ACUTE MESENTERIC ARTERIAL OCCLUSION

Authors:
Gregory Pearl, MD
Ramyar Gilani, MD
Section Editors:
John F Eidt, MD
Joseph L Mills, Sr, MD
Deputy Editor:
Kathryn A Collins, MD, PhD, FACS
All topics are updated as new evidence becomes available and our peer review process is
complete.
Literature review current through: Apr 2017. | This topic last updated: Oct 25, 2016.

INTRODUCTION Acute mesenteric ischemia refers to the sudden onset of small

intestinal hypoperfusion, which can be due to reduction or cessation of arterial inflow.
Ischemia due to acute mesenteric arterial occlusion can be caused by embolic obstruction
of the intestinal blood supply, most commonly to the superior mesenteric artery (SMA).
Acute ischemia can also occur due to acute thrombotic obstruction, often in the setting of
an already diseased mesenteric vessel (eg, atherosclerosis).

Acute mesenteric ischemia due to acute arterial obstruction involving the small intestine
will be reviewed here. Colonic ischemia, chronic mesenteric ischemia, and other forms of
mesenteric ischemia, including mesenteric venous occlusion and nonocclusive mesenteric
ischemia, are reviewed elsewhere. (See "Mesenteric venous thrombosis in
adults" and "Chronic mesenteric ischemia" and "Colonic ischemia" and "Nonocclusive
mesenteric ischemia".)

MESENTERIC ANATOMY AND PHYSIOLOGY The arterial anatomy of the intestinal

circulation is given in the figures (figure 1 and figure 2 and picture 1). Ischemic injury to the
intestine develops when there is insufficient delivery of oxygen and nutrients required for
cellular metabolism. An overview of intestinal anatomy, normal intestinal vascular
physiology, and the response to acute ischemia are discussed in detail elsewhere.
(See "Overview of intestinal ischemia in adults", section on 'Intestinal vascular
anatomy' and "Overview of intestinal ischemia in adults", section on 'Physiology and
mechanisms of ischemia'.)

The intestine may be able to compensate to some extent because of increased oxygen
extraction as well as the presence of collateral flow pathways (figure 3) [1]. The status of
the collateral circulation is particularly important in determining the severity of symptoms
[2]. Acute superior mesenteric arterial occlusion, in the absence of preexisting stenosis
such as with embolism, causes a greater reduction in blood flow compared with other
causes of intestinal ischemia. This is due to the lack of collateralization in the presence of
relatively normal arterial vasculature. By contrast, acute thrombosis of atherosclerotic
lesions may have had the opportunity to develop collateral pathways to provide some
degree of perfusion even in the setting of complete occlusion. Inciting factors such as
dehydration or low cardiac output states can lead to acute thrombosis of even modest
stenosis, causing typical signs and symptoms of acute mesenteric ischemia with no prior
history. For some patients, progression from stenosis to occlusion can be asymptomatic
due largely to a sufficient time course to develop these collaterals.

ETIOLOGY OF MESENTERIC ARTERIAL OCCLUSION The two major causes of

acute mesenteric arterial occlusion are mesenteric arterial embolism and mesenteric
arterial thrombosis. In an autopsy study, the ratio of superior mesenteric embolus to
thrombus ratio was 1.4:1 [3].

Arterial embolism Embolism to the mesenteric arteries, which may partially or

completely occlude the arterial lumen, is most frequently due to dislodged thrombus
from the left atrium, left ventricle, cardiac valves, or proximal aorta. Systemic
embolization occurs in 22 to 50 percent of cases of infected endocarditis, with
embolization to the viscera second only to cerebral embolism [4,5]. A history of prior
embolization is common. In an autopsy series, 19 percent had an acute myocardial
infarction, 48 percent had remnant cardiac thrombus, and 68 percent had
synchronous embolus [3]. Emboli tend to lodge at points of normal anatomical
narrowing, usually at a branching point of an artery. The large diameter and narrow
takeoff angle of the superior mesenteric artery (SMA) make it anatomically most
susceptible to embolism. The inferior mesenteric artery is rarely affected due to its
small caliber [6]. The embolus usually lodges 3 to 10 cm distal to the origin of the
SMA, in a tapered segment distal to the takeoff of the middle colic artery and sparing
the first few jejunal branches, but approximately 15 percent of emboli lodge at the
origin of the SMA [7]. The middle segment of the jejunum, which is most distant from
the collateral circulation of the celiac and inferior mesenteric arteries, is most often
involved in the ischemic process, whereas the proximal jejunum is usually spared.
Jejunal sparing suggests embolic occlusion rather than acute-on-chronic occlusion of
the SMA related to atherosclerotic disease as the underlying cause of acute
mesenteric ischemia (picture 2). Concomitant arteriolar vasoconstriction usually
occurs, further impairing intestinal blood flow and exacerbating the ischemia.
(See "Atrial fibrillation: Anticoagulant therapy to prevent
embolization" and "Antithrombotic therapy for prosthetic heart valves:
Indications" and "Left ventricular thrombus after acute myocardial infarction", section
on 'Prevention of embolic events' and "Embolism from aortic plaque:
Thromboembolism", section on 'Antithrombotic therapy'.)
Arterial thrombosis Arterial thrombosis occurs at areas of severe narrowing most
typically due to atherosclerosis.
Acute thrombosis of the mesenteric circulation often occurs as a superimposed
phenomenon in patients with a history of chronic mesenteric ischemia from
progressive stenosis due to atherosclerotic aortic plaque that involves the takeoff
of the celiac axis and SMA, also referred to as acute-on-chronic ischemia.
Therefore, thrombosis of the SMA or celiac axis usually occurs at the origin of
 the vessel, and involvement of at least two major mesenteric arteries is generally
needed for the patient to have significant symptoms because of the development
of the collateral circulation over time [8]. (See "Chronic mesenteric
ischemia" and "Overview of infected (mycotic) arterial aneurysm", section on
'Visceral arteries'.)
Mesenteric arterial thrombosis can also occur in the setting of vascular injury
related to abdominal trauma, infection, or mesenteric dissection. Septic
embolization from infected heart valves to the visceral arteries can cause
mycotic aneurysm, which can also thrombose. Thrombosis of a previously
placed mesenteric stent can also occur.

