17 Natural History and Management Options of Aneurysmal Subarachnoid Hemorrhage

Michael A. Silva and Nirav J. Patel

Abstract

Aneurysm subarachnoid hemorrhage (aSAH) continues to impose devastating consequences on patients despite increased efforts in recent years to identify and manage aneurysms prior to rupture. The natural history of aSAH is poor with high mortality and rebleed rate. Optimal patient care should be site specific based on the proficiencies of each unique institution.

Aneurysmal subarachnoid hemorrhage (aSAH) is an uncommon but potentially catastrophic neurologic disease. The prevalence of aSAH has been estimated at 2 to 3% of the population, and SAH represents 5% of all stroke.1^{,​ 2,​ 3} The overall incidence is 9 per 100,000, although there is a high regional variability. The average age of patients presenting with SAH is the mid-50 s, with half of the patients younger than 55 years.^{2,​ 4,​ 5} The risk of developing aSAH increases with age,^{1,​ 4} although it has been suggested that there is no significant increase in risk until the age of 80 years.³ Smoking and hypertension are well-established modifiable risk factors for aneurysm formation and rupture. Other risk factors include female sex, family history of aneurysm, diabetes mellitus, excess alcohol consumption, atherosclerosis, and autosomal dominant polycystic kidney disease (ADPCKD).^{1,​ 3,​ 6,​ 7,​ 8,​ 9}

Most SAHs (85%) are due to aneurysmal rupture and are associated with a high mortality rate of up to 50%.² However, not all SAHs are due to aneurysmal rupture, and other causes of SAH such as trauma, nonaneurysmal perimesencephalic SAH, vasculopathy, or other malformations are possible.

Aneurysmal rupture often presents with a sudden-onset headache, classically described by the patient as the “worst headache of their life.” It is imperative to precisely characterize the quality of the headache, which is exquisitely painful and immediate in onset, reaching its maximum intensity of less than 1 minute. One must differentiate this “thunderclap” headache from other forms of severe headache, which may gradually worsen over the course of a day or represent a particularly excruciating iteration of a patient’s chronic headaches. Patients presenting with a sudden-onset severe headache, different in quality compared to prior headaches, should be taken seriously and vascular imaging should be considered. Other symptoms of aSAH include nausea, vomiting, depressed consciousness, focal neurologic deficit, and sometimes a preceding milder “sentinel” headache.¹⁰

A thorough history should be collected, preferably from the patient if their neurologic examination allows. Many patients with a poor Glasgow Coma Scale (GCS) score on presentation will not be able to provide a history, and imaging should be performed immediately. If possible, the patient or their family should be asked about past medical history, with special attention paid to prior known aneurysms, a history of coagulopathy or liver disease, ADPCKD, prior neurosurgical interventions, and adverse reactions to contrast. The patient’s medication list should be reviewed, especially for anticoagulants or antiplatelet agents. Smoking history and family history of intracranial aneurysms should also be probed. A full neurologic examination should be performed. The Hunt-Hess score is a clinical classification that was specifically designed to stratify patients with aneurysmal rupture by mortality based on an initial series of 275 patients.¹¹ Along with the GCS and World Federation of Neurological Societies (WFNS) Score,¹² the Hunt–Hess score is used universally to standardize examinations across patients regardless of institution or examiner (Table 11.1). Patients with a high Hunt–Hess score, especially if grade III or higher, should be considered strong candidates for prompt external ventricular drain (EVD) placement. All reversible factors contributing to a poor neurologic examination must be excluded before assigning a Hunt–Hess score. Correction of hydrocephalus, hypercarbia/hypoxemia, or metabolic factors that may be affecting the patient’s examination is crucial for accurate clinical classification. This is especially true for patient’s presenting with a Hunt–Hess grade V examination in whom a misleading examination due to non-SAH factors risks discouraging intervention in a patient who might benefit from treatment. Correction of reversible causes, such as hydrocephalus and hematoma, can improve the neurologic examination, improve prognosis, and increase the likelihood of successful intervention.

Table 17.1 Clinical grading scales for aneurysmal SAH

Symptoms and history suspicious for aneurysmal rupture should prompt immediate imaging. It is imperative that new-onset, sudden, severe headaches be fully evaluated, and not sent home. Initial imaging should include a noncontrast head computed tomography (CT), which has high sensitivity for detecting hemorrhage and can accurately evaluate the extent, location, and age of subarachnoid blood, if present. The Fisher grade is a radiographic classification of the amount of subarachnoid blood seen on CT and is predominantly used as a predictor of vasospasm.13 A modified Fisher scale is sometimes used, which dispenses of intraventricular hemorrhage as its own category and uses thin versus thick subarachnoid blood as the major differentiator between grades I to II and III to IV^{14,​ 15} (Table 17.2).

