Published online Jan 14, 2027. doi: 10.3748/wjg.123953
Revised: July 21, 2026
Accepted: September 9, 2026
Published online: January 14, 2027
Processing time: 162 Days and 14.6 Hours
Gastroduodenal arterioportal fistula (GDA-APF) is an extremely rare vascular malformation that commonly presents with unexplained upper gastrointestinal bleeding, abdominal pain, ascites, nausea, vomiting, diarrhea, and even con
We report two cases of GDA-APF managed by distinct strategies dictated by lesion characteristics. In case 1, an incidentally detected fistula with a relatively well-defined vascular configuration - comprising a discrete aneurysmal cavity and an accessible draining vein - was cured by combined transarterial and transportal coil embolization with absolute ethanol sclerotherapy with no sym
GDA-APF lacks specific signs. Treatment of choice should be determined by fistula anatomy and concomitant solid-organ pathology.
Core Tip: Gastroduodenal arterioportal fistula is an exceedingly rare vascular malformation with non-specific symptoms. Through two contrasting cases, we highlight that treatment should be individualized by fistula anatomy and coexisting solid-organ pathology rather than a rigid “intervention-first” rule. Anatomically simple lesions with an accessible draining vein are curable by combined transarterial and transportal embolization, whereas complex, multi-fed fistulas with pancreatic arteriovenous malformation warrant upfront pancreaticoduodenectomy.
- Citation: Zhang YP, Lu Y, Wei HZ, Yang M, Liang B, He L, Zhao CB, Deng ZL, Wang JJ, Wang GQ, Wu HS, Yin T. Gastroduodenal arterioportal fistula: Two case reports and review of literature. World J Gastroenterol 2027; 33(2): 123953
- URL: https://www.wjgnet.com/1007-9327/full/v33/i2/123953.htm
- DOI: https://dx.doi.org/10.3748/wjg.123953
Arterioportal fistulas (APFs) cause arterialization and increased pressure in the portal venous system due to an ano
Gastroduodenal APF (GDA-APF) refers to an abnormal communication between the gastroduodenal artery (GDA) and the portal vein or its tributaries, allowing arterial blood to flow directly into the portal venous system[5]. GDA-APF most commonly occurs as a late complication of gastric surgery, possibly due to simultaneous ligation of the artery and adjacent veins[11-15], while cases caused by congenital vascular malformations are extremely rare. Here, we report two cases of GDA-APF that were successfully treated with interventional therapy and surgical treatment, respectively. In this article, we provide valuable insights for establishing standardized treatment protocols for GDA-APF.
Case 1: A 27-year-old woman presented with an arteriovenous malformation incidentally identified during a routine health screening one month prior to admission.
Case 2: A 38-year-old man presented with a one-month history of intermittent, sharp epigastric pain, accompanied by hematemesis and melena for two weeks.
Case 1: Approximately one month before presentation, the patient underwent a routine health screening, during which abdominal imaging incidentally revealed a vascular abnormality suggestive of an APF. Throughout this interval, the patient remained entirely asymptomatic, with no complaints of abdominal pain, distension, hematemesis, melena, jaundice, fatigue, or unintentional weight loss. No prior interventions or treatments was administered before her pre
Case 2: One month prior to admission, the patient developed intermittent, sharp epigastric pain without identifiable precipitating factors. At onset, the pain was not associated with radiation, fever, jaundice, or alterations in bowel habits. Approximately two weeks before admission, the patient developed recurrent episodes of hematemesis and melena, accompanied by progressive fatigue and pallor. Over this one-month symptomatic period, he experienced an unintentional weight loss of approximately 10 kg.
Case 1: The patient had no significant past medical history, including hypertension, diabetes mellitus, hepatitis, pancreatitis, or coagulopathy. She denied any history of abdominal trauma, previous abdominal surgery, or invasive pro
Case 2: The patient had no prior history of peptic ulcer disease, chronic hepatitis, liver cirrhosis, pancreatitis, or coagulation disorders. He denied any history of abdominal trauma or prior abdominal surgery.
Case 1: The patient denied any history of tobacco use, alcohol consumption, or illicit drug use. She reported no known drug or food allergies. Her family history was unremarkable, with no documented hereditary vascular anomalies, hemorrhagic disorders, or malignancies among first-degree relatives.
