Severe Acute Respiratory Distress in a Child with Hypereosinophilic Syndrome: A Case Report.

Hypereosinophilic syndrome with respiratory distress and multiorgan involvement is not so common in children. It is essential to identify this entity based on clinical, laboratory, and imaging features. Corticosteroids should be instituted at the earliest to stabilize the patient and prevent organ damage. Tropical infections are a common secondary cause in children warranting the administration of Diethylcarbamazine. We present a case of an adolescent male in respiratory distress with marked eosinophilia and organs involving the lungs (pulmonary infiltrates with effusion), heart (pericardial effusion), and abdomen (ascites with infiltrates in the liver) which was managed with steroids and anthelmintics. The case highlights the importance of identifying patients with Hypereosinophilic syndrome in pursuing thorough evaluation and commencing therapy.

Definitions of Acute Respiratory Distress Syndrome: Present Recommendations and Challenges.

Acute respiratory distress syndrome (ARDS) is an acute inflammatory process resulting in diffuse lung injury precipitated by an underlying risk factor. However, current definitions may pose barriers to the accurate diagnosis of this syndrome. These include changes in risk factors and associated disease evolution of ARDS, changes in contemporary clinical practice, and access to diagnostic tools required to diagnose ARDS in resource-limited settings. A consensus conference has proposed changes for an expanded global definition of ARDS. In this review article, we review challenges in defining ARDS and present recommendations of the global definition of ARDS.

Environmental Risk Factors for Acute Respiratory Distress Syndrome.

Several environmental exposures increase susceptibility to the acute respiratory distress syndrome (ARDS). Specifically, chronic exposure to ambient air pollution, cigarette smoke, and alcohol "prime" the lung via epithelial injury, endothelial dysfunction, and immunomodulatory mechanisms, increasing the risk and severity of ARDS following an array of acute insults. Future research of these pathways may reveal therapeutic targets. Relevant emerging threats, such as electronic cigarettes and vaping, wildfire smoke, and the environmental hazards associated with climate change, may also be associated with ARDS. Building upon existing public policy interventions can prevent substantial morbidity and mortality from ARDS.

Lung and Diaphragm Protection During Mechanical Ventilation in Patients with Acute Respiratory Distress Syndrome.

Patients with acute respiratory distress syndrome often require mechanical ventilation to maintain adequate gas exchange and to reduce the workload of the respiratory muscles. Although lifesaving, positive pressure mechanical ventilation can potentially injure the lungs and diaphragm, further worsening patient outcomes. While the effect of mechanical ventilation on the risk of developing lung injury is widely appreciated, its potentially deleterious effects on the diaphragm have only recently come to be considered by the broader intensive care unit community. Importantly, both ventilator-induced lung injury and ventilator-induced diaphragm dysfunction are associated with worse patient-centered outcomes.

Acute Respiratory Distress Syndrome in the Immunocompromised Patient.

Improving short- and long-term outcomes in immunosuppressed patients, including patients with cancer, solid-organ transplant recipients, and patients with short- and long-term steroid treatment, has led to a paradigm shift in intensive care unit admission policies. Approximately 20% of patients currently admitted to the ICU carry a diagnosis of immune deficiency. In this population, acute respiratory failure and acute respiratory distress syndrome are the most frequent causes of ICU admission. Intensivists should therefore be aware of etiologies, diagnostics, and management strategies unique to this population.

[Extracorporeal membrane oxygenation (ECMO) in severe acute respiratory distress syndrome due to blunt chest trauma: A case report]. / Oxigenación por membrana extracorpórea (ECMO) en síndrome de dificultad respiratoria aguda grave por traumatismo torácico contuso. Caso clínico.

We report a case of a patient with chest trauma (TT) complicated with severe acute respiratory distress syndrome (ARDS) who required extracorporeal membrane oxygenation (ECMO) as ventilatory support. Clinical case: A 48-year-old man, with no relevant history, after a high-energy vehicle collision admitted with severe TT. He evolved with respiratory failure that required intubation and connection to mechanical ventilation (MV). He persisted with high ventilatory requirements, requiring rescue ECMO and transfer to our center. He evolved with gasometric and ventilatory improvement that allowed disconnection on the ten day. There were no bleeding or thrombotic complications during ECMO. Discussion: ECMO support is complex, expensive, and is performed in high-risk patients. The use of this resource requires trained health workers. Its use must be highly selective, constituting a valuable support tool in some patients with severe ARDS secondary to TT.

