Full Ebook of The Digestive System From Basic Sciences To Clinical Practice 1St Edition Pierre Poitras Online PDF All Chapter

The Digestive System From Basic
Sciences to Clinical Practice 1st Edition

Pierre Poitras
Visit to download the full and correct content document:
https://ebookmeta.com/product/the-digestive-system-from-basic-sciences-to-clinical-p
ractice-1st-edition-pierre-poitras/
More products digital (pdf, epub, mobi) instant
download maybe you interests ...
Testosterone From Basic to Clinical Aspects Alexandre

Hohl
https://ebookmeta.com/product/testosterone-from-basic-to-
clinical-aspects-alexandre-hohl/
Tendinopathy From Basic Science to Clinical Management

Kentaro Onishi
https://ebookmeta.com/product/tendinopathy-from-basic-science-to-
clinical-management-kentaro-onishi/
Anatomy of the Digestive System Quick Study Academic

1st Edition Barcharts
https://ebookmeta.com/product/anatomy-of-the-digestive-system-
quick-study-academic-1st-edition-barcharts/
Neuroscience in the 21st Century From Basic to Clinical

3rd Edition Donald W. Pfaff
https://ebookmeta.com/product/neuroscience-in-the-21st-century-
from-basic-to-clinical-3rd-edition-donald-w-pfaff/
Gynecological Oncology Basic Principles and Clinical
Practice Kavita Singh (Editor)
https://ebookmeta.com/product/gynecological-oncology-basic-
principles-and-clinical-practice-kavita-singh-editor/
DeGroot s Endocrinology Basic Science and Clinical

Practice 8th Edition R. Paul Robertson
https://ebookmeta.com/product/degroot-s-endocrinology-basic-
science-and-clinical-practice-8th-edition-r-paul-robertson/
Polycystic Ovary Syndrome Basic Science to Clinical

Advances Across the Lifespan Rehana Rehman
https://ebookmeta.com/product/polycystic-ovary-syndrome-basic-
science-to-clinical-advances-across-the-lifespan-rehana-rehman/
Basic System Analysis 2nd Edition S. Palani
https://ebookmeta.com/product/basic-system-analysis-2nd-edition-
s-palani/
The Innate Immune System in Health and Disease from the

Lab Bench Work to Its Clinical Implications Volume 1
1st Edition Jorge Morales-Montor
https://ebookmeta.com/product/the-innate-immune-system-in-health-
and-disease-from-the-lab-bench-work-to-its-clinical-implications-
volume-1-1st-edition-jorge-morales-montor/
Pierre Poitras Editor
The Digestive System:

From Basic Sciences
to Clinical Practice
123
The Digestive System: From Basic Sciences to Clinical Practice
Pierre Poitras
Editor
Marc Bilodeau • Mickael Bouin • Jean-Eric Ghia

Co-Editors
The Digestive
System: From Basic
Sciences to Clinical
Practice
Editor Co-Editors
Pierre Poitras Marc Bilodeau
Université de Montréal Professor of Medicine
Montréal, QC, Canada Université de Montréal
Montreal, QC, Canada
Mickael Bouin
Clinical Professor of Medicine
Université de Montréal
Jean-Eric Ghia
Professor of Immunology
University of Manitoba
Winnipeg, MB, Canada
ISBN 978-3-030-98380-2 ISBN 978-3-030-98381-9 (eBook)

https://doi.org/10.1007/978-3-030-98381-9
© The Editor(s) (if applicable) and The Author(s), under exclusive license to Springer Nature Switzerland
AG 2022
0th edition: © Les Presses de l’Universite de Montreal 2020
This work is subject to copyright. All rights are solely and exclusively licensed by the Publisher, whether the
whole or part of the material is concerned, specifically the rights of reprinting, reuse of illustrations, recita-
tion, broadcasting, reproduction on microfilms or in any other physical way, and transmission or informa-
tion storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology
now known or hereafter developed.
The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication
does not imply, even in the absence of a specific statement, that such names are exempt from the relevant
protective laws and regulations and therefore free for general use.
The publisher, the authors and the editors are safe to assume that the advice and information in this book
are believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the
editors give a warranty, expressed or implied, with respect to the material contained herein or for any errors
or omissions that may have been made. The publisher remains neutral with regard to jurisdictional claims in
published maps and institutional affiliations.
This Springer imprint is published by the registered company Springer Nature Switzerland AG
The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland
V
Preface
This book aims to facilitate your learning experience during your undergraduate stud-
ies, as well as to guide you later in your clinical practice as a general practitioner or as
a physician nonspecialist in digestive diseases.
We deliberately chose a direct style, unencumbered by references, hoping to stimu-
late in you the desire to further explore the scientific literature.
As editor, I wanted to offer a personalized version of digestive medicine, as I discov-
ered it with outstanding mentors such as Robert Modigliani, Jean- Claude Rambaud,
John H. Walsh, Charles Code, Morton Grossman, and Serge Bonfils during my years
of training in gastroenterology, and as I evolved within it during 40 years of profes-
sional life with my colleague gastroenterologists, GI surgeons, radiologists, and pathol-
ogists at Hôpital Saint- Luc in Montreal, all passionate like me about the digestive
system.
Our approach is to introduce the disease as a dysregulation of the healthy state.
Anatomy, histology, and physiology illustrate the normal functioning of the organs,
and pathophysiology teaches us the dysregulation process involved. Semiology allows
us to build a differential diagnosis from the patient symptoms. Finally, we confirm the
diagnosis by various measures of investigation, and we use pharmacology to apply the
proper treatment.
The amount of bioscientific knowledge is huge and is growing every day. It is impos-
sible to assimilate and control, quantitatively or qualitatively, all available data from
genetics, molecular biology, etc. Some of these basic discoveries will have an immediate
impact on our medical practice, while others will have to wait. This book seeks to link
basic sciences and clinical practice. The authors made special efforts to highlight the
fundamental notions that impact on current patient care, but, needless to say, this
requires continual reassessment.
We thank you in advance for sending us your comments and suggestions to improve
this work. You can reach us at the following address:
pierre.poitras@umontreal.ca
Pierre Poitras
VII
Acknowledgments
This book was made possible thanks to the contribution of many people, who I would
like to thank here:
Thank you to my teachers and mentors, who taught me to give the best for the care
of my patients.
Thank you to my colleagues at Hôpital Saint-Luc de Montréal, gastroenterologists,
hepatologists, surgeons, radiologists, pathologists, biochemists, and experts in digestive
diseases who have been able to create, during all these years, a hospital environment
conducive to happy and efficient work.
Thank you to the University of Montreal, which has allowed me to have a career
that has been as exciting as it has been fruitful.
Thank you to all the students that I have met throughout my career and who were a
constant stimulus for this profession as a clinician and a teacher.
Thank you to all the colleagues who participated in the writing of this book.
Thank you to all our readers of previous French editions. Your appreciation and
comments have been an inspiration to us.
Thank you to all our past and present sponsors who support us in the dissemination
of knowledge.
Thank you to our publishers, Springer Nature for this English version and Les
Presses de l’Université de Montréal for the French editions, for their editorial expertise
and support.
Finally, special thanks to Monique, an exceptional life companion, psychotherapist,
and constant collaborator, who has taught me so much about life and medical human-
ism, and who has allowed me to become who I am, personally, socially, and profession-
ally. It is to her that I dedicate this book.
Pierre Poitras
IX
Introduction
This book is organized into two parts. In the first part, the eight main organs of the
digestive system are studied, and in the second part, the major clinical symptoms that
afflict the digestive system are revised.
In the first part, each organ is presented in the same way: the first five sections of a
chapter deal with "basic" knowledge of macroscopic and microscopic anatomy, embry-
ology, absorption-secretion, and motor-sensory functions; the clinical disorders are
then listed in three general sections: inflammation, tumor, and function disorders.
In the second part, digestive symptoms are presented in order to facilitate rapid and
effective clinical management.
To guide your readings, colored boxes are used to highlight important issues: blue
for diagnostic key points, orange for therapeutic considerations, green for pediatric
aspects, yellow for tropical specificities, and pink for interactions between basic and
clinical sciences.
Our goal is to make you appreciate the digestive system and thus stimulate your
interest and curiosity. Do not hesitate to increase your knowledge by consulting spe-
cialized books to answer any questions that may arise in you while reading this book.
XI
Contents
I The Digestive Organs

1 The Esophagus......................................................................................................................................3
P. Poitras, M. Bouin, C. Faure, J. P. Galmiche, R. Ratelle, and W. G. Paterson
2 The Stomach...........................................................................................................................................31
P. Poitras, M. Bradette, V. Groleau, R. Ratelle, X. Marchand, and D. Armstrong
3 The Small Intestine............................................................................................................................67

P. Poitras, J. Carrier, V. Marchand, A. Serme, G. Soucy, and J. P. Allard
4 The Colon..................................................................................................................................................125
P. Poitras, J. E. Ghia, A. Sawadogo, C. Deslandres, R. Wassef, M. Dapoigny,
and C. Bernstein
5 The Pancreas..........................................................................................................................................173
R. G. Lahaie, S. Bouchard, P. Poitras, F. Vandenbroucke-Menu, U. Halac,
P. Hammel, and P. D. James
6 The Biliary Tree.....................................................................................................................................205

M. Dagenais, R. G. Lahaie, F. Alvarez, P. Poitras, and A. Barkun
7 The Anorectum.....................................................................................................................................225
M. Bouin, R. Wassef, P. Jantchou, D. Bernard, P. Poitras, and C. N. Andrews
8 The Liver....................................................................................................................................................249
M. Bilodeau, J. Bissonnette, H. Castel, D. Corsilli, D. Fenyves, C. Fournier,
J. M. Giard, G. Huard, P. M. Huet, D. Marleau, G. Pomier-Layrargues,
J. P. Villeneuve, C. Vincent, B. Willems, F. Alvarez, and Mark G. Swain
II Digestive Symptoms, Signs and Other

9 Esophageal Symptoms: Heartburn, Dysphagia, and Chest Pain........................307
P. Poitras and M. Bouin
10 Nausea and Vomiting.......................................................................................................................311

P. Poitras, L. Tremblay, and K. Orlicka
11 Upper Gastrointestinal Bleeding (UGIB).............................................................................315

P. Poitras, J. Bissonnette, and Alan Barkun
12 Dyspepsia.................................................................................................................................................321
P. Poitras
13 Diarrhea....................................................................................................................................................325
P. Poitras
XII Contents
14 Abdominal Distension and Bloating......................................................................................331

P. Poitras
15 Constipation...........................................................................................................................................337
P. Poitras, M. Bouin, C. Faure, and M. Dapoigny
16 Abdominal Pain....................................................................................................................................345
P. Poitras, A. Archambault, and V. Marchand
17 Abdominal Hernias............................................................................................................................353
R. Ratelle
18 Fecal Incontinence.............................................................................................................................359
M. Bouin, R. Wassef, C. Faure, and P. Poitras
19 Anorectal Pain.......................................................................................................................................363
M. Bouin, P. Poitras, and R. Wassef
20 Rectal Bleeding....................................................................................................................................367
R. Wassef and P. Poitras
21 Lower GI Bleeding...............................................................................................................................371
R. Wassef and P. Poitras
22 Food Allergies.......................................................................................................................................377
E. Drouin
23 Undernutrition and Nutritional Support............................................................................381

