Clinical presentation

Prodromal symptoms

  • these symptoms precede the aneurysm rupture in 10-50% of cases; they usually appear 10-20 days before the rupture
    • headaches
    • 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 an intra-aneurysmal thrombus (⇒ TIA symptoms)

Headaches

  • sudden onset of severe headache (typically, patients report the worst headache ever)
    • diffuse or unilateral
    • the pain usually lasts for several days and does not respond to conventional analgesics
    • absence of headache is rare
  • nausea with vomiting
    • symptom of an increased 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, jump, lifting a heavy load) or emotional stress
    •  approximately 30-40% of patients develop SAH during rest

Other symptoms and signs

  • hypertension (usually ≥160/100 mm Hg), tachycardia
  • low-grade fever (usually not in the initial stage) – 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  
    • papillary edema
    • possible monocular vision loss in case of compression of the ipsilateral optic nerve by aneurysm
  • symptomatic epileptic seizures (~ 5-20%), sometimes a non-convulsive status epilepticus (NCSE)
    • provoked by intracranial hypertension or by direct cortical irritation by blood
  • altered level of consciousness, confusional state
    • mild deficit or agitation are often transient
    • patients with severe SAH may be initially comatose (due to intracranial hypertension)
  • focal neurological deficits (depends on the aneurysm location and presence of a simultaneous intraparenchymal hematoma)
    • cranial nerve palsies – in 25% of patients  (mostly n.III, VI)
    • hemiparesis (10-15%), aphasia, neglect syndrome
    • akinetic mutism/abulia, leg mon- or paraparesis (ACA and ACoA aneurysm)
    • eye movement disturbances (from brainstem compression)
  • assess Hunt-Hess clinical score and WFNS SAH scale

Differential diagnosis

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Intracranial complications

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Intracranial hypertension

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

Aseptic meningitis

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Intraparenchymal hemorrhage

Intraventricular bleeding (hemocephalus)

Rebleeding

  • rebleeding is a significant cause of preoperative clinical deterioration or death (linked to 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 first SAH
  • risk of rebleeding is the reason for urgent diagnosis and management of SAH patients
  • clinical manifestation: worsening of headaches, new neurological deficit, impaired consciousness
  • brain CT confirms 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 a 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 CSF pathways     Acute obstructive hydrocephalus
  • an early complication of SAH (appearing < 72hrs), incidence approx. 30%
  • usually caused by a ventricular hemorrhage (hemocephalus) with subsequent blockage of the liquor passage
  • 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 neurologic 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 that represents 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 suspicious of its effects and long-term outcomes   [Tabibkhooei, 2020]
      • does not terminate 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
  • antiepileptic drugs are used when seizures occur; some authors advocate short prophylaxis during the perioperative period
  • long-term prophylactic anticonvulsive therapy is not recommended in patients without prior seizure activity

Extracranial complications

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