C H A P T E R

Peritonitis

80

ANDREW J. DART HANNAH-SOPHIE CHAPMAN

ANATOMY AND PHYSIOLOGY

The peritoneum is a single layer of squamous mesothelial

cells resting on a loose connective tissue containing blood
vessels, lymphatics, and nerves. Anatomically, the peritoneum is divided into a parietal and visceral peritoneum. The
parietal peritoneum lines the diaphragm, abdominal walls,
and pelvic cavity. The parietal peritoneum is continuous
with the visceral peritoneum, which encloses the intraperitoneal organs and forms the omentum and mesenteries of
the abdominal cavities. A small volume of peritoneal fluid
lubricates the surface of the visceral and parietal peritoneum.
Together the peritoneum and fluid are responsible for preventing adhesion formation. Normal peritoneal fluid is a
transparent straw-colored ultrafiltrate of plasma with a total
protein (TP) concentration of less than 1.5g/dL (15g/L) and
total nucleated cell count (TNCC) of less than 2000 cells/L
(2 109 cells/L). The distribution and consistent turnover of
peritoneal fluid ensures a highly effective clearance mechanism for bacteria, cells, and foreign material entering the
peritoneal cavity. Neutrophils represent 24% to 60% of the
cells found in peritoneal fluid. Protein concentrations greater
than 2.0 to 2.5mg/dL (20 to 25g/L) and TNCCs greater than
5000 to10,000 cells/L (5 to 10 109 cells/L) are considered
abnormal.

PATHOPHYSIOLOGY

Peritonitis in the horse may have an infectious (bacterial,

viral, fungal, or parasitic) or noninfectious (traumatic, chemical, or neoplastic) cause (Box 80-1). It is classified as primary
or secondary (defined by cause); peracute, acute, or chronic
(defined by onset and duration); diffuse or localized (defined
by region); and septic or nonseptic (defined by the presence
or absence of bacteria).
Acute, diffuse, septic peritonitis secondary to surgical
manipulation or perforation of the gastrointestinal tract is
the most common manifestation of peritonitis in the horse.
Sepsis usually involves a mixed bacterial population, whether
from gastrointestinal origin or from environmental contamination following trauma (Box 80-2). Common bacterial isolates from exudative peritonitis include the Enterobacteriaceae,
obligate anaerobic bacteria, and gram-positive organisms.
Anaerobic bacteria are reported to be present in at least 20%
to 40% of cases of peritonitis. It has been suggested that
established infections are often characterized by a few organisms despite the variety of organisms that might initially be
introduced. This is proposed to occur through a process of
selective competition between bacteria.
The phases of peritonitis are often separated. The contamination phase lasts 3 to 6 hours and is characterized by
increased vascular permeability and influx of protein-rich
fluid and white cells into the peritoneal cavity, resulting in
the release of mediators of inflammation. Diffuse acute peritonitis lasts up to 5 days and reflects the spread of bacteria

throughout the peritoneal cavity. The inflammatory response

escalates with fluid accumulation and buildup of fibrin and
inflammatory products, resulting in ileus mediated by the
sympathetic nervous system. These processes serve to confine
the spread of contamination. However, if bacteria overwhelm
the immune system, bacteremia and endotoxemia develop,
resulting in hypovolemia and hypoproteinemia and ultimately adhesions and abscess formation. This phase is associated with the highest mortality rate. The acute localizing phase
develops 4 to 10 days after the initial insult. Fibrin aggregates
attempt to localize the infection. Chronic abscess formation
starts as early as 8 days and persists until the body isolates
the infection.

