Peritonitis and Abdominal Sepsis
Author: Brian J Daley, MD, MBA, FACS, FCCP, CNSC; Chief Editor: Praveen K Roy, MD, AGAF
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.
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/μ 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.
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.
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.
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.
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
Spontaneous bacterial peritonitis (SBP) is an acute bacterial infection of ascitic fluid. Contamination of the peritoneal cavity is thought to result from translocation of bacteria across the gut wall or mesenteric lymphatics and, less frequently, via hematogenous seeding in the presence of bacteremia.
SBP can occur as a complication of any disease state that produces the clinical syndrome of ascites, such as heart failure and Budd-Chiari syndrome. Children with nephrosis or systemic lupus erythematosus who have ascites have a high risk of developing SBP. The highest risk of SBP, however is in patients with cirrhosis who are in a decompensated state.[4] In particular, decreased hepatic synthetic function with associated low total protein level, low complement levels, or prolonged prothrombin time (PT) is associated with maximum risk. Patients with low protein levels in ascitic fluid (< 1 g/dL) have a 10-fold higher risk of developing SBP than those with a protein level greater than 1 g/dL. Approximately 10-30% of patients with cirrhosis and ascites develop SBP.[5] The incidence rises to more than 40% with ascitic fluid protein contents of less than 1 g/dL (which occurs 15% of patients), presumably because of decreased ascitic fluid opsonic activity.
More than 90% of cases of SBP are caused by a monomicrobial infection. The most common pathogens include gram-negative organisms (eg, E coli [40%], K pneumoniae [7%], Pseudomonas species, Proteus species, other gram-negative species [20%]) and gram-positive organisms (eg, Streptococcus pneumoniae [15%], other Streptococcus species [15%], and Staphylococcus species [3%]) (see Table 1). However, some data suggest that the percentage of gram-positive infections may be increasing.[6, 7] One study cites a 34.2% incidence of streptococci, ranking in second position after Enterobacteriaceae.[7] 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%.
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
Boerhaave syndrome
Malignancy
Trauma (mostly penetrating)
Iatrogenic*
Peptic ulcer perforation
Malignancy (eg, adenocarcinoma, lymphoma, gastrointestinal stromal tumor)
Trauma (blunt and penetrating)
Cholecystitis
Stone perforation from gallbladder (ie, gallstone ileus) or common duct
Choledochal cyst (rare)
Pancreatitis (eg, alcohol, drugs, gallstones)
Ischemic bowel
Incarcerated hernia (internal and external)
Closed loop obstruction
Malignancy (rare)
Meckel diverticulum
Large bowel and appendix
Ulcerative colitis and Crohn disease
Colonic volvulus
Iatrogenic
Uterus, salpinx, and ovaries
Pelvic inflammatory disease (eg, salpingo-oophoritis, tubo-ovarian abscess, ovarian cyst)
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)
Gram negative
Enterobacter/Klebsiella
Gram positive
Staphylococci
Bacteroides
Eubacteria
Clostridia
Peptostreptococci
Peptococci
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 (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/μ 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
Antibiotic Therapy
(Suggested)
Type of Organism
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
Enterobacter species
Klebsiella species
Proteus species
Second-generation cephalosporin
Penicillins with anaerobic activity
Quinolones with anaerobic activity
Quinolone and metronidazole
Aminoglycoside and metronidazole
Gram-positive
Streptococcus species
Enterococcus species
Bacteroides fragilis
Other Bacteroides species
Eubacterium species
Clostridium species
Anaerobic Streptococcus species
Pseudomonas species
Carbapenems
Triazoles or amphotericin (considered in fungal etiology)
(Alter therapy based on culture results.)
Staphylococcus species
Candida species
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]
Peritonealabscess
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.
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.
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, trimethoprim-sulfamethoxazole); however, whether this improves long-term survival without liver transplantation is unclear.
Secondary peritonitis and peritoneal abscess
Uncomplicated SP and simple abscesses carry a mortality rate of less than 5%, but this rate may increase to greater than 30-50% in severe infections. The overall mortality rate related to intra-abdominal abscess formation is less than 10-20%. Factors that independently predict worse outcomes include advanced age, malnutrition, presence of cancer, a high APACHE II score on presentation, preoperative organ dysfunction, the presence of complex abscesses, and failure to improve in less than 24-72 hours after adequate therapy.
In severe intra-abdominal infections and peritonitis, the mortality rate may increase to greater than 30-50%. The concurrent development of sepsis, SIRS, and MOF can increase the mortality rate to greater than 70%, and, in these patients, more than 80% of deaths occur with an active infection present.
Soriano et al found that cirrhotic patients with SP who underwent surgical treatment tended to have a lower mortality rate than did those who received medical therapy only (53.8% vs 81.8%, respectively).[12] Among the surgically treated patients with SP, the survival rate was greater in those with the shortest time between diagnostic paracentesis and surgery. These researchers concluded that the prognosis of cirrhotic patients with SP could be improved via a low threshold of suspicion on the basis of Runyon's criteria and microbiologic data, prompt use of abdominal CT scanning, and early surgical evaluation.
In comparison with patients with other forms of peritonitis, patients who develop tertiary peritonitis have significantly longer ICU and hospital stays, higher organ dysfunction scores, and higher mortality rates (50-70%).
Other factors affecting prognosis
Several scoring systems (eg, APACHE II, SIRS, multiple organ dysfunction syndrome [MODS], Mannheim peritonitis index) have been developed to assess the clinical prognosis of patients with peritonitis. Most of these scores rely on certain host criteria, systemic signs of sepsis, and complications related to organ failure. Although valuable for comparing patient cohorts and institutions, these scores have limited value in the specific day-to-day clinical decision-making process for any given patient. In general, the mortality rate is less than 5% with an APACHE II of less than 15 and rises to greater than 40% with scores above 15. Rising APACHE II scores on days 3 and 7 are associated with an increase of mortality rates to greater than 90%, whereas falling scores predict mortality rates of less than 20%.
The mortality rate without organ failure generally is less than 5% but may rise to greater than 90% with quadruple organ failure. A delay of more than 2-4 days in instituting either medical therapy or surgical therapy has been clearly associated with increased complication rates, the development of tertiary peritonitis, the need for reoperation, multiple organ system dysfunction, and death.
Outcomes are worse in patients requiring emergent reoperations for persistent or recurrent infections (30-50% increase in the mortality rate); however, patients undergoing early planned second-look operations do not demonstrate this trend.
Persistent infection, recovery of enterococci, and multidrug-resistant gram-negative organisms, as well as fungal infection, are related to worse outcomes and recurrent complications.
Patients older than 65 years have a threefold increased risk of developing generalized peritonitis and sepsis from gangrenous or perforated appendicitis and perforated diverticulitis than younger patients and are 3 times more likely to die from these disease processes. Older patients with perforated diverticulitis are 3 times more likely than younger patients to have generalized rather than localized (ie, pericolic, pelvic) peritonitis. These findings are consistent with the hypothesis that the biologic features of peritonitis differ in elderly persons, who are more likely to present with an advanced or more severe process than younger patients with peritonitis.
Overall, studies suggest that host-related factors are more significant than the type and source of infection with regard to the prognosis in intra-abdominal infections.[13]
For patient education resources, Digestive Disorders Center as well as Abdominal Pain in Adults, Appendicitis, Diverticulosis and Diverticulitis, Cirrhosis, and Sepsis (Blood Infection).
The diagnosis of peritonitis is usually clinical. History should include recent abdominal surgery, previous episodes of peritonitis, travel history, use of immunosuppressive agents, and the presence of diseases (eg, inflammatory bowel disease, diverticulitis, peptic ulcer disease) that may predispose to intra-abdominal infections.
