The World Federation of Neurological Surgeons (WFNS) SAH Scale¹ [4] is

Unlike the WFNS, the most current modification of the Hunt and Hess Classification takes into account comorbid conditions such as hypertension and diabetes which when present place the patient at the next highest risk category. The current patient based on her presentation of moderate headache, nuchal rigidity would place her at an initial Hunt and Hess Grade 2. However, due to her comorbid conditions of hypertension and diabetes, her Hunt and Hess classification is now Grade 3. Her WFNS Grade is 1 based upon a Glasgow Coma Scale of 15 and no motor deficits.

Cerebral autoregulation is the ability to maintain adequate and stable cerebral perfusion pressure over a range of mean arterial pressure (MAP). After SAH, cerebral autoregulation is frequently impaired. Focal reductions in cerebral perfusion may contribute to delayed ischemic neurological deficits (DIND). Elevated blood pressures, both transient and long term, are seen after SAH secondary to sympathetic activation. In a patient with Hunt and Hess Grade III and higher Inadequate cerebral perfusion begins at a higher MAP. Autoregulatory pressure curve is shifted toward a higher BP. In this patient with untreated chronic hypertension, the cerebral pressure curve has already been shifted to higher values but she does not have neurologic findings to suggest a further elevation in MAP is necessary.

Elevated ICP due to increased intracranial volume means a higher MAP is needed to maintain cerebral perfusion pressure (CPP). This sustained, elevated MAP increases the risk of rebleeding or secondary aneurysm rupture. Guidelines for the management of aneurysmal SAH from the onset of symptoms to aneurysm obliteration, recommend blood pressure is best controlled with a titratable agents (e.g., nicardipine, labetolol). This balances the risk of ischemic stroke, hypertension-related rebleeding, and maintenance of global cerebral perfusion pressure [6, 7]. Unfortunately, the MAP goal to achieve these often opposing goals has not been established but a maintaining systolic pressure to <160 mmHg and a MAP above 80–90 mm Hg is often suggested.

The treatment options are interventional or endovascular and surgical; the choice depends upon:

Endovascular techniques are suitable for nearly all accessible aneurysms. Often the choice, endovascular or surgical, is made by the patient or their family prior to the angiogram. Endovascular techniques are often recommended when surgical location (e.g., posterior circulation, cavernous sinus, internal carotid aneurysms) or medical difficulties (e.g., elderly, multiple comorbid conditions) increase the surgical risk. Surgical clipping is suitable when endovascular techniques have limited success (e.g., giant aneurysms (>2.5 cm in diameter), fusiform aneurysms, aneurysms with a wide neck (neck: dome ratio >0.5), and middle cerebral artery aneurysms). In younger patients (<40 years of age), surgical clipping may provide better long-term protection from rebleeding. With ongoing advancements in both microsurgical and endovascular approaches, the methods of determining the proper aneurysm characteristics and patient population for each treatment option continue to change.

When surgical treatment is chosen, a surgical clip is placed to exclude the aneurysm from the cerebral circulation without occluding the primary vessel. An endovascular option involves thrombosis of the aneurysm sac by placement of detachable platinum coils or other devices. Endovascular is an alternative and often a preferred treatment when the aneurysm anatomy and location is favorable.

Unruptured aneurysm is often electively treated. There have been no randomized trials comparing the coiling versus clipping techniques in this population. However, in a retrospective study across 429 centers in the United States, 2535 unruptured aneurysms were evaluated. The results favored endovascular coiling over surgical clipping [9].

SAH treatment is based upon characteristics of both the patient and the aneurysm. Surgical clipping or endovascular coiling of the ruptured aneurysm should be performed as early as possible to reduce the likelihood of rebleeding after SAH. It is worth noting that the International Subarachnoid Trial (ISAT) study [10, 11] was quite influential in favoring change of practice from surgical clipping to coiling. Despite some of its limitations, (small, <1 cm diameter, anterior circulation, good neurological grade), the ISAT study was the first study comparing the outcome measure of endovascular coiling with surgical clipping. Although reported in 2002, the ISAT result showed that fewer patients experienced the primary outcome, death or dependency, in the coiling group (24%) than they clipping group (31%). A strong criticism remains the surgical group contained patients who could not undergo endovascular treatment. The rate of rebleeding at 1 year was higher for the coiling group (2.6%) as compared to clipping (1%). Rebleeding may negate the advantage of the endovascular treatment [12].

