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Management ofFluid Collection inAcute Pancreatitis

Downloaded from https://onlinelibrary.wiley.com/doi/ by Universität Bern, Wiley Online Library on [22/08/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License

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298

Conclusion

Fluid collections that arise in the context of acute pancreatitis generally regress under conservative treatment and do not require interventional treatment in most cases. They may require endoscopic or surgical treatment when they fulfil the morphological criteria of infected (walled- off ) necrosis, when they represent complication- causing or complication- prone pseudocysts, or when they precipitate abdominal compartment syndrome. As supported by the results of the Dutch POINTER trial, an initial conservative approach is

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justifiable: 104 patients with infected pancreatic necrosis occurring within 35days from onset of symptoms were randomized to either receive immediate percutaneous or endoscopic drainage or a delayed approach with antibiotic treatment first and escalation to drainage and necrosectomy if clinically needed. There was no difference with regard to complications, organ failure, or death. Patients in the delayed treatment arm had considerably fewer invasive procedures and were less often taken to necrosectomy. Notably, 39% of patients in the delayed treatment arm did not require any invasive procedures at all[32].

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300

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Management ofPancreatic Fistula inAcute Pancreatitis

Marta Sandini1, Thilo Hackert 2, and Markus W. Büchler

Department of General, Visceral and Transplantation Surgery, Heidelberg University Hospital, Heidelberg, Germany

Department of General, Visceral and Thoracic Surgery, University Hospital Hamburg-Eppendorf, Hamburg, Germany

Introduction

A pancreatic fistula is defined as a leakage of pancreatic juice as a result of disruption of pancreatic ducts or parenchyma. During severe acute necrotizing pancreatitis— associated consequences— the management of local complications plays a major role. Local complications include infected necrosis, and pancreatic absesses which cause destruction of the pancreatic parenchyma and eventually small or larger ducts, leading to a leakage of pancreatic enzyme- rich fluid. This can either provoke the formation of pseudocysts, or— surrounding structures— the onset of a fistula. In most cases parenchyma or duct leakages are self- limiting and can be covered by the surrounding organs, reabsorbed by the serosa, or encapsuled by a fibrous pseudowall with the sequela of a pseudocyst [1]. In case of acute fistulaassociated complications, including arrosional bleeding or bowel perforation, immediate interventional and surgical treatment is required, including angiographic bleeding localization and management (i.e., stent placement in the arroded vessel) or emergency surgery. However, if pancreatic fistula does not cause acute complications, a continous leakage may occur and require therapy that needs to be adapted to the site and clinical symptomatology of the fistula. In this context, internal fistulas to the gastrointestinal tract, bronchi, pleural, mediastinal space, pericardium, and other organs [2–4] have to be differentiated from external— cutaneous— fistulas. As internal fistulas are often clinically asymptomatic, they are more difficult to diagnose and may not immediately be detected[5]. By contrast, external fistulas are more often observed, and can be easily diagnosed through the analysis of pancreatic enzyme content in the fluid[5,6].

besides the systemic SIRS, or sepsis

in case of arrosion of

Pathogenesis andClassification

Pathogenesis

The pathogenesis of pancreatic fistulas is multifactorial and seems to differ according to the site of origin of the fistula and to the timebasis of the necrotizing process in the pancreas, the peripancreatic fat and soft tissue as well as the retroperitoneal space during severe acute pancreatitis, a widespread induction of autodigestion, with interaction between pancreatic exocrine enzymes and inflammatory mediators [7]. Pancreatic parenchyma necrosis is understood as a consequence of oxidative stress and potential calcium overload, leading to a combination of necrosis, apoptosis, pyroptosis and autophagy, in which damage-

