MANAGEMENT OF ACUTE
STROKE
DR. EMMANUEL CHUKWUEMEKA MBAH
HOUSE OFFICER, NEUROLOGY UNIT
UNIVERSITY OF UYO TEACHING HOSPITAL
1
Outline
• Introduction
• Epidemiology
• Risk Factors for Stroke
• Stroke in the Young
• Types of Stroke
• Ischaemic Stroke
• Intracerebral Haemorrhage
• Subarachnoid Haemorrhage
• Complications of Stroke
• Conclusion
• References
2
Introduction
• The definition of stroke over the years has been a subject of debate
and controversy amongst leading experts in neurosciences, neuro
medicine, neurosurgery and neuroradiology.
• The WHO in 1988 defined stroke as a rapidly developed focal or
global cerebral dysfunction of vascular origin lasting more than 24
hours or leading to death while transient ischaemic attack is any focal
cerebral ischaemic event with symptoms lasting less than 24 hours.
• This old definition misclassified at least 1/3 of the patients with stroke
and does not suggest medical emergencies hence impeding the
administration of acute stroke therapies.
3
Introduction
• The 2013 AHA/ASA Expert consensus defined stroke as any objective
evidence of permanent brain, spinal cord, or retinal cell death due to
a vascular cause based upon pathological or imaging evidence with or
without the presence of clinical symptoms.
• This definition, however, fails to take cognizance of the peculiarities
faced by health systems in developing countries where access to this
objective evidence is hampered by financial constraints, and the
unavailability of pathological or imaging devices in many hospitals
and delays in getting results if eventually done.
• Hence, doctors in the aforesaid countries rely on the clinical
symptoms and examination to take decisions.
4
Epidemiology
• Stroke is the leading cause of disability worldwide and the second leading
cause of death.
• The Global Stroke Factsheet released in 2022 reveals that the lifetime risk
of developing a stroke has increased by 50% over the last 17 years and now
1 in 4 people is estimated to have a stroke in their lifetime.
• From 1990 to 2019, there has been a 70% increase in stroke incidence, a
43% increase in deaths due to stroke, a 102% increase in stroke prevalence,
and a 143% increase in Disability Adjusted Life Years (DALY).
• The most striking feature is that the bulk of the global stroke burden (86%
of deaths due to stroke and 89% of DALYs) occurs in lower and lower-
middle-income countries. This disproportionate burden experienced by
lower and lower-middle-income countries has posed an unprecedented
problem to families with fewer resources.
5
Epidemiology
• The current prevalence of stroke in Nigeria is 1.14 per 1000 while the
30-day case fatality rate is as high as 40%.
• 75% – 80% of all strokes are ischaemic while 20% to 25% are
haemorrhagic.
• The rule of “thirds” is used in stroke as a clinical guide: one-third of
the patients who have a stroke recover, either completely or with
minimal residual disability; one-third recover with residual disability;
and about one-third die.
• It is estimated that 87% of stroke deaths occur in the developing
countries
6
Risk Factors for Stroke
• The risk factors for stroke can be modifiable and non-modifiable
• Modifiable risk factors include:
• Hypertension: The most documented modifiable risk factor for stroke.
Risk begins with a BP of 115/75mmHg and doubles with each
20/10mmHg.
• Smoking: The more pack years a patient has, the higher the chances
of having all forms of stroke
• Diabetes: increases the risk of ischaemic stroke independently
• Dyslipidaemia: the higher the number of mmol/l of total cholesterol
the higher the risk of ischaemic stroke.
7
Risk Factors for Stroke
• Diet: meals with high dietary sodium and low potassium increase the risk
of stroke.
• Physical Inactivity: Poor exercise and a sedentary lifestyle increase the risk
of ischaemic stroke.
• Obesity and Body Fat Distribution: Increased adiposity is associated risk of
stroke.
• Atrial fibrillation: associated with 4X to 5X chances of ischaemic stroke.
