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PA RT VI
MESENTERIC VASCULAR DISEASE
CHAPTER
26 Epidemiology and Pathophysiology
of Mesenteric Vascular Disease
Rachel C. Danczyk, Gregory J. Landry, Gregory L. Moneta
Severe acute intestinal ischemia results from sudden symptomatic
reduction in intestinal blood flow of sufficient magnitude to potentially result in intestinal infarction.
bowel and/or right colon may result from mesenteric arterial occlusion (embolus or thrombosis), mesenteric venous occlusion, and
nonocclusive processes, especially vasospasm (
dissections of the superior mesenteric artery (SMA), either in association with cystic medial degeneration of the arteries or, more
commonly, as progression of an existing dissection in the descending thoracic aorta into the SMA and celiac artery, may also result
in acute intestinal ischemia.
Acute Arterial Occlusive Mesenteric
Ischemia
Acute Mesenteric Arterial Embolism
Roughly 25% of all cases of acute mesenteric ischemia are due
to emboli to the SMA, 25% of cases are due to thrombosis of preexisting atherosclerotic lesions, and the remaining 50% are due to
a variety of other etiologies.
left atrial or ventricular mural thrombi or from cardiac valvular
lesions.1 These thrombi are most often associated with cardiac
dysrhythmias such as atrial fibrillation, global myocardial dysfunction with poor ejection fraction, or discrete hypokinetic regions
produced by previous myocardial infarction (MI).3 About 15% of
emboli lodge at the origin of the SMA, but the majority lodge 3
to 10 cm distally in the tapered segment of the SMA just past the
origin of the middle colic artery.2 More than 20% of emboli to the
SMA are associated with concurrent emboli to another arterial bed.
can be compounded by reactive mesenteric vasospasm, further
reducing collateral flow and exacerbating the ischemic insult.
4
Intestinal ischemia due to embolic arterial occlusion
2
1
Acute ischemia of the small
Fig. 26-1). Isolated
Mesenteric emboli can originate from
2,5
cardiac surgery, with a reported mortality rate of greater than 50%
in most series.
by most extracorporeal circuits allows severely stenotic visceral
vessels to occlude during cardiopulmonary bypass. Identified risk
factors for this complication include prolonged cross-clamp times,
use of intraaortic balloon counterpulsation, low cardiac output
syndromes, blood transfusion, triple-vessel disease, coronary artery
disease (CAD), and peripheral artery disease (PAD).
5,7
Presumably, the nonpulsatile perfusion delivered
7
Pathophysiology of Occlusive Acute Mesenteric
Ischemia
Acute mesenteric ischemia, whether the underlying cause is
embolic or thrombotic, may eventually lead to intestinal infarction (
Fig. 26-2). Hypoxia and hypercarbia that occur during flow
interruption, and reperfusion injury once intestinal blood flow
is restored, all contribute to tissue loss
injury is believed to be principally mediated by activation of the
enzyme xanthine oxidase and recruitment and activation of circulating neutrophils (PMNs).
involves production of oxygen-derived free radicals by xanthine
oxidase that then causes profound local tissue injury through lipid
peroxidation, membrane disruption, and increased microvascular permeability.
autocrine and paracrine manner by secreting chemotactic cytokines (tumor necrosis factor [TNF]-α, interleukin [IL]-1, plateletderived growth factor [PDGF]) that perpetuate further damage to
the reperfused tissue. Once activated, PMNs degranulate, releasing
myeloperoxidase, collagenases, and elastases that further injure
already ischemic and vulnerable tissue.
genous inflammatory cascade is not restricted to the injured organ
and may also have deleterious systemic effects, with cardiac,
pulmonary, and other organ system dysfunction.
5,9
The ischemic endothelium recruits PMNs in an
9
The mechanism of injury likely
8
(Fig. 26-3). Reperfusion
5,10
Activation of this endo-
5
Acute Mesenteric Arterial Thrombosis
Thrombosis of the SMA or the celiac artery is usually associated
with preexisting critical stenoses. Many of these patients have histories consistent with chronic mesenteric ischemia (CMI), including postprandial pain, weight loss, “food fear,” and early satiety.
Superior mesenteric artery thrombosis can be regarded as a
complication of untreated chronic intestinal ischemia.
plaque likely progresses slowly to a critical stenosis over years until
thrombosis occurs.
Unlike embolic occlusions, thrombosis of the SMA generally
occurs flush with the aortic origin of the vessel. Aortic dissection
involving the visceral vessels, though rare, can cause acute mesenteric ischemia. The intimal flap of the dissection can extend into,
compress, or exclude the mesenteric orifice.
ischemia is also an uncommon (< 1%) but serious complication of
5
Acute mesenteric
1
The SMA
1,6
Natural History of Acute Mesenteric Arterial
Occlusive Disease
The mortality rate for occlusive acute mesenteric ischemia
exceeds 70% in most series.
emia resulting from SMA embolism has a more favorable prognosis than that resulting from SMA thrombosis.
acute intestinal ischemia due to SMA thrombosis is rare. The more
favorable prognosis associated with embolism is attributable to
the fact that most emboli lodge distally in the SMA (beyond the
origin of the middle colic artery), thus allowing perfusion of the
proximal intestine via middle colic and jejunal artery branches.
Thrombotic occlusion of the SMA usually occurs proximal to the
middle colic artery, and therefore completely interrupts mid-gut
arterial perfusion in patients with poorly developed celiac artery
or inferior mesenteric artery (IMA) collateral flow.
