Brain Edema Research Articles

Differential Diagnoses for Isolated Right Sixth Nerve Palsy in the High Altitude Setting: A Case Report.

This case report describes the presentation and management of a patient with an isolated right sixth nerve palsy while trekking in Nepal. Consideration is made of the anatomy of the sixth nerve and the differential diagnoses afforded to this isolated sign, including high altitude cerebral edema. The case stresses the need to exclude life-threatening pathologies for any symptoms associated with altitude and includes decision-making processes on whether to monitor the patient in the field or evacuate them to a definitive care facility.

Study on the role of peripheral immune cells in cerebral ischemia

Stroke, primarily resulting from the sudden interruption of blood supply to the brain, remains a leading cause of morbidity and mortality worldwide. Following an ischemic stroke, the peripheral immune system significantly contributes to brain damage. Damage-associated molecular patterns (DAMPs) released from ischemic cells activate peripheral immune cells, resulting in increased inflammation and disruption of the blood-brain barrier (BBB). This review highlights the critical immune cells of the peripheral immune system activated after cerebral ischemia, with an emphasis on the roles of T cells, B cells, macrophages, and neutrophils. We discuss the pathophysiological mechanisms of cerebral ischemia, which include reduced blood flow, energy metabolism disorders, neuronal injury and death, and BBB disruption and cerebral edema. The interplay between the peripheral immune system and cerebral ischemia is explored, offering insights into the inflammatory and immunosuppressive responses following ischemic events. Meanwhile, current research advances and future research directions are presented, focusing on potential therapeutic targets within the peripheral immune system to improve outcomes in ischemic brain injury. In summary, this review underscores the necessity of understanding the peripheral immune system's role in cerebral ischemia to develop effective treatment strategies and enhance patient recovery.

Real-time detection of cerebral edema in mice based on low-field nuclear magnetic resonance

Cerebral edema is a secondary symptom of several conditions, including stroke, liver, failure, and severe craniocerebral injury. This study aimed to propose a Low-Field Nuclear Magnetic Resonance (LF-NMR) method for rapid and nondestructive measurement of brain water content and water phase state evaluating animal brain edema models. The water transverse relaxation time (T2) distribution in brain tissues was ascertained by measuring the T2 spectrograms of mouse brain tissues following various drying durations, in accordance with the shifting law of T2 peaks. A methodological study was carried out for the determination of water content in mouse brain tissue by the LF-NMR Peak Area (LF-NMR-PA) method using CuSO4 solution as standard solution. This method was studied in comparison with the wet/dry weight method and the Partial Least Squares Regression (PLSR) prediction method in normal and MCAO model mice, and further applied to the study of mannitol treatment of cerebral edema to validate the precision and accuracy of the hydration measurements as well as the method’s impact on subsequent experiments of cerebral infarct area measurement. In the T2 spectra of mouse brain tissues, the separate peaks T21 (0–10 ms), T22 (10–100 ms), and T23 (100–1000 ms) correspond to fat and bound water, water, and free water in brain tissue, respectively. The LF-NMR-PA method had good specificity, linearity, precision, stability, reproducibility, and recovery. The accuracy and range of use of the LF-NMR-PA method were better than those of the PLSR method, and its results were not significantly different from those of the wet/dry weight method. However, the short measurement time of the LF-NMR-PA method ensured the integrity of the tissues, and the determination of the moisture by this method did not have a significant effect on the subsequent determination of the area of cerebral infarction, which ensured the consistency of the experimental results.

Síndrome da encefalopatia posterior reversível associada à transfusão em anemia falciforme: relato de caso

Sickle Cell Anemia (SCA) is the most common genetic disease in the world, characterized by frequent vaso-occlusive crises that, along with extensive pathophysiology, predispose individuals to neurological events such as Stroke. Posterior Reversible Encephalopathy Syndrome (PRES), on the other hand, is an uncommon manifestation resulting from vasogenic edema whose pathogenesis is not completely understood. Individuals with hemoglobinopathies have a higher chance of developing PRES; however, there are few reports in the literature on the occurrence of PRES related to SCA. The aim of the study is to report a case in which red blood cell transfusion (RBCT) was followed by PRES in a child with SCA. This is a longitudinal single-arm study with systematic research in major databases using the PICO strategy to associate the three events (SCA, RBC, PRES) with their appropriate medical descriptors. The present study evidenced most findings described in the scientific literature, reinforcing the need to expand knowledge of PRES as a differential diagnosis of neurological events in hemoglobinopathies in order to improve healthcare quality and reduce morbidity and mortality in these individuals

CCL4 as a potential serum factor in differential diagnosis of central nervous system inflammatory diseases and gliomas.

