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4.3 Peritonitis (Supplementary)
4.3 Peritonitis (Supplementary)
4.3 Peritonitis (Supplementary)
3
10 February 2014
Peritonitis
Karlos Noel R. Aleta, MD
Schwartz and Sabiston
SCHWARTZ TREATMENT
effective therapy requires:
PERITONITIS o source control to resect or repair the diseased organ
intra-abdominal infection o deridement of necrotic, infected tissue and debris
microbial contamination of the peritoneal cavity o administration of antimicrobial agents directed against
classified according etiology aerobes and anaerobes
this type of antibiotic regimen should be chosen
PRIMARY MICROBIAL PERITONITIS because in most patients the precise diagnosis
occurs when microbes invade the normally sterile cannot be established until exploratory laparotomy is
confines of the peritoneal cavity via hematogenous performed, and the most morbid form of this disease
dissemination from a distant source of infection or direct process is colonic perforation, due to the large
inoculation number of microbes present
o this process is more common among patients who retain a combination of agents or single agents with a
large amounts of peritoneal fluid due to ascites, and in broad spectrum of activity can be used for this
those individuals who are being treated for renal failure purpose; conversion of a parenteral to an oral
via peritoneal dialysis regimen when the patient's ileus resolves will provide
these infections invariably are monomicrobial and rarely results similar to those achieved with IV antibiotics
require surgical intervention effective source control and antibiotic therapy is associated
with low failure rates and a mortality rate of approximately
5 to 6%
DIAGNOSIS
inability to control the source of infection leads to mortality
diagnosis is established based on:
greater than 40%
o patient who has ascites for medical reasons the response rate to effective source control and use of
o physical examination that reveals diffuse tenderness
appropriate antibiotics has remained approximately 70 to
and guarding without localized findings 90% over the past several decades
o absence of pneumoperitoneum on abdominal flat plate Patients in whom standard therapy fails develop an intra-
and upright roentgenograms
abdominal abscess, leakage from a GI anastomosis leading
o presence of more than 100 WBCs/mL to postoperative peritonitis, or tertiary (persistent)
o microbes with a single morphology on Gram's stain
peritonitis
performed on fluid obtained via paracentesis Microbes such as E. faecalis and faecium , S. epidermidis ,
subsequent cultures will typically demonstrate the
C. albicans , and P. aeruginosa can be identified, typically in
presence of gram-positive organisms in patients combination, and may be selected based on their lack of
receiving peritoneal dialysis responsiveness to the initial antibiotic regimen, coupled
with diminished activity of host defenses
TREATMENT Unfortunately, even with effective antimicrobial agent
treatment consists of administration of an antibiotic to therapy, this disease process is associated with mortality
which the organism is sensitive; often 14 to 21 days of rates in excess of 50%
therapy are required surgical intervention is reserved for:
removal of indwelling devices (e.g., peritoneal dialysis o those who harbor multiple abscesses
catheter or peritoneovenous shunt) may be required for o those with abscesses in proximity to vital structures
effective therapy of recurrent infections such that percutaneous drainage would be hazardous
o those in whom an ongoing source of contamination
SECONDARY MICROBIAL PERITONITIS (e.g., enteric leak) is identified
occurs subsequent to contamination of the peritoneal A short course (3 to 7 days) of antibiotics that possess
cavity due to perforation or severe inflammation and aerobic and anaerobic activity seems reasonable, and most
infection of an intra-abdominal organ practitioners leave the drainage catheter in situ until it is
examples include: clear that cavity collapse has occurred, output is less than
o appendicitis 10 to 20 mL/d, no evidence of an ongoing source of
o perforation of any portion of the GI tract contamination is present, and the patient's clinical condition
o diverticulitis has improved.
SABISTON PROGNOSIS
The immediate mortality risk due to SBP is low, particularly
PERITONITIS if recognized and treated expeditiously.
inflammation of the peritoneum and peritoneal cavity o However, the development of other complications of
is most commonly due to a localized or generalized hepatic failure, including gastrointestinal hemorrhage or
infection hepatorenal syndrome, contributes to the death of many
PRIMARY results from bacterial, chlamydial, fungal, of these patients during the hospitalization in which SBP
PERITONITIS or mycobacterial infection in the absence is detected.
