Fichas
Stroke
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- 1Define strokeAn acute, focal neurological deficit of cerebrovascular origin that persists> 24hrs
- 2Define transient ischaemic attack (TIA)- Acute, focal neurological deficit of cerebrovascular origin that persists <1 hour, without signs of cerebral infarction on MRI scanning
- 3Define amaurosis fugax?- Sudden transient loss of vision in one eye
- Often occur with TIAs, and can be the first clinical evidence of ICA stenosis
- This can also occur due to ocular disease or migraine - 4What are the more common risk factors for stroke?- Age
- Personal/Family history
- Hyper-coagulable states
- Atrial fibrillation
- HTN
- Hypercholesterolaemia
- Diabetes
- Smoking & alcohol
- Low exercise & increased weight
- Oestrogen-containing combined contraceptive - 5What are the less common risk factors for stroke?- Endocarditis
- Migraine
- Polycythaemia
- APL syndrome
- Vasculitis
- Amyloidosis - 6What are the risk factors for haemorrhagic stroke?- FH
- Uncontrolled HTN
- Vascular abnormalities (aneurysms, AVMs,HHT)
- Coagulopathies/anticoagulant therapy
- Heavy recent alcohol intake - 7What proportion of strokes are ischaemic/haemorrhagic?- Infarction = 85%
- Haemorrhagic = 15%
> SAH = 10%
> Intra-cerebral haemorrhage = 5% - 8What are the different types of cerebral ischaemia?- Regional infarction: thrombosis/embolus in large vessels, usually cortical areas
- Lacunar: microinfarcts caused bu small vessel disease, usually sub-cortical areas, can be asymptomatic, eventually leading to vascular pseudo-Parkinsonism or vascular dementia
- Global: infarcts at arterial boundary zones due to severe hypotension (watershed infarction), if severe can cause cortical laminar necrosis - 9How is cerebral ischaemic damage divided into zones?- Infarct core: tissue almost certain to die
- Oligaemic periphery tissue: will surive, due to collateral supple
- Ischaemic penumbra: tissue in between; can have either outcome - 10When can infarcts be seen macroscopically?- Can't be seen within 24 hours
- Changes limited to focal swelling and loss of the normal grey-white differentiation - 11How can stroke cause death?- Large infarcts may cause death by associated tissue oedema, leading to herniation and brainstem compression
- Infarcts at critical sites can interfere with vital functions (e.g. breathing)
- Pneumonia secondary to aspiration or immobility - 12What are the clinical features of ischaemic stroke?- Contralateral limb weakness/hemiplegia:
> At first flaccid, but over time reflexes return and become exaggerated, with extensor plantars
> Weakness is maximal at first, and recovery occurs gradually (weeks-months)
- Facial weakness
- Higher dysfunction
- Visual disturbances
- Epileptic fit (rare) - 13In what ways can higher dysfunction manifest?- Expressive aphasia
- Receptive aphasia
- Apraxia: difficulty performing tasks despite intact motor function
- Asterognsois: inability to identify objects in both hands by touch alone despite intact sensation
- Agnosia: inability to recognise objects, people, sounds, shapes or smells despite the specific sense being intact and no memory loss
- Inattention (neglect): inability to attend to stimuli despite intact senses - 14What are the different Oxford (Bamford) classifications of stroke?- Total Anterior Circulation Syndrome (TACS): proximal MCA occlusion
- Partial Anterior Circulation Syndrome (PACS): distal MCA, or ACA occlusion
- Lacunar stroke (LACS): occlusion of a lacunar branch of the MCA
- Posterior Circulation Stroke (POCS): PCA occulsion
* I = confirmed infarct, e.g. TACI, H = confirmed haemorrhage, e.g. TACH - 15Outline the presentation of a TACS strokeMust have all of the following symptoms:
1) Higher dysfunction
2) Homonymous hemianopia
3) Contralateral hemiplegia and/or sensory loss (at least 2 of face/arm/leg) - 16Outline the presentation of a PACS strokeTwo out of three TACS criteria:
a) Higher dysfunction
b) Homonymous hemianopia
c) Hemiplegia and/or sensory loss
OR
Higher dysfunction alone - 17Outline the presentation of a LACS stroke- Pure motor symptoms (≥2/3 face/arm/leg)
- Pure sensory symptoms (≥2/3 face/arm/leg)
- Pure sensorimotor symptoms (≥2/3 face/arm/leg)
- Ataxic hemiparesis - 18Outline how a POCS stroke can present1) Cranial nerve palsy AND contralateral motor/sensory deficit
2) Bilateral motor or sensory deficit
3) Conjugate eye movement problems: nystagmus, diplopia
4) Cerebellar dysfunction
5) Isolated homonymous hemianopia - 19How do the different Oxford (Bamford) classifications relate to prognosis?
