Aortic dissection - A case in images

Aortic dissection is the most common acute emergency condition of the aorta. Early diagnosis and treatment are essential for improving the prognosis. It is recommended that the scanning field include the entire aorta and pelvic vessels to help determine the type and extent of dissection. We presented a case in imagen of acute aortic dissection and showed the most representative TC findings.


Introduction
Acute aortic dissection is caused by the rupture of the intima that causes blood to enter the aortic wall separating the middle layers, thus forming a defined false duct between the outer middle layer and the adventitia outside and the intimate complex, medial or "flap" inside. The new formed channel shows flow in its intervention that returns distally to the light of the vessel through the re-entry hole [1].
Aortic dissection is included in the Acute Aortic Syndrome (AAS), along with intramuralhematoma and penetrating ulcer [1]. These are characterized by: -Intramural hematoma (IH) is a hemorrhage that affects the media layer of the aortic wall. This generates a tear of the vasa vasorum, which is also known as aortic dissection without intimal flap formation [2].
-Aortic dissection (AD) is a tear in the inner layer of aortic wall generating an intimal flap formation, which allows blood to enter into the aortic wall, creating a new passage for blood called false lumen differentiated from the true lumen (also called aortic channel) by a flap [3].
-Penetrating ulcer (PU) refers to an ulcerating atherosclerotic lesion that penetrates the elastic lamina and is associated with hematoma formation within the media of the aortic wall [4].
Two classifications are most commonly used for aortic dissection. The DeBakey system is classified into three types (types I, II, and III) according to the location of the first entry of dissection. Type I has the first entry in the ascending aorta and propagates distally to the descending aorta. Type II has the first entry in the ascending aorta and does not propagate to the aortic arch. Type III has the first entry in the descending aorta and propagates distally above (type IIIa) or below (type IIIb) the diaphragm. The Stanford system is classified into two types (types A and B) based on the involvement of the ascending aorta. Type A includes dissection in the ascending aorta regardless of the site of first entry. Type B does not include dissection in the ascending aorta [5].
It is estimated that in Spain the AAS shows an incidence rate of 20-40 cases per million habitant per year and it is more prevalent in males (80%) that it is in females. Of the AAS subtypes, the most prevalent are AD (80%), followed by IH (15%) and PU (5%). With regards to the location of the first entry of dissection, 68% affects the ascending aorta (type A) and 32% to the descending aorta (type B) [6].
The mortality rate is high in type A and requires urgent surgery. Type B requires antihypertensive treatment [1].
Aortic dissection debuts with chest or abdominal pain that radiates to the back, simulating other pathologies. Up to 20% present with a syncopal picture due to cardiac tamponade or obstruction of supraaortic trunks. Abdominal pain appears by compromise of the abdominal branches.

Imaging findings
According to RESA files [6], Computed Tomography (CT) scan is the most frequently used imaging technique to diagnose patients with AD suspicion. Its multi-slice CT capacity of imaging reconstruction allows for almost 90% sentitivity and 85% specificity [6].

Non-enhanced phase
CT does not provide dynamic information. For instance, it does not provide information on neither the systolic function of the left ventricle or the aortic valve behaviour, which are both key to distinguish between an Intramural Hematoma and an aortic dissection diagnosis. To be able to differentiate between Intramural Hematoma and Aortic Dissection in the presence of active bleeding it would be advisable to obtain images without contrast, because they are clinically indistinguishable.
As we see in figures 1 and 2 no intramural hematoma signs are detectable. Instead we observe a pericardial blood vessel previously shown in the emergency echocardiogram that lead us to request the CT scan. We can also observe the aortic flap, indicative of a dissection.

Arterial phase
The CT Scan sequences are taken with intravenous contrast. The aim of this is to assess the morphology of the aortic channel, the true lumen and be able to observe the new passages of the blood to the false lumen.
The protocol used includes the whole aorta and its main branches, from subclavian artery to the beginning of femoral artery.
In Figure 3, we can clearly observe the aortic flap and how it divides the trajectory of the blood in the aortic channel (red arrow). Figure 4, shows additional information. This includes; (i) a hypoenhanced aortic flap present in the descending aorta (green arrow); (ii) the dissection of the entire intima allows us to observe a circumferential intimal flap and a narrow true lumen in a filiform shape (green arrow) [7]; (iii) the red arrow also shows a typical cobweb sign distribution. The appearance of this distribution is a clear sign of false lumen [8]; (iv) hiperenhanced pulmonary artery (blue arrow).
Following the aortal channel we reach the abdominal aorta: Figures 4 and 5 show a still aortic flap abdominal level (red arrow). This is produced by the dissection, and even though we injected intravenous contrast we see the aortic channel hypo-enhanced. However, we observe both hepatic veins and renal veins as hiperenhanced (green arrow), when, in theory, the venous flow comes after the arterial flow, in a late phase [9].
Additionally, it is evident that the contrast tends to accumulate in the body's dorsal section (blue arrow). Figures 5 and 6 show a liver with no contrast in the ventral area. Instead, the contrast tends to accumulate in the dorsal area. This erratic distribution of the intravenous contrast is also compatible with the asystolic blood pumping idea mentioned earlier.
When cardiac arrest occurs, the blood flow slows down, the blood and venous pressure drop dramatically to undetectable levels and normal pressure gradients between different vascular systems are lost. Therefore, the distribution of the contrast medium injected at this time will be determined by the pressure generated by the injection pump and by the hydrostatic pressure.
In this way, forced contrast reflux accumulates in the declining areas of the right part of the body, especially in the abdominal venous structures (inferior vena cava, hepatic and renal veins) (Figures 5-8) as well as in the hepatic parenchyma (right hepatic lobe) and renal     area. Because there is no dilution of contrast with circulating blood, a markedly dense appearance of these structures is observed. As the blood flow is slowed, the dissection in the portal phase is better visualized [10]. Figure 9 shows internal displacement of intimal calcification.

Late phase
Due to the irregular distribution of the intravenous contrast, we decided to make a late sequence that matches a portal phase.
The difference of enhancements amongst phases are shown in figures 10-13. The flap is visible in both images but is better visualized at portal phase. Figure 14 shows that flap is still present at the end of the aortic artery, just before the aortic bifurcation. However, figure 15 shows a downward trajectory of the flap immediately after the flap bifurcation inside the right iliac common artery. We can therefore confirm that the aortic dissection in this patient is complete and includes all the trajectory of the aortic artery, from the ascending section to the aortic bifurcation and even further in the right iliac common artery.
We can see in figures 16 and 17 almost the entire trajectory of the aortic dissection, including the common iliac arteries. Figures 18-22 shows air in portal system. Its main etiology is the intestinal ischemia. This is generally considered a predictor of intestinal perforation and it may lead to a erroneous prognosis [11][12][13][14]. In our case study, portal pneumatosis suggests intestinal ischemia due to low cardiac output as a result of aortic insufficiency, previous cardiac arrest and/or involvement of abdominal arterial branches by dissection. The abdominal pain presented by our patient could be due to intestinal ischemia [1].

Conclusions
Aortic dissection is the most frequent cause of aortic emergency and as such should always be suspected in these situations. As demonstrated by this case study and in order to avoid future preventable deaths, this must be diagnosed and treated urgently. For, he appropriate diagnosis of aortic dissection, we highly recommend the use of CT imaging with the following sequences: (i) Non-enhanced phase, in order to differentiate between IH and AD; (ii) Arterial phase with intravenous contrast; (iii) Late phase with intravenous contrast matching portal phase; (iv)