54-Management of acute pancreatitis and complications.pdf

8/11/2019 54-Management of acute pancreatitis and complications.pdf

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846 PART 6 PANCREATIC DISEASESection I Inammatory, Infective, and Congenital B. Pancreatitis

the strategy for administration remain uncertain. No recentguidelines relating to the management of acute pancreatitis pro-vide a specic recommendation regarding pain management(Loveday et al, 2010 ).

Fluid ResuscitationAcute pancreatitis can be associated with substantial third-

space uid losses, and the resultant hypovolemia that impairsthe microcirculation of the pancreas is a major determinant ofpancreatic necrosis. The reex splanchnic vasoconstriction inresponse to hypovolemia may compound pancreatic hypoperfu-sion and further predispose to ischemia. Fluid resuscitation isone of the most important aspects of the early management ofacute pancreatitis ( Gardner et al, 2008 ; Talukdar & Vege, 2009 )and is the intervention most likely to improve outcome. Nohigh-level evidence describes the optimal resuscitation uid,required uid rate, or best marker to guide resuscitation andindicate its adequacy ( Banks & Freeman, 2006 ; Pandol et al, 2007 ). It is not even known whether colloids or crystalloids aremore effective in improving pancreatic microcirculation andoutcome. The initial goal of uid resuscitation is to restore cir-

culating blood volume (euvolemia), with the aim of normalizingheart rate, blood pressure, central venous pressure, and urineoutput, even though these do not reect the adequacy of pan-creatic and splanchnic perfusion ( Flint & Windsor, 2003 ). In

morphine in treating the pain associated with acute pancreatitis;however, the NSAID of choice is metamizole (2 g/8 h IV), andthe opioid of choice is buprenorphine (0.3 g/4 h IV). There is

no evidence to support the use of parenterally administeredlocal anesthetics such as procaine in the management ofpain associated with acute pancreatitis. However, the lack ofhigh-quality evidence means that the choice of analgesic and

Table 54.1

Determinants-Based Classication of Acute Pancreatitis

SeverityCategory * Local Determinant

SystemicDeterminant

Mild No local complications and No organfailure

Moderate Sterile pancreatic andperipancreatic complications

or Transientorgan failure

Severe* Infectious pancreatic andperipancreatic complications

or Persistentorgan failure

Critical Infectious pancreatic andperipancreatic complications

and Persistentorgan failure

*Severity is graded on the basis of more severe local or systemic complication (e.g.,sterile pancreatic necrosis without organ failure has to be graded as moderate;sterile pancreatic necrosis with persistent organ failure has to be graded as severe).

Petrov MS, Windsor JA, 2010: Classication of the severity of acute pancreatitis: howmany categories make sense? Am J Gastroenterol 105(1):74-76.

Table 54.2

Randomized Controlled Trials of Analgesics in Patients with Acute Pancreatitis

FirstAuthor Year Setting

InterventionGroup

ControlGroup

NO. PATIENTS

AllocationConcealment

Reduction ofPain Score

Other ImportantFindings

InterventionGroup

ControlGroup

Blamey 1984 U.K. IM buprenorphine IM pethidine 17 15 Single blind No difference No difference interms of adverseeffects

Ebbehoj 1985 Denmark Indomethacin(rectal)

Placebo(rectal)

14 16 Double blind Signicantlygreater in theinterventiongroup over therst 168 h

The number ofopiate injectionswas signicantlyless in theintervention group

Jakobs 2000 Germany IV buprenorphine IV procaine 20 20 Open label Signicantlygreater in theinterventiongroup over therst 48 h

The number ofadditionalanalgesics wassignicantly less inthe interventiongroup

Stevens 2002 U.S. Fentanyl(transdermal)

Placebo(transdermal)

16 16 Double blind Signicantlygreater in theinterventiongroup between36 and 60 h

A signicantlyreduced LOS wasreported in theintervention group

Kahl 2004 Germany IV pentazocine IV procaine 50 51 Open label Signicantlygreater in theinterventiongroup over therst 72 h

The number ofadditionalanalgesics wassignicantly less inthe interventiongroup

Peiro 2008 Spain IV metamizole SC morphine 8 8 Open label Insignicantlygreater in theinterventiongroup over therst 24 h

No differencereported in termsof adverse effects

IM, intramuscular; IV, intravenous; SC, subcutaneous; LOS, length of stay


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B. Pancreatitis Chapter 54 Management of Acute Pancreatitis and Complications 847

controversial for decades. Three RCTs in the 1970s failed todemonstrate a benecial effect of antibiotic prophylaxis, prob-ably because of a small sample size, inappropriate selection ofantibioticssuch as ampicillin, which does not sufciently pen-etrate the pancreasand inclusion of patients with mild pan-creatitis ( Table 54.3 ; Craig et al, 1975 ; Finch et al, 1976 ; Howes et al, 1975 ). Between 1993 and 2009, several randomized, con-trolled, open-label trials were published evaluating the efcacyof prophylactic antibiotic treatment in patients with severeacute 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 trialswere conicting. Although some RCTs demonstrated a signi-cant reduction of infectious complications and mortality withthe use of prophylactic antibiotics, others failed to do so (seeTable 54.3 ). Only three double-blind, placebo-controlled RCTswere published between 2004 and 2009, and all of them wereunable to show a benecial effect of antibiotic prophylaxisregarding infectious pancreatic complications, the need forsurgery, and mortality ( Dellinger et al, 2007 ; Garcia-Barrasa et al, 2009 ; Isenmann et al, 2004 ). This is in line with the

general, urine output should be restored at greater than0.5 mL/h/kg body weight, and the central venous pressureshould be restored to between 8 and 12 cm H 2O. Swan-Ganzmonitoring can be helpful in hemodynamically unstablepatients, and some evidence shows that as an independent riskfactor of pancreatitis severity and a marker of hydrations status,hematocrit might be useful with uid resuscitation ( Pitchumoni et al, 2005 ; Wu et al, 2009 ). Adequate uid resuscitation islikely when the hematocrit is restored to between 30% and35%. A number of other approaches to guide resuscitation offerpromise but have not become established in clinical practice.An example is the use of intramucosal pH (pHi) derived bynasogastric tonometry ( Juvonen et al, 2000a ; van Haren et al, 2007 ), which is predictive of severity and reects the adequacyof perfusion in the splanchnic circulation.

