The treatment of cerebral infarction has been intensified during the recent years. Most patients nowadays regain independence and an ever greater proportion have no residual symptoms. This is mainly a result of thrombolytic therapy in the acute phase and/or thrombectomy and of treatment in stroke units, as well as of effective rehabilitation commenced in the initial phase already.
A previously self-sufficient patient with acute cerebral infarction is investigated at the hospital emergency department where the treatment is also provided and from where a consultation regarding thrombectomy can be made through remote connection.
The patient is transported by ambulance to an adequately equipped hospital where the thrombolytic therapy is administered and where a CT angiography is carried out in order to identify patients suitable for thrombectomy to be further referred to an appropriate tertiary level hospital.
According to the current knowledge, 4 out of 5 cerebral reinfarctions can be prevented by effective secondary prevention.
A healthy lifestyle is the most important factor in the primary prevention of cerebral infarction. Prevention directed at the risk factors of vascular diseases is the best possible treatment.
In many countries, like in Finland, the incidence of cerebral infarction has decreased in recent decades, but increased in the younger age groups (less than 50 years olds), causing concern.
How well secondary prevention is implemented determines the future increase in the number of patients with cerebral infarction, due to the increase in the proportion of aged people in the population.
The most common risk factors for cerebral infarction are advanged age, hypertension, atrial fibrillation, diabetes, hypercholesterolaemia, truncal obesity, and of the living habits unhealthy diet, low level of physical activity, excessive alcohol use and smoking.
Triggering factors include dehydration, surgery, pregnancy, immobilization, the instigation and cessation of anticoagulant therapy, acute excessive alcohol intake and acute infection.
Aetiology
Atherosclerosis of the large vessels, microangiopathy and cardiogenic embolism each account for approximately one third of infarctions with an identified cause. In every third cerebral infarction the cause cannot be found even in thorough investigations.
The aetiology of cerebral infarction is highly dependent on age.
In the younger age groups the underlying cause is more often carotid artery dissection, vasculitis, cerebral vasospasm, hereditary or acquired coagulation disorder, or paradoxical embolism associated with a prothrombotic state, especially in patients with patent foramen ovale or some other rare cause.
In patients aged over 80 years, atrial fibrillation is the causative factor in one out of four cases.
If the cause remains unknown or the only finding is a source of embolism that entails a minor or uknown risk, and imaging findings match an embolic infarction, the condition may be regarded as ESUS (Embolic Stroke of Undetermined Source, about 17% of all cerebral infarctions).
The most common cause of cardiogenic embolism is atrial fibrillation. Other high-risk causes include new or earlier myocardial infarction, sick sinus syndrome, atrial flutter, akinesia/aneurysm of the left ventricle, thrombosis in the left ventricle or atrium or atrial auricle, dilated cardiomyopathy, mechanic valve prosthesis, mitral valve stenosis and endocarditis, as well as atheroma in the ascending aorta or aortic arch.
Microangiopathic infarcts result from thrombosis of the small distal arteries and are located either subcortically or in the basal ganglions or the brain stem. They are most commonly caused by hypertension. Other causes include type 2 diabetes and hypercholesterolemia.
Location of the infarction affects essentially the symptom picture. In 80-90% of the cases the infarction is located in the carotid region (anterior circulation) and in 10-20% to the vertebrobasilar region (posterior circulation).
Cerebral infarction will generally lead to acute hemiplegia and/or sensory disturbance and expressive language impairment. The patient may also present with hemiparesis, a drooping mouth, visual disturbances and disturbed eye movements, dysphagia, vertigo, balance problems, or tetraplegia. An acute neuropsychological deficit, e.g. dyspraxia, memory loss or confusion, may also be indicative, of cerebral infarction.
Vertigo, binocular visual disturbance or swallowing or speech difficulties, when occurring alone, usually do not indicate a disturbance of the cerebral circulation.
Carotid (hemispheral) infarction typically presents with hemiparesis and/or sensory disturbance, often accompanied by weakness in the lower branch of the facial nerve.
Occlusion of the middle cerebral artery is the most common site; paralysis is more pronounced in the upper extremity.
Occlusion of the anterior cerebral artery, which is a rare condition, leads to paralysis most often involving the lower extremity and to urinary incontinence.
An infarction in the dominant hemisphere often involves expressive and receptive language impairment as well as reading and writing difficulties.
