MESENTERIC ISCHEMIA

DR. WALID GANOD

NOV. 2019
ANATOMY:
Celiac Artery : T12, L1
- Three branches : left gastric , Splenic . Common hepatic A
- 25% true trifurcation , 65-75% left gasric branch first
- Presence of fourth branch : dorsal pancreatic , middle colic 5-10%
- 18-20 % of hepatic branches originating from SMA
- Common hepatic A from SMA 2.5%
- Accessory or replaced right or left hepatic artery from SMA 14-18%
SMA & IMA
marginal A of drummond # meandaring A. (arc of riolan )
CLINICAL ANATOMY

• Typicaly SMA embolus ludges just beyond first few jejunal branches as SMA tapers
----------------Sparing of proximal jejunum from ischemia

• In acute thrombotic occlusion usually involve the origin of SMA –widespread ischemia
CLASSIFICATION OF MI

• Arterial : (most common)

- Occlusive MI
• Acute: (surgical emergency)
Embolic 40-50% or thrombotic 20-35%

• Chronic
Atherosclerotic 90% or non atherosclerotic

- Non occlusive MI : colonic ischemia after aortoiliac surgery and abdominal compartment syndrome
• MI due to Venous thrombosis
ACUTE MESENTERIC ARTERIAL EMBOLISM

• Most emboli originate from the cardiac

• associated with atrial fibrillation, myocardial dysfunction, poor ejection fraction, or
cardiac valves due to endocarditis.
• Occasionally emboli generated from an atherosclerotic aorta.
• The majority of emboli lodge 3 to 10 cm distal to the origin of the SMA
• classically sparing the proximal jejunum and colon.
• 20% of emboli to the SMA are associated with concurrent emboli to another arterial bed
including the spleen, or kidney.
ACUTE MESENTERIC ARTERIAL THROMBOSIS

• occurs at areas of severe atherosclerotic narrowing, (origin of the SMA)

named osteal stenosis
• ischemia usually develops from the proximal jejunum to the mid-
transverse colon
• Dehydration, low cardiac output and hypercoagulable states are major
contributing factors to thrombosis as patient had good collateral.
• SMA thrombosis may also occur due to vasculitis, mesenteric dissection,
or a mycotic aneurysm.
CHRONIC MESENTERIC ISCHEMIA

• Atherosclerosis is the most common cause of CMI,

• Patient H/O smoking, hypertension, and hyperlipidemia.
• PMH : coronary, cerebrovascular, renal, aortoiliac, and other peripheral arteries
disease
• Non atherosclerotic CMI as vasculitis, lupus, Buerger disease, and radiation
arteritis.
• Median arcuate ligament syndrome
MESENTERIC VENOUS THROMBOSIS

• 5 to 15% of cases of mesenteric ischemia

• -------impaired venous outflow--------visceral edema, mucosal sloughs, hemorrhage and
abdominal pain.
• primary ( idiopathic) thrombosis
• Secondary : 90% of cases are related to thrombophilia, trauma, or local inflammatory changes
( pancreatitis, diverticulitis, inflammation or infection in the biliary system), obesity or
hypercoagulable state.
• Patients typically have a response to anticoagulation (usually for life) in combination with
treatment for the underlying local or systemic processes.
• Surgical intervention is reserved for patients who are critically ill or whose condition is
deteriorating.
THE THREE CLINICAL PHASES OF ACUTE EMBOLIC MI

Phase 1 is the hyper-peristaltic phase:

severe abdominal pain and minimal abdominal findings, forceful bowel emptying (vomiting
and/or diarrohea) and the presence of a source of embolus (e.g. atrial fibrillation).

Phase 2 is the paralytic phase

Bowels distended and silent abdomen. The pain intensity often decreases.

Phase 3 is the peritonitis phase

continuous pain, peritonitis, rapid general deterioration and acidosis.
CLINICAL PRESENTATION

• Classically, the pain is out of proportion to the findings on physical

• examination.
• Other late findings include fever, oliguria, dehydration, confusion,
tachycardia, and shock
• Metabolic abnormalities can include leukocytosis, metabolic acidosis,
hyperamylasemia, elevated liver function values, and lactic acidemia.
patients with NOMI
• critically ill, hospitalized, intubated patients who experience a sudden deterioration in
their clinical condition. These patients are often administered intravenous vasopressors,
worsening mesenteric vasoconstriction and thus decreasing splanchnic perfusion

patients with MVT,

• fever, abdominal pain and distention, nausea/vomiting, and bloody stools are the most
common findings.
• nonspecific, normal D-dimer levels may help rule out MVT.
CMI

