Classification of pathology
There are several classification systems for aortic dissection.
Cardiac surgeon Michael de Baiki proposed a system based on the anatomical location and extent of damage to the vascular wall. The types of dissection are as follows: • Type I – the pathological process involves the ascending part, the arch and, often, the descending part of the aorta;
• Type II – only the ascending aorta is affected;
• Type III – the descending aorta is subject to dissection:
a – the process is limited to the thoracic region;
b – the process also affects the abdominal region.
The clinical classification, called Stanford, divides two options:
• A – the ascending section is affected, regardless of the location of the initial tear of the internal choroid;
• B – the lesion does not affect the ascending part, that is, it begins below the origin of the left subclavian artery.
According to the course, the process of aortic dissection is divided into acute and chronic . A dissection is considered chronic when more than 14 days have passed since its onset, or it is discovered accidentally in the absence of clinical manifestations.
Moya moya disease
Moyamoya is an insufficiently studied arterial occlusive disease accompanied by damage to large intracerebral vessels, especially the internal carotid artery and the trunk of the middle cerebral and anterior cerebral arteries. The arteries of the lenticular nucleus and striatum form a rich source of collateral blood flow around the obstructed area of the middle cerebral artery, which, on angiography of the cerebral vessels, resembles a puff of smoke (“moya-moya”). Other collaterals include a transdural anastomosis between the superficial cortical branches of the middle cerebral artery and the soft arteries of the skull (scalp). This disease occurs mainly among the peoples of the East, but it should be suspected in the development of transient ischemic attacks (TIA, micro-strokes) or strokes in children and young people.
The etiology of moyamoya disease is unknown. Several pathological studies have been carried out, which show that the narrowing of the lumen of the arteries is accompanied by the deposition of hyaline fibrous material. Anticoagulants should be prescribed to patients with neurological symptoms with particular caution, since subarachnoid hemorrhage is possible when transdural arterial anastomoses rupture. In some cases, operations to create extracranial-intracranial bypasses are recommended, but their effectiveness has not been established. The craniotomy required to create a shunt can lead to interruption of the transdural anastomosis and theoretically can cause an increase in neurological deficit. In addition, extracranial-intracranial shunting can provoke blockage (occlusion) of the proximal (overlying) section of the middle cerebral artery.
Reasons leading to the development of pathology
Dissection of the aortic wall is a multifactorial disease, but almost always occurs against the background of inferiority of its middle choroid. Defects of smooth muscle cells and elastic fibers can be congenital or acquired during life.
The etiological factors for the development of dissection are as follows:
• hypertension, sharp fluctuations in blood pressure;
• atherosclerotic changes;
• genetic defects in the structure of connective tissue (Marfan, Ehlers-Danlos syndromes);
• congenital heart pathology (bicuspid aortic valve, coarctation of the aorta);
• vasculitis (systemic, infectious, toxic);
• damage during diagnostic or therapeutic procedures (catheterization, plastic surgery, prosthetics, etc.);
• chest and abdominal injuries;
• excessive physical and neuro-emotional stress;
• final trimester of pregnancy.
This pathology is diagnosed twice as often in male patients. With age, especially after 60-70 years, the risk of developing the disease increases.
Aortic dissection in people under 40 years of age is usually caused by congenital processes. Women of this age are most susceptible to the disease in the last months of gestation.
Dissecting aortic aneurysm
Aortic dissection is a fairly rare but potentially dangerous disease, occurring in 1 out of 10,000 hospitalized patients (however, a significant proportion of patients die in the hospital stage), in 1 case in 400 autopsies, in 1 out of 100 who die suddenly, 3-4% of all sudden deaths from cardiovascular diseases. Aortic dissection is the most common catastrophe among acute aortic diseases. If left untreated, the early mortality rate for dissection is 1% per hour (one person in a hundred dies every hour) on the first day, 75% within two weeks, and over 90% within the first year. However, the survival rate of patients can now be significantly increased thanks to timely diagnosis and early treatment of this terrible condition. Early clinical recognition and various diagnostic techniques for imaging the aorta are an integral part of the management of patients with aortic dissection.
