Table of Contents  
ORIGINAL ARTICLE
Year : 2014  |  Volume : 7  |  Issue : 5  |  Page : 564-568  

Perforated duodenal ulcer: Emerging pattern


Department of Surgery, Dr. D. Y. Patil Medical College, Hospital and Research Centre, Dr. D. Y. Patil Vidyapeeth, Pimpri, Pune, Maharashtra, India

Date of Web Publication10-Sep-2014

Correspondence Address:
Murtaza Ali Asger Calcuttawala
Department of Surgery, Dr. D.Y. Patil Medical College, Sant Tukaram Nagar, Pimpri, Pune - 411 018, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0975-2870.140385

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  Abstract 

Background: A total of 27 patients of perforated duodenal ulcer admitted in our institution between December 2010 and November 2012 were treated and studied. Materials and Methods: All patients were diagnosed on the basis of clinical and radiological findings, exploratory laparotomy was performed and simple closure of perforation with placement of Graham's omental patch was carried out. This was followed by triple regimen for Helicobacter pylori eradication. Results: All patients were male, maximum incidence (61.54%) was noted in the age group of 21-30, 'O' +ve blood group was most commonly observed in our patients. Eight patients had history suggestive of acute acid peptic disease. Mean time interval between the start of symptoms and surgery was 43 h. No morbidity except minimal pleural effusion was seen in one case. There was no mortality in our series. Conclusion: We conclude that although a number of definitive surgeries have been described for acid peptic disease, but the requirement of such procedures has come down due to increasing use of H. pylori eradication therapy and proton pump inhibitors. However, surgery for complications especially for duodenal ulcer perforation has not reduced concomitantly. Incidence is greater in young males.

Keywords: Duodenal ulcer, Helicobacter pylori, NSAID, perforation


How to cite this article:
Calcuttawala MA, Nirhale DS, Athavale VS, Bhatia M, Kale A, Singh V. Perforated duodenal ulcer: Emerging pattern. Med J DY Patil Univ 2014;7:564-8

How to cite this URL:
Calcuttawala MA, Nirhale DS, Athavale VS, Bhatia M, Kale A, Singh V. Perforated duodenal ulcer: Emerging pattern. Med J DY Patil Univ [serial online] 2014 [cited 2022 Jan 17];7:564-8. Available from: https://www.mjdrdypu.org/text.asp?2014/7/5/564/140385


  Introduction Top


Duodenal ulcer is a common condition characterized by the presence of a well-demarcated break in the mucosa that may extend into the muscularis propria of the duodenum. Despite better understanding of pathophysiology and medical therapy of acid peptic disease, duodenal ulcer perforation remains one of the major cause of peritonitis. [1],[2]

The incidence of perforated peptic ulcer in western countries is 7-9/1, 00,000 population per year. [3] The incidence of perforation of duodenal ulcers in young and middle aged patients appear to be falling but in contrast, there is currently a marked increase in the numbers of elderly. Perforation peritonitis is the most common surgical emergency in India and duodenal ulcer perforation remains the leading cause. [4]

Non-operative treatment of perforated peptic ulcer is associated with a very high incidence of mortality and has no role in the management of this serious life-threatening condition. Patient generally present with acute abdomen and once the diagnosis is confirmed, emergency laparotomy should be performed. [4] Conservative management is reserved for those who cannot withstand stress of surgery. [5] Closure of the perforation with omental patch [4] followed by eradication of Helicobacter pylori is accepted world-wide. [4]


  Materials and Methods Top


All patients of perforated duodenal ulcer admitted under care of all surgical units at Padmashree Dr. D. Y. Patil Medical College and hospital between December 2010 and November 2012 were treated and studied. All patients were initially managed with antibiotics, Ryle's tube aspiration, intravenous fluids and close monitoring of pulse rate, respiratory rate, blood pressure and urine output. Diagnosis was made on the basis of clinical presentation of patient and radiological findings of presence of free gas under diaphragm in erect chest radiograph [Figure 1].
Figure 1: X-ray chest

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Necessary investigations for anesthesia purpose were carried out and patients were prepared for laparotomy. A well-informed and written consent was taken from all patients and their relatives.

