Definition of Stroke
“Stroke is a clinical syndrome characterized by rapidly developing clinical symptoms and/or signs
of focal, and at times global, loss of cerebral function, with symptoms lasting > 24 hours
or leading to death, with no apparent cause other than that of vascular origin”.
Definition of Transient Ischaemic Attack (TIA)
“A Clinical syndrome characterized by an acute loss of focal cerebral or monocular function with
symptoms lasting < 24 hours and which is thought to be due to inadequate cerebral or
ocular blood supply as a result of arterial thrombosis or embolism”.
Cause & Pathophysiology
3 main causes of ischemic stroke:
- Atherothromboembolism (50%)
- Intracranial small vessel disease (penetrating artery disease) (25%)
- Cardiogenic embolism (20%)
- Others ( arterial dissection, trauma, vasculitis (primary/secondary), metabolic disorders, congenital disorders and other less common causes such as migraine, pregnancy, oral contraceptives, etc.)
Atheroma affects mainly the large and medium sized arteries at places of confluence, branching or tortuosity of vessels.
The process begins in childhood as fatty streaks and progresses over years with gradual buildup of fibrolipid plaque and infiltration of inflammatory cells, eventually narrowing the vessel lumen. The final step occurs with ulceration and platelet-fibrin thrombus formation on the plaque surface.
The atherothrombotic plaque can grow to obstruct a vessel, with intraluminal propagation of the thrombus proximally or distally to cause occlusion, or embolism occurs from the plaque surface to occlude smaller distant vessel(s).
Intracranial small vessel disease is thought to be due to lipohyalinosis but other causes may include microatheroma and angionecrosis, or thromboembolism from a larger artery. The clinical syndrome caused by this is lacunar infarction due to occlusion of small perforating arteries.
Vascular risk factors associated with increased risk of stroke: (primary prevention therapy)
|AGE – after 55 yo
|SEX – male>female
||CIGARETTE SMOKING –
|FAMILY Hx of STROKE||AF*|
|OBESITY & PHYSICAL INACTIVITY|
|RAISED HOMOCYSTEINE LEVELS|
|HIGH SALT INTAKE|
|HEAVY ALCOHOL CONSUMPTION –
Embolism from the heart causes approximately 20% of all ischaemic strokes. The most common causes are atrial fibrillation (AF) and valvular heart disease. Not all cardiac sources pose similar threat in causing stroke.
The steps to a diagnosis of ischaemic stroke and the various causes which need investigation to identify the underlying cause for the stroke:
CLASSIFICATION OF STROKE
Based on Oxfordshire Community Stroke Project (OCSP)
|Total Anterior Circulation Stroke (TAC)||All of
|Lacunar Stroke (LAC)||Pathological definition
|Partial Anterior Circulation Stroke (PAC)||Any of
|Posterior Circulation Stroke (POC)||Any of
|Code last letter as follows:|
|Syndrome: Indeterminate pathogenesis, prior to imaging (e.g. TACS)
Infarct (e.g., TACI)
Haemorrhage (e.g., TACH)
- History – from family members, witness, patient
- Physical examination (Full Neurological examination + conscious level + higher mental function test)
- Supplemented with selected diagnostic tests
The diagnosis should provide answers to the following questions: ( 3 what, 1 where, 1 why)