Etiology of aortic dissections
1. Diseases and conditions accompanied by cystic degeneration of the media: a) long-term arterial hypertension (AH) b) congenital connective tissue defects (Marfan, Ellers-Danlos, Turner syndromes, polycystic kidney disease) c) old age (60-70 years) 2. Congenital heart defects: a) coarctation of the aorta b) bicuspid (in 7-14%) and unicuspid valve 3. Atherosclerosis of the aorta 4. Pregnancy 5. Chest trauma, severe physical and emotional stress 6. Systemic vasculitis (especially often granulomatous, giant cell arteritis) 7. Chemical and toxic effects (drugs) 8. Iatrogenic causes. The etiology of aortic dissections is varied, but the main ones are 2 factors that contribute to media degeneration, manifested by disorganization of collagen, smooth muscle elements and elastic fibers: hypertension and age. Hypertension is detected in approximately 84% of patients with RA. The peak incidence of aortic dissection occurs in the 6th–7th decades of life, with men affected 2–3 times more often than women. Marfan syndrome occurs in a small number of cases (6-9% of aortic dissections), most often at a relatively young age with localization of the dissection in the proximal part. A hereditary connective tissue defect is characterized by pathology of the skeletal muscular system (asthenic physique, arachnodactyly, chest deformation, kyphoscoliosis, high arched palate, weakness of the eye ligaments (iridodenosis - lens trembling due to weakness of the ligament of cinnamon), subluxation of the lens, retinal detachment, high myopia), as well as cardiovascular complications (aortic root dilatation, aortic regurgitation, aortic dissection and aneurysm, mitral valve prolapse). Most patients die from complications before reaching 40 years of age, although with timely and adequate correction, life expectancy can be normal. About half of aortic dissections occur in pregnant women over 40 years of age, more often in the third trimester, rarely in the early postpartum period. The reasons for the development of aortic dissections in this category of patients are not completely clear; importance is attached to an increase in blood volume, cardiac output and an increase in blood pressure. Women with Marfan syndrome are at especially high risk of aortic dissection during pregnancy. Sometimes the diagnosis of Marfan syndrome is established after the diagnosis of RA in the postpartum period. Direct trauma to the aorta leads to local tear, hematoma or rupture and only in rare cases to aortic dissection. Various groups of patients after valve replacement suffer from aortic dissection, which usually develops several months and years after surgery. About 18% of acute aortic dissections occur in patients with previous cardiac surgery. Patients with aortic valve replacement are at highest risk. Iatrogenic dissections are associated with angiography and balloon dilatation, aortic cannulation during cardiopulmonary bypass. Delamination in these cases is associated only with technical errors. Aortic dissection also occurs at sites where the aorta has been resected or sutured.
Pathogenesis of aortic dissections
Almost always, aortic dissection begins with a tear in the inner lining in one or two places. In addition to this mechanism, the primary mechanism may be the spontaneous formation of an intramural hematoma due to a rupture of the vasa vasorum, which can lead to the formation of a hematoma without an intimal defect (aortic dissection without an intimal rupture in 3-13%) or with subsequent intimal rupture in the clinical picture of a classic dissection. Intramural hematoma is considered an atypical manifestation of aortic dissection and it is still unclear whether it is an early or subsequent stage of aortic dissection. Rarely, aortic dissection can be promoted by a penetrating atherosclerotic ulcer, most often leading to the formation of a pseudoaneurysm with aortic rupture. Any processes leading to weakening and degeneration of the components of the aortic media, elastic fibers, and smooth muscles predispose to aortic dissection.
RA classification
Aortic dissections are classified by anatomical location and timing. According to the most common classification according to M. DeBakey, aortic dissections are divided according to the place of origin and the degree of involvement of various sections: type I - the place of origin of the rupture is the ascending aorta, and the dissection extends to the arch and often distally to the thoracic and abdominal aorta; type II - the rupture is localized in the ascending part, the dissection is limited only to the ascending aorta; type III - intimal tear is localized in the descending thoracic aorta, spreads more often antegrade distally, along the descending aorta at various lengths, involving either only the entire thoracic region and/or both the thoracic and abdominal regions, and rarely retrogradely to the arch and ascending aorta. Since the treatment tactics for types I and II are similar, anatomical classification is currently common: type A is the proximal or ascending type (which includes DeBakey types I and II), type B is distal or descending (corresponds to DeBakey type III ). According to autopsy data, type A is 2-4 times more common. This type is associated with a relatively high incidence of early complications (rupture with tamponade, stroke, aortic regurgitation), is characterized by high pre-hospital mortality and requires emergency surgical treatment. In most cases, dissection occurs in 2 locations: the ascending aorta - within a few cm of the aortic valve (65%) and the descending aorta - slightly distal to the origin of the left subclavian artery (20%), as the most hemodynamically vulnerable areas. Isolated dissection of the arch (10%) and abdominal aorta (5%), as well as individual arteries arising from the aorta, especially the carotid and coronary, is also possible. For aortic dissections involving the ascending aorta, surgical treatment is indicated, but without its involvement, conservative treatment is recommended. Depending on the time of onset of the disease, acute (less than 2 weeks) and chronic (more than 2 weeks) aortic dissections are distinguished. More than 2/3 of cases of aortic dissection are acute.
