Fast Facts: Acute and Recurrent Pancreatitis

M. Löhr, E. De-Madaria

Description

Acute pancreatitis (AP) is one of the most common disorders of the gastrointestinal tract to result in hospitalization. Although most patients with AP will experience an uneventful disease course, those that develop moderate-to-severe AP can be challenging to manage. Rapid recognition, accurate diagnosis and prediction of severity, together with appropriate treatment, are therefore key in achieving the best outcomes for patients and for preventing subsequent episodes of AP. Written by two pancreatologists with extensive experience of managing patients with AP as well as in clinical research, 'Fast Facts: Acute and Recurrent Pancreatitis' provides a comprehensive, evidence-based guide to: - The pathophysiology and etiology of AP - Fundamentals of diagnosis - Predicting the likely severity of an episode of AP - Monitoring and managing complications in the early and later stages of disease - Preventing recurrence This book will be of interest to all those who may be involved in the care of patients with AP, including internal medicine specialists, gastroenterologists, intensive care specialists, surgeons and endoscopists. Contents: • Pathophysiology • Epidemiology and etiology • Diagnosis • Prognosis • Definitions for complications and severity classification • Early management • Management of symptomatic collections • Management of other local complications • Preventing recurrence and monitoring for late complications after acute pancreatitis

Informations

• Publié par: S. Karger AG
• Date de parution: 31 août 2020
• Nombre de lectures: 3
• EAN13: 9783318066258
• Langue: English
• Poids de l'ouvrage: 2 Mo

Extrait

Fast Facts: Acute and Recurrent Pancreatitis
First published 2020
Text 2020 Enrique de-Madaria, Matthias L hr
2020 in this edition S. Karger Publishers Limited
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ISBN 978-3-318-06624-1
de-Madaria E (Enrique)
Fast Facts: Acute and Recurrent Pancreatitis/
Enrique de-Madaria, Matthias L hr
Medical illustrations by Graeme Chambers, Northern Ireland, UK.
Typesetting by Amnet, Chennai, India.
Printed in the UK with Xpedient Print.
List of abbreviations
Introduction
Pathophysiology
Epidemiology and etiology
Diagnosis
Prognosis
Definitions for complications and severity classification
Early management
Management of symptomatic collections
Management of other local complications
Preventing recurrence and monitoring for late complications after acute pancreatitis
Useful resources
Index
List of abbreviations
ACS: abdominal compartment syndrome
AP: acute pancreatitis
APFC: acute peripancreatic fluid collection
BUN: blood urea nitrogen
CECT: contrast-enhanced computed tomography
CFTR: cystic fibrosis transmembrane regulator
CPA1: carboxypeptidase A1
CT: computed tomography
CTRC: chymotrypsin C
DAMPs: damage-associated molecular patterns
DTS: disconnected tail syndrome
ECG: electrocardiogram
EPI: exocrine pancreatic insufficiency
ERCP: endoscopic retrograde cholangiopancreatography
ESGE: European Society of Gastrointestinal Endoscopy
FiO 2 : fraction of inspired oxygen
FNA: fine-needle aspiration
HTG: hypertriglyceridemia
IAP: intra-abdominal pressure
ICP: idiopathic chronic pancreatitis
IPN: infected pancreatic necrosis
LAMS: lumen-apposing metal stents
MRI: magnetic resonance imaging
NSAID: non-steroidal antiinflammatory drug
OF: organ failure
PaO 2 : partial pressure of oxygen in arterial blood
PEP: post-ERCP pancreatitis
PERT: pancreatic enzyme replacement treatment
PVT: peripancreatic vein thrombosis
RAC: revised Atlanta classification
RCT: randomized controlled trial
SIRS: systemic inflammatory response syndrome
SPINK1: serine protease inhibitor Kazal type 1
VARD: video-assisted retroperitoneal debridement
Introduction
Acute pancreatitis (AP) is one of the most common disorders of the gastrointestinal tract to result in hospitalization. While most patients will experience a mild disease course, up to one-third will develop local and/or systemic complications. Rapid recognition, accurate diagnosis and prediction of severity, followed by appropriate treatment are therefore vital to achieve the best outcomes and to prevent subsequent recurrence. Here, we provide an evidence-based approach to all aspects of AP, reviewing relevant literature and clinical trials that support current methods of diagnosing and treating patients with this condition. We also use our own extensive experience as pancreatologists involved in the management of patients with AP and clinical research to recommend logical approaches in areas where gaps in the evidence exist.
This book is intended to be of interest to a wide range of specialists, from internal medicine specialists, gastroenterologists and intensive care specialists, to surgeons and endoscopists. Each chapter is supported by key learning points and references, and there is a free online FastTest at karger.com/fastfacts to assess your understanding of AP and its diagnosis and management.
1 Pathophysiology
Definitions
Acute pancreatitis (AP) is a disease caused by acute inflammation of the pancreas.
Recurrent AP refers to the development of at least two separate documented episodes of AP with a period of resolution in between, and the absence of definitive changes of chronic pancreatitis. 1
Physiology of normal pancreatic function
The pancreas is an organ with important exocrine and endocrine functions, including being the main source of digestive enzymes. The exocrine pancreas consists of acinar and ductal cells ( Figure 1.1 ).
Pancreatic acinar cells secrete inactive digestive enzymes (zymogens) in order to protect the pancreas from self-digestion. Trypsin is a key pancreatic enzyme and is secreted as a zymogen called trypsinogen. 2 Once in the duodenum, an enterocyte apical membrane enzyme called enterokinase converts pancreatic trypsinogen to trypsin by limited proteolysis of its eight-amino-acid-long N-terminal activation peptide ( Figure 1.2 ). 2 Trypsin then activates other molecules of trypsinogen as well as other zymogens into active enzymes.
Pancreatic ductal cells secrete water and bicarbonate, which neutralize gastric acid and help to flush pancreatic enzymes into the duodenum.
Acinar and ductal secretion is controlled by complex neural (vagal innervation) and endocrine (cholecystokinin, secretin) regulation. Endocrine cells (clustered into the islets of Langerhans) are scattered along the exocrine tissue, and hormones such as insulin interact with acinar cells to further regulate exocrine secretion.