Computed tomography (CT) scans and magnetic resonance imaging (MRI) are commonly utilized to detect brain gliomas and central nervous system inflammation diseases. However, there are instances where depending solely on medical imaging for a precise diagnosis may result in unsuitable medications or treatments. Pathological analysis is regarded as the definitive method for diagnosing brain gliomas or central nervous system inflammation diseases. To achieve this, a craniotomy or stereotaxic biopsy is necessary to collect brain tissue, which can lead to complications such as cerebral hemorrhage, neurological deficits, cerebrospinal fluid leaks, and cerebral edema. Consequently, the advancement of non-invasive or minimally invasive diagnostic techniques is currently a high priority. This study included samples from four glioma patients and five patients with central nervous system inflammatory diseases, comprising both serum and paired cerebrospinal fluid (CSF). A total of 40 human cytokines were identified in these samples. We utilized a receiver operating characteristic (ROC) analysis to assess the sensitivity and specificity for distinguishing central nervous system inflammation diseases and gliomas. Additionally, we examined the correlation of these factors between serum and CSF in the patients. Ultimately, the identified factors were validated using serum from patients with clinically confirmed gliomas and central nervous system inflammation diseases followed by detection and statistical analysis through ELISA. The levels of serum factors IL-4, IFN-α, IFN-γ, IL-6, TNF-α, CCL4, CCL11, and VEGF were found to be significantly higher in gliomas compared with inflammatory diseases of the central nervous system (p < 0.05). Furthermore, a strong correlation was observed between the levels of CCL4 in serum and CSF, with a correlation coefficient of r = 0.92 (95% CI = 0.20-0.99, p = 0.027). We gathered more clinical samples to provide further validation of the abundance of CCL4 expression. A clinical study analyzing serum samples from 19 glioma patients and 22 patients with central nervous system inflammation diseases revealed that CCL4 levels were notably elevated in the inflammatory group compared with the glioma group (p < 0.001). These results suggest that assessing serum CCL4 levels may be useful in distinguishing those patients for clinical diagnostic purposes.

An Analysis of Emergency Surgical Outcomes for Pediatric Traumatic Brain Injury: A Ten-Year Single-Institute Retrospective Study in Taiwan.

Background and Objectives: Pediatric traumatic brain injury (pTBI) remains a major pediatric public health problem, despite well-developed injury prevention programs. The purpose of this study is to analyze the emergency surgical outcomes of pTBI in a single institute ten-year retrospective study to offer a real-world clinical result. Materials and Methods: Our institute presented a clinical retrospective, single-institute research study of 150 pediatric TBI cases that were diagnosed and underwent emergency surgical treatment from 2010 to 2019. Results: The incidence of radiological findings is detailed as follows: brain edema (30%, 45/150), followed by acute subdural hematoma (27.3%, 41/150), epidural hematoma (21.3%, 32/150), chronic subdural hemorrhage (10%, 15/150), skull fracture (6.7%, 10/150), and traumatic subarachnoid hemorrhage (4.7%, 7/150). Surgical intervention data revealed that decompressive craniectomy was still the main effective surgical method. The results showed longer hospital stays and higher morbidity rates in the brain edema, acute subdural hematoma, and chronic subdural hemorrhage groups, which were viewed as poor surgical outcome groups. Epidural hematoma, skull fracture and traumatic subarachnoid hemorrhage were categorized into good surgical outcome groups. Notably, the data revealed gross improvement in Glasgow Coma Scale/Score (GCS) evolution after surgical interventions, and the time to cranioplasty was a significant factor in the development of post-traumatic hydrocephalus (PTH). Conclusions: Our study provided real-world data for the distribution of etiology in pTBI and also categorized it into six groups, indicating disease-orientated treatment. In addition, our data supported that decompressive craniectomy (DC) remains a mainstay surgical treatment in pTBI and early cranioplasty could decrease the incidence of PTH.

