Imaging for Suspected Ruptured Abdominal Aortic Aneurysm

Because of the potential for rapid and sudden hemodynamic collapse, imaging for suspected AAA must be performed as rapidly as possible. Simultaneous with all diagnostic imaging should be patient resuscitation and surgical consultation. As we discuss in detail later, ultrasound is a sensitive modality for the presence of AAA, although it is insensitive for detecting aneurysm rupture.¹⁴ CT without any contrast, or with IV contrast if time allows, is usually definitive. X-rays play little role except in evaluating for other immediate surgical causes of abdominal pain such as free peritoneal air and should be avoided when possible to prevent dangerous delay.

Computed Tomography for Ruptured Abdominal Aortic Aneurysm

CT scan without IV contrast can diagnose the presence of AAA and AAA rupture with high sensitivity and specificity (Figures 11-12 to 11-16).^24-25 An AAA is defined by an aortic diameter 3 cm or greater, but ruptures are rare in aneurysms of this size. The aorta is readily identified as a circular structure in cross section, anterior to the spine. On unenhanced CT, high-density retroperitoneal hematoma can be seen in the perinephric retroperitoneal space, sometimes displacing the kidney anteriorly.²⁶ Without IV contrast, blood shares the same density as the kidney and psoas muscle and can obscure the lower density fat plane that normally separates these two structures from one another and from the aorta. In addition, a high-attenuation crescent within the aortic wall or within mural thrombus predicts rupture.^27-29 Without IV contrast, the crescent is considered to be “high attenuation” if its Hounsfield density exceeds that of unenhanced blood in the aortic lumen.²⁸ If time allows, CT scan with IV contrast provides more anatomic definition to allow open surgical or endovascular intervention (Figures 11-17 and 11-18; see also Figures 11-13 and 11-14). IV contrast also identifies ongoing hemorrhage at the time of CT. Oral contrast should never be used when AAA rupture is suspected, because it introduces an unacceptably long delay before imaging.¹³

Figure 11-12 Unruptured abdominal aortic aneurysm (AAA): Noncontrast computed tomography (CT).

A, noncontrast CT viewed on soft-tissue windows, demonstrating a very large AAA. B, Close-up from A. Characteristic features include a calcified rim and adherent mural thrombus, which is faintly visible on this noncontrast CT as a crescent-shaped rim along the aortic wall. Intravenous (IV) contrast better delineates this in the next figure. This patient does not have an aortic rupture, although it is difficult to be certain of this viewing this noncontrast CT. Retroperitoneal fat (nearly black) bounds the aorta posteriorly and on the patient’s left, but the right and anterior margins of the aorta abut soft-tissue density, so a small amount of extraluminal bleeding could be missed on this scan. CT with IV contrast can evaluate for active bleeding, marked by contrast extravasation. In some cases, aortic rupture can be clearly identified on noncontrast CT. Examples of this are shown in Figures 11-15B and 11-16.

Figure 11-13 Unruptured abdominal aortic aneurysm: Computed tomography (CT) image enhanced by intravenous (IV) contrast.

A, An IV contrast–enhanced CT scan performed immediately after the noncontrast CT in the same patient as Figure 11-12. B, Close-up from A. Both A and B are viewed on soft-tissue windows. With the administration of IV contrast, the true lumen can be clearly differentiated from the adherent mural thrombus, which is nearly circumferential in this patient. Calcifications in the aortic wall are visible. The contrast remains bounded within the rounded aortic contour, ruling out active bleeding from rupture (which would demonstrate contrast extravasation outside of the aortic contour). Oral contrast is not needed for evaluation of the abdominal aorta.

Figure 11-14 Unruptured abdominal aortic aneurysm (AAA): Comparison of noncontrast and intravenous (IV) contrast–enhanced computed tomography (CT).

Noncontrast (A) and IV contrast–enhanced (B) CT scans were performed in the same patient on the same day. These slices are through the same level and demonstrate the additional value of IV contrast in delineating the lumen and adherent mural thrombus, which is faintly visible on the noncontrast scan. This patient does not have active rupture, so contrast is not seen leaving the aorta. A, The presence of an AAA can be confirmed or ruled out without IV contrast. IV contrast assists in the detection of active hemorrhage.

Figure 11-15 Unruptured and ruptured aortic aneurysms: CT without IV or oral contrast.

A, An unruptured but large abdominal aortic aneurysm (AAA), identified by CT without IV contrast. CT without any contrast allows accurate identification of an aortic aneurysm. By definition, an aneurysm has a diameter of 3 cm or greater, though rupture is relatively rare under 4-5 cm. Increasing size is accompanied by increased rupture risk. Typical features include wall calcifications. The surrounding fat should appear nearly black on CT soft-tissue windows. Without IV contrast, blood within the aorta is dark gray on CT soft-tissue windows.

B, A large ruptured AAA, identified on CT without IV contrast. Free peritoneal rupture has occurred, and blood is visible throughout the patient’s left abdomen. Blood without contrast appears gray on CT. In this case, the extravasating blood appears slightly hyperdense (brighter) relative to blood in the aorta, despite the absence of injected contrast. This is a well-described phenomenon in the radiology literature. Rupture of an aneurysm can be detected without any contrast. Blood in the retroperitoneum obscures normal fat planes, such as that separating the aorta and psoas muscle. A retroperitoneal hematoma may also displace the kidneys.

Figure 11-16 Ruptured aortic aneurysm: CT without intravenous or oral contrast.

Free peritoneal rupture has occurred, and blood is visible throughout the patient’s left abdomen.

Figure 11-17 Abdominal aortic aneurysm (AAA) rupture: CT with IV contrast.

A, Axial image. B, Coronal image. C, Sagittal image.

