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Confusion and delirium
— Hypertension
— Chronic liver
— Infection
Pattern of confusion
Delirium develops over 1–2 days. It is characterized by
clouding of consciousness that fluctuates in severity, often worse at night with lucid periods in the day. It can be
accompanied by poor recent memory, disorientation and
hallucinations. Delirium can be hypoactive (patients are
withdrawn, quiet, sleepy), hyperactive (patients are restless,
agitated and aggressive) or mixed (features of both).
Dementia has a gradual onset over months or years. It is
a progressive global deterioration in higher cerebral function, without effect on the level of consciousness. The symp-
familiar surroundings.
HINTS AND TIPS
Severe symptoms of delirium tremens due to
alcohol withdrawal may occur more than 72 hours
after the patient's last drink, and long after the
patient has been admitted to hospital.
Underlying causes
The following should be assessed:
• Age: dementia becomes increasingly common after the
age of 60years.
• Symptoms of infection (see Chapter 8).
• Symptoms of raised intracranial pressure (see
Chapter16).
• Risk factors for, or known, vascular disease (see
Chapter27).
• Alcohol intake: long-term alcohol abuse can cause
dementia; it is also associated with thiamine deficiency
(Wernicke–Korsakoff syndrome) and folate and B12
deficiency, both of which may increase the risk of
dementia.
• Previous head injury or evidence of falls: subdural
haematoma.
• Other neurological symptoms: cerebrovascular
disease, multiple sclerosis, cerebral tumour/abscess,
inflammatory or autoimmune neurological disease.
• Symptoms of endocrine disease: hypothyroidism or
hyperthyroidism, Addison disease.
• Medical history of any disease may be relevant:
long-standing renal disease (uraemia), liver disease
(encephalopathy), malignancy (cerebral metastases,
hypercalcaemia or paraneoplastic syndromes), diabetes
(hypoglycaemia)
• Drug history: use of any sedatives, anticonvulsants and/or
steroids. Might the patient have consumed illicit drugs?
• Social history: confused patients often need a referral
to the safeguarding team, and understanding their
social circumstances may help contextualize the
presentation.
• Family history: Wilson disease (autosomal recessive);
Huntington chorea (autosomal dominant).
• Brief psychiatric history: notably for features of
depression or psychosis.
• Sexual history may provide information regarding the
possibility of HIV infection, hepatitis or syphilis.
CLINICAL NOTES
CONFUSION ASSESSMENT METHOD
The Confusion Assessment Method (CAM) is a
delirium-screening tool that helps identify patients
with the condition. It comprises four questions:
1. Acute onset and fluctuating course?
2. Inattention?
3. Disorganized thinking?
4. Altered level of consciousness?
Delirium is suggested if 1 and 2 and either 3 or 4 is
present. The patient is then said to be ‘CAM positive’.
Examination
The approach to examining a patient presenting with confusion is summarized in Fig.19.1. Attention should be given to:
— Injury
— Cyanosis
— Otoscopy
— Meningism
— Endocarditis
— Heart failure
— Consolidation
disease
— Chronic liver
disease
— Clubbing liver
flap
Fig.19.1 Examining the confused patient.
— Focal signs
— Incontinence
— Hypotension
Skin
— Infection
— Malignancy
— Glasgow coma scale
— Capillary glucose
— Mental state
examination
— Malignancy
— Temperature
— Oxygen saturation
118
History and examination findings
1919
• Consciousness: the level of consciousness should be
recorded. Use the Glasgow Coma Scale score (see
Table18.3).
• Blood pressure: hypotension may be due to sepsis
or cardiac failure. Hypertension is a risk factor for
cerebrovascular events, and can also be a response to
raised intracranial pressure.
• Signs of infection: measure temperature, look for
neck stiffness, consolidation in the chest, signs of
endocarditis, abdominal tenderness, otitis media
on otoscopy and check pressure areas and skin for
evidence of cellulitis (see Chapter8).
• Mental state: The 10-point abbreviated mental test score
is useful to assess the level of confusion, and may be used
serially to monitor progress.
• Focal neurological deficit and the pattern of signs
may give important clues as to the diagnosis (see
Chapters20 and 22): fundoscopy should be performed,
looking for papilloedema (raised intracranial
pressure), optic atrophy (demyelination) or subhyaloid
haemorrhages (subarachnoid haemorrhage).
