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Despite the progress made in medical therapies for treating pulmonary hypertension (PH), a subset of patients remain susceptible to developing a maladaptive right ventricular phenotype. The effective management of end-stage PH presents substantial challenges, necessitating a multidisciplinary approach and early identification of patients prone to acute decompensation. Identifying potential transplant candidates and assessing the feasibility of such a procedure are pivotal tasks that should be undertaken early in the treatment algorithm. Inclusion on the transplant list is contingent upon a comprehensive risk assessment, also considering the specific type of PH and various factors affecting waiting times, all of which should inform the decision-making process. While bilateral lung transplantation is the preferred option, it demands expert intra- and post-operative management to mitigate the heightened risks of pulmonary oedema and primary graft dysfunction in PH patients. Despite the availability of risk assessment tools, the occurrence of acute PH decompensation episodes can be unpredictable, potentially leading to refractory right ventricular failure even with optimal medical intervention, necessitating the use of rescue therapies. Advancements in right ventricular assist techniques and adjustments to graft allocation protocols for the most critically ill patients have significantly enhanced the survival in intensive care, affording the opportunity to endure while awaiting an urgent transplant. Given the breadth of therapeutic options available, specialised centres capable of delivering comprehensive care have become indispensable for optimising patient outcomes. These centres are instrumental in providing holistic support and management tailored to the complex needs of PH patients, ultimately enhancing their chances of a successful transplant and improved long-term prognosis., Competing Interests: Conflict of interest: L. Savale reports grants from Acceleron, Janssen and Merck MSD, and payment or honoraria for lectures, presentations, manuscript writing or educational events from Bayer, Janssen and Merck MSD. A. Benazzo reports grants from XVIVO Perfusion. P. Corris reports participation on a data safety monitoring board or advisory board with MSD and Gossamer. R.D. Davis reports support for attending meetings from WSPHA, and participation on a data safety monitoring board or advisory board with Transmedics Lung EVLP registry. J.T. Granton reports grants from Bayer, Janssen Pharmaceuticals, United Therapeutics, Acceleron, Merck and AstraZeneca, consultancy fees from Merck, and payment or honoraria for lectures, presentations, manuscript writing or educational events from AstraZeneca. The remaining authors have no potential conflicts of interest to disclose., (Copyright ©The authors 2024.)

Luks AM, Grissom CK. Evaluation and Management of the Individual with Recurrent HAPE. High Alt Med Biol. 25:238-246, 2024. Individuals with a history of acute altitude illness often seek recommendations from medical providers on how to prevent such problems on future ascents to high elevation. Although many of these cases can be managed with pharmacologic prophylaxis and counseling about the appropriate rate of ascent alone, there are some situations in which further diagnostic evaluation may also be warranted. One such situation is the individual with recurrent episodes of high altitude pulmonary edema (HAPE), as one of several predisposing factors may be present that warrants additional interventions beyond pharmacologic prophylaxis and slow ascent and may even preclude future travel to high altitude. This review considers this situation in greater detail. Structured around the case of an otherwise healthy 27-year-old individual with recurrent episodes of HAPE who would like to climb Denali (6,190 m), the review examines the known risk factors for disease and then provides guidance regarding when and how to evaluate such individuals and appropriate steps to prevent HAPE on further ascents to high elevation. Except in rare circumstances, a history of recurrent HAPE does not preclude further ascent to high elevation, as a multipronged approach including pharmacologic prophylaxis, careful planning about the rate of ascent, and the degree of physical effort and other strategies, such as preacclimatization, staged ascent, and use of hypoxic tents, can be employed to reduce the risk of recurrence with future travel.

Background: Whether high-flow nasal oxygen can improve clinical signs of acute respiratory failure in acute heart failure (AHF) is uncertain., Objective: To compare the effect of high-flow oxygen with noninvasive ventilation (NIV) on respiratory rate in patients admitted to an emergency department (ED) for AHF-related acute respiratory failure., Design, Settings and Participants: Multicenter, randomized pilot study in three French EDs. Adult patients with acute respiratory failure due to suspected AHF were included. Key exclusion criteria were urgent need for intubation, Glasgow Coma Scale <13 points or hemodynamic instability., Intervention: Patients were randomly assigned to receive high-flow oxygen (minimum 50 l/min) or noninvasive bilevel positive pressure ventilation., Outcomes Measure: The primary outcome was change in respiratory rate within the first hour of treatment and was analyzed with a linear mixed model. Secondary outcomes included changes in pulse oximetry, heart rate, blood pressure, blood gas samples, comfort, treatment failure and mortality., Main Results: Among the 145 eligible patients in the three participating centers, 60 patients were included in the analysis [median age 86 (interquartile range (IQR), 90; 92) years]. There was a median respiratory rate of 30.5 (IQR, 28; 33) and 29.5 (IQR, 27; 35) breaths/min in the high-flow oxygen and NIV groups respectively, with a median change of -10 (IQR, -12; -8) with high-flow nasal oxygen and -7 (IQR, -11; -5) breaths/min with NIV [estimated difference -2.6 breaths/min (95% confidence interval (CI), -0.5-5.7), P  = 0.052] at 60 min. There was a median SpO 2 of 95 (IQR, 92; 97) and 96 (IQR, 93; 97) in the high-flow oxygen and NIV groups respectively, with a median change at 60 min of 2 (IQR, 0; 5) with high-flow nasal oxygen and 2 (IQR, -1; 5) % with NIV [estimated difference 0.8% (95% CI, -1.1-2.8), P  = 0.60]. PaO 2 , PaCO 2 and pH did not differ at 1 h between groups, nor did treatment failure, intubation and mortality rates., Conclusion: In this pilot study, we did not observe a statistically significant difference in changes in respiratory rate among patients with acute respiratory failure due to AHF and managed with high-flow oxygen or NIV. However, the point estimate and its large confidence interval may suggest a benefit of high-flow oxygen., Trial Registration: NCT04971213 ( https://clinicaltrials.gov )., (Copyright © 2024 Wolters Kluwer Health, Inc. All rights reserved.)

