Management of acute pancreatitis and complications

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Chapter 54 Management of acute pancreatitis and complications

Maxim S. Petrov, Benjamin Loveday, John A. Windsor

Overview

The severity of acute pancreatitis (AP) varies from mild uncomplicated disease to critical disease associated with both local and systemic complications (see Chapters 52 and 53). It is important to determine the severity of acute pancreatitis in the individual patient for triage, treatment, and prognosis. Since 1992, when the International Symposium on Acute Pancreatitis in Atlanta published its consensus, it has become customary to define the severity of acute pancreatitis as either mild or severe (Bradley, 1993). Acute pancreatitis is severe when it is associated with local or systemic complications. Although the Atlanta classification was a significant advance, it is now accepted that the dichotomous approach fails to capture clinically relevant categories of patients (Petrov & Windsor, 2010). For instance, it does not allow for discrimination among patients with transient and persistent organ failure, those with sterile and infectious local complications, and those with either local or systemic complications.

A large body of evidence now demonstrates that the two key determinants of severity in acute pancreatitis are organ failure—absent, transient, or persistent—and pancreatic complications—absent, noninfectious, or infectious. Determinants-based classification of the severity of acute pancreatitis composed of four categories (Table 54.1) appears to be more useful for the clinical assessment of severity in individual patients and for comparing groups of patients (Petrov & Windsor, 2010). The distinct advantages of this new classification is that it uses widely accepted and unambiguous terms, it can be applied in both early and late phases of acute pancreatitis, it can facilitate communication between treating physicians, and it promotes standardization for management of acute pancreatitis (Petrov et al, 2010).

Table 54.1 Determinants-Based Classification of Acute Pancreatitis

Although many aspects of the management of acute pancreatitis remain controversial, significant overall progress has been made during the last few decades, evidenced by a reduction in morbidity and mortality rates (Lowenfels et al, 2009; Banks & Freeman, 2006). The improved outcomes have not been due to any treatments based on specific, critical pathophysiology. A wide range of drugs has been evaluated in randomized controlled trials (RCTs) and have proved ineffective in the treatment of acute pancreatitis. These include aprotinin, atropine, calcitonin, fresh frozen plasma, glucagon, gabexate, glucocorticoids, lexipafant, nonsteroidal antiinflammataory drugs (NSAIDs), and octreotide. The overall improvement in outcome for patients with acute pancreatitis has been due to a combination of factors that include improvements in intensive care medicine, imaging techniques, severity prediction, and selection of patients for endoscopic retrograde cholangiopancreatography (ERCP) and surgery.

This chapter describes the current management of acute pancreatitis, and considerable opportunities remain for improvement. The discussion of the evidence base for current practice will highlight these points.

General Management

Pain Management

Pain is the cardinal symptom of acute pancreatitis, and its relief is a clinical priority. The strategy in patients with acute pancreatitis, as for all acute pain, is the staged use of analgesics. Although some debate still surrounds step-up and step-down approaches, it is best practice to use NSAIDs for the management of mild pain (Pezzilli et al, 2007). The potential risk of bleeding as a result of the antiplatelet effect of NSAIDS has not been an issue in practice. For patients with moderate and severe pain, and for those for whom NSAIDs are inadequate, the second step is to use a weak opioid; the third step is to use a strong opioid.

Although experimental findings show that morphine can induce spasm of the sphincter of Oddi and exacerbate the severity of acute pancreatitis, it is worth noting that the avoidance of morphine as an analgesic has not been supported by clinical studies (Economou & Ward-McQuaid, 1971). A comprehensive review of the literature shows that all opiates increase the pressure in the sphincter of Oddi but that physiologic effect is of marginal clinical relevance (Thompson, 2001).

In practice, patients with severe acute pancreatitis require intravenous analgesia, and patient-controlled analgesia should be considered. Epidural analgesia can be considered for patients with severe and critical acute pancreatitis who require high doses of opioids for an extended period. Oral analgesics can be introduced but are less helpful in the acute setting because of the longer onset of action and concerns about variable absorption. Because the pain in acute pancreatitis is continuous, oral analgesics should be prescribed at regular intervals that are at least equal to the half-life of the drug. Although it has been reported that analgesics can also be given transdermally or rectally, no RCTs have compared the different routes of administration of the same analgesic in patients with acute pancreatitis.

Different analgesics have been compared in patients with acute pancreatitis, and the six published RCTs are summarized in Table 54.2 (Blamey et al, 1984; Ebbehoj et al, 1985; Jakobs et al, 2000; Kahl et al, 2004; Peiro et al, 2008; Stevens et al, 2002). These trials had a different study design, evaluated different analgesics, and had small sample sizes; only three of the trials were double-blinded. From these studies it can be said that no credible clinical evidence supports avoiding the use of morphine in treating the pain associated with acute pancreatitis; however, the NSAID of choice is metamizole (2 g/8 h IV), and the opioid of choice is buprenorphine (0.3 g/4 h IV). There is no evidence to support the use of parenterally administered local anesthetics such as procaine in the management of pain associated with acute pancreatitis. However, the lack of high-quality evidence means that the choice of analgesic and the strategy for administration remain uncertain. No recent guidelines relating to the management of acute pancreatitis provide a specific recommendation regarding pain management (Loveday et al, 2010).

Table 54.2 Randomized Controlled Trials of Analgesics in Patients with Acute Pancreatitis

Fluid Resuscitation

Acute pancreatitis can be associated with substantial third-space fluid losses, and the resultant hypovolemia that impairs the microcirculation of the pancreas is a major determinant of pancreatic necrosis. The reflex splanchnic vasoconstriction in response to hypovolemia may compound pancreatic hypoperfusion and further predispose to ischemia. Fluid resuscitation is one of the most important aspects of the early management of acute pancreatitis (Gardner et al, 2008; Talukdar & Vege, 2009) and is the intervention most likely to improve outcome. No high-level evidence describes the optimal resuscitation fluid, required fluid rate, or best marker to guide resuscitation and indicate its adequacy (Banks & Freeman, 2006; Pandol et al, 2007). It is not even known whether colloids or crystalloids are more effective in improving pancreatic microcirculation and outcome. The initial goal of fluid resuscitation is to restore circulating blood volume (euvolemia), with the aim of normalizing heart rate, blood pressure, central venous pressure, and urine output, even though these do not reflect the adequacy of pancreatic and splanchnic perfusion (Flint & Windsor, 2003). In general, urine output should be restored at greater than 0.5 mL/h/kg body weight, and the central venous pressure should be restored to between 8 and 12 cm H₂O. Swan-Ganz monitoring can be helpful in hemodynamically unstable patients, and some evidence shows that as an independent risk factor of pancreatitis severity and a marker of hydrations status, hematocrit might be useful with fluid resuscitation (Pitchumoni et al, 2005; Wu et al, 2009). Adequate fluid resuscitation is likely when the hematocrit is restored to between 30% and 35%. A number of other approaches to guide resuscitation offer promise but have not become established in clinical practice. An example is the use of intramucosal pH (pHi) derived by nasogastric tonometry (Juvonen et al, 2000a; van Haren et al, 2007), which is predictive of severity and reflects the adequacy of perfusion in the splanchnic circulation.

