Acute Mesenteric Ischemia
Isaac George, MD
Resident in Surgery
Department of Surgery
Columbia University
College of Physicians and Surgeons
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Acute Mesenteric Ischemia
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Incidence
Pathophysiology
Diagnosis
Therapy
Treatment Algorithm
Objectives
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Objectives
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Understand pathophysiology
Identify patients at high-risk for mesenteric
ischemia
Develop treatment plan for each patient/apply
treatment algorithm
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Introduction
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Cokkinis (1921):
“occlusion of the mesenteric vessels is regarded as one of those
conditions of which the diagnosis is impossible, the prognosis
hopeless, and the treatment almost useless.”
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Occlusive or non-occlusive mechanism leading to
hypoperfusion of one or more mesenteric vessels
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Rationale
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Incidence
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1-2/1000 hospital admissions
1% of GI admissions1
Mortality
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1960’s - 70-100%2
1970’s - 60-70%3
Morbidity
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Cardiopulmonary, MOSF
Extended LOS, TPN dependence4
Recurrence
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Up to
60%4
1
Ann Surg 2001;233(6):801-808
Ann Surg 1982;195:554-565
3 Ann Surg 1978;188;721-731
4 Ann Vasc Surg 2003;17:72-9
2
Anatomic Considerations
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Pathophysiology: Etiology
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Arterial Embolic Disease
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Arterial Thrombotic Disease
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Venous Thrombotic Disease
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Non-occlusive Mesenteric Ischemia
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Pathophysiology
Arterial Embolism
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Majority of cases (>50%): SMA occlusion
Location: origin of middle colic artery (ischemia from
proximal jejunem to splenic flexure)
Embolic sources: cardiac (80%)1, aortic plaques
Celiac and IMA occlusion usually tolerated
SMA occlusion → death
Most have underlying stenoses as well
1
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Ann Vasc Surg 1990;4:112-116
Pathophysiology
Arterial Thrombotic Disease
15% of acute intestinal ischemia1
Pre-existing atherosclerotic disease
― Worsening chronic mesenteric ischemia
• Found at ostium of SMA
• More delayed onset of symptoms
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1
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Vasc Surg 1996; 4th ed.
Pathophysiology
Venous Thrombotic disease
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5-10% of intestinal ischemia
Younger patient population
80% have hypercoaguable state
Risk factors: oral contraceptives, previous DVT/PE,
malignancy, portal HTN, nephrotic syndrome
May limit arterial flow→edema, segmental infarction
Pathophysiology
Non-Occlusive disease
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20-30% of acute intestinal ischemia
Response to systemic hypoperfusion
― Sympathetic adrenergic system mediated
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Visceral vasoconstriction/shunting for cerebral
protection
Causes: any severe systemic illness, CHF,
dehydration, drugs (cocaine, ergot alkaloids,
digitalis, β-blockers, α-agonist, epo), hemodialysis
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Clinical Presentation:
Physical Examination
Arterial Thromboembolic, Non-Occlusive
• Severe abdominal pain
• Sudden onset
Venous Thrombotic
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Less severe pain
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Subacute
• Symptoms variable
• Abdominal pain-non-specific, crampy vs. steady, anterior
• Gastric emptying/vomiting
• Peritonitis late
• Hypotension, tachycardia
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Clinical Presentation:
Laboratory
Limited clinical utility
• arterial lactate1
• amylase2
• CK, CK-BB3
• Serum phosphate4
• Other useless markers: LDH, PAF, TNF-α, AP, AST/ALT, αglutathione
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1
Eur J Surg 1994;160:381-4
2
Br J Surg 1986;73:219-21
3
Dig Dis Sci 1991;36:1589-93
4
Br J Surg 1982;69:S52-3
Clinical Presentation:
Risk Factors
J Vasc Surg 2002;35:445-52
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Clinical Presentation:
Risk factors
Ann Surg 2001;233(6):801-808
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Clinical Presentation:
Risk factors
Ann Surg 2001;233(6):801-808
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Clinical Presentation
Ann Vasc Surg 2003;17:72-79
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Clinical Presentation
Ann Surg 2001;233(6):801-808
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Diagnosis:
Non-Invasive Imaging
X-ray
Computed Tomography
(helical/angiography)
Ultrasound
MRI/MRA
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Diagnosis:
X-Ray
Plain Films
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pneumatosis
portal venous gas
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thumbprinting →
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Findings late, associated with high mortality
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Diagnosis:
Computed Tomography
Criteria
• pneumatosis
• venous gas
• SMA/celiac/IMA occlusion w/distal
disease
• arterial embolism
Sensitivity: 96%
Specificity: 94%
OR
• bowel wall thickening + one of
following:
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lack of bowel wall
enhancement
solid organ infarction
venous thrombosis
1
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Radiol 2003;229:91-98
Computed Tomography
Radiol 2003;229:91-98
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Computed Tomography
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Radiol 2003;229:91-98
Computed Tomography
Radiol 2003;229:91-98
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Volume Rendering:
Normal
RG 2002;22:161-172
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Volume Rendering:
Ischemia
RG 2002;22:161-172
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Diagnosis:
Ultrasound
High-grade stenosis or occlusion of SMA
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Sensitivity for SMA stenosis: 96% (1993) 1
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Prospective, n=100
Surgically confirmed embolism/thrombus
Sensitivity for SMA stenosis/occlusion: 100% (1999)2
