Acute aortic dissection . The incidence of acute aortic syndrome is approximately 30 cases per million inhabitants per year, of which 80% are dissections of the aorta. Mortality from this cause exceeds 60% in the first week after diagnosis if adequate treatment is not started.
From its initial description by Morgagni in 1761, its correct management continues to represent a challenge.
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- 1 Definition
- 2 predisposing factors
- 3 Classification
- 4 Clinical presentation
- 5 Physical exam
- 6 Complications
- 7 Diagnostic methods
- 8 Sources
- 9 External links
Aortic dissection (DA) is characterized by the creation of a false lumen in the middle layer of the aortic wall. Typically it begins with the formation of a tear in the intima of the aorta, which exposes the underlying middle layer to blood flow, penetrates by dissecting it, and spreads in a false lumen.
- Systemic arterial hypertension.
- Congenital abnormalities of the aortic valve.
- Hereditary connective tissue disorders.
- Turner syndrome
- Noonan syndrome.
- Giant cell aortitis.
- The systemic lupus erythematosus .
- The polyarteritis nodosa .
- Polycystic kidney disease.
- Cocaine ingestion
Most classifications are based on the fundamental fact that they originate from one of the following locations: the ascending aorta, very close to the aortic valve plane; and the descending aorta, just after the origin of the left subclavian artery.
The most commonly used classifications are:
- Type I: DAo originates from the ascending aorta and extends to the aortic arch and even the most distal aorta.
- Type II: DAo originates and is confined only to the ascending aorta.
- Type III: DAo originates from the descending aorta and extends to the distal aorta. Rarely can it spread retrograde to the aortic arch and even to the ascending aorta.
- Type A: DAo involves the ascending aorta regardless of the site of origin.
- Type B: DAo does not involve the ascending aorta.
Proximal descriptive classification
includes DeBakey I and II or Stanford type A. Distal: includes DeBakey type III or Stanford type B.
- The most frequent symptom is sudden-onset, tearing, throbbing-type pain that follows the direction of dissection. The location of the pain depends on the portion of the aorta that is involved.
- In type A dissections, the pain is usually located on the front of the chest (85%), and / or on the back (46%). Abdominal pain (22%), syncope (13%) and stroke (6%) may also be forms of presentation in this type of dissection .
- The dissection affecting the descending aorta (type B) has a clinical presentation similar to that of type A dissection, although sudden onset pain is located in the back in 64% and in the abdomen in 43% of the cases. Strokes and syncope are less frequent.
- Patients with uncomplicated type B dissection have a 30-day mortality of 10%. Conversely, those who develop leg ischemia, kidney failure , visceral ischemia, or contained rupture frequently require urgent aortic repair and mortality is 30%.
There is a group of less common symptoms in the presentation of aortic dissection, with or without associated chest pain, and these are:
- Heart failure due to severe aortic regurgitation in proximal dissections.
- Syncope without focal neurological signs due to rupture of the proximal aortic dissection in the pericardial cavity with tamponade or, less frequently, due to rupture of descending aortic dissection in the left pleural space.
- Cerebrovascular accident, peripheral neuropathy or paraplegia.
- Cardiac arrest or sudden death .
The signs reflect the location of the aortic dissection and the degree of cardiovascular damage. Arterial hypertension appears in 80-90% of distal dissections, being less frequent in proximal ones. The hypotension true is more prevalent in proximal dissections, by cardiac tamponade, although distal aortic dissections also produce hypotension by intrapleural or intraperitoneal rupture. When the dissection occludes the brachiocephalic vessels, we can inaccurately record arterial hypotension (pseudohypootension). The physical signs when the proximal aorta is affected are:
- Pulse deficiency due to occlusion of the vascular lumen by the flap or due to extension of the dissection itself in the artery and compromise of the true lumen by the false channel.
- Musical quality murmur on the right sternal border with intensity dependent on blood pressure caused by aortic regurgitation in proximal dissection (50-60%).
- Neurological manifestations (6-19%): stroke can occur in 3-6% due to direct involvement of the common carotid artery, less commonly coma, paraplegia, and paraparesis.
- Acute myocardial infarction (1-2% of the inferior aspect, due to involvement of the coronary ostium by the flap.
- Renal infarction.
- Ischemia and mesenteric infarction (3-5%).
- Superior vena cava syndrome, sternoclavicular pulsation, pulsatile cervical mass and Horner syndrome.
- Other manifestations: hemothorax, hemoptysis and hematemesis due to ruptures in the pleural space, bronchi or esophagus.
- Limb ischemia.
- Aortic rupture.
- Cardiogenic shock.
- Cardiac tamponade.
- Renal ischemia.
- Visceral ischemia.
It is necessary to have a high index of suspicion because DAo has various forms of presentation. The clinical factors most associated with DAo are: the previous history of high blood pressure, sudden onset and irradiation of chest pain. These clinical factors, together with a normal electrocardiogram, elevated blood pressure, the absence of some of the arterial pulses, the murmur of aortic insufficiency and the widening of the mediastinum evidenced in the chest X-ray, force the clinician to rule out DAo.
It is normal in most cases. There may be signs of left ventricular hypertrophy. It is essential to differentiate this entity from acute myocardial infarction. There may be signs of AMI if the flap occludes the ostium of the coronary artery.
- Chest x-ray
Useful in the differential diagnosis of other entities with similar symptoms.
The unequivocal signs of aortic dissection are less than 30%. Radiographic signs are: aortic button effacement or widening, pleural effusion (usually left), deviation of the trachea, distance greater than 6 mm between intimal calcification and the external contour of the aortic wall, mediastinal widening, or ascending aorta. descending and paraspinal line.
They are very nonspecific. There may be anemia from blood sequestration in the false lumen or from extravasation of blood from the aorta. Creatinine can rise when kidney flow is compromised. Lactodesidrogenase increased by hemolysis within the false lumen.
Transthoracic echocardiography has a sensitivity of 50 to 80% and a specificity of between 70 to 90%. The study should include not only the usual views of the heart, but also the suprasternal, supraclavicular, subcostal views and, if there is a pleural effusion, the subscapular view. Despite this, visualization of the descending aorta is sometimes very difficult.
For this reason, transesophageal echocardiography (TEE) has changed the diagnostic attitude in DAo, due to the closeness of the aorta and the esophagus. The sensitivity and specificity of transesophageal echocardiography is greater than 95%.
- Computed axial tomography
The results obtained by this technique are superimposable to those of the TEE.
The sensitivity and specificity are close to 100%. It has some limitations such as: the use of nephrotoxic contrast, the limited capacity to detect the entrance door and the lack of hemodynamic information regarding the entire state of the aortic valve.
- Nuclear magnetic resonance
It is considered the most complete technique for the diagnosis of DAo, since it allows a detailed evaluation of the aortic morphology and the structures that surround it.
Aortography has been considered for many years the technique of choice in the diagnosis of aortic dissection. This test has a sensitivity of 88%, a specificity of 94%, and a diagnostic accuracy of 98%. The development and refinement of non-invasive techniques has changed this concept.
Currently, transesophageal echocardiography, computed tomography, and magnetic resonance imaging are indispensable allies in the study of the patient with acute aortic syndrome. These non-invasive techniques make it possible to know with certainty the aortic disease of these patients.