|Year : 2014 | Volume
| Issue : 2 | Page : 170-172
Helicobacter pylori in gastroduodenal perforation
Bharat B Dogra, Sunil Panchabhai, Santosh Rejinthal, Sai Kalyan, Siddharth Priyadarshi, Ashwani Kandari
Department of Surgery, Padmashree Dr. D Y Patil Medical College Hospital and Research Centre, Dr. D Y Patil Vidyapeeth, Pimpri, Pune, Maharashtra, India
|Date of Web Publication||4-Feb-2014|
Bharat B Dogra
Prof of Surgery, Padmashree Dr. D Y Patil Medical college Hospital and Research Centre, Pimpri, Pune
Source of Support: None, Conflict of Interest: None
Background:peptic ulcers were earlier believed to be caused by dietary factors, gastric acid, and stress. However, in 1983, Warren and Marshall identified the correlation between Helicobacter pylori (H. pylori) and peptic ulcers. It is now well established that most of the peptic ulcers occur as a result of H. pylori infection. But the co-relation between perforated peptic ulcer and H. pylori infection is not yet fully established. Aims and objectives : to study the prevalence of H. pylori infection in patients with perforated peptic ulcer. Materials and methods: this was a prospective study carried out in all cases of perforated peptic ulcer reporting in surgical wards of a medical college during 2008-2010. A total of 50 cases, presenting as acute perforation of duodenum and stomach during this period, formed the study group. After resuscitation, all the cases were subjected to emergency exploratory laparotomy. The exact site of perforation was identified, biopsy was taken from the ulcer margin from 2-3 sites and the tissue was sent for H. pylori culture and histopathological examination. Simple closure of perforation, omentoplasty, thorough peritoneal lavage and drainage was carried out. Results: out of the 50 cases of perforated peptic ulcer, 38 happened to be males, and only 12 were females. The age of the patients ranged from 20 to 70 years. All the patients underwent only emergency laparotomy. As many as 46 cases (92%) turned out to be positive for H. pylori and only four cases (8%) were negative for this infection. Postoperatively, patients who were found to be positive for H. pylori were put on anti-H. pylori treatment. Conclusion: there was a high prevalence of H. pylori infection in patients with perforated gastroduodenal ulcers.
Keywords: Gastroduodenal perforation, Helicobacter pylori, peptic ulcer
|How to cite this article:|
Dogra BB, Panchabhai S, Rejinthal S, Kalyan S, Priyadarshi S, Kandari A. Helicobacter pylori in gastroduodenal perforation. Med J DY Patil Univ 2014;7:170-2
|How to cite this URL:|
Dogra BB, Panchabhai S, Rejinthal S, Kalyan S, Priyadarshi S, Kandari A. Helicobacter pylori in gastroduodenal perforation. Med J DY Patil Univ [serial online] 2014 [cited 2020 Aug 8];7:170-2. Available from: http://www.mjdrdypu.org/text.asp?2014/7/2/170/126331
| Introduction|| |
Peptic ulcers were earlier believed to be caused by stress, dietary factors, and increased gastric acid secretion till as late as 1983, when Warren and Marshall identified the correlation between Helicobacter pylori infection and peptic ulcers.  It is now well established that most peptic ulcers occur as a result of H. pylori infection. Approximately 50% of the world population is infected with H. pylori.  Prevalence varies with geography, age, race, ethnicity, socioeconomic status and is seen to decrease with improved hygiene.  In developing countries, H. pylori infection is usually acquired during childhood, with infection rates ranging from 13.4% to 24%. There have been recent reports of declining H. pylori infections in developed countries. 