High-altitude pulmonary edema (HAPE) is a deadly form of altitude sickness, and there is no effective treatment for HAPE. Dental pulp stem cells (DPSCs) are a type of mesenchymal stem cell isolated from dental pulp tissues and possess various functions, such as anti-inflammatory and anti-oxidative stress. DPSCs have been used to treat a variety of diseases, but there are no studies on treating HAPE. In this study, Sprague-Dawley rats were exposed to acute low-pressure hypoxia to establish the HAPE model, and SOD1-modified DPSCs (DPSCs HiSOD1 ) were administered through the tail vein. Pulmonary arterial pressure, lung water content (LWC), total lung protein content of bronchoalveolar lavage fluid (BALF) and lung homogenates, oxidative stress, and inflammatory indicators were detected to evaluate the effects of DPSCs HiSOD1 on HAPE. Rat type II alveolar epithelial cells (RLE-6TN) were used to investigate the effects and mechanism of DPSCs HiSOD1 on hypoxia injury. We found that DPSCs could treat HAPE, and the effect was better than that of dexamethasone treatment. SOD1 modification could enhance the function of DPSCs in improving the structure of lung tissue, decreasing pulmonary arterial pressure and LWC, and reducing the total lung protein content of BALF and lung homogenates, through anti-oxidative stress and anti-inflammatory effects. Furthermore, we found that DPSCs HiSOD1 could protect RLE-6TN from hypoxic injury by reducing the accumulation of reactive oxygen species (ROS) and activating the Nrf2/HO-1 pathway. Our findings confirm that SOD1 modification could enhance the anti-oxidative stress ability of DPSCs through the Nrf2/HO-1 signalling pathway. DPSCs, especially DPSCs HiSOD1 , could be a potential treatment for HAPE. Schematic diagram of the antioxidant stress mechanism of DPSCs in the treatment of high-altitude pulmonary edema. DPSCs can alleviate oxidative stress by releasing superoxide dismutase 1, thereby reducing ROS production and activating the Nrf2/HO-1 signalling pathway to ameliorate lung cell injury in HAPE., (© 2024. The Author(s), under exclusive licence to Springer Nature Limited.)

Abstract: Venovenous (VV) ECMO is rarely used during decompensated circulatory states. Although VA ECMO is the routine option, VV ECMO may be an option in selected patients. We present a case of pulmonary edema due to acute heart failure in a patient 4- and 12-year post-lung transplantation who received VV ECMO. Using a thoughtful cannulation strategy, VV ECMO, and aggressive ultrafiltration, the patient was successfully decannulated, extubated, and discharged from the hospital. In cardiogenic pulmonary edema, VV ECMO represents an additional, and likely under-utilized tool, especially in patients who are at high risk for ventilator-associated lung injury. Cannula location and size should be given additional consideration to potentially transition to V-AV ECMO configuration if necessary., (Copyright © 2024 Copyright: © 2024 Annals of Cardiac Anaesthesia.)

Pulmonary edema refers to the accumulation of excessive fluid in the alveolar walls and alveolar spaces of the lungs. It is a life-threatening condition with a high mortality rate and requires immediate assessment and management. Use of intravenous nitroglycerin has been advocated for such cases. The authors present a case series of 3 patients who presented to the emergency department with sympathetic crashing acute pulmonary edema (SCAPE) and were managed with high-dose intravenous nitroglycerin and bilevel positive airway pressure support using the SCAPE treatment protocol, leading to early correction of blood pressure, avoidance of endotracheal intubation, and no episodes of hypotension or rebound hypertension. The authors recommend emergency physicians utilize the SCAPE treatment protocol while managing patients with SCAPE., Competing Interests: Conflicts of Interest None declared

A 24-year-old male patient, without further symptoms or comorbidities presented to the emergency room with acute dyspnea after heavy lifting two days before. On auscultation an attenuated vesicular breath was noticed on the right lung. In the initial chest radiograph a right-sided primary spontaneous pneumothorax with minor mediastinal shift was diagnosed. After insertion of a 12-French chest tube the patient's clinical condition deteriorated. The following chest radiograph and computed tomography of the thorax showed a reexpansion pulmonary edema in the right lung. The patient was admitted to the ICU and supportive treatment was initiated. Pulmonary reexpansion edema after drainage of a pneumothorax is a very rare complication with mortality rates reaching up to 20%. The exact pathophysiology remains unknown. Typical Symptoms include dyspnea, hypotension, and tachycardia. To minimize the risk of a pulmonary reexpansion edema, not more than 1200-1800 ml of air should be drained at once and the drainage should be stopped when the patient starts coughing., Competing Interests: The authors declare that they have no conflict of interest., (Thieme. All rights reserved.)

