Acute pancreatitis radiological approach

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

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  • 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
  • initial
  • Acute pancreatitis radiological approach

    1. 1. Speaker Dr.Krishna SandeepModerator Dr.Kalyan ,Asst Professor
    2. 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. 3.  8 weeks of gestation: Right ventral portion rotates dorsally & fuses with the dorsal outpouching to form the pancreas
    4. 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. 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. 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. 7. Anatomy Located in the anterior pararenal space of the retroperitoneum except the tail (lies in spleno renal lig)
    8. 8. Relationship to surroundingstructures:
    9. 9. 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
    10. 10. 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
    11. 11. Relations - Neck Part of the pancreatic body ventral to the SMA- SMV and portosplenic confluence
    12. 12. Relations - Body Splenic vein (SV), its confluence with the superior mesenteric vein (SMV) superior mesentericartery (SMA)
    13. 13. Relations - Tail Is related to the splenic vien at the hilum
    14. 14. 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
    15. 15. Ductal anatomy
    16. 16.  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.
    17. 17.  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
    18. 18. 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
    19. 19.  Annular pancreas : Baldwins 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 Meckels diverticulum.
    20. 20. Blood supply
    21. 21. Arterial supply Coeliac vessels Superior mesenteric .aHepatic.a Splenic.aGastro duodenal.aSuperior pancreatico-duodenal.a Inferior pancreatico-duodenal.a Anterior Posterior Anterior Posterior Splenic/Coeliac/Superior mesenteric.a Dorsal pancreatic.a Right Left (Transverse pancreatic.a)
    22. 22. Venous drainage Neck, Body & Tail Lymphatic drainage Splenic Vein ---------------- Head Preaortic coeliac nodesSuperior mesenteric & Portal veins
    23. 23. 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)
    24. 24. 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
    25. 25. 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
    26. 26. Clinical features Cullens sign Grey turners sign
    27. 27. 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
    28. 28. Peritoneal lavage Severe pancreatitis Aspiration > 10 -20mL Dark coloured lavaged fluid
    29. 29. Ranson criteria  11 objective signs  Five determined initially, six within 48 hours  < 3 Positive signs no mortality  6 or>6 Positive signs 50% mortality
    30. 30. Other scores Simplified AcutePhysiology  Acute Physiology and Chronic score Health Evaluation (APACHE II)  12 physiologic measurements  > 8 score severe pancreatitis
    31. 31. Imaging Radiograph Sonography Contrast-enhanced computed tomography (CECT)Others Magnetic resonance imaging (MRI) ERCP MRCP Endoscopic ultrasound
    32. 32.  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
    33. 33. Radiographic signs Abdomen Duodenal ileus Sentinel loop sign Colon cutoff sign Abdomenal fat necrosis sign Intra pancreatic gasIncreased gastrocolic separation Gasless abdomen Ascites
    34. 34. Radiographic signsChest Elevated diaphragm Pleural effusion: left sided. Left sided parenchymal changes
    35. 35. Barium studiesSpiculation of posterior wall of stomachEnlargement of duodenal sweep,thickenedirregular mucosal folds Poppel’s Papillary Sign Frostberg’s Sign
    36. 36. Acute pancreatitis Sonology
    37. 37. 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
    38. 38. 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
    39. 39. Pancreatic heterogeneityFocal hypoechoic regions
    40. 40. Enlargement of the pancreas Universal >22 mm (mean plus 3 standard deviations)
    41. 41. 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
    42. 42. acute fluid collections.  Non encapsulated homogenous hypo echoic collections in the pancreas /retroperitoneum /abdomen  Develop in 40% of AP half resolve spontaneouslyDisplaced stomach Lesser sac fluid collection
    43. 43.  Diffrentiation from inflamation convex margins thicker and more localized cause a mass effect through-transmission of sound
    44. 44. 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
    45. 45. Simple pseudocyst following traumaHemorrhagic pseudocystPseudocyst causing CBD obstructionPseudocyst with irregular margins &debris
    46. 46.  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
    47. 47.  Should be differentiated from cystic neoplasms In light of clinical history or imaging evidence of acute or chronic pancreatitis.
    48. 48. Necrosis Necrosis cannot be definitively diagnosed by ultrasound CECT is the modality of choice
    49. 49. Suppuration The Atlanta ClassificationTwo 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
    50. 50. 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”
    51. 51. Pseudo -aneurysm  Encapsulations of arterial haemorrhage which are in communication with the eroded vesselpseudoaneurysm of the gastroduodenal .a.Swirling flow in the center (yin-yang sign)surrounded by a hypoechoic rim of athrombus is clearly shown(arrowhead).
    52. 52. venous thrombosis Splenic vein thrombosis
    53. 53.  Portal vein thrombosis
    54. 54. 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
    55. 55. Short gastric collaterals Gastric mural varices
    56. 56. 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
    57. 57. CT evaluation
    58. 58. 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
    59. 59.  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
    60. 60. 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
    61. 61. Mild pancreatitis
    62. 62. 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
    63. 63. Severe pancreatitis
    64. 64. 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
    65. 65. Complications Fluid collections Pseudocyst Necrosis(liquefactive necrosis) Abcess Phlegmon Haemorrhage Thrombosis Pseudo-aneurysms Pancreatic ascites
    66. 66. Diffuse enlargement with decreased attenuation
    67. 67. Fatstranding and thickening of fascia
    68. 68. Fluid collections Non encapsulated illdefined homogenous collections of fluid attenuation in the pancreas/retroperitoneum/ abdomen
    69. 69. Fluid collections
    70. 70. Fluid collections
    71. 71. 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
    72. 72. Pseudocysts Well defined round/oval collections with fluid attenuation with well defined fibrous capsule persisting greater than 6 weeks which shows contrast enhancement
    73. 73. Pseudocysts Should be differentiated from Fluid collections Necrosis Pseudo aneurysm Fluid filled Stomach /duodenum
    74. 74. 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
    75. 75. Necrosis
    76. 76. Suppurative pancreatitis Two types 1.Pancreatic abcess 2.Infected necrosis/Emphysematous pancreatitis
    77. 77. Pancreatic abcess Infected fluid collection/pseudocyst, which has minimal necrosis. Focal, low-attenuation collection with thick wall that often contains gas bubbles
    78. 78. 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
    79. 79. How to differentiate ? Low-attenuation zone Needle aspiration is crucial Liquid pus Liquefied infected tissueFalse-positive result Contamination by intestinal material when it passes through it
    80. 80. Why to differentiate ? For intervention Abscesses -Percutaneous catheter drainage Infected necrosis surgical necrosectomy & debridement
    81. 81. 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.
    82. 82. Treatment of choice Emergency angiography & selective embolization.
    83. 83. Pseudo-aneurysms Pseudoaneurysm preceeds hemorrhage Encapsulations of arterial haemorrhage which communication with the eroded vessel Swriling and to and fro pattern is seen
    84. 84.  Balthazar A  Balthazar B
    85. 85.  Balthazar C  Balthazar D
    86. 86. Balthazar E
    87. 87. Modified CT severity index stronger prognostic correlation
    88. 88.  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
    89. 89. 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
    90. 90.  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
    91. 91.  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
    92. 92. 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
    93. 93. Neck Anterior  Pylorus  Omental bursa Posterior  SMV  Beginning of portal vein
    94. 94. 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
    95. 95. Tail The tail of the pancreas lies in the splenorenal ligament and enters the hilum of the spleen with splenic vessels.
    96. 96. 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
    97. 97. 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).
    98. 98. Diffuse enlargement with decreased attenuation

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