After the surgery, the patient had an excellent recovery. The partial left third nerve palsy did not resolve, however, no new neurologic deficits were noted. He was observed one night in the intensive care unit then moved to the ward. On the third day after the surgery, he developed slurred speech and a mild right-sided hemiparesis (power 4+/5). A CT scan was done (Fig. 35.3).

• According to the clinical history, it seems that the patient had a “warning headache,” also known as “sentinel hemorrhage” from an aneurysm rupture. These types of headache occur in 30–60% of patients presenting with subarachnoid hemorrhage (SAH).
  
• The SAH may then clear and the patient may not seek medical attention.
  
• Unfortunately, in this case, the patient was not investigated properly initially. A plain CT head should have been performed at the outside hospital.
  
• Newer generation CT scans will detect SAH in more than 95% of cases if scanned within 48 hours of the SAH. The blood will appears as high-density (white) streaks within the subarachnoid spaces.
  
• If the CT turns out to be normal, then a lumbar puncture (LP) is indicated. LP is the most sensitive test for detecting SAH. However, a false-positive may occur such as traumatic taps. Caution must be exerted while performing an LP as intracranial pressure changes may occur and may trigger further bleeding from the rupture site.
  
• The development of ptosis points to specific aneurysm location: this is more common with posterior communicating artery (PCOM) aneurysm, or less commonly basilar apex aneurysm. This is an imminent rupture sign that should be considered seriously and treated as soon as possible.
  
• A CT scan done upon presentation to our ER (not shown here) showed a hyperdensity in the left supraclinoid region. Also, the temporal horns were dilated, which is suggestive of hydrocephalus. Delayed hydrocephalus is one of SAH’s main complications and may be caused by pia-arachnoid adhesions or permanent impairment of the arachnoid granulation function.1,2

• Cerebral angiography is the gold standard for evaluation of SAH and aneurysms. It is an invasive procedure and has inherent risks (e.g., stroke) and may cause delays in treatment.
  
• CTA has a sensitivity of 95% and specificity of 83% in detecting aneurysm as small as 2.2 mm. It is not an invasive procedure and can be done within minutes. The 3D reconstruction of the CTA is very helpful for surgical planning and the head positioning. Even if the endovascular treatment with coiling is considered, CTA can provide further information to determine whether an aneurysm can be treated by coiling.
  
• Magnetic resonance arteriography (MRA) provides the ability to detect aneurysms and determine the size, rate, and direction of flow in an aneurysm relative to the magnetic field. It also helps visualize thrombosis and calcifications within an aneurysm. Its sensitivity to detect aneurysms greater than 3 mm is around 86%, and the false-positive rate is 16%. As the false-positive rate is elevated, this modality may be useful for screening high-risk patients, including first-degree relatives of aneurysm patients.
  
• Magnetic resonance imaging (MRI) alone is not sensitive within the first 24–48 hours. After 4–7 days, MRI is excellent for detecting subacute to remote SAH. It may be helpful to determine which aneurysm bled in cases of multiple aneurysms.^1,2

• 3D CTA shows the presence of a left internal carotid artery (ICA) aneurysm (Fig. 35.2A), most probably at the level of the PCOM segment. The dome of the aneurysm is pointing posteriorly and inferiorly. The left A1 segment is hypoplastic. The aneurysm itself has a wide neck, almost fusiform-like.
  
• There is also a coincidental finding of an arteriovenous malformation (AVM) in the left frontal area (Fig. 35.2B). The major feeders of the AVM appear to be originating from branches of the middle cerebral artery. The drainage of the AVM appears to be via the superior sagittal sinus.

• Aneurysms are present in 2.7–23% of patients with an AVM.
  
• Aneurysm occurring in the presence of AVMs may be flow related, intranidal, or unrelated to the AVM.
  
• In flow-related cases, hemodynamic stress of the increased flow traveling toward the AVM may contribute to the formation of proximal arterial aneurysms. These are more common in males. They arise along the course of arteries that eventually supply the AVM.
  
