Early Restrictive Fluid Resuscitation has no Clinical Advantage in Experimental Severe Pediatric Acute Respiratory Distress Syndrome

2021 ◽  
Author(s):  
Sarah Anne Ingelse ◽  
Marloes M IJland ◽  
Lex M. van Loon ◽  
Reinout A Bem ◽  
Job BM van Woensel ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Pulmonary Edema ◽  
Distress Syndrome ◽  
Dry Weight ◽  
Fluid Restriction ◽  
Arterial Blood ◽  
Early Fluid

Background: Intravenous fluids are widely used to treat circulatory deterioration in pediatric acute respiratory distress syndrome (PARDS). However, the accumulation of fluids in the first days of PARDS is associated with adverse outcome. As such, early fluid restriction may prove beneficial, yet the effects of such a fluid strategy on the cardio-pulmonary physiology in PARDS is unclear. In this study, we compared the effect of a restrictive to a liberal fluid strategy on hemodynamic response and the formation of pulmonary edema in an animal model of PARDS. Methods: Sixteen mechanically ventilated lambs (2-6 weeks) received oleic acid infusion to induce PARDS and were randomized to a restrictive or liberal fluid strategy during a 6-hour period of mechanical ventilation. Transpulmonary thermodilution determined extravascular lung water (EVLW) and cardiac output (CO) Post-mortem lung wet-to-dry weight ratios were obtained by gravimetry. Results: Restricting fluids significantly reduced fluid intake, but increased use of vasopressors among animals with PARDS. Arterial blood pressure was similar between groups, yet CO declined significantly in animals receiving restrictive fluids (p=0.005). There was no difference in EVLW over time (p=0.111) and lung wet-to-dry weight ratio (6.1 IQR 6.0-7.3 vs. 7.1 IQR 6.6-9.4 restrictive vs. liberal, p=0.725) between fluid strategies. Conclusions: Both fluid strategies stabilized blood pressure in this model, yet early fluid restriction abated CO. Early fluid restriction did not limit the formation of pulmonary edema, therefore this study suggests that in the early phase of PARDS a restrictive fluid strategy is not beneficial in terms of immediate cardio-pulmonary effects.

scholarly journals Early effects of ventilatory rescue therapies on systemic and cerebral oxygenation in mechanically ventilated COVID-19 patients with acute respiratory distress syndrome: a prospective observational study

Critical Care ◽  
2021 ◽  
Vol 25 (1) ◽  
Author(s):  
Chiara Robba ◽  
◽  
Lorenzo Ball ◽  
Denise Battaglini ◽  
Danilo Cardim ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Acute Respiratory Distress Syndrome ◽  
Observational Study ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Prospective Observational Study ◽  
Distress Syndrome ◽  
Cerebral Oxygenation ◽  
Arterial Blood ◽  
Early Effects

Abstract Background In COVID-19 patients with acute respiratory distress syndrome (ARDS), the effectiveness of ventilatory rescue strategies remains uncertain, with controversial efficacy on systemic oxygenation and no data available regarding cerebral oxygenation and hemodynamics. Methods This is a prospective observational study conducted at San Martino Policlinico Hospital, Genoa, Italy. We included adult COVID-19 patients who underwent at least one of the following rescue therapies: recruitment maneuvers (RMs), prone positioning (PP), inhaled nitric oxide (iNO), and extracorporeal carbon dioxide (CO2) removal (ECCO2R). Arterial blood gas values (oxygen saturation [SpO2], partial pressure of oxygen [PaO2] and of carbon dioxide [PaCO2]) and cerebral oxygenation (rSO2) were analyzed before (T0) and after (T1) the use of any of the aforementioned rescue therapies. The primary aim was to assess the early effects of different ventilatory rescue therapies on systemic and cerebral oxygenation. The secondary aim was to evaluate the correlation between systemic and cerebral oxygenation in COVID-19 patients. Results Forty-five rescue therapies were performed in 22 patients. The median [interquartile range] age of the population was 62 [57–69] years, and 18/22 [82%] were male. After RMs, no significant changes were observed in systemic PaO2 and PaCO2 values, but cerebral oxygenation decreased significantly (52 [51–54]% vs. 49 [47–50]%, p < 0.001). After PP, a significant increase was observed in PaO2 (from 62 [56–71] to 82 [76–87] mmHg, p = 0.005) and rSO2 (from 53 [52–54]% to 60 [59–64]%, p = 0.005). The use of iNO increased PaO2 (from 65 [67–73] to 72 [67–73] mmHg, p = 0.015) and rSO2 (from 53 [51–56]% to 57 [55–59]%, p = 0.007). The use of ECCO2R decreased PaO2 (from 75 [75–79] to 64 [60–70] mmHg, p = 0.009), with reduction of rSO2 values (59 [56–65]% vs. 56 [53–62]%, p = 0.002). In the whole population, a significant relationship was found between SpO2 and rSO2 (R = 0.62, p < 0.001) and between PaO2 and rSO2 (R0 0.54, p < 0.001). Conclusions Rescue therapies exert specific pathophysiological mechanisms, resulting in different effects on systemic and cerebral oxygenation in critically ill COVID-19 patients with ARDS. Cerebral and systemic oxygenation are correlated. The choice of rescue strategy to be adopted should take into account both lung and brain needs. Registration The study protocol was approved by the ethics review board (Comitato Etico Regione Liguria, protocol n. CER Liguria: 23/2020).

