ruminants peritonitis

1. PERITONITIS
Department of Veterinary Clinical Medicine Ethics and Jurisprudence
College of Veterinary and Animal Sciences

2. PERITONITIS
 Inflammation of the peritoneum
 Abdominal pain, fever, toxemia and reduction in
amount of feces
 Symptoms vary with severity and extent

3. ETIOLOGY
 Primary
 Secondary Specific disease
Injury of serosal surfaces (AT)
Exterior traumatic injury
Perforation of reproductive tract

4.  Cattle
1. Traumatic reticuloperitonitis
2. Secondary to ruminal trocarization
3. Perforation / leakage of abomasal ulcer
4. Concurrent abomasal displacement
5. Necrosis and rupture of abomasal wall after abomasal volvulus
6. Rumenitis subsequent to acute carbohydrate indigestion
7. Complication of caesarean section
8. Rupture of vagina
9. Deposition of semen into peritoneal cavity by any means

5. 10. Injection of sterile hypertonic solutions, e.g. calcium preparations
(chemical peritonitis results lead to constrictive adhesions between
loops)
11. Transection of small intestine (becomes pinched between the
uterus and pelvic cavity at parturition)
12. Intraperitoneal injection of nonsterile solutions
13. Spontaneous uterine rupture
14. Sadistic rupture of vagina
15. Spontaneous rupture of rectum
16. Specific diseases such as tuberculosis

6.  Sheep
1. Intestinal wall abscess – infestation - Esophagostomum sp.
Larvae
2. Serositis-arthritis - Mycoplasma sp.
 Goats
1. Serositis-arthritis - Mycoplasma sp.

7. PATHOGENESIS
 Six factors account for clinical findings
1. Toxemia and septicemia
 Bacteria and breakdown of tissue -toxins - absorbed – peritoneum
 Acute diffuse peritonitis - toxemia is profound
2. Abdominal pain
 Acute, diffuse peritonitis - toxemia - depress - response – pain stimuli
(severe)
 Arched-back posture -evidence of pain on palpation (less severe)
 Inflammation of serous surfaces of the peritoneum causes pain
 Rigidity of abdominal wall and abnormal humped-up posture.

8. 3. Shock and hemorrhage
 Sudden deposition of gut contents, infected uterine contents, Into peritoneal
cavity
 Hemorrhage resulting from the rupture
4. Paralytic ileus
 Result of reflex inhibition of alimentary tract tone and movement in acute
peritonitis
5. Accumulation of fluid exudate
 Accumulation inflammatory exudate - cause visible abdominal distension
 If severe, interfere with respiration - obstruction of diaphragmatic movement

9. 6. Adhesions
Trauma
 Peritoneal mesothelial cells - source of plasminogen activators
 Cattle have a high capacity - respond to trauma with fibrin deposition
 Intra-abdominal fibrin deposition and adhesion formation is the most
important
factor in localizing peritonitis
Serosanguineous exudate
Fibrinogen Plasminogen
Fibrin
Thrombin
Early fibrinous adhesion
plasmin
Plasminogen activato
lysis of the early adhesion
(Fibrinolytic
enzyme )

10. CLINICAL FINDINGS
 Acute and subacute peritonitis
 Inappetence (less severe and chronic cases )
 complete anorexia in acute diffuse peritonitis
 Toxemia and fever
Acute local peritonitis (39.5°C ; 103°F) - first 24-36 hours
Then return to normal - animal may still be partly or completely anorexic.
A high fever (up to 41°c; 106°f) - acute diffuse peritonitis
Terminal stages - falls to subnormal
 Feces
Transit time of ingesta - increased - dry matter increases- amount reduced
In early stages increased frequency of passage of small volumes of soft feces (
X )
Pastured cattle - scant, dark and small fecal balls with thick, jelly-like mucus

11.  Alimentary tract stasis
Acute peritonitis ruminal contractions are reduced or absent
Chronic peritonitis contractions may be present but are weaker than normal
 Abdominal pain evidenced by posture and movement
Acute peritonitis - disinclination to move, lie down
Lying down with great care and grunting with pain.
Posture arched back,
Gait back held rigid and arched.
Grunting at each step
Absence of kicking or bellowing or licking the coat.

12.  Withers pinch test
Abnormal - no movement or kyphosis
Normal – lordosis / dorsiflex back
 Grunt test
Applying pressure to the xyphoid process
to see if the cow grunts

13.  Rectal examination
Palpate slightly distended, saggy, thickwalled loops of intestine
Tough, fibrous adhesions may be present in long-standing cases (usually
caudal part)

14.  Peracute diffuse peritonitis
 Severe weakness,
 Depression
 Circulatory failure
 Recumbent and often unable to rise
 Subnormal temperature (99-100°F)
 High heart rate (1l0-120/min) ; weak pulse
 No abdominal pain is evidenced (Palpation)
 Usually die within 24-48 hours

15.  Chronic peritonitis
 Adhesions - interfere - normal alimentary tract movements
 Adhesions break down- combine – indigestion and toxemia
 Marked abdominal distension with many liters of turbid-infected fluid
(omental bursa)

16. DIAGNOSIS
 Clinical features
 Diagnostic medical imaging
Inflammatory fibrinous changes, and abscesses can be imaged
 Clinical pathology
 Total and differential leukocyte count
Leukopenia, neutropenia and a marked increase in immature
Neutrophils (degenerative left shift)
Normal total leukocyte count,or slight increase (regenerative left shift)
Leukocytosis with marked neutrophilia , occasionally increase in the total
numbers of lymphocytes and monocytes
 Plasma fibrinogen levels tend to increase as severity of acute peritonitis
increases
Acute diffuse
peritonitis
Acute local
peritonitis
Chronic peritonitis

17.  Abdominocentesis and peritoneal fluid
Amount of fluid
Bloodstained- damage to a wall of the viscera
Presence of feed or fecal material - intestinal ischemic necrosis / rupture
Clots and high protein content-inflammation
Number and kinds of leukocytes -presence of inflammation and duration
Microbiological examination

18. DIFFERENTIAL DIAGNOSIS
 Acute local peritonitis –
Traumatic reticuloperitonitis
Acute intestinal
Obstruction
Splenic or hepatic abscess
Simple indigestion
Abomasal
Displacement (right and left)
Postpartum metritis, ketosis
 Acute diffuse peritonitis –
Parturient paresis
coliform mastitis (peracute form)
acute carbohydrate indigestion
perforation /rupture at abomasal ulcer
acute intestinal obstruction
uterine rupture, postpartum metritis

19.  Chronic peritonitis –
Vagus indigestion
lipomatosis or extensive fat
necrosis of the mesentery omentum
persistent minor leakage in intestinal lesion large
ascites
rupture of bladder
chronic pneumonia / toxemias

20. TREATMENT
 Specific cause must be treated
 Exploratory laparotomy - determine - cause of peritonitis
 Anti microbials –
Broad-spectrum antimicrobials (infection and toxemia)
(Choice dependent on ease of administration and drug withdrawal times)
 Administration of antimicrobials into the peritoneal cavity
On the basis higher levels of the drug may be achieved at the site of the
inflammation
 Fluid and electrolytes therapy (severe toxemia and shock)
 Nonsteroidal anti-inflammatory drugs
Flunixin meglumine 0.25-1.1 mg/kg BW intravenously
Every 8-12 hours (peritonitis is accompanied by shock)

21.  Lavage
Peritoneal lavage with large volumes of fluid containing antimicrobials
(large quantities of exudate present)

22. THANK YOU