Mountain sickness in altitude inhabitants of Latin America: A systematic review and meta-analysis.

OBJECTIVE: Chronic and acute mountain sickness is known worldwide, but most of the available information comes from the eastern continent (Himalayas) without taking into account the west which has the most recent group located at altitude, the Andes. The aim of this study was to synthesize the evidence on the prevalence of acute and chronic mountain sickness in Latin American countries (LATAM). METHODS: A systematic search of the variables of interest was performed until July 8, 2023 in the Web of Science, Scopus, PubMed and Embase databases. We included studies that assessed the prevalence of mountain sickness in high-altitude inhabitants (>1500 m.a.s.l) who lived in a place more than 12 months. These were analyzed by means of a meta-analysis of proportions. To assess sources of heterogeneity, subgroup analyses and sensitivity analyses were performed by including only studies with low risk of bias and excluding extreme values (0 or 10,000 ratio). PROSPERO (CRD42021286504). RESULTS: Thirty-nine cross-sectional studies (10,549 participants) met the inclusion criteria. We identified 5 334 and 2 945 events out of 10,000 with acute and chronic mountain sickness in LATAM countries. The most common physiological alteration was polycythemia (2,558 events), while cerebral edema was the less common (46 events). Clinical conditions were more prevalent at high altitudes for both types of MS. CONCLUSION: Acute mountain sickness (AMS) occurs approximately in 5 out of 10 people at high altitude, while chronic mountain sickness (CMS) occurs in 3 out of 10. The most frequent physiological alteration was polycythemia and the least frequent was cerebral edema.

Altitude illnesses.

Millions of people visit high-altitude regions annually and more than 80 million live permanently above 2,500 m. Acute high-altitude exposure can trigger high-altitude illnesses (HAIs), including acute mountain sickness (AMS), high-altitude cerebral oedema (HACE) and high-altitude pulmonary oedema (HAPE). Chronic mountain sickness (CMS) can affect high-altitude resident populations worldwide. The prevalence of acute HAIs varies according to acclimatization status, rate of ascent and individual susceptibility. AMS, characterized by headache, nausea, dizziness and fatigue, is usually benign and self-limiting, and has been linked to hypoxia-induced cerebral blood volume increases, inflammation and related trigeminovascular system activation. Disruption of the blood-brain barrier leads to HACE, characterized by altered mental status and ataxia, and increased pulmonary capillary pressure, and related stress failure induces HAPE, characterized by dyspnoea, cough and exercise intolerance. Both conditions are progressive and life-threatening, requiring immediate medical intervention. Treatment includes supplemental oxygen and descent with appropriate pharmacological therapy. Preventive measures include slow ascent, pre-acclimatization and, in some instances, medications. CMS is characterized by excessive erythrocytosis and related clinical symptoms. In severe CMS, temporary or permanent relocation to low altitude is recommended. Future research should focus on more objective diagnostic tools to enable prompt treatment, improved identification of individual susceptibilities and effective acclimatization and prevention options.

Incidence, predictors, and outcomes of malignant cerebral edema in acute basilar artery occlusion after endovascular treatment: a secondary analysis of the ATTENTION trial.

OBJECTIVE: Malignant cerebral edema (MCE) is a life-threatening complication of ischemic stroke. Few studies have evaluated MCE in patients with acute basilar artery occlusion (BAO) receiving endovascular treatment (EVT). Therefore, the authors investigated the incidence, predictors, and functional outcomes of MCE in BAO patients undergoing EVT. METHODS: This was a post hoc analysis of the Endovascular Treatment for Acute Basilar Artery Occlusion (ATTENTION) trial, a prospective, randomized, multicenter clinical trial that compared endovascular treatment with conventional care of patients with BAO at 36 centers in China. Brain edema was retrospectively assessed using the Jauss score for all available follow-up scans, and patients with a Jauss score ≥ 4 were classified as having MCE. Clinical functional independence was defined as a modified Rankin Scale (mRS) score of 0-2, and a good outcome was defined as an mRS score of 0-3 at the 90-day follow-up. Univariate and multivariate analyses were used to explore the predictors of MCE and the impact of MCE on prognosis. RESULTS: A total of 189 patients were analyzed, and 13.2% of patients developed MCE. Multivariate analysis showed that the baseline Glasgow Coma Scale (GCS) score (OR 0.722, 95% CI 0.548-0.950; p = 0.020) and the number of procedures (OR 1.594, 95% CI 1.051-2.419; p = 0.028) were significantly associated with MCE. After adjusting for confounding factors, the presence of MCE was significantly associated with a lower rate of functional independence (OR 0.115, 95% CI 0.023-0.563; p = 0.008), a lower rate of good outcome (OR 0.092, 95% CI 0.023-0.360; p = 0.001), and a higher rate of mortality (OR 5.373, 95% CI 2.055-14.052; p = 0.001) at the 90-day follow-up. CONCLUSIONS: MCE is not uncommon in BAO patients undergoing EVT and is associated with poor outcomes. Baseline GCS score and the number of procedures were predictors of MCE. In clinical practice, it is crucial that physicians identifying MCE after EVT in patients with BAO and identification of MCE will help in the selection of an appropriate pharmacological treatment strategy and close monitoring.