Acute respiratory failure and acute respiratory distress syndrome

2018 ◽  
Author(s):  
Luciano Gattinon ◽  
Eleonora Carlesso
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Respiratory Failure ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Partial Pressure ◽  
Distress Syndrome ◽  
Gas Analysis ◽  
Chronic Obstructive ◽  
Low Oxygen ◽  
Arterial Blood

Respiratory failure (RF) is defined as the acute or chronic impairment of respiratory system function to maintain normal oxygen and CO2 values when breathing room air. ‘Oxygenation failure’ occurs when O2 partial pressure (PaO2) value is lower than the normal predicted values for age and altitude and may be due to ventilation/perfusion mismatch or low oxygen concentration in the inspired air. In contrast, ‘ventilatory failure’ primarily involves CO2 elimination, with arterial CO2 partial pressure (PaCO2) higher than 45 mmHg. The most common causes are exacerbation of chronic obstructive pulmonary disease (COPD), asthma, and neuromuscular fatigue, leading to dyspnoea, tachypnoea, tachycardia, use of accessory muscles of respiration, and altered consciousness. History and arterial blood gas analysis is the easiest way to assess the nature of acute RF and treatment should solve the baseline pathology. In severe cases mechanical ventilation is necessary as a ‘buying time’ therapy. The acute hypoxemic RF arising from widespread diffuse injury to the alveolar-capillary membrane is termed Acute Respiratory Distress Syndrome (ARDS), which is the clinical and radiographic manifestation of acute pulmonary inflammatory states.

Acute respiratory failure and acute respiratory distress syndrome

2015 ◽  
Author(s):  
Luciano Gattinon ◽  
Eleonora Carlesso
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Respiratory Failure ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Partial Pressure ◽  
Distress Syndrome ◽  
Gas Analysis ◽  
Chronic Obstructive ◽  
Low Oxygen ◽  
Arterial Blood

Respiratory failure (RF) is defined as the acute or chronic impairment of respiratory system function to maintain normal oxygen and CO2 values when breathing room air. ‘Oxygenation failure’ occurs when O2 partial pressure (PaO2) value is lower than the normal predicted values for age and altitude and may be due to ventilation/perfusion mismatch or low oxygen concentration in the inspired air. In contrast, ‘ventilatory failure’ primarily involves CO2 elimination, with arterial CO2 partial pressure (PaCO2) higher than 45 mmHg. The most common causes are exacerbation of chronic obstructive pulmonary disease (COPD), asthma, and neuromuscular fatigue, leading to dyspnoea, tachypnoea, tachycardia, use of accessory muscles of respiration, and altered consciousness. History and arterial blood gas analysis is the easiest way to assess the nature of acute RF and treatment should solve the baseline pathology. In severe cases mechanical ventilation is necessary as a ‘buying time’ therapy. The acute hypoxemic RF arising from widespread diffuse injury to the alveolar-capillary membrane is termed Acute Respiratory Distress Syndrome (ARDS), which is the clinical and radiographic manifestation of acute pulmonary inflammatory states.

scholarly journals Effects of PDE3 Inhibitor Olprinone on the Respiratory Parameters, Inflammation, and Apoptosis in an Experimental Model of Acute Respiratory Distress Syndrome

