Cerebrovascular accident (CVA) Flashcards
What is some epidemiology for CVAs?
More common in: Black Africans (than caucasians) Men After the age of 40 The morning – blood pressure is lowered at night then rises upon waking and is more likely to dislodge any embolism
What are some risk factors for CVA?
Age >65 Hypertension Smoking DM Heart disease – valvular, ischemic, AF Peripheral vascular disease Past TIA Carotid bruit The pill Raised lipids Raised alcohol use Raised clotting (raised plasma fibrinogen, low anti-thrombin etc Syphilis
What are some common aetiologies for CVAs?
Small vessel occlusion/cerebral microangiopathy or thrombosis
Cardiac emboli - AF, endocarditis, prosthetic valve, post MI/mural thrombus Atherothromboembolism i.e. from carotids or vertebrals
CNS bleed - Raised BP, trauma, aneurysm rupture, anticoagulation, thrombolysis
What are some other aetiologies for CVAs?
Sudden drop in blood pressure Carotid artery dissection – spontaneous or from neck trauma Vascultitis Subarachnoid haemorrhage Venous sinus thrombosis Antiphospholipid syndrome Thrombophilia
What is the pathophysiology of a CVA?
Ischemic infarction (80-90%) or haemorrhage (10-20%) into part of the brain
Infarct - Most commonly affected is the MCA or a branch of it
Haemorrhage - due to chronic HTN or AVM rupture
What is cell hypoxia and how does it cause damage in CVAs?
In either type of stroke there is a loss of blood to the tissues → Na/K pumps fail → Na accumulates in cells → upset in osmotic balance → cerebral oedema
i) → cells in area of infarct swell and burst → raised ICP → blood supply affected → vicious cycle
ii) → other local cells swell but do not burst, this area is called the penumbra and the point of treatment is to reduce further swelling and damage to these cells
What is excitotoxicity and how does it cause damage in CVAs?
Accumulation of Na within non lysed cells → continued depolarisation → damage via excitotoxicity
i) Also results in the failure of AMPA and NDMA receptors which allows excessive levels of Ca into the cells
→ release of free radicals → local necrosis.
→ production of cytokines → inflammation → increased oedema.
→ apotosis of cells in the penumbra.
What are some clinical pointers towards a haemorrhagic stroke?
(not necessarily reliable but…)
Meningism, severe headache and coma within hours
More likely to be progressive (whilst still having a sudden onset)
Nearly always due to uncontrolled chronic hypertension
i) Or cocaine, congenital aneurysm, AVM, clotting disorders or tumour
What are some clinical pointers towards an ischemic stroke?
Carotid bruit, AF, past TIA, IHD
What are some features of an MCA stroke?
Contralateral
Hemiplegia - initially flaccid then becoming spastic (as UMN lesion)
Dysphagia
Homonymous hemianopia, visuospatial deficit
Aphasia
Contralateral weakness in arm ± face
What are some features of an ACA stroke?
Dysarthria, aphasia
Unilateral contralateral motor weakness (leg/shoulder > arm/hand/face)
Minimal sensory changes (two-point discrimination) in the same distribution as above
Limb apraxia
Urinary incontinence
What are some features of a PCA stroke?
Visual disturbance
Cortical blindness
What are some features of a brainstem infarct?
Quadriplegia (Corticospinal tract)
Locked-in syndrome (aware but unable to respond) (upper brainstem infarct)
Disturbances of gaze/vision (Oculomotor nuclei)
Sensory loss (Spinothalamic tracts)
Facial weakness and numbness (5th and 7th cranial nerve nuclei)
Nystagmus and vertigo (Vestibular connections)
Dysphagia and dysarthria (9th and 10th cranial nerve nuclei)
Altered consciousness/coma (Reticular activating system)
What are some features of a lacunar infarct (basal ganglia, internal capsule, thalamus, pons)
May be asymptomatic.. otherwise 5x syndromes:
- Ataxic hemiparesis
- Pure motor stroke (only motor deficits)
- Pure sensory stroke
- Sensorimotor
- Dysarthria/clumsy hand
Cognition/consciousness is intact except in thalamic stroke
What do you expect to see on a CT/MRI head of an infarct?
Will always show up as a wedge shaped lesion
What do you expect to see on a CT/MRI head of a haemorrhage?
Appears hyperdense (bright white) but the longer it has been the darker it gets, after a couple of weeks it will be indistinguishable from brain tissue - can use this to estimate the duration of time which the haemorrhage has been present
Hyperdense MCA sign = a direct visualisation of thromboembolic material within the lumen and is the earliest visible sign of the event, appearing 90 mins post
The MCA dot and hyperdense basilar tip signs are the longitudinal equivalents
What are some general features of note when looking at a CT/MRI of a CVA?
Easier to see damage the longer it has been present i.e. 6-12hrs will be clearly visible (maybe not before)
Diffusion MRI scans are more sensitive than normal MRI/CT, especially with infarction - rely on the fact that the damaged cells are filled with water (at least in the early stages)
What cardiac examinations are performed?
ECG for AF? (embolus)
CXR for LA hypertrophy?
Echo for mural thrombus or hypokinetic segment of muscle post MI?
What vascular tests are performed?
Hypertension:
Retinopathy? Nephropathy? Cardiomegaly on CXR?
Carotid artery doppler USS
± CT/MRI angiography:
>70% stenosis is significant
What blood tests are performed?
