Subarachnoid hemorrhage: Difference between revisions
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== Background ==
==Background==
*Abreviation: SAH
*Bleeding into the subarachnoid space (between arachnoid and pia mater)
=== Pearls  ===
*Ruptured cerebral aneurysm accounts for ~85% of nontraumatic SAH
**Most common locations: anterior communicating artery (30%), posterior communicating artery (25%), MCA bifurcation (20%)
*Other causes: arteriovenous malformation, perimesencephalic (benign, ~10%), vasculitis, coagulopathy, drug use
*Mortality: ~50% overall (25% die before reaching hospital, 25% die within 30 days)
*Risk factors:
**[[Hypertension]] (most important modifiable risk factor)
**Smoking, heavy alcohol use
**Family history of SAH or aneurysm (first-degree relative)
**Polycystic kidney disease, Ehlers-Danlos, connective tissue disorders
**Prior SAH (risk of rebleeding)
**Sympathomimetic drug use ([[cocaine]], [[amphetamines]])
*Peak incidence: age 40-60; female predominance (1.6:1)


*Obtain GCS before intubation
==Clinical Features==
*If intubate prevent HTN (rebleeding)  
*"Worst headache of my life" — sudden onset, maximal at onset (thunderclap headache)
**Pretreatment
*'''Sentinel headache''': warning leak days-weeks before major rupture (present in ~30-50%)
***Lidocaine 1-1.5mg/kg (100mg) (blunts incr in BP)  
*Meningismus (neck stiffness, photophobia) — may take 6-12 hours to develop
***Fentanyl 200mcg (sympatholytic)
*Loss of consciousness at onset (~50%)
**Sedation
*Nausea, vomiting (common)
***If pt has high BP - use propofol
*Focal neurologic deficits (CN III palsy → posterior communicating artery aneurysm)
***If pt has adequate BP - use etomidate
*Seizures (~10% at onset)
**Treat pain
*Terson syndrome: intraocular hemorrhage (subhyaloid/vitreous) associated with severe SAH
***Prevents incr catacholamines / incr BP
*'''May present as syncope, cardiac arrest, or altered mental status without headache'''


=== Epidemiology  ===
===Hunt-Hess Grading===
*Grade I: asymptomatic or mild headache
*Grade II: moderate-severe headache, nuchal rigidity, CN palsy
*Grade III: drowsiness, confusion, mild focal deficit
*Grade IV: stupor, moderate-severe hemiparesis
*Grade V: coma, decerebrate posturing


*Of All pts in ED who p/w HA:
==Differential Diagnosis==
**1% will have SAH
*Primary [[headache]] (migraine, tension, cluster)
**10% will have SAH if c/o worst HA of life
*[[Meningitis]] / [[encephalitis]]
**25% will have SAH if c/o worst HA of life + any neuro deficit
*[[Intracerebral hemorrhage]]
*[[Cerebral venous sinus thrombosis]]
*[[Hypertensive emergency]]
*Reversible cerebral vasoconstriction syndrome (RCVS)
*[[Cervical artery dissection]]
*[[Pituitary apoplexy]]


=== Risk Factors  ===
{{Headache DDX}}


*Genetics (polycystic kidney disease, Ehler-Danlos, family hx)
==Evaluation==
*Hypertension
===Non-Contrast CT Head===
*Atherosclerosis
*First-line test
*Cigarette smoking
*Sensitivity ~98% within 6 hours of onset, ~93% at 12 hours, decreasing to ~50% by day 5-7<ref>Perry JJ, et al. Sensitivity of computed tomography performed within six hours of onset of headache for diagnosis of subarachnoid haemorrhage. ''BMJ''. 2011;343:d4277. PMID 21768192</ref>
*Alcohol
*Fisher grade: amount of blood predicts vasospasm risk
*Age &gt;50
*Modern thin-cut CT with experienced radiologist within 6 hours may approach 100% sensitivity
*Cocaine use
*Estrogen deficiency


