Andrew J. Dart, Hannah-Sophie Chapman The peritoneum is a single layer of squamous mesothelial cells resting on a loose connective tissue containing blood vessels, lymphatics, and nerves. Anatomically, the peritoneum is divided into a parietal and visceral peritoneum. The parietal peritoneum lines the diaphragm, abdominal walls, and pelvic cavity. The parietal peritoneum is continuous with the visceral peritoneum, which encloses the intraperitoneal organs and forms the omentum and mesenteries of the abdominal cavities. A small volume of peritoneal fluid lubricates the surface of the visceral and parietal peritoneum. Together the peritoneum and fluid are responsible for preventing adhesion formation. Normal peritoneal fluid is a transparent straw-colored ultrafiltrate of plasma with a total protein (TP) concentration of less than 1.5 g/dL (15 g/L) and total nucleated cell count (TNCC) of less than 2000 cells/µL (2 × 109 cells/L). The distribution and consistent turnover of peritoneal fluid ensures a highly effective clearance mechanism for bacteria, cells, and foreign material entering the peritoneal cavity. Neutrophils represent 24% to 60% of the cells found in peritoneal fluid. Protein concentrations greater than 2.0 to 2.5 mg/dL (20 to 25 g/L) and TNCCs greater than 5000 to10,000 cells/µL (5 to 10 × 109 cells/L) are considered abnormal. Peritonitis in the horse may have an infectious (bacterial, viral, fungal, or parasitic) or noninfectious (traumatic, chemical, or neoplastic) cause (Box 80-1). It is classified as primary or secondary (defined by cause); peracute, acute, or chronic (defined by onset and duration); diffuse or localized (defined by region); and septic or nonseptic (defined by the presence or absence of bacteria). Acute, diffuse, septic peritonitis secondary to surgical manipulation or perforation of the gastrointestinal tract is the most common manifestation of peritonitis in the horse. Sepsis usually involves a mixed bacterial population, whether from gastrointestinal origin or from environmental contamination following trauma (Box 80-2). Common bacterial isolates from exudative peritonitis include the Enterobacteriaceae, obligate anaerobic bacteria, and gram-positive organisms. Anaerobic bacteria are reported to be present in at least 20% to 40% of cases of peritonitis. It has been suggested that established infections are often characterized by a few organisms despite the variety of organisms that might initially be introduced. This is proposed to occur through a process of selective competition between bacteria. The phases of peritonitis are often separated. The contamination phase lasts 3 to 6 hours and is characterized by increased vascular permeability and influx of protein-rich fluid and white cells into the peritoneal cavity, resulting in the release of mediators of inflammation. Diffuse acute peritonitis lasts up to 5 days and reflects the spread of bacteria throughout the peritoneal cavity. The inflammatory response escalates with fluid accumulation and buildup of fibrin and inflammatory products, resulting in ileus mediated by the sympathetic nervous system. These processes serve to confine the spread of contamination. However, if bacteria overwhelm the immune system, bacteremia and endotoxemia develop, resulting in hypovolemia and hypoproteinemia and ultimately adhesions and abscess formation. This phase is associated with the highest mortality rate. The acute localizing phase develops 4 to 10 days after the initial insult. Fibrin aggregates attempt to localize the infection. Chronic abscess formation starts as early as 8 days and persists until the body isolates the infection. Clinical signs are often nonspecific, irrespective of cause, and may include fever, signs of depression, inappetence, tachycardia, dehydration, reduced gastrointestinal motility, signs of abdominal pain, diarrhea, and weight loss. Clinical signs in horses with septic peritonitis are usually more severe than those with nonseptic peritonitis because of the systemic effects of bacteremia and endotoxemia. The exception is peritonitis caused by Actinobacillus equuli—these horses often have malaise, inappetence, fever, and mild signs of abdominal pain with few other localizing signs. Horses with peracute peritonitis may be found dead or showing signs of severe endotoxemia, which leads rapidly to circulatory shock and death in a matter of hours. Typical findings include severe depression, sweating, muscle fasciculations, tachycardia, rapid shallow breathing, cold extremities, and purple or dark red mucous membranes with prolonged capillary refill times. Fever is often not a feature because of the peracute nature of the disease. Acute peritonitis has a slower onset with the gradual spread of bacteria within the abdomen. Horses may have a history of showing signs of intermittent abdominal pain, and may show signs of depression, inappetence, fever, dehydration, tachycardia, tachypnea, congested mucous membranes with delayed refill time, and ileus or diarrhea. Chronic peritonitis may be associated with low-grade and nonspecific signs including intermittent or persistent fever, signs of depression and inappetence, progressive weight loss, dehydration, intermittent mild abdominal pain, reduced fecal output, decreased intestinal motility, intermittent diarrhea, and ventral edema.
Peritonitis
Anatomy and Physiology
Pathophysiology
Clinical Signs
