Subarachnoid Hemorrhage

Extravasation of blood into the subarachnoid space between the arachnoid membrane and the pia mater. It is a neurological emergency associated with high morbidity and mortality. It can be due to Trauma (most common) or vascular malformation.

Primary Category
Neurocritical Care
Secondary Category


  • Extravasation of blood into the subarachnoid space between the arachnoid membrane and the pia mater.
  • It is a neurological emergency associated with high morbidity and mortality.


Traumatic SAH (Most Common Cause!)

Non-traumatic SAH:

  • Aneurysmal SAH (aSAH): 80- 85% of cases. Various types of aneurysms include
    • Saccular aneurysm (a.k.a berry aneurysm)
      • most common type of aneurysms with 5% prevalence.
      • Certain Genetic (connective tissue disorders like Ehler Danlos Syndrome, pseudoxanthoma elasticum, autosomal dominant polycystic kidney disease, familial aldosteronism type 1 and moya moya syndrome) and environmental (smoking, hypertension, estrogen deficiency etc) factors increase the risk of aneurysm formation
      • Rupture rate is ~ 3-25/100,000 population
      • Occurs at branch points of the main arteries of the circle of Willis.
      • Aneurysmal wall lacks an external elastic lamina and contain a very thin adventitia
    • Fusiform aneurysm
      • Occurs due to atherosclerosis
      • Entire circumference of the vessel is enlarged
      • Less likely to rupture
    • Mycotic Aneurysm
      • Occurs most commonly from infectious emboli in patients with infective endocarditis
      • Associated with high morbidity and mortality
  • Non-aneurysmal SAH: 15-20% of cases.
    • Perimesencephalic SAH: Most common type of non-traumatic/non-aneurysmal SAH. Characterized by a localized pattern of blood on CT in the perimesencephalic cisterns anterior to the brainstem with possible extension into the ambient cisterns or basal parts of the sylvian fissures. Normal cerebral angiography, and a benign course is characteristic. Causes include rupture of perforator artery in the posterior circulation, venous origin of blood, rupture of a cryptic vascular malformation, high cervical spinal dural arteriovenous fistula, cavernous angioma, capillary telangiectasia or possibly a small occult aneurysm in some cases.
    • Other causes of non-aneurysmal SAH: Subarachnoid extension of intraparenchymal hemorrhage, occult aneurysm, Intracranial or spinal vascular malformation (Arteriovenous (AV) malformation or dural AV fistula). Intracranial arterial dissection, cerebral vasculitis, Reversible Cerebral Vasoconstriction Syndrome (RCVS) and Posterior Reversible (leuko)Encephalopathy Syndrome (PRES)

Pathophysiology of Aneurysmal SAH

  • Rupture of an aneurysm is the cause of aneurysmal SAH
  • Rupture of an aneurysm releases blood directly into the cerebrospinal fluid (CSF) which then spreads quickly within the CSF leading to increase in intracranial pressure. The blood often spreads into the intraventricular space, but can also spread into the brain parenchyma or rarely, the subdural space, depending on the location of the aneurysm
  • Rebleeding is common and occurs most often within the first day.
  • Secondary events contributing to brain injury include (i) hydrocephalus due to obstruction of CSF flow or decreased reabsorption at the level of arachnoid granulations (ii) vasospasm and delayed cerebral ischemia (iii) increased in intracranial pressure and (iv) spreading cortical depolarization etc

Figure 1: Subarachnoid Hemorrhage on CT Scan

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Figure 1: CT image shows diffuse subarachnoid hemorrhage in all basal cisterns, bilateral sylvian fissures and inter-hemispheric fissure
Source: SAH: Case courtesy of Dr David Cuete, Case Link
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Clinical Presentation

  • Neck Stiffness.
  • Mass effect: Either from the aneurysm itself (e.g. 3rd nerve palsy with posterior communicating artery aneurysm) or as a consequence of increased intracranial pressure.
  • Intraocular hemorrhage: occurs in 20-40% of patients leading to visual disturbances
  • Focal neurological findings
  • Hypertension.
  • Cardiac dysfunction.
  • Pulmonary edema: Neurogenic type.

Table 1: Risk Factors

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Table 2A: Grading Severity of SAH - Initial CT Scan -Modified Fisher Scale

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Table 2B: Grading Severity of SAH - Initial Clinical presentations - Hunt & Hess Scale

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Differential Diagnosis

  • Intracranial hemorrhage.
  • Acute ischemic stroke.
  • Transient ischemic attack.
  • Migraine.
  • Meningitis.
  • Encephalitis.
  • Acute narrow angle closure glaucoma.
  • Reversible cerebral vasoconstriction syndrome.
  • Hypertensive encephalopathy.
  • Idiopathic intracranial hypertension.
  • Pituitary apoplexy.