• Oral contraceptives
• Substance abuse
• Post menopausal state
8
RISK FACTORS
• Non-Modifiable Risk Factors
• Age: the risk of stroke generally increases with age
• Sex: more common in males than in females
• Family history increases the risk of a stroke
• Low Birth Weight
9
STROKE IN THE YOUNG
• Stroke in the young is said to occur in individuals less than 45 years of
age.
• About 40% of stroke in the young are haemorrhagic.
• Some of the causes include:
• Heroine, cocaine, methamphetamine
• Oral contraceptives
• HIV/AIDS
• Coagulopathies
• Vasculitis
• Haemoglobinopathies etc
10
TYPES OF STROKE
• Strokes can be classified into three broad groups:
• Ischaemic Stroke / Cerebral Infarction (80%)
• Haemorrhagic (20%)
• Intracerebral Haemorrhage (15%)
• Primary Subarachnoid Haemorrhage (5%)
11
ISCHAEMIC STROKE
12
Introduction
• Ischaemic stroke is “an episode of neurological dysfunction caused by
focal cerebral, spinal, or retinal infarction” (AHA/ASA)
• Infarction refers to cell death that is attributable to ischaemia and
demonstrated by pathological evidence (during a post-mortem
examination) or imaging evidence (with computed tomography or
magnetic resonance imaging) or clinical evidence (symptoms lasting
24 hours or longer)
• Ischaemic stroke leads to a disruption of cerebral autoregulation
(cerebral perfusion pressure = mean arterial pressure MINUS
intracranial pressure, i.e, CPP = MAP - ICP) 13
Pathogenesis of
Acute Ischaemic
Stroke
14
Pathogenesis
• As necrosis sets in, two portions of the ischaemic brain tissue can be
delineated;
➢The umbra (the already necrosed core; irreversibly dead and cannot be
salvaged)
➢The penumbra (the area surrounding the umbra; can be salvaged if perfusion
is restored quickly enough; otherwise, it eventually undergoes necrosis too)
• Salvaging this ischaemic penumbra is the main aim of the early
treatment of acute ischaemic stroke
15
16
Time is Neuron!
• Normal Cerebral Blood Flow = 55ml/100g/min
• <25ml – diffuse EEG slowing
• <15ml – electrical activity ceases
– Function ceases (Penumbra)
– “functionally impaired but structurally still viable tissue”
– “at risk but still salvageable”
• <10ml - irreversible
– Cell death ensues (Umbra)
17
Mechanisms of Ischaemic Stroke
• Atherothrombosis (50%): It occurs when a blood clot forms on an
atherosclerotic plaque within a blood vessel in the brain and blocks blood
flow to that part of the brain.
• Cerebral small vessel disease (25%): a common cause of stroke and an
important contributor to age-related cognitive decline and risk for
dementia. The common pathologies underlying CSVDs are arteriolosclerosis
caused by aging, hypertension, cerebral amyloid angiopathy etc
• Cardioembolism (20%) from atrial fibrillation, left ventricular thrombi,
cardiac tumors, valvular vegetations, and paradoxical emboli
• Others/Cryptogenic (5%): cerebral ischemia of obscure or unknown origin.
18
Arterial Supply of the Brain
• There are two paired arteries that are responsible for the blood
supply to the brain; the vertebral arteries, and the internal carotid
arteries. These arteries arise in the neck and ascend to the
cranium.
• Within the cranial vault, the terminal branches of these arteries
form an anastomotic circle, called the Circle of Willis. From this
circle, branches arise which supply the majority of the cerebrum.
• Other parts of the CNS, such as the pons and spinal cord, are
supplied by smaller branches from the vertebral arteries
19
Arterial
supply of
the brain
20
Vascular (arterial)
territories of the brain:
ACA = anterior cerebral artery
MCA = middle cerebral artery
PCA = posterior cerebral artery
21
Clinical Features
• Typically, stroke symptoms develop suddenly
• The nature of symptoms depends on the area of the brain that is
affected PLUS the effect(s) of associated conditions like raised
intracranial pressure (arterial/vascular territories). This gives rise
to stroke syndromes which will be highlighted later.
