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Drug reaction with eosinophilia and systemic symptoms (DRESS) is a severe drug reaction where patients present with fever, morbilliform rash and multiorgan manifestations, which may include acute renal failure, acute respiratory distress syndrome and eosinophilic myocarditis. We present a case of a 60‐year‐old woman with acute heart failure, DRESS syndrome features and human herpesvirus 6 reactivation in the absence of a drug trigger. She was diagnosed with eosinophilic myocarditis and successfully treated with corticosteroid therapy. [ABSTRACT FROM AUTHOR]

Medical life-saving techniques include mechanical ventilation. During the COVID-19 epidemic, the lack of inexpensive, precise, and accessible mechanical ventilation equipment was the biggest challenge. The global need exploded, especially in developing nations. Global researchers and engineers are developing inexpensive, portable medical ventilators. A simpler mechanical ventilator system with a realistic lungs model is simulated in this work. A systematic ventilation study is done using the dynamic simulation of the model. Simulation findings of various medical disorders are compared to standard data. The maximum lung pressure (Pmax) was 15.78 cmH2O for healthy lungs, 17.72 for cardiogenic pulmonary edema, 16.05 for pneumonia, 19.74 for acute respiratory distress syndrome (ARDS), 17.1 for AECOPD, 19.64 for asthma, and 15.09 for acute intracranial illnesses and head traumas. All were below 30 cmH2O, the average maximum pressure. The computed maximum tidal volume (TDVmax) is 0.5849 l, substantially lower than that of the healthy lungs (0.700 l). The pneumonia measurement was 0.4256 l, substantially lower than the typical 0.798 l. TDVmax was 0.3333 l for ARDS, lower than the usual 0.497 l. The computed TDVmax for AECOPD was 0.6084 l, lower than the normal 0.700 l. Asthma had a TDVmax of 0.4729 l, lower than the typical 0.798 l. In individuals with acute cerebral diseases and head traumas, TDVmax is 0.3511 l, lower than the typical 0.700 l. The results show the viability of the model as it performs accurately to the presented medical condition parameters. Further clinical trials are needed to assess the safety and reliability of the simulation model. [ABSTRACT FROM AUTHOR]

Introduction. Re-expansion pulmonary edema is a rare complication secondary to rapid pulmonary re-expansion after drainage by thoracentesis and/or closed thoracostomy. As of today, an incidence of less than 1% has been described after closed thoracostomy, with a higher prevalence in the second and third decades of life. Its exact pathophysiological mechanism is unknown; a multifactorial process of lung interstitial damage associated with an imbalance of hydrostatic forces has been proposed. Clinical case. We present the case of a patient who developed pulmonary edema due to re-expansion after closed thoracostomy, conducting a review of the literature on this complication. Results. Although the clinic suggests the diagnosis, the sequence of images plays a fundamental role. In most cases, it tends to be a self-limited disease, so its management is mainly supportive. However, mortality rates of up to 20% have been recorded. Therefore, it is important to identify patients with major risk factors and initiate preventive measures in these patients. Conclusions. Re-expansion pulmonary edema after thoracostomy is a rare complication in cases with pneumothorax; however, it is a complication that can occur in daily practice. Therefore, it must be kept in mind to be able to make the diagnosis and an adequate management. [ABSTRACT FROM AUTHOR]

Introduction: Acute pulmonary edema is a frequent disease among patients in emergency services. Objective: To characterize patients with acute pulmonary edema who attended the emergency services. Methods: A descriptive and cross-sectional study of 37 patients with acute pulmonary edema who attended the emergency services of Dr. Joaquín Castillo Duany Teaching Clinical Surgical Hospital in Santiago de Cuba was carried out, from January to November 2019. The studied variables were age, sex, alive or dead when discharged, noninvasive ventilation usage. Results: There were no differences between the sexes; there was a prevalence of patients older than 60 years of age, who suffered from hypertension. It was demonstrated low noninvasive or invasive ventilation usage. Conclusions: Acute pulmonary edema is more frequent among patients older than 60 years of age in both sexes. Most of the patients suffered from hypertension and there was a deficit in the implementation of noninvasive ventilation in these cases. [ABSTRACT FROM AUTHOR]

The body of a 14-wk-old puppy (Canis familiaris) was submitted to the Animal Health Laboratory, University of Guelph, Ontario for postmortem examination following a history of intermittent anorexia and lethargy progressing to pyrexia, pruritic skin rash, mucoid nasal discharge, decreased mentation, dysphagia, muscle twitches, and focal seizures. Gross examination revealed rhinitis and pulmonary edema. Histologically, there was fibrinonecrotizing bronchopneumonia, tracheitis, and neutrophilic and lymphohistiocytic rhinitis; rarely within the cortical gray and white matter of the brain were small clusters of glial cells, with rare individual neutrophils in the choroid plexus. Although canine distemper was suspected, none of the usual supportive histologic lesions of distinct syncytial cells, viral inclusion bodies, or demyelinating leukoencephalitis were observed. Lung and brain tissues were PCR-positive for canine distemper virus (CDV), and CDV was detected immunohistochemically in the brain. The agent from the PCR-positive sample from the brain was genotyped and was a 99.9% match to the CDV Rockborn strain, indicating that the disease agent in our case was vaccinal in origin. Our unusual case highlights the possibility of reversion to virulence in a modified-live virus vaccine, and the occurrence of a disease in the absence of a full complement of the usual and compatible histologic lesions. [ABSTRACT FROM AUTHOR]

Re-expansion pulmonary edema (RPE) is a rare but potentially life-threatening complication that can occur after rapid lung expansion following the management of lung collapse. This meta-analysis aimed to investigate the risk factors for RPE following chest tube drainage in patients with spontaneous pneumothorax. We conducted a comprehensive systematic literature search in electronic databases of PubMed, ScienceDirect, Cochrane Library, and ProQuest to identify studies that explore the risk factors for RPE following chest tube drainage in spontaneous pneumothorax. Pooled odds ratios (OR) or weighted mean differences (WMD) were calculated to evaluate the risk factors. Statistical analysis was conducted using Review Manager 5.3 software. Five studies involving 1.093 spontaneous pneumothorax patients were included in this meta-analysis. The pooled analysis showed that the following risk factors were significantly associated with increased risk of RPE following chest tube drainage: the presence smoking history (OR=1.94, 95% CI: 1.22-3.10, P =0.005, I2=0%), longer duration of symptoms (WMD=3.76, 95% CI: 2.07-5.45, P <0.0001,> P [ABSTRACT FROM AUTHOR]

