Achalasia

Background: Achalasia is an esophageal motor disorder characterized by increased lower esophageal sphincter (LES) pressure, diminished-to-absent peristalsis in the distal portion of the esophagus composed of smooth muscle, and lack of a coordinated LES relaxation in response to swallowing.

Primary achalasia is the most common subtype and is associated with loss of ganglion cells in the esophageal myenteric plexus. These important inhibitory neurons induce LES relaxation and coordinate proximal-to-distal peristaltic contraction of the esophagus.

Secondary achalasia is relatively uncommon. This condition exists when a process other than intrinsic disease of the esophageal myenteric plexus is the etiology. Examples of maladies causing secondary achalasia include certain malignancies, diabetes mellitus, and Chagas disease.

Sir Thomas Willis first described achalasia in 1674. Willis successfully treated a patient by dilating the LES with a cork-tipped whalebone. Not until 1929 did Hurt and Rake first realize that the primary pathophysiology resulting in achalasia was a failure in LES relaxation.

Pathophysiology: The exact etiology of achalasia is not known. The most widely accepted current theories implicate autoimmune disorders, infectious diseases, or both. The last decade has witnessed much progress in the understanding of the cellular and molecular derangements in achalasia.

Degeneration of the esophageal myenteric plexus of Auerbach is the primary histologic finding. However, with early achalasia, a mixed inflammatory infiltrate of T cells, mast cells, and eosinophils is found in association with myenteric neural fibrosis and with a selective loss of inhibitory postganglionic neurons from the Auerbach plexus. In these patients with early achalasia, neurons of the myenteric plexus are relatively well preserved.

The inhibitory neurons produce nitric oxide (NO) and vasoactive intestinal peptide (VIP). NO and VIP are inhibitory neurotransmitters responsible for relaxation of the LES and for coordinated esophageal peristalsis. The loss of inhibitory neurons allows unopposed excitatory stimulation by postganglionic cholinergic neurons of the Auerbach plexus, which leads to a failure in LES relaxation and, eventually, to aperistalsis of the distal esophagus due to loss of the esophageal body latency gradient. Essentially, this means that this portion of the esophagus is unable to relax and subsequently generate a proper, sequential peristaltic wave.

Clinically important features defined by this pathophysiology include the following:

• Peristalsis in the distal smooth muscle segment of the esophagus may be lost. Contractions occur, but they are weak; simultaneous; uncoordinated; and, therefore, nonpropulsive.
• The LES fails to relax, either partially or completely.
• LES pressure is elevated in some patients.
• The coordination of LES relaxation in response to swallowing and esophageal contraction is lost.

Frequency:

• In the US: Achalasia is a relatively uncommon disease. In the United States, the incidence and prevalence approximate international rates.

• Internationally: Mayberry and Rhodes described the demographics of achalasia for the city of Cardiff, England, in 1926-1977 (Mayberry, 1980). The incidence of achalasia is 4-6 cases per million persons. The disease prevalence is approximately 8 cases per million population. Mayberry and Atkinson also estimated an annual incidence of 1-2 cases per 200,000 persons in the area of Nottingham, England (Mayberry, 1985). Rates may be slightly higher in South America because of the prevalence of Chagas disease there.

Mortality/Morbidity:

• Failure of the LES to relax and decrements in esophageal peristalsis lead to stasis and the retention of foodstuffs and upper gastrointestinal secretions in the esophagus. The primary morbidity associated with this effect is esophagitis, which is readily recognized on endoscopic examination.

• The mass of pooled secretions and solid materials places the patient at risk for aspiration. According to Vantrappen and associates, as many as 30% of patients with achalasia report nocturnal coughing episodes (Vantrappen, 1971). Nocturnal coughing can lead to aspiration pneumonia, which is a serious complication.

• Patients with achalasia are at increased risk for esophageal carcinoma, compared with the general population. According to Wychulis et al and Lortat-Jacob et al, 2-7% of patients with achalasia have an esophageal carcinoma (Wychulis, 1971; Lortat-Jacob, 1969). Esophageal carcinoma and a greatly dilated esophagus are found more frequently in patients with long-standing disease than in patients with early-stage achalasia.

Race: No racial predilection has been described for achalasia.

Sex: Achalasia has no sex predilection.

Age: The incidence of achalasia peaks in those aged 20-40 years. The disease has been diagnosed in infants and in patients well into their 80s (Nihoul-Fekete, 1991).

Anatomy: The average length of the esophagus is 25 cm. As illustrated by Clemente, the esophagus begins just distal to that portion of the inferior pharyngeal constrictor muscle that originates on the cricoid cartilage (Clemente, 1981). The esophagus terminates at the gastroesophageal junction. By convention, the esophagus is typically divided into 3 segments: (1) the cervical esophagus, (2) the thoracic esophagus, and (3) the abdominal esophagus.

The esophageal musculature is composed of an outer longitudinal layer and an inner circular layer. According to Meyer and colleagues, the esophageal musculature is striated in the proximal 5% of the organ (Meyer, 1986). The following 30-40% contains both striated and smooth muscle. The distal 50-60% is composed solely of smooth muscle, which is relevant because the denervation that is the hallmark of achalasia affects the smooth-muscle segment of the esophagus.

Esophageal contraction and peristalsis are mediated by parasympathetic fibers traveling in the vagus nerves. The dorsal motor nucleus of the vagus nerve is responsible for controlling the smooth muscle. In contrast, the nucleus ambiguus controls skeletal muscle.

The esophagus contains 2 major nerve plexuses: the Auerbach plexus and the Meissner plexus. The Auerbach, or myenteric, plexus is embedded between the longitudinal and circular layers of esophageal muscle. Neurons of the Auerbach plexus receive input from vagal preganglionic efferent fibers responsible for smooth muscle control. The Meissner plexus can be found in the submucosa of the esophagus. This plexus of nerves carries afferent information from the esophagus to the vagal parasympathetic and thoracic sympathetic nerves, then onward to the central nervous system.

Clinical Details: Dysphagia is the most common presenting symptom in patients with achalasia. The ingestion of either solids or liquids can result in dysphagia, though dysphagia for solids is more common. Emotional stress and the ingestion of cold liquids are well-known exacerbating or precipitating factors. The natural history varies. Some patients notice that the dysphagia reaches a certain point of severity and then stops progressing. In others, the dysphagia continues to worsen, resulting in decreased oral intake, malnutrition, and inanition. Therefore, weight loss is included in the complex of signs and symptoms associated with achalasia, and it is usually a sign of advanced esophageal disease.

Approximately 25-50% of patients with dysphagia report episodes of chest pain, which are frequently induced by eating. Typically, chest pain is described as being retrosternal; this is a more common feature in patients with early or so-called vigorous achalasia. As the disease progresses and as the esophageal musculature fails, chest pain tends to abate or disappear.

As many as 80-90% of patients with achalasia experience spontaneous regurgitation of undigested food from the esophagus during the course of the disease. Some learn to induce regurgitation to relieve the retrosternal discomfort related to the distended esophagus.

As the disease progresses, the likelihood that aspiration will occur increases. As a result, some patients may present with signs or symptoms of pneumonia or pneumonitis. Lung abscesses, bronchiectasis, and hemoptysis are some of the more severe pulmonary consequences of achalasia-associated aspiration.

Patients with achalasia are at increased risk for esophageal cancer. When esophageal cancer occurs, it is usually found in patients with a long history of achalasia.

Preferred Examination: The radiologic examination of choice in the diagnosis of achalasia is a barium swallow study performed under fluoroscopic guidance.

A diagnosis of achalasia supported by the results of radiologic studies must always be confirmed by performing upper gastrointestinal endoscopy and esophageal manometry. These tests allow the direct evaluation and inspection of the esophageal mucosa and an objective measurement of esophageal contractility.