Antibiotics

Although the use of broad-spectrum antibiotics to treat the established infection in acute pancreatitis is a well-established practice, the use of prophylactic antibiotics has been controversial for decades. Three RCTs in the 1970s failed to demonstrate a beneficial effect of antibiotic prophylaxis, probably because of a small sample size, inappropriate selection of antibiotics—such as ampicillin, which does not sufficiently penetrate the pancreas—and inclusion of patients with mild pancreatitis (Table 54.3; Craig et al, 1975; Finch et al, 1976; Howes et al, 1975). Between 1993 and 2009, several randomized, controlled, open-label trials were published evaluating the efficacy of prophylactic antibiotic treatment in patients with severe acute pancreatitis (Delcenserie et al, 1996; Pederzoli et al, 1993; Rokke et al, 2007; Sainio et al, 1995; Schwarz et al, 1997; Spicak et al, 2003; Xue et al, 2009). The results of these trials were conflicting. Although some RCTs demonstrated a significant reduction of infectious complications and mortality with the use of prophylactic antibiotics, others failed to do so (see Table 54.3). Only three double-blind, placebo-controlled RCTs were published between 2004 and 2009, and all of them were unable to show a beneficial effect of antibiotic prophylaxis regarding infectious pancreatic complications, the need for surgery, and mortality (Dellinger et al, 2007; Garcia-Barrasa et al, 2009; Isenmann et al, 2004). This is in line with the findings of a meta-analysis that showed an inverse relationship between methodologic quality of the studies and impact of antibiotic prophylaxis on mortality (de Vries et al, 2007).

Table 54.3 Randomized Controlled Trials of Intravenous Antibiotic Prophylaxis vs. No Antibiotics in Patients with Acute Pancreatitis

On the other hand, it is worth noting that the three double-blind RCTs mentioned were not without flaws. These include a large crossover to open-label antibiotics in the control group (i.e., a high percentage of patients in the placebo group were treated with intravenous antibiotics) and the inclusion of patients on the basis of predicted severity of acute pancreatitis rather than proven necrotizing pancreatitis. All the studies were underpowered because the power calculation was based on an infection rate of 40%, whereas the actual infection rates in the placebo groups of the trials were only 12% to 17%.

Several attempts have been made to statistically aggregate data on the use of prophylactic antibiotics in acute pancreatitis. Although only two new RCTs were published from 2006 through 2007, it is notable that seven of the 10 meta-analyses were published within this period (Petrov, 2008). Thirteen RCTs were included in these seven meta-analyses. Because of different inclusion criteria and various meta-analysis techniques used, concordance is lacking, and they provide contradictory recommendations regarding the role of prophylactic antibiotics in reducing the risk of pancreatic infectious complications. Overall, it appears that the most recent studies do not support the use of prophylactic antibiotics to reduce the frequency of pancreatic infectious complications, surgical intervention, and death in patients with acute pancreatitis. Therefore routine broad-spectrum prophylactic antibiotics in patients with severe acute pancreatitis cannot be recommended on the basis of current evidence.

Nutritional Management

Severe acute pancreatitis is associated with a cytokine-mediated systematic inflammatory response and a hypercatabolic state (Windsor & Hammodat, 2000; see Chapter 10). The adverse consequences of this include protein-calorie malnutrition, expansion of the extracellular fluid compartment, and immune suppression. A meta-analysis of RCTs showed that nutritional support, both enteral and parenteral, significantly reduced risk of mortality in patients with acute pancreatitis compared with no nutritional support (Petrov et al, 2008c). Nutritional support is thus an essential part of the management of patients with severe acute pancreatitis (Banks & Freeman, 2006; Pandol et al, 2007).

Type of Feeding

The feasibility of providing nutritional support in patients with acute pancreatitis has been known for more than 3 decades. Parenteral nutrition (PN), rather than enteral nutrition (EN), became the standard of care because of the concept of “resting” the pancreas. The rationale for this was to prevent stimulating increased secretion of pancreatic proteolytic enzymes and exacerbating pancreatitis severity. But the use of PN has decreased in the face of well-recognized problems, such as catheter-related sepsis, the high cost of treatment, electrolyte and metabolic disturbances, villous atrophy and gut barrier failure with promotion of bacterial translocation, systemic sepsis, and multiple organ failure.

A number of RCTs compared total PN and total EN in the management of predicted severe AP (Table 54.4; Casas et al, 2007; Doley et al, 2009; Eckerwall et al, 2006; Gupta et al, 2003; Kalfarentzos et al, 1997; Louie et al, 2005; Petrov et al, 2006; Wu et al, 2010). A meta-analysis of high-quality RCTs has shown a significant twofold reduction in the risk of total and pancreatic infectious complications and a 2.5-fold reduction in the risk of death in patients receiving total EN (Petrov et al, 2008f). The basis for the clinical benefits of EN over PN remain unclear, although EN may prevent or attenuate mucosal barrier failure and bacterial translocation (Windsor & Hammodat, 2000). Intestinal permeability studies are a surrogate marker for clinically relevant events and provide conflicting results. Three clinical studies showed increased intestinal permeability to both micromolecules and macromolecules in patients with severe acute pancreatitis when compared with mild acute pancreatitis and healthy volunteers (Ammori et al, 1999; Juvonen et al, 2000b; Nagpal et al, 2006). But an early RCT from the United Kingdom (Powell et al, 2000) in which patients with predicted severe AP were randomized to receive either EN or no artificial nutritional support showed significantly increased intestinal permeability by day 4 in patients allocated to the EN group. Similarly, a recent RCT from Sweden comparing nasogastric EN and PN in patients with predicted severe acute pancreatitis demonstrated impaired gut permeability on day 3 in the EN group (Eckerwall et al, 2006). This difference might be explained by the inclusion of a considerable number of patients with mild AP in whom intestinal permeability is unlikely to change (Petrov et al, 2008f).

