Pulmonary Edema Research Articles

Effect of atorvastatin on lipopolysaccharide-induced lung inflammation and hypoxia in mice; modulation of HIF-1α, CINC and MIP-2

Background Acute lung injury is a crucial pathological state, particularly in some severe infectious respiratory illnesses, distinguished by acute inflammation, pulmonary edema, hypoxia, and neutrophil recruitment. Cytokine-induced neutrophil chemoattractant (CINC) and macrophage inflammatory protein-2 (MIP-2) play a vital role in neutrophil recruitment. Objective Here, we validated the potential repressing effect of atorvastatin on acute lung injury induced by lipopolysaccharide (LPS) in mice. Materials and methods Mice were injected with LPS (250 μg/kg; i.p.) daily for 7 days, and atorvastatin (25 and 50 mg/kg; orally) daily along with LPS. Results Atorvastatin ameliorated oxidative stress as evidenced by increased reduced glutathione (GSH) and nuclear factor-erythroid 2 related factor 2 (Nrf2) levels and decreased malondialdehyde (MDA) levels. Additionally, it lessened inflammatory biomarkers including tumor necrosis factor-alpha (TNF-α), mitogen-activated protein kinase (MAPK), extracellular signal-regulated kinase (ERK), CINC, and MIP-2, as well as hypoxia biomarker hypoxia-inducible factor–1α (HIF-1α). Moreover, atorvastatin slowed the progression of lung tissue histological lesions. Conclusion Collectively, the present study suggests that, atorvastatin effectively protects against LPS-induced acute lung injury through inhibition of oxidative stress, inflammation, hypoxia, and neutrophil recruitment.

Neutral Polysaccharide from Platycodonis Radix-Ameliorated PM2.5-Induced Lung Injury by Inhibiting the TLR4/NF-κB p65 Pathway and Regulating the Lung and Gut Microbiome.

Platycodonis radix (PR) has been reported to play a protective role in lung injury. However, much less is known about the protective effect and mechanism of its main component PR polysaccharides (PRPs) in particulate matter (PM2.5)-induced lung injury. Here, a neutral polysaccharide (MW: 244.56 kDa) was isolated from PR, mainly composed of Rha, Ara, Gal, Glc, Xyl, and Man. PRPs significantly improved PM2.5-induced pulmonary edema, oxidative damage, and cell apoptosis and downregulated inflammatory factor levels in bronchoalveolar lavage fluid. Mechanistically, PRPs reduced intestinal mucosal barrier damage, thereby lowering serum lipopolysaccharide levels and inhibiting the overactivation of the TLR4/NF-κB signaling pathway in the lung tissue. Notably, PRPs could optimize the composition of pulmonary and intestinal microbiota. Oral administration of PRPs resulted in enrichment of short-chain fatty acid (SCFA)-producing bacteria, thereby upregulating the levels of acetate, butyrate, and isovalerate. Taken together, PRPs have great potential in preventing and repairing the lung injury caused by PM2.5.

Human liver stem cells and derived extracellular vesicles protect from sepsis-induced acute lung injury and restore bone marrow myelopoiesis in a murine model of sepsis

BackgroundSepsis is a condition with high mortality and morbidity, characterized by deregulation of the immune response against the pathogen. Current treatment strategies rely mainly on antibiotics and supportive care. However, there is growing interest in exploring cell-based therapies as complementary approaches. Human liver stem cells (HLSCs) are pluripotent cells of mesenchymal origin, showing some advantages compared to mesenchymal stem cells in terms of immunomodulatory properties. HSLC-derived extracellular vesicles (EVs) exhibited a superior efficacy profile compared to cells due to their potential to get through biological barriers and possibly to avoid tumorigenicity and showed to be effective in vivo and ex vivo models of liver and kidney disease. The potential of HLSCs and their EVs in recovering damage to distal organs due to sepsis other than the kidney remains unknown. This study aimed to investigate the therapeutic potential of the intravenous administration of HSLCs or HSLCs-derived EVs in a murine model of sepsis.ResultsSepsis was induced by caecal ligation and puncture (CLP) on C57/BL6 mice. After CLP, mice were assigned to receive either normal saline, HLSCs or their EVs and compared to a sham group which underwent only laparotomy. Survival, persistence of bacteraemia, lung function evaluation, histology and bone marrow analysis were performed. Administration of HLSCs or HLSC-EVs resulted in improved bacterial clearance and lung function in terms of lung elastance and oedema. Naïve murine hematopoietic progenitors in bone marrow were enhanced after treatment as well. Administration of HLSCs and HLSC-EVs after CLP to significantly improved survival.ConclusionsTreatment with HLSCs or HLSC-derived EVs was effective in improving acute lung injury, dysmyelopoiesis and ultimately survival in this experimental murine model of lethal sepsis.

