Cerebral embolism

Atrial fibrillation

Cardiac arrhythmia of any type are combined with symptomatic cerebral and systemic embolism. Particular attention should be paid to the high incidence of embolism in sick sinus syndrome and atrial fibrillation, atrial fibrillation against the background of patients with rheumatic valvular heart disease. Therefore, in order to prevent embolism in such patients show long-term administration of anticoagulants (warfarin sodium). It is noted that most often clinically manifest embolism occur in patients with atrial fibrillation, regardless of the reasons therefor. It is estimated that the incidence of embolism in the vessels of the brain in patients with atrial fibrillation not associated with valvular lesions, reaching 4-7% per year, and in most cases even the first stroke leads to profound disability of the patient.

The formation of the wall blood clot burden embolism, followed by relatively frequent in patients with atherosclerotic lesions of the cardiovascular system and myocardial infarction, regardless of whether with or without dysfunction of papillary muscles, congestive heart failure or ventricular aneurysm.

Patients with atrial fibrillation who are at high risk for stroke now have an alternative to long-term warfarin in the form of a device designed to close the left atrial appendage and prevent blood clots from migrating to the brain and causing a ischemic stroke.

 

Cardiac surgery

Heart valve replacement surgery and are accompanied by a particularly high risk of embolism. Less common cause of cerebral embolism are surgery on the chest, after which it is possible embolism of the pulmonary veins, as well as head and neck (arterioarterialnye emboli from the aorta or carotid arteries). By fat or air embolism of cerebral vessels cause fractures of long bones, surgery on the organs of the chest cavity and diagnostic angiography with intravascular administration of contrast medium through the catheter. Both options provide multiple embolic sites of point hemorrhages. The most significant complication of the use of artificial hearts are embolism from the cavity of the heart vessels in the brain.

Birth defects of the heart walls may be the cause of paradoxical embolism in a patient. Transported through the blood and tumor mogzhet thrombotic material, infectious or fibrous maranticheskie deposits accumulate on the surface of the endocardium in the heart chambers or valves. Layers of the valve of the aorta and the left atrioventricular valve in rheumatic endocarditis or maranticheskom observed simultaneously with systemic or cerebral embolism and diagnosed based on patient history, objective and laboratory examinations. Typical flat sediments under flaps of the left atrioventricular valve and to a lesser extent - aortic valve (Libman-Sacks endocarditis) have been described in patients with systemic lupus erythematosus. They can be a source of emboli in the vessels of the brain, but increasingly the foci of bacterial endocarditis.

Thrombotic deposition in acute and subacute bacterial endocarditis in patients lead to septic embolism. Such emboli can cause extensive brain infarcts, did not differ from non-infectious embolic infarctions with occlusion of major cerebral arteries. They also serve the cause of heart attacks and small to microscopic abscesses. Meanwhile, large abscesses of the brain can not be combined with embolism with subacute bacterial endocarditis. Mycotic (fungal) aneurysms caused by septic emboli are the cause of subarachnoid and intracerebral hemorrhages. If you suspect a cerebral embolism should always be aware of the possibility of endocarditis in a patient and eliminate it.

Atrial myxoma leading to tumor embolism. Substrate with myxoma emboli are deposits on the surface of the endocardium. In the case of myxoma in the differential diagnosis helps to identify signs of pulmonary hypertension, a high erythrocyte sedimentation rate, symptoms of systemic disease (fever, malaise). Mitral valve prolapse in the formation of a thrombus membrane is combined with cerebral embolism, but their formation mechanisms are not well understood in order to predict the incidence of recurrent embolism in patients. It is assumed that it is low. When the diagnosis of mitral valve prolapse in a patient should be performed echocardiography.

 

Cerebral embolism clinical syndromes

If the cause of acute ischemic cerebral embolism is an artery, the progression of clinical neurological deficits in a patient characterized by a sudden and, as a rule, the maximum severity of symptoms. However, neurological deficits may be incomplete, as well as significantly changed after its origin. Thus, in some cases, the neurological deficit may increase or decrease, remaining in the patient for only a few minutes or hours, which is the clinical picture of transient ischemic attack (TIA microstroke) embolic origin.

