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274
A. Chi and J. R. Stone
Fig. 24.2 A 58-year-old female with a past medical history of coronary
artery disease presents with a 6-day history of nausea, vomiting, bloody
diarrhea, and abdominal pain. CTA (a) demonstrates portal venous gas
(arrows) as well as large bowel pneumatosis (arrowheads) (b). Nonselective
angiography demonstrates ush occlusion of the SMA of unknown acuity,
accompanied by proximal high-grade narrowing of the celiac (arrow) (c)
and IMA (arrow) (f) secondary to atherosclerotic disease. Balloon expandable stents were placed in both the celiac (d) and IMA (g) resulting in
restoration of ow through these two vessels (e) and (h)
24 Mesenteric Ischemia
275
botic mesenteric ischemia typically describe a more insidious
onset of symptoms. Imaging usually reveals occlusion within
1–2cm of the origin of the SMA (Fig.24.2). Collateral vessels may be present, indicating an acute on chronic process.
Aortic dissection involving the abdominal aorta accounts
for AMI in less than 5% of cases. The mesenteric arteries
may be supplied by either the true or false lumen. Ischemia
occurs when there is absence of a distal reentry site, insufcient fenestrations (communication) between the true and
false lumina or compression of the vascular lumen supplying
the mesenteric vessel(s). CTA allows for anatomic imaging
of true and false lumens, dissection ap and branch vessels.
Catheter directed DSA allows for dynamic visualization of
contrast within the aorta and branch vessels, measurement of
intravascular pressures within true and false lumens, and
endovascular treatment of this condition.
Nonocclusive Mesenteric Ischemia (NOMI)
Approximately 5–15% of cases of acute mesenteric ischemia are due to NOMI (Fig. 24.3), with the most common
etiology involving prolonged systemic hypotension [16,
17]. Other causes include the use of vasopressor medica-
tions, such as dopamine, and digitalis. Clinically, patients
can present with ileus, increasing abdominal pain, and/or
increasing transaminases. Imaging demonstrates diffuse
arterial vasospasm with “sausage-like” segmental narrowing or diffuse narrowing of the arterial circulation, most
commonly seen at arterial branch points. Delayed lling of
distal branches, asymmetric bowel perfusion, and/or delayed
venous lling are commonly seen. Additionally, high pressure in the mesenteric vascular bed may cause reux of contrast from the SMA into the aorta, during catheter-based
angiography.
Fig. 24.3 A 67-year-old with history of nonoperative lung cancer
admitted primarily for management of multivessel coronary artery disease developed multiple bleeding complications, acute kidney injury,
and fungemia. On hospital day 14, the patient developed severe metabolic acidosis, and an urgent laparotomy was performed which demonstrated dusky appearance of a large portion of the bowel with a segment
of nonviable bowel that was resected. CTA was secondarily performed
demonstrating severe diffuse narrowing of the SMA (arrow) (a), (arrow)
(b), (arrowheads) (c). Catheter-directed angiography demonstrates
attenuated ow through a narrow SMA with severely compromised
bowel perfusion consistent with NOMI (d)
276
A. Chi and J. R. Stone
Key Point
Imaging appearance of NOMI:
• Diffuse arterial vasospasm
• Segmental or diffuse narrowing of arterial
circulation
• Delayed lling of distal arterial branches
• Asymmetric bowel perfusion
• Delayed venous lling
Table 24.3 CT/CTA appearance of acute mesenteric ischemia
CT/CTA ndings of
acute mesenteric
ischemia (general)
Thrombotic AMI Filling defect within 1–2cm of the SMA
Embolic AMI
Mesenteric artery
dissection
NOMI Diffuse arterial narrowing
SMV thrombosis Filling defect in SMV
Bowel ischemia/infarction
Mucosal wall edema
Pneumatosis
Portal venous gas
Pneumoperitoneum
origin
Collateral vessels may be present
Filling defect ≥3cm distal to the SMA
origin
Minimal collateral vessels
Dissection extending into mesenteric
vessels
Absence of distal reentry site
Insufcient fenestrations
Compression of true lumen by false lumen
“Sausage-like” segmental narrowing
Delayed lling of distal branches
Asymmetric bowel perfusion
Delayed venous lling
Lack of ow in SMV
Extensive arterial mucosal enhancement
Portomesenteric Vein Thrombosis
SMV thrombosis accounts for less than 5% of cases of acute
mesenteric ischemia [18]. Risk factors for this condition
include portal hypertension, abdominal inammatory disease, oral contraceptives, prior surgery involving the portal
venous system, trauma, and hypercoagulable states.
