Peritonitis is defined as an inflammation of the serosal membrane that
lines the abdominal cavity and the organs contained therein. The peritoneum, which is an otherwise sterile environment, reacts to various pathologic stimuli with a fairly uniform inflammatory response. Depending on the underlying pathology, the resultant peritonitis may be infectious or sterile (ie, chemical or mechanical). The abdomen is the second most common source of sepsis and secondary peritonitis. [1]Intra-abdominal sepsis is an inflammation of the peritoneum caused by pathogenic microorganisms and their products. [2] The inflammatory process may be localized (abscess) or diffuse in nature. Peritonitis is most often caused by introduction of an infection into the otherwise sterile peritoneal environment through organ perforation, but it may also result from other irritants, such as foreign bodies, bile from a perforated gall bladder or a lacerated liver, or gastric acid from a perforated ulcer. Women also experience localized peritonitis from an infected fallopian tube or a ruptured ovarian cyst. Patients may present with an acute or insidious onset of symptoms, limited and mild disease, or systemic and severe disease with septic shock. Peritoneal infections are classified as primary (ie, from hematogenous dissemination, usually in the setting of an immunocompromised state), secondary (ie, related to a pathologic process in a visceral organ, such as perforation or trauma, including iatrogenic trauma), or tertiary (ie, persistent or recurrent infection after adequate initial therapy). Primary peritonitis is most often spontaneous bacterial peritonitis (SBP) seen mostly inpatients with chronic liver disease. Secondary peritonitis is by far the most common form of peritonitis encountered in clinical practice. Tertiary peritonitis often develops in the absence of the original visceral organ pathology. Infections of the peritoneum are further divided into generalized (peritonitis) and localized (intra-abdominal abscess). This article focuses on the diagnosis and management of infectious peritonitis and abdominal abscesses. An abdominal abscess is seen in the image below.
Peritonitis and abdominal sepsis. A 35-year-old man
with a history of Crohn disease presented with pain and swelling in the right abdomen. In figure A, a thickened loop of terminal ileum is evident adherent to the right anterior abdominal wall. In figure B, the right anterior abdominal wall is markedly thickened and edematous, with adjacent inflamed terminal ileum. In figure C, a right lower quadrant abdominal wall abscess and enteric fistula are observed and confirmed by the presence of enteral contrast in the abdominal wall. The diagnosis of peritonitis is usually clinical. Diagnostic peritoneal lavage may be helpful in patients who do not have conclusive signs on physical examination or who cannot provide an adequate history; in addition, paracentesis should be performed in all patients who do not have an indwelling peritoneal catheter and are suspected of having SBP, because results of aerobic and anaerobic bacterial cultures, used in conjunction with the cell count, are useful in guiding therapy. The management approach to peritonitis and peritoneal abscesses targets correction of the underlying process, administration of systemic antibiotics, and supportive therapy to prevent or limit secondary complications due to organ system failure. Early control of the septic source is mandatory and can be achieved operatively and nonoperatively. Nonoperative interventions include percutaneous abscess drainage, as well as percutaneous and endoscopic stent placements. Operative management addresses the need to control the infectious source and to purge bacteria and toxins. The type and extent of surgery depends on the underlying disease process and the severity of intra-abdominal infection.