Letteratura scientifica selezionata sul tema "Patient self-Inflicted lung injury"

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.

Acute respiratory distress syndrome (ARDS) is characterized by acute-onset rapid-deteriorating inflammatory lung injury. Although the preservation of spontaneous breathing may have physiological benefits in oxygenation, increasing evidence shows that vigorous spontaneous breathing may aggravate lung injury (i.e., patient self-inflicted lung injury). Increased lung stress and pendelluft, which is defined as intrapulmonary gas redistribution without a significant change in tidal volume, are important mechanisms of patient self-inflicted lung injury. The presence of pendelluft may be considered a surrogate marker of vigorous inspiratory effort, which can cause the dependent lung to overstretch. In this review, we summarized three major methods for electrical impedance tomography–based pendelluft monitoring. Future studies are warranted to compare and validate the different methods of pendelluft estimation in patients with ARDS.

Patient self-inflicted lung injury (P-SILI) is a life-threatening condition arising from excessive respiratory effort and work of breathing in patients with lung injury. The pathophysiology of P-SILI involves factors related to the underlying lung pathology and vigorous respiratory effort. P-SILI might develop both during spontaneous breathing and mechanical ventilation with preserved spontaneous respiratory activity. In spontaneously breathing patients, clinical signs of increased work of breathing and scales developed for early detection of potentially harmful effort might help clinicians prevent unnecessary intubation, while, on the contrary, identifying patients who would benefit from early intubation. In mechanically ventilated patients, several simple non-invasive methods for assessing the inspiratory effort exerted by the respiratory muscles were correlated with respiratory muscle pressure. In patients with signs of injurious respiratory effort, therapy aimed to minimize this problem has been demonstrated to prevent aggravation of lung injury and, therefore, improve the outcome of such patients. In this narrative review, we accumulated the current information on pathophysiology and early detection of vigorous respiratory effort. In addition, we proposed a simple algorithm for prevention and treatment of P-SILI that is easily applicable in clinical practice.

Patient self-inflicted lung injury (P-SILI) is a major challenge for the ICU physician: although spontaneous breathing is associated with physiological benefits, in patients with acute respiratory distress syndrome (ARDS), the risk of uncontrolled inspiratory effort leading to additional injury needs to be assessed to avoid delayed intubation and increased mortality. In the present review, we analyze the available clinical and experimental evidence supporting the existence of lung injury caused by uncontrolled high inspiratory effort, we discuss the pathophysiological mechanisms by which increased effort causes P-SILI, and, finally, we consider the measurements and interpretation of bedside physiological measures of increased drive that should alert the clinician. The data presented in this review could help to recognize injurious respiratory patterns that may trigger P-SILI and to prevent it.

We report the case of a patient with injuries to multiple organs as a result of attempted suicide with a nail gun. The patient shot 12 nails into his chest, causing damage to multiple organs, including the heart, lungs, and stomach. With timely emergency surgery, we successfully removed all the nails, and the patient was discharged from the hospital two weeks after surgery.

