Cerebral Artery Vasospasm Research Articles

A prospective pilot study of gut microbiome in cerebral vasospasm and delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage

A recent systematic review indicated that gut–microbiota–brain axis contributes to growth and rupture of intracranial aneurysms. However, gaps were detected in the role of intestinal microbiome in cerebral vasospasm (CVS) after aneurysmal subarachnoid hemorrhage (aSAH). This is the first pilot study aiming to test study feasibility and identify differences in gut microbiota between subjects with and without CVS following aSAH. A prospective nested case–control pilot study with 1:1 matching was conducted recruiting subjects with aSAH: cases with CVS; and controls without CVS based on the clinical picture and structured bedside transcranial Doppler (TCD). Fecal samples for microbiota analyses by means of 16S rRNA gene amplicon sequencing were collected within the first 96 h after ictus. Operational taxonomic unit tables were constructed, diversity metrics calculated, phylogenetic trees built, and differential abundance analysis (DAA) performed. At baseline, the groups did not differ significantly in basic demographic and aneurysm-related characteristics (p > 0.05). Alpha-diversity (richness and Shannon Index) was significantly reduced in cases of middle cerebral artery (MCA) vasospasm (p < 0.05). In DAA, relative abundance of genus Acidaminococcus was associated with MCA vasospasm (p = 0.00013). Two butyrate-producing genera, Intestinimonas and Butyricimonas, as well as [Clostridium] innocuum group had the strongest negative correlation with the mean blood flow velocity in anterior cerebral arteries (p < 0.01; rho = − 0.63; − 0.57, and − 0.57, respectively). In total, 16 gut microbial genera were identified to correlate with TCD parameters, and two intestinal genera correlated with outcome upon discharge. In this pilot study, we prove study feasibility and present the first preliminary evidence of gut microbiome signature associating with CVS as a significant cause of stroke in subjects with aSAH.

The Effect of Age on Cerebral Vasospasm and Delayed Cerebral Ischemia in Patients with Aneurysmal Subarachnoid Hemorrhage

The association between patient age and cerebral arterial vasospasm (CVS) and delayed cerebral ischemia (DCI) risk following aneurysmal subarachnoid hemorrhage (aSAH) remains unclear. This study aims to assess the role of age on aSAH-related complications. Single-center retrospective study comprising aSAH patients treated between January 2009 and March 2023. Age was analyzed as continuous and categorical variables (<60yrs vs. ≥60yrs and by decade). Outcomes of interest included radiographic CVS, DCI, cerebral infarction, in-hospital mortality, length-of-stay, ventriculoperitoneal shunt placement, and modified Rankin Scale (mRS) scores at discharge and 3-month follow-up. 925 aSAH patients were included. Most (n=598; 64.6%) were <60yrs old (46±9.1yrs). CVS likelihood was lower in the older cohort (aOR=0.56 [0.38-0.82]). Patients ≥60yrs had higher mortality rates (aOR=2.24 [1.12-4.47]) and worse mRS scores at discharge (aOR=2.66 [1.91-3.72]) and 3-month follow-up (aOR=2.19 [1.44-3.32]). Advanced age did not have a significant effect on DCI or cerebral infarction risk. Higher in-hospital mortality was documented with increasing age (p<0.001). A significant interaction between CVS and age for the outcome of DCI was documented, with a stronger positive effect on poor outcomes (i.e., higher odds of DCI) among patients aged <60 years compared to those aged ≥60. There is an inverse relationship between patient age and CVS incidence following aSAH. Nonetheless, patients ≥60yrs had comparable DCI rates, higher in-hospital mortality, and worse functional outcomes than their younger counterparts. Routine screening and reliance on radiographic CVS as primary marker for aSAH-related complications should be reconsidered, particularly in older patients.

Cerebral arterial vasospasm complicating supratentorial meningioma resection: illustrative cases.

Cerebral arterial vasospasm is a rare complication after supratentorial meningioma resection. The pathophysiology of this condition may be similar to vasospasm after aneurysmal subarachnoid hemorrhage, and treatment options may be similar. The authors present two cases of cerebral vasospasm after supratentorial meningioma resection and perform a systematic literature review of similar cases. Cerebral arterial vasospasm after supratentorial meningioma resection may be associated with significant morbidity due to cerebral ischemia if not addressed in a timely manner. Treatment paradigms may be adopted from the management of arterial vasospasm associated with subarachnoid hemorrhage.

