MENURadiopaedia.org SEARCH ARTICLES CASES COURSES LOG IN REGISTER NOW ADVERTISEMENT: Supporters see fewer/no ads Acute pancreatitis Last revised by Rohit Sharma on 27 Sep 2023 Citation, DOI, disclosures and article data Acute pancreatitis (plural: pancreatitides) is an acute inflammation of the pancreas and potentially life-threatening. On this page: Article: Terminology Epidemiology Diagnosis Clinical presentation Pathology Radiographic features Treatment and prognosis Differential diagnosis See also Related articles References Images: Cases and figures Terminology Two subtypes of acute pancreatitis are described in the Revised Atlanta Classification 1: interstitial edematous pancreatitis the vast majority (90-95%) most often referred to simply as "acute pancreatitis" or "uncomplicated pancreatitis" necrotizing pancreatitis necrosis develops within the pancreas and/or peripancreatic tissue Epidemiology The demographics of patients affected by acute pancreatitis reflect the underlying cause, of which there are many (see Pathology below). Diagnosis The diagnosis of acute pancreatitis is usually based on clinical criteria or a combination of clinical and radiographic features 1. Diagnostic criteria Two of the following three criteria are required for the diagnosis 1: acute onset of persistent, severe epigastric pain (i.e. pain consistent with acute pancreatitis) lipase/amylase elevation >3 times the upper limit of normal characteristic imaging features on contrast-enhanced CT, MRI, or ultrasound ADVERTISEMENT: Supporters see fewer/no ads Clinical presentation Classical clinical features include 3: acute onset of severe central epigastric pain (over 30-60 min) poorly localized tenderness and pain exacerbated by supine positioning radiates through to the back in 50% of patients Elevation of serum amylase and lipase are 90-95% specific for the diagnosis 3. A normal amylase level (normoamylasaemia) in acute pancreatitis is well-recognized, especially when it occurs on the ground of chronic pancreatitis. A normal lipase level has also been reported (<10 case reports) but is extremely rare 16. (Rare) signs of hemorrhage 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 leads to inflammation of the pancreatic tissue, disruption of small pancreatic ducts, and 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. Etiology gallstone passage/impaction: most common cause of acute pancreatitis (up to 15% develo

1. Sonological features of
pancreatitis
Moderator – Dr Srinivasa Babu
Presentor – Dr Chandrahas

2. Anatomy of the pancreas
• The pancreas is situated on the posterior abdominal wall at approximately L1
level.
• It is described as having a head, neck, body and tail. It is retroperitoneal with the
exception of the tail, which lies in the splenorenal ligament.
• It is over 15 cm long and lies transversely and slightly obliquely, with the tail
higher than the head.
• The pancreas lies obliquely in the anterior pararenal space of the
retroperitoneum, with the head caudal to the body and tail.
• The pancreas is draped over the spine and aorta; thus the neck and body are more
superficial than the head and tail.

4. Anatomy of the pancreas
• The head of the pancreas lies in the curve of the duodenum, with the pylorus and
the duodenal cap overlapping it slightly on its upper surface.
• The uncinate process projects posteriorly and to the left from its lower part to lie
posterior to the superior mesenteric vessels.
• The remainder of the pancreatic head lies anterior to the vessels of the posterior
abdominal wall, that is, the vena cava and renal veins, the aorta and its coeliac and
superior mesenteric branches.
• The common bile duct passes posterior to the head of the pancreas in a groove or
tunnel towards its termination in the second part of the duodenum.

5. Anatomy of the pancreas
• The neck of the pancreas extends from the upper part of the anterior portion of the head.
• It lies anterior to the union of the splenic vein and the superior mesenteric vein to form the
portal vein.
• The body of the pancreas curves over the vertebrae and great vessels to reach the left
paravertebral gutter.
• The splenic vein passes posterior to the body, where it receives the inferior mesenteric vein.
• The body lies anterior to the left kidney and adrenal.
• The tail of the pancreas is related to the splenic hilum. Here it lies in the splenorenal
ligament.
• The lesser sac is anterior to the pancreas and anterior to this lies the stomach and part of the
lesser omentum.

