Emergency Neuro Presentations Flashcards
As the brain and ventricles are enclosed by a rigid skull, they have a limited ability to accommodate additional volume. Additional volume (e.g. haematoma, tumour, excessive CSF) will therefore lead to a rise in intracranial pressure (ICP).
What is normal range for ICP?
7-15 mmHg in adults in the supine position
What is cerebral perfusion pressure?
cerebral perfusion pressure (CPP) is the net pressure gradient causing cerebral blood flow to the brain
CPP = mean arterial pressure - ICP
What causes raised intracranial pressure?
idiopathic intracranial hypertension
traumatic head injuries
infection e.g. meningitis
tumours
hydrocephalus
What features may raised ICP present with?
headache
vomiting
reduced levels of consciousness
papilloedema
Cushing’s triad
What is Cushing’s triad of raised ICP?
widening pulse pressure
bradycardia
irregular breathing
How can raised ICP be investigated?
neuroimaging : CT/MRI
invasive ICP monitoring:
catheter placed into the lateral ventricles of the brain to monitor the pressure
may also be used to take collect CSF samples / drain CSF
a cut-off of > 20 mmHg is often used to determine if further treatment is needed to reduce the ICP
What is the initial management of raised ICP?
investigate and treat the underlying cause
head elevation to 30º
IV mannitol may be used as an osmotic diuretic
controlled hyperventilation
removal of CSF
What is the purpose of controlled hyperventilation in the mx of raised ICP?
aim is to reduce pCO2 → vasoconstriction of the cerebral arteries → reduced ICP
leads to rapid, temporary lowering of ICP
caution needed as may reduce blood flow to already ischaemic parts of the brain
What are the methods for removing excess CSF?
drain from intraventricular monitor
repeated lumbar puncture (e.g. idiopathic intracranial hypertension)
ventriculoperitoneal shunt (for hydrocephalus)
What are the 4 different types of intracranial haemorrhage?
Extradural haemorrhage (bleeding between the skull and dura mater)
Subdural haemorrhage (bleeding between the dura mater and arachnoid mater)
Subarachnoid haemorrhage (bleeding in the subarachnoid space)
Intracerebral haemorrhage (bleeding into brain tissue)
What is a subarachnoid haemorrhage?
bleeding in the subarachnoid space, where the cerebrospinal fluid is located, between the pia mater and the arachnoid membrane
very high mortality (around 30%) and morbidity
may be traumatic or spontaneous
What are the causes of spontaneous subarachnoid haemorrhage?
intracranial aneurysm (saccular ‘berry’ aneurysms): 85% of cases
associated with hypertension, adult PCKD, Ehlers-Danlos and coarctation of the aorta
arteriovenous malformation
pituitary apoplexy
mycotic (infective) aneurysms
In which patient group are subarachnoid haemorrhages more common?
Aged 45 to 70
Women
Black ethnic origin
Give some risk factors for subarachnoid haemorrhage
Family Hx
Hypertension
Smoking and alcohol
Cocaine use
Sickle cell anaemia
Connective tissue disorders (e.g., Marfan syndrome or Ehlers-Danlos syndrome)
Neurofibromatosis
Autosomal dominant polycystic kidney disease
How does subarachnoid haemorrhage typically present?
sudden onset occipital ‘ thunderclap’ headache
often comes on during strenuous activity, such as heavy lifting or sex
nausea and vomiting
meningism (photophobia, neck stiffness)
seizures
coma
ECG changes including ST elevation may be seen
How should a suspected subarachnoid haemorrhage be investigated?
non-contrast CT head is the first-line investigation of choice : blood appears hyperdense/bright on CT
if CT head is done within 6 hours of symptom onset and is normal: do NOT do lumbar puncture
consider an alternative diagnosis
if CT head is done more than 6 hours after symptom onset and is normal: do a lumber puncture (LP) to confirm / exclude diagnosis
SAH seen on CT / confirmed on LP:
CT angiography is used after confirming the diagnosis to locate the source of the bleeding
What findings would you expect on an LP for a patient with SAH?
Raised red cell count (a decreasing red cell count on successive bottles may be due to a traumatic procedure)
Xanthochromia (a yellow colour to the CSF caused by bilirubin)
How can you manage subarachnoid haemorrhage?
bed rest, analgesia
oral nimodipine to prevent vasopasm
discontinuation of antithrombotics (reversal of anticoagulation if present)
intracranial aneurysms require prompt intervention (within 24 hours):
most treated with a coil by interventional neuroradiologists, but a minority require a craniotomy and clipping by a neurosurgeon
What are the complications of aneurysmal SAH?
re-bleeding
hydrocephalus
hyponatraemia
ventriculoperitoneal shunt
vasospasm (also termed delayed cerebral ischaemia)
seizures
What is the risk of rebleeding after aneurysmal SAH?
