Multidetector computed tomography of mesenteric ischaemia

Bowel ischaemia accounts for approximately 0.1 % of all hospital admissions and 1.0 % of admissions for an acute abdomen [1, 2]. Mesenteric ischaemia predominantly affects the elderly, particularly those with comorbid conditions such as congestive heart failure, cardiac arrhythmias, valvular heart disease, coronary artery disease, peripheral vascular disease, dyslipida, recent myocardial infarction or hypotensive episode [2, 3]. Tobacco use is a strongly associated risk factor [2]. In chronic mesenteric ischaemia, women are affected more often than men by a factor of 3–4:1 [2, 3], and there is invariably a background of atherosclerotic disease and often smoking. Younger patients who develop acute or chronic mesenteric ischaemia usually have a predisposing condition such as vasculitis, collagen vascular disease, hypercoagulable state or vasoactive medications [3].

The clinical and laboratory features of acute mesenteric ischaemia (AMI) are nonspecific and make early diagnosis a challenge. Patients present with vague symptoms, such as abdominal pain, nausea, vomiting, diarrhoea and bloating [1, 2]. The physical examination is often benign, with an initially soft and nontender abdomen; the classic hallmark is pain out of proportion to the physical examination [1, 3]. Laboratory tests are neither sensitive nor specific; leukocytosis with leftward shift, acidosis with a high anion gap and elevated amylase may occur late [3, 4]. Though suggestive of ischaemia, an elevated lactate value is also nonspecific and a late marker [1, 2]. Stools may contain occult blood and potentially fatal haemorrhage can occur with bowel infarction [3].

Patients with chronic mesenteric ischaemia have a more insidious onset of disease, with subtle or nonspecific symptoms, an unremarkable physical examination and nonspecific laboratory tests. The classic clinical triad of postprandial abdominal pain, sitophobia (aversion to food) and weight loss may be present [5]. There may also be a history of nausea, vomiting, diarrhoea and signs of malabsorption [6].

A detailed discussion of the complex pathophysiology regarding mesenteric ischaemia is outside the scope of this article, but available elsewhere [2, 7, 8]. Mesenteric ischaemia presents acutely in 95 % of cases and can be arterial or venous in origin according to the following four categories [2]: embolic occlusion of the superior mesenteric artery (SMA), 40–50 % of cases; acute mesenteric arterial thrombosis, 20–30 %; nonocclusive mesenteric ischaemia (NOMI), 25 %; mesenteric venous thrombosis (MVT), 5–15 % [6, 9].

Mesenteric emboli usually originate from left-sided cardiac chambers or valves [2, 3]. Emboli most commonly affect the SMA because of its high flow rate and acute angle with the aorta [2, 4], and they typically lodge distal to the origin of the middle colic artery, resulting in sparing of the duodenum and transverse colon [1]. Twenty per cent of patients may have synchronous emboli to other viscera, such as the spleen or kidneys [2].

Acute mesenteric arterial thrombosis carries the worst prognosis and typically occurs at or near the ostia of the mesenteric arteries. There is usually a background of generalised atherosclerosis and possibly chronic mesenteric ischaemia [1, 2, 10]. NOMI results from low cardiac output and subsequent splanchnic vasoconstriction in such settings as myocardial infarction, congestive heart failure, arrhythmias, shock, sepsis, hypovolaemia and certain drugs [2, 3, 10]. NOMI is associated with a high mortality rate and is often underdiagnosed. Treatment includes administration of vasodilating agents.

MVT involves the SMV in 95 % of cases. MVT may be primary (idiopathic), but is more often secondary to predisposing hypercoagulable conditions such as portal hypertension, trauma, inflammatory or neoplastic processes, and bowel obstruction [3, 9]. With venous thrombosis, bowel ischaemia may be acute, subacute or chronic, with the clinical presentation varying from relatively asymptomatic to acutely ill patients [2]. Thrombosis of small veins draining close to the bowel are more likely to cause bowel infarction [9].

Chronic mesenteric ischaemia (CMI) accounts for 5 % of all mesenteric ischaemia cases and is almost always secondary to severe atherosclerotic disease. Less common, nonatherosclerotic causes of CMI include fibromuscular dysplasia, median arcuate ligament syndrome, radiation-induced injury, tumours encasing or obstructing major vessels, arterial dissection, Takayasu’s arteritis and other vasculitides [3, 5, 11]. As atherosclerotic disease progresses slowly over time, collateral vessels develop throughout the splanchnic circulation. Because of these collateral vessels, intestinal infarction is rare in CMI [3], and typically two of the three main vessels must be affected for symptoms to occur [6].

Three major arteries arise from the ventral abdominal aorta to supply the splanchnic organs: the coeliac artery (CA), superior mesenteric artery (SMA) and inferior mesenteric artery (IMA). The CA (Fig. 1a) arises from the aorta at T12 or L1 and typically divides into three branches: the common hepatic artery, splenic artery and left gastric artery [2, 4]. CA branches supply the liver, distal oesophagus, stomach, pancreas, spleen, stomach and proximal duodenum.

