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Clinical Workup andDifferential Diagnosis 419

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Figure51.1 Inflammatory pancreatic head mass. Computed

tomography showing a large inflammatory pancreatic head mass in a patient with chronic pancreatitis, with typical diffuse pancreatic calcifications and a large pseudocyst in the pancreatic head.

Figure51.2 Impacted stent in the irregular and scarified main

pancreatic duct. Prolonged interventional treatment leading to nonremovable stents in the pancreatic duct with marked pancreatic duct irregularities and narrowing.

Figure51.3 Walled- off necrosis. Magnetic resonance imaging

depicting an inflammatory pancreatic head mass with wallednecrosis which developed after an episode of acute pancreatitis in a patient with chronic pancreatitis. External interventional drainage.

off

pancreatitis. Maldigestion and absorption with steatorrhea, coagulopathy, and malnutrition occurs as a result of persistent cholestasis. Duodenal stenosis is found in about 10% of patients[6], resulting in gastric dilatation, postprandial bloating and vomiting, anorexia and malnutrition. Malnutrition may be exaggerated by pancreatic exocrine insufficiency. Loss of endocrine function typically occurs later and will affect around 80% of patients[9]. Stenosis and finally thrombotic occlusion of the mesentericoportal vessels is usually a late complication. Occlusion of the splenic vein results in left- sided portal hypertension with development of gastric fundal varices and splenomegaly. As complete occlusion of the portal vein usually develops gradually, extensive collaterals develop around the pancreatic head, a phenomenon called cavernous transformation [6]. Patients suffering from chronic pancreatitis have a 10- fold elevated risk of about 3% to develop pancreatic cancer[9].

Clinical Workup andDifferential Diagnosis

Episodes of acute pancreatitis can lead to the development of pancreatic pseudocysts or walled- off necrosis (WON, Fig.51.3)[10], with secondary complications like superinfection, pseudoaneurysm, hemorrhage, compression of the duodenum or bile duct, internal pancreatic fistula, and pancreatic ascites.

Biliary stricture is reported in up to 35% of patients[6], leading to jaundice and recurrent cholangitis. Of note, subclinical common bile duct (CBD) narrowing can be aggravated to frank obstruction by acute edematous swelling of the pancreatic head during episodes of acute

The most important differential diagnoses are pancreatic head cancer and autoimmune pancreatitis. Careful clinical history- taking can yield important hints. Longstanding complaints or recurrent attacks over a period of years rather than months, accompanied by signs of chronic malnutrition points toward benign IPHM, whereas clinical deterioration over weeks to months with weight loss or new- onset diabetes mellitus are suggestive of malignancy. Jaundice can occur with IPHM but should always prompt efforts to rule out malignancy. Associated autoimmune disease points to autoimmune

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pancreatitis [11]. Laboratory workup should include serum amylase and lipase activity and carbohydrate antigen 19- 9 (CA19- 9), as elevated serum enzyme activity indicates an episode of acute pancreatitis, whereas marked elevation of the tumor marker in absence of acute pancreatitis is suggestive of malignancy. Sensitivity and specificity of CA19- 9 for discrimination of chronic pancreatitis from PDAC were reported as 84% and 75% [12]. Serum immunoglobulin G4 (IgG4) can be increased in autoimmune pancreatitis [13]. Because of the risk of tumor spillage and lack of therapeutic consequences, tissue biopsy is not recommended when resectable malignancy is suspected.

Cross- sectional imaging by contrast- enhanced computed tomography (CECT) or magnetic resonance imaging (MRI) is mandatory. In IPHM, the pancreatic head is enlarged with loss of the lobular parenchymal architecture, calcifications, and narrowing of the pancreatic duct (Fig. 51.1). There can be mass-

forming lesions in the pancreatic head virtually indistinguishable from pancreatic cancer. Upstream MPD dilatation is often absent in autoimmune pancreatitis [11]. Accuracy of modern cross- sectional imaging for differentiation of IPHM and pancreatic cancer has been reported in the range of 90% [14]. Magnetic resonance cholangiopancreatography can be a valid substitute for invasive endoscopic retrograde cholangiopancreatography (ERCP) to assess configuration of the biliary tree and MPD (Fig.51.2). In view of eventual surgical intervention, it is of paramount importance to assess mesentericoportal vein status and signs of portal hypertension.