Resolution of Acute Respiratory Distress Syndrome-Induced Takotsubo Cardiomyopathy with Venovenous Extracorporeal Membrane Oxygenation.

INTRODUCTION: Takotsubo cardiomyopathy (TTCM) can occur in acute respiratory distress syndrome (ARDS) and a few cases in literature were reported to be associated with hemodynamic instability. All these patients were managed with venoarterial extracorporeal membrane oxygenation (VA-ECMO).Case presentation: We present two patients with ARDS-induced TTCM who were managed successfully with venovenous ECMO (VV-ECMO). CONCLUSION: Ventricular function in both patients fully recovered three days after ECMO initiation, and they were subsequently weaned from ECMO once pulmonary function improved.

Transpulmonary Plasma Endothelin-1 Arterial:Venous Ratio Differentiates Survivors from Non-Survivors in Critically Ill Patients with COVID-19-Induced Acute Respiratory Distress Syndrome.

Endothelin-1 (ET-1) is a potent vasoconstrictor produced by endothelial cells and cleared from circulating blood mainly in the pulmonary vasculature. In a healthy pulmonary circulation, the rate of local production of ET-1 is less than its rate of clearance. In the present study, we aimed to investigate whether the abnormal pulmonary circulatory handling of ET-1 relates to poor clinical outcomes in patients with coronavirus disease 2019 (COVID-19)-induced acute respiratory distress syndrome (ARDS). To this end, central venous and systemic arterial ET-1 plasma levels were simultaneously measured on Days 1 and 3 following ICU admission in mechanically ventilated COVID-19 patients with ARDS (COVID-19 ARDS, N = 18). Central venous and systemic arterial ET-1 plasma levels were also measured in two distinct SARS-CoV-2-negative mechanically ventilated critically ill patient groups, matched for age, sex, and critical illness severity, with ARDS (non-COVID-19 ARDS, N = 14) or without ARDS (non-COVID-19 non-ARDS, N = 20). Upon ICU admission, COVID-19-induced ARDS patients had higher systemic arterial and central venous ET-1 levels compared to the non-COVID-19 ARDS and non-COVID-19 non-ARDS patients (p < 0.05), yet a normal systemic arterial:central venous (A:V) ET-1 ratio [0.63 (0.49-1.02)], suggesting that pulmonary ET-1 clearance is intact in these patients. On the other hand, the non-COVID-19 ARDS patients demonstrated abnormal ET-1 handling [A:V ET-1 ratio 1.06 (0.93-1.20)], while the non-COVID-19 non-ARDS group showed normal ET-1 handling [0.79 (0.52-1.11)]. On Day 3, the A:V ratio in all three groups was <1. When the COVID-19 ARDS patients were divided based on 28-day ICU mortality, while their systemic arterial and central venous levels did not differ, the A:V ET-1 ratio was statistically significantly higher upon ICU admission in the non-survivors [0.95 (0.78-1.34)] compared to the survivors [0.57 (0.48-0.92), p = 0.027]. Our results highlight the potential importance of ET-1 as both a biomarker and a therapeutic target in critically ill COVID-19 patients. The elevated A:V ET-1 ratio in non-survivors suggests that the early disruption of pulmonary ET-1 handling may be a key marker of poor prognosis.

Rehabilitation for Patients with COVID-19-Associated Acute Respiratory Distress Syndrome During Quarantine: A Single-Center Experience.

