Lower gastrointestinal bleeding pathophysiology: Difference between revisions

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|Angiodysplasia
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* Tortuous dilation of multiple small submucosal and mucosal blood vessels
* Tortuous dilation of multiple small submucosal and mucosal blood vessels  
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* Dilated and thin-walled vessels in mucosa and submucosa often in clusters.
* Dilated and thin-walled vessels in mucosa and submucosa often in clusters.

Revision as of 20:14, 13 December 2017

Lower gastrointestinal bleeding Microchapters

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Overview

Pathophysiology

Blood supply

  • Superior mesentric artery and inferior mesentric artery are the two major blood vessels that supply lower gastrointestinal tract.[1][2][3]
  • The superior mesentric artery and inferior mesentric artery are interconnected through a branch of anatomizing branches which are collectively called as marginal artery of Drummond. 
  • This vascular arcade runs in the mesentery close to the bowel.
Lower GI Tract Arterial Supply Venous Drainage
Midgut
  • Distal duodenum jejunum
  • Ileum
  • Appendix
  • Cecum
  • Ascending colon
  • Hepatic flexure
  • Proximal transverse colon.
  • Superior mesenteric artery (SMA)
    • Ileocolic
    • Right colic
    • Middle colic branches
  • Superior mesenteric vein
Hindgut
  • Distal one-third of the transverse colon
  • Splenic flexure
  • Descending colon,
  • Sigmoid colon
  • Rectumhu
  • Inferior mesenteric artery (IMA)
    • Left colic
    • Sigmoid
    • Superior rectal (hemorrhoidal) branches
  • Portal system ɸ
ɸ -Except lower rectum, which drains into the systemic circulation.
Blood supply to the intestines includes the celiac artery, superior mesenteric artery (SMA), inferior mesenteric artery (IMA), and branches of the internal iliac artery (IIA).
Source: By Anpol42 (Own work) [CC BY-SA 4.0 (https://creativecommons.org/licenses/by-sa/4.0)], via Wikimedia Commons

Pathogenesis

The pathogenesis of lower gastrointestinal bleeding can be discussed based on the etiology. Diverticulosis is the most common etiology of lower GI bleeding accounting for 30% of all cases, followed by anorectal disease, ischemia, inflammatory bowel disease (IBD), neoplasia and arteriovenous (AV) malformations.

  • Diverticulosis
    • The colonic wall weakens with age and results in the formation of saclike protrusions known as diverticula.[4][5][6][7]
    • These protrusions generally occur at the junction of blood vessel penetrating through the mucosa and circular muscle fibers of the colon resulting in painless bleeding
    • Despite the majority of diverticula being on the left side of the colon, diverticular bleeding originates from the right side of the colon in 50% to 90% of instances.
Diagram of sigmoid diverticulum
Source:By Anpol42 (Own work) [CC BY-SA 4.0 (https://creativecommons.org/licenses/by-sa/4.0)], via Wikimedia Commons
  • Anorectal disease
  • Hemorrhoids are engorged vessels in the normal anal cushions. When swollen, this tissue is very friable and susceptible to trauma, which leads to painless, bright red bleeding.[8][9][8]
  • Anal fissures are defined as a tear in the anal mucosa. With the passage of stool, the mucosa continues to tear and leads to bright red bleeding. [10]
  • Mesenteric Ischemia
  • Mesenteric ischemia results when there is inadequate blood supply at the level of the small intestine.[11][12][13][14]
  • 2 or more vessels (celiac ,SMA, or IMA) must be involved for bleeding to occur.
  • Non occlusive mesenetric ischemia affects critically ill patients who are vasopressor-dependent.
  • Venous thrombosis of the visceral vessels can also precipitate an acute ischemic event.
  • Decreased blood flow leads to transmural infarction with necrosis and perforation.
  • Associated mucosal sloughing results in bleeding.
  • Ischemic Colitis
  • Ischemic colitis is caused by poor perfusion of the colon, which results in the inability of that area of the colon to meet its metabolic demands.[15][16][17]
  • It can be gangrenous or nongangrenous, acute, transient, or chronic.
  • The left colon is predominantly affected, with the splenic flexure having increased susceptibility.
  • Intraluminal hemorrhage occurs as the mucosa becomes necrotic, sloughs, and bleeds.
  • Damage to the tissue is caused both with the ischemic insult as well as reperfusion injury.
  • Inflammatory Bowel Disease[18][19]
    • Crohn's diseas
      • In Crohn's disease T cell activation stimulates interleukin (IL)-12 and tumor necrosis factor (TNF)-a, which causes chronic inflammation and tissue injury.[20][21][22][23][24][25]
      • Initially, inflammation starts focally around the crypts, followed by superficial ulceration of the mucosa.
      • The deep mucosal layers are then invaded in a noncontinuous fashion, and noncaseating granulomas form, which can invade through the entire thickness of the bowel and into the mesentery and surrounding structures resulting in bleeding
  • Ulcerative colitis
    • In ulcerative colitis T cells cytotoxic to the colonic epithelium accumulate in the lamina propria, accompanied by B cells that secrete immunoglobulin G (IgG) and IgE.[23][26][27][28]
    • This results in inflammation of the crypts of Lieberkuhn, with abscesses and pseudopolyps along with rupturing of minute blood vessels in mucosa resulting in bleeding.
  • Neoplasia
  • Mutations of multiple genes are required for the formation of adenocarcinoma, including the APC gene, Kras, DCC, and p53.[29][30][31]
  • Certain hereditary syndromes are also classified by defects in DNA mismatch repair genes and microsatellite instability.
  • As tumor grows it invades the surrounding tissue disrupting the normal vasculature along with it
  • Therefore tumors tend to bleed slowly, and patients present with hemocult positive stools and microcytic anemia.
  • AV Malformation/Angiodysplasia
  • In AV malformation direct connections between arteries and veins occur in the colonic submucosa.[32][33][34][35][36]
  • The lack of capillary buffers causes high pressure blood to enter directly into the venous system, making these vessels at high risk of rupture into the bowel lumen.
  • In Angiodysplasia over time, previously healthy blood vessels of the cecum and ascending colon degenerate and become prone to bleeding.

