Hemosuccus Pancreaticus from Large Inferior Pancreaticoduodenal Artery Pseudoaneurysm Complicating Chronic Pancreatitis

Abstract

Hemosuccus pancreaticus is an uncommon cause of upper gastrointestinal bleeding characterized by hemorrhage entering the pancreatic duct and draining into the duodenum. Although pseudoaneurysms may arise from several peripancreatic vessels in the setting of chronic pancreatitis, involvement of the inferior pancreaticoduodenal artery (IPDA) is particularly uncommon and carries a high risk of rupture. A man in his late 30s with a known history of chronic calcific pancreatitis presented with melena, severe anemia, and hemodynamic instability. Side-viewing duodenoscopy revealed intermittent bleeding from the ampulla of Vater, raising suspicion for hemosuccus pancreaticus. Computed tomography angiography identified a 6.4 cm IPDA pseudoaneurysm causing multi-organ compression. Successful endovascular coil embolization achieved complete occlusion of the pseudoaneurysm. This case demonstrates successful minimally invasive management and diagnostic challenges of a life-threatening vascular complication of chronic pancreatitis. High clinical suspicion, early targeted imaging, and prompt intervention are essential for preventing catastrophic hemorrhage.

INTRODUCTION

Hemosuccus pancreaticus represents a rare but potentially fatal cause of upper gastrointestinal haemorrhage, occurring in approximately 1 in 1500 cases of gastrointestinal bleeding.[1] The condition involves bleeding from the pancreatic duct into the duodenum through the ampulla of Vater, most commonly secondary to pseudoaneurysm rupture in chronic pancreatitis patients.[2]

Pseudoaneurysms develop in about 10% of chronic pancreatitis cases through enzymatic erosion of peripancreatic vessels.[3] While the splenic artery is most commonly affected, inferior pancreaticoduodenal artery (IPDA) involvement is exceptionally rare.[4] Early recognition and intervention are crucial, as untreated cases carry mortality rates approaching 90%.[1]

This report presents successful endovascular management of a large IPDA pseudoaneurysm causing hemosuccus pancreaticus with extensive multi-organ involvement.

CASE REPORT

A man in his late 30s with a 2-year history of chronic calcific pancreatitis without endocrine or exocrine insufficiency presented to the emergency department with a 3-day history of progressive dizziness and multiple episodes of melena. The dizziness was gradual in onset, intermittent in nature, and worsened with exertion. He reported progressive dyspnea that had worsened from New York Heart Association Class I to Class III over the same duration.

One day prior to presentation, he experienced a syncopal episode lasting approximately 10–15 min with his wife witnessing the episode. The episode was spontaneous with no history of convulsions, tongue bite, urinary incontinence, or postictal confusion. The patient regained consciousness spontaneously and was immediately oriented on recovery.

He described a 2-year history of intermittent colicky epigastric pain radiating to the back. Each episode was moderate in intensity, lasted several hours, bore no relation to meals, and was partially relieved by analgesics. The episodes were not associated with vomiting or hematemesis. However, the frequency and severity of the epigastric pain had notably increased over the preceding weeks.

His past medical history was significant for chronic alcohol consumption (70 g per day for 7 years), with his last alcohol intake being 2 years prior to presentation. There was no history of recent trauma, fever, nonsteroidal anti-inflammatory drug use, anticoagulant therapy, alcohol binge, or corrosive substance ingestion. He denied any history suggestive of chronic liver disease, gallstone disease, coagulopathy, or peptic ulcer disease. There was no history of chest pain, palpitations, orthopnea, pale stools, dark-colored urine, jaundice, pedal edema, abdominal distention, seizures, focal neurological deficits, head injury, or previous abdominal surgery. Family history was negative for gastrointestinal disease or bleeding disorders.

Examination

On general examination, the patient was conscious, alert, and oriented to time, place, and person. He was hemodynamically unstable with a blood pressure of 80/56 mmHg, requiring vasopressor support with noradrenaline infusion at 0.1 µg/kg/min. He was afebrile with a pulse rate of 90 beats per min, respiratory rate of 20 cycles per min, and oxygen saturation of 97% on room air.

The patient appeared pale and cachectic with signs of generalized wasting. There was no icterus, cyanosis, clubbing, lymphadenopathy, or peripheral edema. Bilateral pupils were equally reactive to light. Neurological examination, including motor system, sensory system, and higher mental functions, was unremarkable.

