Clinical presentation and complications of subarachnoid hemorrhage

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)

Headache

• 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)    
  • 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 (du to brainstem compression)
• assess Hunt-Hess clinical score and WFNS SAH scale

Differential diagnosis

Intracranial complications

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

Intraparenchymal hemorrhage

• this co-occurrence worsens the prognosis, large, superficial ICH may require neurosurgical management

Intraventricular hemorrhage (hemocephalus)

• found in 10-30% of clinical cases of ruptured aneurysms (typically ACA and ICA)
• intraventricular hemorrhage (IVH) is a significant predictor of poor outcome

Rebleeding

• 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 worseing neurological deficit, impaired consciousness
• brain CT confirms the diagnosis

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 cerebrospinal fluid (CSF) pathways    
• an early complication of SAH (occuring 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) 
    • 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

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