Marvin KungBVSc, MANZCVSSurgical Registrar

Peritonitis

Overview

• Normal physiology and anatomy

• Pathophysiology

• Classifications

• Risk factors of GI leakage

Peritoneum - Anatomy

• Serous membrane with mesothelial cells and transversalis fascia

• Lines abdomen, pelvic and scrotal cavities

– Parietal

– Visceral

– Connecting

• Bi-directional and semipermeable

• 150% of total skin surface area

Peritoneum - Physiology

Fluid

• Small amount of viscous fluid present

• Larger amount in immature animals

• Dialysate of plasma – protein <3 g/dl

• <300 cells/µL - macrophages, mesothelialcells , lymphocytes

• Lacks fibrinogen – X clot

Peritoneum - Physiology

Drainage

Absorbed by lymphatics in diaphragm to mediastinal node

Particles <10 microns cleared ( Bacteria 0.5-2.0, RBCs 7-8 microns)

Bacterial peritonitis -> bacteremia

Peritoneum - Physiology

Drainage

Factors affecting drainage : (Hosgood et al 1989)

– Gravity

– Respiratory movements

– Diaphragmatic movement

– Intestinal activity

– Intraperitoneal pressure

Circulation

• Hosgood et al 1989 (Vet Surg)

– General cranial movement of fluid and particles

– Complete dispersion post injection

• 15-30 minutes cranial injection

• 60-120 minutes caudal injection

• Hosgood et al 1989 (Vet Surg)

– General cranial movement of fluid and particles

– Complete dispersion post injection

• 15-30 minutes cranial injection

• 60-120 minutes caudal injection

Healing - Mesothelium

• Injures easily but heals rapidly – denuded areas heal by day 3 (Ellis 1971)

• Adhesions

– Occur with vascular damage -> fibroblasts can migrate

– Normally fibrinolysis occurs 3-4 days after formation, therefore no adhesions

Pathophysiology - Defences

• Innate immunologic mechanisms

• Absorption

• Ability to localise infection

Pathophysiology - Defences

• Innate immunologic mechanisms (Heel & Hall 1996)

– Complement system C3a and C5a • Stimulates chemotaxis of neutrophils

• Degranulation of basophils and mast cells

– Absorption through diaphragmatic lymphatics

– Phagocytosis

– Abscess formation

– Resident natural killer cells

Pathophysiology - Defences

• Secondary amplification system (Heel & Hall 1996)

– Immunoglobin production at omental and peritoneum-associated lymphoid tissue

Pathophysiology – Inflammatory response

• Influx of protein-rich fluid from vascular space along macrophages and neutrophils

• Activation of humoral opsonins, antibodies, and complement

• Complement : ↑inflammatory response(Hall et al 1998) Opsonisation

Clearing immune complexesCell lysisChemotaxis

Pathophysiology – Inflammatory response

• Mast cells degranulation- Histamine and prostaglandin causing increased permeability -> exudation of fluid rich in complement, immunoglobins, fibrin, clotting factors

- Releases complement and opsonins

Pathophysiology – Inflammatory response

Peritoneal fibrinolytic system deactivated

↓ Fibrin clearance

↑Fibrin clumps

Hide bacteria ↓Clearance Adhesions

Pathophysiology – Inflammatory response ( Cytokines)

TNF-αIL-1B

Peritoneal mesothelial cells IL-8

Macrophages

Arachidonic acid metabolism

↑Prostaglandins

Lymphocytes

TNF-α

Monocytes IL-10

Chemotaxis -Neutrophils

↓Proinflammatorymediators

IL-6

(Hall et al 1998)

Pathophysiology – Systemic

Hypovolemia

Increased abdopressure

Reflex rigidityIleus

Hypotension, Tissue hypoxia

– ARF– Metabolic acidosis– Pancreas releases

myocardial depressant factor

– ↓ Ventilation– Respiratory

acidosis– Hypoxemia

↓Cardiac venous return and output

Fluid movement into abdomen

Hypoproteinaemia

Adjuvants of Peritonitis

• Bile salts– Lower surface tension, altering cell adhesion, lysing

RBCs

• Haemoglobin– Interfering chemotaxis,phagocytosis,bacterial

clearance. Release of iron ?

• Gastric mucin– Heparin-like anticomplement effect ->↓phagocytosis

• Barium – Marked chemical peritonitis

Localising infection

• Omentum

• Ileus

• Reflex rigidity

• Adhesion

Pathophysiology - Summary

Classifications

• Primary vs Secondary (Tertiary?)

• Septic vs Aseptic

• Focal vs Generalised

• Acute vs Chronic

Classifications

• Primary : Spontaneous– Cats with FIP– Culp et al (2009) JAVMA

• 15 dogs , 9 cats with PP compared to 49 dogs, 11 cats with SP• Transudates more common in primary• predominantly Gram +ve (80% dogs, 60% cats)• Similar survival rates to SP

– Ruthrauff et al (2009) JAAHA• 12 cats, mortality rate 31% • Oral route suggested -> Bacteroides & Fusobacterium

– Various case reports• Salmonella, Chlamydia , Clostridium,Mycobacterium, Citrobacter,

Blastomyces, fungal, etc.

