JC30 (Surgery) - Cerebrovascular events Flashcards

(36 cards)

1
Q

List 5 types of cranial haemorrhage typically caused by trauma or occur spontaneously

A

Traumatic/ spontaneous:

  • Lobar intracerebral haemorrhage
  • Subarachnoid haemorrhage

Traumatic:
- Extradural or subdural haemorrhage

Spontaneous:

  • Intraventricular haemorrhage
  • Deep intracerebral hemorrhage
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2
Q

Outline major subtypes of ischemic and haemorrhagic stroke

A

Ischemic stroke:

  • Thrombotic
  • Embolic
  • Systemic hypoperfusion

Haemorrhagic stroke:

  • Intracerebral
  • Subarachnoid
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3
Q

Compare onset between ischemic and hemorrhagic stroke subtypes

A

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)
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4
Q

Common sites of lacunar infarct

A

o Pons
o Thalamus
o Internal capsule/ Corona radiata
o Basal ganglia (caudate/ putamen/ globus pallidus/ subthalamic nuclei/ substantia nigra)

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5
Q

Common sites of ischemic stroke due to systemic hypoperfusion

A

Boundary zone (border/ watershed) regions between major cerebral artery supply are most vulnerable to systemic hypoperfusion

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6
Q

Define Transient ischemic attack

A

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

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7
Q

Criteria for risk of ischemic stroke following TIA

A

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%)

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8
Q

Causes of haemorrhagic stroke

A
  • Systemic HTN
  • Amyloid angiopathy (degenerative)
  • Hemorrhagic transformation of infarction
  • Bleeding tendency
  • Tumor bleeding
  • AVM, Moyamoya disease
  • Venous sinus thrombosis
  • Arterial dissection
  • Vasculitis
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9
Q

Incidence of ischemic stroke vs haemorrhagic stroke

A

Ischemic = 75%

Haemorrhagic = 25%
- SAH <5%
- ICH 20%

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10
Q

Non-modifiable risk factors of stroke

A
Advanced age
Higher risk at most ages for men
Higher risk for blacks
Medical history of TIA or stroke
Family history
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11
Q

Modifiable risk factors of stroke

A
  1. Hypertension (promotes athersclerosis) - lacunar infarct
  2. Diabetes mellitus - ischemic stroke, carotid atherosclerosis, carotid plaque
  3. Dyslipidemia - ischemic stroke
  4. Smoking - ischemic stroke and SAH
  5. Alcoholism
  6. Oral contraceptive pills
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12
Q

Etiologies of thrombosis formation in large vessels (intra- and extracranial)

A

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)
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13
Q

Etiologies of thrombosis formation in small intracranial vessels

A

Lipohyalinosis with fibrinoid degeneration
• Lipid deposition and accumulation of foamy macrophages
• Hyalinization and thickening of vessel wall
• Fibrinoid degeneration (necrosis) of vessel wall

Microatheroma

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14
Q

Etiologies/ sources of emboli causing ischemic stroke

A

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

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15
Q

Etiologies of systemic hypoperfusion causing ischemic stroke

A

 Pump failure
• Cardiac arrest
• Cardiac arrhythmia

 Decreased cardiac output (CO)
• Myocardial infarction (MI)
• Pericardial effusion/ Cardiac tamponade
• Pulmonary embolism

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16
Q

Etiologies of subarachnoid haemorrhage

A

□ 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%)
17
Q

Clinical features of SAH

A

Headache: characteristically sudden, severe, ‘thunderclap’
→ Often occipital, hours to days

LOC ± seizures

Focal neurological signs

Meningism: neck stiffness, photophobia

18
Q

Typical description of fundoscopic changes in SAH

A

papilloedema, subhyaloid haemorrhage*

(haemorrhage into space between hyaloid membrane surrounding the vitreous and retina)*

19
Q

Typical description of SAH on NECT

A

Urgent NECT: hyperdensity in subarachnoid space

→ ‘Star sign’: hyperdensity in basal cisterns, Sylvian and interhemispheric fissures
→ Sulcal hyperdensity

20
Q

Investigations for SAH

A

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)

21
Q

3 Complications of SAH and management

A
  1. Rebleeding* (days): endovascular coiling and antifibrinolytic agent
  2. Vasospasm* (1 week): blood in CSF trigger arteriole spasm
    - Nimodepine (cerebral selective CCB)
    - Angioplasty: mechanical or chemical
    - Triple-H therapy: Hypertension + Haemodilution + Hypervolemia
  3. Hydrocephalus (months)
    - CSF drainage

Others: cerebral oedema, seizures (consider prophylactic anticonvulsants), SIADH, arrhythmia

22
Q

Management plan for acute ischemic stroke:

  • Adjuvant
  • Reperfusion therapy
  • Medical therapy
A

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)
23
Q

Therapeutic window for IV tPA thrombolysis and endovascular theombectomy in acute ischemic stroke

A

tPA: 3-4.5 hours from symptom onset

Endovascular thrombectomy: 6 hours from symptom onset

24
Q

List 3 acute cerebral complications of acute ischemic stroke

A

→ Oedema, increased ICP, herniation
→ Haemorrhagic transformation of cerebral infarction
→ Seizures

25
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
26
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
27
How to manage haemorrhagic transformation of ischemic stroke after tPA thrombolysis?
rtPA-related IC, give prothrombin complex concentrate (PCC)
28
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 ```
29
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
30
Surgical treatment options for cerebral anuerysms
Microsurgical clipping Endovascular coiling/ stenting Flow diverter
31
4 types of cerebral vascular malformations
□ Arteriovenous malformation (AVM): most common, highest bleeding risk □ Cavernous angioma □ Venous angioma □ Capillary telangiectasia
32
Cerebral AVM - Cause - Pathological consequences
congenital: no capillaries between arteries and veins ``` Pathological consequences: □ Arteriovenous shunting □ Arterialized veins □ Venous varices □ A/w aneurysms ```
33
Clinical presentation of cerebral AVM
□ Haemorrhage □ Seizures □ Ischaemia due to vascular steal phenomenon □ Headache □ Others: bruit, hydrocephalus, heart failure
34
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
35
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
36
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