Subarachnoid Hemorrhage - StatPearls - NCBI Bookshelf

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Subarachnoid Hemorrhage
Endrit Ziu; Mahammed Z. Khan Suheb; Fassil B. Mesfin.
Author Information and Affiliations

Last Update: June 1, 2023.
Continuing Education Activity

Subarachnoid hemorrhages are life-threatening and result from the accumulation of blood
between the arachnoid and pia mater. The incidence of subarachnoid hemorrhage in the United
States is between 10 to 14 out of 100,000 individuals per year. Although presentations may vary,
the characteristic presenting symptom is the thunderclap headache, which patients may describe
as the “worst headache of my life.” This should prompt further imaging. The headache often is
associated with nausea, vomiting, and diplopia. Quite often signs of meningismus are present due
to the spread of blood into the fourth ventricle and further down the spinal cord, irritating nerves
and causing neck and back pain. Cranial nerve deficits can occur. Practitioners should perform a
detailed exam. The presence of focal deficit increases the grade of subarachnoid hemorrhage and
changes the perspective of post-event recovery. Patients with a high-grade subarachnoid
hemorrhage quite often present in a state of coma that calls for a quick evaluation and urgent
treatment, as the coma can be reversible. In addition to subarachnoid hemorrhage patients may
have a concurrent intraocular hemorrhage, known as Terson syndrome. When Terson syndrome
is present, an ophthalmology service should be consulted to help with the care of the patient.
Eighty percent of patients that develop Terson syndrome require regular follow-up visits but do
not require further intervention. This activity reviews the evaluation and management of
subarachnoid hemorrhages and highlights the essential role of the interprofessional team in
caring for those with this grave condition.
Objectives:
Explain when subarachnoid hemorrhage should be considered on differential diagnosis.
Review the exam findings expected in a patient with a subarachnoid hemorrhage.
Describe the management of a subarachnoid hemorrhage.
Explain the significance of cooperation between the interprofessional team members to

enhance the delivery of care for those with subarachnoid hemorrhage.
Access free multiple choice questions on this topic.
Introduction
Overall, about 20% of strokes are hemorrhagic, with SAH and Intracerebral hemorrhage (ICH)
each accounting for 10%.[1] Subarachnoid space is described as a space between the arachnoid
membrane and the pia mater. It consists of the cerebrospinal fluid and the blood vessels that
supply different areas of the brain. A subarachnoid hemorrhage (SAH) is defined as the
accumulation of blood in the space between the arachnoid membrane and the pia mater around
the brain referred to as the subarachnoid space. The etiology of SAH can be either nontraumatic
https://www.ncbi.nlm.nih.gov/books/NBK441958/#article-29607.s5 1/18
(about 85% are secondary to aneurysm rupture) or traumatic in nature.[2] In this review, we shall
discuss the various aspects of nontraumatic SAH. Most nontraumatic causes of SAH (~ 85%) are
caused by the rupture of an intracranial aneurysm. The remaining 15-20% of patients presenting
with SAH do not have a vascular lesion on the initial digital subtraction angiography.[3]
Regardless of the cause, a SAH is often a devastating clinical event with substantial mortality
and high morbidity among survivors. Prehospital care is critical and involves triaging the patient
with attention to the airway, breathing, and circulation to a hospital with
neurocritical/neurosurgical expertise. The classic presentation is often a sudden-onset, severe
headache typically described as the "worst headache of my life". Treatments are based on
randomized controlled studies and prospective cohort studies. A SAH has a prolonged course of
illness and is complicated by various factors not limited to seizures, vasospasm, hydrocephalus,
and delayed cerebral ischemia (DCI). [4][5]
Etiology
As elucidated earlier, about 85% of nontraumatic SAH cases are secondary to aneurysmal
rupture. The remaining 15-20% have a diverse cause, and the mechanism of bleeding is often not
identified. Determining the precise etiology of the bleeding is very important, as practitioners can
tailor treatment to the cause of the bleeding. The most common causes of nontraumatic SAH are
mentioned below:
1) Aneurysmal Subarachnoid hemorrhage (aSAH)
- An aneurysmal cause of SAH has similar risk factors associated with aneurysm formation.
Hypertension, cigarette smoking, and family history are the most consistently observed risk
factors. Other factors include Alcohol, sympathomimetic drugs, and estrogen deficiency.
- Older age (>60 years), posterior circulation location, atherosclerosis, hypertension, and large
Intra-arterial aneurysm (IA) size (>5 mm) are contributing factors for an IA to rupture. A family
history of IA or SAH, previous history of SAH, or the presence of autosomal dominant
polycystic kidney disease increases the risk of IA rupture.[6]
2) Nonaneurysmal Subarachnoid hemorrhage (NASAH)
i) Perimesencephalic nonaneurysmal subarachnoid hemorrhage: It is characterized by a specific

pattern of localized blood on CT, normal cerebral angiography, and a benign course of illness.[7]
This subtype makes up the majority, up to two-thirds, of patients with NASAH.[3] The CT
findings typically include blood isolated to the perimesencephalic cisterns anterior to the
brainstem.[8]
ii) Occult aneurysm: A small percentage of cases are not diagnosed in initial angiographic
studies but may be identified on repeat angiography and are classified under this group.[9] The
reasons are technical or reading errors, small aneurysm size, and obscuration of aneurysm
because of vasospasm, hematoma, or thrombosis within the aneurysm.[10]
iii) Vascular malformations: These can be intracranial or spinal in location. Most brain vascular
malformations that cause SAH are either arteriovenous malformations (AVM) or dural
arteriovenous fistulae.[11][12] They are usually visualized on cerebral angiography. Dural
arteriovenous fistulae are the most common type of spinal vascular malformation.[13] Vascular
malformation associated with bleeding is usually managed surgically and or with endovascular
interventions.
iv) Intracranial arterial dissection: Dissection of an intracranial artery can produce SAH. When
the dissection of the intracranial artery extends through the adventitia, SAH occurs.[14] In these
situations, the bleeding is massive and often devastating. This condition is diagnosed by
conventional angiography and treated surgically or with endovascular interventions.[14][15][14]
v) Other causes: Cocaine abuse is associated with aneurysmal and nonaneurysmal SAH.[11]
[16][11] Cerebral amyloid angiopathy can cause SAH in older adults.[17] Cerebral venous
thrombosis, sickle cell disorders, moyamoya disease, cerebral vasculitis, and bleeding disorders
are some of the conditions that cause SAH.[18][19][20]
Epidemiology
The overall global incidence of aneurysmal SAH was 7.9 per 100,000 person-years.[21] By time
trends, in 2010 the incidence of SAH was 6.1 per 100,000 person-years, declining from 1980
when the reported incidence was 10.2 per 100,000 person-years. Around the world, Japan and
Finland have higher cases of subarachnoid hemorrhage for reasons unknown.[21]
Most aSAH occur between 40 and 60 years of age, and young children and older adults can be
affected.[22] The mean age of aneurysmal rupture ranges from 50-55 years.[23] It is more
prevalent in the Blacks and Hispanic populations than the white Americans.[22] There is a
slightly higher incidence of aneurysmal SAH in females, which may be related to their hormonal
status.[23] Patients with a history of smoking and previously ruptured intracerebral aneurysm are
highly associated with new subarachnoid hemorrhage.
Pathophysiology
Hemodynamic stress is the initiating factor for intracranial aneurysm (IA) formation. The
observation best illustrates that IAs occur at arterial junctions, bifurcations, or abrupt vascular
angles where excessive hemodynamic stresses are exerted on arterial walls.[24] The typical
locations include the bifurcation of the basilar artery at the junction of the ipsilateral posterior
inferior cerebellar artery (PICA), vertebral artery, and the anterior communicating artery.[25]
Large unruptured aneurysms compress the adjacent cerebral tissue causing neurological signs.
However, the rupture of these lesions creates a state of reduced blood flow and vasospasm
leading to cerebral ischemia. The pathophysiological mechanisms by which these lesions are
formed and eventually rupture are not fully understood. The hemodynamic stress to the vessel
wall caused by increased blood pressure and other risk factors promotes the formation and
rupture of IA.[26] Multiple studies point to inflammation as a dominant factor in the
pathogenesis of IA.[27] A hemodynamic insult initiates the inflammatory process. It leads to
matrix metalloproteinases (MMPs)–mediated degradation of the extracellular matrix and
apoptosis of smooth muscle cells (SMCs), which are the predominant matrix-synthesizing cells
of the vascular wall. These processes significantly weaken the arterial wall, resulting in
dilatation, aneurysm formation, and ultimately rupture (Figure; Table 1). Notably, The two main
constituents of the inflammatory response and the associated degenerative response are
macrophages and SMCs.[27]
Histopathology
Aneurysms are divided according to their morphology into:
i) Saccular aneurysms that are pouch-like protrusions of the vessel wall, usually arising in
cerebral artery bifurcations (A);
ii) Fusiform aneurysms that are dilatations of the vessel wall that do not lead to the formation of
a separate saccular pouch (B); and
iii) dolichoectasias are elongated, tortuous, and sometimes dilated vessel segments (C).
Furthermore, a rare fourth type of cerebral artery aneurysm is the dissecting aneurysm that
usually has a fusiform shape (B), but originates from acute dissection or tearing of the arterial
wall layers.
History and Physical

