Subarachnoid Hemorrhage Clinical Presentation

Updated: Dec 07, 2018
  • Author: Tibor Becske, MD; Chief Editor: Helmi L Lutsep, MD  more...
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The signs and symptoms of subarachnoid hemorrhage (SAH) range from subtle prodromal events to the classic presentation. Prodromal events often are misdiagnosed, while the classic presentation is one of the most pathognomonic pictures in all of clinical medicine.

Prodromal events

Signs and symptoms precede ruptured cerebral aneurysm in anywhere from 10-50% of cases. Premonitory manifestations generally appear 10-20 days prior to rupture. The most common 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 one or more of the following:

  • Sentinel leaks

  • Mass effect of aneurysm expansion

  • Emboli

Sentinel leaks

Sentinel, or "warning," leaks with minor loss of blood from the aneurysm are reported to occur in 30-50% of aneurysmal SAHs. Sentinel leaks produce sudden focal or generalized head pain that may be severe. Sentinel headaches precede aneurysm rupture by a few hours to a few months, with a reported mean of 2 weeks prior to discovery of the SAH.

In addition to headaches, sentinel leaks may produce nausea, vomiting, photophobia, malaise, or, less commonly, neck pain. These symptoms may be ignored by the physician. Therefore, a high index of suspicion is necessary for accurate diagnosis. Sentinel leaks usually do not generate symptoms suggestive of elevated intracranial pressure (ICP) or meningeal irritation. Sentinel leaks usually do not occur in patients with arteriovenous malformations.

Mass effect

Prodromal presentations occasionally are caused by the mass effect of an expanding aneurysm and have characteristic features based on aneurysm location, as follows:

  • Posterior communicating artery/internal carotid artery: focal, progressive retro-orbital headaches and oculomotor nerve palsy

  • Middle cerebral artery: contralateral face or hand paresis, aphasia (left side), contralateral visual neglect (right side)

  • Anterior communicating artery: bilateral leg paresis and bilateral Babinski sign

  • Basilar artery apex: vertical gaze, paresis, and coma

  • Intracranial vertebral artery/posterior inferior cerebellar artery: vertigo, components of lateral medullary syndrome


Emboli originating from intra-aneurysmal thrombus formation can cause transient ischemic attacks.

Classic presentation

The central feature of classic SAH is sudden onset of severe headache (thunderclap headache), often described as the "worst headache of my life." Less severe hemorrhages may cause headache of moderate intensity, neck pain, and nonspecific symptoms. Absence of headache in the setting of a ruptured intracranial aneurysm is rare and probably represents amnesia for the event.

The headache may be accompanied by nausea and/or vomiting from increased ICP and meningeal irritation. Symptoms of meningeal irritation, including nuchal rigidity and pain, back pain, and bilateral leg pain, occur in as many as 80% of patients with SAH but may take several hours to manifest. Photophobia and visual changes are common. Focal neurologic deficits may also occur.

Sudden loss of consciousness (LOC) occurs at the ictus in as many as 45% of patients as intracranial pressure (ICP) exceeds cerebral perfusion pressure. LOC often is transient; however, approximately 10% of patients remain comatose for several days, depending on the location of the aneurysm and the amount of bleeding.

Seizures during the acute phase of SAH occur in 10-25% of patients. Seizures result from the sudden rise in ICP or direct cortical irritation by blood. No correlation exists between the seizure focus and the anatomic site of aneurysm rupture.

A proposed decision rule for diagnosis of SAH focuses on the following 7 characteristics, which are strongly associated with SAH:

  • Aged 40 years or older

  • Witnessed loss of consciousness

  • Complaint of neck pain or stiffness

  • Onset of manifestations with exertion

  • Arrival by ambulance

  • Vomiting

  • Diastolic blood pressure ≥100 mm Hg or systolic blood pressure ≥160 mm Hg

Should one or more of these be present in a patient with an acute nontraumatic headache reaching maximum intensity within 1 hour, the possibility of SAH hemorrhage should be investigated. [12] On the other hand, it may be possible to consider foregoing investigation in patients with none of these characteristics. [12] This decision rule has not yet been validated. Further study is needed before this approach can be recommended.

Approximately 30-40% of patients are at rest at the time of SAH. Physical or emotional strain, defecation, coitus, and head trauma contribute to varying degrees in the remaining 60-70% of cases.


