Secondary peritonitis develops when bacteria contaminate the peritoneum as a result of spillage from an intraabdominal viscus. The organ isms found almost always constitute a mixed flora in which facultative gram-negative bacilli and anaerobes predominate, especially when the contaminating source is colonic. Early in the course of infection, when the host response is directed toward containment, exudate containing fibrin and PMNs is found. Early death in this setting is attributable to gram-negative bacillary sepsis and to potent endotoxins circulating in the bloodstream. Gram-negative bacilli, particularly E. coli, are common bloodstream isolates, but Bacteroides fragilis bacteremia also occurs. The severity of abdominal pain and the clinical course depend on the inciting process. The organisms isolated from the peritoneum also vary with the source of the initial process and the normal flora at that site. Secondary peritonitis can result primarily from chemical irritation and/or bacterial contamination. For example, as long as the patient is not achlorhydric, a ruptured gastric ulcer will release low-pH gastric contents that will serve as a chemical irritant. The normal flora of the stomach comprises the same organisms found in the oropharynx but in lower numbers. Thus, the bacterial burden in a ruptured ulcer is negligible compared with that in a ruptured appendix. The normal flora of the colon below the ligament of Treitz contains ~10¹¹ anaerobic organisms/g of feces but only 10⁸ aerobes/g; therefore, anaerobic species account for 99.9% of the bacteria . Leak age of colonic contents (pH 7–8) does not cause significant chemical peritonitis, but infection is intense because of the heavy bacterial load.

Depending on the inciting event, local symptoms may occur in secondary peritonitis—for example, epigastric pain from a ruptured gastric ulcer. In appendicitis (Chap. 342), the initial presenting symptoms are often vague, with periumbilical discomfort and nausea followed in a number of hours by pain more localized to the right lower quadrant. Unusual locations of the appendix (including a retrocecal position) can complicate this presentation further. Once infection has spread to the peritoneal cavity, pain increases, particularly with infection involving the parietal peritoneum, which is innervated extensively. Patients usually lie motionless, often with knees drawn up to avoid stretching the nerve fibers of the peritoneal cavity. Coughing and sneezing, which increase pressure within the peritoneal cavity, are associated with sharp pain. There may or may not be pain localized to the infected or dis eased organ from which secondary peritonitis has arisen. Patients with secondary peritonitis generally have abnormal findings on abdominal examination, with marked voluntary and involuntary guarding of the anterior abdominal musculature. Later findings include tenderness, especially rebound tenderness. In addition, there may be localized findings in the area of the inciting event. In general, patients are febrile, with marked leukocytosis and a left shift of the WBCs to band forms.

While recovery of organisms from peritoneal fluid is easier in secondary than in primary peritonitis, a tap of the abdomen is rarely the procedure of choice in secondary peritonitis. An exception is in cases involving trauma, where the possibility of a hemoperitoneum may need to be excluded early. Emergent studies (such as abdominal CT) to find the source of peritoneal contamination should be under taken if the patient is hemodynamically stable; unstable patients may require surgical intervention without prior imaging. Results of cultures from chronic drain sites are not reliable for defining the etiology of infections.

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المزيد

مواضيع ذات صلة

Peritonitis in Patients Undergoing Continuous Ambulatory Peritoneal Dialysis

Primary (Spontaneous) Bacterial Peritonitis

Signs and Symptoms of Lyme disease

Pathology and Microbiology of Lung Abscess

Epidemiology of Ventilator-Associated Pneumonia

Epidemiology of Community-Acquired Pneumonia

Etiology of Community-Acquired Pneumonia

Causes of Macrocytosis with Normoblastic Erythropoiesis

Urinary tract infection

Genitourinary malformations

Diabetic Foot Ulcers

Kidney transplantation