Study on the Nasal Drug Delivery System of NMD Liposomes In Situ Thermosensitive Gel.

Nimodipine (NMD) is a 1,4-dihydropyridine calcium antagonist that is effective in the prevention and treatment of cerebral arterial vasospasm and cerebral ischemic injury caused by subarachnoid hemorrhage. Since the drug itself is highly insoluble in water and has low oral bioavailability, while injectable formulations may cause pain and inflammation, the blood-brain barrier (BBB) prevents the effective delivery of therapeutic agents to the brain tissue. Therefore, in the present study, NMD liposomes were prepared by ethanol injection and innovatively lyophilised and loaded into temperature-sensitive in situ gels for intranasal administration as sprays to deliver drugs to brain tissues bypassing the blood-brain barrier. The optimal gel formulation was obtained by screening in which liposomes were divided into lecithin, cholesterol, and NMD in the ratio of 40:10: 1; Pluronic P407, Pluronic P188, Tween 80, polyvinyl ketone and ethyl nipagin in the ratio of (180:20:3:1:1); Pluronic P407, Pluronic P188, Tween 80, polyvinyl ketone, and ethyl nipagin in the ratio of (180:20:3:1:1). The prepared flow gel can form a solidified gel after a temperature of 31.07-32.07°C and a time of 58.51-59.89s. Meanwhile, the NMD liposome gel formulation achieved sustained release over 56h. The pharmacokinetic results of the developed NMD liposomal temperature-sensitive in situ gel and NMD temperature-sensitive in situ gel showed that liposomal nasal mucosal in situ gel is a more effective brain-targeted drug delivery system for NMD.

Abstract 091: Intraventricular milrinone for management of vasospasm following aneurysmal subarachnoid hemorrhage

Introduction Aneurysmal subarachnoid hemorrhage (aSAH) accounts for about 10% of hemorrhagic strokes [1] and holds a high mortality and morbidity rate. [2, 3] Vasospasm is one of the more devastating complications of aSAH. Novel imaging modalities have drastically improved our ability in prompt detection of vasospasm in these patients. However, clinical management of this complication is still debated among experts. [4] Systemic cerebral vasodilators are widely used in aSAH patients, but guidelines for interventional and rescue procedures are not well developed. [5] Methods Here, we report a case of severe vasospasm following aSAH that was successfully treated with intraventricular injection of milrinone through external ventricular drain (EVD) in conjunction to standard therapy. Results A 70‐year‐old man with a history of diabetes, hypertension, and hyperlipidemia was brought to the emergency department after he was found down and unresponsive. He was intubated by EMS on route. Head CT on arrival showed a diffuse subarachnoid hemorrhage, more prominent in the posterior fossa, and grade IV on the modified Fisher scale. An initial DSA showed a ruptured aneurysm in the second segment of the right posterior inferior cerebellar artery, second segment. A right frontal EVD was placed on the second day. Hemodynamic augmentation was achieved with intravenous and intraventricular milrinone. Cerebral arterial patency was evaluated with daily transcranial doppler (TCD). The patient did not show any evidence of vasospasm until day 9 where TCD revealed severe vasospasm in the basilar and bilateral vertebral arteries, as well as mild vasospasm of anterior and middle cerebral arteries. Intraventricular milrinone was injected into the EVD in from day 9 to day 12. Using sterile technique, 4 mL of CSF was removed followed by the injection of 0.87mg (2mL) of milrinone into the EVD via a three way stop cock. EVD was then flushed with 2mL of preservative‐free saline and clamped for 1 hour. This procedure effectively improved vasospasm on serial TCDs and also DSAs (Figure1). The patient underwent several DSA’s on days 10, 14, 19, 20, and 21 with targeted intraarterial milrinone and verapamil injections. His final TCD showed only mild middle cerebral artery and moderate basilar artery vasospasm. At that point, no more intervention was deemed necessary. A ventriculoperitoneal shunt was also placed. CT scan before discharge showed mild improvement in ventricular size and stable SAH blood products. The course of hospitalization was complicated by hyponatremia, atrial fibrillation, and respiratory failure with inability to wean off ventilator, resulting in tracheostomy and gastrostomy tube placement. The patient was discharged in stable condition on day 30 to a rehabilitation center. Conclusion Intraventricular milrinone in addition to standard therapy can be an effective method in treatment of severe vasospasm in aSAH patients.