Table 54.4 Randomized Controlled Trials of Total Enteral vs. Total Parenteral Nutrition in Patients with Predicted Severe Acute Pancreatitis

Route of Enteral Feeding

Nasogastric (NG) tube insertion may be more practical than nasojejunal (NJ), as the latter often requires endoscopy or radiology expertise, the transfer of patients within the hospital, and a delay in starting feeding. However, NJ EN has been preferred to NG EN because of a fear about pancreatic stimulation. Pancreatic response to feeding was studied in human volunteers, and it was shown that all forms of EN, with the exception of NJ feeding, stimulate pancreatic secretion (O’Keefe et al, 2003). By contrast, a study in patients with acute pancreatitis showed a significantly lower rate of secretion of trypsin, amylase, and lipase in comparison with healthy subjects (O’Keefe et al, 2005). Moreover, it was shown that the greater the severity of acute pancreatitis, the greater the reduction in pancreatic enzyme secretion as a response to duodenal feeding, probably reflecting greater injury of acinar cell mass. The possible clinical implication of these findings is that NG EN may not aggravate the course of acute pancreatitis, as was previously suggested.

Two RCTs have compared NG EN with NJ EN in patients with severe acute pancreatitis (Eatock et al, 2005; Kumar et al, 2006). These studies demonstrated the feasibility, safety, and tolerance of NG EN, but a meta-analysis did not demonstrate a statistically significant reduction in risk of death (Petrov et al, 2008b). Before NG EN can be considered the standard of care in the nutritional support of patients with AP, a well-designed and adequately powered RCT comparing mortality and morbidity of NG EN and NJ EN is required. A practical compromise is to start EN through an NG tube after the patient has been resuscitated and for the tube to be advanced when endoscopic or radiologic assistance is available.

Type of Enteral Feeding

The concept of “pancreatic rest” has also influenced decisions about the type and content of enteral feeding. The preferred formulations, elemental and semi-elemental formulas (Roberts, 2001; Petrov, 2007), did not require pancreatic enzymes for digestion and absorption. However, the major disadvantage of elemental and semi-elemental formulas is the cost, which is reportedly threefold to sevenfold higher than that of polymeric formulas. A recent meta-analysis of RCTs compared these two formula types in terms of feeding intolerance, infectious complications, and mortality and found that the use of polymeric over elemental and semi-elemental feedings did not result in reduced tolerance in patients with acute pancreatitis and appeared to reduce the risk of infectious complications and death (Petrov et al, 2009a). Thus the use of elemental and semi-elemental formulas confers no apparent advantage over relatively inexpensive polymeric formulas.

Because the gastrointestinal tract is the largest immune organ, containing approximately 65% of the immune tissue in the body, it has been considered that the use of immune-enhanced enteral formulations might increase the beneficial effects of EN in acute pancreatitis (Bengmark, 1999; Schloerb, 2001). Several trials were performed in different clinical settings, which suggested that immunonutrition might have the potential to modify the inflammatory response. The results of RCTs that compared the use of immune-enhanced and standard enteral formulas were statistically aggregated in several meta-analyses (Beale et al, 1999; Heyland et al, 2001; Heys et al, 1999). The most recent and comprehensive systematic review of 2419 patients from 22 RCTs (Heyland et al, 2001) found that the effect of immune-enhancing EN may depend on the subset of the analyzed patients. In particular, no effect of immunonutrition on the risk of infectious complications or death was reported within the subgroup of critically ill patients. At the same time, administration of a formula high in arginine in a combined group of critically ill and elective surgery patients was associated with a statistically significant reduction in infectious complications and a trend toward lower mortality rates in comparison with other immune-enhancing diets. A recent meta-analysis of RCTs in patients with acute pancreatitis did not show any clinical beneficial effect of immunonutrition when compared with standard EN (Petrov et al, 2008a).

Tolerance of Enteral Feeding

Dieticians generally agree on the caloric target in patients with acute pancreatitis: 30 kcal/kg and 1.5 g/kg of protein daily based on ideal body weight (Andersson et al, 2009; Olah & Romics, 2008). To ensure tolerance of EN, it is usually commenced at a low rate of 25 to 30 mL/h and increased incrementally over a day or more, until the desired caloric intake is reached. Despite this approach, EN can be associated with feeding intolerance in some patients with acute pancreatitis. Most commonly, the intolerance manifests as abdominal distension, delayed gastric emptying, gastroesophageal reflux, and diarrhea, all of which may develop in the presence of sepsis or with a significant clinical deterioration. In general, tolerance is achieved when EN is provided without development of one of these complications (Bankhead et al, 2009; Mallampalli et al, 2000). Various strategies to improve tolerance to EN require clinical studies, which are also needed to investigate markers of gut motility, absorption, and blood flow that can be easily applied at the bedside.

Timing of Enteral Feeding

The best time to start EN in patients with acute pancreatitis has never been studied. The indirect evidence in regard to this is derived from trials of EN versus PN only. Some authors have demonstrated clinical benefits of early enteral nutrition, but others have demonstrated the favorable effects of delayed enteral feeding (Petrov et al, 2009b). Early EN should help maintain gut integrity (enterocyte population) and function (motility) and reduce bacterial translocation and ileus. It should also help to achieve caloric targets more quickly. But early nutrition is not without risk, particularly in hemodynamically unstable patients and in those requiring inotropic support. These patients appear to be at an increased risk of nonocclusive mesenteric ischemia, and it is best to commence EN after adequate resuscitation.

Therapeutic Endoscopic Retrograde Cholangiopancreatography

Endoscopic retrograde cholangiopancreatography (ERCP) with endoscopic sphincterotomy (ES) has been promoted as a proven intervention in patients with acute biliary pancreatitis since the early 1990s (see Chapters 18 and 27). This was based on the findings of two RCTs, from the United Kingdom and Hong Kong, of early ERCP (within 24 to 48 hours of admission) with or without ES versus conservative treatment (Neoptolemos et al, 1988; Fan et al, 1993). Both trials demonstrated that early ERCP was associated with a reduction in complications, but not in mortality, and only in patients with predicted severe acute pancreatitis.

Some evidence suggests that the duration of biliary obstruction, rather than the predicted severity of acute pancreatitis, is the most important determinant of outcome (Acosta et al, 1997, 2006). This is probably due to concomitant cholangitis secondary to the obstruction and probably best explains the usefulness of ERCP in the context of acute biliary pancreatitis (Petrov, 2009). The first multicenter RCT to examine the role of ERCP in acute pancreatitis was designed to include only patients without evidence of biliary obstruction (Folsch & Neoptolemos, 2002). This German study did not find any benefit of early ERCP (within 72 h after onset of symptoms) over conservative treatment. The most recent RCT, from Argentina, found that early ERCP in patients with biliary obstruction, defined by laboratory and radiologic criteria, and without evidence of acute cholangitis conferred no benefit (Oria et al, 2007).

