Objective To set up and to evaluate an acute closed brain injury model in rats. Methods The acute closed brain injury was produced in rats by using an impactor consisting of a stand, a guide tube, a weight and a footplate. Ninetysix SD rats were divided into a control group(n＝32, no impact), a mild injury group(n＝32, impact once at force level of 400 g·cm) and a severe injury group(n＝32, impact once at force level of 800 g·cm) to elucidate the physiological responses, the pathophysiological changes and brain edema after brain injury at different injury levels. Results In the mild injury group and the severe injury group, a sudden rise or reduction of blood pressure, deep and fast breath apnea, and pain reflects inhibition were observed. The responses were more obvious in the severe injury group than in the mild injury group. The water content of the brain increased after 6 hours of injury. The pathological contusion and edema of brain were noted or above the impact force level of 800 g·cm. When the impact force rose to or over 1200g·cm, the animals died of persistent apnea mostly. Conclusion Although the established closed brain injury model with different biomechanical mechanisms as the clinical brain injury, it is in conformity with pathological changes and pathophysiological characteristics of acute clinical brain injury, it can be utilized extensively because of its convenient and practice.
Fifteen rabbits were given a second degree scald on the back, then a large amount of fluid were given rapidly. In this way an acute diluted hyponatremia and a brain edema model were produced. In one group, the magnetotherapy was instituted immediately following the acut injury, while in the other group, it was started after the brain edema being developed. After giving a large quantity of fluid, the Na~+, CI~-, and K~+ concentrations in the blood were decreased and the quantity of water in the brain tissue was increased evidentely. The phenomena of neuron edema and widening of the perivascular space were also found. It was proved that the model of experimental brain edema could be produced on animals and the treatment and the prevention for brain edema could be obtained to advantage to certaiin degree. Also,it was better to use the magnetotherapy in brain edema as early as possidle.
We used near-infrared spectroscopy technology to monitor and assess the treatment effect of dehydrating agent in injured rat brain in real time style. We employed the brain edema model in rats resulting from Feeney's freefall damage, then treated with different doses of mannitol, and collected reduced scattering coefficient (μ's) and intracranial pressure (ICP) values after the injury and during the treatment. The results showed that brain edema happened 1 h after the injury in rats' brain tissue, peaked around 72 h after injury, and then began to decrease gradually. The reduced scattering coefficient and ICP values of the treatment group injected with mannitol all decreased after administration. Compared with the effect of low-dose mannitol treatment, that of high-dose mannitol treatment was much better. The duration of the plateau was longer and most experiments results declined significantly. From this we conclude that the reduced scattering coefficient and ICP are consistent with the trend changes, and the reduced scattering coefficient could be used as an indicator for monitoring cerebral edema.
Objective We modeled superior vena cava (SVC) occlusion in rabbits to observe the effect of different blocking time on brains. Method Forty rabbits were randomly divided into four groups. Group Ⅰ was set as a control group (n=10). Group Ⅱ was set as a 30 minutes SVC blocking time group (n=10). Group Ⅲ was set as a 60 minutes SVC blocking time group (n=10). And group Ⅳ was set as a 90 minutes SVC blocking time group (n=10). We detected the patho- logical and physiological changes in the course of the experiment. After the intervention, malondialdehyde (MDA) and superoxide dismutase (SOD) of brain tissue homogenate in each group were detected. Brain sections were stained with hematoxylin-eosin (HE). And we observed the edema and damage of brain tissue under the microscope. Results There was no obvious change on the content of MDA and SOD within 30 minutes interruption (P>0.05). When the blocking time was longer than 60 minutes, the content of MDA increased significantly (P<0.05) and the SOD decreased significantly (P<0.05). Compared to the group Ⅰ and the group Ⅱ, the brain water content in the group Ⅲ and the group Ⅳ with a interruption time above 60 minutes increased significantly. And under the microscope, the cell edema and damage induced by ischemia and hypoxia increased significantly. Conclusion The blocking time of SVC within 30 minutes is relatively safe. But there would be significant brain edema and neurocyte degeneration when the blocking time is more than 60 minutes.
Massive cerebral infarction with malignant brain edema has poor prognosis with very high mortality, despite aggressive medical treatment. Surgical decompression is recommended by Chinese and international clinical guidelines for patients with massive cerebral infarction, however, there is no standardized diagnosis and treatment protocol in clinical practice. Following the principle of evidence-based medicine and based on the diagnosis and treatment norms of the participating hospitals of Severe Ischaemic Stroke Collaboration in recent years, we recommend this consensus statement of the standardized surgical decompression for malignant brain edema in massive cerebral infarction.
