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Peritonitis Emedscape

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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 theabdominal cavity and the organs contained therein. The peritoneum, which is anotherwise sterile environment, reacts to various pathologic stimuli with a fairlyuniform inflammatory response. Depending on the underlying pathology, theresultant peritonitis may be infectious or sterile (ie, chemical or mechanical). Intra-abdominal sepsis is an inflammation of the peritoneum caused by pathogenicmicroorganisms 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 otherwisesterile peritoneal environment through organ perforation, but it may also result from

    other irritants, such as foreign bodies, bile from a perforated gall bladder or alacerated liver, or gastric acid from a perforated ulcer. Women also experiencelocalized peritonitis from an infected fallopian tube or a ruptured ovarian cyst.Patients may present with an acute or insidious onset of symptoms, limited and milddisease, 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 pathologicprocess in a visceral organ, such as perforation or trauma, including iatrogenictrauma), 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 ofperitonitis encountered in clinical practice. Tertiary peritonitis often develops in theabsence of the original visceral organ pathology. (See Clinical Presentation.)

    Infections in the peritoneum are further divided into generalized (peritonitis) andlocalized (intra-abdominal abscess). This article focuses on the diagnosis andmanagement of infectious peritonitis and abdominal abscesses. An abdominalabscess is seen in the image below.

    The diagnosis of peritonitis is usually clinical. Diagnostic peritoneal lavage may behelpful in patients who do not have conclusive signs on physical examination or whocannot provide an adequate history; in addition, paracentesis should be performed inall patients who do not have an indwelling peritoneal catheter and are suspected ofhaving SBP, because results of aerobic and anaerobic bacterial cultures, used inconjunction with the cell count, are useful in guiding therapy. (See Workup.)

    The current approach to peritonitis and peritoneal abscesses targets correction ofthe underlying process, administration of systemic antibiotics, and supportive therapyto prevent or limit secondary complications due to organ system failure. (SeeTreatment and Management and Medication.)

    Early control of the septic source is mandatory and can be achieved operatively andnonoperatively. Nonoperative interventions include percutaneous abscess drainage,

    as well as percutaneous and endoscopic stent placements. Operative managementaddresses the need to control the infectious source and to purge bacteria and toxins.

    http://emedicine.medscape.com/article/180234-overviewhttp://emedicine.medscape.com/article/180234-overviewhttp://emedicine.medscape.com/article/180234-overview
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    The type and extent of surgery depends on the underlying disease process and theseverity of intra-abdominal infection.

    AnatomyThe 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), bycovering the extraperitoneal structures in the pelvis (inferior), and by covering theundersurface of the diaphragm (superior). This parietal layer of the peritoneumreflects onto the abdominal visceral organs to form the visceral peritoneum. Itthereby creates a potential space between the 2 layers (ie, the peritoneal cavity).

    The peritoneum consists of a single layer of flattened mesothelial cells over looseareolar tissue. The loose connective tissue layer contains a rich network of vascularand lymphatic capillaries, nerve endings, and immune-competent cells, particularlylymphocytes and macrophages. The peritoneal surface cells are joined by junctional

    complexes, thus forming a dialyzing membrane that allows passage of fluid andcertain small solutes. Pinocytotic activity of the mesothelial cells and phagocytosis bymacrophages allow for clearance of macromolecules.

    Normally, the amount of peritoneal fluid present is less than 50 mL, and only smallvolumes are transferred across the considerable surface area in a steady state eachday. The peritoneal fluid represents a plasma ultrafiltrate, with electrolyte and soluteconcentrations similar to that of neighboring interstitial spaces and a protein contentof less than 30 g/L, mainly albumin. In addition, peritoneal fluid contains smallnumbers of desquamated mesothelial cells and various numbers and morphologiesof migrating immune cells (reference range is < 300 cells/ L, predominantly of

    mononuclear morphology).The peritoneal cavity is divided incompletely into compartments by the mesentericattachments and secondary retroperitonealization of certain visceral organs. A largeperitoneal fold, the greater omentum, extends from the greater curvature of thestomach and the inferior aspect of the proximal duodenum downward over a variabledistance to fold upon itself (with fusion of the adjacent layers) and ascends back tothe taenia omentalis of the transverse colon. This peritoneal fold demonstrates aslightly different microscopic anatomy, with fenestrated surface epithelium and alarge number of adipocytes, lymphocytes, and macrophages, and it functions as a fatstorage location and a mobile immune organ.

    The compartmentalization of the peritoneal cavity, in conjunction with the greateromentum, influences the localization and spread of peritoneal inflammation andinfections

    PathophysiologyIn peritonitis caused by bacteria, the physiologic response is determined by severalfactors, including the virulence of the contaminant, the size of the inoculum, theimmune status and overall health of the host (eg, as indicated by the AcutePhysiology and Chronic Health Evaluation II [APACHE II] score), and elements ofthe local environment, such as necrotic tissue, blood, or bile .[2]

    Intra-abdominal sepsis from a perforated viscus (ie, secondary peritonitis orsuppurative peritonitis) results from direct spillage of luminal contents into the

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    peritoneum (eg, perforated peptic ulcer, diverticulitis, appendicitis, iatrogenicperforation). 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 tothe 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 muchdebate since Harold Conn first recognized it in the 1960s. Enteric organisms havetraditionally been isolated from more than 90% of infected ascites fluid inspontaneous bacterial peritonitis (SBP), suggesting that the GI tract is the source ofbacterial contamination. The preponderance of enteric organisms, in combinationwith the presence of endotoxin in ascitic fluid and blood, once favored the argumentthat SBP was due to direct transmural migration of bacteria from an intestinal orhollow 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 ahematogenous source of the infecting organism in combination with an impairedimmune defense system. Nonetheless, the exact mechanism of bacterialdisplacement 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 bacterialgrowth in the ascitic fluid. A key predisposing factor may be the intestinal bacterialovergrowth found in people with cirrhosis, mainly attributed to decreased intestinaltransit time. Intestinal bacterial overgrowth, along with impaired phagocytic function,low serum and ascites complement levels, and decreased activity of thereticuloendothelial system, contributes to an increased number of microorganismsand decreased capacity to clear them from the bloodstream, resulting in theirmigration into and eventual proliferation within ascites fluid.

    Interestingly, adults with SBP typically have ascites, but most children with SBP donot have ascites. The reason for and mechanism behind this is the source ofongoing investigation.

    Fibrinolysis

    Alterations in fibrinolysis (through increased plasminogen activator inhibitor activity)and the production of fibrin exudates have an important role in peritonitis. Theproduction of fibrin exudates is an important part of the host defense, but largenumbers of bacteria may be sequestered within the fibrin matrix. This may retardsystemic dissemination of intraperitoneal infection and may decrease early mortalityrates from sepsis, but it also is integral to the development of residual infection andabscess formation. As the fibrin matrix matures, the bacteria within are protectedfrom host clearance mechanisms.