How should it be managed?
happens in 10% of cases
most common in the first 12 hours
if rebleeding is suspected then a repeat CT should be arranged
associated with a high mortality (up to 70%)
Hydrocephalus refers to increased cerebrospinal fluid, causing expansion of the ventricles.
Treatment options include:
Lumbar puncture
External ventricular drain (a drain inserted into the brain ventricles to drain CSF)
Ventriculoperitoneal (VP) shunt (a catheter connecting the ventricles with the peritoneal cavity)
When does vasopasm most commonly present post SAH?
How should it be managed?
also termed delayed cerebral ischaemia, typically 7-14 days after onset
ensure euvolaemia (normal blood volume)
consider treatment with a vasopressor if symptoms persist (e.g. vasopressin, adrenaline, noradrenaline)
Which are the most important prognostic factors in SAH?
conscious level on admission
age
amount of blood visible on CT head
Meningitis is defined as inflammation of the meninges (lining of the brain and spinal cord).
What are the common causative organisms?
How does it present?
Neisseria meningitidis and Streptococcus pneumoniae
GBS in neonates
Presentation:
fever, neck stiffness, vomiting, headache, photophobia, altered consciousness and seizures
meningococcal septicaemia = non-blanching rash
How may meningitis present differently in neonates?
Neonates and babies can present with very non-specific signs and symptoms
poor feeding, lethargy, hypotonia, hypothermia and a bulging fontanelle
What are the common causes of meningitis in the 0-3 month age group?
Group B Streptococcus (most common cause in neonates)
E. coli
Listeria monocytogenes
What are the common causes of meningitis in the 3 month - 6 year age group?
Neisseria meningitidis
Streptococcus pneumoniae
Haemophilus influenzae
What are the common causes of meningitis in the 6 - 60 year age group?
Neisseria meningitidis
Streptococcus pneumoniae
> 60 age group are more at risk of meningitis caused by which organism?
Listeria monocytogenes
What are the 2 special tests that you can use to assess for meningeal irritation?
Both tests create a slight stretch in the meninges
Kernig’s test:
lying the patient on their back, flexing one hip to 90 degrees and then slowly straightening the knee whilst keeping the hip flexed at 90 degrees.
+ve = spinal pain or resistance to movement
Brudzinski’s test :
lying the patient flat on their back and gently using your hands to lift their head and neck off the bed and flex their chin to their chest
+ve = patient involuntarily flexes their hips and knees
How do bacterial v viral meningitis present on an LP?
(consider appearance, protein, glucose, WCC and culture)
Appearance
Cloudy V Clear
Protein
High V Normal
Glucose
Low V Normal
White Cell Count
Neutrophils V Lymphocytes
Culture
Bacteria Present V Negative
What is the pre-hospital mx of suspected bacterial meningitis?
IM benzylpenicillin urgently
How can meningitis be investigated?
Bloods:
FBC, CRP, U&Es
glucose
lactate
clotting profile
Additional tests that may be helpful include:
blood gases
throat swab for meningococcal culture
Consider LP + CSF analysis
When should a LP not be performed for suspected bacterial meningitis?
signs of severe sepsis or a rapidly evolving rash
severe respiratory/cardiac compromise
significant bleeding risk
signs of raised intracranial pressure
How should patients with suspected bacterial meningitis and no contraindications to LP be managed?
IV access → take bloods and blood cultures
Lumbar puncture to confirm dx
IV antibiotics
3 months - 50 years: ceftriaxone (or cefotaxime)
> 50 years: ceftriaxone + amoxicillin
IV dexamethasone
avoid dexamethasone in septic shock, meningococcal septicaemia, or if immunocompromised
CT scan is not normally indicated
When an LP is taken for suspected bacterial meningitis, what should the CSF be tested for?
glucose, protein, microscopy and culture
lactate
meningococcal and pneumococcal PCR
enteroviral, herpes simplex and varicella-zoster PCR
consider investigations for TB meningitis
How should patients with suspected bacterial meningitis and signs of raised ICP be managed?
get critical care input
secure airway + high-flow oxygen
IV access → take bloods and blood cultures
IV dexamethasone alongside abx (cefotaxime +/- amoxicillin)
Arrange neuroimaging
How should patients with suspected bacterial meningitis and sepsis / rapidly evolving rash be managed?
get critical care input
secure airway + high-flow oxygen
IV access → take bloods and blood cultures
IV fluid resuscitation
IV antibiotics (cefotaxime +/- amoxicillin)
What should be offered to household members and close contacts of an individual with confirmed bacterial meningitis?
oral ciprofloxacin or rifampicin prophylaxis if they have have contact with the individual in the 7 days before sx onset
Viral meningitis is more benign condition than bacterial meningitis and is much more common.