Table 17.2 Radiological grading of aneurysmal SAH

If the CT is positive for subarachnoid blood, CT angiography (CTA) is unequivocally indicated to assess for an underlying vascular source (Fig. 17.1). CTA is highly sensitive for detecting aneurysms; however, the gold standard is conventional angiography. Digital subtraction angiography (DSA) is exquisitely sensitive for aneurysm detection and can characterize the lesion sufficiently to guide treatment. A DSA is also useful in SAH in the setting of a negative CTA (Fig. 17.2 and Fig. 17.3). The angiogram is both diagnostic and potentially therapeutic if the aneurysm is determined to be amenable to endovascular treatment. An alternative to CTA or conventional angiography in patients with contraindications to these imaging modalities is magnetic resonance angiography (MRA), which is typically performed without contrast and characterizes vascular lesions based on the effect of blood flow on magnetic resonance. However, in the acute setting, the acuity of aneurysmal rupture trumps most relative contraindications to CTA or angiography in the majority of patients.

On initial suspicion of aneurysmal rupture, certain laboratory studies and tests should be sent immediately. Coagulation studies, platelet count, platelet function assay, complete blood count (CBC), liver function tests (LFTs) to assess for liver function, and a basic metabolic panel should be part of initial laboratory studies. An electrocardiogram (EKG) is helpful to set a baseline, particularly since some patients present in mild cardiac failure, termed Takotsubo cardiomyopathy. Vital signs should be actively monitored, with particular attention paid to blood pressure. A combination of hypertension and bradycardia (Cushing’s reflex) may be observed in the setting of increased intracranial pressure (ICP) and could be a sign of the need for prompt cerebrospinal fluid (CSF) diversion. Most importantly, the systolic blood pressure (SBP) should be controlled. We advocate aggressive measures to keep SBP less than 140 mm Hg to help prevent rebleeding, which carries a 80% mortality.¹⁶

17.2 Selected Papers on the Natural History of Aneurysmal Subarachnoid Hemorrhage

●Nieuwkamp DJ, Setz LE, Algra A, Linn FHH, de Rooji NK, Rinkel GJ. Changes in case fatality of aneurysmal subarachnoid haemorrhage over time, according to age, sex and region: a meta-analysis. Lancet Neurol 2009;8(7):635–64217

●Korja M, Kivisaari R, Rezai Jahromi B, Lehto H. Natural history of ruptured but untreated intracranial aneurysms. Stroke 2017;48(4):1081–1084

17.3 Natural History of Aneurysmal Subarachnoid Hemorrhage

Mortality after aneurysmal rupture is 50%.² Untreated aSAH carries a 20-day median survival and a 65% 1-year mortality.¹⁷ For patients who survive the initial rupture event, the risk of rerupture is highest in the immediate posthemorrhage period at 8 to 23% within the first 72 hours,¹⁸ with some studies reporting a rate of over 40% within the first 24 hours.¹⁹ After a rebleeding event, 80% of patients die or are permanently disabled.¹⁶ The risk of rerupture decreases progressively with each day after the initial hemorrhage down to less than 1% risk on day 21.¹⁹ After 6 months, there is a 3.5% annual risk of rebleed, and mortality from a late repeat hemorrhage is 67%.²⁰

Higher Hunt–Hess score on presentation, elevated SBP, large aneurysm size, presence of multiple aneurysms, and angiography within 6 hours are associated with increased risk of rerupture.18^{,​ 21} There is a hypothetical and controversial increased risk of rerupture after EVD placement and CSF drainage due to decreased external tamponade of the aneurysm sac resulting in increased transmural pressure²²; however, no studies have definitively demonstrated this association.^{18,​ 21,​ 23,​ 24,​ 25}