AntibioticsAlthough the use of broad-spectrum antibiotics to treat theestablished infection in acute pancreatitis is a well-establishedpractice, the use of prophylactic antibiotics has been

Table 54.3

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

FirstAuthor Year Setting

InterventionGroup

ControlGroup

NO. PATIENTS

AllocationConcealment Main Findings

InterventionGroup

ControlGroup

Howes 1975 U.S. Ampicillin None 48 47 Open label No signicant difference in anyoutcomeCraig 1975 U.S. Ampicillin None 23 23 Open label No signicant difference in any

outcomeFinch 1976 U.S. Ampicillin Placebo 31 27 Double blind No signicant difference in any

outcomePederzoli 1993 Italy Imipenem None 41 33 Open label Signicantly lower rate of

pancreatic infection in theintervention group

Sainio 1995 Finland Cefuroxime None 30 30 Open label Signicantly lower mortality rate,but not pancreatic infection, inthe intervention group

Delcenserie 1996 France Ceftazidime + amikacin + metronidazole

None 11 12 Open label No signicant difference in anyoutcome

Schwarz 1997 Germany Ooxacin + metronidazole

None 13 13 Open label No signicant difference in anyoutcome

Spicak 2003 CzechRepublic

Meropenem None 20 21 Open label No signicant difference in anyoutcome

Isenmann 2004 Germany Ciprooxacin + metronidazole

Placebo 58 56 Double blind No signicant difference in anoutcome

Dellinger 2007 NorthAmericaand Europe

Meropenem Placebo 50 50 Double blind No signicant difference in anyoutcome

Rokke 2007 Norway Imipenem None 36 37 Open label Signicantly lower rate ofpancreatic and extrapancreaticinfection in the interventiongroup

Xue 2009 China Imipenem None 29 27 Open label No signicant difference in anyoutcome

Garcia-Barrasa

2009 Spain Ciprooxacin Placebo 22 19 Double blind No signicant difference in anyoutcome


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suppression. A meta-analysis of RCTs showed that nutritionalsupport, both enteral and parenteral, signicantly reduced riskof mortality in patients with acute pancreatitis compared withno nutritional support ( Petrov et al, 2008c ). Nutritional supportis thus an essential part of the management of patients withsevere acute pancreatitis ( Banks & Freeman, 2006 ; Pandol et al, 2007 ).

Type of Feeding The feasibility of providing nutritional support in patients withacute 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 restingthe pancreas. The rationale for this was to prevent stimulatingincreased secretion of pancreatic proteolytic enzymes and exac-erbating pancreatitis severity. But the use of PN has decreasedin the face of well-recognized problems, such as catheter-relatedsepsis, the high cost of treatment, electrolyte and metabolic dis-turbances, villous atrophy and gut barrier failure with promo-tion of bacterial translocation, systemic sepsis, and multipleorgan failure.

A number of RCTs compared total PN and total EN inthe 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 RCTshas shown a signicant twofold reduction in the risk of total andpancreatic infectious complications and a 2.5-fold reduction inthe risk of death in patients receiving total EN ( Petrov et al, 2008f ). The basis for the clinical benets of EN over PN remainunclear, although EN may prevent or attenuate mucosal barrierfailure and bacterial translocation ( Windsor & Hammodat, 2000 ). Intestinal permeability studies are a surrogate marker forclinically relevant events and provide conicting results. Threeclinical studies showed increased intestinal permeability to bothmicromolecules and macromolecules in patients with severeacute pancreatitis when compared with mild acute pancreatitis

ndings of a meta-analysis that showed an inverse relationshipbetween methodologic quality of the studies and impact of anti-biotic prophylaxis on mortality ( de Vries et al, 2007 ).

On the other hand, it is worth noting that the three double-blind RCTs mentioned were not without aws. These include alarge crossover to open-label antibiotics in the control group(i.e., a high percentage of patients in the placebo group weretreated with intravenous antibiotics) and the inclusion of

patients on the basis of predicted severity of acute pancreatitisrather than proven necrotizing pancreatitis. All the studies wereunderpowered because the power calculation was based on aninfection rate of 40%, whereas the actual infection rates in theplacebo groups of the trials were only 12% to 17%.

Several attempts have been made to statistically aggregatedata on the use of prophylactic antibiotics in acute pancreatitis.Although only two new RCTs were published from 2006through 2007, it is notable that seven of the 10 meta-analyseswere published within this period ( Petrov, 2008 ). ThirteenRCTs were included in these seven meta-analyses. Because ofdifferent inclusion criteria and various meta-analysis techniquesused, concordance is lacking, and they provide contradictoryrecommendations regarding the role of prophylactic antibiotics

in reducing the risk of pancreatic infectious complications.Overall, it appears that the most recent studies do not supportthe use of prophylactic antibiotics to reduce the frequency ofpancreatic infectious complications, surgical intervention, anddeath in patients with acute pancreatitis. Therefore routinebroad-spectrum prophylactic antibiotics in patients with severeacute pancreatitis cannot be recommended on the basis ofcurrent evidence.

Nutritional Management Severe acute pancreatitis is associated with a cytokine-mediatedsystematic inammatory response and a hypercatabolic state(Windsor & Hammodat, 2000 ; see Chapter 10). The adverseconsequences of this include protein-calorie malnutrition,expansion of the extracellular uid compartment, and immune

Table 54.4

Randomized Controlled Trials of Total Enteral vs. Total Parenteral Nutrition in Patients with Predicted SevereAcute Pancreatitis

First Author Year Setting *

NO. OF PATIENTS

RI and Mortality RateInterventionGroup

ControlGroup

Kalfarentzos 1997 Greece 18 20 Signicantly lower RI in the intervention groupGupta 2003 UK 8 9 Insignicantly lower RI in the intervention groupLouie 2005 Canada 10 18 Insignicantly lower RI in the intervention groupEckerwall 2006 Sweden 23 25 No signicant difference in outcomesPetrov 2006 Russia 35 34 Signicantly lower RI and mortality rate in the intervention groupCasas 2007 Spain 11 11 Insignicantly lower RI in the intervention groupDoley 2009 India 25 25 No signicant difference in outcomes Wu 2010 China 53 54 Signicantly lower RI and mortality rate in the intervention group

*Allocation concealment was open-label in all studies.The intervention group received enteral nutrition, whereas the control group received parenteral nutrition.RI, rate of pancreatic infection


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Because the gastrointestinal tract is the largest immuneorgan, containing approximately 65% of the immune tissue inthe body, it has been considered that the use of immune-enhanced enteral formulations might increase the benecialeffects of EN in acute pancreatitis ( Bengmark, 1999 ; Schloerb, 2001 ). Several trials were performed in different clinical set-tings, which suggested that immunonutrition might have thepotential to modify the inammatory response. The results of

RCTs that compared the use of immune-enhanced and stan-dard enteral formulas were statistically aggregated in severalmeta-analyses ( Beale et al, 1999 ; Heyland et al, 2001 ; Heys et al, 1999 ). The most recent and comprehensive systematicreview of 2419 patients from 22 RCTs ( Heyland et al, 2001 )found that the effect of immune-enhancing EN may dependon the subset of the analyzed patients. In particular, no effectof immunonutrition on the risk of infectious complicationsor death was reported within the subgroup of critically illpatients. At the same time, administration of a formula high inarginine in a combined group of critically ill and electivesurgery patients was associated with a statistically signicantreduction in infectious complications and a trend toward lowermortality rates in comparison with other immune-enhancing

diets. A recent meta-analysis of RCTs in patients with acutepancreatitis did not show any clinical benecial effect ofimmunonutrition when compared with standard EN ( Petrov et al, 2008a ).

