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Basics

Basics

Definition

An inflammatory process involving the serous membrane of the abdominal cavity.

Pathophysiology

  • Insult to the peritoneal cavity, whether localized or generalized, leads to an inflammatory process characterized by vasodilation, cellular infiltration, stimulation of pain fibers, and development of adhesions.
  • Extent and severity depend on type and severity of the insult.
  • Bacterial peritonitis is commonly associated with Gram-negative bacterial endotoxin. The lipopolysaccharide (LPS) binds to macrophages, inducing cytokine release such as interleukin 1 (IL-1) and tumor necrosis factor (TNF). Gram-positive bacteria contain peptidoglycan, teichoic acid, and hyaluronic acid. Resultant cytokine release includes IL-1, TNF, and nitric oxide (NO). NO causes vasodilation and can promote hypotension.
  • Release of vasoactive substances (histamine, serotonin, protease, nitric oxide, endotoxin) cause vasodilation and increased vascular permeability. Cytokine release from mast cells, neutrophils, macrophages, and lymphocytes result in chemotaxis, activation of the complement system, and further accumulation of fluid. Activation of the complement system also results in fibrin degradation, damage to the mesothelium in the face of decreased fibrinolysis results in adhesion formation.
  • Bile damages mesothelial cells and inhibits PMN function. Blood in the peritoneal cavity interferes with chemotaxis and phagocytosis and promotes bacterial growth. The result of significant abdominal inflammation can be systemic inflammatory response syndrome (SIRS) and sepsis. With time, SIRS can progress to multiple organ dysfunction (MODS) and can affect the respiratory system (acute respiratory distress syndrome [ARDS] or pulmonary thromboembolism [PTE]), or cause renal dysfunction, reduced cardiac function, and neurologic signs.

Systems Affected

  • Cardiovascular
  • Gastrointestinal
  • Hemic/Lymphatic/Immune
  • Renal/Urologic Hepatobiliary

Genetics

N/A

Incidence/Prevalence

N/A

Geographic Distribution

N/A

Signalment

Species

Dog and cat

Breed Predilections

None

Mean Age and Range

None

Predominant Sex

None

Signs

General Comments

Signs may be vague and nonspecific and signs depend on the time of evaluation in relation to severity of the inflammation and systemic response present.

Historical Findings

Lethargy, depression, anorexia, vomiting, diarrhea, collapse

Physical Examination Findings

  • Abdominal discomfort or pain-localized or generalized; patient usually resents palpation; less common in cats.
  • A “prayer” position-due to abdominal discomfort.
  • Compensatory shock-tachycardia, tachypnea, injected mucus membranes, rapid capillary refill time (CRT).
  • Early decompensatory shock-tachycardia, poor pulse quality, depressed mentation, pallor, prolonged CRT. Cats often show a normal to decreased heart rate (<140/min).
  • Decompensatory shock-bradycardia, weak or absent pulses, severely depressed mentation, pallor or cyanosis, prolonged CRT.
  • Vomiting common.
  • Arrhythmias may be detected.
  • Fever-not consistent; when noted with other signs of peritonitis strongly suggests bacterial contamination of the abdominal cavity.
  • Weight loss-reported in one-third of dogs and cats with secondary peritonitis.

Causes

Primary Peritonitis

  • Uncommon.
  • Primary peritonitis results from hematogenous or lymphatic spread, or due to translocation from the gastrointestinal tract. Feline infectious peritonitis (FIP) is a form of peritonitis in cats.

Secondary Peritonitis

  • Predominant form.
  • Secondary peritonitis is the most common form of the condition and results due to contamination of the peritoneal cavity originating in one of the abdominal organs. Sources include the gastrointestinal tract (up to 75%), perforation of ulcerations, GI tract tumors, perforation secondary to GDV, leakage following GI surgery, penetrating trauma, biliary tract trauma or rupture due to obstruction or mucocele formation, abscessation of the pancreas, kidney, prostate, spleen or liver, ruptured pyometra, and urine leakage. Uroabdomen and bile peritonitis may or may not be septic; regardless, chemical peritonitis is present.