EPIDEMIOLOGY AND RISK FACTORS Thromboembolic occlusion of the superior

mesenteric artery is the most common cause of acute mesenteric ischemia. Acute
mesenteric arterial occlusion accounts for 67 to 95 percent of cases of acute mesenteric
ischemia [3,6,7,9-11].

Risk factors Risk factors for acute mesenteric arterial occlusion include any process
that increases the potential for embolism from the heart or proximal arterial vasculature or
for arterial thrombosis. (See "Overview of intestinal ischemia in adults", section on 'Risk
factors'.)

The risk of embolism is increased in patients with cardiac arrhythmias, cardiac

valvular disease, infective endocarditis, recent myocardial infarction, ventricular
aneurysm, aortic atherosclerosis, and aortic aneurysm.
The risk of thrombotic occlusion is increased in patients with peripheral artery
disease (with or without prior mesenteric stenting), advanced age, and low cardiac
output states [7]. Traumatic injury can also lead to visceral artery thrombosis [12].
Unlike mesenteric venous thrombosis, there does not appear to be a significant
association between inherited coagulation defects and mesenteric arterial thrombosis
[13,14].

Less frequently, acute mesenteric ischemia may also be observed in the setting of an
underlying vasculitis, most commonly polyarteritis nodosa. Vasculitis affects the small- and
medium-diameter arteries and can lead to acute segmental intestinal infarction, but it may
be difficult to determine if acute symptoms are due to arterial occlusion or spasm (ie,
nonocclusive ischemia). Fibrous intimal thickening is typically seen histologically [15,16]. In
most cases, stenoses and/or microaneurysms are detected on arteriography without
obstruction of the main mesenteric arteries. (See "Nonocclusive mesenteric
ischemia" and "Gastrointestinal manifestations of vasculitis" and "Clinical manifestations
and diagnosis of polyarteritis nodosa in adults".)

CLINICAL FEATURES Early symptoms and clinical signs, including laboratory studies
and plain radiographs, are nonspecific, but any patient with acute-onset abdominal pain,
minimal findings on abdominal examination (classically described as pain out of proportion
to the exam), and metabolic acidosis should be regarded as having intestinal ischemia
until proven otherwise. Risk factors for arterial embolism or for atherosclerosis (smoking,
hypertension, hyperlipidemia, diabetes) may be present (see 'Risk factors' above).
Symptoms of chronic mesenteric ischemia such as pain with meals and weight loss may
be noted on the history. Plain films and cross-sectional abdominal imaging do not exclude
mesenteric ischemia but may identify complications related to mesenteric ischemia (eg,
necrosis, perforation) and indicate the need for immediate abdominal exploration, while
also helping to exclude other obvious causes of abdominal pain (eg, volvulus, small bowel
obstruction) [17-28]. (See "Overview of intestinal ischemia in adults", section on
'Laboratory studies' and "Overview of intestinal ischemia in adults", section on 'Plain
radiographs' and "Overview of intestinal ischemia in adults", section on 'Advanced
abdominal imaging'.)