Automatic B-lines: a tool for minimizing time to diuretic administration in pulmonary edema patients in the emergency department of a developing country

BackgroundEffective management of pulmonary edema in the emergency department (ED) is crucial given its significant global impact on health. This study aimed to investigate the hypothesis: “Does the utilization of Automatic B-lines via ultrasonography in patients with pulmonary edema facilitate faster diuretic administration in a developing country?”MethodsThis retrospective observational study was conducted at a tertiary academic center in Thailand. Patients with pulmonary edema admitted to the ED between January 2023 and June 2024 were enrolled. Ultrasound documentation and electronic ED medical records were compared to assess the time of diuretic administration between patients who had lung ultrasounds utilizing automatic B-lines and those who had manual B-lines counted by physician eye inspection. Multivariate logistic regression was employed to examine the relationship between the use of automatic B-lines and early diuretic administration.ResultsThe study included 134 patients with pulmonary edema. The time to diuretic administration was significantly shorter in the automatic B-lines group (median time [Q1-Q3], 55 min; range, 35–110 min) compared to the non-automatic B-lines group (median time, 100 min; range, 75–145 min). In the multivariable logistic regression analysis, early diuretic administration within 60 min of triage was significantly more likely in the automatic B-lines group (adjusted odds ratio, 1.45; 95% confidence interval, 1.10–2.45) than in the non-automatic B-lines group.ConclusionsIn a developing country, patients with pulmonary edema who had lung ultrasound evaluation with automated B lines experienced a fastest diuresis compared to those who utilized ultrasonography without automatic B lines. Implementing automatic B-lines as an early screening protocol could enhance clinical practice in the ED.

Prehospital treatment of autonomic dysreflexia

Autonomic dysreflexia is a potentially life-threatening condition that can affect people with established spinal cord injuries above the level of T6. If left untreated, it can lead to uncontrolled hypertension causing stroke, seizures, pulmonary oedema and death. In Ireland and the UK, there are approximately 60 000 people living with spinal cord injuries who are at risk of developing autonomic dysreflexia. Despite this, there are no prehospital guidelines on treating the condition to date. This educational article aims to address this gap in knowledge and offer potential treatment options for paramedics and ambulance clinicians, which can be effectively applied to this cohort of patients in the future.

Deep learning model for detection acute cardiogenic pulmonary edema in cases of preeclampsia

<span lang="EN-US">The physiological changes during the pregnancy period increase the risk of developing pulmonary edema and acute respiratory failure. This condition falls under critical medical emergencies associated with maternal mortality. This study utilized a convolutional neural networks (CNN) architectural model employing chest Xray dataset images. CNN utilizes the convolution process by moving a convolutional kernel of a certain size across an image, allowing the computer to derive new representative information from the multiplication of portions of the image with the utilized filter.</span><span lang="EN-US">To simplify, the vanishing gradient issue occurs when information dissipates before reaching its destination due to the lengthy path between input and output layers. This study was developed model for detection acute cardiogenic pulmonary Edema in pre-eclampsia cases using chest Xray images, implemented using PyTorch, Keras, and MxNet. The validated model achieved its optimum with accuracy 90.65% and binary cross-entropy loss (BCELoss) value of 0.4538. It exhibited an improved sensitivity value of 83.514% using a 5% dataset and a specificity value of 57.273%. This indicates an increase in sensitivity value by 83.514% using a 5% data set and a specificity value of 57.273%. The research results demonstrate an improvement in accuracy compared to several similar studies that also utilized CNN models.</span>

Unexpected pulmonary edema following sitting position craniotomy: A venous air embolism complication.

