Stroke Flashcards

1
Q

Define a stroke

A

an acute neurological deficit lasting longer than 24 hours due to vascular compromise.

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2
Q

What else is a stroke referred to as?

A

cerebrovascular accident - CVA

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3
Q

What is the aetiology (causes) of stroke?

A

Caused by a transient or permanent critical reduction in cerebral blood flow due to arterial occlusion or stenosis.

Ischaemic (85%) of strokes

  • Reduction in cerebral blood flow due to arterial occlusion or stenosis. Typically divided into lacunar (affecting blood flow in small arteries), thrombotic and embolic
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4
Q

What can the causes (aetiology) of stroke be divided into?

A
  • Cardiac:
    • Atherosclerotic disease: smoking, hypertension, diabetes, high cholesterol
    • Atrial fibrillation
    • Paradoxical embolism due to septal abnormality, such as a patent foramen ovale
  • Vascular
    • Aortic dissection
    • Vertebral dissection
    • Vasculitides
  • Haematological
    • Hypercoagulability, such as antiphospholipid syndrome
    • Sickle cell disease
    • Polycythaemia
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5
Q

What are the types of stroke?

A

Two main types:

Ischaemic and Haemorrhagic

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6
Q

What are ischaemic strokes like?

A
  • Ischaemic stroke → which is when there is a blocked artery that reduces blood flow to the brain
    • Ischaemic strokes arethe most common type of stroke.
    • The amount of damage they cause is related to the parts of the brain that are affected and how long the brain suffers from reduced blood flow.
    If the symptoms self resolve in 24hours this is called a transient ischaemic attack, and there is usually minimal long term damage.
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7
Q

What is a Haemorrhagic stroke like?

A
  • when there is an artery in the brain that breaks crating a pool of blood that damages the brain

They happen when a blood clot blocks the flow of blood and oxygen to the brain. These blood clots typically form in areas where the arteries have been narrowed or blocked over time by fatty deposits known as plaques. This process is known as atherosclerosis.

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8
Q

What are not considered Haemorrhagic strokes?

A

Extradural and subdural

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9
Q

What does the frontal lobe control?

A

The frontal lobe controls movement and executive function, which is our ability to make decisions.

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10
Q

What does the parietal lobe control?

A

The parietal lobe processes sensory information which lets us locate exactly where we are physically and guides movement in a three dimensional space.

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11
Q

What does the temporal lobe control?

A

The temporal lobe plays a role on hearing, smell, memory as wells as visual recognition of faces and language.

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12
Q

What does the occipital lobe control?

A

The occipital lobe is primarily responsible for vision.

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13
Q

What controls the different slides of your body?

A

The right cerebrum controls muscles on the left side of your body.

The left cerebrum controls muscles on the right side of your body

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14
Q

What controls the different slides of your body?

A

The right cerebrum controls muscles on the left side of your body.

The left cerebrum controls muscles on the right side of your body

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15
Q

What does the cerebellum do?

A

The cerebellum helps with muscle co-ordination and balance.

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16
Q

What does the brainstem do?

A

The brain stem plays a vital role in functions like heart rate, blood pressure, breathing, gastrointestinal function and consciousness.

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17
Q

What is the composition of the cerebrum?

A
  • Has 2 hemispheres
  • each has a cortex
  • each cortex has 4 lobes
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18
Q

What is the blood supply of the brain?

A

The Brian receives blood from:

  • L + R internal carotid arteries and L+R vertebral arteries
  • together form basilar artery

Branches of internal carotid arteries:

  • L+R middle cerebral arteries - supply lateral portions of F,P and T lobes
  • anterior cerebral arteries - supply medial portion of the F and P lobes and connect them via the Anterior Communicating Artery
  • Posterior communicating arteries - attach to posterior arteries on each side

Branches of vertebral and basilar arteries supply cerebellum and brianstem.

Basilar artery branches:

  • L+ R posterior cerebral arteries - supplies the O lobe + some T lobe and thalamus

Main + communicating arteries = Circle of Willis

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19
Q

Can the brain operate with less blood?

A

In general the brain can get by on diminished blood flow, especially when it happens gradually as that allow for enough time for the collateral circulation to develop, which is where a nearby blood vessel starts sending out branches of blood vessels to serve an area that is in need. But once the supply of the blood os reduced to below the needs of the tissue it causes tissue damage → which is what we call an ischaemic stroke.

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20
Q

What are the mechanisms for an ischaemic stroke?

A

Endothelial cell dysfunction and embolism

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21
Q

What occurs in an endothelial cell dysfunction?

A

One mechanism is endothelial cell dysfunction, which is when something inflames or irritates the slippery inner lining of the artery (the tunica intima).

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22
Q

Describe endothelial cell dysfunction in action

A

One classic irritant is the toxin found in tobacco. It floats around in the blood damaging the endothelium.

That damage becomes a sight for atherosclerosis which is where a plaque forms. This is when a build up of fat, cholesterol, proteins, calcium and immune cells form and start to obstruct arterial blood flow.

This plaque has two parts to it:

  1. The soft cheesy textured interior
  2. The hard, fibrous cap

Usually it takes years for plaque to build up, and this slow blockage only partially blocks the arteries, and even though less blood makes it to brain tissue, there is still some blood.

Strokes happen when there is sudden and complete or nearly complete blockage of the artery.

Since plaque sit in the lumen of the blood vessel they are constantly being stressed by mechanical forces from blood flow and it is often the smaller plaques that are more dangerous. Their fibrous caps are softer than the larger ones and are more prone to getting ripped off. Once that happens the inner cheesy filling is exposed to the blood, and is thrombogenic, which means they tend to form clots quickly. Platelets adhere to the exposed cheesy material and they release chemicals that enhance the clotting process. Within a minute that artery can be fully blocked.

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23
Q

What are the most common sites for atherosclerosis?

A

Branch points in arteries particularly of the internal carotid and the middle cerebral artery are the most common sites for atherosclerosis.

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24
Q

Describe an embolism

A
  • An embolism stroke typically happens when a blood cot breaks off from one location, travels through the blood and gets lodged in a vessel down stream. Typically an artery arteriole or capillary, with a small diameter.
  • These blood clots typically emerge from atherosclerosis, but they can also form in the heart. For example stagnant blood flow can form a clot, and blood can stagnate due to an atrial fibrillation, or after a heart attack.
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25
Q

Where can embolisms occur?

A
  • If a clot form on the left atrium, it moves into the left ventricle and from there it has a direct route to the brain.
  • On the other hand, if a clot forms in the low-pressure veins or right atrium, then it goes into the tight ventricle and gets lodged in the pulmonary capillaries with no way of getting to the brain.
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26
Q

What exception can affect an embolism route?

A
  • An important exception is if a person has a heart defect like an atrial septal defect that allows blood and potentially a blood clot to go from the right side of the heart over to the left side of the heart.
  • In that situation, a venous or right atrial blood clot will have bypassed the pulmonary circulation and established a route to the brain.
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27
Q

What is a lacunar stroke?

A

A specific type of ischaemic stroke called a Lacunar stroke, they typically involve the deep branches of the middle cerebral artery that feed the basal ganglia.

Lacunar refers to lake, and is called that because after a Lacunar stroke, the damaged brain tissue develops fluid filled pockets called cysts that look like little lakes under the microscope.

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28
Q

What causes a lacunar stroke?

A

Lacunar strokes develop as a result of hyaline atherosclerosis which is when the arteriole wall gets filled with protein. This can happen as a result of hypertension or diabetes, and can make the artery wall quite thick, reducing the size of the lumen.

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29
Q

What is the pathophysiology of symptoms?

A

Patients typically have a focal neurological deficit which corresponds to the region of the brain that’s affected e.g.

  • An anterior cerebral artery stroke affects the feet and legs.
  • A middle cerebral artery stroke affects the hands, arms, face, and the language centers in the dominant hemisphere, including Broca’s and Wernicke’s area.
  • A posterior cerebral artery stroke primarily affects the visual cortex, which affects a person’s ability to see clearly.
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30
Q

What pathways can be affected by stroke?

A

Both motor and sensory fibres may be affected:

  • Damage to motor pathways: flaccid paralysis develops almost immediately. And then over the following days to weeks, there’s spastic paralysis and hyperreflexia due to the hyperexcitable stretch reflex.
  • Damage to sensory pathways: numbness, reduced pain and vibration sensation.
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31
Q

How do pathways present in stroke patients?

A

Both motor and sensory symptoms usually happen on the side that’s contralateral from the stroke, except in rare cases of brain stem stroke, where both sides are affected.

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32
Q

What are some other pathophysiology symptoms?

A
  • Atherosclerosis, migraine, vasculitis-reduce cerebral perfusion and/or result in artery-to-artery embolism
  • Cardiac pathologies (e.g., atrial fibrillation, myocardial ischaemia/infarction, patent foramen ovale) that lead to cerebral arterial occlusion due to embolism
  • Haematological pathologies (e.g., prothrombotic hypercoagulable or hyperaggregable states) that directly precipitate cerebrovascular thrombosis (particularly venous), or facilitate systemic venous or intracardiac thrombus formation and cardioembolism.
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33
Q

What are the statistics on stroke in the UK?

A
  • There are more than 100,000 strokes in the UK each year causing 38,000 deaths, making it a leading cause of death and disability.
  • People are most likely to have a stroke over the age of 55.
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34
Q

What is the epidemiology of all strokes?

A
  • Stroke is the third leading cause of mortality in the US and the UK
  • The average age for a stroke is 68 to 75 years old
  • Stroke rates are higher in Asian and black African populations than in Caucasians
  • M>F
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35
Q

What are the clinical manifestations of stroke?

A

Usually sudden onset followed by gradual decline

Specific symptoms depends on anatomical site of stroke

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36
Q

What are the clinical manifestations in ACA, MCA and PCA stroke?

A
  • Anterior cerebral artery
    • Contralateral hemiparesis and sensory loss with lower limbs > upper limbs
  • Middle cerebral artery
    • Contralateral hemiparesis andsensory loss with upper limbs > lower limbs
    • Homonymous hemianopia
    • Aphasia: if affecting the ‘dominant’ hemisphere (the left in 95% of right-handed people)
    • Hemineglect syndrome: if affecting the ‘non-dominant’ hemisphere; patients fail to be aware of items to one side of space
  • Posterior cerebral artery
    • Contralateral homonymous hemianopia withmacular sparing
    • Visual agnosia
    • Contralateral loss of pain and temperature due to spinothalamic damage
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37
Q

What are teh clinical manifestations in vertebrobasilar artery, webers syndrome and lateral medullary syndrome?

A
  1. Vertebrobasilar artery
    • Cerebellar signs
    • Reduced consciousness
    • Quadriplegia orhemiplegia
  2. Weber’s syndrome (midbrain infarct; branches of osteoporosis cerebral artery)
    • Oculomotor palsy and contralateral hemiplegia
  3. Lateral medullary syndrome (posterior inferior cerebellar artery occlusion)
    • Ipsilateral facial loss of pain and temperature
    • Ipsilateral Horner’s syndrome: miosis (constriction of the pupil), ptosis (drooping of the upper eyelid), and anhidrosis (absence of sweating of the face)
    • Ipsilateral cerebellar signs
    • Contralateral loss of pain and temperature
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38
Q

What are the clinical manifestations in retinal/opthalmic artery and basilar artery stroke?

A
  • Retinal/ophthalmic artery
    Amaurosis fugax
  • Basilar artery
    • ‘Locked in’ syndrome
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39
Q

What are the symptoms of stroke?

