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Treatment of arteriovenous malformations

 
, medical expert
Last reviewed: 04.07.2025
 
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On the one hand, it is quite easy to answer the question of what method to use to treat arteriovenous malformation, since only the surgical method allows the patient to get rid of the AVM itself and the complications it leads to. But, on the other hand, it is often very difficult to assess the risk of surgical intervention and the risk of developing these complications. Therefore, each time it is necessary to take into account many factors, the total assessment of which can incline the doctor to active surgical treatment or refuse it.

Choice of tactics for treatment of arteriovenous malformations

First of all, the variant of clinical manifestation of AVM is important. If the patient has had at least one spontaneous intracranial hemorrhage, conservative treatment can be applied only at a certain stage, but surgical treatment is inevitable. The question may only be in the choice of the method of surgery, which we will discuss below. Other variants of clinical manifestation of AVM pose a lesser danger to the patient's life, but it should not be forgotten that in almost half of such patients, AVM rupture can occur within 8-10 years. But even without taking into account the threat of rupture, the severity of clinical manifestations and the degree of disability of the patient can be such that surgery becomes absolutely indicated. Thus, migraine-like headache of moderate intensity, rarely (1-2 times a month) bothering the patient, cannot be an indication for surgical treatment if the operation itself is associated with a risk to the patient's life and a high probability of developing a neurological defect. At the same time, there are AVMs (usually extra-intro-cranial or associated with the dura mater), which cause persistent, almost constant headaches that are not relieved by simple analgesics. The pain can be so intense that it prevents the patient from performing even simple work and actually disables him. Some patients resort to drugs, while others attempt suicide. In such situations, the risk of even a complex operation is justified and patients willingly agree to it.

Epileptic seizures caused by AVMs may vary in severity and frequency: minor seizures such as absences or twilight consciousness, localized Jackson-type seizures, and full-blown seizures. They may recur with a frequency of once every few years and several times a day. In this case, the patient's social status, profession, and age should be taken into account. If minor rare equivalents do not significantly affect the patient's profession, do not limit his degree of freedom and quality of life, then a complex and dangerous operation should be avoided. But if the risk of surgery is not high, it should be undertaken, since the danger of AVM rupture remains, and in addition, the seizures themselves, even rare ones, gradually lead to a change in the patient's personality, as well as long-term use of anticonvulsants. A high-risk operation can only be performed on patients who suffer from frequent, full-blown epileptic seizures that prevent them from even leaving their apartment on their own and practically turn them into invalids.

Severe and dangerous are pseudotumor and stroke-like variants of the clinical course of AVM, since they lead to patient disability even without hemorrhage, therefore surgery may be contraindicated only if it is associated with a risk to the patient's life or the likelihood of developing a more severe neurological deficit than already exists. Somewhat less dangerous are transient cerebrovascular accidents, especially isolated ones, but it should not be forgotten that with this variant of the course, an ischemic stroke may also develop. Considering the severity of various variants of the clinical course of AVM and the risk of possible complications in an attempt at their radical extirpation, we have developed a simple method for determining indications for surgery.

We have identified 4 degrees of severity of the clinical course and 4 degrees of surgical risk depending on the size and location of the AVM.

Severity of the clinical course.

  1. degree - asymptomatic course;
  2. degree - isolated epileptic seizures, isolated PIMC, rare migraine attacks;
  3. degree - stroke-like course, pseudotumor course, frequent (more than once a month) epileptic seizures, repeated PIMC, frequent persistent migraine attacks;
  4. degree - apoplectic type of course, characterized by one or more spontaneous intracranial hemorrhages.

The degree of surgical risk in radical extirpation of AVM.

  1. degree - AVMs of small and medium size, cortical-subcortical, located in functionally “silent” areas of the brain.
  2. degree - small and medium-sized AVMs located in functionally important areas of the brain, and large AVMs in “silent” areas of the brain.
  3. degree - small and medium-sized AVMs located in the corpus callosum, in the lateral ventricles, in the hippocampus and large AVMs in functionally important areas of the brain.
  4. degree - AVM of any size located in the basal ganglia, AVM of functionally important parts of the brain.

In order to determine the indications for open surgery, a simple mathematical operation must be performed: subtract the surgical risk degree from the clinical course severity indicator. And if this results in a positive result, the operation is indicated; if the result is negative, the operation should be avoided.

Example: Patient K. has an AVM manifested by full-blown epileptic seizures 1-2 times a month (grade III severity). According to angiography, the AVM is up to 8 cm in diameter and is located in the mediobasal regions of the left temporal lobe (grade IV surgical risk): 3-4=-1 (surgery is not indicated).

