Stroke, TIA and SAH

Question 2

Stroke - definition

Answer 2

Ischaemic infarction or bleeding causes rapid onset focal neurological signs and symptoms. The incidence is 1.5 per 1000 per year but rises with age to 10 per 1000 per year at 75 years of age.

Question 3

Stroke - causes

Answer 3

• Ischaemic – small vessel occlusion = thrombosis, cardiac emboli e.g. in AF, endocarditis or MI or atherothromboembolism e.g. from the caroitid arteries.
• Haemorrhagic – hypertension, trauma, aneurysm rupture, anticoagulation or thrombolysis.
• Rarer causes – sudden drop in BP >40mmHg e.g. in sepsis causes a watershed stroke, carotid artery dissection (spontaneous or from neck trauma), vasculitis, subarachnoid haemorrhage, venous sinus thrombosis, antiphospholipid syndrpme, thrombophilia or Fabry’s disease.

Question 4

Stroke - risk factors

Answer 4

Hypertension, smoking, diabetes mellitus, heart disease (valvular, ischaemic or AF), peripheral vascular disease, previous TIA or stroke, increased packed cell volume, carotid bruit, oral contraceptive pill, alcoholism, clotting tendency, increased homocysteine or syphilis.

Question 5

Stroke - signs

Answer 5

• Haemorrhagic indicators – signs of meningism, severe headache and coma within hours.
• Ischaemic indicators – carotid bruits, atrial fibrillation, previous TIA or ischaemic heart disease.
• Cerebral hemisphere infarcts – contralateral hemiplegia – initially flaccid then spastic paralysis, contralateral sensory loss, dysphasia, homonymous hemianopia and visuo-spatial defects.
• Brainstem infarcts – quadriplegia, disturbances in gaze and vision or locked-in syndrome.
• Lacunar infarcts – small infarcts around the basal ganglia, internal capsule, thalamus and pons. 5 lacunar syndromes are described – pure motor, ataxic hemiparesis, pure sensory, mixed sensorimotor and dysarthria. Cognition and consciousness will remain intact.

Question 6

Stroke - differential diagnosis

Answer 6

Head injury, subdural haemorrhage, hypo or hyperglycaemia, intracranial tumours, hemiplegic migraine, epilepsy (Todd’s paralysis), Wernicke’s, hepatic or herpes encephalopathy, drug overdose (if in coma), CNS lymphoma, pneumocephalus (air entry via otitis, mastoid air cells or trauma), HIV, toxoplasmosis (in AIDs) or abscess (e.g. typhoid).

Question 7

Stroke - acute management

Answer 7

• ABC – ensure airway is patent to avoid hypoxia or aspiration.
• Monitor blood glucose – keep between 4-11 mmol/L – give insulin if diabetic or uncontrolled BM.
• Monitor blood pressure – however treatment may result in inadequate cerebral perfusion.
• Urgent CT or MRI – if thrombolysis considered, cerebellar stroke (as requires urgent evacuation), unusual presentation or patient is at high risk of haemorrhage otherwise imaging can wait!
• Thrombolysis – consider if patient is aged 18-80 years and onset of symptoms was <48 hours ago.
• Keep patient nil by mouth until swallowing assessed but ensure adequate hydration.
• Antiplatelet agent – once haemorrhagic stroke is excluded give 300mg aspirin.
• Admission to a stroke unit – for multidisciplinary team e.g. specialist nursing and physiotherapy.

Question 8

Stroke - thrombolysis

Answer 8

Consider when the patient is seen within 4.5 hours and no contraindication exist urgently refer the patient for reperfusion with 0.9mg/kg alteplase (tPA) over 1 hour. Small increased risk of intracranial bleeding - all should have a CT head 24 hours post-thrombolysis to identify haemorrhage.

Contraindications – haemorrhage on CT, mild non-disabling deficits, recent surgery, trauma or obstetric delivery, previous CNS haemorrhage, known aneurysm, severe liver disease, varices or portal hypertension, seizures at presentation, recent arterial or venous puncture at a non-compressible site, anticoagulants or PTT >15 secs, platelets <100 x 10⁹/L or BP >220/130.

Question 9

Stroke - investigations

Answer 9

To identify risk factors for further strokes:

• Hypertension – retinopathy, nephropathy or cardiomegaly – however don’t treat acutely.
• Cardiac source of emboli – 24 hour ECG monitoring for AF, CXR for LA enlargement (causing AF) and echocardiogram for mural thrombus due to AF, hypokinesis post-MI or valve disease.
• Carotid artery stenosis – perform doppler ultrasound and CT/MRI angiography – carotid endarterectomy shows clear benefit for fit patients with >70% stenosis on Doppler.
• Bloods – for evidence of hypo or hyperglycaemia, hyperlipidaemia or hyperhomocysteinaemia.
• Specific investigations – for vasculitis e.g. ESR, ANA, prothrombotic states e.g. thrombophilia or antiphospholipid syndrome or hyperviscosity e.g. polycythaemia or sickle cell disease.

