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 19 November 2017

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View all the figures for this chapter.

ERCP

Peter B. Cotton


9. Complications of pancreatitis

Douglas A. Howell

Top of page Synopsis  Next section

Complications of acute and chronic pancreatitis are varied, often complex, and potentially fatal. This chapter will attempt to summarize all of these feared developments, address their causation, and review current and potential future approaches.

The first section deals with the toxic and metabolic complications. Early death from pancreatitis most frequently follows shock, a poorly understood but dramatic occurrence seen, fortunately, in a small minority. All organ systems may be affected, in a fashion that can range from mild to very severe, resulting in renal failure, respiratory failure, disseminated intravascular coagulation, and severe gastrointestinal bleeding. Prolonged septic-like systemic inflammatory response syndrome may result in coma, and a profound catabolic state untreatable by total parenteral nutrition.

Recent clinical experience has recognized the major difference in clinical course and treatment when pancreatic necrosis complicates the early phase of acute pancreatitis. Diagnosis, treatment, and predictors of outcome are addressed.

The chapter closes with a comprehensive review of the main miscellaneous complications which are often recognized during the later phase of pancreatitis. Patients who appear to be recovering may experience fistula formation, producing acute pancreatic hydrothorax or enteric fistulas. Percutaneous or surgical drainage is a frequent cause of cutaneous fistulas, a particularly difficult and debilitating complication. Finally, dramatic and potentially fatal vascular complication can occur very abruptly, taxing the diagnostic and interventional skills of the treating team.

Throughout this review up-to-date reports of successful approaches to all of these events are addressed. We emphasize that since controlled trials of newer treatment modalities have, in general, not been directly compared to traditional surgical therapy, a multidisciplinary approach with gastroenterology, interventional radiology, and surgery is vital.

Top of page Toxic and metabolic complications  Previous section Next section

Few diseases can produce more varied and severe diffuse metabolic complications than acute pancreatitis. Although the organ weighs only 90 g in the adult, when inflamed, the pancreas can produce such profound systemic effects that respiratory, renal, and circulatory failure can rapidly ensue, producing multiorgan system death within a few days. In patients with severe acute pancreatitis, the likely sequence is peripancreatic leakage of proteolytic juice, activation of proinflammatory cytokines, third space loss secondary to retroperitoneal injury, hypoperfusion, and finally, rapid progression to frank pancreatic necrosis.

This sequence is variable and may appear as partial individual organ compromise or full-blown multiorgan failure. The recognition of these end organ complications served as the basis for the famous 'Ranson's criteria', which has for nearly 30 years remained the most popular clinical measure of the severity of acute pancreatitis (Fig. 1) [1].

A principal drawback to Ranson's scoring system has been the need to reassess the patient at 48 h before a final score can be calculated. In an effort to predict severity as early as possible to help triage patients to the most appropriate level of care, several other clinical scoring systems have been advocated [2–4]. The Acute Physiologic and Chronic Health Evaluation scoring system (APACHE II and III) permits a more comprehensive initial assessment of severity. Khan pointed out recently that since the natural history of pancreatitis varies considerably depending upon underlying etiology, patient responses, and presence of comorbidity, APACHE scoring, when repeated at 48 h, as in Ranson's criteria, more accurately predicts outcome [4].

The modified Glasgow Coma/Imrie score has also been used to predict severity and thus the development of complications. One direct comparison of these three scoring systems recently reported that APACHE III and modified Glasgow/Imrie had a greater magnitude of correlation with length of hospital stay as a measure of severity than did Ranson's traditional criteria [2]. However, death was equally predicted, with fatal cases uniformly having > 5 Ranson criteria, APACHE III scores > 30 at 96 h, and modified Glasgow/Imrie scores > 4.

Alternatively, in a slightly smaller but contemporary study, Ranson's criteria, particularly at 48 h, remained a valid scoring system for severity of pancreatitis when compared to the newest APACHE III scoring [5]. Because of its inherit simplicity, the authors advocated the continued use of the venerable Ranson's criteria and emphasized that elevated BUN, low calcium, base deficit, and third space loss predicted mortality.

In clinical practice currently, a CT-based measure of severity has proved valuable when added to clinical scoring [6]. Robert recently analysed all available clinical scoring systems plus a CT scan score of severity in 130 patients [7]. Multivariate analysis revealed that low serum albumin plus extra pancreatic fluid collections on initial CT scanning within the first 24 h was the best predictor of severe pancreatitis overall.

Although some concern has been raised as to the potential for renal toxicity of contrast-enhanced early CT scanning in acute pancreatitis, the general consensus suggests that the value of the information gained remains worthwhile [8].

Shock and renal failure have traditionally been the most frequent and perhaps the most feared of the potential toxic and metabolic complications of acute pancreatitis. In the mid-1960s, Frey reported a 22% rate of shock and renal failure in his series of 490 patients [9]. At that time mortality followed in nearly 80% of these complications.

Although shock and renal failure are associated in most patients, oliguria and even anuria requiring prolonged dialysis can be seen in euvolemic patients with normal blood pressures throughout their early illness. This dramatic systemic complication is attributed to profound renal cortical vasoconstriction due to poorly understood nephrotoxic vasoactive circulating factors produced by the acute inflammatory response. Permanent renal failure eventuating in renal transplantation rarely occurs.

Respiratory complications occur in a variable percentage and often in a stepwise fashion, with hypoxemia with a normal chest X-ray being the most frequently recognized. Pulmonary infiltrates, atelectasis with elevated diaphragms, and pleural effusions may then ensue and progress to full-blown acute respiratory distress syndrome (ARDS), often requiring ventilatory support. This sequence is again poorly understood but appears to be precipitated by circulating proinflammatory cytokines due to the retroperitoneal proteolytic injury, producing an alveolar capillary leak. The flood of protein-rich fluid can, at times, produce such complete consolidation that mechanical ventilation cannot compensate, resulting in a respiratory death [10].

Disseminated intravascular coagulation (DIC) is a less frequent complication of acute pancreatitis [1]. DIC may produce severe bleeding since extensive retroperitoneal injury is present. The consequence of such hemorrhage can greatly worsen the above outlined systemic complications.

A more recently described toxic reaction to pancreatitis has been termed systemic inflammatory response syndrome (SIRS) [11]. High fever, tachycardia, and delirium may persist for days or even weeks and may be difficult to distinguish from bacterial sepsis. This syndrome can produce a profoundly catabolic state that cannot be adequately reversed with total parenteral nutrition (TPN) [12–14].

In patients with severe SIRS, fine-needle radiologically guided aspiration of retroperitoneal fluid collections has proved to be valuable for distinguishing this syndrome from complicating retroperitoneal infection. To avoid potential contamination of otherwise sterile fluid, a fastidious technique to avoid traversing bowel, particularly colon, and with adequate skin preparation, is mandatory [15,16].