Extensive portomesenteric venous thrombosis causes intestinal venous congestion and mucosal edema leading to arterial
hypoperfusion. Diagnosis is usually made by CTA or MRA
during a venous phase where a lling defect or lack of ow
is seen in the mesenteric veins with associated bowel mucosal edema (Table24.3).
Angiography usually demonstrates high resistance to
arterial ow with diffuse arterial vasospasm, prolonged arterial phase and prolonged mucosal enhancement, lack of
opacication of mesenteric veins, prolonged opacication of
venules or larger regional veins, and/or a xed intraluminal
lling defect(s) within the mesenteric veins.
Chronic Mesenteric Ischemia
Physical exam ndings are often nonspecic for evaluation
of CMI, though an abdominal bruit may be present. The most
common site of ischemia is at the splenic exure watershed
area between the SMA and IMA [24]. Initial imaging examinations can include ultrasound, CTA, and/or MRA.Ultrasound
(US) is a readily available imaging modality which lacks
ionizing radiation and can be used to screen for chronic mesenteric ischemia. US can provide ow data in fasting or postprandial states to detect physiologically signicant stenoses
[19]. The affected vessel may demonstrate an increase in
peak systolic velocity (PSV) and end-diastolic velocity
(EDV) [19]. Signicant stenosis of the SMA can lead to loss
of diastolic ow or ow reversal. Limitations of ultrasound
include overlying bowel gas, variant anatomy, sonographer
experience, patient body habitus, and lack of uniform criteria
for interpretation of ndings [19]. Contrast-enhanced US
may increase the sensitivity and specicity of the study [20].
As for acute ischemia, CTA is usually preferred over
MRA, for its spatial resolution and accessibility. A stenosis
is considered physiologically signicant when stenosis
diameter is greater than 60%; cross-sectional area reduction
is more than 70%; and trans-lesional systolic pressure gradient is greater than 20mmHg [21–23]. An initial noncontrast
CT should be performed to identify calcications, extravascular blood, stents, foreign bodies, surgical clips, and
devices. Negative oral contrast (distended bowel contents
look dark), if tolerated, can aid in evaluation of bowel.
Positive oral contrast (bowel contents look bright) can
degrade CT images by causing streak artifact and obscuring
the difference between the IV contrast enhanced bowel wall
and its luminal contents [6]. CT is also excellent for assessing stent or surgical graft patency [25]. Multiplanar reformation and reconstructions greatly enhance diagnosis and
pre-procedural planning diagnosis [26].
Conventional Therapy
Acute Mesenteric Ischemia
Initial treatment should include making the patient NPO,
uid resuscitation, correction of metabolic acidosis if present, broad-spectrum antibiotics, and avoidance of vasoconstrictive medications [5, 28].
Arterial Occlusive Disease
Historically, treatment of arterial mesenteric ischemia primarily involved surgical exploration, revascularization, and
resection of infarcted bowel [27, 29, 30]. Surgical thrombec-
tomy has been utilized, though this approach does not seem
to benet long-term patency [31, 32]. Recent studies suggest
24 Mesenteric Ischemia
277
that rapid endovascular revascularization demonstrates
relatively favorable outcomes as compared to traditional
open surgical methods [33, 34]. Thus, management is evolving to include early endovascular therapy in the initial management to quickly reestablish ow. If bowel infarction is
present, revascularization should be performed as soon as
possible, followed by surgical exploration with resection of
necrotic bowel. In addition to reestablishing ow, vasodilators such as papaverine may be administered directly into the
SMA to reduce vasoconstriction and vasospasm to optimize
intestinal perfusion. Given the frequent need for adjunctive
procedures and intensive care in this patient population,
treatment of acute mesenteric ischemia requires a multidisciplinary approach involving interventional radiology, surgery,
and critical care teams.
Key Point
Papaverine is a potent vasodilator that can be administered directly to the SMA to relieve vasoconstriction
and optimize intestinal perfusion.
