Peritonitis and Abdominal Sepsis Treatment & Management

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

Approach Considerations

The current approach to peritonitis and peritoneal abscesses targets correction of the underlying process, administration of systemic antibiotics, and supportive therapy to prevent or limit secondary complications due to organ system failure. Treatment success is defined as adequate source control with resolution of sepsis and clearance of all residual intra-abdominal infection.

Early control of the septic source is mandatory and can be achieved by operative and nonoperative means.

Operative management addresses the need to control the infectious source and to purge bacteria and toxins. The type and extent of surgery depends on the underlying disease process and the severity of intra-abdominal infection. Definitive interventions to restore functional anatomy involve removing the source of the antimicrobial contamination and repairing the anatomic or functional disorder causing the infection. This is accomplished by surgical intervention. Occasionally, this can be achieved during a single operation; however, in certain situations, a second or a third procedure may be required. In some patients, definitive intervention is delayed until the condition of the patient improves and tissue healing is adequate to allow for a (sometimes) lengthy procedure.

To see complete information on the Surgical Approach to Peritonitis and Abdominal Sepsis, please go to the main article by clicking here.

Nonoperative interventions include percutaneous abscess drainage, as well as percutaneous and endoscopic stent placements. If an abscess is accessible for percutaneous drainage and if the underlying visceral organ pathology does not clearly require operative intervention, percutaneous drainage is a safe and effective initial treatment approach. With percutaneous treatment, the definition of success includes the avoidance of further operative intervention and, in some cases, the delay of surgery until after resolution of the initial sepsis.

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

  1. Control the infectious source
  2. Eliminate bacteria and toxins
  3. Maintain organ system function
  4. Control the inflammatory process

The treatment of peritonitis is multidisciplinary, with complementary application of medical, operative, and nonoperative interventions. Medical support includes the following:

  • Systemic antibiotic therapy
  • Intensive care with hemodynamic, pulmonary, and renal support
  • Nutrition and metabolic support
  • Inflammatory response modulation therapy

Early control of the septic source is mandatory and can be achieved by operative and nonoperative means. Nonoperative interventional therapies include percutaneous drainage of abscesses and percutaneous and endoscopic stent placements.

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

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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.

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Antibiotic Therapy

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

The optimal duration of antibiotic therapy must be individualized and depends on the underlying pathology, severity of infection, speed and effectiveness of source control, and patient response to therapy. Antibiotics can be discontinued once clinical signs of infection have resolved. Recurrence is a concern with certain infections, such as those from Candida and Staphylococcus aureus, and treatment should be continued for 2-3 weeks.

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Nonoperative Drainage

Drainage refers to evacuation of an abscess. This can be performed operatively or percutaneously under ultrasound or CT guidance. If the abscess is localized at the level of the skin and underlying superficial tissues, simple removal of sutures or opening of the wound may be sufficient. Percutaneous techniques are preferred when an abscess can be completely drained, and debridement and repair of the anatomic structures are not needed. Factors that may prevent successful source control with percutaneous drainage include diffuse peritonitis, lack of localization of the infectious process, multiple abscesses, anatomic inaccessibility, or need for surgical debridement.[4]

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

Most patients with tertiary peritonitis develop complex abscesses or poorly localized peritoneal infections that are not amenable to percutaneous drainage. Up to 90% of patients will require reoperation for additional source control.

For primary percutaneous management of intra-abdominal abscesses, the etiology, location, and morphology of the abscess must be defined; evaluate for the presence of an ongoing enteric leak or fistula formation. With proper indications, most studies have reported success rates of greater than 80% (range 33-100%) for drainage of localized nonloculated abscesses; however, the success rates depend to some degree on the underlying pathology. In these studies, no significant differences were found between operative and primary nonoperative management with regard to the overall morbidity or length of hospital stay (mean duration of drainage 8.5 d).

Common reasons for failure of primary nonoperative management include enteric fistula (eg, anastomotic dehiscence), pancreatic involvement, infected clot, and multiple or multiloculated abscesses. Procedure-related significant complications are reported to occur in less than 10% of cases (range 5-27%), with less than a 1% attributable mortality rate with experienced physicians.

In peritoneal abscess formation caused by subacute bowel perforation (eg, diverticulitis, Crohn disease, appendicitis), primary percutaneous management with percutaneous drainage was successful in most patients. Patients with Crohn disease whose abscesses were drained percutaneously had significantly fewer associated fistulae. Failure in these patients was related to preexisting fistulization and extensive stricture formation.

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

In summary, percutaneous and surgical drainage should not be considered competitive but rather complementary. If an abscess is accessible to percutaneous drainage and the underlying visceral organ pathology does not clearly require an operative approach, percutaneous drainage can be used safely and effectively as the primary treatment modality. In these cases, patients must be closely monitored, and improvement should occur in less than 24-48 hours. With lack of improvement, patients must be reevaluated aggressively (eg, repeat CT scan) and the therapeutic strategy should be altered accordingly.

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Nutrition

In general, patients with peritonitis develop some degree of gut dysfunction (eg, ileus) after exploration. Consider establishing some form of nutritional support early in the course of treatment because most patients have an insufficient enteral intake for a variable amount of time preoperatively. The existing data support that enteral nutrition is superior to parenteral hyperalimentation. Enteral nutrition has been found to have fewer complications in patients who are severely ill. If enteral feeding is contraindicated or not tolerated, parenteral nutrition should be instituted.