Posterior reversible encephalopathy syndrome and parkinsonism as the first manifestation of primary hyperparathyroidism - a report of two cases.

Primary hyperparathyroidism (PHPT) may be asymptomatic or present with renal calculi, secondary osteoporosis, fractures and neuropsychiatric manifestations. Posterior reversible encephalopathy syndrome (PRES) and parkinsonism are atypical manifestations that may be rarely associated with PHPT. We report two patients who presented with the conditions mentioned above. The first patient involved a 38-year-old woman who presented with diminution of vision, seizures, altered behavior and hypertension over eight months. An MRI of the brain done had shown vasogenic edema involving the parieto-occipital regions, suggestive of PRES. A metabolic screen revealed PTH-dependent hypercalcemia that was localized to the left inferior parathyroid gland. Following focused parathyroidectomy, there was improvement in sensorium, vision and normalization of blood pressure. The second patient was of a 74-year-old man who presented with progressive extrapyramidal symptoms of gait abnormalities and rigidity since the past eight months. He was initiated on Selegeline and Levodopa for the same purpose, and subsequently reported minimal improvement in symptoms. Investigations revealed PHPT associated with a right inferior parathyroid adenoma. Within two weeks following surgery, there was an improvement in rigidity and gait and he was able to ambulate without support. PRES has been reported to occur in the context of preeclampsia, hypertension, infection, sepsis and autoimmune conditions. PRES associated with hypercalcemia is rarely reported. While extra-pyramidally related manifestations are described in hypoparathyroidism, PHPT related parkinsonism is not commonly encountered. Identifying the underlying aetiology and initiation of corrective measures may lead to amelioration of patient symptomatology. The occurrence of PRES and parkinsonism is rare in primary hyperparathyroidism; the two patients described above highlight the importance of screening for hypercalcemia in the setting of neurological manifestations.

Activation of the Nrf2/Keap1 signaling pathway mediates the neuroprotective effect of Perillyl alcohol against cerebral hypoxic-ischemic damage in neonatal rats

ABSTRACT Neonatal hypoxic-ischemic encephalopathy (HIE) is a severe disease with a poor prognosis, whose clinical treatment is still limited to therapeutic hypothermia with limited efficacy. Perillyl alcohol (POH), a natural monoterpene found in various plant essential oils, has shown neuroprotective properties, though its effects on HIE are not well understood. This study investigates the neuroprotective effects of POH on HIE both in vitro and in vivo. We established an in vitro model using glucose deprivation and hypoxia/reperfusion (OGD/R) in PC12 cells, alongside an in vivo model via the modified Rice-Vannucci method. Results indicated that POH acted as an indirect antioxidant, reducing inducible nitric oxide synthase and malondialdehyde production, maintaining content of antioxidant molecules and enzymes in OGD/R-induced PC12 cells. In vivo, POH remarkably lessened infarct volume, reduced cerebral edema, accelerated tissue regeneration, and blocked reactive astrogliosis after hypoxic-ischemic brain injury. POH exerted antiapoptotic activities through both the intrinsic and extrinsic apoptotic pathways. Mechanistically, POH activated Nrf2 and inactivated its negative regulator Keap1. The use of ML385, a Nrf2 inhibitor, reversed these effects. Overall, POH mitigates neuronal damage in HIE by combating oxidative stress, reducing inflammation, and inhibiting apoptosis via the Nrf2/Keap1 pathway, suggesting its potential for HIE treatment.

