A c u t e M e s e n t e r i c Is c h e m i a

a,b,
Michael J. Sise, MD *

KEYWORDS
 Acute mesenteric ischemia  Mesenteric arterial occlusion
 Mesenteric venous thrombosis  Nonocclusive mesenteric ischemia
 Ischemic colitis

KEY POINTS
 Acute mesenteric ischemia is uncommon and always occurs in the setting of preexisting
comorbidities. Consequently mortality rates remain high.
 The 4 major types of acute mesenteric ischemia are acute superior mesenteric artery
(SMA) thromboembolic occlusion, mesenteric arterial thrombosis, mesenteric venous
thrombosis, and nonocclusive mesenteric ischemia, including ischemic colitis.
 Delays in diagnosis are common and associated with a high rate of morbidity and
mortality.
 Prompt diagnosis requires attention to the history and physical examination, a high index
of suspicion, and early contract CT scanning.
 Although both open and endovascular techniques have a role, operative management
with exploratory laparotomy to asses bowel viability remains the best tool to prevent
bowel infarction and an associated high mortality rate.
 Selective use of nonoperative therapy with volume resuscitation, optimizing cardiac
output, and vasodilators has an important role in nonocclusive mesenteric ischemia of
both the small bowel and colon.

OVERVIEW

Acute mesenteric ischemia remains a deadly process despite more than 50 years of
advances in the treatment of vascular diseases. Successful management requires
early diagnosis and prompt treatment if there is any chance of survival. The mortality
rate remains more than 50% and there is little room for either delay or errors in man-
agement of this acute care surgical emergency.1–4 Mesenteric ischemia is always sec-
ondary to a preexisting local or remote disease process and the cause ranges from
cardiac source embolism to thrombosis of mesenteric veins in the setting of inherited
or acquired hypercoagulability (Box 1).3–5 Each type of mesenteric ischemia creates a

a
Department of Surgery, University of California San Diego School of Medicine, San Diego, CA,
USA; b Division of Trauma, Scripps Mercy Hospital, 4077 5th Avenue MER-62, San Diego, CA
92103, USA
* 550 Washington Street, Suite 641, San Diego, CA 92103.
E-mail address: [email protected]

Surg Clin N Am 94 (2014) 165–181

http://dx.doi.org/10.1016/j.suc.2013.10.012 surgical.theclinics.com
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166 Sise

Box 1
Associated diseases leading to mesenteric ischemia

Mesenteric arterial occlusion

 Cardiac disease
 Atrial fibrillation
 Recent myocardial infarction
 Congestive heart failure
 Digitalis therapy
 Previous arterial emboli
 Hypercoagulable state
 Hypovolemia, shock
Venous thrombosis
 Portal hypertension
 Intra-abdominal inflammation
 Trauma or major bowel surgery
 Hypercoagulable state
 Chronic renal failure

high risk of mesenteric infarction and death if diagnosis and treatment are delayed.
Symptoms may vary from the sudden onset of diffuse, severe, and constant abdom-
inal pain to the insidious onset of vague generalized abdominal pain. There are 4 com-
mon causes: acute cardiac source embolism to the SMA, acute thrombosis of
preexisting stenotic atherosclerotic lesion, splanchnic vasoconstriction leading to
low flow and regional ischemia (commonly called nonocclusive mesenteric ischemia)
in either small or large bowel, and mesenteric venous thrombosis (Table 1).6
The purpose of this article is to review the pathophysiology, clinical presentation,
diagnostic work-up, effective management, and outcome of acute mesenteric
ischemia. Readers should acquire an increased sense of awareness of mesenteric
ischemia, develop an appropriately high index of suspicion in a variety of clinical set-
tings, and be ready to move with decisive action to promptly make the diagnosis and
effectively manage it in a timely fashion.

