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Neuro > Approach to stroke > Flashcards

Approach to stroke Flashcards

1
Q

What are the stroke mimickers and how to rule them out?

A

Hypoglycaemia

  • Palpitations, SOB, Sweating, N&V, Hunger
  • Good to ask: PMH of diabetes, any skipped meals, vigorous exercise

Infection (meningitis, encephalitis)

  • Travel, Contact;
  • Headache, Fever, Photophobia, Phonophobia, Nuchal rigidity, N&V

Todd’s Paresis:

  • Focal weakness in a part of the body after a focal seizure (Hemiplegia post-seizure)
  • Typically, due to a Partial Seizure / Partial w 2’ generalised seizure
  • Usually lasts < 48 hours

Brain tumour : Slow progression of symptoms, constitutional symptoms

Migraine aura (eg: Hemiplegic migraine)

  • Can have focal neurological deficits as prodrome but usually will disappear when headache appears
  • Migraine symptoms = PPPOUNDS = pounding headache, photophobia/ phonophobia, prodromal aura, one day duration, unilateral, N&V, debilitating, serotonin agonists
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2
Q

What are the investigations to be performed for stroke patients?

A
  • CBG for hypoglycaemia
  • ECG for A Fib
  • FBC, Renal Panel, PT/PTT coagulation profile
  • Non-Contrast CT Brain
  • USS Carotids
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3
Q

What is the acute management of haemorrhagic stroke?

A

1) ABCs

2) Reverse Anticoagulation
- Warfarin reversal: IV vitamin K, unactivated prothrombin complex concentrate (also called factor IX complex)
- NOAC reversal (idarucizumab for dabigatran)
- Heparin reversal: protamine sulfate IV infusion

3) Nurse patient at 30 degrees: heads up (improves drainage), neutral neck position (not kinked to the side)
4) Permissive HTN of <160/ 100 mmHg to maintain CPP

5) Permissive Hyperventilation: im for a low PaCO2 for permissive hyperventilation
to allow for VasoC

6) Keep Normothermic (prevent fever): Higher temp will ↑ Edema & ICP, hence we will prevent hyperthermia
Paracetamol, Cold Saline

7) KIV Osmotic Diuretics eg: Mannitol
8) KIV Surgical Decompression
9) Vitals Monitoring and Conscious Level Charting within the Acute Stroke Unit

10) Keep well sedated: reduce brain metabolic load
- Propofol infusion; Fentanyl Infusion; Remifentanil infusion

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4
Q

What is the acute management of ischemic stroke?

A

1) ABCs
2) Acute Management (Thrombolysis VS Thrombectomy VS None)
3) Nurse patient supine
4) Permissive HTN of <220/120 (<180 if post-thrombolysis)
5) High Dose Statin & Aspirin
6) Vitals Monitoring and Conscious Level Charting within the Acute Stroke Unit

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5
Q

What is the chronic management of stroke?

A

Conservative Multidisciplinary approach

  • PT / OT / Rehab to improve function
  • Speech therapist for speech therapy, for swallowing, consider NGT
  • Insert IDC and teach patient how to perform intermittent catheterization
  • DVT prophylaxis w/ early mobilization, PET stockings and SC Clexane
  • Consider psychiatric referral to screen for depression
  • Central CV RF, and manage HTN, HLD, DM
  • Smoking Cessation, Alcohol Cessation
  • Weight Loss, Improve Diet, - Increase Exercise

Medical

  • Most of patients 🡪 antiplatelet monotherapy, lifelong
  • Intracerebral Atherosclerosis 🡪 3/12 DAPT, lifelong monotherapy
  • Mild Stroke / Severe TIA 🡪 3/52 DAPT, lifelong monotherapy
  • Statin therapy

Assess for and treat underlying:

  • AF – start anticoagulation & rate control; drop antiplatelets
  • Carotid Artery Atherosclerosis 🡪 early endarterectomy
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6
Q

ABCD2 Score for TIA – risk assessment tool to predict risk of stroke for first 2- and 7-days following TIA (refer to diagram)

  • 0-3 = low risk -> can _________________
  • 4-5 = moderate risk -> ____________________
  • 6-7 = high risk -> _____________________
  • If high risk (ABCD2 = 6-7), or 2 recent TIAs (especially if in same vascular territory), pts should have urgent Ix and commencement of 2’ prevention
A

go home w/ 3 wk Aspirin & High dose STATINS;

inpatient evaluation + high dose aspirin 300mg loading dose;

inpatient evaluation + high dose aspirin 300mg loading dose

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7
Q

What is the ABCD2 scores to risk stratify TIA?

