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==Background==
==Background==
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.
*Bleeding into the subarachnoid space (between arachnoid and pia mater)
===Epidemiology===
*Ruptured cerebral aneurysm accounts for ~85% of nontraumatic SAH
The prevalence of SAH in patients presenting with true thunderclap headache is estimated at ~10%. <ref>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</ref>
**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)


===Risk Factors===
==Clinical Features==
*Genetics (polycystic kidney disease, Ehler-Danlos, family history)  
*"Worst headache of my life" — sudden onset, maximal at onset (thunderclap headache)
*Hypertension
*'''Sentinel headache''': warning leak days-weeks before major rupture (present in ~30-50%)
*Atherosclerosis
*Meningismus (neck stiffness, photophobia) — may take 6-12 hours to develop
*Cigarette smoking
*Loss of consciousness at onset (~50%)
*[[Alcohol]]
*Nausea, vomiting (common)
*Age &gt;50  
*Focal neurologic deficits (CN III palsy → posterior communicating artery aneurysm)
*[[Cocaine]] use
*Seizures (~10% at onset)
*Estrogen deficiency
*Terson syndrome: intraocular hemorrhage (subhyaloid/vitreous) associated with severe SAH
 
*'''May present as syncope, cardiac arrest, or altered mental status without headache'''
===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
*Observation and repeat head CT for stable patients


==Clinical Features==
===Hunt-Hess Grading===
*Sudden, severe [[headache]] that reaches maximal intensity within minutes (97% of cases)
*Grade I: asymptomatic or mild headache
**Sudden onset is more important finding than worst [[headache]]
*Grade II: moderate-severe headache, nuchal rigidity, CN palsy
*May be associated with [[syncope]], [[seizure]], [[nausea/vomiting]], meningismus
*Grade III: drowsiness, confusion, mild focal deficit
**Meningismus may not develop until hrs after bleed (blood breakdown -&gt; aseptic meningitis)
*Grade IV: stupor, moderate-severe hemiparesis
*[[Retinal hemorrhage]]
*Grade V: coma, decerebrate posturing
**May be the only clue in comatose patients
*Sentinel bleed headache 6-20 days before serious SAH in 30-50% of patients


==Differential Diagnosis==
==Differential Diagnosis==
{{Intracranial hemorrhage DDX}}
*Primary [[headache]] (migraine, tension, cluster)
*[[Meningitis]] / [[encephalitis]]
*[[Intracerebral hemorrhage]]
*[[Cerebral venous sinus thrombosis]]
*[[Hypertensive emergency]]
*Reversible cerebral vasoconstriction syndrome (RCVS)
*[[Cervical artery dissection]]
*[[Pituitary apoplexy]]


===Other===
{{Headache DDX}}
*Drug toxicity
*Ischemic [[Stroke (Main)|Stroke]]
*[[Meningitis]]
*[[Encephalitis]]
*Intracranial tumor
*Intracranial hypotension
*Metabolic derangements
*[[Cerebral venous thrombosis]]
*Primary headache syndromes (benign thunderclap headache, [[Migraine]], [[Cluster Headache]])


==Diagnosis ==
==Evaluation==
[[File:SubarachnoidP.png|thumb|Noncontrast CT showing subarachnoid hemorrhage (white area in the center stretching into the sulci).]]
===Non-Contrast CT Head===
===Ottawa SAH Rules<ref>Ottawa SAH Rule JAMA. 2013 Sep 25;310(12):1248-55. doi: 10.1001/jama.2013.278018</ref>===
*First-line test
''Never has been externally and prospectively validated, authors caution implementation into routine use''
*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>
*100% sensitive to rule out SAH (97.1%-100%)
*Fisher grade: amount of blood predicts vasospasm risk
*Can exclude SAH if all of the following are true
*Modern thin-cut CT with experienced radiologist within 6 hours may approach 100% sensitivity
**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'''
===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


===Non-Contrast Head CT===
===Ottawa SAH Rule===
{| class="wikitable"
*For alert patients >15 years with new severe nontraumatic headache reaching maximum intensity within 1 hour
| align="center" style="background:#f0f0f0;"|'''Time from onset of symptoms'''
*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>:
| align="center" style="background:#f0f0f0;"|'''Sensitivity of CT'''
**Age ≥40
|-
**Neck pain or stiffness
| <6 hours||~100%<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>  
**Witnessed loss of consciousness
|-
**Onset during exertion
| 6-12 hours||98%
**Thunderclap headache (instant peak)
|-
**Limited neck flexion on exam
| 12-24 hours||93%<ref>van Gijn J and van Dongen KJ. The time course of aneurysmal haemorrhage on computed tomograms. Neuroradiology. 1982; 23:153–156.</ref>
|-
| 24 hours - 5 days||<60%
|}


*SAH due to aneurysm - look in cisterns (esp. suprasellar cistern)  
===CT Angiography (CTA)===
*SAH due to trauma - look at convexities of frontal and temporal cortices
*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


