Successful percutaneous treatment of infected necrosis of the body of the pancreas associated with segmental disruption of the main pancreatic duct Josef Gmeinwieser, MD, Axel Holstege, MD, Hubert Zirngibl, MD, Klaus-Dieter Palitzsch, MD, Sigrun Hügl, MD, Michael Strotzer, MD, Stefan Feuerbach, MD, Jürgen Schölmerich, MD
Survival in the initial phase of acute pancreatitis has improved significantly during the last decade as a result of better intensive care and general management.1 Serial imaging studies usually show “organization” of acute pancreatic necrosis (i.e., liquefaction and encapsulation of necrotic pancreatic tissue). Persistent infection of these cavities despite endoscopic or percutaneous drainage has been ascribed to formation and infection of sequestered solid necrotic tissue that is presumably inaccessible to antibiotics.2,3 The standard procedure in these situations in symptomatic patients is surgery to clear the cavities and to remove the necrotic tissue.3,4 Percutaneous or endoscopic drainage of pancreatic abscesses and infected necrotic areas has been described.2,5-8 However, this approach has been successful only in the minority of cases. Failure was mainly due to the inability to remove solid material. Another problem with a conventional interventional approach is persisting secretion from the remaining tail of the pancreas in cases with necrosis of the body. This is a report of a patient with a large area of infected necrosis of the body of the pancreas. He was successfully treated with a new interventional approach consisting of percutaneous and endoscopic necrosectomy and percutaneous pancreatic duct blockade. CASE REPORT A 17-year-old boy underwent operation for lower abdominal pain because of a suspicion of appendicitis in another hospital. Two days before surgery the patient had consumed an excessive amount of alcohol. No other etiologic factors were found. When the appendix was found not to be inflamed, a diagnosis of necrotizing pancreatitis was made. The patient became septic and was transferred to our intensive care unit. Assisted ventilation was
From the Departments of Radiology, Internal Medicine and Surgery, University of Regensburg, Germany. Reprint requests: Prof. Dr. J. Schölmerich, Department of Internal Medicine, University of Regensburg, 93042 Regensburg, Germany; fax 49-941-944-7002. Copyright © 2000 by the American Society for Gastrointestinal Endoscopy 0016-5107/2000/$12.00 + 0 37/4/108299 doi:10.1067/mge.2000.108299 VOLUME 52, NO. 3, 2000
Figure 1. Bolus contrast abdominal spiral CT at 7 weeks after onset of necrotizing pancreatitis. An abscess-like cavity had formed which comprised the complete necrotic body of the pancreas. Due to the fluid-equivalent density of necrotic tissue, solid material could not be identified within the surrounding fluid. required for 3 weeks and he remained febrile during this entire period despite successive treatment with various antibiotics (imipenem, metronidazole, mezlocillin, later erythromycin and amoxicillin/clavulanic acid). Initial CT revealed complete necrosis of the body of the pancreas and fluid collections in the transverse mesocolon and the paracolic gutters. Two weeks later, a fluid collection had developed around the sequester. CT-guided, fine-needle aspiration revealed sterile greenish fluid. Four weeks after the onset of symptoms the patient was free of pain and all organ functions were normal. However, temperature elevations to approximately 38° C persisted despite antibiotic treatment. Two weeks later he was afebrile and went home free of symptoms. CT at this time demonstrated demarcation of the necrosis and almost complete regression of the acute fluid collections in the transverse mesocolon and the paracolic gutters. The patient was readmitted to another hospital 3 days later with recurrent abdominal pain and temperature elevations to 38° to 39° C. He was immediately transferred to our department. Abnormal laboratory tests (normal values in parentheses) included serum amylase 408 U/L, (<120), lipase 449 U/L (<190), Creactive protein 60 mg/dL (<5), and white blood cell count 17,500/µL (<10,800). CT revealed an increase in the size of the necrotic cavity which now appeared to be an abscess or pseudocyst (Fig. 1). He was treated with metronidazole and mezlocillin and total parenteral nutrition. Because fever persisted although pain ameliorated, aspiration of the necrotic cavity was repeated under CT guidance. Contamination with Staphylococcus suppurativus was found. The patient and his parents strictly declined the surgical procedure that was recommended. Therefore, a percutaneous interventional approach was attempted. Under local anesthesia, a drainage catheter (16F van Sonnenberg, Boston GASTROINTESTINAL ENDOSCOPY