1,2,5,11,12
Occlusive acute intestinal isch-
1
Survival following
1,3,6
1
323
324
Other
Acute blood flow interruption
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10%
Nonocclusive
CH
26
MVT
15%
Embolus
25%
FIGURE 261 Etiology of acute mesenteric ischemia. MVT, mesenteric
venous thrombosis.
Thrombosis
25%
Hypoxia, hypercarbia
Reperfusion
Xanthine oxidase and polymorphonuclear
neutrophil (PMN) activation
25%
Oxygen-derived free radicals
Tissue injury
FIGURE 263 Pathophysiological mechanisms of acute occlusive
mesenteric ischemia.
FIGURE 262 Ischemic bowel. Arrows indicate segments of clearly
infarcted intestine.
Nonocclusive Mesenteric Ischemia
Epidemiology
Nonocclusive mesenteric ischemia (NOMI) accounts for 25% of all
episodes of acute intestinal ischemia.
arterial blood flow is inadequate to supply perfusion to the bowel.
The result is intestinal ischemia and infarction in the presence of a
patent macroscopic vasculature.
tified multiple risk factors for development of NOMI (
Mesenteric arterial vasospasm may occur following elective revascularization procedures for chronic SMA occlusion. In such cases,
vasoconstriction of small and medium-sized vessels is precipitated
by early enteral feeding.
18
Without prompt intervention, NOMI may
1,5,13,14
In NOMI, microscopic
15
Previous reports
15–17
have iden-
Box 26-1).
Box 26-1 Risk Factors for Development of
Nonocclusive Mesenteric Ischemia
Age >50 years
Atherosclerotic mesenteric arterial disease
Digitalis use
Sepsis
Prior hypotensive episodes
Congestive heart failure (CHF)
Coronary artery disease (CAD)
Vasoconstrictive drugs
Recent myocardial infarction (MI)
Cardiac arrhythmias
progress from localized intestinal ischemia to transmural infarction, peritonitis, and death.
ment, owing to the underlying medical conditions that precipitate
NOMI and frequent delays in diagnosis.
19,20
Mortality is high regardless of treat-
5,13–15
Pathophysiology
Nonocclusive mesenteric ischemia was first recognized in autopsies of patients with small-intestinal gangrene in the absence of
arterial or venous occlusion.
mechanisms of mesenteric circulation has demonstrated that the
pathophysiology of NOMI is multifactorial. Virtually all patients
with NOMI have a severe coexisting illness, commonly severe
cardiac failure.
23
It is postulated that hypoperfusion from cardiac failure, resulting in peripheral hypoxemia and splanchnic
vasoconstriction, precipitates intestinal ischemia.
vasoconstriction, intestinal hypoxia, and ischemia-reperfusion
injury all contribute to development of NOMI.
Mesenteric vasoconstriction, the hallmark of NOMI, represents
an exaggerated homeostatic mechanism induced by excessive
sympathetic activity during cardiogenic shock or hypovolemia. The
body attempts to maintain cardiac and cerebral perfusion at the
expense of splanchnic and peripheral circulations. Experimental
evidence suggests that the mediators of this response are
endothelin-1 (ET-1), nitric oxide (NO), vasopressin, and angiotensin (Ang).
24,25
Endothelin-1 is a potent vasoconstrictor secreted
21,22
Investigation of the regulatory
13,14
Mesenteric
from endothelial cells (ECs); in concert with other vasoactive peptides, it regulates myogenic cells in the vascular wall. Nitric oxide
can have paradoxical effects on vascular tone, depending on local
concentration.
26
At low concentrations it acts as a vasodilator,
whereas at higher concentrations it acts as an oxygen-derived free
radical, impairing mitochondrial energy production.
The splanchnic autoregulatory system is affected by local
arteriolar smooth muscle relaxation and vasodilation, as well as
increased cellular oxygen extraction.
27
Adequate oxygen delivery
may be maintained despite declining perfusion pressures until
a critical threshold is reached. In experimental models, maximal extraction is reached at a pressure of 40 mmHg, but beyond
this point, oxygen consumption declines, and ischemia ensues.28
Neri et al. recently demonstrated that postoperative cardiac surgery patients who develop NOMI had persistent deficits between
oxygen delivery (Do2) and consumption (Vo2) because of poor circulatory reserve. In contrast, postoperative cardiac patients who
did not develop NOMI were able to normalize their D
by optimizing their cardiac output.
14
In the presence of impaired
o
:Vo2 ratio
2
perfusion, blood flow is not evenly distributed in the bowel wall.
The mucosa retains its perfusion at the expense of the serosal layers through mucosal production of NO, prostaglandins (PGs), and
stimulation of dopamine-I receptors.
27
Histological damage is first
observed at the villous tip and progresses to the deeper muscularis,
submucosa, and mucosa within a few hours.
Once set in motion, mesenteric vasospasm may persist despite
correction of the precipitating event.
13,14
The etiology of persistent
vasoconstriction once adequate blood flow is restored is unknown,
but it may respond to direct intraarterial papaverine infusion or other
vasodilators, including iloprost.
29
This phenomenon of protracted
vasoconstriction, however, plays an important role in development
and maintenance of occlusive and nonocclusive intestinal ischemia,
and may also complicate mesenteric revascularization.
