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Primary Peritonitis
Pathogenesis. Primary peritonitis is an infection of the peritoneal cavity not directly related to other intraabdominal abnormalities. The vast majority of cases are due to bacterial infection; it is also commonly known as spontaneous bacterial
peritonitis. Usually it occurs in the presence of ascites from
any of a variety of underlying conditions [1]. In the preantibiotic era, primary peritonitis accounted for 10% of all pediatric abdominal emergencies; it now accounts for 1 2% [2].
The decline has been attributed to widespread use of antibiotics
for minor upper respiratory tract illness.
Although primary peritonitis may occur in children without
predisposing disease, it is especially associated with postnecrotic cirrhosis and nephrotic syndrome. In adults, primary
peritonitis develops in up to 25% of patients with alcoholic
cirrhosis but has also been reported to occur in adults with
postnecrotic cirrhosis, chronic active hepatitis, acute viral hepa-
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titis, congestive heart failure, metastatic malignant disease, systemic lupus erythematosus, and lymphedema and, rarely, in
adults with no underlying disease [3]. The presence of ascites
appears to be the common link among these various conditions.
The route of infection in primary peritonitis is usually not
apparent but is thought to be hematogenous, lymphogenous,
via transmural migration through an intact gut wall from the
intestinal lumen, or, in women, from the vagina via the fallopian tubes. In cirrhotic patients the hematogenous route is most
likely. Organisms removed from circulation by the liver may
contaminate hepatic lymph and pass through the permeable
lymphatic walls into the ascitic fluid. In addition, portosystemic
shunting greatly diminishes hepatic clearance of bacteremia,
which would tend to perpetuate bacteremia and increase the
opportunity to cause metastatic infection at susceptible sites
such as the ascitic collection.
The infrequency of primary peritonitis in forms of ascites
other than that due to liver disease emphasizes the importance
of intrahepatic shunting in the pathogenesis of this disease.
The hepatic reticuloendothelial system is known to be a major
site for removal of bacteria from blood, and animal studies
have suggested that destruction of blood-borne bacteria by the
reticuloendothelial system is impaired in experimental cirrhosis
and in alcoholic liver disease. The decrease in phagocytic activity seen in alcoholic cirrhosis is proportional to the severity of
the liver disease.
Enteric bacteria may also gain access to the peritoneal cavity
by directly traversing the intact intestinal wall. In an animal
model, Escherichia coli passes from the bowel into the peritoneal cavity after the introduction of hypertonic solutions into
the peritoneum. The infrequent occurrence of bacteremia and
the multiplicity of species in peritoneal fluid when anaerobic
bacteria are involved suggest that transmural migration of bacteria is the probable route of infection of ascitic fluid in most
of these patients.
In prepubertal girls, the pathogenesis of primary peritonitis
is likely related to an ascending infection of genital origin, as
suggested by the simultaneous presence of pneumococci in
vaginal secretions and peritoneal fluid. Alkaline vaginal secretions that occur in this age group may be less inhibitory to
bacterial growth than the acidic secretions of postpubertal females.
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Peritonitis Update
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examination for additional pathological conditions. Antimicrobial therapy is usually continued for 10 14 days if improvement is noted, but short-course therapy for 5 days has been
shown to be as efficacious as the longer course in some patients.
Administration of intraperitoneal antimicrobials is not necessary.
Treatment of primary peritonitis is successful in more than
one-half of cirrhotic patients, but because of the underlying
liver condition, the overall mortality has been reported as high
as 95% in some series. Those patients with the poorest prognosis were found to have renal insufficiency, hypothermia, hyperbilirubinemia, and hypoalbuminemia [9].
Treatment of peritonitis caused by gram-positive organisms,
as well as of early infections, has been more frequently successful than treatment of gram-negative or late infections. In nephrotic patients with gram-positive infections or in patients
who do not have a preterminal underlying illness, the survival
rate is 90%.
