The patient was admitted to the intensive care unit (ICU) and underwent a therapeutic procedure for the fnding on the previous angiogram. Six days later, the patient developed dysphasia and right-sided hemiparesis (right leg is weaker than right arm). A CT of the head reveals a right frontal hypodensity with surrounding mild edema.

• There is extensive subarachnoid hemorrhage (SAH) involving anterior interhemispheric fissure and bilateral sylvian fissures.

• SAH, likely secondary to aneurysmal rupture

• Hunt & Hess (H&H) and World Federation of Neurosurgical Societies (WFNS)
  
• H & H grading¹:
  
  
  
  • 1: Asymptomatic, or mild headache (H/A) and slight nuchal rigidity
    
  • 2: Cranial nerve palsy, moderate to severe H/A, nuchal rigidity
    
  • 3: Mild focal deficit, lethargy, or confusion
    
  • 4: Stupor, moderate to severe hemiparesis, early decerebrate rigidity
    
  • 5: Deep coma, decerebrate rigidity, moribund appearance
  
  
• WFNS grading²:
  
  
  
  • 1: Glasgow Coma Score (GCS) 15 with no major focal deficit
    
  • 2: GCS 13–14 with no major focal deficit
    
  • 3: GCS 13–14 with major focal deficit
    
  • 4: GCS 7–12 with or without major focal deficit
    
  • 5: GCS 3–6 with or without major focal deficit
  
  
• This patient has an H&H grade 3 and WFNS grade 2.

• Fisher grading system³:
  
  
  
  • 1: No SAH
    
  • 2: Diff use or vertical layer <1 mm thick
    
  • 3: Localized clot and/or vertical layer >1 mm
    
  • 4: Intracerebral hemorrhage or intravenous hemorrhage with minimal diff use or no SAH
  
  
• This patient has Fisher grade 3.
  
• The amount of subarachnoid blood correlates with the risk of vasospasm.
  
• Grade 3 carries the worst prognosis.

• Management includes the steps here⁴:
  
  
  
  • ICU admission
    
  • Arterial and central lines
    
  • Monitor systolic blood pressure (SBP), mean arterial pressure (MAP), and central venous pressure (CVP) closely
    
  • Phenytoin (dilantin™) loading (18 mg/kg) and maintenance doses (100 mg tid × 1 week unless seizures)
    
  • Nimodipine (60 mg by mouth every 4 hours × 21 days)
    
  • Analgesics
    
  • In cases of hydrocephalus or H&H grade >3, an external ventricular drain (EVD) should be inserted.
    
  • Cerebral angiography ± coiling (if the cause of SAH is aneurysm). If the aneurysm is not coilable, then craniotomy and aneurysm clipping.
    
  • In cases of poor H&H grade (V) at presentation, prognosis is very poor unless the comatose state is partly due to hydrocephalus or to a postictal state. Initial management usually consists of an EVD insertion and observation for a few hours. The decision to initiate aggressive management depends on the patient’s clinical improvement.

• The right anteroposterior projection internal carotid artery angiogram reveals an aneurysm at the level of the anterior communicating artery (ACOM) pointing inferiorly.

• The likely diagnosis is vasospasm aff ecting the right anterior cerebral artery (ACA).
  
• Vasospasm is a major complication of SAH.
  
• Clinical vasospasm occurs in 30% of SAH.
  
• Infarction occurs in about half of these cases if vasospasm remains untreated.
  
• 7% of attributed deaths are due to vasospasm.⁵
  
• Very few preventive and therapeutic measures have reproducible benefits in randomized trials.
  
• A cerebral angiogram may be done to confirm the presence of radiographic vasospasm, which may correlate with the clinical picture.

• As suspected clinically and based on the CT scan findings, the angiogram reveals severe stenosis suggesting cerebral vasospasm aff ecting the right A2 segment of the ACA.
  
• Note the occluded right ACOM aneurysm, which has been treated by endovascular coiling.

• The exact pathophysiology is unknown. However, there are two theories that might explain the pathophysiology⁶:
  
• Theories of “spasmogens”
  
  
  
  • Components of erythrocytes
    
  • Oxyhemoglobin
    
  • Plasma and buff y coat (white blood cells) do not induce vasospasm.
  
  
• Structural theories
  
  
  
  • Proliferative vasculopathy
    
  • Immune vasculopathy
    
  • Vessel wall inflammation
    
  • Extracellular lattice contraction
  
  
• Vasoconstriction theories
  
  
  
  • Free-radical lipid peroxidation
    
  • Derangement in eicosanoid production
    
  • Nitric oxide deficit
    
  • Endothelin excess4

• Transcranial Doppler
  
• Electroencephalogram
  
• Cerebral blood flow studies using positron emission tomography and single photon emitted computed tomography scans

• Vasodilation by angioplasty or intraarterial verapamil or papaverine

• Start “triple H” therapy, which traditionally comprises hypervolemia, hypertension, and hemodilution⁷
  
  
  
  • Hypertension: Keep systolic blood pressure at 160 mm Hg, or mean arterial pressure at 120 mm Hg or above
    
  • Hemodilution: Hematocrit 30–35%
  
  
• Alternatively, normovolemia may be used as hypervolemia can increase the risk of cardiorespiratory complications (central venous pressure is kept around 6 mm Hg).
  
• Normonatremia: [Na⁺ ] >140 mEq/L
  
• Normoglycemia: [glucose] <8 mmol/L
  
• Normothermia
  
• Norepinephrine bitartrate (Levophed; Abbott Laboratories, Abbott Park, IL) may be used to maintain blood pressure at pretreatment levels on an as needed basis.
  
• Induced hypertension and/or angioplasty may be performed if the patient is refractory to other treatments.
  
• Milrinone: a phosphodiesterase III inhibitor reducing the incidence of vasospasm may also be used in an intravenous infusion form