18
Use of vasoconstrictor agents and digitalis has been associated
with the majority of cases of NOMI. Vasoactive agents, including
α-adrenergic drugs and vasopressin, produce splanchnic vasoconstriction directly, whereas digoxin preparations alter mesenteric
vasoreactivity by stimulating arterial and venous smooth muscle
cell (SMC) contraction.
lar vasoconstriction in the setting of acute venous hypertension.
27,29
This may enhance mesenteric arterio-
29
Restoration of blood flow to the ischemic intestine may be complicated by reperfusion injury. During critical ischemia, adenosine
triphosphate (ATP) levels are depleted, causing distortion of ATPdependent cell membrane systems. This results in loss of cellular
homeostasis, with cellular swelling and electrolyte imbalances.27
Reduction in ATP levels also generates large amounts of adeno sine,
a precursor of hypoxanthine. Within the swollen cells, calcium
accumulates and triggers hydrolysis of the enzyme xanthine
dehydrogenase into xanthine oxidase, which reacts with intracellular hypoxanthine to produce uric acid and toxic oxygen free
radicals.
5,27
These free radicals exert direct damage to cellular
membranes, causing capillary leak syndrome, and incite endogenous inflammatory cascades that cause widespread tissue
injury. The deleterious effects of free radicals are usually limited
by endogenous scavengers such as glutathione, catalase, superoxide dismutase, and NO.27 However, in cases of prolonged ischemia, the capacity of this scavenger system to eliminate reactive
oxygen species (ROS) is exceeded, and continued damage occurs.
The degree of reperfusion injury is thus related to the frequency
and duration of the ischemic episodes. Clark and Gewertz demonstrated that two short 15-minute periods of low flow followed
by reperfusion resulted in a more severe histological injury than a
single 30-minute period of ischemia.
30,31
In NOMI, a similar scenario exists: hypoperfusion may be partial
and occasionally repetitive. It is believed that episodic reperfusion
creates a local environment replete with primed neutrophils within
the ischemic bed that are capable of degranulating and releasing
superoxide. This concept is substantiated by recent experimental
evidence that reperfusion injury may be attenuated by reperfusion
with leukodepleted blood or by blockade of EC surface receptors
for leukocyte adherence.32 In addition, several compounds including N-acetylcysteine and vitamin E have been shown in animal
models to reduce tissue damage caused by reactive oxygen spe-
33
cies.
Application of these novel approaches in human NOMI
awaits further study.
Mesenteric Venous Thrombosis
Mesenteric venous thrombosis (MVT) refers to thrombosis of the
veins draining the intestine (inferior mesenteric, superior mesenteric, splenic, and portal veins). The obstruction in venous return
leads to edema, distention, and in some cases, infarction of the
affected segments.
Epidemiology
Mesenteric venous thrombosis is a comparatively rare form of
mesenteric ischemia. The presentation may vary from asymptomatic to fulminant with intestinal infarction and hemodynamic collapse. Mesenteric venous thrombosis was first described by Elliot
in 1895 as “thrombosis of the portomesenteric venous system.”34
In 1935, Warren and Eberhard characterized MVT as a distinct clinical entity. These authors reported a 34% mortality rate following
intestinal resection for venous thrombosis.
Mesenteric venous thrombosis currently constitutes no more
than 5% to 15% of all cases of acute mesenteric ischemia.
372 patients with MVT were reported from 1911 to 1984,
accounted for only 6.2% of 1167 patients treated for mesenteric ischemia at the Mayo Clinic from 1972 to 1993.
found that MVT represented 0.006% of hospital admissions.
estimated that intestinal infarction due to MVT is encountered in
less than 1 in 1000 laparotomies for acute abdomen.
Pathophysiology
Mesenteric venous thrombosis can be classified as primary or secondary. Primary MVT is defined as spontaneous idiopathic thrombosis
of mesenteric veins not associated with any other disease or etiological factor.
substantially in the past decade because of increased recognition of
inherited thrombotic disorders and hypercoagulable states.
to have secondary MVT. Currently, however, a causative factor can
be identified in only 35% of patients with MVT.
of secondary MVT are shown in
accounts for 9% to 18% of episodes of MVT in young women.
Protein C and protein S deficiency, antithrombin III deficiency,
dysfibrinogenemia, abnormal plasminogen, polycythemia vera,
thrombocytosis, sickle cell disease (SCD), and factor V Leiden
mutation have all been associated with MVT.
ondary MVT has also been reported, most commonly associated
with volvulus, intussusception, or mechanical bowel strangulation.
Thrombosis due to an intraabdominal cause such as inflammatory
Trauma
Surgery
Cancer
Cirrhosis
Portal hypertension
Inflammatory bowel disease
Oral contraceptive use
Splenomegaly
Pancreatitis
Dehydration
Infection
Diverticular disease
Hypercoagulable states
1,5,36
Patients in whom an etiological factor can be identified are said
Location of the thrombus may be predicted by etiology.
Box 26-2 Causes of Secondary Mesenteric Venous
1,5
35
36
Only
37
and MVT
38
Ottinger and Austen
40
39
It is
The number of patients in this group has decreased
36,38
Known causes
Box 26-2. Oral contraceptive use
1,5,36,41,42
Localized sec-
41
Thrombosis
325
CH
26
EPIDEMIOLOGY AND PATHOPHYSIOLOGY OF MESENTERIC VASCULAR DISEASE
326
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conditions or surgery starts in the larger vessels at the site of compression and propagates distally to involve the smaller venous
arcades and arcuate channels.
underlying hypercoagulable state usually begins in the small vessels and later involves the larger vessels.
rectae and the intramural vessels interferes with adequate venous
CH
drainage, with eventual hemorrhagic infarction of the involved
26
bowel segment. The transition from normal to ischemic bowel is
41
In contrast, thrombosis due to an
36,41
Occlusion of the venae
usually gradual, unlike that seen with acute embolic or thrombotic
occlusion.
