Pulmonary microthrombosis in severe adult respiratory distress syndrome

Vesconi, S.; Rossi, Gianpaolo; Artigas, Antonio; Gattinoni, Luciano

doi:10.1097/00003246-198802000-00002

Cited by 63 publications

(44 citation statements)

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“…9,[11][12][13][14]18,30,31 We looked for some of these readily available factors that could have affected RV function in our patients. In our study, we found that nonsurvivors had a statistically significant lower pH compared with survivors (7.31 ± 0.05 vs. 7.38 ± 0.04).…”

Section: Discussionmentioning

confidence: 99%

Echocardiographic Parameters of Right Ventricular Function Predict Mortality in Acute Respiratory Distress Syndrome: A Pilot Study

et al. 2016

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Right ventricular (RV) dysfunction in acute respiratory distress syndrome (ARDS) contributes to increased mortality. Our aim is to identify reproducible transthoracic echocardiography (TTE) parameters of RV dysfunction that can be used to predict outcomes in ARDS. We performed a retrospective single-center cohort pilot study measuring tricuspid annular plane systolic excursion (TAPSE), Tei index, RV-fractional area change (RV-FAC), pulmonary artery systolic pressure (PASP), and septal shift, reevaluated by an independent blinded cardiologist (JK). Thirty-eight patients were included. Patients were divided on the basis of 30-day survival. Thirty-day mortality was 47%. Survivors were younger than nonsurvivors. Survivors had a higher pH, PaO 2 ∶ FiO 2 ratio, and TAPSE. Acute Physiology and Chronic Health Evaluation II (APACHE II), Simplified Acute Physiology Score II (SAPS II), and Sequential Organ Failure Assessment (SOFA) scores were lower in survivors. TAPSE has the strongest association with increased 30-day mortality from date of TTE. Accordingly, TAPSE has a strong positive correlation with PaO 2 ∶ FiO 2 ratios, and Tei index has a strong negative correlation with PaO 2 ∶ FiO 2 ratios. Septal shift was associated with lower PaO 2 ∶ FiO 2 ratios. Decrease in TAPSE, increase in Tei index, and septal shift were seen in the severe ARDS group. In multivariate logistic regression models, TAPSE maintained a significant association with mortality independent of age, pH, PaO 2 ∶ FiO 2 ratios, positive end expiratory pressure, PCO 2 , serum bicarbonate, plateau pressures, driving pressures, APACHE II, SAPS II, and SOFA scores. In conclusion, TAPSE and other TTE parameters should be used as novel predictive indicators for RV dysfunction in ARDS. These parameters can be used as surrogate noninvasive RV hemodynamic measurements to be manipulated to improve mortality in patients with ARDS and contributory RV dysfunction.Keywords: pulmonary hypertension, tricuspid annular plane systolic excursion, transthoracic echocardiography. Acute respiratory distress syndrome (ARDS) is a life-threatening respiratory syndrome characterized by hypoxemia, noncardiogenic pulmonary edema, pulmonary inflammation, and decreased pulmonary compliance. Despite our best efforts, mortality rates associated with ARDS still remain between 30% and 40%.1,2 Current management of ARDS is mainly supportive with mechanical ventilation and hemodynamic support. 3 Pulmonary hypertension and right ventricular (RV) dysfunction are independent predictors of mortality associated with poorer outcomes in patients with ARDS. [4][5][6][7][8] The increased lung mass in ARDS due to accumulation of inflammatory exudate in the alveolar space compresses not only the dependent alveoli but also the pulmonary vessels, leading to increased pulmonary vascular resistance. 9 In addition to direct compression, pulmonary endothelial cell dysfunction and microvascular thrombosis from systemic inflammatory response lead to development of pulmonary hypertension in ARDS. 10...

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Section: Discussionmentioning

confidence: 99%

Echocardiographic Parameters of Right Ventricular Function Predict Mortality in Acute Respiratory Distress Syndrome: A Pilot Study

et al. 2016

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“…Using selective angiography, the authors have documented prevalent perfusion to the nondependent lung regions, suggesting an important role for extrinsic compression and hypoxic vasoconstriction during ARDS [15]. Indeed, recent data, obtained with more sophisticated techniques suggest prevalent perfusion to the dependent atelectatic lung regions [16].…”

