Monitoring of Cerebral Hemodynamics and Oxygenation to Detect Delayed Ischemic Neurological Deficit After Aneurysmal Subarachnoid Hemorrhage

Author(s):  
Martin Seule ◽  
Carl Muroi ◽  
Christopher Sikorski ◽  
Emanuela Keller
2020 ◽  
Vol 133 (3) ◽  
pp. 773-779
Author(s):  
Christopher Wendel ◽  
Ricardo Scheibe ◽  
Sören Wagner ◽  
Wiebke Tangemann ◽  
Hans Henkes ◽  
...  

OBJECTIVECerebral vasospasm (CV) is a delayed, sustained contraction of the cerebral arteries that tends to occur 3–14 days after aneurysmal subarachnoid hemorrhage (aSAH) from a ruptured aneurysm. Vasospasm potentially leads to delayed cerebral ischemia, and despite medical treatment, 1 of 3 patients suffer a persistent neurological deficit. Bedside transcranial Doppler (TCD) ultrasonography is used to indirectly detect CV through recognition of an increase in cerebral blood flow velocity (CBFV). The present study aimed to use TCD ultrasonography to monitor how CBFV changes on both the ipsi- and contralateral sides of the brain in the first 24 hours after patients have received a stellate ganglion block (SGB) to treat CV that persists despite maximum standard therapy.METHODSThe data were culled from records of patients treated between 2013 and 2017. Patients were included if an SGB was administered following aSAH, whose CBFV was ≥ 120 cm/sec and who had either a focal neurological deficit or reduced consciousness despite having received medical treatment and blood pressure management. The SGB was performed on the side where the highest CBFV had been recorded with 8–10 ml ropivacaine 0.2%. The patient’s CBFV was reassessed after 2 and 24 hours.RESULTSThirty-seven patients (male/female ratio 18:19), age 17–70 years (mean age 49.9 ± 11.1), who harbored 13 clipped and 22 coiled aneurysms (1 patient received both a coil and a clip, and 3 patients had 3 untreated aneurysms) had at least one SGB. Patients received up to 4 SGBs, and thus the study comprised a total of 76 SGBs.After the first SGB, CBFV decreased in 80.5% of patients after 2 hours, from a mean of 160.3 ± 28.2 cm/sec to 127.5 ± 34.3 cm/sec (p < 0.001), and it further decreased in 63.4% after 24 hours to 137.2 ± 38.2 cm/sec (p = 0.007). A similar significant effect was found for the subsequent SGB. Adding clonidine showed no significant effect on either the onset or the duration of the SGB. Contralateral middle cerebral artery (MCA) blood flow was not reduced by the SGB.CONCLUSIONSTo the authors’ knowledge, this is the largest study on the effects of administering an SGB to aSAH patients after aneurysm rupture. The data showed a significant reduction in ipsilateral CBFV (MCA 20.5%) after SGB, lasting in about two-thirds of cases for over 24 hours with no major complications resulting from the SGB.


1998 ◽  
Vol 88 (2) ◽  
pp. 272-276 ◽  
Author(s):  
Joanna M. Wardlaw ◽  
Ruth Offin ◽  
Graham M. Teasdale ◽  
Evelyn M. Teasdale

Object. In this prospective observational study, the authors assess the impact of routine transcranial Doppler (TCD) ultrasound monitoring on the diagnosis, management, and outcome of delayed ischemic neurological deficit complicating subarachnoid hemorrhage (SAH). Methods. Over a 10-month period 186 patients admitted to a regional neurosciences center were included in the study. Three times a week, routine TCD examinations performed by neuroradiographers made an important positive contribution to the diagnosis of delayed ischemic neurological deficit in 72% of patients with this complication and led to altered management for the benefit of the patient in 43%. In 9% of patients with recent SAH, it was believed that the outcome might have been better if the TCD result had been acted upon appropriately. The TCD results did not adversely influence management or outcome and were generally accurate when compared with those obtained on angiography. Conclusions. A routine TCD service provided by neuroradiographers is accurate and useful in diagnosing and managing elevated blood velocities and ischemic neurological deficit following SAH. In addition, it is possible that if the information gleaned from TCD findings was used more often in patient management, outcome might be improved; however, a randomized controlled trial is necessary to assess both these points definitively.


1997 ◽  
Vol 3 (4) ◽  
pp. E3 ◽  
Author(s):  
Joanna M. Wardlaw ◽  
Ruth Offin ◽  
Graham M. Teasdale ◽  
Evelyn M. Teasdale

In this prospective observational study, the authors assess the impact of routine transcranial Doppler (TCD) ultrasound monitoring on the diagnosis, management, and outcome of delayed ischemic neurological deficit complicating subarachnoid hemorrhage (SAH). Over a 10-month period 186 patients admitted to a regional neurosciences center were included in the study. Three times a week, routine TCD examinations performed by neuroradiographers made an important positive contribution to the diagnosis of delayed ischemic neurological deficit in 72% of patients with this complication and altered management for the benefit of the patient in 43%. In 9% of patients with recent SAH, it was believed that the outcome might have been better if the TCD result had been acted upon appropriately. The TCD results did not adversely influence management or outcome and were accurate when compared with those obtained on angiography. The authors conclude that a routine TCD service provided by neuroradiographers is accurate and useful in diagnosing and managing elevated blood velocities and ischemic neurological deficit following SAH. In addition, it is possible that if the information gleened from TCD findings was used more often in patient management, outcome might be improved; however, a randomized controlled trial is necessary to assess this definitively.