Background and Objectives: In this study, we evaluated clinical factors associated with implementing a rehabilitation program for patients with COVID-19-associated acute respiratory distress syndrome (ARDS) requiring mechanical ventilation (MV) during the quarantine period. Materials and Methods: This observational study was conducted in the National Designated Isolated ICU, a dedicated COVID-19 center with 18 beds, from 30 December 2020 to 30 May 2022. One hundred and fifty-four patients (mean age: 67.3 ± 13.4 years; male: 59.7%) were enrolled. The ICU rehabilitation program included early mobilization, chest physiotherapy, and dysphagia treatment. Results: Forty-five patients (29.3%) participated in the rehabilitation program. Multivariate logistic regression identified three significant factors: tracheostomy (odds ratio [OR], 2.796; 95% confidence interval [CI], 1.238-6.316; p = 0.013), body mass index ≥ 25.0 kg/m2 (OR, 2.724; 95% CI, 1.276-5.817; p = 0.010), and extracorporeal membrane oxygenation (OR, 2.931; 95% CI, 1.165-7.377; p = 0.022); patients with all three factors were younger (median 44 vs. 70 years, p < 0.001) and had significantly lower Acute Physiology and Chronic Health Evaluation II scores (median 12 vs. 16, p = 0.002) on the MV day. One-year cumulative mortality rates for patients with 0 to 3 factors were 66.7%, 50.8%, 38.9%, and 15.4%, respectively, with a significant difference among them (log-rank, p < 0.001). Conclusions: Three clinical factors associated with implementing a rehabilitation program during the quarantine period for COVID-19-associated ARDS patients were identified. The program was feasible and beneficial, particularly for younger patients with lower illness severity and fewer comorbidities on the day of MV.

Gut microbiota-derived acetic acids promoted sepsis-induced acute respiratory distress syndrome by delaying neutrophil apoptosis through FABP4.

In patients with sepsis, neutrophil apoptosis tends to be inversely proportional to the severity of sepsis, but its mechanism is not yet clear. This study aimed to explore the mechanism of fatty acid binding protein 4 (FABP4) regulating neutrophil apoptosis through combined analysis of gut microbiota and short-chain fatty acids (SCFAs) metabolism. First, neutrophils from bronchoalveolar lavage fluid (BALF) of patients with sepsis-induced acute respiratory distress syndrome (ARDS) were purified and isolated RNA was applied for sequencing. Then, the cecal ligation and puncture (CLP) method was applied to induce the mouse sepsis model. After intervention with differential SCFAs sodium acetate, neutrophil apoptosis and FABP4 expression were further analyzed. Then, FABP4 inhibitor BMS309403 was used to treat neutrophils. We found CLP group had increased lung injury score, lung tissue wet/dry ratio, lung vascular permeability, and inflammatory factors IL-1ß, TNF-α, IL-6, IFN-γ, and CCL3 levels in both bronchoalveolar lavage fluid and lung tissue. Additionally, FABP4 was lower in neutrophils of ARDS patients and mice. Meanwhile, CLP-induced dysbiosis of gut microbiota and changes in SCFAs levels were observed. Further verification showed that acetic acids reduced neutrophil apoptosis and FABP4 expression via FFAR2. Besides, FABP4 affected neutrophil apoptosis through endoplasmic reticulum (ER) stress, and neutrophil depletion alleviated the promotion of ARDS development by BMS309403. Moreover, FABP4 in neutrophils regulated the injury of RLE-6TN through inflammatory factors. In conclusion, FABP4 affected by gut microbiota-derived SCFAs delayed neutrophil apoptosis through ER stress, leading to increased inflammatory factors mediating lung epithelial cell damage.

NK cells contribute to the resolution of experimental malaria-associated acute respiratory distress syndrome after antimalarial treatment.

In both humans and mice, natural killer (NK) cells are important lymphocytes of the innate immune system. They are often considered pro-inflammatory effector cells but may also have a regulatory or pro-resolving function by switching their cytokine profile towards the production of anti-inflammatory cytokines, including interleukin-10 (IL-10) and transforming growth factor-ß, and by killing pro-inflammatory immune cells. Here, the role of NK cells in the resolution of malaria lung pathology was studied. Malaria complications, such as malaria-associated acute respiratory distress syndrome (MA-ARDS), are often lethal despite the rapid and efficient killing of Plasmodium parasites with antimalarial drugs. Hence, studying the resolution and healing mechanisms involved in the recovery from these complications could be useful to develop adjunctive treatments. Treatment of Plasmodium berghei NK65-infected C57BL/6 mice with a combination of artesunate and chloroquine starting at the appearance of symptoms was used as a model to study the resolution of MA-ARDS. The role of NK cells was studied using anti-NK1.1 depletion antibodies and NK cell-deficient mice. Using both methods, NK cells were found to be dispensable in the development of MA-ARDS, as shown previously. In contrast, NK cells were crucial in the initiation of resolution upon antimalarial treatment, as survival was significantly decreased in the absence of NK cells. Considerably increased IL-10 expression by NK cells suggested an anti-inflammatory and pro-resolving phenotype. Despite the increase in Il10 expression in the NK cells, inhibition of the IL-10/IL-10R axis using anti-IL10R antibodies had no effect on the resolution for MA-ARDS, suggesting that the pro-resolving effect of NK cells cannot solely be attributed to their IL-10 production. In conclusion, NK cells contribute to the resolution of experimental MA-ARDS.

