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242 D. Samsami and E. D. Ehrenpreis
Table 26.3 Physiologic and pharmacologic factors regulating mesenteric blood flow
Decrease blood flow by
splanchnic vasoconstriction
Humoral (endogenous and
exogenous) factors
Neural factors a-Adrenergic receptors b-Adrenergic receptors
Adapted from Oldenburg WA, Lau LL, Rodenberg TJ, Edmonds HJ, Burger CD. Acute
Mesenteric Ischemia. A Clinical Review. Arch Intern Med. 2004;164(10):1054–1062
Epinephrine (high dose) Epinephrine (low dose)
Norepinephrine (moderate to
high dose)
Dopamine (high dose) Dopamine (low dose)
Phenylephrine Dobutamine
Vasopressin Sodium nitroprusside
Angiotensin II Papaverine
Digoxin Nitric oxide
Dopaminergic receptors
Increase blood flow by
splanchnic vasodilation
Norepinephrine (low dose)
The majority of cases of acute intestinal ischemia result from blockage of blood
flow in the superior mesenteric artery. Pharmacologic causes of mesenteric ischemia are also shown in Table 26.3. Reduction in either arterial or venous blood flow
may result in the development of acute mesenteric ischemia, while chronic
mesenteric ischemia is generally caused by arterial narrowing. (See Chap. 25
Mesenteric Arterial Thrombosis and Chap. 24 Mesenteric Venous Thrombosis).
Acute Mesenteric Ischemia of Arterial Origen
There are several mechanisms resulting in the development of an acute decrease in
mesenteric arterial blood flow.
SMA embolus (SMAE): Although controversial, it is currently believed that
SMAE is the most common cause of acute mesenteric ischemia and is responsible
for 50% of cases. The origins of SMAE in these patients are thromboses in the left
atrium, left ventricle, cardiac valves and the abdominal aorta. Atrial fibrillation and
other arrythmias predispose to atrial emboli. Ventricular stasis and poor cardiac
output are associated with venous thrombi. Valvular heart disease, especially when
complicated by endocarditis, may be accom panied by valvular emboli. The SMA is
a relatively large artery and low takeoff angle (25–60 degrees), from the aorta. This
creates ideal condition for embolic obstruction, as emboli tend to become wedged
in areas of anatomic narrowing (Fig. 26.1). In general, embolic obstruction occurs
about 6–8 cm distal to the origin of the SMA, at a narrowed location near the
beginning of the middle colic artery. Emboli to other arterial systems are seen in
20% of cases and diminished circulation to other organs including the spleen, or
kidney may be seen.
26 Ischemic Enteropathy (Also Called Mesenteric Ischemia) 243
Fig. 26.1 Schematic representation of the abdominal aorta and inferior vena cava. The superior
mesenteric artery is shown having a very sharply angulated takeoff from the abdominal aorta
SMA Thrombosis (SMAT)
Approximately 25% of acute intestinal ischemia of arterial origin are due to SMAT.
Thrombosis of the SMA occurs in patients with longstanding atherosclerotic
involvement and narrowing of the SMA. These patients may have chronic symptoms including sitophobia (fear of eating) and post- prandial abdominal pain,
although relative compensation for SMA narrowing takes place by the formation of
collateral blood flow. Decreased blood circulation in the SMA after cardiac
244 D. Samsami and E. D. Ehrenpreis
decompensation from an acute myocardial infarction, congestive heart failure or
vessel dissection results in acute thrombus formation. In general, symptomatic acute
mesenteric ischemia develops when the celiac trunk and SMA are involved.
Nonocclusive Mesenteric Ischemia (NOMI)
20% of cases of ischemic enteropathy of arterial origin are due to NOMI. NOMI
occurs when constriction of the splanchnic bed occurs after an acute cardiovascular
event without the presence of an anatomic obstruction. It is most commonly seen in
critically ill patients with sepsis and markedly diminished cardiac output, in which
failure of normal autoregulation of mesenteric blood flow is present. A variety of
pharmacologic agents that reduce the reginal blood flow within the splanchnic
circulation may result in the development of NOMI. These include vasopressors
such as norepinephrine, epinephrine, vasopressin and phenylephrine, digitalis
(which diminishes splanchnic blood flow), vasoconstrictors such as cocaine and
sumatriptan as well as diuretic medications.
