Clinical presentation

Prodromal symptoms

  • these symptoms precede the aneurysm rupture in 10-50% of cases and usually occur 10-20 days before rupture
    • headache
    • dizziness, nausea, vomiting
    • orbital pain, diplopia, visual loss
    • seizures
    • photophobia
  • etiology of prodrome symptoms:
    • sentinel leaks (“weeping aneurysm”)
    • the mass effect of an aneurysm (see below)
    • embolism from intra-aneurysmal thrombus (⇒ TIA symptoms)


  • sudden onset of severe headache (typically, patients report the worst headache ever)
    • diffuse or unilateral, reaches maximal intensity within minutes
    • pain usually lasts for several days and does not respond to conventional analgesics
    • absence of headache is rare
  • headache is often associated with nausea and vomiting
    • symptom of increased intracranial pressure (ICP) and meningeal irritation
    • unlike migraine, vomiting in SAH does not bring relief
    • take care of aspiration risk
  • headache may be provoked (60-70% of cases) by physical exertion and/or Valsalva maneuver (defecation, coitus, jumping, lifting a heavy load) or emotional stress
    •  approximately 30-40% of patients develop SAH at rest

Other symptoms and signs

  • hypertension (usually ≥160/100 mm Hg), tachycardia
  • low-grade fever (usually not in the early stages) – secondary to chemical meningitis from blood products
  • meningeal syndrome
    • nuchal rigidity and neck pain develop within tens of minutes to several hours
    • Kernig’s sign or Brudzinski’s sign and low back pain develop later (several hours)
    • photophobia
    • absence of meningeal syndrome does not exclude SAH
  • ocular symptoms:
    • conjunctival and subhyaloid retinal hemorrhages (Terson syndrome)   Terson syndrome  
    • papilledema
    • possible monocular vision loss caused by the compression of the ipsilateral optic nerve by the aneurysm
  • symptomatic epileptic seizures (~ 5-20%), sometimes a non-convulsive status epilepticus (NCSE)
    • provoked by intracranial hypertension or direct cortical irritation by blood
  • altered level of consciousness, confusional state
    • mild deficit or agitation are often transient
    • patients with severe SAH may initially be comatose (due to intracranial hypertension)
  • focal neurologic deficits (depending on aneurysm location and presence of concomitant intraparenchymal hematoma)
    • cranial nerve palsies – in 25% of patients (mostly CN III and VI)
    • hemiparesis (10-15%), aphasia, neglect syndrome
    • akinetic mutism/abulia, mon- or paraparesis (ACA and ACoA aneurysm) on lower extremities
    • eye movement disturbances (due to brainstem compression)
  • assess Hunt-Hess clinical score and WFNS SAH scale

Differential diagnosis

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Intracranial complications

Intracranial complications Extracranial complications
aseptic meningitis cardiovascular complications
intraparenchymal hemorrhage
pulmonary complications (ARDS)
intraventricular hemorrhage (IVH)
fluid and electrolytes dysbalance
vasospasms (VSP) +/- cerebral ischemia (DID)
traumatic lesions
mass effect
acute obstructive (non-communicating) hydrocephalus
non-resorptive hydrocephalus
epileptic seizures
intracranial hypertension

Intracranial hypertension

  • increased ICP due to:
    • mass effect of blood (subarachnoid, intracisternal, intraventricular, or subdural hemorrhage)
    • acute hydrocephalus
  • once ICP reaches mean arterial pressure (MAP), cerebral flow ceases ⇒ intracranial circulatory arrest

Aseptic meningitis

  •  a sterile inflammatory response of the meninges to the presence of blood in the subarachnoid space
  • patients may experience headaches, neck stiffness, photophobia (sensitivity to light), fever, and other signs similar to infectious meningitis (all symptoms of SAH itself)
    • it may be difficult to distinguish symptoms of rebleeding from aseptic meningitis
  • lumbar puncture can be performed, which shows an elevated white cell count in the CSF but without the presence of infectious agents
  • meningeal adhesions may lead to hyporesorptive hydrocephalus (see below), which must always be excluded when progressive headaches develop
  • corticosteroids (SOLUMEDROL 250-500mg per day in IV infusion for several days) have a good effect when conventional analgesics fail