Aortic dissection associated acute mesenteric ischemia
approaches a mortality rate of 90% when treated with surgical repair. Early intervention with endovascular techniques
may reduce this mortality [3].
Nonocclusive Mesenteric Ischemia (NOMI)
First-line therapy should focus on reversing any precipitating factors including treating hypotension and discontinuing, if feasible, the use of vasoconstrictors. Endovascular
approaches for management of NOMI include an intraarterial infusion of papaverine directly into the SMA.
Treatment is typically continued until symptoms resolve. If
peritonitis or continued elevation of lactic acid occurs, surgical exploration must be performed to assess for bowel
infarction.
Portomesenteric Vein Thrombosis
Treatment of portomesenteric thrombosis should be guided
by clinical presentation and distribution of thrombus. Most
cases are treated with early anticoagulation and supportive
care, including stabilizing cardiovascular status and correcting any predisposing factors with appropriate hydration. If
symptoms persist or peritoneal signs and/or lactic acidosis
occur, endovascular intervention may be of benet. If the
bulk of the clot is located within the main trunk of the
SMV and portal vein, transhepatic or transjugular portosystemic access to the portal venous system with retrograde
catheterization of the SMV can be considered. Once access
is established into the portal vein and SMV, mechanical,
pharmacomechanical, and/or pharmacologic approaches
may be utilized to debulk clot and reestablish ow, often in
concert with transhepatic portosystemic shunt (TIPS) creation. If clot is distributed peripherally in small venules or
capillaries, thrombolysis through a SMA approach may be
sufcient [6]. Intra-arterial papaverine into the SMA may be
employed when there is concurrent mesenteric arterial vasoconstriction or concern for bowel ischemia. When bowel
infarction is present, surgical exploration to resect nonviable
bowel should be performed. Intra-arterial papaverine may be
a useful adjunct following surgical exploration/bowel resection to prevent additional bowel compromise in the postsurgical period and enhance early recovery.
Chronic Mesenteric Ischemia
Historically, surgical intervention typically involved either
transaortic endarterectomy or mesenteric artery bypass.
With advancements in endovascular techniques, stent placement is considered a rst-line approach. In the setting of
mesenteric arterial occlusion, a proximal stump of the
occluded artery may allow recanalization. If there is a “ush
occlusion,” i.e., no patent segment, proximal arterial surgical intervention may be necessary [6]. In patients who are
surgical candidates and fail endovascular therapy, bypass
generally remains an option.
Surgical revascularization is associated with increased
periprocedural morbidity and mortality compared with transcatheter approaches but may offer more durable results.
Oderich etal. [8] performed a 14-year retrospective review
of outcomes in 229 patients undergoing open surgical vs.
percutaneous transluminal angioplasty (PTA) or stent placement for treatment of CMI. Presumably bare metal stents
were used in all cases, as stent grafts were not mentioned.
Morbidity was 36% in the open surgical group vs. 18% in the
endovascular group (P<0.001). However, 5-year recurrencefree survival was 55% in the endovascular vs. 89% in the
open surgical group (p< 0.05). Additionally, open surgical
repair was associated with improved primary (88% vs. 41%,
p<0.05) and secondary (97% vs. 88%, p < 0.05) patency
rates when compared with endovascular repair. However, a
recent meta-analysis evaluated the comparative effectiveness
and cost-effectiveness of endovascular repair versus operative repair and found that endovascular repair is favored over
operative repair in all age groups [35]. While endovascular
repair is associated with an increased reintervention rate, it is
more cost-effective overall than operative repair [10].
Median arcuate ligament compression of either the celiac
or SMA is generally a contraindication to endovascular therapy due to the forces of diaphragmatic compression leading
to fractured or crushed stents. Surgery is indicated should
revascularization be required in order to decompress the
affected arteries, celiac ganglion, and neural plexus via
release of the median arcuate ligament [37–39].
278
Key Point
Median arcuate ligament compression is a contraindication to placement of a stent in the SMA or celiac
artery due to risk of stent fracture or crushing.
Interventional Therapy
Acute Mesenteric Ischemia
Endovascular management of acute mesenteric ischemia is
an important therapeutic option for early revascularization
and may be used as an adjunct to surgical management.