    Whether fibrin ultimately results in containment or persistent infection may dependon the degree of peritoneal bacterial contamination. In animal studies of mixedbacterial peritonitis that examined the effects of systemic defibrinogenation andthose of abdominal fibrin therapy, heavy peritoneal contamination uniformly led tosevere peritonitis with early death (< 48 h) because of overwhelming sepsis.

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    Bacterial load

    Bacterial load and the nature of the pathogen also play important roles. Somestudies suggest that the number of bacteria present at the onset of abdominalinfections is much higher than originally believed (approximately 2 10 8 CFU/mL,

    much higher than the 5 105

    CFU/mL inocula routinely used for in vitro susceptibilitytesting). 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 abscessformation. Among these virulence factors are capsule formation, facultativeanaerobic growth, adhesion capabilities, and succinic acid production. Synergybetween certain bacterial and fungal organisms may also play an important role inimpairing the host's defense. One such synergy may exist between Bacteroidesfragilis and gram-negative bacteria, particularly E coli (see the image below) ,whereco-inoculation significantly increases bacterial proliferation and abscess formation.

    Gram-negative Escherichia coli.

    Enterococci

    Enterococci may be important in enhancing the severity and persistence ofperitoneal infections. In animal models of peritonitis with E coli and B fragilis, thesystemic manifestations of the peritoneal infection and bacteremia rates wereincreased, as were bacterial concentrations in the peritoneal fluid and rate ofabscess formation. Nevertheless, the role of Enterococcus organisms inuncomplicated intra-abdominal infections remains unclear. Antibiotics that lackspecific activity against Enterococcus are often used successfully in the therapy ofperitonitis, and the organism is not often recovered as a blood-borne pathogen inintra-abdominal sepsis.

    FungiThe role of fungi in the formation of intra-abdominal abscesses is not fullyunderstood. Some authors suggest that bacteria and fungi exist as nonsynergisticparallel infections with incomplete competition, allowing the survival of all organisms.In this setting, treatment of the bacterial infection alone may lead to an overgrowth offungi, which may contribute to increased morbidity.

    Abscess formation

    Abscess formation occurs when the host defense is unable to eliminate the infectingagent and attempts to control the spread of this agent by compartmentalization. Thisprocess is aided by a combination of factors that share a common feature, ie,impairment of phagocytotic killing. Most animal and human studies suggest that

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    abscess formation occurs only in the presence of abscess-potentiating agents. Although the nature and spectrum of these factors have not been studiedexhaustively, certain fiber analogues (eg, bran) and the contents of autoclaved stoolhave been identified as abscess-potentiating agents. In animal models, these factorsinhibit 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 inthe development of the systemic inflammatory response syndrome (SIRS) andmultiple organ failure (MOF) have been a major focus of research over the pastdecade. Comparatively few data exist about the magnitude of theintraperitoneal/abscess cytokine response and implications for the host. Existingdata suggest that bacterial peritonitis is associated with an immense intraperitonealcompartmentalized cytokine response. Higher levels of certain cytokines (ie, tumornecrosis factor-alpha [TNF-alpha], interleukin [IL]-6) have been associated withworse outcomes, as well as secondary (uncontrolled) activation of the systemicinflammatory cascade.

    EtiologyThe etiology of disease depends on the type, as well as location, of peritonitis, asfollows:

    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 ofbacteria across the gut wall or mesenteric lymphatics and, less frequently, viahematogenous seeding in the presence of bacteremia.

    SBP can occur as a complication of any disease state that produces the clinicalsyndrome of ascites, such as heart failure and Budd-Chiari syndrome. Children withnephrosis 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 whoare in a decompensated state .[4] In particular, decreased hepatic synthetic functionwith associated low total protein level, low complement levels, or prolongedprothrombin time (PT) is associated with maximum risk. Patients with low proteinlevels in ascitic fluid (< 1 g/dL) have a 10-fold higher risk of developing SBP thanthose with a protein level greater than 1 g/dL. Approximately 10-30% of patients withcirrhosis and ascites develop SBP .[5] The incidence rises to more than 40% withascitic 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

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    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 beincreasing .[6, 7] One study cites a 34.2% incidence of streptococci, ranking in secondposition 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 isolatesare found in less than 10%.

    Secondary peritonitis

    Common etiologic entities of secondary peritonitis (SP) include perforatedappendicitis; perforated gastric or duodenal ulcer; perforated (sigmoid) colon causedby diverticulitis, volvulus, or cancer; and strangulation of the small bowel (see Table1). Necrotizing pancreatitis can also be associated with peritonitis in the case ofinfection of the necrotic tissue.

    The pathogens involved in SP differ in the proximal and distal GI tract. Gram-positiveorganisms predominate in the upper GI tract, with a shift toward gram-negativeorganisms in the upper GI tract in patients on long-term gastric acid suppressivetherapy. Contamination from a distal small bowel or colon source initially may resultin the release of several hundred bacterial species (and fungi); host defenses quicklyeliminate most of these organisms. The resulting peritonitis is almost alwayspolymicrobial, containing a mixture of aerobic and anaerobic bacteria with apredominance of gram-negative organisms (see Table 1).

    As many as 15% of patients who have cirrhosis with ascites who were initiallypresumed to have SBP have SP. In many of these patients, clinical signs andsymptoms alone are not sensitive or specific enough to reliably differentiate betweenthe 2 entities. A thorough history, evaluation of the peritoneal fluid, and additionaldiagnostic 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*

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    Stomach Peptic ulcer perforation

    Malignancy (eg, adenocarcinoma, lymphoma, gastrointestinalstromal tumor)

    Trauma (mostly penetrating)

    Iatrogenic*

    Duodenum Peptic ulcer perforation

    Trauma (blunt and penetrating)

    Iatrogenic*

    Biliary tract Cholecystitis

    Stone perforation from gallbladder (ie, gallstone ileus) orcommon duct

    Malignancy

    Choledochal cyst (rare)

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    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

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    Trauma (mostly penetrating)

    Large bowel andappendix

    Ischemic bowel

    Diverticulitis

    Malignancy

    Ulcerative colitis and Crohn disease

    Appendicitis

    Colonic volvulus

    Trauma (mostly penetrating)

    Iatrogenic

    Uterus, salpinx, andovaries

    Pelvic inflammatory disease (eg, salpingo-oophoritis, tubo-ovarian abscess, ovarian cyst)

    Malignancy (rare)

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    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 bowelinjury (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:

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    (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-generationcephalosporin

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    Klebsiella species

    Proteus species

    Third-generation cephalosporin

    Penicillins with anaerobic activity

    Quinolones with anaerobicactivity

    Quinolone and metronidazole

    Aminoglycoside andmetronidazole

    Gram-positive

    Streptococcus species

    Enterococcus species

    Anaerobic Bacteroides fragilis

    Other Bacteroides species

    Eubacterium species

    Clostridium species

    Anaerobic Streptococcus species

    Tertiary Gram- Enterobacter species Second-generation

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    negative

    Pseudomonas species

    Enterococcus species

    cephalosporin

    Third-generation cephalosporin

    Penicillins with anaerobic activity

    Quinolones with anaerobicactivity

    Quinolone and metronidazole

    Aminoglycoside andmetronidazole

    Carbapenems

    Triazoles or amphotericin(considered in fungal etiology)

    (Alter therapy based on cultureresults.)