Gas6/Axl signaling promotes hematoma resolution and motivates protective microglial responses after intracerebral hemorrhage in mice

BackgroundIntracerebral hemorrhage (ICH) stands out as the most fatal subtype of stroke, currently devoid of effective therapy. Recent research underscores the significance of Axl and its ligand growth arrest-specific 6 (Gas6) in normal brain function and a spectrum of neurological disorders, including ICH. This study is designed to delve into the role of Gas6/Axl signaling in facilitating hematoma clearance and neuroinflammation resolution following ICH. MethodsAdult male C57BL/6 mice were randomly assigned to sham and ICH groups. ICH was induced by intrastriatal injection of autologous arterial blood. Recombinant mouse Gas6 (rmGas6) was administered intracerebroventricularly 30 min after ICH. Virus-induced knockdown of Axl or R428 (a selective inhibitor of Axl) treatment was administrated before ICH induction to investigate the protective mechanisms. Molecular changes were assessed using western blot, enzyme-linked immunosorbent assay and immunohistochemistry. Coronal brain slices, brain water content and neurobehavioral tests were employed to evaluate histological and neurofunctional outcomes, respectively. Primary glia cultures and erythrophagocytosis assays were applied for mechanistic studies. ResultsThe expression of Axl increased at 12 h after ICH, peaking on day 3. Gas6 expression did not remarkably changed until day 3 post-ICH. Early administration of rmGas6 following ICH significantly reduced hematoma volume, mitigated brain edema, and restored neurological function. Both Axl-knockdown and Axl inhibitor treatment abolished the neuroprotection of exogenous Gas6 in ICH. In vitro studies demonstrated that microglia exhibited higher capacity for phagocytosing eryptotic erythrocytes compared to normal erythrocytes, a process reversed by blocking the externalized phosphatidylserine on eryptotic erythrocytes. The erythrophagocytosis by microglia was Axl-mediated and Gas6-dependent. Augmentation of Gas6/Axl signaling attenuated neuroinflammation and drove microglia towards pro-resolving phenotype. ConclusionsThis study demonstrated the beneficial effects of recombinant Gas6 on hematoma resolution, alleviation of neuroinflammation, and neurofunctional recovery in an animal model of ICH. These effects were primarily mediated by the phagocytotic role of Axl expressed on microglia.

Hypophosphatemia correction reduces ICANS incidence and duration in CAR T-cell therapy: a pooled clinical trial analysis.

A common complication of chimeric antigen receptor (CAR)-T cell therapy is immune effector cell associated neurotoxicity syndrome (ICANS), which presents with encephalopathy, aphasia, inattention, somnolence, seizures, weakness, or cerebral edema. Despite its significant morbidity, there are currently no effective targeted treatments. Given the clinical similarities between ICANS and the neurological manifestations of acute hypophosphatemia, we retrospectively reviewed 499 patients treated with CD19-targeted CAR-T cell therapy across multiple clinical trials between 2015 and 2020. In addition to clinical toxicities experienced by the patients, we also interrogated the impact of serum electrolyte data and repletion of corresponding electrolyte deficiencies with ICANS incidence, severity, and duration. Hypophosphatemia was a common occurrence in CAR T-cell recipients, and the only electrolyte derangement associated with a significantly higher cumulative incidence of ICANS. Moreover, phosphorus repletion in hypophosphatemic patients was associated with significantly decreased ICANS incidence and duration. Hypophosphatemia was uniquely associated with encephalopathy neurological adverse events, which also showed the strongest positive correlation with both ICANS and CRS severity. These findings suggest that serum phosphorus could be a reliable biomarker for ICANS, and expeditious, goal-directed phosphorus repletion in response to serum hypophosphatemia could be a safe, inexpensive, and widely available intervention for such patients.

Association between ASPECTS region of infarction and clinical outcome in non-acute large vessel occlusion ischaemic stroke after endovascular recanalisation

PurposeThis study retrospectively investigated whether infarction in specific Alberta Stroke Program Early CT Score (ASPECTS) regions is associated with clinical outcome in patients with symptomatic non-acute internal carotid or middle...

Epidemiological Profile of Diabetic Ketoacidosis

Diabetic ketoacidosis is a real public health problem in our context with an incidence of 12.67%. Diabetic ketoacidosis is a therapeutic emergency that requires rigorous management, especially in the acute phase, while respecting the therapeutic particularities of each patient and taking care to detect the etiologies. The etiological research of ketoacidotic decompensation has enabled us to determine, as the main triggering factors, therapeutic non-compliance and then infections, predominated by urinary infections and pneumonia. Initial treatment is based on rehydration, insulin therapy and correction of electrolyte and acid-base disorders, of course, with rigorous and essential monitoring combating possible complications, particularly iatrogenic, represented in our context mainly by the hypokalemia, hypoglycemia, cerebral edema and acute renal failure. The analytical statistical study allowed us to conclude that death was essentially linked to complications occurring during the hospital stay, notably septic shock, cerebral involvement, renal failure and the use of mechanical ventilation.