Risk Factors

  • Trauma.
  • Gastrointestinal surgery.
  • Undetected abscess of liver, pancreas, prostate, or uterus.
  • Prior NSAID use is associated with perforation occurring at the pylorus compared to other sites.

Diagnosis

Diagnosis

Differential Diagnosis

Other causes of abdominal pain or distention, sepsis, and shock.

CBC/Biochemistry/Urinalysis

  • Neutrophilic leukocytosis most common finding; may be a left shift; degenerative left shift or development of neutropenia may portend a worsening prognosis.
  • Hemoconcentration or anemia.
  • Hypoproteinemia-owing to exudation of albumin.
  • Hypo- or hyperkalemia and hyponatremia.
  • Azotemia-associated with prerenal, renal, or post-renal causes.
  • Metabolic acidosis.
  • Hypoglycemia-may indicate sepsis; hyperglycemia may be present in cats.
  • Liver enzyme elevations-associated with hepatic causes of peritonitis or due to MODs.
  • Hyperlactatemia-due to poor perfusion associated with shock.

Other Laboratory Tests

  • Coagulation abnormalities may develop-prolonged activated partial thromboplastin time (aPTT) and prothrombin time (PT).
  • Thromboelastography to evaluate for hyper- or hypocoagulability.
  • DIC may also develop-prolonged aPTT, PT, and thrombocytopenia, elevated D-dimers (>1,000 U), low protein C levels.

Imaging

Radiography

  • Findings inconsistent and depend on cause.
  • Loss of serosal detail (ground-glass appearance suggests fluid in the abdominal cavity)-rule out lack of intra-abdominal fat.
  • Generalized ileus may be present.
  • Consider making right and left lateral projections of the abdomen.
  • Pneumoperitoneum-gas in the abdomen may be slight, closely evaluate the region of the diaphragm; consider making lateral beam images in a sternally recumbent or lateral recumbency.
  • Can be diagnostic for GDV, GI foreign bodies, mass lesions, enlargement of organs with abscessation.
  • Contrast procedures-rarely warranted; may complicate management if contrast material enters the abdominal cavity; avoid barium if gastrointestinal perforation is suspected.

Ultrasound

May identify smaller volumes of peritoneal effusion; abscesses of the pancreas, liver, or prostate; rupture of the gallbladder, tumors or mass lesions. Important for aspiration of small volumes of fluid.

DIAGNOSTIC PROCEDURES

  • Abdominocentesis and diagnostic peritoneal lavage-safe and reliable and should be performed as soon as possible.
  • Abdominocentesis-empty the urinary bladder; aseptically clip and prepare the abdomen. Utilize ultrasound guidance if desired. Use a 22- or 20-gauge needle, butterfly catheter or over-the-needle catheter to penetrate the abdominal cavity. Collect the first few drops of fluid for cytology. Use a 3 mL syringe to apply gentle negative pressure if free flow of fluid does not occur.; tap all four quadrants (i.e., four separate needle punctures), with the left side last in an attempt to avoid inadvertent splenic puncture. Ultrasound guidance may be necessary to avoid the falciform fat and spleen and is required when small volumes of fluid are present.
  • Diagnostic peritoneal lavage-if abdominal fluid not recovered by abdominocentesis and the index of suspicion is high (e.g., postoperative complication). Empty the urinary bladder and aseptically prepare the abdomen. Infuse 20 mL/kg warm sterile saline through an 18- or 16-gauge over-the-needle catheter using gravity; gently roll patient from side to side to distribute the lavage fluid. Move the infusion bag to a position below the patient to recover fluid. There is no need to recover entire amount of infused fluid.
  • Cytology-first collect samples into EDTA tube; note color and clarity of the fluid and presence of fibrin.
  • Culture and sensitivity-next, collect sample in a sterile clot tube.
  • Suspected chemical peritonitis-finally, analyze abdominal fluid for creatinine (for uroabdomen), amylase (for pancreatitis), and bilirubin (for bile leakage).
  • Suspected FIP-submit abdominal fluid for protein electrophoresis and globulin determination.

