Abstract
Introduction:
Acute abdomen in pediatric patients presents diagnostic challenges due to the wide range of potential causes and overlapping clinical features. Duodenal ulcer perforation, though rare, can mimic more common conditions like appendicitis, complicating diagnosis and management. Perforated peptic ulcer disease (PUD) in children, especially without chronic nonsteroidal anti-inflammatory drug (NSAID) use or Helicobacter pylori infection, is uncommon but requires prompt recognition.
Case presentation:
A 9-year-old male presented with severe diffuse abdominal pain, fever, and a history of chills. Physical examination revealed tenderness, board-like rigidity, and sluggish bowel sounds. Laboratory tests showed leukocytosis, but radiological findings, including abdominal X-ray, were normal. Ultrasound indicated gaseous abdomen and fluid collection. An exploratory laparotomy revealed a perforation in the first part of the duodenum, which was repaired using a Graham omental patch. Postoperatively, the patient recovered well with intravenous antibiotics and was discharged on the sixth postoperative day.
Clinical discussion:
Duodenal ulcer perforation, though rare, should be considered in pediatric cases of acute abdomen. Common causes of PUD include H. pylori infection, NSAIDs, and stress-related ulcers. Diagnosis is often delayed, particularly when typical radiological signs like pneumoperitoneum are absent, as in this case. Timely surgical intervention is critical to prevent morbidity and mortality.
Conclusion:
Duodenal ulcer perforation should be considered as a potential cause of peritonitis in children with acute abdomen, even in the absence of typical radiographic signs. Early recognition and surgical intervention are essential for favorable outcomes.
Keywords: acute abdomen, case report, duodenal perforation, peptic ulcer, peritonitis
Introduction
Acute abdomen in pediatric patients presents a significant diagnostic challenge due to the wide number of potential etiologies and the overlap of clinical features across various conditions[1]. While appendicitis is the most common cause of surgical abdomen in children, rarer conditions like duodenal ulcer perforation can mimic this presentation, leading to diagnostic uncertainty[2]. These uncommon cases demand attention due to their potential for delayed recognition and significant morbidity. Peptic ulcer disease (PUD) in children is rare, with a prevalence of 8.1% reported in some regions and an annual incidence of 1.55 cases/year in others[2,3]. Complications such as perforation are even rarer, often posing serious diagnostic and management challenges[1,2]. Unlike in adults, pediatric PUD is less frequently linked to chronic Nonsteroidal anti-inflammatory drugs (NSAID) use or Helicobacter pylori infection, making the underlying cause difficult to ascertain[4]. Furthermore, radiological findings typically aid in the diagnosis, but the absence of expected signs, such as pneumoperitoneum on X-ray, can further complicate the clinical evaluation[1].
HIGHLIGHTS
Duodenal ulcer perforation as a cause of acute abdomen in the pediatric population is uncommon and often diagnosed only during surgical exploration.
Typical radiological signs, such as pneumoperitoneum, may be absent, making diagnosis more difficult and highlighting the need for a high index of suspicion.
Surgical intervention, typically involving omental patch repair, remains the mainstay of treatment for perforated duodenal ulcers in children.
Delayed diagnosis and surgery can lead to increased morbidity and mortality, emphasizing the importance of timely intervention.
While H. pylori infection is a common cause of peptic ulcers, no specific risk factors were identified in this case, suggesting the complexity of pediatric PUD.
In this report, we describe the case of a 9-year-old male with acute abdomen due to a perforated duodenal ulcer. Notably, our case lacked radiological evidence of pneumoperitoneum on X-ray, underscoring the diagnostic difficulties in such presentations. This case highlights the need for a high index of suspicion for uncommon causes of acute abdomen in children and demonstrates the importance of timely surgical intervention in achieving favorable outcomes. This work has been reported in line with SCARE guideline[5].
Case presentations
A case of a 9-year-old male who presented to a pediatric emergency with a perforated duodenal ulcer. Visitor and patient give a history of diffuse abdominal pain of severe intensity for the last 1 day associated with on and off fever with chills and rigor. The pain was severe enough to make him bedridden and seek medical attention. There was no history of chronic consumption of NSAIDs. Personal history cannot provide us with a clue about the diagnosis as well. On examination, the patient was looking ill with a pulse rate of 120 beats per minute, his respiratory rate was 20/min and his blood pressure was 100/70 mmHg. Per Abdominal examination shows diffuse tenderness with raised temperature and board-like rigidity. The bowel sound was sluggish, and hernial orifices were intact. Routine investigations were sent which showed leucocytosis of around 13 000, elevated C-reactive proteins level and the rest of the blood investigations were normal as depicted in Table 1. The X-ray of the abdomen and pelvis was done, which was grossly normal with no features of pneumoperitoneum (Fig. 1).