In case of a zero result, subjective factors should be taken into account: the patient's and relatives' willingness to undergo surgery, the surgeon's experience and qualifications. It should not be forgotten that 45% of malformations, regardless of their clinical manifestation, can rupture. Therefore, if a zero result is obtained, surgical treatment should still be considered. Malformations, the open removal of which is associated with a grade IV risk, are best operated on endovascularly, but only if the clinical course of the AVM and the degree of surgical risk allow choosing an adequate treatment tactic. Otherwise, the tactic in the acute period of AVM is determined. In this case, the severity of the patient's condition, the volume and localization of the intracranial hematoma, the presence of blood in the cerebral ventricles, the severity of the dislocation syndrome, the size and localization of the AVM itself are taken into account. The main issue that needs to be addressed is the choice of the optimal timing and scope of surgical intervention.

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Choice of treatment tactics in the acute period of rupture of arteriovenous malformation

Treatment tactics in the acute period of arteriovenous malformation rupture are determined by many factors: the size and location of the AVM, the volume and location of the intracerebral hemorrhage, the time since the rupture, the severity of the patient's condition, age and somatic status, the surgeon's experience in performing such operations, the equipment of the operating room, and many others. In the vast majority of cases, ABM ruptures result in the formation of intracerebral hematomas, which can be limited or can break through into the ventricular system or the subdural space. Much less often, AVM rupture is accompanied by subarachnoid hemorrhage without hematoma formation. In this case, treatment tactics in the acute period should be conservative only. Surgical removal of the arteriovenous malformation can be performed only after 3-4 weeks, when the patient's condition becomes satisfactory and signs of cerebral edema disappear according to ACT. In case of intracerebral hematoma formation, its volume, localization, severity of dislocation syndrome and perifocal cerebral edema should be taken into account. It is necessary to assess the severity of the patient's condition and, if it is severe, to determine the cause: whether the volume of the hematoma and the dislocation of the brain determine the severity of the condition or it is caused by the localization of hemorrhage in functionally important centers, and possibly other reasons. In the first case, the question of surgical intervention is raised, but it is necessary to determine the timing of its implementation and the scope of the operation. Emergency surgical treatment is carried out if the severity of the condition progressively increases and is caused by a hematoma with a volume of more than 80 cm3 and contralateral displacement of the midline structures of the brain by more than 8 mm, and the deformation of the enveloping pontine cistern indicates the initial signs of temporotentorial herniation. The scope of the operation depends on the patient's condition, the size and localization of the malformation itself. The patient's severe condition with severe impairment of consciousness up to stupor and coma, advanced age, severe concomitant pathology do not allow performing the operation in full. It is also impossible if a medium or large arteriovenous malformation has ruptured and its removal requires a multi-hour operation, prolonged anesthesia, and the possibility of blood transfusion cannot be ruled out. In such cases, the necessary operation for vital indications should be performed in a reduced volume: only the hematoma is removed and bleeding from the malformation vessels is stopped. If necessary and there is uncertainty in reliable hemostasis, an inflow-outflow system is installed. The malformation itself is not removed. The entire operation should not exceed one hour. If the source of the hematoma was a rupture of a small AVM, it can be removed simultaneously together with the hematoma, since this will not significantly complicate or prolong the operation.

Thus, emergency surgery for AVM rupture is performed only for large hematomas causing severe compression and dislocation of the brain, threatening the patient's life. In this case, only a small arteriovenous malformation is removed together with the hematoma, and the removal of medium and large AVMs should be postponed for 2-3 weeks, until the patient recovers from a serious condition.

In other cases, when the severity of the condition is determined not by the volume of the hematoma, but by the localization of the hemorrhage in vital structures of the brain (ventricle of the brain, corpus callosum, basal ganglia, pons, cerebral peduncles or medulla oblongata), emergency surgery is not indicated. Only in the case of development of hydrocephalus is bilateral ventricular drainage performed. Emergency surgery is also not indicated if the volume of the hematoma is less than 80 cm3 and the patient's condition, although serious, is stable and there is no direct threat to his life. In such cases, the AVM can be removed together with the hematoma in a delayed period. The larger the size of the AVM and the more technically difficult its removal, the later the surgery should be performed. Usually, these periods fluctuate between the second and fourth weeks from the moment of rupture. Thus, in case of AVM rupture in the acute period, conservative tactics or emergency surgery for vital indications in a reduced volume are more often undertaken. Radical extirpation of AVM should be performed in the delayed period (after 2-4 weeks), if possible.

Intensive care in the acute period of rupture of arteriovenous malformation

Patients with severity of the condition of I and II degrees according to Hunt and Hess do not require intensive care. They are prescribed analgesics, sedatives, calcium antagonists, rheological drugs, nootropics. A more severe category of patients - III, IV and V degrees of severity, require intensive care, which, along with general measures (ensuring adequate breathing and maintaining a stable central hemogram), should include rheological therapy, anti-edematous, neuroprotective, corrective and restorative.

