Multidisciplinary approach for treatment of duodenal perforation complicated with gastrointestinal hemorrhage in pediatric patient and relevant literature review

Abstract

Objective

To investigate the key clinical diagnostic and therapeutic points, challenges and corresponding strategies for duodenal perforation complicated with recurrent gastrointestinal bleeding in children, and to provide a clinical reference for managing this rare pediatric acute critical condition.

Methods

The clinical data of a 2-year-and-7-month-old female child with duodenal perforation and recurrent gastrointestinal bleeding were retrospectively analyzed. A systematic review and analysis were conducted from the perspectives of etiology, diagnosis, treatment and postoperative management, combined with relevant domestic and foreign literature over the past decade.

Results

A 2-year-and-7-month-old Chinese female child presented with viral enteritis initially, which progressed to duodenal perforation complicated with recurrent gastrointestinal bleeding. She received sequential interventions including duodenal perforation repair, gastroscopic exploration, gastrointestinal reconstruction, and transcatheter gastroduodenal artery embolization. Through whole-course multidisciplinary team (MDT) collaboration and refined comprehensive supportive therapy, the child achieved complete recovery with no recurrent bleeding.

Conclusion

The diagnosis and treatment of duodenal perforation complicated with recurrent gastrointestinal bleeding in children should focus on the core features of pediatric physiological particularities, etiological complexity, age-stage specificity and targeted management of clinical challenges. Adopting multimodal localization approaches, rationally selecting therapeutic regimens and relying on whole-course MDT collaboration can effectively reduce the risk of rebleeding and improve the prognosis of affected children.

Supplementary Information

The online version contains supplementary material available at https://doi.org/10.1186/s12887-026-07211-9.

Introduction

Duodenal perforation complicated with recurrent gastrointestinal bleeding is extremely rare in children, with an estimated incidence of less than 1% among all pediatric acute abdominal conditions. Peptic ulcer perforation accounts for only 3%–5% of pediatric gastrointestinal perforations [1], and the median age at presentation is approximately 11 years, making this case in a 2-year-old child even more uncommon.Owing to the immature development of the gastrointestinal mucosal barrier, poor ability to express symptoms, unique anatomical structures, and distinct age-stage characteristics of etiology in children, the clinical diagnosis and treatment of this condition are significantly more challenging than in adults [2, 3]. The early symptoms of the disease are mostly non-specific, making it prone to misdiagnosis and delayed treatment, which can lead to diffuse peritonitis, hemorrhagic shock, and even death [4, 5]. In addition, the duodenum is characterized by abundant blood supply and a thin intestinal wall; thus, ulcer perforation is likely to induce inflammatory adhesions, and ulcer erosion of arterial blood vessels can result in pulsatile bleeding. A single therapeutic approach is associated with a high rate of postoperative rebleeding [6, 7].

The systematic review published by Vidović et al. [1] indicated that the median age of onset for pediatric perforated peptic ulcer is 11 years (range: 3.2–16.5 years). The patient in this case was only 2 years and 7 months old, which is considerably younger than the median age reported in the literature. This study analyzes the diagnosis and treatment of this case based on relevant domestic and international literature over the past decade. We summarize the key clinical points, challenges, and targeted management strategies to provide practical references for pediatric practice.

Clinical data

Present illness

The patient was admitted with a 5-day history of diarrhea, paroxysmal abdominal pain, and fever, followed by hematochezia for half a day. She had 3–4 watery bowel movements daily, with a maximum temperature of 38.5℃. She was initially treated at a local hospital, where laboratory tests revealed the following results: white blood cell (WBC) count 11.62 × 10⁹/L, neutrophil count 8.93 × 10⁹/L, hemoglobin (Hb) 143 g/L, C-reactive protein (CRP) <0.5 mg/L; stool routine showed weakly positive Group A rotavirus and 0–1 red blood cells per high-power field (RBC/HP). A diagnosis of gastroenteritis was made, and the child was administered oral cephalosporin antibiotics plus fluid replacement therapy for 2 days, followed by probiotics and antidiarrheal agents for an additional 3 days, with no clinical improvement. On the 6th day of treatment, the child presented with poor mental status, pale complexion, and passage of dark red blood clots in the stool, and was thus transferred to our hospital for further management.