=== Etiology of Spontaneous SAH  ===
===Lumbar Puncture===
*Required if CT negative and clinical suspicion remains
*Classic finding: xanthochromia (yellow discoloration from bilirubin in CSF)
**Takes 6-12 hours to develop — LP performed <6 hours after onset may miss xanthochromia
*'''Elevated RBCs that do NOT clear''' across sequential tubes (vs traumatic tap which clears)
*Elevated opening pressure
*Traumatic tap vs SAH: controversial; visual xanthochromia and clinical context are most important


*Ruptured aneurysm (85%)  
===Ottawa SAH Rule===
*Nonaneurysmal (15%)
*For alert patients >15 years with new severe nontraumatic headache reaching maximum intensity within 1 hour
**Perimesencephalic hemorrhage (10%) - lower risk of complications
*100% sensitivity (validation study) — if none present, SAH effectively ruled out<ref>Perry JJ, et al. Clinical decision rules to rule out subarachnoid hemorrhage for acute headache. ''JAMA''. 2013;310(12):1248-1255. PMID 24065011</ref>:
**Other: tumor, coagulopathy, dissection, vasculitis, SCD, venous sinus thrombosis
**Age ≥40
**Neck pain or stiffness
**Witnessed loss of consciousness
**Onset during exertion
**Thunderclap headache (instant peak)
**Limited neck flexion on exam


== Clinical Features ==
===CT Angiography (CTA)===
*Sudden, severe [[headache]] that reaches maximal intensity within minutes (97% of cases)  
*Obtain with initial CT if SAH confirmed or high suspicion
**Sudden onset is more important finding than worst [[headache]]
*Identifies aneurysm location and morphology for surgical/endovascular planning
*May be associated with [[syncope]], [[seizure]], [[nausea/vomiting]], meningismus
*Sensitivity >95% for aneurysms >3 mm
**Meningismus may not develop until hrs after bleed (blood breakdown -&gt; aseptic meningitis)
*[[Retinal hemorrhage]]
**May be the only clue in comatose patients
*There is a sentinel bleed headache 6-20 days before serious SAH in 30-50% of patients


== Differential Diagnosis ==
===Labs===
{{Intracranial hemorrhage DDX}}
*CBC, BMP, coagulation studies (PT/INR, PTT)
*Type and screen
*Troponin (neurogenic myocardial stunning)
*Finger stick glucose


===Other===  
==Management==
*Drug toxicity
===ED Management===
*Ischemic [[Stroke (Main)|Stroke]]
*ABCs, IV access, continuous monitoring
*[[Meningitis]]
*Blood pressure control:
*[[Encephalitis]]
**Target SBP <160 mmHg until aneurysm secured (reduce rebleeding risk)
*Intracranial tumor
**Nicardipine infusion (5-15 mg/hr, titrate q5min) — preferred
*Intracranial hypotension
**Labetalol 10-20 mg IV q10-20min
*Metabolic derangements
**Avoid nitroprusside (increases ICP)
*[[Cerebral venous thrombosis]]
*Seizure management: benzodiazepines acutely; prophylactic AEDs controversial
*Primary headache syndromes (benign thunderclap headache, [[Migraine]], [[Cluster Headache]])
*Treat headache: acetaminophen; short-acting opioids cautiously
**Avoid ketorolac (platelet inhibition)
*Aminocaproic acid (tranexamic acid): may reduce rebleeding risk before aneurysm secured — 4g IV loading dose (discuss with neurosurgery)
*Reverse anticoagulation if applicable


== Diagnosis  ==
===Definitive Treatment===
===Ottawa SAH Rules<ref>Ottawa SAH Rule JAMA. 2013 Sep 25;310(12):1248-55. doi: 10.1001/jama.2013.278018</ref>===
*Neurosurgery/neurointerventional consultation emergently
''Never has been externally and prospectively validated, authors caution implementation into routine use''
*Aneurysm securing (within 24 hours ideally):
*100% sensitive to rule out SAH (97.1%-100%)
**Endovascular coiling (preferred for most aneurysms) OR
*Can exclude SAH if all of the following are true
**Surgical clipping
**Age < 40
*ICU admission
**No Neck pain or stiffness
**No Witnessed LOC
**No onset during exertion
**No Thunderclap symptomatology (max intensity at honest)
**No limited neck flexion on physical exam


