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The SMA arises anteriorly from the abdominal aorta, just below the coeliac
artery, at around the level of L1. It has the widest calibre of the three arteries and its
downwards sloping angle of origin makes it the most susceptible to embolic occlusion. The SMA supplies the duodenum from the ampulla of Vater to the distal third
of the transverse colon. Numerous branches arise from the SMA to supply the
bowel, and these form anastomotic arcades in the mesentery. From these arcades,
the vasa recta arise which directly supply the ileal and jejunal walls. There are fewer
jejunal arterial arcades, making the jejunum more vulnerable to ischaemic injury
compared to the ileum (Fig.26.1b).
The IMA has the smallest calibre of the three major arteries and arises from the
anterior abdominal aorta at the level of L3. It supplies the distal two-thirds of the
transverse colon, the descending and sigmoid colon, and supplies the upper twothirds of the rectum (Fig.26.1c). The marginal artery of Drummond along the large
bowel can also be helpful in circumstances of embolism or stenoses.
Anatomical Variants
Both the SMA and coeliac artery can arise as a single trunk from the aorta (coeliacomesenteric trunk), or the SMA can arise from the common hepatic artery. The Arc
of Riolan is a possibility for collateral ow in the event of occlusion, and in these
cases, the splenic exure can be spared [9].
L. R. Howroyd et al.
Venous Anatomy
The portal venous system and the inferior vena cava should be considered. The
portal venous system transports nutrient rich blood from the bowel to the liver for
processing. At the level of the bowel, the veins are paired in the mesentery with the
arteries. The SMV and splenic vein converge at the portovenous or portomesenteric
conuence and form the portal vein.
General Pathophysiology ofAMI
The development of AMI depends on several factors, including how many vessels
are involved, the level at which the vascular occlusion occurs, the quality of the
available arterial collateral network, and crucially, the duration of interrupted arterial supply. Ischaemic injury develops when there is insufcient delivery of oxygen
and nutrients required to support cellular metabolism. The bowel is thought to be
able to tolerate major reduction in mesenteric blood ow for up to 3h without substantial injury [10, 11].
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In the initial stages of hypoxic injury, the mucosa is affected rst and if the vascular obstruction is relieved rapidly, injured cells may recover. If the hypoxia persists, the submucosa, muscularis propria and eventually serosa become involved,
with oedema, haemorrhage and necrosis occurring. Once the muscularis is affected,
the ischaemia is called transmural and is irreversible. This can occur in as little as
6h in cases of complete vascular obstruction [12]. Once the bowel wall is infarcted,
bacterial translocation leads to gangrene, peritonitis, sepsis and multi-organ failure.
The most important prognostic factor is the duration of inadequate blood supply
[13]. Therefore rapid diagnosis and effective intervention are fundamental to an
improved outcome.
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General Management Principles
The management of AMI is primarily focussed on restoring adequate blood ow to
the mesenteric vessels and treating any identiable underlying causes. Adequate
resuscitation and anticoagulation if appropriate are early steps in any case.
With the advent and continuing evolution of image-guided endovascular procedures, the open surgery is not obligatory anymore, as treatment options are
expanding.
Mesenteric Arterial Embolism (MAE)
This is the most common cause of AMI, accounting for approximately 33–50% of
cases [4, 14]. The most common origin of the emboli is cardiac, with around 50%
of patients presenting with MAE having atrial brillation (AF) [8]. Related risk factors include recent myocardial infarct, known cardiac thrombi, mitral valve disease
and previous embolic disease.
Pathophysiology
Due to its wide calibre and narrow take off angle from the aorta, the SMA is particularly vulnerable to embolic events. Usually, the embolus lodges in the proximal
SMA approximately 3–10 cm beyond the vessel origin as it tapers in calibre at
around the level of the middle colic artery branch [15–17]. When this occurs, the
proximal branches of the SMA remain patent and therefore the proximal jejunum
remains partially perfused, whereas the distal jejunum and ileum are vulnerable to
ischaemia [18, 19].
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Clinical Presentation
The typical presentation is with sudden and severe abdominal pain. Nausea, vomiting, tachycardia and hypotension may ensue. Abdominal guarding and rebound tenderness suggest that bowel gangrene is already occurring.