MESENTERIC VASCULAR ANATOMY AND PHYSIOLOGY

The celiac artery and SMA origins from the aorta are in close proximity to the renal artery
origins in the upper abdomen (Fig. 1). The celiac axis lies just below the aortic hiatus of
the diaphragm. The proximal portions of the celiac artery and SMA are each enveloped

Table 1
Causes of mesenteric ischemia

50% Arterial embolism

20% Arterial thrombosis
20% Small vessel occlusion
10% Venous thrombosis
 Acute Mesenteric Ischemia 167

Fig. 1. Mesenteric arterial anatomy demonstrating collateral flow between major branches
of the aorta. (From Creager MA. Atlas of Vascular Disease. 2nd Edition. Philadelphia: Current
Medicine 2003; with kind permission of Springer Science1Business Media.)

in a plexus of lymphatic and neurologic tissue. These vessels are relatively thin walled
compared with extremity arteries. The portal vein and major mesenteric veins are also
thin walled. The inferior mesenteric artery (IMA) arises from the left anterior lateral
aspect of the mid-infrarenal aorta. The arterial blood supply of the gut is divided into
4 major areas (Table 2). Anomalous patterns of mesenteric arterial anatomy occur in
approximately 15% of individuals and, although a replaced right hepatic artery from
the SMA is one of the most commonly reported, there are a variety of anomalies
reported.6,7

Table 2
Gut regions, arterial blood supply, and sources of collateral flow

Region Blood Supply Collateral Connections

Foregut: distal esophagus Celiac artery Pancreaticoduodenal arteries
through the ampulla of Vater and arc of Bühler distally <5%
in the duodenum
Migut: ampulla of Vater region SMA Pancreaticoduodenal arteries
of the duodenum to splenic and arc of Bühler proximally
flexure of the colon Marginal artery of Drummond
and arc of Riolan distally
Hindgut: splenic flexure of the IMA Proximal: marginal artery of
colon to distal sigmoid colon Drummond
Distal: superior hemorrhoidal to
middle hemorrhoidal arteries
arc of Riolan
Cloacal derivatives: distal Branches of the Middle hemorrhoidal to superior
sigmoid colon, rectum colon, internal iliac arteries hemorrhoidal arteries
and anus proximally
168 Sise

