Arteriovenous malformation

Arteriovenous malformation is a congenital defect in vascular development, which is characterized by the presence of an abnormal network of arteriovenous anastomoses. The most common arteriovenous malformation is located in the region of the posterior cranial fossa and have a fairly typical structure - one or two real arteries, an AVM coil and one draining vein.

[1], [2], [3]

Pathogenesis

The most dangerous is the rupture of the walls of the malformation, which is accompanied by a spontaneous intracranial hemorrhage. This is due to the fact that in the vessels of malformation, mixed blood circulates under pressure close to the arterial blood. And it is natural that high pressure leads to a stretching of degenerate altered vessels, an increase in their volume and a thinning of the wall. In the end, in the most thin place there is a gap. According to static data, this occurs in 42-60% of patients with AVM. Mortality at the first break of AVM reaches 12-15%. In others, bleeding can be repeated, without any periodicity. We observed a patient who for eleven years had eleven spontaneous intracranial hemorrhages. Such a relatively "benign" course of AVM rupture in comparison with the rupture of arterial aneurysms is explained by the peculiarities of hemodynamic disorders that appear after the rupture. It is known that the rupture of arterial aneurysm leads most often to subarachnoid hemorrhage (SAH) and the development of angiospasm, which in the first few minutes is protective in nature, contributing to the rapid stopping of bleeding, but in the subsequent represents a major danger to the life of the patient.

It is angiospasm, which leads to brain ischemia and its edema, and determines the severity of the patient's condition and prognosis. In contrast, the angiospasm of the leading AVM arteries, on the contrary, improves blood supply to the brain due to a decrease in arteriovenous discharge. When the AVM is ruptured, intracranial and subdural hematomas are often formed. The breakthrough of blood in the subarachnoid cisterns is secondary. Bleeding from the ruptured wall of the AVM stops faster, because the blood pressure in it is lower than in the main arteries and the wall is more malleable to compression by the bleeding. Naturally, this does not always end safely for the patient. The most dangerous are AVM ruptures near the ventricles of the brain, in the subcortical ganglia and in the brainstem. Angiospasm of the leading arteries in this situation helps stop bleeding.

The determining factor in the pathogenesis of the AVM rupture is the volume of blood flow and localization of the hematoma. The hemispheric intracerebral hematomas, even up to 60 cm ³  , are relatively favorable. They can cause gross focal neurological disorders, but rarely lead to gross vital disorders. Breaking the hematoma into the ventricles of the brain greatly worsens the prognosis. On the one hand, the blood, irritating the ependyma of the ventricles, strengthens the liquor production, on the other hand, acting on the ventricle bottom, leads to gross disorders of the functions of vital centers located in the hypothalamus. The spread of blood throughout the ventricular system leads to tamponade last, which in itself is not compatible with life.

The blood penetrated into the subarachnoid cisterns also violates the liquor circulation, making it harder for the cerebrospinal fluid to be blocked by the pachyon granulations. As a consequence, the resorption of the CSF is slowed and acute cerebrospinal fluid hypertension can develop, followed by internal and external hydrocephalus. As a result of the disintegration of the formed elements of the outflowing blood, a large number of toxic substances are formed, most of which have a vasoactive effect. This, on the one hand, leads to vasoconstriction of small pial arteries, on the other - increases the permeability of capillaries. Blood decay products also affect nerve cells, altering biochemical processes in them and disrupting the permeability of cell membranes. First of all, the function of the potassium-sodium pump changes and the potassium begins to leave the cell, and in its place rushes the sodium cation, which is four times more hydrophilic than potassium.

This leads first to intracellular edema in the zone around the hemorrhage, and then to the swelling of the cells. The development of edema is also promoted by hypoxia, which inevitably joins due to compression of the brain vessels with hematoma and elevated cerebrospinal pressure, as already mentioned. Violation of the functions of the diencephalic parts of the brain and, above all, the regulation of the water-electrolyte balance leads to a delay in the body's fluid, loss of potassium, which also increases the edematous response of the brain. The pathogenesis of AVM rupture is not limited to cerebral disorders. Equally dangerous are extracerebral complications. First of all, it is a cerebro-cardiac syndrome, which can simulate acute coronary insufficiency on an electrocardiogram. 