Aortic dissection clinic
The clinical picture of the disease is determined by 3 pathoanatomical factors underlying the dissection: dissection of the aortic wall, the development of an extensive intramural hematoma and compression or separation of the aortic branches supplying vital organs (heart, brain and spinal cord, kidneys), followed by ischemia. Sudden aortic dissection itself causes pain. The formation of an intramural hematoma in the area of the ascending aorta leads to compression of the coronary arteries, narrowing of the LV outflow tract, acute circulatory failure, and proximal coarctation. An extensive intramural hematoma, containing a large amount of blood, creates a kind of “oligemic syndrome.” Symptoms of aortic dissection can vary, because... dissection is a dynamic process and the initial picture of the disease may differ from the final one. They can mimic almost all cardiovascular, neurological, surgical and urological diseases. The leading and most common (in 90-96% of cases) aortic dissection syndrome is pain (except for patients with impaired consciousness). The pain is unusually intense and occurs suddenly, with maximum severity at the beginning of the dissection, in contrast to myocardial infarction (MI), where it gradually increases. In some cases, the pain can become unbearable. The pain has a tearing, tearing, shooting nature, can be migrating from the site of origin in the direction of the dissection, and may initially be accompanied by vagal manifestations, nausea, vomiting, and increased blood pressure. The localization of pain in RA is determined by the location of the onset of dissection. Pain behind the sternum, in front of the chest, simulating MI, is characteristic of proximal dissection (more than 90% of cases), especially if it extends to the root and causes compression of the coronary arteries. With further dissection (type 1), the pain moves to the interscapular space, then moves along the spine. Migrating pain along the path of dissecting hematoma is observed in 17-70% of patients. Pain in the neck, pharynx, jaw, face, teeth indicates involvement of the ascending aorta and arch. Pain in the chest behind, back, and lower extremities is characteristic of distal dissection, and it is initially localized in the interscapular space. The absence of pain in the interscapular space is sufficient evidence against distal dissection. When aortic dissection types I and II spread to the abdominal aorta, the pain is localized in the epigastrium, hypogastrium, and lower back, simulating acute diseases of the gastrointestinal tract and urological diseases. An asymptomatic (painless) course (except for patients with impaired consciousness) may occur in patients with chronic dissection. Less common initial signs of aortic dissection (with or without pain) may be: - symptoms of cerebral or spinal cord ischemia, peripheral neuropathy, syncope without local neurological symptoms (in 4-5%), which are more often associated with rupture of aortic dissection in pericardium or pleural cavity; - aortic insufficiency and acute circulatory failure; - renal ischemia; — ischemia of the digestive organs; - cardiac arrest and sudden death. Physical examination findings in aortic dissection are variable and, to varying degrees, are related to the location of the aorta and the degree of cardiovascular involvement. In other cases, even in the presence of extensive dissection, objective data may be subtle or completely absent. 1) Hypertension at the onset of the disease (with a possible clinical picture of shock) is observed more often with distal dissection (in 80-90% of cases), less often with proximal dissection. Arterial hypotension is more common with proximal dissection. Its causes are most often cardiac tamponade, or intrapleural or intraperitoneal rupture of the aorta. 2) Asymmetry of the pulse (decrease in its filling or absence) and blood pressure in the upper or lower extremities is observed in half of the patients with proximal and in 15% with distal RA (with the involvement of the femoral or subclavian arteries). The narrowing is caused either by extension of the aortic dissection to one artery or another, with a decrease in the true lumen, or by proximal obstruction by an intimal flap overlying the ostium of the involved artery. Although the presence of pulse asymmetry in a patient with acute pain suggests RA, erroneous interpretations are possible. 