Management Of Subarachnoid Hemorrhage Patients Research Articles

Early management of patients with aneurysmal subarachnoid hemorrhage in a hospital with neurosurgical/neuroendovascular facilities: a consensus and clinical recommendations of the Italian Society of Anesthesia and Intensive Care (SIAARTI)—part 2

BackgroundQuestions remain on the optimal management of subarachnoid hemorrhage (SAH) patients once they are admitted to the referring center, before and after the aneurysm treatment. To address these issues, we created a consensus of experts endorsed by the Italian Society of Anesthesia and Intensive Care (SIAARTI) to provide clinical guidance regarding this topic. Specifically, in this manuscript (part 2), we aim to provide a list of experts’ recommendations regarding the management of SAH patients in a center with neurosurgical/neuroendovascular facilities after aneurysm treatment.MethodsA multidisciplinary consensus panel composed by 24 physicians selected for their established clinical and scientific expertise in the acute management of SAH patients with different specializations (anesthesia/intensive care, neurosurgery, and interventional neuroradiology) was created. A modified Delphi approach was adopted.ResultsA total of 33 statements were discussed, voted, and approved. Consensus was reached on 30 recommendations (28 strong and 2 weak). In 3 cases, where consensus could not be agreed upon, no recommendation was provided.ConclusionsThis consensus provides practical recommendations (and not mandatory standard of practice) to support clinician’s decision-making in the management of SAH patients in centers with neurosurgical/neuroendovascular facilities after aneurysm securing.

Early management of patients with aneurysmal subarachnoid hemorrhage in a hospital with neurosurgical/neuroendovascular facilities: a consensus and clinical recommendations of the Italian Society of Anesthesia and Intensive Care (SIAARTI)\u2013Part 1

BackgroundIssues remain on the optimal management of subarachnoid hemorrhage (SAH) patients once they are admitted to the referring center, before and after the aneurysm treatment. To address these issues, we created a consensus of experts endorsed by the Italian Society of Anesthesia and Intensive Care (SIAARTI). In this manuscript, we aim to provide a list of experts’ recommendations regarding the early management of SAH patients from hospital admission, in a center with neurosurgical/neuro-endovascular facilities, until securing of the bleeding aneurysm.MethodsA multidisciplinary consensus panel composed of 24 physicians selected for their established clinical and scientific expertise in the acute management of SAH patients with different background (anesthesia/intensive care, neurosurgery, and interventional neuroradiology) was created. A modified Delphi approach was adopted.ResultsAmong 19 statements discussed. The consensus was reached on 18 strong recommendations. In one case, consensus could not be agreed upon and no recommendation was provided.ConclusionsThis consensus provides practical recommendations for the management of SAH patients in hospitals with neurosurgical/neuroendovascular facilities until aneurysm securing. It is intended to support clinician’s decision-making and not to mandate a standard of practice.

NEK7 Coordinates Rapid Neuroinflammation After Subarachnoid Hemorrhage in Mice.

Background: Subarachnoid hemorrhage (SAH) is a devastating disease which leads to high morbidity and mortality. Recent studies have indicated that, never in mitosis gene A-related expressed kinase 7 (NEK7), is involved in NLRP3 (NLR family, pyrin domain containing 3) associated inflammation, which may result in subsequent cellular and vascular damage. The aim of this study was to investigate whether NEK7 is involved in the pathophysiology of subarachnoid hemorrhage.Methods: 455 adult male C57B6J mice, weighing 22 to 30 g, were used to investigate the time course of NEK7 expression in the ipsilateral cortex after SAH, and to investigate the intrinsic function and mechanism of NEK7. A vascular puncture model was used to create the mouse SAH model, and intracerebroventricular injection was used to deliver NEK7 recombinant protein, NEK7 small interfering RNA, nigericin, and MCC950. Neurological score, brain water content, Evans blue extravasation, immunofluorescence, and western blot were evaluated for neurological outcome, neuronal apoptosis, blood-brain barrier damage, microglia accumulation, and the mechanism of NEK7 and NLRP3 activation.Results: Our results exhibited that intrinsic NEK7 was elevated after SAH in the cortex of the left/ipsilateral hemisphere and was colocalized with microglia, endothelial cells, neuron, astrocyte, and oligodendrocyte, and highly expressed in microglia and endothelial cells after SAH. NEK7 recombinant protein aggravated neurological deficits, brain edema, neuronal apoptosis, BBB permeability, microglial accumulation, and activated caspase-1 and IL-1β maturation, while NEK7 small interfering RNA injection reversed those effects. Nigericin administration enhanced ASC oligomerization, caspase-1 and IL-1β maturation without increasing the protein level of NLRP3, and ASC oligomerization and caspase-1 IL-1β maturation reduced when combined with NEK7 knockdown or MCC950 delivery. We found the level of NEK7 expression increased after SAH and could activate the downstream NLRP3 pathway to induce caspase-1, IL-1β expression and then increased the BBB opening, microglia accumulation and neuronal apoptosis after SAH.Conclusions: This study demonstrated for the first time that NEK7 mediated the harmful effects of neuronal apoptosis and BBB disruption after SAH, which may potentially be mediated by the NEK7/NLRP3 signal. NEK7 served as a co-component for NLRP3 inflammasome activation after SAH. NEK7 may be a promising target on the management of SAH patients.