Pharmacological Prevention of Delayed Cerebral Ischemia in Aneurysmal Subarachnoid Hemorrhage.

Causes of morbidity and mortality following aneurysmal subarachnoid hemorrhage (aSAH) include early brain injury and delayed neurologic deterioration, which may result from delayed cerebral ischemia (DCI). Complex pathophysiological mechanisms underlie DCI, which often includes angiographic vasospasm (aVSP) of cerebral arteries. Despite the study of many pharmacological therapies for the prevention of DCI in aSAH, nimodipine-a dihydropyridine calcium channel blocker-remains the only drug recommended universally in this patient population. A common theme in the research of preventative therapies is the use of promising drugs that have been shown to reduce the occurrence of aVSP but ultimately did not improve functional outcomes in large, randomized studies. An example of this is the endothelin antagonist clazosentan, although this agent was recently approved in Japan. The use of the only approved drug, nimodipine, is limited in practice by hypotension. The administration of nimodipine and its counterpart nicardipine by alternative routes, such as intrathecally or formulated as prolonged release implants, continues to be a rational area of study. Additional agents approved in other parts of the world include fasudil and tirilazad. We provide a brief overview of agents currently being studied for prevention of aVSP and DCI after aSAH. Future studies may need to identify subpopulations of patients who can benefit from these drugs and perhaps redefine acceptable outcomes to demonstrate impact.

Efficacy and safety of bridging therapy and direct mechanical thrombectomy in large vessel occlusions: a meta-analysis.

Efficacy and safety of bridging therapy and direct mechanical thrombectomy in large vessel occlusions: a meta-analysis.

Relationship between cerebral vasospasm vascular territory and functional outcome after aneurysmal subarachnoid hemorrhage

BackgroundVasospasm following aneurysmal subarachnoid hemorrhage (SAH) contributes significant morbidity and mortality after brain aneurysm rupture. However, the association between vascular territory of vasospasm and clinical outcome has not been studied....

Reversible Cerebral Vasospasm in Acute Intermittent Porphyria: A Case Report and Review of the Literature.

The porphyrias are rare inherited diseases of heme biosynthesis which can involve the nervous system. The most common neurological manifestations of acute intermittent porphyria are autonomic visceral neuropathy, peripheral motor neuropathy, and central nervous system dysfunction. In rare cases, patients with acute intermittent porphyria have presented with cerebral infarction, suggested to be due to vasospasm in cerebral arteries. We report a case of reversible vasospasm in porphyric encephalopathy demonstrated by both magnetic resonance and conventional angiography. Unexplained abdominal pain occurred before the onset of neurological symptoms.LEARNING POINTSAcute intermittent porphyria can affect the central nervous system.Abdominal pain with neurological symptoms should prompt consideration of porphyria.Cerebral vasospasm is implicated in the pathogenesis of cerebral infarction.Heme arginate is the treatment of choice for central nervous system injury.

Role of Nimodipine and Milrinone in Delayed Cerebral Ischemia

The role of nimodipine and milrinone in the management of delayed cerebral ischemia (DCI) after aneurysmal subarachnoid hemorrhage (SAH) was studied using clinical and TCD (transcranial Doppler) parameters. In this prospective observational study, patients with DCI after aneurysmal SAH presenting between November 2020 and June 2021 who were treated by either intra-arterial nimodipine (IAN) or intravenous milrinone (IVM) were included after excluding patients in whom both IAN and IVM had been given or mechanical angioplasty was performed. Twelve-hourly TCD was performed during the course of the therapy. Clinical improvement and the development of new brain infarcts were also assessed. A P value <0.05 was considered statistically significant. Thirty-four patients fulfilled the inclusion criteria (IVM, 13/34 [38%]; IAN, 21/34 [62%]); patients in the IVM group (vs. IAN group) had poorer median Glasgow Coma Scale score (12 vs. 13), poorer motor response (<M6 response, 5/13 [38%] vs. 5/21 [24%]; P= 0.36) and higher grades (modified Fisher grade ≥3) of SAH (12/13 [92%] vs. 8/21 [86%]; P= 0.56). More patients in the IAN group (vs. IVM group) showed clinical improvement (17/21 [81%] vs. 10/13 [77%]; P= 0.77), development of new infarcts (15/21 [71%] vs. 7/13 [54%]; P= 0.29] and discharged to home (13/21 [62%] vs. 6/13 [46%]; P= 0.36) with less mortality (1/21 [9%] vs. 4/13 [23%]; P= 0.037). On TCD analysis, both IAN and IVM protocols showed similar effects in middle cerebral artery vasospasm; however, IAN proved better over time. In group-effect analysis, the IAN protocol was significantly better in anterior cerebral artery and posterior cerebral artery vasospasm compared with IVM protocol. In this single-center small study, patients in the IAN group had significantly less mortality compared with the IVM group in the management of DCI after aneurysmal SAH.