CLINICAL SIGNS

Clinical signs are often nonspecific, irrespective of cause, and

may include fever, signs of depression, inappetence, tachycardia, dehydration, reduced gastrointestinal motility, signs
of abdominal pain, diarrhea, and weight loss. Clinical signs
in horses with septic peritonitis are usually more severe than
those with nonseptic peritonitis because of the systemic
effects of bacteremia and endotoxemia. The exception is
peritonitis caused by Actinobacillus equulithese horses often
have malaise, inappetence, fever, and mild signs of abdominal pain with few other localizing signs.
Horses with peracute peritonitis may be found dead or
showing signs of severe endotoxemia, which leads rapidly to
circulatory shock and death in a matter of hours. Typical
findings include severe depression, sweating, muscle fasciculations, tachycardia, rapid shallow breathing, cold extrem
ities, and purple or dark red mucous membranes with
prolonged capillary refill times. Fever is often not a feature
because of the peracute nature of the disease. Acute peritonitis
has a slower onset with the gradual spread of bacteria within
the abdomen. Horses may have a history of showing signs
of intermittent abdominal pain, and may show signs of
depression, inappetence, fever, dehydration, tachycardia,
tachypnea, congested mucous membranes with delayed
refill time, and ileus or diarrhea. Chronic peritonitis may be
associated with low-grade and nonspecific signs including
intermittent or persistent fever, signs of depression and inappetence, progressive weight loss, dehydration, intermittent
mild abdominal pain, reduced fecal output, decreased intestinal motility, intermittent diarrhea, and ventral edema.

CLINICAL INVESTIGATION AND DIAGNOSIS

Procedures used to confirm a diagnosis may include hematology and serum biochemistry, abdominal paracentesis, rectal
palpation, ultrasonography, urogenital examination, laparoscopy, and exploratory laparotomy.
Changes in hematology and serum biochemistry vary
with the onset, severity, and type of peritonitis. Horses with
peracute peritonitis usually have a markedly high hematocrit

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SECTION

BOX 80-1

VI Gastrointestinal Disease

Common Causes of Peritonitis

in the Horse

Septic
Gastrointestinal
Surgical complications
Gastrointestinal tract rupture
Abdominal abscess
Rectal tear
Enterocentesis
Traumatic
Uterine tears
Reproductive accidents
Abdominal wounds
Other types of infection
Septicemia
Actinobacillus equuli infection
Urachal infection
Nonseptic
Verminous arteritis
Cyathostome migration
Uroperitoneum
Hemorrhage
Chemical agents
Neoplasia
Blunt trauma

BOX 80-2

Bacteria Commonly Isolated From

Horses With Peritonitis

Sole Pathogens
Actinobacillus equuli
Streptococcus equi subsp equi
Rhodococcus equi
Corynebacterium pseudotuberculosis
Escherichia coli
Enterobacteriaceae
Staphylococcus spp
Bacteroides spp
Peptostreptococcus spp
Clostridium spp
Fusobacterium spp

and serum hypoproteinemia associated with acute hypovolemia, fluid shifts, and sequestration of protein in the
abdomen. However, the serum protein concentration may
appear to be within normal range because of the acute concurrent loss of fluid and profound dehydration. A severe
leukopenia with neutropenia and degenerative left shift with
severe toxic changes in the neutrophils is common. Increases
in serum urea and creatinine associated with prerenal azotemia and electrolyte imbalances, including low ionized
calcium, hyponatremia, hypokalemia, and hypochloremia,
may be present and accompany metabolic acidosis. Horses
with acute peritonitis often have a high hematocrit and a
serum hypoproteinemia, characterized by low serum albumin
and a decrease in the albumin-to-globulin ratio. Fibrinogen
usually increases after 48 hours. Leukopenia and neutropenia
may be seen initially, followed by leukocytosis and neutrophilia with a degenerative left shift. Changes in serum electrolytes, urea, and creatinine, and changes in acid-base
balance, usually mirror, but may not be as severe as, those
in horses with peracute peritonitis. Hematology and serum

biochemistry can vary in horses with chronic peritonitis.