Pathologic Findings

  • Intra- or extracellular bacteria, degenerative neutrophils, and plant material are diagnostic of septic peritonitis.
  • Normal peritoneal fluid contains <2,500 cells/µL; peritoneal fluid glucose levels more than 20 mg/dL below that of the peripheral blood are highly suggestive of septic peritonitis.
  • Fluid lactate >2.5 mmol/L in dogs is suggestive of septic peritonitis, but is not useful in cats.
  • Recent surgery results in <10,000 cells/mL; primary peritonitis usually results in 7,000 cells/µL in dogs and 3,000 cells/µL in cats.
  • Fluid bilirubin or creatinine levels higher than that of peripheral blood indicate bile peritonitis or uroabdomen, respectively. Acellular homogenous, laminated, basophilic material on cytology may be mucoid material associated with bile peritonitis.

Treatment

Treatment

Appropriate Health Care

Inpatient-intensive monitoring and supportive care are required.

Intravenous Fluid Therapy

  • Critical for correction of hemodynamic disturbances and electrolyte and acid-base abnormalities prior to considering surgery.
  • Balanced electrolyte solution-lactated Ringer's solution or Normosol-R for initial treatment; evaluate the response to therapy frequently.
  • Potassium and glucose-may need to supplement.
  • Replacement rate-may initially be as high as 55 mL/kg (cats) and 90 mL/kg (dogs); adjust rate frequently as patient status changes; if supplemented with potassium, the rate should not exceed 0.5 mEq/kg/h of potassium.
  • Colloid administration is highly recommended in acute and/or severe cases (up to 20 mL/kg/d in dogs and 15 mL/kg/d in cats).
  • Goals-blood pressure >90 mmHg, heart rate 80–140/min (dogs) and 140–225/min (cats), CRT <2 sec, urine output >1–2 mL/kg/h, serum lactate <2.5 mmol/L in dogs.
  • Inadequate response to therapy prompts vasopressor administration (dopamine, dobutamine, vasopressin, norepinephrine).
  • Whole blood or packed red blood cells (PRBC) -as required for anemia.
  • DIC-remove the inciting cause, support with plasma; consider heparin therapy.
  • Consider canine albumin transfusion in cases of severe hypoalbuminemia.

Nursing Care

  • Significant and dependent upon the severity of systemic signs, SIRS, MODS, ARDS, sepsis.
  • Continue intravenous fluid therapy and maintenance of goals per the above.

Activity

  • Will be significantly decreased depending on the severity of systemic illness.
  • Depends on the inciting cause and surgery necessary.

Diet

  • Dictated by cause, when identified, and any concurrent conditions (e.g., heart disease).
  • Feeding tube placement should be considered and placed at the time of surgery for early nutritional support (e.g., esophagostomy, gastrostomy, jejunostomy).
  • Adequate nutrition-essential to optimize outcome; may attenuate the hypermetabolic state, preserve hepatic antioxidant defenses, prevent protein-calorie malnutrition, and maintain the gastrointestinal barrier function.

Client Education

  • Advise client of the high rate of morbidity and in most cases of septic peritonitis, mortality.
  • Inform client that extensive monitoring and intensive care may be costly.

Surgical Considerations

  • Decision to treat medically or surgically-dictated by etiology, patient's response to initial treatment, and owner's financial constraints.
  • Known bacterial contamination or suspected chemical peritonitis-surgical intervention necessary.
  • Perform surgery as soon as the patient is stable.
  • Exploratory laparotomy-prepare for incision extending from xiphoid to pubis; goals of surgery are to remove the source of contamination, debride and clean the abdomen, collect fluid or tissue for Gram stain and aerobic and anaerobic culture, and providing nutritional support; use monofilament absorbable or non-absorbable suture within the abdomen (avoid multifilament, non-absorbable suture and catgut); before closing, thoroughly lavage the abdomen with 200–300 mL/kg sterile saline solution, warmed to body temperature. Do not add antimicrobials or other products (povidone iodine) to the lavage solution; remove all lavage solution from the abdomen.
  • Surgeon must be able to assess organ viability and resection. Anastomosis of the GI tract should utilize healthy tissue; consider serosal patching, perform omental patching if serosal patching not done.
  • Consider omentalization of pancreatic abscesses, perform omentalization for prostatic abscessation. Remove affected organ or part in other cases of abscessation.
  • Consider open abdominal drainage-based on degree of contamination, ability to debride the abdomen, severity of the illness, and anticipation of septic complications. Allow continued removal of fluid, bacteria, and toxins. Forms include closed suction drains, vacuum-assisted peritoneal drainage (VAPD), and closure of the caudal abdomen with partial closure of the cranial abdomen. Sterile bandaging is required in each form; less external materials for VAPD, but regulate suction and specialized foam and connections to suction required. Requires anesthesia for abdominal closure unless closed suction drains are used.

