevant parameters such as respiratory mechanics, cytokine response, aretrial blood gas (ABG) changes, and observation of postmortem histopathologic changes. This promising new model has the capacity to successfully replicate human ARDS which is a well-known and notoriously multifactorial pathogenic process to reproduce experimentally for an extended period of time. The "two-hit model" is a viable and appropriate model for the research of novel treatments for ARDS. [ABSTRACT FROM AUTHOR]

Background: Postoperative negative pressure pulmonary edema (NPPE) can occur in any patient undergoing general anesthesia. There are several risk factors for it, especially postoperative laryngospasm. The disease is usually benign and quickly reversible. In our case the severity and need for advanced critical care therapy was unusual. Case: We report a severe case of postoperative negative pressure pulmonary edema in a 62-year-old male patient undergoing elective right-sided retroperitoneoscopic adrenalectomy. The patient developed a severe case of acute respiratory distress syndrome (ARDS) after postoperative laryngospasm, possibly in conjunction with a suspected anaphylactic reaction. The patient was consequently treated with a combination of invasive airway pressure release ventilation (APRV) and a prone positioning regimen. After drastic improvement in respiratory function, the patient was discharged from the intensive care unit after 10 days and from the hospital after 14 days. Conclusion: NPPE is a rare but relevant complication of anesthesia and laryngospasm. The disease can basically occur in any patient undergoing general anesthesia and therefore should be considered. [ABSTRACT FROM AUTHOR]

Background: Quantification of pulmonary edema in patients with acute respiratory distress syndrome (ARDS) by chest computed tomography (CT) scan has not been validated in routine diagnostics due to its complexity and time-consuming nature. Therefore, the single-indicator transpulmonary thermodilution (TPTD) technique to measure extravascular lung water (EVLW) has been used in the clinical setting. Advances in artificial intelligence (AI) have now enabled CT images of inhomogeneous lungs to be segmented automatically by an intensive care physician with no prior radiology training within a relatively short time. Nevertheless, there is a paucity of data validating the quantification of pulmonary edema using automated lung segmentation on CT compared with TPTD. Methods: A retrospective study (January 2016 to December 2021) analyzed patients with ARDS, admitted to the intensive care unit of the Department of Anesthesiology and Critical Care Medicine, University Hospital Mannheim, who underwent a chest CT scan and hemodynamic monitoring using TPTD at the same time. Pulmonary edema was estimated using manually and automated lung segmentation on CT and then compared to the pulmonary edema calculated from EVLW determined using TPTD. Results: 145 comparative measurements of pulmonary edema with TPTD and CT were included in the study. Estimating pulmonary edema using either automated lung segmentation on CT or TPTD showed a low bias overall (− 104 ml) but wide levels of agreement (upper: 936 ml, lower: − 1144 ml). In 13% of the analyzed CT scans, the agreement between the segmentation of the AI algorithm and a dedicated investigator was poor. Manual segmentation and automated segmentation adjusted for contrast agent did not improve the agreement levels. Conclusions: Automated lung segmentation on CT can be considered an unbiased but imprecise measurement of pulmonary edema in mechanically ventilated patients with ARDS. [ABSTRACT FROM AUTHOR]

Summary: Although respiratory distress is encountered infrequently in equine practice, it can be serious and potentially fatal, requiring immediate and decisive intervention. History and physical examination can often give sufficient clues to identify the cause of respiratory distress and initiate emergency treatment. Ultrasonography can also be invaluable when assessing distress caused by lower respiratory tract issues. Upper respiratory tract obstruction, tension pneumothorax and occasionally pulmonary oedema can be rapidly fatal and require immediate intervention by emergency tracheotomy, thoracocentesis and evacuation of pleural air or administration of furosemide and oxygen, if available. Acute severe asthma and substantial pleural effusion are often not an immediate threat to life but nonetheless require fast intervention including administration of bronchodilators and corticosteroids or pleurocentesis, respectively. [ABSTRACT FROM AUTHOR]

