Acute pancreatitis varies from a mild uneventful disease to a severe life-threatening illness with multisystemic organ failure (MOF) with shock, renal failure, respiratory failure and death.
The frequency of acute pancreatitis varies among different countries (1).
In the US the rate is 270 cases per 100,000, which accounts for more than 200.000 hospital admissions each year.
In Finland the rate is 70 cases per 100,000 and in the Netherlands the rate is 18 per 100,000.
Gallstones and alcohol abuse are the most common causes of acute pancreatitis, accounting for 80% of cases.
Post-ERCP pancreatitis is the third most common cause of pancreatitis, but usually has a mild course.
In the Netherlands there are approximately 3500 admissions for acute pancreatitis a year.
In the last 10 years the incidence of acute pancreatitis has increased by 75%, due to increased alcohol consumption and increasing obesity.
The 1992 Atlanta Symposium on Acute Pancreatitis has classified this entity into a mild acute pancreatitis and a severe acute pancreatitis.
80-85% of cases of acute pancreatitis run a mild course without the development of multiple organ failure.
This group has a mortality of
15-20% of cases of acute pancreatitis run a serious clinical course with pancreatic necrosis and the development of multiple organ failure.
Of these, pancreatic necrosis remains sterile in 60% of patients, whereas in 40% of these patients the necrosis becomes infected.
This last category of patients has the highest mortality rate of 25-70%.
It is important to realize that severe acute pancreatitis runs a biphasic course (2).
During the first 1-2 weeks there is a pro-inflammatory response, which results in a systemic inflammatory response syndrome (SIRS).
It is a sterile response in which sepsis or infection hardly ever occurs.
If the SIRS is severe it will lead to early multiple organ failure.
After the first 1-2 weeks there is a transition from a pro-inflammatory to an anti-inflammatory response.
It is during this anti-inflammatory response that the patient is at risk for the translocation of intestinal flora and the development of infection of necrotic tissue and fluid collections.
The subsequent sepsis will result in late multiple organ failure.
Early mortality in acute pancreatitis is the result of the systemic inflammatory response with multiple organ failure.
Late mortality is the result of infection of pancreatic necrosis and peripancreatic fluid collections which results in sepsis and is seen in more than 50% of deaths.
Imaging of Acute Pancreatitis
In the diagnosis and staging of acute pancreatitis and its complications CT is the imaging modality of choice.
Ultrasound is important in determining whether gallstones are the cause of the acute pancreatitis (i.e. biliary pancreatitis).
ERCP with sphincterotomy and stone extraction should only be used if a patient has biliary pancreatitis and signs of biliary obstruction.
MRI is as sensitive as CT, but not as practical or accessible.
In certain cases it can be of additional value.
There is no additional value of an early CT (within 72 hours) in patients with acute pancreatitis.
The diagnosis is usually made on clinical and laboratory findings.
An early CT may be misleading concerning the severity of the pancreatitis, since it can underestimate the presence and amount of necrosis.
Early CT is only recommended when the diagnosis is uncertain, or in case of suspected early complications such as perforation or ischemia.
The case on the left shows a normally enhancing pancreas with enhancement comparable to that of the spleen on day 1.
As the patient's condition worsened, a second CT was performed on day 3.
Notice how the majority of the pancreatic body and tail no longer enhance - in fact only a small part of the pancreatic head enhances.
The patient died on day 5 due to severe SIRS and multiple organ failure.
Classification of Acute Pancreatitis
CT Severity Index
It is critical to identify patients who are at high risk for severe disease, since they require close monitoring and possible intervention.
Early staging is based on the presence and degree of systemic organ failure (cardiovascular, pulmonary, renal) and on the presence and extend of pancreatic necrosis (3,4).
Balthazar et al constructed a CT severity index (CTSI) for acute pancreatitis that combines the grade of pancreatitis (A-E) with the extent of pancreatic necrosis.
The CTSI assigns points to patients according to their grade of acute pancreatitis - which can be determined on a non-contrast CT as well as a contrast-enhanced CT - as well as the degree of pancreatic necrosis - which requires the use of intravenous contrast material.
More points are given for a higher grade of pancreatitis and for more extensive necrosis.
Patients with pancreatitis but no collections or necrosis (i.e. Balthazar grade A-C) have a mild pancreatitis.
This is also called 'edematous or interstitial pancreatitis' (no pancreatic necrosis).
It is a self-limiting disease with an uneventfull recovery occurring in 80% of patients with acute pancreatitis.
There is an intermediate form of pancreatitis without pancreatic necrosis with an intermediate clinical course.
This is called extrapancreatic necrosis (EXPN) (5,6).
Sometimes the term exudative pancreatitis is used.
These patients have Balthazar grade D or E.
These patients have a relatively mild course because there is no pancreatic necrosis, but there is higher morbidity than in interstitial pancreatitis, because they have peripancreatic collections, that can become infected (7).
Severe pancreatitis or necrotizing pancreatitis
Severe pancreatitis, also called 'necrotizing pancreatitis' occurs in 20% of patients.