A broad range of signs and symptoms are seen in spontaneous bacterial peritonitis (SBP). A high index of suspicion must be maintained when caring for patients with ascites, particularly those with acute clinical deterioration. As many as 30% of patients are completely asymptomatic. Manifestations of SBP may include the following:
Fever and chills (as many as 80% of patients)
Abdominal pain or discomfort (found in as many as 70% of patients)
Worsening or unexplained encephalopathy
Ascites that does not improve following administration of diuretic medication
Worsening or new-onset renal failure
Abdominal pain, which may be acute or insidious, is the usual chief complaint of patients with peritonitis. Initially, the pain may be dull and poorly localized (visceral peritoneum); often, it progresses to steady, severe, and more localized pain (parietal peritoneum). Abdominal pain may be exacerbated by any movement (eg, coughing, flexing the hips) and local pressure. If the underlying process is not contained, the pain becomes diffuse. In certain disease entities (eg, gastric perforation, severe acute pancreatitis, intestinal ischemia), the abdominal pain may be generalized from the beginning.
Abdominal distention may be noted, as well as signs of dysfunction of other organs. Symptoms may be subtle in patients on corticosteroids, in diabetic patients with advanced neuropathy, and in hospitalized patients, especially the very young and the very old. In the presence of ascites, decreased friction between the visceral and parietal peritoneal surfaces may reduce the symptoms of abdominal pain, as seen in patients with SBP.
Anorexia and nausea are frequent symptoms and may precede the development of abdominal pain. Vomiting may be due to underlying visceral organ pathology (ie, obstruction) or be secondary to peritoneal irritation.
On physical examination, patients with peritonitis generally appear unwell and in acute distress. Many of them have a temperature that exceeds 38° C, although patients with severe sepsis may become hypothermic. Tachycardia may be present, as a result of the release of inflammatory mediators, intravascular hypovolemia from anorexia, vomiting and fever, and third-space losses into the peritoneal cavity. With progressive dehydration, patients may become hypotensive (5-14% of patients), as well as oliguric or anuric; with severe peritonitis, they may present in overt septic shock.
When examining the abdomen of a patient with suspected peritonitis, the patient should be supine. A roll or pillows underneath the patient's knees may allow for better relaxation of the abdominal wall.
On abdominal examination, almost all patients demonstrate tenderness to palpation. In most patients—even those with generalized peritonitis and severe diffuse abdominal pain—the point of maximal tenderness or referred rebound tenderness roughly overlies the pathologic process (ie, the site of maximal peritoneal irritation).
Most patients demonstrate increased abdominal wall rigidity. The increase in abdominal wall muscular tone may be voluntary, in response to or in anticipation of the abdominal examination, or involuntary because of the peritoneal irritation. Patients with severe peritonitis often avoid all motion and keep their hips flexed to relieve the abdominal wall tension. The abdomen is often distended, with hypoactive-to-absent bowel sounds. This finding reflects a generalized ileus and may not be present if the infection is well localized. Occasionally, the abdominal examination reveals an inflammatory mass.
Signs of hepatic failure (eg, jaundice, angiomata) may be noted.
Rectal examination often elicits increased abdominal pain, particularly with inflammation of the pelvic organs, but rarely indicates a specific diagnosis. A tender inflammatory mass toward the right may indicate appendicitis, and anterior fullness and fluctuation may indicate a cul de sac abscess.
In female patients, vaginal and bimanual examination findings may be consistent with pelvic inflammatory disease (eg, endometritis, salpingo-oophoritis, tubo-ovarian abscess), but exam findings are often difficult to interpret in severe peritonitis.
A complete physical examination is important for excluding conditions whose presentation may resemble that of peritonitis. Thoracic processes with diaphragmatic irritation (eg, empyema), extraperitoneal processes (eg, pyelonephritis, cystitis, acute urinary retention), and abdominal wall processes (eg, infection, rectus hematoma) may mimic certain signs and symptoms of peritonitis. Always examine the patient for the presence of external hernias to rule out intestinal incarceration.
Remember that the presentation and the findings on clinical examination may be entirely inconclusive or unreliable in patients with significant immunosuppression (eg, severe diabetes, steroid use, posttransplant status, HIV infection), in patients with altered mental state (eg, head injury, toxic encephalopathy, septic shock, analgesic agents), in patients with paraplegia, and in patients of advanced age. With localized deep peritoneal infections, fever and/or an elevated WBC count may be the only signs present. As many as 20% of patients with SBP demonstrate very subtle signs and symptoms. New onset or deterioration of existing encephalopathy may be the only sign of the infection at the initial presentation. Most patients with tuberculous peritonitis demonstrate vague symptoms and may be afebrile.
Thoracic processes with diaphragmatic irritation (eg, empyema), extraperitoneal processes (eg, pyelonephritis, cystitis, acute urinary retention), and abdominal wall processes (eg, infection, rectus hematoma) may mimic certain signs and symptoms of peritonitis. Always examine the patient for the presence of external hernias to rule out intestinal incarceration.
According to Adler and Gasbarra, the following should be considered in the differential diagnosis[8] :
Chemical irritants (eg, bile, blood, gastric juice, barium, enema or douche contents)
Chronic peritoneal dialysis
Chylous peritonitis
Eosinophilic peritonitis
Familial Mediterranean fever
Fungal infections (eg, histoplasmosis, cryptococcosis, coccidioidomycosis)
Granulomatous peritonitis (eg, parasitic infestations, sarcoidosis, tumors, Crohn disease, starch granules)
Gynecologic disorders (Chlamydia peritonitis, salpingitis, endometriosis, teratoma, leiomyomatosis, dermoid cyst)
HIV-associated peritonitis (from opportunistic organisms)
Mesothelial hyperplasia and metaplasia
Neoplasms (eg, primary mesothelioma, secondary carcinomatosis, Pseudomyxoma peritonei)
Parasitic infections (eg, schistosomiasis, ascariasis, enterobiasis, amebiasis, strongyloidiasis)
Perforated viscus
Peritoneal encapsulation
Peritoneal loose bodies and peritoneal cysts
Peritoneal lymphangiectasis
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-Schönlein purpura], Kohlmeier-Degos disease, polyarteritis nodosa)
Acute Angioedema
Urinary Tract Infection (UTI) and Cystitis (Bladder Infection) in Females
Whipple Disease
Diagnostic paracentesis should be performed in all patients who do not have an indwelling peritoneal catheter and are suspected of having SBP. In peritoneal dialysis patients with a peritoneal catheter, fluid should be withdrawn using sterile technique. Ultrasonography may aid paracentesis if ascites is minimally detectable or questionable.
The results of aerobic and anaerobic bacterial cultures, used in conjunction with the cell count, prove the most useful in guiding therapy for those with SBP.[14] With regard to ascitic fluid culture, direct inoculation of routine blood culture bottles at the bedside with 10 mL of ascitic fluid has been reported to significantly increase the sensitivity of microbiologic studies.
The diagnostic and therapeutic approach to peritonitis and peritoneal abscess is summarized in the algorithm below.
Diagnostic and therapeutic approach to peritonitis and peritoneal abscess.
CBC Count and Other Blood Studies
Most patients will have leukocytosis (>11,000 cells/μ L), with a shift to the immature forms on the differential cell count. Patients who have severe sepsis, are immunocompromised, or have certain types of infections (eg, fungal, cytomegaloviral) may not have leukocytosis or leukopenia. In cases of suspected SBP, hypersplenism may reduce the polymorphonuclear leukocyte count.
Blood chemistry findings may reveal dehydration and acidosis. PT, PTT, and INR are indicated. Liver function tests may be indicated. Amylase and lipase levels should be obtained if pancreatitis is suspected. Blood culture results are positive for the offending agent in as many as 33% of patients with SBP and may help guide antibiotic therapy. Measurement of serum albumin allows calculation of the serum-to-ascites albumin gradient (SAAG). A SAAG of more than 1.1 is noted in SBP.