Specific clinical features that suggest mesenteric arterial embolism or mesenteric arterial
thrombus as a cause of acute mesenteric ischemia are as follows:

Mesenteric arterial embolism The typical clinical triad of acute embolic occlusion in
an older adult patient with atrial fibrillation (or other source for embolism) and severe
abdominal pain out of proportion to the physical examination is present in one-third to
one-half of patients. Bowel emptying, nausea, and vomiting are also common, but
bloody bowel movements are less common, unless advanced ischemia is present.
The patient may be subtherapeutic on previously prescribed antithrombotic therapy. A
prior embolic event is present in approximately one-third of patients. It is particularly
important in these patients to perform a complete vascular examination examining the
carotid, upper extremity, and lower extremity pulses for evidence of reduced perfusion
related to synchronous embolism [29]. Over 20 percent of acute mesenteric emboli
are multiple.
For patients with a history of infective endocarditis, most emboli (cerebral most
common, followed by visceral, then lower extremity) occur within the first two to four
weeks of antimicrobial therapy and may be more common in patients with mitral valve
involvement, larger vegetation size (largest are associated with streptococcus),
staphylococcus independent of vegetation size, and increasing vegetation size while
on treatment [4,5]. (See 'Risk factors' above and "Clinical manifestations and
evaluation of adults with suspected native valve endocarditis".)
Mesenteric arterial thrombosis The typical patient with acute mesenteric
thrombotic occlusion is a patient with risk factors for atherosclerosis and possibly
known peripheral artery disease who may or may not have an established diagnosis
of chronic mesenteric ischemia based upon symptoms of chronic postprandial
abdominal pain, food aversion, and weight loss. However, in contrast to the classic
description, one study noted that patients may not be cachectic, possibly due to
earlier diagnosis or a relatively high proportion of patients who were overweight
before the onset of symptoms. However, obtaining an antecedent history of chronic
mesenteric ischemic symptoms may be helpful for differentiating thrombotic versus
 embolic occlusion and may potentially influence the choice of initial treatment [11,30].
(See 'Endovascular intervention' below and "Chronic mesenteric ischemia".)

Routine laboratory evaluation for abdominal pathology is performed, including complete

blood count, arterial blood gas, and lactate. Classically, patients have leukocytosis,
acidosis, and elevated lactate; however, this occurs in a minority of patients. Normal
laboratory findings do not exclude the diagnosis of acute mesenteric arterial occlusion.
(See "Overview of intestinal ischemia in adults", section on 'Laboratory studies'.)

DIAGNOSIS As with all forms of mesenteric ischemia, the diagnosis of acute

mesenteric arterial occlusion depends upon a high level of clinical suspicion, particularly in
patients with known risk factors for peripheral embolization (eg, atrial fibrillation, recent
myocardial infarction, valvular disease) or a history of peripheral artery disease with or
without a history of chronic abdominal pain. Rapid diagnosis is essential to prevent the
catastrophic events associated with intestinal infarction [31].

A definitive diagnosis of mesenteric arterial occlusion relies upon demonstrating the

occlusion within the mesenteric arteries on imaging studies. High-resolution computed
tomographic (CT) angiography is highly diagnostic for cases of acute mesenteric ischemia.
In addition, based upon the appearance of vessels in the abdomen, it is possible to
differentiate between embolic and thrombotic etiologies. Further information for operative
planning, such as distal arterial reconstitution and choice of inflow vessel for surgical
bypass, can also be obtained. In the setting of equivocal CT angiography findings,
catheter-based angiography may be needed. For patients who present with advanced
ischemia (bowel perforation and peritonitis) and hemodynamic instability, a diagnosis will
necessarily be made in the operating room. (See 'Management' below.)

Embolic mesenteric occlusion Embolic occlusion often appears as an oval-shaped

thrombus surrounded by contrast in a noncalcified arterial segment located in the
middle and distal portion of the proximal superior mesenteric artery (SMA) (image
1 and image 2).
Thrombotic mesenteric occlusion Thrombotic occlusion usually appears as
thrombus superimposed on a heavily calcified occlusive lesion at the ostium of the
SMA (image 3).

In addition to determining the type of mesenteric arterial occlusion (ie, embolism or

thrombus), CT angiography identifies the collateral circulation and potential sources of
inflow and avoidable sites with extensive atherosclerotic lesions in cases that might require
revascularization.

DIFFERENTIAL DIAGNOSIS Acute mesenteric arterial occlusion needs to be

differentiated from other causes of abdominal pain and from mesenteric ischemia due to
nonocclusive mesenteric ischemia or mesenteric venous thrombosis. These distinctions
are reviewed elsewhere. (See "Causes of abdominal pain in adults" and "Overview of
intestinal ischemia in adults", section on 'Differential diagnosis'.)

MANAGEMENT Initial medical management for all patients with acute mesenteric
ischemia includes the following, which are discussed in detail separately (algorithm 1)
(see "Overview of intestinal ischemia in adults", section on 'Initial management'):

Nothing by mouth, nasogastric decompression.

Fluid therapy to maintain adequate intravascular volume and visceral perfusion and
monitored as normal urine output.
Avoidance of vasopressors, which can exacerbate ischemia.
Antithrombotic therapy consists of anticoagulation (unfractionated heparin, weight-
based protocol) to limit thrombus propagation and help alleviate associated arteriolar
vasoconstriction with or without antiplatelet therapy [32].
Empiric broad-spectrum antibiotic therapy.
Proton pump inhibitors [33].
Supplemental oxygen [33].

