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GUIDELINES FOR THE MANAGEMENT OF ACUTE MESENTERIC
ISCHEMIA
Manju Kalra, MBBS, Peter Gloviczki, MD, Thomas C. Bower, MD, Audra
A. Duncan, MD , Gustavo S. Oderich, MD, , Joseph J. Ricotta II M.D.
Division of Vascular and Endovascular Surgery,
Gonda Vascular Center,
Mayo Clinic,
Rochester, MN, USA
Correspondence to:
Manju Kalra, MBBS
Mayo Clinic
200 First Street SW
Rochester, MN 55905
Phone: 507-284-3407
Fax: 507-266-7156
E.mail: [email protected]
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Mortality from acute mesenteric ischemia (AMI) continues to be high in-spite of
advances in surgical and critical care, with an average from published reports being
67% (24 to 96%). Although imaging modalities have advanced tremendously making
earlier diagnosis and treatment feasible, the typical patient with acute mesenteric
ischemia is older with more severe underlying contributing illnesses; younger patients
with embolism from rheumatic valvular heart disease are now a rarity. A high index
of suspicion, prompt diagnosis and treatment are key to improving outcomes of this
grave problem.(1) Too often AMI is suspected only when peritoneal signs in
conjunction with leukocytosis and acidosis are found leading to delayed diagnosis,
septic shock, multisystem organ failure and death, or survival following extensive
bowel resection and short gut syndrome.(2)
A. The hallmark of clinical presentation of a patient with AMI is abrupt onset, severe,
non-localized “abdominal pain out of proportion to physical signs”. This should raise
the possibility of the diagnosis and prompt appropriate evaluation. This being said a
certain percentage of patients will present with insidious abdominal pain causing the
diagnosis to be delayed. Identifying risk factors and important clues in the clinical
history can help make a timely diagnosis. These include atrial fibrillation, recent
myocardial infarction, congestive heart failure, prior embolic events, symptoms of
chronic mesenteric ischemia (postprandial pain, weight loss, food fear), previous
deep venous thromboses, hypercoagulable states, and digoxin / vasopressor therapy.
Laboratory findings are nonspecific in the early stages. In the later stages there is
evidence of hemoconcentration from sequestration of fluid in the bowel wall
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including leukocytosis, elevated serum lactate and amylase. Plain X-rays of the
abdomen serve only to rule out other, more obvious causes of acute abdomen. Duplex
ultrasonography is not useful in this situation because of abdominal tenderness and
bowel distension with gas.
B. Computerized tomography (CTA) scan with intravenous contrast is a fast, effective
and non-invasive way to rule out commoner causes of acute abdomen, confirm the
diagnosis of AMI and potentially identify the etiology.(3) It has replaced mesenteric
arteriography as the definitive diagnostic tool in contemporary practice.(4) Given the
speed with which it can be performed in most centers even patients presenting with
signs of bowel infarction and peritonitis can have the study prior to proceeding to the
operating in order to identify the etiology and plan operative intervention.(5) All
patients should receive appropriate resuscitation with intravenous fluids and broad
spectrum antibiotics simultaneously. Further course of treatment is guided by the
etiology identified and the acuity of presentation. Arterial embolism accounts for
AMI in 40-50% of patients, 25% are secondary to arterial thrombosis and 20% have
nonocclusive, low flow mesenteric ischemia. In 10% of patients mesenteric venous
thrombosis is the etiology.(6)
C. Critical patients with suspicion of acutely ischemic bowel or signs of peritonitis
should be taken to the operating room directly for exploratory laparotomy regardless
of the underlying etiology. Bowel viability is assessed at exploration, definitely
nonviable bowel is resected, equivocally viable bowel is preserved and then the
causative pathology of AMI is addressed.
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D. Non-critical patients with slower symptom progression and no peritoneal signs
should be treated with initial mesenteric revascularization by endovascular means,
surgical intervention or systemic anticoagulation based on the etiology of AMI
identified. Subsequently the ischemic bowel can be addressed with close observation
laparoscopy or laparotomy depending on outcome and progression.