Gross and Microscopic Pathology

Disease Gross Pathology Microscopic Pathology
Diverticulosis
  • Numerous visible flask like protrusions along the intestinal wall.
  • Thick and corrugated circular muscle with mucosal folds.
  • Inflammatory cells
  • Intramucosal ganglion cells
  • Lymphoid infiltrate
  • Lymphoglandular complexes
  • Mucin depletion
  • Mild cryptitis
  • Achitectural distortion
  • Paneth cell metaplasia
  • Ulceration 
Angiodysplasia
  • Tortuous dilation of multiple small submucosal and mucosal blood vessels
  • Dilated and thin-walled vessels in mucosa and submucosa often in clusters.
  • Surrounding mucosa may be eroded
Hemorrhoids
  • Tortuous superficial dilations of multiple blood vessels.
  • Dilated, thick-walled, congested submucosal vessels
  • Papillary endothelial hyperplasia
  • Internal hemorrhoids are lined by rectal or transitional mucosa,
  • External hemorrhoids have a squamous lining
  • Superficial ulcerations
  • Pagetoid dyskeratosis
Mesenteric ischemia 
  • Hemorrhagic infarctions
  • Ulcerations
  • Mucosal plaque
  • Strictures
  • Lamina propria hemorrhage
  • Superficial epithelial necrosis,
  • Deep crypts
  • Minimal inflammation
  • Strictures
Ischemic colitis
  • Discrete or serpiginous ulcerations (may be discrete or serpiginous)
  • Cobblestone pattern resembling Crohn’s disease
  • Pseudopolyps resembling ulcerative colitis
  • Hemorrhagic infractions
  • Frank blood or dark mucus in lumen
  • Late fibrosis and stricture formation
  • Hallmarks of ischemic bowel are necrotizing phlebitis and thrombi formation
  • Necrosis
  • Ulceration and granulation tissue extend into submucosa and surrounding smooth muscle fibers of muscularis mucosa
Crohn's disease 
  • Dull and granular serosa
  • Creeping fat
  • Thick/rubbery intestinal wall (due to edema, inflammation, fibrosis, hypertrophy of muscularis propria)
  • Strictures (string sign on barium enema)
  • Skip areas
  • Aphthous mucosal ulcers
  • Superficial or deep ulceration
  • Adjacent granulation tissue extending into deep submucosa or below.
  • Transmural inflammation with lymphoid aggregates
  • Goblet cells
  • Focal neutrophils in epithelium and overlying lymphoid aggregates and plasmacytosis
  • Edematous mucosa and submucosa
Ulcerative colitis
  • Deep fissuring ulcerations
  • Hemorrhagic mucosa
  • Pseudopolyps
  • Diffuse mononuclear inflammatory infiltrate in lamina propria
  • Crypt abscesses (neutrophils in glandular lumen) and cryptitis
  • Granulation tissue and reepithelialization
  • Submucosal fibrosis
  • Schwann cell proliferation

