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."

Systemic embolization due to non-bacterial thrombotic endocarditis: An autopsy case report and mini review of the literature.

Nonbacterial thrombotic endocarditis is a rare, non-infectious complication associated with hypercoagulable states, such as malignancies and autoimmune diseases. Due to the difficulty distinguishing marantic endocarditis from infective endocarditis, the diagnosis is often delayed or even a postmortem finding. We present the case of a 70-year-old Caucasian female with marantic endocarditis secondary to metastatic duodenal adenocarcinoma. The patient presented with a short history of memory deficits, personality disturbances, and left homonymous hemianopia. Diffusion-weighted magnetic resonance imaging showed multi-territorial bihemispheric cerebral infarctions. Transthoracic echocardiography revealed native mitral valve endocarditis, and serial blood cultures remained negative. Despite antibiotic therapy, the patient's condition continuously deteriorated, and she died within 3 weeks after her initial presentation. Postmortem examination showed a non-bacterial thrombotic endocarditis. Early clinical suspicion and prompt diagnosis are of decisive importance for the survival of the patients.

Case report: Probable toxocariasis in a Swiss adult patient with hypereosinophilic syndrome and multiorgan involvement.

Hypereosinophilic syndromes are a heterogeneous group of rare diseases characterized by eosinophil-related organ damage and peripheral blood hypereosinophilia. Hypereosinophilic syndromes may occur secondary to a variety of clinical entities, for example, drug hypersensitivity reactions, parasitic infections, autoimmune disorders, and malignancies. Toxocariasis is a parasitic infection caused by the larval stage of the Toxocara species. It is usually a childhood disease and invades organs such as the liver but can affect any organ. Hypereosinophilic syndrome and multiorgan involvement are very rare manifestations of Toxocara infection, especially in adults. However, the disease may be underdiagnosed because of different factors, including a lack of laboratory infrastructure in some countries, a lack of uniform case definitions, and limited surveillance infrastructure, with its estimation constituting a challenge. We, therefore, present a probable case of hypereosinophilic syndrome with multiorgan involvement secondary to infection with Toxocara canis in a 79-year-old Swiss female patient with a medical history of ischemic cerebrovascular insult and a curatively resected non-small-cell bronchial carcinoma, successfully treated with albendazole and steroids.

Insights into SARS-CoV-2-associated subacute thyroiditis: from infection to vaccine.

Since the COVID-19 emergence as a global pandemic in March 2020, more than 5 million SARS-CoV-2-related deaths have been globally documented. As the pandemic progressed, it became clear that, although the infection is mainly characterized as a respiratory disease, it also affects other organs and systems, including the thyroid gland. Indeed, emerging evidence suggests that SARS-CoV-2 can act as a trigger for various thyroid disorders, for example, subacute thyroiditis (SAT), Grave's disease, and non-thyroidal illness syndrome. The entry of SARS-CoV-2 into the host cells is mainly mediated by the ACE2-receptor, making organs and systems with high expression of this receptor, such as the thyroid gland, highly vulnerable to COVID-19. Accumulating data propose that SAT may be an underestimated manifestation of COVID-19 infection. Importantly, if SAT remains unrecognized, it may trigger or aggravate potential other complications of the disease, for example, respiratory insufficiency and cardiovascular complications, and thus negatively influence prognosis. Moreover, recent case reports, case series, and systematic reviews highlight SAT as a potential side effect of the vaccination against SARS-CoV-2. The present review aims to raise awareness of SARS-CoV-2-associated- and post-vaccination subacute thyroiditis, to discuss recent evidence regarding its pathophysiology, and to present useful information for this special form of SAT related to daily clinical practice.

Health Status of Afghan Refugees in Europe: Policy and Practice Implications for an Optimised Healthcare.

Four decades of civil war, violence, and destabilisation have forced millions of Afghans to flee their homes and to move to other countries worldwide. This increasing phenomenon may challenge physicians unfamiliar with the health status of this population, which may be markedly different from that of the host country. Moreover, several factors during their migration, such as transport in closed containers, accidental injuries, malnutrition, and accommodation in detention centres and refugee camps have a major influence on the health of refugees. By taking into account the variety of the specific diseases among migrant groups, the diversity of the origins of refugees and asylum seekers, and the increasing numbers of Afghan refugees, in this review we focus on the population of Afghans and describe their health status with the aim of optimising our medical approach and management. Our literature review shows that the most prevalent reported infections are tuberculosis and other respiratory tract infections and parasitic diseases, for example leishmaniasis, malaria, and intestinal parasitic infections. Anaemia, hyperlipidaemia, arterial hypertension, diabetes, smoking, overweight, malnutrition, low socioeconomic status, and poor access to healthcare facilities are additional risk factors for non-communicable diseases among Afghan refugees. With regards mental health issues, depression and post-traumatic stress disorder (PTSD) are the most common diagnoses and culture shock and the feeling of being uprooted modulate their persistence. Further research is needed in order to provide us with extensive, high-quality data about the health status of Afghan refugees. The main objective of this review is to identify protective factors which could ensure key health concepts and good clinical practice.

