On resection of deep duodenal ulcers

1934 ◽  
Vol 30 (2) ◽  
pp. 348-348
Author(s):  
A. Ciminata
Keyword(s):  
Duodenal Ulcer ◽  
Anterior Wall ◽  
Duodenal Stump ◽  
Duodenal Ulcers

The author recommends dissecting the anterior wall of the 12 duodenal ulcer, resecting the crater of the ulcer and then performing atypical closure of the duodenal stump followed by peritonization of the stump with the pancreas and the apex of the omentum.

LAPAROSCOPIC REPAIR OF PERFORATED DUODENAL ULCER PATCH VERSUS CONVENTIONAL SURGERY

2019 ◽  
Vol 3 (1) ◽  
Author(s):  
Dr. Anil Kumar Saxena ◽  
Dr. Devi Das Verma
Keyword(s):  
Duodenal Ulcer ◽  
Laparoscopic Repair ◽  
Open Repair ◽  
Wound Dehiscence ◽  
Duodenal Perforation ◽  
Perforated Duodenal Ulcer ◽  
Conventional Surgery ◽  
Duodenal Ulcers ◽  
Duration Of Operation ◽  
Repair Group

Introduction: For many surgeries for duodenal ulcer Laparoscopic repair has become gold standard for many elective procedures such as ant reflux procedures, laparoscopic cholecystectomy and in colorectal surgery. Although in the emergency setting such as in the management of perforated duodenal ulcer Laparoscopic repair has been slow and limited. Since 1990, for the treatment of perforated peptic ulcer Laparoscopic repair has been used which has been widely accepted as an effective method. Duodenal ulcer is defined as a peptic ulcer which develops in the first part of the small intestine called duodenum and usually present as a perforation of acute abdomen. In perforated duodenal symptoms as severe and sudden onset abdominal pain that is worse in right upper quadrant and epigastrium and usually followed by nausea and vomiting. In this situation there is rapid generalization of pain and in examination shows peritonitis with lack of bowel sounds. Aim: The main objective of this study is to evaluate outcome of laparoscopic surgery in comparison with conventional surgery. Material and methods: All the patients with clinically diagnosed with perforated duodenal ulcers presenting within 24 hours of symptoms and undergoing surgery were included during the study period. Total 50 patients were included with age group 15-65 years. All the patients with perforated duodenal ulcers were included which go through either conventional open or laparoscopic without omental patch repair. Result: Total 50 patients were included in these studies which were divided into two group with 25 patients in each group as laparoscopic duodenal perforation repair group and conventional open repair group. Mean duration of operation (in minutes) was 105.4±10.4 in laparoscopic duodenal perforation repair group whereas mean duration of operation (in minutes) was 67.3±8.6 in conventional open repair group. Mean duration of number of doses of analgesics required in laparoscopic group and conventional open group as 9.5±1.7 and 17.2± 3.1 respectively. Out of 25 patients in each group of laparoscopic duodenal perforation repair group and the conventional open repair group the outcome were noted with their post operative complication as shown in table no 5 below.   In Post-operative complications 21(84%) patients in laparoscopic duodenal perforation repair group and 14(56%) patients in conventional open repair group had no complications. 4 (16%) patients in the laparoscopic duodenal perforation repair group and 2(8%) patients in conventional open repair group showed Post-operative complications as chest infection. In the conventional open repair group  patients present with wound dehiscence and wound infection and Wound dehiscence and chest infection were 4(16%) and 5(20%) respectively whereas nil in Laparoscopic duodenal perforation repair group. Conclusion: Duodenal ulcer perforation is a life-threatening emergency which required urgent management for the patients. Due to the advance in duodenal ulcer perforation closure by laparoscopy it becomes popular and favorite choice. With certain criteria, laparoscopic closure of perforated duodenal ulcer is safe and effective though it was associated with longer operating time and had no impact on the outcome. Hence laparoscopic closure was better in comparison to open repair for the earlier returns to normal daily activities. Keywords:  Duodenal ulcer, Laparoscopic repair, Post-operative analgesia, conventional surgery

RESULTS OF THE SUTURE OF THE PERFORATION BY SINGLE-PORT LAPAROSCOPIC SURGERY (SPLS) FOR THE PERFORATED DUODENAL ULCER TREATEMENT

