Subarachnoid Hemorrhage (SAH)

Epidemiology

Demographic Features of Aneurysmal Subarachnoid Hemorrhage

  • Etiology: most subarachnoid hemorrhages originate from the rupture of saccular aneurysms
  • Incidence: 10-15 per 100k population
  • Mean Age: 55 y/o (most occur between 40-60 y/o)
  • Sex: slightly higher risk of aneurysmal subarachnoid hemorrhage in females than males
  • Race: higher risk of aneurysmal subarachnoid hemorrhage in African-Americans, than in Caucasians

Risk Factors for Aneurysmal Subarachnoid Hemorrhage

  • Estrogen Deficiency
  • Family History of Intracranial Aneurysms
  • Hypertension (see Hypertension, [[Hypertension]])
  • Moderate-Heavy Ethanol Abuse (see Ethanol, [[Ethanol]])
  • Tobacco Abuse (zee Tobacco, [[Tobacco]]): most important preventable risk factor for aneurysmal SAH
  • Use of Caffeine-Containing Medications (see Caffeine, [[Caffeine]])
  • Use of Sympathomimetics: in females

Etiology

  • Brain/Cervical Tumor
    • Epidemiology: rare etiology of SAH
  • Cerebral Amyloid Angiopathy
    • Epidemiology: most commonly occurs in older adults
    • Clinical: bleeding is usually localized to a single sulcus
  • Cerebral Vasculitis
    • Epidemiology: case reports
  • Cerebral Venous Thrombosis (see Cerebral Venous Thrombosis, [[Cerebral Venous Thrombosis]])
    • Epidemiology: rare etiology of SAH
  • Coagulopathy (see Coagulopathy, [[Coagulopathy]])
    • General Comments
      • Coagulopathy is a rare etiology of SAH: it is more commonly associated with intracerebral hemorrhage and subdural hematoma than with subarachnoid hemorrhage (see Intracerebral Hemorrhage, [[Intracerebral Hemorrhage]] and Subdural Hematoma, [[Subdural Hematoma]])
    • Acquired Vitamin K Deficiency (see Vitamin K, [[Vitamin K]])
    • Anticoagulation
      • Coumadin (see Coumadin, [[Coumadin]]): unclear if coumadin increases the risk of SAH [MEDLINE]
        • However, coumadin does appear to increase the severity of SAH, when it does occur
      • Factor IIa (Thrombin) Inhibitors (see Factor IIa Inhibitors, [[Factor IIa Inhibitors]])
      • Factor Xa Inhibitors (see Factor Xa Inhibitors, [[Factor Xa Inhibitors]])
      • Heparins
    • Antiphospholipid Antibody Syndrome (see Antiphospholipid Antibody Syndrome [[Antiphospholipid Antibody Syndrome]])
    • Antiplatelet Agents: unclear if antiplatelet agents increase the risk of SAH [MEDLINE]
      • However, antiplatelet agents appear to increase the severity of SAH when it does occur
    • Disseminated Intravascular Coagulation (DIC) (see Disseminated Intravascular Coagulation, [[Disseminated Intravascular Coagulation]])
    • Platelet Glycoprotein IIb/IIIa Receptor Antagonists (see Platelet Glycoprotein IIb IIIa Receptor Antagonists, [[Platelet Glycoprotein IIb IIIa Receptor Antagonists]])
    • Thrombocytopenia (see Thrombocytopenia, [[Thrombocytopenia]])
    • Thrombolytics (see Thrombolytics, [[Thrombolytics]])
  • Cocaine Abuse (see Cocaine, [[Cocaine]])
    • Epidemiology: associated with both aneurysmal and non-aneurysmal SAH
  • Infection
    • Inhalational Anthrax (see Bacillus Anthracis, [[Bacillus Anthracis]]): may be associated with hemorrhagic meningitis
  • Intracranial Aneurysm (see Intracranial Aneurysm, [[Intracranial Aneurysm]])
    • Epidemiology: saccular aneurysms account for most cases of SAH
    • Clinical: aneurysms may be occult in some cases (due to interpretive errors on studies, small aneurysm size, or obscuration of the aneurysm related to vasospasm, hematoma, or thrombosis within the aneurysm)
  • Intracranial Arterial Dissection
    • Vertebrobasilar Artery Dissection
  • Moyamoya Disease (see Moyamoya Disease, [[Moyamoya Disease]])
    • Epidemiology: associated with cerebral aneurysms which can rupture and produce SAH
      • Rarely SAH occurs due to rupture of fragile transdural anastomotic vessels
  • Perimesencephalic Non-Aneurysmal Subarachnoid Hemorrhage
    • Clinical: usually present with blood isolated to the perimesencephalic cisterns anterior to the brainstem
      • Extension into the ambient cisterns or basal parts of the sylvian fissures may occur
      • Absence of extension into the lateral sylvian fissure, anterior interhemispheric fissure, or lateral ventricles
  • Pituitary Apoplexy (see Panhypopituitarism, [[Panhypopituitarism]])
  • Post-Carotid Endarterectomy Cerebral Hyperperfusion Syndrome
    • Epidemiology: case reports
  • Posterior Reversible Encephalopathy Syndrome (PRES) (see Posterior Reversible Encephalopathy Syndrome, [[Posterior Reversible Encephalopathy Syndrome]])
    • Epidemiology: case reports
  • Reversible Cerebral Vasoconstriction Syndrome (RCVS) (see Reversible Cerebral Vasoconstriction Syndrome, [[Reversible Cerebral Vasoconstriction Syndrome]])
    • Epidemiology: case reports
  • Sickle Cell Disease (see Sickle Cell Disease, [[Sickle Cell Disease]])
  • Spinal Aneurysm
    • Epidemiology: rare etiology of SAH
  • Traumatic Brain Injury (TBI) (see Traumatic Brain Injury, [[Traumatic Brain Injury]])
    • Epidemiology: xxx
  • Vascular Malformation
    • Intracranial Vascular Malformation
      • Arteriovenous Malformation
      • Cavernous Malformation
      • Dural Arteriovenous Fistula
    • Spinal Vascular Malformation
      • Dural Arteriovenous Fistula

Physiology

Rebleeding

  • Rebleeding Following the Initial Aneurysal Subarachnoid Hemorrhage is Common: occurs in 5-10% of cases over the furst 72 hrs [MEDLINE]
  • Risk Factors for Rebleeding
    • Poor-grade SAH
    • Larger Aneurysm
    • Sentinel Bleeds
    • Those who Undergo Catheter Cerebral Angiogram Within 3-6 hrs of the Initial Bleed
  • Factors with No Data Supporting a Relationship to Risk of Rebleeding
    • Blood Pressure: modest BP elevation (SBP <160 mm Hg, MAP <110 mm Hg) is probably not associated with a risk of rebleeding [MEDLINE]

Diagnosis

Head CT (see Head Computed Tomography, [[Head Computed Tomography]])

  • Findings
    • Blood in Cerobrospinal Fluid Spaces
    • Hydrocephalus: may also be present
  • Sensitivity: detects 92% of SAH if performed within 24 hrs of onset of bleed

Recommendations for Aneurysmal Subarachnoid Hemorrhage (American Heart Association/American Stroke Association Aneurysmal SAH Management Guidelines, 2012) (Stroke, 2012) [MEDLINE]

  • Acute diagnostic workup should include noncontrast head CT, which, if nondiagnostic, should be followed by lumbar puncture (Class I; Level of Evidence B)

Head CT Angiogram (see xxxx, [[xxxx]])

  • Useful for Aeurysmal Detection and Presurgical Planning

Recommendations for Aneurysmal Subarachnoid Hemorrhage (American Heart Association/American Stroke Association Aneurysmal SAH Management Guidelines, 2012) (Stroke, 2012) [MEDLINE]