Tolerance of Enteral Feeding Dieticians generally agree on the caloric target in patients withacute pancreatitis: 30 kcal/kg and 1.5 g/kg of protein dailybased on ideal body weight ( Andersson et al, 2009 ; Olah &Romics, 2008 ). To ensure tolerance of EN, it is usually com-menced at a low rate of 25 to 30 mL/h and increased incre-mentally over a day or more, until the desired caloric intake isreached. Despite this approach, EN can be associated withfeeding intolerance in some patients with acute pancreatitis.Most commonly, the intolerance manifests as abdominal dis-tension, delayed gastric emptying, gastroesophageal reux, anddiarrhea, all of which may develop in the presence of sepsis orwith a signicant clinical deterioration. In general, tolerance isachieved when EN is provided without development of one ofthese complications ( Bankhead et al, 2009 ; Mallampalli et al, 2000 ). Various strategies to improve tolerance to EN requireclinical studies, which are also needed to investigate markers ofgut motility, absorption, and blood ow that can be easilyapplied at the bedside.

Timing of Enteral Feeding The best time to start EN in patients with acute pancreatitishas never been studied. The indirect evidence in regard to thisis derived from trials of EN versus PN only. Some authorshave demonstrated clinical benets of early enteral nutrition,but others have demonstrated the favorable effects of delayedenteral feeding ( Petrov et al, 2009b ). Early EN should helpmaintain gut integrity (enterocyte population) and function(motility) and reduce bacterial translocation and ileus. Itshould also help to achieve caloric targets more quickly. Butearly nutrition is not without risk, particularly in hemodynami-cally unstable patients and in those requiring inotropic support.These patients appear to be at an increased risk of nonocclu-sive mesenteric ischemia, and it is best to commence EN afteradequate resuscitation.

and healthy volunteers ( Ammori et al, 1999 ; Juvonen et al, 2000b ; Nagpal et al, 2006 ). But an early RCT from the UnitedKingdom ( Powell et al, 2000 ) in which patients with predictedsevere AP were randomized to receive either EN or no articialnutritional support showed signicantly increased intestinalpermeability by day 4 in patients allocated to the EN group.Similarly, a recent RCT from Sweden comparing nasogastricEN and PN in patients with predicted severe acute pancreatitis

demonstrated impaired gut permeability on day 3 in the ENgroup ( Eckerwall et al, 2006 ). This difference might beexplained by the inclusion of a considerable number of patientswith mild AP in whom intestinal permeability is unlikely tochange ( Petrov et al, 2008f ).

Route of Enteral Feeding Nasogastric (NG) tube insertion may be more practical thannasojejunal (NJ), as the latter often requires endoscopy or radi-ology expertise, the transfer of patients within the hospital, anda delay in starting feeding. However, NJ EN has been preferredto NG EN because of a fear about pancreatic stimulation. Pan-creatic 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 ( OKeefe et al, 2003 ).By contrast, a study in patients with acute pancreatitis showeda signicantly lower rate of secretion of trypsin, amylase, andlipase in comparison with healthy subjects ( OKeefe et al, 2005 ). Moreover, it was shown that the greater the severity ofacute pancreatitis, the greater the reduction in pancreaticenzyme secretion as a response to duodenal feeding, probablyreecting greater injury of acinar cell mass. The possible clinicalimplication of these ndings is that NG EN may not aggravatethe course of acute pancreatitis, as was previously suggested.

Two RCTs have compared NG EN with NJ EN in patientswith severe acute pancreatitis ( Eatock et al, 2005 ; Kumar et al, 2006 ). These studies demonstrated the feasibility, safety, andtolerance of NG EN, but a meta-analysis did not demonstrate astatistically signicant reduction in risk of death ( Petrov et al, 2008b ). Before NG EN can be considered the standard of carein the nutritional support of patients with AP, a well-designedand adequately powered RCT comparing mortality and mor-bidity of NG EN and NJ EN is required. A practical compro-mise is to start EN through an NG tube after the patient hasbeen resuscitated and for the tube to be advanced when endo-scopic or radiologic assistance is available.

Type of Enteral Feeding The concept of pancreatic rest has also inuenced decisionsabout the type and content of enteral feeding. The preferredformulations, elemental and semi-elemental formulas ( Roberts, 2001 ; Petrov, 2007 ), did not require pancreatic enzymes fordigestion and absorption. However, the major disadvantage ofelemental and semi-elemental formulas is the cost, which isreportedly threefold to sevenfold higher than that of polymericformulas. A recent meta-analysis of RCTs compared these twoformula types in terms of feeding intolerance, infectious com-plications, and mortality and found that the use of polymericover elemental and semi-elemental feedings did not result inreduced tolerance in patients with acute pancreatitis andappeared to reduce the risk of infectious complications anddeath ( Petrov et al, 2009a ). Thus the use of elemental and semi-elemental formulas confers no apparent advantage over rela-tively inexpensive polymeric formulas.


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Cholecystectomy Recurrent attacks of gallstone pancreatitis carry a morbidityrate of up to 40% ( Banks & Freeman, 2006 ), and an early lapa-roscopic cholecystectomy is widely advocated within the samehospital admission (see Chapter 30). The optimal timing ofcholecystectomy has been controversial. The U.K. guidelinesfor the management of acute pancreatitis recommend that all

patients with biliary pancreatitis undergo denitive manage-ment of gallstones during the same hospital admission (indexcholecystectomy; Working Group, 2005 ). However, some sur-geons have concerns that early surgery may be associated withan increase in operative difculty and hence morbidity and con-version rate; therefore they advocate cholecystectomy after aperiod of 4 to 6 weeks to allow resolution of the inammatoryprocess (interval cholecystectomy; Green, 2008 ; Larson et al, 2006 ). These two approaches have been compared in severalRCTs, which demonstrated no difference in complication ratesbetween index and interval cholecystectomy; however, indexcholecystectomy resulted in a signicantly shorter length ofhospital stay ( Siddiqui et al, 2008 ). It is worth mentioning thatpatients with acute biliary pancreatitis were excluded from

these trials. An adequately powered RCT of index versus inter-val cholecystectomy is needed to draw a rm conclusion aboutthe optimal timing of cholecystectomy in patients with acutebiliary pancreatitis.

MANAGEMENT OF SYSTEMICCOMPLICATIONS

Most patients with acute pancreatitis have an initial suddeninammatory respiratory syndrome response, others developmultiple organ dysfunction syndrome (MODS) in the rst fewdays, and some develop MODS later in response to infectiouscomplications (see Chapters 52 and 53). Patients with severeand critical acute pancreatitis are best managed in an intensivecare environment to allow for optimal monitoring of uid resus-citation and organ function and the early identication oflife-threatening local or systemic complications. Systemic com-plications and organ failure are not an all-or-nothing phenom-enon, rather a continuous spectrum exists between normalfunction of an organ system and its complete failure ( Table 54.5 ; Marshall et al, 1995 ).

