Chapter 9. Abdominal Aortic Aneurysm

Aneurysm of the abdominal aorta is a relatively common disease in patients over 50 years of age.1–3 Rupture of an abdominal aortic aneurysm (AAA) has a high mortality and causes as many as 30,000 deaths per year in the United States, which is more than AIDS or prostate cancer.4 It is one of the least-known killers in American society.4

More than 100 years ago, William Osler said, “There is no disease more conducive to clinical humility than aneurysm of the aorta.” This remains true today, as the diagnosis of ruptured AAA continues to confound clinicians. Misdiagnosis of ruptured AAA is common because many patients have not had a previously asymptomatic AAA formally diagnosed; they also may present with nonspecific complaints and have normal vital signs.5–7 Mortality due to AAA is decreased if the diagnosis is made prior to rupture or if the diagnosis is made rapidly after rupture of AAA.8–13

The availability of point-of-care ultrasound in the ED has allowed emergency physicians to change their approach to patients at risk for a ruptured AAA. A screening point-of-care ultrasound examination can now be obtained on patients over 50 years of age who present with pain in the abdomen, back, flank, or groin, and on those who present with dizziness, syncope, unexplained hypotension, or cardiac arrest.2,14 This practice is analogous to the immediate acquisition of an ECG for all patients with possible myocardial infarction. In this capacity, ultrasound clearly can save lives, making this application one of the indisputable benefits of emergency point-of-care ultrasound.8,9,13,15

AAA occurs in 2–5% of the population over 50 years of age and about 10% of men over 65 years of age who have risk factors for vascular disease.16–22 The prevalence is even higher in patients with first-degree relatives who have an AAA and those with peripheral vascular disease.4,23 AAA is about four times more prevalent in men than in women.24–26 The prevalence has been steadily rising in both men and women over the past several decades, so despite advances in diagnostic imaging and surgical techniques there has been essentially no change in the number of patients presenting with ruptured AAA.27–31

The risk of AAA rupture is directly related to the largest diameter of the aneurysm and increases dramatically in those >5 cm. Estimates of rupture risk are as follows: <2% per year for aneurysms <4 cm, 1–5% per year for those 4–5 cm, 3–15% per year for those 5–6 cm, 10–20% per year for those 6–7 cm, and 20–50% per year for those >7 cm.32–37 Other factors such as continued smoking, uncontrolled hypertension, and emphysema increase the risk of rupture.38,39 Also, women have a higher risk for rupture than men with the same-size aneurysm.32,40–42 Current guidelines for elective treatment of AAA suggest operative repair of aneurysms 5.5 cm or larger in the “average” patient.43 Of course, each patient's situation is unique and requires an analysis of the risks and benefits prior to elective surgery.4

Most patients with an AAA are asymptomatic until rupture occurs. The overall mortality for ruptured AAA is roughly 80%. About 60% die prior to receiving any medical care and 40–50% of those who have emergent operative repair die.18,44–49 Rapid diagnosis and early surgical management have been shown to decrease mortality.10–13 Unfortunately, 30–60% of patients with a ruptured AAA may be initially misdiagnosed.6,44,50,51 Delayed or misdiagnosis occurs because the symptoms may mimic other common conditions such as renal colic, musculoskeletal back pain, diverticulitis, GI hemorrhage, sepsis, or acute coronary syndrome. Patients do not usually know that they have an aneurysm, and many have normal vital signs and initially appear well.6,18,47,51–53

Emergency physicians routinely manage a large number of patients over 50 years of age who have symptoms that could be consistent with a ruptured AAA. Most of these patients do not have a ruptured AAA, but those who do must be diagnosed rapidly. Even when an aneurysm is suspected, physical examination findings are not reliable for excluding or confirming the diagnosis.6,18,47,51–55 Therefore, clinicians need an accurate diagnostic screening test that can be effectively used on a large number of patients. The diagnostic test must be rapid and easy to obtain so that clinicians will have a low threshold for using it. The only diagnostic test that fits this description is point-of-care ultrasound performed by the clinician who is already caring for the patient.50 Laboratory tests are unhelpful and plain radiographs are unreliable; the two essentially have no place in the diagnostic evaluation for an acute AAA. Computed tomography (CT) is very accurate for detecting AAA but it exposes patients to ionizing radiation, is very expensive, and is not practical in unstable patients. The use of point-of-care ultrasound performed by clinicians has been extensively studied and is nearly 100% accurate for detecting or excluding AAA.5,7,56–59