  • CTA may be considered in the workup of aSAH. If an aneurysm is detected by CTA, this study may help guide the decision for type of aneurysm repair, but if CTA is inconclusive, DSA is still recommended (except possibly in the instance of classic perimesencephalic aSAH) (Class IIb; Level of Evidence C)

Brain MRI with MR Angiogram (see Brain Magnetic Resonance Imaging, [[Brain Magnetic Resonance Imaging]])

  • Sensitivity/Specificity of Brain MRI
    • Brain MRI with proton density and FLAIR sequences may be as sensitive as head CT for the acute detection of SAH
    • Brain MRI FLAIR and T2 sequences have high sensitivity in patients with a subacute SAH presentations (>4 days from the bleed)
  • Brain MR Angiogram: useful for aneurysmal detection and presurgical planning

Recommendations for Aneurysmal Subarachnoid Hemorrhage (American Heart Association/American Stroke Association Aneurysmal SAH Management Guidelines, 2012) (Stroke, 2012) [MEDLINE]

  • Magnetic resonance imaging (fluid-attenuated inversion recovery, proton density, diffusion-weighted imaging, and gradient echo sequences) may be reasonable for the diagnosis of aSAH in patients with a nondiagnostic CT scan, although a negative result does not obviate the need for cerebrospinal fluid analysis (Class IIb; Level of Evidence C)

Lumbar Puncture (LP) (see Lumbar Puncture, [[Lumbar Puncture]])

  • Findings
    • Clearing of Blood in Later Tubes: unreliable means of distinguishing a traumatic lumbar puncture from SAH, since SAH can also manifest a clearing of blood in later tubes
      • This observation is really only useful if the initial tube has lots of blood and the last tube has no blood
    • Xanthochromia (Pink or Yellow Tint Due to Hemoglobin Degradation Products): RBC’s present (and not due to traumatic lumbar puncture)
      • Presence of xanthochromia indicates that blood has been in the cerebrospinal fluid for ≥2 hrs
      • Most sensitive 6 hrs after onset of bleed
      • Other potential cause of xanthochromia: increased cerebrospinal fluid protein (≥150 mg/dL), systemic hyperbilirubinemia (serum bilirubin >10-15 mg/dL), and traumatic lumbar puncture with >100k RBC/μL
      • Xanthochromia can last for 2 or more weeks

Cerebral Angiogram/Digital Subtraction Angiography (DSA) (see Cerebral Angiogram, [[Cerebral Angiogram]])

  • Technique: usually done via femoral arterial approach
  • Findings
    • Identification and Characterization of Aneurysm

Recommendations for Aneurysmal Subarachnoid Hemorrhage (American Heart Association/American Stroke Association Aneurysmal SAH Management Guidelines, 2012) (Stroke, 2012) [MEDLINE]

  • DSA with 3-dimensional rotational angiography is indicated for detection of aneurysm in patients with aSAH (except when the aneurysm was previously diagnosed by a noninvasive angiogram) and for planning treatment (to determine whether an aneurysm is amenable to coiling or to expedite microsurgery) (Class I; Level of Evidence B)

Electroencephalogram (EEG) (see Electroencephalogram, [[Electroencephalogram]])

  • May Be Useful to Define Seizure Activity in Some Cases

Clinical Manifestations

General Comments

Recommendations for Aneurysmal Subarachnoid Hemorrhage (American Heart Association/American Stroke Association Aneurysmal SAH Management Guidelines, 2012) (Stroke, 2012) [MEDLINE]

  • Aneurysmal SAH is a medical emergency that is frequently misdiagnosed. A high level of suspicion for Aneurysmal SAH should exist in patients with acute onset of severe headache (Class I; Level of Evidence B)
  • The initial clinical severity of Aneurysmal SAH should be determined rapidly by use of simple validated scales (eg, Hunt and Hess, World Federation of Neurological Surgeons), because it is the most useful indicator of outcome after Aneurysmal SAH (Class I; Level of Evidence B)

World Federation of Neurological Surgeons Subarachnoid Hemorrhage Grading Scale

  • Grade 1
    • GCS: 15
    • Motor Deficit: Absent
  • Grade 2
    • GCS: 13-14
    • Motor Deficit: Absent
  • Grade 3
    • GCS: 13-14
    • Motor Deficit: Present
  • Grade 4
    • GCS: 7-12
    • Motor Deficit: Absent or Present
  • Grade 5
    • GCS: 3-6
    • Motor Deficit: Absent or Present

Hunt and Hess Subarachnoid Hemorrhage Grading Scale

  • Grade 1: asymptomatic or mild headache and slight nuchal rigidity
  • Grade 2: severe headache, stiff neck, no neurologic deficit except cranial nerve palsy
  • Grade 3: drowsy or confused, mild focal neurologic deficit
  • Grade 4: stuporous, moderate or severe hemiparesis
  • Grade 5: coma, decerebrate posturing

Cardiovascular Manifestations

Arrhythmias

  • Epidemiology: occur in 35% of cases
  • Clinical

Electrocardiographic Abnormalities (see Electrocardiogram, [[Electrocardiogram]])

  • Epidemiology: EKG abnormalities occur in 25-75% of patients with SAH
  • Clinical
    • Prolonged QT (see Torsade, [[Torsade]]): common in SAH (present in 71% of cases)
    • ST Segment Changes
    • T-Wave Inversions

Hypertension (see Hypertension, [[Hypertension]])

  • Epidemiology: may be observed on presentation

Hypovolemia (see Hypovolemic Shock, [[Hypovolemic Shock]])

  • Epidemiology
    • Hypovolemia and Hyponatremia are Common in SAH
    • Hypovolemia is Associated with Increased Incidence of Cerebral Infarction and Worse Outcome [MEDLINE] [MEDLINE]
  • Physiology
    • Due to Cerebral Salt Wasting (see Cerebral Salt Wasting, [[Cerebral Salt Wasting]]: the diagnosis of cerebral salt wasting generally requires the presence of hypovolemia

Elevated Serum Brain Natriuretic Peptide (BNP) Elevation (se Elevated Serum Brain Natriuretic Peptide, [[Elevated Serum Brain Natriuretic Peptide]])

  • Epidemiology
    • Elevated Serum BNP Has Been Observed in SAH
    • Elevated Serum BNP is Associated with Increased Mortality in SAH (Neurology, 2009) [MEDLINE]
  • Physiology

    • BNP Likely Originates from Injured Cardiac Muscle, as BNP Levels are Associated with Myocardial Necrosis, Pulmonary Edema and Both Systolic/Diastolic Left Ventricular Dysfunction (Stroke, 2005) [MEDLINE]

    Elevated Serum Troponin (see Elevated Serum Troponin, [[Elevated Serum Troponin]])

  • Epidemiology

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    Takotsubo Cardiomyopathy (Stress-Induced Cardiomyopathy) (see Takotsubo Cardiomyopathy, [[Takotsubo Cardiomyopathy]])

    • Epidemiology
      • Left Ventricular Dysfunction Occurs in 10-20% of SAH Cases
    • Risk Factors
      • Elevated Troponin Levels (see Elevated Serum Troponin, [[Elevated Serum Troponin]])
      • Female Gender
      • Poor-Grade Subarachnoid Hemorrhage
      • Prior Stimulant Drug Use
    • Physiology: abnormal cerebral blood flow to the hippocampus/brain stem/basal ganglia (suggesting activation of these areas) -> excessive catecholamine release, resulting in sympathetic stimulation of the myocardium