Physical Examination

Physical examination findings may be normal. About half of patients have mild to moderate blood pressure (BP) elevation. BP may become labile as ICP increases. Temperature elevation, secondary to chemical meningitis from subarachnoid blood products, is common after the fourth day following bleeding. Tachycardia may be present for several days after the occurrence of a hemorrhage.

Funduscopy may reveal papilledema. Subhyaloid retinal hemorrhage (small round hemorrhage, perhaps with visible meniscus, near the optic nerve head) is evident in 20-30% of patients. Other retinal hemorrhages may be seen.

Global or focal neurologic abnormalities are found in more than 25% of patients. Global depression of neurologic function may be noted, including altered level of consciousness and confusional state. Motor neurologic deficits occur in 10-15% of patients, usually from middle cerebral artery aneurysms. In 40% of patients, no localizing signs are evident. Seizures may occur.

Focal neurologic findings

Cranial nerve palsies, along with memory loss, are present in 25% of patients. The most frequent is oculomotor nerve palsy with or without ipsilateral mydriasis, which results from rupture of a posterior communicating artery aneurysm. Abducens nerve palsy is usually due to increased ICP rather than a true localizing sign. Monocular vision loss can be caused by an ophthalmic artery aneurysm compressing the ipsilateral optic nerve.

Hemiparesis results from middle cerebral artery (MCA) aneurysm, ischemia or hypoperfusion in the vascular territory, or intracerebral clot. Patients may also have aphasia, hemineglect, or both. Leg monoparesis or paraparesis with or without akinetic mutism/abulia points to anterior communicating aneurysm rupture.


Clinical Grading Scales

Clinical assessment of SAH severity commonly utilizes grading scales. The 2 clinical scales most often employed are the Hunt and Hess and the World Federation of Neurological Surgeons (WFNS) grading systems. A third, the Fisher scale, classifies SAH based on CT scan appearance and quantification of subarachnoid blood.

The WFNS scale is as follows:

  • Grade 1 - Glasgow Coma Score (GCS) of 15, motor deficit absent

  • Grade 2 - GCS of 13-14, motor deficit absent

  • Grade 3 - GCS of 13-14, motor deficit present

  • Grade 4 - GCS of 7-12, motor deficit absent or present

  • Grade 5 - GCS of 3-6, motor deficit absent or present

The Fisher scale (CT scan appearance) is as follows:

  • Group 1 - No blood detected

  • Group 2 - Diffuse deposition of subarachnoid blood, no clots, and no layers of blood greater than 1 mm

  • Group 3 - Localized clots and/or vertical layers of blood 1 mm or greater in thickness

  • Group 4 - Diffuse or no subarachnoid blood, but intracerebral or intraventricular clots are present

The Hunt and Hess grading system is as follows:

  • Grade 0 - Unruptured aneurysm

  • Grade I - Asymptomatic or mild headache and slight nuchal rigidity

  • Grade Ia - Fixed neurological deficit without acute meningeal/brain reaction

  • Grade II - Cranial nerve palsy, moderate to severe headache, nuchal rigidity

  • Grade III - Mild focal deficit, lethargy, or confusion

  • Grade IV - Stupor, moderate to severe hemiparesis, early decerebrate rigidity

  • Grade V - Deep coma, decerebrate rigidity, moribund appearance

In the Hunt and Hess system, the lower the grade, the better the prognosis. Grades 1-3 generally are associated with favorable outcome; these patients are candidates for early surgery. Grades IV and V carry a poor prognosis; these patients need stabilization and improvement to grade III before surgery is undertaken. Some recommend more aggressive management for patients with poor clinical grade.

Survival correlates with the grade of subarachnoid hemorrhage upon presentation. Reported figures include a 70% survival rate for Hunt and Hess grade I, 60% for grade II, 50% for grade III, 40% for grade IV, and 10% for grade V.

The Hunt and Hess and the WFNS grading systems have been shown to correlate well with patient outcome. The Fisher classification has been used successfully to predict the likelihood of symptomatic cerebral vasospasm, one of the most feared complications of SAH. All 3 grading systems are useful in determining the indications for and timing of surgical management. For an accurate assessment of SAH severity, these grading systems must be used in concert with the patient's overall general medical condition and the location and size of the ruptured aneurysm.



Some complications of SAH include the following:

  • Hydrocephalus

  • Rebleeding

  • Vasospasm

  • Seizures

  • Cardiac dysfunction


Hydrocephalus can be an acute or a delayed complication of SAH. Acute obstructive hydrocephalus complicates 20% of SAH cases. Clinical risk factors for the development of hydrocephalus include increased patient age, use of antifibrinolytic drugs, left ventricular systolic dysfunction, and seizures.