All variables related to history suggestive of acid peptic disease, smoking, alcohol consumption, NSAID use, any other associated medical diseases were noted. Then presence of clinical features pain, vomiting, fever, abdominal distension, tenderness, guarding/rigidity, tachycardia, shock was recorded. Distribution of perforated duodenal ulcer in different age groups, gender and blood group were documented. Treatment delay time was duly calculated. Intraoperative findings of peritoneal spillage, location and size of perforation were given due importance.

All laparotomies were done under general anesthesia with supra umbilical midline incision. Peritoneal spillage with bile stained fluid fibrinous exudates and flakes was found in all cases. All perforations were <1 cm in diameter with surrounding tissue edema. Peritoneal toilet was performed and perforation was closed by interrupted sutures with 3-0 silk. Graham's pedicle omental patch was reinforced at the site of perforation with 3-0 silk [Figure 2]. Thorough peritoneal lavage was given in all patients with 2-3 L of normal saline.
Figure 2: Site of perforation

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Intraabdominal drain was placed and abdominal, closure done in single layer. Postoperatively patients were kept nil by mouth until return of bowel sounds and intravenous fluids were supplemented. Intravenous antibiotics were given for 5-7 days. Patients were discharged within 14 days. At the time of discharge, they were advised to refrain from smoking, consumption of alcohol and using NSAIDs. All patients were put on triple regimen for eradication of H. pylori for 2 weeks at the time of discharge from hospital.

Post-operative morbidity, mortality and stay in hospital were assessed. These patients have been followed-up for 9 months, they remained asymptomatic.


  Result Top


In our study, all patients were male and age group varied from 17 years to 68 years with mean age of 30.43 years. Eight cases (61.54%) were seen in age group between 21 and 30 years and only one case over the age of 50 years [Figure 3]. Eight patients (61.54%) were having blood group O-positive, 3 (23.07%) patients of A-positive and 2 (15.38%) patients of 13-positive.
Figure 3: Incidence in different age groups

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Out of these 13 patients, 8 (61.54%) gave a history of symptoms suggestive of acid peptic disease for the duration varying from 1 months to 6 month for which none of them had consulted any doctor nor had taken any treatment. Three patients (23.07%) were chronic alcoholic and they also gave a history of alcohol consumption on the day before the onset of symptoms. Three patients (23.7%) had used NSAID very often and two patients (15.38%) were smoker. None of these 13 patients had any associated medical illness like tuberculosis, chronic obstructive pulmonary disease, diabetes mellitus, hypertension.

All patients came with the complains of severe pain in the abdomen. The pain was associated with multiple episodes of non-bilious vomiting. Surprisingly none of them presented with fever. Out of them 11 (84.61%) had tachycardia at the time of admission and 2 (15.3 8%) patients presented in the state of shock.

On examination, all patients had tenderness all over abdomen, which was most marked in epigastric region. Eight (61.54%) patients were having guarding/rigidity and 4 (30.77%) patients presented with abdominal distension. We studied treatment delay in two parts, one before coming to hospital, i.e., from the onset of symptoms to arrival in emergency department in hours and second delay in hospital, i.e., from the arrival of patient in the emergency department to the start of exploratory laparotomy.

Six patients (46.15%) presented on the second day i.e., (25-48 h) after the onset of symptoms. One patient (7.69%) came to hospital after 93 h and 10 min after onset of symptoms. The mean time delay before the patient came to hospital was 35 h and 30 min [Figure 4]. In hospital four patients (30.77%) were operated within 6 h of admission and nine patients (69.23%) were operated within 24 h of admission. Mean in-hospital delay was 7 h 53 min [Figure 5].