We report a case of a 42-year-old female who had non-cardiogenic pulmonary edema following a setting position craniotomy to remove a left cerebellar pontine angle mass. During the operation, the patient experienced a sudden drop in her end-tidal CO2 levels, which needed an immediate intervention. After ruling out other potential causes, we determined that air venous embolism was the cause of this unexpected and serious complication. However, the condition was self-limited and resolved with supportive treatment after approximately 1 week. This case highlights the importance of recognizing and managing the unexpected complications of venous air embolism, as well as how prompt intervention and supportive treatment are critical for improving patient outcomes.

Verapamil inhibits ferroptosis in septic acute lung injury by blocking L-type calcium channels.

Acute lung injury (ALI) and its severe form, acute respiratory distress syndrome (ARDS), result from pulmonary edema and alveolar-capillary barrier disruption due to inflammation, often triggered by conditions like sepsis. Sepsis-induced ALI (SALI) involves extensive damage to vascular endothelium and alveolar epithelium, leading to respiratory failure. Our study explores ferroptosis, an iron-dependent cell death pathway, and calcium dysregulation in SALI. Elevated cytosolic calcium early in ferroptosis exacerbates lipid peroxidation and cellular damage. We investigated verapamil, a calcium channel blocker, and found it reduces calcium influx, alleviates iron overload, and decreases oxidative stress, protecting against ferroptosis-induced apoptosis in lung cells. These insights suggest targeting ferroptosis pathways, including calcium and iron homeostasis, may offer new therapeutic strategies for SALI, potentially improving outcomes in ALI/ARDS.

A stable rat model of high altitude pulmonary edema established by hypobaric hypoxia combined diurnal temperature fluctuation and exercise.

Hypobaric hypoxia (HH) is regarded as the main cause of high-altitude pulmonary edema (HAPE), however, the effect of diurnal temperature fluctuation and exercise has been overlooked. The aim of current study was to elucidate the role of diurnal temperature fluctuation and exercise in the development of HAPE and establish a reliable experimental rat model. Male SPF Wistar rats were assigned to control group (1400m, 25°C) and five model groups: Model Ⅰ group (6000m, 25°C), Model Ⅱ group (6000m, 2°C), Model Ⅲ group (6000m, 12°C/2°C light/dark cycle), Model IV group (6000m, 2°C, and exercise) and Model V group (6000m, 12°C/2°C light/dark cycle, and exercise). After exposure for 72h, the blood and lung tissues were collected for further research. The rats in Model I group did not show signs of HAPE. Compared with Model I group, the rats in Model II and Model III groups were suffered from more damage, evidence by enhanced oxidative stress and inflammatory reaction, but still did not show signs of HAPE. Model IV and Model V could induce HAPE, display the obvious pathological changes and edema, more serious oxidative stress and inflammatory reaction in lung tissues, suggesting that the key role of exercise in the development of HAPE. The rats in the Model V group showed the best performance in terms of modeling indicators, indicating that diurnal temperature fluctuation could further aggravate the degree of lung edema. In summary, HH combined with diurnal temperature fluctuation and exercise is a stable and reliable modeling method for HAPE, which can be used for subsequent research on the prevention and treatment of HAPE.

Maternal pulmonary hypertension and cardiopulmonary outcomes during delivery hospitalization in the United States: A nationwide study from 2016–2020

