Pancreatic adenocarcinoma complicated by intramural duodenal hematoma: A case report and review of literature

Abstract

BACKGROUND

Intramural duodenal hematoma is an uncommon condition that most frequently occurs secondary to blunt abdominal trauma. The development of intramural duodenal hematoma in patients with pancreatic cancer is exceedingly rare, and its clinical course in this setting remains poorly characterized.

CASE SUMMARY

Here, we report the first case in which the natural history of intramural duodenal hematoma associated with pancreatic cancer was observed beyond the early phase following initial presentation. In this case, the patient ultimately underwent pancreaticoduodenectomy after rebleeding of the hematoma increased the risk of further hemorrhage, which could have compromised the safe administration of neoadjuvant chemotherapy. We also reviewed the relevant literature and discuss the clinical challenges in the management of intramural duodenal hematoma in patients with pancreatic cancer.

CONCLUSION

Up-front surgery should be considered in similar cases due to the risk of rebleeding and limited evidence supporting neoadjuvant therapy.

Key Words: Intramural duodenal hematoma; Pancreatic cancer; Pancreaticoduodenectomy; Neoadjuvant chemotherapy; Natural history; Review of the literature; Case report

Core Tip: Intramural duodenal hematoma in patients with pancreatic cancer is exceedingly rare. We report the first case in which the natural history of intramural duodenal hematoma associated with pancreatic cancer was observed beyond the early phase following initial presentation. In this case, the patient ultimately underwent pancreaticoduodenectomy after rebleeding of the hematoma increased the risk of further hemorrhage, which could have compromised the safe administration of neoadjuvant chemotherapy. In similar cases of resectable pancreatic cancer complicated by intramural duodenal hematoma, up-front surgery should be considered in light of the risk of rebleeding and the limited evidence supporting neoadjuvant therapy.

INTRODUCTION

Intramural duodenal hematoma is a rare clinical entity first described by McLauchlan[1] in 1838. It occurs most frequently in children following blunt abdominal trauma[2]. In adults, trauma likewise represents the most common etiology of intramural duodenal hematoma[3]. Other reported causes include the use of antithrombotic agents, coagulation disorders, and complications associated with upper gastrointestinal endoscopy[4,5]. Intramural duodenal hematoma arising in patients with pancreatic cancer is exceedingly rare, with only a limited number of cases reported in the literature[6-10]. Consequently, the optimal management strategy in this clinical context remains poorly defined. Herein, we report a case of intramural duodenal hematoma occurring in a patient with pancreatic cancer and discuss the diagnostic and therapeutic challenges associated with its management.

CASE PRESENTATION

Chief complaints

A 51-year-old man was noted to be jaundiced by his colleagues at work, prompting a medical consultation at a local clinic.

History of present illness

Blood tests were in keeping with obstructive jaundice, and contrast computed tomography (CT) revealed an ill-defined hypoattenuating mass measuring 40 mm at the head of the pancreas, together with dilatation of both the bile and pancreatic ducts. Obstructive jaundice from cancer at the head of the pancreas was suspected, resulting in his referral to our hospital for further investigations and treatment.

History of past illness

The patient took regular medications for hypertrophic cardiomyopathy, but this did not include antithrombotic drugs. His medications included a beta-blocker, mineralocorticoid receptor antagonist, statin, angiotensin II receptor blocker and sodium-glucose cotransporter-2 inhibitor.

Personal and family history

He also had a previous history of microvascular decompression for trigeminal neuralgia.

Physical examination upon admission

The patient was jaundiced on arrival but was otherwise asymptomatic.

Laboratory examinations

His blood results showed obstructive jaundice as well as elevated tumor markers including carbohydrate antigen 19-9, DUPAN-2 and SPAN-1 (Table 1).

Table 1 Blood results at the time of first presentation.