In 1989, the first report on the use of point-of-care ultrasound by emergency physicians to rapidly diagnose ruptured AAA was published.60 Two prospective studies reported that emergency physicians with limited training could diagnose AAA with sensitivity and specificity approaching 100%.57,61 In 2000, a study analyzed 68 patients over 50 years of age presenting to an ED with symptoms worrisome for a ruptured AAA.56 Point-of-care ultrasound was performed by emergency physicians who had attended a 3-day point-of-care ultrasound training course but had no prior experience performing or interpreting sonograms. They detected 26 AAAs and had 100% sensitivity and 100% specificity. They concluded that relatively inexperienced providers can perform aortic ultrasound examinations accurately. In 2003, a prospective study analyzed 114 patients presenting to an ED with symptoms suggestive of ruptured AAA.7 Point-of-care ultrasound examinations were performed by emergency physicians and senior emergency medicine residents. The investigators diagnosed AAA in 29 patients, had 100% sensitivity, and 98% specificity compared with confirmatory testing, and concluded that emergency physicians could use point-of-care ultrasound to diagnose or exclude AAA. A 2005 study evaluated 238 patients who presented to an ED with symptoms concerning for ruptured AAA.5 Ultrasound examinations were performed by senior emergency medicine residents who had been trained following guidelines of the American College of Emergency Physicians.62 They found 36 ruptured AAAs and had 100% sensitivity for making the diagnosis, although their measurements were not perfect. They correctly measured aneurysm diameter in 34 of 36 patients and incorrectly measured 2 aneurysms, but recognized that the aorta was abnormal, leading to the correct diagnosis in those cases. The investigators concluded that appropriately trained emergency medicine residents can accurately determine the presence of AAA.

A 1998 study conducted by Plummer and colleagues dramatically demonstrated the need for emergency point-of-care ultrasound.13 They reviewed the medical records of 50 consecutive patients presenting to their ED with a ruptured AAA. Twenty-five patients who had an immediate point-of-care ultrasound examination had an average time to diagnosis of 5.4 minutes and a median time to disposition for operative intervention of 12 minutes. Twenty-five patients who did not receive an immediate point-of-care ultrasound examination had an average time to diagnosis of 83 minutes and a median time to disposition for operative intervention of 90 minutes. Their most important finding was that those patients who received an early point-of-care ultrasound examination had a 40% mortality compared with a 72% mortality for those patients who did not receive a point-of-care ultrasound examination.

Although ultrasound is operator dependent and the quality of the examination may be influenced by the expertise of the clinician as well as patient body habitus, point-of-care aortic ultrasound can achieve 100% accuracy with brief training.56,63–66 There is not much inter-observer variability, even in inexperienced hands, though more experienced clinicians tend to be more accurate.64,67 Training in point-of-care ultrasound of the abdominal aorta to evaluate for AAA is now a standard part of the core point-of-care ultrasound curriculum across all US emergency medicine residency programs.68

The main indication for point-of-care aortic ultrasound examination is to rapidly identify patients with an AAA (Figure 9-1). Patients with signs or symptoms that could be attributable to a ruptured AAA should undergo an immediate point-of-care ultrasound examination. Patients with a ruptured AAA have widely varying presentations. Reasonable indications for bedside aortic ultrasound examination include all patients over 50 years of age with the following signs or symptoms:

• The classic presentation of ruptured AAA
• Any pain consistent with ruptured AAA
• Unexplained hypotension, dizziness, or syncope
• Cardiac arrest

It is certainly preferable to diagnose AAA prior to rupture since early recognition and repair carries a much lower mortality. In 2005, the US Preventive Services Task Force published recommendations that endorsed the one-time screening for AAA by ultrasonography in men aged 65–75 who had any history of tobacco use. It has been demonstrated that screening for AAA and surgical repair of large AAAs (5.5 cm or more) in men aged 65–75 with a history of tobacco use (current or former smokers) lead to decreased AAA-specific mortality.8

Classic Presentation of Ruptured AAA

The “classic” presentation of a ruptured AAA is the triad of abdominal, back, or flank pain; a palpable abdominal mass; and hypotension. This “classic” presentation is found in <25% of cases.6,47,50,51,53 Pain is the most consistent part of the triad and is present in >80% of those seeking medical attention.6,51,53 Palpation of an abdominal mass on physical examination is an unreliable finding. One study reported that a palpable mass was noted in only 18% of 329 patients presenting with a ruptured AAA.53 In addition, many thin patients with an apparent pulsatile abdominal mass have a normal abdominal aorta.54 Finally, hypotension is not universally present with ruptured AAA. Most aneurysms rupture into the retroperitoneum, resulting in a transient tamponade effect; thus, 30–50% of patients have a normal blood pressure at the time of presentation with ruptured AAA.6,18,51–53,69