2020 ◽  
Vol 21 (9) ◽  
pp. 3382
Author(s):  
Petra Kosutova ◽  
Pavol Mikolka ◽  
Sona Balentova ◽  
Marian Adamkov ◽  
Andrea Calkovska ◽  
...  
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Arterial Oxygen Saturation ◽  
Oxygenation Index ◽  
Arterial Oxygen ◽  
Arterial Blood ◽  
Respiratory Parameters ◽  
Pde3 Inhibitor

This study aimed to investigate whether a selective phosphodiesterase-3 (PDE3) inhibitor olprinone can positively influence the inflammation, apoptosis, and respiratory parameters in animals with acute respiratory distress syndrome (ARDS) model induced by repetitive saline lung lavage. Adult rabbits were divided into 3 groups: ARDS without therapy (ARDS), ARDS treated with olprinone i.v. (1 mg/kg; ARDS/PDE3), and healthy ventilated controls (Control), and were oxygen-ventilated for the following 4 h. Dynamic lung–thorax compliance (Cdyn), mean airway pressure (MAP), arterial oxygen saturation (SaO2), alveolar-arterial gradient (AAG), ratio between partial pressure of oxygen in arterial blood to a fraction of inspired oxygen (PaO2/FiO2), oxygenation index (OI), and ventilation efficiency index (VEI) were evaluated every hour. Post mortem, inflammatory and oxidative markers (interleukin (IL)-6, IL-1β, a receptor for advanced glycation end products (RAGE), IL-10, total antioxidant capacity (TAC), 3-nitrotyrosine (3NT), and malondialdehyde (MDA) and apoptosis (apoptotic index and caspase-3) were assessed in the lung tissue. Treatment with olprinone reduced the release of inflammatory mediators and markers of oxidative damage decreased apoptosis of epithelial cells and improved respiratory parameters. The results indicate a future potential of PDE3 inhibitors also in the therapy of ARDS.

Gadobutrol-induced acute respiratory distress syndrome rescued by intravenous immunoglobulin and extracorporeal membrane oxygenation

2021 ◽  
Author(s):  
Yu-Chen Chen ◽  
Yi-Chih Hsu ◽  
Hsiang-Cheng Chen ◽  
CHUN-CHI LU
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Extracorporeal Membrane Oxygenation ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Intravenous Immunoglobulin ◽  
Distress Syndrome ◽  
Rapid Progression ◽  
Membrane Oxygenation ◽  
Arterial Blood ◽  
Ige Mediated

Abstract BackgroundGadobutrol-induced life-threatening allergies, such as acute respiratory distress syndrome (ARDS), is rarely reported. The severe allergies publishing in previous literature report involves IgE and tryptase-mediated immune responses. Gadobutrol-related non-IgE-mediated allergy has not been reported.Case presentationA 39-year-old woman underwent Gadobutrol-contrast magnetic resonance imaging of both lower limbs for clinically suspected vasculitis. One hour after injection of 8 ml Gadobutrol, the patient developed dizziness without respiratory symptoms. Eight hours after the contrast injection, she exhibited vomiting, dyspnea, and rapid progression of edema. She visited the emergency room, where chest imaging showed increased infiltration in both lungs. Arterial blood gas analysis revealed hypoxemia when she was given 100% inspired oxygen. The patient was admitted to intensive care unit and received inotropic agents. Extracorporeal membrane oxygenation was applied due to the diagnosis of ARDS and persistent hypoxia after using mechanical ventilation. Systemic intravenous glucocorticoid and antihistamine were prescribed for allergic reaction. Contrast-relevant non-IgE-mediated allergy was confirmed by detailed medical record and laboratory data. An additional 2 days of intravenous immunoglobulin was prescribed. By 3 days after admission, the patient’s shock and acute respiratory distress syndrome had responded great. She was discharged 13 days after admission.ConclusionsHere, we present the first case of gadobutrol-induced non-IgE-mediated allergy complicated by ARDS. This condition was successfully rescued by dual therapy of venovenous extracorporeal membrane oxygenation and intravenous immunoglobulin without any complications.

