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stroke_mx

ED Mx of stroke

patient information sheets

rapid neuro exam to screen for possible acute stroke

  • quick exam for FLAWS (another Dr Gary Ayton acronym)
  • Face and eyes
    • smile, show teeth - symmetry (if this is the ONLY abnormality found consider facial nerve palsy rather than stroke)
    • show both hands low down and ask patient how many fingers (tests lower visual quadrants, hemianopia and neglect)
    • move both hands whilst higher up as ask which hand is moving (tests upper visual quadrants, hemianopia and neglect)
    • if presents with isolated facial weakness, exclude facial nerve palsy / Bell's palsy
    • if presents with vertigo, then consider doing HINTS exam for vertigo and stroke exam:
      • head impulse test
      • nystagmus
      • skew test
  • Legs
    • stand with eyes closed and arms out
  • Arms
    • whilst patient is holding out both arms with eyes closed, touch each hand simultaneously and ask which was touched (tests basic power, sensation and neglect)
  • Walking
    • walk - tests ataxia, gait and basic leg power
  • Speech
    • ask patient to touch nose with little finger (tests for receptive dysphasia and coordination)
    • ask patient to repeat a sentence (tests repetition and expressive dysphasia)

or you can use the silly acronym FAST:

initial considerations in Mx of the stroke patient:

  • Explain to patient and relatives what has happened
  • Consider the kindest level of intervention taking into account:
    • quality of life
    • coexisting conditions
    • prognosis
  • Is there a stroke trial in progress - is pt eligible?
  • Is there a stroke team available to start their Rx and care within the ED, if so do a STROKE CALL ASAP
  • may be eligible for thrombolysis if seen early (must be given within 4.5hrs of onset of stroke) and in appropriate facilities where CT scanning and decision making by a neurologist can be made in a timely manner, if so, go to ED Mx of stroke with possible thrombolytic Rx

resuscitation

  • give oxygen only to maintain SaO2 > 92%
  • ECG, IV line, bloods - FBE, clotting, glucose, U&E
  • if on anticoagulants, IMMEDIATELY REVERSE COAGULOPATHY WITHIN 30min ie. BEFORE CT:
    • if it turns out to be an infarct, reversing the coagulopathy is unlikely to cause harm as it didn't manage to prevent the infarct in the first place anyway

if unconscious:

  • is patient candidate for intubation or is this a terminal event?
  • in general:
    • young patients (<55yrs) are managed aggressively
    • patients 55-75yrs are usually managed aggressively unless they are in a nursing home, or have other substantial premorbid disabilities
    • patients > 75yrs tend to be managed conservatively unless family supports are significant & minimal premorbid disability, or family insistent on resuscitation & need time to adjust to possibility of death within next 24-48hrs.
  • consider lowering intracranial pressure:
    • 500ml 10% glycerol IV over 4hrs daily for 6 days - controversial - 

CT scan ASAP and further supportive measures

  • urgent CT head no contrast
    • within 30-60min of arrival if:
      • coagulopathy (eg. on warfarin)
      • GCS < 13
      • unexplained fluctuating symptoms
      • possible SAH (eg. severe headache at onset)
      • possible meningitis
      • possible thrombolysis candidate - onset within 4.5hrs, etc - see thrombolysis in stroke
      • and patient not for palliative Mx
    • otherwise CT within 24hrs is reasonable
  • analgesia for headache as this will help to reduce acutely elevated BP: eg. panadeine, morphine
  • maintain BP: 
    • maintain MAP < 130 if PH HT - ?labetalol ?nicardipine
    • maintain systolic BP > 90 and < 150
    • maintain cerebral perfusion pressure > 70 (CPP = MAP - ICP)
    • NB. for consideration of thrombolysis, BP must be < 185/110mmHg to qualify
    • if BP > 220/120:
      • avoid ca channel blockers as steal effect
    • if lower BP, do so smoothly to decrease it by no more than 20% to ensure CPP is maintained.
    • lowering BP is debateable, ? do not lower unless:
      • d/w neuro/neurosurgeon as some are keen on lowering BP to prevent further bleeding
      • diastolic consistently > 130mmHg & even then do not lower below 110mmHg diastolic in 1st 48hrs
      • see also: Mx of hypertension in stroke syndromes
  • maintain hydration but do not over-hydrate as risk of cerebral oedema
  • nil by mouth if no gag reflex (& may need PEG tube inserted - usually after assessment by OT)
  • Rx convulsions as per usual
    • 25% pts with ICH have seizures, usually within 1st 72hrs ⇒ phenytoin
  • maintain core temp < 37.5deg C
  • maintain glucose < 10
  • maintain CVP 5-12
  • maintain ICP < 20 - patient position +/- mannitol
  • maintain osmolarity < 310mOsm/L
  • maintain pCO2 30-35.
  • Is there raised intracranial pressure?
    • closely monitor neurologic observations, BP, HR
    • if GCS < 9 and ICH - consider role of ICP monitoring

is it stroke?