Each of the mesenteric vessels interconnects with adjacent areas via preexisting col-
laterals. These collaterals have varying capability of supplying adequate blood supply
to adjacent areas in acute occlusion. The gastroduodenal artery branch of the common
hepatic artery anastomoses with branches of the inferior pancreatic duodenal artery.
The dorsal pancreatic artery, a branch of the splenic artery, anastomoses with the ante-
rior and posterior pancreaticoduodenal arcades via a right transverse branch of the
dorsal pancreatic artery (Kirk’s arcade). The arc of Bühler, which is present in only
1% to 4% of individuals, parallels the aorta proximally connecting the celiac axis to
the SMA.6 There may also be arcs of Barkow, collateral pathway within the omentum
between the epiploic arteries of the splenic artery and SMA.6
In chronic atherosclerotic disease, the celiac axis distribution of flow may be
adequately perfused from the SMA via the collaterals (described previously).
They may also provide reverse flow to collateralize the SMA in chronic stenosis
of its origin. These connections are usually inadequate, however, in acute SMA
occlusion. The mesenteric arcades and the marginal artery of Drummond may
provide adequate flow from the SMA to the IMA in the setting of occlusion at its
origin. An important collateral, the arc of Riolan, develops in chronic occlusive dis-
ease and may provide flow in either direction between the proximal SMA and IMA.
If the proximal IMA is occluded, the hypogastric arteries usually provide adequate
collateral flow to the IMA distribution via the superior hemorrhoidal artery. The arc
of Riolan is also an important collateral via the IMA to the hypogastric and iliac
arteries to supply the lower extremities in chronic atherosclerotic infrarenal aortic
occlusion.
In chronic mesenteric occlusive disease from atherosclerosis, patients may have to-
tal gut perfusion via a single remaining mesenteric artery or the bilateral hypogastric
arteries via collateral flow to the other vessels.7 Many of these patients, however,
have intestinal angina when eating large meals.
The pattern of occlusion also determines if collaterals are adequate (Fig. 2). Emboli
to the SMA usually lodge distal to the proximal jejunal branches and middle colic ar-
tery, thereby preventing celiac artery and IMA collateral contributions from reaching
the small bowel and right colon.6,8 Thrombotic occlusion of an atherosclerotic plaque
at the origin of any of the mesenteric vessels often leaves collateral flow intact so that
symptoms may not occur at bowel rest. If thrombosis extends distally in the SMA,
however, a pattern of ischemia similar to acute embolism may occur.7
Venous drainage of the bowel is via the portal venous system (Fig. 3).8 Gastric
venous drainage is via the splenic vein and small bowel and the proximal colon
through the splenic flexure drain via the superior mesenteric vein. The inferior mesen-
teric vein drains the descending colon and rectum. Collateral venous vessels are pre-
sent between each major area of the portal venous drainage. Connection to the
systemic venous system, however, is limited. Collateral flow via portal-systemic anas-
tomoses in the area of the distal esophagus, the falciform ligament, and the anorectal
area are well developed in chronic portal venous hypertension from hepatic paren-
chymal disease or chronic hepatic vein obstruction. They do not, however, provide
adequate flow in acute total obstruction from portal vein thrombosis.8
Total mesenteric blood flow represents approximately 20% (varying between
10% and 35%) of resting cardiac output.9 Postprandial blood flow may increase by
as much as 200%. Symptoms, therefore, may relate to eating in patients with marginal
collateral flow and acute occlusion.10,11 The splanchnic circulation is also sensitive to
the systemic effects of dehydration, inflammation, catecholamine release, cardiac
insufficiency, and vigorous exercise. Each of these factors may result in nonocclusive
mesenteric ischemia secondary to splanchnic vasoconstriction. In the setting of
 Acute Mesenteric Ischemia 169

Fig. 2. Location of proximal atherosclerotic thrombosis versus embolic occlusion in the SMA.
(From Creager MA. Atlas of Vascular Disease. 2nd Edition. Philadelphia: Current Medicine
2003; with kind permission of Springer Science1Business Media.)

chronic atherosclerotic occlusive disease of the mesenteric vessels, these factors

may precipitate mesenteric infarction from low flow.9

PATHOPHYSIOLOGY

The pathophysiology of mesenteric ischemia is essentially the result of insufficient

blood flow to meet the metabolic demand of the bowel.10,11 Acute ischemia leads
to anaerobic metabolism in the gut, regional acidosis, and initial hyperperistalsis
with cramping pain and gut emptying, followed by intense ischemic pain from gut
wall hypoperfusion. This visceral pain is vague and projected across the area of the
superficial abdominal wall where its innervation is shared with the surface structure
innervation.12 Therefore, foregut structures generate visceral pain in the epigastrium,
midgut in the periumbilical regions, hindgut in the infrabumbilical region, and cloacal
derivatives in the suprapubic region of the abdomen.12
170 Sise

Fig. 3. Mesenteric and portal venous anatomy. (From Creager MA. Atlas of Vascular Disease.
2nd Edition. Philadelphia: Current Medicine 2003; with kind permission of Springer
Science1Business Media.)

