The document discusses the embryology, anatomy, clinical features, investigations and imaging findings of acute pancreatitis. Regarding embryology, it describes how the pancreas develops from dorsal and ventral buds that fuse. For anatomy, it outlines the relationships of different parts of the pancreas. It also summarizes the etiology, pathophysiology and scoring systems used to classify severity of acute pancreatitis. Imaging findings on ultrasound, CT and MRI are summarized to diagnose and characterize acute pancreatitis and its complications.
2. Embryology
4th week embryologic
growth, ventral & dorsal
outpouchings develop at
the junction of the
foregut and midgut.
Ventral bud is divided
into left and right
portions:
the left ventral portion
generally atrophies
3. 8 weeks of gestation:
Right ventral portion
rotates dorsally & fuses
with the dorsal
outpouching to form the
pancreas
4. The dorsal bud develops
into the pancreatic body,
tail, and superior portion of
the pancreatic head
ventral bud develops into
the inferior portion of the
pancreatic head and
uncinate process of the
pancreas.
5. 7th gestational week, the dorsal and ventral
pancreatic ducts fuse in the region of the neck.
Dorsal pancreatic ductal system drains the tail, body,
and anterior portion of the pancreatic head.
Ventral component drains the posterior aspect of the
pancreatic head.
6. The portion of the ventral duct between the dorsal-
ventral fusion point and the major papilla is termed
the duct of Wirsung.
The portion of the dorsal duct proximal to the dorsal-
ventral fusion point is called the main pancreatic duct
(MPD).
If a segment of the dorsal duct persists distal to the
dorsal-ventral fusion point, it is termed the duct of
Santorini, or accessory duct.
7.
8. Anatomy
Located in the anterior pararenal space of the
retroperitoneum except the tail (lies in spleno renal lig)
12. Relations - Head
Dorsally- inferior vena cava (IVC)
Medially - SMA and SMV
Anterolaterally - gastroduodenal
artery (GDA) and
pancreaticoduodenal arcade
Epiploic foramen (foramen of
Winslow) entrance into the lesser
peritoneal sac located Cephalic to
the pancreas adjacent to IVC and PV
13. Relations - Uncinate process
The uncinate process
wraps around behind the
SMA and SMV
The uncinate process is
medial and dorsal to the
SMA and SMV
14. Relations - Neck
Part of the pancreatic
body ventral to the SMA-
SMV and portosplenic
confluence
15. Relations - Body
Splenic vein (SV), its
confluence with the
superior mesenteric vein
(SMV)
superior
mesentericartery (SMA)
17. Normal size and echo texture
Head -6 to 28 mm(17.7 +/- The parenchyma is usually
4.2 mm) isoechoic or hyperechoic
Body - 4 to 23 mm (10.1 +/- compared with hepatic
3.8 mm) parenchyma
Tail - 5 to 28 mm (16.4 +/- pancreatic echogenicity
4.2 mm). increases with age
Size dec with age
19. The duct of Wirsung unites with the CBD and drains
into the major papilla.
The duct of Santorini, or accessory duct, drains the
anterior and superior portion of the head into the
minor papilla.
The distal CBD and duct of Wirsung traverse the
sphincter of Oddi (which consists of three separate
smooth muscles) to enter the duodenum.
20. In most cases (80%–90%),
the CBD and duct of
Wirsung unite within this
sphincteric segment, with
the muscular wrap being
10–15 mm in length.
This common channel may
be long (Y-type
configuration) or short (V
type).
Sphinter of oddi – three
sphinters
21. Anamolies of pancreas and ducts
Ectopic atrophic accessory duct
Pancreas/accessory persists as tiny accessory
nodules duct in 60%;
Annular pancreas accessory (upper)
Pancreas divisum duct atrophies completely
Agenesis of the dorsal - no connection with
pancreatic moiety duodenum (20%);
major and minor ducts
open separately and do not
communicate (10%);
both ducts persist,
communicate and open
separately
22. Annular pancreas : Baldwin's theory -persistence of
the left ventral bud,which normally atrophies
Pancreas divisum :failure of fusion of the dorsal and
ventral moieties
Accessory nodules (pancreatic rests) may occur in the
wall of the stomach, the duodenum, the small
intestine or within a Meckel's diverticulum.