Laboratory test	Result	Reference interval
WBC	6900/μL	3300-8600/μL
Neu (%)	81.6%	42.0%-75.6%
Lym (%)	8.6%	17.4%-48.2%
Mon (%)	7.1%	3.4%-9.0%
Eos (%)	2.3%	0.4%-8.6%
Bas (%)	0.4%	0.2%-1.4%
RBC	511 × 104/μL	435-555 × 104/μL
Hb	16.3 g/dL	13.7-16.8 g/dL
Plt	25.1 × 104/μL	15.8-34.8 × 104/μL
PT INR	1.09	0.90-1.05
TP	7.5 g/dL	6.6-8.1 g/dL
Alb	4.2 g/dL	4.1-5.1 g/dL
Glb	3.3 g/dL	2.2-3.4 g/dL
T-BIL	12.9 mg/dL	0.4-1.5 mg/dL
D-BIL	8.5 mg/dL	≤ 0.4 mg/dL
AST	174 U/L	13-30 U/L
ALT	293 U/L	10-42 U/L
ALP	460 U/L	38-113 U/L
γ-GTP	1540 U/L	13-64 U/L
LDH	256 U/L	124-222 U/L
Amylase	181 U/L	44-132 U/L
Na	139.5 mmol/L	138.0-145.0 mmol/L
K	3.9 mmol/L	3.6-4.8 mmol/L
Cl	101.6 mmol/L	101.0-108.0 mmol/L
BUN	11.6 mg/dL	8.0-20.0 mg/dL
CRE	0.47 mg/dL	0.65-1.07 mg/dL
CRP	0.45 mg/dL	0.00-0.14 mg/dL
CEA	2.8 ng/mL	≤ 5.0 ng/mL
CA19-9	621 U/mL	≤ 37 U/mL
DUPAN-2	512 U/mL	0-150 U/mL
SPAN-1	143 U/mL	0-30 U/mL

WBC: White blood cells; RBC: Red blood cells; Hb: Hemoglobin; Plt: Platelet count; PT: Prothrombin time; TP: Total protein; Alb: Albumin; Glb: Globulin; T-BIL: Total bilirubin; D-BIL: Direct bilirubin; AST: Aspartate aminotransferase; ALT: Alanine aminotransferase; ALP: Alkaline phosphatase; γ-GTP: Gamma-glutamyltranspeptidase; LDH: Lactate dehydrogenase; BUN: Blood urea nitrogen; CRE: Creatinine; CRP: C-reactive protein; CEA: Carcinoembryonic antigen; CA19-9: Carbohydrate antigen 19-9.

Imaging examinations

Contrast CT confirmed the presence of an ill-defined hypoattenuating mass at the head of the pancreas measuring 40 mm in diameter, with local invasion of the distal common bile duct, the duodenum, the adipose tissue adjacent to the anterior peripancreatic surface, and the superior mesenteric vein. The lymph nodes in the hepatoduodenal ligament and around the left gastric artery were enlarged, consistent with localized lymph node metastasis, but there were no features of distant metastasis (Figure 1A).

Figure 1 Abdominal contrast computed tomography. A: Abdominal contrast computed tomography in the coronal plane showing an ill-defined 40 mm hypovascular mass at the head of the pancreas (arrows), together with dilatation of the common bile duct (arrowhead); B: Abdominal contrast computed tomography in the coronal plane revealing a high-density mass in the second part of the duodenum (arrows), consistent with a hematoma in the wall of the duodenum.

Endoscopic retrograde cholangiopancreatography (ERCP) and biliary endoscopic sphincterotomy was conducted to insert a plastic stent in the common bile duct. Histopathology of the biopsy taken from the bile duct showed adenocarcinoma, confirming the diagnosis of a resectable adenocarcinoma at the head of the pancreas. The obstructive jaundice improved without complications, and the patient was discharged from hospital three days after ERCP.

MULTIDISCIPLINARY EXPERT CONSULTATION

Initial plans were to offer the patient neoadjuvant chemotherapy followed by pancreaticoduodenectomy, in keeping with the recommendations from the Japanese clinical practice guidelines for pancreatic cancer[11]. However, ten days following discharge from hospital, the patient presented with severe upper abdominal pain and vomiting. Unenhanced CT showed an elliptical 79 mm × 44 mm × 42 mm mass in the wall of the second part of the duodenum on the opposite side of the ampulla of Vater, demonstrating a non-contrast hyperattenuation measuring approximately 30-81 Hounsfield units (HU), consistent with an acute intramural hematoma. After the administration of intravenous contrast, there was enhancement of the mucosa without internal enhancement of the intramural mass. There was also no active extravasation of contrast media. Although the lumen of the duodenum was narrowed by the hematoma, there was no upstream dilation of the duodenum or stomach suggesting obstruction (Figure 1B).

FINAL DIAGNOSIS

The patient was admitted to hospital for fasting and for observations. Upper gastrointestinal endoscopy was conducted on the third day of hospital admission, and revealed a smooth erythematous submucosal mass arising from the superior duodenal angle on the opposite side from the ampulla of Vater, in keeping with intramural hematoma.

