Approach to stroke Flashcards
What are the stroke mimickers and how to rule them out?
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
What are the investigations to be performed for stroke patients?
- CBG for hypoglycaemia
- ECG for A Fib
- FBC, Renal Panel, PT/PTT coagulation profile
- Non-Contrast CT Brain
- USS Carotids
What is the acute management of haemorrhagic stroke?
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
What is the acute management of ischemic stroke?
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
What is the chronic management of stroke?
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
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
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
What is the ABCD2 scores to risk stratify TIA?
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
[Cortical] What are the symptoms if there is a stroke at the frontal lobe?
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
[Cortical] What are the symptoms if there is a stroke at the parietal lobe?
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
[Cortical] What are the symptoms if there is a stroke at the temporal lobe?
Dominant Lobe (Wernicke’s = superior temporal gyrus): receptive aphasia - Patient may make fully formed words but talk gibberish
Both: contralateral superior quadrantanopia
[Cortical] What are the symptoms if there is a stroke at the occipital lobe?
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)
[Subcortical] What are the symptoms if there is a stroke at the basal ganglia/ thalamus acutely ?
Posterior limb of internal capsule = contralateral hemiparesis
Ventral thalamus = contralateral sensory loss
Pons = ataxia
[Brainstem] Whans happens if CN5 is damaged?
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
[Brainstem] What happens if CN6 is damaged?
I/L weakness in abduction of eye; w/ medial deviation
[Brainstem] What happens if CN7 is damaged?
I/L facial weakness
[Brainstem] What happens if CN8 is damaged?
I/L deafness
[Brainstem] What happens if CN9 is damaged?
I/L loss of pharyngeal sensation / gag reflex
[Brainstem] What happens if CN10 is damaged?
I/L palatal weakness w/ deviation AWAY from side of lesion
[Brainstem] What happens if CN11 is damaged?
I/L weakness of SCM and Trapezius
[Brainstem] What happens if CN12 is damaged?
I/L weakness of the tongue w/ deviation TOWARDS side of lesion
[Brainstem] What are the 4 medial tracts starting with ‘M’?
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
[Brainstem] What are the 4 lateral tracts starting with ‘S’?
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
[Brainstem] What are the 3 loops of cerebellum?
- Vestibular loop: equilibiurm and oculomotor control
- Spinal loop: tone posture gait
- Cortical loop: coordination of articulation, fine movements
[Brainstem] What are the clinical features of someone who has a damaged cerebellum?
Dysmetria/ Dysdiadochokinesia, ataxia, nystagmus, intention tremor, slurred / Staccato speech, hypotonia
[Brainstem] How does lateral pontine syndrome present?
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
[Brainstem] How does lateral medullary syndrome present?
LMS damages:
- Spinothalamic Tract,
- Spinocerebellar Tract,
- Sympathetic Trunk,
- Sensory nuclei (CN5) + CN9, 10, 11
[Brainstem] How does medial medullary syndrome present?
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
What is pyramidal pattern of weakness?
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”
What is a hemiplegia/ circumduction gait?
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
[Brainstem] What is the gait like in a patient with cerebellar damange?
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
What is the parkinson gait like?
- Reduced arm swing
- Turning in steps
- Shuffling Gait
What is the stomping/ stamping gait or sensory gait?
- 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
What is diplegic gait?
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
What is trendeleburg gait?
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
What is a neuropathic/ high steppage gait?
- 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
What features would suggest a thrombotic ischemic stroke?
- 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
What features would suggest an embolic ischemic stroke?
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
What features would suggest a haemorrhagic stroke?
History of coagulopathy, trauma
Signs of ↑ ICP on examination: drowsy, N&V, papilledema, headache
How does an old stroke present on DWI, ADC, T2?
bright in DWI, ADC, T2
How does a new stroke present on DWI, ADC, T2?
bright in DWI, dark in ADC
What is the presentation of subarachnoid haemorrhage?
- Hyper-acute presentation: thunderclap headache with ensuing deficits
- Meningism (nausea & vomiting, nuchal rigidity), back pain/bilateral leg pain (presents later), photophobia/visual changes, LOC
How does intracerebral haemorrhage present?
- Charcot-Bouchard aneurysms (longstanding uncontrolled HTN)
- Progresses for hours/day
- Altered mental status, nausea & vomiting, headache, focal neurological symptoms
Pure motor lacunar syndrome
- Site of lesion
- Clinical features
- Exclude if?
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
Pure sensory lacunar syndrome
- Site of lesion
- Clinical features
- Exclude if?
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
Sensorimotor lacunar syndrome
- Site of lesion
- Clinical features
- Exclude if?
Lesion in: Thalamus,
Posterior limb of internal capsule
Clinical features: Contralateral hemiparesis & contralateral sensory loss (equal brachio-crural distribution)
Exclude if: Crossed signs
Ataxic hemiparesis lacunar syndrome
- Site of lesion
- Clinical features
- Exclude if?
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
Clumsy hand lacunar syndrome
- Site of lesion
- Clinical features
- Exclude if?