In patients with a less severe form of SIRS, TPN can be switched to enteral feeding to further minimize pancreatic stimulation; Takacs demonstrated that adding octreotide to enteric feedings reduces gastrointestinal hormone release (CCK, glucagon, gastrin, and glucose) to baseline [17]. Windsor has developed evidence that this change to the enteral route for nutrition can actually diminish the inflammatory response and lead to more rapid improvement compared to continuing TPN [18]. Tube placement, duodenal edema, and prolonged ileus may all hamper the initiation of enteral feeding in sicker patients, however.

Platelet activating factor (PAF) has been implicated in the pathogenesis of SIRS, possibly by amplifying mediators of inflammation. Unfortunately, an attempt to block this effect by the infusion of lexiphant, a potent inhibitor of PAF, was demonstrated to have no clinical benefit in a placebo-controlled trial [19].

Death due to acute pancreatitis follows two patterns: early (within 1, or in some series, 2 weeks) and late. Early death is secondary to these incompletely understood severe metabolic inflammatory responses leading to multiorgan system failure. Death later than 2 weeks is generally secondary to sepsis and represents about one-half of fatal cases [20]. Death rates in various recent series with variable etiologies range from 2 to 9%, which represents a marked improvement compared to the pre-TPN era [21].

Factors which may be important in the sequence of rapid onset multiorgan system failure are under active research. Ethridge et al. recently studied the impact of cyclo-oxygenase (COX) on pancreatitis severity, especially with regard to lung injury [22]. In their mouse model, inhibition of COX-2 or deletion of the COX gene profoundly decreased severity of pancreatitis and protected against ARDS.

Host response may prove to be a critical determinate of the severity of pancreatitis and the resulting complications [23,24]. A defect in interleukin-10 function has been identified in some patients with severe acute pancreatitis [25]. This defect might result in a failure to down-regulate the initial acute inflammatory reaction once they have been maximally stimulated. If confirmed, this finding would help us to understand why these seemingly unpredictable complications may be seen even after rather trivial injury, such as after simple cannulation or unremarkable sphincterotomy at ERCP.

In an attempt to prevent post-ERCP pancreatitis, an initial randomized trial of a single bolus of interleukin-10 (8 µg/kg) was given to patients 15 min prior to ERCP and compared to a placebo group [26]. Unfortunately, both groups experienced the identical rate of pancreatitis and, furthermore, the severity as measured by length of stay was the same. Nevertheless, a full understanding of the role of pro- and anti-inflammatory cytokines may be the best hope of preventing or at least attenuating the severity of acute pancreatitis.

Top of page Pancreatic fluid collections  Previous section Next section

In the setting of pancreatitis, fluid collections are frequent and have been used as a measure of severity to create a CT-based score as previously discussed [6]. When combined with extent of non-perfusion (equivalent to necrosis) and detection of retroperitoneal complications, CT becomes a vital tool in predicting severity [27].

Fluid collections are at first sterile, amylase rich, and unorganized. They are seen early, often within 24 h, and may persist. Unencapsulated and younger than 4 weeks from the onset of pancreatitis, they are properly watched expectantly (Fig. 2 B). If necrosis is not present, infection is rare. Whether they will persist, organize, and encapsulate beyond 4 weeks into a true pseudocyst largely depends on pancreatic ductal anatomy and the presence of necrosis. Normal ductal and sphincter anatomy predicts spontaneous resolution, whereas fistula, ductal obstruction, or disruption predict persistence and pseudocyst formation [28]. Finally, necrosis will organize slowly and an associated fluid collection will usually become a complex pseudocyst; this might be better termed an area of 'organizing necrosis' to distinguish them [29].

Top of page Pseudocysts and abscesses  Previous section Next section

A pseudocyst of the pancreas is a maturing fluid collection surrounded by granulation tissue which occurs as a consequence of acute or chronic leakage of pancreatic juice (Fig. 2A). In distinction, acute fluid collections may be wholly inflammatory and will frequently resolve. Alternatively, severe ductal disruption with a consequent large fistula will virtually always result in pseudocyst formation [30,31].

Prior to any decision regarding management, a pancreatic pseudocyst must be carefully distinguished from other cystic or fluid-filled collections in the retroperitoneum [32–35]. In the absence of a definite attack of pancreatitis, some pseudocysts may be exceedingly difficult to differentiate from true cystic neoplasms. [36,37]. Inadvertent endoscopic or surgical drainage of true neoplasms is ineffective and occasionally disastrous. Be aware that obstructing neoplasms, usually malignant, can produce acute or chronic pancreatitis and result in a pseudocyst. These combination cases can be extremely challenging to diagnose and treat [38]. In most cases careful clinical history, dynamic CT, and pancreatography are necessary prior to establishing a complete diagnosis. In atypical cases, endoscopic ultrasound (EUS) adds important diagnostic information, especially if a small obstructing tumour or a cystic neoplasm is present [39–42].

The evolving pseudocyst requires time to develop a complete encircling wall which, of course, lacks an epithelial lining (Fig. 2 B). By recent consensus, 4 weeks has been chosen as a minimal time from the onset of acute pancreatitis until this process is reasonably complete and the collection can be termed a pseudocyst [43]. The development of a pseudocyst in chronic pancreatitis is often more difficult to precisely age. These collections often occur more gradually as a consequence of ductal obstruction by stones or fibrotic strictures and are frequently mature upon discovery. Once a secure diagnosis of a mature or maturing pseudocyst is established, the clinician must remember that many pseudocysts will still resolve. Early authors emphasized that pseudocysts larger than 6 cm rarely resolve, but size alone does not always warrant intervention [30]. Etiology remains important since pseudocysts complicating acute pancreatitis are much more likely to resolve than those due to chronic pancreatitis [44]. Clinicians were formerly hesitant to follow pseudocysts for fear of the spontaneous development of complications, especially infection and hemorrhage. However, several authors have reported a surprisingly low incidence of adverse events during follow-ups in asymptomatic patients with stable or slowly resolving pseudocysts [45,46].

In general, patients with continued ductal leakage communicating with the pseudocyst will not stabilize and permit resumption of a diet (Fig. 3). Clinicians should be suspicious if, after initial improvement with symptom resolution on IV therapy (with or without TPN and octreotide), pain returns upon oral feeding. A serious ductal injury or leak is often present in this setting [47].

Unchecked, continued leakage with resulting expansion can produce a series of additional complications. Progressive enlargement in the usual retrogastric position will produce gastric compression resulting in early satiety, nausea, vomiting, pain, and weight loss. Frank outlet obstruction usually occurs at the pylorus or in the duodenal sweep (Fig. 4). When the ampullary area and pancreatic head are involved obstructive jaundice often occurs.