Cyclophilin a signaling induces pericyte-associated blood-brain barrier disruption after subarachnoid hemorrhage

ObjectiveThe potential roles and mechanisms of pericytes in maintaining blood–brain barrier (BBB) integrity, which would be helpful for the development of therapeutic strategies for subarachnoid hemorrhage (SAH), remain unclear. We sought to provide evidence on the potential role of pericytes in BBB disruption and possible involvement and mechanism of CypA signaling in both cultured pericytes and SAH models.MethodsThree hundred fifty-three adult male C57B6J mice weighing 22 to 30 g, 29 CypA−/− mice, 30 CypA+/+ (flox/flox) mice, and 30 male neonatal C57B6J mice were used to investigate the time course of CypA expression in pericytes after SAH, the intrinsic function and mechanism of CypA in pericytes, and whether the known receptor CD147 mediates these effects.ResultsOur data demonstrated both intracellular CypA and CypA secretion increased after SAH and could activate CD147 receptor and downstream NF-κB pathway to induce MMP9 expression and proteolytic functions for degradation of endothelium tight junction proteins and basal membranes. CypA served as autocrine or paracrine ligand for its receptor, CD147. Although CypA could be endocytosed by pericytes, specific endocytosis inhibitor chlorpromazine did not have any effect on MMP9 activation. However, specific knockdown of CD147 could reverse the harmful effects of CypA expression in pericytes on the BBB integrity after SAH.ConclusionsThis study demonstrated for the first time that CypA mediated the harmful effects of pericytes on BBB disruption after SAH, which potentially mediated by CD147/NF-κB/MMP9 signal, and junction protein degradation in the brain. By targeting CypA and pericytes, this study may provide new insights on the management of SAH patients.

LRP1 activation attenuates white matter injury by modulating microglial polarization through Shc1/PI3K/Akt pathway after subarachnoid hemorrhage in rats

White matter injury (WMI) is associated with motor deficits and cognitive dysfunctions in subarachnoid hemorrhage (SAH) patients. Therapeutic strategy targeting WMI would likely improve the neurological outcomes after SAH. Low-density lipoprotein receptor-related protein-1 (LRP1), a scavenger receptor of apolipoprotein E (apoE), is able to modulate microglia polarization towards anti-inflammatory M2 phenotypes during inflammatory and oxidative insult. In the present study, we investigated the effects of LRP1 activation on WMI and underlying mechanisms of M2 microglial polarization in a rat model of SAH. Two hundred and seventeen male Sprague Dawley rats (weight 280–330 g) were used. SAH was induced by endovascular perforation. LPR1 ligand, apoE-mimic peptide COG1410 was administered intraperitoneally. Microglial depletion kit liposomal clodronate (CLP), LPR1 siRNA or PI3K inhibitor were administered intracerebroventricularly. Post-SAH assessments included neurobehavioral tests, brain water content, immunohistochemistry, Golgi staining, western blot and co-immunoprecipitation. SAH induced WMI shown as the accumulation of amyloid precursor protein and neurofilament heavy polypeptide as well as myelin loss. Microglial depletion by CLP significantly suppressed WMI after SAH. COG1410 reduced brain water content, increased the anti-inflammatory M2 microglial phenotypes, attenuated WMI and improved neurological function after SAH. LRP1 was bound with endogenous apoE and intracellular adaptor protein Shc1. The benefits of COG1410 were reversed by LPR1 siRNA or PI3K inhibitor. LRP1 activation attenuated WMI and improved neurological function by modulating M2 microglial polarization at least in part through Shc1/PI3K/Akt signaling in a rat model of SAH. The apoE-mimic peptide COG1410 may serve as a promising treatment in the management of SAH patients.

