Acute pancreatitis
Updates to Article Attributes
Acute pancreatitis refers to is an acute inflammation of the pancreas and is a potentially life threatening-threatening condition.
The diagnosis of acute pancreatitis is made by fulfilling two of the following three criteria 8:
- acute onset of persistent, severe epigastric pain (i.e. pain consistent with acute pancreatitis)
- lipase/amylase elevation >
;3x;3 times the upper limit of normal - characteristic imaging features on
CECTcontrast-enhanced CT, MRI, orUSultrasound
Imaging is only required to establish the diagnosis if the first two criteria are not met. Imaging is crucial for the detection of complications and to help guide treatment.
Terminology
There are two subtypes of acute pancreatitis 8:
-
interstitial oedematous pancreatitis
- the vast majority (90-95%)
- most often referred to simply as "acute pancreatitis" or "uncomplicated pancreatitis"
-
necrotising pancreatitis
- necrosis develops within the pancreas and/or peripancreatic tissue
Epidemiology
The demographics of patients affected by acute pancreatitis reflects the underlying cause, of which there are many, including:
-
gallstone passage/impaction: most common cause of acute pancreatitis (up to 15%
coulddevelop pancreatitis) - idiopathic: 20% (range 10%-30%) of cases of acute pancreatitis
- evidence suggests that most cases are associated with congenital duct abnormalities
- alcohol abuse: most common cause of chronic pancreatitis
- non-linear dose-response relationship 10
- 1.2x risk with ~40 g/day alcohol consumption
- 4x risk with ~100 g/day alcohol consumption
- non-linear dose-response relationship 10
- metabolic disorders
-
hypertriglyceridaemia-induced pancreatitis 13
- 1-4% of cases
- most common cause in pregnancy
- hypercalcemia
-
hypertriglyceridaemia-induced pancreatitis 13
- autoimmune pancreatitis
- penetrating peptic ulcer
- trauma: most common cause in children
- blunt abdominal trauma
- surgery
- endoscopic retrograde cholangiopancreatography (ERCP) 7
penetrating ulcer
- malignancy
- hereditary pancreatitis (autosomal dominant) SPINK1 gene mutation 5
- malnutrition
- infection
- viral: mumps, Coxsackie, hepatitis, infectious mononucleosis, AIDS
- parasitic:
Ascariasis
- structural: not a cause, but associated with increased incidence
- toxins
- scorpion
stingssting: in particular, the Trinidad thick-tailed scorpion,tityusTityus trinitatis - spider
bites (somebite (several species)
- scorpion
- drugs: steroids, tetracycline, frusemide, azathioprine, thiazides, L-asparaginase and many others
- interestingly, NSAIDs, while used for symptomatic treatment of pancreatitis, have been implicated as a possible cause, e.g. diclofenac is used in preventing post-ERCP pancreatitis, but is nonetheless considered the major NSAID responsible for inducing acute pancreatitis in the general population 14
- others
See: causes of pancreatitis (mnemonic).
Clinical presentation
Classical clinical features include 3:
- acute onset of severe central epigastric pain (over 30-60 min)
- poorly localised tenderness and pain
- exacerbated by supine positioning
- radiates through to the back in 50% of patients
Elevation of amylase and lipase are 90-95% specific for the diagnosis 3.
(Rare) signs of haemorrhage on the physical exam include:
- Cullen sign: periumbilical bruising
- Grey-Turner sign: flank bruising
Pathology
There continues to be debate over the precipitating factor leading to acute pancreatitis, with duct occlusion being an important factor, but neither necessary nor sufficient.
Mechanism notwithstanding, activation of pancreatic enzymes within the pancreas rather than the bowel lead to inflammation of the pancreatic tissue, disruption of small pancreatic ducts and in leakage of pancreatic secretions. Because the pancreas lacks a capsule, the pancreatic juices have ready access to surrounding tissues. Pancreatic enzymes digest fascial layers, spreading the inflammatory process to multiple anatomic compartments.
