CVA Flashcards
1
Q
How many types of stroke are there
A
Ischaemic and Haemorrhagic (TIA falls under ischaemic)
2
Q
What are the causes of ischaemic stroke
A
- Thrombotic (atherosclerosis plaque, clot from large vessel like MCA/PCA/ACA, clot from small vessel like lacunar infarct)
- Embolic (carotid plaque, Afib, atherosclerotic plaque)
3
Q
What are the causes for haemorrhagic stroke
A
- Intracerebral (hypertension and thrombolytic drugs)
- Subarachnoid (aneurysm rupture/berry’s aneurysm)
4
Q
What are the indications for CLC
A
- Hypoxia
- Metabolic imbalance (e.g. hypoglycaemia)
- Falls/Trauma to head
- Unresponsiveness
- Neurological disease processes (e.g. stroke, brain tumour)
- Epilepsy
- New admission (to form baseline assessment)
5
Q
Which kind of stroke is CLC mainly used for
A
Haemorrhagic stroke
6
Q
What does CLC measure
A
GCS, VS, Pupil size reaction and accomodation to light, Motor strength
7
Q
What are the score ranges and GCS and what do they mean
A
Mild brain injury: 13-15
Moderate brain injury: 9-12
Severe brain injury: 3-8
8
Q
At what score of the GCS do you need to prepare to secure airway
A
Less than or equals to 8
9
Q
What are the ways to inflict pain on patient to test on their best verbal response
A
- Peripheral stimuli
- put pressure on lateral inner side of the 3/4th finger
- Central stimuli
I) Trapezius squeeze (for spinal cord injury >T4)
II) Pressure on supra-orbital notch/ridge (for spinal cord injury >C5)
10
Q
What are the scores available for best motor response
A
6: obeys command
5: localise pain, moving limb to attempt to remove painful stimuli
- removing pain from peripheral stimulus: either withdraw hand or use another hand to remove stimuli
- removing pain from central stimulus: hand reaches towards painful stimuli and try to remove it
4: flexion to pain, withdraw from stimuli (arms bend but wrist is straight)
3: abnormal flexion/decortication (inward rotation of wrist/flexion of arm/wrist but extension of legs to pain) *injury to midbrain
2: extension to pain/decerebration (extend upper and lower limbs to pain) *injury to brain stem
1: none
11
Q
What are the functions of frontal lobe
A
Movement, intelligence, behaviour, memory
12
Q
What are the functions of parietal lobe
A
Intelligence, language, sensation, reading
13
Q
What are the functions of temporal lobe
A
Speech, behaviour, memory, hearing, vision
14
Q
What are the functions of brain stem
A
Breathing, blood pressure, heartbeat, swallowing and consciousness
15
Q
What are the functions of cerebellum
A
Balance and coordination
16
Q
What are the functions of occipital lobe
A
Vision
17
Q
What are the 3 principles of acute ischaemic stroke
A
- Achieve timely recanalisation of occluded artery and reperfusion of ischaemic tissue
- Optimise collateral flow
- Avoid secondary brain injury
18
Q
How low should bp be maintained pre tPA?
A
<185/110mmHg
19
Q
How low should bp be maintained pre tPA?
A
<185/110mmHg
20
Q
How low should bp be post tPA?
A
<180/105mmHg
21
Q
When should bp be lowered in patients not undergoing tPA?
A
- When bp is >220/120mmHg
- When pt has a hx of ACS, HF, aortic dissection, hypertensive encephalopathy and acute renal failure
22
Q
When should patients not undergo tPA
A
- When pt has a malignant cerebral infarct (symptoms for >4hr)
- When pt have signs of haemorrhage/is haemorrhagic/risk of haemorrhage
23
Q
What are the inclusion criteria for patients to undergo tPA
A
- > /= 18y
- Time from last well seen (<4.5hrs)
- Ischaemic stroke with significant neurological deficit (NIHSS > 4)
24
Q
What are the other alternative treatment for patients who can’t undergo tPA?