A
  • Headache
  • Gaze paresis

Uncommon

  • Nausea and/or vomiting
  • Neck or facial pain
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40
Q

What are the common signs and diagnostic factors?

A
  • Signs/Diagnostic factors
    • Unilateral weakness or paralysis in the face, arm or leg
    • Dysphasia: Slurred speach
    • Ataxia
    • Visual disturbance
    • Dysarthria
    • Arrhythmias, murmurs or pulmonary oedema
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41
Q

What are the uncommon signs and diagnostic factors?

A

Uncommon

- Vertigo
- Miosis, ptosis, and facial anhidrosis (hemilateral)
- Decreased level of consciousness or coma
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42
Q

What are the classifications for stroke?

A

The Bamford classification is commonly used and categorises stroke based on the area of circulation affected.

Bamford classification - blood vessel - criteria

  1. TACS (Total anterior circulation stroke) - anterior or middle cerebral artery - HHH (hemiplegia, homonymous hemianopia and higher cortical dysfunction, such as dysphasia or neglect)
  2. PACS (Posterior anterior circulation stroke) - anterior or middle cerebral artery - two or three from above (HHH)
  3. Lacunar stroke - perforating arteries: usually affects the posterior limb of the internal capsule - there is no higher cortical dysfunction or visual field abnormality. One of the following:
    - pure hemimotor or hemisensory loss
    - pure sensorimotor loss
    - ataxic hemiparesis
  4. Posterior circulation stroke - posterior cerebral or vertebrobasilar artery or branches - One of the following:
    - cerebellar syndrome
    - isolated homonymous hemianopia
    - loss of consciousness
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43
Q

What are the investigations for ischaemic stroke?

A
  • Assessment using ROSIER scale

Recognition of Stroke in the Emergency Room (ROSIER) scale is a variation of FAST (Face, Arm, Speech, Time) and is used to differentiate acute stroke from stroke-mimics

FAST:
- Face: has the face drooped on one side? Can the person smile?
- Arms: can they lift both arms?
- Speech: is the speech slurred or garbled? Can they understand what you’re saying?
- Time: dial 999 immediately if there are any of the features above

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44
Q

What is another way to assess for stroke?

A

A stroke is possible if the score is > 0 and requires an urgent non-contrast CT head. Once hypoglycaemia has been excluded, assess the following:

  • loss of consciousness or syncope -1 point
  • seizure activity -1

New, acute onset of:
- asymmetrical facial weakness +1
- asymmetrical leg weakness +1
- Speech disturbance +1
- Visual field defect +1

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45
Q

What are the primary investigations for stroke?

A
  • Non-contrast CT head: first-line imaging.
  • CT is usuallynormal in the first few hours of ischaemic stroke but allows exclusion of haemorrhage
  • ECG: assess for atrial fibrillation.
  • Bloods:
  • CT angiogram (CTA): identifies arterial occlusion and should be performed in all patients who are appropriate for thrombectomy
  • MRI head: MRI is an alternative to non-contrast CT head; MRI has a higher sensitivity for infarction and the same sensitivity for haemorrhage when compared to CT imaging. MRI is an alternative to con-contrast CT head.
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46
Q

What do you look for when investigating bloods in stroke?

A
  • Screen for risk factors includingHba1c, lipids, clotting screenand rule out stroke mimics such ashypoglycemia and hyponatraemia
    • In younger patients, consider ESR, autoantibody and thrombophilia screen
      • FBC
      • serum glucose
      • serum electrolytes
      • serum urea and creatinine
      • Prothrombin time and PTT (with INR)
      • Cardiac enzymes
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47
Q

What is the difference between MRI and CT in an investigation?

A

Diffusion-weighted MRI is the gold standard imaging technique. More sensitive but CT is safer and easier to obtain

CT is an alternative.

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48
Q

What other investigations can be considered?

A
  • Echocardiogram:for the exclusion of an intracardiac aneurysm or a septal defect
  • Carotid Doppler ultrasound :stenosis of >70% is an indication forendarterectomyin Europe.
    • The stroke must be non-disabling to qualify
  • Lumbar puncture: check for small subarachnoid haemorrhage

Investigations to consider

  • Serum toxicology screen
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49
Q

How is a suspected ischaemic stroke managed?

A
  • Suspected ischaemic stroke
    - Stabilisation and referral to acute stroke unit

Maintain stable blood glucose levels, hydration status and temperature

Blood pressure should not be lowered too much during a stroke because this risks reducing the perfusion to the brain. Unless complications are present, e.g., hypertensive encephalopathy.

-
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50
Q

How do you manage a confirmed ischaemic stroke?

A
  • Confirmed ischaemic stroke
    Presentation within 4.5 hours AND thrombolysis not contraindicated
    - Supportive care + monitoring
  • Thrombolysis: Alteplase (intravenous) (Do not delay)
  • Alteplase is atissue plasminogen activator that rapidly breaks down clots to reestablish blood flow; and can reverse the effects of a stroke if given in time.
  • Given if < 4.5 hours of symptom onset and haemorrhage excluded on imaging
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51
Q

What are the contraindications of thrombolysis?

A
  • Contraindications of thrombolysis
    • Examples of thrombolytics include alteplase, tenecteplase and streptokinase.
    • The key side effect of thrombolysis is haemorrhage, whilst hypotension and allergic reactions can occur and are more common with streptokinase.
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52
Q

What are some absolute contraindications of thrombolysis?

A
  1. intracranial haemorrhage on CT - suspected subarachnoid haemorrhage
  2. Neurosurgery, head trauma or stroke in past 3 months - uncontrolled hypertension (>185 mmHg SBP or >110 mmHg DBP)
  3. History of intracranial haemorrhage - known intracranial arteriovenous malformation, neoplasm or aneurysm
  4. Active internal bleeding - suspected or confirmed endocarditis
  5. known bleeding diathesis: coagulation or bleed disorders - aortic dissection
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53
Q

What are the relative contraindications of thrombolysis?

A
  1. Major surgeries or serious non-head trauma in previous 14 days - history of GI, genitourinary or gynaecological haemorrhage within past 21 days
  2. Recent lumbar puncture (usually in the past 7 days) - pregnancy
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54
Q

When is a thrombectomy offered?

A

Thrombectomy(mechanical removal of the clot) may be offered if an occlusion is confirmed on imaging, depending on the location and the time since the symptoms started. It is not used after 24 hours since the onset of symptoms.

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55
Q

What are the conditions of thrombectomy being offered?

A
  • Confirmation of stroke requires CTA or MR angiogrampriorto thrombectomy
  • Must score > 5 on NIH Stroke Scale/Score (NIHSS) and pre-stroke functional status < 3 on the modified Rankin scale
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56
Q

When is a thrombectomy offered in a Proximal anterior circulation stroke and proximal posterior circulations trike (basilar or PCA stroke)?

A
  • Proximal anterior circulation stroke: offerthrombectomywithin 6 hours with IV thrombolysis (if within 4.5 hours), or within6 to 24 hours without IV thrombolysisif there is potential to salvage brain tissue (demonstrated as limited infarct core on imaging)
  • Proximal posterior circulation stroke (basilar or posterior cerebral artery): considerthrombectomywithin 24 hours with IV thrombolysis (if within 4.5 hours)if there is potential to salvage brain tissue (demonstrated as limited infarct core on imaging)
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57
Q

What else is given for stroke management?

A
  • Antiplatelet agent - aspirin - 300mg daily
    • Given as soon as possible once haemorrhage is excluded on CT
      Iftreated with thrombolysis, start aspirin after 24 hours once haemorrhage is excluded
      Continue until 2 weeks after the onset of stroke symptoms
  • Venous thromboembolism prophylaxis plus early mobilisation
  • High intensity statin (after 48 hours) - atorvastatin
  • Anticoagulation
    • If atrial fibrillation is the cause, anticoagulation should not be started until 14 days post-stroke. Patients should be on aspirin 300mg until then.
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58
Q

What is the management when presentation is after 4.5 hours or thrombolysis contraction indicated?

A
  • Presentation after 4.5 hours OR thrombolysis contra-indicated
    • Supportive care + monitoring
    • Mechanical thrombectomy
    • Antiplatelet agent - aspirin - 300mg daily
    • Venous thromboembolism prophylaxis plus early mobilisation
    • High intensity statin (after 48 hours) - atorvastatin
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59
Q

How is stroke prevented?

A
  • Clopidogreldaily lifelong is first-line
    • Offeraspirin75 mg daily +MR dipyridamoleif clopidogrel is contraindicated
    • OfferMR dipyridamole aloneif aspirin and clopidogrel are contraindicated
  • High-dose statin e.g. atorvastatin 20-80mg, usually after 48 hours of stroke
  • Manage hypertension, diabetes, smoking and other cardiovascular risk factors
  • Carotid endarterectomy or stenting in patients with carotid artery disease
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60
Q

What are some complications of ischaemic stroke?

A
  • Deep venous thrombosis: due to immobility
  • Aspiration pneumonia: due to dysphagia
  • Haemorrhagic transformation of ischaemic stroke
  • Depression
  • Alteplase-related orolingual oedema
  • Neurological sequelae: such as weakness, impaired mobility, Middle cerebral artery syndrome and seizures
  • Requirement for nutritional support: such as nasojejunal feeding
    • Intracerebral haemorrhage
    • Transient ischaemic attack
    • Hypertensive encephalopathy
    • Hypoglycaemia
    • Complicated migraine
    • Seizure and postictal deficits
    • Wernicke’s encephalopathy
    • Brain tumour
    • Sepsis
    • Ingestion of toxic substances
    • Hyponatraemia
    • Hypercalcaemia
    • Uraemia
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61
Q

What are some differential diagnosis of ischaemic stroke?

A
  • Intracerebral haemorrhage
  • Transient ischaemic attack
  • Hypertensive encephalopathy
  • Hypoglycaemia
  • Complicated migraine
  • Seizure and postictal deficits
  • Wernicke’s encephalopathy
  • Brain tumour
  • Sepsis
  • Ingestion of toxic substances
  • Hyponatraemia
  • Hypercalcaemia
  • Uraemia
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62
Q

What are some strong risk factors?

A

Strong

  • Older age: the average age for a stroke is 68 to 75 years old
  • Family history of stroke
  • History of ischaemic stroke
  • Hypertension: the single greatest risk factor
  • Smoking
  • Diabetes
  • Atrial fibrillation
  • Comorbid cardiac conditions
  • Carotid artery stenosis
  • Sickle cell diseases
  • Dyslipidaemia
  • Lower levels of education
  • Hypercholesterolaemia
  • Haematological disease: such as polycythaemia
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63
Q

What are some weak risk factors of ischaemic stroke?

A

Weak

  • Poor dietary nutrition
  • Physical inactivity
  • Obesity
  • Alcohol abuse
  • Medication: such as hormone replacement therapy or the combined oral contraceptive pill
    • Oestrogen-containing therapy
  • Obstructive sleep apnoea
  • Illicit drug use
  • Migraine
  • HyPerhomocysteinaemia
  • Elevated lipoprotein
  • Hypercoagulable states
  • Elevated C-reactive protein
  • Aortic arch plaques
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64
Q

What is the prognosis for ischaemic stroke?

A

For ischaemic stroke, the prognosis depends on the severity.

A total anterior circulation stroke confers the poorest prognosis.

Regarding thrombolysis, if administered within 3 hours, patients are 30% more likely to have minimal or no disability.

In general, mortality for haemorrhagic stroke is significantly higher than for ischaemic stroke and can be as high as 40%.

