scholarly journals Patient-Self Inflicted Lung Injury: A Practical Review

2021 ◽  
Vol 10 (12) ◽  
pp. 2738
Author(s):  
Guillaume Carteaux ◽  
Mélodie Parfait ◽  
Margot Combet ◽  
Anne-Fleur Haudebourg ◽  
Samuel Tuffet ◽  
...  

Patients with severe lung injury usually have a high respiratory drive, resulting in intense inspiratory effort that may even worsen lung damage by several mechanisms gathered under the name “patient-self inflicted lung injury” (P-SILI). Even though no clinical study has yet demonstrated that a ventilatory strategy to limit the risk of P-SILI can improve the outcome, the concept of P-SILI relies on sound physiological reasoning, an accumulation of clinical observations and some consistent experimental data. In this review, we detail the main pathophysiological mechanisms by which the patient’s respiratory effort could become deleterious: excessive transpulmonary pressure resulting in over-distension; inhomogeneous distribution of transpulmonary pressure variations across the lung leading to cyclic opening/closing of nondependent regions and pendelluft phenomenon; increase in the transvascular pressure favoring the aggravation of pulmonary edema. We also describe potentially harmful patient-ventilator interactions. Finally, we discuss in a practical way how to detect in the clinical setting situations at risk for P-SILI and to what extent this recognition can help personalize the treatment strategy.

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Liam Weaver ◽  
Anup Das ◽  
Sina Saffaran ◽  
Nadir Yehya ◽  
Timothy E. Scott ◽  
...  

Abstract Background There is on-going controversy regarding the potential for increased respiratory effort to generate patient self-inflicted lung injury (P-SILI) in spontaneously breathing patients with COVID-19 acute hypoxaemic respiratory failure. However, direct clinical evidence linking increased inspiratory effort to lung injury is scarce. We adapted a computational simulator of cardiopulmonary pathophysiology to quantify the mechanical forces that could lead to P-SILI at different levels of respiratory effort. In accordance with recent data, the simulator parameters were manually adjusted to generate a population of 10 patients that recapitulate clinical features exhibited by certain COVID-19 patients, i.e., severe hypoxaemia combined with relatively well-preserved lung mechanics, being treated with supplemental oxygen. Results Simulations were conducted at tidal volumes (VT) and respiratory rates (RR) of 7 ml/kg and 14 breaths/min (representing normal respiratory effort) and at VT/RR of 7/20, 7/30, 10/14, 10/20 and 10/30 ml/kg / breaths/min. While oxygenation improved with higher respiratory efforts, significant increases in multiple indicators of the potential for lung injury were observed at all higher VT/RR combinations tested. Pleural pressure swing increased from 12.0 ± 0.3 cmH2O at baseline to 33.8 ± 0.4 cmH2O at VT/RR of 7 ml/kg/30 breaths/min and to 46.2 ± 0.5 cmH2O at 10 ml/kg/30 breaths/min. Transpulmonary pressure swing increased from 4.7 ± 0.1 cmH2O at baseline to 17.9 ± 0.3 cmH2O at VT/RR of 7 ml/kg/30 breaths/min and to 24.2 ± 0.3 cmH2O at 10 ml/kg/30 breaths/min. Total lung strain increased from 0.29 ± 0.006 at baseline to 0.65 ± 0.016 at 10 ml/kg/30 breaths/min. Mechanical power increased from 1.6 ± 0.1 J/min at baseline to 12.9 ± 0.2 J/min at VT/RR of 7 ml/kg/30 breaths/min, and to 24.9 ± 0.3 J/min at 10 ml/kg/30 breaths/min. Driving pressure increased from 7.7 ± 0.2 cmH2O at baseline to 19.6 ± 0.2 cmH2O at VT/RR of 7 ml/kg/30 breaths/min, and to 26.9 ± 0.3 cmH2O at 10 ml/kg/30 breaths/min. Conclusions Our results suggest that the forces generated by increased inspiratory effort commonly seen in COVID-19 acute hypoxaemic respiratory failure are comparable with those that have been associated with ventilator-induced lung injury during mechanical ventilation. Respiratory efforts in these patients should be carefully monitored and controlled to minimise the risk of lung injury.