TREATMENT

The intramural hematoma protruded into the duodenal lumen, causing it to be narrow so that it was not possible to pass the endoscope past the hematoma. Nevertheless, the lumen was still patent even in the narrowest part, and gastrografin contrast could pass without significant impedance into the jejunum (Figure 2). The abdominal pain resolved by the second day of hospital admission, and it became possible for the patient to resume oral intake of food. However, on the morning of the eighth day of his admission, the patient complained of sudden onset of upper abdominal pain and nausea. Unenhanced abdominal CT taken immediately after the onset of symptoms showed the enlargement of the intramural duodenal hematoma to 98 mm × 61 mm × 48 mm. The bulk of the hematoma demonstrated a non-contrast hyperattenuation measuring approximately 15-35 HU, demonstrating the evolution of the original bleed that lead to the patient’s hospital admission. There was also a 30 mm × 15 mm × 10 mm area in the middle of the hematoma of non-contrast hyperattenuation measuring approximately 30-61 HU, which was consistent with a recent rebleed (Figure 3). The abdominal pain had settled by the time the patient had undergone the abdominal CT scan, which we interpreted to indicate the cessation of active bleeding.

Figure 2 Upper gastrointestinal endoscopy. A: Upper gastrointestinal endoscopy showing a smooth red swelling arising from the subepithelial layer from the superior duodenal angle on the opposite side of the ampulla of Vater, consistent with an intramural duodenal hematoma; B: The duodenal lumen was narrow because of the subepithelial swelling; C: The contrast was able to pass without significant impedance to the jejunum.

Figure 3  Abdominal computed tomography in the coronal plane showed the enlargement of the intramural duodenal hematoma, consistent with a rebleed (arrows).

However, we considered that there was a risk of further episodes of bleeding into the intramural duodenal hematoma, and advised the patient to undergo pancreaticoduodenectomy on a semi-urgent basis. He underwent surgery and recovered without post-operative complications, being discharged home from hospital on the tenth postoperative day.

The examination of the resected specimen revealed that the intramural hematoma was separate from the pancreatic tumor and the ampulla of Vater (Figure 4). There was one area of the duodenum where there was only the serous membrane covering the intramural hematoma (Figure 5). The pathological stage was pT2N2M0 pStage III (8^th edition Union for International Cancer Control classification of malignant tumors), and R0 resection was achieved.

Figure 4  In the resected specimen, the hematoma (white circle) was separate from the tumor at the head of the pancreas (yellow circle) and the ampulla of Vater.

Figure 5  Histopathology of the resected specimen showed that the hematoma was located mainly within the muscularis propria, but in one area, there was only the subserosa (arrowhead) covering the hematoma (arrow).

OUTCOME AND FOLLOW-UP

The patient commenced adjuvant chemotherapy with S-1 (tegafur/gimeracil/oteracil) after four weeks following surgery. Five months postoperatively, the patient developed multiple liver metastasis, and the chemotherapy was changed to folinic acid, 5-fluorouracil, oxaliplatin, irinotecan (FOLFIRINOX). After two courses of FOLFIRINOX, disease progression was seen, and chemotherapy was changed to gemcitabine and nab-paclitaxel. After three courses of gemcitabine and nab-paclitaxel and ten months following surgery, further disease progression was seen in the form of peritoneal metastasis and massive ascites. The patient’s general condition had also deteriorated to Eastern Cooperative Oncology Group performance status 3, and the patient was referred to palliative care.

DISCUSSION

Intramural duodenal hematoma typically presents with abdominal pain, nausea, and vomiting. Although most patients recover with conservative management alone[3], a minority require interventional treatment such as coil embolization via interventional radiology[12] or surgical intervention to control ongoing bleeding[13,14]. In addition, several reports have described relief of intestinal obstruction caused by intramural duodenal hematoma through CT-guided percutaneous drainage[15,16] or endoscopic drainage[17,18]. Intramural duodenal hematoma may also obstruct the ampulla of Vater, which can lead to jaundice, pancreatitis, and even death[5,19].