Rheological therapy includes the introduction of plasma-substituting solutions (0.9% NaCl solution, Ringer's solution, plasma, polarizing mixture), rheopolyglucin, etc. Isotonic glucose solution can be used in small quantities (200-400 ml per day). The use of hypertonic glucose solutions is accompanied by an increase in metabolic acidosis, so it is not recommended. The total daily volume of intravenous infusion should be 30-40 ml/kg of weight. The main criterion for calculating this volume is hematocrit. It should be within 32-36. With spontaneous intracranial hemorrhages, as a rule, there is thickening of the blood, an increase in its viscosity and coagulability, which leads to difficulty in hemocirculation in the smallest vessels - precapillaries and capillaries, microvascular coagulation and capillary stasis. Rheological therapy is aimed at preventing or minimizing these phenomena. Along with hemodilution, antiplatelet and anticoagulant therapy (trental, sermion, heparin, fraxiparin) are carried out. Anti-edematous therapy includes measures aimed at the maximum elimination of any negative effects on the brain. This is, first of all, hypoxia. It can be caused by both external respiration disorders and hemocirculatory disorders. Intracranial hypertension also complicates blood flow through the cerebral vessels. It contributes to the development of edema and intoxication due to the breakdown of blood cells and the absorption of products of this breakdown into the blood, acidosis (mainly lactic and pyruvic acids), an increase in the level of proteolytic enzymes, vasoactive substances. Therefore, hemodilution itself eliminates some of the listed negative factors (blood thickening, increased viscosity, sludge syndrome, capillary stasis, intoxication). To eliminate acidosis, 4-5% soda is prescribed, the amount of which is calculated based on the acid-base balance. Corticosteroid hormones (prednisolone, dexamethasone, dexazone, etc.) protect neurons well from edema. They are administered intramuscularly 3-4 times a day. Thus, prednisolone is prescribed at a dose of 120-150 mg per day. In this case, arterial pressure may increase slightly, which is well corrected by the introduction of calcium antagonists.

In hypoxic conditions, antihypoxants effectively protect brain cells from edema. These are drugs that slow down the rate of biochemical reactions, thereby reducing the cells' need for oxygen. These include sodium oxybutyrate or GOMC, seduxen, sibazon, sodium thiopental, and hexenal. The daily dose of thiopental and hexenal can reach 2 g. Sodium oxybutyrate is administered at a dose of 60-80 ml per day. These drugs are especially indicated for patients with psychomotor agitation and with the development of diencephalic syndrome. In cases of prevalence of mesencephalobulbar syndrome (low blood pressure, muscle hypotonia, normo- or hypothermia, bulbar type of respiratory failure), antihypoxants are not indicated.

Since all patients with intracranial hemorrhage have a sharp increase in the activity of the kallikrein-kinin system and proteolytic enzymes, it is advisable to prescribe protease inhibitors. Contrycal, trasylol, gordox are administered in Ringer's physiological solution by drip, 30-50 thousand units per day, for 5 days. By this time, the activation of the kallikrein-kinin system decreases.

Calcium antagonists are important in the treatment of spontaneous intracerebral hemorrhages. By blocking calcium channels in cell membranes, they protect the cell from excessive penetration of calcium ions, which always rushes into cells suffering from hypoxia and leads to their death. Calcium antagonists also, by acting on the myocytes of the cerebral arteries, prevent the progression of angiospasm, which is very important in patients with ruptured malformations and the resulting compression of the brain. Various representatives of this group of drugs are used - isoptin, phenoptin, veropamil, nifedipine, corinfar, etc. The most active of them in relation to brain pathology is nimotop by Bayer (Germany). Unlike other similar drugs, nimotop has the ability to penetrate the blood-brain barrier. In the acute period, nimotop is administered intravenously by drip continuously for 5-7 days. For this purpose, nimotop is used in 50 ml vials containing 4 mg of the active substance. It is better to use a dispenser for this purpose. The rate of administration is controlled by the pulse rate (nimotop slows the heart rate) and by arterial pressure. With rapid administration of the drug, hypotension may develop. Arterial pressure should be maintained at the level of moderate hypertension (140-160 mm Hg). On average, one vial of nimotop is diluted in 400 ml of saline and this amount is enough for 12-24 hours. After 5-7 days, if the patient's condition improves, he is prescribed nimotol tablets 1-2 tablets four times a day.

With regard to nootropics and cerebrolysin, glycine, a wait-and-see approach should be followed. In the acute period of rupture, when nerve cells suffer from hypoxia and edema, stimulating their activity is inappropriate. These drugs will play an important role in restoring brain function after surgery.

It is important to prescribe antioxidants: vitamins A, E, selenium preparations. Along with this, corrective therapy is carried out, aimed at normalizing all homeostasis indicators. In cases where the hemorrhage is not classified as incompatible with life, such therapy leads to an improvement in the condition of patients with severity of grades III-IV in 7-10 days, after which the question of the timing of radical surgery can be decided.

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