This is used to rule out urinary tract diseases (eg, pyelonephritis, renal stone disease); however, patients with lower abdominal and pelvic infections often demonstrate WBCs in the urine and microhematuria.
Stool Sample
In patients with diarrhea, evaluate a stool sample—employing a Clostridium difficile toxin assay, a WBC count, and a specific culture (ie, Salmonella, Shigella, cytomegalovirus [CMV])—if the patient's history suggests infectious enterocolitis.
Peritoneal Fluid Analysis
The single best predictor of SBP is an ascitic fluid neutrophil count of greater than 500 cells/µL, which carries a sensitivity of 86% and a specificity of 98%. By lowering the ascitic fluid neutrophil count threshold to 250 cells/μ L, the sensitivity increases to 93% with only a minimal decrease in specificity to 94%.
The fluid should be evaluated for glucose, protein, lactate dehydrogenase (LDH), cell count, Gram stain, and aerobic and anaerobic cultures. If pancreatitis or a pancreatic leak is suspected, amylase analysis should be added to the panel. Bilirubin and creatinine levels can be analyzed as well, if a biliary or urinary leak is suspected as a possible etiology. The peritoneal/ascitic fluid characteristics or levels are then compared with their respective serum values.
The fluid in bacterial peritonitis generally demonstrates a low pH and low glucose levels with elevated protein and LDH levels. Traditionally, ascitic fluid pH of less that 7.34 was consistent with a diagnosis of SBP; however, ascitic pH is less commonly measured because it is unreliable and lacks specificity for the condition.
The diagnosis of SBP is established when the polymorphonuclear neutrophil (PMN) count is 250 cells/µL or greater in conjunction with a positive bacterial culture result. In most of these cases, as mentioned previously, cultures are positive for a single organism. Obviously, these patients should receive antibiotic therapy. Although up to 30% of cultures remain negative, most of these patients are presumed to have bacterial peritonitis; they should be treated. A significantly decreased peritoneal fluid glucose level (< 50 mg/dL), a peritoneal fluid LDH level much greater than the serum LDH, a peritoneal fluid WBC count greater than 10,000 cells/µL, a pH lower than 7.0, high amylase levels, multiple organisms on Gram stain, or recovery of anaerobes from the culture raises the suspicion of SP in these patients. Some authors recommend repeating the paracentesis in 48-72 hours to monitor treatment success (decrease in neutrophil count to < 50% of the original value).
Culture-negative neutrocytic ascites (probable SBP) is established when the ascitic fluid culture results are negative but the PMN count is 250 cells/µL or greater. This may happen in as many as 50% of patients with SBP and may not actually represent a distinctly different disease entity. Rather, it may be the result of poor culturing techniques or late-stage resolving infection. Nonetheless, these patients should be treated just as aggressively as those with positive culture results.
Monomicrobial nonneutrocytic bacterascites exists when a positive culture result coexists with a PMN count of less than 250 cells/µL. Although this may often be the result of contamination of bacterial cultures, 38% of these patients develop SBP. Therefore, monomicrobial nonneutrocytic bacterascites may represent an early form of SBP. All study patients described who eventually developed SBP were symptomatic. For this reason, any patient suspected clinically of having SBP in this setting must be treated.
Tuberculous peritonitis (TP) is identified by ascites with high protein content, a low glucose and low SAAG, elevated ascitic fluid WBC count, and lymphocyte predominance. In TP, the fluid Gram stain and acid-fast stain results are rarely positive, and routine culture results are falsely negative in as many as 80% of cases. A peritoneal fluid protein level greater than 2.5 g/dL, LDH level greater than 90 U/mL, and predominantly mononuclear cell count of more than 500 cells/µL should raise the suspicion of TP, but specificity for the diagnosis is limited. Laparoscopy with visualization of granulomas on peritoneal biopsy and specific culture (which requires 4-6 wk) may be needed for definitive diagnosis.
Peritonitis in patients receiving continuous ambulatory peritoneal dialysis (CAPD) is indicated by contamination of the dialysis catheter; cloudy effluent, total fluid WBC count of greater than 100 neutrophils/µL, or presence of organisms on Gram stain.
Routine intraoperative peritoneal fluid cultures in defined acute disease entities (ie, gastric or duodenal ulcer perforation, appendicitis, diverticulitis or perforation of the colon caused by obstruction or ischemia) are controversial. Several studies found no significant difference in patients with appendicitis, diverticulitis, and other common etiologies for bacterial peritonitis with regard to postoperative complication rates or overall outcomes. The antibiotic regimen was altered only 8-10% of the time based on operative culture data. In patients who had previous abdominal operations or instrumentation (eg, peritoneal dialysis catheter, percutaneous stents) and patients with prolonged antibiotic therapy, critical illness, and/or hospitalization, these cultures may reveal resistant or unusual organisms that should prompt alteration of the antibiotic strategy.
For a summary of ascitic fluid analysis, see Table 4, below.
Table 4. Ascitic Fluid Analysis Summary [4] (Open Table in a new window)
Less Helpful
Cell count
Obtain culture in blood culture (BC) bottles.
Tuberculosis (TB) smear and culture
Cytology
Total protein
Lactate dehydrogenase (LDH)
Gram stain
Alpha 1-antitrypsin
Glycosaminoglycans
Bedside Reagent Strips
An exciting new development in the rapid diagnosis of SBP is the proposed use of bedside reagent strips read by a portable spectrophotometric device. In a pilot study, this combination achieved a 100% sensitivity in diagnosis of spontaneous bacterial peritonitis.[15]
This diagnostic method holds promise in replacing the time-consuming process of manual cell counting, which is often unavailable in many laboratories "after hours". The decreased time to diagnosis may result in a significant reduction of the time from paracentesis to antibiotic treatment of presumptive SBP.
In a small cohort, the average time saved from dipstick to laboratory results ranged from 2.73 hours (dipstick to validated result from automated counter) to 3 hours (dipstick to validated manual cell count of ascitic fluid). Although promising, this diagnostic method has not been investigated in a large-scale study.
Plain films of the abdomen (eg, supine, upright, and lateral decubitus positions) are often the first imaging studies obtained in patients presenting with peritonitis. Their value in reaching a specific diagnosis is limited.
Free air is present in most cases of anterior gastric and duodenal perforation but is much less frequent with perforations of the small bowel and colon and is unusual with appendiceal perforation. Upright films are useful for identifying free air under the diaphragm (most often on the right) as an indication of a perforated viscus. Remember that the presence of free air is not mandatory with visceral perforation and that small amounts of free air are missed easily on plain films.
Abdominal ultrasonography may be helpful in the evaluation of pathology in the right upper quadrant (eg, perihepatic abscess, cholecystitis, biloma, pancreatitis, pancreatic pseudocyst), right lower quadrant, and pelvis (eg, appendicitis, tubo-ovarian abscess, Douglas pouch abscess). However, the examination is sometimes limited because of patient discomfort, abdominal distention, and bowel gas interference.
Ultrasonography may detect increased amounts of peritoneal fluid (ascites), but its ability to detect quantities of less than 100 mL is limited. The central (perimesenteric) peritoneal cavity is not visualized well with transabdominal ultrasonography. Examination from the flank or back may improve the diagnostic yield, and providing the ultrasonographer with specific information about the patient's condition and the suspected diagnosis before the examination is important. With an experienced ultrasonographer, a diagnostic accuracy of greater than 85% has been reported in several series.
Ultrasonographically guided aspiration and placement of drains has evolved into a valuable tool in the diagnosis and treatment of abdominal fluid collections.
Advantages of ultrasound include low cost, portability, and availability. Disadvantages are that the test is operator dependent, and there is reduced visualization in the presence of overlying bowel gas and abdominal dressings.