A typical presenting symptom is a thunderclap headache. Patients usually describe it as the
"worst headache of my life." This problem should prompt further imaging. A headache is
frequently associated with nausea, vomiting (often projectile), nuchal rigidity, and photophobia.
Meningismus is typically present due to blood extending into the fourth ventricle. As the blood
moves further down the spinal cord, it irritates surrounding nerves causing neck pain and
stiffness. Practitioners should perform a detailed exam. The presence of a focal deficit increases
the grade of subarachnoid hemorrhage and changes the perspective of post-event recovery.
Patients with a high-grade subarachnoid hemorrhage often present in a state of coma that calls
for an urgent evaluation and treatment, as in some the coma can be reversible.[28] The presence
of an unruptured IA or increased intracranial pressure (ICP) post rupture may cause cranial nerve
palsies from compression on the third and or sixth cranial nerve (CN III, CN VI).[28] Some
patients also experience seizures with IA rupture.[29]
Evaluation
Initial evaluation of a patient suspected of having a subarachnoid hemorrhage should include a
head computed tomogram (CT).[30] A CT angiography should be performed if an aSAH is
identified to determine the location and size of the aneurysm. However, if the initial Head CT is
negative, a lumbar puncture is performed in case of strong suspicion. A lumbar puncture should
ideally be performed 6 hours after the initial Head CT to detect the presence of xanthochromia.
Often xanthochromia can be assessed at the bedside due to visible cerebrospinal fluid color
change.[31] A CT angiogram helps confirm and identify an intracerebral aneurysm's location. If
the CT angiogram is negative, it should be followed by cerebral angiography or digital
subtraction angiography (DSA).[32] A few factors should be considered in patients allergic to
contrast or who have decreased renal function. These patient populations need pre-procedure
treatment to decrease the risk of an adverse reaction. Time-of-flight magnetic resonance
angiography (TOF-MRA) is another acceptable mode of imaging that does not require contrast
injection.[32][33][34]
The sensitivity of CT scans and red blood cell (RBC) counts are time-dependent and very
sensitive early in the diagnosis. This loss of sensitivity over time can be due to the brisk
physiologic flow of cerebrospinal fluid (CSF). Over time, the RBCs present in the CSF undergo
lysis resulting in breakdown products such as bilirubin and oxyhemoglobin. RBC lysis explains
that xanthochromia becomes increasingly sensitive after a few hours.
Treatment / Management
All Patients presenting with aSAH should be organized according to the severity of disease. In
general, management include medical measures and interventional options like endovascular
coiling or direct surgical clipping of the IA. Patients are typically treated with both medical and
interventional options. More conservative or less invasive interventions may be sufficient for
patients with grade I or II SAH. The key goals for all SAH patients are the prevention of
rebleeding, delayed cerebral ischemia (DCI), supportive care, pain management, and accurate
diagnosis and treatment.
Although immediate care aims to prevent rebleeding and to secure the aneurysm, other common
problems include hydrocephalus and vasospasm. Hydrocephalus is present in up to 30% of
patients with intraventricular hemorrhage.[35] The proposed mechanism is thought to be
secondary to the mechanical blockage of the CSF flow at different levels and an inflammatory
reaction due to the presence of blood in the CSF. This inflammatory reaction eventually leads to
the fibrosis of arachnoid granulations.[35] In patients with a significant SAH and a higher (more
severe) clinical grade, the incidence of rebleeding is higher and may be evident upon admission
to the ED or intensive care unit (ICU). Hydrocephalus often occurs within the first three days
post hemorrhage. At this time, placement of an intraventricular external drainage device is
recommended to relieve the elevated ICP.[36] Another major complication in aSAH is delayed
cerebral ischemia (DCI) development. Approximately 60% of patients with aSAH have
radiographic vasospasm, defined as vasoconstriction and narrowing of the cerebral arteries,
evident with cerebral angiography with or without clinical signs or symptoms.[37] About 39% of
patients will have clinical manifestations of vasospasm. These segments of vasospasm cause
reduced blood flow to the brain, causing DCI.
Osmotic diuretics (i.e., Mannitol) and antihypertensive medications for blood pressure control
are required to stabilize the patient until surgical or endovascular interventions can be initiated to
secure the IA.[36] Grades III, IV, or V require more aggressive and extensive care that may
include intubation and mechanical ventilation to protect the airway and support respiratory effort
in patients with decreased levels of consciousness. It is often recommended to place an arterial
line for close monitoring of blood pressure. Other interventions may include an indwelling
urinary catheter and seizure prophylaxis.[36]
Monitoring
Transcranial Doppler – Transcranial Doppler (TCD) sonography is used for detecting and
monitoring vasospasm in SAH. A TCD is able to detect changes in velocity prior to the clinical
sequelae of vasospasm. However, it is an operator-dependent technology that has imperfect
sensitivity and specificity.[38][39][40][41][38] In general, digital subtraction angiography is
required to diagnose vasospasm and institute treatment.
Imaging studies – In the acute phase of SAH, imaging studies like CT angiography (CTA) and
CT perfusion can detect arterial narrowing or perfusion asymmetry. These methods are sensitive
and help in predicting delayed cerebral ischemia.[42][43] The use of this technique as a
monitoring tool may be limited by risks of recurrent dye loads and radiation exposure.[39] A
finding of perfusion-diffusion mismatch on magnetic resonance imaging may be another method
of detecting brain areas at risk of infarction in this setting.[44] The clinical utility of either of
these methods remains to be established.
Electroencephalography (EEG) – Continuous EEG can be useful to detect subclinical seizures