Presence of cholestasis and its impact on survival in SARS-CoV-2 associated acute respiratory distress syndrome.

Data on cholestasis and biliary injury in patients with COVID-19 are scarce. The primary aim of this study was to evaluate the prevalence of cholestasis and factors associated with its development and outcome in critically ill patients with COVID-19 associated acute respiratory distress syndrome (ARDS). In this retrospective exploratory study, COVID-19 patients with ARDS admitted to an intensive care unit (ICU) at the Medical University of Vienna were evaluated for the development of cholestasis defined as an alkaline phosphatase level of 1.67x upper limit of normal for at least three consecutive days. Simple and multiple logistic regression analysis was used to evaluate parameters associated with development of cholestasis and survival. Of 225 included patients 119 (53%) developed cholestasis during ICU stay. Patients with cholestasis had higher peak levels of alkaline phosphatase, gamma-glutamyl transferase, bilirubin and inflammation parameters. Factors independently associated with cholestasis were extracorporeal membrane oxygenation support, ketamine use, high levels of inflammation parameters and disease severity. Presence of cholestasis and peak ALP levels were independently associated with worse ICU and 6-month survival. Development of cholestasis is a common complication in critically ill COVID-19 patients and represents a negative prognostic marker for survival. It is associated with disease severity and specific treatment modalities of intensive care.

Optimizing the safety and efficacy of the awake venovenous extracorporeal membrane oxygenation in patients with COVID-19-related ARDS.

BACKGROUND: Maintaining the patient awake and not intubated during the venovenous extracorporeal membrane oxygenation (VV ECMO) reduces the risk of ventilation-induced lung injury in patients with ARDS. Currently, there is a lack of data on outcomes and complications associated with the awake ECMO approach. OBJECTIVES: To evaluate outcomes and the occurrence of complications of awake ECMO approach guided by local safety protocol comprising ultrasound-guided cannulation, argatroban-based anticoagulation, respiratory support, and routine sedation targeted to reduce respiratory effort and keeping nurse-to-patient ratio of 1:1. DESIGN: A single-center retrospective case series analysis. METHODS: Consecutive patients with COVID-19-related acute respiratory distress syndrome (ARDS) (CARDS) treated by full awake VV ECMO approach from April 2019 to December 2023 were eligible. RESULTS: Our center treated 10 patients (mean age 54.7 ± 11.6 years) with CARDS with an awake ECMO approach. The reasons for awake ECMO included the presence of barotrauma in six patients, a team consensus to prefer awake ECMO instead of mechanical ventilation in three patients, and the patient's refusal to be intubated in one case. Before ECMO, patients were severely hypoxemic, with a mean value of Horowitz index of 48.9 ± 9.1 mmHg and a mean respiratory rate of 28.8 ± 7.3 breaths per minute on high-flow nasal cannula or noninvasive ventilation support. The mean duration of awake VV ECMO was 558.0 ± 173.6 h. Seven patients (70%) were successfully disconnected from ECMO and fully recovered. Intubation from respiratory causes was needed in three patients (30%), all of whom died eventually. In total, three episodes of delirium, two episodes of significant bleeding, one pneumothorax requiring chest tube insertion, and one oxygenator acute exchange occurred throughout the 5580 h of awake ECMO. No complications related to cannula displacement or malposition occurred. CONCLUSION: The awake ECMO strategy guided by safety protocol appears to be a safe approach in conscious, severely hypoxemic, non-intubated patients with COVID-19-related ARDS.

