Dissection and rupture of the aorta. What causes illness. What it is

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Aortic dissection is considered a very serious pathology and requires immediate treatment. Otherwise there is a big risk lethal outcome. Most often, to completely eliminate the pathology, you have to resort to surgical intervention.

Manifestations of the disease

Most often, the disease occurs under the influence of various other provoking factors. Often these causes are other serious diseases. The signs are somewhat similar to those of other diseases, but they are too severe to ignore. Therefore, in any case, with such phenomena, it is recommended to consult a doctor as soon as possible.

Development of an aortic dissection

Features of the disease

The risk group primarily includes people over 50 years of age. Mostly they are men. According to statistics, the disease occurs several times more often among males than among women.

Dissection of the aorta is manifested by a violation of the integrity of the walls of the vessel. As a result, blood enters under one of the layers of the aorta. The walls of the aorta are constantly subjected to a colossal load. If the integrity of the vessel is broken or the wall is affected by an inflammatory process, atherosclerosis, then under the influence of a strong blood flow that circulates under pressure, the walls can delaminate. This is especially true if a person has hypertension.

Aortic dissection often occurs where blood flow reaches its maximum (in the ascending aorta). In this case, the situation is complicated by the fact that if initially only a small wall defect occurs, then the situation gradually worsens and an increasing area of ​​the vessel wall exfoliates.

The most dangerous for the patient's life is an increase in the diameter of the aorta at this moment. Then we can talk about the dissection of the aneurysm. In this case, it is necessary to immediately resort to surgical intervention. If this is not done in a timely manner, then if the aneurysm ruptures, there is practically no chance to save the patient - the mortality rate for such a pathology is more than 90% even before the patient is admitted to the hospital. Therefore, at the first suspicion of an aneurysm, it is necessary to immediately undergo an examination and, if necessary, perform an immediate operation.

Causes of pathology

Most often, aortic dissection does not even have the main causes of this pathology, but rather provoking factors that increase the risk of developing this problem. These include primarily:

  • men;
  • old people;
  • people with congenital heart valve disease;
  • persons with a hereditary predisposition.

But it is also customary to single out a number of diseases that can provoke the development of this complication:

  • atherosclerosis;
  • diabetes;
  • arterial hypertension;
  • inflammatory process that affects the walls of blood vessels. Most often similar diseases contribute to the death of the middle layer of the vessel wall and therefore gradually leads to its destruction.

According to statistics, men suffer from this disease twice as much as women. This is primarily due to the fact that it is men who more often lead an unhealthy lifestyle, have much more bad habits than women, and do not follow their diet. That is why the risk of developing this pathology increases many times under the influence of these factors.

It is also important in this matter and the presence of hereditary predisposition. Most often, this is accompanied various pathologies in development (problems with valves).

Older people are much more likely to suffer from hypertension and diabetes. hypertension is one of the most common causes of aortic dissection. This is due to the fact that under the influence of increased blood pressure significantly increases the load on the walls of blood vessels, which can quickly lead to a violation of their integrity. If hypertension at the same time also manifests itself in combination with atherosclerosis and the walls of blood vessels are also destroyed under the influence of cholesterol plaques, then the prognosis will be much less encouraging.

The risk increases especially with the development of an aortic aneurysm. In such a case, the risk of its rupture at additional load on the walls of the vessel due to constant hypertension increases simultaneously several times. In this case, not only the inner layer of the vessel is ruptured, but also its entire wall. A person at this moment is able to die literally in a matter of minutes due to severe internal bleeding and significant blood loss.

Main symptoms

Often the main problem is that the signs of aortic dissection are in fact on initial stage may be completely absent. A person may not even be aware of the development of such a serious pathology in his body. When the symptoms become more obvious, it will be too late and there will be very little time for diagnosis and treatment.

By the nature of development, one can distinguish between an acute form of the disease, when the disease progresses in a maximum of two weeks, or chronic (the disease can develop for months). The acute form is the most dangerous for the patient's life and has a less favorable prognosis.

Symptoms often depend primarily on which part of the wall is damaged and how strong the changes are.

Aortic dissection often has the following symptoms:

Pain syndrome
  1. Pain syndrome. Pain may occur in various places: chest, lower back, neck, limbs. Often it can be simply unbearable. Gradually, depending on the spread of the dissection, the pain moves to various other parts of the body.
  2. Fainting state. Just like shock, it can occur due to unbearable pain. Also, a person may faint due to a sharp drop in blood pressure. As a result, cardiac arrest is also possible and quick death sick. A similar condition develops due to the fact that blood begins to flow into false channels, pour out into the body cavity, while the internal organs do not receive enough nutrition. This is what causes fainting. Blood pressure also falls due to massive internal bleeding.
  3. Bradycardia. Heart failure and pulse deficit are also pronounced.
  4. Lack of blood supply internal organs may lead to the most various symptoms depending on the nature of the developed pathology. Myocardial infarction, stroke, renal failure can be expressed in severe cyanosis, a decrease in the amount of urine excreted.

CT, MRI and X-rays allow you to quickly and reliably confirm or refute the alleged diagnosis. In this case, the doctor's actions should be as quick and coordinated as possible, since aortic dissection is an emergency and requires immediate treatment. Otherwise, death is inevitable.

Treatment of the disease

MRI

The problem is always complicated by the fact that not every case allows you to see such a defect during the examination. Very often, during such studies, only external defects can be detected. If the delamination affects only inner wall vessel, it is quite difficult to consider this. But this does not mean at all that such a process will not progress. Gradually, more and more new parts of the aorta are affected, which leads to deformation and thinning of its meshes, which can quickly lead to rupture of the vessel. That is why it is so important when the first symptoms of the disease occur, immediately seek help from a doctor. Only fast and high-quality medical care can save the patient's life.

Operation

Surgery is needed for those patients who have conservative treatment did not give any positive results and the upward delamination continues.

Also, such operations are indicated if there is a significant risk of rupture of the aortic walls.

The operation may consist in prosthetics of the affected area or simply in its removal and further suturing of the ends of the vessel. Most often, they still prefer to simply sew the ends of the damaged vessel, since implants can not easily and quickly take root in any organism. But if there is no other way out, then they are also used. Most often, this may be required if too much of the aortic wall is damaged.


Aortic prosthesis

Postoperative prognosis directly depends on which part of the aortic wall is affected and how much. It is also very important whether further delamination of the wall continues. After such an operation, it is very important for the patient to monitor their blood pressure, diabetics should carefully control their blood sugar levels. It is also important to monitor your lifestyle: give up bad habits, limit your physical activity, follow a diet (especially for fats and carbohydrates).

If treatment is not started in a timely manner, because if the delamination is constantly aggravated, then usually the mortality rate in the first year after the discovery of the disease is 90%.

Conservative treatment

Conservative methods of treatment are usually used in cases where the course of the disease is chronic and there is no risk of rupture of the walls of the vessel. In this case, the main therapy should be aimed at stabilizing blood pressure and reducing the load on the vessel walls. Since hypertension is the main cause of dissection of the aortic walls, when diagnosing this pathology, drugs to stabilize pressure will in any case be prescribed.

Sometimes there are cases when the disease is accompanied by a significant decrease in pressure. In this case, it is necessary to take drugs to increase the pressure to normal acceptable numbers. In some cases, in a hospital setting, patients may be shown taking narcotic drugs to reduce pain syndrome.

If there is a risk of rupture of an aortic aneurysm or the patient's condition is rapidly deteriorating, the blood supply to the internal organs is disrupted, then it is necessary to deliver such a patient to the surgical department as soon as possible and perform the operation. But before that, in any case, to begin with, it is necessary to stabilize its pressure.

The method of treatment is chosen depending on each specific case. Only a qualified physician can determine whether or not an operation is necessary based on the studies performed. Often, alas, to diagnose a disease on early stage fails due to the absence of any significant symptoms at this time. Therefore, treatment is usually carried out already during the acute manifestation of the disease. At this time, it is only necessary surgical intervention, so as to eliminate the defect of the vessel wall conservative methods won't work anyway.

Postoperative care consists of general therapy, which is applied after any surgical intervention. It is also very important to take antibiotics to prevent the development of the inflammatory process of the vessel walls. This phenomenon is very common and leads to even greater complication of the situation.

It is also very important that the therapy be chosen as comprehensively as possible and in the future be aimed not only at solving the main problem, but also at eliminating the root cause that led to the development of this problem.

As long as the root cause persists, no treatment will give full and lasting results, as the problem will come back again.

It is very important not only to know how to properly treat such an ailment, but above all how to properly prevent it. It is usually much easier and more desirable to prevent the development of pathology than to fight it later, even with the most modern and effective methods. To do this, it is enough just to healthy lifestyle life and keep under control those diseases that are the main provoking factors.

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Clinical recognition

We have built the presentation in accordance with the usual course of examination of a patient in an emergency. For example, data from the history and physical examination are presented first. This is followed by laboratory and radiographic data, usually obtained in the emergency department. As the examining physician's suspicion increases, more sophisticated confirmatory studies may be required. If there is a significant possibility that there is a dissection, medical treatment should be started. Thus, the section on the diagnostic strategy is structured in such a way as to illustrate the most effective way for various clinical situations to a timely and correct diagnosis. Although the final treatment strategy is different for proximal and distal dissections, the primary and most secondary evaluations are largely the same.

History and general examination

In most cases, aortic dissection happens unexpectedly. The patient complains of a sudden onset of severe chest pain, but none of the disorders that usually accompany the bundle is manifested. History of high blood pressure or previously diagnosed aneurysm thoracic aorta indicate a possible dissection. Almost all patients with a distal dissection and most with a proximal dissection have a history of hypertension on close examination. Other conditions associated with aortic dissection, such as pregnancy, corrected and uncorrected aortic coarctation, and anomalies aortic valve should also raise suspicion of delamination.

