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Peritonitis http://emedicine.medscape.

com/article/180234-overview
Brian James Daley, MD, MBA, FACS, FCCP, CNSC; Chief Editor: Julian Katz, MD
Background
Peritonitis is defined as 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). Intra-
abdominal sepsis is an inflammation of the peritoneum caused by pathogenic
microorganisms and their products.
[1]
The inflammatory process may be localized
(abscess) or diffuse in nature. (See Pathophysiology.)
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. (See Etiology.)
Peritoneal infections are classified as primary (ie, from hematogenous dissemination,
usually in the setting of immunocompromise), 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) caused by
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. (See Clinical Presentation.)
Infections in 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.
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. (See Workup.)
The current 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. (See
Treatment and Management and Medication.)
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.
Anatomy
The peritoneum is the largest and most complex serous membrane in the body. It
forms a closed sac (ie, coelom) by lining the interior surfaces of the abdominal wall
(anterior and lateral), by forming the boundary to the retroperitoneum (posterior), by
covering the extraperitoneal structures in the pelvis (inferior), and by covering the
undersurface of the diaphragm (superior). This parietal layer of the peritoneum
reflects onto the abdominal visceral organs to form the visceral peritoneum. It
thereby creates a potential space between the 2 layers (ie, the peritoneal cavity).
The peritoneum consists of a single layer of flattened mesothelial cells over loose
areolar tissue. The loose connective tissue layer contains a rich network of vascular
and lymphatic capillaries, nerve endings, and immune-competent cells, particularly
lymphocytes and macrophages. The peritoneal surface cells are joined by junctional
complexes, thus forming a dialyzing membrane that allows passage of fluid and
certain small solutes. Pinocytotic activity of the mesothelial cells and phagocytosis by
macrophages allow for clearance of macromolecules.
Normally, the amount of peritoneal fluid present is less than 50 mL, and only small
volumes are transferred across the considerable surface area in a steady state each
day. The peritoneal fluid represents a plasma ultrafiltrate, with electrolyte and solute
concentrations similar to that of neighboring interstitial spaces and a protein content
of less than 30 g/L, mainly albumin. In addition, peritoneal fluid contains small
numbers of desquamated mesothelial cells and various numbers and morphologies
of migrating immune cells (reference range is < 300 cells/ L, predominantly of
mononuclear morphology).
The peritoneal cavity is divided incompletely into compartments by the mesenteric
attachments and secondary retroperitonealization of certain visceral organs. A large
peritoneal fold, the greater omentum, extends from the greater curvature of the
stomach and the inferior aspect of the proximal duodenum downward over a variable
distance to fold upon itself (with fusion of the adjacent layers) and ascends back to
the taenia omentalis of the transverse colon. This peritoneal fold demonstrates a
slightly different microscopic anatomy, with fenestrated surface epithelium and a
large number of adipocytes, lymphocytes, and macrophages, and it functions as a fat
storage location and a mobile immune organ.
The compartmentalization of the peritoneal cavity, in conjunction with the greater
omentum, influences the localization and spread of peritoneal inflammation and
infections
Pathophysiology
In peritonitis caused by bacteria, the physiologic response is determined by several
factors, including the virulence of the contaminant, the size of the inoculum, the
immune status and overall health of the host (eg, as indicated by the Acute
Physiology and Chronic Health Evaluation II [APACHE II] score), and elements of
the local environment, such as necrotic tissue, blood, or bile.
[2]

Intra-abdominal sepsis from a perforated viscus (ie, secondary peritonitis or
suppurative peritonitis) results from direct spillage of luminal contents into the
peritoneum (eg, perforated peptic ulcer, diverticulitis, appendicitis, iatrogenic
perforation). With the spillage of the contents, gram-negative and anaerobic bacteria,
including common gut flora, such as Escherichia coli and Klebsiella pneumoniae,
enter the peritoneal cavity. Endotoxins produced by gram-negative bacteria lead to
the release of cytokines that induce cellular and humoral cascades, resulting in
cellular damage, septic shock, and multiple organ dysfunction syndrome (MODS).
The mechanism for bacterial inoculation of ascites has been the subject of much
debate since Harold Conn first recognized it in the 1960s. Enteric organisms have
traditionally been isolated from more than 90% of infected ascites fluid in
spontaneous bacterial peritonitis (SBP), suggesting that the GI tract is the source of
bacterial contamination. The preponderance of enteric organisms, in combination
with the presence of endotoxin in ascitic fluid and blood, once favored the argument
that SBP was due to direct transmural migration of bacteria from an intestinal or
hollow organ lumen, a phenomenon called bacterial translocation. However,
experimental evidence suggests that direct transmural migration of microorganisms
might not be the cause of SBP.
An alternative proposed mechanism for bacterial inoculation of ascites suggests a
hematogenous source of the infecting organism in combination with an impaired
immune defense system. Nonetheless, the exact mechanism of bacterial
displacement from the GI tract into ascites fluid remains the source of much debate.
A host of factors contributes to the formation of peritoneal inflammation and bacterial
growth in the ascitic fluid. A key predisposing factor may be the intestinal bacterial
overgrowth found in people with cirrhosis, mainly attributed to decreased intestinal
transit time. Intestinal bacterial overgrowth, along with impaired phagocytic function,
low serum and ascites complement levels, and decreased activity of the
reticuloendothelial system, contributes to an increased number of microorganisms
and decreased capacity to clear them from the bloodstream, resulting in their
migration into and eventual proliferation within ascites fluid.
Interestingly, adults with SBP typically have ascites, but most children with SBP do
not have ascites. The reason for and mechanism behind this is the source of
ongoing investigation.
Fibrinolysis
Alterations in fibrinolysis (through increased plasminogen activator inhibitor activity)
and the production of fibrin exudates have an important role in peritonitis. The
production of fibrin exudates is an important part of the host defense, but large
numbers of bacteria may be sequestered within the fibrin matrix. This may retard
systemic dissemination of intraperitoneal infection and may decrease early mortality
rates from sepsis, but it also is integral to the development of residual infection and
abscess formation. As the fibrin matrix matures, the bacteria within are protected
from host clearance mechanisms.
Whether fibrin ultimately results in containment or persistent infection may depend
on the degree of peritoneal bacterial contamination. In animal studies of mixed
bacterial peritonitis that examined the effects of systemic defibrinogenation and
those of abdominal fibrin therapy, heavy peritoneal contamination uniformly led to
severe peritonitis with early death (< 48 h) because of overwhelming sepsis.
Bacterial load
Bacterial load and the nature of the pathogen also play important roles. Some
studies suggest that the number of bacteria present at the onset of abdominal
infections is much higher than originally believed (approximately 2 10
8
CFU/mL,
much higher than the 5 10
5
CFU/mL inocula routinely used for in vitro susceptibility
testing). This bacterial load may overwhelm the local host defense.
Bacterial virulence
Bacterial virulence factors
[3]
that interfere with phagocytosis and with neutrophil-
mediated bacterial killing mediate the persistence of infections and abscess
formation. Among these virulence factors are capsule formation, facultative
anaerobic growth, adhesion capabilities, and succinic acid production. Synergy
between certain bacterial and fungal organisms may also play an important role in
impairing the host's defense. One such synergy may exist between Bacteroides
fragilis and gram-negative bacteria, particularly E coli (see the image below) ,where
co-inoculation significantly increases bacterial proliferation and abscess formation.
Gram-negative Escherichia coli.
Enterococci
Enterococci may be important in enhancing the severity and persistence of
peritoneal infections. In animal models of peritonitis with E coli and B fragilis, the
systemic manifestations of the peritoneal infection and bacteremia rates were
increased, as were bacterial concentrations in the peritoneal fluid and rate of
abscess formation. Nevertheless, the role of Enterococcus organisms in
uncomplicated intra-abdominal infections remains unclear. Antibiotics that lack
specific activity against Enterococcus are often used successfully in the therapy of
peritonitis, and the organism is not often recovered as a blood-borne pathogen in
intra-abdominal sepsis.
Fungi
The role of fungi in the formation of intra-abdominal abscesses is not fully
understood. Some authors suggest that bacteria and fungi exist as nonsynergistic
parallel infections with incomplete competition, allowing the survival of all organisms.
In this setting, treatment of the bacterial infection alone may lead to an overgrowth of
fungi, which may contribute to increased morbidity.
Abscess formation
Abscess formation occurs when the host defense is unable to eliminate the infecting
agent and attempts to control the spread of this agent by compartmentalization. This
process is aided by a combination of factors that share a common feature, ie,
impairment of phagocytotic killing. Most animal and human studies suggest that
abscess formation occurs only in the presence of abscess-potentiating agents.
Although the nature and spectrum of these factors have not been studied
exhaustively, certain fiber analogues (eg, bran) and the contents of autoclaved stool
have been identified as abscess-potentiating agents. In animal models, these factors
inhibit opsonization and phagocytotic killing by interference with complement
activation.
Cytokines
The role of cytokines in mediation of the body's immune response and their role in
the development of the systemic inflammatory response syndrome (SIRS) and
multiple organ failure (MOF) have been a major focus of research over the past
decade. Comparatively few data exist about the magnitude of the
intraperitoneal/abscess cytokine response and implications for the host. Existing
data suggest that bacterial peritonitis is associated with an immense intraperitoneal
compartmentalized cytokine response. Higher levels of certain cytokines (ie, tumor
necrosis factor-alpha [TNF-alpha], interleukin [IL]-6) have been associated with
worse outcomes, as well as secondary (uncontrolled) activation of the systemic
inflammatory cascade.
Etiology
The etiology of disease depends on the type, as well as location, of peritonitis, as
follows:
Primary peritonitis
Secondary peritonitis
Tertiary peritonitis
Chemical peritonitis
Peritoneal abscess
Primary peritonitis
Spontaneous bacterial peritonitis (SBP) is an acute bacterial infection of ascitic fluid.
Contamination of the peritoneal cavity is thought to result from translocation of
bacteria across the gut wall or mesenteric lymphatics and, less frequently, via
hematogenous seeding in the presence of bacteremia.
SBP can occur as a complication of any disease state that produces the clinical
syndrome of ascites, such as heart failure and Budd-Chiari syndrome. Children with
nephrosis or systemic lupus erythematosus who have ascites have a high risk of
developing SBP. The highest risk of SBP, however is in patients with cirrhosis who
are in a decompensated state.
[4]
In particular, decreased hepatic synthetic function
with associated low total protein level, low complement levels, or prolonged
prothrombin time (PT) is associated with maximum risk. Patients with low protein
levels in ascitic fluid (< 1 g/dL) have a 10-fold higher risk of developing SBP than
those with a protein level greater than 1 g/dL. Approximately 10-30% of patients with
cirrhosis and ascites develop SBP.
[5]
The incidence rises to more than 40% with
ascitic fluid protein contents of less than 1 g/dL (which occurs 15% of patients),
presumably because of decreased ascitic fluid opsonic activity.
More than 90% of cases of SBP are caused by a monomicrobial infection. The most
common pathogens include gram-negative organisms (eg, E coli [40%], K
pneumoniae [7%], Pseudomonas species, Proteus species, other gram-negative
species [20%]) and gram-positive organisms (eg, Streptococcus pneumoniae[15%],
other Streptococcus species [15%], Staphylococcus species [3%]) (see Table 1).
However, some data suggest that the percentage of gram-positive infections may be
increasing.
[6, 7]
One study cites a 34.2% incidence of streptococci, ranking in second
position after Enterobacteriaceae.
[7]
Viridansgroup streptococci (VBS) accounted for
73.8% of these streptococcal isolates. A single organism is noted in 92% of cases,
and 8% of cases are polymicrobial.
Anaerobic microorganisms are found in less than 5% of cases, and multiple isolates
are found in less than 10%.
Secondary peritonitis
Common etiologic entities of secondary peritonitis (SP) include perforated
appendicitis; perforated gastric or duodenal ulcer; perforated (sigmoid) colon caused
by diverticulitis, volvulus, or cancer; and strangulation of the small bowel (see Table
1). Necrotizing pancreatitis can also be associated with peritonitis in the case of
infection of the necrotic tissue.
The pathogens involved in SP differ in the proximal and distal GI tract. Gram-positive
organisms predominate in the upper GI tract, with a shift toward gram-negative
organisms in the upper GI tract in patients on long-term gastric acid suppressive
therapy. Contamination from a distal small bowel or colon source initially may result
in the release of several hundred bacterial species (and fungi); host defenses quickly
eliminate most of these organisms. The resulting peritonitis is almost always
polymicrobial, containing a mixture of aerobic and anaerobic bacteria with a
predominance of gram-negative organisms (see Table 1).
As many as 15% of patients who have cirrhosis with ascites who were initially
presumed to have SBP have SP. In many of these patients, clinical signs and
symptoms alone are not sensitive or specific enough to reliably differentiate between
the 2 entities. A thorough history, evaluation of the peritoneal fluid, and additional
diagnostic tests are needed to do so; a high index of suspicion is required.
Table 1. Common Causes of Secondary Peritonitis (Open Table in a new window)
Source Regions Causes
Esophagus Boerhaave syndrome