associated molecular pattern molecules (DAMP) play a central role. Microvascular perfusion failure, as a consequence of local thrombosis and inflammation, contributes to formation of necrosis. Following parenchyma necrosis, proteases and the entire spectrum of all other activated pancreatic enzymes are released into the retroperitoneum and an autodigestive process is initiated. Local leukocyte recruitment and further activation of inflammation favor the necrotizing process throughout the peripancreatic region and the retroperitoneum, toward the mesocolon, small bowel mesentery, and paracolic retroperitonal gutters. The autodigestive process may extend to the skin, bowel, or any other organs. In addition, the development of colonic fistulas during acute pancreatitis can be a consequence of colonic wall necrosis due to venous ischemia (e.g., following mesenteric thrombosis) or arterial infarction as a consequence of systemic hemodynamic instability in

point when it occurs. On the

The Pancreas: An Integrated Textbook of Basic Science, Medicine, and Surgery, Fourth Edition. Edited by Hans G. Beger, Markus W. Büchler, RalphH. Hruban, Julia Mayerle, John P. Neoptolemos, Tooru Shimosegawa, Andrew L. Warshaw, David C. Whitcomb, and Yupei Zhao. © 2023 John Wiley & Sons Ltd. Published 2023 by John Wiley & Sons Ltd. Companion website: www.wiley.com/go/beger/thepancreas4e

Surgical Treatment 301

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the hyperacute phase. In the end, iatrogenic fistula can be produced during intraoperative manipulation or endoscopic treatment.

Classification

Pancreatitis- associated fistula can be defined as an abnormal communication between the ductal pancreatic systems, and other spaces or organs due to the leakage of pancreatic secretions from damaged pancreatic ducts[8]. In contrast to postoperative pancreatic fistulas, there is no grading system for fistulas associated to acute pancreatitis[9]. Pancreatitis- associated fistulas can be classified into internal and external fistulas. If their orifice is located intracorporally— regardless of the organ or structure affected— they are classified as internal fistulas; in case of a connection to the skin, the fistula is defined as external. External fistulas can be classified as low- or high- output fistulas, according to the daily cutoff of 200 mL[10]. Further characterization of fistulas includes description as simple (straight channel from the pancreas toward the skin or another organ) or complex (multiple channels and tracts to different organs or structures). Moreover, the fluid can be characterized as clear pure pancreatic juice (due to external drainage of a pseudocyst communicating with the pancreatic duct) or as mixed (consisting of pancreatic juice in combination with gastrointestinal secretions or bile). In the latter case, the pancreatic juice might be activated by enterokinase, leading to proteolytic effects of the fluid and a more severe injury. Finally, the unfortunate event of disruption of the main duct can give rise to a persistent pancreatic fistula, in the so- called “disconnected pancreatic duct syndrome”[11].

Diagnosis

External Fistulas

The vast majority of external fistulas form along the tract of interventional or surgically placed drainages that are inserted to treat the complications of pancreatic necrosis. They can easily be recognized by their typical rich content of amylase and lipase. As mentioned earlier, there is no standard defined cutoff for the increase in pancreatic enzyme, amount of fluid, or duration of secretion. To differentiate between simple and complex fistulas radiological imaging should be performed. Conventional fistulography, computed tomography (CT), magnetic resonance cholangiopancreatography (MRCP), and endoscopic retrograde cholangiopancreatography (ERCP) are the most described[12–15]. CT scan is the gold standard in the diagnosis and classification of acute pancreatitis and its complications, namely abscesses, pseudocysts, and walled- off infected necrosis[8]. However, CT scan shows a lower accuracy in fistula detection compared with MRI/

MRCP imaging. Conventional fistulography is useful to determine potential connections to other organs (i.e., colon), and ERCP has the advantage of providing simultaneous diagnostic and therapeutic possibility, namely the placement of a pancreatic stent in cases of pancreatic duct disruption (Fig.36.1).

