Medscape is available in 5 Language Editions – Choose your Edition here.


Peritonitis and Abdominal Sepsis Clinical Presentation

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


The diagnosis of peritonitis is usually clinical. History should include recent abdominal surgery, previous episodes of peritonitis, travel history, use of immunosuppressive agents, and the presence of diseases (eg, inflammatory bowel disease, diverticulitis, peptic ulcer disease) that may predispose to intra-abdominal infections.

A broad range of signs and symptoms are seen in spontaneous bacterial peritonitis (SBP). A high index of suspicion must be maintained when caring for patients with ascites, particularly those with acute clinical deterioration. As many as 30% of patients are completely asymptomatic. Manifestations of SBP may include the following:

  • Fever and chills (as many as 80% of patients)
  • Abdominal pain or discomfort (found in as many as 70% of patients)
  • Worsening or unexplained encephalopathy
  • Diarrhea
  • Ascites that does not improve following administration of diuretic medication
  • Worsening or new-onset renal failure
  • Ileus

Abdominal pain, which may be acute or insidious, is the usual chief complaint of patients with peritonitis. Initially, the pain may be dull and poorly localized (visceral peritoneum); often, it progresses to steady, severe, and more localized pain (parietal peritoneum). Abdominal pain may be exacerbated by any movement (eg, coughing, flexing the hips) and local pressure. If the underlying process is not contained, the pain becomes diffuse. In certain disease entities (eg, gastric perforation, severe acute pancreatitis, intestinal ischemia), the abdominal pain may be generalized from the beginning.

Abdominal distention may be noted, as well as signs of dysfunction of other organs. Symptoms may be subtle in patients on corticosteroids, in diabetic patients with advanced neuropathy, and in hospitalized patients, especially the very young and the very old. In the presence of ascites, decreased friction between the visceral and parietal peritoneal surfaces may reduce the symptoms of abdominal pain, as seen in patients with SBP.

Anorexia and nausea are frequent symptoms and may precede the development of abdominal pain. Vomiting may be due to underlying visceral organ pathology (ie, obstruction) or be secondary to peritoneal irritation.


Physical Examination

On physical examination, patients with peritonitis generally appear unwell and in acute distress. Many of them have a temperature that exceeds 38° C, although patients with severe sepsis may become hypothermic. Tachycardia may be present, as a result of the release of inflammatory mediators, intravascular hypovolemia from anorexia, vomiting and fever, and third-space losses into the peritoneal cavity. With progressive dehydration, patients may become hypotensive (5-14% of patients), as well as oliguric or anuric; with severe peritonitis, they may present in overt septic shock.

When examining the abdomen of a patient with suspected peritonitis, the patient should be supine. A roll or pillows underneath the patient's knees may allow for better relaxation of the abdominal wall.

On abdominal examination, almost all patients demonstrate tenderness to palpation. In most patients—even those with generalized peritonitis and severe diffuse abdominal pain—the point of maximal tenderness or referred rebound tenderness roughly overlies the pathologic process (ie, the site of maximal peritoneal irritation).

Most patients demonstrate increased abdominal wall rigidity. The increase in abdominal wall muscular tone may be voluntary, in response to or in anticipation of the abdominal examination, or involuntary because of the peritoneal irritation. Patients with severe peritonitis often avoid all motion and keep their hips flexed to relieve the abdominal wall tension. The abdomen is often distended, with hypoactive-to-absent bowel sounds. This finding reflects a generalized ileus and may not be present if the infection is well localized. Occasionally, the abdominal examination reveals an inflammatory mass.

Signs of hepatic failure (eg, jaundice, angiomata) may be noted.

Rectal examination often elicits increased abdominal pain, particularly with inflammation of the pelvic organs, but rarely indicates a specific diagnosis. A tender inflammatory mass toward the right may indicate appendicitis, and anterior fullness and fluctuation may indicate a cul de sac abscess.

In female patients, vaginal and bimanual examination findings may be consistent with pelvic inflammatory disease (eg, endometritis, salpingo-oophoritis, tubo-ovarian abscess), but exam findings are often difficult to interpret in severe peritonitis.

A complete physical examination is important for excluding conditions whose presentation may resemble that of peritonitis. Thoracic processes with diaphragmatic irritation (eg, empyema), extraperitoneal processes (eg, pyelonephritis, cystitis, acute urinary retention), and abdominal wall processes (eg, infection, rectus hematoma) may mimic certain signs and symptoms of peritonitis. Always examine the patient for the presence of external hernias to rule out intestinal incarceration.

Remember that the presentation and the findings on clinical examination may be entirely inconclusive or unreliable in patients with significant immunosuppression (eg, severe diabetes, steroid use, posttransplant status, HIV infection), in patients with altered mental state (eg, head injury, toxic encephalopathy, septic shock, analgesic agents), in patients with paraplegia, and in patients of advanced age. With localized deep peritoneal infections, fever and/or an elevated WBC count may be the only signs present. As many as 20% of patients with SBP demonstrate very subtle signs and symptoms. New onset or deterioration of existing encephalopathy may be the only sign of the infection at the initial presentation. Most patients with tuberculous peritonitis demonstrate vague symptoms and may be afebrile.

Contributor Information and Disclosures

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.


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.

  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].

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


Trauma (mostly penetrating)


Stomach Peptic ulcer perforation

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

Trauma (mostly penetrating)


Duodenum Peptic ulcer perforation

Trauma (blunt and penetrating)


Biliary tract Cholecystitis

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


Choledochal cyst (rare)

Trauma (mostly penetrating)


Pancreas Pancreatitis (eg, alcohol, drugs, gallstones)

Trauma (blunt and penetrating)


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



Ulcerative colitis and Crohn disease


Colonic volvulus

Trauma (mostly penetrating)


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
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


Etiologic Organisms Antibiotic Therapy


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


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
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.