The term subarachnoid hemorrhage (SAH) refers to extravasation of blood into the subarachnoid space

between the pial and arachnoid membranes (see the image below). It occurs in various clinical contexts,
the most common being head trauma. However, the familiar use of the term SAH refers to nontraumatic
(or spontaneous) hemorrhage, which usually occurs in the setting of a rupturedcerebral
aneurysm or arteriovenous malformation (AVM).

A 47-year-old woman presented with headache and vomiting; her

CT scan in the emergency department revealed subarachnoid hemorrhage.

Signs and symptoms

Signs and symptoms of SAH range from subtle prodromal events to the classic presentation. The most
common premonitory symptoms are as follows:

Headache (48%)
Dizziness (10%)
Orbital pain (7%)
Diplopia (4%)
Visual loss (4%)
Signs present before SAH include the following:

Sensory or motor disturbance (6%)

Seizures (4%)
Ptosis (3%)
Bruits (3%)
Dysphasia (2%)
Prodromal signs and symptoms usually are the result of sentinel leaks, mass effect of aneurysm
expansion, emboli, or some combination thereof.
The classic presentation can include the following:

Sudden onset of severe headache (the classic feature)

Accompanying nausea or vomiting

Symptoms of meningeal irritation

Photophobia and visual changes
Focal neurologic deficits
Sudden loss of consciousness at the ictus
Seizures during the acute phase
Physical examination findings may be normal or may include the following:

Mild to moderate BP elevation

Temperature elevation
Tachycardia
Papilledema
Retinal hemorrhage
Global or focal neurologic abnormalities
Complications of SAH include the following:

Hydrocephalus
Rebleeding
Vasospasm
Seizures
Cardiac dysfunction
See Clinical Presentation for more detail.

Diagnosis
Diagnosis of SAH usually depends on a high index of clinical suspicion combined with radiologic
confirmation via urgent noncontrast CT, followed by lumbar puncture or CT angiography of the brain. After
the diagnosis is established, further imaging should be performed to characterize the source of the
hemorrhage.
Laboratory studies should include the following:

Serum chemistry panel

Complete blood count
Prothrombin time (PT)/activated partial thromboplastin time (aPTT)
Blood typing/screening
Cardiac enzymes
Arterial blood gas (ABG) determination
Imaging studies that may be helpful include the following:

CT (noncontrast, contrast, or infusion)

Digital subtraction cerebral angiography
Multidetector CT angiography
MRI (if no lesion is found on angiography)
Magnetic resonance angiography (MRA; investigational for SAH)
Other diagnostic studies that may be warranted are as follows:

Baseline chest radiograph

ECG on admission
Lumbar puncture and CSF analysis
See Workup for more detail.

Management
Current treatment recommendations include the following:

Antihypertensive agents (eg, IV beta blockers) when mean arterial pressure exceeds 130 mm Hg
Avoidance of nitrates (which elevate ICP) when feasible
Hydralazine and calcium channel blockers
Angiotensin-converting enzyme (ACE) inhibitors (not first-line agents in acute SAH)
In patients with signs of increased ICP or herniation, intubation and hyperventilation
Other interventions for increased ICP are as follows:

Osmotic agents (eg, mannitol)

Loop diuretics (eg, furosemide)
IV steroids (controversial but recommended by some)
Additional medical management is directed toward the following common complications:

Rebleeding
Vasospasm
Hydrocephalus
Hyponatremia
Seizures
Pulmonary complications
Cardiac complications
Surgical treatment to prevent rebleeding includes the following options:

Clipping the ruptured aneurysm

Endovascular treatment [1] (ie, coiling)
The choice between coiling and clipping usually depends on the location of the lesion, the neck of the
aneurysm, and the availability and experience of hospital staff.
Screening is not recommended in the general population. However, it can lower cost and improve quality
of life in patients at relatively high risk for aneurysm formation and rupture.