2020 ◽  
pp. 243-244
Author(s):  
M.M. Pylypenko ◽  
O.Yu. Khomenko

Background. The success of respiratory support depends on the effectiveness of improving gas exchange, reducing lung damage, and adaptation of the respirator. Reduction of lung damage has previously been reported in the context of ventilator-associated injury: barotrauma in case of high plateau pressure and driving pressure, volume trauma in case of large tidal volume, atelectasis trauma due to the cyclic collapse of lungs on exhalation and opening on inspiration. Objective. To describe the features of lung damage during mechanical lung ventilation (MLV) and the possibility of its prevention. Materials and methods. Analysis of literature sources on this topic. Results and discussion. The main causes of “air hunger” breathing type and shortness of breath include hypoxia, acidosis, increased anatomical and functional dead space, psychomotor agitation and fear. Metabolic acidosis is compensated by hyperventilation and respiratory alkalosis, but it is treated by improving oxygenation. High-flow oxygenation helps to leach CO2 from the dead space. Psychomotor agitation and pain aggravate shortness of breath, so all components of these processes should be influenced by effective analgesia, providing the patient with a comfortable body position (especially obese people), ensuring the absence of hunger and thirst, creating conditions for night sleep and more. If all these measures are taken, but the patient’s agitation is maintained, sedation should be considered. Propofol and dexmedetomidine are increasingly used for short-term sedation. Approaches to sedation have been changing abroad in recent years. First, non-pharmacological methods are used and only then – pharmacological ones. First of all, it is recommended to achieve analgesia, and then – sedation. It is advisable to maintain moderate sedation (from 0 to -2 on the RASS scale) and avoid deep sedation (from -3 to -5 points on the RASS scale). Sedation should be stopped each morning for the wake-up test and the respirator quitting test. To improve the immediate consequences of treatment (duration of MLV and stay in the intensive care unit), it is advisable to minimize the use of benzodiazepines and prefer propofol or dexmedetomidine. The depth of sedation should be constantly monitored, however, even experienced physicians may not always be able to detect asynchrony and excessive sedation. Asynchrony is associated with the increased mortality and prolonged weaning. To assess the intensity of the patient’s respiratory effort, the index of rapid shallow breathing, the maximum vacuum in the airways and the pressure in 0.1 second after the start of the breathing attempt are used. If the latter exceeds 3.5 cm H2O, it indicates the excessive respiratory effort of the patient (Telias I. et al., 2020). Conclusions. 1. The term “self-induced lung injury” has become widely used in the practice of anesthesiologists. 2. The need for respiratory support is determined primarily by the patient’s breathing efforts. 3. The ability to timely identify and respond to asynchrony helps to avoid self-induced lung damage.


2004 ◽  
Vol 51 (3) ◽  
pp. 45-49 ◽  
Author(s):  
Vladimir Bumbasirevic ◽  
V. Bukumirovic ◽  
Nada Popovic ◽  
V. Nikolic ◽  
Nevena Kalezic ◽  
...  

Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) contribute to progressive hypoxemia in critically ill patients. It has been proved that conventional mechanical ventilation with physiological respiratory volume contributes to further lung damage. In this respect, application of protective ventilatory strategy - pulmonary ventilation with limited volume and pressure can avoid mentioned consequences. The aim of this paper is to discuss mechanims by which elements contained in protective mechanical ventilation of patients with ALI/ARDS prevent further progrssive lung injury, to argue the effects of positive end - expiratory pressure and present insturctions for its application.


Author(s):  
Sanjay Mukhopadhyay ◽  
Mitra Mehrad ◽  
Pedro Dammert ◽  
Andrea V Arrossi ◽  
Rakesh Sarda ◽  
...  

Abstract Objectives The aim of this report is to describe the lung biopsy findings in vaping-associated pulmonary illness. Methods Lung biopsies from eight patients with vaping-associated pulmonary illness were reviewed. Results The biopsies were from eight men (aged 19-61 years) with respiratory symptoms following e-cigarette use (vaping). Workup for infection was negative in all cases, and there was no evidence for other etiologies. Imaging showed diffuse bilateral ground-glass opacities in all patients. Most recovered with corticosteroid therapy, while one died. Lung biopsies (seven transbronchial, one surgical) showed acute lung injury, including organizing pneumonia and/or diffuse alveolar damage. Common features were fibroblast plugs, hyaline membranes, fibrinous exudates, type 2 pneumocyte hyperplasia, and interstitial organization. Some cases featured a sparse interstitial chronic inflammatory infiltrate. Although macrophages were present within the airspaces in all cases, this feature was not prominent, and findings typical of exogenous lipoid pneumonia were absent. Conclusions The histopathology of acute pulmonary illness related to e-cigarette use (vaping) is characterized by acute lung injury patterns, supporting the contention that vaping can cause severe lung damage.


Author(s):  
Dietrich Henzler ◽  
Alf Schmidt ◽  
Zhaolin Xu ◽  
Nada Ismaiel ◽  
Haibo Zhang ◽  
...  