Background and Importance: Acute cardiogenic pulmonary oedema (ACPO) is a common indication for non-invasive ventilation (NIV) in the emergency department (ED). HACOR score of >5 is used to predict NIV failure. The predictive ability of HACOR may be affected by altered physiological parameters in ACPO patients due to medications or comorbidities., Objectives: To validate the HACOR scale in predicting NIV failure among acute cardiogenic pulmonary oedema (ACPO) patients., Design, Settings and Participants: This is a prospective, observational study of consecutive ACPO patients requiring NIV admitted to the ED., Outcome Measure and Analysis: Primary outcome was the ability of the HACOR score to predict NIV failure. Clinical, physiological, and HACOR score at baseline and at 1 h, 12 h and 24 h were analysed. Other potential predictors were assessed as secondary outcomes., Main Results: A total of 221 patients were included in the analysis. Fifty-four (24.4%) had NIV failure. Optimal HACOR score was >5 at 1 h after NIV initiation in predicting NIV failure (AUC 0.73, sensitivity 53.7%, specificity 83.2%). As part of the HACOR score, respiratory rate and heart rate were not found to be significant predictors. Other significant predictors of NIV failure in ACPO patients were acute coronary syndrome, acute kidney injury, presence of congestive heart failure as a comorbid, and the ROX index., Conclusions: The HACOR scale measured at 1 h after NIV initiation predicts NIV failure among ACPO patients with acceptable accuracy. The cut-off level > 5 could be a useful clinical decision support tool in ACPO patient. However, clinicians should consider other factors such as the acute coronary and acute kidney diagnosis at presentation, presence of underlying congestive heart failure and the ROX index when clinically deciding on timely invasive mechanical ventilation., Competing Interests: Declaration of competing interest During the preparation of this work, the authors used Chat GPT 4.0 in order to enhance clarity and readability of selected sentences. After using this tool, the authors reviewed and edited the content as needed and take full responsibility for the content of the publication., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Background: Human records describe pulmonary edema as a life-threatening complication of electric shock. Successful management requires prompt recognition and intensive care. However, in companion animals, electrocutions are rarely reported, even though domestic environments are full of electrical devices and there is always the possibility of accidental injury. Therefore, it is important for veterinarians to know more about this condition in order to achieve successful patient outcomes., Case Presentation: A 3-month-old male Labrador Retriever was presented with a history of transient loss of consciousness after chewing on a household electrical cord. On admission, the puppy showed an orthopneic position with moderate respiratory distress. Supplemental oxygen via nasal catheter was provided, but the patient showed marked worsening of respiratory status. Point-of-care ultrasound exams suggested neurogenic pulmonary edema due to electrical shock close to the central nervous system and increased B-lines without evidence of cardiac abnormalities. Mechanical ventilation of the patient was initiated using volume-controlled mode with a tidal volume of 9 to 15 ml/kg until reaching an end-tidal carbon dioxide ≤ 40 mm Hg, followed by a stepwise lung-recruitment maneuver in pressure-controlled mode with increases of the peak inspiratory pressure (15 to 20 cm H 2 O) and positive end-expiratory pressure (3 to 10 cm H 2 O) for 30 min, and return to volume-controlled mode with a tidal volume of 15 ml/kg until reaching a peripheral oxygen saturation ≥ 96%. Weaning from the ventilator was achieved in six hours, and the patient was discharged two days after admission without neurological or respiratory deficits., Conclusions: We present a rather unusual case of a neurogenic pulmonary edema subsequent to accidental electrocution in a dog. Timely diagnosis by ultrasound and mechanical ventilation settings are described. Our case highlights that pulmonary edema should be considered a potentially life-threatening complication of electrical shock in small animal emergency and critical care medicine., (© 2024. The Author(s).)

Abstract: Swimming-induced pulmonary edema (SIPE) is a rare but life-threatening acute illness that can occur in otherwise healthy athletes and individuals. Also known as immersion pulmonary edema, SIPE presents in swimmers, snorkelers, and SCUBA divers. It occurs in persons under heavy exertion in cold water temperatures, leading to coughing, shortness of breath, and sometimes blood-tinged sputum. Under these conditions, there is increased pulmonary vascular pressure, which may ultimately lead to pulmonary edema. This article synthesizes the latest data on the prevalence, pathophysiology, etiology, risks, short- and long-term complications, and the efficacy of supportive medical treatment interventions., (Copyright © 2024 by the American College of Sports Medicine.)

Negative-pressure pulmonary edema (NPPE) is a rare respiratory complication due to acute upper airway obstruction occurring shortly after extubation. We report a case of NPPE in young adult patient who underwent an eventful general anesthesia. The patient presented laryngospasm followed by acute respiratory distress with pink frothy sputum. The NPPE was initially misdiagnosed, and a preventable tracheostomy was performed. NPPE was managed with mechanical ventilation and diuretics, and the patient had full recovery. Every anesthesiologist should be aware of the diagnosis of NPPE. Early recognition and management are essential to prevent the morbidity associated with NPPE in young healthy patients., (© 2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Treatment of high altitude pulmonary edema (HAPE) can be challenging and is further complicated in the pediatric patient in the prehospital environment. The following case presents a decompensating pediatric patient with HAPE in the prehospital aeromedical environment. It illustrates the potential benefit of continuous positive airway pressure (CPAP) as a treatment modality in the treatment of HAPE.

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., (© 2024. The Author(s).)

Competing Interests: Declaration of interests We declare no competing interests.