Pain Consistent with Ruptured AAA

Pain is the most common reason for patients with a ruptured AAA to seek medical care. Most patients complain of pain in the abdomen, back, or flank. Studies have found that about 80% of ruptured AAA patients have abdominal pain, about 60% have back or flank pain, and 22% have groin pain at the time of presentation.6,51 In another study of 329 cases of ruptured AAA, it was found that 49% had abdominal pain and 36% had back pain at the time of presentation.53 Clinicians should be aware that patients often present with referred pain to the scrotum, buttocks, thighs, shoulders, chest, or other locations.2 Many patients with ruptured AAA are misdiagnosed with renal colic, diverticulitis, or musculoskeletal pain.50 When patients present with nonspecific pain and stable vital signs, it is common to miss or delay the diagnosis. In these difficult patients, it is imperative to rapidly diagnose a ruptured AAA because those who develop hypotension prior to surgery have a higher mortality.10,13,18,70 No patient with a known or suspected AAA rupture should be considered stable regardless of initial vital signs.52

Unexplained Hypotension, Dizziness, or Syncope

Hypotension is present in 50% or more of patients presenting with ruptured AAA.6,18,51–53,69 Altered mental status secondary to hypotension can make it difficult to obtain a history of abdominal, back, or flank pain. Therefore, patients may present with unexplained hypotension and no other clues of a ruptured AAA. Many of these patients are misdiagnosed with GI hemorrhage, sepsis, or myocardial infarction.6,50,51,53 Both hypotension and altered mental status prior to surgery are independent predictors of mortality from a ruptured AAA.18,70,71 Multiple protocols for screening ED patients who present with undifferentiated hypotension have been developed.72 One study used an empiric ultrasound examination to screen for pericardial effusion, free intraperitoneal fluid, and AAA. Another study used a similar approach that included additional ultrasound windows to evaluate the inferior vena cava (IVC), perisplenic region, and pelvis.73 Both studies pointed out that empiric abdominal ultrasonography is especially valuable when clinical history is limited or unknown and suggested that it should be a routine part of evaluation of patients with unexplained hypotension.

Relative hypotension, orthostatic hypotension, dizziness, or syncope may be precursors to overt hypotension and are indications for ultrasound examination of the abdominal aorta. Relative hypotension occurs in patients with baseline hypertension who have a decrease in blood pressure level but still have values that are within the “normal” range. These patients may present with altered mental status, vague weakness, dizziness, or syncope. A study that reviewed the records of 23 patients with a ruptured AAA found that 61% were initially misdiagnosed.51 Only 13% of patients had overt hypotension (systolic blood pressure <90 mm Hg) but 26% had syncope and 48% had an initial systolic blood pressure <110 mm Hg or orthostatic hypotension.

Cardiac Arrest

Cardiac arrest is a fairly common presentation in patients with ruptured AAA.18 Clinicians should recognize that patients with pulseless electrical activity may be in a state of severe hypotension that could possibly be reversible if the cause is rapidly identified and aggressively treated.74 A case report described a patient with pulseless electrical activity in whom emergency physicians used point-of-care ultrasound to immediately identify mechanical cardiac activity despite lack of pulses.75 This finding led to aggressive resuscitation and a search for potential hemorrhage. They then used point-of-care ultrasound to detect a large AAA, allowing the patient to proceed directly to the operating room for surgical repair. They concluded that patients presenting with pulseless electrical activity who are found to have mechanical cardiac activity should have immediate ultrasound imaging of their aorta. Multiple approaches to rapid ultrasound exam of the pulseless electrical activity arrest victim have been described. If hypovolemia is suggested by decreased cardiac chamber volume and increased IVC collapsibility, the aorta should be promptly assessed to evaluate for possible AAA rupture.76–79

Some physicians argue that patients who have sustained cardiac arrest from a ruptured AAA have a miniscule chance of survival and that surgical repair is a waste of resources, but this view is not supported by data.70 One study found that preoperative cardiac arrest occurred in 24% of patients with ruptured AAA, but 28% of those survived operative repair.18

Screening for AAA in High-Risk Asymptomatic Patients

Ultrasound screening for AAA and its impact on mortality have been extensively studied.16,80–84 A 2005 evidence-based systematic review of population-based screening for AAA concluded that selective screening for AAA significantly improves AAA-related mortality. When the study extrapolated the findings to the entire US population of men aged 65–74 years, it estimated that 11,392 AAA deaths could be prevented over a 5-year period.9 A 2007 Cochrane review of four randomized controlled trials involving 127,891 men and 9342 women found significant decrease in mortality from AAA in men who were screened, but not for women. Only one of the analyzed trials included women, leading to the conclusion that there is insufficient evidence to determine the benefit of AAA screening in women.85