A
- Antiplatelet/anticoagulation therapy (aspirin/warfarin)
- Warfarin anticoagulant for short term (3mths) before changing to antiplatelet
- Heparin anticoagulant
- Factor Xa (rivaroxaban, apixaban, edoxaban); direct thrombin inhibitor (dabigatran)
- Endovascular therapy (angioplasty/stent)
25
What is the surgical treatment for ischaemic stroke
Thrombectomy
26
What are the preventive measures for recurrent ischaemic strtoke
1. Antiplatelet/anticoagulant
2. Carotid endarterectomy
3. Endovascular angioplasty/stent
27
What investigation results shd be tested for ischaemic stroke
1. FBC
2. PT/aPTT
3. D-dimer (TRO DVT/thrombus)
4. Fibrinogen
5. BNP (signify cardiac failure)
6. TSH (TRO hyperthyroidism which can cause AFib)
28
When is Endovascular therapy done
1. For symptoms lasting >6hrs
2. Large vessel obstruction
3. NIHSS >/= 6hrs
29
How to care for pt post EVT
1. Groin puncture site
a) monitor for bleeding, swelling, haematoma and pain. (Inform dr immediately)
b) keep leg straight and CRIB for 6hrs
2. Monitor for retroperitoneal haematomia (hypotension & flank pain)
3. Monitor for arterial occlusion (leg paraesthesia, pallor, pain, pulseless, cold - do neurovascular assessment for cap refill, pulse etc)
30
What are the benefits of stroke patients staying in acute stroke unit?
More likely to be alive, independent and living at home one year after
31
What are the complications of tPA?
1. Symptomatic intracerebral/intracranial haemorrhage
2. Asymptomatic intracerebral/intracranial haemorrhage
3. Systemic bleeding
4. Other bleeding complications (minor to severe - e.g. clot dissolve but blood vessels start to leak)
5. Angioedema
6. Transient hypotension
32
What are the complications of ischaemic stroke?
1. Cerebral oedema
2. Post-stroke seizure
3. Pneumonia
4. UTI
5. Post-stroke depression
6. Pressure ulcers/bedsores
7. Limb contractures/shortened muscles from decreased movement in affected area
8. Shoulder pain
9. DVT/VTE/blood clot in body (typical legs)
10. Aphasia (difficulty speaking/unds speech)
11. Hemiparesis
12. Hemisensory deficit
13. Muscle spasticity (muscle tightening due to prolonged muscle contraction)
14. Shoulder subluxation (partial shoulder instability)
15. Haemorrhagic transformation (petechial/mutlifocal OR secondary haematoma)
33
How to care for a TIA patient with new stroke symptoms
1. Monitor GCS/NIHSS score regularly
2. Inform medical team
3. KIV hyper acute reperfusion stroke tx (tPA/EVT)
*if patient have new stroke within hyperacute timing, to see if patient is eligible for stroke tx
34
How to care for a ischaemic stroke patient with haemorrhagic transformation
1. Monitor GCS/NIHSS closely and regularly
2. Elevate HOB
3. Inform medical team if
a) decreased GCS/increased NIHSS
b) new pupil changes
c) severe headache
d) N&V
35
How to care for a patient with malignant MCA/cerebellar infarct?
1. Close monitoring for signs of neurological deterioration
2. Osmotic therapy, hyperventilation (for oedema/swelling)
3. Refer to neurosurgeon for decompressive craniotomy (give space for brain to swell)
36
How to care for an stroke patient with seizure
1. Monitor for stroke activity
2. Provide first aid if seizure occurs
3. Administer antiepileptics
4. Prophylactic antiepileptics (usually not given unless HI)
37
How to care for a stroke patient with dehydration?