Case 2: The patient denied any history of long-term tobacco or alcohol use and reported no known drug allergies. There was no family history of gastrointestinal bleeding, vascular malformations, hereditary hemorrhagic conditions, or malignancies.
Case 1: On admission, the patient’s vital signs were within normal limits. Abdominal examination revealed a soft, non-distended, non-tender abdomen. There was no tenderness, rebound tenderness, or guarding on palpation. No abdominal masses or organomegaly were appreciated, and no abdominal bruit was auscultated. The remainder of the systemic examination was unremarkable.
Case 2: On admission, the patient’s vital signs were within normal limits. He appeared pale. Abdominal examination revealed a soft abdomen with localized tenderness in the epigastric region. No rebound tenderness or guarding was elicited. Murphy’s sign was negative, and no palpable masses or organomegaly were detected. Bowel sounds were normoactive, and no abdominal bruit was auscultated.
Case 1: The hemoglobin level was 120 g/L, with no evidence of anemia. Routine urinalysis and stool examination, including fecal occult blood testing, were unremarkable. Serum biochemistry, including hepatic and renal function tests, coagulation profile, immunological markers, and infectious disease markers, demonstrated no clinically significant abnormalities.
Case 2: The hemoglobin level was 95 g/L. Fecal occult blood testing was positive. Serum tumor markers, including carcinoembryonic antigen, carbohydrate antigen 19-9, carbohydrate antigen 125, and neuron-specific enolase, were all within normal limits. Routine urinalysis, serum biochemistry, immunological markers, and infectious disease markers showed no clinically significant abnormalities.
Case 1: Contrast-enhanced abdominal computed tomography (CT) demonstrated thickening of the posterior pancreaticoduodenal vascular arcade, with a saccular dilatation at the arterial end. This saccular structure communicated via a fistulous tract with a draining vein that emptied into the superior mesenteric vein (SMV), with aneurysmal dilatation noted in the proximal segment of the draining vein. Based on these findings, a preliminary diagnosis of GDA-APF with aneurysm formation at the arterial end was established. To further delineate the vascular anatomy, digital subtraction angiography (DSA) was performed. Selective celiac trunk and SMA angiography revealed dilated branches of the superior mesenteric artery and the GDA, with a distal saccular aneurysmal protrusion and opacification of the draining vein (Figure 1). Subsequently, ultrasound-guided percutaneous transhepatic puncture of the right portal vein branch was performed, and venography confirmed that several portal venous branches communicated with the aneurysmal cavity.
Case 2: Magnetic resonance cholangiopancreatography demonstrated a 21 mm × 14 mm T1-hypointense lesion in the pancreatic head (Figure 2). To identify the source of gastrointestinal bleeding, esophagogastroduodenoscopy was performed, revealing fresh blood adherent to the anterior wall at the junction of the duodenal bulb and the descending duodenum; however, no definitive ulcer or neoplastic lesion was identified (Figure 2B). Endoscopic ultrasonography (EUS) further characterized the pancreatic lesion as a nearly round, hypoechoic mass with relatively well-defined margins in the uncinate process of the pancreas. Prominent circumferential blood flow signals were observed around the lesion, and elastography indicated intermediate tissue stiffness (Figure 2C). EUS-fine-needle aspiration (EUS-FNA) was subsequently performed to rule out hypervascular tumors using a 22-gauge needle (Cook Medical, IN, United States) under 5 mL of negative-pressure suction, with two passes comprising 20 to-and-fro movements each. During the procedure, abundant intralesional blood flow signals were noted, and the lesion demonstrated a marked tendency to bleed. Histopathological examination of the aspirate revealed grayish-brown, thread-like tissue fragments measuring approximately 0.8 cm in aggregate length, microscopically composed of hemorrhagic and inflammatory fibrinous tissue; however, a definitive histological diagnosis could not be established (Figure 3A). Given the persistent hematemesis and progressive anemia, celiac and superior mesenteric arteriography was performed. DSA revealed an abnormal vascular network in the descending segment of the GDA, with early opacification of the portal vein, indicating dual arterial supply from both GDA and SMA (Figure 2D).
Based on the combined findings of contrast-enhanced abdominal CT, celiac and superior mesenteric arteriography, and percutaneous transhepatic portal venography, a definitive diagnosis of GDA-APF with aneurysm formation at the portal venous end was established.