Endoscopy, supplemented by biopsy when necessary, helps in excluding gastroesophageal malignancies, fungal or bacterial infections, and other disease processes that can mimic achalasia.

Manometry must be considered the criterion standard for diagnosis of the disease. Manometric findings consistent with achalasia include incomplete LES relaxation, which is present in more than 80% of patients; elevated LES pressure, which is present in some patients; and diminished-to-absent peristalsis in the distal esophagus.

If manometric findings are normal in a patient with clinical symptoms or radiographic evidence of achalasia, a condition termed pseudoachalasia may be present. Causes of pseudoachalasia include esophageal and gastric malignancies and other tumors involving distal esophagus or LES. In patients with these conditions, endoscopy with biopsy analysis and CT can be helpful.

Limitations of Techniques: A fluoroscopically guided barium swallow study that demonstrates 1 or more findings (see X-ray) is highly suggestive of achalasia. However, a definitive diagnosis can be made only by means of esophageal manometry, preferably with the addition of upper endoscopy.

Conversely, normal findings on barium swallow study do not completely exclude achalasia, especially in its early stages. This situation is when esophageal manometry is most valuable, because the physiologic derangements associated with achalasia precede the development of the anatomic findings discernible by using radiographic studies.

RADIOGRAPH

Findings: Plain chest radiographs occasionally offer clues in the diagnosis of achalasia. A double mediastinal stripe is occasionally depicted. An air-fluid level can be seen in the esophagus; this is frequently retrocardiac. Owing to the paucity of air progressing through the hypertensive LES, the gastric air bubble may be small or absent.

Features of achalasia depicted at barium study under fluoroscopic guidance include the following:

• Failure of peristalsis to clear the esophagus of barium with the patient in the recumbent position
• Antegrade and retrograde motion of barium in the esophagus secondary to uncoordinated, nonpropulsive, tertiary contractions
• Pooling or stasis of barium in the esophagus when the esophagus has become atonic or noncontractile (which occurs late in the course of disease)
• LES relaxation that is incomplete and not coordinated with esophageal contraction
• Dilation of the esophageal body, which is typically maximal in the distal esophagus
• Tapering of the barium column at the unrelaxed LES, resulting in the bird beak sign
• Associated epiphrenic diverticula (possible finding)

According to Schima and coworkers, approximately 90% of patients undergoing barium swallow examination for suspected achalasia have some esophageal dilation and a classic bird beak deformity (Schima, 1992).

A recent study from El-Takli and colleagues (2006) contradicts this claim. These investigators reviewed the barium-contrast radiographs of 51 patients with manometrically diagnosed achalasia. In only 58% of these studies was achalasia mentioned as a diagnostic possibility by the interpreting radiologist. The radiographs were then provided to an expert gastrointestinal radiologist, mixed in with normal control studies. This expert determined that typical radiological features of achalasia were absent in 50% of the studies performed on achalasia patients. The authors concluded that barium-contrast radiography is not sensitive for the diagnosis of achalasia, frequently due to the lack of characteristic and detectable radiologic features.

Kostic and coinvestigators (2005) published preliminary data on timed barium esophagograms in patients with achalasia and in normal controls. Subjects were fasted and then given 250 mL of low-density barium sulfate suspension orally. Radiographs were made 1, 2, and 5 minutes after the start of barium administration. The height and width of the barium column and the rate of change over time were recorded. The study was repeated in all subjects after an approximate 1-week interval. The controls uniformly achieved complete esophageal emptying within 2 minutes. The height and width of the barium column and the rate of esophageal emptying were all markedly abnormal in the achalasia patients. The static data were very reproducible between studies, but the functional (esophageal emptying) data were not, with a coefficient of correlation of only 0.50. The authors concluded that further studies were necessary before clinical usefulness of the timed barium esophagograms could be confirmed.

Degree of Confidence: Chest radiographic findings have low sensitivity and specificity for the diagnosis of achalasia. If suspected, achalasia should be confirmed with other radiologic examinations, such as barium swallow study under fluoroscopy, and with upper gastrointestinal endoscopy and manometry.

False Positives/Negatives: No normal variants exist; however, several disease processes can mimic achalasia on chest radiographs or barium swallow studies. These include colon adenocarcinoma, esophageal carcinoma, gastric carcinoma, non–small cell lung cancer, thoracic scleroderma, amyloidosis, Chagas disease, collagen-vascular disease, and lymphoma.

According to Gockel and colleagues (2005), pseudoachalasia, caused by carcinomas and other disease processes or iatrogenic conditions involving the cardia and gastroesophageal junction, may be difficult to differentiate from achalasia. Pseudoachalasia may be indistinguishable from achalasia when conventional endoscopic, manometric, and radiologic diagnostic means are used. In their report, they described that pseudoachalasia was caused by primary malignancies in 53.9%, secondary malignancies in 14.9%, and benign lesions in 12.6% of the 264 cases in the series. The remainder of the cases (11.9%) were due to sequelae of operations involving the distal esophagus or proximal stomach.

Esophageal motor abnormalities can result from tumor infiltration of the esophageal wall and associated nerve damage. If mucosal irregularity or mass effect is present at the tapered gastroesophageal junction, pseudoachalasia should be considered. The use of amyl nitrite can often be helpful, as the LES relaxes in achalasia but remains fixed in pseudoachalasia.

Acetabulum, Fractures

Background

Most acetabular fractures occur in the setting of significant trauma secondary to either a motor vehicle accident or a high-velocity fall. Blunt force is exerted on the femur, passes through the femoral head, and is transferred to the acetabulum. The direction and magnitude of the force, as well as the position of the femoral head, determine the pattern of acetabular injury. The determination of the pattern of injury is key to the classification of an acetabular fracture. Once the acetabular fracture is classified, appropriate therapy can be planned and implemented.

Pathophysiology

One function of the acetabulum is to provide a means of transferring weight-bearing forces from the appendicular skeleton to the axial skeleton via the acetabulum's articulation with the femoral head. The femoral head also transfers high-energy forces to the acetabulum in the setting of trauma. The pattern of acetabular injury is determined by the position of the femoral head at the time of the traumatic event. When the femoral head is rotated internally, the force is transferred to the posterior column. When the femoral head is rotated externally, the force is directed toward the anterior column. If the femoral head is adducted, the force is transmitted to the acetabular roof; if it is abducted, the force is directed inferiorly.

The direction of the force also determines which part of the acetabulum is injured. An anterior force applied to the femoral head is transmitted to the posterior wall and column. Conversely, a posterior force affects the anterior wall and column. A force to the lateral aspect of the femoral head is directed toward the medial wall of the acetabulum, often resulting in transverse acetabular fractures.

Frequency

United States

Table 1. Relative Frequency of Acetabular Fracture Types

Fracture Type	Letournel1* (%)	Matta2** (%)	Dakin et al3† (%)
Both-column	27.9	33.3	14.1
Transverse with posterior wall	20.6	23.5	35.3
Posterior wall	22.4	8.6	12.9
T-shaped	5.3	12.2	3.5
Transverse	3.7	3.5	8.2
Anterior column	3.9	4.7	1.2
Anterior column with posterior hemitransverse	8.8	5.9	3.5
Posterior column with posterior wall	3.5	3.9	18.8
Posterior column	2.3	3.1	1.2
Anterior wall	1.6	1.2	1.2

*n = 567.

**n = 255.

† n = 85.