    Gram-positive

    Staphylococcus species

    Fungal Candida species

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    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, Crohndisease) without bacterial inoculation of the peritoneal cavity. Clinical signs and

    symptoms are indistinguishable from those of SP or peritoneal abscess, and thediagnostic and therapeutic approach should be the same .[9]

    Peritoneal abscess

    Peritoneal abscess describes the formation of an infected fluid collectionencapsulated by fibrinous exudate, omentum, and/or adjacent visceral organs. Theoverwhelming majority of abscesses occurs subsequent to SP. Abscess formationmay be a complication of surgery. The incidence of abscess formation afterabdominal surgery is less than 1-2%, even when the operation is performed for anacute inflammatory process. The risk of abscess increases to 10-30% in cases ofpreoperative perforation of the hollow viscus, significant fecal contamination of theperitoneal cavity, bowel ischemia, delayed diagnosis and therapy of the initialperitonitis, and the need for reoperation, as well as in the setting ofimmunosuppression. Abscess formation is the leading cause of persistent infectionand development of tertiary peritonitis.

    EpidemiologyThe overall incidence of peritoneal infection and abscess is difficult to establish andvaries with the underlying abdominal disease processes. SBP occurs in both childrenand adults and is a well-known and ominous complication of cirrhosis .[5]Of patientswith cirrhosis who have SBP, 70% are Child-Pugh class C. In these patients, thedevelopment of SBP is associated with a poor long-term prognosis.

    Once thought to occur only in those individuals with alcoholic cirrhosis, SBP is nowknown to affect patients with cirrhosis from any cause. In patients with ascites, theprevalence may be as high as 18%. This number has grown from 8% over the past 2decades, most likely secondary to an increased awareness of SBP and heightenedthreshold to perform diagnostic paracentesis.

    Although the etiology and incidence of hepatic failure differ between children andadults, in those individuals with ascites, the incidence of SBP is roughly equal. Twopeak ages for SBP are characteristic in children: one in the neonatal period and theother at age 5 years.

    PrognosisOver the past decade, the combination of better antibiotic therapy, more aggressiveintensive care, and earlier diagnosis and therapy with a combination of operative andpercutaneous techniques have led to a significant reduction in morbidity andmortality related to intra-abdominal sepsis

    Spontaneous bacterial peritonitis

    The mortality rate in SBP may be as low as 5% in patients who receive promptdiagnosis and treatment. However, in hospitalized patients, 1-year mortality ratesmay range from 50-70% .[10] This is usually secondary to the development ofcomplications, such as gastrointestinal bleeding, renal dysfunction, and worsening

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    liver failure .[11] Patients with concurrent renal insufficiency have been shown to be ata higher risk of mortality from SBP than those without concurrent renal insufficiency.

    Mortality from SBP may be decreasing among all subgroups of patients because ofadvances 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 rateis less than 10% in fairly well-compensated patients with early therapy. As many as70% of patients who survive an episode of SBP have a recurrent episode within 1year, and for these patients, the mortality rate approaches 50%. Some studiessuggest that the recurrence rate of SBP may be decreased to less than 20% withlong-term antibiotic prophylaxis (eg, quinolones, trimethoprim-sulfamethoxazole);however, whether this improves long-term survival without liver transplantation isunclear.

    Secondary peritonitis and peritoneal abscess

    Uncomplicated SP and simple abscesses carry a mortality rate of less than 5%, butthis rate may increase to greater than 30-50% in severe infections. The overallmortality 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 toimprove in less than 24-72 hours after adequate therapy.

    In severe intra-abdominal infections and peritonitis, the mortality rate may increaseto greater than 30-50%. The concurrent development of sepsis, SIRS, and MOF canincrease the mortality rate to greater than 70%, and, in these patients, more than80% of deaths occur with an active infection present.

    Soriano et al found that cirrhotic patients with SP who underwent surgical treatmenttended to have a lower mortality rate than did those who received medical therapyonly (53.8% vs 81.8%, respectively) .[12] Among the surgically treated patients withSP, the survival rate was greater in those with the shortest time between diagnosticparacentesis and surgery. These researchers concluded that the prognosis ofcirrhotic patients with SP could be improved via a low threshold of suspicion on thebasis of Runyon's criteria and microbiologic data, prompt use of abdominal CTscanning, and early surgical evaluation.

    Tertiary peritonitis

    In comparison with patients with other forms of peritonitis, patients who developtertiary peritonitis have significantly longer ICU and hospital stays, higher organdysfunction scores, and higher mortality rates (50-70%).

    Other factors affecting prognosis

    Several scoring systems (eg, APACHE II, SIRS, multiple organ dysfunctionsyndrome [MODS], Mannheim peritonitis index) have been developed to assess theclinical prognosis of patients with peritonitis. Most of these scores rely on certainhost 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 givenpatient. In general, the mortality rate is less than 5% with an APACHE II of less than

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    15 and rises to greater than 40% with scores above 15. Rising APACHE II scores ondays 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 ininstituting either medical therapy or surgical therapy has been clearly associated withincreased complication rates, the development of tertiary peritonitis, the need forreoperation, multiple organ system dysfunction, and death.

    Outcomes are worse in patients requiring emergent reoperations for persistent orrecurrent infections (30-50% increase in the mortality rate); however, patientsundergoing early planned second-look operations do not demonstrate this trend.

    Persistent infection, recovery of enterococci, and multidrug-resistant gram-negativeorganisms, as well as fungal infection, are related to worse outcomes and recurrentcomplications.

    Patients older than 65 years have a threefold increased risk of developinggeneralized peritonitis and sepsis from gangrenous or perforated appendicitis andperforated diverticulitis than younger patients and are 3 times more likely to die fromthese disease processes. Older patients with perforated diverticulitis are 3 timesmore likely than younger patients to have generalized rather than localized (ie,pericolic, pelvic) peritonitis. These findings are consistent with the hypothesis thatthe biologic features of peritonitis differ in elderly persons, who are more likely topresent with an advanced or more severe process than younger patients withperitonitis.

    Overall, studies suggest that host-related factors are more significant than the typeand source of infection with regard to the prognosis in intra-abdominal infections .[13]

    HistoryThe diagnosis of peritonitis is usually clinical. History should include recentabdominal surgery, previous episodes of peritonitis, travel history, use ofimmunosuppressive agents, and the presence of diseases (eg, inflammatory boweldisease, diverticulitis, peptic ulcer disease) that may predispose to intra-abdominalinfections.