All images are viewed on CT soft-tissue windows. Administration of IV contrast allows recognition of active contrast extravasation—ongoing hemorrhage at the moment of CT. However, IV contrast is not generally needed for recognition of AAA rupture. In this patient, blood is seen throughout the abdomen and retroperitoneum. Blood that escaped from the aorta before the administration of IV contrast appears dark gray. Abdominal and retroperitoneal fat appears nearly black on CT soft-tissue windows. Injected contrast appears bright white. Adherent thrombus within the aorta appears dark gray, whereas white contrast material defines the patent lumen. Contrast outside of the aorta indicates active hemorrhage. Compare the patient’s right psoas muscle with the left. On the left, blood obscures the normal fat plane surrounding the psoas. The diagnosis of AAA rupture could have been made in this patient without any contrast. Multiplanar reconstructions with IV contrast are useful if the patient is sufficiently stable, because these allow sizing of endovascular grafts.

Figure 11-18 Abdominal aortic aneurysm (AAA): Three-dimensional CT reconstructions.

Three-dimensional reconstructions can be generated and rotated in space to visualize the aorta for preoperative planning. Measurements from these three-dimensional models and from two-dimensional axial, coronal, and sagittal plane reconstructions are used to size endovascular grafts. Three-dimensional modeling requires fine CT slice acquisition, around 1.25 mm per slice, for high-quality rendering. Multiple software packages allow three-dimensional modeling from standard CT datasets. Here, a sacular AAA is viewed from the front (A) and side (B).

Alternative Imaging Modalities for Abdominal Aortic Aneurysm Rupture

Magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) can be used to diagnose AAA with excellent sensitivity and specificity, but the delay before imaging is unacceptably long in most institutions using this modality.³⁰ Noncontrast CT should always be preferred over MRI, because it is highly sensitive and specific for AAA and AAA rupture. Catheter-based formal angiography can be used to diagnose AAA with or without rupture, although in most institutions this has been replaced by ultrasound or CT imaging for diagnostic purposes, as angiography is both time-consuming and invasive. Plain radiographs play virtually no role in the diagnosis of AAA and should be avoided whenever possible, because they may introduce unacceptable diagnostic delay. Rarely, the calcified outline of an aortic aneurysm may be seen on x-ray, but the sensitivity is unknown and plain x-ray should not be used for this diagnosis (Figure 11-19). An exception to this rule is in the unstable patient in whom a competing diagnosis such as perforation of a hollow viscus is being considered. In this case, an upright portable chest x-ray to assess for pneumoperitoneum can be rapidly performed (see Figure 11-1).

Figure 11-19 Abdominal aortic aneurysm (AAA): Plain radiograph.

X-rays should not be used to diagnose the presence of AAA, because the sensitivity is unknown and the ability to detect rupture is likely poor. Occasionally, x-ray obtained for other suspected diagnoses may reveal a calcified aortic contour. A, Supine abdominal x-ray. B, Close-up from A.

Imaging of Patients With Prior Endovascular Abdominal Aortic Aneurysm Repairs: Endoleaks

Following endovascular repair of AAAs, an endoleak may occur (Figures 11-20 and 11-21).³³ An endoleak is defined as the continued flow of blood into the aneurysm sac. Endoleaks are graded as one of four types. Type 1 endoleaks occur immediately, at the time of placement of an endovascular graft, usually because of mis-sizing of the graft, such that the proximal or distal ends of the graft are not sealed against the aorta. This requires placement of a larger graft, because type 1 endoleak leaves the aneurysm sac subject to systemic vascular pressures with continued risk of acute rupture. Type 2 endoleaks result from retrograde flow of blood through collateral vessels into the aneurysm sac (see Figure 11-21). Common examples include filling of the aneurysm sac from lumbar perforating arteries. Type 2 endoleaks are often observed without treatment, because they do not subject the aneurysm sac to full systemic vascular pressures and are at relatively low risk of rupture. Type 2 endoleaks that do not resolve spontaneously can be treated with angiographic embolization. Type 3 endoleaks occur when a tear in the fabric of the graft occurs or if separation occurs between grafts consisting of multiple modules. This type of leak is relatively rare but leaves the aneurysm sac subject to systemic vascular pressures, requiring replacement of the graft because of continued risk of aneurysm rupture. Type 4 endoleaks occur from leaks through pores of the graft material and usually do not require repair.³³

Figure 11-20 CT evaluation of patients with prior endovascular aortic aneurysm repair.

A, B, CT scout images showing the radiodense graft.

C, CT with intravenous (IV) contrast, showing contrast contained within the graft.

CT is useful for assessment of patients with prior endovascular aortic aneurysm repair. Although the graft material is visible without IV contrast, detection of a leak of blood within the aneurysm sac but outside of the graft material (an endoleak) requires IV contrast. Here, contrast appears contained within the graft material.

Figure 11-21 Type 2 endoleak following aortic aneurysm endovascular repair: CT without and with intravenous (IV) contrast.

A, A noncontrast CT shows the endograft within the aortic aneurysm but cannot detect an endoleak (leak of blood within the aneurysm sac, outside of the graft).

B, C, IV contrast–enhanced CT shows contrast outside of the graft but within the aneurysm sac—confirming an endoleak. Some slow leaks are not seen on arterial phase imaging but are visible on delayed images.

Definitive diagnosis of an endoleak can be made with IV contrast–enhanced CT (see Figures 11-20 and 11-21). Without IV contrast, the presence of an endoleak will go unrecognized on CT, because leaking blood will have a similar Hounsfield density to thrombus outside of the stent but contained within the aneurysm sac. With the addition of IV contrast, blood flow within the aneurysm sac outside of the stent is evident. Because retrograde filling of the aneurysm sac is often slow (e.g., with type 2 endoleaks described earlier), some endoleaks can be difficult to detect on arterial-phase CT with IV contrast. Additional delayed images (acquired approximately 5 minutes after initial contrast injection) may be required.^34-35 Some authors have argued against the need for delayed phase images, because most endoleaks detected with this technique resolve spontaneously without intervention.³⁶ Contrast-enhanced ultrasound can be used to assess for endoleak in patients with contraindications to IV contrast for CT. Contrast-enhanced ultrasound performs favorably compared with CT.^23,37 MRI can also be used to assess for endoleaks, because graft materials are MRI compatible. Contraindications to gadolinium contrast are discussed elsewhere in this chapter.