Objectives: The number and distribution of lung ultrasound (LUS) imaging artifacts termed B‐lines correlate with the presence of acute lung disease such as infection, acute respiratory distress syndrome (ARDS), and pulmonary edema. Detection and interpretation of B‐lines require dedicated training and is machine and operator‐dependent. The goal of this study was to identify radio frequency (RF) signal features associated with B‐lines in a cohort of patients with cardiogenic pulmonary edema. A quantitative signal indicator could then be used in a single‐element, non‐imaging, wearable, automated lung ultrasound sensor (LUSS) for continuous hands‐free monitoring of lung fluid. Methods: In this prospective study a 10‐zone LUS exam was performed in 16 participants, including 12 patients admitted with acute cardiogenic pulmonary edema (mean age 60 ± 12 years) and 4 healthy controls (mean age 44 ± 21). Overall,160 individual LUS video clips were recorded. The LUS exams were performed with a phased array probe driven by an open‐platform ultrasound system with simultaneous RF signal collection. RF data were analyzed offline for candidate B‐line indicators based on signal amplitude, temporal variability, and frequency spectrum; blinded independent review of LUS images for the presence or absence of B‐lines served as ground truth. Predictive performance of the signal indicators was determined with receiving operator characteristic (ROC) analysis with k‐fold cross‐validation. Results: Two RF signal features—temporal variability of signal amplitude at large depths and at the pleural line—were strongly associated with B‐line presence. The sensitivity and specificity of a combinatorial indicator were 93.2 and 58.5%, respectively, with cross‐validated area under the ROC curve (AUC) of 0.91 (95% CI = 0.80–0.94). Conclusion: A combinatorial signal indicator for use with single‐element non‐imaging LUSS was developed to facilitate continuous monitoring of lung fluid in patients with respiratory illness. [ABSTRACT FROM AUTHOR]

Background: Mediastinal lymphatic tumors are relatively rare. The prognosis is poor but has improved due to recent advances in treatment strategies. Herein, we report a case of mediastinal lymphoma diagnosed using surgical biopsy, which was complicated by mediastinal mass syndrome due to general anesthesia. Case presentation: A 25-year-old man with cough, fever, dyspnea, and night sweats was transferred to our hospital for resection of a large anterior mediastinal tumor. Although his preoperative diagnosis was WHO type B1 thymoma, the clinical findings suggested a lymphoma. A repeat surgical biopsy was performed under general anesthesia. Immediately after extubation, the patient developed acute respiratory failure with hypolucency of the right lung field on chest radiography. He was reintubated immediately and was diagnosed with negative pressure pulmonary edema in the right lung. He was managed with positive-pressure ventilation and his respiratory distress resolved within 5 days. Pathological examination of surgical specimens confirmed the diagnosis of lymphoma. Conclusion: Surgical biopsy is useful for the diagnosis of mediastinal tumors. However, the risk of perioperative mediastinal mass syndrome should be carefully assessed before administering general anesthesia. [ABSTRACT FROM AUTHOR]

Background: Peripartum cardiomyopathy (PPCM) is a potentially life-threatening pregnancy-related condition characterized by left ventricular dysfunction and heart failure, typically occurring in the peripartum period. Individuals with a history of preeclampsia and hypertension are particularly prone to developing PPCM. Recent research suggests that the condition may be triggered by vascular dysfunction influenced by maternal hormones in the late stages of gestation. The onset of left heart failure results in decreased cardiac output, leading to insufficient perfusion, which in turn, contributes to pulmonary edema and exacerbates tissue hypoxia. This cardiovascular response activates the neurohumoral system, causing peripheral vasoconstriction and elevating both mean capillary filling pressure (MCFP) and central venous pressure (CVP). Early administration of furosemide reduces volume overload due to negative cumulative fluid balance gaining and vasodilation, which increases the velocity of intravascular refilling and causes interstitial edema to resolve. This will decrease interstitial fluid pressure, resulting in decreased mechanical compression to systemic capillary and systemic vein pressure, thus decreasing MCFP and CVP subsequently. Reduced CVP also contributes to increased venous return by decreasing the gradient pressure between MCFP and CVP, resulting in increased cardiac output (CO) and improved tissue oxygenation. Case: A 33-year-old Asian woman, para 3 at full term pregnancy, admitted to the intensive care unit (ICU) after c-section and tubectomy due to shortness of breath and palpitation. Based on history taking, physical examination and echocardiography the patient fulfilled the criteria of PPCM which was also complicated by pulmonary edema. Despite impending respiratory failure, the patient rejected intubation and continuous positive airway pressure (CPAP), and was given oxygen supplementation through nasal cannula. Furosemide was given rapidly continued by maintenance dose and CVP was monitored. Antihypertensive drug, anticoagulants, and bromocriptine were also administered. After achieving negative cumulative fluid balance the patient's symptoms resolved and was discharged one week later. Conclusion: There is a correlation between negative cumulative fluid balance and reduced central venous pressure after early furosemide therapy. Suspicion for PPCM should not be lowered in the presence of preeclampsia, it could delay appropriate treatment and increase the mortality. [ABSTRACT FROM AUTHOR]

Lung infection by influenza A virus (IAV) is a major cause of global mortality from lung injury, a disease defined by widespread dysfunction of the lung's air-blood barrier. Endocytosis of IAV virions by the alveolar epithelium - the cells that determine barrier function - is central to barrier loss mechanisms. Here, we address the current understanding of the mechanistic steps that lead to endocytosis in the alveolar epithelium, with an eye to how the unique structure of lung alveoli shapes endocytic mechanisms. We highlight where future studies of alveolar interactions with IAV virions may lead to new therapeutic approaches for IAV-induced lung injury. [ABSTRACT FROM AUTHOR]

Background: Lung ultrasound (LUS) is a simple bedside tool to assess overhydration. Our study aimed to assess extravascular lung water (EVLW) using B-lines and correlate it with weaning, duration of mechanical ventilation, and mortality in critically ill patients admitted to the intensive care unit (ICU). Patients and methods: 150 mechanically ventilated ICU patients prospectively observed over 18 months, with their demographic and clinical data noted. Extravascular lung water was monitored using LUS in four intercostal spaces (ICS) from day 1 to day 5, day 7, day 10, and weekly thereafter. Pulmonary fluid burden was graded as low (1-10), moderate (11-20), and high (21-32). Weaning outcome, duration of weaning, mechanical ventilation, ICU stay, and mortality were compared in patients with and without EVLW. Results: Out of 150, 54 patients (36.0%) had EVLW. The mean lung score amongst our patients was 8.57 ± 6.0. The mean time for detection of EVLW was 1.43 ± 2.24 days. Lung score was low in 40 (26.67%) patients, moderate in 9 (6.00%) patients, and high in 5 (3.33%) patients. Incidence of weaning failure (p-value = 0.006), duration of weaning, mechanical ventilation, ICU stay (p-value < 0.0001 each), and overall mortality were significantly higher in patients with EVLW (p-value = 0.006). Conclusion: We conclude that a good proportion of critically ill patients have EVLW. Extravascular lung water significantly increases the duration of weaning, mechanical ventilation days, ICU stay, and overall mortality in critically ill patients. [ABSTRACT FROM AUTHOR]

A monolayer of endothelial cells (ECs) lines the lumen of blood vessels and, as such, provides a semi-selective barrier between the blood and the interstitial space. Compromise of the lung EC barrier due to inflammatory or toxic events may result in pulmonary edema, which is a cardinal feature of acute lung injury (ALI) and its more severe form, acute respiratory distress syndrome (ARDS). The EC functions are controlled, at least in part, via epigenetic mechanisms mediated by histone deacetylases (HDACs). Zinc-dependent HDACs represent the largest group of HDACs and are activated by Zn2+. Members of this HDAC group are involved in epigenetic regulation primarily by modifying the structure of chromatin upon removal of acetyl groups from histones. In addition, they can deacetylate many non-histone histone proteins, including those located in extranuclear compartments. Recently, the therapeutic potential of inhibiting zinc-dependent HDACs for EC barrier preservation has gained momentum. However, the role of specific HDAC subtypes in EC barrier regulation remains largely unknown. This review aims to provide an update on the role of zinc-dependent HDACs in endothelial dysfunction and its related diseases. We will broadly focus on biological contributions, signaling pathways and transcriptional roles of HDACs in endothelial pathobiology associated mainly with lung diseases, and we will discuss the potential of their inhibitors for lung injury prevention. [ABSTRACT FROM AUTHOR]

