Splanchnic venous anatomy parallels the arterial system to drain into the portal venous system. The

splenic and superior mesenteric veins join to form the portal vein. Hepatic venous blood is drained by

the right, middle and left hepatic veins. Portal–systemic connections are multiple and important when

considering portal hypertension.

Physiologic intestinal function relies on adequate perfusion and oxygenation of the microvascular

splanchnic circulation. Splanchnic blood flow is estimated as 300 to 1,200 mL/min, or about 10% to

35% of the cardiac output, with approximately 70% of this blood flow supplying the mucosa and

submucosa.1,2 Various intrinsic and extrinsic autoregulatory mechanisms including tissue metabolites,

myogenic mechanisms, and the autonomic nervous system ensure adequate gut circulation through both

vasoconstriction and relaxation of arterial smooth muscle. The degree of visceral artery dilation and

constriction determines the relatively large fluctuations in splanchnic blood flow during fasting and

postprandial states.

Duplex ultrasound demonstrates moderate to high arterial resistance in the SMA, with low diastolic

flow and slight flow reversal during fasting states. Figure 91-2 demonstrates duplex ultrasonography of

normal aorta and SMA. Vessel diameter, flow velocity, calculated volumetric blood flow, spectral

analysis, and response to physiologic stimuli allow for precise assessment of the visceral circulation. In

the postprandial period (30 to 90 minutes), low-resistance signals are noted throughout systole and

diastole, indicative of dilated splanchnic arteriolar beds. Flow reversal does not occur. In contrast, low

arterial resistance signals are noted in the celiac artery circulation regardless of feeding, likely due to

the influence of the low resistance hepatic vascular bed.

2 Intestinal ischemia may result from presplanchnic conditions that decrease total mesenteric blood

flow (i.e., heart failure and hypovolemia), splanchnic conditions that decrease regional blood flow

through the mesenteric circulation (i.e., thromboembolism) or postsplanchnic venous congestion (i.e.,

mesenteric vein thrombosis [MVT] and cirrhosis). Regardless of the mechanism, impaired perfusion of

the intestine results in hypoxia-associated sequelae that include cytokine release, free radial production,

microcirculatory damage, and bacterial translocation. Mucosal barrier function is compromised

secondary to physical disruption of the mucosa, a change in normal intestinal microflora resulting from

treatment with broad spectrum antibiotics, and impairment of host immune defenses.3 Intestinal

ischemia may rapidly progress to tissue necrosis causing severe metabolic derangements and ultimately

multiple organ dysfunction and death. In addition to ischemia-related bowel injury, splanchnic

reperfusion exaggerates injury patterns. Reperfusion injury is associated with increased microvascular

permeability, increased epithelial permeability with leaking of fluid and molecules into the bowel

lumen, and decreased intestinal blood flow.

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ACUTE MESENTERIC ISCHEMIA

“Occlusion of the mesenteric vessels is apt to be regarded as one of those conditions of which … the diagnosis is

impossible, the prognosis hopeless and the treatment almost useless”.4 AMI remains an uncommon event but

carries catastrophic potential as illustrated by AJ Cokkinis’ statement above from 1926. Klass is credited

with the first successful restoration of arterial blood supply in an attempt to salvage AMI in 1951 by

SMA embolectomy.5,6 While clear medical and technologic progress has been made in the interim,

delayed diagnosis and treatment continues to impede improvements in contemporary patient morbidity

and mortality rates that approach 80%.6,7

AMI accounts for <1 in every 1,000 hospital admissions, presents most commonly during the seventh

and eighth decades of life, and epidemiologic study suggests that women are affected with three times

the frequency of males, at least in part attributed to relative female longevity.6 A Swedish

epidemiologic study cites an AMI incidence of 12.9/100,000 people years (as diagnosed by autopsy or

operation).8

3 The most common causes of AMI are referenced above and include: embolization (40% to 50%),

arterial thrombosis (25% to 30%), nonocclusive mesenteric ischemia (NOMI) (15% to 20%), and

mesenteric venous thrombosis (5% to 15%).6,8 Additional causes may include visceral malperfusion

associated with aortic dissection, mesenteric arterial dissection, and trauma. Historic mortality rates for

