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Peritonitis and Abdominal Sepsis Treatment & Management

  • Author: Brian J Daley, MD, MBA, FACS, FCCP, CNSC; Chief Editor: Julian Katz, MD  more...
 
Updated: Feb 23, 2015
 

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 infections are 4-fold, as follows[13] :

  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 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.

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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.[19]

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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.[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.

Further outpatient care

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]

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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.[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]

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Contributor Information and Disclosures
Author

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

Disclosure: Nothing to disclose.

Specialty Editor Board

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, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Chief Editor

Julian Katz, MD Clinical Professor of Medicine, Drexel University College of Medicine

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, Physicians for Social Responsibility

Disclosure: Nothing to disclose.

Acknowledgements

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.

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.

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.

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.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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.

References
  1. Pavlidis TE. Cellular changes in association with defense mechanisms in intra-abdominal sepsis. Minerva Chir. 2003 Dec. 58(6):777-81. [Medline].

  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. 2010 Apr. 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. 2009 Dec 22. 9:212. [Medline]. [Full Text].

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

  5. Lata J, Stiburek O, Kopacova M. Spontaneous bacterial peritonitis: a severe complication of liver cirrhosis. World J Gastroenterol. 2009 Nov 28. 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. 2005 Sep. 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. 2005 Feb. 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. 2010 Jan-Feb. 30(1):19-22. [Medline].

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

  11. Cheruvattath R, Balan V. Infections in Patients With End-stage Liver Disease. J Clin Gastroenterol. 2007 Apr. 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. 2010 Jan. 52(1):39-44. [Medline].

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

  14. Riggio O, Angeloni S. Ascitic fluid analysis for diagnosis and monitoring of spontaneous bacterial peritonitis. World J Gastroenterol. 2009 Aug 21. 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. 2007 Apr. 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. Swank HA, Vermeulen J, Lange JF, Mulder IM, van der Hoeven JA, Stassen LP, et al. The ladies trial: laparoscopic peritoneal lavage or resection for purulent peritonitis and Hartmann's procedure or resection with primary anastomosis for purulent or faecal peritonitis in perforated diverticulitis (NTR2037). BMC Surg. 2010 Oct 18. 10:29. [Medline]. [Full Text].

  18. Angenete E, Thornell A, Burcharth J, et al. Laparoscopic lavage is feasible and safe for the treatment of perforated diverticulitis with purulent peritonitis: the first results from the randomized controlled trial DILALA. Ann Surg. 2014 Dec 8. [Medline].

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

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

  21. Biondo S, Lopez Borao J, Millan M, Kreisler E, Jaurrieta E. Current status of the treatment of acute colonic diverticulitis: a systematic review. Colorectal Dis. 2012 Jan. 14(1):e1-e11. [Medline].

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

  23. Maconi G, Barbara G, Bosetti C, Cuomo R, Annibale B. Treatment of diverticular disease of the colon and prevention of acute diverticulitis: a systematic review. Dis Colon Rectum. 2011 Oct. 54(10):1326-38. [Medline].

  24. [Guideline] Cohen MJ, Sahar T, Benenson S, Elinav E, Brezis M, Soares-Weiser K. Antibiotic prophylaxis for spontaneous bacterial peritonitis in cirrhotic patients with ascites, without gastro-intestinal bleeding. Cochrane Database Syst Rev. 2009 Apr 15. CD004791. [Medline].

  25. 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.

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

  27. 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. 2010 Mar. 66(3):308-13. [Medline].

  28. Wiggins KJ, Craig JC, Johnson DW, Strippoli GF. Treatment for peritoneal dialysis-associated peritonitis. Cochrane Database Syst Rev. 2008 Jan 23. 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. After surgery, the patient 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 Regions Causes
Esophagus Boerhaave syndrome



Malignancy



Trauma (mostly penetrating)



Iatrogenic*



Stomach Peptic ulcer perforation



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



Trauma (mostly penetrating)



Iatrogenic*



Duodenum Peptic ulcer perforation



Trauma (blunt and penetrating)



Iatrogenic*



Biliary tract Cholecystitis



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



Malignancy



Choledochal cyst (rare)



Trauma (mostly penetrating)



Iatrogenic*



Pancreas Pancreatitis (eg, alcohol, drugs, gallstones)



Trauma (blunt and penetrating)



Iatrogenic*



Small bowel Ischemic bowel



Incarcerated hernia (internal and external)



Closed loop obstruction



Crohn disease



Malignancy (rare)



Meckel diverticulum



Trauma (mostly penetrating)



Large bowel and appendix Ischemic bowel



Diverticulitis



Malignancy



Ulcerative colitis and Crohn disease



Appendicitis



Colonic volvulus



Trauma (mostly penetrating)



Iatrogenic



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



Malignancy (rare)



Trauma (uncommon)



*Iatrogenic trauma to the upper GI tract, including the pancreas and biliary tract and colon, often results from endoscopic procedures; anastomotic dehiscence and inadvertent bowel injury (eg, mechanical, thermal) are common causes of leak in the postoperative period.
Table 2. Microbial Flora of Secondary Peritonitis
Type Organism Percentage
Aerobic    
Gram negative Escherichia coli 60%
  Enterobacter/Klebsiella 26%
  Proteus 22%
  Pseudomonas 8%
Gram positive Streptococci 28%
  Enterococci 17%
  Staphylococci 7%
Anaerobic Bacteroides 72%
  Eubacteria 24%
  Clostridia 17%
  Peptostreptococci 14%
  Peptococci 11%
Fungi Candida 2%
Table 3. Microbiology of Primary, Secondary, and Tertiary Peritonitis
Peritonitis



(Type)



Etiologic Organisms Antibiotic Therapy



(Suggested)



Class Type of Organism
Primary Gram-negative E coli (40%)



K pneumoniae (7%)



Pseudomonas species (5%)



Proteus species (5%)



Streptococcus species (15%)



Staphylococcus species (3%)



Anaerobic species (< 5%)



Third-generation cephalosporin
Secondary Gram-negative E coli



Enterobacter species



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-positive Streptococcus species



Enterococcus species



Anaerobic Bacteroides fragilis



Other Bacteroides species



Eubacterium species



Clostridium species



Anaerobic Streptococcus species



Tertiary Gram-negative Enterobacter 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-positive Staphylococcus species
Fungal Candida species
Table 4. Ascitic Fluid Analysis Summary [4]
Routine Optional Unusual Less Helpful
Cell count Obtain culture in blood culture (BC) bottles. Tuberculosis (TB) smear and culture pH
Albumin Glucose Cytology Lactate
Total protein Lactate dehydrogenase (LDH) Triglyceride Cholesterol
  Amylase Bilirubin Fibronectin
  Gram stain   Alpha 1-antitrypsin
      Glycosaminoglycans
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