Peritonitis and Abdominal Sepsis Workup

  • Author: Brian James Daley, MD, MBA, FACS, FCCP, CNSC; Chief Editor: Julian Katz, MD   more...
 
Updated: Mar 29, 2011
 

Approach Considerations

Diagnostic paracentesis should be performed in all patients who do not have an indwelling peritoneal catheter and are suspected of having SBP. In peritoneal dialysis patients with a peritoneal catheter, fluid should be withdrawn using sterile technique. Ultrasonography may aid paracentesis if ascites is minimally detectable or questionable.

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

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

Diagnostic and therapeutic approach to peritonitisDiagnostic and therapeutic approach to peritonitis and peritoneal abscess.
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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.

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Urinalysis

This is used to rule out urinary tract diseases (eg, pyelonephritis, renal stone disease); however, patients with lower abdominal and pelvic infections often demonstrate WBCs in the urine and microhematuria.

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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.

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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.

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 250 cells/µL or greater. Although this may often be the result of contamination of bacterial cultures, 38% of these patients develop SBP. Therefore, monomicrobial nonneutrocytic bacterascites may represent an early form of SBP. All study patients described who eventually developed SBP were symptomatic. For this reason, any patient suspected clinically of having SBP in this setting must be treated.

Tuberculous peritonitis is identified by ascites with high protein content, a low glucose and low SAAG, elevated ascitic fluid WBC count, and lymphocyte predominance. In TP, the fluid Gram stain and acid-fast stain results are rarely positive, and routine culture results are falsely negative in as many as 80% of cases. A peritoneal fluid protein level greater than 2.5 g/dL, LDH level greater than 90 U/mL, and predominantly mononuclear cell count of more than 500 cells/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)

RoutineOptionalUnusualLess Helpful
Cell countObtain culture in blood culture (BC) bottles.Tuberculosis (TB) smear and culturepH
AlbuminGlucoseCytologyLactate
Total proteinLactate dehydrogenase (LDH)TriglycerideCholesterol
AmylaseBilirubinFibronectin
Gram stainAlpha 1-antitrypsin
Glycosaminoglycans
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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.

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Radiography

Plain films of the abdomen (eg, supine, upright, and lateral decubitus positions) are often the first imaging studies obtained in patients presenting with peritonitis. Their value in reaching a specific diagnosis is limited.

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

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Ultrasonography

Abdominal ultrasonography may be helpful in the evaluation of pathology in the right upper quadrant (eg, perihepatic abscess, cholecystitis, biloma, pancreatitis, pancreatic pseudocyst), right lower quadrant, and pelvis (eg, appendicitis, tubo-ovarian abscess, Douglas pouch abscess). However, the examination is sometimes limited because of patient discomfort, abdominal distention, and bowel gas interference.

Ultrasonography may detect increased amounts of peritoneal fluid (ascites), but its ability to detect quantities of less than 100 mL is limited. The central (perimesenteric) peritoneal cavity is not visualized well with transabdominal ultrasonography. Examination from the flank or back may improve the diagnostic yield, and providing the ultrasonographer with specific information about the patient's condition and the suspected diagnosis before the examination is important. With an experienced ultrasonographer, a diagnostic accuracy of greater than 85% has been reported in several series.

Ultrasonographically guided aspiration and placement of drains has evolved into a valuable tool in the diagnosis and treatment of abdominal fluid collections.

Advantages of ultrasound include low cost, portability, and availability. Disadvantages are that the test is operator dependent, and there is reduced visualization in the presence of overlying bowel gas and abdominal dressings.

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CT Scanning

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

Whenever possible, the CT scan should be performed with enteral and intravenous contrast. CT scans can detect small quantities of fluid, areas of inflammation, and other GI tract pathology, with sensitivities that approach 100%. (See the image below.) CT scanning can be used to evaluate for ischemia, as well as to determine bowel obstruction. An abscess is suggested by the presence of fluid density that is not bound by the bowel or other known structures. Gas within an abdominal mass or the presence of an enhancing wall and adjacent inflammatory changes are also highly suggestive of an abscess. Ischemia can be demonstrated by a clot in a large vessel or by the absence of blood flow. Gas within the intestinal wall or in the portal vein may also suggest ischemia.

A 78-year-old man was admitted with a history of pA 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.

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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.

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MRI

MRI is an emerging imaging modality for the diagnosis of suspected intra-abdominal abscesses. Abdominal abscesses demonstrate decreased signal intensity on T1-weighted images and homogeneous or heterogeneous increased signal intensity on T2-weighted images; abscesses are observed best on gadolinium-enhanced, T1-weighted, fat-suppressed images as well-defined fluid collections with rim enhancement.

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

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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.

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Contributor Information and Disclosures
Author

Brian James Daley, MD, MBA, FACS, FCCP, CNSC  Professor, Associate Program Director, Department of Surgery, Division of Trauma and Critical Care, University of Tennessee Health Science Center College of Medicine

Brian James Daley, MD, MBA, FACS, FCCP, CNSC is a member of the following medical societies: American Association for the Surgery of Trauma, American College of Chest Physicians, American College of Surgeons, American Medical Association, Association for Academic Surgery, Association for Surgical Education, Eastern Association for the Surgery of Trauma, Shock Society, Society of Critical Care Medicine, Southeastern Surgical Congress, and Tennessee Medical Association

Disclosure: Nothing to disclose.