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Figure 2. Fluoroscopic image during percutaneous necrosectomy. Scientific International, Natick, Mass.) was placed by a retroperitoneal approach. However, only a little putrid fluid could be evacuated. The patient remained febrile. Two days later injection of contrast showed a large, solid mass within the cavity. Because it was not adherent to the wall of the cavity, the risk of life-threatening bleeding during an attempt of percutaneous removal was considered to be low. Furthermore bolus contrast CT had ruled out the possibility of a pseudoaneurysm or splenic vein thrombosis. The 16F catheter was replaced with a 26F peel-away sheet (Cook Inc., Bloomington, Ind.) under light systemic intravenous sedation (Sufentanil, 150 γ) and local anesthesia with surgical stand-by. Under fluoroscopic guidance, the necrotic pancreatic body and fatty tissue were fragmented (Fig. 2) and extracted using a snare catheter (Lassos, Osypka Company, Grenzach-Whylen, Germany) and a Dormia basket. A bronchoscope was inserted and no necrotic tissue was visualized. Pathologic examination of the extracted material showed necrotic pancreatic and fatty tissue, weighing 30 gm (Fig. 3). A 26F double-lumen drainage catheter (Sherwood Medical Company, St. Louis, Mo.) was left in place for continuous lavage of the cavity with normal saline solution. The patient became afebrile after this procedure. Six days after extraction, contrast injection into the cavity revealed slight shrinkage and, as expected, a connection to the pancreatic duct in the remaining tail of the pancreas. Pancreatic secretions drained at a rate of 80 to 100 mL/day through the catheter. Percutaneous blockade of the duct was undertaken to stop secretion. In a first attempt 3 weeks after percutaneous necrosectomy, the duct could not be cannulated because the residual cavity was still too large. The patient was sent home free of symptoms with an 8F drainage tube in place for 4 weeks. Subsequently, the cavity was found to be almost closed (Fig. 4). It was then possible to cannulate the pancreatic duct in the tail which was completely filled with 4 mL Ethibloc (Ethibloc; Ethicon Company, Norderstedt, Germany). Thereafter, the drainage was removed and octreotide was administered for 4 days in addition to parenteral nutrition and antibiotics. Slight left upper quadrant pain was present for 3 days and the patient went home 5 days after the duct occlusion. He has remained free of symptoms for 3 years. 414
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Figure 3. A 26F sheet and “Lassos” snare catheters and removed necrotic tissue.
DISCUSSION Infected necroses of the body of the pancreas together with segmental disruption of the main pancreatic duct is considered an unequivocal indication for surgery.3,6 Besides debridement, the persistent excretory function of the vital tail of the pancreas necessitates that it be resected along with the body of the pancreas. As a rule, splenectomy is indispensable during this operation. Interventional approaches to therapy until now have been restricted to percutaneous drainage and necrosectomy carried out in small steps over several weeks by lavage and aspiration. Using this procedure, Freeny et al.6 were only able to cure 4 of 14 patients with infected necroses of the pancreatic body. In these cases, the excretory function of the pancreatic tissue upstream to the pancreatic duct disruption stopped spontaneously. Persistent secretion required resection of the functioning tail of the pancreas in 10 patients. The risk of diabetes increases with the loss of functioning pancreatic tissue. Splenectomy increases the susceptibility to infection. Owing to the risk of these long-term complications, our adolescent patient and his parents refused to agree to the operation that had originally been planned. Percutaneous debridement of an abscess cavity with a snare was described for the first time by Dixon et al.9 in 1994. Although percutaneous necrosectomy with lavage and aspiration alone as applied by Freeny et al.6 requires several weeks, even large necrotic tissue collections can be removed percutaneously in one session using the snare technique. Because abscess cavities heal only when they are completely cleansed of necrotic tissue, the duration of drainage required can be appreciably shortened by the active procedure. In contrast to surgical debridement, this technique of percutaneous necrosectomy requires complete sequestration of the necrotic tissue. In our case, a necrosis of the body of the pancreas only became infected 6 weeks after the VOLUME 52, NO. 3, 2000
