The Invisible Menace – The Lion in the Savannah

“A little internal bleeding never hurt anyone. – Valkyrie.” Derek Landy

It is 7.30 PM, after a long day on call when a colleague of the Medicine Department calls you…

“Hi, it’s Doctor Green speaking. I’m sorry to bother you. I’m calling you because of a patient admitted about 5-6 days ago with acute pancreatitis and a peripancreatic necrotic collection. He was doing well until this morning when he started complaining of abdominal pain. We repeated the lab exams that were good. Now he is becoming tachycardic and the blood gas analysis showed increased lactates. Can you come to evaluate him?”

The first thing you think about is an infection of the peripancreatic collection and you ask yourself why this needs a surgical evaluation… But you are wrong…

Oh yes, you are so wrong…

And you don’t know yet that what’s waiting for you there can become a living Hell…

Introduction

Anatomically speaking, the pancreas is enclosed in a tangle of vessels, both arterials and venous, and it leans over the main branches of the portal vein and the aorta (Figure 1). Its vascularization derives mainly from the pancreaticoduodenal arteries, connecting the gastroduodenal artery and the superior mesenteric one, and from the dorsal pancreatic, greater pancreatic, and transverse pancreatic arteries, branches of the splenic artery. The outflow involves branches of the portal system.

As already stated in one of our previous posts, although we know quite well the pathophysiology of acute pancreatitis, it still maintains a high mortality rate, counting about 1-7% in mild cases, and reaching 18% in severe cases.

Analyzing the complications of acute pancreatitis, only a few of them involve vascular complications, in particular:

• Splenic and/or mesenteric vein thrombosis
• Disseminated intravascular coagulation
• Gastric varices
• Pancreatic arterial pseudoaneurysm

It is clear that hemorrhagic complications of acute pancreatitis are unique events. So, why speak about them?

Bleeding Complications of Pancreatitis

Speaking about hemorrhagic complications of pancreatitis is like telling ghost stories around a bonfire. In fact, their prevalence is reported to be between 1.2-14.5%, and usually, when the gap is so wide in the literature, it means that the event is exceptional. Moreover, the mortality rate secondary to these bleeding complications reaches 34-52%… Flipping a coin…

According to the literature, the hemorrhagic complications of pancreatitis are caused by:

• Ruptured pseudoaneurysms (60%)
• Hemorrhagic pseudocysts without pseudoaneurysms (20%)
• Capillary, venous, or small vessel bleeding (20%)

The pseudoaneurysms may involve basically all arteries surrounding the pancreatic gland:

• Splenic artery (35-50%)
• Gastroduodenal and pancreaticoduodenal arteries (20-25%)
• Mesenteric, colic, and hepatic arteries (5%)
• Aorta (0.5%)

In these patients, the bleeding may occur early after the onset of acute pancreatitis. However, it is usually seen as a late complication (26-27 days after the onset of acute pancreatitis), and sometimes it might even happen in patients with chronic pancreatitis.

As previously stated, hemorrhage has a high mortality rate, accounting for more than 50% of the overall deaths in patients with acute pancreatitis. The mortality is usually higher if the bleeding is intra-abdominal compared to gastrointestinal, it manifests lately, more than >7 days after the onset of pancreatitis, and/or if it is managed with an acute phase surgical operation.

Risk Factors & Pathophysiology

Known risk factors for bleeding in patients with acute pancreatitis are:

• Pancreatic necrosis
• Peripancreatic infection
• Disease severity and multiorgan failure
• Pancreatic surgery
• Long-term anticoagulation
• Fungal sepsis

The pathophysiology of bleeding in acute pancreatitis may involve different pathways (Figure 2)… Let’s try to keep things easy:

• Acute pancreatitis involves the release of lipolytic and proteolytic enzymes that, on one side, digest the pancreatic gland and the peripancreatic tissues, creating pseudocysts or walled-off necrosis. If the wall of these collections is disrupted, it may cause direct bleeding. On the other side, the enzymes may cause arterial wall erosion giving birth to a pseudoaneurysm that may bleed.
• Peripancreatic collections can be treated with radiologically inserted drains. These drains may cause direct trauma to vessels or perpetuate local inflammation, thus increasing the risk of pseudoaneurysm formation.
• In severe cases, necrosectomy may be necessary, but it carries a high risk of vascular damage.
• Acute pancreatitis increases the risk of developing spleno-porto-mesenteric venous thrombosis, which may evolve into portal hypertension, a condition that can be already present because of chronic alcohol consumption, a known causative agent for pancreatitis. If portal hypertension develops, varices will appear and can potentially bleed.
• Patients with acute pancreatitis might assume non-steroidal anti-inflammatory drugs (NSAIDs) that, together with the increased stress due to pancreatitis itself, may increase the risk of bleeding peptic ulcer.

Classification

Bleeding in patients with acute pancreatitis may be classified according to:

• Origin: arterial or venous
• Site: intraluminal (i.e. gastrointestinal) or extraluminal (i.e. intra-abdominal)
• Correlation: spontaneous or post-procedural (i.e. postoperative or post-drainage)
• Severity: minor or major (i.e. acute reduction in Hb level of at least 2 g/dL and/or new onset of hemodynamic instability)
• Timing: early or late (the cut-off is 7 days from the onset of acute pancreatitis)

Clinical Presentation

The clinical presentation may vary greatly depending on whether the bleeding is secondary to an invasive procedure (i.e. surgery or percutaneous drainage) or spontaneous, as well as if it is intra- or extraluminal.