Internal Fistulas

Internal pancreatic fistulas are mostly asymptomatic, and may be difficult to recognize. In case of persisting ascites and/or a pleural effusion an internal fistula should be ruled out. In rare cases also acute mediastinitis arising from a pancreato- me diastinal fistula can be observed[16]. Unfortunately, unrecognized internal fistulas can lead to life- threatening conditions, if the activation of pancreatic enzymes leads to arrosional bleeding or bowel perforation[17]. Once an internal fistula is suspected, further imaging work- up needs to be tempestively done. CT scan remains the gold standard for diagnosis and treatment, and the biochemical analysis of collected fluid can confirm the suspected diagnosis[18,19]. For internal fistulas, MRCP or ERCP can be useful for the diagnosis and as well as ERCP for ultimate treatment[20].

Surgical Treatment

The treatment of pancreatits associated fistulas refers mainly to the international guidelines for the management of severe acute pancreatitis[8,21–24]. Supportive care management, namely adequate fluid resuscitation, pain control, nutritional support, and antibiotic treatment in cases of infected necrosis are the recommended strategies. In cases of failure of the conservative treatment, either due to organ compression from a fluid collection, or to persistent systemic infection, the so- called “step- up approach” is recommended, involving first of all an endoscopic attempt, followed by radiologic effort and, in case of failure of the first two, leading to a surgical minimally invasive or open intervention[25].

Open surgery in acute pancreatitis is no longer a gold standard in acute pancreatitis and should be cautiously evaluated just for those patients in whom all other options were not successful. However, a short overview on classical surgical approaches is mandatory [26]. The historically used open surgical techniques are the necrosectomy combined with open packing[27], the planned staged relaparotomies with repeated lavage [28], the placement of “kissing- drains” in the lesser sac and closed continuous lavage[29,30], and the closed packing [31], with mortality rates of up to 15% in referral centers [27,32–34]. In the first two techniques several consequent re- laparotomies are mandatory in order to achieve a satisfactory debridement of necrotic tissues.

Management ofPancreatic Fistula inAcute Pancreatitis

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302

Figure36.1 Internal pancreatic fistula to

the retroperitoneal space after severe necrotizing pancreatitis. Endoscopic retrograde cholangiopancreatography (ERCP) showing the pancreatic duct (broken white arrow) and the leakage with contrast medium extravasation (white arrow).

The last two, conversely, allow a progressive and continuous lavage of the necrotic region, without the need of subsequent surgeries. As the mortality rate and the risk of following injuries increases with the number of relaparotomies, the last two techniques should be preferred.

Drain Management

Once a pancreatitis- associated fistula is diagnosed, the amount and duration of drain in place are related to the size of the involved duct (main duct or branches of first, second, or third order), the localization of duct rupture (head, body, or tail of the pancreas), and the functionality of the sphincter of Oddi. In the acute phase of the disease, edema or spasm of the sphincter of the papilla may impair outflow, leading to increased pressure within the ductal system and subsequent rupture of the duct or maintenance of the outlet via the fistula. Once outflow via the papilla is restored, secondary to resolution of either the edema or spasm, spontaneous healing of the fistula can be observed in most cases.

Management ofInternal Fistulas

Most fistulas (80–100%) close spontaneously within 2–3 months [35]. Failure to heal is mainly due to larger defects of the pancreatic duct system, resulting in highvolume output. Endoscopic trangastric drainage, or surgical treatments should be considered. The surgical approach to internal fistulas focuses mainly on treatment of the underlying disease, as once infected necrosis is treated adequately, internal fistulas will close rapidly [36,37]. As

suggested in international guidelines, the surgical approach is indicated only after failure of all conservative strategies and should be deferred at least for 4weeks after the onset of acute pancreatitis.

