Outcomes of high-grade aneurysmal subarachnoid hemorrhage patients treated with coiling and ventricular intracranial pressure monitoring

BACKGROUND High-grade aneurysmal subarachnoid hemorrhage is a devastating disease with a low favorable outcome.Elevated intracranial pressure is a substantial feature of high-grade aneurysmal subarachnoid hemorrhage that can result to secondary brain injury.Early control of intracranial pressure including decompressive craniectomy and external ventricular drainage had been reported to be associated with improved outcomes.But in recent years,little is known whether external ventricular drainage and intracranial pressure monitoring after coiling could improve outcomes in high-grade aneurysmal subarachnoid hemorrhage.AIM To investigate the outcomes of high-grade aneurysmal subarachnoid hemorrhage patients with coiling and ventricular intracranial pressure monitoring.METHODS A retrospective analysis of a consecutive series of high-grade patients treated between Jan 2016 and Jun 2017 was performed.In our center,followed by continuous intracranial pressure monitoring,the use of ventricular pressure probe for endovascular coiling and invasive intracranial pressure monitoring in the acute phase is considered to be the first choice for the treatment of high-grade patients.We retrospectively analyzed patient characteristics,radiological features,intracranial pressure monitoring parameters,complications,mortality and outcome.RESULTS A total of 36 patients were included,and 32(88.89%)survived.The overall mortality rate was 11.11%.No patient suffered from aneurysm re-rupture.The intracranial pressure in 33 patients(91.67%)was maintained within the normal range by ventricular drainage during the treatment.A favorable outcome was achieved in 18 patients(50%)with 6 mo follow-up.Delayed cerebral ischemia and Glasgow coma scale were considered as significant predictors of outcome(2.066 and-0.296,respectively,P<0.05).CONCLUSION Ventricular intracranial pressure monitoring may effectively maintain the intracranial pressure within the normal range.Despite the small number of cases in the current work,high-grade patients may benefit from a combination therapy of early coiling and subsequent ventricular intracranial pressure monitoring.

Blast-Induced Traumatic Brain Injury Triggered by Moderate Intensity Shock Wave Using a Modified Experimental Model of Injury in Mice

Background： The increasing frequency of explosive injuries has increased interest in blast-induced traumatic brain injury （bTBI）. Various shock tube models have been used to study bTBI. Mild-to-moderate explosions are often overlooked because of the slow onset or mildness of the symptoms. However, heavy gas cylinders and large volume chambers in the model may increase the complexity and danger. This study sought to design a modified model to explore the effect of moderate explosion on brain injury in mice. Methods： Pathology scoring system （PSS） was used to distinguish the graded intensity by the modified model. A total of 160 mice were randomly divided into control, sham, and bTBI groups with different time points. The clinical features, imaging features, neurobehavior, and neuropathology were detected after moderate explosion. One-way analysis of variance followed by Fisher＇s least significant difference posttest or Dunnett＇s t 3-test was performed for data analyses. Results： PSS of mild, moderate, and severe explosion was 13.4 ± 2.2, 32.6 ± 2.7 （t = 13.92, P 〈 0.001; vs. mild group）, and 56.6 ± 2.8 （t = 31.37, P 〈 0.001; vs. mild group）, respectively. After moderate explosion, mice showed varied symptoms of malaise, anorexia, incontinence, apnea, or seizure. After bTBI, brain edema reached the highest peak at day 3 （82.5% ± 2.1% vs. 73.8% ± 0.6%. t - 7.76, P 〈 0.001）, while the most serious neurological outcomes occurred at day 1 （Y-maze： 8.25 ±2.36 vs. 20.00 ± 4.55, t = -4.59, P=0.048; 29.58% ± 2.84% vs. 49.09% ±11.63%, t = -3.08, P = 0.008; neurologic severity score： 2.50 ± 0.58 vs. 0.00±0.00, t = 8.65, P = 0.016）. We also found that apoptotic neurons （52.76% ± 1.99% vs. 1.30% ± 0.11%, t =57.20, P 〈 0.001 ） and gliosis （2.98 ± 0.24 vs. 1.00 ± 0.00, t = 14.42, P = 0.021） in the frontal were significantly higher at day 3 post-bTBI than sham bTB1. Conclusions： We provide a reliable, reproducible bTBI model in mice that can produce a graded explosive waveform similar to the free-field shock wave in a controlled laboratory environment. Moderate explosion can trigger mild-to-moderate blast damage of the brain.