    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 withascites, particularly those with acute clinical deterioration. As many as 30% ofpatients are completely asymptomatic. Manifestations of SBP may include thefollowing:

    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 ofpatients with peritonitis. Initially, the pain may be dull and poorly localized (visceral

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    peritoneum); often, it progresses to steady, severe, and more localized pain (parietalperitoneum). Abdominal pain may be exacerbated by any movement (eg, coughing,flexing the hips) and local pressure. If the underlying process is not contained, thepain becomes diffuse. In certain disease entities (eg, gastric perforation, severeacute 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 withadvanced neuropathy, and in hospitalized patients, especially the very young andthe very old. In the presence of ascites, decreased friction between the visceral andparietal peritoneal surfaces may reduce the symptoms of abdominal pain, as seen inpatients with SBP.

    Anorexia and nausea are frequent symptoms and may precede the development ofabdominal pain. Vomiting may be due to underlying visceral organ pathology (ie,obstruction) or be secondary to peritoneal irritation.

    Physical ExaminationOn physical examination, patients with peritonitis generally appear unwell and inacute distress. Many of them have a temperature that exceeds 38 C, althoughpatients with severe sepsis may become hypothermic. Tachycardia may be present,as a result of the release of inflammatory mediators, intravascular hypovolemia fromanorexia vomiting and fever, and third-space losses into the peritoneal cavity. Withprogressive dehydration, patients may become hypotensive (5-14% of patients), aswell as oliguric or anuric; with severe peritonitis, they may present in overt septicshock.

    When examining the abdomen of a patient with suspected peritonitis, the patientshould be supine. A roll or pillows underneath the patient's knees may allow forbetter relaxation of the abdominal wall.

    On abdominal examination, almost all patients demonstrate tenderness to palpation.In most patients even those with generalized peritonitis and severe diffuseabdominal pain the point of maximal tenderness or referred rebound tendernessroughly overlies the pathologic process (ie, the site of maximal peritoneal irritation).

    Most patients demonstrate increased abdominal wall rigidity. The increase inabdominal 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 torelieve the abdominal wall tension. The abdomen is often distended, with hypoactive-to-absent bowel sounds. This finding reflects a generalized ileus and may not bepresent if the infection is well localized. Occasionally, the abdominal examinationreveals an inflammatory mass.

    Signs of hepatic failure (eg, jaundice, angiomata) may be noted.

    Rectal examination often elicits increased abdominal pain, particularly withinflammation of the pelvic organs, but rarely indicates a specific diagnosis. A tenderinflammatory mass toward the right may indicate appendicitis, and anterior fullnessand fluctuation may indicate a cul de sac abscess.

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    In female patients, vaginal and bimanual examination findings may be consistentwith pelvic inflammatory disease (eg, endometritis, salpingo-oophoritis, tubo-ovarianabscess), 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 diaphragmaticirritation (eg, empyema), extraperitoneal processes (eg, pyelonephritis, cystitis, acuteurinary retention), and abdominal wall processes (eg, infection, rectus hematoma)may mimic certain signs and symptoms of peritonitis. Always examine the patient forthe presence of external hernias to rule out intestinal incarceration.

    Remember that the presentation and the findings on clinical examination may beentirely inconclusive or unreliable in patients with significant immunosuppression (eg,severe diabetes, steroid use, posttransplant status, HIV infection), in patients withaltered mental state (eg, head injury, toxic encephalopathy, septic shock, analgesicagents), in patients with paraplegia, and in patients of advanced age. With localizeddeep peritoneal infections, fever and/or an elevated WBC count may be the onlysigns present. As many as 20% of patients with SBP demonstrate very subtle signsand symptoms. New onset or deterioration of existing encephalopathy may be theonly sign of the infection at the initial presentation. Most patients with TPdemonstrate vague symptoms and may be afebrile.

    Diagnostic ConsiderationsThoracic processes with diaphragmatic irritation (eg, empyema), extraperitonealprocesses (eg, pyelonephritis, cystitis, acute urinary retention), and abdominal wallprocesses (eg, infection, rectus hematoma) may mimic certain signs and symptomsof 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 thedifferential 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

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    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 anindwelling peritoneal catheter and are suspected of having SBP. In peritonealdialysis patients with a peritoneal catheter, fluid should be withdrawn using steriletechnique. Ultrasonography may aid paracentesis if ascites is minimally detectableor questionable.

    The results of aerobic and anaerobic bacterial cultures, used in conjunction with thecell count, prove the most useful in guiding therapy for those with SBP . [14]With regardto ascitic fluid culture, direct inoculation of routine blood culture bottles at the bedsidewith 10 mL of ascitic fluid has been reported to significantly increase the sensitivity ofmicrobiologic studies.

    The diagnostic and therapeutic approach to peritonitis and peritoneal abscess issummarized in the algorithm below.

    http://emedicine.medscape.com/article/756735-overviewhttp://emedicine.medscape.com/article/756735-overviewhttp://emedicine.medscape.com/article/756261-overviewhttp://emedicine.medscape.com/article/756261-overviewhttp://emedicine.medscape.com/article/773895-overviewhttp://emedicine.medscape.com/article/773895-overviewhttp://emedicine.medscape.com/article/758674-overviewhttp://emedicine.medscape.com/article/758674-overviewhttp://emedicine.medscape.com/article/233101-overviewhttp://emedicine.medscape.com/article/233101-overviewhttp://emedicine.medscape.com/article/183350-overviewhttp://emedicine.medscape.com/article/183350-overviewhttp://emedicine.medscape.com/article/183350-overviewhttp://emedicine.medscape.com/article/233101-overviewhttp://emedicine.medscape.com/article/758674-overviewhttp://emedicine.medscape.com/article/773895-overviewhttp://emedicine.medscape.com/article/756261-overviewhttp://emedicine.medscape.com/article/756735-overview
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    Diagnostic and therapeutic approach to peritonitis and peritoneal abscess.

    CBC Count and Other Blood StudiesMost patients will have leukocytosis (>11,000 cells/ L), with a shift to the immatureforms on the differential cell count. Patients who have severe sepsis, areimmunocompromised, or have certain types of infections (eg, fungal,cytomegaloviral) may not have leukocytosis or leukopenia. In cases of suspectedSBP, hypersplenism may reduce the polymorphonuclear leukocyte count.

    Blood chemistry findings may reveal dehydration and acidosis. PT, PTT, and INR areindicated. Liver function tests may be indicated. Amylase and lipase levels should beobtained if pancreatitis is suspected. Blood culture results are positive for theoffending agent in as many as 33% of patients with SBP and may help guideantibiotic 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.

    UrinalysisThis is used to rule out urinary tract diseases (eg, pyelonephritis, renal stonedisease); however, patients with lower abdominal and pelvic infections oftendemonstrate WBCs in the urine and microhematuria.

    Stool SampleIn patients with diarrhea, evaluate a stool sample employing a Clostridiumdifficile toxin assay, a WBC count, and a specific culture (ie, Salmonella,Shigella, cytomegalovirus [CMV]) if the patient's history suggests infectiousenterocolitis.

