haemorrhagic stroke diagram

Definition of stroke/cardiovascular accident

Acute neurologic injury that occurs as a result of ischemic infarction or bleeding into part of the brain manifested by rapid onset of focal CNS signs and symptoms with or without a focal higher cerebral dysfunction (e.g. aphasia, hemisensory loss, visual defect) lasting >24 hours.

Epidemiology

  • It is a common medical emergency with an annual incidence of between 180 – 300 per 100,000
  • Stroke is the third most common cause of death in the developed world after cancer and ischemic heart disease

Race

  • In US  stroke has a higher incidence in the black population than in the white population. Hispanics have a lower overall incidence of stroke

Sex

  • In patients younger than 60 years, the incidence of stroke is greater in males (3:2 ratio).

Age

  • Stroke can occur in patients of all ages, including children.
  • Risk of stroke increases with age, especially in patients older than 64 years, in whom 75% of all strokes occur.

Risk factors

Unmodifiable factors

  • Age
  • Sex: Male>female
  • Ethnicity- lowest risk among Hispanics
  • History of prior stroke
  • Heredity
  • Pregnancy

MODIFIABLE

  • Hypertension
  • Diabetes mellitus
  • Heart disease
  • Atrial fibrillation
  • Carotid disease- Asymmetrical bruit Stenosis
  • Smoking
  • Obesity
  • Physical inactivity
  • Excessive alcohol consumption
  • Hypercholesterolemia
  • Blood disorders

Clinical Classification

  • Transient ischemic attack(TIA)

                The standard definition of TIA requires that all neurologic signs and symptoms resolve within 24 hours regardless of whether there is imaging evidence of new permanent brain injury.

  • Stroke: reserved for events in which symptoms last for > 24 hours.
  • RIND (Reversible Ischemic Neurological Deficit); symptoms persist beyond 24hrs but resolve within one week.
  • Stroke-in-evolution (progressing stroke): Stroke in which the focal deficit worsens after the patient first presents (i.e. increasing volume of infarction).
  • Completed stroke: Means a focal deficit persists and is not progressing.

Types  of Stroke

  • Two major types:
    1. Ischemic stroke (85%) occurs either due to;
  • thrombosis
  • embolism
  • systemic hypoperfusion

2)Hemorrhagic  strokes (15%)which can occurs in following areas;

  • intracerebral
  • subarachnoid

Ischemic stroke: Thrombosis

  • Thrombosis refer to local in situ obstruction of an artery
  • Are either large or small vessel disease.

 

1) Large vessel disease ;

Large vessels include both the extracranial (common and internal carotids, vertebral).  And intracranial arterial system (Circle of Willis and proximal branches)

  • Pathologies affecting large extracranial vessels include: Atherosclerosis, Dissection , Takayasu arteritis , Giant cell arteritis , Fibromuscular dysplasia.
  • Pathologies affecting large intracranial vessels include: Atherosclerosis, Dissection, Arteritis/vasculitis, Noninflammatory vasculopathy, Moyamoya syndrome Vasoconstriction.

   Note – atherosclerosis is most commonest in both.

Extracranial  large  vessels

  • In patients with thrombosis, the neurologic symptoms often fluctuate, remit, or progress in a sputtering fashion

 

Small vessel disease (30%): affect the intra cerebral arterial system, specifically the penetrating arteries of the vertebral, basilar and arteries of circle of Willis.

  • Deep Structures supplied are : Basal ganglia, internal capsule, thalamus & pons
  • Thrombosis in small vessels is due to

a.) lipohyalinosis : lipid hyaline built up distally due to hypertension & fibrinoid degeneration

b.) atheroma formation at their origin or in the parent large artery, extending into the orifices of the small arteries (atheromatous branch  disease).

  • Stroke due to obstruction of these vessels is referred to as a lacunar infarct.
  • Symptoms develop quickly, within hrs to a few days.

 

Ischemic strokes: Embolic

  • Divided into four categories
    1. Known cardiac source; eg patient with heart disease, congestive cardiac failure.
    2. Possible cardiac / aortic source after TTE/TEE (Transthoracic Echocardiography/ Transesophageal Echocardiography)
    3. Artery to artery embolism
    4. Unknown source of embolism
    5. Symptoms are abrupt, maximal at onset & depend upon the region of the brain rendered ischemic.