Introduction Au cours de l’insuffisance respiratoire aiguë (IRA) de novo ou du syndrome de détresse respiratoire aiguë (SDRA), la ventilation invasive (VI) appliquée au patient pour pallier aux altérations sévères de l’hématose, de même que les efforts respiratoires spontanés, peuvent paradoxalement aggraver les lésions alvéolaires initiales et provoquer alors des lésions dénommées ventilator induced lung injury (VILI) ou patient self-inflicted lung injury (P-SILI).L’exacerbation aiguë de pneumopathie interstitielle diffuse (EAPID), bien que proche sémiologiquement, histologiquement et radiologiquement du SDRA et ayant bénéficié de l’amélioration des connaissances du VILI et du P-SILI, reste grevée d’une mortalité bien plus élevée. MéthodeNous nous sommes donc intéressés aux conséquences de la ventilation et des efforts respiratoires spontanés au cours des EAPID.RésultatsNous avons tout d’abord étudié les conséquences des stratégies d’oxygénation non invasives au cours de l’IRA de novo et montré que la ventilation non invasive (VNI) augmentait le volume courant par rapport à l’oxygénothérapie à haut débit (OHD) sans augmentation du recrutement alvéolaire, donc exposant le poumon à un risque de surdistention. Nous avons ensuite mis au point un modèle de poumon artificiel mécanique reproduisant la ventilation spontanée au cours de l’IRA de novo et les mécanismes physiopathologiques impliqués dans le P-SILI.Nous avons ensuite utilisé ces connaissances acquises au cours de l’IRA de novo pour modéliser la ventilation spontanée des patients atteints de PID au repos, au cours d’un exercice maximal et d’une EAPID. Nous avons mis en évidence que l’hétérogénéité de l’atteinte pulmonaire, et donc de la compliance dans les PID, était associée tant à l’effort qu’au cours de l’EAPID à la présence de mécanismes impliqués dans le P-SILI : recrutement/dérecrutement alvéolaires, surdistension, concentration du stress pulmonaire, et phénomène de Pendelluft.Nous avons ensuite soumis ce modèle d’EAPID aux contraintes de la VI. Nous avons ainsi pu montrer que celle-ci, appliquée avec des volumes courants supérieurs à 5 ml/kg de poids prédit sur la taille, des niveaux de pressions expiratoire positive supérieure à 4 cmH2O et une fréquence respiratoire supérieure à 25/min, était potentiellement délétère selon notre modèle. Nous avons parallèlement évalué, au cours d’une étude clinique rétrospective, les conséquences de la stratégie d’oxygénation non invasive appliquée au cours de l’EAPID. A contrario de ce que nous avions pu montrer dans l’IRA de novo, nous n’avons pas retrouvé de différence entre la VNI et l’OHD en termes de mortalité ou de recours à la VI. Grace à notre modèle expérimental d’EAPID, nous devrions pouvoir comprendre les mécanismes physiopathologiques expliquant ce résultat et envisager une stratégie d’oxygénation optimisée et personnalisée pour la prise en charge de l’EAPID. ConclusionNotre travail de recherche, à la fois expérimental et clinique, a donc permis de mettre en évidence la possibilité de P-SILI et de VILI au cours des EAPID, de montrer que le risque de surdistension est majeur dans cette pathologie au cours de la VI. La stratégie d’oxygénation non invasive optimale reste encore à déterminer
IntroductionIn the course of de novo acute respiratory failure (ARF) or acute respiratory distress syndrome (ARDS), invasive mechanical ventilation (IMV) and spontaneous respiratory efforts, may paradoxically worsen initial alveolar lesions and cause ventilator induced lung injury (VILI) or patient self-inflicted lung injury (P-SILI). Acute exacerbation of diffuse interstitial lung disease (AE-ILD) presents similar characteristics to ARDS in semiology, histology and radiology. However, the risk of mortality remains higher in AE-ILD despite improved knowledge of VILI and P-SILI. MethodsWe were interested in the effects of ventilation and spontaneous respiratory effort during AE-ILD.ResultsWe first studied the effects of non-invasive oxygenation strategies during de novo ARF, and showed that non-invasive ventilation (NIV) increased tidal volume compared to high flow nasal canulae oxygen therapy (HFNC) without increasing alveolar recruitment, thus exposing the lung to the risk of overdistention. We then developed a mechanical artificial lung model reproducing spontaneous ventilation during de novo ARF and studied the pathophysiological mechanisms involved in P-SILI.We then used this knowledge learned from de novo ARF to model spontaneous ventilation in patients with ILD at rest, during maximal exercise and AE-ILD. We demonstrated that the inhomogeneity of lung injury and of compliance in ILD was associated during exercise and AE-ILD, with the presence of mechanisms involved in P-SILI: recruitment/derecruitment, overdistension, stress concentration and Pendelluft phenomenon.We then exposed this AE-ILD model to the challenges of IMV. We showed that IMV applied with tidal volumes of more than 5 ml/kg PBW, positive expiratory pressure levels of more than 4 cmH2O and respiratory rates of more than 25 cpm were deleterious in our model. At the same time, we evaluated the effects of non-invasive oxygenation strategies during AE-ILD in a retrospective clinical study. We found no difference between NIV and HFNC in mortality or use of invasive ventilation. ConclusionOur research has highlighted the occurence of P-SILI and VILI during AE-ILD and has shown a major risk of overdistension in AE-ILD during IMV. Our model of AE-ILD could help us to develop optimized and personalized oxygenation strategies for AE-ILD patients