Focal Segmental Ischemia (FSI)
FSI refers to the development of damage to short segments of the small intestine as
a result of vascular compromise. Causes of FSI may be thrombotic, embolic,
traumatic and vasculitic. FSI may occur secondary to medications such as oral
contraceptives. It may also be seen with strangulated intestinal hernias.
Acute Mesenteric Ischemia of Venous Origen (MVT)
Approximately 10% of all cases of ischemic enteropathy result from mesenteric
venous thrombosis. The superior mesenteric vein is the most common site of
occurrence of MVT. A variety of conditions that are associated with hypercoagulable states predispose to the development of MVT. These include neoplastic disorders, cirrhosis of the liver, acute pancreatitis, and hereditary hypercoagulable
states including Factor V Leiden, prothrombin gene mutation, deficiencies of
anticlotting clotting (such as antithrombin, protein C and protein S), and elevated
levels of homocysteine or fibrinogen or dysfibrinogenemia. Acute MVT has an
expected 30% survival at 30 days and a poor longt-erm prognosis. For additional
information see Chap. 24, Mesenteric Vein Thrombosis.
26 Ischemic Enteropathy (Also Called Mesenteric Ischemia) 245
Table 26.4 Causes of
chronic mesenteric ischemia
Causes of chronic mesenteric ischemia
Occlusion from atherosclerosis
Dissection of mesenteric vasculature
Inflammation of the vessels (vasculitis)
Fibromuscular dysplasia of the mesenteric vessels
Radiation-induced vascular injury
Chronic cocaine abuse
Chronic mesenteric ischemia: Chronic mesenteric ischemia is an insidious process
and is usually related to arterial occlusion from atherosclerosis. Additional causes of
chronic mesenteric ischemia include dissection of mesenteric vasculature, inflammation of the vessels (vasculitis), fibromuscular dysplasia of the mesenteric vessels,
radiation-induced vascular injury, and chronic cocaine abuse (Table 26.4).
Since the development of mesenteric atherosclerosis is a slow process, collateralization of mesenteric vessels occurs. This process results in clinical compensation for loss of flow in vessels affected by atherosclerosis. Because of this
phenomenon, signs and symptoms of intestinal ischemia typically occur when at
least two and sometimes three arteries are affected.
Signs and Symptoms of Ischemic Enteropathy
The medical history usually does not provide enough information to secure the
diagnosis of acute ischemic enteropathy. Acute mesenteric ischemia and nonocclusive mesenteric ischemia should always be considered in patients with rapidly
developing and diffuse abdominal pain. This is particularly true in patients with risk
factors for acute mesenteric ischemia including patients with cardiovascular disease
such as congestive heart failure or recent myocardial infarction, hereditary hypercoagulable states, vasculitis or the use of vasoconstricting medications including
cocaine. Patients with acute ischemic enteropathy present with abdominal pain that
is out of proportion to the physical exam. Associated symptoms may include
nausea, vomiting, fever, and gastrointestinal hemorrhage. As ischemia persists,
symptoms may evolve and the pain may temporarily disappear indicating that
significant bowel necrosis has occurred. The classic presentation of chronic
ischemic enteropathy is recurrent post-prandial pain. Signs and symptoms typically
appear when at least two arteries are affected. The pain is often described as dull,
crampy, located in the epigastric region, and occurring approximately one hour
after eating. Symptoms often resolve within a couple of hours. Patients often
develop food aversion (sitophobia) due to anticipation of post-prandial pain, thus
leading to weight loss.