Treatment

Asymptomatic IPHM virtually does not exist; however, symptom- free periods of weeks to months are common. Indications for invasive treatment are persistent pain or dependence on analgesics, recurrent acute pancreatitis, obstructive cholestasis, gastric outlet obstruction, development of persistent large or symptomatic pancreatic pseudocysts or walled- off pancreatic necrosis (WON), and suspicion of malignancy. Conservative management is chosen in case of inoperability or as a strategy to avoid operative treatment during a period of recovery, either after an episode of acute pancreatitis or as a bridge to operation.

Medical therapy consists of pain control and eventual substitution of pancreatic enzymes and insulin. It must be stressed that clinical remission of symptoms can be achieved by cessation of alcohol consumption in alcoholinduced chronic pancreatitis. Furthermore, the role of tobacco smoke as a causal agent has recently been recognized[15]. At least initially, surveillance of a pancreatic

head mass by cross-

sectional imaging should be per-

formed every 3 to 6months to rule out malignancy.

Endoscopic stenting of the MPD can be effective to induce remission of pancreatic cysts, pancreatic fistula as well as pain by decompression of the MPD. However, randomized trials have shown that surgical treatment provides more effective and durable pain control[16–18] and has been included in international guidelines[19,20]. For example, patients with obstructive chronic pancreatitis, who recently started opioid treatment (no longer than 6months) were randomized to either early surgical drainage (by a lateral pancreaticojejunostomy or duodenumpreserving pancreatic head resection) or endoscopic drainage (stent, lithotripsy) within 6weeks of randomization. Izbicki pain score [21] was significantly lower in patients treated with surgery than with endoscopic intervention[18]. In addition, the Izbicki pain score was found to be able to identify those patients who benefit most from surgery [21]. Another disadvantage of endoscopic therapy is the necessity of regular stent exchange every 3 to 6months to prevent cholangitis and tissue overgrowth; however, while efficacy is similar between plastic stents and metal stents, reintervention is lower in fully covered

expanding metal stents as shown in a recent rand-

selfomized controlled trial for benign biliary strictures due to chronic pancreatitis[22]. When a stent cannot be removed due to incrustation or migration, surgical intervention is needed (Fig. 51.1). Stenting of the CBD for obstructive jaundice is only a short- term option as remission of CBD obstruction can only be expected in cases of acute edematous swelling of the IPHM in acute pancreatitis.

Operative therapy can be divided into drainage procedures and those procedures that involve resecting a part of the pancreas. While drainage procedures aim at decompression of the MPD by pancreatojejunostomy, removal of the IPHM is the goal of resectional procedures, which can be combined with MPD drainage. On surgical exploration, the IPHM is usually found to be heavily indurated, and the inflammatory fibrotic process may extend into the peripancreatic tissues causing heavy adhesions to the organs in vicinity, like the retropancreatic blood vessels, duodenum, and hepatoduodenal ligament. These conditions render operative procedures involving the pancreatic head very challenging and in rare cases even technically impossible, especially when associated mesentericoportal hypertension leads to diffuse bleeding.

Radical pancreatoduodenectomy (PD) with (LongmireTraverso[23]) or without (Kausch- Whipple[24,25]) preservation of the pylorus is the procedure of choice when malignancy is suspected and offers very good long- term pain control in chronic pancreatitis. For the IPHM, duodenum- pre serving pancreatic head resection (DPPHR) was developed by Beger and colleagues [3]. In the Frey modification [26], pancreatic parenchyma is spared by

References 421

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excoriation of the IPHM without transsection at the pancreatic neck, and laterolateral pancreatojejunostomy ensures adequate MPD decompression. In the Hamburg modification of DPPHR [6], drainage of the MPD is further optimized by a V- shaped excision along the MPD. Randomized trials have shown reduced perioperative and short- term morbidity in DPPHR compared to PD with comparable long- term results [6]; however, long- term quality of life and serious adverse events after 24months were equal between PD and DPPHR[27]. Equality in this context clearly speaks for duodenum- preserving procedures as organ preservation should be in the focus of every surgeon whenever possible. Equality was also reported for Beger versus Frey procedures[28,29] and so far no randomized trial has involved other DPPHR modifications.

