Abstract
A pancreatic pseudoaneurysm can occur following an attack of pancreatitis. This occurs due to erosion of the pancreatic or peripancreatic artery by the pancreatic enzyme-rich pancreatic secretion pseudocyst. If left untreated, it may cause massive and even fatal haemorrhage. Interventional radiology with coil embolisation of the pseudoaneurysm is the standard of care in such cases. We describe a patient who developed a pseudoaneurysm involving the origin of the gastroduodenal artery (GDA). This was successfully managed by coil embolisation of the pseudoaneurysm along with placement of a flow diverter-like stent in the common hepatic artery across the origin of the GDA leading to exclusion of the diseased segment.
Keywords: Gastroenterology, Pancreatitis, Interventional radiology
Background
Endovascular treatment with transarterial embolisation or placement of covered stent is used in the treatment of visceral artery aneurysm (VAA) or visceral artery pseudoaneurysm (VAPA), and the two methods can be combined for achieving higher clinical success.1 Recently, flow diverting stents have been used for the treatment of VAA and VAPA. The unique properties of flow diverting stents allow for rapid and significant flow reduction within the aneurysm without compromising blood flow in the parent artery and they can be effective in the treatment of large or complex aneurysms.1 2
We present our patient who had a giant peripancreatic pseudoaneurysm involving the origin of the gastroduodenal artery (GDA). We combined transarterial coil embolisation of the GDA with the placement of a flow diverter-like stent across the common hepatic artery (CHA) to successfully treat this patient.
Case presentation
A man in his 30s presented with abdominal pain of 20-day duration. The pain was located in the epigastrium and was moderate to severe in intensity. It radiated to the back and increased following a meal. It was associated with vomiting and was relieved with bending forward. Over the past 7 days, he began passing dark-coloured urine and noticed yellow discolouration of his eyes. He also developed itching over his body. He reported occasionally passing black, tarry stools for the past 4 months. He also reported vomiting about 100–200 mL of blood, 4 days prior to presentation.
He used to consume 80–100 g per day of country liquor (alcohol) daily for the past 10 years which he claimed to have stopped 1 month before presentation.
On clinical examination, his pulse was 110/min, regular with a blood pressure of 110/50 mm Hg. He was pale and jaundiced. He had parotid gland swelling with a few spider angiomas over the face and upper trunk. He had pitting pedal oedema.
On abdominal examination, there was tenderness in the epigastrium. A firm, smooth and ill-defined lump, 5×6 cm in size located in the epigastrium and extended to the right hypochondrium, was palpable. His liver and spleen were not palpable and he had no ascites.
Cardiovascular and respiratory system examination was unremarkable.
Given the spider angiomas, parotid swelling, jaundice and history of upper gastrointestinal (GI) bleed with significant alcohol intake, a presumptive diagnosis of upper GI bleed probably from oesophagogastric varices with chronic liver disease with acute exacerbation of chronic pancreatitis was made.
Investigations
The patient’s blood investigations revealed a haemoglobin of 58 g/L (140–180 g/L), a white cell count of 7.2×109/L (4–11×109/L) and a platelet count of 426×109/L (150–450×109/L); while his total bilirubin was 153.9 µmol/L (5.1–17.1 µmol/L) and his direct bilirubin was 102.6 µmol/L (1.7–5.1 µmol/L). His aspartate aminotransferase was 46 U/L (5–40 U/L), alanine aminotransferase was 30 U/L (5–40 U/L), alkaline phosphatase was 438 U/L (80–310 U/L), total protein was 66 g/L (60–75 g/L) and albumin was 27 g/L (30–45 g/L).
His Contrast enhanced computerised tomography (CECT) of the abdomen showed a large, heterogeneous, well-defined, rounded, partially thrombosed pseudoaneurysm posterior to the head and neck of the pancreas, which was extending up to the subhepatic region. It measured 7.9×8.2×7.3 cm (Cranio-caudal/Transverse/Anterior-posterior (CC×Trans×AP)). It was seen to have a small communication with a branch of the CHA and showed progressive filling in the portovenous phase. The surrounding collection appeared non-enhancing suggestive of haematoma formation. The neck of the lesion measured 7 mm. The haematoma was seen to cause mass effect, compressing the pancreas and main pancreatic duct (MPD) in the head and neck region with resultant dilatation of MPD in the body and tail of the pancreas. It was seen to compress the distal common bile duct (CBD) causing proximal dilatation of the CBD, common hepatic duct and intrahepatic biliary radicals. The CBD measured 11.3 mm. The portal vein and the splenic vein were not visualised and were replaced by multiple collaterals. There were multiple dilated periportal, peripancreatic, intrahepatic and subhepatic collaterals with oesophageal and gastric varices. The pancreas was atrophic with few calcific foci suggestive of chronic calcific pancreatitis (figure 1). His procoagulant workup was negative. His upper GI endoscopy revealed large oesophageal varices.