Brain-lung interactions and mechanical ventilation in patients with isolated brain injury.

During the last decade, experimental and clinical studies have demonstrated 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 brain injury (BI). The pathophysiology of these brain-lung interactions are complex and involve neurogenic pulmonary oedema, inflammation, neurodegeneration, neurotransmitters, immune suppression and dysfunction of the autonomic system. The systemic effects of inflammatory mediators in patients with BI create a systemic inflammatory environment that makes extracranial organs vulnerable to secondary procedures that enhance inflammation, such as mechanical ventilation (MV), surgery and infections. Indeed, previous studies have shown that in the presence of a systemic inflammatory environment, specific neurointensive care interventions-such as MV-may significantly contribute to the development of lung injury, regardless of the underlying mechanisms. Although current knowledge supports protective ventilation in patients with BI, it must be born in mind that ABI-related lung injury has distinct mechanisms that involve complex interactions between the brain and lungs. In this context, the role of extracerebral pathophysiology, especially in the lungs, has often been overlooked, as most physicians focus on intracranial injury and cerebral dysfunction. The present review aims to fill this gap by describing the pathophysiology of complications due to lung injuries in patients with a single ABI, and discusses the possible impact of MV in neurocritical care patients with normal lungs.

Midthoracic Pain, Sentinel Arterial Haemorrhage and Exsanguination after a Symptom-Free Interval (Chiari's Triad) is Diagnostic of Arterio-Oesophageal Fistula: A Life-Threatening Cause of Gastrointestinal Bleeding.

INTRODUCTION: Arterio-oesophageal fistulae are a very uncommon cause of severe gastrointestinal bleeding, and mostly result from an aberrant right subclavian artery and mediastinal surgery or prolonged endotracheal/nasogastric intubation. MATERIAL AND METHODS: We present the case of a patient with an oesophageal adenocarcinoma and haematemesis due to a subclavian arterio-oesophageal fistula after mediastinal radiotherapy. CONCLUSION: We discuss the rare, life-threatening condition of acute erosion of the left subclavian artery caused by an oesophageal tumour and presenting with Chiari's triad. LEARNING POINTS: Subclavian arterio-oesophageal fistula is an uncommon, life-threatening cause of gastrointestinal bleeding.Knowledge of Chiari's triad enables early recognition of potentially fatal gastro-intestinal bleeding.A high level of suspicion is essential for prompt diagnosis and referral for surgical treatment especially in patients with malignancies of the upper gastrointestinal tract.

High-Tidal-Volume Mechanical Ventilation and Lung Inflammation in Intensive Care Patients With Normal Lungs.

BACKGROUND: This study was conducted to investigate whether high-tidal-volume mechanical ventilation is associated with increased lung inflammation compared with low-tidal-volume mechanical ventilation in critically ill patients with no evidence of lung injury. METHODS: In this prospective, single-blind, randomized (1:1), parallel-group study, 18 critically ill patients with normal lungs were randomly assigned to receive mechanical ventilation with a tidal volume of either 6 mL/kg (low tidal volume) or 12 mL/kg (high tidal volume) during the first 4 days in the intensive care unit. RESULTS: At baseline and at 24, 48, and 96 hours, exhaled breath condensate was collected to measure interleukin 1ß, interleukin 10, tumor necrosis factor α, and total nitric oxide metabolites. Interleukin 1ß levels in exhaled breath condensate were significantly increased at 24 hours compared with baseline in the high-tidal-volume group but not in the low-tidal-volume group. The interleukin 1ß increase in the high-tidal-volume group was transient. Exhaled breath condensate levels of interleukin 1ß, interleukin 10, tumor necrosis factor α, and total nitric oxide metabolites did not differ significantly between the high-tidal-volume and low-tidal-volume groups at any time point. CONCLUSION: Short-term mechanical ventilation with a tidal volume of 12 mL/kg may trigger inflammatory responses in the lungs of intensive care unit patients without preexisting lung injury.