Pulmonary Edema II: Noncardiogenic Pulmonary Edema

2017 ◽  
Author(s):  
Annette Esper ◽  
Greg S Martin ◽  
Gerald W. Staton Jr
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Pulmonary Edema ◽  
Distress Syndrome ◽  
Diffuse Alveolar Damage ◽  
Lung Resection ◽  
Upper Airway ◽  
Experimental Models ◽  
Lung Mechanics

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

2017 ◽  
Author(s):  
Annette Esper ◽  
Greg S Martin ◽  
Gerald W. Staton Jr
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Pulmonary Edema ◽  
Distress Syndrome ◽  
Diffuse Alveolar Damage ◽  
Lung Resection ◽  
Upper Airway ◽  
Experimental Models ◽  
Lung Mechanics

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

Clinical and pathological features of fat embolism with acute respiratory distress syndrome

2007 ◽  
Vol 113 (6) ◽  
pp. 279-285 ◽  
Author(s):  
Shang Jyh Kao ◽  
Diana Yu-Wung Yeh ◽  
Hsing I. Chen
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Partial Pressure ◽  
Alveolar Macrophages ◽  
Distress Syndrome ◽  
Fat Embolism ◽  
Arterial Partial Pressure ◽  
Arterial Blood ◽  
Blood Ph

FES (fat embolism syndrome) is a clinical problem, and, although ARDS (acute respiratory distress syndrome) has been considered as a serious complication of FES, the pathogenesis of ARDS associated with FES remains unclear. In the present study, we investigated the clinical manifestations, and biochemical and pathophysiological changes, in subjects associated with FES and ARDS, to elucidate the possible mechanisms involved in this disorder. A total of eight patients with FES were studied, and arterial blood pH, PaO2 (arterial partial pressure of O2), PaCO2 (arterial partial pressure of CO2), biochemical and pathophysiological data were obtained. These subjects suffered from crash injuries and developed FES associated with ARDS, and each died within 2 h after admission. In the subjects, chest radiography revealed that the lungs were clear on admission, and pulmonary infiltration was observed within 2 h of admission. Arterial blood pH and PaO2 declined, whereas PaCO2 increased. Plasma PLA2 (phospholipase A2), nitrate/nitrite, methylguanidine, TNF-α (tumour necrosis factor-α), IL-1β (interleukin-1β) and IL-10 (interleukin-10) were significantly elevated. Pathological examinations revealed alveolar oedema and haemorrhage with multiple fat droplet depositions and fibrin thrombi. Fat droplets were also found in the arterioles and/or capillaries in the lung, kidney and brain. Immunohistochemical staining identified iNOS (inducible nitric oxide synthase) in alveolar macrophages. In conclusion, our clinical analysis suggests that PLA2, NO, free radicals and pro-inflammatory cytokines are involved in the pathogenesis of ARDS associated with FES. The major source of NO is the alveolar macrophages.

scholarly journals Acute Respiratory Distress Syndrome after Onyx Embolization of Arteriovenous Malformation

2011 ◽  
Vol 2011 ◽  
pp. 1-5 ◽  
Author(s):  
Isaac Tawil ◽  
Andrew P. Carlson ◽  
Christopher L. Taylor
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Arteriovenous Malformation ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Pulmonary Edema ◽  
Distress Syndrome ◽  
Ventilatory Support ◽  
Volume Overload ◽  
Embolization Procedure ◽  
Onyx Copolymer

Purpose. We report a case of a 60-year-old male who underwent sequential Onyx embolizations of a cerebral arteriovenous malformation (AVM) which we implicate as the most likely etiology of subsequent acute respiratory distress syndrome (ARDS).Methods. Case report and literature review.Results. Shortly after the second Onyx embolization procedure, the patient declined from respiratory failure secondary to pulmonary edema. Clinical entities typically responsible for pulmonary edema including cardiac failure, renal failure, iatrogenic volume overload, negative-pressure pulmonary edema, and infectious etiologies were evaluated and excluded. The patient required mechanical ventilatory support for several days, delaying operative resection. The patient met clinical and radiographic criteria for ARDS. After excluding other etiologies of ARDS, we postulate that ARDS developed as a result of Onyx administration. The Onyx copolymer is dissolved in dimethyl sulfoxide (DMSO), a solvent excreted through the lungs and has been implicated in transient pulmonary side effects. Additionally, a direct toxic effect of the Onyx copolymer is postulated.Conclusion. Onyx embolization and DMSO toxicity are implicated as the etiology of ARDS given the lack of other inciting factors and the close temporal relationship. A strong physiologic rationale provides further support. Clinicians should consider this uncommon but important complication.

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