Subarachnoid hemorrhage

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Anatomy of the meninges

Defined as hemorrhage into the subarachnoid space (between the arachnoid membrane and the pia mater). This may occur spontaneously, usually from a ruptured cerebral aneurysm, or may result from head injury.


The prevalence of SAH in patients presenting with true thunderclap headache is estimated at ~10%. [1]

Risk Factors

  • Genetics (polycystic kidney disease, Ehler-Danlos, family history)
  • Hypertension
  • Atherosclerosis
  • Cigarette smoking
  • Alcohol
  • Age >50
  • Cocaine use
  • Estrogen deficiency

Etiology of Spontaneous SAH

  • Ruptured aneurysm (85%)
  • Nonaneurysmal (15%)
    • Perimesencephalic hemorrhage (10%) - lower risk of complications
    • Other: tumor, coagulopathy, dissection, vasculitis, SCD, venous sinus thrombosis

Traumatic Subarachnoid Hemorrhage

  • Differentiate from aneurysmal rupture
  • Supportive care with prevention of hypertension, elevated ICP, and vasospasm with PO nimodipine
  • Patients with normal neurologic exam NOT on anticoagulation may not need a repeat head CT[2][3]
    • Recommend 6 hour observation

Clinical Features

  • Sudden, severe headache that reaches maximal intensity within minutes (97% of cases)
    • Sudden onset is more important finding than worst headache
  • May be associated with syncope, seizure, nausea/vomiting, meningismus
    • Meningismus may not develop until hrs after bleed (blood breakdown → aseptic meningitis)
  • Retinal hemorrhage
    • May be the only clue in comatose patients
  • Sentinel bleed headache 6-20 days before serious SAH in 30-50% of patients

Differential Diagnosis

Intracranial Hemorrhage Types



Noncontrast CT showing subarachnoid hemorrhage (white area in the center stretching into the sulci).
More subtle CT showing subarachnoid hemorrhage (white area in the frontal area stretching into the sulci).

Ottawa SAH Rules[4]

Never has been externally and prospectively validated, authors caution implementation into routine use

  • 100% sensitive to rule out SAH (97.1%-100%)
  • Can exclude SAH if all of the following are true
    • Age < 40
    • No neck pain or stiffness
    • No witnessed LOC
    • No onset during exertion
    • No thunderclap symptomatology (max intensity at onset)
    • No limited neck flexion on physical exam

If concerned for SAH and CT normal strongly consider LP, especially if CT obtained >6 hrs after symptom onset

Non-Contrast Head CT

Time from onset of symptoms Sensitivity of CT
<6 hours ~100%[5]
6-12 hours 98%
12-24 hours 93%[6]
24 hours - 5 days <60%
  • SAH due to aneurysm - look in cisterns (esp. suprasellar cistern)
  • SAH due to trauma - look at convexities of frontal and temporal cortices

Lumbar Puncture

  • Elevated RBC count that does not decrease from tube one to four
    • Note: decreasing RBCs in later tubes can occur in SAH; only reliable if RBC count in final tube is nl
  • Opening pressure >20 (60% of patients)
    • Can help differentiate from a traumatic tap (opening pressure expected to be normal)
    • Elevated opening pressure also seen in cerebral venous thrombosis, IIH
  • Xanthochromia
    • May help differentiate between SAH and a traumatic tap
    • Takes at least 2hr after bleed to develop (beware of false negative if measure early)
    • Sn (93%) / Sp (95%) highest after 12hr
  • If unable to obtain CSF consider CTA
    • CTA also highly sensitive for predicting delayed cerebral ischemia
  • If traumatic tap is suspected
    • Tube 4 RBC count <500 has negative predictive value of 100% for SAH. Tube 4 RBC decrease of 70% compared to tube 1 excludes a radiographically detectable SAH.[7]
    • One study found that >2000 RBCs had a sensitivity of 93% and specificity of 93% for SAH, sensitivity increased to 100% when xanthochromia added.[8]

CT Angiogram

  • A CT followed by CTA is an acceptable alternative to CT and LP[9]
  • CTA has a 98% sensitivity for aneurysms >3mm


Physiologic derangements, such as hypoxemia, metabolic acidosis, hyperglycemia, BP instability, and fever, can worsen brain injury and has been independently associated with increased M&M, but no studies showing benefit of corrections.