L. D’Aoust, M. Lemoyne, and Johane P. Allard
24 Obesity.......................................................................................................................................................389
L. D’Aoust, V. Groleau, and F. S. Hould
25 Genes and Digestive Cancers......................................................................................................397

B. Panzini
26 Jaundice....................................................................................................................................................403
P. Poitras and S. Paquin
27 Abnormal Liver Tests........................................................................................................................407

J. P. Villeneuve
28 Ascites........................................................................................................................................................413
J. Bissonnette
29 Diets and Digestive Diseases......................................................................................................417

L. D’Aoust and P. Poitras
Supplementary Information
Index.............................................................................................................................................................. 427
XIII
Contributors
Johane P. Allard, MD Division of Gastroenterology and Hepatology, Toronto General

Hospital, University Health Network, Toronto, ON, Canada
Professor of Medicine, University of Toronto, Toronto, ON, Canada
Fernando Alvarez, MD Department of Gastroenterology, Hepatology and Nutrition, CHU

Sainte-Justine, Montreal, QC, Canada
Professor of Pediatrics, Université de Montréal, Montreal, QC, Canada
Christopher N. Andrews, MD Division of Gastroenterology & Hepatology, Foothills Medical

Centre, Calgary, AB, Canada
Clinical Professor of Medicine, University of Calgary, Calgary, AB, Canada
André Archambault, MD Department of Anesthesiology, Centre Hospitalier de l’Université de

Montréal (CHUM), Montreal, QC, Canada
Assistant Clinical Professor of Anesthesiology, Université de Montréal, Montreal, QC, Canada
David Armstrong, MA, MB, BChir Division of Gastroenterology & Farncombe Family
Digestive Health Research Institute, McMaster University Medical Centre, Hamilton, ON,
Canada
Professor of Medicine, McMaster University, Hamilton, ON, Canada
Alan Barkun, MD Division of Gastroenterology, McGill University Health Center, Montreal,

QC, Canada
Professor of Medicine, McGill University, Montreal, QC, Canada
Denis Bernard, MD Digestive and Colorectal Surgery, CHUM, Montreal, QC, Canada
Professor of Surgery, Université de Montréal, Montreal, QC, Canada
Charles N. Bernstein, MD Director, University of Manitoba IBD Clinical and Research Cen-
tre, Winnipeg, MB, Canada
Distinguished Professor of Medicine, Bingham Chair in Gastroenterology, University of Mani-
toba, Winnipeg, MB, Canada
Marc Bilodeau, MD Liver Unit, CHUM, Montreal, QC, Canada

Professor of Medicine, Université de Montréal, Montreal, QC, Canada
Julien Bissonnette, MD Liver Unit, CHUM, Montreal, QC, Canada

Assistant Clinical Professor of Medicine, Université de Montréal, Montreal, QC, Canada
Simon Bouchard, MD GI Unit, CHUM, Montreal, QC, Canada

Mickael Bouin, MD, PhD GI Unit, CHUM, Montreal, QC, Canada

Clinical Professor of Medicine, Université de Montréal, Montreal, QC, Canada
Marc Bradette, MD Division of Gastroenterology, CHU Québec, Quebec, QC, Canada

Clinical Professor of Medicine, Université Laval, Quebec, QC, Canada
XIV Contributors
Julie Carrier, MD Division of Gastroenterology, CHU Sherbrooke, Sherbrooke, QC, Canada

Professor of Medicine, Université de Sherbrooke, Sherbrooke, QC, Canada
Hélène Castel, MD Liver Unit, CHUM, Montreal, QC, Canada

Daniel Corsilli, MD Liver Unit and Intensive Care Service, CHUM, Montreal, QC, Canada
Michel Dagenais, MD Liver and Pancreatic Surgery, CHUM, Montreal, QC, Canada
Associate Clinical Professor of Medicine, Université de Montréal, Montreal, QC, Canada
Louise D’Aoust, MD GI Unit, CHUM, Montreal, QC, Canada

Michel Dapoigny, MD, PhD Digestive Medicine, CHU Estaing, Clermont-Ferrand, France
Professor Emeritous of Medicine, Université Clermont Auvergne, Clermont-Ferrand, France
Renée Déry, MD Department of Radiology, CHUM, Montreal, QC, Canada

Associate Clinical Professor of Radiology, Université de Montréal, Montreal, QC, Canada
Consultant in Radiology and responsable for the radiology material in the entire manual
Colette Deslandres, MD Department of Gastroenterology, Hepatology and Nutrition, CHU

Clinical Professor of Pediatrics, Université de Montréal, Montreal, QC, Canada
Éric Drouin, MD Department of Gastroenterology, Hepatology and Nutrition, CHU

Associate Clinical Professor of Pediatrics, Université de Montréal, Montreal, QC, Canada
Philippe Ducrotté, MD, PhD Gastroenterology Unit, Hopital Charles-Nicolle, Tunis, Tunisia
Professor of Medicine, Université de Rouen-Normandie, Rouen, France
Christophe Faure, MD Department of Gastroenterology, Hepatology and Nutrition, CHU

Professor of Pediatrics, Université de Montréal, Montreal, QC, Canada
Daphna Fenyves, MD Liver Unit, CHUM, Montreal, QC, Canada

Claire Fournier, MD Liver Unit, CHUM, Montreal, QC, Canada

Jean-Paul Galmiche, MD Professeur d’Hépatogastroentérologie, Institut des maladies de

l’appareil digestif, Université de Nantes, Nantes, France
Jean-Eric Ghia, PhD Department of Immunology, Internal Medicine (Gastroenterology),

Rady Faculty of Health Sciences, Winnipeg, MB, Canada
University of Manitoba, Winnipeg, MB, Canada
Consultant in Physiology for the entire manual
Jeanne-Marie Giard, MD, MPH Liver Unit, CHUM, Montreal, QC, Canada
XV
Contributors
Véronique Groleau, MD Department of Gastroenterology, Hepatology and Nutrition, CHU

Assistant Clinical Professor of Pediatrics, Université de Montréal, Montreal, QC, Canada
Ugur Halac, MD Department of Gastroenterology, Hepatology and Nutrition, CHU

Associate Clinical Professor of Pediatrics, University of Montreal, Montreal, QC, Canada
Pascal Hammel, MD, PhD Digestive and Medical Oncology, Hop Paul Brousse, Villejuif,
France
Professor of Medicine, Université Paris-Saclay, Gif-sur-Yvette, France
Frédéric-Simon Hould, MD Department of Digestive Surgery, University Institute of Cardiology

and Pneumology, Quebec, QC, Canada
Associate Professor of Surgery, Université Laval, Quebec, QC, Canada
Geneviève Huard, MD Liver Unit, CHUM, Montreal, QC, Canada

Pierre-Michel Huet, MD, PhD Liver Unit, CHUM, Montreal, QC, Canada
Paul James, MD, MSc Division of Gastroenterology and Hepatology, Toronto General Hospi-
tal, University Health network, Toronto, ON, Canada
Assistant Professor of Medicine, University of Toronto, Toronto, ON, Canada
Prévost Jantchou, MD, PhD Department of Gastroenterology, Hepatology and Nutrition,

CHU Sainte-Justine, Montreal, QC, Canada
Raymond G. Lahaie, MD GI Unit, CHUM, Montreal, QC, Canada

Michel Lemoyne, MD GI Unit, CHUM, Montreal, QC, Canada

Christiane Malo, PhD Professor of Physiology, Department of Physiology, Faculty of Medi-

cine, Université de Montréal, Montreal, QC, Canada
Valérie Marchand, MD Department of Gastroenterology, Hepatology and Nutrition, CHU

Xavier Marchand, MD Emergency Medicine, CH Centre-de-la-Mauricie, Shawinigan-Sud,

QC, Canada
Medical student 2010–2014, Université de Montréal, Montreal, QC, Canada
Responsible for the anatomical illustration in the entire manual
Denis Marleau, MD Liver Unit, CHUM, Montreal, QC, Canada

Katarzyna Orlicka, MD GI Unit, CHUM, Montreal, QC, Canada

XVI Contributors
Benoit Panzini, MD GI Unit, CHUM, Montreal, QC, Canada

Sarto C. Paquin, MD GI Unit, CHUM, Montreal, QC, Canada

William G. Paterson, MD GI Division, Kingston Health Sciences Centre, Kingston, ON,

Canada
Professor Emeritus of Medicine, Biology and Biomedical & Molecular Sciences, Queen’s
University, Kingston, ON, Canada
Pierre Poitras, MD Professor of Medicine, Université de Montréal, Montréal, QC, Canada
Gilles Pomier-Layrargues, MD Liver Unit, CHUM, Montreal, QC, Canada

Richard Ratelle, MD Digestive Surgery, CHUM, Montreal, QC, Canada

Associate Professor of Surgery, Université de Montréal, Montreal, QC, Canada
Appolinaire Sawadogo, MD Department of Hepatogastroenterology, CHU – Sourô SANOU

of Bobo-Dioulasso, Bobo-Dioulasso, Burkina Faso
Professor of Medicine, Université de Ouagadougou, Ouagadougou, Burkina Faso
Consultant in Tropical Medicine for the entire manual
Abdel Karim Sermé, MD Gastroenterology Hospitalization Service, CHU Yalgado-Ouédraogo

of Ouagadougou, Ouagadougou, Burkina Faso
Professor of Gastroenterology and Hepatology, Université de Ouagadougou, Ouagadougou,
Burkina Faso
Consultant in Tropical medicine for the entire manual
Geneviève Soucy, MD Department of Anatomical Pathology, CHUM, Montreal, QC,

Canada
Associate Professor of Pathology and Cell Biology, Université de Montréal, Montreal, QC,
Canada
Consultant in Pathology and responsible for histopathology material in the entire manual
Mark G. Swain, MD, MSc Division of Gastroenterology and Hepatology, Foothills Medical
Centre, Calgary, AB, Canada
Professor of Medicine, University of Calgary, Calgary, AB, Canada
Lydjie Tremblay, BPharm, MSc Department of Pharmacy, CHUM, Montreal, QC, Canada
Clinical Associate Professor of Pharmacy, Université de Montréal, Montreal, QC, Canada
Consultant in Pharmacological Sciences for the entire manual
Franck Vandenbroucke-Menu, MD Liver and Pancreatic Surgery, CHUM, Montreal, QC,

Canada
Clinical Professor of Surgery, Université de Montréal, Montreal, QC, Canada
Consultant in Embryology for the entire manual
Jean-Pierre Villeneuve, MD Liver Unit, CHUM, Montreal, QC, Canada