Malignancy



Trauma (mostly penetrating)



Iatrogenic*


Stomach Peptic ulcer perforation



Malignancy (eg, adenocarcinoma, lymphoma, gastrointestinal
stromal tumor)



Trauma (mostly penetrating)



Iatrogenic*


Duodenum Peptic ulcer perforation



Trauma (blunt and penetrating)



Iatrogenic*


Biliary tract Cholecystitis



Stone perforation from gallbladder (ie, gallstone ileus) or
common duct



Malignancy



Choledochal cyst (rare)



Trauma (mostly penetrating)



Iatrogenic*


Pancreas Pancreatitis (eg, alcohol, drugs, gallstones)



Trauma (blunt and penetrating)



Iatrogenic*


Small bowel Ischemic bowel



Incarcerated hernia (internal and external)



Closed loop obstruction



Crohn disease



Malignancy (rare)



Meckel diverticulum



Trauma (mostly penetrating)


Large bowel and
appendix
Ischemic bowel



Diverticulitis



Malignancy



Ulcerative colitis and Crohn disease



Appendicitis



Colonic volvulus



Trauma (mostly penetrating)



Iatrogenic


Uterus, salpinx, and
ovaries
Pelvic inflammatory disease (eg, salpingo-oophoritis, tubo-
ovarian abscess, ovarian cyst)



Malignancy (rare)



Trauma (uncommon)


*Iatrogenic trauma to the upper GI tract, including the pancreas and biliary tract and colon,
often results from endoscopic procedures; anastomotic dehiscence and inadvertent bowel
injury (eg, mechanical, thermal) are common causes of leak in the postoperative period.
Common organisms cultured in secondary peritonitis are presented in Table 2,
below.
[8]

Table 2. Microbial Flora of Secondary Peritonitis (Open Table in a new window)
Type Organism Percentage
Aerobic
Gram negative Escherichia coli 60%
Enterobacter/Klebsiella 26%
Proteus 22%
Pseudomonas 8%
Gram positive Streptococci 28%
Enterococci 17%
Staphylococci 7%
Anaerobic Bacteroides 72%
Eubacteria 24%
Clostridia 17%
Peptostreptococci 14%
Peptococci 11%
Fungi Candida 2%
Other rare, nonsurgical causes of intra-abdominal sepsis include the following:
Chlamydia peritonitis
Tuberculosis peritonitis
Acquired immunodeficiency syndrome (AIDS)-associated peritonitis
The most common cause of postoperative peritonitis is anastomotic leak, with
symptoms generally appearing around postoperative days 5-7. After elective
abdominal operations for noninfectious etiologies, the incidence of SP (caused by
anastomotic disruption, breakdown of enterotomy closures, or inadvertent bowel
injury) should be less than 2%. Operations for inflammatory disease (ie, appendicitis,
diverticulitis, cholecystitis) without perforation carry a risk of less than 10% for the
development of SP and peritoneal abscess. This risk may rise to greater than 50% in
gangrenous bowel disease and visceral perforation.
After operations for penetrating abdominal trauma, SP and abscess formation are
observed in a small number of patients. Duodenal and pancreatic involvement, as
well as colon perforation, gross peritoneal contamination, perioperative shock, and
massive transfusion, are factors that increase the risk of infection in these cases.
Peritonitis is also a frequent complication and significant limitation of peritoneal
dialysis.
[3]
Peritonitis leads to increased hospitalization and mortality rates.
Tertiary peritonitis
Tertiary peritonitis (see Table 3, below) develops more frequently in
immunocompromised patients and in persons with significant preexisting comorbid
conditions. Although rarely observed in uncomplicated peritoneal infections, the
incidence of tertiary peritonitis in patients requiring ICU admission for severe
abdominal infections may be as high as 50-74%.
Tuberculous peritonitis (TP) is rare in the United States (< 2% of all causes of
peritonitis), but it continues to be a significant problem in developing countries and
among patients with human immunodeficiency virus (HIV) infection. The presenting
symptoms are often nonspecific and insidious in onset (eg, low-grade fever,
anorexia, weight loss). Many patients with TP have underlying cirrhosis. More than
95% of patients with TP have evidence of ascites on imaging studies, and more than
half of these patients have clinically apparent ascites.
In most cases, chest radiographic findings in patients with TP peritonitis are
abnormal; active pulmonary disease is uncommon (< 30%). Results on Gram stain of
ascitic fluid are rarely positive, and culture results may be falsely negative in up to
80% of patients. A peritoneal fluid protein level greater than 2.5 g/dL, a lactate
dehydrogenase (LDH) level greater than 90 U/mL, or a predominantly mononuclear
cell count of greater than 500 cells/ L should raise suspicion of TP but have limited
specificity for the diagnosis. Laparoscopy and visualization of granulomas on
peritoneal biopsy specimens, as well as cultures (requires 4-6 wk), may be needed
for the definitive diagnosis; however, empiric therapy should begin immediately.
Table 3. Microbiology of Primary, Secondary, and Tertiary Peritonitis (Open Table in
a new window)
Peritonitis Etiologic Organisms Antibiotic Therapy



(Type)


Class Type of Organism


(Suggested)


Primary Gram-
negative
E coli (40%)



K pneumoniae (7%)



Pseudomonas species (5%)



Proteus species (5%)



Streptococcus species (15%)



Staphylococcus species (3%)



Anaerobic species (< 5%)


Third-generation cephalosporin
Secondary Gram-
negative
E coli



Enterobacter species
Second-generation
cephalosporin






Klebsiella species



Proteus species


Third-generation cephalosporin



Penicillins with anaerobic activity



Quinolones with anaerobic
activity



Quinolone and metronidazole



Aminoglycoside and
metronidazole


Gram-
positive
Streptococcus species



Enterococcus species


Anaerobic Bacteroides fragilis



Other Bacteroides species



Eubacterium species



Clostridium species



Anaerobic Streptococcusspecies


Tertiary Gram- Enterobacter species Second-generation
negative


Pseudomonas species



Enterococcus species


cephalosporin



Third-generation cephalosporin



Penicillins with anaerobic activity



Quinolones with anaerobic
activity



Quinolone and metronidazole



Aminoglycoside and
metronidazole



Carbapenems



Triazoles or amphotericin
(considered in fungal etiology)



(Alter therapy based on culture
results.)