Mortality/Morbidity

• Associated injuries
• • Significant trauma is required to cause a fracture of the acetabulum. Therefore, acetabular fractures are most often observed in the setting of major trauma, in which injuries elsewhere in the body are common.
  • Intracranial, spinal, intrathoracic, and intra-abdominal injuries often are observed in conjunction with acetabular fractures.
  • Pelvic ring and extremity fractures also are common in patients with acetabular fractures.
  • Bladder injury and clinically significant pelvic hemorrhage are not routinely observed in the setting of acetabular fracture unless a concomitant pelvic ring injury also is present.
• Complications of acetabular fracture include the following:
• • Immediate posttraumatic complications include injuries to the sciatic, femoral, or superior gluteal nerves.
  • Immediate postsurgical complications include nerve injuries, such as sciatic, femoral, and superior gluteal nerve injuries; wound infection; and thromboembolic disease.
  • Late complications include heterotopic ossification, osteonecrosis (avascular necrosis) of the femoral head or acetabular fracture fragment, chondrolysis, posttraumatic osteoarthritis, and acetabular implant failure.

Age

Elderly patients and persons with osteoporosis may occasionally have an acetabular fracture as a result of low-energy trauma, such as a fall from a standing height.

Anatomy

Gross anatomy

The acetabulum is formed from 3 ossification centers; the ilium, ischium, and pubis each contribute to its development at the triradiate cartilage. The important anatomic components of the acetabulum are the columns, walls, dome, and quadrilateral plate. The acetabulum is divided into 2 columns: anterior and posterior. The 2 columns are described as having the shape of an inverted Y, or of the Greek letter lambda (l).

The anterior column is the larger of the 2 columns. It begins at the iliac wing and extends down the anterior portion of the acetabulum to incorporate the superior pubic ramus. The posterior column begins at the sciatic notch and extends down the posterior acetabulum into the ischium. Both columns are attached to the axial skeleton by the sciatic buttress, which connects the acetabulum to the sacroiliac joint. The column concept is appreciated more easily on the lateral view (see Image 1).

The posterior wall is larger than the anterior wall. The lateral portion of either wall is termed the acetabular rim. The walls help to stabilize the hip joint. The quadrilateral plate is the medial wall of the acetabulum. The dome of the acetabulum is the superior aspect that carries most of the weight-bearing forces. The obturator ring is an important landmark because some acetabular fractures spare the ring, while others disrupt it. The iliac wing is considered part of the anterior column.

Radiographic anatomy

The anteroposterior (AP) view of the pelvis is the primary tool for radiographic evaluation of the acetabulum (see Images 2-3). The iliopectineal, or iliopubic, line is the radiographic landmark for the anterior column. It begins at the sciatic notch and travels along the superior pubic ramus to the symphysis pubis. The ilioischial line demarcates the posterior column. It also begins at the sciatic notch, coursing inferiorly to the medial border of the ischium. The ilioischial line should pass through the acetabular teardrop. If it does not overlap the teardrop, the ilioischial line and, thus, the posterior column are disrupted.

The iliac wing is considered to be part of the anterior column. An iliac wing fracture in the setting of an acetabular injury indicates anterior column involvement. An iliac oblique radiograph provides a better view of the iliac wing. The posterior wall of the acetabulum is more visible than the anterior wall on the AP view because of its more lateral position. The anterior wall can be difficult to appreciate on the AP view. The obturator oblique view better depicts the posterior wall, and the iliac oblique view better depicts the anterior wall. The integrity of the obturator ring is an important feature to recognize. Certain fracture patterns (such as those of column and T-shaped fractures) characteristically include fractures through the obturator ring.

The oblique, or Judet, views of the pelvis are named relative to the side of interest (see Images 4-5). For example, if the acetabular fracture is on the left side, the views are named with reference to the left side. The left posterior oblique radiograph displays the iliac wing en face; therefore, this view is termed the left iliac oblique view. The right posterior oblique radiograph shows the obturator ring en face; therefore, this view is the left obturator oblique view. The iliac oblique view clearly demonstrates the iliac wing, sciatic notch, and ischial spine. In addition, the posterior column and anterior wall of the acetabulum are seen in profile. The obturator oblique radiograph provides the best depiction of the obturator ring and shows the anterior column and posterior wall in profile.

Clinical Details

Fractures of the acetabulum are most commonly classified according to the system described by Judet and colleagues.⁴ The system is based on the orientation of the fractures and the structures involved. In this system, the orientation of the fracture is based on its depiction on a lateral view of the acetabulum. In order to arrive at the correct classification, AP and oblique (Judet) radiographs of the pelvis are obtained and analyzed. Some authors have questioned the necessity of oblique views of the pelvis in the age of multidetector CT scanning. ⁵ Harris and colleagues have proposed a new classification system based on the multidetector CT scan appearance.^{6, 7} Other authors have defended the utility of the standard radiographic series in the evaluation of acetabular fractures.⁸ The Judet system will be presented in the remainder of this article.

In the system described by Judet and colleagues, 10 patterns of acetabular fracture are defined. The 10 patterns are divided into 5 elementary and 5 associated patterns (see Image 6). Elementary patterns include fractures with a single fracture orientation, whereas associated patterns usually involve combinations of the elementary fractures. Elementary patterns include anterior wall, posterior wall, anterior column, posterior column, and transverse fractures. Associated patterns include both-column fractures, posterior column fractures with posterior wall fractures, transverse fractures with posterior wall fractures, T-shaped fractures, and anterior column fractures with posterior hemitransverse fractures. For simplicity, the 10 patterns can be grouped into 3 categories: wall, column, and transverse fractures. Some fractures fit into 2 categories. The following fractures are indicated by pattern type:

• Wall fractures
• • Anterior wall
  • Posterior wall
  • Posterior column with posterior wall (also a column fracture)
  • Transverse with posterior wall (also a transverse fracture)
• Column fractures
• • Anterior column
  • Posterior column
  • Both-column
  • Posterior column with posterior wall (also a wall fracture)
  • Anterior column with posterior hemitransverse (also a transverse fracture)
• Transverse fractures
• • Transverse
  • T-shaped
  • Transverse with posterior wall (also a wall fracture)
  • Anterior column with posterior hemitransverse (also a column fracture)

Fracture patterns

Isolated acetabular wall fractures typically do not involve the weight-bearing articular portion of the acetabulum (see Image 6). Fractures of the posterior wall are more common than are those of the anterior wall because of the preponderance of posteriorly directed forces responsible for acetabular fractures. Posterior wall fractures may occur in isolation (see Images 10-12) or in combination with posterior column or transverse fractures. Anterior wall fractures are rare (see Image 9).

Both-column fractures are the most common acetabular injury. As the name implies, the anterior and posterior columns are involved (see Image 6). On AP radiographs, a disruption of the iliopectineal and ilioischial lines, as well as the obturator ring, can be seen (see Image 24). An iliac wing fracture may be seen on the AP view, but often, it is appreciated only on the iliac oblique radiograph (see Image 25). The pathognomonic spur sign (see Radiograph Findings) is present on the obturator oblique view (see Image 26) and confirmed on a computed tomography (CT) scan (see Images 27-29).

Isolated anterior and posterior column fractures are uncommon. Anterior column fractures disrupt the iliopectineal line while preserving the ilioischial line. Conversely, posterior column fractures disrupt the ilioischial line but not the iliopectineal line (see Images 18-23). Column fractures divide the acetabulum into front and back halves (see Image 7). The posterior column fracture with a posterior wall fracture has the features of each of its components (see Image 6). The slightly more common anterior column fracture with a posterior hemitransverse fracture is the most complex acetabular fracture to classify.

The combination of column fractures and transverse fractures can be difficult to appreciate radiographically (see Image 30). The iliopectineal and ilioischial lines are broken, and an iliac wing fracture should be evident. Unlike the both-column fracture, which shares these features, the obturator ring is intact and the spur sign is not present. On CT scans, the anterior column and the posterior transverse fracture planes can be appreciated (see Image 31).