Connective tissue pathology and other genetic defects may also predispose to aneurysm formation and aortic dissection. Currently, many patients with Marfan syndrome are well trained to recognize the clinical symptoms. It is not uncommon for a patient with Marfan's syndrome to come to the emergency department, stating: "I have Marfan's syndrome and pain typical of aortic dissection." Unfortunately, such claims are sometimes ignored by emergency room physicians, with disastrous consequences. Even without a statement from the patient, the characteristic stigmata of Marfan syndrome, including high costal arch, long arms and legs, increased mobility in the joints, visual disturbances, in the presence of chest pain should lead the examining physician to the idea of ​​a possible aortic dissection. Patients with osteogenesis imperfecta and systemic lupus erythematosus, as well as those with Ehlers-Danlos syndrome, are usually detected during history taking or during physical examination. Turner and Noonan syndromes are also easily recognizable with some attention. More difficult to diagnose are cases with only one or two characteristic features of Marfan syndrome and those with familial dissection syndrome. In any case, pain in the chest, back, or pulse deficit in each of the above groups should be the reason for a thorough examination for aortic dissection.

Characteristics of pain

Consideration of the possibility of acute aortic dissection in a patient with chest pain is a general clinical principle. Intense chest pain is a cardinal sign of aortic dissection that occurs in more than 90% of patients. Pain usually has a characteristic localization. Pain in the anterior chest, is most often combined with a proximal dissection, and pain in the back or scapular space is most often associated with a distal variant. In patients with type I dissection according to DeBakey, pain is usually localized in front and in the scapular region, since both the ascending and descending portions of the aorta are involved in the process. Dissection of only the proximal aorta is characterized by a concentration pain symptoms in the middle substernal region. As the dissection spreads distally, the pain moves to the neck and lower jaw(sometimes there are difficulties with swallowing), then - into the interscapular region and finally captures most back, lumbar region and even smell. This migration of pain from the anterior chest to the scapular region is common in type I dissection and reflects the involvement of new portions of the aorta in the process. The presence of migratory pain should increase the physician's suspicion of aortic dissection. With distal dissection, pain usually occurs in the interscapular region with some anterior irradiation. There may also be intense abdominal pain due to renal and visceral ischemia. Occlusion of the thoracoabdominal aorta and iliac arteries leads to peripheral ischemia and very severe pain in the extremities. There may be numbness and paraparesis of both legs. More often, however, hypoperfusion due to unilateral proximal occlusion of the artery ischemic and painful in one leg, usually the left leg.

Rarely, aortic dissection is painless. This is usually observed in patients with an already formed large aneurysm of the ascending aorta, when the dissection is localized only in its proximal section.

The most important clinical problem is differential diagnosis pain in the chest due to aortic dissection with pain in angina pectoris, myocardial infarction and others. According to Eagle, when an aortic dissection was initially suspected, the most common subsequent findings were acute myocardial infarction, aortic regurgitation without dissection, aortic aneurysm without dissection, musculoskeletal pain, mediastinal cyst or swelling, pericarditis, angina pectoris, gallbladder pathology, and pulmonary embolism(in descending order of probability).

Pain during dissection is usually intense, occurs suddenly and for the first time. It is interesting that often the patient, when describing the nature of pain, uses such a definition as “tearing”. Usually very intense from the very beginning, the pain does not subside, unlike angina pectoris. Patients are usually restless and constantly change their position in an attempt to reduce discomfort. In comparison, angina pain usually comes on slowly and may improve with restriction. motor activity. In the era of immediate treatment of acute coronary ischemia with thrombolysis, extreme care must be taken to ensure that a patient with aortic dissection is not inadvertently diagnosed with coronary ischemia and prescribed thrombolytics. Although uncommon, the clinical picture of proximal aortic dissection can be greatly complicated by concomitant total or partial coronary artery occlusion with symptoms of typical angina or heart failure due to severe myocardial ischemia. This situation can be exacerbated by acute aortic regurgitation, which is also often associated with proximal aortic dissection. Although dissection may present with pain typical of myocardial ischemia, the history of the former is usually less specific. We have had several patients who received thrombolytics for "acute myocardial infarction with ventricular clot embolization" in whom "subsequent femoral embolectomy failed." It turned out that these patients had type I dissection according to De Backy with the involvement of the coronary arteries. Such patients often have pronounced "ischemic" ECG changes and chest pain, but many are younger than 50 and do not have risk factors for CAD.

Patients with chronic proximal aortic dissection usually do not complain of severe pain. A sudden increase in the size of a proximal aortic aneurysm may be the only sign that a dissection has occurred. They may have a feeling of "fullness" in the chest and moderate Blunt pain caused by congestive insufficiency due to aortic regurgitation. In rare cases of advanced dissection, large aneurysms of the ascending aorta can press on the sternum and chest, causing severe bone pain.

Chronic distal aortic dissection is usually asymptomatic and is found on examination for an enlarged aneurysm of the affected segment. However, an increase in the diameter of the aorta can lead to compression of adjacent structures, which can be expressed in back pain from erosion of the vertebral bodies and irritation of the nerve roots.

Sometimes there is an obstruction of the left main bronchus, leading to recurrent pneumonia. Occasionally, the patient notes a pulsation in the abdomen. When a secondary dissection of dilated aortic segments occurs, symptoms similar to those of an acute dissection may occur. In Marfan syndrome, the presence of a proximal dissection or aneurysm increases the likelihood of a distal dissection and vice versa. Often, the primary lesion remains unrecognized, manifesting itself only as bone pain from erosion by an aneurysm of the bodies and processes of the vertebrae.

Both proximal and distal chronic dissection can lead to a hypoperfusion syndrome, which is manifested by abdominal pain after eating due to intestinal ischemia, chronic kidney failure and hypertension, as well as intermittent claudication due to occlusion of the aorta or iliac arteries, or any other of the peripheral vascular disorders described.

Arterial pressure

Most patients with acute proximal aortic dissection have normal or moderately elevated pressure. In the absence of connective tissue disease, virtually all patients with acute distal dissection have either a history or presenting history of hypertension. Patients may be pale, have circulatory failure and shock. However, measuring their blood pressure usually gives normal or high numbers. High blood pressure may be the result of essential hypertension, mechanical occlusion of the renal artery, or occlusion of the thoracoabdominal aorta. Moreover, due to the pain and the nature of the aortic dissection, there is usually a significant release of catecholamines.

In large series, 20% of patients with acute proximal dissection had hypotension and even severe shock on examination, usually signifying pericardial rupture with tamponade or rupture. Patients with acute distal dissection and hypotension always have aortic rupture and retroperitoneal bleeding or chest cavity. Secondary "pseudo-hypotension" has also been reported, resulting from compression or occlusion of one or both subclavian arteries by a dissecting membrane. Hypotension may also result from the sudden development of severe heart failure due to aortic valve insufficiency or coronary artery disease.

In chronic proximal aortic dissection, congestive heart failure due to aortic regurgitation is common. This can be expressed in a slight or moderate decrease in pressure with sometimes severe diastolic hypotension. In chronic distal dissection, the most common cause of hypotension is aortic rupture, which occurs imperceptibly and is accompanied by blood leakage into the pleural cavity and mediastinum.

peripheral pulse

One of the important signs when examining a patient with suspected acute aortic dissection is a pulse deficit. According to different authors, up to 60% of patients have this sign. A pulse deficit on one of the supra-aortic branches usually indicates a proximal dissection. However, with retrograde spread of the distal dissection, there may be a decrease in the pulse in the left subclavian artery.

The fact that the nature of the pulse deficit changes as the dissection spreads distally and secondary communications form is well known. Such changes in the patient's pulse make one suspect an aortic dissection and should encourage the doctor to further research. The pulse on the femoral vessels may be absent due to occlusion of the thoracoabdominal aorta or iliac arteries due to the expansion of the false lumen. Often the patient presents after a recent exploratory operation with a negative result or an attempted Fogarty embolectomy for acute femoral artery occlusion when no thrombus is detected. Then, with a careful reassessment of the patient's condition, a diagnosis of aortic dissection is made.

Pulse deficits are relatively uncommon in patients with chronic aortic dissection. This feature probably indicates the presence of distal secondary communications that decompress the false canal. Pulsus paradoxus should be considered as a sign of pericardial involvement.

auscultatory picture

In addition to the murmur of aortic regurgitation, patients with proximal aortic dissection may have several other findings on cardiac auscultation. Acute regurgitation can lead to an increase in LV end pressure, thereby reducing the intensity of the first heart sound, and sometimes making it completely inaudible. Moreover, the gallop rhythm is usually heard at the Botkin point. Absence of murmur in severe aortic regurgitation was described, which was explained by severe congestive heart failure. The presence of a pericardial rub makes one think of pericardial hemorrhage or, in subacute cases, fibrous pericarditis. A continuous murmur usually indicates a ruptured right ventricular or right atrial dissection. In our practice, we have observed a rupture of the dissection into the pulmonary artery, leading to the appearance of a loud blowing noise and severe pulmonary edema.

Auscultation of the rest of the chest and abdomen can reveal some important details in both acute and chronic dissections. Congestive heart failure can lead to pulmonary edema in both the acute and chronic phases. The absence of vesicular breathing in the left half of the chest may indicate a hemorrhage into the cavity. Various auscultatory murmurs can be caused by hypoperfusion of large branches of the aorta. Suspicious findings can be assessed using Doppler ultrasound. Obtaining a complete auscultatory picture is vital.

Aortic valve insufficiency

An aortic regurgitation murmur develops in 50-70% of patients with acute proximal aortic dissection. The presence of a new murmur, combined with chest pain and pulse deficit, should lead the clinician to the high probability of an aortic dissection involving the ascending aorta. The pathophysiological mechanisms of aortic regurgitation are different. Noises are best heard along the right or left edges of the sternum. In acute onset, many peripheral signs of aortic insufficiency are absent. If there is severe congestive heart failure, there may also be no murmur. The presence and degree of aortic insufficiency is detected by transesophageal or even external echocardiography.

Anyone who survives an acute dissection and enters the chronic phase of the disease develops all the signs of aortic insufficiency. In fact, this complication may be the reason for the admission of such a patient to a medical institution. It should be noted that 10% of patients with chronic distal aortic dissection have secondary aortic insufficiency due to dilatation of the ascending aorta and its root.

Pericardial signs

Because of the sinister nature of pericardial fluid accumulation in acute aortic dissection, looking for signs of this process is of the utmost importance. In the course of a general examination of the patient, swelling of the jugular veins and a paradoxical pulse can serve as suggestive moments. As mentioned above, there may be a pericardial friction rub. Additional important features are low voltage waveforms on the ECG or an increase in the shadow of the heart on the x-ray. However, these data alone do not help confirm the diagnosis of acute proximal dissection. Moreover, in the absence of a previously recorded electrocardiogram, low voltage due to tamponade is not specific sign. Today, the availability of transthoracic and transesophageal echocardiography makes it easy to detect blood in the pericardium.