A 
A: Age > 60 years (1 Point) 
B: Blood pressure >140/80 (1 Point) 
C: Clinical features 
- unilateral weakness = 2 point 
- speech impairment without weakness = 1 point 
D: Duration of sx 
- >60 minutes = 2 points
- 10- 59 minutes = 1 point 
D: diabetes = 1 point
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8
Q

[Cortical] What are the symptoms if there is a stroke at the frontal lobe?

A

Ipsilateral gaze preference (TOWARDS side of lesion)

Dominant lobe (Broca’s = inferior frontal gyrus): expressive aphasia

Unequal brachio-crural weakness (due to human homunculus)

Note: WILL HAVE C/L FACIAL DROOP – Facial droop =/= always CN lesion

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9
Q

[Cortical] What are the symptoms if there is a stroke at the parietal lobe?

A

Both: contralateral inferior quandrantanopia

Both: visual neglect (do line bisection test) and tactile neglect (‘close both eyes and tell me which hand I’m touching’ -> when you touch both sides they won’t feel the neglected side) -> is usually contralateral

Dominant: Gerstmann’s syndrome

  • R-L dissociation
  • Acalculia
  • Agraphia
  • Finger agnosia

Non-dominant:

  • Dressing apraxia
  • Facial agnosia
  • Insight lacking into illness,]
  • Spatial neglect (tested by visual field or sensory – touch or auditory) causing construction apraxia
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10
Q

[Cortical] What are the symptoms if there is a stroke at the temporal lobe?

A 
Dominant Lobe (Wernicke’s = superior temporal gyrus): receptive aphasia
- Patient may make fully formed words but talk gibberish

Both: contralateral superior quadrantanopia

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11
Q

[Cortical] What are the symptoms if there is a stroke at the occipital lobe?

A

Visual field defect: contralateral homonymous hemianopia w macular sparing (MCA + PCA supply part of occipital lobe that represents macula but rest of occipital lobe supplied by PCA only)

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12
Q

[Subcortical] What are the symptoms if there is a stroke at the basal ganglia/ thalamus acutely ?

A

Posterior limb of internal capsule = contralateral hemiparesis

Ventral thalamus = contralateral sensory loss

Pons = ataxia

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13
Q

[Brainstem] Whans happens if CN5 is damaged?

A

I/L loss of pain, temp and touch sensation on the face back as far as the anterior 2/3 of the scalp and sparing the angle of the jaw

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14
Q

[Brainstem] What happens if CN6 is damaged?

A

I/L weakness in abduction of eye; w/ medial deviation

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15
Q

[Brainstem] What happens if CN7 is damaged?

A

I/L facial weakness

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16
Q

[Brainstem] What happens if CN8 is damaged?

A

I/L deafness

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17
Q

[Brainstem] What happens if CN9 is damaged?

A

I/L loss of pharyngeal sensation / gag reflex

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18
Q

[Brainstem] What happens if CN10 is damaged?

A

I/L palatal weakness w/ deviation AWAY from side of lesion

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19
Q

[Brainstem] What happens if CN11 is damaged?

A

I/L weakness of SCM and Trapezius

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20
Q

[Brainstem] What happens if CN12 is damaged?

A

I/L weakness of the tongue w/ deviation TOWARDS side of lesion

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21
Q

[Brainstem] What are the 4 medial tracts starting with ‘M’?

A

Medial Lemniscus: contralateral loss of proprioception and vibration

Motor pathway (corticospinal): contralateral limb weakness

Motor nuclei and nerves: ipsilateral loss of CN 3/4/6/12

Medial Longitudinal Fasciculus (MLF): ipsilateral internuclear ophthalmoplegia

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22
Q

[Brainstem] What are the 4 lateral tracts starting with ‘S’?

A

Spinocerebellar: ipsilateral limb ataxia

Spinothalamic : contralateral loss of pain and temperature

Sensory nucleus of CNV: ipsilateral alteration of pain and temp in the face

Unlike all other sensory nuclei, CN5 nuclei spans across entire brainstem, hence will be affected by lesion at pontine / medullary level

Sympathetic tract: Ipsilateral Horner’s syndrome

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23
Q

[Brainstem] What are the 3 loops of cerebellum?

