NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.

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

Cover of Surgical Treatment

Surgical Treatment: Evidence-Based and Problem-Oriented.

Show details

Early complications of severe acute pancreatitis

, , , and .

Author Information

20% of cases of acute pancreatitis are clinically severe (SAP), associated with a high morbidity and mortality.

In most cases this clinically severe form corresponds to the pathological picture of pancreatic necrosis. Here surgery may take on a fundamental therapeutic role (3, 4).

Early complications

SAP can be seen as a biphasic disease: firstly the “early” or “toxico-enzymatic” phase - generally in the first two weeks and then, the “later” or “septic” phase - from the third to fourth week onwards.

Not all cases of pancreatic necrosis, however, are infected, whereas all, present a toxic phase to different extent. This may range from rapidly self-limiting situations or situations immediately responsive to abundant rehydration, to the swift evolution of severe systemic inflammatory response syndrome (SIRS) and multi-organ failure (MOF) with sterile necrosis.

We have learnt - particularly as a result of the advent of computerized tomographic (CT) imaging - that there is not necessarily any direct correlation between morphological and clinical severity of SAP. Typically, indeed, in the socalled fulminating forms CT scans are not yet characterized by a frank necrotic component, because definite demarcation of the necrosis takes a longer time.

Pancreatic toxemia is the result of the release of the “pancreatic broth” into the bloodstream, being responsible for the impairment of cardiocirculatory, pulmonary, renal, and central nervous system functions, and its reabsorption by the retroperitoneum and peritoneum. In the first two weeks the clinical situation may vary, affecting one or more organ systems and sometimes super-imposing itself upon or mimicking early sepsis (sepsis-like syndrome).

In these situations, the presence of infected necrosis must be confirmed by radiologically guided fine-needle aspiration and bacteriological cultures of the specimens, since the presence of pathogenic bacteria is an absolute indication for surgery (1, 2).

Table I summarizes the main complications in the early phases of SAP necessitating prompt surgical intervention.

Table I. Early complications in SAP (within the first 2 weeks).

Table I

Early complications in SAP (within the first 2 weeks).

Early surgery

Early complications are defined by us as those occurring within the first 15 days of disease (1, 2).

Biliary obstruction

The endoscopist has a better view than the surgeon of both the papilla and the bile sludge (surgically impalpable and radiologically difficult to demonstrate intraoperatively).

In all forms of biliary SAP emergency endoscopic surgery (ES) within 36–48 hours is mandatory (Neoptolemos 1994), before the pancreatic damage becomess “ireversible”. With ES it is possible to improve the patients clinical course, possibly avoiding open surgery in some cases.

“Open” treatment is necessary only in those unfortunate cases in which ES has failed. Though a recent Spanish multicentre study reports a mortality rate of 29.4% for early surgery versus a zero mortality rate for delayed surgery for biliary SAP, according to the current opinion the timing of surgery is not a critical factor for the outcome of severe gallstone pancreatitis (Kg 1988).

It can be inferred from a review of the literature that the patients operated on earlier are operated in this phase because they had more severe disease than those treated later, and that only in those treated early (approximately 20% of cases) choledochal stones could be found. In most cases of biliary SAP the “criminal” stone has already passed (14). Ideally, however, the patients labeled as “biliary” by ultrasonographic and particularly by laboratory findings, should, if affected by the severe form, be treated with ES and then, as soon as the pancreatitis has subsided, should undergo laparoscopic cholecystectomy. We have adopted this policy in view of the fact that the relapse risk during the traditionally suggested six-to-eight-week waiting period has been found to range from 20 to 60% (13).

Multi-organ failure (MOF), failure to improve, deterioration

Among the more controversial indications for early surgery is progressive clinical deterioration and severe SIRS despite adequate support therapy.

This situation is often associated with very extensive sterile necrosis, since MOF due to infected pancreatic necrosis is rare in the early phase and typically manifests itself from the third week onwards.

There are no reliable clinical guidelines for the surgeon (51). Even the use of scoring systems, such as for instance APACHE II, rather than simple clinical observation, does not seem to make a contribution. The scale of the problem is now somewhat less serious than it was, in that many patients who were once doomed to die within 36–48 hours now survive the early toxic phase thanks to sophisticated resuscitation techniques. Those who “fare badly” today, however, are the exremely ill.