Regardless of etiology, catheter-based intervention may provide benet; however, the specic interventional approach
depends on underlying cause.
All patients treated for AMI should be admitted to an
ICU. Laboratory assays should include a CBC, CMP, liver
enzymes, lipase, serum lactic acid, and coagulation panel.
Goals include hydration and hemodynamic resuscitation,
avoiding reperfusion injury, preventing clot propagation and
sepsis, and minimizing the extent of bowel injury.
Anticoagulation may be used to prevent clot propagation.
Low molecular weight heparin (LMWH) is not recommended due to its longer half-life and renal-dependent excretion. In the setting of mesenteric venous thrombosis,
intestinal wall breakdown may seed venous clot and lead to
portal thrombophlebitis from gram-negative and anaerobic
organisms; thus, broad-spectrum antibiotics with piperacillin/tazobactam, metronidazole, and levooxacin are recommended [3]. Close monitoring with serial lactic acid and
frequent abdominal exams should be performed to evaluate
for peritoneal signs and monitor for bowel infarction.
With successful improvement in mesenteric blood ow,
reperfusion injury should be considered in all patients [39].
Local inammation from ischemia interacts with increased
blood oxygen to form reactive oxygen species (ROS), which
directly injures cells and may lead to cell death. Free radical
scavenger medications, such as allopurinol and enalapril,
may help decrease injury, though experience is limited for
this particular application.
When papaverine or other vasodilators are used, close
monitoring is indicated to assess for hypotension, although
this is uncommon, as papaverine has greater than 90% rstpass clearance through the liver. Monitoring of central
venous pressures may be considered. Vasopressors or cardiotonic agents, such as dopamine or dobutamine, may be
needed. Vasopressin and α-agonists should be avoided as
they may worsen mesenteric ischemia. Glucagon has been
used to decrease oxygen demand of the intestines via vasodilation and hypotonicity; however, glucagon may also cause
nausea and vomiting.
A. Chi and J. R. Stone
For mesenteric venous occlusion, supportive care with
early anticoagulation is adequate. Asymptomatic or mildly
symptomatic patients may be managed with anticoagulation
and supportive care alone [44, 45]. If persistent abdominal
pain, peritonitis, or increasing lactic acidosis occurs, endovascular approaches may be considered. Transhepatic or
transjugular intrahepatic portosystemic approaches can provide access for clot lysis and TIPS.If there is peripheral distribution of clot, SMA thrombolysis may be sufcient for
small vessel clearance [30, 46–51]. If signs of bowel infarction are present, surgical intervention should be performed
after or in place of endovascular therapy. Anticoagulation
before and after surgery should be used to prevent rethrombosis, as these patients are typically hypercoagulable;
relevant diagnostic assays should be considered.
The nal common pathway of mesenteric ischemia
involves bowel infarction, which, if left untreated, will lead
to systemic inammatory response syndrome (SIRS) [40].
Decreased blood ow causes accumulation of lactic acid,
loss of cellular homeostasis, cell death through necrosis, and
a resultant inammatory response. This response may overwhelm normal inhibitory feedback loops, causing a cytokine
storm that manifests as SIRS. If unchecked, this leads to
hypotension, multi-organ failure, and death.
Chronic Mesenteric Ischemia
The natural history and factors affecting the progression of
mesenteric artery stenoses are not well dened. Progression
from chronic to acute mesenteric ischemia is associated with
>50% mortality. However, given the risks of both surgical
and endovascular treatment techniques, indications for treatment of asymptomatic mesenteric arterial disease remain
controversial. For symptomatic patients with chronic mesenteric ischemia, endovascular approaches are generally
applied due to relative lower periprocedural morbidity and
mortality, particularly for those who are poor surgical candidates or with a history of previous abdominal surgery. The
primary goal of treatment is to provide adequate revascularization of the mesenteric arterial bed. Endovascular management has taken on an increasing role if CMI is caused by
atherosclerosis or bromuscular dysplasia [41].