Given the common occurrence and high mortality of primary
peritonitis in the setting of cirrhosis with ascites, prevention is
a desirable strategy. This is particularly true for patients who
are awaiting liver transplantation. Selective decontamination
of the gut with oral norfloxacin (400 mg daily) has been shown
to reduce the incidence of spontaneous bacterial peritonitis.
Norfloxacin has the disadvantage of selecting for gram-positive
organisms, including S. aureus, and quinolone-resistant gramnegative organisms. More recently, trimethoprim-sulfamethoxazole (double-strength, given once daily for 5 days each week)
has been shown to reduce the incidence of peritonitis and be
well tolerated [10]. A survival-rate advantage has not been
demonstrated for any of these preventive regimens.
Secondary and Tertiary Peritonitis
Pathogenesis. Secondary intraabdominal infection usually is
due to spillage of gastrointestinal or genitourinary microorganisms into the peritoneal space as a result of loss of integrity of
the mucosal barrier. Examples include appendicitis, diverticulitis, cholecystitis, penetrating wound of the bowel, and perforation of a gastric or duodenal ulcer. Secondary infection is relatively common, taking the form of either generalized peritonitis
or localized abscesses. Abscesses may be restricted to the immediate peritoneal space around a diseased intraabdominal organ, such as pericholecystic, periappendiceal, or peridiverticular abscesses, or to certain peritoneal recesses, such as
interloop, subdiaphragmatic, subhepatic, lesser sac, or pelvic
abscesses.
Peritoneal signs suggestive of appendicitis in immunocompromised patients, e.g., patients with AIDS, organ transplant
recipients, and those receiving chemotherapy or corticosteroids
for neoplasms (especially myelosuppressive drugs), may be due
to typhlitis, an inflammation of the cecum [11]. Cecal ulceration
in these patients may progress to perforation and secondary
peritonitis with colonic flora. Perforation complicating penetrat-
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ing cytomegalovirus enterocolitis has been described as a common cause of acute abdomen in patients with AIDS [12].
Tertiary peritonitis has been conceived as a later stage in
the disease, when clinical peritonitis and systemic signs of
sepsis (e.g., fever, tachycardia, tachypnea, hypotension,
elevated cardiac index, low systemic vascular resistance, leukopenia or leukocytosis, and multiorgan failure) persist after treatment for secondary peritonitis and either no organisms or lowvirulence pathogens, such as enterococci and fungi, are isolated
from the peritoneal exudate. These organisms may gain access
to the peritoneal cavity by contamination during operative interventions, by selection from the initial polymicrobial peritoneal inoculum by antibiotic therapy, or by translocation of
bowel flora. Translocation may be promoted by intestinal ischemia, endotoxemia, malnutrition, or proliferation of resistant
bowel flora by antibiotic pressure.
The cytokine response in peritonitis has been the subject of
a recent excellent review [13]. Undoubtedly, many of the systemic as well as abdominal manifestations of peritonitis are
mediated by cytokines, such as TNF, IL-1, IL-6, IFN-g, and
others. Cytokines appear in the systemic circulation of patients
with peritonitis and to a much greater extent in the peritoneal
exudate [14]. These cytokines are produced by macrophages
and other host cells in response to bacteria or bacterial products,
such as endotoxin [15], or by tissues traumatized during the
operative procedure [16]. Another potential source is direct
translocation of cytokines through the intestinal barrier.
Cytokine responses have been studied in the peritoneal exudate in experimental animal models of peritonitis [17 20], in
patients with spontaneous bacterial peritonitis [21, 22], in patients undergoing continuous ambulatory peritoneal dialysis
(CAPD) [23 25], and in patients with severe secondary bacterial peritonitis who were undergoing planned relaparotomy
[14]. Antibodies to TNF have been found to fail to protect
against death [26] and failed to reduce serum levels of IL-1
and IL-6 in an experimental model of peritonitis [17, 20, 27].
In contrast, antibodies to endotoxin were found to prevent death
in this model, as well as to reduce bacterial numbers in the
peritoneal exudate [28]. Antibodies to IFN-g also afforded a
protective effect both in this model of experimental peritonitis
and following intravenous injection of endotoxin [29].
