Gut-derived immune cells and the gut-lung axis in ARDS.

The gut serves as a vital immunological organ orchestrating immune responses and influencing distant mucosal sites, notably the respiratory mucosa. It is increasingly recognized as a central driver of critical illnesses, with intestinal hyperpermeability facilitating bacterial translocation, systemic inflammation, and organ damage. The "gut-lung" axis emerges as a pivotal pathway, where gut-derived injurious factors trigger acute lung injury (ALI) through the systemic circulation. Direct and indirect effects of gut microbiota significantly impact immune responses. Dysbiosis, particularly intestinal dysbiosis, termed as an imbalance of microbial species and a reduction in microbial diversity within certain bodily microbiomes, influences adaptive immune responses, including differentiating T regulatory cells (Tregs) and T helper 17 (Th17) cells, which are critical in various lung inflammatory conditions. Additionally, gut and bone marrow immune cells impact pulmonary immune activity, underscoring the complex gut-lung interplay. Moreover, lung microbiota alterations are implicated in diverse gut pathologies, affecting local and systemic immune landscapes. Notably, lung dysbiosis can reciprocally influence gut microbiota composition, indicating bidirectional gut-lung communication. In this review, we investigate the pathophysiology of ALI/acute respiratory distress syndrome (ARDS), elucidating the role of immune cells in the gut-lung axis based on recent experimental and clinical research. This exploration aims to enhance understanding of ALI/ARDS pathogenesis and to underscore the significance of gut-lung interactions in respiratory diseases

Pathophysiology of acute lung injury in patients with acute brain injury: the triple-hit hypothesis.

It has been convincingly demonstrated in recent years that isolated acute brain injury (ABI) may cause severe dysfunction of peripheral extracranial organs and systems. Of all potential target organs and systems, the lung appears to be the most vulnerable to damage after ABI. The pathophysiology of the bidirectional brain-lung interactions is multifactorial and involves inflammatory cascades, immune suppression, and dysfunction of the autonomic system. Indeed, the systemic effects of inflammatory mediators in patients with ABI create a systemic inflammatory environment ("first hit") that makes extracranial organs vulnerable to secondary procedures that enhance inflammation, such as mechanical ventilation (MV), surgery, and infections ("second hit"). Moreover, accumulating evidence supports the knowledge that gut microbiota constitutes a critical superorganism and an organ on its own, potentially modifying various physiological functions of the host. Furthermore, experimental and clinical data suggest the existence of a communication network among the brain, gastrointestinal tract, and its microbiome, which appears to regulate immune responses, gastrointestinal function, brain function, behavior, and stress responses, also named the "gut-microbiome-brain axis." Additionally, recent research evidence has highlighted a crucial interplay between the intestinal microbiota and the lungs, referred to as the "gut-lung axis," in which alterations during critical illness could result in bacterial translocation, sustained inflammation, lung injury, and pulmonary fibrosis. In the present work, we aimed to further elucidate the pathophysiology of acute lung injury (ALI) in patients with ABI by attempting to develop the "double-hit" theory, proposing the "triple-hit" hypothesis, focused on the influence of the gut-lung axis on the lung. Particularly, we propose, in addition to sympathetic hyperactivity, blast theory, and double-hit theory, that dysbiosis and intestinal dysfunction in the context of ABI alter the gut-lung axis, resulting in the development or further aggravation of existing ALI, which constitutes the "third hit.

The Heart Is at Risk: Understanding Stroke-Heart-Brain Interactions with Focus on Neurogenic Stress Cardiomyopathy-A Review.