• The most common clinical features include the inability to
speak, unilateral facial weakness, hemiparesis/hemiplegia, and
unilateral sensory disturbance.
• Others include visual field deficits, dysphagia, ataxia, headache,
vomiting, seizures, alteration in level of consciousness, etc.
22
Symptoms and Signs of Anterior Cerebral Artery
syndrome
• Weakness and Sensory loss
– Usually of the contralateral leg, worse distally
– Sensory loss is usually discriminative
– Pain and temperature and non-discriminative touch are
usually preserved or mildly perturbed.
• Language disturbance
• Callosal disconnection syndrome
• Incontinence
• Emotional disturbance and cognitive impairment
23
Clinical Syndromes of Middle Cerebral Artery
• Note that when collaterals have developed the deficits may
not be severe
• Contralateral hemiplegia
• Ipsilateral conjugate deviation of the eyes
• Hemianesthesia
• Hemianopia
• Aphasia
• Neglect
24
Clinical Syndromes of Posterior Cerebral Artery
• Hyperaesthesia
– Note that the ventral-tier thalamic nuclei are supplied by posterior
cerebral artery
• Dejerine – Roussy Syndrome
– Rapidly improving hemiparesis
– Hypesthesia
– Dyesthesia
– Hyperpathia
25
Clinical Syndromes of Posterior Cerebral Artery
• Visual field defects
• Visual Agnosia
• Prosopagnosia
• Kluver-Bucy Syndrome
– Infarction of undersurface of temporal lobe
– Restlessness, agitation, delirium, excessive reaction to visual,
auditory, and cutaneous stimuli
26
Vertebrobasilar Stroke Syndromes
• Double vision, gaze palsies
• Facial numbness; Facial weakness;
• Vertigo; Dysphagia, Dysarthria
• Crossed sensory loss (face and opposite side
of body)
• Crossed motor deficits (face and opposite side
of body)
• Ataxia, in-coordination; drop attacks;
• Motor or sensory loss in both arms or legs.
27
Initial Evaluation
• The goal of the initial evaluation of stroke patients includes:
• Ensuring medical stability, with particular attention to airway,
breathing, and circulation
• Quickly reversing any conditions that are contributing to the
patient's problem
• Determining if patients with acute ischemic stroke are
candidates for thrombolytic therapy
• Moving toward uncovering the pathophysiologic basis of the
patient's neurologic symptoms
28
Initial Evaluation
• Acute ischaemic stroke is a
medical emergency
• Early recognition (BEFAST
campaign) and prompt
intervention (time is brain!)
favour good outcome
• Ideally, initial evaluation and
treatment should begin with
pre-hospital emergency
medical services (where
available)
29
Initial Evaluation
• Assessing vital signs and ensuring stabilization of airway, breathing, and
circulation is part of the initial evaluation of all patients with critical
illness, including those with stroke.
• Give supplemental oxygen if SpO2 is less than 95%
• Check the random blood glucose (and correct hypoglycaemia or
hyperglycaemia as applicable)
• Do urgent Brain non-contrast computed tomography scan of the brain
or brain MRI
• Establish intravenous access and send blood for initial investigations
(clotting profile, serum electrolytes, etc)
30
Initial Evaluation
• Take a short focused history to emphasize the following;
➢Confirm symptom(s) of stroke
➢Actual time of onset of symptom(s) (e.g, 8.24am, 6.37pm, etc; not
merely expressing it as 5 hours ago, 2 days ago, etc). Key in determining
eligibility for thrombolysis.