Hypo/hyperglycaemia
Hyperlipidaemia
Hyperhomocysteinaemia (elevated homocysteine = amino acid who’s increased levels are associated with certain disease states as well as nutrient deficiencies such as B12, B6 and folic acid)
Vascultits – raised ESR, ANA+ve
Prothrombotic states:
Thrombophilia
Hyperviscosity:
Polycythaemia
Sickle cell disease
Thrombocytopenia + other bleeding disorders
What is the first stage of acute management?
Give aspirin 300mg PO once haemorrhagic stroke excluded
Protect the airway – to avoid hypoxia or aspiration
NBM
If swallowing attempts can lead to chocking
Hydrate with IVI: But don’t overhydrate – cerebral oedema
Pulse, BP:
Treating high BP may cause harm in this instance as too much of a drop can compromise cerebral perfusion as autoregulation is impaired
Stop HRT if on
Aim for glucose 4-11mmol/L
What circumstances is a sub 1hr CT/MRI needed?
If thrombolysis is considered
High risk of haemorrhage: Low GCS Raised ICP Severe headache Meningism Progressive symptoms Known bleeding tendency or anticoagulated
Suspected haemorrhagic cerebellar stroke
Unusual presentation with alternative diagnoses likely: Head injury Hypo/hyperglycaemia SDH Tumour Hepatic encephalopathy etc
When is thrombolysis considered?
If found to be ischemic stroke with symptom onset <4.5hrs
Give alterplase 900 micrograms/kg over 60mins via IVI; first 10% of dose given IV injection
(fibrinolytic)
What are some absolute contraindications to thrombolysis?
Previous intracranial haemorrhage
Seizure at onset of stroke
Intracranial neoplasm
Suspected SAH
Stroke or TBI in previous 3m
LP in past 7 days
GI haemorrhage in past 3w
Active bleeding
Pregnancy
Oesophageal varicies
When is thrombectomy considered?
If found to be ischemic stroke within the proximal anterior circulation, with symptom onset <6hrs
Surgical extraction of clot
+
thrombolysis (within 4.5hr window)
What other surgery may be indicated in the event of an ischemic stroke?
Carotid endarterectomy
If carotid Doppler shows stenosis >70% and patient has suffered a stroke or TIA in the carotid territory and is not severely disabled
How do you manage a haemorrhagic stroke in a patient on anticoagulants?
Stop warfarin and give vit K
Stop heparin and give protamine sulphate
Seek specialist advice if on NOAC
What pharmacological secondary prevention is recommended following an ischemic stroke?
1st line antiplatelet:
Clopidogrel
2nd line antiplatelet:
Aspirin + dipyridamole
If secondary to AF:
Warfarin - start 2wks post stroke
What non pharmacological prevention is recommended following any kind of stroke?
Manage underlying pathology:
Hypertension
DM
Raised lipids – give statins
Exercise increase – increases HDL and glucose tolerance
Quit smoking
What kind of rehab might be required after a stroke?
Physiotherapy:
Prevent spasticity and contractures and teaches patients to cope with current level of function
SALT:
Dysphagia
?PEG feeding if persistent
Dysphasia
OT:
Looks at level of function and makes home and lifestyle alterations
Optometry:
For any hemianopias etc
Psychiatry:
For any depression following – SSRIs/therapy
What is the Bamford classification of stroke?
Classification system using clinical features only (and not imaging) to diagnose a stroke
4 clinical pictures: Total anterior circulation stroke (TACS) Partial anterior circulation stroke (PACS) Posterior circulation syndrome (POCS) Lacunar syndrome (LACS)
What is required for a TACS diagnosis?
A total anterior circulation stroke (TACS) involves a large cortical stroke affecting the areas of the brain supplied by both the middle and anterior cerebral arteries.
All three of the following need to be present for a diagnosis of TACS:
Unilateral weakness (and/or sensory deficit) of the face, arm and leg Homonymous hemianopia Higher cerebral dysfunction (dysphasia, visuospatial disorder)
What is required for a PACS diagnosis?
A partial anterior circulation stroke (PACS) is a less severe form of TACS, in which only part of the anterior circulation has been compromised.
Two of the following need to be present for a diagnosis of PACS:
Unilateral weakness (and/or sensory deficit) of the face, arm and leg Homonymous hemianopia Higher cerebral dysfunction (dysphasia, visuospatial disorder)
What is required for a POCS diagnosis?
A posterior circulation syndrome (POCS) involves damage to the area of the brain supplied by the posterior circulation (e.g. cerebellum and brainstem).
One of the following need to be present for a diagnosis of POCS:
Cranial nerve palsy and a contralateral motor/sensory deficit
Bilateral motor/sensory deficit
Conjugate eye movement disorder (e.g. horizontal gaze palsy)
Cerebellar dysfunction (e.g. vertigo, nystagmus, ataxia)
Isolated homonymous hemianopia
What is required for a LACS diagnosis?
A lacunar syndrome (LACS) involves a subcortical stroke that occurs secondary to small vessel disease. There is no loss of higher cerebral functions (e.g. dysphasia).
One of the following needs to be present for a diagnosis of LACS:
Pure sensory stroke
Pure motor stroke
Senori-motor stroke
Ataxic hemiparesis
What territories do each of the cerebral arteries supply?
The anterior cerebral arteries supply the anteromedial area of the cerebrum
The middle cerebral arteries supply the majority of the lateral cerebrum
The posterior cerebral arteries supply a mixture of the medial and lateral areas of the posterior cerebrum