1. Administer IV therapy - isotonic saline to increase intravascular vol
(*avoid hypotonic saline as free water will worsen cerebral oedema
*avoid dextrose as hyperglycaemia will worsen o/c)
2. Monitor I/O (& inform Dr if there is a huge -ve)
3. Commence feeding (oral/NGT) if permissible
38
How to manage BP for ischaemic stroke pts
If pt has undergone hyperacute tx
- IV thrombolysis/tPA = <180/105mmHg
- EVT = differing BP depending on patient profile/how successful is the tx
If pt has not undergone hyperacute tx, shd only tx bp if:
- >220/120mmHg for acute ischaemic stroke (permissive HTN up to 220/120mmHg)
*need to cautiously lower bp by 15% within first 24hrs post stroke (lowering bp too fast can cause hypotension)
-> to give slow acting bp meds to prevent prolonged lowering of bp + still can reverse if bp goes down too fast
39
What happens if a stroke patient has fever afterwards?
Having a fever post stroke is associated with increased mortality and morbidity attributed to:
1. Increased cerebral metabolic demand
2. Cellular acidosis
3. Changes in BBB permeability
4. Increase vol in infarcted tissue
*increase temp within 24hrs will cause poor o/c and large cerebral infarct
40
What are the causes of fever in post stroke patients?
1. Infection (aspiration pneumonia/UTI)
2. Cell necrosis
3. Thermoregulatory mechanism of hypothalamus affected post stroke
41
How often should temperature and blood sugar level be monitored?
4hrly
42
What are the causes of hyperglycaemia in post stroke patients
1. Stress hyperglycaemia
2. Increased tissue necrosis
3. Free radical generation with increased oxidation stress
(either produced naturally or accelerated due to a. exposure to toxic chemicals, b. smoking, c. alcohol, d. fried food)
4. Increased BBB permeability
5. Underlying undetected hyperglycaemia (pt nvr check)
43
What is the range of blood sugar level to maintain for post stroke patients
7.8-10mmol/L
44
When and how should blood sugar level be controlled for post stroke patients?
BGL >10mmol/L to be treated with IV insulin (not bolus because it will cause BGL to crash)
45
What is a major risk factor of aspiration pneumonia?
Dysphagia
46
What are the signs of dysphagia?
1. Excessive drooling
2. No attempts to swallow/bolus holding
3. Multiple swallows for each mouthful
4. Coughing
5. Choking
6. Throat clearing for more than once
7. Breathless/turning blue post swallowing
8. Wet gurgly voice post swallow when asked to cough
47
How should dysphagia be assessed?
Using bedside assessment/swallowing protocol
48
When should dysphagia assessment be done to be most effective reducing risk of aspiration pneumonia?
Before eating, drinking or receiving oral meds
49
What is another way to prevent aspiration pneumonia for patients with dysphagia?
Intensive oral hygiene protocol
50
How should a stroke patient be prevented from getting pneumonia?
1. Early dysphagia screening & refer to ST for reassessment PRN
2. Good pulmonary care via regular suctioning/chest physio (can do chest physio regularly to clear oropharyngeal secretions)
3. HOB elevation and sit pt out during feeding
4. Advise pt to take influenza and pneumococcal vaccine unless contraindicated
5. Good oral hygiene; freq oral toilet (helps reduce HAP [*aspiration of oropharyngeal secretions is the primary mechanism for development of stroke associated pneumonia])
51
How should a stroke patient be prevented from getting UTI?
1. Avoid IDC to prevent CAUTI (do intermittent catheterisation if needed)
2. Adhere to bladder protocol
3. Remove IDC as soon as possible
4. PVRU screening for all stroke pts
5. Encourage early mobilisation if no contraindication
6. SOOB regularly and encourage voiding in commode/toilet
7. Ensure adequate fluid intake and daily bowel movement + Good perineal hygiene
*ask Dr to give laxative if no BO despite adequate fluid intake - constipation can cause urinary retention and lead to UTI
8. Toilet re-training
9. Monitor for UTI
a) Fever
b) Painful urination
c) Cloudy & smelly urine
d) Pt keep gg to toilet; (x) clear urine
10. Send urine for FEME & culture if suspect UTI - to tx accordingly with abx
52
How to prevent constipation in post-stroke patients?
