Jurnal Neuroanestesi Indonesia Literature Review Diagnosis and Management of Cerebral Vasospasm Following Aneurysmal SAH Mirza Oktavian.
Dewi Yulianti Bisri.
Iwan Abdul Rachman Department of Anesthesiology and Intensive Care.
Faculty of Medicine.
Padjadjaran University.
Bandung.
Indonesia Received: February 10, 2025.
Accepted: September 24, 2025.
Publish: October 21, 2025 Correspondence: neurologyuph@gmail.
Abstract Cerebral Vasospasm, characterized by the progressive constriction of cerebral arteries, often occurs following a subarachnoid hemorrhage (SAH) and is a leading cause of morbidity and mortality in affected patients.
This condition can be resulted in cerebral ischemia, the severity of which correlates with the degree of vasospasm.
The underlying pathophysiology involves the encasement of arteries by blood clots, although the intricate interactions between the hematoma and adjacent structures remain incompletely understood.
The delayed onset of vasospasm offers a potential window for preventive interventions.
However, recent randomized controlled trials have been discouraging, as they failed to demonstrate any significant improvement in patient outcomes with the use of clazosentan .
n endothelin antagonis.
, simvastatin .
cholesterol-lowering agen.
, or magnesium sulfate .
Current best practices for managing vasospasm include minimizing ischemia by maintaining adequate blood volume and pressure, administering nimodipine .
calcium channel blocke.
, and, when necessary, performing balloon angioplasty.
Over the past two decades, advancements in the management of vasospasm have significantly reduced associated morbidity and mortality rates.
Nevertheless, vasospasm remains a critical determinant of clinical outcomes following aneurysmal rupture.
Keywords: Diagnosis, cerebral vasospasm, management neuroanestesi Indones 2025.
: 108Ae16 Introduction Cerebral vasospasm represents a severe complication following subarachnoid hemorrhage (SAH), often leading to delayed cerebral ischemia and infarction, and continues to be a central concern in neurocritical care.
1 The diagnosis of cerebral vasospasm poses considerable challenges due to its intricate pathophysiology and the difficulties associated with its early Nevertheless, recent advancements in imaging modalities, such as CT perfusion.
MRI, and transcranial Doppler ultrasonography (TCD), have significantly enhanced the precision and speed of detection.
These technological improvements have created new opportunities for timely interventions, thereby improving the potential for more effective clinical management of this critical condition.
Vasospasm is observed in roughly 40Ae50% of patients following SAH, with its peak occurrence typically between days 4 and 5 after the initial bleeding event.
2 Despite extensive research, the precise mechanisms driving vasospasm are still being elucidated.
Earlier investigations have established that vasospasm is a key contributor to delayed cerebral ischemia, one of the most dreaded outcomes associated with SAH.
Vasospasm is essentially a reactive process marked by abnormal or localized constriction of cerebral arteries.
This phenomenon is thought to be resulted from the release of hemolytic byproducts, which activate smooth muscle cells in the arterial walls.
These effects are primarily mediated through calcium doi: https://doi.
org/10.
24244/jni.
ISSN (Prin.
: 2088-9674 ISSN (Onlin.
: 2460-2302 This is an open access article under the CC-BY-NC-SA licensed: https://creativecommons.
org/licenses/by-nc-sa/4.
JNI is accredited as Sinta 2 Journal: https://sinta.
id/journals/profile/796 Mirza Oktavian.
Dewi Yulianti Bisri.
Iwan Abdul Rachman Copyright A2025 How to cite: Oktavian M, et al, "Diagnosis and Management of Cerebral Vasospasm Following Aneurysmal SAH".
Diagnosis and Management of Cerebral Vasospasm Following Aneurysmal SAH ion (CaA ) signaling pathways and the action of prostaglandins, particularly prostaglandin E2 (PGE.
Cerebral vasospasm is strongly influenced by various predisposing factors, with the volume of subarachnoid blood detected on CT imaging being a critical determinant.
This highlights the necessity of timely and precise diagnostic imaging in the clinical management of high-risk patients.
Contemporary therapeutic approaches emphasize both the prevention and treatment of vasospasm.