Quite quickly, patients with intracerebral hemorrhages develop pneumonia and respiratory failure. Moreover, the bacterial flora plays a secondary role. Primary is the central effect on the lungs, consisting of widespread bronchospasm, increased production of sputum and mucus, ischemia of pulmonary parenchyma due to a widespread spasm of small pulmonary arteries, which quickly leads to dystrophic disorders, desquamation of the alveolar epithelium, a decrease in the gas exchange function of the lungs.

If this is accompanied by oppression of the cough reflex, bulbar type of respiratory failure, then there is a serious threat to the life of the patient. In most cases, the subsequent purulent trachyronchitis badly lends itself to antibacterial therapy and aggravates respiratory failure, which immediately affects the intensification of brain hypoxia. Thus, violation of external respiration, even with a relative compensation of cerebral disorders, can lead to death. Often, patients after coma regain consciousness, but then die from increasing respiratory failure and hypoxic brain edema.

Dystrophic changes quickly develop not only in the lungs, but also in the liver, the gastrointestinal tract, the adrenal gland and kidneys. A threat to the life of a patient is a urinary infection and pressure sores that develop rapidly in the absence of good care for the patient. But these complications can be avoided if doctors remember about them and know the methods of fighting them.

Summing up the examination of the pathogenesis of the AVM rupture, it should be emphasized that mortality with such intracranial hemorrhages is lower than with rupture of arterial aneurysms and hypertensive hemorrhagic strokes, although it reaches the figure of 12-15%. For AVM are characterized by repeated, sometimes multiple hemorrhages with different frequency, which can not be foreseen. In the unfavorable course of the posthemorrhagic period, the listed pathogenetic mechanisms can lead to a fatal outcome.

[4], [5], [6], [7], [8], [9], [10], [11], [12], [13], [14]

Symptoms of the arteriovenous malformation

Hemorrhagic type of course of the disease (50-70% of cases). This type is characterized by the presence of a patient with arterial hypertension, a small size of the malformation node, draining it into deep veins, arteriovenous malformation of the posterior cranial fossa quite often.

Hemorrhagic type in 50% of cases is the first symptom of manifestation of arteriovenous malformation, causes a detailed result and 10-15% and disability of 20-30% of patients (N. Martin et al.). The annual risk of hemorrhage in patients with arteriovenous malformation is 1.5-3%. The risk of re-hemorrhage during the first year reaches 8% and increases with age. Bleeding from arteriovenous malformation is responsible for 5-12% of all maternal mortality and 23% of all intracranial hemorrhages in pregnant women. The picture of subarachnoid hemorrhage is observed in 52% of patients. 17% of patients have complicated forms of hemorrhage: the formation of intracerebral (38%), subdural (2%) and mixed (13%) hematomas, ventricular gemotamponade develops in 47%.

Torpid flow type is characteristic for patients with arteriovenous malformation of large size, localization in the cortex. Blood supply of arteriovenous malformation is carried out by branches of the middle cerebral artery.

For the torpid current type, convulsive syndrome is most common (in 26-27% of patients with arteriovenous malformation), cluster headaches, progressive neurological deficit, as in brain tumors.

Variants of clinical manifestation of arteriovenous malformations

As already indicated, the most frequent first clinical manifestation of AVM is spontaneous intracranial hemorrhage (40-60% of patients). It arises more often without any precursors, amid overall health. Provocative moments can be physical stress, stressful situation, neuropsychic stress, taking large doses of alcohol, etc. At the moment of the AVM rupture, the patients feel a sudden sharp headache, like a stroke or a rupture. The pain quickly builds up, causing dizziness, nausea and vomiting.

In a few minutes, loss of consciousness may occur. In rare cases, the headache may be non-intensive, the patient's consciousnesses do not lose, but they feel how limbs weaken and grow numb (usually contralateral to the focus of hemorrhage), speech is broken. In 15% of cases, hemorrhage manifests as a developed epiprip, after which patients can remain in a coma.