2014 ◽  
pp. 126-132
Author(s):  
Huu Tri Nguyen ◽  
Van Lieu Nguyen
Keyword(s):  
Duodenal Ulcer ◽  
Laparoscopic Surgery ◽  
Single Port ◽  
Previous History ◽  
University Hospital ◽  
Safe Procedure ◽  
Perforated Duodenal Ulcer ◽  
Analgesic Requirement ◽  
Duodenal Ulcers ◽  
The Mean

Background Single-port laparoscopic surgery (SPLS) was increasingly used on several surgical diseases. The aim of this study is evaluation of the results of the suture of the perforation by SPLS for the perforated duodenal ulcer treatement. Methods From January 2012 to July 2014, 35 patients with perforated duodenal ulcers underwent simple suture of the perforations by SPLS at Hue University Hospital and Hue Central Hospital. Results The mean age was 45.9 ± 14.4 years. The sex ratio (male/female) was 16.5 and the mean of BMI was 19.2 ± 2.3. There was one patient (2.9%) with previous history of laparoscopic repair of perforated duodenal ulcer. The duration of the symptoms was 9.9 ± 12.3 hours. 97.1% of patients had the perforations of the anterior wall of the duodenum. The mean size of the perforation was 4.7 ± 3.4 mm (2 – 22mm). 2.9% of patients had the perforations of the posterior wall of the duodenum. The rate of the conversion to the open surgery was 2.9%. The mean operative time was 75.8 ± 33.7min, and the mean hospital stay was 5.8 ± 1.4 days. The mean of the analgesic requirement time was 2.9 ± 0.8 days. The wound length was 1.9 ± 0.1 cm. There was 5.9% of the patients had wound infection. There was no operation-related mortality. Conclusions Simple suture of the perforation by single-port laparoscopic surgery is a feasible and safe procedure, and it may be a scarless surgical technique for perforated duodenal ulcers treatement. Key words: single-port laparoscopic surgery, perforated duodenal ulcer

scholarly journals Causes and Management of Gastric and Duodenal Ulcer in Adolescents

2021 ◽  
pp. 289-297
Author(s):  
Bader Maiedh Mohsen Aladainan ◽  
Mahdi Turki Bin Ali Alfataih ◽  
Alhassan Ahmed Mohammed Aldundur ◽  
Rashed Saleh Mohammed Balhareth ◽  
Eisa Yazeed Ghazwani
Keyword(s):  
Duodenal Ulcer ◽  
Helicobacter Pylori ◽  
Peptic Ulcer ◽  
Review Literature ◽  
Peptic Ulcers ◽  
Significant Progress ◽  
Duodenal Ulcers ◽  
Ulcer Disease ◽  
Last 300 Years ◽  
Made In

Many etiological hypotheses have been suggested to explain the development of peptic ulcers during the last 300 years (including gastric ulcer and duodenal ulcer). In the last two decades, significant progress has been made in understanding the pathophysiology of peptic ulcer disease, particularly with regard to the involvement of Helicobacter pylori and nonsteroidal anti-inflammatory medications (NSAIDs). This study will attempt to review literature on etiology and management of gastric and duodenal ulcers among adolescents.

scholarly journals Prevalence of Helicobacter pylori infection among patients undergoing upper gastrointestinal endoscopy

2015 ◽  
Vol 3 (1) ◽  
Author(s):  
Vudumula Vijaya Lakshmi
Keyword(s):  
Duodenal Ulcer ◽  
Helicobacter Pylori ◽  
Normal Population ◽  
Gastric Ulcers ◽  
Upper Gastrointestinal Endoscopy ◽  
Contributing Factors ◽  
Duodenal Ulcers ◽  
Female Ratio ◽  
Ulcer Disease ◽  
H Pylori

Helicobacter pylori (H. pylori) has a role in the multifactorial etiology of peptic ulcer disease. A link between H. pylori infection and duodenal ulcer disease is now established. Other contributing factors and their interaction with the organism may initiate the ulcerative process. The fact that eradication of H. pylori infection leads to a long-term cure in the majority of duodenal ulcer patients and the fact that the prevalence of infection is higher in ulcer patients than in the normal population are cogent arguments in favor of it being the primary cause of the ulceration. This study was under taken at the Department of surgery, Narayana medical college, Nellore from January 2007 to July 2008. A total of 150 patients with duodenal ulcers, gastric ulcers, antral gastritis, gastric carcinoma and dyspepsia of any kind were studied. Maximum number of cases were in the age group of 31 years to 50 years among both sexes and number of cases gradually decreased after 50 years of age in males and females. Males were more in number and male to female ratio is (2.75:1) approximately 3:1.