Natural History
The natural history of MVT varies based on the etiology. In most
cases, it usually does not result in gangrenous bowel.
symptomatic manifestations are diverse. Patients may present with
a benign abdominal examination and few symptoms or with profound hemodynamic collapse. Most patients have abdominal pain.
Although it can be sudden in onset, most frequently it begins insidiously and worsens over time. Approximately 50% of patients have
pain from 5 to 30 days before seeking medical attention, and 27%
report abdominal pain for more than 1 month.43 In a recent review,
only 16% of patients had severe peritonitis, and 33% required bowel
resection.
42
Despite improved diagnostic modalities and more
aggressive treatment regimens, symptomatic acute MVT is an indicator of poor prognosis, with an approximate 10% to 20% 30-day
mortality rate and a 3-year survival rate of 35%.
evidence of chronic thrombosis fare somewhat better because
collateral venous channels form and thereby augment intestinal
venous drainage.
1,5,41,42
42,44
Patients with
Chronic Mesenteric Ischemia
Symptomatic chronic mesenteric arterial insufficiency is a
well-described but infrequently encountered clinical problem.
Although the earliest report of chronic intestinal ischemia was
by Councilman in 1894,
the first individual to correctly associate postprandial pain with
CMI. Eighteen years later, Dunphy suggested that the abdominal
pain associated with chronic mesenteric arterial occlusion was a
possible precursor of later intestinal infarction.
Maynard performed the first successful endarterectomy for CMI.
Morris et al. described the technique of retrograde aortovisceral
bypass in 1962.
48
Epidemiology
Chronic mesenteric ischemia results from atherosclerosis in 90% of
1,5,49–51
cases.
Nonatherosclerotic etiologies have been described in young adults
Neurofibromatosis
Middle aortic syndrome
Median arcuate ligament compression
Visceral artery dissection
Buerger's disease
Rheumatoid arthritis
Cocaine abuse
Systemic lupus erythematosus (SLE)
Thoracic aortic aneurysm (TAA)
Cogan's syndrome
Polyarteritis nodosa
Aortic coarctation repair
Radiation injury
Thrombosis associated with TAA repair
Mesenteric arteritis
Congenital afibrinogenemia
Ergot poisoning
Nonathero sclerotic causes of CMI are listed in Box 26-3.
Box 26-3 Nonatherosclerotic Conditions Associated
45
in 1918, Goodman credited Baccelli as
46
Later, Shaw and
with Chronic Mesenteric Ischemia
Similarly,
and children as young as 30 months of age.
49–51
In general, Risk
factors for atherosclerotic-associated CMI are similar to those of other
atherosclerotic conditions, including a positive family history, sedentary lifestyle, hypertension, hypercholesterolemia, and smoking.
In contrast to other atherosclerotic vascular diseases, approximately
60% of patients with CMI are female, and nearly 50% of patients have
a history of earlier cardiovascular surgery.
ally manifests at a mean age of about 58 years.
third of patients have hypertension, coronary artery disease, and/or
cerebrovascular disease.
1,5,53–56
Nearly 20% have evidence of chronic
renal insufficiency, and 10% have diabetes.
51
Symptomatic CMI gener-
1,5,46,52–56
More than one
49,56
Although there is a high prevalence of mesenteric atherosclerosis, the clinical syndrome of symptomatic mesenteric ischemia is
uncommon.
significant stenoses in approximately 50% of celiac arteries, 30%
of SMAs, and 30% of IMAs.
1,54,55
An autopsy series of unselected patients found
52
In a more recent series of 120 consecutive autopsies, however, rates of significant stenoses in the
celiac, SMA, and IMA were not quite as high, with 22%, 16%, and
10% incidence, respectively.
55
The prevalence of potentially flowlimiting stenosis within the mesenteric vessels increases with age,
with up to 67% of those older than 80 years of age having more
than 50% stenosis in some mesenteric artery.55 Aortograms performed for aortic aneurysmal or occlusive disease demonstrate
significant stenosis of the celiac artery in 33% of cases and SMA
lesions in nearly 20%.
54–56
Pathophysiology and Natural History
Chronic mesenteric ischemia occurs when the blood supply
is insufficient to meet the metabolic demands of the bowel,
resulting from increased motility, secretion, and absorption
after meals.
ease may be explained in part by the extensive mesenteric collateral circulation, which includes both viscerovisceral (celiac
artery-SMA-IMA), and parietovisceral (hypogastric-IMA) blood
flow.
sis or occlusion of one or more of the major mesenteric vessels
may thus be fully compensated by collateral blood flow. In addition, recent evidence suggests that preexisting significant stenoses in even remote arterial beds may provide protective effects
through the mechanism of ischemic preconditioning.