Horses may have a high hematocrit, although anemia associated with chronic disease may be a feature. Invariably there
will be leukocytosis and neutrophilia with, or without, a left
shift. In some cases the white cell count may be normal.
Serum protein may be elevated, with a hypergammaglobulinemia and increased fibrinogen offsetting any loss of
albumin, which may be mild. Serum electrolytes may be
normal even in the presence of prerenal azotemia and metabolic acidosis.
Abdominocentesis is central to the definitive diagnosis
of peritonitis. Fluid should be collected in an EDTA tube
for cytologic analysis, protein analysis, and Gram stain, in
plain sterile tubes for aerobic and anaerobic culture, and
in a lithium heparin tube if biochemical analysis is to be
requested. Routine evaluation of peritoneal fluid should
include a total protein concentration and both the total
nucleated and differential cell count. If the cell counts are
suggestive of a septic process, cytologic analysis and a Gram
stain should be performed and an anaerobic and aerobic
culture submitted.
Immediate visual examination of the peritoneal fluid
can be strongly indicative of peritonitis. Fluid is usually
abundant, cloudy, and turbid or may be thick and purulent.
In horses with vascular lesions of the intestine, fluid may
be red-tinged, bloody, or, in long-standing cases, take on a
darker appearance and develop an odor of necrotic tissue.
Brown-green fluid or fluid with green particulate matter may
indicate intestinal rupture. Blood contamination of normal
fluid should be distinguished from truly abnormal fluid or
fluid collected after internal hemorrhage. A sample contaminated by a splenic puncture usually has a hematocrit higher
than that of the peripheral blood. With blood contamination, platelets will be seen in the fluid, whereas with internal
hemorrhage, platelets are rarely seen, and erythrophagocytosis may be seen on the cytology smear.
Total protein values greater than 2 to 2.5mg/dL (20 to
25g/L) suggest inflammation and, with septic peritonitis,
may increase to 5mg/dL (50g/L) or higher. Fibrinogen
concentrations may be greater than 10mg/dL, reflecting
the acute inflammatory process. Total nucleated cell count
is usually markedly high in acute peritonitis (100,000 to
800,000 cells/L or 100 to 800 109 cells/L), whereas in
chronic peritonitis, TNCC is typically lower (20,000 to 40,000
cells/L or 20 to 40 109 cells/L). The TNCC does not always
reflect the etiology, severity, or prognosis, and the results of
peritoneal fluid analysis should be correlated with the clinical signs and progression of the disease. An example is peritonitis caused by A equuli, in which fluid is highly turbid and
often purulent, with a TNCC greater than 50,000 cells/L
(>50 109 cells/L). However, these horses characteristically
show mild clinical signs, have few changes on hematology
and serum biochemistry, and respond well to treatment.
In most cases of peritonitis, neutrophils account for more
than 90% of cells and, in septic peritonitis, have marked
degenerative changes on cytology. Free or phagocytosed bacteria may be cultured or cytologically identified in about 70%
of cases, whereas a positive culture alone may only be
obtained in as few as 16% to 25% of cases. Anaerobes are
isolated in only 20% of cases. A Gram stain may aid identification of bacteria and assist in choice of antimicrobial
therapy, particularly in the absence of a positive culture.
Failure to identify or culture bacteria should not rule out a
diagnosis of septic peritonitis.
Measurement of peritoneal fluid pH and comparison of
plasma and peritoneal glucose concentrations may be useful

CHAPTER

to distinguish septic from nonseptic peritonitis. A serum

to peritoneal glucose difference of greater than 50mg/dL
(2.8mmol/L) suggests septic peritonitis. Similarly, a peritoneal fluid pH of less than 7.3 with a peritoneal glucose of less
than 30mg/dL (1.7mmol/L) and fibrinogen of more than
200mg/dL may also suggest sepsis.
Ultrasound of the abdomen may show loops of intestine
in hyperechoic to echoic peritoneal fluid, fibrin deposits,
adhesions, and on occasion, an abdominal abscess. Rectal
palpation is usually not specific for the cause or type of peritonitis, and should not be relied on to make a definitive
diagnosis.