Two important meta-analyses were published in 2008. The first found that compared with conservative treatment, early ERCP in patients with both predicted mild and predicted severe acute pancreatitis did not decrease the incidence of local pancreatic complications or mortality rate (Petrov et al, 2008d). The second meta-analysis was designed to negate the confounding effect of acute cholangitis and demonstrated no benefit of early ERCP over conservative treatment in terms of complications and mortality in patients with predicted mild and predicted severe acute pancreatitis (Petrov et al, 2008e). The conclusion to be drawn from these studies is that early ERCP is indicated in patients with acute pancreatitis if acute cholangitis is evident (see Chapter 43) but not for those with just cholestasis (Petrov, 2009). Although cholestasis can reflect a persisting main bile duct stone, it might also be due to edema of the ampulla secondary to stone passage to the duodenum and may thus be expected to improve over the first few days of admission. Persistent cholestasis without cholangitis may require an ERCP but not usually in the acute setting.

Cholecystectomy

Recurrent attacks of gallstone pancreatitis carry a morbidity rate of up to 40% (Banks & Freeman, 2006), and an early laparoscopic cholecystectomy is widely advocated within the same hospital admission (see Chapter 30). The optimal timing of cholecystectomy has been controversial. The U.K. guidelines for the management of acute pancreatitis recommend that all patients with biliary pancreatitis undergo definitive management of gallstones during the same hospital admission (index cholecystectomy; Working Group, 2005). However, some surgeons have concerns that early surgery may be associated with an increase in operative difficulty and hence morbidity and conversion rate; therefore they advocate cholecystectomy after a period of 4 to 6 weeks to allow resolution of the inflammatory process (interval cholecystectomy; Green, 2008; Larson et al, 2006). These two approaches have been compared in several RCTs, which demonstrated no difference in complication rates between index and interval cholecystectomy; however, index cholecystectomy resulted in a significantly shorter length of hospital stay (Siddiqui et al, 2008). It is worth mentioning that patients with acute biliary pancreatitis were excluded from these trials. An adequately powered RCT of index versus interval cholecystectomy is needed to draw a firm conclusion about the optimal timing of cholecystectomy in patients with acute biliary pancreatitis.

Management of Systemic Complications

Most patients with acute pancreatitis have an initial sudden inflammatory respiratory syndrome response, others develop multiple organ dysfunction syndrome (MODS) in the first few days, and some develop MODS later in response to infectious complications (see Chapters 52 and 53). Patients with severe and critical acute pancreatitis are best managed in an intensive care environment to allow for optimal monitoring of fluid resuscitation and organ function and the early identification of life-threatening local or systemic complications. Systemic complications and organ failure are not an all-or-nothing phenomenon, rather a continuous spectrum exists between normal function of an organ system and its complete failure (Table 54.5; Marshall et al, 1995).

Table 54.5 Modified Marshall Scoring System

Some of the systemic complications of acute pancreatitis—coagulation abnormalities that may range from intravascular thrombosis to disseminated intravascular coagulation, metabolic disturbances (hyperlipidemia, hypocalcemia), liver failure, encephalopathy, and Purtscher retinopathy—are rare in clinical practice and beyond the scope of this chapter. In contrast, respiratory, cardiovascular, renal, and intestinal dysfunction are the most common systemic complications (Banks & Freeman, 2006; Pandol et al, 2007).

Respiratory failure is the most common systemic complication. The pathogenesis involves inflammatory cytokines released from the pancreas and the action of phospholipase A₂ and other pancreatic catabolic enzymes on the lung. The clinical diagnosis of incipient respiratory failure is based on tachypnea and low oxygen saturation. A chest radiograph may confirm pleural effusions, pulmonary edema, and features of acute respiratory distress syndrome. Management is supportive, with oxygen supplementation and analgesia, and some patients will ultimately require endotracheal intubation and mechanical ventilation. Lung-protective ventilation strategies should be instituted, such as adequate positive end-expiratory pressures, permissive hypercapnia, and tidal volumes of 6 mL/kg ideal body weight (Nathens et al, 2004).

Patients with severe and critical acute pancreatitis can develop hypotension (arterial pressure <90 mm Hg) secondary to vasodilation and decreased systemic vascular resistance, and sometimes as a result of cardiotoxicity. Appropriate management consists of close hemodynamic monitoring, intravenous fluid resuscitation, and inotropic medications—dopamine at 2 to 10 µg/kg/min or dobutamine at 2 to 10 µg/kg/min—if indicated (Tonsi et al, 2009).

In the setting of acute pancreatitis, acute renal failure is usually secondary to decreased renal perfusion pressure with hypovolemia and is sometimes secondary to ischemic acute tubular necrosis. The clinical diagnosis is based on acute oliguria and an acute elevation in blood urea nitrogen and serum creatinine (>0.5 mg/dL or 44 mmol/L; Nathens et al, 2004; Tonsi et al, 2009). Treatment is supportive and focused on restoring renal perfusion and providing dialysis if required.

The failure of the intestine is usually due to ischemia secondary to hypovolemia and reflex splanchnic vasoconstriction. The clinical diagnosis is based on the development of nausea and vomiting, increased NG losses, tympanic distension of the abdomen, reduced bowel sounds, and reduced tolerance to EN. Intestinal failure with the breakdown in intestinal barrier function and bacterial translocation can result in bacteremia and the infection of pancreatic necrosis.

Management of Local Complications

Because local complications can develop at any time, frequent assessment and continuous monitoring of patients is necessary. When a local complication occurs, it is necessary to make an accurate diagnosis and to decide whether intervention is required, when it is required, and what intervention is appropriate. Managing the local complications of acute pancreatitis requires a number of considerations.

Type of Complication

The first consideration is the type of local complication and its prognostic significance. Early peripancreatic fluid collections often resolve without intervention and usually have little bearing on disease course. As such, this is more a manifestation of the disease than a complication per se. Fluid collections may persist, often to the result of ductal injury and pancreatic leak; they may cause symptoms because of a mass effect (e.g., gastric outlet obstructions) and from secondary infection. Patients with pancreatic necrosis show signs of clinical deterioration: persistent abdominal discomfort, intolerance to oral feeding, and failure to thrive. The local complication in these patients is often a mature (thick-walled) collection predominantly filled with sterile necrosis. In these patients, intervention might expedite recovery. Intervention is very rarely indicated in patients with sterile necrosis but may be required in those who continue to deteriorate despite maximal supportive care. In contrast, patients with extensive infected pancreatic or peripancreatic necrosis almost always require intervention, as this complication is the most significant determinant of outcome. Although infected pancreatic necrosis has been considered an absolute indication for surgical intervention, cases successfully managed nonsurgically have been reported. Any necrotizing process, regardless of the infectious status, may cause significant hemorrhage (e.g., pseudoaneurysm) or bowel perforation (e.g., duodenum or transverse colon), both of which require urgent intervention. Thus the type of local complication has a direct bearing on the indication for treatment.