Anterior limb of internal capsule, ventral pons
Lesion in: Facial involvement, Sensory loss
Dysarthria and Contralateral UL ataxia (most prominent when writing)
[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
aphasia, agnostic, neglect, apraxia, hemianopia
ataxic hemiparesis & clumsy hand dysarthria
What are the differentials of dysarthria?
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
What are the clinical features of bulbar palsy?
- 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
What are the clinical features of pseudobulbar palsy?
- Speech:
- Emotions:
- Palatal movement:
- Gag reflex:
- Tongue:
- Jaw jerk:
- 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
How can Posterior Circulation Syndrome / Posterior Circulation Infarct (POCI) present?
- 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
What are the syndromes caused if there is a stroke at the Anterior cerebral artery?
- Motor and/or sensory deficit (leg > arm, face usually spared)
- Grasp, sucking reflexes
- Abulia, paratonic rigidity, gait apraxia (inability to plan)
What are the syndromes caused if there is a stroke at the middle cerebral artery in the dominant hemisphere?
- Aphasia (Broca’s + Wernicke’s),
- Motor and sensory deficit (face, arm > leg > foot), may be complete hemiplegia if internal capsule involved
- Homonymous hemianopia
What are the syndromes caused if there is a stroke at the middle cerebral artery in the non dominant hemisphere?
- Neglect,
- Anosognosia,
- Motor and sensory deficit (face, arm > leg > foot),
- Homonymous hemianopia
What are the syndromes caused if there is a stroke at the posteriorcerebral artery in the non dominant hemisphere?
- 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
What are the syndromes caused if there is a stroke at the vertebrobasilar artery (supplies brainstem & cerebellum)?
- 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
What are the syndromes caused if there is a stroke at the internal carotid artery?
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)
What do you need to examine for in a patient with ischemic stroke?
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
What are the 2’ causes to rule out in a young ischemic stroke?
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
What are the investigations required to confirm diagnosis of ischemic stroke?
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
What are the investigations required to determine etiology of ischemic stroke?
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
What are the basic blood investigations required for ischemic stroke?
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 =
What are the contraindications of statins?
decompensated cirrhosis, ALF and worsening obstructive biliary disease
What are the side effects of statins?
rhabdomyolysis, transaminitis, memory impairment
What is the inclusion criteria for thrombolysis with rtPA (alteplase) in HDU?
- 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
What is the exclusion criteria for thrombolysis with rtPA (alteplase) in HDU?
- 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
What is the inclusion criteria for intra-arterial mechanical thrombectomy in HDU?
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)
What is the exclusion criteria for intra-arterial mechanical thrombectomy in HDU?
- 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
What is the management to prevent ischemic stroke progression?
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
What is the management to prevent ischemic stroke complications?
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
Complications of ischemic stroke: Epileptic seizures
- Prevention
- Management
Prevention -> maintain cerebral oxygenation and avoid metabolic disturbance
Management -> AED
Complications of ischemic stroke: Psychiatric, anxiety, depression
- Prevention
- Management
Prevention -> maintain positive attitude and provide information
Management -> anti-depressants
Complications of ischemic stroke: Aspiration pneumonia
- Prevention
- Management
Prevention -> nurse patient semi-erect, avoid aspiration (nil by mouth, nasogastric tube, gastrostomy)
Management -> antibiotics, chest PT, treat fever (hyperthermia can worsen cerebral oedema)
Complications of ischemic stroke: Neurogenic pulmonary oedema (acute pulmonary oedema after CNS insult)
- Pathogenesis
- Prevention
- Management
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
Complications of ischemic stroke: stress ulcer
- Prevention
- Management
Prevention -> PPI
Management -> PPI
Complications of ischemic stroke: UTI
- Prevention
- Management
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
Complications of ischemic stroke: Constipation
- Prevention
- Management
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)
Complications of ischemic stroke: DVT/ PE
- Prevention
- Management
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)
Complications of ischemic stroke: Painful shoulder (subluxation vs frozen shoulder)
- Prevention
- Management
Prevention -> avoid traction injury, shoulder/arm supports, physiotherapy
Management -> physiotherapy, local corticosteroid injections
Complications of ischemic stroke: Pressure ulcers
- Prevention
- Management
Prevention -> frequent turning, monitor pressure areas, avoid urinary damage to skin
Management -> nursing care, pressure-relieving mattresses
What are the is the management to prevent recurrence of ischemic stroke?
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
When is antitherapy monotherapy contraindicated in the prevention of ischemic stroke? Why?
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
When is DAPT indicated for prevention of ischemic stroke?
- 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
What is the history to elicit in a patient with haemorrhagic stroke?
- 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
What is the are the signs to look out for on examination of a patient with haemorrhagic stroke?
Look for focal neurological deficits
Assess for Cushing’s Triad of Hypertension, Bradycardia, Bradypnoea
What are the investigations to conduct for in a patient with haemorrhagic stroke?
- ATLS Protocol if trauma, Cervical Brace
- Non-Contrast CT Scan
- Capillary Blood Glucose
- Lumbar Puncture if subarachnoid if suspected but -ve CT Scan