TREATMENT

Treatment aims are to identify and treat the underlying

cause; eliminate infection; reduce inflammation and relieve
pain; address hypovolemia, hypoproteinemia, and any electrolyte abnormalities; treat endotoxemia; and provide nutritional support.
Whether to treat peritonitis surgically or medically is controversial. In most cases, irrespective of cause, horses will
benefit from stabilization with medical therapy while the
cause is being investigated. Surgical treatment should be
reserved for horses in which surgical intervention is clearly
indicated or when the underlying cause cannot be determined and there is a failure to respond to medical therapy.
Isotonic balanced electrolyte solutions should be administered to replace the fluid deficit and meet ongoing losses.
Additional potassium and calcium can be added to the fluids
as required. Horses will require colloids, preferably plasma,
when the plasma protein concentration falls below 4g/dL
(40g/L). Administration of fresh or hyperimmune plasma
products will address some of the negative effects of bacteremia and endotoxemia. Restoration of the circulating fluid
volume will address the metabolic acidosis and prerenal azotemia in most cases. In ideal circumstances, the hematocrit,
total protein, acid-base balance, and electrolyte balance
should be monitored every 4 to 6 hours to assess the response
to treatment.
Antimicrobial therapy should be instituted immediately
after diagnosis and directed at treating a mixed infection of
gram-positive, gram-negative, and anaerobic bacteria (Table
80-1). Intravenous antimicrobials are preferred because they
TABLE 80-1 Dosages for Common Antimicrobial

Drugs Used to Treat Peritonitis

in the Horse
Antimicrobial

Dosage

Route

Interval

Sodium penicillin

22,00044,000IU/kg
22,00044,000IU/kg
22,000IU/kg
2-4mg/kg
6.6mg/kg
9-12mg/kg
15-25mg/kg
11-25mg/kg
5mg/kg
1.5-2.5mg/kg
30mg/kg

IV

q 6hr

IV

q 6hr

IM
IV
IV
IV
PO
IV
IV
PO
PO

q
q
q
q
q
q
q
q
q

Potassium penicillin
Procaine penicillin
Ceftiofur sodium
Gentamicin sulfate
Amikacin sulfate
Metronidazole
Sodium ampicillin
Enrofloxacin
Trimethoprim
sulfadiazine

12hr
8-12hr
24hr
8hr
6-12hr
6-8hr
24hr
12hr
12hr

80 Peritonitis

351

provide more reliable concentrations in the peritoneal fluid.