or nonconvulsive status epilepticus, particularly for patients with poor-grade SAH who develop
unexplained neurologic deterioration or fail to improve.[40]
Frequency of neuro checks – Patients with acute SAH should be carefully examined every one
to two hours, especially during the high-risk period for delayed cerebral ischemia.[45]
Symptomatic vasospasm and delayed cerebral ischemia are manifested clinically by neurologic
decline, including the onset of focal neurologic abnormalities.
A development of neurologic deficits should be evaluated with an urgent head CT scan (to
identify rebleeding, cerebral infarction, hydrocephalus), angiography (to identify symptomatic
vasospasm), and/or EEG (to detect subclinical seizures). Medical complications can also
contribute to a change in neurologic status.
Even in the absence of clinical change, it is important to identify cerebral vasospasm and
decreased cerebral perfusion. Therefore, some centers monitor all patients with aneurysmal SAH
with TCD sonography daily and head CT, CTA, and CT perfusion on admission and between
days 3 to 5 and days 7 to 10 to screen for evidence of decreased cerebral perfusion or vasospasm.
[45] Digital subtraction angiography can be used in place of CTA/CTP in situations of high
suspicion. Additional monitoring may be employed for high-risk patients with poor neurologic
status, including EEG, and invasive monitoring of brain tissue oxygenation and cerebral blood
flow.[46]
Intracranial pressure monitoring – It is recommended to perform a ventriculostomy in patients

with enlarged ventricles on CT or with WFNS scale score ≥3; this allows direct measurement of
ICP and also allows treatment by drainage of cerebrospinal fluid (CSF) when appropriate.[47]
Medical Management
The significant concerns after an aSAH are rebleeding, hydrocephalus, and vasospasm. The most
immediate problem is rebleeding. The most significant risk of rebleeding and mortality is within
the first 6 hours of the initial hemorrhage.[48] Commonly, patients risk rebleeding with elevated
systolic blood pressure, poor Hunt-Hess grades, intracerebral or intraventricular hematomas,
aneurysms > 10 mm in size, and aneurysms in the posterior circulation.[48]] About 9% to 17% of
patients risk rebleeding in the first 72 hours. Rebleeding carries a mortality rate of up to 50%.
Nearly 15% of patients rebleed in the first few hours after the initial hemorrhage; however, once
the IA is secured, the risk of rebleeding is about 1%.[49] Blood pressure control is a significant
component in the prevention of rebleeding.[49] The following section discusses drug therapy
used for aSAH, including blood pressure control, vasospasm, and anticoagulants.
Drug Therapy
Historically, tertiary and academic medical centers have had specialized neuroscience units. In
recent years, smaller community hospitals that previously cared for neuroscience patients in
general medical or surgical ICUs are becoming specialized. With this, the number of
neuroscience/neurological ICUs and specialty medical-surgical units are increasing. The role of
neuroscience-specialized pharmacists is growing, providing an additional level of expertise to
understand the effects of neurological illness or injury, drug interactions, and the impact on the
patient.[50] The pharmacist is vital in managing drugs such as antiepileptics, anticoagulants,
antibiotics, pain control, and medications that require pharmacy-dosing services. Patients in the
ICU often have multiple continuous intravenous infusions for blood pressure control and
sedation and pain medication in addition to scheduled medicines for the prevention of seizures,
treatment of hyponatremia, or other complications of aSAH.[50] Neuroscience ICUs have
evidence-based, drug-specific protocols to reduce medication errors and decrease provider
variability. Optimizing drug protocols can increase patient safety and improve outcomes.[50]
Blood Pressure Control
Blood pressure control is critical to reducing the risk of rebleeding until the IA is secured and
during the first 24 to 48 hours postoperative period.[49] The sudden surge in central sympathetic
stimulation associated with aSAH results in hypertension, and the generally accepted goal is to
maintain the systolic blood pressure to less than 160 mm Hg.[51] The risk of rebleeding is
highest in the first 24 hours of the initial hemorrhage and carries a mortality rate up to 78%.
Opioid pain medications may help to decrease the blood pressure and promote patient comfort;
however, administering rapid-acting intravenous (IV) antihypertensive medications given as
needed or via continuous infusion work to maintain the blood pressure within ordered
parameters.[49] Nitrates and nitroprusside have fallen out of favor as first-line agents for blood
pressure control due to the potential for increased ICP and toxic side effects, particularly with
prolonged nitroprusside infusions.[52]
Labetalol and hydralazine are often the favored intermittent dosing medications, whereas
nicardipine (Cardene) and clevidipine (Cleviprex) are continuous infusions used for blood
pressure control.[49] Labetalol is a beta-blocker that may be administered over 2 minutes in
doses ranging from 5 to 20 mg IV every 15 minutes.[53] Hydralazine is given in incremental IV
doses of 20 to 40 mg every 30 to 60 minutes. The action of hydralazine is also vasodilation, but
with a direct effect on arterioles to decrease systemic resistance and reduce blood pressure.[53]
The duration of action is more prolonged than labetalol and lasts 1 to 4 hours with a half-life of 2
to 8 hours. Contraindications include coronary artery disease (CAD). The precaution for stroke
patients is to avoid a sudden drop in blood pressure related to antihypertensive medications,
particularly in ischemic stroke, that may result in a hypoperfusion injury to the brain.
Nicardipine (Cardene) is given via continuous IV infusion in titrated doses from 5 to 15 mg/hr to
maintain the systolic blood pressure of 150 to 160 mm Hg to prevent rebleeding. Some clinicians
prefer to maintain a blood pressure of less than 140 mm Hg to prevent rebleeding.[54]
Clevidipine (Cleviprex) is also a calcium channel blocker with a similar mechanism of action as
nicardipine.[55] The onset of action is about 2 to 4 minutes, with a half-life of about 15 minutes.
Dosing and titration begin at 1 to 2 mg/hr and repeated every 90 seconds. Clevidipine is in a lipid
base without preservatives.
Vasospasm Prevention and Treatment
The drug categories that prevent and treat vasospasm include calcium channel blockers,
magnesium, endothelin antagonists, and statins. These categories are revieNimodipine following
sections to describe their current use, if any, in vasospNimodipinement.
Calcium Channel Blockers
Calcium channel blockers (CCBs) reduce cardiac and smooth muscle contraction without an
effect on skeletal muscle. The effectiveness of this classification of drugs in the management of
aSAH has been a source of many studies over the years. Still, it is considered that CCBs mitigate
the abnormal vasoconstriction of cerebral vascular smooth muscle. Oral administration of the
dihydropyridine-type calcium channel blocker nimodipine is the only treatment with consistent,
high-quality evidence for decreasing DCI and is now standard of care in patients with aSAH.
However, these results are advocated by one large trial.[56][57] These early studies showed the
role of oral Nimodipine in reducing DCI and improving outcomes without affecting vasospasm.
[58] This suggests nimodipine may have an important vessel-independent effect not completely
understood. A recent trial (NEWTON [Nimodipine microparticles to enhance recovery while
reducing toxicity after subarachnoid hemorrhage] involving administration of intraventricular
nimodipine showed no improvements over standard oral administration.[59] Oral nimodipine is