A
  • Vestibular loop: equilibiurm and oculomotor control
  • Spinal loop: tone posture gait
  • Cortical loop: coordination of articulation, fine movements
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24
Q

[Brainstem] What are the clinical features of someone who has a damaged cerebellum?

A

Dysmetria/ Dysdiadochokinesia, ataxia, nystagmus, intention tremor, slurred / Staccato speech, hypotonia

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25
Q

[Brainstem] How does lateral pontine syndrome present?

A

LPS damages Spinothalamic Tract, Spinocerebellar Tract, Sympathetic Trunk, Sensory nuclei (CN5) + CN7 & CN8 lesion

Hence p/w:

  • Ipsilateral Horner’s
  • Ipsilateral cerebellar ataxia
  • Ipsilateral Loss of sensation over the face
  • Ipsilateral weakness of facial muscles
  • Ipsilateral sensorineural hearing loss
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26
Q

[Brainstem] How does lateral medullary syndrome present?

A

LMS damages:

  • Spinothalamic Tract,
  • Spinocerebellar Tract,
  • Sympathetic Trunk,
  • Sensory nuclei (CN5) + CN9, 10, 11
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27
Q

[Brainstem] How does medial medullary syndrome present?

A

Injury to CN12, MLF, Corticospinal Tract, Medial lemniscus pathway

Presents w/

  • deviation on tongue protrusion towards side of lesion
  • contralateral weakness of the body w/ PYRAMIDAL PATTERN OF WEAKNESS,
  • Ipsilateral Internuclear Opthalmoplegia
  • Loss of light tough sensation on C/L side of body
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28
Q

What is pyramidal pattern of weakness?

A

UL: shoulder adducted to the chest wall, elbow and wrist flexed and fingers adducted together

LL: When walking, the weak leg is extended, with the foot plantar flexed and internally rotated. All this makes the limb “too long”- so the only way to walk is to throw the foot outwards- a “circumductive gait”

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29
Q

What is a hemiplegia/ circumduction gait?

A

In hemiplegia

  • Contralateral Pyramidal pattern of weakness
  • Hence UL Flexor Hypertonia, LL Extensor Hypertonia
  • Associated with distal weakness > proximal weakness 🡪 hence foot drop

Patient thus presents with

  • Flexed arm held close to the body
  • Extended and internally rotated leg + foot drop
  • Walking in a circumducting position
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30
Q

[Brainstem] What is the gait like in a patient with cerebellar damange?

A

Broad based, VERY UNSTABLE gait. This is compared to broad based gait in proximal muscle weakness, where there is less overt imbalance issues

Cerebellar Ataxia is I/L to lesion, and patient tends to fall towards the same side

May be a/w truncal ataxia (causing massive swaying when walking)
- More medial the cerebellar lesion = ↑ truncal ataxia

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31
Q

What is the parkinson gait like?

A
  • Reduced arm swing
  • Turning in steps
  • Shuffling Gait
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32
Q

What is the stomping/ stamping gait or sensory gait?

A
  • Patient STAMPS on the ground with each step
  • A/w loss of proprioception
  • Stamping sends vibration to the trunk to ascertain that contact between foot and floor has been made
  • Seen in peripheral neuropathy eg: Diabetes, VitB12/Folate Def, Syphilis
  • Much more prominent in the DARK when there is LESS VISUAL CUES
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33
Q

What is diplegic gait?

A

Seen in the context of CEREBRAL PALSY

They present with Pyramidal pattern of weakness

  • Arms are barely affected unlike a quadriplegic
  • Legs extended, toes pointed inwards, but with knees bent

They also have lots of ADDUCTOR SPASM

  • This keeps the legs close together
  • Hence they walk with legs CLOSE TOGETHER on TIPTOES
  • If no adductor release surgery is done, may even have a SCISSOR GAIT where leg swings over to opposite side
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34
Q

What is trendeleburg gait?

A

Weakness of the Gluteus medius

Patient p/w

  • When patient steps down on affected side
  • Causes the sagging of the normal, non-weak side
  • i.e. the SOUND SIDE SAGS
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35
Q

What is a neuropathic/ high steppage gait?

A
  • Lifting of the leg very high in order to overcome the foot drop
  • Occurs when there is foot drop, as a result of distal weakness / peripheral neuropathy
36
Q

What features would suggest a thrombotic ischemic stroke?

