in this pppt there is imaging approach and diagnosis of acute pancreatitis

1. Speaker Dr.Krishna Sandeep
Moderator Dr.Kalyan ,Asst Professor

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.

8. Anatomy
 Located in the anterior pararenal space of the
retroperitoneum except the tail (lies in spleno renal lig)

10. Relationship to surrounding
structures:

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)

16. Relations - Tail
 Is related to the splenic
vien at the hilum

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

18. Ductal anatomy

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.

24. Blood supply

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)

28. Etiology
 Gallstones 40%
 Alcoholism 40%
 Idiopathic 10%
 Other 10%
- Congenital:Annular pancreas
Pancreas divisium
- Infections : Viral :Mumps,CMV,Glandular fever
Parasitic:ascariasis,clonorchis
- Inflamations:SLE,Polyarteritis
- Traumatic:Injury,Surgery,ERCP
- Malignancy:Pancreatic adenocarcinoma
Lymphoma
- Metabolic &Endocrine:Hyperlipidemia
Hypercalcemia
Hyperparathyroidism
Heriditary pancreatitis -AD
- Drugs:Steriods,azathioprine,Thiazides

29. Pancreatic Injury: Pathophysiology
Premature activation of pancreatic enzymes
Interstitial fat necrosis necrotizing vasculitis &thrombosis
autodigestion &devitalisation
pancreatic parenchyma & peripancreatic tissues
Cytokines
Interleukin (IL)-1
Tumor necrosis factor (TNF)
Plateletactivating factor
Organ dysfunction

30. Clinical features
Cullens sign Grey turners sign

31. Biochemical markers
 Pancreatic enzymes
amylase(sensitive but not specific),
lipase(> sensitivity and specificity)
not useful in assessment of disease severity
 Urinary trypsinogen activated peptide
 Methemalbumin - hemorrhagic pancreatitis
 Pancreatic ribonuclease - necrotic tissue.
 IL-6 and phospholipase A2 Concentrations

32. Peritoneal lavage
 Severe pancreatitis
Aspiration
> 10 -20mL
Dark coloured lavaged fluid

33. Ranson criteria
 11 objective signs
 Five determined initially, six
within 48 hours
 < 3 Positive signs
no mortality
 6 or>6 Positive signs
50% mortality

34. Other scores
 Simplified AcutePhysiology  Acute Physiology and Chronic
score Health Evaluation (APACHE II)
 12 physiologic measurements
 > 8 score
severe pancreatitis

35. Imaging
 Radiograph
 Sonography
 Contrast-enhanced computed tomography (CECT)
Others
 Magnetic resonance imaging (MRI)
 ERCP
 MRCP
 Endoscopic ultrasound

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

37. Radiographic signs
Abdomen
 Duodenal ileus
 Sentinel loop sign
 Colon cutoff sign
 Abdomenal fat necrosis
sign
 Intra pancreatic gas
Increased gastrocolic
separation
 Gasless abdomen
 Ascites

38. Radiographic signs
Chest
 Elevated diaphragm
 Pleural effusion: left
sided.
 Left sided
parenchymal changes

39. Barium studies
Spiculation of posterior wall of stomach
Enlargement of duodenal sweep,thickened
irregular mucosal folds
 Poppel’s Papillary Sign
 Frostberg’s Sign

40. Acute pancreatitis
Sonology

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

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

45. Pancreatic heterogeneity
Focal hypoechoic regions

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

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”

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).

60. venous thrombosis
 Splenic vein thrombosis

61.  Portal vein thrombosis

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

63. Short gastric collaterals Gastric mural varices

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

65. CT evaluation

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

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

70. Mild pancreatitis

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

72. Severe pancreatitis

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

74. Complications
 Fluid collections
 Pseudocyst
 Necrosis(liquefactive necrosis)
 Abcess
 Phlegmon
 Haemorrhage
 Thrombosis
 Pseudo-aneurysms
 Pancreatic ascites

75. Diffuse enlargement with decreased attenuation

76. Fatstranding and thickening of fascia

77. Fluid collections
 Non encapsulated illdefined homogenous collections
of fluid attenuation in the pancreas/retroperitoneum/
abdomen

78. Fluid collections

79. Fluid collections

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

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

85. Necrosis

86. Suppurative pancreatitis
 Two types
1.Pancreatic abcess
2.Infected necrosis/Emphysematous pancreatitis

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.

92. Treatment of choice
 Emergency angiography & selective embolization.

93. Pseudo-aneurysms
 Pseudoaneurysm preceeds
hemorrhage
 Encapsulations of arterial
haemorrhage which
communication with the
eroded vessel
 Swriling and to and fro pattern
is seen

95.  Balthazar A  Balthazar B

96.  Balthazar C  Balthazar D

97. Balthazar E

100. Modified CT severity index
stronger prognostic correlation

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

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

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

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).

114. Diffuse enlargement with decreased attenuation