Peritonitis is inflammation of the serous membranes of the peritoneal cavity. It may be a primary disease or caused secondarily by other pathologic conditions. Clinical manifestations (eg, acute or chronic, septic or nonseptic, local or diffuse, adhesive or exudative) progression, and outcome vary based on etiology.

Etiology

Primary peritonitis may be infectious or idiopathic. In infectious primary peritonitis, specific infectious agents spread via the bloodstream into the peritoneal cavity of animals that often are immunocompromised. Primary peritonitis is less common than secondary peritonitis and may be caused by infectious agents such as feline coronavirus causing feline infectious peritonitis, Nocardia spp, Mycobacterium spp, Haemophilus parasuis, and other infectious agents. Progression of primary peritonitis tends to be chronic.

Secondary peritonitis can occur as a result of exposure of the peritoneal cavity to nonspecific infectious or noninfectious agents. It is often acute and frequently results in progressive, systemic disease.

Secondary septic peritonitis is commonly associated with perforation of and leakage from GI organs (eg, perforated gastric or abomasal ulcers; traumatic reticuloperitonitis in cattle) or the uterus in animals with uterine tears resulting from parturition. Peritonitis can also result from transmural migration of bacteria (eg, neoplasia, intestinal ischemia) or perforation, rupture, or leakage from other infected viscera (eg, abscesses in liver, spleen, or omentum; cystitis; endometritis; and pyometra). Furthermore, migration of parasites through the abdominal cavity may also result in leakage of chymus with subsequent septic peritonitis. Perforating wounds of the abdominal wall (eg, dog bites) or dehiscence of abdominal wound closure may result in laceration of viscera and inoculation of foreign material and microorganisms into the peritoneal cavity.

Microorganisms associated with septic peritonitis normally reflect the source of contamination. A mixed bacterial population is seen in GI tract perforation, whereas perforation of nongastrointestinal viscera (eg, urinary bladder, gall bladder, uterus, prostate) or hematogenic infection of the peritoneal cavity may be more typically associated with aerobic organisms including Escherichia coli, Streptococcus zooepidemicus equi, Staphylococcus, Proteus, Rhodococcus, Klebsiella, Salmonella, Enterobacter, Pseudomonas, or Corynebacterium.

Secondary aseptic peritonitis occurs after contamination of the abdominal cavity with chemical irritants (eg, bile, urine, drugs) or intestinal ischemia. Common conditions are urolithiasis and rupture of the urinary or gall bladder; however, these conditions are not always aseptic. An aseptic peritoneal inflammation may later become septic.

In large animals, peritonitis is most commonly seen in cattle, less often in horses, and rarely in pigs, sheep, and goats. Peritonitis is a serious and often fatal condition in cats. see Peritonitis: Common Causes of Peritonitis in Cattle, Horses, Small Ruminants, Pigs, Dogs, and Cats summarizes common causes of peritonitis in animals.

Table 1
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Common Causes of Peritonitis in Cattle, Horses, Small Ruminants, Pigs, Dogs, and Cats Species Cause Cattle Traumatic reticuloperitonitis; rumenitis; abomasal ulcer (perforation); abomasal volvulus, cecocolic volvulus; dystocia (uterine torsion, cesarean section); metritis or pyometra; abdominal surgery; intestinal, rectal, or uterine rupture; liver or abdominal abscess rupture; omphalitis (calves); fat necrosis; intraperitoneal injection; neoplasia (eg, mesothelioma) Horses Parasitic (larval) migration; intestinal injury and ischemia (colic); abdominal abscess rupture (Rhodococcus, Streptococcus); abdominal surgery (colic surgery, castration); gastric, intestinal, or uterine rupture; gastroduodenoenteritis, colitis; omphalitis, persistent urachus, bladder rupture (foals); gastric ulcer (perforation); intraperitoneal injection; neoplasia (eg, cholangiocellular carcinoma); penetrating trauma to the abdominal wall; iatrogenic (rectal perforation) Small ruminants Primary peritonitis (Mycoplasma spp); parasitic (larval) migration; abdominal abscess rupture; neoplasia (eg, mesothelioma) Pigs Glässer's disease (Haemophilus parasuis); intestinal (ileal) perforation; dystocia; sequela of septicemic infections (Salmonella choleraesuis) Dogs and cats Feline infectious peritonitis (cat); ingested intestinal foreign bodies; gastric, intestinal, rectal, or uterine rupture; abdominal neoplasia; pancreatitis; fat necrosis; gastric dilatation volvulus (dog); penetrating trauma to abdominal wall