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65
Q

What are the driving rules for car and motor cycle?

A

Car or motorcycle(type 1 license):

  • Patients must not drive for1 monthafter a TIA or stroke
  • Driving may resume after 1 month if there has beensatisfactory clinical recovery
  • Patientsmay not need toinform the DVLA if there is no residual neurological deficit beyond 1 month
  • Multiple TIAsover a short period requires no driving for 3 months and the DVLA must be notified
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66
Q

What are the driving rules for heavy good vehicles?

A

Heavy goods vehicle(type 2 license):

  • Patients must not drive for1 yearafter a TIA or stroke and the DVLA must be notified.
  • Relicensing may be considered after 1 year if there isno significant residual neurologicalimpairment andno other significant risk factors
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67
Q

What is a haemorrhagic stroke?

A
  • If blood leaks from a blood vessel in or around the brain, this is called a haemorrhagic stroke.
  • Bleeding from a single vessel within the brain.
  • High blood pressure is the main cause of intracerebral haemorrhagic stroke
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68
Q

What are the subtypes of haemorrhagic stroke?

A
  • Intracerebral: bleeding within the brain parenchyma
  • Subarachnoid: bleeding into the subarachnoid space
  • Intraventricular: bleeding within the ventricles; prematurity is a very strong risk factor.
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69
Q

What is the circle of Willis comprised of?

A

The Circle of Willis comprises an anterior circulation, which consists of the branches of the internal carotid, and a posterior circulation which consists of the branches of the vertebrobasilar arteries.

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70
Q

What is the anterior circulation?

A
  • Anterior circulation
    • Anterior choroidal artery
    • Anterior cerebral artery (ACA)
    • Middle cerebral artery (MCA)
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71
Q

What is the posterior circulation?

A
  • Posterior circulation
    • Posterior cerebral artery (PCA)
    • Basilar artery
    • Superior cerebellar artery
    • Anterior inferior cerebellar artery
    • Posterior inferior cerebellar artery
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72
Q

What is a berry aneurysm?

A
  • Rupture of a saccular ‘berry’ aneurysm is the most common cause of a spontaneous subarachnoid haemorrhage
  • ## These occur at points of arterial bifurcation within the Circle of Willis; the junction between theanterior communicatingarteryandACAis the most common location
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73
Q

What are watershed zones?

A

Watershed zones: account for 5-10% of infarcts
- These areas are furthest from arterial supply and are most vulnerable to reduced perfusion
- Cortical border zone infarction: border of ACA/MCA and MCA/PCA
- Internal border zone infarction: borders of penetrating MCA branches,orborders of the deep branches of the MCA and ACA (resulting in deep white matter infarction)

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74
Q

What is the Broca’s area?

A
  • in the frontal lobe
    function: - motor production of speech
    Arterial supply: middle cerebral artery
    Effects of a lesion: patients can understand speech but can’t produce it themselves (Broca’s aphasia - non-fluent)
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75
Q

What is Wernicke’s area?

A
  • parietal and temporal lobe
    Superior temporal gyrus in the dominant hemisphere (brodmann area 22)

Function: understanding speech and using correct words to express thoughts

Arterial supply: middle cerebral artery
Effects of a lesion: patients can produce speech but do not grasp the meaning of spoken words (wernickes aphasia ‘fluent’)

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76
Q

What is cerebral dominance?

A
  • Cerebral dominance
  • Majority of people are ‘left dominant’ (95%): this means that the Wernicke’s and Broca’s areas are located in theleft cerebral hemisphere
  • A stroke affecting theleft MCAcauses expressive aphasia (Broca’s area) or receptive aphasia (Wernicke’s area)
  • In contrast,left-handed peopleare more likely to be ‘right dominant’, meaning that these areas are more likely to be on the right
  • Therefore, in left-handed people, aright MCAstroke usually causes aphasia
  • MCA stroke affecting a patient’s ‘non-dominant’ hemisphere often results in hemisensory neglect, not aphasia
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77
Q

What is macular sparing?

A
  • The occipital pole is responsible for supplying the macula and has arich anastomosis; this region is also supplied by theMCA
  • The macular is often spared in aposterior circulation stroke(e.g. PCA infarct), resulting incontralateral homonymous hemianopia with macular sparing
  • This is because of the dual blood supply of the occipital lobe (MCA and PCA)
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78
Q

What is locked in syndrome? (Pseudocoma)

A
  • A condition whereby the patient is fully aware but cannot move or communicate verbally due to almost complete paralysis
  • All voluntary muscles are generally affected, except for vertical eye movements and blinking
  • It may be caused by a stroke affecting thebasilar artery, thusdenying blood to the pons
  • There are also numerous other causes, such as central pontine myelinosis and traumatic brain injury
  • In contrast, persistent vegetative state affects the upper portions of the brain but spares the lower portions
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79
Q

What is locked in syndrome? (Pseudocoma)

A
  • A condition whereby the patient is fully aware but cannot move or communicate verbally due to almost complete paralysis
  • All voluntary muscles are generally affected, except for vertical eye movements and blinking
  • It may be caused by a stroke affecting thebasilar artery, thusdenying blood to the pons
  • There are also numerous other causes, such as central pontine myelinosis and traumatic brain injury
  • In contrast, persistent vegetative state affects the upper portions of the brain but spares the lower portions
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80
Q

What is the aetiology of Haemorrhagic stroke?

A

Ruptured blood vessel leading to reduced blood flow.

  • Aetiology
    • Haemorrhagic (15%) of strokes
      • Ruptured blood vessel leading to reduced blood flow
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81
Q

What is the aetiology of an intracerebral HS?

A
  • Intracerebral: bleeding within the brain parenchyma
    • Trauma
    • Arteriovenous malformation
    • Cerebral amyloid
    • Hypertension
82
Q

What is the aetiology of Subarachnoid and intraventricular HS?

A
  • Subarachnoid: bleeding between the pia mater and arachnoid mater
    • Trauma
    • Berry aneurysm
    • Arteriovenous malformation
  • Intraventricular: bleeding within the ventricles
83
Q

What is the other aetiology of HS?

A
  • Brain bleeds
    • Aneurysm rupture → SAH
    • Anticoagulation
    • Thrombolysis
    • Carotid artery dissection
  • Atherothromboembolism
  • Vasculitis
84
Q

What is the epidemiology of HS?

A

In the UK, around 15% of strokes are haemorrhagic (due to a bleed), and about 85% are ischaemic (due to a blockage to the blood supply in the brain).

Haemorrhagic stroke tends to affect younger people than ischaemic stroke, and is most common in people aged between 45 and 70. Most strokes in the UK happen over the age of 70.

85
Q

What are the types of HS?

A

There are two main types of haemorrhagic stroke:

  • Bleeding within the brain: called an intracerebral haemorrhage, or intracranial haemorrhage (ICH).
  • Bleeding on the surface of the brain: called a subarachnoid haemorrhage (SAH)
86
Q

What is the pathophysiology of HS?

A

Primarily intracerebral haemorrhage. Risk factors -> small vessel disease and aneurysms -> rupture and haemorrhage

  • Compression of the internal capsule with no death of cells
  • Large territory of loss of motor and sensory function
  • Possibility of complete recovery
87
Q

What is the pathophysiology of symptoms for HS?

A

Patients typically have a focal neurological deficit which corresponds to the region of the brain that’s affected e.g.

  • An anterior cerebral artery stroke affects the feet and legs.
  • A middle cerebral artery stroke affects the hands, arms, face, and the language centers in the dominant hemisphere, including Broca’s and Wernicke’s area.
  • A posterior cerebral artery stroke primarily affects the visual cortex, which affects a person’s ability to see clearly.
88
Q

How can pathways (M+S) be affected in HS?

A

Both motor and sensory fibres may be affected:

  • Damage to motor pathways: flaccid paralysis develops almost immediately. And then over the following days to weeks, there’s spastic paralysis and hyperreflexia due to the hyperexcitable stretch reflex.
  • Damage to sensory pathways: numbness, reduced pain and vibration sensation.

Both motor and sensory symptoms usually happen on the side that’s contralateral from the stroke, except in rare cases of brain stem stroke, where both sides are affected.

89
Q

What are the clinical manifestations of HS?

A

Usually sudden onset followed by gradual decline

Specific symptoms depends on anatomical site of stroke

  1. Anterior cerebral artery
    • Contralateral hemiparesis and sensory loss with lower limbs > upper limbs
  2. Middle cerebral artery
    • Contralateral hemiparesis andsensory loss with upper limbs > lower limbs
    • Homonymous hemianopia
    • Aphasia: if affecting the ‘dominant’ hemisphere (the left in 95% of right-handed people)
    • Hemineglect syndrome: if affecting the ‘non-dominant’ hemisphere; patients fail to be aware of items to one side of space
  3. Posterior cerebral artery
    - Contralateral homonymous hemianopia withmacular sparing
    - Contralateral loss of pain and temperature due to spinothalamic damage
    -
90
Q

What are some other clinical manifestations of HS?

A
  • Vertebrobasilar artery
    • Cerebellarsigns
    • Reduced consciousness
    • Quadriplegiaorhemiplegia
  • Weber’s syndrome (midbrain infarct)
    • Oculomotor palsy and contralateral hemiplegia
  • Lateral medullary syndrome (posterior inferior cerebellar artery occlusion)
    • Ipsilateralfacial loss of pain and temperature
    • IpsilateralHorner’s syndrome: miosis (constriction of the pupil), ptosis (drooping of the upper eyelid), and anhidrosis (absence of sweating of the face)
    • Ipsilateralcerebellar signs
    • Contralateralloss of pain and temperature
91
Q

What are the symptoms of HS?

A

Patients tend to have headaches,

Altered mental status,

Seizures,

Nausea and Vomiting

92
Q

What are the signs of HS?

A
  • Slurred speech
  • Arm/leg weakness
  • Facial drooping
93
Q

What other investigations can be considered for HS?

A
  • Pulse, BP and ECG
    • Look for AF
94
Q

What is the management for HS?

A

Haemorrhagic stroke management

The exact management of haemorrhagic stroke depends on the subtype (refer to haemorrhage topics)

  • Admit to neurocritical care: patients will need intensive monitoring due to the risk of raised intracranial pressure and airway compromise
  • If features of raised intracranial pressure: consider intubation with hyperventilation, head elevation (30°) and IV mannitol (IV hypertonic saline)
  • Surgical intervention: decompression may be needed
95
Q

What are some other managements for HS?

A
  • Control BP – Beta blocker/ARB
  • Stop anticoagulants.
  • Beriplex or vitamin K if warfarin related
  • Surgery – clot evasion
96
Q

What are the complications of HS?

A
  • Deep venous thrombosis / pulmonary embolism
  • Aspiration pneumonia: due to dysphagia
  • Infection
  • Seizures
  • Delirium
  • Neurological sequelae: such as weakness, impaired mobility, MCA syndrome and seizures
  • Requirement for nutritional support: such as nasojejunal feeding
  • Depression
97
Q

What are some diagnosis for HS?

A
  • Ischaemic stroke
  • Stroke mimics e.g.
    • Hypoglycaemia
    • Hyponatraemia
    • Hypercalcaemia
    • Uraemia
    • Hepatic encephalopathy
    • Brain tumours
    • Seizure disorder
    • Complicated migraine
  • Conversion and somatisation disorders
98
Q

What are the strong RF for HS?