• Signs of chronic liver disease (CLD): hepatic
encephalopathy can cause confusion. The presence
of CLD may also indicate long-term alcohol abuse or
rarer disorders, such as Wilson disease.
CLINICAL NOTES
ABBREVIATED MENTAL TEST SCORE
One point is awarded for each correct answer.
A score of less than 7/10 strongly suggests
confusion.
• Age.
• Date of birth.
• Time (to nearest hour).
• Current year.
• Address for recall at end of test – to be repeated
by the patient to ensure it has been heard
correctly (e.g. 42 West Street).
• Name of the place where we are.
• Recognition of two people (e.g. nurse and
doctor).
• Beginning of First World War or similar.
• Name of monarch.
• Count backwards from 20 to 1.
Investigations
The investigations used in the diagnosis of delirium and dementia are very similar, although the urgency with which
they are required is different. The following tests should be
considered.
Bedside investigations
Routine observations, including oxygen saturation, capillary glucose, urinalysis and ECG, can all be performed
quickly, and may give an almost immediate clue as to the
underlying cause.
Blood tests
• Full blood count: infection or inflammation; anaemia
with raised mean corpuscular volume in vitamin B12 or
folate deficiency.
• Erythrocyte sedimentation rate: raised in malignancy,
infection, inflammation.
• Urea and electrolytes: hyponatraemia or
hypernatraemia, renal failure, uraemia.
• Liver function rests: abnormal results in liver disease.
• Thyroid function tests: thyroid-stimulating hormone
level usually raised in hypothyroidism and low in
hyperthyroidism.
• Serum calcium: hypercalcaemia or hypocalcaemia.
• Glucose: hypoglycaemia or hyperglycaemia; diabetic
ketoacidosis or hyperosmolar hyperglycaemic state.
• Arterial blood gas: hypoxia and/or CO2 retention.
• Blood cultures if indicated.
• Vitamin B12 and folate levels: deficiency.
• Syphilis serology: tertiary syphilis may cause dementia.
Further tests
Consider the following when clinically indicated:
• Chest X-ray: pneumonia, cardiac failure, malignancy.
• CT/MRI of the head: tumour, stroke, age related changes.
• Urine: toxicology screen, culture for urinary infection.
• Lumbar puncture and CSF examination: protein,
glucose, microscopy, culture and oligoclonal bands.
• Ammonia – level often raised in liver disease and
metabolic disorders (see Chapter33).
• Serum copper and caeruloplasmin (reduced) and 24-hour
urinary copper excretion (increased): Wilson disease.
• Borrelia serology for Lyme disease.
• Thick and thin blood films: malaria.
• HIV serology.
CLINICAL NOTES
CONFUSION SCREEN
Patients presenting with new-onset confusion
should undergo a variety of tests that are
collectively termed the ‘confusion screen’. These
include:
• full blood count, urea and electrolytes, liver
function tests, clotting, thyroid function tests,
calcium, vitamin B12 and folate, glucose.
• CT of the head.
• urine dipstick.
119
Confusion and delirium
Chapter Summary
• Delirium is very common amongst hospital patients.
• Delirium is difficult to diagnose and can often go unnoticed for prolonged periods. It is
also challenging to treat. Pharmacological interventions should be used only as a last
resort.
• As opposed to delirium, dementia is a condition of gradual onset that progresses over
time. It is most common in the elderly population.
• There can be many causes of dementia, but the most common one is Alzheimer disease.
120
Stroke and TIA
20
INTRODUCTION
Stroke is a clinical syndrome where acute focal or global signs
of cerebral dysfunction develop rapidly and persist for more
than 24 hours. Deficits lasting less than 24 hours are termed
‘transient ischaemic attacks’ (TIAs). Different types of stroke
and their causes are described in Table20.1. Eighty-five per-
cent of strokes are ischaemic, and 15% are haemorrhagic.
The annual incidence of stroke is about 115 in 100,000
but rises with age; the incidence of TIA is approximately
Table20.1 Types of stroke
Type Causes
Haemorrhagic Hypertension
Ischaemic
(thrombotic,
hypotensive,
occlusive)
Ischaemic
(embolic)
MI, Myocardial infarction; PAN, polyarteritis nodosa; SLE,
systemic lupus erythematosus.