Figure 1.
CT of the Abdomen done initially showing a large (7.9x8.2x7.3 cm) heterogenous, well-defined partially thrombosed pseudoaneurysm, posterior to the head and neck of the pancreas with compression on distal common bile duct with intrahepatic biliary radical dilatation with the pancreas showing changes of atrophy, calcific foci in the head and dilated pancreatic duct. (A) Plain study, (B) Arterial phase, (C) Portal phase, (D) Venous phase.
Differential diagnosis
A presumptive diagnosis of upper GI bleed with oesophageal varices with acute exacerbation of chronic pancreatitis with peripancreatic pseudoaneurysm with obstructive jaundice secondary to distal CBD compression with extrahepatic portovenous obstruction (EHPVO) was made.
Cirrhosis was unlikely in view of normal platelets, with no evidence of cirrhosis on imaging and the jaundice being attributed to biliary obstruction.
The cause of the upper GI bleed was either from oesophageal varices or bleeding from the peripancreatic pseudoaneurysm.
Treatment
The patient was stabilised with transfusions of packed red blood cells and a continuous infusion of somatostatin. After stabilisation, an upper GI endoscopy was done, which showed large oesophageal varices with red colour signs. This was treated with variceal band ligation.
Conventional angiography revealed a large fusiform aneurysm involving the GDA and its origin from the CHA. A microcatheter was passed in the CHA and distal to the origin of the GDA aneurysm. A 7×30 mm C guard embolic protection stent was deployed in the CHA to cover the origin of the GDA. This was combined with selective embolisation of GDA with four coils (6×0.5 inches) and glue injection. Post-procedure angiography showed complete exclusion of the diseased segment. Following the procedure, the patient was immobilised for 8 hours and was kept nil per oral for 48 hours. He received intravenous fluids and intravenous antibiotics (videos 1 and 2).
Video 1. Showing a large fusiform aneurysm involving the origin of the gastroduodenal artery(GDA).
Video 2. Post procedure video: Following the placement of 7 x 30 mm C guard embolic protection system in the common hepatic artery(CHA) across the origin of the Gastroduodenal artery (GDA) with simultaneous coiling and selective embolization of GDA with 4 coils (6 X 0.5 inch) and 50% glue done showing complete exclusion of diseased segment on angiography.
Outcome and follow-up
Forty-eight hours after the procedure, the patient was started on a soft diet. After 3–4 days, his pain started decreasing, his icterus started improving and he had no further requirement for blood transfusion.
A repeat CT scan of the abdomen done on day 10 following the procedure showed a persistent large and thrombosed pseudoaneurysm arising from GDA (9.8×8.9×9.8 cm). Multiple hyperdense coils were seen in the pseudoaneurysm. Hyperdense areas suggestive of haemorrhage were seen inside the aneurysm. The stent was seen in the CHA covering and blocking the origin of GDA. The CHA was dilated. The CBD was dilated with Intrahepatic biliary radical dilatation (IHBRD). The MPD was dilated (figure 2).
Figure 2.
Repeat CT of the abdomen on Day 10 shows large thrombosed pseudoaneurysm arising from the gastroduodenal artery (GDA) (Size- 9.8x8.9x9.8cm) with multiple hyperdense coils in the pseudoaneurysm. Stent is seen in the common hepatic artery (CHA), across the origin of the GDA. The CHA is dilated. Common bile duct is dilated with IHBRD and dilated main pancreatic duct. (A) Plain study, (B) Arterial phase, (C) Portal phase, (D) Venous phase.
On follow-up after 4 months, the patient was asymptomatic. His CT of the abdomen done at 4 months showed CHA stent and coils in situ with significant regression of the pseudoaneurysm. Additionally, the superior mesenteric vein was not visualised and replaced by collaterals (figure 3). The patient was started on anticoagulation for the same.
Figure 3.
Repeat CT of the abdomen done at 4 months shows common hepatic artery stent and coils in situ and regression of the pseudoaneurysm. (A) Plain study, (B) Arterial phase, (C) Portal phase, (D) Venous phase.
His laboratory parameters are shown in table 1.
Table 1.