The incidence of cerebral arterial vasospasm following aneurysmal subarachnoid haemorrhage: a systematic review and meta-analysis

PurposeTo describe a pooled estimated incidence of cerebral arterial vasospasm (aVSP) following aneurysmal subarachnoid haemorrhage (aSAH) and to describe sources of variation in the reported incidence.MethodsWe performed a systematic review and meta-analysis of randomised clinical trials (RCTs) and cohort studies. The primary outcome was the proportion of study participants diagnosed with aVSP. We assessed for heterogeneity based on mode of imaging, indication for imaging, study design and clinical characteristics at a study level.ResultsWe identified 120 studies, including 19,171 participants. More than 40 different criteria were used to diagnose aVSP. The pooled estimate of the proportion of patients diagnosed with aVSP was 0.42 (95% CI 0.39 to 0.46, I2 = 96.5%). There was no evidence that the incidence aVSP was different, nor that heterogeneity was reduced, when the estimate was assessed by study type, imaging modalities, the proportion of participants with high grade CT scores or poor grade clinical scores. The pooled estimate of the proportion of study participants diagnosed with aVSP was higher in studies with routine imaging (0.47, 95% CI 0.43 to 0.52, I2 = 96.5%) compared to those when imaging was performed when indicated (0.30, 95% CI 0.25 to 0.36, I2 = 94.0%, p for between-group difference < 0.0005).ConclusionThe incidence of cerebral arterial vasospasm following aSAH varies widely from 9 to 93% of study participants. Heterogeneity in the reported incidence may be due to variation in the criteria used to diagnose aVSP. A standard set of diagnostic criteria is necessary to resolve the role that aVSP plays in delayed neurological deterioration following aSAH.PROSPERO registrationCRD42020191895

Left Ventricular Outflow Tract Obstruction in Patients Treated With Milrinone for Cerebral Vasospasm: Case Report and Literature Review.

Subarachnoid hemorrhage is associated with high morbidity and mortality, and cerebral arterial vasospasm is one of its main complications that determines neurological prognosis. The use of intravenous milrinone is becoming more common in the treatment of vasospasm. This molecule has positive inotropic and vasodilating properties by inhibiting phosphodiesterase-3. Its most described side effects are cardiac arrhythmias and arterial hypotension. In this paper, we raise a new issue concerning milrinone and discuss an undescribed side effect of this treatment, left ventricular outflow tract obstruction (LVOTO). Dynamic LVOTO is a clinical situation favored by hypovolemia, decreased left ventricular afterload, and excessive inotropism that can lead to severe hemodynamic failure and pulmonary edema. To our knowledge, this is the first study describing milrinone-induced LVOTO. This could compromise cerebral perfusion and therefore the neurological prognosis of patients. While it is known that catecholamines may induce LVOTO, milrinone-induced LVOTO appears to be a new pathophysiological entity of which neurosurgical intensivists should be aware.

Hypercoagulable state in COVID-19 and diabetes: Cerebral vasospasm, intracardiac clot, and pulmonary embolism

Background: Hypercoagulable state in the form of venous and arterial thromboembolism, associated with poor prognosis, could be a severe sequel of COVID-19 infections. We present representative cases that show hypercoagulable state in COVID-19 and the negative effects of diabetes and age on outcomes of anticoagulation therapy. Our aim is to understand the role of predisposing factors for the successful use of anticoagulants. Methods: We applied clinical history, examination, laboratory tests, noninvasive ultrasound imaging, and computer-assisted tomography to characterize hypercoagulable state in patients with COVID-19. Results: One patient (83 years) was diabetic of the elderly group (>64 years), who developed sepsis-induced coagulopathy (SIC), cerebral arterial vasospasm, intracardiac clots, coronary ischemia, and pulmonary embolism with fatal outcome despite the use of anticoagulation. The second patient (60 years) was diabetic of the middle-age group (48–63 years), who developed SIC, cerebral arterial vasospasm, intracardiac clots, and coronary ischemia and had good outcome with the use of anticoagulation. The third case was a patient (22 years) without diabetes of the youth group (15–47 years) who developed cardiomyopathy, heart valve vegetations, and cerebral arterial vasospasm, received anticoagulation, and had good outcome. The difference in outcome with the application of anticoagulation with lower molecular weight heparin could be related to the greater burden of disease including diabetes, age, and chronic obstructive pulmonary disease. Conclusion: Noninvasive ultrasound imaging modalities in combinations with computed axial tomography scans provided insightful characterization of the hypercoagulable state of COVID-19 infection, which helped guide therapeutic intervention.

