Subarachnoid hemorrhage (SAH) is defined as hemorrhage into the subarachnoid space surrounding the brain. This can be either nontraumatic or traumatic in nature. Cerebral aneurysms are the most common cause of nontraumatic SAH (up to 85%) and have the most devastating consequences. Other causes include venous bleed, which have less severe sequelae. Here we will focus on aneurysmal nontraumatic subarachnoid hemorrhage.

Subarachnoid bleed

SAH

• The primary symptom is a sudden, severe headache in >90% of cases. About 50% have a headache that is classically described as the “worst headache of my life” and reaches maximal intensity within 1 min-the so-called thunderclap headache. This headache may be associated with nausea/vomiting, neck pain, seizure, or complete loss of consciousness.
• Most patients report a history of headaches during the weeks preceding the actual hemorrhage event. These are most likely sentinel bleeds that represent microhemorrhages.
• A posterior communicating artery aneurysm may present as oculomotor (cranial nerve III) palsy, typically involving the pupillary fibers, even in a nonruptured setting.
• The World Federation of Neurosurgeons (WFNS) score and the Hunt and Hess score are clinical scores that correlate with mortality (higher numbers indicating higher mortality) (Table 1).

• Trauma.
• About 85% of nontraumatic SAHs are caused by a ruptured berry aneurysm, whereas 10% do not reveal a bleeding source despite modern imaging techniques. About 5% are due to other causes, which include arteriovenous malformations (AVMs), tumors, vasculitis, reversible cerebrovascular vasoconstriction syndrome, cerebral sinus venous thrombosis, and coagulopathies.
• Table 2 summarizes nonaneurysmal causes of subarachnoid hemorrhage.

• Other headache syndromes: Thunderclap headaches due to reversible cerebral vasoconstriction syndrome (often with recurrent thunderclap headaches), migraine headache, sexual headache, cough headache, exertional headache, secondary causes including, but not limited to, pituitary apoplexy or acute hydrocephalus.

• Basic laboratory values, including CBC, chemistry panel, prothrombin time, partial thromboplastin time, and platelet count.
• Serum troponin to evaluate for severe cardiac stress; elevated troponins indicate cardiac damage secondary to a catecholamine surge and can be associated with poor outcomes.
• Patients with SAH are prone to developing cerebral salt wasting, resulting in hyponatremia. Sodium levels should be monitored frequently.

• Airway, breathing, and circulation
• Once stabilized, good neurologic exam
• Cerebrospinal fluid (CSF) drainage may be required for patients who develop hydrocephalus and increased intracranial pressure. It is also recommended for patients with Hunt and Hess grade 3 or higher

• Critical care management: Initial management strategies are geared toward stabilizing the patient and preventing re-hemorrhage and hydrocephalus. Re-hemorrhage occurs within 72 hr in up to 23% and is associated with very high mortality rates.
• Blood pressure control: Tight blood pressure control is paramount before securing the aneurysm to protect against re-rupture. Blood pressure control can be achieved with the use of antihypertensive infusions such as intravenous nicardipine. A systolic blood pressure of less than 140 mm Hg is recommended. Placement of arterial line is recommended. After securing of the aneurysm, liberalization of blood pressure parameters is the standard.
• Intracranial pressure control: Raised intracranial pressure occurs in more than 50% of patients with subarachnoid hemorrhage secondary to hydrocephalus, cerebral edema, cerebral infarction or other causes. Insertion of a ventricular catheter to treat acute hydrocephalus and maintain intracranial pressure <20 mm Hg can be lifesaving. Patients who are unable to be weaned may require permanent CSF diversion.
• In cases of aneurysmal SAH, treatment focuses on occlusion/exclusion of the aneurysm to prevent rebleeding. Most aneurysms currently are treated endovascularly. The most common treatment methods are:
  1. Microsurgical clipping: Performed through a craniotomy by placing a clip around the neck of the aneurysm
  2. Endovascular coiling (Fig. E6): Performed via digital subtraction angiography; it consists of deploying platinum coils inside the aneurysm (Fig. E7) or stents in the parent artery to cause thrombosis of the aneurysmal sac.
  3. Flow diverters and the Woven EndoBridge (WEB) device are also treatment options.
• Vasospasm: Cerebral vasospasm is a morbid complication leading to cerebral ischemia, disability, and death after SAH. It typically develops between day 4 and 14 (but may occur up to day 21) after the hemorrhage, and it reaches a peak on day 6 to 8. Treatment strategies include:
  1. Induced hypertension with typical mean arterial pressure goals of 90 to 100 (after aneurysm is secured) and with euvolemia instead of hypervolemia, as the latter was found to lead to significant cardiopulmonary and hemodynamic complications. “Triple H” therapy-Hypertension, Hypervolemia, and Hemodilution-was originally employed to maintain cerebral perfusion, but it has fallen out of favor due to its many complications.
  2. Nimodipine (60 mg q4h or 30 mg q2h if blood pressure is low) has been shown to improve outcomes if it is administered between days 4 and 21 after the hemorrhage. Nimodipine has not been shown to reduce the incidence of vasospasm but does have a mortality benefit, likely acting as a neuroprotective agent.
  3. Intraarterial therapies such as intraarterial calcium channel blockers and balloon angioplasty may be employed as needed for symptomatic vasospasm.
• Seizures occur in about 3% of patients during the acute phase. Use of prophylactic antiepileptics is controversial and not recommended, but patients presenting with seizures should be treated appropriately with anticonvulsants.
• Pain control: Use short-acting and less-sedating medications (e.g., codeine, low-dose morphine).
• Monitor and treat for cerebral salt wasting and any other electrolyte abnormalities or anemia.
• Maintain normothermia.
• Avoid hyperglycemia or hypoglycemia.
• Management of SAH is complex and requires a multidisciplinary approach that includes expertise from neurology, critical care, neurosurgery, neuro-interventionalists, cardiologists, and endocrinologists, to name a few. A brief summary of the management is outlined above, but a detailed discussion is outside the scope of this text. The authors recommend supplementing this material with society guidelines such as those laid out by the Neurocritical Care Society.⁶

• Management of reversible risk factors mentioned earlier (smoking, hypertension, drug use)
• Management of neurologic disability through physical therapy and rehabilitation

• Outcomes after SAH have been improving over the years, with a 17% to 50% decrease in case fatality. The prehospital and 30-day mortality rates are still reported at around 15% to 33%.
• Almost half of those who survive hospitalization have cognitive impairments or disability that affect their lifestyles.⁷

All patients should be managed at high-volume SAH centers, which are defined as having a case volume of more than 35 SAHs a year. Patients who present to alternative facilities should be transferred to a high-volume SAH center as soon as possible.

• “Thunderclap” headaches should be considered SAH until proven otherwise and evaluated by CT of the head with/without LP. MRI FLAIR sequence is also a helpful modality.
• All SAH should be managed in a critical care setting (preferably neurocritical care unit) with neurosurgical care available.
• Measures to prevent rebleeding include adequate control of blood pressure and aneurysm treatment with the use of coiling or clipping.

Controlling some of the modifiable risk factors, especially smoking and blood pressure, may help to decrease the risk of aneurysmal rupture.

• SAH is a devastating condition, with most survivors developing significant neurologic or cognitive deficits. A good support system and an adequate physical and cognitive rehabilitation program may prove useful to survivors.
• Screening may be useful for patients with two or more first-degree relatives with SAH.

Subarachnoid Hemorrhage (Patient Information)