Subarachnoid Hemorrhage

Definition:

Bleeding within subarachnoid space, between arachnoid and pia mater and is normally filled with cerebrospinal fluid.

Epidemiology:

• 4th most frequent cerebrovascular disorder
  • Atherothrombosis
  • Emoblism
  • Primary Intracerebral Hemorrhage
  • Subarachnoid Hemorrhage
• Third most common cause of nonobstetric maternal death
  • Half occur postpartum (1–5 per 10,000 pregnancies)
• Age: Between ages 40 and 60
• Gender: Women > Men
• Genetics:
  • 2-5x increased risk of SAH in 1st degree relatives
  • Polycystic kidney, Ehlers-Danlos type II, neurofibromatosis type I, and Marfan’s

• Traumatic SAH (tSAH)
  • Most common cause of SAH by far!
  • Traumatic Brain Injury (TBI)
    • 150-250 (~200) per 100,000 per year worldwide
    • ~40% develop SAH following head trauma
    • ~80 per 100,000 people develop tSAH per year

• Aneurysmal SAH (aSAH)
  • ~10 per 100,000
  • 1–5 per 10,000 pregnancies; half occur postpartum

• 33-45% die within 30 days
  • 12% die prior to hospital arrival
  • 15% die in the first 24 hours after arrival
• Of survivors only 1/3 remain functionally independent

• Primary Spontaneous SAH
  • Aneurysmal subarachnoid hemorrhage (aSAH) 85%
    • Most common at vessel bifurcation in circle of Willis
    • Anterior (internal carotid artery) circulation – 85%
    • Posterior (vertebrobasilar) circulation – 15%
  • Nonaneurysmal SAH
    • Perimesencephalic hemorrhage (10%) - lower risk of complications
    • Other (5%) - AV malformations, sickle cell disease, bleeding diatheses, pituitary apoplexy, trauma, cocaine abuse, and intracranial arterial dissection.
• Secondary SAH – Parenchymal bleed → rupture into ventricular system
• Traumatic Subarachnoid Hemorrhage (tSAH) – trauma

Clinical Syndromes: Aneurysmal rupture → rush of blood into subarachnoid space

1. immediate LOC → no preceding complaint
2. excruciating generalized headache and vomiting → then LOC
3. severe generalized headache → remains relatively lucid with varying degrees of stiff neck (most common presentation

Symptoms:

• Acute "thunderclap" or "worst headache[1] of my life"
• Nuchal rigidity - neck stiffness
• Loss of consciousness
• Nausea/vomiting
• Photophobia.
• Fever[2]

[1] Rupture usually occurs while patient is active; rarely during sexual intercourse, straining at stool, lifting heavy objects, or other sustained exertion

[2] Fever in absence of discernible infective etiology is common in subarachnoid hemorrhage, and in some instances, may be confused with florid meningitis

CT Head without contrast:

• Sensitivity/Specificity
  • Within 6 hours → 100% sensitivity and specificity
  • 24 hours → 93% sensitivity
  • 3 days → 80%
  • 7 days → 50%
• Findings: hyperdensity in the subarachnoid space
• There are four different patterns:

1. Adjacent to intraparenchymal or extraparenchymal hematomas – severe trauma
2. Overlying the cerebral hemispheres in isolation – mod trauma
3. Extensive hemorrhage within the basal cisterns and subarachnoid space – SAH, AVM
4. Nontraumatic perimesencephalic hemorrhage
   • focal small hemorrhage in the interpeduncular cistern can be seen in patients presenting with headache without aneurysm. It usually results in no long-term clinical sequelae.