1. Assess pre-stroke bowel habits
2. Increase mobility
3. Increase fibre intake
4. Prophylactic stool softeners
5. Monitor stool chart - Bristol stool chart
53
What are signs of bowel dysfunction in post stroke patients?
Constipation/Diarrhoea
*spurious diarrhoea can occur if patient have been constipated for too long = keep having diarrhoea (to do abdo xray to assess severity)
54
How to prevent pressure ulcer/bedsore in post-stroke patients?
1. Air mattress
2. Frequent turning
3. Use of wheelchair cushion - refer to OT
4. Use Alleyvn cushion
5. Skin hydration with moisturiser
6. Regular skin assessment (Braden scale)
7. Adequate nutrition
55
How to prevent venous thromboembolism (VTE) - PE & DVT in post-stroke patients?
General measures:
1. Early mobilisation (for those who can - be cautious cos it can cause bleeding if bp is too high)
2. Leg exercises
3. Adequate hydration
+ Mechanical intermittent pneumonic compression/IPC devices (calf pump)
56
Who are at risk of VTE?
1. Immobilised
2. Dehydrated
3. Infection (at risk for/having)
4. Elderly
5. History of malignancy
6. Prev DVT/clotting disorder
57
Is graduated compression stockings useful in VTE prophylaxis in stroke pt?
No
58
How will depression affect post-stroke patients?
It can be severe enough to affect functioning and slow down rehab
59
Where are the common sites for intracerebral haemorrhage?
*usually from small arteries deep in white matter
1. Basal ganglia
2. Thalamus
3. Pons
4. Cerebellum
*bleeding sure may not be identifiable for large haemorrhage (bleeding of major artery)
60
What are the causes of intracerebral haemorrhage?
1. HTN
2. Blood disorders
61
What is the pathophysiology behind intracerebral haemorrhage?
Expanding blood clot dissects & destroys brain tissue
=
Acts like space occupying lesion
=
Increased ICP
(May affect cerebral perfusion = condition deteriorate)
*high ICP in one compartment may displace structures and cause herniation (pressure and vol effect; one of the major fatalities of haemorrhagic stroke)
=
Brain stem compression (with a lot of vital centres)
=
Death (mortality is high in haemorrhage)
62
What is the compensatory mechanism behind increased intracranial pressure?
Brain parenchymal volume takes up about 80% of intracranial volume (1400ml), followed by blood volume and CSF volume which both takes up abt 10% (150ml) each.
With an intracranial pathology (tumour/haemorrhage), this cause an
- increase in CSF drainage via ventricular system
which leads to an
- increase in venous drainage via dural venous sinuses
With increasing size of intracranial pathology, there will be no further compensatory mechanisms, resulting in a rise of intracranial pressure
63
What are the signs and symptoms of intracranial haemorrhage?
Often associated with sever headache & vomiting
+
Seizures are common
*usually occurs while patient is awake/exerting - sudden onset within minutes
*ss usually depend on
a) site of bleed
b) site of extravasation of blood
64
How many types of ruptures are in intracranial haemorrhage?
2 (small and major)
65
What symptom do small rupture cause?
Leaking of blood into subarachnoid space leading to headache
66
What symptoms can major rupture cause?
LOC -> severe headache & severe exertion
*usually without focal deficits (no nerve, spinal cord/brain problem)
67
What are the complications of major rupture?
1. Vasospasm (presence of blood may irritate one or more arteries causing vasospasm and ischaemia within 1-2wks)
2. Hydrocephalus (blockage of reabsorption of CSF with blood clots outside vessel from haemorrhage can result in hydrocephalus and increase in ICP)
3. Re-rupture (chances are higher in another part of the same blood vessels)
68
How does HTN precipitate haemorrhagic stroke?
1. Vessel weakening and rupture
- chronic HTN can exert constant pressure on blood vessel walls, causing them to weaken over time
- this increases the risk of rupture and hence increase the risk of haemorrhagic stroke
2. Aneurysm formation
3. Microbleed and microangiography
- HTN can cause microbleeds and damage to blood vessels in brain (microangiography) leading to an increase risk of haemorrhagic stroke
4. BBB breakdown
- chronic HTN can disrupt integrity of BBB = easier for blood to leak into brain tissue if vessel is damaged
69
What is the cause of epidural haemorrhage?