    Echocardiographic Wall Motion Abnormalities (see Echocardiogram, [[Echocardiogram]])

    • Epidemiology
      • Echocardiographic Wall Motion Abnormalities Occur in 25% of SAH Cases
      • Echocardiographic Wall Motion Abnormalities are Associated with Worse Mortality in SAH (Neurology, 2009) [MEDLINE]
    • Physiology
      • Myocardial Injury Commonly Occurs in SAH
      • Mechanism: sympathetic stimulation and catecholamine discharge

    Endocrinologic Manifestations

    Adrenal Insufficiency (see Adrenal Insufficiency, [[Adrenal Insufficiency]])

    • Epidemiology: occurs in a minority of SAH patients
    • Clinical
      • Vasopressor-Unresponsive Hypotension (see Hypotension, [[Hypotension]])

    Hyperglycemia (see Hyperglycemia, [[Hyperglycemia]])

    • Epidemiology: common
      • Hyperglycemia on Admission is Associated with Poor-Grade of SAH and Worse Outcome

    Panhypopituitarism (see Panhypopituitarism, [[Panhypopituitarism]])

    • Epidemiology: incidence of panhypopituitarism occurring in SAH varies widely between studies

    Gastrointestinal Manifestations

    Nausea/Vomiting (see Nausea and Vomiting, [[Nausea and Vomiting]])

    • Clinical: may be associated with the onset of headache

    Hematologic Manifestations

    Anemia (see Anemia, [[Anemia]])

    • Epidemiology
      • Anemia with Hemoglobin <11 g/dL Occurs in >80% of Cases
      • On Average, Hemoglobin Decreases 3 g/dL After SAH

    Heparin-Induced Thrombocytopenia (HIT) (see Heparin-Induced Thrombocytopenia, [[Heparin-Induced Thrombocytopenia]])

    • Epidemiology
      • May Occur in Some Cases

    Neurologic Manifestations

    Hydrocephalus (see Hydrocephalus, [[Hydrocephalus]])

    • Epidemiology: common complication of SAH
    • Physiology: xxxx

    Increased Intracranial Pressure (ICP) (see Increased Intracranial Pressure, [[Increased Intracranial Pressure]])

    • Physiology
      • Due to Acute Hydrocephalus and Reactive Hyperemia After SAH
    • Diagnosis
      • External Ventricular Drain (EVD) (see External Ventricular Drain, [[External Ventricular Drain]]): generally indicated for patients with evidence of hydrocephalus (on head CT) or World Federation of Neurological Surgeons Subarachnoid Hemorrhage Grade ≥3

    Ischemic Cerebrovascular Accident (CVA) (see Ischemic Cerebrovascular Accident, [[Ischemic Cerebrovascular Accident]])

    • Epidemiology
      • Cerebral Infarction Demonstrated on Neuroimaging is Associated with Poorer Clinical Outcome [MEDLINE]

    Meningeal Signs

    • Epidemiology: may occur
    • Physiology
      • Breakdown of Blood Products within the Cerebrospinal Fluid, Leading to an Aseptic Meningitis
    • Clinical
      • Meningismus/Nuchal Rigidity (see Meningismus, [[Meningismus]])
        • Although Meningismus May Occur in Association with the Onset of Headache, It Typically Does Not Develop Until Several (4-6) Hours After the Initial Bleed: due to breakdown of blood products in the cerebrospinal fluid
      • Low Back Pain (see Back Pain, [[Back Pain]])
        • May Develop Several (4-6) Hours After the Initial Bleed: due to breakdown of blood products in the cerebrospinal fluid

    Photophobia (see Photophobia, [[Photophobia]])

    • Epidemiology: common

    Seizures (see Seizures, [[Seizures]])

    • Epidemiology
      • Seizures Occur in Only 1-7% of Cases After Initial Aneurysmal Rupture
      • When Seizures Occur in Patients with an Unsecured Aneurysm, They are Usually Due to a Aneurysmal Rebleeding
    • Risk Factors for Seizures
      • Intraparenchymal Hematoma/Infarction: possible risk factor
      • Surgical Aneurysm Repair in Patient >65 y/o
      • Thick Subarachnoid Clot
    • Clinical
      • Differentiation of True Seizures from Posturing is Crucial

    Severe Headache (see Headache, [[Headache]])

    • Epidemiology
      • Headache is a Common Presenting Symptom
    • Clinical Features
      • “Sentinel Headache”: 30-50% of patients report a history of a sudden/severe headache which precedes a major SAH by a period of 6-20 days
      • Abrupt Onset
      • Commonly Presents as the “Worse Headache of My Life”
      • Headache is Lateralized to Side of Aneurysm in 30% of Cases
      • Headache May Be Associated with Brief Loss of Consciousness/Meningismus/Nausea and Vomiting

    Vasospasm and Delayed Cerebral Ischemia (DCI)

    • Definitions
      • General Comments: since the current definitions of these entities are inconsistent, clinical trials instead should use radiographic evidence of cerebral infarction and functional outcome as the primary outcome measures
      • Vasospasm: post-SAH arterial narrowing, as demonstrated by radiographic images or ultrasound -> narrowing may produce cerebral ischemia or infarction
        • The Term “vasospasm” Defines a Finding on Diagnostic Studies
        • Vasospasm May Be Asymptomatic
      • Delayed Cerebral Ischemia (DCI): any neurological deterioration (hemiparesis, aphasia, altered consciousness), presumably related to ischemia, which persists for >1 hr and cannot be explained by other physiological abnormalities (on standard radiographic, electrophysiologic, or laboratories)
        • The Term “Delayed Cerebral Ischemia” Defines a Clinical Finding
        • Delayed Cerebral Ischemia May Be Asymptomatic: or at least difficult to detect in patients in poor neurologic condition or on sedation

    Vasospasm

    • Epidemiology: occurs after 72 hrs (peak at 7-8 days)
    • Risk Factors
      • Age <50
      • Higher Severity of SAH
      • Hyperglycemia (see Hyperglycemia, [[Hyperglycemia]])

    Pulmonary Manifestations

    Aspiration Pneumonia (see Aspiration Pneumonia, [[Aspiration Pneumonia]])

    • Epidemiology: common

    Atelectasis (see Atelectasis, [[Atelectasis]])

    • Epidemiology: common

    Neurogenic Pulmonary Edema/Acute Respiratory Distress Syndrome (ARDS) (see Neurogenic Pulmonary Edema, [[Neurogenic Pulmonary Edema]] and Acute Respiratory Distress Syndrome, [[Acute Respiratory Distress Syndrome]])

    • Epidemiology
      • Risk Factors for Pulmonary Complications After Subarachnoid Hemorrhage
        • Poor-Grade Subarachnoid Hemorrhage
    • Physiology: due to sympathetic hyperactivity or cardiac failure
    • Clinical
    • Prognosis
      • In General, Pulmonary Complications in SAH are Associated with Higher Degree of Symptomatic Vasospasm (Neurosurgery, 2003) [MEDLINE]
      • In General, Pulmonary Complications in SAH are Associated with Higher Mortality Rate (Neurosurgery, 2003) [MEDLINE]: however, at least some of the increased mortality risk is related to older age and worse clinical grade at admission
      • Acute Lung Injury in SAH is Associated with Increased ICU Length of Stay (Crit Care Med, 2006) [MEDLINE]

    Renal Manifestations

    Hyponatremia (see Hyponatremia, [[Hyponatremia]])