Complications
- pancreatic fluid collections are defined by presence or absence of necrosis:
- necrosis absent (i.e. interstitial oedematous pancreatitis)
- acute peripancreatic fluid collections (APFCs) (in the first 4 weeks)
- pseudocysts: encapsulated fluid collections after 4 weeks
- necrosis present (i.e. necrotising pancreatitis)
- acute necrotic collections (ANCs): develop in first 4 weeks
- walled-off necrosis (WON): encapsulatedcollections after 4 weeks
- necrosis absent (i.e. interstitial oedematous pancreatitis)
- liquefactive necrosis of pancreatic parenchyma (e.g. necrotising pancreatitis)
- increased morbidity and mortality
- may become secondarily infected (emphysematous pancreatitis)
- pancreatic abscess
- a presence of infection without significant necrosis
- extremely rare
- term not in current use 8
- vascular complications
- haemorrhage: resulting from erosion of blood vessels and tissue necrosis
- pseudoaneurysm: autodigestion of arterial walls by pancreatic enzymes results in pulsatile mass that is lined by fibrous tissue and maintains communication with parent artery
- splenic vein thrombosis
- portal vein thrombosis
- fistula formation with pancreatic ascites: leakage of pancreatic secretions into the peritoneal cavity
Radiographic features
The role of imaging is manifold:
- to clarify the diagnosis when the clinical picture is confusing
- to assess severity (Balthazar score) and thus to determine prognosis
- to detect complications
- to determine possible causes
Imaging studies of acute pancreatitis may be normal in mild cases. Contrast-enhanced CT provides the most comprehensive initial assessment, typically with a dual phase (arterial and portal venous) protocol. However, US is useful for follow-up of specific abnormalities, such as fluid collections and pseudocysts.
CT
Abnormalities that may be seen in the pancreas include:
- typical findings
- focal or diffuse parenchymal enlargement
- changes in density because of oedema
- indistinct pancreatic margins owing to inflammation
- surrounding retroperitoneal fat stranding
- liquefactive necrosis of pancreatic parenchyma
- lack of parenchymal enhancement
- often multifocal
- infected necrosis
- difficult to distinguish from aseptic liquefactive necrosis
- the presence of gas is helpful
- FNA helpful
- abscess formation
- circumscribed fluid collection
- little or no necrotic tissues (thus distinguishing it from infected necrosis)
- haemorrhage
- high-attenuation fluid in the retroperitoneum or peripancreatic tissues
MRI
Contrast-enhanced MR is equivalent to CT in the assessment of pancreatitis.
Ultrasound
The main role of ultrasound is:
- to identify gallstones as a possible cause
- diagnosis of vascular complications, e.g. thrombosis
- identify areas of necrosis which appear as hypoechoic regions
Treatment and prognosis
Treatment is largely supportive, often requiring ICU care in severe cases for respiratory and cardiovascular support and careful management of glucose, calcium, and fluid balance.
Recommendations include 11:
- aggressive fluid resuscitation in first 24 hours
- no need for prophylactic antibiotics
- enteral feeding strongly preferred over parenteral feeding, especially in severe acute pancreatitis
- no need for ERCP in acute gallstone pancreatitis unless evidence of ascending cholangitis
- image-directed catheter placement is an alternative to surgical drainage of pancreatic fluid collections
- cholecystectomy before discharge in patients with acute pancreatitis and gallstones found on imaging
Prognosis for acute pancreatitis varies according to severity. Overall mortality is 5-10% per attack 3. Various scoring systems exist that attempt to stratify severity (e.g. Ranson's criteria and APACHE II).
The newly revised Atlanta classification (new international classification system), attempts to establish uniformity in reporting for both clinical practice and research 8.