E. At exploratory laparotomy the entire bowel is inspected carefully. Irreversible
ischemia of extensive areas of the bowel is incompatible with life and closure of the
abdomen without revasclarization or bowel resection is recommended in this
situation. Segments of obviously necrotic bowel are resected and bowel continuity is
restored only after revascularization is completed and vascularity of the ends has been
determined to be satisfactory. Alternately a decision may be made to exteriorize the
ends of the bowel with re-anastomosis at a delayed secondary procedure, especially if
a surgical bypass is performed. Ischemic, discolored bowel segments are preserved
and re-evaluated following revascularization after remaining covered with warm
saline soaked laparotomy pads for 15-20 minutes. Visual inspection of normal color
and peristalsis alone is sometimes misleading and other modalities to assess bowel
viability include palpable pulses in the mesentery, dopplerable arterial signals on the
antimesenteric border of the bowel, bleeding from the cut ends, inspection for
perfusion under a Wood’s lamp after fluoroscein injection, surface oximetry and laser
tissue flowmetry.(7) In most instances it is prudent to preserve all equivocal segments
of bowel for reassessment at a second look laparotomy in 24 -48 hours. In this
instance the abdomen is packed open for subsequent secondary closure.
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F. Arterial embolism usually originates in the heart in a patient with atrial fibrillation,
recent myocardial infarction, congestive heart failure, left ventricular aneurysm or
valvular heart disease and lodges in the superior mesenteric artery (SMA) a few
centimeters distal to the orifice near the origin of the middle colic artery. On CTA the
proximal SMA is patent and without calcification, with a filling defect at the site of
the embolus. Upon diagnosis of embolism exploratory laparotomy is performed and
the bowel is assessed for viability. The proximal jejunum is usually spared in
embolism. The SMA is exposed in the root of the small bowel mesentery, a transverse
arteriotomy is made in the SMA and the embolus is delivered with Fogarty catheters
passed proximally as well as distally. After reconstitution of flow the bowel is
definitively addressed.
G. Acute mesenteric arterial thrombosis occurs in patients with pre-existing
mesenteric arterial stenoses. Symptoms of chronic mesenteric ischemia can be
elicited in 25-50% of patients. Patients frequently present with a slower progression
of symptoms, the acuity and severity of the situation depending on the extent of preexisting arterial stenoses and degree of collateralization. Severely symptomatic
patients with an acute abdomen should be taken directly to the operating room after
diagnostic CTA which usually reveals ostial SMA occlusion in a calcified artery.
Options for surgical revascularization include antegrade or retrograde bypass to the
SMA from the supraceliac / infrarenal aorta or iliac arteries respectively depending
upon the status of these inflow vessels. Dacron can be used as the conduit if the
bowel is not necrotic; saphenous vein is preferable if concomitant bowel resection is
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necessary.(8) Alternately, retrograde stenting of the SMA with vein patch angioplasty
of the access site can be performed in the latter situation.(9)
In patients with less acute symptoms presumably because of well developed
collaterals mesenteric arteriography with stenting of the SMA is a viable option. Postprocedure the patient is observed or taken to laparoscopy / laparatomy to evaluate the
bowel based upon the clinical status.(10) Support for the safety of this approach in
severely symptomatic acute mesenteric ischemia with suspicion of necrotic bowel is
lacking given the unavoidable delay .
H. Nonocclusive mesenteric ischemia (NOMI) is associated with the highest mortality
rates due to
associated co-morbidities,
incomplete understanding of the
pathophysiology and not unusual delay in diagnosis. A high index of suspicion is
essential to improve outcomes as no diagnostic evaluation, including CTA is
confirmatory for the diagnosis except to rule out proximal SMA occlusion and other
causes of the acute symptoms.(11) When a low flow state is suspected the patient
should be taken to angiography; selective SMA arteriography reveals spasm and low
flow with a “chain of sausages” appearance. Treatment is with intra-arterial
papaverine infusion till relief of symptoms or confirmation of relief of spasm on
repeat arteriography, in conjunction with avoidance of vasopressors and aggressive
management of the underlying pathology.
I. Mesenteric venous thrombosis still carries a significant mortality and should be
suspected in the setting of hypercoagulable states, abdominal trauma, surgery or
inflammation as well as pancreatic / colon cancer.(12) Systemic anticoagulation is the
treatment of choice with improvement in the majority of patients. Surgical /
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endovenous/ thrombectomy / thrombolysis have not proved to be advantageous when
attempted.(13) Laparotomy is performed in cases with suspected bowel infarction.
References
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surgery for acute mesenteric ischemia. Surgery. 1997 Mar;121(3):239-43.
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