PARAPANCREATITIS WITHOUT CT-SIGNS OF PANCREATIC NECROSIS IN PATIENTS WITH ACUTE PANCREATITIS

Aim. To study the nature of peripancreatic lesions and its course in patients with AP without CT-signs of pancreatic necrosis.

Material and Methods. We had analyzed the treatment of 38 patients with AP in whom contrast-enhanced CT did not reveal disorders of contrast accumulation by pancreatic tissue. Peripancreatic changes were assessed by presence of inhomogeneous acute necrotic collections and homogeneous acute peripancreatic fluid collections. Balthazar (2002) and K. Ishikawa et al. (2006) classification was used to estimate prevalence of parapancreatitis.

Results. Acute necrotic collections were revealed in 15 patients. Balthazar index was 3.7 ± 0.1, K. Ishikawa index — 2.46 ± 0.45 on the left side and 0.86 ± 0.4 on the right side (p < 0.01). 7 (47%) patients were treated conservatively.

8 (53%) patients were exposed to interventions including percutaneous punctures alone in 3 cases and 5 patients underwent surgery after puncture. The indication for surgery (in 21—34 days) was the increase of collections' volume and signs of infection. 1 patient died. Patients after conservative treatment had less severe parapancreatitis (2.0 ± 0.8) compared with patients who underwent puncture and surgery (3.7 ± 1.5, p < 0.5) according to gradation of Japanese authors. There were no such differences in Balthazar index (3.4 ± 0.5 and 3.9 ± 0.4, p > 0.05). Patients were discharged after 34 ± 5 days. Acute peripancreatic fluid collections were in 23 patients. Balthazar index was 2.5 ± 0.2, the gradation by Japanese classification — 1.3 ± 0.2 on the left side and 0.8 ± 0.2 on the right side. Conservative treatment was applied in 22 (96%) patients, 1 patient was exposed to percutaneous puncture. All patients were discharged after 16 ± 1 day.

Conclusion. Our data evidence the importance to identify acute necrotic collections in the absence of pancreatic necrosis as a marker of peripancreatic necrosis. 33% of these patients required surgery due to infection. Classification of parapancreatitis by Kazuo Ishikawa reflects parapancreatitis development and its localization more precisely than Balthazar index.

1. Thoeni R.F. The revised Atlanta Classification of acute pancreatitis: its importance for the radiologist and its effect on treatment. Radiology. 2013; 262 (3): 751-764. doi: 10.1148/radiol.11110947.

2. Balthazar E.J., Robinson D.L., Megibow A.J., Ranson J.H. Acute pancreatitis: value of CT in establishing prognosis. Radiology. 1990; 174 (2): 331-336.

3. Ishikawa K., Idoguchi K., Tanaka H., Tohma Y., Ukai I., Watanabe H., Matsuoka T., Yokota J., Sugimoto T. Classification of acute pancreatitis based on retroperitoneal extension: Application of the concept of interfascial planes. Eur. J. Radiol. 2006; 60 (3): 445-452.

4. Banks P.A., Bollen T.L., Dervenis C., Gooszen H.G., Johnson C.D., Sarr M.G., Tsiotos G.G., Vege S.S. Classification of acute pancreatitis - 2012: revision of the Atlanta classification and definitions by international consensus. Gut. 2013; 62 (1): 102-111. doi: 10.1136/gutjnl-2012-302779.

5. Bradley E.L. A clinically based classification system for acute pancreatitis: summary of the International Symposium on Acute Pancreatitis, Atlanta, Ga, September 11 through 13, 1992. Arch. Surg. 1993; 128 (5): 586-590.

6. O'Connor O.J., McWilliams S., Maher M.M. Imaging of acute pancreatitis. AJR. 2011; 197 (2): W221-W225. doi: 10.2214/AJR.10.4338.

7. Balthazar E.J. Acute pancreatitis: assessment of severity with clinical and CT evaluation. Radiology. 2002; 223 (3): 603-613.

8. Bruennler T., Hamer O.W., Lang S., Gruene S., Wrede C.E., Zorger N., Herold T., Siebig S., Rockmann F., Salzberger B., Feuerbach S., Schoelmerich J., Langgartner J. Outcome in a large unselected series of patients with acute pancreatitis. Hepatogastroenterology. 2009; 56 (91-92): 871-876.