In recent years, it has been convincingly demonstrated that acute brain injury may cause severe cardiac complications-such as neurogenic stress cardiomyopathy (NSC), a specific form of takotsubo cardiomyopathy. The pathophysiology of these brain-heart interactions is complex and involves sympathetic hyperactivity, activation of the hypothalamic-pituitary-adrenal axis, as well as immune and inflammatory pathways. There have been great strides in our understanding of the axis from the brain to the heart in patients with isolated acute brain injury and more specifically in patients with stroke. On the other hand, in patients with NSC, research has mainly focused on hemodynamic dysfunction due to arrhythmias, regional wall motion abnormality, or left ventricular hypokinesia that leads to impaired cerebral perfusion pressure. Comparatively little is known about the underlying secondary and delayed cerebral complications. The aim of the present review is to describe the stroke-heart-brain axis and highlight the main pathophysiological mechanisms leading to secondary and delayed cerebral injury in patients with concurrent hemorrhagic or ischemic stroke and NSC as well as to identify further areas of research that could potentially improve outcomes in this specific patient population

ARDS associated acute brain injury: from the lung to the brain.

A complex interrelation between lung and brain in patients with acute lung injury (ALI) has been established by experimental and clinical studies during the last decades. Although, acute brain injury represents one of the most common insufficiencies in patients with ALI and acute respiratory distress syndrome (ARDS), the underlying pathophysiology of the observed crosstalk remains poorly understood due to its complexity. Specifically, it involves numerous pathophysiological parameters such as hypoxemia, neurological adverse events of lung protective ventilation, hypotension, disruption of the BBB, and neuroinflammation in such a manner that the brain of ARDS patients-especially hippocampus-becomes very vulnerable to develop secondary lung-mediated acute brain injury. A protective ventilator strategy could reduce or even minimize further systemic release of inflammatory mediators and thus maintain brain homeostasis. On the other hand, mechanical ventilation with low tidal volumes may lead to self-inflicted lung injury, hypercapnia and subsequent cerebral vasodilatation, increased cerebral blood flow, and intracranial hypertension. Therefore, by describing the pathophysiology of ARDS-associated acute brain injury we aim to highlight and discuss the possible influence of mechanical ventilation on ALI-associated acute brain injury

The Role of Thrombelastography in Multiple Trauma

Hemorrhage and traumatic coagulopathyis are major causes of early death in multiply injured patients. Thrombelastography (TEG) seems to be a fast and accurate coagulation test in trauma care. We suggest that multiply injured trauma patients would benefit the most from an early assessment of coagulation by TEG, mainly RapidTEG, to detect an acute traumatic coagulopathy and especially primary fibrinolysis, which is related with high mortality. This review gives an overview on TEG and its clinical applications

The Heart Is at Risk: Understanding Stroke-Heart-Brain Interactions with Focus on Neurogenic Stress Cardiomyopathy—A Review

In recent years, it has been convincingly demonstrated that acute brain injury may cause severe cardiac complications—such as neurogenic stress cardiomyopathy (NSC), a specific form of takotsubo cardiomyopathy. The pathophysiology of these brain-heart interactions is complex and involves sympathetic hyperactivity, activation of the hypothalamic-pituitary-adrenal axis, as well as immune and inflammatory pathways. There have been great strides in our understanding of the axis from the brain to the heart in patients with isolated acute brain injury and more specifically in patients with stroke. On the other hand, in patients with NSC, research has mainly focused on hemodynamic dysfunction due to arrhythmias, regional wall motion abnormality, or left ventricular hypokinesia that leads to impaired cerebral perfusion pressure. Comparatively little is known about the underlying secondary and delayed cerebral complications. The aim of the present review is to describe the stroke-heart-brain axis and highlight the main pathophysiological mechanisms leading to secondary and delayed cerebral injury in patients with concurrent hemorrhagic or ischemic stroke and NSC as well as to identify further areas of research that could potentially improve outcomes in this specific patient population