Section: Effects On Oxygenationmentioning

confidence: 98%

Prone position in acute respiratory distress syndrome

Pelosi¹,

Brazzi²,

Gattinoni³

2002

Eur Respir J

273

167

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In the last few years prone positioning has been used increasingly in the treatment of patients with acute respiratory distress syndrome (ARDS) and this manoeuvre is now considered a simple and safe method to improve oxygenation. However, the physiological mechanisms causing respiratory function improvement as well as the real clinical benefit are not yet fully understood. The aim of this review is to discuss the physiological and clinical effects of prone positioning in patients with ARDS.The main physiological aims of prone positioning are: 1) to improve oxygenation; 2) to improve respiratory mechanics; 3) to homogenise the pleural pressure gradient, the alveolar inflation and the ventilation distribution; 4) to increase lung volume and reduce the amount of atelectatic regions; 5) to facilitate the drainage of secretions; and 6) to reduce ventilator-associated lung injury.According to the available data, the authors conclude that: 1) oxygenation improves iny70-80% of patients with early acute respiratory distress syndrome; 2) the beneficial effects of oxygenation reduce after 1 week of mechanical ventilation; 3) the aetiology of acute respiratory distress syndrome may markedly affect the response to prone positioning; 4) extreme care is necessary when the manoeuvre is performed; 5) pressure sores are frequent and related to the number of pronations; 6) the supports used to prone and during positioning are different and nonstandardised among centres; and 7) intensive care unit and hospital stay and mortality still remain high despite prone positioning. Eur Respir J 2002; 20: 1017-1028. Acute respiratory distress syndrome (ARDS) is characterised by radiographical diffuse bilateral infiltrates, decreased respiratory compliance, small lung volumes and severe hypoxaemia. Correction of lifethreatening hypoxia and improvement of respiratory mechanics and lung volumes are the main treatment goals. To achieve these ends, it is important to select the most appropriate means of ventilatory support, thereby minimising the damaging effects of mechanical ventilation. Currently, ventilatory support using small tidal volumes and low plateau pressures and respiratory rate, to control arterial carbon dioxide tension (Pa,CO 2 ) and pH, are considered optimal [1]. Moreover, the application of relatively high levels of positive end-expiratory pressure (PEEP) seems to be beneficial in reducing ventilator-associated lung injury (VALI) and improving survival [2]. In 1974, BRYAN [3] suggested that anaesthetised and paralysed patients in the prone position should exhibit better expansion of the dorsal lung regions with a consequent improvement in oxygenation. In 1976, PIEHL and BROWN [4] showed, in a retrospective study, that the prone position improved oxygenation in five patients with ARDS without deleterious effects. One year later, DOUGLAS et al. [5] demonstrated, in a prospective study with a limited group of ARDS patients, that prone positioning could effectively improve oxygenation in ARDS. Starting from these repor...

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“…In contrast, pulmonary deposition of microemboli (ME) often does not cause acute symptoms (silent ME). Nevertheless, pulmonary ME is a relatively common accompaniment to acute lung injury (adult respiratory distress syndrome), hyperoxia, bleomycin toxicity, sepsis, trauma, surgery on the lower extremities, and angioplasty (2,21,30,33,36,39,40,44,52,53). Microembolism may lead to inflammation and edema acutely and contribute to the development of pulmonary fibrosis and hypertension over time (4,9,22,27,31).…”

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confidence: 99%

Platelets inhibit the lysis of pulmonary microemboli

Murciano

Harshaw

Neschis

et al. 2002

American Journal of Physiology-Lung Cellular and Molecular Phys

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Using tracings of 125 I-labeled fibrin(ogen) in rodents, we examined the hypothesis that platelets impede the lysis of pulmonary emboli.125 I-Microemboli (ME, 3-10 micron diameter) lodged homogeneously throughout the lungs after intravenous injection in both rats and mice (60% of injected dose), caused no lethality, and underwent spontaneous dissolution (50 and 100% within 1 and 5 h, respectively). Although lung homogenates displayed the most intense fibrinolytic activity of all the major organs, dissolution of ME was much slower in isolated perfused lungs (IPL) than was observed in vivo. Addition of rat plasma to the perfusate facilitated ME dissolution in IPL to a greater extent than did addition of tissue-type plasminogen activator alone, suggesting that permeation of the clot by plasminogen is the rate-limited step in lysis. Platelet-containing ME injected in rats lysed much more slowly than did ME formed from fibrin alone.125 I-Thrombi, formed in the pulmonary vasculature of mice in response to intravascular activation of platelets by injection of collagen and epinephrine, were essentially resistant to spontaneous dissolution. Moreover, injection of the antiplatelet glycoprotein IIb/IIIa antibody 7E3 F(abЈ) 2 facilitated spontaneous dissolution of pulmonary ME and augmented fibrinolysis by a marginally effective dose of Retavase (10 g/kg) in rats. These studies show that platelets suppress pulmonary fibrinolysis. The mechanism(s) by which platelets stabilize ME and utility of platelet inhibitors to facilitate their dissolution deserves further study. pulmonary embolism; plasminogen activators; platelets; fibrinolysis; animal model; glycoprotein IIb/IIIa THE LUNG SERVES as a natural filter for thromboemboli of diverse sizes (12). Thrombotic occlusion of the main or lobar pulmonary arteries by large clots (massive pulmonary embolism, PE) is a common cause of morbidity and mortality (15,20). In contrast, pulmonary deposition of microemboli (ME) often does not cause acute symptoms (silent ME). Nevertheless, pulmonary ME is a relatively common accompaniment to acute lung injury (adult respiratory distress syndrome), hyperoxia, bleomycin toxicity, sepsis, trauma, surgery on the lower extremities, and angioplasty (2,21,30,33,36,39,40,44,52,53). Microembolism may lead to inflammation and edema acutely and contribute to the development of pulmonary fibrosis and hypertension over time (4,9,22,27,31).The treatment of PE, as with other venous thromboembolic conditions, is typically restricted to agents such as heparin that retard fibrin clot formation, with a relatively limited use of agents that promote fibrinolysis. Despite the effectiveness of such therapy, PE remains a common cause of mortality and morbidity. Thus there is a continuing need for more effective means to prevent and treat both PE and ME, based on a more thorough understanding of the mechanisms that regulate clot dissolution in the lung.For example, the role of platelets in PE and ME has received relatively little study. Recently, it has been shown tha...

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Pulmonary microthrombosis in severe adult respiratory distress syndrome

Cited by 63 publications

References 0 publications

Echocardiographic Parameters of Right Ventricular Function Predict Mortality in Acute Respiratory Distress Syndrome: A Pilot Study

Echocardiographic Parameters of Right Ventricular Function Predict Mortality in Acute Respiratory Distress Syndrome: A Pilot Study

Prone position in acute respiratory distress syndrome

Platelets inhibit the lysis of pulmonary microemboli

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