Imaging for Aortic Dissection

Because the clinical presentation of AAA rupture and abdominal aortic dissection can overlap substantially, diagnostic imaging for aortic dissection should begin with bedside ultrasound to assess for AAA. Ultrasound can sometimes visualize the intimal flap of dissection (Figures 11-22 and 11-23). However, the sensitivity is relatively low, around 70% with use of B scan and color Doppler techniques. Contrast-enhanced ultrasound has been reported to be 97% sensitive compared with CT, although the technique is not widely used.⁵⁶ CT without IV contrast cannot rule out aortic dissection, because the intimal flap typically shares the same density with blood in the true and false lumens (Figure 11-24). Rare case reports document aortic dissection on noncontrast CT, based on displacement of calcified atheromatous plaques or high attenuation clot within the false lumen, but the sensitivity of these findings is unknown and should not be relied upon.⁵⁷ Administration of a rapid bolus of IV contrast should be considered critical to the diagnosis. Thus if a noncontrast CT is first performed to evaluate for AAA and is negative, CT with IV contrast must be performed if possible. With IV contrast, the intimal flap is highlighted as an unenhanced line separating the true and false lumens of the aorta (see Figure 11-24). A normal aorta is circular in cross section, filling uniformly with bright contrast. When an intimal flap is present, the circular cross section appears divided into two lumens. These may be unequal in size. Both lumens may enhance with contrast, or one or both lumens may be thrombosed and fail to enhance (Figure 11-25). In addition to initial arterial phase images, delayed images are usually obtained to assess the perfusion of organs such as the kidneys. Failure of the kidneys to enhance on delayed images indicates hypoperfusion related to the dissection and may require emergency surgery or intravascular techniques to fenestrate the dissection flap and restore blood flow (Figure 11-26).

Figure 11-22 Abdominal aortic dissection: Ultrasound.

This sagittal or long-axis ultrasound demonstrates the intimal flap of an aortic dissection in the proximal abdominal aorta.

Figure 11-23 Abdominal aortic dissection: Ultrasound with Doppler flow.

Same patient as Figure 11-22. Ultrasound demonstrates the intimal flap of an aortic dissection in the proximal abdominal aorta. Color Doppler shows differential blood flow in the true and false lumens.

Figure 11-24 Aortic dissection involving the abdominal aorta: CT without and with intravenous (IV) contrast.

Soft-tissue windows. A, On CT without IV contrast, the intimal flap of dissection is not visible.

B, When IV contrast is administered, the intimal flap separating the true and false lumens of the aorta becomes visible. No oral contrast is needed to make this diagnosis.

Figure 11-25 Aortic dissection: Stanford type B with involvement of the left renal artery.

CT with IV contrast, soft-tissue windows. A, B, Sequential images at the level of the renal artery. C, Close-up from A.

This patient has a dissection of the abdominal aorta. An intimal flap and false lumen appear to involve the origin of the left renal artery, although the kidney does enhance with contrast.

Figure 11-26 Aortic dissection with end-organ ischemia: Delayed phase, intravenous-contrasted CT images.

Aortic dissection involving the abdominal aorta can result in ischemia of end organs, including bowel and kidneys. A, Arterial phase images obtained immediately following contrast administration can reveal the dissection flap, including major branch vessel involvement. In this case, the initial scan was terminated inadvertently above the level of the renal arteries. B, Close-up from A showing intimal flap in detail. C, Delayed images can show evidence of hypoperfusion. In this case, the right kidney does not show normal enhancement, indicating hypoperfusion. The left kidney enhances and shows contrast in the renal collecting system, indicating normal perfusion.

MRI or MRA is also highly sensitive and specific for abdominal aortic disease, including aortic dissection.^58-59 In patients with contraindications to iodinated contrast for CT, such as renal insufficiency or iodinated contrast allergy, MRI or MRA is a reasonable alternative if its performance can be timely. Typical MRI or MRA for aortic dissection requires approximately 25 minutes to complete, compared with fewer than 6 minutes for CT.⁶⁰ This does not take into account the limited availability of MRI outside of normal business hours in many centers, with additional time often required for technicians to arrive. Three-dimensional MRA with injected gadolinium contrast is usually used to demonstrate the intimal flap.^58-59 In patients with renal insufficiency at risk for gadolinium-associated complications (discussed at the end of this chapter), MRI without IV gadolinium can be performed to assess for aortic dissection. New sequences that require no contrast material perform favorably compared with gadolinium-enhanced MRA.^58-61 These protocols include steady-state, two-dimensional, gradient–recall echo⁶⁰; two-dimensional turbo spin echo; and two-dimensional, balanced, steady-state free precession.⁶¹

Acute Mesenteric Artery Occlusion

Acute mesenteric artery occlusion and ischemia can occur from in situ thrombosis or embolic events. Atrial fibrillation is likely the most common cause, accounting for 95% of cases in one prospective study.⁶² Dissection of mesenteric vessels can complicate aortic dissection or rarely may occur in isolation. The superior mesenteric artery (SMA) is the most commonly affected vessel in the setting of atrial fibrillation (see Figures 11-31 to 11-35).⁶³ Occlusion of the SMA may be more common than previously believed. In a population-based study using autopsy results, the incidence was 8.6 per 100,000 person years, with a cause-specific mortality of 6 in 1000 deaths. Suspicion of intestinal ischemia before death was noted in only 33%, possibly reflecting a variable presentation not fitting the classically described signs and symptoms.⁶⁴

Classically, acute mesenteric ischemia from arterial occlusion is characterized by sudden and severe abdominal pain without significant abdominal tenderness. This is often described as “pain out of proportion to exam.” This may be a misleading myth that could result in misdiagnosis or delayed diagnosis in many patients. In a retrospective review from Wake Forest University,⁶⁵ 63% of cases had a delay of greater than 24 hours from symptom onset until treatment, reflecting the difficulty of the diagnosis. Of 77 cases presenting with acute mesenteric ischemia, 64% were described in their initial emergency department record as having peritonitis–suggesting that exam findings were severe, not mild. In a second study of 43 patients with mesenteric ischemia, 48% had diffuse tenderness, and 52% had peritonitis by exam.⁶⁶ One explanation is that these are late findings and patients often present after a delay of many hours from onset of ischemia. In any case, mesenteric ischemia should never be ruled out because the physical examination demonstrates too much tenderness.