1. What is the neurological deficit?
2. Where is the lesion?
3. What is the lesion?
4. Why has the lesion occurred?
5. What are the potential complications and prognosis?
Clinical features of stroke:
- Anterior artery circulation (carotid artery)
- Middle cerebral artery
- i. Aphasia (dominant hemisphere)
- ii. Hemiparesis / plegia
- iii. Hemisensory loss/disturbance
- iv. Homonymous hemianopia
- v. Parietal lobe dysfunction, e.g. astereognosis, agraphaesthesia, impaired two-point discrimination, sensory and visual inattention, left-right dissociation and acalculia
- Middle cerebral artery
- Anterior cerebral artery
- i. Weakness of lower limb more than upper limb
- Posterior (vertebrobasilar) artery circulation
- i. Homonymous hemianopia
- ii. Cortical blindness
- iii. Ataxia
- iv. Dizziness or vertigo
- v. Dysarthria
- vi. Diplopia
- vii. Dysphagia
- viii. Horner’s syndrome
- ix. Hemiparesis or hemisensory loss contralateral to the cranial nerves palsy
- x. Cerebellar signs
- Confirm the diagnosis
- Determine the stroke mechanism
- Risk stratification and prognostication
- Identify potentially treatable large obstructive lesions of the cerebrovascular circulation
|FBC||Exclude anemia, polycythaemia, thrombocytosis, thrombocytopenia, etc|
|Random Blood Glucose||Exclude hypoglycaemia, new diagnosis of DM|
|Urea & Electrolyte||Hydration status, excludes electrolyte imbalances|
|Clotting profile ( if thrombolysis is considered)||Baseline|
|Lipid profile (fasting)|
|OPTIONAL TESTS (in selected patients)|
|Autoimmune screen||ESR, ANA, RF, anti ds-DNA antibody, C3-C4 levels, etc|
|Thrombophilia screen & Lupus anticoagulants||Serum fibrinogen, anti-thrombin III, Protein C, Protein S, factor IV leyden, Antiphospholipid Ab,|
|12 lead ECG||Mandatory|
|Ambulatory ECG||For suspected arrhythmias or SAN diease|
|FOR ALL SUSPECTED STROKE|
|IN SELECTED PATIENTS|
|ECHO cardiography||For suspected cardioembolism, assess cardiac function|
|MRI (magnetic resonance imaging)||
|Carotid duplex Ultrasound||Allows identification of extracranial vessel disease|
|Transcranial Doppler Ultrasound||Identifies intracranial vessel disease with prognostic and therapeutic implications|
|MR angiography (MRA)||
|CT angiography (multislice CT scan)||
|MR venography||In suspected cerebral venous thrombosis|
DIFFERENTIAL DIAGNOSIS OF STROKE
- Metabolic/toxic encephalopathy (hypoglycaemia, non-ketotic hyperglycaemia,
- Wernicke-Korsakoff syndrome, drug intoxication)
- Epileptic seizures (postictal Todd’s paresis)
- Hemiplegic migraine
- Structural intracranial lesions ( e.g. subdural haematoma, brain tumour, arteriovenous malformation)
- Encephalitis (e.g. herpes simplex virus), brain abscess, tuberculoma
- Head injury
- Hypertensive encephalopathy
- Relapsing Multiple Sclerosis
- Conversion disorders
- Hyperviscosity syndrome
- Peripheral nerve lesions (e.g. Guillain-Barre Syndrome)
REPERFUSION OF ISCHAEMIC BRAIN
Aim: to save the adjacent dysfunctional tissue by restoration of circulation and normalization of the metabolism.
Regime for treatment of Acute Ischemic Stroke with Intravenous Thrombolysis rt-PA (recombinant tissue PA – alteplase)
- IV bolus over 1 min rt-PA 10% (0.9mg/kg, maximum 90mg);
- Followed by an infusion over 1hr is recommended for carefully selected patients within 3hrs of the acute onset of ischaemic stroke.
- Admit the patient to an ICU or a **stroke unit for monitoring.
- Perform neurological assessments q 15 min during the infusion of rt-PA (1 hr) and q 30 min for the next 6 hrs and then q hr until 24 hr from Rx.
- If the patient develops severe headache, acute hypertension, nausea or vomiting discontinue the infusion if agent is still being administered and obtain a CT scan of brain.
- Measure bp q 15 min for the 1st 2 hrs, q 30 min for the next 6 hrs and then q hr until 24 hrs from Rx.
- If B.p systolic > 180mm Hg or diastolic >105mm Hg, administer anti-hypertensive medications to maintain bp at or below these levels.
- Delay placement of nasogastric tubes, indwelling bladder catheters or intra-arterial pressure catheters.
- Avoid antiplatelet drugs for the first 24 hrs after administration of rt-PA.
* C/I of streptokinase in acute ischemic stroke because of poor clinical outcome*
**STROKE UNIT – unit in the hospital only managing stroke patients. The core disciplines of the stroke team are: medical (neurologist, geriatrician or general physicians with interest in stroke), nursing, physiotherapy, occupational therapy and speech therapy. In bigger centres, it may include neurosurgeon, social worker and dietitian.
IV rt-PA can be given ONLY if the following is available:
1. A physician with expertise in the diagnosis and management of stroke.
2. Appropriate neuroimaging tests are available 24 hours a day
3. Capability to manage the complications of thrombolysis, particularly intracranial
Characteristics of Patients with Ischaemic Stroke Who Could Be Treated With rt-PA
1. Diagnosis of ischaemic stroke causing measurable neurological deficit
2. The neurological signs should not be clearing spontaneously, minor and isolated
3. Caution should be exercised in treating a patient with major deficits
4. Onset of symptoms❤ hours before beginning treatment
5. No contraindication for thrombolytic therapy
6. Sys Bp < 185mm Hg and/or dia. Bp < 110mm Hg
7. Brain CT is normal
8. The patient or family understand the potential risks and benefits from treatment
Contraindications for intravenous thrombolytic therapy
1. Current use of oral anticoagulant or PT > 15sec (INR > 1.7)
2. Use of heparin in the previous 48 hrs and a prolonged aPTT
3. A platelet count < 100,000/mm3
4. Another stroke or any serious head injury in the previous 3/12
5. Major surgery within the preceding 14 days
6. Arterial puncture at noncompressible site within the last 21 days
7. Pre-treatment sys. bp > 185mmHg or dia. bp > 110mmHg
8. Neurological signs that are improving rapidly
9. Isolated mild neurological deficits, such as ataxia alone, sensory loss alone, dysarthria alone or minimal weakness
10. Prior intracranial haemorrhage
11. A blood glucose < 2.7mmol/l or > 22.2mmol/l
12. Seizure at the onset of stroke
13. GIT or UT bleeding within the preceding 24 days
14. Recent MI
- Supportive care
- Treatment of acute complications.