AMI are as high as 93%, although more contemporary series suggest in-hospital mortality rates of 17%

to 62% and a systematic review of 45 observational studies cites a mean mortality rate of 71.6% for

3,692 patients with AMI.8–13 While there is no validated prediction model for mortality in this clinical

setting, authors have shown with logistic regression models that age, duration of symptoms, ageadjusted comorbidity, specific EKG markers, and shock index may be associated with higher

mortality.12,14,15

Figure 91-1. Mesenteric collateral circulation.

Patients with AMI complain predominantly of abdominal pain followed by nausea, vomiting, and

diarrhea. Pain is often described as “out of proportion” to the clinical examination as tenderness to

palpation may be minimal until transmural necrosis of the intestine develops. Patients can be

tachycardic and demonstrate melena or heme positive stools. Fever, guarding, and rebound are typically

late findings associated with bowel infarction.

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Laboratory abnormalities may include hemoconcentration, leukocytosis, lactic acidosis, and elevated

anion gap, amylase, aspartate aminotransferase, and lactate dehydrogenase. While a reliable biomarker

for AMI remains elusive, D-dimer offers 96% to 100% sensitivity as an exclusionary test for early AMI

with low specificity.16,17 Intestinal fatty acid binding globulin (I-FABP), α-glutathione S-transferase, and

D-lactate are currently promising plasma markers.16,18 I-FABP and α-glutathione S-transferase are

located in the small bowel mucosa while D-lactate originates from bacteria in the intestinal lumen as a

normal product of bacterial fermentation. These markers leak into the blood stream during early

ischemia from damaged enterocytes and may offer increased specificity for small bowel ischemia.

Figure 91-2. Mesenteric duplex ultrasound of a normal aorta and SMA that demonstrates moderate to high arterial resistance in

the SMA, with low diastolic flow and slight flow reversal during fasting states. AO, aorta; SMA, superior mesenteric artery; PSV,

peak systolic velocity; EDV, end-diastolic velocity; RI, resistive index; OR, origin.

Diagnostic work-up often starts with a plain abdominal radiograph which may reveal ileus and

vascular calcifications; bowel wall edema (i.e., thumbprinting), pneumatosis (Fig. 91-3), pneumobilia,

and pneumoperitoneum may become evident with advanced ischemia and infarction, respectively. Highquality computed tomography angiography (CTA) has become the gold standard for imaging AMI given

near-universal availability and its ability to assess for bowel perfusion while excluding alternate sources

of abdominal pain. Additionally, “biphasic” CT offers arterial and delayed phase imaging that permits

visualization of the portal venous system in addition to arterial stenosis, occlusions, and bowel wall

features that support the diagnosis of AMI with a negative and positive predictive value reported up to

96% and 100%, respectively.19,20 Duplex ultrasonography, magnetic resonance angiography (MRA),

diagnostic peritoneal lavage, and diagnostic laparoscopy may serve as adjuncts for diagnosis but

secondary to intrinsic limitations should not be considered first line. Finally, the role for arteriography

remains important and will be described further as it allows for simultaneous therapeutic measures.

Mesenteric emboli most commonly affect the SMA given its oblique orientation off the aorta. Most

emboli are cardiac in origin; less common embolic sources may include proximal aortic aneurysm, atrial

myxoma, and paradoxical embolus secondary to venous thromboembolism with cardiac shunting.

Patient history will likely reveal atrial fibrillation, myocardial infarction, congestive heart failure or

cardiomyopathy, rheumatic heart disease or ventricular aneurysm. Most emboli will spare the SMA

origin and lodge distal to the middle colic artery and early jejunal branches. This pattern of ischemia, in

the absence of well-formed collaterals, results in a classic pattern of ischemia that compromises the bulk

of small bowel and ascending colon while sparing the proximal jejunum and distal transverse colon (Fig.