Diagnostic Evaluation

  • Routine labs including CBC, CMP, coagulation panel, baseline troponin and CXR
  • Non-contrast CT Scan of head:
    • Sensitivity decreases with time. When performed within 6 hours of symptom onset, it has 100% sensitivity and specificity. Sensitivity decreases to 93% within 24 hours of onset, 80% at 3 days, and 50% at 1 week.
    • Findings can be negative in 10-15% of patients. False negative scan may be related to severe anemia or low volume of blood.
    • Location of SAH directly correlates with location of aneurysm. Generally, rupture of saccular aneurysm results in blood in the basal cisterns, sylvian fissure and the interhemispheric fissure.
    • May identify Hematoma or hydrocephalus that requires immediate urgent surgical interventions.
  • MRI of Head:
    • More sensitive than CT for chronic bleeding
  • Lumbar puncture:
    • Used when a non-contrast CT scan of the head is equivocal, negative or non-diagnostic.
    • Used in negative CT to rule out SAH.
    • Invasive, time-consuming.
    • Elevated RBCs in the CSF diagnostic for SAH.
    • Xanthochromia:
      • Yellow discoloration of CSF due to breakdown of hemoglobin into bilirubin.
      • Seen 12 hours after the onset of bleeding.
      • Observed in centrifuged CSF or by spectrophotometry.
      • Increased CSF pressure in 2/3rd of cases of SAH that helps in differentiating true SAH from traumatic taps.
  • Cerebral angiography and Multidetector CT angiography:
    • Identify an aneurysmal source of the bleed. Although Cerebral angiography(CA) and Multi detector CT angiography (MD CTA) have comparable sensitivity, CA is more useful for detection of small aneurysms or distal aneurysms such as mycotic aneurysms.
    • Provides information on cerebrovascular anatomy, aneurysm shape, size, orientation and relation to the parent artery and any other proximal branches


General Management

  • Treatment in high volume centers with an experienced team of neurosurgeons, endovascular specialists, interventional neuro-radiologists, and multi-disciplinary neurointensive care units.
  • Immediate resuscitation and stabilization of the patient.
  • Emergency neurosurgical consultation.
  • Intubation if concerned for airway protection or GCS <8.
  • Consideration of external ventricular drain if evidence of hydrocephalus
  • Admit patient to the ICU, preferably in the Neurological Critical care unit.
  • Reducing environmental noise to minimum until aneurysm is repaired.
  • Seizure prophylaxis and blood pressure control <140 mm hg until aneurysm secured
  • Antifibrinolytic agents (e.g aminocaproic acid) may be considered if unable to secure aneurysm within 24-48 hours
  • Adequate pain control
  • Intravenous fluid to keep patient euvolemic. Carefully monitor intake and urine output hourly
  • Calcium channel blocker: Nimodipine-60mg q4hr for 21 days.
  • BP Monitoring: After securing aneurysm, BP management is dependent on risk of vasospasm/delayed cerebral ischemia guided by clinical evaluation.
  • Blood glucose: administer sliding scale or continuous insulin infusion; Target glucose range 80-140mg/dl.
  • Fever: Temperature control to maintain normothermia.
  • Optimization of intracranial pressure using osmotic agents as needed (mannitol or hypertonic saline)
  • Sedation as needed for control of intracranial pressure or to maintain ventilator synchrony in intubated patients
  • Anxiolytic as needed to treat delirium
  • Control of nausea/vomiting as needed
  • Scheduled stool softeners to ensure regular bowel movements
  • Stress ulcer prophylaxis
  • DVT Prophylaxis: Pneumatic compression stockings and subcutaneous heparin or lovenox.
  • Bedside Swallowing assessment: oral or enteral feeding depending upon the condition.
  • Physical Therapy, Occupational Therapy, Speech and Cognitive Therapy consults
  • Nutritional consult to ensure adequate calorie intake

Definitive management of aneurysm

  • Surgical Clipping or endovascular coiling as early as possible

Long term effects

  • Many Survivors of SAH experience poor cognitive function, mood disorders, impaired daily activities, and lassitude.
  • 15 fold increased likelihood of developing another episode of hemorrhagic SAH in comparison to the general population.
  • Long term risk of dying from cardiovascular and cerebrovascular disease is increased.


  • Repair aneurysms before rupture if identified as high risk for rupture (based on shape, size, location, family history and personal risk factors).
  • Control of modifiable risk factors: control of high blood pressure, stopping smoking, avoiding stimulants, decreasing alcohol intake.
  • Screening with CT angiography or MR angiography in high risk populations.
  • Annual screening for 1-3 years then less common screening in those whose aneurysms remain stable in size.
  • Screening of patients with coarctation of aorta, and ADPKD every 5 years


  • increased risk of long term neurological dysfunction.
  • ~50% Death rate.
  • Timely treatment of aneurysm is necessary to prevent rebleeding

Delayed cerebral ischemia

  • Oral nimodipine q4hr for 21 days for prevention.
  • Maintain euvolemia
  • Daily monitoring of vasospasm with the help of Transcranial doppler.
  • DSA: Gold standard to identify vasospasm.
  • Induction of hypertension if permissible in patients suspected with delayed cerebral ischemia.
  • Intra-arterial vasodilator therapy and/or cerebral angioplasty in patients with delayed cerebral ischemia not responding to induced hypertension.