Pathogenesis

The pathogenesis of peritonitis is species-dependent (eg, peritoneal inflammatory response in cattle is characterized by extensive fibrin formation; horses tend to develop exudative peritonitis) and mainly influenced by etiology (eg, primary or secondary, septic or nonseptic). Due to the release of inflammatory mediators after contact with mechanical, chemical, or infectious agents, serosal capillary permeability is increased, resulting in leakage of plasma proteins, solutes, and water into the peritoneal cavity. Exudation of protein-rich fluid may result in hypoproteinemia and facilitates bacterial proliferation. The combined effect of large fluid losses into the peritoneal cavity and vasodilatory effects of absorbed toxins may produce profound hypotension and hypovolemia.

Rupture or perforation of the forestomach, stomach, or intestine with spillage of large volumes of gastric or intestinal contents and rupture or perforation of the contaminated uterus leads to an acute septic peritonitis. Toxins produced by bacteria and tissue breakdown are readily absorbed through the peritoneum and have severe systemic effects leading to hypotension, shock, systemic inflammatory response syndrome, and disseminated intravascular coagulation (DIC). Endotoxins and acid-base and electrolyte disturbances directly affect cardiac function, leading to reduced cardiac output and circulatory failure. Gastrointestinal hypomotility or ileus is a frequent result of acute peritonitis and can cause functional obstruction and increased mortality. 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.

Chronic peritonitis is often characterized by extensive secretion of fibrinogen and subsequent formation of fibrinous or fibrous adhesions. Such adhesions help localize the inflammation (eg, traumatic reticuloperitonitis in cattle) but may cause mechanical or functional obstruction of the GI tract. Chronic peritonitis in horses often results in recurrent colic.

Clinical Findings

Clinical signs vary depending on the type and etiology of peritonitis. Affected animals may develop toxemia and septicemia, shock, hemorrhage, abdominal pain, paralytic ileus, fluid accumulation, and adhesions in varying degrees.

Shock, hypotension, acid-base disturbances, and circulatory collapse after acute septic peritonitis associated with rupture of intestines or uterus often lead to sudden death. Affected animals normally show only limited clinical signs. In less severe cases abdominal pain and fever are common signs. Hypothermia can also be seen as a result of dehydration, hypovolemia, and sepsis. Abdominal pain may be continuous, severe, and characterized by guarding the abdomen, a stiff gait, or recumbency. In all species pain responses are most evident in the early stages of the disease. Abdominal distention, which may be inapparent, usually is due to accumulation of peritoneal exudates, GI hypomotility or ileus, or peritoneal adhesions. Fecal output is often decreased, although an increased frequency of defecation may be noted in the early stages. Animals with secondary peritonitis may also show clinical signs associated with the primary disease.

Palpation per rectum is a useful diagnostic technique for evaluation of the peritoneum and accessible abdominal organs in large animals. Abdominal radiography may be used in small animals. Generally, ultrasonography is the most useful way to examine the abdominal cavity and assess size, extent, location, and character of peritonitis. Additionally, ultrasonography allows a guided abdominocentesis. Abdominocentesis should be used in large and small animals to obtain fluid for cytologic and biochemical examination and bacteriologic culture. Diagnostic peritoneal lavage can be used if peritoneal fluid cannot be obtained by abdominocentesis. Diagnostic laparoscopy or laparotomy can be considered to verify the diagnosis. These primary diagnostic procedures can often be combined with therapeutic measures.

Cattle

Clinical signs of peritonitis in cattle are often nonspecific and characterized by reduced feed intake, sudden decrease in milk production, and decreased rumination. In chronic cases, ruminal contractions may be present but with reduced intensity. Abdominal percussion may reveal ruminal tympany or pneumoperitoneum. Moderate fever is typical in cattle with peritonitis; a subnormal temperature suggests a terminal acute diffuse peritonitis. Common signs in cattle with peritonitis are a shuffling, cautious gait with a rigid, arched back and grunting when walking or passing urine or feces. Deep palpation of the abdominal wall and pain provocation tests result in a pain response. Chronic peritonitis is associated with development of fibrous adhesions. Depending on localization, rectal palpation may reveal adhesions between intestinal loops and peritoneum. Cattle may develop clinical signs of vagal indigestion or toxemia, with periods of acute, severe illness caused by partial intestinal obstruction. The majority of cattle develop a localized peritonitis with extensive fibrin formation; however, in a few cases the abdominal cavity contains large volumes of turbid, infected peritoneal fluid.

