Peritonitis: Update On Pathophysiology, Clinical Manifestations, and Management
Peritonitis: Update On Pathophysiology, Clinical Manifestations, and Management
Peritonitis: Update On Pathophysiology, Clinical Manifestations, and Management
Transfallopian spread is also suggested by the development ings of peritoneal irritation. Fever (temperature of ú1007F) is
of primary peritonitis in women with intrauterine devices. The the most common presenting sign, occurring in 50% – 80% of
route of spread in women with gonococcal or chlamydial peri- cases and even in the absence of abdominal signs or symptoms.
hepatitis (Fitz-Hugh – Curtis syndrome) is presumably via the Primary peritonitis should always be considered in the differen-
fallopian tubes and paracolic gutters to the subphrenic space, tial diagnosis of decompensation of previously stable chronic
but it may also be hematogenous. liver disease, especially hepatic encephalopathy.
Although tuberculous peritonitis may result from direct entry Primary tuberculous peritonitis usually is gradual in onset,
into the peritoneal cavity of tubercle bacilli (from the lymph causing fever, weight loss, malaise, night sweats, and abdomi-
nodes, intestine, or genital tract in patients with active disease nal distension. The abdomen may not be rigid and is often
of these organs), it is more likely to be disseminated hematoge- characterized as being ‘‘doughy’’ on palpation. The findings
nously from remote foci of tuberculosis, most commonly in at surgery or laparoscopy consist of multiple nodules scattered
the lung. Tuberculous peritonitis may become clinically evident over the peritoneal surface and omentum. Adhesions and a
generally indicated to rule out possible intraabdominal sources examination for additional pathological conditions. Antimicro-
of continuing peritoneal contamination. However, in end-stage bial therapy is usually continued for 10 – 14 days if improve-
cirrhotic patients, exploratory laparotomy may be life-threaten- ment is noted, but short-course therapy for 5 days has been
ing, and the likelihood of finding a primary intraabdominal shown to be as efficacious as the longer course in some patients.
focus may be small. Administration of intraperitoneal antimicrobials is not neces-
Surgery for these patients can be deferred while the response sary.
to antimicrobial therapy is awaited. Patients with primary peri- Treatment of primary peritonitis is successful in more than
tonitis usually respond within 48 hours to appropriate antimi- one-half of cirrhotic patients, but because of the underlying
crobial therapy. The observation of an exponential rate of de- liver condition, the overall mortality has been reported as high
cline in the number of ascitic fluid leukocytes after initiation as 95% in some series. Those patients with the poorest progno-
of antimicrobial therapy for primary peritonitis has been found sis were found to have renal insufficiency, hypothermia, hyper-
to help differentiate primary from secondary bacterial peritoni- bilirubinemia, and hypoalbuminemia [9].
ing cytomegalovirus enterocolitis has been described as a com- can undergo alteration as a result of the primary disease process
mon cause of acute abdomen in patients with AIDS [12]. or previous antimicrobial therapy. For example, diseases of the
Tertiary peritonitis has been conceived as a later stage in stomach that result in obstruction, the loss of gastric acidity
the disease, when clinical peritonitis and systemic signs of (e.g., bleeding, gastric ulcer, or carcinoma), or use of acid-
sepsis (e.g., fever, tachycardia, tachypnea, hypotension, reducing drugs may cause gastric colonization with oral anaer-
elevated cardiac index, low systemic vascular resistance, leuko- obes, such as non-fragilis Bacteroides and Fusobacterium
penia or leukocytosis, and multiorgan failure) persist after treat- species and other oropharyngeal organisms, e.g., viridans strep-
ment for secondary peritonitis and either no organisms or low- tococci, microaerophilic streptococci, Candida species, and
virulence pathogens, such as enterococci and fungi, are isolated lactobacilli.
from the peritoneal exudate. These organisms may gain access Gastric perforation is associated with either sterile chemical
to the peritoneal cavity by contamination during operative in- peritonitis or peritonitis due to the above-mentioned pathogens,
terventions, by selection from the initial polymicrobial perito- depending on the underlying gastric condition. Similarly, the
function who are unresponsive to initial management [33]. therapeutic attempts [46]. This has led to investigation of endo-
However, monomicrobial infection with microorganisms that toxin and cytokine levels in circulation to predict outcome.
have low pathogenicity, such as Candida species, enterococci, However, the magnitude of levels of endotoxin, TNF, and
and coagulase-negative staphylococci, has been noted even in IL-6, in circulation in patients with peritonitis, has not been
acute peritonitis in patients with severely impaired defenses invariably related to prognosis [14, 47 – 51]. It has been sug-
[34]. P. aeruginosa usually is thought of as a nosocomial patho- gested that cytokine levels in the peritoneal exudate, rather than
gen that emerges under the selective pressure of broad- the blood, better reflect the severity of the compartmentalized
spectrum antimicrobial agents. In several studies, however, this peritoneal infection and predict outcome [14].