A study analyzing the cost-effectiveness of a “quick-screen” program for AAA found that the cost-effectiveness ratio (cost per life saved) was lower than the cost of breast cancer screening. A study evaluating the efficacy and cost of a large-scale screening effort in men between the ages of 65 and 75 years who had smoked at least 100 cigarettes in their lifetime found that AAA was diagnosed in 5.1% of screened patients. The cost of the exam per patient was $53.86 Properly trained emergency physicians can perform limited AAA screening examinations with 100% sensitivity.7,56 The rapidity and accuracy of an ED screening exam was reported to have an average time of 141 seconds and a mean size discrepancy of 3.9 mm between the ED exam and comprehensive imaging.87 Other trainees, such as internal medicine and surgery residents, can learn to perform accurate AAA screening examinations with little training.88,89

The Society for Vascular Surgery, the American Association of Vascular Surgery, and the Society for Vascular Medicine and Biology endorse screening of the following patient groups (based on a review of six prospective randomized trials):4,16,25,80,82,84,90–92

1. all men aged 60–85 years;

2. women aged 60–85 years with CV risk factors;

3. men and women older than 50 years with a family history of AAA.

They also recommended that patients found to have an AAA 3–4 cm in diameter have an annual follow-up ultrasound examination, those with an AAA 4–4.5 cm have a follow-up examination every 6 months, and those with an AAA >4.5 cm be referred to a vascular surgeon. While these guidelines are widely accepted and adhered to in the United States, a systematic review of seven national or international guidelines for AAA screening published in 2012 found consensus only in screening men over the age of 65 for AAA and in referring patients with AAAs >5.5 cm for surgical repair.93

The abdominal aorta is entirely a retroperitoneal structure. It begins at the aortic hiatus of the diaphragm at approximately the 12th thoracic vertebrae and courses anterior to the spine before bifurcating into the common iliac arteries. The IVC courses to the right of the abdominal aorta and may be confused for the abdominal aorta by inexperienced operators. The psoas muscle and kidney are posterior–lateral to the abdominal aorta on the left side. The left lobe of the liver is located anterior to the proximal abdominal aorta and acts as the primary acoustic window for this area of the vessel. More caudal, the aorta is posterior to the transverse colon, the pancreas, and proximal duodenum. The distal duodenum crosses over the abdominal aorta distal to the superior mesenteric artery (SMA). Other areas of the small bowel lie anterior to the abdominal aorta as it courses distally to its bifurcation at approximately the 2nd lumbar vertebrae (or umbilicus). Components of the GI system may contain air that can block visualization of the abdominal aorta and its branches.

The abdominal aorta is 10–20 cm in length in adults with a maximum external diameter that is normally <3.0 cm (2.1 cm for men over 55 years and 1.8 cm for women over 55 years). It tapers to approximately 1.5 cm at the bifurcation, but it can be <1.0 cm in diameter in smaller adults. The first large branch of the abdominal aorta is the celiac trunk (Figure 9-2). It comes off the anterior wall of the abdominal aorta approximately 1–2 cm below the level of the diaphragm and courses anteriorly for 1–2 cm before splitting into the common hepatic and splenic arteries. The splenic artery courses to the left and follows the superior border of the pancreas before entering the spleen. The common hepatic artery courses to the right and supplies blood to the liver, stomach, pancreas, and duodenum. The SMA arises from the anterior wall of the aorta approximately 1–2 cm distal from the celiac trunk and courses caudally to supply blood to the small bowel. Both renal arteries come off the lateral wall of the abdominal aorta, just distal to the SMA; the right renal artery courses under the IVC. The paired gonadal arteries (testicular and ovarian) come off the anterior wall distal to the renal vessels. The inferior mesenteric artery comes off the anterior wall 2–3 cm proximal to the iliac bifurcation and supplies blood to the lower GI tract. Both the gonadal vessels and inferior mesenteric artery are usually difficult to visualize by ultrasound and rarely contribute to evaluation and management of the patient.

The bedside scenario when performing an ultrasound examination of the aorta can vary from a calm physician's office to a resuscitation bay crowded with medical personnel working together to provide simultaneous components of patient care. There are a variety of protocols that clinicians may adopt to complete an examination; however, an abbreviated examination of the aorta is usually easy to complete in <1 or 2 minutes. Ideally, evaluate the entire length of the abdominal aorta from the diaphragm to the bifurcation in both the longitudinal and transverse planes.

Examine most patients in the supine position; however, place the patient into the right or left decubital positions if excessive bowel gas is present. Bowel gas is the most common cause for inability to view the abdominal aorta; by placing the patient in either decubitus position, bowel gas may be displaced from the aorta.

Since there are no ribs or other bony structures overlying the abdominal aorta, a variety of transducers can be used for the examination, ranging from curvilinear transducers with large footprints to small phased array transducers typically designed for echocardiography. Most examiners use abdominal “presets” for the examination. Focal zones and frequency may need to be augmented to accommodate the patient's body habitus.

