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MBBS IV - Junior Clerkship WCS > JC30 (Surgery) - Cerebrovascular events > Flashcards

JC30 (Surgery) - Cerebrovascular events Flashcards

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
Q

List 3 delayed cerebral complications of ischemic stroke with rapid deterioration in mental status*

A

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
Q

Haemorrhagic transformation of ischemic stroke

  • Cause
  • Time course
  • S/S
  • Management
A

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
Q

How to manage haemorrhagic transformation of ischemic stroke after tPA thrombolysis?

A

rtPA-related IC, give prothrombin complex concentrate (PCC)

28
Q

Cerebral anuerysms:

  • Sites
  • Etiologies
A

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
Q

Compare surgical and medical CNIII palsy

A

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
Q

Surgical treatment options for cerebral anuerysms

A

Microsurgical clipping

Endovascular coiling/ stenting

Flow diverter

31
Q

4 types of cerebral vascular malformations

A

□ Arteriovenous malformation (AVM): most common, highest bleeding risk
□ Cavernous angioma
□ Venous angioma
□ Capillary telangiectasia

32
Q

Cerebral AVM

  • Cause
  • Pathological consequences
A

congenital: no capillaries between arteries and veins

Pathological consequences:
□ Arteriovenous shunting
□ Arterialized veins
□ Venous varices
□ A/w aneurysms
33
Q

Clinical presentation of cerebral AVM

A

□ Haemorrhage
□ Seizures
□ Ischaemia due to vascular steal phenomenon
□ Headache
□ Others: bruit, hydrocephalus, heart failure

34
Q

Modalities of surgical treatment of cerebral AVM

A

Modalities:
→ Surgical excision: usually for smaller AVMs

→ Embolization of feeder artery: usually for larger AVMs

→ Radiosurgery: better response for smaller AVMs

35
Q

Moyamoya disease

  • Cause
  • Pathological consequences
  • Presentation in children and adults
  • Management
A

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
Q

Cervical arterial dissection

  • 2 major causes
  • Symptoms
  • Pathological consequences
  • Management
A

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

MBBS IV - Junior Clerkship WCS (131 decks)

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