BackgroundMaternal pulmonary hypertension can pose substantial morbidity and mortality risks, particularly during labor and delivery. Although maternal pulmonary hypertension is conventionally considered a contraindication to pregnancy, advances in the management of pH may contribute to improving outcomes. ObjectivesIn this nationwide study, we aim to characterize the prevalence of maternal pulmonary hypertension in the United States and its association with adverse cardiopulmonary outcomes during delivery hospitalizations. Study DesignIn this cross-sectional cohort study, we analyzed delivery hospitalizations in the National Inpatient Sample from 2016 to 2020. The primary exposure was maternal pulmonary hypertension. The primary outcome was a composite of maternal cardiopulmonary morbidity events during the delivery hospitalization including: death, heart failure, intraoperative heart failure, pulmonary edema, cardiac arrest, myocardial infarction, ventricular fibrillation, respiratory failure, pneumonia, acute kidney injury, and cardiac conversion. Propensity score matching was used to estimate the association between maternal pulmonary hypertension and adverse cardiopulmonary outcomes, adjusting for sociodemographic variables and validated clinical comorbidities as covariates. Secondary outcomes included mechanical circulatory support utilization, length of stay, and total hospitalization costs. ResultsAmong 18,161,315 delivery hospitalizations, 4,630 patients had pulmonary hypertension, yielding a maternal pulmonary hypertension prevalence of 25 per 100,000 delivery hospitalizations with a yearly trend of increasing prevalence (odds ratio = 1.06, 95 % CI 1.01 to 1.11, P = 0.028). After propensity score matching to create well-balanced groups, 4,560 patients with pulmonary hypertension were compared to 4,560 patients without pulmonary hypertension. In this confounder-adjusted analysis, the primary composite outcome of cardiopulmonary morbidity and mortality occurred in 41.1 % of the PH group compared to 14.4 % in the no PH group (adjusted odds ratio = 4.16, 95 % CI 3.32 to 5.23, P < 0.001). Additionally, patients with PH had a higher incidence of mechanical circulatory support use (adjusted odds ratio = 9.08, 95 % CI 1.14 to 71.81, P = 0.037), longer length of stay (length of stay ratio = 2.82, 95 % CI 2.74 to 2.9, P < 0.001) and higher total hospitalization costs (total cost ratio = 1.67, 95 % CI 1.52 to 1.85, P < 0.001). ConclusionsMaternal pulmonary hypertension is increasing in prevalence and is strongly associated with adverse cardiopulmonary outcomes in the United States, with 41.1% of pH patients experiencing a composite outcome of cardiopulmonary morbidity and mortality during delivery hospitalization. Our findings emphasize the importance of caring for patients with maternal pulmonary hypertension in a multidisciplinary setting at high-acuity centers to ensure appropriate management of cardiopulmonary complications that arise during labor and delivery.

Lysophosphatidylcholine 14:0 Alleviates Lipopolysaccharide-Induced Acute Lung Injury via Protecting Alveolar Epithelial Barrier by Activation of Nrf2/HO-1 Pathway.

Acute lung injury (ALI) is characterized by diffuse alveolar injury and acute non-cardiac pulmonary edema, with high morbidity and mortality. Lysophosphatidylcholine 14:0 (LPC14:0) has anti-inflammatory and anti-oxidative effects in sepsis and bacteremia. We hypothesized that LPC14:0 could be a potential treatment for ALI. Therefore, the effects of LPC14:0 on lung epithelial cells and the underlying mechanism on ALI were investigated. Lipopolysaccharide (LPS) was instilled intratracheally in vivo while the Murine Lung Epithelial-12 was stimulated by tert-butyl hydroperoxide (t-BHP) in vitro to induce the ALI model. In vivo, lung injury was evaluated by histopathological changes and pulmonary edema was assessed by wet/dry ratio. Evans blue infiltration in lung tissue, total protein content, total cell counts and inflammatory factors in bronchoalveolar lavage fluid were evaluated for alveolar permeability. In vitro, cell viability and cell death rate were assessed by cell counting kit-8 and Calcein-AM/PI stain respectively. The expression of ZO-1, Occludin, Nrf2, and HO-1 was evaluated by Western blot. LPC14:0 attenuated the LPS-stimulated lung injury and oxidative stress in vivo, and alleviated the t-BHP-induced cell damage in vitro. Moreover, LPC14:0 significantly inhibited the degradation of the tight junction proteins and activated the Nrf2/HO-1 signaling pathway both in vivo and in vitro. Mechanistically, ML385, the Nrf2 inhibitor, inhibited the protective effects of LPC14:0 on barrier function in vitro. This study first demonstrated that LPC14:0 mitigated LPS-induced ALI and the destruction of tight junctions, at least in part through up-regulation of the Nrf2/HO-1 pathway.

Dexamethasone alleviates acute lung injury in a rat model with venovenous extracorporeal membrane oxygenation support

BackgroundIn recent years, dexamethasone (Dex) has been used to treat acute respiratory distress syndrome (ARDS) in patients with COVID-19 and achieved promising outcomes. Venovenous extracorporeal membrane oxygenation (VV ECMO) support...