The accumulating fresh enzyme-rich pancreatic juice from a ductal leak can lead to damage and digestion of additional retroperitoneal structures such as blood vessels, or adjacent hollow organs such as the duodenum or colon, or lead to spontaneous perforation into the peritoneal cavity resulting in pancreatic ascites.

Spontaneous infection of a pseudocyst is a feared late complication. Formerly termed infected pseudocyst, the preferred term now is pancreatic abscess [43]. The source of the infecting organism is often unknown, presumably from transmigration of nearby colonic bacteria or from transient bacteremia, but may follow line sepsis or fine-needle aspiration. Gas-producing organisms produce multiple small air bubbles in the pseudocyst, but the presence of gross air within the cavity is often due to fistulization to the duodenum or colon (Fig. 5)[48].

Gaining an understanding of the pancreatic ductal anatomy earlier in the course of pseudocyst patients holds the promise of allowing earlier necessary intervention in pancreatitis patients [28,49]. Traditionally, diagnostic ERCP has been the major test for defining pancreatic ductal anatomy, but most clinicians would not perform early ERCP due to the fear of introducing potentially catastrophic infection. Magnetic resonance pancreatography (MRP) is proving useful in detecting major disruption and predicting the need for intervention without this risk. In our experience MRP does not permit reliable ductal anatomy in lesser leaks since communicating fistulas may contain very little of the static fluid upon which MRCP depends for imaging.

Once the need for intervention has become apparent, the choice of drainage has gradually yielded to endoscopic transmural and transpapillary techniques [50,51]. Clear indications for intervention in well-defined pseudocysts are summarized in Fig. 6. Radiological drainage remains popular in some centres but risks include prolonged drainage, introducing infection, and establishing a fistula when ductal obstruction or disruption is present [30,52].

The detailed techniques of endoscopic drainage are outlined completely in several recent comprehensive reviews [53,54]. To summarize, transmural endoscopic puncture begins with first identification of the appropriate site, then proceeds to needle localization with injection of contrast, puncture (Fig. 7 A, B) 10 mm balloon dilation of the tract, and, finally, multiple stent placement (Fig. 8 A, B, C, D).

Transpapillary therapy involves pancreatic stent placement with or without pancreatic sphincterotomy [55–57]. We have employed pancreatic sphincterotomy alone when the anatomy suggests that complete decompression of the duct by transecting the sphincter muscle should be adequate, thus avoiding the risks of pancreatic stent placement.

A recent long-term follow-up of such endoscopically treated pseudocysts reported excellent results with 15% (6 of 38) recurrence, all in alcohol-induced and therefore, chronic pancreatitis [58]. Complications of endoscopic drainage include perforation when the true lumen of the pseudocyst is missed or the pseudocyst is not adherent or sufficiently organized. Severe bleeding, especially from the gastric wall was a former frequent complication when simple diathermic puncture was followed by extension of the entry point using a sphincterotome [59]. A recently described technique of drainage to avoid any cautery advocated placing a guidewire through a special needle used for the initial localizing puncture. Once the guidewire is within the cavity, balloon dilation alone is used to create the endoscopic cystenterostomy drainage site [60].

Overall, the success rates for endoscopic pseudocyst drainage are summarized in Fig. 9 and approach 80%. The complication risk and recurrence rates stated in these studies are included in Fig. 10 and were 12 and 16%, respectively. Finally, recurrences could be retreated endosurgically about 50% of the time, relegating surgery to only 8 patients out of the 141 cases selected and reported.

The role of EUS pseudocyst management remains in evolution (Fig. 11). Some authors report rarely needing or using EUS but others consider EUS valuable in selecting appropriate drainage sites, excluding intervening blood vessels, and determining depth of puncture [53,61]. However, when collected as diagnostic this information may be difficult to transfer to actual therapy, which is generally done with larger-channel therapeutic endoscopes whose angle of view and therefore alignment for puncture is different from EUS [62,62]. Direct EUS therapeutic drainage but placing 7 Fr stents has been reported, but results are unlikely to equal 10 Fr drainage [63]. Finally, the development of a therapeutic 4.2 channel EUS endoscope has permitted complete therapy, including 10 Fr stent placement in pseudocyst patients [64]. As EUS becomes a more available therapeutic technique this approach may compete well with our current endoscopic transmural drainage procedure.

Finally, laparoscopically directed pseudocyst drainage has been reported but appears to be more invasive, more costly, and has not defined a superior outcome [65].

Top of page Pancreatic necrosis  Previous section Next section

Necrosis of pancreatic tissue complicates acute pancreatitis in a variable percentage of cases, is seen less often in acute exacerbations of chronic pancreatitis, and accounts for many of the complications and much of the mortality (Fig. 12). Etiologies may have an impact on severity with the pancreatitis caused by hypertriglyceridemia producing necrosis in perhaps the highest percentage of at-risk cases [66].

In a large single institutional review, Blum et al.[21] reported a respectably low overall mortality rate of 5% amongst 368 cases of acute pancreatitis, again with about half being earlier than 2 weeks and the remainder later. To emphasize the importance of necrosis, only 36 cases (10%) had documented necrosis but accounted for 9 of the overall 17 deaths. Thus, presence of necrosis resulted in an eventual death rate of 25%. Finally, the authors noted that late deaths in the absence of necrosis were seen in only 4 of 212 patients at risk (2%).

At present, the exact mechanism of necrosis is unknown but ischemic infarction is held as most likely. Poor perfusion secondary to rapid third space loss has been postulated but recent data suggest that the process of necrosis may be underway very rapidly before perfusion is affected. In a retrospective case analysis, patients with necrosis presented earlier but had a similar incidence of hemoconcentration compared to patients with interstitial pancreatitis [67]. Resuscitation volumes were similar retrospectively in both groups. However, patients whose hematocrits continued to rise despite large volumes of fluid resuscitation were all subsequently proven to have necrosis. A cause and effect of inadequate resuscitation could not be established.

The consequence of necrosis is a high likelihood of developing infection in the devitalized tissue, and the loss of a functioning pancreas with consequent diabetes, fistula formation, and various vascular injuries. Many of these complications result in the need for operative and, more recently, ensodcopic management.

Since pancreatic necrosis produces significant morbidity and a large proportion of the late mortality caused by acute pancreatitis, a search for necrosis using dynamic CT is generally felt justified [68].

