1 / 72

Role of CT in acute pancreatitis

Role of CT in acute pancreatitis. Dr. Ahmed Refaey. Consultant radiologist Riyadh Military Hospital. MBBCh , MS, FRCR . Normal CT anatomy of the upper abdomen. Anterior pararenal space. Pancreas is located in the anterior pararenal space Head adjacent to duodenum

galia
Télécharger la présentation

Role of CT in acute pancreatitis

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  1. Role of CT in acute pancreatitis Dr. Ahmed Refaey Consultant radiologist Riyadh Military Hospital MBBCh, MS, FRCR

  2. Normal CT anatomy of the upper abdomen

  3. Anterior pararenal space

  4. Pancreas is located in the anterior pararenal space Head adjacent to duodenum Tail extending toward spleen Splenic vein posterior to body and tail Normal Anatomy by CT

  5. Normal Morphology by CT • No capsule • AP dimensions • Head 2-2.5 cm • Body and tail 1-2 cm • Pancreatic duct • Maximal diameter 3 mm in adults (5 mm in elderly)

  6. Evaluation of Acute Pancreatitis • Contrast-enhanced CT is imaging modality of choice • Oral and IV contrast differentiate pancreatic tissue from adjacent blood vessels and duodenum

  7. There is no additional value of an early CT (within 72 hours) in patients with acute pancreatitis. • The diagnosis is usually made on clinical and laboratory findings. • An early CT may be misleading concerning the severity of the pancreatitis, since it can underestimate the presence and amount of necrosis.

  8. Etiology

  9. Pathophysiology • Activated pancreatic enzymes escaping the ductal system and auto digesting the pancreas and adjacent structures ( mainly amylase, lipase & trypsin ). • Lack of capsule facilitates spread

  10. Acute pancreatitis • Mild acute pancreatitis ----- 80 % * edematous ( interstitial ) * exudative • Severe acute pancreatitis ----20 %

  11. Mild acute pancreatitis - run a mild course without development of multiple organ failure - improvement within 3 days following conservative therapy with gradual decrease of elevated enzymes. - has a mortality rate of < 1%

  12. Severe acute pancreatitis “ necrotizing “ - run a serious clinical course with pancreatic necrosis and the development of multiple organ failure - of these, 60% of pancreatic necrosis remain sterile , while 40% becomes infected - this last category ( infected necrosis ) , has the highest mortality rate ( 25-70%)

  13. Clinical outcome

  14. CT Imaging of acute pancreatitis

  15. Mild acute pancreatitis • Acute edematous “interstitial” pancreatitis • Acute exudative pancreatitis

  16. Acute edematous “interstitial” pancreatitis • Edematous pancreas with/without peripancreatic fat stranding. • No collections or necrosis

  17. Acute exudative pancreatitis • an intermediate form of pancreatitis without pancreatic necrosis with an intermediate clinical course. • This is called extrapancreatic necrosis (EXPN)

  18. Avoid early drainage of collections and avoid introducing infection! • 50% of these collections show spontaneous regression The other 50% either remain stable ( pseudocyt ) or develop infection ( abscess ) .

  19. Peripancreatic fluid 50% spontaneous regression 50% stable sterile ( pseudocyst) infection ( asbscess )

  20. Spontaneous regression of peripancreatic collection

  21. Severe pancreatitis “ necrotizing pancreatitis” occurs in 20% of patients. * partial necrotizing pancreatitis * total necrotizing pancreatitis

  22. Partial necrotizing Total necrotizing • Delayed or no response to conservative therapy • Delayed or no normalization of enzymes • Mortality : 30 – 75 % • Deterioration under conservative therapy • Mortality : 100 % - 40% by 2nd day - 75% by 5th day - 100% by 10th day

  23. Central gland necrosis

  24. Central gland necrosis • Subtype of necrotizing pancreatitis. • Necrosis between the pancreatic head and tail and is nearly always associated with disruption of the pancreatic duct. • This leads to persistent collections as the viable pancreatic tail continues to secrete pancreatic juices. • These collections react poorly to endoscopic or percutaneousdrainage. • Definitive treatment often requires distal pancreatectomy.

  25. An early CT may be misleading concerning the severity of the pancreatitis, since it can underestimate the presence and amount of necrosis.

  26. Mortality • Early mortality in acute pancreatitis is the result of the systemic inflammatory response with multiple organ failure.Late mortality is the result of infection of pancreatic necrosis and peripancreatic fluid collections which results in sepsis and is seen in more than 50% of deaths.

  27. CT Severity Index • It is critical to identify patients who are at high risk for severe disease, since they require close monitoring and possible intervention

  28. Balthazar et al constructed a CT severity index (CTSI) for acute pancreatitis that combines the grade of pancreatitis (A-E) with the extent of pancreatic necrosis.

  29. CT Severity Index • 1- 3 …………….. Mild • 4-6 …………….. Moderate • 7-10 ……………. Severe

More Related