Study of bacterial flora and their antibiotic sensitivity in peritonitis of various causes
DOI:
https://doi.org/10.18203/2349-2902.isj20175399Keywords:
Antibiotic sensitivity, Bacterial flora, Intra-abdominal sepsis, PeritonitisAbstract
Background: Peritonitis is a common emergency encountered by surgeons the world over. Despite a better understanding of pathophysiology, advances in diagnosis, surgery, antimicrobial therapy and intensive care support, peritonitis remains a potentially fatal affliction. Intra-abdominal sepsis is important causes of mortality and morbidity. The treatment is based on rapid fluid resuscitation, initiation of antibiotic therapy and surgical intervention. The antibiotic chosen must cover the most frequently expected bacterial species depending upon the site of perforation. Objectives of the study was done to identify the type of organism present in bowel perforation and their sensitivity pattern to different antibiotics. A guideline will be framed for advising antibiotics to be used for different kinds of perforation.
Methods: This was a prospective study of one year on 50 patients of secondary peritonitis due to bowel perforation, conducted in Amaltas institute of Medical Sciences, Dewas.
Results: This study included 50 patients with an average age of 36 years (range: 3 days-75 years). There were 40 males and 10 females. The mean duration of hospitalization was 10.6 days (range: 3-25 days) with predominant site of perforation was ileum. E. coli emerged as main pathogenic microbe even in site specific culture, was closely followed by Klebsiella. A combination of third generation cephalosporins with sulbactam and metronidazole has been the most promising therapy to treat secondary bacterial peritonitis due to bowel perforation. It needs to be emphasized that although the sensitivity studies reveal an edge for meropenem over cefaperazone sulbactam, yet the preference of cephalosporin with sulbactam over meropenem is justified, considering the economic constraints and with a suitable foresight, to keep meropenem as a reserve drug because trends indicate that our microbes are fast becoming resistant to the promising combination of third generation cephalosporin with sulbactam and metronidazole.
Conclusions: This study suggests that the current recommended empirical antibiotics need to be reassessed.
References
Simmen HP, Heinzelmann M, Largiader F. Peritonitis: classification and causes. Dig Surg. 1996;13:381-3.
Gupta S, Kaushik R. Peritonitis- the Eastern experience. World J Emerg Surg. 2006;26:1-13.
European Association for the Study of the Liver, EASL clinical practice guidelines on the management of ascites, spontaneous bacterial peritonitis, and hepatorenal syndrome in cirrhosis. Journal of Hepatology. 2010;53(3):397-417.
Ageloni S, Leboffe C, Parente A. Efficacy of current guidelines for the treatment of spontaneous bacterial peritonitis in the clinical practice. World Journal of Gastroenterology. 2008;14(17):2757-62.
Lee JM, Han KH, Ahn SH. Ascites and spontaneous bacterial peritonitis: an Asian perspective. J Gastroenterol Hepatol. 2009;24(9):1494-503.
Garcia-Tsao G. Current management of the complications of cirrhosis and portal hypertension: variceal hemorrhage, ascites, and spontaneous bacterial peritonitis. Gastroenterol. 2001;120 (3):726-48.
Park MK, Lee JH, Byun YH. Changes in the profiles of causative agents and antibiotic resistance rate for spontaneous bacterial peritonitis: an analysis of cultured microorganisms in recent 12 years. The Korean Journal of Hepatology. 2007;13(3):370-7.
Singh N, Wagener MM, Gayowski T. Changing epidemiology and predictors of mortality in patients with spontaneous bacterial peritonitis at a liver transplant unit. Clin Microbiol Infection. 2003;9(6):531-7.
Lee JH, Yoon JH, Kim BH. Enterococcus: not an innocent bystander in cirrhotic patients with spontaneous bacterial peritonitis. Eu J Clin Microbiol Infectious Dis. 2009;28(1):21-6.
Alexopoulou A, Papadopoulos N, Eliopoulos DG. Increasing frequency of gram-positive cocci and gram-negative multidrug- resistant bacteria in spontaneous bacterial peritonitis. Liver International. 2013;33(7):975-81.
Mosdell DM, Morris DM, Voltura A. Antibiotic treatment for surgical peritonitis. Ann Surg. 1991;214(5):543-9.
Nathens AB, Rotstein OD. Therapeutic options in peritonitis. Surg Clin North Am. 1994;74(3):677-92.
Laroche M, Harding G. Primary and secondary peritonitis: an update. Eur J Clin Microbiol Infect Dis. 1998;17(8):542-50.
Christou NV, Barie PS, Dellinger EP. Surgical Infection Society Intra-Abdominal Infection Study: prospective evaluation of management techniques and outcome. Arch Surg. 1993;128(2):193-9.
Altemeier WA. The bacterial flora of acute perforated appendicitis with peritonitis: a bacteriologic study based upon one hundred cases. Ann Surg. 1938;107(4):517-28.
Genné D, Menetrey A, Jaquet A, Indino P, Sénéchaud C, Siegrist H. Treatment of Secondary Peritonitis: Is a Less Expensive Broad-Spectrum Antibiotic as Effective as a Carbapenem? Dig Surg. 2003;20:415-20.
Solomkin JS, Dellinger EP, Christou NV, Busuttil RW. Results of a multicentre trial comparing imipenem/cilastatin to tobramycin/clindamycin for intra-abdominal infections. Ann Surg. 1990; 212(5):581-91.
Solomkin JS, Flohr AM, Simmons RL. Indications for Therapy for Fungemia in Postoperative Patients. Arch Surg. 1982;117(10):1272-5.
Peoples JB. Candida and perforated peptic ulcers. Surgery. 1986;100(4):758-64.
Krobot K, Yin D, Zhang Q, et al. Effect of inappropriate initial empiric antibiotic therapy on outcome of patients with community-acquired intra-abdominal infections requiring surgery. Eur J Clin Microbiol Infect Dis. 2004;23:682-7.