What can cause it?
non-polio enteroviruses e.g. coxsackie virus, echovirus
mumps, measles
herpes simplex virus (HSV), cytomegalovirus (CMV), herpes zoster viruses
HIV
What are the risk factors for developing viral meningitis?
patients at the extremes of age (< 5 years and the elderly)
immunocompromised, e.g. patients with renal failure, with diabetes
intravenous drug users
How can viral meningitis be managed?
If there is any question of bacterial meningitis while waiting for LP results the patient should be commenced on broad-spectrum abx with CNS penetration e.g. ceftriaxone and aciclovir IV
viral meningitis is generally self-limiting, with symptoms improving over the course of 7 - 14 days and complications are rare in immunocompetent patients
aciclovir may be used if the patient is suspected of having meningitis secondary to HSV
What complications may arise as a result of meningitis?
sensorineural hearing loss (most common)
seizures
focal neurological deficit
infective: sepsis, intracerebral abscess
pressure: brain herniation, hydrocephalus
Patients with meningococcal meningitis are at risk of developing what condition?
Waterhouse-Friderichsen syndrome (adrenal insufficiency secondary to adrenal haemorrhage)
Encephalitis is inflammation of the brain tissue itself, that is primarily caused by HSV-1 in adults.
What features does it present with?
fever, headache, psychiatric symptoms, seizures, vomiting
focal features e.g. aphasia
peripheral lesions (e.g. cold sores) have no relation to the presence of HSV encephalitis
How can suspected encephalitis be investigated?
PCR for HSV, VZV and enteroviruses
CSF: high WCC and protein
MRI
medial temporal and inferior frontal changes (e.g. petechial haemorrhages)
EEG
lateralised periodic discharges at 2 Hz
How can encephalitis be managed?
IV aciclovir
A stroke represents a sudden interruption in the vascular supply of the brain.
What are the different types of stroke?
ISCHAEMIC: 85%
Thrombotic stroke - from large vessels e.g. carotid
Embolic stroke - AF is an important risk factor
HAEMORRHAGIC: 15%
Intracerebral haemorrhage
Subarachnoid haemorrhage
Give some risk factors for developing an ischaemic stroke
General risk factors for cardiovascular disease:
age
smoking
hypertension
hyperlipidaemia
diabetes mellitus
Risk factors for cardioembolism:
atrial fibrillation
Give some risk factors for developing a haemorrhagic stroke
age
hypertension
arteriovenous malformation
anticoagulation therapy
What features may someone present with when they are having a stroke?
motor weakness
dysphasia, dysphagia
visual field defects (homonymous hemianopia)
balance problems
How may cerebral hemisphere infarcts present?
contralateral hemiplegia: initially flaccid then spastic
contralateral sensory loss
homonymous hemianopia
dysphasia
What system can be used to classify strokes based on their presenting symptoms?
The Oxford Stroke Classification (also known as the Bamford Classification)
Which part of the circulation is involved in a Total anterior circulation stroke (TACS)?
involves middle and anterior cerebral arteries
What are the diagnostic criteria for a Total anterior circulation stroke (TACS) according to the Oxford Stroke Classification System?
All 3 of:
1. unilateral hemiparesis and/or hemisensory loss of the face, arm & leg
2. homonymous hemianopia
3. higher cognitive dysfunction e.g. dysphasia
Which part of the circulation is involved in a Partial anterior circulation stroke (PACS)?
involves smaller arteries of anterior circulation e.g. upper or lower division of middle cerebral artery
What are the diagnostic criteria for a Partial anterior circulation stroke (PACS) according to the Oxford Stroke Classification System?