To determine the severity of hemorrhage from AVM, the above Hunt-Hess scale can be taken as a basis with some amendments. In view of the fact that hemorrhages from AVM can have very different symptoms, focal neurological symptoms can prevail over cerebral palsy. Therefore, patients who are at the level of consciousness on the I or II stages of the scale may have gross focal neurological disorders (hemiparesis, hemi-hypesthesia, aphasia, hemianopsia). In contrast to aneurysmal hemorrhages, when the AVM is ruptured, it is not the extent and prevalence of angiospasm that is determined by the extent and location of the intracerebral hematoma.

Meningeal syndrome develops in a few hours and its severity may be different. Arterial pressure, as a rule, increases, but not so dramatically and not as long as with the rupture of arterial aneurysms. Usually this rise does not exceed 30-40 mm Hg. Art. On the second-third day there is a hyperthermia of the central genesis. The condition of patients regularly deteriorates with the growth of brain edema and the intensification of the decomposition of blood. This lasts up to 4-5 days. With a favorable course after stabilization on the 6th-8th day, the condition of patients begins to improve. The dynamics of focal symptoms depends on the location and size of the hematoma.

When hemorrhaging into functionally important areas of the brain or the destruction of motor conductors, the symptoms of prolapse appear immediately and are maintained for a long time without any dynamics. If the symptoms of prolapse do not appear immediately, but increase in parallel with the edema of the brain, you can expect a deficit recovery in 2-3 weeks, when the edema completely regresses.

The clinical picture of AVM rupture is very diverse and depends on many factors, the main of which are: the volume and localization of hemorrhage, the severity of edematous brain reaction, the degree of involvement of stem structures in the process.

Arteriovenous malformations can be manifested by epileptiform seizures (30-40%). The cause of their development can be hemocirculatory disorders in neighboring areas of the brain due to the phenomenon of stealing. In addition, the malformation itself can act irritatingly on the cerebral cortex, generating epi-discharges. And as we have already talked about individual types of AVM around which gliosis of brain tissue develops, which is also often manifested by epi-seizures.

For an episodrom, due to the presence of AVM, the causelessness of emergence in adulthood, often in the total absence of a provoking factor, is characteristic. Seizures can be generalized or focal. The presence of a clear focal component in the epiprip if there are no cerebral symptoms should lead to the idea of a possible AVM. Even generalized seizures, if they start with seizures mainly in the same limbs with a violent turn of the head and eyes in one direction or another, are often a manifestation of AVM. Less often in patients there are small seizures such as absences or twilight consciousness. Frequency and periodicity of epipriplets can be different: from single to repetitive.

[15], [16], [17], [18], [19]

Forms

V.V. Lebedev and co-workers. Identified three variants of cerebro-cardial syndrome according to ECG data:

• I type - a violation of the functions of automatism and excitability (sinus tachy- or bradycardia, arrhythmia, atrial fibrillation);
• Type II - changes in repolarization processes, transient changes in the end phase of the ventricular complex by type of ischemia, damage to the myocardium with a change in the T wave and the position of the ST segment;
• III type - a violation of the conductivity (blockade, signs of increased stress on the right heart). These ECG changes can be combined and their severity correlates with the severity of the general condition of the patients.

[20], [21], [22], [23], [24]

Diagnostics of the arteriovenous malformation

The presence in the patient of at least one of the clinical signs of AVM, which was mentioned in the symptoms, is a serious reason for a detailed examination, which is carried out according to a certain scheme. You should begin with a careful history. In this case, the diseases of parents and close relatives are clarified, since hereditary predisposition to AVM is not excluded. Anamnesis of the patient's life is revealed from the moment of his birth: how the childbirth passed, what he suffered in childhood, diseases and injuries, when the first signs of the disease appeared, etc. When a neurological examination, unless the patient has a pseudotumorous and non-insult-like variant of the clinical course of AVM, there may not be a rough focal symptomatology.

