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Treatment of TEPA

In order to prevent a clot formation heparin and its low-molecular fractions (clexane) are applied. Streptokinase, celliase, urokinase, actilise are used for thrombolysis.

Application of anticoagulants starts with a bolus intravenous administration of NFH (5000 U) with subsequent dose selection by laboratory findings (APTT). It is important that a therapeutic level will be achieved within the first 24 hours. APTT must be increased, at least, 1.5-2.5 times compared with the norm. It is optimal to use subcutaneous administration of LMH (clexane 1 mg/kg) in the dose selected by the patient's body mass. It is expedient to start treatment with indirect anticoagulants in 5-7 days of heparin therapy. Under usual conditions a treatment with heparin must be discontinued when patient's INR is within therapeutic limits (i.e. from 2 to 3), at least, for two days. Treatment with oral anticoagulants must be continued no less than for three months under INR control every 10-14 days in the patients with the first episode of venous thrombosis and absence of preserved risk factors. The patients with repeated episode of venous thrombosis should be treated with heparin in the same therapeutic regimen as the patients with the first episode, however, an optimal duration of treatment with oral anticoagulants must be no less than 6 months.

ACUTE DISORDERS OF CEREBRAL CIRCULATION (ADCC)

ADCC are subdivided into transitory disorders of cerebral circulation (TDCC) and insults.

TDCC — it is acutely arising disorders of cerebral functions of vascular genesis, characterized by general cerebral, focal or mixed symptomatology that pass in the course of 24 hours after its development.

TDCC may manifest themselves by the central vascular crises and transitory ischemic attacks (TIA).

Vascular crises may be general, regional and mixed.

In clinical picture of general vascular crises overall cerebral and vegetovascular disorders prevail.

Regional crises are subdivided depending on localization into carotid and vertebrobasilar ones. They are accompanied by both overall cerebral and organic microsymptoms. Patients with hypertonic crises make up a large group.

TIA arise as a result of pathology of great arteries of the brain (atherosclerotic stenosis and occlusion, thrombosis). Clinical picture — primarily focal symptomatology (numbness, pareses, paresthesias). Transitory aphasia or cortical dysarthria may be observed in injury of the left hemisphere.

In injury of the internal carotid artery a reduced vision up to blindness and weakness in the extremities on the side of affection are diagnosed. Fits of systemic dizziness, vegetovascular and ocular disorders (visual field defects, diplopia, pareses), as well as bulbar and cerebellar symptoms are typical for lesions in the pool of vertebrobasillar artery.

Diagnosis of TDCC may be established only retrospectively.

Treatment of TDCC:

1) Normalization of AP — hypotensive agents (dibasolum, lasix, ganglioblockers, halidor 50-75 mg, curantyl, aminazine intravenously drop-by-drop, euphillin, droperidol);

2) Improvement of cardiac activity — cardiac glycosides;

3) Timely and adequate restoration of cerebral circulation (cavinton 2-4 ml, instenon 2 ml intravenously);

4) Improvement of rheologic properties of blood, its viscosity, micro­circulation and collateral blood circulation (aspirin 325 mg, curantyl, pentoxyphylline, rheopoliglucin, in TIA — direct anticoagulants — heparin, low molecular heparins, clexane et al. in preventive dosages 20 or 40 mg once a day depending on the degree of risk of thrombosis);

5) Normalization of cerebral metabolism (nootropil or pyracetam, instenon, cerebrolysin, in brain edema — mannite, lasix);

6) Prevention of brain edema, improvement of venous outflow;

7) Elimination of vegetovascular disorders.

INSULT — it is ADCC accompanied by structural alterations in cerebral tissue, persistent organic neurologic symptoms for more than 24 hours since the onset of the disease.

Intracerebral hemorrhage may be parenchymatous as a result of rupture of vessels (85%) or diapedetic (15%).

Clinical picture: acute onset, without precursors, more frequently in the daytime (emotional or physical exertion). Overall cerebral or focal symptoms are developed.

Consciousness: from stunning to coma, defining the prognosis. In bursting of blood into ventricles of the brain — a sharp aggravation of general state in the form of elevation of temperature, respiratory disorders, deepening of vegetative disorders, hormetonia are noted. Hemorrhages into cerebral hemispheres are complicated by a secondary truncal syndrome, and into the trunk — by tetraparesis or tetraplegia, oculomotor disorders.

Electroencephalography, echoencephalography, angiography, computerized and nucleic magnetic resonance tomography help in the diagnosis. A shift of intracerebral vessels into avascular zones is noted. Computerized tomography allows to diagnose parenchymatous hemorrhage in the form of foci of increased density in cerebral parenchyma. Erythrocytes are determined in liquor in spinal puncture.