Lab abnormalities associated with mesenteric ischemia include substantial leukocytosis, elevated anion gap, elevated lactate level, and hyperphosphatemia, but small studies on the topic limit the value of these findings in ruling out a potentially lethal process. Ritz et al.³² found that marked leukocytosis and elevated serum lactate occurred in 93% of patients with acute mesenteric ischemia and were prognostic of mortality. Lange and Jackel⁶⁷ found serum lactate to be elevated in 100% of 20 patients with mesenteric ischemia, although the specificity was only 42%. Merle et al.⁶⁸ found a serum lactate level of greater than 5 mmol/L to be associated with death within 72 hours. High inorganic phosphate levels have long been reported to be associated with mesenteric ischemia, based primarily on animal studies.^69-72 Phosphate is believed to originate from sloughing intestinal mucosa. The sensitivity has not been studied in well-designed human trials but is inadequate for screening in case series. May and Berenson⁷³ reported elevations in only 25% of cases of intestinal ischemia. Gorey and O’Sullivan⁷⁴ reported hyperphosphatemia in only 15% of 65 patients with extensive intestinal ischemia, leukocytosis in 65%, and metabolic acidosis in 67%.

Pitfalls in laboratory screening can occur. Although marked leukocytosis can suggest acute mesenteric ischemia, this is likely a late finding that may occur after frank bowel necrosis has occurred, in which case patient prognosis is poor. Thus patients with normal white blood cell counts should not be dismissed as not having mesenteric ischemia. Patients with significant leukocytosis may be mistakenly suspected of infectious or inflammatory conditions of the abdomen, such as diverticulitis, abdominal abscess, or appendicitis. Although these patients undoubtedly would undergo additional observation or diagnostic imaging, the absolute time criticality of the diagnosis of ischemia might be missed. For example, observation of several hours in the case of SMA thrombosis can result in complete loss of the small bowel, with high morbidity and mortality.

When considering the screening sensitivity of laboratory tests, it is extremely important to remember the methodologic limitations of most studies on the subject, which are usually small, retrospective reviews. In addition, mesenteric ischemia is a spectrum of disease including partial and incomplete vascular occlusions. The elapsed time from the moment of vascular occlusion until emergency department presentation, as well as the degree of bowel hypoperfusion, may affect the sensitivity of laboratory testing and diagnostic imaging.

Imaging for Mesenteric Ischemia

In any patient with suspected acute mesenteric ischemia, immediate surgical consultation and definitive imaging must be performed. Plain radiographs play a limited role in the diagnosis. In retrospective reviews of patients ultimately diagnosed with mesenteric ischemia, plain films are both insensitive and nonspecific.^75-76 In one study of 187 patients, 35% had normal plain films and 42% showed signs of small-bowel obstruction.³² Common plain film abnormalities in acute mesenteric ischemia include an appearance of intestinal ileus, which should come as little surprise given that intestinal motility would be expected to cease in the absence of intestinal blood flow (Figures 11-27 and 11-28; see Figure 11-3). Findings in one small study included air–fluid levels (84%), dilated bowel loops (48%), thickened and unchanging loops (20%), gastric distension and gasless abdomen (12%), and small-bowel pseudo-obstruction (8%).⁷⁶ Findings of ileus may give false reassurance that no critical abnormality is present in the abdomen. The finding of intestinal pneumatosis is likely a relatively rare and late finding, occurring after the onset of intestinal necrosis (see Figures 11-3, 11-27, and 11-28). In one study, only 4% of patients with mesenteric ischemia had pneumatosis on x-ray.⁷⁷ Although pneumatosis should prompt immediate surgical consultation, reliance on this finding likely results in diagnosis at such a late time that exceedingly high morbidity and mortality result.⁷⁸ Ironically, in addition to being insensitive for mesenteric ischemia, pneumatosis is not specific for the diagnosis, occurring sometimes from a variety of less emergent causes (see Figures 11-43 and 11-46).⁷⁸ As with other syndromes of acute abdominal pain, an upright portable chest x-ray is reasonable to detect pneumoperitoneum resulting from intestinal perforation (see Figure 11-1). A negative chest x-ray must be followed by immediate definitive imaging. Abdominal plain films should not be routinely obtained but should be considered in patients too unstable to undergo CT.

Figure 11-27 Bowel infarction (ischemic colitis with pneumatosis): X-ray.

This image depicts classic findings of mesenteric ischemia, including gross distension of bowel, bowel wall thickening, and frank pneumatosis.

Pneumatosis is a late finding, representing the penetration of gas-forming organisms into necrotic bowel wall. How can gas be recognized to be within the bowel wall? The gas is organized in a curved line—indicating that the gas is trapped within the bowel wall, not scattered at random as would be expected if gas were distributed in stool within the bowel. See magnified view, Figure 11-28.

Figure 11-28 Bowel infarction (ischemic colitis with pneumatosis): X-ray.

Close-up from Figure 11-27. This image depicts classic findings of mesenteric ischemia, including gross distension of bowel, bowel wall thickening, and frank pneumatosis.

Computed Tomography for Mesenteric Ischemia

Definitive imaging for mesenteric ischemia is CT with IV contrast (Figures 11-29 to 11-34; see also Figures 11-36 to 11-43, 11-45, 11-46, and 11-48). Oral contrast is not necessary for the diagnosis and should be avoided because of substantial delay, more than 2 hours in some institutions, that can result.¹³ Because of the overlapping presentation of AAA rupture, aortic dissection, and mesenteric ischemia, an immediate CT scan with no contrast agents can be performed to assess for AAA. If this test is negative, immediate CT with IV contrast should be performed unless the patient has significant contraindications to iodinated contrast. As with aortic dissection, the extreme morbidity and mortality of mesenteric ischemia means that the risks and benefits of IV contrast must be carefully weighed. Because this is a time-critical diagnosis with a mortality as high as 60% to 70%,^65-66 some patients with moderate or severe renal insufficiency or contrast allergies should receive immediate IV contrast after a discussion and informed consent from the patient or patient family. Contrast allergies and renal insufficiency are discussed in more detail later.