An infarction in the non-dominant hemisphere may include impairment in the sense of direction and spatial orientation as well as anosognosia (lack of a sensation of illness) and sensory neglect (ignoring the affected side of the body).
Vertebrobasilar (brainstem) infarction typically presents as acute and severe vertigo, nausea, diplopia, dysphagia, dysarthria and sensory disturbance, weakness or paresis in the contralateral extremities. The symptoms are caused by the progressive (often lasting for several days) occlusion of vertebral artery, basilar artery and cerebellar arteries. Homonymous hemianopia without paralysis is most often caused by the occlusion of the posterior cerebral artery.
The symptom picture of lacunar (microangiopathic) infarctions may involve pure motor or sensory hemiparesis which often fluctuates, as well as ataxia and hemiparesis or dysarthria- clumsy hand syndrome. See also Vascular dementia Vascular Cognitive Impairment (Vci).
Cerebral infarctions rarely involve a headache, particularly at the initial stage. A large infarction may cause increased intracranial pressure, headache, nausea and lowered consciousness, but usually with a delay. The symptoms of a severe cerebral infarction may progress in up to 3 days after the incident.
Sinus thrombosis (cerebral venous thrombosis) may occur during pregnancy or puerperium, or in association with hormone therapy, dehydration, coagulopathies, or malignancy. Sinus thrombosis causes symptoms of increased intracranial pressure: headache, lowered consciousness, or seizures with associated unconsciousness as well as paralysis inconsistent with the arterial distribution areas.
Diagnostic work-up at the emergency department
Is the condition caused by disturbed cerebral circulation or some other illness (migraine, epilepsy, encephalitis, brain tumour, or MS)?
Does the patient suffer from an ischaemic disturbance of cerebral circulation or haemorrhage? The two conditions need to be differentiated with the use of a CT scan, which still is the primary investigation in an emergency setting.
Is the patient's condition during examination stable, progressive or recurring?
An unstable phase usually persists until the occluded vessel is opened either spontaneously or through thrombolysis. Improved symptoms do not always translate to reduced risk.
Start aetiological investigations.
Cardiogenic?
An acute onset (e.g. whilst getting out of bed or during straining), loss of consciousness, seizures, and a history of a potentially embolic cardiac disorder suggest cardiogenic embolism. The symptom may also be isolated aphasia, visual field defect or tetraparesis, even as a transient symptom. A CT scan may show, for instance, a haemorrhagic infarction or multiple infarctions. Anticoagulant therapy is indicated.
Find stenoses of the carotid arteries.
Other, more rare causes
Neck pain, Horner's syndrome Neurological Eye Symptoms, and neck trauma prior to the stroke are suggestive of carotid dissection.
All previously self-sufficient patients are transported by ambulance to the care of a specialist team at the nearest appropriate hospital where the patient should primarily be cared for in dedicated wards (stroke units).
A previously self-sufficient patient suitable for thrombolytic therapy is given thrombolytic therapy and, when needed, also thrombectomy is performed. Find out about local treatment locations and policies.
Airways must be open, if necessary with the aid of an oral airway or the patient must be intubated. Oxygen therapy is instigated in the casualty department and continued, should there be problems with ventilation or oxygenation.
Intravenous fluids should always be administered during the acute phase. The patient must be kept nil by mouth before the swallowing function has been tested. Continuous ECG and blood pressure monitoring are commenced. Maintenance fluid in the acute phase is 0.9% sodium chloride or Ringer's solution.
Management of blood glucose
Normoglycaemia is the target The Prognostic Value of Glucose Levels in Acute Stroke. In a diabetic patient with insulin therapy (irrespecive of the type of diabetes), the basal insulin therapy must not be discontinued, but rather it is continued using individual dosage (monitor glucose levels carefully and adjust insulin therapy and glucose administration as required).
Normothermia should be the target, although there is not enough evidence on the effect of cooling down the increased body temperature (by drugs or cooling techniques) on the recovery.
Reducing fever (Ttymp> 37 °C), e.g. paracetamol intravenously or orally 1 g 3-4 times daily)
If required, the body temperature is lowered by airing of the room, cold compresses or with an external cooling device.
Management of fever, combined with the management of hyperglycaemia and with testing of the pharyngeal function, improves the prognosis.