'''If concerned for SAH and CT normal strongly consider LP'''
===Complications (Post-Hemorrhage)===
*'''Rebleeding''': highest risk in first 24 hours (~4%); '''most devastating complication'''
*Vasospasm: occurs days 3-14 (peak day 7); monitor with daily TCDs
**Treat with nimodipine 60 mg PO/NG q4h x 21 days (improves outcomes; does not prevent vasospasm)
**Triple-H therapy (hypertension, hypervolemia, hemodilution) — only after aneurysm secured
*Hydrocephalus: acute (requires EVD) or chronic (VP shunt)
*Hyponatremia: cerebral salt wasting vs SIADH
*Neurogenic cardiac dysfunction: Takotsubo-like, neurogenic pulmonary edema


===Non-Contrast Head CT ===
==Disposition==
====Sensitivity====
*All confirmed SAH: emergent neurosurgical consultation and ICU admission
*Within 6hr of onset of symptoms: Near 100% Sn<ref>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.
</ref>
*Transfer to neurosurgical center if local capabilities unavailable
*Within 12hr of onset of symptoms: 98% Sn
*SAH ruled out (negative CT + negative LP): may discharge with headache precautions and PCP follow-up
*Within 24hr of onset of symptoms: 93% Sn<ref>van Gijn J and van Dongen KJ. The time course of aneurysmal haemorrhage on computed tomograms. Neuroradiology. 1982; 23:153–156.</ref>
*Within 5d of onset of symptoms: <60% Sn
*Not as sensitive/specific for minor bleeds


====Findings====
== Calculators ==
*SAH due to aneurysm - look in cisterns (esp. suprasellar cistern)
{{Ottawa SAH Calculator}}
*SAH due to trauma - look at convexities of frontal and temporal cortices
{{Fisher Scale Calculator}}


===Lumbar Puncture===
==See Also==
====Findings====
*[[Intracerebral hemorrhage]]
*Elevated RBC count that doesn't decrease from tube one to four
*[[Subdural hemorrhage]]
**Note: decreasing RBCs in later tubes can occur in SAH; only reliable if RBC count in final tube is nl
*[[Epidural hemorrhage]]
*Opening pressure &gt;20 (60% of pts)
*[[Headache]]
**Can help differentiate from a traumatic tap (opening pressure expected to be normal)
*[[Thunderclap headache]]
**Elevated opening pressure also seen in cerebral venous thrombosis, IIH
*[[Lumbar puncture]]
*Xanthrochromia
**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


==Workup==
==References==
*Brain CT without contrast
*[[LP]]
 
== Treatment  ==
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.
 
#Avoid hypotension
#*Maintain MAP &gt;80
#*Give [[IVF]]
#*Give [[pressors]] if IVF ineffective
#Discontinue/reverse all anticoagulation
#*[[Coumadin]] --> (Prothrombin complex conc or [[FFP]]) + vitamin K
#*[[Aspirin]] --> [[DDAVP]]
#*[[Plavix]] --> [[Platelets]]
#[[Nimodipine]]
#*Prevents vasospasm (associated with improved neuro outcomes and decreased cerebral infarction)
#*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
#[[Magneisum sulfate]]
#*Controversial; prevents vasospasm acting as NMDA antagonist and a calcium channel blocker; maintain b/w 2-2.5 mmol/L
#Seizure prophylaxis
#*Controversial; 3 day course may be preferable
#*[[Phenytoin]], [[levetiracetam]], [[carbamazepine]] and [[phenobarb]]. Phenytoin can be associated with worse neurologic & cognitive outcome
#Glucocorticoid therapy
#*Controversial; evidence suggests is neither beneficial nor harmful
#Glycemic control
#*Controversial; consider sliding scale if long pt stay in ED while awaiting ICU bed
#Keep head of bed elevated
#Aneurysm treatment
#*Surgical clipping and endovascular coiling are definitive tx
#*Antifibrinolytic - Controversial; if delayed aneurysmal tx, consider short term therapy (<72 hrs) with TXA or aminocaproic acid
 