given in doses of 60 mg every 4 hours or 30 mg every 2 hours for 21 days. If hypotension is a
recurring problem, the recommendation is to administer smaller, more frequent dosing.
Magnesium
The use of Magnesium sulfate has shown to have mixed results on neuroprotective and its
vasodilatation properties—vasodilation results from an inhibition of Voltage-gated
calcium channel-mediated smooth muscle contractions. Various spasmogenic agents such as
endothelin-1, norepinephrine, angiotensin II, and serotonin are counteracted by magnesium. The
Magnesium for Aneurysmal Subarachnoid Hemorrhage (MASH-2) trial was a phase 3,
randomized, placebo-controlled trial. A total of 1,204 patients were enrolled. The study
concluded with no improvement in outcomes in the intervention group.[60] Additionally, An
updated Cochrane meta-analysis of seven prior randomized trials from MASH-2 and those
randomized trials that were eligible for inclusion since the MASH-2 trial involved 2,047 patients
demonstrated that magnesium was not superior to a placebo in reducing poor outcomes after
aSAH. Therefore, magnesium cannot be recommended for routine administration in aSAH.[61]
Endothelin Antagonists
Endothelin antagonists (ET-A) are another potential treatment under investigation. ET-A
receptors mediate vasoconstriction in arterial smooth muscle. Clazosentan is a selective ET-A
receptor antagonist that demonstrated a decrease and a reversal in vasospasm after SAH. One
study, CONSCIOUS-1 (Clazosentan to Overcome Neurological Ischemia and Infarct Occurring
after Subarachnoid Hemorrhage), found a significant dose-dependent effect on vasospasm when
evaluated with angiography. The 413 patients in this study were randomized and given placebo
or clazosentan within 56 hours and continued on their assigned protocol for up to 14 days.[62]
Subsequent studies with clazosentan have reported no benefit with this drug.
Statins
Research with statin drugs have also demonstrated a lack of efficacy and have shown no benefit
in the treatment of vasospasm and neither does it improve short term or long term outcomes in
aSAH[63][64]; however, studies are ongoing. To date, the recommendations have been to
continue the statin medication if the patient had been taking it prior to the onset of the SAH.[65]
Anticoagulants
As per the 2015 guidelines from the Neurocritical Care Society (NCS) and Society of Critical
Care Medicine (SCCM), it is recommended to discontinue all antithrombotic agents and reverse
all anticoagulation until the aneurysm is definitively repaired by surgery or coiling.[66] Patients
presenting with aSAH on anticoagulant therapy have a worse prognosis and outcomes.
Anticoagulants tend to increase the amount of bleeding at the time of rupture, thereby increasing
the overall amount of blood in the subarachnoid space, basal cisterns, and the parenchyma.[67]
On the other hand, thrombotic complications related to venous thromboembolism (VTE) may be
equally as lethal in patients with stroke. An accepted clinical practice is to
initiate pharmacological prophylaxis therapy 24 to 48 hours after surgery with unfractionated or
a low-molecular-weight heparin. Nurse-driven protocols often support VTE prevention measures
intermittent pneumatic compression (IPC) devices on admission to the critical care unit.
Additional measures may consist of early mobilization and prevention of dehydration. Stroke
units that promote early mobilization have demonstrated lower rates of DVT.[68]
Pain Control
Pain management is an essential aspect of patient care. With complaints of the “worst headache
of my life”, the interprofessional health care team needs to provide interventions to make the
patient as comfortable as possible. Nonopioid medications such as acetaminophen (650 mg PO
or 1,000 mg IV) are first line medications and be administered every 4 to 6 hours; however,
consideration must be given to contraindications, that is, liver diseaase.[69] NSAIDs like aspirin
should be avoided until the aneurysm is secured.[40] Opioid medications such as fentanyl (12.5
to 25 mg IV every hour as needed), Dilaudid (0.2 to 4 mg IV every 3 to 4 hours as needed), and
morphine sulfate (2 to 4 mg IV every 1 to 2 hours as required) may provide pain relief as well as
a degree of sedation and serve to decrease anxiety. Patients response to pain medications must be
monitored closely to avoid oversedation and an inability to accurately assess the patients’
neurological status. Pain management is essential but with caution so that worsening in
neurological status is not masked.
Surgical management
Once an aSAH or a ruptured aneurysm is identified, repair with surgical clipping or endovascular
coiling is the only effective treatment and should be performed as early as feasible, preferably
within 24 hours [39]; some expert centers report a median time to aneurysm repair of 7 hours
from admission.[39] Patients in whom aneurysm treatment is not possible or must be delayed
may be candidates for antifibrinolytic therapy, but these agents should not be used for more than
72 hours.[45]
Differential Diagnosis
Bacterial and tuberculous meningitis
Granulomatous meningitis
Neurosarcoidosis
Pseudo-subarachnoid hemorrhage
Staging
Several grading scales are used in clinical practice to standardize the classification of patients
with aSAH and to monitor progression and change in condition. These scales are based on the
initial clinical neurological examination and the appearance of blood on the initial head CT.
These scales include the Glasgow Coma Scale, the Hunt and Hess grading scale, the WFNS
scale, the Fisher grading scale, and the modified Fisher grading scale.
I) The Glasgow Coma Scale (GCS), introduced in 1974, is designed as a reliable and objective
scale of neurological function in three subscales of level of consciousness, eye-opening, and
motor function.[70] The scale ranges from 3 to 15, and points are denoted based on the level of
response. A higher score correlates to a better patient's neurological condition. The GCS is
commonly used for the initial and ongoing assessment of a patient with possible or confirmed
brain injury. It is used to determine neurological deficits and their changes over time.
II) The World Federation of Neurosurgical Societies (WFNS) developed the WFNS grading
scale, which describes the clinical presentation of SAH patients. The scale includes
consciousness and motor deficits in its scoring system. The WFNS grading system uses a
combination of consciousness and motor deficits from the GCS and the presence of focal
neurological deficits to grade the severity of SAH.[71] The scale helps predict recovery and
response to treatment. For example, elderly patients with a WFNS grade of I to III have the best
clinical recovery and seem to benefit from aggressive treatment compared to patients younger
than 70 years with a WFNS score of IV or V.
III) The Hunt and Hess grading scale, introduced in 1968, helps to classify the severity of
aSAH based on the patient's clinical condition. It is used as a predictor of a patient's prognosis
and outcome. A higher score (grade) correlates to a lower survival rate. [72]
IV) The Fisher grading scale is a numerical scale from 0 to 4 that provides insight into the
amount of subarachnoid blood on a CT scan. These grading scales correlate to the hemorrhage's
severity, the IA's clinical grade, and the vasospasm's incidence after the SAH. In comparison, the
modified Fisher grading scale provides more specific descriptions of the amount and location
of blood seen on a CT scan.[73]
Prognosis
SAH is associated with a high early mortality rate.[74] A population-based study published in
2017 found that approximately 18 percent of patients with SAH died suddenly before being
evaluated in a hospital.[75] Among patients who reach the hospital alive, much of the subsequent
early mortality is caused by the common complications of aneurysmal SAH related to initial
bleeding, rebleeding, vasospasm and delayed cerebral ischemia, hydrocephalus, increased
intracranial pressure, seizures, and cardiac complications.[75]
Long-term complications of SAH include neurocognitive dysfunction, epilepsy, and other focal
neurologic deficits. In one registry, more than 10 percent of patients with SAH remained
moderately or severely disabled.[76]
Complications
Seizures
Vasospasm
Rebleed
Hydrocephalus
Increased intracranial pressure
Brain herniation
Cerebral infarction
Medical complications
Neurogenic pulmonary edema[77]
Death
Consultations
A neurosurgical and neurointerventional consult is essential in the early management of this
condition. An interprofessional team can help in making early decisions like coiling or clipping
of the culprit aneurysm.
Deterrence and Patient Education

A patient with an aneurysm, who is being conservatively managed should be advised on all the
complications that can occur if it ruptures.
Any patient and relatives getting admitted with subarachnoid hemorrhage secondary to an
aneurysm rupture should be aware of the chance of rebleed and the morbidity and mortality
associated with any intervention.
Enhancing Healthcare Team Outcomes

The majority of patients with subarachnoid hemorrhage present to the emergency department.
Thus, the emergency department physician and nurse practitioner must know the workup for
these patients. Because of its high mortality, an interprofessional team that includes a
Neurosurgeon, Interventional radiologist, Neurologist, Intensivist, and Intensive Care Unit nurses
is recommended. Unfortunately, despite optimal care, most patients die within 30 days. Even
those who survive are left with severe complications that are disabling.[78][79]
Review Questions
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Comment on this article.
Figure
Head CT Revealing Subarachnoid Hemorrhage. The image

depicts a head CT scan of a patient revealing a subarachnoid
hemorrhage. Contributed by S Dulebohn, MD
Figure
The illustration shows how a hemorrhagic stroke can occur in

the brain. An aneurysm in a cerebral artery breaks open,
which causes bleeding in the brain. The pressure of the blood
causes brain tissue death. Contributed by National Heart
Lung and Blood (more...)
Figure
STAR Sign Subarachnoid Hemorrhage Flynn L, Andrews P.

