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Acute Pancreatitis Associated withCongenital Anomalies

(a)

(b)

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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188

proximity rather than mucosal content[51]. Duplication cysts within the pancreas have been reported and are generally termed as duodenal or gastric duplications since they lack a contiguous structure (Fig.20.3a, b)[59]. Although most enteric duplications do not present with pancreatitis, multiple cases have been identified[65,66]. Duodenal duplication occurs in 10% or fewer cases and may cause “obstructive pancreatitis” from compression between the duodenal wall and the biliopancreatic duct[67,68]. Juxta- pancreatic duplications with pancreatic ductal communication may shed blood or mucous into the main pancreatic duct resulting in obstruction[69–71]. Pancreatitis may occur within the duplication itself, as is found in esophageal duplications containing gastric mucosa and pancreatic tissue (43%)[72]. Local resection is preferred; however, marsupialization of cysts with removal of mucosa, either surgical or endoscopic, may be employed if local resection is not possible[73,74].

Figure20.3 (a) CT scan in a 21- year- old woman with a history of

several years of recurrent acute pancreatitis. The circle indicates an abnormal thick- walled cystic structure adjacent to the head of the pancreas. (b) Operative photograph of a pancreatic duplication cyst bulging into the duodenal lumen, as previously identified on abdominal CT. The catheter has been introduced through the ampulla into the pancreatic duct. Excision of the cyst with suture ligation of its narrow neck was curative of her recurrent pancreatitis.

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Acute Pancreatitis inChildren

Mark E. Lowe1 and Véronique D. Morinville

Department of Pediatrics, Division of Gastroenterology, Hepatology and Nutrition, Washington University School of Medicine, St. Louis, MO, USA

Department of Pediatrics, McGill University Health Center, Montreal, QC, Canada

Division of Pediatric Gastroenterology and Nutrition, Montreal Children’s Hospital, Montreal, QC, Canada

2,3

191

Introduction

The Second International Symposium in Marseilles in 1984 defined acute pancreatitis (AP) as acute abdominal pain accompanied by the finding of increased pancreatic enzymes in blood or urine[1]. However, the pathophysiology of acute pancreatic inflammation has remained difficult to describe, partly due to the relative inaccessibility of the pancreas on physical examination, and to the frequently nonspecific nature of symptoms resulting from diseases of the pancreas. Despite these difficulties, understanding of adult pancreatitis has increased in an exponential manner in recent decades. Unfortunately, the understanding of the pediatric counterpart has lagged, although much progress has been made in recent years.

Pediatric AP poses a challenge to clinicians. Depending on the age and developmental level of a child, it can be extremely difficult to assess the nonspecific symptoms of abdominal pain and nausea or vomiting. Defining the location and nature of the pain and identifying factors that aggravate or alleviate the pain can be particularly challenging in a pediatric patient. Compounding this challenge is that many healthcare professionals still do not consider pancreatitis in the differential diagnosis of pediatric abdominal pathology. Hence, children may experience symptoms from pancreatic inflammation and be diagnosed with “viral gastroenteritis.” For all these reasons, unraveling the complexities of pediatric AP remains an ongoing process.

The challenges in pediatric AP lie in three major areas:

● potential etiologies, many of which are more particu-

lar to children;

● diagnosis, including serum biochemistry and imaging

techniques;

● assessing and following for disease severity and

complications.

This chapter will strive to cover these areas as they pertain to pediatric AP.

Incidence

The prevailing impression amongst pediatric specialists is that the incidence of pediatric acute AP is increasing. A number of population- based series have attempted to quantify the incidence of AP[2–13]. These studies suggest that the incidence of AP in children has truly increased over the past several decades. Since the initial study by Lopez showing a steady increase in the absolute number of cases of AP per year in a single institution, a number of other centers throughout the world have reported similar observations [2] (Table21.1). An estimate of incidence ranged from 1 to 3 cases per 10,000 children. Proposed explanations for the increasing diagnosis of AP in children include increased awareness that AP occurs in children, a true rise in new cases of pediatric AP, increased referral of children to tertiary care centers, and an increase of AP in children with other systemic diseases[2,12,13]. Likely, a combination of these events explains the increased incidence.

Etiology

An adult presenting with a first episode of AP is questioned and investigated to identify the presence of one of two major etiologies for adult AP: biliary disease and

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

Acute Pancreatitis inChildren

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192

Table21.1 Series looking at theincidence ofAP. Studies reporting increase innumber ofcases ofAP diagnosed inchildren over time.