Neurological signs

The neurological manifestations associated with aortic dissection were discussed as early as 1944 in a review by Weisman and Adams. These included syncope, stroke, ischemic paraparesis and paralysis, paraplegia due to dissection and rupture of the vessels supplying the spinal cord, and Horner's syndrome.

According to Slater and DeSanctis, 10% of patients presenting with acute aortic dissection are syncope. Five out of every six such patients subsequently have a ruptured dissection of the ascending aorta into the pericardial cavity. Thus, a history of syncope, combined with signs suggestive of aortic dissection, should lead the clinician to the possibility of rupture of the dissection into the pericardial cavity and tamponade, which is a purely surgical problem.

Neurological deficits may result from a syndrome of hypoperfusion of one or more branches of the aortic arch.

Acute cerebral vascular occlusion is more often found in proximal aortic dissection. Fortunately, neurological deficits develop in less than 20% of these cases. In stroke, there is some chance of improvement after the removal of acute occlusion. However, reperfusion can also lead to massive intracerebral hemorrhage, edema, and global cerebral damage, including coma and brain death.

Paralysis of the limbs develops due to detachment or compression large arteries that feed the spinal cord, or due to ischemia of the peripheral nerves during occlusion of the thoracoabdominal aorta. It is important to establish the etiology, because. restoration of blood circulation in ischemic muscles and nerves of the lower limb usually leads to the restoration of function. Conversely, in patients with circulatory disorders spinal cord the prognosis for the recovery of the neurological function of the lower limb is very unfavorable. The defeat of the intercostal or lumbar arteries, and in particular the Adamkevich artery, can manifest itself as flaccid or spastic motor paraplegia. There is also usually an absence of pain and temperature response below the level of the affected segment of the spinal cord, although sensitivity may be restored over time. As with other spinal lesions, the Babinski reflex may appear on both sides. The tone of the sphincters may also disappear. The sense of position is generally preserved, as is the blood supply to the extremities and the pulse in the femoral vessels.

Acute violation of the patency of the thoracoabdominal aorta is manifested by pain in the lower extremities, acute paralysis, lack of pulsation of the femoral arteries, impaired and reduced sensitivity up to complete anesthesia. Patients are in a very critical condition and may also have impaired renal and visceral blood flow. They usually result from extensive dissection involving most or all of the distal aorta. The limbs are usually marbled and deep tendon reflexes are absent. The marbling sometimes extends proximally to the navel or even to the nipples and may be accompanied by a distinct line of demarcation.

Despite the general severe clinical picture in such patients at admission, with timely surgical intervention, the prognosis for the restoration of functions in them is better than in patients with occlusion of the spinal arteries. This is because blood flow to the aortic bifurcation can usually be restored, and such patients can recover completely.

In patients with chronic dissection in the acute stage, both major and minor strokes can occur, which will manifest as persistent neurological deficits or mild symptoms. Chronic aortic dissection rarely results in paralysis or paraplegia. However, embolic strokes were noted with thrombi accumulating in the proximal pockets of the false lumen of the aorta formed in the acute phase.

Other symptoms

Various unusual physical findings have been described in connection with aortic dissection. They include pathological pulsation in the sternoclavicular junction, superior vena cava syndrome when it is obstructed by a dilated ascending aorta, paralysis vocal cords and hoarseness due to compression of the recurrent nerve, compression of the trachea and bronchi with lung collapse, copious hemoptysis with erosion of the tracheobronchial tree, vomiting of blood with erosion of the esophagus and various pulsations in the neck. These manifestations result from the expansion of the false lumen and compression of adjacent structures. Not uncommon subfebrile temperature, and sometimes it can be noted high fever due to the release of pyrogenic compounds from ischemic organs or as a result of the collapse of hematomas.

Electrocardiography

The classic sign of acute aortic dissection is intense chest pain, but ECG evaluation of acute proximal dissection usually does not reveal ischemic changes. However, significant changes in the ST segment and T wave are sometimes observed, indicating severe ischemia or infarction due to obstruction of the coronary artery by dissection. Sometimes as a result of hematoma spreading to the aortic root, atrial septum or atrioventricular node may develop heart block. Patients with coronary artery disease or hypertension on the ECG may have signs of old myocardial infarction or hypertrophy. In acute or chronic distal dissection, the ECG usually indicates left ventricular hypertrophy associated with chronic hypertension.

Chest x-ray

Conventional radiography, which is available in most admissions offices often provides important information in making a diagnosis of aortic dissection.

Although standard chest x-rays and lateral chest x-rays cannot provide a definitive diagnosis, their evaluation reveals some of the details associated with aortic dissection. In cases of asymptomatic or chronic dissection, x-rays may generally serve as the first source of information about the existence of aortic pathology. Moreover, when older radiographs are available, comparing them with recent ones can provide important information, especially in the context of clinical picture bundles.

In 1932, Wood proposed criteria for the interpretation of plain chest X-ray data, which are still used today. Signs accompanying aortic dissection include changes in the shadow adjacent to the descending thoracic aorta, deformity of the shadow of the aorta and other parts of the supracardiac shadow, tightness adjacent to the brachiocephalic trunk, enlargement of the heart shadow, displacement of the esophagus, mediastinal changes, abnormal contour of the aorta, indistinctness of the aortic shadow , displacement of the trachea or bronchi and pleural effusion.

Most often, changes are found in the region of the aortic arch. They include enlargement of the aortic diameter, the presence of double density due to the expansion of the false lumen, and irregular and indistinct contour. Most of these changes are the result of expansion of the false lumen of the aorta or localized hemorrhages.

According to the Mayo Clinic, of the 74 cases of aortic dissection, 61 chest x-rays had abnormalities in these areas. In 13 cases, there were no signs to suspect a dissection. However, 8 of them had other changes, including heart enlargement, congestive heart failure, and pleural effusion. Thus, only 5 patients had normal chest radiographs. Although the aortic shadow was normal in 18% of patients, this is not surprising, because. often the diameter of the aorta in acute dissection increases only slightly. Thus, an intact aortic shadow and mediastinum should not deter the clinician from further investigation if the patient's history and clinical findings suggest a dissection. In addition, a clearly enlarged aorta in a direct picture may be hidden by the shadow of the heart. This is especially true for cases of type II deBakey stratification. Lem-on and White noted that a significant number of patients with Marfan's syndrome with large aneurysms involving the sinus segment of the aorta had a "normal" aortic caliber on plain radiographs.

The shadow of the aorta, which x-ray at first appears normal, over time it can change greatly, rapidly increasing in size. Local protrusions can be detected.

Separation of calcified intimal plaques greater than 1 cm from the border of the aortic shadow, giving the impression of a thickened aorta, as well as the presence of a double density of the aorta are signs of a dissection with a double channel. Unfortunately, various manifestations of thoracic aortic atherosclerosis and aortic aneurysm without dissection can also have such features, making them nonspecific.

A small pleural effusion, usually on the left, is a very common finding in both chronic and acute proximal and distal dissections. It is the result of diapedesis of erythrocytes through a weakened stratified wall of the aorta in the acute variant, and periaortic inflammation in subacute and chronic. A large effusion may indicate a tear into the pleural space, in which case it is always accompanied by mediastinal enlargement.

An increase in the mediastinal shadow due to bleeding or aortic dilatation, especially when seen on a direct posteroanterior image, is an important finding. It occurs in 10-50% of cases.

An enlarged heart shadow is a common finding in aortic dissection, which may result from pericardial effusion, cardiac dilatation with aortic valve insufficiency and cardiomegaly in chronic cases, and hypertension and left ventricular hypertrophy. If older images are available and the comparison reveals enlargement of the cardiac shadow, pericardial bleeding should be suspected. Unfortunately, the enlargement of the cardiac shadow in acute dissection may be barely noticeable due to the non-distensibility of the pericardium. Moreover, due to the high prevalence of hypertension in these patients, this symptom is also not specific.

Displacement of the tracheobronchial tree and esophagus during dissection is observed in 60% of cases. The displacement can occur both to the right and to the left, depending on the location of the bundle. The course of the gastric tube may show displacement of the esophagus.

Laboratory data

Due to the accumulation of blood in the false lumen and diapedesis of erythrocytes through the wall of the aorta, mild anemia is relatively common. The outpouring of a significant amount of blood into the pleural space leads to severe anemia. A large number of clots may form, leading to a decrease in the content of clotting factors. Occasionally, due to the consumption of platelets and coagulation factors in the false lumen, DIC develops. Blood that accumulates in the false lumen can hemolyze, which leads to an increase in the level of bilirubin and LDH in the blood. Often there is a slight leukocytosis of the order of 10-15 thousand. The level of transaminases is usually normal or slightly elevated. Electrolytes are usually normal. Blood gas analysis may reveal metabolic acidosis due to anaerobic metabolism in ischemic areas. If the kidneys are involved, hematuria may occur.

Surgical treatment of aortic dissection
Hans Georg Borst, Markus K. Heinemann, Christopher D. Stone

cardiolog.org

What it is?

Aortic dissection can be primary or secondary, but in any case it occurs due to hemorrhage within the middle membrane. A fissure can occur in any segment of the aorta and then spread distally and proximally to other arteries. An important symptom is arterial hypertension.

Surgery and prosthetics with synthetic implants is necessary for a fissure in the ascending aorta and for specific dissections of the descending aorta.

Causes and risk factors

Dissection may occur if the patient has a history of degenerative disease of the middle aortic membrane. Causes may be connective tissue abnormalities or trauma. In a third of patients previously noted signs of atherosclerosis and arterial hypertension.

As a result of rupture of the inner membrane, which becomes the primary factor in dissection in some patients, and secondary to hemorrhage in middle shell in others, the blood flow enters the middle layers. A false channel of blood flow is created, leading to expansion of the distal or proximal arterial site.

During the stratification vascular lumen may form through the rupture of the intima in the area distant from the center of the aorta, and thus the initial intensity of blood flow is maintained. But a person has practically no chance of surviving, since serious consequences develop: the process of blood flow in dependent arteries is disrupted, the aortic valve expands, regurgitation appears, heart failure and a fatal rupture occurs.

it called acute dissection and is dangerous if at least two weeks old. The risk of death is significantly reduced if the rupture was more than two weeks ago and there are clear signs of thrombosis in the area of ​​the false lumen and loss of communication routes between the true and false vessel.

