Cardiogenic Edema Research Articles

Predictors for prescription of noninvasive ventilation in the postoperative period of cardiac surgery: a systematic review

Introduction The postoperative (PO) period after cardiac surgery is associated with the occurrence of respiratory complications. Noninvasive positive pressure ventilation (NIPPV) is largely used as a ventilatory support strategy after the interruption of invasive mechanical ventilation. However, the variables associated with NIPPV prescription are unclear. Objective To describe the literature on predictors of NIPPV prescription in patients during the PO period of cardiac surgery. Materials and methods This systematic review was registered on the International Prospective Register of Systematic Reviews (PROSPERO) platform in December 2021 (CRD42021291973). Bibliographic searches were performed in February 2022 using the PubMed, Lilacs, Embase and PEDro databases, with no year or language restrictions. The Predictors for the prescription of NIPPV were considered among patients who achieved curative NIPPV. Results A total of 349 articles were identified, of which four were deemed eligible and were included in this review. Three studies were retrospective studies, and one was a prospective safety pilot study. The total sample size in each study ranged from 109 to 1657 subjects, with a total of 3456 participants, of whom 283 realized NIPPV. Curative NIPPV was the only form of NIPPV in 75% of the studies, which presented this form of prescription in 5–9% of the total sample size, with men around 65 years old being the majority of the participants receiving curative NIPPV. The main indication for curative NIPPV was acute respiratory failure. Only one study realized prophylactic NIPPV (28% of 32 participants). The main predictors for the prescription of curative NIPPV in the PO period of cardiac surgery observed in this study were elevated body mass index (BMI), hypercapnia, PO lung injury, cardiogenic oedema and pneumonia. Conclusions BMI and lung alterations related to gas exchange disturbances are major predictors for NIPPV prescription in patients during the PO period of cardiac surgery. The identification of these predictors can benefit clinical decision-making regarding the prescription of NIPPV and help conserve human and material resources, thereby preventing the indiscriminate use of NIPPV.

Quantitative lung ultrasound spectroscopy, an in vivo clinical study conducted over 101 patients

Lung ultrasound (LUS) is widely adopted to assess the state of the lung surface. However, as standard ultrasound imaging assumptions are unmet in the lung due to the presence of air, essentially this organ cannot be anatomically investigated. Indeed, LUS is mainly based on the analysis of imaging artifacts (horizontal and vertical). Of particular interest is the analysis of vertical artifacts, as they correlate with several pathologies. More specifically, their dependence on frequency was demonstrated to carry important diagnostic information capable to improve LUS specificity. In this study, a new dataset was generated acquiring raw radiofrequency (RF) data from 101 patients (affected by different pathologies, e.g., COVID-19 pneumonia and cardiogenic edema). The ULA-OP research platform was used to collect the data, and a multifrequency approach implemented on both linear and convex probes was adopted. Ultrasound data were thus acquired utilizing orthogonal sub-bands with a 1-MHz bandwidth and with different center frequencies (2–6 MHz). About 12 000 and 3600 multifrequency frames were acquired with convex and linear probes, respectively. Clinical parameters (e.g., FIO2 and LDH) were also stored for all patients. During this meeting, the dataset will be presented together with preliminary results, and its potential applications discussed.

Unconventional interactions of the TRPV4 ion channel with beta-adrenergic receptor ligands.

The transient receptor potential vanilloid 4 (TRPV4) ion channel is present in different tissues including those of the airways. This channel is activated in response to stimuli such as changes in temperature, hypoosmotic conditions, mechanical stress, and chemicals from plants, lipids, and others. TRPV4's overactivity and/or dysfunction has been associated with several diseases, such as skeletal dysplasias, neuromuscular disorders, and lung pathologies such as asthma and cardiogenic lung edema and COVID-19-related respiratory malfunction. TRPV4 antagonists and blockers have been described; nonetheless, the mechanisms involved in achieving inhibition of the channel remain scarce, and the search for safe use of these molecules in humans continues. Here, we show that the widely used bronchodilator salbutamol and other ligands of β-adrenergic receptors inhibit TRPV4's activation. We also demonstrate that inhibition of TRPV4 by salbutamol is achieved through interaction with two residues located in the outer region of the pore and that salbutamol leads to channel closing, consistent with an allosteric mechanism. Our study provides molecular insights into the mechanisms that regulate the activity of this physiopathologically important ion channel.

