God put the pancreas in the back because He did not want surgeons messing with it.Moshe Schein
Beware of the pancreas… That bastard… You can never know when it will burst out… And how things will go…
The term acute pancreatitis (AP) refers to an acute inflammation of the pancreas.
The biggest issue with AP is that it may give a wide spectrum of manifestations and may evolve in very severe forms. Approximately 80% of patients develop just minor forms, where one-fifth develop the severe disease, reaching 20% of mortality. Translating this into bare numbers, we can say that among 25 patients with acute pancreatitis, 5 patients will have a severe disease, one of whom will die… Not bad odds at all… Or maybe it was the contrary?!…
Acute pancreatitis may be the consequence of many insults to the pancreatic tissue. The most common cause is a gallstone (21-33%), obstructing the pancreatic duct. This will activate an enzymatic cascade that will lead to the autodigestion of the pancreatic parenchyma.
Other less frequent but still common causes are alcohol consumption (16-27%), hypercalcemia, hypertriglyceridemia (2-5%), iatrogenic (e.g. ERCP), autoimmune, viral infection, medications (e.g. acetaminophen, tetracycline, valproic acid, etc…).
It is important to remember that the etiology of this disease is often not identified.
According to the revised Atlanta classification, the diagnosis of AP needs the presence of two of three criteria:
- Typical pain (i.e. acute onset of persistent, severe, epigastric pain radiating to the back);
- Elevation of serum amylase or lipase of at least 3 times the upper limit of normal;
- Characteristic findings on imaging (i.e. CEACT scan, MRI, US).
From this, it is quite clear that a patient presenting with typical abdominal pain and elevated serum amylase and/or lipase does not need immediate imaging to confirm the diagnosis… Because the diagnosis has already been made. Moreover, if a CT scan is made too early (within the first 72 h after the onset of AP), it may underestimate the severity of the disease. A contrast-enhanced abdominal CT scan should be asked to make a diagnosis only in case of uncertainty. Abdominal MRI with gadolinium can be an alternative to CT scan in patients with severe contrast allergy or renal failure.
A couple of information about the two pancreatic digestive enzymes:
- Serum amylase – it has a short half-life (about 10 h), reducing the chances of making diagnosis in patients presenting later after the onset of pancreatitis (>24 h);
- Serum lipase – it has a longer half-life (about 8-14 days) and, thanks to this, it has a higher sensitivity for acute pancreatitis, especially in those presenting after 24 h and in those with alcoholic pancreatitis.
Remember that if AP shifts intravascular fluids into the so-called third space, causing hemoconcentration, which may manifest with leukocytosis and increased hematocrit. This is to remember that increased white cell count at presentation may not reflect an ongoing infection, but “just” fluid extravasation. Moreover, an AP will induce a deep activation of cytokines creating a “SIRS” (we know this term actually shouldn’t be used anymore, but still pretty works in this case), so expect elevated CRP, white cells counts, and fever.
From the clinical point of view, you have to remember that the clinical manifestations of AP are extremely aspecific (i.e. nausea, vomiting, dyspnea, etc…) and the same can be said about the physical findings (i.e. epigastric tenderness). However, there are some characteristic signs usually taught during med school: ecchymosis in the periumbilical region (i.e. Cullen’s sign) or bilaterally along the flanks (Grey-Turner’s sign)… Well, you can just forget them… Their prevalence is about 3% and they represent the physical manifestation of advanced retroperitoneal bleeding… Basically, they are angels of death…
Once the diagnosis of acute pancreatitis has been made, the second step is to try to identify the cause behind it. This can be (easily) accomplished by collecting a complete history (e.g. alcohol consumption, recent use of medications, recent ERCP), laboratory exams (e.g. blood alcohol levels, triglyceridemia, calcemia), and ultrasound (i.e. gallstones). More advanced tests may be useful in case of unknown etiology (e.g. tests for viral infections, IgG4).
Classification & Complications
Acute pancreatitis can be classified according to severity into three categories:
- Mild acute pancreatitis – no organ failure, no local or systemic complication;
- Moderately severe acute pancreatitis – transient organ failure (<48 h) and/or local or systemic complications;
- Severe acute pancreatitis – persistent organ failure (>48 h).
We don’t think we need to define what an organ failure is… So, let’s just skip it and go directly to complications…
Systemic complications are quite straightforward… They represent the sudden worsening of preexisting conditions (e.g. chronic renal failure, heart failure, etc…). Obviously, this exacerbation is the direct consequence of the systemic inflammatory response syndrome secondary to AP.
On the other hand, local complications represent the changes in the pancreatic parenchyma and peripancreatic tissues due to the inflammatory process. Acute pancreatitis may appear in two different forms: acute interstitial edematous pancreatitis (85%) and necrotizing pancreatitis (15%). These two forms may evolve, leading to different local complications: peripancreatic fluid collections and acute necrotic collections, respectively. These two distinct entities usually develop within the first 4 weeks after the onset of AP. Similar to their initial forms, these “early” local complications may further evolve, giving birth to distinct “late” local complications. Accordingly, after at least 4 weeks, they may progress into pancreatic pseudocyst and walled-off necrosis, respectively.
|Initial Form||Interstitial Edematous Pancreatitis |
Acute inflammation of the pancreatic parenchyma and peripancreatic tissues, but without necrosis.
Pancreatic parenchyma enhanced by contrast.
|Necrotizing Pancreatitis |
Inflammation associated with pancreatic parenchymal necrosis and/or peripancreatic necrosis.