Management of necrosis initially is conservative, with the expectation of most patients who do not develop infection eventually spontaneously resolving [69]. However, once the necrotic tissue becomes infected, intervention is almost always required. At present, the majority of these patients are still best managed with surgical debridement and drainage, almost always externally [15]. Prolonged hospitalization with multiple procedures often follows, with surgical centers favouring either closed drainage with subsequent radiologically assisted catheter drainage or open drainage with surgically placed abdominal mesh to permit planned repeated debridements [70].

A few cases of attempted retroperitoneal laparoscopic necrosectomy have been reported [71,72]. At present this experience is anecdotal and no comparative trials have yet been reported. The risk of sudden and severe bleeding, and the need for multiple repeat interventions have prevented wide adoption of the technique.

In an attempt to prevent the development of infection in the setting of necrosis, the use of broad-spectrum antibiotics, especially imipenem, has reached a consensus. All eight recently reviewed trials demonstrated benefit in the patients receiving broad-spectrum antibiotics [73]. Many questions remain as to the use of newer antibiotics, the duration of therapy, the timing of onset of use, and the need for fungal coverage [74,75].

Organizing necrosis  Previous section Next section

As stated earlier, persistent necrotic material organizes and encapsulates into a complex collection containing a mixture of solid and semisolid debris and fluid. Simple catheter drainage will be insufficient to evacuate this material and infection will often complicate such efforts. When approaching apparent pseudocyst patients, it is of paramount importance to assess for necrosis, then plan and treat patients appropriately [76]. Endoscopic treatment of organizing necrosis is possible but demands techniques of wider drainage such as the placement of multiple stents, creation of a large cyst gastrostomy, and at times nasocystic lavage [29] (Fig. 13 A, B, C, D).

Repeated endoscopic procedures should be anticipated since cavity infections will occur in greater than 50%. When prompt reintervention is performed, these infections can usually be managed with lavage and repeat or additional stent placement. Nevertheless, a multidisciplinary approach to these cases is mandatory for optimal patient outcome. The interventional disciplines of surgery, gastroenterology, and radiology all have roles to play in specific situations [66].

Top of page Miscellaneous complications  Previous section Next section

Pancreatic fistulas  Previous section Next section

These occur in both interstitial and necrotizing pancreatitis. In the presence of an intact pancreatic sphincter or a ductal stricture, the initial leak continues and, as discussed earlier, is often the etiology of pseudocyst formation. At times and for unclear reasons, some collections do not wall-off and the fistula may track throughout the retroperitoneum. Fistulous communication under the diaphragmatic cruri can result in amylase-rich pleural effusions, broncho-pleural fistulas, or even pericardial tamponade [77,78]. Cases of inguinal, scrotal, femoral, and other hernias developing with amylase-rich fluid tracking down these potential spaces have been reported.

Internal fistulas adjacent to hollow organs are perhaps the most frequently recognized. Fistulization to the duodenum may result in resolution of an otherwise expanding pseudocyst as mentioned earlier [48]. Communication between a pseudocyst and the colon will be complicated by sepsis and generally will require surgery. However, Howell et al. reported successful endoscopic treatment of two such cases without requiring surgery [79].

Perhaps, the most dramatic consequence of a pancreatic ductal fistula is pancreatic ascites. Easily diagnosed by routine testing of paracentesis fluid for amylase, these rather rare cases are often overlooked and treated mistakenly as cirrhotic ascites since liver and pancreatic disease often coexist in the alcoholic.

Finally, cutaneous pancreatic fistulas occur after attempts at external drainage are performed. Although these very severe, disabling fistulas are occasionally unavoidable, they are often a consequence of imprecise knowledge of the true diagnosis or the lack of appreciation of the importance of ductal anatomy (Fig. 14).

Currently, many of these complex fistulas can be managed endoscopically providing the duct is intact to the papilla. Various authors advocate pancreatic stent placement or nasopancreatic drainage with or without pancreatic sphincterotomy. Rapid closure of these fistulae can be expected with effective endoscopic transpapillary drainage. If no infection is present, endoscopic management is often definitive and should be attempted before external drainage establishes a cutaneous fistula [80].

Ductal disruption  Previous section Next section

Severe ductal disruption is the rule in necrosis cases but can be seen in well-perfused interstitial pancreatitis. To define the term, disruption occurs when the main pancreatic duct has been transected by the inflammatory process of pancreatitis, most likely by direct proteolytic digestion or ischemic infarction. Ductal disruption greatly complicates the approach to treatment and worsens outcome in both acute and chronic pancreatitis. Spontaneous resolution without intervention is very unlikely to occur. External cutaneous fistulae usually follow a percutaneous or surgical drainage approach due to the presence of a viable but disconnected gland. Although the downstream pancreas can be drained and diverted endoscopically by transpapillary therapy, the upstream pancreas continues to contribute to persistence of the fistula. This so-called 'disconnected tail syndrome' often results in pseudocyst recurrence after internal transmural endoscopic or surgical internal cystgastrostomy drainage [51] (Fig. 15). A few authors have reported successful endoscopic drainage by bridging the disruption to reconnect the tail, but the long-term outcome of these efforts remains unclear. More often these patients will experience a long illness with TPN and repeated interventions until the disconnected tail eventually autolyses, atrophies due to stricturing, or is surgically resected [81].

Vascular complications  Previous section Next section

Venous thrombosis  Previous section Next section

A frequent vascular complication of acute pancreatitis is thrombosis of the splenic vein and, less frequently, of the portal vein [82]. The cause is an intense inflammatory response surrounding these venous structures, often with compression by the resulting edematous reaction. Stasis and activation of clotting factors then produce acute thrombosis with resulting left-sided portal hypertension. Because the obstruction to portal inflow to the liver is usually partial, esophageal varices usually do not occur. Nonetheless, bleeding from gastric varices can be severe, especially when coagulopathy coexists (Fig. 16).

During the period of convalescence, where often surgical debridement or pseudocyst drainage must be undertaken, a secondary venous thrombosis may be a major determinant in treatment selection. Furthermore, the failure to recognize this form of portal hypertension prior to such interventions can prove disastrous. Significant gastric wall varices often contraindicate endoscopic or even surgical pseudocyst gastrostomy. Helical dynamic contrast CT scanning should detect venous thrombosis and predict left-sided portal hypertension accurately (Fig. 17). EUS has proven particularly valuable in assessing for gastric varices. One or both studies should be performed near the time of any invasive intervention.

Top of page Arterial complications  Previous section Next section

Thrombotic arterial complications secondary to acute pancreatitis are less common, but when they occur they can be severe. Splenic artery thrombosis with resulting splenic infarction is generally survivable with splenectomy. However, superior mesenteric artery thrombosis resulting in small and, at times, large bowel infarction is accompanied by a high mortality. The middle colic artery is perhaps the most frequent artery to thrombose, often resulting in a more limited large bowel infarction which may respond to resection and temporary surgical colostomy.

