Xinhua Ma

Rationale: Cardiac arrest (CA) is an acute emergency with high mortality and is closely associated with the risk of brain damage or systemic ischemia–reperfusion injury, post-traumatic stress symptoms. Patient concerns: Targeted temperature management in the intensive care unit can improve the neurological outcomes of patients who are comatose after resuscitation from CA. However, there is often a lack of specific evaluation methods for optimal target temperature settings. Diagnoses: From November 2021 to October 2022, 9 CA patients received prompt cardiopulmonary resuscitation and return of spontaneous circulation after approximately 10 to 30 minutes of cardiopulmonary resuscitation in Xiangya Hospital, Central South University. Interventions: We retrospectively reviewed 9 CA patients’ medical data, including demographic characteristics, hemodynamic change, clinically relevant score, imageological examination, transcranial Doppler ultrasonography, electroencephalogram (EEG), somatosensory-evoked potential, and laboratory data. Outcomes: According to the result of each patient’s transcranial Doppler ultrasonography, somatosensory-evoked potential, and EEG to formulate an individualized target temperature. Contrary to the internationally recommended target of hypothermia, we found that not all patients require hypothermia therapy to maintain normal cerebrovascular autonomic regulation function. And neuron-specific enolase and S100β in patients showed a downward trend after hypothermia therapy. Compared with before hypothermia treatment, clinically relevant scores were reduced in patients with good prognosis. Intracranial congestion or ischemia was improved and intracranial pressure was reduced in all patients during hypothermia treatment. For patients with good EEG response, the ratio of gray matter in the brain increased and the neurological prognosis was significantly improved. Finally, after 6 months of follow-up, we found 3 patients died and 1 patient had a long-term vegetative state, the other patients had a good prognosis. Lessons: Individualized targeted temperature management under the guidance of multimodal brain monitoring plays an important role in brain protection of patients with CA.

Introduction: The purpose of this study is to describe sedation and analgesia management, and identify the factors associated with increased demand for medication in acute respiratory distress syndrome (ARDS) patients receiving venovenous extracorporeal membrane oxygenation (VV-ECMO). Methods: This retrospective, single-center study included consecutive adult ARDS patients who received VV-ECMO for at least 24 hours from January 2018 to December 2020 in a comprehensive intensive care unit. The electronic medical records were retrospectively reviewed to collect data. Results: Forty-two adult patients meeting the inclusion criteria were included in the study. Midazolam, sufentanil, and remifentanil were main sedatives and analgesics used in the patient population. The morphine equivalents, representative of the demand for opioids, was 512.9 (IQR, 294.5, 798.2) mg/day. The midazolam equivalents, representative of benzodiazepine requirement, was 279.6 (IQR, 208.8, 384.5) mg/day. The levels of serum creatinine, total bilirubin, lactic acid, SOFA score, and APACHE Ⅱ score at cannulation were found to be associated with opiate or benzodiazepine requirements. Multiple linear regression analysis revealed a linear correlation between midazolam equivalents and morphine equivalents (p < 0.001). In addition, there was a negative linear correlation between Acute Physiology and Chronic Health Evaluation Ⅱ (APACHE Ⅱ) score and midazolam equivalents (p = 0.024). Conclusions: The sedation and analgesia requirements of ARDS patients receiving VV-ECMO often increase simultaneously. More large-scale studies are needed to confirm the risk factors for increased sedation and analgesia needs in patients supported on VV-ECMO.

The high mortality rate associated with acute respiratory distress syndrome (ARDS) is a major challenge for intensive care units. In the present study, we applied bioinformatics and animal models to identify core genes and potential corresponding pathways in ARDS. Using bioinformatics analysis, IL-1β was identified as the core gene of ARDS. Cell experiments showed that up-regulation of IL-1β downregulates claudin18 to promote lung barrier function damage by regulating the IL-1β-HER2/HER3 axis, further promoting the development of ARDS. This was validated in the animal models. IL-1β promotes the development of ARDS by regulating the IL-1β-HER2/HER3 axis. These findings deepen the understanding of the pathological mechanisms of ARDS. Transcription data sets related to ARDS were subjected to differential expression gene analysis, functional enrichment analysis, and receiver operating characteristic curve analysis and, so as to identify core genes in ARDS. Cell experiments were used to further explore the effects of core genes on lung barrier function damage. Animal models were applied to validate the effects of core gene in mediating biological signal pathways in ARDS.