Background: Hyperbaric oxygen therapy (HBOT) has several hemodynamic effects including increases in afterload (due to vasoconstriction) and decreases in cardiac output. This, along with rare reports of pulmonary edema during emergency treatment, has led providers to consider HBOT relatively contraindicated in patients with reduced left ventricular ejection fraction (LVEF). However, there is limited evidence regarding the safety of elective HBOT in patients with heart failure (HF), and no existing reports of complications among patients with HF and preserved LVEF. We aimed to retrospectively review patients with preexisting diagnoses of HF who underwent elective HBOT, to analyze HBOT-related acute HF complications., Methods: Research Ethics Board approvals were received to retrospectively review patient charts. Patients with a history of HF with either preserved ejection fraction (HFpEF), mid-range ejection fraction (HFmEF), or reduced ejection fraction (HFrEF) who underwent elective HBOT at two Hyperbaric Centers (Toronto General Hospital, Rouge Valley Hyperbaric Medical Centre) between June 2018 and December 2020 were reviewed., Results: Twenty-three patients with a history of HF underwent HBOT, completing an average of 39 (range 6-62) consecutive sessions at 2.0 atmospheres absolute (ATA) (n = 11) or at 2.4 ATA (n = 12); only two patients received fewer than 10 sessions. Thirteen patients had HFpEF (mean LVEF 55 ± 7%), and seven patients had HFrEF (mean LVEF 35 ± 8%) as well as concomitantly decreased right ventricle function (n = 5), moderate/severe tricuspid regurgitation (n = 3), or pulmonary hypertension (n = 5). The remaining three patients had HFmEF (mean LVEF 44 ± 4%). All but one patient was receiving fluid balance therapy either with loop diuretics or dialysis. Twenty-one patients completed HBOT without complications. We observed symptoms consistent with HBOT-related HF exacerbation in two patients. One patient with HFrEF (LVEF 24%) developed dyspnea attributed to pulmonary edema after the fourth treatment, and later admitted to voluntarily holding his diuretics before the session. He was managed with increased oral diuretics as an outpatient, and ultimately completed a course of 33 HBOT sessions uneventfully. Another patient with HFpEF (LVEF 64%) developed dyspnea and desaturation after six sessions, requiring hospital admission. Acute coronary ischemia and pulmonary embolism were ruled out, and an elevated BNP and normal LVEF on echocardiogram confirmed a diagnosis of pulmonary edema in the context of HFpEF. Symptoms subsided after diuretic treatment and the patient was discharged home in stable condition, but elected not to resume HBOT., Conclusions: Patients with HF, including HFpEF, may develop HF symptoms during HBOT and warrant ongoing surveillance. However, these patients can receive HBOT safely after optimization of HF therapy and fluid restriction., Competing Interests: I have read the journal’s policy and the authors of this manuscript have the following competing interests: RK is a shareholder in the Rouge Valley Hyperbaric Medical Center, Toronto, ON. This does not alter our adherence to PLOS ONE policies on sharing data and materials., (Copyright: © 2024 Schiavo et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)

Background: Because of their high morbidity and mortality, patients with acute pulmonary oedema (APE) require early recognition of symptoms, identification of precipitating factors and admission to specialized care units (cardiac critical care or intensive care). APE is at the crossroads of different specialties (cardiology, emergency medicine and intensive care medicine). Although multidisciplinary expertise and management may be a strength, it can also be a source of confusion, with unexpected heterogeneity in patient care. We hypothesized that the management of severe APE may be heterogeneous between specialties and, in some situations, may differ from international recommendations., Aim: We designed a survey to compare management of different APE phenotypes according to the physicians' medical specialty, and to compare the results with what experts would do and European guidelines., Methods: Four clinical cases of typical APE with questions pertaining to the latest guidelines were designed by a Scientific Committee designated by the French Scientific Societies for Cardiology, Emergency Medicine and Intensive Care Medicine. We focused on oxygenation and ventilation strategies, management of precipitating factors, including timing of coronary revascularization, use of diuretics and management of diuretic resistance, and discharge coverage. From 20 June 2022 until 09 September 2022, the four cases of APE (two during hypertensive crises, two during acute coronary syndromes) were proposed to French physicians involved in APE care, and to experts, using an open online survey. To avoid any diagnostic ambiguity, the diagnosis of APE was given at the beginning of each clinical case., Results: The intention is to present the results at national and international conferences and publish them in a peer-reviewed journal., Conclusions: The results of this survey are intended to pave the way for the generation of novel hypotheses for future clinical trials in case of equipoise between subsets of therapeutic procedures in APE., (Copyright © 2024 Elsevier Masson SAS. All rights reserved.)

Opinion Statement: Individuals who have ever been diagnosed with cancer are at increased risk for cardiovascular conditions during and after cancer treatment. Especially during cancer treatment, cardiovascular conditions can manifest in many ways, including peripheral or pulmonary edema. Edema can indicate volume overload affecting the heart even without other unequivocal evidence of apparent diastolic or systolic left ventricular dysfunction, particularly at rest. We propose a novel algorithm to streamline the diagnostic evaluation and cardiovascular classification for cancer patients with edema. We initially advise prompt evaluation with a chest X-ray and echocardiogram. We then suggest classification into one of five categories based on the timing of presentation of edema relative to cancer treatment, as well as echocardiography results and the presence or absence of hypertension or lymphatic causes of edema. This classification tool can then be utilized to guide further cardiovascular management suggestions. These concurrent syndromes presenting as edema may indicate the development or aggravation of undiagnosed diastolic dysfunction with or without hypertension, even if transiently present only while on cancer treatment., (© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Introduction: Negative pressure pulmonary edema (NPPE) is a potentially life-threatening complication that develops rapidly following acute upper airway obstruction. The condition is rare, dramatic but resolves quickly. Prompt recognition and appropriate supportive treatment may prevent unnecessary investigations and iatrogenic complications., Methods: We describe a spectrum of etiologies and clinical manifestation of pediatric NPPE in our center and review of previous publications., Conclusion: The etiology for the development of NPPE in children has shifted over the years. Although dramatic in presentation, this type of pulmonary edema often resolves quickly with minimal support., (© 2023 The Authors. Pediatric Pulmonology published by Wiley Periodicals LLC.)

