This document provides an overview of the management of acute stroke. It defines stroke and transient ischemic attack, and discusses the epidemiology, classification, risk factors, pathophysiology, clinical presentation, diagnosis, management, complications and prognosis of stroke. The management involves resuscitation, reperfusion therapies like thrombolysis and thrombectomy, treating complications, secondary prevention including blood pressure and diabetes control, and rehabilitation. The document emphasizes the importance of specialized stroke units and timely management to improve outcomes for patients with acute stroke.

1. Management of Acute
Stroke
BY
DR. IBRAHIM ADAMU
DEPT. OF INTERNAL MEDICINE
STATE SPECIALIST HOSPITAL, GOMBE
31ST JANUARY, 2023

2. OUTLINE
 Introduction
 Epidemiology
 Classification
 Risk factors
 Pathophysiology
 Clinical presentation
 Management
 Conclusion
 References

3. INTRODUCTION
 Cerebrovascular diseases include some of the most common and
devastating disorders
 Major cause of adult disability
 The word “stroke” was first introduced into medicine in 1689 by
William Cole in a ‘physico-medical essay concerning apoplexies’
Apoplexy, from the Greek word meaning “to struck down with
violence," first appeared in Hippocratic Circa 400 BC writings
which describe this phenomenon.

4. DEFINITION
Stroke
◦ ‘Rapidly developing focal (or global) disturbance of cerebral
function, lasting 24 hours or longer, or leading to death, with no
apparent cause other than of vascular origin’ (WHO 1970)
Transient Ischemic attack (TIA)
◦ ‘Episodes of temporary and focal dysfunction of vascular origin,
which are variable in duration, commonly lasting from 2 to 15
minutes, but occasionally lasting as long as a day (24 hours)
(WHO 1975)

5. DEFINITION
Stroke : Clinical syndrome of rapidly evolving focal disturbance of
cerebral function, with no apparent cause other than of vascular
origin with an objective neuroimaging evidence of infarcton
irrespective of duration of symptoms.
TIA : a transient episode of neurological dysfunction caused by focal
brain, spinal cord, or retinal ischemia without objective evidence of
acute infarction
The risk of developing a stroke after a hemispheric TIA can be as high as 20% within the first month, with
the greatest risk within the first 48 hours.

6. EPIDEMIOLOGY
 Common neurological emergency associated with morbidity and
mortality
 Stroke is the 4th most common neurological disorder after
headache, epilepsy and neuropathy
 Someone suffers a stroke every 53 seconds and someone dies
from stroke every 3.3 minutes
 Second leading cause of preventable deaths in adults worldwide.
 15 million cases annually [WHO]
- 5 million deaths
- 5 million left with disability
- 5 million recover

7. EPIDEMIOLOGY
 Male : Female = 1.7:1
 Incidence Increases with rising age (0.5/1000 at <40yrs, 10-
12/1000 at 40yrs, 70/1000 at 70yrs)
3rd leading cause of death in USA and 0.6% of admission
 In Africa, stroke accounts for 0.9- 4% of hospital admissions and
2.8-4.5% of total deaths
 A study in Lagos reported that stroke accounts for 1.14 per 1000
medical admissions and 1 out of every 14.8 deaths
 In a study conducted in FTHG showed that stroke account for 8.9%
of medical admissions and 62% of the subjects where male

8. EPIDEMIOLOGY
 Among stroke survivors
- 30% require assistance with activities of daily living
- 20% require assistance with ambulation and
- 16% institutional care.

9. CLASSIFICATION
Broadly classified into pathologic types
1. Infarctive/Ischemic stroke (80%)
i) Thrombotic (50%)
ii) Embolic (30%)
iii) Small vessel stroke( lacunar)
iv) Hypoperfusion
2. Haemorrhagic Stroke (20%)
i) Intra-cerebral haemorrhage (ICH)-15%
ii) Subarachnoid haemorrhage (SAH)-5%

10. CLASSIFICATION OF STROKE

11. CLASSIFICATION
 Anterior Circulation stroke
◦ Total (TACS)
◦ Partial (PACS)
 Posterior Circulation Stroke (POCS)
(OxfordshireCommunityclassification)

