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

1. Micky Trent DVM DACVS

2.  What are the histologic layers of normal
peritoneum?
 Which vary by species?

3.  Layers
 Mesothelial Cells
 Basement membrane
 Submesothelial
connective tissue
 Loose c.t.
 Species variation

4.  What are the layers of peritoneum?
 What is the peritoneal space?

5.  Peritonal cavity
 Layers
 Parietal
 Visceral

6.  How is peritoneum innervated?
 Why should we as surgeons care?

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.  What abdominal structures are considered
retroperitoneal?
 Why should we as surgeons care?

9.  List 4 critical functions that depend on the
peritoneum.

10.  Cell nutrition
 Peritoneal fluid production
 Maintain gliding surfaces
 Waste control

11.  Cell Nutrition
 Diffusion
 Produce Peritoneal
Fluid
 Transudate from
blood
 Inflammation
changes volume and
character

12.  Maintain Gliding
Surface
 Surface villi trap
fluid
 Peritoneal fluid
 Plasminogen
activators
 Mesothelial cells
 Fibrin break down
 Depressed with
peritoneal trauma

13.  How is waste removed from the peritoneal
cavity?
 Low MW compounds?
 Cells?
 Foreign bodies?

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.  Functional Removal
 Localization
 Omental Trapping
 Fibrin Trapping
 Phagocytosis
 PMNs
 Macrophages
 Bacterial kill

16.  Functional Removal
 Localization
 Omental Trapping
 Fibrin Trapping
 Phagocytosis
 PMNs
 Macrophages
 Bacterial kill

17.  How does the peritoneum respond initially
(24hrs) to trauma?
 Vascular phase?
 Inflammatory cascade?
 Coagulation cascade?
 Link between inflammation and coagulation?

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.  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.  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.  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.  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.  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.  Species variation?

25.  tPA vs PAI baseline
 Human, horses, dogs – tPA high
 Cows – PAI high
 Post-injury
 Most: tPA down, PAI up
 Cow: PAI up

26.  Describe the steps in adhesion formation.
 What key enzymes are involved?
 How are these enzymes affected by trauma?

28.  What is the incidence of post-op adhesions?
 In people?
 In horses?
 Which structures are most commonly involved
in identified cases in horses?
 Why?

29.  Humans
 67%-93%
 Horses
 9%-32%
 Caveats?
 Canine/Feline
 Low

30.  Equine
 SI procedures
 Regardless of procedure
 SI
 Ventral incision
 Why??

31.  Are there any beneficial effects of peritoneal
adhesions?

32. Beneficial Effects
 Seal Breaks in
continuity
 Prevent visceral
leakage
 Neovascularization
 Stabilize mobile
viscera
 Bovine, canine,
equine

33. Beneficial Effects
 Seal Breaks in
continuity
 Prevent visceral
leakage
 Neovascularization
 Stabilize mobile
viscera
 Bovine, canine,
equine

34.  What are common stimuli for adhesions?

35.  Suturing
Peritoneum!!
 Ischemia
 Serosal trauma
 Drying
 Abrasion
 Others
 Foreign bodies
 Bacteria

36.  List preventative methods (and mechanisms)
for reduction of adhesions

37.  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)

38.  Solid barriers
 Seprafilm (CMC & HA)
 Interceed (oxidized cellulose)
 Hyaluronate membranes
 CMC
 Omentectomy(x)
 Antiticoagulants - Heparin (x)
 Fibrinolytics – tPA (cost)
 Antiinflammatories (~)
 Lavage (?)
 Antioxidants (?)

39.  Fucoidan
 Chitosan dextran
 Hydrogel (PCEC)
 Aldehyde dextran
 Parecoxib
 Alginate gell
 Statins