Transverse fractures are transverse because of their appearance when the acetabulum is examined from the lateral view (see Image 6). The iliopectineal and ilioischial lines are interrupted, but the obturator ring is spared. On CT scans, the fracture is oriented vertically (front to back).

Transverse fractures divide the acetabulum into top and bottom halves, as seen on the lateral view of the acetabulum (see Image 7). The transverse fracture with a posterior wall fracture is a common fracture that incorporates the features of transverse and posterior wall elementary fractures (see Images 13-15). The T-shaped fracture is a fairly common acetabular injury. This fracture has the characteristics of an elementary transverse fracture with the addition of a medial acetabular wall fracture extending through the obturator ring (see Images 16-17). The anterior column with posterior hemitransverse fracture is discussed earlier.

In a study by Brandser and colleagues, the following 3 most common types of acetabular fracture accounted for roughly two thirds of all fractures: both-column fractures, transverse fractures with posterior wall fractures, and posterior wall fractures.² This number increased to 90% when the next 2 most common fracture types were considered: T-shaped and transverse fractures. The frequency of the fractures types is as follows:

• Commonly occurring acetabular fractures (90%)
• • Both-column
  • Transverse with posterior wall
  • Posterior wall
  • T-shaped
  • Transverse
• Uncommonly occurring acetabular fractures (10%)
• • Anterior column
  • Anterior column with posterior hemitransverse
  • Posterior column with posterior wall
  • Posterior column
  • Anterior wall

Preferred Examination

AP radiography of the pelvis is used in the initial radiographic assessment of patients with major trauma that is suggestive of pelvic and/or acetabular injury (see Images 2-3). Images are obtained with the patient in the supine position and with the radiographic beam passing in an AP direction. Abnormalities depicted on the AP pelvis radiograph direct the need for the next set of radiographs. Acetabular fractures are imaged by using oblique (ie, Judet) views of the pelvis. Pelvic ring fractures are imaged by using inlet and outlet views of the pelvis (see Pelvic Ring Fractures).

Oblique, or Judet, radiographs of the pelvis are obtained with the patient in the left posterior oblique and right posterior oblique positions (see Images 4-5). The patient should be at a 45º angle relative to the radiographic beam, which remains perpendicular to the cassette. This technique results in 2 orthogonal radiographs of the pelvis. The patient must be moved to the oblique position; the radiographic tube is not moved so as to be at a 45º angle relative to the patient and film cassette. Angling the tube results in unacceptable radiographic distortion. A common mistake in this radiographic technique is the positioning of the patient in an oblique position that is not steep enough, with a resultant angle of less than 45º. On an oblique view obtained with good positioning, the coccyx should project over the femoral head.

Pelvic CT scans may be obtained alone or in combination with abdominal CT scans during the initial trauma evaluation. Axial CT scans may be obtained, but helical CT scanning yields better 2-dimensional and 3-dimensional reformatted images. Pelvic CT scans allow the detection of subtle fractures and displacements that are not appreciated on radiographs.

Limitations of Techniques

Virtually all acetabular fractures can be correctly classified after careful interpretation of AP and oblique radiographs of the pelvis. Intra-articular fracture fragments can be difficult to recognize on radiographs.

Compared with radiography, pelvic CT scanning allows a more precise determination of the degree of articular involvement, as well as of fragment displacement and orientation. Pelvic CT scanning also permits the identification of intra-articular fracture fragments. In complex acetabular fractures, 3-dimensional reformatted images may help conceptualize the fracture pattern and, thereby, aid in the planning of orthopedic surgery.

RADIOGRAPH

Findings

Brandser and Marsh devised a system of observations leading to the correct classification of most acetabular fractures.⁹ The answers to the following questions about the radiographic observations are used to determine the acetabular fracture pattern:

• Is a fracture of the obturator ring present? A fracture of the obturator ring indicates either a T-shaped or a column fracture (with the exception of the hemitransverse type of fracture). An intact obturator ring eliminates these fractures from consideration.
• Is the ilioischial line disrupted? Disruption of the ilioischial line occurs in fractures involving the posterior column or fractures in the transverse group.
• Is the iliopectineal line disrupted? Disruption of the iliopectineal line indicates anterior column involvement or 1 of the transverse-type fractures.
• Is the iliac wing above the acetabulum fractured? Iliac wing fractures are observed in fractures involving the anterior column.
• Is the posterior wall fractured? Posterior wall fractures can occur in isolation or in combination with posterior column or transverse fractures.
• Is the spur sign present? The spur sign is observed exclusively in the both-column fracture. The spur is a strut of bone extending from the sacroiliac joint. Usually, this strut of bone connects to the articular surface of the acetabulum. In the both-column fracture, this connection is disrupted; a fractured piece of bone that resembles a spur remains. The spur sign is best depicted on the obturator oblique view (see Image 26). In addition, the spur sign can be appreciated on CT scans (see Image 27).

Table 2 shows the combined set of radiographic and CT scan observations that are useful in acetabular fracture classification.

Table 2. Radiographic Features of Acetabular Fracture Types⁹

Fracture Type	Obturator

Ring

Fracture	Ilioischial

Line

Disrupted	Iliopectineal

Line

Disrupted	Iliac

Wing

Fracture	Posterior

Wall

Fracture	Pelvis

Into

Halves	Spur

Sign	CT Scan

Fracture

Orientation
Both-column	Yes	Yes	Yes	Yes	No	Front/back	Yes	Horizontal
Anterior column	Yes	No	Yes	Yes	No	Front/back	No	Horizontal
Posterior

column	Yes	Yes	No	No	No	Front/back	No	Horizontal
Posterior

column with

posterior wall	Yes	Yes	No	No	Yes	Front/back	No	Horizontal
T-shaped	Yes	Yes	Yes	No	No	Top/bottom	No	Vertical
Transverse with

posterior wall	No	Yes	Yes	No	Yes	Top/bottom	No	Vertical
Transverse	No	Yes	Yes	No	No	Top/bottom	No	Vertical
Posterior wall	No	No	No	No	Yes	No	No	Oblique
Anterior wall	No	No	Yes	No	No	No	No	Oblique
Anterior column

with posterior

hemitransverse

No

Yes

Yes

Yes

No

N/A*

No

N/A

*N/A indicates not applicable.

Degree of Confidence

By using Brandser and Marsh's system, the accurate classification of acetabular fractures is possible in almost every patient.

False Positives/Negatives

An accessory ossification center, the os acetabulum, can mimic an acetabular wall fracture. Its differentiating features include its characteristic superolateral location and well-corticated margins. Fractures of the anterior puboacetabular junction can be observed in pelvic ring fractures. These fractures may extend into the anterior column of the acetabulum, but they are not anterior column fractures per se. Such fractures are more correctly considered to be superior pubic ramus fractures.

Abdominal Aortic Aneurysm, Rupture

Background

Abdominal aortic aneurysms (AAAs) are segmental dilatations of the aortic wall that cause the vessel to be larger than 1.5 times its normal diameter or that cause the distal aorta to exceed 3 cm. These can continue to expand and rupture spontaneously, exsanguinate, and cause death.

AAA rupture is an important cause of unheralded deaths in people older than 55 years, claiming more than 15,000 lives annually in the United States alone.

Pathophysiology

A marked decrease in aortic elastin, an increase in collagen production and degradation, inflammatory changes, and imbalances of matrix metalloproteinases and their inhibitors have been noted in pathologic studies. Atherosclerosis may be only a facilitating factor.

Genetic predisposition plays some role, especially in disorders such as Marfan disease and type IV Ehlers-Danlos syndrome. Familial clustering of cases also has been documented.

