Peritonitis
Peritonitis: Excerpt from Handbook of Diseases
Peritonitis is an acute or chronic inflammation of the peritoneum, the membrane that lines the abdominal cavity and covers the visceral organs. Inflammation may extend throughout the peritoneum, or it may be localized as an abscess.
Peritonitis commonly decreases intestinal motility and causes intestinal distention with gas. Mortality is 10%, with death usually resulting from bowel obstruction; the mortality was much higher before the introduction of antibiotics.
Causes
Although the GI tract normally contains bacteria, the peritoneum is sterile. In peritonitis, however, bacteria invade the peritoneum. Generally, such infection results from inflammation and perforation of the GI tract, allowing bacterial invasion. Usually, this is a result of appendicitis, diverticulitis, peptic ulcer, ulcerative colitis, volvulus, strangulated obstruction, perforated or ruptured gallbladder, gangrenous gallbladder, abdominal neoplasm, or a penetrating wound.
Peritonitis may also result from chemical inflammation, as in the rupture of a fallopian tube or the bladder, perforation of a gastric ulcer, or release of pancreatic enzymes.
With chemical and bacterial inflammation, accumulated fluids containing protein and electrolytes make the transparent peritoneum opaque, red, inflamed, and edematous. Because the peritoneal cavity is so resistant to contamination, such infection is often localized as an abscess instead of disseminated as a generalized infection.
Signs and symptoms
The key symptom of peritonitis is sudden, severe, and diffuse abdominal pain that tends to intensify and localize in the area of the underlying disorder.
CLINICAL TIP: Direct or rebound tenderness may be elicited over an area affected by diverticulitis.
Pain may be accompanied by anorexia, nausea, vomiting, abdominal distention, and altered bowel habits (particularly constipation). For example, if appendicitis causes the rupture, pain eventually localizes in the right lower quadrant. The patient commonly displays weakness, pallor, excessive sweating, and cold skin because of excessive loss of fluid, electrolytes, and protein into the abdominal cavity.
Decreased intestinal motility and paralytic ileus result from the effect of bacterial toxins on the intestinal muscles. Intestinal obstruction causes nausea, vomiting, and abdominal rigidity.
Other clinical characteristics
Typical features include hypotension, tachycardia, signs of dehydration (oliguria, thirst, dry swollen tongue, pinched skin), acutely tender abdomen associated with rebound tenderness, temperature of 103° F (39.4° C) or higher, and hypokalemia. Inflammation of the diaphragmatic peritoneum may cause shoulder pain and hiccups.
Abdominal distention and resulting upward displacement of the diaphragm may decrease respiratory capacity. Typically, the patient with peritonitis tends to breathe shallowly and move as little as possible to minimize pain.
Diagnosis
Severe abdominal pain in a patient with direct or rebound tenderness suggests peritonitis. Abdominal computed tomography scan or X-rays showing edematous and gaseous distention of the small and large bowel support the diagnosis. In the case of perforation of a visceral organ, the X-ray shows air in the abdominal cavity.
Other tests include the following:
❑ Chest X-ray may show elevation of the diaphragm.
❑ Blood studies reveal leukocytosis (greater than 20,000/µl).
❑ Paracentesis reveals bacteria, exudate, blood, pus, or urine.
❑ Laparotomy may be necessary to identify the underlying cause.
Treatment
Early treatment of GI inflammatory conditions and preoperative and postoperative antibiotic therapy help prevent peritonitis. After peritonitis develops, emergency treatment must combat infection, restore intestinal motility, and replace fluids and electrolytes.
Empiric antibiotic therapy usually includes the administration of appropriate antibiotics, depending on the infecting organisms. To decrease peristalsis and prevent perforation, the patient should receive nothing by mouth; I.V. fluids are administered. Other supportive measures include preoperative and postoperative administration of analgesia and nasogastric (NG) decompression.
When peritonitis results from perforation, surgery is necessary. The aim of surgery is to eliminate the source of infection by evacuating the spilled contents and repairing any organ perforation.
Special considerations
❑ Monitor vital signs, fluid intake and output, and the amount of NG drainage or vomitus.
❑ Place the patient in semi-Fowler’s position to facilitate comfort.
❑ Encourage the patient to deep-breathe, cough effectively, and use an incentive spirometer.
❑ Teach the patient how to splint the incision.
❑ Counteract mouth and nose dryness due to fever and NG intubation with regular cleaning and lubrication.
After surgery to evacuate the peritoneum:
❑ Administer parenteral fluid and electrolytes as ordered. Accurately record fluid intake and output, including drainage from the NG tube and the incision.
❑ Place the patient in Fowler’s position to promote drainage (through drainage tube) by gravity.
❑ Encourage and assist ambulation as ordered, usually on the first postoperative day.
❑ Observe for signs of dehiscence (may complain that, “something gave way”) and abscess formation (persistent abdominal tenderness and fever).
❑ Frequently assess for peristaltic activity by listening for bowel sounds and evaluating for passage of flatus, bowel movements, and soft abdomen.
❑ When peristalsis returns and temperature and pulse rate are normal or when NG output diminishes (less than 200 ml/24 hr), the NG tube is removed.
❑ Gradually decrease parenteral fluids and increase oral intake.
Book Source Details
- Book Title: Handbook of Diseases
- Author(s): Springhouse
- Year of Publication: 2003
- Copyright Details: Handbook of Diseases, Copyright © 2003 Lippincott Williams & Wilkins.
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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More About This Book:
Title: Handbook of Diseases
Authors: Springhouse
Publisher: Lippincott Williams & Wilkins
Copyright: 2003
ISBN: 1-58255-266-5
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