A
  • Hypertension
  • Older Age: the average age for a stroke is 68 to 75 years old
  • Male sex
  • Ethnicity – Asian, black and/or Hispanic
  • Heavy Alcohol use
  • Illicit sympathomimetic drugs
  • Family history of intracerebral haemorrhage
  • Haemophilia
  • Cerebral amyloid angiopathy
  • Autosomal dominant mutations in the COL4A1 gene
  • Hereditary Haemorrhagic telangiectasia
  • Autosomal dominant mutations in the KRIT1 gene, CCM2 gene, or PDCD10 gene
  • Anticoagulation
  • Vascular malformations
  • Moyamoya disease
99
Q

What are the weak RF for HS

A
  • Smoking
  • Non-steroidal anti-inflammatories
  • Diabetes mellitus
  • Sympathomimetic medications
  • Cerebral vasculitis
  • Thrombocytopenia
  • Leukaemia
  • Past TIA
  • Heart disease

Atrial fibrillation – stasis of blood in poorly contracting atria → thrombus formation

  • Hypercholesterolaemia
  • Vasculitis
  • Haematological disease: such as polycythaemia
  • Medication: such as hormone replacement therapy or the combined oral contraceptive pill
100
Q

What is the prognosis for HS?

A

In general, mortality for haemorrhagic stroke is significantly higher than for ischaemic stroke and can be as high as 40%.

101
Q

What is a Transient ischaemic attack (TIA)?

A

A transient ischaemic attack (TIA) is a transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischaemia, without acute infarction.

It usually resolves spontaneously within 24 hours.

defined as transient neurological dysfunction secondary toischaemiawithoutinfarction.

102
Q

What do TIA signal?

A

Transient ischaemic attacks often precede a full stroke.

Acrescendo TIAis where there are two or more TIAs within a week. This carries a high risk of developing in to a stroke.

It is a medical emergency, within the first week following a TIA, the risk of stroke is up to 10%.

103
Q

When defining stroke what is important?

A

The definition is now ‘tissue-based’ rather than ‘time-based’ with the incoporation of the phrase ‘without evidence of acute infarction’. Thus, the end-point is biological tissue damage, not an arbitrary time cut-off.

104
Q

What is the aetiology of TIA?

A
  1. In situ thrombosis of an intracranial artery or artery-to-artery embolism of thrombus as a result of stenosis or unstable atherosclerotic plaque (16%).
  2. Cardioembolic events (29%).
  3. Small-vessel occlusion (16%).
  4. Uncertain mechanism (36%).
105
Q

What cardioembolic events can cause TIA?

A
  • Intracardiac thrombus may form in response to some secondary risk factor such as stasis from impaired ejection fraction or atrial fibrillation.
    • The precipitating factor may be a thrombogenic nidus within the heart such as an infectious vegetation or artificial valve.
    • Rarely, thrombus can pass from the venous system across a cardiac shunt to create paradoxical emboli.
106
Q

What small vessel occlusion causes TIA?

A
  • Microatheromas, fibrinoid necrosis, and lipohyalinosis of small penetrating vessels are seen.
    • Hypertension and diabetes predispose to small ischaemic lesions.
    • Because these may occur in the brainstem and internal capsule, a small lesion can result in significant symptoms.
  • Occlusion due to hypercoagulability, dissection, vasculitis, vasospasm, or sickle cell occlusive disease (3%). These are less common aetiologies.
107
Q

How is the aetiology of TIA similar to an ischaemic stroke?

A

Ischaemia refers to the absence of blood flow to an organ, which deprives it of oxygen. Cerebral ischaemia may be due to in situ thrombosis, emboli, or rarely, dissection.

Thrombosis: local blockage of a vessel due to atherosclerosis. Precipitatedby cardiovascular risk factors (e.g. hypertension, smoking) or small vessel disease (e.g. vasculitis, sickle cell).

Emboli: propagation of a blood clot that leads to acute obstruction and ischaemia. Typically due to atrial fibrillationor carotid artery disease.

Dissection: a rare cause of cerebral ischaemia from tearing of the intimal layer of an artery (typically carotid).This leads to an intramural haematoma that compromisescerebral blood flow. May be spontaneous or secondary to trauma.

108
Q

What is the pathophysiology of TIA?

A

TIA is caused by temporary blockage to blood flow, which leads to ischaemia.

During a TIA, there is a transient reduction in blood flow to an area of cerebral tissue that causes neurological symptoms.

TIA commonly occurs secondary to embolisation from atrial fibrillation or carotid artery disease.

109
Q

What decides the severity of a TIA?

A

The severity of clinical neurological impairment after arterial occlusion depends on the complex interplay between the degree of obstruction, area and function of tissue supplied by the vessel, the length of time thrombus obstructs the vessel, and the ability of collateral circulation to provide supplemental perfusion to the area at risk.

110
Q

What decides the severity of a TIA?

A

The severity of clinical neurological impairment after arterial occlusion depends on the complex interplay between the degree of obstruction, area and function of tissue supplied by the vessel, the length of time thrombus obstructs the vessel, and the ability of collateral circulation to provide supplemental perfusion to the area at risk.

111
Q

What is the epidemiology of a TIA?

A
  • The age-adjusted annual incidence rate for transient ischemic attack in the UK has been estimated at 190 cases per 100,000 population
  • Often called a ministroke, a transient ischemic attack may be a warning.
    • About 1 in 3 people who has a transient ischemic attack will eventually have a stroke, with about half occurring within a year after the transient ischemic attack.
    • It is estimated that approximately 15% of patients have at least one TIA prior to a stroke.
  • The estimated incidence of TIA within the UK is 50 per 100,000 people per year.
  • M>F
112
Q

What are the symptoms of TIA?

A
  • Unilateral weakness or paralysis
    • Facial weakness
    • Limb weakness
  • Dysphasia: slurred speech
  • Ataxia, vertigo, loss of balance or incoordination
  • Homonymous hemianopia: visual field loss on the same side of both eyes
  • Sudden transient loss of vision in one eye (amaurosis fugax)**a painless temporary loss of vision, usually in one eye
    • This is a classical syndrome of short-lived monocular blindness, which is often described as a black curtain coming across the vision.
    • It is a term usually reserved for transient visual loss of ischaemic origin.
    • The principle cause of amaurosis fugax is transient obstruction of the ophthalmic artery, which is a branch of the internal carotid artery.
    • However, other ischaemic causes to consider include giant cell arteritis (i.e. temporal arteritis) and central retinal artery occlusion.
    • An important differential of transient visual loss, particularly in young patients, is migraine.
  • Contralateral sensory/ motor deficits
113
Q

What are the symptoms of TIA?

A
  • Unilateral weakness or paralysis
    • Facial weakness
    • Limb weakness
  • Dysphasia: slurred speech
  • Ataxia, vertigo, loss of balance or incoordination
  • Homonymous hemianopia: visual field loss on the same side of both eyes
  • Sudden transient loss of vision in one eye (amaurosis fugax)**a painless temporary loss of vision, usually in one eye
    • This is a classical syndrome of short-lived monocular blindness, which is often described as a black curtain coming across the vision.
    • It is a term usually reserved for transient visual loss of ischaemic origin.
    • The principle cause of amaurosis fugax is transient obstruction of the ophthalmic artery, which is a branch of the internal carotid artery.
    • However, other ischaemic causes to consider include giant cell arteritis (i.e. temporal arteritis) and central retinal artery occlusion.
    • An important differential of transient visual loss, particularly in young patients, is migraine.
  • Contralateral sensory/ motor deficits
114
Q

What are the signs and key diagnostic factors of TIA?

A
  • Sudden onset and brief duration of symptoms
  • Patient / witness report of focal neurological deficit
    • Focal neurology: on examination
  • Homonymous hemianopia: visual field loss on the same side of both eyes
  • Diplopia
  • Irregular pulse: suggests atrial fibrillation as an underlying cause
  • Carotid bruit: suggests carotid artery stenosis
  • Hypertension
115
Q

What are the primary investigations of a TIA?

A
  • The Face Arm Speech Time Test (FAST test): check for/ ask about facial weakness, arm weakness, speech difficulty
  • ECG: rule out Atrial fibrillation as an underlying cause
  • Auscultation: listen for carotid bruit
  • Bloods:
    • Screen for risk factors with bloods includingHba1c, lipids, clotting screenand rule out TIA mimics such ashypoglycemia and hyponatraemia
      • Blood glucose
      • Full blood count and platelet count
      • Prothrombin time, INR, Partial thromboplastin time
      • Fasting and lipid profile
      • Serum electrolytes
  • TIA clinic:
    • If the suspected TIA occurredlessthan a week ago: urgent assessment within24 hours
    • If the suspected TIA occurredmorethan a week ago: urgent assessment within7 days
    • At TIA clinic, a specialist assessment is conducted and further imaging is arranged, such as anMRI headandcarotid doppler
116
Q

What other investigations can you consider for a TIA?

A
  • CT head: imaging isnot advocated until the patient is seen in the TIA clinic. However, imaging is indicated if other pathology is suspected, or to rule out an intracranial haemorrhage
  • Echocardiogram: for the exclusion of an intracardiac aneurysm or a septal defect
  • ABCD2: arisk stratifying tool to determine the risk of future stroke.
117
Q

What other investigations can you consider for a TIA?

A
  • CT head: imaging isnot advocated until the patient is seen in the TIA clinic. However, imaging is indicated if other pathology is suspected, or to rule out an intracranial haemorrhage
  • Echocardiogram: for the exclusion of an intracardiac aneurysm or a septal defect
  • ABCD2: arisk stratifying tool to determine the risk of future stroke.
118
Q

What are the acute managements for a TIA?

A
  • Antiplatelet:initiallyaspirin 300mg daily - the first-line, immediate managementDonotoffer aspirin in these circumstances:
    • Bleeding disorder or taking an anticoagulant: needs immediate admission and assessment
    • Taking low-dose aspirin regularly: continue the current dose and arrange a specialist review
    • Aspirin is contraindicated: needs specialist advice
  • Discuss urgently with a stroke specialistfor admission/observation in the case of:They should be referred and seen within 24 hours by a stroke specialist.
    • More than one TIA (crescendo TIA)
    • Suspected cardioembolic source
    • Severe carotid stenosis
  • Carotid endarterectomy:surgical procedure to remove the blockage, **stenosis of > 70% on Doppler is an indication for urgent endarterectomy
119
Q

What is the secondary prevention for a TIA?

A
  • Clopidogrel (antiplatelet) 75 mgdaily is first-line
    • Offeraspirin75 mg daily withMR dipyridamoleif clopidogrel is contraindicated
    • OfferMR dipyridamole aloneif both aspirin and clopidogrel are contraindicated
    • Offeraspirin 75mgdaily if both clopidogrelandMR dipyridamole are contraindicated
  • High-dose statin: for lipid modification e.g. atorvastatin 20-80mg
  • Manage hypertension, diabetes, smoking and other cardiovascular risk factors
120
Q

What is the secondary prevention for a TIA?

A
  • Clopidogrel (antiplatelet) 75 mgdaily is first-line
    • Offeraspirin75 mg daily withMR dipyridamoleif clopidogrel is contraindicated
    • OfferMR dipyridamole aloneif both aspirin and clopidogrel are contraindicated
    • Offeraspirin 75mgdaily if both clopidogrelandMR dipyridamole are contraindicated
  • High-dose statin: for lipid modification e.g. atorvastatin 20-80mg
  • Manage hypertension, diabetes, smoking and other cardiovascular risk factors
121
Q

What are the driving rules after a TIA?