Pure MPD drainage procedures like the PuestowGillesby[30] (pancreatic left resection with splenectomy and laterolateral pancreatojejunostomy), PartingtonRochelle [31] (laterolateral pancreatojejunostomy) or Izbicki[32] (longitudinal V- shaped excision and laterolateral pancreatojejunostomy) operations do not remove the IPHM. MPD drainage in unselected patients only achieved 50–65% permanent pain control[6], which is inferior to that of pancreatic head resection with 75–95% [33–45]. Although no randomized trial has compared drainage versus resection procedures, drainage procedures are therefore reserved for patients without IPHM.

However, in case of mesentericoportal vein occlusion with portal hypertension and cavernous transformation, pancreatic head resection becomes impossible and therapy is limited to operative or endoscopic MPD drainage. Preoperative recanalization of the portal vein can be performed in selected patients with short- segment portal vein occlusion[46]. Gastroenterostomy and hepaticojejunostomy are measures of last choice for biliary or duodenal obstruction.

Adequate timing is an important aspect in the management of patients with IPHM. Maximum duration of a trial of nonoperative management of IPHM should be 6months, as optimal operative treatment usually becomes impossible in an advanced stage. In the presence of

mesentericoportal

vein narrowing or partial thrombosis, elective surgery should be performed as soon as possible, and prophylactic anticoagulation is advocated until surgery.

Certain contraindications impede early surgery.

Cachexia should be treated by high-

caloric nutrition with adequate simultaneous supplementation of pancreatic enzymes and vitamins, and in case of gastric outlet obstruction by jejunal tube feeding, to achieve adequate nutritional status for operation. Elective surgery is also not indicated before at least 3months have passed since the last episode of acute pancreatitis. Serum pancreatic enzyme activity can be used to monitor acute pancreatitis activity.

On histopathological workup, IPHM is characterized by fibrotic atrophy of exocrine acinar epithelium, the remaining ductal and islet epithelia becoming “skeletonized” in fibrous connective tissue. Strong inflammatory granulocytic or lymphocytic infiltration is uncommon. In contrast, autoimmune pancreatitis typically shows duct- centric inflammation, with IgG4 positive plasma cells or granulocytic epithelial lesions[11]. As overall tissue organization is heavily disturbed and chronic pancreatitis can be associated with pancreatic intraepithelial neoplasia (PANIN), distinction from PDAC can be difficult even for experienced pathologists. Intraoperative frozen section examination at least of the surgical resection margins is mandatory and in case of any doubt, radical oncologic resection is warranted.

Summary

Chronic pancreatitis with inflammatory pancreatic head mass is a domain of surgical therapy. The main differential diagnoses are pancreatic head cancer and autoimmune pancreatitis. Best results are achieved by resection of the pancreatic head mass with adequate drainage of the pancreatic duct, but pancreatic head resection may become impossible in advanced stages of the disease. Adequate workup and timing of conservative and surgical therapy is of paramount importance for successful management.

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Structural Complications: Strictures, Stones, Pseudocysts, andVascular Complications

Xiaodong Tian1, Xiaochao Guo 2, and Yinmo Yang

Department of General Surgery, Peking University First Hospital, Beijing, China

Department of Radiology, Peking University First Hospital, Beijing, China

Introduction

Chronic pancreatitis (CP) is a chronic inflammatory process in the pancreas, during which the pancreatic parenchyma is pathologically replaced by fibrous connective tissue, resulting in a series of structural complications and progressive insufficiency of exocrine and endocrine function [1]. Morphologic changes of the pancreas are one of the important features during CP, though they are usually not apparent in the early phase. The typical structural complications include, but are not limited to, strictures of pancreatic duct and/or biliary tract, intraductal stones, development of pseudocysts, and peripancreatic vascular complications. These structural changes will lead to dilation of the pancreatic duct, intraductal high pressure, and parenchyma atrophy of the pancreas. The corresponding clinical manifestations are malnutrition and pain syndromes.