This case presents a rare occurrence of re-expansion pulmonary edema following a drainage of pyo-pneumothorax in a 33-year-old patient. The diagnosis was established through a thoracic radiography, and the treatment consisted of symptomatic management, showing positive progress. Later on, the patient was diagnosed with pleural tuberculosis via GeneXpert testing and subsequently initiated on anti-bacterial therapy.This case report aims to shed light on the infrequent pulmonary edema ex vacuo as a complication of pleural drainage. It explores its causes, risk factors, diagnostic approaches, and treatment options. this study highlights the necessity of effective prevention and management strategies., (© 2023. The Author(s).)

Background: Veno-arterial extracorporeal membrane oxygenation (VA-ECMO) flows are titrated to achieve adequate perfusion while attempting to ideally maintain arterial pulse pressure (PP). We assessed risk in patients with low PP defined as <10 mmHg within the first 2 days of support., Methods: Demographics, haemodynamics, echocardiographic and radiological findings were recorded retrospectively in cases conducted between 2014 and 2016. Outcomes were hospital mortality, requirement for renal replacement therapy (RRT) and severe pulmonary oedema (PO)., Results: Of 101 patients, 66.3% were male, mean age was 56 (range 18-71 years), mean duration of support was 6.3 days ± 4.1 days, 37.6% died prior to hospital discharge, 39.6% needed RRT and 11.9% had severe PO. Areas under the receiver operating curves of PP at 48 h for hospital mortality, RRT and severe PO were (respectively): 0.69 (95% CI 0.58-0.80, p = .001), 0.64 (95% CI 0.50-0.77, p = .044), 0.69 (95% CI 0.55-0.82, p = .009). The odds ratio for mortality, RRT, severe PO for those with low PP were (respectively) 2.8 (95% CI 1.01-7.5, p = .04), 3.1 (95% CI 1.11-8.40, p = .026), 7.6 (95% CI 2.06-27.89, p = .001). Central venous pressure, mean arterial pressure were not predictive., Conclusion: PP during the first 2 days of support is predictive of clinically important outcomes in patients supported with VA-ECMO., Competing Interests: Declaration of conflicting interestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Cardiogenic pulmonary edema (CPE) is characterized by the development of acute respiratory failure associated with the accumulation of fluid in the lung's alveolar spaces due to an elevated cardiac filling pressure. All cardiac diseases, characterized by an increasing pressure in the left side of the heart, can cause CPE. High capillary pressure for an extended period can also cause barrier disruption, which implies increased permeability and fluid transfer into the alveoli, leading to edema and atelectasis. The breakdown of the alveolar-epithelial barrier is a consequence of multiple factors that include dysregulated inflammation, intense leukocyte infiltration, activation of procoagulant processes, cell death, and mechanical stretch. Reactive oxygen and nitrogen species (RONS) can modify or damage ion channels, such as epithelial sodium channels, which alters fluid balance. Some studies claim that these patients may have higher levels of surfactant protein B in the bloodstream. The correct approach to patients with CPE should include a detailed medical history and a physical examination to evaluate signs and symptoms of CPE as well as potential causes. Second-level diagnostic tests, such as pulmonary ultrasound, natriuretic peptide level, chest radiograph, and echocardiogram, should occur in the meantime. The identification of the specific CPE phenotype is essential to set the most appropriate therapy for these patients. Non-invasive ventilation (NIV) should be considered early in the treatment of this disease. Diuretics and vasodilators are used for pulmonary congestion. Hypoperfusion requires treatment with inotropes and occasionally vasopressors. Patients with persistent symptoms and diuretic resistance might benefit from additional approaches (i.e., beta-agonists and pentoxifylline). This paper reviews the pathophysiology, clinical presentation, and management of CPE.

Re-expansion pulmonary edema (RPE) after chest drain insertion is rare. The objective of this clinical case report is to highlight the importance of this chest drain insertion complication. A 35-year-old man presented to the emergency department with a chief complaint of shortness of breath and pleuritic chest pain. Further physical examination and radiographic investigations showed a left-sided hemipneumothorax. A chest drain was inserted, but subsequently the patient developed worsening shortness of breath, desaturation, and coughed out pink frothy sputum. Repeated chest radiographic and computed tomographic thorax findings suggested RPE. A nonrebreathable mask with high-flow oxygen was given to the patient to maintain his oxygen saturation. The patient was referred to the cardiothoracic team and was admitted to the hospital. Despite conservative management in the ward, the patient underwent lung decortication. Postdecortication, the left-sided lung re-expanded well, and the patient was discharged home. This case highlighted this rare, potentially fatal complication of chest drain insertion for spontaneous pneumothorax., Competing Interests: Disclosure: The author reports no conflicts of interest., (Copyright © 2023 Wolters Kluwer Health, Inc. All rights reserved.)