Trajectory of Patient

The second consideration is the clinical status and trajectory of the patient. If supportive measures, such as those discussed above, bring about clinical improvement—evidenced by serial clinical assessment and inflammatory markers, such as C-reactive protein (CRP)—intervention is unnecessary. If, however, the patient continues to deteriorate despite maximum intensive care support, survival will depend on effective intervention. Related to this is a consideration of the physiologic reserve of the patient. Elderly patients with significant preexistent morbidity have less physiologic reserve to withstand prolonged severe illness and invasive interventions.

Timing of Intervention

The timing of intervention is an important consideration and one of the most difficult decisions to make in the management of patients with acute pancreatitis. Early intervention of local complications is often fraught with difficulty in patients with more severe necrotizing pancreatitis because of the risk of hemorrhage when necrotic tissue is less well demarcated from viable tissue. Delaying intervention allows this demarcation and thus reduces the risks of bleeding, dissemination of infection, and collateral damage to adjacent organs as the necrotic process has stopped extending, and infected necrotic tissues become organized and “walled off.” Appreciation of this has resulted in a notable trend toward delayed intervention, which is uncommonly performed before 4 weeks from the onset of symptoms.

Another emerging concept related to timing is the increasing use of percutaneous catheter drainage in patients with infected fluid collections and those with infected necrosis. Preemptive drainage with one or more catheters often produces an improvement in the patient’s overall clinical status, or at least it arrests clinical deterioration. In this way drainage buys time and allows the more definitive necrosectomy to be delayed, until the patient is more stable, and the lesion is better defined. If required, repeat intervention can be undertaken on a programmed basis (e.g., every second day) or with an on-demand strategy, wherein the intervention is repeated only if and when it is clinically indicated. The former is often necessary if intervention has occurred earlier in the disease course, when immature necrosum does not readily debride.

Type of Intervention

Another important consideration is the type of intervention. There are many different interventions, and the challenge is to select the intervention that is appropriate for the particular local complication, taking into account the anatomic location, infection status, complexity of any target lesions, the physiologic status and comorbidity of the individual patient, and the availability of expertise with the type of intervention. A review of current guidelines highlights the absence of level 1 evidence to guide decision making regarding the types of intervention (Loveday et al, 2008). Two broad philosophies are evolving in this regard. Many consider open surgical drainage with necrosectomy to be the gold standard in the management of infected pancreatic necrosis, and they reserve less invasive interventions for subsequent complications, such as percutaneous tube drainage of residual fluid complications. Such a step-down approach contrasts with the approach that advocates starting with less invasive interventions, such as percutaneous or endoscopic drainage, and only employing open surgical techniques later in the disease course in those who fail to respond (i.e., the step-up approach). These two approaches have been subjected to an RCT demonstrating that a minimally invasive step-up approach results in a reduced rate of the composite endpoint of major complications or death in patients with necrotizing pancreatitis and suspected or confirmed infected necrotic tissue (van Santvoort et al, 2010).

There are a number of variations to open surgical necrosectomy. More recently a number of less invasive approaches to treatment have been developed. The advocates for a less invasive approach argue that open surgery adds insult to injury and pushes a patient closer to or beyond their physiologic reserve; they point to the need to tailor treatment to specific lesions in individual patients and to the opportunities afforded by the development and convergence of minimally invasive technologies. Enthusiasts must be cautious not to overstate the benefits of less invasive approaches in the absence of high-level evidence. The reported improvement in outcomes with less invasive approaches might be due to a number of factors, including improvements in the early management of acute pancreatitis, such as resuscitation and EN; better intensive care to prevent and treat organ failure; more aggressive and appropriate use of percutaneous drainage; and better timing and selection of patients for intervention.

Classification of Interventions

In response to the need to standardize the description of invasive interventions to facilitate communication, comparison, and controlled trials (Windsor, 2007), progress has been made with the introduction of the VRP classification system, based on the ICD-10 approach (Loveday et al, 2011). It uses three dimensions, combining the method of visualization of the lesion, route taken to reach the lesion, and the purpose of the intervention (Table 54.6). Visualization includes open procedures, in which the operative site is exposed through the skin incision; endoscopic procedures, in which the operative site is visualized with an endoscope (gastroscope, laparoscope, or nephroscope); radiologic procedures that use computed tomography (CT), ultrasound, or fluoroscopy to visulalize lesions; and hybrid procedures that combine endoscopic and radiologic techniques. The routes taken by these interventions include the external route into the body, by mouth or gastrostomy tube, or the percutaneous route, through the skin; the internal routes used to reach a target lesion might pass through the gastrointestinal wall, peritoneum, or retroperitoneum.

Table 54.6 VRP Classification of Invasive Procedures

V1 Radiologic	Using only radiologic modalities (e.g., fluoroscopy, CT, US, MR) to visualize and assist entering the target lesion
V2 Endoscopic	Using any white-light endoscopic instrument (e.g., flexible or rigid endoscope, urologic endoscope) to visualize the target lesion
V3 Combined	Using an endoscopic technique as the primary mode of visualization, assisted by a real-time radiologic modality
V4 Open	Using any method in which skin and any other body layers are cut to expose the site of the procedure
Vx	Insufficient information
Vz	Other visualization technique
R1 Per os transpapillary	External orifice entry point, internal route traversing papilla to enter pancreatic duct
R2 Per os transmural	External orifice entry point, internal route traversing gastrointestinal wall
R3 Percutaneous retroperitoneal	Skin external entry point, internal route traversing retroperitoneum
R4 Percutaneous transperitoneal	Skin external entry point, internal route traversing peritoneum
R5 Percutaneous transmural	Skin external entry point, internal route traversing gastrointestinal wall
Rx	Insufficient information
Rz	Other route
P1 Drainage	Letting out fluid and/or solid necrotic matter, externally out of the body or internally into the gastrointestinal tract
P2 Lavage	Flushing away solid necrotic matter with fluid to facilitate external or internal drainage
P3 Fragmentation	Breaking down solid necrotic matter by instrumental or mechanical disruption to facilitate external or internal drainage
P4 Debridement	Taking or cutting out solid necrotic matter with either sharp or blunt dissection
P5 Excision	Cutting out all or part of the pancreas, including healthy tissue, with the intention to fully remove all necrotic matter
Px	Insufficient information
Pz	Other purpose

Procedures should be classified using a single value from each component, and the highest applicable value should be selected.

CT, computed tomography; US, ultrasound; MR, magnetic resonance

Loveday BP, et al, 2011: A comprehensive classification of invasive procedures for treating the local complications of acute pancreatitis based on visualization, route, and purpose. Pancreatology 11:406-413.