Approach to treatment Clinical evaluation and vascular imaging determine whether

the patient is a candidate for vascular intervention and whether the occlusion is embolic or
thrombotic (algorithm 2 and algorithm 3), which has a bearing on the type of intervention
offered. The goal of vascular intervention is to restore intestinal blood flow as rapidly as
possible. The specific treatment chosen depends upon the clinical status of the patient and
the etiology and location of the occlusion. Optimal treatment may include open,
endovascular, or a combined approach. The ability to offer an endovascular approach
depends upon local resources and the availability of vascular specialists. A hybrid
interventional suite/operating room may be the ideal setting to manage acute mesenteric
arterial occlusion, but these are generally available only at large vascular centers.
(See 'Diagnosis' above and 'Surgical versus endovascular intervention' below.)

Some patients (eg, acute-on-chronic occlusion) who are hemodynamically stable

and do not have clinical signs of advanced bowel ischemia can be observed while on
heparin anticoagulation, if there is evidence of good collateral blood flow on vascular
imaging studies. Antiplatelet therapy may be justified in this setting if the risk of
progressive ischemia appears to be greater than the risk of bleeding [32,34]. The
patient should have serial clinical assessment (laboratory, physical examination) with
a low threshold to repeat abdominal imaging studies or, if abdominal symptoms
progress, surgical or endovascular intervention. (See 'Surgical versus endovascular
intervention' below.)
A palliative approach may be the best option for poor-risk surgical candidates with
extensive transmural infarction (eg, small bowel up to the midtransverse colon).
Extensive bowel resection would be inappropriate for these patients and may also be
inappropriate for a subset of patients who might otherwise be expected to tolerate the
 procedure but for whom lifelong parenteral nutrition would be unacceptable (picture
3). (See "Palliative care: The last hours and days of life".)
Patients who are good-risk surgical candidates with indications for immediate
laparotomy such as peritonitis or radiologic features of advanced bowel ischemia
(free air, extensive pneumatosis) should be taken directly to the operating room for
exploration. Resection of bowel should ideally be delayed until after mesenteric
arterial revascularization can be performed to salvage as much bowel as possible;
however, in practice, this sequence does not commonly occur. In situations where an
individual with appropriate vascular expertise is not immediately available, resection
of grossly necrotic or perforated bowel (leaving any questionable bowel) while
awaiting intraoperative consultation is appropriate, or, alternatively, following
resection, abdominal closure and transfer is also a reasonable option when required.
(See 'Abdominal exploration/damage control' below.)
The traditional treatment for mesenteric embolism is open surgical
embolectomy, which, in addition to expeditiously clearing the thrombus, allows
direct assessment of bowel viability. (See 'Embolectomy' below.)
Open surgical treatment of mesenteric artery thrombosis is treated principally
with mesenteric bypass. Thrombectomy alone is unlikely to offer a durable
solution due to the presence of thrombogenic atherosclerotic plaques.
Intraoperative retrograde superior mesenteric artery angioplasty and stenting is
another option, particularly in the presence of gross contamination where bypass
is more problematic. (See 'Mesenteric bypass' below.)
Patients who are hemodynamically stable and who do NOT have clinical or
radiologic signs of advanced intestinal ischemia may be candidates for a primary
endovascular approach.
Although we prefer open surgical thrombectomy for patients with acute
embolism, percutaneous aspiration of the clot or catheter-directed thrombolytic
therapy is another approach that has been used successfully with reasonable
outcomes. (See 'Embolectomy' below and 'Pharmacomechanical
thrombolysis' below.)
For patients with acute mesenteric thrombosis, we suggest a primary
endovascular approach. (See 'Mesenteric angioplasty/stenting' below.)

Surgical versus endovascular intervention Reports indicate that endovascular

intervention may be as effective as traditional surgical approaches in patients with acute
mesenteric arterial occlusion [35,36]. This approach remains somewhat controversial as
direct visualization of the bowel is not an option during percutaneous interventions. The
long-term outcome after percutaneous treatment (eg, reocclusion after thrombolysis, stent
thrombosis) has not been well studied [35-42].

In a review from Sweden, there has been a steady increase in mesenteric

revascularizations for acute mesenteric ischemia since 2004. In 2009, endovascular
treatment surpassed open surgery [30]. The authors noted that this shift in treatment has
not yet taken place in other countries [35]. No randomized trials are available to guide
treatment, but there are six nonrandomized studies that have compared open versus
endovascular revascularization for acute mesenteric ischemia [30,35,36,43-45].