Abstract Background An on-going debate exists as to whether partial ventilatory support is lung protective in an acute phase of ARDS. So far, the effects of different respiratory efforts on the development of ventilator-associated lung injury (VALI) have been poorly understood. To test the hypothesis whether respiratory effort itself promotes VALI, acute lung injury (ALI) was induced in 48 Sprague Dawley rats by hydrochloric acid aspiration model. Hemodynamics, gas-exchange, and respiratory mechanics were measured after 4 h of ventilation in pressure control (PC), assist-control (AC), or pressure support with 100% (PS100), 60% (PS60), or 20% (PS20) of the driving pressure during PC. VALI was assessed by histological analysis and biological markers. Results ALI was characterized by a decrease in PaO2/FiO2 from 447 ± 75 to 235 ± 90 mmHg (p < 0.001) and dynamic respiratory compliance from 0.53 ± 0.2 to 0.28 ± 0.1 ml/cmH2O (p < 0.001). There were no differences in hemodynamics or respiratory function among groups at baseline or after 4 h of ventilation. The reduction of mechanical pressure support was associated with a compensatory increase in an inspiratory effort such that peak inspiratory transpulmonary pressures were equal in all groups. The diffuse alveolar damage score showed significant lung injury but was similar among groups. Pro- and anti-inflammatory proteins in the bronchial fluid were comparable among groups. Conclusions In experimental ALI in rodents, the respiratory effort was increased by reducing the pressure support during partial ventilatory support. In the presence of a constant peak inspiratory transpulmonary pressure, an increased respiratory effort was not associated with worsening ventilator-associated lung injury measured by histologic score and biologic markers.


2021 ◽  
Author(s):  
Anup Das ◽  
Liam Weaver ◽  
Sina Saffaran ◽  
Nadir Yehya ◽  
Timothy E. Scott ◽  
...  

There is ongoing controversy regarding the potential for increased respiratory effort to generate patient self-inflicted lung injury (P-SILI) in spontaneously breathing patients with COVID-19 acute respiratory failure. However, direct clinical evidence linking increased inspiratory effort to lung injury is scarce. We adapted a recently developed computational simulator that replicates distinctive features of COVID-19 pathophysiology to quantify the mechanical forces that could lead to P-SILI at different levels of respiratory effort. In accordance with recent data, the simulator was calibrated to represent a spontaneously breathing COVID-19 patient with severe hypoxaemia (SaO2 80.6%) and relatively well-preserved lung mechanics (lung compliance of 47.5 ml/cmH2O), being treated with supplemental oxygen (FiO2 = 100%). Simulations were conducted at tidal volumes (VT) and respiratory rates (RR) of 7 ml/kg and 14 breaths/min (representing normal respiratory effort) and at VT/RR of 15/14, 7/20, 15/20, 10/30, 12/30, 10/35, 12/35, 10/40, 12/40 ml/kg / breaths/min. Lung compliance was unaffected by increased VT but decreased significantly at higher RR. While oxygenation improved, significant increases in multiple indicators of the potential for lung injury were observed at all higher VT/RR combinations tested. Pleural pressure swing increased from 10.1 cmH2O at baseline to 30 cmH2O at VT/RR of 15 ml/kg / 20 breaths/min and to 54.6 cmH2O at 12 ml/kg / 40 breaths/min. Dynamic strain increased from 0.3 to 0.49 at VT/RR of 12 ml/kg / 30 breaths/min, and to 0.6 at 15 ml/kg / 20 breaths/min. Mechanical power increased from 7.83 J/min to 17.7 J/min at VT/RR of 7 ml/kg / 20 breaths/min, and to 240.5 7 J/min at 12 ml/kg / 40 breaths/min. Our results suggest that the forces generated during increased inspiratory effort in severe COVID-19 are compatible with the development of P-SILI. If conventional oxygen therapy or non-invasive ventilation is ineffective in reducing respiratory effort, control of driving and transpulmonary pressures with invasive ventilation may reduce the risk of P-SILI and allow time for the resolution of the underlying condition.


2021 ◽  
Vol 99 ◽  
pp. 108033
Author(s):  
Ramazan Ozdemir ◽  
Ismail Kursat Gokce ◽  
Asli Cetin Taslidere ◽  
Kevser Tanbek ◽  
Cemile Ceren Gul ◽  
...  

Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 3561-3561
Author(s):  
Rick Kapur ◽  
Michael Kim ◽  
Shanjee Shanmugabhavananthan ◽  
Edwin R. Speck ◽  
Rukhsana Aslam ◽  
...  