Past medical history

The child had an unremarkable past medical history, with no history of peptic ulcer or congenital digestive tract malformation. There was no history of taking non-steroidal anti-inflammatory drugs (NSAIDs), hormonal agents, or other special medications, no history of food or drug allergy, and no history of abdominal trauma or surgery.

Physical examination

Body temperature (T): 37.8℃, pulse (P): 150 beats/min, respiration (R): 30 breaths/min, blood pressure (BP): 100/53 mmHg, body weight: 12.5 kg. The child was conscious but lethargic. She appeared acutely ill, with pale skin, palpebral conjunctiva, and oral mucosa.Tachypnea was noted; a grade 3/6 blowing systolic murmur was auscultated over the precordium. The abdomen was slightly distended, with no abdominal wall varices, gastrointestinal pattern, or peristaltic waves. Abdominal muscles were mildly rigid, and no abdominal mass was palpable upon deep palpation. Mild tenderness was present in the right upper abdomen with no fixed tender point, and rebound tenderness was weakly positive (±). The liver and spleen were not palpable below the costal margin, Murphy’s sign was negative, shifting dullness was weakly positive (±), Bowel sounds were decreased, with only 2 audible per minute (normal: 4–6 per minute), with no hyperactive bowel sounds or metallic tinkling.

Auxiliary examinations

Laboratory tests

On the 6th day of illness, laboratory examination revealed the following results: Hb 60 g/L、CRP 22.62 mg/L、WBC count 13.62 × 10⁹/L、neutrophil ratio 78.5%; fecal occult blood test (++++); coagulation profile, liver and renal function, serum electrolytes, and myocardial enzyme spectrum were all within normal limits.

Imaging examinations

Abdominal plain computed tomography (CT) demonstrated free intraperitoneal gas, hyperdense lesions within the gallbladder, intraperitoneal effusion, and hyperdense foci in the descending to horizontal duodenum, which was highly suggestive of gastrointestinal perforation (Fig. 1).

Fig. 1.

The position indicated by the red arrow is the scattered free gas shadow in the abdominal cavity

Preliminary diagnosis

1. Gastrointestinal perforation complicated with gastrointestinal bleeding

2. Moderate anemia

3. Intraperitoneal effusion

4. Cholelithiasis

Clinical course and management

First operation: laparoscopic duodenal perforation repair

The child was initially diagnosed with gastrointestinal perforation, and laparoscopic minimally invasive surgery was selected as the first-line therapeutic approach. Intraoperative exploration revealed partial adhesions between the descending duodenum and the liver/gallbladder duct, with the serosal surface covered by yellowish-white purulent exudate. A 1.5 × 1.5 cm perforation was identified on the anterior wall of the descending duodenum, with intestinal mucosal eversion; bile, purulent exudate, food residue, and blood clots were extruding from the perforation, with no obvious active bleeding (Fig. 2). Surgical interventions included resection of inflammatory necrotic tissue at the duodenal perforation site (with pathological examination, Fig. 3) plus primary perforation repair. The surgical field was repeatedly irrigated with warm normal saline until the irrigant became clear, and one gastric decompression tube and one abdominal drainage tube were indwelled postoperatively.

Fig. 2.

Intraoperative image of the first operation: duodenal perforation with mucosal eversion, surrounding inflammatory adhesions, and serosal coverage of purulent exudate

Fig. 3.

Histopathological examination of the necrotic tissue surrounding the duodenal perforation (×10 magnification) demonstrated extensive neutrophilic infiltration, with focal infiltration of a small number of lymphocytes and plasma cells

However, intraluminal exploration or intraoperative endoscopy was not performed during the first laparoscopic operation. Therefore, we cannot definitively confirm whether a more extensive ulcerative lesion, an exposed vessel, or a posterior duodenal ulcer was already present at that time. Two possibilities cannot be excluded: first, an occult posterior duodenal ulcer with an underlying exposed artery might have pre-existed but remained unrecognized due to the lack of intraluminal evaluation; second, persistent postoperative inflammation, secondary infection, increased intraduodenal pressure, and insufficient gastrointestinal decompression might have gradually aggravated mucosal injury, leading to progressive ulceration and arterial exposure. This situation strongly indicates that thorough intraluminal exploration or intraoperative endoscopic assessment is essential for pediatric patients with duodenal perforation to identify occult lesions at an early stage.

