Aortic Aneurysm & Dissection

Presented by : Feryal AlKhateeb

Samah AlKhateeb

Anatomy

Histoloogy

Thoracic Aortic Aneurysm

Aortic aneurysm is defined as a permanent, localized dilatation of the aorta to a diameter that is at least 50% greater than is normal at that anatomic level.

The annual incidence of thoracic aortic aneurysms is estimated to be 5.9 per 100,000 persons.

Aneurysms can be localized to a single aortic segment, or they can involve multiple segments. In the most extreme cases, the entire aorta is aneurysmal; this condition is often called mega-aorta.

Aortic aneurysms can be either “true” or “false.”

True aneurysms can take two forms: fusiform and saccular.

1. Fusiform aneurysms are more common and can be described as symmetrical dilatations of the aorta.

2. Saccular aneurysms are localized outpouchings of the aorta.

False aneurysms, also called pseudoaneurysms, are leaks in the aortic wall that are contained by the outer layer of the aorta and/or the periaortic tissue; they are caused by disruption of the aortic wall and lead blood to collect in pouches of fibrotic tissue.

Causes and Pathogenesis Nonspecific medial degeneration

Aortic dissection

Genetic disorders

1. Marfan syndrome

2. Loeys-Dietz syndrome

3. Ehlers-Danlos syndrome

4. Familial aortic aneurysms

5. Aneurysms-Osteoarthritis syndrome

6. Congenital bicuspid aortic valve

7. Bovine aortic arch

Poststenotic dilatation

Infection

Aortitis

Takayasu arteritis

Giant cell arteritis

Rheumatoid aortitis

Trauma

Clinical Manifestation In many patients with thoracic aortic aneurysms, the aneurysm is discovered

incidentally when imaging studies are performed for unrelated reasons. And they are asymptomatic at time of diagnosis.

1. Local compression and erosion. - anterior chest discomfort. - left vocal cord paralysis and hoarsness. - interscapular back pain. - middle back and epigastric pain.

2. Aortic valve regurgetation. - progressive heart failure. - widened pulse pressure. - diastolic murmer.

3. Distal embolization. - occlusion and thrombosis of the visceral, renal, or lower extremity branches.

4. Rupture. - sudden, severe pain in the anterior chest (ascending aorta), upper back or left chest (descending thoracic aorta), or left flank or abdomen (thoracoabdominal aorta). - acute cardiac tamponade and death. - severe hemorrhagic shock.

Diagnostic Evaluation

Plain radiography. - (CXRs) may appear normal in patients with thoracic aortic disease and, thus, cannot exclude the diagnosis of aortic aneurysm. 1- convexity in the right superior mediastinum 2- loss of the retrosternal space (on lateral view) 3- widening of the descending thoracic aortic shadow 4- a rim of calcification outlining the dilated aneurysmal aortic wall. - Once a thoracic aortic aneurysm is detected on plain radiographs, additional studies are required to define the extent of aortic involvement.

Echocardiography and Abdominal Ultrasonography.

Computed Tomography. - CT is the most common—and arguably the most useful—imaging modality for evaluating thoracic aortic aneurysms. - provides information about an aneurysm’s location, extent, anatomic anomalies, and relationship to major branch vessels.

Magnetic Resonance Angiography. - It is the best method of diagnosing aneurysms, but have more limitations than CT.

- MRA environment is not appropriate for many critically ill patients. - MRA imaging is suboptimal in patients with extensive aortic calcification.

Invasive Aortography and Cardiac Catheterization.

- the use of invasive aortography in patients with thoracic aortic disease is generally limited to those undergoing endovascular therapies or when other types of studies are contraindicated or have not provided satisfactory results. - A key limitation of aortography is that it : images only the lumen and may therefore underrepresent the size of large aneurysms that contain laminated thrombus. Manipulation of intraluminal catheters can result in embolization of laminated thrombus or atheromatous debris.

Treatment

Once a thoracic Aortic aneurysm is detected, management begins with patient education, particularly if the patient is asymptomatic. - strict control of hypertension. - cessation of smoking.