Species classification

The dissection process is classified according to anatomical features, for this the generally accepted DeBakey system is used:

  • The dissection begins in the ascending part and extends to the aortic arch;
  • Begins and is limited only within the ascending department;
  • It begins in the descending thoracic aorta, slightly below the outgoing left subclavian artery and spreads proximally and distally;
  • In pregnant women, it can be localized in a specific single artery, for example, carotid or coronary.

Danger and complications

Every patient who has undergone surgery, until the end of life, must periodically undergo courses of antihypertensive therapy. Often the treatment regimen includes: ACE inhibitor, ß-blocker, blocker calcium channels.

These drugs are combined with antihypertensive agents. Recommended abstaining from excessive physical activity. Every two years, the patient is required to undergo a complete examination by MRI.

As late complications allocate repeated relapses dissection, the occurrence of a limited aneurysm in the body of a weakened aorta, progress of regurgitation aortic processes. With the development of such pathologies, the patient again inevitably ends up on the surgical table.

Symptoms

The first symptom of an aortic dissection is sharp pain between the shoulder blades or in the precordial region, patients often describe it as "tearing". It often radiates as the fissure propagates through the aorta.

The pain is so severe that some people lose consciousness from pain shock , as well as due to irritation of the aortic baroreceptors and extracranial obstruction of the cerebral artery. Cardiac tamponade develops.

Some patients experience partial loss of pulse in an artery. BP varies significantly for each limb. Regurgitation murmurs are heard.

Acute heart failure occurs in one third of cases.. Blood entering the left pleural cavity causes pleural effusion. Arterial occlusions cause signs of ischemia or neuralgia in the extremities, anuria, and oliguria if the renal artery is involved.

When and which doctor to contact?

Dissection is so dangerous and painful that the patient himself is not able to attend to the issues of emergency medical care. It is necessary to immediately call doctors or independently deliver the victim to a medical facility, where he will be admitted to the intensive care unit or intensive care unit.

Urgent surgeon consultation, vascular surgeon, cardiologist and anesthesiologist.

Diagnostics

Symptoms are differentiated from stroke, intestinal and myocardial infarction, paraparesis and paraplegia with impaired blood flow in the spinal cord, limb ischemia due to acute distal arterial occlusion.

The patient is assigned emergency chest x-ray, which will show the widening of the mediastinal shadow and the limited bulge characteristic of an aneurysm. In most cases, a pleural effusion is found on the left side.

After stabilization, the patient needs to do transesophageal echocardiography, MRA and CTA. The result of which may be to obtain data on the severity of the tear of the inner shell and the formation of a double lumen.

contrast angiography carried out immediately before the operation. With its help, the degree of involvement of the main aortic branches is clarified. Aortography is needed to confirm the diagnosis and helps to determine whether the patient needs coronary artery bypass surgery. With the help of echocardiography, the intensity of regurgitation processes is determined, as well as the need for valve replacement.

Laboratory determine the level of CPK-MB serum and troponin, this will help differentiate a dissection from an infarction, unless the rupture was caused by the infarct itself. General analysis blood shows the presence of leukocidosis and anemia.

Treatment Methods

If the patient did not die during transport to the hospital, then his placed in the intensive care unit and connect an intra-arterial pressure monitor. A catheter is placed to excrete urine. The blood type and Rh factor are immediately determined, since during the operation there is a need for a red blood cell mass. With unstable hemodynamics, a person is intubated.

Prescribe drugs to lower blood pressure, relieve spasm arterial walls, pain syndrome and ventricular contractility. Add to list medicines usually includes b-blockers, for example, Propranolol, or Metroprolol and Labetalol. As an alternative, calcium channel blockers are used - Verapamil and Diltiazem.

The use of exclusively medical treatment is justified only with uncomplicated and stable dissection. Surgery is indicated in 98% of cases. Indications for surgical intervention serve:

  • Ischemia of a limb or organ;
  • uncontrolled hypertension;
  • Prolonged expansion of the aorta;
  • Bundle propagation;
  • Signs of aortic rupture;
  • Marfan syndrome.

During the operation the surgeon eliminates the entrance to the false canal and replaces the aorta. With regurgitation, the aortic valve undergoes plasty or prosthetics.

Forecasts and preventive measures

Some patients do not survive until the ambulance arrives. If no action is taken, the person will die. within the next 24 hours at 3% of total cases, in the first week - in 30%, during two weeks - in 80%, and within one year - in 90%.

In-hospital mortality rates are somewhat lower, with proximal dissection on the surgical table, 30% of patients die, with distal dissection - 12%.

As a prevention of delamination it is recommended to have an annual medical examination for the detection of diseases of the cardiovascular system. Aortic fissure can be prevented through continuous cardiac surveillance, including daily monitoring of blood pressure and cholesterol levels. And also by periodically undergoing ultrasound or ultrasound procedures.

Symptoms of aortic dissection are found in approximately 3% of total autopsies.. The group at particular risk includes men, older people of both sexes and representatives of the black race. Peak rates occur at the age of 55-65 years, and with connective tissue pathologies - at 25-45 years.

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The reasons

The most common cause decrease in the strength of the aortic wall is a long-term arterial hypertension. More than 60% of patients with aortic dissection have high blood pressure. However, to date, exact reasons the development of a dissecting aortic aneurysm is not discussed, but only about the possible factors of its occurrence. Thus, the possible reasons may be the following:

  • arterial hypertension.
  • Congenital malformations of the heart and blood vessels (open aortic duct, coarctation of the aorta, aortic valve defects).
  • Connective tissue diseases (Ehlers-Danlos syndrome, Marfan syndrome).
  • Systemic vasculitis.
  • Atherosclerosis.
  • Chest injury.

Risk factors include elderly age(over 60 years old).

Classification

According to the DeBakey classification, which is most often used today, there are three types of dissecting aortic aneurysm:

  1. The place of rupture of the inner membrane is the ascending aorta, the dissection reaches the thoracic and abdominal segments.
  2. Rupture and dissection in the ascending aorta.
  3. Rupture and dissection in the descending aorta. Two types are distinguished: the bundle does not extend below the diaphragm, the bundle goes below the diaphragm.

There is an alternative classification of dissecting aneurysm, in which two types of aortic dissection are distinguished:

  1. Type A - dissection in the ascending aorta.
  2. Type B - aortic dissection limited to the descending segment.

signs

Symptoms depend on the extent of dissection and intramural hematoma, organ ischemia, compression of the aortic branches.

Dissecting aortic aneurysm can occur in several ways:

  • the formation of a large unruptured hematoma;
  • stratification of the wall with a breakthrough of the hematoma into the aortic lumen;
  • dissection with breakthrough hematoma in the tissue around the aorta;
  • aortic rupture in the absence of dissection.

The disease usually begins suddenly. The first symptoms are similar to manifestations of cardiovascular, urological, neurological diseases. The main symptom is an unbearable rapidly growing pain behind the sternum, in the spine, between the shoulder blades, in the lower back, in the epigastrium. The pain migrates along the dissection.

In addition, it is possible the following symptoms dissecting aneurysm:

  • increase and then decrease in blood pressure;
  • heavy sweating;
  • asymmetric pulse in the arms;
  • general weakness;
  • cyanosis of the skin;
  • loss of consciousness, coma;
  • shortness of breath and hoarseness.

Dissecting aneurysm occurs in acute, subacute and chronic form. Acute can be fatal within hours or days. Subacute lasts from several days to three to four weeks. Chronic illness may last several months.

In the acute form of aortic dissection, the patient experiences severe incessant pain in the chest and epigastric region, then in the back and along the spine. The pain increases in waves, which indicates that the process of separation continues. Sometimes there is a shock. Aortic valve insufficiency may develop, an asymmetric pulse in the limbs is observed, and heart failure progresses rapidly.

Diagnostics

If a dissecting aortic aneurysm is suspected, urgent diagnostics, the main methods of which are:

  • chest x-ray;
  • UZDG;
  • echocardiography;
  • CT scan;
  • Magnetic resonance imaging;
  • aortography.

Chest x-ray allows you to determine the signs of a dissecting aneurysm: aortic dilation, pleural effusion, absence of pulsation, deformation of the aortic contours.

Echocardiography is a more informative and accessible method that allows you to detect a detached flap, determine the true and false canals, assess atherosclerotic lesions, the condition of the aortic valve, and the condition of the thoracic aorta.

Aortography makes it possible to determine the location of the initial rupture, the extent and location of the dissection, the condition of the aortic valve, aortic branches, and coronary arteries.

Differential diagnosis is carried out with renal colic, myocardial infarction, kidney infarction, acute aortic insufficiency, stroke, non-dissecting aneurysm and others.

With the help of electrocardiography, signs of pathologies associated with a dissecting aneurysm or its consequences can be detected.

A highly sensitive method - nuclear magnetic resonance imaging, which takes about 40 minutes, is not applicable for unstable and severe pathology.

Treatment

As already mentioned, aortic dissection - acute condition life-threatening. Often patients need urgent operation. The first step is an emergency hospitalization in the intensive care unit.

For all types of dissecting aneurysms, treatment begins with drug therapy, the purpose of which is to relieve pain and get out of a state of shock. For this, the patient is administered analgesics. Pain during vessel dissection is very severe, so preoperative anesthesia involves narcotic drugs. If the pain is not relieved, this indicates that the aortic dissection is ongoing.

In addition, the task of doctors is to prevent further separation of the wall and its external rupture and to stabilize the patient's condition. Hemodynamics, diuresis, heart rate, pulmonary artery pressure, central venous pressure are constantly monitored. The indications for urgent surgical intervention are assessed.

Indications for emergency surgical treatment relate:

  • Ascending aortic dissection.
  • External break.
  • Acute heart failure.
  • Violation of blood flow in the branches of the aorta.
  • Stratification progression.

In uncomplicated types of aneurysm with distal dissection, the main treatment is medication. If treatment is ineffective and in case of acute proximal dissection, immediately after the patient's condition has stabilized, a surgical operation is performed. Depending on the indications, prosthetics or plastic surgery of the aortic valve, prosthetics of the ascending aorta, aortic arch, descending aorta, reimplantation of the coronary arteries is performed. Any operation for all types of disease is complex, lengthy, accompanied by large blood loss.