➢The course/evolution of the symptom(s)
➢Any previous stroke or transient ischaemic attack
➢Risk factors for stroke
➢Ask about possible stroke mimics
➢Current medications
➢Any treatment already given
31
Initial Evaluation
• Stroke Mimics • Stroke Chameleons
• Post-Ictal paralysis • Vertigo
• Hypoglycaemia • Isolated Monoplegia
• Delirium
• Migraine
• Functional disorders
• Brain Tumours
32
Initial Evaluation & Management…4
• A quick examination should go on simultaneously with the
history (determine the level of consciousness; ascertain the
presence and degree of neurological deficits; do a quick
cardiovascular system examination).
• The level of neurologic deficit is commonly assessed using
the NIHSS (National Institute of Health Stroke Scale)
33
34
Brain CT scan in Ischaemic stroke
35
Management of Ischaemic Stroke
• Resuscitation
• Reperfusion therapy
• Prevention of secondary brain injury
• Other supportive care
• Rehabilitation
• Secondary prevention of stroke
***Stroke care is essentially multidisciplinary in approach (a team
of different health professionals cooperate to provide stroke care)
***The best outcome is obtained when a stroke patient is
admitted into a “stroke unit” (a dedicated ward with specific staff)
36
Management of Ischaemic Stroke
• Stroke Unit
• Mounting evidence suggests that patients with acute stroke have better
outcomes when admitted to a hospital unit that is specialized for the care
of patients with all types of acute stroke.
• The precise components of an acute stroke unit vary between centers and
countries, but generally include a hospital ward with dedicated telemetry
beds that is continuously staffed by a team of physicians, nurses and other
personnel who specialize in stroke care.
• Additional components include prompt availability of neuroimaging (eg,
CT, MRI, various types of angiography, ultrasound, transcranial Doppler)
and cardiac imaging.
37
Management of Ischaemic Stroke
• Resuscitation
➢ABC of resuscitation
➢Give supplemental oxygen if SpO2 is < 94%
➢Establish intravenous access
➢Start IV 0.9% saline 1L 8hrly
➢Start IV 20% Mannitol 1g/kg amounting to 350mls x 6doses in a 70kg
man followed by 20mg of IV Frusemide
38
Management of Ischaemic Stroke
• Reperfusion therapy (this is the specific treatment of acute
ischaemic stroke aimed at the recanalization of the obstructed
artery and salvaging brain tissue): two evidence-based forms;
➢Intravenous thrombolysis
➢Mechanical thrombectomy
39
Management of Ischaemic Stroke
• Intravenous thrombolysis
➢Involves the urgent administration of intravenous alteplase (also known
as recombinant tissue plasminogen activator – rtPA) to lyse the clot
➢Must be given within 4.5 hours of the onset of stroke symptoms
(preferably within 3 hours)
➢It improves outcomes after a stroke
➢The patient must be at least 18 years old
➢The stroke deficit should be disabling
➢Brain CT should have excluded any form of intracranial haemorrhage
➢There are other equally important considerations
40
Contraindications to the use of IV alteplase
➢ Severe head trauma within 3 ➢ Blood pressure > 185/110
months mmHg
➢ Previous intracranial ➢ International normalized ratio
haemorrhage > 1.7
➢ Recent brain/spinal surgery ➢ Platelets < 100,000/mm3
(within 3 months) ➢ Brain CT scan showing an
➢ Gastrointestinal malignancy or extensive hypodensity > one-
bleeding (within 21 days) third of the cerebral
➢ Bleeding diathesis hemisphere
41
Management of Ischaemic Stroke
• Intravenous thrombolysis
➢Total dose given: 0.9 mg per kg body weight (MAXIMUM POSSIBLE
DOSE is 90 mg)
➢Give 10% of the calculated dose as a bolus
➢Give the remaining 90% as an infusion over 60 minutes
➢The most important complication is intracranial bleeding
➢There may also be angioedema 42
Management of Ischaemic Stroke
• Mechanical thrombectomy
➢Involves the use of a device attached to a catheter to remove the blood
clot
➢The approach is endovascular
