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Peritonitis in Animals

ByThomas Wittek, Dr Med Vet, DECBHM
Reviewed/Revised Dec 2024

Peritonitis is inflammation of the serous membranes of the peritoneal cavity. It may be primary or caused by infectious or noninfectious agents. Clinical signs can include localized pain, increased abdominal wall tension, abdominal distention, kyphosis, listlessness, fever, and anorexia. Clinical diagnosis may be supported by ultrasonography and laboratory analysis of blood or abdominal fluid. Treatment includes peritoneal lavage, surgery, antimicrobials, and anti-inflammatory medications.

Peritonitis is defined as inflammation of the serous membranes of the peritoneal cavity. It may be a primary disease or secondary to other pathological conditions. Various infectious and noninfectious agents can cause peritonitis; therefore, clinical signs, disease progression pathways, and outcomes may vary. Peritonitis can be acute or chronic, septic or nonseptic, local or diffuse, or adhesive or exudative. The term “tertiary peritonitis,” used in human medicine for particular cases of chronic peritonitis with a small number of bacteria or fungi, is not used in veterinary medicine.

Etiology of Peritonitis in Animals

Primary peritonitis is less common than secondary peritonitis and may be infectious or idiopathic. In infectious primary peritonitis, infectious agents spread hematogenously into the peritoneal cavity of animals that are often immunocompromised. Such infectious agents include feline coronavirus (FCoV), which leads to feline infectious peritonitis (FIP); Nocardia spp; Mycobacterium spp; Haemophilus parasuis; and others. Progression of primary peritonitis tends to be chronic.

Secondary peritonitis occurs when the peritoneal cavity is exposed to nonspecific infectious or noninfectious agents associated with other conditions. It is often acute and frequently results in progressive, systemic disease. Secondary septic peritonitis is commonly associated with perforation of, and subsequent leakage from, GI organs (as in traumatic reticuloperitonitis in cattle, for example), which can lead to transmural migration of bacteria. Examples of infected abdominal structures that may leak or rupture include abscesses, the bladder, and the uterus. Furthermore, migration of parasites through the abdominal cavity can result in leakage of chyme and subsequent septic peritonitis. Perforating wounds of the abdominal wall (eg, dog bites) or dehiscence of abdominal wound closure can result in laceration of viscera and inoculation of foreign material and microorganisms into the peritoneal cavity.

Microorganisms associated with septic peritonitis usually reflect the source of contamination. A mixed bacterial population is present in cases of GI tract perforation, whereas perforation of non-GI viscera (eg, urinary bladder, gallbladder, uterus, prostate) and hematogenous infection of the peritoneal cavity are more typically associated with aerobic organisms, including Escherichia coli, Streptococcus equi zooepidemicus, Staphylococcus, Proteus, Rhodococcus, Klebsiella, Salmonella, Enterobacter, Pseudomonas, and Corynebacterium.

Secondary aseptic peritonitis occurs after contamination of the abdominal cavity with chemical irritants (eg, bile, urine, drugs). Common conditions leading to such contamination are rupture of the urinary bladder or gallbladder from uroliths or choleliths, respectively; however, these conditions are not always aseptic. Initially aseptic peritoneal inflammation resulting from intestinal ischemia may later become septic. In addition, intraperitoneal administration of drugs or fluids can result in temporary peritoneal inflammation. Aseptic peritonitis can also result from abdominal surgery.

Among large animals, peritonitis most commonly occurs in cattle, less often in horses, and rarely in pigs, sheep, and goats. Because South American camelids show severe inflammatory reactions to infections with Dicrocoelium dendriticum, peritonitis can develop subsequent to severe hepatitis. Peritonitis is also a serious and often fatal condition in cats (FIP).

See the table Common Causes of Peritonitis for causes of this disease in various species.

Table
Table

Pathogenesis of Peritonitis in Animals

Peritoneal inflammation results from a variety of possible pathogenetic pathways. These pathways are species dependent (eg, peritoneal inflammatory response in cattle is characterized by extensive fibrin formation, and horses tend to develop exudative peritonitis) and mainly influenced by etiology (eg, primary or secondary, septic or nonseptic, acute or chronic). Because the peritoneum releases inflammatory mediators after contact with mechanical, chemical, or infectious agents, serosal capillary permeability is increased and results in leakage of plasma proteins, solutes, and water into the peritoneal cavity. Exudation of protein-rich fluid can result in hypoproteinemia and facilitates bacterial proliferation. The combined effect of large fluid losses into the peritoneal cavity and vasodilatory effects of absorbed toxins can produce profound hypotension and hypovolemia. Inflammation can also decrease antioxidative capacity and result in oxidative stress.

