Includes Both the Acute And the Chronic

1. Mesenteric Ischaemia
- By KARTIK GULERIA
ROLL NO.-42

2. Anatomy:
• Superior Mesenteric Artery:
• Artery of Midgut
• Supplies all derivative of midgut:
 Lower part of Duodenum below the opening of Bile Duct
 Jejunum
 Ileum
 Appendix
 Caecum
 Ascending Colon
 Right 2/3rd of transverse colon
 Lower half of the head of pancreas

3. Origin,course termination:
• Arises from front of Abdominal aorta behind the body of pancreas at level
of vertebra L1, 1cm below the coeliac trunk
• Then run downwards to the right forming a curve with convexity towards
left
• At origin -Lies behind the body of pancreas
• Then in front of uncinate process
• Next crosses the third part of duodenum enters the root of mesentry runs
between the two layers
• Terminates in Right iliac fossa by anastomosing with a branch of ileocolic
artery

5. Relations:
• ABOVE THE ROOT OF THE MESENTERY:
• Anteriorly-Related to body of pancreas and Splenic Vein
• Posteriorly-Related to Aorta ,left renal vein ,the uncinate process and 3rd part of
the duodenum.
• WITHIN THE ROOT OF THE MESENTRY:
• Crosses the IVC and Right psoas
• Along the coarse accompanied by superior mesenteric vein on the right side
• Surrounded by superior mesenteric plexus of nerves.

7. Branches:
• Gives 5 set of branches both from right and left sides
• Arising from right side are:
Inferior pancreaticoduodenal
• 1st branch of SMA from rt. side
• Supplies both duodenum and pancreas
Middle colic
• Branch of SMA from rt side passes in tranverse mesocolon dividing into rt. and lt.
branches
• Supplies tranverse colon
Right Colic
• Branch of SMA passes rt. to reach ascending colon dividing into ascending and
decending arteries.
• Supplies hepatic flexure and ascending colon.

9. Ileocolic Artery
• Arises from rt. side of SMA runs downwards and to right till the caecum and ends
by dividing into superior and inferior branches .Inferior branch further
anastomoses with SMA.
• Supplies ascending colon,caecum,vermiform appendix and terminal ileum
Rising from left are 12-15 jejunal and ileal branches.
• Arise from lt. side of SMA between layers of mesentry to reach jejunum and ileum
• Supply of both surfaces of jejunum and ileum

10. Superior Meseneteric vein:
• Large vein drains blood from Small Intestine,appendix,caecum,ascending
colon and tranverse colon.
• Begins in Rt. Iliac fossa by union of tributaries from ileocaecal
region.Terminates, behind the neck of pancreas by joining the splenic vein
to form portal vein
• Tributaries as follows :
• Veins corresponding to branches of SMA
• Rt. Gastroepiploic vein
• Inferior pancreaticoduodenal vein.

11. Mesenteric Ischaemia:
ACUTE MESENTERIC ISCHAEMIA CHRONIC MESENTERIC ISCHAEMIA
ARTERIAL OCCLUSION VENOUS OCCLUSION NON-OCCLUSIVE
EMBOLISM
50%
THROMBOSIS
15-25%
MESENTERIC
VENOUS
THROMBOSIS(MVT)
5-15%
NON-OCCLUSIVE
MESENTERIC
ISCHAEMIA(NOMI)
15-20%

12. Acute Mesenteric Ischaemia
• Acute mesenteric ischemia (AMI) is a vascular emergency that is
caused by an interruption of the blood supply to the small intestine.
• There is sudden interruption of the blood supply to a segment of the
small intestine, leading to ischemia, cellular damage,intestinal
necrosis, and eventually patient death if untreated.
• It can be either Occlusive or without occlusion
• It has a high Mortality Rate Ranging from 50-70%.
• So prompt diagnosis and interventions are to be done in order to
lower the mortality rates.

14. Occlusive Mesenteric Ischaemia:
• AMI only applies to approximately 1% of all patients with an “acute
abdomen”
• Incidence rises significantly >70 yrs of age
• Risk factors are reported for It such as :
• Heart Failure
• Atrial Fibrillation
• Coronary Heart Disease
• Arterial Hypertension
• Peripheral Vascular Disease
• AMI is a time-critical emergency resulting in irreversible hypoperfusion of
the mesenteric organs within a few hours, leading to a high mortality
rate.