Aneurysm (particularly Charcot–
Bouchard microaneurysms; also berry
and mycotic aneurysms)
Arteriovenous malformation
Tumours
Bleeding tendency
(thrombocytopenia, coagulopathy,
anticoagulants)
Drugs (amphetamines, ecstasy,
cocaine)
Haemorrhagic transformation of
infarction
Hypertension
Intracranial arterial atheroma
Vasculitis (e.g., temporal arteritis,
SLE, PAN, neurosyphilis)
Prolonged hypotension (e.g., cardiac
arrest)
Thrombophilia (hyperviscosity,
antiphospholipid syndrome)
Drugs (amphetamines, ecstasy,
cocaine)
Arterial dissection (cervical or
vertebral)
Carotid or vertebral atheroma
Cardiac:
• Atrial fibrillation with left atrial
thrombosis
• Endocarditis
• Ventricular thrombus, e.g., due to
MI or ventricular aneurysm
• Atrial myxoma
Paradoxical:
• Venous thrombus can reach the
cerebral circulation via an atrial
septal defect
Table20.2 ABCD2 score for transient ischaemic attack
Feature Severity Score
Age >60years 1
Blood pressure
≥140/90 mmHg
Clinical features Unilateral weakness 2
Duration of
symptoms
Diabetes 1
Score 0–3, low risk; score 4–7, high risk.
1
Speech disturbance without
weakness
Other 0
<10 min 0
10–59 min 1
≥60 min 2
1
190 in 100,000. The risk of developing a stroke following a
TIA is around 17% at 3months. To aid the decision- making
process regarding inpatient or outpatient management in
patients after a TIA, risk stratification for experiencing a
subsequent stroke is performed with a scoring system such
as ABCD2 (Table20.2).
Stroke patients are at increased risk of experiencing
another event. The 5-year recurrence rate is around 25%.
shows the main risk factors for stroke; many are common to
all vascular diseases (see Chapter27).
CLINICAL NOTES
RISK FACTORS FOR STROKE
• Previous stroke or transient ischaemic attack.
• Poorly controlled hypertension.
• Atrial fibrillation.
• Established vascular disease (carotid bruit,
coronary artery disease, peripheral vascular
disease).
• Diabetes mellitus.
• Hypercholesterolaemia.
• Thrombophilia.
• Family history.
• Smoking.
• Oral contraceptive pill use.
• Obesity.
• Excessive alcohol intake.
121
Stroke and TIA
CAUSES AND PATHOPHYSIOLOGY
The main causes of ischaemic stroke are thromboembolism
from arteries and heart emboli (in atrial fibrillation, myocardial infarction or infective endocarditis). Uncommon causes
of cerebral infarction include vasculitis, arterial dissection, venous sinus thrombosis (which may also cause haemorrhage),
polycythaemia and meningovascular syphilis (see below).
Thrombus in situ may also occur in perforating arteries, often due to lipohyalinosis as a complication of hypertension.
Around 20% of ischaemic strokes occur in the posterior cerebral circulation. The risk factors for TIA are identical, and the
underlying disease processes are very similar, the main cause
being embolism from a distant source. Other possible causes
include thrombotic occlusion of small perforating vessels, low
flow through stenosed vessels, vasculitis and haematological
conditions such as sickle cell disease. Two or more TIAs occurring closely together (within 1week) may be due to an unstable
plaque and are termed ‘crescendo TIA’. Crescendo TIA signifies
a high risk of stroke.
Cerebral haemorrhage is usually due to rupture of perforating arteries or intracerebral vessels (primary intracerebral haemorrhage); underlying causes include hypertension
(causing vessel fragility and microaneurysms), cerebral amyloid angiopathy and arteriovenous malformations.
CLINICAL NOTES
DIFFERENTIAL DIAGNOSIS OF STROKE
• Transient ischaemic attack in the first 24 hours.
• Drug overdose.
• Hypoglycaemia.
• Subdural haemorrhage.
• Space occupying lesion.
• Epilepsy.
• Hemiplegic migraine.
HINTS AND TIPS
Amaurosis fugax is a so-called retinal TIA. It is an
episode of transient monocular visual loss, and is
most frequently a result of ischaemia.