Suppression of Cardiogenic Edema with Sodium-Glucose Cotransporter-2 Inhibitors in Heart Failure with Reduced Ejection Fraction: Mechanisms and Insights from Pre-Clinical Studies.

In heart failure with reduced ejection fraction (HFrEF), cardiogenic edema develops from impaired cardiac function, pathological remodeling, chronic inflammation, endothelial dysfunction, neurohormonal activation, and altered nitric oxide-related pathways. Pre-clinical HFrEF studies have shown that treatment with sodium–glucose cotransporter-2 inhibitors (SGLT-2i) stimulates natriuretic and osmotic/diuretic effects, improves overall cardiac function, attenuates maladaptive cardiac remodeling, and reduces chronic inflammation, oxidative stress, and endothelial dysfunction. Here, we review the mechanisms and effects of SGLT-2i therapy on cardiogenic edema in various models of HFrEF. Overall, the data presented suggest a high translational importance of these studies, and pre-clinical studies show that SGLT-2i therapy has a marked effect on suppressing the progression of HFrEF through multiple mechanisms, including those that affect the development of cardiogenic edema.

Acute Unilateral Lung Edema Following Reperfusion in a Lung Transplant Recipient: A Case Report Discussing the Role of Double Chambered Right Ventricle

<h3>Introduction</h3> Acute unilateral lung edema immediately following reperfusion of newly transplanted lung is rare. We present a case of a hemodynamic collapse with acute lung edema during a sequential single lung transplantation (LTx) for emphysema in a patient with post-operatively diagnosed double-chambered right ventricle (DCRV). <h3>Case Report</h3> A 61-year old woman underwent LTx. Pre-operative trans-thoracic echocardiography (ECHO) showed only mild signs of pulmonary hypertension with a septal bounce sign. Invasively measured pulmonary pressures were normal at induction. One hour following reperfusion of the first transplanted right lung (RL) the graft developed severe edema and the patient developed severe systemic hypotension. Therefore, urgent VA-ECMO was installed. Trans-esophageal ECHO excluded pulmonary vein stenosis (PVS) of the congested lung (<i>Fig 1, A</i>). A biopsy excluded hyperacute rejection (HAR). After 30 minutes of ECMO support recovery of the graft occured (<i>Fig 1, B</i>). ECMO was continued until post-operative day (POD) 2. Computed tomography (CT) on POD 32 revealed RV hypertrophy, RV outflow tract stenosis causing DCRV (<i>Fig 1, D&E</i>) and reduced sternum-spine diameter. (<i>Fig 1, G</i>). Heart catheterization on POD 87 showed a RVOT gradient of 26 mmHg and severe left ventricular (LV) diastolic dysfunction (DD) (end diastolic pressure 33mmHg). <h3>Summary</h3> The differential diagnosis of intra-operative acute unilateral edema after LTx includes primary graft dysfunction (PGD), PVS, HAR or cardiogenic edema. PGD was unlikely due to the nature and evolution of the edema. Cardiogenic origin is possible based on LV DD. This can be due to underlying cardiac disease, acute ischemia or the effect of DCRV (reverse Bernheim effect: <i>Fig 1, F</i>). It is not clear if the DCRV was present before LTx. Our case demonstrates the essential role of proper assessment of both LV and RV morphology and function before LTx.