A
  • History: risk factors (smoking, hypertension, hyperlipidaemia, diabetes)
  • History of TIA in same territory
  • Clots arise at site of occlusion
  • Preceded by warning / milder signs
  • Stuttering course of progressive neurological deficit over several hrs
37
Q

What features would suggest an embolic ischemic stroke?

A

History of VHD e.g. mitral stenosis, prosthetic valves

AF -> consider HTN, rheumatic heart disease, thyroid

Hx of TIA in more than one vascular territory

Onset

  • Sudden in onset
  • Maximal deficits at onset
  • Onset while getting up to pee, coughing/sneezing
38
Q

What features would suggest a haemorrhagic stroke?

A

History of coagulopathy, trauma

Signs of ↑ ICP on examination: drowsy, N&V, papilledema, headache

39
Q

How does an old stroke present on DWI, ADC, T2?

A

bright in DWI, ADC, T2

40
Q

How does a new stroke present on DWI, ADC, T2?

A

bright in DWI, dark in ADC

41
Q

What is the presentation of subarachnoid haemorrhage?

A
  • Hyper-acute presentation: thunderclap headache with ensuing deficits
  • Meningism (nausea & vomiting, nuchal rigidity), back pain/bilateral leg pain (presents later), photophobia/visual changes, LOC
42
Q

How does intracerebral haemorrhage present?

A
  • Charcot-Bouchard aneurysms (longstanding uncontrolled HTN)
  • Progresses for hours/day
  • Altered mental status, nausea & vomiting, headache, focal neurological symptoms
43
Q

Pure motor lacunar syndrome

  • Site of lesion
  • Clinical features
  • Exclude if?
A

Lesion in: Posterior limb of internal capsule (i.e. opp to spinal cord)

Clinical features: Contralateral hemiparesis (equal brachio-crural distribution)

Exclude if: Crossed signs, Sensory loss

44
Q

Pure sensory lacunar syndrome

  • Site of lesion
  • Clinical features
  • Exclude if?
A

Lesion in: Ventral thalamus (i.e. opp to spinal cord)

Clinical features: Contralateral sensory loss (equal brachio-crural distribution)

Exclude if: Crossed signs, Motor involvement

45
Q

Sensorimotor lacunar syndrome

  • Site of lesion
  • Clinical features
  • Exclude if?
A

Lesion in: Thalamus,
Posterior limb of internal capsule

Clinical features: Contralateral hemiparesis & contralateral sensory loss (equal brachio-crural distribution)

Exclude if: Crossed signs

46
Q

Ataxic hemiparesis lacunar syndrome

  • Site of lesion
  • Clinical features
  • Exclude if?
A

Lesion in: Posterior limb of internal capsule, pons

Clinical features

  • Contralateral UL/LL weakness and cerebellar ataxia (equal brachio-crural weakness from hemiparesis)
  • Note: ataxia can actually either be I/L or C/L

Exclude if: Facial involvement, Dysarthria

47
Q

Clumsy hand lacunar syndrome

  • Site of lesion
  • Clinical features
  • Exclude if?
A

Anterior limb of internal capsule, ventral pons

Lesion in: Facial involvement, Sensory loss

Dysarthria and Contralateral UL ataxia (most prominent when writing)

48
Q

[OCSP classification = LACI (Lacunar Circulation Infarct)]

Do not expect: Any cortical signs (e.g. _______, __________, ___________, ___________, __________), brainstem signs or obtundation of sensorium

Lacunar syndromes will have equal loss of sensation /weakness in UL and LL with exceptions being __________ & __________

Monoplegia, stupor, coma, loss of consciousness, and seizures also are typically absent

A

aphasia, agnostic, neglect, apraxia, hemianopia

ataxic hemiparesis & clumsy hand dysarthria

49
Q

What are the differentials of dysarthria?

A

Pseudobulbar (UMN lesion for CN 5/9/10/11/12) -> bulb = medulla

  • bilateral CVAs affecting internal capsule
  • multiple sclerosis
  • motor neuron disease
  • high brainstem tumours
  • head injuries

Bulbar (LMN lesion for CN 5/9/10/11/12)

  • motor neurone disease
  • syringobulbia
  • guillain barre syndrome
  • poliomyelitis
  • subacute meningitis (carcinoma, lymphoma)
  • neurosyphilis
  • brainstem CVA

Extrapyramidal (Parkinson’s)

  • Typical slow, stuttering speech
  • Look for cardinal Parkinsonian features (TRAP)

Cerebellar

  • Staccato, scanning speech
  • Look for cerebellar signs: Dysmetria/ dysdiadochokinesia, ataxia, nystagmus, intention tremor, slurred/ staccato speach, hypotonia
50
Q

What are the clinical features of bulbar palsy?