Enhancing the safety and effectiveness of extracorporeal membrane oxygenation (ECMO) therapy in awake, spontaneously breathing patients with the most severe form of COVID-19-related acute respiratory distress syndrome (ARDS)Why Was the Study Done? Extracorporeal membrane oxygenation (ECMO) represents a life-saving therapeutic approach that ensures appropriate gas exchange in patients with the most severe form of respiratory failure ­ acute respiratory distress syndrome (ARDS). Typically, patients are connected to ECMO when already deeply sedated and mechanically ventilated. The awake ECMO approach (keeping the patient awake, not intubated, and breathing spontaneously during ECMO support) minimizes the risks associated with mechanical ventilation and provides several relevant physiological benefits. However, the awake ECMO approach is also associated with several significant risks, including delirium, bleeding, and cannula displacement. Published papers have reported relatively frequent complications and method failures. What Did the Researchers Do? To address safety concerns regarding the awake ECMO approach, we present a single-center retrospective analysis of ten COVID-19-related ARDS patients treated with the awake ECMO approach, guided by the local safety protocol. What Did the Researchers Find? The awake ECMO approach yielded success (i.e., the patient was not intubated for respiratory causes, was successfully disconnected from ECMO, and fully recovered in seven patients (70.0%), outperforming previously published efficacy ranges. Three patients were intubated due to the progression of respiratory failure and eventually died. The incidence of adverse events during the 5,580 hours of awake ECMO was considered low. No cannula displacement or malposition occurred despite routine active physiotherapy, including walking during ECMO treatment in three patients. What Do the Findings Mean? The general applicability of the study is limited by the low number of patients and the retrospective monocentric design. However, the presented data illustrate real-life clinical scenarios and could aid clinicians in managing severely hypoxemic but still conscious and cooperative patients.

NAT10-mediated ac4C acetylation of TFRC promotes sepsis-induced pulmonary injury through regulating ferroptosis.

BACKGROUND: Sepsis-induced pulmonary injury (SPI) is a common complication of sepsis with a high rate of mortality. N4-acetylcytidine (ac4C) is mediated by the ac4C "writer", N-acetyltransferase (NAT)10, to regulate the stabilization of mRNA. This study aimed to investigate the role of NAT10 in SPI and the underlying mechanism. METHODS: Twenty-three acute respiratory distress syndrome (ARDS) patients and 27 non-ARDS volunteers were recruited. A sepsis rat model was established. Reverse transcription-quantitative polymerase chain reaction was used to detect the expression of NAT10 and transferrin receptor (TFRC). Cell viability was detected by cell counting kit-8. The levels of Fe2+, glutathione, and malondialdehyde were assessed by commercial kits. Lipid reactive oxygen species production was measured by flow cytometric analysis. Western blot was used to detect ferroptosis-related protein levels. Haematoxylin & eosin staining was performed to observe the pulmonary pathological symptoms. RESULTS: The results showed that NAT10 was increased in ARDS patients and lipopolysaccharide-treated human lung microvascular endothelial cell line-5a (HULEC-5a) cells. NAT10 inhibition increased cell viability and decreased ferroptosis in HULEC-5a cells. TFRC was a downstream regulatory target of NAT10-mediated ac4C acetylation. Overexpression of TFRC decreased cell viability and promoted ferroptosis. In in vivo study, NAT10 inhibition alleviated SPI. CONCLUSION: NAT10-mediated ac4C acetylation of TFRC aggravated SPI through promoting ferroptosis.

TGF-ß1 overexpression in severe COVID-19 survivors and its implications for early-phase fibrotic abnormalities and long-term functional impairment.

Introduction: In post-COVID survivors, transforming growth factor-beta-1 (TGF-ß1) might mediate fibroblast activation, resulting in persistent fibrosis. Methods: In this study, 82 survivors of COVID-19-associated ARDS were examined at 6- and 24-months post-ICU discharge. At 6-months, quantitative CT analysis of lung attenuation was performed and active TGF-ß1 was measured in blood and exhaled breath condensate (EBC). Results: At 6-months of ICU-discharge, patients with reduced DmCO/alveolar volume ratio exhibited higher plasma and EBC levels of active TGF-ß1. Plasma TGF-ß1 levels were elevated in dyspneic survivors and directly related to the high-attenuation lung volume. In vitro, plasma and EBC from survivors induced profibrotic changes in human primary fibroblasts in a TGF-ß receptor-dependent manner. Finally, at 6-months, plasma and EBC active TGF-ß1 levels discriminated patients who, 24-months post-ICU-discharge, developed gas exchange impairment. Discussion: TGF-ß1 pathway plays a pivotal role in the early-phase fibrotic abnormalities in COVID-19-induced ARDS survivors, with significant implications for long-term functional impairment.