Microbiology. With gastrointestinal perforation as the precipitating event, the number and types of microorganisms isolated from the peritoneal cavity depend on the level of the
perforation. The stomach in the fasting state contains a sparse
microflora of a few relatively more acid-resistant species, e.g.,
lactobacilli or Candida species. Similarly, the duodenum and
proximal small bowel contain a sparse microflora in the fasting
state, whereas the colon contains a high microbial density, i.e.,
about 1012/g, of which 99.9% are obligate anaerobes, mainly
of the B. fragilis group.
E. coli, the predominant colonic facultative anaerobe, is
found at counts of 106 8/g, while enterococci are less numerous
at counts of 104 6/g. The characteristic microflora, however,
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therapeutic attempts [46]. This has led to investigation of endotoxin and cytokine levels in circulation to predict outcome.
However, the magnitude of levels of endotoxin, TNF, and
IL-6, in circulation in patients with peritonitis, has not been
invariably related to prognosis [14, 47 51]. It has been suggested that cytokine levels in the peritoneal exudate, rather than
the blood, better reflect the severity of the compartmentalized
peritoneal infection and predict outcome [14].
Management and prevention. A skeptical attitude is necessary when reviewing reports on clinical trials of antimicrobial
therapy for intraabdominal sepsis. Surgical therapy alone may
be sufficient to cure many otherwise healthy, young patients
with intraabdominal infection who have no signs of severe
sepsis; even antimicrobial agents to which the pathogens are
resistant may be associated with a good outcome for these
patients.
To establish a specific role for antimicrobial regimens requires clinical trials with sufficient numbers of high-risk patients whose severity of illness has been stratified by APACHE
II scoring. Clinical trials are frequently diluted by low-risk
patients, since the sickest patients who would test the efficacy
of the antimicrobial agent are often excluded by strict enrollment requirements.
Medical management of secondary peritonitis includes use
of antimicrobial therapy and supportive measures to maintain
vital functions, e.g., to improve or maintain circulation, nutrition, and oxygenation to vital organs. Antimicrobial agents
must penetrate to the site of infection in concentrations that
are sufficient to overcome the effects of high bacterial density,
metabolic inactivity and slow growth rate of the bacterial
inoculum, low pH, low redox potential, necrotic tissue, and
bacterial products that may lower the drugs activity. For
example, aminoglycosides and clindamycin are less active at
acid pH values, aminoglycosides are less active at low redox
potentials, and b-lactam drugs are less active against high
bacterial densities.
The animal model of intraabdominal sepsis demonstrated the
necessity of treating both the facultative enteric gram-negative
bacilli, namely E. coli, and the anaerobic gram-negative bacilli,
namely B. fragilis. Empirical use of an antimicrobial regimen
active against these organisms has been well established. Indeed, the need for intraoperative cultures to document etiological microbes and their antimicrobial susceptibilities has been
questioned, because the results are rarely available to influence
clinical decisions [52].
Early clinical trials have established the therapeutic regimen
of clindamycin plus aminoglycoside as the gold standard
[53, 54]. Aminoglycosides are frequently underdosed because
of fear of nephrotoxicity or because of underestimation of the
expanded volume of distribution in critically ill patients with
intraabdominal sepsis. Once-daily aminoglycoside therapy
in which the total daily dose is given to patients with normal
renal function as a single dose every 24 hours rather than as
multiple smaller, divided doses obviates these dosing prob-
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Clinical presentation and evaluation. Criteria for the diagnosis of CAPD-associated peritonitis are (1) signs and symptoms
of peritoneal irritation, (2) cloudy dialysate effluent with a
leukocyte count of 100/mm3, and (3) a positive culture of
dialysate fluid. Any two of these criteria may be adequate to
establish the diagnosis [82]. Clinical manifestations of peritonitis vary from mild to severe, depending largely on the virulence
of the pathogen and the time course of the infection [67].
Generally, turbid dialysate is the first and most common symptom to appear, followed shortly thereafter by abdominal pain
and tenderness.