Gabapentinoid-induced peripheral edema and acute heart failure: A translational study combining pharmacovigilance data and in vitro animal experiments

IntroductionGabapentinoids are ligands of the α2-δ subunit of voltage-gated calcium channels (Cav) that have been associated with a risk of peripheral edema and acute heart failure in connection with a potentially dual mechanism, vascular and cardiac. Objectives & methodsAll cases of peripheral edema or heart failure involving gabapentin or pregabalin reported to the French Pharmacovigilance Centers between January 1, 1994 and April 30, 2020 were included to describe their onset patterns (e.g., time to onset). Based on these data, we investigated the impact of gabapentinoids on the myogenic tone of rat third-order mesenteric arteries and on the electrophysiological properties of rat ventricular cardiomyocytes. ResultsA total of 58 reports were included (gabapentin n = 5, pregabalin n = 53). The female-to-male ratio was 4:1 and the median age was 77 years (IQR 57–85, range 32–95). The median time to onset were 23 days (IQR 10–54) and 17 days (IQR 3–30) for non-cardiogenic edema and acute heart failure, respectively. Cardiogenic and non-cardiogenic peripheral edema occurred frequently after a dose escalation (27/45, 60%), and the course was rapidly favorable after discontinuation of gabapentinoid (median 7 days, IQR 5–13). On rat mesenteric arteries, gabapentinoids significantly decreased the myogenic tone to the same extent as verapamil and nifedipine. Acute application of gabapentinoids had no significant effect on Cav1.2 currents of ventricular cardiomyocytes. ConclusionGabapentinoids can cause concentration-dependent peripheral edema of early onset. The primary mechanism of non-cardiogenic peripheral edema is vasodilatory edema secondary to altered myogenic tone, independent of Cav1.2 blockade under the experimental conditions tested.

Pulmonary Edema II: Noncardiogenic Pulmonary Edema

There are two categories of pulmonary edema: edema caused by increased capillary pressure (hydrostatic or cardiogenic edema) and edema caused by increased capillary permeability (noncardiogenic pulmonary edema, or acute respiratory distress syndrome [ARDS]). This review focuses on noncardiogenic pulmonary edema and describes the general approach to patients with suspected pulmonary edema. The pathogenesis, diagnosis, treatment, and outcome of noncardiogenic pulmonary edema are reviewed. Miscellaneous causes of pulmonary edema are discussed, including neurologic insults, exposure to high altitude, reexpansion of a collapsed lung, lung transplantation, upper airway obstruction, drugs, and lung resection. Figures include chest scans showing pulmonary edema and noncardiogenic pulmonary edema, an illustration of the differences between cardiogenic and noncardiogenic edema, and a chart comparing lung mechanics and other variables in experimental models of cardiogenic pulmonary edema and noncardiogenic edema. Tables show clinical characteristics of patients with noncardiogenic pulmonary edema, the definition of ARDS, causes of ARDS, and treatments for ARDS that do not involve ventilation. This review contains 3 figures, 9 tables, and 55 references. Key words: acute respiratory distress syndrome, diffuse alveolar damage, noncardiogenic pulmonary edema, pulmonary edema

Pulmonary Edema II: Noncardiogenic Pulmonary Edema

There are two categories of pulmonary edema: edema caused by increased capillary pressure (hydrostatic or cardiogenic edema) and edema caused by increased capillary permeability (noncardiogenic pulmonary edema, or acute respiratory distress syndrome [ARDS]). This review focuses on noncardiogenic pulmonary edema and describes the general approach to patients with suspected pulmonary edema. The pathogenesis, diagnosis, treatment, and outcome of noncardiogenic pulmonary edema are reviewed. Miscellaneous causes of pulmonary edema are discussed, including neurologic insults, exposure to high altitude, reexpansion of a collapsed lung, lung transplantation, upper airway obstruction, drugs, and lung resection. Figures include chest scans showing pulmonary edema and noncardiogenic pulmonary edema, an illustration of the differences between cardiogenic and noncardiogenic edema, and a chart comparing lung mechanics and other variables in experimental models of cardiogenic pulmonary edema and noncardiogenic edema. Tables show clinical characteristics of patients with noncardiogenic pulmonary edema, the definition of ARDS, causes of ARDS, and treatments for ARDS that do not involve ventilation. This review contains 3 figures, 9 tables, and 55 references. Key words: acute respiratory distress syndrome, diffuse alveolar damage, noncardiogenic pulmonary edema, pulmonary edema