Postoperative management included nil per os (NPO), gastrointestinal decompression, intravenous fluid replacement, anti-infection therapy with broad-spectrum antibiotics, high-dose acid suppression with a proton pump inhibitor (PPI), and parenteral nutritional support. On postoperative days (POD) 1–4, the child’s vital signs remained stable, with no significant drainage from the abdominal tube. Hb increased to 110 g/L and stabilized, CRP decreased to 1.12 mg/L, and the WBC count gradually elevated from 13.62 × 10⁹/L to 23.67 × 10⁹/L (Fig. 10).

Fig. 10.

Dynamic trends of hemoglobin (Hb), C-reactive protein (CRP), and white blood cell (WBC) count from admission to the 6-month follow-up. All indicators were detected using standard clinical laboratory methods. Horizontal axis: detection date; left vertical axis: Hemoglobin (unit: g/L); middle vertical axis: CRP (unit: mg/L); right vertical axis: WBC count (unit: ×10⁹/L)

Operation: digestive tract reconstruction

On POD 5, approximately 80 mL of bright red blood was drained from the gastric tube, and the child passed about 100 g of tarry stools, with Hb dropping to 82 g/L. Active gastrointestinal bleeding was suspected, and the child was immediately administered 2 units of packed red blood cells, 100 mL of fresh frozen plasma, and 1 unit of cryoprecipitate to correct anemia and coagulation dysfunction.

An emergency gastroscopy was performed to localize the bleeding source (Fig. 4), but the visual field was severely obscured by a large volume of blood in the narrow duodenal lumen, precluding the identification of the bleeding point. The procedure was thus converted to open surgery. Intraoperative exploration identified pulsatile arterial bleeding from the posterior wall of the duodenal bulb, approximately 2 cm proximal to the original perforation site; the bleeding point was about 0.3 cm in diameter, with a 4 × 2 cm area of mucosal ulceration in the surrounding region. Superficial suture ligation failed to achieve effective hemostasis, and full-thickness suture ligation was subsequently performed. Given the extensive mucosal ulceration and the inability to identify the opening of the major duodenal papilla (to avoid iatrogenic injury to the pancreaticobiliary duct during suture ligation), proximal duodenal closure and exclusion, partial gastrectomy (with pathological examination, Figs. 5 and 6), and gastrojejunal Roux-en-Y anastomosis were performed with written informed parental consent. One nasointestinal feeding tube and two abdominal drainage tubes were indwelled postoperatively. Postoperative systemic management included gastrointestinal decompression, total parenteral nutrition, acid suppression, gastric mucosal protection, hemostasis, hepatoprotection, and anti-infection therapy.

Fig. 4.

Findings of the first emergency gastroscopy: no abnormal lesions were found in the esophageal, cardiac, gastric fundus, or gastric angular mucosa; a large volume of bright and dark red bloody fluid was present in the gastric cavity; gastric antral mucosa showed red predominance with red and white mottling; pyloric contraction and relaxation were normal; a large amount of bloody fluid was noted in the duodenal bulb

Fig. 5.

Gross specimen of the resected partial gastric tissue

Fig. 6.

Microscopic examination of the resected gastric tissue at 10× magnification revealed the following findings: In the duodenal mucosa, partial congestion and edema were observed, accompanied by submucosal hemorrhage and hematoma formation, with evident congestion of blood vessels on the serosal surface. For the gastric wall, mucosal edema was noted, along with scattered inflammatory cell infiltration; the submucosa showed loose edema, vascular proliferation and congestion, and the serosal surface also presented vascular congestion

Interventional therapy: gastroduodenal artery embolization

On the 8th day after the second operation, the child developed massive recurrent gastrointestinal bleeding, passing tarry stools three times (total volume: ~150 g), with approximately 150 mL of dark red bloody fluid drained from the gastric tube; Hb decreased progressively to 66 g/L. A hospital-wide multidisciplinary team (MDT) discussion was convened, involving specialists from the Medical Administration Department, Pediatric Surgery, Pediatric Endocrinology and Gastroenterology, Pediatric Rheumatology and Immunology, Gastrointestinal Surgery, Hepatobiliary and Pancreatic Surgery, Adult Gastroenterology, Interventional Radiology, Anesthesiology, and Transfusion Medicine. The MDT conducted a systematic analysis of the child’s clinical condition, including key diagnostic and therapeutic points, clinical management measures, and postoperative care strategies, and a refined comprehensive treatment plan was formulated.