CSF-Based Volumetric Imaging Biomarkers Highlight Incidence and Risk Factors for Cerebral Edema After Ischemic Stroke.

BACKGROUND: Cerebral edema has primarily been studied using midline shift or clinical deterioration as end points, which only captures the severe and delayed manifestations of a process affecting many patients with stroke. Quantitative imaging biomarkers that measure edema severity across the entire spectrum could improve its early detection, as well as identify relevant mediators of this important stroke complication. METHODS: We applied an automated image analysis pipeline to measure the displacement of cerebrospinal fluid (ΔCSF) and the ratio of lesional versus contralateral hemispheric cerebrospinal fluid (CSF) volume (CSF ratio) in a cohort of 935 patients with hemispheric stroke with follow-up computed tomography scans taken a median of 26 h (interquartile range 24-31) after stroke onset. We determined diagnostic thresholds based on comparison to those without any visible edema. We modeled baseline clinical and radiographic variables against each edema biomarker and assessed how each biomarker was associated with stroke outcome (modified Rankin Scale at 90 days). RESULTS: The displacement of CSF and CSF ratio were correlated with midline shift (r = 0.52 and - 0.74, p < 0.0001) but exhibited broader ranges. A ΔCSF of greater than 14% or a CSF ratio below 0.90 identified those with visible edema: more than half of the patients with stroke met these criteria, compared with only 14% who had midline shift at 24 h. Predictors of edema across all biomarkers included a higher National Institutes of Health Stroke Scale score, a lower Alberta Stroke Program Early CT score, and lower baseline CSF volume. A history of hypertension and diabetes (but not acute hyperglycemia) predicted greater ΔCSF but not midline shift. Both ΔCSF and a lower CSF ratio were associated with worse outcome, adjusting for age, National Institutes of Health Stroke Scale score, and Alberta Stroke Program Early CT score (odds ratio 1.7, 95% confidence interval 1.3-2.2 per 21% ΔCSF). CONCLUSIONS: Cerebral edema can be measured in a majority of patients with stroke on follow-up computed tomography using volumetric biomarkers evaluating CSF shifts, including in many without visible midline shift. Edema formation is influenced by clinical and radiographic stroke severity but also by chronic vascular risk factors and contributes to worse stroke outcomes.

Efficacy of propofol-based anesthesia against risk of brain swelling during craniotomy: A meta-analysis of randomized controlled studies.

STUDY OBJECTIVE: This meta-analysis aimed to compare the risk of brain swelling during craniotomy between propofol-based and volatile-based anesthesia. DESIGN: Meta-analysis of randomized controlled trials (RCTs). SETTING: Operating room. INTERVENTION: Propofol-based anesthesia. PATIENTS: Adult patients undergoing craniotomy. MEASUREMENTS: Databases, including EMBASE, MEDLINE, Google Scholar, and Cochrane Library, were searched from inception to April 2023. The primary outcome was the risk of brain swelling, while the secondary outcomes included the impact of anesthetic regimens on surgical and recovery outcomes, as well as the risk of hemodynamic instability. MAIN RESULTS: Our meta-analysis of 17 RCTs showed a significantly lower risk of brain swelling (risk ratio [RR]: 0.85, p = 0.03, I2 = 21%, n = 1976) in patients receiving propofol than in those using volatile agents, without significant differences in surgical time or blood loss between the two groups. Moreover, propofol was associated with a lower intracranial pressure (ICP) (mean difference: -4.06 mmHg, p < 0.00001, I2 = 44%, n = 409) as well as a lower risk of tachycardia (RR = 0.54, p = 0.005, I2 = 0%, n = 822) and postoperative nausea/vomiting (PONV) (RR = 0.59, p = 0.002, I2 = 19%, n = 1382). There were no significant differences in other recovery outcomes (e.g., extubation time), risk of bradycardia, hypertension, or hypotension between the two groups. Subgroup analysis indicated that propofol was not associated with a reduced risk of brain swelling when compared to individual volatile agents. Stratified by craniotomy indications, propofol reduced brain swelling in elective craniotomy, but not in emergency craniotomy (e.g., traumatic brain injury), when compared to volatile anesthetics. CONCLUSIONS: By reviewing the available evidence, our results demonstrate the beneficial effects of propofol on the risk of brain swelling, ICP, PONV, and intraoperative tachycardia. In emergency craniotomy for traumatic brain injury and subarachnoid hemorrhage, brain swelling showed no significant difference between propofol and volatile agents. Further large-scale studies are warranted for verification.