17.3.1 Vasospasm

After the immediate posthemorrhage period, patients must be monitored closely for vasospasm. Even after promptly and successfully treating a patient’s aneurysm and observing an improvement in their neurologic examination, subsequent vasospasm can erase the patient’s progress and leave them with lifelong debilitation. Vasospasm is one of the most feared, yet most common complications of aSAH. As many as 40% of patients experience delayed cerebral ischemia due to vasospasm after SAH, and it is associated with significant morbidity and mortality.^{2,​ 26,​ 27,​ 28} Predictors of vasospasm include amount (but not location) of subarachnoid blood, hypotension, hypovolemia, and loss of consciousness at the time of hemorrhage.^{28,​ 29,​ 30,​ 31} It is unclear whether clipping or coiling has any effect on the rate of vasospasm or infarction.^{32,​ 33,​ 34} Magnesium is used by some groups to prevent vasospasm, but studies have shown no clear evidence of improved outcomes.³⁵ Nimodipine is the only vasospasm prophylaxis supported by the literature, having been shown to improve neurologic outcomes due to vasospasm when given to patients before onset of symptoms.^{36,​ 37}

The peak incidence of vasospasm occurs 4 to 14 days after aneurysm rupture.² Patients should be monitored for vasospasm in the hospital through this high-risk period before being discharged. The most crucial aspect of vasospasm management is precise and dependable serial neurological examination. Serial transcranial Doppler measurements (TCDs) provide a noninvasive means of screening for and monitoring vasospasm.³⁸ Although questions have been raised regarding the lack of sensitivity of TCDs,³⁹ they remain the workhorse of vasospasm monitoring. CTA or conventional angiography, as part of posttreatment follow-up imaging, may detect arterial irregularity or stenosis suggestive of vasospasm. Importantly, clinical vasospasm differs from radiographic vasospasm, and treatment of vasospasm should be reserved for patients with clinically significant vasospasm. Detailed neurologic examination of the posthemorrhage patient will identify patients with clinical vasospasm requiring treatment. If TCDs are persistently elevated, a more thorough evaluation of the extent of vasospasm can be attained with targeted CTA or conventional angiography. Hyponatremia is often a harbinger of vasospasm, as well as increased blood pressure. Finally, it is most imperative that any change in examination be taken seriously, presuming first vasospasm, and working to resolve the deficit.

The primary goal of vasospasm treatment is to prevent infarction as a result of prolonged ischemia. Intra-arterial calcium antagonists, nimodipine being the most well studied, have been shown to reduce the risk of secondary ischemia and poor clinical outcome.⁴⁰ Permissive or induced hypertension is used at some institutions to maximize cerebral perfusion in the setting of vasospasm; however, no studies have successfully demonstrated a clinical benefit for this practice.^{41,​ 42} Normovolemia should be maintained; in fact, positive fluid balance is associated with poorer outcomes.^{43,​ 44} The use of statins in patients with vasospasm is controversial.^{45,​ 46}

17.3.2 Chronic Hydrocephalus

Patients who fail EVD clamping trials and cannot be weaned off of the EVD should undergo shunt placement. Rates of chronic hydrocephalus and shunting vary wildly across institutions, ranging from 4 to 64% in the literature.^{47,​ 48} In one series of 2,842 patients, 16.3% of patients who underwent EVD placement on presentation ultimately required a shunt.⁴⁷ Predictors of shunt-dependent hydrocephalus after SAH include intraventricular hemorrhage, higher Hunt–Hess score and Fisher grade, prolonged CSF drainage, bicaudate index  > 0.2, and hyperglycemia on admission.^{47,​ 49,​ 50,​ 51} Endoscopic third ventriculostomy (ETV) and fenestration of the lamina terminalis (FLT) during aneurysm treatment are debated as tools for reducing shunt-dependent hydrocephalus. Some studies have demonstrated a benefit, whereas others have shown no reduction in shunt dependency.^{52,​ 53}

17.3.3 Seizure

As many as 10 to 20% of patients with SAH suffer posthemorrhage seizures.⁵⁴ In a series of 7,002 patients with aSAH, 2.3% of patients experienced a seizure in the early posthemorrhage period, and an additional 5.5% of patients had late seizures.⁵⁵ Increased age, history of prior seizure, anterior circulation SAH locations, and hydrocephalus are associated with increased risk of seizure after SAH.⁵⁶ At many institutions, prophylactic antiepileptics are given; however, as previously discussed, there is insufficient evidence to support universal use of AEDs in patients with SAH. If a seizure is detected, prompt treatment and subsequent secondary prevention with AEDs should be initiated. Long-term electroencephalographic (EEG) monitoring should be considered in patients with an otherwise unexplained change in level of consciousness and neurologic examination.