    Peritoneal Fluid AnalysisThe single best predictor of SBP is an ascitic fluid neutrophil count of greater than500 cells/L, which carries a sensitivity of 86% and a specificity of 98%. By loweringthe ascitic fluid neutrophil count threshold to 250 cells/ L, the sensitivity increases to93% with only a minimal decrease in specificity to 94%.

    The fluid should be evaluated for glucose, protein, lactate dehydrogenase (LDH), cellcount, Gram stain, and aerobic and anaerobic cultures. If pancreatitis or a pancreaticleak is suspected, amylase analysis should be added to the panel. Bilirubin andcreatinine levels can be analyzed as well, if a biliary or urinary leak is suspected as apossible 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 glucoselevels with elevated protein and LDH levels. Traditionally, ascitic fluid pH of less that7.34 was consistent with a diagnosis of SBP; however, ascitic pH is less commonlymeasured because it is unreliable and lacks specificity for the condition.

    SBP is established when the polymorphonuclear neutrophil (PMN) count is 250cells/L or greater in conjunction with a positive bacterial culture result. In most ofthese cases, as mentioned previously, cultures are positive for a single organism.Obviously, these patients should receive antibiotic therapy. Although up to 30% ofcultures remain negative, most of these patients are presumed to have bacterialperitonitis; they should be treated. A significantly decreased peritoneal fluid glucoselevel (< 50 mg/dL), a peritoneal fluid LDH level much greater than the serum LDH, a

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    peritoneal fluid WBC count greater than 10,000 cells/L, a pH lower than 7.0, highamylase levels, multiple organisms on Gram stain, or recovery of anaerobes fromthe culture raises the suspicion of SP in these patients. Some authors recommendrepeating the paracentesis in 48-72 hours to monitor treatment success (decrease inneutrophil count to < 50% of the original value).

    Culture-negative neutrocytic ascites (probable SBP) is established when the asciticfluid culture results are negative but the PMN count is 250 cells/L or greater. Thismay happen in as many as 50% of patients with SBP and may not actually representa distinctly different disease entity. Rather, it may be the result of poor culturingtechniques or late-stage resolving infection. Nonetheless, these patients should betreated just as aggressively as those with positive culture results.

    Monomicrobial nonneutrocytic bacterascites exists when a positive culture resultcoexists with a PMN count 250 cells/L or greater. Although this may often be theresult of contamination of bacterial cultures, 38% of these patients develop SBP.Therefore, monomicrobial nonneutrocytic bacterascites may represent an early formof SBP. All study patients described who eventually developed SBP weresymptomatic. For this reason, any patient suspected clinically of having SBP in thissetting must be treated.

    Tuberculous peritonitis is identified by ascites with high protein content, a lowglucose and low SAAG, elevated ascitic fluid WBC count, and lymphocytepredominance. In TP, the fluid Gram stain and acid-fast stain results are rarelypositive, 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 raisethe suspicion of TP, but specificity for the diagnosis is limited. Laparoscopy withvisualization of granulomas on peritoneal biopsy and specific culture (which requires4-6 wk) may be needed for definitive diagnosis.

    Peritonitis in patients receiving continuous ambulatory peritoneal dialysis (CAPD) isindicated by contamination of the dialysis catheter; cloudy effluent, total fluid WBCcount 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 thecolon caused by obstruction or ischemia) are controversial. Several studies found nosignificant difference in patients with appendicitis, diverticulitis, and other common

    etiologies for bacterial peritonitis with regard to postoperative complication rates oroverall outcomes. The antibiotic regimen was altered only 8-10% of the time basedon operative culture data. In patients who had previous abdominal operations orinstrumentation (eg, peritoneal dialysis catheter, percutaneous stents) and patientswith prolonged antibiotic therapy, critical illness, and/or hospitalization, these culturesmay reveal resistant or unusual organisms that should prompt alteration of theantibiotic 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)

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    Routine Optional Unusual Less Helpful

    Cell count Obtain culture in blood culture(BC) bottles.

    Tuberculosis (TB) smearand culture

    pH

    Albumin Glucose Cytology Lactate

    Totalprotein

    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 ofbedside reagent strips read by a portable spectrophotometric device. In a pilot study,this combination achieved a 100% sensitivity in diagnosis of spontaneous bacterialperitonitis .[15]

    This diagnostic method holds promise in replacing the time-consuming process ofmanual 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 fromparacentesis to antibiotic treatment of presumptive SBP.

    In a small cohort, the average time saved from dipstick to laboratory results rangedfrom 2.73 hours (dipstick to validated result from automated counter) to 3 hours(dipstick to validated manual cell count of ascitic fluid). Although promising, thisdiagnostic method has not been investigated in a large-scale study.

    RadiographyPlain films of the abdomen (eg, supine, upright, and lateral decubitus positions) areoften the first imaging studies obtained in patients presenting with peritonitis. Theirvalue in reaching a specific diagnosis is limited.

    Free air is present in most cases of anterior gastric and duodenal perforation but ismuch less frequent with perforations of the small bowel and colon and is unusualwith appendiceal perforation. Upright films are useful for identifying free air under thediaphragm (most often on the right) as an indication of a perforated viscus.Remember that the presence of free air is not mandatory with visceral perforationand 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-

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    ovarian abscess, Douglas pouch abscess). However, the examination is sometimeslimited because of patient discomfort, abdominal distention, and bowel gasinterference.

    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 providingthe ultrasonographer with specific information about the patient's condition and thesuspected diagnosis before the examination is important. With an experiencedultrasonographer, a diagnostic accuracy of greater than 85% has been reported inseveral series.

    Ultrasonographically guided aspiration and placement of drains has evolved into avaluable 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 reducedvisualization in the presence of overlying bowel gas and abdominal dressings.

    CT ScanningIf the diagnosis of peritonitis is made clinically, a CT scan is not necessary andgenerally delays surgical intervention without offering clinical advantage. However,CT scanning is indicated in all cases in which the diagnosis cannot be established onclinical grounds and findings on abdominal plain films. CT scans of the abdomen andpelvis remain the diagnostic study of choice for peritoneal abscess and relatedvisceral pathology.

    Whenever possible, the CT scan should be performed with enteral and intravenouscontrast. CT scans can detect small quantities of fluid, areas of inflammation, andother GI tract pathology, with sensitivities that approach 100%. (See the imagebelow.) CT scanning can be used to evaluate for ischemia, as well as to determinebowel obstruction. An abscess is suggested by the presence of fluid density that isnot bound by the bowel or other known structures. Gas within an abdominal mass orthe presence of an enhancing wall and adjacent inflammatory changes are alsohighly suggestive of an abscess. Ischemia can be demonstrated by a clot in a largevessel or by the absence of blood flow. Gas within the intestinal wall or in the portalvein may also suggest ischemia.

    In abscess formation subsequent to secondary peritonitis (SP), approximately half ofpatients have a simple abscess without loculation, and the other half have complexabscesses secondary to fibrinous septation and organization of the abscessmaterial. Abscess formation occurs most frequently in the subhepatic area, thepelvis, and the paracolic gutters, but it may also occur in the perisplenic area, thelesser sac, and between small bowel loops and their mesentery.