Mesenteric Arterial Thrombus (MAT)
Accounts for approximately 25–30% of cases [4, 5], often in association with coronary artery disease, peripheral arterial disease, or diabetic arteriopathy.
Due to the chronic nature of the underlying cause, there is usually a wellestablished collateral arterial supply, and ischaemia usually only develops when two
of the three major mesenteric arteries suffer severe stenosis or occlusion (usually the
coeliac artery and SMA).
Alternatively, ischaemia can develop in the absence of complete occlusion in the
setting of generalised reduction in blood ow to the bowel, for example, in states of
hypotension or low cardiac output.
Given that the patients with MAT tend to be older, with multiple co-morbidities,
and a larger portion of the bowel is affected, the prognosis of MAT is worse when
compared to MAE [5].
Clinical Presentation
As there is a sudden obstruction to an already stenosed artery, the typical presentation is that of an acute exacerbation of pain on a background of longstanding
abdominal angina. However previous angina is not obligatory, and new onset of
pain can be the only evidence of the trouble.
Mesenteric Venous Thrombosis (MVT)
Incidence andRisk Factors
MVT accounts for 5–11% of cases [4, 5]. Of all the causes of AMI detailed here,
this has the youngest peak age of onset. In up to 75% of these patients a background
derangement is present [20].
Approximately 50% of patients have a history of previous venous thrombus, that
is a deep vein thrombus (DVT) or pulmonary embolus (PE) [21]. Risk factors for
venous thromboembolism in general are risk factors for MVT, such as oral contraceptive pill use and pregnancy [22]. Portal hypertension, hypercoagulable states
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(e.g. inherited diseases such as Factor V Leiden and antiphospholipid syndrome),
intraabdominal infection, intraabdominal inammation (e.g. pancreatitis), malignancy, and abdominal trauma or recent surgery are all common risk factors.
Pathophysiology
Propensity to thrombosis is classically attributed to a combination of Virchow’s
triad (stagnant ow, hypercoagulability and endothelial damage). The above risk
factors/secondary causes can all be understood within this framework. Thrombosis
starts in the intramural venules, vasa recta and venous arcades [20]. The SMV and
ileal loops it drains are most affected, with the IMV and colon rarely affected,
thought in part due to collateral ow in the pelvic systemic veins making the IMV
less vulnerable.
Bowel wall oedema and luminal distention in the affected bowel are the consequence. The oedema and distention lead to increased tissue pressure and the arterial
inow is compromised, thus leading to ischaemia. MVT may not necessarily cause
intestinal infarction, instead collateral venous drainage can form. Chronic venous
thrombosis can lead to raised portal venous pressures (portal hypertension) and
dilated venous collaterals, prone to bleeding.
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Clinical Presentation
Typically, there is a subacute presentation with abdominal pain over a period of
days to weeks.
Non-occlusive Mesenteric Ischaemia
NOMI accounts for 15–20% of cases of AMI [4, 5].It classically occurs in critically
unwell or physiologically vulnerable patients. Notably, it complicates 0.5–1% of all
cardiac operations [23] and heart failure is a strong risk factor. Cocaine use has also
been identied in younger patients presenting with NOMI [24].
Pathophysiology
NOMI used to be attributed to prolonged and severe mesenteric arterial spasm;
however, hypoperfusion with no spasm seems to be the major driver. This is a poorly
understood phenomenon typically occurring in critically ill patients with deranged
tissue perfusion. The combination of the often vulnerable physiological state of the
patient with the difculties in identifying and treating NOMI effectively lead to a
mortality rate of NOMI of around 50% [25, 26].
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Presentation
NOMI is difcult to identify as patients are usually already very unwell or post
surgical, and as such are likely intubated and ventilated, unable to communicate any
symptoms, and the signs can be masked. It should be suspected in any critically
unwell patient with a sudden and unexpected deterioration. If the patient is conscious, this may be in the form of nonspecic pain, bloating and nausea and acute
confusion. If the patient is sedated, the warning signs include an unexplained metabolic acidosis and need for more inotropic support.
L. R. Howroyd et al.
Other Causes ofAMI
Arterial Dissection
Approximately 5% of patients with an aortic dissection develop AMI [4, 27].