Acute Respiratory Distress Syndrome (ARDS) is initiated by a primary insult that triggers a cascade of pathological events, including damage to lung epithelial and endothelial cells, extracellular matrix disruption, activation of immune cells, and the release of pro-inflammatory mediators. These events lead to increased alveolar-capillary barrier permeability, resulting in interstitial/alveolar edema, collapse, and subsequent hypoxia and hypercapnia. ARDS not only affects the lungs but also significantly impacts the cardiovascular system. We conducted a comprehensive literature review on heart-lung crosstalk in ARDS, focusing on the pathophysiology, effects of mechanical ventilation, hypoxemia, and hypercapnia on cardiac function, as well as ARDS secondary to cardiac arrest and cardiac surgery. Mechanical ventilation, essential for ARDS management, can increase intrathoracic pressure, decrease venous return and right ventricle preload. Moreover, acidemia and elevations in transpulmonary pressures with mechanical ventilation both increase pulmonary vascular resistance and right ventricle afterload. Cardiac dysfunction can exacerbate pulmonary edema and impair gas exchange, creating a vicious cycle, which hinders both heart and lung therapy. In conclusion, understanding the heart-lung crosstalk in ARDS is important to optimize therapeutic strategies. Future research should focus on elucidating the precise mechanisms underlying this interplay and developing targeted interventions that address both organs simultaneously. [ABSTRACT FROM AUTHOR]

Acute lung injury (ALI) is a serious acute respiratory disease that can cause alveolar-capillary barrier disruption and pulmonary edema, respiratory failure and multiple organ dysfunction syndrome. However, there is no effective drugs in clinic until now. GSK3179106 has been reported can alleviate intestinal stress syndrome, but the protective effect of GSK3179106 on ALI has not been elucidated. The present study will evaluate the pharmacological activity of GSK3179106 on lipopolysaccharide (LPS)-induced inflammation and lung injury and clarify its underlying mechanism. We found that GSK3179106 significantly attenuated LPS-induced lung injury in vivo, accompanied by inhibited infiltration of inflammatory cells and reduced expression of inflammatory cytokines. Meanwhile, GSK3179106 dose-dependently reduced the LPS-induced IL-6 expression both in protein and gene levels in macrophages. Mechanistically, GSK3179106 could inhibited the phosphorylation of P38 MAPK induced by LPS. Importantly, results showed that there is a direct combination between GSK3179106 and P38 MAPK. Together, our findings not only clarified the anti-inflammatory activity of GSK3179106 but also discovered its new clinical indications. Therefore, compound GSK3179106 may be a potential candidate for the treatment of acute inflammatory diseases. [ABSTRACT FROM AUTHOR]

Background: Pulmonary oedema is a feared and difficult to predict complication of severe malaria that can emerge after start of antimalarial treatment. Proinflammatory mediators are thought to play a central role in its pathogenesis. Methods: An exploratory study was conducted to evaluate the predictive capacity of biomarkers for development of clinical pulmonary oedema in patients with severe falciparum malaria at two hospitals in Bangladesh. Plasma concentrations of interleukin-6 (IL-6), IL-8, tumour necrosis factor (TNF), soluble Receptor of Advanced Glycation End-products (sRAGE), surfactant protein-D (SP-D), club cell secretory protein (CC16), and Krebs von den Lungen-6 (KL-6) on admission were compared with healthy controls. Correlations between these biomarker and plasma lactate and Plasmodium falciparum histidine-rich protein 2 (PfHRP2) levels were evaluated. Receiver Operating Characteristic (ROC) curves were constructed to assess the predictive capacity for clinical pulmonary oedema of the biomarkers of interest. Results: Of 106 screened patients with falciparum malaria, 56 were classified as having severe malaria with a mortality rate of 29%. Nine (16%) patients developed clinical pulmonary oedema after admission. Plasma levels of the biomarkers of interest were higher in patients compared to healthy controls. IL-6, IL-8, TNF, sRAGE, and CC16 levels correlated well with plasma PfHRP2 levels (rs = 0.39; P = 0.004, rs = 0.43; P = 0.001, rs = 0.54; P < 0.001, rs = 0.44; P < 0.001, rs = 0.43; P = 0.001, respectively). Furthermore, IL-6 and IL-8 levels correlated well with plasma lactate levels (rs = 0.37; P = 0.005, rs = 0.47; P < 0.001, respectively). None of the biomarkers of interest had predictive capacity for development of clinical pulmonary oedema. Conclusions: IL-6, IL-8, TNF, sRAGE, SP-D, CC16 and KL-6 cannot be used in predicting clinical pulmonary oedema in severe malaria patients. [ABSTRACT FROM AUTHOR]