Based on the clinical presentation, imaging findings, intraoperative observations, and postoperative histopathological examination, a definitive diagnosis of GDA-APF with concomitant pancreatic arteriovenous malformation (P-AVM) was established.
Although the patient was clinically asymptomatic, there was potential for massive gastrointestinal bleeding from the GDA-APF in the future. Given the patient’s young age, the lesion location, and its anatomical characteristics, interventional embolization was selected as the definitive therapeutic strategy. Under local anesthesia, the right femoral artery was accessed using the Seldinger technique, and catheters were sequentially advanced into the celiac trunk and SMA for arteriography and DSA imaging. Subsequently, under ultrasound guidance, the right portal vein branch was punctured, and a 5F sheath was introduced. The catheter was then advanced through the SMV into the aneurysmal cavity and its draining vein, where multiple coils were deployed to embolize both the aneurysm and the draining vein. A microcatheter was then advanced through the GDA into the aneurysmal cavity for sclerotherapy with absolute ethanol, followed by coil embolization of the feeding branches arising from SMA and GDA (Figure 1B). Completion angiography demonstrated satisfactory embolization with complete occlusion of the lesion (Figure 1C). Finally, two additional coils were deployed to occlude the transhepatic puncture tract to prevent post-procedural hemorrhage.
Given the patient’s persistent hematemesis and progressive anemia, celiac arteriography combined with transcatheter arterial embolization was initially performed as the first-line therapeutic approach. Under local anesthesia, the right femoral artery was accessed using the Seldinger technique, and a 5F Yashiro catheter and microcatheter (Terumo, Tokyo, Japan) were sequentially advanced into the celiac trunk and SMA for angiography and DSA imaging. Through superselective microcatheter cannulation of the feeding branches arising from GDA and SMA, a total of 17 coils (Cook Medical, IN, United States) measuring 6, 8, and 10 mm in diameter were deployed for embolization. Immediate post-embolization angiography demonstrated acceptable occlusion of the abnormal vascular network. However, the patient subsequently experienced recurrent hematemesis with further decline in hemoglobin levels, indicating failure of endovascular therapy. Given the lesion location and persistent bleeding, a multidisciplinary team consultation recommended definitive surgical management, and pancreaticoduodenectomy (Whipple procedure) was performed. Postoperative histopathological examination of the resected specimen confirmed the presence of numerous malformed arteriovenous vessels within the pancreatic parenchyma, consistent with P-AVM (Figure 3B).
The patient’s post-procedural course was uneventful with no complications. The post-procedure hospital stay was one week. The patient did not return to our institution for imaging follow-up; telephone follow-up at 24 months confirmed that she remained entirely asymptomatic, with no gastrointestinal bleeding, abdominal pain, or ascites.
Following pancreaticoduodenectomy, the patient’s hematemesis and melena resolved completely, and no recurrent gastrointestinal bleeding was observed throughout the postoperative period. At one month postoperatively, both body weight and hemoglobin levels had returned to normal range. Contrast-enhanced CT at 12 (Figure 4A) and 24 months (Figure 4B) showed expected post-pancreaticoduodenectomy changes with a patent pancreaticojejunal anastomosis and only mild main-pancreatic-duct dilatation. Critically, no recurrent arterioportal shunt, abnormal vascular network, or early portal-venous opacification was identified, and there was no evidence of portal hypertension. The patient remained asymptomatic with normal hemoglobin throughout the 24-month follow-up. The comparative information of the two patients in this study is presented in (Table 1).