47
It has been proposed that the pathophysiology of symptomatic
CMI involves a regional vascular steal phenomenon.
have used tonometric assessment of splanchnic blood flow in dogs
with 50% stenoses of both the celiac artery and SMA to show that
food intake reduced intestinal perfusion by 50%. This reduction
was associated with a significant decrease in intestinal intramural
pH that was attributed to steal from the intestinal to the gastric circulation stimulated by a food bolus within the stomach.
Rarely, single-vessel disease of the SMA may produce symptoms
characteristic of CMI. The vast majority of patients who present
with symptomatic CMI, however, have arteriographic evidence of
multivessel visceral artery disease.
A variety of pain syndromes characterize patients with CMI. In
general, the symptoms consist of upper abdominal cramping or
aching pain beginning 20 to 30 minutes after eating. At first the
pain may be of short duration, but later it may become more persistent and last for 3 to 4 hours after eating. As the disease progresses, the amount of food that precipitates abdominal pain may
decrease. Patients avoid eating to prevent the resulting abdominal
pain. Most patients with CMI suffer weight loss secondary to diminished nutritional intake; malabsorption is not the primary mechanism of weight loss.
No form of bowel activity is “classic” for CMI. Patients may have
diarrhea (which can potentially exacerbate their nutritional depletion), constipation, or normal bowel habits. Without intervention,
such patients develop severe protein-calorie malnutrition, and CMI
can progress to visceral infarction.
Most fatal cases of CMI occur in patients with a prolonged history of chronic abdominal complaints.
57
The infrequent occurrence of symptomatic dis-
1,5,55–57
The slow development of a chronic high-grade steno-
61
1,5,49–52,55,56
57
49,50,55–57
1,49–51,55–57
Such cases are
Investigators
58–60
61
1,5,46–51
frequently characterized by months of abdominal complaints
and multiple negative endoscopies, CT scans, and other diagnostic tests. In retrospect, the diagnosis is usually obvious. A high
index of suspicion and prompt intervention are clearly indicated
in cases of unexplained abdominal pain and weight loss. Early
diagnosis may prevent acute thrombosis of stenotic vessels and
the often fatal complication of intestinal infarction.
1,49–51,55–57
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Philadelphia, 1995, WB Saunders, p 526.
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43. Morasch MD, Ebaugh JL, Chiou AC, et al: Mesenteric venous thrombosis: a changing clinical
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44. Harnik IG, Brandt LJ: Mesenteric venous thrombosis, Vasc Med 15:407–418, 2010.
45. Councilman WT: Three cases of occlusion of the superior mesenteric artery, Boston Med
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46. Taylor LM, Porter JM: Treatment of chronic intestinal ischemia, Semin Vasc Surg 3:186, 1990.
47. Shaw RS, Maynard EP III: Acute and chronic thrombosis of the mesenteric arteries
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thromboendarterectomy, N Engl J Med 258:874, 1958.
48. Morris GC, Crawford ES, Cooley DA, et al: Revascularization of the celiac and superior
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49. White CJ: Chronic mesenteric ischemia: diagnosis and management, Prog Cardiovasc Dis
54:36–40, 2011.
50. Sanders BM, Dalsing MC: Mesenteric ischemia affects young adults with predisposition,
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51. Zeller T, Rastan A, Sixt S: Chronic atherosclerotic mesenteric ischemia, Vasc Med 15:333–338,
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52. Crawford ES, Morris GC, Myhre HO, et al: Celiac axis, superior mesenteric artery, and inferior
mesenteric artery occlusion: surgical considerations, Surgery 82:856, 1977.
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56. Chang JB, Stein TA: Mesenteric ischemia, Asian J Surg 26:55, 2003.
57. van Bockel JH, Geelkerken RH, Wasser MN: Chronic splanchnic ischemia, Best Pract Res Clin
Gastroenterol 15:99, 2001.
58. Heusch G, Schulz R: Remote preconditioning, J Mol Cell Cardiol 34:1279, 2002.
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27 Clinical Evaluation and Treatment
of Mesenteric Vascular Disease
Rachel C. Danczyk, Gregory L. Moneta
Evaluation
Clinical evaluation of possible mesenteric ischemia begins
with a careful history and physical examination and—above
all—an appropriate index of suspicion for the diagnosis. The
major etiologies of mesenteric ischemia include mesenteric
venous thrombosis (MVT), acute mesenteric ischemia, nonocclu-
sive mesenteric ischemia (NOMI), and chronic mesenteric isch-
emia (CMI). These differ in their underlying pathologies and
the clinical settings in which they occur, but there may be significant overlap in their clinical presentation. The most crucial
point is to understand the variety of clinical settings in which
intestinal ischemia can occur and to include mesenteric ischemia in the differential diagnosis of patients presenting with
abdominal pain. The goal is to achieve a diagnosis prior to the
onset of bowel infarction. Without consideration of intestinal
ischemia, the appropriate diagnostic evaluation is unlikely to
be obtained, resulting in needless additional morbidity and
mortality.
Acute Occlusive Mesenteric Ischemia
SIGNS AND SYMPTOMS
Acute occlusive mesenteric ischemia is caused by embolism to the
superior mesenteric artery (SMA) or acute thrombotic occlusion
of an atherosclerotic SMA. Mortality exceeds 60%.
Thrombotic occlusion of the SMA carries a worse prognosis
than embolism to the SMA because with thrombotic occlusion,
the SMA occludes proximal to the middle colic artery and interrupts arterial flow to the entire small intestine. Emboli, which
usually originate from the heart, typically lodge in the SMA distal
to the origin of the middle colic artery, thereby maintaining some
perfusion to the small intestine via the middle colic and jejunal
artery branches.