15. SMA EMBOLISM SMA THROMBOSIS
• AORTIC OSTIUM(15%)
• AROUND MIDDLE COLIC
ARTERY(40%)
• DISTAL BRANCHES(45%)
• AORTIC OSTIUM(60-80%)
• AROUND MIDDLE COLIC
ARTERY(15%)
• DISTAL BRANCHES(5%)
ACUTE SMA OCCLUSION:

16. Aetiologies: EMBOLISM
• Cardiac
Cardiac Dyrhythmias such as Atrial Fibrillation
Mural Thrombus following MI
Vegetations on mitral and aortic valves assosciated with endocarditis
• Proximal Aortic Disease eg Atheromatous plaque from an aortic
aneurysm.
• Iatrogenic eg Arteriography

17. Pathophysiology:EMBOLISM
• Emboli typically lodge at points of normal anatomic narrowing, and
the SMA is particularly vulnerable because of its relatively large
diameter and low takeoff angle from the aorta.
• The majority of emboli lodge 3 to 10 cm distal to the origin of the
SMA, thus classically sparing the proximal jejunum and colon.

18. Aetiologies:THROMBOSIS
• Atherosclerosis
• Vasculitis
• Thrombangitis Obliterans
• Polyarteritis Nodosa

19. Pathophysiology:THROMBOSIS
• Many of these patients have a history consistent with chronic
mesenteric ischemia (CMI) or intestinal angina including postprandial
pain, weight loss, or food fear and thus a systematic history is
important when evaluating a patient suspected to have AMI.
• If there is Involvement of the ileocolic artery will result in necrosis of
the proximal colon.

20. Presentation:
• The initial clinical stage of AMI is characterized by the sudden onset of
strong, spasmodic abdominal pain after 3–6 h, this phase is followed by
a painless interval due to the damage of the intramural pain receptors
as a result of prolonged hypoperfusion.(nausea ,vomiting,diarrhea)
• Acute complete circulatory disruption of the intestine leads to
irreversible mucosal ischemia with leukocyte infiltration and formation
of oxygen radicals within 6 h.
• The collapse of the mucosal barrier further contributes to bacterial
translocation and gangrene of the intestinal wall. In addition, bacterial
infiltration leads to peritonitis, ileus, sepsis, and multiorgan failure
• Classical Triad Pain,Fever,Hemocult+ve Stools

22. Diagnostics
• TIME IS CRUCIAL!!!!!!!
• Therefore focused diagnostic are vital in detecting AMI as soon as
possible unspecific routine diagnostics may further contribute to increase
in mortality rate.
• So Focused Medical H/o,the recognition of predisposing factors, and a
precise clinical examination are the key to time-saving diagnostics and
improved survival in patients with AMI.
• If there is any suspicion of acute occlusive mesenteric ischemia, biphasic
contrast-enhanced computed tomography with three dimensional
multiplanar reconstruction computed tomography (CT) is the diagnostic
tool of choice

24. Laboratory Studies:
• They are not definitive but may be helpful to corroborate clinical suspicion.
• More than 90% of patients will have an abnormally elevated leukocyte count. The second
most commonly encountered abnormal finding is metabolic acidosis with elevated lactate
level, which occurred in 88%
• Patients may present with lactic acidosis due to dehydration and decreased oral intake.
Thus, differentiation of early ischemia versus irreversible bowel injury based upon the
lactate level alone is not reliable unless accompanied by other clinical evidence
• Elevated serum lactate levels >2 mmol/l was associated in irreversible intestinal ischemia.
• D-dimer has been reported to be an independent risk factor of intestinal ischemia tells clot
formation and endogenous degradation via fibrinolysis. No patient presenting with a
normal D-dimer had intestinal ischemia and D-dimer >0.9 mg/L had a specificity, sensitivity,
and accuracy of 82, 60, and 79%, respectively.
• Elevated amylase has been reported in roughly a half of patients with AMI.

25. Other Investigations:
• X-RAY--
• Straight X-Ray Abdomen to be done
• Absence of gas in the lumen of the thickened small intestine
• Dilated Bowel Loops
• THUMB PRINTING SIGN which signifies Bowel wall edema and
thickening
• Pneumatosis Intestinalis(Gas in the wall of small bowel)

27. CT Angiography:
• The CT scan should include the whole abdomen in both the arterial
and venous phases.
• The venous phase is required for the diagnosis of mesenteric venous
thrombosis
• MRI can be done but CT is preferred to safe time
• In addition to detailed imaging of the intestinal wall, the main
advantages of CT angiography over catheter angiography is the ability
to rule out other differential diagnoses of AMI.

28. • In the presence of advanced AMI, the CTA findings reflect irreversible
ischemia (intestinal dilatation and thickness, reduction or absence of
visceral enhancement,pneumatosis intestinalis, and portal venous
gas) and free intraperitoneal air.
• CTA should be performed despite the presence of renal failure, as the
consequences of delayed diagnosis, missed diagnosis, or
mismanagement are far more detrimental to the kidneys and the
patient then exposure to the iodinated contrast agent.