Situate the machine at the patient's right side. Place a liberal amount of gel in the area from the xiphoid process to the umbilicus. By convention, scan the abdominal aorta in the longitudinal (sagittal) plane by pointing the transducer marker dot toward the patient's head and in the transverse (axial) plane by pointing the transducer marker dot toward the patient's right side. The vast majority of imaging of the abdominal aorta is performed on the anterior surface along the patient's midline (Figure 9-3). The critical portion of the abdominal aorta examination (just above the bifurcation) is accomplished in the transverse orientation with the transducer indicator pointed toward the patient's right side.

A curved array transducer is typically used to examine the aorta. Base frequency selection on body habitus to achieve the best balance of resolution and penetration. An average-sized adult is usually scanned at approximately 3.5 MHz. Select a lower frequency for greater penetration in patients with a large body habitus. Scan smaller or thinner adults at resolutions as high as 5 MHz. Standard two-dimensional gray scale imaging is adequate; additional features such as color Doppler and power Doppler are not required but can facilitate differentiation of the abdominal aorta from other structures. Select a sufficient depth at the beginning of the examination until the abdominal aorta is identified. Upon visualizing the aorta, adjust the depth, focal zone, and frequency to optimize the image.

Although not required for all examinations of the abdominal aorta, identification of landmark structures including arterial branches, venous structures, and other abdominal organs can ensure that an adequate segment of the aorta has been imaged. Visualization of this entire length of abdominal aorta is required to exclude AAA. Should its diameter be adequately visualized and appear normal over this length, then a ruptured AAA can be confidently excluded.

There are two primary obstacles to obtaining adequate images of the abdominal aorta: bowel gas and obesity. Bowel gas may require the examiner to move the transducer slightly to either side of the midline to acquire views. Another option is to apply gentle, continuous pressure in order to compress the bowel with the transducer and move bowel gas away from the area of interest. This may require 1–2 minutes of continuous pressure on the abdominal wall with the transducer.

Strategies to overcome obesity include using firm pressure to decrease the distance from the skin–transducer interface to the target organ and rolling the patient in a left lateral decubitus position to swing the pannus away from the midline. Firm pressure on the transducer will allow visualization of the aorta in nearly all patients. Iatrogenic rupture of an AAA by firm pressure during physical examination or an ultrasound examination has not been reported.52

If time permits for a complete examination of the abdominal aorta, initially place the transducer just caudal to the xiphoid process (Figures 9-4 and 9-5; Video 9-1: Aorta). In the transverse plane, an excellent point of reference is the spine. It appears as a posteriorly oriented concave structure that is highly reflective (hyperechoic) and casts a shadow. The abdominal aorta is easily found immediately anterior and slightly to the left of the spine. It is pulsatile and round to ovular in shape. This usually makes it easy to differentiate from the IVC, which is thin-walled, varies in size with respiration, and is often flattened by minimal pressure from the transducer. This view also provides an opportunity to angle the transducer beam into the frontal plane (i.e., toward the head) in order to acquire a subcostal view of the heart. Superficial to the most proximal abdominal aorta will be the subcutaneous tissue and left lobe of the liver. The left lobe of the liver acts as the acoustic window for imaging the proximal portion of the abdominal aorta (See Video 9-1: Abdominal Aorta).

As the transducer is moved more caudal, branches of the abdominal aorta come into view starting with the celiac trunk and then the SMA. The latter is in close proximity to several other vascular structures in the transverse plane (Figure 9-6A). The left renal vein courses under the SMA and over the abdominal aorta joining the IVC. The splenic vein crosses over the SMA along the body of the pancreas before joining the superior mesenteric vein to create the portal vein in the liver. One or both renal arteries and veins may be seen just inferior to the take-off of the SMA coursing posterior and lateral to the kidneys. When the renal arteries are not visible, involvement of an aneurysm with these branch vessels can be predicted on the basis of proximity to the SMA. The renal arteries are likely to be involved if the aneurysm is within 2 cm of the branching point for the SMA.

Since the distal abdominal aorta is the most common location of an AAA, clinicians may opt to examine the distal aorta first in the hemodynamically unstable patient. The distal aorta is best viewed by placing the transducer just superior to the umbilicus in the transverse plane (Figure 9-3). However, there is much to be said for starting in the epigastric region every time and taking the additional seconds to orient to the anatomy before moving distally. The distal transverse view often visualizes only the abdominal aorta and posterior spine as the IVC may be collapsed because of compression from the transducer (Figure 9-6B). Anterior–posterior (AP) diameter from outer wall to outer wall in transverse section provides the most accurate measurement of the diameter of the abdominal aorta. In contrast, measurement of the longitudinal dimension may cause a “cylinder tangent” error (described in Pitfalls section). If a careful measurement is required, then use the freeze frame option on the ultrasound machine along with the caliper measurement software. In some patients, the bifurcation of the aorta can be seen, and iliac arteries followed to exclude iliac artery aneurysm if suspected (Figure 9-7).

