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Peritonitis and Abdominal Sepsis Medication

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

Medication Summary

The goals of pharmacotherapy in patients with peritonitis and abdominal sepsis are to reduce morbidity and prevent complications. The agents used are antimicrobials such as cefotaxime, gentamicin, ampicillin, and sulfamethoxazole.

Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting. Traditionally, a combination of an aminoglycoside and ampicillin was used to treat SBP. This regimen affords excellent empiric coverage of more than 90% of SBP cases caused by gram-negative aerobes or gram-positive cocci. More recently, the third-generation cephalosporin cefotaxime has been demonstrated to be as effective as the ampicillin/aminoglycoside combination, and it does not carry the increased risk of nephrotoxicity in cirrhotic patients. Cefotaxime does not cover enterococci, which are the pathogen in up to 5% of cases.



Class Summary

Cephalosporins are structurally and pharmacologically related to penicillins. They inhibit bacterial cell wall synthesis, resulting in bactericidal activity. Cephalosporins are divided into first, second, third, and fourth generation. First-generation cephalosporins have greater activity against gram-positive bacteria, and succeeding generations have increased activity against gram-negative bacteria and decreased activity against gram-positive bacteria.

Cefotaxime (Claforan)


Cefotaxime is a third-generation cephalosporin with a broad gram-negative spectrum, lower efficacy against gram-positive organisms, and higher efficacy against resistant organisms. Thus, it provides excellent empiric coverage of SBP.

Cefuroxime (Ceftin, Kefurox, Zinacef)


Second-generation cephalosporin; maintains gram-positive activity of first-generation cephalosporins; adds activity against P mirabilis, H influenzae, E coli, K pneumoniae, and M catarrhalis.

Binds to penicillin binding proteins and inhibits final transpeptidation step of peptidoglycan synthesis, resulting in cell wall death. Condition of patient, severity of infection, and susceptibility of microorganism determines proper dose and route of administration. Resists degradation by beta-lactamase.

Ceftriaxone (Rocephin)


Ceftriaxone is a third-generation cephalosporin with broad-spectrum, gram-negative activity; lower efficacy against gram-positive organisms; and higher efficacy against resistant organisms. Its bactericidal activity results from inhibiting cell wall synthesis by binding to one or more penicillin-binding proteins. It exerts an antimicrobial effect by interfering with synthesis of peptidoglycan, a major structural component of bacterial cell walls. Bacteria eventually lyse due to the ongoing activity of cell wall autolytic enzymes while cell wall assembly is arrested.

Ceftriaxone is highly stable in the presence of beta-lactamases, both penicillinase and cephalosporinase, of gram-negative and gram-positive bacteria. Approximately 33-67% of the dose is excreted unchanged in the urine; the remainder is secreted in bile and ultimately in feces as microbiologically inactive compounds. Ceftriaxone reversibly binds to human plasma proteins, and the binding decreases from 95% bound at plasma concentrations of less than 25 mcg/mL to 85% bound at 300 mcg/mL.



Cefotetan is a second-generation cephalosporin used as single-drug therapy to provide broad gram-negative coverage and anaerobic coverage. Also provides some coverage of gram-positive bacteria. Half-life is 3.5 h. Inhibits bacterial cell wall synthesis by binding to one or more of the penicillin-binding proteins; inhibits final transpeptidation step of peptidoglycan synthesis, resulting in cell wall death.



Cefepime is a fourth-generation cephalosporin. Gram-negative coverage comparable to ceftazidime but has better gram-positive coverage (comparable to ceftriaxone). Cefepime is a zwitter ion; rapidly penetrates gram-negative cells. Best beta-lactam for IM administration.



Class Summary

Aminoglycosides are bactericidal antibiotics used primarily to treat gram-negative infections. They interfere with bacterial protein synthesis by binding to 30S and 50S ribosomal subunits.

Gentamicin (Gentacidin, Garamycin)


Gentamicin is an aminoglycoside antibiotic effective against Pseudomonas aeruginosa; E coli; and Proteus, Klebsiella, and Staphylococcus species. Gentamicin is also variably effective against some strains of certain gram-positive organisms, including S aureus, enterococci, and L monocytogenes. Dosing regimens are numerous; adjust the dose based on creatinine clearance and changes in volume of distribution. Gentamicin may be given IV/IM. Gentamicin has been reported to offer additive or synergistic activity against enterococci when used with ampicillin.



Class Summary

The penicillins are bactericidal antibiotics that work against sensitive organisms at adequate concentrations and inhibit the biosynthesis of cell wall mucopeptide.

Piperacillin and Tazobactam sodium (Zosyn)


Piperacillin is a semisynthetic extended-spectrum penicillin that inhibits bacterial cell wall synthesis by binding to specific penicillin-binding proteins; it is the most effective of the antipseudomonal penicillins.

Tazobactam increases piperacillin activity against S aureus, Klebsiella, Enterobacter, and Serratia species; the greatest increase is in activity against B fragilis. However, it does not increase anti–P aeruginosa activity.

Amoxicillin and clavulanate (Augmentin)


Amoxicillin inhibits bacterial cell wall synthesis by binding to penicillin-binding proteins; clavulanate inhibits beta-lactamase producing bacteria. This combination is a good alternative antibiotic for patients allergic or intolerant to the macrolide class. Usually, it is well tolerated, and provides good coverage for most infectious agents. It is not effective against Mycoplasma and Legionella species. The half-life of the oral dosage form is 1-1.3 hours. It has good tissue penetration but does not enter cerebrospinal fluid.

Ticarcillin and clavulanate potassium (Ticar)


This combination of an antipseudomonal penicillin with a beta-lactamase inhibitor provides coverage against most gram-positive and gram-negative organisms, as well as most anaerobes. It inhibits biosynthesis of cell wall mucopeptide and is effective during the stage of active growth.