Pulmonary Edema I: Cardiogenic Pulmonary Edema

There are two categories of pulmonary edema: edema caused by increased capillary pressure (hydrostatic or cardiogenic edema) and edema caused by increased capillary permeability (noncardiogenic pulmonary edema, or acute respiratory distress syndrome). This review focuses on cardiogenic pulmonary edema and describes the general approach to patients with suspected cardiogenic pulmonary edema. The pathogenesis, diagnosis, treatment, and outcome of cardiogenic pulmonary edema are reviewed. Figures include chest scans showing pulmonary edema and noncardiogenic pulmonary edema, an illustration of the differences between cardiogenic and noncardiogenic edema, and a chart comparing lung mechanics and other variables in experimental models of cardiogenic pulmonary edema and noncardiogenic edema. Tables show clinical characteristics of patients with cardiogenic pulmonary edema and treatment options. This review contains 3 figures, 4 tables, and 24 references. Key words: cardiogenic pulmonary edema, congestive heart failure, pulmonary edema, Starling’s law

Pulmonary Edema I: Cardiogenic Pulmonary Edema

There are two categories of pulmonary edema: edema caused by increased capillary pressure (hydrostatic or cardiogenic edema) and edema caused by increased capillary permeability (noncardiogenic pulmonary edema, or acute respiratory distress syndrome). This review focuses on cardiogenic pulmonary edema and describes the general approach to patients with suspected cardiogenic pulmonary edema. The pathogenesis, diagnosis, treatment, and outcome of cardiogenic pulmonary edema are reviewed. Figures include chest scans showing pulmonary edema and noncardiogenic pulmonary edema, an illustration of the differences between cardiogenic and noncardiogenic edema, and a chart comparing lung mechanics and other variables in experimental models of cardiogenic pulmonary edema and noncardiogenic edema. Tables show clinical characteristics of patients with cardiogenic pulmonary edema and treatment options. This review contains 3 figures, 4 tables, and 29 references Keywords: cardiogenic pulmonary edema, congestive heart failure, pulmonary edema, Starling’s law

Pulmonary Edema I: Cardiogenic Pulmonary Edema

There are two categories of pulmonary edema: edema caused by increased capillary pressure (hydrostatic or cardiogenic edema) and edema caused by increased capillary permeability (noncardiogenic pulmonary edema, or acute respiratory distress syndrome). This review focuses on cardiogenic pulmonary edema and describes the general approach to patients with suspected cardiogenic pulmonary edema. The pathogenesis, diagnosis, treatment, and outcome of cardiogenic pulmonary edema are reviewed. Figures include chest scans showing pulmonary edema and noncardiogenic pulmonary edema, an illustration of the differences between cardiogenic and noncardiogenic edema, and a chart comparing lung mechanics and other variables in experimental models of cardiogenic pulmonary edema and noncardiogenic edema. Tables show clinical characteristics of patients with cardiogenic pulmonary edema and treatment options. This review contains 3 figures, 4 tables, and 24 references. Key words: cardiogenic pulmonary edema, congestive heart failure, pulmonary edema, Starling’s law

NON-CARDIOGENIC PULMONARY EDEMA FOLLOWING CARDIAC ABLATION: WILL THE REAL CULPRIT PLEASE STAND UP?