The bowel can tolerate marked reductions in blood flow.9 At bowel rest, up to
80% of capillaries are not perfused without compromising adequate oxygen delivery.
The intestinal mucosa extracts increasing amounts of oxygen during hypoperfusion
and preserves mucosal integrity during initial periods of ischemia. Prolonged ischemia
produces an inflammatory reaction, which disrupts the intestinal mucosal barrier and
ultimately allows translocation of bacteria. Local peritoneal and systemic inflammatory
sequelae follow quickly once transmural necrosis has occurred.13
Ischemia visceral pain is intense and constant, does not increase with palpation,
and is not associated with abdominal wall rigidity or peritoneal signs on physical ex-
amination during its initial phases.12 This results in the classic “pain out of proportion
to physical findings” attributed to acute mesenteric ischemia. The initial gut emptying
with vomiting may confuse an examining physician and divert attention to other
gastrointestinal diagnoses. In the later stages with peritoneal inflammation, localiza-
tion of pain in the abdomen and the presence of associated physical findings occur.
Cardiac source emboli have a predilection to enter the orifice of SMA most likely
because of both its size and angle of origin from the aorta. SMA emboli typically lodge
distal to the origin of proximal jejunal branches and the middle colic artery (see Fig. 2).7
This gives rise to a pattern of small intestine and colon ischemia with sparing of the
proximal jejunum and perfusion of the transverse colon and distal colon. Celiac artery
and IMA emboli are less common and hypogastric artery emboli rarely cause ischemia
due to the extent of pelvic collateral arteries.7 Acute thrombosis of chronic atheroscle-
rotic mesenteric arterial occlusive disease may result in a spectrum of symptoms from
vague pain worsened by meals to sudden and intense pain identical to that of acute
embolic occlusion. These symptoms depend on the preexisting collateral flow.
Mesenteric venous thrombosis is usually partially occlusive in its initial stages and
causes symptoms with eating, including vague abdominal pain and nausea.14,15 Acute
total occlusion of the portal vein causes abdominal pain similar to acute SMA
 Acute Mesenteric Ischemia 171

occlusion in addition to producing abdominal distension and diffuse tenderness due to

intestinal venous engorgement and fluid sequestration in the abdomen. The late
stages of intestinal ischemic syndromes are the result of intestinal infarction and sys-
temic inflammatory response. Cardiovascular collapse may result if resection of
necrotic bowel is not promptly performed. Mortality rates are prohibitively high with
intestinal infarction.
Colon ischemia, usually resulting from either chronic mesenteric arterial insuffi-
ciency or nonocclusive mesenteric ischemia, is most common in the descending
and sigmoid colon.16,17 Regional hypoperfusion results in a spectrum of sequelae
from mucosal sloughing to transmural infarction. The spectrum of symptoms often
mimics diverticular disease. Bleeding, local inflammation, perforation with peritonitis,
and late stricture may occur depending on the extent, severity, and duration of the
ischemia. Transverse colon and right colon involvement may also occur in nonocclu-
sive mesenteric ischemia.

CLINICAL PRESENTATION AND DIAGNOSIS

Acute intestinal ischemia from sudden embolic occlusion of the SMA causes the
classic findings (described previously). Acute superimposed on chronic occlusion of
a preexisting atherosclerotic disease often results in a more insidious onset of pain
due to preexisting collateral flow, which mitigates the severity of ischemia.10,11,18 A
history of intestinal angina (postprandial pain), fear of food, and weight loss often ac-
companies acute on chronic mesenteric occlusive ischemia. Mesenteric venous
thrombosis causes an insidious onset of initially vague symptoms, which worsen pro-
gressively over time.14,15 In patients with inherited hypercoagulability, it may occur
spontaneously or after a brief episode of gastreoenteritis or other illness. Mesenteric
venous thrombosis from acquired hypercoagulability may occur in the conjunction
with abdominal or multisystem trauma, intra-abdominal inflammation, or oral contra-
ceptives. The most common causes are listed in Box 1.14,15 Nonocclusive acute
mesenteric ischemia from vasoconstriction occurs in the setting of critical illness
with reduced cardiac output with or without preexisting mesenteric arterial stenosis.
It is particularly difficult to diagnose in the critical care setting because it is associated
with vague symptoms or undetectable symptoms in an intubated patient.
Atrial fibrillation is the most common cause of cardiac source embolism.10,11,18
These patients describe a sudden onset of pain associated with nausea, vomiting,
and diarrhea. The most common initial findings are mild abdominal distension and
hypoactive bowel sounds without abdominal tenderness. In patients with acute wors-
ening of chronic mesenteric ischemia, almost all have a history of postprandial pain
and weight loss (Table 3).
Profound leukocytosis may be the only initial abnormal laboratory studies in patients
with acute mesenteric ischemia and the white blood cell counts often exceed 20,000
cmm.10,18 All patients with abdominal pain and a profound leukocytosis should have
intestinal ischemia included in their differential diagnoses. Metabolic acidosis is a