25. Arterial supply
Coeliac vessels Superior mesenteric .a
Hepatic.a Splenic.a
Gastro duodenal.a
Superior pancreatico-duodenal.a Inferior pancreatico-duodenal.a
Anterior Posterior Anterior Posterior
Splenic/Coeliac/Superior mesenteric.a
Dorsal pancreatic.a
Right Left (Transverse pancreatic.a)
26. Venous drainage
Neck, Body & Tail
Lymphatic drainage
Splenic Vein
----------------
Head Preaortic coeliac nodes
Superior mesenteric
&
Portal veins
27. ACUTE PANCREATITIS
An acute inflammatory process of the pancreas with variable
involvement of other regional tissues or remote organ systems
Severity
Mild acute pancreatitis
Minimal organ dysfunction
lacks the features of severe acute pancreatitis.
Usually normal enhancement of pancreatic parenchyma on CECT
uneventful recovery
Severe acute pancreatitis
local complications such as necrosis, abscess or pseudocyst
organ failure
Mortality
(ref: The Atlanta Classification of acute pancreatitis revisited)
36. Ultrasound - First line invstigation
To detect gallstones and bile duct obstruction
CECT - Investigation of choice
To diagnose pancreatic necrosis.
MRI
Best to differentiate fluid from solid lesions
Magnetic resonance cholangiopancreatography
accurate means of detecting stones in the gallbladder and bile ducts.
Endoscopic ultrasound
more sensitive than TAS for the detection of common bile duct stones
41. Scanning techniques
Compression scanning
Left lateral decubitus position -Head of the
pancreas and the distal (ampullary) pancreatic and
bile ducts
Right lateral decubitus position -pancreatic tail
through the spleen and left kidney
Right anterior oblique position -through the water
filled stomach for tail
Scanning during a Valsalva maneuver
oral water or contrast administration
Color Doppler sonography for the tail related to
splenic artery and vein
42.
43. Ultrasonogram-features
Echogenicity
Typically decreases due to interstitial edema.
Rarely, echogenicity may increase
Hemorrhage or fat saponification
Pseudopancreatitis
Normal pancreas may appear hypoechoic due to fatty
infiltration of the liver
46. Enlargement of the pancreas
Universal
>22 mm (mean plus 3
standard deviations)
47. Inflamation
Pancreatic inflammation is
typically hypoechoic
Extrapancreatic inflammation -
ventral and adjacent to pancreas
Prepancreatic retroperitoneum
Rt & lt anterior pararenal spaces
Perirenal spaces
Transverse mesocolon
Diffrentiation from fluid collections
48.
49. acute fluid collections.
Non encapsulated homogenous hypo echoic collections
in the pancreas /retroperitoneum /abdomen
Develop in 40% of AP half resolve spontaneously
Displaced stomach
Lesser sac fluid
collection
50. Diffrentiation from inflamation
convex margins
thicker and more localized
cause a mass effect
through-transmission of sound
51. Pseudocyst
Well defined round/oval collections with hypo
echogenicity with well defined fibrous capsule
persisting greater than 6 weeks
Purely cystic or with mural irregularity ,septations
,internal echoes - debris from necrosis, hemorrhage or
infection
52. Simple pseudocyst following trauma
Hemorrhagic pseudocyst
Pseudocyst causing CBD obstruction
Pseudocyst with irregular margins &
debris
53. Conservative management
Indications for drainage of a pseudocyst
abdominal pain - growth /hemorrhage
biliary obstruction
gastrointestinal obstruction (usually duodenal)
Internal or external fistula formation - pancreatic ascites
or pleural effusion
54. Should be differentiated from cystic neoplasms
In light of clinical history or imaging evidence of acute
or chronic pancreatitis.
55. Necrosis
Necrosis cannot be definitively diagnosed by
ultrasound
CECT is the modality of choice
56. Suppuration
The Atlanta Classification
Two types -
1.Pancreatic abscess, an infected fluid
collection/pseudocyst, which has minimal necrosis.