However, even a slight anisoreflexia, reflexes of oral automatism, a violation of the functions of the cranial nerves may indicate an organic lesion of the brain. If the patient feels a pulsating noise in the head, it is necessary to perform auscultation over the paranasal sinuses and in the temporal areas. However, such noise can rarely be objectified. It occurs only with extranitranial and giant AVM. A special study of the patient begins with non-invasive methods.

First of all, this is an electrophysiological examination. Rheoencephalography (REG) often does not give an indication of AVM, but the asymmetry of the blood filling of various arterial basins, the asymmetry of vascular tone can indirectly confirm a presumptive diagnosis. More informative is the electroencephalography (EEG), it can detect irritative changes in bioelectrical activity with an accent in some area of the brain. In pseudotumorous or stroke-like flow, a focus of pathological bioactivity may appear on the EEG, often in the form of recording slow high-amplitude waves. In patients with epileptic type of course, a focus of epileptic activity is possible, especially with functional loads (hyperventilation of the lungs, sound and light stimuli).

Thus, the electrophysiological methods of brain research, although not specific, nevertheless, with the correct interpretation of the results can confirm the diagnosis of AVM, but the absence of any changes in REG and EEG does not exclude AVM.

In recent years, ultrasonic methods have been widely used in the diagnosis of cerebrovascular diseases. Ultrasonic dopplerography of extracranial arteries can reveal the acceleration of blood flow in this or that arterial basin by 1.5 times or more, since with medium and large AVM - the velocity of blood flow in the leading arteries is much higher than normal values. However, small-size AVMs do not significantly affect the rate of blood flow in the extracranial arteries, therefore they are not detected by extracranial dopplerography.

More informative is the method of transcranial Doppler. It can detect not only a significant acceleration of blood flow in the arteries that supply blood to the AVM, but also the so-called "shunting phenomenon".

The presence of free shunting causes the emergence of a number of hemodynamic phenomena, which are recorded in the Doppler study in the form of a pattern of lightweight perfusion or shunting. 

It is characterized by:

• significant increase (mainly due to diastolic), the linear velocity of blood flow is proportional to the level of arteriovenous discharge;
• a significant reduction in the level of peripheral resistance (due to organic damage to the vascular system at the level of resistive vessels, which determined the low level of circulatory resistance in the system);
• relative safety of kinematics indexes of the flow;
• the absence of pronounced changes in the Doppler spectrum (the broadening of the spectrum is observed with the AVM of the "large flux" causing turbulent rotation in the zones of bifurcations of the main arteries of the head, up to the formation of non-pulsating turbulent patterns);
• a sharp decrease in cerebrovascular reactivity, due to the absence in the AVM system of vessels possessing contractile properties.

The sensitivity of TCD in the diagnosis of arteriovenous malformations according to the described criterion is 89.5%, with a specificity of 93.3% and error-freeness of 90.8%.

The next non-invasive method of investigation is X-ray tomography. It allows you to identify AVM from 2 cm in diameter and more, but it is better to identify large and giant. Computerogram AVM is quite typical, they can not be compared to any other pathology. They look like foci of heterogeneous density (hyper- and hypodensitive), irregular in shape, sometimes worm-like interwoven without the phenomena of perifocal edema and without mass effect, that is, without displacements and deformations of the ventricles of the brain and subarachnoid cisterns.

Often in the body of malformation, sharply hyperdense inclusions are revealed - these are the centers of calcification. They have almost bone density, irregular shape and a variety of sizes. If all of these signs occur - it is pathognomonic for AVM. Intravenous administration of iodine-containing contrast agent allows for better visualization of arteriovenous malformations. In this case, the hyperdense focus becomes even more dense and may even reveal enlarged drainage veins.

With ruptures of AVM and spontaneous intracranial x-ray hemorrhages, computed tomography is also highly informative. The main significance is given to the localization of intracerebral hemorrhage, its shape and appearance. So, if the aneurysmal hemorrhages are located mainly near the basal cisterns, and the hypertensive hemorrhages are near the basal ganglia, then the hematomas due to the AVM rupture can be localized anywhere, like on convection, reaching the cerebral cortex, and near the median structures of the brain.

