Acute pancreatitis

Acute pancreatitis refers to acute inflammation of the pancreas and is a potentially life threatening condition. Imaging is often required to not only confirm the diagnosis but also to guide treatment.

Epidemiology

The demographics of patients affected by acute pancreatitis reflects the underlying cause. Causes include:

alcohol abuse: most common cause of chronic pancreatitis

gallstone passage/impaction: most common cause of acute pancreatitis (up to 15% could develop pancreatitis) 

metabolic disorders 

hereditary pancreatitis (autosomal dominant) SPINK-1 gene mutation 5

hypercalcemia

hyperlipidemia (types 1 and 5)

malnutrition

trauma : most common cause in children

blunt abdominal trauma

surgery

endoscopic retrograde cholangiopancreatography (ERCP) 7

penetrating ulcer

malignancy

pancreatic adenocarcinoma

lymphoma

infection

viral: mumps, coxsackie, hepatitis, infectious mononucleosis, AIDS

parasitic: Ascariasis 5, Clonorchis

structural

choledochocoele

pancreas divisum

toxins

scorpion bites

spider bites (some)

idiopathic: 20% of cases of acute pancreatitis

drugs: steroids, tetracycline, frusemide, azathioprine, thiazides, L-asparaginase and many others

others

cystic fibrosis

systemic lupus erythematosus (SLE) 4

haemolytic uremic syndrome (HUS)

Reye's syndrome 6

Clinical presentation

Acute pancreatitis is generally diagnosed clinically. Classical features include 3:

gradual development 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.

Signs of haemorrhage 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 not withstanding, 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 (collections of enzyme-rich pancreatic juice)

acute: resolve spontaneously in 50% of cases; may be intrapancreatic, anterior pararenal space, lesser sac, or extend anywhere in the abdomen, into solid organs, or even into the chest

in the remaining 50% of cases, these fluid collections progress to pseudocysts

pseudocyst formation

a round or oval, encapsulated pancreatic fluid collection encased by a distinct fibrous capsule

requires at least 4 weeks to develop

about 50% will spontaneously resolve, whereas the remainder will require catheter or surgical drainage.

liquefactive necrosis of pancreatic parenchyma

morbidity and mortality increase dramatically when necrosis is present

may become secondarily infected (emphysematous pancreatitis)

abscess - peripancreatic abscess

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 peritoneal cavity

Radiographic features

Role of imaging is either to clarify the diagnosis when the clinical picture is confusing, to assess severity (Balthazar score), to determine prognosis, or to detect complications.

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

indistinctness of the margins of the gland owing to inflammation

surrounding retroperitoneal stranding

liquefactive necrosis of pancreatic parenchyma

lack of parenchymal enhancement

often multifocal.

infected necrosis

difficult to distinguish from aseptic liquefactive necrosis

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

May be used to monitor patient's progress:

diagnosis of vascular complications, ie. thrombosis

identify gallstones

hypoechoic lesions may indicate necrotic change

Treatment and prognosis

Prognosis for acute pancreatitis varies according to severity. Overall mortality is 5-10% per attack 3. Ranson's criteria are useful in prognosticating.

The newly revised Atlanta classification system makes the scene for a new international classification system, trying to uniform reporting for both clinical practice and research 8.

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.

Ultrasound or CT directed aspiration biopsy may be needed to confirm the presence of pancreatic abscess. Image-directed catheter placement is an alternative to surgical drainage of pancreatic fluid collections.