Gram-
positive
Staphylococcus species
Fungal Candida species
Chemical peritonitis
Chemical (sterile) peritonitis may be caused by irritants such as bile, blood, barium,
or other substances or by transmural inflammation of visceral organs (eg, Crohn
disease) without bacterial inoculation of the peritoneal cavity. Clinical signs and
symptoms are indistinguishable from those of SP or peritoneal abscess, and the
diagnostic and therapeutic approach should be the same.
[9]

Peritoneal abscess
Peritoneal abscess describes the formation of an infected fluid collection
encapsulated by fibrinous exudate, omentum, and/or adjacent visceral organs. The
overwhelming majority of abscesses occurs subsequent to SP. Abscess formation
may be a complication of surgery. The incidence of abscess formation after
abdominal surgery is less than 1-2%, even when the operation is performed for an
acute inflammatory process. The risk of abscess increases to 10-30% in cases of
preoperative perforation of the hollow viscus, significant fecal contamination of the
peritoneal cavity, bowel ischemia, delayed diagnosis and therapy of the initial
peritonitis, and the need for reoperation, as well as in the setting of
immunosuppression. Abscess formation is the leading cause of persistent infection
and development of tertiary peritonitis.
Epidemiology
The overall incidence of peritoneal infection and abscess is difficult to establish and
varies with the underlying abdominal disease processes. SBP occurs in both children
and adults and is a well-known and ominous complication of cirrhosis.
[5]
Of patients
with cirrhosis who have SBP, 70% are Child-Pugh class C. In these patients, the
development of SBP is associated with a poor long-term prognosis.
Once thought to occur only in those individuals with alcoholic cirrhosis, SBP is now
known to affect patients with cirrhosis from any cause. In patients with ascites, the
prevalence may be as high as 18%. This number has grown from 8% over the past 2
decades, most likely secondary to an increased awareness of SBP and heightened
threshold to perform diagnostic paracentesis.
Although the etiology and incidence of hepatic failure differ between children and
adults, in those individuals with ascites, the incidence of SBP is roughly equal. Two
peak ages for SBP are characteristic in children: one in the neonatal period and the
other at age 5 years.
Prognosis
Over the past decade, the combination of better antibiotic therapy, more aggressive
intensive care, and earlier diagnosis and therapy with a combination of operative and
percutaneous techniques have led to a significant reduction in morbidity and
mortality related to intra-abdominal sepsis
Spontaneous bacterial peritonitis
The mortality rate in SBP may be as low as 5% in patients who receive prompt
diagnosis and treatment. However, in hospitalized patients, 1-year mortality rates
may range from 50-70%.
[10]
This is usually secondary to the development of
complications, such as gastrointestinal bleeding, renal dysfunction, and worsening
liver failure.
[11]
Patients with concurrent renal insufficiency have been shown to be at
a higher risk of mortality from SBP than those without concurrent renal insufficiency.
Mortality from SBP may be decreasing among all subgroups of patients because of
advances in its diagnosis and treatment. The overall mortality rate of patients with
SBP may exceed 30% if diagnosis and treatment are delayed, but the mortality rate
is less than 10% in fairly well-compensated patients with early therapy. As many as
70% of patients who survive an episode of SBP have a recurrent episode within 1
year, and for these patients, the mortality rate approaches 50%. Some studies
suggest that the recurrence rate of SBP may be decreased to less than 20% with
long-term antibiotic prophylaxis (eg, quinolones, trimethoprim-sulfamethoxazole);
however, whether this improves long-term survival without liver transplantation is
unclear.
Secondary peritonitis and peritoneal abscess
Uncomplicated SP and simple abscesses carry a mortality rate of less than 5%, but
this rate may increase to greater than 30-50% in severe infections. The overall
mortality rate related to intra-abdominal abscess formation is less than 10-20%.
Factors that independently predict worse outcomes include advanced age,
malnutrition, presence of cancer, a high APACHE II score on presentation,
preoperative organ dysfunction, the presence of complex abscesses, and failure to
improve in less than 24-72 hours after adequate therapy.
In severe intra-abdominal infections and peritonitis, the mortality rate may increase
to greater than 30-50%. The concurrent development of sepsis, SIRS, and MOF can
increase the mortality rate to greater than 70%, and, in these patients, more than
80% of deaths occur with an active infection present.
Soriano et al found that cirrhotic patients with SP who underwent surgical treatment
tended to have a lower mortality rate than did those who received medical therapy
only (53.8% vs 81.8%, respectively).
[12]
Among the surgically treated patients with
SP, the survival rate was greater in those with the shortest time between diagnostic
paracentesis and surgery. These researchers concluded that the prognosis of
cirrhotic patients with SP could be improved via a low threshold of suspicion on the
basis of Runyon's criteria and microbiologic data, prompt use of abdominal CT
scanning, and early surgical evaluation.
Tertiary peritonitis
In comparison with patients with other forms of peritonitis, patients who develop
tertiary peritonitis have significantly longer ICU and hospital stays, higher organ
dysfunction scores, and higher mortality rates (50-70%).
Other factors affecting prognosis
Several scoring systems (eg, APACHE II, SIRS, multiple organ dysfunction
syndrome [MODS], Mannheim peritonitis index) have been developed to assess the
clinical prognosis of patients with peritonitis. Most of these scores rely on certain
host criteria, systemic signs of sepsis, and complications related to organ failure.
Although valuable for comparing patient cohorts and institutions, these scores have
limited value in the specific day-to-day clinical decision-making process for any given
patient. In general, the mortality rate is less than 5% with an APACHE II of less than
15 and rises to greater than 40% with scores above 15. Rising APACHE II scores on
days 3 and 7 are associated with an increase of mortality rates to greater than 90%,
whereas falling scores predict mortality rates of less than 20%.
The mortality rate without organ failure generally is less than 5% but may rise to
greater than 90% with quadruple organ failure. A delay of more than 2-4 days in
instituting either medical therapy or surgical therapy has been clearly associated with
increased complication rates, the development of tertiary peritonitis, the need for
reoperation, multiple organ system dysfunction, and death.
Outcomes are worse in patients requiring emergent reoperations for persistent or
recurrent infections (30-50% increase in the mortality rate); however, patients
undergoing early planned second-look operations do not demonstrate this trend.
Persistent infection, recovery of enterococci, and multidrug-resistant gram-negative
organisms, as well as fungal infection, are related to worse outcomes and recurrent
complications.
Patients older than 65 years have a threefold increased risk of developing
generalized peritonitis and sepsis from gangrenous or perforated appendicitis and
perforated diverticulitis than younger patients and are 3 times more likely to die from
these disease processes. Older patients with perforated diverticulitis are 3 times
more likely than younger patients to have generalized rather than localized (ie,
pericolic, pelvic) peritonitis. These findings are consistent with the hypothesis that
the biologic features of peritonitis differ in elderly persons, who are more likely to
present with an advanced or more severe process than younger patients with
peritonitis.
Overall, studies suggest that host-related factors are more significant than the type
and source of infection with regard to the prognosis in intra-abdominal infections.
[13]

