Peritonitis: Introduction

Etiology
Pathogenesis
Clinical Findings
Diagnosis
Treatment

Inflammation of the peritoneum may be acute or chronic, local or diffuse, and most commonly is
secondary to contamination of the peritoneal cavity. It is often accompanied by abdominal pain,
fever, toxemia, and reduced fecal output.
Etiology:
Primary peritonitis is infrequent. It may be caused by infectious agents such as feline
infectious peritonitis virus ( Feline Infectious Peritonitis and Pleuritis: Introduction),
Nocardia spp , or Mycobacterium spp . Access to the peritoneal cavity is generally by the
hematogenous route. Progression of primary peritonitis tends to be chronic (days to
weeks).
Secondary peritonitis is often acute and results in rapid, progressive, systemic illness. It is
most commonly associated with GI perforation or dehiscence of abdominal wound
closure, or with perforation of other infected viscera (eg, prostatic or hepatic abscess,
pyometra). Penetrating abdominal injuries may lacerate viscera or inoculate the peritoneal
cavity with foreign material and microorganisms. Peritonitis may also occur secondary to
chemical irritants (eg, bile, urine) and to other disease processes that allow transmural
migration of bacteria (eg, neoplasia, visceral ischemia). Peritonitis from chemical
irritation or foreign bodies (eg, sponge) may be septic or nonseptic. Septic peritonitis may
remain localized if the omentum or mesentery contains the septic process, which
sometimes results in formation of an abdominal abscess.
In large animals, peritonitis is most commonly seen in cattle, less often in horses, and
rarely in pigs, sheep, and goats. As well, it is a serious and often fatal condition in small
animals, with mortality suggested to be as high as 68%.
In large animals, peritonitis most commonly results from injury to the serosal surface of
the GI tract, which allows intestinal contents to leak into the peritoneal cavity. Other
causes include traumatic perforations of the abdominal wall or reproductive tract and
introduction of pathogens or irritants via injection or surgery (Table: Common Causes of
Peritonitis in Livestock).
Microorganisms associated with septic peritonitis reflect the source of contamination. A
mixed bacterial population is seen in GI perforation (coliforms, anaerobes), whereas
perforation of nongastrointestinal viscera (eg, gallbladder, uterus, prostate) may be
associated with aerobic organisms including Escherichia coli , Staphylococcus , Proteus
spp , and less commonly, Klebsiella , Enterobacter , Pseudomonas , and Corynebacterium
. In horses, Streptococcus equi and Rhodococcus equi may be associated with peritonitis.
Pathogenesis:
Toxemia and septicemia, shock, hemorrhage, abdominal pain, paralytic ileus, fluid
accumulation, and adhesions all contribute to the clinical signs and progression of
peritonitis. Toxins produced by bacteria and tissue breakdown are readily absorbed
through the peritoneum. Bacterial or chemical irritants increase serosal capillary
permeability resulting in leakage of plasma proteins, solutes, and water into the peritoneal
cavity. Exudation of protein-rich fluid can result in hypoproteinemia and bacterial
proliferation. Endotoxins absorbed from the peritoneal cavity have systemic effects
leading to hypotension, shock, and systemic inflammatory response syndrome (SIRS) and
disseminated intravascular coagulation (DIC). Endotoxins, myocardial depressant factor,
acid-base, and electrolyte disturbances directly affect the cardiac function, leading to
reduced cardiac output. The combined effect of large fluid losses into the peritoneal
cavity and vasodilatory effects of absorbed toxins can produce profound hypotension and
hypovolemia. Rupture of the GI tract, with spillage of large volumes of intestinal
contents, leads to acute peritonitis. Death due to endotoxic shock may occur suddenly
with limited clinical signs or lesions. Shock and hemorrhage associated with rupture of
the gut or uterus often lead to death in animals with infection of the GI or reproductive
tracts; however, shock and hemorrhage may be minor following uterine rupture in cows.
Peritonitis may not develop if the uterine contents are not contaminated, but it may follow
if the uterus is not repaired or healed within a few days. Paralytic ileus is a frequent result
of acute peritonitis and may also follow intestinal obstruction or surgery, leading to
functional obstruction and increased mortality rate if it persists. Large volumes of
inflammatory exudates may be secreted into the peritoneal cavity during peritonitis and
may lead to impaired respiration by impinging on the diaphragm. Peritoneal trauma leads
to secretion of fibrinogen and formation of fibrinous adhesions. Such adhesions help
localize the inflammation but may cause mechanical or functional obstruction of the GI
tract.