Small Ruminants and Pigs

Generally, the clinical signs in small ruminants and pigs are similar to those in other animals; however, peritonitis is rarely diagnosed in pigs, sheep, or goats.

Horses

Clinical signs include colic, ileus, distended intestines on rectal examination, gastric reflux, and occasionally diarrhea. Rectal palpation may reveal tacky, dry mucosa and in some cases fibrinous or fibrous adhesions between intestinal loops and other abdominal organs. Intestinal peristaltic sounds are reduced. Tachycardia, weak pulses, poor peripheral perfusion, and fever are common. Weight loss and intermittent abdominal pain (colic) may be observed in horses with chronic peritonitis.

Dogs and Cats

In small animals, anorexia and depression are nonspecific signs of peritonitis; often accompanied by vomiting and decreased defecation. The abdomen may be distended. Abdominal palpation may be painful, and abdominal masses may be detected. Icterus may be present in generalized biliary peritonitis in small animals. Abdominal radiographs may reveal GI obstruction, bowel dilatation, free abdominal air, ascites, or radiodense foreign material. Loss of serosal details in radiographs indicates abdominal fluid.

Diagnosis

Laboratory analyses to confirm the clinical diagnosis and determine the severity of peritonitis should include WBC, RBC, and several biochemical parameters in blood and peritoneal fluid.

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. Anemia may occur due to hemorrhage into the peritoneal cavity but is also commonly associated with chronic inflammation. Abnormalities of serum biochemical parameters (eg, total protein, albumin, fibrinogen, bilirubin, lactic acid dehydrogenase [LDH], alkaline phosphatase [ALP], CPK) may accompany peritonitis. Hypoalbuminemia, hyperglobulinemia, and hyperbilirubinemia are frequently present. Generally, the changes in hematologic and biochemical parameters indicate inflammatory processes and tissue damage, but they are not pathognomonic for peritonitis.

Peritoneal fluid is a plasma dialysate with specific physical and chemical properties that result from the membrane permeability, concentrations and electrical charges of ions, and osmotic pressure. The fluid contains cells deriving from the mesothelium and the blood or lymphatic vessels. Under physiologic conditions peritoneal fluid is a transudate, whereas peritonitis results in a fluid that can be normally characterized as an exudate. A peritoneal fluid showing properties of both transudate and exudate is termed a modified transudate. Analysis of peritoneal fluid is a useful diagnostic method in gastroenterology because the fluid generally reflects abdominal conditions. The volume of peritoneal fluid is frequently increased when peritonitis is present. In cases of septic peritonitis, samples of peritoneal fluid should be examined microbiologically in order to characterize infectious pathogens.

The parameters of the classic transudate-exudate categorization system are shown in (see Peritonitis: Characteristics of Transudates and Exudates in Cattle, Horses, Dogs, and Cats). Use of a scoring system allows further classification as mild, moderate, or severe peritonitis. In practice, however, analysis of peritoneal fluid may be inconsistent, leading to inconclusive results. Therefore, the diagnostic value of this traditional concept is limited. To improve the sensitivity of the distinction between an exudate and transudate of pleural and peritoneal effusions in human medicine, Light's criteria (fluid to serum protein ratio >0.5, fluid to serum LDH ratio >0.6, or fluid LDH activity >200 U/L), cutoff values for ratios between peritoneal fluid and plasma or serum of various parameters (eg, lactate, glucose, enzymes), and the serum-ascites albumin gradient (SAAG) have been established. These concepts have been applied to some animal species (ie, horses, small animals).

Table 2
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Characteristics of Transudates and Exudates in Cattle, Horses, Dogs, and Cats Parameter Species Transudate Exudate Total protein (g/dL) All <2.5 >3.0 Specific gravity All <1.020 >1.025 Cell count (109/L) Cattle 0.5–5.0 >8.0 Horses 0.5–5.0 >8.0 Dogs, cats <3.0 >5.0 Color All Colorless to yellow Variable Turbidity All Clear to moderate Moderate to opaque Bacteria All Absent May be present

Under physiologic conditions, the ratio between lymphocytes and neutrophils is close to 1:1. Acute peritonitis usually results in an increased number of leukocytes and the percentage of neutrophils can be 60–90%. However, in cases of peracute septic inflammation the number of leukocytes may decrease due to necrosis and cell damage. Histologically, a high rate of degenerative leukocytes (cytolysis, karyorrhexis, or karyolysis) can be found. In chronic peritoneal inflammation, the proportion of neutrophils decreases and the proportion of monocytes increases. The presence of intra- or extracellular bacteria confirms septic peritonitis. Gram-staining enables differentiation between gram-positive and gram-negative bacteria and facilitates early antibiotic treatment.

