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Peritonitis and Abdominal Sepsis Differential Diagnoses

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

Diagnostic Considerations

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
  • Pyelonephritis
  • Sclerosing peritonitis
  • Splenosis
  • Vascular conditions (eg, mesenteric embolus, mesenteric nonocclusive ischemia, ischemic colitis, portal vein thrombosis, mesenteric vein thrombosis)
  • Vasculitis (eg, systemic lupus erythematosus, allergic vasculitis [Henoch-Schönlein purpura], Kohlmeier-Degos disease, polyarteritis nodosa)

Differential Diagnoses

 
 
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 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 stain Alpha 1-antitrypsin
   Glycosaminoglycans
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