3) Aortic regurgitation with a diastolic murmur of aortic insufficiency is an important sign of proximal dissection and occurs in 50-75% of patients. The murmur may have a musical tone and is better heard along the right edge of the sternum. It can be increasing, decreasing, of varying intensity, depending on the value of blood pressure. In severe aortic insufficiency, there may be peripheral signs: fast, galloping and high pulse and high pulse pressure. In some cases, with the development of congestive heart failure, due to acutely developed aortic insufficiency, the diastolic murmur may be subtle or absent. Four mechanisms can lead to the development of aortic insufficiency during proximal dissection: - expansion of the aortic root and aortic annulus, as a result of which the aortic valve leaflets cannot close in diastole; - asymmetrical dissection, when the pressure of the dissecting hematoma can reduce the location (or weaken the function) of one leaflet below the line of closure of the others; - rupture of the ring supporting the leaflet, or a tear in the leaflet of the aortic valve itself, resulting in a “dangling” leaflet; - prolapse through the aortic valve of a mobile intimal flap, which prevents complete closure of the valve leaflets during diastole, which can cause severe aortic insufficiency. In severe aortic regurgitation, sudden onset of heart failure may be an objective sign of RA. 4) Neurological disorders occur in 6-19% of all aortic dissections and include cerebrovascular disorders, peripheral neuropathy, disturbances of consciousness, and paraplegia. Cerebrovascular disorders occur in 3-6% of cases, due to involvement of the innominate or left common carotid artery. Less commonly, there may be disturbances of consciousness or even coma. When the spinal arteries are involved (usually with distal dissection), there may be paraplegia or paraparesis due to spinal cord ischemia. 5) More rare manifestations of aortic dissection may be: MI, renal infarction, etc. In 1-2% of cases of proximal dissection, the ostia of the coronary arteries may be involved and secondary MI may develop (more often - posterior/inferior, due to more frequent damage to the right coronary artery). Due to the presence of symptoms of aortic dissections, myocardial infarction may not be clinically evident. On the other hand, the ECG of acute MI may not recognize aortic dissection, and the use of thrombolysis can lead to fatal consequences. Therefore, in case of posterior/inferior myocardial infarction, one should not forget about the possibility of RA, and before thrombolysis, some authors consider it necessary to conduct an X-ray examination to exclude aortic dissection. The spread of dissection to the abdominal aorta can cause various vascular disorders: renal ischemia and infarction, leading to severe hypertension and acute renal failure; mesenteric ischemia and infarction of the corresponding area (in 3-5% of aortic dissections); acute ischemia of the lower extremities (with the spread of dissection to the iliac arteries). 6) The clinical manifestation of aortic dissection may be pleural effusions, usually on the left, due to either a secondary exudative reaction around the affected aorta or as a result of rupture or leakage of blood into the pleural cavity. 7) Very rare manifestations of aortic dissection can be: - pulsation of the sternoclavicular joint - hoarseness of voice - compression of the trachea and bronchi with symptoms of stridor or bronchospasm - hemoptysis with a rupture in the tracheobronchial tree - dysphagia - vomiting of blood with a rupture in the esophagus - Horner's syndrome - syndrome superior vena cava - pulsation of neck tissue - atrioventricular block (if the septum is involved) - fever of unknown origin caused by exposure to pyrogenic substances from the hematoma or associated effusion - murmurs caused by rupture of the dissected aorta in the cavity of the atria or right ventricle with the development of heart failure. Despite the variety of clinical manifestations of aortic dissection, it should be borne in mind that various diseases manifested by chest pain can mimic aortic dissection: MI, acute aortic regurgitation without aortic dissection, non-dissecting thoracic or abdominal aortic aneurysm, mediastinal tumors, pericarditis, bone muscle pain.
