Peritonitis: Introduction - The Merck Veterinary Manual

Peritonitis: Introduction

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.