Everything depends on the localization of the AVM itself. In appearance, such hemorrhages have a non-uniform density (against a background of hyperdense hemorrhage, foci of normal or decreased density are determined), irregular shape, uneven contours. Against the background of hemorrhage, the body of the AVM itself can not be determined, but in rare cases the body of malformation can look like a "filling fault" of the hematoma cavity with blood. It has long been proven that spontaneous hemorrhages occupy a certain volume, stratifying the brain. Therefore, their boundaries, as a rule, are even, clear, and the shapes approach an ellipse or ball. When the AVM ruptures, the blood, as it were, exfoliates the brain substance from the body of the malformation and, therefore, sometimes the contours of the AVM itself can be traced in the center or along the periphery of the hemorrhage.

In cases where arteriovenous malformation is located near the ventricles of the brain or basal cisterns, when it is ruptured, blood can flow directly into them. In these situations, computed tomography only ascertains the presence of subarachnoid or intraventricular hemorrhage, but it is impossible to distinguish it from aneurysmal or hypertensive.

When the AVM ruptures, computed tomography (CT) is not only diagnostic, but also prognostic, and therefore allows you to choose adequate therapeutic tactics.

Evaluating the computerogram, in addition to the size of the hemorrhage, it is necessary to take into account the severity and prevalence of perifocal edema, the condition of the ventricles of the brain and the degree of their displacement, changes on the part of subarachnoid cisterns. The hemispheric hemorrhage usually causes compression of the homolateral lateral ventricle until complete nonvisualization, while the contralateral and third ventricles are displaced in the opposite direction. The degree of displacement depends on the volume of the hematoma and the severity of the brain edema.

The displacement of the median brain structures in the opposite direction from the hematoma by more than 10 mm indirectly indicates a threat to the life of the patient and, if it is caused by a large volume of hematoma (more than 100 cm ³ ), it is necessary to decide the question of an emergency operation. But if the volume of the hematoma is less than 60 cm ³, and the displacement of the median structures exceeds 10 mm, it should be interpreted as a result of cerebral edema, and in this situation the operation will only exacerbate its course and worsen the prognosis. More favorable in the diagnostic plan is the case when large hematoma sizes (80-120 cm ³ ) cause a moderate displacement of the median structures (less than 8 mm). In this case, as a rule, perifocal edema is not clearly expressed and this allows you not to rush with the operation.

An important prognostic value is the visualization of the bridge covering the cistern. Until it is clearly visible, you can stick to expectant tactics. But if one of its sides is not visualized (amputation of half of the enclosing tank on the side of the hematoma), emergency measures should be taken to save the life of the patient, since such a picture indicates the development of temporo-tentorial injection (axial displacement of the brain with a hiccampal convolution in the gap between the brain stem and the edge of the tentorial opening), which is a direct threat to the life of the patient. If the covering tank of the bridge is not visualized at all - the situation is critical and even an emergency operation can no longer save the patient.

Thus, X-ray computed tomography is an important method in the routine diagnosis of arteriovenous malformations and in the diagnosis and prediction of the outcome of intracranial hemorrhages due to rupture of arteriovenous malformations.

The most informative and up to date indispensable method of diagnosis of arteriovenous malformations is angiography. Cerebral angiography is an invasive method of research, associated with the risk of developing a number of complications (embolism of the cerebral arteries, angiospasm in response to the introduction of a catheter or contrast medium into the artery, thrombosis of the artery at the site of its puncture, allergic reaction to contrast, etc.). Therefore, for its conduct, there should be clear indications.

Angiography is absolutely indicated to all patients with spontaneous intracranial hemorrhages, since only it allows to establish the true cause of hemorrhage. Exception is made only by those patients, in whom irrespective of the result of angiography operative intervention is not expedient. These are patients in the terminal state, patients of senile age and with gross decompensated somatic pathology.