    • Epidemiology
      • Hyponatremia is the Most Common Electrolyte Imbalance in Aneurysmal SAH: occurs in 30-50% of cases
      • Hyponatremia Increases the Risk of Cerebral Ischemia in SAH, Even if Fluid Restriction is Not Applied (Ann Neurol, 1990) [MEDLINE]
    • Physiology
      • Cerebral Salt Wasting and Syndrome of Inappropriate Anti-Diuretic Hormone Secretion (SIADH) (see Cerebral Salt Wasting, [[Cerebral Salt Wasting]] and Syndrome of Inappropriate Antidiuretic Hormone Secretion, [[Syndrome of Inappropriate Antidiuretic Hormone Secretion]])
        • Both Cerebral Salt Wasting and SIADH May Exist in the Same Patient: with excessive urine output and simultaneous excessive free water retention (Anesth Analg, 2009) [MEDLINE]
        • The Clinical Entity of Cerebral Salt Wasting Was First Described in 1950 (While SIADH Was First Described in 1959)
        • Diagnosis of Cerebral Salt Wasting Generally Requires the Presence of Hypovolemia, While the Diagnosis of SIADH Requires the Presence of Euvolemia or Modest Hypervolemia

    Vascular Manifestations

    Deep Venous Thrombosis (DVT) (see Deep Venous Thrombosis, [[Deep Venous Thrombosis]])

    • Epidemiology
      • Incidence of DVT in SAH is 1.5-18%
    • Risk Factors for DVT
      • Poor-Grade Subarachnoid Hemorrhage
    • Physiology: SAH induces a prothrombotic state

    Other Manifestations

    Fever (see Fever, [[Fever]])

    • Epidemiology: occurs in 41-72% of cases
    • Risk Factors for Fever
      • Intraventricular Hemorrhage
      • Poor Hunt–Hess Grade SAH
    • Physiology: due to a non-infectious, systemic inflammatory reaction
    • Prognosis
      • Fever is Associated with Increased Incidence of Cerebral Infarction
      • Fever is Associated with Worse Outcome

    Prevention

    Recommendations for Aneurysmal Subarachnoid Hemorrhage (American Heart Association/American Stroke Association Aneurysmal SAH Management Guidelines, 2012) (Stroke, 2012) [MEDLINE]

    • Treatment of high blood pressure with antihypertensive medication is recommended to prevent ische- mic stroke, intracerebral hemorrhage, and cardiac, renal, and other end-organ injury (Class I; Level of Evidence A)
    • Hypertension should be treated, and such treatment may reduce the risk of Aneurysmal SAH (Class I; Level of Evidence B)
    • Tobacco use and alcohol misuse should be avoided to reduce the risk of Aneurysmal SAH (Class I; Level of Evidence B)
    • In addition to the size and location of the aneurysm and the patient’s age and health status, it might be reasonable to consider morphological and hemodynamic characteristics of the aneurysm when discussing the risk of aneurysm rupture (Class IIb; Level of Evidence B)
    • Consumption of a diet rich in vegetables may lower the risk of Aneurysmal SAH (Class IIb; Level of Evidence B)
    • It may be reasonable to offer noninvasive screening to patients with familial (at least 1 first-degree relative) Aneurysmal SAH and/or a history of Aneurysmal SAH to evaluate for de novo aneurysms or late regrowth of a treated aneurysm, but the risks and benefits of this screening require further study (Class IIb; Level of Evidence B)
    • After any aneurysm repair, immediate cerebrovascular imaging is generally recommended to identify remnants or recurrence of the aneurysm that may require treatment (Class I; Level of Evidence B)

    Treatment

    General Hospital Care of Subarachnoid Hemorrhage

    Clinical Data

    • Management of Subarachnoid Hemorrhage in High-Volume Centers
      • Only 15% of SAH Patients are Transferred From the Lowest Volume Centers and Only 4.5% are Sent to the Highest Volume Centers [MEDLINE]
      • Mortality is 10-20% Higher at Low Volume Centers [MEDLINE]
      • SAH Should Be Therefore Treated at High-Volume Centers [MEDLINE]: due to need for neurointensive care unit, neurointensivists, vascular neurosurgeons and interventional neuroradiologists

    Recommendations for Aneurysmal Subarachnoid Hemorrhage (American Heart Association/American Stroke Association Aneurysmal SAH Management Guidelines, 2012) (Stroke, 2012) [MEDLINE]

    • Low-volume hospitals (eg, <10 aSAH cases per year) should consider early transfer of patients with aSAH to high-volume centers (eg, >35 aSAH cases per year) with experienced cerebrovascular sur- geons, endovascular specialists, and multidisciplinary neuro-intensive care services (Class I; Level of Evidence B)
    • The risk of early aneurysm rebleeding is high, and rebleeding is associated with very poor outcomes. Therefore, urgent evaluation and treatment of patients with suspected Aneurysmal SAH is recommended (Class I; Level of Evidence B)
    • Annual monitoring of complication rates for surgical and interventional procedures is reasonable (Class IIa; Level of Evidence C)
    • A hospital credentialing process to ensure that proper training standards have been met by indi- vidual physicians treating brain aneurysms is reasonable (Class IIa; Level of Evidence C)

    Anemia Management (see Anemia, [[Anemia]])

    Recommendations (Neurocritical Care Society Guidelines, 2011) [MEDLINE]

    • Minimize Blood Loss
    • Maintain Hemoglobin >8-10 g/dL: higher targets may be required for patient with delayed cerebral ischemia, but data are lacking

    Recommendations for Aneurysmal Subarachnoid Hemorrhage (American Heart Association/American Stroke Association Aneurysmal SAH Management Guidelines, 2012) (Stroke, 2012) [MEDLINE]

    • The Use of Packed Red Blood Cell Transfusion to Treat Anemia Might Be Reasonable in Patients with Aneurysmal SAH Who are at Risk of Cerebral Ischemia (Class IIb Recommendation, Level of Evidence B)
      • The Optimal Hemoglobin Goal is Undetermined (Class IIb Recommendation, Level of Evidence B)

    Aneurysmal Repair

    Indications

    Techniques

    • Coil Embolization
    • Microsurgical Clip Ligation

    Clinical Efficacy

    • Aneurysmal Repair Markedly Decreases the Risk of Aneurysmal Rebleeding: clip ligation is slightly more efficacious than coil embolization in preventing rebleeding [MEDLINE]

    Recommendations (Neurocritical Care Society Guidelines, 2011) [MEDLINE]

    • Early Aneurysm Repair is Recommended to Prevent Rebleeding

    Recommendations for Aneurysmal Subarachnoid Hemorrhage (American Heart Association/American Stroke Association Aneurysmal SAH Management Guidelines, 2012) (Stroke, 2012) [MEDLINE]