Coauthor(s)

Alex Jacocks, MD  Program Director, Professor, Department of Surgery, University of Oklahoma School of Medicine

Disclosure: Nothing to disclose.

Chandler Long, MD  Resident Physician, Department of Surgery, University of Tennessee Medical Center, Knoxville

Disclosure: Nothing to disclose.

Lena M Napolitano, MD, FACS, FCCP, FCCM  Professor of Surgery, University of Michigan School of Medicine; Chief, Surgical Critical Care, Program Director, Surgical Critical Care Fellowship, Associate Chair, Department of Surgery, University of Michigan Health System

Lena M Napolitano, MD, FACS, FCCP, FCCM is a member of the following medical societies: Alpha Omega Alpha, American Association for the Surgery of Trauma, American College of Chest Physicians, American College of Critical Care Medicine, American College of Physicians, American College of Surgeons, American Medical Association, American Society for Parenteral and Enteral Nutrition, Association for Academic Surgery, Association of VA Surgeons, Association of Women Surgeons, California Professional Society on the Abuse of Children, Eastern Association for the Surgery of Trauma, Phi Beta Kappa, Shock Society, Society of Critical Care Medicine, and Society of University Surgeons

Disclosure: Pfizer, Wyeth, Schering Plough, Merck, Ortho-McNeil Honoraria Speaking and teaching

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

Disclosure: Nothing to disclose.

Ruben Peralta, MD, FACS  Professor of Surgery, Anesthesia and Emergency Medicine, Senior Medical Advisor, Board of Directors, Program Chief of Trauma, Emergency and Critical Care, Consulting Staff, Professor Juan Bosch Trauma Hospital, Dominican Republic

Ruben Peralta, MD, FACS is a member of the following medical societies: American Association of Blood Banks, American College of Healthcare Executives, American College of Surgeons, American Medical Association, Association for Academic Surgery, Eastern Association for the Surgery of Trauma, Massachusetts Medical Society, Society of Critical Care Medicine, and Society of Laparoendoscopic Surgeons

Disclosure: Nothing to disclose.

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

Disclosure: Nothing to disclose.

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

Disclosure: Nothing to disclose.

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

Disclosure: Nothing to disclose.

Specialty Editor Board

David L Morris, MD, PhD, FRACS  Professor, Department of Surgery, St George Hospital, University of New South Wales, Australia

David L Morris, MD, PhD, FRACS is a member of the following medical societies: British Society of Gastroenterology

Disclosure: RFA Medical None Director; MRC Biotec None Director

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

BS Anand, MD  Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine

BS Anand, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American Gastroenterological Association, and American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

John Geibel, MD, DSc, MA  Vice Chairman, Professor, Department of Surgery, Section of Gastrointestinal Medicine and Department of Cellular and Molecular Physiology, Yale University School of Medicine; Director of Surgical Research, Department of Surgery, Yale-New Haven Hospital

John Geibel, MD, DSc, MA is a member of the following medical societies: American Gastroenterological Association, American Physiological Society, American Society of Nephrology, Association for Academic Surgery, International Society of Nephrology, New York Academy of Sciences, and Society for Surgery of the Alimentary Tract

Disclosure: AMGEN Royalty Consulting; ARdelyx Ownership interest Board membership

Chief Editor

Julian Katz, MD  Clinical Professor of Medicine, Drexel University College of Medicine; Consulting Staff, Department of Medicine, Section of Gastroenterology and Hepatology, Hospital of the Medical College of Pennsylvania

Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Geriatrics Society, American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law, Medicine & Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility

Disclosure: Nothing to disclose.

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  15. Gaya DR, David B Lyon T, Clarke J, Jamdar S, Inverarity D, Forrest EH, et al. Bedside leucocyte esterase reagent strips with spectrophotometric analysis to rapidly exclude spontaneous bacterial peritonitis: a pilot study. Eur J Gastroenterol Hepatol. Apr 2007;19(4):289-95. [Medline].

  16. Blot S, De Waele JJ. Critical issues in the clinical management of complicated intra-abdominal infections. Drugs. 2005;65(12):1611-20. [Medline].

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  18. Runyon B. Ascites and spontaneous bacterial peritonitis. In: Feldman M, Friedman LS, Sleisenger MH, eds. Sleisenger & Fordtran's Gastrointestinal and Liver Disease. Vol 2. 8th ed. Philadelphia, Pa: Saunders; 2006:1935-64.

  19. Colizza S, Rossi S. Antibiotic prophylaxis and treatment of surgical abdominal sepsis. J Chemother. Nov 2001;13 Spec No 1(1):193-201. [Medline].