17.4 Selected Papers on the Management Options for Aneurysmal Subarachnoid Hemorrhage

●Molyneux A, Kerr R, Stratton I, et al; International Subarachnoid Aneurysm Trial (ISAT) Collaborative Group. International Subarachnoid Aneurysm Trial (ISAT) of neurosurgical clipping versus endovascular coiling in 2143 patients with ruptured intracranial aneurysms: a randomised trial. Lancet 2002;360(9342):1267–1274

●McDougall CG, Spetzler RF, Zabramski JM, et al. The Barrow Ruptured Aneurysm Trial. J Neurosurg 2012;116(1):135–144

17.5 Management Options for Aneurysmal Subarachnoid Hemorrhage

Initial evaluation of the patient, assessment of Hunt–Hess or WFNS and Fisher grade, and review of key laboratory values allow for prioritization of immediate management steps. Regardless of clinical or radiographic grade, all patients should have their blood pressure closely monitored with an arterial line and systolic pressure maintained below 140 mm Hg before treatment. Central venous access should be considered in patients with a poor examination on presentation who are likely to require hypertonic agents. If a patient is on anticoagulation, reversal (if possible and safe, depending on the initial indication for anticoagulation) can be considered. Antifibrinolytic therapy might mitigate the risk of rerupture before definitive aneurysm treatment18; however, there is insufficient evidence in the literature to support universal use of antifibrinolytics.⁵⁷ Similarly, if the patient is on antiplatelet therapy or if laboratory studies showed low platelet count or function, platelet transfusion or desmopressin (DDAVP) can be considered. This decision should be weighed against the risk of reversing antiplatelet therapy in patients requiring it for preexisting stents or other reasons.

17.5.1 Intracranial Pressure Management

Control of ICP is critical to the management of SAH. Approximately 20% of patients with SAH develop acute hydrocephalus within 72 hours of hemorrhage.^{22,​ 58} Proposed mechanisms of hydrocephalus in the SAH patient include stimulation of choroid plexus CSF production and obstruction of CSF resorption due to interference of arachnoid granulations, but numerous other mechanisms have been proposed.⁵⁹ The typical presentation of acute hydrocephalus is depressed consciousness after an initially alert state.⁶⁰ Although 50% of patients recover spontaneously within 24 hours,⁵⁸ acute hydrocephalus after SAH is associated with a higher rate of mortality and cerebral infarction.⁶⁰

Initial measures to control ICP should include elevating the head of the bed, relieving venous outflow compression (e.g., cervical collars), and maintaining normotension and normocapnia. Although different institutions and surgeons have diverse algorithms for timing or EVD placement, certain principles are nearly universal. Radiographic evidence of acute hydrocephalus, high Hunt–Hess score on presentation (III or higher) or WFNS score of III or higher, and decline in neurologic examination (especially development of somnolence, worsening headache, nausea, vomiting, or up-gaze palsy) should prompt repeat CT and strong consideration of EVD placement. Placement of an EVD serves several benefits beyond ICP monitoring and CSF drainage to relieve elevated ICP. The EVD can drain blood from the ventricle in Fisher grade IV patients with intraventricular extension of their SAH. The decreased ICP also relieves external pressure on the vasculature, which may be contributing to ischemia from vasospasm. The EVD should be set to drain at 20 cm H₂O to prevent malignant ICP but without excessively dropping transmural pressure and running the theoretical risk of promoting rerupture.^{22,​ 58}

Sedation (and subsequent intubation) may be required for refractory ICPs. Sedation should be used judiciously to avoid respiratory depression that would depress breathing and increase pCO₂, thus increasing ICPs. Sedation may also confound neurological examinations. Intubation and direct control of pCO₂ can combat this dilemma. If the patient becomes somnolent or is unable to maintain their airway for other reasons, intubation should be pursued. Administration of mannitol or hypertonic saline should be initiated if ICPs remain elevated. Close monitoring of laboratory values is essential. SAH is associated with hyper- and hyponatremia, which are each independently associated with poor outcomes.⁶¹

17.5.2 Seizure Prophylaxis

Seizure prophylaxis in the acute setting is controversial. A majority of institutions use antiepileptic drugs (AEDs) for seizure prophylaxis, but many do not.⁶² In a retrospective propensity score-matched study of 353 patients, prophylactic AEDs did not significantly decrease the risk of seizure in SAH patients.⁶³ In a separate study of 7,002 patients, perioperative AEDs did not decrease seizure risk.⁵⁵ Similarly, a Cochrane review showed insufficient evidence and a lack of randomized trials to support or refute the use of AEDs as primary or secondary seizure prophylaxis in SAH patients.⁶⁴ When used, there is evidence to suggest that a brief course (3 days) of AEDs may be superior to extended seizure prophylaxis in these patients.⁵⁴