If the diagnosis of peritonitis is made clinically, a CT scan is not necessary and generally delays surgical intervention without offering clinical advantage. However, CT scanning is indicated in all cases in which the diagnosis cannot be established on clinical grounds and the findings on abdominal plain films. CT scans of the abdomen and pelvis remain the diagnostic study of choice for peritoneal abscess and related visceral pathology.
Whenever possible, the CT scan should be performed with enteral and intravenous contrast. CT scans can detect small quantities of fluid, areas of inflammation, and other GI tract pathology, with sensitivities that approach 100%. (See the image below.) CT scanning can be used to evaluate for ischemia, as well as to determine bowel obstruction. An abscess is suggested by the presence of fluid density that is not bound by the bowel or other known structures. Gas within an abdominal mass or the presence of an enhancing wall and adjacent inflammatory changes are also highly suggestive of an abscess. Ischemia can be demonstrated by a clot in a large vessel or by the absence of blood flow. Gas within the intestinal wall or in the portal vein may also suggest ischemia.
A 78-year-old man was admitted with a history of prior surgery for small bowel obstruction and worsening abdominal pain, distended abdomen, nausea, and obstipation. In figure A, a marked amount of portal venous gas within the liver, mesenteric venous gas, and pneumatosis intestinalis are consistent with ischemic small intestine. The superior mesenteric artery appears patent. The liver has a nodular contour consistent with cirrhosis. In figures B and C, markedly distended loops of small intestine containing fluid and air-fluid levels are consistent with a small bowel obstruction. No focal fluid collections are identified.
In abscess formation subsequent to secondary peritonitis (SP), approximately half of patients have a simple abscess without loculation, and the other half have complex abscesses secondary to fibrinous septation and organization of the abscess material. Abscess formation occurs most frequently in the subhepatic area, the pelvis, and the paracolic gutters, but it may also occur in the perisplenic area, the lesser sac, and between small bowel loops and their mesentery.
Peritoneal abscesses and other fluid collections may be aspirated for diagnosis and drained under CT guidance; this technique has become a mainstay of therapy.
Nuclear Scanning
These diagnostic studies have little use in the initial evaluation of patients with suspected peritonitis or intra-abdominal sepsis. They are most frequently used in the evaluation of fever of unknown origin or in patients with persistent fever despite adequate antibiotic treatment and negative CT scan findings.
MRI is an emerging imaging modality for the diagnosis of suspected intra-abdominal abscesses. Abdominal abscesses demonstrate decreased signal intensity on T1-weighted images and homogeneous or heterogeneous increased signal intensity on T2-weighted images; abscesses are observed best on gadolinium-enhanced, T1-weighted, fat-suppressed images as well-defined fluid collections with rim enhancement.
Limited availability and high cost, as well as the need for MRI-compatible patient support equipment and the length of the examination, currently limit its usefulness as a diagnostic tool in acute peritoneal infections, particularly for patients who are critically ill.
Contrast Studies
Conventional contrast studies (ie, Gastrografin swallow, upper GI tract study with follow-through, colorectal contrast enema, fistulogram, contrast studies of drains and stents) are reserved for specific indications in the setting of suspected peritonitis or peritoneal abscess.
The current approach to peritonitis and peritoneal abscesses targets correction of the underlying process, administration of systemic antibiotics, and supportive therapy to prevent or limit secondary complications due to organ system failure. Treatment success is defined as adequate source control with resolution of sepsis and clearance of all residual intra-abdominal infection.
Early control of the septic source is mandatory and can be achieved by operative and nonoperative means.
Operative management addresses the need to control the infectious source and to purge bacteria and toxins. The type and extent of surgery depends on the underlying disease process and the severity of intra-abdominal infection. Definitive interventions to restore functional anatomy involve removing the source of the antimicrobial contamination and repairing the anatomic or functional disorder causing the infection. This is accomplished by surgical intervention. Occasionally, this can be achieved during a single operation; however, in certain situations, a second or a third procedure may be required. In some patients, definitive intervention is delayed until the condition of the patient improves and tissue healing is adequate to allow for a (sometimes) lengthy procedure.
See Surgical Approach to Peritonitis and Abdominal Sepsis for more information.
Nonoperative interventions include percutaneous abscess drainage, as well as percutaneous and endoscopic stent placements. If an abscess is accessible for percutaneous drainage and if the underlying visceral organ pathology does not clearly require operative intervention, percutaneous drainage is a safe and effective initial treatment approach. With percutaneous treatment, the definition of success includes the avoidance of further operative intervention and, in some cases, the delay of surgery until after resolution of the initial sepsis.
The general principles guiding the treatment of infections are 4-fold, as follows[13] :
Control the infectious source
Eliminate bacteria and toxins
Maintain organ system function
Control the inflammatory process
The treatment of peritonitis is multidisciplinary, with complementary application of medical, operative, and nonoperative interventions. Medical support includes the following:
Systemic antibiotic therapy
Intensive care with hemodynamic, pulmonary, and renal support
Nutrition and metabolic support
Inflammatory response modulation therapy
Early control of the septic source is mandatory and can be achieved by operative and nonoperative means. Nonoperative interventional therapies include percutaneous drainage of abscesses and percutaneous and endoscopic stent placements.
Treatment of peritonitis and intra-abdominal sepsis always begins with volume resuscitation, correction of potential electrolyte and coagulation abnormalities, and empiric broad-spectrum parenteral antibiotic coverage.
Hemodynamic Resuscitation
Aggressive fluid resuscitation to treat intravascular fluid depletion should be instituted. Pressor agents are avoided if possible. Fluid administration requires frequent monitoring of blood pressure, pulse, urine output, blood gases, hemoglobin and hematocrit, electrolytes, and renal function.
Antibiotic therapy is used to prevent local and hematogenous spread of infection and to reduce late complications.[16] Several different antibiotic regimens are available for the treatment of intra-abdominal infections.[16] Both single-agent broad-spectrum therapy and combination therapies have been used. However, no specific therapy has been found to be superior to another therapy. Infection of the abdominal cavity requires coverage for gram-positive and gram-negative bacteria, as well as for anaerobes. Antipseudomonal coverage is recommended in patients who have had previous treatment with antibiotics or who have had a prolonged hospitalization.
The optimal duration of antibiotic therapy must be individualized and depends on the underlying pathology, severity of infection, speed and effectiveness of source control, and patient response to therapy. Antibiotics can be discontinued once clinical signs of infection have resolved. Recurrence is a concern with certain infections, such as those from Candida and Staphylococcus aureus, and treatment should be continued for 2-3 weeks.
Nonoperative Drainage
Drainage refers to evacuation of an abscess. This can be performed operatively or percutaneously under ultrasound or CT guidance. If the abscess is localized at the level of the skin and underlying superficial tissues, simple removal of sutures or opening of the wound may be sufficient. Percutaneous techniques are preferred when an abscess can be completely drained, and debridement and repair of the anatomic structures are not needed. Factors that may prevent successful source control with percutaneous drainage include diffuse peritonitis, lack of localization of the infectious process, multiple abscesses, anatomic inaccessibility, or the need for surgical debridement.[4]
In some instances, success of nonoperative drainage also includes the ability to delay surgery until the acute process and sepsis are resolved and a definitive procedure can be performed under elective circumstances.
Most patients with tertiary peritonitis develop complex abscesses or poorly localized peritoneal infections that are not amenable to percutaneous drainage. Up to 90% of patients will require reoperation for additional source control.
For primary percutaneous management of intra-abdominal abscesses, the etiology, location, and morphology of the abscess must be defined; evaluate for the presence of an ongoing enteric leak or fistula formation. With proper indications, most studies have reported success rates of greater than 80% (range 33-100%) for drainage of localized nonloculated abscesses; however, the success rates depend to some degree on the underlying pathology. In these studies, no significant differences were found between operative and primary nonoperative management with regard to the overall morbidity or length of hospital stay (mean duration of drainage 8.5 d).