- 20What points need to be covered when taking a history of a patient who has suffered a stroke?- HPC: time/speed of onset, body parts affected, seizure at onset
- PMH: previous stroke/MI, AF, DM, abscess, tumour
- DH: warfarin, heparin, OCP
- Social: alcohol, smoking, illicit drugs - 21What needs to be included in your examination of a stroke patient?- GCS
- NHISS (national institute of health stroke scale)
- CVS: murmurs (endocarditis), BP, HR, signs of dissection
- Resp: SpO2, RR, crackles
- Neuro: UMN/LMN, CNS, cerebellar - 22What investigations would you do for a patient with suspected stroke?- FBC, U&Es, glucose + HbA1c, lipids, coagulation, ESR
- Brain imaging within 1 hour if: considering thrombolysis, bleeding risk/headache at onset, ↓ consciousness, neck stiffness
> MRI gold standard but CT commonly used, if visible on CT (50%) lesions will be seen by day 7
- ECG - 23Outline the acute management of stroke- A-E (always check glucose)
- Withhold anti-platelet therapy until haemorrhage excluded, as soon as excluded, give aspirin 300mg
- Then arrange for thrombolysis if symptoms for >30mins but onset within 4.5hrs - 24What is involved in thrombolysis?- First check for contra-indications: must have lab results back
- Alteplase 0.9mg/kg, as per clinical pathway within hospital
- 10% bolus over 1 minute, remainder over 60 mins - 25Outline the ward management of a patient post-stroke- SALT (swallow) within 2 hours
- Physiotherapy + early mobilisation
- Occupational therapy: limb splinting, ward groups
- Nursing: SSKIN bundle, early nutrition required if NBM
- LMWH started on day 3 post-ischaemic stroke + TED stockings - 26What is done following thrombolysis- Monitor closely over 24hrs via cardiac monitor and using STOC chart
- If pt develops severe headache, acute HTN, nausea or vomiting then discontinue infusions and get emergency CT
- Avoid catheterisation during infusion
- Avoid aspirin or heparin for 24hrs
- Avoid NG tube insertion for first 24hrs - 27What should you do if thrombolysis is contra-indicated?- Manage supportively on ward
- Continue 300mg aspirin daily while implementing secondary prevention measures - 28Outline the secondary prevention of future strokes- Identify and tackle lifestyle RFs
- Antihypertensive therapy: start 2 weeks following stroke if elevated BP, lower slowly
- Antiplatelet therapy: aspirin 300mg daily for 2 weeks, clopidogrel 75mg therafter
- Statin: offer from 48hrs post-stroke
- Manage co-morbidities e.g. AF or DM - 29What is the policy with regards to driving after a stroke?- Must not drive for 4 weeks following a stroke
- After this period, may return to driving if clinical improvement is satisfactory, without needing to inform the DVLA - 30Give post-stroke complications- Malignant MCA syndrome
- DVT/PE
- Aspiration & hydrostatic pneumonia
- Pressure sores
- Depression
- Seizures
- Incontinence
- Post-stroke pain: worsens outcomes, multi-factorial, often needs pain team input - 31What is malignant MCA syndrome?- Rapid neurologcial deterioration due to cerebral oedema following MCA stroke
- High morbidity/mortality, mainly <60yrs
- Presentation:
> Increased agitation/restlessness
> Reducing GCS
> Haemodynamic/thermal instability
- Signs of raised ICP - 32How do you manage malignant MCA syndrome?- Decompressive hemicraniectomy
- If CT/MRI shows infarct of at least 50% of MCA territory in a pt <60yrs with any ↓ in consciousness NICE recommends immediate referral for decompressive hemicraniectomy - 33Following a TIA, what features suggest high risk of future strokes?- Recurrent TIAs within a short period of time
- AF, or TIA whilst anticoagulated
- ABCD2 score of 4 or more:
> Age: >60 (1 point)
> BP @ presentation: >140/90 (1 points)
> Clinical features: unilateral weakness (2p), speech disturbance w.out weakness (1p)