A

Driving:

  • Cars and motorcycles: stop driving one month, do not need to inform DVLA
  • Larger vehicles (e.g. buses, lorries): stop driving, inform the DVLA
  • Lifestyle advice: increase physical activity, smoking cessation, diet optimisation and advice on alcohol intake
  • Startsecondary preventionmeasures for cardiovascular disease.
122
Q

What is the management for a suspected vs a confirmed transient ischaemic attack?

A
  • Suspected transient Ischaemic attack
    • Antiplatelet therapy
    • Referral for specialist assessment
  • Confirmed transient Ischaemic attack
    • Anti platelet therapy
    • High-intensity statin
    • Anticoagulant (for atrial fibrillation)
123
Q

What are the different diagnosis for a TIA?

A
  • Toxic/metabolic
    • Hypoglycaemia
    • drug and alcohol consumption
  • Neurological:
    • Seizures with post-seizure (Todd’s) paralysis
    • Complex migraine
    • Bell’s palsy
    • Stroke
  • Space occupying lesion: tumour, haematoma
    • Intercranial Haemorrhage
    • Abscess
    • Mass
  • Global hypoperfusion / syncope
  • Conversion disorder
  • Labyrinthine disorders
  • Multiple sclerosis
  • Peripheral neuropathy
  • Infection: meningitis/encephalitis, systemic infection with ‘decompensation’ of old stroke
124
Q

What are the complications for a TIA?

A
  • Stroke
    • TIA is a medical emergency as the risk of recurrent stroke is up to 10% in the next week
  • Myocardial infarction
    • TIA represents underlying atherosclerotic disease, thus increasing the risk of acute coronary syndrome
125
Q

What are the RFs for a transient ischaemic attack?

A
  • Atrial fibrillation
  • Valvular disease
  • Carotid stenosis
  • Congestive heart failure
  • Hypertension
  • Diabetes mellitus
  • Cigarette smoking
  • Alcohol use disorders
  • Increasing age
  • Hyperlipidaemia
  • Patent foramen ovale (PFO)
  • Inactivity
  • Obesity
  • Hypercoagulability

Risk factors for TIA are dueto conditions that affect theintegrity of vessels or increase the risk of embolisation

  • Hypercholesterolaemia
  • Thrombophilic disorders e.g. antiphospholipid syndrome
  • Sickle cell disease
126
Q

What is the prognosis for a TIA?

A
  • Over 10% of TIA patients seen in the emergency department will have a stroke within 3 months.
  • Additionally, a TIA is a marker of underlying atherosclerotic disease, therefore these patients are at risk for ischaemic heart disease.
127
Q
A

Migraine with an aura → Opthamic artery involvement → Contraindicated oestrogen birth control → as it increases the risk of stroke.

They should only have pogesterone based birth control.

128
Q

What are the different types of intracranial haemorrhage?

A

Extradural - bleeding into the potential space between dura mater and skull
- typically due to trauma to the temporal area and pterion resulting in middle meningeal artery rupture
- patients present with loss of consciousness followed by a lucid interval, followed by deterioration

Subdural - bleeding into the space between the dura and arachnoid mater
- due to rupture of bridging veins
- acute < 3 days
- chronic > 21 days ans seen in elderly or alcoholics

Subarachnoid - bleeding into the space between the arachnoid and pia mater
- usually small volume and occurs at the site of impact (coup) or opposite side (countercoup)
- trauma is teh most common cause of a subarachnoid haemorrhage
- atraumatic causes include berry aneurysms and AVMs

129
Q

What are some other intracranial haemorrhages?

A

Intraparenchymal/intracerebral - bleeding with the brain parenchyma itself
- a traumatic causes include hypertension

Contusions - represent bruises of the brain parenchyma
- they are typically found in the anterior fossa floor or the temporal pole
- contusion can be coup (site of impact) or countercoup (opposite side of impact)

Intraventricular - bleeding into the ventricular system - usually originates from extension form an intraparenchymal or subarachnoid bleed

130
Q

What is an intracerebral haemorrhage?

A

Intracerebral haemorrhage describes bleeding within the cerebrum.

Haemorrhagic strokes can be split into two types: an intracerebral haemorrhage which is when bleeding occurs within the cerebrum, and a subarachnoid haemorrhage which is when bleeding occurs between the pia mater and arachnoid mater of the meninges.

An intracerebral haemorrhage that involves just the brain tissue is called an intraparenchymal haemorrhage, whereas if the blood extends into the ventricles of the brain which store cerebrospinal fluid, it’s called an intraventricular haemorrhage.

131
Q

When does an intracerebral haemorrhage occur?

A
  • An intracerebral haemorrhage occurs when the blood vessel bursts inside the brain. The blood then spills into the nearby brain tissue. This can cause the affected brain cells to lose their oxygen supply. They become damaged or die.

Intraparenchymal/intracerebral → Bleedingwithin the brain parenchymaitself → Atraumatic causes include hypertension

132
Q

What is the primary aetiology of Intracerebral haemorrhage?

A

Rupture due to:

  1. Cerebral amyloid angiopathy (CAA) accounts for a significant number of primary Intracerebral haemorrhages, specifically in the older population.
    - A degenerative disease where abnormal protein deposits in the walls of arterioles making them less compliant.
  2. Hypertension can cause haemorrhage in any intracranial location.
    - Hypertension, causing:
    - Arteriosclerosis: stiffening of vessels
    - Microaneurysms: called Charcot-Bouchard aneurysms, most likely to be found on small arteries
  3. Vasculitis
133
Q

What are some secondary aetiology for an IC Haemorrhage?

A

Arises from an identifiable vascular malformation or as a complication of other medical or neurological diseases that either impair coagulation or promote vascular rupture.

  • Arteriovenous malformations: blood vessels that directly connect an artery to a vein. Over time these abnormal vessels dilate and can rupture
  • Secondary to ischaemic stroke: ischaemia causes brain tissue death. If there is reperfusion, there’s an increased chance that the damaged blood vessel might rupture. Bleeding into dead tissue is called haemorrhagic conversion.
  • Cerebral infarction or cerebral tumour with haemorrhage into the diseased tissue.
    • Vascular tumours
  • Drug misuse-cocaine
134
Q

What is the pathophysiology of Intracerebral haemorrhage?

A
  • Intracerebral haemorrhage (ICH) is caused by vascular rupture with bleeding into the brain parenchyma, resulting in a primary mechanical injury to the brain tissue.

Once there’s an intracerebral haemorrhage, blood starts to spew out from a damaged blood vessel creating a pool of blood which increases pressure in the skull and puts direct pressure on nearby tissue cells and blood vessels.

Haemorrhage also means that less blood is flowing downstream to the cells that need it, which leaves the downstream tissue deprived of oxygen-rich blood. Healthy tissue can die from both the direct pressure and the lack of oxygen within a few hours.

Increased pressure within the skull can also lead to brain herniation, which is when the brain moves across structures in the skull.

135
Q

Where can an Intracerebral haemorrhage occur?

A

This can occur anywhere, e.g.

  • Lobar intracerebral haemorrhage
  • Deep intracerebral haemorrhage
  • Intraventricular haemorrhage
  • Basal ganglia haemorrhage
  • Cerebellar haemorrhage
136
Q

What is the epidemiology of an intracerebral haemorrhage?

A
  • Epidemiology
    • There are more than 100,000 strokes in the UK each year causing 38,000 deaths, making it a leading cause of death and disability.
    • People are most likely to have a stroke over the age of 55.
    • Stroke is the second largest cause of death globally (5.5 million deaths) after ischaemic heart disease.
137
Q

What are the symptoms of an IC Haemorrhage?

A
  • Headache
  • Nausea
  • Vomiting
  • Weakness
  • Seizures
  • Reduced consciousness
138
Q

What are the signs and diagnostic factors of an IC Haemorrhage?

A
  • Unilateral weakness or paralysis in the face, arm, or leg
  • Sensory loss (numbness)
  • Dysphasia
  • Dysarthria
  • Visual disturbance
  • Photophobia
  • Ataxia

Specific stroke symptoms depend on part of brain affected e.g.

  • Anterior or middle cerebral artery stroke: numbness and sudden muscle weakness.
  • Broca’s area or Wernicke’s area stroke: slurred speech or difficulty understanding speech, respectively.
  • Posterior cerebral artery stroke: vision disturbances.
139
Q

What are the investigations of an IC Haemorrhage?

A
  • non-contrast CT head
    • CT/ MRI: to confirm size and location of haemorrhage
  • Angiography: visualise the exact location of haemorrhage
  • FBC
  • Clotting screen
  • Serum glucose
  • Serum electrolytes
  • Serum urea and creatinine
  • Liver function tests
  • ECG
140
Q

What is the management of a suspected vs confirmed Haemorrhage?

A
  • Suspected intracerebral haemorrhage
    • Stabilisation
    • Urgent referral to hyperacute or acute stroke unit
  • Confirmed intracerebral haemorrhage
    • Supportive care
    • Monitoring
    • Immediate referral for neurosurgery assessment
    • Consider
      • Rapid blood pressure control
      • Urgent reversal of anticoagulation
141
Q

What are the managements of an IC Haemorrhage?

A
  • Consider intubation, ventilation and ICU care if they have reduced consciousness
  • Correct any clotting abnormality
  • Correct severe hypertension but avoid hypotension
  • Drugs to relieve intracranial pressure e.g. Mannitol
  • Craniotomy: part of the skull bone is removed to drain any accumulated blood and relieve pressure. Good for if the bleed is close to the surface of the skull
  • Stereotactic aspiration: aspirate off blood and relieve intracranial pressure, guided by CT scanner. Good for bleeding that is located deeper in brain tissue
142
Q

What are the complications of an IC Haemorrhage?

A
  • Delirium
  • Infection
  • DVT
  • Pulmonary embolism
  • Seizures
  • Aspiration pneumonia
143
Q

What are the RFs of an Intracerebral Haemorrhage?

A
  • Hypertension
  • Older age
  • Male sex
  • Asian, black and/or Hispanic
  • Heavy alcohol use
  • Family history
  • Head injury
  • Aneurysms
  • Ischaemic stroke can progress to haemorrhage
  • Brain tumours
  • Anticoagulants such as warfarin
144
Q

What are some differential diagnosis of an intracerebral haemorrhage?

A
  • Ischaemic stroke
  • Hypertensive encephalopathy
  • Hypoglycaemia
  • Complicated migraine
  • Seizure disorder
145
Q

What is the structure of the meninges?

A

The outer layer of the meninges is the dura mater, the middle layer is the arachnoid mater, and the inner layer is the pia mater. These last two, the arachnoid and pia maters, are the leptomeninges.

Between the leptomeninges there’s the subarachnoid space, which houses cerebrospinal fluid, or CSF.

CSF is a clear, watery liquid which is pumped around the spinal cord and brain, cushioning them from impact and bathing them in nutrients.

146
Q

How can a subarachnoid Haemorrhage affect the meninges?

A

Subarachnoid haemorrhages can lead to a pool of blood under the arachnoid mater that increases the intracranial pressure and prevents more blood from flowing into the brain.

147
Q

What is a subarachnoid haemorrhage?

A

Subarachnoid haemorrhage (SAH) is a type of intracranial haemorrhage characterised by blood within the subarachnoid space.

148
Q

What does a SAH involve?

A

Spontaneous arterial bleeding into the subarachnoid space

Subarachnoid haemorrhage involves bleeding in to thesubarachnoid space, where thecerebrospinal fluid is located, between thepia mater and thearachnoid membrane. This is usually the result of a rupturedcerebral aneurysm.

149
Q

What is the aetiology of a SAH?