Abdominal pain is the most common presenting symptom in
patients with occlusive acute mesenteric ischemia, and physical
findings can range from nonspecific tenderness to an acute abdomen. Distention, rigidity, and rebound tenderness occur, particularly when the diagnosis of acute mesenteric ischemia is delayed.
The classic presentation is sudden onset of acute abdominal pain
out of proportion to the physical findings. This reflects profound
intestinal ischemia without associated bowel perforation and peritonitis. Vomiting, fever, and diarrhea are present in one third of
patients with acute mesenteric ischemia. Patients with embolism
tend to present with an acute onset of abdominal pain, whereas
patients with thrombosis of a stenotic SMA may have a more
delayed presentation.
Laboratory values are typically nonspecific. The majority of
patients will have moderate to marked leukocytosis, but about
10% of patients will have a normal white blood cell (WBC) count.
Elevated serum amylase and metabolic acidosis may occur in
patients with necrotic bowel, but an absence of these findings does
not exclude bowel necrosis.
RADIOLOGICAL DIAGNOSIS
Ultrasound has a limited role in diagnosing acute occlusive mesenteric ischemia. Duplex ultrasonography in the setting of an acute
abdomen is limited by abdominal distention, excessive bowel gas,
and patient discomfort.
1
An abdominal computed tomography (CT) scan is often obtained
during evaluation of a patient with abdominal pain. In addition
to finding other abdominal pathologies causing abdominal pain,
CT scans can detect late findings of acute mesenteric ischemia
with a sensitivity of 90%, including bowel luminal dilation, bowel
wall thickening, submucosal edema or hemorrhage, pneumatosis
intestinalis, and portal venous gas.
with some degree of intestinal infarction. Emboli tend to lodge
distally, and thus the sensitivity of CT scanning in detecting mesenteric arterial embolic occlusion is low and ranges from 37% to
3
80%
(Fig. 27-1). In patients with early ischemia, there may be mini-
mal findings on CT scans. These patients benefit most from early
diagnosis and definitive mesenteric revascularization before the
onset of intestinal infarction. Therefore, a high index of suspicion
and thorough physical examination is of the utmost importance in
this population of patients.
Mesenteric angiography remains the gold standard for diagnosing vascular lesions associated with acute mesenteric ischemia,
but its use is predicated on clinical judgment. In a patient with
obvious peritoneal findings and suspected necrotic bowel, as
evidenced by hypotension and acidosis, an urgent exploratory
laparotomy is required to resect necrotic bowel and perform
revascularization. In this emergent situation, preparation and performance of a mesenteric angiogram may delay definitive operative treatment and increase mortality.
In patients without peritoneal findings but clinically suspected
to have mesenteric ischemia, angiography can be performed
to make the definitive diagnosis and plan additional therapy.
Abrupt occlusion of the SMA distal to the origin of the middle
colic artery is typically seen in patients with an embolus (Figs. 27-2
through 27-4), whereas patients with thrombotic occlusion of a
chronically stenotic SMA show signs of occlusion beginning at its
origin from the aorta.
TREATMENT
Treatment of acute mesenteric occlusive ischemia is aimed at
the etiology of the disease. With acute embolic disease, embolectomy can be performed. Thrombotic disease should generally
be addressed with a bypass operation. Bypass as an option for
acute mesenteric occlusive ischemia treatment is discussed later
in the chapter.
Operative Embolectomy
Once angiography has identified embolic disease, the patient is
taken to the operating room for abdominal exploration and embolectomy. When performing an SMA embolectomy, a midline incision in the abdomen is made, followed by a thorough examination
of the abdominal contents. This may or may not reveal intestinal
infarction. The transverse colon is then reflected superiorly, and
the SMA is approached at the root of the small-bowel mesentery.
The ligament of Treitz is divided and the proximal SMA mobilized.
If the embolus is located more distally, the distal SMA may be
exposed at the root of the small-bowel mesentery. Embolectomy
is performed through a transverse arteriotomy using standard balloon catheters, and the embolus is extracted. The arteriotomy is
then closed, and the intestines are again inspected for viability;
any nonviable bowel is resected. A Doppler probe can be used
to assess the antimesenteric border for intestinal arterial flow. If
the bowel viability is equivocal, a “second look” operation can be
planned in the following 24 to 48 hours to reassess the bowel and
resect if necessary.
4
2
These findings are associated
328
FIGURE 271 Axial computed tomography (CT) scan demonstrating
a mid-aortic thrombus that caused embolic occlusion of superior
mesenteric artery (SMA).
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CliniCAl EvAluATion And TREATmEnT of mEsEnTERiC vAsCulAR disEAsE
FIGURE 274 Anteroposterior angiogram of superior mesenteric artery
(SMA) after operative embolectomy demonstrating filling of distal SMA.
Embolic
occlusion
FIGURE 272 Anteroposterior angiogram demonstrating abrupt
embolic occlusion of superior mesenteric artery (SMA).
Embolic occlusion
FIGURE 273 Anteroposterior angiogram of the superior mesenteric
artery (SMA) demonstrating embolic occlusion of distal SMA.