TOPIC: Diffuse Lung Disease TYPE: Medical Student/Resident Case Reports INTRODUCTION: Non-cardiogenic pulmonary edema (NCPE) is an entity with a variety of etiologies and pathology that include alveolar damage due to direct toxicity or catecholamine surge. We present a case of non-cardiogenic pulmonary edema 48 hours following ablation for atrial fibrillation. CASE PRESENTATION: A 72-year-old woman with a history of atrial fibrillation, coronary artery disease with bypass grafting, and heart failure with preserved ejection fraction presented with sudden onset shortness of breath for a few hours. She had undergone cardiac ablation with pulmonary vein isolation and cavotricuspid isthmus line 2 days prior, with no periprocedural complications. She was tachypneic and hypoxic (oxygen saturation 51% on room air), with reduced breath sounds on auscultation but no peripheral edema or jugular venous distension. Laboratory workup was notable for leukocytosis, elevated N-terminal proBNP (9,853 pg/mL), elevated C-reactive protein (257 mg/L), with normal procalcitonin and negative viral panel, including SARS-CoV-2. Electrocardiography showed no acute abnormalities. Computed tomography (CT) of the chest did not show pulmonary embolism but demonstrated bilateral ground glass opacities. Oxygen was administered via high-flow nasal cannula, and diuresis was initiated in the inpatient setting. Echocardiography revealed mild left ventricular diastolic dysfunction, with left atrial enlargement and mild pulmonary hypertension (39 mm of Hg). Right heart catheterization demonstrated normal filling and pulmonary artery pressures (pulmonary capillary wedge pressure (PCWP) of 6 mm Hg and mean pulmonary artery pressure or 16 mm Hg). Systemic corticosteroids were empirically initiated for suspicion of an inflammatory etiology. The combination of steroids and diuresis produced symptomatic and radiographic improvement, and she was discharged with supplemental oxygen. Her oxygen was unable to be completely weaned off as of follow-up 6 weeks later. DISCUSSION: Catheter ablation for atrial fibrillation is a widely adopted rhythm control strategy with a favorable safety profile. NCPE appears to be an exceedingly rare complication of ablation, with only a few cases being reported in our literature review. The diagnosis of NCPE can be challenging to make, as it must be distinguished for cardiogenic edema. The lack of peripheral edema or jugular venous distension in our patient suggested the absence of cardiac etiology, but a right heart catheterization demonstrating normal PCWP definitively excluded it. Hypotheses for mechanisms for this reaction include a systemic inflammatory response syndrome, autoimmune reaction to ablation, and vagus nerve injury with consequent dysregulation of immunomodulation. Treatment is primarily supportive, including adequate ventilation, with consideration for diuresis and corticosteroids. CONCLUSIONS: NCPE is a rare adverse effect of ablation, and treatment is primarily supportive. REFERENCE #1: Weber R, Minners J, Restle C, et al. Pulmonary edema after extensive radiofrequency ablation for atrial fibrillation. J Cardiovasc Electrophysiol. 2008 Jul;19(7):748-52. DISCLOSURES: No relevant relationships by Dan Kazmierski, source=Web Response No relevant relationships by jacob miller, source=Web Response No relevant relationships by Pius Ochieng, source=Web Response No relevant relationships by NISHANT SHARMA, source=Web Response

The Diagnostic Contribution of Systematic Lung Ultrasonography in Patients Admitted to a Conventional Pulmonology Hospitalization Unit.

Although the evidence to date remains limited, we hypothesized that performing protocolized lung ultrasound (LUS) in patients, admitted to a conventional pulmonology hospitalization unit, could improve diagnostic precision. The main objectives of this study were to evaluate the diagnostic contribution and changes in the treatments administered after performing a protocolized LUS in patients hospitalized in a Pulmonology Department ward. This was a prospective, observational study, which included patients admitted from the Emergency Department to a conventional Pulmonology Department hospitalization unit, after first being evaluated by a pulmonologist. LUS was performed within the first 48 hours of admission. The diagnosis at the time of discharge was used as the reference diagnosis. A total of 180 patients were included in this study. The admitting diagnoses were the decompensation of an underlying obstructive disease in 60 patients (33.3%), respiratory infection in 93 (51.7%), pulmonary thromboembolism (PE) in 9 (5%), exacerbation of an interstitial lung disease in 14 (7.8%), and other causes in 4 cases (2.2%). Ultrasonography provided new information, unsuspected at the patient's admission, in 117 (65%) of the patients by capturing images suggestive of infection in 63 patients (35%), 1 new case of ILD, 23 (12.7%) cases of cardiogenic edema, and pleural pathology in 19 (10.5%), as well as two tumors and indirect data related to a PE. The use of LUS resulted in the decision to change the already established treatment in 17.2% of the cases. LUS provided additive information in more than half of patients that ended up reclassifying or potentially changing diagnosis or treatment. Thus, including LUS in management algorithms could reduce the need for other complementary tests or unnecessary treatments.