Serial laboratory parameters
| Parameters | On admission | Day 7 (day 3 post-procedure) | Day 14 (day 11 post-procedure) | 4 months post-procedure |
| Haemoglobin (g/L) (140–180 g/L) | 58 | 82 | 79 | 134 |
| Leucocytes (×109/L) (4–11×109/L) | 7.2 | 8.6 | 7.3 | 5.6 |
| Platelets (×109/L) (150–450×109/L) | 426 | 230 | 429 | 271 |
| Total/direct bilirubin (µmol/L) (5.1–17.1 µmol/L)/(1.7–5.1 µmol/L) |
123.1/68.4 | 104.3/82.08 | 78.66/42.74 | 35.9/6.84 |
| Aspartate aminotransferase (U/L) (5–40 U/L) | 46 | 51 | 85 | 26 |
| Alanine aminotransferase (U/L) (5–40 U/L) | 30 | 36 | 54 | 39 |
| Alkaline phosphatase (U/L) (80–310 U/L) | 438 | 620 | 1145 | 201 |
| Total protein (g/L) (60–75 g/L) | 66 | 69 | 68 | 81 |
| Serum albumin (g/L) (30–45 g/L) | 27 | 29 | 29 | 39 |
| International normalised ratio | 1.1 | 1.1 | 1.0 | 2.3 |
| Amylase (U/L) (20–120 U/L) | 84 | 92 | 86 | – |
Bold font values denote abnormal values.
Discussion
Our patient had Acute exacerbation of chronic pancreatitis with pseudoaneurysm involving the origin of the GDA with EHPVO. We could successfully treat our patient with the placement of a flow diverter-like stent in the CHA to cover and block the origin of the GDA (C guard embolic protection system) together with coil embolisation of the pseudoaneurysm (Wilson Cook Hilal Embolisation coils). We decided not to do an endoscopic retrograde cholangiopancreatography (ERCP) and bile duct stenting in view of portal cavernoma and the associated risk of bleeding during ERCP and also the likelihood of resolution of biliary obstruction following the treatment of the pseudoaneurysm. As anticipated, the bile duct obstruction and jaundice resolved following treatment of the pseudoaneurysm.
A diagrammatic representation of various pseudoaneurysms in relation to the pancreas is shown in figure 4. Pancreatic pseudoaneurysm is a relatively rare condition and occurs due to the weakening of the peripancreatic arteries as it comes in contact with enzyme-rich pancreatic juice and inflammatory exudate following an attack of acute or chronic pancreatitis. It can also occur after pancreatobiliary surgery when there is an anastomotic leak leading to the formation of a peripancreatic haematoma. Infection of the haematoma leads to a gradual erosion of the vessel in contact, which leads to the formation of a pseudoaneurysm. It can also occur following abdominal trauma leading to intraperitoneal infection, which may similarly cause erosion of the artery in contact and pseudoaneurysm formation.
Figure 4.
Diagrammatic representation of various pseudoaneurysms in relation to the pancreas (illustrated by authors SC and SP).IVC; inferior vena cava.
The distribution of various arterial pseudoaneurysms, which can occur in pancreatitis, is shown in table 2.
Table 2.
Frequency of various arterial pseudoaneurysms which can occur in pancreatitis
| Splenic artery (%) | Gastroduodenal artery/pancreaticoduodenal artery (%) | Common hepatic artery/proper hepatic artery (%) | Superior mesenteric artery (%) | Other (%) | Total number of pseudoaneurysms noted | |
| Mallick et al7 | 39.2 | 47.8 | 2.2 | 6.5 | 6.5 | 46 |
| Gambiez et al8 | 29 | 57 | – | – | 7 | 14 |
| De Perrot et al9 | 60 | 30 | – | – | 10 | 10 |
| Carr et al10 | 23 | 70 | – | 8 | – | 13 |
| Beattie et al11 | 23 | 62 | – | – | 15 | 13 |
| Bergert et al12 | 27 | 43 | 11 | 11 | 8 | 37 |
| Lermite et al13 | 35 | 47 | 6 | 6 | 6 | 17 |
| Udd et al14 | 42 | 58 | – | – | – | 33 |
| Sethi et al15 | 44 | 19 | 19 | – | 19 | 16 |
A pseudoaneurysm can have varied presentations depending on the vessel involved and its location. It may rupture resulting in major or even fatal haemorrhage. When located retroperitoneally, it can lead to retroperitoneal haematoma formation and the patient may present with abdominal pain or signs of hypovolaemia. When it is in contact with a hollow viscus like the stomach or duodenum, the patient may present with haematemesis or melaena. It can erode into the pancreas and present as hemosuccus pancreaticus or erode into the bile duct and present as haemobilia. Occasionally, it may present as an initial minor bleed, known as herald bleed, which may be followed by exsanguinating haemorrhage. Hence, when detected, pancreatic pseudoaneurysms should be treated. Intravascular intervention with coil embolisation is preferred due to low associated morbidity and high technical and clinical success. Surgical intervention may be required due to failure of vascular intervention or lack of expertise locally in interventional radiology. Surgery consists of ligation of the involved vessel. When this is not possible, major surgery like pancreatic resection may be required with its associated morbidity and mortality.