A comprehensive understanding of the natural history of CP is also important, since the evolution of changes in morphology and function may take years to manifest.

Pathophysiologic Basis and Morphological Features ofthe Pancreas

The pathogenic mechanism of CP remains elusive and controversial. Several theories have been proposed in the past several decades: toxic- metabolic, oxidative stress, stone and duct obstruction, necrosis- fibrosis, primary duct hypothesis, and sentinel acute pancreatitis event hypothesis[2]. Each of these models is compelling and provides a certain mechanism to explain the diverse etiologies of CP, providing rationale for the cardinal

pathologic changes of fibrosis, loss of acinar tissue (atrophy), stones, and duct changes. Grossly, the pancreas becomes firm and shrunken, with an irregular contour. Dilated pancreatic duct is usually presented due to the obstruction of main pancreatic duct caused by either inflammatory fibrosis around the duct or intraductal stones. Fibrous scarring may result in the distortion or disappear of the normal macroscopic lobulation. Parenchyma calcifications and pseudocysts formation may be related to specific etiologies.

Strictures ofPancreatic Duct, Biliary Tract or Duodenum

Pancreatic parenchyma is replaced by fibrosis in advanced CP patients, and the recurrent inflammatory episodes might develop periductal fibrotic strictures, leading eventually to pancreatic duct stricture. The most common reasons for pancreatic duct strictures are inflammation, fibrosis, and previous stone[6]. However, Kalady etal.[7] had reported that nearly 12% of the CP patients with isolated pancreatic duct strictures were associated with malignancy, especially for those without pancreatitis history or irregular pancreatic duct side branches, as well as those with stricture located only in the head or neck. Therefore, all newly developed pancreatic duct strictures should be further evaluated by EUS or CT/MRI before treatment. The endoscopic management (ERCP or EUSsuited for CP patients with localized strictures, and surgical approaches remain the key choice for selected patients[8,9].

Stricture of common bile duct (CBD) is reported to be

usually caused by fibrosis of the pancreatic head, which

guided pancreatic drainage) is

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

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exerts extrinsic pressure on the intrapancreatic CBD. Moreover, inflammation caused by either pancreatic calculi or pseudocysts in the pancreatic head was also reported to contribute to significant biliary stricture during the acute phase[10]. The incidence of CBD stricture in CP patients ranges from 3% to 46%, and approximately 17% present as asymptomatic cholestasis[6]. Treatment of CBD stricture depends on the patients’ manifestation and morphologic changes of the pancreas. The indications for biliary decompression include cholangitis, severe and persistent jaundice, and occurrence of CBD stones. The drainage of bile duct can be accomplished either endoscopically or surgically. Despite the minimally invasive advantages of endoscopic therapy, there is still no evidence on which is the better strategy for CPassociated biliary stricture, while surgical interventions showed superior results in terms of long- term pain relief[11]. In a multicenter randomized study of multiple plastic stents versus covered self- expandable metallic stent (cSEMS) in the treatment of biliary stricture in CP patients, Haapamäki and colleagues found that a 6- month treatment with either multiple plastic stents or cSEMS produced good long- term relief of biliary stricture[12]. Surgical treatment should also be considered if bile duct obstruction recurs after long- term endoscopic therapy. Moreover, surgery must be undertaken if malignancy cannot be excluded.

Around 5% of CP patients developed duodenal stenosis due to paraduodenal pancreatic inflammation, named groove pancreatitis (GP), which is characterized by scarring between the duodenum and pancreatic head, accompanied by blood vessels compression, CBD stricture, duodenal wall rigidity, and luminal narrowing (Fig.52.1)[13,14]. Patients

with GP usually complain of upper abdominal pain, nausea, recurrent vomiting with weight loss for weeks to years. The characteristic manifestation is duodenal stenosis resulting in gastric outlet obstruction. Although tubular stricture of CBD is frequent, obstructive jaundice is rarely presented, and the main pancreatic duct is normal in most patients, which helps differentiate it from pancreatic adenocarcinoma. However, differentiating GP from pancreatic cancer is difficult because both of these two diseases are associated with similar clinical presentation, radiologic findings, as well as gross pathologic features [14]. Conservative and endoscopic treatments are helpful in many cases, while surgical intervention may be necessary in cases either with diagnostic uncertainty or severe obstructive symptoms.