The physiologic total protein concentration in peritoneal fluid is 20–25 g/L. The normal protein ratio between peritoneal fluid and serum is lower than 1:2. The SAAG is calculated by subtracting the peritoneal fluid albumin concentration from the serum concentration. The cutoff value of 11 g/L for humans seems suitable for monogastric animals. However, the reference values for protein ratio and SAAG are not applicable in dairy cattle, mainly due to their higher serum protein and albumin concentrations compared with those of monogastric animals and humans.

In healthy individuals, glucose concentration is the same in both serum and peritoneal fluid. Bacterial infection of the peritoneal cavity results in a major decrease of peritoneal glucose concentration. A peritoneal fluid:serum ratio of glucose concentrations lower than 0.5 is highly sensitive and specific for septic peritonitis.

Intestinal ischemia results in an increase of l-lactate concentration in plasma and peritoneal fluid. Although an association exists between l-lactate concentration in peritoneal fluid and plasma, l-lactate in peritoneal fluid is considered to be more closely correlated to the severity of intestinal ischemia. Physiologically, l-lactate concentration in peritoneal fluid is lower than in plasma (in healthy horses it is ~1:2). This ratio is reversed in colicky horses with intestinal ischemia, cows with abomasal volvulus, and dogs with gastric dilatation volvulus. Lactate is also a bacterial metabolite (predominately d-lactate); therefore, increased lactate concentration in peritoneal fluid may also indicate septic peritonitis. The accuracy of peritoneal lactate concentration in differentiating septic and nonseptic peritonitis varies between species (eg, 90–95% in dogs but 65–70% in cats).

Inflammation can be monitored using acute phase proteins such as C-reactive protein or haptoglobin (in cattle) as markers. Acute phase protein concentrations are increased in peripheral blood and in peritoneal fluid in animals with peritonitis; however, these parameters are general indicators for inflammation and not specific for peritonitis.

Fibrinogen concentration in peritoneal fluid may be increased in animals with peritonitis. However, fibrinogen concentration has limited diagnostic value because there is only a weak association between peritoneal and blood fibrinogen concentration. An increased concentration of the fibrin degradation product d-dimer indicates intestinal ischemia and inflammation with high sensitivity and specificity. Normal values for human plasma are <0.3 mg/L. Reference values for animals are not completely known but seem to be similar to those for humans.

Inflammation, intestinal ischemia, and reperfusion affect the activities of several enzymes (ALP, AST, CPK, LDH) in peritoneal fluid and peripheral blood. CPK activity is primarily increased in serum and peritoneal fluid in cases of intestinal ischemia. The origin of CPK is thought to be the muscular layer of the strangulated, ischemic intestines. However, other tissues (eg, striated muscle after colic episodes in horses) may be sources of higher CPK activities; therefore, the sensitivity and specificity of CPK are low.

LDH activity is a measure of inflammatory response and has been used to differentiate exudate from transudate (peritoneal fluid:serum LDH ratio >0.6; LDH activity of peritoneal fluid >200 U/L). The reference values for monogastric animals, but not those for cattle, are similar to those for humans.

An increase of ALP during intestinal ischemia and reperfusion has been found in peritoneal fluid of horses with colic and cows with displaced abomasum. However, the origin of the ALP was not exclusively the damaged stomach or intestine. Other sources for the increased ALP activity in these cases include hepatocytes and granulocytes. Normally, the serum ALP activity does not show major changes during intestinal ischemia.