Medications

Medications

Drug(s) Of Choice

  • Antimicrobials-early and aggressive therapy for suspected septic peritonitis; broad-spectrum (against Gram-positive and Gram-negative, aerobic, and anaerobic organisms); final therapy must be based on culture and susceptibility testing.
  • Initial therapy-gram negative (enrofloxacin, cefotaxime, amikacin); gram positive (ampicillin, clindamycin); anaerobes (metronidazole).
  • Ampicillin 22 mg/kg IV q8h.
  • Clindamycin 12 mg/kg IV q12h.
  • Cefotaxime 20–80 mg/kg IV q8h.
  • Enrofloxacin 10–20 mg/kg IV q12h (5 mg/kg/d IV in cats).
  • Amikacin 10–15 mg/kg IV q24h.
  • Metronidazole 10 mg/kg IV q8–12h.
  • Pain control-depending on the severity of pain; may be intermittent or via continuous rate infusion (CRI). Significant pain is usually present; opioids recommended.
  • Multimodal CRI for pain; dogs, morphine-0.05–0.2 mg/kg/h, ketamine (0.2–0.6 mg/kg/h), lidocaine (2–4 mg/kg/h); cats, fentanyl (2–4 µg/kg/h), ketamine (0.05–0.2 mg/kg/h).
  • GI protectants-often recommended due to poor perfusion and stress. Required for cases of GI ulceration.
  • Famotidine-0.5–1.0 mg/kg IV q12–24h for rapid onset of action.
  • Pantoprazole 1 mg/kg IV q24h for more complete decrease in gastric acid.
  • Sucralfate: dogs, 0.5–1.0 mg PO q8h; cats, 0.25–0.5 mg PO q8h.

Contraindications

  • Glucocorticoids-use is controversial.
  • NSAIDs are not recommended.
  • Heparin therapy for the treatment of DIC-less effective in the case of insufficient antithrombin levels.

Precautions

  • Aminoglycosides-use with caution if renal function is impaired.
  • Adequate hydration-essential to enhance safety of these drugs.
  • Antiemetic use should be avoided if gastrointestinal foreign body or rupture is at all suspected. Use indicated when GI cause is eliminated.

Possible Interactions

Time sucralfate and gastric acid reducer so that sucralfate is given when the pH is lower. Also avoid oral medications at the same time as sucralfate as required.

Alternative Drug(s)

Fluoroquinolone-enrofloxacin or orbifloxacin; substitute for an aminoglycoside, especially with impaired renal function.

Follow-Up

Follow-Up

Patient Monitoring

  • Fluid balance, electrolyte balance, acid-base status-depending on the severity of the condition.. Blood gas, electrolyte, lactate measurements as necessary.
  • Frequency of monitoring-varies with severity of the condition and response to treatment. May be frequent (1h).
  • Maintain urine output 1–2 mL/kg/h and goals described in fluid therapy section above.
  • Replace fluid losses (vomiting, diarrhea) as necessary.
  • Change recumbency every 4–6h as necessary.
  • Enteral nutrition as soon as possible via oral feeding or nasoesophageal, gastrostomy, or jejunostomy tube feeding promotes enterocyte health and decreases bacterial migration through the intestinal wall.
  • Repeat ultrasound and cytologic evaluation depending on index of suspicion for leakage of intestinal surgery sites.
  • CBC, chemistry profile, urinalysis-every 1–2 days during periods of intensive monitoring, even in patients that are responding.

Prevention/Avoidance

Prevention-difficult except when specific risk factors are identified (e.g., pyometra).