A more frequent arterial complication of pancreatitis is the formation of a pseudoaneurysm resulting in hemorrhage. Various series report this serious complication in up to 10% of cases of severe acute pancreatitis and it can complicate chronic pancreatitis as well [83,84].

If the pseudoaneurysm formed in an expanding pseudocyst wall, sudden hypotension with syncope followed by intense pain has been termed 'pancreatic apoplexy. If the pseudocyst into which the pseudoaneurysm ruptures communicates with the pancreatic duct, frank gastrointestinal bleeding can be the presenting symptom. Termed 'hemosuccus pancreaticus', such bleeding is amongst the rarest causes of gastrointestinal hemorrhage [85].

Finally, the presence of a pseudoaneurysm may be silent, only to acutely rupture during any invasive intervention where the surrounding tamponade is decompressed. This can be especially devastating in endoscopic pseudocyst drainage since prompt control of bleeding in general is not possible. Delayed rupture may also occur, resulting in exsanguinating gastrointestinal bleeding if a pseudocyst enterostomy has been created or if a surgical or radiological external drain has been placed [86].

To avoid these severe bleeding complications, it is imperative that the presence of a pseudoaneurysm is carefully searched for before intervention. All drainage procedures are strictly contraindicated until such a vascular lesion can be addressed and resolved. Dynamic, arterial phase, thin-section helical CT scanning through the pancreatic region is likely the best diagnostic study [87] (Fig. 18). Doppler ultrasound can be confirmatory but does not have the comprehensive screening power of CT. MRI with an arteriography protocol has been little reported but would likely visualize these lesions [8].

Once detected, preoperative angiography with embolization of the pseudoaneurysm has become a popular approach [88] (Fig. 19). These procedures can be technically challenging if the pancreatico-duodenal artery is the affected vessel since embolization may be necessary from both the celiac trunk and the superior mesenteric artery. Pseudoaneurysm of the celiac trunk can present a nearly insurmountable problem since gallbladder, gastric, and even hepatic infarction may follow embolization. If portal vein thrombosis is also present, the risk of hepatic infarction increases dramatically. Successful treatment of hemosuccus pancreaticus radiological embolization at angiography is the preferred approach as well [89].

Once the pseudoaneurysm is thoroughly embolized and thrombosed, interventions can then be safely carried out [84]. Elton et al. reported successful endoscopic pseudoaneurysm/pseudocyst drainage following radiological embolization in three such cases [90]. In all three patients, thrombosis following embolization was documented by repeat dynamic contrast CT or Doppler ultrasound prior to endoscopic intervention. Successful endoscopic drainage of the obstructing pseudocyst, stent management of strictures, and clearance of obstructing clots within the pancreatic duct resulted in symptom resolution and avoided surgery in these cases.

Finally, massive diffuse retroperitoneal bleeding may be seen in the setting of necrotizing pancreatitis, often with coincident coagulopathy. This so-called 'hemorrhagic pancreatitis' is less often reported since better radiology more often identifies a focal arterial source. However, when true diffuse hemorrhagic pancreatitis does occur, mortality rates exceed 35%, even in the modern era [88].

Top of page Summary  Previous section Next section

Complications of pancreatitis vary widely, are of complex etiology, and involve multiple organ systems. Avoiding these complications remains the basic goal for all treating physicians, but once present their expert detection and appropriate management is the key to optimizing patient outcome [91]. Great progress has been made in treating these supremely ill patients but early and specific treatments to prevent complications are still lacking. Prolonged hospitalizations, TPN, dialysis, ventilatory support, antibiotic therapy, and radiological, endoscopic, and surgical treatments all have had a role in reducing mortality to less than 10% of afflicted patients. However, much needs to be discovered [92].

Top of page Outstanding issues and future trends  Previous section Next section

The major need in pancreatology remains a full understanding of the pathophysiology of acute pancreatitis that results in the dramatic cascade of events outlined in the chapter. Once the earliest events are identified, specific medical interventions, possibly extremely specific pharmacological agents, can be developed that can prevent progression to shock, end organ compromise, necrosis, and the other late complications outlined. More basic research is needed.

Lacking this knowledge, research will continue to look for methods of preventing the complications of pancreatitis once severe disease has been established. A major need is an effective way to prevent progression to necrosis, beyond aggressive fluid resuscitation.

Trends in the future will continue to be innovations in minimally invasive therapies. Debridement of infected necrosis, intervention prior to infection, and management of ductal disruption resulting in a disconnected tail are all areas of considerable confusion and often subjects of interdisciplinary debate. Therapeutic, endoscopic, percutaneous laparoscopic debridement and transgastric endoscopic therapy are the newest players on a seemingly crowded field.