17.5.3 Timing of Treatment

Optimal timing of treatment is not known, and no randomized controlled trials exist to study whether early or delayed treatment is best. Hunt and Hess postulated that delaying treatment in the higher-grade SAH would be beneficial, which inspired their namesake Hunt and Hess scale.¹¹ Although some studies have shown no difference in outcomes between early and delayed treatment,^{65,​ 66} it is generally thought that prompt treatment is beneficial.^{67,​ 68} A large observational study by Nieuwkamp et al found no significant difference between early and late observation.⁶⁶ However, Laidlaw and Siu studied outcomes after surgery within 24 hours of rupture and argue that ultra-early surgery may reduce the risk of rebleeding since the rate of rebleeding is highest in the early postrupture period.⁶⁷ This risk must be weighed against the increased surgical risk of operating in the immediate postbleed period.¹¹ Studies that compare outcomes between early and delayed treatment will be unavoidably confounded by the clinical improvement that patients treated early would have regardless of intervention, an effect not captured in the delayed treatment group. Ultimately, a randomized controlled trial is needed to credibly compare early versus delayed treatment, yet such a study is ethically challenging and unlikely to occur in the era of endovascular treatment, which avoids the risks of surgical intervention in the early postbleed period.

17.5.4 Overview of Treatment Modalities

The workhorses of aneurysm treatment are clipping, revascularization, endovascular coiling, and endovascular flow diversion (Table 17.3). Microsurgical clipping, the oldest of these modalities, is a safe and reliable treatment option in many patients.^{19,​ 69,​ 70,​ 71,​ 72,​ 73} However, clipping carries the inherent risks of open surgery, requires manipulation of intact brain tissue when exposing the aneurysm, and can be challenging for aneurysms that are difficult to access surgically, but does lend itself to immediate and robust treatment (Fig. 17.4). Endovascular coiling, the oldest and most widely used endovascular treatment modality, is a reliable and safe technique for treating most aneurysms.^{74,​ 75,​ 76,​ 77,​ 78} In general, a key benefit of endovascular treatment is that it is a safe alternative for patients who are otherwise not healthy enough for open surgery or general anesthesia (Fig. 17.5). Some aneurysms are not amenable to coiling due to a wide neck (which can lead to coil reflux and incomplete occlusion) or distal location (which limits catheter control). The use of endovascular treatment has expanded dramatically over the past few decades and even more so in the past several years as a result of new devices, improved outcomes data, and increased interventionist comfort with endovascular techniques. Flow diversion, such as with the Pipeline Embolization Device (PED), is a recent advancement in endovascular aneurysm treatment. Deployment of the PED stent within the parent vessel across the aneurysm neck diverts blood flow away from the aneurysm sac without directly manipulating the aneurysm sac like with clipping or coiling. Branching vessels off of the parent vessel covered by the stent remain perfused due to the pressure gradient driving flow through the stent wall into the branching vessel. Flow diversion has proven particularly useful in the treatment of wide-necked aneurysms that are not amenable to coiling. However, PED placement requires initiation of antiplatelet therapy, which is controversial in patients with aSAH.

17.5.5 Comparing Treatment Modalities

A summary of key studies on aneurysm treatment modalities is provided in Table 17.3. The International Subarachnoid Aneurysm Trial (ISAT), published in 2002, randomized 2,143 patients to clipping or coiling. This audit showed a survival benefit at 1 and 7 years posttreatment, with a higher rate of disability-free survival at 10 years for coiling, but a higher rate of rebleeding in the coiling cohort.^{79,​ 80,​ 81} Another prospective randomized controlled trial comparing clipping to coiling in 109 patients with SAH showed comparable clinical outcomes at 1 year.⁸² Similarly, the Barrow Ruptured Aneurysm Trial (BRAT) randomized 471 patients to clipping or coiling and found similar outcomes for anterior circulation aneurysms, but improved outcomes for coiling over clipping for aneurysms of the posterior circulation.^{83,​ 84} Coiling demonstrated a lower rate of occlusion and higher rate of retreatment, but there were zero cases of rerupture at 6 years of follow-up.⁸⁴ Another randomized controlled trial demonstrated no difference in clinical outcome between coiling and clipping despite a lower rate of complete occlusion, a lower rate of symptomatic vasospasm, and a lower rate of cerebral infarction in the coiling cohort⁸⁵ (Table 17.3).