Rationale: Flash pulmonary edema is a critical medical condition characterized by sudden and severe fluid accumulation in the lungs, which poses an immediate and life-threatening emergency. This can arise from a variety of underlying causes. This manuscript presents a case of recurrent pulmonary edema that was successfully managed through the insertion of a renal artery stent., Patient Concerns: A 78-year-old woman visited the emergency room with recurrent acute dyspnea. Computed tomography renal angiography revealed renal artery stenosis of a single-functioning kidney., Diagnoses: Flash pulmonary edema caused by renal artery stenosis of a functioning single kidney., Interventions: Percutaneous transluminal angioplasty and stenting were performed for the renal artery stenosis., Outcomes: The patient's kidney function rapidly improved, and she has been free of flash pulmonary edema for 2 years., Lessons: Flash pulmonary edema can have various causes and can immediately be a life-threatening emergency. However, it can be treated with percutaneous revascularization if it is caused by renal artery stenosis. This case report reinforces the importance of accurate and immediate diagnosis when dealing with flash pulmonary edema. This case emphasizes the potential therapeutic benefit of renal artery stenting in the management of flash pulmonary edema caused by renal artery stenosis in patients with a single-functioning kidney., Competing Interests: The datasets generated during and/or analyzed during the current study are publicly available.The authors have no conflicts of interest to disclose., (Copyright © 2023 the Author(s). Published by Wolters Kluwer Health, Inc.)

Competing Interests: Disclosures Dr Toggweiler serves as a consultant for Medtronic, Biosensors, Abbott, Boston Scientific, Medira, AtHeart Medical, Veosource, Teleflex, and Shockwave, has received institutional research grants from Boston Scientific and Fumedica, and holds equity in Hi-D Imaging. Dr Cuculi has received consulting and speaker fees from SIS and Abbott Vascular. The other authors report no conflicts.

Re-expansion pulmonary edema is a serious complication that can occur after minimally invasive cardiac surgery through a right mini-thoracotomy. Herein, we describe two paediatric cases where re-expansion pulmonary edema was observed after simple atrial septal defect closure through a right mini-thoracotomy. This is the first case report of re-expansion pulmonary edema after a paediatric cardiac surgery.

Objective: To retrospectively compare efficacy of a continuous positive airway pressure (CPAP) helmet against standard oxygen supplementation (STD) administered by nasal cannulae in dogs with acute cardiogenic pulmonary edema (ACPE)., Animals: 83 dogs (STD group, n = 41; CPAP group, 42) hospitalized for ACPE (January 2019 to April 2021)., Methods: Mean respiratory rate, heart rate, systolic arterial pressure, and rectal body temperature were compared between and within groups before and at 1 (T1), 2 (T2), 3 (T3), 6 (T6), and 12 (T12) hours from the beginning of STD/CPAP therapy. Duration of oxygen supplementation, hospitalization time, total diuretic dose, additional pharmacological interventions and mortality rates were compared between groups. The veterinary bedside lung ultrasound in emergency score, thoracic radiographs, and arterial blood parameters were compared between and within groups before and at the end of CPAP/STD therapy., Results: Within both groups, clinical parameters decreased during the observation period. Mean respiratory rate and heart rate were significantly lower in the CPAP group than the STD group at T1, T2, T3, T6, and T12. Mean systolic arterial pressure was significantly lower in the CPAP group than the STD group at T2, T3, T6, and T12. Mean oxygen supplementation duration, cumulative loop diuretic dose, and both veterinary bedside lung ultrasound in emergency score and arterial PaCO2 at the end of CPAP/STD therapy were significantly lower in the CPAP group than the STD group. No significant differences were observed in hospitalization time and mortality rates., Clinical Relevance: The addition of helmet CPAP compared with standard oxygen administration showed a faster clinical improvement with lower cumulative loop diuretic and shorter oxygen supplementation in dogs hospitalized for ACPE.

Negative pressure pulmonary edema and alveolar hemorrhage are potentially life-threatening complications after relief of upper airway obstruction. The laryngeal-pharyngeal obstruction results in high negative intrapleural pressures. The increased intrapleural pressures affect the integrity of the alveolo-capillary membrane due to various factors. This review describes clinical symptoms, etiologic factors, pathophysiology and treatment strategies associated with each of these factors. The aim of this review is to equip clinicians with the knowledge base necessary to identify patients at increased risk for negative pressure pulmonary edema and alveolar hemorrhage., Competing Interests: Die Autorinnen/Autoren geben an, dass kein Interessenkonflikt besteht., (Thieme. All rights reserved.)

Background: High-flow nasal cannula (HFNC), which overcomes the disadvantages of the existing low flow mask, is an efficient method that can immediately provide a high volume of heated oxygen to the patient.[1] Therefore, this case reports a case in which HFNC was applied to a pregnant with acute respiratory failure., Case: A 37-year-old woman pregnant (GA 30 + 5 weeks) with twin was diagnosed with preeclampsia. It was decided to perform an emergency Cesarean-section under combined spinal-epidural technique worsening respiratory failure. After delivery, maternal dyspnea was not alleviated applying of O28 L/min via facial mask. Thus, high-flow nasal cannula (HFNC) oxygen therapy was applied (60 L/min, partial pressure of oxygen (FiO2) 80%) and SpO2 subsequently rose to 98% and the patient's dyspnea was resolved., Conclusions: HFNC is a safe device that can effectively provide oxygen to pregnant with acute respiratory failure., Competing Interests: The authors have no funding and conflicts of interest to disclose., (Copyright © 2023 the Author(s). Published by Wolters Kluwer Health, Inc.)