  1. Avoid hypotension
    • Maintain MAP>80 (CPP of 60 as long as ICP<20)
    • Give IVF
    • Give pressors if IVF ineffective
  2. Hypertension
    • AHA/ASA has no formal recommendations but states that decreasing to SBP <160 is reasonable[10]
    • Rapid SBP lowering <140 has been advocated with early research showing improved functional outcome[11], but more recent work has found no difference between SBP <140 and <180[12]
    • Ensure appropriate pain control and sedation before adding antihypertensives
  3. Discontinue/reverse all anticoagulation
  4. Nimodipine
    • Only CCB studied that has been shown improve outcomes (contrary to popular belief, it does not affect large-vessel vasospasm but does decrease incidence of delayed cerebral ischemia)[13]
    • Give 60mg q4hr PO or NGT only (never IV) within 96hr of symptom onset. NNT 13 to prevent one poor outcome
    • Keep an eye on BP for fluctuations
  5. Magnesium sulfate
    • Controversial; prevents vasospasm acting as NMDA antagonist and a calcium channel blocker; maintain between 2-2.5 mmol/L
  6. Seizure prophylaxis
  7. Glucocorticoid therapy
    • Controversial; evidence suggests is neither beneficial nor harmful
  8. Glycemic control
    • Controversial; consider sliding scale if long patient stay in ED while awaiting ICU bed
  9. Keep head of bed elevated
  10. Aneurysm treatment
    • Surgical clipping and endovascular coiling are definitive treatment
    • Antifibrinolytic - Controversial; if delayed aneurysmal treatment, consider short term therapy (<72 hrs) with TXA or aminocaproic acid


  • Consider neuroprotective intubation
  • Ensure patient is pain-free for post-intubation sedation
    • Propofol with fentanyl
    • Try to prioritize pain control with fentanyl

AHA Aneurysmal SAH BP Guidelines[15]

  1. No well-controlled studies exist that answer whether BP control influences rebleeding
  2. BP should be controlled to balance the risk of stroke, hypertension-related rebleeding, and maintenance of cerebral perfusion pressure (Class I, Level of Evidence B).
  3. Nicardipine, labetalol, and esmolol are appropriate choices for BP control (Sodium nitroprusside may raise intracranial pressure and cause toxicity with prolonged infusion and should be avoided)


  • Admit



  • Risk is highest within first 24 hours (2.5-4%), particularly within first 6 hours
  • Usually diagnosed by CT after acute deterioration in neuro status
  • Only aneurysm treatment is effective in preventing rebleeding


  • Leading cause of death and disability after rupture
  • Typically begins no earlier than day three after hemorrhage
  • Characterized by decline in neuro status
  • Aggressive treatment can only be started after aneurysm has been treated
    • treatment for symptomatic vasospasm: Triple-H therapy (hemodilution + induced hypertension (pressors) + hypervolemia), balloon angioplasty, or intra-arterial vasodilators[citation needed]
    • Studies have not provided strong evidence of benefit Triple-H therapy[citation needed]

Cardiac abnormalities

Most likely related to the release of catecholamines due to hypoperfusion of hypothalamus


  • Consider ventricular drain placement for deteriorating LOC + no improvement within 24hr


  • Hyponatremia is seen in 10%-40% of the patients with subarachnoid hemorrhage who are admitted to the ICU.[16]
  • Cerebral Salt Wasting and SIADH are the two most common causes[17]