Location Years Author Incidence in last year Further study details

United States: Children’s Medical Center of Dallas

United States:

Children’s Hospital of Pittsburgh of

Australia:

Royal Children’s Hospital, Melbourne

United States:

Children’s Hospital of Wisconsin

Mexico:

Hospital of Pediatrics, Guadalajara

United States:

New Haven Hospital

Yale-

United States:

Healthcare Cost and Utilization Project Kids’ Inpatient Database

United States:

Nationwide Emergency Department Sample

United Kingdom:

Liverpool

India:

Sanjay Gandhi Postgraduate Institute of Medical Science

United States:

Cincinnati Children’s Hospital Medical Center

Taiwan:

Taiwan National Health Insurance Research Database

1993–1998 Lopez[2] Not reported Total cases/yr: 5, 19, 20, 38, 79,

1993–2004 Morinville[13] 1.3 per 10,000

1993–2002 Nydegger[3] 0.35 per 10,000

1996–2011 Werlin[5] Not reported Noted a consistent increase in

1990–2005 Sanchez- Ramirez[4] 53 per 10,000

1994–2007 Park[12] 8.9 per 10,000 ED

2000–2009 Pant[6] 35 per 10,000

2006–2011 Pant[7] 1.6 per 10,000 ED

1999–2009 Wilkinson[8] 0.3 per 10,000

2003–2014 Poddar[9] Not reported 5- fold increase in AP cases

2006, 2009, 2012

2000–2013 Cheng[11] 0.3 per 10,000

El- Haija[10] Not reported Kids’ Inpatient Database

Abu-

children

hospitalizations

visits

hospitalizations

visits

children

113 (1993–98)

Number of cases increased from 28 to 141 per year

Consistent, progressive increase in cases of AP per year over the study period

number of AP cases over study period with the exception of 2001

Reported a nonlinear increase in new cases over the study years

Increase in number of patients admitted for AP over time. Normalization to number of ED visits showed same rate per 10,000 visits

Relied on ICD9 codes to identify 55,012 patients

Relied on ICD9 codes to identify 78,787 patients with ED visits for AP

Identified patients by ICD10 codes from Hospital Episode Statistics database

Significant increase in diagnosis of AP over the study period

Incidence increased steadily from age 13 to 18 years

AP: acute pancreatitis; ED: Emergency Department.

alcohol ingestion. These, in fact, appear to account for most cases of AP in adults. In children, by contrast, the etiologies of AP are more broadly divided (Table21.2). Figure21.1 summarizes the breakdown of presumed etiologies based on previously published series from multiple countries. In general, the largest categories are divided up amongst idiopathic (24%), trauma (17%), systemic (15%), structural (14%), and medications (10%). A recent single- center study suggested that drug- induced pancreatitis is the leading known cause of AP [14]. The same center also reported that first attack of pancreatitis was

associated with genetic risk factors in 18% of patients[14]. Since genetic testing is not often done with the initial episode of AP, many studies may underestimate the role of genetic variants. The various risk factors may act alone or jointly to lead to a clinical episode of AP[15].

Pathophysiology

The pathophysiology of pediatric AP is believed to be identical to that of adult AP.

Pathophysiology 193

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Table21.2 Potential etiologies ofacute pancreatitis. Thedifferential list is extensive. Aclinician must consider theparticular patient’s

history ofpresent illness, past medical history, andfamily history inconsidering thepotential trigger ofan attack ofAP.

Category Examples

Anatomic abnormalities Annular pancreas

Anomalous choledochopancreaticoductal junction

Choledochal cyst, choledochocoele

Intestinal duplication or cyst

Pancreas divisum

Biochemical abnormalities Diabetic ketoacidosis

Hypercalcemia (hyperparathyroidism, familial hypocalciuric hypercalcemia)

Hypertriglyceridemia

Uremia

Gallstone disease Biliary sludge

Choledocholithiasis

Microlithiasis

Genetic Hereditary pancreatitis: PRSS1

SPINK1

CFTR

CTRC

Others

Iatrogenic Following ERCP

Following liver transplant (postsurgery anatomy + medications)

Following nongastrointestinal surgery (Fontan heart operation, spinal fusion surgery)

Idiopathic Unidentified infections, toxins, drugs or trauma, genetic risks

Inborn errors of metabolism Acute intermittent porphyria

Branched-

chain ketoaciduria (maple syrup urine disease)

Cationic aminoacidurias

Cystinuria

Glycogen storage disorders

Homocystinuria

3- Hydroxy- 3- methylglutaryl- CoA lyase deficiency

Pyruvate kinase deficiency

Infectious agents Bacteria (Campylobacter fetus, Escherichia coli, legionella, Mycoplasma pneumoniae,