In the Swedish study, the 30-day mortality rate was similar after open versus
endovascular surgery for embolic occlusions (37 versus 33 percent), whereas the
mortality rate was significantly higher after open than endovascular treatment for
thrombotic occlusions (56 versus 23 percent) [30]. Differences in disease severity
may have existed between the treatment groups, but the authors speculated that it is
possible that the endovascular approach is better for thrombotic occlusions in older
adult and fragile patients.
A retrospective review found no significant difference in mortality between open and
endovascular approaches for patients treated over a 20-year period [35].
In another single-center study, endovascular compared with open surgery led to
significantly lower rates of mortality for patients with acute thrombotic occlusions [36].
Three other multicenter reviews showed a lower frequency of bowel resection and
death rates with endovascular therapy for acute thrombotic occlusion [43-45]. The
long-term survival at five years after endovascular treatment and open vascular
surgery was 40 and 30 percent, respectively [43]. Independent risk factors for
decreased long-term survival were short bowel syndrome and advanced age.
In a series of 70 patients with acute mesenteric ischemia, 56 initially underwent
endovascular treatment with a technical success rate of 84 percent. Immediate
procedure (in-hospital) mortality was significantly lower for endovascular compared
with open surgical treatment (36 versus 50 percent) [36].

ENDOVASCULAR INTERVENTION Initial catheter-based arteriography and possible

endovascular treatment can only be considered for patients who are hemodynamically
stable and who do not have clinical signs of advanced ischemia (eg, radiographic,
peritonitis). For those who undergo endovascular intervention, there should be a low
threshold to terminate the procedure if problems arise or to convert to open surgical
exploration if the patient's clinical condition deteriorates at any time.

Endovascular options for patients with mesenteric arterial occlusion include [46-51]:

Pharmacologic or mechanical thrombectomy

Balloon angioplasty, typically with arterial stent placement

An antegrade approach to the superior mesenteric artery (SMA) can be performed via
femoral or brachial artery access. Brachial access may be preferred if there is a sharp
downward angle between the aorta and the superior mesenteric artery or if the ostium of
the SMA is calcified; each scenario would make the approach from the femoral artery very
difficult. (See 'Mesenteric angioplasty/stenting' below.)
If an antegrade approach from the femoral or brachial artery fails, a retrograde approach
through the exposed SMA at the time of laparotomy is another option. (See 'Mesenteric
angioplasty/stenting' below.)

Pharmacomechanical thrombolysis Pharmacomechanical thrombolysis should only

be considered in patients who can undergo arteriography within eight hours of the onset of
abdominal pain and who do not have clinical evidence of advanced ischemia or other
contraindications to thrombolytic therapy.

After gaining access, the SMA is cannulated and catheterized. To directly aspirate the
thrombus, a series of wires and catheters are used to place a relatively stiff wire into the
ileocolic branch of the SMA over which an introducer with a removable hub is placed
proximal to the embolus in the SMA (typically a 7-Fr, 45-cm introducer [eg, Destination,
Terumo]) [9]. Inside the introducer, a 6-Fr guiding catheter is introduced into the clot. The
clot is then aspirated into the guiding catheter with a 20-mL syringe as the catheter is
withdrawn over the wire. The hub of the introducer can be removed to clear any residual
clots. Repeat arteriography is performed, and, if needed, repeated aspirations can be
performed. An alternative to this method is an over-the-wire double lumen aspiration
catheter (eg, Export), which may allow removal of smaller, more peripheral clots (image 4).

Catheter-directed thrombolysis is an alternative for cases of incomplete aspiration

embolectomy or distal mesenteric embolization. In cases of incomplete aspiration
embolectomy or distal embolization, local thrombolysis is a reasonable alternative in
patients without peritonitis [52]. With the introducer placed in the proximal SMA, a 4-Fr
end-hole catheter can be advanced up to the clot or a multiple sidehole catheter (holes
over 10 cm) advanced through the clot. The catheter is secured at its exit site and a
dressing applied to the access site. Low-dose heparin (500 units/hour) administered
through the sheath prevents its thrombosis. Papaverine infusion should not be used
concomitantly, as it can precipitate in the presence of heparin. Termination of the infusion
and abdominal exploration are indicated for any patient who develops progressive
symptoms or signs of ischemia. Provided the patient remains clinically stable,
arteriography should be repeated within four hours, and if clot lysis is not demonstrated,
the patient should be taken to the operating room for abdominal exploration.
(See 'Surgery' below.)

A review of 20 case reports and seven small series using thrombolytic therapy for acute
SMA occlusion reported angiographic resolution of the SMA occlusion in 43 out of 48
patients (90 percent) [53]. Most were treated with infusions of urokinase. The overall 30-
day survival rate was 43 out of 48 patients (90 percent).

Mesenteric angioplasty/stenting Mesenteric artery angioplasty/stenting can be

performed in an antegrade fashion (device introduced via the aorta into the SMA) or
retrograde (device introduced via the SMA distal to the obstruction) [38,54]. Open
mesenteric stenting for acute mesenteric ischemia is discussed below. Antegrade stenting,
which is more typically performed in the setting of chronic ischemia (or acute-on-chronic
ischemia), is discussed separately. (See "Chronic mesenteric ischemia", section on
'Management'.)