  • DDx:
  • Pointers to haemorrhagic stroke rather than infarct:
    • PH hypertension
    • meningism
    • severe headache
    • vomiting
    • tend to progress
    • coma within hours
  • Pointers to ischaemic infarction rather than haemorrhagic stroke:

search for aetiologic factors

  • AF (50% of embolic strokes) ⇒ ECG
  • valvular heart disease
  • ventricular aneurysm post-AMI (mural thrombus)
  • carotid bruit ⇒ carotid doppler as outpatient if TIA?
  • evidence of chronic hypertension - HT retinopathy, cardiomegaly ⇒ CXR
    • NB. acutely elevated BP may be due to stroke
  • temporal arteritis - temporal headaches, raised ESR ⇒ give steroids ASAP
  • thrombocytopenia, coagulopathy, thrombolytic Rx ⇒ FBE, clotting
  • polycythaemia ⇒ FBE
  • SBE
  • migraine
  • metabolic causes (usually not focal neuro. deficits though) - hypoglycaemia ⇒ glucose, U&E
  • severe hypotension - usually systolic BP < 50mmHg
  • ICH:
    • lobar - usually due to amyloid angiopathy - apolipoproteinaemia E4 ⇒ 4x risk of ICH
    • non-lobar - chronic hypertension

determine extent of clinical deficit:

  • 50% of ischaemic strokes are cerebral hemisphere infarcts:
    • contralateral hemiplegia - usually flaccid before it becomes spastic
    • sensory loss
    • homonymous hemianopia
    • dysphasia
  • 25% of ischaemic strokes are lacunar syndromes:
    • small infarcts around basal ganglia, thalamus & pons
    • pt conscious
    • may cause pure motor, pure sensory, mixed sensorimotor or ataxia
  • 25% of ischaemic strokes are brainstem infarcts:
    • wide range of effects including:
      • quadriplegia, disturbances of gaze & vision, locked-in syndrome

Mx if infarct on CT brain

consider thrombolysis

otherwise consider anti-thrombotic Rx

  • no evidence to support heparin or enoxaparin Rx for evolving infarct but consider if AF or risk of DVT
  • consider aspirin or heparin or warfarin if embolic or chronic AF - see AF thromboembolic stroke Mx
  • for infarct or TIA and not starting anticoagulation or thrombolysis:
    • aspirin 300mg o/NGT daily for 14 days at least
    • +/- dipyridamole 200mg o bd (but does give more side effects such as headache)

disposition

  • admit under stroke unit / neurology unit
  • use of a dedicated stroke centre increases likelihood of independent discharge by 6% with NTT = 16 pts

Mx if haemorrhagic stroke on CT brain

  • how big (cm - see scale on film, how many views is it visible in, how many mm between each view)?
  • volume in mls approx. equal to A x B x C / 2 where A,B,C are the 3D linear measurements.
  • NB. bleeds are DYNAMIC and may increase over next few hours
  • ? role of rFactorVIIa:
    • decreases growth of haemorrhage by 50%
    • BUT 5% risk of AMI or secondary ischaemic stroke
  • where is it? - see Interpreting the head CT
  • does it extend into ventricles?
  • are there ventricular casts & if so in which ventricles? (may need evacuation to prevent obstructive hydrocephalus)
  • mass effect with midline shift?
  • if small bleed in cerebrum & pt unconscious then likely that pt actually has an infarct which has become haemorrhagic, as need to involve a large majority of cerebrum for it to cause unconsciousness (unless patient is coning) whereas small bleeds in brain stem, posterior fossa may cause pressure laterally on brainstem resulting in unconsciousness without coning.
  • discuss with neurosurgeon ASAP:
    • may be candidate for urgent surgical evacuation
    • patients not usually suitable for surgery:
      • unlikely to get placement for rehabilitation & be discharged home:
        • age > 75 yrs, particularly if few social supports
        • age > 55 yrs & unlikely to be able to learn eg. speech centres involved
      • site of bleed not readily amenable for Sx:
        • brainstem
        • near posterior limb of internal capsule on LEFT side as must go through speech centres to get to it
        • small bleeds (< 2cm) not causing significant problems may be closely watched
    • STICH Trial 2005:
      • early surgery < 60hrs only likely to be beneficial if:
        • decreased GCS with large volume haemorrhage near the surface with secondary midline shift but no IVH & no hydrocephalus
      • ? role of aspiration of deep lesion

further investigations as suggested by clinical features:

  • echocardiogram - if AF, valvular heart disease or possible mural thrombus post AMI
  • carotid doppler
  • cerebral angiogram
  • clotting screen for ATIII deficiency, protein C or S deficiency, lupus anticoagulant
  • SLE serology
  • syphilis serology

prognosis:

  • overall mortality:
    • 20% at 1 month;
    • 5-10% per year thereafter
    • 40% complete recovery
  • Poor prognostic features:
    • drowsiness
    • head & eye deviation
    • hemiplegia
  • ICH:
    • >60ml bleed with GCS < 9 ⇒ 91% 30 day mortality
    • 30-60ml bleed ⇒ 1% independent living at 30D
    • presence of IVH ⇒ 50% worse prognosis
  • MCA infarct:
    • > 20% mortality; > 70% permanently disabled;
  • lacunar infarct with no aphasia/neglect:
    • 20% have a stuttering course
    • 0% mortality
    • usually reasonable recovery 
stroke_mx.txt · Last modified: 2018/01/23 14:18 (external edit)