91-4).

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Figure 91-3. Abdominal radiograph demonstrating diffuse ileus and intestinal pneumatosis (arrow) in a patient with acute

mesenteric ischemia.

Figure 91-4. Pattern of embolic mesenteric ischemia – SMA emboli typically spare the middle colic artery (arrow) and proximal

jejunal branches (bracket) resulting in an ischemic pattern that spares the jejunum and distal transverse colon.

Acute in situ arterial thrombosis typically coincides with pre-existing atherosclerotic disease. Up to

20% to 50% of patients will describe antecedent postprandial abdominal pain and weight loss consistent

with CMI.2,6,9 Clinical presentation may be more subacute given the presence of preformed collaterals

that are typically absent in cases of embolic AMI. Patient history will likely reveal common

cardiovascular risk factors. Figure 91-5 demonstrates the highly calcified aorta of a patient presenting

with AMI and chronic celiac artery occlusion, SMA thrombosis (encircled), and IMA occlusion.

MANAGEMENT OF AMI

4 Patients with AMI warrant immediate medical management that includes the establishment of

adequate intravenous (IV) access and hemodynamic monitoring, systemic anticoagulation with heparin,

fluid resuscitation, correction of electrolyte abnormalities, and administration of broad-spectrum IV

antibiotics. Further vasoconstrictive insult with vasopressors should be avoided if possible. Patients with

AMI and evidence of threatened bowel viability warrant immediate surgical exploration. Frankly

necrotic or perforated bowel should be resected and left in discontinuity to limit contamination while

definitive intestinal management should never delay revascularization.

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Figure 91-5. CT imaging demonstrating in situ SMA thrombosis in the setting of highly calcified aortoiliac occlusive disease and

chronic celiac and IMA occlusions presenting as acute mesenteric ischemia.

SMA thromboembolectomy is the standard technique for embolic disease. Figure 91-6 illustrates

anterior exposure of the SMA at the base of the colonic mesentery. Typically venous tributaries, small

lymphatics, and autonomic nerve fibers require ligation to facilitate arterial exposure. The inferior

pancreatic border may require mobilization for more proximal SMA exposure. The SMA is exposed and

controlled proximal to the middle colic artery; the middle colic artery and jejunal branches are similarly

controlled. After a therapeutic level of systemic anticoagulation is confirmed a transverse arteriotomy is

created sharply (Fig. 91-7). The proximal SMA is vented; in the absence of robust and pulsatile

antegrade flow a balloon thromboembolectomy should be performed with a 3-Fr or 4-Fr catheter. Distal

vasculature is fragile and thromboembolectomy is best accomplished with a smaller catheter (i.e., 2 Fr

or 3 Fr). During balloon thromboembolectomy the balloon should be inflated with heparinized saline

(not air) as the catheter is withdrawn. The same person should control the balloon inflation that is

controlling catheter removal. Finally, consider flushing regional heparin or thrombolytic agent directly

into the distal SMA and branches. Balloon thromboembolectomy should be repeated until the balloon is

withdrawn free of thrombus burden. Following the successful clearance of all macroscopic thrombus the

arteriotomy can be repaired primarily with simple sutures of 5-0 or 6-0 monofilament suture placed in

an interrupted fashion. Vein patch angioplasty should be considered over primary repair for diminutive

vessels.

In cases of SMA occlusive disease with in situ thrombosis, bypass is typically required for successful

revascularization. In cases of such acuity, typically single-vessel reconstruction (SMA) is all that is

required. While there are multiple options for graft orientation and conduit, a retrograde bypass off the

right common iliac artery oriented in a “lazy-C” configuration is most often favored (Fig. 91-8). The

lateral portion of SMA is exposed cephalad to the fourth portion of the duodenum. This exposure

requires opening of the peritoneum adjacent to the duodenum with full exposure of the terminal aorta

and iliac arteries. Synthetic graft (i.e., 6- or 8-mm externally supported polytetrafluoroethylene) is

typically favored over autogenous conduit given its favorable size match, ready availability, and

resistance to kinking. Saphenous vein graft may be considered for cases of gross enteric contamination.

