Cerebrovascular accident

 

Abrupt loss of function of part of the NS due to a vascular lesion

Brain cells die if deprived of blood supply for four minutes, cerebral necrosis

 

 

Physiology

Brain is 2% of body weight but consumes 20% of absorbed oxygen

Brain has no anaerobic capacity

Anoxia rapidly leads to neuronal necrosis

Focal anoxia / hypoxia leads to CVA or stroke

Global hypoxia / anoxia leads to anoxic encephalopathy

 

 

 

Normal defence mechanisms

Cerebral vasodilation is a response to hypoxia or hypercapnia

Extensive collateral circulation

 

 

 

Pathophysiology

Cerebral infarct                          85%

Intracerebral haemorrhage          7 - 17%

Subarachnoid haemorrhage       5 - 13%

Embolism                                 3 - 14%

Emboli, detached vegetation from heart valves in sub-acute bacterial endocarditis

May be exacerbated by anaemia

Infarction takes several hours due to compensatory vascular mechanisms.

Oedema around lesions, maximal after about 2 days

Ischaemia may damage vascular endothelium leading to secondary heamorrhage

Necrosed brain tissue undergoes outolysis

Large vessel or lacunar infarcts.

 

 

Risk factors

Age

Gender male > female

Race Afro > Asian > White

Heredity

Previous vascular event

High fibrinogen

Hypertension

Heart disease, (AF, failure, endocarditis)

Hyperlipidaemia

Smoking

Alcohol

Polycythaemia

Oral contraceptives

Social deprivation

 

 

 

Epidemiology

Third most common cause of death in the West

1 - 2 per 1000 per year

Incidence increases sharply over the age of 60

Women over 60 years    - 17% of deaths

Men over 60 years         - 10% of deaths

30 - 40% of patients are alive 3 years after an initial stroke

 

 

Clinical classification

Transient ischaemic attack (resolves within 24 hours)

Progressive stroke (or stroke in evolution)

Completed stroke

 

 

Clinical features

 

 

Focal deficit of brain function

 

Headache may precede neurological defect

 

Onset of stroke is typically over minutes

 

Effects vary from mild TIAs too coma and complete hemiplegia.

 

TIAs recover within 24 hours      

 

Hemiplegia       

 

Hemiparesis

 

Hemisensory loss

 

Confusion (common)                

 

Loss of consciousness (rare)

 

Visual field defects

 

Aphasia or dysphasia may occur if dominant hemisphere is effected. This is usually in the left side of the brain. In right handed people 90% are in the left, in left handed people it is left in approx 60% of individuals.

 

Other symptoms include epilepsy, receptive dysphasia, giddiness, dysarthria, dysphagia, ataxia and blindness.

 

Gradual improvement may occur

 

 

 

Investigations

Clinical history and picture

CT / MRI

EEG/ ECG

Cerebral angiography

 

 

 

Differential diagnosis

Tumour

Abcess

Subdural haemotoma

Demylination

 

 

 

Management

Anticoagulation after scanning  

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Nursing points

 

 

Airway

Check GCS, care of unconscious patient, check swallowing, aspiration, NBM if swallowing unsafe

 

 

Breathing

Check ventilations, O2 Sats, keep above 95%

 

 

Circulation

Check perfusion of peripheries, are P and BP adequate, possible fluid replacement and correction of heart problems.

 

 

Hydration

Check for dehydration, hydrate using enteral, NG, parenteral

 

 

Nutrition

Assess status, give diet, consider supplements, NG feeding for dysphagia

 

 

Medication

Check swallowing or use other routes

 

 

Blood pressure

Probably best not to lower BP in first week unless causing specific complications, maintain cerebral perfusion.

 

 

Blood glucose

Hyperglycaemia may increases infarct volume, give insulin or GKI, watch out for iatrogenic hypoglycaemia

 

 

Temperature

Raised temperature may increase infarct volume, investigate cause of pyrexia, give early antipyuretics

 

 

Pressure areas

Formally assess risk. Treat infection, give hydration and nutrition.

Position to relieve pressure, prevent disturbance to circulation, support effected limbs, prevent contractures and maintain normal body alignment

 

 

Incontinence

Check of constipation and urinary retention. Avoid urinary catheterisation if possible.

 

General points

Maximise mobility and independence

Aids to communication

Take time to communicate

Prevent complications of immobility

Move patients using proximal holds

 

Rehabilitation

Physiotherapy

Speech therapy

Relieve spasticity, prevent contractures, use of walking aids

OT - a range of aids and adaptations

 

Prevention

Prevention of arterial disease    

Recognise and treat hypertension, diabetes, obesity, hyperlipidaemia

Daily aspirin?                           

Stop smoking

Oral contraception                                

Alcohol

Pharmacology in CVA

 

 

Aetiology of thrombosis

 

Interacting effects of three factors, i.e. Virchow’s Triad.

 

 

Disorders of vascular endothelium

Hypertension, atheroma, infection may all lead to endothelial injury.

Blood flow turbulence, underlying collagen will be exposed.

 

Sluggish or abnormal blood flow

Reduced or turbulent blood flow.          

Platelets and other clotting factors have time to accumulate.

 

Increased blood coagulabilit

Increased proportion of cells to plasma.

Increased red cell count as in hypoxia. 

Thrombocytosis.

Too many young platelets after haemorrhage.

Consider aspirin.

 

 

Antiplatelet drugs

Low dose aspirin 300mg  from day one.

Dipyridamole, alone or with aspirin.

Clopidogrel, reduces primary ischaemic events more than aspirin.

 

 

Anticoagulants

Heparin, side effects outweigh advantages

Warfarin

 

 

Thrombolysis in acute presentation, e.g. TPA, alteplase.

Dangerous to give more that 3 hours after onset.

 

 

Baclofen acts at spinal level as a GABA derivative to block activation of motor neurones via pre-synaptic receptors.

 

Correction of haemorrhagic disorders.

 

 

Surgery, decompressive crainectomy, carotid endarterectomy

 

 

Treat risk factors

 

ACE inhibitors such as captopril, lisinopril.

 

Hypoglycaemics, e.g. insulin,

Glibenclamide to stimulate insulin secretion.

Metformin to reduce hepatic gluconeogenesis.

 

Statins such as simvastatin to lower LDL cholesterol by inhibition of hepatic synthesis.

 

Omega 3 oils.

 

Ca++ antagonists such as nifedipine.

 

 

Stroke is a clinical term for the acute loss of perfusion to the vascular territories of the brain, leading to ischemia and loss of neurologic function in the affected areas. Resulting from hemorrhagic or ischemic insults, patients present with focal neurologic deficits to hospitals every day. Prompt recognition and treatment are necessary to return blood flow to deprived areas in order to restore neurologic function.

 

Strokes are grossly divided into ischemic and hemorrhagic types. Ischemic strokes are responsible for roughly 70% of all strokes and occur from thromboembolic occlusion of cerebral arteries. Blood flow occlusion begins an ischemic cascade that, if unchecked, will result in irreversible infarction. Hypoxic-induced cell death causes inflammatory swelling, which may alter the brain architecture, producing a midline shift as shown.

 

Hemorrhagic strokes are responsible for roughly 30% of all strokes, more commonly from intracerebral rather than subarachnoid etiologies. Patients present similarly to those with ischemic stroke except that they tend to appear more ill with signs of increased intracranial pressure. The most common etiologies are trauma, leakage from small intracerebral arteries secondary to chronic hypertension, aneurysmal rupture, iatrogenic anticoagulation, cocaine abuse, or cerebral amyloidosis.