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Peritonitis is defined as an inflammation of the serosal membrane that lines the abdominal cavity and the

organs contained therein. The peritoneum, which is an otherwise sterile environment, reacts to various
pathologic stimuli with a fairly uniform inflammatory response. Depending on the underlying pathology, the
resultant peritonitis may be infectious or sterile (ie, chemical or mechanical). 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
an immunocompromised state), secondary (ie, related to a pathologic process in a visceral organ, such as
perforation or trauma, including iatrogenic trauma), or tertiary (ie, persistent or recurrent infection after
adequate initial therapy). Primary peritonitis is most often spontaneous bacterial peritonitis (SBP) seen mostly
inpatients with chronic liver disease. Secondary peritonitis is by far the most common form of peritonitis
encountered in clinical practice. Tertiary peritonitis often develops in the absence of the original visceral organ
pathology. (See Clinical Presentation.)
Infections of the peritoneum are further divided into generalized (peritonitis) and localized (intra-abdominal
abscess). This article focuses on the diagnosis and management of infectious peritonitis and abdominal
abscesses. An abdominal abscess is seen in the image below.

A 35-year-old man with a history of Crohn disease presented with pain and swelling in the
right abdomen. In figure A, a thickened loop of terminal ileum is evident adherent to the right anterior abdominal wall. In
figure B, the right anterior abdominal wall is markedly thickened and edematous, with adjacent inflamed terminal ileum. In
figure C, a right lower quadrant abdominal wall abscess and enteric fistula are observed and confirmed by the presence of
enteral contrast in the abdominal wall.

The diagnosis of peritonitis is usually clinical. Diagnostic peritoneal lavage may be helpful in patients who do
not have conclusive signs on physical examination or who cannot provide an adequate history; in addition,
paracentesis should be performed in all patients who do not have an indwelling peritoneal catheter and are

suspected of having SBP, because results of aerobic and anaerobic bacterial cultures, used in conjunction with
the cell count, are useful in guiding therapy. (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 the 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
108 CFU/mL, much higher than the 5 105 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 the 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 grampositive organisms (eg, Streptococcus pneumoniae [15%], other Streptococcus species [15%],
and Staphylococcus species [3%]) (see Table 1). However, some data suggest that the percentage of grampositive infections may be increasing.[6, 7] One study cites a 34.2% incidence of streptococci, ranking in second
position after Enterobacteriaceae.[7] Viridans group 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*

Peptic ulcer perforation

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

Stomach

Trauma (mostly penetrating)

Iatrogenic*

Peptic ulcer perforation

Trauma (blunt and penetrating)


Duodenum
Iatrogenic*

Cholecystitis

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

Malignancy

Biliary tract

Choledochal cyst (rare)

Trauma (mostly penetrating)

Iatrogenic*

Pancreas

Pancreatitis (eg, alcohol, drugs, gallstones)

Trauma (blunt and penetrating)

Iatrogenic*

Ischemic bowel

Incarcerated hernia (internal and external)

Closed loop obstruction

Crohn disease
Small bowel
Malignancy (rare)

Meckel diverticulum

Trauma (mostly penetrating)

Ischemic bowel

Diverticulitis

Malignancy

Ulcerative colitis and Crohn disease

Large bowel and appendix

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

Escherichia coli

60%

Enterobacter/Klebsiella

26%

Proteus

22%

Pseudomonas

8%

Streptococci

28%

Enterococci

17%

Staphylococci

7%

Bacteroides

72%

Eubacteria

24%

Clostridia

17%

Peptostreptococci

14%

Peptococci

11%

Candida

2%

Aerobic
Gram negative

Gram positive

Anaerobic

Fungi

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

(Type)

Etiologic Organisms

Class

Antibiotic Therapy

Type of Organism

(Suggested)

E coli (40%)

K pneumoniae (7%)

Pseudomonas species (5%)

Proteus species (5%)


Primary

Gram-negative

Third-generation cephalosporin
Streptococcus species (15%)

Staphylococcus species (3%)

Anaerobic species (< 5%)

Secondary

Gram-negative

E coli

Second-generation cephalosporin

Enterobacter species

Third-generation cephalosporin

Klebsiella species

Penicillins with anaerobic activity

Proteus species

Quinolones with anaerobic activity

Streptococcus species

Gram-positive

Enterococcus species

Bacteroides fragilis

Quinolone and metronidazole

Other Bacteroides species

Aminoglycoside and metronidazole

Eubacterium species
Anaerobic
Clostridium species

Anaerobic Streptococcusspecies

Enterobacter species

Second-generation cephalosporin

Pseudomonas species

Third-generation cephalosporin

Enterococcus species

Penicillins with anaerobic activity

Gram-negative

Quinolones with anaerobic activity


Gram-positive

Staphylococcus species
Quinolone and metronidazole

Tertiary
Aminoglycoside and metronidazole

Carbapenems
Fungal

Candida species
Triazoles or amphotericin (considered in fungal etiology)

(Alter therapy based on culture results.)

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 occur 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 in patients with SBP may exceed 30% if the 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 in 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, trimethoprimsulfamethoxazole); 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 (5070%).

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