Injury patterns and mortality associated with near-hanging in children.

BACKGROUND: The pathophysiology of near-hanging in children is different from that of adults due to anatomic, physiologic, and injury-related mechanisms, with evidence suggesting that blunt cerebrovascular injuries (BCVI) and cervical spine injuries (CSI) are uncommon. We sought to estimate the incidence of secondary injuries and their association with mortality in pediatric near-hanging victims. METHODS: We performed a retrospective observational study of children (≤17 years) with a diagnosis code for hanging between October 1, 2015 and February 28, 2023 who presented to one of 47 geographically diverse US children's hospitals. We evaluated the incidence of the following secondary injuries: cerebral edema, pneumothorax, pulmonary edema, BCVI, and CSI. We performed Fisher's exact test with Bonferroni correction to identify associations between intentionality, sex, age, and secondary injuries with mortality. RESULTS: We included 1929 children, of whom 33.8% underwent neuroimaging, 45.9% underwent neck imaging, and 38.7% underwent neck angiography. The most common injury was cerebral edema (24.0%), followed by pulmonary edema (3.2%) and pneumothorax (2.8%). CSI (2.1%) and BCVI (0.9%) occurred infrequently. Cerebral edema, pneumothorax, pulmonary edema, and younger age (≤12 years) were associated with mortality. CONCLUSIONS: In this multi-center study of pediatric near-hanging victims, BCVI and CSI occurred rarely and were not associated with mortality. While children in our study underwent neck imaging more frequently than head imaging, cerebral edema occurred more often than other injury types and imparted the highest mortality risk. Given the rarity of BCVI and CSI, a selective approach to neck imaging may be warranted in pediatric near-hanging events.

Acute Mountain Sickness and High Altitude Cerebral Edema in Women: A Scoping Review-UIAA Medical Commission Recommendations.

Derstine, Mia, Dominique Jean, Beth A. Beidleman, Jacqueline Pichler Hefti, David Hillebrandt, Lenka Horakova, Susi Kriemler, Kasté Mateikaité-Pipiriené, Peter Paal, Alison Rosier, Marija Andjelkovic, and Linda E. Keyes. Acute mountain sickness and high altitude cerebral edema in women: A scoping review-UIAA Medical Commission recommendations. High Alt Med Biol. 24:259-267, 2023. Background: Acute mountain sickness (AMS) and high-altitude cerebral edema (HACE) are illnesses associated with rapid ascent to altitudes over 2,500 m in unacclimatized lowlanders. The aim of this scoping review is to summarize the current knowledge on sex differences in the epidemiology, pathophysiology, symptomatology, and treatment of AMS and HACE, especially in women. Methods and Results: The UIAA Medical Commission convened an international author team to review women's health issues at high altitude and to publish updated recommendations. Pertinent literature from PubMed and Cochrane was identified by keyword search combinations (including AMS, HACE, and high altitude), with additional publications found by hand search. The primary search focus was for articles assessing lowland women sojourning at high altitude. Results: The literature search yielded 7,165 articles, 37 of which were ultimately included. The majority of publications included did not find women at increased risk for AMS or HACE. There was extremely limited sex-specific data on risk factors or treatment. Conclusions: There is a limited amount of data on female-specific findings regarding AMS and HACE, with most publications addressing only prevalence or incidence with regard to sex. As such, general prevention and treatment strategies for AMS and HACE should be used regardless of sex.

Epidemiology and Outcomes of Cerebral Edema in Hospitalized Children.