    Peritoneal abscesses and other fluid collections may be aspirated for diagnosis anddrained 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 withsuspected peritonitis or intra-abdominal sepsis. They are most frequently used in the

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    evaluation of fever of unknown origin or in patients with persistent fever despiteadequate antibiotic treatment and negative CT scan findings.

    MRIMRI 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 onT2-weighted images; abscesses are observed best on gadolinium-enhanced, T1-weighted, fat-suppressed images as well-defined fluid collections with rimenhancement.

    Limited availability and high cost, as well as the need for MRI-compatible patientsupport equipment and the length of the examination, currently limit its usefulness asa diagnostic tool in acute peritoneal infections, particularly for patients who arecritically ill.

    Contrast StudiesConventional contrast studies (ie, Gastrografin swallow, upper GI tract study withfollow-through, colorectal contrast enema, fistulogram, contrast studies of drains andstents) are reserved for specific indications in the setting of suspected peritonitis orperitoneal abscess.

    Approach ConsiderationsThe current approach to peritonitis and peritoneal abscesses targets correction ofthe underlying process, administration of systemic antibiotics, and supportive therapyto prevent or limit secondary complications due to organ system failure. Treatmentsuccess 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 operativeand nonoperative means.

    Operative management addresses the need to control the infectious source and topurge bacteria and toxins. The type and extent of surgery depends on the underlyingdisease process and the severity of intra-abdominal infection. Definitive interventionsto restore functional anatomy involve removing the source of the antimicrobialcontamination and repairing the anatomic or functional disorder causing theinfection. This is accomplished by surgical intervention. Occasionally, this can beachieved during a single operation; however, in certain situations, a second or a thirdprocedure may be required. In some patients, definitive intervention is delayed untilthe 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 AbdominalSepsis, please go to the main article by clicking here.

    Nonoperative interventions include percutaneous abscess drainage, as well aspercutaneous and endoscopic stent placements. If an abscess is accessible forpercutaneous drainage and if the underlying visceral organ pathology does notclearly require operative intervention, percutaneous drainage is a safe and effective

    initial treatment approach. With percutaneous treatment, the definition of success

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    includes the avoidance of further operative intervention and, in some cases, thedelay of surgery until after resolution of the initial sepsis.

    The general principles guiding the treatment o f [13] infections are 4-fold, as follows:

    1. Control the infectious source2. Eliminate bacteria and toxins3. Maintain organ system function4. Control the inflammatory process

    The treatment of peritonitis is multidisciplinary, with complementary application ofmedical, operative, and nonoperative interventions. Medical support includes thefollowing:

    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 operativeand nonoperative means. Nonoperative interventional therapies includepercutaneous drainage of abscesses and percutaneous and endoscopic stentplacements.

    Treatment of peritonitis and intra-abdominal sepsis always begins with volumeresuscitation, correction of potential electrolyte and coagulation abnormalities, andempiric broad-spectrum parenteral antibiotic coverage.

    Hemodynamic Resuscitation Aggressive fluid resuscitation to treat intravascular fluid depletion should beinstituted. Pressor agents are avoided if possible. Fluid administration requiresfrequent monitoring of blood pressure, pulse, urine output, blood gases, hemoglobinand hematocrit, electrolytes, and renal function.

    Antibiotic Therapy Antibiotic therapy is used to prevent local and hematogenous spread of infection andto reduce late complications .[16] Several different antibiotic regimens are available forthe treatment of intra-abdominal infections .[16] Both single-agent broad-spectrumtherapy and combination therapies have been used. However, no specific therapyhas been found to be superior to another therapy. Infection of the abdominal cavityrequires coverage for gram-positive and gram-negative bacteria, as well as foranaerobes. Antipseudomonal coverage is recommended in patients who have hadprevious treatment with antibiotics or who have had a prolonged hospitalization.

    The optimal duration of antibiotic therapy must be individualized and depends on theunderlying pathology, severity of infection, speed and effectiveness of sourcecontrol, and patient response to therapy. Antibiotics can be discontinued onceclinical signs of infection have resolved. Recurrence is a concern with certaininfections, such as those from Candida and Staphylococcus aureus, and treatmentshould be continued for 2-3 weeks.

    Nonoperative Drainage

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    Drainage refers to evacuation of an abscess. This can be performed operatively orpercutaneously under ultrasound or CT guidance. If the abscess is localized at thelevel of the skin and underlying superficial tissues, simple removal of sutures oropening of the wound may be sufficient. Percutaneous techniques are preferredwhen an abscess can be completely drained, and debridement and repair of the

    anatomic structures are not needed. Factors that may prevent successful sourcecontrol with percutaneous drainage include diffuse peritonitis, lack of localization ofthe infectious process, multiple abscesses, anatomic inaccessibility, or need forsurgical debridement .[4]

    In some instances, success of nonoperative drainage also includes the ability todelay surgery until the acute process and sepsis are resolved and a definitiveprocedure can be performed under elective circumstances.

    Most patients with tertiary peritonitis develop complex abscesses or poorly localizedperitoneal infections that are not amenable to percutaneous drainage. Up to 90% ofpatients 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 presenceof an ongoing enteric leak or fistula formation. With proper indications, most studieshave reported success rates of greater than 80% (range 33-100%) for drainage oflocalized nonloculated abscesses; however, the success rates depend to somedegree on the underlying pathology. In these studies, no significant differences werefound between operative and primary nonoperative management with regard to theoverall 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 drainplacement and/or resection with or without anastomosis is under evaluation . [17]

    Common reasons for failure of primary nonoperative management include entericfistula (eg, anastomotic dehiscence), pancreatic involvement, infected clot, andmultiple or multiloculated abscesses. Procedure-related significant complications arereported 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 withpercutaneous drainage was successful in most patients. Patients with Crohn disease

    whose abscesses were drained percutaneously had significantly fewer associatedfistulae. Failure in these patients was related to preexisting fistulization andextensive stricture formation.

    Concerns regarding the transgression of small or large bowel with drainagecatheters in deep abscesses or ileus have been addressed in animal studies, whichhave found no increase in abscess formation, independent of whether cathetersremained for 5 days or longer. Similar data are not available for human patients.

    In summary, percutaneous and surgical drainage should not be consideredcompetitive but rather complementary. If an abscess is accessible to percutaneousdrainage and the underlying visceral organ pathology does not clearly require anoperative approach, percutaneous drainage can be used safely and effectively asthe primary treatment modality. In these cases, patients must be closely monitored,

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    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 therapeuticstrategy 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 earlyin the course of treatment because most patients have an insufficient enteral intakefor a variable amount of time preoperatively. The existing data support that enteralnutrition is superior to parenteral hyperalimentation. Enteral nutrition has been foundto have fewer complications in patients who are severely ill. If enteral feeding iscontraindicated or not tolerated, parenteral nutrition should be instituted.