Clinical risk factors that predispose individuals to these degenerative changes in the arterial wall include smoking, advanced age, male sex, chronic obstructive pulmonary disease (COPD), hypertension, and family history.Females, African-Americans, and persons with diabetes appear to have a lower prevalence of AAA.

Larger aneurysms tend to enlarge at a higher rate, as noted by Bernstein.

Table 1. Growth Rate of AAAs

Initial Size of AAA, cm	Mean Growth Rate, cm/y	95% Confidence Interval of the Mean Growth Rate
3.0–3.9	0.39	0.20, 0.57
4.0–4.9	0.36	0.21, 0.50
5.0–5.9	0.43	0.27, 0.60
6.0–6.9	0.64	0.16, 1.1

The natural history of an individual case is difficult to predict, and AAAs can have intervals of stability and slow and rapid expansion. The general recommendation is to consider elective aneurysmorrhaphy for aneurysms with a diameter of 5 cm or greater or for small aneurysms that have an average growth rate of more than 0.5 cm/y. Approximately 20% of aneurysms expand faster than 0.4 mm/y; the rest do so at slower rates.

AAA rupture

In addition to the initial aneurysm diameter, independent predictors of rupture include current smoking, lower forced expiratory volume (FEV-1), and higher mean blood pressure, all risk factors possibly amenable to modification. Findings from various series have suggested that diabetes mellitus, elevated levels of serum markers such as amino-terminal type III procollagen propeptide (PIIINP), a rapid rate of AAA expansion, and unfavorable morphology and aortic wall compliance are also predictive of rupture. Of note, the prevalence of diabetes in the population with AAAs is relatively low.

Attempts have been made to index the aneurysmal diameter to individual body size or anatomic points of reference (eg, body surface area, supraceliac aortic diameter, aneurysm length), but no feature has been found to be highly predictive of rupture. Rupture has been observed in some AAAs smaller than 5 cm in diameter but wider than the transverse dimension of the third lumbar vertebral body.

Findings from a few studies have suggested that most AAAs rupture into the left retroperitoneum. The retroperitoneum contains the leak by means of mechanisms that cause clotting or tamponade. This rupture can also cause abdominal, back, or flank pain; this symptom is related to impingement of the hematoma on adjacent structures.

Aneurysms that continue to leak or those that rupture into the peritoneal cavity can result in hemodynamic collapse and, often, death.

Frequency

United States

The estimated incidence of ruptured AAA in a population study from Sweden was 0.06 case per 1000 people.This rate increased with age; the age-adjusted incidences were less than 0.01, 0.37, or 1.36 per 1000 people younger than age 60 years, those aged 70-79 years, and those older than 90 years, respectively.

The best-known predictor of rupture rate is the maximal aneurysm diameter. Simplified estimates for the annual rupture rates based on size are as follows:

Table 2. Annual Rupture Rates Based on Size

Maximum Aneurysmal Diameter, cm	5-Year Rupture Rate, %
<4.0	2
4.0–4.9	3–12
5.0–5.9	25
6.0–6.9	35
>7.0	75

The annual rupture rate in the UK Small Aneurysm Trial (N = 2257, with about half in randomized arm and half in the registry) was 2.2% per year for the first 3 years of follow-up. The initial aneurysm diameter was 3-6 cm, and the mean was approximately 4.4 cm.

AAA rupture after stent-graft placement has been observed with specific devices, but device evolution and operator experience in both patient selection and device placement make it difficult to provide any stable estimates of the incidence at this time.

Mortality/Morbidity

The mortality rate for ruptured AAA is substantial. As many as 2 of 3 patients with ruptured AAA die before arriving at the hospital.Of those who reach the hospital, as many as one fifth of those who die do so before the operation, and the overall mortality rate still averages approximately 49%.

Multivariate analyses by Harris and coworkers revealed adverse predictors for early mortality, as shown in Table 3 below.

Table 3. Predictors of Early Mortality

Risk Factor	Percentage of Patients With Factor, %	Associated Mortality Rate, %	Mortality Rate in Patients Without Factor, %
Cardiac arrest	19	81	26
Loss of consciousness	26	72	24
Intraoperative BP <>	28	62	24

Note: For all comparisons, P <.05 unless otherwise noted. BP indicates blood pressure.

*P value <.10.

Deaths that occurred after the second postoperative day were predicted by variables shown in Table 4 below.

Table 4. Variables Predictive of Mortality

Risk Factor	Percentage of Patients With Factor, %	Associated Mortality Rate, %	Mortality Rate in Patients Without Factor, %
Renal failure	30	75	8
Respiratory failure	28	69	19

In the consecutive series of 180 patients with ruptured AAA, the following factors were independently related to the mortality rate: age; systolic BP less than 80 mm Hg; and a history of hypertension, angina, or myocardial infarction (MI). In patients who survived the surgery, the causes of death were as follows:

• Renal failure or multisystem failure (32%)



• Cardiac failure (29%)



• Respiratory failure, including pneumonia (17%)



• Coagulopathy (12%)



• GI hemorrhage (3%)



• Perforated duodenal ulcer (1.5%)



• Renal hemorrhage (1.5%)



• Hemorrhage from graft anastomosis (1.5%)



• Stroke (1.5%)



• Aspiration (1.5%)

Major postoperative complications observed in a series of 174 patients at the Mayo Clinic are shown in Table 5 below.

Table 5. Major Postoperative Complications

Event	Percentage of Patients Affected, %	Case Fatality Rate, %
Respiratory failure	48	34
Tracheostomy	14	44
Renal failure	29	76
Sepsis	24	45
MI/CHF*	24	66
Bleeding	17	90
Stroke	6	50
Ischemic colitis	5	67
Lower extremity ischemia	3	17
Paraplegia/paraparesis	2	50

*CHF indicates congestive heart failure.

Other major postoperative morbidities reported in the literature include the following:

• Delayed hemorrhage from iatrogenic injuries



• GI or genitourinary tract injuries



• Pancreatitis



• Duodenal obstruction



• Prosthetic graft infection

One in 5 patients undergo a repeat operation. One half undergo repeat laparotomy, and the other half undergo a tracheostomy or vascular procedure.

Late in-hospital deaths occur at a mean of 25 days ± 23.

The long-term outlook for patients is grim. Table 6 below shows survival statistics of the 147 patients with ruptured AAA (defined as blood outside the aortic wall) in the prospective Canadian Aneurysm Study.Younger age and total intraoperative urine output were the only factors that were independently predictive of survival.

Table 6. Cumulative Survival of Ruptured AAA Patients, as Determined at Kaplan-Meier Analysis

Time Since First Diagnosis	Survival Rate of Cohort, %	Patients Surviving > 1 mo After Surgery, %
1 month	49	96
1 year	41	87
2 years	37	77
3 years	36	73
4 years	29	60
5 years	26	53

Roughly 40% of early and late ( <5>

The availability of vascular surgeons, as opposed to general surgeons, was independently associated with a decreased 30-day mortality rate.

Sex

• In 2001, the National Center for Health Statistics reported that annual deaths attributable to AAA are almost 2-fold higher for males compared with females.



• An autopsy study revealed that the peak incidence of AAA was a decade later for women compared with men. Specifically, the peak incidence for women was at 90 years (4.5%) and 80 years in men (5.9%).



• Females were noted to have 3 times more ruptures than males in the UK Small Aneurysm Trial.In addition, females who have ruptured AAA may have a higher mortality rate than that of their male counterparts.

Age

• The incidence of AAA increases significantly after age 55 years in men and after age 70 years in women.



• The mean age of men with ruptured AAA is 70.6 years (range, 44-89 y) versus 77.3 years (range, 67-86 y) for women.