A fatal pediatric case of acute fulminant cerebral edema with COVID-19 in Korea: a case report

Although most children with coronavirus disease 2019 (COVID-19) infection present with mild symptoms, a few pediatric patients develop severe neurological manifestations. Herein, we describe the case of a pediatric patient who presented with rapidly progressive diffuse and fatal cerebral edema associated with COVID-19. A previously healthy 6-year-old boy was diagnosed with acute fulminant cerebral edema (AFCE), which resulted in transtentorial downward herniation within 48 hours after the initial onset of fever. Detailed history-taking, close monitoring of the consciousness level with serial neurological examinations, and prompt diagnosis and treatment are required in patients suspected to have AFCE. Further research is needed to identify the pathogenesis of AFCE associated with COVID-19 and the related risk factors.

No difference in 6-month functional outcome between early and late decompressive craniectomies following acute ischaemic stroke in a national neurosurgical centre: a single-centre retrospective case-cohort study.

Decompressive craniectomies (DCs) are recommended for the treatment of raised intracranial pressure after acute ischaemic stroke. Some studies have demonstrated improved outcomes with early decompressive craniectomy (< 48h from onset) in patients with malignant cerebral oedema following middle cerebral artery infarction. Limited data is available on suboccipital decompressive craniectomy after cerebellar infarction. Our primary objective was to determine whether the timing of DCs influenced functional outcomes at 6months. Our secondary objectives were to analyse whether age, gender, the territory of stroke, or preceding thrombectomy impacts functional outcome post-DC. We conducted a retrospective study of patients admitted between January 2014 and December 2020 who had DCs post-acute ischaemic stroke. Data was collected from ICU electronic records, individual patient charts, and the stroke database. Twenty-six patients had early DC (19 anterior/7 posterior) and 21 patients had late DC (17 anterior/4 posterior). There was no difference in the modified Rankin Scale (mRS) score of the two groups at 90 (p = 0.318) and 180 (p = 0.333) days post early vs late DC. Overall outcomes were poor, with 5 out of 46 patients (10.9%) having a mRS score ≤ 3 at 6months. There was no difference in mRS scores between the patients who had hemicraniectomies for anterior circulation stroke (n = 35) and suboccipital DC for posterior circulation stroke (n = 11) (p = 0.594). In this single-centre retrospective study, we found no significant difference in functional outcomes between patients who had early or late DC after ischaemic stroke.

Effects of intestinal flora on cerebral hemorrhage area and brain tissue inflammation in acute hemorrhagic stroke.

To explore the impacts of intestinal flora on cerebral hemorrhage area and brain tissue inflammation in acute hemorrhagic stroke, seventy-two male C57BL/6 mice were randomly separated into 6 groups (n=12), the experimental group (EG, day 1, day 3 and day 7) and the control group (CG, day 1, day 3 and day 7). The mouse cerebral hemorrhage model was established by collagenase injection, and the EG received 0.4 mL fecal filtrate of healthy mice once a day, and the CG received the same amount of normal saline transplantation. The mNSS score, hematoma volume and cerebral edema content were used to evaluate nerve function injury and brain injury degree at each time point after operation. The expressions of inflammatory factors were detected by western blot. We found that at each time point after operation, compared with the CG, nerve function deficit scores of mice in the EG declined (P<0.05), the water content of mice brain tissue in the EG declined (P<0.05), and the protein expressions of inflammatory factors in the EG were decreased (P<0.05). Relative to the CG, the volume of hematoma in the EG declined on day 3 along with day 7 after operation (P<0.05). In conclusion, intestinal flora can reduce cerebral hemorrhage area and brain tissue inflammation, and then improve the performance of nerve function deficit in acute hemorrhagic stroke.