Table 3
Frequency of signs and symptoms in chronic mesenteric arterial occlusive disease

1. Postprandial pain 100%

2. Weight loss 85%
3. Abdominal bruit 70%
4. Nausea, vomiting 60%
172 Sise

late finding and indicates intestinal infarction. Because of the liver’s ability to clear lac-
tic acid, however, the early stages of intestinal infarction do not result in systemic
metabolic acidosis. Hyperamylasemia and elevated serum lipase may also occur in
the early course of mesenteric ischemia.1,2,10,19
An early diagnosis of acute mesenteric ischemia in patients at risk requires a
promptly performed CT scan of the abdomen with intravenous contrast.20,21 This ex-
amination effectively evaluates mesenteric arterial and venous patency and perfu-
sion of the bowel and indicates if one of the other possible causes of clinical
findings is present. Early CT scanning both allows timely diagnosis before significant
bowel compromise occurs and makes appropriate interventions more likely to suc-
ceed.1,2,20,21 Intestinal necrosis may cause an overwhelming inflammatory response
and shock with an associated high mortality rate.13,22 One of the primary reasons
why the outcome of acute mesenteric ischemia has not significantly improved in
the past 4 decades is the all too common delay in diagnosis and intestinal infarction
in this group of patients who are all at risk because of the high incidence of signifi-
cant comorbidities.12,22–24 The best strategy to improve outcomes remains prompt
recognition, early diagnosis, and successful management prior to bowel
necrosis.1,2,12
The role of catheter angiography of the mesenteric vessels has diminished with the
availability of CT angiography. The timesavings with immediately available CT imaging
and the morbidity of catheterization both make this traditional diagnostic technique
unnecessary. Endovascular techniques have a role, however, in managing mesenteric
ischemia (discussed later). The widespread use of CT imaging has resulted in
improved early diagnosis and an improvement in outcomes.

MANAGEMENT OF MESENTERIC ISCHEMIA

The key principles of management of acute mesenteric ischemia are summarized in

Fig. 4. The decision for an immediate open surgical approach versus an endovascular
approach requires consideration of 3 key factors. First and foremost is the duration
and severity of bowel ischemic, followed by the nature of the occlusive lesion, and
equally important is consideration of the ready availability and the capability of an

Fig. 4. Key elements of decision making in the management of mesenteric ischemia.

 Acute Mesenteric Ischemia 173

emergency center’s interventional radiology or vascular surgical intervention pro-

gram.1,2,10,25 In patients with suspected bowel infarction or impending infarction, im-
mediate exploratory laparotomy is mandatory.2,25 At exploration, the cause of
mesenteric ischemia is found and remedied and bowel viability is assessed. Embolic
occlusion usually is due to a relatively organized cardiac thrombus, which is not
amenable to thrombolytic therapy. Thrombolysis also risks fragmentation and further
distal embolization, which cannot be further lysed or retrieved by catheter thrombec-
tomy. Bowel infarction is likely to result. Therefore, prompt operation with SMA embo-
lectomy combined with inspection of the bowel for necrosis is the best approach. The
operative technical aspects of the management of each major cause of acute mesen-
teric ischemia are summarized in Fig. 5.
Acute thrombosis of chronic atherosclerotic occlusive disease may be managed
with endovascular techniques, with stenting the mesenteric arterial lesion.10,11,26–29
Thrombolytic therapy has a role in the treatment of fresh thrombus in this cause of
acute mesenteric ischemia.10,11,28,29 Successful use of these endovascular tech-
niques requires, however, an active preexisting program with adequate personnel,
equipment, and timely staffing at the emergency center. Even if thrombolysis and
stenting are successful, exploratory laparotomy may be required to assess the recov-
ery of ischemic bowel. The risk of bowel necrosis and subsequent peritonitis requires
prompt abdominal exploration in those patients who do not have complete relief
of symptoms and the absence of signs of ongoing ischemia after endovascular
techniques. Laparoscopy has a limited role in the management of mesenteric
ischemia.10,11,25
Intraoperative assessment of intestinal blood flow includes running the bowel and
inspection of the entire intestinal tract by assessing color and peristaltic activity and
palpating the mesenteric arterial arcades. The main trunk of the SMA is located by up-
ward retraction the transverse colon and downward retraction of the small bowel. The
trunk of the artery is palpated at 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 in the midline over the aorta just below the left lobe of the liver. The IMA is