• Consequently, a number of competing comorbidities occur in this elderly cohort. These diminish the long-term survival rates even after successful AAA repair. On average, two thirds of postoperative patients died within the next 5 years, mostly due to causes related to cardiovascular disease.

Anatomy

Approximately one third of AAAs originate close to or at the level of the renal arteries, and suprarenal involvement has been reported in as many as 10% of patients.

In an old series by Rosch, 1 in 3 patients had accessory renal arteries, of which 7% arose from the AAA, and 1 in 5 patients had celiac or superior mesenteric artery stenosis. As many as 30% of patients with AAA can have renal artery stenosis. These are relevant findings because colon ischemia, as well as renal failure, can occur after aneurysmectomy.

A Japanese series of 97 cases of ruptured AAA revealed the following distribution of sites of rupture:

• Right lateral wall - 28%



• Pelvic arteries - 22%



• Posterior wall - 19%



• Left lateral wall - 17%



• Anterior wall - 10%



• Suprarenal - 4%

In a series of 226 AAAs in Italy, bleeding occurred into the following regions⁴¹:

• Retroperitoneal - 85.3%



• Peritoneal - 7.1%



• Inferior vena cava (IVC) or iliac vein - 5.8%



• Enteric - 1.8%

Although ruptures into the retroperitoneum typically originate from the left posterior aspect of the AAA, ruptures into the intestine tend to occur from the right anterior aspect.

Clinical Details

As many as three fourths of AAAs are initially asymptomatic. Most aneurysms are incidentally discovered during routine physical examination, during a diagnostic imaging study, or during surgery for other abdominal pathology.

Hypotension, pulsatile abdominal mass, and flank or back pain constitute the classic triad for ruptured AAA. However, this triad may be incomplete in as many as 50% of patients. Cardiac arrest can be the clinical presentation in a fourth of patients. In 1985, Donaldson et al described the presentation of their series of 81 patients that survived to undergo surgery for ruptured AAA.

Symptoms

• Abdominal pain - 58%



• Back pain - 70%



• Syncope - 30%



• Vomiting - 22%

Findings

• Mass - 91%



• Tenderness - 78%



• Systolic blood pressure less than 80 mm Hg - 42%



• White blood cell count greater than 10,000/µL - 79%



• Hematocrit less than 38-42%



• AAA apparent on abdominal plain film - 74%

Atypical presentations

• Pain radiating to the groin



• Back pain from AAA erosion into the vertebral body, with rare false aneurysm formation into the left psoas muscle



• Acute femoral neuropathy with or without thigh ecchymosis due to femoral nerve compression as blood dissects inferiorly between the iliacus and psoas muscles and the overlying fascial pockets



• Partial upper GI obstruction from AAA compression of the third portion of the duodenum



• Lower extremity ischemia and visceral thromboembolism caused by embolization of AAA mural thrombi



• Acute bilateral limb ischemia from aortic thrombosis



• GI bleeding secondary to aortoenteric fistula, usually involving the third part of the duodenum



• High output CHF, widened pulse pressure with machinery-like murmur, hematuria, rectal bleeding, priapism, or lower extremity swelling related to a fistula from the aorta to IVC or renal, lumbar, or common iliac vein

Preferred Examination

Intravenous access with 2 large-bore catheters should be established if a ruptured AAA is suspected. Blood should be drawn for stat determination of the CBC and kidney profile and for blood typing and screening. The vascular surgery team should be involved from the outset.

Ideally, in a hemodynamically stable patient, nonenhanced and enhanced helical or spiral CT of the thorax, abdomen, and pelvis should be expeditiously performed. This examination provides key information about the extent of aneurysmal disease, and it can be used to confirm and localize the site of rupture.

In the patient with an unstable presentation, an emergency operation is indicated. Time may permit only rapid bedside ultrasonography (US) and Doppler study of abdominal aorta and iliac arteries to confirm the presence of aneurysms.

The maximal aneurysm diameter is adequately assessed by using B-mode ultrasonography, CT scanning, and MRI. Aortography reveals only the lumen of the AAA because laminated clot obscures the outer limit of the aneurysm wall. Therefore, it often causes underestimation of the true aortic diameter.

Limitations of Techniques

Although CT and MRI provide detailed information about the blood vessels and their surrounding structures, these examinations require time; therefore, they may be unsuitable for use in patients in unstable condition. When contrast material is used in conjunction with CT to delineate blood-filled structures, it poses a risk of acute renal failure, particularly in hypovolemic elderly patients who may already have baseline nephrosclerosis or diabetic nephropathy.

Sonography is a quick and convenient modality, but it is much less sensitive and specific for the diagnosis of aneurysmal rupture. The absence of sonographic evidence of rupture does not rule out this entity if clinical suspicion is high.

Abdominal Aortic Aneurysm, Diagnosis

Background: Approximately 40,000 patients undergo aneurysmorrhaphy each year. In the United States, 15,000 deaths per year are attributed to abdominal aortic aneurysms (AAAs).

Since 1951, when Dubost first performed repair of an AAA with a homograft, surgery has been the mainstay of treatment. Many refinements in technique have occurred during the interval, but none as significant as the stent-graft. In 1991, Parodi et al described a novel, less invasive technique for repairing AAAs by placing a graft from within the vessel. This technique was labor intensive and involved the customized construction of the graft for each patient by sewing the graft material to self-expanding metal skeleton. Today, designs are approved by the US Food and Drug Administration, and numerous devices are being used in clinical investigations.

Pathophysiology: Classically, AAAs have been attributed to a weakening of the arterial wall as a result of atherosclerotic vascular disease caused by the atheromatous lesions seen on pathologic examination. Recent evidence supports a multifactorial process in which atherosclerosis is involved. Other etiologic cofactors under investigation include changes in the matrix of the aortic wall with age, proteolysis, metalloproteinase changes, inflammation, infectious agents (eg, syphilis, mycotic infections), and a genetic predisposition (eg, Marfan syndrome, Ehlers-Danlos syndrome).

True aneurysms involve dilation of all 3 layers of the vessel wall, whereas false aneurysms are caused by the disruption of 1 or more layers of the vessel wall. Elastin and collagen are the primary structural elements of the aortic wall. Experimental findings have shown that the relative content of elastin and collagen are lowest in the infrarenal aorta and that, with the destruction of collagen and elastin, dilatation of the aorta ensues. Increased concentrations of several proteases capable of degrading collagen and/or elastin have been found in the walls of AAAs and in aortic occlusive disease; both are manifestations of atherosclerosis.

An immunologic component to atherosclerotic vascular disease has been recognized and is characterized by infiltration of the aortic wall by macrophages, T lymphocytes, and B lymphocytes; these are known to activate proteolytic activity. The nature of this response has led researchers to investigate autoimmunity in the pathogenesis of AAA. Recent reports describe Chlamydia pneumoniae antigens, in contrast to active infection, in the walls of AAA. After the infectious agent is cleared, an antigenic stimulus remains, stimulating proteolytic activity with weakening of the vessel wall and aneurysm formation.

Inflammatory aneurysms, once believed to be distinct entities, are currently considered one extreme in the spectrum of atherosclerotic aneurysms; these account for 3-10% of all AAAs. Clinical and imaging characteristics differentiate inflammatory from noninflammatory aneurysms.

The familial pattern of AAA has long been recognized with a 15-19% incidence among first-degree relatives. This observation suggests that one or more genes are related to AAA and atherosclerosis. The identification of these genes may enable the early detection and prevention of AAA in high-risk patients.

Frequency:

• In the US: AAA is usually asymptomatic and detected on routine physical examination or during an unrelated radiologic examination. Therefore, the condition is likely underdiagnosed. In most studies, prevalence increases in those older than 60 years. In the United States, the reported incidence is 5-7% with a mean patient age of 70-75 years.