2.Infected necrosis with a fluid collection due to
infection of necrotic pancreatic tissue
57. Vascular Complications
Haemorrhage
Clinically insignificant hemorrhage
- related to venous &small vessel
disease
Potentially fatal hemorrhage
- related to major vessels
splenic& gastroduodenal arteries.
Vascular erosion
sudden pain expansion of the cyst
gastrointestinal (GI) bleeding-bleeding into the pancreatic
duct-“Hemosuccus pancreaticus”
58.
59. Pseudo -aneurysm
Encapsulations of arterial haemorrhage which are in
communication with the eroded vessel
pseudoaneurysm of the gastroduodenal .a.
Swirling flow in the center (yin-yang sign)
surrounded by a hypoechoic rim of a
thrombus is clearly shown
(arrowhead).
62. Secondary changes due to thrombosis
Splenic vein thrombosis
Left sided (“sinistral”) portal hypertension
Hepatopetal pathway to bypass
the splenic vein clot includes
Short gastric collaterals
gastric mural varices
coronaryVein
then flow toward the liver
Isolated gastric varices - GI
bleeding
64. Secondary changes due to thrombosis
Portal vein Thrombosis
Main portal vein is clotted,
blood flows to the liver
around the clot.
Cavernous transformation
of the portal vein
Gallbladder wall varices
66. CT Evaluation
Water is the preffered oral contrast media but it
obscures the small stones at ampullary region
Iv contrast is used
Three phases
arterial phase 20 s delay
Pancreatic parenchymal phase 40s delay(optimum for
pancreatic study)
Portal venous phase 65 s delay
67. Normal pancreas enhances uniformly
Pancreatic duct is seen as linear non enhancing
structure
Pit fall normal fat plane between the splenic vein and
the posterior surface of the gland should not be
mistaken for duct
68.
69. Mild pancreatitis
Interstitial / Edematous pancreatitis
Pathology –interstitial inflamation & edema with
microscopic necrosis-
-low attenuation &enlarged pancreatic gland
intact capillary network with vasodilation
- uniform enhancement of the pancreatic gland
71. Severe pancreatitis
Necrotising /Suppurative /Hemorrhagic pancreatitis
Pathology – severe inflamation,acinar necrosis &
necrosis of vessel wall
Low attenuation ,Non enhancing areas indicate
decreased blood flow and relate to pancreatic zones of
ischemia or necrosis
73. Acute pancreatitis
Pancreatic changes- (due to inflamation)
diffuse enlargement of gland
decrease in density
blurring of margins
Peripancreatic changes –
fat stranding (mucky fat)
blurring of fatplanes
thickening of involved fascia
80. Fluid collections
Resolve spontaneously /develop into pseudocysts
Should be differentiated from pseudocyst
lack capsule
confined to the anatomical space –lesser sac/ant para
renal space
time of appearance
81. Pseudocysts
Well defined round/oval collections with fluid
attenuation with well defined fibrous capsule
persisting greater than 6 weeks which shows contrast
enhancement
82. Pseudocysts
Should be differentiated from
Fluid collections
Necrosis
Pseudo aneurysm
Fluid filled Stomach /duodenum
83.
84. Necrosis /Necrotising pancreatitis
Focal /diffuse areas of nonenhancement on CECT
Considered significant on CECT
More than 30% of the gland is affected
or
An area larger than 3 cm is present
Appears with in first 24 to 48 hours
So CT should be performed after 2-3 days
Initial CT with in 12 hrs only show equivocal findings
87. Pancreatic abcess
Infected fluid collection/pseudocyst, which has
minimal necrosis.
Focal, low-attenuation collection with thick wall that
often contains gas bubbles
88. Infected necrosis
Emphysematous pancreatitis
Infected necrosis with a fluid collection, which arises
from infection of necrotic pancreatic tissue
Heterogenous low attenuation areas with gas bubbles
89. How to differentiate ?
Low-attenuation zone
Needle aspiration is crucial
Liquid pus Liquefied infected tissue
False-positive result
Contamination by intestinal material when it passes
through it
90. Why to differentiate ?
For intervention
Abscesses -Percutaneous catheter drainage
Infected necrosis surgical necrosectomy &
debridement
91. Hemorrhage
Leakage from Infected granulation tissue
Enzymatic digestion of blood vessels
Splenic arteries
Gastro duodenal arteries
High-attenuation fluid (blood) within the
peritoneal cavity
retroperitoneum
preexisting fluid collection
pseudocyst.