• Where is the anatomical site of the lesion?
• Are any risk factors present?
Symptoms usually develop rapidly, but a stepwise progressive neurological worsening over hours or days can
also occur. Established deficit remains stable and usually
abates over time. If there has been gradual neurological
deterioration, consider one of the differential diagnoses or
hydrocephalus secondary to the stroke (oedema or blood
preventing free drainage of cerebrospinal fluid).
Any intracranial artery can be involved in stroke. The
symptoms and signs will reflect which artery and therefore
which part of the brain has been involved. This is summarized in Fig.20.1. The most common presentation is with
hemiplegia due to occlusion of the middle cerebral or internal carotid artery causing infarction of the internal capsule.
Motor deficit is initially in the form of flaccid paralysis that
later develops into spasticity. The presence of collateral arteries leads to variation in the presentation.
COMMUNICATION
Taking a history from a patient with a stroke can
be challenging. The patient may have a receptive
or expressive dysphasia, and could have visual
impairment from a homonymous hemianopia. It
is important to position yourself where the patient
can see you to maximize communication with the
patient. A collateral history may be required.
PATIENT SAFETY
FAST is a validated screening tool for the presence
of neurological symptoms in patients presenting
acutely. It stands for ‘face, arm, speech, time’,
and is mostly used in an out-of-hospital setting
for patients in whom a diagnosis of stroke is
suspected.
HISTORY AND EXAMINATION FINDINGS
History
The history taking should focus on three distinct areas:
• Does the history fit with the diagnosis of stroke?
122
HINTS AND TIPS
If the patient has atrial fibrillation, calculate the
patient’s risk of further stroke with a risk-scoring
system such as the CHA2DS2-VASc score
(Table20.3) to allow a reasoned decision regarding
anticoagulation.
History and examination findings
— Sudden ataxia, sudden dysnomia
— Spinothalamic sensory loss
Circle of Willis
2020
Anterior cerebral artery
— Contralateral hemiparesis
and hemisensory loss
leg > arm
— If dominant−−expressive
dysphasia
Carotid artery
Posterior communicating
Carotid territory
artery
Posterior cerebral artery
— Contralateral
homonymous hemianopia
— Cortical blindness
(Anton syndrome)
— Contralateral hemisensory
disturbance (thalamic
syndrome)
Vertebrobasilar territory
— Involuntary movements
Vertebral artery
Lacunar infarcts
— Particularly in patients with hypertension
— Small vessel occlusion
— Internal capsule, basal ganglia,
thalamus, brainstem can be affected
— Pure motor or pure sensory disturbance
Anterior spinal artery
— Paraparesis
Anterior communicating
artery
Middle cerebral artery
— Contralateral hemiparesis
± hemisensory loss
arm and face > leg
— If dominant−−expressive
dysphasia
— Contralateral homonymous
hemianopia
Basilar artery
— Pontine stroke
— Pinpoint pupils
— Coma
— Quadriplegia
— Cardiorespiratory disturbance
— Cranial nerve palsies
Posterior inferior
cerebellar artery
— Lateral medullary syndrome
(Wallenberg syndrome)
— Ipsilateral 5th (sensory), 6th, 8th,
9th, 10th nerve palsy, nystagmus,
ataxia, Horner syndrome
— Contralateral spinothalamic
sensory loss, hemiparesis
(rare)
Fig.20.1 Symptoms and signs associated with different strokes. Note that haemorrhagic strokes have symptoms and
signs determined by the site of the bleed. Patients may also develop headache, loss of consciousness and vomiting
because of raised intracranial pressure.
Table20.3 CHA2DS2-VASc score for stroke risk with
atrial fibrillation
Feature Score
Congestive heart failure 1
Hypertension history 1
Age 65–74years 1
Age ≥75years 2
Diabetes 1
Previous stroke/TIA/thromboembolism 2
Vascular disease history 1
• Is there any evidence of an underlying cause?
• Have any complications arisen because of the stroke?
• What immediate treatment is needed?
Fig.20.2 summarizes this examination approach.