References

  1. ↑ Geboes K, Geboes KP, Maleux G (2001). "Vascular anatomy of the gastrointestinal tract". Best Pract Res Clin Gastroenterol. 15 (1): 1–14. doi:10.1053/bega.2000.0152. PMID 11355897.
  2. ↑ Granger DN, Holm L, Kvietys P (2015). "The Gastrointestinal Circulation: Physiology and Pathophysiology". Compr Physiol. 5 (3): 1541–83. doi:10.1002/cphy.c150007. PMID 26140727.
  3. ↑ "The Gastrointestinal Circulation - NCBI Bookshelf".
  4. ↑ Hobson KG, Roberts PL (2004). "Etiology and pathophysiology of diverticular disease". Clin Colon Rectal Surg. 17 (3): 147–53. doi:10.1055/s-2004-832695. PMC 2780060. PMID 20011269.
  5. ↑ Maykel JA, Opelka FG (2004). "Colonic diverticulosis and diverticular hemorrhage". Clin Colon Rectal Surg. 17 (3): 195–204. doi:10.1055/s-2004-832702. PMC 2780065. PMID 20011276.
  6. ↑ Comparato G, Pilotto A, Franzè A, Franceschi M, Di Mario F (2007). "Diverticular disease in the elderly". Dig Dis. 25 (2): 151–9. doi:10.1159/000099480. PMID 17468551.
  7. ↑ Matrana MR, Margolin DA (2009). "Epidemiology and pathophysiology of diverticular disease". Clin Colon Rectal Surg. 22 (3): 141–6. doi:10.1055/s-0029-1236157. PMC 2780269. PMID 20676256.
  8. ↑ 8.0 8.1 Lohsiriwat V (2012). "Hemorrhoids: from basic pathophysiology to clinical management". World J. Gastroenterol. 18 (17): 2009–17. doi:10.3748/wjg.v18.i17.2009. PMC 3342598. PMID 22563187.
  9. ↑ Sanchez C, Chinn BT (2011). "Hemorrhoids". Clin Colon Rectal Surg. 24 (1): 5–13. doi:10.1055/s-0031-1272818. PMC 3140328. PMID 22379400.
  10. ↑ Holland RA, Rimes AF, Comis A, Tyndale-Biscoe CH (1988). "Oxygen carriage and carbonic anhydrase activity in the blood of a marsupial, the Tammar wallaby (Macropus eugenii), during early development". Respir Physiol. 73 (1): 69–86. PMID 3140330.
  11. ↑ Krupski WC, Selzman CH, Whitehill TA (1997). "Unusual causes of mesenteric ischemia". Surg. Clin. North Am. 77 (2): 471–502. PMID 9146726.
  12. ↑ Walker TG (2009). "Mesenteric ischemia". Semin Intervent Radiol. 26 (3): 175–83. doi:10.1055/s-0029-1225662. PMC 3036494. PMID 21326562.
  13. ↑ Berland T, Oldenburg WA (2008). "Acute mesenteric ischemia". Curr Gastroenterol Rep. 10 (3): 341–6. PMID 18625147.
  14. ↑ Mastoraki A, Mastoraki S, Tziava E, Touloumi S, Krinos N, Danias N, Lazaris A, Arkadopoulos N (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.
  15. ↑ FitzGerald JF, Hernandez Iii LO (2015). "Ischemic colitis". Clin Colon Rectal Surg. 28 (2): 93–8. doi:10.1055/s-0035-1549099. PMC 4442720. PMID 26034405.
  16. ↑ Theodoropoulou A, Koutroubakis IE (2008). "Ischemic colitis: clinical practice in diagnosis and treatment". World J. Gastroenterol. 14 (48): 7302–8. PMC 2778113. PMID 19109863.
  17. ↑ Rania H, Mériam S, Rym E, Hyafa R, Amine A, Najet BH, Lassad G, Mohamed TK (2014). "Ischemic colitis in five points: an update 2013". Tunis Med. 92 (5): 299–303. PMID 25504381.
  18. ↑ Kim DH, Cheon JH (2017). "Pathogenesis of Inflammatory Bowel Disease and Recent Advances in Biologic Therapies". Immune Netw. 17 (1): 25–40. doi:10.4110/in.2017.17.1.25. PMC 5334120. PMID 28261018.