Some of the systemic complications of acute pancreatitis coagulation abnormalities that may range from intravascularthrombosis to disseminated intravascular coagulation, meta-bolic disturbances (hyperlipidemia, hypocalcemia), liver failure,encephalopathy, and Purtscher retinopathyare rare in clinicalpractice and beyond the scope of this chapter. In contrast,

Therapeutic Endoscopic RetrogradeCholangiopancreatography Endoscopic retrograde cholangiopancreatography (ERCP)with endoscopic sphincterotomy (ES) has been promoted as aproven intervention in patients with acute biliary pancreatitissince the early 1990s (see Chapters 18 and 27). This was basedon the ndings of two RCTs, from the United Kingdom

and Hong Kong, of early ERCP (within 24 to 48 hours ofadmission) with or without ES versus conservative treatment(Neoptolemos et al, 1988 ; Fan et al, 1993 ). Both trials demon-strated that early ERCP was associated with a reduction incomplications, but not in mortality, and only in patients withpredicted severe acute pancreatitis.

Some evidence suggests that the duration of biliary obstruc-tion, 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 cholangitissecondary to the obstruction and probably best explains theusefulness of ERCP in the context of acute biliary pancreatitis(Petrov, 2009 ). The rst multicenter RCT to examine the roleof ERCP in acute pancreatitis was designed to include only

patients without evidence of biliary obstruction ( Folsch &Neoptolemos, 2002 ). This German study did not nd anybenet of early ERCP (within 72 h after onset of symptoms)over conservative treatment. The most recent RCT, from Argen-tina, found that early ERCP in patients with biliary obstruction,dened by laboratory and radiologic criteria, and without evi-dence of acute cholangitis conferred no benet ( Oria et al, 2007 ).

Two important meta-analyses were published in 2008. Therst found that compared with conservative treatment, earlyERCP in patients with both predicted mild and predicted severeacute pancreatitis did not decrease the incidence of local pan-creatic complications or mortality rate ( Petrov et al, 2008d ).The second meta-analysis was designed to negate the con-founding effect of acute cholangitis and demonstrated nobenet of early ERCP over conservative treatment in terms ofcomplications and mortality in patients with predicted mild andpredicted severe acute pancreatitis ( Petrov et al, 2008e ). Theconclusion to be drawn from these studies is that early ERCP isindicated in patients with acute pancreatitis if acute cholangitisis evident (see Chapter 43) but not for those with just cholesta-sis ( Petrov, 2009 ). Although cholestasis can reect a persistingmain bile duct stone, it might also be due to edema of theampulla secondary to stone passage to the duodenum and maythus be expected to improve over the rst few days of admis-sion. Persistent cholestasis without cholangitis may require anERCP but not usually in the acute setting.

Table 54.5

Modied Marshall Scoring System

Organ System 0 1 2 3 4

Respiratory (PaO2/FiO2) >400 301-400 201-300 101-200 90


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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 isoften a mature (thick-walled) collection predominantly lledwith sterile necrosis. In these patients, intervention might expe-dite recovery. Intervention is very rarely indicated in patientswith sterile necrosis but may be required in those who continueto deteriorate despite maximal supportive care. In contrast,

patients with extensive infected pancreatic or peripancreaticnecrosis almost always require intervention, as this complica-tion is the most signicant determinant of outcome. Althoughinfected pancreatic necrosis has been considered an absoluteindication for surgical intervention, cases successfully managednonsurgically have been reported. Any necrotizing process,regardless of the infectious status, may cause signicant hemor-rhage (e.g., pseudoaneurysm) or bowel perforation (e.g., duo-denum or transverse colon), both of which require urgentintervention. Thus the type of local complication has a directbearing on the indication for treatment.

Trajectory of Patient The second consideration is the clinical status and trajectory ofthe patient. If supportive measures, such as those discussedabove, bring about clinical improvementevidenced by serialclinical assessment and inammatory markers, such asC-reactive protein (CRP)intervention is unnecessary. If,however, the patient continues to deteriorate despite maximumintensive care support, survival will depend on effective inter-vention. Related to this is a consideration of the physiologicreserve of the patient. Elderly patients with signicant preexis-tent morbidity have less physiologic reserve to withstand pro-longed severe illness and invasive interventions.

Timing of InterventionThe timing of intervention is an important consideration andone of the most difcult decisions to make in the managementof patients with acute pancreatitis. Early intervention of localcomplications is often fraught with difculty in patients withmore severe necrotizing pancreatitis because of the risk ofhemorrhage when necrotic tissue is less well demarcated fromviable tissue. Delaying intervention allows this demarcationand thus reduces the risks of bleeding, dissemination of infec-tion, and collateral damage to adjacent organs as the necroticprocess has stopped extending, and infected necrotic tissuesbecome organized and walled off. Appreciation of this hasresulted in a notable trend toward delayed intervention, whichis uncommonly performed before 4 weeks from the onset ofsymptoms.

Another emerging concept related to timing is the increasinguse of percutaneous catheter drainage in patients with infecteduid collections and those with infected necrosis. Preemptivedrainage with one or more catheters often produces an improve-ment in the patients overall clinical status, or at least it arrestsclinical deterioration. In this way drainage buys time and allowsthe more denitive necrosectomy to be delayed, until the patientis more stable, and the lesion is better dened. If required,repeat intervention can be undertaken on a programmed basis(e.g., every second day) or with an on-demand strategy, whereinthe intervention is repeated only if and when it is clinically indi-cated. The former is often necessary if intervention has occurred

respiratory, cardiovascular, renal, and intestinal dysfunction arethe most common systemic complications ( Banks & Freeman, 2006 ; Pandol et al, 2007 ).

Respiratory failure is the most common systemic complica-tion. The pathogenesis involves inammatory cytokines releasedfrom the pancreas and the action of phospholipase A 2 and otherpancreatic catabolic enzymes on the lung. The clinical diagnosisof incipient respiratory failure is based on tachypnea and low

oxygen saturation. A chest radiograph may conrm pleural effu-sions, pulmonary edema, and features of acute respiratorydistress syndrome. Management is supportive, with oxygensupplementation and analgesia, and some patients will ulti-mately require endotracheal intubation and mechanical ventila-tion. Lung-protective ventilation strategies should be instituted,such as adequate positive end-expiratory pressures, permissivehypercapnia, and tidal volumes of 6 mL/kg ideal body weight(Nathens et al, 2004 ).

Patients with severe and critical acute pancreatitis candevelop hypotension (arterial pressure 0.5 mg/dL or 44 mmol/L; Nathens et al, 2004 ;Tonsi et al, 2009 ). Treatment is supportive and focused onrestoring renal perfusion and providing dialysis if required.

The failure of the intestine is usually due to ischemia sec-ondary to hypovolemia and reex splanchnic vasoconstriction.The clinical diagnosis is based on the development of nauseaand vomiting, increased NG losses, tympanic distension of theabdomen, reduced bowel sounds, and reduced tolerance to EN.Intestinal failure with the breakdown in intestinal barrier func-tion and bacterial translocation can result in bacteremia and theinfection of pancreatic necrosis.

MANAGEMENT OF LOCAL COMPLICATIONSBecause local complications can develop at any time, frequentassessment and continuous monitoring of patients is necessary.When a local complication occurs, it is necessary to makean accurate diagnosis and to decide whether intervention isrequired, when it is required, and what intervention is appropri-ate. Managing the local complications of acute pancreatitisrequires a number of considerations.

