Coarctation of the aorta accounts for 4-15% of all congenital heart defects. The origin of this defect is associated with an abnormality in the transformation of the aortic isthmus during the formation of extrauterine circulation. The disease is 2–2.5 times more common in males. Bonnet proposed to distinguish between two types of coarctation of the aorta: 1) “infantile”, in which the aorta is narrowed over a large distance above the place of discharge of the OAP; 2) “adult”, in which the narrowing is observed only on a short segment of the aorta (segment), usually in the area of transition of the arch to the descending part below the site of the OAA (isthmus of the aorta). For practical purposes, it is convenient to consider 4 options for coarctation of the aorta: I) isolated, 2) coarctation of the aorta in combination with OAP; 3) coarctation of the aorta in combination with DMS; 4) coarctation of the aorta in combination with other congenital heart defects.
Circulatory disorder is manifested by severe hypertension in the arterial vascular pool above coarctation and hypoperfusion below it. In this case, hemodynamic compensation is achieved due to the development of collateral arteries connecting the upper and lower parts of the body (intercostal, internal mammary arteries, internal mammary arteries). Decompensation is manifested by malignant hypertension, deep sclerotic changes in the walls of the arteries. HELL sometimes reaches 300 mm Hg . (40 kPa). The consequence of this are cerebrovascular disorders up to the development of hemorrhagic stroke, heart and kidney failure. The expansion of the intercostal arteries leads to a compressed – NIJ roots of the spinal cord, severe spinal disorders (paralysis, disruption of the pelvic organs). In the origin of arterial hypertension, in addition to the mechanical cause, a significant role is given to renal vasopressor , a weed factor that is a direct consequence of renal ischemia.
Depending on the type of defect, various hemodynamic disorders occur. With the “adult” type of coarctation with a closed arterial duct, systolic overload of the left ventricle comes to the fore. In the “infantile” type, when there is OAP, pulmonary hypertension develops rapidly with an outcome in cyanosis of the lower half of the body. The combination of defect with defects of the septa significantly accelerates the onset of pulmonary hypertension.
In most cases, with this defect, imbalance is detected due to the pronounced development of the muscles of the shoulder girdle in comparison with the relative underdevelopment of the muscular system of the lower extremities. Moreover, blood pressure in the upper extremities is significantly increased. The pulse on the arteries of the thigh is sharply weakened or absent. The pulsation of the abdominal aorta is also not determined. In some cases, it is possible to detect the pulsation of the dilated intercostal arteries during tissue capture in the subscapular region. When ascultation is determined: a pronounced accent of II tone above the aorta, systolic murmur under the right clavicle, in the interscapular space on the left and on the vessels of the neck. The rest of the clinical picture in adult patients repeats all the signs of defects stenosing the outlet arterial tract of the left ventricle (aortic stenosis) with its pronounced systolic overload. In general, the physical picture is changeable and meager. That is why this anomaly requires special attention of doctors, since it is associated with frequent diagnostic errors.
Under normal conditions, blood pressure in the lower extremities is 29-30 mm Hg higher . (2.7-4 kPa) than on the top. When comparing blood pressure levels under coarctation of the aorta, the pressure on the lower extremities (the auscultation point in the popliteal fossa with the location of the cuff on the thigh) is not determined or significantly reduced. Coarctation should be considered pronounced if the pressure gradient between the upper and lower extremities reaches 40 mm Hg . (5.3 kPa). Depending on the level of blood pressure, 3 stages of the defect are distinguished: I – moderate (blood pressure below 150 mmHg (20 kPa); II – moderate severity (blood pressure – 150-200 mmHg (20-28.7 kPa ); III – severe (blood pressure greater than 200 mmHg (26.6 kPa). X-ray and ECG data for this anomaly are characteristic of hypertension and are signs of left ventricular hypertrophy. Dopplerography and chest tomography are of great help in the diagnosis in the sagittal plane.With a typical isolated form, the anomalies of the listed means are sufficient to establish final diagnoza.V doubtful cases should resort to aortography . Thus aorta contrasted through the arterial branch of the shoulder belt with a mandatory recording layer the pressure gradient in the coarctation . When concomitant congenital heart diseases shows angiocardiography and sensing cardiac cavities.
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The most common causes of non-traumatic aneurysms are atherosclerosis and syphilis. Traumatic aneurysms, or false, are formed after gunshot and stab wounds, less often – due to a blunt injury. Their development is possible in the presence of a narrow wound channel, a small area of damage to soft tissues, covering the wound opening with skin or tissues. Under these conditions, blood poured from the damaged vessel accumulates in the surrounding tissues, exfoliating them, and a periarterial pulsating hematoma occurs . The clots that form in it are pushed to the periphery by a stream of blood, condense, organize, as a result of which a connective tissue capsule is formed and a pulsating hematoma turns into a false aneurysm . Pathological anatomy. Three types of traumatic aneurysms are distinguished: arterial, arteriovenous and combined . An arterial aneurysm has an aneurysmal sac that communicates with the lumen of the artery. Arteriovenous aneurysm is the result of simultaneous damage artery and vein, which leads to the formation or arteriovenous – th fistula or aneurysms intermediate. With combined aneurysms, a combination of these types of aneurysms is observed. With the prolonged existence of an arteriovenous aneurysm, the wall of the leading artery changes significantly , which is manifested by its thinning, a change in the internal elastic membrane, resulting in an increase in the diameter of the artery. On the contrary, in the wall of the vein extending from the aneurysm, hypertrophy of the muscle membrane and the development of the internal elastic membrane are noted. The diameter of the vein also increases.
Arteriovenous and combined aneurysms cause severe hemodynamic disorders. In this case, not only peripheral blood circulation is disturbed, but also central hemodynamics. A pathological discharge of arterial blood into the venous system leads to difficulty in the outflow of venous blood from the affected limb, as well as to an increase in the volume of blood flowing to the right atrium. Due to venous stasis, superficial veins expand, swelling and trophic changes in the distal extremities occur. Working myocardial hypertrophy develops, which is then replaced by myogenic dilatation with cardiac decompensation.
The main complaint of patients is the presence of a pulsating formation in one or another segment of the limb. When viewed at the site of an arterial aneurysm, a swelling is visible, often pulsating. On palpation, it has a densely elastic consistency, is clearly delimited, round or oval, pulsates synchronously with the contractions of the heart. With auscultation over the area of the aneurysm, systolic murmur is determined, which disappears when the leading artery is compressed. Ripple to the periphery from the aneurysm is often weakened. Hand applied to the site of the aneurysm, the jitter can be felt or purling (symptom of feline purring) .Patognomonichnym symptomatic arteriovenous aneurysm is a slowing of heart rate for 15-30 min in 1, combined with an increase in blood pressure in the artery leading cross-clamping (Dobrovolskaya symptom). The slowdown of the pulse is due to an improvement in cardiac activity due to a decrease in blood flow to the right atrium.
Complications of the aneurysm are rupture of the aneurysmal sac, accompanied by profuse, life-threatening bleeding, thromboembolism and thrombotic masses contained in the aneurysm. With a traumatic aneurysm, an outbreak of a dormant infection, the development of soft tissue phlegmon are possible. A number of patients develop severe trophic disorders and cardiac disturbances, depriving them of their ability to work.
Diagnosis is not difficult when there is a pulsating swelling and vascular noise. To clarify the true shape and size of the aneurysm, localization, the state of the distal and proximal arterial bed and the degree of development of collateral blood flow, arteriography is necessary .