2 of 3 are present:
1. unilateral hemiparesis and/or hemisensory loss of the face, arm & leg
2. homonymous hemianopia
3. higher cognitive dysfunction e.g. dysphasia
What part of the circulation is involved in a Lacunar Infarct?
involves perforating arteries around the internal capsule, thalamus and basal ganglia
What are the diagnostic criteria for a Lacunar infarct (LACS) according to the Oxford Stroke Classification System?
presents with 1 of the following:
1. pure motor stroke
2. pure sensory stroke
3. ataxic hemiparesis
What part of the circulation is involved in a Posterior Circulation Stroke?
vertebrobasilar arteries
What are the diagnostic criteria for a Posterior Circulation Stroke (POCS) according to the Oxford Stroke Classification System?
presents with 1 of the following:
1. cerebellar or brainstem syndromes (e.g. vertigo, nystagmus, ataxia)
2. loss of consciousness
3. isolated homonymous hemianopia
What is the likely site of the lesion for a stroke patient presenting with:
Contralateral hemiparesis and sensory loss, lower extremity > upper
Anterior cerebral artery
What is the likely site of the lesion for a stroke patient presenting with:
Contralateral hemiparesis and sensory loss, upper extremity > lower
Contralateral homonymous hemianopia
Aphasia
Middle cerebral artery
(MCA supplies Wernicke’s and Broca’s areas)
What is the likely site of the lesion for a stroke patient presenting with:
Contralateral homonymous hemianopia with macular sparing
Visual agnosia
Posterior cerebral artery
(PCA supplies area that contains visual cortex in the occipital lobe)
What is the likely site of the lesion for a stroke patient presenting with:
Ipsilateral CN III palsy
Contralateral weakness of upper and lower extremity
branches of the posterior cerebral artery that supply the midbrain - Weber’s syndrome
What is the likely site of the lesion for a stroke patient presenting with:
Ipsilateral: facial pain and temp loss
Contralateral: limb/torso pain and temp loss
Ataxia, nystagmus, double vision
Horner’s syndrome
Posterior inferior cerebellar artery (lateral medullary syndrome, Wallenberg syndrome)
What is the likely site of the lesion for a stroke patient presenting with:
Ipsilateral: facial paralysis and deafness
Contralateral: limb/torso pain and temperature loss
Anterior inferior cerebellar artery (lateral pontine syndrome)
What is the likely site of the lesion for a stroke patient presenting with:
Amaurosis fugax
Retinal/ophthalmic artery
What is the likely site of the lesion for a stroke patient presenting with:
‘Locked-in’ syndrome
Basilar artery
How do lacunar strokes present?
present with either isolated hemiparesis, hemisensory loss or hemiparesis with limb ataxia
strong association with hypertension
common sites include the basal ganglia, thalamus and internal capsule
Whilst symptoms alone cannot be used to differentiate haemorrhagic from ischaemic strokes, patients who’ve suffered haemorrhages are more likely to have:
decrease in the level of consciousness: seen in up to 50% of patients with haemorrhagic stroke
headache is also much more common
nausea and vomiting
seizures occur in up to 25% of patients
What scoring tools can be used to identify strokes quickly in the community and in ED?
FAST tool:
F – Face
A – Arm
S – Speech
T – Time (act fast and call 999)
ROSIER Tool:
The ROSIER tool (Recognition Of Stroke In the Emergency Room) gives a score based on the clinical features and duration
stroke is possible in patients scoring one or more
How should suspected strokes be investigated?
Urgent non-contrast CT head scan to exclude haemorrhage
acute ischaemic strokes:
‘hyperdense artery’ sign corresponding with the responsible arterial clot - this tends to visible immediately
may show areas of low density in the affected territory once ischaemia has set in
acute haemorrhagic strokes:
typically show areas of hyperdense material (blood) surrounded by low density (oedema)
How should a confirmed ischaemic stroke be managed?
aspirin 300mg orally or rectally should be given as soon as possible (continued daily for 2 weeks)
Thrombolysis with alteplase should be given if:
* it is administered within 4.5 hours of onset of stroke symptoms
* haemorrhage has been definitively excluded (i.e. Imaging has been performed)
What is recommend for patients with an acute ischaemic stroke who present within 4.5 hours?
A combination of thrombolysis AND thrombectomy
What are the absolute contraindications to delivering thrombolysis?
Previous intracranial haemorrhage
Uncontrolled hypertension >200/120mmHg
Seizure at onset of stroke
Intracranial neoplasm
Suspected subarachnoid haemorrhage
Stroke or traumatic brain injury in preceding 3 months
Lumbar puncture in preceding 7 days
Active bleeding
Oesophageal varices
Pregnancy
How may you investigate for an underlying cause of stroke?