The How To: Acute Mesenteric Ischemia
Embolic and Thrombotic AMI:
1. Femoral arterial access is obtained via the Seldinger
technique, with or without ultrasound guidance. If
distal aortoiliac occlusive disease or unfavorable
(continued)
24 Mesenteric Ischemia
279
angle of mesenteric arterial branches, may consider
brachial arterial access. If brachial arterial access is
used, small catheters and sheaths should be employed
to prevent brachial artery thrombosis. (Refer to
Chap. 8 for a review of access techniques.)
2.
enteric arterial vasculature and diameter to accommodate balloon catheters, stents, or pharmacological
thrombectomy devices is advanced over the wire.
3. A diagnostic aortogram is obtained in both AP and
lateral projections. These provide information
regarding the overall perfusion of the mesenteric
circulation, the key information concerning the
anatomy of the stenosis or occlusion, and a “working view” for crossing any pre-existing lesion.
4. The affected artery is catheterized; a hydrophilic
steerable guidewire may be used to cross the lesion.
This guidewire may be exchanged for a stiff exchange
wire once the lesion is traversed with a catheter.
5. With a stiff wire in place, the sheath may be
advanced beyond the lesion to aid with balloon and/
or stent delivery. Predilation of the lesion may be
required to facilitate passage of the sheath.
6.
lished to the occluded artery via selective injection
thrombectomy, or mechanical thrombolysis.
7.
lesion, percutaneous transluminal angioplasty and
balloon-expandable stents are employed. If the
lesion is too narrow to allow passage of a balloon-
used to predilate. Stent grafts are often preferred.
8. ography is repeated to assess the downstream circulation. If mesenteric arterial vasoconstriction is
noted, intra-SMA papaverine may be used. In adults,
Key Point
The goal of endovascular therapy is to rapidly reestablish flow into the proximal arterial segments.
Aortic Dissection:
1. Creation of fenestrations at the level of the mesenteric
vessels or increasing the caliber of the true lumen can
be used alone or in combination with endograft
placement to equilibrate flow between the true and
-
-
false lumen and increase intestinal perfusion [43].
2. Endograft placement can be used to cover the
primary aortic defect to depressurize the false lumen
and enhance true lumen flow into the SMA.
Intravascular ultrasound (IVUS) may be used to map
the course of the planned endograft deployment.
Stents or stent grafts can be placed within the SMAto
reestablish blood flow.
Nonocclusive Mesenteric Ischemia (NOMI)
1. Reverse any existing causes of hypotension and/or
pharmacological sources of vasoconstriction.
2. Intra-arterial SMA infusion of papaverine may be
used until symptoms resolve.
3. Development of peritonitis or increasing lactic acidosis
should prompt exploratory laparotomy to evaluate and
resect nonviable bowel.
Portomesenteric Vein Thrombosis
1. Transhepatic or transjugular intrahepatic portosystemic
approaches may provide the greatest benefit for
direct lysis, thrombectomy and adjunctive TIPS
creation to restore patency. If there is peripheral distri bution of clot, SMA thrombolysis may be sufficient
for small vessel clearance [30, 46–51]. However, direct
transhepatic or transjugular approaches to SMV
thrombosis are complex and require specific expertise
due to risks of intraperitoneal bleeding and liver
injury. Of the two, transhepatic approaches to SMV
thrombosis is associated with the highest risk of
bleeding; transjugular portosystemic approaches
should be used when at all possible.
2. Endovascular options include systemic, transarterial
or transvenous infusion of thrombolytics depending
on the location and extent of the lesion (Fig. 24.4).
3. Mechanical thrombectomy, angioplasty and stent
placement, and TIPS creation may be used with portal
access to the mesenteric venous system.
280
A. Chi and J. R. Stone
Fig. 24.4 A 62-year-old female with adenocarcinoma of the pancreas
presenting with malaise, nausea, vomiting, and diarrhea. CTA demonstrates SMV thrombosis in axial (arrows) (a, b) and coronal (arrowheads) (c) planes. Access was established into the portal system through
a transjugular portosystemic approach (d). SMV thrombotic segment
was traversed (e), and aspiration thrombectomy was performed (f) with
a Penumbra Indigo device (Penumbra, Inc., Alameda, CA).