A
  • Rupture of saccular aneurysms (70%)
  • Idiopathic (<15%)
  • Trauma → It is most commonly caused bytrauma(traumatic SAH).
  • Atraumaticcases are referred to asspontaneousSAH and are caused by the following:
    • Berry aneurysm: saccular aneurysm is the most common cause of spontaneous SAH (80% of spontaneous SAH)
      • Arise at points of arterial bifurcation within the Circle of Willis; the junction between the anterior communicating and anterior cerebral arteries is the most common location
      • Associated with adult polycystic kidney disease, coarctation of the aorta and Ehlers-Danlos/ Marfan’s syndrome
    • Arterio-venous malformations (10%)
      • Arteriovenous malformation(AVM) - abnormal connections between artery and vein can dilate and cause rupture
    • Perimesencephalic: venous bleeding with normal CT and excellent prognosis
    • Mycotic aneurysm: due to bacterial infection e.g. secondary to emboli from infective endocarditis
    • Vertebral artery dissection
    • Pituitary apoplexy: bleeding into the pituitary gland, often associated with a tumour
150
Q

What is the pathophysiology of a SAH?

A
  • Rupture of the arteries forming the circle of Willis
    • Rupture of the junction of the anterior communicating artery and the anterior cerebral artery or the posterior communicating artery and the internal carotid artery
    • Leads to tissue ischaemia (since less blood can reach the tissue) as well as rapid raised ICP as the blood acts like a space-occupying lesion and puts pressure on the brain → neurological deficits
  • Arteriovenous malformations (AVM)
    • Vascular development malformation often with a fistula between arterial and venous systems causing high flow through the AVM and high-pressure arterialisation of draining veins → rupture
  • Subarachnoid haemorrhages can lead to a pool of blood under the arachnoid mater that increases the intracranial pressure. This puts direct pressure on nearby tissue cells and blood vessels as well as preventing more blood from flowing into the brain.
  • Healthy tissue can die from both the direct pressure and the lack of oxygen within a few hours.
  • Blood vessels that are “bathing” in a pool of blood can start to intermittently vasoconstrict - vasospasm. If the vasospasm affects arteries in the circle of Willis, it will reduce the supply of blood flow to the brain, causing further ischaemic injury.
  • Over time, blood in the subarachnoid space can irritate the meninges and cause inflammation which leads to scarring of the surrounding tissue. The scar tissue can obstruct the normal outflow of cerebrospinal fluid, causing fluid build up which dilates the ventricles at the centre of the brain. This is referred to as hydrocephalus.
151
Q

What is the epidemiology of a SAH?

A
  • Typical age 35-65 – mean age 50
  • Account for ~5% of strokes
  • The incidence of Subarachnoid haemorrhage in most populations is between 6-8 cases out of 100,000 per year

Subarachnoid haemorrhage is more common in:

  • Black patients
  • Female patients
  • Most commonly presents in people age 45-70
152
Q

What are the symptoms of a SAH?

A
  • Sudden onset severe occipital “thunderclap” headache – like being kicked in the head
    • Severe, sudden onset
    • Occipital
    • ‘Thunderclap’ headache
  • Neck stiffness
    • Meningism: photophobia and neck stiffness
  • Seizures
  • Vision changes
  • Nausea and vomiting
  • Speech changes
  • Loss of consciousness
  • Weakness
  • Confusion
  • Coma
  • Drowsiness
153
Q

What are the signs of a SAH?

A
  • 3rd nerve palsy
    An aneurysm arising from the posterior communicating artery will press on the 3rd nerve, causing apalsy with afixed dilated pupil
  • 6th nerve palsy
    A non-specific sign which indicates raised intracranial pressure
  • Reduced GlasgowComa Scale
  • Meningeal irritation
    Kernig’s sign – unable to extend patient’s leg at the knee when the thigh is flexed
    Neck stiffness
  • Brudzinski’s sign – when patient’s neck is flexed, patient will flex their hips and knees
  • Subhyaloid haemorrhages (bleeding between retina and vitreous membrane) ± papilloedema
154
Q

What are the primary investigations for SAH?

A
  • FBC
  • Serum glucose
  • Clotting screen
  • Urgent non-contrast CT head:
    • Diagnostic (but can be negative in a minority of patients)
    • CT imaging typically shows blood in the basal cisterns
    • Shows subarachnoid or intraventricular blood in 95% of cases undergoing scanning within 24 hours, sensitivity decreases after that time, spider or 5 star sign.
  • ECG: should be requested forallpatients and may demonstrate arrhythmias, ischaemia and ST-elevation
155
Q

What are some other investigations for a SAH?

A
  • Other investigations to consider
  • Lumbar puncture (LP):perform if CT head isnegative and clinical suspicion remains
    If CT normal but SAH still suspected → Perform from12 hours of symptom onset (not earlier)

Findings - RBCs or xanthochromia (yellow pigmentation due to degradation of haemoglobin to bilirubin and is present at 12 hours post-bleed) with normal or raised opening pressure
Xanthochromia helps to differentiate SAH from a ‘traumatic tap’, which is simply blood in the CSF due to the procedure itself
CSF in Subarachnoid haemorrhage is uniformly blood early on and becomes xanthrochromic (yellow) after several hours due to the breakdown products of haemoglobin (bilirubin)

  • CT angiogram or digital subtraction angiography (DSA): after spontaneous SAH has been confirmed, further imaging may be conducted to find the source, such as an aneurysm or AVM; this is usually done in aspecialist neurosurgical unit
  • ABG – to rule out hypoxia
156
Q

What is the management for SAH?

A
  • Refer to neurosurgeon
    • On confirmation of SAH, all patients must beimmediately
      referred toneurosurgery.

Intervention should generally be performed within 24 hours due to the risk of rebleeding.

  • Nimodipine (calcium channel blocker) – reduces cerebral artery spasm, used to prevent vasospasm
    • 60mg 4-hourly should be offered to all patients immediately upon diagnosis; this is thought to prevent vasospasm and a 21-day course**is usually offered
  • Early intervention to prevent re-bleeding
    • Radiologically
    • Surgically – surgical clipping or endovascular coiling
      • Intervention: first-line isendovascular coilingof the aneurysm; second-line issurgical clippingvia craniotomy
  • If features of raised intracranial pressure: consider intubation with hyperventilation, head elevation (30°) and IV mannitol
  • Conservative:
    • Bed rest
    • Antitussive (anti-cough) agent and stool softeners: prevents straining and therefore reduce the risk of rebleeding
157
Q

What is the differential diagnosis for SAH?

A
  • Differential diagnosis
    • Migraine
    • Meningitis
    • Corticol vein thrombosis
158
Q

What are the complications for a SAH?

A
  • Rebleeding: 22% risk at 1 month
  • Vasospasm: accounts for 23% of deaths; at highest risk for the first 2-3 weeks after SAH; treated with (induced)hypertension,hypervolaemia andhaemodilution (triple-H therapy).
  • Hydrocephalus: acutely managed with external ventricular drain (CSF drainage into an external bag) or a long-term ventriculoperitoneal shunt, if required
  • Seizures: seizure-prophylaxis is often administered (e.g. Keppra)
  • Hyponatraemia: commonly due to syndrome of inappropriate antidiuretic hormone secretion (SIADH)
  • Death
159
Q

What are the RFs for SAH?

A

Hypertension and smoking are the two most important modifiable risk factors.

  • Smoking
  • Hypertension
  • Increasing age: most commonly presents in people > 50 years old
  • Alcohol misuse
    • Alcohol excess: there is a significantly increased risk withcurrentalcohol abuse
  • Bleeding disorders
  • Mycotic aneurysm
  • Cocaine use
  • Family history
  • Polycystic kidney disease(PKD): 5 times more common in autosomal dominant PKD
  • Connective tissue disorders: such as Marfan syndrome or Ehlers-Danlos
  • Neurofibromatosis: tumours form on your nerve tissues
160
Q

What is the prognosis for SAH?

A
  • At 6 months, 25% of patients are dead and 50% are moderately to severely disabled.
  • Importantpredictors of 30-day mortalityinclude age, level of consciousness on admission and the amount of blood visible on CT.
  • Causes of mortalityinclude medical complications (23%), vasospasm (23%), rebleeding (22%) and initial haemorrhage (19%)
161
Q

What does the dura mater consist of?

A
  • The outer membrane, the dura mater consists of two layers. The internal layer of the dura mater lies above the arachnoid mater - the two are separated by the subdural space.
  • The external layer of the dura mater adheres to the inner surface of the skull. These two layers of the dura mater travel together, but at certain spots, the internal layer of the dura mater separates from the external one to form the meningeal folds.
162
Q

What is the role of the subdural space?

A
  • The subdural space plays a major role in venous blood drainage in the brain.
  • The surface of the brain is supplied by numerous arteries in the subarachnoid space that provides oxygen rich blood to the brain. After the brain tissue has taken up the oxygen and nutrients, the blood drains into superficial cerebral veins, or bridging veins, that also sit in the subarachnoid space.
  • These veins travel through the arachnoid mater, pass through the subdural space and penetrate the inner layer of the dura mater to drain into the dural venous sinuses located between the two layers of the dura mater.
  • Eventually the blood in the venous sinuses drain into the internal jugular vein and returns to the heart.
163
Q

What is the role of the subdural space?

A
  • The subdural space plays a major role in venous blood drainage in the brain.
  • The surface of the brain is supplied by numerous arteries in the subarachnoid space that provides oxygen rich blood to the brain. After the brain tissue has taken up the oxygen and nutrients, the blood drains into superficial cerebral veins, or bridging veins, that also sit in the subarachnoid space.
  • These veins travel through the arachnoid mater, pass through the subdural space and penetrate the inner layer of the dura mater to drain into the dural venous sinuses located between the two layers of the dura mater.
  • Eventually the blood in the venous sinuses drain into the internal jugular vein and returns to the heart.
164
Q

What is an extradural Haemorrhage?

A

Bleeding above the dura mater.

Anextradural haemorrhage (also known as an ‘epidural’ haemorrhage) is bleeding into the potential space between the skull and the dura mater. The blood then collects in this space and is referred to as anextradural haematoma (EDH).

165
Q

What is the aetiology of an extradural Haemorrhage?

A
  • Traumatic head injury – typically after trauma to temple
    • Usually at the pterion
    • Ruptures middle meningeal artery

EDH is usually caused bytrauma,e.g. blunt trauma to the head

  • Arterial bleeding:the majority of EDHs occur as a result of rupture of the middle meningeal artery. This is commonly affected through trauma to the temporal region or pterion (thinnest part of the skull)
  • Venous bleeding:this is rarer and usually due to venous bleeding from dural venous sinus laceration and is usually seen at the vertex, middle cranial fossa or posterior cranial fossa

Rarely, EDH can be due tonon-traumaticevents such as:

  • Haemorrhagic tumour
  • Coagulopathy
  • Infection
  • Vascular malformation
166
Q

What is the pathophysiology of an ED Haemorrhage?

A
  • Head injury leading to fracture in temporal/parietal bone resulting in laceration of middle meningeal artery
  • Blood accumulates rapidly over minutes-hours between the bone and the dura
167
Q

What is the presentation of an ED Haemorrhage?

A

The classic presentation is aninitial loss of consciousness followed by a lucid interval

  • Initial loss of consciousness on trauma to the temporal region
  • Lucid interval:patient regains consciousness as there isvenous shuntingdirecting blood out of the epidural space
  • Continued expansion of haematoma:leads to local compression of the temporal lobe and eventual cerebral herniation, e.g.uncal herniation
  • Uncal herniation results in compression of third nerve resulting in afixed, dilated ipsilateral pupil
  • Uncal herniation results in compression of the ipsilateral cerebral peduncle resulting incontralateral hemiparesis
  • Further compression will lead to brainstem compression, Cushing’s reflex, tonsillar herniation, and eventual death
168
Q

What is the epidemiology of an extradural haemorrhage?