A repeat gastroscopy was performed to rule out anastomotic bleeding or secondary peptic ulcer (Fig. 7), with no definite bleeding point identified. The child was then transferred to the Interventional Radiology Department for selective gastroduodenal artery embolization (Figs. 8 and 9).

Fig. 7.

Findings of the repeat gastroscopy: a gastric tube was present in the esophageal lumen with smooth mucosal surface and a clear submucosal vascular network; the dentate line was distinct; the cardiac orifice had normal opening and closure with smooth mucosa; moderate mucus and brown retained fluid were noted in the residual stomach; mild congestion of the residual gastric mucosa with natural rugal folds; the gastrojejunal anastomosis was patent with mucosal congestion and edema but no active bleeding; advancement of the endoscope 20 cm past the gastrojejunal anastomosis revealed no obvious abnormalities in the efferent loop mucosa, a clear intestinal lumen with no bloodstains; further endoscopic advancement was technically difficult, the jejunojejunal anastomosis was not visualized, and no definite bleeding point was identified throughout the examination

Fig. 8.

Angiographic findings: multiple angiograms of the superior mesenteric artery showed no contrast medium extravasation or vascular malformations; the gastroduodenal artery was clearly opacified, and angiography at the catheter opening revealed intense staining in the blood supply area of the artery and accelerated venous return, with no obvious contrast medium extravasation. A 2.0 F microcatheter was used to superselect the branches of the gastroduodenal artery, and embolization was performed with a coil system [8510-0410/MicroVention]. A follow-up angiogram 5 minutes later showed complete occlusion of the embolized artery, and no new compensatory collateral branches were observed on superior mesenteric artery angiography (Fig. 9).

Fig. 9.

Interventional embolization results

Postoperative comprehensive support and rehabilitation

No recurrent gastrointestinal bleeding occurred after selective gastroduodenal artery embolization. In accordance with the refined treatment plan formulated by the hospital-wide MDT, the child’s Hb gradually increased and stabilized above 110 g/L, and WBC count and CRP levels returned to normal ranges. The abdominal drainage tubes and nasointestinal feeding tube were removed sequentially, and the diet was gradually transitioned from liquid to semi-liquid diets, with no abdominal distension, vomiting, or other adverse symptoms. The child was discharged from the hospital with complete clinical recovery after 6 weeks of inpatient treatment. During a 6-month follow-up after discharge, the child achieved normal growth and development, and all relevant laboratory test indicators remained within normal limits (Fig. 10).

Discussion

Based on the clinical management of this case and a review of recent domestic and international literature, we summarize the core features of duodenal perforation complicated with recurrent gastrointestinal bleeding in children. These features include unique pediatric physiological characteristics, complex etiology, age-related specificity, and distinct diagnostic and therapeutic challenges. This section analyzes the disease from three aspects: etiological and pathophysiological mechanisms, core diagnostic and therapeutic points, as well as clinical difficulties and corresponding strategies, and conducts a comparative discussion in combination with case reports by scholars worldwide.

Analysis of etiology and pathophysiological mechanisms

The etiology of duodenal perforation with recurrent gastrointestinal bleeding in children differs significantly from that in adults. In adults, the main causes are Helicobacter pylori (Hp) infection and non-steroidal anti-inflammatory drug (NSAID) use [8], whereas in children, the disease is mostly driven by the synergistic effect of multiple factors—centered on infectious etiologies, mucosal barrier injury, and anatomical particularities. These factors interact and superimpose to form a vicious cycle of mucosal injury → ulcer formation → perforation → vascular involvement → recurrent bleeding.

