This document discusses the histology, innervation, functions, and healing process of the peritoneum. It covers the layers of the peritoneum, how it is innervated leading to pain perception, its roles in nutrient diffusion, fluid production, and waste removal. The document also summarizes the inflammatory and coagulation cascades triggered by peritoneal trauma, as well as preventative methods for reducing post-operative adhesions.

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