Trial of Org 10172 in Acute Stroke Treatment
(TOAST) CLASSIFICATION

  • It classifies ischemic strokes into 5 subtypes using clinical features & ancillary diagnostic studies including neuro-imaging
    1. Large artery atherosclerosis (LAA)
    2. Cardioembolism
    3. Small vessel occlusion
    4. Strokes of other determined etiology
    5. Strokes of other undetermined etiology (cryptogenic) which can be due to; negative evaluation, Incomplete evaluation

Pathophysiology of Ischemic Stroke

  • Acute occlusion of vessel> reduction in blood flow to brainà> ischemia / infarction
  • A fall in cerebral blood flow to zero causes death of brain tissue within 4–10 min
  • Values <16–18 mL /100 g tissue / min cause infarction within an hour; & values <20 mL/100 g tissue / min cause ischemia without infarction unless prolonged for several hours or days.
  • NB – tissue surrounding the core region (umbra) of infarction is ischemic but reversibly dysfunctional and is referred to as ischemic penumbra

Pathways of Focal Cerebral Infarction in ischemic strokes

Distinct pathways

  1. Necrotic pathway in which cellular cytoskeleton breakdown is rapid, due principally to energy failure of the cell. Occur in umbra region.
  2. Apoptotic pathway in which cells become programmed to die. Occur in the penumbra.

Necrotic pathway: ischemic cascade

  • Ischemia produces necrosis by starving neurons of glucose, which results in failure of mitochondria to produce ATP. Without ATP, membrane ion pumps fail & neurons depolarize, allowing intracellular calcium to raise ↑.
  • Cellular depolarization also cause glutamate release from synaptic terminals; ↑ EC glutamate induce neurotoxicity by activating postsynaptic glutamate receptors that increase neuronal calcium influx.
  • Free radicals are produced by membrane lipid degradation & mitochondrial dysfunction: cause catalytic destruction of membranes & likely damage other vital functions of cells

Net effect

  • The resultant overload in intracellular Ca2+ appears to be especially toxic & may exceed the ability of the neuron to extrude or sequester the cation.
  • This results in sustained activation of a variety of calcium-sensitive enzymes, including proteases, phospholipases, and endonucleases, leading to cell death.

Hemorrhagic strokes

Two subtypes:

  1. Intra – cerebral (ICH) / parenchymal
  2. Subarachnoid Hemorrhage (SAH)

Causes/Etiology

  • Hypertension (about 60%)
  • Trauma
  • Bleeding diathesis
  • Amyloid angiopathy
  • Illicit drug use (cocaine, amphetamin)
  • Vascular malformations.

Less frequent causes: bleeding into tumor, aneurysmal rupture & Vasculitis

Pathophysiology

  • The bleeding is directly into the brain, forming a localized hematoma that spreads along white matter pathways.
  • Accumulation of blood occurs over minutes or hours; the hematoma gradually enlarges by adding blood at its periphery.
  • Headache, vomiting, and a decreased level of consciousness develop if the hematoma becomes large enough to increase intracranial pressure or cause shifts in intracranial contents.

Diagnosis involves the following;

History taking

Symptoms include the following:

  1. Sudden numbness or weakness of face, arm, or leg, especially on one side of the body.
  2. Confusion of sudden onset, difficulty in speaking or understanding.
  3. Progressive sudden deterioration of vision of one or both eyes.
  4. Sudden difficulty in walking, dizziness, and loss of balance or coordination.
  5. Severe headache with no known cause.

 

Establish the time the patient was last normal is especially critical when thrombolytic therapy is an option.

Rule out risk factors for atherosclerosis and CVS D’SES e.g.  hypertension  and diabetes( DM).

Also rule out history of smoking, alcohol, high cholesterol levels. History of drugs, trauma.

Physical exam;

Physical examination is directed toward 5 major areas:

  • Assessing the airway, breathing, and circulation (ABCs),
  • Defining the severity of the patient’s neurologic deficits
  • Identifying potential causes of the stroke
  • Identifying potential stroke mimic; e.g seizures, brain tumor, systemic infections and
  • Also identifying comorbid conditions

 

General exam; vitals *blood pressure.

  • Head and neck exam; Contusions, lacerations, and deformities may suggest trauma as the cause for the patient’s symptoms. Auscultation of the neck may elicit a bruit, suggesting carotid disease as the cause of the stroke.
  • Cardiac: Cardiac arrhythmias, such as atrial fibrillation, are found commonly in patients with stroke.

Neurological exam;

The neurologic examination must be thorough; able to localise  which site has been affected based on neurological deficits.

  • A useful tool in quantifying neurological impairment is the National Institutes of Health Stroke Scale (NIHSS).
  • It focuses on 6 major areas of the neurologic examination: (1) level of consciousness, (2) visual function, (3) motor function, (4) sensation and neglect, (5) cerebellar function, and (6) language. The NIHSS is used most by stroke teams.