Nimodipine is regarded as the cornerstone of prophylactic therapy, while hemodynamic augmentation through induced hypertension is commonly employed to manage symptomatic Aneurysmal rupture leading to SAH affects approximately 10 in 10,000 individuals annually, with a mortality rate nearing 40%.
Survivors of the initial hemorrhagic episode face a substantial risk of neurological deficits due to delayed cerebral vasospasm.
Approximately twothirds of SAH patients develop arterial narrowing indicative of vasospasm between days 3 and 14 following the rupture.
however, only about onethird of these individuals manifest clinically significant neurological symptoms.
Patients with posterior circulation aneurysms are at heightened risk, with nearly 75% experiencing symptomatic vasospasm.
The temporal profile of complications varies, with intracranial hemorrhage or vasospasm peaking within the first 24 to 48 hours after traumatic injury and rebleeding risk highest in the first 24 hours post-rupture.
6 Additionally, patients undergoing craniotomy for tumor resection are vulnerable to vasospasm or hemorrhage within 48 to 72 hours post-surgery.
7 While existing therapies are effective, novel strategiesAiincluding endothelin receptor antagonists, magnesium sulfate, statins, and endovascular interventions like transluminal angioplastyAiare being explored.
8Ae10 Despite progress, cerebral vasospasm remains a leading cause of morbidity and mortality in SAH patients, necessitating ongoing research and innovation in neurocritical care.
11,12
Literature Review Definition Cerebral vasospasm is characterized by abnormal and sustained constriction of cerebral arteries, commonly occurring after SAH.
13 This narrowing of blood vessels significantly threatens cerebral perfusion, increasing the risk of ischemia, which can lead to stroke, neurological deficits, or death if not promptly managed.
Symptomatic vasospasm presents as new neurological deficits or a decline in consciousness, both resulting from ischemic injury.
14 Accurate diagnosis requires ruling out other potential causes of deterioration, such as hydrocephalus, seizures, metabolic disturbances, infection, or excessive sedation.
Angiographic vasospasm is defined by moderate to severe arterial narrowing seen on DSA, distinct from changes caused by atherosclerosis, catheter-induced spasm, or congenital vascular 15 Typically associated with blood flow velocities exceeding 120 cm/s, it emerges between days 3 and 14 following hemorrhage and serves as a critical predictor of clinical outcomes and prognosis.
Risk factor The extent of clot burden within the subarachnoid space is the most important predictor for the development of cerebral vasospasm following SAH.
The Fisher scale and its modified version are commonly used to evaluate this risk by Table 1.
Stages of Cerebral Vasospasm Development2,16 Timeframe Stage of development Day 0 Initiation - Following SAH due to aneurysm rupture Days 3-5 Early Vasospasm - Spasms begin to develop, possibly with mild Days 6-8 Peak Vasospasm - Maximum intensity, highest risk of ischemic Days 9-14 Resolution - Spasms subside, clinical symptoms decrease After Day Post-Vasospasm Recovery - Blood vessels return to normal, recovery from brain damage progresses After 2 Rehabilitation - Patients may require Weeks rehabilitation for residual effects Jurnal Neuroanestesi Indonesia classifying CT findings.
the modified Fisher scale assigns scores from 0 to 4 based on subarachnoid blood thickness and the presence of IVH, offering a more precise assessment of vasospasm Additional risk factors include delayed clot resolution, which is challenging to assess clinically, along with variables such as loss of consciousness at aneurysm rupture, poor neurological status on admission, and comorbidities like smoking, diabetes mellitus, hyperglycemia, hypertension, younger age, and cocaine use.
Aneurysm location also plays a significant role, with distal anterior cerebral artery aneurysms posing a higher risk due to their proximity to major cerebral vessels vulnerable to post-hemorrhagic hemodynamic changes.
In a study of 370 SAH patients, left ventricular hypertrophy and hypertension were identified as strong predictors of severe vasospasm, underscoring the importance of proactive monitoring and management.
17 Understanding these risk factors is crucial for developing targeted strategies to prevent and treat cerebral vasospasm, ultimately reducing its incidence and improving clinical outcomes in SAH patients.
Pathophysiology Cerebral vasospasm can be classified by type and underlying cause.