The Centers for Medicare and Medicaid Services (CMS) developed the Severe Sepsis and Septic Shock Performance Measure bundle (SEP-1) metric to improve sepsis care, but evidence supporting this bundle is limited and harms secondary to compliance have not been investigated. This study investigates the effect of an emergency department (ED) sepsis quality-improvement (QI) effort to improve CMS SEP-1 compliance, looking specifically at antibiotic overtreatment and harm from fluid resuscitation. This was a retrospective observational study conducted between March and July 2021 with patients for whom a sepsis order set was initiated. The primary outcomes included the number of patients treated with antibiotics who were ultimately deemed nonseptic and the number of patients who developed pulmonary edema, with or without need for positive pressure ventilation (PPV), within 48 h of receiving a 30 mL/kg fluid bolus. Data were collected via nonblinded chart reviews, with a free marginal κ-calculation indicating excellent interrater reliability. The study cohort included 273 patients, 170 (62.3%) who were ultimately determined to be septic and 103 (37.7%) who were nonseptic. Of the 103 nonseptic patients, 82 (79.6%) received antibiotics in the ED. Of the 121 patients (44.3%) who received a 30 mL/kg bolus, 5 patients (4.1%) developed pulmonary edema and 0 of 121 patients required PPV within 48 h. The QI effort led to moderate rates of antibiotic overtreatment and very few patients developed pulmonary edema due to a 30 mL/kg fluid bolus. [ABSTRACT FROM AUTHOR]

Pulmonary endarterectomy (PEA) is the guideline-recommended treatment for patients with chronic thromboembolic pulmonary hypertension (CTEPH). However, some patients develop severe cardiopulmonary compromise before surgery, intraoperatively, or early postoperatively. This may result from advanced CTEPH, reperfusion pulmonary edema, massive endobronchial bleeding, or right ventricular (RV) failure secondary to residual pulmonary hypertension. Conventional cardiorespiratory support is ineffective when these complications are severe. Since 2005, we used extracorporeal membrane oxygenation (ECMO) as a rescue therapy for this group. We review our experience with ECMO support in these patients. This study was a retrospective analysis of patients who received perioperative ECMO for PEA from a single national center from August 2005 to July 2022. Data were prospectively collected. One hundred and ten patients (4.7%) had extreme cardiorespiratory compromise requiring perioperative ECMO. Nine were established on ECMO before PEA. Of those who received ECMO postoperatively, 39 were for refractory reperfusion lung injury, 20 for RV failure, 31 for endobronchial bleeding, and the remaining 11 were for "other" reasons, such as cardiopulmonary resuscitation following late tamponade and aspiration pneumonitis. Sixty-two (56.4%) were successfully weaned from ECMO. Fifty-seven patients left the hospital alive, giving a salvage rate of 51.8%. Distal disease (Jamieson Type III) and significant residual pulmonary hypertension were also predictors of mortality on ECMO support. Overall, 5- and 10-year survival in patients who were discharged alive following ECMO support was 73.9% (SE: 6.1%) and 58.2% (SE: 9.5%), respectively. Perioperative ECMO support has an appropriate role as rescue therapy for this group. Over 50% survived to hospital discharge. These patients had satisfactory longer-term survival. [ABSTRACT FROM AUTHOR]

Respiratory complications such as noncardiogenic pulmonary edema, acute respiratory distress syndrome and pneumonia are frequently seen in drowning. No additional disease was noted in the history of a 37-year-old male patient who was brought to the emergency department with cardiopulmonary arrest after drowning at sea. Spontaneous circulation returned following 12 minutes of cardiopulmonary resuscitation. Bedside point-of-care ultrasound (POCUS) revealed multiple and confluent B lines, an irregularity on the pleural line, disappearance in the A-lines, and subpleural hypoechoic areas predominantly in the 2nd, 3rd, 4th and 6th zones of the right lung and the 3rd, 4th and 6th zones of the left lung. The ventilator mode and settings were adjusted according to the POCUS findings, being a safe option in emergency departments for the diagnosis of noncardiogenic pulmonary edema due to drowning and for the management of such patients. [ABSTRACT FROM AUTHOR]

Endoscopic transsphenoidal resection of craniopharyngioma is a commonly used technique. Cerebral vasospasm may occur in nearly 10% of cases leading to adverse neurological outcomes. Cardiopulmonary dysfunction may be seen in patients with severe vasospasm. The literature describing the occurrence of neurogenic stunned myocardium following craniopharyngioma resection in pediatric patients is very sparse. Here, we describe such a case managed with a combination of milrinone (to relieve vasospasm and improve cardiac pump function), noradrenaline (to obtain target blood pressure), and vasopressin (to control urine output). This case report proposes the treatment plan of neurogenic stunned myocardium following vasospasm in pediatric patients. [ABSTRACT FROM AUTHOR]

The article explores the use of lung ultrasonography (LUS) in diagnosing and differentiating types of pulmonary edema. LUS has gained popularity in diagnosing lung diseases, but there is debate over its ability to accurately distinguish between alveolar and interstitial pulmonary edema. Factors such as probe types, scanning depth, and focus position can impact the appearance of B-lines, making it challenging to make definitive judgments. While LUS cannot differentiate cardiogenic and pulmonary lung edema based on B-lines, cardiac ultrasound can be used to distinguish cardiogenic pulmonary edema caused by left heart failure. Further research is needed to better understand the relationship between B-lines and pulmonary edema. [Extracted from the article]

The homeostasis and health of an organism depend on the coordinated interaction of specialized organs, which is regulated by interorgan communication networks of circulating soluble molecules and neuronal connections. Many diseases that seemingly affect one primary organ are really multiorgan diseases, with substantial secondary remote organ complications that underlie a large part of their morbidity and mortality. Acute kidney injury (AKI) frequently occurs in critically ill patients with multiorgan failure and is associated with high mortality, particularly when it occurs together with respiratory failure. Inflammatory lung lesions in patients with kidney failure that could be distinguished from pulmonary oedema due to volume overload were first reported in the 1930s, but have been largely overlooked in clinical settings. A series of studies over the past two decades have elucidated acute and chronic kidney–lung and lung–kidney interorgan communication networks involving various circulating inflammatory cytokines and chemokines, metabolites, uraemic toxins, immune cells and neuro-immune pathways. Further investigations are warranted to understand these clinical entities of high morbidity and mortality, and to develop effective treatments. Here, the authors review the current understanding of interorgan crosstalk mechanisms, with a focus on interorgan communication in the kidney–lung axis during acute or chronic disease of the kidney or lung. Key points: Interorgan communication networks consist of soluble circulating factors, the immune system and the nervous system, and involve neuro-immune and neuro-endocrine interactions. Acute kidney injury (AKI) causes long-recognized complications, such as uraemia and volume overload, and less well understood "non-traditional" complications, such as remote organ dysfunction and immune dysfunction, which contribute to increased morbidity and mortality. AKI-induced remote lung inflammation depends on the actions of soluble circulating factors that are released by the kidney and other organs, including osteopontin, HMGB1, IL-6, IL-8 and TNF, and of immune cells, including neutrophils, monocytes, macrophages and T cells. Primary lung injury due to infection, acid aspiration, ischaemia–reperfusion injury or barotrauma can lead to AKI in rodents and humans; some of the mechanisms of lung–kidney crosstalk are similar to those implicated in kidney–lung crosstalk, but more mechanistic studies are required. Studies in preclinical models and correlative evidence from clinical studies suggest a bidirectional detrimental relationship between chronic kidney disease and chronic lung disease; however, the molecular mechanisms are largely unknown. [ABSTRACT FROM AUTHOR]