Neuroinflammation as a Target for Intervention in Subarachnoid Hemorrhage.

Aneurysmal subarachnoid hemorrhage (SAH) is a sub-type of hemorrhagic stroke associated with the highest rates of mortality and long-term neurological disabilities. Despite the improvement in the management of SAH patients and the reduction in case fatality in the last decades, disability and mortality remain high in this population. Brain injury can occur immediately and in the first days after SAH. This early brain injury can be due to physical effects on the brain such as increased intracranial pressure, herniations, intracerebral, intraventricular hemorrhage, and hydrocephalus. After the first 3 days, angiographic cerebral vasospasm (ACV) is a common neurological complication that in severe cases can lead to delayed cerebral ischemia and cerebral infarction. Consequently, the prevention and treatment of ACV continue to be a major goal. However, most treatments for ACV are vasodilators since ACV is due to arterial vasoconstriction. Other targets also have included those directed at the underlying biochemical mechanisms of brain injury such as inflammation and either independently or as a consequence, cerebral microthrombosis, cortical spreading ischemia, blood–brain barrier breakdown, and cerebral ischemia. Unfortunately, no pharmacologic treatment directed at these processes has yet shown efficacy in SAH. Enteral nimodipine and the endovascular treatment of the culprit aneurysm, remain the only treatment options supported by evidence from randomized clinical trials to improve patients’ outcome. Currently, there is no intervention directly developed and approved to target neuroinflammation after SAH. The goal of this review is to provide an overview on anti-inflammatory drugs tested after aneurysmal SAH.

Corticosteroids in the Management of Hyponatremia, Hypovolemia, and Vasospasm in Subarachnoid Hemorrhage: A Meta-Analysis

Background: Cerebral vasospasm and sodium and fluid imbalances are common sequelae of aneurysmal subarachnoid hemorrhage (SAH) and cause of significant morbidity and mortality. Studies have shown the benefit of corticosteroids in the management of these sequelae. We have reviewed the literature and analyzed the available data for corticosteroid use after SAH. Methods: PubMed, EMBASE, and Cochrane electronic databases were searched without language restrictions, and 7 observational, controlled clinical studies of the effect of corticosteroids in the management of SAH patients were identified. Data on sodium and fluid balances, symptomatic vasospasm (SVS), and outcomes were pooled for meta-analyses using the Mantel-Haenszel random effects model. Results: Corticosteroids, specifically hydrocortisone and fludrocortisone, decreased natriuretic diuresis and incidence of hypovolemia. Corticosteroid administration is associated with lower incidence of SVS in the absence of nimodipine, but does not alter the neurological outcome. Conclusions: Supplementation of corticosteroids with mineralocorticoid activity, such as hydrocortisone or fludrocortisone, helps in maintaining sodium and volume homeostasis in SAH patients. Larger trials are warranted to confirm the effects of corticosteroids on SVS and patient outcomes.

Hemoglobin induced NO/cGMP suppression Deteriorate Microcirculation via Pericyte Phenotype Transformation after Subarachnoid Hemorrhage in Rats.

Subarachnoid hemorrhage (SAH) usually results from ruptured aneurysm, but how leaked hemoglobin regulates the microcirculation in the pathophysiology of early brain injury after SAH is still unclear. In the present study, we sought to investigate the role and possible mechanism of hemoglobin induced pericyte phenotype transformation in the regulation of microcirculation after SAH. Endovascular perforation SAH rat model, brain slices and cultured pericytes were used, and intervened with endothelial nitric oxide synthase (eNOS) antagonist L-NNA and its agonist scutellarin, hemoglobin, DETA/NO (nitric oxide(NO) donor), PITO (NO scavenger), 8-Br-cGMP (cGMP analog). We found modulating eNOS regulated pericyte α-SMA phenotype transformation, microcirculation, and neurological function in SAH rats. Modulating eNOS also affected eNOS expression, eNOS activity and NO availability after SAH. In addition, we showed hemoglobins penetrated into brain parenchyma after SAH. And hemoglobins significantly reduced the microvessel diameters at pericyte sites, due to the effects of hemoglobin inducing α-SMA expressions in cultured pericytes and brain slices via inhibiting NO/cGMP pathway. In conclusion, pericyte α-SMA phenotype mediates acute microvessel constriction after SAH possibly by hemoglobin suppressing NO/cGMP signaling pathway. Therefore, by targeting the eNOS and pericyte α-SMA phenotype, our present data may shed new light on the management of SAH patients.

