Acute mesenteric arterial disease can result from occlusion of the mesenteric arteries or veins, reducing or stopping blood flow to the intestines. It has high morbidity and mortality rates of 60-70% despite aggressive treatment. Diagnosis involves clinical evaluation, lab tests, CT angiography and mesenteric angiography. Treatment depends on the severity and includes resuscitation, antibiotics, surgery to remove dead bowel and restore blood flow, and endovascular procedures in some cases. Prompt diagnosis and treatment is needed to prevent intestinal infarction and improve outcomes.

1. ACUTE MESENTERIC ARTERIAL
DISEASE

2. HISTORICAL BACKGROUND
• First description of mesenteric vascular occlusion -Antonio Beniviene (Florence)
fifteenth century.
• Sporadic case reports appeared in the literature in the 1800s from Tiedman and
Virchow.
• Successful treatment with resection of infarcted intestine was reported in 1895 by
Elliott.
• The first SMA embolectomy was performed in 1951 however success rates over the
next few decades were poor and mortality was 70-90%
• In the 1970s liberal use of angiography with adjuncts like vasodilators decreased the
mortality and mortality rates to about 50%.

3. • Acute mesenteric ischemia (AMI) - abrupt reduction in or cessation of the delivery
of oxygen to the intestine. Either from
• an occlusion of the mesenteric arterial supply or venous drainage
• as well as hypo-perfusion during shock states
• Frequency in patients with acute abdomen varies
• 2.1% in suspected peritonitis
• 17.7 % in emergency laparotomies
• 31% in damage control laparotomies in non-trauma patients.
INTRODUCTION

4. Acute mesenteric ischemia
Occlusive mesenteric ischemia
SMA embolus
SMA thromosis
Aortic dissection occluding
visceral arteries or isolated
dissection of the mesenteric
arteries
Vascular trauma
Arteriopathies like FMD, TA,
PAN
Non- occlusive mesenteric
ischemia (NOMI)
Colonic ischemia after aorto-
iliac surgery
Abdominal compartment
syndrome
PATHOPHYSIOLOGICAL CLASSIFICATION

5. Acute mesenteric ischemia carries a 60 – 70% morbidity and mortality rate that has
not changed for many decades despite early aggressive treatment
• The mortality rates have been shown to be less where endovascular techniques
were routinely used.
• Traditionally treatment of AMI
• surgical with intensive medical support and
• use of interventional options for non occlusive mesenteric ischemia (NOMI)
• Endovascular and hybrid procedures can be applied in well selected patients.
INTRODUCTION

6. • Uncommon accounting for less than 1:1000 admissions
• Females :males::3:1
• Usually in the 7th decade
• Comorbid conditions
• h/o atrial fib/flutter, recent MI, CCF, peripheral arterial emboli
• If the patient has symptom suggestive of previous chronic mesenteric ischemia –
an acute on chronic ischemia should be considered
INCIDENCE AND RISK FACTORS

7. • Irrespective of the cause- infarction is from mucosa outward.
• Virchow’s triad – endothelial injury or dysfunction(atherosclerosis), haemodynamic
changes and hypercoagulability cause thrombosis.
• Most common – 40-50% of cases , mostly thrombo-emboli or athero-emboli
• SMA -most commonly involved because -wide caliber, narrow takeoff angle from the
aorta.
• Embolus typically lodges in proximal SMA distal to the takeoff of the middle colic artery
(as the artery tapers) thus sparing the duodenum and transverse colon.
• Only few emboli lodge in the proximal SMA i.e.15% at the SMA origin.
• 1/3 have an antecedent embolic event usually a cardiac source
• Atrial tachyarrhythmia, low EF (CCF, Cardiomyopathy), recent MI, Ventricular
aneurysm.
PATHOPHYSIOLOGY OF ARTERIAL EMBOLISM

