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Abstracts
| Prevention and Management of Infection Complicating
Acute Pancreatitis* Henry L. Laws, MD Acute pancreatitis varies in etiology, severity, response to therapy, and onset of complicating infection. A typical breakdown of etiology is as follows: gallstones, 50 percent; ethanol, 30 percent; hyperlipidemia, 5 percent; trauma, 3 percent; and iodiopathic, 12 percent. The process usually begins abruptly. Findings on physical examination may vary depending on severity, time from onset and habitus of the patient. Early deaths result from hypovolemia and shock. Deaths occurring after the first few days stem from complicating infections. In the emergency room many patients may look surprisingly fit, even with a severe pancreatitis. Forty percent will exhibit some abnormality in gas exchange. Most patients can be divided fairly readily into those with severe pancreatitis and mild pancreatitis, but sometimes the severity of the inflammatory process may not be evident for two or three days. A grading system such as that of Ranson allows prediction of eventual outcome and comparison of one series of patients to another. Severity features of Ranson include: at admission or diagnosis, age over 55 years, white blood cell count over 16,000/m3, blood glucose over 200 mg %, serum lactic dehydrogenase over 350 IU/L, and serum glutamic oxaloacetate transaminase over 250 Sigma-Franke units %; during the initial 48 hours, hematocrit fall greater than 10 percentage points, blood urea nitrogen rise more than 5 mg%, serum calcium level below 8 mg %, arterial PO2 below 60 mmHg, base deficit greater than 4 mEq/L, and estimated fluid sequestration more than 6000 mL. A contrast-enhanced CT (CECT) scan done after 48 hours, but preferably one week after onset, provides a fairly good estimation of the degree of nonperfused pancreatic tissue. Levels of necrosis by CECT are defined by Balthazar as follows: no necrosis, all pancreatic tissue is perfused; mild necrosis, 30 percent or less of pancreatic tissue is nonperfused; moderate necrosis, 30 to 50 percent of pancreatic tissue is nonperfused; and severe necrosis, > 50 percent of pancreatic tissue is nonperfused. On the CT scan 20 to 30 percent of people will demonstrate peripancreatic fluid collection. The classification of peripancreatic fluid collections by Stanten and Frey can suggest severity of the peripancreatic inflammation: 0, no peripancreatic inflammation; 1, peripancreatic extension within the pericapsullary space; 2, extension into a single space beyond the capsule; 3, extension into two or more spaces above the lower level of the kidneys; and 4, retroperitoneal extension below the level of the kidneys. Infection rarely supervenes within one week of onset of the pancreatitis and generally becomes evident two or three weeks after the beginning. Aspiration from the area of the pancreas or peripancreatic area with smear and culture can reliably demonstrate the evidence of infection and the need for surgical intervention. If infection supervenes, mortality approaches 100% unless the patient receives surgical management and appropriate antibiotic therapy. The preferable prophylactic regimen is imipenem-cilastatin 500 mg q6h for two or more weeks according to most collective reviews on this subject. We also employ fluconazole 400 mg/day. If infection supervenes, management consists of debridement and/or drainage of the pancreas and peripancreatic area through an upper abdominal transverse incision, generally with open intra-abdominal packing combined with appropriate antibiotic therapy. Our indications for operation include: 1) positive percutaneous smear and/or culture from the affected area; 2) septicemia with no other apparent source; 3) gas in pancreatic or peripancreatic area; and 4) development of the septic syndrome (deteriorating function of multiple organs) even without a proven organism within the pancreas of peripancreatic area. References 1. Ranson JHC. Acute pancreatitis. In: Current Problems in Surgery. Chicago: Year Book Medical Publishers, Inc. 1979. 2. Balthazar EJ. Contrast-enhanced computed tomography in severe acute pancreatitis. In: Bradley EL III, ed. Acute Pancreatitis: Diagnosis and Therapy. New York: Raven Press, 1994, pp 57-68. 3. Stanten R, Frey CF. Comprehensive management of acute necrotizing pancreatitis and pancreatic abscess. Arch Surg 1990; 125:1269-75. 4. Banks PA. The role of needle aspiration bacteriology in the management of necrotizing pancreatitis. In: Bradley EL III, ed. Acute Pancreatitis: Diagnosis and Therapy. New York: Raven Press, 1994, pp 99-103. 5. Pederzoli P, Bassi C, Vesentini S, Campedelli A. A randomized multicenter clinical trial of antibiotic prophylaxis of septic complications in acute necrotizing pancreatitis with imipenem. Surg Gynecol Obstet 1993; 176:480-3. 6. Kramer KM, Levy H. Prophylactic antibiotics for severe acute pancreatitis: The beginning of an era. Pharmacotherapy 1999; 19:592-602. 7. Stone HH, Strom PR, Mullins RJ. Pancreatic abscess management by subtotal resection and packing. World J Surg 1984; 8:340-5. 8. Laws HL, Kent RBIII. Acute Pancreatitis: Management of Complicating Infection. The American Surgeon 2000, 66:145-152. |
