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Holzheimer RG, Mannick JA, editors. Surgical Treatment: Evidence-Based and Problem-Oriented. Munich: Zuckschwerdt; 2001.

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Surgical Treatment: Evidence-Based and Problem-Oriented.

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Acute pancreatitis

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Acute pancreatitis

Acute pancreatitis is an acute inflammation of the pancreas resulting from an auto-digestion of the gland. In 75–80% of cases acute pancreatitis is a self-limiting disease which subsides spontaneously, but 20–25% of acute pancreatitis are severe, characterized by the development of pancreatic or peri-pancreatic necrosis, resulting in general and local complications responsible for a mortality rate of 8 to 35% (1, 2).

Etiology - pathogenesis

The main causes of acute pancreatitis are alcohol intake and gallstones. Other causes have been implicated: hyperlipemia, trauma of the pancreas, infectious diseases, drugs, postoperative pancreatitis, pancreatitis induced by ERCP or endoscopic sphincterotomy, congenital anomalies such as pancreas divisum.

The pathogenic phenomenons leading to autodigestion of the pancreas and surrounding tissues result from premature activation of pancreatic enzymes. The mechanisms by which intracellular activation of enzymes occur, irrespective of the etiology of pancreatitis, remain unclear (3).

Severe pancreatitis develops in two phases: a first phase characterized by the consequences of systemic inflammatory response resulting in organ failures, and a second phase dominated by the local complications of pancreatic and peri-pancreatic auto-digestion, mainly infection of fluid collections and necrosis. Infection of necrosis is the major cause of death (4).


The diagnosis of acute pancreatitis is usually easy: rapid onset of unremitting abdominal pain radiating to the back in 40–70% of patients, associated with vomiting. Physical examination may seem relatively poor compared with the importance of pain and often finds a moderate abdominal tenderness. in severe forms. An increase of serum pancreatic enzymes (amylase, lipase) is usually present.

Plain X rays of the abdomen may show a dilatation of the small bowel in the left hypocondrium.

CT scan is not necessary for the diagnosis of acute pancreatitis. It may be helpful when there is no rise of pancreatic enzymes or in post-operative pancreatitis.


The Atlanta classification is the new, clinically based classification of acute pancreatitis (5).

Acute pancreatitis

  • mild
  • severe

Interstititial edematous pancreatitis

is characterized by interstitial edema associated infrequently with fat necrosis.

necrotizing pan creatitis

  • sterile
  • infected

The main feature is necrosis of the pancreas and/or peripancreatic tissues. Necrosis can be sterile or infected.

Fluid collections

are defined as collections occurring early in the course of pancreatitis with no defined wall. More than half of these fluid collections disappear spontaneously in the course of the disease.

Post-acute pseudocysts

are defined as a collection of pancreatic juice limited by a fibrotic wall.

Pancreatic abscess

is a circumscribed collection of pus with minimal or no necrotic debris, developed in the peripancreatic spaces.


Severity of acute pancreatitis cannot be assessed only by clinical presentation because extra-pancreatic complications, although more frequent in necrotizing pancreatitis, may be observed in mild pancreatitis (6). Many scoring systems have been described to differentiate between mild and severe pancreatitis.

Multiple prognostic factors

Specific: some multiple scoring systems have been assessed in patients with acute pancreatitis. The Ranson (PPV: 94%, NPV: 80%) and Glasgow (PPV: 57%, NPV: 90%) scores have been thoroughly evaluated and remain a reference for evaluation of severity. The presence of 3 or more criteria, in each system, indicates a severe pancreatitis (7, 8).

Non specific prognostic factors: The Acute Physiology and Chronic Health Evaluation score (APACHE score) was developed to evaluate critically ill patients in intensive care units. This score and other scores derived from it (APACHE II score, SAPS: Simplified Acute Physiology Score) are as accurate as specific scores in determining severity of acute pancreatitis (9, 10). An APACHE II score exceeding 8 points indicates a severe form of pancreatitis.

The specific multiple factors scoring systems requiring 48 hours to be established and APACHE II score comprising 14 parameters, more practical scoring systems have been developed.

Single prognostic factors

Numerous biological parameters (pancreatic enzymes, markers of the inflammatory response) have been shown to have prognostic significance but cannot be measured routinely. Among the routinely available laboratory examinations the most reliable is C reactive protein (CRP) which rises significantly at 48 hours after onset of pancreatitis. The cut-off point discriminating between mild and severe pancreatitis varies from 100 mg/l to 210 mg/l.

Imaging techniques

Computed tomography (CT scan)

The introduction of CT scan realized a revolution in the prognostic evaluation of acute pancreatitis. Ranson and Balthazar described two scoring systems. The first one was based on the presence of extra-pancreatic collections and the second associated both extra-pancreatic collections and non-enhancement of the pancreas on angioscanner (11).