8. • Thrombosis superimposed on atherosclerosis accounts for 25-30% AMI with many
patients being asymptomatic.
• Usually insidious in onset due to extensive collaterals and maintenance of viability until
closure of the critically stenotic vessel or collateral.
• Acute on chronic presentations are common- history of chronic mesenteric ischemia in
these patients – abdominal pain, food avoidance and weight loss prior to presentation
-20%
• Complications of mesenteric revascularization can also lead to acute ischemia
• Endovascular failures- distal embolization, vessel perforation, dissection, stent
migration, thrombosis
PATHOPHYSIOLOGY OF ARTERIAL THROMBOSIS

9. • Only 1/5th of bowel capillaries are open at any given time and normal oxygenation is
maintained at just 20%of maximal blood flow.
• Intestinal mucosa can extract increasing amounts of oxygen during hypoperfusion.
• Prolonged ischemia leads to disruption of intestinal mucosal barrier – reactive
oxygen metabolites and neutrophil activation.
FINAL COMMON PATHWAY OF BOWEL ISCHEMIA

10. • AMI is usually not included initially as a diagnosis in elderly with abdominal pain and
tenderness
• Survival is less when it is diagnosed after 24 hours of onset of symptoms (50- 30%)
• Only about 1/3 are diagnosed before surgical exploration or death and bowel necrosis
indicates a delay in diagnosis.
• High index of suspicion with history and physical examinations needed.
• Prompt investigation and treatment is cornerstone.
DIAGNOSTIC EVALUATION

11. • Clinical presentation
• Laboratory investigations
• ECHO
• Diagnostic imaging
• Radiograph
• Duplex ultrasound
• CT
• Arteriography
• MRA
• Diagnostic Laparoscopy
DIAGNOSTIC EVALUATION

12. • Symptoms out of proportion with signs.
• Abdominal pain and tenderness and no peritoneal signs in early presentation.
• Embolic episode has a abrupt presentation
• May be a forceful and sudden bowel evacuation after onset of pain.
• Thrombosis may have subacute presentation due to collaterals – pain distension,
diarrhea, acidosis, sepsis and GI bleed
CLINICAL PRESENTATION

13. • leukocytosis, lactic acidosis, amylasemia, and coagulopathy (become apparent as
bowel ischemia proceeds to infarction, tissue death, and sepsis)
• Assess fluid status, electrolyte and acid base balance, infection.
• Hemoconcentration, leukocytosis and high anion gap, lactic acidosis.
• D Dimer – within 24 hours of presentation (exclusion test)
• Amylase, AST and LDH but non specific
• Intestinal fatty acid- binding protein (FABP) plasma and urinary are found to be
elevated
• Also liver FABP and ileal bile acid- binding protein (specific for ileum)
• Not yet clinically used.
LABORATORY EVALUATION

14. XRay
25% have normal xray , ileus, bowel wall edema (thumb-printing) or
pneumatosis.
• Mainly used to exclude other diagnosis.
Duplex ultrasound
• Accurately identifies high grade stenosis of Celiac and SMA but may miss
embolus beyond proximal segment.
• Not much use in AMI due to pain, user dependency, bowel gas obscuring the
field etc.
DIAGNOSTIC EVALUATION - XRAY

15. • High resolution CT -Excludes or identifies various pathologies including bowel infarction
(presence of mural thickening, intraperitoneal fluid, pneumatosis intestinalis, portal
venous air, and pneumoperitoneum)
• Arterial phase CTA for Ischemia. Oral contrast should be replaced by “negative” oral
contrast like water before the scan
• Delayed phase -bowel wall enhancement and portal system. – Biphasic CT
DIAGNOSTIC EVALUATION - CT

16. • Biphasic Multidetector CTA 100 % sensitive and 89% specific for AMI,
• no one sign was diagnostic but presence of
• pneumatosis,
• SMA or Celiac+IMA occlusion, arterial embolism,
• SMA or portal venous gas,
• focal lack of bowel wall enhancement, free air,
• solid organ infarction,
• SMV or PV thrombosis,
• bowel obstruction/dilatation, mucosal enhancement, mesenteric stranding and ascites as
indirect signs.
DIAGNOSTIC EVALUATION - CT

