P atients with ESRD are at higher risk of brain hemorrhage. Hemodialysis per se is associated with a 10 times higher incidence of intracranial hemorrhage in these patients than in the general population. 15 , 16 Furthermore, the occurrence of brain hemorrhage in ESRD patients carries a poor prognosis with high morbidity and mortality of up to 60%. 15 Among all therapeutic strategies for brain hemorrhage, management of blood pressure and ICP are 2 important but not easily achieved tasks for ESRD patients due to the influence of RRT. Renal replacement
Vin-Cent Wu, Tao-Min Huang, Chih-Chung Shiao, Chun-Fu Lai, Pi-Ru Tsai, Wei-Jie Wang, Hui-Yu Huang, Kuo-Chuan Wang, Wen-Je Ko, Kwan-Dun Wu and NSARF Group
Daniel M. Caruso, A. Giancarlo Vishteh, Karl A. Greene, Marc R. Matthews and Carlos A. Carrion
to continuous arteriovenous hemofiltration and hemodiafiltration in acute renal failure. Am J Kidney Dis 18: 451–458, 1991 10. Ojemann RG , Heros RC : Spontaneous brain hemorrhage. Stroke 14 : 468 – 475 , 1983 Ojemann RG, Heros RC: Spontaneous brain hemorrhage. Stroke 14: 468–475, 1983 11. Tindall GT , Craddock A , Greenfield JC Jr : Effects of the sitting position on blood flow in the internal carotid artery of man during general anesthesia. J Neurosurg 26 : 383 – 389
Philip Cheng, Li Ma, Sonali Shaligram, Espen J. Walker, Shun-Tai Yang, Chaoliang Tang, Wan Zhu, Lei Zhan, Qiang Li, Xiaonan Zhu, Michael T. Lawton and Hua Su
(approximately 8 mm Hg) immediately after the anastomosis of the CCA and the EJV, and was sustained for up to 2 weeks. Brain samples were collected 2 weeks after VH. We found massive hemorrhage in the bAVM lesions of mice subjected to VH ( Fig. 4 ). VH also caused some microhemorrhages in the angiogenic region of the wild-type (WT) brain. VH did not cause hemorrhage in the brain of mice injected with Ad-Cre and AAV-LacZ. Therefore, deletion of Alk1 alone or injection of AAV vector does not cause brain hemorrhage. VH increased mortality of bAVM mice; 50% of mice in the bAVM
Mentor Petrela, Arben Rroji, Eugen Enesi, Artur Xhumari and Artid Lame
immediately recognized. 8 They are most often incidentally discovered but may occasionally cause pulmonary emboli, endocarditis, dysrhythmias, cardiac tamponade, 2 or even a brain hemorrhage, as in the present case. To our knowledge, this is the first report of guidewire-induced brain hemorrhage. The guidewire spontaneously found the route from the heart to the brain and beyond to the scalp where it then exited the patient’s head. Given that the patient had been well before he attempted to pull out the wire, it would appear that until then the spontaneous and original
Samuel S. Shin, Geoffrey Murdoch, Ronald L. Hamilton, Amir H. Faraji, Hideyuki Kano, Nathan T. Zwagerman, Paul A. Gardner, L. Dade Lunsford and Robert M. Friedlander
Stereotactic radiosurgery (SRS) is a therapeutic option for repeatedly hemorrhagic cavernous malformations (CMs) located in areas deemed to be high risk for resection. During the latency period of 2 or more years after SRS, recurrent hemorrhage remains a persistent risk until the obliterative process has finished. The pathological response to SRS has been studied in relatively few patients. The authors of the present study aimed to gain insight into the effect of SRS on CM and to propose possible mechanisms leading to recurrent hemorrhages following SRS.
During a 13-year interval between 2001 and 2013, bleeding recurred in 9 patients with CMs that had been treated using Gamma Knife surgery at the authors' institution. Microsurgical removal was subsequently performed in 5 of these patients, who had recurrent hemorrhages between 4 months and 7 years after SRS. Specimens from 4 patients were available for analysis and used for this report.
Histopathological analysis demonstrated that vascular sclerosis develops as early as 4 months after SRS. In the samples from 2 to 7 years after SRS, sclerotic vessels were prominent, but there were also vessels with incomplete sclerosis as well as some foci of neovascularization.
Recurrent bleeding after SRS for CM could be related to incomplete sclerosis of the vessels, but neovascularization may also play a role.
