Saudi Journal of Gastroenterology
Home About us Instructions Submission Subscribe Advertise Contact Login    Print this page  Email this page Small font sizeDefault font sizeIncrease font size 
Users Online: 908 

ARTICLES Table of Contents   
Year : 1998  |  Volume : 4  |  Issue : 1  |  Page : 1-7
Treatment of acute pancreatitis

Department of Medicine, College of Medicine, King Saud University, Riyadh, Saudi Arabia

Click here for correspondence address and email

Date of Submission20-Aug-1997
Date of Acceptance22-Sep-1997


There is no specific treatment for acute pancreatitis. Majority of patients with acute pancreatitis respond to medical therapy. Supportive measures and close observations represent the cornerstone of the medical therapy. Failure to respond to medical treatment may indicate choledocholithiasis or infected necrosis. Endoscopic papillotomy with stone retrieval is beneficial in patients with severe biliary pancreatitis. Image-guided fine needle aspiration and bacteriological examination of aspirate is reliable in detecting infection and deliniating causative pathogen. Surgical debridement is the method of choice for treatment of infected necrosis. In contrast, in pancreatic abscess, surgery is preserved for those, who do not respond to percutaneous drainage combined with antibiotics. The benefit of antisecretory and antiproteolytic agents is debatable. A combination of antioxidants, calcium channel antagonists and antibiotics may play a major role in the treatment of acute pancreatitis in the future.

How to cite this article:
Al-Mofleh IA. Treatment of acute pancreatitis. Saudi J Gastroenterol 1998;4:1-7

How to cite this URL:
Al-Mofleh IA. Treatment of acute pancreatitis. Saudi J Gastroenterol [serial online] 1998 [cited 2022 Dec 9];4:1-7. Available from:

Early diagnosis of acute pancreatitis, determining the etiology and assessing its severity are important to choose and initiate the appropriate therapy. Majority of pancreatitis cases run a mild course, requiring supportive therapy only and resolve within few days. Approximately 20 % become severe and require intensive care monitoring and supportive treatment. The effect of antisecretory agents, such as somatostatin, octreotide and H,-receptor antagonists is debatable [1] . Protease inhibitors including aprotonin and gabexate mesilate have also not proven to be effective [2],[3] . In contrast, antioxidants, calcium channel antagonists, angiotensin converting enzyme inhibitors, dopamin, hypertonic dextran, and antibiotics seem to have a promising effect in future management of acute pancreatitis [4],[5],[6],[7],[8],[9] . Infection of pancreatic necrosis is the leading cause of mortality [10] . Recent knowledge relating to the infection source, transmission route, nature of microorganisms and selection of appropriate antibiotics may reduce morbidity and mortality. Surgery is no longer the only method to treat severe acute pancreatitis. Advances in medical therapy as well as in the endoscopic and percutaneous approaches to treat pancreatitis and its complications brought up new therapeutic alternatives.

The aim of this article is to provide an overview on the current therapeutic advances of acute pancreatitis.

   General Principles of Treatment Top

There is no specific treatment for acute pancreatitis. The aim of medical treatment is to rest the organ and reduce the release of digestive and proteolytic enzymes, supportive care and prevention of local and systemic complications. In the vast majority of cases acute pancreatitis is a self-limiting disease and resolves within one week. All patients with acute pancreatitis require close observation, adequate intravenous volume replacement, analgesia and withholding oral feeding. Only patients with severe disease, evidenced by development of local and/ or systemic complications, require intensive care monitoring and treatment [11] . Total parenteral nutrition (TPN) may be required, however the use of TPN is associated with a number of complications and high cost. Total enteral nutrition (TEN) via a tube placed endoscopically in the jejunum has been found to be safe, effective and cost effective compared to TPN. Jejunal tube feeding has no considerable stimulatory effect on pancreatic secretion [12] . Clinical assessment, multifactorial scoring system (MFSS), biological markers and contrast-enhanced computed tomography (CECT) provide valuable information about the severity, prognosis and probably the choice of therapeutic approach.