Abdominal examination revealed splenomegaly and a soft abdomen with moderate epigastric tenderness. There was no guarding, rigidity, or peritoneal signs. Cardiovascular and respiratory system examinations were unremarkable.

Investigations

Initial laboratory investigations revealed severe anemia with hemoglobin of 5.9 g/dL on presentation, requiring transfusion of two units of cross-matched packed red blood cells. Renal function tests, liver function tests, and serum electrolytes were within normal limits. Hypoproteinemia was noted with serum total protein of 4.5 g/dL and albumin of 2.5 g/dL. Glycated hemoglobin was 4.8%, and fasting lipid profile was within normal limits. Pancreatic enzymes were not elevated (serum lipase 10 U/L and serum amylase 56 U/L), consistent with chronic pancreatitis. Iron studies showed serum iron of 72 µg/dL, total iron-binding capacity of 172 µg/dL, transferrin saturation of 41.8%, and ferritin of 260 ng/mL, making iron deficiency anemia unlikely. Direct and indirect Coombs tests were negative with a reticulocyte count of 7% and serum lactate dehydrogenase of 201 U/L, making hemolytic anemia less likely. Prothrombin time (International normalized ratio), Vitamin B12 levels, and inflammatory markers (erythrocyte sedimentation rate, C-reactive protein, and procalcitonin) were within normal limits, making active sepsis unlikely.

Chest radiograph (PA view), electrocardiogram, and computed tomography (CT) of the brain were all normal. Urinalysis was unremarkable.

Emergency upper gastrointestinal endoscopy performed on day 1 showed no ulcers, varices, strictures, or masses in the esophagus or stomach. Side-viewing duodenoscopy revealed intermittent blood at the major duodenal papilla (papillary orifice), suggestive of hemosuccus pancreaticus[Figure 1].

Figure 1.

Sideview duodenoscopy image showing blood (black arrow) emerging from major papillary orifice consistent with hemosuccus pancreaticus

Contrast-enhanced computed tomography of the abdomen and pelvis with CT angiography demonstrated:

Acute-on-chronic calcific pancreatitis with associated inflammatory changes and ill-defined fluid collections. Main pancreatic duct dilatation (maximum diameter 9 mm) with multiple intraductal calculi [Figure 2].

Figure 2.

Noncontrast computed tomography abdomen (axial section) showing multiple calcifications (blue arrow) within the pancreas, consistent with chronic calcific pancreatitis

Localized fluid collection (approximately 21 mm × 18 mm) with a peripheral enhancing wall posteroinferior to the pancreatic body, suggestive of a pseudocyst [Figure 3].

Figure 3.

Non-contrast-enhanced computed tomography abdomen (axial section) showing a well-defined hypodense cystic lesion arising from the pancreas, consistent with a pancreatic pseudocyst (blue arrow)

Well-defined iso- to mildly hyperdense lesion in the posteroinferior aspect of the pancreatic head measuring 63.5 mm × 52 mm × 58 mm (Anteroposterior [AP] × Transverse [TR] × Craniocaudal [CC]). The lesion demonstrated a relatively hypodense center showing contrast opacification in the arterial phase, communicating with the IPDA through a small neck (diameter 2.5 mm). No enhancement of the peripheral portion was noted, suggestive of a pseudoaneurysm with peripheral thrombus. The patent-enhancing lumen measured approximately 36 mm × 31 mm × 29 mm (AP × TR × CC) [Figure 4].

Figure 4.

Contrast-enhanced computed tomography angiography (coronal section) showing an inferior pancreaticoduodenal artery pseudoaneurysm with peripheral thrombus (blue arrow) and active contrast extravasation (yellow arrow). The inferior pancreaticoduodenal artery (pink arrow) is visualised arising from the superior mesenteric artery (SMA) (red arrow). A vascular variant is also noted, with a replaced right hepatic artery (green arrow) originating from the SMA

Compression of the main pancreatic duct in the head region and compression with displacement of the first and second parts of the duodenum toward the right side. Compression and displacement of the inferior portion of the common bile duct with resultant dilatation of the proximal common bile duct (15 mm maximum diameter), common hepatic duct, hepatic ducts, and central intrahepatic biliary radicles [Figure 5].

Figure 5.