Thrombectomy was followed by PTA (g) resulting in restoration of ow
through the SMV trunk (h)
24 Mesenteric Ischemia
281
The How To: Chronic Mesenteric Ischemia
1. Follow steps 1–4 from arterial occlusive disease AMI.
2. If the lesion is too narrow to allow passage of the
sheath, a lower profile balloon may be used to predilate
the lesion. Care should be taken in passing a balloon expandable stent across a high-grade lesion to avoid
the stent becoming dislodged from the balloon in the
process. Treatment of I MA lesions may require
microcatheter techniques with 0.018 or 0.014 inch
wires given the relatively s mall caliber of this vessel.
3. Significant lesions are defined by >60% diameter
narrowing or with 70–80% reduction in cross-sectional
area, in combination with at least 15–20 mmHg
systolic trans-lesion pressure gradients at rest
(Fig. 24.5). A systolic peak measurement of <10 mmHg
is considered not significant, and 10–20 mmHg is
considered borderline with treatment guided primarily
by symptoms.
4. If stent placement is required, the choice of stent
depends upon the location and type of lesion. For
ostial lesions, balloon-expandable stents are generally
preferred. Lesions within the trunk of the mesenteric
arteries may be treated with either balloon-expandable
or selfexpanding stents. Although bare metal stents are
often used, covered stents may be superior in the
setting of soft plaque, arteries <6 mm in diameter (to
reduce risk for in-stent restenosis) or for treatment of
in-stent restenosis secondary to intimal hyperplasia
(Fig. 24.6).
5. Pharmacologic adjuncts include IV heparin of
3000–5000 IU with a target activated clotting time
(ACT) of >220 s. Intra-arterial nitroglycerin in boluses
of 100–200 µg may be used to prevent or minimize
spasm. If a stent was deployed, aspirin 325 mg and
clopidogrel 300 mg may be administered in the recov ery room. Aspirin 81–325 mg/day for life and clopi dogrel 75 mg/day for at least 3–6 months should also
be prescribed.
Key Point
Signicant stenotic lesions are dened as:
• >60% diameter narrowing
• 70–80% reduction in cross-sectional area
• ≥20 mmHg systolic trans-lesional pressure gradient at rest
Long-term management following treatment of mesenteric ischemia should include follow-up in an outpatient
clinical setting at regular intervals. At 1month, a follow-up
CTA may be performed to assess for vessel patency. If a stent
was placed, CTA or duplex US at 6–12 months is recommended to evaluate for in-stent stenosis. Patients with stents
should be prescribed clopidogrel (Plavix) using a 300 mg
loading dose followed by 75 mg/day for 3–6 months and
aspirin 81–325mg/day for life. Patients should also follow
up with a gastroenterologist, particularly in the setting of
extensive bowel resection with risk of short gut syndrome
given the potential need for dietary modications.
Complications of endovascular therapy for mesenteric
ischemia include general angiographic risks such as access
site injury (hematoma or pseudoaneurysm) and contrast
nephropathy. Thrombolysis and anticoagulation increase
risk of access site complications, and dehydration increases
the risk of contrast-induced nephropathy. Thrombolysis
complications also include embolization and stroke.
Papaverine and other vasodilators may lead to hypotension
in some cases. Additional complications include infection,
sepsis, and reperfusion injury.
Complications associated with angioplasty and distal
stent placement include dissection, embolization, thrombosis, perforation, and stent dislodgement [3]. Although
complication rates are low (<10%), the occurrence of anatomical complications within the mesenteric artery
increases the risk of morbidity and mortality. The most
common causes of death following mesenteric artery stent
placement include myocardial infarction and multi-organ
system failure secondary to bowel ischemia from distal
embolization, dissection, or stent thrombosis. Despite the
rare morbidity and mortality associated with distal
embolic events, the use of distal embolic protection
remains controversial [42].
282
A. Chi and J. R. Stone
Fig. 24.5 A 73-year-old female with history of central abdominal pain
after eating. CTA demonstrates severe narrowing of the celiac and SMA
secondary to atherosclerotic disease (a). Aortogram also demonstrates
severe narrowing (arrow) (b), which was treated with a balloonexpandable stent (c), resulting in restoration of ow (d)
24 Mesenteric Ischemia
283
Fig. 24.6 A 59-year-old female with chronic abdominal pain and pre-
viously placed IMA and left colic artery stents. Abdominal pain has
recently worsened, prompting angiography. Select angiogram of the
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