Top of page References  Previous section

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Historical background
The changing world of pancreatic–biliary medicine
  The impact of scanning radiology
  Extending the indications for therapeutic ERCP
  Improvements in surgery
  Patient empowerment
  Current focus
Benefits and risks
  Degree of difficulty and expertise
  Report cards
  Unplanned events
  Clinical success and value
The future
References
Synopsis
Introduction
  Imaging of the pancreatico-biliary system
   ERCP
   ERCP vs. PTC
   MRCP
   EUS
Section I: Preparation for ERCP
  Room set-up and floor plan (Figs 1, 2)
   Space
   Position of monitors and endoscopy cart (Fig. 2)
  Essential equipment for ERCP
   Side-viewing duodenoscopes
   Forward-viewing scopes
  Medication
   Sedatives and analgesics
   Anesthesia
   Smooth muscle relaxants
   Reversal agents
  Monitoring during conscious sedation
  Contrast agents
   Syringes for aspiration and irrigation
  Organization and storage of accessories (Fig. 4)
  Organization of the worktop (Fig. 5)
  Fluoroscopy for ERCP
   Fluoroscopy units (Fig. 6)
   KV and mA
   Split screen
   Magnified view
   Orientation of fluoroscopic images
   Personnel protection (Fig. 8)
   Other protective gear
   Positioning of the patient
  Radiological interpretation
   Scout film (Fig. 7)
   Contrast studies
   Drainage films
   The pancreatogram
   Normal anatomy
   Pathological changes
   Congenital anomalies
   The cholangiogram
   Normal anatomy
   Pathological strictures
   Bile duct stones (Fig. 11)
   Gallbladder
   Underfilling and delayed drainage
Section II: Diagnostic and therapeutic ERCP
  Diagnostic ERCP
   Scopes
   Accessories (Fig. 13)
   Preparation of patient
   Informed consent
   Fasting
   Antibiotics
  ERCP procedure
   Intubation and examination of the stomach
   Approaching the main papilla
   Cannulation of the papilla
   Ease and success in cannulation
   Minor papilla cannulation
  Complications of diagnostic ERCP
   Respiratory depression and other complications
   Pancreatitis
   Cholangitis
  Failed cannulation and special situations
   What to do with a difficult intubation
   Failure to insert the duodenoscope
   Lost in the stomach
   Failure to identify the papilla
   Tip of endoscope is too proximal
   Tip of scope is too distal
   Obscured papilla
   What to do if cannulation is difficult
   Abnormal papilla
   Failed common duct cannulation
   Failed pancreatic duct cannulation
   Failed accessory (minor) papilla cannulation
   Failure to obtain get deep CBD cannulation
   Precut sphincterotomy to assist in CBD cannulation
   Needle-knife precut technique
   Selective cannulation of the intrahepatic system (IHBD)
   Cannulation of the papilla in a Billroth II situation(Fig. 17)
  Therapeutic ERCP
   Standard endoscopic sphincterotomy or papillotomy (Fig. 18)
   Preparation of patients
   Laboratory tests
   The sphincterotome (or papillotome)
   Electrosurgical unit
   Adequacy of sphincterotomy
   Wire-guided sphincterotomes
   Periampullary diverticula and sphincterotomy
   Distorted anatomy
   Precut sphincterotomy for impacted stone
   Indications for sphincterotomy and results
   Complications of sphincterotomy
   Post sphincterotomy bleeding
   Pancreatitis
   Cholangitis
   Perforation
   What to do if the sphincterotomy fails to cut
   The risk of a half cut
   What to do with a deviated cut
   Sphincterotomy in Billroth II cases
   Stone extraction (Figs 19, 20)
   Equipment
   Procedure
   Endoscopic nasobiliary catheter drainage for bile duct obstruction (Fig. 24)
   Procedure
   Endoscopic plastic stent insertion for malignant biliary obstruction (Fig. 26)
   Equipment
   Preparation of patient
   Procedure
   One-step introducer system
   Bilateral stenting for hilar obstruction
   Brushing cytology for bile duct strictures (Fig. 27)
   Single-lumen system
   Double-lumen system
   Assessment of response to biliary stenting
   Results of biliary stenting
   Complications of stenting
   Early complications
   Late complications
   Self-expandable metal stents
   Stent configurations
   Lengths of stents
   Introducer system for SEMS
   Balloon dilation of biliary strictures (Fig. 28)
   Equipment
   Procedure
   Endoscopic management of bile leaks
Outstanding issues and future trends
References
Synopsis
Background
  Incidence of CBD stones
  Traditional management
  Non-operative approach to CBD stones
Pathogenesis
  Classification of CBD stones
   Primary CBD stones
   Bacteriology of primary CBD stones
   Secondary CBD stones
Clinical presentations
  Asymptomatic biliary stones
  Symptomatic biliary stones
   Obstructive jaundice
   Pain
   Clinical cholangitis
   Biliary pancreatitis
   Oriental cholangitis or recurrent pyogenic cholangitis
Diagnosis
  Clinical diagnosis
  Imaging
   Abdominal ultrasound scan
   Endoscopic retrograde cholangiopancreatography (ERCP)
   Magnetic resonance cholangiogram (MRC) for CBD stones
   Endoscopic ultrasonography (EUS) for CBD stones
Management for CBD stones
  ERCP, sphincterotomy, and stone extraction
   Endoscopic sphincterotomy
   Choice of endoscopes
   Cannulation with sphincterotome
   Sphincterotomy
   Stone extraction
   Basket stone extraction
   Balloon stone extraction
Complications
  Acute pancreatitis
  Bleeding
Controversies
  Sphincterotomy vs. balloon sphincteroplasty
   Balloon sphincteroplasty
   Balloon sphincteroplasty for CBD stones
   Sphincterotomy for CBD stones
   Long-term complications of sphincterotomy
  ERCP vs. laparoscopic common duct exploration for retained CBD stones
   Preoperative ERCP
   Operative removal of CBD stones
   Factors that predict CBD stones
   MRC for detection of CBD stones
   Risk scores for prediction of CBD stones
Alternative approaches to CBD stones
  Precut sphincterotomy for failed deep cannulation
   Complications of precut sphincterotomy
  Percutaneous transhepatic cholangiogram and drainage
   Rendezvous procedure (two-hands technique)
   Percutaneous stone extraction
The challenge: giant CBD stones
  Basket mechanical lithotripsy (BML)
  Through-the-scope BML using a metal sheath
   Results of BML
  Mother and baby choledochoscopy and intraductal lithotripsy
   Electrohydraulic lithotripsy (EHL)
   Intraductal laser lithotripsy
  Stenting and interval endoscopic lithotripsy
   Effects of stenting on CBD stones
   The need for stone extraction after stenting
  Extracorporeal shock-wave lithotripsy (ESWL)
   Results of ESWL for CBD stones
  Open surgery
Intrahepatic duct stones
  ERCP and basket removal
  Wire-guided basket
  Percutaneous transhepatic cholangioscopy (PTC)
   Results of percutaneous treatment of intrahepatic stones
ERCP and sphincterotomy in Billroth II gastrectomy
  Precaution and alternatives for Billroth II gastrectomy
  Side-viewing vs. forward-viewing scope for ERCP in Billroth II gastrectomy
Cholangitis
  Pathophysiology
   Effect of biliary obstruction on the reticuloendothelial system
   Bacteriology of cholangitis
