David E. Manthey
ABDOMINAL AORTIC ANEURYSMS
The incidence of abdominal aortic aneurysm (AAA) increases with age.
Most patients are older than 60.
Males are at increased risk.
Eighteen percent of patients have a family history of aneurysm in a first-degree relative.
Other risk factors include connective tissue disease, Marfan’s syndrome, and atherosclerotic risk factors (smoking, hypertension, hyperlipidemia, and diabetes).
Thinning of the media of the aorta with a reduction in elastin, collagen, and fibrolamellar units results in a decrease in tensile wall strength.
Laplace’s law (wall tension = [pressure × radius]) dictates that as the aorta dilates, the force on the aortic wall increases, causing further aortic dilation.
The rate of aneurysmal dilation is variable, with larger aneurysms expanding more quickly. An average rate may be 0.25 to 0.5 cm per year.
Asymptomatic AAAs may be found on physical examination or during an unrelated radiologic evaluation. Those larger than 5 cm are at higher risk of rupture.
Three clinical scenarios exist for symptomatic aneurysms: acute rupture, aortoenteric fistula, and chronic contained rupture.
Sudden death most commonly occurs with intraperi-toneal rupture of the aneurysm.
The classic presentation is an older male with severe back or abdominal pain who presents with syncope or hypotension.
Pain, described as abrupt and severe at onset, is the most common presenting symptom; 50% describe this pain as “tearing” or “ripping.”
Many patients present with a complaint of unilateral flank or groin pain, hip pain, or abdominal pain localized to a specific quadrant. An AAA is most commonly misdiagnosed as renal colic.
The presence of an AAA does not alter the femoral arterial pulsations.
Lack of tenderness does not imply an intact aorta.
There may be signs of retroperitoneal hemorrhage such as periumbilical (Cullen’s sign) or flank ecchy-mosis (Grey-Turner’s sign) or scrotal hematoma.
Aortoenteric fistulas may present with a deceptively minor “sentinel” bleed or massive GI hemorrhage. This is classically seen after prior aortic grafting.
Chronic contained rupture is uncommon, but is seen when an AAA ruptures retroperitoneal with significant fibrosis that limits blood loss.
DIAGNOSIS AND DIFFERENTIAL
The differential for AAA depends on its presentation. The key is to keep AAA in your differential when evaluating patients for symptoms such as back pain, syncope, and renal colic.
Diagnostic studies should never unnecessarily delay the surgical repair of an AAA. They are only needed when the diagnosis of AAA is unclear.
In the unstable patient, bedside abdominal ultrasound has >90% sensitivity for demonstrating the presence of an aneurysm and measuring its diameter. Ultrasound cannot reliably determine the presence of retroperito-neal hemorrhage and rupture (see Fig. 29-1).
Computed tomographic (CT) scanning, approximately 100% accurate in determining the presence or absence of an AAA, is preferred in the stable patient as it better delineates the anatomic details of the aneurysm and any associated rupture (see Fig. 29-2).
FIG. 29-1. Bedside US image of an abdominal aortic aneurysm. This aneurysm measures 6.5 cm.
FIG. 29-2. CT scan of a patient with a 12-cm abdominal aortic aneurysm. Calcification of the aortic wall is seen anterior to the spinal column. Evidence of hemorrhage and surrounding inflammation (arrow) is seen in the left side of the abdomen.
EMERGENCY DEPARTMENT CARE AND DISPOSITION
Stabilize the patient with volume resuscitation with isotonic fluids and/or blood transfusion through multiple large-bore IV lines.
Immediate surgical consultation or transfer to an appropriate institution is warranted for suspected rupturing AAA or aortoenteric fistula.
Symptomatic aneurysms of any size should be considered emergent.
Control pain appropriately with narcotics. Utilize a short acting β-blocker if elevated BP remains after pain control.
Type and cross patient with rupturing AAA or aortoenteric fistula for several units of blood.
Consult a vascular surgeon for urgent repair of chronically contained ruptured AAAs.
For an incidentally discovered AAA, consultation with a vascular surgeon for admission or close outpatient follow-up based on the size of the aneurysm is appropriate.
Aortic dissection has a bimodal distribution. First peak is of younger patients with predisposing conditions, and a larger number in the second peak with age > 50 years.
A major risk factor for the older group is chronic hypertension.
