Management of Bleeding from the Pancreas



Acute hemorrhage originating from the pancreas is the least common form of upper gastrointestinal bleed [1,2]. Specifically, hemorrhage from the pancreatic duct through the papilla of Vater is rare with approximately 100 cases having been reported in the literature. The first report by Lower and Farrell in 1931 identified a splenic artery aneurysm as the cause [3].


Pancreatic Duct Main Pancreatic Duct Splenic Artery Coil Embolization Endovascular Technique 
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1 Introduction

Acute hemorrhage originating from the pancreas is the least common form of upper gastrointestinal bleed [1, 2]. Specifically, hemorrhage from the pancreatic duct through the papilla of Vater is rare with approximately 100 cases having been reported in the literature. The first report by Lower and Farrell in 1931 identified a splenic artery aneurysm as the cause [3]. This phenomenon has been described in various terms including wirsungorrhagia and hemowirsungia, highlighting the identification of hemorrhage from the pancreatic duct into the duodenum [4, 5]. Hemosuccus pancreaticus was first proposed by Sandblom in 1970 signifying emission of blood from the pancreatic ducts through the ampulla of Vater [6]. Longmire proposed hemoductal pancreatitis as another synonymous term [7].

2 Surgical Anatomy

The pancreas was first described by Eristratos in 300 BC. The origin of the word pancreas is Greek for pan meaning all and kreas defined as meat/flesh. The pancreas is a retroperitoneal organ situated at the level of the L2 vertebrae. The pancreas is commonly divided into segments consisting of the head, uncinate process, neck, body, and tail. The head of the pancreas lies nestled in the c-loop of the duodenum and the uncinate process is the portion of the head that extends posterior to the superior mesenteric vessels. The neck overlies the superior mesenteric vessels. The body begins at the level of the superior mesenteric vessels and the tail extends into the splenic hilum.

The duct of Wirsung (main pancreatic duct) was first described in 1642 and the duct of Santorini (accessory duct) in 1734. These are the two main ducts that drain exocrine secretions into the duodenum. The duct of Wirsung drains most of the head, body, and tail of the pancreas, while the duct of Santorini drains the superior portion of the head. Most possess branching that connects these two major ducts. Vater described the common bile duct and ampulla in 1720. However, it was not until 1919 that a pathologist from Johns Hopkins by the name of Oddi described the common duct theory where the common bile duct and main pancreatic duct joined together to drain via the ampulla of Vater into the duodenum. Of note, the accessory duct empties directly into the duodenum (minor papilla) several centimeters proximal to the ampulla of Vater.

The arterial blood supply of the pancreas is both redundant and profound. The celiac axis provides the common hepatic artery which in turn supplies the gastroduodenal artery as the origin of the superior branches of the pancreaticoduodenal artery. The pancreaticoduodenal branches supply the head of the pancreas. In addition the splenic artery provides the dorsal pancreatic, the great pancreatic, and the caudal pancreatic arteries as it travels toward the splenic hilum. These branches supply the body and tail of the pancreas. The superior mesenteric artery supplies the inferior branches of the pancreaticoduodenal artery as well as the inferior pancreatic artery. The venous anatomy parallels the arterial supply. Specifically, the superior pancreaticoduodenal veins drain into the portal vein, meanwhile the inferior pancreaticoduodenal veins unite to form the Henle trunk just proximal to the superior mesenteric vein. The veins from the body and tail drain directly into the splenic vein.

3 Clinical Presentation

Hemosuccus pancreaticus (HP) is a rare cause of upper gastrointestinal hemorrhage seen predominantly in men (sex ratio 7:1) [8]. Most of these cases are related to chronic consumption of alcohol. Frayssinet et al. reported the mean age of onset as 50 or 60 years when the site of pathology was the pancreatic parenchyma or the pancreatic arterial supply, respectively [9]. HP can present with an abrupt onset of epigastric abdominal pain to be later followed by acute gastrointestinal hemorrhage. The epigastric pain begins and radiates posteriorly [10] due to increased intraductal pressure by the presence of blood in the main pancreatic duct [11]. Within 48 h, gastrointestinal hemorrhage ensues as either hematemesis or melena; the onset of hemorrhage is usually associated with improvement of the abdominal pain. The amelioration of the abdominal pain is considered pathognomonic for HP. In addition, the intermittent nature of hemorrhage is specific for HP as a result of the cyclic balance between clot formation and dissolution within the pancreatic duct [1, 5]. Other possible associated symptoms include jaundice, weight loss, and a palpable pulsatile, epigastric mass with a systolic thrill.

