Lecture-8

Systemic Pathology I
VPM 221
PATHOLOGY
OF THE
PERITONEUM
November 2008
Normal structure and function
• peritoneal
i
l cavity
i incompletely
i
l l divided
di id d into
i
compartments by
b
mesentery, omentum and ligaments, which are all lined by
mesothelium;; surface area greater
g
than that of the skin;;
• normal peritoneum: smooth, shiny membrane with just enough
fluid to keep it moist;
• fibrinolytic activity of mesothelium;
• resident population of
macrophages,
h
replenished
l i h d by
b
blood monocytes;
Normal structure and function (cont’d)
• partial compartmentalization of peritoneal cavity + adhesive ability
and blood supply of omentum / mesentery → possible sequestration
of bacterial infections;
• ascites (hydroperitoneum), due to
overproduction
d ti or diminished
di i i h d removall
of intraperitoneal fluid;
• hemoperitoneum in acute
traumatic injury;
• peritonitis.
Ascites
Hemoperitoneum
Chylous ascites
Abdominal fat necrosis (steatonecrosis)
Damage to adipocytes → formation of soaps,
soaps free cholesterol,
cholesterol free
radicals → marked inflammation, acute (hyperemia, neutrophils,
cellular debris) to chronic (macrophages, multinucleated giant cells,
fibrosis).
Abdominal fat necrosis (cont’d)
1. Enzymatic
y
Fat Necrosis.
ƒ acute pancreatic necrosis releases proteolytic and lipolytic
enzymes;
ƒ grossly:
• multifocal to confluent white masses of necrotic adipose tissue,
associated with inflammatory reaction (hyperemia
(hyperemia, fibrin);
• peripancreatic and, possibly, distant locations.
Multifocal fat necrosis (white areas) disseminated throughout the abdominal fat, pancreatitis, cat.
2. Multifocal Fat Necrosis.
ƒ
especially in fat sheep,
sheep occasionally in other species;
ƒ
pathogenesis: probably related to pressure ischemia (necrosis) of
the fat and subsequent inflammation;
ƒ
grossly: small, white, dry, firm or gritty plaques associated with
chronic inflammation.
(bovine –
perirenal fat)
http://w3.vet.cornell.edu
3. Massive Fat
Necrosis (diffuse lipogranulomatosis).
ƒ especially in fat cattle of the Channel Island breeds.
breeds
ƒ pathogenesis: increased production of saturated fatty acids in rumen
→ fat
at sto
stores
es so
solid
d at body te
temperature
pe atu e → pprone
o e to trauma
t au a / ischemic
sc e c
necrosis.
ƒ grossly: hard masses of necrotic fat in abdomen and elsewhere;
incidental, or may cause intestinal obstruction, compression of
ureters, or dystocia.
Steatitis (yellow fat disease)
ƒ seen in manyy species.
p
ƒ diet high in polyunsaturated fat and low in vitamin E, allowing
peroxidation of body fatty acids (e.g. cats on all-fish diet).
ƒ all fat stores are affected (= pansteatitis, including panniculitis).
http://w3.vet.cornell.edu
Great blue heron – pansteatitis? or massive fat necrosis
secondary to obesity?
cross section of stomach and perigastric fat
Inflammation - peritonitis
ƒ Very common in large animals,
animals less so in dogs and cats;
ƒ most often caused by bacteria, but also viruses, helminths and
cchemicals
e c s (e.g. bile,
b e, pancreatic
p c e c enzymes);
e y es);
ƒ classified as: primary or secondary, acute or chronic, localized or
diffuse, septic or nonseptic;
Inflammation - peritonitis (cont’d)
ƒ common causes:
►
bacteremia / septicemia, particularly in young animals:
serosal surfaces (peritoneum, pleura, pericardium), synovial
membranes of joints, and meninges normally have a large population
of macrophages,
macrophages replenished by blood monocytes; in young animals,
animals
monocytes phagocytize well but have limited bactericidal power,
and they end up transporting bacteria from other sites (e.g.
omphalitis,
h li i mucous membranes)
b
) to these
h
sites;
i
►
intestinal accident;
►
perforated viscera (stomach / abomasum, reticulum, uterus);
ƒ if the animal survives, sequelae may include fibrous adhesions /
intestinal obstruction.
Cattle
• high capacity for sequestration of infections;
• common causes: omphalophlebitis / septicemia (newborns);
pperforated reticulum / abomasum / uterus.