   Drugs Top

Secretory inhibitors:

Somatostatin has been used for two decades in the treatment of acute pancreatitis. However, the benefit of somatostatin and its analogue octreotide remain uncertain. Kay et al reviewed physiological properties, and the effect of somatostatin in experimental models and in man, but they did not find enough evidence to support the use of somatostatin or its analogue in the treatment or prophylaxis of acute pancreatitis [13] . On the other hand, the effect of octreotide may worsen the outcome of idopathic recurrent pancreatitis. Di Francesco et al have studied the effect of administration of octreotide on  Sphincter of Oddi More Details motor response [14] . They found that acute administration of octreotide was associated with an increase of sphincter pressure. They suggested that this increase may impair pancreatic outflow and thus trigger or worsen pancreatitis.

Other antisecretory drugs including H2 receptor antagonists have not proven to be effective in treatment of acute pancreatitis [1] .

In experimental studies, gilanin, a 29 amino acid peptid has inhibited rat pancreatic enzymes. This antisecretory action of gilanin is mediated by its inhibitory effect on the cholinergic transmission [15] .

Nasogastric suction reduces gastrin release and gastric emptying, but it has not been beneficial in mild and moderate acute pancreatitis. However in severe pancreatitis, it may be beneficial. Therefore it has to be used selectively [1] .

Protease inhibitors:

Aprotonin was the first protease inhibitor applied clinically with disappointing results [2] . In the same multicenter study glucacon, another protease inhibitor, has also not been found effective in acute pancreatitis.

Effect of gabexate mesilate, a low molecular weight synthetic protease inhibitor, has been evaluated in a multicenter study in patients with moderate and severe acute pancreatitis randomized after a median of 21 hours after the onset of the abdominal pain. Results showed that despite the use of a high dose of 4g/day for one week, gabexate was not effective in preventing complications and mortality [3] . The authors explained the lack of effect by the delayed admission and induction of treatment. Meanwhile, the prophylactic treatment with gabexate in patients undergoing ERCP has been found effective in reducing the frequencies of acute pancreatitis and pain [16] . Thus cost effectiveness and the identification of patients at risk to develop pancreatitis post ERCP have yet to be determined. A gabexate treatment course costs approximately US $ 260 [17] .

Oxygen-free radicals scavengers:

Oxygen free radicals (OFR) play an important role in the pathogenesis of acute pancreatitis. Ischemia is known to enhance the release of OFR which contribute to pancreatic damage and multiple organ failure (MOF). Antioxidants, OFR scavengers, have a protective role on the endothelial barrier [4] .

Calcium channel antagonists:

Cytosolic calcium also plays a role in the endothelial permeability regulation [18] . Pretreatment of animals with calcium channel antagonists has also been associated with protective effect against endothelial permeability alteration on acute pancreatitis. However, there has been no correlation between the protective activity of antioxidants or calcium channel antagonists and organ improvement [4] .

Angiotensin converting enzyme (ACE) inhibitors:

They inhibit the bradykinin degrading enzymes and therefore, they may have a promising role in the treatment of acute pancreatitis [5] .


In an experimental model of alcoholic acute pancreatitis, dopamine has significantly reduced the inflammatory score and the 24 hours urinary TAP. This reduction is dose independent. The authors have suggested to use depamine, in a renal dose in all patients with acute pancreatitis [6] .


Micro circulation is impaired in patients with necrotizing pancreatitis. In an experimental model, dextran 6 % (60,000) has maintained capillary perfusion in tissue surrounding necrotic nodules [19] . Furthermore, hypertonic dextran 10% (500,000) given early (30 minutes after experimental induction of pancreatitis) reduces typsinogen activation, acinar necrosis and mortality. A combination of aprotinin with dextran has no additional effect [7] .

[Figure - 1],[Figure - 2] summarize the therapeutic approach of acute pancreatitis and local complications.

   Treatment of local complications Top

Sterile necrosis:

In the absence of infection, pancreatic necrosis is treated medically with sufficient hydration and treatment of complications. In case there is no improvement or rather the patient condition deteriorates, infection of necrosis has to be suspected. A CT-guided fine needle aspiration for Gram stain and culture is accurate and safe to prove infection and plan for further management. If the aspirate is sterile medical treatment is continued. Failure to respond to medical treatment require surgical debridement. Surgical treatment is no longer considered as the treatment of choice for sterile necrosis [11] . A recent metaanalysis of five prospective studies constituting 287 patients, surgical debridement has failed to improve morbidity and the overall mortality [20].