It is characterized by a protacted clinical course, a high incidence of local complications and a high mortality rate.
On the left there is normal enhancement of the entire pancreatic gland with only mild surrounding fatty infiltration.
There are no fluid collections or necrosis
(Balthazar grade C, CTSI: 2).
In exudative pancreatitis, or better called EXPN, there is normal enhancement of the entire pancreas associated with extensive peripancreatic collections.
These are often heterogeneous in appearance and may be progressive.
EXPN consists of necrosis of peripancreatic fat, extravasated pancreatic fluid and inflammatory and hemorrhagic components.
When peripancreatic collections persist or increase, it is usually due to the presence of fat necrosis (i.e. EXPN).
Since fat does not enhance on CT, we cannot diagnose fat necrosis.
In the case on the left on day 18 there is expansion of the peripancreatic collections.
There are two or more collections, but no pancreatic necrosis.
(Balthazar grade E, CTSI: 4)
On the left a patient with acute necrotizing pancreatitis.
There are 2 or more fluid collections and more than 50% of the gland does not enhance
(Balthazar grade E, CTSI :10).
This patient died two days later due to severe systemic inflammatory response syndrome (SIRS) and multi organ failure.
The detection of pancreatic necrosis in clinical practice is important because most life-threatening complications occur in patients with pancreatic necrosis (1,2).
Necrotizing Pancreatitis (2)
In the case on the left the body and tail of the pancreas do not enhance after i.v. contrast (blue arrows).
There is however normal enhancement of the pancreatic head (yellow arrow).
More than 50% of the pancreas is necrotic and there are at least two collections (CTSI : 10).
Central gland necrosis
Central gland necrosis is a subtype of necrotizing pancreatitis.
It represents necrosis between the pancreatic head and tail and is nearly always associated with disruption of the pancreatic duct.
This leads to persistent collections as the viable pancreatic tail continues to secrete pancreatic juices.
These collections react poorly to endoscopic or percutaneous drainage.
Definitive treatment often requires distal pancreatectomy.
The images on the left illustrate a case of central gland necrosis.
There is a fluid collection in the omental bursa, adjacent to the stomach.
Notice the normal enhancement of the pancreatic head and tail, but the lack of enhancement of the majority of the pancreatic body.
Two weeks later the collection in the omental bursa and pancreatic body has increased significantly.
The pancreatic tail still enhances and so does the pancreatic head (arrows).
This patient developed septicaemia and underwent surgery.
Intraabdominal fluid collections and collections of necrotic tissue are common in acute pancreatitis.
These collections develop early in the course of acute pancreatitis.
In the early stage such a collection does not have a wall or capsule.
Preferred locations are the omental bursa and the retroperitoneal space (anterior and posterior pararenal space).
These collections are the result of the release of activated pancreatic enzymes (namely lipase, trypsin and amylase) which also causes necrosis of the surrounding tissues.
This explains why a lot of these collections contain solid debris.
50% of these collections show spontaneous regression (image on the left).
The other 50% either remain stable or increase and undergo organization and demarcation with liquefaction.
They may remain sterile or develop infection.
Based on imaging alone it is often not possible to determine whether these collections contain fluid or necrotic tissue and whether they are infected or not.
Consequently, instead of naming them as 'pseudocysts', 'abscesses' or 'necrosis', it is better to describe them as 'peripancreatic collections'.
On the left CT scans of a patient with acute pancreatitis.
There is a collection in the area of the pancreatic head in the right anterior pararenal space.
On a follow up scan the collection in the right anterior pararenal space is larger.
It has a fluid density and a thin enhancing wall.
One day later the patient developed septicaemia and percutaneous drainage was performed.
After drainage the collection has barely diminished in size and consequently there was suspicion of necrotic tissue.
The patient therefore underwent surgery and the collection was found to consist of necrotic debris, which was not appreciated on CT.
The necrotic debris was too thick for successful percutaneous drainage.
- Infected necrosis is:
- Infection of necrotic pancreatic parenchyma
- And/or necrotic extrapancreatic fatty tissue
- Usually occurs in the 2nd-3rd week.
- Most severe local complication of acute pancreatitis
- Most common cause of death in patients with acute pancreatitis
- Air bubbles are seen in 20% of cases with infected necrosis.
The case on the left is a typical example of infected pancreatic necrosis.
On day 3 there is no enhancement of the pancreas, consistent with necrosis (compare to enhancing spleen).
On follow up the peripancreatic collections increase in size and finally there are air bubbles in the heterogeneous collection, consistent with infected pancreatic necrosis.
Infected necrosis (2)
In the patient on the left there is a normal enhancement of the pancreas with surrounding septated heterogeneous peripancreatic collections with fluid- and fat densities (images on the left).
Two weeks later (images on the right) there are air bubbles in the peripancreatic collection, consistent with infected necrosis.
This patient underwent surgery.
The surgeon had to remove a lot of necrotic tissue and estimated he had removed over 90% of the pancreas.
Remarkably, a CT performed 6 months after surgery showed a normal pancreas.