A

They are about half as common as a subdural hematomas and usually occur in young adults.

  • Usually occurs in young adults (rare < 2 and > 60)

EDHs occur in approximately 2% of all head injuries and up to 15% of all fatal head injuries

169
Q

What are the symptoms of an ED Haemorrhage?

A
  • Characteristic history
    - Head injury
    - Loss of consciousness following trauma or initial drowsiness
    - Lucid interval – period of time between traumatic brain injury and decrease in consciousness
    - Occurs in ~ 20% of patients
    - Patients regain full consciousness
    • Signs of raised ICP – headache, vomiting, nausea, seizure
      • ± hemiparesis with brisk reflexes
    • Ipsilateral pupil dilation
      • Pupil dilation if bleeding continues
    • Confusion
170
Q

What are the signs of an ED Haemorrhage?

A

Worsening neurological status

  • Cushing’s reflex:hypertension and bradycardia
    • Bradycardia and raised BP
  • Decreased Glasgow coma scale
    • Reduced GCS: loss of consciousness after the trauma due to concussion
      • There might be a lucid interval after initial trauma if there is a slower bleed. This is followed by rapid decline.
  • Uncal herniation:ipsilateral, fixed dilated pupil and contralateral hemiparesis
  • Local compression results in mass effect and brain herniation
  • Coning of brain through foramen magnum
  • May be focal neurological symptoms e.g. muscle weakness, hemiparesis, abnormal plantar reflex (upgoing plantar) or sensory problems
  • Signs of raised ICP – headache, vomiting, nausea, seizure
    • ± hemiparesis with brisk reflexes

Evidence of head injury:

  • Bruising or scalp haematoma
  • Battle’s sign (bruising behind mastoid process)
  • Bleeding from one/both ears
  • Haemotympanum
  • Periorbital haematoma (Racoon eyes)
  • Rhinorrhea or otorrhea
171
Q

What are the investigations for an ED Haemorrhage?

A
  • Non-contrast CT head scan – shows biconvex hypodense haematoma that is adjacent to the skull
    • Blood forms a more rounded/biconvex shape compared with the sickle-shaped subdural haematomas as the tough dural attachments to the skull keep it more localised
    • Don’t cross suture linesFindings:
      • Hyperdense mass = looks “more white” than the surrounding healthy brain tissue
  • EDH appears as a hyperdense well-demarcated biconvex collection, most frequently beneath the temporal bone, and the bleed should be limited by the cranial sutures
    • Can also assess for skull fracture
    • Features of mass effect, such as uncal herniation, may be present
    • Venous bleeds may be located at the vertex, middle cranial fossa, or posterior cranial fossa
  • Epidural haemorrhages cause blood to build up between the outer layer of the dura mater and the skull so epidural haematomas don’t cross suture lines and they push on the brain forming a biconvex shape. This is not the case with subdural haematomas.
  • Skull X-ray – may be normal or show fracture lines crossing the course of the middle meningeal artery
    • Skull fracture increases the extradural haemorrhage risk so do an urgent CT on anyone with suspected skull fracture
  • Check FBC and clotting
172
Q

What is the management if an ED Haemorrhage?

A

Definitive management

  • Refer to neurosurgeon - Clot evacuation
    • Burr hole craniotomy and Irrigation/removal of haematoma via burr twist drill
      • Craniotomy and haematoma evacuation: part of the skull bone is removed in order to remove accumulated blood below.
        • Indicated if the EDH is greater than 30cm3should be regardless of the GCS score
        • An EDH less than 30cm3and with less than 15-mm thickness with less than a 5-mm midline shift in patients with a GCS score greater than 8 without focal deficitcan be managed non-operativelywithserial CT scanningandclose neurological observationin a neurosurgical centre
    • Ligation of bleeding vessel
      • Followed by ligation of the vessel.
  • Stabilise patient – ABCDE management
  • IV mannitol – to reduce ICP
  • Consider intubation, ventilation and ICU care if they have reduced consciousness
  • Correct any clotting abnormality
  • Correct severe hypertension but avoid hypotension

General principles:aim to reduce/control intracranial pressure

  • Bed position:have the head of the bed tilted up at ~30 degrees
  • Intubation:if the patient has reduced GCS
  • Oxygen:ensure adequate oxygenation
  • Maintain adequate cerebral perfusion (Perfusion = MAP - ICP)
    • Hyperventilation:may be considered in a deteriorating patient; hyperventilation can reduce pCO2which causes cerebral vasoconstriction and reduces ICP
    • Inotropes and vasopressors
    • Fluids
    • Osmotherapy:hypertonic saline or mannitol help shift extracellular fluid and CSF into the vascular compartment, reducing ICP
  • Decrease cerebral metabolic rate:hypothermia and sedation/paralysis
  • Burr hole:temporising measure to reduce ICP prior to definitive management
173
Q

What are the complications of an ED Haemorrhage?

A
  • Death due to respiratory arrest
    • Brain displacement
    • Raised ICP
    • Herniation – supratentorial (cerebrum pushed against skull or tentorium) or infratentorial (cerebellum pushed against brainstem)
      • Increased intracranial pressure can also cause the brain to herniate, these can be lethal:
        • Supratentorial herniation: cerebrum is pushed against the skull or the tentorium, can compress the arteries that nourish the brain leading to an ischaemic stroke
        • Infratentorial herniation: cerebellum is pushed against the brainstem, can compress the vital area in the brainstem that control consciousness, respiration, and heart rate.
          • Patients present with deep irregular breathing, high BP, low HR
  • Coma

Secondary injury refers to theevolving consequencesof primary injury and includes the following:

  • Cerebral oedema
  • Raised intracranial pressureandherniation
  • Ischameia:can occur due to mass effect, herniation, hypoperfusion, vasospasm
  • Seizures
  • Infection
174
Q

What are the RFs of an extradural haemorrhage?

A
  • Age:mean age of affected patients is 20-30 years of age. As patients get older the dura becomes more adherent to the skull, making EDH less likely.
  • Male sex:men are more often affected than females
  • Anticoagulant usage:patients on anticoagulants who sustain a head injury are at an increased risk of developing a haemorrhage.

Usually occurs in young adults

General risk Factors

  • Head injury
  • Hypertension
  • Aneurysms
  • Ischaemic stroke can progress to haemorrhage
  • Brain tumours
  • Anticoagulants such as warfarin
175
Q

What is the prognosis of an ED Haemorrhage?

A
  • Themortality rate for acute EDH isapproximately 25%.
  • Prognosis is good if diagnosed and operated on early.
    • Most patients with an EDH have agood prognosis if they receive early evacuation of the haematoma.
  • Poor prognosis factors include reduced GCS on arrival, older age, large haematomas, rapid clinical progression, pupillary abnormalities and raised intracranial pressure.
  • Poor prognosis if coma, pupil abnormalities or decerebrate rigidity are present pre-op.
176
Q

What is a subdural haemorrhage?

A

Bleeding below the dura mater

Asubdural haemorrhage occurs when blood accumulates between the dura and arachnoid mater (subdural space), forming a collection known as asubdural haematoma (SDH).

177
Q

What does a subdural haemorrhage involve?

A
  • A subdural haematoma is a collection of clotting blood that forms in the subdural space. This is the space between two of the meninges, which form the protective lining that covers the brain.
178
Q

How is a subdural haemorrhage classified?

A
    • Acute- where the blood collects quickly after a head injury; symptoms can occur immediately or within hours.
    • Subacute- where symptoms develop between 3-7 days after the injury.
    • Chronic- the blood collects slowly after a head injury; symptoms can occur 2-3 weeks after the initial injury.
    SDH can be classified in terms of acuity
179
Q

What are the classifications for a SDH?

A

Acute - <3 days old
- traumatic rupture of bridging cortical veins

Chronic - >21 days old
- traumatic rupture of bridging cortical veins
- associate with cortical atrophy e.g. elderly or alcoholics
- bridging veins are more prone to rupture with cortical atrophy
- requires lower impact trauma compared to acute
- because there is cortical atrophy, the subdural space is larger; these haematoma can enlarge significantly over time whilst patients remain asymptomatic

Subacute SDH - 3-21 days

180
Q

What is the epidemiology of a SDH?

A
  • Occurs more frequently in the elderly or alcoholics.
  • Acute subdural haematoma is found in about 11% to 20% of patients admitted to hospital with mild to severe traumatic brain injury.
181
Q

What is the aetiology of a subdural haemorrhage?

A

Subdural haemorrhage commonly occurs aftertrauma. The subdural space containsbridging veins which take blood from the brain to the dural venous sinuses. If these veins rupture, they can bleed into the subdural space.

Rupture of bridging veins, usually caused by:

  • Brain atrophy: in the elderly the brain shrinks in size which means that the bridging veins are stretched across a wider space where they are largely unsupported
  • Alcohol abuse: caused the wall of the veins to thin out, and make them more likely to break.
  • Trauma/ injury e.g.
    • Falls
    • Shaken baby syndrome
    • Acceleration-deceleration injury: speeding on the road and then suddenly slamming the brakes. Causes damage to the front of the brain as the body jerks forward, and then the back of the brain as the body moves backwards.
182
Q

What is the pathophysiology of a SDH?

A
  • The meninges are the protective lining that surrounds the brain within the skull, and the spinal cord within the backbone.
  • There are three layers of meninges
  • There are also three thin spaces between the layers of meninges
    • The main cause of a subdural haemorrhage is a rupture of the bridging veins located in the subdural space. This can be due to trauma or without trauma e.g. reduced intracranial pressure or dural metastases
    • When there is active bleeding, it’s called a haemorrhage, and the collection of blood that results is called a haematoma.
    • As the damaged bridging veins are under low pressure, the bleeding can be slow causing delayed onset of symptoms which might develop over the course of days to weeks as the haematoma gradually expands.
    • An acute subdural haematoma causes symptoms within 2 days, a subacute subdural haematoma causes symptoms between 3 and 14 days, and a chronic subdural haematoma causes symptoms after 15 days.
    • The haematoma can compress the brain and cause increased intracranial pressure.A large subdural haematoma on one side of the skull can cause a midline shift which is a displacement of the whole brain towards the opposite side of the skull.The increased intracranial pressure can also cause the brain to herniate.
183
Q

What is the pathophysiology of a SDH?

A
  • The meninges are the protective lining that surrounds the brain within the skull, and the spinal cord within the backbone.
  • There are three layers of meninges
  • There are also three thin spaces between the layers of meninges
    • The main cause of a subdural haemorrhage is a rupture of the bridging veins located in the subdural space. This can be due to trauma or without trauma e.g. reduced intracranial pressure or dural metastases
    • When there is active bleeding, it’s called a haemorrhage, and the collection of blood that results is called a haematoma.
    • As the damaged bridging veins are under low pressure, the bleeding can be slow causing delayed onset of symptoms which might develop over the course of days to weeks as the haematoma gradually expands.
    • An acute subdural haematoma causes symptoms within 2 days, a subacute subdural haematoma causes symptoms between 3 and 14 days, and a chronic subdural haematoma causes symptoms after 15 days.
    • The haematoma can compress the brain and cause increased intracranial pressure.A large subdural haematoma on one side of the skull can cause a midline shift which is a displacement of the whole brain towards the opposite side of the skull.The increased intracranial pressure can also cause the brain to herniate.
184
Q

What are the spaces between the meninges?