Question 10

Stroke - primary prevention

Answer 10

Encourage patients to exercise and stop smoking. Treat hypertension, diabetes mellitus, hyperlipidaemia and cardiac disease. Consider lifelong anticoagulation if rheumatic or prosthetic heart valves on the left side or chronic atrial fibrillation

Question 11

Stroke - secondary prevention

Answer 11

• Aim to lower blood pressure and cholesterol even if not significantly raised.
• Anti-platelets – unless imaging shows primary haemorrhage give 300mg aspirin for 2 weeks and 75mg for life. 200mg dipyridamole BD in combination with aspirin improves outcome.
• Anticoagulation – warfarin should be used instead of aspirin for embolic stroke or chronic AF but should not be started for the first 2 weeks (use anti-platelet therapy until this time).

Question 12

TIA - definition

Answer 12

Sudden onset focal neurological signs due to temporary occlusion of cerebral circulation usually by emboli. In order for this to be a TIA and not a stroke the symptoms must last <24 hours.

Question 13

TIA - signs

Answer 13

Mimic those of a stroke in the same arterial territory. Global events such as syncope or dizziness are not typical of TIAs.

Emboli may pass to the retinal artery and cause amaurosis fugax – vision is progressively lost ‘like a curtain descending over the field of view’.

Question 14

TIA - causes

Answer 14

Most commonly atherothromboembolism (from carotid arteries), cardioembolism (mural thrombus post-MI or in AF or valve disease) or hyperviscosity (polycythaemia or sickle cell anaemia).

Question 15

TIA - differential diagnosis

Answer 15

Hypoglycaemia, migraine aura (symptoms spread over minutes), focal epilepsy (symptoms spread over seconds and include twitching or jerking), hyperventilation or retinal bleeds.

Question 16

TIA - investigations

Answer 16

Aim to find the cause and define vascular risk – FBC, ESR, Us and Es, glucose, lipids, CXR, ECG and carotid Doppler ± angiography, CT or diffusion weighted MRI and echocardiogram.

Question 17

TIA - stroke risk

Answer 17

ABCD2 score – if >6 this strongly predicts a stroke (8.1% in 2 days and 35.5% in 1 week). Patients with a score >4 should be assessed by a specialist within 24 hours and all patients seen within 7 days.

• Age >65 years = 1 point
• Blood pressure >140/90 = 1 point
• Clinical features - unilateral weakness = 2 points and speech disturbance = 1 point
• Duration of symptoms - >1 hour = 2 points and between 10-59 mins = 1 point
• Diabetes = 1 point

Question 18

TIA - management

Answer 18

Time to intervention is crucial – risk of stroke within 90 days of TIA is 2% in those treated within 72 hours compared to 10% in those treated within 3 weeks of the TIA.

• Control risk factors – hypertension, hyperlipidaemia, diabetes mellitus and stop smoking.
• Antiplatelets – 300mg aspirin OD for 2 weeks followed by 75mg aspirin OD for life and 200mg dipyridamole BD for 2 years. If patient is aspirin intolerant 75mg clopidogrel OD can be given.
• Anticoagulation – patients with cardiac emboli e.g. AF or mitral stenosis will require warfarin.
• Carotid endarterectomy – if >70% stenosis of internal carotid artery and patient fit for surgery.
• Driving – should be avoided for 1 month – only inform DVLA if multiple attacks in short period.

Question 19

TIA - prognosis

Answer 19

The combined risk of stroke and MI is 9% per year. If carotid artery stenosis is >70% the risk of stroke rises to 12% in the first year and 10% in subsequent years.

Question 20

SAH - definition and causes

Answer 20

Spontaneous bleeding in the subarachnoid space – the typical age of patient is between 35-65 years.

Causes – rupture of saccular aneurysms (80%) or AV malformations (15%) but often no cause is found.

Question 21

SAH - risk factors

Answer 21

Smoking, alcohol misuse, hypertension, bleeding disorders, mycotic aneurysm (due to an infectious process), family history of SAH and possibly being post-menopausal due to low oestrogen.

Berry aneurysms - common sites – junction of posterior communicating and internal carotid or of the anterior communicating and the anterior cerebral or at the bifurcation of the middle cerebral artery. Associations – polycystic kidney disease, co-arctation of the aorta or Ehlers-Danlos syndrome.