7. The pancreatic ducts
• The pancreatic duct begins in the tail by the union of ductules and passes transversely
towards the head, closer to the anterior than the posterior surface of the gland.
• It receives smaller ducts along its length at right-angles and increases in size as it
approaches the head.
• At the neck the duct turns inferiorly, some what posteriorly and to the right, and joins the
bile duct to form a terminal, common dilated portion called the ampulla (of Vater) before
entering the duodenum at the papilla.
• An accessory duct (of Santorini) arises in the lower part of the head, which it drains, and
then passes upwards anterior to the main duct, to which it is connected by a communicating
duct, and drains to the duodenum about 2 cm proximal to the papilla.

10. The development of the pancreas
• The pancreas arises from the junction of the primitive foregut and midgut as a larger dorsal
division and two smaller ventral buds.
• The ventral buds arise in common with the biliary duct.
• The left ventral bud atrophies and the right ventral bud swings posteriorly to unite with the
inferior aspect of the dorsal division, trapping the superior mesenteric vessels between
divisions.
• The duct of the smaller ventral portion becomes the main duct and the proximal part of the
duct of the larger dorsal division becomes the accessory duct.

12. Arterial supply of the pancreas
• The pancreas is supplied by branches of the coeliac and superior mesenteric arteries.
• The coeliac supplies branches via its hepatic and splenic arteries.
• The gastroduodenal artery, arising from the hepatic artery, divides into the right gastroepiploic artery and the
superior pancreaticoduodenal artery.
• The inferior pancreaticoduodenal artery arises from the right side of the superior mesenteric artery.
• It divides early into anterior and posterior branches that anastomose with those of the superior
pancreaticoduodenal artery.

13. Venous drainage of the pancreas
• The neck, body and tail of the pancreas drain to the splenic vein and the head drains to the
superior mesenteric and portal veins.
Lymphatic drainage
• Lymphatic drainage is to nodes along the course of the supplying arteries to preaortic coeliac
nodes.

14. Ultrasonography of the pancreas
• Pancreatic Body
• Compression scanning with a “large footprint,”
curved linear transducer is the key technique in
visualizing the body of the pancreas.
• The key vascular landmarks for the body of the
pancreas are the splenic vein, its confluence
with the superior mesenteric vein (SMV), and
the superior mesenteric artery (SMA).
• The region between the body and head of the
pancreas the “neck,” generally referring to the
part of the pancreatic body ventral to the SMA-
SMV and portosplenic confluence

15. • Pancreatic Head
• The head is the key pancreatic structure; common bile duct stones, periampullary
neoplasms, and pancreatic/extrahepatic duct obstructions occur here.
• Vascular landmarks for the pancreatic head are the inferior vena cava (IVC) dorsally, the
SMA and SMV medially, and the gastroduodenal artery and the pancreaticoduodenal
arcade anterolaterally.
• The pancreatic head is usually directly ventral to the IVC. Cephalic to the pancreas, the IVC
is adjacent to the portal vein; this location is the entrance into the lesser peritoneal sac, the
epiploic foramen (foramen of Winslow).
• The uncinate process (or uncinate) is a portion of the caudal pancreatic head that wraps
around behind the SMA and SMV, ending in a point oriented medially. The uncinate process
is medial and dorsal to the SMA and SMV
• The GDA is a landmark for the ventrolateral pancreatic head; the GDA courses between the
pancreas and the second portion of the duodenum.

20. • Pancreatic Parenchyma
• The sonographic appearance of the normal pancreas varies widely in parenchymal echogenicity and texture,
shape, and size.
• The pancreatic parenchyma is usually isoechoic or hyperechoic compared with the hepatic parenchyma
• The parenchymal texture varies widely from homogeneous to a lobular internal architecture.
• Pancreatic size varies considerably from individual to individual. The shape of the pancreas can also vary
considerably.
• The size of the head of the pancreas ranged from 6 to 28 mm (17.7 ± 4.2 mm), body size from 4 to 23 mm
(10.1 ± 3.8 mm), and tail size from 5 to 28 mm (16.4 ± 4.2 mm).

