Approach

SAH requires emergency treatment and early referral to a dedicated neurocritical care unit.[37]​​[96]​ When patients are evaluated in rural or community settings, strong consideration should be made for expedited referral to high-volume tertiary care centers with multidisciplinary neurointensive care services, comprehensive stroke center capabilities, and experienced cerebrovascular surgeons/neuroendovascular interventionalists.[37][97]​​​ Surgical or endovascular treatment of the ruptured aneurysm should be performed as early as feasible after presentation, preferably within 24 hours of onset, to improve outcome.[37]

Stabilization and cardiopulmonary support

Stabilization of patients simultaneously with workup is vital to prevent unwanted early complications. It is essential to establish the need for endotracheal intubation and mechanical ventilation as the first priority.[38] Consciousness level should be assessed using the Glasgow Coma Scale, in addition to airway adequacy and cardiovascular function.[39]​ A poor level of awareness and seizures on presentation are risk factors for aspiration. A large hemorrhage burden and the presence of a subdural hematoma are associated with the occurrence of seizures after aneurysm rupture.[41] A full neurologic exam should be performed with special attention to pupillary reaction. Fixed and dilated pupils in comatose patients are associated with a poor prognosis, especially when present bilaterally.[42]​ Intraocular hemorrhages (secondary to increased intracranial pressure) are seen in 10% to 40% of patients with SAH.[43]​ They cause visual loss in the affected eye. This is associated with worse prognosis and increased mortality.[43]​ Isolated dilation of one pupil and loss of the pupillary light reflex may indicate brain herniation as a result of rising intracranial pressure. A poor neurologic status on admission seems to predict cardiac abnormalities thought to be secondary to overwhelming sympathetic activation.[44][45][46][47]​​​​ Close monitoring of vital signs should be instituted (e.g., blood pressure, heart rate and rhythm, and respiratory rate).[37][48]​​​​​

In patients with aneurysmal SAH (aSAH) and unsecured aneurysm, frequent blood pressure (BP) monitoring and BP control with short acting medication(s) is recommended to avoid severe hypotension, hypertension, and BP variability.[37]

Tracheal intubation: animated demonstration
Tracheal intubation: animated demonstration

How to insert a tracheal tube in an adult using a laryngoscope.

Bag-valve-mask ventilation: animated demonstration
Bag-valve-mask ventilation: animated demonstration

How to use bag-valve-mask apparatus to deliver ventilatory support to adults. Video demonstrates the two-person technique.

​​ There is insufficient evidence to recommend a particular BP target.[37] Sudden, profound reduction of BP should be avoided.[37][101]​​ In patients who are receiving anticoagulants, emergency reversal with appropriate agents should be performed to prevent rebleeding.[37] Reversal strategies should follow current published standards for life-threatening bleeding.[37][102]​​​ If present, coagulopathy should be treated aggressively using prothrombin complex concentrate (PCC) or fresh frozen plasma (FPP), and vitamin K. See Anticoagulation management principles.

Electrolytes and fluids

Close monitoring and goal-directed treatment of volume status are reasonable to maintain euvolemia.[37][103][104][105]​​​​ Induction of hypertension and hypervolemia is potentially harmful because of the association with excess morbidity including cerebral edema, hemorrhagic transformation in areas of infarction, reversible leukoencephalopathy, myocardial infarction, and congestive heart failure.[37][39]​​[106][107][108][109]​​​​ Therefore, prophylactic hemodynamic augmentation should not be performed to reduce iatrogenic patient harm.[37]

Electrolyte imbalances (e.g., hyponatremia) are common and should be corrected.[37] If present, coagulopathy should be treated aggressively using prothrombin complex concentrate or fresh frozen plasma, and vitamin K. American Heart Association states that use of mineralocorticoids such as fludrocortisone is reasonable to treat natriuresis and hyponatremia, as supported by several RCTs.[37]​ However, although fludrocortisone use reduces excess sodium excretion, urine volume, and intravenous fluid use in patients with SAH, it has not been found to consistently affect outcome.[37][110][111][112][113] Some guidelines state there is insufficient evidence to support its use in maintaining normal serum sodium concentrations or improving functional outcome.[113] See Hyponatremia​.

Analgesia

Analgesia should be provided to conscious patients. Acetaminophen can be used as a first-line option.[39]​ For severe pain, opioids such as codeine or tramadol should be given.[39]​ If a patient is still in pain, morphine or oxycodone may be required.[39] Aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs) should be avoided before aneurysm occlusion.[39] Mental status also needs to be closely monitored, especially in patients at risk of acute hydrocephalus or vasospasm. Judicious use of analgesia is therefore recommended.