Purpose: A human cadaveric model combining standard lung protective mechanical ventilation and modified cardiac bypass techniques was developed to allow investigation into automated modes of detection of venous air emboli (VAE) prior to in vivo human or animal investigations. Methods: In this study, in order to create an artificial cardiopulmonary circuit in a cadaver that could mimic VAE physiology, the direction of flow was reversed from conventional cardiac bypass. Normal saline was circulated in isolation through the heart and lungs as opposed to the peripheral organs by placing the venous cannula into the aorta and the arterial cannula into the inferior vena cava with selective ligation of other vessels. Results: Mechanical ventilation and this reversed cardiac bypass scheme allowed preliminary detection of VAE independently but not in concert in our current simulation scheme due to pulmonary edema in the cadaver. A limited dissection approach was used initially followed by a radical exposure of the great vessels, and both proved feasible in terms of air signal detection. We used electrical impendence as a preliminary tool to validate detection in this cadaveric model however we theorize that it would work for echocardiographic, intravenous ultrasound or other novel modalities as well. Conclusion: A cadaveric model allows monitoring technology development with reduced use of animal and conventional human testing. [ABSTRACT FROM AUTHOR]

Background: Preterm infants are at risk for bronchopulmonary dysplasia (BPD) due to prolonged respiratory support. Studies have described differences in the regional distribution of lung ventilation (non-dependent (NDL) vs. dependent (DL)). The aim of this study was to use LUS to compare regional distribution of pulmonary edema and atelectasis in infants with evolving BPD. Methods: We prospectively performed LUS in premature infants with evolving BPD. On each side, three lung areas (NDL/anterior, lateral, and DL/posterior) were examined for the presence of pulmonary edema and atelectasis. Pulmonary edema scores were assigned based on the number of B-lines, and atelectasis scores were assigned based on the presence/absence of atelectasis. Results: 38 premature infants were enrolled. The NDL showed more pulmonary edema and atelectasis compared to the DL (p = 0.003, p = 0.049, respectively) and compared to the lateral lung (p =< 0.001, p = 0.004, respectively). There was no difference between the lateral and DL (p = 0.188, p = 0.156, respectively). There was no difference between the right and the left lung (p = 0.223, p = 0.656, respectively). Conclusions: In this cohort of preterm infants with evolving BPD, lung disease was unevenly distributed, with more pulmonary edema and atelectasis in the NDL regions compared to the DL or lateral regions. [ABSTRACT FROM AUTHOR]

End stage kidney disease (ESKD) patients in the developing countries often present late for dialysis initiation with advanced uremia and life‐threatening complications. Urgent start dialysis in such emergent situations exposes the patient to risk of uremia related complications as well as iatrogenic insults. We report the case of a middle‐aged man with ESKD who presented late with acute pulmonary edema and hyperkalemia and developed osmotic demyelination syndrome following urgent start hemodialysis. Osmotic demyelination syndrome in this patient is noteworthy since there was no accompanying hyponatremia, the most commonly recognized antecedent. We propose that rapid lowering of serum osmolality by aggressive hemodialysis is sufficient to incite osmotic demyelination syndrome in patients who have long‐standing uremia and high blood urea level. Malnutrition resulting from uremia might be a compounding factor in this scenario. Our patient had a characteristic initial presentation of osmotic demyelination syndrome with locked‐in‐state which later progressed to respiratory failure and death. [ABSTRACT FROM AUTHOR]

Objective: To clarify the incidence of excessive distension absorption in hysteroscopic surgery using 5% mannitol solution, evaluate the associated risks, and help to establish a safe fluid deficit threshold for such complication. Design: Retrospective descriptive study. Setting: Academic medical center. Patients: Ten thousand six hundred ninety-three patients underwent inpatient hysteroscopic surgery with 5% mannitol perfusion using a monopolar electrosurgical instrument from Jan. 2015 to Sep. 2020. Intervention(s): None. This study has been approved by the Ethics Committee of Sun Yat-sen Memorial Hospital. Measurements and main results: A fluid deficit of more than 1000 mL was defined as the diagnostic criteria for excessive distension absorption. The overall incidence of excessive distension absorption in this study was 0.46% (49/10693). The incidence was 2.57% (16/623) for transcervical resection of fibroid (TCRF), 2.36% (9/381) for retained products of conception (RPOC) removal, 1.20% (6/501) for hysteroscopic uterine septum resection (HSR), 0.48% (4/828) for transcervical resection of the endometrium (TCRE), and 0.53% (14/2621) for transcervical resections of adhesion (TCRA). Excessive distension absorption could occur within seven minutes in HSR. Among the patients diagnosed with excessive distension absorption, 30.77% (12/39) exhibited signs or symptoms related to circulation overload with a fluid deficit under 2500 mL, and 10.26% (4/39) developed pulmonary edema. Conclusion: Excessive distension absorption could happen in all kinds hysteroscopic surgical treatment including RPOC removal and TCRA which were rarely reported. The overall incidence of excessive distension absorption could be low. But it would be five times higher in certain procedures such as TCRF, RPOC removal and TCRA. Resection using a needle electrode in HSR and TCRA may contribute to the short time development of excessive distension absorption. 30.77% of the patients could not tolerate the fluid deficit of less than 2500 mL which was set as a threshold for isotonic distending media and presented with circulation overload related signs or symptoms. [ABSTRACT FROM AUTHOR]