    Nutritional demands increase during sepsis, with caloric requirements of 25-35kcal/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]

    ConsultationsThe treatment of intra-abdominal sepsis requires a multidisciplinary approach. In thetreatment of secondary peritonitis, a surgeon must be consulted. Interventionalradiology may need to be consulted if ultrasound or CT-guided drainage of anabscess is being considered.

    Other consultations may include the following:

    Gastroenterology Infectious disease Critical care Diet/nutrition

    ComplicationsComplications of peritonitis include tertiary peritonitis, infection or dehiscence of thesurgical site, enterocutaneous fistula, abdominal compartment syndrome, andenteric 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. Abdominalcompartment syndrome is a well-recognized disease entity related to acutelyincreased 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 toenteric insufficiency because of short gut, pancreatic insufficiency, or hepaticdysfunction.

    Long-term MonitoringDepending on the type of perforation causing secondary peritonitis, patients mayrequire further surgical care or repeat abscess drainage by interventional radiology.Follow-up care depends on the cause of the intra-abdominal sepsis. In simpleinfections, such as those caused by cholecystitis or appendicitis, once the infection iscleared, no follow-up care is necessary. However, in patients with perforated

    duodenal ulcer, chronic pancreatitis, or Crohn disease, lifelong follow-up care isneeded.

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    Repeat paracentesis is not required in SBP if the patient has advanced cirrhosis withsigns and symptoms of infection, a positive bacterial isolate with monomicrobialtypical 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 notrequired, a repeat peritoneal fluid analysis is recommended to verify decliningpolymorphonuclear 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-abdominalabscess. 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 directedmostly by specifics of the underlying disease process and the presence or absenceof chronic complications (eg, enterocutaneous fistulae). Patients with simpleperitoneal infections after appendicitis or cholecystitis are usually cured and do notrequire long-term follow-up care. Patients with peritoneal operations for perforatedpeptic ulcer disease, Crohn disease, pancreatitis, and others often require lifelongmedical therapy and treatment of recurrent complications.

    Further inpatient care

    Further care of the hospitalized patient is dependent on the etiology of the peritonitisand 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 ofperitonitis, diverticulitis is probably the entity most frequently treated in an outpatientsetting. A recent review outlines both inpatient and outpatient therapy . [20]

    ProphylaxisOutpatient prophylaxis, although not routinely recommended, has been shown toprevent 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 withfluoroquinolones, often norfloxacin, has led to selective intestinal decontamination

    and high-level fluoroquinolone resistance. This has been supported by published

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    data that show a higher predominance of gram-positive pathogens in ascitic fluidcultures than previously reported .[21]

    Deterrence and prevention

    The prevention of peritonitis centers on causes that are acquired, most of whichinvolve longstanding behaviors that despite all best efforts, remain uncontrolled.Diverticula develop in the Western population with increasing age at a prevalence of80% in the eighth decade of life. Although increasing fiber and fluid intake has beenpromoted, the evidence to support this regimen is inadequate .[22] In cirrhotic patientswith ascites, similar results of unclear efficacy of prophylaxis haunt effectiveprevention .[23]

    Medication SummaryThe goals of pharmacotherapy in patients with peritonitis and abdominal sepsis areto reduce morbidity and prevent complications. The agents used are antimicrobialssuch as cefotaxime, gentamicin, ampicillin, and sulfamethoxazole.

    Empiric antimicrobial therapy must be comprehensive and should cover all likelypathogens in the context of the clinical setting. Traditionally, a combination of anaminoglycoside and ampicillin was used to treat SBP. This regimen affords excellentempiric coverage of more than 90% of SBP cases caused by gram-negative aerobesor gram-positive cocci. More recently, the third-generation cephalosporin cefotaximehas been demonstrated to be as effective as the ampicillin/aminoglycosidecombination, and it does not carry the increased risk of nephrotoxicity in cirrhoticpatients. Cefotaxime does not cover enterococci, which are the pathogen in up to 5%of cases.

    CephalosporinsClass Summary

    Cephalosporins are structurally and pharmacologically related to penicillins. Theyinhibit bacterial cell wall synthesis, resulting in bactericidal activity. Cephalosporinsare divided into first, second, third, and fourth generation. First-generationcephalosporins have greater activity against gram-positive bacteria, and succeedinggenerations have increased activity against gram-negative bacteria and decreasedactivity against gram-positive bacteria.

    Cefotaxime (Claforan)

    Cefotaxime is a third-generation cephalosporin with a broad gram-negativespectrum, lower efficacy against gram-positive organisms, and higher efficacyagainst resistant organisms. Thus, it provides excellent empiric coverage of SBP.

    Cefuroxime (Ceftin, Kefurox, Zinacef)

    Second-generation cephalosporin; maintains gram-positive activity of first-generationcephalosporins; adds activity against P mirabilis , H influenzae , E coli ,K pneumoniae ,and M catarrhalis .

    http://reference.medscape.com/drug/claforan-cefotaxime-342506http://reference.medscape.com/drug/claforan-cefotaxime-342506http://reference.medscape.com/drug/ceftin-zinacef-cefuroxime-342500http://reference.medscape.com/drug/ceftin-zinacef-cefuroxime-342500http://reference.medscape.com/drug/ceftin-zinacef-cefuroxime-342500http://reference.medscape.com/drug/claforan-cefotaxime-342506
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    Binds to penicillin binding proteins and inhibits final transpeptidation step ofpeptidoglycan synthesis, resulting in cell wall death. Condition of patient, severity ofinfection, and susceptibility of microorganism determines proper dose and route ofadministration. Resists degradation by beta-lactamase.

    Ceftriaxone (Rocephin)

    Ceftriaxone is a third-generation cephalosporin with broad-spectrum, gram-negativeactivity; lower efficacy against gram-positive organisms; and higher efficacy againstresistant organisms. Its bactericidal activity results from inhibiting cell wall synthesisby binding to one or more penicillin-binding proteins. It exerts an antimicrobial effectby interfering with synthesis of peptidoglycan, a major structural component ofbacterial cell walls. Bacteria eventually lyse due to the ongoing activity of cell wallautolytic enzymes while cell wall assembly is arrested.

    Ceftriaxone is highly stable in the presence of beta-lactamases, both penicillinaseand cephalosporinase, of gram-negative and gram-positive bacteria. Approximately33-67% of the dose is excreted unchanged in the urine; the remainder is secreted inbile and ultimately in feces as microbiologically inactive compounds. Ceftriaxonereversibly 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 300mcg/mL.

    Cefotetan

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

    Cefepime

    Cefepime is a fourth-generation cephalosporin. Gram-negative coverage comparableto ceftazidime but has better gram-positive coverage (comparable to ceftriaxone).Cefepime is a zwitter ion; rapidly penetrates gram-negative cells. Best beta-lactamfor IM administration.

    AminoglycosidesClass Summary

    Aminoglycosides are bactericidal antibiotics used primarily to treat gram-negativeinfections. They interfere with bacterial protein synthesis by binding to 30S and 50Sribosomal subunits.