Rupture or perforation of the forestomach, stomach, intestine, or infected uterus results in spillage of ingesta or contaminated contents into the abdomen, leading to 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 (SIRS), and DIC. Endotoxins, acid-base disturbances, and electrolyte disturbances directly affect cardiac function, resulting in decreased cardiac output and circulatory failure. Acute peritonitis frequently results in paralytic ileus, leading to functional GI obstruction and increased mortality.

With peritonitis, large volumes of inflammatory exudates secreted into the peritoneal cavity can impair respiration by impinging on the diaphragm. Spillage of small amounts of gastric or intestinal content (eg, after transcutaneous rumenocentesis or when bar-suture techniques are used in left displaced abomasum surgery) normally result in localized peritonitis.

Chronic peritonitis is often characterized by extensive secretion of fibrinogen and subsequent formation of fibrinous or fibrous adhesions. Such adhesions help localize the inflammatory process (as in traumatic reticuloperitonitis in cattle or type 3 abomasal ulcers in cattle); however, they can lead to mechanical or functional GI tract obstruction. Chronic peritonitis in horses often results in recurrent colic episodes.

Clinical Findings of Peritonitis in Animals

Clinical signs of peritonitis vary, depending on disease type and etiology. Affected patients may develop the following:

  • increased abdominal wall tension

  • kyphosis

  • decreased general activity and feed intake

  • abdominal pain or pain reaction to abdominal palpation

  • abdominal fluid accumulation and distention

  • paralytic ileus

  • fever

  • toxemia and septicemia

  • hemorrhage

  • shock, SIRS

  • adhesions

With acute septic peritonitis associated with intestinal or uterine rupture, peracute death may result from shock, hypotension, acid-base disturbances, and circulatory collapse. In such cases, patients typically show limited clinical signs of peritonitis. In less severe cases, abdominal pain and fever are common. Hypothermia can also occur as a result of dehydration, hypovolemia, and sepsis. Abdominal pain can be permanent and severe and is characterized by abdominal guarding, stiff gait, or recumbency.

In all species, pain responses are most evident in the early stages. Abdominal distention, which may be inapparent, is usually due to accumulation of peritoneal exudates, paralytic ileus, or peritoneal adhesions. Fecal output often decreases, although frequency of defecation may increase in the early stages of peritonitis. Patients with secondary peritonitis may also show clinical signs associated with the primary disease. However, cases of chronic bacterial peritonitis developing in apparently clinically healthy patients have been reported.

Cattle

Clinical signs of peritonitis in cattle are often nonspecific and include decreased feed intake, milk production, and rumination activity. In chronic cases, ruminal contractions can be present but are of low intensity. Abdominal percussion may reveal ruminal tympany or pneumoperitoneum. Moderate fever is typical during the first 24–36 hours in cattle with acute, local peritonitis. High fever suggests acute, diffuse peritonitis.

Cattle with peritonitis often have a shuffling, cautious gait and a rigid, arched back, and they may grunt when walking or passing urine or feces. Deep palpation of the abdominal wall and pain provocation tests elicit a pain response. Calves with peritonitis due to a perforated abomasal ulcer deteriorate rapidly and show clinical signs of sepsis and SIRS.

Cattle with chronic peritonitis may develop fibrous adhesions. Depending on disease localization, rectal palpation may reveal adhesions between intestinal loops and peritoneum. Cattle may suffer from chronic indigestion (Hoflund syndrome, abomasal impaction) or toxemia, and periods of acute, severe illness can result from partial intestinal obstruction. Most cattle develop localized peritonitis by extensive fibrin formation; however, occasionally, the abdominal cavity contains large volumes of turbid, infected peritoneal fluid. A specific form of the disease in cattle is localized between omental layers and can be diagnosed using ultrasonography.

Small Ruminants, South American Camelids, and Pigs

Generally, clinical signs of peritonitis in small ruminants, South American camelids, and pigs are similar to those in other animals. However, peritonitis is rarely diagnosed clinically in pigs, sheep, or goats, although it is not an uncommon finding during routine meat inspection after pig slaughter. Peritonitis is more common in llamas and alpacas, in which liver flukes (Fasciola and Dicrocoelium) are the cause.

Horses

Clinical signs of peritonitis in horses include colic, palpably 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 decreased. Tachycardia, weak pulses, poor peripheral perfusion, and fever are common. Weight loss and intermittent abdominal pain (colic) can occur in horses with chronic peritonitis.

