Subarachnoid hemorrhage

Background

• Abreviation: SAH

Pearls

• Obtain GCS before intubation
• If intubate prevent HTN (rebleeding)
  • Pretreatment
    • Lidocaine 1-1.5mg/kg (100mg) (blunts incr in BP)
    • Fentanyl 200mcg (sympatholytic)
  • Sedation
    • If pt has high BP - use propofol
    • If pt has adequate BP - use etomidate
  • Treat pain
    • Prevents incr catacholamines / incr BP

Epidemiology

• Of All pts in ED who p/w HA:
  • 1% will have SAH
  • 10% will have SAH if c/o worst HA of life
  • 25% will have SAH if c/o worst HA of life + any neuro deficit

Risk Factors

• Genetics (polycystic kidney disease, Ehler-Danlos, family hx)
• 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

Clinical Features

• Sudden, severe headache that reaches maximal intensity within minutes (97% of cases)
  • Sudden onset is more important finding than worst HA
• May be a/w 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/HA 6-20d before SAH (30-50% of pts)

Differential Diagnosis

Intracranial Hemorrhage Types

• Intra-axial
  • Hemorrhagic stroke (Spontaneous intracerebral hemorrhage)
  • Traumatic intracerebral hemorrhage
• Extra-axial
  • Epidural hemorrhage
  • Subdural hemorrhage
  • Subarachnoid hemorrhage (aneurysmal intracranial hemorrhage)

Other

• Drug toxicity
• Ischemic Stroke
• Meningitis
• Encephalitis
• Intracranial tumor
• Intracranial hypotension
• Metabolic derangements
• Cerebral venous thrombosis
• Primary headache syndromes (benign thunderclap headache, Migraine, Cluster Headache)

Diagnosis

Ottawa SAH Rules

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 honest)
  • No limited neck flexion on physical exam

If concerned for SAH and CT normal strongly consider LP

Non-Contrast Head CT

Sensitivity

• Within 6hr of onset of symptoms: Near 100% Sn
• Within 12hr of onset of symptoms: 98% Sn
• Within 24hr of onset of symptoms: 93% Sn
• Within 5d of onset of symptoms: <60% Sn
• Not as sensitive/specific for minor bleeds

Findings

• SAH due to aneurysm - look in cisterns (esp. suprasellar cistern)
• SAH due to trauma - look at convexities of frontal and temporal cortices

Lumbar Puncture

Findings

• Elevated RBC count that doesn't 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 pts)
  • Can help differentiate from a traumatic tap (opening pressure expected to be normal)
  • 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

Workup

• 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.

AHA Aneurysmal SAH BP Guidelines

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)

• Avoid hypotension
  • Maintain MAP >80
  • Give IVF
  • Give pressors if IVF ineffective
• Discontinue/reverse all anticoagulation
  • Coumadin - (Prothrombin complex conc or FFP) + vit K
  • Aspirin - DDAVP
  • Plavix - Platelets
• Nimodipine
  • Prevents vasospasm (a/w 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
  • 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 a/w 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 Tx
  • 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

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

• Grade 0: Unruptured aneurysm
• Grade 1: Asymptomatic or mild HA and slight nuchal rigidity

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
• Grade 3: Mild mental status change (drowsy or confused), mild focal neurologic deficit
• Grade 4: Stupor or moderate to severe hemiparesis
• Grade 5: Coma or decerebrate rigidity

Survival Rate

• Grade 1: 70%
• Grade 2: 60%
• Grade 3: 50%
• Grade 4: 20%
• Grade 5: 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

• 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