Mesenteric ischemia pathophysiology: Difference between revisions

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{{familytree| | | | X01 | | | | | | | | | | | X02 |X01=Hypovolemia|X02= Cardiac failure|}}
{{familytree| | | | X01 | | | | | | | | | | | X02 |X01=[[Hypovolemia]]|X02= [[Cardiac failure]]|}}
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{{familytree| | | | | | | | | |A01| | | | | | | | |A01= Endogenous vasoconstriction|}}
{{familytree| | | | | | | | | |A01| | | | | | | | |A01= [[Endogenous]] [[vasoconstriction]]|}}
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{{familytree| | | | | | | | | |B01| | | | | | | | |B01= Splanchnic vasoconstriction|}}
{{familytree| | | | | | | | | |B01| | | | | | | | |B01= [[Splanchnic]] [[vasoconstriction]]|}}
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{{familytree| | | | | | | | | |C01| | | | | | | | |C01= Gut mucosal hypoperfusion|}}
{{familytree| | | | | | | | | |C01| | | | | | | | |C01= Gut mucosal hypoperfusion|}}
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{{familytree| | |D01| | | | | | | | | | | | | |D02|D01= Restoration of blood by vasodialtion of collaterals|D02= Gut mucosal barrier disruption|}}
{{familytree| | |D01| | | | | | | | | | | | | |D02|D01= Restoration of blood by [[vasodialtion]] of collaterals|D02= Gut [[mucosal]] barrier disruption|}}
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{{familytree| | | |!| | | | | | | | | | | | | | |!|}}
{{familytree| | |E01| | | | | | | | | | | | | |E02|E01= Ischemia-reperfusion injury|E02= Increased mucosal perfusion to bacterial toxins|}}
{{familytree| | |E01| | | | | | | | | | | | | |E02|E01= [[Ischemia]]-reperfusion injury|E02= Increased [[mucosal]] perfusion to [[bacterial]] [[toxins]]|}}
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{{familytree| | | | | | | | | |F01| | | | | | | | |F01= Activation of inflammatory response|}}
{{familytree| | | | | | | | | |F01| | | | | | | | |F01= Activation of [[inflammatory]] response|}}
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Revision as of 15:35, 11 January 2018


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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Feham Tariq, MD [2]

Overview

The factors that regulate the intestinal blood flow play a vital role in the development of mesenteric ischemia. Mucosa of the intestines has a high metabolic activity and accordingly a high blood flow requirement. The majority of blood supply of the intestine comes from the superior mesenteric artery, with a collateral blood supply from superior and inferior pancreaticoduodenal arteries (branches of the celiac artery) as well as the inferior mesenteric artery. The splanchnic circulation (arteries supplying the viscera) receives 15-35% of the cardiac output, making it sensitive to the effects of decreased perfusion. Mesenteric ischemia occurs when intestinal blood supply is compromised by more than 50% of the original blood flow without activation of adaptive responses. This can lead to disruption of mucosal barrier, allowing the release of bacterial toxins (present in the intestinal lumen) and vasoactive mediators which ultimately lead to complete necrosis (cell death) of the intestinal mucosa. This can further progress to depression in myocardial activity, sepsis, multiorgan failure, and without prompt intervention, even death.

Pathophysiology

Pathogenesis

Factors contributing in the pathogenesis of mesenteric ischemia:[7][8]

(A) Mesenteric blood supply (General circulation)

Arterial Region supplied
Superior mesenteric artery (SMA) Small intestine, proximal and mid colon upto the splenic flexure.
Inferior mesenteric artery (IMA) Hind gut starting from the splenic flexure to the rectum.
Celiac artery (CA) Foregut, hepatobiliary system and spleen.
Venous supply
The venous system parallels the arterial branches and drains into the portal venous system.

