Micky Trent DVM DACVS
 What are the histologic layers of normal
peritoneum?
 Which vary by species?
 Layers
 Mesothelial Cells
 Basement membrane
 Submesothelial
connective tissue
 Loose c.t.
 Species variation
 What are the layers of peritoneum?
 What is the peritoneal space?
 Peritonal cavity
 Layers
 Parietal
 Visceral
 How is peritoneum innervated?
 Why should we as surgeons care?
 Sensory Innervation
 Parietal Layer
 Sharp & Deep pain,
Stretch
 Localizable
 Not blocked by local or
regional block...
 What abdominal structures are considered
retroperitoneal?
 Why should we as surgeons care?
 List 4 critical functions that depend on the
peritoneum.
 Cell nutrition
 Peritoneal fluid production
 Maintain gliding surfaces
 Waste control
 Cell Nutrition
 Diffusion
 Produce Peritoneal
Fluid
 Transudate from
blood
 Inflammation
changes volume and
character
 Maintain Gliding
Surface
 Surface villi trap
fluid
 Peritoneal fluid
 Plasminogen
activators
 Mesothelial cells
 Fi...
 How is waste removed from the peritoneal
cavity?
 Low MW compounds?
 Cells?
 Foreign bodies?
 Physical Removal
 Transmesothelial
 Small molecules
 H20
 Stomata/Lymphatics
 Peritoneal flow to
diaphragm 10 route...
 Functional Removal
 Localization
 Omental Trapping
 Fibrin Trapping
 Phagocytosis
 PMNs
 Macrophages
 Bacterial k...
 Functional Removal
 Localization
 Omental Trapping
 Fibrin Trapping
 Phagocytosis
 PMNs
 Macrophages
 Bacterial k...
 How does the peritoneum respond initially
(24hrs) to trauma?
 Vascular phase?
 Inflammatory cascade?
 Coagulation cas...
 Brief vasoconstriction
 Histamine, PGE2 release
 Local vasodilation & cell influx
 Procoagulant factors
 Platelets a...
 Local release of cytokines
 Cell migration to wound bed
 Platelet aggregation
 Coagulation cascade activation
 Initi...
 Close overlap with Inflammatory response
 Two pathways converging to one
 Intrinsic pathway
 BM damage & collagen exp...
 Thrombin
 Cleaves soluble circulating fibrinogen into insoluble
fibrin clots
 Factor XII stimulates clot formation and...
 How does a peritoneal defect heal?
 What is the timing?
 Where do new cells come from?
 Are there differences in cell...
 12-24 hrs – PMNs
 24 hrs + macrophages
 Cytokine release
 Day 3
 Mesothelial and fibroblast cells appear
 Area of l...
 Species variation?
 tPA vs PAI baseline
 Human, horses, dogs – tPA high
 Cows – PAI high
 Post-injury
 Most: tPA down, PAI up
 Cow: PAI...
 Describe the steps in adhesion formation.
 What key enzymes are involved?
 How are these enzymes affected by trauma?
 What is the incidence of post-op adhesions?
 In people?
 In horses?
 Which structures are most commonly involved
in i...
 Humans
 67%-93%
 Horses
 9%-32%
 Caveats?
 Canine/Feline
 Low
 Equine
 SI procedures
 Regardless of procedure
 SI
 Ventral incision
 Why??
 Are there any beneficial effects of peritoneal
adhesions?
Beneficial Effects
 Seal Breaks in
continuity
 Prevent visceral
leakage
 Neovascularization
 Stabilize mobile
viscera
...
Beneficial Effects
 Seal Breaks in
continuity
 Prevent visceral
leakage
 Neovascularization
 Stabilize mobile
viscera
...
 What are common stimuli for adhesions?
 Suturing
Peritoneum!!
 Ischemia
 Serosal trauma
 Drying
 Abrasion
 Others
 Foreign bodies
 Bacteria
 List preventative methods (and mechanisms)
for reduction of adhesions
 Avoid serosal trauma
 Reduce/avoid foreign bodies
 Minimize ischemic tissue
 Minimize bacterial contamination
 Consi...
 Solid barriers
 Seprafilm (CMC & HA)
 Interceed (oxidized cellulose)
 Hyaluronate membranes
 CMC
 Omentectomy(x)
 ...
 Fucoidan
 Chitosan dextran
 Hydrogel (PCEC)
 Aldehyde dextran
 Parecoxib
 Alginate gell
 Statins
Peritoneal Healing, Cow/Horse
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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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Transcript of "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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