Methods for diagnosing aortic dissections
If aortic dissection is suspected, it is important to quickly and accurately verify the diagnosis. Chest X-ray, while not a method of verifying the diagnosis, can nevertheless be the first to reveal signs suspicious of aortic dissection. X-ray examination data are not specific, but may provide grounds for other research methods. The main radiological signs indicating the possibility of RA are: I. Expansion of the aortic shadow (in 81-90% of cases, according to our data), better identified in the left oblique projection (sometimes local protrusion in the area of dissection, less often - expansion of the upper mediastinum). Expansion of the aortic shadow was detected in 50% of patients with type I dissection (- and in 10% - type III. There was unevenness of the contours of the descending aorta, deformation of its shadow. 2. Separation (separation) of the calcified intima in the area of protrusion from the adventitia by more than 1 cm (normally up to 0.5 cm) - a presumptive, but also not diagnostic sign. 3. Change in the shadow of the contours of the aorta or mediastinum when compared with the data of a previous study. 4. Deviation of the trachea or pleural effusion (usually left-sided). 5. Sharply decreased or absent pulsations of an abnormally wide aorta. Although most patients with RA have one or more radiographic findings, 12% of patients have an unchanged chest x-ray. Absence of x-ray changes does not exclude the diagnosis of aortic dissection. Standard 12-lead electrocardiography reveals signs nonspecific for RA left ventricular hypertrophy and associated changes (ST segment depression, negative T wave).In 1/3 of patients, the ECG remains normal!!! However, taking an ECG is important for two reasons: - the absence of changes on the ECG in a patient with severe pain in the chest is the reference differential diagnostic criterion for RA with MI; — the presence of signs of AMI on the ECG (usually lower localization), when compared with X-ray data, allows not only to assume that the patient has aortic dissection, but also indicates the involvement of the coronary arteries. Laboratory signs are not very indicative in the diagnosis of aortic dissection: a. anemia - with significant sequestration of blood in the false canal or rupture in the cavity; b. small (moderate) neutrophilic leukocytosis (up to 12-14 thousand/mm3); V. increased LDH and bilirubin (due to hemolysis of blood in the false channel); d. normal levels of CPK and transaminases; D. Occasionally, the development of disseminated intravascular coagulation syndrome is possible. According to objective and routine examination methods, the diagnosis of aortic dissection can be made in only 62% of patients. The rest at the onset of the disease have signs of myocardial ischemia, congestive circulatory failure, non-dissecting aneurysm of the thoracic or abdominal aorta, symptoms of aortic stenosis, pulmonary embolism, etc. Among these patients with initially undiagnosed aortic dissection, 2/3 of aortic dissections were diagnosed by other research methods used to resolve other clinical issues. In 1/3 the diagnosis was made only at autopsy. The main methods for diagnosing aortic dissections are currently considered to be methods that allow visualization of the aorta: - aortography - contrast-enhanced computed tomography (CT) - nuclear magnetic resonance (NMR) - transthoracic and transesophageal echocardiography. Each technique has its own advantages and disadvantages. The choice of method depends on opportunity and experience. Aortography has long been considered the standard and the only accurate, highly sensitive method for diagnosing aortic dissections. Direct signs of aortic dissection during aortography are: visualization of two lumens (true and false), intimal flap, and indirect signs are deformation of the aortic lumen, expansion and deformation of its wall, abnormal origin of vascular branches, the presence of aortic regurgitation. Aortography allows: 1. to determine the extent of dissection 2. to identify the involvement of aortic branches 3. to determine the location of the initial rupture and the exact location of the proximal fenestration 4. the presence or absence of distal fenestration 5. to assess the degree of consistency of the aortic valve and coronary arteries. However, the false lumen, most often detected in the descending aorta, thromboses in 10-15% of cases; the true lumen is narrowed. With transfemoral access, the catheter may not enter the true lumen of the aorta. It is possible to detect the presence of an intimal flap (i.e., a detached inner membrane between the true and false lumen) in 1/3 of patients. The disadvantage of aortography is the possibility of obtaining false-negative results, which happens with weak contrast of the false lumen (due to its possible thrombosis), equally uniform contrast of both channels, small and local dissection. The difficulties of using this method include the risk of an invasive procedure and the introduction of a contrast agent (its intolerance), the impossibility of performing aortography in unstable (non-transportable) patients. In addition, the introduction of alternative diagnostic techniques has shown that the sensitivity and specificity of aortography are 77-88% and 