Background: Peripheral veno-arterial extracorporeal membrane oxygenation (pECMO) has become the first-line device in refractory cardiogenic shock (rCS). Some pECMO complications can preclude any bridging strategies and a peripheral-to-central ECMO (cECMO) switch can be considered as a bridge-to-decision. We conducted this study to appraise the in-hospital survival and the bridging strategies in patients undergoing peripheral-to-central ECMO switch. Methods: This retrospective monocenter study included patients admitted to a ECMO-dedicated intensive care unit from February 2006 to January 2023. Patients with rCS requiring pECMO switched to cECMO were included. Patients were not included when the cECMO was the first mechanical circulatory support. Results: Eighty patients, with a median [IQR25-75] age of 44 [29–53] years at admission and a female-to-male sex ratio of 0.6 were included in the study. Refractory pulmonary edema was the main switching reason. Thirty patients (38%) were successfully bridged to: heart transplantation (n = 16/80, 20%), recovery (n = 10/80, 12%) and ventricle assist device (VAD, n = 4/30, 5%) while the others died on cECMO (n = 50/80, 62%). The most frequent complications were the need for renal replacement therapy (76%), hemothorax or tamponade (48%), need for surgical revision (34%), mediastinitis (28%), and stroke (28%). The in-hospital and one-year survival rates were 31% and 27% respectively. Myocardial infarction as the cause of the rCS was the only variable independently associated with in-hospital mortality (HR 2.5 [1.3–4.9], p = 0.009). Conclusions: The switch from a failing pECMO support to a cECMO as a bridge-to-decision is a possible strategy for a very selected population of young patients with a realistic chance of heart function recovery or heart transplantation. In this setting, cECMO allows patients triage preventing from wasting expensive and limited resources. [ABSTRACT FROM AUTHOR]

Hydrogen sulfide (H2S), as a key gas signaling molecule, plays an important role in regulating various diseases, with appropriate concentrations providing antioxidative, anti-inflammatory, and anti-apoptotic effects. The specific role of H2S in acute hypoxic injury remains to be clarified. This study focuses on the H2S donor sodium hydrosulfide (NaHS) and explores its protective effects and mechanisms against acute hypoxic lung injury. First, various mouse hypoxia models were established to evaluate H2S's protection in hypoxia tolerance. Next, a rat model of acute lung injury (ALI) induced by hypoxia at 6500 m above sea level for 72 h was created to assess H2S's protective effects and mechanisms. Evaluation metrics included blood gas analysis, blood routine indicators, lung water content, and lung tissue pathology. Additionally, LC-MS/MS and bioinformatic analyses were combined in performing quantitative proteomics on lung tissues from the normoxic control group, the hypoxia model group, and the hypoxia model group with NaHS treatment to preliminarily explore the protective mechanisms of H2S. Further, enzyme-linked immunosorbent assays (ELISA) were used to measure oxidative stress markers and inflammatory factors in rat lung tissues. Lastly, Western blot analysis was performed to detect Nrf2, HO-1, P-NF-κB, NF-κB, HIF-1α, Bcl-2, and Bax proteins in lung tissues. Results showed that H2S exhibited significant anti-hypoxic effects in various hypoxia models, effectively modulating blood gas and blood routine indicators in ALI rats, reducing pulmonary edema, improving lung tissue pathology, and alleviating oxidative stress, inflammatory responses, and apoptosis levels. [ABSTRACT FROM AUTHOR]