Fibromuscular Dysplasia (FMD)
FMD is a rare but well-recognised cause of CMI which can develop into MAT. If the
patient is not known to have FMD the appearances on imaging are the same as in the
more common renal artery manifestation of the disease, with a classically described
‘string of beads’ appearance to the affected arteries [28].
Inammatory
Takayasu’s arteritis and Ehlers Danlos syndrome have both been reported as causes
for AMI [29, 30]. Cases of trauma, retroperitoneal brosis, abdominal coarctation,
neurobromatosis and post irradiation arteritis have all been identied as possible
causes for AMI [27].
Diagnostic Imaging
Double or Triple-Phase CT with CT Angiography
CT can distinguish between AMI and other causes of abdominal pain, as well as
demonstrate specic features of causes of AMI.Furthermore, CT is key in establishing potential options for management, in planning endovascular procedures, or
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identifying irreversible damage which will indicate that the situation cannot be
rectied by simply restoring mesenteric blood ow and will require open surgical
resection.
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Contrast-Enhanced Phases
The contrast given in CT contains iodine, which absorbs X-rays differently to tissues in the body and appears denser or brighter on the acquired images, acting to
highlight the vessels or organ it is in. Altering the time delay between when the
contrast is given intravenously and when the CT is then acquired gives different
phases of imaging.
Arterial Phase
A time delay of 20–40s will result in an arterial phase scan, where the contrast is
mainly in the abdominal aorta and mesenteric arteries. This is often known as a CT
Angiogram (CTA) and in AMI will enable assessment for intravascular lling
defects. In cases of AMI the sensitivity for CTA alone is as much as 93.3% and the
specicity 95.9% [31].
Portal Venous Phase
If the interval between contrast administration and image acquisition is delayed to
60–90s, the contrast bolus has had time to pass through the capillary beds and is
within the mesenteric venous system. This phase provides information about endorgan perfusion and allows for assessment of venous patency.
Enteric Contrast Administration
Administration of oral or per rectum contrast has no role in suspected cases of
AMI.High-density contrast in the lumen of the bowel can mask features of ischaemia.
Unenhanced/Non-contrast Phase
A possible pitfall with contrast-enhanced images is differentiating structures that
are inherently dense, like calcium in atherosclerotic plaque, with iodine contrast. To
differentiate between contrast and pre-existing densities, an unenhanced scan before
any contrast is given is necessary. In AMI, this enables detection of vascular calcication or high-density intravascular thrombus that may be masked by contrast
administration.
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If these three phases are acquired in the same study, non-contrast or unenhanced,
arterial and portal venous phases, this is known as a triple-phase study. The downside is that the three phases require three separate acquisitions through the scanner,
and so the dose of ionising radiation is greater. Techniques such as dual-energy CT
and iodine mapping can further increase accuracy in diagnosis of AMI [32].
In suspected cases of AMI, a clinical conversation with the radiologist in the vetting process facilitates appropriate protocolling of the study. A decision can be
made about whether a single phase, for example, just an arterial (i.e., just a CTA) or
just a portal venous phase study is sufcient to make the diagnosis, or whether a
triple phase will enable more detailed conclusions to be drawn.
CT inAMI
General CT Features
Bowel wall thickening is the most common nding in AMI representing mural
oedema, haemorrhage, or infection but this is not specic to AMI and is seen in
other scenarios such as inammation [33]. Importantly, not all causes of AMI result
in bowel wall thickening. Indeed, in cases of complete arterial occlusion, the bowel
wall can be thinned [34]. Wall thickening is most prominent in cases of MVT, and
in cases of MAE and MAT wall thickening is usually only seen once the perfusion
has been restored. [35]
Bowel wall enhancement patterns are variable. High density on the unenhanced
phase is indicative of intramural haemorrhage. High density on the contrastenhanced images is indicative of congestion or reperfusion. A target or halo appearance is the classical description.
Reduced bowel wall enhancement is specic, but not sensitive for ischaemia
[36]. In arterial causes, decreased enhancement will occur early and is not necessarily indicative of irreversible ischaemia. Conversely, in venous causes decreased
enhancement occurs late and is more indicative of irreversible ischaemia [37].
The presence of mesenteric stranding is also variable and does not correlate with
the severity of ischaemia. Stranding is more prominent in MVT and NOMI, and if
present in arterial causes of occlusion, it is a later sign and may indicate more
advanced irreversible ischaemia [34].