This is important to improve mortality and functional disability.
- Oxygen and Airway Support
- To prevent hypoxia and potential worsening of the neurological injury.
- Regular Observation
- To recognise impaired pulmonary function (pulse oxymeter), circulatory function (PR, bp) and to recognise complications from mass effect.
- First treated with bed rest, but mobilisation should begin as soon as the patient’s condition is judged to be stable.
- This involves passive and full-range-of-motion exercises, frequent turning, the use of alternating pressure mattresses (ripple mattress), and close surveillance of the skin. Measures to avoid falls are an important part of mobilisation.
- Blood Pressure
- Hypertension following stroke is quite common.
- However, its optimal management has not been established.
- Very high blood pressure should be reduced gradually.
- Proposed drugs: Labetolol 10-20 mg boluses at 10 min intervals up to 150-300 mg or 1 mg/ml infusion, 1-3 mg/min or Captopril 6.25-12.5 mg orally.
- Sublingual use of a calcium antagonist, such as nifedipine, should be avoided because of rapid decline in blood pressure.
- Blood Glucose
- Hyperglycaemia following acute stroke is strongly associated with subsequent mortality and impaired neurological recovery.
- This applies to diabetics and non-diabetics.
- Sustaining nutrition is important as malnutrition after a stroke might interfere with recovery.
- Persons with infarctions of the brain stem, multiple strokes, large hemispheric lesions, or depressed consciousness are at the greatest risk for aspiration.
- Swallowing impairments are associated with an increased mortality.
- Early initiation of PEG feeding has not been shown to improve long-term outcome.
- A water swallow test should be performed before the patient is allowed to eat or drink.
- A wet voice after swallowing, incomplete oral-labial closure, or coughing reflex on swallowing indicates high risk of developing aspiration.
- A videofluoroscopic modified barium swallow examination can be performed later if indicated.
- If the patient fails the swallowing test, a nasogastric tube should be inserted to prevent aspiration.
- Percutaneous placement of an endogastric (PEG) tube is superior to nasogastric tube feeding if a prolonged need for devices is anticipated.
- The commonest complication = pneumonia and UTI.
- The appearance of fever should prompt a search for infection and appropriate antibiotic therapy should be administered early. Bladder catheters should be avoided if possible.
- A meta-analysis suggested that fever after stroke onset is associated with marked increase in mortality and morbidity.
- Anti-pyretics should be used to control elevated temperatures in acute stroke patients.
- Raised Intracranial Pressure
- Cerebral oedema and increased intracranial pressure largely occur with large cerebral infarctions.
- The head of the bed can be elevated by 20 to 30 degrees in an attempt to help venous drainage.
- Hyperventilation is an emergency measure that acts almost immediately; a reduction of the PCO2 by 5 to 10 mm Hg can lower intracranial pressure by 25% to 30%.
- Mannitol (0.25 to 0.5 g/kg) IV administered over 20 minutes lowers intracranial pressure and can be given 1 6 hrs.
- The usual max daily dose is 2 g/kg.
- If hydrocephalus is present, drainage of CSF via an intraventricular catheter can rapidly lower intracranial pressure.
- Hemicraniectomy and temporal lobe resection have been used to control intracranial pressure and prevent herniation among those patients with very large infarctions of the cerebral hemisphere.
- Ventriculostomy and suboccipital craniectomy is effective in relieving hydrocephalus and brain stem compression caused by large cerebellar infarctions
MANAGEMENT OF BLEEDING COMPLICATION
- Haemorrhagic transformation should be considered as a cause of neurological deterioration following the use of a thrombolytic agent.
- If an urgent brain CT confirms a haemorrhage, stop the rt-Pa infusion.
- Obtain blood samples for coagulation tests, infuse fresh frozen plasma and cryoprecipitate, and seek immediate neurosurgical opinion.
- Depends on the stroke type, size and location.
- Haemorrhagic stroke has a higher mortality than ischaemic stroke. However patients with haemorrhagic stroke show a better neurological and functional recovery.
- Brainstem infarct, large hemispheric infarct and cardio embolic stroke also carry a poor prognosis.
- Lacunar infarct has the lowest mortality rate.