Transcript for Aortic aneurysm and dissection
Content Reviewers:Evan Debevec-McKenney, Sam Gillespie, Rishi Desai, MD, MPH, Jake Ryan, Antonella Melani, MD, Kaia Chessen, MScBMC, Robyn Hughes, MScBMC
Aortic aneurysm and dissection
An aneurysm is a full-thickness dilation of a segment of a blood vessel so that it’s 50 percent greater than its normal diameter, and it’s usually caused by a weakness in the blood vessel wall.
True aneurysms involve all three layers of the arterial wall - the tunica intima, which has endothelial cells; the tunica media, which has smooth muscle; and the tunica adventitia, which has connective tissue as well as vasa vasorum which are the vessels nourishing the aortic wall itself.
There are two major types of aneurysms: fusiform aneurysms, which are uniform in shape with symmetrical dilatation and involves the entire circumference of the aortic wall; and saccular aneurysms, which are localized outpouchings of only a portion of the aortic wall.
Most individuals with Abdominal aortic aneurysm, or AAA, have no symptoms and are only detected as an incidental finding on imaging studies performed to evaluate an unrelated condition.
Some cases, especially in thinner individuals, may be discovered on a routine physical examination as a pulsating abdominal mass that can be felt on palpation and heard as a bruit on auscultation.
One-time screening with ultrasound can be done in individuals with risk factors like hypertension, increasing age, male gender, smoking, atherosclerosis, genetic syndromes - such as Turner syndrome or connective tissue diseases like Marfan’s syndrome or Ehlers-Danlos syndrome, familiarity for aneurysmal diseases, and having aneurysms in other arteries.
Aortic dissection is defined as a separation of the layers of the aortic wall due to an intimal tear, creates a second blood flow channel.
Blood may flow in between the layers of the blood vessel wall as the tear extends, which can lead to aortic rupture or decreased blood flow to the organs.
Dissection in most cases is associated with a sudden onset of severe pain, often described as tearing.
Aortic dissection can quickly evolve to full-thickness tearing due to the weakening of the aortic wall to the extent that it can no longer support the forces imposed upon it, leading to a complete rupture.
Most cases of aortic rupture present with the classical triad of severe acute pain, a pulsatile abdominal mass, and hypotension.
This may rapidly cause a massive hemorrhage, possibly evolving into shock and death.
Aortic aneurysms are classified by their location along the aorta.
Abdominal aortic aneurysms involve the segment of the aorta within the abdominal cavity.
Thoracic aortic aneurysms are found within the chest; and these are further classified as ascending or descending aneurysms.
Finally, there’s thoracoabdominal aortic aneurysms, which involve both the thoracic and abdominal aorta.
AAAs are the most common form of aneurysm, usually involving the infrarenal segment of the aorta, inferior to the renal arteries and superior to the iliac bifurcation.
A AAA is defined as dilation with a transverse diameter exceeding 3 centimeters.
Symptoms of a AAA, include abdominal pain that can radiate.
For proximal aneurysms, there’s upper abdominal or back pain, and for distal aneurysms, there’s lower abdominal or pelvic pain.
The pain is typically unrelated to movement or body position.
Unruptured aneurysms typically present with an indolent onset of pain that is vague and nonspecific, while ruptured aneurysms cause sudden-onset severe pain.
AAAs that cause symptoms may be about to rupture or may have already ruptured - and so all of them are considered medical emergencies.
Aneurysms cause turbulent blood flow and that can lead to vessel wall damage, areas of stagnant blood flow, and the formation of thrombi.
Thrombi can also embolize to various sites causing symptoms like claudication, painful blue digits due to recurrent focal ischemia - known as blue toe syndrome - or a painful pulseless cool extremity due to acute limb ischemia.
Rarely, AAA can lead to acute aortic thrombosis leading to bilateral lower extremity ischemia, or rarely, spinal cord ischemia.
Finally, large aneurysms can cause local compression of nearby structures, like the gastrointestinal tract or the spine.
A definitive diagnosis of AAA requires seeing a focal aortic dilation on imaging.
Small aneurysms have a diameter smaller than 4 centimeters; medium aneurysms have a diameter between 4 and 5.5 centimeters; and large aneurysms have a diameter larger than 5.5 centimeters.
Based on prior imaging, a rapidly expanding aneurysm is defined as one that grows more than 0.5 centimeters per year.
For symptomatic individuals, a diagnosis of AAA is guided by their hemodynamic status.
Hemodynamically stable individuals with symptoms of a AAA should get an urgent abdominal CT scan with contrast.
CT scan findings consistent with a ruptured AAA include a retroperitoneal hematoma, indistinct aortic walls, retroperitoneal fat stranding, loss of the fat plane between the aorta and surrounding tissue, and extravasation of IV contrast outside the aorta into the retroperitoneum, into a vein, or even into the bowel.
On the other hand, findings that may be associated with potentially unstable aneurysms or impending rupture include a crescent sign of layering hematoma within the aorta, aortic blebs that bulge from the surface of the aorta, "draping" of the aorta over a vertebral body, irregularity of the aortic wall, breaks in the calcification of the aortic wall, and localized areas of higher attenuation within a mural thrombus.
Now, in hemodynamically unstable individuals with symptoms of a AAA, they should be taken right away for surgical management.
On the other hand, if it’s not clear that they have an aneurysm, then a bedside ultrasound should be obtained.
The treatment options for asymptomatic AAA include conservative management, surveillance with a plan for eventual repair, and immediate repair.
Conservative treatment involves management of modifiable risk factors like smoking cessation, antihypertensive therapy to control blood pressure, statin therapy to lower cholesterol levels, and antiplatelet therapy for cardiovascular disease.
Asymptomatic AAA smaller than 5.5 centimeters in diameter should be followed up with annual ultrasound with periodic clinical evaluation and surveillance of aneurysm diameter.
Repair is recommended if the aneurysm is or becomes bigger than 5.5 centimeters or is rapidly expanding, which is defined as an increase in maximal aortic diameter of 5 millimeters or more over a six-month period of time or more than 1 centimeter over one year.
For a symptomatic unruptured AAA of any size, urgent AAA repair should be performed, because the presence of symptoms suggests that the aneurysm is rapidly changing and might rupture.
A ruptured AAA can be fatal and needs emergency repair.
For individuals with ruptured AAA, the systolic blood pressure should be maintained between 80 and 100 mm Hg prior to repair, which is known as permissive hypotension, to minimize further tearing of the aorta and reduce blood loss.
There are two modes of repair: open aneurysm repair, and endovascular aneurysm repair or EVAR.
Open aneurysm repair involves replacement of the diseased aortic segment with a prosthetic graft through a midline abdominal or retroperitoneal incision depending on the location of the aneurysm.
The dilated portion of the aorta is opened for insertion of a synthetic graft.
Once the graft is sewn into the proximal and distal portions of the aneurysm, the aneurysmal sac is closed around the graft to avoid adhesions or fistulization, especially with the duodenum.