BACKGROUND: Cerebral edema can be a consequence of multiple disease processes. Untreated cerebral edema can be fatal, and even with aggressive management, it can be devastating. The objective of this study was to describe the prevalence, underlying causes, and outcomes of cerebral edema in hospitalized children. METHODS: A retrospective cross-sectional study using the 2016 Kids' Inpatient Database was performed. Children aged one month to 20 years were included. Sample weighting was employed to produce national estimates. Univariate analyses were used to compare those who died and survived. Multivariable logistic regression was performed to assess the influence of demographic variables and etiologic factors on mortality. RESULTS: Cerebral edema was documented in 4903 children of 2,210,263 (2.2 of 1000) discharges. Among children with cerebral edema, males were 57%, white children were 47.9%, and adolescents were 48.9%. The three most common etiologies associated with cerebral edema in this cohort were stroke (21.7%), anoxic injury (21.4%), and central nervous system (CNS) malignancy (16%). The overall hospital mortality rate was 29.4%. The adjusted mortality rate was significantly higher when cerebral edema was associated with anoxic injury (84%). The mortality was lower when cerebral edema was associated with CNS malignancy (9.5%) or diabetic ketoacidosis (DKA) (4.3%). CONCLUSIONS: Cerebral edema is uncommon in hospitalized children but has a high mortality. Stroke and anoxic brain injury are the two most common etiologies for cerebral edema in hospitalized children in the United States. Among all etiologies for cerebral edema in children, anoxic brain injury has the highest mortality, whereas DKA has the lowest mortality.

Efficacy of two hemodialyses in patients with chronic renal failure complicated by massive intracerebral hemorrhage.

OBJECTIVE: To compare the efficacy of intermittent hemodialysis (IHD) and continuous veno-venous hemofiltration (CVVH) in patients with chronic renal failure complicated by massive intracerebral hemorrhage. METHODS: Sixty-two patients were randomly and equally divided into IHD and CVVH groups. The clinical variables were compared, including National Institutes of Health Stroke Scale (NIHSS) score as the primary indicator, cerebral edema volume, hospital-acquired pneumonia (HAP) incidence, acute heart failure (AHF) incidence, rehemorrhage incidence, hospital stay length, and modified Rankin Scale (mRS) score. RESULTS: The CVVH group had lower NIHSS scores and edema volumes than the IHD group on postoperative days 7 and 14. Moreover, in the CVVH group, (i) the NIHSS scores on postoperative days 3 and 7 were higher than those on postoperative day 1; (ii) there was no significant difference in NIHSS scores between days 14 and 1; and (iii) no significant difference in cerebral edema volume was found between postoperative days 1 and 3, 7, and 14. In the IHD group, the NIHSS scores and cerebral edema volume on postoperative days 7 and 14 were significantly higher than those on postoperative day 1. The CVVH group had a lower incidence of HAP, AHF, and adverse events and shorter hospital stay length than the IHD group. The proportions of patients with mRS scores of 1 and 2 in the CVVH group were higher than those in the IHD group on day 30 after discharge. INTERPRETATION: CVVH is more effective than IHD in the treatment of patients with chronic renal failure complicated by massive intracerebral hemorrhage.

Increased volume of cerebral oedema is associated with risk of acute seizure activity and adverse neurological outcomes in encephalitis - regional and volumetric analysis in a multi-centre cohort.

BACKGROUND: Seizures can occur unpredictably in patients with acute encephalitis syndrome (AES), and many suffer from poor long-term neurological sequelae. Establishing factors associated with acute seizures risk and poor outcomes could support clinical care. We aimed to conduct regional and volumetric analysis of cerebral oedema on magnetic resonance imaging (MRI) in patients with AES. We assessed the relationship of brain oedema with acute seizure activity and long-term neurological outcome. METHODS: In a multi-centre cohort study, adults and children presenting with an AES were recruited in the UK. The clinical and brain MRI data were retrospectively reviewed. The outcomes variables were inpatient acute seizure activity and neurological disability at six-months post-discharge. A poor outcome was defined as a Glasgow outcome score (GOS) of 1-3. We quantified regional brain oedema on MRI through stereological examination of T2-weighted images using established methodology by independent and blinded assessors. Clinical and neuroimaging variables were analysed by multivariate logistic regression to assess for correlation with acute seizure activity and outcome. RESULTS: The study cohort comprised 69 patients (mean age 31.8 years; 53.6% female), of whom 41 (59.4%) had acute seizures as inpatients. A higher Glasgow coma scale (GCS) score on admission was a negative predictor of seizures (OR 0.61 [0.46-0.83], p = 0.001). Even correcting for GCS on admission, the presence of cortical oedema was a significant risk factor for acute seizure activity (OR 5.48 [1.62-18.51], p = 0.006) and greater volume of cerebral oedema in these cortical structures increased the risk of acute seizures (OR 1.90 [1.12-3.21], p = 0.017). At six-month post-discharge, 21 (30.4%) had a poor neurological outcome. Herpes simplex virus encephalitis was associated with higher risk of poor outcomes in univariate analysis (OR 3.92 [1.08-14.20], p = 0.038). When controlling for aetiology, increased volume of cerebral oedema was an independent risk factor for adverse neurological outcome at 6 months (OR 1.73 [1.06-2.83], p = 0.027). CONCLUSIONS: Both the presence and degree of cerebral oedema on MRIs of patients with AES may help identify patients at risk of acute seizure activity and subsequent long-term morbidity.