XVII
Contributors
Catherine Vincent, MD Liver Unit, CHUM, Montreal, QC, Canada

Ramses Wassef, MD Digestive and Colorectal Surgery, CHUM, Montreal, QC, Canada
Professor of Surgery, Université de Montréal, Montreal, QC, Canada
Bernard Willems, MD Liver Unit, CHUM, Montreal, QC, Canada

XIX
Abbreviations
5-ASA 5-amino salicylic acid (mesalamine)
5-HIAA 5-hydroxy indole acetic acid

5-HT 5-hydroxytryptamine (serotonin)
6mp 6-mercaptopurine
AA Amino acid
AB Antibody
ac Ante cibum (before meal)
ACE Angiotensin converting enzyme
Ach Acetylcholine
ADP Adenosine diphosphate
Ag Antigen
Ag Silver
AIH Autoimmune hepatitis
Al Aluminum
alk phos Alkaline phosphatase
ALT Alanine aminotransferase
am Before noon
AMA Anti-mitochondria (antibody)
AMP Adenosine monophosphate
ANS Autonomic nervous system
APC Adenomatosis polyposis coli (gene)
APUD Amine precursor uptake decarboxylase
ASA Aminosalicylic acid (Aspirin®)
ASBT Apical sodium bile acid transporter
ASM Anti-smooth muscle (antibody)
ASO Atherosclerosis obliterans
AST Aspartate aminotransferase
ATP Adenosine triphosphate
AZA Azathioprine
BA Bile acid
BAO Basal acid output
BBM Brush border membrane
BCRP breast cancer resistant protein
BD Bile duct
bid (bis in die) 2 times a day
BLM Basolateral membrane
BMI Body mass index
BP Blood pressure
BS Bile salt
C Carbon (atom)
C4 7α-Hydroxy-4-cholesten-3-one
Ca Calcium
XX Abbreviations
cAMP Cyclic AMP (adenosine monophosphate)

CBD Common bile duct
CCK Cholecystokinin (also called CCK-PZ)
CCK-PZ Cholecystokinin-pancreozymin
CD Crohn’s disease
CFTR Cystic fibrosis transmembrane conductance regulator
Cl Chloride (ion)
ClC Chloride channel
CMV Cytomegalo virus
CN (or cn) Cranial nerve
CNS Central nervous system
CO2 Carbon dioxide
COX Cyclo-oxygenase enzyme
CP Chronic pancreatitis
Cr Chromium
CRF Corticotropin releasing factor
CSA Cyclosporin
CT Celiac trunk
CTscan Computerized axial tomography
Cu Copper
Cx Surgery
CYP Cytochrome P450
D2 (D3, D4) Duodenum second (third, fourth) portion
DMT Divalent metal ion transporter
DRE Digital rectal examination
DU Duodenal ulcer
Dx Diagnosis
E+ Electrolytes
E coli Escherichia coli
EC Enterochromaffin
ECEH Enterohemorrhagic Escherichia coli
ECL Enterochromaffin-like
EGF Epidermal growth factor
EHBD Extrahepatic bile duct
ENS Enteric nervous system
ENT Ear-nose-throat (medical specialist)
EPS Epigastric pain syndrome
ERCP Endoscopic retrograde cholangio-pancreatography
ETOH Ethanol
FA Fatty acid
FATP Fatty acid transport protein
FDA Food and Drug Administration (USA)
Fe Iron
FGF19 Fibroblast growth factor 19
FGID Functional gastro-intestinal disorder
XXI
Abbreviations
FODMAP Fermentables, oligosaccharides, disaccharides, monosaccharides, and

polyols
FXR Farnesoid X
g (or gm) Gram
GABA Gamma-aminobutyric acid
GERD Gastroesophageal reflux disease
GDA Gastro-duodenal artery
GRP Gastrin releasing peptide
GU Gastric ulcer
H Hydrogen (atom)
H. pylori Helicobacter pylori
H 2O Water
H2RA Histamine H2 receptor antagonist
HAMP Hepcidin antimicrobial peptide
Hb Hemoglobin
HbsAg Hepatitis B surface antigen (Australian antigen)
HCC Hepatocellular carcinoma
HCl Hydrochloric acid
HCO3 Bicarbonate
HCP Heme carrier protein
HFE gene High iron gene (hemochromatosis gene)
HIV Human immunodeficiency virus
HLA Human leukocyte antigen
HNPCC Hereditary non-polyposis colon cancer
Hp Helicobacter pylori
hr Hour
HR Heart rate
HS (or hs) (hora somni) at bedtime
Ht Hematocrit
HUS Hemolytic uremic syndrome
IBABP Ileal bile acid binding protein
IBD Inflammatory bowel disease
IBS Irritable bowel syndrome
ICU Intensive-care unit
id (in die) once a day
IF Intrinsic factor
Ig Immunoglobulin
IHBD Intrahepatic bile duct
IL Interleukin
IM (or im) Intra-muscular
INR International normalized report (prothrombin coagulation test)
IPAN Intrinsic primary afferent neuron
IPMN Intraductal papillary mucinous neoplasm (of the pancreas)
IR (or ir) Intra-rectal
ITP Inositol triphosphate
XXII Abbreviations
IV (or iv) Intra-venous

K Potassium
Kg Kilogram
L Liter
LDH Lactate dehydrogenase
LES Lower esophageal sphincter
LGIB Lower Gi bleeding
LH Left hypochondrium
LIF Left iliac fossa
LKM Liver-kidney microsomes
LT Leukotriene
LUQ Left upper quadrant (abdomen)
MALT Mucosa associated lymphoid tissue
MAO Maximum acid output
max Maximum
MDR Multidrug resistance (gene)
MELD Model end-stage liver disease
MEN Multiple endocrine neoplasia
min Minute
min Minimum
Mg Magnesium
MgOH Magnesium hydroxide
MgSO4 Magnesium sulfate
MMC Migrating motor complex
MMF Mycophenolate mofetil
Mn Manganese
MRI Magnetic resonance imaging
N Nitrogen
Na Sodium
NALFD Non-alcoholic fatty liver disease
NASH Nonalcoholic steatohepatitis
NET Neuroendocrine tumor
NG tube Nasogastric tube
NH3 Ammonia
NH4 Ammonium
NHE Na (sodium) – hydrogen exchanger
NK Neurokinin
NMR Nuclear magnetic resonance
NO Nitric oxide
NPO (nil per os) nothing by mouth, fasting
NPY Neuropeptide Y
NSAID Non-steroidal anti-inflammatory drug
OST Organic solute transporter
PACAP Pituitary adenylate cyclase-activator peptide
PBC Primary biliary cholangitis
XXIII
Abbreviations
PC (or pc) (post cibum) after meal

PCFT Proton coupled folate transporter
PDS Postprandial distress syndrome
PEG Polyethylene glycol
PEPT-1 Peptide transporter-1
PET Positron emission tomography
PgE Prostaglandin E
PGP P-glycoprotein
PLC Phospholipase C
pm Afternoon
plt Platelets
PO (or po) (per os) oral
PO4 Phosphate
PPI Proton pump inhibitor
PRN (or prn) (pro re nata) as needed
PSC Primary sclerosing cholangitis
PYY Peptide YY
Q 3-4 hrs (quaque) every 3 to 4 hours
QID(or qid) (quater in die) four times a day
RBC Red blood cells
RH Right hypochondrium
RIF Right iliac fossa
ROH Alcohol
RR Relative risk
RUQ Right upper quadrant (abdomen)
RX Radiology
Rx Treatment
SB Small bowel
SC (or sc) Subcutaneous
SGLT-1 Sodium glucose transporter 1
SIBO Small intestinal pullulation overgrowth
SMA Superior mesenteric artery
SO Sphincter of Oddi
SP Substance P
SPINK Serine peptidase inhibitor, Kazal type 5
SSRI Selective serotonin reuptake inhibitor
T4 Thyroxine
TCA Tacrolimus
TG Triglycerides
TID (or tid) (ter in die) three times a day
TIPS Transjugular intrahepatic portal shunt
TLESR Transient lower esophageal sphincter relaxation
TNF Tumor necrosing factor
TNM Tumor-node-metastasis (classification)
TPMT Thiopurine methyl transferase
XXIV Abbreviations
TPN Total parenteral nutrition

TRPM Transient receptor potential melastatin
UC Ulcerative colitis
UES Upper esophageal sphincter
UGIB Upper GI bleeding
VHA Hepatitis A virus
VHB Hepatitis B virus
VHC Hepatitis C virus
VHD Hepatitis D virus
VIP Vasointestinal polypeptide
vit Vitamin
WHO World Health Organization
X-ray Radiography, radiology
ZE Zollinger-Ellison
ZES Zollinger-Ellison syndrome
XXV
Warning
This book is not a “tricks list” for your exams.

It is not a “recipe book” for the treatment of your patients on the ward.
This book is to discover, learn, understand, and appreciate the digestive system.
Enjoy.
Pierre Poitras
1 I
The Digestive Organs

Contents
Chapter 1 The Esophagus – 3

P. Poitras, M. Bouin, C. Faure, J. P. Galmiche, R. Ratelle,
and W. G. Paterson
Chapter 2 The Stomach – 31

P. Poitras, M. Bradette, V. Groleau, R. Ratelle,
X. Marchand, and D. Armstrong
Chapter 3 he Small Intestine – 67

T
P. Poitras, J. Carrier, V. Marchand, A. Serme, G. Soucy,
and J. P. Allard
Chapter 4 The Colon – 125

P. Poitras, J. E. Ghia, A. Sawadogo, C. Deslandres,
R. Wassef, M. Dapoigny, and C. Bernstein
Chapter 5 The Pancreas – 173

R. G. Lahaie, S. Bouchard, P. Poitras,
F. Vandenbroucke-Menu, U. Halac, P. Hammel,
and P. D. James
Chapter 6 The Biliary Tree – 205

M. Dagenais, R. G. Lahaie, F. Alvarez, P. Poitras,
and A. Barkun
Chapter 7 The Anorectum – 225

M. Bouin, R. Wassef, P. Jantchou, D. Bernard, P. Poitras,
and C. N. Andrews
Chapter 8 The Liver – 249

M. Bilodeau, J. Bissonnette, H. Castel, D. Corsilli,
D. Fenyves, C. Fournier, J. M. Giard, G. Huard,
P. M. Huet, D. Marleau, G. Pomier-Layrargues,
J. P. Villeneuve, C. Vincent, B. Willems, F. Alvarez,
and Mark G. Swain
3 1
The Esophagus
P. Poitras, M. Bouin, C. Faure, J. P. Galmiche, R. Ratelle,
and W. G. Paterson
Contents
1.1 Macroscopic Anatomy – 5