Pancreatic Ductal Stones

Pancreatic ductal stones are a direct consequence of CP and occur in approximately 50% of cases, with the prevalence increasing over time to reach 50% at 5 years and nearly 100% after 14 years of the disease onset [16]. Pancreatic stones can cause outflow obstruction and produce upstream ductal hypertension and subsequent parenchymal hypertension, thus result in pseudocysts or fistula formation, recurrent exacerbations or contribution to the pathogenesis of pain.

Long- term alcohol consumption has been identified to be a major cause of calcium stone formation, which is possibly through disturbing the cholinergic regulation of pancreatic secretions and aggravating the loss of endocrine and exocrine functions[17]. Noticeably, pancreatic ductal stones are also common in nonalcoholic CP

Figure52.1 Groove pancreatitis. Left: coronal reconstruction image of contrast- enhanced CT. “Sheet- like” hypodense and “patchy”

enhanced soft tissue are shown in the pancreatic- duodenal groove (asterisk). Medial duodenal wall is thickened with intramural cyst (arrowhead). Right: schematic diagram of groove pancreatitis. Source: Yinmo Yang.

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patients. Maruyama reported that pancreatic stone formation in autoimmune pancreatitis was associated with narrowing of both Wirsung and Santorini ducts, which may subsequently result in pancreatic juice stasis and stone formation[18]. Pancreatic duct stenosis promotes the formation of intraductal stones, while the stones lead to intraductal ulcers and scars, which aggravate the pancreatic duct narrowing and cause more stone formation, resulting in CP progression and even increasing risk of cancer[19]. In a retrospective analysis of risk factors for pancreatic duct stones formation, both the main pancreatic duct narrowing and chronic alcohol consumption were identified as significant independent risk factors, and the period between diagnosis of CP and pancreatic stones formation seemed significantly shorter in alcoholic CP patients than in nonalcoholic patients[20]. Hao and colleagues [21] constructed a pancreatic stonepredicting nomogram for CP patients, and found that the age at onset of CP, body mass index, smoking, diabetes mellitus, pancreatic pseudocyst, biliary stricture, severe acute pancreatitis, and type of pain were significantly associated with intraductal stone development.

Symptomatic CP patients and those with duct obstruction caused by the pancreatic ductal stones were eligible for endoscopic or surgical treatments[22]. To remove the intraductal stones, endoscopic therapy should be the first choice, especially for patients without other complications. While for patients with multiple strictures, calculi in the body/tail region, concerns of associated solid mass, or failure of endoscopic therapy, surgery should be considered.

Pseudocyst inCP

Pancreatic pseudocyst is a fluid accumulation with high concentration of amylase that is surrounded by a fibrous capsule (Fig. 52.2). Pseudocyst usually arises from the disruption of the main pancreatic duct or major duct branches. In contrast to real cyst, it has no internal epithelial cell lining and the patients might have a history of clinical manifestations related to acute or chronic pancreatitis. Pseudocyst is considered to be one of the most common complications of both AP and CP with the prevalence of 20–40% in CP patients [23]. It is more commonly presented in patients with alcoholic CP.

The symptoms of a pseudocyst are usually nonspecific, most patients only complain about vague abdominal pain, nausea, or vomiting [24]. In up to 40% of CP patients, the pseudocysts will spontaneously resolve after 6weeks, and only conservative supportive care is needed. However, large cysts are more likely to become symptomatic or cause complications. When the pseudocyst persists for longer than 12weeks, there will be rare possibility for it to disappear spontaneously, and the additional complications include infection, hemorrhage, pseudocyst rupture, and disruptions of the pancreatic duct system[24,25]. In cases where symptoms worsen or complications occur, multiple modalities of treatments including percutaneous drainage, endoscopic procedures, and surgical drainage can be offered depending on the individual patient profile.