Laboratory evaluation of dialysate effluent is critical to establishing the diagnosis of CAPD-associated peritonitis. A dialysate leukocyte count of 100/mm3 is the traditional diagnostic
value but is not specific. The differential cell count of dialysate
may have a better predictive value. In one study, polymorphonuclear leukocytes comprised 50% of the total cell count
(mean, 85%) in infected patients, while in uninfected patients
the proportion was 40% (mean, 12%) [82]. A preponderance
of eosinophils in the fluid is seen in the self-limited condition
eosinophilic peritonitis, which often follows placement of
the Tenckhoff catheter and may represent allergy to the tubing
[83, 84].
Peritoneal eosinophilia also occurs with fungal peritonitis
or recent intraperitoneal administration of antibiotics. Gram
staining of dialysis fluid detects only 20% 30% of peritonitis
episodes. Gram-positive organisms, especially S. aureus, are
more likely to be detected than are gram-negative ones [85].
Cultures offer a greater yield than gram stains but require
concentration of the dialysate by centrifugation, filtration, or
lysis-centrifugation [86].
Even with these specialized methods, 3% 30% of CAPDrelated peritonitis episodes are culture-negative. Presumably,
most are due to fastidious, low-virulence organisms or coagulase-negative staphylococci that survive less well in dialysis
fluid [70]. Cases of culture-negative peritonitis that do not
respond to empirical antibiotic treatment should be further investigated by performance of dialysate fluid cultures for mycobacteria and fungi. Blood cultures are usually negative, regardless of the etiologic agent.
Management and prevention. The increased use of intraperitoneal antibiotics as therapy for peritonitis has allowed most patients to be treated on an ambulatory basis. Hospitalization is
indicated for those who are severely ill or who are unable to
manage administration of intraperitoneal antibiotics at home. A
variety of antimicrobial agents have been used successfully for
treatment, including penicillins, cephalosporins, aztreonam, imipenem, aminoglycosides, fluoroquinolones, and macrolide and
glycopeptide antibiotics. Initial therapy may be guided by results
of the dialysis fluid gram staining, but since these are uncommonly positive, empirical treatment with a cephalosporin or vancomycin plus aminoglycoside is typically initiated.
In relatively mild episodes of peritonitis, a single agent with
antistaphylococcal activity may also be suitable. Antibiotic se-
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factors may also be important in the pathogenesis of this infection [73]. Microbial pathogens that reach the dialyzed peritoneal cavity are removed by three major lines of defense. First,
despite the dilution of fibrinogen and coagulation proteins, fibrin trapping and sequestration of microorganisms operate efficiently in the dialyzed peritoneum. Second, removal of the
dialysate serves to eliminate or decrease the inoculum of contaminating organisms. Finally, a complex interplay of opsonization, phagocytosis, and intracellular killing by peritoneal
macrophages, mesothelial cells, and neutrophils serves to combat bacterial invasion and prevent infection.
Unfortunately, the dialyzed peritoneal cavity is not a supportive milieu for operation of these cellular and immunologic
defense mechanisms because of its low pH (5.5 6.0), high
osmolarity (300 400 mOsmol/kg), and decreased levels of IgG
and complement (1% of their normal levels). A correlation
between deficiencies in these host defenses and patient risk for
peritonitis has not been conclusively identified [73].
Microbiology. In patients undergoing CAPD, peritonitis is
usually caused by a single pathogen that originates from the
normal flora of the skin or upper respiratory tract. Approximately 60% 70% of cases are caused by gram-positive cocci,
20% 30% by gram-negative bacilli, and the remainder by various other bacteria, fungi, and mycobacteria [74]. Coagulasenegative Staphylococcus is the single most common pathogen,
followed by S. aureus and species of Streptococcus. Among
the gram-negative organisms, most Enterobacteriaceae species
have been associated with CAPD peritonitis, but no single
species predominates in all reported series. Although a rare
pathogen in other types of peritonitis, P. aeruginosa occurs
with relative frequency in CAPD peritonitis (5% 10% of
cases). It warrants special note because of its association with
significant morbidity and late complications [75, 76].