We believe that in these critically ill and rapidly deteriorating cases an attempt at surgery, however disparate, is justified to remove the endo-retroperitoneal “enzymatic broth” responsible for the toxemia (11, 12). Unfortunately, it is impossible to find scientific evidence definitely supporting this approach, partly because the planning of prospective, randomized, controlled trials is ethically questionable and also limited in its statistical validity due to the small numbers of patients who can be recruited over a reasonable time period.

In one non-randomized study (8) no statistically significant difference in mortality rates between operated and not operated patients (46 vs. 31%) was found, but in view of the low number of patients and the fact that the surgical timing was not exactly early (20.5 days after onset of disease) no conclusive indications can be established.

Neither could the pancreatic resection techniques used in a Finnish study (17) modify the outcome in patients with MOF depending upon their early or late implementation.

We treated 59 patients for MOF unresponsive to intensive medical therapy within the first two weeks of the disease, using the procedure defined as retro-endoperitoneal drainage and postoperative lavage (11, 12). We had a mortality rate of 30.5% (18/59 patients) which seems acceptable in view of the severity of disease (mean Ranson score 4.9 and mean APACHE II score 19.1).

In conclusion, not all patients with MOF in the course of SAP will benefit from early surgery.

Theoretically, in these cases, peritoneal lavage might potentially exert a beneficial effect, but it is not aimed at the retroperitoneum, the main site of the inflammatory-toxic process. Despite initial enthusiasm for this approach (15), there have been no satisfactory results later (7).

Early infected necrosis

Among the cases of infected SAP treated in our department only 15% have shown signs of infection in the first two weeks of the disease, thus confirming what we have already said about the typical timing of onset of this complication.

The therapeutic principles are the same as in later infections, though it is important to recall that recognition of this complication may be rendered more difficult by the simultaneous presence and activity of toxemia. Generally, in these particular patients a delay in the diagnosis may prove fatal.

Hemorrhage and peritonitis

A decision to operate or, in selected cases, for angiographic embolization, appears indisputable in those fortunately rare cases who bleed, whereas the clinical picture of peritonitis (on an enzymatic basis) must be carefully assessed before opting for a surgical solution. The later mentionel patients often improve or even recover after the acute phase after 24–48 hours of intensive medical therapy.

Peritonitis itself in the course of SAP is not an absolute indication of laparotomy.

Occasionally, a diagnostic laparatomy to exclude other etilogies of the “acute abdomen” may be required. Explorative laparotomy seems not to exacerbate the pancreatitis, though, understandably, it may “convert” sterile necrosis to infected pancreatic necrosis (14).

Extensive sterile necrosis

For most authors sterile necrosis extending to more than 50% of the pancreatic volume is a possible surgical indication (14).

We agree with others (14), that the extent of necrosis, which can be reliably estimated by CT findings and C-reactive protein levels, is highly indicative of the risk of infection itself. However, since there is no direct correlation between morphological and clinical severity, the extent of the necrosis itself cannot be used as a basis for a surgical indication, especially in the early situation.

In contrast to the data reported by Warshaw's team (16) - who claim that early debridement of sterile necrosis is beneficial - others report that in a prospective study of eleven patients with extensive sterile necrosis, medical therapy was successful even in cases with additional pulmonary and renal failure (3, 4).

Thus, pancreatic necrosis even when accompanied by organ failure, is not an absolute indication for surgery.

Identification of predictive prognostic factors is important in order to be able to better tarfon therapy approaches to particular disease severity scores. In this sense shock appears to be the most negative prognostic factor (8).

Rupture of Wirsung duct

Rupture of the Wirsung's duct is viewed by some as an indication, for a resective procedure, in that drainage would inevitably expose the patient to the formation of an external pancreatic fistula. Today with endoscopic retrograde cholangiopancreatography (FRCP) it can be demonstrated that in the acute phase of SAP the main duct is actually more frequently involved than it was once believed (10). In our experience it seems to be more reasonable to wait one to two months after the acute pancreatitis has subsided and then to drain the pseudocyst (the “natural” outcome of Wirsung rupture), than to try to treat the lesion in the acute phase of SAP. This appears more prudent than resectionwith its associated high morbidity and mortality rates is proposed.


Whereas in the 1970s surgery was believed to be the only treatment providing some chance of survival in necrotizing SAP, in recent years the more conservative approach has led to a new judgement of surgical timing, now depending much more on the actual nature of the complications. In the initial phase of the disease, severe toxemia with subsequent MOF and early clinical deterioration may demands early surgery. The - generally later occurring - onset of infected necrosis will lead to later surgery.