Features ofAdvanced Ischaemia
An important role of CT is in identifying advanced and likely irreversible ischaemia. Imaging features of this are ileus, with bowel wall dilatation being the best
predictor of transmural necrosis in arterial occlusions [38]. Thinning of the bowel
wall indicative of muscular and neurological ischaemia is highly specic [37]. Late
signs are intramural gas (pneumatosis intestinalis) and portal venous gas. Free intraperitoneal air is another late sign signifying perforation (Fig.26.2).
26 Acute Mesenteric Ischaemia: Imaging andIntervention
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a
b
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Fig. 26.2 Features of advanced mesenteric ischemia. (a), (b) and (c) are contrast-enhanced axial
CT images. (a) Distended, uid-lled small bowel loops indicating adynamic ileus (white arrowheads). These loops show absent mural enhancement and paper-thin bowel wall. Note nondistended small bowel loops in the right hemipelvis showing normal bowel wall thickness and
enhancement (white arrows). (b) Circumferential small bowel pneumatosis (white arrowheads).
(c) A large locule of gas within the left portal vein (white arrow) with gas-lled peripheral portal
vein branches in the anterior liver (white arrowheads)
c
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Specic Features oftheSubtypes ofAMI
MAE: emboli may be visualised as high-density material within the arterial lumen
on the unenhanced CT, or as either luminal lling defects or an abrupt transition to
completely non-opacied artery on the arterial phase CT.As described above, the
SMA is the most affected vessel due to its anatomy. CT in these patients may reveal
further emboli elsewhere, such as the peripheral arteries causing limb ischaemia, or
in solid abdominal organs—causing hepatic, splenic, or renal infarcts. The vascular
territory affected will determine the segments of bowel that are affected (Fig.26.3).
MAT: Calcication at the ostia of the major splanchnic vessels is typical in atherosclerotic disease and can point towards MAT as a potential underlying cause.
Arterial stenosis or occlusion is well-visualised in arterial phase imaging. However
acute and chronic occlusion can look identical and can only be reliably distinguished if there are bowel or mesenteric changes suggestive of acute ischaemia.
Additionally, the clinical picture must be considered when differentiating the two
(Fig.26.4).
MVT: In >90% of cases [39] a lling defect is evident in the portal venous sys-
tem on a portal venous phase CT.Additional features include mural rim enhancement in the wall of the vein at the site of thrombus, mesenteric engorgement and
ascites. Prominent bowel wall thickening reecting marked mural oedema is not
uncommon (Fig.26.5).
a
Fig. 26.3 Features of mesenteric arterial embolism. (a) Coronal arterial phase CT showing an
occlusive lling defect within the SMA lodged at the orice of the middle colic artery (white
arrow) with poorly enhancing ileal loops in the right lower abdomen. Note that the proximal jejunal branches remain patent (white arrowhead) and the jejunal loops in the left upper abdomen have
preserved normal enhancement. (b) Axial arterial phase CT shows a lling defect within the SMA
with a characteristic peripheral rim of enhancement representing contrast between the embolus and
the vessel wall (white arrow)
b
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a
c
b
d
Fig. 26.4 Intervention for mesenteric arterial thrombus. (a) Sagittal arterial phase CT showing
non-occlusive lling defect within the proximal SMA (white arrowheads). The origin of the coeliac axis is patent (white arrow). (b) Lateral projection digital subtraction angiogram performed via
a ush catheter in the abdominal aorta. Proximal SMA non-occlusive thrombus is again demonstrated (white arrowheads). The proximal celiac axis is again shown to be patent (white arrow). (c)
Angiogram performed after suction thrombectomy shows improved patency of proximal SMA and
its branches but with residual vessel wall irregularity (white arrowheads) and an underlying stenosis in the proximal SMA (white arrow). (d) Completion angiogram performed following deployment of a balloon-expandable metal stent in the proximal SMA (white arrowheads) showing
signicantly improved vessel calibre and ow
NOMI: NOMI is a diagnosis of exclusion, and occlusive causes must be actively
ruled out. Classically the distribution of the bowel ischaemia is segmental and discontinuous and there is no occlusive cause evident. Watershed areas tend to be
affected rst, and arterial diameters tend to be particularly small [5, 33, 34, 40].
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