Lumbar Puncture:

• 65% specificity
• Findings
  • Elevated RBC:
    • CSF becomes grossly bloody within 30 mins of the hemorrhage
    • RBC counts up to 1 million/mm3 or even higher
    • RBC count that does not diminish from tube 1 to tube 4
    • Xanthochromia[1]
  • Opening pressure:
    • CSF between 250-500 mm H2O
• Limitations
  • inability to diagnosis:
    • pituitary apoplexy
    • cerebral venous sinus thrombosis
    • arterial dissection
    • unruptured aneurysm

Computed tomography angiography (CTA)

• 98% sensitive and 100% specific for detecting aneurysms larger than 3 mm.
• CTA to the right shows vasospasm
• Angio-negative SAH
  • 10% of spontaneous SAHs are perimesencephalic[2]

[1] Xanthochromia is produced by hemoglobin product breakdown, resulting in a yellow tinge/color of the CSF. The presence of xanthochromia in the setting of SAH greatly reduces the chance of traumatic LP.

[2] Blood is seen in a stereotypical pattern around the brainstem and angiogram findings are negative. The theory is that these are venous in nature and low pressure. This is considered mostly a benign phenomenon without the complication of “clinical vasospasm”

• Prevent Early Rebleeding
  • Anticoagulant reversal - If the patient is on an anticoagulant or antiplatelet agent, stop the drug before performing any interventions
• Hemodynamic management: Blood pressure control prior to aneurysm coiling or clipping
  • Place arterial line
  • BP Goal: Avoid hypotension and hypertension –MAPS < 110 or SBP 120-140
  • Etiologies of HTN
    • Pain
    • headache
    • elevated ICP in patients with hydrocephalus
    • increased sympathetic nervous system activity
    • preexisting hypertension
  • Interventions
    • Pain Control
      • Short-acting analgesic such as fentanyl
    • Antihypertensives 
      • Intermittent IV bolus
        • Labetolol 5-10mg IV PRN
        • Hydralazine 5-10mg doses IV
        • Enalapril
      • IV Drip[1]
        • Nicardipine/Cardene (2.5-20mg/hour)
• Prevent delayed cerebral ischaemia
  • “Symptomatic vasospasm” typically manifests between days 3-14 (peak day 7)
  • Symptoms:
    • fluctuating mental status
    • multi-focal neurological complaints
    • low grade fever
    • increased BP (body tries to autoregulate)
    • increased ICP
  • Severe vasospasm leads to strokes and death.
  • Treatment:
    • Nimodipine - 60 mg every 4 hours for 14–21 days after SAH

[1] NOTE: Sodium nitroprusside is usually avoided because of its tendency to increase ICP and thus reduce the cerebral perfusion pressure

Acute Hydrocephalus

• Etiology: Intracranial hypertension or herniation
• Pathophysiology: large amount of blood ruptures into ventricular system or floods basal subarachnoid space → find its way into ventricles through the foramina of Luschka and Magendie
• Management:
• • Hyperventilation - temporizing measure
    • Decreased PCO2 effectively decreases ICP by causing cerebral arteriolar constriction and reducing cerebral blood volume.
    • Effect generally lasts for less than 24 hours
    • Level II evidence discourages maintaining PCO2 levels below 25 mm Hg in TBI patients given the risk for global ischemia
  • Osmotherapy
    • Mannitol 20%
      • Dose: 0.5-1.0 g/kg hourly
      • Decreases intravascular volume and brain water and may transiently reduce ICP
    • Hypertonic Saline
      • 23.4% hypertonic saline solution 0.5–2.0 ml/kg
      • maintaining the head of the bed at greater than a 30° angle
• • Consider placement of ICP monitor/ventriculostomy
    • External ventricular drain (EVD)
    • Transorbital ventricular decompression. A. The upper eyelid is retracted and the globe is displaced downward. B. Insertion of the needle.
  • Seizure Prophylaxis
    • Phenytoin (Dilantin)
      • • Loading dose of 1000 mg, then
        • 100 mg every 8 hours.
    • Keppra, or levetiracetam (LEV)
      • • 1000 mg doses every 12 hours

Aneurysm Treatment/Neurosurgical Management:

• Early surgery (days 1-3) for patients who have a grade of I to III on the Hunt-Hess scale
  • Surgical clipping – before hypertensive therapy for vasospasm
  • Endovascular coil insertion into bleeding vessel
    • Electrolytically detachable coils placed directly in aneurysm, where they induce thrombosis.