The document discusses mesenteric ischemia, describing the anatomy and blood supply of the intestines, various causes of mesenteric ischemia including arterial thromboembolism, thrombosis, venous thrombosis, and non-occlusive mesenteric ischemia. Diagnostic imaging workup and various treatment approaches are outlined, including supportive care, restoring blood flow through endovascular or surgical revascularization, and resection of non-viable intestine. Early diagnosis and treatment are emphasized for improved outcomes in mesenteric ischemia.

1. BY
RES
Steven Nabil Fouad

2. --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.
-- early dianosis result in better outcome
--Intestinal ischemia occurs when the splanchnic
perfusion fails to meet the metabolic demands of the
intestines resulting in ischemic tissue injury
--Occlusive or non-occlusive mechanism leads to
hypo perfusion of one or more mesenteric vessels

3.  Incidence
⚫ 1-2/1000 hospital admissions
⚫ 1% of GI admissions
⚫ increased incidence with age
 Mortality
⚫ 1960’s - 70-100%
⚫ 1970’s - 60-70%
⚫
21st century > 50%
 Morbidity
⚫ Poor quality of life
 Recurrence
⚫ Up to 60% in the long run

5. • Celiac artery, SMA, and IMA supply foregut, midgut, and
hindgut, respectively
• Splanchnic circulation can receive up to 30% of the cardiac
output
• Celiac artery: Supplies lower esophagus, stomach, duodenum,
liver, pancreas, and spleen
• SMA : Supplies the ileum, cecum, ascending colon, the
transverse colon and communicates with the IMA.
• Communication between superior and inferior
pancreaticoduodenal arteries is an important anastomosis that
helps to maintain bowel perfusion in atherosclerotic disease of
the mesenteric vessels
• Right and middle colic arteries are an important supply of
blood to the marginal artery of Drummond

6. • IMA:
• Smallest mesenteric vessel
• Supplies distal transverse, descending, sigmoid colon,
rectum
• SMV drains the small intestine, cecum, ascending colon,
transverse colon, stomach, pancreas and duodenum
• IMV drains descending colon, sigmoid colon, rectum
• IMV joins the splenic vein, which then joins the SMV to form
the portal vein. The portal vein enters the liver

9.  Abrupt Cessation of mesenteric blood flow
lead to malperfusion of bowel associated with
bowel necrosis.

10. Insufficient blood perfusion of small bowel or colon may
result from:
 Arterial Embolic Disease (50%)
 Arterial Thrombotic Disease (25%)
• Venous Thrombotic Disease (10%)
 Non-occlusive Mesenteric Ischemia
(20%)

11. • Injury severity is inversely proportional to mesenteric blood flow
• Number of vessels involved, mean arterial pressure, duration of
ischemia, and extent of collateral circulation all determine mesenteric
blood flow
• SM vessels are more frequently involved than the IM vessels (larger
diameter and better collaterals with inferior vessels)
• Damage may range from reversible ischemia to transmural infarction with
necrosis and perforation
• Arterial insufficiency causes tissue hypoxia, leading to bowel wall spasm
initially(vomiting or diarrhea)
• Injury complicated by reactive vasospasm in SMA after initial occlusion
• Mucosal sloughing may cause bleeding into the GIT

12. • Minimal abdominal tenderness is present despite symptoms of
intense visceral pain
• If ischemia persists disruption of mucosal barrier occurs and
bacteria, toxins, and vasoactive substances are released into the
systemic circulation
• This can cause septic shock, cardiac failure, or multi-organ failure
before bowel necrosis actually occurs
• With worsening hypoxic damage the bowel wall becomes edematous
and cyanotic
• Bowel necrosis occurs in 8-12 hours from onset of symptoms
• Transmural necrosis leads to peritonitis and indicates grave
prognosis

15.  Majority of cases (>50%): SMA occlusion
 Location: origin of middle colic artery (ischemia from
proximal jejunam to splenic flexure)
 Occlusion is sudden and no time to develop
compensatory increase in collateral flow
 Ischemia is more severe in SMA occlusion
 Celiac and IMA occlusion usually less severe and is
tolerated
 Most have underlying stenosis as well

16.  Embolic sources: cardiac (80%), aortic plaques
 Typical causes:
 Mural thrombi - MI
 Atrial thrombi - mitral stenosis and AF, vegetative
endocarditis
 Aortic thrombi - mycotic aneurysm, thrombi at sites of
atheromatous plaques, sites of vascular aortic prosthetic
grafts interposed between heart and SMA

17. • 15%-25% of acute intestinal ischemia
• Pre-existing atherosclerotic disease
— Worsening chronic mesenteric ischemia
— Late complication of pre existing visceral
atherosclerosis
• Found at ostium of SMA
• More delayed onset of symptoms - Slow process of
atherosclerotic stenosis before acute occlusion allows
time for development of collateral circulation

18. • Symptoms do not develop until 2 of 3 arteries are stenosed
or completely blocked
• Patients usually have history of atherosclerotis at other sites
(eg, CAD, strokes, PVD) or other vascular disease (Aortic
Aneurysms, dissections, trauma)
• Patients frequently present with history of chronic mesenteric
ischemia and symptoms of intestinal angina (POST PRANDIAL
PAIN )before acute event