Abstract Transfusion-related acute lung injury (TRALI), a syndrome characterized by respiratory distress triggered by blood transfusions, is the leading cause of transfusion-related mortality. Mostly, TRALI has been attributed to passive infusion of human leucocyte antigen (HLA) and human neutrophil antigen (HNA) antibodies present in the transfused blood product. Several animal models have been developed to study the pathogenesis of antibody-mediated TRALI and various mechanisms for TRALI induction have been suggested, including involvement of endothelial cells, neutrophils and monocytes. In 2006, a murine of model of antibody-mediated TRALI was developed using a monoclonal MHC class I antibody (clone 34-1-2s). This antibody was shown to cause significant lung damage (excess lung water: pulmonary edema) within 2 hours of administration into BALB/c mice, which in follow-up studies was only reproducible after initial priming with the gram-negative endotoxin lipopolysaccharide (LPS). 34-1-2s was also shown to cause severe lung damage in severe combined immunodeficient (SCID) mice. We investigated 34-1-2s mediated TRALI in BALB/c mice, without LPS priming, and found no difference in TRALI severity when compared with injection with an control isotype antibody for 34-1-2s (Isotype Mouse IgG2a antibody), as examined by lung wet-to-dry ratios, a measure for pulmonary edema. Recently it was described that the acute phase protein C-reactive protein (CRP), heavily up-regulated during acute infections and also present at lower levels in healthy individuals, was able to enhance antibody-mediated platelet destruction both in vitro and in vivo via Fc-receptor mediated phagocytic responses. Considering the fact that TRALI has been shown to be mainly antibody-mediated, plus the fact that it has been suggested to be an Fc-dependent process as well, we investigated the effect of CRP in a murine antibody-mediated TRALI. We tested if CRP would be able to enhance antibody-mediated TRALI in the murine 34-1-2s based BALB/c TRALI model. For that purpose, we co-injected CRP together with 34-1-2s and compared that to co-injection of CRP together with control isotype mouse IgG2a or to injection with CRP alone. We found that CRP+34-1-2s injection resulted in significantly higher lung damage than CRP+isotype antibody, as well as than CRP alone, with at least 43% of the mice in the CRP+34-1-2s group having a lung wet-to-dry ratio of higher than 5, which is considered to represent severe lung damage. As the monocyte-derived neutrophil chemoattractant macrophage inflammatory protein 2 (MIP-2: murine equivalent of human IL-8) was recently shown to play a central role in murine (SCID) 34-1-2s-mediated TRALI induction, we measured MIP-2 values in our BALB/c TRALI model and found that CRP alone was capable of producing high levels of MIP-2, which were found to be even more increased when 34-1-2s was co-injected with CRP. We propose a mechanism in which CRP plays a synergistic role with 34-1-2s antibody to significantly increase the induction of antibody-mediated TRALI via enhanced stimulation of monocyte-derived MIP-2 secretion. Disclosures No relevant conflicts of interest to declare.


2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Shinichiro Ohshimo

AbstractAcute respiratory distress syndrome (ARDS) is a fatal condition with insufficiently clarified etiology. Supportive care for severe hypoxemia remains the mainstay of essential interventions for ARDS. In recent years, adequate ventilation to prevent ventilator-induced lung injury (VILI) and patient self-inflicted lung injury (P-SILI) as well as lung-protective mechanical ventilation has an increasing attention in ARDS.Ventilation-perfusion mismatch may augment severe hypoxemia and inspiratory drive and consequently induce P-SILI. Respiratory drive and effort must also be carefully monitored to prevent P-SILI. Airway occlusion pressure (P0.1) and airway pressure deflection during an end-expiratory airway occlusion (Pocc) could be easy indicators to evaluate the respiratory drive and effort. Patient-ventilator dyssynchrony is a time mismatching between patient’s effort and ventilator drive. Although it is frequently unrecognized, dyssynchrony can be associated with poor clinical outcomes. Dyssynchrony includes trigger asynchrony, cycling asynchrony, and flow delivery mismatch. Ventilator-induced diaphragm dysfunction (VIDD) is a form of iatrogenic injury from inadequate use of mechanical ventilation. Excessive spontaneous breathing can lead to P-SILI, while excessive rest can lead to VIDD. Optimal balance between these two manifestations is probably associated with the etiology and severity of the underlying pulmonary disease.High-flow nasal cannula (HFNC) and non-invasive positive pressure ventilation (NPPV) are non-invasive techniques for supporting hypoxemia. While they are beneficial as respiratory supports in mild ARDS, there can be a risk of delaying needed intubation. Mechanical ventilation and ECMO are applied for more severe ARDS. However, as with HFNC/NPPV, inappropriate assessment of breathing workload potentially has a risk of delaying the timing of shifting from ventilator to ECMO. Various methods of oxygen administration in ARDS are important. However, it is also important to evaluate whether they adequately reduce the breathing workload and help to improve ARDS.


1999 ◽  
Vol 341 (11) ◽  
pp. 848-849 ◽  
Author(s):  
David A. Tanen ◽  
Kimberlie A. Graeme ◽  
Robert Raschke
Keyword(s):  

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