95%, respectively. Thus, the false tract is visualized in 87% of patients, the intimal flap in 70%, and the site of the initial intimal tear in only 50% of patients with aortic dissections. Echocardiography is an accessible and non-invasive method for diagnosing RA. According to the literature, transthoracic echocardiography can detect 80% of aortic dissections. Currently, a special role in the diagnosis of aortic dissection is given to transesophageal echocardiography (the sensitivity of the method is 95%, and the specificity is 75%), which is the method of choice in case of an unstable patient’s condition, because can be quickly performed at the patient’s bedside, in the operating room, immediately before surgery, and does not require cessation of monitoring and ongoing therapeutic measures. Echocardiography allows visualization of dilation of the aortic bulb, increased aortic wall thickness, aortic valve function, identification of the mobile flap in the aortic lumen, and also provides additional information about cardiac structures and function. If transesophageal echocardiography is not possible, computed tomography with contrast injection is the method of choice. On contrast-enhanced CT, aortic dissection is identified by the presence of two distinct lumens, apparently separated by an intimal flap, or by a different rate (degree) of contrast opacification. The method has a sensitivity of 83-94% and a specificity of 87-100%. The advantages of CT are: non-invasiveness, although IV contrast is required; availability; the ability to establish a diagnosis of aortic dissection in the case of false lumen thrombosis; the ability to determine the presence of pericardial effusion. The main disadvantages of CT are: relatively low sensitivity for diagnosing aortic dissections; inability to identify an intimal flap in 1/3 of cases; the rarity of identifying the location of the initial rupture; inability to detect the presence of aortic regurgitation and involvement of vascular branches. NMR is a non-invasive technique that does not require IV contrast, while providing high-quality images in several planes. NMR facilitates the recognition of RA, allows the identification of branch involvement, and also diagnoses aortic dissection in patients with pre-existing aortic diseases. The sensitivity and specificity of the method are about 98%, while the sensitivity is 88% for identifying the site of intimal rupture and aortic regurgitation, 98% for diagnosing the presence of thrombosis and 100% for detecting pericardial effusion. The unusually high accuracy makes NMR the modern “gold standard” in the diagnosis of RA, especially in stable patients and with chronic dissection. However, the method still has a number of disadvantages: NMR is contraindicated in patients with a pacemaker, in the presence of a certain type of vascular staples, and some old types of prosthetics with metal artificial valves; is not a widely available method. Some authors consider the unstable condition of the patient, requiring intravenous administration of antihypertensive drugs and blood pressure monitoring, to be a relative contraindication to NMR.
Treatment of aortic dissections
Treatment for aortic dissection is aimed at stopping the progression of the dissecting hematoma. Death is usually caused not by the intimal rupture itself, but by subsequent vascular complications or aortic rupture. Without treatment, aortic dissection has a high mortality rate. The main cause of death in the proximal type of dissection is cardiac tamponade, less often - occlusion of the main branches of the aorta, and in the distal type - bleeding into the left pleural cavity and renal failure. Mortality in the proximal type among those treated conservatively is approximately 4 times higher than among those operated on. All patients with aortic dissection should be hospitalized in an intensive care unit to stabilize hemodynamics, monitor blood pressure, heart rate and diuresis, and, if necessary, monitor central venous pressure or pulmonary artery wedge pressure, regardless of further treatment tactics. Intensive therapy for acute dissection is aimed at relieving pain and reducing blood pressure (systolic - up to 100-120 mm Hg), using various schemes. The pain should be relieved with IV morphine. To reduce cardiac output and reduce the rate of LV ejection, b-blockers are used in increasing doses until the heart rate decreases to 60-80 per minute. Propranolol (Obsidan) is used intravenously at an initial dose of 1 mg every 3-5 minutes. The maximum initial dose should not exceed 0.15 mg/kg. Maintenance therapy - every 4-6 hours in doses from 2 to 6 mg, depending on heart rate. You can also prescribe metoprolol at a dose of 5 mg IV every 5 minutes. (up to three times). Labetalol, as an α-blocker, is 2-7 times less active than phentolamine, and as a β-blocker, it is 5-18 times less active than propranolol. Blocks α- and b-adrenergic receptors in a ratio of 1:3. Blood pressure decreases, mainly due to a decrease in peripheral resistance, with virtually unchanged cardiac output. Intravenous administration is carried out either as a bolus - 100-125 mg, or as a slow drip - 50-200 mg / day. in 200 ml of saline or glucose. The drug is contraindicated in cases of AV conduction disorders, a tendency to