  20. Ginés P, Rimola A, Planas R, Vargas V, et al. Norfloxacin prevents spontaneous bacterial peritonitis recurrence in cirrhosis: results of a double-blind, placebo-controlled trial. Hepatology. Oct. 1990;12(4 Pt 1):716-24.

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  23. [Best Evidence] Wiggins KJ, Craig JC, Johnson DW, Strippoli GF. Treatment for peritoneal dialysis-associated peritonitis. Cochrane Database Syst Rev. Jan 23 2008;CD005284. [Medline].

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Diagnostic and therapeutic approach to peritonitis and peritoneal abscess.
A 48-year-old man underwent suprapubic laparotomy, right hemicolectomy, and gastroduodenal resection for right colon cancer invading the first portion of the duodenum. He developed abdominal pain and distention. Computed tomography (CT) scanning was used to confirm an anastomotic dehiscence. Figure A shows a contrast-enhanced scan of the abdomen and pelvis that reveals multiple fluid collections, perihepatic ascites, and mild periportal edema. A collection of fluid containing an air-fluid level is visible anterior to the left lobe of the liver. A second collection is anterior to the splenic flexure of the colon. In figure B, a third fluid collection is present in the inferior aspect of the lesser space and in the transverse mesocolon. Figure C shows the pelvis with a collection of free fluid in the rectovesical pouch.
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.
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.
Gram-negative Escherichia coli.
Table 1. Common Causes of Secondary Peritonitis
Source RegionsCauses
EsophagusBoerhaave syndrome



Malignancy



Trauma (mostly penetrating)



Iatrogenic*



StomachPeptic ulcer perforation



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



Trauma (mostly penetrating)



Iatrogenic*



DuodenumPeptic ulcer perforation



Trauma (blunt and penetrating)



Iatrogenic*



Biliary tractCholecystitis



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



Malignancy



Choledochal cyst (rare)



Trauma (mostly penetrating)



Iatrogenic*



PancreasPancreatitis (eg, alcohol, drugs, gallstones)



Trauma (blunt and penetrating)



Iatrogenic*



Small bowelIschemic bowel



Incarcerated hernia (internal and external)



Closed loop obstruction



Crohn disease



Malignancy (rare)



Meckel diverticulum



Trauma (mostly penetrating)



Large bowel and appendixIschemic bowel



Diverticulitis



Malignancy



Ulcerative colitis and Crohn disease



Appendicitis



Colonic volvulus



Trauma (mostly penetrating)



Iatrogenic



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



Malignancy (rare)



Trauma (uncommon)



*Iatrogenic trauma to the upper GI tract, including the pancreas and biliary tract and colon, often results from endoscopic procedures; anastomotic dehiscence and inadvertent bowel injury (eg, mechanical, thermal) are common causes of leak in the postoperative period.
Table 2. Microbial Flora of Secondary Peritonitis
TypeOrganismPercentage
Aerobic
Gram negativeEscherichia coli60%
Enterobacter/Klebsiella26%
Proteus22%
Pseudomonas8%
Gram positiveStreptococci28%
Enterococci17%
Staphylococci7%
AnaerobicBacteroides72%
Eubacteria24%
Clostridia17%
Peptostreptococci14%
Peptococci11%
FungiCandida2%
Table 3. Microbiology of Primary, Secondary, and Tertiary Peritonitis
Peritonitis



(Type)



Etiologic OrganismsAntibiotic Therapy



(Suggested)



ClassType of Organism
PrimaryGram-negativeE coli (40%)



K pneumoniae (7%)



Pseudomonas species (5%)



Proteus species (5%)



Streptococcus species (15%)



Staphylococcus species (3%)



Anaerobic species (< 5%)



Third-generation cephalosporin
SecondaryGram-negativeE coli



Enterobacter species



Klebsiella species



Proteus species



Second-generation cephalosporin



Third-generation cephalosporin



Penicillins with anaerobic activity



Quinolones with anaerobic activity



Quinolone and metronidazole



Aminoglycoside and metronidazole



Gram-positiveStreptococcus species



Enterococcus species



AnaerobicBacteroides fragilis



Other Bacteroides species



Eubacterium species



Clostridium species



Anaerobic Streptococcus species



TertiaryGram-negativeEnterobacter species



Pseudomonas species



Enterococcus species



Second-generation cephalosporin



Third-generation cephalosporin



Penicillins with anaerobic activity



Quinolones with anaerobic activity



Quinolone and metronidazole



Aminoglycoside and metronidazole



Carbapenems



Triazoles or amphotericin (considered in fungal etiology)



(Alter therapy based on culture results.)



Gram-positiveStaphylococcus species
FungalCandida species
Table 4. Ascitic Fluid Analysis Summary[4]
RoutineOptionalUnusualLess Helpful
Cell countObtain culture in blood culture (BC) bottles.Tuberculosis (TB) smear and culturepH
AlbuminGlucoseCytologyLactate
Total proteinLactate dehydrogenase (LDH)TriglycerideCholesterol
AmylaseBilirubinFibronectin
Gram stainAlpha 1-antitrypsin
Glycosaminoglycans
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