DUODENAL ULCER IN CHILDHOOD

PEDIATRICS ◽  
1970 ◽  
Vol 45 (2) ◽  
pp. 283-286
Author(s):  
Mary Loretta Rosenlund ◽  
C. Everett Koop
Keyword(s):  
Duodenal Ulcer ◽  
Common Symptom ◽  
Peptic Ulcers ◽  
Older Children ◽  
Duodenal Ulcers ◽  
X Ray ◽  
Ulcer Disease ◽  
The Past ◽  
Younger Age ◽  
The Central Nervous System

There has been some disagreement concerning the admittedly rare incidence of duodenal ulcer disease in children. Because of conflicting reports from other pediatrics centers, we have reviewed the records of all patients admitted to The Children's Hospital of Philadelphia in the past 20 years (1948 through 1967) in whom duodenal ulcer was diagnosed by x-ray, at operation or on postmortem examination (Table I). There were 27 children between the ages of 15 days and 15½ years, with well established duodenal ulcers. Six of these were female (22%). The age at presentation was scattered, but the majority were between 2 and 11 years of age. Presenting complaints were varied: gastrointestinal bleeding was most common in the younger age group, while abdominal pain, usually persistent and intermittent, was the most common symptom in the older children. The diagnosis of duodenal ulcer was made by x-ray examination in 22 patients and at operation in 2; and the ulcers were discovered only at autopsy in 3 children. All the ulcers were duodenal; the precise location was not specified in 9, but 11 were bulbar and 7 were postbulbar. Complications of the ulcer were noted in 9 patients. Perforation occurred in 7 patients, leading to death in 4 (all had disease of the central nervous system) and repeated bleeding in 2. Etiology of the ulcer disease was determined in 15 of the children, but the cause was unknown in 12. Our series is concerned only with duodenal ulcers which, admittedly, comprise the greatest percentage of peptic ulcers.

scholarly journals ABO blood group, secretor status and detection ofHelicobacter pyloriamong patients with gastric or duodenal ulcers

1991 ◽  
Vol 106 (2) ◽  
pp. 221-229 ◽  
Author(s):  
A. Mentis ◽  
C. C. Blackwell ◽  
D. M. Weir ◽  
C. Spiliadis ◽  
A. Dailianas ◽  
...  
Keyword(s):  
Duodenal Ulcer ◽  
Helicobacter Pylori ◽  
Gastric Ulcer ◽  
Blood Group ◽  
Local Population ◽  
Abo Blood Group ◽  
Duodenal Ulcers ◽  
Secretor Status ◽  
Gastric Or Duodenal Ulcers ◽  
H Pylori

SUMMARYPatients (454) referred for gastroscopy to the General Hospital of Athens were examined to determine (1) if non-secretors were over-represented among patients with ulcers and (2) is there was an association with ABO blood group or secretor status and carriage ofHelicobacter pylori.Compared with the local population, among patients with either gastric ulcer (51) or duodenal ulcer (96) there was a significant increase in the proportion of those who were blood group O (P< 0·025); however, there were no significant differences in the proportions of non-secretors.H. pyloriwas identified in 62 % of the 454 patients: 59·5 % of those without evidence of ulcers; 62·5 % of those with gastric ulcer; 88% of those with duodenal ulcer (P< 0·0005). These bacteria were cultured more often and in higher numbers from patients with duodenal ulcer (P< 0·025). There was no association between ABO blood group and prevalence ofH. pylori. The prevalence ofH. pyloriamong non-secretors with gastric ulcer (12·5%) was significantly lower than that for non-secretors with duodenal ulcer (100%) (P< 0·0005). This was not observed for secretors.