Symptomatic vasospasm involves clinical signs such as headache, neurological deficits, or altered consciousness resulting from arterial narrowing, which, if untreated, can progress to delayed cerebral ischemia and infarction.
19 Angiographic vasospasm, in contrast, is detected through imaging modalities like angiography and may not present with symptoms but can still impair cerebral blood flow and lead to ischemic injury.
The etiology is multifactorial, with SAH as the primary trigger due to blood accumulation in the subarachnoid space and the release of vasoactive substances like oxyhemoglobin, which induce prolonged vasoconstriction.
20 Trauma, surgical manipulation, and infection may also lead to vasospasm via mechanical injury, inflammation, or endothelial disruption.
20 Inflammatory mediators, cytokines, and oxidative stress further impair vascular tone and function, while hydrocephalus may elevate intracranial pressure, increasing vasospasm risk.
Genetic predisposition and endothelial dysfunction also play contributory roles.
At the core of vasospasm pathophysiology is smooth muscle contraction, largely driven by increased intracellular calcium within vascular smooth muscle cells.
Following SAH, blood breakdown products such as oxyhemoglobin and deoxyhemoglobin heighten contractility, resulting in sustained vasoconstriction.
Concurrent endothelial injury impairs the release of vasodilators like NO and prostacyclin while promoting vasoconstrictors such as endothelin-1, worsening arterial narrowing.
Inflammation further exacerbates this process through cytokine-mediated smooth muscle activation and endothelial damage, increasing the likelihood of delayed cerebral ischemia.
19 Recurrent vasospasm may eventually lead to vascular remodeling, marked by structural alterations that impair vessel reactivity.
Additionally, early brain injury (EBI), occurring shortly after hemorrhage or trauma, initiates oxidative stress and disrupts cerebral autoregulation, amplifying the severity and persistence of vasospasm.
This complex interplay of vascular, cellular, and biochemical mechanisms underlies the development of cerebral vasospasm and informs strategies for its clinical management.
Clinical manifestation Cerebral vasospasm presents clinically with symptoms resulting from reduced cerebral perfusion, commonly beginning with a sudden, severe "thunderclap" headache that may resemble the initial SAH episode.
As the condition progresses, focal neurological deficits such as hemiparesis, aphasia, or sensory disturbances may appear, along with changes in consciousness ranging from confusion to coma.
Seizures, either focal or generalized, can occur due to ischemic injury, while cognitive and behavioral changesAi such as memory loss and irritabilityAimay also be observed.
In severe or prolonged cases, delayed cerebral ischemia may develop, leading to permanent deficits including motor, sensory, language, and cognitive impairments, with possible visual disturbances like blurred vision or Diagnosis and Management of Cerebral Vasospasm Following Aneurysmal SAH field loss.
Prompt recognition and management of these signs are critical to reducing morbidity and improving outcomes.
Diagnosis Cerebral vasospasm is a critical complication of aSAH that requires vigilant monitoring and timely intervention, guided by AHA/ASA recommendations for managing vasospasm and DCI.
Standard surveillance includes TCD, with CTA.
CT perfusion.
EEG, and biochemical markers used for further assessment in complex Management strategies center on enteral nimodipine and maintaining euvolemia, with more aggressive treatments like induced hypertension or endovascular therapy reserved for severe or refractory cases, while routine use of statins, magnesium, or prophylactic hemodynamic manipulation is not recommended.
The American College of Radiology (ACR) Appropriateness Criteria provide a framework for selecting optimal imaging strategies in patients with suspected cerebral vasospasm.
Standard imaging methods typically encompass cervicocerebral angiography and contrastenhanced CTA.
Supplementary imaging modalities that may be considered appropriate include transcranial Doppler ultrasound, contrast-enhanced head MRI perfusion, noncontrast head MRI, and non-contrast head CT.
These diagnostic tools play a critical role in facilitating precise identification and effective management of cerebral vasospasm, as well as mitigating potential complications arising from this condition.
Figure 1.
Modified Fisher CT Grading Scale Figure 2.
Differences Between the Classic and Modified Fisher Scales.
(Source: https://pbrainmd.
com/2015/02/) The modified Fisher scale predicts the risk of vasospasm in aSAH patients by scoring the extent of SAH and presence of IVH, with higher scores indicating greater risk.