Difficult Course of a Teenager’s Cardiogenic Shock

Abstract Fulminant myocarditis is a peculiar condition characterized by sudden-onset diffuse myocardial inflammation leading to hemodynamic compromise. We report the case of a 15-year-old male adolescent, without any cardiovascular history, who presented sudden-onset severe biventricular systolo-diastolic dysfunction leading to cardiogenic shock, 2 weeks after an episode of respiratory tract infection. A comprehensive treatment regimen was initiated including heart failure treatment, inotropic and vasoactive support, antibiotics, antiviral treatment, intravenous immunoglobulin, and glucocorticoids, but with poor evolution. Bridge-to-transplantation therapy was taken into consideration for hemodynamic stabilization. Veno-arterial extracorporeal membrane oxygenation (VA-ECMO) support was initiated, first peripherally, via femoral artery and femoral vein access, but secondary to left ventricle (LV) distension, the patient developed pulmonary edema. To decompress the LV, an echocardiography-guided atrial septostomy was performed, and after 2 days, central cannulation (right atrium – ascending aorta) with another cannula for left atrial venting was done, and the patient remained with open sternum. Five days from the initiation of VA-ECMO the patient underwent an orthotopic heart transplantation by bicaval technique with favorable evolution in the follow-up period. Early initiation of VA-ECMO is a salvage intervention in pediatric patients with fulminant myocarditis, but with multiple possible complications. This paper highlights strategies for the optimization of VA-ECMO.

Hyperbaric Oxygen Protects Acute Lung Injury Secondary to Deinagkistrodon Acutus Venom Poisoning by Regulating Th17/Treg Balance.

To explore the mechanism of hyperbaric oxygen (HBO) intervention on acute lung injury secondary to Deinagkistrodon acutus snake venom poisoning and provide more toxicological and clinical evidence for Deinagkistrodon acutus venom poisoning. Male Kunming mice (n = 96) were randomly divided into four groups: the control group which was not given any interventional treatments, venom group in which each mouse was injected with Deinagkistrodon acutus venom (1 mg/kg) through the tail vein, antivenom group in which each mouse was injected with anti-Deinagkistrodon acutus venom immediately after the model was successfully established, and HBO+antivenom group in which each mouse was given HBO treatment at 1 h, 5 h, 11 h and 23 h following the injection of antivenom. Lung tissues of mice were obtained and processed for the detection of the lung coefficient, the levels of inflammatory factors such as interleukin (IL)-6, IL-10 and IL-17, and the protein expression of retinoic acid receptor (RAR)-related orphan receptor gamma (RORγt) and forkhead box P3 (FOXP3). Separate lung tissue specimens were acquired for hematoxylin-eosin staining. Compared with the venom group, HBO+antivenom group exhibited (1) improved survival rate within 24 h; (2) resolution of pulmonary edema, integrity restoration of alveolar structure, and reduced number of infiltrated inflammatory cells; (3) diminished levels of pro-inflammatory factors and increased abundance of anti-inflammatory factors beginning 2 h after envenomation; and (4) balanced expression of RORγt protein and FOXP3 protein at 24 h after envenomation. HBO combined with antivenom can significantly relieve secondary lung injury in mice poisoned with Deinagkistrodon acutus venom by immediately regulating the balance of helper T cell 17 (Th17)/regulatory T cell (Treg) related proteins.

Lung parenchymal and pleural findings on computed tomography after out-of-hospital cardiac arrest

IntroductionLung injury and the acute respiratory distress syndrome (ARDS) are common after out-of-hospital cardiac arrest (OHCA), but the imaging characteristics of lung parenchymal and pleural abnormalities in these patients have not been well-characterized. We aimed to describe the incidence of lung parenchymal and pleural findings among patients who had return of spontaneous circulation (ROSC) and who underwent computed tomography (CT) of the chest after OHCA. MethodsThis was a retrospective cohort study conducted at two academic hospitals from 2014 to 2019. We included adults successfully resuscitated from OHCA who received a head-to-pelvis or dedicated chest CT scan. The composite primary outcome was the incidence of lung parenchymal and pleural abnormalities. CT scans were overread by attending radiologists and lung parenchymal and pleural findings were categorized based on predefined criteria. Data are presented as absolute numbers and percentages. We examined the associations between CPR duration, time to successful intubation, and outcome using multivariable analyses. ResultsWe evaluated 204 eligible patients. Mean age was 54 years and 33 % were women. An initial shockable rhythm was found in 27 % and in 72 patients (36 %) the presumed etiology of OHCA was cardiac. A total of 133 patients underwent head-to-pelvis CT and 71 patients had dedicated chest CT. The median time from 911 call to CT scan was 2.5 (IQR 2.0–3.4) hours. A total of 160 (78 %) of patients had abnormal lung parenchyma or pleural findings. Patients with longer CPR duration or longer time to successful intubation had a higher incidence of abnormal lung findings on CT. ConclusionOver three-quarters of patients who survived to the hospital post OHCA and received a chest CT had lung parenchymal or pleural abnormalities, the most common of which were aspiration, pulmonary edema, and consolidation/pneumonia. Future planned research will characterize the clinical impact of these findings and whether early chest CT could identify patients at risk for ARDS or other pulmonary complications.

