Flow diversion of ruptured intracranial aneurysms: a single-center study with a standardized antithrombotic treatment protocol.

BACKGROUND: The use of antithrombotic medication following acute flow diversion for a ruptured intracranial aneurysm (IA) is challenging with no current guidelines. We investigated the incidence of treatment-related complications and patient outcomes after flow diversion for a ruptured IA before and after the implementation of a standardized antithrombotic medication protocol. METHODS: We conducted a single-center retrospective study including consecutive patients treated for acutely ruptured IAs with flow diversion during 2015-2023. We divided the patients into two groups: those treated before the implementation of the protocol (pre-protocol) and those treated after the implementation of the protocol (post-protocol). The primary outcomes were hemorrhagic and ischemic complications. A secondary outcome was clinical outcome using the modified Ranking Scale (mRS). RESULTS: Totally 39 patients with 40 ruptured IAs were treated with flow diversion (69% pre-protocol, 31% post-protocol). The patient mean age was 55 years, 62% were female, 63% of aneurysms were in the posterior circulation, 92% of aneurysms were non-saccular, and 44% were in poor grade on admission. Treatment differences included the use of glycoprotein IIb/IIIa inhibitors (pre-group 48% vs. post-group 100%), and the use of early dual antiplatelets (pre-group 44% vs. 92% post-group). The incidence of ischemic complications was 37% and 42% and the incidence of hemorrhagic complications was 30% and 33% in the pre- and post-groups, respectively, with no between-group differences. There were three (11%) aneurysm re-ruptures in the pre-group and none in the post-group. There were no differences in mortality or mRS 0-2 between the groups at 6 months. CONCLUSION: We found no major differences in the incidence of ischemic or hemorrhagic complications after the implementation of a standardized antithrombotic protocol for acute flow diversion for ruptured IAs. There is an urgent need for more evidence-based guidelines to optimize antithrombotic treatment after flow diversion in the setting of subarachnoid hemorrhage.

Comparison of high versus low frequency cerebral physiology for cerebrovascular reactivity assessment in traumatic brain injury: a multi-center pilot study.

Current accepted cerebrovascular reactivity indices suffer from the need of high frequency data capture and export for post-acquisition processing. The role for minute-by-minute data in cerebrovascular reactivity monitoring remains uncertain. The goal was to explore the statistical time-series relationships between intra-cranial pressure (ICP), mean arterial pressure (MAP) and pressure reactivity index (PRx) using both 10-s and minute data update frequency in TBI. Prospective data from 31 patients from 3 centers with moderate/severe TBI and high-frequency archived physiology were reviewed. Both 10-s by 10-s and minute-by-minute mean values were derived for ICP and MAP for each patient. Similarly, PRx was derived using 30 consecutive 10-s data points, updated every minute. While long-PRx (L-PRx) was derived via similar methodology using minute-by-minute data, with L-PRx derived using various window lengths (5, 10, 20, 30, 40, and 60 min; denoted L-PRx_5, etc.). Time-series autoregressive integrative moving average (ARIMA) and vector autoregressive integrative moving average (VARIMA) models were created to analyze the relationship of these parameters over time. ARIMA modelling, Granger causality testing and VARIMA impulse response function (IRF) plotting demonstrated that similar information is carried in minute mean ICP and MAP data, compared to 10-s mean slow-wave ICP and MAP data. Shorter window L-PRx variants, such as L-PRx_5, appear to have a similar ARIMA structure, have a linear association with PRx and display moderate-to-strong correlations (r ~ 0.700, p < 0.0001 for each patient). Thus, these particular L-PRx variants appear closest in nature to standard PRx. ICP and MAP derived via 10-s or minute based averaging display similar statistical time-series structure and co-variance patterns. PRx and L-PRx based on shorter windows also behave similarly over time. These results imply certain L-PRx variants may carry similar information to PRx in TBI.

Perioperative Treatment of Brain Arteriovenous Malformations Between 2006 and 2014: The Helsinki Protocol.

OBJECTIVE: We reviewed retrospectively the perioperative treatment of microsurgically resected brain arteriovenous malformations (bAVMs) at the neurosurgical department of Helsinki University Hospital between the years 2006 and 2014. We examined the performance of the treatment protocol and the incidence of delayed postoperative hemorrhage (DPH). METHODS: The Helsinki protocol for postoperative treatment of bAVMs was used for the whole patient cohort of 121. The patients who had subsequent DPH were reviewed in more detail. RESULTS: Five out of 121 (4.1%) patients had DPH. These patients had a higher Spetzler-Martin grade (SMG) (p = 0.043) and a more complex venous drainage pattern (p = 0.003) as compared to those who had no postoperative bleed. Patients with DPH had 43% larger intravenous fluid intake in the neurosurgical intensive care unit (p = 0.052); they were all male (p = 0.040) and had longer stay in the intensive care unit (p = 0.022). CONCLUSIONS: The Helsinki protocol for postoperative treatment of bAVMs was found to produce comparable results to a more complex treatment algorithm. DPH was associated with high SMG, complex venous drainage pattern, male gender and high intravenous fluid intake. Our findings support the use of SMG in defining patient's postoperative treatment as the DPHs in our study occurred in patients with grade 2-5.