Ultrasonography gives less precise informations on pancreatic and peri-pancreatic lesions than CT-scan but is necessary for the search of gallstones. It may be helpful to guide percutaneous fine-needle aspiration of collections or insert drains.

Magnetic Resonance Imaging

MRI gives informations equivalent to that of CT scan but its prognostic value is not yet thoroughly evaluated in acute pancreatitis


The aim of treatment is to treat and try to prevent the systemic manifestations of the first phase and detect the occurrence of local infection which will require surgical treatment during the second phase. The type of treatment depends on the severity of pancreatitis. In mild pancreatitis, general complications occur in less than 10% of patients and pancreatic inflammation subsides spontaneously. In severe pancreatitis intensive-care measures are required and must be associated with treatment of local infection.

Intensive-care measures

Their aim is to treat organ failures. Up to now, no treatment reducing the inflammatory response, antienzymes therapy or measures inducing a decrease of pancreatic secretions (somatostatine, nasogastric suction) were shown to improve the prognosis.

Hypovolemia is treated by perfusion of crystalloid and colloid solutions that are sufficient in most cases. Human albumin may be indicated when there is a severe hypoprotidemia.

Controlled ventilation is often necessary and may be prolonged in patients with ARDS.

Nutritional support is essential in the treatment of severe acute pancreatitis which realize an hypermetabolic state. Parenteral nutrition is used at the beginning of the disease when ileus precludes enteral nutrition. Enteral nutrition is started as soon as possible via a surgical feeding jejunostomy or a feeding tube placed in the jejunum under fiberoptic guidance. The advantages of enteral nutrition are the protection of the gut-mucosal barrier and the decrease of bacterial translocation which causes infection of pancreatic and peri-pancreatic necrosis and fluid collections (12).

The role of antibiotics in preventing infection of necrosis is not yet demonstrated. Four prospective, randomized studies showed a decrease in the number of extra-pancreatic infections and pancreatic infections but no decrease in the mortality rate. Antibioprophylaxy using digestive decontamination resulted in a decrease of pancreatic infection with no reduction of the mortality rate (13).

Treatment of local complications

Early extensive pancreatomies have been abandoned because of an unacceptable mortality rate (30–50%) and because they did not reach their aim that was to prevent initial systemic complications by resection of the necrotic pancreas, nor late local infectious complications (14). Resection of sterile pancreatic necrosis is unnecessary and may aggravate the prognosis (15).

At present, for most authors, the indication for surgical drainage is infection of necrosis.

The diagnosis of local infection is difficult. Clinical parameters do not allow to discriminate between sterile and infected necrosis. Hyperleucocytosis, fever, organ failures resulting from the inflammatory response, can be observed in sterile pancreatic necrosis. The diagnosis of infection relies on bacteriological studies of aspirates yielded by percutaneous aspiration under CT scan or ultrasonography guidance. Percutaneous aspiration gives the right bacteriological status in 90% of cases. When several collections or pancreatic areas of hypodensity are present all of them must be examined unless there is a technical impossibility (interposition of digestive or vascular structures). Percutaneous aspirations can be performed systematically every 3 or 4 days or when clinical signs of sepsis are present (16).

Several techniques of drainage have been proposed:

  • Percutaneous drainage: it is best indicated for the treatment of infected fluid collections, especially for pancreatic abscesses. Nonetheless, the presence of necrotic debris, often associated with fluid collections, justify the use of large drains (> 20 french). It has no indication in the treatment of sterile fluid collections because of an almost constant occurrence of superinfection (17).
  • Surgical drainage: it must remove all necrotic material and collections. Necrosectomy can be performed through a transperitoneal or a retroperitoneal approach (18, 19). Most often several operations are necessary to remove all necrotic tissues. The choice of the surgical approach depends on the location of necrosis and collections. Retroperitoneal approach is best indicated when collections develop to the left. Some authors favor planned relaparotomies, others reoperate only if clinical, biological and radiological parameters lead to a suspicion of persisting infected collections and necrosis. Laparoscopic techniques are not yet widely used but allow a limited approach, thus avoiding large wound dehiscence and bowel fistulas.

Etiological treatment

It concerns mainly biliary pancreatitis and its modalities are based on the severity of pancreatitis.

In mild pancreatitis, most authors recommend biliary surgery during the same admission, after normalization of clinical and biological parameters. Laparoscopic cholecystectomy is associated with peroperative cholangiography which can show a common bile duct stone. When operation is performed within 48 hours of onset of pancreatitis, common bile duct stones are found in up to 75% of patients, falls to 45% between day 2 and 4 and to 5% between day 5 and 7 because of spontaneous duodenal migrations of stones.