> Duration of Sx: ≥60mins (2p), 10-59mins (1p)
> Diabetes: 1 point for pre-existing DM - 34What is the management of a patient with any of the high-risk features post-TIA?- Statin e.g. simvastatin 40mg
- 300mg aspirin or continue low-dose if already taking
- Arrange referral to specialist clinic within 24hrs
- Advise pt not to drive until seen by specialist
*Management of low risk is sam but referral to specialist less urgent (1 week) - 35Discuss assessment for carotid stenosis post-TIA- Done at specialist clinic
- If stenosis is >50%, carotid endarterectomy should be offered:
> Reduces risk of TIA/stroke by 75%
> Risks: procedure-related stroke and mortality risks
> Alternative = percutaneous luminal angioplasty +/- stenting - 36What are the RFs for venous sinus thrombosis?- Pro-thrombotic RF (85%):
> Oral contraceptives
> Pregnancy/puerperium
> Malignancy
> Genetic thrombophilia
- Head injury
- Recent LP
- Infection - 37What is the pathology of a venous sinus thrombosis?- Venous infarction leads to vascular congestion
- Eventually there is haemorrhagic necrosis
- It can be split into cortical venous thrombosis and dural venous thrombosis - 38How would a cortical venous thrombosis present?- Headache: may be thunderclap
- Focal signs
- Seizures
- Fever
- Encephalopathy - 39How would a dural sinus thrombosis present?- Cavernous sinus thrombosis:
> Ocular pain, worse on movement
> Proptosis and chemosis
> Opthalmoplegia
> Papilloedema
- Fever
- Sagittal and lateral sinus thrombosis:
> Signs of raised ICP: headache, vomiting, fever, papilloedema, seizures - 40What investigations would you do for a suspected venous sinus thrombosis?- CT: often normal
- LP: raised ICP
- MRI angiography: may be required for diagnosis - 41Discuss deep intra-cerebral haemorrhage: causes, areas affected- Mainly caused by rupture of micro-aneurysms (Charcot-Bouchard aneurysms) and degeneration of small deep penetrating arteries
- Occur in sub-cortical areas - 42Discuss lobar intra-cerebral haemorrhage- Occurs in normotensive individuals >60, in the cerebral cortex
- Rarely can be caused by cerebral amyloid angiopathy - 43How would intra-cerebral haemorrhage present?- As per haemorrhagic stroke
- No reliable way to differentiate at bedside
- More likely to present with severe headache and ensuing coma - 44Outline the investigations for suspected intra-cerebral haemorrhage- CT: haemorrhage seen immediately
- MRI: very reliable after 2 hours from symptom onset - 45Outline the management of an intra-cerebral haemorrhage- As per cerebral infarction, with antiplatelets/anticoagulants contraindicated
- Reverse any anticoagulation
- Lower BP to <140/90 within 1hr (use IV betolol)
- Neurosurgical intervention may be required (if deepening coma and coning) - 46Describe the presentation of a subarachnoid haemorrhage (SAH)- 'Thunderclap' headache: develops over seconds, devastating in intensity, often occipital, often comes on during transient HTN e.g. exercise or sex
- Vomiting (after headache)
- Photophobia
- Increasing drowsiness/coma
- Focal signs may point to location of lesion (may also instead reflect ↑ ICP or cerebral vasospasm) - 47What might you see on examination of a pt with SAH?- Neck stiffness
- Positive Kernig's sign: takes 6 hours to develop
- Papilloedema: may be present, along with retinal haemorrhages - 48List abnormalities which predispose to SAHs- Berry aneurysms (70%)
- Arteriovenous malformations (10%)
- No lesion found (20%) - 49Discuss berry aneurysms: locations, RFs, causes what nerve palsy- Developmental rather than congenital
- Develop in Circle of Willis and adjacent arteries: ant. communicating aa (most common), post. communicating aa (@ bifurcation from ICA), middle cerebral aa (@bifurcation/trifurcation)