Fungi have become an important cause of CAPD-related
peritonitis in recent years because of their increasing frequency
and problematic management. Although many different fungi
have been isolated, including Aspergillus, Mucor, Rhizopus,
Alternaria, Fusarium, Penicillium, and Drechslera species,
C. albicans accounts for 80% 90% of cases [74, 76]. Risk
factors for acquisition of fungal peritonitis are bacterial peritonitis within the preceding month, recent hospitalization, presence of extraperitoneal infection, use of immunosuppressive
agents, and concomitant HIV infection, but diabetes mellitus
does not pose a special risk [77, 78].
Mycobacteria have been described as pathogens in fewer than
3% of cases of CAPD-related peritonitis, but they may also
account for a portion of cases labeled as culture-negative [79].
Overall, 86% of mycobacterial isolates reported in the literature
have been of group IV (rapid growers), such as M. fortuitum and
M. chelonae [80]. One particularly large outbreak involved 17
patients who developed infection with M. chelonae following
treatment with contaminated intermittent peritoneal dialysis machines [81]. Other rare causes of peritonitis in patients undergoing
CAPD are viruses, algae, and M. tuberculosis.
Peritonitis Update
References
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lections are adjusted when the results of cultures and susceptibility tests are known. A single specific agent is adequate treatment in the majority of cases of bacterial peritonitis.
P. aeruginosa, however, has been associated with a high therapeutic failure rate and frequent relapses [75, 76]. A synergistic
combination of antibiotics, such as an antipseudomonal b-lactam drug plus an aminoglycoside, has been recommended in
addition to removal of the dialysis catheter.
Intraperitoneal administration of antibiotics is the preferred
method for drug delivery in CAPD-associated peritonitis because it achieves high local concentrations and permits selftreatment by the patient [87 89]. Therapy is usually continued
for 10 14 days but may need to be extended with unusually
severe or slow-to-respond infections. Recommendations for
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Treatment of fungal peritonitis is controversial because of the
lack of controlled studies and the small numbers of cases seen
at any single center. Although there are reports of successful
treatment with intraperitoneal and/or systemic antifungal agents
alone [91, 92], removal of the dialysis catheter is usually prudent
to prevent relapse [68, 93]. A short course of systemic amphotericin B (250500 mg) is often given following catheter removal.
Some evidence has suggested that catheter removal alone may
be curative in selected patients. Mycobacterial peritonitis also
requires removal of the dialysis catheter for cure. Most of these
organisms are resistant to conventional antituberculous agents,
and susceptibilities vary greatly among the species. Antibiotic
selections should be guided by either in vitro susceptibility test
results or published recommendations [7981].
Prevention of peritonitis in patients undergoing CAPD requires
intensive education regarding aseptic technique and catheter care.
Efforts to reduce the incidence of peritonitis by using oral or
intraperitoneal antibiotics have largely been unsuccessful [9497].
Although a decrease in the number of random positive dialysate
cultures has been observed in clinical studies, occurrence of clinical peritonitis was unaffected by prophylactic antibiotics. In addition, topical mupirocin has been used to eliminate nasal colonization with S. aureus but has yet to be shown to significantly impact
the incidence of CAPD-related peritonitis [98].
The most significant advances in the prevention of dialysisrelated peritonitis involve instrumentation changes, including
(1) devices that facilitate connection of tubing, such as titanium
adapters; (2) devices that help maintain field sterility during
exchanges, such as ultraviolet light systems and in-line filters;
and (3) devices that protect intraluminal sterility during
exchanges, such as connector systems with disinfectant
(Y-connector, O-set). Most such devices have been shown to
favorably impact the incidence of peritonitis but add appreciably to the overall cost of CAPD.
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Peritonitis Update
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05-07-97 17:21:37
The Conflict-of-Interest Policy of the Office of Continuing Medical Education, UCLA School of Medicine,
requires that faculty participating in a CME activity disclose to the audience any relationship with a pharmaceutical or equipment company which might pose a potential, apparent, or real conflict of interest with regard to
their contribution to the program. The author reports no
conflict of interest.
cida
UC: CID
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