It is somewhat more difficult to give indications for angiography in a planned manner. All patients with one of the described variants of the clinical manifestation of AVM, except for the asymptomatic, are subject to all non-invasive methods of examination.

If at the same time there is at least one sign confirming the presence of arteriovenous malformation, angiography should be considered as shown. If none of the methods indicates a possible presence of AVM, you should not immediately abandon angiography. It is necessary to evaluate the clinical picture. So, if the patient had only one epicopa and without a focal component, total cerebral angiography should be discarded.

At the same time, even one epiproduct, but with a clear focal component (weakness or numbness of one of the limbs or hemitip, numbness of the half of the face, short-term speech or seizure of Jackson type, coming hemianopsia, etc.), gives grounds for angiography. The same applies to the migraine-like course of AVM. If seizures of hemicranialgia are rare and occur with moderate severity, angiography can be abstained. But frequent and severe migraine attacks, practically disabling the patient, require an angiographic examination.

Transient impairment of cerebral circulation (PNMC) in the vertebrobasilar department is often the result of circulatory insufficiency in it due to impaired permeability of vertebral arteries or angiospasm. Therefore, it is not advisable to examine these patients with angiographic examination for AVM. At the same time, even single PNMCs in one of the cerebral hemispheres in young people require angiography, since more often they are caused not by an occlusive-stenotic lesion of the arteries, but by arteriovenous malformation.

As for patients with pseudotumorous and stroke-like clinical manifestations of arteriovenous malformation, angiography is also shown.

Thus, any suspicion of the presence of AVM in most cases requires an angiographic examination, except for those situations where surgical treatment is contraindicated.

Angiographic examination of patients with AVM has a number of characteristics. When examining a patient, it must be remembered that the velocity of blood flow in the leading arteries of medium and large AVM can several times exceed the normal values, so the speed of angiographic survey should be higher than usual. With multi-fistular malformations, after 2 seconds the contrast can pass through her body and the draining veins. Modern angiographic devices allow tracing the passage of contrast in any period of time.

This gives very important information about the direction of various flows in the body of the malformation, the sequence of filling its vessels. Each of the feeding arteries supplies only a part of the arteriovenous malformation, while the remaining vessels of the malformation are not visible. Therefore, the second important feature of angiography is that despite obtaining information about the presence of AVM in one of the arterial basins, it is necessary to contrast other pools. Hemodynamically active AVM can be filled not only from one carotid and vertebrobasilar basin, but also from the contralateral carotid artery.

Therefore, to obtain complete information about the size of AVM and the sources of its blood supply, it is necessary to contrast both carotid and vertebrobasilar basins, which is easier to achieve with selective angiography. The same can be achieved with right-sided axillary and left-sided direct carotid angiography. With right-sided axillary angiography, the contrast retrograde under pressure enters the brachiocephalic trunk and simultaneously the vertebral artery and carotid contrasts. Thus, one introduction of contrast allows one to immediately obtain information about two basins. The left carotid artery departs from the arch of the aorta independently, so for its contrasting, direct puncture angiography can be performed. Such a partial angiography, although longer than the selective one, but in patients with severe atherosclerosis of the aorta and its branches, is more acceptable, since conducting a catheter in such situations, on the one hand, presents great technical difficulties, and on the other - is fraught with danger either damage to the atherosclerotic plaque, or detachment of the parietal thrombus with subsequent embolism of the cerebral arteries.

When assessing angiography, you need to pay attention to the following points:

1. The size of arteriovenous malformation is determined in two projections by measuring the greatest distance from the outer boundaries of the AVM body. At the same time contrast data of all basins are compared and supplemented. For example, AVM, having a total size of 8x8 cm, with carotid angiography is contrasted only by 2/3 of the volume, and by 1/3 - from the posterior cerebral artery. Comparison of these images by imposing allowed to obtain information about its true dimensions.
2. Determining the sources of blood supply, it is necessary to establish not only the pools from which the AVM is filled with contrast, but also the direct leading arteries: their number, diameter, location in relation to the cerebral cortex and the main furrows and cisterns, the peculiarities of their branching and the place of approach to the AVM body. In some cases, two standard folds are not enough, because the arteries are superimposed one on top of the other and simultaneously on the body of malformation, so repetition of angiography with a rotation of the head 45 degrees in one direction or another is possible. Modern angiographic devices allow, with a single administration of contrast medium, to obtain an image of the brain arteries from any angle, rotating the image on the display around both the vertical and horizontal axes. Of all the leading arteries, it is necessary to identify the main arteries (they usually are from one to three) and secondary. The latter can be several dozen. And not all arteries are detected angiographically. Some of them because of smaller diameter and less hemodynamic significance are not detected, but during surgery the surgeon inevitably encounters them and must be able to coagulate and cross without damaging them. Bleeding if such arteries is damaged by a spatula or suction tip delivers a lot of trouble to the surgeon.
3. By determining the draining veins, their number, sizes and venous sinuses are counted, into which these veins flow.
4. The spatial arrangement of the draining veins and the leading arteries is compared to determine the correct surgical tactics.
5. The hemodynamic activity of AVM is determined. The more active the arteriovenous malformation, the more pronounced "stealing" of the brain. With large multi-fistular AVM on an angiogram, only the leading and draining vessels and the body of the AVM can be seen, and the other cerebral arteries are not at all in contrast, which creates the illusion of their absence. Medium and small AVMs do not cause a large "stealing", so they tend to be detected against the background of a normal cerebral vascular pattern.
6. It is necessary to remember the existence of hemodynamically inactive AVM. These are usually venous malformations, telangiectasias, certain types of cavernous malformations, the so-called cavern. Their angiographic detection is very difficult. Typically, typical angiographic signs in the form of hypertrophic leading arteries, enlarged drainage veins, contrasted in the arterial phase, are absent. However, upon closer examination of the angiogram, one can see pathological vessels reminiscent of either a fine mesh, sprouts, jellyfish or individual vessels, atypically located, uneven in diameter and twisted in the most bizarre manner. In this case, the draining veins may be absent. It is also difficult to see micromalformation (less than 5 mm); since they are often superimposed on larger main vessels and the summation of the image does not allow them to be identified.
7. The ruptured arteriovenous malformations can be thrombosed. With partial thrombosis, the malformation is still visible on the angiogram, but its true dimensions may be several times greater than the detected angiographic dimensions. The surgeon must always remember this when going to surgery, and be prepared for the fact that the malformation will be considerably larger. In a number of cases (according to our data, 12%), the ruptured malformation is subjected to total thrombosis. This is especially true for small and medium AVMs. They are not detected angiographically or a weakly contrasting draining vein can be seen in the arterial phase. In such difficult situations, anamnesis, the age of the patient, the nature and localization of computed tomography data, the detection of petrificata next to hematoma can help to think about the possibility of an AVM rupture. On the operation, removing the hematoma, the surgeon should always examine its walls in order to detect AVM.
8. Angiography is performed in the postoperative period to confirm the radical nature of extirpation. The presence of at least one draining vein, revealed in the arterial phase, indicates a non-surgical operation.

Diagnosis of arteriovenous malformations requires the doctor, first of all, the knowledge of the clinic, the morphology of AVM and the possibilities of existing methods. For correct choice of medical tactics and successful surgical treatment, information about AVM should be complete and comprehensive.

[25], [26], [27], [28], [29]

Treatment of the arteriovenous malformation

Open (transcranial) interventions:

• Stage I - coagulation of afferents;
• II stage - isolation of the nucleus of arteriovenous malformation;
• Stage III - dressing and coagulation with efferent and removal of arteriovenous malformation,

Endovascular interventions:

• stationary balloon-occlusion of feeding arteries - embolization in the flow (uncontrolled);
• combination of temporary or permanent balloon occlusion with embolization in the flow;
• super selective embolization.

Arteriovenous malformation is also treated by radiosurgery (Gamma-knife, Cyber-knife, Li nas, etc.).