Background: Pulmonary surfactant (PS) plays an important role in the treatment of sepsis-induced acute lung injury (ALI). Liraglutide, a glucagon-like peptide-1 (GLP-1) analog, improves the secretion and function of PS in ALI, but the underlying mechanism remains unknown. This study aimed to investigate how liraglutide regulates PS secretion in ALI. Methods: C57BL/6 mice were injected subcutaneously with normal saline containing different concentrations of liraglutide after the establishment of the ALI model. MLE-12 cells were treated with liraglutide after LPS stimulation. The survival rate of mice, wet/dry weight ratio, inflammatory factors in bronchoalveolar lavage fluid (BALF), pulmonary injury, and apoptosis were analyzed. Cell viability, proliferation, apoptosis, the expression of SP-A, SP-B, and expression of autophagy-related proteins in cells were measured. Results: ALI mice showed reduced pulmonary injury, less apoptosis, and less inflammation compared to the controls. Liraglutide prolonged survival, decreased the wet/dry weight ratio, reduced inflammatory responses, and attenuated pulmonary edema compared with the ALI group. Moreover, LPS-induced cell damage and reduction of SP-A and SP-B expression were markedly reversed by liraglutide in MLE-12 cells. Furthermore, the protective effects of liraglutide were reversed by rapamycin. Conclusion: Liraglutide alleviate sepsis-induced ALI by inhibiting autophagy and regulating PS. [ABSTRACT FROM AUTHOR]

Objective: Real‐world data on cardiopulmonary events among pregnant women receiving β‐agonist therapy are scarce. In the present study, we aimed to examine the absolute and relative risks of maternal cardiopulmonary events associated with the use of β‐agonist ritodrine during pregnancy. Methods: By linking Taiwan's National Birth Certificate Application Database with National Health Insurance data, 1 831 564 pregnancies at ≥20 weeks' gestation were identified. Age‐standardized incidence rates of cardiopulmonary events among pregnant women exposed to ritodrine were estimated. Nested case–control analyses were conducted to evaluate the relative risk of pulmonary edema, heart failure, and arrhythmia associated with prior ritodrine use. Cases and controls were matched using risk set sampling, and adjusted odds ratios were estimated using conditional logistic regression models. Results: A total of 189 cases of pulmonary edema, 126 cases of heart failure, and 162 cases of arrhythmia were identified (corresponding age‐standardized incidence rates: 20.90, 8.35, and 16.63 per 100 000 among pregnant women only exposed to oral ritodrine; 91.28, 36.01, and 14.61 per 100 000 among those ever exposed to intravenous ritodrine). Exposure to oral ritodrine was associated with a lower increased risk of pulmonary edema (aOR 1.76; 95% CI: 1.12–2.76) and arrhythmia (2.21; 1.47–3.32) whereas exposure to ritodrine injection was associated with a significantly higher risk of pulmonary edema (10.56; 6.39–17.45), arrhythmia (4.15; 1.99–8.64), and heart failure (5.58; 2.27–13.74). Conclusions: Pregnant women receiving intravenous ritodrine therapy had higher cardiopulmonary risks and should be intensively monitored. While the relative risk associated with oral ritodrine is not pronounced, it should be used judiciously among pregnant women as well. Synopsis: Oral ritodrine exposure in pregnancy doubles the risk of pulmonary edema and arrhythmia, while ritodrine injections pose a higher risk—11‐fold for pulmonary edema and four‐ to six‐fold for heart failure/arrhythmia. [ABSTRACT FROM AUTHOR]

Aim: Sodium–glucose cotransporter 2 inhibitors (SGLT2is), used as a glucose‐lowering therapy in people with type 2 diabetes (T2D), have significant cardiorenal benefits, reducing hospitalization for heart failure (HF) and cardiovascular mortality in patients with and without T2D. Recent clinical trial evidence suggests their potential utility in preventing incident T2D among the high‐risk HF populations. Therefore, we aimed to assess whether this finding was reproducible in a real‐world setting. Methods: We performed a retrospective cohort analysis of 484 643 patients with HF, without baseline diabetes, prescribed either angiotensin‐converting enzyme inhibitors or angiotensin II receptor blockers with/without SGLT2is (treatment, n = 42 018; reference, n = 442 625) across 95 global health care organizations, using a large real‐world ecosystem. Propensity score matching balanced arms 1:1 for confounders (n = 39 168 each arm). Subgroup analysis further evaluated the impact on patients with prediabetes and the efficacy of dapagliflozin/empagliflozin, specifically, on incident T2D and secondary outcomes, including all‐cause mortality, acute pulmonary oedema and hospitalization. Results: Treatment with SGLT2is significantly reduced incident T2D {hazard ratio (HR) 0.71 [95% confidence interval (CI) 0.63, 0.75]} in patients with HF. The analysis of patients with prediabetes found that SGLT2is further reduced incident T2D [HR 0.62 (95% CI 0.45, 0.80)]. The magnitude of reduction in incident T2D was higher in patients prescribed dapagliflozin [HR 0.47 (95% CI 0.39, 0.56)] versus empagliflozin [HR 0.81 (95% CI 0.70, 0.93)]. Conclusion: Treatment with SGLT2is in patients with HF was associated with a reduced risk of incident T2D, most strikingly in people with prediabetes. [ABSTRACT FROM AUTHOR]