| Case 1 | Case 2 | |
| Basic information | ||
| Age | 27 years | 38 years |
| Gender | Female | Male |
| Chief complaint | Incidental detection on health screening | Epigastric pain, hematemesis and melena |
| Clinical manifestations | ||
| Main symptoms | Asymptomatic | Intermittent sharp epigastric pain, hematemesis, melena |
| Weight change | No significant change | Weight loss of 10 kg |
| Significant past history | No | No |
| Significant personal and family history | No smoking, alcohol, or allergies; family history unremarkable | No smoking, alcohol, or allergies; family history unremarkable |
| Physical examination | Soft abdomen; no tenderness or bruit | Pale; epigastric tenderness; no bruit |
| Imaging studies | ||
| Primary examinations | Contrast-enhanced abdominal CT, DSA, percutaneous transhepatic portal venography | MRCP, EGD, EUS, EUS-FNA, DSA |
| Lesion report | CT: Thickening of posterior pancreaticoduodenal vascular arcade with saccular dilatation; DSA: Thickening of branches of superior mesenteric artery and gastroduodenal artery, with “saccular” aneurysmal protrusion distally and visualization of draining veins; portal venography: Several portal branches communicating with the aneurysm | MRCP: 21 mm × 14 mm T1 hypointense lesion in pancreatic head; EGD: Fresh blood at duodenal bulb-descending junction, no ulcer/tumor; EUS: Round, well-defined hypoechoic uncinate mass with prominent peripheral flow; EUS-FNA: Hemorrhagic and inflammatory fibrinous tissue, non-diagnostic DSA: Abnormal vascular network with early portal vein opacification in the vertical course of gastroduodenal artery, supplied by gastroduodenal and superior mesenteric arteries |
| Laboratory tests | ||
| Hemoglobin | 120 g/L | 95 g/L (mild anemia) |
| Other labs | Fecal occult blood negative; other panels unremarkable | Fecal occult blood positive; tumor markers (CEA, CA19-9, CA-125, NSE) normal; other panels unremarkable |
| Complications | ||
| Surrounding organ pathology | None | Concomitant pancreatic arteriovenous malformation |
| Treatment plan | ||
| Interventional approach | Combined arterial and portal venous embolization | Arterial embolization alone |
| Treatment method | Endovascular embolization (coils + absolute ethanol sclerosant) | Endovascular embolization (coils) failed, followed by pancreaticoduodenectomy |
| Treatment outcome | Successful single interventional treatment | Interventional treatment failed, cured by surgery |
| Prognosis | ||
| Follow-up results | Satisfactory embolization with complete occlusion of lesion. Telephonic follow-up at 12 months and 24 months; patient remained entirely asymptomatic | Weight recovered and hemoglobin normalized at 1 month postoperatively. Contrast-enhanced CT at 12 months and 24 months showed no recurrent arterioportal shunt and no portal hypertension |
Extrahepatic APF involving GDA and SMV is an uncommon disorder characterized by abnormal communication between the arterial and portal circulation[16], allowing high-pressure arterial blood to flow directly into the venous system. This may weaken or rupture the venous wall and reduce perfusion to surrounding tissues, potentially leading to portal hypertension and regional intestinal ischemia. Since only a minority of patients with APFs manifest symptoms and the clinical manifestations lack specificity, misdiagnosis and missed diagnosis are common. Most patients complain of abdominal pain, caused by either the pulsatile fistulous mass or intestinal ischemia. Other common symptoms of intestinal ischemia are diarrhea, weight loss, or gastrointestinal bleeding[15].
Conventional imaging modalities (such as ultrasound, CT, and magnetic resonance imaging) can provide useful information for diagnosing APFs. Doppler ultrasound can not only detect the location of APFs but also assess blood flow direction[16]. The CT scan depicts the vascular nature of the pathology on contrast enhanced images and may reveal underlying abnormalities such as pancreatitis or pseudocyst[8]. Magnetic resonance angiography can be used in cases with contraindications to conventional angiography. However, endoscopy often reveals only varices or active bleeding, making it difficult to identify the underlying cause. For patients with recurrent gastrointestinal bleeding of unknown etiology or when routine examinations fail to identify a clear source of bleeding, vascular malformations should be highly suspected and included in the differential diagnosis. DSA can directly visualize dilated feeding arteries, abnormal vascular networks, and early portal vein opacification, representing the gold standard for diagnosing APFs. Ultrasound or CT can serve as initial screening tools, while DSA plays a central role in confirming the diagnosis and formulating treatment strategies.
The diagnostic pitfalls of these lesions are well illustrated by case 2. EUS-FNA was performed because cross-sectional imaging revealed a hypervascular hypoechoic mass in the pancreatic head with negative tumor markers, and histological characterization was sought to exclude a neuroendocrine or other solid neoplasm before definitive management. In retrospect, the prominent circumferential Doppler flow signals should have raised suspicion of a vascular lesion. FNA of a hypervascular pancreatic lesion carries a substantial risk of bleeding and a low diagnostic yield, as reflected by the marked intraprocedural bleeding tendency and the non-diagnostic, purely hemorrhagic aspirate obtained in this case. We therefore caution that abundant intralesional flow on EUS should prompt consideration of a vascular malformation, in which case contrast-enhanced imaging or angiography - rather than FNA - should be prioritized to avoid procedure-related hemorrhage.