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Specificity: 98%
PPV: 93%, NPV: 100%
N=82, prospective
Confirmed with angiography
1
J Vasc Surg 1993;17:780-788
2
Radiol 1999;211:405-410
Diagnosis:
MRI
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Poor delineation of smaller vessels
Limited clinical application
Perfusion flow contrast studies show promise1
1
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Radiol 2004;234:569-575
Diagnosis: Angiography
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1
Gold Standard
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Anatomic delineation of
occlusion and collaterals
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Plan operative
revascularization
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Allow infusion of
therapeutic agents (lytics,
vasodilators)
Ann Surg 2001;233(6):801-808
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Principles of Treatment
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Diagnose
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Restore Flow
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Resect non-viable tissue
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Supportive Care
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Second-Look
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Therapy
Supportive measures
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IV resuscitation
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Optimize cardiac status
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Broad-spectrum antibiotics (no data)
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Nasogastric decompression
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Therapy:
Pharmacologic
Anticoagulation
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Heparin IV
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Prevents clot propagation
Systemic vs. intra-arterial
Timing of initiation
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Immediately vs. 48 hr delay1,2
Restart 48 hrs after surgical intervention
Warfarin
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Prevents clot propagation
Give for 6-12 mos if no clotting disorder (no data)
1
Surg Gynecol Obstet 1981;153:561-569
2
Vascular Emergencies. 1982;553-561
Therapy:
Pharmacologic
Vasodilators
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Papaverine (30-60 mg/hr)
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Increases cAMP, relaxes smooth muscle
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Primary indication: Non-occlusive arterial disease
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Criterion for use:
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Peritoneal signs absent
Cannot undergo surgery
Must have good distal perfusion bed
Therapy:
Pharmacologic
Vasodilators (cont.)
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Papaverine
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Early SMA infusion reduces mortality to 40-50%1
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Directed infusion via angiography
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Rx: 24-48 hrs
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Endpoints both clinical and angiographic
Subsequent surgery
1
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Surg 1977;82:848-855
Therapy:
Pharmacologic
Thrombolysis
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urokinase>streptokinase, rtPA
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Short t½, easily reversed
Dose: high vs. low
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5,000 U/hr - 600,000 U/hr
Direct SMA infusion vs. operative placement
Am Surg 2004;70(7):600-604
Therapy:
Pharmacologic
Thrombolysis
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Duration: minutes – 48 hrs1
– too long → risk of bowel necrosis
– Treat to re-establish flow vs. complete dissolution
– > 48 hrs
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Greater risk of bleeding
Discontinue
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Worsening abdominal symptoms without evidence of
thrombolysis
Bleeding
No angiographic improvement
1
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JVIR 2005;16:317-329
Pooled Data
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JVIR 2005;16:317-329
Outcomes
• Technical success: 43/48
• Technical failure: 5/48
• Outcome most dependent on
age of thrombus/embolus
• Improvement of abd pain in
1st hour is a favorable
prognostic sign
• Technical success does not
equal clinical success
• Survival: 43/48
• Safety
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JVIR 2005;16:317-329
Therapy:
Pharmacologic
Thrombolysis
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Criterion for use:
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Embolic/thrombotic disease
Poor operative candidates
No contraindications to fibrinolytics
No bowel infarction (no peritonitis/acidosis)
Expansion of use to all patients without bowel
infarction
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Therapy:
Endovascular
Angioplasty/Stenting
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Long-term durability questioned vs. surgical
repair
Utility in acute ischemia setting
Advantages:
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Shorter duration of treatment than
thrombolysis
Definitive treatment
JVIR 1999;10(7):861-867
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Therapy:
Endovascular
Angioplasty/Stenting
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Ideal for thrombotic lesions
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Calcified ostial lesions
Flow-limiting dissections
Chronic occlusion
Advanced techniques for embolic lesions
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Flow-limiting dissections
Embolectomy w/distal protection
Therapy:
Endovascular
J Vasc Surg 2003;38:692-8
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Therapy:
Endovascular
Stenting Outcomes (Chronic, SMA/Celiac)
1998: Primary patency 100% at 14 mos (n=3)1
0% mortality
1999: Primary patency 74% at 18 mos (n=12)2
8.3% mortality <30 days
2003: Technical success 96% (n=26)3
Clinical success 88%
Primary patency at 34 mos 65%
Restenosis at 34 mos 12%
1
The PVD . org
Cardiovasc Int Radiol 1998;21:305-313
2 JVIR 1999;10(7):861-867
3 J Vasc Surg 2003;38:692-8I
Therapy:
Endovascular Stenting
Indications
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Simple stenotic lesions
Complex lesions (long-segment, irregular, heavily
calcified)
Total occlusion
Contraindications
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Suspected bowel necrosis (peritonitis, acidosis, etc)
diffuse distal disease
Median arcuate ligament compression syndrome
1
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J Vasc Surg 2003;38(4):692-8
Surgery
Anyone with peritonitis needs to be explored.