   Effect of raised intrabiliary pressure and cholangiovenous reflux
  Clinical presentation
   Simple cholangitis: Charcot's triad
   Suppurative cholangitis: Reynold's pentad
  Clinical management
   Initial conservative management
   Urgent biliary decompression
   Role of ERCP
   Endoscopic drainage vs. surgery
   ERCP vs. PTBD
   Nasobiliary catheter drainage vs. stenting in acute cholangitis
   Surgery to prevent recurrent cholangitis
   Types of operation
Conclusion
Outstanding issues and future trends
References
Synopsis
ERCP in diagnosis of pancreatico-biliary malignancies
  Radiological diagnosis
   Significance of 'double duct stricture' sign
  Tissue diagnosis
   Brush cytology, biopsy, and FNA
  Tumor markers in bile or pancreatic juice
Direct endoscopic examination of pancreatico-biliary malignancies
  Choledochoscopy
  Pancreatoscopy
Intraductal ultrasound [IDUS]
Magnetic resonance cholangiopancreatography
  MRCP vs. ERCP
Palliation of inoperable pancreatico-biliary malignancies
  Endoscopic stenting for malignant jaundice
   Technique of endoscopic stent insertion
   Types of stents
   Plastic stents
   Metal stents
   Metal vs. plastic stents
   Covered and uncovered metal stents
   Biodegradable stents
   Endoscopic stenting for hilar strictures
   Bismuth classification for hilar obstruction
   Unilateral vs bilateral drainage for hilar obstruction
  Other techniques of endoscopic palliation
   Intraductal photodynamic therapy
   Brachytherapy
ERCP in management of ampullary neoplasms
  Benign tumors
   Ampullary carcinoma
Outstanding issues and future trends
References
Synopsis
Introduction
Classification of bile duct injuries
  Presentation
Diagnostic protocol
Management of bile duct leakage after cholecystectomy
  Type A injury (peripheral leaks)
  Type B injury (main duct leaks)
  Type C injuries (postoperative biliary strictures)
  Type D injury (transections)
   Delayed reconstruction
Surgical treatment of postoperative biliary strictures
Percutaneous treatment of postoperative strictures
Endoscopic treatment of postoperative biliary strictures
  Reported results
  Phases of endoscopic treatment
   Stent insertion phase
   Stenting phase
   Follow-up phase
Postoperative biliary strictures: surgery or endoscopy [43]?
  Recurrent strictures after surgery
Metal stents for benign strictures
A more aggressive treatment protocol?
Conclusions
Outstanding issues and future trends
References
Synopsis
Introduction
Definitions
  Sphincter of Oddi dysfunction
  Sphincter of Oddi stenosis
Classification of SOD
Epidemiology
  SOD in patients with gallbladder disease
  SOD after cholecystectomy
  SOD in the biliary or pancreatic sphincter, or both
  SOD and pancreatitis
Clinical presentation
  The Rome criteria
Initial evaluation
  Serum chemistries
  Standard imaging
Non-invasive diagnostic methods for SOD
  Morphine–prostigmin provocative test (Nardi test)
  Radiographic assessment of extrahepatic bile duct and main pancreatic duct diameter after secretory stimulation
   Ultrasound provocation testing
   Endoscopic ultrasound monitoring
   MRCP monitoring
  Quantitative hepatobiliary scintigraphy
   Results
   Adding morphine provocation
  Comparing non-invasive tests
  Current status of non-invasive methods
Invasive diagnostic methods for SOD
  Cholangiography
  Endoscopy
  Pancreatography
  Intraductal ultrasonography (IDUS)
Sphincter of Oddi manometry
  Sphincter of Oddi manometry: technique and indications
   Drug interactions
   Manometry catheters
   Cannulation techniques
   Study both sphincters
  Interpretation of manometry traces
   Normal values
  Complications of SOM
   Methods to reduce complications
   Aspirating catheter system
   Prophylactic stenting
  Sphincter of Oddi manometry; conclusion
   Type I patients
   Type II patients
   Type III patients
Therapy for sphincter of Oddi dysfunction
  Medical therapy
   Nifedipine
   Electrical nerve stimulation
  Surgical therapy
  Endoscopic balloon dilation and biliary stent trials
  Endoscopic sphincterotomy
   Randomized controlled trials of endoscopic sphincterotomy for SOD
   Is pancreatic sphincterotomy necessary?
  Risks and benefits of endoscopic treatment for SOD
  Botulinum toxin injection
Sphincter of Oddi dysfunction in recurrent pancreatitis
  Endoscopic sphincterotomy for SOD in pancreatitis
   Lans and colleagues
   Guelrud and colleagues
   Kaw and Brodmerkel
   Toouli and colleagues
   Okolo and colleagues
  Endoscopic sphincterotomy as a cause of pancreatic sphincter stenosis
  Endoscopic Botox injection
  SOD in recurrent pancreatitis: conclusion
Conclusion
Outstanding issues and future trends
References
Synopsis
Introduction
Interdisciplinary management; complex ERCP
Acute gallstone pancreatitis
  Clinical diagnosis of acute gallstone pancreatitis
  Predicting severity of acute pancreatitis
  Acute treatment
  The role of early ERCP
   British study
   Hong Kong study
   Polish study
   German study
   Meta-analysis of studies of early ERCP, and current consensus
   ERCP is rarely indicated before cholecystectomy in patients with gallstone pancreatitis
   Acute pancreatitis postcholecystectomy
   Treatment by biliary sphincterotomy alone?
Pancreatic duct disruptions
  Stenting for duct disruption
Smoldering pancreatitis
Acute recurrent pancreatitis
  'Idiopathic' pancreatitis
  Microlithiasis and occult gallstones
   Detecting microlithiasis
   Bile crystals
   Empiric cholecystectomy?
  Sphincter of Oddi dysfunction (SOD)
   Diagnosis of SOD
   Endoscopic therapy for SOD
   Sphincterotomy without sphincter manometry?
   Is sphincter manometry dangerous?
   SOD in patients with intact gallbladders
  Pancreas divisum
   Does pancreas divisum cause pancreatitis?
   Endoscopic treatment for pancreas divisum
   Stenting for pancreas divisum
   Problems with endoscopic therapy
  Chronic pancreatitis (idiopathic, alcohol, familial, other)
   Endoscopic therapy for chronic pancreatitis
  Pancreatitis due to neoplastic obstruction
   Endoscopic management of neoplastic obstruction
   Stenting for smoldering pancreatitis due to malignancy
  Choledochocele
  Other rare causes of pancreatitis
Overall approach to unexplained acute pancreatitis
  Concerns about ERCP and empiric sphincterotomy in recurrent acute pancreatitis
   Risks of ERCP
  Investigations other than ERCP
   MRCP
   EUS
  Recommended approach to ERCP for acute recurrent pancreatitis
  Final diagnosis in recurrent acute pancreatitis after extensive investigation
   Our experience
   Occult neoplasms
   Endoscopic treatment and results
Outstanding issues and future trends
References
Synopsis
Chronic pancreatitis
Treatments for chronic pancreatitis
  Medical therapy
  Surgical therapy
  Endoscopic treatment for chronic pancreatitis
   Safety issues
   Indications for endoscopic treatment
   Results of endoscopic treatment
Pancreatic ductal strictures
  Pancreatic stent placement techniques
  Efficacy of pancreatic duct stenting
   Cremer and colleagues
   Ponchon and colleagues