===Lumbar Puncture===
===Labs===
*Elevated RBC count that doesn't decrease from tube one to four
*CBC, BMP, coagulation studies (PT/INR, PTT)
**Note: decreasing RBCs in later tubes can occur in SAH; only reliable if RBC count in final tube is nl
*Type and screen
*Opening pressure &gt;20 (60% of patients)
*Troponin (neurogenic myocardial stunning)
**Can help differentiate from a traumatic tap (opening pressure expected to be normal)
*Finger stick glucose
**Elevated opening pressure also seen in cerebral venous thrombosis, IIH
*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
*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.<ref>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.</ref>
**One study found that >2000 RBCs had a sensitivity of 93% and specificity of 93% for SAH, sensitivity increased to 100% when xanthochromia added.<ref>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.</ref>


==Management==
==Management==
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.
===ED Management===
 
*ABCs, IV access, continuous monitoring
#Avoid hypotension
*Blood pressure control:
#*Maintain MAP>80 (CPP of 60 as long as ICP<20)
**Target SBP <160 mmHg until aneurysm secured (reduce rebleeding risk)
#*Give [[IVF]]
**Nicardipine infusion (5-15 mg/hr, titrate q5min) — preferred
#*Give [[pressors]] if IVF ineffective
**Labetalol 10-20 mg IV q10-20min
#Hypertension
**Avoid nitroprusside (increases ICP)
#*AHA/ASA has no formal recommendations but states that decreasing to SBP <160 is reasonable<ref>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.</ref>
*Seizure management: benzodiazepines acutely; prophylactic AEDs controversial
#*Rapid SBP lowering <140 has been advocated with early research showing improved functional outcome<ref>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.</ref>, but more recent work has found no difference between SBP <140 and <180<ref>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].</ref>
*Treat headache: acetaminophen; short-acting opioids cautiously
#*Ensure appropriate pain control and sedation before adding antihypertensives
**Avoid ketorolac (platelet inhibition)
#Discontinue/reverse all anticoagulation
*Aminocaproic acid (tranexamic acid): may reduce rebleeding risk before aneurysm secured — 4g IV loading dose (discuss with neurosurgery)
#*[[Coumadin]] --> (Prothrombin complex conc or [[FFP]]) + vitamin K
*Reverse anticoagulation if applicable
#*[[Aspirin]] --> [[DDAVP]]
#*[[Plavix]] --> [[Platelets]]
#*Dabigitran ([[Pradaxa]]) --> [[Idarucizumab]] (Praxbind): 5 grams IV
#[[Nimodipine]]
#*Only CCB studied that has been shown to prevent 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 patient 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


===Intubation===
===Definitive Treatment===
*Consider neuroprotective intubation
*Neurosurgery/neurointerventional consultation emergently
**3 minutes before intubation
*Aneurysm securing (within 24 hours ideally):
***[[Lidocaine]] 1-2 mg/kg to blunt sharp MAP increase
**Endovascular coiling (preferred for most aneurysms) OR
***Fentanyl 1-2 mcg/kg as sympatholytic
**Surgical clipping
**Sedation
*ICU admission
***Etomidate if blood pressure normal
***Propofol if blood pressure high
**Succinylcholine without defasciculating dose
*Ensure patient is pain-free for post-intubation sedation
**Propofol with fentanyl
**Try to prioritize pain control with fentanyl


{{AHA SAH BP Guidelines}}
===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==
==Disposition==
*Admit
*All confirmed SAH: emergent neurosurgical consultation and ICU admission
 
*Transfer to neurosurgical center if local capabilities unavailable
==Complications ==
*SAH ruled out (negative CT + negative LP): may discharge with headache precautions and PCP follow-up
===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), balloon angioplasty, or intra-arterial vasodilators{{Citation needed|reason=Reliable source needed|date=February 2016}}
**Studies have not provided strong evidence of benefit Triple-H therapy{{Citation needed|reason=Reliable source needed|date=February 2016}}
 
===Cardiac abnormalities===
Most likely related to the 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]]===
*Hyponatremia is seen in 10%-40% of the patients with subarachnoid hemorrhage who are admitted to the ICU.<ref>Woo, M.H, Kale-Pradhan, P.B. Fludrocortisone in the treatment
of subarachnoid hemorrhage-induced hyponatremia. Annals of Pharmacotherapy. 1997.  31, 637–639.</ref>
*Cerebral Salt Wasting and [[SIADH]] are the two most common causes<ref>Albanese, A. et al. . Management of hyponatremia in patients with acute cerebral insults. Archives of Disease in Childhood, 85. (2001). 246–251.</ref>
 
==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'''
|-
|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 (HTN, DM, severe atherosclerosis, COPD)
 
===World Federation of Neurosurgical Societies (WFNS) ===
Objective terminology, and fair interobserver variability
{| class="wikitable"
|-
!width="50"| 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 ==
== Calculators ==
*[[Intracranial Hemorrhage (Main)]]
{{Ottawa SAH Calculator}}
*[[Head Trauma]]
{{Fisher Scale Calculator}}


==External Links==
==See Also==
*[http://emcrit.org/podcasts/sah/ EMCrit Podcast - Subarachnoid Hemorrhage]
*[[Intracerebral hemorrhage]]
*[[Subdural hemorrhage]]
*[[Epidural hemorrhage]]
*[[Headache]]
*[[Thunderclap headache]]
*[[Lumbar puncture]]


==References==
==References==
<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:Neurology]]
[[Category:Neurology]]
[[Category:Critical Care]]
[[Category:Neurosurgery]]

Revisión actual - 09:56 22 mar 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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