Clinical presentation and complications of subarachnoid hemorrhage

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, jumping, 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)    
  • 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

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

Intraparenchymal hemorrhage

Intraventricular bleeding (hemocephalus)

Rebleeding

Cerebral ischemia

Vasospasms

→ see Vasospasms in subarachnoid hemorrhage

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

Acute obstructive hydrocephalus

• acute dilatation of the lateral ventricles due to obstruction of CSF pathways    
• 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) 
    • 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

Epileptic seizures

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