➢Recommended only for ischaemic stroke due to occlusion of large
arteries
➢Must be carried out within 6 hours of onset of stroke symptoms
➢May be performed after initially giving alteplase
43
Management of Ischaemic Stroke
• Prevention of secondary brain injury
➢Treat hypoglycaemia (IV glucose)
➢Treat hyperglycaemia (soluble insulin or GKI infusion)
➢Treat fever (parenteral paracetamol)
➢Address possible raised intracranial pressure (nurse 30 degrees
head up; consider IV mannitol 0.5–1 g per kg body weight per
dose over 10-15 minutes; repeat 8-hourly; follow each dose with
20 mg of IV frusemide)
44
Management of Ischaemic Stroke
• Management of blood pressure
➢The optimal approach to the management of BP in acute ischaemic
stroke has not been determined
➢BP > 220/120 mmHg warrants a mild reduction
➢Any evidence of ongoing end organ damage (grade 3 or 4 hypertensive
retinopathy OR acute left ventricular failure) warrants a reduction
➢A mild hypertension (permissive hypertension) is allowed in the acute
phase
➢Use IV antihypertensives (like labetalol, nicardipine, esmolol, etc) when
indicated 45
Management of Ischaemic Stroke
• Other supportive care
➢Intermittent urethral catheterization
➢NPO in the first 24 hours (swallowing test; consider nasogastric tube,
percutaneous endoscopic gastrostomy tube)
➢Active infection surveillance (urinary tract infection, aspiration
pneumonia – prophylactic antibiotics not routinely recommended)
➢Deep venous thrombosis prophylaxis (ideally with intermittent
pneumatic compression device; consider Sc. Clexane 40 iu daily if no
contraindications)
➢Prevent decubitus ulcers (regular turning in bed, water bed/air bed)
46
Management of Ischaemic Stroke
Guggling Swallowing Score (GUSS)
47
Management of Ischaemic Stroke
• Rehabilitation
➢Physiotherapy
➢Occupational therapy
➢Speech therapy
48
Management of Ischaemic Stroke
• Secondary prevention of ischaemic stroke
➢Measures taken to prevent another stroke (via modification of risk
factors)
➢Oral aspirin 300 mg within 48 hours of stroke onset (continue with
300mg daily; an alternative is clopidogrel 75 mg daily)
➢Ensure BP and glycaemic control (where indicated)
➢Consider anticoagulation (in arrhythmias)
➢Treat dyslipidaemia
➢Lifestyle modification (healthier diet, weight reduction, smoking
cessation, alcohol cessation, adequate physical activity)
➢Carotid endarterectomy (in carotid artery occlusive disease) 49
SPONTANEOUS INTRACEREBRAL
HAEMORRHAGE
50
Introduction
• Stroke due to intracerebral haemorrhage (ICH) is defined as
“rapidly developing clinical signs of neurological dysfunction
attributable to a focal collection of blood within the brain
parenchyma or ventricular system that is not caused by
trauma” (AHA/ASA)
• If bleeding occurs within the brain parenchyma due to trauma,
it is not stroke
51
Aetiology
• Hypertension is by far the most important cause of
spontaneous intracerebral haemorrhage
• With chronic high blood pressure, degenerative changes occur
within intracerebral arteries that over time lead to the
development of aneurysms (Charcot-Bouchard aneurysms)
which can rupture to cause intracerebral haemorrhage (ICH)
52
Aetiology
• Hypertensive ICH tends to occur more commonly in the deeper
parts of the brain (thalamus, pons, basal ganglia and
cerebellum)
• Other important causes of spontaneous ICH
➢Cerebral amyloid angiopathy
➢Bleeding disorders
➢Anticoagulant use
➢Use of sympathomimetic drugs (amphetamine, cocaine, etc)
➢Haemorrhagic transformation of cerebral infarct
➢Arteriovenous malformations 53
Clinical Features
• The clinical features of ICH are similar to those of acute
ischaemic stroke (and will be determined by the area of the
brain affected)
• To a large extent, ICH patients tend to be more severely ill at
presentation with more severe depression in level of
consciousness and other features of raised intracranial
pressure as well as more marked elevations in blood
pressure.
