60 Peritonitis
Overview/pathophysiology
Peritonitis is the inflammatory response of the peritoneum to offending chemical and bacterial agents invading the peritoneal cavity. The inflammatory process can be local or generalized and may be classified as primary, secondary, or tertiary, depending on pathogenesis of the inflammation. Primary peritonitis, such as spontaneous bacterial peritonitis, occurs without a recognizable cause. Secondary peritonitis is caused by abdominal injury or rupture of abdominal organs. Common events include abdominal trauma, postoperative leakage of gastrointestinal (GI) content or blood into the peritoneal cavity, intestinal ischemia, ruptured or inflamed abdominal organs, poor sterile techniques (e.g., with peritoneal dialysis), and direct contamination of the bloodstream. Tertiary peritonitis is a persistent abdominal sepsis without a focus of infection, and it may follow treatment of a previous episode of peritonitis. The peritoneum responds to invasive agents by attempting to localize the infection with a shift of the omentum (the “guardian of the abdominal cavity”) to wall off the inflamed area. Inflammation of the peritoneum results in tissue edema, development of fibrinous exudate, and hypermotility of the intestinal tract. As the disease progresses, paralytic ileus occurs, and intestinal fluid, which then cannot be reabsorbed, leaks into the peritoneal cavity. As a result of the fluid shift, cardiac output and tissue perfusion are reduced, leading to impaired cardiac and renal function. If infection or inflammation continues, respiratory failure and shock can ensue. Peritonitis often is progressive and can be fatal. It is the most common cause of death following abdominal surgery, and mortality is dictated by the patient’s overall health, including nutritional and immune status and organ function.
Assessment
Signs and symptoms:
Early findings:
Acute abdominal pain with movement, anorexia, nausea, vomiting, chills, fever, rigor, malaise, weakness, hiccoughs, diaphoresis, absence of bowel sounds, and abdominal distention and rigidity (often described as boardlike).
Physical assessment:
Presence of tachycardia, hypotension, and shallow and rapid respirations caused by abdominal distention and discomfort. Often the patient assumes a supine position with knees flexed or side-lying with knees drawn up toward the chest. Palpation usually reveals peritoneal irritation as shown by distention, abdominal rigidity with general or localized tenderness, guarding, and rebound or cough tenderness. However, as many as one fourth of these patients will have minimal or no indications of peritoneal irritation. Auscultation findings include hyperactive bowel sounds during the gradual development of peritonitis and absence of bowel sounds or infrequent high-pitched sounds (“tinkling” or “squeaky”) during later stages if paralytic ileus occurs. Ascites may be present as demonstrated by shifting areas of dullness on percussion.
Diagnostic tests
Serum tests:
May reveal presence of leukocytosis, usually with a shift to the left (may be the only sign of tertiary peritonitis); hemoconcentration; elevated blood urea nitrogen (BUN); and electrolyte imbalance, particularly hypokalemia. Hypoalbuminemia and prolonged prothrombin time (PT), in combination with leukocytosis, are especially characteristic.
Arterial blood gas (ABG) values:
May reveal hypoxemia (Pao2 less than 80 mm Hg) or acidosis (pH less than 7.40).
Paracentesis for peritoneal aspiration with culture and sensitivity and cell count:
May be performed to determine presence of blood, bacteria, bile, pus, and amylase content and identify causative organism. Gram stain of ascitic fluid is positive in only about 25% of these patients. Diagnosis of bacterial peritonitis is confirmed by positive culture of ascitic fluid and cell count and differential of the ascitic fluid notable for elevated polymorphonuclear (PMN) count of 250 cells/mm3 or greater. Ascitic fluid also may be tested for total protein, glucose concentration, and lactate dehydrogenase to differentiate spontaneous bacterial peritonitis from secondary bacterial peritonitis.
Abdominal x-ray examination:
To determine presence of distended loops of bowel and abnormal levels of fluid and gas, which usually collect in the large and small bowel in the presence of a perforation or obstruction. “Free air” under the diaphragm also may be visualized, which indicates a perforated viscus.
Computed tomography (CT) scan, ultrasound, and magnetic resonance imaging (MRI):
May be used to evaluate abdominal pain and more clearly delineate nondistinct areas found by plain abdominal x-ray examination.
Chest x-ray examination:
Abdominal distention may elevate the diaphragm. Pain from peritonitis may limit respiratory excursion and lead to associated infiltrates in the lower lobes. In later stages, changes in serum osmolality allow for pleural effusions to occur.
Contrast x-ray examination:
May be used to identify specific intestinal pathologic conditions. Water-soluble contrast (e.g., meglumine diatrizoate) may be used to evaluate suspected upper GI perforation.
Radionuclide scans:
Gallium, hepatoiminodiacetic acid (HIDA) (lidofenin) and liver-spleen scans may be used to identify intraabdominal abscess.
Nursing diagnoses:
Risk for shock
related to potential for worsening/recurring peritonitis or development of inflammatory process
Desired Outcome: Patient is free of symptoms of worsening/recurring peritonitis or septic shock as evidenced by normothermia, blood pressure (BP) at least 90/60 mm Hg (or within patient’s normal range), heart rate (HR) 100 bpm or less, absence of chills, presence of eupnea, urinary output at least 30 mL/hr, central venous pressure (CVP) 2-6 mm Hg (5-12 cm H2O), decreasing abdominal girth measurements, and minimal tenderness to palpation.