Increased concentrations of protein and globulin in serum and peritoneal fluid are often observed in cats with FIP. However, neither parameter is accurate enough for diagnosis, especially if measured in serum. Calculation of the albumin:globulin ratio may improve the diagnostic value. The traditional Rivalta's test simply differentiates transudates from exudates. Although it produces false-positive results in cats with septic bacterial peritonitis, it still seems useful for FIP diagnosis. The widely used parameter α-1-acid glycoprotein indicates inflammation but is not specific for FIP. Serum anti-feline coronavirus (FCoV) antibody titers must be interpreted critically because many healthy cats are anti-FCoV-antibody positive. The diagnostic value of anti-FCoV antibody titers in peritoneal fluid is still under discussion. A number of advanced diagnostic methods (eg, immuno-fluorescent staining of FCoV antigen in peritoneal macrophages, ELISA to detect antigen-antibody complexes in serum, reverse transcriptase-PCR) have been introduced as diagnostic measures to improve accuracy of FIP diagnosis. Generally the laboratory tests performed on peritoneal fluid are superior to those that use serum.

Prognosis

Generally peritonitis is a severe, life-threatening disease with a guarded prognosis. However, prognosis strongly depends on the character and severity of the disease and must be determined individually. Survival rates of 50–70% have been reported, with much lower rates for return to productivity in farm animals. Despite new developments in therapy during recent years, FIP is still a lethal disease for which there is no effective longterm treatment, and the prognosis for cats with FIP remains poor.

Treatment

Adequate therapy depends on the diagnosis and the results of physical examinations and laboratory analyses. In severe cases of septic peritonitis, the initial treatment must be directed toward saving life and stabilizing the circulation and organ function. Therapy should include treatment of hypovolemic or toxemic shock, aggressive anti-inflammatory therapy, and treatment of metabolic and rheologic disturbances (eg, electrolyte and acid-base imbalances, coagulopathies). Replacement fluids, electrolytes, plasma, or whole blood may be necessary to maintain cardiac output and improve circulation.

Appropriate antimicrobial therapy should be started once septic peritonitis is suspected or confirmed. Peritoneal fluid samples should be obtained for culture and susceptibility testing. Parenteral broad-spectrum antimicrobial therapy should be applied initially. Aminoglycoside or fluoroquinolone antibiotics are effective against gram-negative organisms, and penicillins or cephalosporins are effective against gram-positive bacteria. The antimicrobial drug may be changed later based on the results of cytology and culture and sensitivity testing. Antimicrobial and anti-inflammatory treatment should be continued through the healing period.

If possible, specific therapy should be directed at the cause of peritonitis. In animals with suspected leakage of abdominal organs, surgery should be performed immediately to explore the abdomen and repair any defects. This should be followed by a peritoneal lavage with an isothermic, isotonic, balanced electrolyte solution. Although frequently performed, there is no proven clinical benefit in adding antimicrobial drugs to the lavage solution. Solutions containing antiseptics (eg, povidone-iodine) also have no proven clinical benefit and may function as chemical irritants that worsen inflammation. Heparin treatment may be considered in cases of DIC and may prevent extensive fibrin formation within the peritoneal cavity.

The application of abdominal drains and subsequent lavage in small and large animals may help treat severe peritonitis by removing septic and pro-inflammatory material from the abdominal cavity. The decision to manage peritoneal drainage is based on the severity of the case, experience level, intensive care options, and equipment. Maintenance of drain patency can be difficult, especially in cattle, due to extensive fibrin formation. In animals treated by peritoneal drainage, serum protein and electrolyte levels should be monitored periodically, because both are lost with drainage of exudate.

Nutritional support should be anticipated, as many animals with peritonitis will not eat. Enteral nutrition helps maintain the health of the intestinal mucosa; however, vomiting (in dogs and cats) or anorexia may force the consideration of alternatives. In certain patients, total or partial parenteral nutrition may be necessary to provide a portion of the nutritional requirements while enteral nutrition is being initiated. Antioxidants and vitamins should also be considered. Vomiting is sometimes caused by peritonitis in small animals; antiemetic treatment is indicated in such cases.

Feline coronaviral infection may cause a primary feline infectious peritonitis (FIP), which remains a fatal disease. The therapy is palliative (eg, interferon, glucocorticoids, supportive care) and directed toward reducing the inflammation. However, there is no effective longterm therapy. Commercial vaccines are available for prophylaxis in some countries; however, there are conflicting reports on their efficacy. The vaccines are not effective when administered to animals that have already been exposed to feline coronavirus, but they may offer some protection when administered to seronegative animals.

In chronic adhesive peritonitis, laparoscopy or laparotomy may be considered to cut adhesions that prevent intestinal motility or to remove or drain intestinal abscesses.

Last full review/revision March 2012 by Thomas Wittek, PD DrMedVetHabil, DECBHM, MRCVS