Post-mortem distribution of MDPHP in a fatal intoxication case.

The synthetic cathinone (SC) 3,4-methylenedioxy-α-pyrrolidinohexanophenone (MDPHP), is structurally correlated to the 3,4-methylenedioxypyrovalerone (MDPV). In recent years, the number of intoxication cases has increased even if little is known about the pharmacokinetics properties. The post-mortem (PM) distribution of MDPHP remains largely unexplored. In these reports, MDPHP levels were quantified in blood, gastric content and urine. This study aimed to describe the MDPHP PM distribution in several specimens, i.e. central and peripheral blood (CB and PB), right and left vitreous humor (rVH and lVH), gastric content (GCo), urine (U) and hair. The samples were collected from a cocaine-addicted 30-year-old man with a PM interval estimated in 3-4 h. Autopsy examination revealed unspecific findings, i.e. cerebral and pulmonary edema. No injection marks were observed. Toxicological analyses were performed using a multi-analytical approach: headspace gas chromatography for blood alcohol content (BAC); gas chromatography-mass spectrometry (GC-MS) for the main drugs of abuse; liquid chromatography-tandem mass spectrometry (LC-MS/MS) for benzodiazepines and new psychoactive substances (NPS). BAC was negative (0.02 g/L). MDPHP concentrations were: 1,639.99 ng/mL, CB; 1,601.90 ng/mL, PB; 12,954.13 ng/mL, U; 3,028.54 ng/mL, GCo; 1,846.45 ng/mL, rVH; 2,568.01 ng/mL, lVH; 152.38 (0.0-1.5 cm) and 451.33 (1.5-3.0 cm) ng/mg, hair. Moreover, hair segments were also positive for 3,4-dimethylmethcathinone (DMMC < limit of quantification: 0.01 ng/mg), α-PHP (0.59 ng/mg, 0.0-1.5 cm; 3.07 ng/mg, 1.5-3.0 cm), cocaine (6.58 ng/mg, 0.0-1.5 cm; 22.82 ng/mg, 1.5-3.0 cm), and benzoylecgonine (1.13 ng/mg, 0.0-1.5 cm; 4.30 ng/mg, 1.5-3.0 cm). MDPHP concentrations were significantly higher than those reported in the literature for fatal cases. For these reasons, the cause of death was probably the consumption of a lethal amount of MDPHP. Because CB and PB were similar, PM redistribution was not relevant.

Эффективность алгоритма назначения диуретической терапии под контролем натрийуреза у пациентов с острой декомпенсацией сердечной недостаточности в отделении реанимации и интенсивной терапии: проспективное интервенционное контролируемое исследование

INTRODUCTION: The European Society of Cardiology suggests using early and repeated assessment of sodium content in urine in patients admitted with heart failure to evaluate diuretic therapy. OBJECTIVES: Evaluation of the effectiveness of the algorithm for diuretic therapy under the control of natriuresis in patients with acute decompensation of chronic heart failure (ADCHF) in the intensive care unit (ICU). MATERIALS AND METHODS: A prospective study included 150 patients hospitalized in the ICU with ADCHF. All patients underwent standard physical, laboratory and instrumental examinations. The starting dose of furosemide was 20 mg i/v. After 2 hours, a quantitative assessment of sodium in urine was performed. If the natriuresis was ≥ 70 mmol/l, furosemide was continued at the same dose every 12 hours. If the natriuresis was &lt; 70 mmol/L, the dose of furosemide was doubled. Natriuresis was monitored every 12 hours. RESULTS: In the natriuresis-controlled group the duration of patients' stay in the ICU was significantly shorter (3 vs. 5 days, p = 0.01), achieving euvolemia was significantly more frequent (42 % vs. 12 %, p &lt; 0.05), the daily diuresis in patients was significantly higher on more daily (120 mg vs. 80 mg, p &lt; 0.05) and the total dose of furosemide (420 mg vs. 240 mg, p &lt; 0.05). There was a pronounced decrease in congestion in the group of patients with natriuresis control with less pulmonary (number of B-lines 9.6 ± 1.2 versus 23.4 ± 2.5) and venous congestion (GRADE 0–56 %, 1–20 %, 2–24 %, 3–0 % against 0–20 %, 1–35 %, 2–18 %, 3–27 %) on the 3rd day of hospitalization. CONCLUSION: The inclusion of an algorithm for diuretic therapy under the control of natriuresis in patients with ADCHF in the ICU is effective and contributes to a more pronounced and rapid reduction of congestion, as well as a 1.5-fold reduction of time in the ICU.