Leptospirosis and melioidosis coinfection presenting as acute respiratory distress syndrome and osteomyelitis: Case report and systematic review.

INTRODUCTION: Leptospirosis and melioidosis are common in tropical and temperate climates and can be acquired by exposure to contaminated water and soil. However, concomitant leptospirosis and melioidosis infection is rarely described in the literature. We report a case of leptospirosis-melioidosis coinfection and systematically review the literature. CASE PRESENTATION: A 42-year-old male presented with fever associated with chills and rigor, dull aching pain in the right thigh, myalgia, progressive breathlessness, and dry cough for 10 days. At presentation, he was tachypneic and had tachycardia, and oxygen saturation was 46% in room air. Chest radiography and computed tomography scan showed interstitial involvement. Magnetic resonance imaging for thigh pain revealed right femur osteomyelitis. Leptospira serology was positive, and blood culture grew Burkholderia pseudomallei, confirming the diagnosis of melioidosis. Thus, a diagnosis of presumptive leptospirosis based on modified Faine's criteria and systemic melioidosis was made. He received doxycycline and intravenous meropenem and improved. RESULTS: We performed a systematic review to understand the spectrum of leptospirosis-melioidosis coinfection. We identified only nine cases of coinfection described in literature. Only one patient had septic arthritis, and our case is the only one presenting with osteomyelitis. Serology diagnosed leptospirosis, whereas melioidosis was confirmed by blood culture in most patients. The majority of coinfected patients developed some complications, and six died. CONCLUSIONS: Leptospirosis-melioidosis coinfection is rarely reported in the literature. Physicians should maintain a high index suspicion of leptospirosis-melioidosis coinfection in patients presenting with acute febrile illness following exposure to soil or freshwater, particularly in tropical and endemic regions.

Acute respiratory distress syndrome as the initial symptom of hepatic angiosarcoma with Kasabach-Merritt syndrome: A case report.

RATIONALE: Hepatic angiosarcoma (HSA) has a poor prognosis. Our understanding of its clinical features, diagnosis, treatment, and prognosis remains limited. In certain cases, vascular tumors such as HSA can induce bleeding complications due to thrombocytopenia, known as Kasabach-Merritt syndrome (KMS). When KMS symptoms occur in the lungs, its clinical manifestations closely resemble those of ARDS, leading to misdiagnosis and poor outcomes. Unfortunately, this condition is extremely rare and there is a lack of relevant case reports, which further adds to the difficulty of its diagnosis and treatment. PATIENT CONCERNS: This case report describes a patient who initially presented with symptoms of ARDS. Due to the unique nature of these symptoms, the patient underwent a complex diagnostic and treatment process before finally being diagnosed with HSA complicated by KMS through pathological examination. DIAGNOSES: The patient was eventually diagnosed with HSA by pathology and KMS with multiorgan hemorrhage. INTERVENTIONS: Highly misleading clinical manifestations were recorded during the diagnosis and treatment, which, to our knowledge, have not been previously reported. OUTCOMES: The patient died from a massive pulmonary hemorrhage. LESSONS: Dysfunction of a single organ or system may be the external manifestation of a multi-system clinical disease. Therefore, in the clinical diagnosis and treatment process, especially during early diagnosis, while it is important to focus on the primary or typical clinical symptoms, it is equally crucial not to underestimate or ignore accompanying symptoms that lack specificity. When diagnosis and treatment reach an impasse, these "atypical" symptoms often prove to be key in solving the puzzle.

Successful rapid improvement of acute respiratory distress syndrome induced by EGFR-mutated non-small cell lung cancer with almonertinib: a case report.