Figure 11-29 Bowel infarction (ischemic colitis with pneumatosis): CT with oral and IV contrast.

Same patient as in Figures 11-27 and 11-28.

A, A slice viewed on typical CT soft-tissue windows. B, Close-up from A. C, The same slice viewed on an intermediate window setting designed to highlight air. D, Close-up from C. Air is visible within the bowel wall, indicating a bowel segment with frank necrosis whose wall has been infiltrated with gas-forming organisms. This is a dire imaging finding that should prompt immediate surgical consultation. The mortality exceeds 70% for mesenteric ischemia.

Why choose different CT window settings? Standard soft-tissue windows render fat dark—nearly black. This is useful because it allows the identification of subtle fat stranding, which lightens the color of fat. But air can be less noticeable on this setting, because air (black) and fat (nearly black) have little contrast with each other. The window settings in C and D make fat a lighter gray, helping to differentiate it from gas.

Figure 11-30 Bowel infarction (ischemic colitis with pneumatosis): CT with intravenous and oral contrast (soft-tissue windows).

Same patient as Figures 11-27 through 11-29.

This 61-year-old female presented with sepsis, lactic acidosis, and frank pneumatosis on x-ray caused by ischemic colitis. Unstable, on pressor medications, she underwent exploratory laparotomy, extensive lysis of adhesions, subtotal colectomy with end ileostomy, small-bowel resection with primary anastomosis, and splenectomy. Miraculously, she survived, given the severity of her illness on presentation. The operative findings suggested that her ischemia may have been caused by extensive adhesions rather than a single vascular obstruction.

Coronal reconstructions show massive dilatation of the large bowel, as well as frank pneumatosis. A, An anterior slice shows the bowel to be dilated and air filled (remember, the patient was supine during CT, so an anterior coronal plane represents the superior portion of the abdomen). B, A more posterior coronal plane shows a dilated, fluid-filled ascending colon with gas infiltrating its wall—pneumatosis. C, Close-up from B.

Figure 11-31 Superior mesenteric artery (SMA) occlusion: CT with intravenous (IV) contrast.

This 77-year-old male presented in atrial fibrillation with abdominal pain and bright red blood from his colostomy, beginning abruptly after dinner. He had recently been discontinued from warfarin therapy because of falls. Mesenteric ischemia from an embolic occlusion was suspected, given the abrupt onset, atrial fibrillation, gastrointestinal bleeding, and an elevated lactate level (twice the upper limit of normal). CT with IV and oral contrast was performed. The SMA was noted to be completely obstructed with thrombus approximately 6 cm distal to its origin. No secondary bowel findings of ischemia were noted, likely because of the rapidity with which CT was performed after the onset of symptoms. This series of axial views follows the SMA from its origin (A, cephalad slice) to the point of thrombus obstruction (N, caudad slice). Because the SMA tracks anteriorly and diagonally from cephalad to caudad, it is visible in short-axis cross section in most of the slices. Note the sudden change from a widely patent, contrast-filled SMA to a completely unopacified vessel. The finding is the same one that would be noted with an occlusive pulmonary embolism.

Figure 11-32 Superior mesenteric artery (SMA) occlusion: CT with IV contrast.

Same patient as Figure 11-31. This series of axial views (cropped to the region of interest) tracks the SMA from its origin (A) to the point of thrombosis (O).

Figure 11-33 Superior mesenteric artery (SMA) occlusion: CT with IV contrast.

Same patient as in Figures 11-31 and 11-32. This coronal CT captures the SMA at a point where it travels almost perfectly parallel to the coronal plane (A). The patent proximal portion is visible, and the abrupt thrombosed section is also seen. Compare with the angiogram in Figure 11-34. B, Close-up.

Was contrast needed for this diagnosis? Oral contrast played no role here. This patient had a normal CT with the exception of the SMA thrombus, with no secondary bowel findings. IV contrast was essential to the diagnosis, because the SMA thrombosis would not have been visible without a well-timed, high-quality bolus through a large-bore IV catheter.

Figure 11-34 Superior mesenteric artery (SMA) occlusion: Computed tomography (CT) with intravenous contrast.

Same patient as in Figures 11-31 through 11-33. Maximal intensity projection (MIP) images show the thrombosed SMA section in more detail. MIP images are created after the CT scan is performed using the original CT dataset. They “thicken” the image slab, allowing tortuous anatomic structures that cross through multiple routine CT slices to be seen in a single image. Your radiologist can create these upon request to improve diagnostic capabilities. Your local institution may already be performing this postprocessing “behind the scenes.”

A, Coronal reconstruction and enlargement. B, Close-up from A.

C, Sagittal reconstruction and enlargement. D, Close-up from C.

Figure 11-35 Superior mesenteric artery (SMA) occlusion: Angiogram.

Same patient as in Figures 11-31 through 11-34. A catheter has been inserted into the aorta through a femoral artery. The catheter tip has been positioned at the origin of the SMA, and contrast has been injected. The proximal SMA fills, but contrast does not fill the vessel beyond approximately 6 cm—indicating complete thrombotic occlusion. Compare with Figure 11-34, a coronal maximal intensity projection image created from computed tomography reconstruction.

A, Digital angiography. B, The same image using a digital subtraction technique, which digitally removes static portions of the image to allow better inspection of the dynamic contrast injection.

Figure 11-36 Mesenteric ischemia resulting from superior mesenteric artery (SMA) thrombosis: CT without and with contrast.