In this case, rotavirus infection combined with secondary bacterial infection was the primary inducement of initial mucosal injury, which is highly consistent with the age-specific feature that infectious mucosal injury is the main cause of gastrointestinal bleeding in early childhood. Rotavirus infection was considered an important precipitating and associated factor, which triggered initial intestinal mucosal injury and systemic inflammatory response, thereby promoting ulcer formation and perforation [4], Although the exact pathophysiological mechanism is not yet fully understood, according to the study by Boshuizenet et al. [9, 10], rotavirus infection can induce apoptosis of intestinal epithelial cells, damage the integrity of the mucosal barrier, and lead to the occurrence of perforation/ulcer; meanwhile, the systemic inflammatory response induced by viral infection stimulates excessive gastric acid secretion, and gastric acid together with pepsin further erodes the submucosa. Secondary bacterial infection triggers suppurative inflammation of the intestinal wall, leading to mucosal erosion and ulcer formation; the progressive deepening of ulcers penetrates the muscular layer and causes duodenal perforation. This is consistent with the etiology of pediatric duodenal ulcer perforation reported by Suraj et al. [11], in which 8 out of 12 pediatric perforation cases had a history of intestinal viral or bacterial infection, confirming that infection is the primary risk factor for duodenal perforation in children. After perforation, gastrointestinal contents leak into the abdominal cavity, inducing diffuse peritonitis and exacerbating the systemic inflammatory response, which forms a positive feedback loop of inflammation → gastric acid secretion and results in refractory ulcers [12].

In addition, postoperative intestinal dysmotility, inadequate decompression, and impaired distal intestinal passage may have contributed to the clinical course. Rotavirus enteritis and postoperative peritonitis can induce intestinal ileus, resulting in impaired distal intestinal transit and increased intraduodenal pressure. Elevated duodenal pressure may have caused mechanical stress on the repaired perforation site, leading to delayed healing, ulcer progression, and eventual rupture of exposed blood vessels, which promoted recurrent bleeding. This mechanism has also been reported in pediatric patients with duodenal perforation, where persistent intestinal dysmotility increases the risk of postoperative complications [10].

The duodenal bulb and descending duodenum are directly supplied by branches of the gastroduodenal artery. This region is characterized by a thin intestinal wall and superficial submucosal blood vessels; in children, blood vessel walls are thin and poor in elasticity, making ulcers highly prone to eroding arterial vessels and causing pulsatile bleeding [13, 14]. Additionally, surgical procedures such as perforation repair and ulcer suture ligation can lead to local vascular adhesion and malformation; the persistent postoperative inflammatory response stimulates the vascular wall, easily triggering recurrent vascular rupture and bleeding, which forms the pathophysiological basis for recurrent bleeding. Furthermore, children have a small blood volume (approximately 80–100 mL/kg), and recurrent bleeding can rapidly lead to hemorrhagic shock, induce coagulation dysfunction in the body, further reduce hemostatic efficiency, and exacerbate bleeding risk [15]. Severe bleeding in children can lead to coagulation disorders and increase the risk of bleeding [16], which is consistent with the coagulation abnormality observed in the present case with a cumulative blood loss of approximately 1500 mL (accounting for about 120% of the total blood volume).

Core diagnostic and therapeutic points, clinical difficulties and corresponding strategies

The diagnosis and treatment of duodenal perforation with recurrent gastrointestinal bleeding in children should follow the principles of early identification, early diagnosis, accurate localization, precise hemostasis, emphasis on supportive care, and strong multidisciplinary collaboration. Combined with case reports in the literature over the past decade, the core points of each link are analyzed comparatively as follows:

Early diagnosis: vigilance for non-specific symptoms and timely completion of key examinations

Difficulty

Children have poor ability to express symptoms and only present with non-specific manifestations such as diarrhea, abdominal pain, and fever in the early stage, which is easily misdiagnosed as common intestinal viral infection. Clinical practitioners need to pay close attention to warning signs of ineffective conventional treatment. Vidović S et al. reported in a systematic review that the early misdiagnosis rate of duodenal perforation in children is as high.