Objective: To mine and analyze the adverse reaction signals of human serum albumin (HSA) using the FDA adverse event reporting system (FAERS) database for the safe clinical use of this drug. Methods: Data cleaning and analysis of adverse event reports in the FAERS database for a total of 76 quarters from Q1 2004 to Q4 2022 were performed using the reporting odds ratio (ROR), Medicines and Healthcare Products Regulatory Agency (MHRA), and Bayesian confidence propagation neural network (BCPNN). Gender-differentiated signal detection was used to investigate the gender differences in the occurrence of HSA adverse events. Results: Through a combination of three methods, a total of 535 adverse event reports were identified. These reports involved 1,885 cases of adverse reactions, with respiratory, thoracic, and mediastinal disorders, as well as general disorders and administration site conditions, as the most common. One noteworthy new signal was the occurrence of transfusion-related acute lung injury. Additionally, gender-differentiated signals were present, with females experiencing paraesthesia, hypertension, pulmonary oedema, loss of consciousness, and vomiting. Conclusion: This study has revealed that HSA poses a risk of causing transfusionrelated acute lung injury. It has also been observed that adverse reactions, including paraesthesia, hypertension, pulmonary oedema, loss of consciousness, and vomiting, are more prevalent in females. These findings should be taken into account when using HSA in a clinical setting. [ABSTRACT FROM AUTHOR]

Acute Respiratory Distress Syndrome (ARDS) is a sudden onset of lung injury characterized by bilateral pulmonary edema, diffuse inflammation, hypoxemia, and a low P/F ratio. Epithelial injury and endothelial injury are notable in the development of ARDS, which is more severe under mechanical stress. This review explains the role of alveolar epithelial cells and endothelial cells under physiological and pathological conditions during the progression of ARDS. Mechanical injury not only causes ARDS but is also a side effect of ventilator-supporting treatment, which is difficult to model both in vitro and in vivo. The development of lung organoids has seen rapid progress in recent years, with numerous promising achievements made. Multiple types of cells and construction strategies are emerging in the lung organoid culture system. Additionally, the lung-on-a-chip system presents a new idea for simulating lung diseases. This review summarizes the basic features and critical problems in the research on ARDS, as well as the progress in lung organoids, particularly in the rapidly developing microfluidic system-based organoids. Overall, this review provides valuable insights into the three major factors that promote the progression of ARDS and how advances in lung organoid technology can be used to further understand ARDS. [ABSTRACT FROM AUTHOR]

Acute respiratory distress syndrome (ARDS) is a common condition associated with critically ill patients, characterized by bilateral chest radiographical opacities with refractory hypoxemia due to noncardiogenic pulmonary edema. Despite significant advances, the mortality of ARDS remains unacceptably high, and there are still no effective targeted pharmacotherapeutic agents. With the outbreak of coronavirus disease 19 worldwide, the mortality of ARDS has increased correspondingly. Comprehending the pathophysiology and the underlying molecular mechanisms of ARDS may thus be essential to developing effective therapeutic strategies and reducing mortality. To facilitate further understanding of its pathogenesis and exploring novel therapeutics, this review provides comprehensive information of ARDS from pathophysiology to molecular mechanisms and presents targeted therapeutics. We first describe the pathogenesis and pathophysiology of ARDS that involve dysregulated inflammation, alveolar-capillary barrier dysfunction, impaired alveolar fluid clearance and oxidative stress. Next, we summarize the molecular mechanisms and signaling pathways related to the above four aspects of ARDS pathophysiology, along with the latest research progress. Finally, we discuss the emerging therapeutic strategies that show exciting promise in ARDS, including several pharmacologic therapies, microRNA-based therapies and mesenchymal stromal cell therapies, highlighting the pathophysiological basis and the influences on signal transduction pathways for their use. [ABSTRACT FROM AUTHOR]

Background: Pulmonary metabolic dysfunction can cause lung tissue injury. There is still no ideal drug to protect against hypoxia-induced lung injury, therefore, the development of new drugs to prevent and treat hypoxia-induced lung injury is urgently needed. We aimed to explore the ameliorative effects and molecular mechanisms of vitamin D3 (VD3) on hypoxia-induced lung tissue injury. Methods: Sprague–Dawley (SD) rats were randomly divided into three groups: normoxia, hypoxia, and hypoxia + VD3. The rat model of hypoxia was established by placing the rats in a hypobaric chamber. The degree of lung injury was determined using hematoxylin and eosin (H&E) staining, lung water content, and lung permeability index. Transcriptome data were subjected to differential gene expression and pathway analyses. In vitro, type II alveolar epithelial cells were co-cultured with hepatocytes and then exposed to hypoxic conditions for 24 h. For VD3 treatment, the cells were treated with low and high concentrations of VD3. Results: Transcriptome and KEGG analyses revealed that VD3 affects the complement and coagulation cascade pathways in hypoxia-induced rats, and the genes enriched in this pathway were Fgb/Fga/LOC100910418. Hypoxia can cause increases in lung edema, inflammation, and lung permeability disruption, which are attenuated by VD3 treatment. VD3 weakened the complement and coagulation cascade in the lung and liver of hypoxia-induced rats, characterized by lower expression of fibrinogen alpha chain (Fga), fibrinogen beta chain (Fgb), protease-activated receptor 1 (PAR1), protease-activated receptor 3 (PAR3), protease-activated receptor 4 (PAR4), complement (C) 3, C3a, and C5. In addition, VD3 improved hypoxic-induced type II alveolar epithelial cell damage and inflammation by inhibiting the complement and coagulation cascades. Furthermore, VD3 inhibited hypoxia-induced autophagy in vivo and in vitro, which was abolished by the mitophagy inducer, carbonyl cyanide-m-chlorophenylhydrazone (CCCP). Conclusion: VD3 alleviated hypoxia-induced pulmonary edema by inhibiting the complement and coagulation cascades and autophagy pathways. [ABSTRACT FROM AUTHOR]