Figure52.2 Pseudocysts in CP patients (contrast- enhanced CT). Left: pseudocysts (asterisks) can be seen in the pancreatic area, and

splenic vein is occluded (white arrow). Right: pseudocyst (white triangle) is shown in the pancreatic head, with calcifications of the cystic wall and surrounding tissues (white arrow). Source: Yinmo Yang.

Vascular complications ofCP 427

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Vascular complications ofCP

Peripancreatic inflammation may affect the vessels in closest proximity to the pancreas, resulting in venous thrombosis most commonly involving the splenic vein, or pseudoaneurysm most commonly involving the splenic artery. Vascular complications occur in about 8.4–12.2% of CP patients, with the incidence of venousthrombosis and pseudoaneurysm approximately

7.6~10.9% and 0.8~2.5%, respectively[26,27]. Vascular complications were more commonly shown in males and alcoholic CP, while less commonly in patients with pancreatic atrophy and calcification [26]. Pseudocysts and alcoholic CP have been found to be risk factors for vascular complications in CP cases[27,28]. In a retrospective analysis of the database of 1363 patients with CP, alcoholic CP, presence of pseudocyst and inflammatory head mass were shown to be independent risk factors for venous thrombosis, whereas alcoholic CP and pseudocyst were identified as independent risk factors for pseudoaneurysm[26].

Consequences of pancreatitisthrombosis include gastroesophageal varices, venous collaterals, splenomegaly, and gastrointestinal bleed, with prevalences of 28.9%, 44.3%, 18.1%, and 14.1%, respectively[26]. Patients with pseudoaneurysm usually present with gastrointestinal bleeding, or are incidentally detected on contrast- enhanced CT done for other indications.

associated splenic vein

Sinistral portal hypertension (SPH), also known as regional, segmental, splenoportal, localized or left- sided portal hypertension, is a pathological condition of splenic vein hypertension localized in the left- sided gastrosplenic region, presents in less than 5% of all patients with portal hypertension (Fig. 52.3) [29]. In contrast to cirrhosis- related portal hypertension, SPH is characterized by normal hepatic function, isolated gastric varices, and splenomegaly. The CP- related SPH accounts for

31.8–53.8% of all cases, and the main etiology is splenic vein occlusion caused by venous thrombosis, extrinsic splenic vein compression by pseudocysts, inflammatory changes in the vascular endothelium, or relatively low perfusion associated with pancreatic fibrosis [30–31]. The incidence of SPH in patients with CP ranges from

9.7% to 22%, among which 4–17% develop severe gastrointestinal bleeding [26,31–35]. Splenomegaly is frequently observed in patients with SPH, while the incidence of hypersplenism is not as common as in portal hypertension. The site of gastrointestinal bleeding in patients with SPH is mainly located in the proximal stomach due to gastric varices, which is different from the lower esophageal hemorrhage in portal hypertension. Generally, CP- related SPH patients without history of gastrointestinal bleeding do not require surgical intervention [35]. Splenectomy is the most common therapeutic choice for SPH patients who experience gastrointestinal bleeding. Endoscopic therapy and splenic artery embolization could be the choices for patients

Figure52.3 Schematic diagram of sinistral portal hypertension (SPH) caused by CP- related splenic vein thrombosis. PV: portal vein;

CV:gastric coronary vein; RGV:right gastric vein; SV:splenic vein; SMV:superior mesenteric vein;IMV: inferior mesenteric vein; GEV:gastroepiploic vein. Source: Yinmo Yang.

Structural Complications: Strictures, Stones, Pseudocysts, andVascular Complications

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428

who are not suitable for surgery. However, for patients with SPH as the initial manifestation, the possibility of pancreatic cancer should be considered, because the involvement of splenic vein by pancreatic cancer is another important etiology of SPH.

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Acknowledgment

We kindly thank Dr Yuting Hou from Peking University First Hospital for making the colored drawings for this chapter.

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