1.1.1 S hape and Structure – 5
1.1.2 Vascular Supply – 6
1.1.3 Innervation – 7
1.2 Microscopic Anatomy – 7

1.2.1 E sophageal Mucosa – 7
1.2.2 Muscularis – 8
1.2.3 Serosa – 8
1.3 Embryology/Development – 8
1.3.1 ormal Development – 8
N
1.3.2 Atresias of the Esophagus – 8
1.3.3 Esophageal Stenosis/Strictures – 9
1.3.4 Duplications and Cysts – 9
1.3.5 Rings and Webs – 9
1.4 Secretion/Absorption – 9
1.5 Motility/Sensitivity – 9
1.5.1 ropharyngeal (Transfer) Motility – 9
O
1.5.2 Esophageal (Transport) Motility – 9
1.5.3 Sphincters: Upper and Lower – 11
1.5.4 Sensory Function – 11
1.6 Inflammation Disorders – 11

1.6.1 eptic Esophagitis – 11
P
1.6.2 Infectious Esophagitis – 13
1.6.3 Eosinophilic Esophagitis – 14
1.6.4 Caustic Esophagitis – 14
1.6.5 Drug-Induced Esophagitis – 15
1.6.6 Radiation Esophagitis – 15
1.7 Tumor Disorders – 15

1.7.1 T ypes of Esophageal Neoplasia – 15
1.7.2 Clinical – 16
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2022

P. Poitras (ed.), The Digestive System: From Basic Sciences to Clinical Practice,
https://doi.org/10.1007/978-3-030-98381-9_1
1.7.3 iagnosis of Esophageal Cancer – 16
D
1.7.4 Treatment of Esophageal Cancer – 16
1.8 Function Disorders – 17

1.8.1 astroesophageal Reflux Disease (GERD) – 17
G
1.8.2 Oropharyngeal (Transfer) Dysmotility – 22
1.8.3 Esophageal (Transport) Dysmotility – 22
1.8.4 Sensitivity Disorders – 26
1.9 Miscellaneous – 26
1.9.1 iatal Hernia – 26
H
1.9.2 Diverticulum – 27
1.9.3 Esophageal Rupture – 28
1.9.4 Esophageal Bleeding – 28
1.9.5 Mallory-Weiss – 28
1.9.6 Schatzki’s Ring – 28
The Esophagus
5 1
1.1 Macroscopic Anatomy At the cervical level, the esophagus is located in front
of the vertebral column and behind the trachea. On
1.1.1 Shape and Structure each side, we find the carotid arteries and the recurrent
laryngeal nerves, branches of the vagus nerve control-
1
ling motility of the pharynx and upper esophagus.
The digestive tract begins, we often forget, with the oral
The thoracic esophagus then passes into the poste-
cavity. The teeth grind the food before the tongue and
rior mediastinum in front of the spine, behind the tra-
the striated muscles of the pharynx push it into the
chea, the carina, the heart, the aortic arch, then to the
esophagus.
right of the aorta, and bordered by the pulmonary
pleura (. Fig. 1.1b).
(a) Esophagus. The esophagus is a tube with an approxi-
The abdominal esophagus is made up of a short seg-
mate diameter of 2.5 cm, which allows the passage of
ment (1–2 cm long) between the diaphragm and the stom-
food from the oral cavity through the thoracic cavity into
ach. The two branches of the vagus nerve descend from the
the stomach. The esophagus starts at the cricopharyngeal
central nervous system by running on both sides of the
muscle (or upper esophageal sphincter) located at about
esophagus; at the level of the diaphragmatic hiatus, the left
15 cm of the incisors, anterior to the C6 vertebra, and
and right branches of the vagus nerve are found on the
continues until the lower esophageal sphincter (positioned
anterior and posterior walls, respectively, of the esophagus
at the cardia, approximately 40 cm from the incisors at the
(due to the rotation of the stomach during its fetal devel-
level of T11 vertebra) before its entry in the abdominal
opment; see 7 Sect. 2.3 in 7 Chap. 2). The surgical proce-
cavity and the stomach. The esophagus is classically
dure of truncal vagotomy, once used to reduce gastric acid
divided into three relatively identical segments identified
secretion and treat peptic ulcer, consisted of sectioning
as the upper, middle, and lower thirds of the esophagus
both of these vagal branches in the lower esophagus.
(. Fig. 1.1a).
a b
.. Fig. 1.1 a (left figure). Esophagus anatomy: front view. b (right figure). Esophagus anatomy: side view
6 P. Poitras et al.
(b) Sphincters. At both ends of the esophageal tube, we phragm, mainly on its abdominal side. This sphincter
find sphincters, areas of high pressure designed to close area is made up of muscle fibers from the lower esopha-
1 the tube entrance and acting as a one-way valve.
The upper esophageal sphincter (UES) or cricopha-
gus (“internal” sphincter), and muscle fibers from the
gastric fundus as well as the diaphragm pillars (“exter-
ryngeal muscle is composed of fibers from pharyngeal nal” sphincter). Its role in gastroesophageal reflux dis-
muscles aligned transversally and of transverse fibers ease (GERD) will be discussed subsequently.
from the esophagus that encircle the esophageal tube
and form a high-pressure zone probably intended to
protect the tracheal airway from possible gastroesopha- 1.1.2 Vascular Supply
geal regurgitations. Between the oblique muscle fibers
from the pharynx and the transverse fibers from the (a) Arteries. The esophagus is supplied in its upper seg-
upper esophageal sphincter, we find an area of potential ment by four to six small arteries derived from the thyroid
weakness, Killian’s triangle, that may give rise to Zenk- arteries, by arteries originating directly from the aorta or
er’s diverticulum (discussed later in this chapter), espe- derived from intercostal or bronchial arteries in the middle
cially in the presence of a high pressure within the UES segment, and by gastric arteries in the distal segment
that generates an obstacle to food swallowing. (. Fig. 1.2a). The arteries form a dense irrigation network
The lower esophageal sphincter (LES) is an area of which protects the esophagus from an ischemic process.
high pressure, approximately 2 cm long, located at the
esophagogastric junction that prevents regurgitation of (b) Veins.An extensive network of small veins drains
gastric contents into the esophagus. It is normally located the esophagus via the thyroid veins at its upper part and
at the thoracoabdominal junction, at the level of the dia- toward the azygos and intercostal veins in its middle
a b
.. Fig. 1.2 a (left figure). Arteries of the esophagus. b (right figure). Veins of the esophagus
The Esophagus
7 1
part. At the lower portion, esophageal veins may drain (regulating muscle contractions for motility), as else-
toward the abdomen to the short gastric veins or to the where in the gastrointestinal tract (see 7 Chap. 3).
Extrinsic innervation depends on sympathetic and
left gastric vein and thus toward the portal circulation;
this explains then the possible formation of venous dila- parasympathetic systems. Cervical and thoracic sympa-
1
tations in the lower esophagus (called esophageal vari- thetic ganglia provide motor and sensitive innervation to
ces) in the setting of portal hypertension due to liver the entire esophagus. The vagus nerve exerts a parasympa-
cirrhosis (. Fig. 1.2b). thetic motor innervation to the upper esophagus as well as
in the pharynx. Afferent fibers of the vagus nerve are also
(c) Lymphatics. Lymphatic channels arise in the mucosa probably important in esophageal sensory transmission.
and muscular region of the esophagus and drain to par- At the buccopharyngeal level, cranial nerves IX and
aesophageal lymph nodes distributed all along the XII are responsible, respectively, for sensitive and motor
organ. In case of neoplasia, the lymphatic flow from the innervation. A damage of these nerves, after a vascular
upper 2/3 of the esophagus moves upward (cervical stroke of the brain stem, for example, will create swal-
lymph nodes, paratracheal lymph nodes of the upper lowing dysfunction.
mediastinum, paraesophageal lymph nodes of the mid-
dle or inferior mediastinum, etc.), while the lower esoph-
agus may drain into the abdomen to celiac and perigastric 1.2 Microscopic Anatomy
lymph nodes.
The abdominal lymphatic secretions are channeled, Like the rest of the digestive tract, the esophagus is
via the thoracic duct running up along the esophagus, to made up of an internal mucosa layer resting on a mus-
join the left subclavian vein near by the jugular vein. cular structure. The peculiarities of the esophagus are as
Trauma, surgical or otherwise induced, of the cervical follows:
esophagus, may therefore damage this structure and
lead to chylothorax and even intestinal lymphangiecta-
sias. 1.2.1 Esophageal Mucosa
The esophageal mucosa is made of a stratified squamous

1.1.3 Innervation epithelium (. Fig. 1.3). This squamous mucous mem-
brane is also found at the very distal end of the digestive
Intrinsic innervation of the esophagus is provided by the tract, at the anus, while the columnar (glandular)
enteric nervous system (ENS) with a relatively sparse epithelium is the normal histology of the entire gastro-
Meissner’s submucosal plexus (controlling microcircula- intestinal tract from the stomach to the rectum. At
tion and secretion) and Auerbach’s myenteric plexus approximately 40 cm from the incisor teeth, at the gas-
tric cardia level, we find the Z line that marks the transi-
tion, clearly visible macroscopically (e.g., in endoscopy;
. Fig. 1.4), between the whitish squamous mucosa of
.. Fig. 1.3 Esophagus normal histology: squamous mucosa of the

esophagus (on the right part of the figure) and columnar mucosa of
the stomach (on the left part) as seen at the gastroesophageal junc- .. Fig. 1.4 In endoscopy, the meeting junction between the gastric
tion. (Photo from W. Bloom and D.W. Fawcett, Textbook of Histol- reddish mucosa (at the center of the image) and of the esophageal
ogy, 1968) whitish mucosa is obvious. (Photo by P.Poitras)
8 P. Poitras et al.
the esophagus and the reddish columnar epithelium of 1.3 Embryology/Development