Ampicillin (Omnipen, Marcillin)


Ampicillin interferes with bacterial cell wall synthesis during active multiplication, causing bactericidal activity against susceptible organisms. Dose adjustments may be necessary in renal failure. Rash should be evaluated carefully to differentiate nonallergic ampicillin rash from hypersensitivity reaction.



Class Summary

Macrolide antibiotics have bacteriostatic activity and exert their antibacterial action by binding to the 50S ribosomal subunit of susceptible organisms, resulting in inhibition of protein synthesis

Tobramycin (Nebcin)


Tobramycin is used in skin, bone, and skin structure infections, caused by S aureus, P aeruginosa, Proteus species, E coli, Klebsiella species, and Enterobacter species. It is indicated in the treatment of staphylococcal infections when penicillin or potentially less-toxic drugs are contraindicated and when bacterial susceptibility and clinical judgment justifies its use. Like other aminoglycosides, tobramycin is associated with nephrotoxicity and ototoxicity.

Clindamycin (Cleocin)


Clindamycin is a semisynthetic antibiotic produced by 7(S)-chloro-substitution of 7(R)-hydroxyl group of its parent compound lincomycin. It inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. Clindamycin distributes widely in the body without penetration of the CNS. Clindamycin is protein bound and is excreted by the liver and kidneys.



Class Summary

Carbapenems are structurally related to penicillins and have broad-spectrum bactericidal activity. The carbapenems exert their effect by inhibiting cell wall synthesis, which leads to cell death. They are active against gram-negative bacteria, gram-bacteria, and anaerobes.

Meropenem (Merrem IV)


A bactericidal broad-spectrum carbapenem antibiotic that inhibits cell-wall synthesis, meropenem is effective against most gram-positive and gram-negative bacteria. Compared with imipenem, meropenem has slightly increased activity against gram-negative organisms and slightly decreased activity against staphylococci and streptococci.

Aztreonam (Azactam)


Aztreonam is a monobactam, not a beta-lactam, antibiotic that inhibits cell wall synthesis during bacterial growth. It is active against gram-negative bacilli but has very limited gram-positive activity and is not useful for anaerobes. Aztreonam lacks cross-sensitivity with beta-lactam antibiotics. It may be used in patients allergic to penicillins or cephalosporins. Transient or persistent renal insufficiency may prolong serum levels.

Ertapenem (Invanz)


The bactericidal activity of ertapenem results from inhibition of cell wall synthesis and is mediated through binding to penicillin-binding proteins. Ertapenem is stable against hydrolysis by a variety of beta-lactamases, including penicillinases, cephalosporinases, and extended spectrum beta-lactamases; it is hydrolyzed by metallo-beta-lactamases.

Imipenem and cilastatin (Primaxin)


This combination is used for treatment of infections with multiple organisms because other agents do not have wide spectrum coverage or are contraindicated due to potential for toxicity.



Class Summary

Fluoroquinolones have broad-spectrum activity against gram-positive and gram-negative aerobic organisms. They inhibit DNA synthesis and growth by inhibiting DNA gyrase and topoisomerase, which is required for replication, transcription, and translation of genetic material.

Ciprofloxacin (Cipro)


Ciprofloxacin, a fluoroquinolone, inhibits bacterial DNA synthesis and, consequently, growth, by inhibiting DNA gyrase and topoisomerase, which is required for replication, transcription, and translation of genetic material. Quinolones have broad activity against gram-positive and gram-negative aerobic organisms. It has no activity against anaerobes. Continue treatment for at least 2 days (7-14 d typical) after signs and symptoms have disappeared. In prolonged therapy, perform periodic evaluations of organ system functions (eg, renal, hepatic, hematopoietic); adjust the dose in the presence of renal function impairment. Superinfections may occur with prolonged or repeated antibiotic therapy.

Norfloxacin (Chibroxin, Noroxin)


Norfloxacin is a fluoroquinolone with activity against pseudomonads, streptococci, MRSA, S epidermidis, and most gram-negative organisms, but it has no activity against anaerobes. It inhibits bacterial DNA synthesis and, consequently, growth.



Class Summary

Anti-infectives such as metronidazole and sulfamethoxazole/trimethoprim are effective against some types of bacteria that have become resistant to other antibiotics.

Sulfamethoxazole and trimethoprim (Bactrim, Bactrim DS, Cotrim, Cotrim DS, Septra, Septra DS)


Trimethoprim-sulfamethoxazole inhibits bacterial growth by inhibiting the synthesis of dihydrofolic acid. Its antibacterial activity includes common urinary tract pathogens, except Pseudomonas aeruginosa.

Metronidazole (Flagyl)


Metronidazole is an imidazole ring-based antibiotic active against various anaerobic bacteria and protozoa. It is used in combination with other antimicrobial agents (but is used as monotherapy in C difficile enterocolitis).


Glycylcycline Antibiotic

Class Summary

Glycylcycline antibiotics are structurally similar to tetracycline antibiotics and were developed to overcome bacterial mechanisms of tetracycline resistance. Tigecycline is the first drug approved in this class.

Tigecycline (Tygacil)


Tigecycline is a glycylcycline antibiotic that is structurally similar to tetracycline antibiotics. It is used for complicated intra-abdominal infections caused by C freundii, E cloacae, E coli, K oxytoca, K pneumoniae, E faecalis (vancomycin-susceptible isolates only), S aureus (methicillin-susceptible isolates only), S anginosus group. (includes S anginosus, S intermedius, and S constellatus), B fragilis, B thetaiotaomicron, B uniformis, B vulgatus, C perfringens, and P micros. Use with caution in patients with severe hepatic impairment.

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
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