bronchospasm, and in the first months of pregnancy. If there are contraindications to the use of b-blockers (bradycardia, AV block, bronchospasm), calcium channel antagonists are now increasingly used. Nifedipine sublingual can be used immediately while other drugs are prepared for administration. The disadvantage of nifedipine is its weak negative inotropic and chronotropic effects, and therefore diltiazem and verapamil can be used. If beta blockers are ineffective, sodium nitroprusside can be used at a dose of 0.5-10 mg/kg*min IV. For refractory hypertension, as a result of involvement of the renal arteries, the most effective is the use of ACE inhibitors (enalapril - 0.625 mg intravenously every 4-6 hours with a gradual increase in dose). With normal blood pressure, only b-blockers are used (and if they cannot be used, diltiazem or verapamil) to reduce the rate of LV ejection. In case of hypotension, one should think about the possibility of cardiac tamponade, aortic rupture, which, if possible, requires rapid restoration of blood volume. For refractory hypotension, it is preferable to use norepinephrine and mesaton. Dopamine is used to improve kidney function and only in small doses. When the patient's condition is stabilized, diagnostic studies are immediately carried out to verify the diagnosis. If the patient's condition is unstable, it is preferable to perform TEE, against the background of continuous monitoring and therapeutic measures. Further tactics are determined by the type of separation. Sudden deterioration in patients with aortic dissection is associated with tamponade or aortic rupture. As has been proven in a number of retrospective studies, pericardiocentesis during hemotamponade worsened the prognosis and patients died suddenly after 5-40 minutes. after the procedure, therefore, carrying out this procedure in urgent conditions is possible only in the operating room with direct surgical intervention. In extreme cases, with severe hypotension, careful aspiration of only enough pericardial fluid to produce an acceptable rise in blood pressure is possible.
Surgical treatment of aortic dissection
In all cases, patients should be consulted by a vascular surgeon. Surgery is the treatment of choice for acute proximal aortic dissections, which may lead to complications such as rupture, tamponade, acute aortic regurgitation, or neurological impairment. Surgical treatment is also indicated for chronic ascending dissection with severe aortic regurgitation and localized aneurysm. In chronic distal dissection, surgery is indicated for aneurysms larger than 6 cm in diameter. For distal dissection, conservative therapy is justified due to the lower risk of early death, older age of patients, and the presence of severe atherosclerosis or pulmonary heart disease, which increases the risk of surgical intervention. With this type of dissection, surgical treatment is indicated when a saccular aneurysm forms, when vital organs are involved, limb ischemia continues despite conservative therapy, dissection, or retrograde spread to the ascending aorta. Surgical treatment is indicated for all patients with Marfan syndrome. Conservative (medical) treatment is the treatment of choice for uncomplicated distal dissection, stable isolated aortic arch dissection, and stable uncomplicated chronic dissection (more than two weeks old). The risk of surgical intervention increases in the presence of concomitant diseases, especially pulmonary emphysema, violation of the integrity of the aneurysm, cardiac tamponade, shock, and involvement of vital organs. Postoperative mortality with rapid surgical treatment was significantly lower (3%) than with long-term preoperative preparation (20%). The goals of surgical treatment are: - resection of the most damaged segment of the aorta containing an intimal rupture; — removal of the intimal flap; — obliteration of the entrance to the false canal; — prosthetics of the excised area of the aorta; - restoration of the aortic valve (valvuloplasty). Possible complications of surgery for aortic dissection include: 1. Early bleeding, infections, pulmonary and renal failure, and sometimes spinal cord ischemia with paraplegia. 2. Progression of aortic regurgitation. 3. Formation of a local aneurysm. 4. Repeated delamination. With the introduction of new surgical methods, postoperative survival is 80% for proximal dissection and 90% for distal dissection. Such methods that have reduced mortality in operated patients with aortic dissection are: thromboexclusion in typical cases of dissection of the descending aorta, the use of endovascular methods (balloon dilatation of the renal arteries), the use of special glue to fill the false lumen. Further long-term treatment of all patients after discharge from the hospital includes maintaining systolic blood pressure at a level not higher than 130-140 mm Hg. Art., prescription of antihypertensive drugs with a negative inotropic effect (beta blockers, calcium antagonists), repeated thorough examination, control radiography, CT, MRI every three months during the first year, then every 6 months. Late complications include: aneurysm formation after surgical repair at the site of repair 1/3 of late deaths may be associated with rupture of the false lumen after successful surgery.