Negative pressure pulmonary edema (NPPE) can occur rapidly after the release of an upper airway obstruction. In general anesthesia, NPPE can be caused by laryngospasm after extubation. This report describes a case in which NPPE was thought to have occurred after extubation during general anesthesia in a disabled person. The patient was a 28-yearold man, 160 cm in height and 56 kg in weight, who was scheduled for dental caries treatment under ambulatory general anesthesia due to intellectual disability. After induction of general anesthesia, nasal intubation was performed after sufficient oral suctioning to remove a large amount of serous secretion. After completion of dental treatment, pressurized extubation was performed after oral suctioning as sufficient spontaneous breathing and body movement were observed. Immediately after extubation, SpO 2 dropped to 80%, subsequently recovering to 99% under oxygen administration at 5 liter/min with an oxygen mask. It dropped to approximately 85% again, however, when administration of oxygen was discontinued. Although communication with the patient was difficult, no expression of anguish or dyspnea was observed. A chest radiograph showed symmetric middle-lobe and lingular segment infiltrates, and the patient was transferred to the nearest general hospital. No obvious clinical findings other than a decrease in SpO 2 were observed, suggesting NPPE as a result of airway narrowing due to secretions.

Objective: To characterize the clinical features of noncardiogenic pulmonary edema (NCPE), etiology, and outcome in dogs and cats. The study also aimed to evaluate associations with mortality., Design: Retrospective study., Setting: University teaching hospital., Animals: Thirty dogs and 1 cat, all client owned., Interventions: None., Measurements and Main Results: Data collected included animal characteristics, clinical history, evaluation of oxygenation, radiographic features, treatments, and outcomes. Causes of NCPE included upper airway obstruction, electrocution, drowning, neurogenic etiology, and unknown. The etiology was known in 21 of 31 cases (68%), while the etiology of the remaining 10 cases (32%) was classified as unknown. The most common cause for NCPE was upper airway obstruction, found in 14 of 31 cases (45%). The majority of thoracic radiographs showed a mixed interstitial-to-alveolar pulmonary pattern with a diffuse distribution (52%). Oxygen therapy was administered to 27 dogs (90%). Furosemide was administered to 12 dogs (40%). The median duration of hospitalization was 48 hours (range: 1-192). Twenty-three animals (74%) survived to discharge. Six dogs were mechanically ventilated, with only 2 of them (33%) surviving to discharge. The requirement for mechanical ventilation was the only parameter associated with mortality (P = 0.03)., Conclusions: NCPE is a heterogenous disease process that is most common in dogs. There are a variety of causes, but upper airway obstruction appears to be the most common. The overall prognosis is good in animals that do not require mechanical ventilation., (© Veterinary Emergency and Critical Care Society 2023.)

Background: Adequate fluid removal to achieve euvolemic status can be difficult in patients with incident peritoneal dialysis (PD). Limited treatments such as increased high dextrose PD solutions and icodextrin are currently available. We reported four incident PD patients whose' ultrafiltration volume was increased after sodium-glucose cotransporter-2 inhibitors., Case Presentation: The four reported cases were diabetic kidney disease stage 5 (cases 1-3) and IgA nephritis (case 4) patients whostartedt PD because of acute pulmonary edema (case 1 and 3), nausea vomiting (case 2), and hyperkalemia (case 4). They had an ultrafiltration volume of 700-1000 ml per day but hpersistentted peripheral pitting edema or pulmonary edema. Their ultrafiltration volincreased after dapagliflozin 5 mg daily, and the fluid overload symptoms ere improved. No hypotension, or hypoglycemia was found, and the urine was not increased during dapagliflozin treatment., Conclusions: SGLT-2 inhibitors may increase ultrafiltration in incident PD patients. More studies are needed to support the safety of SGLT-2 inhibitors in PD patients., (© 2023. The Author(s).)

Background: Scorpion envenomation is associated with several complications. One of the most serious complications is the cardiac involvement in the form of myocarditis that remains the main reason for mortalities associated with scorpion envenomation. The present review aims to elucidate clinical and paraclinical findings associated with scorpion-related myocarditis, and to explore different management strategies and subsequent outcomes., Methods: We searched PubMed, Web of Science, Scopus, and Google Scholar for articles related to keywords of myocarditis associated with scorpion envenomation up to May 1, 2022. Each article was carefully reviewed by two independent researchers. In case of disagreement for inclusion, we sought a third researcher opinion., Results: A total of 703 cases from 30 case reports and 34 case series were included in our review. Myocarditis associated with scorpion envenomation was usually reported in children presenting with cardiopulmonary symptoms including pulmonary edema (60.7%) and shock or hypotension (45.8%). The most common ECG findings are sinus tachycardia (82%) followed by ST-T changes (64.6%). The management typically included inotropes (especially dobutamine), prazosin, diuretics, nitroglycerine and digoxin, when indicated. Mechanical ventilation was required in 36.7% of the patients. Mortality in confirmed scorpion-related myocarditis cases is estimated at 7.3%. Almost all survived cases showed rapid recovery and improvement in the left ventricular function., Conclusion: Even though myocarditis associated with scorpion envenomation is rare, it remains a serious and in some of cases a fatal consequence of scorpion sting. In case of relative presentations, particularly in envenomed children, diagnosis of myocarditis should be considered. Early screening using serial cardiac markers and echocardiography can guide the treatment. Prompt treatment that focuses on cardiogenic shock and pulmonary edema usually results in a favorable outcome., Competing Interests: The authors have declared that no competing interests exist., (Copyright: © 2023 Fereidooni et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)