93. Pseudo-aneurysms
Pseudoaneurysm preceeds
hemorrhage
Encapsulations of arterial
haemorrhage which
communication with the
eroded vessel
Swriling and to and fro pattern
is seen
101. CT
overall accuracy of 87%
sensitivity of 100% for the extended necrotic areas
sensitivity of 50% for minor necrotic areas
specificity of 100% -no false-positives
102. Pit falls in CT
Enhancement values of the pancreas with a bolus of contrast material
can be substantially decreasedin Healthy patients with fatty
infiltrationof the pancreas Patients with interstitial pancreatitis,due
to parenchymal edema
Slight variation in the enhancementvalues of the head, body, andtail of
the pancreas (usually 30 HU) is sometimes seen in healthy individuals.
Pancreatic necrosis should not be diagnosedin these cases unless a
localized or diffuse change in the texture of the gland is recognized
103.
104. Pancreatic necrosis develops early, within the first 24–48
hours after the onset of clinical symptoms
CT performed during the initial 12 hours may show only
equivocal findings, with a slight heterogeneous decrease in
attenuation of the pancreas (ischemia) but a normal
parenchymal texture
2–3 days after the initial onset pancreatic necrosis develops,
zones of tissue liquefaction become better defined and
more easily recognized
Thus CT scans obtained 3 days after clinical onset yield
higher accuracy in the depiction of necrotizing pancreatitis
105.
106. CT cannot be used to help reliably diagnose
retroperitoneal fat necrosis.
In clinical practice all heterogeneous peripancreatic
collections should be considered areas of fat necrosis
untilproven otherwise
107.
108. HEAD
Posterior
SMV
Splenic vein
IVC
Terminal portion of renal vein
Right crus of diaphragm
Anterior
Transverse colon
Uncinate process passes in
front of aorta
Lateral
Bile duct
109. Neck
Anterior
Pylorus
Omental bursa
Posterior
SMV
Beginning of portal vein
110. Body
Anterior
Stomach separated by
omental bursa
Posterior
Aorta
SMA
Left crus of diaphragm
Left adrenal
Left kidney
Left renal vein
Splenic vein
Inferior
Transverse mesocolon
Duodeno-jejunal junction
Left colic flexure
Superior border
Splenic artery
111. Tail
The tail of the
pancreas lies in the
splenorenal ligament
and enters the hilum
of the spleen with
splenic vessels.
112. Scanning techniques
Compression scanning
left lateral decubitus position view the
rightmost portion of the pancreas and the
distal (ampullary) pancreatic and bile
ductsmay also be useful, especially to see the
left part of the body and more central tail.
Position the transducer to the right of the
midline and angle “down the barrel”
(longitudinal axis) of the pancreatic body and
tail
Scanning during a Valsalva maneuver
oral water or contrast administration
Right anterior oblique position and scan
through the waterfilledstomach for tail
pancreatic tail is coronal imaging through the
spleen and left kidney, with the patient in a
right lateral decubitus position
Color Doppler sonography can reveal the
splenic artery and vein, facilitating
identification of the tail
113. Relations
Vascular landmarks for the
pancreatic
head are the inferior vena cava
(IVC) dorsally,
the SMA and (SMV medially,
and the gastroduodenal
artery (GDA) and the
pancreaticoduodenal arcade
anterolaterally
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).