In the longitudinal plane at the xiphoid process (Figures 9-8 and 9-9), angle the transducer from left to right to image the proximal IVC and the aorta. Some clinicians utilize a “sniff” test to help with differentiation of these structures as well. By having the patient quickly sniff, a sudden drop in thoracic pressure is created that pulls blood from the IVC into the thorax and causes the IVC to collapse. In addition, the IVC is often seen directly entering the right atrium of the heart (Figure 9-10), while the abdominal aorta will demonstrate the celiac trunk and SMA exiting from its anterior surface. The splenic vein and left renal vein may be seen in their short axes above and below the SMA, respectively, and the left renal vein may be seen coursing under the IVC. When rotating the transducer from a transverse to longitudinal view of the aorta, avoid inadvertently sliding the transducer over the IVC. In some patients, the IVC may appear pulsatile due to cardiac motion.

A final option for ultrasound imaging of the aorta is the coronal view. Place the transducer in the right anterior axillary line and, using the hepatic acoustic window, scan the aorta in the coronal plane. Initiate the examination with the image display at maximum depth. This will yield an image with the IVC toward the top of the screen and the aorta lying deeper (Figures 9-11 and 9-12).

Abdominal Aortic Aneurysm

The primary abnormality is aneurysmal enlargement of the abdominal aorta. This is most frequently seen in the transverse view as an aorta >3.0 cm in diameter (Figure 9-13). Aneurysmal dilation is usually fusiform, resulting in a uniform concentric enlargement of the circumference (Figure 9-14). Localized outpouching of a segment of the aortic wall results in the more unusual saccular aneurysm formation (Figure 9-15). Aneurysmal dilatation is most often confined to the infrarenal aorta and usually terminates proximal to the bifurcation. Contiguous thoracoabdominal aneurysm occurs in a minority of cases (2%) and involves the thoracic aorta in addition to the abdominal aorta, including the segment involving the celiac, superior mesenteric, and renal arteries. The iliac arteries are involved in some patients with AAA (Figure 9-16A), and occasionally, iliac artery aneurysms occur in an isolated fashion. More than 90% of AAAs occur in the distal abdominal aorta, inferior to the renal arteries. An AAA may rarely be detected only in the proximal abdominal aorta (Figure 9-16B). Rupture most commonly occurs into the left retroperitoneum. Less commonly, intraperitoneal rupture can occur.94 Ultrasonography is inadequate to demonstrate the presence of extraluminal retroperitoneal blood associated with rupture, which is found with a sensitivity <5%.95 However, in the appropriate clinical setting, a large AAA should be considered ruptured until proven otherwise.52,96

Intraluminal Thrombus

With increasing diameter, the laminar flow rate decreases at the periphery, resulting in blood stagnation and thrombus formation. This intraluminal thrombus is well visualized on ultrasound and is more common anteriorly and laterally but may be circumferential (Figure 9-13). Thrombus is found in both ruptured and unruptured AAAs. It is not an indication of rupture or dissection, and is not a false lumen. Complete occlusion of the abdominal aorta has also been described and has been successfully diagnosed with point-of-care ultrasound.97

Hemoperitoneum

Rupture into the peritoneal cavity may present with acute hemoperitoneum that may be visualized with the right intercostal oblique window of the FAST examination (Figure 9-17) or other windows.

Tortuosity of the Aorta

Variations in the position and size of vessels are common. The aorta often becomes tortuous with age. This can cause difficulty with following the course of the vessel and finding the correct plane for transverse and longitudinal views (Figure 9-18).

Contained Aortic Rupture

A contained rupture of an AAA is not commonly diagnosed with ultrasound. When present, it may be seen as a hypoechoic mixed density area (from contained hemorrhage and hematoma) surrounding the aorta (Figure 9-19).

Hydronephrosis

A large AAA can cause secondary complications by compressing surrounding structures. Compression of the left ureter can lead to hydronephrosis and eventually to a perinephric urinoma from calyceal rupture (Figure 9-20). Hydronephrosis is, of course, a much more common finding in patients being imaged for suspected ureterolithiasis. Thus, the finding of hydronephrosis in a patient with AAA risk factors and flank pain should not reassure the clinician that the cause is an obstructing ureteral stone.

Acute Abdominal Aortic Dissection

This disease entity may be confused with ruptured AAA and can occur with or without a coexisting aneurysm. Only 2%–4% of patients with an aortic dissection experience it in the abdominal aorta. The presenting symptoms are similar to those seen in ruptured AAA but may mimic other disease entities such as pancreatitis.98 Occasionally, clinicians will encounter mild aortic dilation caused by an aortic dissection and mistakenly diagnose an early AAA thought to be too small for rupture. Care should thus be taken to examine for a flap in the lumen (Figure 9-21). Utilizing color Doppler will occasionally show flow in only one portion of the abdominal aorta in transverse orientation. Even if the flap cannot be well visualized, a finding of mild aortic dilatation in the correct clinical scenario should raise the suspicion for an abdominal aortic dissection.