The overall purpose of treatment is to eliminate areas of necrotic and infected tissue or fluid and inflammatory and enzyme-rich exudates. However, the way in which this is achieved varies considerably, and some procedures are much more aggressive than others. Therefore the purpose of individual treatment procedures for PN may be to effect simple drainage alone or to lavage the necrotic cavity to assist drainage of necrotic debris, fragment necrotic tissue to facilitate its drainage, debride necrotic tissue, or excise or resect the pancreas. The overall aim of intervention is to control the septic focus and preserve pancreatic function.

Open Surgical Necrosectomy

Three general variations of open necrosectomy are currently practiced: 1) open necrosectomy with open or closed packing, 2) open necrosectomy with continuous closed postoperative lavage, and 3) programmed open necrosectomy. Although these are broadly similar in terms of the necrosectomy, they differ in terms of how they provide egress routes for infected fluid, debris, and tissue. The abdomen is entered though a midline or bilateral subcostal incision. The latter is preferred, as it minimizes contamination of the greater sac and allows easy access to the extremities of the gland. The pancreas is exposed by dividing the gastrocolic omentum or gastrohepatic omentum to access the pancreas through the lesser sac. The body and tail of the pancreas (Fig. 54.1) can also be exposed by elevating the transverse colon and gaining access to the lesser sac via the transverse mesocolon (Fig. 54.2). Inflammatory adhesions may exist between the pancreas and stomach or transverse mesocolon, and great care is required during exposure. It is generally useful to take down both the hepatic and splenic flexures, if possible, as this will facilitate exposure and reduce the risk of colonic fistula secondary to drain erosion. When the process involves the head of the pancreas, access might require medial mobilization of the duodenum.

FIGURE 54.1 Access to the pancreas via the gastrocolic omentum.

(From Uhl W, et al, 2007: Necrosectomy. In Clavien P-A, et al (eds): Atlas of Upper Gastrointestinal and Hepato-Pancreato-Biliary Surgery. New York, Springer, pp 893-915.)

FIGURE 54.2 Access to the pancreas via the transverse mesocolon.

(From Mithofer K, et al, 1997: Interventional and surgical treatment of pancreatic abscess. World J Surg 21[2]:162-168.)

Open Necrosectomy with Closed Packing

The goal of necrosectomy with closed packing is to perform a single operation by performing a thorough debridement and removal of necrotic and infected tissue to minimize the need for reoperation or subsequent drainage (Pezzilli et al, 2007). Primary closure of the abdomen is the intention. Once the necrotic cavity is opened, fluid collections are drained, and the exposure is enlarged to allow debridement of all areas of necrosis, including those in the perirenal and paracolic spaces. Early advocates used gauze-stuffed Penrose drains placed via separate stab incisions, but many variations are in practice with regard to the type and number of drains. Between 2 and 12 drains are placed with the intention to fill the cavity and provide some compression. Additional silicone drains (Jackson-Pratt) are placed in the pancreatic bed and lesser sac for fluid drainage. The stuffed Penrose drains are removed one every other day, starting 5 to 7 days postoperatively, allowing a slow collapse of the cavity. The silicone drains are removed later.

Open Necrosectomy with Open Packing

The difference with this approach is that the abdomen is left open after debridement and packing of the pancreatic bed, lesser sac, and retroperitoneum (Gotzinger, 2008). Drains are placed in addition to the packing. Sometimes the abdomen is closed, and the packing is accessed via separate flank incisions (Nakasaki et al, 1999). Open packing techniques have been reported to have higher incidences of fistulae, bleeding, and incisional hernias as well as a slightly higher mortality rate (Heinrich et al, 2006). However, it should be noted that no prospective trials have compared open packing with any other technique.

Open Necrosectomy with Continuous Closed Postoperative Lavage

In this approach, debridement is followed by continuous peripancreatic lavage to remove infected necrotic debris, peripancreatic exudates, and extravasated pancreatic exocrine fluid (Fernandez-del Castillo et al, 1998). The large silicone drainage catheters are placed into the pancreatic bed to inflow and outflow isotonic irrigation fluid (Fig. 54.3). During closure, a closed peripancreatic compartment is made by resuturing the gastrocolic and duodenocolic ligaments. Postoperative continuous lavage is instituted at 1 to 10 L per day and should be continued until the effluent is clear and the patient shows improvement in clinical and laboratory parameters (Wig et al, 2004). No evidence is available to suggest the best irrigation fluid, the optimal number or caliber of drains, or the duration of irrigation.

FIGURE 54.3 Open necrosectomy with continuous closed postoperative lavage.

(From Uhl W, et al, 2007: Necrosectomy. In Clavien P-A, et al (eds): Atlas of Upper Gastrointestinal and Hepato-Pancreato-Biliary Surgery. New York, Springer, pp 893-915.)

Programmed Open Necrosectomy

The principle of this approach is to be more conservative with debridement, particularly if necrosum has not fully demarcated, with the intention of performing repeat procedures every 48 hours until debridement is no longer required. The pancreatic bed is drained or packed, and the abdomen is closed by suturing mesh or a zipper to the fascial edges of the wound. This allows multiple reentries and helps to prevent wound retraction, which aids in later delayed primary wound closure. In a proportion of patients, primary closure is not possible, and secondary intention healing is allowed to occur, accepting that this may require elective scar excision and repair of an incisional hernia. This procedure may be modified with the addition of intraabdominal vacuum sealing (negative pressure 50 to 75 mm Hg) to encourage granulation of the pancreatic bed, potentially reducing the number of operations and mortality (Olejnik et al, 2008).

Several approaches to open surgical necrosectomy are possible. Comparing them has limited value in the absence of controlled trials because of variations in referral patterns, selection criteria, patient comorbidities, and the use of presurgical percutaneous management. Most techniques are associated with a 15% to 25% mortality rate, but this can be higher in patients with multiple organ failure and in those who have had early surgery. The important principles are adequate exposure guided by high-quality preoperative CT scanning, gentle debridement of demarcated dead tissue, preservation of viable pancreatic tissue, and thorough irrigation of the pancreatic bed, lesser sac, and retroperitoneum. Packing is probably best reserved to control hemorrhage, as it is associated with an increased risk of enteric fistulae. The placement of wide-bore dependent drains allows further egress of necrotic and infected material, aided by continuous irrigation, which may reduce the need for reoperation. In rare cases, when a necrosectomy is indicated within the first 2 weeks, an open approach should be considered because of the higher probability of requiring multiple procedures.