Clinical Neurochemistry of Subarachnoid Hemorrhage: Toward Predicting Individual Outcomes via Biomarkers of Brain Energy Metabolism.

The functional outcome of patients with subarachnoid hemorrhage is difficult to predict at the individual level. The monitoring of brain energy metabolism has proven to be useful in improving the pathophysiological understanding of subarachnoid hemorrhage. Nonetheless, brain energy monitoring has not yet clearly been included in official guidelines for the management of subarachnoid hemorrhage patients, likely because previous studies compared only biological data between two groups of patients (unfavorable vs favorable outcomes) and did not determine decision thresholds that could be useful in clinical practice. Therefore, this Viewpoint discusses recent findings suggesting that monitoring biomarkers of brain energy metabolism at the level of individuals can be used to predict the outcomes of subarachnoid hemorrhage patients. Indeed, by taking into account specific neurochemical patterns obtained by local or global monitoring of brain energy metabolism, it may become possible to predict routinely, and with sufficient sensitivity and specificity, the individual outcomes of subarachnoid hemorrhage patients. Moreover, combining both local and global monitoring improves the overall performance of individual outcome prediction. Such a combined neurochemical monitoring approach may become, after prospective clinical validation, an important component in the management of subarachnoid hemorrhage patients to adapt individualized therapeutic interventions.

Effect of Insular Injury on Autonomic Functions in Patients With Ruptured Middle Cerebral Artery Aneurysms

Insular injuries are known to cause autonomic derangements. Patients with ruptured middle cerebral artery aneurysms frequently develop temporal hematomas (THs) in addition to subarachnoid hemorrhages, and those with TH may sustain autonomic derangements more frequently than those without TH. Hemispheric lateralization in autonomic derangements has been reported in patients with insular ischemic stroke, and this study was conducted to clarify whether such lateralization was also observed in patients with TH resulting from middle cerebral artery aneurysm rupture. A retrospective analysis on the medical records of 79 patients with ruptured middle cerebral artery aneurysms was performed on the basis of lateralization and presence of TH. They were quadrichotomized as left TH+ (LTH+; n=17), right TH+ (n=25), left TH- (n=15), and right TH- (n=22). Comparisons, mainly between LTH+ and right TH+, were made on demographic variables, autonomic/cardiac parameters, plasma catecholamine and glucose levels, and outcomes. There were no significant differences in demographic or cardiac parameters between the 2 groups. Systolic blood pressures were lower in LTH+ (139±34 versus 174±47 mm Hg; P=0.05). The LTH+ group also tended to be more bradycardiac (80±19 versus 101±22 bpm; P=0.13). The LTH+ group exhibited significantly lower plasma norepinephrine (1008±975 versus 2549±2133 pg/mL; P=0.03) and glucose levels (9.3±1.8 versus 12.2±4.5 mmol/L; P=0.04). However, in-hospital mortality did not differ significantly (41% versus 44%; P=1.00). Lateralization of autonomic derangements observed might not have had a significant effect on the outcomes. Nevertheless, autonomic derangements associated with insular injury should be considered in the management of subarachnoid hemorrhage patients with TH.