12. RISK FACTORS
Non-modifiable
◦ Age
◦ Gender
◦ Race Black
◦ Prior stroke
◦ Family History
◦ Migraine with aura

13. RISK FACTORS
Modifiable risk factors
High blood pressure
Cigarette smoking
Transient ischemic attacks
Heart disease
Diabetes mellitus
Hypercoagulopathy
Systemic illnesses e.g CKD, SCDx
Alcohol consumption
Obesity
Sedentary life style
Homocystenaemia
Antiphospholipid syndrome
Drugs e.g OCP, HRT, cocaine, and
steroids
Infectons e.g HIV, CMV, Herpes
simplex

14. PATHOPHYSIOLOGY
Infarctive Stroke
 Cerebral auto-regulation is lost and cerebral blood flow will
depend on blood pressure
 There is attempt at mobilization of collateral circulation following
occlusion of cerebral blood vessel:
 Inner core of infarct (umbra) has CBF 10 mls/100g/min, this area
is energy depleted with disruption membrane ion transport and
mitochondrial failure leading to release of proteolytic enzymes and
ultimately liquefactive necrosis

15.  The surrounding core area
(penumbra) has CBF 10-
20mls/100g/min
 The penumbra tissue looses
electrical activity but can be
salvaged if blood flow is
restored during the
therapeutic window period
(3-6hrs)
 Reduction in BP or
dehydration will thus worsen
ischemia
PATHOPHYSIOLOGY

16. PATHOPHYSIOLOGY
Hemorrhagic stroke
 Chronic hypertension with
charcot-bouchard aneurysms and
berry/saccular aneurysms,
congenital AV malformations,
amyloid angiopathy,
anticoagulant therapy and drugs
all results to rupture of cerebral
vessels
 Bleeding into the surface of the
brain is commonly due to
aneurysm while bleeding into the
tissue of the brain is commonly
caused by HTN

17. PATHOPHYSIOLOGY
Explosive entry of blood into the brain parenchyma with structural
disruption of neuronal activity by
• Compression of neurons and vessels leading to additional ischemic
damage
• Vasospasm from direct neurotoxicity of blood
• Raised ICP from Cerebral oedema
• Large hemorrhages can cause trans-tentorial coning and rapid death due
to severely elevated intracranial pressure
Predilection sites for bleed includes putaminal (35%), lobar (25%), thalamic (20%), cerebellar (8%),
pontine (7%)

18. Hemorrhagic
 - Longstanding hypertension with poor compliance
 - Associated with emotional excitement/activity
 - Headache & vomiting
 - Alteration in level of consciousness
 - Seizures
CLINICAL PRESENTATION

19. CLINICAL PRESENTATION
Thrombotic
- History of TIA
- Stroke is progressive
- Usually happens in the early morning hours

20. CLINICAL PRESENTATION
Embolic
- Abrupt with no warning
- Patients with known heart disease like VHDx, AF, IHD etc.
- Maximal deficit at onset
- Rapid recovery

21. Stroke Syndromes
1. MCA Stroke Syndrome
- Dominant hemisphere
- Non-dominant hemisphere
2. ACA Stroke Syndrome
3. PCA Stroke Syndrome

22. CLINICAL PRESENTATION
General signs
 Fever
 Hypertension
 Elevated blood sugar
 Precordium- murmurs, cardiac arrhythmias
 Altered level of consciousness or coma
 Neck- carotid bruit, nuchal rigidity
 Eye- retinal hemorrhages
Anisocoria (pupillary dilatation/constriction)

23. PHYSICAL EXAMINATION
Physical is directed toward 5 major areas:
(1) assessing the airway, breathing, and circulation (ABCs)
(2) defining the severity of the patient's neurologic deficits (level of
consciousness, visual function, motor function, sensation and
neglect, cerebellar function, and language)
(3) identifying potential causes of the stroke
(4) identifying potential stroke mimics
(5) identifying comorbid conditions

24. DIAGNOSIS
 History
 Exam
 Imaging
◦ CT Scan
◦ MRI
◦ CT/MR Angiography

25. CT SCANS
 CT is highly sensitive for the diagnosis of haemorrhage in the
acute setting
 Early CT Scan is valuable to make diagnosis and to exclude stroke
mimics

26. MRI
 MRI is more sensitive than CT for the diagnosis of stroke but
changes are not imminent in the early acute stage
 Although new generation CT scanners may identify subtle
indicators of infarction within six hours of stroke onset in a
significant number of patients