Risk factors for development of cerebral edema following cardiac arrest.

BACKGROUND: Cerebral edema following cardiac arrest is a well-known complication of resuscitation and portends a poor outcome. We identified predictors of post-cardiac arrest cerebral edema and tested the association of cerebral edema with discharge outcome. METHODS: We performed a retrospective chart review including patients admitted at a single center between January 2015-March 2020 following resuscitation from in-hospital and out-of-hospital cardiac arrest who had head computed tomography imaging. Our primary outcome was moderate-to-severe cerebral edema, which we defined as loss of grey-white differentiation with effacement of the basal and ambient cisterns and radiographic evidence of uncal herniation. We used logistic regression to test associations of demographic information, clinical predictors and comorbidities with moderate-severe cerebral edema. RESULTS: We identified 727 patients who met the inclusion criteria, of whom 102 had moderate-to-severe cerebral edema. We identified six independent predictors of moderate-to-severe cerebral edema: younger age, prolonged arrest duration, pulseless electrical activity/asystole as initial rhythm, unwitnessed cardiac arrest, hyperglycemia on admission, and lower Glasgow coma score on presentation. Of patients with moderate-to-severe cerebral edema, 2% survived to discharge, 56% had withdrawal of life-sustaining therapies and 42% progressed to death by neurological criteria. CONCLUSIONS: Our study identified several risk factors associated with the development of cerebral edema following cardiac arrest. Further studies are needed to determine the benefits of early interventions in these high-risk patients.

The need to be alert to complications of peri-lead cerebral edema caused by deep brain stimulation implantation: A systematic literature review and meta-analysis study.

BACKGROUND: The compatibility of deep brain stimulation (DBS) hardware and MRI scans has greatly improved the diagnostic rate of postoperative peri-lead edema (PLE). However, the etiology, incidence, and prognostic outcomes of this complication have not been established. OBJECTIVE: The incidence of PLE and associated symptoms, the process of occurrence and progression of this complication, as well as treatment strategies were evaluated. METHODS: We conducted a Preferred Reporting Items for Systematic Reviews and Meta-Analyses compliant systematic review of all studies that reported on incidences of PLE and associated symptoms after DBS implantation. Through systematic literature review, we evaluated its causes, neuropsychiatric symptoms, duration, treatment methods, and prognostic outcomes. RESULTS: Our search retrieved 10 articles, including 5 articles on PLE and 10 articles on symptomatic PLE. The incidence of PLE was 35.8% (95% CI: 17.0%-54.6%), while the incidence of symptomatic PLE was 3.1% (95% CI: 1.5%-4.7%) accounting for 8.7% of PLE. CONCLUSIONS: This complication is not as rare as previously reported. Therefore, it requires significant attention after DBS implantation. The correlation between its causes, duration, symptoms, and the area involved in edema should be assessed in long-term prospective clinical studies with large sample sizes.

Acute Ischemic Stroke and COVID-19: An Analysis of 27 676 Patients.

BACKGROUND AND PURPOSE: Acute ischemic stroke may occur in patients with coronavirus disease 2019 (COVID-19), but risk factors, in-hospital events, and outcomes are not well studied in large cohorts. We identified risk factors, comorbidities, and outcomes in patients with COVID-19 with or without acute ischemic stroke and compared with patients without COVID-19 and acute ischemic stroke. METHODS: We analyzed the data from 54 health care facilities using the Cerner deidentified COVID-19 dataset. The dataset included patients with an emergency department or inpatient encounter with discharge diagnoses codes that could be associated to suspicion of or exposure to COVID-19 or confirmed COVID-19. RESULTS: A total of 103 (1.3%) patients developed acute ischemic stroke among 8163 patients with COVID-19. Among all patients with COVID-19, the proportion of patients with hypertension, diabetes, hyperlipidemia, atrial fibrillation, and congestive heart failure was significantly higher among those with acute ischemic stroke. Acute ischemic stroke was associated with discharge to destination other than home or death (relative risk, 2.1 [95% CI, 1.6-2.4]; P<0.0001) after adjusting for potential confounders. A total of 199 (1.0%) patients developed acute ischemic stroke among 19 513 patients without COVID-19. Among all ischemic stroke patients, COVID-19 was associated with discharge to destination other than home or death (relative risk, 1.2 [95% CI, 1.0-1.3]; P=0.03) after adjusting for potential confounders. CONCLUSIONS: Acute ischemic stroke was infrequent in patients with COVID-19 and usually occurs in the presence of other cardiovascular risk factors. The risk of discharge to destination other than home or death increased 2-fold with occurrence of acute ischemic stroke in patients with COVID-19.