Type of ComplicationThe rst consideration is the type of local complication and itsprognostic signicance. Early peripancreatic uid collectionsoften resolve without intervention and usually have little bearingon disease course. As such, this is more a manifestation of thedisease than a complication per se. Fluid collections may persist,often to the result of ductal injury and pancreatic leak; theymay cause symptoms because of a mass effect (e.g., gastricoutlet obstructions) and from secondary infection. Patients


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There are a number of variations to open surgical necrosec-tomy. More recently a number of less invasive approaches totreatment have been developed. The advocates for a less inva-sive approach argue that open surgery adds insult to injury andpushes a patient closer to or beyond their physiologic reserve;they point to the need to tailor treatment to specic lesions inindividual patients and to the opportunities afforded by thedevelopment and convergence of minimally invasive technolo-

gies. Enthusiasts must be cautious not to overstate the benetsof less invasive approaches in the absence of high-level evidence.The reported improvement in outcomes with less invasiveapproaches might be due to a number of factors, includingimprovements in the early management of acute pancreatitis,such as resuscitation and EN; better intensive care to preventand treat organ failure; more aggressive and appropriate use ofpercutaneous drainage; and better timing and selection ofpatients for intervention.

Classication of InterventionsIn response to the need to standardize the description of inva-sive interventions to facilitate communication, comparison,

and controlled trials ( Windsor, 2007 ), progress has been madewith the introduction of the VRP classication system, basedon the ICD-10 approach (Loveday et al, 2011). It uses threedimensions, combining the method of visualization of thelesion, route taken to reach the lesion, and the purpose of theintervention ( Table 54.6 ). Visualization includes open proce-dures, in which the operative site is exposed through the skinincision; endoscopic procedures, in which the operative site is

earlier in the disease course, when immature necrosum does notreadily debride.

Type of InterventionAnother important consideration is the type of intervention.There are many different interventions, and the challenge is toselect the intervention that is appropriate for the particular local

complication, taking into account the anatomic location, infec-tion status, complexity of any target lesions, the physiologicstatus and comorbidity of the individual patient, and the avail-ability of expertise with the type of intervention. A review ofcurrent guidelines highlights the absence of level 1 evidence toguide decision making regarding the types of intervention(Loveday et al, 2008 ). Two broad philosophies are evolving inthis regard. Many consider open surgical drainage with necro-sectomy to be the gold standard in the management of infectedpancreatic necrosis, and they reserve less invasive interventionsfor subsequent complications, such as percutaneous tube drain-age of residual uid complications. Such a step-down approach contrasts with the approach that advocates starting with lessinvasive interventions, such as percutaneous or endoscopic

drainage, and only employing open surgical techniques later inthe disease course in those who fail to respond (i.e., the step-upapproach ). These two approaches have been subjected to anRCT demonstrating that a minimally invasive step-up approachresults in a reduced rate of the composite endpoint of majorcomplications or death in patients with necrotizing pancreatitisand suspected or conrmed infected necrotic tissue ( van Sant-voort et al, 2010 ).

Table 54.6

VRP Classication of Invasive Procedures

V1 Radiologic Using only radiologic modalities (e.g., uoroscopy, CT, US, MR) to visualize and assist entering the target lesion V2 Endoscopic Using any white-light endoscopic instrument (e.g., exible 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 Insufcient information Vz Other visualization techniqueR1 Per os transpapillary External orice entry point, internal route traversing papilla to enter pancreatic ductR2 Per os transmural External orice entry point, internal route traversing gastrointestinal wallR3 Percutaneous retroperitoneal Skin external entry point, internal route traversing retroperitoneumR4 Percutaneous transperitoneal Skin external entry point, internal route traversing peritoneumR5 Percutaneous transmural Skin external entry point, internal route traversing gastrointestinal wall

Rx Insufcient informationRz Other routeP1 Drainage Letting out uid and/or sol id necrotic matter, externally out of the body or internal ly into the gastrointestinal tractP2 Lavage Flushing away solid necrotic matter with uid to facilitate external or internal drainageP3 Fragmentation Breaking down solid necrotic matter by instrumental or mechanical disruption to facilitate external or internal drainageP4 Debridement Taking or cutting out solid necrotic matter with either sharp or blunt dissectionP5 Excision Cutting out al l or part of the pancreas, including heal thy tissue, with the intention to fu lly remove al l necrotic matter Px Insufcient informationPz Other purpose

Procedures should be classied 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 classication of invasive procedures for treating the local complications of acute pancreatitis based on visualization, route, and purpose.Pancreatology 11:406-413.


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transverse mesocolon ( Fig. 54.2 ). Inammatory adhesions mayexist between the pancreas and stomach or transverse mesoco-lon, and great care is required during exposure. It is generallyuseful to take down both the hepatic and splenic exures, ifpossible, as this will facilitate exposure and reduce the risk ofcolonic stula secondary to drain erosion. When the processinvolves the head of the pancreas, access might require medialmobilization of the duodenum.

Open Necrosectomy with Closed Packing The goal of necrosectomy with closed packing is to perform asingle operation by performing a thorough debridement andremoval of necrotic and infected tissue to minimize the needfor reoperation or subsequent drainage ( Pezzilli et al, 2007 ).Primary closure of the abdomen is the intention. Once thenecrotic cavity is opened, uid collections are drained, and theexposure is enlarged to allow debridement of all areas ofnecrosis, including those in the perirenal and paracolic spaces.Early advocates used gauze-stuffed Penrose drains placed viaseparate stab incisions, but many variations are in practicewith regard to the type and number of drains. Between 2and 12 drains are placed with the intention to ll the cavityand provide some compression. Additional silicone drains(Jackson-Pratt) are placed in the pancreatic bed and lessersac for uid drainage. The stuffed Penrose drains are removedone every other day, starting 5 to 7 days postoperatively, allow-ing a slow collapse of the cavity. The silicone drains areremoved later.

Open Necrosectomy with Open Packing The difference with this approach is that the abdomen is leftopen after debridement and packing of the pancreatic bed,lesser sac, and retroperitoneum (Gotzinger, 2008). Drains areplaced in addition to the packing. Sometimes the abdomen isclosed, and the packing is accessed via separate ank incisions(Nakasaki et al, 1999 ). Open packing techniques have beenreported to have higher incidences of stulae, bleeding, andincisional hernias as well as a slightly higher mortality rate(Heinrich et al, 2006 ). However, it should be noted that no pro-spective trials have compared open packing with any othertechnique.

visualized with an endoscope (gastroscope, laparoscope, ornephroscope); radiologic procedures that use computedtomography (CT), ultrasound, or uoroscopy to visulalizelesions; and hybrid procedures that combine endoscopic andradiologic techniques. The routes taken by these interventionsinclude the external route into the body, by mouth or gastros-tomy tube, or the percutaneous route, through the skin; theinternal routes used to reach a target lesion might pass through

the gastrointestinal wall, peritoneum, or retroperitoneum.The overall purpose of treatment is to eliminate areas of

necrotic and infected tissue or uid and inammatory andenzyme-rich exudates. However, the way in which this isachieved varies considerably, and some procedures are muchmore aggressive than others. Therefore the purpose of individ-ual treatment procedures for PN may be to effect simple drain-age alone or to lavage the necrotic cavity to assist drainage ofnecrotic debris, fragment necrotic tissue to facilitate its drain-age, debride necrotic tissue, or excise or resect the pancreas.The overall aim of intervention is to control the septic focus andpreserve pancreatic function.