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High-altitude pulmonary edema (HAPE) is a fatal threat for sojourners who ascend rapidly without sufficient acclimatization. Acclimatized sojourners and adapted natives are both insensitive to HAPE but have different physiological traits and molecular bases. In this study, based on GSE52209, the gene expression profiles of HAPE patients were compared with those of acclimatized sojourners and adapted natives, with the common and divergent differentially expressed genes (DEGs) and their hub genes identified, respectively. Bioinformatic methodologies for functional enrichment analysis, immune infiltration, diagnostic model construction, competing endogenous RNA (ceRNA) analysis and drug prediction were performed to detect potential biological functions and molecular mechanisms. Next, an array of in vivo experiments in a HAPE rat model and in vitro experiments in HUVECs were conducted to verify the results of the bioinformatic analysis. The enriched pathways of DEGs and immune landscapes for HAPE were significantly different between sojourners and natives, and the common DEGs were enriched mainly in the pathways of development and immunity. Nomograms revealed that the upregulation of TNF-α and downregulation of RPLP0 exhibited high diagnostic efficiency for HAPE in both sojourners and natives, which was further validated in the HAPE rat model. The addition of TNF-α and RPLP0 knockdown activated apoptosis signaling in endothelial cells (ECs) and enhanced endothelial permeability. In conclusion, TNF-α and RPLP0 are shared biomarkers and molecular bases for HAPE susceptibility during the acclimatization/adaptation/maladaptation processes in sojourners and natives, inspiring new ideas for predicting and treating HAPE. [ABSTRACT FROM AUTHOR]

Staying in or underwater can lead to acute pulmonary complaints, which clinically present as an acute immersion-induced pulmonary edema (IPE), particular in strenuous swimming (SIPE) or diving (DIPE). › The IPE presents as a cardiac pulmonary edema and is induced by several pathophysiological processes during immersion, including fluid-shift, severe breathing, strenuous exercise, ambient cold, and aggravating cardiac pathologies. › This clinical review summarizes current evidence about the incidence of IPE in general, SIPE, and DIPE, the main aspects of its complex underlying pathophysiology, clinical symptoms, outcome and prognosis. It furthers provides recommendations for emergency treatment and indication of hospital admission. [ABSTRACT FROM AUTHOR]

Freediving (synonyms: breath-hold diving, apnea diving) has become a popular leisure activity and continues to gain popularity and recognition as both a competitive and recreational sport. Formal freediving competitions are sanctioned by the international Confédération Mondiale des Activités Subaquatiques (CMAS) or the Association Internationale pour le Développement de l'Apnée (AIDA). Both organizations have set up rules and guidelines for competitive pool disciplines where athletes compete for maximum submerged breath-hold time or underwater swimming distance with or without fins. › In freshwater disciplines athletes strive for maximum depth using different freediving techniques. These aquatic breath-holding activities carry unique medical risks that are related to environmental factors eliciting extreme physiological challenges. Pool disciplines carry an increased risk of hypoxemia and, consequently, loss of consciousness, particularly in untrained individuals. Hypoxic complications are reported to occur in up to 10% of dives during freediving competitions. Shallow water blackout following hyperventilation to extend breathhold capability is a serious risk applying to all aquatic breath-hold activities, however, is more common during recreational freediving. › Deep freediving poses the athlete to further risks such as barotrauma of ear drums or lungs, immersion pulmonary edema, nitrogen narcosis, and decompression sickness when reaching great depths. While serious complications in competitive freediving are rare, however, the risk clearly rises with increasing depth. Special breathing techniques to increase lung volumes such as glossopharyngeal insufflation carry additional risks. › This article reviews possible complications and injury that may occur in competitive freedivers and discusses strategies for management and prevention of possible injury. [ABSTRACT FROM AUTHOR]