• Internationally: In Europe and Asia, the reported incidence is 5-7%, with a mean patient age of 70-75 years.

Mortality/Morbidity: In the United States 15,000 deaths per year are attributed to AAAs.

• When AAAs are repaired electively, the overall mortality rate is 0.9-5%.

• If repair is delayed until rupture, mortality rates as high as 75% are reported.

• In aneurysms 4-5 cm in diameter, the risk of rupture is almost 25%, with an associated mortality rate as high as 75%.

Race:

• Worldwide, AAA is more common in white males than in others. In the United States, AAA is far more common in white males than in black males. This difference may be partially caused by increased detection in white males, resulting from better access to medical care.

• The prevalence in white and black females is almost identical.

• Etiologic explanations for these race-related differences include different genetic susceptibility, as well as exposure to environmental risk factors. Note that, in the United States, other clinical manifestations of atherosclerosis do not have this racial predilection.

Sex: Depending on the published series, the male-to-female ratio is 1.6-4.5:1.

• Inflammatory aneurysms represent 3-10% of atherosclerotic AAAs and have a male-to-female ratio of 6-30:1.

• The reasons for male preponderance of AAA are not clear; however, hormonal factors, genetic susceptibility, and exposure to environmental factors are believed to play a role.

Age:

• AAAs occur in 5-7% of the population older than 60 years.

• AAAs are seen most often in patients aged 60-80 years.

• The mean age of patients with inflammatory aneurysms is 62-65 years; these patients are 5-10 years younger than those with noninflammatory AAA.

Anatomy: An aneurysm is defined as a localized dilation of an artery by at least 50% as compared with the expected normal diameter of the vessel. The term ectasia is used when the dilatation is less than 50%. If the arteries are diffusely enlarged by 50% or more, the condition is called arteriomegaly.

The Society for Vascular Surgery and the International Society for Cardiovascular Surgery have suggested the classification of aneurysms by their site, origin, histologic features, and clinicopathologic manifestations. The anatomic site and morphology of an aneurysm can be preoperatively determined by radiologic means.

The site of an aneurysm is related to its natural history, clinical presentation, and means of treatment. The site of abdominal aneurysms should be characterized as suprarenal, juxtarenal or pararenal, or infrarenal. Approximately 90-95% of AAAs involve the infrarenal abdominal aorta. Rarely do they extend above the renal arteries; however, extension into the common iliac arteries is fairly common.

Clinical Details: AAAs occur in 5-7% of the population older than 60 years. Although most patients with AAA are asymptomatic, they can present with symptoms of mass effect, compression of abdominal organs, or visceral or peripheral emboli originating from the wall of the aneurysm. Rarely, patients present with back pain, which can represent rupture of the aneurysm, a surgical emergency. Patients older than 60 years who smoke and who are known to have atherosclerosis, hypertension, and/or chronic obstructive pulmonary disease are at increased risk for AAA. Routine screening of these patients is warranted.

Once an aneurysm is identified, it should be repaired or followed up with imaging, depending on the clinical scenario and the size of the aneurysm at the time of diagnosis. Most aneurysms (80%) demonstrate progressive enlargement. The diameter of an aneurysm is directly related to its risk of rupture. For aneurysms smaller than 4 cm in diameter, the risk of rupture is less than 10%. Once an aneurysm is 4-5 cm in diameter, the risk of rupture increases to almost 25%, with an associated mortality rate as high as 75%. The accepted surgical mortality rate remains less than 5% with the elective repair of these 4- to 5-cm aneurysms.

The morphologic features, including the maximum diameter in both the anteroposterior and lateral dimensions and the length of the aneurysm, should be reported. The shape of the aneurysm (fusiform or saccular) and its relationship to branch vessels should be described. Arterial wall complications such as the expansion over time, compression or erosion into adjacent structures, rupture, dissection, and thrombotic occlusion should be documented as well.

With the advent of the endoluminal repair of aneurysms, several additional morphologic characteristics should be recorded. These determine if endovascular repair is possible, and if so, what type of device can be used. These features include the following: (1) greatest mural diameter, (2) extent of aneurysm (eg, length of proximal and distal neck, extension into iliac arteries), (3) tortuosity of the aorta, (4) anatomy of the iliac arteries (eg, iliac artery occlusive disease, tortuosity, caliber, patency of internal iliac arteries and relation of aneurysm to them, presence of concomitant iliac artery aneurysms), (5) presence and degree of intraluminal thrombus, (6) presence and degree of calcification in the neck and iliac arteries, and (7) anatomy of the femoral arteries (eg, caliber, degree of calcification or occlusive disease).

Preferred Examination: Because of portability, lack of ionizing radiation, cost, and availability, ultrasonography (US) should be the initial imaging modality when an asymptomatic, pulsatile abdominal mass is palpated.

If the aneurysm is approaching 5 cm or more or if rapid enlargement is seen on serial US images, a CT or CT angiogram (CTA) should be ordered to better delineate the extent of disease prior to conventional surgery or treatment with the insertion of an endovascular graft. In patients whose renal function does not permit the administration of iodinated contrast material, MRI and magnetic resonance angiography (MRA) provide good alternatives.

Angiographic examination may be requested because of a clinical concern that concomitant renal artery stenosis or peripheral vascular disease may require surgical intervention during AAA repair. At some institutions, CTA and MRA have replaced routine diagnostic angiography in the preoperative evaluation of AAA.

In urgent situations in which the clinical diagnosis is fairly certain or rupture is imminent or suspected and in which the patient's condition is stable, CT and/or CTA may be the initial and only examination required.

Imaging of the aorta does not end with the repair of the aneurysm. After repair with, either a traditional open surgical procedure or an endovascular procedure, follow-up imaging is necessary. In the case of conventional surgical repair, follow-up imaging is performed yearly, usually with US. For endovascular grafts, the follow-up is more stringent, with immediate postprocedural CT as well as 6-month and then yearly CT follow-up.

When the evaluation for AAA is performed with CT or MRI, note the extent of the aneurysm, any involvement of major branch vessels, and the existence of a retroaortic or circumaortic left renal vein. Note if the aneurysm has significant wall thickening, a typical characteristic of an inflammatory aneurysm, because the surgical approach for this condition differs from that needed for the more common, predominately atherosclerotic aneurysm.

Limitations of Techniques: With conventional radiography in the anteroposterior or lateral projection, calcification of both opposing abdominal aortic walls must be present to outline an AAA. However, this finding is present in less than 50% of cases. A tortuous, calcified aorta may mimic an AAA unless both walls can be seen clearly. The lack of overlying bony structures in the lateral projection may allow clearer definition of the aneurysm.

US is considered the screening examination of choice; however, it may not adequately depict the entire abdominal aorta if a large amount of bowel gas is present or if the patient is obese.

With or without contrast enhancement, CT is an excellent screening examination for AAA. CT depicts the absolute size of the aneurysm. However, the extent of mural thrombus and the presence of dissection cannot be evaluated without the administration of contrast material.

MRI with contrast enhancement provides an alternative to CT in patients with renal insufficiency. MRI has several absolute contraindications, including cardiac pacemakers and intracranial aneurysm clips. Claustrophobia and a patient's inability to remain motionless are likely to yield a nondiagnostic study. MRI is not as available as CT and US.

Angiography is also a safe procedure. However, because it is an invasive procedure, a small but definite risk to the patient exists. The true size of the aneurysm may not be discernible because of a mural thrombus; therefore, underestimation of the true extent of the aneurysm is possible. The role of angiography is in planning surgical or endovascular repair.