Advances in the understanding of delayed cerebral ischaemia
after aneurysmal subarachnoid haemorrhage. F1000Research.
2015;4. doi:10.12688/f1000research.6635.1.(CC By S.A.
4.0 https://creativecommons.org/licenses/by/4.0) (more...)
Figure
Computed tomography image of a horizontal section through

the head, showing a large aneurysm of the anterior
communicating artery. (Reproduced with permission from
deGroot J: Correlative Neuroanatomy of Computed Tomography and Magnetic

Resonance Imaging. (more...)
Figure
Cerebral aneurysm (CA) formation and rupture. Aneurysm

formation is initiated by hemodynamically triggered
endothelial dysfunction. An inflammatory response
implicating several cytokines and inflammatory mediators as
well as macrophages, T cells, and (more...)
Figure
Glasgow coma scale Contributed by Mahammed khan suheb
Figure
Fischer and modified Fischer scale Contributed by

Mahammed khan suheb
Figure
Hunt and Hess scale Contributed by Mahammed khan suheb
Figure
World Federation of Neurological Societies Grading Scale

(WFNS) Contributed by Mahammed Khan suheb
References
1. de Rooij NK, Linn FH, van der Plas JA, Algra A, Rinkel GJ. Incidence of subarachnoid
haemorrhage: a systematic review with emphasis on region, age, gender and time trends. J
Neurol Neurosurg Psychiatry. 2007 Dec;78(12):1365-72. [PMC free article: PMC2095631]
[PubMed: 17470467]
2. Ikawa F, Michihata N, Matsushige T, Abiko M, Ishii D, Oshita J, Okazaki T, Sakamoto S,
Kurogi R, Iihara K, Nishimura K, Morita A, Fushimi K, Yasunaga H, Kurisu K. In-hospital
mortality and poor outcome after surgical clipping and endovascular coiling for aneurysmal
subarachnoid hemorrhage using nationwide databases: a systematic review and meta-
analysis. Neurosurg Rev. 2020 Apr;43(2):655-667. [PubMed: 30941595]
3. Schwartz TH, Solomon RA. Perimesencephalic nonaneurysmal subarachnoid hemorrhage:
review of the literature. Neurosurgery. 1996 Sep;39(3):433-40; discussion 440. [PubMed:
8875472]
4. Kowalski RG, Claassen J, Kreiter KT, Bates JE, Ostapkovich ND, Connolly ES, Mayer SA.
Initial misdiagnosis and outcome after subarachnoid hemorrhage. JAMA. 2004 Feb
18;291(7):866-9. [PubMed: 14970066]
5. Gallas S, Tuilier T, Ebrahiminia V, Bartolucci P, Hodel J, Gaston A. Intracranial aneurysms in
sickle cell disease: Aneurysms characteristics and modalities of endovascular approach to
treat these patients. J Neuroradiol. 2020 May;47(3):221-226. [PubMed: 30904450]
6. Vlak MH, Rinkel GJ, Greebe P, van der Bom JG, Algra A. Trigger factors for rupture of
intracranial aneurysms in relation to patient and aneurysm characteristics. J Neurol. 2012
Jul;259(7):1298-302. [PMC free article: PMC3390687] [PubMed: 22186848]
7. Rinkel GJ, Wijdicks EF, Vermeulen M, Ramos LM, Tanghe HL, Hasan D, Meiners LC, van
Gijn J. Nonaneurysmal perimesencephalic subarachnoid hemorrhage: CT and MR patterns
that differ from aneurysmal rupture. AJNR Am J Neuroradiol. 1991 Sep-Oct;12(5):829-34.
[PMC free article: PMC8333493] [PubMed: 1950905]
8. Canhão P, Ferro JM, Pinto AN, Melo TP, Campos JG. Perimesencephalic and
nonperimesencephalic subarachnoid haemorrhages with negative angiograms. Acta
Neurochir (Wien). 1995;132(1-3):14-9. [PubMed: 7754850]
9. Tatter SB, Crowell RM, Ogilvy CS. Aneurysmal and microaneurysmal "angiogram-negative"
subarachnoid hemorrhage. Neurosurgery. 1995 Jul;37(1):48-55. [PubMed: 8587690]
10. Jung JY, Kim YB, Lee JW, Huh SK, Lee KC. Spontaneous subarachnoid haemorrhage with
negative initial angiography: a review of 143 cases. J Clin Neurosci. 2006 Dec;13(10):1011-
7. [PubMed: 16931020]
11. Rinkel GJ, van Gijn J, Wijdicks EF. Subarachnoid hemorrhage without detectable
aneurysm. A review of the causes. Stroke. 1993 Sep;24(9):1403-9. [PubMed: 8362440]
12. Cordonnier C, Al-Shahi Salman R, Bhattacharya JJ, Counsell CE, Papanastassiou V, Ritchie
V, Roberts RC, Sellar RJ, Warlow C., SIVMS Collaborators. Differences between
intracranial vascular malformation types in the characteristics of their presenting
haemorrhages: prospective, population-based study. J Neurol Neurosurg Psychiatry. 2008
Jan;79(1):47-51. [PubMed: 17488785]
13. Koch C. Spinal dural arteriovenous fistula. Curr Opin Neurol. 2006 Feb;19(1):69-75.
[PubMed: 16415680]
14. Caplan LR. Dissections of brain-supplying arteries. Nat Clin Pract Neurol. 2008
Jan;4(1):34-42. [PubMed: 18199995]
15. Santos-Franco JA, Zenteno M, Lee A. Dissecting aneurysms of the vertebrobasilar system.
A comprehensive review on natural history and treatment options. Neurosurg Rev. 2008
Apr;31(2):131-40; discussion 140. [PubMed: 18309525]
16. Nolte KB, Brass LM, Fletterick CF. Intracranial hemorrhage associated with cocaine abuse:
a prospective autopsy study. Neurology. 1996 May;46(5):1291-6. [PubMed: 8628469]
17. Karabatsou K, Lecky BR, Rainov NG, Broome JC, White RP. Cerebral amyloid angiopathy
with symptomatic or occult subarachnoid haemorrhage. Eur Neurol. 2007;57(2):103-5.
[PubMed: 17179713]
18. Beitzke M, Gattringer T, Enzinger C, Wagner G, Niederkorn K, Fazekas F. Clinical
presentation, etiology, and long-term prognosis in patients with nontraumatic convexal
subarachnoid hemorrhage. Stroke. 2011 Nov;42(11):3055-60. [PubMed: 21921284]
19. Marcolini E, Hine J. Approach to the Diagnosis and Management of Subarachnoid
Hemorrhage. West J Emerg Med. 2019 Mar;20(2):203-211. [PMC free article:
PMC6404699] [PubMed: 30881537]
20. Kuroda H, Mochizuki T, Shimizu S, Kumabe T. Rupture of Thrombosed Cerebral
Aneurysm During Antithrombotic Therapy for Ischemic Stroke: Case Report and Literature
Review. World Neurosurg. 2019 Jun;126:468-471. [PubMed: 30898732]
21. Etminan N, Chang HS, Hackenberg K, de Rooij NK, Vergouwen MDI, Rinkel GJE, Algra
A. Worldwide Incidence of Aneurysmal Subarachnoid Hemorrhage According to Region,
Time Period, Blood Pressure, and Smoking Prevalence in the Population: A Systematic
Review and Meta-analysis. JAMA Neurol. 2019 May 01;76(5):588-597. [PMC free article:
PMC6515606] [PubMed: 30659573]
22. Shea AM, Reed SD, Curtis LH, Alexander MJ, Villani JJ, Schulman KA. Characteristics of
nontraumatic subarachnoid hemorrhage in the United States in 2003. Neurosurgery. 2007
Dec;61(6):1131-7; discussion 1137-8. [PubMed: 18162891]
23. Rinkel GJ, Djibuti M, Algra A, van Gijn J. Prevalence and risk of rupture of intracranial
aneurysms: a systematic review. Stroke. 1998 Jan;29(1):251-6. [PubMed: 9445359]
24. Chalouhi N, Ali MS, Jabbour PM, Tjoumakaris SI, Gonzalez LF, Rosenwasser RH, Koch
WJ, Dumont AS. Biology of intracranial aneurysms: role of inflammation. J Cereb Blood
Flow Metab. 2012 Sep;32(9):1659-76. [PMC free article: PMC3434628] [PubMed:
22781330]
25. Brisman JL, Song JK, Newell DW. Cerebral aneurysms. N Engl J Med. 2006 Aug
31;355(9):928-39. [PubMed: 16943405]
26. Penn DL, Komotar RJ, Sander Connolly E. Hemodynamic mechanisms underlying cerebral
aneurysm pathogenesis. J Clin Neurosci. 2011 Nov;18(11):1435-8. [PubMed: 21917457]
27. Chalouhi N, Hoh BL, Hasan D. Review of cerebral aneurysm formation, growth, and
rupture. Stroke. 2013 Dec;44(12):3613-22. [PubMed: 24130141]
28. Green DM, Burns JD, DeFusco CM. ICU management of aneurysmal subarachnoid
hemorrhage. J Intensive Care Med. 2013 Nov-Dec;28(6):341-54. [PubMed: 22328599]
29. Diringer MN. Management of aneurysmal subarachnoid hemorrhage. Crit Care Med. 2009
Feb;37(2):432-40. [PMC free article: PMC2820121] [PubMed: 19114880]
30. Vermeulen M, van Gijn J. The diagnosis of subarachnoid haemorrhage. J Neurol Neurosurg
Psychiatry. 1990 May;53(5):365-72. [PMC free article: PMC488050] [PubMed: 2191083]
31. Edlow JA. Managing Patients With Nontraumatic, Severe, Rapid-Onset Headache. Ann
Emerg Med. 2018 Mar;71(3):400-408. [PubMed: 28601276]
32. Kumar A, Niknam K, Lumba-Brown A, Woodruff M, Bledsoe JR, Kohn MA, Perry JJ,
Govindarajan P. Practice Variation in the Diagnosis of Aneurysmal Subarachnoid
Hemorrhage: A Survey of US and Canadian Emergency Medicine Physicians. Neurocrit
Care. 2019 Oct;31(2):321-328. [PubMed: 30790225]
33. Li K, Barras CD, Chandra RV, Kok HK, Maingard JT, Carter NS, Russell JH, Lai L, Brooks
M, Asadi H. A Review of the Management of Cerebral Vasospasm After Aneurysmal
Subarachnoid Hemorrhage. World Neurosurg. 2019 Jun;126:513-527. [PubMed: 30898740]
34. Dodson V, Majmundar N, El-Ghanem M, Amuluru K, Gupta G, Nuoman R, Wainwright J,
Kaur G, Cole C, Santarelli J, Chandy D, Bowers C, Gandhi C, Al-Mufti F. Intracranial
Administration of Nicardipine After Aneurysmal Subarachnoid Hemorrhage: A Review of
the Literature. World Neurosurg. 2019 May;125:511-518.e1. [PubMed: 30708083]
35. Chen S, Luo J, Reis C, Manaenko A, Zhang J. Hydrocephalus after Subarachnoid
Hemorrhage: Pathophysiology, Diagnosis, and Treatment. Biomed Res Int.
2017;2017:8584753. [PMC free article: PMC5360938] [PubMed: 28373987]
36. Bederson JB, Connolly ES, Batjer HH, Dacey RG, Dion JE, Diringer MN, Duldner JE,
Harbaugh RE, Patel AB, Rosenwasser RH., American Heart Association. Guidelines for the
management of aneurysmal subarachnoid hemorrhage: a statement for healthcare
professionals from a special writing group of the Stroke Council, American Heart
Association. Stroke. 2009 Mar;40(3):994-1025. [PubMed: 19164800]
37. Dodd WS, Laurent D, Dumont AS, Hasan DM, Jabbour PM, Starke RM, Hosaka K, Polifka
AJ, Hoh BL, Chalouhi N. Pathophysiology of Delayed Cerebral Ischemia After
Subarachnoid Hemorrhage: A Review. J Am Heart Assoc. 2021 Aug 03;10(15):e021845.
[PMC free article: PMC8475656] [PubMed: 34325514]
38. Djelilovic-Vranic J, Basic-Kes V, Tiric-Campara M, Djozic E, Kulenovic J. Follow-up of
Vasospasm by Transcranial Doppler Sonography (TCD) in Subarachnoid Hemorrhage
(SAH). Acta Inform Med. 2017 Mar;25(1):14-18. [PMC free article: PMC5402374] [PubMed:
28484291]
39. Connolly ES, Rabinstein AA, Carhuapoma JR, Derdeyn CP, Dion J, Higashida RT, Hoh BL,
Kirkness CJ, Naidech AM, Ogilvy CS, Patel AB, Thompson BG, Vespa P., American Heart
Association Stroke Council. Council on Cardiovascular Radiology and Intervention.
Council on Cardiovascular Nursing. Council on Cardiovascular Surgery and Anesthesia.
Council on Clinical Cardiology. Guidelines for the management of aneurysmal
subarachnoid hemorrhage: a guideline for healthcare professionals from the American Heart
Association/american Stroke Association. Stroke. 2012 Jun;43(6):1711-37. [PubMed:
22556195]
40. Diringer MN, Bleck TP, Claude Hemphill J, Menon D, Shutter L, Vespa P, Bruder N,
Connolly ES, Citerio G, Gress D, Hänggi D, Hoh BL, Lanzino G, Le Roux P, Rabinstein A,
Schmutzhard E, Stocchetti N, Suarez JI, Treggiari M, Tseng MY, Vergouwen MD, Wolf S,
Zipfel G., Neurocritical Care Society. Critical care management of patients following
aneurysmal subarachnoid hemorrhage: recommendations from the Neurocritical Care
Society's Multidisciplinary Consensus Conference. Neurocrit Care. 2011 Sep;15(2):211-40.
[PubMed: 21773873]
41. Krejza J, Kochanowicz J, Mariak Z, Lewko J, Melhem ER. Middle cerebral artery spasm
after subarachnoid hemorrhage: detection with transcranial color-coded duplex US.
Radiology. 2005 Aug;236(2):621-9. [PubMed: 16040918]
42. van der Schaaf I, Wermer MJ, van der Graaf Y, Velthuis BK, van de Kraats CI, Rinkel GJ.
Prognostic value of cerebral perfusion-computed tomography in the acute stage after
subarachnoid hemorrhage for the development of delayed cerebral ischemia. Stroke. 2006
Feb;37(2):409-13. [PubMed: 16373646]
43. van der Schaaf I, Wermer MJ, van der Graaf Y, Hoff RG, Rinkel GJ, Velthuis BK. CT after
subarachnoid hemorrhage: relation of cerebral perfusion to delayed cerebral ischemia.
Neurology. 2006 May 23;66(10):1533-8. [PubMed: 16717213]
44. Vatter H, Güresir E, Berkefeld J, Beck J, Raabe A, du Mesnil de Rochemont R, Seifert V,
Weidauer S. Perfusion-diffusion mismatch in MRI to indicate endovascular treatment of
cerebral vasospasm after subarachnoid haemorrhage. J Neurol Neurosurg Psychiatry. 2011
Aug;82(8):876-83. [PubMed: 21436228]
45. Suarez JI. Diagnosis and Management of Subarachnoid Hemorrhage. Continuum (Minneap
Minn). 2015 Oct;21(5 Neurocritical Care):1263-87. [PubMed: 26426230]
46. Francoeur CL, Mayer SA. Management of delayed cerebral ischemia after subarachnoid
hemorrhage. Crit Care. 2016 Oct 14;20(1):277. [PMC free article: PMC5064957] [PubMed:
27737684]
47. Hellingman CA, van den Bergh WM, Beijer IS, van Dijk GW, Algra A, van Gijn J, Rinkel
GJ. Risk of rebleeding after treatment of acute hydrocephalus in patients with aneurysmal
subarachnoid hemorrhage. Stroke. 2007 Jan;38(1):96-9. [PubMed: 17122426]
48. Tang C, Zhang TS, Zhou LF. Risk factors for rebleeding of aneurysmal subarachnoid
hemorrhage: a meta-analysis. PLoS One. 2014;9(6):e99536. [PMC free article:
PMC4049799] [PubMed: 24911172]
49. D'Souza S. Aneurysmal Subarachnoid Hemorrhage. J Neurosurg Anesthesiol. 2015
Jul;27(3):222-40. [PMC free article: PMC4463029] [PubMed: 25272066]
50. Rhoney DH. Introduction: neurologic critical care. J Pharm Pract. 2010 Oct;23(5):385-6.
[PubMed: 21507843]
51. Bath PM, Song L, Silva GS, Mistry E, Petersen N, Tsivgoulis G, Mazighi M, Bang OY,
Sandset EC. Blood Pressure Management for Ischemic Stroke in the First 24 Hours. Stroke.
2022 Apr;53(4):1074-1084. [PubMed: 35291822]