Comparison of ETCO2 Value and Blood Gas PCO2 Value of Patients Receiving Non-invasive Mechanical Ventilation Treatment in Emergency Department.

Capnography is the non-invasive measurement and graphic representation of the partial pressure of CO2 in expiration. Although there are many studies in the literature comparing the partial pressure of carbon dioxide (pCO2) and end-tidal CO2 (ETCO2) values in patients who underwent IMV (invasive mechanical ventilation), there are no studies showing their interchangeable applicability in patients who received NIMV (non-IMV). We aimed to evaluate whether the use of ETCO2 in the treatment process can replace pCO2 use in patients scheduled for NIMV treatment in the emergency department. Patients who applied to the emergency department with respiratory distress between March 2019 and January 2020, who were diagnosed with acute cardiogenic edema or acute chronic obstructive pulmonary disease (COPD) exacerbation, and who needed NIMV were included in the study. General characteristics of the patients and the pCO2 and ETCO2 values were measured in the blood gas 1 h after the NIMV application was started. 64.2% (99 patients) of the patients included in the study were male, and 35.8% (55 patients) were female. The mean age of the patients included in the study was 69.1 ± 12.2 years. The mean pCO2 values ​​were measured as 52.6 ± 13.2. The mean of ETCO2 values ​​measured simultaneously was 33.6 ± 10.1. There was a significant difference between the controlled pCO2 values ​​and ETCO2 values ​​at the first hour of NIMV treatment (Z: − 10.640, p < 0.001). The ETCO2 level was found to be different in our patients who received NIMV treatment, which could not be used instead of the pCO2 level.

Acute lung injury - from pathophysiology to treatment.

Acute lung injury is characterized by acute respiratory insufficiency with tachypnea, cyanosis refractory to oxygen, decreased lung compliance, and diffuse alveolar infiltrates on chest X-ray. The 1994 American-European Consensus Conference defined "acute respiratory distress syndrome, ARDS" by acute onset after a known trigger, severe hypoxemia defined by PaO2/FiO2</=200 mm Hg, bilateral infiltrates on chest X-ray, and absence of cardiogenic edema. Milder form of the syndrome with PaO2/FiO2 between 200-300 mm Hg was named "acute lung injury, ALI". Berlin Classification in 2012 defined three categories of ARDS according to hypoxemia (mild, moderate, and severe), and the term "acute lung injury" was assigned for general description or for animal models. ALI/ARDS can originate from direct lung triggers such as pneumonia or aspiration, or from extrapulmonary reasons such as sepsis or trauma. Despite growing understanding the ARDS pathophysiology, efficacy of standard treatments, such as lung protective ventilation, prone positioning, and neuromuscular blockers, is often limited. However, there is an increasing evidence that direct and indirect forms of ARDS may differ not only in the manifestations of alterations, but also in the response to treatment. Thus, individualized treatment according to ARDS subtypes may enhance the efficacy of given treatment and improve the survival of patients.

Penggunaan Ventilasi Mekanik non Invansif Untuk Mengatasi Kegagalan Pernafasan pada Pasien dengan Edema Pulmo Akut Kardiogenik

Background: Cardiogenic Pulmo edema can cause a heterogeneous syndrome with a mortality rate of up to 9.5% (Aliberti et all., 2018).Objective: The purpose of this paper was to explain how effective the use of non-invasive mechanical ventilation in patients with acute pulmonary edema with respiratory failure.&#x0D; Methods: The literature review was compiled by synthesizing and comparing various relevant scientific articles from the literature search results using the online database of Proquest and Clinicalkey Elsevier that have significance related to the management of acute cardiogenic pulmo edema.&#x0D; Result: Compared with conservative therapy, noninvasive mechanical ventilation has been shown more effective in improving oxygenation in patients with acute cardiogenic pulmo edema Non-invasive ventilation can reduce dyspnea, acidosis and hypercapnea faster than standard oxygen therapy. Studies show that compared to endotracheal intubation, non-invasive mechanical ventilation is associated with a lower risk of nosocomial infection, lower antibiotic use, shorter length of stay in intensive care units and lower mortality. Study found that there were no differences betwen the two setting of non-invasive mechanical ventilation used, Bilevel positive Airway Pressure (BiPAP) and Continues positive Airway Pressure (CPAP) in patients outcomes. However, there are absolute and relative contraindications that must be considered, including the effectiveness of the therapy being insignificant when given too late&#x0D; Conclusion: Noninvasive mechanical ventilation can be considered as the first choice in the management of acute cardiogenic pulmonary edema because of its high clinical effectiveness representing a rescue action for patients not improving with conventional oxygen therapy.