Introduction: Medico legal deaths including burns claim a substantial number of lives in central Karnataka. 'A prospective Study of Histo-Pathological changes in Lungs, Liver and Kidneys in Burns Cases' was carried out at the Department of Forensic Medicine & Toxicology, SS hospital, SSIMS & RC, Davangere. Material & methods: The present study was carried out for the period of 3 years from January 2021 to December 2023. Totally 100 cases with burns and scalds injuries brought to the mortuary for autopsy was the material for study and collection of tissues for histopathological examination. Observations & Results: In the present study, histopathological changes in lungs showed congestion, pulmonary edema, Diffuse alveolar damage or ARDS changes, bronchopneumonia, interstitial pneumonitis, anthracotic pigment, carbon laden macrophages, intravascular thrombi, septic emboli, interstitial & intra alveolar hemorrhage. Histopathological changes in liver showed congestion, fatty change, centrilobular necrosis, cloudy swelling, focal hemorrhage, necrosis, portal inflammation. Histopathological changes in kidneys showed ATN in majority of cases, cloudy degeneration, congestion, tubularcasts and acute pyelonephritis in rest of the cases. Conclusion: The effect of burns on vital organs can be assessed through histopathological examination, which helps in determining the post burn complications and which aid in better treatment outcome of the burn's patients. [ABSTRACT FROM AUTHOR]

This study examines the anti‐inflammatory activity of cynaropicrin against lipopolysaccharide (LPS) in vitro and ovalbumin (OVA)‐challenged asthma in mice. Cynaropicrin's antimicrobial effects were tested on Escherichia coli (E. coli) and Streptococcus pyogenes (S. pyogenes) using the disc diffusion technique. Cytotoxicity was assessed with an (3‐(4, 5‐dimethylthiazolyl‐2)‐2, 5‐diphenyltetrazolium bromide) assay. The anti‐inflammatory property was evaluated in LPS‐induced RAW264.7 cells, while OVA‐challenged asthmatic mice were treated with 10 mg/kg of cynaropicrin. Key inflammatory and antioxidant markers were quantified, and lung histology was examined to confirm therapeutic roles. The antimicrobial studies proved that cynaropicrin effectively inhibited the growth of E. coli and S. pyogenes. Cynaropicrin displayed no cytotoxicity on RAW264.7 cells. Furthermore, it significantly inhibited inflammatory cytokine synthesis upon LPS induction. Cynaropicrin treatment decreased the inflammatory cell counts and also suppressed specific allergic markers in OVA‐challenged mice. It also decreased nitric oxide and myeloperoxidase levels and reduced pulmonary edema. Cynaropicrin increased antioxidant levels and decreased proinflammatory cytokines in the asthmatic mice. Lung histological examination confirms the ameliorative potency of cynaropicrin against OVA‐induced asthmatic pulmonary inflammation in mice. Our findings suggest cynaropicrin possesses significant ameliorative potency against allergen‐induced pulmonary inflammation. [ABSTRACT FROM AUTHOR]

Background: Newborns with critical congenital heart disease (CCHD) with increased pulmonary blood flow (PBF) are at high risk for congestive heart failure. In this study, we aimed to evaluate the presence and degree of pulmonary edema in newborns with CCHD using lung ultrasound (LUS) during the perioperative period. Methods: Prospective clinical trial, 44 newborn patients with CCHD were evaluated in this prospective clinical trial. LUS was repeatedly performed to determine the course of pulmonary edema during the perioperative period. LUS was performed simultaneously with chest radiography (CXR), which was the main part of patient management. The primary outcome of this study was to identify whether a correlation existed between LUS and CXR findings. The secondary outcomes were to determine the relationship between LUS and the need for respiratory support, diuretic use, vasoactive inotropic score (VIS), and pro-B-type natriuretic peptide (pro-BNP) levels during the perioperative period. Results: The mean gestational age of the patients was 38.3 ± 1.7 weeks, with a mean birth weight of 3026 ± 432 g. In the preoperative period, both LUS and CXR images were consistent with clinical signs of pulmonary edema. On the first postoperative day, pulmonary edema increased compared to the preoperative period but gradually decreased by the 6th day of surgery (p