   Smits and colleagues
   Ashby and Lo
   Hereditary and early onset pancreatitis
   Predicting the outcome
  Duration of stenting
  Does response to stenting predict the outcome of surgery?
  Long-term follow-up
  Complications associated with pancreatic stents
   Occlusion
   Migration
   Stent-induced duct changes
   Brief mini-stents
Pancreatic ductal stones
  Causes of pancreatic ductal stones
  Stones cause obstruction
  Endoscopic techniques for stone extraction
   Pancreatic sphincterotomy
   Biliary sphincterotomy also?
   Pancreas divisum
   Stone removal
   Results of endoscopic treatment for stones
   Sherman and colleagues
   Smits and colleagues
   Cremer and colleagues
   Summary results
   Endoscopic therapy with ESWL
   Sauerbruch and colleagues
   The Brussels group
   Kozarek and colleagues
   Farbacher and colleagues
   Intraductal lithotripsy
   Medical treatment for stones
   Citrate
   Trimethadione
   Overall results for stone treatment
Pancreatic pseudocysts
  Endoscopic treatment for pseudocysts
Biliary obstruction in chronic pancreatitis
  Standard biliary stents
   Deviere and colleagues
   The Amsterdam group
   Barthet and colleagues
  Metal stents for biliary obstruction?
  Biodegradable stents
  Stenting for biliary strictures and chronic pancreatitis: conclusion
Sphincter of Oddi dysfunction in chronic pancreatitis
  Pathogenesis of SOD in chronic pancreatitis
  Frequency of SOD in chronic pancreatitis
  Surgical sphincter ablation
  Endoscopic pancreatic sphincterotomy
Pancreas divisum
  Pancreas divisum: a cause of pancreatitis?
  Minor papilla ablation
Outstanding issues and future trends
  Acknowledgement
References
Synopsis
Toxic and metabolic complications
Pancreatic fluid collections
Pseudocysts and abscesses
Pancreatic necrosis
  Organizing necrosis
Miscellaneous complications
  Pancreatic fistulas
  Ductal disruption
  Vascular complications
   Venous thrombosis
Arterial complications
Summary
Outstanding issues and future trends
References
Synopsis
Introduction
Patient preparation
  Sedation for ERCP in children
  Antibiotic prophylaxis
  Other medication
Instruments
Technique
  Indications
  Biliary indications
  Pancreatic indications
Success rates for ERCP in children
Complications
Biliary findings (Fig. 3)
  Biliary atresia vs. neonatal hepatitis
   ERCP findings
  Miscellaneous genetic cholestatic diseases
  Bile plug syndrome
  Choledochal cyst
   Pathogenesis of choledochal cyst
   Classification of anomalous ductal union
   Classification of choledochal cysts
   Type I
   Type II
   Type III
   Type IV
   Type V
   Choledochocele
   Treatment of choledochal cysts
   Fusiform choledochal dilatation and carcinoma
  Primary sclerosing cholangitis
  Parasitic infestation
  Choledocholithiasis
   ERCP for stones
  Biliary strictures and leaks
   Primary stricture
   Malignant strictures
   Liver transplantation
   Bile leaks
Pancreatic findings (Fig. 17)
  Recurrent pancreatitis
   Choledochal cyst and anomalous pancreatico-biliary union
   Pancreas divisum
   Prevalence of pancreas divisum
   Significance of pancreas divisum
   ERCP diagnosis of pancreas divisum
   Treatment of pancreas divisum
   Other pancreatic congenital anomalies
   Duodenal duplication cyst
   Sphincter of Oddi dysfunction
   Pancreatic trauma
   Acquired immunodeficiency syndrome
  Chronic pancreatitis
   Endoscopic treatment of chronic pancreatitis in children
  Pancreatic pseudocysts
Outstanding issues and future trends
References
Synopsis
Introduction
The risks of ERCP
  Risks for endoscopists and staff
  Technical failure
   Expertise
   Complexity
   Degree of difficulty scale for ERCP procedures (Fig. 1)
   Level 1
   Level 2
   Level 3
   Defining intent
   Risk consequences of technical failure
  Clinical failure
Unplanned adverse clinical events—complications
  When does an event become a complication?
   Complication definition
   Severity criteria
  Types of adverse clinical events
  Timing of events and attribution
  A dataset for unplanned events
Overall complication rates
  Accuracy of data collection
  Changes in complications over time
  Complication rates at MUSC
General risk issues
  Operator-related issues
  Patient-related issues; clinical status, indications, and comorbidities
   Age
   Illness and associated conditions
   Indication
   Anatomical factors
   Complication-specific risk factors
  Procedure performed
   Diagnostic or therapeutic?
   Biliary sphincterotomy
   Pancreatic sphincterotomy
   Precut sphincterotomy
   Repeat sphincterotomy
   Balloon sphincter dilation
   Endoscopic papillectomy
   Stenting
   Pseudocyst drainage
Reducing the risks of ERCP: general issues
  The contract with the patient; informed consent
   Educational materials
   Humanity
  Care after ERCP
   Admission?
   Early refeeding?
Pancreatitis after ERCP
  Definitions
  Incidence of pancreatitis after ERCP
  Risk factors for pancreatitis
   Patient factors increasing the risk [114,115,122,123]
   Procedure factors increasing the risk
   Pancreatic manipulation
   Sphincter manometry
   Sphincterotomy
   Biliary sphincter dilation
   Biliary stenting
   Pancreatic stenting
   Combining patient- and procedure-related factors
  Prevention of pancreatitis after ERCP
   Avoiding ERCP, especially in high-risk patients
   Mechanical factors
   Contrast agents
   Pharmacological prophylaxis
   Pancreatic stenting to prevent pancreatitis
   Feeding and monitoring
  Post-ERCP pancreatitis, recognition, and management
  Post-ERCP pancreatitis, conclusion
Perforation
  Duct and tumor 'penetrations'
  Sphincterotomy-related perforation
   Risk factors for sphincterotomy perforation
   Recognition of sphincterotomy perforation
   Reducing risks of sphincterotomy perforation
   Management of sphincterotomy perforation
   Surgery?
  Perforation remote from the papilla
   Recognition and management of endoscopic perforation
  Stent migration perforation
Infection after ERCP
  Nosocomial infection
  Cholangitis
  Cholecystitis
  Pancreatic sepsis
  Prophylactic antibiotics
  Delayed infection
Bleeding after ERCP
  Definition of bleeding, and incidence
  Risk factors for bleeding, and avoidance
   Prevention
  Management of sphincterotomy bleeding
   Delayed bleeding
Complications of stents
  Blockage of (plastic) biliary stents
  Stent migration
  Duct damage due to stents
  Cholecystitis
Basket impaction
Cardiopulmonary complications and sedation issues
Rare complications
Deaths after ERCP
Late complications
  Diagnostic error
  Late infection
  Late effects of sphincterotomy
  Sphincterotomy with the gallbladder in place
  Pancreatic sphincterotomy
Managing adverse events
  Prompt recognition and action
  Professionalism and communication
  Documentation
Learning from lawsuits
  Communication
  Financial concerns
  Standard of care practice
   Indications
   The procedure
   Postprocedure care
Conclusion
Outstanding issues and future trends
References

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