A
  • Speech- nasal, indistinct (flaccid) dysarthria, lacks modulation and has a nasal twang
  • Emotions: normal
  • Palatal movement- absent
  • Check for other brainstem signs eg. Facial palsy
  • Gag reflex - absent
  • Tongue: wasted, fasciculations, wrinkled, thrown into folds and increasingly motionless
  • Jaw jerk: absent or normal
51
Q

What are the clinical features of pseudobulbar palsy?

  • Speech:
  • Emotions:
  • Palatal movement:
  • Gag reflex:
  • Tongue:
  • Jaw jerk:
A
  • Speech: spastic (monotonous, slurred, high pitched), donald duck dysarthria (the patient is trying to squeeze out words from tight lips
  • Emotions: labile
  • Palatal movement: absent
  • Gag reflex: increased or normal
  • Tongue: spastic (cannot be protruded, lies on the floor of the mouth and is small and tight)
  • Jaw jerk: increased
52
Q

How can Posterior Circulation Syndrome / Posterior Circulation Infarct (POCI) present?

A
  • Cerebellar syndrome
  • Isolated internuclear opthalmoplegia
  • Lateral medullary syndrome (PICA)
  • Lateral Pontine syndrome (AICA)
  • Isolated homonymous hemianopsia w/ macular sparing (occipital lobe)
  • Brain stem syndrome
  • Lock in syndrome
53
Q

What are the syndromes caused if there is a stroke at the Anterior cerebral artery?

A
  • Motor and/or sensory deficit (leg > arm, face usually spared)
  • Grasp, sucking reflexes
  • Abulia, paratonic rigidity, gait apraxia (inability to plan)
54
Q

What are the syndromes caused if there is a stroke at the middle cerebral artery in the dominant hemisphere?

A
  • Aphasia (Broca’s + Wernicke’s),
  • Motor and sensory deficit (face, arm > leg > foot), may be complete hemiplegia if internal capsule involved
  • Homonymous hemianopia
55
Q

What are the syndromes caused if there is a stroke at the middle cerebral artery in the non dominant hemisphere?

A
  • Neglect,
  • Anosognosia,
  • Motor and sensory deficit (face, arm > leg > foot),
  • Homonymous hemianopia
56
Q

What are the syndromes caused if there is a stroke at the posteriorcerebral artery in the non dominant hemisphere?

A
  • Homonymous hemianopia
  • Alexia (problems reading) without agraphia (dominant hemisphere)
  • Visual hallucinations, visual perseverations (calcarine cortex)
  • Sensory loss, choreoathetosis, spontaneous pain (thalamus)
  • CN III palsy, paresis of vertical eye movement, motor deficit (cerebral peduncle, midbrain). Remember that CN3 passes under PCA and above superior cerebellar artery
57
Q

What are the syndromes caused if there is a stroke at the vertebrobasilar artery (supplies brainstem & cerebellum)?

A
  • Crossed signs (CN palsy + contralateral sensory/motor deficit)
  • Diplopia, dizziness, nausea, vomiting, dysarthria, dysphagia, hiccup (lateral medullary syndrome)
  • Limb and gait ataxia (cerebellar sign)
  • Coma (oedema causes compression on brainstem)
  • Bilateral signs suggest basilar artery disease
58
Q

What are the syndromes caused if there is a stroke at the internal carotid artery?

A

Progressive or stuttering onset of MCA syndrome, occasionally ACA syndrome as well if insufficient collateral flow

TACI = 3/3 of

  • Contralateral motor/ sensory deficit
  • Contralateral homonymous hemianopia
  • Higher cortical dysfunction Gerstmann syndrome (R-L dissociation, acalculia, agraphia, finger agnosia) or DISC Face (Dressing apraxia, facial agnosia, insight lacking into illness, spatial neglect causing construction apraxia)
59
Q

What do you need to examine for in a patient with ischemic stroke?

A

Neuro: UL LL + CN + cerebellar + cortical signs (aphasia and neglect for MCA, visual field defects for PCA)

CVS for embolic source: AF, new murmurs

Carotid bruit

Fundoscopy: for papilledema

60
Q

What are the 2’ causes to rule out in a young ischemic stroke?