Abstract Background Quantification of pulmonary edema in patients with acute respiratory distress syndrome (ARDS) by chest computed tomography (CT) scan has not been validated in routine diagnostics due to its complexity and time-consuming nature. Therefore, the single-indicator transpulmonary thermodilution (TPTD) technique to measure extravascular lung water (EVLW) has been used in the clinical setting. Advances in artificial intelligence (AI) have now enabled CT images of inhomogeneous lungs to be segmented automatically by an intensive care physician with no prior radiology training within a relatively short time. Nevertheless, there is a paucity of data validating the quantification of pulmonary edema using automated lung segmentation on CT compared with TPTD. Methods A retrospective study (January 2016 to December 2021) analyzed patients with ARDS, admitted to the intensive care unit of the Department of Anesthesiology and Critical Care Medicine, University Hospital Mannheim, who underwent a chest CT scan and hemodynamic monitoring using TPTD at the same time. Pulmonary edema was estimated using manually and automated lung segmentation on CT and then compared to the pulmonary edema calculated from EVLW determined using TPTD. Results 145 comparative measurements of pulmonary edema with TPTD and CT were included in the study. Estimating pulmonary edema using either automated lung segmentation on CT or TPTD showed a low bias overall (− 104 ml) but wide levels of agreement (upper: 936 ml, lower: − 1144 ml). In 13% of the analyzed CT scans, the agreement between the segmentation of the AI algorithm and a dedicated investigator was poor. Manual segmentation and automated segmentation adjusted for contrast agent did not improve the agreement levels. Conclusions Automated lung segmentation on CT can be considered an unbiased but imprecise measurement of pulmonary edema in mechanically ventilated patients with ARDS.

Abstract Background Postoperative negative pressure pulmonary edema (NPPE) can occur in any patient undergoing general anesthesia. There are several risk factors for it, especially postoperative laryngospasm. The disease is usually benign and quickly reversible. In our case the severity and need for advanced critical care therapy was unusual. Case We report a severe case of postoperative negative pressure pulmonary edema in a 62-year-old male patient undergoing elective right-sided retroperitoneoscopic adrenalectomy. The patient developed a severe case of acute respiratory distress syndrome (ARDS) after postoperative laryngospasm, possibly in conjunction with a suspected anaphylactic reaction. The patient was consequently treated with a combination of invasive airway pressure release ventilation (APRV) and a prone positioning regimen. After drastic improvement in respiratory function, the patient was discharged from the intensive care unit after 10 days and from the hospital after 14 days. Conclusion NPPE is a rare but relevant complication of anesthesia and laryngospasm. The disease can basically occur in any patient undergoing general anesthesia and therefore should be considered.

Aim. Using the CHAID (Chi Squared Automatic Interaction Detection) method to develop a classification tree for predicting hospital mortality in patients with non-ST-elevation myocardial infarction (non-STEMI) aged 75 years and older and compare the quality of the constructed model with the logistic regression model.Material and methods. A retrospective analysis of the case histories of 119 sequentially enrolled patients aged ≥75 years who were hospitalized in a cardiology department due to non-STEMI in 2020-2021 was carried out. The construction of a predictive model of probability of dying was carried out using the logistic regression method. To assess the impact of various predictors affecting the probability of dying during the of hospitalization period in patients with non-STEMI, a classification tree was developed using the CHAID method. To compare the quality of logistic regression models and the classification tree, the areas under the ROC curve and confidence intervals were estimated.Results. Based on the construction of a binary logistic regression, it was found that the factors increasing hospital mortality were cardiogenic shock (CS): odds ratio (OR) 47.55; 4.00-589.16; p=0.002; new-onset atrial fibrillation: OR 6.45; 1.39-30.42; p=0.018; and the number of points on the GRACE scale: for each increase by 1 point: OR 1.03; 1,00-1,05; p=0.046. Similar data were obtained when analyzing the classification tree: in patients with CS, the predicted mortality was 91.7%. The probability of an unfavorable outcome based on the constructed classification tree was higher than the average in the analyzed sample in persons without CS, 2-3 degree atrioventricular blocks, and pulmonary edema, but with right bundle branch block on the electrocardiogram (25.0%) and in persons without CS and atrioventricular blockages of 2-3 degrees, but with pulmonary edema and a Q wave on the electrocardiogram (50.0%). Both methods of predicting hospital mortality are applicable. There were no statistically significant differences in the quality of both constructed models; the difference in the areas under the ROC curves was 0.043±0.268 with a 95% confidence interval of -0.055-0.141, p=0.387.Conclusion. Both developed methods can be used to determine the probability of dying in a hospital. Currently, the recruitment of patients into a prospective study of a similar design has begun and is continuing, during which validation of the constructed forecasting models is planned.