CT perfusion imaging has shown superior accuracy in detecting delayed cerebral ischemia compared to noncontrast CT and CTA.
However, postoperative intra-aortic counterpulsation balloon therapy has not demonstrated significant benefits over hypervolemic therapy in improving outcomes.
Transcranial Doppler ultrasonography (TCD) is the primary non-invasive method for detecting cerebral vasospasm, relying on increased blood flow velocity as arteries narrow.
It is commonly used in SAH patients to identify early signs of vasospasm through velocity changes detected via Doppler frequency shifts.
TCD employs a 2 MHz ultrasound probe applied to cranial acoustic windows, such as transtemporal or submandibular regions, where the skull is thinner.
TCD is highly effective in detecting proximal cerebral vasospasm by identifying segmental and diffuse increases in blood flow velocity, particularly in vessels like the MCA, where velocities above 120 cm/s suggest vasospasm and those over 200 cm/s indicate severe vasospasm.
Differentiating vasospasm from hyperemia requires comparing intracranial velocities with those of the cervical ICA, using parameters like the Lindegaard ratio and SVIRI ratio.
While TCD is reliable for major arteries, it is less effective for distal branches, limiting its correlation with perfusion Jurnal Neuroanestesi Indonesia Table 1.
Breakdown of Diagnostic Modalities for Cerebral Vasospasm Cases Modality Serial Psychological Assessment Description Repeated evaluation of cognitive function and mental status TCD (Transcranial Doppler Ultrasoun.
A non-invasive ultrasound tech-nique that measures cerebral blood flow velocity.
CTA (CT Angiograph.
Imaging technique that provides detailed images of brain blood vessels CTP (CT Perfusion Imaging that evaluates Imagin.
cerebral blood flow, volume, and transit time MRI (Magnetic A non-invasive imaging Resonance Imagin.
technique using a magnetic field to produce brain images PWI (Perfusion-Weighted Assesses brain perfusion Imagin.
using MRI to evaluate blood flow and volume DSA (Digital Subtraction An invasive technique Angiograph.
providing detailed images of blood vessels using contrast dye Brain Tissue Oxygenation Monitors brain tissue Monitoring oxygenation using sensors placed in brain Cerebral Microdialysis Measures metabolites in Catheter brain interstitial fluid to detect ischemia Near-Infrared A non-invasive method Spectroscopy (NIRS) using near-infrared light to monitor cerebral deficits seen in CBF studies.
DSA, especially 2D-DSA, remains the gold standard for definitive diagnosis and therapeutic intervention.
it carries a complication rate of 1.
3Ae2.
4%, with 5% of patients experiencing potentially permanent deficits.
Due to its invasiveness and associated risks.
DSA is best reserved for selected cases requiring diagnostic confirmation or resistant to medical therapy.
Advantages Non-invasive, identifies early neurocognitive Real-time monitoring, portable, cost-effective Limitations Subjective, dependent on patient cooperation, does not directly detect Operator-dependent, indirect measurement, limited to large vessels High spatial resolution, can detect vasospasm and Can detect areas at risk of infarction, complements CTA No radiation exposure, high tissue resolution Involves radiation and contrast dye, less suitable for continuous monitoring Involves radiation, contrast dye, limited Time-consuming, expensive, does not directly detect vasospasm Non-invasive, no radiation, good tissue Gold standard for vasospasm detection, high accuracy Expensive, longer scan time, limited availability Direct tissue oxygenation monitoring, identifies Invasive, risk of infection, limited availability Invasive, risk of complications, expensive, time-consuming Sensitive to metabolic Invasive, risk of infection, changes, local monitoring limited localized data Continuous monitoring, portable, non-invasive Limited penetration depth, indirect measurement, sensitive to artifacts A.
Preoperative maximum intensity projection (MIP) image from a CTA study demonstrates an anterior communicating artery aneurysm .
Postoperative CTA shows successful clipping of the aneurysm and narrowing of the anterior cerebral artery .
, consistent with C.