22. Pancreatitis
• Pancreas is an exocrine and endocrine organ with vital role in functioning of the body.
• Inflammation of the pancreas is called pancreatitis.
• Incidence:
Acute pancreatitis - 13- 45 per lakh population
Chronic pancreatitis - 5-12 per lakh population
• Acute pancreatitis
• “An acute inflammatory process of the pancreas with variable involvement of other regional
tissues or remote organ systems associated with raised pancreatic enzyme levels in blood
and/or urine.”

23. Pathogenesis of Acute pancreatitis

24. AETIOLOGY OF ACUTE PANCREATITIS
• Gallstones (30-45%)
• Alcohol abuse (30-35%)
• Post-operative.
• Trauma.
• Metabolic causes: hypertriglyceridemia, hypercalcemia, renal failure, after renal
transplantation.
• Infections : Viral (mumps, coxsackie), ascariasis.
• Drugs : Azathioprine, thiazide diuretics, furosemide.
• Vascular causes : Ischaemic-hypoperfusion state (after cardiac surgery).
• Penetrating peptic ulcer.
• Vasculitis : Systemic lupus erythematosis

25. Clinical features
Symptoms:
• Upper abdominal pain radiating to
back and shoulder tips.
• Nausea/vomiting.
• Fever.
• Weakness.
Signs:
• Tachycardia/tachypnea.
• Hypotension.
• Abdominal distension
• Gray turners sign, Cullen's sign and
fox’s sign.

26. ROLE OF ULTRASOUND
• Pancreatic sonography can be an efficient and valuable tool in many common diseases, such
as pancreatitis and pancreatic neoplasm.
• Sonography is often the first test used in patients with jaundice or abdominal pain.
• Evaluation of the gallbladder and bile ducts is the focus of most sonographic examinations
performed in patients with acute pancreatitis.
• Detect gallstones as a cause of acute pancreatitis
• Detect bile duct dilation and obstruction
• Diagnose unsuspected acute pancreatitis or confirm diagnosis of acute pancreatitis Guide
aspiration and drainage

27. Sonological features
• Pancreatic echogenicity typically decreases in patients who have acute pancreatitis because of interstitial
edema. In some patients, echogenicity is normal.
• In rare cases, echogenicity may increase, possibly because of hemorrhage, necrosis, or fat saponification.
• Enlargement of the pancreas is almost universal in acute pancreatitis.
• when there is fatty infiltration of the liver, the normal pancreas may appear hypoechoic, a pattern called
“pseudopancreatitis”

28. • Pancreatic heterogeneity is a subjective but common finding, present in more than
50% of patients.

29. • Focal hypoechoic regions
are noted in some patients.

30. • Other most common and most useful finding is pancreatitis-associated inflammation.
• Extra pancreatic inflammatory changes may be detected even when the pancreatic contour is normal and the
pancreas is not obviously enlarged.
• Pancreatic inflammation is typically hypoechoic or anechoic and conforms to a known retroperitoneal or
peritoneal space.
• Inflammation is most often seen ventral and adjacent to the pancreas in the prepancreatic retroperitoneum ,
the right and left anterior pararenal spaces, the perirenal spaces, and the transverse mesocolon.
• Areas of inflammation within the anterior pararenal space are often seen immediately adjacent to the
echogenic fat within the perirenal space.
• Acute pancreatic inflammation within the anterior pararenal space occasionally outlines Gerota fascia.
• An inflammatory mass (formerly called a phlegmon), may be present.
• The transverse mesocolon region can be seen well in most patients on longitudinal scans. Inflammation can
extend caudal to the pancreas and behind the stomach and may reach the transverse colon.