Stroke in gliomas: a case report and literature review

A 60-year-old patient presented to the emergency department with sudden onset neurological symptoms suggestive of a cerebrovascular event. Initial diagnostic imaging revealed a complex clinical picture with an unclear diagnosis, with differentials including aneurysm, neoplasm, ischaemia accompanied by cerebral oedema. CT angiography revealed a small aneurysm, while subsequent MRI demonstrated findings consistent with diffuse multifocal glioma and areas of restricted diffusion, suggesting post-compressive ischaemia. This case highlights both the diagnostic challenges of using CT imaging for early suspected stroke and the importance of multimodal imaging when the clinical diagnosis is uncertain.

Polydatin ameliorates early brain injury after subarachnoid hemorrhage through up-regulating SIRT1 to suppress endoplasmic reticulum stress.

This study aims to investigate the inhibitory effect of Polydatin (PD) on endoplasmic reticulum (ER) stress following subarachnoid hemorrhage (SAH) and to elucidate the underlying mechanisms. A standard intravascular puncture model was established to mimic SAH in mice. Neurological functions were assessed using neurological scoring, Grip test, and Morris water maze. Brain edema and Evans blue extravasation were measured to evaluate blood-brain barrier permeability. Western blot and quantitative real-time polymerase chain reaction (PCR) analyses were performed to examine protein and mRNA expressions related to ER stress. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining was used to detect cell apoptosis, and transmission electron microscopy was used to observe the ultrastructure of the endoplasmic reticulum. The results indicated that PD significantly reduced brain edema and Evans blue extravasation after SAH, improving neurological function. Compared to the SAH group, the expression levels of ER stress-related proteins including glucose-regulated protein 78 (GRP78), phosphorylated protein kinase R-like endoplasmic reticulum kinase (p-PERK), phosphorylated eukaryotic initiation factor 2α (p-eIF2α), activating transcription factor 4 (ATF4), and C/EBP homologous protein (CHOP), were significantly lower in the PD-treated group. Moreover, PD significantly enhances the protein expression of Sirtuin 1 (SIRT1). Validation with sh-SIRT1 confirmed the critical role of SIRT1 in ER stress, with PD's inhibitory effect on ER stress being dependent on SIRT1 expression. Additionally, PD attenuated ER stress-mediated neuronal apoptosis and SAH-induced ferroptosis through upregulation of SIRT1. PD alleviates ER stress following SAH by upregulating SIRT1 expression, thereby mitigating early brain injury. The protective effects of PD are mediated through SIRT1, which inhibits ER stress and reduces neuronal apoptosis and ferroptosis.

Remote ischemic preconditioning prevents high-altitude cerebral edema by enhancing glucose metabolic reprogramming.

Incidence of acute mountain sickness (AMS) ranges from 40%-90%, with high-altitude cerebral edema (HACE) representing a life-threatening end stage of severe AMS. However, practical and convenient preventive strategies for HACE are lacking. Remote ischemic preconditioning (RIPC) has demonstrated preventive effects on ischemia- or hypoxia-induced cardiovascular and cerebrovascular diseases. This study aimed to investigate the potential molecular mechanism of HACE and the application of RIPC in preventing HACE onset. A hypobaric hypoxia chamber was used to simulate a high-altitude environment of 7000 meters. Metabolomics and metabolic flux analysis were employed to assay metabolite levels. Transcriptomics and quantitative real-time PCR (q-PCR) were used to investigate gene expression levels. Immunofluorescence staining was performed on neurons to label cellular proteins. The fluorescent probes Mito-Dendra2, iATPSnFR1.0, and CMTMRos were used to observe mitochondria, ATP, and membrane potential in cultured neurons, respectively. TUNEL staining was performed to detect and quantify apoptotic cell death. Hematoxylin and eosin (H&E) staining was utilized to analyze pathological changes, such as tissue swelling in cerebral cortex samples. The Rotarod test was performed to assess motor coordination and balance in rats. Oxygen-glucose deprivation (OGD) of cultured cells was employed as an invitro model to simulate the hypoxia and hypoglycemia induced by RIPC in animal experiments. We revealed a causative perturbation of glucose metabolism in the brain preceding cerebral edema. Ischemic preconditioning treatment significantly reprograms glucose metabolism, ameliorating cell apoptosis and hypoxia-induced energy deprivation. Notably, ischemic preconditioning improves mitochondrial membrane potential and ATP production through enhanced glucose-coupled mitochondrial metabolism. Invivo studies confirm that RIPC alleviates cerebral edema, reduces cell apoptosis induced by high-altitude hypoxia, and improves motor dysfunction resulting from cerebral edema. Our study elucidates the metabolic basis of HACE pathogenesis. This study provides a new strategy for preventing HACE that RIPC reduces brain edema through reprogramming metabolism, highlighting the potential of targeting metabolic reprogramming for neuroprotective interventions in neurological diseases caused by ischemia or hypoxia.

