The aortic dissection is the routing of blood through a crack in the aortic wall and into the intima of the aorta with a pitch of the intima and media and creating a false lumen. The Intimariss may be a primary event or occur secondary to a hemorrhage in the media back. The dissection can occur anywhere along the aorta, and proximal and distal to expand into other arteries. Decisively contributes to hypertension do so. Symptoms are a sudden onset of chest and back pain caused by the crack, the dissection can lead to aortic insufficiency (AI) and affect blood flow to the Seitenastarterien. The diagnosis is made by imaging methods (eg. As transesophageal echocardiography, CT angiography, MRI, Kontrastaortographie). The treatment always includes an aggressive blood pressure control and serial imaging for monitoring the progress of the dissection; a surgical repair of the aorta and the placement of a synthetic grafts are required for the dissection of the ascending aorta, and for certain dissection A. descendens. Endovascular stent grafts are used in certain patients, especially if the dissection relates to the descending, thoracic aorta. One fifth of patients die before they reach the hospital, up to one third of patients die of operative or postoperative complications.
Evidence of dissection are found in 1-3% of all autopsies. Dark-skinned people, men, the elderly and people with hypertension are at particularly high risk. The highest incidence is in the age from 50 to 65 years or in patients with congenital connective tissue diseases (eg. As Marfan syndrome, Ehlers-Danlos syndrome) aged 20 to 40 years.
The aortic dissection is the routing of blood through a crack in the aortic wall and into the intima of the aorta with a pitch of the intima and media and creating a false lumen. The Intimariss may be a primary event or occur secondary to a hemorrhage in the media back. The dissection can occur anywhere along the aorta, and proximal and distal to expand into other arteries. Decisively contributes to hypertension do so. Symptoms are a sudden onset of chest and back pain caused by the crack, the dissection can lead to aortic insufficiency (AI) and affect blood flow to the Seitenastarterien. The diagnosis is made by imaging methods (eg. As transesophageal echocardiography, CT angiography, MRI, Kontrastaortographie). The treatment always includes an aggressive blood pressure control and serial imaging for monitoring the progress of the dissection; a surgical repair of the aorta and the placement of a synthetic grafts are required for the dissection of the ascending aorta, and for certain dissection A. descendens. Endovascular stent grafts are used in certain patients, especially if the dissection relates to the descending, thoracic aorta. One fifth of patients die before they reach the hospital, up to one third of patients die of operative or postoperative complications. Evidence of dissection are found in 1-3% of all autopsies. Dark-skinned people, men, the elderly and people with hypertension are at particularly high risk. The highest incidence is in the age from 50 to 65 years or in patients with congenital connective tissue diseases (eg. As Marfan syndrome, Ehlers-Danlos syndrome) aged 20 to 40 years. Classification The aortic dissections are classified anatomically. The DeBakey classification system is used most often. (Editor’s note: For the German-speaking countries the Stanford classification is more common!) Type I (50% of dissections): These dissections begin in the ascending aorta and extend at least to the aortic arch and sometimes beyond. Type II (35%): These dissections begin in the ascending aorta and are limited only to this. Type III (15%): This Disektionen begin in the descending thoracic aorta just behind the origin of the left subclavian artery and extend distally or, less commonly, the proximal end. The Stanford system is easier. Type A: This dissection include the ascending aorta. Type B: These dissections are limited to the descending thoracic aorta. Although the dissection can be anywhere spring along the aorta, it most often occurs in the proximal ascending aorta (within the first 5 cm distal to the aortic valve) or the descending thoracic aorta (immediately after the origin of the left subclavian artery) on. Rarely dissection is confined to individual arteries (z. B. coronary arteries, carotid arteries), typically occurs in pregnant women or post partum. Etiology The aortic dissection always occurs in the context of a pre-existing degeneration of the tunica media of the aorta. Causes are connective tissue diseases and injuries (see Table: Factors that contribute to aortic dissection). Factors that contribute to aortic dissection category Examples atherosclerotic risk factors cocaine dyslipidemia hypertension Smoking acquired connective tissue disease Behcet’s disease giant cell arteritis Takayasu’s arteritis congenital or hereditary connective tissue diseases bicuspid aortic coarctation Cystic Mediannekrose Ehlers-Danlos syndrome Marfan syndrome Turner syndrome Familial Thoracic aortic aneurysm Iatrogenic cardiac catheterization heart valve surgery injury Dezelerationstrauma atherosclerotic risk factors, especially hypertension, the patients have more than two-thirds of an impact. After Intimaruptur that in some patients a primary and in other patients is a secondary event after Mediaeinblutung, blood flows into the media and creates a false channel that extends distally or less frequently and proximally along the artery. Pathophysiology dissections can communicate with the true lumen of the aorta via a Intimaruptur at distal site and so maintain the systemic blood flow. But serious consequences are common: restriction of blood supply to the arteries that branch off from the aorta (including coronary arteries) aortic heart valve dilation and regurgitation heart failure Fatal rupture of the aorta through the adventitia in the pericardium, the right atrium or the left pleural space Acute dissections and those that present themselves within <2 weeks, these complications cause most likely. The risk increases beyond on ? 