Intramural duodenal hematomas are rare and are most commonly caused by blunt abdominal trauma[2,3]. Other reported etiologies include antithrombotic therapy, coagulation disorders, and complications of upper gastrointestinal endoscopy[3,4]. Intramural duodenal hematomas occurring in patients with pancreatic cancer are exceedingly rare, with only five cases reported in the literature to date[6-10]. To identify these cases, we searched the medical database PubMed for articles published between 1970 and 2025 using the MeSH terms “pancreatic cancer” and “hematoma”. The NPO Japan Medical Abstracts Society database was also searched for articles in Japanese during the same period using the terms “pancreatic cancer” and “duodenal intramural hematoma”. Additional relevant reports were identified through citation tracking of the retrieved literature.

In one case reported by Khurana et al[9], an early pancreatic neck cancer was identified in a patient receiving warfarin therapy. In that case, warfarin was considered the most likely cause of the intramural duodenal hematoma, as the pancreatic lesion was small (19 mm × 15 mm) and anatomically distant from the hematoma. In another report by Tanaka et al[6], trauma was suspected as the cause of the intramural duodenal hematoma, with pancreatic cancer regarded as an incidental finding. In contrast, the remaining four cases including the present case involved large tumors in the pancreatic head with local invasion of the duodenum (Table 2)[6-10].

Table 2 Summary of pancreatic adenocarcinoma complicated by intramural duodenal hematoma.

Ref.	Location of pancreatic cancer	Stage1 and size	Duodenal invasion	Prior history of trauma	Antithrombotic medication	Prior endoscopy	Location of duodenal hematoma	Contact between hematoma and tumor	Treatment
Tanaka et al[6], 2002	Head of the pancreas	pT1N0M0: 15 mm × 15 mm × 12 mm	No	Presumed	No	No	Second part, anterior wall	No	Pancreatico-duodenectomy
Chou et al[7], 2007	Uncinate process	30 mm × 30 mm × 28 mm	Yes	No	No	No	Second part, opposite to ampulla of Vater	Yes	Pancreatico-duodenectomy
Kitamura et al[8], 2013	Head of the pancreas (pancreaticoduodenal groove)	pT2N?M1, pStage IV: 30 mm × 30 mm × 25 mm	Yes	No	No	No	Second and third part	No	Pancreatico-duodenectomy
Khurana et al[9], 2014	Neck of the pancreas	pT1N1M0, pStage IIB 19 mm × 15 mm	No	No	Warfarin (for deep vein thrombosis)	No	Second part	No	Distal pancreatectomy
Nitta et al[10], 2019	Head of the pancreas	pT3N2M0, pStage III 60 mm	Yes	No	No	No	Second part	No	Pancreatico-duodenectomy
Current case	Head of the pancreas	pT2N2M0 pStage III 40 mm	Yes	No	No	ERCP, 11 days prior	Second and third part, opposite to ampulla of Vater	No	Pancreatico-duodenectomy

¹8^th edition Union for International Cancer Control classification of malignant tumors.

ERCP: Endoscopic retrograde cholangiopancreatography.

In the present case, the possibility that direct blunt trauma during ERCP contributed to the development of the intramural duodenal hematoma cannot be entirely excluded. However, the interval of 11 days between ERCP and the onset of symptoms favors pancreatic cancer as the underlying cause rather than ERCP-related injury. In previously reported cases of ERCP-associated intramural duodenal hematoma, symptoms typically developed immediately or within two days after the procedure[20-24]. Although one report described a diagnosis made one week after ERCP[18], that patient presented with vomiting without abdominal pain, suggesting the possibility of delayed symptom recognition rather than delayed hematoma formation. Among the other three reported cases involving pancreatic head tumors, no prior endoscopic procedures or other known risk factors for intramural duodenal hematoma were identified (Table 2)[6-10]; this suggests the direct role of the pancreatic cancer in the etiology of intramural duodenal hematoma.

The mechanism by which pancreatic head tumors may cause intramural duodenal hematoma has not been previously discussed. We hypothesize that the hematoma may result from shearing forces exerted on small vessels penetrating the duodenal wall. Such forces could arise when a pancreatic head tumor pulls the duodenum in a direction opposite to its retroperitoneal fixation at the second portion of the duodenum. This hypothesis is consistent with observations from the current and previously reported cases that the hematoma tends to occur on the second part of duodenum on the opposite side to the ampulla of Vater[6,7]. In addition, the pancreatic lesions implicated in the etiology of the hematoma were all above 30 mm in diameter and located in the head or the uncinate process of the pancreas (Table 2)[6-10]; the size and the location of the lesion would enable it to exert the shearing force on the wall of the second part of the duodenum to cause the hematoma. It is also possible that the pancreatic lesions located in the head or the uncinate process of the pancreas could lead to regional venous congestion by the tumor mass effect, causing the engorgement of the small vessels penetrating the duodenal wall to make them more susceptible to bleeding.