Anticonvulsants

Prophylactic use of anticonvulsants following SAH is controversial.[114][115]​​ 

US guidelines suggest that prophylactic anticonvulsants may be considered in patients with aSAH and high-seizure-risk features (i.e., ruptured middle cerebral artery aneurysm, high-grade SAH, intracranial hemorrhage, hydrocephalus, and cortical infarction).[37] These guidelines recommend against the routine use of anticonvulsants in patients with aSAH without high-seizure-risk features since phenytoin for seizure prophylaxis is associated with excess morbidity and mortality.[37][88][116]​​​ The risk of seizures is significantly lower after coil embolization than following surgical clipping of aneurysm.[37] Short-course treatment may be adequate prophylaxis, and some evidence suggests that it is better tolerated than a longer course.[87][117]​​​ Routine long-term use of anticonvulsants is not recommended, but may be considered for patients with known risk factors for delayed seizure disorder.[37] In patients with aSAH who present with seizures, treatment with anticonvulsants for ≤7 days is reasonable to reduce seizure-related complications in the perioperative period.[37] In patients with aSAH without prior epilepsy who present with seizures, treatment with anticonvulsants beyond 7 days is not effective for reducing future aSAH-associated seizure risk.[37][39][114]​​

There is some evidence that in the US levetiracetam may be the most commonly prescribed agent for the prevention of seizures following SAH.[118] One small prospective study comparing levetiracetam with phenytoin for seizure prophylaxis after neurologic injury (including SAH) found the same outcomes with respect to mortality and seizure control, but levetiracetam-treated patients experienced better long-term functional outcomes than those treated with phenytoin (as as evaluated by the Glasgow Outcome Scale-Extended and Disability Rating Scale).[119]

Nimodipine

Early initiation of enteral nimodipine (a calcium-channel blocker) is beneficial in preventing vasospasm, delayed cerebral ischemia and improving functional outcomes in patients with aneurysmal SAH.[37] [ Cochrane Clinical Answers logo ]

Post stabilization

Once stabilized, the patient should be admitted to a dedicated neurocritical care unit.[97] These units significantly reduce in-hospital mortality and length of stay.[120] On admission to ICU, neurologic status should be graded using scales such as the Hunt and Hess Scale or the World Federation of Neurological Surgeons (WFNS) Scale.[37] These scales are recommended to determine initial clinical severity and predict outcome.[37] The higher the grade, the poorer the outcome.[121] The WFNS scale is preferred over the Hunt and Hess scale; it is more reliable because it uses the GCS score in defining the mental status.[35]​ In contrast, the Hunt and Hess Scale grades level of consciousness into drowsiness, stupor, and deep coma.[35]​ The modified Fisher Scale can be used to document and grade the quantity and distribution of subarachnoid blood on admission CT.[94]​ Although not definitive, it helps to predict the potential risk of vasospasm, which is a serious complication.

Antitussives and stool softeners

Cough may be suppressed with antitussives to prevent potential rebleeding. Cough and cold medications that include opioids, such as codeine or hydrocodone, should not be used in children ages 18 years or younger as the risks (slowed or difficult breathing, misuse, abuse, addiction, overdose, and death) outweigh the benefits when used for cough in these patients.[122]​ Stool softeners are used routinely, as straining to defecate can potentially cause rebleeding.

Surgery and coil embolization

A neurosurgeon and interventional neuroradiologist should be involved in the decision about how to treat an aneurysm. Complete obliteration of the ruptured aneurysm is indicated whenever feasible to reduce the risk of rebleeding and retreatment.[37][123][124][125]​​ Most surgeons operate on patients with good neurologic status during the first 72 hours to prevent rebleeding, a practice that also seems to be associated with improved outcome.[126]  Treatment should be individualized according to patient-specific factors such as medical comorbidities and pre-hemorrhage functional status, and should incorporate shared decision-making with the family or surrogate decision makers.[37]

AHA/ASA recommends:[37]

  • In patients with high-grade aSAH, aneurysm treatment is reasonable, after careful discussion of likely prognosis with family members, to optimize patient outcome

  • In patients with aSAH and advanced age, aneurysm treatment is reasonable, after careful discussion of prognosis with family members, to improve survival and outcome.

  • In patients with aSAH who do not improve after correction of modifiable conditions and are deemed unsalvageable because of evidence of irreversible neurologic injury, treatment of the aneurysm is not beneficial.

