Scandinavian Journal of Surgery 99: 106110, 2010

Mesenteric ischemia: the whole spectrum

M. J. Sise
Department of Surgery, Scripps Health, San Diego, CA, U.S.A.
Key words: Superior mesenteric artery; thrombosis; embolism; intestinal necrosis; intestinal ischemia;
arterial occlusion

Background
Mesenteric ischemia remains a deadly process which
requires early diagnosis and prompt treatment if the
patient is to have any chance of survival. The overall
mortality rate remains approximately 40% and there
is little room for either delay or error in the management of this acute care surgical emergency (1, 2).
There are a variety of causes which ultimately, if left
untreated, lead to mesenteric infarction and death.
Symptoms vary from the insidious onset of vague
generalized abdominal pain to the sudden onset of
diffuse, severe, and constant pain. There are four
common causes: acute cardiac source embolism to the
superior mesenteric artery, acute thrombosis of an
atherosclerotic lesion with previous partial occlusion,
splanchnic vasoconstriction leading to low flow and
regional ischemia (commonly called non-occlusive
mesenteric ischemia), and mesenteric venous thrombosis (Table 1). All of these causes are secondary phenomena which result from other major diseases and
occur in a high risk setting.
Mesenteric Vascular Anatomy
The arterial blood supply of the gut is divided into
four major areas each defined by the major arteries
which supply them. Important collaterals link the
perfusion of each area (Table 2). These collaterals are
not sufficient to provide adequate flow if the superior
mesenteric artery is acutely occluded. However, in
chronic, progressive atherosclerotic occlusive disease,
they can steadily increase in size to prevent ischemia.
Patients occasionally will have total gut perfusion via
a single remaining mesenteric artery or the bilateral
hypogastric arteries in the presence of a gradual progression to total occlusion of the other proximal aor-

Correspondence:
Michael J. Sise, M.D.
550 Washington St, Suite 641
San Diego, CA 92103, U.S.A.
Email: sise.mike@scrippshealth.org

Table 1
Etiology of acute mesenteric ischemia.
50%
20%
20%
10%

Arterial embolism
Arterial thrombosis
Small vessel occlusion
Venous thrombosis

tic branches to the foregut, midgut, and hindgut.

However, many of these patients have intestinal angina when eating large meals. The venous drainage
of the gut is via the portal venous system. Gastric
drainage is via the splenic vein. The small bowel and
the proximal colon through the splenic flexure drain
via the superior mesenteric vein. The remainder of
the colon drains via the inferior mesenteric vein. Collateral venous vessels are present between each major
area.
The celiac and mesenteric artery origins from the
aorta are closely associated with the renal artery origins in the upper abdomen just below the aortic hiatus of the diaphragm. Their proximal portions each
have a closely applied plexus of lymphatic and neurologic tissue. These vessels are relatively thin-walled,
unlike similarly sized extremity arteries, and must be
handled with care. The portal vein and major mesenteric veins are also thin-walled, easily torn, and
equally easily injured during exposure.
Clinical presentation
The pathophysiology of mesenteric ischemia is based
upon insufficient blood flow to meet the metabolic
demand of the bowel. Acute ischemia leads to initial
hyperperistalsis, gut emptying, followed by intense
ischemia pain from gut wall hypoperfusion. Since
this is visceral pain, it is vague and projected across
the area of the superficial abdominal wall with innervation shared with the visceral innnervation. Foregut structures generate visceral pain in the epigastrium, midgut in the periumbilical regions, hindgut
in the infraumbilical region, and cloacal derivatives
in the supra-pubic region of the abdomen. Ischemia

Mesenteric ischemia: the whole spectrum

107

Table 2
Gut regions, their blood supply, and collateral connections.
Region

Blood supply

Collateral connections

Foregut
Distal esophagus through the ampulla
of Vater in the duodenum

Celiac artery

Pancreatico-duodenal arteries and Arc

of Buhler distally

Migut
Ampulla of Vater region of the duodenum
to splenic flexure of the colon

Superior mesenteric artery

Pancreatico-duodenal arteries and Arc

of Buhler proximally. Marginal artery of
Drummond and Arc of Rioland distally

Hindgut
Splenic flexure of the colon to distal
sigmoid colon

Inferior mesenteric artery

Marginal artery of Drummond and Arc

of Rioland proximally
Superior hemorrhoidal to middle
hemorrhoidal arteries distally