52. Osgood ML. Aneurysmal Subarachnoid Hemorrhage: Review of the Pathophysiology and
Management Strategies. Curr Neurol Neurosci Rep. 2021 Jul 26;21(9):50. [PubMed:
34308493]
53. MacCarthy EP, Bloomfield SS. Labetalol: a review of its pharmacology, pharmacokinetics,
clinical uses and adverse effects. Pharmacotherapy. 1983 Jul-Aug;3(4):193-219. [PubMed:
6310529]
54. Huang RQ, Jiang FG, Feng ZM, Wang TY. Nicardipine in the treatment of aneurysmal
subarachnoid haemorrhage: a meta-analysis of published data. Acta Neurol Belg. 2013
Mar;113(1):3-6. [PubMed: 23111775]
55. Varelas PN, Abdelhak T, Corry JJ, James E, Rehman MF, Schultz L, Mays-Wilson K,
Mitsias P. Clevidipine for acute hypertension in patients with subarachnoid hemorrhage: a
pilot study. Int J Neurosci. 2014 Mar;124(3):192-8. [PubMed: 24007334]
56. Dorhout Mees SM, Rinkel GJ, Feigin VL, Algra A, van den Bergh WM, Vermeulen M, van
Gijn J. Calcium antagonists for aneurysmal subarachnoid haemorrhage. Cochrane Database
Syst Rev. 2007 Jul 18;2007(3):CD000277. [PMC free article: PMC7044719] [PubMed:
17636626]
57. Pickard JD, Murray GD, Illingworth R, Shaw MD, Teasdale GM, Foy PM, Humphrey PR,
Lang DA, Nelson R, Richards P. Effect of oral nimodipine on cerebral infarction and
outcome after subarachnoid haemorrhage: British aneurysm nimodipine trial. BMJ. 1989
Mar 11;298(6674):636-42. [PMC free article: PMC1835889] [PubMed: 2496789]
58. Petruk KC, West M, Mohr G, Weir BK, Benoit BG, Gentili F, Disney LB, Khan MI, Grace
M, Holness RO. Nimodipine treatment in poor-grade aneurysm patients. Results of a
multicenter double-blind placebo-controlled trial. J Neurosurg. 1988 Apr;68(4):505-17.
[PubMed: 3280746]
59. Carlson AP, Hänggi D, Wong GK, Etminan N, Mayer SA, Aldrich F, Diringer MN,
Schmutzhard E, Faleck HJ, Ng D, Saville BR, Bleck T, Grubb R, Miller M, Suarez JI,
Proskin HM, Macdonald RL., NEWTON Investigators. Single-Dose Intraventricular
Nimodipine Microparticles Versus Oral Nimodipine for Aneurysmal Subarachnoid
Hemorrhage. Stroke. 2020 Apr;51(4):1142-1149. [PubMed: 32138631]
60. Dorhout Mees SM, Algra A, Vandertop WP, van Kooten F, Kuijsten HA, Boiten J, van
Oostenbrugge RJ, Al-Shahi Salman R, Lavados PM, Rinkel GJ, van den Bergh WM.,
MASH-2 Study Group. Magnesium for aneurysmal subarachnoid haemorrhage (MASH-2):
a randomised placebo-controlled trial. Lancet. 2012 Jul 07;380(9836):44-9. [PMC free
article: PMC3391717] [PubMed: 22633825]
61. Dorhout Mees SM, Algra A, Wong GK, Poon WS, Bradford CM, Saver JL, Starkman S,
Rinkel GJ, van den Bergh WM, writing groups of MASH-I, IMASH, MASH-II, MASH and
FAST-MAG. van Kooten F, Dirven CM, van Gijn J, Vermeulen M, Rinkel GJ, Boet R, Chan
MT, Gin T, Ng SC, Zee BC, Al-Shahi Salman R, Boiten J, Kuijsten H, Lavados PM, van
Oostenbrugge RJ, Vandertop WP, Finfer S, O'Connor A, Yarad E, Firth R, McCallister R,
Harrington T, Steinfort B, Faulder K, Assaad N, Morgan M, Starkman S, Eckstein M,
Stratton SJ, Pratt FD, Hamilton S, Conwit R, Liebeskind DS, Sung G, Kramer I, Moreau G,
Goldweber R, Sanossian N. Early Magnesium Treatment After Aneurysmal Subarachnoid
Hemorrhage: Individual Patient Data Meta-Analysis. Stroke. 2015 Nov;46(11):3190-3.
[PubMed: 26463689]
62. Rhoney DH, McAllen K, Liu-DeRyke X. Current and future treatment considerations in the
management of aneurysmal subarachnoid hemorrhage. J Pharm Pract. 2010 Oct;23(5):408-
24. [PubMed: 21507846]
63. Kirkpatrick PJ, Turner CL, Smith C, Hutchinson PJ, Murray GD., STASH Collaborators.
Simvastatin in aneurysmal subarachnoid haemorrhage (STASH): a multicentre randomised
phase 3 trial. Lancet Neurol. 2014 Jul;13(7):666-75. [PubMed: 24837690]
64. Wong GK, Chan DY, Siu DY, Zee BC, Poon WS, Chan MT, Gin T, Leung M., HDS-SAH
Investigators. High-dose simvastatin for aneurysmal subarachnoid hemorrhage: multicenter
randomized controlled double-blinded clinical trial. Stroke. 2015 Feb;46(2):382-8.
[PubMed: 25516195]
65. Liu J, Chen Q. Effect of statins treatment for patients with aneurysmal subarachnoid
hemorrhage: a systematic review and meta-analysis of observational studies and
randomized controlled trials. Int J Clin Exp Med. 2015;8(5):7198-208. [PMC free article:
PMC4509204] [PubMed: 26221259]
66. Frontera JA, Lewin JJ, Rabinstein AA, Aisiku IP, Alexandrov AW, Cook AM, del Zoppo GJ,
Kumar MA, Peerschke EI, Stiefel MF, Teitelbaum JS, Wartenberg KE, Zerfoss CL.
Guideline for Reversal of Antithrombotics in Intracranial Hemorrhage: A Statement for
Healthcare Professionals from the Neurocritical Care Society and Society of Critical Care
Medicine. Neurocrit Care. 2016 Feb;24(1):6-46. [PubMed: 26714677]
67. Rinkel GJ, Prins NE, Algra A. Outcome of aneurysmal subarachnoid hemorrhage in patients
on anticoagulant treatment. Stroke. 1997 Jan;28(1):6-9. [PubMed: 8996479]
68. Xu T, Yu X, Ou S, Liu X, Yuan J, Chen Y. Efficacy and Safety of Very Early Mobilization in
Patients with Acute Stroke: A Systematic Review and Meta-analysis. Sci Rep. 2017 Jul
26;7(1):6550. [PMC free article: PMC5529532] [PubMed: 28747763]
69. Muehlschlegel S. Subarachnoid Hemorrhage. Continuum (Minneap Minn). 2018
Dec;24(6):1623-1657. [PubMed: 30516599]
70. Teasdale G, Murray G, Parker L, Jennett B. Adding up the Glasgow Coma Score. Acta
Neurochir Suppl (Wien). 1979;28(1):13-6. [PubMed: 290137]
71. Teasdale GM, Drake CG, Hunt W, Kassell N, Sano K, Pertuiset B, De Villiers JC. A
universal subarachnoid hemorrhage scale: report of a committee of the World Federation of
Neurosurgical Societies. J Neurol Neurosurg Psychiatry. 1988 Nov;51(11):1457. [PMC free
article: PMC1032822] [PubMed: 3236024]
72. Hunt WE, Hess RM. Surgical risk as related to time of intervention in the repair of
intracranial aneurysms. J Neurosurg. 1968 Jan;28(1):14-20. [PubMed: 5635959]
73. Claassen J, Bernardini GL, Kreiter K, Bates J, Du YE, Copeland D, Connolly ES, Mayer
SA. Effect of cisternal and ventricular blood on risk of delayed cerebral ischemia after
subarachnoid hemorrhage: the Fisher scale revisited. Stroke. 2001 Sep;32(9):2012-20.
[PubMed: 11546890]
74. van Gijn J, Kerr RS, Rinkel GJ. Subarachnoid haemorrhage. Lancet. 2007 Jan
27;369(9558):306-18. [PubMed: 17258671]
75. Lindbohm JV, Kaprio J, Jousilahti P, Salomaa V, Korja M. Risk Factors of Sudden Death
From Subarachnoid Hemorrhage. Stroke. 2017 Sep;48(9):2399-2404. [PubMed: 28739833]
76. Schatlo B, Fung C, Stienen MN, Fathi AR, Fandino J, Smoll NR, Zumofen D, Daniel RT,
Burkhardt JK, Bervini D, Marbacher S, Reinert M, D Alonzo D, Ahlborn P, Mendes Pereira
V, Roethlisberger M, Seule M, Kerkeni H, Remonda L, Weyerbrock A, Woernle K, Venier
A, Perren F, Sailer M, Robert T, Rohde V, Schöni D, Goldberg J, Nevzati E, Diepers M,
Gralla J, Z'Graggen W, Starnoni D, Woernle C, Maldaner N, Kulcsar Z, Mostaguir K,
Maduri R, Eisenring C, Bernays R, Ferrari A, Dan-Ura H, Finkenstädt S, Gasche Y,
Sarrafzadeh A, Jakob SM, Corniola M, Baumann F, Regli L, Levivier M, Hildebrandt G,
Landolt H, Mariani L, Guzman R, Beck J, Raabe A, Keller E, Bijlenga P, Schaller K.
Incidence and Outcome of Aneurysmal Subarachnoid Hemorrhage: The Swiss Study on
Subarachnoid Hemorrhage (Swiss SOS). Stroke. 2021 Jan;52(1):344-347. [PubMed: 33272133]
77. Al-Dhahir MA, M Das J, Sharma S. StatPearls [Internet]. StatPearls Publishing; Treasure
Island (FL): Jul 17, 2023. Neurogenic Pulmonary Edema. [PubMed: 30422579]
78. Pratt AK, Chang JJ, Sederstrom NO. A Fate Worse Than Death: Prognostication of
Devastating Brain Injury. Crit Care Med. 2019 Apr;47(4):591-598. [PubMed: 30855326]
79. Zheng K, Zhong M, Zhao B, Chen SY, Tan XX, Li ZQ, Xiong Y, Duan CZ. Poor-Grade
Aneurysmal Subarachnoid Hemorrhage: Risk Factors Affecting Clinical Outcomes in
Intracranial Aneurysm Patients in a Multi-Center Study. Front Neurol. 2019;10:123. [PMC
free article: PMC6400833] [PubMed: 30873104]
Disclosure: Endrit Ziu declares no relevant financial relationships with ineligible companies.
Disclosure: Mahammed Khan Suheb declares no relevant financial relationships with ineligible companies.
Disclosure: Fassil Mesfin declares no relevant financial relationships with ineligible companies.
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1) Aneurysmal Subarachnoid hemorrhage (aSAH)

