Disease: Ischaemic stroke affecting the dominant left cerebral hemisphere

 

 

Definition : An ischaemic stroke is death of brain tissue resulting from an occluded artery caused either by an atherosclerotic obstruction or embolus that interrupts blood supply to the area of the brain supplied by the occluded artery. The sudden loss of blood circulation results in a corresponding loss of neurologic function (Jauch, 2014).

 

AETIOLOGY:

A depletion of blood flow in a cerebral artery resulting from a:

· Thrombus –atherosclerotic plaque that has ruptured in a cerebral artery

· Embolus

· from heart e.g. left atrial thrombus, left ventricular thrombus, atrial fibrillation

· from carotid artery (Craft &Gordon,2011)

 

PATHOGENESIS:

· Interruption of blood flow to cerebral tissue initiates a biochemical ischaemic cascade.

· Mitochondrial production of ATP ceases depolarisation  influx of sodium and calcium and efflux of potassium. Passive inflow of water into cells causes cytotoxic oedema and destruction of cells in infarct core.

· Membrane depolarization also stimulates the release of neurotransmitters. Glutamate release excessive calcium influx into nearby neurons (exocitotoxicity) destruction of cells by lipolysis, proteolysis and free radicals.

· Mitochondria break down releasing toxins and apoptotic factors.

· Injured brain tissue triggers inflammatory response release of inflammatory mediators cell death and oedema

destruction of cells in infarct core necrosis

ischaemic penumbra around core has diminished blood flow but preserved cellular metabolism.

 

Areas of necrotic tissue are not able to conduct nerve impulses so functions such as initiating and conveying motor impulses, receiving and interpreting sensory information and speech control will be interrupted.

(Bautista, 2014; Craft & Gordon, 2011; Maas & Safdieh,2009).

 

CLINICAL MANIFESTATIONS:

 

Just superior to the medullary junction, 90% of axons in the left pyramid cross to the right right motor dysfunction.

The middle cerebral artery supplies the frontal, temporal and parietal lobes as well as the basal ganglia and internal capsule. (Tocco,2011).

 

Therefore specific clinical manifestations include:

· Hemiplegia and weakness on right side of body

· Sensory loss on right side

· Inability to see the right visual field of each eye

· Aphasia

· Apraxia

· Dysarthria

· Impaired reasoning

· Behavioural changes

· Problems with memory

(Bautista, 2014; Craft & Gordon, 2011).

 

DIAGNOSIS

· Complete history

· Physical and neurological examination

· Brain MRI or CT scan – Essential in differentiating cerebral haemorrhage from ischaemic stroke. MRI is superior as cerebral ischaemia can be identified within minutes and can identify small areas of stroke.

· Other tests for vascular imaging can be used e.g. CT angiography, magnetic resonance angiography

(Silverman & Rymer, 2009).

 

TREATMENT

The emphasis of ischaemic stroke treatment is placed on salvaging potentially reversible ischemic penumbra brain tissue, preventing secondary stroke and minimising longterm disability. (Jaunch, 2014).

 

· Reperfusion

· thrombolytic agent (e.g.tPA)

· intra-arterial technique

 

· Neuroprotection

-antithrombotic therapy (e.g. aspirin)

 

· Nursing management

Acute phase

· frequent evaluation of neurological status

· frequent evaluation of vital signs

· Monitor oxygen saturation – administer oxygen if required

· Screen for swallowing deficits and manage appropriate hydration and nutrition strategies

· Manage activities of daily living

· Screen for communication deficits and address appropriate communication strategies

· Prevent complications e,g pressure areas, contractures, DVT

· Assess urinary and faecal continence and address appropriately

 

Rehabilitation

· begin as early as possible by preventing complications, passive and active movement and mobilizing as early as possible.

· Support and encourage activities provided by physiotherapists, occupational therapists and speech therapists

· Education – e.g. lifestyle modification, adherence to medications

(National Stroke Foundation, 2010).

 

 

COURSE OF DISEASE

 

· With reperfusion – blood is restored to the area and signs and symptoms gradually resolve

 

· Without treatment – Course is determined by severity of stroke. Ischaemia will extend to penumbra as stroke evolves, signs and symptoms worsen. As cerebral oedema resolves, and with structural and functional reorganisation recovery may continue for 6 months to a year. (peak recovery in about 3 months). Requires rehabilitation to optimise function.

 

(Teasell & Hussein, 2014).

· Complications

Contractures

Fatigue

Incontinence

Mood disturbances

Falls

Dysarthria and aphasia

 

PROGNOSIS

· Stroke prognosis is influenced by factors such as age and stroke severity.

· One in five likely to die within one month of suffering ischaemic stroke.

· Of those who recover about 90% will experience some impairment

(Dashe,2014)

 

PREVENTION

Eliminating modifiable risk factors will prevent an ischaemic stroke.

· Don’t smoke

· Diet high in fruit and vegetables, low in fats and salt

· 30 minutes of moderate-intensity physical activity on most days of the week

· Maintain healthy BMI

· Limit alcohol to no more than two standard drinks per day

(National Stroke Foundation, 2010)

 

If a history of atrial fibrillation – ensure adherence to anticoagulation therapy.

 

 

 

 

 

 

 

References

Bautista, C. (2014). Disorders of Brain Function. In S. Grossman & C. Porth (Eds),

Porth’s pathophysiology: Concepts of altered health states (9th ed.). (pp489-

524). Philadelphia: Lippincott Williams & Wilkins.

Craft, J. & Gordon, C. (2011), Alterations of Neurological Function across the

Lifespan. In J.Craft, C.Gordon & A. Tiziani (Eds). Understanding

Pathophysiology (pp 188-226). Sydney, Australia:Elsevier Australia.

Dashe, J. F. (2014). Stroke prognosis in adults. UpToDate. Retrieved from:

http://www.uptodate.com/contents/stroke-prognosis-in-adults

Jaunch, E.C. (2014). Ischemic stroke treatment and management, Retrieved from:

http://emedicine.medscape.com/article/1916852-overview

Maas, E.B. & Rymer, M.M. (2009). Ischaemic stroke: Pathophysiology and Principles

of Localization. Neurology 13 .Retrieved from:

http://www.turner-white.com/pdf/brm_Neur_V13P1.pdf

National Stroke Foundation (2010). Clinical guidelines for stroke management

2010. Melbourne Australia.

Silverman, I.E. & Rymer, M.M. (2009). An atlas of investigation and treatment.

Ischaemic stroke. Clinical publishing:Oxford,U.K.

Teasell, R.& Hussein, N. (2014)Brain reorganization, recovery and organizecare.

In Stroke rehabilitation clinician handbook 2014. Retrieved from:

http://www.ebrsr.com/sites/default/files/Chapter%202_Brain%20Reorganization,%20Recovery%20and%20Organized%20Care_June%2018%202014.pdf

Tocco, S. (2011). Identify the vessel recognize the stroke. American Nurse Today

9 (6).