Head injury or traumatic brain injury is a ubiquitous phenomenon in all societies and affects up to 2 per cent of the population per year (Bullock et al. 2006). Although the causes of head injury and its distribution within populations vary, it can have devastating consequences both for the patient and family (Tagliaferri et al. 2006). In some countries severe traumatic brain injury is the commonest cause of death in people under 40 years (Lee et al. 2006), and it is estimated that the sequelae of head injury cost societies billions of dollars per year. Understanding of the pathophysiology, diagnosis, and management have all improved dramatically in the last few decades (Steudel et al. 2005). However within western society, perhaps one of the greatest benefits has been the reduction in severe craniocerebral injuries following motor vehicle accidents. This has arisen because of increased safety in car design, seat-belt legislation, the introduction of air-bags, enforcement of speed limits, and the societal conformity to drink-driving legislation. For instance, because of these changes, in the last 15 years the number of severe head injuries managed in the Clinical Neuroscience unit in Edinburgh has decreased by around 66 per cent. Unfortunately in some developing countries one legacy of increased traffic, particularly of motor cycles, is an epidemic of head injuries amongst young adults (Lee et al. 2006). With the number of severe head injuries declining in many countries the challenge will be to provide better care for patients with minor head injury, about 10 times more common than severe injury (Steudel et al. 2005).Ageing patients who tend to fall over, falls associated with increased alcohol consumption, and domestic or social assaults probably now contribute to the majority of head injuries (Flanagan et al. 2005; Steudel et al. 2005; Tagliaferri et al. 2006). Sporting injuries are fortunately uncommon as a cause of severe craniocerebral injury, although horse riding accidents can sometimes be devastating particularly in teenage girls. In some countries injuries from hand guns and other missiles are common (Aryan et al. 2005), but in European countries many such injuries are self-inflicted. Prompt management of intracranial haematoma, which occurs in 25–45 per cent of severe head injuries, 3–12 per cent of moderate injuries, and 0.2 per cent of minor injuries, and the rehabilitation of patients with head injury are now important areas in clinical neuroscience (Flanagan et al. 2005; Bullock et al. 2006b, c).

Ventilatory therapy plays a critical role in managing patients with Acute Respiratory Distress Syndrome (ARDS). The primary goal of ventilator therapy is to assist in ventilation while preventing ventilator-induced lung injury (VILI) and ventilator-induced diaphragm dysfunction (VIDD). Volutrauma and atelectrauma are the main mechanisms responsible for VILI. Recently, respiratory rate and flow rate have been highlighted as possible elements contributing to VILI, and the concept of mechanical power was proposed. Once patients are able to breathe spontaneously, efforts should focus on avoiding patient self-inflicted lung injury (P-SILI). Prolonged paralysis of the diaphragm or patient-ventilator dyssynchrony can lead to VIDD or P-SILI. To achieve less injurious ventilation, careful selection of Positive End-Expiratory Pressure (PEEP) and tidal volume is crucial. However, determining the optimal ventilator settings remains a challenge, as it depends on the specific characteristics of each patient and the judgment of the physician. Therefore, critical care physicians should have a comprehensive understanding of the pathophysiological basis of ARDS and be aware of the current consensus regarding ventilator management for these patients.

Abstract Chapter 8 examines posttraumatic stress disorder (PTSD) in relation to respiratory conditions such as respiratory distress syndrome and acute lung injury, asthma symptoms, or attacks. It also examines the association between PTSD and severe acute respiratory syndrome (SARS) in patients, healthcare workers, and hospital staff. Factors explaining differential levels of distress in SARS patients include demographic variables, risk exposure to SARS, coping strategies, self-efficacy, self-esteem, and altruism. The association between PTSD and Covid-19 is also being investigated in hospitalised patients, health care workers, the general population, and some specific populations such as pregnant women, military veterans, and psychiatric patients. The risk factors for these individuals include demographic variables, a history of mental health problems, previous trauma, level of exposure to traumatic Covid-19, experience of hospitalisation for Covid-19, loss of a loved one, lockdown, domestic violence, and media exposure, and various coping strategies. Interventions for people with Covid-19 are also discussed.