Head trauma causing skull fracture (blunt trauma) and laceration of arterial vessels (most commonly meningeal artery)
*more tremendous force is required than subdural haemorrhage
70
What are the SS of epidural haemorrhage?
Triphasic presentation:
Brief LOC -> lucid interval -> headache + progressive obtundation (altered LOC) + hemiparesis (contralateral)
*blown pupil (ipsilateral) secondary to uncal herniation
71
What is the cause of subdural haemorrhage?
Head trauma leading to rupture of bulging veins (*elderly/alcoholics/pt on anticoagulation meds are more susceptible & can occur with minor head trauma)
72
What are the SS of subdural haemorrhage?
*non-specific clinical signs (e.g sleep a lot/behavioural change)
1. Headache
2. AMS
3. Hemiparesis
4. Non-convulsive seizures (may occur in 20% of SDH pts)
*can be subacute/chronic
*gradual change in mental status may present as delirium/dementia in elderly - need to do hx taking
73
What are the causes of intraparenchymal haemorrhage?
Damaged blood vessels due to:
1. HTN
2. Head trauma
3. Cerebral amyloid angiopathy
4. Ruptured aneurysm
5. Blocked vessels (atherosclerosis)
74
What are the presentation of intraparenchymal haemorrhage?
Fast & headache
*SS depend on location affected
75
What does ganglionic haemorrhage cause?
Contralateral hemiparesis which worsens to drowsiness & coma
76
What happens in thalamic haemorrhage?
Contralateral hemiplegia with involvement of 3rd nerve
77
Why is there changes in personality for thalamic bleed?
1. Impact on emotion regulation
- thalamus plays a key role in processing and relaying sensory information to cerebral cortex
- incl areas involved in emotion & behaviour
- bleed = disrupt pathway = altered emotional regulation & personality traits
2. Connection to limbic system
- thalamus is closely connected to limbic system responsible for emotions, mood and behaviour
- damage = mood swings, irritability/other changes in personality
3. Cognitive & executive functioning
- thalamus is involved in cognitive functions (attention, memory & decision making)
- haemorrhage = impair function = change in thinking, responding & interactions
4. Effect on frontal lobe connections
*thalamus has connection to frontal lobe
- crucial for higher order functions (planning, judgement and social behaviour)
- distribution of these connections = disinhibition, impulsivity & changes in social behaviour - perceived as changes in personality)
78
What does pontine haemorrhage cause?
Paraplegia, pinpoint pupils, death
79
What does cerebellar haemorrhage cause?
Ataxia, altered sensorium, death
80
What are the causes of SAH?
1. Arterial causes
a) rupture of saccular/berry aneurysm
b) rupture of arteriovenous malformation (AVM)
2. Venous in nature - trauma/RTA/TBI
81
What are the risk factors for aneurysm rupture?
1. Tobacco use
2. Alcohol abuse
3. HTN caused by cocaine & other stimulants
4. Large aneurysm size
82
What are the SS of SAH?
1. Sudden onset of worst headache ever experienced/thunderclap headache (esp aneurysmal SAH)
2. Vomiting
3. May/May not LOC
4. Commonly no focal neurological deficits
5. Oedema & mass effect can result
6. N&V
7. Truncal ataxia
8. Vertigo
9. Dysarthria (unclear articulation of speech)
10. Neck pain/nuchal rigidity
11. AMS
*mainly associated with activities
83
What are the mgt for haemorrhagic stroke?