The terminal aorta or left common iliac artery may also be used for inflow. Antegrade bypass off the

supraceliac aorta may be considered in cases of prohibitive anatomy, but this exposure adds additional

technical complexity and operative time combined with the physiologic stress of aortic cross-clamping.

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Figure 91-6. SMA exposure at the base of the colonic mesentery (SMA encircled proximal to the middle colic artery).

Figure 91-7. Illustration of balloon SMA thromboembolectomy through a transverse arteriotomy.

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Figure 91-8. Retrograde bypass off the right common iliac artery oriented in a ‘lazy-C’ configuration.

While surgery has remained the standard of care for AMI over previous decades, a hybrid procedure

for SMA thrombosis has become widely embraced for its efficiency and decreased invasiveness for

mesenteric revascularization. This approach negates the need for aortic cross-clamping, prosthetic

conduit, and difficulty with arterial quality. Retrograde open mesenteric stenting (ROMS) was first

described by Milner et al. in 2006 and further popularized by Wyers et al. in a 2007 case series.21,22 The

infracolic SMA is exposed at the base of the transverse colonic mesentery as previously described for

retrograde cannulation following local patch angioplasty with vein or bovine pericardium. This hybrid

approach allows for simultaneous assessment and treatment of nonviable intestine with mesenteric

revascularization by way of SMA stenting. The largest and most contemporary series on ROMS reports a

technical success rate of 93% and primary-assisted patency rates of 91% at 12 months.23

Regardless of the approach to successful revascularization, intestinal viability must be assessed; this

decision is typically deferred for 20 to 30 minutes following reperfusion and aided by Doppler

interrogation of the mesenteric arcade, observation of serosal color, and the presence of peristalsis.

Adjuncts also include the use of fluorescein with a modified Wood’s lamp or perfusion fluorometer.6

Nonviable bowel is resected and in cases of unclear viability the intestine may be left in discontinuity,

the abdomen left open, and plans for a second-look laparotomy at 24 to 48 hours secured for definitive

intestinal management.

Exclusive endovascular treatments for AMI are increasingly reported despite historic concerns that

this approach increases time to revascularization, prohibits assessment of bowel viability, and that

endovascular failure might delay traditional revascularization thereby worsening patient outcomes.

Successful cases of percutaneous mechanical thrombectomy, aspiration thrombectomy, and intra-arterial

thrombolysis, with or without adjuvant angioplasty and stenting, have been reported in patients without

evidence of advanced bowel ischemia.24–29 The largest single center experience with endovascular

therapy for AMI reported a success rate of 87%, with failures most often requiring surgical

embolectomy.30 These authors compared outcomes following open and endovascular therapies for AMI

and identified a reduction in need for laparotomy, length of bowel resected, and morbidity including

acute renal failure and pulmonary failure in the endovascular group. Additionally, successful

endovascular therapy was associated with improved mortality (36% vs. 50%) and those endovascular

failures succumbed to similar mortality rates as the open surgical group. Most recently a National

Inpatient Sample (NIS) review identified a significant increase in the utilization of endovascular therapy

for AMI and reported that mortality, hospital length of stay, need for bowel resection, and need for

postoperative parenteral nutrition were reduced in those patients receiving endovascular therapy in

comparison to traditional open surgical revascularization.31

Nonatherosclerotic Mesenteric Arterial Occlusive Disease

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Intestinal ischemia may result from iatrogenic injury (i.e., arterial dissection or thromboembolism

during endovascular techniques), aortic dissection resulting in visceral malperfusion, trauma,

inflammatory arteritides, and fibromuscular dysplasia (FMD). Indeed, these patients warrant an

individualized approach to treatment. In cases of aortic dissection branch revascularization or aortic

fenestration is essential. Traumatic injuries often require urgent surgical repair or revascularization.