Intraoperatively peritoneal spillage, tissue edema were common findings.
Figure 4: Delay before surgery

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Figure 5: Delay in hospital

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First part of duodenum was the most common site of perforation as seen in 11 (84.61%) patients and 1 (7.69%) each in pyloric region and second part of duodenum. All these perforations were found to be on the anterior wall and there was no evidence of concomitant posterior wall perforation or bleeding through it.

All patients were discharged within 14 days with healing of wound by primary intension and uneventful post-operative period except one case.

This case had minimal pleural effusion on the right side, which seemed to be reactionary and resolved without any intervention.

The mortality rate was zero in our study.


  Discussion Top


Duodenal ulcer perforation is one of the most common causes of generalized peritonitis. [1] Though it has been seen that incidence of peptic ulcer disease as such is decreased; epidemiological data suggest that incidence of ulcer complications has remained stable or has increased slightly over last decade. [6] However, controversy exist regarding the incidence of perforated peptic ulcer: Most authors [7] reports that the number of operations for perforated peptic ulcer remains constant, whereas others [8] claim that it has risen and some state that it has fallen. [9]

Despite the decrease in surgical volume, due to decrease in elective surgery for peptic ulcer disease, [10] there is an increase in proportion of emergency operations performed for which most common indication was perforated peptic ulcer. [9],[10],[11]

Eight cases (61.54%) in our study were in the age group of 21-30 years, which is contrary to the figures in literature, which states that the incidence of duodenal ulcer perforation is decreasing in youngsters and increasing in elderly'. [2] This preponderance in youngsters may be due to life-style pattern with increased stress, smoking habits, alcohol consumption, irregularity in meals etc. In literature, it was noticed that hospital admissions and mortality is increasing in older patients. [13] In our study, we have only one case over the age of 50 and he had uneventful recovery. Svanes [14] had correlated it with cohort stating that ulcer perforation risk is common in cohort born after turn of 20 th century and less common in previous and succeeding birth cohort.

All our patients were male; as also seen in many studies. [12] This could be because of greater acid secretion in men than women [13] or because of more stress and increased indulgence in smoking by men. [12] Earlier male:female ratio was 10: 1 [13] which is now 1.5:1. [13] This may be the effect of changing pattern of smoking and increased stress in the working women which is rising in western countries. [12] Smoking is a causal factor for ulcer perforation and accounts for a major part of ulcer perforation. [16] In our study we had only two patients who used to smoke.

Eight patients had history suggestive of acid peptic disease for the duration varying from 1 month to 6 months; this suggest that all of them had acute peptic ulcer disease. Watkins et al. [9] study suggested that the majority of perforations are now of acute peptic ulcer and are unlikely to be prevented by improved therapy.

We observed that 8 (61.54%) patients in our study had "0 positive" blood group. Our observation is strongly supported by other authors. [11] Peptic ulcer has been shown to be associated with increased Lewis blood group antigen expression. [18] It is not done routinely and we did not have facilities to perform Lewis antigen expression test.

In spite of the overall decline in the incidence of peptic ulcer disease, the incidence of perforated duodenal ulcer has not been reduced in western countries; this may be due to the increased use of NSAIDs. [19] In our study, three patients (23.1%) gave a history of use of NSAIDs frequently. About one of four-ulcer perforation can be attributing to the use of NSAID. [14]

The use of NSAID has been found to be the most, common cause of peptic ulcer among patients who test negative for H. pylori. [20]

Some studies find no correlation between H. pylori infection and ulcer perforation and reports that, the eradication of H. pylori does not involve any significant reduction in the incidence of patients with perforated peptic ulcer. [21] Marshall [22] stated that H. pylori has been detected in almost 100% of patients with duodenal ulcers but in patients presenting with perforated peptic ulcer, the prevalence of H. pylori can be as low as 50%. [21] Considering all these facts and proven benefits of triple regimen for eradication of H. pylori [23] we also put all our patients on triple regimen for eradication of H. pylori post operatively. Also recurrent ulcer disease in patients with a history of perforated duodenal ulcer is related to H. pylori infection. [15]

All perforations we treated were of <1 cm in diameter. Mortality has significant bearing to the size of perforation. [24] Size of perforation greater than 5 mm was identified as risk factor for releak. [25] We did not come across a single releak in our patients.