17. • Angiography -most sensitive diagnostic modality-no flow in SMA a short distance
from origin, at the branching point of the middle colic artery- “ mercury meniscus ”
sign
• Lateral views -delineating the embolus. Anterior views allow visualization of distal
mesenteric vessels. In 1/3 patients, additional emboli can be identified in other
arterial beds -renal, cerebral, or peripheral extremities
DIAGNOSTIC EVALUATION - ARTERIOGRAPHY

18. • Patients with strongly suspected NOMI may benefit as long as there is no immediate
need to explore.
• Nowadays used in conjunction with therapy
• Injection of vasodilators
• Thrombolysis
• Angioplasty +/- stenting
• Angiography followed by open, hybrid and exploration can also be done based on
clinical presentation.
DIAGNOSTIC EVALUATION - ARTERIOGRAPHY

19. • Can be both functional or anatomical
• Gadolinium- enhanced is appealing as it is non invasive, non nephrotoxic and less
allergic.
• However its lengthy and need lots of post processing not ideal for emergency setting.
DIAGNOSTIC EVALUATION - MRA

20. • Has limited ability to assess bowel viability.
• Walking the bowel and serosal colour may be difficult.
• Fluorescein dye with ultraviolet light may help delineate nonviable bowel but not
widely used.
DIAGNOSTIC LAPAROSCOPY

21. DIAGNOSTIC RECOMMENDATIONS
• In acute abdominal pain D-Dimer measurement to exclude AMI – IB
• In suspected AMI triphasic CTA with 1mm slices to detect arterial occlusion – IB
• In suspected AMI with elevated creatinine levels CTA can be done wit risk to save
life – IIbC
• NOMI – clinical suspicion should be the mainstay for diagnosis- IIaC
• In NOMI , DSA is the most reliable method to verify the diagnosis - IIaC

22. • Initial resuscitation and critical care
• Treatment of NOMI
• Surgical treatment
• SMA embolectomy
• SMA Bypass
• Assessment of bowel viability
• Endovascular treatment
• SMA Embolus treatment
• SMA Thrombosis treatment
• Hybrid procedures
TREATMENT

23. • Fluid resuscitation with isotonic crystalliods -Aggressive fluid resuscitation
as bowel ischemia results in significant fluid shifts and sequestration.
• Nasogastric tube decompression to decrease intraluminal pressure and
minimize reduction of blood flow to the bowel wall should be performed
• Correct electrolyte imbalances
• CVP monitoring, urine output, arterial pressure
• Broad spectrum antibiotics - as ischemia leads to bacterial translocation
• Heparin
• Try to avoid vasopressors as they worsen ischemia
TREATMENT – INITIAL RESUSCITATION

24. • The main goals are revascularization, assessment of bowel viability, and resection of
necrotic bowel.
• Endovascular therapies are an option if there is no evidence of bowel ischemia.
• Obvious bowel ischemia needs surgery – revascularization before bowel resection.
Bowel is re - examined after blood flow is restored
• Infra pancreatic SMA can be exposed based on need ie embolectomy versus bypass.
With or without mobilization of the 4th part of duodenum.
• Preparation should include both thighs for vein graft harvest
• Midline laparotomy
TREATMENT – SURGERY

25. • Omentum and transverse colon elevated and small bowel moved to the right.
• Transverse incision at base of transverse mesocolon in mesentry. Vein is usually
encountered first, artery is to the left of the vein and is covered by a plexus of
lymphatics.
• proximal exposure of artery -gentle upward retraction of lower border of pancreas.
• Proximal SMA between the middle and right colic branches is isolated
TREATMENT – SURGERY – SMA EMBOLECTOMY

26. • Heparinisation followed by transverse arteriotomy
• Distal embolectomy with 2-3 Fr catheter is done, proximal venting is preferred to
embolectomy.
• Milking of the clot can also be attempted ( to prevent damage to smaller branches) and
one time instillation of thrombolytic agent into the distal vessels.
• Primary closure or vein patch is done.
TREATMENT – SURGERY – SMA EMBOLECTOMY

