Emergent Management of Subarachnoid Hemorrhage

Updated: Oct 08, 2020
  • Author: Rami C Zebian, MD; Chief Editor: Andrew K Chang, MD, MS  more...
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Emergent management of subarachnoid hemorrhage (SAH), including prehospital care, is critical. Headache caused by SAH from a ruptured aneurysm is one of the most deadly, with a median case-fatality of 27%–44%. [1] This is rare, however, and comprises only 1% of all headaches presenting to the ED. [2]  On initial presentation, the one-year mortality of untreated SAH is up to 65%. [3] Mortality may be reduced to 18% with appropriate diagnosis and treatment. [4] An estimated 10%–15% of patients die before reaching the hospital. Moreover, mortality rate reaches as high as 40% within the first week, and about 50% die in the first 6 months. [5, 6, 7, 8, 9]

The common medical use of the term subarachnoid hemorrhage (SAH) refers to the nontraumatic presence of blood within the subarachnoid space from some pathologic process, usually from rupture of a berry aneurysm or arteriovenous malformation (AVM) (see the following image).

Brain computed tomography (CT) scan showing subtle Brain computed tomography (CT) scan showing subtle finding of blood at the area of the circle of Willis consistent with acute subarachnoid hemorrhage. Image courtesy of Dana Stearns, MD, Massachusetts General Hospital.

SAH classification

Subarachnoid hemorrhage (SAH) is classified according to 5 grades, as follows:

  • Grade I: Mild headache with or without meningeal irritation

  • Grade II: Severe headache and a nonfocal examination, with or without mydriasis

  • Grade III: Mild alteration in neurologic examination, including mental status

  • Grade IV: Obviously depressed level of consciousness or focal deficit

  • Grade V: Patient either posturing or comatose

See also Subarachnoid Hemorrhage, Subarachnoid Hemorrhage Surgery, Arteriovenous Malformation, and Cerebral Aneurysms.


Prehospital Care

Advances in the management of subarachnoid hemorrhage (SAH) have resulted in a relative reduction in mortality rate that exceeds 25%. However, more than one third of survivors have major neurologic deficits. Mortality and morbidity rates increase with age and poorer overall health of the patient.

Prehospital care is critical and includes the following:

  • Address the patient's airway, breathing, and circulatory status (ABCs)

  • Triage and transport patients with altered level of consciousness or an abnormal neurologic examination to the closest medical center with a computed tomography (CT) scan and neurosurgical backup

  • Ideally, avoid sedating these patients en route


Emergency Department Care

Grade I or II SAH

In patients with a suspected grade I or II subarachnoid hemorrhage (SAH), emergency department (ED) care essentially is limited to diagnosis and supportive therapy.

Early identification of sentinel headaches is key to reduced mortality and morbidity rates. Use sedation judiciously.

Secure intravenous access, and closely monitor the patient's neurologic status.

Grade III, IV, or V SAH

In patients with a grade III, IV, or V subarachnoid hemorrhage (SAH) (ie, altered neurologic examination), ED care is more extensive.

Address the patient's airway, breathing, and circulatory status (ABCs). In addition, reliable neurologic examinations before and after initial treatment are critically important to optimizing management and to deciding on the appropriate neurosurgical intervention.


Endotracheal (ET) intubation of obtunded patients protects them from aspiration caused by depressed airway protective reflexes. Also intubate to hyperventilate patients with signs of herniation.

Thiopental and etomidate are the optimal induction agents in subarachnoid hemorrhage (SAH) during an intubation. Thiopental is short-acting and has a barbiturate cytoprotective effect. It should be used only in hypertensive patients because of its propensity to drop systolic blood pressure (SBP), which is the leading cause of secondary brain injury. In hypotensive and normotensive patients, use etomidate.

Use rapid sequence intubation if possible. In the process, to blunt intracranial pressure (ICP) increase, ideally use sedation, defasciculation, short-acting neuromuscular blockade, and other agents with ICP-blunting properties (such as intravenous lidocaine).


Avoid excessive or inadequate hyperventilation. Target the partial pressure of carbon dioxide (pCO2) at 30-35 mm Hg to reduce elevated ICP. Excessive hyperventilation may be harmful to areas of vasospasm.

Avoid excessive sedation. It makes serial neurologic exams more difficult and has been reported to increase ICP directly. However, avoid any increase in ICP due to excessive agitation from pain and discomfort.