2 weeks if Advice for thrombosis of the false lumen and loss of communication between true and false lumen occur. Variants of the aortic dissection include the separation of the intima and media by an intramural hematoma without unique Intimariss or lobes, a Intimariss and a protrusion without hematoma or false lumen and a dissection or a hematoma, which is caused by the rupture of atherosclerotic plaque. This Varienten be regarded as precursors of the classic aortic dissection. Typically, symptoms and discomfort arises suddenly a violent, unbearable precordial or localized between the shoulder blades pain, often described as "tearing" or "ripping". The pain often wanders away from the original site when the dissection extends along the aorta. Up to 20% of patients presenting with syncope due to severe pain due to activation of aortic baroreceptors, due to obstruction of the extracranial cerebral vessels or due to cardiac tamponade. Occasionally, patients presenting with symptoms of stroke, myocardial infarction, intestinal infarction, with paraparesis or paraplegia due to an interruption of the blood supply to the spinal cord, or an ischemic leg due to an acute distal arterial occlusion. Approximately 20% of patients have partial or complete loss of the larger arterial pulses, as amended and may decrease. The blood pressures of the limbs can differ, sometimes by> 30 mmHg; This finding suggests a poor prognosis. A Aortenklappeninsuffizienzgeräusch is heard in 50% of patients with a proximal dissection. Peripheral signs of aortic insufficiency may be present. Rarely results in a heart failure as a result of severe acute aortic regurgitation. The leakage of blood and inflammatory serous fluid in the left pleural can lead to signs of pleural effusion; the closure of a limb artery can cause signs of peripheral ischemia or neuropathy. A closure of the renal artery can cause oliguria or anuria. The cardiac tamponade may result in the paradoxical pulse and expand the jugular veins. Tips and risks Only about 20% of patients with aortic dissection have pulse deficits. Diagnosis Transesophageal echocardiography (TEE), CT angiography (CTA) or magnetic resonance angiography (MRA) A aortic dissection must be considered in any patient with chest pain, thoracic back pain, unexplained syncope or abdominal pain, stroke and acute onset of cardiac insufficiency, v , a. when the pulses or the blood pressure of the limbs are different. These patients require chest x-ray images; at 60 to 90% of the mediastinum is extended, usually with a localized bulge that marks the origin of the dissection. Often a left-sided pleural effusion. In patients presenting with acute chest pain, ECG changes of acute inferior MI and a previously documented sound of aortic insufficiency (AI), a type I aortic dissection should be in the right coronary artery (causing inferior MI) and the aortic valve (caused AI) are considered. When the thorax X-ray image indicates a dissection immediately after the patient a TEE, CTA or MRA is stabilized performed. The findings of a Intimalappens and a double lumen confirm the dissection. The multiplanar TEE has a sensitivity of 97-99%, together with an M-mode it is virtually 100% specific. The process can be performed at the bedside in <20 minutes and does not require contrast agents. If the TEE is not available, a CTA is recommended; it has a positive predictive value of 100% and a negative predictive value of 86%. An MRA has nearly 100% sensitivity and specificity for aortic dissection. But it is time consuming and not very suitable in emergencies. You will probably use the most sense in stable patients with subacute or chronic chest pain when dissection is suspected. The contrast angiography is an option if a surgical procedure is considered. In addition to identifying the origin and extent of the dissection, to assess the severity of aortic regurgitation and the extent to which the larger Aortenseitenäste are concerned, the aortography helps determine whether simultaneous coronary bypass surgery is required. Echocardiography should be performed to detect an aortic regurgitation and thus to decide whether the aortic valve should be accompanying reconstructed or replaced. An ECG is performed almost anywhere. The findings are, however, between normal and high pathologically (in acute coronary occlusion or aortic regurgitation), so that this investigation is not helpful diagnostically. Studies of soluble Elastinkomponenten and smooth muscle Myosinschwerekettenproteine ??be made; they appear promising, but are not routinely available. Serum CK-MB and troponin may help distinguish aortic dissection from myocardial infarction, except if the dissection causes the myocardial infarction. Routine laboratory analysis can detect a slight leukocytosis and anemia when blood from the aorta has emerged. An increased LDH can be a non-specific signs of involvement of the trunk of the celiac artery or mesenteric artery. A heart surgeon should be involved early on during diagnostic tests. Forecast die Approximately 20% of patients with aortic dissection before they reach the hospital. Without treatment, the mortality rate is 1- 3% / h in the first 24 h, at 30% in the 1st week, 80% in the 2nd week and at 90% after one year. The hospital mortality for patients treated is 30% for proximal dissection and at 10% for distal. In treated patients that survive the acute phase, the survival rate is 60% after 5 years and 40% after 10 years. About a third of late deaths occurs due to complications of dissection, the rest due to other diseases. Treating ?