Digital subtraction angiography (DSA), in an anteroposterior view, confirms vasospasm involving the A1 segment of the anterior cerebral Diagnosis and Management of Cerebral Vasospasm Following Aneurysmal SAH Advanced neuroimaging techniques, such as perfusion-weighted MRI .
w-MRI), have demonstrated utility in identifying discrete areas of early ischemic damage indicative of Diffusion-weighted MRI further contributes by revealing reductions in relative cerebral blood volume (CBV) and mean transit time, thereby assisting in the identification of candidates for triple-H therapy.
Historically.
MRA was primarily employed for diagnosing intracranial aneurysms and atherosclerosisrelated vascular stenosis.
However, its application in vasospasm diagnosis became more widespread after 1995.
Modern MRA protocols utilize flow-independent strategies and offer the dual advantage of assessing radiographic vessel narrowing and providing physiological insights into vasospasm-related changes.
The therapeutic strategy for managing vasospasm extends beyond pharmacological interventions to include non-pharmacological methods that target the root causes of the condition.
Central to this approach is hemodynamic optimization, which focuses on maintaining euvolemia and employing hypervolemic therapy to ensure sufficient blood volume and cerebral perfusion Additionally, blood pressure modulation through the controlled elevation of systolic levels may be utilized to enhance cerebral blood flow.
In critical scenarios, endovascular cerebral angioplasty serves as an effective intervention to dilate constricted arterial segments and reestablish normal circulation.
The drainage of CSF via EVD plays a pivotal role in alleviating hydrocephalus, lowering intracranial pressure, and potentially reducing vasospasm severity.
Continuous monitoring of neurological function is indispensable for informing clinical decisionmaking and addressing potential complications.
For refractory cases, decompressive craniectomy may be considered to mitigate intracranial hypertension and improve cerebral perfusion.
A multidisciplinary framework that integrates both pharmacological and non-pharmacological modalities is vital for achieving optimal patient outcomes and effectively managing this intricate Management The 2023 AHA/ASA guidelines for managing patients with SAH advocate the use of nimodipine, a calcium channel blocker (CCB) that has demonstrated efficacy in reducing DCI.
Additionally, the guidelines emphasize the importance of maintaining optimal cerebral perfusion pressure and euvolemic conditions to ensure sufficient cerebral blood flow and mitigate complications associated with reduced perfusion.
In patients with aSAH, management begins with oral nimodipine (Class 1*) and regular neurological examinations (Class 1A).
If the neurological exam is reliable, transcranial Doppler (TCD) monitoring is recommended (Class 2aA).
if unreliable.
TCD monitoring with continuous EEG .
EEG) should be considered (Class 2aA).
Invasive multimodality neuromonitoring may be an option (Class 2bA), but prophylactic hemodynamic augmentation should be avoided (Class 3: Harm*).
If neurological status worsens or monitoring indicates decline when exams are unreliable, clinicians should address confounders by elevating blood pressure, ensuring euvolemia, and obtaining further imaging as needed (Class 2a*).
If the patient improves, monitoring continues (Class 1A).
if not, endovascular rescue therapy with intra-arterial spasmolytic agents with or without angioplasty may be pursued (Class 2b*).
Improvement after intervention leads back to continued monitoring, while persistent deficits prompt further imaging to determine DCI or another cause for the neurological decline.
Nimodipine is the cornerstone pharmacological treatment for vasospasm following SAH, administered orally at 60 mg every four hours for 21 days to reduce both the incidence and severity of vasospasm.
In acute settings, intraarterial vasodilators such as nicardipine and papaverine are delivered via catheterization for localized arterial relief, while clazosentan, an endothelin-1 receptor antagonist, serves as an alternative by inhibiting vasoconstriction.
Although not universally adopted, agents like statins and magnesium sulfate have been explored for their endothelial-stabilizing and neuroprotective effects.
Non-pharmacological Jurnal Neuroanestesi Indonesia Figure 3.
Management of Cerebral Vasospasm and DCI in Patients with aSAH as Outlined by the AHA/ASA Table 2.
Description of Management Approaches for Patients with Cerebral Vasospasm Aspect Approach Description and Key Strategies Pharmacological Nimodipine.
Nicardipine.
Nimodipine as the primary treatment.
Approach Papaverine.
Clazosentan.
Statins.
Nicardipine and Papaverine for acute Magnesium Sulfate management.