History
The diagnosis of peritonitis is usually clinical. History should include recent
abdominal surgery, previous episodes of peritonitis, travel history, use of
immunosuppressive agents, and the presence of diseases (eg, inflammatory bowel
disease, diverticulitis, peptic ulcer disease) that may predispose to intra-abdominal
infections.
A broad range of signs and symptoms are seen in spontaneous bacterial peritonitis
(SBP). A high index of suspicion must be maintained when caring for patients with
ascites, particularly those with acute clinical deterioration. As many as 30% of
patients are completely asymptomatic. Manifestations of SBP may include the
following:
Fever and chills (as many as 80% of patients)
Abdominal pain or discomfort (found in as many as 70% of patients)
Worsening or unexplained encephalopathy
Diarrhea
Ascites that does not improve following administration of diuretic medication
Worsening or new-onset renal failure
Ileus
Abdominal pain, which may be acute or insidious, is the usual chief complaint of
patients with peritonitis. Initially, the pain may be dull and poorly localized (visceral
peritoneum); often, it progresses to steady, severe, and more localized pain (parietal
peritoneum). Abdominal pain may be exacerbated by any movement (eg, coughing,
flexing the hips) and local pressure. If the underlying process is not contained, the
pain becomes diffuse. In certain disease entities (eg, gastric perforation, severe
acute pancreatitis, intestinal ischemia), the abdominal pain may be generalized from
the beginning.
Abdominal distention may be noted, as well as signs of dysfunction of other organs.
Symptoms may be subtle in patients on corticosteroids, in diabetic patients with
advanced neuropathy, and in hospitalized patients, especially the very young and
the very old. In the presence of ascites, decreased friction between the visceral and
parietal peritoneal surfaces may reduce the symptoms of abdominal pain, as seen in
patients with SBP.
Anorexia and nausea are frequent symptoms and may precede the development of
abdominal pain. Vomiting may be due to underlying visceral organ pathology (ie,
obstruction) or be secondary to peritoneal irritation.
Physical Examination
On physical examination, patients with peritonitis generally appear unwell and in
acute distress. Many of them have a temperature that exceeds 38 C, although
patients with severe sepsis may become hypothermic. Tachycardia may be present,
as a result of the release of inflammatory mediators, intravascular hypovolemia from
anorexia vomiting and fever, and third-space losses into the peritoneal cavity. With
progressive dehydration, patients may become hypotensive (5-14% of patients), as
well as oliguric or anuric; with severe peritonitis, they may present in overt septic
shock.
When examining the abdomen of a patient with suspected peritonitis, the patient
should be supine. A roll or pillows underneath the patient's knees may allow for
better relaxation of the abdominal wall.
On abdominal examination, almost all patients demonstrate tenderness to palpation.
In most patientseven those with generalized peritonitis and severe diffuse
abdominal painthe point of maximal tenderness or referred rebound tenderness
roughly overlies the pathologic process (ie, the site of maximal peritoneal irritation).
Most patients demonstrate increased abdominal wall rigidity. The increase in
abdominal wall muscular tone may be voluntary, in response to or in anticipation of
the abdominal examination, or involuntary because of the peritoneal irritation.
Patients with severe peritonitis often avoid all motion and keep their hips flexed to
relieve the abdominal wall tension. The abdomen is often distended, with hypoactive-
to-absent bowel sounds. This finding reflects a generalized ileus and may not be
present if the infection is well localized. Occasionally, the abdominal examination
reveals an inflammatory mass.
Signs of hepatic failure (eg, jaundice, angiomata) may be noted.
Rectal examination often elicits increased abdominal pain, particularly with
inflammation of the pelvic organs, but rarely indicates a specific diagnosis. A tender
inflammatory mass toward the right may indicate appendicitis, and anterior fullness
and fluctuation may indicate a cul de sac abscess.
In female patients, vaginal and bimanual examination findings may be consistent
with pelvic inflammatory disease (eg, endometritis, salpingo-oophoritis, tubo-ovarian
abscess), but exam findings are often difficult to interpret in severe peritonitis.
A complete physical examination is important for excluding conditions whose
presentation may resemble that of peritonitis. Thoracic processes with diaphragmatic
irritation (eg, empyema), extraperitoneal processes (eg, pyelonephritis, cystitis, acute
urinary retention), and abdominal wall processes (eg, infection, rectus hematoma)
may mimic certain signs and symptoms of peritonitis. Always examine the patient for
the presence of external hernias to rule out intestinal incarceration.
Remember that the presentation and the findings on clinical examination may be
entirely inconclusive or unreliable in patients with significant immunosuppression (eg,
severe diabetes, steroid use, posttransplant status, HIV infection), in patients with
altered mental state (eg, head injury, toxic encephalopathy, septic shock, analgesic
agents), in patients with paraplegia, and in patients of advanced age. With localized
deep peritoneal infections, fever and/or an elevated WBC count may be the only
signs present. As many as 20% of patients with SBP demonstrate very subtle signs
and symptoms. New onset or deterioration of existing encephalopathy may be the
only sign of the infection at the initial presentation. Most patients with TP
demonstrate vague symptoms and may be afebrile.
Diagnostic Considerations
Thoracic processes with diaphragmatic irritation (eg, empyema), extraperitoneal
processes (eg, pyelonephritis, cystitis, acute urinary retention), and abdominal wall
processes (eg, infection, rectus hematoma) may mimic certain signs and symptoms
of peritonitis. Always examine the patient for the presence of external hernias to rule
out intestinal incarceration.
According to Adler and Gasbarra, the following should be considered in the
differential diagnosis
[8]
:
Chemical irritants (eg, bile, blood, gastric juice, barium, enema or douche contents)
Chronic peritoneal dialysis
Chylous peritonitis
Eosinophilic peritonitis
Familial Mediterranean fever
Fungal infections (eg, histoplasmosis, cryptococcosis, coccidioidomycosis)
Granulomatous peritonitis (eg, parasitic infestations, sarcoidosis, tumors, Crohn
disease, starch granules)
Gynecologic disorders (Chlamydia peritonitis, salpingitis, endometriosis, teratoma,
leiomyomatosis, dermoid cyst)
HIV-associated peritonitis (from opportunistic organisms)
Mesothelial hyperplasia and metaplasia
Neoplasms (eg, primary mesothelioma, secondary carcinomatosis, Pseudomyxoma
peritonei)
Parasitic infections (eg, schistosomiasis, ascariasis, enterobiasis, amebiasis,
strongyloidiasis)
Perforated viscus
Peritoneal encapsulation
Peritoneal loose bodies and peritoneal cysts
Peritoneal lymphangiectasis
Pyelonephritis
Sclerosing peritonitis
Splenosis
Vascular conditions (eg, mesenteric embolus, mesenteric nonocclusive ischemia,
ischemic colitis, portal vein thrombosis, mesenteric vein thrombosis)
Vasculitis (eg, systemic lupus erythematosus, allergic vasculitis [Henoch-Schnlein
purpura], Kohlmeier-Degos disease, polyarteritis nodosa)
Differential Diagnoses
Aneurysm, Abdominal
Angioedema
Appendicitis, Acute
Mesenteric Ischemia
Urinary Tract Infection in Females
Whipple Disease
Approach Considerations
Diagnostic paracentesis should be performed in all patients who do not have an
indwelling peritoneal catheter and are suspected of having SBP. In peritoneal
dialysis patients with a peritoneal catheter, fluid should be withdrawn using sterile
technique. Ultrasonography may aid paracentesis if ascites is minimally detectable
or questionable.
The results of aerobic and anaerobic bacterial cultures, used in conjunction with the
cell count, prove the most useful in guiding therapy for those with SBP.
[14]
With regard
to ascitic fluid culture, direct inoculation of routine blood culture bottles at the bedside
with 10 mL of ascitic fluid has been reported to significantly increase the sensitivity of
microbiologic studies.
The diagnostic and therapeutic approach to peritonitis and peritoneal abscess is
summarized in the algorithm below.
Diagnostic and therapeutic approach to peritonitis and peritoneal abscess.
CBC Count and Other Blood Studies
Most patients will have leukocytosis (>11,000 cells/ L), with a shift to the immature
forms on the differential cell count. Patients who have severe sepsis, are
immunocompromised, or have certain types of infections (eg, fungal,
cytomegaloviral) may not have leukocytosis or leukopenia. In cases of suspected
SBP, hypersplenism may reduce the polymorphonuclear leukocyte count.
Blood chemistry findings may reveal dehydration and acidosis. PT, PTT, and INR are
indicated. Liver function tests may be indicated. Amylase and lipase levels should be
obtained if pancreatitis is suspected. Blood culture results are positive for the
offending agent in as many as 33% of patients with SBP and may help guide
antibiotic therapy. Measurement of serum albumin allows calculation of the serum-to-
ascites albumin gradient (SAAG). A SAAG of more than 1.1 is noted in SBP.
Urinalysis
This is used to rule out urinary tract diseases (eg, pyelonephritis, renal stone
disease); however, patients with lower abdominal and pelvic infections often
demonstrate WBCs in the urine and microhematuria.
Stool Sample
In patients with diarrhea, evaluate a stool sampleemploying a Clostridium
difficile toxin assay, a WBC count, and a specific culture (ie, Salmonella,
Shigella, cytomegalovirus [CMV])if the patient's history suggests infectious
enterocolitis.
Peritoneal Fluid Analysis
The single best predictor of SBP is an ascitic fluid neutrophil count of greater than
500 cells/L, which carries a sensitivity of 86% and a specificity of 98%. By lowering
the ascitic fluid neutrophil count threshold to 250 cells/ L, the sensitivity increases to
93% with only a minimal decrease in specificity to 94%.
The fluid should be evaluated for glucose, protein, lactate dehydrogenase (LDH), cell
count, Gram stain, and aerobic and anaerobic cultures. If pancreatitis or a pancreatic
leak is suspected, amylase analysis should be added to the panel. Bilirubin and
creatinine levels can be analyzed as well, if a biliary or urinary leak is suspected as a
possible etiology. The peritoneal/ascitic fluid characteristics or levels are then
compared with their respective serum values.
The fluid in bacterial peritonitis generally demonstrates a low pH and low glucose
levels with elevated protein and LDH levels. Traditionally, ascitic fluid pH of less that
7.34 was consistent with a diagnosis of SBP; however, ascitic pH is less commonly
measured because it is unreliable and lacks specificity for the condition.
SBP is established when the polymorphonuclear neutrophil (PMN) count is 250
cells/L or greater in conjunction with a positive bacterial culture result. In most of
these cases, as mentioned previously, cultures are positive for a single organism.
Obviously, these patients should receive antibiotic therapy. Although up to 30% of
cultures remain negative, most of these patients are presumed to have bacterial
peritonitis; they should be treated. A significantly decreased peritoneal fluid glucose
level (< 50 mg/dL), a peritoneal fluid LDH level much greater than the serum LDH, a
peritoneal fluid WBC count greater than 10,000 cells/L, a pH lower than 7.0, high
amylase levels, multiple organisms on Gram stain, or recovery of anaerobes from
the culture raises the suspicion of SP in these patients. Some authors recommend
repeating the paracentesis in 48-72 hours to monitor treatment success (decrease in
neutrophil count to < 50% of the original value).
Culture-negative neutrocytic ascites (probable SBP) is established when the ascitic
fluid culture results are negative but the PMN count is 250 cells/L or greater. This
may happen in as many as 50% of patients with SBP and may not actually represent
a distinctly different disease entity. Rather, it may be the result of poor culturing
techniques or late-stage resolving infection. Nonetheless, these patients should be
treated just as aggressively as those with positive culture results.
Monomicrobial nonneutrocytic bacterascites exists when a positive culture result
coexists with a PMN count 250 cells/L or greater. Although this may often be the
result of contamination of bacterial cultures, 38% of these patients develop SBP.
Therefore, monomicrobial nonneutrocytic bacterascites may represent an early form
of SBP. All study patients described who eventually developed SBP were
symptomatic. For this reason, any patient suspected clinically of having SBP in this
setting must be treated.
Tuberculous peritonitis is identified by ascites with high protein content, a low
glucose and low SAAG, elevated ascitic fluid WBC count, and lymphocyte
predominance. In TP, the fluid Gram stain and acid-fast stain results are rarely
positive, and routine culture results are falsely negative in as many as 80% of cases.
A peritoneal fluid protein level greater than 2.5 g/dL, LDH level greater than 90 U/mL,
and predominantly mononuclear cell count of more than 500 cells/L should raise
the suspicion of TP, but specificity for the diagnosis is limited. Laparoscopy with
visualization of granulomas on peritoneal biopsy and specific culture (which requires
4-6 wk) may be needed for definitive diagnosis.
Peritonitis in patients receiving continuous ambulatory peritoneal dialysis (CAPD) is
indicated by contamination of the dialysis catheter; cloudy effluent, total fluid WBC
count of greater than 100 neutrophils/L, or presence of organisms on Gram stain.
Routine intraoperative peritoneal fluid cultures in defined acute disease entities (ie,
gastric or duodenal ulcer perforation, appendicitis, diverticulitis or perforation of the
colon caused by obstruction or ischemia) are controversial. Several studies found no
significant difference in patients with appendicitis, diverticulitis, and other common
etiologies for bacterial peritonitis with regard to postoperative complication rates or
overall outcomes. The antibiotic regimen was altered only 8-10% of the time based
on operative culture data. In patients who had previous abdominal operations or
instrumentation (eg, peritoneal dialysis catheter, percutaneous stents) and patients
with prolonged antibiotic therapy, critical illness, and/or hospitalization, these cultures
may reveal resistant or unusual organisms that should prompt alteration of the
antibiotic strategy.
For a summary of ascitic fluid analysis, see Table 4, below.
Table 4. Ascitic Fluid Analysis Summary
[4]
(Open Table in a new window)
Routine Optional Unusual Less Helpful
Cell count Obtain culture in blood culture
(BC) bottles.
Tuberculosis (TB) smear
and culture
pH
Albumin Glucose Cytology Lactate
Total
protein
Lactate dehydrogenase (LDH) Triglyceride Cholesterol
Amylase Bilirubin Fibronectin
Gram stain Alpha 1-antitrypsin
Glycosaminoglycans
Bedside Reagent Strips
An exciting new development in the rapid diagnosis of SBP is the proposed use of
bedside reagent strips read by a portable spectrophotometric device. In a pilot study,
this combination achieved a 100% sensitivity in diagnosis of spontaneous bacterial
peritonitis.
[15]