Retrograde open mesenteric stenting In selected patients, retrograde catheter-based

mesenteric revascularization may be appropriate [36,55-58]. In settings where
thrombectomy is unsuccessful in restoring arterial inflow and autogenous bypass conduit
(saphenous vein, femoral [deep] vein) to perform surgical bypass is not available or cannot
be expeditiously harvested, it may be possible to establish arterial inflow using retrograde
catheterization of the superior mesenteric artery. If successful, this approach avoids the
risk of contaminating a prosthetic vascular graft. With appropriate endovascular equipment
and fluoroscopic imaging, the procedure is relatively straightforward, with reported results
competitive with those of open surgical bypass.

SURGERY Immediate surgery is indicated for patients with acute mesenteric ischemia
with clinical symptoms or signs of advanced ischemia (eg, peritonitis, sepsis, pneumatosis
intestinalis) [59].

Abdominal exploration/damage control Laparotomy is indicated for patients with

acute abdominal findings on exam indicating peritonitis. Laparotomy, rather than
laparoscopy, may be safer and more expedient for evaluating the viscera in the face of
grossly dilated bowel. The intestinal tract should be evaluated first for areas of impending
or gross perforation; these areas should be immediately resected using a stapler to
contain gross spillage. A general abdominal exploration should be performed, looking for
obvious pathology or other signs of visceral embolization.

The extent and severity of intestinal ischemia, including the appearance of the abdominal
contents (color, distention), peristalsis, arterial pulsations in the mesenteric arcades, and
bleeding from cut surfaces, should be assessed. Although mesenteric arterial
revascularization is preferably performed before bowel resection, areas of the small or
large intestine that are clearly nonviable (ie, full-thickness ischemia with dilated, dark,
paralyzed bowel (picture 4)) can be quickly resected using a damage control approach.
Bowel of questionable viability that peristalses even a little should be left intact until after
perfusion is restored, after which bowel viability should be reassessed. (See "Overview of
damage control surgery and resuscitation in patients sustaining severe injury".)

Revascularization

Embolectomy Open superior mesenteric artery (SMA) embolectomy remains a good

option and should be performed in those with indications for open surgical intervention.
Mesenteric embolectomy is performed through a midline abdominal incision that allows full
inspection of the bowel. The proximal superior mesenteric artery can be exposed at the
root of the mesentery by retracting the transverse colon cephalad, mobilizing the distal
duodenum, and palpating the SMA in the root of the mesentery (picture 5).
A transverse arteriotomy is made, through which 3-Fr or 4-Fr Fogarty embolectomy
catheters can be introduced to extract the clot (picture 6). The catheters should be
advanced distally as well as proximally. Absence of additional thrombus with multiple
passes and restoration of pulsatile inflow confirms clearance of the artery. The vessel is
flushed with heparin and the arteriotomy repaired primarily. If arterial inflow cannot be
obtained, repeat mesenteric arteriography may be necessary. If inflow cannot be restored,
bypass from the aorta or other location can be necessary. (See 'Mesenteric
bypass' below.)

Mesenteric bypass Revascularization of the SMA can be achieved in several ways

[60-63]. Superior mesenteric artery bypass is the most practical method in the setting of
acute mesenteric arterial occlusion. Other options include thromboendarterectomy and
translocation; however, these techniques are less commonly used in the setting of acute
mesenteric ischemia. Translocation (transection of the SMA distal to the occlusive lesion
with reimplantation into the infrarenal aorta) is unlikely to be feasible in acute
circumstances given the typically distal level of obstruction. For patients with chronic
mesenteric ischemia (or possibly acute-on-chronic disease), thromboendarterectomy may
be an option if disease is confined to the origin of the visceral vessels. (See "Chronic
mesenteric ischemia", section on 'Management'.)

Mesenteric bypass constructs a graft from the chosen inflow vessel (eg, aorta, iliac artery)
to a site distal to the occlusive lesion. Autologous reversed saphenous vein may be the
preferred conduit, but polytetrafluoroethylene (PTFE) grafts reinforced with rings are a
reasonable option for retrograde revascularizations to prevent kinking. However, in
general, prosthetic reconstruction is discouraged in the acute setting, particularly in the
face of abdominal contamination because of an increased high risk for graft infection. If
native conduit is not available, angioplasty and stenting (antegrade or retrograde) may be
a better option rather than placing a prosthetic graft within a contaminated field.
(See 'Mesenteric angioplasty/stenting' above.)

Antegrade bypass The inflow is from the supraceliac aorta.

Retrograde bypass The inflow is from the infrarenal aorta or iliac arteries.

Mesenteric artery bypass has good long-term patency rates and high rates of symptom-
free survival; however, perioperative mortality in the face of acute intestinal ischemia
remains high [64]. (See 'Morbidity and mortality' below.)

Bowel and abdominal closure Following open revascularization, the small bowel
should be carefully reexamined for areas of irreversible ischemic injury, which may require
resection. In one review of 83 patients requiring revascularization for acute mesenteric
ischemia, 24 percent required resection of a median length of 43 cm of bowel [60]. The
presence of Doppler signals over the serosal surface may be helpful in identifying
potentially salvageable ischemic segments to be left in place for reevaluation at second-
look operation; however, surgeon experience and visual inspection have been shown to be
as accurate as other adjunctive diagnostic techniques in the intraoperative assessment of
bowel viability. At the time of definitive abdominal closure, intravenous injection
of fluorescein dye with inspection of the intestine illuminated via a Wood's lamp can assist
in determining remaining bowel viability (picture 7).