Figure 1.1 Anatomy of the pancreas. The exocrine pancreas consists of acinar and ductal cells. The acinar cells constitute the bulk of the pancreatic tissue. They are organized into grape-like clusters, branching from a ductal system. The acinar cells produce inactive digestive enzymes (zymogens), which protect the pancreas from self-digestion. The ductal cells add water and bicarbonate to the enzyme mixture, neutralizing gastric acid and flushing acinar cell secretions into the duodenum.
Pathogenesis
The etiology of AP is discussed in detail in Chapter 2 . However, the initial step in the pathogenesis of AP is acinar cell injury, which has several important consequences ( Figure 1.3 ). 3
Altered calcium signaling. In the early phase of AP there is a peak in the cytosolic Ca 2+ concentration; this calcium is released from internal stores and is followed by Ca 2+ influx through the store-operated Ca 2+ channels in the plasma membrane. 4 Altered calcium signaling is associated with destabilization of the secretory zymogen granules and intracellular activation of trypsinogen to trypsin. 4

Figure 1.2 Activation of trypsinogen to trypsin by duodenal enterokinase. Trypsinogen is the inactive precursor (zymogen) form of trypsin. Activation of trypsinogen to trypsin is catalyzed by enterokinase, an enzyme located in the duodenal mucosa, which cleaves the N-terminal activation peptide. Trypsin can also activate other molecules of trypsinogen.
Necrosis. When an injured cell becomes necrotic, it releases substances that activate inflammation, including so-called damage-associated molecular patterns (DAMPs). DAMPs induce local inflammation and may also be associated with systemic inflammation.
Induction of proinflammatory transcription factors. Acinar cell injury is associated with the activation of transcription factors such as nuclear factor kappa B, 5 which in turn induce the secretion of proinflammatory molecules such as cytokines, chemokines and adhesion molecules. These substances are involved in immune cell recruitment to the damaged tissue: neutrophils, monocytes and other cells infiltrate the pancreas and produce inflammation. Proinflammatory cytokines greatly contribute to systemic toxicity.
Autophagy blockade appears to be another important step in the pathogenesis of AP. Autophagy is a general term for several pathways through which cytoplasmic materials are delivered to the lysosome to be self-digested by lysosomal hydrolases. 3 The initial injury to the acinar cells can block this process of autophagy, leading to trypsinogen activation, cell death and inflammation. 3 The exact mechanisms underlying the relationship between autophagy and pancreatitis are subject to ongoing research.

Figure 1.3 Pathogenesis of acute pancreatitis: injury to pancreatic acinar cells triggers multiple detrimental consequences. DAMPs, damage-associated molecular patterns.
Premature intrapancreatic activation of zymogens Altered calcium signaling, inflammation, altered autophagy and genetic mutations in certain proteins (see page 19-22 ) are associated with intrapancreatic activation of trypsinogen to trypsin. In turn, trypsin can activate other zymogens in a cascade reaction that leads to mitochondrial malfunction, cell necrosis and direct self-diges