Abstract WP435: Acute Blood Pressure Reduction and Cerebral Infarction After Aneurysmal Subarachnoid Hemorrhage

Background: Radiographic cerebral infarction (RCI) is a prominent cause of disability after aneurysmal subarachnoid hemorrhage (SAH). Current guidelines for acute blood pressure (BP) management of SAH patients are intended to prevent rebleeding, but their potential impact on RCI is unknown. HYPOTHESIS: RCI after SAH is associated with more acute BP reduction and lower BP. METHODS: We evaluated 49 patients with SAH. Clinical and radiographic data were prospectively collected. BP data were electronically retrieved from the medical record. BP was compared with multivariate generalized linear models. RESULTS: RCI was detected in 19 of 49 patients (38.8%). No rebleeding occurred in any of the patients during their hospital stay. Vasospasm occurred in 8 (16.3%) of patients and was associated with higher systolic and diastolic BP (P<0.001 for both) between days 4 and 14. Historical hypertension was associated with RCI (52.6% vs. 23.3%, P=0.036), although initial systolic (168±37 vs. 151±26 mm Hg, P=0.1) and diastolic BP (90±20 vs. 83±19, P=0.2) were not. In a generalized linear model accounting for time from symptom onset, vasospasm, historical hypertension and a vasospasm by time interaction (since BP augmentation depended on the time from symptom onset), lower systolic (-7, 95%CI -8 to -6 mm Hg, (P<0.001) and diastolic BP (-5, 95%CI -6 to -4 mm Hg, P<0.001) were associated with RCI. There were similar data for change in BP from initial BP. CONCLUSIONS: RCI after SAH is associated with greater BP reductions and historical hypertension may contribute to this risk. More aggressive BP reduction than recommended by current guidelines, while potentially decreasing the risk of aneurysm rebleeding, may be associated with RCI. Routine perfusion scanning to determine the risk of RCI from reduced perfusion may be warranted.

Basic and Translational Research on Proteinase-Activated Receptors: The Role of Thrombin Receptor in Cerebral Vasospasm in Subarachnoid Hemorrhage

Cerebral vasospasm is one of the major complications of subarachnoid hemorrhage (SAH). The prevention and treatment of cerebral vasospasm thus plays a critical role in the management of SAH patients. However, the mechanism of cerebral vasospasm still remains elusive, while effective therapeutic strategies also remain to be established. The role of thrombin and its receptor proteinase-activated receptor 1 (PAR1) in cerebral vasospasm was investigated using a rabbit double hemorrhage SAH model. The expression of PAR1 was up-regulated and the contractile response to thrombin was markedly enhanced in the basilar artery of SAH models. The intrathecal administration of a PAR1 antagonist prevented the up-regulation of PAR1 and the enhancement of the contractile responses to thrombin in SAH. These observations thus suggest that PAR1 may play a pivotal role in post-hemorrhagic cerebral vasospasm in SAH. Following SAH, thrombin activates PAR1, thereby up-regulating the expression of PAR1, which culminates in the increased contractile response to thrombin in the basilar artery. PAR1 antagonists are thus anticipated to be a novel therapeutic strategy for cerebral vasospasm. However, further studies are needed before establishing the clinical usefulness of PAR1 antagonists.

Current advances in the diagnosis of vasospasm

Symptomatic vasospasm leading to delayed ischemia and neurological deficits is one of the most serious complications after aneurysmal subarachnoid hemorrhage (SAH). Reliable and early detection of symptomatic vasospasm is one of the major goals in the management of patients with SAH. In awake patients, the close clinical neurological examination still remains the most important diagnostic measure. In comatous or sedated patients, cerebral angiography remains the mainstay of the diagnostic workup for vasospasm. However, angiography does not allow assessing the hemodynamic relevance of vasospasm and is not suited for early identification of cerebral hypoperfusion and ischemia. Therefore, a large panel of new monitoring techniques for the assessment of regional cerebral perfusion has been recently introduced into the clinical management of SAH patients. This article briefly reviews the most relevant methods for monitoring cerebral perfusion and discusses their clinical predictive value for the diagnosis of vasospasm. On the basis of the currently available monitoring technologies, an algorithm for the diagnosis of vasospasm is presented.

Perfusion-weighted Magnetic Resonance Imaging in Patients with Vasospasm: A Useful New Tool in the Management of Patients with Subarachnoid Hemorrhage.