Restoration of bowel continuity can be performed during the index surgery for well-
demarcated, clearly viable bowel segments. If bowel viability is in question or the patient is
hemodynamically unstable, a damage control approach can be undertaken by resecting
the nonviable segments and stapling the small bowel closed awaiting a second-look
procedure to restore bowel continuity.

The abdominal wall is left open when repeat laparotomy is planned, which is particularly
likely if there has been a significant interval of ischemia that leads to bowel edema with
reperfusion. If closure is elected (eg, no necrotic bowel, minimal ischemic time), abdominal
compartment pressures should be monitored. A planned "second-look" laparotomy is
frequently needed to reassess and resect irreversibly ischemic bowel. (See 'Second-look
laparotomy and abdominal wall closure' below.)

POSTPROCEDURE CARE AND FOLLOW-UP Patients with acute mesenteric

ischemia are often very ill post-intervention, requiring intensive care management and
nutritional support. In one study, the mean length of hospital stay was 23 days [35].

Second-look laparotomy and abdominal wall closure A second-look laparotomy is

needed for most patients after mesenteric revascularization for acute mesenteric arterial
occlusion to reevaluate the bowel 24 to 48 hours after the initial operation. In a review of
93 patients undergoing arterial revascularization for mesenteric ischemia, 80 percent of
patients underwent a second-look laparotomy, and among those patients, 28 percent had
necrotic bowel requiring resection at the second operation [35]. (See "Management of the
open abdomen in adults".)

If primary abdominal closure was elected (eg, no necrotic bowel, minimal ischemic time),
abdominal compartment pressures should be monitored. (See "Abdominal compartment
syndrome in adults", section on 'Measurement of intra-abdominal pressure'.)

Long-term medical management Long-term management is aimed at the prevention

of future embolic events, typically with the use of vitamin K antagonists or novel oral
anticoagulants [32]. Patients who survive after acute mesenteric embolic occlusion need
long-term medical treatment [32]. (See "Atrial fibrillation: Anticoagulant therapy to prevent
embolization".)

Following revascularization of thrombotic arterial occlusion due to atherosclerosis, medical

management of peripheral artery disease includes antiplatelet therapy and statin therapy
as part of a cardiovascular risk reduction strategy.
Stent surveillance Patients who have a stent inserted in the mesenteric artery should
have periodic surveillance either using duplex ultrasound or computed tomography (CT)
angiography. There are few data to guide a specific surveillance interval. There are no
data to guide follow-up surveillance following mesenteric stenting. We perform follow-up
imaging at three months post-intervention, then every six months for up to two years, and
annually thereafter provided there is no evidence for restenosis. For those with recurrent
stenosis, reintervention may be needed to prevent stent occlusion, which may lead to
recurrent symptoms.

MORBIDITY AND MORTALITY Mortality from acute mesenteric ischemia remains

high, with most series not showing appreciable improvement despite an aggressive
treatment regardless of approach.

For open surgical approaches to revascularization, perioperative mortality in contemporary

studies ranges between 31 and 62 percent [31,33,65-70]. In a series limited to patients
undergoing intervention for acute mesenteric arterial occlusion, perioperative mortality
(open and endovascular) was 22 percent, and complications occurred in 68 percent [35].
Perioperative mortality was similar for open and endovascular approaches. The causes of
perioperative death included ongoing mesenteric ischemia with intra-abdominal sepsis and
multiorgan failure, cardiac causes, hemorrhage, and termination of care. At one year,
overall survival was 38 percent. On multivariate analysis, independent predictors of any or
major postoperative complications were bowel resection at initial surgery (hazard ratio
[HR] 17.14, 95% CI 2.00-147) and prior transient ischemic attack (TIA)/stroke (HR 9.99,
95% CI 1.86-53.7). On univariate analysis, acute-on-chronic mesenteric ischemia
appeared protective for mortality.

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Basics topic (see "Patient education: Ischemic bowel disease (The Basics)")