Strategy

Based on the present case, if diarrhea, abdominal pain accompanied by fever fails to relieve after 3–5 days of anti-infection and antidiarrheal treatment, or if symptoms such as poor mental status, pale complexion, hematochezia, and coffee-ground vomiting occur, abdominal plain CT, dynamic monitoring of hemoglobin + CRP, and fecal occult blood test should be completed immediately. Zhang et al. [17] reported 32 cases of pediatric gastrointestinal perforation, in which the diagnostic accuracy of abdominal CT reached 96.9%, much higher than the 62.5% of abdominal X-ray plain film. Demir M et al. [18] also confirmed in a study on laparoscopic repair of duodenal perforation in children that abdominal CT can clearly identify the perforation site and surrounding inflammatory adhesions, providing an important basis for the formulation of surgical plans. Dynamic changes in hemoglobin and CRP can reflect disease progression: for example, the sharp drop in hemoglobin from 143 g/L to 60 g/L and the increase in CRP from < 0.5 mg/L to 22.62 mg/L in the present case indicated aggravated mucosal injury and complicated severe infection, which provided a critical basis for emergency surgery.

We acknowledge that intraoperative endoscopy was not performed during the first operation, which represents a potential limitation. The decision was based on the emergency clinical scenario, severe peritoneal contamination, and the need for rapid control of perforation and sepsis in a critically ill 2-year-old child. At that time, intraoperative endoscopy would have significantly prolonged anesthesia time and increased the risk of hemodynamic instability. However, we recognize that this may have led to missed detection of occult posterior duodenal ulcer and exposed arterial vessels, which were likely already present but unrecognized. This unrecognized ulcerative lesion was an important contributing factor to postoperative recurrent bleeding. Future studies may consider selective intraoperative endoscopy in hemodynamically stable children with duodenal perforation to exclude occult ulcerative lesions.

Emergency surgery: perforation repair + infection control with concurrent vascular assessment

The core objectives of emergency surgery are to repair the perforation, thoroughly clear abdominal infection, and assess vascular involvement. Duodenal perforation in children is mostly complicated with abdominal suppurative infection; during surgery, it is necessary to completely remove abdominal effusion, purulent exudate, and food residue, and repeatedly irrigate the surgical field with warm normal saline postoperatively until the irrigant becomes clear, to avoid residual infection leading to refractory ulcers [19]. Meanwhile, special attention should be paid to the assessment of blood vessels around the perforation; for patients with severe mucosal eversion and erosion, vigilance for vascular involvement is required to predict postoperative bleeding. Laparoscopic repair has become the preferred surgical method for pediatric gastrointestinal perforation due to its minimal trauma and rapid recovery. Chan KS et al. [20] reported Laparoscopic surgery has far fewer complications than open surgery. However, open surgery is still required for cases complicated with severe adhesions or massive bleeding. Sermonesi G et al. [21] suggests laparoscopy as the first approach for stable patients undergoing emergency abdominal surgery for general surgery emergencies and abdominal trauma.

Management of recurrent bleeding: localization as priority, combined multimodal approaches, and individualized selection

A critical contributing factor to recurrent bleeding was unrecognized posterior duodenal ulcer and exposed arterial vessels at the first surgery. The anterior perforation was obvious and repaired, while the posterior ulcer remained undetected due to inflammatory adhesions and lack of intraoperative endoscopic evaluation.

Difficulty

The pediatric gastrointestinal lumen is narrow and intestinal mobility is high; bloody fluid obscures the visual field during active bleeding, leading to high failure rate of single examination. Inflammatory adhesions after perforation cause disorder of vascular anatomical structure, resulting in difficulty in localization during surgical exploration [22].

Strategy

Follow the multimodal localization approach of gastroscopy → abdominal CTA → angiography [23]. Endoscopy is the preferred method for diagnosis and treatment, however, the procedure is technically difficult in children and is suitable for cases with moderate blood loss and clear visual field. Novak et al. [24] proposed that for massive gastrointestinal bleeding in children, angiography can be performed directly, which achieves both localization and embolization hemostasis and effectively improves diagnostic and therapeutic efficiency. For interventional procedures, small-caliber catheters ( 2.0 F microcatheters) should be selected and operated by experienced interventional physicians; superselective catheterization should avoid damaging surrounding normal blood vessels.