Principles of neuroanesthesia in aneurysmal subarachnoid hemorrhage: The Helsinki experience.

BACKGROUND: Aneurysmal subarachnoid hemorrhage is a devastating disease that is followed by a marked stress response affecting other organs besides the brain. The aim in the management of patients with aSAH is not only to prevent rebleedings by treating the aneurysm by either microneurosurgery or endovascular surgery, but also to evacuate acute space-occupying hematomas and to treat hydrocephalus. METHODS: This review is based on the experience of the authors in the management of more than 7500 patients with aSAH treated in the Department of Neurosurgery at Helsinki University Central Hospital, Finland. RESULTS: The role of the neuroanesthesiologist together with the neurosurgeon may begin in the emergency department to assess and stabilize the general medical and neurologic status of the patients. Early preoperative management of patients in the NICU, prevention of rebleeding, and providing a slack brain during microneurosurgical procedures are further steps. Postoperative management, prevention, and treatment of possible medical complications and cerebrovascular spasm are as necessary as high-quality microsurgery. CONCLUSION: Multidisciplinary and professional teamwork is essential in the management of patients with cerebral aneurysms.

External validation of the international mission for prognosis and analysis of clinical trials model and the role of markers of coagulation.

BACKGROUND: Markers of coagulation have shown to have important value in predicting traumatic brain injury outcome. OBJECTIVE: To externally validate and investigate the role of markers of coagulation for outcome prediction by using the International Mission for Prognosis and Analysis of Clinical Trials (IMPACT) model while adjusting for overall injury severity. METHODS: A retrospective chart analysis of traumatic brain injury patients admitted to Helsinki University Central Hospital between 2009 and 2010 was performed. Outcome was estimated by using the criteria of the IMPACT model. Admission international normalized ratio (INR) and platelet count were used as markers of coagulation. Overall injury severity was categorized with the injury severity score (ISS). Variables were added to the calculated IMPACT risk, generating new models. Model performance was assessed by analyzing and comparing the area under the curve (AUC) of the models. RESULTS: For 342 included patients, 6-month mortality was 32% and unfavorable neurological outcome was 36%. Patients with a poor outcome had lower platelets and higher INR and ISS than those with good outcome (P < .001). The IMPACT model had an AUC of 0.85 for predicting mortality and 0.81 for neurological outcome. Addition of INR but not ISS or platelets to the IMPACT predicted risk improved the predictive validity for mortality ([INCREMENT]AUC 0.02, P = .034) but not neurological outcome ([INCREMENT]AUC 0.00, P = .401). In multivariate analysis, INR remained significant for mortality but not for neurological outcome when adjusting for IMPACT risk and ISS (P = .012). CONCLUSION: The IMPACT model showed excellent performance, and INR was an independent predictor for mortality, independent of overall injury severity.

Effect of the combination of mannitol and ringer acetate or hydroxyethyl starch on whole blood coagulation in vitro.

Mannitol is administered to decrease the intracranial pressure and to improve surgical conditions during craniotomy. Simultaneously a crystalloid infusion is always given and sometimes hydroxyethyl starch (HES) is indicated for intravascular volume replacement. As normal coagulation profile is required during craniotomy, we aimed at determining the effect of mannitol with or without HES or Ringer acetate on blood coagulation in this randomized cross-over in vitro study. Blood samples were withdrawn from 10 volunteers. From whole blood we prepared 10 vol.% and 20 vol.% dilutions of mannitol (15% Mannitol) alone, mannitol and Ringer acetate, and mannitol and HES 130/0.4 (Voluven) at a ratio of 1:1. Blood samples were analyzed by modified thromboelastometry. Coagulation parameters: clotting time, clot formation time, and maximum clot firmness (MCF), were registered. Clot formation time was prolonged in all dilutions compared with control (P<0.05). MCF decreased in all dilutions compared with control (P<0.05). MCF in 20 vol.% dilution of mannitol with HES was lower than MCF in the corresponding dilution with Ringer acetate (P<0.05). Fibrinogen-dependent MCF in 10 vol.% dilution of mannitol with HES was lower than MCF in the corresponding dilution with Ringer acetate (P<0.05). We conclude that mannitol in combination with HES 130/0.4 impairs clot propagation and clot strength in vitro. Fibrin clot strength impairment is more pronounced when mannitol is combined with HES than Ringer acetate. Our findings indicate that HES in combination with mannitol should be avoided whenever a disturbance in hemostasis is suspected during craniotomy.