Aortovenous Fistula

Formation of an arteriovenous fistula occurs when an AAA ruptures into an adjacent vein; the left renal vein or the IVC is most often involved. Because these aneurysms are usually large (11–13 cm on average), a pulsatile mass can often be palpated on physical examination. The presenting symptoms are similar to those seen in AAA rupture. An ultrasound examination demonstrating a large AAA, along with a CT scan documenting a retroaortic left renal vein and an IVP showing absence of left renal filling, may help confirm the diagnosis.

Isolated Iliac Artery Aneurysm

Iliac artery aneurysms are present in up to 20% of AAAs but are found in the absence of AAA in 2–7% of cases. Thus, include careful examination of the bifurcation of the abdominal aorta (found posterior to the umbilicus) as well as the proximal iliac arteries in every bedside aorta ultrasound exam. The normal diameter of the iliac arteries is about 1 cm. Aneurysms measure >1.5 cm and elective repair is generally considered at 3.5 cm.99

Endoleak

In a patient with a previously grafted AAA, abdominal pain may occur from expansion of the aneurysm sac due to leakage of blood through or around the endoluminal graft. The ability to detect endoleak by ultrasound is limited, but if comparison images are available, an expanding aneurysm sac post-repair should prompt further investigation by CT. If no comparison images are available, an endoleak may be definitively diagnosed by demonstrating flow out of the graft by color Doppler.94

1. Contraindication. The only absolute contraindication to performing this ultrasound examination of the abdominal aorta is if it delays clearly indicated, immediate surgical intervention.

2. Overreliance on examination. The finding of an enlarged aorta alone is not sufficient to diagnose rupture of the abdominal aorta. There are no reliable ultrasound findings of retroperitoneal hematoma associated with the most common form of AAA rupture. However, the finding of AAA (especially with a diameter >5 cm) accompanied by other clinical manifestations, such as acute hemodynamic compromise, strongly suggests the diagnosis of AAA rupture. Correlate the location of the aneurysm with the SMA origin and recognize that if dilation is within 2 cm inferior to the SMA, the renal arteries are likely to be involved. When hemodynamically stable, patients with contained rupture may be diagnosed by definitive imaging prior to surgical intervention.

3. Patient factors limiting imaging. Obesity and bowel gas always render ultrasound imaging more difficult. Failure to determine the involvement of the major branches of the aorta makes operative planning more difficult for the surgeon. When bowel gas or other technical factors prevent a complete systematic real-time scan through all tissue planes, identify and document these limitations. Such limitations may mandate further evaluation by alternative methods, as clinically indicated.100

4. Errors in imaging. Two common errors in imaging must be avoided. First, the physician must take care not to inadvertently sweep the plane of the beam into a right parasagittal plane, which may result in a long-axis view of the IVC. The IVC here is thin walled and easily compressed, and can be mistaken for the abdominal aorta. The examiner can avoid this error by visualizing the aorta and IVC in the transverse plane (Figure 9-22), or when in longitudinal plane by visualizing the celiac trunk and SMA at the proximal abdominal aorta (Figure 9-23). The second error may result from the “cylinder tangent” effect (Figure 9-24). Limited window accessibility may result in a situation in which the plane of the beam enters the cylinder of the aorta at a tangent and displays an incorrect AP diameter. This is not an artifact error but an operator error. Measure the aorta in both sagittal and transverse planes to avoid this error.

5. A small aneurysm does not preclude rupture. A patient with symptoms and signs consistent with acute AAA and an aortic diameter >3.0 cm should have this diagnosis (or alternative vascular catastrophes) fully investigated.

6. Large paraaortic nodes may be confused for AAA. Large paraaortic nodes usually occur anterior to the aorta, but may be posterior, displacing the aorta away from the vertebral body. They can be distinguished by an irregular nodular shape, which is identifiable in real time. If color flow Doppler is utilized, the nodes will not demonstrate luminal flow.

Case 1

Patient Presentation

A 65-year-old man presented to the ED after a witnessed syncopal episode. Upon awaking in the morning, the patient complained of feeling weak and constipated. The patient had a history of well-controlled hypertension.

On physical examination, the patient was awake, alert, and oriented. His blood pressure was 110/50 mm Hg, pulse 100 beats per minute, respirations 18 per minute, and temperature 98.9°F. He appeared pale and slightly diaphoretic. His lungs were clear to auscultation, neck veins flat, and abdomen soft and nontender with no peripheral edema. The remainder of his physical examination was unremarkable.