In other cases, a slight deficiency can significantly increase the extent of myocardial and a Big artery in the brain. Whatever it was, the nature of the neurological deficit corresponds to the damage of a particular vascular bed due to the localization of embolus, such as large or small vnemozgovyh penetrating arteries. As a result of neurological deficit corresponds to the occlusion of large or small cerebral vessels. Obviously, the size of embolus determine vessel diameter, which is subject to occlusion.

With the development of several neurological syndromes can be assumed that the reason for this is embolism of cerebral arteries. Syndromes damage pool of middle cerebral artery include:

• Frontal opercular syndrome, manifested by tilting the person with aphasia and dysarthria rough;
• Shoulder syndrome or carpal paralysis, which does not movable entire arm, forearm and wrist or hand only in the presence or absence of cortical disorders of sensitivity, depending on whether involved in the kill zone sensory cortex along with the motor;
• Isolated syndrome or Wernicke aphasia Broca in the dominant hemisphere lesion in a patient;
• The syndrome of denial left halves of the visual fields with lesions of the occipital lobe non-dominant hemisphere in the patient.

Full awareness of patients suddenly appeared in his visual field defect shows the posterior cerebral artery embolism, whereas Acute ataxia or weakness in the leg indicate the anterior cerebral artery embolism. Acutely evolved unsteady gait may be due to embolism of cerebellar artery.

Much more difficult to establish the cause of stroke in the pool of small arteries - whether it embolism or atherothrombotic occlusion or lipogialinoticheskaya that occurs much more frequently. However, the sharp upcoming sleepiness along with the inability to look up in conjunction with the omission of bilateral upper eyelid (ptosis ) suggests embolism top of the basilar artery with the electoral damage of the artery Percheron. Artery Percheron - a small vessel coming from the upper portion of the main arteries supplying the brain and medial divisions subtalamusa and thalamus on both sides.

Septic emboli in endocarditis or fat embolism often occur neochagovoy symptoms, including disorientation, agitation, delirium.

Consequence of surgery on the heart may be of particular neurological syndrome: the patient wakes up slowly, in the waking state he has slowed thinking, confusion, there may be excitement, pugnacity, memory deteriorates, there are often visual hallucinations. Most symptoms resolved within a week, but persistent deficits of visual perception is often indicative of an existing adjacent zone myocardial blood flow in the middle cerebral artery parietal - occipital localization that developed presumably due to hypotension or multiple small emboli.

Convulsions in cerebral infarction are more frequently observed after embolic infarction and lacunar infarctions occur when, localized deep in the white matter. Epileptic seizures in a patient accompany the supratentorial cortical localization of heart attacks, but they are never pathognomonic symptom. Often obscure origin epilepsy in the elderly is the result of chronically occurring silent cortical infarcts of the brain and is easily eliminated by phenytoin.

 

Cerebral embolisms clinical examination and laboratory studies

Before treatment with anticoagulants should be patient magnetic resonance (MRI) or computed tomography (CT) scan of the brain. This is to prevent a small hemorrhage that makes the same symptoms as embolic stroke.

Lumbar puncture to detect red blood cells in cerebrospinal fluid (CSF) is indicated only in cases where the supposed small (possibly hemorrhagic ) infarction in the area of the pons, accompanied by dysarthria, clumsy hand syndrome or other syndromes of the posterior cranial fossa. In connection with bone artifacts in computed tomography (CT) scan of the brain in a patient can "skip" hemorrhage, take it for a small heart attack. Through magnetic resonance (MR) brain patient can distinguish acute from chronic hemorrhage and a stroke, get more reliable data for the early detection of cerebral infarction.

If the diagnosis of cerebral artery embolism is justified and necessary to establish its alleged source of arterial, cerebral angiography is justified conduct. However, after 24 h embolus may be subject to transfer, dissolution (lysis), splitting, and the conclusion of embolism as a cause of embolic stroke is only conjectural. Intravenous contrast angiography does not have sufficient resolution to detect cerebral emboli.