27. • Lateral retroperitoneum is opened down over the aorta and onto left CIA
• Peritoneal soilage and the suitability of the inflow vessels is the main deciding factor
for type of bypass.
• Single vessel bypass is preferred in emergency setting and graft orientation is based on
the atherosclerosis and occlusive disease in the inflow vessel.
• Lazy C – lie of the graft from Rt CIA, Left CIA or distal aorta can all be used, end to end
graft to SMA anastomosis can be done.
TREATMENT – SURGERY – SMA BYPASS

28. • Short retrograde aorto SMA bypass using larger graft 8- 10 from infra renal aorta –
kinking of shorter graft after removal of retractors is a problem
• Antegrade bypass from supraceliac aorta is an option but exposure and supraceliac
clamping of aorta is difficult in such a setting
• 6-8 mm dacron or externally supported PTFE is preferred, use omental flap to cover
• Rifampicin coated dacron in contamination or a good quality vein graft. ( deep vein
preferred to GSV but may not be ideal in emergency settings)
TREATMENT – SURGERY – SMA BYPASS

29. • Bowel viability should be done about 20-30 min after reperfusion
• Pulsations, colour, peristalisis, bleeding from cut edges
• Combined with Doppler signals at the antimesenteric border of the bowel gives better
results
• Fluorescein dye is accurate but needs special equipment.
• Finally clinical judgement and reassessment is advised
• Minimal resection of non viable bowel with delaying reanastamosis to a second relook
procedure has also been highlighted.
TREATMENT – SURGERY – BOWEL VIABILITY

30. • Decision is made at the initial surgery
• Is done irrespective of the clinical improvement of the patient
• 12- 48 ours after initial procedure
• Resection of non viable bowel and anastomosis
• Reassess revascularization
• Abdominal closure
RELOOK LAPAROTOMY

31. • In acute settings -Percutaneous endovascular catheter based thrombolysis and
chemical thrombectomy is being done is a few centers with results varying and there
being a lot of shortcomings.
• Thrombolysis takes long ( bowel necrosis can occur in a few hours if circulation is not
re-established)
• Technically more difficult than an open embolectomy and time consuming
• Bowel viability cannot be assessed and patient may still need a laparotomy. (main
cause of mortality)
TREATMENT – ENDOVASCULAR

32. • Sub acute and chronic conditions have a better outcome with endovascular
• Especially in surgically high risk patients
• In thrombotic AMI may have a role as the occlusion is at the origin in the initial 3 – 6
cm of the vessel.
• It is technically more difficult and results in acute setting are not favourable even
with stenting.
TREATMENT – ENDOVASCULAR

33. • An open- interventional approach, in patients who are too sick for a bypass.
• Midline laparotomy with exposure and control of the SMA at the root of the
transverse mesocolon
• Thrombo-endarterectomy done if needed, patch plasty with a retrograde cannulation
with a flexible sheath placement towards the aorta.
• Lesion crossing is 100% due to sheath proximity and then balloon expandable stent is
deployed
• Morbidity and mortality is much better than with open bypass.
• Restenosis of the stent is known and close follow-up is recommended with
percutaneous treatment if needed.
TREATMENT – HYBRID – RETROGRADE OPEN
MESENTERIC STENTING (ROMS)

34. • Rare condition where patients present with acute abdominal pain but intestinal angina
with weight loss in chronic cases is also reported.
• It may also be an incidental finding on CT.
• Can be diagnosed by MRA, Angiography and duplex US also.
• Risk factors include – hypertension, male, atherosclerosis, pregnancy, CTD, FMD,
vasculitis and trauma
• Males in their 6th decade, almost 50% having aneurysmal dilataion of SMA
• Clinically spontaneous dissections may range from being asymptomatic to catastrophic
bowel ischemia or aneurysmal rupture.
SPONTANEOUS VISCERAL DISSECTION