Table 1.
Laboratory investigations
| Investigation | Result | Reference range | Remarks |
|---|---|---|---|
| Complete blood count (CBC) | |||
| Hemoglobin | 12.5 g/dL | 11.5–15.5 g/dL | Normal |
| Total leukocyte count (TLC) | 13 000/mm3 | 4000–11 000/mm3 | Elevated |
| Platelet count | 250 000/mm3 | 150 000–450 000/mm3 | Normal |
| C-reactive protein (CRP) | 62 mg/L | <10 mg/L | Elevated |
| Liver function tests (LFTs) | |||
| Total bilirubin | 0.8 mg/dL | 0.2–1.2 mg/dL | Normal |
| Aspartate aminotransferase (AST) | 32 U/L | 10–40 U/L | Normal |
| Alanine aminotransferase (ALT) | 28 U/L | 10–40 U/L | Normal |
| Renal function tests (RFTs) | |||
| Blood urea | 20 mg/dL | 10–50 mg/dL | Normal |
| Serum creatinine | 0.6 mg/dL | 0.2–0.9 mg/dL | Normal |
| Serum electrolytes | |||
| Sodium (Na+) | 137 mEq/L | 135–145 mEq/L | Normal |
| Potassium (K+) | 4.0 mEq/L | 3.5–5.1 mEq/L | Normal |
| Pancreatic enzymes | |||
| Serum amylase | 58 U/L | 30–110 U/L | Normal |
| Serum lipase | 42 U/L | 10–140 U/L | Normal |
| Typhoid serology | |||
| Widal test (Salmonella typhi O) | 1:80 | <1:160 | Negative |
| Widal test (Salmonella typhi H) | 1:80 | <1:160 | Negative |
| Rapid typhoid IgM/IgG | Negative | Negative | No evidence of acute/recent infection |
Figure 1.

Chest X-ray PA view showing normal findings.
Ultrasound of the abdomen and pelvis was done which showed a gaseous abdomen, mild fluid with internal echoes in the abdomen and pelvis with prominent bowel loops. USG-guided aspiration of pus yielded pus mixed collection. There was also a blind-ending tubular, non-compressing peristaltic structure of diameter 5.4 mm that seemed to be arising from the base of the caecum with minimal surrounding inflammation. After the above workup, he was planned for an exploratory laparotomy and proceeded. A right-sided supraumbilical transverse incision was given and the abdominal layer opened. He was found to have moderate pyoperitoneum, so peritoneal lavage was done with 3 L of warm saline. The appendix was found to be healthy with no signs of inflammation and there was no fecolith as well. Exploration was continued and he was found to have a perforation at the first part of the duodenum (Fig. 2). Margins were refreshed and Graham omental patch repair was done (Fig. 3). A 14 Fr abdominal drain was placed and the abdominal layer was closed. He was shifted to a ward and managed with intravenous antibiotics and analgesics. The patient passed flatus, bowel sound was present and there was minimal nasogastric output, so oral feeding was started on the third postoperative day, which he tolerated well. The abdominal drain was removed on the fifth postoperative day and he was discharged on the sixth postoperative day on triple regimen therapy considering H. Pylori infection to be the more common cause of duodenal perforation. At the 2-week follow-up, the patient remained asymptomatic with no signs of complications, and by the 1-month follow-up, they had regained normal dietary habits with no recurrence of symptoms.
Figure 2.

Picture showing perforation at D1 of size 0.5 × 0.5 cm with bile leakage (black arrow).
Figure 3.

Picture showing Graham’s omental patch repair (black arrow).
Discussion
Acute abdomen in pediatrics due to peptic ulcer perforation is a rare presentation and requires prompt diagnosis and management due to potentially life-threatening consequences. In this case report, we describe a 9-year-old male who presented with acute abdomen due to peptic ulcer perforation diagnosed intraoperatively with no findings of pneumoperitoneum on X-ray. This case study discusses the clinical presentation, diagnostic evaluation, therapeutic interventions, and the management of this challenging case.