Penicillin or ceftiofur and gentamicin or amikacin are
commonly combined with metronidazole to provide broadspectrum coverage. Antimicrobial therapy can be modified
on the basis of the results of culture and sensitivity and
response to treatment. Aminoglycosides reach peritoneal
fluid concentrations that are 50% to 80% of serum levels
following intravenous administration. However, although
aminoglycosides can penetrate the capsule of intraabdominal abscesses, they are minimally active in the acidic environment within an abscess. Enrofloxacin may be more
effective for treatment of abdominal abscesses in adult
horses. Antimicrobial treatment should be continued until
clinical signs resolve and clinicopathologic parameters
return to normal. Monitoring peritoneal fluid total protein
concentration and TNCC may also indicate the response to
therapy, but repeated abdominocentesis causes peritoneal
inflammation, which may complicate interpretation of
results. Treatment may be protracted and continue for weeks
to months.
Peritonitis caused by A equuli commonly responds well
and rapidly to treatment with penicillin. However, resistance
to penicillin has been reported, so it is advisable to combine
penicillin with gentamicin to cover all contingencies until
culture and sensitivity results become available.
Flunixin meglumine (0.25 to 1.1mg/kg, IV, every 6 to 24
hours) is often used for pain relief and to reduce the effects
of prostaglandins. At the higher doses (1mg/kg, every 6 to
8 hours), it provides excellent pain relief, and at lower doses
(0.25mg/kg, every 4 to 6 hours), it is reported to ameliorate
some of the adverse effects of endotoxemia on cardiovascular
function.
Abdominal drainage and lavage removes excess fluid, bacteria, foreign material, degenerative neutrophils, inflammatory byproducts, blood, and fibrin. The effectiveness of
lavage solutions in dispersing and treating the extensive peritoneal surfaces has been debated, and there are concerns that
lavage solution may disseminate localized infection. Nonetheless drainage and lavage are likely to have beneficial
effects, particularly early in the disease process.
A 32-French thoracic catheter, Foley catheter, or mushroom drain is often used. Drains are usually placed on the
ventral midline and used as both the ingress and egress port.
However, addition of an ingress drain in the paralumbar
fossa has been used to improve the distribution of the lavage
solution. The drains can be inserted in the standing horse
with the use of regional anesthesia.
Isotonic balanced electrolyte solutions are used as the base
for the lavage solution. There is little evidence that the addition of antiseptics, antimicrobials, or heparin to the lavage
solution provides additional benefit. Lavage is commonly
performed twice daily. Ten to 30L of warmed isotonic electrolyte solution is gravity-fed into the abdomen, the drain is
plugged or clamped, and the horse is walked for 15 to 30
minutes to distribute the fluid within the abdomen before
draining. The volume of fluid retrieved should be similar to
the volume infused, and the color of the fluid provides an
indication of the response to therapy. After drainage, the
drain can be filled with heparinized saline before it is resealed.
Lavage is continued for several days, until the fluid retrieved
is more clear or the drain ceases to function. Complications
of peritoneal drainage and lavage include puncture of the
viscera during insertion, patient discomfort during infusion
of the lavage solution, subcutaneous edema fluid accumulation, infection or cellulitis around the insertion site, ascending infection, and herniation of omentum into the drain or

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VI Gastrointestinal Disease

out of the site of insertion. These complications can be minimized with diligent drain management.
Anthelmintic treatment may be required if there is suspicion of verminous arteritis secondary to migration of Strongylus vulgaris larvae or larval cyathostomes. Fenbendazole (10
to 15mg/kg, PO, for 5 days, or 50mg/kg, PO, for 3 days) and
ivermectin (0.2mg/kg, PO) may be suitable anthelmintics.

PROGNOSIS

Reported mortality rates vary from 25% to 75%. Horses with

peracute peritonitis have a poor prognosis. In general, horses
with peritonitis that develops after gastrointestinal surgery
and horses that respond poorly to initial treatment for peritonitis have a poorer prognosis. There is no single clinical or
laboratory parameter that can be reliably used to assess the
prognosis, but factors like endotoxemia, severe signs of
abdominal pain, and coagulopathies, and complications like
laminitis, ileus, and diarrhea will be associated with a poorer
prognosis. Horses with A equuli peritonitis usually respond
reliably and consistently to appropriate antimicrobial therapy
and have a favorable prognosis.

Suggested Readings
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Medicine. 2nd ed. St Louis: Mosby, 1996:742-749.
Dabareiner R. Peritonitis. In: Robinson NE, ed. Current
Veterinary Therapy. 4th ed. Philadelphia: WB Saunders,
1997;206-214.
Dabareiner R. Peritonitis. In: Smith B, ed. Large Animal
Internal Medicine. 4th ed. St Louis: Mosby, 2009:
761-767.
Davis JL. Treatment of peritonitis. Vet Clin North Am 2003;19:
765-778.
Mair T. Other conditions. In: Mair T, Divers T, Ducharme N,
eds. Manual of Gastroenterology. Philadelphia: WB Saunders,
2002;317-363.
Matthews S, Dart AJ, Dowling BA, et al. Peritonitis associated
with Actinobacillus equuli in horses: 51 cases. Aust Vet J
2001;79:536-539.
Murray MJ. Peritonitis. In: Reed SM, Bayly WM, eds.
Equine Internal Medicine. Philadelphia: WB Saunders,
1998:700-705.
Nogradi N, Toth B, Cole Macgilivray K. Peritonitis in horses:
55 cases. Acta Vet Hung 2011;55:181-193.