Lack of pancreatic parenchyma enhancement by contrast, presence of necrosis.
|“Early” Local Complication |
|Acute Peripancreatic Fluid Collection (APFC) |
Homogeneous fluid collection confined by peripancreatic fascial planes and without a clear wall.
|Acute Necrotic Collection (ANC) |
Collection containing variable amounts of both fluid and necrosis.
Heterogeneous, non-liquid collection with no definable wall, involving intrapancreatic and/or extrapancreatic tissues.
|“Late” Local Complication |
|Pancreatic Pseudocyst |
Encapsulated collection of fluid with a well-defined inflammatory wall.
Completely encapsulated, well-circumscribed, homogeneous fluid collection.
|Walled-Off Necrosis (WON) |
Mature, encapsulated collection of pancreatic and/or peripancreatic necrosis.
Heterogeneous, liquid, and non-liquid, loculated collection with a complete and well-defined wall.
It is good to remember that necrotic degeneration of pancreatic parenchyma may become infected.
Other possible local complications are porto-spleno-mesenteric venous thrombosis (in 50% of necrotizing pancreatitis), gastric outlet syndrome, and colonic necrosis.
All these local complications are recognizable with a CEACT scan, which should be made 72-96 h after the onset of acute pancreatitis not to underestimate the extension of the ongoing inflammatory process. However, in patients with a “simple” mild AP there is no need to perform a CEACT scan. Therefore, the practice of performing routine CT scans should be abandoned in favor of a more targeted strategy.
For what concerns systemic complications and organ failure, a close and strict monitoring should be set up for the first 48-72 h to identify as soon as possible initial signs of organ failure. Organ failure may be defined as a Modified Marshall Score ≥2 for that specific system.
Modified Marshall Scoring System for Organ Dysfunction:
|Kidney (umol/L or mg/dL)||<134 <1.4||134-169 1.4-1.8||170-310 1.9-3.6||311-439 3.7-4.9||>439 >4.9|
|Cardiovascular (systolic blood pressure in mmHg)||>90||<90, fluid responsive||<90, not fluid responsive||<90, pH <7.3||<90, pH <7.2|
Predictors of Severity
Needless to say, complications and severity grading of acute pancreatitis correlate with mortality… And quick and appropriate treatments may decrease the death rate in patients with severe AP… So, it appears obvious that predicting AP severity might be useful in providing immediate and proper treatments to these patients.
Before starting this, it is mandatory to remember that serial measurements of serum amylase and/or lipase in AP are not useful… This practice does not predict severity or prognosis, and either helping us in altering our management. Serum amylase and lipase are elements that help us in making diagnosis… That’s it… This is because they might drop to normal levels pretty fast because of their reduced production or because there is no more pancreatic parenchyma to produce them (think about massive necrosis of the gland)…
During the years, many scores have been created to predict AP severity and determine the most appropriate level of care.
The most common scores are the Acute Physiology and Chronic Health Evaluation II (APACHE II), the Bedside Index of Severe Acute Pancreatitis (BISAP), and the Ranson Score. However, every single one of them has a major pitfall that makes them not-so-user-friendly to use. APACHE II has been designed for patients admitted in the Intensive Care Unit, it requires a large number of variables to fill in and it is not specific for AP. BISAP, although specific for AP and easy to calculate, does not reach great sensitivity for predicting severe AP. Ranson score requires particular variables not always collected routinely in non-ICU patients and it needs at least 48 hours to calculate.
An easy and alternative way to predict severe pancreatitis is using C-Reactive Protein levels. In fact, a CRP level >190 mg/L within the first 48 h or an absolute increase of >90 mg/L are associated with severe pancreatitis.
We cannot advise in favor of or against one score over the others. Our advice is to use mainly your clinical judgment to determine if a patient is at major risk of severe disease. However, if you want to use something to help your judgment and to protect you from the legal point of view, you can always use one of them. Nowadays, with our cell phones they are quite easy to calculate (and you don’t have to remember them by heart).
Ok guys… We think that is enough now… Next time we are going to see how to properly treat patients with mild AP and how to manage local complications…
Until next time: be good, be brave, be an acute care surgeon…
- Mederos MA, et al. Acute pancreatitis – a review. JAMA 2021;325:382-90.
- Greenberg JA, et al. Clinical practice guideline: management of acute pancreatitis. J Can Chir 2016;59:128-40.
- Working Group IAP/APA Acute Pancreatitis Guidelines. IAP/APA evidence-based guidelines for the management of acute pancreatitis. Pancreatology 2013;13:e1-e15.
- Banks PA, et al. Classification of acute pancreatitis – 2012: revision of the Atlanta classification and definitions by international consensus. Gut 2013;62:102-11.
- Crockett SD, et al. American Gastroenterological Association Institute guideline on initial management of acute pancreatits. Gastroenterology 2018;154:1096-101.
- Vivian E, et al. Acute pancreatitis task force on quality. Am J Gastroenterol 2019;114:1322-42.
- Ketwaroo G, et al. Quality of care indicators in patients with acute pancreatitis. Dig Dis Sci 2019;64:2514-26.
How to Cite This Post
Bellio G, Marrano E. The Awakening of the Sleeping Lion – Part 1. Surgical Pizza. Published on July 10, 2021. Accessed on July 31, 2021. Available at [https://surgicalpizza.org/emergency-surgery/the-awakening-of-the-sleeping-lion-part-1/].