{{AHA SAH BP Guidelines}}
 
== Complications  ==
 
*Rebleeding
**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
*Vasospasm
**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
***Tx for symptomatic vasospasm: Triple-H therapy (hemodilution + induced hypertension (pressors) + hypervolemia), ballon angioplasty, or intra-arterial vasodilators.
****Studies have not provided strong evidence of benefit Triple-H therapy
*Cardiac abnormalities (?2/2 release of catecholamines due to hypoperfusion of hypothalamus)
**Ischemia
***Elevated troponin (20-40% of cases)
***ST segment depression
**Rhythm disturbances
***Torsades, A-fib/flutter
**QT prolongation
**Deep, symmetric TWI
**Prominent U waves
*Hydrocephalus
**Consider ventricular drain placement for deteriorating LOC + no improvement w/in 24hr
*Hyponatremia
**Usually due to SIADH
***Treat via isotonic, or if necessary, hypertonic saline (do not treat via H2O restriction)
**Rarely due to cerebral salt-wasting
***Volume depleted, so treat with isotonic saline
 
== Prognosis  ==
 
=== Hunt and Hess  ===
Subjective terminology, but good interobserver variability
{| class="wikitable"
| align="center" style="background:#f0f0f0;"|'''Grade'''
| align="center" style="background:#f0f0f0;"|'''Description'''
| align="center" style="background:#f0f0f0;"|'''Survival Rate'''
|-
| Grade 0: ||Unruptured aneurysm||-
|-
| Grade 1: ||Asymptomatic or mild HA and slight nuchal rigidity||70%
|-
| Grade 1a: ||No acute meningeal/brain reaction, with fixed neurological def||-
|-
| Grade 2: ||Moderate to severe HA, stiff neck, no neurologic deficit except CN palsy||60%
|-
| Grade 3: ||Mild mental status change (drowsy or confused), mild focal neurologic deficit||50%
|-
| Grade 4: ||Stupor or moderate to severe hemiparesis||20%
|-
| Grade 5: ||Coma or decerebrate rigidity||10%
|}
<br>
 
:Grade 1 or 2 have curable disease
 
:Add one grade for serious systemic disease (HTN, DM, severe atherosclerosis, COPD)
 
=== World Federation of Neurosurgical Societies (WFNS)  ===
Objective terminology, and fair interobserver variability
*Grade 1: GCS of 15, no motor deficits
*Grade 2: GCS of 13 or 14, no motor deficits
*Grade 3: GCS of 13 or 14, with motor deficits
*Grade 4: GCS of 7–12, with or without motor deficits
*Grade 5: GCS of 3–6, with or without motor deficits
 
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  ==
*[[Intracranial Hemorrhage (Main)]]
*[[Head Trauma]]
 
== Source  ==
<references/>
<references/>
*Connolly ES Jr, et al. Guidelines for the management of aneurysmal subarachnoid hemorrhage: a guideline from the AHA/ASA. ''Stroke''. 2012;43(6):1711-1737. PMID 22556195
*Edlow JA, et al. Diagnosis of subarachnoid hemorrhage. ''Stroke''. 2023;54(4):1058-1072. PMID 36848423
*van Gijn J, et al. Subarachnoid haemorrhage. ''Lancet''. 2007;369(9558):306-318. PMID 17258671


[[Category:Neuro]]
[[Category:Neurology]]
[[Category:Critical Care]]
[[Category:Neurosurgery]]

