JC30 (Surgery) - Cerebrovascular events Flashcards
List 5 types of cranial haemorrhage typically caused by trauma or occur spontaneously
Traumatic/ spontaneous:
- Lobar intracerebral haemorrhage
- Subarachnoid haemorrhage
Traumatic:
- Extradural or subdural haemorrhage
Spontaneous:
- Intraventricular haemorrhage
- Deep intracerebral hemorrhage
Outline major subtypes of ischemic and haemorrhagic stroke
Ischemic stroke:
- Thrombotic
- Embolic
- Systemic hypoperfusion
Haemorrhagic stroke:
- Intracerebral
- Subarachnoid
Compare onset between ischemic and hemorrhagic stroke subtypes
Ischemic:
- Thrombosis: Stuttering progression with periods of improvement
- Embolic: Sudden onset, deficit maximal at onset
- Systemic hypoperfusion: Diffuse, gradual onset
Haemorrhagic:
- Intracerebral haemorrhage: Gradual progression (mins or hours)
- Subarachnoid haemorrhage: Sudden onset (seconds)
Common sites of lacunar infarct
o Pons
o Thalamus
o Internal capsule/ Corona radiata
o Basal ganglia (caudate/ putamen/ globus pallidus/ subthalamic nuclei/ substantia nigra)
Common sites of ischemic stroke due to systemic hypoperfusion
Boundary zone (border/ watershed) regions between major cerebral artery supply are most vulnerable to systemic hypoperfusion
Define Transient ischemic attack
Transient episode of neurological dysfunction caused by focal brain, spinal cord or retinal ischemia without an acute infarction
Fully reversible neurological deficit lasting < 24 hours with no structural brain damage
NO evidence of infarction on neuroimaging
Criteria for risk of ischemic stroke following TIA
ABCD2 score (Guidelines by (AHA/ASA)
Estimate the risk of ischemic stroke in the first 2 days after TIA
o Score 0 – 3: Low 2-day stroke risk (1%)
o Score 4 – 5: Moderate 2-day stroke risk (4%)
o Score 6 – 7: High 2-day stroke risk (8%)
Causes of haemorrhagic stroke
- Systemic HTN
- Amyloid angiopathy (degenerative)
- Hemorrhagic transformation of infarction
- Bleeding tendency
- Tumor bleeding
- AVM, Moyamoya disease
- Venous sinus thrombosis
- Arterial dissection
- Vasculitis
Incidence of ischemic stroke vs haemorrhagic stroke
Ischemic = 75%
Haemorrhagic = 25%
- SAH <5%
- ICH 20%
Non-modifiable risk factors of stroke
Advanced age Higher risk at most ages for men Higher risk for blacks Medical history of TIA or stroke Family history
Modifiable risk factors of stroke
- Hypertension (promotes athersclerosis) - lacunar infarct
- Diabetes mellitus - ischemic stroke, carotid atherosclerosis, carotid plaque
- Dyslipidemia - ischemic stroke
- Smoking - ischemic stroke and SAH
- Alcoholism
- Oral contraceptive pills
Etiologies of thrombosis formation in large vessels (intra- and extracranial)
Intracranial:
- Atherosclerosis
- Arterial dissection
- Vasospasm/ Vasoconstriction
- Moyamoya disease
Extracranial
- Atherosclerosis
- Arterial dissection
- Vasculitis
- Fibromuscular dysplasia (abnormal alternating thick and thin fibromuscular ridges with collagen in vessels/ string on beads sign)
Etiologies of thrombosis formation in small intracranial vessels
Lipohyalinosis with fibrinoid degeneration
• Lipid deposition and accumulation of foamy macrophages
• Hyalinization and thickening of vessel wall
• Fibrinoid degeneration (necrosis) of vessel wall
Microatheroma
Etiologies/ sources of emboli causing ischemic stroke
Cardiac causes:
- Myocardial infarction
- Arrhythmia
- Valvular heart diseases: prosthetic valve, infective endocarditis or non-bacterial thrombotic endocarditis
- Dilated cardiomyopathy
- Atrial or ventricular thrombus
- Left atrial myxoma
Aortic cause:
- Atheroma from PAD
Etiologies of systemic hypoperfusion causing ischemic stroke
Pump failure
• Cardiac arrest
• Cardiac arrhythmia
Decreased cardiac output (CO)
• Myocardial infarction (MI)
• Pericardial effusion/ Cardiac tamponade
• Pulmonary embolism
Etiologies of subarachnoid haemorrhage
□ Trauma: the most common cause of SAH (not aneurysm)
□ Spontaneous SAH: → (Berry) aneurysm (75%) → Arteriovenous malformation (AVM) (5%) → Tumours or bleeding tendency (5%) → Idiopathic (15%)
Clinical features of SAH
Headache: characteristically sudden, severe, ‘thunderclap’
→ Often occipital, hours to days
LOC ± seizures
Focal neurological signs
Meningism: neck stiffness, photophobia
Typical description of fundoscopic changes in SAH
papilloedema, subhyaloid haemorrhage*
(haemorrhage into space between hyaloid membrane surrounding the vitreous and retina)*
Typical description of SAH on NECT
Urgent NECT: hyperdensity in subarachnoid space
→ ‘Star sign’: hyperdensity in basal cisterns, Sylvian and interhemispheric fissures
→ Sulcal hyperdensity
Investigations for SAH
Urgent NECT