54
Initial Evaluation & Diagnosis
• The initial approach to the workup (brain imaging & other
investigations) of a patient with suspected ICH should be as
previously discussed for acute ischaemic stroke
• The diagnosis of acute spontaneous ICH is confirmed if urgent
brain CT scan reveals a focal hyperdense lesion within the brain
parenchyma (that may or may not involve one/more
ventricles)
55
Brain CT scan in intracerebral
haemorrhage
56
Management
• Most general aspects of management of acute ICH are as for
acute ischaemic stroke (initial resuscitation and mgt of fever,
glucose derangements, and hypoxaemia)
• It is now recommended to rapidly reduce the blood pressure to
slightly less than 140/90 mmHg (persistently elevated BP favours
expansion of the haematoma leading to poor outcome)
• Use reasonable doses of short-acting intravenous
antihypertensives (such as labetalol, nicardipine or esmolol)
57
Management
• Address raised intracranial pressure (nurse 30 degrees head
up; IV mannitol)
• Stop any pro-bleeding medication (such as antiplatelets or
anticoagulants)
• Some patients with acute ICH may benefit from surgery
(ventriculostomy; haematoma evacuation; or
decompressive craniectomy) 58
Management
• Sometimes, a repeat brain CT scan is warranted if patients
deteriorate (to exclude worsening bleeding or severely raised
intracranial pressure
• Generally, the poor prognostic factors in ICH include:
➢Glasgow coma score ≤ 8 (*please manage in the intensive care unit)
➢Old age (especially ≥ 80 years)
➢Ventricular extension of the haemorrhage
➢Large haematoma volume (≥ 30 ml)
➢Haematoma in the posterior cranial fossa
➢Persistently elevated blood pressure
➢Others (such as seizures, infections, cardiac arrhythmias, etc)
59
Management
• Treat seizures if they occur (prophylactic anticonvulsants are
not recommended)
• Institute secondary preventive measures (BP control; review
antiplatelet or anticoagulant medications; dietary
modification and other aspects of lifestyle)
• Provide rehabilitation as required (physiotherapy,
occupational therapy, speech therapy)
60
PRIMARY SUBARACHNOID HAEMORRHAGE
61
Introduction
• Stroke due to subarachnoid haemorrhage (SAH) is defined as “rapidly
developing signs of neurological dysfunction and/or headache
because of bleeding into the subarachnoid space, which is not
caused by trauma” (AHA/ASA)
• Overall, the most common cause of SAH is trauma. However,
traumatic SAH is not stroke
• Non-traumatic SAH (stroke) = primary SAH or spontaneous SAH
62
Introduction
• SAH is the least common type of stroke but it may be the most
catastrophic in terms of outcome
• Subarachnoid haemorrhage occurs when there is a rupture of
one of the vessels that float within the subarachnoid space
• By far the commonest cause of non-traumatic primary SAH is
rupture of berry (saccular) aneurysm (and the term “aneurysmal
SAH” is frequently used synonymously with “primary SAH”
63
An illustration
of the
subarachnoid
space
64
65
66
Aetiology
• The following are conditions where brain aneurysms (and
possible rupture leading to SAH) tend to develop:
➢Autosomal dominant polycystic kidney disease
➢Ehlers-Danlos syndrome
➢Sickle cell anaemia
➢Neurofibromatosis type 1
➢Tuberous sclerosis
➢Arteriovenous malformations
➢Systemic lupus erythematosus
***Collagen component of the arterial wall
67
Clinical Features
• Headache (typically sudden and severe; “the worst headache of my
life”)
• Neck pain (due to meningeal irritation)
• Nausea/Vomiting
• Photophobia
• Alteration in level of consciousness (may range from drowsiness to
coma; due to raised intracranial pressure)
• Seizures
• Focal neurologic deficits (not commonly present; often indicates a
complication) 68
Clinical Features