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onset of the disease. The dead tissue no longer adhered to the surrounding vital tissue and could therefore be mobilized percutaneously, fragmented, and extracted without major risk of hemorrhage. The safest place to perform percutaneous necrosectomy would be an operating room. Fluoroscopy equipment that provides images of excellent quality is mandatory. This was not the case with the mobile fluoroscopy units in our operating theater. Therefore the procedure was performed in the radiology department with surgical stand-by. Necrotic tissue attached to the cavity wall was ruled out by endoscopic inspection of the necrotic cavity. Intraoperative blockade of the pancreatic duct with Ethibloc or fibrin tissue sealant is an accepted method for elimination of excretory activity of remaining tissue in resections of the head of the pancreas.10 However, a prerequisite for success is that the Ethibloc plug fill the remaining duct system entirely. Percutaneous blockade with fluoroscopic guidance therefore requires that an occluding catheter be pushed as far as possible into the duct in the tail of the pancreas to apply the viscous blocking agent with sufficiently high pressure during retraction. In our patient the duct was not dilated. Therefore the diameter of a 5F catheter was sufficient for blocking. A prerequisite for duct cannulation is almost complete obliteration of the cavity around the drain. The length of time required for healing of the cleansed abscess cavity when the drainage of pancreatic juice is not impaired depends in particular on the size of the cavity. In our case, this process took 7 weeks. During this period, the volume of pancreatic juice formed by the tail of the pancreas was at least 80 mL per day. Spontaneous cessation of exocrine activity was therefore improbable. Ethibloc, instead of fibrin glue, was used because of the good results obtained by our surgeon with the use of this agent in several hundred partial duodenopancreatectomies.11 Presumably the effect of fibrin glue would have been the same. Successful blockade of the pancreatic duct in the tail of the pancreas was crucial to the long-term success of this interventional therapy. Because neither complete demarcation or sequestration of the necrotic tissue nor the obliteration of the cleansed cavity can be hastened, the interventional therapy described requires appreciably more patience on the part of the patient and physicians compared with surgery. The disadvantage of a longer duration of treatment is balanced by the long-term lower risk of diabetes and infection. To
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Figure 4. Contrast filling of the abscess cavity 7 weeks after percutaneous necrosectomy. The duct of the remaining tail of the pancreas drains into the markedly shrunken cavity.
our knowledge, this is the first report of successful interventional treatment of an infected necrosis involving the entire body of the pancreas associated with a segmental disruption of the main pancreatic duct with persistent excretory function of the vital tail of the pancreas. REFERENCES 1. Niederau C, Schulz H-U. Current conservative treatment of acute pancreatitis: evidence from animal and human studies. Hepato-Gastroenterology 1993;40:538-49. 2. Baron TH, Thaggard WG, Morgan DE, Stanley RJ. Endoscopic therapy for organized pancreatic necrosis. Gastroenterology 1996;111:755-64. 3. Farthmann EH, Lausen M, Schöffel U. Indications for surgical treatment of acute pancreatitis. Hepato-Gastroenterology 1993;40:556-62. 4. Balthazar EJ, Freeny PC. Imaging and intervention in acute pancreatitis. Radiology 1994;193:297-306. 5. Adams DB, Harvey TS, Anderson MC. Percutaneous catheter drainage of infected pancreatic and peripancreatic fluid collections. Arch Surg 1990;125:1554-7. 6. Freeny PC, Hauptmann E, Althaus SJ, Traverso LW, Sinanan M. Percutaneous CT-guided catheter drainage of infected acute necrotizing pancreatitis: techniques and results. AJR Am J Roentgenol 1998;170:969-75. 7. Steiner E, Mueller PR, Hahn PF. Complicated pancreatic abscesses: problems in interventional management. Radiology 1988;167:443-6. 8. Rotman N, Mathieu D, Anglade MC, Fagniez PL. Failure of percutaneous drainage of pancreatic abscesses complicating severe acute pancreatitis. Surg Gynecol Obstet 1992;174:141-4. 9. Dixon G. Nitinol snare for removal of abscess debris. JVIR 1994;5:647-8. 10. Gebhardt C. Surgical treatment of pain in chronic pancreatitis. Role of the Whipple procedure. Acta Chir Scand 1990;156:303-6. 11. Gall FP, Gebhardt C, Meister R, Zirngibl H, Schneider MU. Severe chronic cephalic pancreatitis: use of partial duodenopancreatectomy with occlusion of the pancreatic duct in 289 patients. World J Surg 1989;13:809-16.
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