Cloacal derivatives

Branches of the bilateral hypogastric

arteries

Middle hemorrhoidal to superior

hemorrhoidal arteries proximally

pain is intense and constant. It is does not increase

with palpation and not associated with abdominal
wall rigidity. Thus the classical pain out of proportion with physical findings attributed to acute mesenteric ischemia. The initial reflex gut emptying with
vomiting and diarrhea also diverts the examining
physicians attention to other diagnoses. Finally, when
ischemia leads to necrosis, inflammation of the gut
surface leads to localization of pain in the abdomen
and the presence of associated physical findings.
Acute intestinal ischemia from sudden complete
occlusion of the celiac or superior mesenteric arteries
from a cardiac source embolism causes the classical
findings outlined above. Acute on chronic occlusion
of a previously stenotic atherosclerotic lesion may
lead to a less drastic and more insidious onset of pain
because of pre-existing collateral flow which mitigates, to a certain extent, the severity of the resulting
ischemia. In this setting, there may be a history of
intestinal angina including post prandial pain, fear of
food, and weight loss. Similarly, venous occlusion is
usually insidious in onset and causes more vague
symptoms which worsen progressively over time.
Non-occlusive acute mesenteric ischemia from vasoconstriction always occurs in the setting of critical
illness with reduced cardiac output and is associated
with vague symptoms at first.
Concurrent cardiac disease is the common element
of these patients medical history. Atrial fibrillation is
the most commonly associated cardiac diagnosis
(Table 3) (36). Patients usually report rapid onset of
pain associated with nausea, vomiting, loose stools.
Abdominal distension, hypoactive bowel sounds, and
guaiac positive stools are also commonly found on
physical examination early in the course of mesenteric ischemia. In patients with acute worsening of
chronic mesenteric ischemia there is always a history
of long standing post prandial pain and weight loss
occurs in close to 90% of patients. A history of nausea
and vomiting in the past is present in over 50% and
an abdominal bruit is found on physical examination
in over two thirds of these patients. Approximately
50% of patients with mesenteric venous thrombosis
have a history of hypercoagulability, 25% a history of
hepatitis, 25% thrombocytosis, and 10% pancreatic

Table 3
Risk factors for mesenteric ischemia.
Arterial embolism or thrombosis

Venous thrombosis

Cardiac disease:
atrial figrillation
recent myocardial infarction
congestive heart failure
digitalis therapy

Portal hypertension

Previous arterial emboli

Hypercoagulable state
Hypovolemia, shock

Inflammation
Postop period, trauma
Prothrombotic state
Chronic renal failure
Congestive heart failure

cancer (3, 4). These patients have findings similar to

those with acute arterial occlusion in the later stages
of this disease. Early, the findings are less distinct and
the use of CT scanning allows timely diagnosis before
significant bowel compromise occurs.
End stage intestinal necrosis causes severe shock
and an overwhelming inflammatory response with
an attendant high mortality rate (7, 9). Because acute
mesenteric ischemia usually occurs in the setting of
significant pre-existing diseases, outcome with intestinal necrosis is poor and has not significantly improved in the last four decades (5, 6). The goal remains prompt recognition and successful management prior to bowel necrosis.
Diagnosis
The classical pain out of proportion to findings is not
always present as previously discussed. Hypoactive
bowel sounds are usually encountered and signs of
peritoneal irritation occur late. The onset of intestinal
ischemia often produces a profound leukocytosis
with peripheral WBC elevation in excess of 20,000. In
fact, any patient with abdominal pain and a WBC in
excess of 20,000 should have acute mesenteric ischemia included in their differential diagnosis. Serum
amylase elevation occurs, however, serum lactate elevations and systemic acidosis are later findings.
Plain film radiography is not helpful until late in the

M. J. Sise

108

course of mesenteric ischemia when an ileus pattern,

distented bowel, and bowel wall thickening are seen.
High resolution abdominal CT scan with contrast is
very accurate and specific in delineating not only the
extent of visceral ischemia but the status of flow in
the mesenteric vasculature (10). Both mesenteric arterial and portal venous blood flow is accurately assessed with contrast CT scanning (11). Findings of
abnormal intestinal wall blood flow, arterial intraluminal defects, or a halo sign in the mesenteric veins
are very well demonstrated and accurately diagnose
the presence and the causes of mesenteric ischemia.
Visceral CT angiography has largely replaced catheter
angiography in the work up of acute and chronic
mesenteric ischemia. Although catheter angiography
is somewhat more accurate, it is time consuming and
does not produce results of significantly more usefulness than those of high resolution scans with coronal,
sagital, and VTR reconstructions. Catheter angiography is particularly less accurate is assessing venous
phase blood flow compared to CT scanning. Other
diagnoses in the differential for acute mesenteric ischemia include pancreatitis, small bowel obstruction,
and acute biliary tract disease among others. CT scanning is very accurate in excluding these diagnoses in
patients with mesenteric ischemia.
Management
The key to successful management of acute mesenteric ischemia from major arterial occlusion is prompt