Somatosensory evoked potentials and transcranial color Doppler monitoring in subarachnoid hemorrhage

The outcome of patients with subarachnoid hemorrhage (SAH) is broadly influenced by the complications that may result from the hemorrhage. We describe a series of subjects, in which neurophysiological monitoring executed by simultaneous recording of somatosensory evoked potentials (SEPs) and transcranial color Doppler (TCD) was performed to reveal possible, early complications following acute SAH. We described the absolute and interhemispheric values of SEPs from the upper limb and TCD examinations of the cerebral arteries in 13 subjects with acute SAH. In cases with middle cerebral artery (MCA) vasospasm, N20 SEP amplitude absolute values for the hemisphere involved in the vasospasm were much lower than the contralateral ones. The N20 amplitude ratio reduction correlated with reciprocal of MCA mean flow velocity values detected within each patient. In the subjects with early ischemic damage following SAH, the affected hemisphere showed N20 amplitude drop; in addition, the relationship between SEPs and TCD findings was missing. Our findings emphasize the utility of simultaneous evaluation of SEPs and TCD in SAH follow-up, since the two methods reflect different pathomechanisms of possible secondary brain damage in aneurysmal SAH.

Vasospasm after transsphenoidal adenoma removal: risk factors and new treatment perspectives for this rare event.

Cerebral vasospasm is an uncommon complication following transsphenoidal surgery (TSS) of a pituitary adenoma. Therefore, neither its physiopathology nor its management are clear. We present a case of vasospasm after TSS and we discuss about its etiology and treatment. A 52-year-old woman presented with hirsutism, without neurologic symptoms. A MRI showed a pituitary macroadenoma. The patient underwent an endoscopic transsphenoidal approach. Post-operative CT scan revealed an extensive subarachnoid haemorrhage (SAH). On postoperative 7th day, she developed an abrupt mixed aphasia. An urgent arteriography showed left middle cerebral artery vasospasm, so intra-arterial nimodipine was administered. After that, vasospasm disappeared and the patient recovered completely. The key to successful management of this rare complication is a high index of suspicion. The presence of postoperative SAH seems to definitely contribute to its apparition. Therefore, treatment in concordance with protocols for vasospasm due to aneurysmal SAH is recommended.

NLRP3 inhibition attenuates early brain injury and delayed cerebral vasospasm after subarachnoid hemorrhage

BackgroundThe NLRP3 inflammasome is a critical mediator of several vascular diseases through positive regulation of proinflammatory pathways. In this study, we defined the role of NLRP3 in both the acute and delayed phases following subarachnoid hemorrhage (SAH). SAH is associated with devastating early brain injury (EBI) in the acute phase, and those that survive remain at risk for developing delayed cerebral ischemia (DCI) due to cerebral vasospasm. Current therapies are not effective in preventing the morbidity and mortality associated with EBI and DCI. NLRP3 activation is known to drive IL-1β production and stimulate microglia reactivity, both hallmarks of SAH pathology; thus, we hypothesized that inhibition of NLRP3 could alleviate SAH-induced vascular dysfunction and functional deficits.MethodsWe studied NLRP3 in an anterior circulation autologous blood injection model of SAH in mice. Mice were randomized to either sham surgery + vehicle, SAH + vehicle, or SAH + MCC950 (a selective NLRP3 inhibitor). The acute phase was studied at 1 day post-SAH and delayed phase at 5 days post-SAH.ResultsNLRP3 inhibition improved outcomes at both 1 and 5 days post-SAH. In the acute (1 day post-SAH) phase, NLRP3 inhibition attenuated cerebral edema, tight junction disruption, microthrombosis, and microglial reactive morphology shift. Further, we observed a decrease in apoptosis of neurons in mice treated with MCC950. NLRP3 inhibition also prevented middle cerebral artery vasospasm in the delayed (5 days post-SAH) phase and blunted SAH-induced sensorimotor deficits.ConclusionsWe demonstrate a novel association between NLRP3-mediated neuroinflammation and cerebrovascular dysfunction in both the early and delayed phases after SAH. MCC950 and other NLRP3 inhibitors could be promising tools in the development of therapeutics for EBI and DCI.