A thorough neurological examination should be performed. The initial Glasgow Coma Scale (GCS) score
should be recorded and then any changes should be documented. The GCS is imperfect in stroke as dysphasia and
aphasia reduce the verbal score. Does the pattern of neurological deficit fit with disruption of the cerebral vascular
supply (see Fig.20.1)?
Female sex 1
A score of 2 or greater is generally taken as an indication for
anticoagulation.
TIA, transient ischaemic attack.
CLINICAL NOTES
STROKE CLASSIFICATION
Numerous different systems are used to classify
Examination
Clinical examination gives information regarding four important areas in the stroke patient:
stroke. The Bamford classification is one of
the more commonly used (Table20.4). One
of its advantages is that it gives prognostic
estimation.
• What are the neurological abnormalities, and do they
fit with the diagnosis of stroke?
123
Stroke and TIA
Pulse
— Atrial fibrillation
r
Neurology
— Swallow assessment
— Focal deficit
Neck
— Carotid artery bruits
Chest
— Signs of aspiration
Heart
— Murmur
General
— Glasgow coma scale
— Capillary glucose
Head
— Injury
— Xanthelasmata
— Temporal artery
tenderness
Blood pressure
— Hypotension
— Hypertension
Hands
— Nicotine staining
— Xanthomata
Legs
— Peripheral vascula
disease
— Femoral bruits
Fig.20.2 Examining the stroke patient.
Table20.4 The Bamford classification of stroke
Category
Total anterior circulation
stroke
Middle/anterior cerebral
artery territory
Partial anterior circulation
stroke
124
Percentage of
overall strokes Clinical findings
20 All of (1) unilateral weakness of two
or more of face, arm and leg; with or
without sensory deficit;
(2) homonymous hemianopia;
(3) disturbance of higher cerebral
function, e.g., dysphasia, dyspraxia,
inattention.
If the patient is drowsy, then
(2) and (3) are assumed
35 Any of the following: (1) two of the
components of total anterior
circulation stroke; (2) higher cortical
function deficit alone;
(3) limited sensory or motor deficit
Percentage at 1year
Living
Deceased
independently
60 5
15 55
History and examination findings
Table20.4 The Bamford classification of stroke—Cont’d
Category
Lacunar stroke
Infarcts involving: basal
ganglia, internal capsule,
thalamus and pons
Posterior circulation stroke 25 Brainstem and/or cerebellar deficits
Percentage of
overall strokes Clinical findings
20 Pure motor or sensory stroke
or mixed affecting two-thirds
of the face/arm/leg
Sensorimotor stroke affecting twothirds or more of the face/arm/leg
Ataxic hemiparesis
Dysarthria – clumsy hand syndrome
No disturbance of higher function
(motor deficits of any combination of
upper and lower limbs or the whole
of the face; sensory deficits in any
combination of upper and lower limbs
or the whole of the face; or cerebellar
signs – ataxia, imbalance, vertigo,
diplopia, dysarthria, dysphagia)
Isolated homonymous hemianopia
Percentage at 1year
Deceased
10 60
20 60
Living
independently
2020
There are many causes of and risk factors for stroke.
Particular attention should be paid to:
• Carotid bruits: carotid atheroma.
• Murmurs: endocarditis, valvular disease, atrial septal
defect.
• Pulse: atrial fibrillation.
• Blood pressure: hypertension can be the cause or
result of stroke; prolonged hypotension is also a risk
factor.
• Diminished peripheral pulses and femoral bruits:
peripheral vascular disease.
• Xanthelasmata, xanthomata: underlying
hyperlipidaemia.
• Tar-stained fingers from smoking.
Complications are very common following stroke, both in
the short term and during recovery, and are related to the
extent of cerebral damage and the degree of neurological
deficit. The more common problems, and prophylactic
measures, are outlined in Table20.5.
Investigations
The diagnosis of stroke is clinical. The aim of immediate
investigations is to look for treatable causes and to offer the
best supportive care. The following investigations should be
performed for any patient with an acute stroke:
Bedside investigations
• Capillary blood glucose: to rule out hypoglycaemia.
Diabetes is associated with increased risk of stroke.
Hypoglycaemia may present with stroke-like symptoms
or signs, and prolonged severe hypoglycaemia may
result in permanent brain injury.