Younger patients have identifiable risk factors such as bicuspid aortic valve, connective tissue disease, and familial history of aortic dissection.
Aortic dissection occurs when the intima is violated, allowing blood to enter the media and dissect between the intimal and adventitial layers, developing a false lumen.
The false lumen may dissect proximally and/or distally and may rupture back through the intima or out through the adventitia.
The Stanford classification system categorizes type A dissections as any involvement of the ascending aorta, and type B dissections as restricted to the descending aorta. The DeBakey system classifies type I dissections as those that involve the ascending aorta, the arch, and the descending aorta. Type II involves only the ascending aorta, and type III only the descending aorta.
Intramural hematomas result from injury to the vasa vasorum with subsequent infarction of the media. They are often precursors to aortic dissection.
Penetrating atherosclerotic ulcers involve the intima and can lead to hematomas, dissection, or perforation of the aorta.
More than 85% of patients have abrupt onset of severe or the worst pain ever. It is more commonly described as “sharp” followed by tearing or ripping.
Type A dissection presents with chest pain (80%), more commonly anterior (71% of those with chest pain). Patients also report back (47%) and abdominal pain (21%>). Type B dissections present with back pain (64%), chest pain (63%), and abdominal pain (43%).
Syncope occurs in up to 10% of patients. Interruption of blood supply may alter the presentation by the area affected such as coronary artery occlusion with MI, stroke symptoms with carotid involvement, or paraplegia with occlusion of the vertebral blood supply. The dissection may progress distally, causing abdominal or flank pain or limb ischemia.
Proximal retrograde dissection into the aortic root may lead to cardiac tamponade.
An aortic insufficiency murmur may be heard in 32%. Fifteen percent of patients have decreased radial or femoral pulse deficits.
Hypertension (49%) and tachycardia are common, but hypotension (18%) may also be present.
Very few patients with aortic dissection have involvement of a coronary artery (6%). The ratio of acute coronary syndrome to aortic dissection is about 3000:5.
DIAGNOSIS AND DIFFERENTIAL
Ischemic end-organ manifestations associated with dissections may confuse the differential diagnosis, including myocardial infarction, pericardial disease, and spinal cord injuries.
Rupture of the dissection back through the intima into the true lumen may cause a cessation of symptoms, leading to false reassurance.
Most patients with a thoracic dissection will have an abnormal chest x-ray, but up to 37% will be normal. More common findings include a widening of the mediastinum, abnormal aortic contour, pleural effusion, apical capping, and depression of the left main stem bronchus (see Fig. 29-3).
CT scanning, with and without contrast, is the imaging modality of choice. It can reliably diagnose dissection as well as location of flap and extension into great vessels (see Fig. 29-4).
CT scanning will also diagnose intramural hematomas and penetrating atherosclerotic ulcers.
Transesophageal echocardiography may be as sensitive and specific as CT in experienced hands.
FIG. 29-3. Abnormal aortic contour on chest radiography. Frontal and lateral radiographs of the chest in a patient with type B aortic dissection reveal an abnormal aortic contour (arrow). A right pleural effusion is present, and multiple postoperative clips and wires are also seen.
FIG. 29-4. Type B dissection into the iliac arteries. Contrast CT image of dissection extending into the iliac arteries (anterior to vertebral body). True and false lumens are visible in both arteries (arrows).
EMERGENCY DEPARTMENT CARE AND DISPOSITION
Patients with suspected aortic dissection require prompt radiographic confirmation of the diagnosis and early consultation with the CT surgeon.
Hypertension must be controlled with drugs that will not increase the shear force on the intimal flap. β-Blockers are the first-line choice, with nitroprus-side added if the blood pressure remains elevated. Calcium channel blockers can be used if there is a contraindication to β-blockers.
Dissection of the ascending aorta requires prompt surgical repair. Repair may include surgical repair, endovascular treatment or fenestration of the intimal flap.
As acute coronary syndrome and dissection may present with anterior chest pain, a chest radiograph should be assessed for signs of dissection before administering heparin or fibrinolytics.
For further reading in Emergency Medicine: A Comprehensive Study Guide, 7th ed., see Chapter 62, “Aortic Dissection and Related Aortic Syndromes,” by Gary A. Johnson and Louise A. Prince. Please also see Chapter 63, “Aneurysms of the Aorta and Major Arteries”, by Louise A. Prince and Gary A. Johnson.