OBJECTIVE Cerebral vasospasm (VSP) is one of the most important risk factors for the development of a delayed neurological deficit after subarachnoid hemorrhage (SAH). Perfusion-weighted magnetic resonance imaging (pwMRI) provides the possibility of detecting tissue at risk for infarction. The objective of our study was to evaluate the feasibility and impact of pwMRI in the management of SAH patients. METHODS From a consecutive series of 180 patients experiencing SAH and treated at our institution over a 3-year period, we identified 20 who underwent pwMRI during their acute illness. For these 20 patients, the results of pwMRI were compared with the results of diffusion-weighted MRI, transcranial Doppler sonography, and neurological examinations performed at the same time and with repeated pwMRI examinations of the same patient at different times. RESULTS Nineteen of 20 patients showed perfusion changes predominantly in the time maps. Fifteen of 19 patients with changes in pwMRI had a neurological deficit at the same time. In 7 of 15 patients with neurological deterioration, transcranial Doppler sonography showed signs of VSP, whereas all 15 patients showed alterations in pwMRI. The areas of perfusion changes in pwMRI correlated well with the neurological deficits of the patients and were larger than the areas of changed diffusion in diffusion-weighted MRI performed at the same time. There were no clinical complications with regard to the pwMRI examinations. CONCLUSION pwMRI is safe and helpful in the management of patients with VSP after SAH. The sensitivity of pwMRI is higher than that of transcranial Doppler sonography in the detection of decreased perfusion as a result of VSP. pwMRI can detect tissue at risk before definitive infarction occurs and therefore may lead to a change of therapy in those patients.

Perfusion-weighted Magnetic Resonance Imaging in Patients with Vasospasm: A Useful New Tool in the Management of Patients with Subarachnoid Hemorrhage

Cerebral vasospasm (VSP) is one of the most important risk factors for the development of a delayed neurological deficit after subarachnoid hemorrhage (SAH). Perfusion-weighted magnetic resonance imaging (pwMRI) provides the possibility of detecting tissue at risk for infarction. The objective of our study was to evaluate the feasibility and impact of pwMRI in the management of SAH patients. From a consecutive series of 180 patients experiencing SAH and treated at our institution over a 3-year period, we identified 20 who underwent pwMRI during their acute illness. For these 20 patients, the results of pwMRI were compared with the results of diffusion-weighted MRI, transcranial Doppler sonography, and neurological examinations performed at the same time and with repeated pwMRI examinations of the same patient at different times. Nineteen of 20 patients showed perfusion changes predominantly in the time maps. Fifteen of 19 patients with changes in pwMRI had a neurological deficit at the same time. In 7 of 15 patients with neurological deterioration, transcranial Doppler sonography showed signs of VSP, whereas all 15 patients showed alterations in pwMRI. The areas of perfusion changes in pwMRI correlated well with the neurological deficits of the patients and were larger than the areas of changed diffusion in diffusion-weighted MRI performed at the same time. There were no clinical complications with regard to the pwMRI examinations. pwMRI is safe and helpful in the management of patients with VSP after SAH. The sensitivity of pwMRI is higher than that of transcranial Doppler sonography in the detection of decreased perfusion as a result of VSP. pwMRI can detect tissue at risk before definitive infarction occurs and therefore may lead to a change of therapy in those patients.

Intracranial pressure monitoring in patients with subarachnoid haemorrhage

ICP monitoring is part of intensive care management of subarachnoid hemorrhage patients (SAH). However, patterns of ICP and their relationship with cerebral ischemia or quality of outcome have not yet been clearly defined.

Microsensor and Microdialysis Technology: Advanced Techniques in the Management of Severe Head Injury

Neuroscientists continue the search for the "magic bullet" that will prevent the deleterious effects of primary and secondary brain injury. Indirect measurement of the effects of primary and secondary brain injury through the study of ICP- or CPP-directed management, CBF monitoring, Sjo2 monitoring, and TCD monitoring has led to improved care of persons with brain injury. Although the findings from brain injury research using microsensor and microdialysis technology are only preliminary and extensive research is still needed, these technologies have dramatically expanded knowledge about brain injury at the cellular level. Extended neuromonitoring is poised to enter a new and exciting phase because of the growth in knowledge regarding the cellular events associated with brain injury. The recent approval of NeuroTrend by the FDA will further promote this growth. Applications of the technology have already expanded to include uses beyond the management of traumatic brain injury. Microsensor and microdialysis technology is being used intraoperatively to determine "safe" temporary clipping times for aneurysm surgery and is also being used within the critical care setting to improve the monitoring and management of subarachnoid hemorrhage patients who are experiencing vasospasm. The ultimate application of this new technology is to improve long-term outcomes for patients with brain injury through the reduction of secondary brain injury. If that goal is to be accomplished, then it will be important for nurses caring for patients with brain injury to become immersed in this exciting new phase in brain injury monitoring. Nurses must obtain a comprehensive knowledge base of brain injury pathophysiology and how extended neuromonitoring can lead to improved outcomes. Technical proficiency will also be important to ensure that treatment and research conclusions are based on accurate data. Finally and perhaps most importantly, it will be critical for nurses to participate in and develop research studies that explore the impact of interventions, especially nursing care activities, on the injured brain if these exciting new advances are to be translated into tangible benefits for brain-injured patients.