Controversy exists over the choice between surgical clipping and endovascular coil embolization. The ruptured aneurysm should be evaluated by specialist(s) with endovascular and surgical expertise to determine the relative risks and benefits of surgical or endovascular treatment according to patient (e.g., age, neurologic status on admission, comorbid conditions) and aneurysm characteristics (e.g., size and location).[37] The results of a major international prospective and randomized trial have sparked major controversies.[127][128][129]​​ The International Subarachnoid Aneurysm Trial (ISAT) included over 1000 patients in each treatment group. At 1 year, 23.7% of patients were dead or dependent following coiling compared with 30.6% in the clipping group.[128] Criticisms of the study included uneven distribution of enrolled patients (almost all came from Europe), differing levels of expertise among the interventionists and surgeons, and enrollment criteria that aneurysms be considered suitable for either surgical or endovascular repair.[127] Long-term follow-up of patients enrolled in ISAT has revealed that despite an increased risk of recurrent bleeding in the coiling group, the 5-year death risk remained significantly lower compared with the clipping group.[130] Another publication assessing long-term follow-up (10 years and beyond) after ISAT concluded that despite a higher risk of rebleeding, the probability of disability-free survival was significantly greater in the endovascular group than in the neurosurgical group.[131]

​In surgical clipping, a craniotomy is performed to expose the aneurysm, and a clip is placed on its neck to exclude it from the circulation. Complications of clipping include aneurysm rupture, injury to vascular structures, postoperative stroke, and clipping of arterial perforators. A craniotomy is not needed for endovascular coil embolization. An arterial catheter is advanced to the aneurysm lumen where titanium coils are deposited. A thrombus forms in the lumen, excluding the aneurysm from the circulation. Ongoing technological advances have refined coil embolization of aneurysms, making it a therapeutic option for complex aneurysms that were only amenable to surgical clipping in the past.[132] Yet there remain drawbacks to coil embolization, mainly incomplete embolization and recurrences requiring reintervention.[133][134][135][136][137]​​ Potential adverse events of the procedure itself are stroke, vessel rupture, and dissection.

For patients with good-grade SAH from ruptured aneurysms of the anterior circulation equally suitable for both primary coiling and clipping, AHA/ASA recommends primary coiling in preference to clipping to improve 1-year functional outcome.[37][128][138]​​​​ However, the guideline notes both treatment options are reasonable in this patient group to achieve a favorable long-term outcome.[37]

AHA/ASA recommends coiling in preference to clipping in patients with aSAH from ruptured aneurysms of the posterior circulation that are amenable to coiling, to improve both short- and long-term outcomes.[37][138][139][140]​​

Patient age may inform the modality of treatment. For aSAH patients <40 years of age, clipping of the ruptured aneurysm might be considered the preferred mode of treatment to improve durability of the treatment and outcome. Longer life expectancy and better long-term protection from re-rupture favor consideration of clipping in younger patients.[37][128]​​​[141]​ However, for patients >70 years of age, the superiority of coiling or clipping to improve outcome is not well established.[37][128][142]​ 

For patients with aSAH deemed salvageable and with depressed level of consciousness due to large intraparenchymal hematoma, emergency clot evacuation should be performed to reduce mortality.[37]

Venous thromboembolism (VTE) prophylaxis

In patients with aSAH whose ruptured aneurysm has been secured, pharmacologic or mechanical venous (intermittent pneumatic compression) VTE prophylaxis is recommended to reduce the risk for VTE.[37] See Venous thromboembolism (VTE) prophylaxis​.

Other investigated therapies

Statins and magnesium sulfate have been investigated for their presumed neuroprotective effect in the treatment of SAH. However, neither has been shown to be beneficial in terms of mortality and clinical outcomes in SAH patients.[113][143][144][145][146]​​​​​​ AHA/ASA recommends against routine use of statin therapy or intravenous magnesium sulfate to improve outcomes.[37]

Endothelin receptor antagonists have not been shown to improve functional outcomes or mortality in meta-analysis of randomized controlled trials.[145][147] [ Cochrane Clinical Answers logo ] ​​ Several organizations strongly recommend against endothelin receptor antagonists based on this lack of benefit and an increased risk of adverse events.[113]​ The most common adverse effects in phase 3 trials included pulmonary complications related to fluid retention, hypotension, and anemia.[113]​ However, based on two Japanese phase 3 trials of endovascular coiling and surgical clipping clazosentan has been approved in Japan for the prevention of vasospasm, vasospasm-related cerebral infarction, and ischemic symptoms after aneurysmal SAH.​[148] In contrast to most other trials, the investigator found clazosentan resulted in a decrease in morbidity and mortality with no unexpected safety findings.[148]​ Endothelin receptor antagonists have not been approved for this indication in the US and Europe.​

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