Introduction: Chronic thromboembolic pulmonary hypertension (CTEPH), characterized by thromboembolic changes affecting the pulmonary bed, leads to ventricular function deterioration and premature death. The introduction of balloon pulmonary angioplasty (BPA) has significantly improved the prognosis of CTEPH patients. Aim: The authors of this article decided to summarize the experience of the BPA program, conducted between 2014 and 2022, at the reference center. Material and methods: Among 111 CTEPH patients, 55 were included in the analysis. A total of 226 sessions were performed, with a significant percentage of intravascular imaging and pressure catheter use. Results: Mean pulmonary pressure decreased significantly from 42 (22–66) to 26.5 mm Hg (11–54) (p < 0.05). Pulmonary vascular resistance and natriuretic peptide concentration decreased from 6.67 (1.66–14) to 3.295 Wood units (1.09–11.11), respectively, and from 1934 (60–16963) to 296 (21–9901) ng/ml (p < 0.05). There was also an improvement in the functional class (WHO) from 2.85 ±0.61 to 2.15 ±0.62 and an increase in the 6-minute walking distance from 300 ±131 to 367 ±154 m (p < 0.05). There were no in-hospital deaths or within 30 days of the procedure. Arterial damage occurred during nine sessions (n = 9/226, 4%), while 0.9% (n = 2/226) were complicated by acute right ventricular failure. Post-reperfusion pulmonary edema (RPE 0 – none) was observed in almost 90% of the sessions, grade 1 to 3 RPE occurred in 10.2%, and grade 4 RPE was not noted. Conclusions: BPA programs conducted in experienced centers are a safe and effective treatment option for inoperable CTEPH patients. [ABSTRACT FROM AUTHOR]

Introduction: Polyethylene glycol 3,350 and electrolytes is a commonly prescribed bowel regimen for colonoscopy preparation with an overall excellent safety profile, though prior reports have demonstrated risk of volume overload. Case Presentation: A 55-year-old man with significant cardiopulmonary co-morbidities was admitted for acute hypoxic respiratory failure and subsequent evaluation for lung transplant. As part of his pretransplant evaluation, colon cancer screening was advised. Despite multiple days of bowel preparation, his stools contained sediment. Unfortunately, he developed pulmonary edema due to prolonged bowel preparation. Conclusion: While bowel preparation is considered generally safe, our case report highlights the importance of judicious use with monitoring in high-risk individuals. [ABSTRACT FROM AUTHOR]

OBJECTIVE To document any discordance between the set temperature and independently measured temperature of neonatal incubators in order to determine the potential of neonatal incubators to cause hypothermia or hyperthermia in neonatal animals. SAMPLE 5 different veterinary neonatal incubators from 2 separate manufacturers. METHODS Internal temperatures of 5 incubators from 2 manufacturers were monitored with both internal and external motiitoring devices to determine how much incubator temperatures might vary from what is reported on the incubator thermostat. The study was conducted on May 25, 2022. RESULTS Increases in temperature as measured by thermocouple and infrared sensors of > 2 °C were detected in 3 of the 5 (60%; 95% Cl, 17% to 93%) tested incubators. Temperatures exceeded 41 QC at times, despite the incubator thermostat being set to 35 DC. CLINICAL RELEVANCE Neonatal puppies have a decreased capacity to thermoregulate and are susceptible to both hypothermia and hyperthermia if environmental temperatures are not kept within a proper range. Core temperatures below 35.0 °C lead to bradycardia, dyspnea, loss of suckle reflex, hypoglycemia, gastrointestinal ileus, and multiple organ failure; temperatures above 41.1 °C lead to pulmonary edema, petechial and ecchymotic hemorrhage in multiple organs, and death. [ABSTRACT FROM AUTHOR]

The aim of this report was to document the presentation of a 12-week-old pyometra in an 11-year-old female Chihuahua with hyperadrenocorticism and endocardiosis. The patient presented with clinical and paraclinical signs consistent with chronic hyperadrenocorticism. An adrenocorticotropic hormone (ACTH) stimulation test confirmed the hyperadrenocorticism (post-stimulation cortisol of 27.79 μg/dl). However, the progression of subclinical pyometra was evident at 12 weeks of evolution (Acute Patient Physiologic and Laboratory Evaluation - fast [APPLE-fast] of 15; Quick Sequential Organ Failure Assessment [qSOFA] of 1) with additional signs of pulmonary edema secondary to endocardiosis. At 48 hours post-surgery, the patient exhibited lethargy, anorexia, an APPLE-fast of 26, and clinical criteria of SIRS-3. After the therapeutic failure of the previous approach with enrofloxacin plus ampicillin/sulbactam, and later cefovecin, it was decided to administer gentamicin for 3 days, with a favorable clinical and paraclinical response, and an APPLE-fast of 19. The result of the urine culture revealed the presence of enterohemorrhagic Escherichia coli (EHEC) with a multidrugresistant profile suggestive of extended spectrum beta-lactamase (ESBL). At the clinical follow-up 4 weeks after starting trilostane post-discharge, the tutor reported improvement in clinical signs of chronic polydipsia, polyuria, and polyphagia, with an appropriate quality of life score for monitoring hyperadrenocorticism. It is presumed that the classic clinical expression of pyometra and infectious cystitis was mitigated by the uncontrolled underlying hyperadrenocorticism, and the clinical course of the disease progressed to sepsis due to EHEC with apparent production of ESBL. [ABSTRACT FROM AUTHOR]

The dramatic changes in physiology at high altitude (HA) as a result of the characteristic hypobaric hypoxia condition can modify innate and adaptive defense mechanisms of the body. As a consequence, few sojourners visiting HA with mild or asymptomatic infection may have an enhanced susceptibility to high-altitude pulmonary edema (HAPE), an acute but severe altitude sickness. It develops upon rapid ascent to altitudes above 2500 m, in otherwise healthy individuals. Though HAPE has been studied extensively, an elaborate exploration of the HA disease burden and the potential risk factors associated with its manifestation are poorly described. The present review discusses respiratory tract infection (RTI) as an unfamiliar but important risk factor in enhancing HAPE susceptibility in sojourners for two primary reasons. First, the symptoms of RTI s resemble those of HAPE. Secondly, the imbalanced pathways contributing to vascular dysfunction in HAPE also participate in the pathogenesis of the infectious processes. These pathways have a crucial role in shaping host response against viral and bacterial infections and may further worsen the clinical outcomes at HA. Respiratory tract pathogenic agents, if screened in HAPE patients, can help in ascertaining their role in disease risk and also point toward their association with the disease severity. The microbial screenings and identifications of pathogens with diseases are the foundation for describing potential molecular mechanisms underlying host response to the microbial challenge. The prior knowledge of such infections may predict the manifestation of disease etiology and provide better therapeutic options. [ABSTRACT FROM AUTHOR]