Prevalence of cerebral edema among diabetic ketoacidosis patients. / Prevalencia de edema cerebral en pacientes con cetoacidosis diabética.

Introduction: Cerebral edema (CE) is the most severe complication of diabetic ketoacidosis (DKA) in children. There is no accurate knowledge of CE pathogenesis and its onset has been related to intravenous rehydration therapy during the initial treatment. Objectives: To estimate the prevalence of CE among DKA patients treated at Hospital General de Niños Pedro de Elizalde with intravenous rehydration and analyze potential risk factors for the development of CE. Materials and methods: Cross-sectional prevalence study and exploratory analysis to compare clinical and laboratory characteristics between patients with and without CE. Patients aged 1-18 years hospitalized with the diagnosis of DKA between January 1st, 2005 and December 31st, 2014 were included. Results: A total of 693 DKA events from 561 medical records were analyzed. Ten patients had evidence of CE (1.44 %; 95 % confidence interval: 0.8-2.6). Patients with CE had higher serum urea levels (p < 0.001), lower carbon dioxide pressure (p < 0.001), and lower serum sodium levels (p < 0.001) than those without CE. Conclusion: The prevalence of CE among DKA patients was 1.44 %, smaller than that reported in our country (1.8 %). The risk factors at admission associated with CE development were high serum urea levels, hyponatremia, and hypocapnia.

Introducción. El edema cerebral (EC) es la complicación más grave de la cetoacidosis diabética (CAD) en niños. La patogénesis del EC no se conoce con exactitud y su aparición ha sido relacionada con la terapia de rehidratación endovenosa en el tratamiento inicial. Objetivos. Estimar la prevalencia de EC en pacientes con CAD tratados en el Hospital General de Niños Pedro de Elizalde mediante rehidratación endovenosa y analizar potenciales factores de riesgo para el desarrollo de EC. Materiales y método. Estudio de diseño transversal para prevalencia y un análisis exploratorio para comparar las características clínicas y de laboratorio entre los pacientes con y sin EC. Se incluyeron pacientes de 1 a 18 años hospitalizados con diagnóstico de CAD desde el 1 de enero de 2005 hasta el 31 de diciembre de 2014. Resultados. Se analizaron 693 episodios de CAD en 561 historias clínicas. En 10 pacientes, se evidenció EC (el 1,44 %; intervalo de confianza del 95 %: 0,8-2,6). Los pacientes con EC presentaron mayor uremia (p < 0,001), menor presión de dióxido de carbono (p < 0,001) y menor natremia (p < 0,001) que aquellos pacientes sin EC. Conclusión. La prevalencia de EC en pacientes con CAD fue del 1,44 %, menor que la reportada en nuestro país (del 1,8 %). Los factores de riesgo al ingresar asociados a su desarrollo fueron la presencia de uremia elevada, hiponatremia e hipocapnia.

Luteolin Protects Against CIRI, Potentially via Regulation of the SIRT3/AMPK/mTOR Signaling Pathway.

Mitochondrial abnormalities accelerate the progression of ischemic brain damage. Sirtuin 3 (SIRT3) is mainly found in mitochondria and affects almost all major aspects of mitochondrial function. Luteolin, a flavonoid with diverse biological properties, including antioxidant activity, inhibition of cell apoptosis and regulation of autophagy. It also modulates the activity of AMP activated kinase and/or sirtuin 1 (SIRT 1) by regulating the expression of sirtuins. We investigated the protective effects of luteolin on cerebral ischemia-reperfusion. It was found through experiments that luteolin reduced the infarcted area of MCAO rat model, and based on the experimental results, it was inferred that luteolin affected the AMPK, mTOR and SIRT3 pathways, thereby protecting brain cells. As expected, we found that luteolin can reduce the neurological function score, the degree of cerebral edema, the cerebral infarction volume, alleviate morphological changes in the cortex and hippocampus, increase neuron survival and decrease the number of apoptotic neurons. At the same time, luteolin significantly reduced the number of GFAP and Iba-1 positive glial cells in the hippocampus while enhanced the scavenging of oxygen free radicals and the activity of SOD in mitochondria. Addtionally, it can also enhance antioxidant capacity via the reversal of mitochondrial swelling and the mitochondrial transmembrane potential. Moreover, luteolin can increase SIRT3-targeted expression in mitochondria, decrease the phosphorylation of AMPK, and increase phosphor-mTOR (p-mTOR) levels, which may have occurred specifically through activation of the SIRT3/AMPK/mTOR pathway. We speculate that luteolin reduces the pathological progression of CIRI by increasing SIRT3 expression and enhancing mitochondrial function. Therefore, the results indicate that luteolin can increase the transduction of SIRT3, providing a potential mechanism for neuroprotective effects in patients with cerebral ischemia.