This diagnostic method holds promise in replacing the time-consuming process of
manual cell counting, which is often unavailable in many laboratories "after hours".
The decreased time to diagnosis may result in a significant reduction of the time from
paracentesis to antibiotic treatment of presumptive SBP.
In a small cohort, the average time saved from dipstick to laboratory results ranged
from 2.73 hours (dipstick to validated result from automated counter) to 3 hours
(dipstick to validated manual cell count of ascitic fluid). Although promising, this
diagnostic method has not been investigated in a large-scale study.
Radiography
Plain films of the abdomen (eg, supine, upright, and lateral decubitus positions) are
often the first imaging studies obtained in patients presenting with peritonitis. Their
value in reaching a specific diagnosis is limited.
Free air is present in most cases of anterior gastric and duodenal perforation but is
much less frequent with perforations of the small bowel and colon and is unusual
with appendiceal perforation. Upright films are useful for identifying free air under the
diaphragm (most often on the right) as an indication of a perforated viscus.
Remember that the presence of free air is not mandatory with visceral perforation
and that small amounts of free air are missed easily on plain films.
Ultrasonography
Abdominal ultrasonography may be helpful in the evaluation of pathology in the right
upper quadrant (eg, perihepatic abscess, cholecystitis, biloma, pancreatitis,
pancreatic pseudocyst), right lower quadrant, and pelvis (eg, appendicitis, tubo-
ovarian abscess, Douglas pouch abscess). However, the examination is sometimes
limited because of patient discomfort, abdominal distention, and bowel gas
interference.
Ultrasonography may detect increased amounts of peritoneal fluid (ascites), but its
ability to detect quantities of less than 100 mL is limited. The central (perimesenteric)
peritoneal cavity is not visualized well with transabdominal ultrasonography.
Examination from the flank or back may improve the diagnostic yield, and providing
the ultrasonographer with specific information about the patient's condition and the
suspected diagnosis before the examination is important. With an experienced
ultrasonographer, a diagnostic accuracy of greater than 85% has been reported in
several series.
Ultrasonographically guided aspiration and placement of drains has evolved into a
valuable tool in the diagnosis and treatment of abdominal fluid collections.
Advantages of ultrasound include low cost, portability, and availability.
Disadvantages are that the test is operator dependent, and there is reduced
visualization in the presence of overlying bowel gas and abdominal dressings.
CT Scanning
If the diagnosis of peritonitis is made clinically, a CT scan is not necessary and
generally delays surgical intervention without offering clinical advantage. However,
CT scanning is indicated in all cases in which the diagnosis cannot be established on
clinical grounds and findings on abdominal plain films. CT scans of the abdomen and
pelvis remain the diagnostic study of choice for peritoneal abscess and related
visceral pathology.
Whenever possible, the CT scan should be performed with enteral and intravenous
contrast. CT scans can detect small quantities of fluid, areas of inflammation, and
other GI tract pathology, with sensitivities that approach 100%. (See the image
below.) CT scanning can be used to evaluate for ischemia, as well as to determine
bowel obstruction. An abscess is suggested by the presence of fluid density that is
not bound by the bowel or other known structures. Gas within an abdominal mass or
the presence of an enhancing wall and adjacent inflammatory changes are also
highly suggestive of an abscess. Ischemia can be demonstrated by a clot in a large
vessel or by the absence of blood flow. Gas within the intestinal wall or in the portal
vein may also suggest ischemia.
In abscess formation subsequent to secondary peritonitis (SP), approximately half of
patients have a simple abscess without loculation, and the other half have complex
abscesses secondary to fibrinous septation and organization of the abscess
material. Abscess formation occurs most frequently in the subhepatic area, the
pelvis, and the paracolic gutters, but it may also occur in the perisplenic area, the
lesser sac, and between small bowel loops and their mesentery.
Peritoneal abscesses and other fluid collections may be aspirated for diagnosis and
drained under CT guidance; this technique has become a mainstay of therapy.
Nuclear Scanning
These diagnostic studies have little use in the initial evaluation of patients with
suspected peritonitis or intra-abdominal sepsis. They are most frequently used in the
evaluation of fever of unknown origin or in patients with persistent fever despite
adequate antibiotic treatment and negative CT scan findings.
MRI
MRI is an emerging imaging modality for the diagnosis of suspected intra-abdominal
abscesses. Abdominal abscesses demonstrate decreased signal intensity on T1-
weighted images and homogeneous or heterogeneous increased signal intensity on
T2-weighted images; abscesses are observed best on gadolinium-enhanced, T1-
weighted, fat-suppressed images as well-defined fluid collections with rim
enhancement.
Limited availability and high cost, as well as the need for MRI-compatible patient
support equipment and the length of the examination, currently limit its usefulness as
a diagnostic tool in acute peritoneal infections, particularly for patients who are
critically ill.
Contrast Studies
Conventional contrast studies (ie, Gastrografin swallow, upper GI tract study with
follow-through, colorectal contrast enema, fistulogram, contrast studies of drains and
stents) are reserved for specific indications in the setting of suspected peritonitis or
peritoneal abscess.
Approach Considerations
The current 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. Treatment
success is defined as adequate source control with resolution of sepsis and
clearance of all residual intra-abdominal infection.
Early control of the septic source is mandatory and can be achieved by operative
and nonoperative means.
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. Definitive interventions
to restore functional anatomy involve removing the source of the antimicrobial
contamination and repairing the anatomic or functional disorder causing the
infection. This is accomplished by surgical intervention. Occasionally, this can be
achieved during a single operation; however, in certain situations, a second or a third
procedure may be required. In some patients, definitive intervention is delayed until
the condition of the patient improves and tissue healing is adequate to allow for a
(sometimes) lengthy procedure.
To see complete information on the Surgical Approach to Peritonitis and Abdominal
Sepsis, please go to the main article by clicking here.
Nonoperative interventions include percutaneous abscess drainage, as well as
percutaneous and endoscopic stent placements. If an abscess is accessible for
percutaneous drainage and if the underlying visceral organ pathology does not
clearly require operative intervention, percutaneous drainage is a safe and effective
initial treatment approach. With percutaneous treatment, the definition of success
includes the avoidance of further operative intervention and, in some cases, the
delay of surgery until after resolution of the initial sepsis.
The general principles guiding the treatment of
[13]
infections are 4-fold, as follows:
1. Control the infectious source
2. Eliminate bacteria and toxins
3. Maintain organ system function
4. Control the inflammatory process
The treatment of peritonitis is multidisciplinary, with complementary application of
medical, operative, and nonoperative interventions. Medical support includes the
following:
Systemic antibiotic therapy
Intensive care with hemodynamic, pulmonary, and renal support
Nutrition and metabolic support
Inflammatory response modulation therapy
Early control of the septic source is mandatory and can be achieved by operative
and nonoperative means. Nonoperative interventional therapies include
percutaneous drainage of abscesses and percutaneous and endoscopic stent
placements.
Treatment of peritonitis and intra-abdominal sepsis always begins with volume
resuscitation, correction of potential electrolyte and coagulation abnormalities, and
empiric broad-spectrum parenteral antibiotic coverage.
Hemodynamic Resuscitation
Aggressive fluid resuscitation to treat intravascular fluid depletion should be
instituted. Pressor agents are avoided if possible. Fluid administration requires
frequent monitoring of blood pressure, pulse, urine output, blood gases, hemoglobin
and hematocrit, electrolytes, and renal function.
Antibiotic Therapy
Antibiotic therapy is used to prevent local and hematogenous spread of infection and
to reduce late complications.
[16]
Several different antibiotic regimens are available for
the treatment of intra-abdominal infections.
[16]
Both single-agent broad-spectrum
therapy and combination therapies have been used. However, no specific therapy
has been found to be superior to another therapy. Infection of the abdominal cavity
requires coverage for gram-positive and gram-negative bacteria, as well as for
anaerobes. Antipseudomonal coverage is recommended in patients who have had
previous treatment with antibiotics or who have had a prolonged hospitalization.
The optimal duration of antibiotic therapy must be individualized and depends on the
underlying pathology, severity of infection, speed and effectiveness of source
control, and patient response to therapy. Antibiotics can be discontinued once
clinical signs of infection have resolved. Recurrence is a concern with certain
infections, such as those from Candida and Staphylococcus aureus, and treatment
should be continued for 2-3 weeks.
Nonoperative Drainage
Drainage refers to evacuation of an abscess. This can be performed operatively or
percutaneously under ultrasound or CT guidance. If the abscess is localized at the
level of the skin and underlying superficial tissues, simple removal of sutures or
opening of the wound may be sufficient. Percutaneous techniques are preferred
when an abscess can be completely drained, and debridement and repair of the
anatomic structures are not needed. Factors that may prevent successful source
control with percutaneous drainage include diffuse peritonitis, lack of localization of
the infectious process, multiple abscesses, anatomic inaccessibility, or need for
surgical debridement.
[4]