Classifications

• Secondary – most common – many causes

(neoplastic, necrosis, penetrating wounds, abscesses, etc)

***Leakage of gastrointestinal contents *** 47%-63%

Pathophysiology – GI leakage

• Severity of peritonitis related to site of leakage

• Colon – anaerobes:aerobes ≈ 1000:1

• Polymicrobial with predominance of E.coli and Bacteroides fragilis

• Early mortality – > high [endotoxin]

• Presence of B fragilis enhances lethality of E. coli (Hall et al 1998)

• Adjuvants also enhance bacterial growth

Pathophysiology – GI leakage

Exotoxin by E.coli : α-Hemolysin

– Toxic, allowing tissue invasion and destruction

– Decrease intraperitoneal pH

– Lyse intraperitoneal erythrocytes

– Reduce viable leukocytes

– Increases mortality

Risk factors of leakage

• Ralphs et al 2003 JAVMA– Anastomosis leakage risk factors

– 90 dogs, 25 cats

– 14% dogs developed leakage, none in cats

– Risk factors identified• Hypoalbuminaemia

• Preoperative peritonitis

• Presence of foreign body

• Blood products

• Left shift

Risk factors of leakage

• Grimes et al 2011 JAVMA – 197 dogs (225 surgeries)

- Full thickness GI incision (enterotomy, resection, biopsy)

- Risk factors identified :- Preoperative peritonitis

- Hypoalbuminaemia and hypoproteinaemia

- Hypotension

- Surgery and GA time

- Foreign body : protective

Risk factors of leakage

• Mouat et al 2014 JAAHA

– Longer section of bowel resected ?

– 35 dogs

• Humans

– Colorectal surgeries

Finishing up…

• Hypoproteinaemia** and hypovolemia

• Mortality 20-50 % (later studies)

• Poor prognostic indicators (various studies)– Anastomotic leakage (Ralphs et al 2003 )

– Lactate and clearance ( Cortellini et al 2014)

– Septic shock (Dickinson et al 2015)

– Etc

• Important to know risk factors of GI leakage

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Marvin KungBVSc, MANZCVSSurgical Registrar

References

1. Hosgood G, Salisbury SK, Cantwell HD: Intraperitoneal circulation and drainage in the dog. Vet Surg 18:261, 1989

2. Ellis H: Wound repair: reaction of the peritoneum to injury. Ann R Coll Surg Engl 60:219, 1978.

3. Heel KA, Hall JC: Peritoneal defences and peritoneum-associated lymphoid tissue. Br J Surg 83:1031, 1996.

4. Members ACCP/SCCM Consensus Conference Committee: American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference: Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. Crit Care Med 20:864, 1992.

5. Culp WT(1), Zeldis TE, Reese MS, Drobatz KJ. Primary bacterial peritonitis in dogs and cats: 24 cases (1990-2006). J Am Vet Med Assoc. 2009 Apr 1;234(7):906-13. doi: 10.2460/javma.234.7.906.

6. Ruthrauff CM, Smith J, Glerum L.. Primary bacterial septic peritonitis in cats: 13 cases. J Am Anim Hosp Assoc. 2009 Nov-Dec;45(6):268-76

7. Ralphs SC, Jessen CR, Lipowitz AJ: Risk factors for leakage following intestinal anastomosis in dogs and cats: 115 cases (1991–2000). J Am Vet Med Assoc223:73, 2003

8. Grimes JA, Schmiedt CW, Cornell KK, et al. Identification of risk factors for septic peritonitis and failure to survive following gastrointestinal surgery in dogs. Journal of the American Veterinary Medical Association. 2011;238:486–494.

9. Mouat EE, Davis GJ, Drobatz KJ, Wallace KA. Evaluation of data from 35 dogs pertaining to dehiscence following intestinal resection and anastomosis. J Am Anim Hosp Assoc. 2014 Jul-Aug;50(4):254-63

10. Dickinson AE, Summers JF, Wignal J, Boag AK, Keir I. Impact of appropriate empirical antimicrobial therapy on outcome of dogs with septic peritonitis.. J Vet Emerg Crit Care (San Antonio). 2015 Jan;25(1):152-9. doi:10.1111/vec.12273. Epub 2014 Dec 26.

11. Cortellini S, Seth M, Kellett-Gregory LM. Plasma lactate concentrations in septic peritonitis: A retrospective study of 83 dogs (2007-2012).J Vet EmergCrit Care (San Antonio). 2014 Sep 11. doi: 10.1111/vec.12234. [Epub ahead of print]