Latest revision as of 09:56, 22 March 2026

Background

  • Bleeding into the subarachnoid space (between arachnoid and pia mater)
  • Ruptured cerebral aneurysm accounts for ~85% of nontraumatic SAH
    • Most common locations: anterior communicating artery (30%), posterior communicating artery (25%), MCA bifurcation (20%)
  • Other causes: arteriovenous malformation, perimesencephalic (benign, ~10%), vasculitis, coagulopathy, drug use
  • Mortality: ~50% overall (25% die before reaching hospital, 25% die within 30 days)
  • Risk factors:
    • Hypertension (most important modifiable risk factor)
    • Smoking, heavy alcohol use
    • Family history of SAH or aneurysm (first-degree relative)
    • Polycystic kidney disease, Ehlers-Danlos, connective tissue disorders
    • Prior SAH (risk of rebleeding)
    • Sympathomimetic drug use (cocaine, amphetamines)
  • Peak incidence: age 40-60; female predominance (1.6:1)

Clinical Features

  • "Worst headache of my life" — sudden onset, maximal at onset (thunderclap headache)
  • Sentinel headache: warning leak days-weeks before major rupture (present in ~30-50%)
  • Meningismus (neck stiffness, photophobia) — may take 6-12 hours to develop
  • Loss of consciousness at onset (~50%)
  • Nausea, vomiting (common)
  • Focal neurologic deficits (CN III palsy → posterior communicating artery aneurysm)
  • Seizures (~10% at onset)
  • Terson syndrome: intraocular hemorrhage (subhyaloid/vitreous) associated with severe SAH
  • May present as syncope, cardiac arrest, or altered mental status without headache

Hunt-Hess Grading

  • Grade I: asymptomatic or mild headache
  • Grade II: moderate-severe headache, nuchal rigidity, CN palsy
  • Grade III: drowsiness, confusion, mild focal deficit
  • Grade IV: stupor, moderate-severe hemiparesis
  • Grade V: coma, decerebrate posturing

Differential Diagnosis

Headache

Common

Killers

Maimers

Others

Aseptic Meningitis

Evaluation

Non-Contrast CT Head

  • First-line test
  • Sensitivity ~98% within 6 hours of onset, ~93% at 12 hours, decreasing to ~50% by day 5-7[1]
  • Fisher grade: amount of blood predicts vasospasm risk
  • Modern thin-cut CT with experienced radiologist within 6 hours may approach 100% sensitivity

Lumbar Puncture

  • Required if CT negative and clinical suspicion remains
  • Classic finding: xanthochromia (yellow discoloration from bilirubin in CSF)
    • Takes 6-12 hours to develop — LP performed <6 hours after onset may miss xanthochromia
  • Elevated RBCs that do NOT clear across sequential tubes (vs traumatic tap which clears)
  • Elevated opening pressure
  • Traumatic tap vs SAH: controversial; visual xanthochromia and clinical context are most important

Ottawa SAH Rule

  • For alert patients >15 years with new severe nontraumatic headache reaching maximum intensity within 1 hour
  • 100% sensitivity (validation study) — if none present, SAH effectively ruled out[2]:
    • Age ≥40
    • Neck pain or stiffness
    • Witnessed loss of consciousness
    • Onset during exertion
    • Thunderclap headache (instant peak)
    • Limited neck flexion on exam

CT Angiography (CTA)

  • Obtain with initial CT if SAH confirmed or high suspicion
  • Identifies aneurysm location and morphology for surgical/endovascular planning
  • Sensitivity >95% for aneurysms >3 mm

Labs

  • CBC, BMP, coagulation studies (PT/INR, PTT)
  • Type and screen
  • Troponin (neurogenic myocardial stunning)
  • Finger stick glucose