    • Management Decisions
      • Determination of aneurysm treatment, as judged by both experienced cerebrovascular surgeons and endovascular specialists, should be a multidisciplinary decision based on characteristics of the patient and the aneurysm (Class I; Level of Evidence C)
    • Timing of Intervention
      • Surgical clipping or endovascular coiling of the ruptured aneurysm should be performed as early as feasible in the majority of patients to reduce the rate of rebleeding after Aneurysmal SAH (Class I; Level of Evidence B)
    • Technique
      • Complete obliteration of the aneurysm is recommended whenever possible (Class I; Level of Evidence B)
      • For patients with ruptured aneurysms judged to be technically amenable to both endovascular coiling and neurosurgical clipping, endovascular coiling should be considered (Class I; Level of Evidence B)
      • In the absence of a compelling contraindication, patients who undergo coiling or clipping of a ruptured aneurysm should have delayed follow-up vascular imaging (timing and modality to be individualized), and strong consideration should be given to retreatment, either by repeat coiling or microsurgical clipping, if there is a clinically significant (eg, growing) remnant (Class I; Level of Evidence B)
      • Microsurgical clipping may receive increased consideration in patients presenting with large (>50 mL) intraparenchymal hematomas and middle cerebral artery aneurysms. Endovascular coiling may receive increased consideration in the elderly ( 70 years of age), in those presenting with poor-grade (World Federation of Neurological Surgeons classi- fication IV/V) aSAH, and in those with aneurysms of the basilar apex (Class IIb; Level of Evidence C)
    • Aneurysmal Stenting
      • Stenting of a ruptured aneurysm is associated with increased morbidity and mortality, and should only be considered when less risky options have been excluded (Class III; Level of Evidence C)
    • Anesthesia Management During Surgical/Endovascular Management
      • Minimization of the degree and duration of intraop- erative hypotension during aneurysm surgery is probably indicated (Class IIa; Level of Evidence B)
      • There are insufficient data on pharmacological strategies and induced hypertension during temporary ves- sel occlusion to make specific recommendations, but there are instances when their use may be considered reasonable (Class IIb; Level of Evidence C)
      • Induced hypothermia during aneurysm surgery is not routinely recommended but may be a reasonable option in selected cases (Class III; Level of Evidence B)
      • Prevention of intraoperative hyperglycemia during aneurysm surgery is probably indicated (Class IIa; Level of Evidence B)
      • The use of general anesthesia during endovascular treatment of ruptured cerebral aneurysms can be beneficial in selected patients (Class IIa; Level of Evidence C)

    Anticonvulsants

    Agents

    Recommendations (Neurocritical Care Society Guidelines, 2011) [MEDLINE]

    • Consider Anticonvulsant Prophylaxis for Short Course (3-7 Days)
      • Avoid Phenytoin (Dilantin) (see Phenytoin, [[Phenytoin]])
    • Anticonvulsant Use in Patients with Seizures Occurring After Presentation: standard management
    • Continuous EEG Monitoring (see Electroencephalogram, [[Electroencephalogram]]): may be considered in patients with poor-grade SAH who fail to improve or have neurological deterioration of unclear etiology

    Recommendations for Aneurysmal Subarachnoid Hemorrhage (American Heart Association/American Stroke Association Aneurysmal SAH Management Guidelines, 2012) (Stroke, 2012) [MEDLINE]

    • The use of prophylactic anticonvulsants may be considered in the immediate posthemorrhagic period (Class IIb; Level of Evidence B)
    • The routine long-term use of anticonvulsants is not recommended (Class III; Level of Evidence B) but may be considered for patients with known risk factors for delayed seizure disorder, such as prior seizure, intracerebral hematoma, intractable hypertension, infarction, or aneurysm at the middle cerebral artery (Class IIb; Level of Evidence B)

    Anti-Fibrinolytic Therapy

    Agents

    Clinical Efficacy

    • Anti-Fibrinolytic Therapy Significantly Decreases the Risk of Rebleeding , But Does Not Impact Outcome: likely due to higher incidence of cerebral ischemia with anit-fibrinolytic thearpy
    • Anti-Fibrinolytic Therapy Also Increases the Risk of Deep Venous Thrombosis (see Deep Venous Thrombosis, [[Deep Venous Thrombosis]]) [MEDLINE]

    Recommendations (Neurocritical Care Society Guidelines, 2011) [MEDLINE]

    • Early Short Course of Anti-Fibrinolytics May Be Considered Prior to Aneurysmal Repair: begin at diagnosis and continue until aneurysmal reapir (or 72 hrs, whichever is shorter)
    • Avoid Delayed Start of Anti-Fibrinolytics (>48 hrs After Bleed) or Prolonged Anti-Fibrinolytics (>3 Days): since the risk of rebleeding during this later period is less
    • Avoid Anti-Fibrinolytics in Patients with Risk Factors for Thromboembolic Complications

    Recommendations for Aneurysmal Subarachnoid Hemorrhage (American Heart Association/American Stroke Association Aneurysmal SAH Management Guidelines, 2012) (Stroke, 2012) [MEDLINE]

    • For patients with an unavoidable delay in obliteration of aneurysm, a significant risk of rebleeding, and no compelling medical contraindications, short-term (<72 hours) therapy with tranexamic acid or aminocaproic acid is reasonable to reduce the risk of early aneurysm rebleeding (Class IIa Recommendation, Level of Evidence B)

    Antiplatelet Therapy

    Rationale

    • Antiplatelet Therapy Decreases the Risk of Delayed Cerebral Ischemia

    Agent

    Clinical Efficacy

    • Meta-Analysis Examining Antiplatelet Therapy (Cochrane Database Syst Rev, 2007) [MEDLINE]: antiplatelet therapy was associated with a non-significant trend toward improved outcome
      • Antiplatelet therapy had a small non-significant reduction in brain ischemia
      • Antiplatelet therapy had a non-significant increase in hemorrhagic complications

    Nutrition Support

    • Aspiration Precautions
    • Speech Therapy with Swallowing Evaluation

    Venous Thromboembolism Prophylaxis (see Deep Venous Thrombosis, [[Deep Venous Thrombosis]])

    Clinical Efficacy

    • Meta-Analysis of DVT Prophylaxis in Mixed Neurosurgical Population (Chest, 2008) [MEDLINE]
      • SCD’s, Unfractionated Heparin, and Low Molecular Weight Heparin were Similarly Effective in Preventing DVT
      • There Was a Trend Toward Higher Rates of Intracerebral Hemorrhage and Non-Cerebral Minor Hemorrhage with Low Molecular Weight Heparin, as Compared to SCD’s and Unfractionated Heparin

    Recommendations (Neurocritical Care Society Guidelines, 2011) [MEDLINE]

    • DVT Prophylaxis with Sequential Compression Devices (SCD’s) Should Be Used in All Patients
    • Pharmacologic Prophylaxis Should Be Withheld in Patients with Unsecured Aneurysms Who are Expected to Undergo Surgery
    • Pharmacologic Prophylaxis with Unfractionated Heparin Can Be Started 24 hrs Post-Op
    • Unfractionated Heparin/Low Molecular Weight Heparin Prophylaxis Should Be Withheld 24 hrs Before/After Intracranial Procedures
    • Recommended Duration of DVT Prophylaxis is Unclear

    Recommendations for Aneurysmal Subarachnoid Hemorrhage (American Heart Association/American Stroke Association Aneurysmal SAH Management Guidelines, 2012) (Stroke, 2012) [MEDLINE]

    • Deep Venous Thrombosis is a Relatively Frequent Complication After Aneurysmal SAH
      • Early Identification and Targeted Treatment are Recommended, But Further Research is Needed to Identify the Ideal Screening Paradigm (Class I Recommendation, Level of Evidence B)

    Management of Heparin-Induced Thrombocytopenia (HIT) (see Heparin-Induced Thrombocytopenia, [[Heparin-Induced Thrombocytopenia]])

    Recommendations for Aneurysmal Subarachnoid Hemorrhage (American Heart Association/American Stroke Association Aneurysmal SAH Management Guidelines, 2012) (Stroke, 2012) [MEDLINE]

    • Heparin-Induced Thrombocytopenia is a Relatively Frequent Complication After Aneurysmal SAH
      • Early Identification and Targeted Treatment are Recommended, But Further Research is Needed to Identify the Ideal Screening Paradigm (Class I Recommendation, Level of Evidence B)

    Fever Management (see Fever, [[Fever]])

    Recommendations (Neurocritical Care Society Guidelines, 2011) [MEDLINE]

    • Routine Surveillance for Sources of Fever
      • Treat Source Promptly
    • Anti-Pyretics: first line therapy
      • Acetaminophen (Tylenol) (see Acetaminophen, [[Acetaminophen]])
      • Ibuprofen (Motrin) (see Ibuprofen, [[Ibuprofen]])
    • Surface Cooling: used in cases where anti-pyretics are ineffective
    • Intravascular Cooling: used in cases where anti-pyretics are ineffective
    • Monitoring/Treatment of Shivering