Refugee, Migrant and Ethnic Minority Health

International migration, particularly to Europe, has increased in the last few decades, making research on aspects of this phenomenon, including numbers, challenges, and successes, particularly vital. This Special Issue highlights this necessary and relevant area of research. It presents 37 articles including studies on diverse topics relating to the health of refugees and migrants. Most articles (28) present studies focusing on European host countries. The focus on Europe is justified if we take into consideration the increased number of refugees and migrants who have come to Europe in recent years. However, there are also articles which present studies from countries in other continents. The topics discussed in the Issue include healthcare utilization, infectious diseases, mother and child health, mental health, and chronic diseases. Finding from the included articles indicate that further development of guidelines and policies at both local and international levels is needed. Priorities must be set by encouraging and funding in-depth research that aims to evaluate the impact of existing policies and interventions. Such research will help us formulate recommendations for the development of strategies and approaches that improve and strengthen the integration of migrants and refugees into the host countries

The Difficult Diagnosis of Ischaemic Papillary Muscle Rupture : Case report from an urban emergency department

We present a rare case of severe ischaemic papillary muscle rupture in a 67-year-old male patient who was admitted to the Emergency Department of the University Hospital Bern, Switzerland, in November 2013 with acute chest pain. On admission, the patient’s blood pressure was 60/40 mm/Hg, his pulse was 110 beats per minute and his respiratory rate was 20 breaths per minute. An electrocardiogram was normal and focused assessment with sonography in trauma was negative. Transthoracic echocardiography showed possible thickening of the mitral valve leaflet with no indications of severe mitral insufficiency or wall motion abnormalities. Triple-ruleout computed tomography angiography revealed no pulmonary emboli or aortic dissection, although coronary atherosclerosis was present. Finally, severe insufficiency of the mitral valve with rupture of the papillary muscle, likely due to ischaemia, was observed via transoesophageal echocardiography. The patient underwent a successful surgical intervention and was discharged 10 days later in stable condition

Fuchs Syndrome with Isolated Oral Mucosa Lesions due to Severe Herpes Simplex Cheilitis in a Patient with Idiopathic Thrombocytopenic Purpura.

Stevens-Johnson syndrome (SJS) is a severe dermatological disease classically characterized by erythematous target lesions and mucosal involvement. Fuchs syndrome is an incomplete presentation of SJS which has oral, conjunctival and genital manifestations but no skin lesions. To the best of our knowledge, our case of Fuchs syndrome in an 80-year-old man is the first such case related to herpes simplex virus (HSV)-1 infection to be described. Our patient quickly recovered following IVIG therapy, although specific treatment is still a topic of discussion. Research is required on this poorly understood dermatological disease to determine optimum therapy. LEARNING POINTS We report a case of Fuchs syndrome in an elderly man after HSV-1 cheilitis.Therapy always includes discontinuation of the causative drug.Specific therapy for Stevens-Johnson syndrome and Fuchs syndrome is still a topic of discussion, although we noted marked improvement following the administration of IVIG therapy

Injury patterns of non-fatal accidents related to ice hockey, an analysis of 7 years of admission to a Level-1 Emergency Centre in Switzerland

Objective This study was carried out to identify the frequency and types of injuries in adult ice hockey, in order to better understand injury patterns and identify potential areas for injury prevention. Methods We conducted a retrospective database review of acute injuries reported in ice hockey in patients presenting to a Level-1 adult Emergency Centre in Switzerland. Patients between January 1, 2013 and December 31, 2019 and over 16 years of age were identified in our computerised patient database. Each consultation was reviewed to derive information on demographics, playing level and the features of the injury, including location, type, mechanism and consequences. Different age groups were compared, as were amateur and professional players. A statistical analysis was performed. Results A total of 230 patients were identified. The most common diagnoses were fracture (28.3%), contusion/abrasion (23.9%), laceration (12.6%) and concussion (10.4%). The most commonly affected body parts were the face (31.3%), the shoulder/clavicle (13.0%) and the head (12.2%). Most lesions were caused by player-player contact (37.4%), contact with the puck (24.3%) and falls (10.9%). In comparison to the younger cohorts, patients >36 years of age more frequently suffered injuries caused by falls, (p Conclusions Injuries continue to play a major role in ice hockey, especially in the face and due to player-player contact. Future investigations should focus on player-player contact and possible effective preventive measures. Players must be encouraged to employ face protection and to wear a mouth guard at all times