Infected necrosis:

How a sterile pancreatic necrosis becomes infected? Experimental and clinical observations demonstrated the majority of microorganisms found in infected necrosis are of enteric origin suggesting translocation from the gut [21],[22],[23],[24],[25]. The presence of Gram-negative bacteria in infected pancreatic necrosis is preceded by gut colonization with the same bacteria [22] . Other routes of pancreatic necrosis infection include translocation through biliary and duodenal reflux from ascitis fluid, hematogenous and lymphagenous spread [25],[26],[27],[28] .

Infection may complicate 40-60 % of cases of necrotizing pancreatitis. In the majority of patients, pancreatic infection takes place within the first two weeks of acute pancreatitis [29] .

Infection is the most important cause of death in acute pancreatitis [10] . US or CT-guided FNA is safe and highly effective in the diagnose of infection [21],[30] . Gram stain has been highly accurate and was positive in 98% of infected aspirate confirmed by culture [31] . Most secondary infections are originating from the GUT. E. Coli and pseudomonas spp. have been the commonest gram negative while enterococci and staph. epidermidis were the commonest gram positive aerobics. Candida albicans has been also among the commonest causes of secondary infection of pancreatic necrosis [22] .

Ciproflaxin, oloflaxin and imipenem are the best antibiotics in regard to their high pancreatic tissue concentration and high bacterial activity against the majority of organisms found in pancreatic infection [23] . Despite this progress in the knowledge about the germs and antibiotics, the effect of antibiotics in the treatment of infected necrotizing pancreatitis remains debatable. Early studies have failed to prove that antibiotics have a benificial effect on the overall morbidity and mortality of acute pancreatitis. However, some recent experimental and clinical studies revealed a significant decrease in morbidity and mortality [8],[9] . Furthermore, selective prophylaxis has been associated with reduction of morbidity without a significant reduction in the mortality [9],[21],[32]. Selective decontamination has been effective in reducing the morbidity and mortality in patients with severe acute necrotizing pancreatitis. The selective decontamination regimen has been a combination of oral colistin sulfate, norfloxacin, amphotericin and systemic application of cefotaxime sodium [22].

Surgical debridement has been considered as the gold standard for treating infected necrosis [11] . Three main surgical procedures are used: (a) debridement with close sump drainage, (b) debridement with open packing, and (c) debridement with continuous lavage have been compared. Debridement with open packing has been more suitable to be performed repeatedly with lower mortality [33],[34] . Indications for surgical debridment are listed in tablel. Patients with infected pancreatic necrosis have responded well to extensive debridement with continuous lavage and suction drainage combined with supportive treatment and appropriate antimicrobial agents [35] . External percutaneous drainage with large pigtail catheters has been considered as alternative method to surgery in patients at high risk [36] .


Majority of pancreatic pseudocysts (PPC) resolve spontaneously within a variable period which may exceed six months. Nowadays, there is an agreement to treat symptomatic PPC only, regardless the size of PPC and the duration of persistence [37].

Previously surgery was the only method of treatment of PPC. However, in recent years radiologic and endoscopic alternatives have been successfully applied, to decompress PPC. The perantaneous approach require a prior ERCP to prove a patent, nonobstructed pancreatic, duct for a successful drainage [38] .

Percutaneous drainage of PPC has been effective in 90 % of cases. Infection and hemorrhage are the major while mild bleeding, PPC colonization and pleura effusion are the minor complications which occur in 5 % of patients each [39] .

Endoscopic approach consisting of cyst gastrostomy, cyst duodenostomy, main pancreatic duct stenting or combination of techniques has been associated with lower morbidity. Therefore it has been considered as the first line approach especially in the presence of bulging into the upper gastrointestinal tract lumen or duct communication. The success rate of various endoscopic approaches ranges between 80 and 94% [40],[41],[42],[43] . Cyst gastrostomy and cyst duodenostomy approach can be improved by endosonographic guide [44] . Complication in the form of bleeding, perforation, gallbladder puncture, stent clogging and abscess formation have been encountered in around 12% of patients [42],[43] compared to 38 % post surgical morbidity [40].