27. Ancillary investigation
1. Lipid profile
2. Glucose
3. Urea/electrolytes/creatinine
4. Urinalysis
5. ECG /Echocardiography
6. Chest X-ray
7. FBC & Clotting profile
Others: Carotid USS, Homocysteine levels, Cardiac troponins,
Genotype, Viral screen

28. DIFFERENTIALS
 Hypoglycemia
 ICSOL
 Brain abscess
 Seizure disorder
 CNS Tumour
 Hypertensive encephalopathy
 Wernicke’s encephalopathy
 Drugs e.g Phenytoin

29. MANAGEMENT
 Management of stroke should ideally be in a dedicated ‘stroke
unit’
 The principles of management of stroke
- Resuscitation
- Reperfusion
- Treat or prevent acute complications
- Secondary prevention
- Rehabilitation

30. Reperfusion therapies
1. Thrombolysis - IV recombinant tissue plasminogen activator -
rTPA, (0.9mg/kg)
2. Thrombectomy - (mechanical removal)
3. Hemicraniectomy – Massive cerebral edema, cerebellar
hematoma

31. Treatment of acute complications
Neurological
•Raised ICP
•Seizure
•Hydrocephalus
Non-neurological
CHEST: Aspiration pneumonia, P.E
ENDOCRINE: SIADH, Hyperglycemia, Hypoglycemia
CVS: Arrhythmias, Hypertension
GIT: Constipation

32. Treatment of acute complications
 Hypertension: Target is <220/120mmHg (MAP <145) in ischemic
stroke and <160/90mmHg (MAP 135) in hemorrhagic stroke.
Presence of end organ damage may require urgent BP reduction
 Studies have shown that use of Aspirin as 300mg in the first 24
hrs improves morbidity. It is given for 2 weeks then tapered
 The use of anti-oxidant has no place now in management of
stroke. Infact Vit-E may worsen hemorrhagic stroke
 The IVF of choice in stroke is N/S

33. Secondary prevention
 Prevent late complications e.g depression, decubitus ulcer, joint
contractures
 Blood pressure control
◦ Diuretics +/- ACE inhibitors or ARBs
 Diabetes management
 Lipid management
 Smoking cessation
 Alcohol moderation
 Weight reduction
 Anti-platelet agents/Anti-coagulants

34. Rehabilitation
 The aim is to restore function
- Physiotherapy
- Speech therapy
- Occupational therapy

35. COMPLICATIONS
 Acute (< 7 days) e.g Cerebral edema, Aspiration pneumonitis,
Hypoglycemia
 Subacute (2wk – 3mo) e.g DVT, UTI, Chest infections, Sores,
Malnutrition
 Chronic ( > 3mo) e.g Contractures, Depression, Paraplegia

36. PROGNOSIS
The following are associated with poor prognosis
◦ Increased patient age
◦ Raised temperature
◦ Hyperglycemia
◦ Increased blood pressure
◦ Increased stroke severity
◦ Access to specialist care
◦ Availability of stroke facilities
Chances of mortality decreases significantly after the first week

37. CONCLUSION
 Stroke is a common neurological emergency and a major cause of
adult disability and mortality world-wide
 Despite newer drugs and advances in medical intensive care
technology, the mortality and long-term morbidity rates is still
significantly high
 Incidence varies among different parts of the world and increases
with age
 Risk factors can be modifiable and non-modifiable, with
hypertension and diabetes as one of the most recognized risk
factors especially among the elderly
 Outcome depends on type, time of presentation, facilities available
and presence of co-morbid states
 In poor countries, the problem is compounded by increasing level
of poverty, ignorance and poor drug compliance etc.

38. REFERENCES
 Lecture notes on cerebrovascular disorders by Dr. Fadimatu Kabir
delivered on 24th February, 2022
 Robert M. Kliegman, Bonita F. Stanton, Joseph W. St. Geme III,
Nina F. Schor, & Richard E. Behrman ‘Update on management of
Stroke’ The New England Journal of Medicine. Article No.
10.1056/NEJMoa223456
 Professor Parveen Kumar, Dr. Micheal Clark MD Textbook of
Clinical Medicine 8th edition
 CT Patterns of Stoke in Adults Patients at FTHG by Dr Yunusa
Dahiru Mohammed
 Website: http://www.emedicine/medscape.com/stroke50763.
Accessed on Friday, 27th March 2023, 3:36pm