the stomach. The Z line corresponds to the lower por-
1 tion of the lower esophageal sphincter.
The epithelial structure of the esophagus explains
1.3.1 Normal Development
the relative paucity of absorptive or secretory phenom-
The oropharynx, trachea, lungs, and esophagus develop
ena so common to the rest of the digestive tract. This
from a common tube: the endoderm. In the 4th week of
squamous mucous membrane also explains the presence
fetal life, a bud forms at the ventral part of the tube to
of squamous cell neoplasia at this site level of the diges-
become the respiratory system. The dorsal part of the
tive tract. In Barrett’s esophagus (secondary to GE
tube will turn into the esophagus and a foregut from
reflux as discussed later), the squamous mucosa is
which the stomach will arise. The separation of the two
replaced by a columnar mucosa allowing then the devel-
tubes in respiratory and digestive organs is carried out
opment of adenocarcinomas.
around the 6th week. Esophageal lumen is formed
In the submucosa, we find blood vessels, lymphatics,
around week 10 and will be epithelialized with squa-
some nerves of Meissner’s plexus, as well as glandular
mous cells from the 16th week. From week 18 to 20, the
cells secreting mucus and bicarbonate involved in the
fetus can swallow up to 500 ml amniotic fluid per day;
defense of mucosal integrity.
the impossibility to perform this function (e.g., due, to
esophageal atresia) may lead to an increase in this fluid
and of uterine volume. Mechanisms of suction-
1.2.2 Muscularis deglutition and of esophageal peristalsis are mature
enough at 34 weeks to allow bottle-feeding from that
The esophagus, as most of the digestive tract, is made
point onward.
up mainly of smooth muscles organized in a circular
We will now describe different malformations that
inner layer and a longitudinal outer layer. The upper
may arise during development.
esophagus, however, contains striated muscles that are
in fact an extension of the pharyngeal muscles. Diseases
of the smooth muscles can thus affect the middle and
distal esophagus, while pathologies of the striated mus- 1.3.2 Atresias of the Esophagus
cles can affect the proximal region of the esophagus.
As elsewhere in the gastrointestinal tract, the intrin- Atresias of the esophagus are often accompanied by a
sic enteric nervous system is made up of the myenteric tracheoesophageal fistula (. Fig. 1.5). They affect
and submucous plexuses, respectively, located between 1/3000 to 1/4500 births; 50% of the children carriers of
the longitudinal and circular muscle layers and between these manifestations also have other abnormalities such
the circular muscles and the mucous membrane. as imperforate anus and heart defects.
Atresia of the esophagus results from an impaired
canalization of the esophageal lumen, while broncho-
1.2.3 Serosa esophageal fistulas are more likely the result of a separa-
tion failure of the two tubes.
The serosa, usually lining the external muscle layer of These malformations will be suspected in a newborn
digestive cavities, is absent in the esophagus. It is replaced baby that regurgitates saliva and liquids after ingestion.
by a thin adventitia (thin connective tissue layer). Passage through the bronchial tubes will cause coughing
.. Fig. 1.5 Congenital atresia of the esophagus: various malformations are possible
The Esophagus
9 1
and choking. Surgical correction will be required Swallowing, however, benefits from saliva secretion.
promptly. The parotid, submaxillary, and sublingual glands pro-
duce 1–2 liters of liquid daily, often in response to chew-
ing, which will help the swallowing by lubricating the
1
1.3.3 Esophageal Stenosis/Strictures food. Saliva also contains enzymes, such as amylase and
lipase, which initiate the digestion process. Bicarbonate-
These are rare congenital malformations that occur in rich saliva plays an important role in the esophagus’s
1/50,000 births. Stenoses are most often short and of ability to neutralize the gastric acid that could backflow
fibrous or cartilaginous in nature (tracheobronchial into it.
remnant). They are often tolerated in the very young age
when feeding only liquid food, but they will be revealed
subsequently when dysphagia occurs when taking solid 1.5 Motility/Sensitivity
food.
The role of the esophagus is to transport food from the
mouth to the stomach. The act of swallowing (degluti-
1.3.4 Duplications and Cysts tion) involves a transfer of the food bolus from the oral
cavity to the esophageal cavity and then a transport of
Duplications and cysts are found in 1/8000 births. the bolus through the esophageal body toward the stom-
Double esophageal tubes are rare; most of the time, it ach.
consists in “cystic” structures located in the paraoesoph-
ageal region and without communication with the real
esophagus. Patients are often asymptomatic (the condi- 1.5.1 Oropharyngeal (Transfer) Motility
tion being discovered accidentally during a radiological
examination) or may suffer from symptoms due to com- The food undergoes a first transformation in our plate
pression by these additional structures. Surgical treat- (shredding by our utensils) before its form is again
ment will be required to control symptoms. altered by dental chewing. This is how the food bolus is
formed. The transfer of this bolus into the esophageal
cavity initially involves a voluntary action of the striated
1.3.5 Rings and Webs muscles of the tongue and oropharynx, controlled
mainly by the cranial nerve XII (hypoglossal nerve), fol-
The most common ring is Schatzki’s ring, an annular lowed by involuntary movements of the palate, the
fibrous ring located at the esophagogastric junction. pharynx, the larynx, as well as the upper esophagus, all
However, the congenital nature of Schatzki’s ring is regulated by the vagus nerve (CN X) and glossopharyn-
being questioned; there is increasing evidence that this geal nerve (CN IX). The stages of swallowing are repre-
band is the consequence of gastroesophageal reflux dis- sented in . Fig. 1.6.
ease (GERD). See 7 Sect. 1.9, point 6. Any damage to neural structures (brain stem dam-
The membrane, or web, is a noncircumferential age by vascular stroke, amyotrophic lateral sclerosis,
band, found mostly in the upper esophagus or middle Parkinson’s, etc.) or striated muscles (oculopharyngeal
esophagus. It can be solitary, sometimes associated with dystrophy, myasthenia gravis, etc.) of this region may
iron deficiency anemia, then called Plummer-Vinson’s disrupt the physiology of swallowing and lead to a
syndrome (or Paterson-Kelly’s syndrome), or they can proximal dysphagia with possible false routes to the
be multiple. upper (nasal regurgitations) or lower (cough, choking)
Esophageal dilatation per endoscopy is the usual airways.
treatment of symptomatic rings and webs.
1.5.2 Esophageal (Transport) Motility

1.4 Secretion/Absorption
Once the voluntary swallowing of the bolus provided by
Although some secretion of bicarbonates and mucus by the striated muscles of the oropharynx has pushed the
submucosal glands occurs, overall the esophagus has food bolus into the esophageal cavity, the smooth mus-
minimal absorptive or secretory function. cles of the esophagus will ensure the progression of the
10 P. Poitras et al.
a b c
.. Fig. 1.6 Swallowing: a The bolus is pushed by the tongue towards the pharynx. b The soft palate rises to block the nasopharynx (and
avoid regurgitation of food through the nose). c The larynx moves upward and anteriorly, while the epiglottis goes down to block the entrance
to the trachea (and avoid intrabronchial aspiration of food resulting in acute airway obstruction, or complicated by aspiration pneumonia);
the upper esophageal sphincter, normally closed and under tension, relaxes to let the food bolus get into the esophageal cavity where trans-
port motility will take over. Swallowing is controlled by cranial nerves IX, X, and XII and cervical sympathetic ganglion
bolus along the organ. As explained extensively in

7 Chap. 3, this peristalsis is mainly involuntary and
relies on the enteric nervous system of Auerbach’s
plexus. The following steps are involved:
55 Detection of the intraluminal food bolus with activa-
tion of sensitive afferent neural fibers [usually CGRP
(calcitonin gene-related peptide)] in mucosa and
muscle layers of the intestinal wall.
55 The information is transmitted to the efferent motor
neurons that will activate, via acetylcholine and neu-
rokinins, the contraction of the circular muscles of
the esophagus upstream of the bolus.
55 At the same time, the efferent neural fibers will cause
the relaxation, via VIP (vasointestinal polypeptide)
and NO (nitric oxide), of the circular muscles local-
ized downstream of the bolus to allow a well-
synchronized propulsion forward.
Esophageal motility can be easily analyzed in clinical or .. Fig. 1.7 Normal motility (on standard classical manometry) of
the esophagus recorded using a probe inserted through the nose into
research settings using manometry with the help of pres- the esophagus and the stomach to measure, at various levels of the
sure sensors (installed on a thin tube or a wire intro- organ, the intraluminal pressure variations secondary to contrac-
duced, usually nasally, into the esophagus to the tions of the esophageal wall during swallowing a sip of water
stomach) that record the contractions of the esophagus
at different points along the organ. Various contractile toward the stomach (and thus forcing a vertical posi-
waves are identified (. Fig. 1.7): tion when eating).
55 The primary wave is a peristaltic contraction nor- 55 The secondary wave is identical to the primary wave
mally initiated in response to the ingestion of the above described, but not induced by swallowing. Initi-
food bolus. It migrates, at a rate of 3–4 cm/second, ated by local distension, it can start at any level of the
all along the esophagus, from top to bottom, push- esophagus and migrate downward. It can be triggered
ing the bolus in front of it. The primary wave thus experimentally by the infusion of a liquid or by local
allows eating in a lying down position (“Roman” distension (with a balloon) of an esophageal segment.
style), or even upside down as the opossum. In case It is generated strictly by the sensory and motor func-
of disappearance of this contractile wave, usually by tions of the peristaltic reflex described before. In prac-
damage to the smooth muscles of the esophagus tice, it will occur during episodes of reflux to “clean”
(e.g., scleroderma), gravity becomes the only factor the esophagus of material refluxed by the stomach
allowing the descent of food along the esophagus that could irritate or inflame the esophagus.
The Esophagus
11 1
55 Tertiary waves are nonperistaltic simultaneous con- quency is responsible for most cases of GE reflux dis-
tractions. They are independent of swallowing and ease (GERD) as discussed later.
have no obvious motor function. They are encoun-
tered during pathological states such as achalasia or
1
diffuse spasm. 1.5.4 Sensory Function
Sensory function is essential to detect the presence of