Forecast

Without treatment, the disease in most cases ends in death. Most patients die from a dissecting aneurysm during the first months and even days, about 10% can live for a year. modern medicine has quite effective methods for diagnosing and treating dissecting aneurysms. After surgery, the survival rate reaches 80-90%. At timely treatment the prognosis is considered quite favorable: the 10-year survival rate is 60%.

Prevention

The main prevention of a dissecting aneurysm is the prevention of the development of cardiovascular diseases, examinations by a cardiologist, and the maintenance of normal levels of arterial and cholesterol in the blood.

It is estimated that 24,000 acute aortic dissections occur annually in the United States alone, exceeding even the incidence of ruptured abdominal aortic aneurysms.

Unfortunately, only about 2,000 are correctly diagnosed in their lifetime. Such a high mortality that accompanies untreated dissections makes their timely recognition the responsibility of the examining physician.

Despite notable advances in the accuracy of diagnosing aortic dissections and the availability of modern imaging modalities, most an important factor, providing the correct intravital diagnosis, is the suspicion of the examining doctor. If such a suspicion arises, it is important to seek timely advice from a surgeon familiar with the detailed assessment of aortic dissection.

About the first lifetime diagnosis of aortic dissection in the early 1900s. Swaine and Latham reported. However, real progress in clinical recognition only occurred with the advent of more efficient radiographic techniques, which provided clinicopathological correlation prior to autopsy. To the moment clinical manifestations in 2/3 of patients, the ascending aorta is involved in the process, and in 1/3 - only the distal one. In men, stratification occurs 2-3 times more often and in most cases at the age of 40-60 years.

The following sections deal primarily with the clinical manifestations and diagnosis of acute aortic dissection. Notable differences between acute and chronic dissection are also highlighted.

Clinical recognition

We have built the presentation in accordance with the usual course of examination of a patient in an emergency. For example, data from the history and physical examination are presented first. This is followed by laboratory and radiographic data, usually obtained in the emergency department. As the examining physician's suspicion increases, more sophisticated confirmatory studies may be required. If there is a significant possibility that there is a dissection, medical treatment should be started. Thus, the section on the diagnostic strategy is structured in such a way as to illustrate the most effective way for various clinical situations to a timely and correct diagnosis. Although the final treatment strategy is different for proximal and distal dissections, the primary and most secondary evaluations are largely the same.

History and general examination

In most cases, aortic dissection happens unexpectedly. The patient complains of a sudden onset of severe chest pain, but none of the disorders that usually accompany the bundle is manifested. A history of high blood pressure or a previously diagnosed thoracic aortic aneurysm suggests a possible dissection. Almost all patients with a distal dissection and most with a proximal dissection have a history of hypertension on close examination. Other conditions associated with aortic dissection, such as pregnancy, corrected and uncorrected aortic coarctation, and aortic valve anomalies, should also raise the suspicion of dissection.

Connective tissue pathology and other genetic defects may also predispose to aneurysm formation and aortic dissection. Currently, many patients with Marfan syndrome are well trained to recognize the clinical symptoms. It is not uncommon for a patient with Marfan's syndrome to come to the emergency department, stating: "I have Marfan's syndrome and pain typical of aortic dissection." Unfortunately, such claims are sometimes ignored by emergency room physicians, with disastrous consequences. Even without a statement from the patient, the characteristic stigmata of Marfan syndrome, including high costal arch, long arms and legs, increased mobility in the joints, visual disturbances, in the presence of chest pain, should lead the examining physician to the idea of ​​a possible aortic dissection. Patients with osteogenesis imperfecta and systemic lupus erythematosus, as well as those with Ehlers-Danlos syndrome, are usually detected during history taking or during physical examination. Turner and Noonan syndromes are also easily recognizable with some attention. More difficult to diagnose are cases with only one or two characteristic features of Marfan syndrome and those with familial dissection syndrome. In any case, pain in the chest, back, or pulse deficit in each of the above groups should be the reason for a thorough examination for aortic dissection.

Characteristics of pain

Consideration of the possibility of acute aortic dissection in a patient with chest pain is a general clinical principle. Intense chest pain is a cardinal sign of aortic dissection that occurs in more than 90% of patients. Pain usually has a characteristic localization. Anterior chest pain is most commonly associated with proximal dissection, while pain in the posterior or scapular space is most common with distal dissection. In patients with type I dissection according to DeBakey, pain is usually localized in front and in the scapular region, since both the ascending and descending portions of the aorta are involved in the process. With dissection of only the proximal aorta, the concentration of pain symptoms in the middle substernal region is characteristic. As the dissection spreads distally, the pain moves to the neck and lower jaw (sometimes there are difficulties with swallowing), then to the interscapular region, and finally captures most of the back, lumbar region, and even the groin. This migration of pain from the anterior chest to the scapular region is common in type I dissection and reflects the involvement of new portions of the aorta in the process. The presence of migratory pain should increase the physician's suspicion of aortic dissection. With distal dissection, pain usually occurs in the interscapular region with some anterior irradiation. There may also be intense abdominal pain due to renal and visceral ischemia. Occlusion of the thoracoabdominal aorta and iliac arteries results in peripheral ischemia and severe pain in the extremities. There may be numbness and paraparesis of both legs. More often, however, hypoperfusion due to unilateral proximal occlusion of the artery ischemic and painful in one leg, usually the left leg.

Rarely, aortic dissection is painless. This is usually observed in patients with an already formed large aneurysm of the ascending aorta, when the dissection is localized only in its proximal section.

The most important clinical problem is the differential diagnosis of chest pain due to aortic dissection with pain in angina pectoris, myocardial infarction, and others. According to Eagle, at initial suspicion of aortic dissection, the most frequently reported subsequent findings were acute, aortic regurgitation without dissection, aortic aneurysm without dissection, musculoskeletal pain, mediastinal cyst or swelling, pericarditis, gallbladder pathology, and pulmonary embolism (in decreasing order of probability).

Pain during dissection is usually intense, occurs suddenly and for the first time. It is interesting that often the patient, when describing the nature of pain, uses such a definition as “tearing”. Usually very intense from the very beginning, the pain does not subside, unlike angina pectoris. Patients are usually restless and constantly change their position in an attempt to reduce discomfort. By comparison, angina pain usually comes on slowly and may improve with limited movement. In the era of immediate treatment of acute coronary ischemia with thrombolysis, extreme care must be taken to ensure that a patient with aortic dissection is not inadvertently diagnosed with coronary ischemia and prescribed thrombolytics. Although uncommon, the clinical picture of proximal aortic dissection can be greatly complicated by concomitant total or partial coronary artery occlusion with symptoms of typical angina or heart failure due to severe myocardial ischemia. This situation can be exacerbated by acute aortic regurgitation, which is also often associated with proximal aortic dissection. Although dissection may present with pain typical of myocardial ischemia, the history of the former is usually less specific. We have had several patients who received thrombolytics for "acute myocardial infarction with ventricular clot embolization" in whom "subsequent femoral embolectomy failed." It turned out that these patients had type I dissection according to De Backy with the involvement of the coronary arteries. These patients often have marked "ischemic" ECG changes and chest pain, but many are under 50 years of age and do not have risk factors for coronary artery disease.

Patients with chronic proximal aortic dissection usually do not complain of severe pain. A sudden increase in the size of a proximal aortic aneurysm may be the only sign that a dissection has occurred. They may have a feeling of "fullness" in the chest and mild dull pain caused by congestive insufficiency due to aortic regurgitation. In rare cases of advanced dissection, large aneurysms of the ascending aorta can press on the sternum and chest, causing severe bone pain.

Chronic distal aortic dissection is usually asymptomatic and is found on examination for an enlarged aneurysm of the affected segment. However, an increase in the diameter of the aorta can lead to compression of adjacent structures, which can be expressed in back pain from erosion of the vertebral bodies and irritation of the nerve roots.

Sometimes there is an obstruction of the left main bronchus, leading to recurrent pneumonia. Occasionally, the patient notes a pulsation in the abdomen. When a secondary dissection of dilated aortic segments occurs, symptoms similar to those of an acute dissection may occur. In Marfan syndrome, the presence of a proximal dissection or aneurysm increases the likelihood of a distal dissection and vice versa. Often, the primary lesion remains unrecognized, manifesting itself only as bone pain from erosion by an aneurysm of the bodies and processes of the vertebrae.

Both proximal and distal chronic dissection can lead to a hypoperfusion syndrome, which presents with postprandial abdominal pain due to intestinal ischemia, chronic renal failure and hypertension, and intermittent claudication due to occlusion of the aorta or iliac arteries, or any other of the described peripheral vascular disorders.


Arterial pressure

Most patients with acute proximal aortic dissection have normal or moderately elevated pressure. In the absence of connective tissue disease, virtually all patients with acute distal dissection have either a history or presenting history of hypertension. Patients may be pale, have circulatory failure and shock. However, measuring their blood pressure usually gives normal or high numbers. High blood pressure may be the result of essential hypertension, mechanical occlusion of the renal artery, or occlusion of the thoracoabdominal aorta. Moreover, due to the pain and the nature of the aortic dissection, there is usually a significant release of catecholamines.

In large series, 20% of patients with acute proximal dissection had hypotension and even severe shock on examination, usually signifying pericardial rupture with tamponade or rupture. Patients with acute distal dissection and hypotension always have aortic rupture and bleeding into the retroperitoneum or chest cavity. Secondary "pseudo-hypotension" has also been reported, resulting from compression or occlusion of one or both subclavian arteries by a dissecting membrane. Hypotension may also result from the sudden development of severe heart failure due to aortic valve insufficiency or coronary artery disease.

In chronic proximal aortic dissection, congestive heart failure due to aortic regurgitation is common. This can be expressed in a slight or moderate decrease in pressure with sometimes severe diastolic hypotension. In chronic distal dissection, the most common cause of hypotension is aortic rupture, which occurs imperceptibly and is accompanied by blood leakage into the pleural cavity and mediastinum.

peripheral pulse

One of the important signs when examining a patient with suspected acute aortic dissection is a pulse deficit. According to different authors, up to 60% of patients have this sign. A pulse deficit on one of the supra-aortic branches usually indicates a proximal dissection. However, with retrograde spread of the distal dissection, there may be a decrease in the pulse in the left subclavian artery.