Hunt and Hess

Subjective terminology, but good interobserver variability

Grade Description Survival Rate
0 Unruptured aneurysm -
1 Asymptomatic or mild HA and slight nuchal rigidity 70%
1a No acute meningeal/brain reaction, with fixed neurological def -
2 Moderate to severe HA, stiff neck, no neurologic deficit except CN palsy 60%
3 Mild mental status change (drowsy or confused), mild focal neurologic deficit 50%
4 Stupor or moderate to severe hemiparesis 20%
5 Coma or decerebrate rigidity 10%
Grade 1 or 2 have curable disease
Add one grade for serious systemic disease (hypertension, DM, severe atherosclerosis, COPD)

World Federation of Neurosurgical Societies (WFNS)

Objective terminology, and fair interobserver variability

Grade GCS Focal neurological deficit
1 15 Absent
2 13–14 Absent
3 13–14 Present
4 7–12 Present or absent
5 <7 Present or absent

Other scales are also available, including the Ogilvy and Carter scale (comprehensive, yet complex), and the Fisher scale or Claassen grading system (vasospasm index risk).

Note: First-degree relatives are at 2-5 fold increase in SAH, so screening is considered on individual basis.

See Also

External Links


  1. Dubosh NM et al. Sensitivity of Early Brain Computed Tomography to Exclude Aneurysmal Subarachnoid Hemorrhage: A Systematic Review and Meta-Analysis. Stroke 2016. PMID: 26797666
  2. Borczuk, et al. Patients with traumatic subarachnoid hemorrhage are at low risk for deterioration or neurosurgical intervention. J Am Coll Surg. 2014; 219.
  3. Nahmias JT, et al. Mild Traumatic Brain Injuries Can Be Safely Managed Without Neurosurgical Consultation: The End of a Neurosurgical "Nonsult"? American Association for the Surgery of Trauma. Annual Meeting. 2016
  4. Ottawa SAH Rule JAMA. 2013 Sep 25;310(12):1248-55. doi: 10.1001/jama.2013.278018
  5. Perry JJ, et al. Sensitivity of computed tomography performed within six hours of onset of headache for diagnosis of subarachnoid haemorrhage: prospective cohort study. BMJ. 2011; 343:d4277.

  6. van Gijn J and van Dongen KJ. The time course of aneurysmal haemorrhage on computed tomograms. Neuroradiology. 1982; 23:153–156.
  7. Gorchynski J, Oman J, and Newton T. Interpretation of traumatic lumbar punctures in the setting of possible subarachnoid hemorrhage: who can be safely discharged? Cal J Emerg Med. 2007; 8(1): 3–7.
  8. Perry JJ, Alyahya B, Sivilotti MLA, et al. Differentiation between traumatic tap and aneurysmal subarachnoid hemorrhage: prospective cohort study. BMJ : British Medical Journal. 2015;350:h568.
  9. Walsh B, Vilke GM, Coyne CJ. Clinical Guidelines for the Emergency Department Evaluation of Subarachnoid Hemorrhage. Meurer WJ, JEM. 2016; 50(4) 696-701.
  10. 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):1711-1737.
  11. Anderson CS, Heeley E, Huang Y, et al. Rapid blood-pressure lowering in patients with acute intracerebral hemorrhage. N Engl J Med. 2013; 368:2355-2365.
  12. Qureshi AI, Palesch YY, Barsan WG, et al. Intensive Blood-Pressure Lowering in Patients with Acute Cerebral Hemorrhage. N Engl J Med. 2016; 1-11. [Epub ahead of print].
  13. Francoeur CL, Mayer SA. Management of delayed cerebral ischemia after subarachnoid hemorrhage. Crit Care. 2016;20(1):277.
  14. Bucher J and Koyfman A. Intubation of the neurologically injured patient. J Emerg Med. 2016; 49:920-927.
  15. Bederson J. et al. 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;40:994-1025 PDF
  16. Woo, M.H, Kale-Pradhan, P.B. Fludrocortisone in the treatment of subarachnoid hemorrhage-induced hyponatremia. Annals of Pharmacotherapy. 1997. 31, 637–639.
  17. Albanese, A. et al. . Management of hyponatremia in patients with acute cerebral insults. Archives of Disease in Childhood, 85. (2001). 246–251.