Causal relationship between lipidome and acute respiratory distress syndrome

Acute respiratory distress syndrome (ARDS), with high morbidity and mortality, is a common clinical syndrome of acute respiratory failure caused by diffuse lung inflammation and edema. ARDS can precipitate in various ways. The complex pathophysiology of ARDS involves the activation and dysregulation of multiple metabolisms and immune responses. Using summary-level data from a genome-wide association study (GWAS), a two-sample Mendelian randomization (MR) analysis of 179 genetically predicted lipid species and ARDS (375 cases, 406,518 controls) was performed and validated in plasma and pulmonary edema fluid from 24 patients. Furthermore, we used a two-step MR to quantify the effect of immune cell-mediated lipids on ARDS. We identified 8 lipids (Cholesterol, Phosphatidylcholine (14:0_16:0), Phosphatidylcholine (16:0_20:5), Phosphatidylcholine (18:0_18:2), Phosphatidylethanolamine (18:1_18:1), Triacylglycerol (51:2), Triacylglycerol (52:4), and Triacylglycerol (54:3) ) associated with ARDS. The proportions of genetically-predicted lipids mediated by the four types of immune cells were determined. Sensitivity analysis did not reveal any obvious pleiotropy or heterogeneity. Our study demonstrates the power of multivariate genetic analysis in correlated lipidomic data and reveals genetic links between ARDS and lipid species beyond standard lipids.

Edema pulmonar neurogénico secundario a una convulsión: Descripción de un caso y revisión de la literatura

Dyspnea is a common reason for consultation in the emergency department, may be the main manifestation of pulmonary edema, which can be classified as cardiogenic or non-cardiogenic. Within the latter, neurogenic pulmonary edema has been described as a rare complication evidenced in patients with central nervous system lesions, which usually resolves within 48-72 hours after the onset of symptoms. This paper presents a case of a 53-year-old female patient admitted to the emergency department with a generalized tonic epileptic seizure and desaturation, chest imaging showing multilobar alveolar opacities. During the hospitalization, cardiogenic pulmonary edema, pulmonary infection and aspiration pneumonia were ruled out. The clinical and imaging course of the patient confirms self-limited neurogenic pulmonary edema.

Celostna ultrazvočna ocena kongestije pri bolnikih s srčnim popuščanjem – kaj moramo vedeti?

In clinical practice, the assessment of congestion in patients with heart failure is most often based on history, clinical examination, and chest X-ray. Clinical symptoms and signs of congestion or signs of congestion on the radiograph appear only in moderate or severe congestion, which can lead to a delay in the diagnosis and appropriate treatment of patients with heart failure. Ultrasound assessment of pulmonary and systemic venous congestion enables more accurate and early identification of congestion, enables better adjustment of diuretic therapy, and represents an important risk assessment for predicting the treatment outcome in patients with heart failure. For clinical use, ultrasound evaluates systemic venous congestion in the inferior vena cava, internal jugular, hepatic, portal, and interlobar renal veins. In contrast, pulmonary congestion is evaluated with lung ultrasound. Due to the ease of implementation and interpretation, the ultrasound assessment of congestion is accessible to both beginners and those who are not skilled in ultrasound examination of the heart and opens the possibility of using the method to a wide range of doctors who encounter patients with heart failure. In the article, we present individual ultrasound methods for assessing systemic venous and pulmonary congestion, their advantages and disadvantages, and explain the interpretation of the obtained values.