• Complications of acute spontaneous SAH
➢Rebleeding
➢Hydrocephalus
➢Delayed cerebral ischaemia (due to vasospasm as a result blood
being in contact with the outside of intact arteries; if severe enough
may lead to focal infarction and, hence, focal neurologic deficits)
69
Brain with generalized atrophy & Hydrocephalus
Normal brain
70
Initial Evaluation & Diagnosis
• Resuscitate and offer prompt general measures
• Do urgent brain CT scan (as in any patient with suspected
stroke)
• Acute SAH is revealed as hyperdensities within the
subarachnoid space (including cerebrospinal fluid cisterns) on
CT scan
71
Brain CT scan appearance in Primary SAH
72
Diagnosis
• Occasionally, the brain CT scan may be negative even when
SAH has actually occurred (anaemia, mild bleeding, etc)
• If the suspicion for SAH remains strong and the CT is
negative, perform a lumbar puncture immediately (as long
as the CT scan has excluded raised intracranial pressure)
• The cerebrospinal fluid is initially bloody but later becomes
xanthochromic (and remains so for a few weeks) 73
Management
• Maintain blood pressure at about 150/90 mmHg
• Prevent the Valsalva manoeuvre which transiently raises the
intracranial pressure (a laxative such as liquid paraffin;
antitussive to prevent coughing; and catheterize the urethra to
prevent straining at micturition)
• Strict bed rest
74
Management
• Start oral nimodipine (a calcium channel blocker) 60 mg 4-
hourly for 21 days (to reduce the chance of vasospasm and
delayed cerebral ischaemia)
• Consider giving IV mannitol to treat raised ICP
• If severely ill, transfer to the ICU
• Perform a ventriculostomy if hydrocephalus has developed
75
Management
• A brain CT angiography (or magnetic resonance
angiography) is necessary to identify the culprit aneurysm
(and possibly other unruptured ones)
• Definitive treatment (which should be done as soon as
possible) involves one of the following;
➢Aneurysym coiling (an endovascular approach)
➢Aneurysm clipping (an open neurosurgical procedure)
76
77
Complications of Stroke
• Many different complications may arise in patients with
stroke from the time of onset all the way to weeks or
months after the stroke
• Some of these complications are immediately life-
threatening while others merely add to the morbidity of
stroke and the burden of the patient’s caregiver(s)
• It is recommended to be proactive in the prevention and/or
management of stroke complications 78
Complications of Stroke
• Stroke complications:
➢Nervous system – cerebral oedema, cerebral herniation
➢Cardiovascular system – cardiac arrhythmias, deep venous thrombosis
➢Respiratory system – aspiration pneumonia, orthostatic pneumonia,
central sleep apnoea, pulmonary embolism
➢Gastrointestinal system – regurgitation, constipation, faecal
incontinence, malnutrition
➢Genitourinary system – urinary tract infection, urinary incontinence
➢Musculoskeletal system – joint contractures, muscle spasticity,
decubitus ulcers
79
Conclusion
• Stroke is a disease of major public health importance in
Nigeria & mortality is still very high
• Recognition by patients and care providers that stroke is
a medical emergency will change the current picture
• Stroke is preventable and prevention is the only
affordable option for developing countries
80
References
1. ASA/AHA 2019 Guidelines on Management of Acute Stroke
2. Ekeh, Bertha. (2015). Stroke Recovery and its predictors in a
Nigerian Teaching Hospital. J of Clin and App Neuro 2015;
1:17-22. Journal of Clinical and Applied Neurosciences. 1. 17-
22.
3. Dr. A. Adebowale’s lecture note on Cerebrovascular Diseases
(2021)
4. Dr. M.B Fawale’s lecture note on Cerebrovascular Diseases
(2015)
81
Thank You for your time….
Any Question???
82