Indecations for operation : 1. Elective operation in asymptomatic patients when the

diameter of an ascending aortic aneurysm is >5.5 cm, or diameter of a descending thoracic aortic aneurysm is >6.0 cm.

2. The rate of dilatation is >0.5 cm/y. 3. Emergent intervention for patients who present with

aneurysm rupture or superimposed acute dissection. 4. patients who present with symptoms may need urgent

operation

Traditional open operations to repair proximal aortic aneurysms performed through a midsternal incision and require cardiopulmonary bypass.

The spectrum of operations ranges from simple graft replacement of the tubular portion of the ascending aorta to graft replacement of the entire proximal aorta, including the aortic root, and reattachment of the coronary arteries and brachiocephalic branches.

Open repair vs. endovascular repair.

Stent graft repair of descending thoracic aortic aneurysms has become the accepted treatment option

Operative Complications

Bleeding is a potential complication for all aneurysm repairs. Stroke is a major cause of morbidity and mortality and

typically results from embolization of atherosclerotic debris or clot.

Myocardial infarction may occur with technical problems with coronary ostia implantation during root replacement for ascending aortic aneurysms and may require reoperation.

Pulmonary dysfunction. Renal dysfunction. Paraparesis and paraplegia, either acute or delayed, are the

most devastating complications. Complications specific to endovascular stenting include

endoleaks, stent fractures, stent graft migration or thrombosis, iliac artery rupture, retrograde dissection, microembolization, aortoesophageal fistula.

Long Term Monitoring

serial evaluations (ie, CT or MRI for ascending, arch, or descending aneurysms; echocardiography for ascending aneurysms) may be performed every 3-6 months during the first postoperative year and every 6 months thereafter.

Aortic Dissection

By Samah AlKhateeb

Pathology and Classification

Aortic dissection, the most common catastrophic event involving the aorta, is a progressive separation of the aortic wall layers that usually occurs after a tear forms in the intima and inner media, resulting in blood tracking into the aortic tissues splitting the medial layer and creating a false lumen.

Figure 22-17. Illustration of longitudinal sections of the aortic wall and lumen. Blood

flows freely downstream in normal aortic tissue. In classic aortic dissection, blood entering

the media through a tear creates a false channel in the wall. Intramural hematomas arise

when hemorrhage from the vasa vasorum causes blood to collect within the media; the

intima is intact. Penetrating aortic ulcers are deep atherosclerotic lesions that burrow into

the aortic wall and allow blood to enter the media. In each of these conditions, the outer

aortic wall is severely weakened and prone to rupture.

The extensive disruption of the aortic wall has severe anatomic consequences. First, the outer wall of the false lumen is extremely thin, inflamed, and fragile, which makes it prone to expansion or rupture in the face of ongoing hemodynamic stress. Second, the expanding false lumen can compress the true lumen and cause malperfusion syndrome by interfering with blood flow in the aorta or any of its branch vessels, including the coronary, carotid, intercostal, visceral, renal, and iliac arteries. Finally, when the separation of layers occurs within the aortic root, the aortic valve commissures can become unhinged, which results in acute valvular regurgitation.

Dissection vs. Aneurysm.

Dissection and aneurysm are separate entities, although they often coexist and are mutual risk factors. In most cases, dissection occurs in patients without aneurysms. The subsequent progressive dilatation of the weakened outer aortic wall results in an aneurysm. On the other hand, in patients with degenerative aneurysms, the ongoing deterioration of the aortic wall can lead to a superimposed dissection. The overused term dissecting aneurysm should be reserved for this specific situation.

Classification.

For management purposes, aortic dissections are classified according to their location and chronicity.

Location. To guide treatment, dissections are categorized according to their anatomic location and extent.

Chronicity. Dissection is considered acute within the first 14 days after the initial tear; after 14 days, the dissection is considered chronic.

Figure 22-19. Illustration of the classification

schemes for aortic dissection based on which portions of the aorta are

involved. Dissection can be confined to the ascending aorta (left) or

descending aorta (middle), or it can involve the entire aorta (right).