Guzman et al[3] have proposed a novel classification for APFs with therapeutic implications: Type I APFs are small peripheral intrahepatic fistulas with minimal physiological impact, typically asymptomatic, and generally close spontaneously within 1 month. They commonly occur following percutaneous liver biopsy. For these fistulas, clinical follow-up with Doppler ultrasound monitoring for 1 month is appropriate; if the fistula persists for longer than 1 month or if the patient becomes symptomatic, transcatheter embolization is recommended. Type II APFs are larger and more centrally located, and can be either intrahepatic or extrahepatic. They commonly occur following penetrating abdominal trauma or result from splenic artery aneurysm erosion into the portal venous system. These fistulas can lead to portal hypertension and hepatic fibrosis. To prevent irreversible complications from portal hypertension, treatment should consist of embolization or conventional surgery as seen in this case series. Type III APFs are rare congenital fistulas and typically present as diffuse intrahepatic lesions that can cause severe portal hypertension during childhood. These patients require a specialized pediatric hepatobiliary center where treatment may consist of hepatic artery ligation, embolization, resection, or liver transplantation.
All extrahepatic APFs should be treated, as they do not close spontaneously under normal circumstances[17]. In general, APFs require early treatment, particularly in asymptomatic patients with high-flow fistulas, to prevent the development of complications. Both open and endovascular management of APFs has been well described[5,18,19], but endovascular interventional techniques are increasingly being used as the preferred treatment approach, including embolization and stent placement (Table 2)[5,19,20]. Earlier reports relied predominantly on surgical excision, which generally proved curative, whereas the majority of recent cases have been managed with transcatheter embolization, yielding favorable outcomes in most patients. Currently, endovascular therapy as emerged as the initial treatment of choice for the majority of GDA-APF.
| Case | Ref. | Age (years) | Gender | Etiology | Symptoms | Aneurysm/pseudoaneurysm (angiographic) | Therapy | Outcome |
| 1 | [15] | 48 | M | Partial gastrectomy, V | Pain | - | Excision | Good |
| 2 | [15] | 52 | F | Partial gastrectomy, V | Pain, hematochezia | Small aneurysm | Excision | Good |
| 3 | [15] | 53 | M | BI, V | - | - | Excision | Good |
| 4 | [15] | 48 | M | Whipple pancreaticoduodenectomy | Hematemesis | Large aneurysm | Balloon + surgery | Death by exsanguination (postoperative) |
| 5 | [15] | 61 | F | Partial gastrectomy, BII | Diarrhea, pain, abdominal claudication | Small aneurysm | Excision | Good |
| 6 | [15] | 54 | M | Trauma (stab wound) | - | Large aneurysm | Spontaneous thrombosis | Good |
| 7 | [15] | 62 | M | Partial gastrectomy, BII | Hematemesis, melena | Venous ectasia | None, inoperable | Death by liver failure (5 months) |
| 8 | [15] | 60 | M | partial gastrectomy, BII | Pain | - | Excision | Good |
| 9 | [15] | 36 | M | Partial gastrectomy, BII | - | Small aneurysm | Coil embolization | Good |
| 10 | [15] | 46 | F | Gastrectomy | Pain, weight loss | - | Coil embolization | Good |
| 11 | [15] | 48 | M | “Congenital” | Hematemesis | - | Portocaval shunt | Good |
| 12 | [15] | 53 | F | Rupture of pancreatic pseudocyst | Pain, hematemesis | (40 mm, diameter of cyst) | Detachable balloon embolization | Death (20 days) by volvulus and perforation |
| 13 | [18] | 44 | M | Total gastrectomy | Acute variceal bleeding | Large aneurysm | Coil embolization | Good |
| 14 | [20] | 45 | M | Laparoscopic cholecystectomy, laparotomy | Hematemesis, pain, diarrhea, weight loss | - | Microspheres embolization | Good |
| 15 | [16] | 70 | M | Cholecystectomy | Pain, melena | Large aneurysm | Coil embolization | Improved after embolization; recurrent bleeding at 3 years; good after TIPS |
| 16 | [21] | 39 | F | Chronic pancreatitis | Pain, chills, anemia | Approximately 4.5 cm GDA pseudoaneurysm | Coil/NBCA embolization + portal vein stenting | Good |
| 17 | [22] | 61 | M | Chronic pancreatitis | Pain, fevers, anemia | Approximately 7 cm GDA pseudoaneurysm | Coil embolization | Good |
| 18 | Present study, case 1 | 27 | F | - | - | Saccular aneurysm | Coil embolization + ethanol sclerotherapy | Good |
| 19 | Present study, case 2 | 38 | M | - | Pain, hematemesis, melena, weight loss | - | Coil embolization failed; Whipple pancreaticoduodenectomy | Good |