Massive and severe cerebral infarction can lead to a high mortality and disability rate, and it is the bottleneck of preventing and treating cerebrovascular disease. Once the malignant brain edema of massive cerebral infarction or the critical status of severe cerebral infarction occurs, the treatment effect is very poor. Therefore, we should not only focus on the treatment of critical cerebral infarction, but also prevent its occurrence. It is clinically important to prevent the occurrence of this critical condition in advance and to prevent the occurrence of massive cerebral infarction and severe cerebral infarction. This article points out that some patients with massive or severe cerebral infarction can be prevented from becoming critically ill. The definition, key risk factors and corresponding prevention and treatment strategies of critical cerebral infarction have also been proposed. Critical cerebral infarction can be divided into two categories with or without malignant brain edema, and the risk factors and prediction and prevention strategies by categories andphases can be studied separately.
Objective To understand the dynamic changes of inflammatory indicators in the peripheral blood of patients with malignant cerebral edema at different time points after acute cerebral infarction, and provide a basis for early prediction and prevention of malignant cerebral edema. Methods Consecutive patients with acute cerebral infarction within 24 h of onset who were admitted to the Department of Neurology, West China Hospital of Sichuan University between January 1st, 2017 to December 31st, 2018 were collected. The basic clinical data of the patients were collected, and the data of inflammatory cells (white blood cell count, absolute neutrophil count, absolute lymphocyte count, and neutrophil to lymphocyte ratio) and acute phase reactants (blood glucose, fibrinogen, albumin, and fibrinogen to albumin ratio) were dynamically collected at admission and 1, 3, and 7 d after admission, respectively. Differences between groups were compared using generalized estimating equations. Results A total of 798 patients with acute cerebral infarction were included, of whom 93 (11.65%) developed malignant cerebral edema. At all time points examined, the white blood cell counts, absolute neutrophil counts, and neutrophil to lymphocyte ratios were higher in the malignant cerebral edema group than those in the non-malignant cerebral edema group (Wald χ2=63.737, P<0.001; Wald χ2=91.848, P<0.001; Wald χ2=75.197, P<0.001); 1 and 3 d after admission, the absolute lymphocyte counts were lower in the malignant cerebral edema group than those in the non-malignant cerebral edema group (Wald χ2=18.580, P<0.001). The blood glucose levels were higher in the malignant cerebral edema group compared with the non-malignant cerebral edema group 1, 3, and 7 d after admission (Wald χ2=16.722, P<0.001); no significant between-group effect was found in the albumin levels (Wald χ2=3.643, P=0.056); the fibrinogen levels were significantly different between groups 3 d after admission (Wald χ2=8.923, P=0.003), and the fibrinogen to albumin ratios differed between the two groups 3 and 7 d after admission (Wald χ2=6.739, P=0.009). Dynamic analysis of multiple time points in the malignant cerebral edema group found that these inflammatory markers mostly reached their extreme values 3 d after admission. Conclusions Compared with the non-malignant cerebral edema group, the inflammatory cell-related indicators (except lymphocytes) and the acute phase inflammatory reactant-related indicators in malignant cerebral edema patients are significantly higher, and the absolute lymphocyte count is significantly lower. Three days after admission to hospital is probably the most significant time point for the change of each inflammatory indicator.
Objective To explore the association between procalcitonin (PCT) level and the development of malignant brain edema (MBE) after acute cerebral infarction. Methods The data on patients with stroke admitted to the Department of Neurology of West China Hospital, Sichuan University between January 1, 2017 and December 31, 2018 were retrospective collected. Patients were divided into MBE group and non-MBE group based on whether MBE had occurred. The basic information and neuroimaging data of two groups of patients were compared and analyzed. Results A total of 798 patients were included. Among them, there were 93 cases of MBE (11.65%) and 705 cases of non-MBE (88.35%). The median time of MBE occurrence (lower quartile, upper quartile) was 29 (24, 54) hours after onset. The difference in the National Institutes of Health Stroke Scale, large-scale middle cerebral artery infarction, dysarthria, low fever, consciousness status, chronic heart failure, TOAST typing, mechanical ventilation, gastric tube placement, PCT on the first and third day of admission between the two groups were statistically significant (P<0.05). There was no statistically significant difference in the other indicators between the two groups (P>0.05). The results of multivariate logistic regression analysis showed that both day 1 PCT and large-scale middle cerebral artery infarction were associated with MBE. Conclusions Elevated PCT within 24 hours from onset is independently associated with the development of MBE after acute cerebral infarction. Patients with elevated PCT after cerebral infarction may require careful clinical management.