Pulmonary edema

  • Oxygen, mechanical ventilation.
  • Monitor PCWP and ventricular function.


  • Initial lorazepam-0.1mg/kg IV at 2mg/min to stop the seizure. Both phenytoin and levetiracetam are commonly used for maintenance therapy
  • Hydrocephalus: Treat with External ventricular drain

Cardiopulmonary complications

  • Takotsubo cardiomyopathy: enhances possibility of delayed cerebral ischemia.
  • Neurogenic Pulmonary edema or Acute Respiratory Distress Syndrome (ARDS): manage with mechanical ventilation and careful diuresis.
  • Ensure normal CPP in heart failure patients to prevent delayed cerebral ischemia
  • Hemodynamic support with inotropes or pressors as needed


  • Use Compressive devices.
  • Use unfractionated heparin or lovenox for DVT prophylaxis

Stress induced hyperglycemia

  • Avoid oral hypoglycemic agents
  • Target glucose level: 80-200mg/dl using sliding scale or scheduled insulin

Hyponatremia/Cerebral salt wasting syndrome

  • Hydrocortisone or fludrocortisone to prevent natriuresis.
  • Hypertonic saline where needed. hypertonic fluids.


  • Packed RBCs to keep hemoglobin above 8 mg/dl


  • most common non-neurological complication.
  • associated with a worse prognosis.
  • Acetaminophen use (scheduled or PRN)
  • Surface cooling or intravascular devices to control fever when antipyretics fail.

Further Reading

  • Macdonald, R. L. & Schweizer, T. A. Spontaneous subarachnoid haemorrhage. Lancet 389, 655–666 (2017)
  • Connolly, E. S., Jr et al. Guidelines for the management of aneurysmal subarachnoid hemorrhage: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke 43, 1711–1737 (2012)


  • Lovelock CE, Rinkel GJ, Rothwell PM. Time trends in outcome of subarachnoid hemorrhage: population-based study and systematic review. Neurology 2010;74(19):1494Y1501. doi:10.1212/WNL.0b013e3181dd42b3.
  • Bambakidis NC, Selman WR. Subarachnoid hemorrhage. In: Suarez JI, ed. Critical care neurology and neurosurgery.
  • Etminan N, Macdonald RL. Medical complications after aneurysmal subarachnoid hemorrhage: an emerging contributor to poor outcome. World Neurosurg 2014;pii:S1878-8750(14)00577-4. doi:10.1016/j.wneu.2014.06.031.
  • Connolly ES Jr, Rabinstein AA, Carhuapoma JR, et al Guidelines for the management of aneurysmal subarachnoid hemorrhage: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke 2012;43(6):1711Y1737. doi:10.1161/STR.0b013e3182587839.
  • Nieuwkamp DJ, Setz LE, Algra A, Linn FH, de Rooij NK, Rinkel GJ. Changes in case fatality of aneurysmal subarachnoid haemorrhage over time, according to age, sex, and region: a meta-analysis. Lancet Neurol 2009; 8: 635–42.
  • Al-Khindi T, Macdonald RL, Schweizer TA. Cognitive and functional outcome after aneurysmal subarachnoid hemorrhage. Stroke 2010; 41: e519–36.
  • Rinkel GJ, Algra A. Long-term outcomes of patients with aneurysmal subarachnoid haemorrhage. Lancet Neurol 2011; 10: 349–56.
  • Thompson BG, Brown RD Jr, Amin-Hanjani S, et al. Guidelines for the management of patients with unruptured intracranial aneurysms: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke 2015; 46: 2368–400.
  • Huhtakangas J, Lehto H, Seppä K, et al. Long-term excess mortality after aneurysmal subarachnoid hemorrhage: patients with multiple aneurysms at risk. Stroke 2015; 46: 1813–18.
  • Diringer MN, Bleck TP, Claude Hemphill J 3rd, et al. Critical care management of patients following aneurysmal subarachnoid hemorrhage: recommendations from the Neurocritical Care Society’s Multidisciplinary Consensus Conference. Neurocrit Care 2011;15(2):211Y240. doi:10.1007/s12028-011-9605-9.
  • Diringer MN, Bleck TP, Claude Hemphill J 3rd, et al. Critical care management of patients following aneurysmal subarachnoid hemorrhage: recommendations from the Neurocritical Care Society’s Multidisciplinary Consensus Conference. Neurocrit Care 2011;15(2):211Y240. doi:10.1007/s12028-011-9605-9.
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Manish KC

Written by

Manish KC

ECFMG Certified Physician, Clinical Research Coordinator at the Division of Gastroenterology, Hepatology, and Nutrition at the University of Louisville, Remote Researcher at the Larkin Health System, Miami, Florida

Shraddha Mainali

Associate professor of Neurology in the division of stroke and Neurocritical care at The Virginia Commonwealth University

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