The choice of treatment depends on the characteristics of the patient and the fistula, and comprises several drainage techniques. Endoscopic transmural drainage and percutaneous drainage (Fig.36.2) have become the procedures of choice in cases of internal fistula with symptomatic pseudocyst formation [38]. Furthermore, endoscopic sphincterotomy with or without transpapillary stent placement facilitates the drainage of pancreatic juice into the duodenum and can consequently release pressure from the disruption site. This accelerates the healing and may even allow the closure of partially disrupted pancreatic ducts within a median interval of 10 days [39

-41]. In case of severe damage and disconnected pancreatic duct syndrome endoscopic treatment cannot be sufficient. An early surgical treatment may be considered after initial drainage of a fluid collection by endoscopic therapy. Surgical treatment (i.e., central pancreatectomy or distal pancreatectomy) has a long-

term success rate of approximately 90%; however, atrophy of the pancreatic gland is a frequent and early complication after disrupted duct syndrome, leading to chronic pancreatits and diabetes in up to 30% of cases[42].

Management ofExternal Fistulas

Simple fistulas do not necessarily lead to complications; therefore, a conservative management should be pursued. Complex fistulas are more likely to develop

Figure36.2 Internal pancreatic fistula during severe necrotizing

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pancreatitis. X- ray after percutaneous catheter drainage (black arrow) of a large fluid collection (white star). Transition of contrast medium to the descending colon (broken black arrow).

References 303

Nutritional Support

Nutritional support care can be added to improve not only healing of a fistula but also patients’ general performance status, which is often reduced after acute pancreatitis. If chosen, the enteral route should be preferred in all phases of the disease. A total parenteral nutrition regimen should only be considered if the enteral route is not tolerated or if the enteral feeding alone cannot achieve the expected nutritional daily requirements. When parenteral nutrition is indicated, a glutamine supplement should be administered, at 0.20 g/kg per day of L- glutamine. Otherwise, there is no role for immunonutrition in pancreatitis- associated fistula[44].

According to international nutritional guidelines, pancreatic enzymes should not be generally supplemented, except in patients with obvious pancreatic exocrine insufficiency. A debatable aspect in the management of internal fistula is the role of somatostatin analogs. No clear benefit of octreotide has been demonstrated[45], with the exception of the pancreaticopleural fistula, where it has been shown to reduce the output and decrease the time to fistula closure[46].

dangerous complications because of high risk of free activation of pancreatic enzymes in the abdominal cavity and digest surrounding structures. The aim of surgical therapy of external pancreatic fistulas is to redirect the drainage into the intestinal tract[43]. The surgical procedure chosen is based on the site of the fistula, the thickness and nature of the fistula tract, as well as the texture of the pancreatic tissue. If the fistula tract is located on the right side of the body of the pancreas or even in the head, resection should be avoided and internal drainage into a Roux- en- Y jejunal loop is preferred[6,43]. For persisting fistulas located in the body or tail of the pancreas, central or distal pancreatetomies are suitable procedures to remove the fistula-

bearing part of the pancreas[24]. Crucial for surgical treatment of external pancreatic fistula is the timing of the procedure. Formal pancreatic resections should be avoided in the early phase of fistula occurrence, as fistulas may spontaneusly close even 6months after an acute episode.

References

Conclusions

Pancreatic fistulas are common sequelae following acute pancreatitis and, in most cases, self- limiting processes. Pancreatic fistulas can occur spontaneously or be the consequence of interventions required to manage infected walled- off necrosis in severe acute pancreatitis. The majority of fistulas present with low output and tend to close spontaneously within a few months. For this reason, a conservative approach is recommended. After failure of the conservative treatment, a step- up approach is the gold standard, including a wide range of minimally invasive therapeutic options. Endoscopic and percutaneous interventions should be preferred, as surgeryremains high even at referral centers. The surgical option remains the ultimate treatment when the endoscopic and percutaneous intervention are not successful. The type and extent of resection must be considered and tailored for each case. Surgery should be delayed by at least 4–6weeks following the onset of an acute episode.