In the treatment of diverticular disease, the use of laparoscopic drainage and drain placement and/or resection with or without anastomosis continues to be evaluated.[17]
In preliminary results from the Swedish DILALA (DIverticulitis LAparoscopic LAvage) trial, Angenete et al reported that in the short term, laparoscopic lavage may be safe and effective in treating perforated diverticulitis with purulent peritonitis (Hinchey III classification).[18] The investigators found no differences in 12-week morbidity and mortality between 39 patients who underwent laparoscopic lavage and 39 patients who underwent a Hartmann procedure (colon resection and stoma). However, the laparoscopic lavage procedure resulted in decreased operative times and reduced recovery time and hospital stays.[18]
Common reasons for failure of primary nonoperative management include enteric fistula (eg, anastomotic dehiscence), pancreatic involvement, infected clot, and multiple or multiloculated abscesses. Procedure-related significant complications are reported to occur in less than 10% of cases (range 5-27%), with less than a 1% attributable mortality rate with experienced physicians.
In peritoneal abscess formation caused by subacute bowel perforation (eg, diverticulitis, Crohn disease, appendicitis), primary percutaneous management with percutaneous drainage was successful in most patients. Patients with Crohn disease whose abscesses were drained percutaneously had significantly fewer associated fistulae. Failure in these patients was related to preexisting fistulization and extensive stricture formation.
Concerns regarding the transgression of small or large bowel with drainage catheters in deep abscesses or ileus have been addressed in animal studies, which have found no increase in abscess formation, independent of whether catheters remained for 5 days or longer. Similar data are not available in human patients.
In summary, percutaneous and surgical drainage should not be considered competitive but rather complementary. If an abscess is accessible to percutaneous drainage and the underlying visceral organ pathology does not clearly require an operative approach, percutaneous drainage can be used safely and effectively as the primary treatment modality. In these cases, patients must be closely monitored, and improvement should occur in less than 24-48 hours. With lack of improvement, patients must be reevaluated aggressively (eg, repeat CT scan) and the therapeutic strategy should be altered accordingly.
In general, patients with peritonitis develop some degree of gut dysfunction (eg, ileus) after exploration. Consider establishing some form of nutritional support early in the course of treatment because most patients have an insufficient enteral intake for a variable amount of time preoperatively. The existing data support that enteral nutrition is superior to parenteral hyperalimentation. Enteral nutrition has been found to have fewer complications in patients who are severely ill. If enteral feeding is contraindicated or not tolerated, parenteral nutrition should be instituted.
Nutritional demands increase during sepsis, with caloric requirements of 25-35 kcal/kg/d. Patients with sepsis should be fed a high-protein isocaloric diet. Hypercaloric diets cannot prevent the intense protein catabolism associated with sepsis.[19]
The treatment of intra-abdominal sepsis requires a multidisciplinary approach. In the treatment of secondary peritonitis, a surgeon must be consulted. Interventional radiology may need to be consulted if ultrasound or CT-guided drainage of an abscess is being considered.
Other consultations may include the following:
Complications of peritonitis include tertiary peritonitis, infection or dehiscence of the surgical site, enterocutaneous fistula, abdominal compartment syndrome, and enteric insufficiency. Enterocutaneous fistulae can lead to ongoing (potentially large) volume, protein, and electrolyte losses; inability to use the gut for nutritional support; and associated long-term complications of intravenous alimentation. Abdominal compartment syndrome is a well-recognized disease entity related to acutely increased abdominal pressure (ie, intra-abdominal hypertension) and is associated with the development of multiple organ dysfunction. Extensive initial (gastrointestinal) disease, chronic recurrent infections, and associated reoperations may lead to enteric insufficiency because of short gut, pancreatic insufficiency, or hepatic dysfunction.
Depending on the type of perforation causing secondary peritonitis, patients may require further surgical care or repeat abscess drainage by interventional radiology. Follow-up care depends on the cause of the intra-abdominal sepsis. In simple infections, such as those caused by cholecystitis or appendicitis, once the infection is cleared, no follow-up care is necessary. However, in patients with perforated duodenal ulcer, chronic pancreatitis, or Crohn disease, lifelong follow-up care is needed.
Repeat paracentesis is not required in SBP if the patient has advanced cirrhosis with signs and symptoms of infection, a positive bacterial isolate with monomicrobial typical organism, and a good response to treatment.[20] If the course is atypical, repeat paracentesis should be performed in 48 hours.
For SBP, a 10-day to 14-day course of antibiotics is recommended. Although not required, a repeat peritoneal fluid analysis is recommended to verify declining polymorphonuclear neutrophil (PMN) counts and sterilization of ascitic fluid.
If improvement in ascitic fluid or clinical condition does not occur within 48 hours, further evaluation is required to rule out bowel perforation or intra-abdominal abscess. Evaluation may include a combination of radiography, CT scanning, intraluminal contrast studies, or surgical exploration.
After resolution of peritonitis and peritoneal abscesses, follow-up care is directed mostly by specifics of the underlying disease process and the presence or absence of chronic complications (eg, enterocutaneous fistulae). Patients with simple peritoneal infections after appendicitis or cholecystitis are usually cured and do not require long-term follow-up care. Patients with peritoneal operations for perforated peptic ulcer disease, Crohn disease, pancreatitis, and others often require lifelong medical therapy and treatment of recurrent complications.
Further inpatient care
Further care of the hospitalized patient is dependent on the etiology of the peritonitis and the clinical response to therapy. Whenever cultures have been obtained, antibiotic therapy should be appropriately focused on the organisms present. Appropriate resuscitation following known guidelines for sepsis should be instituted as soon as the diagnosis of sepsis is entertained.
Outpatient treatment of peritonitis is very limited; however, of the common causes of peritonitis, diverticulitis is probably the entity most frequently treated in an outpatient setting. A recent review outlines both inpatient and outpatient therapy.[21]
Prophylaxis
Outpatient prophylaxis, although not routinely recommended, has been shown to prevent SBP in the following high-risk groups:
Patients with ascites admitted with acute GI bleeding
Patients with ascitic fluid protein levels of less than 1 g/dL
Patients with a prior episode of SBP
Suggested outpatient prophylactic regimens include the following:
Norfloxacin - 400 mg daily
Ciprofloxacin - 750 mg weekly
Five doses of double-strength trimethoprim-sulfamethoxazole per week (Monday through Friday)
Evidence suggests that the long-term prophylaxis of patients with cirrhosis with fluoroquinolones, often norfloxacin, has led to selective intestinal decontamination and high-level fluoroquinolone resistance. This has been supported by published data that show a higher predominance of gram-positive pathogens in ascitic fluid cultures than previously reported.[22]
Deterrence and prevention
The prevention of peritonitis centers on causes that are acquired, most of which involve longstanding behaviors that despite all best efforts, remain uncontrolled. Diverticula develop in the Western population with increasing age at a prevalence of 80% in the eighth decade of life. Although increasing fiber and fluid intake has been promoted, the evidence to support this regimen is inadequate.[23] In cirrhotic patients with ascites, similar results of unclear efficacy of prophylaxis haunt effective prevention.[24]
The goals of pharmacotherapy in patients with peritonitis and abdominal sepsis are to reduce morbidity and prevent complications. The agents used are antimicrobials such as cefotaxime, gentamicin, ampicillin, and sulfamethoxazole.
Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting. Traditionally, a combination of an aminoglycoside and ampicillin was used to treat SBP. This regimen affords excellent empiric coverage of more than 90% of SBP cases caused by gram-negative aerobes or gram-positive cocci. More recently, the third-generation cephalosporin cefotaxime has been demonstrated to be as effective as the ampicillin/aminoglycoside combination, and it does not carry the increased risk of nephrotoxicity in cirrhotic patients. Cefotaxime does not cover enterococci, which are the pathogen in up to 5% of cases.