Question 22

SAH - symptoms and signs

Answer 22

Symptoms – sudden (usually within secs) devastating typically occipital headache, vomiting, collapse, seizures, drowsiness and coma often follows and may last for months.

Signs – neck stiffness, Kernig’s sign – hip is flexed and pain occurs when patient attempts to straighten the leg (takes 6 hours to develop) and focal neurology e.g. pupil changes caused by 3rd nerve palsy.

Question 23

SAH - differential diagnosis

Answer 23

Only 25% of patients who present with thunderclap headache have SAH – in 50-60% no cause is found and the rest have meningitis, migraine, intracerebral bleeds or vein thrombosis.

Question 24

SAH - investigations

Answer 24

Head CT detects >90% of SAH within 48 hours. Perform lumbar puncture if patient remains CT negative and there are no contraindications after 12 hours from onset – CSF is uniformly bloody to begin with and becomes xanthochromic (yellow) after several hours due to Hb breakdown.

Question 25

SAH - management

Answer 25

• Re-examine CNS – monitor BP, pupils and GCS – repeat CT if the patient is deteriorating.
• Maintain cerebral perfusion – keep well hydrated and aim for blood pressure of >160mmHg.
• Give either 1mg/hour IVI or 60mg/4 hours PO nimodipine – a calcium antagonist that reduces vasospasm and subsequent morbidity from cerebral ischaemia.
• Endovascular coiling is preferable to surgical clipping where possible (7% increase in survival).
• Catheter or CT angiography will identify single vs multiple aneurysms prior to intervention.

Question 26

SAH - complications

Answer 26

• Re-bleeding – commonest cause of death that occurs in 20% often within the first 48 hours.
• Cerebral ischaemia – due to vasospasm and may cause a permanent neurological deficit.
• Hydrocephalus – due to blockage of arachnoid granulations – requires lumbar drainage.
• Hyponatraemia – this is common but should not be managed with fluid restriction.

Question 27

SAH - mortality rates

Answer 27

• Grade I - no signs - 0%
• Grade II - neck stiffness or cranial nerve palsy - 11%
• Grade III - drowsiness - 37%%
• Grade IV - drowsiness with hemiplegia - 71%
• Grade V - prolonged coma - 100%

Question 28

SAH - unruptured aneurysms

Answer 28

In most cases the risk of surgery outweighs the benefit. Except when patient <45 years and aneurysm >7mm – especially when at junction of internal carotid and posterior communicating artery or basilar artery bifurcation, uncontrolled hypertension or previous bleeding.

Question 29

Dural venous sinus thrombosis

Answer 29

Symptoms come on gradually over days or weeks. Thrombosis within a dural venous sinus may extend into cortical veins and cause infarction within a venous territory:

• Sagittal sinus thrombosis (47%) – headache, vomiting, seizures, vision change or papilloedema.
• Transverse sinus thrombosis (35%) – headache ± mastoid pain, seizures or papilloedema.
• Sigmoid sinus – cerebellar signs and lower cranial nerve palsies.

Question 30

Cortical vein thrombosis - definition and signs

Answer 30

Cause infarcts with stroke-like focal symptoms that usually develop over days (however thunderclap headache can also occur).

Signs – focal seizures, encephalopathy, headache and slowly evolving focal deficits – paresis, speech disorders, decreased cognition and change in vision.

Question 31

CVT - causes

Answer 31

• Common causes – pregnancy, oral contraceptives, head injury, dehydration, blood dyscrasias, intracranial (local invasions) or extracranial (hypercoagulability) malignancies or recent LP.
• Systemic causes – heart failure, hyperthyroidism, inflammatory bowel disease, SLE, anti-phospholipid syndrome, homocystinuria, hyperviscosity, ketoacidosis or nephrosis.
• Infectious causes – meningitis, cerebral abscess, septicaemia, fungal infections or otitis media.
• Drug causes – androgens e.g. oxymetholone, antifibrinolytics e.g. tranexamic acid or infliximab.

Question 32

CVT - differential

Answer 32

Subarachnoid haemorrhage, meningitis, encephalitis, abscess or arterial stroke.

Question 33

CVT - investigations

Answer 33

• Exclude SAH if thunderclap headache and ensure there’s no signs of meningism.
• T2 weighted CT or MRI venography – the thrombus and infarction can be visualised – but can be normal for 1 week when delta sign appears – transversely cut sinus shows a filling defect.
• Lumbar puncture – may be normal, contain red blood cells or xanthochromia.

Question 34

CVT - management

Answer 34

Get expert help - heparin improves outcome even in haemorrhagic venous infarction. In addition fibrinolytics (e.g. streptokinase) have been used via selective catheterisation.