246 D. Samsami and E. D. Ehrenpreis
Diagnosis
The diagnostic approach is largely dependent on the clinical presentation. If a
patient is hemodynamically stable, without signs of sepsis, the first recommended
imaging study is a contrast en hanced computerized tomogram (CT) or CT
angiography (CTA). Although a CT scan is a sensitive test, it can be negative in
early stages of bowel ischemia. If the CT scan is non-diagnostic and suspicion for
mesenteric ische mia remains high, the next diagnostic test would be a mesenteric
angiogram with arterial and venous phases. On the other hand, if a patient presents
with hemodynamic instability, plain abdominal films can be of utility to show free
air and other signs of advanced ischemia. If these signs are present, a laparotomy is
indicated.
Physical Findings
In early acute mesenteric ischemia, even in the presence of severe pain, the
abdominal examination may be normal or only mildly abnormal with minimal
abdominal distention and tenderness. This is why the term “pain out of proportion
to exam” has become a classic description of acute mesenteric ischemia. As
intestinal ischemia progresses and transmural bowel infarction develops, the
abdomen can become grossly distended, bowel sounds are diminished or absent,
and peritoneal signs can develop. There are a few other pertinent exam findings. For
instance, occult blood may also be present in the stool. A feculent odor of the breath
can also be observed with bowel ische mia. In addition, there can be non-specific
signs consistent with dehydration and shock that indicate a deteriorating clinical
course. On the other hand, physical exam findings for chronic mesenteric ischemia
are usually nonspecific. Due to the fear of eating from postprandial pain, these
patients can be undernourished and cachectic appearing. The abdominal exam is
soft and non-tender however may be slightly distended. An abdominal bruit is
commonly present but this is also a nonspecific finding.
Laboratory Findings
Laboratory values are typically non-specific. While abnormal laboratory findings
can support the diagnosis of acute ischemic enteropathy, normal laboratory values
should not exclude the diagnosis or delay further workup. The reason for this is
because most abnormalities only arise once ischemic enteropathy has progressed to
bowel necrosis. The most common findings for mesenteric ische mia include
leukocytosis, elevated amylase, phosphorus, and metabolic acidosis. Leukocytosis
can be moderate to markedly elevated, however 10% of patient have a normal white
blood cell count. Elevated lactic acid is 86% sensitive and 44% specific for acute
mesenteric ischemia. The specificity increases once other causes of lactic acidosis
26 Ischemic Enteropathy (Also Called Mesenteric Ischemia) 247
are ruled out such as shock and diabetic ketoacidosis. Elevated serum amylase has
been observed in 50% of patients. Studies have shown that the bowel contains high
concentrations of both organic and inorganic phosphate. When there is ischemia,
phosphate is released from the bowel, and elevated phosphorus has been observed
in 80% of patients. D-dimer can also be checked, as it is an early marker for
ischemia, increasing as early as 30 minutes after an ischemic event. While a normal
d-dimer can help exclude acute mesenteric ischemia, an elevated level is not
diagnostic as there are many other conditions that increase d-dimer levels.
Imaging
A plain abdominal radiograph is often the initial test ordered in patients with acute
abdominal pain however it has very little diagnostic role in mesenteric ischemia. Its
primary purpose is to rule out other diagnoses such as perforated viscus or a bowel
obstruction. Findings suggestive of mesenteric ischemia include presence of an
ileus, bowel wall thickening, as well and pneumatosis intestinalis. A plain radiograph can also show free intraperitoneal air, a late sign of ischemia indicating that
intestinal perforation has already occurred and that urgent surgical exploration is
required (Fig. 26.2).
For patients with suspected acute mesenteric ischemia who are hemodynamically stable, a contrast enhanced CT scan, especially a CTA is performed. Findings
on CT that are associated with mesenteric ischemia include bowel wall thickening,
submucosal edema or hemorrhage, pneumatosis intestinalis, portal vein gas,
porto-mesenteric thrombosis, mesenteric arterial calcification, and mesenteric artery
occlusion. Findings consistent with intestinal infarction include discontinuous
mucosal enhancement and adjacent mesenteric stranding (Fig. 26.3).