This 37-year-old male with no prior medical or surgical history presented with abdominal pain with nausea, vomiting, and diarrhea. He underwent noncontrast CT that was interpreted as normal—despite a white blood cell count of 24.5 x 10⁹, an anion gap of 19 mEq/L, and a lactate level of 3.5 mmol/L. The emergency physicians then suspected mesenteric ischemia. CT with contrast was performed, revealing complete thrombosis of the SMA near its origin from the aorta. The two CT scans are displayed side by side to allow comparison of the images. A key point is the need for injected contrast to allow recognition of filling defects within vascular structures. When reviewing the images, compare the noncontrast CT (A) to the CT with intravenous (IV) contrast (B). Slices are numbered from cephaladmost (1) to caudadmost (12). Each slice is shown with an enlarged view centered on the vascular structures of interest. Track the SMA from its origin off the aorta. Without IV contrast, patency of the SMA cannot be assessed, because liquid blood and thrombus have nearly identical density and appear dark gray. With the addition of IV contrast, the patent lumen appears bright white, whereas the filling defect resulting from a thrombus appears dark gray.

Oral contrast is not needed for the diagnosis. In this patient, oral contrast was given but did not progress beyond the stomach—likely because of ileus in the face of bowel ischemia. Oral contrast results in unnecessary delay that can worsen the severe morbidity and mortality of mesenteric ischemia. Operatively, this patient was found to have SMA thrombosis with gangrene of the small intestine and right and transverse colon. He underwent resection of more than 200 cm of small bowel and was left dependent on total parenteral nutrition.

Figure 11-37 Ischemic colitis: CT without IV contrast.

CT soft-tissue windows. This 86-year-old female presented with abdominal pain, vomiting, altered mental status, and hypotension. The patient had an elevated lactate level of 5.7 mmol/L, although this could represent sepsis, rather than mesenteric ischemia. A, The patient did not receive IV contrast because of renal insufficiency (creatinine 2 mg/dL), so vascular structures are not well seen. Although the patient received oral contrast, none reached the distal bowel before CT scan. B, Close-up.

The descending colon shows circumferential wall thickening with a doughnut-like configuration, suggesting colitis, though the cause is not certain (ischemic or infectious). Some surrounding fat stranding is seen. Other images showed portal venous gas (Figure 11-38). The radiologist interpreted the CT scan as suggestive of ischemic colitis.

Because of a concurrent non–ST-elevation myocardial infarction (NSTEMI), the patient was treated solely with fluid resuscitation and antibiotics. She survived the illness. Was the CT diagnosis correct? Was the portal venous gas real, or was it misrecognized air in biliary ducts? These questions remain unanswered. Perhaps this was a case of infectious colitis.

Figure 11-38 Portal venous gas in setting of ischemic colitis: CT without IV contrast.

Same patient as in Figure 11-370. A, Portal venous gas does not require any contrast for identification. This patient had an elevated creatinine and received no IV contrast. She did receive oral contrast, but this did not contribute to the diagnosis. B, Close-up.

Figure 11-39 Portal venous gas and possible ischemic colitis.

CT with IV contrast, soft-tissue windows. This 65-year-old female presented with nausea and epigastric pain. CT with intravenous contrast was performed and showed concerning findings, including thickening of the entire ascending colon, pneumatosis of the colon, and portal venous gas. Laparoscopy was performed because of concern for ischemic colitis—but after inspection of the entire bowel, no resection was performed. The patient was treated for likely infectious colitis. Stool cultures, Clostridium difficile testing, and fecal leukocyte testing were all negative. She recovered uneventfully. Look carefully at these images, which demonstrate portal venous gas. A collection of gas is seen at a branch point in the portal vein (A) and extending to the patient’s left portal vein (B). C, Close-up from A. D, Close-up from B.

Figure 11-40 Portal venous gas and possible ischemic colitis.

Same patient as Figure 11-39. Gas has spread through the portal system. Normally, this is an ominous sign, possibly indicating mesenteric ischemia. Remarkably, this patient had a nontherapeutic laparoscopy and recovered with fluids and antibiotic therapy. These images do not readily distinguish portal vein gas from gas in the biliary tree, which can have a similar appearance. However, Figure 11-39 showed gas more proximally in the portal vein, so these gas collections presumably are present in peripheral portal vein branches, not bile ducts A and C, two adjacent axial CT images through the cephalad portion of the liver, viewed on soft-tissue windows. IV contrast has been administered. B, Close-up from A. D, Close-up from C.

Figure 11-41 Thickening of right colon and ischemic colitis: CT with intravenous contrast only.

Same patient as Figures 11-39 and 11-40. Did this patient have ischemic or infectious colitis? This is uncertain, but patients with her concerning constellation of CT findings should be pursued as possible mesenteric ischemia, because delay in treatment could be catastrophic. A, Axial CT viewed on soft-tissue windows. B, Close-up from A.

Figure 11-42 Thickening of right colon and ischemic colitis.

Same patient as Figures 11-39 through 11-41. As the ascending colon transitions to the transverse colon beyond the hepatic flexure, it relatively rapidly resumes a normal wall thickness. A, Axial CT with IV contrast viewed on soft-tissue windows. B, Close-up from A.

Figure 11-43 Thickening of right colon and ischemic colitis.

Same patient as Figures 11-39 through 11-42. A, Axial CT with IV and oral contrast. B, Close-up from A. Bowel wall thickening is accompanied by an even more concerning finding—pneumatosis (air within the bowel wall). Normally, this finding is associated with bowel wall necrosis, usually in the face of ischemia. Remarkably, this patient recovered without bowel resection or revascularization, but pneumatosis should be treated as a possible surgical indication because of the extreme mortality of untreated mesenteric ischemia. Bowel wall thickening and inflammatory stranding may be seen in infectious, inflammatory, or ischemic colitis. Yersina, Campylobacter, and Salmonella have been described as causing pneumatosis.

Remember that air appears black on all CT window settings. Fat also appears nearly black on soft-tissue window settings. When in doubt, inspect the same slice using lung or bone window settings, as fat appears gray on these window settings. In this case, a standard soft-tissue window setting has been adjusted slightly to make fat brighter in appearance, thereby making black gas more evident.