In some instances, success of nonoperative drainage also includes the ability to
delay surgery until the acute process and sepsis are resolved and a definitive
procedure can be performed under elective circumstances.
Most patients with tertiary peritonitis develop complex abscesses or poorly localized
peritoneal infections that are not amenable to percutaneous drainage. Up to 90% of
patients will require reoperation for additional source control.
For primary percutaneous management of intra-abdominal abscesses, the etiology,
location, and morphology of the abscess must be defined; evaluate for the presence
of an ongoing enteric leak or fistula formation. With proper indications, most studies
have reported success rates of greater than 80% (range 33-100%) for drainage of
localized nonloculated abscesses; however, the success rates depend to some
degree on the underlying pathology. In these studies, no significant differences were
found between operative and primary nonoperative management with regard to the
overall morbidity or length of hospital stay (mean duration of drainage 8.5 d).
In the treatment of diverticular disease, the use of laparoscopic drainage and drain
placement and/or resection with or without anastomosis is under evaluation.
[17]

Common reasons for failure of primary nonoperative management include enteric
fistula (eg, anastomotic dehiscence), pancreatic involvement, infected clot, and
multiple or multiloculated abscesses. Procedure-related significant complications are
reported to occur in less than 10% of cases (range 5-27%), with less than a 1%
attributable mortality rate with experienced physicians.
In peritoneal abscess formation caused by subacute bowel perforation (eg,
diverticulitis, Crohn disease, appendicitis), primary percutaneous management with
percutaneous drainage was successful in most patients. Patients with Crohn disease
whose abscesses were drained percutaneously had significantly fewer associated
fistulae. Failure in these patients was related to preexisting fistulization and
extensive stricture formation.
Concerns regarding the transgression of small or large bowel with drainage
catheters in deep abscesses or ileus have been addressed in animal studies, which
have found no increase in abscess formation, independent of whether catheters
remained for 5 days or longer. Similar data are not available for human patients.
In summary, percutaneous and surgical drainage should not be considered
competitive but rather complementary. If an abscess is accessible to percutaneous
drainage and the underlying visceral organ pathology does not clearly require an
operative approach, percutaneous drainage can be used safely and effectively as
the primary treatment modality. In these cases, patients must be closely monitored,
and improvement should occur in less than 24-48 hours. With lack of improvement,
patients must be reevaluated aggressively (eg, repeat CT scan) and the therapeutic
strategy should be altered accordingly.
Nutrition
In general, patients with peritonitis develop some degree of gut dysfunction (eg,
ileus) after exploration. Consider establishing some form of nutritional support early
in the course of treatment because most patients have an insufficient enteral intake
for a variable amount of time preoperatively. The existing data support that enteral
nutrition is superior to parenteral hyperalimentation. Enteral nutrition has been found
to have fewer complications in patients who are severely ill. If enteral feeding is
contraindicated or not tolerated, parenteral nutrition should be instituted.
Nutritional demands increase during sepsis, with caloric requirements of 25-35
kcal/kg/d. Patients with sepsis should be fed a high-protein isocaloric diet.
Hypercaloric diets cannot prevent the intense protein catabolism associated with
sepsis.
[18]

Consultations
The treatment of intra-abdominal sepsis requires a multidisciplinary approach. In the
treatment of secondary peritonitis, a surgeon must be consulted. Interventional
radiology may need to be consulted if ultrasound or CT-guided drainage of an
abscess is being considered.
Other consultations may include the following:
Gastroenterology
Infectious disease
Critical care
Diet/nutrition
Complications
Complications of peritonitis include tertiary peritonitis, infection or dehiscence of the
surgical site, enterocutaneous fistula, abdominal compartment syndrome, and
enteric insufficiency. Enterocutaneous fistulae can lead to ongoing (potentially large)
volume, protein, and electrolyte losses; inability to use the gut for nutritional support;
and associated long-term complications of intravenous alimentation. Abdominal
compartment syndrome is a well-recognized disease entity related to acutely
increased abdominal pressure (ie, intra-abdominal hypertension) and is associated
with the development of multiple organ dysfunction. Extensive initial (gastrointestinal)
disease, chronic recurrent infections, and associated reoperations may lead to
enteric insufficiency because of short gut, pancreatic insufficiency, or hepatic
dysfunction.
Long-term Monitoring
Depending on the type of perforation causing secondary peritonitis, patients may
require further surgical care or repeat abscess drainage by interventional radiology.
Follow-up care depends on the cause of the intra-abdominal sepsis. In simple
infections, such as those caused by cholecystitis or appendicitis, once the infection is
cleared, no follow-up care is necessary. However, in patients with perforated
duodenal ulcer, chronic pancreatitis, or Crohn disease, lifelong follow-up care is
needed.
Repeat paracentesis is not required in SBP if the patient has advanced cirrhosis with
signs and symptoms of infection, a positive bacterial isolate with monomicrobial
typical organism, and a good response to treatment.
[19]
If the course is atypical,
repeat paracentesis should be performed in 48 hours.
For SBP, a 10-day to 14-day course of antibiotics is recommended. Although not
required, a repeat peritoneal fluid analysis is recommended to verify declining
polymorphonuclear neutrophil (PMN) counts and sterilization of ascitic fluid.
If improvement in ascitic fluid or clinical condition does not occur within 48 hours,
further evaluation is required to rule out bowel perforation or intra-abdominal
abscess. Evaluation may include a combination of radiography, CT scanning,
intraluminal contrast studies, or surgical exploration.
After resolution of peritonitis and peritoneal abscesses, follow-up care is directed
mostly by specifics of the underlying disease process and the presence or absence
of chronic complications (eg, enterocutaneous fistulae). Patients with simple
peritoneal infections after appendicitis or cholecystitis are usually cured and do not
require long-term follow-up care. Patients with peritoneal operations for perforated
peptic ulcer disease, Crohn disease, pancreatitis, and others often require lifelong
medical therapy and treatment of recurrent complications.
Further inpatient care
Further care of the hospitalized patient is dependent on the etiology of the peritonitis
and the clinical response to therapy. Whenever cultures have been obtained,
antibiotic therapy should be appropriately focused on the organisms present.
Appropriate resuscitation following known guidelines for sepsis should be instituted
as soon as the diagnosis of sepsis is entertained.
Further outpatient care
Outpatient treatment of peritonitis is very limited; however, of the common causes of
peritonitis, diverticulitis is probably the entity most frequently treated in an outpatient
setting. A recent review outlines both inpatient and outpatient therapy.
[20]

Prophylaxis
Outpatient prophylaxis, although not routinely recommended, has been shown to
prevent SBP in the following high-risk groups:
Patients with ascites admitted with acute GI bleeding
Patients with ascitic fluid protein levels of less than 1 g/dL
Patients with a prior episode of SBP
Suggested outpatient prophylactic regimens include the following:
Norfloxacin - 400 mg daily
Ciprofloxacin - 750 mg weekly
Five doses of double-strength trimethoprim-sulfamethoxazole per week (Monday
through Friday)
Evidence suggests that the long-term prophylaxis of patients with cirrhosis with
fluoroquinolones, often norfloxacin, has led to selective intestinal decontamination
and high-level fluoroquinolone resistance. This has been supported by published
data that show a higher predominance of gram-positive pathogens in ascitic fluid
cultures than previously reported.
[21]