Chronic Mesenteric Ischemia
SIGNS AND SYMPTOMS
Patients with CMI are typically women (3:1 female-to-male ratio)
between the ages of 40 and 70 years, and a history of recurrent
abdominal pain is the most critical factor in the diagnosis. The
pain associated with CMI is mid-abdominal or epigastric in origin
and is described as colicky or a dull intense ache that may radiate to the back. Pain is postprandial and generally begins 15 to 30
minutes after eating and lasts up to 4 hours. There are no signs of
peritonitis, and the degree of pain may reflect the volume of the
ingested meal.
Patients may ingest some meals without pain early in the course
of CMI, so pain may be initially attributed to cholelithiasis, peptic ulcer disease, or malignancy. Patients often undergo extensive
evaluation with endoscopy, CT, barium studies, and abdominal
ultrasonography prior to reaching a diagnosis of CMI. As the disease
progresses, patients begin to experience pain with each meal and
may develop a fear of food. Weight loss, the hallmark of CMI,
results from limited nutritional intake, not malabsorption; patients
with CMI will have normal gastrointestinal absorption test results.
RADIOLOGICAL DIAGNOSIS
Mesenteric Angiography
Chronic mesenteric ischemia is a clinical diagnosis. There are no
absolute confirmatory tests, but contrast mesenteric angiography
is the standard to diagnose arterial lesions associated with CMI.
Radiographs are obtained in the lateral and anteroposterior projections. Findings on angiography suggestive of CMI include stenosis or occlusion of the celiac artery (CA) and/or the SMA (
When the origins of the CA or SMA are occluded, the more distal
vessels are often patent through filling by enlarged and easily visualized pancreaticoduodenal arterial collaterals. Occasionally, one
can find mid-SMA stenosis with a normal proximal SMA (Fig. 27-6)
or a “coral reef” aorta with associated SMA occlusion (
all patients with mesenteric artery obstruction, however, have mesenteric ischemia. It is vitally important to differentiate high-grade
mesenteric artery stenosis from the clinical entity of CMI.
Duplex Ultrasonography
Duplex ultrasonography can serve as a valuable noninvasive
screening test for splanchnic artery stenosis and for follow-up
in patients with mesenteric artery reconstructions. Despite the
Fig. 27-5).
Fig. 27-7). Not
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SMA
stenosis
FIGURE 275 Lateral aortogram demonstrating long-segment stenosis
of superior mesenteric artery (SMA).
SMA
stenosis
FIGURE 276 Lateral aortogram demonstrating long-segment stenosis
of middle superior mesenteric artery (SMA).
accuracy of duplex detection of mesenteric artery stenoses, an
appropriate history and physical examination and angiographic
confirmation of high-grade stenoses or occlusion of the splanchnic vessels are still required for the diagnosis of CMI. Duplex examination of the mesenteric arteries can be technically difficult and
should be performed by vascular technologists with extensive
experience in abdominal ultrasound techniques.
Celiac stenosis
Aortic coral reef
plaque
SMA occlusion
FIGURE 277 Lateral aortogram demonstrating “coral reef” atherosclerotic
plaque in aorta, with associated superior mesenteric artery (SMA) occlusion
and celiac artery (CA) stenosis.
In healthy individuals, fasting blood flow velocity waveforms differ between the SMA and the CA. Arterial waveforms reflect endorgan vascular resistance. The liver and spleen have relatively high
constant metabolic requirements and are therefore low-resistance
organs. As a result, CA waveforms are generally biphasic with a
peak systolic component, no reversal of end-systolic flow, and a
relatively high end-diastolic velocity (EDV). The normal fasting
SMA velocity waveform is triphasic, reflecting the high vascular
resistance of the intestinal tract at rest (
Figs. 27-8 and 27-9). There
is a peak systolic component, often an end-systolic reverse flow
component, and a minimal diastolic flow component.
Changes in Doppler-derived arterial waveforms in response to
feeding are different in the CA and SMA. Because the liver and
spleen have fixed metabolic demands, there is no significant
change in CA velocity waveform after eating. Blood flow in the
SMA, however, increases markedly after a meal, reflecting a marked
decrease in intestinal arterial resistance. Waveform changes in the
SMA postprandially include a near doubling of systolic velocity,
tripling of the EDV, and loss of end-systolic reversal of blood flow.
In addition, there is a small but detectable increase in the diameter of the SMA postprandially. The diameter of the SMA has been
shown to be 0.60 ±
after a meal. These changes are maximal at 45 minutes after ingestion of a test meal
0.09 cm in the fasting state and 0.67 ± 0.09 cm
5
and are dependent on the composition of the
meal ingested. Mixed composition meals produce the greatest flow
increase in the SMA when compared with equal caloric meals
composed solely of fat, glucose, or protein.
Detection of Splanchnic arterial StenoSiS
6
Duplex ultrasound can detect hemodynamically significant stenoses in splanchnic vessels. In 1986, investigators at the University of
Washington found that flow velocities in stenotic SMAs and CAs
were significantly increased when compared with normal SMAs and
7
CAs.
Quantitative criteria for splanchnic artery stenosis were first
developed and validated at Oregon Health & Science University.
8
In a blinded prospective study of 100 patients who underwent
mesenteric artery duplex scanning and lateral aortography, a peak
systolic velocity (PSV) in the SMA of 275 cm/s or more indicated
70% or greater SMA stenosis with a sensitivity of 92%, specificity of
Aorta/Superior Mesenteric Artery
FIGURE 278 Duplex ultrasonography of aorta and superior
mesenteric artery (SMA).