Duodenal ulcer is the defect in the mucosa extending deeper upto muscularis mucosa of duodenal wall and can present variably from asymptomatic, dyspepsia, and upper gastrointestinal (GI) bleeding to perforation[6]. Various causes of PUD are H. pylori infection, steroidal anti-inflammatory drugs, stress response, and gastrinoma[3,7,8]. H. pylori infection is the most common cause of peptic ulcer and often has family aggregation. The H. pylori infection rate is high, accounting for up to 30%[7,9]. Duodenal ulcers associated with H. pylori infection are rarely seen in children under 10 years of age, but due to overuse of NSAIDS, NSAID-related ulcers are now being seen more frequently[10]. Interestingly in a retrospective study by Yeh et al[6], about half of the patients were H. pylori negative and NSAID negative but there is lack of proper evidence on “Idiopathic DU” in children. Complications of duodenal ulcers include upper GI bleeding, perforation, and obstruction. These issues are relatively more common in children, likely because the condition is often diagnosed later in this age group[11]. Between 0% and 9% of PUD with duodenal ulcers develop perforation and are more common in age group older than 7 years[12].
The differential diagnoses considered included acute appendicitis with perforation, as ultrasound showed a blind-ending tubular, noncompressible peristaltic structure mimicking an inflamed appendix; however, intraoperative findings confirmed an intact and healthy appendix. Typhoid ileal perforation was also considered due to the fever history, but the absence of terminal ileum perforation intraoperatively ruled it out. Necrotizing enterocolitis or intestinal perforation, though a possibility in neonates and infants, was unlikely in this previously healthy 9-year-old. Spontaneous bacterial peritonitis was deemed unlikely due to the absence of predisposing conditions such as nephrotic syndrome or chronic liver disease. Pancreatitis was another consideration, as epigastric pain could suggest this condition; however, the patient did not exhibit classic symptoms such as vomiting, and laboratory tests showed no elevation in pancreatic enzymes.
Among uncommonly diagnosed conditions in children, duodenal ulcer perforation is one of them with an incidence of 1.55 cases/year as per the literature review[13]. PUD is rarely suspected as an entity of abdominal complaints in the pediatric population. The diagnosis is, therefore, done once a child develops complications but in our case, we diagnosed the case only during the intraoperative period[6,14]. Peptic ulcers are found to be associated with systemic conditions, such as sepsis, severe head or body trauma, or burns however no risk factor was seen in our case[14,15]. A perforated peptic ulcer is a surgical emergency with a mortality of up to 30%[16]. Usually, diagnosis is missed because of variable symptoms and due to suspicion[17]. Peritoneal signs and radiographic findings of free subdiaphragmatic air, when observed, the most likely pathology is supposed to be perforated appendix rather than duodenal ulcer perforation[1,2]. Mortality and morbidity are expected if there is a delay of more than 12 hours for surgery, smaller age, female gender, and perforations of larger diameter[4,15]. The mainstay of ulcers of perforated duodenal ulcers is surgical repair. Various surgical techniques like simple omental patch closure, truncal vagotomy, and drainage procedure, hemi-gastrectomy can be done[18]. Since 1990, laparoscopic treatment for perforated peptic ulcers has been reported to be a safe option in many centers[19]. So open versus laparoscopic surgery is dependent upon the health center and surgeons’ expertise. In this case, perforated margins were refreshed and Graham omental patch repair was done.
Table 2 shows the comparative analysis of the duodenal ulcer perforations cases in pediatric populations.
Table 2.