Fig. 5. Summary of intraoperative management of acute mesenteric ischemia.

174 Sise

located by inspection along left anterior-lateral area of the infrarenal aorta at the base
of the left colon mesentery. Assessment of the distal mesenteric at the bowel for
Doppler signals aids in the assessment of areas of questionable perfusion. Fluorescein
angiography with an ultraviolet lamp can be helpful in further assessing the return of
perfusion.30
If mesenteric ischemia is first encountered in the operating room, the pattern and
appearance of ischemic bowel are essential in determining the cause (Fig. 6).1,10,11
Embolism to the SMA usually lodges in the main trunk of the vessel distal to the origin
of the proximal jejunal branches and the middle colic artery. This results in proximal
sparing of the jejunum and distal sparing of the transverse colon with ischemia of
the remaining small bowel and ascending colon. Thrombosis of the SMA origin leads
to ischemia throughout its distribution from the duodenum to the splenic flexure of the

Fig. 6. Patterns of acute mesenteric ischemia relative to site of arterial occlusion. Location of
SMA occlusion (A) Ostium, (B) Below middle colic artery, (C) At ileocolic vessels, (D) Multiple
arcades or vas rectum. (From Creager MA. Atlas of Vascular Disease. 2nd Edition. Philadel-
phia: Current Medicine 2003; with kind permission of Springer Science1Business Media.)
 Acute Mesenteric Ischemia 175

colon. Total visceral ischemia from the distal esophagus through the rectum results if
the celiac artery and the IMA are also occluded. This rare phenomenon may present
with a hungry and hypoglycemic patient secondary to the loss of liver perfusion and
access to glycogen stores and carries a poor prognosis.

EMBOLIC MESENTERIC ARTERIAL OCCLUSION

SMA emboli are best removed through a transverse incision in the main trunk of the
artery at the mesenteric root below the pancreas (Fig. 7).11,31 Fogarty catheter embo-
lectomy must be performed with caution (Fig. 8). This visceral artery is fragile and
catheters should be used gently proximally and distally to avoid arterial injury from
tears and dissections. Once thrombectomy is completed, careful flushing with hepa-
rinized saline (10 units of heparin per mL) proximally and distally is performed. Avoid
flushing forcibly proximally to prevent dislodging thrombus into the aorta and causing
distal embolism. Closure of the arteriotomy should be performed in a tension-free
manner with either running or interrupted monofiliament sutures by placing proximial
and distal vascular clamps and gently retracting the artery toward the arterotomy
site. After re-establishing flow, placing warm laparotomy packs and waiting 10 to
15 minutes to reassess are helpful in relieving spasm. Damage control closure and
reinspection in 24 to 36 hours is advised unless there is prompt complete restoration
of normal intestinal blood flow without questionable areas of bowel at the initial
operation.10,11

THROMBOTIC MESENTERIC ARTERIAL OCCLUSION

Proximal mesenteric arterial thrombosis and acute bowel ischemia discovered in the
operating room require experience in advanced vascular surgical technique.10,11,26
If an acute care surgeon is not comfortable and capable of performing the necessary
aortomesenteric bypass, a vascular surgeon colleague should be called for assis-
tance. There are a variety of bypass options. Retrograde iliac artery to mesenteric
artery bypass is seemingly easier to perform than antegrade supraceliac arotomesen-
teric bypass. Retrograde bypasses may, however, yield inferior results.32–35 In

