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Peritoneal Healing, Cow/Horse

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Brief quiz/review of peritoneum and adhesions, specific to the horse and cow.

Published in: Health & Medicine, Technology
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Peritoneal Healing, Cow/Horse

  1. 1. Micky Trent DVM DACVS
  2. 2.  What are the histologic layers of normal peritoneum?  Which vary by species?
  3. 3.  Layers  Mesothelial Cells  Basement membrane  Submesothelial connective tissue  Loose c.t.  Species variation
  4. 4.  What are the layers of peritoneum?  What is the peritoneal space?
  5. 5.  Peritonal cavity  Layers  Parietal  Visceral
  6. 6.  How is peritoneum innervated?  Why should we as surgeons care?
  7. 7.  Sensory Innervation  Parietal Layer  Sharp & Deep pain, Stretch  Localizable  Not blocked by local or regional blocks  Visceral Layer  Deep pain, stretch  NO sharp pain  Poorly localizable  Can block with direct application
  8. 8.  What abdominal structures are considered retroperitoneal?  Why should we as surgeons care?
  9. 9.  List 4 critical functions that depend on the peritoneum.
  10. 10.  Cell nutrition  Peritoneal fluid production  Maintain gliding surfaces  Waste control
  11. 11.  Cell Nutrition  Diffusion  Produce Peritoneal Fluid  Transudate from blood  Inflammation changes volume and character
  12. 12.  Maintain Gliding Surface  Surface villi trap fluid  Peritoneal fluid  Plasminogen activators  Mesothelial cells  Fibrin break down  Depressed with peritoneal trauma
  13. 13.  How is waste removed from the peritoneal cavity?  Low MW compounds?  Cells?  Foreign bodies?
  14. 14.  Physical Removal  Transmesothelial  Small molecules  H20  Stomata/Lymphatics  Peritoneal flow to diaphragm 10 route  Diaphram lymphatics  Thoracic duct to vena cava  Larger molecules  Particles/cells  Fluid  Omental alternative
  15. 15.  Functional Removal  Localization  Omental Trapping  Fibrin Trapping  Phagocytosis  PMNs  Macrophages  Bacterial kill
  16. 16.  Functional Removal  Localization  Omental Trapping  Fibrin Trapping  Phagocytosis  PMNs  Macrophages  Bacterial kill
  17. 17.  How does the peritoneum respond initially (24hrs) to trauma?  Vascular phase?  Inflammatory cascade?  Coagulation cascade?  Link between inflammation and coagulation?
  18. 18.  Brief vasoconstriction  Histamine, PGE2 release  Local vasodilation & cell influx  Procoagulant factors  Platelets adhere to wound bed  Alpha corpuscles degranulate  Release PDGF, TGF-β, dense corpuscles  Release epinephrine, serotonin  Contribute to PG & leukotriene release
  19. 19.  Local release of cytokines  Cell migration to wound bed  Platelet aggregation  Coagulation cascade activation  Initial clot formation  Fibrin deposition  Temporary matrix for signaling molecules & inflammatory cells  Temporary bridge between tissues
  20. 20.  Close overlap with Inflammatory response  Two pathways converging to one  Intrinsic pathway  BM damage & collagen exposure  Factor XII (Hagemen factor)  Activation of factor II (prothrombin)  Activation of factor IIa (thrombin precursor)  Thrombin production
  21. 21.  Thrombin  Cleaves soluble circulating fibrinogen into insoluble fibrin clots  Factor XII stimulates clot formation and activation of the fibrinolytic system  Fibrinolysis determined by:  tPA (mesothelial cells, leukocytes, tissue)  PAI1&2
  22. 22.  How does a peritoneal defect heal?  What is the timing?  Where do new cells come from?  Are there differences in cells shed in a dialysate?  How is ECM formed?
  23. 23.  12-24 hrs – PMNs  24 hrs + macrophages  Cytokine release  Day 3  Mesothelial and fibroblast cells appear  Area of lesion regresses  Day 7-10  Mesothelial layer reestablished  ECM follows cell migration
  24. 24.  Species variation?
  25. 25.  tPA vs PAI baseline  Human, horses, dogs – tPA high  Cows – PAI high  Post-injury  Most: tPA down, PAI up  Cow: PAI up
  26. 26.  Describe the steps in adhesion formation.  What key enzymes are involved?  How are these enzymes affected by trauma?
  27. 27.  What is the incidence of post-op adhesions?  In people?  In horses?  Which structures are most commonly involved in identified cases in horses?  Why?
  28. 28.  Humans  67%-93%  Horses  9%-32%  Caveats?  Canine/Feline  Low
  29. 29.  Equine  SI procedures  Regardless of procedure  SI  Ventral incision  Why??
  30. 30.  Are there any beneficial effects of peritoneal adhesions?
  31. 31. Beneficial Effects  Seal Breaks in continuity  Prevent visceral leakage  Neovascularization  Stabilize mobile viscera  Bovine, canine, equine
  32. 32. Beneficial Effects  Seal Breaks in continuity  Prevent visceral leakage  Neovascularization  Stabilize mobile viscera  Bovine, canine, equine
  33. 33.  What are common stimuli for adhesions?
  34. 34.  Suturing Peritoneum!!  Ischemia  Serosal trauma  Drying  Abrasion  Others  Foreign bodies  Bacteria
  35. 35.  List preventative methods (and mechanisms) for reduction of adhesions
  36. 36.  Avoid serosal trauma  Reduce/avoid foreign bodies  Minimize ischemic tissue  Minimize bacterial contamination  Consider protective coatings  Carboxymethyl cellulose most common  Use of heparin debatable (little support)
  37. 37.  Solid barriers  Seprafilm (CMC & HA)  Interceed (oxidized cellulose)  Hyaluronate membranes  CMC  Omentectomy(x)  Antiticoagulants - Heparin (x)  Fibrinolytics – tPA (cost)  Antiinflammatories (~)  Lavage (?)  Antioxidants (?)
  38. 38.  Fucoidan  Chitosan dextran  Hydrogel (PCEC)  Aldehyde dextran  Parecoxib  Alginate gell  Statins

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