4 Diagnostic Studies

The diagnosis of HP is a clinical dilemma due to the nature of intermittent hemorrhage from a source that is difficult to detect by common diagnostic studies. Upper gastrointestinal endoscopy can visualize active hemorrhage from the papilla in 30% of patients [1] (Figs. 1 and 2). This confirms either HP or hemobilia, while blood seen in the second portion of the duodenum provides evidence suggestive of these diagnoses. Endoscopy can also disclude other causes of upper gastrointestinal hemorrhage, such as gastritis, ulcers, and varices. Endoscopic retrograde cholangiopancreatography (ERCP) can also sort through HP as a cause of hemorrhage; pancreatic duct filling defects can represent the presence of blood clot or opacification of pseudocysts and/or communicating arterial aneurysms can identify the etiology of HP. Abdominal CT angiography rarely provides direct evidence of HP. However, pseudocysts and aneurysms are sometimes visible which can lead to a diagnosis with correlating symptoms. Technetium 99m-labeled red cell scintigraphy can identify a zone when active hemorrhage is present, yet the intermittent nature of HP makes this test unlikely to yield any helpful data [11].
Fig. 1

Hemobilia visualized at the ampulla of Vater on endoscopic exam

Fig. 2

Substantial hemobilia is more difficult to localize

Selective mesenteric arteriography provides the best opportunity for diagnosis of HP. This modality is capable of providing definitive proof by opacification of the main pancreatic duct [4]; arteriography has a 96% sensitivity in diagnosis of HP. However, identifying a direct vascular communication with the pancreatic duct is rare [12, 13]. Pseudoaneurysms of the common hepatic, gastroduodenal, or splenic arteries seen by arteriography in the setting of gastrointestinal hemorrhage are suggestive of HP.

5 Pathophysiology

There are various etiologies to HP. Pseudoaneurysms of the common hepatic, gastroduodenal, pancreaticoduodenal, or splenic arteries have been reported [14, 15, 16, 17]. Acute or chronic pancreatitis is the most common cause of pseudoaneurysm formation [18]. Pseudoaneurysms occur due to exocrine enzyme autodigestion and erosion into peripancreatic vessels [14, 18]. The most common cause of hemorrhage is due to a rupture of the splenic artery (60–65%) followed by gastroduodenal (20–25%), pancreaticoduodenal (10–15%), and hepatic artery (5–10%) [17, 19, 20, 21]. Ruptured pseudoaneurysms portend a poor prognosis with a reported mortality of 12–57% [17]. Other uncommon causes include pancreatic pseudocysts and pancreaticolithiasis [22, 23].

6 Management

Upon confirmation of HP, intervention generally consists of a combination of endovascular control of arterial hemorrhage and subsequent operative intervention. Hemodynamically stable patients can be temporized with endovascular techniques for control of hemorrhage. Interventional radiographic methods provide the optimal first line of treatment. Transcatheter balloon occlusion, coil embolization, and vascular stent deployment are several distinct methods for treatment. Balloon occlusion obstructs the artery prior to surgery, limiting blood loss and shortening operative times [1]. Coil embolization induces thrombus formation within the diseased vessel inducing complete obliteration of the artery [24, 25]. Thus embolization of the celiac axis, common hepatic artery, and superior mesenteric artery are contraindicated. Nevertheless, embolization of hemorrhage secondary to pancreatitis or pseudocysts has been shown to be very effective [25, 26, 27]. Some argue that coil embolization can be used as a definitive therapy as an alternative to operative intervention [26, 27]. Stent deployment allows for exclusion of a pathologic segment of an artery with continued distal perfusion of vital organs. Overall success of endovascular techniques for treatment of visceral aneurysms or pseudoaneurysms is 75–80% [8, 28]. There is a reported 17–37% recurrence rate associated following coil embolization [29].

Surgery is considered the definitive treatment and first-line therapy for hemodynamically unstable patients. Surgical management can include management of pancreatic parenchymal disease by drainage of pseudocysts, arterial disease by ligation of bleeding arterial disease, or a combination of drainage procedure and arterial ligation. The risk of recurrent bleeding, infection, and necrosis is possible after these procedures [30, 31]. A more aggressive and preferable approach is pancreatic resection which would address both problems [32]. Disease involving the pancreaticoduodenal arteries requires ligation of arterial bleeding, resection of the head, and drainage of the distal pancreas. Splenic artery etiologies require distal pancreatectomy. Nevertheless, surgical management of HP is technically difficult with a 70–85% success rate and associated 20–25% mortality [17, 19, 21, 26].

7 Conclusion

HP is a rare cause of upper gastrointestinal hemorrhage. Diagnosis is often delayed due to intermittent hemorrhage and the limitations of diagnostic studies to identify active hemorrhage. Most patients have previously suffered from acute or chronic pancreatitis, thus these patients should have a higher index of suspicion for HP as the cause of gastrointestinal hemorrhage. Endovascular techniques have increased the available therapeutic options with less invasive alternatives; these serve well as first-line therapies in hemodynamically stable patients. Endovascular techniques can also be used as a bridge to more definitive surgical treatment. Surgical drainage of pancreatic disease, arterial ligation of peripancreatic vessels, and pancreatic resection are all valid options. Ideally, anatomic pancreatic resections have the best outcomes but are still associated with a significant mortality.


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Copyright information

© Springer Science+Business Media, LLC 2010

Authors and Affiliations

  1. 1.Department of General & Thoracic SurgeryDuke University Medical CenterDurhamUSA
  2. 2.Department of SurgeryDuke University Medical CenterDurhamUSA

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