surgical therapy (Fig. 1) (12). Although there is a limited role for endovascular management, it cannot be
successful without also performing an exploratory
laparotomy except in the very earliest stages of ischemia when necrosis is not a significant risk. The risk
of bowel necrosis and subsequent peritonitis and
generalized inflammatory response requires prompt
abdominal exploration to assess bowel viability even
when arterial flow has been restored by endovascular
techniques. Endovascular management has a role in
chronic mesenteric ischemia from atherosclerotic lesions without the presence of acute intestinal ischemia (13, 14). Laparoscopy has a little, if any role, in
the management of mesenteric ischemia. Prompt exploratory laparotomy is the key to successful management.
The intraoperative assessment of blood flow of the
bowel begins with an inspection of the entire intestinal tract by running the bowel, assessing color, peristaltic activity, and palpating the mesenteric arcade
arteries (Fig. 2) . The main trunk of the superior mesenteric artery is then palpated by cephalad retraction
of the transverse colon, caudal retraction of the small
bowel, and palpation of the root of the mesentery
along the inferior margin of the body of the pancreas.
The celiac artery and its branches are palpated
through the lesser sac below the left lobe of the liver
and above the lesser curve of the stomach. The inferior mesenteric is palpated along the left side of the
infra-renal aorta and the base of the left colon mesenMichael
J. Sise,
MD,
FACS border for
tery. Doppler
assessment
of the
mesenteric
pulsatile signals is helpful in areas of questionable

Figure 1. Decision-making in the management of mesenteric ischemia

Classical signs of
mesenteric ischemia

Abdominal pain
out of proportion
to findings
CT scan evidence of
arterial occlusion

Direct to OR

Unstable patient

Insidious onset,
vague symptoms

Mesenteric venous
thrombosis
Non-occlusive
mesenteric
ischemia

Fig. 1. Decision-making in the management of mesenteric ischemia.

Anticoagulation,
resuscitation, bowel
rest, serial
examinations, treatment
of underlying low-flow
state or inflammatory
processes,
exploratory laparotomy
for failure to improve

Michael J. Sise, MD, FACS

Figure 2. Intra-operative management
mesenteric
ischemia
Mesenteric of
ischemia:
the whole spectrum
Superior mesenteric
artery embolism

Mesenteric arterial
thrombosis

109

Embolectomy of superior mesenteric

artery, reassessment for bowel viability,
resect bowel as needed, damage control
closure, re-operation, anticoagulation

Aorto- mesenteric bypass as needed,

reassessment for bowel viability, resect
bowel as needed, damage control
closure, reoperation, anticoagulation

Fig. 2. Intra-operative management of mesenteric ischemia.

perfusion. Fluorescein angiography with an ultraviolet lamp has also been used (15).
The pattern and appearance of ischemic bowel is
helpful in determining the cause of mesenteric ischemia. Cardiac source embolism to the superior mesenteric artery usually lodges in the vessel distal to the
origin of the middle colic artery. Therefore, sparing
of the proximal jejunum and the transverse colon
with ischemia of the remaining small bowel and ascending colon are seen. Thrombosis of the origin of
the superior mesenteric artery leads to ischemia
throughout its distribution from the duodenum to the
splenic flexure of the colon. If the celiac artery and
the inferior mesenteric artery are also stenotic or occluded, more proximal and distal areas are also ischemic. In the worst case scenario, acute thrombosis
leads to total intestinal ischemia from the distal
esophagus to the rectum.
Embolism in the superior mesenteric artery is retrieved through a transverse incision in the main
trunk of the artery in the mesenteric root below the
pancreas (16). This area is exposed in the manner
outlined above. Care should be taken in handling this
relatively fragile artery. Balloon embolectomy catheters should also be used gently proximally and distally to avoid arterial injury. Gentle flushing distally
with heparinzed saline (10 units of heparin per ml)
should be performed. Do not flush proximally for
fear of dislodging thrombus into the aorta and causing distal embolism. The closure of the arterotomy
must be done with either a tension-free running
monofilament suture or interrupted sutures. This is
best accomplished by placing proximal and distal
vascular clamps and gently retracting the artery towards the arterotomy site to minimize tension. Once
flow has been re-established, the bowel may not immediately appear perfused. Placing warm laparotomy packs and waiting 10 to 15 minutes to reassess
is helpful. Injection of papaverine hydrochloride into
the superior mesenteric artery (two ml of a 30 mg per
ml solution) is a helpful adjunct to reduce vasospasm
and improve reperfusion.