Hemostatic regimens should be selected individually according to bleeding type and location: ① For pulsatile bleeding, superficial suture ligation has poor efficacy, and full-thickness suture ligation is required while avoiding injury to important anatomical structures such as the pancreaticobiliary duct. In the present case, full-thickness suture ligation was performed after ineffective superficial suture ligation during the second operation, which is consistent with the suture principle for duodenal arterial bleeding in children proposed by Li et al. ② For refractory recurrent bleeding, transcatheter arterial embolization (TAE) is the preferred option. Superselective embolization of the bleeding vessel has high hemostatic efficiency and minimal impact on the blood supply of abdominal organs in children. which is consistent with the successful hemostasis after interventional embolization in the present case. Meanwhile, the application of pediatric-specific small-caliber catheters can significantly reduce the technical difficulty; the 2.0 F microcatheter used for superselective catheterization in the present case effectively avoided vascular injury.

Gastrointestinal reconstruction: balancing hemostasis and protection of pediatric digestive function

When ulceration is extensive with mucosal erosion and hemostasis carries the risk of pancreaticobiliary duct injury, gastrointestinal reconstruction surgery is indicated, with the core principle of excluding the diseased intestinal segment and preserving the normal digestive structure. The pediatric gastrointestinal tract is in the developmental stage; reconstruction surgery should simplify the procedure as much as possible to avoid long-term malnutrition and digestive dysfunction caused by excessive surgery, which is consistent with the principle of “minimal trauma and maximal functional preservation” for pediatric gastrointestinal reconstruction proposed by Dong et al. In the present case, gastrointestinal reconstruction was performed during the second operation, which fundamentally avoided re-erosion of blood vessels by ulcers and minimized the long-term impact on the child’s digestive function. The child had normal digestive function during the 6-month postoperative follow-up. In addition, gastrointestinal reconstruction for complex peptic ulcers in children that the postoperative rebleeding rate of gastrojejunal Roux-en-Y anastomosis is only 5.6%, making it the preferred reconstruction method for refractory duodenal ulcers in children.

Whole-course management: MDT collaboration + refined comprehensive support to reduce rebleeding risk

The multidisciplinary team (MDT) collaborative diagnosis and treatment model is the core guarantee for such diseases, which can realize standardized whole-course management from diagnosis to treatment and rehabilitation, and avoid the limitations of single-department diagnosis and treatment. The Pediatric Branch of the Chinese Medical Association proposed in the consensus on pediatric MDT diagnosis and treatment that whole-course MDT collaboration is required for rare pediatric acute abdominal diseases, which can improve diagnostic and therapeutic efficiency by more than 60%. The three key clinical decisions for the present case (second operation, interventional therapy, and postoperative comprehensive plan) were all formulated through hospital-wide MDT discussion, effectively avoiding clinical risks. This is consistent with the results of MDT diagnosis and treatment for pediatric gastrointestinal bleeding reported by Novak et al. In which the rebleeding rate of children with refractory gastrointestinal bleeding treated by MDT collaboration was 58.3% lower than that of single-department treatment.

Postoperative refined comprehensive support is the key to reducing the risk of rebleeding, with four key aspects to be focused on: ① Acid suppression therapy: High-dose intravenous PPI infusion for a course of no less than 4–6 weeks to inhibit gastric acid secretion and promote ulcer healing. Jiang et al. [23] proposed that the PPI dosage for acid-related diseases in children is 0.8–1.0 mg/(kg·dose) q12h, which is consistent with the medication regimen of the present case. ② Nutritional support: Parenteral nutrition is given during the fasting period to ensure a caloric supply of 100 kcal/(kg·d); enteral nutrition is gradually transitioned to when the condition is stable, with nasointestinal tube infusion preferred to avoid gastric stimulation. which is in line with the Guidelines for Pediatric Enteral Nutritional Support formulated by the Gastroenterology Group of the Pediatric Branch of the Chinese Medical Association. ③ Coagulation support: Vitamin K1, fibrinogen, and prothrombin complex are administered to children with recurrent bleeding to correct the vicious cycle of bleeding → coagulation disorder, consistent with the diagnostic and therapeutic principles for pediatric coagulation dysfunction proposed by the Hematology Group of the Pediatric Branch of the Chinese Medical Association [25]. ④ Infection control: Adjust the antibiotic regimen according to inflammatory indicators and bacterial culture results until inflammatory indicators return to normal, to avoid residual infection stimulating the mucosa. Wong, Beatrice P. Y. et al. [26] confirmed in their study that postoperative anti-infection treatment until CRP < 5 mg/L in children with gastrointestinal perforation can increase the ulcer healing rate by 30%.