Dogs and Cats

In dogs and cats, anorexia and listlessness are nonspecific clinical signs of peritonitis and are often accompanied by vomiting and decreased defecation. The abdomen may be distended. Abdominal palpation may elicit pain, and abdominal masses may be detected. Icterus may be present in generalized biliary peritonitis.

Diagnosis of Peritonitis in Animals

  • Physical examination

  • Abdominal ultrasonography

  • Laboratory analyses

Diagnosis of peritonitis is based primarily on characteristic clinical findings during physical examination that are then verified by advanced diagnostic procedures.

Pearls & Pitfalls

  • Diagnosis of peritonitis is based primarily on characteristic clinical findings during physical examination that are then verified by advanced diagnostic procedures.

Rectal palpation is a useful diagnostic technique for evaluating the peritoneum and accessible abdominal organs; however, local peritonitic processes in the cranial abdomen (eg, traumatic reticuloperitonitis in cattle) are too far cranial to be diagnosed by rectal examination.

Advanced Diagnostic Procedures

In addition to physical examination, several advanced diagnostic procedures, especially abdominal ultrasonography, can help verify a peritonitis diagnosis and visualize the extent and character of disease. They may also provide information on disease etiology.

Generally, ultrasonography is the most valuable diagnostic tool for examining the abdominal cavity and assessing the extent, localization, and character of peritonitis. Ultrasonography of the abdominal cavity and abdominal organs allows visualization of ascites and inflammation products (fibrin formation). Especially in small animals, ultrasonography can provide information on etiology (eg, intestinal distention, urinary bladder rupture, liver and gallbladder diseases, pancreatic diseases, or neoplasms). In addition, it allows for guided abdominocentesis.

Abdominocentesis is performed in both large and small animals to obtain fluid for cytological and biochemical examination and for bacteriological culture. Diagnostic peritoneal lavage can be used if peritoneal fluid cannot be obtained by abdominocentesis.

Abdominal radiography can be used in small animals and may reveal GI tract obstruction, bowel dilatation, free abdominal air, ascites, or radiodense foreign material; loss of serosal detail in radiographs indicates abdominal fluid. In large animals, such as horses and cattle, radiography is also useful, though high-power x-ray machines are required; therefore, this technique is limited to stationary units in veterinary clinics. Although radiography is still a suitable diagnostic tool in all animals, it has been partially replaced by ultrasonography.

Diagnostic laparoscopy or laparotomy can help confirm the diagnosis. Diagnostic laparotomy is frequently used in cattle because it is inexpensive, can be performed with the patient in a standing position, and is associated with few or minor complications. It also makes additional diagnostic procedures unnecessary and can often be combined with therapeutic measures.

Laboratory Analyses

Laboratory analyses can help confirm the clinical diagnosis, determine the severity of peritonitis, and guide treatment decisions. Tests should include a CBC and several biochemical parameters in both blood and peritoneal fluid.

Acute, diffuse peritonitis with toxemia is usually accompanied by leukopenia, neutropenia, and marked immature neutrophilia (degenerative left shift). In less severe cases of acute peritonitis, leukocytosis can occur as a result of increased neutrophil production. Patients with acute, localized peritonitis may have a normal WBC count with a regenerative left shift. Total WBC count in patients with chronic peritonitis may be normal, but occasionally these patients have lymphocytosis and monocytosis.

Several abnormal serum biochemical parameters can accompany peritonitis. Hypoalbuminemia, hyperglobulinemia, and hyperbilirubinemia are frequently present.

Peritoneal fluid is a plasma dialysate with specific physical and chemical properties that depend on membrane permeability, concentrations and electrical charges of ions, and osmotic pressure.Under normal physiological conditions, peritoneal fluid is a transudate, whereas in patients with peritonitis it is typically characterized as an exudate. In cases of septic peritonitis, samples of peritoneal fluid should be examined microbiologically to characterize infectious pathogens.

The traditional transudate-exudate categorization system is shown in the table Characteristics of Transudates and Exudates in Cattle, Horses, Dogs, and Cats.