Pang et al proposed a management-based classification system for peripancreatic pseudoaneurysms that is based on the following three elements3:
Type of artery from which the pseudoaneurysm arises.
Presence or absence of communication with the GI tract.
Presence or absence of a high concentration of pancreatic juice at the bleeding site.
In this system, originating artery type is specified as follows:
Type I: pseudoaneurysm arises from a minor artery but must be at least 5 mm away from its junction of origin from a type II or III artery.
Type II: aneurysm arises from a major artery that may be sacrificed without physiological consequences (eg, the splenic and GDAs).
Type III: aneurysm arises from a major artery that cannot be sacrificed without significant consequences for the patient (eg, the superior mesenteric artery or the hepatic artery proper).
GI tract communication is specified as follows:
Type A: no communication with the GI tract.
Type B: communication with the GI tract.
Exposure to pancreatic juice is specified as follows:
Type 1: no exposure to pancreatic juice.
Type 2: exposure to pancreatic juice.
Our patient had a pseudoaneurysm involving the GDA. This artery can be sacrificed without much risk of visceral ischaemia. However, as the aneurysm involved the origin of the GDA, it indicated weakness in the wall of the CHA. This artery cannot be sacrificed. Our patient also had EHPVO and a sacrifice of the CHA could have led to severe hepatic ischaemia or infarction. Conventional covered stents have high porosity and high radial expansion force. They are more suitable for straight clogged vessels as they are difficult to place in tortous vessels and can clot or kink easily. Besides, they are not effective in occluding wide-mouthed aneurysms. Hence, a conventional covered stent was considered unsuitable for our patient. Flow diverters are used in interventional neurology to cover aneurysms involving the intracranial vessels. These stents have a braided metallic design with low porosity (<18 pores/mm2) and low radial expansion force in comparison with conventional covered stents. They are effective in covering wide-mouthed aneurysms and can be deployed in tortuous vessels without kinking or clotting thereby effectively covering the aneurysm and also ensuring adequate blood supply distally. Treatment with isolated coil embolisation of the vessel involved has good initial success. However, there may be delayed bleeding if pancreatic juice and inflammatory exudate continue to be in contact with the artery involved as was the case in our patient. To prevent such an occurrence, coil embolisation needs to be combined with the placement of a covered vascular stent so as to completely occlude the aneurysm. Placement of flow diverter-like stents for treatment of VAA has been reported by other workers. Baldino et al reported its use in the treatment of symptomatic superior mesenteric artery-dissecting aneurysm with good clinical success.4 In a comparative study, Zang et al demonstrated that the flow diverter may be a preferred treatment option for large and giant unruptured aneurysms.5 Venturini et al have suggested in their review article that endovascular treatment should be based on the morphology of the aneurysm for good technical and clinical success.6
We could achieve good technical and clinical success in our patient by adapting the treatment based on the morphology and location of the aneurysm.
Patient’s perspective.
I had come to the hospital with abdominal pain, bleeding and yellowish discoloration of eyes. I was in bad shape and was told previously that I may require surgery and the disease could progress with fatal consequences. I am glad that this intervention could relieve me of my great suffering, avoid surgery and help me have had such a dramatic improvement. I would like to thank all the doctors and staff who were extremely cooperative throughout and helped me never lose faith and overcome my suffering.
Learning points.
A high index of suspicion is needed to diagnose peripancreatic pseudoaneurysm following pancreatitis.
Endovascular treatment should be the preferred treatment option.
When the involved artery cannot be sacrificed and a wide-mouthed aneurysm is present, placement of a flow diverter-like stent should be considered.
Isolated coil embolisation of the pseudoaneurysm may lead to delayed bleeding if it continues to be in contact with pancreatic juice or inflammatory exudate.
Endovascular treatment should be combined with specific treatment of the underlying disease.
Footnotes
Contributors: SP—case management, concept, literature search, manuscript preparation, editing and review. SC—case management, concept, literature search, manuscript editing and review. AG—case management (radiological intervention), concept, manuscript editing and review. PMR—case management, concept, manuscript editing and review.
Funding: The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Case reports provide a valuable learning resource for the scientific community and can indicate areas of interest for future research. They should not be used in isolation to guide treatment choices or public health policy.
Competing interests: None declared.
Provenance and peer review: Not commissioned; externally peer reviewed.
Ethics statements
Patient consent for publication
Obtained.
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