A TACO PRESENTATION MIMICKING NEW DIAGNOSIS OF ACUTE MYELOID LEUKEMIA WITH TUMOR LYSIS

SESSION TITLE: Medical Student/Resident Cardiovascular Disease Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Transfusion-associated circulatory overload (TACO) should be suspected in patients who progress into acute respiratory distress and decompensate within several hours of a blood transfusion. TACO is separated from transfusion-related acute lung injury (TRALI) physiologically in development of hydrostatic cardiogenic edema rather than permeability edema. According to the NHSN (National Healthcare Safety Network) 2016-TACO clinical definition, the criteria consists of new onset dyspnea and cough, positive fluid balance, elevation in brain natriuretic peptide (BNP), and radiographic findings of pulmonary edema with evidence of left heart failure. Unfortunately, patients with leukemia, previous stem cell transplants, and other hematologic disorders can be more predisposed to TRALI; the risk factors are unclear although HLA incompatibility is theorized to be associated. Although TRALI has been mentioned in a few case reports for leukemia patients, interestingly TACO has not been described at all. CASE PRESENTATION: A 58-year-old male, otherwise healthy, initially presented with fatigue and shortness of breath. He was hemodynamically stable, and labs showed hemoglobin of 4.2 (normal 13.5—17.5), white blood cell count 20.1 (4.5—11.0), and platelet count 43 (160—420), BNP 617 (0—900 pg/ml). He received one unit of packed red blood cells and in several hours became hypoxic and tachypneic, hypertensive to 233/160, and required intubation. Repeat BNP was 1,676. Chest CT (Figure 1) showed bilateral pleural effusions and concern for ARDS. An echocardiogram showed new severely reduced systolic function with ejection fraction (EF) of 29% along with grade 2 diastolic dysfunction (Figure 2). Given flash pulmonary edema and a rising WBC count, he was given aggressive diuresis and broad spectrum antibiotics. WBC trended as high as 71.7, creatinine worsened to 2.0 (0.8—1.4 mg/dl), uric acid increased to 11.1 (3.7—7.0 mg/dl) and LDH worsened to 2,907 (87-241 units/L). Bone marrow biopsy showed hypercellular marrow with 21% blasts, trilineage dyspoiesis, consistent with acute myeloid leukemia with myelodysplasia related changes (AML-MRC) with positive CD117 stain. Patient was treated with rasburicase and allopurinol for tumor lysis. Repeat echo showed recovered EF to 55%, and patient was started on daunorubicin and cytarabine for chemotherapy. DISCUSSION: Signs of volume overload such as shortness of breath can occasionally be the clinical presentation of AML. Transfusion of packed RBCs was thought to contribute to acute cardiogenic pulmonary edema. This patient fulfilled all criteria of TACO surveillance diagnosis including acute respiratory distress within 6 hours of transfusion, pulmonary edema, volume overload, and BNP elevation. CONCLUSIONS: This case aims to remind the clinician to be cognizant of underlying etiologies that can "tip over” the threshold for TACO, such as leukemia. Reference #1: Semple JW, Rebetz J, Kapur R. Transfusion-associated circulatory overload and transfusion-related acute lung injury. Blood. 2019 Apr 25;133(17):1840-1853. doi:10.1182/blood-2018-10-860809. Epub 2019 Feb 26. Review. Reference #2: Ido, K., Aoyama, Y., Nagasaki, J., Koh, S., Ichihara, H., Harada, H., … Mugitani, A. (2017). Pulmonary Involvement of Acute Myeloid Leukemia Mimicking Transfusion-related Acute Lung Injury. Internal medicine (Tokyo, Japan), 56(18), 2493–2496. doi:10.2169/internalmedicine.8505-16 Reference #3: Kuriyan M. Commentary on TRALI in leukemia. J Pediatr Hematol Oncol. 2006 Jun;28(6):328-30. DISCLOSURES: No relevant relationships by Jonathan Chang, source=Web Response No relevant relationships by JENNIFER CHIURCO, source=Web Response No relevant relationships by Hanyuan Shi, source=Web Response No relevant relationships by Justin Spraglin, source=Web Response