The treatment of proximal mesenteric arterial

thrombosis requires experience and skill in advanced
vascular surgical technique. Call for a vascular surgeon colleague to assist if you are not comfortable
and capable to perform the necessary aorto-mesenteric bypass. There are a variety of bypasses described. Retrograde iliac artery to mesenteric artery
bypass appears easier to perform than antegrade
supra-celiac aorto-mesenteric bypass. It is, in reality,
a poor second choice. The iliac arteries are often involved with atherosclerotic occlusive disease in this
setting and the bypass is difficult to complete without
kinking or placing synthetic graft in proximity to the
duodenum with the risk of later erosion.
Antegrade aorto-mesenteric bypass from the supra-celiac aorta is the best choice for restoring flow in
acute mesenteric ischemia form proximal mesenteric
arterial thrombosis (1719). This approach requires
exposure of the retro-crural aorta by mobilizing the
left lobe of the liver and retracting it to the right. The
lesser omentum is opened, the stomach retracted caudally, and the crura of the diaphragm divided over
the aorta. The tunnel for the graft is relatively easily
made with gentle blunt dissection behind the pancreas along the left anterior margin of the aorta to the
superior mesenteric artery at the root of the mesentery below the pancreas. It is also feasible to dissect
directly down the superior mesenteric artery behind
the pancreas if the stenotic area of the artery is of
short duration. The celiac artery at its bifurcation into
the splenic and common hepatic branches may also
be exposed for a second limb of the bypass if needed.
The proximal synthetic graft bypass anastomosis is
performed end to side to the aorta after
17 systemic
heparinization and placement of totally occluding
proximal and distal aortic clamps. Partial occluding
clamps run the risk of damaging the aorta, causing
distal emboli, and make the proximal anastomosis
difficult to perform by compressing the aorta into a
narrow space. The distal anastomoses are performed
end to side. Prior to completion, careful flushing and,
if indicated, balloon catheter thrombectomy should

110

M. J. Sise

be perfomed. Once flow has been re-established to

the bowel, it is inspected for viability as outlined
above.
The management of the bowel after restoration of
arterial blood flow should include damage control
techniques (Fig. 2.). There is little or no advantage to
immediate closure of the abdominal wall even if all
of the bowel initially appears viable. Damage control
temporary closure carries little or no morbidity and
insures that there is no delayed bowel necrosis that
goes unrecognized. Obviously necrotic bowel should
be resected by stapling and dividing at healthy margins. Anastomosis of bowel segments should be deferred until reoperation at 24 to 36 hours. Temporary
abdominal wall closure should be performed followed by prompt transfer to the intensive care unit
for appropriate postoperative critical care management. Early anticoagulation with intravenous heparin
should be added despite the risk of operative site
hemorrhage in order to prevent re-thrombosis of
mesenteric vessels.
Mesenteric venous thrombosis leading to ischemic
bowel is much more difficult to manage than arterial
source mesenteric ischemia (3, 4). By the time intestinal ischemia occurs from venous engorgement and
impeded arterial flow, there are few, if any, options
that will relieve venous obstruction. Portal or mesenteric venous thrombectomy is not effective and very
dangerous. The only choice is systemic anticoagulation coupled with resection of necrotic bowel, damage control closure, and aggressive resuscitative measures. Patients that survive this dreadful complication
of an underlying hypercoagulability often require extensive bowel resection and are left with shot-gut
syndrome. Multiple reoperations to reassess bowel
for viability are the rule in the early management of
mesenteric venous thrombosis.
Outcome
The initial results following mesenteric ischemia are
related to both the absence or presence of intestinal
infarction and the underlying causes of vascular compromise. Little has changed in the last four decades
with regard to overall survival. Perioperative mortality remains approximately 40% (4, 6, 20, 21). Recurrent cardiac source embolism occurs in 30% of patients with this complication (20, 21). Mesenteric arterial thrombosis is a harbinger or advanced systemic
atherosclerosis and the risk of death from coronary
artery disease is high. Mesenteric venous thrombosis
is always a secondary phenomenon and life-long risk
of thrombotic complications follows for those who
are fortunate enough to survive (24, 7).
The mainstay of post-event care of patients with
acute mesenteric ischemia is management of their
underlying comorbidities. All will require some form
of anticoagulation or antiplatelet therapy. Cardiac

disease must be aggressively treated. The causes of

hypercoagulability need to be thoroughly investigated in those with mesenteric venous thrombosis.
Life-long medical management is essential for all survivors of the various forms of mesenteric ischemia.
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Received: May 4, 2010