Local microvascular invasion by the cancer and broader tumor induced coagulopathy are other possible theories of intramural duodenal hematoma formation in patients with pancreatic cancer, but these can be refuted from the current and previous cases given that these features were not always observed (Table 2)[6-10].

The Japanese guidelines recommend neoadjuvant chemotherapy with gemcitabine and S-1 for patients with resectable pancreatic cancer[11], based on evidence from a randomized phase II/III trial demonstrating improved overall survival in patients with resectable disease[25,26]. Given that most intramural duodenal hematomas resolve with conservative management[3], we initially considered neoadjuvant chemotherapy in the present case.

However, following a second episode of bleeding from the intramural duodenal hematoma, we recommended semi-urgent pancreaticoduodenectomy because further bleeding could have compromised the safe administration of neoadjuvant chemotherapy. Furthermore, rupture of the hematoma could theoretically result in peritoneal dissemination of cancer cells. Although postoperative findings revealed that the hematoma did not directly contact the pancreatic tumor, this relationship could not be reliably determined from preoperative imaging. In cases of recurrent intramural duodenal hematoma unrelated to malignancy, interventional radiology or endoscopic drainage might be considered; however, in the presence of resectable pancreatic cancer, upfront surgery was deemed the most appropriate strategy. The timing of surgery was justified retrospectively by findings in the resected specimen, which showed that the hematoma was covered only by the serosal membrane in one area of the duodenum, indicating a substantial risk of imminent rupture (Figure 5).

In previously reported cases of intramural duodenal hematoma associated with pancreatic cancer, pancreaticoduodenectomy was also performed on a semi-urgent basis. The present case is unique in that the natural course of the intramural duodenal hematoma was observed beyond the initial days after presentation in a patient with pancreatic cancer. Based on this experience, we suggest that upfront surgery may be the preferred management strategy for patients with resectable pancreatic head cancer presenting with intramural duodenal hematoma.

Although the Japanese guidelines recommend neoadjuvant chemotherapy for resectable pancreatic cancer[11], evidence supporting this approach remains inconsistent across regions. Several clinical trials conducted outside Japan have failed to demonstrate a clear survival benefit of neoadjuvant therapy in resectable disease[27,28]. Consequently, recommendations differ among international guidelines. For example, the National Comprehensive Cancer Network guidelines state that neoadjuvant therapy may be considered for resectable pancreatic cancer, particularly in patients with high-risk features such as markedly elevated carbohydrate antigen 19-9 levels, large primary tumors, significant regional lymphadenopathy, excessive weight loss, or severe pain[29]. In contrast, the European Society for Medical Oncology guidelines indicate that current evidence is insufficient to support routine neoadjuvant chemotherapy for resectable pancreatic cancer[30]. Considering these differences, together with the risk of rebleeding and potential rupture of the intramural duodenal hematoma demonstrated in the present case, upfront surgery may represent a reasonable and pragmatic treatment strategy for patients with resectable pancreatic head cancer complicated by intramural duodenal hematoma.

In the current case, transcatheter arterial embolization was not performed because there was no indication of ongoing active bleeding at the time of imaging for the first episode of hematoma formation. After the rebleed, the option of performing prophylactic transcatheter arterial embolization was considered, which in this case would have likely involved the embolization of both the branches of the superior and inferior pancreaticoduodenal arteries given the lack of visualization of the bleeding vessel on contrast CT. While prophylactic transcatheter arterial embolization was not conducted in the end because surgery could be performed promptly in the current case, it may play an important role in the future as a bridge to surgery, particularly in cases when surgery cannot be undertaken immediately. Furthermore, the role of transcatheter arterial embolization should actively be explored to treat and prevent the recurrence of intramural duodenal hematoma for patients with locally advanced or metastatic pancreatic cancer, where pancreaticoduodenectomy would be the treatment of last resort.

CONCLUSION

We report a rare case of intramural duodenal hematoma associated with pancreatic head cancer. In cases of resectable pancreatic cancer complicated by intramural duodenal hematoma, up-front surgery should be considered in light of the risk of rebleeding and the limited evidence supporting neoadjuvant therapy. Given the potential risk of rupture of the intramural duodenal hematoma leading to peritoneal seeding of cancer cells and haemorrhagic shock, surgery should be conducted on a semi-urgent basis.