19. • 5-10% of intestinal ischemia
• Younger patient population
• 80% have hypercoagulable state (Secondary
MVT)
• Primary MVT occurs in the absence of any
identifiable predisposing factor

20. • Common Causes:
• Malignancy
• Blood disorders - Sickle cell disease, Protein C & S
deficiency
• Post surgery
• oral contraceptives, previous DVT/PE
• Nephrotic syndrome

21. • Decreased venous outflow impedes inflow of
arterial blood and also causes bowel wall edema
leading to bowel ischemia
• Fluid sequestration and bowel wall edema are more
pronounced than in arterial occlusion
• Infarction rarely observed with isolated SMV
thrombosis, unless collateral flow in peripheral
arcades or vasa recta is also affected
• Colon rarely involved due to good collateral supply

22.  20-30% of acute intestinal ischemia
 Precipitated by severe reduction in mesenteric
perfusion secondary to arterial spasm or decreased
cardiac output
-Sympathetic adrenergic system mediated
 Visceral vasoconstriction/shunting for cerebral
protection
 Bowel perfusion, like cerebral perfusion, is preserved
till late in hypotension therefore NOMI represents a
failure of autoregulation

23. • Causes:
• Cardiac failure
• Shock
• Use of potent vasopressors in critically ill patients
• Vasoactive drugs (eg, digitalis, cocaine, diuretics, and
vasopressin) may also cause regional vasoconstriction

25. • All-cause mortality 71% (59-93%)
• Once bowel wall infarction has occurred the mortality is as
high as 90%
• Survivors have a high risk of re-thrombosis and poor QOL
due to short-gut syndrome

26. *Predictors of mortality:
1.older age
2.Atieology of ischemia;
-Mortality is highest for thrombotic AMI followed by NOMI and
embolic AMI.
-Venous thrombotic AMI carries a relatively better prognosis
3.Labaratory indicators;
-hepatic and renal impairment
-metabolic acidosis (LDH)
-lecucytosis (sepsis)
4. radilogical indicators;
-intramural pneumatosis
-free IP fluid collection (PERFPRATION)

27. 5.Time of intervention
• Early and aggressive diagnosis and treatment
shown to reduce mortality if diagnosis made before
onset of peritonitis.
• The timeliness of diagnosis and treatment is the
most significant indicator of survival.
• Madrid study - described 21 patients with SMA
embolus
• Intestinal viability achieved in 100% of patients if
symptoms <12 hours, 56% if <12-24 hours, and
18% if > 24 hour

28. Arterial Thromboembolic, Non-Occlusive
• Severe abdominal pain
• Sudden onset
• Pain out of proportion of pysical
examination
Venous Thrombotic
 Less severe pain
 Subacute
• Symptoms variable
• Abdominal pain
• vomiting
• Peritonitis & acidosis (late)
• Hypotension, tachycardia

33. Limited clinical utility
 CBC
 PC &INR
 LIVER FUNCTION
 KIDNEY FUNCTION
 ELECTROLYTE
 arterial blood gases
 D.dimer ,CRP
 Other markers : LDH, TNF
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

34. Non-Invasive Imaging
 Plain X-ray
Computed Tomography
(helical/angiography)
 Ultrasound
 MRI/MRA
Invasive
 Endoscopic procedures
 Angiography

35. Plain Films
 pneumatosis
 portal venous gas
 thumbprinting →
 Findings late, associated with high mortality

36. Sensitivity: 96%
Specificity: 94%
Criteria
• pneumatosis
• venous gas
•SMA/celiac/IMA occlusion w/distal
disease
• arterial embolism
OR
•bowel wall thickening + one of
following:
– lack of bowel wall
enhancement
– solid organ infarction
– venous thrombosis
1 Radiol 2003;229:91-98
Ct Angio with 3D reconstruction
is a highly sensitive test for
intestinal ischemia

37. Radiol 2003;229:91-98

38. ⚫ A mesenteric duplex scan demonstrating a high peak
velocity of flow in SMA is associated with 80% PPV of
mesenteric ischemia
⚫ More significantly, a negative duplex scan virtually
precludes the diagnosis of mesenteric ischemia
⚫ Body habitus is an important limitation of duplex
scan. Poor yield in obese patients
⚫ Mainly used as a screening test
⚫ Confirmed with angiography

39.  Poor delineation of smaller vessels
 Limited clinical application
 Perfusion flow contrast studies show promise1
1 Radiol 2004;234:569-575

40. ENDOSCOPIC PROCEDURES
 Endoscopic techniques using visible light
spectroscopy can be used in the diagnosis of
chronic ischemia
 When suspecting mesenteric ischemia involving the
colon performing an endoscopy to evaluate up to
the splenic flexure is high yield
 This is an excellent diagnostic tool in pts with
chronic renal insufficiency who cannot tolerate iv
contrast

41.  Gold Standard
⚫ Anatomic delineation of
occlusion and collaterals
⚫ Plan operative
revascularization
⚫ Allow infusion of therapeutic
agents (thrombolytics,
vasodilators)
1 Ann Surg 2001;233(6):801-808