Endoscopic Techniques

In 1996, Gagner described the first true endoscopic treatment of necrotizing pancreatitis, in which the pancreas was debrided using a laparoscopic approach. Over the last decade, a wide range of endoscopic approaches for pancreatic necrosectomy have been described, including infracolic laparoscopy, transgastric laparoscopy, hand-assisted laparoscopy, retroperitoneal laparoscopy, transgastric flexible endoscopy, flexible endoscopy via a percutaneous endoscopic gastrostomy, and retroperitoneal nephroscopy (Ammori, 2002; Baron & Morgan, 1999; Charnley et al, 2006; Cuschieri et al, 1998; Horvath et al, 2001; Parekh, 2006). This array of endoscopic techniques can be classified by the type of scope that is used: laparoscope, nephroscope, or flexible endoscope (Windsor, 2007). Although some endoscopic procedures do not utilize radiologic modalities, many are hybrid procedures that incorporate fluoroscopy or endoscopic ultrasound into the procedure.

Laparoscopic Techniques

Most laparoscopic techniques are minimally invasive versions of open surgical techniques, and they use an anterior or lateral approach. In Gagner’s original (1996) description of laparoscopic necrosectomy, two anterior routes—retrogastric retrocolic and transgastric—and one lateral route were described. In the retrogastric retrocolic route, a 30-degree laparoscope is introduced through the umbilical port following CO₂ insufflation (15 mm Hg). Placement of additional ports depends on the location of the necrosis. Following necrosectomy, large sump drains are placed in the necrotic beds, and continuous lavage may be established to remove peritoneal contaminants. In the transgastric route, the stomach is opened anteriorly and posteriorly. Endoluminal ports are used, which maintain the tip of the port inside the stomach. Debridement is performed internally through the posterior stomach wall, in a technique akin to an open cystogastrostomy. It is also possible to use a transduodenal route for necrosis of the pancreatic head, although this can be more difficult. No drains are left in the stomach, but a drain may be placed over the incision in the anterior gastric wall. With the retroperitoneal route, the patient is placed in the left or right lateral position, and a small flank incision made. The three muscle layers of the abdominal wall are split, and a trocar is inserted. Using a 0-degree laparoscope and CO₂ insufflation (10 to 15 mm Hg), a tract is made through to the pancreas. Once the necrotic areas have been identified, necrosectomy proceeds as when approached via a retrogastric retrocolic route.

These techniques have subsequently been modified. Of the lateral approaches, one of the most widely used laparoscopic techniques is videoscopic-assisted retroperitoneal debridement (VARD; Fig. 54.4), which was first described by Horvath and colleagues in 2001. The purpose of this procedure differs from those of open necrosectomy. Rather than performing complete removal of all infected and necrotic tissue, the purpose of VARD is to facilitate percutaneous drainage. In this technique, radiologic drainage of the lesion is first instituted. In the operating room, the patient is placed in a modified left lateral decubitus position, and a 4- to 5-cm incision is made in the left flank at the site of the drain. A finger is used to probe and confirm entry into the necrotic cavity. Fluid and loose necrotic debris are removed by suction, and two ports (10 to 12 mm) are inserted through the incision. The incision is sealed with wet sponges and towel clips to allow insufflation with CO₂. Debridement of necrotic tissue is performed with hydrodissection and 10 mm forceps. Drains are placed for postoperative continuous lavage: a 10-Fr red rubber drain is brought through a separate anterolateral incision, and two 1.3-cm (0.5-inch) Penrose drains are placed in the original skin incision. An ostomy bag is then positioned over the flank incision and Penrose drains, and continuous lavage is performed through the red rubber drain at 200 mL/h for 5 days or until the effluent is clear.

FIGURE 54.4 Videoscopic-assisted retroperitoneal debridement technique.

(From van Santvoort HC, et al, for the Dutch Acute Pancreatitis Study Group, 2007: Case-matched comparison of the retroperitoneal approach with laparotomy for necrotizing pancreatitis. World J Surg 31:1635-1642.)

Variations of the anterior laparoscopic approaches are well described. In addition to the retrogastric, recolic, and transgastric routes, a transmesocolic route may be used, in which the transverse colon is elevated to expose the pancreatic lesion in the lesser sac (Cuschieri et al, 1998). Laparoscopic ultrasound may be used to confirm the position of the lesion, and the transverse mesocolon is usually opened to the left of the middle colic vessels. Following necrosectomy, two or more drains are placed in the pancreatic bed for postoperative lavage of the lesser sac. Anterior approaches may also incorporate a hand-assist device; this is termed hand-assisted laparoscopic surgery (HALS; Parekh, 2006). Another recent publication described single-port laparoscopic necrosectomy (Bucher et al, 2008). Port placement (12 mm) is through postlaparotomy drain tracts, allowing introduction of both a 4-mm laparoscope and 5-mm instruments. Insufflation pressures are kept to 8 mm Hg, as higher pressures may promote bacterial translocation from the cavity. Debridement is performed with both hydrodissection and atraumatic grasping forceps, hemostasis is achieved with monopolar diathermy, and a sump drain is placed for continuous postoperative lavage.

Nephroscopic Techniques

Nephroscopic techniques utilize warmed fluid to expand the necrotic cavity, irrigate turbid fluid, and maintain a clear visual field. Carter and colleagues (2000) were the first to describe the use of a nephroscope during necrosectomy, terming the procedure percutaneous necrosectomy. The principle underlying this procedure is the same as for an open procedure: debridement of devitalized tissue and establishment of a system for continuous postoperative lavage—with reduced physiologic stress on the patient. Percutaneous necrosectomy may only be used when the area of necrosis is accessible to percutaneous puncture, and it is contraindicated in the presence of bowel ischemia, perforated viscus, or significant preoperative hemorrhage. The first step is to insert a drainage catheter into the pancreatic lesion under CT guidance. The preferred path for drainage is between the lower pole of the spleen and the splenic flexure (Fig. 54.5), although in right-sided necrosis, a path through the gastrocolic omentum, anterior to the duodenum, may occasionally be used. The patient is then transferred to the operating room and positioned in the left lateral position, or for right-sided necrosis, in the right lateral position. A nephrolithotomy drape is used to collect irrigant fluid, and the drain tract is dilated to allow insertion of a 34-Fr Amplatz sheath. A nephroscope is inserted through the sheath into the cavity, and lavage is used to clear away debris and suppurative fluid (Fig. 54.6). Following necrosectomy, a 32-Fr soft drainage tube is left in the cavity. A smaller (8-Fr) catheter can be inserted through or alongside the larger drain to allow continuous postoperative lavage. This might be commenced at 250 mL/h with warmed dialysis fluid. Repeat procedures are often required after 2 to 10 days (Carter & Wysocki, 2008).

FIGURE 54.5 Insertion of a drainage catheter under CT guidance.

(From Bruennler T, et al, 2008: Percutaneous necrosectomy in patients with acute, necrotizing pancreatitis. Eur Radiol 18[8]:1604-1610.)