Noncontrast computed tomography abdomen (coronal section) showing dilated intrahepatic biliary radicles (red arrow) and a dilated common bile duct (blue arrow), consistent with obstructive biliary dilatation

Posterior compression of the right renal vein and inferior vena cava, with non-enhancing outpouching extending to the lower pole of the right kidney, causing compression of the right pelviureteric junction and proximal ureter with resultant right-sided hydronephrosis [Figures 6 and 7].

Figure 6.

Contrast-enhanced computed tomography abdomen (axial section) showing compression of the right pelvi-ureteric junction (pink arrow) with associated hydronephrosis

Figure 7.

Contrast-enhanced computed tomography abdomen (axial section) showing extrinsic compression of the inferior vena cava and right renal vein (green arrow)

Medial compression of the proximal superior mesenteric vein, portal confluence, and proximal main portal vein.

Compression of the splenic vein in its proximal portion with hypodense filling defects suggestive of partial thrombosis. The distal splenic vein segment showed normal contrast opacification measuring approximately 7.5 mm.

Multiple portosystemic collaterals in the perigastric, peripancreatic, perisplenic, splenorenal, periportal regions, and mesentery.

Splenomegaly with a splenic index measuring 930 cc.

Anatomical vascular variation with the left hepatic artery arising from the celiac trunk and the right hepatic artery from the superior mesenteric artery (SMA). Mild compression of the proximal right hepatic artery by the lesion was noted.

Differential diagnosis

• Peptic ulcer disease with arterial erosion

• Esophageal or gastric varices

• Pancreatic neoplasm with vascular invasion

• Aortoenteric fistula.

Treatment

Following the presentation, immediate resuscitation was initiated. Two wide-bore intravenous lines were secured, and fluid resuscitation was started with isotonic crystalloids (0.9% normal saline and Ringer’s lactate) with a rapid bolus of 1000 mL. The patient was started on noradrenaline at 0.1 µg/kg/min, adjusted according to mean arterial pressure (MAP) to maintain MAP >65 mmHg. Two units of packed red blood cells were transfused on day 1 to correct the anemia. Once hemodynamic stability was achieved, maintenance isotonic crystalloids were continued, and noradrenaline was tapered and discontinued.

The patient was started on intravenous pantoprazole 40 mg twice daily and tramadol 50 mg in 100 mL of 0.9% normal saline three times daily for pain management. Following hemodynamic stabilization and diagnostic workup confirming hemosuccus pancreaticus secondary to an IPDA pseudoaneurysm, the patient underwent emergency endovascular coil embolization on day 3.

Under local anesthesia, right femoral arterial access was obtained. Celiac and SMA angiograms confirmed a large pseudoaneurysm arising from the posterior IPDA branch of the SMA [Figures 8 and 9]. Selective endovascular coil embolization of the IPDA and pseudoaneurysm was performed under fluoroscopic guidance using multiple free coils, employing the sandwich technique with embolization of both afferent and efferent vessels. Postembolization angiograms demonstrated complete occlusion of the pseudoaneurysm-bearing segment of the IPDA [Figure 10].

Figure 8.

Digital subtraction angiography demonstrating a replaced right hepatic artery (blue arrow) arising from the superior mesenteric artery (yellow arrow). A contrast-filled pseudoaneurysm with active extravasation (red arrow) is seen arising from the inferior pancreaticoduodenal artery (green arrow)

Figure 9.

Roadmap fluoroscopic angiography image demonstrating a replaced right hepatic artery (blue arrow) arising from the superior mesenteric artery (yellow arrow). A contrast-filled pseudoaneurysm with active extravasation (red arrow) is seen arising from the inferior pancreaticoduodenal artery (green arrow)

Figure 10.

Postembolisation digital subtraction angiography demonstrating a replaced right hepatic artery (blue arrow) and inferior pancreaticoduodenal artery (green arrow) arising from the superior mesenteric artery (yellow arrow). Coils placed within the pseudoaneurysm are visible (red arrow), with no residual aneurysm sac or contrast extravasation, confirming successful embolization

The procedure was uneventful. Postprocedure, the patient was monitored in the intensive care unit with stable vital signs and no evidence of rebleeding or access site complications. The patient was kept nil per oral until the following morning, and the right lower limb was immobilized for 6 h postprocedure. Antibiotic prophylaxis was administered for 7 days postprocedure. Following hemodynamic stabilization, the patient was started on pancreatic enzyme supplementation (lipase 25,000 IU, amylase 40,000 IU, protease 40,000 IU three times daily) and multivitamin supplementation once daily.