34. Sonological features of pancreatitis
• Spread of inflammation along perivascular spaces, especially the splenic vein and splenoportal confluence, is
characteristic of acute pancreatitis
• This perivascular inflammation may explain why some patients develop thrombosis of the portal veins.
• Occasionally, retroperitoneal findings similar to those seen in acute pancreatitis can be seen in patients with
ascites, perhaps because of a “leaky” peritoneum.
• In contrast to inflammation, fluid collections often have convex margins, are thicker and more localized, may
cause a mass effect, and sometimes have through transmission of sound

36. Complications of Acute pancreatitis
• Complications of acute pancreatitis can be classified as systemic complications (those
related to organ failure) and local complications.
Local complications :
• Acute fluid collections
• Pseudocysts
• Pancreatic abscess
• Necrosis
• Infected necrosis
• Hemorrhage
• Venous thrombosis
• Pseudoaneurysms

38. Pseudocyts
• Pancreatic pseudocysts are a well-known complication of acute
and chronic pancreatitis.
• Pseudocysts comprise 75% to 90% of all cystic lesions of the
pancreas. The “wall” of pancreatic pseudocysts consists of
fibrous and granulation tissue.
• Pseudocysts do not have an epithelial lining.
• Pseudocysts are more common in patients with chronic than
acute pancreatitis.

39. Chronic pancreatitis
• Chronic pancreatitis is characterized by intermittent pancreatic inflammation with progressive, irrevers- ible
damage to the gland.
• Chronic pancreatitis ultimately leads to permanent structural change and deficient endocrine and exocrine
function.
• Alcoholism is the predominant cause of chronic pancreatitis
• Other causes include pancreatic duct obstruction caused by strictures, hypertriglyceridemia, hypercalcemia,
autoimmune pancreatitis, tropical pancreatitis, and other genetic mutations
• The key histologic features are fibrosis, acinar atrophy, chronic inflammation, and distorted and blocked
ducts.
• Chronic pancreatitis ultimately leads to permanent structural change and deficient endocrine and exocrine
function.
• Some lasting morphologic changes include alterations in parenchymal texture, glandular atrophy, glandular
enlargement, focal masses, dilation and beading of the pancreatic duct (often with intraductal calcifications),
and pseudocysts.
• Chronic pancreatitis is characterized clinically by pain, malabsorption, and diabetes.

40. Sonological features of chronic pancreatitis
• The hallmark of chronic pancreatitis is ductal dilation and calcifications, which can be in the branch ducts ,
main duct or both.
• CT is superior to sonography in detecting calcifications and ductal dilation.
• Calcifications are often made much more conspicuous on ultrasound images by looking for the colour comet-
tail artifact, also known as the “twinkling artifact”.
• Areas of increased and decreased echogenicity are related to the effects of patchy fibrosis.

41. • Pseudocysts
• Pseudocysts are more common in patients with
chronic (20%- 40%) than with acute (5%-16%)
pancreatitis.
• Pseudocysts may present with various shapes,
contain necrotic debris , hemorrhage (≈5%), or
even have a completely solid pattern.
• Portal and Splenic Vein Thrombosis
• Thrombosis of the portal venous system can
occur in chronic pancreatitis because of
(1) intimal injury from recurrent acute inflammation,
(2) chronic fibrosis and inflammation, or
(3) compression by either a pseudocyst or an
enlarged pancreas.
Splenic vein thrombosis is relatively common in
patients with chronic pancreatitis.
Portal vein thrombosis occurs less frequently.

43. • Splenic vein thrombosis will often result in left-sided portal
hypertension.
• This can result in isolated gastric varices, which can cause life-
threatening gastrointestinal bleeding.
• The hepatopetal pathway to bypass the splenic vein clot includes
short gastric collaterals that lead to the gastric mural varices,
then flow toward the liver in the coronary vein.
• Gallbladder wall varices were present in 30% of patients with
portal vein thrombosis.

44. Masses associated with chronic pancreatitis
• Focal pancreatic masses occur in approximately 30% of patients who have chronic pancreatitis.
• The presence of calcification within a mass makes the diagnosis of chronic pancreatitis likely.
• In chronic pancreatitis calcifications are multiple and ductal.
• Hyperechoic masses, even without discrete calcifications, are usually related to chronic pancreatitis.

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