Changes in bodily fluid pressures, such as pulmonary artery pressure, play key roles in high-altitude pulmonary edema (HAPE) and other disorders. Smart delivery systems releasing a drug in response to these pressures might facilitate early medical interventions. However, pressure-responsive delivery systems are unavailable. We here constructed hydrostatic pressure-sensitive multivesicular liposomes (PSMVLs) based on the incomplete filling of the internal vesicle space with neutral lipids. These liposomes were loaded with amlodipine besylate (AB), a next-generation calcium channel inhibitor, to treat HAPE on time. AB-loaded PSMVLs (AB-PSMVLs) were destroyed, and AB was released through treatment under hydrostatic pressure of at least 25 mmHg. At 25 mmHg, which is the minimum pulmonary artery pressure value in HAPE, 38.8% of AB was released within 1 h. In a mouse HAPE model, AB-PSMVLs concentrated in the lung and released AB to diffuse into the vascular wall. Intravenously injected AB-PSMVLs before HAPE modeling resulted in a stronger protection of lung tissues and respiratory function and lower occurrence of pulmonary edema than treatment with free drug or non-pressure-sensitive AB-loaded liposomes. This study offers a new strategy for developing smart drug delivery systems that respond to changes in bodily fluid pressures. [Display omitted] • Pressure-sensitive multivesicular liposome was designed to carry amlodipine besylate. • Pressure sensitivity was due to loss of separate tricaprylin region in lipid structure. • Liposome rupture and drug release were triggered by hydrostatic pressure > 25 mmHg. • This system trapped in the lung can release drug by increased pulmonary artery pressure. • This system prevented the occurrence of high altitude pulmonary edema in mice. [ABSTRACT FROM AUTHOR]

Background: The incidence of lung pathology is the most common autopsy finding and is responsible for a great deal of mortality and morbidity. It is affected by a wide variety of respiratory pathogens and is involved in many systemic diseases. It is secondarily involved in almost all forms of terminal disease. Radiological findings are usually nonspecific in lung diseases and need prompt histopathological examination to find out the exact cause of death. Aims and Objectives: The aim is to study the spectrum of histopathological findings in lung in autopsy cases. Materials and Methods: This is a retrospective study done in the Department of Pathology at Government Kilpauk Medical College and Hospital during the year 2022. Lung specimens were received from the Forensic medicine department. Gross findings were noted. Following adequate formalin fixation, the tissue specimens were processed and paraffin sectioning was done followed by hematoxylin and eosin staining. The findings were documented and the results were analyzed. Results: Among 100 cases studied during year maximum cases were seen in the age group of 31-40 years (32%). Males (72%) were more commonly affected than females (28%). The most common findings are Pulmonary edema (34%) followed by congestion (32%) and other findings include emphysematous change (13%), pneumonia (10%), tuberculosis (6%), metastatic adenocarcinomatous deposits (1%), primary well-differentiated adenocarcinoma (1%), pulmonary chondroma (1%), and bronchiectasis (1%). Conclusion: The most common finding observed was pulmonary edema. In our study, male preponderance was noted. This study emphasizes to scrutinize the histopathological findings in the lung, especially following a sudden death. [ABSTRACT FROM AUTHOR]

A 27-year-old Japanese woman with a history of depression and an eating disorder presented to our emergency department with a chief complaint of generalized weakness. Electrocardiography showed prominent QT prolongation with multiple ventricular contractions. Chest X-ray plain computed tomography revealed pulmonary edema. Echocardiography showed decreased left ventricular systolic function. Suspecting acute myocarditis, we performed a myocardial biopsy from the right ventricular septum. The biopsy histology revealed extensive myocardial fibrosis and a very mild inflammatory cell infiltrate. In an additional detailed medical interview, the patient admitted that she had consumed three bottles of a first-aid liquid containing naphazoline approximately ~12 h before her presentation, in a suicide attempt. Her QTc and left ventricular ejection fraction improved during hospitalization. Acute drug intoxication can cause QT prolongation and ventricular arrhythmias, cardiomyopathy, and pulmonary edema. When acute QT prolongation, myocardial damage, and pulmonary edema are seen (suggesting acute myocarditis), naphazoline intoxication should be investigated in the differential diagnosis. [ABSTRACT FROM AUTHOR]

Background: Sepsis is a clinical disease characterized by systemic inflammatory reactions following infection that can lead to multiorgan failure. Acute Lung Injury (ALI) is a common ailment with increased morbidity and fatality rates worldwide. Objectives: The present investigation was planned to investigate the salutary activities of uvaol against Lipopolysaccharide (LPS)-exposed ALI in mice. Materials and Methods: The 5 mg/kg of LPS was exposed to the mice for 3 days through the intra-tracheal route to initiate the ALI, and 5 and 10 mg/kg, respectively, of uvaol were administered orally for 3 days the LPS challenge. The mice were scarified under anesthesia, lungs were excised, and wet and dry weights were weighed accurately. All the biochemical parameters, including apoptosis, inflammation, and oxidative stress marker levels, were assessed using the respective assay kits. Results: The uvaol (5 and 10 mg/kg) treatment effectively diminished pulmonary edema, total protein, and LDH activity in the ALI mice. The MDA was reduced, and the GSH and SOD levels were increased by the uvaol. The uvaol effectively reduced the inflammatory cytokines and infiltrations in the ALI mice. The PGE-2, iNOS, and COX-2 levels in the BALF of ALI mice were effectively reduced by the uvaol. The Bax and caspase-3 expression was reduced, and the Bcl-2 was elevated by the uvaol. The outcomes of histopathological analysis also supported the therapeutic potential of uvaol against ALI. Conclusion: In conclusion, the outcomes of the current exploration highlighted that uvaol considerably prevented the LPS-exposed ALI in mice via its antioxidant and anti-inflammatory effects. Hence, it can be concluded that uvaol can be employed in the treatment of ALI in the future. [ABSTRACT FROM AUTHOR]

Acute lung injury is a life-threatening condition characterized by hypoxemia, pulmonary edema, and inflammation. This comprehensive review delves into the intricate landscape of Acute Lung Injury (ALI) and Acute Respiratory Distress Syndrome (ARDS), shedding light on the multifaceted challenges and advancements in their understanding and treatment. The exploration of pathological features, pharmacological interventions, and long-term outcomes unveils the complexities inherent in managing these critical respiratory conditions. The etiology of ALI/ARDS is diverse and includes direct and indirect insults to the lungs. Key findings underscore the hurdles posed by the heterogeneous patient population, emphasizing the imperative of tailoring interventions based on individual characteristics. Ambiguities surrounding optimal timing, dosing, and duration of pharmacological interventions highlight the need for standardized protocols to ensure consistency in treatment approaches. While advancements in mechanical ventilation, fluid management, and pharmacological agents show promise, the absence of reliable biomarkers for treatment response prediction remains a significant limitation. Recommendations for clinical practice encompass personalized and targeted approaches, leveraging technological advancements for individualized care, and advocating for standardized protocols. The pharmacology of ALI/ARDS is complex and challenging, as no specific drug has been proven to be effective in treating ALI. However, several pharmacological agents have been tested or are under investigation for modulating the inflammatory response, reducing oxidative stress, enhancing alveolar fluid clearance, and preventing fibrosis. On a policy level, there is a call for increased research initiatives, specifically in biomarker identification and large-scale trials for emerging treatments. Acknowledging limitations in the evolving nature of research and study heterogeneity, this review stands as a timely and informative resource, providing valuable insights for healthcare practitioners and policymakers navigating the intricate landscape of ALI and ARDS. Implementing the outlined recommendations holds the potential to enhance patient care and guide future research endeavors in this critical field. [ABSTRACT FROM AUTHOR]