Clinical Findings:
Signs are nonspecific and vary depending on the type of peritonitis (primary or
secondary). Abdominal pain may be generalized and severe, so that the animal guards the
abdomen, walks with a stiff gait, or is recumbent. Cattle may have a shuffling, cautious
gait, with a rigid, arched back; grunting when walking or when passing urine or feces is
common. Deep, firm palpation of the abdominal wall results in an easily recognized pain
response in cattle. Pain responses in all species are most evident in the early stages of the
disease. Fever is common but may be suppressed by prostaglandin inhibitors. Fever
(103.5-106°F [39.7-41.1°C]) is a common clinical finding in dogs with peritonitis, while
cats may be hypothermic with peritonitis and concomitant shock. Abdominal distention,
which may be inapparent, usually is due to accumulation of peritoneal exudate and may
be accompanied by hemorrhage, septicemia, toxemia, paralytic ileus, shock, and
adhesions. Fluid transudation sequesters electrolytes and protein in the abdominal cavity
and atonic gut, and venous stasis leads to hypotension, acid-base disturbances, and
circulatory collapse. Toxemia and bacteremia contribute to shock. Icterus may be present
in generalized biliary peritonitis. Animals with secondary peritonitis may also exhibit
signs of the primary illness.
In small animals, anorexia and depression are often accompanied by vomiting, and feces
may not be passed. Dehydration, hypovolemia, and sepsis may result in hypothermia and
death due to loss of extravascular fluid volume. In large animals, complete anorexia may
be seen in acute, diffuse peritonitis, while decreased appetite may occur in less severe and
chronic cases.
In horses, clinical signs include severe colic, ileus, distended intestines on rectal
examination, gastric reflux, and occasionally diarrhea. Intestinal stasis leads to reduced
peristaltic sounds but sounds of paralytic ileus may be audible and should be
differentiated from normal gut sounds. The horse is restless and may lie down and roll
intermittently. Tachycardia, weak pulses, poor peripheral perfusion, and fever are
common. Septic peritonitis is frequently fatal, despite intensive treatment.
In cattle, rumination ceases and milk production drops. In chronic cases, ruminal
contractions may be present but reduced in intensity. Abdominal percussion may detect
ruminal tympany. Fever (103°F [39.5°C]) is typical during the first 24-36 hr in cattle with
acute, local peritonitis. High fever (up to 106°F [41.5°C]) suggests acute, diffuse
peritonitis.
Fecal output in large animals is reduced, although there may be an increased frequency of
defecation in the early stages of peritonitis that gives the impression of increased
production. Feces may be completely absent for as long as 3 days, even in animals that
recover. Rectal palpation may reveal tacky, dry mucosa and fibrinous adhesions between
intestinal loops.
Peracute, diffuse peritonitis is associated with extreme weakness, depression, and
circulatory failure (tachycardia with a weak pulse). Body temperature is often subnormal
(99-100°F [37-37.5°C]). Abdominal pain is not evident. In cases of cecal rupture during
foaling, mares suddenly stop straining, and progress toward parturition stops. Shock
develops, followed by death in 4-5 hr.
Chronic peritonitis is associated with development of fibrous adhesions. Cattle may have
chronic indigestion and toxemia, with periods of acute, severe illness caused by partial
intestinal obstruction. Liters of turbid, infected peritoneal fluid may be produced but may
be difficult to distinguish from ruminal contents on physical examination. Weight loss,
intermittent pain, and diminished gut sounds may be observed in horses with chronic
peritonitis.
Diagnosis:
Diagnosis can be difficult because the clinical signs are nonspecific.The most reliable
indicators of peritonitis include abnormal feces (in large animals, amount and
composition), intestinal stasis, abdominal pain (diffuse or focal), fibrinous or fibrous
abdominal adhesions, abnormal peritoneal fluid with an increased WBC count, and a
normal or low peripheral WBC count with a degenerative left shift. Peritonitis is rarely
diagnosed antemortem in pigs, sheep, or goats.
In dogs with septic effusion, peritoneal glucose concentration is often lower than blood
glucose concentration. A blood-to-fluid glucose difference of >20 mg/dL has been found
to be 100% sensitive and specific for diagnosis of septic peritonitis. In addition, a blood-
to-fluid lactate difference of <2.0 mmol/L is equally sensitive and specific. In cats, blood-
to-fluid glucose difference was 86% sensitive and 100% specific for septic peritonitis.
Abdominal radiographs may reveal GI obstruction (bowel dilatation, free abdominal air),
ascites, or radiodense foreign material. Loss of serosal detail (a “ground glass”
appearance) is indicative of abdominal fluid. Ultrasonography is a valuable adjunct test to
evaluate size, shape, and contents of other viscera (eg, gallbladder, prostate gland)
suspected to be the source of peritonitis. Rectal palpation in large animals is a useful
means of evaluating the intestines. Abdominal paracentesis should be used in large and
small animals to obtain fluid for cytologic examination and culture (Table:
Characteristics of Adult Bovine and Equine Peritoneal Fluid, Table: Peritoneal Fluid
Characteristics and Classification in Dogs and Cats). Diagnostic peritoneal lavage is
used when small amounts of fluid cannot be obtained by paracentesis. Cytologic
examination of abdominal fluid may reveal septic or nonseptic suppurative inflammation
with one or more bacterial infections. Neutrophils are degenerative in the presence of
sepsis.