Pancreatic abscess:

Pancreatic abscess is a circumscribed intra­abdominal collection of pus with little or no pancreatic necrosis, usually in the proximity of the pancreas [45] . Majority of pancreatic abscess (upto 70%) respond to percutaneous drainage [46] . In patients who need surgery, percutaneous drainage may help to delay surgery till improvement of the general condition. Furthermore, percutaneous drainage may minimize the surgical procedure.

   Other therapeutic procedures Top

Long peritoneal lavage:

Infection, the major cause of morbidity may occur later in the course of a necrotizing pancreatitis, has been considered as the effect of peritoneal lavage, that has been applied over the last three decades, is debatable. However, a recent controlled clinical trial of long (7 days) peritoneal lavage application has strongly suggested a dramatic decline in pancreatic sepsis and related mortality in severe acute pancreatitis [47] .

Endoscopic Retrograde Cholangio Pancreatography (ERCP):

The value of ERCP and endoscopic papillotomy (EPT) in acute biliary pancreatitis has been controversial. Neoptolemos et al reported a reduction of morbidity in patients predicted to develop severe acute pancreatitis when early ERCP and stone retrieval have been performed [48] . Fan et al have compared early ERCP and EPT with conventional treatment in patients with acute pancreatitis. Complications and mortality have been similar in both treatment groups. However, biliary sepsis related morbidity has declined significantly in the endoscopic treated group. The authors suggested emergency ERCP to reduce biliary sepsis in acute pancreatitis irrespective of the course and severity [49] . The role of early ERCP and biliary decompression is generally accepted in patients with severe acute biliary pancreatitis.

Furthermore, EPT has been accepted as alternative for cholecystectomy in the prevention of recurrences in the elderly [50],[51],[52] .


The risk of recurrence of acute pancreatitis in the presence of the gallbladder is 35%. Cholecystectomy during the same admission, effectively prevents recurrence in the elderly. Endoscopic papillotomy has been accepted as an alternative for cholecystectomy to prevent further attacks of acute pancreatitis [51] . In pregnancy, acute biliary pancreatitis is managed medically and cholecystectomy is rarely required. However, it can be safely performed after the first trimester. Endoscopic stone removal is also possible [53] .

Laparascopic cholecystectomy (LC) has been extensively evaluated in the past few years. Early LC is safe but associated with technical difficulties [54] , increase in the surgical complications, conversion rate and longer postoperative hospital study when performed in patients with acute biliary pancreatitis (ABP) during the first week of admission [55] . Combined endoscopic and laparascopic management is effective and safe [56],[57] and recommended as the primary approach in ABP [58] . A combined approach has also been performed to manage recurrent biliary pancreatitis in pregnancy [59]

   Conclusion Top

Majority of cases of acute pancreatitis respond to medical treatment. Deterioration of necrotizing pancreatitis and infection of necrosis require surgical debridement. Gram stain and culture of fine needle aspirate are highly accurate in confirming infections, identifying causative organisms and helping to select appropriate antibiotics. Long peritoneal lavage may reduce sepsis and related mortality. Majority of pancreatic abscess cases respond to percutaneous drainage and antibiotics. Only symptomatic pseudocysts, irrespective of size and duration, are treated endoscopically percutaneously or surgically, dextran, antibiotics, antioxidants, calcium channel blockers and dopamine may be beneficial. Early endoscopic papillotomy is mandatory in severe biliary pancreatitis. Laparoscopic as well as combined laparoscopic endoscopic approach are effective and safe.