 

Cerebral embolisms treatment

Treatment of patients with embolic cerebral infarction of the brain designed to help with the available stroke in the acute and the chronic stage of its occurrence and prevention of embolic strokes in this patient in the future. If you suspect a cerebral embolism physician efforts should be aimed primarily at maintaining perfusion of the brain in the zone of ischemia, as far as possible, to be adequate. We should not reduce high blood pressure if it is a matter of malignant hypertension. At low pressure should take steps to improve it. However, this should be done with caution, as excessive increase in pressure may increase cerebral edema. As soon as cerebral infarction pattern becomes apparent edema rarely causes problems to the 2- 3rd day, but then can be stored up to 10 days.

Although there is an assumption that the recovery of blood in the recycling of tissue infarction in connection with the dissolution (lysis ) embolus leads to increased swelling, in fact, edema of the brain embolism is distributed according to two rules:

• In the supratentorial embolic cerebral infarction larger the area of ??infarction, the more likely the development of edema. After contact with emboli in the trunk of the middle cerebral artery more likely to develop symptomatic cerebral edema, which can lead to coma and death from herniation of the temporal lobes than one branch of embolic middle cerebral artery.
• The formation of a small swelling of the cerebellum after the embolic infarction, usually in the back of the pool inferior cerebellar artery (lower parts of the cerebellum), can cause a sharp rise in intracranial pressure in the posterior fossa. The resulting compression of the brainstem can cause sudden onset of coma and respiratory arrest. In such situations require urgent surgical decompression.

In both the above cases, the patient should be advised as soon as possible to limit fluid intake and taking medications that increase the osmotic pressure. Often to increase the osmolarity of blood plasma to 300-310 mOsm / l of mannitol administered intravenously. Mannitol is administered every 2-4 hours.

The need to treat patients with anticoagulants depends on are embolic material fragments of the thrombus from the heart or from an unknown source. The reason for conflicting judgments on the issue of appointment of anticoagulants was the fear of the possibility of the development of hemorrhagic infarct and, more importantly, bleeding in the infarcted area. According to the conservative point of view, repeated embolism rarely occur in the first few days, therefore, the use of anticoagulants can be postponed for 3-4 days. According to other sources, significant bleeding in the infarcted area found only rarely, usually with extensive infarcts involving the basal ganglia, for example, due to embolism of the trunk of the middle cerebral artery. Therefore it is unwise to refrain from the use of anticoagulants for several days except those cases, when the area of infarction is large. But undoubtedly, anticoagulant therapy, both immediate and deferred, are contraindicated in septic emboli due to the threat of intracerebral or subarachnoid hemorrhage from mycotic aneurysm.

All of embolism of cardiac origin, except maranticheskih, septic and tumor (myxoma), result from the formation of wall thrombi. It can be mikrotrombov in the eye of the left atrium, such as atrial fibrillation, large blood clots on the surface of the wall near the site of ventricular myocardial or thrombotic mass in the ventricular cavity of the aneurysm, the left atrium -ventricular valve or aortic valve. In the formation of blood clots in the parietal embolism should be treated with anticoagulants for as long as the threat disappears repeated embolism. It is believed that in cases of acute myocardial infarction rather use anticoagulants for 6 months. In chronic or intermittent atrial fibrillation, these medications must be taken indefinitely.

Rarely observed in the present atrial fibrillation against the background of rheumatic heart valve is an indication for long-term, for life, receiving anticoagulants, even if the patient was no embolism. Among patients with asymptomatic atrial fibrillation caused by coronary artery disease or other diseases of the heart, also have an increased incidence of cerebral embolism in comparison with a control group of patients of similar age. However, in such a case there are conflicting opinions regarding the potential risk of long-term use of anticoagulants.

With any form of heart disease and cerebral embolism from an unidentified source usually recommend warfarin sodium in low doses. At the same time the prothrombin time should not exceed the reference value by more than 1.5 times and must take account of contraindications to warfarin. It should be noted that there are no reliable guidance on duration of use of anticoagulants in patients with cerebral embolism from unclarified source. But when it comes to patients younger than 50 years, it seems reasonable period of time from 6 months to 1 year.