A

FHx of stroke

Cerebral venous thrombosis: recurrent miscarriages, PMHx of DVT

Vasculitis (not much specific symptoms, so ask general AI things e.g. rash)

Arterial dissections after trauma

Heart problems - “have you been told that you have heart probs”, palpitations, chest pain

  • MS, MR
  • Patent foramen ovale can cause cardioembolic strokes
  • AF!!!

Coagulopathy, illicit drugs e.g. Cocaine

61
Q

What are the investigations required to confirm diagnosis of ischemic stroke?

A

If Urgent: CT brain TRO acute haemorrhage 🡪 in so doing Rules in Ischaemic Stroke

If Non-urgent: MRI brain (more sensitive to infarcts, + demonstrates extent of infarct)

  • For pt presenting BEYOND therapeutic window
  • If MRI done, don’t do CT
  • If CT done, do MRI stroke protocol (FLAIR/DWI to visualize oedema)
  • “Do A Great MRI Test” = DWI (infarct?), ADC (old or new?), GRE/haem (any bleeds?), MRA (any stenosis/occlusion?), T2W (any old infarcts)

Hypocount at bedside -> TRO hypoglycemia/DKA

62
Q

What are the investigations required to determine etiology of ischemic stroke?

A

Evaluate CVRF: BP, fasting lipids, fasting glucose or HBA1c (if known DM)

Cardiac enzymes, ECG – if aetiology is an AMI

If suspected embolic stroke

  • ECG (for AF or IHD) and CXR (cardiomegaly)
  • If no A-Fib picked up: 2D-Echo (for clots, valvular dz) & 24h telemetry x3/7 for paroxysmal AF
  • Consider TFT for RF for AF

If anterior circulation (ACA or MCA territory) stroke, do U/S carotids

Young stroke workup (<55yo)

  • Vasculitis: ANCA, lupus anticoagulant, ASA, ANA
  • Anti-phospholipid syndrome: lupus anticoagulant, anti-cardiolipin, anti B2-glycoprotein
  • Thrombophilia : cardiolipin (more for arterial thrombus), F5 leiden, protein C and S (more for venous thrombosis)
  • ECG, 24h telemetry (for AF / Other arrhythmias)
  • CTA/MRA
63
Q

What are the basic blood investigations required for ischemic stroke?

A

CT Angiogram (if indicated, for thrombectomy!) but do not delay thrombolysis

FBC

  • Hb (anaemia)
  • Plt (thrombocytopenia) -> may affect antiplatelet treatment

PT/APTT if patient on anticoagulants

Renal function (U/E/Cr) to see baseline renal function and need for dose adjustment

LFT for liver function prior to starting statins
- Statin induced hepatitis =

64
Q

What are the contraindications of statins?

A

decompensated cirrhosis, ALF and worsening obstructive biliary disease

65
Q

What are the side effects of statins?

A

rhabdomyolysis, transaminitis, memory impairment

66
Q

What is the inclusion criteria for thrombolysis with rtPA (alteplase) in HDU?

A
  • Clinical diagnosis of ischemic stroke causing measurable neurologic deficit
  • Ability to start Tx within <4.5 hours of onset of S&S
  • Age ≥18 years
67
Q

What is the exclusion criteria for thrombolysis with rtPA (alteplase) in HDU?

A
  • Significant head trauma or previous stroke in last 3 months
  • Symptoms suggest SAH
  • CT demonstrates multilobar infarct (hypodensity >⅓ cerebral hemisphere)
  • Arterial puncture in non-compressible site in last 7 days
  • History of intracranial haemorrhage
  • Intracranial neoplasm, arteriovenous malformation or aneurysm
  • Recent intracranial or intraspinal surgery
  • Elevated blood pressure (systolic > 185 or diastolic > 110 mmHg)
  • Active internal bleeding
  • Acute bleeding diathesis (platelets<100x103, heparin therapy with aPTT greater than normal upper limit, current anticoagulation with INR > 1.7 or PT > 15, or current use of direct thrombin/factor Xa inhibitors)
  • Hypoglycaemia -> blood glucose < 2.7 mmol/L
68
Q

What is the inclusion criteria for intra-arterial mechanical thrombectomy in HDU?

A

ONLY if pt presents within 6-24 hours of stroke symptoms (old guidelines = within 6hrs)

AND stroke is caused by a large artery occlusion in the proximal anterior circulation (i.e. proximal MCA/ACA occlusion 🡪 confirmed on CT angiogram)

69
Q

What is the exclusion criteria for intra-arterial mechanical thrombectomy in HDU?