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Long-

Christin Tjaden1 and Thilo Hackert

Introduction

Term Outcome After Acute Pancreatitis

Department of General, Visceral and Transplantation Surgery, University of Heidelberg, Heidelberg, Germany Department of General, Visceral and Thoracic Surgery, University Hospital Hamburg-Eppendorf, Hamburg, Germany

preexisting signs of subclinical chronic pancreatitis may be found in terms of fibrosis or calcifications and

Most patients with acute pancreatitis recover completely without any further symptoms or morphological alterations within days or weeks after discharge. This observation was described in the original definition of acute pancreatitis by the Consensus Symposium 1963 in Marseille[1]. However, recent reports on long- term outcome after acute pancreatitis show growing evidence that there is a certain risk for late pancreatitis- associated complications even after mild clinical courses[2–5].

Functional impairments can occur immediately or even years after sustaining acute pancreatitis[2,3,5–8], specifically loss of endocrine function resulting in diabetes mellitus type 3 or exocrine insufficiency with the need for pancreatic enzymes substitution, have been described in numerous studies [2,9–11]. Etiology or severity of the index episode are not clearly associated with the overall risk for an impairment of pancreatic function. In addition, episodes of pain with a considerable impact on quality of life can occur at any point of time after the initial event of acute pancreatitis. These possibly recurrent pain sensations bear a high risk for chronification and may be associated with recurrent pancreatitis; there is also a certain overlap with clinical courses of chronic pancreatitis[2,5,12,13]. This latter correlation has been examined in several recent publications[2–5,14–20]. It is sometimes difficult to distinguish between the primary episode of acute pancreatitis as a symptom of a chronic disease and chronic pancreatitis developing as a long-

term consequence of pancreatitis. Morphological characteristics (i.e., those found in cross- sectional imaging at the initial episode of pancreatitis) can be useful for this differentiation as

can be clearly distinguished from typical signs of newonset acute pancreatitis.

In contrast to chronic pancreatitis, little is known about histomorphologic pathways and alterations of recurrent acute pancreatitis. One hypothesis is the socalled necrosis–fibrosis sequence [21], which suggests that acute inflammatory changes after an initial and acute damage of the pancreas result in mesenchymal cell activation with various patterns of subsequent fibrosis development and obstruction of pancreatic ducts. Another model is based on a “sentinel acute pancreatitis event (SAPE),” postulating a long- lasting intrapancreatic activation of immunomodulatory and stellate cells during the index episode. These alterations lead to hypersensitivity of the pancreas when responding to potential stimuli, resulting in recurrent attacks of acute and eventually chronic pancreatitis[22]. Despite these hypotheses, the possible pathophysiologic link between acute and chronic pancreatitis remains controversial and is not well understood[23].

Because there are no follow- up guidelines for clinical examinations and imaging after acute pancreatitis and histopathologic findings for such patients are rare due to the infrequent need for operations with respective tissue harvesting, the frequency of such alterations is unknown. In available cross- sectional imaging, alterations of the pancreatic duct, parenchyma, or surrounding areas (i.e., formation of pseudocysts or fluid collections) can be observed during both short- and long- term courses. These morphological findings may be correlated with the severity of the first attack and the type of treatment, in particular interventional or surgical necrosectomy.

Exocrine Dysfunction 307

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Their extent and the underlying initial etiology of the primary acute pancreatitis episode determine clinical outcome patterns. In alcohol- related acute pancreatitis a recurrent and eventually chronic course is observed more often than it is in a biliary genesis of the disease[13,15,19,20]. This fact underlines the importance of avoiding further exposure to risk factors such as alcohol and nicotine as a basic precaution following a first pancreatitis episode [14,24,25]. Furthermore, patient education can be regarded as a simple method to reduce the lifelong risk of recurrence and associated healthcare costs[20,24]. Follow- up examinations should therefore address the above- mentioned topics and should include clinical and laboratory as well as imaging examinations, when necessary. This chapter gives an overview of the long- term sequelae of acute pancreatitis with regard to risk factors, diagnosis, and management.