Deterrence and prevention
The prevention of peritonitis centers on causes that are acquired, most of which
involve longstanding behaviors that despite all best efforts, remain uncontrolled.
Diverticula develop in the Western population with increasing age at a prevalence of
80% in the eighth decade of life. Although increasing fiber and fluid intake has been
promoted, the evidence to support this regimen is inadequate.
[22]
In cirrhotic patients
with ascites, similar results of unclear efficacy of prophylaxis haunt effective
prevention.
[23]

Medication Summary
The goals of pharmacotherapy in patients with peritonitis and abdominal sepsis are
to reduce morbidity and prevent complications. The agents used are antimicrobials
such as cefotaxime, gentamicin, ampicillin, and sulfamethoxazole.
Empiric antimicrobial therapy must be comprehensive and should cover all likely
pathogens in the context of the clinical setting. Traditionally, a combination of an
aminoglycoside and ampicillin was used to treat SBP. This regimen affords excellent
empiric coverage of more than 90% of SBP cases caused by gram-negative aerobes
or gram-positive cocci. More recently, the third-generation cephalosporin cefotaxime
has been demonstrated to be as effective as the ampicillin/aminoglycoside
combination, and it does not carry the increased risk of nephrotoxicity in cirrhotic
patients. Cefotaxime does not cover enterococci, which are the pathogen in up to 5%
of cases.
Cephalosporins
Class Summary
Cephalosporins are structurally and pharmacologically related to penicillins. They
inhibit bacterial cell wall synthesis, resulting in bactericidal activity. Cephalosporins
are divided into first, second, third, and fourth generation. First-generation
cephalosporins have greater activity against gram-positive bacteria, and succeeding
generations have increased activity against gram-negative bacteria and decreased
activity against gram-positive bacteria.
Cefotaxime (Claforan)

Cefotaxime is a third-generation cephalosporin with a broad gram-negative
spectrum, lower efficacy against gram-positive organisms, and higher efficacy
against resistant organisms. Thus, it provides excellent empiric coverage of SBP.
Cefuroxime (Ceftin, Kefurox, Zinacef)

Second-generation cephalosporin; maintains gram-positive activity of first-generation
cephalosporins; adds activity against P mirabilis, H influenzae, E coli,K pneumoniae,
and M catarrhalis.
Binds to penicillin binding proteins and inhibits final transpeptidation step of
peptidoglycan synthesis, resulting in cell wall death. Condition of patient, severity of
infection, and susceptibility of microorganism determines proper dose and route of
administration. Resists degradation by beta-lactamase.
Ceftriaxone (Rocephin)

Ceftriaxone is a third-generation cephalosporin with broad-spectrum, gram-negative
activity; lower efficacy against gram-positive organisms; and higher efficacy against
resistant organisms. Its bactericidal activity results from inhibiting cell wall synthesis
by binding to one or more penicillin-binding proteins. It exerts an antimicrobial effect
by interfering with synthesis of peptidoglycan, a major structural component of
bacterial cell walls. Bacteria eventually lyse due to the ongoing activity of cell wall
autolytic enzymes while cell wall assembly is arrested.
Ceftriaxone is highly stable in the presence of beta-lactamases, both penicillinase
and cephalosporinase, of gram-negative and gram-positive bacteria. Approximately
33-67% of the dose is excreted unchanged in the urine; the remainder is secreted in
bile and ultimately in feces as microbiologically inactive compounds. Ceftriaxone
reversibly binds to human plasma proteins, and the binding decreases from 95%
bound at plasma concentrations of less than 25 mcg/mL to 85% bound at 300
mcg/mL.
Cefotetan

Cefotetan is a second-generation cephalosporin used as single-drug therapy to
provide broad gram-negative coverage and anaerobic coverage. Also provides some
coverage of gram-positive bacteria. Half-life is 3.5 h. Inhibits bacterial cell wall
synthesis by binding to one or more of the penicillin-binding proteins; inhibits final
transpeptidation step of peptidoglycan synthesis, resulting in cell wall death.
Cefepime

Cefepime is a fourth-generation cephalosporin. Gram-negative coverage comparable
to ceftazidime but has better gram-positive coverage (comparable to ceftriaxone).
Cefepime is a zwitter ion; rapidly penetrates gram-negative cells. Best beta-lactam
for IM administration.
Aminoglycosides
Class Summary
Aminoglycosides are bactericidal antibiotics used primarily to treat gram-negative
infections. They interfere with bacterial protein synthesis by binding to 30S and 50S
ribosomal subunits.
Gentamicin (Gentacidin, Garamycin)

Gentamicin is an aminoglycoside antibiotic effective against Pseudomonas
aeruginosa; E coli; and Proteus, Klebsiella, and Staphylococcus species. Gentamicin
is also variably effective against some strains of certain gram-positive organisms,
including S aureus, enterococci, and L monocytogenes. Dosing regimens are
numerous; adjust the dose based on creatinine clearance and changes in volume of
distribution. Gentamicin may be given IV/IM. Gentamicin has been reported to offer
additive or synergistic activity against enterococci when used with ampicillin.
Penicillins
Class Summary
The penicillins are bactericidal antibiotics that work against sensitive organisms at
adequate concentrations and inhibit the biosynthesis of cell wall mucopeptide.
Piperacillin and Tazobactam sodium (Zosyn)

Piperacillin is a semisynthetic extended-spectrum penicillin that inhibits bacterial cell
wall synthesis by binding to specific penicillin-binding proteins; it is the most effective
of the antipseudomonal penicillins.
Tazobactam increases piperacillin activity against S aureus, Klebsiella, Enterobacter,
and Serratia species; the greatest increase is in activity against B fragilis. However, it
does not increase antiP aeruginosa activity.
Amoxicillin and clavulanate (Augmentin)

Amoxicillin inhibits bacterial cell wall synthesis by binding to penicillin-binding
proteins; clavulanate inhibits beta-lactamase producing bacteria. This combination is
a good alternative antibiotic for patients allergic or intolerant to the macrolide class.
Usually, it is well tolerated, and it provides good coverage to most infectious agents.
It is not effective against Mycoplasma and Legionella species. The half-life of the oral
dosage form is 1-1.3 hours. It has good tissue penetration but does not enter
cerebrospinal fluid.
Ticarcillin and clavulanate potassium (Ticar)

This combination of an antipseudomonal penicillin with a beta-lactamase inhibitor
provides coverage against most gram-positive and gram-negative organisms, as well
as most anaerobes. It inhibits biosynthesis of cell wall mucopeptide and is effective
during the stage of active growth.
Ampicillin (Omnipen, Marcillin)

Ampicillin interferes with bacterial cell wall synthesis during active multiplication,
causing bactericidal activity against susceptible organisms. Dose adjustments may
be necessary in renal failure. Rash should be evaluated carefully to differentiate
nonallergic ampicillin rash from hypersensitivity reaction.
Macrolides
Class Summary
Macrolide antibiotics have bacteriostatic activity and exert their antibacterial action
by binding to the 50S ribosomal subunit of susceptible organisms, resulting in
inhibition of protein synthesis
Tobramycin (Nebcin)

Tobramycin is used in skin, bone, and skin structure infections, caused by S aureus,
P aeruginosa, Proteus species, E coli, Klebsiella species, and Enterobacter species.
It is indicated in the treatment of staphylococcal infections when penicillin or
potentially less-toxic drugs are contraindicated and when bacterial susceptibility and
clinical judgment justifies its use. Like other aminoglycosides, tobramycin is
associated with nephrotoxicity and ototoxicity.
Clindamycin (Cleocin)

Clindamycin is a semisynthetic antibiotic produced by 7(S)-chloro-substitution of
7(R)-hydroxyl group of its parent compound lincomycin. It inhibits bacterial growth,
possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-
dependent protein synthesis to arrest. Clindamycin distributes widely in the body
without penetration of the CNS. Clindamycin is protein bound and excreted by the
liver and kidneys.
Carbapenems
Class Summary
Carbapenems are structurally related to penicillins and have broad-spectrum
bactericidal activity. The carbapenems exert their effect by inhibiting cell wall
synthesis, which leads to cell death. They are active against gram-negative bacteria,
gram-bacteria, and anaerobes.
Meropenem (Merrem IV)

A bactericidal broad-spectrum carbapenem antibiotic that inhibits cell-wall synthesis,
meropenem is effective against most gram-positive and gram-negative bacteria.
Compared with imipenem, meropenem has slightly increased activity against gram-
negative organisms and slightly decreased activity against staphylococci and
streptococci.
Aztreonam (Azactam)

Aztreonam is a monobactam, not a beta-lactam, antibiotic that inhibits cell wall
synthesis during bacterial growth. It is active against gram-negative bacilli but has
very limited gram-positive activity and is not useful for anaerobes. Aztreonam lacks
cross-sensitivity with beta-lactam antibiotics. It may be used in patients allergic to
penicillins or cephalosporins. Transient or persistent renal insufficiency may prolong
serum levels.
Ertapenem (Invanz)

The bactericidal activity of ertapenem results from inhibition of cell wall synthesis and
is mediated through binding to penicillin-binding proteins. Ertapenem is stable
against hydrolysis by a variety of beta-lactamases, including penicillinases,
cephalosporinases, and extended spectrum beta-lactamases; it is hydrolyzed by
metallo-beta-lactamases.
Imipenem and cilastatin (Primaxin)