The presence of intra- or extracellular bacteria confirms septic peritonitis. A number of
serum biochemical abnormalities may accompany peritonitis. Anemia is commonly
associated with any inflammatory disease process in dogs and cats. Hypoglycemia may
develop but is not reliably present. Cats <6 mo of age appear more likely to present with a
low blood glucose concentration (likely due to decreased glycogen and body fat reserves).
Hypoalbuminemia and hyperbilirubinemia are frequently present in dogs and cats. Many
septic dogs show cholestasis histopathologically, but this has not been found in septic
cats. In contrast to reported findings in other species, cats rarely have an associated
increase in serum alkaline phosphatase. Additional causes of icterus in septic animals
might include hemolysis (immune-mediated, toxic, or secondary to electrolyte
derangements), with or without a decreased capacity for hepatic hemoglobin metabolism.
Total and differential WBC counts are helpful in establishing a diagnosis and determining
severity of peritonitis. Acute, diffuse peritonitis with toxemia is usually accompanied by
leukopenia, neutropenia, and a marked increase in immature neutrophils (degenerative
left shift). In less severe acute peritonitis, leukocytosis may occur as a result of increased
neutrophil production. Acute, localized peritonitis may reveal a normal WBC count with
a regenerative left shift. The total WBC count in chronic peritonitis may be normal, with
an occasional increase in lymphocytes and monocytes.
Treatment:
Initial treatment must be directed toward stabilizing the metabolic consequences of
peritonitis (electrolytes, acid-base, coagulation abnormalities) as well as determining the
nidus of inflammation/infection and correcting or excising it. Replacement fluids,
electrolytes, plasma, or whole blood may be necessary to maintain cardiac output. Broad-
spectrum antimicrobial therapy should be initiated, usually by a parenteral route, once
appropriate samples have been collected for cytologic evaluation and culture and
sensitivity. Aminoglycoside or quinoline antibiotics are effective against gram-negative
organisms, and penicillins or cephalosporins are effective against gram-positive
organisms. The antimicrobial selected may be changed after sensitivity testing has been
performed. There are no published clinical reports of the effectiveness of antimicrobials
for treating peritonitis in cattle and horses. Cattle are typically treated with broad-
spectrum antimicrobials; the specific choice depends on ease of use and drug withdrawal
times. Antimicrobials used for peritonitis in horses include gentamicin (2.2-3.3 mg/kg,
IV, bid-tid ), penicillin (22,000 IU/kg, IV or IM, bid-qid ), and metronidazole (15-25
mg/kg, PO).
In small animals, antimicrobial choice is often empirical initially. Multiple isolates are
likely, including gram-negative, gram-positive, aerobic, and anaerobic organisms. For
combination therapy, enrofloxacin or aminoglycosides (for gram-negative organisms)
may be combined with penicillins, first-generation cephalosporins, or clindamycin (for
gram-positive anaerobic organisms). Second- or third-generation cephalosporins or
imipenum are good candidates for single-agent therapy. Appropriate antibiotics should be
started once septic peritonitis is confirmed and fluid samples are obtained for culture and
sensitivity.
Once the animal is stabilized, surgery is done to explore the abdomen and to repair any
defects (eg, a ruptured viscus). This is followed by thorough peritoneal lavage with an
isothermic, isotonic, balanced electrolyte solution. There is no proven clinical benefit in
adding an antimicrobial to the lavage solution. Solutions containing antiseptics (eg,
povidone-iodine) may induce chemical peritonitis and likewise have no proven clinical
benefit. Abdominal drains to allow postoperative lavage and open peritoneal drainage
(small animals) are sometimes used to treat severe peritonitis. Survival in dogs and cats
managed with closed versus open drainage is very similar. The decision to manage a
small animal patient with open peritoneal drainage is often based on experience level and
severity of the case. Maintaining patency of drains can be difficult, especially in cattle. In
animals treated by open peritoneal drainage, serum protein and electrolyte levels should
be monitored periodically, because both are lost with drainage of exudate. Parenteral
antimicrobials are continued postoperatively based on either empiric choice or culture and
sensitivity data if available. Nutritional support should be anticipated, as many animals
with peritonitis will not eat postoperatively. Enteral nutrition helps maintain the health of
the intestinal mucosa; however, vomiting or anorexia may force the consideration of
alternatives. Feeding tube placement in small animals (esophagostomy, gastrostomy, or
jejunostomy tubes) at the time of surgical closure is easily performed. In certain patients,
parenteral nutrition (total or partial) may be viewed as a way to provide a portion of the
nutritional requirements while enteral nutrition is being initiated. Hyperalimentation, or
alimentation by feeding-tube gastrostomy and catheter jejunostomy may be needed in
anorectic animals.
In animals with toxemia and shock, IV fluids and electrolytes are crucial elements of
treatment, especially during the first 24-72 hr following surgery in horses. Flunixin
meglumine (0.25-1.1 mg/kg, IV, bid-tid ) is recommended for treatment of shock,
although efficacy is unknown.