Commonly affected arteries:

(B) Collateral circulation

The role of collateral circulation in the development of mesenteric ischemia is as follows:[11][12][13][14][15][14]

(C) Response of mesenteric vasculature to ischemia

The sequence of events that take place in the small intestine subsequent to decreased blood flow:



 
 
 
Ischemic insult
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Decreased delivery of oxygen and nutrients
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Disruption in cellular metabolism
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Tissue injury due to hypoxia and reperfusion
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Full thickness necrosis of the bowel
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Perforation of the bowel wall
 
 
 
 


Post ischemic cellular changes:
Time duration since ischemia Pathological changes in the small intestine
3-4 hours Necrosis of the mucosal villi
6 hours Transmural, mural or mucosal infarction
1-4 days Bowel hemorrhage

Reperfusion injury:

(D) Vasoactive and humoral factors regulating the mesenteric blood flow

Intrinsic regulation:

(a) Metabolic factors:

(b) Myogenic factors:

Extrinsic regulation:

(a) Neural component:

(b) Humoral component:

Factors regulating mesenteric blood flow
Extrinsic reguatory system
Humoral (endogenous and exogenous) Neural component
Decrease blood flow Increase blood flow Decrease blood flow Increase blood flow
Intrinsic regulatory component
Decrease blood flow (Myogenic factors) Increase blood flow (Metabolic factors)
  • Arteriolar tension receptors

Areas prone to ischemia:

Areas prone to ischemia Blood supply
Splenic flexure End arteries of superior mesenteric artery
Rectosigmoid junction End arteries of inferior mesenteric artery

Watershed areas lacking collateralization:

  • Splenic flexure
    • Supplied by the end arteries of SMA with no collateral circulation.
  • Rectosigmoid junction
    • Supplied by the end arteries of IMA with no collateral circulation.
  • Middle segment of jejunum[24]
    • This area is the farthest from collateral circulation and hence prone to ischemia as compared to other segments of jejunum.

Pathogenesis of occlusive mesenteric ischemia:



 
 
 
 
 
 
 
 
 
Vascular occlusion
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Blood flow<metabolic demand
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Mucosal barrier disruption and bacterial translocation into the circulation
 
 
 
 
Anaerobic glycolysis in mucosa and lactate production
 
 
 
 
 
 
Activation of vascular and humoral factors leading to vasoconstriction
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Systemic activation of inflammatory response
 
 
 
 
Lactic acidosis
 
 
 
 
 
 
Intestinal necrosis
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Multiorgan failure
 
 
 
 
 
 
 
 

Pathogenesis of non-occlusive mesenteric ischemia:



 
 
 
Hypovolemia
 
 
 
 
 
 
 
 
 
 
Cardiac failure
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Endogenous vasoconstriction
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Splanchnic vasoconstriction
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Gut mucosal hypoperfusion
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Restoration of blood by vasodialtion of collaterals
 
 
 
 
 
 
 
 
 
 
 
 
 
Gut mucosal barrier disruption
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Ischemia-reperfusion injury
 
 
 
 
 
 
 
 
 
 
 
 
 
Increased mucosal perfusion to bacterial toxins
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Activation of inflammatory response
 
 
 
 
 
 
 
 

Gross Pathology

Gross pathology shows following changes:

  • Early stage of ischemia: Intestinal wall in congested.
  • Late stage of ischemia: Edematous, friable and hemorrhagic bowel wall.