In summary, the recurrent gastrointestinal bleeding in this patient was likely multifactorial, including unrecognized posterior duodenal ulcer at the first surgery, infectious mucosal injury, persistent postoperative inflammation, inadequate gastrointestinal decompression, and intestinal dysmotility. These factors interacted synergistically, leading to delayed ulcer healing, progressive mucosal erosion, and eventual arterial bleeding. A balanced consideration of these mechanisms is essential for understanding the clinical course and optimizing management strategies for similar pediatric patients.

Conclusion

Duodenal perforation complicated with recurrent gastrointestinal bleeding is a rare acute and critical condition in pediatrics, whose etiology is mainly based on infection, mucosal barrier injury, and anatomical particularities. Its pathophysiological process presents a vicious cycle of mucosal injury → ulcer formation → perforation → vascular involvement → recurrent bleeding, and the disease predominantly occurs in infants aged 1–3 years, which is highly consistent with the etiological and pathophysiological characteristics of cases reported by scholars worldwide. The core clinical difficulties in diagnosis and treatment include high early misdiagnosis rate, difficulty in localizing bleeding points, limitations of surgical and interventional procedures due to pediatric physiological characteristics, and high risk of postoperative rebleeding—these are common challenges faced by pediatric clinicians globally.

The diagnosis and treatment of duodenal perforation with recurrent gastrointestinal bleeding in children must fully consider the physiological characteristics of children, integrate the advantages of multiple disciplines, and realize standardized whole-course management from diagnosis to treatment and rehabilitation, so as to effectively reduce the mortality and rebleeding risk and improve the long-term prognosis of children. Meanwhile, it is necessary to strengthen health education for parents, avoid self-medication, cultivate reasonable eating habits, and reduce risk factors for gastrointestinal mucosal stimulation in early childhood and school age.

Abbreviations

BP

Blood Pressure

CT

Computed Tomography

CRP

C-reactive Protein

Hb

Hemoglobin

Hp

Helicobacter pylori

MDT

Multidisciplinary Team

NSAIDs

Non-steroidal Anti-inflammatory Drugs

NPO

Nil Per Os

P

Pulse

PPI

Proton Pump Inhibitor

POD

Postoperative Day

R

Respiration

RBC/HP

Red Blood Cells per High-power Field

TAE

Transcatheter Arterial Embolization

T

Temperature

WBC

White Blood Cell

Authors’ contributions

Rongkun Zhu and Yanan Zhang contributed equally to this work and share first authorship. Conceptualization: Xiwei Hao; Data Curation: Rongkun Zhu, Yanan Zhang, Di Wang, Xiaoxuan Ma; Formal Analysis: Rongkun Zhu, Yanan Zhang; Investigation: Rongkun Zhu, Yanan Zhang, Xiwei Hao; Methodology: Rongkun Zhu,; Project Administration: Xiwei Hao; Software: Rongkun Zhu, Yanan Zhang; Validation: Xiwei Hao; Funding Acquisition: Qian Dong; Writing – Original Draft: Rongkun Zhu, Yanan Zhang; Writing – Review & Editing: Qian Dong, Xiwei Hao.All authors have read and approved the final version of the manuscript and confirm the order of authorship as listed.

Funding

This work was supported by Taishan Scholar Climbing Program Expert of Shandong Province (Grant No. tspd20240820);

Data availability

The datasets used and/or analyzed during the current study are available from the corresponding authors on reasonable request.

Declarations

Ethics approval and consent to participate

This study was conducted in accordance with the Declaration of Helsinki. Ethical approval was obtained from the Ethics Committee of The Affiliated Hospital of Qingdao University (Approval No.: QYFY WZLL 42319).

Consent for publication

Written informed consent was obtained from the patient’s legal guardian for publication of this case report and any accompanying images.

Competing interests

The authors declare no competing interests.