The delay before surgical treatment is a strong determinant for lethality, complication rates and hospital cost. Patients who receive treatment within 6 h have better prognosis. Delay of more than 24 h increases morbidity and mortality. [17],[23],[24] We were fortunate that out of 13; 10 patients who were operated more than 24 h after the onset of symptoms survived without any major complication. These results should not undermine need of immediate operative management for peptic ulcer perforation for better outcome.

In our study, the cause of delay before coming to hospital were mainly lack of transportation services, unawareness of seriousness and indulgence of quacks in management of such patients in villages. The principal causes of in hospital delay were absence of accompanying relative for consent and financial support.

The significant risk factors that lead to death have been cited as presence of shock at admission and co-existent significant illness. [24] In our study, two patients came in shock but none with any coexistent disease. Out of these two, one of our patients developed a post-operative complication of minimal pleural effusion, which resolved on its own.

A study by Oribabor et al. concluded that simple omental patch and H. pylori eradication is no longer appropriate as a mode of treatment for the youths who are mostly affected in the center. Therefore advocated more widespread use of definitive ulcer surgery for most of their patients with no pre-operative risk factors. [25]

A recent study by Parmar et al. which concluded that commonest site of the perfration was at the anterior wall of the first part of the duodenum. They concluded that outcome of simple closure with omental graft was excellent as compared with definitive surgery. [26]


  Conclusion Top


We conclude that although a number of definitive surgeries have been described for acid peptic disease, but requirement of such procedures has come down due to increasing use of H. pylori eradication therapy and proton pump inhibitors. However surgery for complications especially for duodenal ulcer perforation has not reduced concomitantly. Incidence has been greater in young males. Now-a-days perforations are seen more in acute peptic ulcer disease. NSAID is one of the contributing etiological factors. Early diagnosis and timely management is advocated to reduce morbidity and mortality.

 
  References Top

1.Gupta BS, Talukdar RN, Neupane HC. Cases of perforated duodenal ulcer treated in College of Medical Sciences, Bharatpur over a period of one year. Kathmandu Univ Med J (KUMJ) 2003;1:166-9.  Back to cited text no. 1
    
2.Simmen HP, Heinzelmann M, Largiader F. Pentonitis: classification and causes. Dig Surg 1996;13:381-3.  Back to cited text no. 2
    
3.Watkins RM, Dennison AR, Collin J. What has happened to perforated peptic ulcer? Br J Surg 1984;71:774-6.  Back to cited text no. 3
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4.Jhobta RS, Attri AK, Kaushik R, Sharma R, Jhobta A. Spectrum of perforation peritonitis in India - Review of 504 consecutive cases. World J Emerg Surg 2006;1:26.  Back to cited text no. 4
    
5.Keane TE, Dillon B, Afdhal NH, McCormack CJ. Conservative management of perforated duodenal ulcer. Br J Surg 1988;75:583-4.  Back to cited text no. 5
    
6.Paimela H, Paimela L, Myllykangas-Luosujärvi R, Kivilaakso E. Current features of peptic ulcer disease in Finland: Incidence of surgery, hospital admissions and mortality for the disease during the past twenty-five years. Scand J Gastroenterol 2002;37:399-403.  Back to cited text no. 6
    
7.Sacco R, Giovanelli A, Giuliano L, Piazzalunga D, Poletti EM, Arrigoni F, et al. Epidemiological behavior of perforated peptic ulcer before and after the introduction of the antisecretory drug therapy. Our experience. Minerva Chir 1995;50:871-8.   Back to cited text no. 7
    
8.Andersen IB, Bonnevie O, Jørgensen T, Sørensen TI. Time trends for peptic ulcer disease in Denmark, 1981-1993. Analysis of hospitalization register and mortality data. Scand J Gastroenterol 1998;33:260-6.  Back to cited text no. 8
    