A
  • Blood pressure > 185/110 mmHg
  • Blood glucose < 2.7 or > 22.2 mmol/L
  • IV treatment with thrombolytic therapy in a dose >0.9 mg/kg alteplase or 90mg
  • Platelet < 40,000 mL or INR > 3.0
70
Q

What is the management to prevent ischemic stroke progression?

A

High Dose Aspirin within 48 hours (always cover with PPIs)

  • Aspirin loading dose 300mg -> 100mg OM to reduce mortality/recurrent stroke
  • If intolerant to aspirin, use clopidogrel (Plavix) 75mg

High dose statin therapy (SPARCL)

  • Reduce LDLs and risk of atherothrombus, also has anti-inflammatory effect
  • Atorvastatin 40-80mg, Simvastatin 20-40mg

Vitals monitoring

GCS / Conscious level charting
- If sudden raised ICP, ?haemorrhagic conversion/ cerebral oedema -> refer neurosurgery

71
Q

What is the management to prevent ischemic stroke complications?

A

Prevent further brain hypoperfusion

  • IV fluids -> maintain fluid status
  • Permissive hypertension for 2 weeks to encourage cerebral perfusion: <220/120 if no revascularisation therapy, <180/105 if post-thrombolysis
  • Transient HTN after stroke lasts ~24h due to dysautoregulation & is an expected phenomenon 🡪 try not to correct in first 24h unless >220/120 (lower by 15% after 48-72 hours)
  • After 72 hours 🡪 BP is expected to drop 🡪 only then control any supra-physiological BP readings
  • Optimise head position (Flat position for ischemic stroke)

Optimise BGL

  • Hyperglycemia may occur even in non-diabetics due to cortisol-mediated stress response -> worsens clinical outcomes due to increased anaerobic metabolism, lactic acidosis, and free radical production
  • Hypoglycemia: neuroglycopenic symptoms may mask neurological symptoms

Assess for dysphagia -> aspiration risk

  • Swallow evaluation, speech therapist input, NG tube + small feeds
  • RF: Low GCS, swallowing impairment from stroke

Miscellaneous

  • UTI: clear bowels, aseptic catheter if needed, PVRU
  • RF: Neurogenic bladder, bed bound
  • DVT: Intermittent Pneumatic Compression -> i.e. calf pumps. Clexane if stroke is not large
  • Bedsores, contractures, subluxation
  • Depression -> give anti-depressants (e.g. SSRI - fluoxetine). RF: stroke itself, loss of function
72
Q

Complications of ischemic stroke: Epileptic seizures

  • Prevention
  • Management
A

Prevention -> maintain cerebral oxygenation and avoid metabolic disturbance

Management -> AED

73
Q

Complications of ischemic stroke: Psychiatric, anxiety, depression

  • Prevention
  • Management
A

Prevention -> maintain positive attitude and provide information

Management -> anti-depressants

74
Q

Complications of ischemic stroke: Aspiration pneumonia

  • Prevention
  • Management
A

Prevention -> nurse patient semi-erect, avoid aspiration (nil by mouth, nasogastric tube, gastrostomy)

Management -> antibiotics, chest PT, treat fever (hyperthermia can worsen cerebral oedema)

75
Q

Complications of ischemic stroke: Neurogenic pulmonary oedema (acute pulmonary oedema after CNS insult)

  • Pathogenesis
  • Prevention
  • Management
A

Pathogenesis = especially abrupt severe rise in ICP -> neuronal compression, ischemia or damage -> increased sympathetic discharge -> catecholamine surge -> increased SVR and decreased left ventricular contractility + alveolar-capillary leakage

Prevention -> monitor SpO2

Management -> supplemental O2 if SpO2 < 94%, diuretics

76
Q

Complications of ischemic stroke: stress ulcer

  • Prevention
  • Management
A

Prevention -> PPI

Management -> PPI

77
Q

Complications of ischemic stroke: UTI

  • Prevention
  • Management
A

Prevention -> avoid catheterisation (use penile sheath if possible), monitor urinary retention via bladder scan to check for post-void retention of urine (PVRU)

Management -> antibiotics

78
Q

Complications of ischemic stroke: Constipation

  • Prevention
  • Management
A

Prevention -> appropriate aperients (anti-constipation drugs) and diet

Management -> appropriate aperients e.g. senna (15-25mg PO), lactulose (15-30ml PO qday), bisacodyl (5-15mg PO qday)