Inflammatory arteritides are typically managed medically (i.e., immunosuppression) with surgical

bowel resection reserved for nonviability.

Mesenteric Vein Thrombosis

Splanchnic vein thrombosis is defined by thrombosis of the portal venous system which includes the

superior mesenteric, inferior mesenteric, splenic, and portal veins. The sequelae of such may include

bowel or splenic infarction and chronic portal hypertension. MVT is a less common form of intestinal

ischemia that may present in a more subacute fashion. While AMI symptoms are similar to those

aforementioned, patients with MVT may also complain of days to weeks of a prodrome that includes

crampy abdominal pain, distension, nausea, and malaise. Whether thrombosis originates in the small or

large splanchnic veins, intestinal infarction requires the involvement of venous arcades and vasa recta

resulting in occlusion of venous return, venous engorgement of the bowel wall, cyanosis, and mucosal

ischemia that can progress to transmural infarction.32 Idiopathic MVT represents a minority of cases as

more than 50% of patients have at least one predisposing risk factor. Risk factors for MVT include

heritable and acquired thrombophilia, hypercoagulable states resulting from systemic disorders

(including malignancy and heparin-induced thrombocytopenia), and local intra-abdominal processes

(i.e., pancreatitis or trauma). A high index of suspicion is necessary for diagnosis given the nonspecific

nature of presenting symptoms, signs, and laboratory studies.32 CT imaging with portal phase venous

contrast (CT venogram) is the imaging modality of choice. Findings suggestive of MVT include a

sharply defined, enhancing venous wall with central low attenuation.32,33 MRA, angiography, and

laparoscopy are useful adjuncts. Emergent laparotomy should be considered for signs of advanced

intestinal ischemia; intraoperatively blood-tinged ascites is likely to be encountered and the bowel will

appear dusky, thick, and rubbery. Systemic anticoagulation is the mainstay of treatment as it reduces

mortality, decreases recurrent thrombosis rates from approximately 30% to <5%, and decreases

mortality associated with recurrent thrombosis.32,34–37 Additionally, with anticoagulation most patients

will demonstrate partial or complete venous recanalization with time. In the absence of a defined risk

factor, patients with MVT should undergo a work-up for thrombophilia. A finite duration of

anticoagulation is recommended for those with a reversible provoking risk factor with cessation of

anticoagulation encouraged after 3 months; remaining cases of idiopathic MVT or persistent risk

warrant indefinite anticoagulation.38 Historically open venous thrombectomy was employed for

advanced cases of MVT at the time of laparotomy. More recently various systemic and percutaneous

thrombolytic techniques have been applied to cases of large vessel disease; however, no large or wellcontrolled trials exist to guide recommendations for such over anticoagulation alone.32,39–42

Nonocclusive Mesenteric Ischemia

NOMI results from diffuse mesenteric vasospasm. This rare form of intestinal ischemia most often

affects critically ill patients with hemodynamic instability. Risk factors include decreased cardiac output

(i.e., heart failure or arrhythmia), hemodialysis, shock, vasoactive medications (i.e., vasopressors or

digitalis), and drug abuse (i.e., cocaine). Angiography is required for diagnosis and will demonstrate

diffuse vasoconstriction and nonopacification of branch vessels (Fig. 91-9). Treatment centers on

improving mesenteric perfusion by optimizing volume status, limiting vasoactive medications and

correcting contributing comorbidities. Intra-arterial infusion of vasodilators (i.e., papaverine or

nitroglycerin) or IV infusion of glucagon or prostaglandin E2, which selectively increases splanchnic

blood flow, have been advocated in treating this form of intestinal ischemia without robust large or

well-controlled trials to support treatment guidelines.43–45

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