The SMA (Fig. 1b) arises from the aorta at the level of L1 and courses inferiorly to the right lower quadrant where it terminates as the ileocolic artery [2]. The major SMA branches are the inferior pancreaticoduodenal artery, jejunal and ileal arteries, and the right and middle colic arteries. The SMA partially supplies the pancreas and distal duodenum, as well as the entire jejunum, ileum, caecum, ascending colon and the majority of the transverse colon to the splenic flexure [4]. The SMA collateralises with the CA via the pancreaticoduodenal arteries and collateralises with the IMA via the marginal artery of Drummond. Closer to the mesenteric root, the SMA and IMA variably collateralise via the arc of Riolan, which connects the middle colic artery to a left colic artery branch.

The IMA (Fig. 1b) arises a few centimetres above the aortic bifurcation at approximately L3. The IMA branches into the left colic and sigmoid arteries, and terminates as the superior rectal branch, which collateralises with the internal iliac artery [4]. Thus, the IMA supplies the splenic flexure, descending and sigmoid colon and proximal rectum. The splenic flexure is a watershed zone between the SMA and IMA perfusion territories and is at risk for ischaemia [2].

In addition to the aforementioned collateral systems, severe, chronic stenosis or occlusion of all three mesenteric arteries can result in phrenic, lumbar and internal iliac collaterals [11] (Fig. 2).

Mesenteric venous blood drains via the superior and inferior mesenteric veins, which parallel the arteries, and into the portal vein (Fig. 1c). The left colic, sigmoid and superior haemorrhoidal veins drain into the inferior mesenteric vein (IMV), which joins the splenic vein. The duodenal, pancreatic, right gastroepiploic, jejunal, ileal, right and middle colic veins drain into the superior mesenteric vein (SMV).

The American College of Radiology Appropriateness Criteria advocate computed tomography angiography (CTA) as the first-line imaging modality to evaluate both acute and chronic mesenteric ischaemia [6]. CTA is fast, readily available, noninvasive and highly accurate, and it can be used to evaluate other causes of abdominal pain or provide anatomic mapping for preoperative planning [6]. CTA is also less dependent on operator and patient factors [2] than other imaging modalities.

Although previously considered the gold standard diagnostic test, and despite the added benefit of potentially guiding therapy, conventional angiography is now considered a second-line test to diagnose acute or chronic mesenteric ischaemia [6]. In the acute setting, angiography is controversial if signs of peritonitis are present and not recommended if the patient is unstable [2, 6]. The main drawbacks of angiography are that it is invasive, time consuming and not available at all medical centres, particularly after routine working hours [1].

Contrast-enhanced magnetic resonance angiography (MRA) can evaluate stenoses and occlusions of the proximal CA and SMA. However, MRA is limited in assessing smaller calibre arteries including much of the IMA and also less sensitive to detecting gas bubbles and signs of NOMI [6]. The availability and lengthy imaging times of MRA also limit its usefulness in the acute setting, where delayed diagnosis can affect patient care.

Abdominal radiographs and ultrasound (US) are of limited value, with poor sensitivity and specificity in diagnosing mesenteric ischaemia, but may be performed in patients with nonspecific abdominal pain [2, 6]. Radiographs are usually only abnormal with frank bowel infarction [6]. Although Doppler US can be used to assess for proximal mesenteric artery occlusion and signs of bowel compromise, this can be technically challenging and dependent on a number of factors, including patient body habitus, patient compliance and mobility, the presence of bowel gas and local expertise [2]. In patients with CMI, Doppler US peak systolic velocity measurements of greater than 275 cm/s in the SMA and 200 cm/s in the CA correspond to at least 70 % stenosis of these vessels. Like MRA, US cannot be used to assess for distal arterial occlusion or NOMI.

Although the majority of abdominal MDCT applications benefit from positive oral contrast with barium or iodine suspension, such intraluminal contrast makes it difficult to assess enhancement of the bowel mucosa. Evaluation of the intestinal wall is thus best performed with a neutral oral contrast agent, such as water or methylcellulose solution [3, 10, 12].

Although initial CT protocols for mesenteric ischaemia recommended an initial, unenhanced phase to assess for intramural haematoma, calcified plaque and bowel enhancement, recent articles suggest that the unenhanced phase can be omitted [9, 10, 13, 14], as a loop of normally enhancing bowel can often be found to compare and act as an internal control [13]. The multiphasic MDCT imaging protocol includes both arterial and portal venous phase acquisitions: the arterial phase is required for optimal assessment of the mesenteric arterial supply, as thromboembolic disease may account for 60–80 % of acute mesenteric ischaemia cases, and the venous phase is used for assessing bowel wall enhancement and venous drainage. Typical CT parameters are as follows: 120 ml of non-ionic iodinated contrast material is power injected at a rate of 3–5 ml/s, followed by a saline chaser; 120 kVp; 270–300 mAs with automatic tube current modulation whenever possible; as thin a collimation as possible (e.g. 0.625 mm in 64-slice scanners) because of the small size of mesenteric branches [9, 10, 12]. The arterial and portal-venous phases are acquired at approximately 30 and 60 s after injection, respectively, often triggered by a specific attenuation threshold in a region of interest placed over the abdominal aorta [13, 14].

Raw images are reconstructed into 3–5-mm-thick slices for review of the abdominal viscera. Sagittal and coronal reformatted images are generated, as well as three-dimensional maximum-intensity projection (MIP) and volume-rendered images. Sagittal reformats are particularly useful for assessing the origin of the mesenteric arteries from the aorta [10].

MDCT imaging features of mesenteric ischaemia can be classified as intestinal, vascular and mesenteric (Table 1) [9].