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| Year : 2009 | Volume
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| Issue : 4 | Page : 573-574 |
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| Pancreatic abscess secondary to gall stones caused by Escherichia coli |
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VP Baradkar, M Mathur, S Kumar
Department of Microbiology, Lokmanya Tilak Municipal Medical College and General Hospital, Sion, Mumbai - 400 002, India
Click here for correspondence address and email
| Date of Web Publication | 1-Oct-2009 |
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How to cite this article:
Baradkar V P, Mathur M, Kumar S. Pancreatic abscess secondary to gall stones caused by Escherichia coli. Indian J Pathol Microbiol 2009;52:573-4 |
Pancreatic abscess is defined as an acute inflammatory process of the pancreas, with variable involvement of other regional tissues or remote organ system. [1] The causes of pancreatic abscess and acute pancreatitis include cholelithiaisis, ethanol abuse, trauma, metabolic causes such as hypercalcemia, diabetic ketoacidosis, uremia, hyperparathyroidism, autoimmune diseases and idiopathic causes. [1] Acute pancreatitis following pancreatic abscess is classified as either mild (85% cases) or severe (15% cases). [1],[2],[3],[4],[5] The organisms reported from cases of pancreatic abscesses include Escherichia More Details coli,Klebsiella species, Proteus species, Pseudomonas species, Enterobacter species, Candida species, Staphylococcus aureus, Enterococcus fecalis, Citrobacter species, Bacteroides species, Haemophilus influenzaeand Mycobacterium tuberculosis. [1],[2],[3],[4],[5] Specific treatment for acute pancreatitis currently does not exist and management is still supportive and varies from case to case.
Here we report a case of pancreatic abscess due to E. coli, secondary to bile stones, which was managed successfully with supportive therapy, antibiotics, endoscopic retrograde cholangiopancreatography (ERCP) and surgical drainage.
A 36-year-old male was admitted for evaluation with a one-month history of fever, abdominal discomfort, anorexia, nausea and vomiting. The patient was non-diabetic and there was no history of any major illness in the past. On examination the patient was febrile, with a pulse rate of 100/min, blood pressure of 130/80 mm/Hg. There was no pallor, icterus or cyanosis. The findings of the cardio-respiratory and nervous system examination were within normal limits. There was no abdominal distension or any obvious organomegaly but a mild tenderness was noted in the epigastric region. Total leukocyte counts was 9800/ mm 3 , with 78% polymorphs and 22% lymphocytes. The erythrocyte sedimentation rate was slightly raised at 20 mm at the end of one hour. The liver and renal function tests were within normal limits. The level of serum amylase was raised, at 297.76 IU/ L (normal upto 220 IU/L) and serum lipase was 797.07 U/L (normal value for adults < 190 IU/L).
Ultrasonography (USG) of the abdomen was performed which showed, partially distended gallbladder with multiple calculi. There was no evidence of pericholecystic fluid. The pancreas was partially obscured by bowel gas, but appeared bulky, showing hypoechoic parenchyma. No solid or cystic lesion was noted. The pancreatic duct was not dilated. Approximately 9.4 X 4.5 cm-sized hypoechoic collections were observed anterior to the pancreas. Grade 4 fatty degeneration was also observed. There was moderate ascites, left-sided basal consolidation was noted in the left lung along with mild left pleural effusion. USG liver showed diffuse Grade 1 increase in echotexture. No local solid or cystic lesion was seen. The intrahepatic part of the biliary radicals was not dilated. The portal veins were normal [Figure 1].