This combination is used for treatment of infections with multiple organisms because
other agents do not have wide spectrum coverage or are contraindicated due to
potential for toxicity.
Fluoroquinolones
Class Summary
Fluoroquinolones have broad-spectrum activity against gram-positive and gram-
negative aerobic organisms. They inhibit DNA synthesis and growth by inhibiting
DNA gyrase and topoisomerase, which is required for replication, transcription, and
translation of genetic material.
Ciprofloxacin (Cipro)

Ciprofloxacin, a fluoroquinolone, inhibits bacterial DNA synthesis and, consequently,
growth, by inhibiting DNA gyrase and topoisomerase, which is required for
replication, transcription, and translation of genetic material. Quinolones have broad
activity against gram-positive and gram-negative aerobic organisms. It has no
activity against anaerobes. Continue treatment for at least 2 days (7-14 d typical)
after signs and symptoms have disappeared. In prolonged therapy, perform periodic
evaluations of organ system functions (eg, renal, hepatic, hematopoietic); adjust the
dose in the presence of renal function impairment. Superinfections may occur with
prolonged or repeated antibiotic therapy.
Norfloxacin (Chibroxin, Noroxin)

Norfloxacin is a fluoroquinolone with activity against pseudomonads, streptococci,
MRSA, S epidermidis, and most gram-negative organisms, but it has no activity
against anaerobes. It inhibits bacterial DNA synthesis and, consequently, growth.
Anti-Infectives
Class Summary
Anti-infectives such as metronidazole and sulfamethoxazole/trimethoprim are
effective against some types of bacteria that have become resistant to other
antibiotics.
Sulfamethoxazole and trimethoprim (Bactrim, Bactrim DS, Cotrim, Cotrim DS,
Septra, Septra DS)

Trimethoprim-sulfamethoxazole inhibits bacterial growth by inhibiting the synthesis of
dihydrofolic acid. Its antibacterial activity includes common urinary tract pathogens,
except Pseudomonas aeruginosa.
Metronidazole (Flagyl)

Metronidazole is an imidazole ring-based antibiotic active against various anaerobic
bacteria and protozoa. It is used in combination with other antimicrobial agents (but
is used as monotherapy in C difficile enterocolitis).
Glycylcycline Antibiotic
Class Summary
Glycylcycline antibiotics are structurally similar to tetracycline antibiotics and were
developed to overcome bacterial mechanisms of tetracycline resistance. Tigecycline
is the first drug approved in this class.

Tigecycline (Tygacil)

Tigecycline is a glycylcycline antibiotic that is structurally similar to tetracycline
antibiotics. It is used for complicated intra-abdominal infections caused by C freundii,
E cloacae, E coli, K oxytoca, K pneumoniae, E faecalis (vancomycin-susceptible
isolates only), S aureus (methicillin-susceptible isolates only), S anginosus group.
(includes S anginosus, S intermedius, and S constellatus), B fragilis, B
thetaiotaomicron, B uniformis, B vulgatus, C perfringens, and P micros. Use with
caution in patients with severe hepatic impairment.

References
1. Pavlidis TE. Cellular changes in association with defense mechanisms in intra-abdominal
sepsis. Minerva Chir. Dec 2003;58(6):777-81. [Medline].
2. Appenrodt B, Grnhage F, Gentemann MG, Thyssen L, Sauerbruch T, Lammert F.
Nucleotide-binding oligomerization domain containing 2 (NOD2) variants are genetic risk
factors for death and spontaneous bacterial peritonitis in liver cirrhosis. Hepatology. Apr
2010;51(4):1327-33. [Medline].
3. Barretti P, Montelli AC, Batalha JE, Caramori JC, Cunha Mde L. The role of virulence factors
in the outcome of staphylococcal peritonitis in CAPD patients. BMC Infect Dis. Dec 22
2009;9:212. [Medline].[Full Text].
4. [Guideline] Runyon BA. Management of adult patients with ascites due to
cirrhosis. Hepatology. Mar 2004;39(3):841-56. [Medline].
5. Lata J, Stiburek O, Kopacova M. Spontaneous bacterial peritonitis: a severe complication of
liver cirrhosis.World J Gastroenterol. Nov 28 2009;15(44):5505-10. [Medline]. [Full Text].
6. Bert F, Noussair L, Lambert-Zechovsky N, Valla D. Viridans group streptococci: an
underestimated cause of spontaneous bacterial peritonitis in cirrhotic patients with
ascites. Eur J Gastroenterol Hepatol. Sep 2005;17(9):929-33. [Medline].
7. Cholongitas E, Papatheodoridis GV, Lahanas A, Xanthaki A, Kontou-Kastellanou C,
Archimandritis AJ. Increasing frequency of Gram-positive bacteria in spontaneous bacterial
peritonitis. Liver Int. Feb 2005;25(1):57-61. [Medline].
8. Adler SN, Gasbarra DB. A Pocket Manual of Differential Diagnosis. Philadelphia, Pa:
Lippincott Williams & Wilkins; 2005.
9. Nouri-Majalan N, Najafi I, Sanadgol H, Ganji MR, Atabak S, Hakemi M, et al. Description of
an outbreak of acute sterile peritonitis in Iran. Perit Dial Int. Jan-Feb 2010;30(1):19-
22. [Medline].
10. Evans LT, Kim WR, Poterucha JJ, Kamath PS. Spontaneous bacterial peritonitis in
asymptomatic outpatients with cirrhotic ascites. Hepatology. Apr 2003;37(4):897-
901. [Medline].
11. Cheruvattath R, Balan V. Infections in Patients With End-stage Liver Disease. J Clin
Gastroenterol. Apr 2007;41(4):403-11. [Medline].
12. Soriano G, Castellote J, Alvarez C, et al. Secondary bacterial peritonitis in cirrhosis: a
retrospective study of clinical and analytical characteristics, diagnosis and management. J
Hepatol. Jan 2010;52(1):39-44.[Medline].
13. Marshall JC. Intra-abdominal infections. Microbes Infect. Sep 2004;6(11):1015-25. [Medline].
14. Riggio O, Angeloni S. Ascitic fluid analysis for diagnosis and monitoring of spontaneous
bacterial peritonitis. World J Gastroenterol. Aug 21 2009;15(31):3845-50. [Medline]. [Full
Text].
15. Gaya DR, David B Lyon T, Clarke J, Jamdar S, Inverarity D, Forrest EH, et al. Bedside
leucocyte esterase reagent strips with spectrophotometric analysis to rapidly exclude
spontaneous bacterial peritonitis: a pilot study. Eur J Gastroenterol Hepatol. Apr
2007;19(4):289-95. [Medline].
16. Blot S, De Waele JJ. Critical issues in the clinical management of complicated intra-
abdominal infections.Drugs. 2005;65(12):1611-20. [Medline].
17. Swank HA, Vermeulen J, Lange JF, Mulder IM, van der Hoeven JA, Stassen LP, et al. The
ladies trial: laparoscopic peritoneal lavage or resection for purulent peritonitis and Hartmann's
procedure or resection with primary anastomosis for purulent or faecal peritonitis in perforated
diverticulitis (NTR2037). BMC Surg. Oct 18 2010;10:29. [Medline]. [Full Text].
18. Hawker FH. How to feed patients with sepsis. Curr Opin Crit Care. Aug 2000;6(4):247-
252. [Medline].
19. Runyon B. Ascites and spontaneous bacterial peritonitis. In: Feldman M, Friedman LS,
Sleisenger MH, eds. Sleisenger & Fordtran's Gastrointestinal and Liver Disease. Vol 2. 8
th
ed.
Philadelphia, Pa: Saunders; 2006:1935-64.
20. Biondo S, Lopez Borao J, Millan M, Kreisler E, Jaurrieta E. Current status of the treatment of
acute colonic diverticulitis: a systematic review. Colorectal Dis. Jan 2012;14(1):e1-
e11. [Medline].
21. Colizza S, Rossi S. Antibiotic prophylaxis and treatment of surgical abdominal sepsis. J
Chemother. Nov 2001;13 Spec No 1(1):193-201. [Medline].
22. [Best Evidence] Maconi G, Barbara G, Bosetti C, Cuomo R, Annibale B. Treatment of
diverticular disease of the colon and prevention of acute diverticulitis: a systematic review. Dis
Colon Rectum. Oct 2011;54(10):1326-38. [Medline].
23. [Best Evidence] [Guideline] Cohen MJ, Sahar T, Benenson S, Elinav E, Brezis M, Soares-
Weiser K. Antibiotic prophylaxis for spontaneous bacterial peritonitis in cirrhotic patients with
ascites, without gastro-intestinal bleeding. Cochrane Database Syst Rev. Apr 15
2009;CD004791. [Medline].
24. Gins P, Rimola A, Planas R, Vargas V, et al. Norfloxacin prevents spontaneous bacterial
peritonitis recurrence in cirrhosis: results of a double-blind, placebo-controlled
trial. Hepatology. Oct. 1990;12(4 Pt 1):716-24.
25. Soares-Weiser K, Brezis M, Leibovici L. Antibiotics for spontaneous bacterial peritonitis in
cirrhotics.Cochrane Database Syst Rev. 2001;CD002232. [Medline].
26. Tubau F, Liares J, Rodrguez MD, Cercenado E, Aldea MJ, Gonzlez-Romo F, et al.
Susceptibility to tigecycline of isolates from samples collected in hospitalized patients with
secondary peritonitis undergoing surgery. Diagn Microbiol Infect Dis. Mar 2010;66(3):308-
13. [Medline].
27. [Best Evidence] Wiggins KJ, Craig JC, Johnson DW, Strippoli GF. Treatment for peritoneal
dialysis-associated peritonitis. Cochrane Database Syst Rev. Jan 23
2008;CD005284. [Medline].