1986 ◽  
Vol 65 (1) ◽  
pp. 48-62 ◽  
Author(s):  
S. Sam Finn ◽  
Sigurdur A. Stephensen ◽  
Carole A. Miller ◽  
Laura Drobnich ◽  
William E. Hunt

✓ Thirty-two patients with aneurysmal subarachnoid hemorrhage (SAH) were managed according to a protocol based on pain control and hemodynamic manipulation, monitored by an arterial line and Swan-Ganz catheter. Hemodynamic parameters were adjusted to four clinical situations. 1) For the unoperated patient with no neurological deficit, the regimen aims to maintain pulmonary wedge pressure (PWP) at 10 to 12 mm Hg, and the cardiac index (CI) and blood pressure (BP) at normal levels. 2) For the unoperated patient presenting with or developing neurological deficit, the PWP is increased until the deficit is reversed or the CI falls; the CI is high, and the BP normal. 3) For the postoperative patient with no neurological deficit, the PWP is maintained at 12 to 14 mm Hg, the CI is a high normal, and the BP is normal. 4) For the postoperative patient developing neurological deficit but showing no surgical complication on the computerized tomography scan, the PWP is increased until the deficit is reversed or the CI falls; the CI is high and the BP is increased with vasopressors if necessary. Fourteen patients developed neurological deficits either preoperatively, postoperatively, or both. Neurological deficits were repeatedly reversed by increasing the PWP, as measured hourly. In several patients an optimal wedge pressure was determined, below which deficits would reappear. In one patient whose neurological deficit was reversed on several occasions by increasing the PWP, the optimal PWP rose after each episode until it reached 22 mm Hg. Detailed event-related analysis of these patients' course illustrates these phenomena well. The optimal PWP varied from patient to patient, but ranged most frequently from 14 to 16 mm Hg. Meticulous monitoring of the patients' neurological status coupled with prompt correction of low PWP (assuming an adequate CI) has proven to be an effective way to prevent and reverse neurological deficits following aneurysmal SAH.


2019 ◽  
pp. S58-S66
Author(s):  
Dewi Prahaztuti ◽  
Hanik Badriyah Hidayati ◽  
Achmad Firdaus Sani

Subarachnoid hemorrhage (SAH) has been shown to result in cerebral vasospasm at day 4 to day 14, which is the main cause of mortality and morbidity after SAH. Outcome after SAH depends on many factors, including the severity of the event, medical management, and prevention of several serious complications. The principal goal in management of vasospasm after SAH is to prevent delayed ischemic neurological deficit (DIND) by decreasing intracranial pressure (ICP), optimizing cerebral oxygen demand rate and improving cerebral blood flow (CBF). Therapeutic management has been applied to prevent or treat vasospasm, including hemodynamic therapy, and endovascular therapy. Endovascular therapies, including mechanical angioplasty and chemical angioplasty with administration of intra-arterial (IA) vasodilator, have been widely used and given a good outcome. The purpose of this article is to describe the management of vasospasm including medical management and endovascular treatment. This review will describe the treatment modalities and management strategies to treat vasospasm.Abbreviations: SAH – subarachnoid hemorrhage; aSAH – aneurysmal subarachnoid hemorrhage; TCD – transcranial Doppler; ROS – reactive oxygen species; ICAM – intercellular adhesion molecule; VCAM – vascular cell adhesion molecule; IL – interleukin; CTA – computed tomography angiography; MRA – magnetic resonance angiography; CBF – cerebral blood flow; DIND – delayed ischemic neurological deficit; RCT - randomized controlled trialsCitation: Prahaztuti D, Hidayati HB, Sani AF. Management of cerebral vasospasm in subarachnoid hemorrhage. Anaesth Pain & Intensive Care 2018;22(3 Suppl 1):S58-S66.Received: 19 Oct 2018 Reviewed: 4, 11 Nov 2018 Accepted: 12 Nov 2018


2020 ◽  
Vol 10 (8) ◽  
pp. 495
Author(s):  
Petr Vachata ◽  
Jan Lodin ◽  
Aleš Hejčl ◽  
Filip Cihlář ◽  
Martin Sameš

Cerebral vasospasm and subsequent delayed ischemic neurological deficit is a typical sequela of acute subarachnoid hemorrhage after aneurysm rupture. The occurrence of vasospasms after uncomplicated surgery of an unruptured aneurysm without history of suspected rupture is extremely rare. The pathogenesis and severity of cerebral vasospasms is typically correlated with the amount of blood breakdown products extravasated during subarachnoid hemorrhage. In rare cases, where vasospasms occur after unruptured aneurysm surgery, the pathogenesis is most likely multifactorial and unclear. We present two cases of vasospasms following uncomplicated clipping of middle cerebral artery (MCA) aneurysms and a review of literature. Early diagnosis and therapy of this rare complication are necessary to achieve optimal clinical outcomes.


QJM ◽  
2020 ◽  
Vol 113 (Supplement_1) ◽  
Author(s):  
A N Elshaer ◽  
I S Habil ◽  
A A Moharram ◽  
M A Menshawe ◽  
A M Marzouk

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.


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