Acute hydrocephalus usually occurs within the first 24 hours after hemorrhage but may occur as late as 7 days afterward. It presents as a relatively abrupt mental status change, including lethargy, stupor, or coma. CT scan differentiates hydrocephalus from rebleeding.

Acute hydrocephalus can precipitate life-threatening brainstem compression and occlusion of blood vessels. It is associated with lower preoperative Hunt and Hess grade and poorer prognosis. Consequently, any change in the level of consciousness requires an emergent CT scan to evaluate ventricular size. An obtunded patient with dilated ventricles deserves an immediate ventriculostomy.

Late or chronic hydrocephalus, caused by scarring of the arachnoid granulations and alterations in CSF absorption, occurs in 10-15% of patients with SAH. Typically, late hydrocephalus is of the communicating type and develops 10 or more days after SAH. Patients may present with incontinence, gait instability, and cognitive deterioration. It may be impossible to distinguish late hydrocephalus from vasospasm clinically.


The incidence of the complication of rebleeding is greatest in the first 2 weeks. The peak is within 24-48 hours following initial SAH (approximately 6%), with a rate of 1.5% per day for the next 12-13 days. Clinical factors that increase the likelihood of rebleeding include the following:

  • Hypertension

  • Anxiety [5]

  • Agitation

  • Seizures


Currently, delayed ischemia from arterial smooth muscle contraction of the large capacitance vessels at the base of the brain is the leading cause of death and disability following aneurysmal SAH. Vasospasm is symptomatic in 36% of patients. The incidence of angiographic vasospasm is 30-70%; of these patients, 20-36% become symptomatic.

Risk factors for vasospasm include the following:

  • Larger volumes of blood in the subarachnoid space

  • Clinically severe SAH

  • Female sex

  • Young age

  • Smoking

Vasospasm may be clinically indistinguishable from rebleeding. Symptoms vary with the arterial territory involved, but patients typically present with a new-onset general decrease in consciousness or focal neurologic deficit. Lethargy, with or without focal neurologic deficit, is a manifestation of vasospasm, until proven otherwise.

Overall, vasospasm typically has its onset on day 3 after SAH, is maximal at about days 6-8, and usually resolves around day 12. However, the time of clinical onset differs according to whether the patient has had a prior SAH. In patients with previous SAH, the incidence of vasospasm is 38.7% in the first 3 days and only 20% between days 10 and 17. In patients with no prior SAH, most frequent time of onset is between days 10 and 17, with only a 4.2% incidence on day 3.

Overall, close to 50% of patients develop vasospasm in the peak period. Correlation between the initial CT scan and the incidence of vasospasm is well established. When the CT scan fails to demonstrate blood or shows only a thin layer, vasospasm is unlikely. If the CT scan shows a significant blood clot of 5 X 3 mm or larger, severe angiographic spasm and clinical deficits follow in nearly all cases.

Conventional angiography is the definitive imaging study for vasospasm. The diagnosis of vasospasm can be made reliably at the bedside in a noninvasive fashion with transcranial Doppler.

Other tests, such as single-photon emission computed tomography (SPECT), positron emission tomography (PET), xenon CT scan, and radioactive xenon clearance, can be useful for evaluation of regional cerebral blood flow in patients with vasospasm. However, these tests often are difficult to perform on critically ill patients.


Seizures occur in 13-24% of patients with SAH, commonly in the first 24 hours after the bleed. [13] They are most common after rupture of middle cerebral artery aneurysms. Generalized, partial, and complex-partial seizures are observed after SAH. Seizures can lead to increased cerebral blood flow, hypertension, and elevated ICP, thereby escalating the risk of rebleeding and neurologic deterioration.

Cardiac dysfunction

Cardiac dysfunction occurs in a significant number of people with SAH. Neurogenic sympathetic hyperactivity, as well as increased levels of systemic catecholamines, has been implicated in SAH-associated cardiac dysfunction. Arrhythmias occur in as many as 90% of patients and most commonly include the following:

  • Premature ventricular complexes (PVCs)

  • Bradyarrhythmias

  • Supraventricular tachycardia

Arrhythmias are most prevalent in the first 48 hours following SAH. Only a small percentage of arrhythmias (usually those associated with hypokalemia) are life-threatening.