-blockers and other medications of blood pressure setting Surgical procedures patients who die of the aortic dissection immediately should an intensive care unit with intraarterial (vascular access: Procedure) A blood pressure monitor to be laid; a bladder catheter is applied to the monitoring of urine. A blood-typing and cross blood test should be carried out for four to six canned when a surgical care is likely. Hemodynamically unstable patients should be intubated. It will be immediately recognized drugs to lower blood pressure, arterial shear stress, for ventricular contractility and for the pain to hold 110 mmHg or as deep as possible blood pressure at ? as long as it is compatible with an adequate cerebral, coronary and renal blood flow is. A ?-blocker commonly used first. The options are metoprolol 5 mg iv Up to four doses with an interval of 15 minutes or esmolol 50 to 200 ug / kg / min in a constant i.v. Infusion or labetalol (an ?- and ?-adrenergic blockers), 1-2 mg / min in a constant i.v. Infusion was given as an initial bolus of 5-20 mg with additional doses of 20-40 mg every 10-20 min to the blood pressure control, or until a total dose of 300 mg or followed by an additional 20-40 mg every 4-8 hours. Alternatives for ?-blockers are calcium antagonists (eg., Verapamil 0.05-0.1 mg / kg iv bolus or diltiazem 0.25 mg / kg [up to 25 mg] iv bolus or 5-10 mg / h as a continuous iv infusion). If the systolic blood pressure, despite the use of ?-blockers remains> 110 mmHg, nitroprusside may be in a constant i.v. Infusion of 0.2-0.3 ug / kg / min and titrated as needed up (often 200-300 g / min) to control the blood pressure. Nitroprusside should not be given without ?-blockers or calcium channel blockers as an increase Reflexsympathikusaktivierung in response to the vasodilation ventricular inotropic and aortic shear stress and can degrade the dissection. to regulate tips and risks In order blood pressure in aortic dissection, no vasodilator (eg. as nitroprusside) should be used without a ?-blockers or calcium channel blockers, because the vasodilator may cause a knee-jerk sympathetic activation, which increases the shearing of the aorta. The attempt of a sole drug therapy is justified in uncomplicated, stable dissection that is limited to the descending aorta (type B), and for the stable, isolated dissection of the aortic arch. The surgical treatment is always indicated in fact, when the dissection affects the proximal aorta. The surgical procedure is also indicated in a limb ischemia or visceral ischemia, uncontrollable hypertension, a permanent enlargement of the aorta, an increasing expansion of the dissection and instructions for aortic rupture, regardless of the type of dissection. The surgical care may also represent the best care of acute distal dissection in patients with Marfan syndrome. The goal of surgery is to close the entrance to the false lumen and restore the aorta with a synthetic graft. When present, a significant aortic valve insufficiency must be treated by a Aortenrekonstruktion or valve replacement. The surgical results are best in early, aggressive intervention; the mortality rate is 7-36%. Predictors of poor results are hypotension, renal failure, age> 70 years, sudden onset of chest pain, pulse deficit and ST-segment elevation in the ECG. Stent-grafts, which seal the entrance to the false lumen and improve the openness of the true lumen, the Ballonfenestrierung (is in an opening in the Dissektionslappen that separates true and false lumen introduced), or both can be less invasive alternatives for patients with type B dissection who develop peripheral ischemic complications be. All patients, incl. Of patients treated with surgical or endovascular methods, for antihypertensive medication long-term therapy, usually with ?-blockers, calcium channel blockers and ACE inhibitors. Almost all combinations of antihypertensive drugs are acceptable. Exceptions are the antihypertensive agents which act mainly vasodilatory (z. B. hydralazine, minoxidil), and ?-blockers, which have an intrinsic sympathomimetic activity (eg. As acebutolol, pindolol). The Avoid strenuous physical activity is often recommended. Before discharge, an MRI can be performed and after six months and one year and then repeated every one to two years. The most important late complications are redissection, the formation of localized aneurysms in the aorta wall weak and progressive aortic regurgitation. These complications may require surgical or endovascular repair. Summary The aortic dissection can be anywhere along the aorta spring, but it is most common in the proximal ascending aorta (within the first 5 cm distal to the aortic valve) or the descending thoracic aorta (immediately after the origin of the left subclavian artery). The dissection requires a pre-existing degeneration of the medial aorta (eg., Caused by connective tissue disease, injury), but hypertension is also often involved. Patients have intolerable, tearing precordial or interscapular pain usually. Other manifestations depend on whether the aortic root and / or aortic branches are affected, and the presence and position of any rupture; Heart failure, Organischämie and hemorrhagic shock can occur. The diagnosis is made by means of TEA, CTA or MRA. ?-blockers and other drugs as required to control blood pressure should be administered immediately. A sole drug therapy in uncomplicated, stable dissection that is limited to the descending aorta or the aortic arch (type B), appropriate. In other cases, surgery is necessary.