Asymmetric cerebral edema presenting with severe neurologic impairment and seizures after cardiac and thoracic interventions.

INTRODUCTION: A syndrome of focal neurologic deficits with characteristic imaging features, acute encephalopathy, and seizures after cardiac and thoracic interventions has been previously briefly reported in the literature. In a retrospective observational study, we aim to identify the prevalence and characteristics of this syndrome, in addition to discussing the possible underlying pathophysiology. METHODS: In a retrospective study, we reviewed records of consecutive adult patients (≥18 years old) who underwent cardiac and thoracic procedures at a single institution between September 2014 to September 2019 and found to have evidence of focal cerebral edema following their procedure. We included and reported clinical course of patients who developed post-operative neurologic dysfunction and underwent magnetic resonance imaging (MRI) showing (1) asymmetric cerebral edema with (2) cortical diffusion restriction and (3) T2 cortical or subcortical hyperintensity and (4) no proximal vascular occlusion. RESULTS: Three out of 107 patients (2.8%) met our inclusion criteria. These represented one male and two females with age at presentation of 63, 81 and 69, respectively. All patients developed severe neurologic impairment on the same day following their procedure (sternotomy with valve or bypass surgery in 2 patients; esophageal dilatation procedure in 1 patient). All patients underwent MRI of the brain and vessel imaging qualifying our inclusion criteria. Two patients improved neurologically prior to discharge, and one patient expired after family elected to withdraw care. CONCLUSION: We present a series of cases with a rare syndrome after cardiac and thoracic interventions. Although the exact mechanism of this syndrome remains unclear, we believe it to be related to relative cerebral hyperperfusion and cerebral dysautoregulation following anesthesia and thoracic manipulation. Future studies should focus on understanding the true prevalence and pathophysiology of this syndrome.

Clinical and Imaging Features of Contrast-Induced Neurotoxicity After Neurointerventional Surgery.

BACKGROUND: Contrast-induced neurotoxicity (CIN) is an infrequent complication of endovascular procedures, and its understanding remains poor. We aimed to study and characterize the clinical and imaging features of a case series of CIN after neurointerventional surgery. METHODS: We reviewed all neuroendovascular consecutive procedures from September 2014 to November 2018. CIN was defined as new onset of neurologic deficits that occurred postoperatively after excluding other conditions. All demographic, clinical, procedural, and radiologic data were retrospectively analyzed and collected. RESULTS: Eleven cases of CIN in 1587 patients were identified out of 2510 procedures. The median age was 76 years (interquartile range [IQR], 65-81). The most common comorbidity was hypertension (82%). Median procedure time was 100 minutes (IQR, 80-130.5 minutes). All patients showed wide variability in intraprocedural blood pressure (BP) recordings with fluctuations from the baseline BP. Systolic BP ranged from 83 mm Hg below the patient baseline to 80 mm Hg above baseline. The median symptom onset was 4 hours (IQR, 0.8-9.5 hours). The CIN signs and symptoms presented gradually, initially with encephalopathy and later with focal signs. All patients had an initial computed tomography scan, which showed ipsilateral cerebral edema in 82% of patients. Two had contrast enhancement. Complete resolution of CIN symptoms was obtained in a median time of 3 days (IQR, 2.5-3 days). CONCLUSIONS: CIN should be considered in the context of the progressive onset of neurologic deficits after neuroendovascular procedures. A distinct imaging pattern of ipsilateral hemisphere edema in the absence of ischemia is usually identified. Variability in procedural BP might be a predisposing factor.

Effectiveness of Endovascular Therapy for Patients with Acute Ischemic Stroke: A Meta-Analysis of Randomized Controlled Trials.

