This patient’s clinical presentation suggests subarachnoid hemorrhage (SAH) due to rupture of an intracranial aneurysm. He should be admitted to the neurological intensive care unit (NeuroICU). Two large bore IV lines as well as an arterial line for blood pressure management should be established. An initial systolic blood pressure goal of < 140 mm Hg should be instituted. Coagulopathy or platelet inhibition should be reversed if present. Intubation is reserved for patients who are unable to adequately protect their airway because of depressed mention. Ventricular drainage is also a consideration for patients with hydrocephalus who are unable to follow commands or present in poor neurological status.

In the first 12 hours after the initial bleed, noncontrast head CT has a 98% to 100% sensitivity for the detection of SAH. This sensitivity decreases to 93% at 24 hours and to 57% to 85% after 6 days.^1–7 If the initial head CT does not reveal SAH, a lumbar puncture with analysis of the cerebrospinal fluid (CSF) for xanthochromia should be performed.⁸

Imaging of the cerebral vasculature must be obtained to determine the source of the SAH. The gold standard for evaluation of cerebral vascular lesions remains catheter angiography. Less invasive modalities including magnetic resonance angiography (MRA) and CT angiography (CTA) may be initially utilized depending on availability and patient stability. Three-dimensional time-of-flight MRA has a sensitivity to detect cerebral aneurysms of between 55% and 93%.^9–12 Dichotomizing by size, the sensitivity is 85% to 100% for aneurysms ≥ 5 mm but only 56% for those < 5 mm.^11,13,14 CTA is more frequently utilized in the setting of SAH as it is faster and more readily available. In addition, it has an aneurysm detection sensitivity of between 77% and 100% and specificity between 79% and 100%.^15–21

Newly diagnosed cranial nerve (CN) III palsy in the setting of a posterior communicating artery aneurysm suggests aneurysm instability and expansion (Figure 24-2). A noncontrast head CT should be immediately obtained to rule out rebleeding. Rebleeding is the major cause of death in patients who survive the initial hemorrhage but do not undergo surgical intervention. Early intervention is thus warranted in patients with aneurysmal SAH and especially in those demonstrating aneurysm instability.^22–25

In untreated aneurysmal SAH, the greatest risk of rebleeding occurs on the first day (4%), with a daily frequency of 1.5% until 13 days. By 2 weeks after initial hemorrhage, the rebleed rate is 15% to 20% and up to 50% by 6 months.²⁴ In modern tertiary care medical centers, the rate of rebleeding is nearly 7% when prehospital events are excluded.²⁶ If these prehospital events are included, a 10% to 20% incidence of “ultra-early” rebleeds has been suggested.^27–30 Overall, rebleed events in the first day are associated with a drastically reduced chance of survival.²⁶ The goal of surgical and endovascular treatment is to prevent this occurrence, and since the 1980s there has been a shift toward early intervention.³¹

The use of antifibrinolytic therapy for the prevention of rebleeding is controversial. Although it has been shown to significantly decrease the incidence of rebleeding by 40% to 60%, it has also been shown to increase the risk of ischemic neurologic deficits by a similar margin.^32,33 However, it has also been shown that when antifibrinolytic therapy is prophylactically administered before early surgery, preoperative rebleeding rates can be reduced effectively, and ischemic complications can be minimized by postsurgical discontinuation of antifibrinolytics.^28,34 ε-Aminocaproic acid (36 g/d) or tranexamic acid (6-12 g/d) can be used for these purposes.³⁵

When the patient’s clinical status permits, early aneurysm surgery is recommended to prevent rebleeding and enable expedient institution of vasospasm therapy.^36–42 Although no strict criteria exist, it may be unwise to proceed with surgery in patients who are moribund, present with severe vasospasm, or have significant cardiopulmonary compromise (Table 24-1). Conversely, although surgical outcomes are more favorable for patient presenting in good neurological and medical status, good outcomes can also be achieved in poor-grade patients.^43,44 Indeed, up to 40% patients with Hunt and Hess grade IV and V have been shown to have a good clinical outcome (modified Rankin score, 0-3) after surgical intervention.^45,46

A 41-year-old woman presents after the sudden onset of worst headache of life and brief loss of consciousness with limb shaking. Noncontrast head CT shows diffuse SAH in the basal cisterns. CTA and catheter angiography show a 6- to 7-mm anterior communicating artery aneurysm (Figure 24-3). After initial stabilization in the NeuroICU, the patient’s baseline blood pressure of 145/90 mm Hg increases to 205/152 mm Hg. Routine laboratory evaluation is significant for serum sodium concentration of 130 mEq/L, hematocrit of 45%, and normal coagulation studies.

A definitive target blood pressure should be established by taking the patient’s baseline into account.⁴⁷ Although some studies have found that rebleeding is more common when the systolic blood pressure is > 150 to 160 mm Hg, others have found no relationship between blood pressure and rebleed rates.^26,27,29 Differences among these studies are related to the variable use of antihypertensive medications and inconsistent observation times.⁴⁸ Blood pressure control with short-acting continuous infusion agents such as nicardipine, labetalol, or esmolol are appropriate.

Prophylactic anticonvulsants are indicated in all patient with SAH. Nearly 8% of patients experience seizures at SAH onset and > 20% of patients experience seizures at some time after the initial hemorrhage.^49,50 Meperidine (Demerol) should be avoided because it can lower the seizure threshold. In patients presenting with status epilepticus, it is important to halt seizure activity expeditiously to mitigate associated neurological injury.

Hematocrit levels > 40% significantly increase serum viscosity, as so do levels of serum fibrinogen > 250 mg/dL. Serum viscosity may play an important role in the setting of vasospasm prevention and treatment, but this hypothesis has not been definitively evaluated.⁵¹ A hematocrit > 40% at admission can be corrected with delivery of 5% IV colloids or hypertonic saline.^52,53 Hematocrit levels often decrease upon admission because of frequent diagnostic blood draws and the initiation standard isotonic saline infusions. A hematocrit between 28% and 32% is often considered ideal.⁵⁴

This patient exhibits two common complications of SAH: hydrocephalus and hyponatremia. A CTA should be obtained to exclude vasospasm as another contributor to the patient’s clinical status. Hydrocephalus is common in the setting of aneurysm rupture, occurring in 20% to 30% of cases.³⁵ Class I evidence indicates that ventriculostomy placement improves the neurologic status of patients who are symptomatic.^55–57 The hyponatremia, which may be due to either syndrome of inappropriate antidiuretic hormone (SIADH) or cerebral salt wasting, should also be addressed. Urine electrolyte studies are helpful for determining the etiology of hyponatremia. Although SIADH is typically treated with fluid restriction, one must be wary of this strategy in patients with SAH because volume contraction has been shown to correlate with symptomatic vasospasm.⁵⁸ In the acute setting, normal or hypertonic saline as well as fludrocortisone therapy may be sufficient to correct the serum sodium concentrations.^59,60