Genetic polymorphism and prostate cancer (PC) are the most pernicious and recurrently malignancy worldwide. It is the most dominating cause of cancer related casualty among men in the US. Asian countries are inflicted with PC at an alarming rate though still the prevalence of PC is lower than European and American men. Some of the genetic and environmental factors that might play a role in PC risk include: age genetic predilection, family history, race/ethnicity, lifestyle, and dietary habits and non-dietary environmental risk factors such as smoking. Socio-economic factors including economic, scholastic and intellectual factors do not, intrinsically seem to straight away influence the risk of acquiring PC. Other genetic changes that may support an increased risk of developing PC include HPC1, HPC2, HPCX, CAPB, ATM,s HOXB13 and mismatch repair genes. PC occurrence rates are highly variable. Almost all PC mortalities are due to metastatic disease, generally through tumors the progress to be hormone refractory or castrate resistant. PC, developing research has acknowledged a number of candidate genes and biological pathways associated with PC. Indirect pathways such as P13K/AKT signaling pathway is one of most well known alternate pathway in PC Vascular endothelial growth factor (VEGF) is widely known to be potent stimulator of angiogenesis. The over expression of EGFR in a very large majority of cases is accompanied by the succession of PC, implying that this may play a mechanistic role. Numerous occupational factors have been proposed to cause PC. Some of the risk factors include; farmers/agricultural workers, pesticides, shift work and flight personnel. PC treatment can be done through surgery, radical prostatectomy is the main type of surgery. Risks of injury are many – reactions to anesthesia, loss of blood, blood clumps in the legs/lungs, injury to surrounding organs, infection at the site of surgery and many more. The other treatments are hormone therapy, chemotherapy and radio therapy chemotherapy. Chemotherapeutic drugs are typically used one at a time for PC such as transurethral resection of prostate (TURP). Some of the chemotherapeutic drugs are Docetaxel, Cabazitaxel, Mitoxantrone and Estramustine. Among the score of biomarkers being studied, numerous markers and techniques deserve awareness and acceptability for both patients and urologists in clinical practice.

The aim of this chapter is to provide nurses with the knowledge to be able to assess, manage, and care for people with chronic obstructive pulmonary disease (COPD) in an evidence-based and person-centred way. The chapter will provide a comprehensive overview of the causes, risk factors, and impact of COPD, before exploring best practice to deliver care, as well as to prevent or minimize further ill-health. Nursing assessments and priorities are highlighted throughout, and the nursing management of the symptoms and common health problems associated with COPD can be found in Chapters 2, 15, 18, and 22, respectively. Chronic obstructive pulmonary disease (COPD) is predominantly caused by smoking and is characterized by airflow obstruction that is not fully reversible (National Institute for Health and Clinical Excellence (NICE), 2010). This broad definition embraces previously used definitions such as chronic bronchitis, emphysema, and chronic asthma. Historically, perceptions of the treatment for and care of the patient with COPD were negative, because of the chronic nature of this progressive disease, which was often viewed as self-inflicted through its links with smoking. Current emphasis, regardless of aetiology, is that it is both preventable and treatable (National Institute for Health and Clinical Excellence (NICE), 2010). Currently around 1 million UK citizens are diagnosed with COPD; prevalence data are higher, at 1.7 million (Britton, 2003). This appears to be underreported because it is thought that there could be as many as another 2 million people currently undiagnosed (British Lung Foundation, 2006). COPD is already a significant burden of disease area, with expectations that, by 2020, it will be the third largest cause of mortality (Murray and Lopez, 1997). Reasons for increasing prevalence include that:… ● an ageing population increases the likelihood of chronic disease development; ● diagnosis of COPD is better guided by both national and international COPD guidelines, with inclusion in the Quality and Outcomes Framework (QOF) in general practice bringing financial incentives for maintaining COPD registers and improving COPD care; ● increasing public awareness leads to more people seeking help on symptom presentation; ● more women being diagnosed, correlating to more women smoking, perhaps owing to greater social acceptability; ● other as yet unknown causes....