Table
Table

Peritoneal fluid with both transudate and exudate properties is commonly called a modified transudate. Peritonitis is also commonly classified as mild, moderate, or severe. In practice, however, analysis of peritoneal fluid can be inconsistent, leading to inconclusive results. Therefore, the diagnostic value of this traditional system is limited. To improve the sensitivity of the transudate-exudate distinction for peritoneal effusions, the following have been established:

  • the Light criteria (peritoneal fluid:serum protein ratio > 0.5, peritoneal fluid:serum LDH ratio > 0.6, or peritoneal fluid LDH activity > 200 U/L)

  • cutoff values for peritoneal fluid:serum (or peritoneal fluid:plasma) ratios for various parameters (eg, lactate, glucose, enzymes)

  • serum-ascites albumin gradient

Under normal physiological conditions, the lymphocyte:neutrophil ratio in peritoneal fluid is close to 1:1. Acute peritonitis usually results in a high WBC count, and the percentage of neutrophils can be as high as 60–90% of the total WBC count. However, in cases of peracute septic inflammation, the WBC count may decrease because of necrosis and cell damage. Histologically, a high number of degenerative WBCs can be found in peritoneal fluid. With chronic peritoneal inflammation, the proportion of neutrophils decreases, and the proportion of monocytes increases.

The presence of intra- or extracellular bacteria in peritoneal fluid confirms septic peritonitis. A Gram stain enables differentiation between gram-positive and gram-negative bacteria and facilitates early antimicrobial treatment.

The physiological total protein concentration in peritoneal fluid is 2–2.5 g/dL. The normal ratio of peritoneal fluid protein to serum protein is < 1:2.

In healthy patients, glucose concentration is the same in both serum and peritoneal fluid. Septic peritonitis, however, results in a major decrease in peritoneal glucose concentration, as the inflammatory response triggered by infection leads to increased glucose uptake by inflammatory cells. A ratio of peritoneal fluid glucose concentration to serum glucose concentration < 0.5 is highly sensitive and specific for septic peritonitis. Because the glucose concentration in peritoneal fluid frequently falls below the detection limit in patients with septic peritonitis, it is often not necessary to measure serum glucose concentration.

Pearls & Pitfalls

  • A ratio of peritoneal fluid glucose concentration to serum glucose concentration < 0.5 is highly sensitive and specific for septic peritonitis.

Intestinal ischemia results in increased l-lactate concentration in both plasma and peritoneal fluid. Although an association exists between l-lactate concentrations in peritoneal fluid and plasma, the level of l-lactate in peritoneal fluid is more closely correlated to the severity of intestinal ischemia. Physiologically, in healthy animals, l-lactate concentration is lower in peritoneal fluid than in plasma (in healthy horses, the ratio is approximately 1:2). This ratio is reversed in colicky horses with intestinal ischemia, cows with abomasal volvulus, and dogs with gastric dilatation volvulus.

Increased concentration of the fibrin degradation product D dimer indicates intestinal ischemia and inflammation with high sensitivity and specificity. Normal D-dimer concentration in human plasma is < 0.3 mg/L. Reference values for small animals and horses seem to be similar to those for humans. Peritoneal fluid D-dimer concentration in healthy cows is < 0.6 mg/L; increased values indicate peritonitis with high sensitivity and specificity.

Inflammation, intestinal ischemia, and reperfusion affect the activities of several enzymes (alkaline phosphatase, AST, CK, and LDH) in peritoneal fluid and peripheral blood. CK activity is primarily increased in serum and peritoneal fluid in cases of intestinal ischemia. The origin of this increased CK is thought to be the muscular layer of strangulated, ischemic intestines.

LDH activity is a measure of inflammatory response and can be used to differentiate exudate from transudate (peritoneal fluid:serum LDH ratio > 0.6; peritoneal fluid LDH activity > 200 U/L). The reference values for monogastric animals, but not for cattle, are similar to those for humans. For cattle, a cutoff value of 960 U/L has been identified.

Increased concentrations of albumin and globulin in serum and peritoneal fluid are often observed in cats with feline infectious peritonitis. However, neither parameter is accurate enough for definitive diagnosis, especially if measured in serum. Calculation of the albumin:globulin ratio may improve the diagnostic value of either parameter individually. The traditional Rivalta test (mixing a sample of abdominal effusion with acetic acid and distilled water to look for a precipitate in cases of FIP) simply differentiates transudates from exudates; although it produces false-positive results in cats with septic bacterial peritonitis, it still seems useful for FIP diagnosis. Presence in blood of alpha-1-acid glycoprotein (a widely used parameter) indicates inflammation but is not specific for FIP.

Prognosis of Peritonitis in Animals

Although the mesothelium of the peritoneum is able to regenerate rapidly, peritonitis must be considered a severe, life-threatening disease with a guarded prognosis. The prognosis depends strongly on the character and severity of disease and, therefore, must be determined individually. Survival rates are generally considered to be 50–70% across species, with much lower rates for return of productivity in farm animals. In horses, the prognosis for further use in equestrian sport is guarded. Furthermore, horses that survive peritonitis frequently suffer from recurrent colic episodes. Advancements in treatment of FIP are changing the prognosis for this disease, such that many cats are now successfully treated.