Possible Complications

  • If underlying cause is not identified and managed, patient is at risk for complications.
  • Open peritoneal drainage-increased cost and required intensive care, repeated sedation or anesthesia for aseptic bandage changes, ascending/nosocomial infection, hypoproteinemia, electrolyte imbalances, enterocutaneous fistulation, and abdominal hernia formation.
  • Adhesions.

Expected Course and Prognosis

  • Prognosis-depends on rapid identification and successful management of the underlying cause and appropriate follow-up care.
  • Septic peritonitis-mortality of 30–68%. Prognosis worse in animals with pre-existing septic peritonitis, incorrectable hypotension, low serum albumin and total protein, respiratory dysfunction, DIC, low protein C, low antithrombin, MODS, and better survival in patients with lower pre-operative alanine aminotransferase, gamma-glutamyl transferase, packed cell volume, total solids, thromboelastography consistent with hypercoagulation, and albumin.
  • Septic peritonitis-open peritoneal drainage may improve survival.
  • Septic bile peritonitis-27% survival compared to 100% with non-septic bile peritonitis.
  • Antibiotic treatment within the first hour in cases of suspected septic peritonitis per a specific treatment protocol based on hospital cultures reduced mortality from approximately 80% to 42%.
  • Plasma lactate >2/5 mmol/L or inability to normalize plasma lactate-poorer survival in septic peritonitis.
  • Feeding tube complications depend on the site of placement. Esophagostomy (localized infection or abscessation), gastrostomy and jejunostomy (leakage or premature dislodgement associated peritonitis), nasoesophageal (sneezing, epistaxis). Refeeding syndrome-decreased magnesium, phosphorus, potassium. Warrants close monitoring.
  • Bradycardia and hypothermia in cats with primary septic peritonitis were associated with mortality.

Miscellaneous

Miscellaneous

Associated Conditions

N/A

Age-Related Factors

N/A

Zoonotic Potential

N/A

Pregnancy/Fertility/Breeding

N/A

Abbreviations

  • aPTT = activated partial thromboplastin time
  • ARDS = acute respiratory distress syndrome
  • CRI = continuous rate infusion
  • CRT = capillary refill time
  • DIC = disseminated intravascular coagulation
  • EDTA = ethylene diamine tetraacetic acid
  • FIP = feline infectious peritonitis
  • GDV = gastric dilatation volvulus
  • IL-1 = interleukin 1
  • LPS = lipopolysaccharide
  • MODS = multiple organ dysfunction
  • NO = nitric oxide
  • NSAID = nonsteroidal anti-inflammatory drug
  • PT = prothrombin time
  • PTE = pulmonary thromboembolism
  • SIRS = systemic inflammatory response syndrome
  • TNF = tumor necrosis factor
  • VAPD = vacuum assisted peritoneal drainage

Suggested Reading

Bentley AM, Mayhew PD, Culp WT, Otto CM. Alterations in the hemostatic profiles of dogs with naturally occurring septic peritonitis. J Vet Emerg Crit Care 2013, 23:1422.

Cortellini S, Seth M, Kellett-Gregory LM. Plasma lactate concentrations in septic peritonitis: a retrospective study of 83 dogs (2007–2012). J Vet Emerg Crit Care 2014, epub ahead of print.

Dayer T, Howard J, Spreng D. Septic peritonitis from pyloric and non-pyloric gastrointestinal perforation: prognostic factors in 44 dogs and 11 cats. J Small Anim Pract 2013, 54:625629.

Grimes JA, Schmiedt CW, Cornell KK, Radlinsky MA. Identification of risk factors for septic peritonitis and failure to survive following gastrointestinal surgery in dogs. J Am Vet Med Assoc 2011, 238:486494.

Ragetly GR, Bennett RA, Ragetly CA. Septic peritonitis: etiology, pathophysiology, and diagnosis. Comp Cont Ed Pract Vet 2011, 33:16.

Ragetly GR, Bennett RA, Ragetly CA. Septic peritonitis: treatment and prognosis. Comp Cont Ed Pract Vet 2011, 33:E15.

Author MaryAnn G. Radlinsky

Consulting Editor Stephen C. Barr

Acknowledgment The author and editors acknowledge the prior contribution of Sharon Fooshee Grace.

Client Education Handout Available Online