1.5.3 Sphincters: Upper and Lower the intraluminal food bolus (or refluxed gastric mate-
rial) which then triggers peristaltic contractions that will
Sphincters are areas of high intraluminal pressure that harmoniously propel esophageal content toward the
act as barriers functioning like unidirectional valves stomach.
being closed and contracted in the resting state to pre- In normal situations, we are not consciously aware
vent reflux, but getting relaxed and opened during swal- of the passage of food or other sensations within the
lowing to allow the passage of the bolus across. esophagus. Painful sensations can be perceived in abnor-
mal situations, such as strong spastic contractions, food
(a) Upper esophageal sphincter or cricopharyngeal muscle. blockage, or prolonged acid exposure to the esophageal
The upper esophageal sphincter (UES), which is com- mucosa. Sensory or painful sensation can also be facili-
posed of striated muscles, forms a barrier between the tated by visceral hypersensitivity as documented in vari-
esophageal and oropharyngeal cavities, thus serving to ous functional digestive disorders.
protect the trachea of unexpected reflux from the esoph-
agus.
When the bolus arrives from the oropharynx, the 1.6 Inflammation Disorders
sphincter relaxes and opens to let the bolus enter the
esophageal cavity. The cranial nerves IX, X, and XII Inflammation of the esophagus can appear under differ-
play an important role in this coordination. Impaired ent forms in response to different causal factors.
relaxation or opening of the UES will result in upper
(oropharyngeal/ transfer) dysphagia, and possibly the
creation of a diverticular pouch (Zenker’s diverticulum; 1.6.1 Peptic Esophagitis
see 7 Sect. 1.9.1) in the area of wall weakness (Killian’s
triangle) between the oblique pharyngeal muscle fibers Peptic esophagitis is secondary to the reflux of acidic
and the transverse fibers of the cricopharyngeus. gastric content into the esophagus [GERD (gastro-
esophageal reflux disease) extensively discussed in this
(b) Lower esophageal sphincter. LES is a high-pressure chapter in the Sect. 7 1.8]. Peptic esophagitis is the most
area, created by tonic contraction of specialized circular common form of esophagitis met in practice.
smooth muscle, that separates the stomach from the
esophagus to prevent reflux of gastric material to the (a) Symptoms of peptic esophagitis. Esophagitis is clini-
esophagus. cally revealed by sensations of chest discomfort. Regur-
Hypotension or defective contraction of this sphinc- gitation of food or acidic-bilious liquid, retrosternal
ter will result in gastroesophageal reflux and possibly burning, and pyrosis (burning sensation along the
secondary esophagitis. esophagus from the bottom to the top) suggest GERD
The LES normally contracted during the “resting (with or without esophagitis); odynophagia (pain dur-
state” must relax to open in a coordinated manner at the ing the passage of food bolus) or dysphagia (feeling of
arrival of the esophageal bolus for its passage into the food getting stuck during passage to the stomach) sug-
stomach. This highly coordinated relaxation relies on gests esophagitis (secondary to acid GE reflux).
the NO and VIP inhibitory neurons of the enteric ner-
vous system. Insufficient relaxation of the LES (as (b) Diagnosis of esophagitis. Esophageal endoscopy is
encountered in achalasia discussed later) will compro- the best way to diagnose esophagitis. The macroscopic
mise esophageal transit, and this will result in lower appearance of esophageal mucosa seen at endoscopy
(esophageal/transport) dysphagia. (. Fig. 1.8) and/or its microscopic aspect on mucosal
Transient inappropriate lower sphincter relaxation biopsies obtained during endoscopy will establish the
(TILSR) not triggered by swallowing may occur “spon- diagnosis.
taneously” (or due to distension of the gastric fundus;
2–3/hr in normal individuals) and allow the retrograde (c) Pathophysiology of peptic esophagitis. Acid-peptic
passage of air (belching) or, unfortunately, of gastric reflux from the stomach is the dominant cause of peptic
fluid (gastroesophageal reflux). Their increased fre- esophagitis. However, all individuals with GERD are
a b c
.. Fig. 1.8 Peptic esophagitis seen in endoscopy: a re-epithelialized ulceration (arrow) at the gastroesophageal junction (the gastric colum-
nar and esophageal squamous mucosa are, respectively, of reddish and whitish coloration); b Barrett’s esophagitis with columnar-type
mucosa extending up above the GE junction into the esophagus; c normal GE junction. (Photos by P. Poitras)
not victims of esophagitis. A balance between aggres- gren’s disease or after maxillary gland radiotherapy
sion factors and esophageal defense probably explains treatment) can confirm its clinical importance in the
this situation. genesis of esophagitis.
Aggression Factors:
55 Quantity of reflux: Quantification of gastroesopha- (d) Complications of esophagitis. Acute bleeding from an
geal reflux, by continuous recording of esophageal esophagitis lesion is rare. More severely ulcerated areas or
pH, reveals a certain relationship between the magni- the use of anticoagulants may be contributing factors.
tude of the refluxed acid material into the esophagus Chronic occult bleeding from ulcerated esophagitis may
and the severity of the esophagitis. explain some cases of iron deficiency anemia.
55 Quality of reflux: Although the degree of acidity is Stenosis is a narrowing of esophageal lumen due to
paramount, bile, under experimental conditions, acts local inflammation or scar from healed ulceration. It
as a potentiating agent to acid in inducing esopha- will be suspected in the presence of dysphagia, typically
geal inflammation, so it may contribute to the sever- more with solid than with liquid foods, and it will be
ity of esophagitis. Hypersecretion of gastric acid confirmed by endoscopy or radiology. The treatment of
could be, in rare cases (such as a gastrinoma that stenosis requires control of esophagitis and acid reflux,
causes a major hypersecretion of gastric acid; see usually by proton pump inhibitors (PPIs). In some cases,
Zollinger–Ellison syndrome in 7 Chap. 2), a factor mechanical dilatation with bougies or balloons will be
promoting mucosal damage to the esophagus. required.
Barrett’s esophagus: The squamous esophageal
Defense of the Esophagus: mucosa, in this condition, is replaced by an intestinal-
55 Mucosal resistance of the esophagus to aggression, type columnar mucosa.
for example, by secreting local mucus or bicarbon- The diagnosis is suspected during endoscopy which
ates, could be a protective factor. The concept of reveals a reddish, gastric-looking mucosa above the car-
“mucosal barrier” so important in gastric patho- dia, in esophageal territory. The esophagus may thus
physiology (see 7 Chap. 2) is however not as well appear short (hence the name endo-brachy-esophagus)
developed in esophageal pathology. since the junction of the esophageal and gastric mucosa
55 Esophageal peristalsis contributes to the defense of is higher than the usual endoscopic Z line classically
the esophagus by promoting the flow of refluxed located at 40 cm from the incisor teeth. The differential
gastric material back into the stomach (esophageal diagnosis will be made with a hiatal hernia raising the
clearance). The loss of peristaltic secondary con- cardia (and thus the Z line) into the thorax above the
tractions, normally initiated during a backflow, usual diaphragmatic location. Endoscopic biopsies will
probably contributes to the severe esophagitis seen confirm histological presence of intestinal metaplasia,
in patients with esophageal muscle disease due to in an anatomical segment otherwise identified as the
scleroderma. esophagus.
55 Saliva, rich in bicarbonate and with a neutral or Barrett’s esophagus is important since it is consid-
alkaline pH, is a factor favoring the neutralization of ered preneoplastic, precursor to the development of a
gastric acid refluxed into the esophagus. However, no local adenocarcinoma. The risk of malignant evolution
clinical situation (e.g., during hyposalivation by Sjo- is estimated at 1/200 patients.
The Esophagus
13 1
Treatment of Barrett’s esophagus is disappointing with predominant regurgitation). The role of novel
since the suppression of reflux by medication or surgery endoscopic anti-reflux procedures remains to be defined.
does not seem to induce regression of the re-epithelialized
glandular mucosa of the esophagus. Follow-up of this
1
condition (with endoscopy and biopsies every 3–5 years) 1.6.2 Infectious Esophagitis
is often recommended hoping for early detection of
high-grade dysplasia or early adenocarcinoma lesions Infectious esophagitis is usually of viral or mycotic ori-
allowing treatment of an early-stage cancer disease. The gin, more rarely bacterial.
benefit of this monitoring strategy is however unclear. (a) Symptoms of infectious esophagitis. Odynophagia
as well as dysphagia or chest pain is found in infec-
(e) Treatment of peptic esophagitis. Treatment of peptic tious esophagitis. Heartburn or pyrosis is rare.
esophagitis is based on the reduction of acid exposure in (b) Viral esophagitis.
the esophagus. This is usually achieved satisfactorily by 55 Herpes simplex 1 can cause esophagitis in immu-
inhibiting the activity of the proton pump located on gas- nosuppressed patients, often by chemotherapeu-
tric parietal cells secreting HCl in the stomach cavity and tic agents. It can also be seen during a primary
abnormally refluxed in the esophagus (see 7 Chap. 2). infection to herpes in healthy subjects.
Healing of inflammation is seen in 80–90% of cases of Endoscopy may reveal along the esophagus
peptic esophagitis after 4–8 weeks of treatment with pro- vesicular lesions similar to herpes skin lesions, or
ton pump inhibitors (PPIs). small ulcers surrounded by healthy mucosa.
In case of failure of the usual therapy with a PPI Biopsies will reveal typical intranuclear inclu-
administered at least 30 min before breakfast for opti- sions on histological analysis, and culture can
mal bioefficacy, various pharmacological strategies are confirm the diagnosis of the virus (but is rarely
possible: (a) doubling the PPI dose (in a single morning done).
dose or, preferably, in divided doses, 30 min before Esophagitis usually resolves spontaneously in
breakfast and dinner); (b) addition of an H2 blocker 1 to 2 weeks. Acyclovir (400 mg po 5 times/day
(e.g., ranitidine 150–300 mg at bedtime) to optimize or IV 5 mg/kg q 8 h for 7–14 days) will accelerate
nocturnal acid suppression; and (c) addition of proki- resolution of the infection, as well as foscarnet
netics (e.g., domperidone 10–20 mg before meals and at or other antiviral agents.
bedtime) to facilitate gastric emptying and possibly 55 Cytomegalovirus: CMV esophagitis is encoun-
increase the tone of the lower esophageal sphincter can tered mainly in patients immunosuppressed by
sometimes be tried, although evidence for efficacy is lim- HIV. It is often a source of severe esophageal
ited. Medication failure is usually not an indication for pain.
surgery since the results are often disappointing, except Endoscopy may reveal long, penetrating ulcers
in cases where the control of incapacitating regurgita- of esophageal mucosa, and biopsies will show
tion is sought. characteristic intracytoplasmic viral inclusions.
Discontinuation of PPIs results in clinical and/or Treatment requires the use of ganciclovir or
endoscopic recurrence in 2/3 of patients, unless a predis- foscarnet.
posing condition (e.g., obesity, drugs reducing sphincter 55 Human Immunodeficiency Virus: The HIV has
tone) was present and can be corrected. Continuation of been implicated in some cases of viral-looking
PPI therapy appears to be the optimal solution (at the esophagitis in HIV-positive patients when it was
present time); PPIs are considered as safe drugs for not possible to identify CMV or herpes. Tran-
chronic prolonged use (even for years). However, long- sient symptoms of esophagitis may accompany
term disadvantages to chronic PPI therapy (based on the primary HIV infection.
retrospective case-control and cohort studies) are pres- (c) Mycotic esophagitis.
ent, such as an increased risk of enteric infections 55 Candida albicans is responsible for esophagitis in
(Salmonella RR 3, Clostridium difficile RR 2, etc.) or patients with AIDS or immunosuppressed by
pneumonia (RR 4), as well as a possible risk of hip frac- undernutrition, systemic diseases, chemother-
ture; malabsorption of iron, calcium, and vitamin B12; apy, etc., but also in subjects whose immunity is
or interaction with certain drugs including the antiplate- only partially or locally compromised, such as
let agent clopidogrel (interaction on P450 cytochrome) asthmatics using corticosteroids administered by
or drugs requiring gastric acid milieu for optimal bronchial inhalation or people treated with anti-
absorption (e.g., ketoconazole). biotics.
Anti-reflux surgery does not offer medical or eco- The infection is often localized more in the
nomic benefits at the present time (aside for patients proximal esophagus and may include the oral
Dysphagia for solid foods and/or food impaction