Patients with a TIA or stroke are investigated for carotid artery stenosis and atrial fibrillation with:
Carotid imaging (e.g., carotid ultrasound, or CT or MRI angiogram)
ECG or ambulatory ECG monitoring
What secondary prevention should be offered to patients who have had a stroke?
Clopidogrel 75mg once daily (alternatively aspirin plus dipyridamole)
Atorvastatin 20-80mg (not started immediately – usually delayed at least 48 hours)
Blood pressure and diabetes control
Addressing modifiable risk factors (e.g., smoking, obesity and exercise)
How can you measure someone’s functional status post-stroke?
Barthel index (BI): an outcome measure for stroke
Describes 10 tasks, and is scored according to amount of time or assistance required by the patient for each given task
Tasks: feeding, moving from wheelchair to bed, personal toileting, getting on/off toilet, bathing, walking on level surface, ascending/descending stairs, dressing, controlling bowels and controlling bladder
The total score is from 0 to 100, with 0 being completely dependent, and 100 being completely independent
Cauda equina syndrome (CES) is a serious condition in which the lumbosacral nerve roots that extend below the spinal cord are compressed.
What may cause it?
the most common cause is a central disc prolapse
this typically occurs at L4/5 or L5/S1
other causes include:
tumours: primary or metastatic
infection: abscess, discitis
trauma
haematoma
What features may CES present with?
low back pain
bilateral sciatica: around 50% of cases
reduced sensation/pins-and-needles in the perianal area
decreased anal tone
urinary dysfunction
incontinence is a late sign that may indicate irreversible damage
How should CES be investigated and managed?
urgent MRI whole spine
surgical decompression
How may a primary brain injury be classified?
focal (contusion/ haematoma) or diffuse (diffuse axonal injury)
Diffuse axonal injury occurs as a result of mechanical shearing following deceleration, causing disruption and tearing of axons
How may cerebral contusions be classified?
adjacent to (coup) or contralateral (contre-coup) to the side of impact
What is secondary brain injury?
When cerebral oedema, ischaemia, infection, or herniation exacerbates the original injury
The normal cerebral auto regulatory processes are disrupted following trauma, making the brain more susceptible to blood flow changes and hypoxia
What is shown here?
Extradural haematoma
Bleeding into the space between the dura mater and the skull
Most occur in the temporal region where skull fractures cause a rupture of the middle meningeal artery
What is shown here?
What are the risk factors?
Subdural haematoma
Bleeding between the dura mater and the arachnoid mater
Risk factors include old age, alcoholism and anticoagulation
Slower onset of symptoms than a epidural haematoma, +/- fluctuating consciousness
What is shown here?
Subarachnoid haemorrhage
Which patients with head injuries require a CT head within 1 hour?
GCS < 13 on initial assessment
GCS < 15 at 2 hours post-injury
suspected open or depressed skull fracture
any sign of basal skull fracture
post-traumatic seizure
focal neurological deficit
more than 1 episode of vomiting
Give some signs of basal skull fracture
haemotympanum, ‘panda’ eyes, cerebrospinal fluid leakage from the ear or nose, Battle’s sign
If a patient is on warfarin who have sustained a head injury with no other indications for a CT head scan, what should you do?
perform a CT head scan within 8 hours of the injury
How should traumatic head injuries be managed?
Life threatening rising ICP : consider IV mannitol/ furosemide while theatre is being prepped
Diffuse cerebral oedema may require decompressive craniotomy
Depressed skull fractures:
open = formal surgical reduction and debridement
closed injuries may be managed nonoperatively
Which patients should receive ICP monitoring following head injury?
ICP monitoring is appropriate in those who have GCS 3-8 and normal CT scan.
ICP monitoring is mandatory in those who have GCS 3-8 and abnormal CT scan.
What is the most likely cause of hyponatraemia in a patient with a traumatic head injury?
SIADH
What is the minimum cerebral perfusion pressure in children and adults?
Minimum of cerebral perfusion pressure of 70mmHg in adults and between 40 and 70 mmHg in children.