A

The epidural space is the space between the vertebral column and the dura mater. (There is only a potential epidural space in the skull.)
- The subdural space is the space between the dura mater and the arachnoid mater.
- The subarachnoid space is the space between the arachnoid mater and the pia mater.

185
Q

What are the clinical features of an acute and chronic subdural haemorrhage?

A

Acute - symptom onset within 3 days of inciting event
- may have lucid interval
- reduced consciousness
- headaches and vomiting
- slurred speech
- focal neurological deficit, e.g. weakness or fixed dilated pupil
- cushing’s reflex
- seizures

Chronic - insidious onset usually in the elderly or alcoholics
- progressive confusion and cognitive deficit
- headaches and vomiting
- focal neurological deficit e.g. weakness or fixed dilated pupils

186
Q

What are the clinical features of an acute and chronic subdural haemorrhage?

A

Acute - symptom onset within 3 days of inciting event
- may have lucid interval
- reduced consciousness
- headaches and vomiting
- slurred speech
- focal neurological deficit, e.g. weakness or fixed dilated pupil
- cushing’s reflex
- seizures

Chronic - insidious onset usually in the elderly or alcoholics
- progressive confusion and cognitive deficit
- headaches and vomiting
- focal neurological deficit e.g. weakness or fixed dilated pupils

187
Q

What are the symptoms of a SDH?

A
  • headache
  • nausea/vomiting
  • Confusion
  • Seizure
  • Loss of consciousness
188
Q

What are the signs/Diagnostioc factors of a SDH?

A
  • Reduced GCS: loss of consciousness right after the injury or in the ensuing days to weeks as the haematoma increases in size.
  • Sometimes there can be focal neurological symptoms e.g. muscle weakness, unequal pupils, hemiparesis or sensory problems
  • evidence of trauma
  • Diminished eye response
  • Diminished verbal response
  • Diminished motor response
189
Q

What are the investigations for a SDH?

A
  • Non-contrast CT head scan
    • Immediate CT head to establish the diagnosis. Shows clot and midline shift.
      Findings:
      A hyperdense crescent shaped haematoma suggestive of an acute subdural haematoma as indicated by red arrows on this CT head.
  • SDH appears as acrescentic collectionaround the surface of the brain which isnot limited by the suture linesof the skull unlike in anextradural haemorrhage. There may be evidence of mass effect such as midline shift or herniation
    • Acute:hyperdense (bright)
    • Subacute:as the clot matures, the density starts to drop until it is isodense to the brain cortex
    • Chronic:becomes hypodense (dark)
  • Acute subdural haematoma: hyperdense mass = looks “more white” than the surrounding healthy brain tissue
  • Chronic subdural haematoma: hypodense masses = “less white” than the surrounding brain tissue.
  • Acute on chronic bleeding: combination of hyperdense and hypodense, seen in individuals who have a rebleed in the bridging veins after a chronic haematoma has already formed.

Bleeding is between the dura and arachnoid so subdural haematomas follow the contour of the brain and form a crescent-shape and cross suture lines. This is different to an epidural haemorrhage!

190
Q

What are the investigations for a SDH?

A
  • Non-contrast CT head scan
    • Immediate CT head to establish the diagnosis. Shows clot and midline shift.
      Findings:
      A hyperdense crescent shaped haematoma suggestive of an acute subdural haematoma as indicated by red arrows on this CT head.
  • SDH appears as acrescentic collectionaround the surface of the brain which isnot limited by the suture linesof the skull unlike in anextradural haemorrhage. There may be evidence of mass effect such as midline shift or herniation
    • Acute:hyperdense (bright)
    • Subacute:as the clot matures, the density starts to drop until it is isodense to the brain cortex
    • Chronic:becomes hypodense (dark)
  • Acute subdural haematoma: hyperdense mass = looks “more white” than the surrounding healthy brain tissue
  • Chronic subdural haematoma: hypodense masses = “less white” than the surrounding brain tissue.
  • Acute on chronic bleeding: combination of hyperdense and hypodense, seen in individuals who have a rebleed in the bridging veins after a chronic haematoma has already formed.

Bleeding is between the dura and arachnoid so subdural haematomas follow the contour of the brain and form a crescent-shape and cross suture lines. This is different to an epidural haemorrhage!

Check FBC and clotting

191
Q

What is the management for a SDH?

A

Anurgent neurosurgical opinionis required.

  • General principlesGeneral principles:aim to reduce/control intracranial pressure
    • Bed position:have the head of the bed tilted up at ~30 degrees
    • Intubation:if the patient has reduced GCS
    • Oxygen:ensure adequate oxygenation
    • Maintain adequate cerebral perfusion (Perfusion = MAP - ICP)
      • Hyperventilation:may be considered in a deteriorating patient; hyperventilation can reduce pCO2which causes cerebral vasoconstriction and reduces ICP
      • Inotropes and vasopressors
      • Fluids
      • Osmotherapy:hypertonic saline or mannitol help shift extracellular fluid and CSF into the vascular compartment, reducing ICP
    • Decrease cerebral metabolic rate:hypothermia and sedation/paralysis
    • Burr hole:temporising measure to reduce ICP prior to definitive management
192
Q

What is the management for a SDH?

A

Anurgent neurosurgical opinionis required.

  • General principlesGeneral principles:aim to reduce/control intracranial pressure
    • Bed position:have the head of the bed tilted up at ~30 degrees
    • Intubation:if the patient has reduced GCS
    • Oxygen:ensure adequate oxygenation
    • Maintain adequate cerebral perfusion (Perfusion = MAP - ICP)
      • Hyperventilation:may be considered in a deteriorating patient; hyperventilation can reduce pCO2which causes cerebral vasoconstriction and reduces ICP
      • Inotropes and vasopressors
      • Fluids
      • Osmotherapy:hypertonic saline or mannitol help shift extracellular fluid and CSF into the vascular compartment, reducing ICP
    • Decrease cerebral metabolic rate:hypothermia and sedation/paralysis
    • Burr hole:temporising measure to reduce ICP prior to definitive management
193
Q

What is the definitive management for a SDH?

A
  • Conservative:small acute and chronic SDHs which are not causing neurological deficit can be observed
  • Surgery:involves craniotomy and evacuation. Indications for acute SDH are as follows
    • Acute SDH with athickness>10mmor amidline shift>5mm
    • GCS < 9 and GCS score decreased between the time of injury and hospital admission by 2 or more points
    • Patient presents with asymmetric or fixed and dilated pupils
    • ICP > 20 mmHg
    • A patient with a chronic SDH should be considered for evacuation, particularly if the hematoma is producing mass effect or the patient is symptomatic
194
Q

What is the definitive management for a SDH?

A
  • Conservative:small acute and chronic SDHs which are not causing neurological deficit can be observed
  • Surgery:involves craniotomy and evacuation. Indications for acute SDH are as follows
    • Acute SDH with athickness>10mmor amidline shift>5mm
    • GCS < 9 and GCS score decreased between the time of injury and hospital admission by 2 or more points
    • Patient presents with asymmetric or fixed and dilated pupils
    • ICP > 20 mmHg
    • A patient with a chronic SDH should be considered for evacuation, particularly if the hematoma is producing mass effect or the patient is symptomatic
195
Q

What are some other managements for a SDH?

A
  • Observation, monitoring and follow-up imaging-CT
    • Correct any clotting abnormality
    • Correct severe hypertension but avoid hypotension
    • Address cause of trauma/ injury
  • Prophylactic antiepileptics
  • Mannitol: used to reduce ICP
  • Surgery
    • Drainage:
      • Small subdural haematomas are drained via burr hole washout - by placing a small tube called a catheter, through a drilled hole in the skull.
      • Large subdural haematomas require a craniotomy, which is when part of the skull bone is removed in order to remove accumulated blood below
  • Consider intubation, ventilation and ICU care if they have reduced consciousness
196
Q

What are some other managements for a SDH?

A
  • Observation, monitoring and follow-up imaging-CT
    • Correct any clotting abnormality
    • Correct severe hypertension but avoid hypotension
    • Address cause of trauma/ injury
  • Prophylactic antiepileptics
  • Mannitol: used to reduce ICP
  • Surgery
    • Drainage:
      • Small subdural haematomas are drained via burr hole washout - by placing a small tube called a catheter, through a drilled hole in the skull.
      • Large subdural haematomas require a craniotomy, which is when part of the skull bone is removed in order to remove accumulated blood below
  • Consider intubation, ventilation and ICU care if they have reduced consciousness
197
Q

What are the complications for a SDH?

A
  • Complications
    • Epilepsy related to trauma
    • Neurological deficits
    • Coma
    • Increased intracranial pressure can also cause the brain to herniate, these can be lethal:
      • Supratentorial herniation: cerebrum is pushed against the skull or the tentorium, can compress the arteries that nourish the brain leading to an ischaemic stroke
      • Infratentorial herniation: cerebellum is pushed against the brainstem, can compress the vital area in the brainstem that control consciousness, respiration, and heart rate
    • Stroke
    Secondary injury refers to theevolving consequencesof primary injury and includes the following:
    • Cerebral oedema
    • Raised intracranial pressureandherniation
    • Ischameia:can occur due to mass effect, herniation, hypoperfusion, vasospasm
    • Seizures
    • Infection
198
Q

What are the complications for a SDH?

A
  • Complications
    • Epilepsy related to trauma
    • Neurological deficits
    • Coma
    • Increased intracranial pressure can also cause the brain to herniate, these can be lethal:
      • Supratentorial herniation: cerebrum is pushed against the skull or the tentorium, can compress the arteries that nourish the brain leading to an ischaemic stroke
      • Infratentorial herniation: cerebellum is pushed against the brainstem, can compress the vital area in the brainstem that control consciousness, respiration, and heart rate
    • Stroke
    Secondary injury refers to theevolving consequencesof primary injury and includes the following:
    • Cerebral oedema
    • Raised intracranial pressureandherniation
    • Ischameia:can occur due to mass effect, herniation, hypoperfusion, vasospasm
    • Seizures
    • Infection
199
Q

What are some differential diagnosis for a SDH?

A
  • Epidural haematoma
  • Intracerebral haematoma
  • Diffuse axonal injury (DAI)
  • Stroke
  • Seizure
  • Substance abuse
  • Dementia
  • CNS masses e.g. tumours or abscesses
  • Subarachnoid haemorrhage
200
Q

What are some differential diagnosis for a SDH?

A
  • Epidural haematoma
  • Intracerebral haematoma
  • Diffuse axonal injury (DAI)
  • Stroke
  • Seizure
  • Substance abuse
  • Dementia
  • CNS masses e.g. tumours or abscesses
  • Subarachnoid haemorrhage
201
Q

What is a prognosis for a subdural haemorrhage?

A
  • Mortality following acute and chronic SDHincreases with age; those above 80 have a mortality of almost 90% if they have an acute SDH.
  • Poor prognostic factors for acute and SDH includereduced GCS on arrival,size of the SDH, andincreasing age.
  • For chronic SDH, the prognosis is more favourable.
202
Q

What is a prognosis for a subdural haemorrhage?

A
  • Mortality following acute and chronic SDHincreases with age; those above 80 have a mortality of almost 90% if they have an acute SDH.
  • Poor prognostic factors for acute and SDH includereduced GCS on arrival,size of the SDH, andincreasing age.
  • For chronic SDH, the prognosis is more favourable.