SUMMARY AND RECOMMENDATIONS

Acute mesenteric ischemia refers to the sudden onset of small intestinal

hypoperfusion. Risk factors for acute mesenteric arterial occlusion include any
process that increases the potential for embolism from the heart or proximal arterial
vasculature or the risk for mesenteric arterial thrombosis. (See 'Introduction' above
and 'Risk factors' above.)
Embolism to the mesenteric arteries most commonly lodges 3 to 10 cm distal to
the origin of the superior mesenteric artery (SMA) in a tapered segment distal to
the takeoff of the middle colic artery.
Thrombosis of the mesenteric arteries is often superimposed on a preexisting
stenosis due to atherosclerotic plaque. Mesenteric arterial thrombosis can also
occur in the setting of vascular injury, spontaneous mesenteric dissection,
aneurysm, or a previously placed mesenteric stent.
Early symptoms and clinical signs are nonspecific. Specific clinical features that
suggest mesenteric arterial embolism or mesenteric arterial thrombus as a cause of
acute mesenteric ischemia include:
For acute embolic occlusion, the typical triad is an older adult patient with atrial
fibrillation (or other source for embolism) and severe abdominal pain out of
proportion to the physical examination.
For mesenteric thrombosis, the typical patient is a patient with atherosclerosis
risk factors and known peripheral artery disease who may or may not have an
established diagnosis of chronic mesenteric ischemia based upon symptoms of
chronic postprandial abdominal pain, food aversion, and weight loss.
A definitive diagnosis of mesenteric arterial occlusion relies upon demonstrating the
occlusion within the mesenteric arteries on imaging studies. For patients who present
with acute abdominal findings on exam indicative of bowel infarction and peritonitis,
the diagnosis will necessarily be made in the operating room at the time of emergent
exploratory laparotomy. Multidetector computed tomography (CT) angiography
(without oral contrast) is the initial study of choice for evaluating hemodynamically
stable patients with acute abdominal pain and clinical features suggestive of acute
mesenteric ischemia. (See "Overview of intestinal ischemia in adults", section on
'Diagnosis'.)
Embolic occlusion appears as an oval-shaped thrombus surrounded by contrast
in a noncalcified arterial segment located in the middle and distal portion of the
proximal SMA.
Thrombotic occlusion appears as thrombus superimposed on a calcified
occlusive lesion at the origin of the SMA.
The goal of treatment for patients with acute mesenteric ischemia is to restore
intestinal blood flow as rapidly as possible after initial management that includes
systemic anticoagulation and empiric broad-spectrum antibiotic therapy, among
others. Specific treatment depends upon the clinical status of the patient and the
etiology and location of the occlusion. (See 'Management' above.)
Patients who are good-risk surgical candidates with indications for immediate
laparotomy should be taken directly to the operating room for exploration.
Mesenteric arterial revascularization is preferably performed before bowel
 resection, but areas of the small or large intestine that are clearly nonviable can
be quickly resected using a damage control approach. (See 'Surgery' above.)
-For mesenteric embolism, the traditional treatment is open surgical
embolectomy. We prefer open surgical thrombectomy, but percutaneous
aspiration of the clot and catheter-directed thrombolytic therapy are
alternative approaches.
-For patients with mesenteric artery thrombosis, mesenteric bypass is the
treatment of choice. Thrombectomy alone is unlikely to be durable.
Intraoperative retrograde superior mesenteric artery angioplasty and
stenting is another option, particularly in the presence of gross
contamination where surgical bypass is more problematic.
Some hemodynamically stable patients with acute-on-chronic mesenteric artery
occlusion, who do not have clinical signs of advanced bowel ischemia, can be
observed while maintained on systemic anticoagulation, provided there is
evidence of good collateral blood flow on vascular imaging studies. The patient
should have serial clinical assessment with a low threshold to repeat abdominal
imaging studies or, if abdominal symptoms progress, surgical or endovascular
intervention.
Patients who are hemodynamically stable and who do not have clinical or
radiologic signs of advanced intestinal ischemia may be candidates for a primary
endovascular approach, which may include pharmacomechanical thrombectomy
and balloon angioplasty (typically with arterial stent placement). For those who
undergo endovascular intervention, there should be a low threshold to convert to
open surgical exploration at any time if problems arise or the patient's clinical
condition deteriorates. (See 'Surgical versus endovascular intervention' above.)
A palliative approach may be the best option for poor-risk surgical candidates
with extensive transmural infarction (eg, small bowel up to the midtransverse
colon).
For most patients after mesenteric revascularization, a second-look laparotomy 24
to 48 hours after the initial operation is needed to reevaluate the bowel.
(See 'Second-look laparotomy and abdominal wall closure' above.)
Long-term management is aimed at preventing future embolic events with
anticoagulation, and cardiovascular risk reduction strategies in those with thrombotic
arterial occlusion related to atherosclerosis. (See 'Long-term medical
management' above.)
Following mesenteric artery stenting, the patient should have periodic surveillance.
We obtain follow-up imaging, either using duplex ultrasound or CT angiography, at
three months post-intervention, then every six months for up to two years, and
annually thereafter provided there is no evidence for restenosis. For those with
recurrent stenosis, reintervention may be needed to prevent stent occlusion, which
can lead to recurrent symptoms. (See 'Stent surveillance' above.)
Mortality from acute mesenteric ischemia remains high, with most series not
showing appreciable improvement despite an aggressive treatment regardless of
approach. For open surgical approaches to revascularization, perioperative mortality
ranges between 31 and 62 percent. The causes of perioperative death included
ongoing mesenteric ischemia with intra-abdominal sepsis and multiorgan failure,
cardiac causes, hemorrhage, and termination of care. (See 'Morbidity and
mortality' above.)
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