    Gentamicin (Gentacidin, Garamycin)

    http://reference.medscape.com/drug/rocephin-ceftriaxone-342510http://reference.medscape.com/drug/rocephin-ceftriaxone-342510http://reference.medscape.com/drug/cefotetan-342496http://reference.medscape.com/drug/cefotetan-342496http://reference.medscape.com/drug/maxipime-cefepime-342511http://reference.medscape.com/drug/maxipime-cefepime-342511http://reference.medscape.com/drug/gentak-garamycin-gentamicin-342517http://reference.medscape.com/drug/gentak-garamycin-gentamicin-342517http://reference.medscape.com/drug/gentak-garamycin-gentamicin-342517http://reference.medscape.com/drug/maxipime-cefepime-342511http://reference.medscape.com/drug/cefotetan-342496http://reference.medscape.com/drug/rocephin-ceftriaxone-342510
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    Gentamicin is an aminoglycoside antibiotic effective against Pseudomonasaeruginosa; E coli; and Proteus, Klebsiella, and Staphylococcus species. Gentamicinis also variably effective against some strains of certain gram-positive organisms,including S aureus, enterococci, and L monocytogenes. Dosing regimens arenumerous; adjust the dose based on creatinine clearance and changes in volume of

    distribution. Gentamicin may be given IV/IM. Gentamicin has been reported to offeradditive or synergistic activity against enterococci when used with ampicillin.

    PenicillinsClass Summary

    The penicillins are bactericidal antibiotics that work against sensitive organisms atadequate concentrations and inhibit the biosynthesis of cell wall mucopeptide.

    Piperacillin and Tazobactam sodium (Zosyn)

    Piperacillin is a semisynthetic extended-spectrum penicillin that inhibits bacterial cellwall synthesis by binding to specific penicillin-binding proteins; it is the most effectiveof 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, itdoes not increase anti P aeruginosa activity.

    Amoxicillin and clavulanate (Augmentin)

    Amoxicillin inhibits bacterial cell wall synthesis by binding to penicillin-bindingproteins; clavulanate inhibits beta-lactamase producing bacteria. This combination isa 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 oraldosage form is 1-1.3 hours. It has good tissue penetration but does not entercerebrospinal fluid.

    Ticarcillin and clavulanate potassium (Ticar)

    This combination of an antipseudomonal penicillin with a beta-lactamase inhibitorprovides coverage against most gram-positive and gram-negative organisms, as wellas most anaerobes. It inhibits biosynthesis of cell wall mucopeptide and is effectiveduring 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 maybe necessary in renal failure. Rash should be evaluated carefully to differentiatenonallergic ampicillin rash from hypersensitivity reaction.

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    MacrolidesClass Summary

    Macrolide antibiotics have bacteriostatic activity and exert their antibacterial actionby binding to the 50S ribosomal subunit of susceptible organisms, resulting in

    inhibition of protein synthesisTobramycin (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 orpotentially less-toxic drugs are contraindicated and when bacterial susceptibility andclinical judgment justifies its use. Like other aminoglycosides, tobramycin isassociated with nephrotoxicity and ototoxicity.

    Clindamycin (Cleocin)

    Clindamycin is a semisynthetic antibiotic produced by 7(S)-chloro-substitution of7(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 bodywithout penetration of the CNS. Clindamycin is protein bound and excreted by theliver and kidneys.

    CarbapenemsClass Summary

    Carbapenems are structurally related to penicillins and have broad-spectrumbactericidal activity. The carbapenems exert their effect by inhibiting cell wallsynthesis, 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 andstreptococci.

    Aztreonam (Azactam)

    Aztreonam is a monobactam, not a beta-lactam, antibiotic that inhibits cell wallsynthesis during bacterial growth. It is active against gram-negative bacilli but hasvery limited gram-positive activity and is not useful for anaerobes. Aztreonam lackscross-sensitivity with beta-lactam antibiotics. It may be used in patients allergic to

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    penicillins or cephalosporins. Transient or persistent renal insufficiency may prolongserum levels.

    Ertapenem (Invanz)

    The bactericidal activity of ertapenem results from inhibition of cell wall synthesis andis mediated through binding to penicillin-binding proteins. Ertapenem is stableagainst hydrolysis by a variety of beta-lactamases, including penicillinases,cephalosporinases, and extended spectrum beta-lactamases; it is hydrolyzed bymetallo-beta-lactamases.

    Imipenem and cilastatin (Primaxin)

    This combination is used for treatment of infections with multiple organisms becauseother agents do not have wide spectrum coverage or are contraindicated due topotential for toxicity.

    FluoroquinolonesClass Summary

    Fluoroquinolones have broad-spectrum activity against gram-positive and gram-negative aerobic organisms. They inhibit DNA synthesis and growth by inhibitingDNA gyrase and topoisomerase, which is required for replication, transcription, andtranslation of genetic material.

    Ciprofloxacin (Cipro)

    Ciprofloxacin, a fluoroquinolone, inhibits bacterial DNA synthesis and, consequently,growth, by inhibiting DNA gyrase and topoisomerase, which is required forreplication, transcription, and translation of genetic material. Quinolones have broadactivity against gram-positive and gram-negative aerobic organisms. It has noactivity against anaerobes. Continue treatment for at least 2 days (7-14 d typical)after signs and symptoms have disappeared. In prolonged therapy, perform periodicevaluations of organ system functions (eg, renal, hepatic, hematopoietic); adjust thedose in the presence of renal function impairment. Superinfections may occur withprolonged 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 activityagainst anaerobes. It inhibits bacterial DNA synthesis and, consequently, growth.

    Anti-Infectives

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    Class Summary

    Anti-infectives such as metronidazole and sulfamethoxazole/trimethoprim areeffective against some types of bacteria that have become resistant to otherantibiotics.

    Sulfamethoxazole and trimethoprim (Bactrim, Bactrim DS, Cotrim, Cotrim DS,Septra, Septra DS)

    Trimethoprim-sulfamethoxazole inhibits bacterial growth by inhibiting the synthesis ofdihydrofolic acid. Its antibacterial activity includes common urinary tract pathogens,except Pseudomonas aeruginosa.

    Metronidazole (Flagyl)

    Metronidazole is an imidazole ring-based antibiotic active against various anaerobicbacteria and protozoa. It is used in combination with other antimicrobial agents (butis used as monotherapy in C difficile enterocolitis).

    Glycylcycline AntibioticClass Summary

    Glycylcycline antibiotics are structurally similar to tetracycline antibiotics and weredeveloped to overcome bacterial mechanisms of tetracycline resistance. Tigecyclineis the first drug approved in this class.

    Tigecycline (Tygacil)

    Tigecycline is a glycylcycline antibiotic that is structurally similar to tetracyclineantibiotics. It is used for complicated intra-abdominal infections caused by C freundii,E cloacae, E coli, K oxytoca, K pneumoniae, E faecalis (vancomycin-susceptibleisolates 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 withcaution in patients with severe hepatic impairment.

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