Fig. 26.2 Anterior–posterior radiographic images of the abdomen show massive pneumoperi-
toneum with air under the right hemidiaphragm (white arrows) and lucent air outlining the small
bowel walls (black arrows). The latter finding is call Rigler’s sign
248 D. Samsami and E. D. Ehrenpreis
Fig. 26.3 Coronal,
contrast-enhanced computed
tomography image shows a
dilated small bowel loop with
discontinuous mucosal
enhancement (arrows) and
adjacent mesenteric
fat-stranding suggestive of
small bowel infarction in this
patient with SMA thrombosis
(not shown). With permission
from Dr. Abraham Dachman
and Dr. Justin Ramirez
CTA is the imaging modality of choice and should be performed without delay.
A meta-analysis of six studies published between 1996 and 2009 on the diagnostic
accuracy of multidetector CT in acute mesenteric ischemia showed a pooled sensitivity of 93% and specificity of 96%. It is important to note that the CT angiogram
should not be performed with oral contrast. This is because oral contrast can
obscure the mesenteric vessels and bowel wall enhancement. Disadvantages of CT
include radiation exposure, the risk of contrast nephropathy, and allergic reactions
to iodinated contrast. CT angiography should still be performed in patients despite
renal failure as the consequences of delayed diagnosis outweigh detrimen tal renal
affects. If CT angiography findings are equivocal, catheter directed angiography
may be necessary.
MRA is a good option in in patients to avoid radiation exposure and for those
who cannot have iodinated contrast, however it takes significantly longer to perform. MRA additionally appears to be more sensitive at identifying venous
occlusions. By contrast, CT demonstrates better visualization of the IMA, the
peripheral splanchnic vessels, calcified plaques, and previously placed stents.
Duplex ultrasonography is another imaging modality used in the appropriate
clinical setting. It can identify occlusions in the celiac or superior mesenteric
arteries or arterial stenosis. Duplex ultrasonography has limitations based on body
habitus, presence of bowel gas, effects of respiration, and operator expertise.
26 Ischemic Enteropathy (Also Called Mesenteric Ischemia) 249
Histologic Findings
Histological specimens demonstrate the pathophysiologic processes associated with
mesenteric ischemia, and may provide useful information regarding the extent and
severity of intestinal injury. Findings differ by temporal occurrence ischemia as well
as the site of diminished mesenteric blood flow. In the small intestine, ischemic
changes due to arterial insufficiency initially occur at the tips of the intestinal villi.
Early stages of injury show minor surface epithelial degeneration and mild
hyalinization of the lamina propria caused by leakage of plasma proteins from
injured capillaries. With further ischemic insult, the necrosis extends through the
entire length of the villi and starts to involve the bases of the crypts. “Crypt ghosts”
are empty spaces within the mucosa and represent remnants of intestinal crypts at
this stage. The submucosa is typically edematous and erythematous with engorged
veins. It is described as friable, and may have associated hemorrhage. The muscularis propria is the last layer to be affected. As this layer undergoes necrosis, the
intestinal wall becomes thin, friable, and easily disrupted. Organizing thrombi may
be detected within blood vessels (Figs. 26.4 and 26.5).
Acute intestinal ischemia due to venous obstruction ultimately acts in a manner
similar to arterial insufficiency. However, it is differentiated by an initial phase that
is characterized by severe vascular congestion, hemorrhage, and marked tissue
edema. With progressive tissue insult, arterial flow ceases.
Chronic mesenteric ischemia has a histologically distinct appearance when
compared to acute causes of mesenteric ischemia. Chronic mesenteric ischemia is
characterized by fibrosis that usually involves all layers of the intestinal wall,
including the mucosa. Hemosiderin deposits may also be present. These indicate
previous episodes of hemorrhage. Chronic intestinal ischemia may also be characterized by the presence of linear ulcerations and strictures.