1. Stop antiplatelet & anticoagulation
2. BP mgt (target SBP <140mmHg)
- ICH = SBP <160/>120mmHg
- SAH = MAP <130/>80mmHg
*initiate tx within 2hrs of ICH symptom onset and reach target within 1hr
*lowering SBP to 140mmHg is safe and may improve functional o/c in pt with mild to mod ICH and SBP <220mmHg
*lowering SBP to <130mmHg in pt with ICH & increased bp/mild ICH = potentially harmful and shd be avoided
3. Monitor neurological condition
4. Control ICP (CPP [>60] = MAP - ICP; ICP is managed by maintaining CPP)
**- Controlling MAP**
*a) Normovolemia*
I) Administer IV N/S 0.9%
II) Monitor for f & e (CVP, blood electrolytes, I/O [ensure no overload/dehydration], BGL [6-10mmol/L; increase BGL from stress = decreased hydration)
*b) Maintain BP (within 140-160mmHg)*
I) Monitor BP to prevent hypotension
II) Administer antihypertensives
**- Controlling ICP**
*a) CSF drainage by EVD*
*b) Decompressive craniectomy*
> for patients who need brain to swell up to decrease ICP (*don’t do unnecessarily)
I) Ischaemic stroke
II) Malignant MCA/bad stroke
III) SAH
IV) Hydrocephalus
> life saving measure; decreases mortality but have no significant benefit in functional o/c - pt will not return to premorbid state
*c) Osmotic therapy*
> Administer hyperosmolar fluid/osmotic diuretic (IV mannitol 20%)
~ achieve plasma osmolarity to draw water out of brain and reduce swelling
*monitor renal function to ensure kidney is normal/due to withdrawing fluid
~ monitor for AE (f&e imbalance)
I) HypoNa (mannitol get excreted out too fast)
II) Hypotension
III) PE (fluid move out too fast)
IV) CHF
~ monitor serum osmolarity (<320mm osm)
*d) Facilitate venous drainage*
I) HOB 30
II) Neck and head in neutral position
III) Knees straight
**- Controlling CPP**
*a) Control cerebral perfusion*
I) decrease brain need for oxygen and glucose = sedate pt adequately
II) administer, titrate and monitor SE of sedative, analgesic, neuromuscular blocker agents, prophylactic antiepileptics & abx
III) avoid cluster of activities
IV) ensure rest period btwn procedures
V) maintain normothermia (increase tempt = increase cerebral metabolism)
~ control fever with antipyretics and prevent HAI (VAP, CAUTI, CLABSI)
*b) Ventilation & oxygenation*
I) keep clear airway (*hyperoxygenate before suctioning)
II) monitor ventilator setting, blood ABG, SpO2
III) hyperventilate & keep PCO2 25-30mmHg temporarily (too long = decrease perfusion to brain)
~ decrease CO2 lead to decreased blood flow, bp and eventually ICP
~ increase RR on ventilator settings to increase exhalation of CO2
84
What symptoms will be caused if stroke is due to clot in anterior cerebral artery?
Anterior cerebral artery supplies blood flow to medial aspect of frontal lobe
1. Contralateral hemiparesis
2. Contralateral sensory loss
3. Aphasia
4. Urinary incontinence (bilateral lesions)
5. Confusion
6. Disorientation
7. Apraxia
8. Aphasia
9. Contralateral paralysis and sensory loss in opposite leg
*deep branch will be ok cos of collateral flow
85
What symptoms will be seen if stroke is caused by a clot in the middle cerebral artery?
Middle cerebral artery supplies to most lateral aspect of cerebral hemisphere, internal capsule and basal ganglia
1. Contralateral hemiplegia
2. Contralateral sensory loss
3. Aphasia
4. Homonygous hemianopsia
5. Neglect syndrome
6. Face and hand paralysis
7. Conjugate gaze paralysis
8. Motor aphasia
9. Conductive aphasia
10. Sensory aphasia (wernike aphasia)
11. Conductive apraxia
12. Dressing apraxia
13. Contralateral paralysis
86
What symptoms will be seen if a stroke is caused by clot in vertebral-basilar territory?
Vertibro-basilar territory supplies blood to thalamus, brainstem and cerebellum
1. Sensory loss
2. Mild hemiparesis
3. Disturbances in gait, speech, swallowing and vision
4. Cerebellar symptoms (ataxia, intentional tremor, in-coordination)
5. Brain lesion symptoms (Contralateral paralysis and sensory loss)
87
What is the symptoms seen if stroke is caused by posterior cerebral artery?