Cephalosporins are structurally and pharmacologically related to penicillins. They inhibit bacterial cell wall synthesis, resulting in bactericidal activity. Cephalosporins are divided into first, second, third, and fourth generation. First-generation cephalosporins have greater activity against gram-positive bacteria, and succeeding generations have increased activity against gram-negative bacteria and decreased activity against gram-positive bacteria.
Cefotaxime (Claforan)
Cefotaxime is a third-generation cephalosporin with a broad gram-negative spectrum, lower efficacy against gram-positive organisms, and higher efficacy against resistant organisms. Thus, it provides excellent empiric coverage of SBP.
Cefuroxime (Ceftin, Kefurox, Zinacef)
Second-generation cephalosporin; maintains gram-positive activity of first-generation cephalosporins; adds activity against P mirabilis, H influenzae, E coli, K pneumoniae, and M catarrhalis.
Binds to penicillin binding proteins and inhibits final transpeptidation step of peptidoglycan synthesis, resulting in cell wall death. Condition of patient, severity of infection, and susceptibility of microorganism determines proper dose and route of administration. Resists degradation by beta-lactamase.
Ceftriaxone (Rocephin)
Ceftriaxone is a third-generation cephalosporin with broad-spectrum, gram-negative activity; lower efficacy against gram-positive organisms; and higher efficacy against resistant organisms. Its bactericidal activity results from inhibiting cell wall synthesis by binding to one or more penicillin-binding proteins. It exerts an antimicrobial effect by interfering with synthesis of peptidoglycan, a major structural component of bacterial cell walls. Bacteria eventually lyse due to the ongoing activity of cell wall autolytic enzymes while cell wall assembly is arrested.
Ceftriaxone is highly stable in the presence of beta-lactamases, both penicillinase and cephalosporinase, of gram-negative and gram-positive bacteria. Approximately 33-67% of the dose is excreted unchanged in the urine; the remainder is secreted in bile and ultimately in feces as microbiologically inactive compounds. Ceftriaxone reversibly binds to human plasma proteins, and the binding decreases from 95% bound at plasma concentrations of less than 25 mcg/mL to 85% bound at 300 mcg/mL.
Cefotetan
Cefotetan is a second-generation cephalosporin used as single-drug therapy to provide broad gram-negative coverage and anaerobic coverage. Also provides some coverage of gram-positive bacteria. Half-life is 3.5 h. Inhibits bacterial cell wall synthesis by binding to one or more of the penicillin-binding proteins; inhibits final transpeptidation step of peptidoglycan synthesis, resulting in cell wall death.
Cefepime
Cefepime is a fourth-generation cephalosporin. Gram-negative coverage comparable to ceftazidime but has better gram-positive coverage (comparable to ceftriaxone). Cefepime is a zwitter ion; rapidly penetrates gram-negative cells. Best beta-lactam for IM administration.
Aminoglycosides are bactericidal antibiotics used primarily to treat gram-negative infections. They interfere with bacterial protein synthesis by binding to 30S and 50S ribosomal subunits.
Gentamicin (Gentacidin, Garamycin)
Gentamicin is an aminoglycoside antibiotic effective against Pseudomonas aeruginosa; E coli; and Proteus, Klebsiella, and Staphylococcus species. Gentamicin is also variably effective against some strains of certain gram-positive organisms, including S aureus, enterococci, and L monocytogenes. Dosing regimens are numerous; adjust the dose based on creatinine clearance and changes in volume of distribution. Gentamicin may be given IV/IM. Gentamicin has been reported to offer additive or synergistic activity against enterococci when used with ampicillin.
The penicillins are bactericidal antibiotics that work against sensitive organisms at adequate concentrations and inhibit the biosynthesis of cell wall mucopeptide.
Piperacillin and Tazobactam sodium (Zosyn)
Piperacillin is a semisynthetic extended-spectrum penicillin that inhibits bacterial cell wall synthesis by binding to specific penicillin-binding proteins; it is the most effective of the antipseudomonal penicillins.
Tazobactam increases piperacillin activity against S aureus, Klebsiella, Enterobacter, and Serratia species; the greatest increase is in activity against B fragilis. However, it does not increase anti–P aeruginosa activity.
Amoxicillin and clavulanate (Augmentin)
Amoxicillin inhibits bacterial cell wall synthesis by binding to penicillin-binding proteins; clavulanate inhibits beta-lactamase producing bacteria. This combination is a good alternative antibiotic for patients allergic or intolerant to the macrolide class. Usually, it is well tolerated, and provides good coverage for most infectious agents. It is not effective against Mycoplasma and Legionella species. The half-life of the oral dosage form is 1-1.3 hours. It has good tissue penetration but does not enter cerebrospinal fluid.
Ticarcillin and clavulanate potassium (Ticar)
This combination of an antipseudomonal penicillin with a beta-lactamase inhibitor provides coverage against most gram-positive and gram-negative organisms, as well as most anaerobes. It inhibits biosynthesis of cell wall mucopeptide and is effective during the stage of active growth.
Ampicillin (Omnipen, Marcillin)
Ampicillin interferes with bacterial cell wall synthesis during active multiplication, causing bactericidal activity against susceptible organisms. Dose adjustments may be necessary in renal failure. Rash should be evaluated carefully to differentiate nonallergic ampicillin rash from hypersensitivity reaction.
Macrolide antibiotics have bacteriostatic activity and exert their antibacterial action by binding to the 50S ribosomal subunit of susceptible organisms, resulting in inhibition of protein synthesis
Tobramycin (Nebcin)
Tobramycin is used in skin, bone, and skin structure infections, caused by S aureus, P aeruginosa, Proteus species, E coli, Klebsiella species, and Enterobacter species. It is indicated in the treatment of staphylococcal infections when penicillin or potentially less-toxic drugs are contraindicated and when bacterial susceptibility and clinical judgment justifies its use. Like other aminoglycosides, tobramycin is associated with nephrotoxicity and ototoxicity.
Clindamycin (Cleocin)
Clindamycin is a semisynthetic antibiotic produced by 7(S)-chloro-substitution of 7(R)-hydroxyl group of its parent compound lincomycin. It inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. Clindamycin distributes widely in the body without penetration of the CNS. Clindamycin is protein bound and is excreted by the liver and kidneys.
Carbapenems are structurally related to penicillins and have broad-spectrum bactericidal activity. The carbapenems exert their effect by inhibiting cell wall synthesis, which leads to cell death. They are active against gram-negative bacteria, gram-bacteria, and anaerobes.
Meropenem (Merrem IV)
A bactericidal broad-spectrum carbapenem antibiotic that inhibits cell-wall synthesis, meropenem is effective against most gram-positive and gram-negative bacteria. Compared with imipenem, meropenem has slightly increased activity against gram-negative organisms and slightly decreased activity against staphylococci and streptococci.
Aztreonam (Azactam)
Aztreonam is a monobactam, not a beta-lactam, antibiotic that inhibits cell wall synthesis during bacterial growth. It is active against gram-negative bacilli but has very limited gram-positive activity and is not useful for anaerobes. Aztreonam lacks cross-sensitivity with beta-lactam antibiotics. It may be used in patients allergic to penicillins or cephalosporins. Transient or persistent renal insufficiency may prolong serum levels.
Ertapenem (Invanz)
The bactericidal activity of ertapenem results from inhibition of cell wall synthesis and is mediated through binding to penicillin-binding proteins. Ertapenem is stable against hydrolysis by a variety of beta-lactamases, including penicillinases, cephalosporinases, and extended spectrum beta-lactamases; it is hydrolyzed by metallo-beta-lactamases.
Imipenem and cilastatin (Primaxin)
This combination is used for treatment of infections with multiple organisms because other agents do not have wide spectrum coverage or are contraindicated due to potential for toxicity.