Salmonella typhii, Yersinia)

Vir uses (coxsackievirus, cytomegalovirus, enterovirus, echovirus, Epstein–Barr, hepatitis A, influenza A,influenza B, measles, mumps, rubella, rubeola, varicella

Other (Ascaris lumbricoides (obstruction), clonorchis ninensis (obstruction), leptospirosis, malaria)

Immunocompromised host (mycobacterium avium intracellulare, pneumocystis carinii, cryptosporidium parvum)

Medications Analgesics (acetaminophen overdose, aminosalicylic acid, sulindac, indomethacin,

propoxyphene)

Anti-

acid (cimetidine, ranitidine)

Anticonvulsants (fosphenytoin, phenytoin, valproic acid)

Antimicrobials (erythromycin, sulfonamides, trimethoprim- sulfamethoxazole, tetracycline,

isoniazid, metronidazole, nitrofurantoin, pentamidine)

(Continued)

Acute Pancreatitis inChildren

Structural/

12%

Hereditary

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194

Table21.2 (Continued)

Category Examples

Chemotherapeutics (- asparaginase, cytarabine)

Diuretics (furosemide, ethacrynic acid, ACE-

Illicit drugs (amphetamines, cocaine, heroin)

Immunomodulators and anti-

mercaptopurine, azathioprine, gold)

Sex hormone-

related (estrogen, tamoxifen, danazol, corticosteroids)

Others: cholestyramine, cyproheptadine, diazoxide, diphenoxylate, histamine, interleukin,

methyldopa, phenformin, procainamide

Obstruction, acquired Neoplasm- associated

Periampullary obstruction (celiac disease, Crohn disease, mucosal inflammation)

Sphincter of Oddi problem (stenosis; dysfunction?)

Systemic illness Crohn disease

Hemolytic uremic syndrome

Henoch–Schonlein purpura

Kawasaki syndrome

Polyarteritis nodosum

Sarcoidosis

Systemic lupus erythematosus

Sickle cell disease

Toxi n s Boric acid

Ethanol and methanol

Methylene chloride

Organophosphates/insecticides

Scorpion bite

Tra u m a Accidental (bicycle handle bar injury, MVA)

Child abuse

I, thiazides, chlorthalidone)

inflammatories (sulfasalazine, 5- ASA products,

ACE- I: angiotensin- converting enzyme inhibitors; 5- ASA: 5- aminosalicylic acid; MVA: motor vehicle accident.

Idiopathic/

Other

24%

Systemic

15%

Figure21.1 Etiology of acute pancreatitis (AP) in

children. Contrary to adults where biliary tree pathology and alcohol account for more than two- thirds of cases, children have a greater spread among the etiologic categories of AP. The following

Biliary/Stones

11%

reflects distribution of etiologies of AP in 1961 children from different countries. Please refer to Table21.2 for examples of subcategories in each of

Metabolic

Iatrogenic

Trauma

16%

Medications

Anatomic

Infectious

the included series.

Imaging 195

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Investigations

A great diversity of potential etiologies of AP is demonstrated in Table21.2. Clinical finesse is involved in determining which causes should be considered for each child presenting with a first episode of AP. Unlike many pediatric diseases, the etiology of AP does not vary significantly among individual age groups[16–18]. A stepwise consideration of probable, possible, and rare etiologies in conjunction with elicited history of present illness, past medical history, family history, and findings on physical examination will direct investigations and limit invasive and sometimes painful procedures for the pediatric patient, as well as minimize unnecessary costs. Since genetic risk factors are common in children, a thorough family history for documented pancreatitis, pancreatic cancer, pancreatic insufficiency including insulin-

dependent diabetes, and/or family members exhibiting symptoms that could be consistent with acute recurrent pancreatitis is particularly important.

Diagnosis

In 2012, an international group of pediatric gastroenterologists published a consensus statement defining AP in childhood[19]. The clinical diagnosis of AP requires the presence of at least two out of three criteria:

● A combination of abdominal pain that is consistent

with pancreatic origin;

● The presence of elevated amylase or lipase or both to

at least three times the upper limit of normal;

● Radiological imaging with findings consistent with AP.

Even with these criteria, the diagnosis of AP can present challenges for the clinician. History and physical examination findings are variable: there may be epigastric to right upper quadrant pain, left upper quadrant pain, back pain, nausea, vomiting, jaundice, tachycardia, guarding, or even signs of shock. In children under the age of three, pain may present as increased irritability, and abdominal distension and fever were more common than in older children[16]. Clinicians must maintain a high degree of suspicion, especially in younger children in whom verbal communicative skills may be limited.