The emerging role of lung ultrasound in COVID-19 pneumonia.

In the last decades lung ultrasound (LUS) has become of crucial importance in the evaluation and monitoring of a widely range of pulmonary diseases. One of the major benefits which favours this examination, is that this is a non-invasive, low-cost and radiation-free imaging modality which allows repeated imaging. LUS plays an important role in a wide range of pathologies, including cardiogenic oedema, acute respiratory distress syndrome and fibrosis. Specific LUS findings have proved useful and predictive of acute respiratory distress syndrome which is of particular relevance in the suspicion and monitoring of patients with lung disease. Furthermore, several studies have confirmed the role of LUS in the screening of interstitial lung diseases in connective tissue diseases. Given these data, LUS will likely play an important role in the management of COVID-19 patients from identification of specific abnormalities corresponding to definite pneumonia phases and CT scans findings. In addition, LUS could allow reduction in the exposure of health-care workers to potential infection. Herein, we provide a summary on emerging role of lung ultrasound in COVID-19 pneumonia.

Urgent reconsideration of lung edema as a preventable outcome in COVID-19: inhibition of TRPV4 represents a promising and feasible approach.

Lethality of coronavirus disease (COVID-19) during the 2020 pandemic, currently still in the exponentially accelerating phase in most countries, is critically driven by disruption of the alveolo-capillary barrier of the lung, leading to lung edema as a direct consequence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. We argue for inhibition of the transient receptor potential vanilloid 4 (TRPV4) calcium-permeable ion channel as a strategy to address this issue, based on the rationale that TRPV4 inhibition is protective in various preclinical models of lung edema and that TRPV4 hyperactivation potently damages the alveolo-capillary barrier, with lethal outcome. We believe that TRPV4 inhibition has a powerful prospect at protecting this vital barrier in COVID-19 patients, even to rescue a damaged barrier. A clinical trial using a selective TRPV4 inhibitor demonstrated a benign safety profile in healthy volunteers and in patients suffering from cardiogenic lung edema. We argue for expeditious clinical testing of this inhibitor in COVID-19 patients with respiratory malfunction and at risk for lung edema. Perplexingly, among the currently pursued therapeutic strategies against COVID-19, none is designed to directly protect the alveolo-capillary barrier. Successful protection of the alveolo-capillary barrier will not only reduce COVID-19 lethality but will also preempt a distressing healthcare scenario with insufficient capacity to provide ventilator-assisted respiration.

Semiquantitative Ultrasound Assessment of Lung Aeration Correlates With Lung Tissue Inflammation

We studied the relationship between ultrasound-assessed lung aeration and inflammation in a particular population of ventilated preterm neonates with mild-to-moderate lung inflammation and no congenital heart defect. Lung aeration estimated by a semiquantitative lung ultrasound score significantly correlated with several inflammatory markers both at cellular (neutrophil count in bronchoalveolar lavage: ρ = 0.400, p = 0.018) and molecular level (total proteins: ρ = 0.524, p = 0.021; interleukine-8: ρ = 0.523, p = 0.021; granulocytes-macrophages colony stimulating factor: ρ = 0.493, p = 0.020; all measured in bronchoalveolar lavage and expressed as epithelial lining fluid concentrations). Lung ultrasound might detect changes in lung aeration attributable to mild-to-moderate local inflammation if cardiogenic lung edema is excluded. Thus, it is possible to describe some levels of lung inflammation with semiquantitative lung ultrasound.