Common signs are:

• Hematemesis
• Melena
• Hematochezia
• Blood in the nasogastric tube or drains
• Drop in Hb level
• Hemodynamic impairment

During Med school, our luminary professors taught us that patients with bleeding due to acute pancreatitis have two pathognomonic signs: Cullen and Grey-Turner signs. The Cullen sign refers to a purplish ecchymotic lesion in the periumbilical area, whereas the Grey-Turner sign refers to the same discoloration along the flanks. These signs are the manifestation of a retroperitoneal hemorrhage that has diffused through fascial planes to the skin along the gastrohepatic and falciform ligaments to the umbilicus (i.e. Cullen sign) or along the pararenal space to the lateral edge of the quadratus lumborum muscles (i.e. Grey-Turner sign). Although they are quite known and usually related to bleeding from acute pancreatitis, they are neither sensitive nor specific, and their prevalence is less than 1% singularly and around 0.65% in association. However, if present, they are related to a mortality rate higher than 50%.

Diagnosis

Once the suspicion of bleeding in a patient with acute pancreatitis arises, it is important to understand where it is bleeding to choose the best diagnostic option:

• Endoscopy: option of choice in the case of intraluminal bleeding
• 3-phase contrast-enhanced abdominal computed tomography (CEACT) scan: it gives information about the patient’s intra-abdominal status and it may highlight contrast extravasation (Figure 3), determining the site of bleeding and helping in planning the following treatment
• Angiography: it usually follows the CEACT scan

It should be noted that, in about 30% of the cases, the bleeding will not be identified and will remain occult, resulting in a (more) difficult management.

Treatment

As in the diagnostic pathway, the treatment strategy depends on where the patient is bleeding from (Figure 4):

• Endoscopy: this option may identify and treat the bleeder at the same time
• Angiography: if the bleeder is identified and it is arterial, it is possible to address it with angioembolization. Usually, angioembolization requires the patient to be hemodynamically stable; however, recent studies have shown how this procedure is feasible and safe even in hemodynamically unstable patients. Nevertheless, angioembolization in hemodynamically unstable patients may be attempted only in dedicated hospitals with available expertise and after careful patient selection.
• Surgery: this option should be the last resort. In fact, in patients with acute pancreatitis, the anatomy is completely subverted by the inflammatory process, creating a hostile environment, reasons why surgery in these patients carries high morbidity and mortality rates.
  Surgery is usually reserved if endoscopic treatment and angioembolization fail, in not-embolizable (e.g. venous or occult) bleeding, or hemodynamically unstable patients.
  The damage control surgery techniques (i.e. retroperitoneal packing with moist gauzes) may be the best choice if suture-ligation of the bleeder is not possible. Sometimes, in extreme cases, a pancreatectomy may be necessary (e.g. proximal, distal, or total).

Prevention

Preventing bleeding in these patients is fundamental to decreasing the death burden on these patients. However, it is anything but easy to do… Just consider that a too-aggressive approach to a pancreatic collection may lead to post-procedural bleeding, but a too-conservative approach to a pancreatic collection may lead to spontaneous bleeding.

One thing we can do is to be careful when drainage is required:

• Prefer soft drains
• Do not place the drain close to big vessels
• Mobilize and remove the drain as soon as possible

And this is it for this time. We really hope you have enjoyed this post on a rare but fearsome complication of pancreatitis.

See you soon.

References

1. Mederos MA, et al. Acute pancreatitis – a review. JAMA 2021;325:382-90.
2. Evans RPT, et al. Pancreatitis: preventing catastrophic haemorrhage. World J Gastroenterol 2017;23:5460-8.
3. Quinlan JD. Acute pancreatitis. Am Fam Physician 2014;90:632-9.
4. Albulushi A, et al. Pattern of acute pancreatitis in a tertiary care center in Oman. Oman Med J 2014;29:358-61.
5. Gupta V, et al. Hemorrhage complicating the course of severe acute pancreatitis. Ann Hepatobiliary Pancreat Surg 2020;24:292-300.
6. Wright WF. Cullen sign and Grey Turner sign revisited. J Am Osteopath Assoc 2016;116:398-401.
7. Bassi M, et al. Skin signs in acute pancreatitis: a case report. Italian Journal of Medicine 2013;4:265-8.
8. Rana SS, et al. Gastrointestinal bleeding in acute pancreatitis: etiology, clinical features, risk factors and outcome. Tropical Gastroenterology 2015;36:31-5.
9. Andersson E, et al. Major haemorrhagic complications of acute pancreatitis. Br J Surg 2010;97:1379-84.
10. Flati G, et al. Potentially fatal bleeding in acute pancreatitis: pathophysiology, prevention, and treatment. Pancreas 2003;26:8-14.
11. Dohan A, et al. Role and effectiveness of percutaneous arterial embolization in hemodynamically unstable patients with ruptured splanchnic artery pseudoaneurysms. Cardiovasc Intervent Radiol 2015;38:862-70.
12. Mejaddam AY, et al. Outcomes following “rescue” superselective angioembolization for gastrointestinal hemorrhage in hemodynamically unstable patients. J Trauma Acute Care Surg 2013;75:398-403.

How to Cite This Post

Bellio G, Marrano E, Cioffi SPB. The Invisible Menace. Surgical Pizza. Published on October 6, 2024. Accessed on March 15, 2025. Available at [https://surgicalpizza.org/emergency-surgery/the-invisible-menace/].