Open Surgical Necrosectomy Three general variations of open necrosectomy are currentlypracticed: 1) open necrosectomy with open or closed packing,2) open necrosectomy with continuous closed postoperativelavage, and 3) programmed open necrosectomy. Although theseare broadly similar in terms of the necrosectomy, they differ interms of how they provide egress routes for infected uid,debris, and tissue. The abdomen is entered though a midline orbilateral subcostal incision. The latter is preferred, as it mini-mizes contamination of the greater sac and allows easy access tothe extremities of the gland. The pancreas is exposed by divid-ing the gastrocolic omentum or gastrohepatic omentum toaccess the pancreas through the lesser sac. The body and tail ofthe pancreas ( Fig. 54.1 ) can also be exposed by elevating thetransverse colon and gaining access to the lesser sac via the

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): Atlasof 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 patic abscess. World J Surg 21[2]:162-168.)

Middle colicartery

Transversemesocolon


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reducing the number of operations and mortality ( Olejnik et al, 2008 ).

Several approaches to open surgical necrosectomy are pos-sible. Comparing them has limited value in the absence of con-trolled trials because of variations in referral patterns, selectioncriteria, patient comorbidities, and the use of presurgical percu-taneous management. Most techniques are associated with a15% to 25% mortality rate, but this can be higher in patients

with multiple organ failure and in those who have had earlysurgery. The important principles are adequate exposure guidedby high-quality preoperative CT scanning, gentle debridementof demarcated dead tissue, preservation of viable pancreatictissue, and thorough irrigation of the pancreatic bed, lesser sac,and retroperitoneum. Packing is probably best reserved tocontrol hemorrhage, as it is associated with an increased risk ofenteric stulae. The placement of wide-bore dependent drainsallows further egress of necrotic and infected material, aided bycontinuous irrigation, which may reduce the need for reopera-tion. In rare cases, when a necrosectomy is indicated within therst 2 weeks, an open approach should be considered becauseof the higher probability of requiring multiple procedures.

Endoscopic TechniquesIn 1996, Gagner described the rst true endoscopic treatmentof necrotizing pancreatitis, in which the pancreas was debridedusing a laparoscopic approach. Over the last decade, a widerange of endoscopic approaches for pancreatic necrosectomyhave been described, including infracolic laparoscopy, trans-gastric laparoscopy, hand-assisted laparoscopy, retroperitoneallaparoscopy, transgastric exible endoscopy, exible endoscopyvia a percutaneous endoscopic gastrostomy, and retroperitonealnephroscopy ( Ammori, 2002 ; Baron & Morgan, 1999 ; Charn-ley et al, 2006 ; Cuschieri et al, 1998 ; Horvath et al, 2001 ;Parekh, 2006 ). This array of endoscopic techniques can be clas-sied by the type of scope that is used: laparoscope, nephro-scope, or exible endoscope ( Windsor, 2007 ). Although someendoscopic procedures do not utilize radiologic modalities,many are hybrid procedures that incorporate uoroscopy orendoscopic ultrasound into the procedure.

Laparoscopic TechniquesMost laparoscopic techniques are minimally invasive versions ofopen surgical techniques, and they use an anterior or lateralapproach. In Gagners original (1996 ) description of laparo-scopic necrosectomy, two anterior routes retrogastric retrocolic and transgastric and one lateral route were described. In theretrogastric retrocolic route, a 30-degree laparoscope is intro-duced through the umbilical port following CO 2 insufation(15 mm Hg). Placement of additional ports depends on thelocation of the necrosis. Following necrosectomy, large sumpdrains are placed in the necrotic beds, and continuous lavagemay be established to remove peritoneal contaminants. In thetransgastric route, the stomach is opened anteriorly and poste-riorly. Endoluminal ports are used, which maintain the tip ofthe port inside the stomach. Debridement is performed inter-nally through the posterior stomach wall, in a technique akin toan open cystogastrostomy. It is also possible to use a transduo-denal route for necrosis of the pancreatic head, although thiscan be more difcult. No drains are left in the stomach, but adrain may be placed over the incision in the anterior gastricwall. With the retroperitoneal route, the patient is placed in the

Open Necrosectomy with Continuous ClosedPostoperative LavageIn this approach, debridement is followed by continuous peri-pancreatic lavage to remove infected necrotic debris, peripan-creatic exudates, and extravasated pancreatic exocrine uid(Fernandez-del Castillo et al, 1998 ). The large silicone drainagecatheters are placed into the pancreatic bed to inow andoutow isotonic irrigation uid ( Fig. 54.3 ). During closure, aclosed peripancreatic compartment is made by resuturing thegastrocolic and duodenocolic ligaments. Postoperative continu-ous lavage is instituted at 1 to 10 L per day and should becontinued until the efuent is clear and the patient showsimprovement in clinical and laboratory parameters ( Wig et al, 2004 ). No evidence is available to suggest the best irrigationuid, the optimal number or caliber of drains, or the duration ofirrigation.

Programmed Open Necrosectomy The principle of this approach is to be more conservative withdebridement, particularly if necrosum has not fully demarcated,with the intention of performing repeat procedures every 48hours until debridement is no longer required. The pancreaticbed is drained or packed, and the abdomen is closed by sutur-ing mesh or a zipper to the fascial edges of the wound. Thisallows multiple reentries and helps to prevent wound retraction,which aids in later delayed primary wound closure. In a propor-tion of patients, primary closure is not possible, and secondaryintention healing is allowed to occur, accepting that this mayrequire elective scar excision and repair of an incisional hernia.This procedure may be modied with the addition of intra-abdominal vacuum sealing (negative pressure 50 to 75 mm Hg)to encourage granulation of the pancreatic bed, potentially

FIGURE 54.3. Open necrosectomy with continuous closed post-operative lavage. (From Uhl W, et al, 2007: Necrosectomy. In Clavien P-A,et al (eds): Atlas of Upper Gastrointestinal and Hepato-Pancreato-BiliarySurgery. New York, Springer, pp 893-915.)


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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 laparo-scopic necrosectomy ( Bucher et al, 2008 ). Port placement(12 mm) is through postlaparotomy drain tracts, allowing intro-duction of both a 4-mm laparoscope and 5-mm instruments.Insufation pressures are kept to 8 mm Hg, as higher pressuresmay promote bacterial translocation from the cavity. Debride-

ment is performed with both hydrodissection and atraumaticgrasping forceps, hemostasis is achieved with monopolar dia-thermy, and a sump drain is placed for continuous postopera-tive lavage.