Key differences between rebleeding and aseptic meningitis:

  • onset – rebleeding is usually sudden and severe, whereas aseptic meningitis has a more gradual onset
  • symptom severity – the headache from rebleeding is typically more intense than that from aseptic meningitis.
  • neurological symptoms – new or worsening neurological deficits are more indicative of rebleeding
  • CSF analysis and imaging – CSF analysis shows signs of inflammation in meningitis and fresh blood in rebleeding; rebleeding can further be verified through imaging

Intraparenchymal and subdural hemorrhage

  • ICH is present in ~ 30% of cases and worsens the prognosis
  • management of large ICHs:
    • hematoma evacuation with simultaneous aneurysm clipping
    • immediate endovascular coiling or aneurysm occlusion followed by hemicraniectomy
  • acute subdural hematoma is rare; immediate evacuation may be necessary for life-threatening hematomas

Intraventricular hemorrhage (hemocephalus)


  • rebleeding is a significant cause of preoperative clinical deterioration or death (associated with 50% mortality)
    • 20-30% of patients rebleed within the first 30 days
    • 4% within the first 12-24 hours,  ~70%  within 5 days from the initial SAH
  • the risk of rebleeding is the reason for urgent diagnosis and treatment of SAH patients
  • clinical manifestation: worsening headache, new or worsening neurological deficit, impaired consciousness
  • brain CT confirms the diagnosis

Cerebral ischemia

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Intracranial traumatic lesions

  • contusions or hemorrhagic contusions, subdural and epidural hematoma
  • sometimes, it is difficult to distinguish traumatic SAH from spontaneous SAH with subsequent head trauma

Mass effect and neurovascular compression syndromes

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Acute obstructive hydrocephalus

  • acute dilatation of the lateral ventricles due to obstruction of cerebrospinal fluid (CSF) pathways     Acute obstructive hydrocephalus
  • an early complication of SAH (occurring usually in the first 72 hours), incidence ~ 30%
  • usually caused by ventricular hemorrhage (hemocephalus) with subsequent CSF passage obstruction
  • it is triventricular and leads to clinical deterioration (mainly impaired consciousness) within the first days after SAH
  • treatment includes:
    • external ventricular drainage (EVD)  Acute obstructive hydrocephalus before and after external ventricular drain
      • depending on clinical neurological dysfunction and CT scan findings
      • avoid rapid lowering of ICP during intraventricular catheter placement (higher risk of rebleeding)
    • endoscopic third ventriculostomy (ETV)
      • an endoscopic procedure is an alternative to EDV
      • it comprises fenestrating the floor of the third ventricle (Lamina Terminalis Fenestration – LTF) and thus establishing a free flow of  CSF from the ventricles to the site of resorption in the subarachnoid space
      • may reduce the rate of shunt-needed hydrocephalus, some authors remain skeptical about its effects and long-term outcomes   [Tabibkhooei, 2020]
      • does not stop or delay the fibrotic process of the leptomeninges and arachnoid granulations

Non-resorptive hydrocephalus

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Epileptic seizures

  • focal or generalized seizures
  • risk factors: MCA aneurysm, intraparenchymal bleeding, ischemic lesion
  • antiseizure medications (ASMs) are used if seizures occur; some authors advocate short-term prophylaxis during the perioperative period
  • long-term prophylactic therapy is not recommended in patients without a history of seizure activity