The fact that the nature of the pulse deficit changes as the dissection spreads distally and secondary communications form is well known. Such changes in the patient's pulse make one suspect an aortic dissection and should encourage the doctor to further research. The pulse on the femoral vessels may be absent due to occlusion of the thoracoabdominal aorta or iliac arteries due to the expansion of the false lumen. Often the patient presents after a recent exploratory operation with a negative result or an attempted Fogarty embolectomy for acute femoral artery occlusion when no thrombus is detected. Then, with a careful reassessment of the patient's condition, a diagnosis of aortic dissection is made.

Pulse deficits are relatively uncommon in patients with chronic aortic dissection. This feature probably indicates the presence of distal secondary communications that decompress the false canal. Pulsus paradoxus should be considered as a sign of pericardial involvement.

auscultatory picture

In addition to the murmur of aortic regurgitation, patients with proximal aortic dissection may have several other findings on cardiac auscultation. Acute regurgitation can lead to an increase in LV end pressure, thereby reducing the intensity of the first heart sound, and sometimes making it completely inaudible. Moreover, the gallop rhythm is usually heard at the Botkin point. Absence of murmur in severe aortic regurgitation was described, which was explained by severe congestive heart failure. The presence of a pericardial rub makes one think of pericardial hemorrhage or, in subacute cases, fibrous pericarditis. A continuous murmur usually indicates a ruptured right ventricular or right atrial dissection. In our practice, we have observed a rupture of the dissection into the pulmonary artery, leading to the appearance of a loud blowing noise and severe pulmonary edema.

Auscultation of the rest of the chest and abdomen can reveal some important details in both acute and chronic dissections. Congestive heart failure can lead to pulmonary edema in both the acute and chronic phases. The absence of vesicular breathing in the left half of the chest may indicate a hemorrhage into the cavity. Various auscultatory murmurs can be caused by hypoperfusion of large branches of the aorta. Suspicious findings can be assessed using Doppler ultrasound. Obtaining a complete auscultatory picture is vital.

Aortic valve insufficiency

An aortic regurgitation murmur develops in 50-70% of patients with acute proximal aortic dissection. The presence of a new murmur, combined with chest pain and pulse deficit, should lead the clinician to the high probability of an aortic dissection involving the ascending aorta. The pathophysiological mechanisms of aortic regurgitation vary. Noises are best heard along the right or left edges of the sternum. In acute onset, many peripheral signs of aortic insufficiency are absent. If there is severe congestive heart failure, there may also be no murmur. The presence and degree of aortic insufficiency is detected by transesophageal or even external echocardiography.

Anyone who survives an acute dissection and enters the chronic phase of the disease develops all the signs of aortic insufficiency. In fact, this complication may be the reason for the admission of such a patient to a medical institution. It should be noted that 10% of patients with chronic distal aortic dissection have secondary aortic insufficiency due to dilatation of the ascending aorta and its root.

Pericardial signs

Because of the sinister nature of pericardial fluid accumulation in acute aortic dissection, looking for signs of this process is of the utmost importance. In the course of a general examination of the patient, swelling of the jugular veins and a paradoxical pulse can serve as suggestive moments. As mentioned above, there may be a pericardial friction rub. Additional important features are low voltage waveforms on the ECG or an increase in the shadow of the heart on the x-ray. However, these data alone do not help confirm the diagnosis of acute proximal dissection. Moreover, in the absence of a previously recorded electrocardiogram, low voltage due to tamponade is not a specific finding. Today, the availability of transthoracic and transesophageal echocardiography makes it easy to detect blood in the pericardium.

Neurological signs

The neurological manifestations associated with aortic dissection were discussed as early as 1944 in a review by Weisman and Adams. These included syncope, stroke, ischemic paraparesis and paralysis, paraplegia due to dissection and rupture of the vessels supplying the spinal cord, and Horner's syndrome.

According to Slater and DeSanctis, 10% of patients presenting with acute aortic dissection are syncope. Five out of every six such patients subsequently have a ruptured dissection of the ascending aorta into the pericardial cavity. Thus, a history of syncope, combined with signs suggestive of aortic dissection, should lead the clinician to the possibility of rupture of the dissection into the pericardial cavity and tamponade, which is a purely surgical problem.

Neurological deficits may result from a syndrome of hypoperfusion of one or more branches of the aortic arch.

Acute cerebral vascular occlusion is more often found in proximal aortic dissection. Fortunately, neurological deficits develop in less than 20% of these cases. In stroke, there is some chance of improvement after the removal of acute occlusion. However, reperfusion can also lead to massive intracerebral hemorrhage, edema, and global cerebral damage, including coma and brain death.

Paralysis of the extremities develops due to separation or compression of large arteries supplying the spinal cord, or due to ischemia of peripheral nerves during occlusion of the thoracoabdominal aorta. It is important to establish the etiology, because. restoration of blood circulation in ischemic muscles and nerves of the lower limb usually leads to the restoration of function. On the contrary, in patients with impaired blood supply to the spinal cord, the prognosis for the restoration of the neurological function of the lower limb is very unfavorable. The defeat of the intercostal or lumbar arteries, and in particular the Adamkevich artery, can manifest itself as flaccid or spastic motor paraplegia. There is also usually an absence of pain and temperature response below the level of the affected segment of the spinal cord, although sensitivity may be restored over time. As with other spinal lesions, the Babinski reflex may appear on both sides. The tone of the sphincters may also disappear. The sense of position is generally preserved, as is the blood supply to the extremities and the pulse in the femoral vessels.

Acute violation of the patency of the thoracoabdominal aorta is manifested by pain in the lower extremities, acute paralysis, lack of pulsation of the femoral arteries, impaired and reduced sensitivity up to complete anesthesia. Patients are in a very critical condition and may also have impaired renal and visceral blood flow. They usually result from extensive dissection involving most or all of the distal aorta. The limbs are usually marbled and deep tendon reflexes are absent. The marbling sometimes extends proximally to the navel or even to the nipples and may be accompanied by a distinct line of demarcation.

Despite the general severe clinical picture in such patients at admission, with timely surgical intervention, the prognosis for the restoration of functions in them is better than in patients with occlusion of the spinal arteries. This is because blood flow to the aortic bifurcation can usually be restored, and such patients can recover completely.

In patients with chronic dissection in the acute stage, both major and minor strokes can occur, which will manifest as persistent neurological deficits or mild symptoms. Chronic aortic dissection rarely results in paralysis or paraplegia. However, embolic strokes were noted with thrombi accumulating in the proximal pockets of the false lumen of the aorta formed in the acute phase.

Other symptoms

Various unusual physical findings have been described in connection with aortic dissection. They include pathological pulsation in the area of ​​the sternoclavicular junction, superior vena cava syndrome with its obstruction by the enlarged ascending aorta, vocal cord paralysis and hoarseness due to compression of the recurrent nerve, compression of the trachea and bronchi with lung collapse, profuse hemoptysis with erosion of the tracheobronchial tree, vomiting of blood with erosion of the esophagus and various pulsations on the neck. These manifestations result from the expansion of the false lumen and compression of adjacent structures. Subfebrile temperature is not uncommon, and sometimes there may be a strong fever due to the release of pyrogenic compounds from ischemic organs or as a result of the collapse of hematomas.

Electrocardiography

The classic sign of acute aortic dissection is intense chest pain, but ECG evaluation of acute proximal dissection usually does not reveal ischemic changes. However, significant changes in the ST segment and T wave are sometimes observed, indicating severe ischemia or infarction due to obstruction of the coronary artery by dissection. Sometimes, as a result of the spread of a hematoma to the aortic root, interatrial septum, or atrioventricular node, a heart block may develop. Patients with coronary artery disease or hypertension on the ECG may have signs of old myocardial infarction or hypertrophy. In acute or chronic distal dissection, the ECG usually indicates left ventricular hypertrophy associated with chronic hypertension.

Chest x-ray

Plain x-rays, which are available in most emergency departments, often provide important information in making a diagnosis of aortic dissection.

Although standard chest x-rays and lateral chest x-rays cannot provide a definitive diagnosis, their evaluation reveals some of the details associated with aortic dissection. In cases of asymptomatic or chronic dissection, x-rays may generally serve as the first source of information about the existence of aortic pathology. Moreover, when old radiographs are available, comparison with recent radiographs can provide important information, especially in the context of the clinical presentation of the dissection.

In 1932, Wood proposed criteria for the interpretation of plain chest X-ray data, which are still used today. Signs accompanying aortic dissection include changes in the shadow adjacent to the descending thoracic aorta, deformity of the shadow of the aorta and other parts of the supracardiac shadow, tightness adjacent to the brachiocephalic trunk, enlargement of the heart shadow, displacement of the esophagus, mediastinal changes, abnormal contour of the aorta, indistinctness of the aortic shadow , displacement of the trachea or bronchi and pleural effusion.

Most often, changes are found in the region of the aortic arch. They include enlargement of the aortic diameter, the presence of double density due to the expansion of the false lumen, and irregular and indistinct contour. Most of these changes are the result of expansion of the false lumen of the aorta or localized hemorrhages.

According to the Mayo Clinic, of the 74 cases of aortic dissection, 61 chest x-rays had abnormalities in these areas. In 13 cases, there were no signs to suspect a dissection. However, 8 of them had other changes, including heart enlargement, congestive heart failure, and pleural effusion. Thus, only 5 patients had normal chest radiographs. Although the aortic shadow was normal in 18% of patients, this is not surprising, because. often the diameter of the aorta in acute dissection increases only slightly. Thus, an intact aortic shadow and mediastinum should not deter the clinician from further investigation if the patient's history and clinical findings suggest a dissection. In addition, a clearly enlarged aorta in a direct picture may be hidden by the shadow of the heart. This is especially true for cases of type II deBakey stratification. Lem-on and White noted that a significant number of patients with Marfan's syndrome with large aneurysms involving the sinus segment of the aorta had a "normal" aortic caliber on plain radiographs.

The shadow of the aorta, which initially appears normal on x-rays, can change dramatically over time, rapidly increasing in size. Local protrusions can be detected.