A particular pediatric consideration is that newborn levels of pancreatic type isoamylase are very low to nondemonstrable, and total amylase levels reach normal adult values by only approximately 8–16 months of age [20,21]. Pancreatic isoamylase activity might not even reach adult values until the age of 10 to 15 years[22]. In a similar fashion, lipase values at birth are significantly lower than those observed for adults and appear to have

the greatest increase within the first year of life[23,24]. Hence, in a young patient, amylase and lipase levels may not always reflect potential pancreatic inflammation particularly if adult ranges of normal enzyme levels are used as references[25].

Clinical scales are utilized to classify adults as having mild or severe disease. Several different scales for children have been proposed over the years. None have been widely applied. Two recent reports suggested that BUN levels or the lipase level and the presence of a pediatric systemic inflammatory response syndrome on admission were prognostic indicators for severe AP in children [14,26]. There was considerable overlap between mild and severe AP for both. It remains to be seen if either gains widespread acceptance and utilization, and thus pediatric severity indices represent an area of necessary research[25].

Imaging

Imaging methods may be helpful in (a) diagnosis, (b) determining severity and complications, and (c) visualizing any anatomic factors leading to AP[27].

Transabdominal ultrasonography (TUS) is widely available, relatively inexpensive, and does not expose a child to radiation or contrast agent. Historically, TUS has often been the initial diagnostic modality in suspected AP. It can repeatedly be performed in almost any setting to follow the course of illness and does not require procedural sedation. Ultrasonography may demonstrate enlargement of the pancreas, altered echogenicity, duct diameter abnormalities, and fluid collections (intra- or extrapancreatic) [28], abnormalities of the pancreaticobiliary drainage system, including the presence of a choledochal cyst, or common bile duct stones[27]. Limitations include air within the stomach interfering with image acquisition from the body and tail of the pancreas, and differentiation of normal from abnormal pancreas in cases of pancreatitis where echogenic changes may or may not be present. A recent study showed that TUS is only moderately sensitive for diagnosing AP and that crosssuch as computed tomography (CT) provided higher sensitivity[29]. In addition, CT with contrast may be more useful in more severe cases of AP to assess for local complications. The main drawback to more widespread CT scan utilization is its radiation exposure.

The capability of magnetic resonance cholangiopancreatography (MRCP, with or without secretin) to diagnose most cases of pancreas divisum, choledochal cyst, cholelithiasis, pancreaticobiliary junction anomalies and obstructive abnormalities has decreased the use of endoscopic retrograde cholangiopancreatography (ERCP) for diagnostic purposes even though MRCP might not be as sensitive

sectional imaging

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196

as ERCP in detecting pancre atobiliary abnormalities[30,31]. Although MRCP offers imaging without radiation, there are still pediatric factors to take into consideration. Due to the relatively long duration of the procedure (15 to 45minutes), younger children will require sedation, ranging from oral sedatives to intravenous general anesthesia and intubation. Additionally, the quality of MRCP images depend on the protocol utilized for image acquisition as well as the radiologist’s interpretation of these[32].

When indicated, pediatric ERCP in experienced hands is safe and effective at all ages, although infants and young toddlers may require slimmer pediatric duodenoscopes [33,34]. Pediatric uses include stone removal, assessment of pancreatic duct anatomy and injuries, drainage of nonresolving pancreatic pseudocysts, sphincterotomy, and stent placement. ERCP at the time of cholecystectomy is safe and effective in pediatric patients[35]. The obvious difficulties with ERCP include the need for sedation (typically general anesthesia), and the use of ionizing radiation during fluoroscopy.

Experience with pediatric EUS has increasingly been reported in recent years [36]. EUS provides detailed imaging of pancreatic parenchyma and ducts without the use of radiation, but with the need for sedation. Its benefits include not only its role in imaging, but also in interventions, with the capacity to sample tissue and fluid collections through fine needle aspiration and biopsy, as well as accomplish drainage of fluid collections such as pseudocysts. As endoscopists increasingly become comfortable with pediatric use of EUS, its role in diagnosis and management of AP will become better defined.