One rule, however, is now universally accepted by all surgeons operating on the pancreas: the longer you wait, or rather the longer you can wait, the better it will be in terms of reducing intraoperative complications and perioperative morbidity.

With the passing of hours, days, and, even better, weeks, the necrotic foci are progressively isolated from the bloodstream, forming areas of parenchymal sequestration allowing the surgeon to give up earlier necrosectomy with its associated risks of hemorrhage and fistula formation in favor of later and safer sequestrectomy by “digitoclasia” (1, 2).


Bassi C. Infected pancreatic necrosis. Int J Pancreatol. (1994);16:1–10. [PubMed: 7806908]
Bassi C, Falconi M, Sartori N, Bonora A, Caldiron E, Butturini G, Salvia R, Pederzoli P. The role of surgery in the major early complications of severe acute pancreatitis. Eur J Gastroenterol Hepat. (1997);9:131–136. [PubMed: 9058622]
Bradley E L, Allen K. A prospective longitudinal study of observation versus surgical intervention in the management of necrotizing pancreatitis. Am J Surg. (1991);161:19–25. [PubMed: 1987854]
Bradley E L. A clinically based classification system for acute pancreatitis: summary of the Atlanta Symposium. Arch Surg. (1993);128:586–590. [PubMed: 8489394]
D’Egidio A, Schein M. Surgical strategics in the treatment of pancreatic necrosis and infections. Br J Surg. (1991);78:133–137. [PubMed: 2015459]
Fernandez-Cruz L, Navarro S, Valderrama R. et al. Acute necrotizing pancreatitis: a multicenter study. Hepatogastroenterology. (1994);41:185–189. [PubMed: 8056412]
Imrie C W. Peritoneal lavage in severe acute pancreatitis. Br J Surg. (1985);72:677–680. [PubMed: 4041722]
Karimgani I, Kathaleen A, Porter A, Langevin R E, Banks F A. Prognostic factors in sterile pancreatic necrosis. Gastroenterology. (1992);103:1636–1640. [PubMed: 1426885]
Kim U, Shen H Y, Bodner B. Timing of surgery for acute gallstone pancreatitis. Am J Surg. (1988);156:393–396. [PubMed: 2461106]
Neoptolemos JP, Bain IA, Sagar G (1994) Endoscopic retrograde cholangiopancreatography in acute pancreatitis. In: Pederzoli P, Bassi C, Cavallini G (eds) Facing the Pancreatic Dilemma. Springer, Berlin Heidelberg, pp 433–447 .
Pederzoli P, Bassi C, Vesentini S. et al. Retroperitoneal and peritoneal drainage and lavage in the treatment of severe acute pancreatitis. Surg Gynecol Obstet. (1990);170:197–203. [PubMed: 2305344]
Pederzoli P, Cavallini G, Bassi C, Falconi M (1994) Sterile necrosis: surgical indications? In: Pederzoli P, Bassi C, Cavallini C (eds) Facing the pancreatic dilemma. Springer, Berlin Heidelberg, pp 43–65 .
Pellegrini C A. Surgery for gallstone pancreatitis. Am J Surg. (1993);165:515–518. [PubMed: 8480893]
Poston G J, Williamson C N. Surgical management of acute pancreatitis. Br J Surg. (1990);77:5–12. [PubMed: 2405934]
Ranson J H C, Spencer F C. The role of peritoneal lavage in severe acute pancreatitis. Ann Surg. (1978);187:565–575. [PMC free article: PMC1396548] [PubMed: 646497]
Rattner D W, Legermate D A, Lee M J, Mueller P L, Warshaw A L. Early surgical debridement of symptomatic pancreatic necrosis is beneficial irrespective of infection. Am J Surg. (1992);163:105–110. [PubMed: 1733356]
Teerenhovi O, Nordback I, Isolauri J. Influence of pancreatic resection on systemic complications in acute pancreatitis. Br J Surg. (1988);75:793–795. [PubMed: 3167531]
Copyright © 2001, W. Zuckschwerdt Verlag GmbH.
Bookshelf ID: NBK6978


  • PubReader
  • Print View
  • Cite this Page

Related information

  • PMC
    PubMed Central citations
  • PubMed
    Links to PubMed

Recent Activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...