An early adolescent boy with chronic kidney disease on haemodialysis was referred to the surgical clinic for the creation of an arteriovenous fistula. He was undergoing treatment for dilated cardiomyopathy and extrapulmonary tuberculosis. The patient was haemodynamically stable during the procedure, but he developed rapidly progressing dyspnoea, tachycardia and tachypnoea about 10 min after the vessels were declamped. His blood pressure rapidly rose above 220/120 mm Hg and saturation dropped below 90%. A multidisciplinary team (MDT) constituted of surgeons, nephrologists and intensivists was quickly activated. The patient was put on a mechanical ventilator and resuscitated with parenteral antihypertensives, diuretics, amiodarone and haemodialysis. The patient improved clinically and was discharged on the third postoperative day. Thus, a rapidly activated MDT approach was key in breaking the vicious cycle caused by hypertensive crisis, myocardial dysfunction and impending ventilatory failurethat occurred following access surgery., Competing Interests: Competing interests: None declared., (© BMJ Publishing Group Limited 2023. No commercial re-use. See rights and permissions. Published by BMJ.)

Objective: To review various types of noncardiogenic pulmonary edema (NCPE) in cats and dogs., Etiology: NCPE is an abnormal fluid accumulation in the lung interstitium or alveoli that is not caused by cardiogenic causes or fluid overload. It can be due to changes in vascular permeability, hydrostatic pressure in the pulmonary vasculature, or a combination thereof. Possible causes include inflammatory states within the lung or in remote tissues (acute respiratory distress syndrome [ARDS]), airway obstruction (post-obstructive pulmonary edema), neurologic disease such as head trauma or seizures (neurogenic pulmonary edema), electrocution, after re-expansion of a collapsed lung or after drowning., Diagnosis: Diagnosis of NCPE is generally based on history, physical examination, and diagnostic imaging. Radiographic findings suggestive of NCPE are interstitial to alveolar pulmonary opacities in the absence of signs of left-sided congestive heart failure or fluid overload such as cardiomegaly or congested pulmonary veins. Computed tomography and edema fluid analysis may aid in the diagnosis, while some forms of NCPE require additional findings to reach a diagnosis., Therapy: The goal of therapy for all types of NCPE is to preserve tissue oxygenation and reduce the work of breathing. This may be achieved by removing the inciting cause (eg, airway obstruction) and cage rest in mild cases and supplemental oxygen in moderate cases and may require mechanical ventilation in severe cases., Prognosis: Prognosis is generally good for most causes of veterinary NCPE except for ARDS, although data are scarce for some etiologies of NCPE., (© Veterinary Emergency and Critical Care Society 2023.)

Background: Improvement of oxygenation is the aim in the therapy of high-altitude pulmonary edema (HAPE). However, descent is often difficult and hyperbaric chambers, as well as bottled oxygen, are often not available. We compare Auto-PEEP (AP-Pat), a special kind of pursed lips breathing, against the application of bottled oxygen (O 2 -Pat) in two patients suffering from HAPE., Methods: We compare the effect of these two different therapies on oxygen saturation measured by pulse oximetry (SpO 2 ) over time., Result: In both patients SpO 2 increased significantly from 65-70% to 95%. Above 80% this increase was slower in AP-Pat compared with O 2 -Pat. Therapy started immediately in AP-Pat but was delayed in O 2 -Pat because of organizational and logistic reasons., Conclusions: The well-established therapies of HAPE are always the option of choice, if available, and should be started as soon as possible. The advantage of Auto-PEEP is its all-time availability. It improves SpO 2 nearly as well as 3 L/min oxygen and furthermore has a positive effect on oxygenation lasting for approximately 120 min after stopping. Auto-PEEP treatment does not appear inferior to oxygen treatment, at least in this cross-case comparison. Its immediate application after diagnosis probably plays an important role here.

This case demonstrates the value of perioperative point-of-care ultrasound for rapid bedside evaluation and treatment of pulmonary oedema in an infant. A nine-week-old male infant undergoing cleft lip repair received significant intravenous fluid resuscitation for intraoperative hypotension. After uneventful extubation, he developed increased work of breathing and a gradual decline in oxygen saturation despite supplemental oxygen by way of a facemask. Lung point-of-care ultrasound revealed confluent B-lines in multiple lung fields, consistent with pulmonary oedema, likely from fluid overload. He was treated with furosemide resulting in clinical improvement within 30 minutes.

Acute brain injury (ABI) consists of any acquired insult to the brain and is a significant cause of morbidity and mortality worldwide. Approximately 20% to 30% of patients with ABI develop a lung injury called neurogenic pulmonary edema (NPE), and its development often results in poor outcomes. This article provides a narrative review of the evidence regarding proposed mechanisms of injury, diagnosis, and treatment of NPE in the critical care setting. PubMed and Ovid databases were searched for observational or prospective studies relevant to the diagnosis and treatment of NPE. Overall, studies showed that although the specific mechanisms responsible for NPE remain uncertain, putative mechanisms include vaso- and venoconstriction, catecholamine release with resultant pulmonary vasoconstriction called the "blast injury theory," increased vagal tone, and increased capillary permeability. Diagnosis involves identifying signs of pulmonary edema in patients who experienced a neurologic insult. Management strategies aim to address both brain and lung injury, and treatment modalities appear to work best when balanced toward maintaining a normal physiologic state. In summary, NPE is an often underdiagnosed but important sequela of ABI, which may result in additional long-term morbidity. It is therefore an important entity for providers to recognize and tailor their clinical approach toward.