Cerebrovascular pathophysiology of delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage.

Aneurysmal subarachnoid hemorrhage (SAH) remains a serious cerebrovascular disease. Even if SAH patients survive the initial insults, delayed cerebral ischemia (DCI) may occur at 4 days or later post-SAH. DCI is characteristics of SAH, and is considered to develop by blood breakdown products and inflammatory reactions, or secondary to early brain injury, acute pathophysiological events that occur in the brain within the first 72 hours of aneurysmal SAH. The pathology underlying DCI may involve large artery vasospasm and/or microcirculatory disturbances by microvasospasm, microthrombosis, dysfunction of venous outflow and compression of microvasculature by vasogenic or cytotoxic tissue edema. Recent clinical evidence has shown that large artery vasospasm is not the only cause of DCI, and that both large artery vasospasm-dependent and -independent cerebral infarction causes poor outcome. Animal studies suggest that mechanisms of vasospasm may differ between large artery and arterioles or capillaries, and that many kinds of cells in the vascular wall and brain parenchyma may be involved in the pathogenesis of microcirculatory disturbances. The impairment of the paravascular and glymphatic systems also may play important roles in the development of DCI. As pathological mediators for DCI, glutamate and several matricellular proteins have been investigated in addition to inflammatory molecules. Glutamate is involved in excitotoxicity contributing to cortical spreading ischemia and epileptic activity-related events. Microvascular dysfunction is an attractive mechanism to explain the cause of poor outcomes independently of large cerebral artery vasospasm, but needs more studies to clarify the pathophysiologies or mechanisms and to develop a novel therapeutic strategy.

The association between hyponatraemia and long-term functional outcome in patients with aneurysmal subarachnoid haemorrhage: A single centre prospective cohort study

To assess the association between hyponatraemia and long-term functional outcome and other relevant outcomes in patients with aneurysmal subarachnoid haemorrhage (aSAH) we conducted a prospective cohort study in a Neurosciences Intensive Care Unit (ICU) in Sydney, Australia. The primary exposure variable was hyponatraemia (Na+ <135 mmol/L). The primary outcome was favourable outcome, a score of 5–8 on the extended Glasgow Outcome Score (GOSe) at 12 months. We also measured mortality, the incidence of delayed cerebral ischaemia (DCI) and cerebral arterial vasospasm and duration of ICU and hospital admission. There were 200 participants, 111 (56%) developed hyponatraemia. Hyponatraemia was not associated with favourable outcome at 12 months (unadjusted odds ratio [OR] OR 1.31, 95% confidence interval [CI] 0.65–2.65, p = 0.56). The result was similar after adjustment for baseline covariates (adjusted OR 0.60, 95% CI 0.16–1.99, p = 0.43). There was no association between hyponatraemia and the incidence of DCI (OR 0.95, 95% CI 0.46 to 2.0, p > 0.99) nor cerebral arterial vasospasm (OR 1.4, 95% CI 0.8 to 2.5, p = 0.27). Those who developed hyponatraemia had a longer median duration of ICU admission (17 days, interquartile range [IQR] 12 to 20, compared to 13 days, IQR 8–21, p = 0.02) and longer median duration of hospital admission (24 days, IQR 21–30, compared to 22 days IQR 14–31, p = 0.05). While hyponatraemia is common following aSAH, it is not associated with worse long-term functional outcome, increased rate of DCI, nor cerebral arterial vasospasm. Hyponatraemia in patients with aSAH was associated with longer duration of ICU and hospital admission.