are cardinal symptoms of eosinophilic esophagitis.
(c) Diagnosis of eosinophilic esophagitis. Endoscopy
1 may reveal, surprisingly considering the symptoms,
an almost normal mucosa macroscopically (but
microscopically infiltrated by eosinophils) or reveal
suggestive changes such as longitudinal furrows, a
trachea-like appearance with multiple thin rings dis-
tributed along the esophagus, or a diffuse narrowing
of the esophagus. Biopsies are necessary and diag-
nostic.
(d) Treatment of eosinophilic esophagitis. The etio-
pathogenesis of eosinophilic esophagitis is poorly
known, as is its treatment. PPIs appear to help in
40% of cases. Corticosteroid therapy is effective,
preferably by topical application (fluticasone or
.. Fig. 1.9 Candida esophagitis: endoscopic view, white and flaky budesonide) rather than oral in order to minimize
membranes attached to the esophageal mucosa. (Photo by P. Poitras)
steroid side effects. Exclusion diets (wheat, milk,
eggs, peanuts, soy, seafood) have given very encour-
cavity. The diagnosis is suspected at endoscopy aging results (75–95% success in children, but diet
in front of whitish and flaky membranes compa- compliance is difficult), thus supporting an allergic
rable to the thrush of oral candidiasis. Biopsies origin of the problem. Hypoallergenic elemental diet
or cytological analyses reveal the presence of is also an option. Dilatation of stenosis by bougie or
Candida albicans (. Fig. 1.9). endoscopic balloon seems hazardous.
The treatment can be done, in milder cases, with (e) Evolution. The long-term evolution is poorly known;
a topical solution of nystatin (500,000 U qid for some patients, unfortunately, seem to deteriorate,
7–14 days). In severe cases or in HIV patients, flu- while many others seem to have a favorable sponta-
conazole (100–200 mg per os id for 2 weeks) will be neous evolution.
preferable.
55 Others: Histoplasmosis, aspergillosis, cryptococ-
cosis, and blastomycosis can occasionally affect 1.6.4 Caustic Esophagitis
the esophagus.
Ingestion of caustic acid or alkali often results in severe
esophageal damage. It is usually accidental in children
1.6.3 Eosinophilic Esophagitis and linked to suicidal acts in adults. Corrosive house-
hold products, such as ammonia, laundry detergents,
(a) Definition of eosinophilic esophagitis. Eosinophilic pipe cleaners, and pool acids, are frequently involved.
esophagitis refers to an infiltration of the esophagus (a) Symptoms. In the acute initial period, dysphagia,
by eosinophils as detected by microscopic analysis of chest pain, and/or sore mouth are often present.
endoscopic biopsies. It is characterized by massive Esophagitis is often severe and can lead to perfora-
eosinophilic infiltration (>15 eosinophils/high- tion with secondary mediastinitis and its lethal com-
powered field) distributed all along the esophagus. plications if not treated. Perforation can also occur
Eosinophil infiltration can also be found in gastro- in the gastric area or intestine if these organs have
esophageal reflux, but it is usually moderate (less been in contact with the corrosive agent.
than five eosinophils/field) and restricted to the lower Long-term symptoms include parietal healing
esophagus, as well as in eosinophilic gastroenteritis with fibrosis and strictures of the esophageal lumen,
(with or without blood eosinophilia) damaging other which often requires mechanical dilatations, often
digestive organs. repeated, or even surgical replacement of the esoph-
(b) Clinic. Eosinophilic esophagitis was first described agus. In the very long term, there is an increased risk
in the 1970s, but its incidence has been rising steadily developing squamous cell cancer.
since then. Well known in pediatrics where it affects (b) Investigation. Alkaline or acidic agents are equally
often atopic or allergic children, it is encountered toxic (even if their mechanisms of toxicity are differ-
now more and more frequently in the adult (often ent). Domestic bleach, fortunately, rarely leads to
young men). severe complications.
The Esophagus
15 1
Endoscopy may be used to confirm the extent Lady”: 15–30 mL of antacid and 15–30 mL of vis-
and severity of the caustic burns in order to assist in cous Xylocaine), can help relieve pain.
(b) Bisphosphonates. Frequently used bisphosphonates
prognosis and care planning. Endoscopy (if one
decides to do it) should be performed with great del- for the treatment of osteoporosis are associated with
1
icacy in order to avoid perforating necrotic and frag- chemical esophagitis often more diffuse than those
ile organs. described above. The esophagitis mechanism remains
(c) Treatment of caustic esophagitis. Careful monitor- unclear and implies, among other things, the reflux
ing of the patient is recommended so that early in the esophagus of the drug once dissolved in the
intervention can be initiated if complications ensue. stomach. To counteract this complication occurring
Preventive maneuvers seem to be ineffective: forcing mainly with alendronate, it is suggested to take the
vomiting may make worse contact of the toxic agent drug in a standing position (and stay in this position
with the esophagus; diluting or neutralizing solu- for at least 1 hr) and to ingest a large quantity of
tions seem to be ineffective and may also promote fluids to promote passage of the drug through the
harmful vomiting. Reducing the inflammatory reac- intestine and avoid its reflux in the esophagus or its
tion with systemic steroids (e.g., methylprednisolone stagnation in the stomach.
20–40 mg q 6 h IV) remains a debated therapeutic
issue.
Esophageal and/or gastrointestinal perforations 1.6.6 Radiation Esophagitis
will require emergency, and often morbid, surgery.
Depending on the condition of the tissue, drainage Radiotherapy for the treatment of thoracic neoplasia
with suture of the perforation or more or less (lymphoma, cancer of the lung/esophagus, etc.) can
extensive removal of the affected organs will be affect the esophagus. In the acute phase, during the
required. treatment period, mucositis causing pain, odynopha-
gia, and dysphagia can occur. Treatment with local
analgesics and antacids helps relieve these symptoms.
1.6.5 Drug-Induced Esophagitis In some cases, dysphagia can be severe enough to
compromise food ingestion, and temporary artificial
(a) Pill esophagitis. This is due to a medication pill tube feeding may be required. Delayed complications
“trapped” or stagnating in an esophageal segment such as stenosis may require mechanical dilatations.
that induces a local corrosive damage. It occurs
most often in the upper esophagus, and it is charac-
terized by localized chest pain, often with odyno- 1.7 Tumor Disorders
phagia and dysphagia, starting few hours after
ingestion of the drug. 1.7.1 Types of Esophageal Neoplasia
Endoscopy usually shows a well-circumscribed
ulcer (or two “kissing” ulcers) surrounded by healthy Squamous cell (epidermoid) carcinoma and adenocarci-
mucosa, reflecting the “burn” by the stagnant pill. noma are the two main malignant neoplasms that affect
Aggravating factors are as follows: the esophagus (. Fig. 1.10).
55 Some medications seem more irritating or cor- (a) Squamous cell neoplasia develops from the esopha-
rosive; this includes potassium supplements, tet- geal squamous epithelium. It is most commonly
racycline and its derivatives, aspirin, and located to the middle and upper thirds of the organ.
NSAIDs. It preferentially affects males over 50. Its prevalence
55 Certain conditions are known to favor poor is high in some parts of the world including China,
transport of the pill down the esophagus and the northeast of France, or in the black population
“stagnation of the pill” with secondary corrosive of North America. Predisposing factors involving
damage. Any condition associated with abnormal chronic mucosal damage are well recognized: heavy
esophageal transit is a risk factor. alcohol ingestion, smoking, ingestion of hot tea,
55 Most of the time, taking the medication in a lying caustic esophagitis, etc. Previously established as
down position, and with insufficient fluid bolus the most important type of esophageal cancers, the
to promote trans-esophageal passage, is involved frequency of the epidermoid carcinoma seems to
in pill-induced ulceration. have regressed in the recent decades (perhaps in
The ulcer usually heals spontaneously in a few days. response to a decreased exposition to predisposing
Antacids, possibly with local anesthetics (“Pink factors).
.. Fig. 1.10 Histology and characteristics of esophageal neoplasms: (1) The picture on the left shows a well-differentiated squamous cell
carcinoma {(a); compared with the normal squamous cells (present on d)} with formation of keratin pearls (b); squamous cell cancer is most
often located in the upper or middle esophagus. (2) the right picture shows adenocarcinoma cells (c) infiltrating the mucosa under a normal
squamous epithelium (d). (Photos by G.Soucy)
(b) Adenocarcinoma was classically considered as a rare 1.7.3 Diagnosis of Esophageal Cancer
esophageal tumor, but it is now the most common
esophageal cancer in the Western world. X-rays of the esophagus (. Fig. 1.11) can reveal the
Adenocarcinoma develops from glandular tissue; it luminal obstruction by the tumor (although not as sen-
is therefore more readily seen during the re- sitive as endoscopy), but will not be able to differentiate
epithelialization of the normal squamous esopha- the nature of the cancer.
geal epithelium by the glandular lining seen in Endoscopy is the best test to diagnose esophageal
Barrett’s esophagitis. This type of cancer mainly cancer; biopsies and/or cytology are required to confirm
affects the distal esophagus. It develops more read- the diagnosis.
ily in male subjects, of Caucasian origin, aged over The progression of the disease is usually toward the
50 years and suffering from chronic gastroesopha- adjacent lymph nodes and thus to the cervical, thoracic,
geal reflux. or abdominal regions depending on the location of the
primary tumor. Extent of the disease will be evaluated
by axial tomography (CT scan), positron emission
1.7.2 Clinical tomography (PET), or echo-endoscopy.
Esophageal neoplasia grows intra-luminally to obstruct

the esophageal channel, thus causing progressive dys- 1.7.4 Treatment of Esophageal Cancer
phagia, initially presenting with solid food and later on
affecting also liquids. Weight loss, due to a deficient Unfortunately, no curative treatment can be offered for
caloric intake, is common. Anemia caused by chronic esophageal cancer in a large proportion of patients.
bleeding from the ulcerated tumor may occur. Survival after treatment is 30 to 40% at 5 years.
The Esophagus
17 1
a b c d
.. Fig. 1.11 a Radiography of a normal esophageal appearing as a cylinder about 25 cm long and 2.5 cm wide. b Peptic stricture is seen here
in the distal esophagus with a typical smooth and symmetrical narrowing of the lumen. c Achalasia (1) the lumen of the esophagus is dis-
tended; (2) the cardia is slim and slender, appearing as a bird’s beak. d Neoplasia (epidermoid here): the esophagus is narrowed by a prolif-
erative mass protruding into the lumen of the organ and mimicking an “apple core.” (Photos by R. Déry)
The overall therapeutic strategy is comparable for 1.8 Function Disorders

the epidermoid carcinoma or adenocarcinoma.
Faced with a disease that is believed to be limited and 1.8.1 astroesophageal Reflux Disease
G
curable, the therapeutic procedures include radiation
therapy, usually combined with chemotherapy (with cis-
(GERD)
platin) frequently followed by excision surgery.
(a) Definition. GERD is defined as the reflux of gastric
Esophagectomy, with different reconstruction tech-
niques (esophagogastric anastomosis with a pull-up of material into the esophagus, resulting in troublesome
the stomach, interposition of a colonic or jejunal seg- symptoms.
ment, etc.), is a complex and unfortunately often morbid
procedure to be carried out in expert centers. (b) Symptoms of GERD. Regurgitation of food with a feel-
In the case of an advanced, unresectable disease, the ing of retrosternal discomfort or with bitter taste in the
strategies of palliation include chemotherapy ± radio- mouth, heartburn (retrosternal burning sensation due to
therapy to decrease the volume of the obstructive mass the acidic pH of the refluxed material), and pyrosis (heart-
and secondary dysphagia, or stent placement, using burn radiating upward, progressing from the bottom to
endoscopic or radiological guidance, that re-establishes the top of the esophagus) are indicative of GERD (with
the esophageal lumen to allow an oral feeding. or without esophagitis). Odynophagia (retrosternal pain
at the passage of food) or dysphagia (blockage sensation
at the passage of food) is suggestive of esophagitis (a com-