- Much more common in polycystic kidney disease
- RFs: FH, smoking, HTN, Ehlers-Danlos/Marfans
- Most common causes of painful CN III palsy (mass effect) - 50Discuss AVMs- Congenital abnormalities in arteries/veins
- Tendency to rebleed if symptomatic once: 10% rebleed annually
- Can also cause epilepsy, often focal - 51What are the complications of SAH?- Death (30% die immediately)
- Rebleed:
> Aneurysms: clot can form if vasospasm sufficient which holds for 3-4 days before rebleeding
> AVMs: generally rebleed within a few years rather than days
- Hydrocephalus
- Cerebral vasospasm (can be severe leading to ischaemic damage) - 52What investigations should you do for a suspected SAH?- FBC, U&E, LFT, ESR, clotting
- CT head
- LP (if CT is normal): >12hrs after symptom onset - look for xanthochromia
- CT/MRI angiography for a pts fit for surgery - 53Outline the management of an SAH- 4 weeks bed rest
- HTN control
- Nimodipine to prevent vasospasm
- IV fluids
- Analgesia + anti-emetics
- Stool softeners to prevent straining
- Discuss with neurosurgery: usual procedure is coiling by interventional radiology - 54Discuss acute subdural haematoma: who?, acute management, consequences- Occurs in severe acceleration-deceleration head injury
- Pts often young, come in with dilated pupil and no lucid interval before ↓ GCS
- Craniotomy and early evacuation of clot is required
- Often seriously ill even with early intervention - require ICU with intracranial pressure monitoring
- High incidence of subsequent epilepsy, permanent neuro disability and high mortality - 55Discuss subacute/spontaneous subdural haematoma: cause and risk factors- May occur spontaneously or after minor trauma
- Can be bilateral
- RFs: elderly, alcohol abuse, coagulopathy - 56Discuss the presentation of subacute/spontaneous subdural haematoma- Sx/signs of ↑ ICP develop ~3 weeks after insult or start of bleed, often fluctuant
- Headache
- Drowsiness
- Confusion
- Focal neurological signs
- Eventually, stupor and coma due to coning - 57Discuss the management of a subacute/spontaneous subdural haematoma- Chronic subdural haemorrhage may resolve spontaneously
- Progress can be assessed with imaging but liason with neurosurgery is essential - 58How do CT heads of acute and chronic subdural haematomas differ?- Acute: classic cresenteric shape with ↑ density (white), conforming to contour of skull. May have accompanying midline shift and compression of the ventricles
- Chronic: blood becomes more radiolucent (dark), and assumes a lentiform shape similar to that of an extradural haematoma - 59CT of acute subdural
- 60CT of chronic subdural
- 61How do extradural haemorrhages occur?- Most common in young pts following minor assault or sporting injury
- Blow to the side of the head, enough to cause a fracture and associated tearing of the middle meningeal artery
- Blood accumulates rapidly over minutes to hours in extradural space - 62Describe the presentation of an extradural haemorrhage- Brief duration of unconsciousness and then a lucid recovery period
- Progressive hemiparesis and stupor develops due to transtentorial coning
- First there is ipsilateral dilated pupil then bilateral fixed dilated pupil
- Untreated, there is hemiplegia and respiratory arrest - 63Outline investigations and management of an extradural haemorrhage- Ix: CT (shows characteristic lentiform shape + midline shift/ventricle compression as it enlarges)
- Mx: Urgent neurosurgical referral, burr hole to release pressure (v. good prognosis if done early), can be treated conservatively with regular monitoring if very minor
Información
- Descripción
- (Neurology) Medicine Fichas sobre Stroke, creado por Liam Musselbrook el 10/11/2017.
- Creado por
- Liam Musselbrook
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