   References Top

1.Greenberger NJ, Toskes PP, Isselbacker KJ. Acute and chronic pancreatitis. In: Isselbacher KJ, Braunwald E, Wilson JD, Martin JB, Fauci AS, Kasper DL (Eds). Harrison's principles of internal medicine. McGraw-Hill, New York 1994;1520-7.  Back to cited text no. 1    
2.Cox AG. Death from acute pancreatitis. MRC multicenter trial of glucagon and aprotinin. Lancet 1977;24:632-5.  Back to cited text no. 2    
3.Buehler M, Malfertheiner P, Uhl W, et al. Gabexate mesilate in human acute pancreatitis. Gastroenterology 1993;104:1165-70.  Back to cited text no. 3    
4.Wang XD, Deng XM, Haraldsen R, Andersson R, Ihse I. Antioxidant and calcium channel blockers counteract endothelial barrier injury induced by acute pancreatitis in rats. Scand J Gastroenterol 1995;30:1129-36.  Back to cited text no. 4    
5.Weidenbach H, Lerch MM, Gress TM, Pfaff D, Turi S, Adler G. Vasoactive mediators and progression from edematous to necrotizing experimental acute pancreatitis. Gut 1995;37:434-40.  Back to cited text no. 5  [PUBMED]  [FULLTEXT]
6.Karanajia ND, Widdison AL, Lutrin FJ, Reber HA. Dopamine in models of alcoholic acute pancreatitis. Gut 1994;35:547-51.  Back to cited text no. 6    
7.Huch K, Schmidt J, Schrat W, Sinn HP, Buhr H, Herfarth C, Klar E. Hypertonic dextran and systemic aprotinin in necrotizing rodent pancreatitis. Scand J Gastroenterol 1995;30:812-6.  Back to cited text no. 7    
8.Mithofer K, Fernandez-del Castillo C, Ferraro MJ, et al. Antibiotic treatment improves survival in experimental acute necrotizing pancreatitis. Gastroenterology 1996; 110:232-40.  Back to cited text no. 8    
9.Sainio V, Kemppainen E, Puolakkainen M, et al. Early antibiotic treatment in acute necrotizing pancreatitis. The Lancet 1995;346:663-7.  Back to cited text no. 9    
10.Berger HG. Surgery in acute pancreatitis. Hepatogastroenterology 1991;38:92-6.  Back to cited text no. 10    
11.Banks PA. Practice guidelines in acute pancreatitis. Am J Gastroenterol 1997;92:377-86.  Back to cited text no. 11  [PUBMED]  
12.McClave SA, Greene LM, Snidar HL, et al. Comparison and safety of early enteral vs parenteral nutrition in mild acute pancreatitis. J Parent Ent Nutr 1997;21:14-20.  Back to cited text no. 12    
13.McKay C J, Imrie CW, Baxter JN, Somatostatin and somatostatin analogues-are they indicated in the management of acute pancreatitis ? Gut 1993;34:1622-6.  Back to cited text no. 13    
14.Di Francesco V, Angelini G, Bovo P, et al. Effect of octreotide on sphincter on Oddi motility in patients with acute recurrent pancreatitis: a manometric study. Dig Dis Sci 1996;41:2392-6.  Back to cited text no. 14  [PUBMED]  
15.Herzig KH, Brunke G, Schon 1, Schaffer M, Folsch UR. Mechanism of galanin's inhibitory action on pancreatic enzyme secretion : Modulation of cholinergic transmission studies in vivo and in vitro. Gut 1993;34:1616-21.  Back to cited text no. 15    
16.Cavallini G, Tittobello A, Frulloni L, Masci E, Mariani A, Di Francesco V and Gabaxate in Digestive endoscopy - Italian Group N Engl J Med 1996;335:919-23.  Back to cited text no. 16    
17.Huibregstse K. Complications of endoscopic sphincterotomy and their prevention (Editorial) N Engl J Med 1996;335:961-2.  Back to cited text no. 17    
18.Lum H, Aschner JL, Phillips PG. Time course of thrombin­induced increase in endothelial permeability: relationship to Ca2+ and inositol polyphosphates. Am J Physiol 1992;263:L219-25.  Back to cited text no. 18    
19.Klar E, Herfarth C, Messmer K. Therapeutic effect of isovolemic hemodilution with dextran 60 on the impairment of pancreatic microcirculation in acute biliary pancreatitis. Ann Surg 1990;211:346-53.  Back to cited text no. 19  [PUBMED]  [FULLTEXT]
20.Bradley EL III. Debridement is rearly necessary in patients with sterile pancreatic necrosis. Pancreas 1996;13:220-3.  Back to cited text no. 20    