Acute: hyperemia
/ hemorrhage;
h
h
fibrin, (fibrinous
peritonits), cow
Cattle
Rupture of liver abscesses causes
septic peritonitis
subacute / chronic
fibrinopurulent
peritonitis – hardware
(adult)
subacute / chronic fibrinopurulent peritonitis –
perforated abomasal ulcer (calf)
Horse
• poor capacity for sequestration of infections;
• usually
ll acute andd fatal;
f l
• common causes: rupture of stomach;
intestinal accident (torsion,
(torsion volvulus,
volvulus sequestration);
• septicemia in foals: Rhodococcus equi, Actinobacillus equuli.
Pig
• neonatall septicemia
i
i (e.g.
(
colibacillosis);
lib ill i )
• fibrinous / fibrinosuppurative peritonitis (and polyserostitis / arthritis),
e g Hemophilus parasuis (Glasser
e.g.
(Glasser’ss disease)
disease), Mycoplasma spp.,
spp
Streptococcus suis type 2.
Focal foreign body (granulomatous) reaction (forgotten gauze)
Dog, Cat
• nocardiosis;
• uterine rupture, intestinal accidents.
Perforated gastric ulcers in a dog.
Nocardiosis, note the yellow granular
material (“sulfur granules”)
characteristic of this condition
Feline infectious peritonitis
p
ƒ incidence is low and sporadic;
• caused by feline coronaviruses – broad spectrum of virulence,
spontaneous mutations
i
are common → potential
i l for
f emergence off
more virulent strains;
• persistently infected healthy cats carry the virus in their intestine,
intestine
blood and tissues - reservoirs;
• disease is more common in young and aged cats, especially in
environments with close continuous contact among many cats.
Feline infectious peritonitis
Pathogenesis:
• ingestion
gest o oor inhalation
a at o of
o FCoV
CoV → replication
ep cat o in to
tonsils,
s s, intestinal
test a
epithelium, mesenteric lymph nodes → hematogenous spread and
some replication in monocytes / macrophages;
• ability of individual strains of FCoV to cause disease appears to
correlate with their ability to invade and replicate in monocytes /
macrophages;
• animal’s immune response, i.e humoral vs cell-mediated, determines
outcome of infection;;
• immune-complex disease → vasculitis;
• activated macrophages may have central in development of lesions.
lesions
Effusive form:
• serofibrinous pperitonitis ((upp to 1 litre of exudate)) and ppleuritis;;
• fluid is clear, viscous, pale to deep yellow, and contains fibrin strands;
• foci of necrosis or inflammatory nodules on serosal surfaces of viscera.
Marked abdominal distension due to the presence of fluid,
fluid FIP,
FIP
effusive form.
Effusive form (cont’d)
Both examples (top and left bottom)
show abundant clear yellow fluid
and abundant fibrin deposited on the
serosal surface
White foci of necrosis or nodules are
Sometimes present on serosal surfaces of
visceral organs
Effusive form (cont’d): vasculitis - fibrinoid necrosis of
several arterioles, necrosis of tissue ((mesenteric lymph
y p node).
)
Noneffusive form:
• nodular to locally extensive pyogranulomatous inflammation in
several organs;
• less severe peritoneal exudate.
Examples of pyogranulomatous nephritis resembling neoplastic
lesions (lymphoma), cats, FIP, dry form.
Noneffusive form (cont’d): meningitis, with vasculitis
Noneffusive form (cont’d): myocarditis, with vasculitis
Neoplasia
Mesothelioma
• rare malignant
li
t tumor;
t
seen mostt commonly
l as congenital
it l neoplasia
l i in
i calves;
l
• spread is usually by exfoliation / implantation, rather than by blood / lymph;
• must be differentiated from granulomatous peritonitis (e.g. tuberculosis) or
secondary neoplasia (e.g. carcinomatous implantation).
Lipoma
• common in horses;; arises from the mesentery,
y, often large
g and
pedunculated;
Lipoma (cont’d)
• can cause intestinal strangulation when peduncle winds around
loop of intestine.
http://w3.vet.cornell.edu
Secondary tumors
• Usually arise from exfoliation / implantation,
implantation rather than by
lymphogenous or hematogenous metastasis;
• carcinomas are more common than sarcomas.
Uterine carcinoma with metastases to the omentum,
bovine
Peritoneal carcinomatosis
3 examples of direct seeding of the peritoneal surface (cavity)
in two dogs (left) and a chicken (top right)
Disseminated hemangiosarcoma
(omentum), dog