Flow diversion, one of the newest endovascular treatment options, has been used sparingly in the treatment of ruptured aneurysms due to concerns for the need for antiplatelet therapy after treatment in patients with a recent bleed. Some studies have shown a high rate of periprocedural complications for ruptured aneurysms treated with PED.⁸⁶ However, flow diversion has demonstrated opportunity when compared to clipping and coiling for both ruptured and unruptured aneurysms.^{87,​ 88,​ 89}

Ultimately, the choice of treatment cannot always be dictated by an external study. Each patient decision depends on patient-specific context, institutional expertise, provider proficiency, and many other factors. At our institution, we favor prompt treat for aSAH. The safest manner of achieving long-term treatment is best, but this is dependent on the patient, the case, and the team. We work to achieve excellence in endovascular, open surgical and hybrid techniques such that each is ready when the need arises. Treatment choice should be largely guided by retrospective and prospective review of outcomes by each provider at each institution, through keeping a database.

Surgical and endovascular aneurysm treatment each carry their own risks. Intraoperative rerupture is seen with both treatment modalities90^{,​ 91}; it is associated with more favorable outcomes compared to spontaneous rupture.⁹⁰ Periprocedural complications are higher for ruptured aneurysms than unruptured aneurysms.⁹² Coiling is associated with a 5.9% rate of procedural complications resulting in disability or death. Patients undergoing clipping have a higher rate of in-hospital complications, which may be related to increased length of stay⁹³ (Table 17.3).

Table 17.3 Summary of the treatment modalities and outcome of SBC reported in NCDB and the SEER database

17.5.7 Rerupture after Treatment

Assuming complete aneurysm obliteration, the rate of rerupture is low after either clipping or endovascular treatment.94^{,​ 95} Angiographically stable aneurysms have a 0.4% risk of rerupture, compared to 7.9% for recurrent aneurysms.⁹⁶ Late rebleeding (> 1 month) after successfully coiled aneurysms is rare at around 1%; thus, angiographic follow-up of angiographically stable aneurysms beyond 6 months may be of limited use (Fig. 17.6).^{97,​ 98}

17.6 Authors’ Recommendations

Many basic principles of managing aSAH are evidence based, relatively uncontroversial, and nearly universal. However, differences in regional expertise and resources lead to distinct practice patterns across institutions. Optimal patient care should be site specific based on the proficiencies of each unique institution. Treatment algorithms should be specific to each institution and each provider such that the unique capabilities of each institution are maximally employed.

A possible paradigm of aneurysm care would be for neurovascular neurosurgeons to be well trained in both open and endovascular techniques such that they can personally offer all treatment options to patients and their families and counsel them in all options.^{99,​ 100,​ 101} A single surgeon providing both endovascular and open vascular options does not remove bias, but can better navigate indications for applying the different technology. A potentially equivalent alternative is to have a team well versed in all options, who can work well together in an outcome-driven manner. Increased specialization within vascular neurosurgery runs the risk of limiting the scope of unbiased counseling that patients and their families can receive from a single surgeon. The obligation to offer comprehensive perspective on the scope of treatment options is particularly burdensome in the care of a ruptured aneurysms when the responsibility of management often lies with one or a handful of neurosurgeons at one institution, and the patient usually lacks the opportunity to shop around for different opinions. With these circumstantial constraints in mind, each institution should develop and embrace their own unique treatment algorithm based on transparent, prospective outcomes. This benchmarking provides direction for future decisions.

This chapter provides an overview of the basic principles of aSAH management and ruptured aneurysm treatment. By no means is this intended to be a universal guideline; rather, it represents the treatment algorithm used at one specific institution. Each provider and institution should adopt a treatment algorithm that best utilizes their unique expertise and resources.

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Natural History and Management Options for Cushing’s Disease Natural History and Management Options of Angionegative Subarachnoid Hemorrhage Natural History and Management Options of Chronic Subdural Hematoma Natural History and Management Options of Ruptured Brain Arteriovenous Malformation Natural History and Management Options of Cranial Dural Arteriovenous Fistulas Natural History and Management Options of Unruptured Brain Arteriovenous Malformation

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