    Recommendations for Aneurysmal Subarachnoid Hemorrhage (American Heart Association/American Stroke Association Aneurysmal SAH Management Guidelines, 2012) (Stroke, 2012) [MEDLINE]

    • Aggressive Control of Fever to a Target of Normothermia by the Use of Standard or Advanced Temperature Modulating Systems is Reasonable in the Acute Phase of Aneurysmal SAH (Class IIa, Level of Evidence B)

    Glucose Management

    Recommendations (Neurocritical Care Society Guidelines, 2011) [MEDLINE]

    • Avoid Hypoglycemia (<80 mg/dL)
    • Avoid Hyperglycemia (>200 mg/dL)
    • If Cerebral Microdialysis is Being Used: serum glucose may be adjusted to avoid cerebral hypoglycemia

    Recommendations for Aneurysmal Subarachnoid Hemorrhage (American Heart Association/American Stroke Association Aneurysmal SAH Management Guidelines, 2012) (Stroke, 2012) [MEDLINE]

    • Careful Glucose Management with Strict Avoidance of Hypoglycemia is Recommended in Aneurysmal SAH (Class IIb, Level of Evidence B)

    Blood Pressure Management

    Agents

    • Nicardipine (Cardene) (see Nicardipine, [[Nicardipine]]): most commonly used agent

    Considerations if Intracranial Pressure (ICP) Monitoring is Not Employed

    • Alert Patient (Without ICP Measurement): cerebral perfusion pressure is deemed to be adequate -> lowering blood pressure in this setting may decrease the risk of re-rerupture
    • Obtunded Patient (Without ICP Measurement): withhold antihypertensive therapy -> lowering blood pressure in this setting may be hazardous, since this may result in decreased cerebral perfusion pressure

    Clinical Efifcacy

    • Prospective Randomized Trial Comparing Hypertensive/Hypervolemic/Hemodilution (Hyperdynamic) Therapy with Normovolemic Therapy (Neurosurgery, 2001) [MEDLINE]: n = 32
      • No Difference with Respect to Cerebral Vasospasm or Outcome at 1 Year
      • Hyperdynamic Group Had Higher Costs and Complication Rate

    Recommendations (Neurocritical Care Society Guidelines, 2011) [MEDLINE]

    • In Unsecured, Recently Ruptured Aneurysms: target MAP <110
      • Avoid Hypotension (see Hypotension, [[Hypotension]])
      • Use Pre-Morbid Baseline Blood Pressure as a Guide to Refine the Blood Pressure Target

    Recommendations for Aneurysmal Subarachnoid Hemorrhage (American Heart Association/American Stroke Association Aneurysmal SAH Management Guidelines, 2012) (Stroke, 2012) [MEDLINE]

    • Between the time of aSAH symptom onset and aneurysm obliteration, blood pressure should be controlled with a titratable agent to balance the risk of stroke, hypertension-related rebleeding, and maintenance of cerebral perfusion pressure (Class I; Level of Evidence B)
    • The magnitude of blood pressure control to reduce the risk of rebleeding has not been established, but a decrease in systolic blood pressure to <160 mm Hg is reasonable (Class IIa; Level of Evidence C)

    Intravascular Volume Management

    • Techniques to Monitor Intravascular Volume Status
      • Central Venous Pressure (CVP) (see Hemodynamics, [[Hemodynamics]]): unreliable indicator of intravascular volume status [MEDLINE] [MEDLINE]
      • Swan-Ganz Catheter (see Swan-Ganz Catheter, [[Swan-Ganz Catheter]]): not usually necessary
      • FloTrac Assessment of Cardiac Index in Post-Operative SAH is Inferior to Thermodilution Cardiac Output (see FloTrac, [[FloTrac]]) [MEDLINE]
      • Echocardiographic Assessment of Inferior Vena Cava Distensibility May Be a Better Predictor of Fluid Responsiveness in SAH (see Echocardiogram, [[Echocardiogram]]) [MEDLINE]

    Clinical Efifcacy

    • Prospective Randomized Trial Comparing Hypertensive/Hypervolemic/Hemodilution (Hyperdynamic) Therapy with Normovolemic Therapy (Neurosurgery, 2001) [MEDLINE]: n = 32
      • No Difference with Respect to Cerebral Vasospasm or Outcome at 1 Year
      • Hyperdynamic Group Had Higher Costs and Complication Rate

    Recommendations (Neurocritical Care Society Guidelines, 2011) [MEDLINE]

    • Euvolemia is Recommended: this is especially true in the setting of neurogenic pulmonary edema/ARDS
      • Avoid Hypovolemia: due to risk of increased harm
      • Avoid Hypervolemia: due to risk of cerebral infarction
    • Normal Saline is the Preferred Agent to Maintain Euvolemia (see Normal Saline, [[Normal Saline]])
    • In Cases with Persistent Negative Fluid Balance Despite Standard Measures, Fludrocortisone or Hydrocortisone May Be Considered (see Fludrocortisone, [[Fludrocortisone]] and Hydrocortisone, [[Hydrocortisone]])

    Recommendations for Aneurysmal Subarachnoid Hemorrhage (American Heart Association/American Stroke Association Aneurysmal SAH Management Guidelines, 2012) (Stroke, 2012) [MEDLINE]

    • Administration of Large Volumes of Hypotonic Intravenous Fluid and Intravascular Volume Contraction are Not Recommended After Aneurysmal SAH (Class III Recommendation, Level of Evidence B)
    • Monitoring Volume Status in Certain Patients with Recent Aneurysmal SAH by Some Combination of Central Venous Pressure, Pulmonary Capillary Wedge Pressure (PCWP), and Fluid Balance is Reasonable (Class IIa Recommendation, Level of Evidence B)
      • Treatment of Volume Contraction with Intravenous Crystalloid/Colloid is Reasonable (Class IIa Recommendation, Level of Evidence B)

    Hyponatremia Management (see Hyponatremia, [[Hyponatremia]])

    Clinical Data

    • Retrospective Study of the Impact of Fluid Restriction in SAH (Ann Neurol, 1985) [MEDLINE]
      • Fluid Restriction Increases the Risk of Cerebral Infarction in SAH
    • Data from Traumatic Brain Injury (TBI) Suggests that Hypertonic Saline Lowers ICP and May Improve Cerebral Perfusion (see Traumatic Brain Injury, [[Traumatic Brain Injury]])
    • Limited Data in in Poor-Grade SAH Suggests Clinical Benefit from 23.5% Hypertonic Saline (Stroke, 2010) [MEDLINE]

    Recommendations (Neurocritical Care Society Guidelines, 2011) [MEDLINE]

    • Do Not Use Fluid Restriction to Treat Hyponatremia in SAH (Strong Recommendation, Weak Quality Evidence)
    • Minimize Free Water Intake (Strong Recommendation, Very Low Quality Evidence)
    • Early Treatment with Hydrocortisone or Fludrocortisone May Be Used to Limit Natriuresis and Hyponatremia (Weak Recommendation, Moderate Quality Evidence) (see Hydrocortisone, [[Hydrocortisone]] and Fludrocortisone, [[Fludrocortisone]])
    • Hypertonic Saline May Be Used to Correct Hyponatremia (Strong Recommendation, Very Low Quality Evidence) (see Hypertonic Saline, [[Hypertonic Saline]])
    • While Vasopressin-Receptor Antagonists May Be Considered to Correct Hyponatremia, Extreme Caution Should Be Exercised to Avoid Hypovolemia (Strong Recommendation, Weak Quality Evidence) (see Conivaptan, [[Conivaptan]] and Tolvaptan, [[Tolvaptan]])