21.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.  Back to cited text no. 21  [PUBMED]  
22.Luiten EJ, Hop WCJ, Lange JF, Bruining HA. Controlled clinical trial of selective decontamination for the treatment of severe acute pancreatitis. Ann Surg 1995;222:57-65.  Back to cited text no. 22    
23.Buehler M, Malfertheiner P, Friess H, et al. Human pancreatic tissue concentration of bactericidal antibiotics. Gastroenterology 1992;103:1902-8.  Back to cited text no. 23    
24.Runkel NS, Moody FG, Smith GS, et al. The role of gut in the development of sepsis in acute pancreatitis. J Surg Res 1991;51:18-23.  Back to cited text no. 24  [PUBMED]  [FULLTEXT]
25.Tarpila E, Nystrom P O, Franzen L, et al. Bacterial translocation during acute pancreatitis in rats. Eur J Surg 1993;159:109-13.  Back to cited text no. 25    
26.Knock CP, Thrompson AG. Pancreatic ductal mucosa as a protective barrier in the pathogenesis of acute pancreatitis. Am J Surg 1969;117:18-23.  Back to cited text no. 26    
27.Byrne JJ, Joison J. Bacterial regurgitation in experimental pancreatitis. Am J Surg 1964;107:317-20.  Back to cited text no. 27  [PUBMED]  
28.Webster MW, Pasculle AW, Myerowitz RL, et al. Post induction bacteremia in experimental acute pancreatitis. Am J Surg 1979;138:418-20.  Back to cited text no. 28  [PUBMED]  [FULLTEXT]
29.Gerzof SG, Banks PA, Robbins AH, et al. Early diagnosis of pancreatic infection by computed tomography-guided aspiration. Gastroenterology 1987;93:1315-20.  Back to cited text no. 29  [PUBMED]  
30.Banks PA. Infected necrosis: Mortality and therapeutic consequences. Hepatogastroenterol 1991;38:116-9.  Back to cited text no. 30    
31.Banks PA. The role of needle aspiration bacteriology in the management of acute pancreatitis. In Bradley (Ed) Acute pancreatitis: principles and practice. New York; Raven Press; 1993:99-104.  Back to cited text no. 31    
32.McClelland P, Murray A, Yagoob M, et al. Prevention of bacterial infection and sepsis in acute severe pancreatitis. Ann R Coll Surg Engl 1992; 4:329-34.  Back to cited text no. 32    
33.Bradley EL III. A fifteen year experience with open drainage for infected pancreatic necrosis. Surg Gynec Obstet 1993;177:215-22.  Back to cited text no. 33    
34.Hwang TL, Cniu CT, Chen HM, et al. Surgical results for severe acute pancreatitis using different surgical procedures. Hepatogastroenterology 1995;42:1026-9.  Back to cited text no. 34    
35.Farkas G, Marton J, Mandi Y, Szederkeny E-Surgical strategy and management of infected pancreatic necrosis. Br J Surg 1996;38:930-3.  Back to cited text no. 35    
36.Banks PA. Acute pancreatitis: Medical and surgical management. Am J Gastroenterol 1994;89:S78-85.  Back to cited text no. 36  [PUBMED]  
37.Vitas GJ, Sarr MG. Selected management of pancreatic pseudocysts: operative versus expectant management. Surgery 1992;11:23-30.  Back to cited text no. 37    
38.Ahearne PM, Baillie JM, Cotton PB, et al. An endoscopic retrograde cholangiopancreatography (ERCP) based algorithm for the management of pancreatic pseudocysts. AmJ Surg 1992;163:11-6.  Back to cited text no. 38    
39.Van Sonnenberg E, Wittich G, Gasola G, et al. Percutaneous drainage of infected and non-infected pancreatic pseudocysts: Experience in 101 cases. Radiology 1989;170:757-61.  Back to cited text no. 39    
40.Catalono MF, Geenen JE, Schmalz MJ, Johnson JK, Dean RS, Hogan WJ. Treatment of pancreatic pseudocysts with ductal communication by transpapillary pancreatic duct endoprothesis. Gastrointest Endosc 1995;42:214-8.  Back to cited text no. 40    
41.Barthel M, Sahel J, Bodiou-Bertei C, Bernard JP. Endoscopic transpapillary drainage of pancreatic pseudocysts. Gastrointest Endosc 1995;42:208-13.  Back to cited text no. 41    