Treatment of Peritonitis in Animals

  • Anti-inflammatories

  • Antimicrobials

  • Peritoneal lavage

  • Surgery

Adequate treatment for peritonitis depends on the diagnosis and the results of both physical examination and laboratory analyses.

In severe cases of septic peritonitis, initial treatment must be directed at saving the life of the patient and stabilizing cardiovascular and other organ functions. In severe cases, euthanasia is a consideration. Patients should be treated for hypovolemic or toxemic shock and any metabolic and rheological disturbances (eg, electrolyte and acid-base disorders, DIC). Aggressive use of anti-inflammatories is also recommended. Replacement fluids, electrolytes, plasma, or whole blood may be necessary to maintain cardiac output and improve circulation. Prevention of circulatory failure from complications of DIC is essential. Treatment with the antioxidants vitamin C (20–60 mg/kg, SC, IM, or IV,) and vitamin E (0.5–3.0 mg/kg, SC, IM, or IV) can be useful, as can administration of short-acting glucocorticoids. In addition, prokinetic drugs may be necessary to increase and coordinate motility of the GI tract. Supportive treatment with antioxidants, short-acting glucocorticoids, and prokinetic drugs is administered as long as required and can be modified depending on the patient's general condition, clinical signs, and laboratory results.

Treatment with appropriate antimicrobials should be started once septic peritonitis is suspected or confirmed. Peritoneal fluid samples should be obtained for culture and susceptibility testing. Parenteral broad-spectrum antimicrobials must be administered initially. Antimicrobial drugs can be changed later according to the results of both cytological testing and culture and susceptibility testing. Antimicrobial and anti-inflammatory treatment should continue through the healing period.

If possible, treatment should be initiated to eliminate the cause of peritonitis. In patients with suspected leakage of abdominal organs, surgery should be performed immediately to explore the abdomen and repair defects, followed by peritoneal lavage with an isothermic, isotonic, balanced electrolyte solution before the abdominal cavity is closed. Although antimicrobial drugs are frequently added to the lavage solution, there is no clinical benefit to adding them. Solutions containing antiseptics (eg, povidone-iodine) also have no proven clinical benefit and can even function as chemical irritants that exacerbate inflammation. Heparin treatment may be considered in cases of DIC and may prevent extensive fibrin formation within the peritoneal cavity.

In both small and large animals, placement of abdominal drains and subsequent lavage can help treat severe peritonitis by removing septic and proinflammatory material from the abdominal cavity. Whereas the removal of septic peritoneal fluid is generally accepted as beneficial, the efficacy of repeated peritoneal lavage is under debate. Some reports describe positive effects; however, others claim that intensive lavage can disturb epithelial healing and result in further spread of inflammation. The composition of the lavage solution is also under debate; there is no evidence that the addition of antimicrobials or antiseptics to this solution provides any advantage.

The decision to manage peritoneal drainage is based on the severity of the case, the veterinarian's experience level, the potential need for intensive care, and the availability of equipment. Maintenance of drain patency can be difficult, especially in cattle, because of extensive fibrin formation in the abdominal cavity. In patients treated by peritoneal drainage or lavage, serum protein and electrolyte concentrations should be monitored periodically, because both protein and electrolytes are lost with drainage of exudate.

Nutritional support should be anticipated, because many patients with peritonitis will not eat. Enteral nutrition helps to maintain the health of the intestinal mucosa; however, vomiting (in dogs and cats) or anorexia may force the consideration of alternatives. In ruminants and South American camelids, transfaunation using either rumen fluid obtained from other animals or commercially available products has proved beneficial. In certain patients, total or partial parenteral nutrition may be necessary to provide all or a portion of their nutritional requirements while enteral nutrition is being initiated. Administration of antioxidants and vitamins also should be considered. Vomiting is sometimes a sequela of peritonitis in small animals; therefore, antiemetic treatment is indicated in such cases.

In chronic adhesive peritonitis, laparoscopy or laparotomy can be considered to cut adhesions that prevent intestinal motility or to remove or drain intestinal abscesses. However, the success of such interventions might be limited because adhesions can reform.

Key Points

  • Acute peritonitis is frequently a severe, life-threatening condition.

  • Diagnostic procedures are directed at determining the etiology and character of peritonitis.

  • Aggressive treatment is often required.

  • Animals with chronic peritonitis may show disturbed GI motility with recurrent clinical signs of abdominal pain.

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