If the patient has an absolute contraindication to administration of iodinated contrast, noncontrast CT can be performed to assess for mesenteric ischemia. There are no large trials of this approach. Several letters to the editors of radiology journals have commented on the ability to diagnose mesenteric ischemia based on the presence of mural pneumatosis, thickening of the bowel wall, free air, and fat stranding surrounding regions of the small bowel corresponding to vascular territories (see Figures 11-37 and 11-45).^79-81 It is likely that these findings occur relatively late in the presentation, so although their presence may be helpful, their absence does not rule out the possibility of acute mesenteric ischemia. A red flag for mesenteric ischemia is a normal noncontrast abdominal CT in the presence of significant abdominal pain or concerning laboratory findings, such as profound leukocytosis, anion gap, or elevated lactate (Figure 11-36).

When ordering CT for evaluation of mesenteric ischemia, it is important to communicate the diagnostic concern to the radiologist and CT technician so that the CT can be performed appropriately. Modern protocols specifically tailored for evaluation of mesenteric ischemia have been developed.^63,82-84 These use thin-section imaging through the region of the celiac, superior and inferior mesenteric, and middle colic arteries, as well as a rapid contrast bolus to ensure proper opacification of these vessels. Some protocols use arterial phase imaging to evaluate for acute arterial occlusion, followed by delayed images obtained approximately 60 seconds later to evaluate contrast filling of the mesenteric veins and portal venous system.⁸² Kirkpatrick et al.⁸² reported high sensitivity (96%) and specificity (94%) in a small study of 62 patients. Zandrino et al.⁸⁵ reported sensitivity of 92% and specificity of 100% using a similar protocol. However, because of the rarity of mesenteric arterial occlusion and resulting small studies, wide confidence intervals exist around these point estimates. In addition, no studies to date have evaluated the interobserver variability in recognizing these findings. In the setting of intestinal ischemia associated with small-bowel obstruction, the prospective sensitivity of CT for detecting ischemic changes is relatively low in clinical practice (15%),⁸⁶ in contrast to high sensitivity of CT in a pure research setting, which has been reported as high as 96%.⁸⁷ This may reflect the increased vigilance of radiologists when assessing specifically for ischemic changes in a research study.

What Are the CT Findings of Mesenteric Ischemia?

The CT findings of acute mesenteric ischemia include arterial vascular occlusion with an intravascular filling defect similar to that observed with pulmonary embolism (see Figures 11-31 to 11-34 and 11-36). The normal celiac, superior mesenteric, and inferior mesenteric arteries fill uniformly with injected contrast. At their origins from the aorta, these are relatively large vessels with predictable locations. Failure of these vessels to fill, or partial filling, is generally readily recognized, and CT images correlate closely with formal angiography (see Figure 11-35). More distal branches are smaller and more difficult to assess. Secondary findings like bowel wall thickening, regional fat stranding, free air, and mural pneumatosis can be seen in advanced cases. Hypoperfused bowel may also fail to enhance with IV contrast. The portal venous system should be inspected for gas, which can also indicate mesenteric ischemia (Figures 11-38 to 11-40).⁸⁸

Primary findings of a filling defect in mesenteric arteries are highly specific (see Figures 11-31 to 11-34 and 11-36). Unfortunately, some secondary CT findings of mesenteric ischemia are nonspecific and can sometimes be confused with those of inflammatory bowel disease such as Crohn’s disease or ulcerative colitis. In addition, infectious causes such as infectious enteritis can cause bowel wall thickening and fat stranding, similar in appearance to ischemic changes (Figures 11-41 to 11-43; see also Figure 11-46). However, it is essential that the clinician consider ischemia and avoid delay in surgical consultation if the presentation remotely suggests an ischemic cause. If mesenteric ischemia is mistaken for a less dire condition such as inflammatory bowel disease, the outcome can be disastrous (see Figure 11-36).

Figure 11-44 Mesenteric ischemia with free air: Nondiagnostic chest x-ray.

This 81-year-old female presented with diffuse abdominal pain and vomiting. Her electrocardiogram showed new atrial fibrillation, and her lactate level was elevated. A chest x-ray was performed and showed no pneumoperitoneum. Compare this x-ray with the CT in Figure 11-45.

How Sensitive Is Ultrasound for the Diagnosis of Mesenteric Ischemia? What Are the Ultrasound Findings?

Doppler ultrasound can be used to assess thrombosis or stenosis of the celiac artery and SMA. The proximal portions of these vessels at their origins from the aorta are readily seen on ultrasound. The examination can be technically difficult but is a reasonable initial approach in patients with contraindications to CT with IV contrast. In one prospective study of 100 patients, Moneta et al.⁸⁹ reported that mesenteric duplex ultrasound was able to visualize 93% of superior mesenteric arteries and 83% of celiac arteries. Using a threshold of 70% or greater stenosis, duplex ultrasound was 92% sensitive and 96% specific for SMA stenosis and 87% sensitive and 80% specific for celiac stenosis. Danse et al.⁹⁰ reported that Doppler ultrasound confirmed mesenteric ischemia in 8 of 21 patients (38%) and suggested ischemia in an additional 11 of 21 patients (52%)—although this study did not include blinding to other clinical data. More recently, Hata et al.¹⁹ assessed the performance of contrast-enhanced ultrasound for the diagnosis of bowel ischemia. In this study, patients with evidence of small-bowel dilatation were imaged using an injected ultrasound contrast agent. Rather than imaging blood vessels, the investigators assessed bowel wall for normal, diminished, or absent enhancement. The pooled sensitivity of diminished or absent enhancement was 85% (95% CI = 62%-97%), with a specificity of 100% (95% CI = 91%-100%). Contrast-enhanced ultrasound may gain a role in the assessment of unstable patients or those with contraindications to CT contrast agents.

How Sensitive Is Magnetic Resonance Imaging or Angiography for Mesenteric Ischemia?