Clinical manifestations
Many variants of localization and extent of dissection, the possibility of occlusion of various branches of the aorta give such a variety of clinical manifestations that they make their systematization quite difficult. The most typical symptoms are:
• sharp pain, most intense at the moment of occurrence, more often - behind the sternum, in the heart area, less often - in the interscapular region, epigastrium, lower back;
• motor excitement;
• shortness of breath;
• pale or bluish skin;
• increased blood pressure (higher values are typical for a low location of the dissection);
• hypotension (often the result of cardiac tamponade and aortic valve insufficiency);
• loss of consciousness;
• arrhythmia;
• pulse asymmetry;
• transient disturbances of sensitivity and movements in the limbs;
• visual and speech disorders.
Systemic hypotension
Systemic hypotension due to Morgagni-Adams-Stokes attacks and other causes can sometimes lead to ischemia distal to the site of stenosis (narrowing of the arterial lumen). Cerebral infarction (ischemic stroke) develops only in conditions of long-term hypotension, such as during cardiac arrest. Cerebral infarctions (ischemic strokes) tend to be localized in remote (distal) segments of large intracerebral arteries, including in the distal zones of the blood supply of the middle, anterior and posterior cerebral arteries. This is what causes the development of cerebral infarctions (ischemic strokes) in the areas of adjacent blood supply to the middle and anterior or middle and posterior cerebral arteries. Proximal limb weakness and distal parietal deficits support this diagnosis.
Treatment
Aortic dissection requires prompt transfer of the patient to the vascular surgery department. Equipping with high-tech equipment and the qualifications of our specialists allow us to provide the necessary assistance at the proper level and in full compliance with modern standards.
An emergency operation is performed on a dissection affecting the ascending part and the arch. The duration of the disease is not taken into account in this case - the risk of complications is too high. The same tactics are also required by the pathology of the descending section, when the possibility of further detachment of the vascular wall is real. If there is no direct threat to life, the operation can be delayed.
Severe concomitant pathology forces patients to be treated conservatively. It should be noted that, nevertheless, the most effective method of treatment is surgical .
The essence of the operation is to eliminate the false passage and replace the affected area with a synthetic prosthesis, and, if necessary, restore the function of the aortic valve.
Binswanger's disease
Binswanger disease (chronic progressive subcortical encephalopathy) is a rare condition in which the subcortical white matter of the brain is infarcted. In Binswanger's disease, U-fibers remain intact. A computed tomography (CT) scan of the brain reveals periventricular (around the ventricles of the brain) areas of low x-ray absorption. In small arteries of the deep white matter, as happens with arterial hypertension, lipohyalinosis invariably develops. In Binswanger's disease, infarctions may be observed in the deep white and gray matter of the brain, which belongs to the zone of adjacent blood supply to the penetrating arteries of the circle of Willis and the cerebral cortex. The pathophysiological essence of the disease and even the underlying pathological changes remain unclear. This disease is one of the causes of abulia and disability in older people.
Diagnostics
Correct diagnosis will make it possible to accurately determine the type and location of dissecting aortic aneurysm, which is of decisive importance for the choice of further tactics.
The acute form, due to its pronounced clinical manifestations, is determined quite easily, while the chronic form is often disguised as other diseases. This requires a careful differential diagnosis.
A physical examination reveals the following signs:
- cyanosis or pale skin;
- pulse difference in peripheral arteries;
- high blood pressure, a significant difference in the arms and legs, in some cases it is not determined;
- percussion – expansion of the boundaries of cardiac dullness.
To confirm, the following diagnostic methods must be used:
electrocardiography (ECG);- chest x-ray;
- echocardiography – this technique is the gold standard;
- Ultrasound of the abdominal organs;
- CT or MRI;
- contrast angiography.
Prognosis and prevention
Unfortunately, abdominal aortic aneurysm is one of the most insidious and unpredictable vascular pathologies, in which the probability of death exceeds 50%. Prevention and timely detection of an aneurysm are essential for a positive outcome. Quitting nicotine addiction, as well as monitoring blood pressure and taking timely measures to normalize it, helps reduce the risk of developing an aneurysm.
Technological progress is helping to reduce the number of diagnostic errors: modern research methods make it possible to identify pathology even in the absence of symptoms. Therefore, people who are at risk - smokers, hypertensive patients, elderly people, as well as those who have a high probability of developing a congenital pathology - should consult a doctor more often for a diagnostic examination. Often, patients are unaware of the development of an aneurysm until it ruptures, but then medical care may not be provided in a timely manner.
Be sure to consult a cardiac surgeon about being examined for the presence of an abdominal aortic aneurysm. Timely detection of the disease can save your life and in any case preserve your health and performance.
