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.
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 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.