29. SMA
OCCLUSION

30. SMA
STENOSIS
PARTIAL THROMBOSIS OF SMA

31. Treatment:
• FLUID RESUSCITATION:
Fluid resuscitation with crystalloid and blood products is essential for
the management of the patient with suspected AMI.
Preoperatively resuscitation is important to prevent cardiovascular
collapse on induction of anesthesia.
Assessment of electrolyte levels and acid–base status should be
performed.
In patients with AMI, there is severe metabolic acidosis and
hyperkalemia may be present due to underlying bowel infarction and
reperfusion.

32. . Vasopressors should be used with caution, and only to avoid fluid
overload and abdominal compartment syndrome
The fluid volume requirement in these patients may be high, due to
extensive capillary leakage, but extensive crystalloid overload should
be avoided to optimize bowel perfusion.

33. • Broad-spectrum antibiotics should be administered immediately. Unless
contraindicated, patients should be anticoagulated with intravenous
unfractionacted heparin.
• High risk of infection among patients with AMI outweighs the risks of
acquired antibiotic resistance, and therefore broad-spectrum antibiotics
should be administered early in the course of treatment
• Intestinal ischemia leads to early loss of the mucosal barrier, which
facilitates bacterial translocation and the risk of septic complications.
• If there are no signs of peritonitis or intestinal gangrene, interventional
pharmacotherapy with local fibrinolysis should be considered in case of
peripheral embolism.
• If Peritonitis then Emergency Surgery is to be preferred.

34. • Prompt Laparotomy is to be done to overt peritonitis
• The goal of surgical intervention for AMI includes:
• Re-establishment blood supply to the ischemic bowel.
• Resection of all non-viable regions
• Preservation of all viable bowel.
• After initial resuscitation, midline laparotomy should be performed
followed by assessment of all areas of the intestine with decision for
resection of all clearly necrotic areas.
• .Embolectomy and either primary or patch angioplasty is a well
established definitive treatment for SMA emboli.
• If thrombosis of SMA will require Bypass procedure

35. Surgical Options:
• Clinical signs of peritonitis, any evidence of intestinal gangrene,
central occlusion of the SMA, or failure of endovascular options
require an immediate surgical treatment.
• The irreversibly ischemic parts of the intestine need to be resected in
order to control the septic focus.
• The underestimation of an ischemic segment that might lead to an
anastomotic leak further contributes to a high morbidity and
mortality

36. • In case of unavoidable major bowel resections, critical residual length
limits must be kept in mind:
• 100 cm in case of a terminal jejunostomy (ileum and colon removed)
• 65 cm in case of a jejuno-colonic anastomosis (colon retained)
• 35 cm in case of a jejuno-ileal anastomosis (ileo-cecal region retained)
• Resection beyond these critical lengths inevitably leads to short
bowel syndrome with need for permanent parenteral nutrition or
small bowel transplantation.
• The primary treatment for intestinal failure due to major bowel
resections is total parenteral nutrition.

38. Endovascular Techniques:
• The therapeutic endovascular approach consists of angiographic
catheter aspiration embolectomy and catheter lysis with recombinant
tissue plasminogen activator, urokinase, or pharmacotherapy with
prostaglandin E1.
• Fractioning of the thrombus with a guide wire can additionally
increase the effect of the fibrinolytic agent.

40. Non-Occlusive Mesenteric Ischaemia:
• Etiology:
• Low flow states eg shock
• Drugs e.g digitalis,vasopressors
• PATHOPHYSIOLOGY:
• NOMI occurs in approximately 20% of cases and is usually a consequence of SMA vasoconstriction
associated with low splanchnic blood flow
• The compromised SMA blood flow often involves the proximal colon as well due to involvement of
the ileocolic artery.
• Its incidence is increased in two different patient groups in patients on chronic hemodialysis with
consecutive hypovolemia and intestinal vasospasm as well as in patients after cardiac surgery
including extracorporeal circulation.
• Presentation:
Right-sided abdominal pain associated with the passage of maroon or bright red blood in the stool is
highly suggestive of NOMI in these patients.

41. Diagnosis
• Clinical examination in these patients is challenging and of limited
value due to intubation and sedation. Abdominal distension, signs of
sepsis, and inflammatory parameters need to be assessed carefully.
• For stable patients with NOMI, interventional catheter angiography is
recommended
• In NOMI CTA may demonstrate bowel ischemia and free fluid in the
face of patent mesenteric vessels.
• Sausage Sign is seen in NOMI on CT angiogram

43. Managment:
• Management of NOMI is based on treatment of the underlying
precipitating cause.
• Fluid resuscitation, optimization of cardiac output, and elimination of
vasopressors remain important primary measures.
• Additional treatment may include systemic anticoagulation and the
use of catheter directed infusion of vasodilatory and antispasmodic
agents,most commonly papaverine hydrochloride.
• The decision to intervene surgically is based on the presence of
peritonitis, perforation, or overall worsening of the patient’s
condition
• In case of peritoneal signs an exploratory laparotomy is required for
resection of frankly necrotic bowel.