Subarachnoidal hemorrhage. An acute onset without precursors, sharp headache (more often in the occipital region), dizziness, nausea, vomiting, short loss of consciousness, meningeal symptoms are observed.

Local symptoms may appear on the 3-5 days as a result of spasm, as well as elevation of body temperature, leukocytosis. Recurrent subarachnoidal hemorrhages are typical in 7-14 days.

Persistent focal disorders develop in subarachnoidal-parenchymatous hemorrhage.

Blood has a xanthochromic tint in liquor on the 3-5 day of the disease. Changes in the form of hemorrhages and congestion are seen in the fundus of the eye.

Ischemic insult (cerebral infarction) is the result of atherosclerotic lesion of great cerebral vessels on the background of arterial hypertension, diabetes mellitus. By the mechanism of development we distinguish thrombotic and nonthrombotic insult.

The up-to-date conception of pathogenesis of ischemic insult — is the conception of threshold ischemic blood flow. The threshold is defined by critically low level of cerebral blood flow and insufficient supply of oxygen to the cerebral tissue.

The upper ischemic threshold is observed in the blood flow < 20-18 ml/ 100 g of the brain per min. A further decrease of this index leads to disappearance of somato-sensory generated potentials and EEG-activity,

disorder of synaptic transmission. At the same time, energy potential and function of ion pumps are maintained.

The lower ischemic threshold arises in blood flow of 10-12ml/100 g of the brain per min. ATP, here, is not synthetized, function of cell membranes is broken: neurons lose K^, absorb Ca^+T, Na^T and water by osmosis. The increase of Ca⁺^ content in neurons activates membrane phospholipases, contributes to the formation of toxic fatty acids that are the link of many processes leading to the death of cerebral cells (cerebral infarction).

The conception of "ischemic penumbra".

It is a zone that is formed around ischemic center or infarction nucleus. A blood flow is reduced in it and is between two ischemic thresholds. As a result of this neurons function ceases. Disturbances of neurons' function bear a reversible nature only for 6 hours. A timely increase of cerebral blood flow in the zone of ischemic "penumbra" allows to restore a normal functioning of neurons in this region, and decrease of cerebral blood flow leads to the death of neurons' cells and neuroglia. This occurs as a result of disproportion between cerebral blood flow and neuronal metabolism.

A region of cerebral infarction, in a day after its development, consists of two different areas — ischemic and hyperemic. In other words, zones of "miserable" perfusion or hypoperfusion with a low blood flow, high coefficient of oxygen extraction in the tissue of ischemic area of the brain, as well as zones of excessive perfusion and hyperperfusion with obligatory elevation of partial pressure of oxygen, signs of decrease of A-V difference by oxygen and carbon dioxide are revealed.

More frequent cerebral infarction occurs in the pool of the middle meningeal artery. A gradual onset, in the course of several hours, sometimes, 2-3 days is typical.

Growing focal neurologic symptoms prevail over general cerebral ones. Pseudotumorous form of cerebral infarction develops in 1/3 of cases.

Vegetative disorders and meningeal signs on the background of maintained or stunned consciousness are registered in development of cerebral edema.

Embolic infarction arises acutely, without any precursors, a loss of consciousness is possible, often convulsions. A loss of functions is incomplete, but rapid.

Diagnosis is based on the study of preinsult period, rate of insult development, the state of focal and general cerebral symptoms, as well as the dynamics of their reverse development, investigations of the fundus of the eye, lumbar puncture, echoencephalography, computerized and nucleic magnetic resonance tomography.

In cerebral infarction foci of reduced density are revealed at the end of the first day by means of positron emission tomography. Here, we may judge not only of cerebral blood flow, but of cerebral metabolism as well.

Treatment: A success of treatment is defined with time factor and intensity of treatment.

One should not prescribe preparations, which efficiency is not proved (steroids, glycerol, glycosides). In sub-, epi- and intracerebral hematomas patients' hopitalization is indicated to neurosurgical department.

Basic (nondifferentiated) therapy

1) Arresting of disorders of vitally important functions (respiration, hemo­dynamics);

2) Normalization of WEE and AAB in patients being in comatous state;

3) Decrease of intracranial hypertension;

4) Decrease of complications rate.
Differentiated therapy of hemorrhagic insult:

— Dehydration (saluretics);

— Hypotensive therapy (clophelinum, etc.);

— Hemostasis (vicasol, CaCl₂, dicynone, vitamin C);

— Agents inhibiting fibrinolysis (ACA);

— Sedation — diazepam, sibazonum, relanium;

— For prevention of ischemia — vasodilators, calcium antagonists (nino-dopin, nimotop);

— Surgical treatment in lateral hematomas or hemorrhages into the cerebellum.

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