Posterior cerebral artery supplies blood to occipital and medial aspect of temporal lobe
1. Vision deficits (homonygous central blindness, colour blindness)
2. Memory impairment
3. Vision loss
4. Memory loss
5. Agraphia
6. Thalamic syndrome (sensation of tempt affected - burning/tingling pain)
88
What are the early signs of increased ICP?
1. Headache
2. N & V
3. Confusion
4. Irritability
5. Restlessness
6. Photophobia
7. Diplopia
89
What are the late signs of increased ICP?
1. Deterioration in LOC/Decreased GCS
2. Changes in pupil size, shape and responsiveness to light (papilloedema/dilated pupils)
3. Cushing reflex (to tell Dr cos need to do scan)
a) increased SBP
b) widened pulse pressure
c) Bradycardia
d) irregular respi
4. Decorticate/decerebrate posturing
5. Flaccid (end stage)
90
What are the indications for EVD?
1. Hydrocephalus
2. Relieving/monitoring increased ICP in SAH/ICH pts (occurs due to impaired absorption of CSF)
3. Drain infected/blood stained CSF following infection (bacterial meningitis)/neurosurgery
4. Administer medications (abx and thrombolytics) for pts with CSF infection/significant intraventricular clot volume
91
What are the contraindications for EVD?
1. Pts on anticoagulants/hx of coagulation disorders
2. Pt with scalp/brain infections
92
Which stopcock can nurses touch?
Main system and drip chamber stopcock
93
What to look out for when patient is on EVD?
Monitor their conscious level and VS
1. Check for lethargy, restlessness, paleness, level of interaction, posture and movement
2. Check GCS
3. Pupil size, shape and reaction to light
- dilated pupil = midbrain compression
- one pupil dilated and unreactive = ipsilateral brainstem compression/uncal herniation due to temporal lobe bleed
4. Movement of all limbs and document any diff
5. VS showing late sign of brain deterioration
- increased bp = increased ICP
- tempt changes = dysfunction of hypothalamus/brain
- respi pattern is a clear indication of brain functioning
- pulse raises temporarily as a compensatory mechanism (slow down when ICP increases)
94
How does CSF get drained into EVD
When intraventricular pressure exceeds height of collection drip chamber height (the lower the height = the more the drainage -> gravity concept)
95
When does flow of CSF stop?
When pressure in CSF compartment of brain equalises with collection chamber
96
Why do you need to document prescribed pressure level and check collection chamber frequently?
To ensure pressure level is not too high (lead to under drainage of CSF) or too low (lead to over drainage of CSF)
97
How to care for EVD?
1. Ensure EVD chamber is facing foot of bed
2. Check and observe at frequent intervals for drainage tube for
a) patency (EVD column oscillation/CSF moving through tubing, ICP waveform, CSF drainage/vol lvl)
b) free from kinks
c) traction
d) leaks
*coil EVD to prevent dislodgement and blockage
3. Ensure prescribed height is maintained at all times
4. All connections must be tight to maintain close system
5. Touching of EVD components must be aseptic (sterile surgical gloves)
*handling of EVD shd be kept to a minimum
98
How to do dressing for EVD?
1. Check for redness/swelling
2. To maintain aseptic technique when changing dressing
3. Check EVD dressing at least once per shift - change with wet/soiled
4. Ensure tubing is free from traction
5. Document in notes
99
What is the normal rate of CSF drainage in EVD?
25ml/hr
100
What does increase drainage of CSF mean?
Overdrainage/Intracranial HTN
Ventricles will collapse -> pull tissue away from brain -> vessel tear -> subdural haemorrhage/haematoma -> change in pressure gradient -> herniation
*herniation is the abnormal displacement of brain tissue from one component of skull to the other
101
What does under drainage of CSF lead to?
Increased ICP/herniation then eventually complications of increased ICP
102
When should you change the drainage bag of EVD?