Metabolic theory of preeclampsia: implications for maternal cardiovascular health.

Preeclampsia (PE) is a multisystemic disorder of pregnancy that not only causes perinatal mortality and morbidity but also has a long-term toll on the maternal and fetal cardiovascular system. Women diagnosed with PE are at greater risk for the subsequent development of hypertension, ischemic heart disease, cardiomyopathy, cerebral edema, seizures, and end-stage renal disease. Although PE is considered heterogeneous, inefficient extravillous trophoblast (EVT) migration leading to deficient spiral artery remodeling and increased uteroplacental vascular resistance is the likely initiation of the disease. The principal pathophysiology is placental hypoxia, causing subsequent oxidative stress, leading to mitochondrial dysfunction, mitophagy, and immunological imbalance. The damage imposed on the placenta in turn results in the "stress response" categorized by the dysfunctional release of vasoactive components including oxidative stressors, proinflammatory factors, and cytokines into the maternal circulation. These bioactive factors have deleterious effects on systemic endothelial cells and coagulation leading to generalized vascular dysfunction and hypercoagulability. A better understanding of these metabolic factors may lead to novel therapeutic approaches to prevent and treat this multisystemic disorder. In this review, we connect the hypoxic-oxidative stress and inflammation involved in the pathophysiology of PE to the resulting persistent cardiovascular complications in patients with preeclampsia.

Evaluation of optic nerve sheath diameter in patients undergoing laparoscopic surgery in the Trendelenburg position: a prospective observational study.

The Trendelenburg position and pneumoperitoneum may cause cerebral edema and increased intracranial pressure. Non-invasive measurement of the diameter of the optic nerve sheath by ultrasonography can provide early recognition of intracranial pressure. Evaluate the optic nerve sheath diameter (ONSD) changes in patients who undergo laparoscopic surgery in the Trendelenburg position and make indirect conclusions about changes in intracranial pressure. Prospective, observational. Laparoscopic surgeries. Patients aged 18-75 years who underwent laparoscopic surgery in the Trendelenburg position under general anesthesia were included in our study. The ONSD was measured four times: Immediately after tracheal intubation, in the neutral position (baseline value) (T0), 10 minutes after pneumoperitoneum and Trendelenburg position (T1), 60 minutes after pneumoperitoneum and Trendelenburg position (T2), and 10 minutes after the pneumoperitoneum is terminated and placed in the neutral position (T3). Compare ONSD measured by ultrasonography at different times of surgery. 40. Arterial carbon dioxide pressure increased with laparoscopy and Trendelenburg position in parallel with ONSD measurements and decreased again after returning to the neutral position. It was still higher than the baseline value at the T3. There was also a significant difference[a] between the measurement made at the T2 and the measurement made at T1. This difference showed that the prolongation of the Trendelenburg time was associated with an increase in ONSD. At the end of the operation it was observed that the decreased statistically significantly (T3) 10 minutes after the pneumoperitoneum was terminated and the position was corrected. However, the ONSD was still higher at the end of the operation (T3) compared to the baseline value measured at the beginning of the operation (T0). The ONSD increased in relation to Trendelenburg position and pneumoperitoneum. With these results, we think the ultrasonographic measurement of ONSD, a non-invasive method, can be used for clinical follow-up when performing laparoscopic surgery in the Trendelenburg position in cases requiring intracranial pressure monitoring. There may be variations in the measurement of ONSD, even in the measurements of the same practitioner, as in all imaging with an ultrasonography device.