OBJECTIVE: This meta-analysis of published randomized controlled trials (RCTs) aimed to investigate the efficacy and safety of endovascular therapy (ET) for patients with acute ischemic stroke. METHODS: The summary relative risks (RRs) with corresponding 95% confidence intervals were calculated to measure the effectiveness of ET using a random-effects model. RESULTS: Thirteen RCTs including 3408 patients were identified among 2851 initial electronic citations. Overall, the summary RR indicated that ET significantly increased the incidence of a modified Rankin Scale score of 0-2 (RR, 1.50; P < 0.001), asymptomatic intracerebral hemorrhage (IH) (RR, 1.42; P = 0.001), subarachnoid hemorrhage (RR, 2.36; P = 0.001), and major complications due to non-intracerebral bleeding (RR, 1.47; P = 0.014). However, ET had no significant effects on the risk of 7-day death (P = 0.827); death after 30 days (P = 0.085); symptomatic IH (P = 0.288); type 1 (P = 0.413), type 2 (P = 0.300), and total parenchymal hematoma (P = 0.160); intraventricular hemorrhage (P = 0.244); early neurologic deterioration (P = 0.570); recurrent stroke (P = 0.830); and symptomatic edema (P = 0.485). CONCLUSIONS: The findings of this meta-analysis suggest the incidence of a modified Rankin Scale score of 0-2 in patients who received ET was significantly increased. Moreover, the harmful effects of ET might exist due to greater risk of asymptomatic IH, subarachnoid hemorrhage, and non-intracerebral bleeding, and these results should be verified by further large-scale long-term RCT.

Docosahexaenoic Acid Protects Traumatic Brain Injury by Regulating NOX2 Generation via Nrf2 Signaling Pathway.

Docosahexaenoic acid (DHA) is verified to have neuroprotective effects on traumatic brain injury (TBI) rats by activating Nrf2 signaling pathway, but the role of NOX2 in this effect has not been illuminated. So this study explored the role of NOX2 in TBI models treated with DHA, aiming to complete the mechanism of DHA. TBI rat models were constructed with or without DHA treatment, and H2O2-induced hippocampal neurons were pretreated with DHA alone or in combination with Nrf2 inhibitor brusatol. The neurological function, cognitive ability, and cerebral edema degree of rats were assessed. The apoptosis rate and viability of cells was measured. The generation of NOX2, Nrf2, HO-1 and NQO-1 expression levels, and ROS content in hippocampal CA1 region and hippocampal neurons were detected. DHA could not only improve the neurological function, brain edema and cognitive ability in TBI rats, but also decrease effectively the contents of NOX2 and ROS in hippocampal CA1 region and hippocampal neurons. DHA promoted the nuclear transposition of Nrf2 and the expression levels of HO-1 and NQO-1 in hippocampal CA1 region and hippocampal neurons. On the contrary, Nrf2 inhibitor brusatol inhibited the nuclear transposition of Nrf2 and the expression levels of HO-1 and NQO-1 in hippocampal neurons, promoted the generation of ROS and NOX2, and accelerated cell apoptosis. Both in vivo and in vitro experiments demonstrated that DHA treated TBI by reducing NOX2 generation that might function on Nrf2 signaling pathway, providing a potential evidence for its clinical application.

MCC950 Inhibits NLRP3 Inflammasome and Alleviates Axonal Injures in Early Stages of Diffuse Axonal Injury in Rats.

Increasing evidence has revealed that neuroinflammation plays a pivotal role in axonal injures. Nucleotide oligomerization domain (NOD)-like receptor protein (NLRP3) inflammasome is reported to be widely involved with the pathology of central nervous system disorders. But the role of NLRP3 in diffuse axonal injury (DAI) are rarely reported. The purpose of this study was to investigate the expression of NLRP3 after diffuse axonal injury and the role of NLRP3 in axonal injures. The lateral head rotation device was used to establish DAI model of rats. Immunohistochemical staining for ß-amyloid precursor protein and Bielschowsky silver staining were used to assess axonal injures and axonal loss. Terminal Deoxynucleotidyl Transferase-Mediated Digoxigenin-dUTP-Biotin Nick-End Labelling Assay was used to detect cell apoptosis. Brain water content was used to assess cerebral edema and the modified Neurologic Severity Score was used to assess the neurological deficits. Components of NLRP3 inflammasome, such as NLRP3, apoptosis-associated speck-like (ASC) adapter protein and caspase-1, and pro-inflammatory cytokines, for example IL-18 and IL-1ß, were over-expressed in early stages of DAI. MCC950, a selective small-molecule inhibitor of NLRP3 inflammasome, inhibited the over-expression of NLRP3 inflammasome and pro-inflammatory cytokines after DAI. MCC950 alleviated axonal injures and cell apoptosis. MCC950 also decreased brain water content and alleviated neurologic deficits 1 day and 3 days after DAI but not 7 days after DAI. These results suggest that MCC950 treatment in the early stages of DAI has a time limiting effect in preventing from axonal injuries and neurological deficits, and that NLRP3 inflammasome plays an important role in axonal injures and may be a potential candidate for axonal injures following DAI.