organism has been isolated in up to 24% of patients with acute Management and prevention. A skeptical attitude is neces-
community-acquired perforating appendicitis [35, 36]. sary when reviewing reports on clinical trials of antimicrobial
Although enterococci are found in 20% of intraabdominal therapy for intraabdominal sepsis. Surgical therapy alone may
infections, their exact role in polymicrobial infection and the be sufficient to cure many otherwise healthy, young patients
lems, because both the bactericidal activity and postantibiotic as the appendix or gallbladder, after resection of the organ.
effect of aminoglycosides are concentration-dependent, while Similarly, contamination of the peritoneum from a defect in
their nephrotoxicity is time-dependent. However, too few se- the intestinal wall, such as immediately following penetrating
verely ill patients with intraabdominal sepsis have been studied abdominal trauma, may also require only operative intervention
to allow recommendation of the general use of single daily to remove the diseased organ and a brief course of antimicrobial
doses of these drugs. therapy [53]. Persistent signs of sepsis suggest formation of
Regimens in which a third-generation cephalosporin is substi- an intraabdominal abscess that requires drainage, continued
tuted for the aminoglycoside or metronidazole is substituted for contamination of the peritoneum from an inadequately con-
clindamycin compare favorably to the ‘‘gold standard.’’ Resis- trolled source, superimposed nosocomial infection with a resis-
tance, however, emerges readily under selective pressure of anti- tant pathogen, or tertiary peritonitis.
microbial therapy with third-generation cephalosporins among Treatment against Enterococcus or Candida species in-
certain gram-negative bacilli that produce inducible b-lacta- volved in polymicrobial infections is controversial. Identifi-
Abscesses that present as localized peritonitis may be drained nias, and tertiary peritonitis with organisms such as enterococci
percutaneously with the aid of ultrasonography or CT, followed or Candida species [63 – 65]. Indeed, repeated entry into the
by definitive surgery, if necessary. Percutaneous drainage of inflamed peritoneum may further escalate the cytokine cascade.
a peridiverticular abscess may permit a subsequent one-stage A review concluded that in the absence of randomized con-
procedure of primary resection and immediate anastomosis. trolled prospective trials with appropriate stratification of pa-
Peritonitis caused by colonic perforation due to diverticuli- tients by severity of illness, there is insufficient evidence to
tis or colon cancer has been treated with one of three proce- determine if these procedures improve outcome of severe dif-
dures, depending on the particular clinical situation: (1) a fuse peritonitis [66].
three-stage procedure, which involves an initial proximal co-
lostomy to decompress the bowel and divert the fecal stream,
Peritonitis Complicating Peritoneal Dialysis
followed by resection of the diseased bowel, and finally anas-
tomosis to restore bowel continuity several months later; (2) Pathogenesis. Since its development in the late 1970s,
factors may also be important in the pathogenesis of this infec- Clinical presentation and evaluation. Criteria for the diagno-
tion [73]. Microbial pathogens that reach the dialyzed perito- sis of CAPD-associated peritonitis are (1) signs and symptoms
neal cavity are removed by three major lines of defense. First, of peritoneal irritation, (2) cloudy dialysate effluent with a
despite the dilution of fibrinogen and coagulation proteins, fi- leukocyte count of ú100/mm3, and (3) a positive culture of
brin trapping and sequestration of microorganisms operate ef- dialysate fluid. Any two of these criteria may be adequate to
ficiently in the dialyzed peritoneum. Second, removal of the establish the diagnosis [82]. Clinical manifestations of peritoni-
dialysate serves to eliminate or decrease the inoculum of con- tis vary from mild to severe, depending largely on the virulence
taminating organisms. Finally, a complex interplay of opsoni- of the pathogen and the time course of the infection [67].
zation, phagocytosis, and intracellular killing by peritoneal Generally, turbid dialysate is the first and most common symp-
macrophages, mesothelial cells, and neutrophils serves to com- tom to appear, followed shortly thereafter by abdominal pain
bat bacterial invasion and prevent infection. and tenderness.
Unfortunately, the dialyzed peritoneal cavity is not a support- Laboratory evaluation of dialysate effluent is critical to estab-
lections are adjusted when the results of cultures and suscepti- 2. Nohr CW, Marshall DG. Primary peritonitis in children. Can J Surg 1984;
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tam drug plus an aminoglycoside, has been recommended in
6. Runyon BA, Umland ET, Merlin T. Inoculation of blood culture bottles
addition to removal of the dialysis catheter. with ascitic fluid: improved detection of spontaneous bacterial peritoni-
Intraperitoneal administration of antibiotics is the preferred tis. Arch Intern Med 1987; 147:73 – 5.
method for drug delivery in CAPD-associated peritonitis be- 7. Stassen WN, McCullough AJ, Bacon BR, et al. Immediate diagnostic
cause it achieves high local concentrations and permits self- criteria for bacterial infection of ascitic fluid: evaluation of ascitic fluid
polymorphonuclear leukocyte count, pH, and lactate concentration,
treatment by the patient [87 – 89]. Therapy is usually continued
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