SUBARACHNOID HEMORRHAGE
Clinical presentation and complications of subarachnoid hemorrhage
Created 29/03/2021, last revision 05/03/2023
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, 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:
- symptomatic epileptic seizures (~ 5-20%), sometimes a non-convulsive status epilepticus (NCSE)
- provoked by intracranial hypertension or by direct cortical irritation by blood
- 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)
- 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 (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 the diagnosis
Cerebral ischemia
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Vasospasms
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 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
- external ventricular drainage (EVD)
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 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
Extracranial complications
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