Decreased relapse rate after antibacterial treatment of Helicobacter pylori-associated duodenal ulcers. Munich duodenal ulcer trial

1993 ◽  
Vol 5 (3) ◽  
pp. 145-154 ◽  
Author(s):  
Gerd A. Marines ◽  
Ekkehard Bayerdörffer ◽  
Wilhelm Höchter ◽  
Josef Weingart ◽  
Walter Heldwein ◽  
...  
Keyword(s):  
Duodenal Ulcer ◽  
Helicobacter Pylori ◽  
Relapse Rate ◽  
Antibacterial Treatment ◽  
Duodenal Ulcers

A novel small molecule CFTR inhibitor attenuates HCO3− secretion and duodenal ulcer formation in rats

2005 ◽  
Vol 289 (4) ◽  
pp. G753-G759 ◽  
Author(s):  
Yasutada Akiba ◽  
Michael Jung ◽  
Samedy Ouk ◽  
Jonathan D. Kaunitz
Keyword(s):  
Duodenal Ulcer ◽  
Duodenal Mucosa ◽  
Mutant Mice ◽  
Protective Mechanism ◽  
Ulcer Formation ◽  
Apparent Paradox ◽  
Duodenal Ulcers ◽  
Buffering Power ◽  
Ph Stat ◽  
Cf Transmembrane Conductance Regulator

The cystic fibrosis (CF) transmembrane conductance regulator (CFTR) plays a crucial role in mediating duodenal bicarbonate (HCO3−) secretion (DBS). Although impaired DBS is observed in CF mutant mice and in CF patients, which would predict increased ulcer susceptibility, duodenal injury is rarely observed in CF patients and is reduced in CF mutant mice. To explain this apparent paradox, we hypothesized that CFTR dysfunction increases cellular [HCO3−] and buffering power. To further test this hypothesis, we examined the effect of a novel, potent, and highly selective CFTR inhibitor, CFTRinh-172, on DBS and duodenal ulceration in rats. DBS was measured in situ using a standard loop perfusion model with a pH stat under isoflurane anesthesia. Duodenal ulcers were induced in rats by cysteamine with or without CFTRinh-172 pretreatment 1 h before cysteamine. Superfusion of CFTRinh-172 (0.1–10 μM) over the duodenal mucosa had no effect on basal DBS but at 10 μM inhibited acid-induced DBS, suggesting that its effect was limited to CFTR activation. Acid-induced DBS was abolished at 1 and 3 h and was reduced 24 h after treatment with CFTRinh-172, although basal DBS was increased at 24 h. CFTRinh-172 treatment had no effect on gastric acid or HCO3− secretion. Duodenal ulcers were observed 24 h after cysteamine treatment but were reduced in CFTRinh-172-pretreated rats. CFTRinh-172 acutely produces CFTR dysfunction in rodents for up to 24 h. CFTR inhibition reduces acid-induced DBS but also prevents duodenal ulcer formation, supporting our hypothesis that intracellular HCO3− may be an important protective mechanism for duodenal epithelial cells.

scholarly journals Specific Antibodies in Sera and Gastric Aspirates of Symptomatic and Asymptomatic Helicobacter pylori-Infected Subjects

1998 ◽  
Vol 5 (3) ◽  
pp. 288-293 ◽  
Author(s):  
A. Mattsson ◽  
A. Tinnert ◽  
A. Hamlet ◽  
H. Lönroth ◽  
I. Bölin ◽  
...  
Keyword(s):  
Duodenal Ulcer ◽  
Helicobacter Pylori ◽  
Membrane Proteins ◽  
Immunosorbent Assay ◽  
Antibody Responses ◽  
Enzyme Linked Immunosorbent Assay ◽  
Duodenal Ulcers ◽  
Specific Antibodies ◽  
Antibody Titers ◽  
H Pylori

ABSTRACT In this study we have determined systemic and local antibody responses against different Helicobacter pylori antigens inH. pylori-infected and noninfected subjects. In addition, we studied whether differences in antibody responses between patients with duodenal ulcers and asymptomatic H. pylori carriers might explain the different outcomes of infection. Sera and in most instances gastric aspirates were collected from 19 duodenal ulcer patients, 15 asymptomatic H. pylori carriers, and 20 noninfected subjects and assayed for specific antibodies against different H. pylori antigens, i.e., whole membrane proteins (MP), lipopolysaccharides, flagellin, urease, the neuraminyllactose binding hemagglutinin HpaA, and a 26-kDa protein, by enzyme-linked immunosorbent assay. The H. pylori-infected subjects had significantly higher antibody titers against MP, flagellin, and urease in both sera and gastric aspirates compared with the noninfected subjects. Furthermore, the antibody titers against HpaA were significantly elevated in sera but not in gastric aspirates from the infected subjects. However, no differences in antibody titers against any of the tested antigens could be detected between the duodenal ulcer patients and the asymptomatic H. pyloricarriers, either in sera or in gastric aspirates.

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