Clazosentan as an endothelin antagonist, with Statins and Magnesium Sulfate providing additional benefits Non-Pharmacological Hemodynamic Management.
Maintaining euvolemia, hypervolemic therapy.
Approach Cerebral Angioplasty.
CSF controlled blood pressure, cerebral angioplasty.
Drainage.
Decompressive CSF drainage, and decompressive craniectomy Craniectomy to regulate pressure and blood flow Triple-H Therapy Hypervolemia.
Hypertension.
Increasing blood volume and pressure while Hemodilution reducing blood viscosity to improve circulation and prevent ischemia Advanced Techniques Intra-Aortic Balloon IABP for hemodynamic support, endovascular Counterpulsation (IABP), angioplasty, and intra-arterial vasodilator Endovascular Vasospasm administration to manage severe vasospasm Reversal.
Intravenous Milrinone Timing Strategy Golden Period .
Ae5 Day.
Early Early treatment within the first 3Ae5 days is Late Treatment crucial to reduce the severity of delayed cerebral ischemia (DCI).
late treatment is less effective and carries a higher risk of complications Multidisciplinary Combined Pharmacological and Integrating pharmacological and nonApproach Non-Pharmacological Strategies, pharmacological approaches with routine Personalized Care Plans monitoring and personalized treatment plans for optimal outcomes Diagnosis and Management of Cerebral Vasospasm Following Aneurysmal SAH approaches focus on hemodynamic optimization through euvolemia and induced hypertension to preserve cerebral perfusion, and in severe cases, endovascular interventions such as angioplasty may be employed to mechanically restore blood Induced hypertension remains the mainstay hemodynamic strategy for refractory cases to augment cerebral perfusion, whereas routine hypervolemia and hemodilution, previously included in the so-called AoTriple-H therapy,Ao are no longer recommended due to unfavorable riskAe benefit profiles.
IABP is also used in refractory cases to augment systemic and cerebral circulation by enhancing diastolic pressure.
Endovascular approaches, including angioplasty and intra-arterial vasodilator infusion, are indicated in severe or refractory vasospasm, with balloon dilation restoring vessel caliber and direct drug delivery improving localized perfusion.
milrinone, a phosphodiesterase i inhibitor, is another option under investigation for its dual role in increasing cardiac output and reducing cerebral vasoconstriction.
Optimal treatment depends on timely intervention, ideally within the 3Ae5-day post-SAH "golden period" when the risk of DCI peaks and response to therapy is greatest.
Delayed interventions beyond this window are often less effective, as irreversible cerebral injury may have already occurred, correlating with worse outcomes and higher morbidity and mortality.
To improve prognosis, continuous clinical monitoring and early imaging diagnostics are essential for prompt detection and implementation of individualized treatment Conclusion Cerebral vasospasm is a severe and potentially life-threatening observed following SAH, characterized by sustained constriction of cerebral blood vessels that compromises cerebral blood flow and may progress to DCI, which, if untreated, can cause profound neurological deficits or mortality.
Key risk factors include the extent of blood accumulation in the subarachnoid space, the presence of hydrocephalus, demographic variables such as age and sex, and comorbidities like hypertension and smoking, with clinical manifestations ranging from severe headaches and focal neurological deficits to altered mental status, seizures, or cognitive dysfunction in advanced cases.
Management integrates non-pharmacological approaches, with nimodipine serving as the cornerstone pharmacotherapy to prevent vasospasm and reduce morbidity, while acute interventions may involve intra-arterial vasodilators such as nicardipine or papaverine, and endothelin receptor antagonists like clazosentan to counteract vasoconstriction.
Nonpharmacological strategies focus on optimizing hemodynamics through euvolemic management, controlled blood pressure modulation, and advanced interventions including endovascular angioplasty or cerebrospinal fluid drainage to relieve intracranial pressure.
Preventive efforts rely on strict hemodynamic control, timely prophylactic pharmacotherapy, and advanced monitoring with modalities such as TCD and CTA to detect early vasospasm, as early intervention in the initial days post-SAH is crucial to improving clinical outcomes and minimizing long-term neurological sequelae, thereby enhancing recovery and mitigating the burden of this complex condition.
References