MRI or MRA has excellent sensitivity and specificity for arterial mesenteric ischemia and for portal venous thrombosis.^30,58,63,84 Gadolinium contrast is generally given.^63,84 CT should be the first-line test because of higher spatial resolution and speed. Indications for MRI include nondiagnostic CT or contraindications for iodinated contrast, particularly severe allergy. Because mesenteric ischemia is extremely time dependent, no time should be wasted performing steroid prep for patients with iodinated contrast allergy (most protocols require 6 hours or more of delay); therefore, emergency MRI is sometimes required. Gadolinium is contraindicated in patients with renal insufficiency, as described later. In this circumstance, MRA can be performed without gadolinium contrast using special sequences as described earlier for aortic dissection—although the sensitivity of these sequences has not been extensively evaluated in mesenteric ischemia.

Variations in Mesenteric Ischemia

Ischemic Colitis

Ischemic colitis accounts for more than half of cases of intestinal ischemia, occurring in about 0.3% of acute hospital admissions. It particularly affects elderly patients with volume depletion and other medical illnesses. Ischemic colitis can also mimic infectious colitis such as Clostridium difficile colitis. Common features of ischemic colitis include hematochezia, abdominal pain, and diarrhea. Remarkably, many patients recover with IV fluid resuscitation and antibiotics. Nonetheless, morbidity is high, and mortality can occur in elderly patients with this condition. Emergent colectomy is sometimes required.⁹¹ Moreover, the presentation can be indistinguishable from SMA occlusion, so the same urgency of diagnostic evaluation is essential. Ischemic colitis has similar noncontrast CT findings, with thickening of the large-bowel wall, surrounding regional fat stranding, pneumatosis, and sometimes pneumoperitoneum (Figures 11-45 and 11-46; see also Figures 11-29, 11-30, and 11-37 to 11-43). CT with IV contrast should be used when possible, because this may reveal a filling defect in vessels supplying the affected large bowel.⁹² The findings are not specific and can mimic infectious colitis or inflammatory bowel disease.

Figure 11-45 Ischemic colitis: CT without IV contrast.

A, Axial CT, viewed on soft-tissue windows. B, Close-up from A. Same patient as Figure 11-44. The patient’s presentation suggested mesenteric ischemia.

Because of the patient’s renal insufficiency, no IV contrast was given. Oral contrast was administered but did not progress beyond the small bowel before CT. This CT scan shows pneumoperitoneum, with a large amount of free air visible within a perihepatic fluid collection. Compare this with the chest x-ray in Figure 11-44, which showed no sign of pneumoperitoneum. Chest x-ray is relatively insensitive for pneumoperitoneum, whereas CT is exquisitely sensitive for this without any contrast agents. Also note the thickened descending colon with surrounding fat stranding. Pneumatosis is also visible in the wall of the descending colon, though no oral contrast has reached the colon. Laparotomy showed perforated ischemic colitis. The patient died of multiorgan failure and sepsis 4 days later.

Figure 11-46 Pneumatosis: CT with oral and intravenous (IV) contrast.

This 56-year-old male with end-stage renal disease on hemodialysis, diabetes, and peripheral vascular disease presented with abdominal pain. He reported similar episodes managed with antibiotics.

His CT demonstrates pneumatosis intestinalis, concerning for ischemic bowel. Given his previous history, this patient was managed nonoperatively and improved with IV antibiotics (ciprofloxacin and metronidazole). CT findings of pneumatosis, though not specific for ischemic bowel, should prompt surgical consultation and consideration of surgical exploration. All panels are displayed with CT soft-tissue windows. Mesenteric ischemia has a mortality rate greater than 70%.

A, Axial view. B, Coronal view. C, Close-up from A. D, Close-up from B.

What Is Contrast Nephropathy? Which Patients Are at Risk?

Contrast nephropathy is defined as a 25% increase in baseline serum creatinine or an absolute rise of 0.5 mg/dL following administration of parenteral iodinated contrast.^106-107 It complicates 15% of contrast procedures, accounts for 10% of in-hospital renal failure, and affects more than 150,000 patients annually in the United States. Although a minority of these patients progress to permanent renal failure or require dialysis, contrast nephropathy is responsible for significant morbidity.¹⁰⁶

Contrast nephropathy risk becomes significant at creatinine clearance rates below 60 mL per minute. Measured serum creatinine is a poor surrogate for creatinine clearance, because it is just one variable in the formula for creatinine clearance (Box 11-1), which is also affected by patient mass, age, gender, and race. In a study of 765 emergency department patients, of whom nearly 1 in 8 had a creatinine clearance rate of less than 60 mL per minute, a serum creatinine limit of 1.8 mg/dL missed 55% of at-risk patients.¹⁰⁸ Even using a highly conservative limit of 1.0 mg/dL would have failed to identify 9% of at-risk patients—highlighting the importance of using creatinine clearance rather than measured serum creatinine.

How Can Contrast Nephropathy Be Prevented?

Multiple means of reducing the risk of contrast nephropathy have been investigated. Early work suggested a benefit to hydration with sodium bicarbonate,¹⁰⁹ but a larger randomized, controlled trial showed no advantage over hydration with normal saline.¹¹⁰ N-acetyl cysteine has been shown in some trials to reduce the incidence of contrast nephropathy, but studies have not demonstrated improvements in patient-oriented outcomes such as need for dialysis.¹¹¹ Most studies on N-acetyl cysteine focus on oral administration 24 hours before contrast administration and thus have no role in emergency department patients with suspected acute abdominal vascular catastrophes requiring immediate imaging. Only one study has investigated the use of IV N-acetyl cysteine 30 minutes before contrast administration and showed a small benefit.¹¹²

Low-osmolality and nonionic contrast agents have lower associated risks of contrast nephropathy than higher-osmolality and ionic contrast agents.¹¹³ Hydration with sodium chloride has been shown to reduce the risk of contrast nephropathy and should be used whenever possible, unless contraindicated by comorbidities such as heart failure or anuria.^113-115 Reducing the volume of contrast administered is also beneficial.¹⁰⁶