Cerebral infarction is often accompanied by an acute reactive increase in blood pressure, which acts as a defence mechanism. A reduction of blood pressure is not generally advisable during the first 48 hours of treatment Blood Pressure Alteration in Acute Stroke.
If the diastolic pressure is below 120 mmHg and the systolic pressure below 220 mmHg, no antihypertensive medication is needed. If, however, thrombolytic or anticoagulant therapy is instigated the upper limit should be around 185/110 mmHg. A lower blood pressure level (< 160/110 mmHg) should be considered after thrombolytic therapy if the risk of intracranial bleeding is particularly high or if the vessel can be opened with thrombectomy.
The first-line antihypertensive agents are intravenous labetalol or enalapril. Vasodilators and other forms of abrupt blood pressure reduction should be avoided (no chewable nifedipine).
If systolic pressure exceeds 220 mmHg, blood pressure should be reduced during the acute stage, and also whenever necessary from the cardiovascular viewpoint.
Arrhythmias
Patients with cerebral infarction often suffer from arrhythmias (tachycardia) and myocardial ischaemia during the acute phase, including ST changes in an ECG. Beta-blockade is usually indicated.
Automatic ECG monitoring, capable of recognizing atrial fibrillation and with alarm function, is recommended at least during the first 24 hours within the stroke unit.
Prevention of pneumonia
The risk of aspiration is high and nothing must be given to the patient orally before the swallowing function has been tested. Prophylactic intravenous antimicrobial for possible aspiration is started for all patients who have vomited, who have been lying on the ground for a longer time, or who were unconscious when found.
Prevention of deep venous thrombosis and pulmonary embolism
Use of medical stockings (“anti-embolic stockings”) is no longer recommended, since they have not been shown to be of benefit in the treatment of patients with disturbances in cerebral circulation, but they do cause local complications.
Use of intermittent pneumatic compression stockings (IPC) has been shown to reduce the risk of deep venous thrombosis.
Their use should be started no later than within 12 hours from the start of immobilization; otherwise an ultrasonography examination of the lower extremity veins should be performed before using the stockings.
If IPCs cannot be used, if the patient's risk of bleeding complication is low or if the patient has, in addition to immobilization, a known prothrombotic state, starting subcutaneous low molecular weight heparin with thromboprofylaxis dosing should be considered, unless there are contraindications to it.
Brain oedema
Brain oedema is a life-threatening condition in an extensive cerebral infarction. It can be treated with temperature reduction, blood glucose control, osmotic preparations Mannitol for Acute Stroke, positional therapy, prevention of restlessness and seizures, maintenance of optimal blood gas values, ventilation support, or, in the most severe cases, hemicraniectomy, which is, besides thrombolytic and thrombectomy therapy and treatment carried out in a stroke unit, an evidence-based effective treatment modality in the acute phase Surgical Decompression for Cerebral Oedema in Acute Ischaemic Stroke.
Rehabilitation
Rehabilitation is introduced at an early stage.
It is most effective if carried out by a multidisciplinary team at a stroke unit where every patient is assessed within a week from the onset concerning the rehabilitation needs and measures.
In a cerebral infarction with mild symptoms, a combination therapy of aspirin 100 mg per day + clopidogrel 75 mg per day may be used for a period of 3 weeks, after which only one antithrombotic drug is used http://www.bmj.com/content/363/bmj.k5130.
The direct oral anticoagulants or permanent warfarin therapy are used for the prevention of AF-induced cerebral infarction.
Blood pressure medication http://www.dynamed.com/management/secondary-prevention-of-stroke-or-transient-ischemic-attack#ANTIHYPERTENSIVE_DRUGS (especially the combination of an ACE inhibitor and a diuretic, or therapy based on an AT receptor blocker) are beneficial for patients who have suffered ischaemic disturbance of the cerebral circulation. A beta blocker should not be used as the only blood pressure medication. A general target is below 140/90 mmHg, but after a cerebral infarction the target is below 130/80 mmHg (in home measurements < 125/80 mmHg), if the target can be reached without adverse effects. Hypotension with symptoms should be avoided.
The treatment goal in other aetiologies than atherosclerosis is <1.8-2.5 mmol/l, with the exception of atrial fibrillation or other cardioembolic aetiology.
The most important changes in living habits include smoking cessation, Mediterranean or Baltic diet, treatment of obesity and increasing the amount of physical exercise.
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