Outcome and follow-up

The hemoglobin level on day 3 was 9.1 g/dL with no further decline thereafter. The patient was discharged on day 6 with a hemoglobin level of 10 g/dL. At 1-month follow-up, repeat hemogram showed hemoglobin of 11 g/dL [Table 1]. The patient remained pain-free, ambulatory, and reported no bleeding manifestations, delayed adverse vascular events, or procedural complications at the latest follow-up.

Table 1.

Serial hemogram values during hospitalisation and at 1-month follow-up

Hemogram	Day 1	Day 2	Day 3	Day 4	Day 5	Day 6	1 month follow up visit
Hemoglobin (g/dL)	5.9	8.3	8.9	9.1	9.4	10	11
WBC count (/µL)	9100	13,600	4800	6000	8000	8700	6600
Platelet count (/µL)	188,000	207,000	178,000	170,000	233,000	208,000	190,000
RBC count (×106/µL)	2.28	3.28	3.38	3.46	3.66	3.77	4.10
Hematocrit (%)	18.3	26.1	27	27.5	29.3	30.7	34

RBC=Red blood cell, WBC=White blood cell

DISCUSSION

This case demonstrates several unique features that merit detailed discussion. The pseudoaneurysm size (6.4 cm) significantly exceeds typical reports in the literature. A systematic review by Balachandra and Siriwardena analyzing 214 cases found mean diameters of 2.8 cm for visceral artery pseudoaneurysms in pancreatitis.[5] The extensive multi-organ compression observed in this case represents an unusual set of complications, with simultaneous biliary obstruction, venous compression, and hydronephrosis rarely reported together in the literature.[6]

Pathophysiology of pseudoaneurysm formation

True aneurysms maintain all three arterial wall layers (intima, media, and adventitia), whereas pseudoaneurysms are characterized by contained hematomas with walls composed of fibrous tissue, adventitia, and surrounding perivascular structures rather than native vascular components.

The primary mechanism underlying pseudoaneurysm formation involves the extravasation of activated pancreatic enzymes such as elastase, trypsin, and lipase – from damaged pancreatic ducts into the surrounding peripancreatic tissues. These proteolytic and lipolytic enzymes cause elastolytic erosion of adjacent vascular walls, progressively weakening the structural integrity of peripancreatic vessels. This enzymatic autodigestion is perpetuated by ongoing inflammation in chronic calcific pancreatitis, creating a sustained risk for vascular complications.[7]

Pancreatic pseudocysts, present in 20%–40% of chronic pancreatitis patients and in up to 60% of those with pseudoaneurysms, play a dual role in pseudoaneurysm formation. First, established pseudocysts can directly erode into adjacent visceral arteries through mechanical pressure and enzymatic degradation, converting the pseudocyst into a pseudoaneurysm. Second, pseudocyst formation creates a microenvironment rich in pancreatic enzymes that accelerates vascular wall breakdown. Recent multivariate analyses have identified pseudocyst presence as an independent predictor of pseudoaneurysm formation.[8]

Anatomical considerations and vessel involvement

IPDA involvement is exceptionally rare among visceral artery pseudoaneurysms. In a comprehensive review of vascular complications in pancreatitis, pseudoaneurysms most commonly affected the splenic artery (40%), gastroduodenal artery (30%), and pancreaticoduodenal arteries collectively (20%), with isolated IPDA pseudoaneurysms comprising <5% of cases.[9] Splenic artery pseudoaneurysms, in particular, have been extensively reported in the literature, highlighting their clinical significance.[10] The anatomical proximity of the IPDA to the pancreatic head and its involvement in the pancreaticoduodenal vascular arcade make it particularly susceptible to inflammatory complications in chronic pancreatitis.

The pancreaticoduodenal arcade represents a critical collateral pathway connecting the celiac trunk circulation (via the gastroduodenal artery and superior pancreaticoduodenal arteries) with the SMA circulation (via the inferior pancreaticoduodenal arteries). This collateral network explains why IPDA embolization rarely results in end-organ ischemia. Barge and Lopera demonstrated that collateral flow maintains adequate perfusion in 94% of cases following IPDA embolization,[11] which contributed to the successful outcome in this case without ischemic complications.