Fig. 7. (A) Palpation of SMA at the base of the mesentery. (B) Exposure of the proximal SMA.
(From Rutherford RB. Atlas of Vascular Surgery. Philadelphia, W.B. Saunders 1993; with
permission.)
176 Sise

Fig. 8. Balloon catheter embolectomy of the SMA. (From Creager MA. Atlas of Vascular Dis-
ease. 2nd Edition. Philadelphia: Current Medicine 2003; with kind permission of Springer
Science1Business Media.)

patients with proximal mesenteric atherosclerotic occlusive disease, the iliac arteries
are usually also involved. It may be difficult to find a suitable graft origin site in the iliac
arteries and it is also difficult to complete without kinking. This bypass route also pla-
ces synthetic graft in proximity to the duodenum, and eventual and graft erosion and
graft infection or graft-enteric fistula are risks.
Antegrade aortomesenteric bypass from the supraceliac aorta is the best choice for
restoring flow in acute mesenteric ischemia from proximal mesenteric arterial throm-
bosis (Fig. 9).32 This bypass should be performed by experienced surgeons and re-
quires exposure of the retrocrural aorta by mobilizing the left lobe of the liver. The
lesser omenetum is incised and the left hepatic lobe is retracted medially with the
stomach retracted caudally. The aorta is palpated through the crura of the diaphragm
and its fibers divided longitudinally to expose the area for the proximal end-to-side
anastomosis to the aorta. Bypass to the SMA is performed by tunneling the graft
with blunt dissection along the left anterior lateral aspect of the aorta behind the
pancreas to the artery at the root of the mesentery. More proximal exposure of the
SMA is achieved by direct dissection down the SMA behind the pancreas. There is
dense plexus of lymphatic and neural tissue at the proximal SMA, which must be
dissected free to expose as sufficient length of artery for distal anastomosis. If needed,
the celiac artery origin is exposed in a similar fashion to its bifurcation into the splenic
 Acute Mesenteric Ischemia 177

Fig. 9. Antegrade aortomesenteric artery bypass. (A) Exposure aorta behind crura of the dia-
phragm, (B) Create aortic site for anastomosis, (C) Graft for single vessel bypass, (D) Graft for
bypass to both celiac artery and superior mesenteric artery. (From Wylie EJ, Stoney RJ, Ehren-
feld WK. Manual of Vascular Surgery Vol.1. New York: Springer-Verlag 1980; with kind
permission of Springer Science1Business Media.)

and common hepatic branches in order to place a second bypass limb. Patients
should be systemically heparinized (5000 units of heparin intravenous bolus) prior to
arterial clamping the aorta. Proximal and distal totally occluding aortic clamps are
preferred because partially occluding clamps may make anastomosis difficult and
damage the aorta, causing dissection or distal emboli. The distal anastomoses should
be performed in an end-to-side fashion with careful antegrade and retrograde flushing
and, if indicated, balloon catheter thrombectomy. The bowel is then inspected for
viability (described previously).

MESENTERIC VENOUS THROMBOSIS

The management of mesenteric ischemia from acute on chronic occlusive lesions

should also include damage control techniques.5,10,11,36 If there is any doubt regarding
178 Sise