35. • Treatment options range from conservative management, anticoagulation,
endovascular stenting and open surgical repair.
• Conservative management has only a 50% success rate , anticoagulation 65%.
• Endovascular stenting for symptomatic patients and those with aneurysm >2cm ,
anticoagulation for failed stenting and open surgery for unsuccessful
anticoagulation is recommended.
• Asymptomatic and symptomatic patients can be regularly followed up with short
course anticoagulation and lifelong antiplatelet therapy if no mesenteric ischemia.
TREATMENT

36. • Mesenteric ischemia in the absence of structural - vessel occlusion may occur in low
- flow states, most commonly owing to poor cardiac output, usually in hospitalized
critically ill patients
• Recent cardiac surgery and haemodialysis patients are at highest risk for NOMI
• Less common - mesenteric vasospasm following elective revascularization - chronic
SMA occlusion, of small and medium-size vessels is precipitated by early enteral
feeding.
• older mean age of the population with severe medical problems at risk for this type
of mesenteric ischemia.
NOMI

37. • Vasospasm usually in the distribution of SMA is a must.
• 20% of AMI and highest mortality as it is usually associated with multisystem organ
failure.
• Hypothesis is that cardiac failure, peripheral hypoxemia, paradoxical splanchnic
vasospasm and reperfusion injury all contribute to its development.
• Excessive sympathetic activity due to cardiogenic shock/hypovolemia leads to
vasospasm to maintain cerebral and cardiac perfusion at the expense of visceral and
peripheral organs
• Vasopressin and angiotensin are the neurohumoral mediators (Vasoactive
medications like adrenaline, noradrenaline and vassopresin are associated with the
development of NOMI. )
PATHOPHYSIOLOGY OF NOMI

38. • Vasospasm may continue even after the initiating insult is corrected.
• The exact mechanism for this is not known but it plays an important role in occlusive as
well as non occlusive mesenteric ischemia and reperfusion as well.
• Frequency and duration of ischemic episodes affects the ischemia reperfusion injury.
• Episodic reperfusion primes the ischemic tissue with leucocytes that react to and
produce reactive oxygen species.
PATHOPHYSIOLOGY OF NOMI

39. • NOMI have insidious onset and seen in hospitalized patients who are critically ill.
NOMI – CLINICAL PRESENTATION

40. • Diagnosis -CT or angiography.
• Angiography should not be performed until the patient has been
adequately resuscitated.
• As hypotension or hypovolemia will demonstrate similar findings on
the angiogram
• Radiographic criteria include
• Narrowing of the origins of multiple branches of the SMA
• Alternate dilatation and narrowing of the intestinal branches (the
“string-of-sausages” sign)
• Spasm of the mesenteric arcades
• Impaired filling of the intramural vessels.
INVESTIGATIONS-NOMI

41. • Angiography – 4 criteria for diagnosis
• Narrowing of origins of multiple branches of the SMA - lesions
themselves are smooth in contour without total occlusion
• Alternate dilation and narrowing of the intestinal branches –
string of sausages sign
• Spasm of mesenteric arcades
• Impaired filling of intramural vessels
NOMI INVESTIGATIONS

42. • Mainly medical , with critical care management and arteriography
• Surgery is only for peritonitis and bowel gangrene
• Direct angiographic infusion of intra-arterial vasodilators until there is improvement.
• Papaverine 30-60mg/hr ( HR/BP monitoring)
• Heparin should not be given through the same catheter simultaneously.
• Check angio at the end of treatment.
TREATMENT – NOMI

43. • NOMI – no surgical intervention unless the patient has bowel infarction.
• Treatment of choice –catheter guided papaverine perfusion of the SMA
• Initial bolus of 30 mg, followed by infusion of 30 - 60 mg/hr for a 24 - hour
period.
• Repeat angiogram to determine if the spasm has improved and vascular
perfusion has returned to a normal - appearing state.
• Cardiac support is needed to improve general condition.
• Some series have reported the use of papaverine for up to 5 days without
complication
NOMI TREATMENT