This document discusses mesenteric vascular ischemia, including: 1. It describes the anatomy of the celiac artery, superior mesenteric artery, and inferior mesenteric artery which supply the foregut, midgut, and hindgut respectively. 2. The pathophysiology section explains that mesenteric ischemia can be caused by embolic or thrombotic arterial occlusion, thrombotic venous occlusion, or non-occlusive processes which result in insufficient blood perfusion to the small bowel or colon. 3. The signs and symptoms include severe abdominal pain, vomiting, fever, abdominal distension and tenderness, with potential progression to shock, peritonitis, and multi

1. Mesenteric vascular ischemia

2. BASIC ANATOMY
• Celiac artery , Superior mesenteric artery and
Inferior mesenteric artery supplies fore gut ,
mid gut and hind gut respectively
• Celiac artery:
• Supplies lower esophagus, stomach,
duodenum, liver, pancreas, and spleen

4. • SMA:
• Communication between superior and inferior
pancreaticoduodenal arteries is an important
anastomosis that helps to maintain bowel perfusion
in atherosclerotic disease of the mesenteric vessels
• Supplies the ileum, cecum, ascending colon, the
transverse colon and communicates with the IMA.
• 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
• Rectal branches offer anastomosis between
visceral blood supply and the common
supply

8. • 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. PATHOPHYSIOLOGY
• Insufficient blood perfusion of small bowel or
colon – Causes are :
• Embolic (50%) or Thrombotic arterial (25%)
occlusion
• Thrombotic venous occlusion (10%)
• Non-occlusive processes (20%)

10. • Injury severity is inversely proportional to
mesenteric blood flow (number of vessels
involved, systemic mean blood pressure,
duration of ischemia, and collateral
circulation)
• SM vessels are more frequently involved than
the IM vessels (larger diameter and better
collaterals with inferior vessels)

11. • Damage may range from reversible ischemia to
transmural infarction with necrosis and
perforation
• Injury complicated by reactive vasospasm in SMA
after initial occlusion and Arterial insufficiency
causes tissue hypoxia, leading to bowel wall
spasm initially(vomiting or diarrhea)
• Mucosal sloughing may cause bleeding into the
GIT

12. • Abdominal pain and tenderness present.
• 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

13. • 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 peritonism and
indicates bad prognosis

14. • MESENTERIC ARTERIAL ISCHAEMIA
– Occlusive
• Acute mesenteric arterial embolism
• Acute mesenteric arterial thrombosis
– Non occlusive

15. ACUTE MESENTERIC ARTERIAL
EMBOLISM
• Caused by embolism
• 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

16. • Occlusion is sudden and no time to develop
compensatory increase in collateral flow
• Ischemia is more severe
• SMA is most susceptible to emboli due to
small angle and greater diameter, with IMA
less commonly affected

17. ACUTE MESENTERIC ARTERIAL
THROMBOSIS
• Late complication of preexisting visceral
atherosclerosis
• Symptoms do not develop until 2 of 3 arteries
are stenosed or completely blocked
• Slow process of atherosclerotic stenosis before
acute occlusion allows time for development
of collateral circulation

18. • Thrombus formation results in acute cessation
of blood flow to GIT resulting initially in
mucosal ischaemia and necrosis causing
bloody stools
• Bowel wall also becomes necrotic leading to
bacterial overgrowth and bowel perforation,
sepsis and death

19. • Patients usually have history of atherosclerotis at
other sites (eg, CAD, strokes, PVD) or other
vascular disease (Aortic Aneurysms, dissections,
trauma)
• Drops in cardiac output after MI, CCF may cause
AMI in pre-existing visceral atherosclerosis
• Patients frequently present with history of chronic
mesenteric ischemia and symptoms of intestinal
angina before acute event

20. NONOCCLUSIVE MESENTERIC
ISCHEMIA
• Precipitated by severe reduction in mesenteric
perfusion secondary to arterial spasm or decreased
cardiac output
• Causes:
• Cardiac failure
• Shock
• Use of potent vasopressors in critically ill patients

21. • Vasoactive drugs (eg, digitalis, cocaine,
diuretics, and vasopressin) may also cause
regional vasoconstriction
• Gross pathologic arterial or venous occlusions
are not observed

22. MESENTERIC VENOUS THROMBOSIS
• Causes:
• Malignancy
• Blood disorders - Sickle cell disease, Protein
C & S deficiency
• Post surgery - after ligation of the splenic
vein, portal vein or SMV

23. • Mechanism for ischemia is a massive influx of
fluid into the bowel wall and lumen, resulting
in systemic hypovolemia and
haemoconcentration
• Subsequent bowel edema and decreased
venous outflow impedes inflow of arterial
blood and leads to bowel ischemia
• Much younger population

24. • Symptoms may be present longer
• Infarction rarely observed with isolated SMV
thrombosis, unless collateral flow in peripheral
arcades or vasa recta is also affected
• Fluid sequestration and bowel wall edema are
more pronounced than in arterial occlusion
• Colon rarely involved due to good collateral
supply

26. http://drkeyurbhatt.blogspot.com/2012/12/case-acute-mesenteric-ischemia-due-to.html
http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S11
30-01082010000500007

27. How patient present to you?
• Symptoms-
– Severe generalized abdominal pain
– Not relieved by anything
– Vomiting
– Fever
– Distension of abdomen
– Diarrhoea blood stained

28. • Signs
– Tachycardia
– Tachypnoea
– Hypotension
– shock
– Generalised tenderness in abdomen
– Decreased bowel sound
– No gaurding ,rigidity but in late case there will be
signs of peritonitis due to bowel perforation

29. INVESTIGATIONS
• CBC – Leukocytosis due to sepsis
• Electrolytes- Imbalance due to 3rd space fluid
loss , dehydration , increased blood urea
• S. creatinine – may raised due to dehydration
and hypotension
• ABGA – metabolic acidosis , anion gap acidosis
due to intravascular fluid depletion

30. INITIAL MANAGEMENT

31. Radiological investigations
• Plain x ray abdomen (erect)
– Multiple air- fluid level with dilated bowel loops
– Some air seen in left colon and rectum
– No free gas
• CT angiogram / Mesenteric angoigram / MR
angiogram
– Exact site of blockage
– Sensitivity 75% and specificity 100%
– Additionally detect thickened and dilated bowel loops

35. MANAGEMENT
• Pre- operative management
– Resuscitation
– Monitor vitals / urine output
• Operative management
– Urgent exploration – midline exploratory
laparotomy
• surgical embolectomy
• Assess bowel viability

40. THE END