Plain and contrast-enhanced axial computerized tomographic (CT) scan of abdomen was performed which showed a loss of pancreatic architecture, with replacement of entire pancreatic tail, body and neck by 12 X 17.7 X 7.6 cm-sized , hypodense irregular cystic density. The lesion was thin walled and showed air specks extending into the lesser sac, causing a mass effect on the greater curvature of the stomach [Figure 2]. There was another similar pseudocyst within the acinar process of the pancreas with small ill-defined pseudocysts in the peripancreatic region inferior to the 'C' loop of the duodenum communicating with the large cyst. There was extensive peripancreatic free fluid and thickening of bilateral Gerota's fascia. A small spared part of the pancreatic head was noted to be bulky showing suboptimal contrast enhancement. The gallbladder was noted to be distended with multiple calculi. The spleen was normal in size and density. No focal lesions were seen. The adrenals, ureters and visualized bones were normal. The conclusion from the imaging was of acute pancreatitis with intra- and extra-pancreatic pseudocyst as described, the largest one completely replacing the neck, body and tail of the pancreas.
A CT scan-guided percutaneous aspiration biopsy was performed. The fluid was sent for cytology and culture. Cytology showed inflammatory cells without evidence of malignancy. Culture on Blood and MacConkey agar yielded colonies of E. coli which was sensitive to amikacin, amoxycillin + alavulanic acid, ciprofloxacin, cefotaxime. The patient was started on Cefotaxime which was continued for two weeks. ERCP and sphincterotomy was done and the bile calculi were removed. Percutaneous drainage was performed for two weeks. The patient meanwhile showed signs of recovery with complete remission of fever and subsidence of the epigastric pain. The patient was later discharged after two weeks on oral ciprofloxacin and was asked to follow up on outdoor patient basis. On the last follow-up, one month after admission the patient was doing well and there were no symptoms of any relapse during this period.
Cholelithiaisis-associated pancreatitis accounts for approximately 45% of cases of pancreatitis followed by ethanol abuse for 35%, other causes for up to 10% and in up to 10% no cause may be found (idiopathic). In the present case, multiple gallstones acted as the cause of pancreatitis and abscess formation. There was no other metabolic abnormality observed. The clinical presentation of pancreatitis varies from case to case, with epigastric pain, nausea and vomiting being the commonest symptoms as observed in the present case. Respiratory signs of pleural effusion and basal collapse are found in 10-20% of patients as observed in the present case. [1],[3],[5]
Blood/ plasma amylase levels are elevated which confirms the diagnosis. Plasma lipase levels are increased and are a specific marker of pancreatitis. It differentiates acute pancreatitis from other causes of hyperamylasemia. This was observed in the present study. The diagnosis was performed by USG and CT scanning followed by diagnostic aspiration which yielded E. coli. Our patient responded to Cefotaxime along with gallstone removal by ERCP, sphincterotomy. The percutaneous drain was kept for two weeks.
Early diagnosis and prompt treatment of pancreatitis or pancreatic abscess is necessary to prevent any associated morbidity or mortality.
 References | |  |
| 1. | van Sonnenberg E, Wittich GR, Chon KS, D'Agostino HB, Casola G, Easter D, et al. Percutaneous radiological drainage of pancreatic abscess. AJR Am J Roentgenol 1997;168:979-84.  |
| 2. | Birck R, Keim V, Fiedler F, van der Woude FJ, Romeiss P. Pancreatitis after Losartan. Lancet 1998;351:1178. |
| 3. | Hartwig W, Werner J, Uhl W, Buchler MW. Management of infection in acute pancreatitis. J Hepatobiliary Pancreat Surg 2002;9:423-8. |
| 4. | Baker S. Diagnosis& management of acute pancreatitis. Crit Care Resusc 2004;6:17-27. |
| 5. | Folsch UR, Nitsche R, Ludtke R, Hilgers RA, Creutzfeldt W. Early ERCP& papillotomy compared with conservative treatment for acute biliary pancreatitis. The German Study Group on Acute Biliary Pancreatitis. N Eng J Med 1997;336:237-42. |
Correspondence Address:
V P Baradkar
Department of Microbiology, L.T.M.M.C and L.T.M.G.H, Sion, Mumbai - 400 022
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0377-4929.56162
[Figure 1], [Figure 2] |
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| This article has been cited by | | 1 |
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