In severe pancreatitis, early biliary surgery worsens the prognosis (20). It has been suggested that early ERCP (Endoscopic Retrograde Cholangio-Pancreatography) associated with ES (Endoscopic Sphincterotomy) may improve the evolution by decompressing the pancreatic duct obstructed by the migrating gallstone. Three prospective, randomized studies have been performed to assess the role of early ERCP and ES. Morbidity is decreased by this approach but there is no difference in mortality or percentage of infected necrosis. The only indication of urgent ERCP and ES is the presence of acute cholangitis (21).


Beger H G, Büchler M, Bittner R. et al. Necrosectomy and postoperative local lavage in patients with necrotizing pancreatitis: results of a prospective multicentre trial. World J Surg. (1998);12:255–262. [PubMed: 3394351]
D'Edigio A, Schein M. Surgical strategies in the treatment of pancreatic necrosis and infection. Br J Surg. (1991);78:133–137. [PubMed: 2015459]
Steer M L. How and where does pancreatitis begin? Arch Surg. (1992);127:1–4. [PubMed: 1280081]
Renner I A, Savage W T, Pantoja J L, Renner V J. Death due to acute pancreatitis. A retrospective analysis of 405 autopsy cases? Dig Dis Sci. (1985);30:1005–1018. [PubMed: 3896700]
Bradley E L III. A clinically based classification system for acute pancreatitis. Arch Surg. (1993);128:586–590. [PubMed: 8489394]
Rau B, Pralle U, Uhl W, Schoenberg M H, Beger H G. Management of sterile necrosis in instances of severe acute pancreatitis. Am J Coll Surg. (1995);181:279–288. [PubMed: 7551320]
Ranson H C, Rifkind K M, Turner J W. Prognostic signs and nonoperative peritoneal lavage in acute pancreatitis. Surg Gynecol Obstet. (1976);143:209–219. [PubMed: 941075]
Blamey S L, Imrie C W, O'Neill J, Gilmour W h, Carter D C. Prognostic factors in acute pancreatitis. Gut. (1984);25:1340–1346. [PMC free article: PMC1420197] [PubMed: 6510766]
Knaus W A, Draper E A, Wagner D P, Zimmerman J E. APACHE II: a severity of disease classification. Crit Care Med. (1985);13:218–229. [PubMed: 3928249]
Le Gall J R, Loirat P, Alperovitch A. et al. A simplified acute physiologic score for intensive care patients. Crit Care Med. (1984);12:975–977. [PubMed: 6499483]
Balthazar E J, Robinson D L, Megibow A J, Ranson J H C. Acute pancreatitis: value of CT in establishing prognosis. Radiology. (1990);174:331–336. [PubMed: 2296641]
Sigurdsson G. Prevention of sepsis and multiple organ failure in critically ill patients. Acta Anaesthesiol Scand. (1995);39 (suppl 105):23–30.
Bassi C, Falconi M, Talami G. et al. Controlled clinical trial of pefloxacin versus imipenem in severe acute pancreatitis. Gastroenterology. (1998);115:1513–1517. [PubMed: 9834279]
Pellegrini A C. The treatment of acute pancreatitis: a continuing challenge. N Engl J Med. (1985);312:436–438. [PubMed: 3969098]
Mier J, Lucque-de Léon E, Castillo A, Robledo F, Blanco R. Early versus late necrosectomy in severe necrotizing pancreatitis. Am J Surg. (1997);173:71–75. [PubMed: 9074366]
Rau B, Pralle U, Mayer J M, Beger H G. Role of ultrasonographically guided fine-needle aspiration cytology in the diagnosis of infected necrosis. Br J Surg. (1998);85:179–184. [PubMed: 9501810]
Paye F, Rotman N, Radier C, Nouira R, Fagniez P L. Percutaneous aspiration for bacteriological studies in patients with acute pancreatitis. Br J Surg. (1998);85:755–759. [PubMed: 9667700]
Bradley E L III. A fifteen year experience with open drainage for infected pancreatic necrosis. Surg Gynecol Obstet. (1993);177:215–222. [PubMed: 8356492]
Fagniez P L, Rotman N. Retroperitoneal approach to the management of necrotizing pancreatitis. Problems in General Surgery. (1997);13:146–152.
Kelly T R, Wagner D S. Gallstones pancreatitis: a prospective randomized trial of the timing of surgery. Surgery. (1988);104:600–605. [PubMed: 3175860]
Fölsh U R, Nitsche R, Lüdke R, Hilgers R A, Creutzfeld W. the German Study Group on Acute Biliary Pancreatitis. Early ERCP and papillotomy compared with conservative treatment for acute biliary pancreatitis. N Engl J Med. (1997);336:237–242. [PubMed: 8995085]
Copyright © 2001, W. Zuckschwerdt Verlag GmbH.
Bookshelf ID: NBK6932


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