Background: Clazosentan, an endothelin receptor antagonist, has been shown to prevent cerebral vasospasms following subarachnoid hemorrhage (SAH) effectively. However, clazosentan-induced pulmonary edema is a frequently reported adverse effect and a primary reason for discontinuing treatment. The presence of preexisting heart conditions predisposes patients to severe pulmonary edema; thus, the administration of clazosentan is generally contraindicated. Case Description: We report the successful administration of clazosentan in a 58-year-old female patient with SAH and severe heart failure (Takotsubo cardiomyopathy). The patient initially presented with a ruptured left internal carotid posterior communicating artery aneurysm, leading to SAH. She successfully underwent neck clipping, and postoperative treatment to prevent cerebral vasospasm, including clazosentan, was initiated. Following the emergency surgical intervention, she exhibited pulmonary edema and diffused left ventricular hypokinesis with an ejection fraction of 10-20%. Although drug-induced pulmonary edema emerged after the administration of clazosentan, tailored fluid management based on daily cardiac function and ventilator management in response to pulmonary edema enabled the completion of a 2-week clazosentan therapy regimen. This approach guaranteed the patient's stability throughout the treatment period. Neither cerebral vasospasm nor cardiopulmonary complications were observed. Conclusion: This case highlights the importance of a multidisciplinary approach in managing complex patients with severe cardiac comorbidities undergoing clazosentan therapy. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

The aim. To establish the relationship between structural-functional and laboratory parameters in patients with myocardial infarction (MI) and heart failure (HF) undergoing percutaneous coronary intervention (PCI). Materials and methods. We examined 308 MI patients who were divided into 3 groups: 161 patients without signs of acute heart failure (AHF) (group I), 99 with Killip class II-III AHF (group II) and 48 with Killip class IV (cardiogenic shock) (group III). All the patients underwent general clinical examinations: complete blood count, lipid profile, creati-nine, quantitative determination of troponin I, D-dimer, creatine kinase-MB, electrocardiography, coronary angiography with PCI, focused cardiac ultrasound and standard echocardiography over 3-5 days. Results. According to the focused cardiac ultrasound, the majority of MI patients with signs of AHF had preserved left ventricle function, and only 8.2% of patients had left ventricle ejection fraction (LVEF) ˂40%. The most significant structural and functional changes were observed in group II. After PCI, a significant increase in left ventricle contractility was found in all groups, but in the group II, the increase in LVEF was more pronounced. The severity of HF manifestations increased depending on the severity of diastolic dysfunction. Many correlations were established: an inverse relationship between LVEF and the presence of HF, the number ofaffected vessels, proximal left anterior descending artery lesions, low-density lipoprotein cholesterol, and atrium fibrilla-tion; a direct relationship between LVEF and hemoglobin levels and glomerular filtration rate. Conclusions. The vast majority of patients with MI and signs of AHF had preserved left ventricle contractile function. High-grade HF manifestations increase depending on the severity of diastolic dysfunction. Myocardial revascularization in MI pa-tients significantly improves functional and volumetric parameters of myocardial function. Numerous correlations between structural-functional and laboratory parameters in patients with MI and HF who underwent PCI have been established.

A 47-year-old man had localized pulmonary edema (LPE) and a massive pulmonary embolism. The cause of LPE was believed to be a high blood supply to the spared pulmonary artery territories without a thrombus. The patient was successfully treated with unfractionated heparin and thrombolytic agents.

Background: Takotsubo syndrome, which is often induced by physical or psychological stress, is typically a cardiac syndrome with transient left ventricular dysfunction in the absence of obstructive coronary artery disease. Subarachnoid hemorrhage with typical symptoms and signs is frequently reported, whereas the incidence of subarachnoid hemorrhage with Takotsubo syndrome as the prominent manifestation without a typical headache is rarely reported. Case description: We present a rare case of a 63-year-old male patient with cough and fever as the first manifestations, accompanied by mild dizziness, headache, and mental discomfort; however, the patient was eventually diagnosed with atypical subarachnoid hemorrhage with Takotsubo syndrome. The patient underwent general anesthesia downwards stent-assisted spring coil embolization and was discharged from the hospital after postoperative treatment consisting of anti-cerebrovascular spasm, anti-platelet aggregation, and cerebrospinal fluid replacement. Conclusion: This case demonstrates the association between Takotsubo syndrome and subarachnoid hemorrhage. When patients present with unexplained pulmonary edema with mild neurologic symptoms, clinicians should be alerted to subarachnoid hemorrhage and Takotsubo syndrome.

Negative pressure pulmonary edema (NPPE), also known as post-obstructive pulmonary edema, is a rare and life-threatening condition. It occurs when a person breathes against an obstructed glottis, causing negative thoracic pressure in the lungs. This negative pressure can lead to fluid accumulation in the lungs, resulting in pulmonary edema. The obstructed glottis might be caused by laryngospasm, which occurs when the muscles around the larynx involuntarily spasm and can lead to complete upper airway occlusion. This report shares the case of a 33-year-old woman hospitalized for periapical dental abscess, facial swelling, and shortness of breath. The patient exhibited signs of poor oral hygiene. After the exacerbation of her symptoms, she showed signs of asphyxia and decreased oxygen saturation, which led to her intubation. Imaging revealed bilateral pleural effusion and patchy ground glass opacities favoring NPPE. After three days of treatment with diuretics and other conservative measures, her condition was alleviated, and she was extubated. Laryngospasm in the presence of a dental abscess is uncommon. Identification of imaging favoring NPPE in this setting is even more rare. In cases of laryngospasm, prompt intubation is crucial. Therapy with diuretics and other conservative measures can effectively treat NPPE following laryngospasm.

The term transfusion-related acute lung injury (TRALI) was coined in 1985 to describe acute respiratory distress syndrome (ARDS) after transfusion, when another ARDS risk factor was absent; TRALI cases were mostly associated with donor leukocyte antibody. In 2001, plasma from multiparous donors was implicated in TRALI in a randomized controlled trial in Sweden. In 2003 and in many years thereafter, the U.S. Food and Drug Administration reported that TRALI was the leading cause of death from transfusion in the United States. In 2003, the United Kingdom was the first among many countries to successfully reduce TRALI using male-predominant plasma. These successes are to be celebrated. Nevertheless, questions remain about the mechanisms of non-antibody TRALI, the role of blood products in the development of ARDS in patients receiving massive transfusion, the causes of unusual TRALI cases, and how to reduce inaccurate diagnoses of TRALI in clinical practice. Regarding the latter, a study in 2013-2015 at 169 U.S. hospitals found that many TRALI diagnoses did not meet clinical definitions. In 2019, a consensus panel established a more precise terminology for clinical diagnosis: TRALI type I and TRALI type II are cases where transfusion is the likely cause, and ARDS are cases where transfusion is not the likely cause. For accurate diagnosis using these clinical definitions, critical care or pulmonary expertise is needed to distinguish between permeability versus hydrostatic pulmonary edema, to determine whether an ARDS risk factor is present, and, if so, to determine whether respiratory function was stable within the 12 hours before transfusion.

A sympathetic crashing pulmonary edema (SCAPE) is an emergency medical situation necessitating early recognition and treatment. We present a case of a 15-years old male who underwent a toenail excision of his left big toe and who developed SCAPE postoperatively. The low incidence of SCAPE intraoperatively makes it challenging for anesthesiologists to diagnose it. It occurs unexpectedly and precipitously, and it may increase the risks of morbidity and mortality if it is not treated promptly. Our aim is to raise awareness of how to abruptly manage such cases.

