Acute pancreatitis is defined as an acute inflammatory process of the pancreas with variable involvement of other local tissues and remote organ systems.
It is one of the most common causes of hospital admission for gastrointestinal disorders.
It has a variety of causes (gallstones and alcohol in the vast majority) and can range in severity from mild to severe and life threatening.
Despite the fact that mild acute pancreatitis (the most common form) has a very low mortality rate,
organ failure presence and infected necrosis can bring this rate up to 20%-30% [1].
The revised Atlanta classification system is an international consensus which provides clear definitions when assessing acute pancreatitis type,
phase,
severity and complications,
using easily identifiable clinical and radiological criteria [2].
Diagnosis
According to this classification,
the diagnosis of acute pancreatitis requires at least two of the following three features [2]:
- abdominal pain consistent with acute pancreatitis;
- serum lipase and/or amylase activity at least 3 times greater than the upper limit of normal;
- characteristic findings on contrast-enhanced CT (CECT) or MRI,
or less commonly on transabdominal US.
Course and severity of the disease
The onset of acute pancreatitis is considered to be the 1st day of pain.
Two distinct clinical phases of evolution,
the early phase and the late phase,
are reflected by the two peaks in mortality: one very early after onset (usually within the first week) and another after 2-6 weeks from onset [3].
The two phases are:
- the early phase (1st week) – severity is based on clinical/functional parameters,
because treatment is determined primarily by the presence and duration of organ failure secondary to the host’s systemic inflammatory response (SIRS)
- the late phase (after the 1st week) – morphological data (as seen on CECT or MRI) guides therapy and must be used in conjunction clinical criteria [4]
During the early phase (1st week after the onset),
the pathological process in and around the pancreas evolves from the initial state of inflammation and variable degrees of ischemia and/or edema to either resolution or to irreversible necrosis and liquefaction,
and/or development of fluid collections in and around the pancreas.
Systemic inflammatory response syndrome (SIRS) development can lead to organ failure,
the presence and duration of which determines the severity and the need for treatment.
Over the course of the 1st week,
organ failure either resolves or becomes more severe.
The modified Marshall scoring system is used to assess organ failure.
There is not always a direct correlation between clinical severity with or without organ failure and extent of morphological characteristics in and around the pancreas [5,
6].
During the late phase (after the 1st week) the pathological process either resolves (interstitial edematous pancreatitis - IEP) or tends to stabilise or progress (necrotising pancreatitis).
The progression is characterised by extension and/or infection of the necrosis and persistent multiorgan failure.
Infected necrosis can lead to bacteraemia and sepsis.
The main determinant of severity and the need for treatment continues to be persistent organ failure,
but local complications may have direct implications in choosing the type of treatment.
Thus,
the late phase requires both clinical and morphological,
image-based criteria [2].
This classification defines three degrees of severity [7,
8]:
- mild - absence of organ failure and of local or systemic complications
- moderately severe - presence of transient (<48h) organ failure and/or local or systemic complications
- severe - persistent organ failure (>48h)
Imaging
Imaging is required to confirm the diagnostic if suggestive abdominal pain is present but the amylase/lipase level is under the threshold value (e.g.
in case of delayed presentation).
Imaging is also useful early in the disease course when the cause of the disease is unclear,
to look for causative factors such as choledocholithiasis and pancreatic cancer [4].
Imaging is fundamental in staging acute pancreatitis,
assessing complications,
guiding catheter placement for drainage,
and monitoring treatment response through follow-up studies.
Because of the wide availability and high accuracy,
contrast-enhanced CT plays the leading role in acute pancreatitis imaging,
while MRI is usually reserved for a better characterisation of collections and for choledocholithiasis not seen in CT.
MRI should also be used in patients in whom contrast-enhanced CT is contraindicated (e.g.
due to pregnancy or iodinated intravenous contrast agents allergy).
Transabdominal US can evaluate the presence of gallbladder stones [9,
10].
The ideal time for assessing local complications with CT is 72 hours after onset and the examination should be repeated whenever the clinical picture drastically changes.
Sometimes,
in the early phase of the disease,
the heterogeneous enhancement of the parenchyma can impede the differentiation between IEP and ill-defined necrosis.
CECT performed 5-7 days later allows for a definitive characterisation.
The radiologist report should include the following: the presence/absence of pancreatic necrosis,
characterisation of fluid collection in and around the pancreas,
other findings such as ascites,
gallstones,
biliary dilatation,
venous thrombosis (splenic,
portal,
mesenteric etc.),
varices,
pseudoaneurysms,
pleural effusions and inflammatory involvement of the gastrointestinal tract,
liver,
spleen,
kidneys or ureters [2].
There are two types of acute pancreatitis:
- interstitial edematous pancreatitis (IEP)
- necrotising pancreatitis
Four types of pancreatic and peripancreatic collections are described:
- acute peripancreatic fluid collection (APFC)
- pancreatic pseudocyst
- acute necrotic collection (ANC)
- walled-off necrosis