Nephroscopic TechniquesNephroscopic techniques utilize warmed uid to expand thenecrotic cavity, irrigate turbid uid, and maintain a clear visualeld. Carter and colleagues (2000 ) were the rst to describe theuse of a nephroscope during necrosectomy, terming the proce-dure percutaneous necrosectomy. The principle underlying thisprocedure is the same as for an open procedure: debridement ofdevitalized tissue and establishment of a system for continuouspostoperative lavagewith reduced physiologic stress on the

patient. Percutaneous necrosectomy may only be used when thearea of necrosis is accessible to percutaneous puncture, and it iscontraindicated in the presence of bowel ischemia, perforatedviscus, or signicant preoperative hemorrhage. The rst step isto insert a drainage catheter into the pancreatic lesion underCT guidance. The preferred path for drainage is between thelower pole of the spleen and the splenic exure ( Fig. 54.5 ),although in right-sided necrosis, a path through the gastrocolicomentum, anterior to the duodenum, may occasionally be used.The patient is then transferred to the operating room and posi-tioned in the left lateral position, or for right-sided necrosis, inthe right lateral position. A nephrolithotomy drape is used tocollect irrigant uid, and the drain tract is dilated to allow inser-tion of a 34-Fr Amplatz sheath. A nephroscope is insertedthrough the sheath into the cavity, and lavage is used to clearaway debris and suppurative uid ( Fig. 54.6 ). Following necro-sectomy, a 32-Fr soft drainage tube is left in the cavity. A smaller(8-Fr) catheter can be inserted through or alongside the largerdrain to allow continuous postoperative lavage. This might becommenced at 250 mL/h with warmed dialysis uid. Repeatprocedures are often required after 2 to 10 days (Carter &Wysocki, 2008).

Flexible Endoscopic TechniquesThe use of exible endoscopy to treat patients with PN has along history. In 1991, Prinz and Olen recognized that someareas of the abdomen were difcult to access during opennecrosectomy as a result of the inammatory process, thereforea choledochoscope was passed through the open abdomen todebride necrosis located in the lower retroperitoneum followingopen necrosectomy ( Prinz & Olen, 1991 ). Since that time, theuse of exible endoscopes has developed considerably, withmany different techniques currently available, as discussedbelow. In these procedures, the endoscope is either inserted viaan external or ice, usually the mouth, or a skin incision is made.

Peroral exible endoscopic techniques follow an internalroute through either the gastric/duodenal wall or duodenalpapilla, and some authors consider this to be a form of naturalorice transluminal endoscopic surgery ( Friedland et al, 2009 ).Initial descriptions of exible endoscopic treatment of PN used

left or right lateral position, and a small ank incision made.The three muscle layers of the abdominal wall are split, and atrocar is inserted. Using a 0-degree laparoscope and CO 2 insuf-ation (10 to 15 mm Hg), a tract is made through to the pan-creas. Once the necrotic areas have been identied, necrosectomyproceeds as when approached via a retrogastric retrocolic route.

These techniques have subsequently been modied. Of thelateral approaches, one of the most widely used laparoscopictechniques is videoscopic-assisted retroperitoneal debridement (VARD; Fig. 54.4 ), which was rst described by Horvath and colleagues in 2001 . The purpose of this procedure differs fromthose of open necrosectomy. Rather than performing completeremoval of all infected and necrotic tissue, the purpose ofVARD is to facilitate percutaneous drainage. In this technique,radiologic drainage of the lesion is rst instituted. In the operat-ing room, the patient is placed in a modied left lateral decubi-tus position, and a 4- to 5-cm incision is made in the left ankat the site of the drain. A nger is used to probe and conrmentry into the necrotic cavity. Fluid and loose necrotic debrisare removed by suction, and two ports (10 to 12 mm) areinserted through the incision. The incision is sealed with wetsponges and towel clips to allow insufation with CO 2. Debride-ment of necrotic tissue is performed with hydrodissection and10 mm forceps. Drains are placed for postoperative continuouslavage: a 10-Fr red rubber drain is brought through a separateanterolateral incision, and two 1.3-cm (0.5-inch) Penrose drainsare placed in the original skin incision. An ostomy bag is thenpositioned over the ank incision and Penrose drains, and con-tinuous lavage is performed through the red rubber drain at200 mL/h for 5 days or until the efuent is clear.

Variations of the anterior laparoscopic approaches are welldescribed. In addition to the retrogastric, recolic, and transgas-tric routes, a transmesocolic route may be used, in which thetransverse colon is elevated to expose the pancreatic lesion inthe lesser sac ( Cuschieri et al, 1998 ). Laparoscopic ultrasoundmay be used to conrm the position of the lesion, and the trans-verse mesocolon is usually opened to the left of the middle colicvessels. Following necrosectomy, two or more drains are placedin the pancreatic bed for postoperative lavage of the lesser sac.

FIGURE 54.4. Videoscopic-assisted retroperitoneal debridementtechnique. (From van Santvoort HC, et al, for the Dutch Acute PancreatitisStudy Group, 2007: Case-matched comparison of the retroperitoneal approachwith laparotomy for necrotizing pancreatitis. World J Surg 31:1635-1642.)

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Endoscopic retrograde pancreatography (ERP) can be usedto diagnose any communication between the duct and cavity orduct stenosis or disruption, and transpapillary stenting can beemployed to decompress the duct. Puncture of the posteriorgastric wall into the pancreatic lesion may be performed at thepoint of maximal bulging, although conrmation of the locationwith endoscopic ultrasound helps achieve correct placement ofthe perforation and avoids injury to vessels. A successful punc-ture is conrmed with aspiration of suppurative uid from thecavity.

The injection of contrast with uoroscopy can be used todetermine the extent of the cavity. The gastric perforation isdilated with balloons up to 20 mm. For lavage and drainage, a7-Fr nasocystic (lavage) and a 10-Fr pigtail drain (drainage) are

lavage and drainage without instrumental debridement ( Baron et al, 1996 ). A more aggressive approach was subsequentlyintroduced, which demonstrated that necrotic tissue may bedebrided with baskets, snares ( Fig. 54.7 ), forceps, and suction(Seewald et al, 2005 ). A recent long-term multicenter study oftransluminal endoscopic necrosectomy described 93 patientswho underwent a mean of six interventions, starting at a meanof 43 days after the onset of severe acute pancreatitis ( Seifert et al, 2009 ). Initial clinical success was obtained in 80% ofpatients but with a complication rate of 26% over 43 months offollow-up; 16% developed recurrent pancreatitis, 10% requiredfurther endoscopic procedures, 4% required surgical treatment,and the mortality rate was 7.5% at 30 days. Surgical necrosec-tomy was required in 12% of patients.

FIGURE 54.5. Insertion of a drainage catheter under CT guidance. (From Bruennler T, et al, 2008: Percutaneous necrosectomy in patients with anecrotizing pancreatitis. Eur Radiol 18[8]:1604-1610.)

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procedures are usually required to clear the cavity of necrotictissue. A similar procedure may be performed with externalentry into the body via a percutaneous endoscopic gastrostomy(PEG) tube ( Baron & Morgan, 1999 ).