79
Q

Complications of ischemic stroke: DVT/ PE

  • Prevention
  • Management
A

Prevention -> maintain hydration, early mobilization/SOOB, TED stockings, LMWH, intermittent pneumatic compression (C/I in those with overt evidence of leg ischemia -> not to be used in patients who have been immobilised for more than 72h without VTE prophylaxis)

Management -> anticoagulants (exclude haemorrhagic stroke first)

80
Q

Complications of ischemic stroke: Painful shoulder (subluxation vs frozen shoulder)

  • Prevention
  • Management
A

Prevention -> avoid traction injury, shoulder/arm supports, physiotherapy

Management -> physiotherapy, local corticosteroid injections

81
Q

Complications of ischemic stroke: Pressure ulcers

  • Prevention
  • Management
A

Prevention -> frequent turning, monitor pressure areas, avoid urinary damage to skin

Management -> nursing care, pressure-relieving mattresses

82
Q

What are the is the management to prevent recurrence of ischemic stroke?

A

Lifestyle

  • BP: aim 140/90 (SBP <130 if lacunar)
  • Lipids: aim LDL <2.1
  • Reduce Na <1.2g/day
  • Smoking cessation 🡪 MOST SIGNIFICANT RISK REDUCTION (50% at 1Y, baseline by 5Y)
  • HLD: simvastatin 80mg for ALL within 24h unless C/I, aim total cholesterol <4mmol/L. Aim LDL <1.8 (SPARCL trial)
  • DM: consider OHGA/ insulin

Anti-platelet MONO-therapy (C/I if active bleed): lifelong antiplatelet therapy

  • Aspirin loading dose 300mg FOR ALL 24h after thrombolysis (or immediately after if no thrombolysis was given), continue x2/52
  • If DAPT, add clopidogrel loading dose 600mg
  • Start after 24 hours if post-TPA (to allow it to wash out)
  • Start immediately if not post-TPA

Anticoagulation if

  • Anti-coagulation 2 weeks after stroke
  • Warfarin vs NOACs
    1. cardioembolic stroke
    2. AF (stroke in CHADVASC=2 -> anticoagulate)
    3. Stroke recurrence on max DAPT

Carotid stenosis:

  • Carotid endarterectomy if >70% stenosis, good candidates for Sx
  • Carotid angioplasty and stenting if not good Sx candidates
83
Q

When is antitherapy monotherapy contraindicated in the prevention of ischemic stroke? Why?

A

Contraindicated if pt has AF (Cardioembolic stroke)

  • Anti-plt does NOT ↓ risk of Stroke in AF! And yet it ↑ risk of bleed by 1% – hence we do NOT start antiplatelet therapy
  • Instead, aim to start anticoagulation 3-14 days AFTER the stroke!

C/I in active bleed; if large ischaemic stroke, consider holding off for critical period (1wk) in case of haemorrhage conversion

84
Q

When is DAPT indicated for prevention of ischemic stroke?

A
  • Mild Stroke (NIHSS <5) or High-risk TIA 🡪 3/52 DAPT then lifelong monoTx
  • For pt w/ evidence of intracranial atherosclerosis (>50% occlusion of large vessel) 🡪 3/12 DAPT then lifelong monoTx
85
Q

What is the history to elicit in a patient with haemorrhagic stroke?

A
  • Any recent trauma / falls
  • Any anticoagulation / antiplatelet therapy / Blood disorders
  • Any focal neurological Deficits
  • Features of raised ICP: headache, N&V, worse in morning & straining, night-time awakening
  • SAH: thunderclap, worst headache of life, meningism 🡪 may NOT have neuro deficits
  • EDH: lucid interval before falling into unconsciousness, focal neuro deficits, raised ICP
86
Q

What is the are the signs to look out for on examination of a patient with haemorrhagic stroke?

A

Look for focal neurological deficits

Assess for Cushing’s Triad of Hypertension, Bradycardia, Bradypnoea

87
Q

What are the investigations to conduct for in a patient with haemorrhagic stroke?

A
  • ATLS Protocol if trauma, Cervical Brace
  • Non-Contrast CT Scan
  • Capillary Blood Glucose
  • Lumbar Puncture if subarachnoid if suspected but -ve CT Scan

Neuro (13 decks)

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