One of the complications of peptic ulcer disease is perforation and such patients used to be managed earlier by definitive surgical procedures in the form of vagotomy and gastrojejunostomy or pyloroplasty. But since the identification of H. pylori as the causative agent, the treatment protocol has also changed dramatically to simple closure of perforation followed by full course of anti- H. pylori treatment by administration of standard triple therapy. This method has reduced the incidence of residual and recurrent ulcers. 
| Materials and methods|| |
This was a prospective study carried out in patients with gastroduodenal perforation who were admitted to a medical college hospital from July 2008 to Sep 2010. A pro forma was designed, which included demographic data, signs, symptoms, confirmatory investigations, diagnosis, and management. All the patients were managed by surgical exploration through midline supra-umbilical incision and sucking out or mopping off the peritoneal fluid. Stomach and duodenum were scanned in all the cases to locate perforation in the anterior or posterior wall. A note was made about the exact site and size of perforation. Three biopsy samples were taken from 3, 6, and 9 o'clock positions of the perforation and subjected to Giemsa stain, urease test, and culture, respectively. Closure of perforation was carried out by using 3-4 simple interrupted sutures followed by omentoplasty by using a pedicled omental patch to augment and cover the suture line. Peritoneal toilet was carried out with saline and a pelvic drain was kept in all the cases for 48 h. Patients found to be positive for H. pylori were put on medical therapy that comprised of Cap Lansoprazole 30 mg, Tab Tinadazole 500 mg, and Tab Clarithromycin 250 mg twice daily for 14 days. These patients were followed up for a period of 6 months and subjected to endoscopic evaluation on review at 8, 16, and 24 weeks postoperatively.
| Results|| |
A total of 50 patients who developed perforation were operated during the study period. Out of these, 38 were males and 12 were females, in the ratio of 3:1. The highest incidence was found in the age group of 41-50 years (mean age being 49.2 years) [Table 1]. Severe pain in epigastrium was the main symptom. In our study, 64% of patients gave the history of smoking and as many as 40% of patients had history of alcohol consumption. Out of 50 cases studied, 42 patients (84%) were found to be having duodenal ulcer perforation and only eight patients (16%) had gastric ulcer perforation. Duodenal perforation was found on the anterior wall of first part of duodenum in all the cases. Of cases having involvement of stomach, five had perforation over anterior wall in a prepyloric region, two had posterior wall perforation, and one patient had perforation over lesser curvature. In our study, 46 (92%) patients were positive for H. pylori, out of which 42 patients were of duodenal perforation and only four were having gastric perforation [Table 2].
H. pylori was detected by Giemsa stain in 42 patients. However, urease test was positive only in 30 patients and culture was positive in 10 patients. Giemsa stain showed 91.3% sensitivity, 100% specificity, and high positive predictive value of 100% in detecting H. pylori [Table 3].
All the 46 patients detected positive for H. pylori were given anti-H. pylori medical treatment for 14 days while the remaining four patients were given only Cap Lansoprazole 30 mg BD for 14 days postoperatively. The patients were called for follow up at 8, 16, and 24weeks, respectively. All the 50 patients reported for 8-week follow up and most of them were asymptomatic, but dyspeptic symptoms were present in 4 patients. Endoscopic evaluation was carried out in all the cases. There was evidence of satisfactory healing of ulcer in 42 patients. Four cases that reported with persistent dyspeptic symptoms showed incomplete healing on endoscopic examination. Such patients were put on second course of anti-H. pylori treatment for another 14 days. In their subsequent follow up they showed evidence of healing of ulcers.
| Discussion|| |
In this study of 50 cases of gastro-duodenal perforation, H. pylori infection, most of the patients were middle-aged. Male to female ratio was 3:1. This is comparable with studies reported earlier by Ng et al. and Aman et al. ,
Prevalence of H. pylori infection in peptic ulcer perforation, in our study, was 92%, whereas, Aman et al., in their study, found the prevalence of 85.1%.  The association of H. pylori infection with duodenal ulcer perforation was even more striking in that out of 42 cases of duodenal ulcer perforation, H. pylori was detected in 40 cases (95%). Ng et al., in their series found 70% prevalence of H. pylori infection with duodenal perforation. 
Kumar et al. conducted a study on 49 patients with duodenal perforation by the means of three diagnostic methods (rapid urease test, histology, and culture method), and reported infection rate of 57%. He found rapid urease test as the most sensitive diagnostic method with reported prevalence of 70%. 