FIGURE 54.6 Percutaneous necrosectomy technique.

(From Uhl W, et al, 2007: Necrosectomy. In Clavien P-A, et al (eds): Atlas of Upper Gastrointestinal and Hepato-Pancreato-Biliary Surgery. New York, Springer, pp 893-915.)

Flexible Endoscopic Techniques

The use of flexible endoscopy to treat patients with PN has a long history. In 1991, Prinz and Olen recognized that some areas of the abdomen were difficult to access during open necrosectomy as a result of the inflammatory process, therefore a choledochoscope was passed through the open abdomen to debride necrosis located in the lower retroperitoneum following open necrosectomy (Prinz & Olen, 1991). Since that time, the use of flexible endoscopes has developed considerably, with many different techniques currently available, as discussed below. In these procedures, the endoscope is either inserted via an external orifice, usually the mouth, or a skin incision is made.

Peroral flexible endoscopic techniques follow an internal route through either the gastric/duodenal wall or duodenal papilla, and some authors consider this to be a form of natural orifice transluminal endoscopic surgery (Friedland et al, 2009). Initial descriptions of flexible endoscopic treatment of PN used lavage and drainage without instrumental debridement (Baron et al, 1996). A more aggressive approach was subsequently introduced, which demonstrated that necrotic tissue may be debrided with baskets, snares (Fig. 54.7), forceps, and suction (Seewald et al, 2005). A recent long-term multicenter study of transluminal endoscopic necrosectomy described 93 patients who underwent a mean of six interventions, starting at a mean of 43 days after the onset of severe acute pancreatitis (Seifert et al, 2009). Initial clinical success was obtained in 80% of patients but with a complication rate of 26% over 43 months of follow-up; 16% developed recurrent pancreatitis, 10% required further endoscopic procedures, 4% required surgical treatment, and the mortality rate was 7.5% at 30 days. Surgical necrosectomy was required in 12% of patients.

FIGURE 54.7 Pancreatic necrosis debridement with the use of flexible endoscope.

(From Seewald S, et al, 2005: Aggressive endoscopic therapy for pancreatic necrosis and pancreatic abscess: a new safe and effective treatment algorithm [videos]. Gastrointest Endosc 62[1]:92-100.)

Endoscopic retrograde pancreatography (ERP) can be used to diagnose any communication between the duct and cavity or duct stenosis or disruption, and transpapillary stenting can be employed to decompress the duct. Puncture of the posterior gastric wall into the pancreatic lesion may be performed at the point of maximal bulging, although confirmation of the location with endoscopic ultrasound helps achieve correct placement of the perforation and avoids injury to vessels. A successful puncture is confirmed with aspiration of suppurative fluid from the cavity.

The injection of contrast with fluoroscopy can be used to determine the extent of the cavity. The gastric perforation is dilated with balloons up to 20 mm. For lavage and drainage, a 7-Fr nasocystic (lavage) and a 10-Fr pigtail drain (drainage) are placed in the cavity (Fig. 54.8). Continuous lavage with 1500 mL/day saline is established. Necrosectomy may be performed with endoscopic instruments, such as a Dormia basket or polypectomy snare, and introduction of a forward-viewing endoscope into the necrotic cavity can be used for better visualization during the necrosectomy. Multiple necrosectomy procedures are usually required to clear the cavity of necrotic tissue. A similar procedure may be performed with external entry into the body via a percutaneous endoscopic gastrostomy (PEG) tube (Baron & Morgan, 1999).

FIGURE 54.8 Transmural drainage of organized pancreatic necrosis.

(From Baron TH, et al, 2002: Outcome differences after endoscopic drainage of pancreatic necrosis, acute pancreatic pseudocysts, and chronic pancreatic pseudocysts. Gastrointest Endosc 56[1]:7-17.)

Several techniques using flexible endoscopy through skin incisions have been described. The first was by Prinz and Olen (1991) after open necrosectomy, as detailed above. Following percutaneous necrosectomy with a nephroscope, subsequent debridement may be undertaken using a flexible endoscope, a so-called sinus-tract endoscopy (Carter et al, 2000). The drain tract is dilated to 45 Fr, and a flexible endoscope is inserted into the cavity for necrosectomy. A similar technique has been described following open necrosectomy via a translumbar incision, in which a flexible endoscope is inserted into the cavity for debridement of ongoing necrosis (Jakobs et al, 2000). These endoscopic debridements were initiated 10 days after the open necrosectomy and were carried out every 3 days for 4 weeks (approximately 8 to 10 sessions).

The plethora of endoscopic approaches to necrosectomy and the absence of formal comparison make a recommendation for the optimal approach problematic. The selection of an endoscopic technique will be influenced by training, experience, and the availability of equipment, but it will also be determined by the location and complexity of the target lesion and the clinical status of the patient.

Radiologic Techniques

Interventional radiology techniques are assuming greater importance, particularly for initial sepsis control to allow definitive necrosectomy to be performed more electively (Jakobs et al, 2000). Ultrasound, fluoroscopy, or CT is used to guide the interventional radiologist into the pancreatic lesion. These radiologic modalities are also used to define the extent and composition of the lesion, visualize the instruments used, and determine the efficacy of the treatment procedure. The purpose of radiologic techniques may be to achieve either drainage, with or without lavage, or debridement.

Radiologic Drainage Techniques

Drainage techniques are most effective if target lesions have a significant fluid component. They can be located in many sites but are most often in the lesser sac, anterior and left pararenal spaces, and other parts of the retroperitoneum (Fig. 54.9; Jakobs et al, 2000). Image-guided needle puncture of the lesion may involve a retroperitoneal or transperitoneal route and may be transmural (transgastric or transduodenal), but a retroperitoneal approach is preferred to reduce the risk of contamination and possible peritonitis (Jakobs et al, 2000). A guidewire is passed down the needle, and the tract is dilated to accommodate a catheter. Because catheters readily block with necrosum and debris, it is advisable to maximize catheter diameter to improve patency. Typically, catheters should have multiple sideholes and a minimum diameter of 12 Fr (Jakobs et al, 2000). Drain tracts may be serially dilated to accommodate larger catheters (20 to 24 Fr). Often multiple catheters are required, especially for large or complex lesions. To increase the efficacy of the drainage procedure, remove toxic factors, and help maintain catheter patency, lavage should be considered (Eatock et al, 2005; Jakobs et al, 2000). Theoretical concerns have been raised that lavage may spread infection, either from infected fluid spilling over into previously sterile cavities or from the increased intracavity pressure, resulting in translocation of bacteria into surrounding tissues. However, this has not been demonstrated as a major problem clinically, most likely because the pancreatic lesion is walled off in a fibrous capsule 4 to 6 weeks after the onset of acute pancreatitis.