Rebleeding is a major cause of morbidity in SAH with mortality rates nearing 70%. Without intervention, the risk of rebleeding reaches 40% within the first month. The highest daily rate (4%) occurs within the first 24 h followed by a daily rate of 1–2% for the next 28 days. Early surgery (0–3 days) is associated with reduced frequency of rebleeding. All but the most difficult aneurysms are treated with endovascular approach at the time of diagnosis. Consequently, the difficult surgical exposure caused by local edema and blood increases risk of intraoperative bleeding and long surgery. Once secured, the ability to treat vasospasm and eliminate rebleeding improve outcomes. Late surgery (>10 days posthemorrhage) has the advantage of better surgical conditions with increased risk occurring during days 4–9.

The current standard practice is intervention as soon as the aneurysm has been diagnosed. Studies consistently support early surgery and showing its association with improved clinical outcome in low-grade as well as high-grade SAH patients. Patients who were coiled or clipped within 24 h of SAH presentation had improved clinical outcomes compared with treatment after 24 h [13]. In the Netherlands, 1500 patients from eight hospitals, found no difference in low-risk patients but better outcomes in patients with poor clinical condition on admission after early surgery [14].

Vasospasm, a complication following SAH, is severe vasoconstriction cerebral vessels of distal from the original aneurysm. Its severity is associated with the amount of blood present on the CT scan and occurs beginning 2–3 days after SAH.

One can divide the vasospasm into (1) “clinical vasospasm” which refers to “delayed ischemic neurologic deficit” (DIND) or delayed cerebral ischemia (DCI) and (2) angiographic vasospasm, detected only on arteriogram. After surviving SAH treatment, vasospasm is a dreaded late complication. DCI can occur following SAH with or without angiographic evidence of narrowed of the cerebral vessels. Vasospasm on cerebral angiography is seen as a narrowing of the lumen of cerebral arteries. Daily studies with transcranial doppler (TCD) use increased blood flow velocity to detect narrowed arterial lumens or vasospasm in the anterior and posterior circulation. TCD changes can anticipate clinically symptomatic vasospasm.

Delayed cerebral ischemia is a clinical diagnosis that presents as confusion, depressed consciousness often with focal neurologic deficits on imaging. DCI symptoms typically begin as early as 3 days but the highest frequency is between 6 and 8 days post SAH. Seizures, hydrocephalus, cerebral edema, hypoxemia, hyponatremia, and sepsis can mimic DCI.

Persistent, untreated clinically symptomatic vasospasm is associated with increased morbidity and mortality due to cerebral ischemia and infarction. The major causes of morbidity and death in patients with aneurysmal SAH as cited by The International Cooperative Study on the timing of Aneurysm Surgery were:

The amount of hemorrhage seen on Computed Tomography (CT) is a very powerful predictor of vasospasm. The Fisher Scale is the most well-known grading scale and provides a correlation between the amount of blood on CT and the risk of vasospasm.

Other predictive factors of an increase risk are systemic hypertension, age <50 years old [15], cigarette smoker, cocaine use, and female.

This patient is at low risk of vasospasm.

Assuming the aneurysm has been secured, the initial treatment for vasospasm is administration of nimodipine, maintenance of euvolemia, and induced hypertension to improve cerebral perfusion [6]. Nimodipine has been shown to improve neurological outcomes but not cerebral vasospasm (Class I, Level of Evidence A). The efficacy of other calcium channel blockers, oral or IV, remains uncertain. The intravenous calcium channel blocker in widespread use is nicadipine, used for blood pressure control and vasospasm treatment [16].