Between 2006 and 2019, over 200 000 patients were admitted for acute pancreatitis (AP) in Australia. [1] In the general population of Australia, gallstones are the leading cause of acute pancreatitis, followed by alcohol, at a ratio of 2 to 1. [2, 3, 4] However, amongst the indigenous population of Australia, alcohol is the leading cause of acute pancreatitis. [5] Additionally, the age of onset tends to be younger in indigenous individuals, with hereditary pancreatitis being almost 70 times more prevalent. [5, 6] A 2021 study demonstrated that the prevalence of both acute and chronic pancreatitis was higher in the Indigenous population in Central Australia, compared to the non-Indigenous population. [7] This study also demonstrated that complications of pancreatitis, including post-pancreatitis diabetes mellitus, in this region of Australia were under investigated. [7]
Diagnosis of acute pancreatitis requires two of the following three features;
- Abdominal pain characteristic of the disease (epigastric pain, typically radiating posteriorly)
- Serum lipase three times the upper limit of normal
- Characteristic findings on abdominal imaging (typically CT in the first instance). [8]
The two sub-divisions of acute pancreatitis are interstitial and necrotizing pancreatitis. A key distinction between the two is, as the names suggest, the presence of focal necrosis. This can be seen on contrast enhanced CT imaging, as an area of hypodensity within the pancreas. Both interstitial and necrotising pancreatitis are associated with local complications, which are defined in the Atlanta Classification. [8]
Within 4 weeks from onset of acute interstitial pancreatitis, acute peripancreatic fluid collection may occur. This is a result of inflammation and rupture of pancreatic side ducts, and results in the presence of non-encapsulated fluid surrounding the pancreas. Within 4 weeks from onset of acute necrotising pancreatitis, an acute necrotic collection may develop. This manifests as a non-encapsulated, heterogenous collection on contrast enhanced CT imaging. The collection consists of both fluid and necrotic material.
In the case of acute interstitial pancreatitis, after 4 weeks, a pancreatic pseudocyst may develop. On contrast enhanced CT imaging, this is seen as a well-defined, fluid density collection, with an enhancing wall. Finally, in the case of acute necrotising pancreatitis, a walled off necrosis may develop. Like a pseudocyst, this manifests as a fluid density lesion, with an enhancing wall. The context of the case allows for one to distinguish between a pancreatic pseudocyst and walled-off necrosis, as a pseudocyst will develop following an episode of interstitial pancreatitis whereas walled off necrosis will develop following an episode of necrotising pancreatitis.
This presentation will explore the case of a 37-year-old male with a known pancreatic pseudocyst, on a background of recurrent episodes of acute pancreatitis, secondary to alcohol consumption. The patient presented to the emergency department (ED) with acute abdominal pain. CT on presentation demonstrates interval reduction in size of the pseudocyst with abdominal free fluid, concerning for rupture. Pseudocyst rupture is rare but potentially lethal, and may occur secondary to trauma, infection, recurrence of acute pancreatitis or intra-cystic haemorrhage. [9] Given the patient continues to consume alcohol, the concern for recurrence of acute pancreatitis was raised.