Differential diagnosis
General imaging differential considerations include:
- pancreatic ductal adenocarcinoma
- autoimmune pancreatitis
- peptic ulcer disease with posterior perforation
- pancreatic lymphoma (diffuse pattern)
-<p><strong>Acute pancreatitis</strong> refers to acute inflammation of the <a href="/articles/pancreas">pancreas </a>and is a potentially life threatening condition.</p><p>The diagnosis of acute pancreatitis is made by fulfilling two of the following three criteria <sup>8</sup>:</p><ul>- +<p><strong>Acute pancreatitis</strong> is an acute inflammation of the <a href="/articles/pancreas">pancreas </a>and is a potentially life-threatening condition.</p><p>The diagnosis of acute pancreatitis is made by fulfilling two of the following three criteria <sup>8</sup>:</p><ul>
-<li>lipase/amylase elevation >3x the upper limit of normal</li>-<li>characteristic imaging features on CECT, MRI, or US</li>- +<li>lipase/amylase elevation >3 times the upper limit of normal</li>
- +<li>characteristic imaging features on contrast-enhanced CT, MRI, or ultrasound</li>
-</ul><h4>Epidemiology</h4><p>The demographics of patients affected by acute pancreatitis reflects the underlying cause, of which there are many including: </p><ul>- +</ul><h4>Epidemiology</h4><p>The demographics of patients affected by acute pancreatitis reflects the underlying cause, of which there are many, including: </p><ul>
-<a href="/articles/gallstones-1">gallstone</a> passage/impaction: most common cause of acute pancreatitis (up to 15% could develop pancreatitis) </li>-<li>idiopathic: 20% of cases of acute pancreatitis</li>- +<a href="/articles/gallstones-1">gallstone</a> passage/impaction: most common cause of acute pancreatitis (up to 15% develop pancreatitis)</li>
- +<li>idiopathic: 20% (range 10%-30%) of cases of acute pancreatitis<ul><li>evidence suggests that most cases are associated with congenital duct abnormalities </li></ul>
- +</li>
- +<li><a title="Autoimmune pancreatitis" href="/articles/autoimmune-pancreatitis">autoimmune pancreatitis</a></li>
- +<li>penetrating peptic ulcer</li>
-<li>penetrating ulcer</li>-<li>parasitic: <em>Ascariasis</em> <sup>5</sup>, <em>Clonorchis</em>- +<li>parasitic: ascariasis <sup>5</sup>, <em>Clonorchis</em>
-<li>structural<ul>- +<li>structural: not a cause, but associated with increased incidence<ul>
-<li>scorpion stings: in particular, the Trinidad thick-tailed scorpion, <em>tityus trinitatis</em>- +<li>scorpion sting: in particular, the Trinidad thick-tailed scorpion, <em>Tityus trinitatis</em>
-<li>spider bites (some)</li>- +<li>spider bite (several species)</li>
-<li>drugs: steroids, tetracycline, frusemide, azathioprine, thiazides, L-asparaginase and many others</li>- +<li>drugs: steroids, tetracycline, frusemide, azathioprine, thiazides, L-asparaginase and many others<ul><li>interestingly, NSAIDs, while used for symptomatic treatment of pancreatitis, have been implicated as a possible cause, e.g. diclofenac is used in preventing post-ERCP pancreatitis, but is nonetheless considered the major NSAID responsible for inducing acute pancreatitis in the general population <sup>14</sup>
- +</li></ul>
- +</li>
-</ul><p>See: <a href="/articles/causes-of-pancreatitis-mnemonic">causes of pancreatitis (mnemonic)</a>.</p><h4>Clinical presentation</h4><p>Classical clinical features include <sup>3</sup>:</p><ul>- +</ul><p>See: <a href="/articles/causes-of-pancreatitis-mnemonic">causes of pancreatitis (mnemonic)</a></p><h4>Clinical presentation</h4><p>Classical clinical features include <sup>3</sup>:</p><ul>
References changed:
- 14. Pezzilli R, Morselli-Labate A, Corinaldesi R. NSAIDs and Acute Pancreatitis: A Systematic Review. Pharmaceuticals (Basel). 2010;3(3):558-71. <a href="https://doi.org/10.3390/ph3030558">doi:10.3390/ph3030558</a> - <a href="https://www.ncbi.nlm.nih.gov/pubmed/27713268">Pubmed</a>
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