44. Mesenteric Venous Thrombosis:
• Etiology:
Inheited Hypercoagulable States:
• Factor V Leiden mutation
• Protein C,S,Antithrombin III deficiency
Acquired Hypercoagulable States:
• Malignancy
• Oral Contraceptives
• Portal Hypertension
• Intra-Abdominal Sepsis e.g acute pancreatitis
• Postoperative States e.g Abdominal Surgery
 Thrombosis is attributed to a combination of Virchow’s triad, i.e. stagnated blood flow,
hypercoagulability, and vascular inflammation
PRESENTATION:
Patients with MVT present with a mixture of nausea, vomiting, diarrhea, and abdominal cramping.

45. Diagnosis :
• In MVT, the most common positive radiological finding on venous
phase CTA is thrombus in the superior mesenteric vein on venous
phase CTA. This has been described as the target sign

47. Treatment:
• The first-line treatment for mesenteric venous thrombosis is anticoagulation.
• Early use of heparin has been associated with improved survival.
• When clinical signs demand operative intervention, necrotic bowel is to be resected and
use damage control techniques as anticoagulation therapy may improve the clinical
picture over the ensuing 24–48 h.
• Second-look laparotomy, 24–48 h later, may avoid the resection of bowel that may be
viable.
• Trans-jugular intrahepatic portosystemic shunt can be used for MVT with the rationale of
decreasing portal pressure, which works as a vacuum of clot fragments and improves the
effectiveness of thrombolysis in the case of acute thrombosis
• Supportive measures include nasogastric suction, fluid resuscitation, and bowel rest.

48. Chronic Mesenteric Ischaemia
• Dure to advanced atherosclerotic disease of multiple mesenteric
arteries
• Good Collateral Circulatory -Symptomatic chronic mesenteric ischemia
is rare
• Risk Factors:
• +ve Family H/o
• Smoking
• Hypertension
• Hypercholesterolemia
• Mc in Females between Age 50 and 70 yrs

49. • Non Atherosclerotic Causes are less frequent
• Inflammatory arterial disease
• middle aortic syndrome
• celiac artery compression
• chronia aortic dissection,aortic coarctation
• fibromuscular dysplasis
• neurofibromatosis
• PATHOPHYSIOLOGY:
• Mesenteric Circulation consists of 3 primary vessels:celiac artery,SMA,IMA
• Blood flow increases within an hour after eating food due to increase in
metabolic demand
• Diffuse atherosclerosis responsible for 95% of CMI
• Chronic Occlusion of single vessel allows collateral blood flow to compensate
• Symptoms not present till 2 primary vessels are occluded

50. Clinical Features:
• Classical picture:
• Postprandial Abdominal Pain
• Weight Loss
• Pain -Intestinal angina/intestinal claudication
• Diffuse-Midabdominal,Midepigastric and crampy in nature
• Develops 30-60 minutes of eating
• Severity depends on size of meal ingested
• Early onset pain with coeliac artery ischaemia
• Late onset pain-diffuse ischaemic disease

51. Clinical Features:
• Nausea
• Vomiting
• Diarrhea
• Bloating
• Constipation
• Occult blood in stool and ischaemic colitis

52. Diagnosis:
• Non Invasive Mesenteric Duplex Scan
• Fasted State
• Sensitivity 75%
• Specificity 92%
• Aortography
• CT angiogram
• Magnetic Resonace Angiography

53. Treatment:
• Therapeutic Goal with CMI is to revascularize mesenteric circulation
and prevent development of bowel infarction.Mesenteric occlusive
disease can be treated successfully by either transaortic
endarterectomy or mesenteric artery bypass
• For occlusive lesions located 1-2cm distal to mesenteric origin
mesenteric arterybypass is to be performed.So both the Coeliac
artery and SMA are to be revascularised
• Smoking Cessation is also helpful

54. Endovascular Treatment:
• Done for mesenteric Artery Stenosis/Short segment occlusion by
balloon dilatation or stent placement as a less invasive alternative to
open surgical intervention .
• It is also suited to patients with recurrent disease following previous
mesenteric vascularization
• Mesenteric angioplasty and stenting is also heplful

55. SOURCES:
• BAILEY AND LOVE’s SHORT PRACTICE OF SURGERY(27TH EDITION)
• Acute mesenteric ischemia: guidelines of the World Society of
Emergency Surgery
• Review article on Acute mesenteric ischemia