Mild includes –edematous and interstitial pancreatitisSevere includes-necrotising,haemorrhagic,suppurative pancreatitis
premature activation of pancreatic enzymes leading to autodigestion of the pancreatic parenchyma and peripancreatic tissuesextensive interstitial fat necrosis, necrotizing vasculitis with occlusions and thrombosis of small feeding arteries and draining veins, areas of hemorrhage, and devitalized pancreatic parenchymaCytokines interleukin (IL)-1, tumor necrosis factor (TNF), and plateletactivating factor organ dysfunction
increased amylase: sensitive but not specificincreased lipase: > sensitivity and specificity – and stays elevated longer
pancreatic enzymes amylase and lipase, while useful diagnostic indicators, have no role in the assessment of disease severityurinary trypsinogen activated peptide levels has recently been shown to be promising in identifying patients with severe pancreatitiscorrelates directly with premature activation of trypsinogenmethemalbumin hemorrhagic pancreatitis pancreatic ribonuclease necrotic tissue.IL-6 and phospholipase A2 Concentrations and the clinical severity of pancreatitis
The presence, volume, and color of aspirated intraperitoneal fluid has beenused as an indicator of the severity of anattack of acute pancreatitis
Glasgow original or modified system
Necrosis appears as nonenhancement of the pancreas considered significant,when more than 30% of the gland is affected,on CECT or an area larger than 3 cm is present
increased gastrocolic separation in the left upper quadrant (region marked by stars). This separation between the stomach and the transverse colon is consistent with a fluid collection in the lesser sacCOLON CUT OFF SIGN: is paucity of gas distal to the splenic flexure caused by functional colonic spasm secondary to spread of the pancreatic inflammation into the phrenocolic ligament.SENTINAL LOOP: A mildly dilated ,gas-filled segment of small bowel with or with out air fluid levels is seen.ABDOMINAL FAT NECROSIS SIGN: presence of innumerable mottled radiolucencies and ill defined densities scattered over large areas of upper abdomenGas-less abdomen: multiple loops of fluid-filled bowel
Spiculated appearance of posterior wall of stomachEnlargement of duodenal sweep, atony, thickened irregular spiculated mucosal folds.Poppel’s Papillary Sign-enlargement of papilla of vaterFrostberg’s Sign- Inverted configuration of duodenal loopInduration of root of mesentery may compress 3rd duodenal segment leading onto proximal dilatation.
Compression scanningLeft lateral decubitus position view the rightmost portion of the pancreas and the distal (ampullary) pancreatic and bile ducts may also be useful, especially to see the left part of the body and more central tail.Right anterior oblique position and scan through the waterfilledstomach for tail Right lateral decubitus position coronal imaging of pancreatic tail through the spleen and left kidneyScanning during a Valsalva maneuveroral water or contrast administrationColor Doppler sonographycan reveal the splenic artery and vein, facilitating identification of the tailPosition the transducer to the right of the midline and angle “down the barrel” (longitudinal axis) of the pancreatic body and tail
Extrapancreatic inflammatory changes most often seen ventral and adjacent to the pancreas in the prepancreaticretroperitoneum, right and left anterior pararenal spaces, the perirenal spaces, and the transverse mesocolon
Pancreatic abscess” is reserved for infected fluid collections, essentially pseudocysts that become infected.
Splenic vein thrombosis is most common than portal vein thrombosis,Clot at the splenicvien not extending to the confluence
Diagnosis of splenic vein clot may depend on detection of collaterals, such as short gastric varices or an enlarged coronary vein
Cavernous transformation of the portal vein -If the portal veinclot persists, these hepatopetal collaterals may enlargeGallbladder wall varices were present in 30% of patients with portal vein thrombosis
Fluid collections –non encapsulated homogenous collections of fluid attenuation in the pancreas/retroperitoneum/abdomenPseudocyst-well defined round/oval collections with fluid attenuation with well defined fibrous capsule persisting greater than 6 weeksNecrosis- (liquefactive necrosis) areas with lack of contrast enhancement on bolus contrast Necrosis appears as nonenhancement of the pancreas considered significant,when more than 30% of the gland is affected,on CECT or an area larger than 3 cm is presentAbcess- loculated fluid collections may contain gasPhlegmon –mass of edema&inflamation –illdefinedheterogenous soft tissue and fluid densitiesHaemorrhage – high attenuation in retroperitoneum /peritoneumThrombosis –the vessels are distended &fail to enhance on venous phase scansPseudo-aneurysms-encapsulations of arterial haemorrhage which are in communication with the eroded vessel-swriling and to and fro pattern is seenPancreatic ascites-due to leakage
Necrosis by low attenuation with out surrounding enhancing capsule and acute condition