Separation of calcified intimal plaques greater than 1 cm from the border of the aortic shadow, giving the impression of a thickened aorta, as well as the presence of a double density of the aorta are signs of a dissection with a double channel. Unfortunately, various manifestations of thoracic aortic atherosclerosis and aortic aneurysm without dissection can also have such features, making them nonspecific.

A small pleural effusion, usually on the left, is a very common finding in both chronic and acute proximal and distal dissections. It is the result of diapedesis of erythrocytes through a weakened stratified wall of the aorta in the acute variant, and periaortic inflammation in subacute and chronic. A large effusion may indicate a tear into the pleural space, in which case it is always accompanied by mediastinal enlargement.

An increase in the mediastinal shadow due to bleeding or aortic dilatation, especially when seen on a direct posteroanterior image, is an important finding. It occurs in 10-50% of cases.

An enlarged heart shadow is a common finding in aortic dissection, which may result from pericardial effusion, cardiac dilatation with aortic valve insufficiency and cardiomegaly in chronic cases, and hypertension and left ventricular hypertrophy. If older images are available and the comparison reveals enlargement of the cardiac shadow, pericardial bleeding should be suspected. Unfortunately, the enlargement of the cardiac shadow in acute dissection may be barely noticeable due to the non-distensibility of the pericardium. Moreover, due to the high prevalence of hypertension in these patients, this symptom is also not specific.

Displacement of the tracheobronchial tree and esophagus during dissection is observed in 60% of cases. The displacement can occur both to the right and to the left, depending on the location of the bundle. The course of the gastric tube may show displacement of the esophagus.

Laboratory data

Due to the accumulation of blood in the false lumen and diapedesis of erythrocytes through the wall of the aorta, mild anemia is relatively common. The outpouring of a significant amount of blood into the pleural space leads to severe anemia. A large number of clots may form, leading to a decrease in the content of clotting factors. Occasionally, due to the consumption of platelets and coagulation factors in the false lumen, DIC develops. Blood that accumulates in the false lumen can hemolyze, which leads to an increase in the level of bilirubin and LDH in the blood. Often there is a slight leukocytosis of the order of 10-15 thousand. The level of transaminases is usually normal or slightly elevated. Electrolytes are usually normal. Blood gas analysis may reveal metabolic acidosis due to anaerobic metabolism in ischemic areas. If the kidneys are involved, hematuria may occur.

Surgical treatment of aortic dissection
Hans Georg Borst, Markus K. Heinemann, Christopher D. Stone

This largest blood vessel originates in the left ventricle of the heart, consists of the ascending part, the arc, the thoracic and abdominal departments(descending part). The mouth of the vessel is also the beginning of a large circle of blood circulation, which nourishes most of the body.

There are three layers in the wall:

  • intima (internal);
  • media (middle layer with muscle fibers, the most powerful);
  • adventitia (external).

Aortic dissection can be described by the following mechanism: cracks form in the inner shell, then they deepen into the middle and outer, and an abnormal lumen is created. Blood rushes into it, under its pressure, the crack expands and a gap is formed. But there is also reverse process- thickening of the aorta. How dangerous this phenomenon can be read.



Background and symptoms of the disease


The etiology of the disease consists of the following factors:

  • atherosclerotic damage to the vessel wall;
  • arterial hypertension;
  • connective tissue lesions;
  • injury.

There is also an anatomical classification. Its principle lies in the levels of distribution. The simplest and strictest - Stanford, divides the pathology into stratification of the ascending part (type A) and the descending part (type B).

The descending department is most often affected. Layering variations include separating the inner and middle

  • shells from each other under the action of:
  • internal hematoma;
  • intimal tear without hematoma;
  • ulceration of an atherosclerotic plaque leading to stratification with a hematoma.

Symptoms of the disease

Aortic dissection has clear symptoms, the causes make some differences in them.
Often, everything starts suddenly, with the appearance of a sharp burning pain in the region of the heart, radiating into the interscapular space. Migration of pain is characteristic, this is associated with the spread of aortic dissection.

Patients suddenly lose consciousness, this is due to unbearable pain. Loss of consciousness can be caused by irritation of the aortic baroreceptors, blockage of the arteries that feed the brain, cardiac tamponade (abnormal filling of the heart cavities with blood).

Pathology is often accompanied by signs of a stroke, myocardial infarction, circulatory disorders of the spinal cord.


Clinically, in some patients there is a pulse deficit, blood pressure indicators on the right and left arms differ by more than 30 mm Hg. Art.

Auscultation of the heart reveals a noise in the area of ​​​​attachment of the 2nd rib to the sternum on the right, that is, aortic. Gradually develops heart failure, shortness of breath due to effusion of fluid into the pleural cavity. With blockage of the renal arteries, oliguria is observed, up to anuria.

Differential Diagnosis

Aortic dissection, although it has pathognomonic symptoms, can be difficult to diagnose.
Suspicion can be caused by any person with signs of severe chest pain, especially if he has not presented any complaints before. Sharp fainting or pain in the abdomen, described as "dagger", sudden shortness of breath, differences in blood pressure - all this suggests an aortic dissection.

After examining the patient, the doctor prescribes an ECG, chest x-ray, TPE, angiography.

On the ECG, you can get signs of ischemia and myocardial infarction, but these changes can be interpreted in different ways. In addition to this, a test for cardiac troponins (CPK, alkaline phosphatase, LDH 1.2) will also not give a specification of the result, because all indicators appear at different times.

An x-ray of the chest will reveal the area of ​​the aneurysm (bulging) as well as the presence of fluid in the pleural cavity.

CAG - coronary angiography, is one of the best methods for diagnosing the pathology of the heart vessels. Its disadvantage is a large list of contraindications and the impossibility of carrying out outside a specialized hospital.

TEE - transesophageal echocardiography is also a fairly informative method, but it becomes available only when the patient's condition stabilizes.

It can also cause aortic dissection. A cardiac surgeon advises and treats such patients.

Treatment of aortic dissection

Aortic dissection is a serious disease. Symptoms, causes and very complex treatment clearly prove this.

Such patients are hospitalized strictly in the intensive care unit, where they control all vital statistics. Tracheal intubation is performed, a urinary catheter is placed, and the blood type is determined. Administer drugs that reduce blood pressure: B-blockers or nitrates. However, it makes no sense to use only drug treatment, the condition can worsen at any moment.

Surgery includes aortic valve repair, valve replacement, and aortic stenting. It all depends on the location of the split.

After the operation, the patient receives for life drug therapy, most often these are ß-blockers, calcium channel blockers and ACE inhibitors. Diagnostic control includes ECG and CT or MRI.

The prognosis is often unfavorable. 30% of patients, and sometimes no longer survive to hospitalization. Another 30% die in the hospital. This is due to the severity of the condition.

Get timely examinations and treatment. Do not ignore prescribed therapy.

- a defect in the inner membrane of the aneurysmically dilated aorta, accompanied by the formation of a hematoma, longitudinally exfoliating the vascular wall with the formation of a false canal. A dissecting aortic aneurysm is manifested by sudden intense pain migrating along the course of dissection, an increase in blood pressure, signs of ischemia of the heart, brain and spinal cord, kidneys, and internal bleeding. Dissection Diagnosis vascular wall based on echocardiography, CT and MRI of the thoracic/abdominal aorta, aortography. Treatment of a complicated aneurysm includes intensive drug therapy, resection of the damaged aortic area, followed by reconstructive plasty.

Treatment of a dissecting aortic aneurysm

Patients with complicated aortic aneurysm are urgently hospitalized in the cardiac surgery department. Conservative therapy is indicated for any form of the disease at the initial stage of treatment in order to stop the progression of the stratification of the vascular wall, to stabilize the patient's condition. Intensive therapy of a dissecting aortic aneurysm is aimed at stopping the pain syndrome (by administering non-narcotic and narcotic analgesics), removing from a state of shock, lowering blood pressure. Hemodynamic monitoring is carried out, heart rate, diuresis, CVP, pressure in the pulmonary artery. For clinically significant hypotension, fast recovery OCC at the expense intravenous infusion solutions.

Medical treatment is essential in most patients with uncomplicated type B dissecting aneurysms (with distal dissection), stable isolated aortic arch dissection, and stable uncomplicated chronic dissection. With the ineffectiveness of the therapy, the progression of dissection and the development of complications, as well as patients with acute proximal dissection of the aortic wall (type A), immediately after stabilization of the condition, urgent surgical intervention is indicated.

In case of dissecting aortic aneurysm, resection of the damaged aortic area with tear, removal of the intimal flap, elimination of the false lumen and restoration of the excised aortic fragment (sometimes simultaneous reconstruction of several branches of the aorta) are performed by prosthetics or convergence of the ends. In most cases, the operation is performed under cardiopulmonary bypass. According to the indications, valvuloplasty or aortic valve replacement, coronary artery reimplantation are performed.

Forecast and prevention

In the absence of treatment of a dissecting aortic aneurysm, mortality is high, during the first 3 months it can reach 90%. Postoperative survival for type A dissection is 80%, and for type B dissection, 90%. The long-term prognosis is generally favorable, with a 10-year survival rate of 60%. Prevention of the formation of a dissecting aortic aneurysm is to control the course cardiovascular diseases. Prevention of aortic dissection includes observation by a cardiologist, monitoring of blood pressure and blood cholesterol levels, periodic ultrasound or aortic ultrasound.

Aortic dissection most often affects older people. But there are cases when such a disease is detected among young people. Therefore, in order to prevent the development of complications, it is necessary to know how this disease manifests itself.

And for this you need to learn everything about the causes, symptoms and treatment of aortic dissection.

What causes disease

Allocate congenital and acquired causes of aortic aneurysm. The first ones are associated with the presence in a person of pathologies of the cardiovascular system, which manifest themselves in defective development or its narrowing (stenosis) and congenital malformations of the aorta itself - tortuosity and coarctation. In addition, congenital or acquired heart disease can serve as a cause. In addition, the following diagnosed diseases associated with connective tissue pathologies affect the development of an aneurysm:

  • Ehlers-Danlos syndrome;
  • annuarticular ectasia;
  • polycystic kidney disease;
  • osteogenesis;
  • Turner syndrome;
  • homocystinuria.

Etiopathogenic factors also influence the local expansion of the site, such as:

  • fluctuations in blood pressure caused by hypertension,
  • atherosclerosis;
  • syphilis;
  • chest and abdominal trauma;
  • damage to the aorta by a foreign body or adjacent pathological process(cancer of the esophagus, spondylitis, peptic ulcer of the esophagus).