Objective To investigate the protective effect of dexmedetomidine on pulmonary edema in rats with hemorrhagic shock after exposure to a plateau environment. Methods A total of 280 SD male rats (10 weeks old, 200~220 g) were randomly divided into 4 groups: the plateau control (sham) group, the hemorrhagic shock after exposure to the plateau environment (HS) group, the lactated Ringer's resuscitation (LR) group, and the dexmedetomidine+lactated Ringer's resuscitation (DEX+LR) group.Using a low-pressure hypoxic chamber to simulate 5 000 m altitude, the rats have stayed the chamber for 48 h to accept pretreatment, injecting oleic acid treatment via the tail vein.After 0.5 h of induction of oleic acid, the rats were slowly drawn blood via the femoral artery (40% to 50% of the blood volume) to establish a model of hemorrhagic shock after exposure to the plateau environment.The effect of dexmedetomidine on pulmonary vascular permeability was observed by changes in lung water content, pulmonary microvascular permeability and alveolar lavage fluid protein concentration after prophylactic administration of dexmedetomidine; The effect of dexmedetomidine on respiratory function was observed by measuring respiratory rate and tidal volume; Pathological changes of lung tissue was detected by HE staining; Blood gas analysis was used to detect the effect of dexmedetomidine on arterial blood gases and survival rate. Results Compared with the sham group, the lung water content, pulmonary microvascular permeability and alveolar lavage fluid protein concentration of the rats in the HS group increased (P < 0.05).The respiratory rate increased (P < 0.05), and the tidal volume and minute ventilation decreased (P < 0.05). Results of HE staining showed that the alveolar wall was thickened, and the lumen of alveoli was partially narrowed, with infiltration of inflammatory cells. Results of arterial blood gas suggested there was acidosis, and rats were in a hypoxic state (P < 0.05).Compared with the HS group, the rats in the LR group had aggravated pulmonary oedema.HE staining showed there was a fusion of alveolar sacs, lung tissue structure was destroyed and appeared obvious inflammatory cell infiltration.Respiratory rate and tidal volume increased, and arterial blood gas got deteriorated (P < 0.05).Dexmedetomidine significantly improved the lung function of rats with hemorrhagic shock pulmonary oedema after exposure to the plateau environment, and there was a decreased in pulmonary microvascular permeability, lung water content and alveolar lavage fluid protein concentration, compared with the lactated Ringer's solution resuscitation group (P < 0.05).The tidal volume, respiratory rate and minute ventilation of the rats tended to be higher than that of the plateau control group (P < 0.05).HE staining results showed that the alveolar structure tended to be intact, and the exudation in the alveolar lumen was reduced or even disappeared.Arterial blood gas analysis suggested that the level of acidosis was improved (P < 0.05), which eventually improved the survival rate. Conclusion Pulmonary edema is more likely to be induced during the resuscitation of rats with hemorrhagic shock after exposure to the plateau environment, and prophylactic administration of dexmedetomidine (10 μg/kg) is effective in preventing the development of pulmonary oedema.

Abstract Background Differentiating cardiogenic vs noncardiogenic causes of respiratory signs can be challenging when echocardiography is unavailable. Radiographic vertebral left atrial size (VLAS) and vertebral heart size (VHS) have been shown to predict echocardiographic left heart size, with VLAS specifically estimating left atrial size. Hypothesis/Objectives Compare the diagnostic accuracy of VLAS and VHS to predict left‐sided congestive heart failure (CHF) in dogs presenting with respiratory signs. Animals One‐hundred fourteen dogs with respiratory signs and radiographic pulmonary abnormalities. Methods Retrospective cross‐sectional study. Dogs had to have an echocardiogram and thoracic radiographs obtained within 24 hours. Diagnosis of CHF was confirmed based on the presence of respiratory signs, cardiac disease, LA enlargement, and cardiogenic pulmonary edema. Results Fifty‐seven dogs had CHF and 57 did not have CHF. Compared to VHS (area under the curve [AUC] 0.85; 95% confidence interval [CI], 0.77‐0.91), VLAS was a significantly (P = .03) more accurate predictor of CHF (AUC, 0.92; 95% CI, 0.85‐0.96). Optimal cutoff for VLAS was >2.3 vertebrae (sensitivity, 93.0%; specificity, 82.5%). Murmur grade (P = .02) and VLAS (P

Background Endobronchial ultrasound (EBUS) is widely used to diagnose lung cancer. Monitored anesthesia care (MAC) can enhance patient comfort and procedural conditions during EBUS. EBUS under MAC is usually safe but can lead to various complications. Case A 34-year-old male who had increased sputum for two months showed an enlarged paratracheal lymph node and planned for lymph node biopsy by EBUS. During EBUS under MAC, an unexpected oxygen saturation decline required intervention. After intubation, copious frothy fluid was suctioned from the bronchi, and oxygenation was recovered. A narrowed trachea and the EBUS bronchoscope might have resulted in upper airway obstruction, and suction performed under these conditions might have caused pulmonary edema. The patient received non-invasive ventilation and high-flow nasal cannula and recovered without complications. Conclusions When there is an expected risk of upper airway obstruction during EBUS, careful preoperative evaluation and preparation are essential to prevent negative pressure pulmonary edema.

Abstract Background Lung ultrasound (LUS) can detect pulmonary edema and it is under consideration to be added to updated acute respiratory distress syndrome (ARDS) criteria. However, it remains uncertain whether different LUS scores can be used to quantify pulmonary edema in patient with ARDS. Objectives This study examined the diagnostic accuracy of four LUS scores with the extravascular lung water index (EVLWi) assessed by transpulmonary thermodilution in patients with moderate-to-severe COVID-19 ARDS. Methods In this predefined secondary analysis of a multicenter randomized-controlled trial (InventCOVID), patients were enrolled within 48 hours after intubation and underwent LUS and EVLWi measurement on the first and fourth day after enrolment. EVLWi and ∆EVLWi were used as reference standards. Two 12-region scores (global LUS and LUS–ARDS), an 8-region anterior–lateral score and a 4-region B-line score were used as index tests. Pearson correlation was performed and the area under the receiver operating characteristics curve (AUROCC) for severe pulmonary edema (EVLWi > 15 mL/kg) was calculated. Results 26 out of 30 patients (87%) had complete LUS and EVLWi measurements at time point 1 and 24 out of 29 patients (83%) at time point 2. The global LUS (r = 0.54), LUS–ARDS (r = 0.58) and anterior–lateral score (r = 0.54) correlated significantly with EVLWi, while the B-line score did not (r = 0.32). ∆global LUS (r = 0.49) and ∆anterior–lateral LUS (r = 0.52) correlated significantly with ∆EVLWi. AUROCC for EVLWi > 15 ml/kg was 0.73 for the global LUS, 0.79 for the anterior–lateral and 0.85 for the LUS–ARDS score. Conclusions Overall, LUS demonstrated an acceptable diagnostic accuracy for detection of pulmonary edema in moderate–to–severe COVID-19 ARDS when compared with PICCO. For identifying patients at risk of severe pulmonary edema, an extended score considering pleural morphology may be of added value. Trial registration: ClinicalTrials.gov identifier NCT04794088, registered on 11 March 2021. European Clinical Trials Database number 2020–005447-23.