9.Watkins RM, Dennison AR, Collin J. What has happened to perforated peptic ulcer? Br J Surg 1984;71:774-6.  Back to cited text no. 9
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10.Paimela H, Oksala NK, Kivilaakso E. Surgery for peptic ulcer today. A study on the incidence, methods and mortality in surgery for peptic ulcer in Finland between 1987 and 1999. Dig Surg 2004;21:185-91.   Back to cited text no. 10
    
11.Kleeff J, Friess H, Büchler MW. How Helicobacter pylori changed the life of surgeons. Dig Surg 2003;20:93-102.  Back to cited text no. 11
    
12.Koo J, Ngan YK, Laun SK. Trends in hospital admission, perforation and mortality of peptic ulcer in Hong Kong from 1970 to 1980. Gastroenterol 1983;84:1558-62.  Back to cited text no. 12
    
13.Svanes C, Salvesen H, Stangeland L, Svanes K, Søreide O. Perforated peptic ulcer over 56 years. Time trends in patients and disease characteristics. Gut 1993;34:1666-71.  Back to cited text no. 13
    
14.Svanes C. Trends in perforated peptic ulcer: Incidence, etiology, treatment, and prognosis. World J Surg 2000;24:277-83.  Back to cited text no. 14
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15.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.  Back to cited text no. 15
    
16.Svanes C, Søreide JA, Skarstein A, Fevang BT, Bakke P, Vollset SE, et al. Smoking and ulcer perforation. Gut 1997;41:177-80.  Back to cited text no. 16
    
17.Sharma SS, Mamtani MR, Sharma MS, Kulkarni H. A prospective cohort study of postoperative complications in the management of perforated peptic ulcer. BMC Surg 2006;6:8.  Back to cited text no. 17
    
18.Zheng PY, Tang FA, Qi YM, Li J. Association of peptic ulcer with increased expression of Lewis antigens, but not vacuolating cytotoxin activity or babA2 gene status, in Helicobacter pylori strains from China. Chin J Dig Dis 2006;7:61-5.  Back to cited text no. 18
    
19.Bjorkman DJ. Current status of nonsteroidal anti-inflammatory drug (NSAID) use in the United States: Risk factors and frequency of complications. Am J Med 1999;107:3S-8.  Back to cited text no. 19
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20.McColl KE, el-Nujumi AM, Chittajallu RS, Dahill SW, Dorrian CA, el-Omar E, et al. A study of the pathogenesis of Helicobacter pylori negative chronic duodenal ulceration. Gut 1993;34:762-8.  Back to cited text no. 20
    
21.Reinbach DH, Cruickshank G, McColl KE. Acute perforated duodenal ulcer is not associated with Helicobacter pylori infection. Gut 1993;34:1344-7.  Back to cited text no. 21
    
22.Marshall BJ. Helicobacter pylori. Am J Gastroenterol 1994;89:S116-28.  Back to cited text no. 22
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23.Svanes C, Lie RT, Svanes K, Lie SA, Søreide O. Adverse effects of delayed treatment for perforated peptic ulcer. Ann Surg 1994;220:168-75.  Back to cited text no. 23
    
24.Subedi SK, Afaq A, Adhikary S, Niraula SR, Agrawal CS. Factors influencing mortality in perforated duodenal ulcer following emergency surgical repair. JNMA J Nepal Med Assoc 2007;46:31-5.  Back to cited text no. 24
    
25.Oribabor FO, Adebayo BO, Aladesanmi T, Akinola DO. Perforated duodenal ulcer; management in a resource poor, semi-urban nigerian hospital. Niger J Surg 2013;19:13-5.  Back to cited text no. 25
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26.Parmar H, Prajapati M, Shah R. Recent trends in peptic perforation. Int J Med Sci Public Health 2013;2:110-2.  Back to cited text no. 26
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]



 

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