42.  Diagnosis
 Supportive Care
 Restoring Blood Flow
 Resection of non-viable gut
 Second-Look

43. Supportive measures
 IV resuscitation
 Optimize cardiac status
 Broad-spectrum antibiotics (no data)
 Nasogastric decompression
 Correction of electrolyte imbalances

44. Anticoagulation
 Heparin IV
⚫ Prevents clot propagation
⚫ Systemic vs. intra-arterial
⚫ Restart 48 hrs after any surgical intervention
 Warfarin
⚫ 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

45. Vasodilators
 Papaverine
⚫ Increases cAMP, relaxes smooth muscle
⚫ Primary indication: Non-occlusive arterial disease
⚫ Early SMA infusion reduces mortality to 40-50%
⚫ Directed infusion via angiography
⚫ Not commonly used nowadays
⚫ Criterion for use:
 Peritoneal signs absent
 Cannot undergo surgery

46. Thrombolysis
 urokinase>streptokinase, rtPA
⚫ Short t½, easily reversed
⚫ Dose: high vs. low
 5,000 U/hr - 600,000 U/hr
⚫ Direct SMA infusion vs. operative placement

47. Thrombolysis
 Duration: minutes – 48 hrs1
⚫ Risk of bowel necrosis if treatment delayed
⚫ Treat to re-establish flow vs. complete dissolution
⚫ > 48 hrs-Greater risk of bleeding
Discontinue if
 Worsening abdominal symptoms without evidence of
thrombolysis
 Bleeding
 No angiographic improvement
1 JVIR 2005;16:317-329

48.  Criterion for use:
⚫ 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 and
without contraindications to thrombolysis

49. Endovascular therapy includes:
 Embolectomy
 Angioplasty and stenting
 Thrombectomy via fogarty
cateter
 Catheter based thrombolysis
 If trombectomy failed by pass
by autologous vein or
protestic graft.

50. Indications
 Simple stenotic lesions - ideal
 Complex lesions (long-segment, irregular, heavily
calcified)without distal disease
 Total occlusion of short segment
Contraindications
 Suspected bowel necrosis (peritonitis, acidosis, etc)
 Diffuse distal disease
 Median arcuate ligament compression syndrome

51. Advantages
 Significantly low peri-procedure mortality
 Shorter hospital stay
 Technical success rate 91%
 Immediate symptom relief 82%
Disadvantages
 One third developed restenosis at 26months
 Long term outcome better in open repair (5 year patency
rate was 3.8 times greater in open repair)
 Potential serious complication of endovascular repair is
occlusion of stent itself which manifests as AMI

52. Indications
 Prohibitive operative risk
 No clinical signs of peritoneal inflammation
 Those with no autologous vessel available for graft
even with contaminated peritoneal cavity

53. Advantages
 Technical success rate 87%
 Significantly lower in hospital mortality and morbidity
 Lesser complications
 Outcomes (both short term and long term) comparable to
open repair
 Successful endovascular repair resulted in a mortality rate of
36% which was significantly lower compared to that of 50% in
those treated surgically
 Patients who failed endovascular repair had a mortality rate of
about 50% which was equivalent to that of traditional surgical
repair
Disadvantages
 There is a slight theoretical risk of ischemia reperfusion injury
which might lead to worsening clinical outcome

54. Angioplasty/Stenting
 Ideal for thrombotic lesions
⚫ Calcified ostial lesions
⚫ Chronic or acute occlusion
 Advanced techniques for embolic lesions
⚫ Embolectomy w/distal protection
 Long-term durability questioned vs. surgical repair
 Utility in acute ischemia setting
 Advantages:
⚫ Shorter duration of treatment than thrombolysis
⚫ Definitive treatment

55.  Prior heparinisation
 Trans femoral or trans brachial puncture
 Visceral vessels are selectively cannulated and
visualised in lateral view
 Lesion identified and crossed with 0.014-0.032 inch
guide wire
 Balloon angioplasty with appropriate size balloon
performed
 Balloon expandable stent is preferred over self-
expanding stent
 Following intervention patient is to be put on dual
antiplatelet therapy for 3 months at least
 Follow up surveillance by ultrasound Doppler or upper gi
endoscopic ultrasound to check for patency

56. Anyone with peritonitis needs to be explored
 Midline incision
 Evaluate extent of ischemia
 Doppler of entire SMA if possible
 Revascularization (embolectomy vs. bypass)
 Re-evaluate ischemia
 Lastly, non-viable bowel must be resected
** therapeutic anticoagulation and surgical
exploartion of choice .

58.  Mesenteric ischemia is diagnosis which is often missed
and even today it carries a relatively grim prognosis.
 Mesenteric ischemia is to be suspected in any patient
presenting with pain abdomen out of proportion to the
physical findings.
 The timeliness of diagnosis and treatment is vitally
important.
 Surgical procedures have been the mainstay of
treatment over the years but the advent of endovascular
treatment options offer great promise in reducing the
mortality and morbidity without compromising on the
efficacy of treatment.

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