Causes and Clinical History

Aortic dissection is a lethal condition. Without appropriate modern medical or surgical treatment, most patients (approximately 90%) die within 3 months of dissection, mostly from rupture.

the specific causes remain unknown. Ultimately, any condition that weakens the aortic wall increases the risk of aortic

dissection.

Risk Factors:

Common general cardiovascular risk factors; Smoking

Hypertension

Atherosclerosis

Hypercholesterolemia

Connective tissue disorders.

Bicuspid aortic valve.

Preexisting medial degenerative disease.

Iatrogenic dissection; aortic injury during cardiac catheterization, surgery, or endovascular aortic repair.

Cocaine and amphetamine abuse.

Severe emotional stress or extreme physical exertion such as during weightlifting.

Clinical Manifestations

The onset of dissection often is associated with sudden severe chest or back pain, classically described as “tearing”, that migrates distally as the dissection progresses along the length of the aorta.

The location of the pain often indicates which aortic segments are involved.

Clinical Manifestations

The dissection may track proximally to involve:

the head and neck vessels (symptoms and signs of a stroke or transient ischemic attack).

the coronary vessels (myocardial infarction).

the aortic root (aortic regurgitation).

The dissection can extend distally down the aorta to involve:

the renal arteries (renal failure).

the mesenteric arteries (abdominal pain and bowel ischemia).

the spinal arteries (paraplegia, incontinance).

the iliac arteries (leg pain, pallor, loss or reduced pulses and limb ischemia).

Investigations

Diagnosis is confirmed by:

Chest X- ray shows widening of the mediastinum in two-thirds of patients and a small left pleural effusion.

Contrast CT shows a flap across the aortic lumen with distal aneurysmal change. (it is probably the investigation of choice)

Echocardiography may also demonstrate a flap and aortic regurgitation. Transoesophageal echocardiography (TOE)

Figure 1. Chest X-ray (postero-anterior projection) showing that

the descending thoracic aorta is extremely dilated and tortuous.

Figure 22-21. Computed tomographic scans showing that the aorta has been separated

into two channels—the true (T) and false (F) lumens— in two patients with different phases

of aortic dissection. A. An acute DeBakey type I aortic dissection. The dissecting membrane

appears wavy (arrows) in the early phase of dissection. Here, the true lumen of the proximal

aorta can be seen to be extensively compressed. This may lead to malperfusion of the heart.

B. A chronic DeBakey type III aortic dissection. In the chronic phase, the membrane

appears straighter and less mobile (arrow) because it has stabilized over time.

Figure 2. Sagittal computed tomography images demonstrating the

thoracic (A) and abdominal (B) portions of the involved dissecting aorta

with arrows indicating the dissecting intimal flap.

Treatment

Once the diagnosis is made, treatment depends largely upon the type of dissection.

In the emergency situation, before further imaging, blood pressure (which is usually high at presentation) should be brought under control to prevent extension of the dissection.

Surgical options

Type A (or type I and II)

Should be managed surgically because of the risk that the dissection may extend back across the aortic root resulting in tamponade, and to correct aortic incompetence.

The surgery aims to interpose a prosthetic tube graft at the aortic root to prevent further dissection.

Illustration of proximal aortic repair for acute ascending aortic dissection

Illustration of distal aortic repair of a chronic dissection.

(Continued)

Type B (or type III) Usually treated conservatively. Hypertensive drugs are used, reducing systolic pressure to 100

–120 mmHg to prevent further extension of the dissection. Any organ, limb or mesenteric ischemia resulting from the

dissection is treated by revascularization. An aneurysm resulting from a chronic dissection may require

treatment if it enlarges or produces pressure symptoms. In cases where there is evidence of impending aortic rupture

or non-perfusion of a visceral artery, endovascular placement of a covered stent (a stent – graft) is appropriate.

The stent is placed to cover the proximal entry into the false lumen, and to re-establish blood flow through the collapsed true lumen.

The End

Thank You!

Resource : schwartz’s principles of surgery , 10th edition.