Management of subarachnoid hemorrhage patients: is early surgery better than delayed?

Management of subarachnoid hemorrhage patients: is early surgery better than delayed?

Management of subarachnoid hemorrhage patients who presented with respiratory arrest resuscitated with bystander CPR.

The sudden death rate from aneurysmal subarachnoid hemorrhage (SAH) is 10%. Since 1989, 26 SAH patients who were witnessed to collapse into coma with respiratory arrest and required cardiopulmonary resuscitation (CPR) at the scene survived to reach the hospital and be diagnosed. Although reports on hospital management of grade V SAH suggest improved outcome, no report has previously addressed the issue of respiratory arrest after acute SAH. We analyze our experience with this unique subgroup of aneurysmal SAH patients. This is a retrospective analysis of 26 consecutive SAH patients who collapsed at the scene and required CPR for respiratory arrest and survived to reach the hospital and be diagnosed. Statistical analysis was performed using the t test and Mann-Whitney rank-sum test. All patients were grade V on arrival at the emergency department. Twenty-one patients received mouth-to-mouth resuscitation only, and 5 received chest compressions as well. The mean duration of bystander CPR was 12 to 15 minutes. CT scan showed diffuse, thick SAH in all patients, an associated subdural hemorrhage in 2, and an intraparenchymal hemorrhage in 4. After CT scan, an intracranial pressure (ICP) monitor was placed in 24, and 2 were taken to emergency surgery for subdural and intracerebral hemorrhage. ICP was elevated in 24 patients (mean, 54 mm Hg), and a ventriculostomy was placed in all 24. ICP was unresponsive in 12, and all suffered brain death. ICP lessened to < 25 mm Hg in 12, and all underwent angiography. All 12 had an aneurysm and underwent emergency surgical clipping. Time to surgery from SAH was < or = 11 hours in all 12 patients. All were managed with calcium channel blockers and hyperdynamic therapy in addition to aggressive control of ICP. The outcome at 12 months in the 14 surgical cases was normal in 3 patients (21%), good in 2 (14%), vegetative in 1 (7%), and death in 8 (57%). Aneurysmal SAH patients that present with respiratory arrest present as grade V patients with elevated ICP. Bystander CPR coupled with early retrieval, diagnosis, and therapy can lead to 20% functional survival in what used to be sudden death from aneurysmal SAH.

&lt;I&gt;Postoperative Luxury Perfusion Syndrome in Patients with Severe Subarachnoid Hemorrhage Treated by Early Aneurysmal Clipping&lt;/I&gt;

Cerebral blood flow (CBF) was measured in 90 patients who underwent early aneurysmal clipping after subarachnoid hemorrhage (SAH). Measurements were made by a noninvasive, two-dimensional method involving intravenous injection of 133Xe. Patients of Hunt and Hess grades I and II exhibited normal to slightly subnormal CBF, without significant changes, during the study period. Grades III-V patients had almost normal CBF in the early postoperative period, but their CBF gradually decreased, becoming significantly low after day 31. It is noteworthy that in grades IV and V patients, CBF was abnormally high in the acute stage, relative to their poor neurological condition; these patients were considered to have the "global luxury perfusion syndrome." The syndrome was not uncommon in patients with severe SAH. Possible causative or contributory factors are attempts to surgically reduce intracranial pressure, which leads to increased cerebral perfusion pressure, and concomitant global dysautoregulation. In patients with this syndrome, maneuvers intended to increase CBF should be avoided, as they may aggravate brain swelling or cause hemorrhagic events. Positron emission tomographic studies will provide more accurate and useful information concerning the management of SAH patients.