RADIOGRAPH

Findings: Calcification of the abdominal aortic wall is frequently evident on plain radiographs of the abdomen. Calcification is best seen on lateral views when the spine does not obscure the opposing walls of the vessel. When calcification can be clearly identified in the opposing aortic walls, AAA can be diagnosed with the plain radiographic findings.

Degree of Confidence: If the classic eggshell appearance is present (see Image 2), the degree of confidence is approximately 100%; however, this finding is present only in 50% of patients. Occasionally, only the anteroposterior or lateral abdominal image demonstrates the findings clearly. If AAA is suspected, perform abdominal US or CT for confirmation. As such, negative plain radiographic findings do not exclude the diagnosis in any way.

False Positives/Negatives: A tortuous, calcified aorta can mimic AAA unless both walls can be seen clearly. If the opposing walls are not calcified, the diagnosis cannot be made with certainty. In these cases US, CT or MRI must be performed if AAA is clinically suspected.

CT SCAN

Findings: CT accurately demonstrates dilation of the aorta , and involvement of major branch vessels proximally and distally. This information helps in determining the appropriate intervention, which may be either surgical or endovascular repair. CT also shows the other organs in the abdomen and demonstrates involvement or displacement of organs that can confuse the clinical picture. The location and number of the renal arteries, caliber of the aneurysm, degree of calcification, lengths of the neck and iliac artery, and presence of mural thrombus are readily assessed. CTA allows multiplanar assessment of the aneurysm and associated relevant vessels (visceral arteries, iliac and femoral arteries).

Degree of Confidence: CT has emerged as the diagnostic imaging standard for the evaluation of AAA with an accuracy that approaches 100%. A well-performed CT examination can reveal the extent of the aneurysm, as well as the involvement of other organs. Intravenously administered contrast agent is needed to obtain the full benefit of CT; however, a nonenhanced study accurately depicts AAAs. Three-dimensional reconstructions of state-of-the-art, multidetector-row, helical CT scans can help in preoperative planning and may replace the need for preoperative diagnostic angiography.

False Positives/Negatives: The administration of contrast material is essential for detecting dissection or ulceration of a vessel that might be missed without it. In the acute setting (eg, in a patient with back pain or an aneurysm), a false-positive diagnosis of rupture is possible if fluid resulting from another cause is seen in the abdomen. Conversely, an aneurysm or rupture can be missed in a patient who has recently undergone barium study because artifact can obscure the aorta.

MRI

Findings: MRI and MRA can be used to define the extent of AAA, similarly CT . The absence of iodinated contrast material and radiation are advantages of this modality. However, MRI is more sensitive to motion than CT because a patient must remain motionless for longer than with current multidetector-row helical CT technology. In addition, the remaining organs in the abdomen are not seen as well on MRIs because of motion.

Degree of Confidence: In technically well performed MRI and MRA, degree of confidence approaches 100%. These examinations clearly reveal the extent of the aneurysm; however, motion can cause artifacts that can render the results nondiagnostic. Patients must be able to remain motionless for longer periods than with CT to enable a diagnostic examination.

False Positives/Negatives: If prior abdominal surgery has been performed and if metal clips or devices were used, MRI may not be possible. If the metal is close to the aneurysm or if branch vessels or heavy calcification is seen, artifacts may obscure the vessel and result in a nondiagnostic study.

ULTRASOUND

Findings: US is the screening examination of choice as a result of its relative availability, speed, and low cost ). US is operator dependent, unlike other modalities; therefore, operator experience is important. The abdominal aorta normally tapers as it extends distally. Any increase in its diameter exists is considered abnormal.

Degree of Confidence: If the abdominal aorta can be seen in its entirely, US provides a reliable, low-cost screening examination. Any increase in the size as the aorta travels distally is abnormal. However, in a patient who is obese or in whom the bowel is distended with gas, a complete examination of the aorta and proximal iliac arteries may not be technically possible. In such instances, another cross sectional imaging study (eg, CT, MRI) should be obtained.

False Positives/Negatives: A technically unsatisfactory examination may result from a large patient body habitus or a large amount of bowel gas, which results in incomplete visualization of the aorta. Thus, a false-negative result is possible if these limitations are not recognized.

INTERVENTION

Intervention: The Society for Vascular Surgery and the International Society for Cardiovascular Surgery guidelines for the repair of AAA include the following: (1) Any patient with a documented rupture or suspected rupture; (2) a symptomatic or rapidly expanding aneurysm, regardless of its size; (3) aneurysms larger than 4 cm in diameter; (4) complicated aneurysms with embolism, thrombosis, or symptomatic occlusive disease; and (5) atypical aneurysms (eg, dissecting, mycotic, saccular). These guidelines must be weighed against the existing clinical risk factors in each patient. With the advent of endoluminal repair, patients who are poor surgical candidates have a possible alternative to open repair. Careful screening of these patients is critical for good outcomes.

Endovascular repair, such as stent-graft placement, is evolving as an alternative to conventional, open surgical repair (see Image 6). The US Food and Drug Administration has approved several devices for use in the endovascular repair of aneurysms. Each device has benefits and limitations.

The primary factors that determine suitability for endovascular repair are the diameter and length of the proximal neck of the aneurysm, the tortuosity of the aorta, and the anatomy of the iliac arteries.

Endovascular devices rely on radial force (and, for some devices, hooks) to engage the more normal segments of the aorta and iliac arteries and to exclude blood flow from the aneurysmal sac. If the proximal neck is too wide or too short or densely calcified, a good seal cannot be achieved at the attachment site. The sac remains pressurized, and the aneurysm is still at risk of rupture, with endotension or an endoleak.

The flexibility of an endovascular graft is an important consideration in selecting a patient for endovascular repair. If the angle between the neck of the aneurysm and the aorta is too great, the graft may be displaced from its intended position with a subsequent leak at the attachment site. The leak can occur acutely (type I) or later, as aneurysm shrinkage and remodeling occurs.

The tortuosity of one or both of the iliac arteries can also preclude endovascular repair. If the common iliac arteries are too large, the limb of the stent is not well opposed to the wall of the artery, and a leak at the attachment site results. Embolization of a hypogastric artery can be performed to allow extension of a graft limb to a nonaneurysmal external iliac artery if needed. If the iliac arteries are too small or too tortuous, advancing the stent-graft deployment system into position may be impossible.

The presence of circumferential calcification at the neck is increasingly recognized as a negative prognostic indicator for primary seal formation, and it may indicate an increased risk of rupture during the procedure. Extensive intraluminal thrombus may similarly affect the ability to obtain a secure, long-term seal at the proximal part of the neck.

Concomitant embolization of one or, rarely, both internal iliac arteries may be required prior to graft placement if the iliac arteries are aneurysmal to or beyond the distal common iliac artery. Embolization can lead to buttock claudication and, in rare cases, colonic ischemia or infarction.

Medical/Legal Pitfalls:

• Clinicians order radiologic studies during the course of patient examinations. The clinical history should be considered when reviewing the radiologic studies, though it may be misleading in some cases. When AAA is suspected, it is rarely missed.

• When an examination, especially a plain radiograph is ordered for a reason other than the evaluation of AAA, curvilinear calcifications should be carefully assessed because most AAAs are asymptomatic. When they are discovered, the referring clinicians should be notified of the abnormal and unexpected findings. In some cases, referring clinician might be reminded of the need for appropriate follow-up and the time interval.

• At minimum, radiologists should follow several guidelines to ensure good patient care:

• The ordering physician should be notified and US or CT should be recommended when findings suggestive of AAA are seen on plain radiographs.

• Recommend appropriate surveillance for aneurysms both before and after their repair.

• Notify the ordering physician when evidence of arterial wall complications is present. Such evidence includes expansion over time, compression or erosion into adjacent structures, rupture, dissection, and thrombosis.