Fluoroquinolones have broad-spectrum activity against gram-positive and gram-negative aerobic organisms. They inhibit DNA synthesis and growth by inhibiting DNA gyrase and topoisomerase, which is required for replication, transcription, and translation of genetic material.
Ciprofloxacin (Cipro)
Ciprofloxacin, a fluoroquinolone, inhibits bacterial DNA synthesis and, consequently, growth, by inhibiting DNA gyrase and topoisomerase, which is required for replication, transcription, and translation of genetic material. Quinolones have broad activity against gram-positive and gram-negative aerobic organisms. It has no activity against anaerobes. Continue treatment for at least 2 days (7-14 d typical) after signs and symptoms have disappeared. In prolonged therapy, perform periodic evaluations of organ system functions (eg, renal, hepatic, hematopoietic); adjust the dose in the presence of renal function impairment. Superinfections may occur with prolonged or repeated antibiotic therapy.
Norfloxacin (Chibroxin, Noroxin)
Norfloxacin is a fluoroquinolone with activity against pseudomonads, streptococci, MRSA, S epidermidis, and most gram-negative organisms, but it has no activity against anaerobes. It inhibits bacterial DNA synthesis and, consequently, growth.
Anti-infectives such as metronidazole and sulfamethoxazole/trimethoprim are effective against some types of bacteria that have become resistant to other antibiotics.
Sulfamethoxazole and trimethoprim (Bactrim, Bactrim DS, Cotrim, Cotrim DS, Septra, Septra DS)
Trimethoprim-sulfamethoxazole inhibits bacterial growth by inhibiting the synthesis of dihydrofolic acid. Its antibacterial activity includes common urinary tract pathogens, except Pseudomonas aeruginosa.
Metronidazole (Flagyl)
Metronidazole is an imidazole ring-based antibiotic active against various anaerobic bacteria and protozoa. It is used in combination with other antimicrobial agents (but is used as monotherapy in C difficile enterocolitis).
Glycylcycline Antibiotic
Glycylcycline antibiotics are structurally similar to tetracycline antibiotics and were developed to overcome bacterial mechanisms of tetracycline resistance. Tigecycline is the first drug approved in this class.
Tigecycline (Tygacil)
Tigecycline is a glycylcycline antibiotic that is structurally similar to tetracycline antibiotics. It is used for complicated intra-abdominal infections caused by C freundii, E cloacae, E coli, K oxytoca, K pneumoniae, E faecalis (vancomycin-susceptible isolates only), S aureus (methicillin-susceptible isolates only), S anginosus group. (includes S anginosus, S intermedius, and S constellatus), B fragilis, B thetaiotaomicron, B uniformis, B vulgatus, C perfringens, and P micros. Use with caution in patients with severe hepatic impairment.
What is peritonitis?
What are causes of peritonitis?
How are peritoneal infections classified?
How is peritonitis diagnosed?
What are the treatment approaches to peritonitis?
What is the anatomy of the peritoneum relevant to peritonitis and abdominal sepsis?
What is the role of peritoneal fluid in peritonitis and abdominal sepsis?
What is the anatomy of the peritoneal cavity relative to peritonitis and abdominal sepsis?
Which bacterial virulence factors are involved in the pathogenesis of peritonitis and abdominal sepsis?
What is the pathophysiology of peritonitis?
What is the pathophysiology of abdominal sepsis?
What is the role of bacterial inoculation of ascites in the pathogenesis of peritonitis and abdominal sepsis?
Which factors contribute to the formation of inflammation and bacterial growth in the pathogenesis of peritonitis and abdominal sepsis?
What is the role of fibrinolysis in the pathogenesis of peritonitis and abdominal sepsis?
What is the significance of bacterial load in the pathogenesis of peritonitis and abdominal sepsis?
What is the role of enterococci in the pathogenesis of peritonitis and abdominal sepsis?
What is the role of fungi in the pathogenesis of peritonitis and abdominal sepsis?
How does abscess formation occur in peritonitis and abdominal sepsis?
What is the role of cytokines in the pathogenesis of peritonitis and abdominal sepsis?
What causes peritonitis and abdominal sepsis?
What is spontaneous bacterial peritonitis (SBP)?
How does spontaneous bacterial peritonitis (SBP) occur?
What are the most common pathogens causing spontaneous bacterial peritonitis (SBP)?
What are the common etiologies of secondary peritonitis (SP)?
Which pathogens are involved in the etiology of secondary peritonitis (SP)?
How is secondary peritonitis (SP) differentiated from SBP in patients with cirrhosis?
Which pathogens are common causes of secondary peritonitis (SP)?
What are rare, nonsurgical causes of intra-abdominal sepsis?
What is the most common cause of postoperative peritonitis?
Which factors increase the risk of peritonitis and abdominal sepsis following surgery for penetrating abdominal trauma?
How frequently does peritonitis complicate peritoneal dialysis?
What are the risk factors for tertiary peritonitis?
What is tuberculosis peritonitis (TP)?
How is tuberculosis peritonitis (TP) diagnosed?
What causes chemical (sterile) peritonitis?
What is the role of peritoneal abscess in the etiology of tertiary peritonitis?
What is the overall incidence of peritoneal infection?
What is the prevalence of spontaneous bacterial peritonitis (SBP)?
Which factors have reduced morbidity and mortality of intra-abdominal sepsis?
What is the mortality rate in spontaneous bacterial peritonitis (SBP)?
What is the mortality rate in uncomplicated secondary peritonitis (SP)?
What is the mortality rate in severe intra-abdominal sepsis and peritonitis?
How do the mortality rates of peritonitis vary among treatments?
What is the prognosis of tertiary peritonitis?
Which prognostic scoring systems are used for peritonitis and abdominal sepsis?
What is the mortality rate for peritonitis and abdominal sepsis without organ failure?
What is the prognosis of peritonitis and abdominal sepsis in patients requiring emergent reoperations?
Which medical conditions are related to worse outcomes and recurrent complications of peritonitis and abdominal sepsis?
What is the risk of developing peritonitis and abdominal sepsis in patients who are older than 65 years?
What are the most significance factors in the prognosis of peritonitis and abdominal sepsis?
Where can patient education resources for peritonitis and abdominal sepsis be found?
What are the signs and symptoms of spontaneous bacterial peritonitis (SBP)?
How is pain characterized in peritonitis?
What are abdominal symptoms of peritonitis?
Which symptoms of peritonitis may precede the development of abdominal pain?
Which physical findings suggest peritonitis and abdominal sepsis?
How should an abdominal exam be performed for suspected peritonitis?
Which abdominal exam findings are characteristic of peritonitis and abdominal sepsis?
Which rectal exam findings are characteristic of peritonitis and abdominal sepsis?
Which findings are characteristic of peritonitis and abdominal sepsis in females?
How can the differential diagnosis of peritonitis and abdominal sepsis be narrowed on physical exam?
Which diseases may mimic the signs and symptoms of peritonitis and abdominal sepsis?
Which medical conditions should be considered in the differential diagnoses of peritonitis and abdominal sepsis?
What are the differential diagnoses for Peritonitis and Abdominal Sepsis?
What is the role of paracentesis in the diagnosis of peritonitis and abdominal sepsis?
Which lab tests are used in the diagnosis and management of spontaneous bacterial peritonitis (SBP)?
What algorithm is useful in the diagnosis and treatment of peritonitis and peritoneal abscess?
What is the role of CBC count in the evaluation of peritonitis and abdominal sepsis?
What is the role of blood chemistry tests in the evaluation of peritonitis and abdominal sepsis?
What is the role of urinalysis in the diagnosis of peritonitis?
What is the role of a stool sample in the diagnosis of peritonitis and abdominal sepsis?
Which finding on ascetic fluid analysis is highly sensitive and specific for spontaneous bacterial peritonitis (SBP)?