In this study, Giemsa stain had high validity for detecting H. pylori. Lofelld et al. conducted study on 302 patients with perforated peptic ulcers and found 78% accuracy in detecting H. pylori by Giemsa stain from biopsy sample. 
In our study, out of 50 patients 46 (92%) were positive for H. pylori. They were given anti-H. pylori treatment by administration of standard triple therapy for 14 days, the remaining four patients were given only Capsule Lansoprozole 30 mg BD for 14 days. There was significant decrease in postoperative symptoms in patients who were given anti-H. pylori treatment, following closure of perforation. Ng et al. in their series found that out of 99 H. pylori patients, 51 were assigned to an anti-H. pylori therapy, and 48 to Omeprazole alone. After 1 year, ulcer relapse was significantly lower in patient treated with an anti-H. pylori therapy.  Likewise, Chu et al. concluded that recurrent ulcer disease in patients with history of perforated duodenal ulcer is related to H. pylori infection.  In our study, all the patients were subjected to endoscopic evaluation after 8 weeks of completion of anti-H. pylori regimen and satisfactory healing was observed in 42 out of 46 cases. Four cases were still symptomatic at 8 weekly review and the ulcers had not healed on endoscopic evaluation. These patients were given another course of anti-H. pylori drugs for 2 weeks and subsequent review revealed healing of ulcer. Therefore, definitive surgeries such as truncal vagotomy and pyloroplasty or gastrojejunostomy were avoided in all the cases.
| Conclusion|| |
Our study indicates a high prevalence of H. pylori infection in patients with perforated peptic ulcers, duodenal as well as gastric ulcers.
The high positive predictive value of 100% of Giemsa stain indicates potential for it being a screening test for H. pylori infections. However, because of high overall prevalence of H. pylori infection in developing countries giving rise to high prior probability, this needs to be validated in other settings.
An early detection of H. pylori and potent anti-H. pylori therapy postoperatively has been found to be adequate in complete healing of these ulcers after simple closure of the ulcer.
| References|| |
|1.||Marshall BJ, Warren JR. Unidentified curved bacilli in the stomach of patients with gastric and peptic ulcerations. J Clin Pathol 1984;323:1311-5. |
|2.||Rauwi EJ, Tygat GN. Helicobacter Pylori in Duodenal and Gastric Ulcer Disease. J Gastroenterol 1995;9:529-47. |
|3.||Goodwin CS, Mendall MM, Northfield TC. Helicobacter Pylori Infection. J Clin Pathol 1997;349:265-9. |
|4.||Brown LM. Helicobacter Pylori Epidemiology and Modes of Transmission. J Gastroenterol 2000;22:283-97. |
|5.||Svanes C. Trends in Perforated Peptic Ulcer: Incidence, Etiology, Treatment, and Prognosis. World J Surg 2000;24:277-83. |
|6.||Ng EK, Lam YH, Sung JJ, Yung MY, To KF, Chan AC, et al. Eradication of Helicobacter pylori prevents recurrence of ulcer after simple closure of duodenal ulcer perforation: Randomized controlled trial. Ann Surg 2000;231:153-8. |
|7.||Aman Z, Afridi V, Khan J. Prevalence of H. Pylori in Perforated Peptic Ulcer. J Postgrad Med Inst 2002;16:195-9. |
|8.||Kumar D, Sinha AN. Helicobacter pylori infection delays ulcer healing in patients operated on for perforated duodenal ulcer. Indian J Gastroenterol 2002;21:19-22. |
|9.||Loffeld RJ, Stobberingh E, Flendrig JA, Arends JW. Helicobacter pylori in gastric biopsy specimens. Comparison of culture, Modified giemsa stain and immune histo-chemistry: A retrospective study. J Pathol 1991;165:60-73. |
|10.||Chu KM, Kwok KF, Law SY, Tuen HH, Tung PH, Branicki FJ, et al. Helicobacter pylori status and endoscopy follow-up of patients having a history of perforated duodenal ulcer. Gastrointest Endosc 1999;50:58-62. |
[Table 1], [Table 2], [Table 3]