Management of stroke include the following measures;

Investigations

  • CBC- anemia, SCD, polycythemia, thrombocytosis,
  • RBS- hypoglycemia may mimic stroke
  • Coagulation profile
  • Cardiac enzymes- MI may occur concurrently
  • ABG(Arterial blood gas test)
  • EEG (Electroencephalogram)
  • Renal function tests
  • HIV test
  • Pregnancy test
  • ECG

Imaging

  • CT scan remains the commonest modality used
  • Not very sensitive in the first 6 hours
  • Findings that can suggest ischemic changes relatively early include loss of the gray-white matter interface, loss of sulci, and loss of the insular ribbon are subtle signs of early ischemia

CT scan may demonstrate other causes of the patient’s symptoms including;

  •   Neoplasm
  •   Epidural
  •   Subdural hemorrhage
  •   Eneurysm
  •   Abscess
  •   Arteriovenous malformation
  •   Hydrocephalus.

CT angiography can demonstrate the vascular occlusion and areas of perfusion deficits .

Diffusion-weighted MRI (DW-MRI) can detect areas of ischemic brain injury earlier in the evolution of ischemia than standard T1/T2-weighted MRI images or CT scan by detecting changes in water molecule mobility

Treatment

  • Observe ABCs principles
  • Stabilize the patient

Supportive cares

1)Do Blood glucose levels

  • Correct hypoglycemia if present.
  • Treat hyperglycemia if rbs >11mmol/l because it may increase the infarct volume therefore use insulin to normalize levels.

2)Correct BP- see below.

3)Cardiac monitor- continuous monitoring for ischemic changes or Atrial fibrillation.

4)Hydration; intravenous fluids- avoid D5W and excess fluid admin- use normal saline  ( not >50ml/h).

Nil per oral initially due to  risk of aspiration; avoid oral intake until swallowing is assessed because dysphagia is common after stroke.

6) Oxygen  therapy if SaO2 <90% or patient is hypotensive.

7) Temp- ensure normothermia-use acetaminophen intravenous. Raised temp increase infarct volume.

8) Rehabilitation

  • Physiotherapy – It helps to prevent pressure sore, Contractures
  • Occupational Therapy- Speech therapy, Recreational therapy

9) Catheterization –to  prevent urinary tract infection

10) Fibrinolytics within 3 hrs of ischaemic stroke, antiplatelets, anticoagulants  for Ischaemic strokes

10) Surgical  intervention – Craniotomy, surgical evacuation, Neurosurgical decompression

Some to note;

BP control:

  • Hypertensive ischemic stroke patients with a moderate elevation of Bp (up to 180/110 mmHg) may not require antihypertensive therapy. Early BP reduction may decrease cerebral perfusion and increase infarction.also the BP normalizes with few
  • If any of the following is present treat HTN regardless of BP; hypertensive encephalopathy, aortic dissection, acute renal failure, acute pulmonary edema, acute myocardial infarction, severe hypertension ( > 220/120 mmHg).
  • Avoid >10% reduction in diastolic blood pressure or >25% reduction in systolic blood pressure within first 24%hrs unless values exceed SBP >220, DBP >115
  • Drugs of choice: labetalol, Enalapril, Sodium nitroprusside, Nicardipine

Antiplatelatet

  • The Chinese Acute Stroke Trial (CAST) and the International Stroke Trial (IST) are 2 large studies in which investigators evaluated aspirin 160-300 mg/d within 48 hours of ischemic stroke symptom onset.
  • Compared with no treatment, aspirin resulted in a 1% absolute reduction in risk of stroke and death in the first few weeks.
  • At later time points (e.g. 6 months), aspirin had absolute reduction of approximately 1% for death or dependence.
  • Aspirin reduces the risk of early recurrence .

Rehabilitation

  • The American Stroke Association guidelines for rehabilitation focus on 6 major areas, as follows;
    • Preventing, recognizing, and managing comorbid conditions and medical complications
    • Training for maximum independence
    • Facilitating maximum psychosocial coping and adaptation by patient and family
    • Preventing secondary disability by promoting community reintegration, including resumption of home, family, recreational, and vocational activities
    • Enhancing quality of life in view of residual disability
    • Preventing recurrent stroke and other vascular conditions

Types of  stroke rehabilitation

Physical Therapy (PT)

  • Walking, range of movement

Occupational Therapy (OT)

  • Taking care of one’s self

Speech Language Therapy

  • Communication skills, swallowing, cognition

Recreational Therapy

  • Cooking, gardening

Stroke recovery

  • 10% of stroke survivors recover almost completely
  • 25% recover with minor impairments
  • 40% experience moderate to severe impairments requiring special care
  • 10% require care within either a skilled-care or other long-term care facility
  • 15% die shortly after the stroke

Written by Doc  Bob

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