Table20.5 Complications of stroke and measures
to prevent them
Complications Prophylactic measures
Acute
Cerebral oedema
(malignant middle cerebral
artery syndrome)
Aspiration pneumonia Patients should be kept
Seizures None. Can be treated with
Subacute and long term
Pressure sores Careful nursing with regular
Contractures and spasticity Regular skilled
Malnutrition Feeding via a nasogastric
Depression Provision of adequate
Deep vein thrombosis Physiotherapy,
Particularly in
haemorrhagic stroke and
usually not preventable
(avoid overenthusiastic
rehydration). Surgical
decompression is
becoming more commonly
performed
nil by mouth until they can
swallow safely
antiepileptics. They may
also occur later in the
illness course as the brain
remodels
turning on an air mattress
physiotherapy
tube or, later, gastrostomy
social and practical
support
antiembolism stockings
Heparin not used routinely
125
Stroke and TIA
• Routine bedside observations: blood pressure, pulse
and oxygen saturations.
• ECG: this may show atrial fibrillation, or potentially
(and much more rarely) ventricular aneurysm
following recent myocardial infarction (persistent ST
elevation, more than 2weeks after an ST-elevation
myocardial infarction with pathological Q waves
suggests a ventricular aneurysm).
Blood tests
• Full blood count: polycythaemia or thrombocytopenia
may cause a stroke; a reactive picture may indicate
inflammation (e.g., temporal arteritis).
• Erythrocyte sedimentation rate/C-reactive protein:
level elevated in inflammation, vasculitis, infection and
malignancy.
• Urea and electrolytes: renal impairment may either be
due to or the cause of hypertension. It may also result
from reduced oral intake or concurrent sepsis.
• Fasting lipids: hypercholesterolaemia is an important,
treatable risk factor for stroke.
• Clotting: to assess the level of anticoagulation if the
patient is receiving warfarin or to investigate suspected
coagulopathy.
• Arterial blood gas: hypoxia should be treated. Seizure
can lead to an increased lactate level.
Imaging
• Chest X-ray: an enlarged heart could indicate
hypertension; an enlarged left atrium could suggest this
being the point of origin for emboli.
• CT of the head: CT findings are often normal in the first
few hours following an ischaemic stroke. The accuracy of
the investigation increases after about 6 hours. Indications
for immediate brain imaging are outlined in red flag:
indications for urgent CT brain scan.
• MRI of the brain: this is preferred if a posterior
circulation stroke is suspected as it provides better
images of the posterior fossa. It is also helpful in cases of
diagnostic uncertainty (especially to exclude tumour).
Further investigations
Depending on the patient and the clinical scenario, further
tests may be required. The following further investigations
should be considered, especially in young patients with no
obvious risk factors:
• Blood cultures: infective endocarditis.
• Autoantibodies: to investigate the patient for vasculitis
(antinuclear antibodies, antineutrophil cytoplasmic
antibodies), antiphospholipid syndrome (anticardiolipin
antibodies) or cerebral lupus (anti-double-stranded DNA).
• Carotid imaging: to look for carotid stenosis in patients
with anterior circulation events (carotid territory);
all patients considered as candidates for carotid
endarterectomy (with or without stenting) should have
this investigation.
• Cerebral angiography/venography or radiological
equivalent: if there are additional signs or symptoms
suggesting an unusual cause of infarction or
haemorrhage, such as venous sinus thrombosis, arterial
dissection or subarachnoid haemorrhage.
• Echocardiography: if cardiac embolus is suspected (e.g.,
after myocardial infarction, in endocarditis, in atrial
fibrillation).
• Twenty-four-hour ECG monitoring: paroxysmal atrial
fibrillation.
• Syphilis serology: neurosyphilis.
RED FLAG
INDICATIONS FOR URGENT CT BRAIN SCAN
• Thrombolysis or early anticoagulation treatment
are considered.
• The patient is taking anticoagulants or has a
known bleeding tendency.
• There is uncertainty as to the diagnosis (e.g.,
subdural or subarachnoid haemorrhage).
• There was severe headache at the onset of
symptoms.
• There are progressive or fluctuating neurological
signs.
• There is a reduced conscious level (Glasgow
Coma Score <13).
• There is papilloedema, neck stiffness or fever.