Risk factors and clinical and neurological consequences of intraoperative rupture of brain aneurysms in microsurgical operations

Objective. to assess the frequency, risk factors and clinical and neurological consequences of intraoperative rupture of arterial aneurysm (AA) of the brain (B) in clipping operations of the B AA .&#x0D; Materials and approaches. A retrospective analysis of microsurgical operations clipping of cerebral aneurysms in 1449 (100%) patients for the period from 2011 to 2018 was performed, of which 141 (9.73%) cases had intraoperative rupture of the aneurysm (IORA). Preoperative examination: clinical and neurological examination, CT of the brain, cerebral angiography( CAG), duplex scanning of the main vessels of the head and neck. The analyzed criteria are risk factors of IORA: AA size, localization, shape, duration of surgery after the primary rupture of AA, the presence of hypertension and the patient's condition before surgery.&#x0D; Results. The frequency of IORA in clipping operations of B AA was 9.73% (141 patients) in a series of observations 1441 (100%). Most often IORA-141 (100%) was registered in clipping operations of AA of complex ACA-AcomA (86 (61%) cases out of 141 (100%)). IORA is possible at all stages of the operation with the maximum frequency of contact breaks – 135 (95.74%); the rarest-6 ( 4.26%) - non - contact IORA (at the stage of craniotomy) was recorded. At the preoperative stage, the vast majority of patients with subsequent IORA were diagnosed with cerebral edema, AA of large size, atherosclerotic changes in the aneurysm-affected segment of the artery and cervical areas of the aneurysm, high blood pressure during surgery, adhesive arachnoid changes. At the time of discharge from the hospital, according to the Glasgow results scale: 69 (48.94%) full or partial restoration of labor activity, 18 (12.77%) had limited daily activities without the need for outside assistance, 37 (26 24%) deep disability ) Deaths were in the group of "contact" IORA - 17 (12.06%). At 6 ( 4.26%) of "non-contact" IORA, a deepening of initial neurological symptoms was recorded with a suppression of the level of consciousness, the addition of pyramidal insufficiency, speech impairment and psycho-organic syndrome, and a deepening of the phenomena of initial cerebral arterial vasospasm.&#x0D; Conclusions. IORA is predominantly in contact with a frequency of occurrence-9.73 %. The most common risk factors for IORA were: cerebral edema, large AA, atherosclerotic changes in the aneurysm-affected artery segment and cervical aneurysm sites, high blood pressure during surgery, adhesions arachnoid changes. IORA leads to deepening of initial neurological symptoms, phenomena of initial vasospasm of cerebral arteries with the level of total mortality-17 (12.06%).

Continous local Intra –arterial Nimodipine administration in severe symptomatic vasospasm after spontanous subarachnoid hemorrhage:a meta-analysis

Abstract Background Subarachnoid hemorrhage (SAH) is bleeding into the subarachnoid space (the area between the arachnoid membrane and the pia mater surrounding the brain). SAH is a potentially life threatening condition. Hemorrhage may occur as a result of a head injury or spontaneously (usually from a ruptured cerebral aneurysm). Spontaneous subarachnoid hemorrhage occurs in about one per 10,000 people per year. Females are more commonly affected than males. While it becomes more common with age, about 50% of people present under 55 years old. It is a form of stroke and comprises about 5 % of all strokes. Disturbed conscious level, specially that associated with cerebral arterial vasospasm, remains a major cause of death and disability in the patients with aneurysmal subarachnoid hemorrhage.The classical modality of management for vasospasm was oral calcium channel blockers (nimodipine) with triple-H therapy (Hypedynamic augmentation therapy). Aim To evaluate the effect of Continous local Intra –arterial nimodipine administration in severe symptomatic vasospasm after spontanous subarachnoid hemorrhage on mortality and morbidity (symptomtic cerebral ischemia). Methodology: Studies and participants In the current meta-analysis, we searched for interventional clinical trials in critically ill adult patients that evaluated to have aneurysmal subarachnoid hemorrhage complicated by severe symptomatic vasospasm (causing delayed cerebral ischemia and neurological deficits) which was refractory to standard hyper dynamic therapy (triple- H therapy) and oral calcium channel blockers (CCBS). Results In the current meta-analysis, the duration of infusion of nimodipine was at least for 72 hours. The onset of occurance of cerebral vasodilation after the infusion in all studies by their different doses was 12 hours detected by transcranial doppler. The time of termination of nimodipine infusion is different from patient to other patient depending on clinical improvement ( improvement of consious level or disappearance of the newly developed neurological deficit) and radiological findings that refers to the relief of vasospasm assesed by transcranial doppler and cerebral angiography. Reinfusion of the nimodipine was done in all included studies in case of recurrence of vasospasm causing new neurological deficit or deterioration in the conscious level . Conclusion It concluded from the current meta-analysis that, intra-arterial nimodipine infusion is effective and safe treatment for syptomatic refractory vasospasm after aneurysmal subarachnoid hemorrhage.