Nutritional demands increase during sepsis, with caloric requirements of 25-35 kcal/kg/d. Patients with sepsis should be fed a high-protein isocaloric diet. Hypercaloric diets cannot prevent the intense protein catabolism associated with sepsis.[17]

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Consultations

The treatment of intra-abdominal sepsis requires a multidisciplinary approach. In the treatment of secondary peritonitis, a surgeon must be consulted. Interventional radiology may need to be consulted if ultrasound or CT-guided drainage of an abscess is being considered.

Other consultations may include the following:

  • Gastroenterology
  • Infectious disease
  • Critical care
  • Diet/nutrition
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Complications

Complications of peritonitis include tertiary peritonitis, infection or dehiscence of the surgical site, enterocutaneous fistula, abdominal compartment syndrome, and enteric insufficiency. Enterocutaneous fistulae can lead to ongoing (potentially large) volume, protein, and electrolyte losses; inability to use the gut for nutritional support; and associated long-term complications of intravenous alimentation. Abdominal compartment syndrome is a well-recognized disease entity related to acutely increased abdominal pressure (ie, intra-abdominal hypertension) and is associated with the development of multiple organ dysfunction. Extensive initial (gastrointestinal) disease, chronic recurrent infections, and associated reoperations may lead to enteric insufficiency because of short gut, pancreatic insufficiency, or hepatic dysfunction.

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Long-term Monitoring

Depending on the type of perforation causing secondary peritonitis, patients may require further surgical care or repeat abscess drainage by interventional radiology. Follow-up care depends on the cause of the intra-abdominal sepsis. In simple infections, such as those caused by cholecystitis or appendicitis, once the infection is cleared, no follow-up care is necessary. However, in patients with perforated duodenal ulcer, chronic pancreatitis, or Crohn disease, lifelong follow-up care is needed.

Repeat paracentesis is not required in SBP if the patient has advanced cirrhosis with signs and symptoms of infection, a positive bacterial isolate with monomicrobial typical organism, and a good response to treatment.[18] 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.

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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.[19]

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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.

References
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  2. Appenrodt B, Grünhage F, Gentemann MG, Thyssen L, Sauerbruch T, Lammert F. Nucleotide-binding oligomerization domain containing 2 (NOD2) variants are genetic risk factors for death and spontaneous bacterial peritonitis in liver cirrhosis. Hepatology. Apr 2010;51(4):1327-33. [Medline].

  3. Barretti P, Montelli AC, Batalha JE, Caramori JC, Cunha Mde L. The role of virulence factors in the outcome of staphylococcal peritonitis in CAPD patients. BMC Infect Dis. Dec 22 2009;9:212. [Medline]. [Full Text].

  4. [Guideline] Runyon BA. Management of adult patients with ascites due to cirrhosis. Hepatology. Mar 2004;39(3):841-56. [Medline].

  5. Lata J, Stiburek O, Kopacova M. Spontaneous bacterial peritonitis: a severe complication of liver cirrhosis. World J Gastroenterol. Nov 28 2009;15(44):5505-10. [Medline]. [Full Text].

  6. Bert F, Noussair L, Lambert-Zechovsky N, Valla D. Viridans group streptococci: an underestimated cause of spontaneous bacterial peritonitis in cirrhotic patients with ascites. Eur J Gastroenterol Hepatol. Sep 2005;17(9):929-33. [Medline].

  7. Cholongitas E, Papatheodoridis GV, Lahanas A, Xanthaki A, Kontou-Kastellanou C, Archimandritis AJ. Increasing frequency of Gram-positive bacteria in spontaneous bacterial peritonitis. Liver Int. Feb 2005;25(1):57-61. [Medline].

  8. Adler SN, Gasbarra DB. A Pocket Manual of Differential Diagnosis. Philadelphia, Pa: Lippincott Williams & Wilkins; 2005.

  9. Nouri-Majalan N, Najafi I, Sanadgol H, Ganji MR, Atabak S, Hakemi M, et al. Description of an outbreak of acute sterile peritonitis in Iran. Perit Dial Int. Jan-Feb 2010;30(1):19-22. [Medline].

  10. Evans LT, Kim WR, Poterucha JJ, Kamath PS. Spontaneous bacterial peritonitis in asymptomatic outpatients with cirrhotic ascites. Hepatology. Apr 2003;37(4):897-901. [Medline].

  11. Cheruvattath R, Balan V. Infections in Patients With End-stage Liver Disease. J Clin Gastroenterol. Apr 2007;41(4):403-11. [Medline].

  12. Soriano G, Castellote J, Alvarez C, et al. Secondary bacterial peritonitis in cirrhosis: a retrospective study of clinical and analytical characteristics, diagnosis and management. J Hepatol. Jan 2010;52(1):39-44. [Medline].

  13. Marshall JC. Intra-abdominal infections. Microbes Infect. Sep 2004;6(11):1015-25. [Medline].

  14. Riggio O, Angeloni S. Ascitic fluid analysis for diagnosis and monitoring of spontaneous bacterial peritonitis. World J Gastroenterol. Aug 21 2009;15(31):3845-50. [Medline]. [Full Text].

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

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

  17. Hawker FH. How to feed patients with sepsis. Curr Opin Crit Care. Aug 2000;6(4):247-252. [Medline].

  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.

  21. Soares-Weiser K, Brezis M, Leibovici L. Antibiotics for spontaneous bacterial peritonitis in cirrhotics. Cochrane Database Syst Rev. 2001;CD002232. [Medline].

  22. Tubau F, Liñares J, Rodríguez MD, Cercenado E, Aldea MJ, González-Romo F, et al. Susceptibility to tigecycline of isolates from samples collected in hospitalized patients with secondary peritonitis undergoing surgery. Diagn Microbiol Infect Dis. Mar 2010;66(3):308-13. [Medline].

  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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