    Recommendations for Aneurysmal Subarachnoid Hemorrhage (American Heart Association/American Stroke Association Aneurysmal SAH Management Guidelines, 2012) (Stroke, 2012) [MEDLINE]

    • Administration of Large Volumes of Hypotonic Intravenous Fluid and Intravascular Volume Contraction are Not Recommended After Aneurysmal SAH (Class III Recommendation, Level of Evidence B)
    • Use of Fludrocortisone Acetate and Hypertonic Saline Solution is Reasonable for Preventing and Correcting Hyponatremia After Aneurysmal SAH (Class IIa Recommendation, Level of Evidence B)

    Hypothalamic Dysfunction Management

    Recommendations (Neurocritical Care Society Guidelines, 2011) [MEDLINE]

    • Management of Adrenal Insufficiency with Standard Therapy
    • Fludrocortisone May Be Used to Inhibit Natriuresis and Hyponatremia: see Hyponatremia Management above
    • Consider Stress-Dose Corticosteroids for Patients with Vasospasm and Vasopressor-Unresponsive Hypotension

    Increased Intracranial Pressure Management (see Increased Intracranial Pressure, [[Increased Intracranial Pressure]])

    External Ventricular Drain (EVD) (see External Ventricular Drain, [[External Ventricular Drain]])

    • Indications
      • Evidence of Hydrocephalus (on Head CT)
      • World Federation of Neurological Surgeons Subarachnoid Hemorrhage Grade ≥3
    • Rationale: allows for intracranial pressure monitoring and treatment by drainage of cerebrospinal fluid

    Hydrocephalus Management (see Hydrocephalus, [[Hydrocephalus]])

    Recommendations for Aneurysmal Subarachnoid Hemorrhage (American Heart Association/American Stroke Association Aneurysmal SAH Management Guidelines, 2012) (Stroke, 2012) [MEDLINE]

    • SAH-Associated acute symptomatic hydrocephalus should be managed by cerebrospinal fluid diversion (EVD or lumbar drainage, depending on the clinical scenario) (Class I; Level of Evidence B)
    • Aneurysmal SAH-associated chronic symptomatic hydrocephalus should be treated with permanent cerebrospinal fluid diversion (Class I; Level of Evidence C)
    • Weaning EVD over >24 hrs does not appear to be effective in reducing the need for ventricular shunting (Class III; Level of Evidence B)
    • Routine fenestration of the lamina terminalis is not useful for reducing the rate of shunt-dependent hydrocephalus and therefore should not be routinely performed (Class III Recommendation, Level of Evidence B)

    Serum Magnesium Level Management

    Rationale

    • Magnesium Acts as a Non-Competitive Calcium Antagonist: may have vascular and potentially neuroprotective effects

    Agents

    Recommendations (Neurocritical Care Society Guidelines, 2011) [MEDLINE]

    • Induction of Hypermagnesemia is Not Recommended
    • Avoid Hypomagnesemia

    Respiratory Support

    • Hyperventilation is Generally Avoided Since it May Precipitate or Exacerbate Vasospasm

    Other Measures

    • Decompressive Craniectomy (see Decompressive Craniectomy, [[Decompressive Craniectomy]])
      • May Be Required in Some Cases with Severe Cerebral Edema
    • Mannitol (see Mannitol, [[Mannitol]]): osmotic diuretic

    Statins (see HMG-CoA Reductase Inhibitors, [[HMG-CoA Reductase Inhibitors]])

    • Recommendations (Neurocritical Care Society Guidelines, 2011) [MEDLINE]
      • Patients on Statins Prior to Presentation with Aneurysmal SAH Should Have Statin Continued in the Acute Phase
      • Consider Acute Statin Therapy in Statin-Naive Patients: may decrease the incidence of delayed cerebral ischemia after aneurysmal SAH

    Vasospasm and Delayed Cerebral Ischemia (DCI) Management

    Monitoring and General Management of Delayed Cerebral Ischemia

    • Recommendations (Neurocritical Care Society Guidelines, 2011) [MEDLINE]
      • Patients at Risk for Delayed Cerebral Ischemia Should Be Monitored in the ICU
      • Nimodipine (Nimotop) (see Nimodipine, [[Nimodipine]]): cerebral vessel vasodilator
        • Nimodipine Has Been Demonstrated to Improve Outcome, But Does Not Affect the Incidence or Either Angiographic or Symptomatic Vasospasm
        • Dose: 60 mg PO q4hrs begun within 4 days on onset and continued x 21 days
      • Transcranial Dopplers May Be Used to Monitor for Large Artery Vasospasm (see Transcranial Doppler Ultrasound, [[Transcranial Doppler Ultrasound]])
      • Imaging of Vascular Anatomy and/or Perfusion Can Be Used to Confirm a Diagnosis of DCI in Monitored Good-Grade Patients Who Exhibit a Change in Neurologic Exam or Trans-Cranial Doppler Studies (see Transcranial Doppler Ultrasound, [[Transcranial Doppler Ultrasound]])
      • Digital Subtraction Angiogram is the Gold Standard for Detection of Large Artery Vasospasm
      • High-Quality CT Angiogram Can Be Used For Vasospasm Screening: due to its high specificity, it may reduce the need for digital subtraction angiogram studies
      • EEG/Cerebral Microdialysis/CT Perfusion May Be Used to Monitor for Delayed Cerebral Ischemia
    • Recommendations for Aneurysmal Subarachnoid Hemorrhage (American Heart Association/American Stroke Association Aneurysmal SAH Management Guidelines, 2012) (Stroke, 2012) [MEDLINE]
      • Oral nimodipine should be administered to all patients with aSAH (Class I; Level of Evidence A)
      • Maintenance of euvolemia and normal circulating blood volume is recommended to prevent DCI (Class I; Level of Evidence B)
      • Prophylactic hypervolemia or balloon angioplasty before the development of angiographic spasm is not recommended (Class III; Level of Evidence B)
      • Transcranial Doppler is reasonable to monitor for the development of arterial vasospasm (Class IIa; Level of Evidence B)
      • Perfusion imaging with CT or magnetic resonance can be useful to identify regions of potential brain ischemia (Class IIa; Level of Evidence B)

    Hemodynamic Management of Delayed Cerebral Ischemia

    • Recommendations (Neurocritical Care Society Guidelines, 2011) [MEDLINE]
      • Maintain Euvolemia
      • Intravenous Normal Saline Infusion May Be Used as a Measure to Increase Cerebral Blood Flow in Advance of Other Interventions
      • Consider Trial of Induced Hypertension: proceed in a stepwise manner with assessment of neurologic function
        • If Nimodipine Induces Hypotension, Should Change to Lower Dose at a More Frequent Interval: if hypotension persists, may discontinue nimodipine
        • Choice of Vasopressor Should Be Based on Other Clinical Parameters
        • In Cases with Unsecured Aneurysm (Which Was Responsible for the Initial SAH), Caution Should Be Exercised with Induced Hypertension
      • Inotropic Support to Maintain Cardiac Output (Inotropes, Intra-Aortic Balloon Pump): may be considered in select cases
      • Avoid Hemodilution: except in cases of polycythemia
    • Recommendations for Aneurysmal Subarachnoid Hemorrhage (American Heart Association/American Stroke Association Aneurysmal SAH Management Guidelines, 2012) (Stroke, 2012) [MEDLINE]
      • Maintenance of euvolemia and normal circulating blood volume is recommended to prevent DCI (Class I; Level of Evidence B)
      • Induction of hypertension is recommended for patients with DCI unless blood pressure is elevated at baseline or cardiac status precludes it (Class I; Level of Evidence B)