Risk factors also include:

Symptoms

Aortic dissection can be either acute or chronic. They are distinguished by pain during seizures.

The acute form is characterized sudden manifestation symptoms of aortic dissection (the reasons for this can be both acquired and congenital), which cause pain, and this condition lasts up to two weeks.

The chronic form is also characterized by pain, but the duration can last indefinitely without treatment until death. Due to that

that when the aorta is dissected, blood circulation to nearby organs is lost, strokes or fainting may develop, as well as severe shortness of breath and unexplained weakness.

With the proximal form of pain, they have a compressive or stabbing character in the areas of the chest and retrosternal space. In this case, they can also give in the back. In the distal form, symptoms of abdominal aortic dissection occur: pain in the stomach, back, which often radiate to the neck.

In the acute form of the course of the disease, high blood pressure and increased heart rate are manifested. If at this stage the disease has not been cured, then the symptoms become chronic.

Ascending aortic dissections

Violations in this department aorta are divided into:

  1. Dissection of an aortic aneurysm, that is, inflammation of the area from the fibrous ring of the aortic valve to the sinotubular ridge. This diagnosis is often accompanied
  2. Dissection of the tubular part of the ascending aorta, that is, inflammation of the area from the sinotubular ridge to its arch. This type of disease of the ascending aorta is not accompanied by valve insufficiency.
  3. The bundle is treated with medication if its diameter does not exceed 45 mm. If this parameter is exceeded, then surgical intervention is recommended. This is due to the fact that, according to statistics, when the ascending section is stratified with a diameter of 55 mm or more, the risk of rupture increases.
  4. Dissection of an aortic aneurysm ruptures more often than others. If a bilateral stratification is found in this department, then a third of patients with such a disease die.
  5. When dissecting the ascending section, a reverse reflux of the contrast agent from the aorta into the left ventricle is observed. It's connected with high blood pressure in the aorta.

descending aorta

Descending aortic dissection is more common in older people with cardiovascular disease.

The reverse direction of the dissection of the descending aorta does not occur, as a result of which aortic regurgitation is not observed. During dissection, the pulse carotid arteries and blood pressure in the upper part remains unchanged.

The first symptom of the initial stage of descending aortic dissection is the onset of sudden pain behind the sternum or between the shoulder blades, which is transmitted to the front of the chest. Patients with such a bundle, as a rule, are not prescribed emergency surgery, but drug treatment is carried out. With such therapy, a prerequisite is the normalization of blood pressure.

If the diameter has reached four centimeters, then the doctor has the right to prescribe surgical treatment. This is due to the fact that if this diameter is exceeded, then the risk increases many times over.

Classification

Michael Ellis DeBakey is an American cardiac surgeon who studied the disease and proposed the following classification of aortic dissection by type:

  1. The first is that the dissection starts from the sinus of Valsava and extends higher to the curvature of the aorta, that is, it can leave the border of the ascending aorta.
  2. The second type - the disease is localized in the ascending aorta.
  3. The third is a dissection that descends below the origin of the left subclavian artery.

The third type is divided into:

  1. 3A - dissection is localized in the thoracic aorta.
  2. 3B - the disease is located below the thoracic aorta. Sometimes the third type can approach the left subclavian artery.

Recently, Stanford University has developed more simple classification which includes two options:

  • Aortic dissection type A is a disease that is localized in the ascending aorta.
  • Type B aortic disease is a lesion that descends below the origin of the left subclavian artery.

Traditional surgical treatment of aortic dissection carries a poor prognosis. In a non-critical condition, this approach is traumatic for the patient and is associated with great difficulties during the operation.

Modern therapeutic methods for the treatment of aortic dissection have a better prognosis. The technology of such intervention is constantly improving, which facilitates the rehabilitation of the patient.

Diagnostics

Aortic dissection is one of the most serious vessel defects, it is a lethal danger to human existence.

According to statistics, 65-70% of patients who do not seek support die from internal bleeding. Of those who undergo surgery, approximately 30% of patients die. The prognosis for such a disease is far from pleasant. A timely diagnosis is considered essential for survival in aortic dissection. Despite the rather ordinary ways of finding a defect, episodes of non-recognition are not uncommon.

The aorta contains three covers: external, middle and internal. The stratification is combined with the inferiority of the middle cover over this or that particular place. Due to this defect, a tear of the inner cover (intima) and the development of an erroneous lumen in the middle of its epithelium are likely. The tear can occupy part of the aorta or spread throughout the entire internal volume.

Dissection, in other words, a dissecting aneurysm, has the ability to form in an arbitrary lobe of the aorta and ends with a rupture of the vessel at any time. Predominantly sensitive areas are the original segments of the aortic arch.

Surgery

Surgery indicated for acute aortic dissection. During this period, the risk of its rupture is possible. Surgical intervention is also acceptable to treat the chronic form of the course of the disease, which has passed from the acute one.

In the initial stage of development, the operation of aortic dissection is not justified, since it is amenable to drug treatment. At this stage, it can be prescribed only if there is a threat of damage to vital organs.

In the chronic form, the operation is indicated for dissection of more than 6 cm in diameter.

According to statistics, if surgery is performed immediately after an acute form is detected, then the risk of death is only three percent, and if you prepare for surgery for a longer time, then a 20 percent risk of death is possible.

Surgical intervention includes:

  • resection of the aorta at the site of dissection;
  • elimination of false lumen;
  • restoration of the excised fragment of the aorta.

Medication treatment

Medical treatment for aortic dissection is recommended for all patients with any form of aortic aneurysm. This approach is indicated to stop the progression of the disease.

Therapy for aortic dissection is aimed at reducing pain by administering non-narcotic and narcotic analgesics, getting rid of shock and lowering blood pressure.

During drug treatment, monitoring of heart rate and pressure dynamics is mandatory. To reduce the cardiac volume of blood circulation and reduce the rate of expulsion of the left ventricle, b and p blockers are used to reduce the heart rate within 70 beats per minute. .In the treatment of aortic dissection, "Propranolol" is administered intravenously at a dose of 1 mg every 3-5 minutes. Maximum effective rate should not exceed 0.15 mg/kg. With maintenance therapy, Propranolol is administered every 4-6 hours at a dose of 2 to 6 mg, which depends on the heart rate. You can also use Metoprolol at a dose of 5 mg IV every 5 minutes.

Also, for the treatment of aortic dissection, Labetalol is used drip from 50 to 200 mg / day per 200 ml of saline.

Alternative treatment

To get to the pharyngeal abscess and treat it with folk remedies, you must regularly use the following decoctions and tinctures inside:

  1. Yellowberry tincture. To prepare the product, we take two tablespoons of dried and chopped grass and pour it with a cup of boiling water. The resulting mixture is wrapped thick cloth and put in a warm place, for example, near the battery. After two hours of infusion, the mixture must be filtered and one tablespoon can be consumed up to five times a day. If your tincture is bitter, then sugar can be added to it.
  2. Viburnum tincture. In the presence of attacks of suffocation, an infusion of viburnum berries should be used. They can also be eaten raw, mixed with honey or sugar.
  3. Dill tincture. To prepare the product, we take a spoonful of fresh or dry dill, if desired, you can add its seeds. One part of the greens will require about three hundred milliliters of boiling water. After infusion for about an hour, the mixture is consumed three times throughout the day.
  4. Infusion of hawthorn. To prepare, take four tablespoons of chopped dry hawthorn fruits and pour three cups of boiling water. We infuse the resulting mixture for several hours, after which it must be divided into two days, and one part should be consumed in three divided doses during the day, half an hour before meals.
  5. A decoction of elderberry. To prepare a decoction, we take the dried root of Siberian elderberry and grind it. Then pour a spoonful of powder with a cup of dill. We put the resulting mixture to infuse, and then finish cooking by boiling for fifteen minutes in a water bath. We filter the finished mixture and take one tablespoon at a time.
  6. A decoction of primrose. For cooking, we take the crushed dry rhizomes of the plant. Pour a spoonful of powder into a mug hot water and continue boiling for half an hour in a water bath. Strain the broth, then squeeze out the moisture from the prepared powder. Use finished product follows three times a day for a tablespoon.

If, in the acute form of the course of the disease, an increase in temperature is observed, then to reduce it, you can take remedies from garlic and a leaf of a golden mustache. To do this, take the peeled garlic and finely chop. Then you need to grind the leaves of the golden mustache and mix with garlic. Add thirty grams of honey to the resulting composition. Leave the finished mixture to brew in a warm place. Then mix and consume one tablespoon with water.

Complications

A complication of aortic dissection is complete break. Mortality from aortic rupture is up to 90%. 65-75% of patients die before they arrive at the hospital, and the rest before they reach the operating room. The walls of the aorta are an elastic structure that requires complete integrity. A gap occurs when its strength is lost. This can happen when the internal or external pressure is greater than the walls can withstand.

Pressure builds up as the tumor progresses. Bleeding can be retroperitoneal or intraperitoneal and can create a fistula between the aorta and intestines.

Prevention

In order to warn yourself against this disease, it is necessary to do prevention, namely:

  • timely treat atherosclerosis;
  • check the level of lipids in the blood;
  • maintain an active, healthy lifestyle;
  • make a proper diet, without the content of fried and fatty foods in the menu. Exclude convenience foods, fast food, soda, alcohol, all foods that exceed the cholesterol content from the diet;
  • give up cigarettes;
  • to control blood pressure, cholesterol in the blood;
  • every year, mostly after forty, undergo an examination of the body to identify cardiovascular abnormalities;
  • Set aside time for physical exercise, but do not allow overwork.

To prolong the life of the heart long term, it is also necessary to carry out the prevention of infectious and catarrhal diseases, since they, in turn, give complications to it.

It is recommended to take food in small portions so that the stomach and intestines do not squeeze the heart, which leads to a deterioration in the blood circulation of the vessels, heart and abdominal organs. Toxins accumulate in the body, which increase the load on the heart. To avoid this, you need to release the intestines in time.

Although physical activity is recommended, people with a disease cardiovascular system it is necessary to reduce them and not lift weights. Otherwise, there will be an overload of blood vessels, which in the future will lead to a stroke and heart attack.

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