Unilaterally dilated pupil that is sluggish to respond to light (or fixed) =
3rd nerve compression secondary to tentorial herniation
Bilaterally dilated pupils that are sluggish to respond to light (or fixed) =
Poor CNS perfusion
Bilateral 3rd nerve palsy
Unilaterally dilated pupil that is cross reactive (Marcus - Gunn) in response to light =
Optic nerve injury
Bilaterally constricted pupils =
Opiates
Pontine lesions
Metabolic encephalopathy
Unilaterally constricted pupil with preserved light reflex =
Sympathetic pathway disruption (e.g. Horner’s)
What is temporal arteritis? (also known as giant cell arteritis)
a vasculitis of unknown cause that affects medium and large-sized vessels
peak incidence is in 70yr olds
requires early recognition as may be sight threatneing
Which patient group is at risk of developing temporal arteritis?
patients with Polymyalgia Rheumatica
around 50% of TA patients have features of PMR such as aching and morning stiffness in proximal limb muscles
What features does temporal arteritis typically present with?
typically patient > 60 years old
usually rapid onset (e.g. < 1 month)
headache
jaw claudication
tender, palpable temporal artery
also lethargy, depression, low-grade fever, anorexia, night sweats
How should temporal arteritis be investigated?
vision testing is a key investigation in all patients
inflammatory markers : raised ESR (> 50 mm/hr) and raised CRP
temporal artery biopsy: skip lesions may be present
What are the potential ocular complications of temporal arteritis?
anterior ischemic optic neuropathy is most common: occlusion of the posterior ciliary artery (branch of the ophthalmic artery) → ischaemia of the optic nerve head
swollen pale disc and blurred margins on fundoscopy
diplopia
temporary visual loss - amaurosis fugax
permanent visual loss may develop suddenly
How should temporal arteritis be managed?
urgent high-dose glucocorticoids should be given as soon as the diagnosis is suspected and before the temporal artery biopsy
no visual loss = high-dose prednisolone
evolving visual loss = IV methylprednisolone prior to starting high-dose prednisolone
there should be a dramatic response, if not the diagnosis should be reconsidered
urgent ophthalmology review
patients with visual symptoms should be seen the same-day by an ophthalmologist
What is bulbar palsy ?
signs and symptoms linked to the impaired function of the lower cranial nerves arising from the brainstem
Glossopharyngeal (9), vagus (10), accessory (11) and hypoglossal (12) are affected
due to the lower part of cranial nerves or their lower motor neurones being damaged
What symptoms might someone present with if they have a bulbar palsy?
dysphagia (glossopharyngeal nerve damage)
difficulty chewing
lack of gag reflex
nasal regurgitation
difficulty in handling secretions / aspiration of secretions
slurred speech, dysphonia and dysarthria
What may cause someone to develop a bulbar palsy?
Brainstem stroke
Brainstem tumour
Degenerative diseases e.g. ALS
Autoimmune diseases e.g. Guillain Barre
Genetic Conditions
How can bulbar palsies be investigated and managed?
consider CSF testing to rule out multiple sclerosis (may present similarly)
MRI to investigate for brainstem strokes and tumours
treat the underlying cause
manage sxs - NG tube for feeding, SALT team input, medications to reduce drooling
Name 4 conditions that are stroke mimics. How are they differentiated from an acute stroke?
HEMI:
- Hypoglycaemia
- Epilepsy
- Migraine (hemiplegic)
- Intracranial tumours/infections
The Recognition of Stroke in the Emergency Room (ROSIER) scale
Define TIA
TIA: a transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischaemia, without acute infarction.
How are TIAs managed acutely?
Immediate antithrombotic therapy:
give aspirin 300 mg immediately, unless contraindicated e.g. the patient has a bleeding disorder or is taking an anticoagulant (needs immediate admission for imaging- CT head- to exclude a haemorrhage)
If the patient has had more than 1 TIA (‘crescendo TIA’) or has a suspected cardioembolic source or severe carotid stenosis:
discuss urgently with a stroke specialist
If the patient has had a suspected TIA in the last 7 days:
arrange assessment within 24 hours by a stroke specialist
If the patient has had a suspected TIA which occurred more than a week previously:
refer for specialist assessment as soon as possible within 7 days
In cases of stroke, thrombolysis with alteplase should only be given if:
it is administered within 4.5 hours of onset of stroke symptoms (unless as part of a clinical trial)
haemorrhage has been definitively excluded (i.e. Imaging has been performed)
How is GCS scored?
In GCS, take the best response from each side!
MoVE 654
Motor:
6. Obeys commands
5. Localises to pain
4. Withdraws from pain
3. Abnormal flexion to pain (decorticate posture)
2. Extending to pain
1. None
Verbal:
5. Orientated
4. Confused
3. Words
2. Sounds
1. None
Eye opening:
4. Spontaneous
3. To speech
2. To pain
1. None