Management Course

On arrival, two large-bore IVs were established in the upper extremities, while the primary examination was simultaneously performed. As part of his secondary survey, a rapid cardiac view by the subcostal window revealed a hyperdynamic heart. Repositioning of the transducer immediately revealed an enlarged abdominal aorta with an AP diameter of 7.2 cm (Figure 9-25). There was no free intraperitoneal fluid. Surgical consultation was initiated.

Reassessment revealed a decline in blood pressure to 80/50 mm Hg. No other diagnostic maneuvers were employed and the patient was transported directly to the operating room for exploratory laparotomy. Operative findings included a ruptured 7.4 cm AAA that was successfully grafted.

Commentary

Case 1 is an example of a patient presenting to the ED with hemodynamic alteration from a ruptured AAA. This type of syncope followed by near-normalization of vital signs with subsequent decline in perfusion parameters is one of the most common presentations for ruptured AAA. This patient exemplifies an hemodynamically unstable profile that requires limited diagnostic evaluation and rapid surgical intervention. It is important to note that the same ultrasound examination was used to demonstrate marked global hyperkinesis of the heart, essentially excluding left ventricular failure as a cause of gradual hemodynamic decline. This was done before performing either an ECG or a chest radiograph.

Case 2

Patient Presentation

A 74-year-old man presented to the ED at 2 AM, complaining of left “hernia” pain. The patient said that he had been diagnosed with a left inguinal hernia more than 10 years earlier, and he had decided against surgical repair, because it did not cause him pain. He said that he began having left groin pain last night after supper and it had gradually worsened. He denied any other medical history.

On physical examination, the patient was awake and alert and was in no distress. His blood pressure was 160/80 mm Hg, pulse rate 85 beats per minute, respirations 20 per minute, and temperature 99.0°F. He had a left inguinal hernia that was moderately tender to palpation. The hernia sac was firm and protruded into his scrotum about 3–4 cm and could not be reduced on examination. His abdomen was mildly obese and nontender. The remainder of his examination was unremarkable.

Management Course

An IV line was established and the patient was given fentanyl 50 micrograms IV with good relief of his pain. A second attempt to reduce the hernia was unsuccessful. Basic laboratory tests, including a urinalysis, were unremarkable and a plain radiograph revealed no signs of bowel obstruction. The on-call surgeon was consulted because the patient was thought to have an incarcerated inguinal hernia. While awaiting surgical consultation, the patient became diaphoretic and dizzy, his blood pressure dropped to 100/60 mm Hg, and he began complaining of left flank pain. A point-of-care ultrasound examination was performed in the ED and he was noted to have an 8-cm AAA (Figure 9-26). The surgeon was called again and informed of the new information. The patient had an additional large-bore IV placed and was aggressively resuscitated and taken to the operating room within 20 minutes. Despite these efforts, he died on the operating table.

Commentary

This case demonstrated a complex presentation of a ruptured AAA. The patient's long-standing inguinal hernia convinced both the patient and the emergency physician that the etiology of his pain was the hernia. It is common to delay or miss the diagnosis of ruptured AAA because referred pain to the groin, back, or flank is thought to be caused by another disease process. In this case, the physician did not initially consider the diagnosis of ruptured AAA because of the patient's atypical symptoms and normal vital signs.

Case 3

Patient Presentation

An emergency physician was giving his 62-year-old father a tour of his ED. While showing off for his father, he performed a bedside abdominal aortic ultrasound examination on his father and was surprised to discover a 4.2-cm AAA (Figure 9-27). His father had a history of smoking, but was asymptomatic and had no other medical history or risk factors.

Management Course

The AAA was monitored every 6 months with serial ultrasound examinations. Two years after it was initially discovered, the AAA measured 5.2 cm in AP diameter. The patient was referred to a surgeon who advised that he delay elective repair until the AAA became 5.5 cm. The patient saw another surgeon for a second opinion and was advised to have the AAA repaired as soon as possible. The second surgeon also recommended having an open repair rather than an angiographic stent because he was otherwise healthy and a good surgical candidate. The patient had an open repair and placement of a Gortex graft without complications and had an uneventful recovery. He was able to play golf just a few months later and continues to be asymptomatic.

Commentary

This case demonstrated the importance of screening asymptomatic patients who are at risk for AAA. Men over 60 years of age who have ever smoked are at higher risk for AAA (up to 10%). There are over 50,000 elective AAA repairs per year in the United States, with a very low surgical mortality rate. Conversely, the mortality rate after AAA rupture is 80%.

The authors would like to thank Ben Dolan, MD, and Scott Joing, MD, for their contributions to this chapter. The authors additionally thank Dave Plummer, MD, for his contributions to this chapter in previous editions.