Use the following interventions early and judiciously to decrease elevated ICP when herniation is suspected:

  • Use osmotic agents, such as mannitol, which reduces ICP 50% in 30 minutes, peaks after 90 minutes, and lasts 4 hours

  • Loop diuretics, such as furosemide, also decrease ICP without increasing serum osmolality

  • Intravenous steroid therapy to control brain edema is controversial and debated

Provide supplemental oxygen for all patients with central nervous system (CNS) impairment.


Obtain emergent neurosurgical consultation for definitive treatment of subarachnoid hemorrhage (SAH).

Interventional radiology may be needed when surgical intervention is deemed necessary by the neurosurgical consultant (eg, a large clot causing a mass effect is present and needs to be evacuated emergently).

Many centers opt for early angiography in all patients. [10, 11]



Monitor the patient's cardiac activity, oximetry, automated blood pressure (BP), and end-tidal carbon dioxide, when applicable. End-tidal carbon dioxide monitoring of intubated patients enables the clinician to avoid excessive or inadequate hyperventilation. Target the partial pressure of carbon dioxide (pCO2) at about 30-35 mm Hg to reduce elevated intracranial pressure (ICP).

Invasive arterial line monitoring is indicated when dealing with labile BP (common in high-grade subarachnoid hemorrhage).

Antihypertensive agents were previously advocated for a systolic blood pressure (SBP) greater than 160 mm Hg or a diastolic BP (DBP) greater than 90 mm Hg.

Keep systolic blood pressure 90-140 mm Hg before aneurysm treatment, then allow hypertension to keep the SBP less than 200 mm Hg. [12] Use medications that can be titrated rapidly.

Vasopressors may be indicated to keep the SBP over 120 mm Hg; this avoids central nervous system (CNS) damage in the ischemic penumbra from the reactive vasospasm seen in subarachnoid hemorrhage (SAH).

Consult critical care providers who will be involved in ongoing care of the patient, as individual practices vary.


Adjunctive Therapies and Measures

Keep the patient's core body temperature at 37.2°C; administer oral (PO) acetaminophen (325-650 mg q4-6h), and use cooling devices if necessary. [12]

Consider antiemetics for nausea or vomiting.

Elevate the head of the bed 30° to facilitate intracranial venous drainage. Emergent ventricular drainage by the neurosurgeon may be necessary.

Maintain the patient's serum glucose level at 80-120 mg/dL; use sliding or continuous infusion of insulin if necessary. [12]

Fluids and hydration

Maintain euvolemia (central venous pressure [CVP], 5-8 mm Hg); if cerebral vasospasm is present, maintain hypervolemia (CVP of 8-12 mm Hg, or pulmonary capillary wedge pressure [PCWP] of 12-16 mm Hg). [12, 13]

Do not overhydrate patients because of the risks of hydrocephalus.

Patients with subarachnoid hemorrhage (SAH) may also have hyponatremia from cerebral salt wasting.

Seizure prevention

Prophylactic use of anticonvulsants does not acutely prevent seizures after subarachnoid hemorrhage (SAH), but use anticonvulsants in patients who have had a seizure or if local practice dictates routine use.

Begin with anticonvulsants that do not change the level of consciousness (ie, phenytoin first; use barbiturates or benzodiazepines only to stop active seizures).

Controversial measures

A randomized study of patients in an intensive care unit (ICU) demonstrated fewer ischemic events after aneurysmal subarachnoid hemorrhage (SAH) when high-dose magnesium was given for 10 days. The presumed mechanism was decreased cerebral vasospasm. [14] A meta-analysis demonstrated similar findings. [15] However, other studies have shown no benefit from magnesium. [16] Clearly, further study is indicated.

Use of antifibrinolytics, such as epsilon aminocaproic acid, to prevent rebleeding is controversial. These agents competitively inhibit plasminogen activation and have been reported to reduce the incidence of rebleeding. Other reports warn of their detrimental vasospastic effect and increased occurrence of hydrocephalus. Consult a neurosurgeon concerning their use.


Hospitalization and Transfer

Admit patients with suspected subarachnoid hemorrhage (SAH) to an intensive care unit (ICU) for serial neurologic examinations and for hemodynamic monitoring. Emergent imaging and intervention may be necessary if mass effect or rebleeding develops.

Patients with possible ruptured or leaking subarachnoid hemorrhage (SAH) should be transferred emergently to the closest center with computed tomography (CT) scanning and neurosurgical staff.

Stabilize patients promptly for transfer in an advanced cardiac life support (ACLS)–monitored unit. Address airway and the possible need for intubation or other emergent interventions, such as mannitol and hyperventilation, prior to transfer.