3 bottle Lumbar puncture if CT negative: Uniformly blood stained progress to Xanthochromia (bilirubin in CSF)
Angiography: digital subtraction angiography
(MRI not sensitive at early stage)
3 Complications of SAH and management
- Rebleeding* (days): endovascular coiling and antifibrinolytic agent
- Vasospasm* (1 week): blood in CSF trigger arteriole spasm
- Nimodepine (cerebral selective CCB)
- Angioplasty: mechanical or chemical
- Triple-H therapy: Hypertension + Haemodilution + Hypervolemia - Hydrocephalus (months)
- CSF drainage
Others: cerebral oedema, seizures (consider prophylactic anticonvulsants), SIADH, arrhythmia
Management plan for acute ischemic stroke:
- Adjuvant
- Reperfusion therapy
- Medical therapy
Adjuvant:
- ABC and ICP control with Mannitol, permissive HTN
- Surgical decompression by CSF drainage, decompressive craniectomy
Reperfusion therapy:
- IV tissue plasminogen activator (tPA, Alteplase) thrombolysis
- Endovascular mechanical thrombectomy (anterior circulation, large arteries only)
Medical therapy:
- Antiplatelet: aspirin
- (Anticoagulant: only for venous thrombosis, cardioembolism, arterial dissection)
Therapeutic window for IV tPA thrombolysis and endovascular theombectomy in acute ischemic stroke
tPA: 3-4.5 hours from symptom onset
Endovascular thrombectomy: 6 hours from symptom onset
List 3 acute cerebral complications of acute ischemic stroke
→ Oedema, increased ICP, herniation
→ Haemorrhagic transformation of cerebral infarction
→ Seizures
List 3 delayed cerebral complications of ischemic stroke with rapid deterioration in mental status*
Malignant MCA syndrome: vasogenic and cytotxic edema causing large hemispheric infarct in MCA
Posterior fossa infarct: obstructive hydrocephalus, coning
Haemorrhagic transformation*: reperfusion with disrupted BBB with raised ICP
Haemorrhagic transformation of ischemic stroke
- Cause
- Time course
- S/S
- Management
Cause: reperfusion with disrupted BBB → extravasation of blood with ↑ICP
S/S: rapid deterioration in mental status (i.e. ↓GCS) on day 1-2 after stroke
Mx:
→ Medical: ABC, elevate bed head, IV mannitol, hyperventilation (salvage)
→ Surgical: external ventricular drainage, emergency hemicraniectomy
How to manage haemorrhagic transformation of ischemic stroke after tPA thrombolysis?
rtPA-related IC, give prothrombin complex concentrate (PCC)
Cerebral anuerysms:
- Sites
- Etiologies
Site: usually at arterial bifurcations
□ Majority along circle of Willis
□ 90% anterior circulation
Aetiology: unknown but related to □ Haemodynamic stress □ Connective tissue diseases, eg. Ehler-Danlos, Marfan’s □ Adult polycystic kidney disease □ Coarctation of aorta □ Family history
Compare surgical and medical CNIII palsy
Surgical CNIII palsy: due to tumor or aneurysm compression
- Peripheral parasympathetic fibers damage
- Central fibers intact (eye movement intact)
> Dilated pupil and ptosis
Medical CNIII palsy: vascular disease e.g. DM
- Central fibers damage
> Loss of eye movement without ptosis
Surgical treatment options for cerebral anuerysms
Microsurgical clipping
Endovascular coiling/ stenting
Flow diverter
4 types of cerebral vascular malformations
□ Arteriovenous malformation (AVM): most common, highest bleeding risk
□ Cavernous angioma
□ Venous angioma
□ Capillary telangiectasia
Cerebral AVM
- Cause
- Pathological consequences
congenital: no capillaries between arteries and veins
Pathological consequences: □ Arteriovenous shunting □ Arterialized veins □ Venous varices □ A/w aneurysms
Clinical presentation of cerebral AVM
□ Haemorrhage
□ Seizures
□ Ischaemia due to vascular steal phenomenon
□ Headache
□ Others: bruit, hydrocephalus, heart failure
Modalities of surgical treatment of cerebral AVM
Modalities:
→ Surgical excision: usually for smaller AVMs
→ Embolization of feeder artery: usually for larger AVMs
→ Radiosurgery: better response for smaller AVMs
Moyamoya disease
- Cause
- Pathological consequences
- Presentation in children and adults
- Management
Progressive occlusion of cerebral vasculature, esp CoW and its feeding vessels
Fragile collaterals develop late in adulthood → ‘puff-of-smoke’ appearance on angiogram
Presentation:
□ Ischaemic symptoms in young
□ Haemorrhagic symptoms in adults
Synangiosis: connection of extracerebral arteries onto pia to allow revascularization of brain
Cervical arterial dissection
- 2 major causes
- Symptoms
- Pathological consequences
- Management
Causes:
- Spontaneous: connect tissue disorder
- Traumatic: neck rotation injury
Symptoms:
- ICA: retroorbital pain, Horner’s syndrome
- VA: occipital pain, vertevrobasilar symptoms
Consequences:
- Ischemia
- Dissecting aneurysm rupture and SAH
Mx:
- Anticoagulant (stable)
- Endovascular or bypass surgery