42.Smits ME, Rauws EAJ, Tytgat GNJ, Huibregste K. The efficacy of endoscopic treatment of pancreatic pseudocysts. Gastrointest Endosc 1995;42:202-7.  Back to cited text no. 42    
43.Binmoeller KF, Seifert H, Walter A, Sochendra N. Transpapillary and transmural drainage of pancreatic pseudocysts. Gastrointest Endosc 1995;42:219-24.  Back to cited text no. 43    
44.Grimm H, Binmoeller KF, Soehendra N. Endosonography­ guided drainage of pancreatic pseudocysts. Gastrointest Endosc 1995;38:170-1.  Back to cited text no. 44    
45.Bradley EL III. A clinically based classification system for acute pancreatitis. Arch Surg 1993;128:586-90.  Back to cited text no. 45    
46.VanSonnenberg E, Wittich GR, Chon K, et al. Complicated pancreatic inflammatory disease: diagnostic and therapeutic role of interventional radiology 1985;155:335-40.  Back to cited text no. 46    
47.Ranson JHC, Berman RS. Long peritoneal lavage decreases pancreatic sepsis in acute pancreatitis. Ann Surg 1990;211:708-18.  Back to cited text no. 47    
48.Neoptolemos JP. Endoscopic sphincterotomy in acute gallstone pancreatitis. Br J Surg 1993;80:547-9.  Back to cited text no. 48  [PUBMED]  
49.Fan ST, Lai ESC, Mok FPT, Lo CM, Zheng SS, Wong J. Early treatment of acute biliary pancreatitis by endoscopic papillotomy N Engl J Med 1993;328:228-32.  Back to cited text no. 49    
50.Lipschitz J, Gecelter GR. Does endoscopic sphincterotomy prevent recurrent biliary pancreatitis ? S Afr J Surg 1993;31:94-7.  Back to cited text no. 50  [PUBMED]  
51.Welbourn CR, Beckly DE, Eyre-Brook IA. Endoscopic sphincterotomy without cholecystectomy for gallstone pancreatitis. Gut 1995;37:119-20.  Back to cited text no. 51  [PUBMED]  [FULLTEXT]
52.Uomo G, Manes G, Laccetti M, Cavallera A, Rabitti PG. Endoscopic sphincterotomy and recurrent of acute pancreatitis in gallstone patients considered unfit for surgery. Pancreas 1997;14:28-31.  Back to cited text no. 52  [PUBMED]  [FULLTEXT]
53.Scott LD, Gallstone disease and pancreatitis in pregnancy. Gastroenterol Clin North Am 1992;21:803-15.  Back to cited text no. 53    
54.Tate JJ, Lau WY, Li AK. Laparoscopic cholecystectomy for biliary pancreatitis. BJ Surg 1994;81:720-2.  Back to cited text no. 54    
55.Tang E, Stain SC, Tang G, Froes E, Berue TV. Timing of laparoscopic surgery in gallstone pancreatitis. Arch Surg 1995;130:496-9.  Back to cited text no. 55    
56.McGrath MF, McGrath JC, Gabbay J, Phillips EH, Hiatt JR. Safe laparoendoscopic approach to biliary pancreatitis in older patients. Arch Surg 1996;131:826-31.  Back to cited text no. 56  [PUBMED]  
57.Liu CL, Lo CM, Fan ST. Acute biliary pancreatitis: diagnosis and management. World J Surg 1997;21:149-54.  Back to cited text no. 57  [PUBMED]  [FULLTEXT]
58.Soper NJ, Brunt LM, Callery MP, Edmundowicz SA, Aliperti E. The role of laparoscopic cholecystectomy in the management of acute gallstone pancreatitis. Am J Surg 1994;167:42-50.  Back to cited text no. 58    
59.Anderoli M, Sayegh SK, Hoefer R, Mathews G, Man WJ. Laparoscopic cholecystectomy for recurrent gallstone pancreatitis during pregnancy. South Med J 1996;89:1114-5.  Back to cited text no. 59    

Correspondence Address:
Ibrahim Abdulkarim Al-Mofleh
Gastroenterology Division (59), King Khalid University Hospital, P.O. Box 7805, Riyadh 11472
Saudi Arabia
Login to access the Email id

Source of Support: None, Conflict of Interest: None

PMID: 19864778

Rights and PermissionsRights and Permissions


  [Figure - 1], [Figure - 2]

  [Table - 1]


    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
    Email Alert *
    Add to My List *
* Registration required (free)  

    General Principl...
    Treatment of loc...
    Other therapeuti...
    Article Figures
    Article Tables

 Article Access Statistics
    PDF Downloaded2    
    Comments [Add]    

Recommend this journal