BACKGROUND: Acute respiratory distress syndrome (ARDS) is a life-threatening condition frequently encountered in critically ill patients, including those with advanced non-small cell lung cancer (NSCLC). Almonertinib, a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), has shown promise as a first-line treatment for NSCLC with classical EGFR mutations. However, its efficacy in NSCLC patients suffering from ARDS has not been well-documented. CASE PRESENTATION: We report the case of a 63-year-old Chinese Han female with severe NSCLC complicated by ARDS. Upon hospital admission, the patient exhibited progressive dyspnea and required intubation to maintain oxygenation. Pathological analysis of bronchoalveolar lavage fluid sediment confirmed lung adenocarcinoma, and genetic testing of blood identified an EGFR E19 mutation. The patient was treated with almonertinib, resulting in significant clinical improvement and successful extubation after nine days. Radiographic imaging showed substantial reduction in pulmonary lesions, highlighting the efficacy of almonertinib. CONCLUSION: This case represents the first documented successful treatment of ARDS induced by EGFR E19 mutated NSCLC using almonertinib. The favorable clinical response observed in this critically ill patient suggests that almonertinib may be a viable therapeutic option for managing severe complications in NSCLC. Further research is necessary to corroborate these findings and optimize dosage and toxicity management strategies for broader clinical application.

Complex Interplay of COVID-19 ARDS with Guillain-Barré Syndrome and Cerebral Infarction: A Case Study.

BACKGROUND Coronavirus disease (COVID-19) can cause various complications. We report a case of severe COVID-19 acute respiratory distress syndrome (ARDS) in a patient receiving veno-venous extracorporeal membrane oxygenation (V-V ECMO), complicated by Guillain-Barre syndrome (GBS) and cerebral infarction, as well as pulmonary embolism. CASE REPORT A 55-year-old Japanese man with a history of ulcerative colitis was admitted for COVID-19. His respiratory status worsened and progressed to ARDS, requiring intubation on hospital day (HD) 3. On HD 16, contrast computed tomography revealed PE. On HD 18, his respiratory condition worsened, and V-V ECMO was initiated. On HD 23, V-V ECMO was successfully discontinued. He regained consciousness on HD 44, but he had quadriplegia. Deep-tendon reflexes were absent in all limbs. Cranial nerve involvement, specifically bilateral facial nerve weakness, was noted. Magnetic resonance imaging showed bilateral scattered cerebral infarctions on HD 76. Nerve conduction studies indicated severe axonal neuropathy. Cerebrospinal fluid examination showed albuminocytologic dissociation. The antibody to the ganglioside GD1a was positive. These findings were consistent with the diagnosis of GBS. He received immunoglobulin treatment on HD 89, and his neurological findings slightly improved. CONCLUSIONS This study emphasized that in COVID-19, neurological complications are not rare, are difficult to diagnose, and are prone to delays in detection.

Delayed admission to hospital with proper prehospital treatments prevents severely burned patients from sepsis in China: A retrospective study.

BACKGROUND: Sepsis is one of the major causes of morbidity and mortality in burn patients. However, the optimal timing of admission which can minimize the probability of sepsis is still unclear. This study aims to determine the optimal time period of admission for severely burned patients and find out the possible reasons for it. METHOD: 185 victims to the Kunshan factory aluminum dust explosion accident, which happened on August 2nd, 2014, were studied. The optimal cutpoint for continuous variables in survival models was determined by means of the maximally selected rank statistic. Univariate and multivariate analyses were further conducted to verify that admission time was not a risk factor for sepsis. Subgroup analyses were performed to find out possible contributing factors for the result. RESULT: The cutoff point for admission time was determined as seven hours, which was supported by the survival curve (p < 0.001). Multivariate analysis showed that, in our study population, delayed admission time was not a risk factor for sepsis (HR = 0.610, 95 %CI = 0.415 - 0.896, p = 0.012). Subgroup analyses showed that "Tracheotomy before admission" (p = 0.002), "Whole blood transfusion" (p < 0.001), "Hemodynamic instability before admission" (p = 0.02), "Has a burn department in the hospital" (p = 0.009), "Has a burn ICU in the hospital" (p < 0.001), "Acute heart failure (AHF)" (p = 0.05), "acute respiratory distress syndrome (ARDS)" (p = 0.05) and "GI bleeding" (p = 0.04) were all statistically significant. CONCLUSION: In our study population, we found that delayed admission time was not a risk factor associated with a reduced incidence of sepsis among severely burned patients. This might be attributed to variations in prehospital treatments (whole blood transfusion and tracheotomy), whether the hospital had a burn department/ICU, and certain complications (AHF, ARDS and GI bleeding). It can be inferred that early prehospital care plays a crucial role in reducing sepsis risk among severe burn patients.