96%, positive predictive value of 80%, negative predictive value of
99%, and accuracy of 96%
9
(Fig. 27-10). In the same study, a PSV of
200 cm/s or higher identified 70% or greater angiographic CA stenosis with a sensitivity of 87%, specificity of 80%, positive predictive
value of 63%, negative predictive value of 94%, and accuracy of 82%
(
Fig. 27-11).
Other duplex criteria for mesenteric artery stenoses are also
in use. An SMA EDV greater than 45 cm/s correlates with 50% or
greater SMA stenosis with 92% specificity and 100% sensitivity. A
CA EDV of 55 cm/s or higher predicts 50% or greater CA stenosis
with 93% sensitivity, 100% specificity, and 95% accuracy.
10,11
Postprandial mesenteric duplex scanning has been used as an
adjunct to fasting duplex scanning to aide in the diagnosis of mesenteric artery stenoses.
12
In patients with less than 70% SMA stenosis, postprandial SMA PSV increases by more than 20% over
baseline velocity. The percent increase in SMA PSV is less in patients
with 70% or greater SMA stenosis. Specificity for the combination
of fasting SMA PSV and postprandial PSV, however, is marginally
improved over that provided by a fasting duplex scan alone.
Therefore, although theoretically attractive, postprandial duplex
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FIGURE 279 Duplex ultrasonography of superior mesenteric
artery (SMA), with peak systolic
velocity (PSV) of 208 cm/s signifying
a normal SMA.
FIGURE 2710 Duplex ultrasonography of superior mesenteric
artery (SMA), with peak systolic
velocity (PSV) of 389 cm/s signifying
70% or greater SMA stenosis.
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FIGURE 2711 Duplex ultrasonography of celiac artery (CA), with
peak systolic velocity (PSV) of
331 cm/s signifying 70% or greater
CA stenosis.
scanning offers no significant improvement over fasting mesenteric
duplex scanning; its routine use as part of ultrasound assessment
of mesenteric artery stenosis is unnecessary. Postprandial examinations are occasionally useful in technically difficult ultrasound
studies in that if there is a postprandial response, the insonated
vessel can be confirmed as being the SMA.
Duplex ultrasonography is best used as an initial screening study to
evaluate for visceral artery stenosis in patients with chronic abdominal pain that may be consistent with CMI. Angiography is required to
establish a definitive diagnosis of mesenteric artery stenosis.
Computed Tomography
Standard CT imaging can be of some value in mesenteric artery stenosis evaluation (also see Chapter 14). Currently, however, no studies have compared the accuracy of spiral CT with angiography in
assessing visceral artery stenoses. Computed tomography angiography can detect but not precisely quantify proximal stenosis of the
CA and SMA, and it is limited by lower resolution and bowel motion
artifact in its ability to detect lesions involving more distal branches.
Computed tomography scans are often obtained to evaluate abdominal pain. Findings suggestive of mesenteric artery stenosis include
calcification at the origin of the CA and SMA and lack of contrast
enhancement within the vessel lumen (
Magnetic Resonance Imaging
Development of fast breath-hold three-dimensional gadoliniumenhanced magnetic resonance angiography (3D Gd-enhanced
MRA) has improved the ability of MRA to detect proximal splanchnic artery lesions (also see Chapter 13). Magnetic resonance angiography is limited in its ability to image more distal visceral branches
because of limited spatial resolution, peristaltic and respiratory
motion, and chemical shift changes between the vessels and fat.
The accuracy of 3D Gd-enhanced MRA in detecting visceral artery
stenosis has been well studied. Overall sensitivity and specificity for
detecting 75% or greater stenosis or occlusion of the CA, SMA, or
inferior mesenteric artery (IMA) were 100% and 95%, respectively.
In addition to providing anatomical details, magnetic resonance
(MR) technology can quantify arterial flow using the phase-contrast
magnetic resonance imaging (MRI) technique, which provides
information about the presence, magnitude, and direction of blood
flow and has been studied in patients with CMI.
prandial flow in the SMA have been compared in patients with
documented atherosclerotic disease and normal volunteers. Mean
fasting SMA blood flow has been shown to be higher in atherosclerotic patients than in normal individuals. This difference can be
used to evaluate for CMI. The addition of MR oximetry technology,
where increased oxygen extraction after a meal is seen in those
with significant mesenteric vessel atherosclerosis, is promising with
Fig. 27-12).
15
Fasting and post-
13
FIGURE 2712 Computed tomographic angiogram (CTA) demonstrating
a patent supraceliac aorta to common hepatic artery, and superior
mesenteric artery (SMA) bypass. Proximal SMA is occluded.
regard to diagnosing CMI.15 Further validation studies correlating
the degree of change in mesenteric blood flow and oxygenation
with angiographic percentage of stenosis will be necessary before
phase-contrast MRI and MR oximetry are universally adopted as
routine noninvasive diagnostic methods for patients with CMI.
14
Treatment
Chronic and Acute Mesenteric Occlusive Disease
The available literature includes no randomized or controlled
clinical trials of surgical intervention for treatment of mesenteric
ischemia, and none are likely to be performed. Published clinical
reports include varied recommendations for treatment, and many
do not include descriptions of operative methods. Others describe
technically demanding procedures requiring extensive dissections
in difficult areas.
postoperative graft patency been included in clinical series.
For all these reasons, there is no current consensus regarding the
surgical details of treatment for intestinal ischemia.
16,17
Only recently has objective determination of
18,19
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