What should be included in the evaluation of the peritoneal fluid for the diagnosis of spontaneous bacterial peritonitis (SBP)?
Which findings on peritoneal fluid analysis are characteristic of bacterial peritonitis?
How is the diagnosis of spontaneous bacterial peritonitis (SBP) established?
What is the significance of a finding of culture-negative neutrocytic ascites in the evaluation of peritonitis?
What is the significance of a finding of monomicrobial nonneutrocytic bacterascites in the evaluation of peritonitis?
How is peritonitis diagnosed in patients receiving continuous ambulatory peritoneal dialysis (CAPD)?
When are intraoperative peritoneal fluid cultures indicated?
How is spontaneous bacterial peritonitis (SBP) diagnosed rapidly?
What is the average time saved with bedside reagent strips in the diagnosis of peritonitis and abdominal sepsis?
What is the role of radiography in the diagnosis of peritonitis and abdominal sepsis?
What is the role of abdominal ultrasonography in the diagnosis of peritonitis and abdominal sepsis?
What are the limitations of ultrasonography in the diagnosis of peritonitis and abdominal sepsis?
What are the advantages of ultrasound in the diagnosis of peritonitis and abdominal sepsis?
When is CT scanning indicated for the diagnosis of peritonitis and abdominal sepsis?
How is CT scanning performed in the diagnosis of peritonitis and abdominal sepsis?
What findings on CT scanning are characteristic of secondary peritonitis (SP)?
What is the role of nuclear scanning in the diagnosis of peritonitis and abdominal sepsis?
What is the role of MRI in the diagnosis of peritonitis and abdominal sepsis?
What is the role of contrast studies in the diagnosis of peritonitis and abdominal sepsis?
What is focus of treatment in peritonitis and peritoneal abscesses?
How is early control of the septic source of peritonitis achieved?
What is the role of surgery in the treatment of peritonitis and abdominal sepsis?
Which nonoperative interventions are used in the treatment of peritonitis and abdominal sepsis?
What are the general principles guiding the treatment of peritonitis and abdominal sepsis infections?
What is included in medical support for peritonitis and abdominal sepsis?
Which nonoperative therapies are used for early control of the septic source in peritonitis and abdominal sepsis?
What is the initial treatment of peritonitis and abdominal sepsis?
How is hemodynamic resuscitation used in the treatment of peritonitis and abdominal sepsis?
What is the role of antibiotic therapy in the treatment of peritonitis and abdominal sepsis?
What is the optimal duration of antibiotic therapy for peritonitis and abdominal sepsis?
How is abscess drainage performed for the treatment of peritonitis and abdominal sepsis?
When is it advisable to delay surgery for peritonitis and abdominal sepsis?
When is percutaneous drainage of abscesses contraindicated in the treatment of peritonitis and abdominal sepsis?
What is the role of primary percutaneous management in the treatment peritonitis and abdominal sepsis?
What is the role of laparoscopic drainage in the treatment of diverticular peritonitis and abdominal sepsis?
What is the efficacy of laparoscopic lavage in the treatment of peritonitis and abdominal sepsis?
What are the common reasons for failure of primary nonoperative management of peritonitis and abdominal sepsis?
When is primary percutaneous drainage most likely to succeed for the treatment of peritonitis and abdominal sepsis?
Which studies have addressed concerns regarding drainage catheters in deep abscesses the management of peritonitis and abdominal sepsis?
When should percutaneous drainage be considered for primary treatment of peritonitis and abdominal sepsis?
What nutritional support is needed during the treatment of peritonitis and abdominal sepsis?
Which specialist consultations are needed for the treatment of peritonitis and abdominal sepsis?
What are the complications of peritonitis?
What is included in follow-up care for peritonitis and abdominal sepsis?
When is repeat paracentesis indicated in the treatment of spontaneous bacterial peritonitis (SBP)?
What is included in the long-term monitoring of spontaneous bacterial peritonitis (SBP)?
How is follow-up care directed after treatment of peritonitis and abdominal sepsis?
What is included in inpatient care following treatment of peritonitis and abdominal sepsis?
What is included in outpatient care following treatment of peritonitis and abdominal sepsis?
Which groups at high risk of spontaneous bacterial peritonitis (SBP) benefit from outpatient prophylaxis?
What are the suggested regimens for spontaneous bacterial peritonitis (SBP) prophylaxis?
What are adverse effects of long-term SBP prophylaxis?
How is peritonitis prevented?
What are the goals of drug treatment for peritonitis and abdominal sepsis?
Which medications are used in the treatment of peritonitis and abdominal sepsis?
Which medications in the drug class Glycylcycline Antibiotic are used in the treatment of Peritonitis and Abdominal Sepsis?
Which medications in the drug class Anti-Infectives are used in the treatment of Peritonitis and Abdominal Sepsis?
Which medications in the drug class Fluoroquinolones are used in the treatment of Peritonitis and Abdominal Sepsis?
Which medications in the drug class Carbapenems are used in the treatment of Peritonitis and Abdominal Sepsis?
Which medications in the drug class Macrolides are used in the treatment of Peritonitis and Abdominal Sepsis?
Which medications in the drug class Penicillins are used in the treatment of Peritonitis and Abdominal Sepsis?
Which medications in the drug class Aminoglycosides are used in the treatment of Peritonitis and Abdominal Sepsis?
Which medications in the drug class Cephalosporins are used in the treatment of Peritonitis and Abdominal Sepsis?
Brian J Daley, MD, MBA, FACS, FCCP, CNSC Professor and Program Director, Department of Surgery, Chief, Division of Trauma and Critical Care, University of Tennessee Health Science Center College of Medicine
Brian J Daley, MD, MBA, FACS, FCCP, CNSC is a member of the following medical societies: American Association for the Surgery of Trauma, Eastern Association for the Surgery of Trauma, Southern Surgical Association, American College of Chest Physicians, American College of Surgeons, American Medical Association, Association for Academic Surgery, Association for Surgical Education, Shock Society, Society of Critical Care Medicine, Southeastern Surgical Congress, Tennessee Medical Association
Praveen K Roy, MD, AGAF Chief of Gastroenterology, Presbyterian Hospital; Medical Director of Endoscopy, Presbyterian Medical Group; Adjunct Associate Research Scientist, Lovelace Respiratory Research Institute; Clinical Assistant Professor of Medicine, University of New Mexico School of Medicine
Praveen K Roy, MD, AGAF is a member of the following medical societies: American Gastroenterological Association, American Society for Gastrointestinal Endoscopy
Alex Jacocks, MD Program Director, Professor, Department of Surgery, University of Oklahoma School of Medicine
Chandler Long, MD Resident Physician, Department of Surgery, University of Tennessee Medical Center-Knoxville
Ketul R Patel, MD Resident, Department of Internal Medicine, Providence Hospital
Ketul R Patel, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, and American Medical Association
Michael H Piper, MD, FACG, FACP Clinical Assistant Professor, Department of Internal Medicine, Division of Gastroenterology, Wayne State University School of Medicine; Consulting Staff, Digestive Health Associates PLC
Michael H Piper, MD, FACG, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Gastroenterology, American College of Physicians, and Michigan State Medical Society
Kenneth L Reed, DO Fellow in Gastroenterology, Providence Hospital, Michigan
Kenneth L Reed, DO is a member of the following medical societies: American College of Gastroenterology, American College of Osteopathic Internists, American Gastroenterological Association, American Osteopathic Association, American Society for Gastrointestinal Endoscopy, and Crohns and Colitis Foundation of America
Bradley J Warren, DO, FACG, FACOI Consulting Staff, Digestive Health Associates, PLC
Bradley J Warren, DO, FACG, FACOI is a member of the following medical societies: American College of Gastroenterology, American Osteopathic Association, and American Society for Gastrointestinal Endoscopy
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