Several techniques using exible endoscopy through skinincisions have been described. The rst was by Prinz and Olen (1991) after open necrosectomy, as detailed above. Followingpercutaneous necrosectomy with a nephroscope, subsequentdebridement may be undertaken using a exible endoscope, aso-called sinus-tract endoscopy ( Carter et al, 2000 ). The draintract is dilated to 45 Fr, and a exible endoscope is inserted intothe cavity for necrosectomy. A similar technique has beendescribed following open necrosectomy via a translumbar inci-sion, in which a exible endoscope is inserted into the cavity fordebridement of ongoing necrosis ( Jakobs et al, 2000 ). Theseendoscopic debridements were initiated 10 days after the opennecrosectomy and were carried out every 3 days for 4 weeks(approximately 8 to 10 sessions).

The plethora of endoscopic approaches to necrosectomyand the absence of formal comparison make a recommendationfor the optimal approach problematic. The selection of an endo-scopic technique will be inuenced by training, experience, andthe availability of equipment, but it will also be determined bythe location and complexity of the target lesion and the clinicalstatus of the patient.

Radiologic TechniquesInterventional radiology techniques are assuming greaterimportance, particularly for initial sepsis control to allow deni-tive necrosectomy to be performed more electively ( Jakobs et al, 2000 ). Ultrasound, uoroscopy, or CT is used to guide theinterventional radiologist into the pancreatic lesion. These

placed in the cavity ( Fig. 54.8 ). Continuous lavage with1500 mL/day saline is established. Necrosectomy may be per-formed with endoscopic instruments, such as a Dormia basketor polypectomy snare, and introduction of a forward-viewingendoscope into the necrotic cavity can be used for better visual-ization during the necrosectomy. Multiple necrosectomy

FIGURE 54.6. Percutaneous necrosectomy technique. (From Uhl W,et al, 2007: Necrosectomy. In Clavien P-A, et al (eds): Atlas of Upper Gastro-intestinal and Hepato-Pancreato-Biliary Surgery. New York, Springer, pp893-915.)

30 F Balloon Catheter

34 F Trocar Sheath

Irrigation Setup

Operating Nephroscopeand Sheath

Balloon Inflator

FIGURE 54.7. Pancreatic necrosis debridement with the use of exi-ble endoscope. (From Seewald S, et al, 2005: Aggressive endoscopic therapy for pancreatic necrosis and pancreatic abscess: a new safe and effective treatmentalgorithm [videos]. Gastrointest Endosc 62[1]:92-100.)

FIGURE 54.8. Transmural drainage of organized pancreatic necro-sis. (From Baron TH, et al, 2002: Outcome differences after endoscopicage of pancreatic necrosis, acute pancreatic pseudocysts, and chronic p pseudocysts. Gastrointest Endosc 56[1]:7-17.)


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surrounding tissues. However, this has not been demonstratedas a major problem clinically, most likely because the pancreaticlesion is walled off in a brous capsule 4 to 6 weeks after theonset of acute pancreatitis.

The efcacy of radiologic drainage procedures is reducedwith more solid lesions. In patients with PN treated withpercutaneous catheter drainage, approximately half will be suc-cessful and will not require surgical intervention ( Jakobs et al,

2000 ). Indications for surgical intervention in patients whohave undergone percutaneous catheter drainage include persis-tent systemic or local manifestations of infected PN, physiologicdeterioration despite the placement of a patent drain, persistentabdominal pain, and intolerance of oral intake after the sys-temic inammatory response syndrome has resolved ( Jakobs et al, 2000 ).

Radiologic Debridement TechniquesIn some specialized centers, radiologic techniques have beenused to debride PN. These procedures are similar to percuta-neous catheter drainage, as described above, but they alsoinclude removal of necrotic material with snares, baskets, oreven by applying suction to a catheter during its removal

(Economou & Ward-McQuaid, 1971 ; Jakobs et al, 2000 ;Thompson, 2001 ). Necrotic tissue may be fragmented withwires before attempting its extraction ( Blamey et al, 1984 ;

Jakobs et al, 2000 ), and lavage is recommended to ush outloosened necrotic debris.

A tailored approach to the treatment of the local complica-tions of acute pancreatitis is required and must take into accountthe specic lesion, the patients status, and the operators exper-tise. Strong trends toward delayed intervention and less invasiveintervention have been seen. Radiologic drainage has assumeda more important role for the denitive treatment of predomi-nantly uid-lled lesions and to delay denitive necrosectomy,either by minimally invasive or open methods. The convergenceof technologies is apparent, and the plethora of minimally inva-sive techniques can now be classied to facilitate accuratedescription and much needed RCTs.

CONCLUSIONThe management of acute pancreatitis remains a formidablechallenge and continues to evolve. Although specic treatmentsfor acute pancreatitis remain elusive, progress has been made inthe management of pain, uid resuscitation, antibiotic prophy-laxis, enteral nutrition, therapeutic ERCP, and cholecystec-tomy. Progress has also been made in the intensive caremanagement of systemic complications and in the developmentof less invasive interventions for the treatment of local compli-cations, particularly infected pancreatic necrosis. This chapterhas highlighted the need for more evidence to guide decisionmaking, quell persisting controversies, and reduce variations inpractice, particularly in patients with severe and critical acutepancreatitis.

References are available at expertconsult.com .

radiologic modalities are also used to dene the extent andcomposition of the lesion, visualize the instruments used, anddetermine the efcacy of the treatment procedure. The purposeof radiologic techniques may be to achieve either drainage, withor without lavage, or debridement.

Radiologic Drainage TechniquesDrainage techniques are most effective if target lesions have asignicant uid component. They can be located in many sitesbut are most often in the lesser sac, anterior and left pararenalspaces, and other parts of the retroperitoneum ( Fig. 54.9 ;

Jakobs et al, 2000 ). Image-guided needle puncture of the lesionmay involve a retroperitoneal or transperitoneal route and maybe transmural (transgastric or transduodenal), but a retroperi-toneal approach is preferred to reduce the risk of contaminationand possible peritonitis ( Jakobs et al, 2000 ). A guidewire ispassed down the needle, and the tract is dilated to accommo-date a catheter. Because catheters readily block with necrosumand debris, it is advisable to maximize catheter diameter toimprove patency. Typically, catheters should have multiple side-holes and a minimum diameter of 12 Fr ( Jakobs et al, 2000 ).Drain tracts may be serially dilated to accommodate largercatheters (20 to 24 Fr). Often multiple catheters are required,especially for large or complex lesions. To increase the efcacyof the drainage procedure, remove toxic factors, and help main-tain catheter patency, lavage should be considered ( Eatock et al, 2005 ; Jakobs et al, 2000 ). Theoretical concerns have been raisedthat lavage may spread infection, either from infected uid spill-ing over into previously sterile cavities or from the increasedintracavity pressure, resulting in translocation of bacteria into

FIGURE 54.9. Common percutaneous access routes for drainage ofpancreas and peripancreatic sites. A, Transhepatic. B, Transgastric.C, Retroperitoneal from left ank. D, Paravertebral. E, Subhepatic.(Modied from Lee MJ, Wittich GR, Mueller PR, 1998: Percutaneous interven-tion in acute pancreatitis. Radiographics 18[3]:711-724.)

A B

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