All radiological and endoscopic tests may offer complementary information regarding the cause or complications associated with pediatric AP. Clinicians must weigh the potential benefits offered by an imaging technology against the drawbacks particular to each technique and decide on an algorithm for a particular patient. Typically, pediatric patients are first assessed by TUS. Subsequently, with a prolonged AP course, there may be a need for either MRCP or CT to better delineate anatomy and to visualize potential complications. With the need for a therapeutic maneuver, both ERCP and EUS are becoming increasingly childto date shows they are safe and effective.

friendly and experience

Management

Society of Pediatric Gastroenterology, Hepatology, and Nutrition Studies published a position paper on the management of pediatric AP[37]. The role of i.v. fluids in the treatment of AP has been the subject of several studies in adults and children. However, details of i.v. therapy such as volume, rate, timing, and composition of the fluid are not firmly established. In one pediatric study, fluid rates

1.5 to 2 times maintenance in the first 24 h shortened length of stay and severity of disease[38]. A second study showed that patients given lactated Ringers solution had a shorter length of stay compared to patients given normal saline [39]. Another major change in management is the recognition that early enteral feeding whether by mouth or feeding tube is safe and may improve outcome[38,40–42]. Early feeds did not increase pain or length of stay and may shorten length of stay. Additionally, patients with higher fat intake did not have higher pain scores.

Outcomes

Overall, children generally have a mild clinical course and only a small fraction have severe complications. Pseudocysts represent the most frequent complication occurring in 10–30% of cases [4,5,43]. They typically present as a persistent abdominal discomfort, abdominal mass on physical examination, continued elevation of pancreatic enzymes, or identified on follow- up imaging. Pseudocysts usually resolve spontaneously and rarely require intervention. When indicated, potential therapeutic options include percutaneous catheter drainage (radiological placement or surgical), cyst- gastrostomy stent placement via EUS guidance, pancreatic duct stenting via ERCP, open surgical cyst- enteric anastomosis drainage and, perhaps, antibiotic therapy[44,45].

Despite a generally positive outcome for pediatric AP, up to 6% of children develop multiorgan failure or pancreatic necrosis[46]. Some studies have found an association between particular triggers of AP and serious complications. As might be predicted, it appears that children who have complex medical histories, including those experiencing AP post liver transplantation, or in the context of a systemic disease, are more susceptible to severe and potentially fatal courses[46]. Mortality data has rarely been reported in children. A database study from 2000 to 2009 of 55,012 children hospitalized with AP reported a mortality rate of about 1.0%[6].

The general measures undertaken in children with AP are similar to those in adults. In most pediatric AP cases, clinical improvement occurs within a few days and discharge is possible in less than a week. Several changes in management of patients with AP have occurred in recent years. In 2018, the Pancreas Committee of the North American

Acute Recurrent Pancreatitis

Acute recurrent pancreatitis (ARP) is defined as at least two distinct episodes of AP separated by a return to normal baseline status [19]. It has been estimated that

References 197

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10–35% of children have recurrent episodes of AP[46]. Most often the second episode occurs within 5months of the first one[47]. Upon the first presentation, etiologies that are amenable to therapy should be sought and if identified, managed appropriately (including hypercalcemia, hypertriglyceridemia, biliary factors, and structural abnormalities). Any reversible cause should be eliminated whenever possible (including culprit medications). With additional attacks other investigations should be considered. Secretin- stimulated MRCP may unveil anatomic abnormalities predisposing to ARP. After a second episode of AP, genetic testing for known risk variants should be done [48]. In a large multi- center study, almost half of patients with ARP had mutations in PRSS1, SPINK1, CFTR, or CTRC [49].

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Since not all patients in this cohort had genetic testing or were screened for fewer than four genes, the percentage of patients harboring gene mutations is likely higher. In the same study, 75% of patients with chronic pancreatitis (CP) had genetic mutations. Mutational analysis is now commercially available for these genetic loci. It is anticipated that a high proportion of children with ARP and CP will have genetic predispositions eventually identified. Along with mutational analysis, a comprehensive search for rare causes of AP is typically indicated[50]. As it is believed that recurrent attacks of AP may eventually lead to morphological changes of CP, prevention of further pancreatic injury is a key interventional goal, and identification of etiologic factors represents the first step.

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acute pancreatitis in Taiwan: a nationwide populationstudy. J Pediatr Gastroenterol Nutr 2019;68(1):e7–e12.

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incidence of acute pancreatitis at an American pediatric tertiary care center: is greater awareness among physicians responsible? Pancreas 2010;39(1):5–8.

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Bhandari V, Husain SZ. A comparison of presentation and management trends in acute pancreatitis between infants/ toddlers and older children. J Pediatr Gastroenterol Nutr 2010;51(2):167–170.

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