Risk Factors

Risk factors for long- term complications of acute pancreatitis have been examined in several cohort studies in recent years[4,5,7,14]. With regard to recurrent episodes of acute pancreatitis, a recent meta- analysis including nearly 8500 patients showed an overall risk of 22% with a nearly twofold increase in alcoholic etiology (38%) and a lower risk for biliary etiology (17%)[4]. With regard to biliary etiology, early removal of the gallbladder after the index episode of pancreatitis reduces the risk of recurrence[5,14]. In nonbiliary etiology, persistence of smoking and alcohol consumption are well- documented risk factors for both recurrent acute episodes as well as progression of primary acute to chronic pancreatitis in the long term [5,7,14]. Nevertheless, some authors report experience with patients who show a progression to chronic pancreatitis despite stopping consumption of alcohol and nicotine[14,15]. In addition, male patients seem to have a higher risk of progression to chronic pancreatitis, even when lifestyleexcluded [4]. Risk factors for functional failure after acute pancreatitis include preceding necrosectomy, which leads to both exocrine and endocrine insufficiency due to the procedure- associated loss of tissue itself and the disease- specific damage to the remaining tissue[5,26,27]. Again, the risk for developing progressive pancreatic dysfunction and diabetes mellitus or exocrine dysfunction is increased in men[4,6]. Moreover, a subset of patients may also have unrecognized genetic risk alterations leading to increased risk of progressive pancreatic failure and chronic pancreatitis through an effect on trypsinogen activation [28]. Tables 37.1 and 37.2 summarize studies on patterns and risk factors for longterm sequelae after acute pancreatitis.

associated risk factors are

Endocrine Pancreatic Dysfunction

Hyperglycemia, impaired glucose tolerance, and diabetes mellitus occur frequently as a consequence of acute pancreatitis and have therefore been investigated as primary or secondary endpoints of several large studies on the loss of pancreatic function on long- term follow- up. A recent review analysed 34 studies focusing on diabetes mellitus after acute pancreatitis[3]. The authors concluded that especially pancreatic diabetes mellitus (type III) and impaired glucose metabolism after acute pancreatitis are increasingly recognized clinical findings requiring more detailed research on it as the published data are inconsistent. Of interest, one of two included meta- analyses had examined 24 prospective studies published between 1968 and 2009, and revealed that nearly 40% of patients showed a prediabetic metabolic situation or a full clinical manifestation of diabetes mellitus[2]. Within 12months after the index episode of acute pancreatitis the prevalences of hyperglycemia and diabetes mellitus were 19% and 15%, respectively. After a 5for diabetes mellitus showed a twofold increase compared with the prevalence after 12 months. A Dutch cohort study on 669 patients described a new onset of diabetes mellitus in 20% of the patients during a median follow- up time of 57months[7]. These data are consistent with findings of a Taiwanese study, which showed a comparable twofold increase of diabetes risk after 10 years in nearly 3000 acute pancreatitis patients, regardless of the severity of the initial course of the disease[6].

In severe courses characterized by extensive parenchyma necrosis and the need for necrosectomy, the correlation between loss of tissue and function seems to provide an explanation for these observations, especially when the body and tail of the pancreas are affected. Decay of a considerable amount of islets predisposes for functional deterioration and 15–30% of patients undergoing extensive necrosectomy show insulin- dependency soon after recovery[5]. This is comparable to outcomes following distal pancreatectomy for other indications, with a rate of postoperative diabetes mellitus of approximately 10%[30–32], and underlines the relevance of the pancreatic body and tail for the endocrine function of the gland due to the pronounced location of islet cells in these segments of the pancreas. In contrast, the pathophysiologic explanation for mild episodes of acute pancreatitis resulting in endocrine insufficiency and an increased risk of diabetes mellitus remains unclear.

year observation period, the risk

Exocrine Dysfunction

In the early phase after acute pancreatitis, exocrine function is often compromised and is easily diagnosed

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