of perforation of the gastrointestinal tract
SECONDARY occurs in the setting of gastrointestinal TUBERCULOUS PERITONITIS
PERITONITIS perforation Peritoneal tuberculosis is the sixth most common site of
frequent causes of secondary bacterial extrapulmonary tuberculosis after lymphatic, genitourinary,
peritonitis include: bone and joint, miliary, and meningeal
o peptic ulcer disease Most cases of tuberculous peritonitis result from
o acute appendicitis reactivation of latent peritoneal disease that had been
o colonic diverticulitis previously established hematogenously from a primary
o pelvic inflammatory disease pulmonary focus
About one-sixth of cases are associated with active
SPONTANEOUS BACTERIAL PERITONITIS (SBP) pulmonary disease
defined as a bacterial infection of ascitic fluid in the The illness often presents insidiously, with patients having
absence of an intra-abdominal, surgically treatable had symptoms for several weeks to months at the time
source of infection of presentation
although most commonly associated with cirrhosis, SBP MOST COMMON SYMPTOM: Abdominal swelling due to
may also occur in patients with nephrotic syndrome and, ascites formation occurring in >80% of instances
less commonly, congestive heart failure Similarly, most patients complain of a nonlocalized,
it is extremely rare for patients with ascitic fluid containing vague abdominal pain
a high protein concentration to develop SBP, such as those Constitutional symptoms reported in about 60% of
with peritoneal carcinomatosis patients:
most common pathogens in adults with SBP: o low-grade fever and night sweats
o Escherichia coli o weight loss
o Klebsiella pneumonia o anorexia
in children with nephrogenic or hepatogenic ascites: o malaise
o group A streptococcus Abdominal tenderness is present upon palpation in about
o Staphylococcus aureus half of patients with peritoneal tuberculosis
o Streptococcus pneumonia A positive tuberculin skin test is present in most cases,
whereas only about half of these patients will have an
DIAGNOSIS abnormal chest radiograph.
The ascitic fluid SAAG is <1.1 g/dL, consistent with a high
made initially by demonstrating more than 250
protein concentration within the ascitic fluid.
neutrophils/mm3 of ascitic fluid in a clinical setting
Microscopic examination of the ascites shows:
consistent with this diagnosis (abdominal pain, fever, or
o erythrocytes
leukocytosis in a patient with low-protein ascites)
o increased number of leukocytes, most of which are
lymphocytes
TREATMENT
Broad-spectrum antibiotics, such as a third-generation DIAGNOSIS
cephalosporin
o are started immediately in patients suspected of having
ULTRASOUND CT
ascitic fluid infection
may demonstrate the will demonstrate the
o these agents cover about 95% of the flora most
presence of echogenic thickened and nodular
commonly associated with SBP material within the ascitic mesentery with
o the spectrum of the antibiotic coverage may be fluid, seen as fine mobile mesenteric
narrowed once the results of antibiotic sensitivity tests strands or particulate lymphadenopathy and
are known matter omental thickening.
Repeat paracentesis with ascitic fluid analysis is not needed may suggest the diagnosis but lacks the sensitivity and
in the usual case in which there is rapid improvement in specificity to be diagnostic
response to antibiotic therapy. The diagnosis is made by laparoscopy with directed
If the setting, symptoms, ascitic fluid analysis, or response biopsy of the peritoneum.
to therapy are atypical, repeat paracentesis may be helpful o in more than 90% of cases, laparoscopy demonstrates
in detecting secondary peritonitis. multiple whitish nodules (<5 mm) scattered over
Multiple bacterial isolates, particularly of gram-negative the visceral and parietal peritoneum; histologic
enteric organisms, combined with a poor response to examination of these nodules demonstrates caseating
antibiotic therapy, suggests the presence of secondary granulomas
peritonitis.
DIAGNOSIS
Gram stain detects organisms in only about 10% to 40%
of cases
About 75% of infections are due to gram-positive
organisms, with Staphylococcus epidermidis
accounting for 30% to 50% of cases
o S. aureus, gram-negative bacilli, and fungi are also
important causes of dialysis-associated peritonitis
TREATMENT
Peritoneal dialysis–associated peritonitis is treated by the
intraperitoneal administration of antibiotics, most
commonly a first-generation cephalosporin
75% of infections are cured by culture-directed
antibiotic therapy
The cure rate for peritonitis due to coagulase-negative
staphylococcus is nearly 90%, compared with the rates for
peritonitis due to S. aureus, gram-negative bacilli, or fungi
of 66%, 56%, and 0%, respectively
Recurrent or persistent peritonitis requires removal
of the dialysis catheter and resumption of
hemodialysis.