intestinal viability, damage control closure may be performed without increasing the
risk of bypass infection. Necrotic bowel is best resected by stapling and dividing at
healthy margins and anastamosis of bowel segments deferred until reoperation at
24 to 36 hours to make certain further necrosis and failure of the anastomosis do
not occur. Expeditious temporary abdominal wall closure followed by prompt transfer
to an ICU for further postoperative critical care management is crucial to manage
these patients who are invariably hemodynamically unstable. Intravenous administra-
tion of heparin for anticoagulation hemorrhage to prevent rethrombosis of mesenteric
vessels should occur early with damage control closures despite the risk of
hemorrhage.
Mesenteric venous thrombosis leading to bowel necrosis is best treated nonopera-
tively with anticoagulation and adequate restoration of circulating blood volume.14,15
Operative management is reserved for patients with sign of bowel infraction. Bowel
resection of necrotic bowel segments is the only option in these advanced cases.
Extensive resection is common when forced to operate and the prognosis is poor.
Prompt recognition is frequently difficult because of the insidious onset of this form
of deep venous thrombosis. It may be more difficult to manage than arterial source
mesenteric ischemia.14,15 By the time intestinal infarction occurs from venous
engorgement and impeded arterial flow, there are few, if any, options that relieve
venous congestion. The few mesenteric and portal venous thrombectomies reported
have had poor results and this procedure is dangerous and not effective. Early recog-
nition with systemic anticoagulation coupled with resection of necrotic bowel, damage
control closure, and aggressive resuscitative measures are all essential for successful
management of this often devastating type of mesenteric ischemia. Multiple reopera-
tions to reassess bowel for viability are invariably required. Patients who survive often
have undergone extensive bowel resection and are often left with short gut
syndrome.37

NONOCCLUSIVE MESENTERIC ISCHEMIA

The setting of nonocclusive mesenteric ischemia, including ischemic colitis, almost

always involves critical illness. Severe cardiopulmonary insufficiency and septic shock
with the use of vasoconstricting drugs are the most common critical illnesses associ-
ated with this entity. The treatment is based on improving mesenteric perfusion and
watchful waiting for the presence of bowel infarction. Optimizing volume status and
limiting vasoconstriction by weaning vasopressor drug infusions are essential to
improving mesenteric blood flow. The decision to perform exploratory laparotomy is
based on the presence of signs of perforation or overall worsening status suggestive
of bowel infarction.
At exploratory laparotomy for suspected bowel infarction, obvious areas of nonvi-
able bowel must be expeditiously resected. Unless a patient is stable and the area
of resection is adjacent to normal bowel on each margin, stapling across bowel, per-
forming a damage control closure, and returning in 24 to 36 hours to reassess for the
need for further resection are essential to successful management. This is particularly
important when multiple areas of bowel resection are required.
Ischemic colitis is managed in a similar fashion to other areas of nonocclusive
mesenteric ischemia. Bowel rest, antibiotics, and adequate fluid infusion lead to suc-
cessful nonoperative management in more than 60% of patients. Signs of peritonitis or
deteriorating hemodynamic status should prompt immediate exploratory laparotomy
with appropriate bowel resection. Colostomy and a Hartmann procedure are often
warranted.
 Acute Mesenteric Ischemia 179

OUTCOME

The frequently associated significant health problems and all too common delays in
diagnosis have made acute mesenteric ischemia a highly morbid and often fatal dis-
ease process. The initial results are related to both the presence of intestinal infarction
and the underlying causes of vascular compromise. Overall survival has not signifi-
cantly changed in the past 4 decades. Perioperative mortality approaches
50%.15,18,23,24,38–40 Recurrent cardiac source embolism occurs in 30% of patients
with acute SMA embolism.23,24 Mesenteric arterial thrombosis is a harbinger of sys-
temic atherosclerosis and the risk of death from coronary artery disease is high.
Mesenteric venous thrombosis is usually a secondary phenomenon and lifelong risk
of thrombotic complications follows for those who survive.3,14,15,37
The most important factor in the care of patients with acute mesenteric ischemia is
management of their underlying comorbidities. Some form of anticoagulation or anti-
platelet therapy is required. Cardiac disease should be aggressively treated. The un-
derlying causes of hypercoagulability must be delineated in those with mesenteric
venous thrombosis. Lifelong medical management of their comorbidities is essential
for all survivors of the various forms of mesenteric ischemia.

REFERENCES

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