  19. ↑ Hendrickson BA, Gokhale R, Cho JH (2002). "Clinical aspects and pathophysiology of inflammatory bowel disease". Clin. Microbiol. Rev. 15 (1): 79–94. PMC 118061. PMID 11781268.
  20. ↑ Woźniak-Parnowska W, Werakso B (1974). "[Comparative studies of microbiological purity of ointments by the direct culture method and use of membrane filters]". Acta Pol Pharm (in Polish). 31 (6): 819–23. PMID 4447044.
  21. ↑ Mazal J (2014). "Crohn disease: pathophysiology, diagnosis, and treatment". Radiol Technol. 85 (3): 297–316, quiz 317–20. PMID 24395894.
  22. ↑ Jewell DP (1989). "Aetiology and pathogenesis of ulcerative colitis and Crohn's disease". Postgrad Med J. 65 (768): 718–9. PMC 2429831. PMID 2694136.
  23. ↑ 23.0 23.1 Sartor RB (2006). "Mechanisms of disease: pathogenesis of Crohn's disease and ulcerative colitis". Nat Clin Pract Gastroenterol Hepatol. 3 (7): 390–407. doi:10.1038/ncpgasthep0528. PMID 16819502.
  24. ↑ Head K, Jurenka JS (2004). "Inflammatory bowel disease. Part II: Crohn's disease--pathophysiology and conventional and alternative treatment options". Altern Med Rev. 9 (4): 360–401. PMID 15656711.
  25. ↑ Zhang YZ, Li YY (2014). "Inflammatory bowel disease: pathogenesis". World J. Gastroenterol. 20 (1): 91–9. doi:10.3748/wjg.v20.i1.91. PMC 3886036. PMID 24415861.
  26. ↑ Ungaro R, Mehandru S, Allen PB, Peyrin-Biroulet L, Colombel JF (2017). "Ulcerative colitis". Lancet. 389 (10080): 1756–1770. doi:10.1016/S0140-6736(16)32126-2. PMID 27914657.
  27. ↑ Farrell RJ, Peppercorn MA (2002). "Ulcerative colitis". Lancet. 359 (9303): 331–40. doi:10.1016/S0140-6736(02)07499-8. PMID 11830216.
  28. ↑ Rönnblom LE, Janson ET, Perers A, Oberg KE, Alm GV (1992). "Characterization of anti-interferon-alpha antibodies appearing during recombinant interferon-alpha 2a treatment". Clin. Exp. Immunol. 89 (3): 330–5. PMC 1554468. PMID 1516252.
  29. ↑ Itzkowitz S (2003). "Colon carcinogenesis in inflammatory bowel disease: applying molecular genetics to clinical practice". J. Clin. Gastroenterol. 36 (5 Suppl): S70–4, discussion S94–6. PMID 12702969.
  30. ↑ Ullman TA, Itzkowitz SH (2011). "Intestinal inflammation and cancer". Gastroenterology. 140 (6): 1807–16. doi:10.1053/j.gastro.2011.01.057. PMID 21530747.
  31. ↑ Kraus S, Arber N (2009). "Inflammation and colorectal cancer". Curr Opin Pharmacol. 9 (4): 405–10. doi:10.1016/j.coph.2009.06.006. PMID 19589728.
  32. ↑ Foutch PG (1993). "Angiodysplasia of the gastrointestinal tract". Am. J. Gastroenterol. 88 (6): 807–18. PMID 8389094.
  33. ↑ Dodda G, Trotman BW (1997). "Gastrointestinal angiodysplasia". J Assoc Acad Minor Phys. 8 (1): 16–9. PMID 9048468.
  34. ↑ Kheterpal S (1991). "Angiodysplasia: a review". J R Soc Med. 84 (10): 615–8. PMC 1295562. PMID 1744847.
  35. ↑ Athanasoulis CA, Galdabini JJ, Waltman AC, Novelline RA, Greenfield AJ, Ezpeleta ML (1977). "Angiodysplasia of the colon: a cause of rectal bleeding". Cardiovasc Radiol. 1 (1): 3–13. PMID 311247.
  36. ↑ Sami SS, Al-Araji SA, Ragunath K (2014). "Review article: gastrointestinal angiodysplasia - pathogenesis, diagnosis and management". Aliment. Pharmacol. Ther. 39 (1): 15–34. doi:10.1111/apt.12527. PMID 24138285.

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