Comparative analysis of duodenal perforation cases in pediatric patients
| Parameter | Present case | Shrestha and Shrestha[2] | Hattingh et al[15] | Kadian et al[20] | Rai et al[21] |
|---|---|---|---|---|---|
| Age | 9-year-old | 12-year-old | 14-year-old | 4-month-old | 3-year-old |
| Initial complaint | Diffuse abdominal pain, fever with chills | Central abdominal pain, vomiting, bloating | Severe abdominal pain, periumbilical region | Pain, distension, vomiting, non-passage of flatus/stool | Fever, abdominal pain, generalized distension |
| Duration of symptoms | 1 day | 3 days (generalized over 2 days) | 2 days (sudden onset) | 2 days | 17 days of fever, abdominal pain |
| Vital signs on admission | Pulse: 120 bpm, RR: 20/min, BP: 100/70 mmHg | Tachycardiac, normotensive, afebrile | Normal vital signs | Tachycardic, tachypnoea, dehydrated | Normal vital signs |
| Abdominal findings | Diffuse tenderness, board-like rigidity, sluggish bowel sounds | Generalized tenderness, board-like rigidity, absent bowel sounds | Diffuse rebound tenderness and rigidity | Guarding and rebound tenderness | Tender abdomen, sluggish bowel sounds |
| Laboratory findings | Leucocytosis (13 000), elevated CRP (62 MG/L) normal blood tests | Leucopenia (1480), elevated CRP (>90 mg/L), mild hyponatremia | Elevated WBC (14 900), normal CRP | Normal gastrin levels | High WBC count (28 400), normal blood tests |
| Radiology | Normal X-ray, USG: Gaseous abdomen, fluid collection | X-ray: Free air under diaphragm, abdominal distension | CT scan: Pneumoperitoneum, large air collection | X-ray: Free air under diaphragm | X-ray: Free gas under both domes of diaphragm |
| Diagnosis | Perforated duodenal ulcer, pyoperitoneum | Perforated duodenal ulcer, peritonitis | Perforated duodenal ulcer with bile leak | Perforated duodenal ulcer | Perforated duodenal ulcer |
| Surgical intervention | Exploratory laparotomy, Graham patch repair | Laparotomy, Graham patch repair, FJ placement | Diagnostic laparoscopy, Graham patch repair | Omental patch repair for duodenal perforation | Graham patch repair |
| Postoperative management | IV antibiotics, analgesics, nasogastric output, oral feeding on POD 3 | FJ feeds, IV fluids, antibiotics, oral feeds on POD 5 | No complications, started diet on POD 4 | IV fluids, antibiotics, NG decompression | Drain in subhepatic region, gradual recovery |
| Outcome | Discharged on POD 6 with triple therapy for H. Pylori | Discharged on POD 11, FJ removed at follow-up | Discharged on POD 7, H. Pylori eradication therapy | Discharged on POD 7 with smooth recovery | Discharged on POD 12 with uneventful recovery |
| Follow-up | Follow-up at OPD in 2 weeks,1 month doing well | Follow-up at OPD, FJ removed | Symptoms free, 1-year follow-up, doing well | Not mentioned | Not mentioned |
CRP, C-reactive protein; FJ, feeding jejunostomy; IV; intravenous; POD, postoperative day; WBC, white blood cells.
Such cases are reported less in the literature and further cases should be reported for generalizability. This case deals with duodenal ulcer perforation as a rare cause of acute abdomen in the pediatric population that too with no findings suggestive of pneumoperitoneum on X-ray. It is recommended that clinicians should consider peptic ulcer perforation as a cause of presentation as acute abdomen even if typical findings of pneumoperitoneum are absent.
Conclusion
Duodenal perforation peritonitis should also be considered a cause of peritonitis in the pediatric population when attending cases of acute abdomen. Typical pneumoperitoneum and right subdiaphragmatic air may not be observed, as in our case. Adequate resuscitation, prevention of sepsis, and timely surgical intervention remain the mainstays of management, and the patient requires close follow-up postoperatively as well.
Footnotes
Sponsorships or competing interests that may be relevant to content are disclosed at the end of this article.
Published online 29 April 2025
Ethical approval
The study is exempt/waived from ethical approval in our institution as it poses minimal risk to the patient and the study is for educational purposes/activities.
Consent
Written informed consent was obtained from the patient’s parents/legal guardian for publication and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal on request.
Sources of funding
Not applicable.
Author contributions
Literature review, follow-up the patient, writing the manuscript, and final approval of the manuscript: K.C.S.; surgery of the patient, literature review, follow-up the patient, writing the manuscript, and final approval of the manuscript: T.N.Y.; literature review, follow-up the patient, writing the manuscript, and final approval of the manuscript: K.R.; surgery of the patient, literature review, follow-up the patient, writing the manuscript, and final approval of the manuscript: R.P.S.; literature review, follow-up the patient, writing the manuscript, and final approval of the manuscript: A.B.; follow-up the patient, writing the manuscript: R.K.; follow-up the patient, writing the manuscript: N.M.; follow-up the patient, writing the manuscript: M.G.
Conflicts of interest disclosure
The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
Research registration unique identifying number (UIN)
Not applicable.
Guarantor
Rajesh Prasad Sah.
Provenance and peer review
Not commissioned, externally peer-reviewed.
Data availability statement
Not applicable.
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