Ruobing Xu, Shu Wang, Weishan Li, Zhen Liu, Jiaxin Tang and Xiaobo Tang
the first study to show that the expression of 12/15-LOX and levels of 15(S)-HETE are increased in the ipsilateral brain area after ICH in an animal model. The induction of the 12/15-LOX product 15(S)-HETE may be associated with PPARγ activation and may downregulate brain hemorrhage–induced proinflammatory signaling. These observations raise the intriguing possibility that the induction of the 12/15-LOX pathway may reflect a response to counterbalance the brain hemorrhagic insult and may represent a biologically important damage-repair response in the brain. These
Giuseppe M. V. Barbagallo, Mario Piccini, Alessandro Gasbarrini, Pietro Milone and Vincenzo Albanese
be associated with intraoperative or postoperative complications, 3 , 17 , 29 , 31 , 38 , 42 , 47 , 49 , 56 most frequently in the form of intercostal neuralgia, retained disc fragments, inadvertent durotomies, atelectasis, extensive bleeding, and emergency conversion to open thoracotomy for vascular injuries. 29 , 39 , 56 Moreover, given the increasing number of thoracoscopic surgeries performed, even rare complications not previously documented, such as chylorrhea or brain hemorrhagic infarction, have been reported. 3 , 16 , 17 We describe a very rare and
John S. Norris, Taufik A. Valiante, M. Christopher Wallace, Robert A. Willinsky, Walter J. Montanera, Karel G. terBrugge and Michael Tymianski
Object. The authors sought to establish prospectively whether there is a simple relationship between radiological features of brain arteriovenous malformation (AVM) hemodynamics and a patient's clinical presentation.
Methods. Thirty-one consecutive patients with AVMs underwent cerebral angiography at 3.8 frames/second during each standardized injection of contrast material. Contrast dilution curves were derived from the image sequences by using regions of interest (ROIs) traced on arteries feeding and veins draining the AVM nidus. Angiographic parameters were then analyzed in a blinded fashion. These parameters included the times required to reach the peak contrast density, the contrast decay time, and fractions thereof, in the ROI for each vessel. The authors determined whether these parameters, the arteriovenous transit time, and/or AVM size were related to patients' presentation with hemorrhage (11 patients), seizure (11 patients), or other clinical symptoms (nine patients). Statistically significant results were found only in analyses of arterial phase times to reach peak contrast density. Analyses of venous parameters, AVM size, and nidus transit time showed trends but no statistical significance. Arterial filling with contrast material was significantly slower in patients presenting with hemorrhage (mean 50%, 80%, and 100% of time to peak ± standard error [SE] = 1.19 ± 0.13, 1.97 ± 0.18, and 3.04 ± 0.34 seconds, respectively) compared with patients presenting with seizures (mean 50%, 80%, and 100% of time to peak ± SE = 0.80 ± 0.12, 1.32 ± 0.18, and 1.95 ± 0.29 seconds, respectively) according to analysis of variance (p < 0.05) and post-hoc t-tests (p < 0.05) for each parameter. Patients who presented with other symptoms had intermediate arterial filling times.
Conclusions. These simple hemodynamic parameters, which can be obtained without added risk to the patient, may help identify a subset of individuals in whom AVMs pose a higher risk of future hemorrhage and who may therefore warrant more expeditious treatment.
Douglas Kondziolka, Eugene Bonaroti, Susan Baser, Fran Brandt, Young Soo Kim and L. Dade Lunsford
use by the United States Food and Drug Administration. To date, no outcome data have substantiated the role or utility of microelectrode recording. We feared that the larger number of brain trajectories necessary during microelectrode recording might translate into a higher risk of brain hemorrhage. On one hand, such an increased risk has not been documented; 23 on the other hand micro-recording has not reduced morbidity rates or improved clinical outcomes. 20, 21 In our series we found no incidence of hemiparesis, no clinically noted visual field deficits, and no
Robert A. Solomon, Christopher M. Loftus, Donald O. Quest and James W. Correll
✓ In a consecutive series of 1930 carotid endarterectomies there were eight cases of postoperative intracerebral hemorrhage. One of these patients was operated on 2 weeks following cerebral infarction and had severe uncontrollable hypertension after surgery. A second patient had an intraoperative embolus and bled while fully heparinized on the 3rd postoperative day. Only one patient in the series bled into an area of documented cerebral infarction. The remainder of the cases represented hemorrhage into essentially normal brain.
Seven of the eight patients with intracerebral hemorrhage had high-grade internal carotid artery stenosis preoperatively. Although several factors have contributed to the brain hemorrhages in this series of patients, postoperative cerebral hyperperfusion which often follows endarterectomy may have played an important role. Defective cerebrovascular autoregulation in chronically ischemic brain regions may predispose patients to intracerebral hemorrhage after removal of a high-grade stenosis of the internal carotid artery.