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Midline incision
Evaluate extent of ischemia
Doppler of entire SMA
Revascularization (embolectomy vs. bypass)
Re-evaluate ischemia
Lastly, non-viable bowel must be resected
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Surgery:
Options for Revascularization
Ann Vasc Surg 2003;17:72-79
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Surgery:
Principles
If embolus suspected,
transverse arteriotomy
proximal to middle colic
takeoff
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• Embolectomy
• Allow reperfusion for
20-30 minutes and then
re-assess bowel viability
Curr Opin Cardiol 1999;14(5):453-460
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Surgery:
Options for Revascularization
• Thrombosis requires a
bypass
• Longitudinal arteriotomy
• Thrombectomy
• Inflow adequate: 
• Inflow inadequate:
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Bypass
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Vein vs. graft
Curr Opin Cardiol 1999;14(5):453-460
Surgery:
Options for Revascularization
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Curr Opin Cardiol 1999;14(5):453-460
Surgery:
Damage Control
24-hr second look operation
• Ischemia continues after acute
event and reperfusion
• No way to determine viability
initially
• Allows time for supportive
measures to recover tissue
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Surgery:
Options
Case Reports
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Angiography + Laparoscopy
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Outcomes After Surgery
20011
30 day mortality
Embolic
Thrombotic
59%
62%
20022
30 day mortality
1 year mortality
3 year mortality
32%
57%
68%
20033
Peri-op mortality
62%
20034
Peri-op mortality
15%
20055
Peri-op mortality
35%
1
Ann Surg 2001;233(6):801-808
J Vasc Surg 2002;35:445-52
3 Ann Vasc Surg 2003;17:72-79
4 Vasc Endovasc Surg 2003;37:245-252
5 W J Surg 2005;29:645-648
2
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Outcomes After Surgery
J Vasc Surg 2002;35:445-52
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Outcomes After Surgery
Ann Vasc Surg 2003;17:72-79
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Outcomes
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TPN dependence:
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8-31%1,2
Significant morbidity
No studies comparing
stenting vs. open
surgery
No studies comparing
embolectomy vs.
bypass
Early intervention most
important factor for
survival
1J
2
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Vasc Surg 2002;35:445-52
Ann Surg 2001;233:801-808
Management of Mesenteric Vein Thrombosis
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5-10% of mesenteric ischemia
Subacute vs. chronic
Better prognosis
Diagnosis: CT scanning, venography
Therapy: anticoagulation, thrombolysis
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surgery if bowel compromise suspected
No role for venous thrombectomy
Long-term anticoagulation
Hypercoaguable workup
1 JVIR
2
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2005;16:317-329
Surg Lap Endo Perc Tech 2003;13(3):215-217
What Should You Do?
Supportive
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IV heparin
Broad-spectrum antibiotics
Hemodynamic optimization
― Volume status
― Cardiac function
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Supportive Measures
AXR
Other cause
(perforated
viscous)
Peritonitis
Yes
Not sure??
No
(? Laparoscopy)
•Prompt laparotomy
•Open bypass vs.
Angiography ±
Stenting
± Second look
Suspect arterial
occlusion
Abdominal angiogram
•Filling of SMA
•Good collaterals
Thrombolysis
Anticoagulation
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CT Angio
Arterial occlusion
Venous
occlusion
•SMA occluded
•No collaterals
•Open bypass vs.
Angiography ± Stenting
Anticoagulation
Anticoagulation