Interventional embolization offers significant advantages, including minimal invasiveness, repeatability, and rapid postoperative recovery. This technique involves superselective catheterization of feeding arteries and embolization using coils, embolic agents (such as tissue glue, Onyx), and other materials to occlude feeding arteries and arteriovenous fistula orifices, thereby blocking abnormal blood flow[21-25]. In the present series, the two cases were managed with markedly different endovascular strategies, the choice of which was guided by the vascular anatomy and hemodynamic characteristics of each lesion. In case 1, the lesion had a relatively well-defined configuration, with a discrete aneurysmal cavity and a draining vein accessible via the portal route; it was therefore treated with a dual-access approach - combined transarterial and percutaneous transhepatic transportal embolization - that simultaneously occluded the arterial inflow and the venous outflow, achieving complete and durable obliteration. In case 2, by contrast, the lesion had a complex architecture and was associated with P-AVM; occlusion of the arterial side alone failed to eliminate the residual shunting arising from the intraparenchymal nidus and collateral feeders, ultimately resulting in rebleeding. These contrasting outcomes highlight the inherent limitations of embolization: For multiple and complex fistulas, especially those with abundant arterial supply or deep-seated locations, interventional embolization often fails to achieve complete occlusion, with risks of vascular recanalization and symptom recurrence.
The reasons for interventional treatment failure in case 2 may include: First, the distal feeding arteries are often tortuous and small, making it difficult to achieve complete dense packing with coils[26]; second, the abnormal vascular network was supplied by multiple arteries, making residual shunting likely after single arterial route embolization, leading to post-embolization rebleeding; third, case 2 had concomitant P-AVM in addition to GDA-APF, which may have contributed to persistent bleeding after intervention[23,24,27,28]; fourth, the patient had extensive lesions, making it difficult to achieve comprehensive and durable embolization with coils alone.
The surgical treatment for multiple or complex fistulas includes fistula ligation and fistula excision[29-31]. For certain extrahepatic APFs, conventional surgery with direct fistula ligation while preserving the involved artery is considered the optimal choice[17,32]. When concomitant solid organ pathology is present (as in case 2 with P-AVM), pancreaticoduodenectomy (Whipple procedure) can serve as the definitive curative approach. This procedure can completely resect the diseased tissue containing the abnormal vascular network, with a high cure rate. Despite the significant surgical trauma and intraoperative bleeding risk, its therapeutic effect is definitive. Case 2 underwent pancreaticoduodenectomy after interventional failure, with complete resolution of hematemesis and normalization of hemoglobin levels postoperatively, fully demonstrating the irreplaceable role of surgery in treating APFs with concomitant solid organ involvement. Therefore, rather than applying a universal “intervention-first” hierarchy, the treatment of GDA-APF should be stratified according to the vascular anatomy and coexisting solid-organ pathology. For fistulas with a simple anatomical structure and accessible draining veins, in which endovascular embolization can achieve a curative effect (as in case 1), interventional therapy should be the treatment of choice. Conversely, for lesions with multiple feeders, high-flow hemodynamics, or an associated solid-organ vascular malformation such as P-AVM (as in case 2), upfront surgical resection may be the more direct and definitive option, as a preliminary attempt at embolization may merely delay curative treatment while increasing patient burden and cost.
GDA-APF is rare but can lead to severe complications, and high index of suspicion is warranted to diagnose it in patients with unexplained upper gastrointestinal bleeding. Precise imaging localization and combined (transarterial and transportal) embolization are effective for single fistula lesions; the failure rate with interventional therapy is high for high-flow, multi-source feeding lesions or those with concomitant solid organ pathology, and early surgical intervention should be considered. Treatment should be individualized, with intervention and surgery complementing each other to improve patient outcomes.
The authors express their gratitude to the contributing investigators and to the patients’ families for their cooperation.
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