When it’s 3/4 full
103
What is the normal finding of CSF?
Clear and colourless
104
What are examples of abnormal CSF findings?
1. Xanthochromia discoloured
- pale yellow/straw coloured
- from RBC breakdown from prev bleeding
2. Slightly blood tinged
3. Moderate blood tinged
4. Heavily blood tinged
5. Turbid/cloudy
- from CNS infection (meningitis)
6. Bright red
- acute haemorrhage/aneurysm bleeding
105
When should you report to Dr for EVD drainage?
1. When there’s no CSF drainage
2. When there’s a leak from EVD insertion
3. When CSF drainage is more than 30ml/hr
4. When there’s blood clot/debris/change in CSF colour
106
What happens if intraventricular pressure is raised?
It will lead to an overdrainage of CSF
107
How to prevent increased/decreased drainage of intraventricular pressure?
1. Maintain regular bowel habits using stool softeners (straining will lead to increased ICP)
2. Take precaution before doing anything that cause patient movement (e.g walking, sudden bed position changes, coughing, suctioning)
- turn off collection chamber briefly during such activities
3. Utilise “lock out” bed controls to avoid bed position changes/place do not adjust bed signage
4. Gentle and calm nursing approach
5. Dim and quiet environment
6. Sedate agitated patient if needed
108
What to look out for when transporting patient with EVD?
1. Maintain it at upright position, air vent of EVD system to be maintained dry at all times
2. Empty drip chamber to drainage bag before procedure (CT/MRI)/in situations where EVD needs to be placed down
3. Do not clamp EVD during transportation
4. Clamp/turn off patient stopcock to stop drainage before transferring from one area to another (turn on after adjusting EVD at prescribed level)
109
What are some patient education to give pt with EVD and their family?
1. Purpose of EVD
2. Maintain head and neck and bed position
3. Control external stimuli (noise, light, approach)
4. No touching of EVD and its components (will cause infection)
5. Mittens/restrainers may be used
6. To inform if any signs of increased ICP
110
What are the evaluations and documentations to be done for EVD?
1. Hourly drainage of CSF in drip chamber
2. Progressive total drainage in 24hr period
3. Patency of drainage system
4. Dressing dry and intact
5. Height of drip chamber in cmH20
6. EVD levelled to tragus of ear
7. Symptoms of increased ICP
111
What are the two types of drainage in EVD?
Ventricular and lumbar
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What is CSF drainage dependent on?
1. Gravity (impt to prevent over/under drainage of CSF)
I) height of EVD placement relative to tragus of ear
II) EVD drainage set at prescribed level
2. Intracerebral pressure
113
What to note before using EVD?
Prime EVD lines and stopcocks with N/S 0.9% and ensure they are free from air bubble
114
When will a patient stopcock be closed?
After medication infusion/B4 removal of EVD
115
What can a nurse do with drip chamber?
Sampling of CSF
116
What is attached to system main stopcock and why?
Transducer to measure ICP in ICU
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What are the complications from EVD?
1. Mechanical complications
- dislodgement and blockage
2. Infective complications
- ventriculitis and meningitis
3. Under drainage of CSF
- Increased ICP/herniation/brain damage
4. Over drainage of CSF
- subdural haemorrhage (due to ventricular collapse)
5. Trauma by EVD insertion
a) parenchymal haemorrhage
b) intraventricular haemorrhage
c) aneurysm rupture
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What are the aims of EVD?
1. Promote healing
2. Prevent harm
119
What are signs of over/under drainage of CSF?
1. Headache
2. New weakness in any limb
3. Decreased GCS/CLC score
4. Changes in pupil size & equality
5. Vision changes (double/blurred vision)
6. Papilloedema
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How many months after stroke will it have the highest recurrence of stroke?
1 month
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What are some activities/conditions to avoid 1 month post stroke?
1. Air travel
2. Strenuous exercise
3. Insomnia
4. Dehydration
5. Driving
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How early should rehab start for post stroke patients?
24hrs post stroke