Extracranial complications

Cardiovascular complications

  • caused by sympathetic activation, risk increases with the severity of SAH
    • arrhythmias (atrial fibrillation or flutter, SV tachycardia) – 35% → arrhythmias
    • T-wave inversion, ST-segment elevation/depression (46%) – can mimic myocardial infarction (MI) but can also be a sign of true MI (check enzymes, clinical presentation, serial ECG)
    • impaired wall kinetics (15%) – left ventricular systolic dysfunction is associated with abnormal sympathetic innervation
  • cardiac monitoring is required:
    • ECG
    • cardiac enzymes + troponin
    • TTE to exclude focal or global hypokinesis
  • administer beta-blockers if necessary

Respiratory complications

  • neurogenic pulmonary edema (in ~ 30%, usually developing within hours of the hemorrhage)
    • the sympathetic nervous system triggers a rapid cascade of events leading to interstitial and intraalveolar edema with a hemorrhagic component ⇒ hypoxemia and hypotension
  • cardiogenic pulmonary edema
  • pneumonia
  • pulmonary embolism


  • SAH-induced hyponatremia is present in up to 30-40% of cases
  • etiology:
    • Cerebral Salt Wasting Syndrome (CSWS) –  excessive natriuresis with subsequent dehydration due to elevated atrial or cerebral natriuretic peptide (ANP) levels
    • Syndrome of inappropriate secretion of antidiuretic hormone (SIADH)
    • adrenal insufficiency (hyper-renin hypoaldosteronism) [Zipser, 1981]
  • therapy
    • depending on etiology, DDx of CSWS and SIADH may be challenging in some cases; severe cases require specialist consultation
    • in mild hyponatremia, use mildly hypertonic sodium chloride (1.5% sodium chloride)
    • avoid fluid restriction

Other systemic complications

  • hypernatremia
    • hyperosmolality from the water loss can lead to neuronal cell shrinkage and brain injury;  volume loss can lead to circulatory problems (e.g., tachycardia, hypotension)
    • acute symptomatic hypernatremia (lasting < 24h) should be corrected rapidly
    • chronic hypernatremia (>48 h) should be corrected gradually because of the risks of cerebral edema due to rapid correction
  • hypomagnesemia (↑ risk of VSP)
  • hypokalemia
  • diabetes insipidus (DI)
  • hyperglycemia
  • fever
  • anemia (Hb < 90 g/L worsens clinical outcome; threshold is < 100g/L if VSPs are present)
  • deep vein thrombosis (check calves regularly)
  • hospital-acquired infections


  • the most common symptom of SAH is a sudden, severe headache often described as “the worst headache of my life”
  • headache is typically very intense and peaks within seconds to minutes
  • yes, SAH can present with neurological deficits such as confusion, blurred vision, double vision, weakness on one side of the body, and seizures, depending on the severity and location of the SAH and complications
  • SAH can lead to a loss of consciousness at onset in about 45% of patients
  • the level of consciousness can vary from drowsiness to deep coma, depending on the severity of the hemorrhage
  • ves, neck stiffness or pain is a common symptom of SAH, occurring due to irritation of the meninges (meningismus)
  • this symptom typically develops several hours after the initial hemorrhage
  • photophobia, or light sensitivity, is a symptom that can be associated with SAH, along with other symptoms like headache and neck stiffness
  • vasospasm refers to the narrowing of blood vessels, which can occur after SAH
  • it typically develops 4-12 days post-hemorrhage and can lead to reduced blood flow, potentially causing secondary brain ischemia and stroke
  • rebleeding is a recurrence of bleeding from the same aneurysm and is a serious complication of SAH
  • the risk is highest in the first 24 hours and remains significant within the first 2 weeks
  • hyponatremia is a common complication of SAH, often resulting from syndrome of inappropriate antidiuretic hormone secretion (SIADH) or cerebral salt-wasting syndrome (CSWS)
  • Yes, patients with SAH are at increased risk of DVT and PE due to immobility, especially in those with severe neurological impairment
  • prophylactic measures should be employed to mitigate this risk.
  • long-term complications can include cognitive impairment, memory deficits, mood changes, and persistent headaches
  • the extent varies based on the severity of the initial hemorrhage and complications

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Clinical presentation and complications of subarachnoid hemorrhage