    Endovascular Management of Delayed Cerebral Ischemia

    • Recommendations (Neurocritical Care Society Guidelines, 2011) [MEDLINE]
      • Balloon Angiplasty May Be Considered
      • Intra-Arterial Nicardipine May Be Considered (see Nicardipine, [[Nicardipine]]): may be used for vasospasm
      • Recommendations for Aneurysmal Subarachnoid Hemorrhage (American Heart Association/American Stroke Association Aneurysmal SAH Management Guidelines, 2012) (Stroke, 2012) [MEDLINE]
      • Cerebral angioplasty and/or selective intra-arterial vasodilator therapy is reasonable in patients with symptomatic cerebral vasospasm, particularly those who are not rapidly responding to hypertensive therapy (Class IIa; Level of Evidence B)

    Post-Admission Evaluation/Rehabilitation

    Recommendations for Aneurysmal Subarachnoid Hemorrhage (American Heart Association/American Stroke Association Aneurysmal SAH Management Guidelines, 2012) (Stroke, 2012) [MEDLINE]

    • After discharge, it is reasonable to refer patients with Aneurysmal SAH for a comprehensive evaluation, including cognitive, behavioral, and psychosocial assessments (Class IIa; Level of Evidence B)

    Prognosis

    • xxx

    Worse with age >50, aneurysm >10 mm, etc.


    References

    General

    • Avoiding pitfalls in the diagnosis of subarachnoid hemorrhage. N Engl J Med. 2000 Jan 6;342(1):29-36 [MEDLINE]
    • Aneurysmal subarachnoid hemorrhage. N Engl J Med. 2006 Jan 26;354(4):387-96 [MEDLINE]

    Epidemiology

    • Antiplatelet drugs and risk of subarachnoid hemorrhage: a population-based case-control study. J Thromb Haemost. 2010;8(7):1468 [MEDLINE]

    Diagnosis

    • Complications of Swan-Ganz catheterization for hemodynamic monitoring in patients with subarachnoid hemorrhage. Neurosurgery. 1995;37: 872–5 [MEDLINE]
    • Plasma B-type natriuretic peptide levels are associated with early cardiac dysfunction after subarachnoid hemorrhage. Stroke. 2005;36(7):1567. Epub 2005 Jun 9 [MEDLINE]
    • Evaluation of the FloTrac uncalibrated continuous cardiac output system for perioperative hemodynamic monitoring after subarachnoid hemorrhage. J Neurosurg Anesthesiol. 2009;21:218–25 [MEDLINE]
    • Inferior vena cava distensibility as a predictor of fluid responsiveness in patients with subarachnoid hemorrhage. Neurocrit Care. 2010;13:3–9 [MEDLINE]

    Clinical

    • Hyponatremia and cerebral infarction in patients with ruptured intracranial aneurysms: is fluid restriction harmful? Ann Neurol. 1985 Feb;17(2):137-40 [MEDLINE]
    • Volume depletion and natriuresis in patients with a ruptured intracranial aneurysm. Ann Neurol. 1985;18:211–6 [MEDLINE]
    • Hyponatremia is associated with cerebral ischemia in patients with aneurysmal subarachnoid hemorrhage. Ann Neurol. 1990;27:106–8 [MEDLINE]
    • Medical complications of aneurysmal subarachnoid hemorrhage: a report of the multicenter, cooperative aneurysm study. Participants of the Multicenter Cooperative Aneurysm Study. Crit Care Med. 1995; 23:1007–17 [MEDLINE]
    • Ultra-early rebleeding in spontaneous subarachnoid hemorrhage. J Neurosurg. 1996;84:35–42 [MEDLINE]
    • Hyponatraemia in a neurosurgical patient: syndrome of inappropriate antidiuretic hormone secretion versus cerebral salt wasting. Nephrol Dial Transplant. 2000;15:262–8 [MEDLINE]
    • Hyponatremia in critically ill neurological patients. Neurologist. 2003;9:290–300 [MEDLINE]
    • Pulmonary complications of aneurysmal subarachnoid hemorrhage. Neurosurgery. 2003;52:1025–31 [MEDLINE]
    • Neurogenic pulmonary edema and other mechanisms of impaired oxygenation after aneurysmal subarachnoid hemorrhage. Neurocrit Care. 2004;1:157–70 [MEDLINE]
    • Acute lung injury in patients with subarachnoid hemorrhage: incidence, risk factors, and outcome. Crit Care Med. 2006;34:196–202 [MEDLINE]
    • Neurogenic pulmonary edema in patients with subarachnoid hemorrhage. J Neurosurg Anesthesiol. 2008;20: 188–92 [MEDLINE]
    • Hyponatremia in neurological patients: cerebral salt wasting versus inappropriate antidiuretic hormone secretion. Intensive Care Med. 2008;34:125–31 [MEDLINE]
    • Impact of cardiac complications on outcome after aneurysmal subarachnoid hemorrhage: a meta-analysis. Neurology. 2009;72(7):635 [MEDLINE]
    • Endocrine response after severe subarachnoid hemorrhage related to sodium and blood volume regulation. Anesth Analg. 2009;108:1922–8 [MEDLINE]
    • Lower incidence of cerebral infarction correlates with improved functional outcome after aneurysmal subarachnoid hemorrhage. J Cereb Blood Flow Metab. 2011;31:1545–53 [MEDLINE]

    Treatment

    • Hyponatremia and cerebral infarction in patients with ruptured intracranial aneurysms: is fluid restriction harmful? Ann Neurol. 1985;17: 137–40 [MEDLINE]
    • Hypervolemic therapy prevents volume contraction but not hyponatremia following subarachnoid hemorrhage. Ann Neurol. 1992;31:543–50 [MEDLINE]
    • Prophylactic hyperdynamic postoperative fluid therapy after aneurysmal subarachnoid hemorrhage: a clinical, prospective, randomized, controlled study. Neurosurgery. 2001 Sep;49(3):593-605; discussion 605-6 [MEDLINE]
    • Outcomes after cerebral aneurysm clip occlusion in the United States: the need for evidence-based hospital referral. J Neurosurg. 2003;99:947–52 [MEDLINE]
    • International subarachnoid aneurysm trial (ISAT) of neurosurgical clipping versus endovascular coiling in 2143 patients with ruptured intracranial aneurysms: a randomised comparison of effects on survival, dependency, seizures, rebleeding, subgroups, and aneurysm occlusion. Lancet. 2005;366:809–17 [MEDLINE]
    • Antiplatelet therapy for aneurysmal subarachnoid haemorrhage. Cochrane Database Syst Rev, 2007 Oct 17;(4):CD006184 [MEDLINE]
    • Impact of a protocol for acute antifibrinolytic therapy on aneurysm rebleeding after subarachnoid hemorrhage. Stroke. 2008;39:2617–21 [MEDLINE]
    • Prevention of venous thromboembolism in neurosurgery: a metaanalysis. Chest. 2008;134:237–49 [MEDLINE]
    • Hypertonic saline in patients with poor-grade subarachnoid hemorrhage improves cerebral blood flow, brain tissue oxygen, and pH. Stroke. 2010;41(1):122 [MEDLINE]
    • 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. doi: 10.1161/STR.0b013e3182587839. Epub 2012 May 3 [MEDLINE]
    • 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. doi: 10.1007/s12028-011-9605-9 [MEDLINE]

    Prognosis

    • Association between subarachnoid hemorrhage outcomes and number of cases treated at California hospitals. Stroke. 2002; 33:1851–6 [MEDLINE]