References

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  2. Savlania A, Tripathi RK (2017). "Acute mesenteric ischemia: current multidisciplinary approach". J Cardiovasc Surg (Torino). 58 (2): 339–350. doi:10.23736/S0021-9509.16.09751-2. PMID 27901324.
  3. Yasuhara H (2005). "Acute mesenteric ischemia: the challenge of gastroenterology". Surg Today. 35 (3): 185–95. doi:10.1007/s00595-004-2924-0. PMID 15772787 : 15772787 Check |pmid= value (help).
  4. Deitch, Edwin A. (2012). "Gut-origin sepsis: Evolution of a concept". The Surgeon. 10 (6): 350–356. doi:10.1016/j.surge.2012.03.003. ISSN 1479-666X.
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  6. Granger DN, Granger HJ (1983). "Systems analysis of intestinal hemodynamics and oxygenation". Am J Physiol. 245 (6): G786–96. PMID 6660300.
  7. 7.0 7.1 Granger DN, Richardson PD, Kvietys PR, Mortillaro NA (1980). "Intestinal blood flow". Gastroenterology. 78 (4): 837–63. PMID 6101568.
  8. Rosenblum JD, Boyle CM, Schwartz LB (1997). "The mesenteric circulation. Anatomy and physiology". Surg Clin North Am. 77 (2): 289–306. PMID 9146713.
  9. Kumar S, Sarr MG, Kamath PS (2001). "Mesenteric venous thrombosis". N Engl J Med. 345 (23): 1683–8. doi:10.1056/NEJMra010076. PMID 11759648.
  10. Ha C, Magowan S, Accortt NA, Chen J, Stone CD (2009). "Risk of arterial thrombotic events in inflammatory bowel disease". Am J Gastroenterol. 104 (6): 1445–51. doi:10.1038/ajg.2009.81. PMID 19491858.
  11. McKinsey JF, Gewertz BL (1997). "Acute mesenteric ischemia". Surg Clin North Am. 77 (2): 307–18. PMID 9146714.
  12. Walker TG (2009). "Mesenteric vasculature and collateral pathways". Semin Intervent Radiol. 26 (3): 167–74. doi:10.1055/s-0029-1225663. PMC 3036491. PMID 21326561.
  13. Fisher DF, Fry WJ (1987). "Collateral mesenteric circulation". Surg Gynecol Obstet. 164 (5): 487–92. PMID 3554567.
  14. 14.0 14.1 Bulkley GB, Womack WA, Downey JM, Kvietys PR, Granger DN (1985). "Characterization of segmental collateral blood flow in the small intestine". Am J Physiol. 249 (2 Pt 1): G228–35. PMID 4025549.
  15. Bulkley GB, Womack WA, Downey JM, Kvietys PR, Granger DN (1986). "Collateral blood flow in segmental intestinal ischemia: effects of vasoactive agents". Surgery. 100 (2): 157–66. PMID 3738747 : 3738747 Check |pmid= value (help).
  16. Mastoraki A, Mastoraki S, Tziava E, Touloumi S, Krinos N, Danias N; et al. (2016). "Mesenteric ischemia: Pathogenesis and challenging diagnostic and therapeutic modalities". World J Gastrointest Pathophysiol. 7 (1): 125–30. doi:10.4291/wjgp.v7.i1.125. PMC 4753178. PMID 26909235.
  17. Corcos, Olivier; Nuzzo, Alexandre (2013). "Gastro-Intestinal Vascular Emergencies". Best Practice & Research Clinical Gastroenterology. 27 (5): 709–725. doi:10.1016/j.bpg.2013.08.006. ISSN 1521-6918.
  18. Hansen MB, Dresner LS, Wait RB (1998). "Profile of neurohumoral agents on mesenteric and intestinal blood flow in health and disease". Physiol Res. 47 (5): 307–27. PMID 10052599.
  19. Schoenberg MH, Beger HG (1993). "Reperfusion injury after intestinal ischemia". Crit Care Med. 21 (9): 1376–86. PMID 8370303.
  20. Patel, Amit; Kaleya, Ronald N.; Sammartano, Robert J. (1992). "Pathophysiology of Mesenteric Ischemia". Surgical Clinics of North America. 72 (1): 31–41. doi:10.1016/S0039-6109(16)45626-4. ISSN 0039-6109.
  21. Takala J (1996). "Determinants of splanchnic blood flow". Br J Anaesth. 77 (1): 50–8. PMID 8703630.
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  23. Granger HJ, Shepherd AP (1973). "Intrinsic microvascular control of tissue oxygen delivery". Microvasc Res. 5 (1): 49–72. PMID 4684756.
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