The anatomical vascular variation identified in this case – with the left hepatic artery originating from the celiac trunk and the right hepatic artery arising from the SMA – is clinically significant. While the right hepatic artery commonly arises from the SMA in 10%–15% of individuals, awareness of such variations is crucial for interventional planning. The mild compression of the proximal right hepatic artery by the pseudoaneurysm, though not requiring specific intervention, highlights the importance of comprehensive vascular mapping in complex cases.

Diagnostic approach

The diagnostic approach followed in this case represents best practice. While standard upper endoscopy has limited sensitivity (approximately 30%) for detecting hemosuccus pancreaticus, the visualization of intermittent ampullary bleeding on side-viewing duodenoscopy provided a definitive diagnosis. This finding is pathognomonic for hemosuccus pancreaticus and distinguishes it from other causes of upper gastrointestinal bleeding.[1,2,3,4,12]

Contrast-enhanced CT angiography demonstrates 94% sensitivity and 98% specificity for detecting visceral artery pseudoaneurysms.[13] In this case, CT angiography was crucial not only for confirming the pseudoaneurysm but also for comprehensive anatomical assessment of the extensive multi-organ involvement. The detailed imaging revealed compression of the common bile duct (resulting in 15 mm dilatation), right renal vein, and inferior vena cava compression leading to hydronephrosis, portal venous compression, and splenic vein thrombosis with portosystemic collateral formation. This comprehensive assessment was essential for procedural planning and anticipating potential complications. The presence of peripheral thrombus within the pseudoaneurysm sac underscores the dynamic nature of pseudoaneurysm formation and partial thrombosis in chronic pancreatitis patients. This finding carries both prognostic and therapeutic implications, as partially thrombosed pseudoaneurysms may have a slightly lower immediate rupture risk but require careful endovascular navigation.

Endovascular management and technical considerations

Endovascular management has emerged as the first-line treatment for visceral artery pseudoaneurysms in hemodynamically stable patients. A multicenter analysis of 46 visceral artery pseudoaneurysms by Omar et al. demonstrated 93.5% technical success with endovascular embolization, with significantly lower mortality (10% vs. 43%) compared to surgical intervention.[14] These outcomes are consistent with long-term institutional experiences reported in the literature.[15] The less invasive nature of endovascular therapy is particularly advantageous in patients with chronic pancreatitis who often have poor nutritional status, chronic inflammation, and compromised physiological reserve.

Several embolization strategies are employed based on anatomical considerations and pseudoaneurysm characteristics

Sandwich technique – This method, used in our case, involves embolizing both afferent and efferent vessels to fully exclude the pseudoaneurysm. A major cause of treatment failure is retrograde filling through collateral pathways, which is avoided in this technique.

Other methods include the sac packing technique and liquid embolic agents.

Venturini et al., in their comprehensive series of 100 patients with visceral artery aneurysms and pseudoaneurysms, reported that the sandwich technique achieved 96% primary success with only 6% recurrence compared to 19% with proximal embolization alone.[16] These findings support the technical approach employed in this case. Additional case reports, such as those by Mitrovic Jovanovic et al. and Camejo et al., further support endovascular treatment success in IPDA pseudoaneurysms.[17,18]

Role of surgical management

Surgery is reserved for hemodynamically unstable patients unable to undergo emergent endovascular intervention, failed endovascular therapy, or cases with large accompanying pseudocysts requiring drainage. Surgical options include arterial ligation, resection, revascularization, or organ resection (splenectomy and distal pancreatectomy). While surgery offers definitive treatment with success rates approaching 89%, it carries substantially higher morbidity and mortality rates (20%–40% vs. 5%–15% for endovascular therapy), particularly in patients with active inflammation or compromised nutritional status as seen in this case. Historical data also emphasize the increased risk profile of surgical intervention in hemorrhagic pancreatitis.[6]

CONCLUSION

• Consider hemosuccus pancreaticus in any chronic pancreatitis patient presenting with GI bleeding

• Side-viewing duodenoscopy and CT angiography are essential diagnostic tools

• Pseudoaneurysms may cause a significant mass effect requiring comprehensive imaging

• Endovascular embolization is a safe and effective first-line therapy

• Long-term surveillance is warranted given the recurrence risk with large pseudoaneurysms.

Conflicts of interest

There are no conflicts of interest.

Funding Statement

Nil.