Management

ED Management

  • ABCs, IV access, continuous monitoring
  • Blood pressure control:
    • Target SBP <160 mmHg until aneurysm secured (reduce rebleeding risk)
    • Nicardipine infusion (5-15 mg/hr, titrate q5min) — preferred
    • Labetalol 10-20 mg IV q10-20min
    • Avoid nitroprusside (increases ICP)
  • Seizure management: benzodiazepines acutely; prophylactic AEDs controversial
  • Treat headache: acetaminophen; short-acting opioids cautiously
    • Avoid ketorolac (platelet inhibition)
  • Aminocaproic acid (tranexamic acid): may reduce rebleeding risk before aneurysm secured — 4g IV loading dose (discuss with neurosurgery)
  • Reverse anticoagulation if applicable

Definitive Treatment

  • Neurosurgery/neurointerventional consultation emergently
  • Aneurysm securing (within 24 hours ideally):
    • Endovascular coiling (preferred for most aneurysms) OR
    • Surgical clipping
  • ICU admission

Complications (Post-Hemorrhage)

  • Rebleeding: highest risk in first 24 hours (~4%); most devastating complication
  • Vasospasm: occurs days 3-14 (peak day 7); monitor with daily TCDs
    • Treat with nimodipine 60 mg PO/NG q4h x 21 days (improves outcomes; does not prevent vasospasm)
    • Triple-H therapy (hypertension, hypervolemia, hemodilution) — only after aneurysm secured
  • Hydrocephalus: acute (requires EVD) or chronic (VP shunt)
  • Hyponatremia: cerebral salt wasting vs SIADH
  • Neurogenic cardiac dysfunction: Takotsubo-like, neurogenic pulmonary edema

Disposition

  • All confirmed SAH: emergent neurosurgical consultation and ICU admission
  • Transfer to neurosurgical center if local capabilities unavailable
  • SAH ruled out (negative CT + negative LP): may discharge with headache precautions and PCP follow-up

Calculators

Template:Ottawa SAH Calculator

Modified Fisher Scale

Modified Fisher Scale — SAH Vasospasm Risk
CT Findings Select Grade
Grade

1 Grade 0 — No SAH or IVH (0)

Grade 1 — Thin SAH, no IVH (1)

Grade 2 — Thin SAH with IVH (2)

Grade 3 — Thick SAH, no IVH (3)

Grade 4 — Thick SAH with IVH (4)

Modified Fisher Grade
Interpretation — Risk of Symptomatic Vasospasm
Grade Vasospasm Risk Description
0 | ~0% | No subarachnoid blood detected.
1 | ~24% | Focal or diffuse thin SAH, no intraventricular hemorrhage (IVH).
2 | ~33% | Focal or diffuse thin SAH with IVH.
3 | ~33% | Focal or diffuse thick SAH (>1mm), no IVH.
4 | ~40% | Focal or diffuse thick SAH with IVH. Highest vasospasm risk.
References
  • Fisher CM, Kistler JP, Davis JM. Relation of cerebral vasospasm to subarachnoid hemorrhage visualized by computerized tomographic scanning. Neurosurgery. 1980;6(1):1-9. PMID 7354892.
  • Frontera JA, Claassen J, Schmidt JM, et al. Prediction of symptomatic vasospasm after subarachnoid hemorrhage: the modified Fisher scale. Neurosurgery. 2006;59(1):21-27. PMID 16823296.

See Also

References

  1. ↑ Perry JJ, et al. Sensitivity of computed tomography performed within six hours of onset of headache for diagnosis of subarachnoid haemorrhage. BMJ. 2011;343:d4277. PMID 21768192
  2. ↑ Perry JJ, et al. Clinical decision rules to rule out subarachnoid hemorrhage for acute headache. JAMA. 2013;310(12):1248-1255. PMID 24065011
  • Connolly ES Jr, et al. Guidelines for the management of aneurysmal subarachnoid hemorrhage: a guideline from the AHA/ASA. Stroke. 2012;43(6):1711-1737. PMID 22556195
  • Edlow JA, et al. Diagnosis of subarachnoid hemorrhage. Stroke. 2023;54(4):1058-1072. PMID 36848423
  • van Gijn J, et al. Subarachnoid haemorrhage. Lancet. 2007;369(9558):306-318. PMID 17258671
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