• Postprandial abdominal pain and Progressive weight loss are the most common
symptoms
• Pain is often described as dull and crampy located in the mid epigastric region.
• Pain often occurs 15 to 45 minutes after a meal, Patients typically develop “food
fear”
• Weight loss can help to distinguish CMI from other functional bowel disorders
• Changes in bowel habits, nausea, and vomiting are less common findings.
• CMI is seen more frequently in elderly women 70%
LABORATORY EVALUATION

• AMI cause many laboratory changes but non specific

• Most times associated with persistent leukocytosis >15000 , and
heamoconcentration
• Elevation of Intestinal fatty acid binding protein offer some promise as
diagnostic tool
• albumin, transthyretin, transferrin, and C-reactive protein, are the only
studies of value in cases of chronic mesenteric ischemia,
NON INVASIVE STUDY

• Pain x-ray : in late stage , free air , small bowal obstruction

• Duplex U/S : need fasting well prepared patient and long time with
pressure on abd. So reserved for evaluation of patients with CMI and for
monitoring after intervention.
• CT angio : failure of proximal mesenteric vessel to opacify, bowel edema ,
stranding in mesentery, pneumatosis are clue to diagnosis with 95 to 100%
accuracy
INVASIVE EVALUATION

• Conventional angiography remains the “gold standard” with

Anteroposterior and lateral views of the visceral aorta
• Selective catheterization of the celiac trunk, SMA, and IMA, provide the
most accurate and specific localization of stenotic and occlusive lesions.
• Therapeutic alternatives such as balloon angioplasty, stenting, and
thrombolysis and percutaneous thrombus extraction can all be used to
restore luminal visceral blood flow.
: MANEGMENT

• The goal of therapy for patients with mesenteric ischemia is the prompt restoration
of blood flow to the visceral organs not resection of ischemic visceral ONLY.

• Medical treatment alone is not effective in patients with symptomatic mesenteric

ischemia.
MEDICAL MANEGMENT :
Before Operation
• invasive monitoring, aggressive fluid resuscitation with restoration of adequate
urine output is required,
• Electrolyte abnormalities and metabolic acidosis should also be corrected.
• Broad-spectrum intravenous antibiotics with aggressive fluid resuscitation can lead
to decreased mortality in these patients.
• Treatment against gram-negative and anaerobic organisms is especially important.
• Patients are also started and maintained on palvix, aspirin and high dose statins
indefinitely.
Endovascular Therapeutic Options In Acute
Or Chronic Mesenteric Ischaemia
• In those with short segment stenoses, cardiac and pulmonary co-morbidities, prior
abdominal surgery, coagulopathy, or malnutrition, endovascular therapy is often favored
• Balloon angioplasty and stenting has favored than open surgery as the dominant method
of revascularization for CMI
ACCE SS TO THE SMA
• via the femoral and brachial routes, although sometimes local exposure of the SMA in
• the abdomen is also needed. Brachial access may be preferable.
ASPIRATION EMBOLECTOMY OF SMA
• Endovascular aspiration embolectomy is a treatment option in patients without peritonitis.
LOCAL SMA THROMBOLYSIS
• In cases of incomplete aspiration embolectomy or distal embolization, local thrombolysis
is a viable treatment alternative in patients without peritonitis.
RECANALIZATION & STENTIN G OF THE SMA after removal of a thrombotic clot
by aspiration or thrombolysis.
CASE 1

• A patient with acute on chronic mesenteric

ischaemia who had first undergone an exploratory
laparotomy and resection of the distal small bowel
and proximal large bowel due to mesenteric
ischaemia.
• Post-operative CT angiography identified a 7 cm
long thrombotic occlusion from the origin of the
SMA.
• The arrow indicates the calcified SMA mixed with
thrombotic clots (a).
• Recanalization and stenting of the proximal
part of the occlusive SMA lesion was
performed but was complicated by a long
dissection (multiple black arrows) ending up
with an occlusion of the distal part of the
SMA
• Re-exploratory laparotomy was performed
and the entire small bowel was ischemic.
• A peripheral arterial SMA branch was punctured and a
guidewire entered the true lumen up to the aorta and snared with
devices from a transfemoral approach, creating a through-and-
through access.
• The long dissection was stented extensively from the true lumen
from the aorta into a non-dissected site in the ileocolic artery
• The patient is still alive and has been asymptomatic during the
4 years of follow-up with repeated CT angiographies.
SURGICAL THERAPY

A.Exploration and define the cause

• Confirm the cause and extent of mesenteric occlusion
• Assessment of bowel viability by inspection
• If no frank necrosis or perforation, start by revascularization before
resection, otherwise resect of affected part without contamination
B. REVASCULARIZATION
1- SMA embolectomy
2- SMA bypass
- supra celiac aorta inflow
- Infra renal aorta inflow
- Iliac artery inflow
C. Determine of intestinal viability
D. Second look surgery
E. Mangment of short bowal syndrome
THANKS