RED FLAG
Patients with a suspected transient ischaemic attack
should be assessed by a specialist urgently. Most
patients require brain imaging. If the vascular territory
or pathology is uncertain, imaging may be done at an
urgent follow-up appointment. Imaging is helpful to
exclude other causes of transient symptoms and to
look for areas of previous silent infarction. Diffusionweighted MRI is the investigation of choice. CT is
used if MRI is contraindicated.
Management
Patients with established stroke should be admitted to hospital, ideally to a stroke unit.
Acute treatment
• An ABCDE approach should be instituted to
ensure adequate oxygen saturations (≥95% unless
contraindicated), haemodynamic stability (see clinical
notes: blood pressure control in acute stroke), glucose
126
History and examination findings
2020
control (between 4 and 11 mmol/L), normothermia and
electrolyte levels within the reference range.
• Thrombolysis with alteplase in selected patients with
ischaemic stroke is beneficial when given up to 4.5 hours
after symptom onset. Brain imaging is required before
commencement of treatment to exclude haemorrhage.
• Antiplatelet agents: in acute ischaemic stroke, aspirin
therapy (usually 300 mg daily) should be started
immediately and no later than within 24 hours and
should be continued for 2weeks, after which long-term
secondary prevention is implemented (see later). Unless
contraindicated, antiplatelet therapy should be started
in all patients with TIA. In postthrombolysis patients,
aspirin therapy is started 48 hours after the intervention.
Patients with a suspected TIA who are at high risk of
stroke (ABCD2 score ≥4) should also be given aspirin (usually 300 mg daily). Specialist assessment and investigations
should occur within 24 hours of onset of symptoms but can
be done in an outpatient setting.
• Anticoagulants: unless contraindicated, patients
with cerebral venous sinus thrombosis should be
anticoagulated to an international normalized ratio
target of 2–3.
• Swallow assessment: required to assess the risk of
aspiration. Give intravenous fluids if swallowing is
compromised to maintain hydration. The speech
and language therapy team and a dietitian should be
involved early.
• Supportive therapy: monitoring for infection and
complications such as hydrocephalus; care of pressure
areas, nutrition; physiotherapy; occupational therapy.
• Neurosurgical intervention may be indicated for
intracerebral haemorrhage or severe middle cerebral
artery infarction. Malignant middle cerebral artery
syndrome is a life-threatening cerebral oedema
following ischaemic stroke.
encephalopathy, hypertensive nephropathy,
hypertensive cardiac failure/myocardial
infarction, aortic dissection, preeclampsia/
eclampsia, intracerebral haemorrhage with
systolic blood pressure exceeding 200 mmHg.
• In patients considered for thrombolysis, the
aim is to maintain the blood pressure below
185/100 mmHg.
Prevention
Secondary prevention following stroke and TIA should be
initiated at diagnosis.
• Patient education and lifestyle changes: smoking
cessation, physical activity, optimization of diet.
• Antiplatelet therapy: unless the patient has atrial
fibrillation, clopidogrel (usually 75 mg daily) is used
following ischaemic stroke or TIA. Dipyridamole is an
alternative to aspirin and clopidogrel.
• Anticoagulant therapy: should be started in patients
with atrial fibrillation or atrial flutter; this is started
14days after the event in the case of stroke and
immediately in the case of TIA. Other indications for
initiating anticoagulation include a cardiac source
of embolism, cerebral venous thrombosis or arterial
dissection. The risks and benefits of anticoagulation
need to be considered and discussed with the patient.
Anticoagulation is avoided in the first 2weeks
following an acute cardioembolic stroke because of the
risk of haemorrhagic transformation.
• Statins are recommended as primary prevention for
patients with a 10-year risk of developing cardiovascular
disease of 10% or more. In people with established
cardiovascular disease, statin therapy should be started.
CLINICAL NOTES
BLOOD PRESSURE CONTROL IN ACUTE
STROKE
• According to National Institute for Health and
Care Excellence guidelines, antihypertensive
medication is not recommended unless a
hypertensive emergency occurs and at least
one of the following is present: hypertensive
COMMUNICATION
If the patient is unconscious or consciousness
is severely impaired, a decision as to the most
appropriate degree of intervention should involve
relatives/the next of kin. Factors to consider
include prognosis, quality of life and if the patient
had expressed any wishes in this regard.
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