Diagnosis and Surgical Management of Peritonitis

John D. Wooldridge, DVM, Dipl. ACVS

 

The peritoneum is a bi-directional, semipermeable barrier and it is important for the surgeon to consider that the circulation and dispersal of fluids within the peritoneal cavity are dynamic processes. Water and low molecular weight solutes diffuse between submesothelial capillaries and the peritoneal fluid according to Starlings Law. Pressure in the capillaries of the visceral peritoneum are higher than elsewhere in the body due to resistance to portal blood flow; therefore, the peritoneal cavity is more susceptible to the accumulation of excessive fluid than most other body cavities.

Fluids move ventrally and cranially as a result of gravity and diaphragm movement. Lymphatic drainage from the diaphragmatic peritoneum is the most important means of keeping the peritoneal cavity from filling with fluid; the diaphragm acts as a muscular pump which contracts to drive fluid into the lymphatics. Inflammation within the peritoneal cavity will result in blockage of the lymphatics, which causes fluid accumulation. Increased protein in the peritoneal fluid and therefore increased colloid oncotic pressure, leads to the attraction of still more fluid from the intravascular and interstitial spaces.

Peritonitis can be classified as either primary or secondary. Primary peritonitis is inflammation of the peritoneum without initial intra-abdominal pathology, such as feline infectious peritonitis. Secondary peritonitis, which makes up 99% of all cases of peritonitis, is inflammation of the peritoneum subsequent to contamination due to abdominal cavity disruption or hollow viscus disruption. Secondary peritonitis can be further classified as aseptic (due to foreign body, chemical, or mechanical irritation), septic/infectious peritonitis, or miscellaneous (including contamination secondary to vascular diseases, neoplasms, allergy, etc.).

Septic peritonitis occurs when bacterial endotoxin and cellular proteases activate the complement cascade. This causes peritoneal vascular dilation and increased capillary permeability, which allows significant quantities of fluid, electrolytes, plasma proteins and red blood cells to accumulate in the peritoneal cavity. As the free abdominal fluid becomes turbid/purulent, the lymphatics are blocked with fibrin and cellular debris, and even more fluid accumulates. Systemic hypovolemic and septic shock results as there is loss of circulating fluid volume and further absorption of bacterial endotoxins and exotoxins.

Clinical signs of a patient with peritonitis can range from extremely mild and non-specific, to severe. Symptoms may include lethargy, anorexia, vomiting, diarrhea, abdominal pain, pyrexia, collapse and shock. History and signalment in combination with the above symptoms should prompt further diagnostics.

The diagnosis of peritonitis can be made by visualization of free air or fluid in the abdomen on plain radiographs, by abdomenocentesis and cytology, and by diagnostic peritoneal lavage. It is important to remember that a mild inflammatory reaction is produced every time the peritoneal cavity is entered surgically, and that air introduced into the abdomen during surgery can be seen on radiographs for at least one week post-operatively. Cytologic evaluation of abdominal fluid can reveal the hallmarks of septic peritonitis: degenerate neutrophils with intracellular bacteria, and possibly organic debris. Bile peritonitis can be diagnosed reliably by comparing the bilirubin concentration of the abdominal effusion to the serum bilirubin concentration: the abdominal effusion will yield a bilirubin concentration at least twice that of the serum.

Immediate medical management prior to emergency surgery should include aggressive shock therapy, and correction of metabolic and acid-base imbalances, Colloids and/or blood products may be indicated based on clinical signs and initial bloodwork results. Potassium and blood glucose concentrations must be evaluated. Broad spectrum antibiotic therapy should be initiated immediately, unless emergency surgery can be performed promptly and there is desire for abdominal fluid culture/sensitivity. A “safe” antimicrobial protocol includes a fluoroquinolone plus metronidazole.

The goals of exploratory surgery are to arrest ongoing contamination, remove all foreign and purulent material, and to provide drainage of the peritoneal exudate. Provision for enteral nutritional support should also be considered via placement of gastrostomy or jejunostomy feeding tubes. Complete exploration and assessment of all abdominal structures is vital. Leaking viscus structures must be repaired or resected. Cholecystectomy is preferred to repair of a necrotizing gall bladder with poor viability. A thorough and exhaustive lavage of the entire peritoneal cavity is absolutely crucial, with complete removal of all free fluid.

Drainage of the abdomen may be accomplished by placement of peritoneal drains or by open abdominal management. Most peritoneal drains will seal within 6 hours due to fibrin/adhesions or omentum, and Penrose drains are relatively worthless to maintain abdominal fluid drainage. Commercial silastic peritoneal column disc catheters seem the preferable method of providing continuous drainage; omentectomy must be performed to allow any drains to function. Open abdominal drainage has been the mainstay of management of peritonitis, but the morbidity and effort/expense to manage these patients is not to be underestimated. Open drainage requires aseptic technique and usually general anesthesia during bandage changes, which may be as frequent as every 4 hours initially.