• Proximal flow-related aneurysms are typically located at these sites:
  
  
  
  • Supraclinoid internal carotid artery
    
  • Circle of Willis
    
  • Middle cerebral artery up to bifurcation
    
  • Anterior cerebral artery up to anterior communicating artery
    
  • Vertebrobasilar trunk
  
  
• All flow-related aneurysms beyond these locations are distal flow-related aneurysms.
  
• Intranidal aneurysms lie within the AVM nidus and are also more common in males.
  
• Unrelated aneurysms are remote to the AVM and more common in females.
  
• The pathogenesis of AVM and concomitant aneurysms may relate to a combination of factors such as underlying vascular defect, hemodynamic stress, vasoactive substances, and locally generated growth factors.
  
• Distal flow-related aneurysms are the most likely to regress with definitive AVM treatment, but the proximal flow-related aneurysms are unlikely to change.
  
• The treatment plan in this case will involve repair of the imminently ruptured internal carotid-posterior communicating artery (IC-PC) aneurysm and then continue with the AVM resection, if safely achievable in the same sitting. The wide neck of the aneurysm excludes the endovascular treatment option in this case.³

• Extended pterional approach is used.
  
• Image guidance may aid in planning the incision and the bone flap.
  
• Ventriculostomy insertion may be performed as a first step.
  
• Sylvian fissure dissection from proximal to distal is performed to visualize parent vessels and the aneurysm neck (see Case 32).
  
• It may be necessary to put temporary clips on parent vessels and the aneurysm’s major branches to reconstruct the aneurysm.
  
• After the clipping, always confirm the flow of all surrounding vessels with intraoperative Doppler; also confirm that there is no flow in the aneurysm dome.
  
• Then, if safely feasible, one may continue with the resection of the AVM.
  
• Note that this step can be done in a separate sitting if difficulties are encountered during aneurysm clipping.
  
• Follow the general principles of AVM surgery.
  
  
  
  • Always try to identify the feeder at the first stage. If one is not sure whether a vessel is a feeder, a temporary clip may be used on that vessel, and observation for changes in the AVM or surrounding brain can then be noted.
    
  • The surrounding gliotic brain presents a good cleavage plane for dissection of the nidus.
    
  • Avoid getting into the nidus.
    
  • The draining veins are taken as a last step in the resection. Again, temporary clips may be used in a similar fashion.^2,4

• The CT scan (Fig. 35.3) shows artifact from the clip placement in the left paraclinoid region; no intracranial hematoma or hypodensities are noted.
  
• Ventriculostomy placement appears adequate with expected size of ventricles.
  
• At the site of the previous AVM location, there is again no hemorrhage and minimal surgical artifact.

• The most probable cause of his condition is vasospasm.
  
• Other possibilities include
  
  
  
  • Normal pressure perfusion breakthrough (secondary to changes in autoregulation post-AVM surgery)
    
  • Seizure
    
  • Infection (meningitis, encephalitis, sepsis)
    
  • Electrolyte abnormalities
    
  • Hyperacute infarction not visible on CT scan yet
  
  
• Management should include
  
  
  
  • Ensure adequate oxygenation and circulation
    
  • Involve seizure prophylaxis
    
  • Check and correct electrolytes
    
  • Further laboratory investigations: complete blood count; electrolytes; prothrombin time/partial thromboplastin time; culture blood, urine, sputum, cerebrospinal fluid (CSF)
    
  • Ensure adequate antibiotic coverage
    
  • Monitor and control intracranial pressure (ICP)
    
    
    
    • Head of bed elevated 30 degrees
      
    • Drain CSF
      
    • May need to sedate or hyperventilate if ICP is elevated
    
    
  • Optimize the hematocrit
    
  • Nimodipine 60 mg by mouth every 4 hours
    
  • “Triple H maneuver” with mild hypertension, hypervolemia, and hemodilution.
    
  • May need to repeat the cerebral angiogram to check for vasospasm and possibly for therapeutic purposes (angioplasty or papaverine injection)
    
  • May also consider MRI if the clip is MRI compatible and if the patient does not improve1,4
  
  
• The patient is this case gradually improved with triple H therapy and physiotherapy. He had an almost complete recovery one month later, except for the left partial third nerve palsy.