2) Nonaneurysmal Subarachnoid hemorrhage (NASAH)

i) Perimesencephalic nonaneurysmal subarachnoid hemorrhage: It is characterized by a specific

History and Physical

Electroencephalography (EEG) – Continuous EEG can be useful to detect subclinical seizures

Intracranial pressure monitoring – It is recommended to perform a ventriculostomy in patients

Blood Pressure Control

Vasospasm Prevention and Treatment

Calcium Channel Blockers

nimodipine showed no improvements over standard oral administration.[59] Oral nimodipine is

Bacterial and tuberculous meningitis

Increased intracranial pressure

Neurogenic pulmonary edema[77]

Deterrence and Patient Education

Enhancing Healthcare Team Outcomes

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Head CT Revealing Subarachnoid Hemorrhage. The image

The illustration shows how a hemorrhagic stroke can occur in

STAR Sign Subarachnoid Hemorrhage Flynn L, Andrews P.

Computed tomography image of a horizontal section through

deGroot J: Correlative Neuroanatomy of Computed Tomography and Magnetic

Cerebral aneurysm (CA) formation and rupture. Aneurysm

Glasgow coma scale Contributed by Mahammed khan suheb

Fischer and modified Fischer scale Contributed by

Hunt and Hess scale Contributed by Mahammed khan suheb

World Federation of Neurological Societies Grading Scale

2022 Apr;53(4):1074-1084. [PubMed: 35291822]

Subarachnoid Hemorrhage (Swiss SOS). Stroke. 2021 Jan;52(1):344-347. [PubMed: 33272133]

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