This indicates that during surgery the differentiation between pancreatic necrosis and necrosis of the peripancreatic tissue is sometimes impossible.
- Collection of pancreatic juice enclosed by a wall of fibrous tissue
- Absence of necrotic tissue is imperative for its diagnosis
- Often communication with the pancreatic duct
- Requires 4 or more weeks to develop
- On CT we cannot diagnose a collection with certainty as a pseudocyst, since it is usually not possible to determine what the content of a collection is
- Differential diagnosis includes abscess, necrosis and sometimes also pseudoaneurysm or cystic tumor.
The patient on the left presented with a gastric outlet obstruction 2 months after an episode of acute pancreatitis.
There is a large, homogeneous, well-demarcated peripancreatic collection which abuts the stomach and the pancreas.
The patient did not have a fever.
The collection underwent successful percutaneous drainage and subsequently resolved along with the patient's symptoms.
This collection therefore proved to be a pancreatic pseudocyst.
On the other hand on the left a CT of an ICU patient on day 40 with central gland necrosis with a spiking fever.
The CT shows a similar collection to that of the previous patient, exept for its pancreatic location.
The collection is homogeneous and well-demarcated with a thin wall abutting the stomach.
During endoscopic debridement this collection contained fluid and necrotic tissue which was removed from the area of the pancreas (image on the right).
Although the imaging characteristics in this case are similar to the previous case, this proved to be infected necrosis.
The patient on the left also has a homogeneous pancreatic and peripancreatic collection, well-demarcated with an enhancing wall, on day 25 of an episode of acute pancreatitis.
Since this patient had fever and multiple organ failure, this collection was suspected to be infected necrosis and not a pseudocyst.
At surgery the collection contained a lot of necrotic debris, which was not recognizable on CT.
These cases illustrate that CT cannot reliably differentiate between collections that consist of pure fluid and those that contain fluid and solid debris with or without infection.
MRI is superior to CT in differentiating between fluid and solid debris.
On the left a patient with several homogeneous peripancreatic collections on CT.
Since these collections show homogeneous high signal intensity on a fat-suppressed T2 MRI sequence, they must be fluid-filled.
On the left another patient 2 months after an episode of acute exudative pancreatitis with also a homogeneous peripancreatic collection in the transverse mesocolon (arrow).
A T2-weighted MRI sequence however, shows that the collection has low signal intensity (arrow), and is therefore mainly solid.
This patient had no fever or signs of sepsis. If endoscopic or percutaneous drainage were attempted in this patient, there would be little or no effect on its size.
The only result would be an increased risk of infection when the collection is colonized following drain placement.
The current management of acute pancreatitis is to be conservative for as long as possible.
During the first two weeks patients with severe acute pancreatitis and multi organ failure should be stabilized in the ICU (8).
Interventions should be delayed for as long as possible.
Allow for demarcation of collections.
Remember that many collections will resorb spontaneously.
FNA and Drainage
Once the clinical condition of the patient deteriorates and the patient is febrile, fine needle aspiration (FNA) can be used to differentiate between sterile and infected collections.
Important remarks concerning FNA:
- No role for FNA in early collections
- Not transgastric for diagnosis only
- Be sure no pseudoaneurysm
- Think ahead - What is the plan:
- Pus > tube
- Indeterminate or clear > Gram stain, culture
- No flow > solid > saline > culture
Important remarks concerning Drainage:
- Indications for access to evolving fluid collections or necrosis decided on full evaluation of clinical, lab, and imaging
- No role for drainage in early collections
- Can be used as a guide for surgical approach
Collections can be approached through the transhepatic, transgastric or transabdominal route, but the preferred approach is to stay in the retroperitoneal compartment.
This approach has some advantages over the others:
- Same abdominal compartment as the pancreas
- No contamination with intestinal flora
- Drain runs parallel to pancreatic bed
- This route can be used to guide surgery
Surgical intervention in infected necrotizing pancreatitis generally consists of necrosectomy
via laparotomy (2,9).
The morbidity and mortality after this procedure might be reduced by minimally invasive strategies.
In the Netherlands there is a nationwide study into the optimal treatment of patients with infected necrotizing pancreatitis: the PANTER trial. (10).
The 20 hospitals of the Dutch Acute Pancreatitis Study Group are currently enrolling patients in a randomised trial to compare:
- Laparotomy with necrosectomy and continuous postoperative lavage with
- CT-guided or endoscopic transgastric drainage, if necessary, followed by videoscopic assisted retroperitoneal debridement (VARD).
Take home messages
- Severity of acute pancreatitis and pancreatic necrosis can only be reliably assessed by imaging after 72 hours.
- Absence of pancreatic parenchymal necrosis does not preclude a serious course of the illness.
- CT can not reliably differentiate between collections that consist of fluid and those that contain solid debris.
In these cases MRI can be of additional value.
- Avoid words such as 'pseudocyst' or 'pseudocyst formation' and 'pancreatic abscess' in the early stages of the disease.
These are rare complications!
- Central gland necrosis is a subtype of necrotizing pancreatitis with important implications.
- Avoid early drainage of collections and avoid introducing infection!