Fig. 26.4 Granulation tissue,
ulcerations, and necrosis
extend into submucosa and
surrounding smooth muscle
fibers of muscularis mucosa.
There is a surface exudate of
neutrophils, fi brin, and
mucosal necrosis (H&E, 4x)
250 D. Samsami and E. D. Ehrenpreis
Fig. 26.5 Organizing
thrombi in the blood vessels
(H&E, 20x) (Histology). With
permission from Dr. Ismail
Mohamed Ahmed Elbaz
Younes
Treatments for Acute Mesenteric Ischemia
Acute mesenteric ischemia is a medical emergency. Once the diagnosis is made,
intervention should be initiated without delay.
Medical
Initial management is focused on resuscitation and stabilization. This consists of
intravenous fluid management with crysta lloids to correct volume deficits and
metabolic derangement and blood products. Fluid volume requirements may be
high due to significant capillary leakage. Early intubation should be considered in
unstable patients to improve oxygenation and allow for more aggressive fluids
resuscitation. Vasopressors should be avoided if possible as they worsen ischemia
by producing vasoconstriction. However, if necessary, dobutamine, low dose
dopamine, and milrinone all improve cardiac function and have been shown to have
less impact on mese nteric blood flow. Additionally, all patients with possible
intestinal ischemia should be started on broad spectrum antibiotics as early as
possible. This is because intestinal ischemia leads to loss of the mucosal barrier,
facilitating bacterial translocation.
Pharmacologic therapy for acute ischemic enteropathy typically consists of
papaverine, thrombolytics, and anticoagulants. Papaverine is a vasodilator that is
indicated to treat arterial spasm. Therefore, it is useful for all arterial forms of acute
mesenteric ischemia, and it is the only treatment for NOMI. Papaverine is usually
infused directly into the SMA resulting in an improvement of intestinal blood flow.
Thrombolytic agents have been shown to be beneficial in SMAE but they have
shown no benefit in SMAT. The infusion must be started within 8 hours of
26 Ischemic Enteropathy (Also Called Mesenteric Ischemia) 251
symptom onset. If symptoms do not improve within 4 hours, or if peritonitis
develops, then the infusion is stopped and surgical treatment should be initiated.
Heparin anticoagulation is the first-line treatment for MVT and early use has
been associated with improved survival. There are no studies that explore the use of
enoxaparin or another low molecular weight heparin as a substitute for heparin.
Surgical
If there are peritoneal signs on physical examination, this usually indicates bowel
infarction rather than ischemia alone. There is a significant reduction in survival in
these patients and emergency laparotomy is required. Goals for surgical intervention in acute mesenteric ischemia include re-establishment of the blood supply to
the ischemic intestine, preservation of viable intestine, and resection of non-viable
organs.
Treatments for Chronic Mesenteric Ischemia
Medical
Medical therapy alone is usually reserved for patients who are asymptomatic or
those who are not good surgical candidates. In these patients, treatment consists of
long-term anticoagulation therapy with medications such as warfarin. Novel oral
anticoagulants have not been studied extensively for this indication.
Surgical
Traditionally, surgical repair has been the standard method of treatment for chronic
mesenteric ischemia. However, published success rates as well as decrease in
morbidity and mortality have shifted practices toward endovascular therapy as
primary treatment for chronic mesenteric ischemia.
Open surgical repair consists of several different procedures including transaortic
endarterectomy, direct reimplantation of the aorta, and anterograde or retrograde
bypass grafting. Two of the most favored techniques include anterograde or retrograde bypass grafting. The anterograde bypass originates from the supraceliac
aorta and should revascularize multiple visceral arteries. Benefits of this technique
include reduction in kinking and turbulent blood flow, along with greater ease of
multivessel revascularization. However, this technique does increase the risk of
renal ischemic injury due to brief cross-clamping of the aorta above the renal
vessels. Retrograde bypass originates from either the infrarenal aorta or the iliac
arteries and it usually only revascularizes the SMA.