plication of GERD).
1 GERD symptoms are common, being reported in 30
to 50% of the population, and their frequency appears
to be increasing with age. GERD is considered as an ill-
ness when symptoms occur at least weekly and have an
impact on the quality of life.
(c) Pathophysiology of GERD. Gastric content, made of

ingested food and secretions produced by the stomach
(HCl, pepsin) or refluxed from the intestine (e.g., bile),
will be, under normal conditions, pushed to the duode-
num by propulsive contractions of the stomach. The
lower esophageal sphincter (LES) works as a unidirec-
tional valve that relaxes to allow the swallowed food to .. Fig. 1.12 Pathophysiology of gastroesophageal reflux disease
(right of the picture in red characters) and of its most frequent com-
enter the stomach cavity and then contracts back to its
plication, esophagitis (left of picture in blue)
basal state in order to close the upper end of the stom-
ach and thereby prevent reflux of gastric contents back
up into the esophagus. The reflux from the stomach into 55 Decreased barrier pressure. The LES normally has a
the esophagus thus occurs when the gate capacity of the basal tone of 20–25 mmHg to impede reflux of gas-
valve is insufficient to impede the passage of gastric tric contents into the esophagus. Sphincter hypoto-
material. nia (pressure below 10 mmHg) is a logical and
The LES measures 2 cm in length and is located at obvious cause for reflux; it is found, however, in only
the diaphragm, mainly on the abdominal side of the a small percentage of cases. Smooth muscle esopha-
thoracoabdominal junction. The sphincter can be seen geal diseases, such as scleroderma, can reduce the
as a two-component structure. The “internal” sphincter pressure of the lower esophageal sphincter (even to 0
corresponds to an area made of specialized smooth mmHg) and result in marked gastroesophageal
muscles of the lower esophagus, which, although not reflux. Some drugs (e.g., theophylline, calcium chan-
identified histologically, generate a short high-pressure nel blockers, nicotine) as well as certain foods (e.g.,
zone between the positive intra-abdominal and the neg- chocolate, mint) can lower the pressure of the sphinc-
ative intrathoracic pressures. The “external” sphincter is ter and may promote reflux.
made of various anatomical factors of the lower esoph- Hiatal hernia (intrathoracic displacement of the
agus that bolster this physiological high-pressure zone: esophageal-gastric junction) seems to be a condition
the diaphragm (making a constrictive ring around the that alters the tension resistance of the LES, proba-
esophagus), the right crus of the diaphragm as well as bly by compromising the anatomic factors that pro-
the phreno-esophageal membrane (surrounding and fix- duce the “external sphincter.”
ing the lower esophagus to the thoracoabdominal junc- 55 Normotensive but incompetent barrier. The lower
tion), the size of the angle of His (allowing compression esophageal sphincter normally relaxes during swal-
of the distal esophagus by the gastric fundus), and the lowing to let the food bolus migrate from the esopha-
intra-abdominal localization of the sphincter. gus to the stomach. Transient and inappropriate
Circumstances favoring reflux are shown in . Fig. relaxation, i.e., without being induced by swallow-
1.12 and discussed here: ing, may occur. This phenomenon usually occurs in
55 Increased intragastric pressure exceeding the lower response to fundic distension, via a vagal reflex
esophageal sphincter retention capacity. The pres- involving VIP and the GABA (gamma-aminobutyric
sure is naturally positive in the abdomen and nega- acid). Studies have confirmed that the gastric content
tive in the thorax. Pregnancy, abdominal obesity, could use these transient and inappropriate relax-
and tight waist clothing are factors that increase ations to reflux into the esophagus. TILSR (transient
intra-abdominal and, consequently, intragastric inappropriate lower sphincter relaxation) which
pressures. Gastric emptying failure by either distal occurs 2–3 times/hr in normal subjects are more fre-
obstruction or gastroparesis will result in stagnation quent in GERD (8–12/hr); increased number of
of gastric contents and promote reflux into the TILSRs is now considered the main pathophysiolog-
esophagus. The recumbent position will shift the gas- ical mechanism for GERD.
tric content into the upper stomach, facilitating its 55 The acid pocket is a concept born in 2001. It results
reflux upward. from the simple observation that acid reflux occurs
often after the meal, a paradoxical situation since the
The Esophagus
19 1
gastric pH is then high due to the food present in the a reflux is suspected, a therapeutic test (using a twice
stomach. Studies have shown that acid secretions daily PPI regimen for 4–8 weeks) could be useful in
accumulate on top of food to form an acidic pocket
in the upper part of the stomach. If the acid pouch is
establishing the contribution of gastroesophageal reflux
in the genesis of these extra-esophageal symptoms. The
1
located in a hiatus hernia, chances for gastroesopha- very limited effectiveness of PPIs (success of less than
geal reflux are clearly increased. PPIs raise the pH of 40% and comparable to placebo in several studies) to
the pocket secretions (from pH 1 to pH 4). Alginate relieve coughs, hoarse voice, or asthma raises doubts
foam (Gaviscon®, discussed below) works by form- about the importance of GERD in these symptoms in a
ing a raft on this pocket (rather than mixing with the majority of patients.
food chyme as other antacids) to “locally” neutralize
the acid in the pocket. (e) Investigation of GERD. Gastroesophageal reflux dis-
ease is a very common condition, but fortunately in
(d) Complications of GERD. Esophageal as well as extra- most patients the diagnosis can be made based on clini-
esophageal complications are seen: cal presentation, and further investigations are not
Esophageal complications: required. Investigations need to be pursued in patients
55 Peptic esophagitis is the main complication of gas- who do not respond appropriately to treatment, or in
troesophageal reflux, as previously discussed in the those with features suggesting complications (e.g., dys-
section of inflammatory diseases (7 Sect. 1.6.1); ste- phagia, odynophagia, weight loss, anemia). Although of
nosis or neoplasia is then possible. unproven value, many experts suggest screening endos-
55 Nonerosive reflux disease (NERD) refers to GERD copy to rule out Barrett’s esophagus be performed in
without esophagitis as established at endoscopy certain higher risk patients (e.g., male Caucasians older
(endoscopy is positive in only 30% of patients sus- than 50 years of age with chronic reflux symptoms for
pected of GERD; among the patients with negative more than 5 years).
endoscopy, 50% have reflux documented on pH stud- Modes of Investigation:
ies and are therefore identified as NERD). Since 55 Endoscopy is the most useful examination to confirm
these patients seldom develop peptic complications the diagnosis of GERD (if esophagitis is present in
(including esophagitis), even in the long run, NERD the esophagus), to guide management of esophagitis
requires only a symptomatic treatment. (in order to avoid long-term complications), to iden-
tify subjects at risk for adenocarcinoma (Barrett’s
Extra-esophageal complications: esophagus), and to reassure the reflux patient with-
55 ENT: Hoarse voice, pharyngeal pain, and cough out esophagitis (since these individuals usually con-
may be symptoms of posterior laryngitis believed to tinue to live without ever developing inflammation
be due to a reflux of irritating gastric material in and its complications). In patients with heartburns,
some cases. endoscopy reveals esophagitis in 30% of cases; oth-
55 Lungs: Asthma may possibly be exacerbated by gas- ers suffer from either NERD (nonerosive reflux dis-
troesophageal reflux. The mechanisms proposed are ease) or esophageal hypersensitivity or functional
either intrabronchial aspiration of material refluxed heartburn.
into the hypopharynx or bronchiolar spasms trig- 55 Recording of esophageal reflux can be done when the
gered by a vagal reflex possibly induced by distension diagnosis is still unclear following endoscopy (e.g.,
or irritation of the esophagus secondary to reflux. In normal endoscopy) or when other conditions justify
rare cases, aspiration of the refluxed material may to confirm the diagnosis (e.g., poor response to anti-
cause aspiration pneumonia. reflux treatment). GERD can be confirmed by vari-
55 Chest pain: Retrosternal pain, sometimes even ous methods that measure reflux of gastric material
mimicking that of angina pectoris (including irra- into the esophagus. Esophageal pHmetry, the most
diation to the left arm or jaw), may be due to commonly used of these methods, continuously
reflux. It is assumed that the pain is due to an measures the esophageal pH using an electrode
esophageal spasm triggered by reflux. The possi- either installed on a catheter that is passed transna-
bility of coronary spasms in response to a vagal sally into the lower esophagus and connected to a
reflex triggered by GERD has also been proposed device worn on a belt or shoulder strap, or clipped to
in some patients. the distal esophageal mucosa endoscopically. Esoph-
ageal pH is then monitored over a period of usually
In presence of a clearcut gastroesophageal reflux, a 24 hours or more. Detecting episodes of esophageal
good response of these extra-esophageal symptoms to pH < 4 indicates reflux of gastric acid into the
treatment with acid suppression can be expected. When esophagus.
Other methods, such as using the concentration downregulation of histamine receptors after a
of bile in the esophagus or esophageal impedance, few days of pharmacological treatment. H2
1 can also be used in select cases, particularly if non-
acidic reflux is suspected.
blockers may be useful to control mild to moder-
ate reflux symptoms (ranitidine 150–300 mg bid
55 Radiography of the esophagus (or barium meal) can or famotidine 20–40 mg bid). They can also be
demonstrate reflux of the barium substance from the used “on demand” for the relief of occasional
stomach into the esophagus. It can occur spontane- reflux or peptic symptoms (in many countries,
ously (mainly in the recumbent position) or can be H2RA can be conveniently purchased over the
induced by different maneuvers increasing abdomi- counter without a prescription). Occasional use
nal pressure (raising legs, etc.). However, the barium of these drugs will prevent tachyphylaxis, but
meal is neither specific nor sensitive for the diagnosis because they require gut absorption and sys-
of GERD or esophagitis, and it rarely helps in the temic circulation, it takes 30 to 60 minutes before
management of these diseases. It can be of some they begin to inhibit acid production. Accord-
interest, however, in the study of dysphagia, as dis- ingly, they are not well suited for the prompt
cussed subsequently. relief of symptoms when taken on a prn basis. In
case of nocturnal symptoms uncontrolled by
(f) Treatment of GERD. PPI, an H2RA taken at bedtime can help in
(a) Correction of risk factors and life style habits that some people.
promote GERD is important. Correcting an exces- 55 Proton pump inhibitors (PPIs): These are potent
sive intra-abdominal pressure (losing weight if inhibitors of gastric acid secretion (see 7 Chap.
obese, abandoning tight clothing, etc.), avoiding 2). Since their introduction in the 1980s, they
reclining positions favoring reflux (no lying down have revolutionized the treatment of GERD and
after meals, elevating the head of the bed, etc.), and currently constitute the most effective treatment
minimizing LES hypotension (avoiding fatty foods, for reflux esophagitis. The usual doses of dexlan-
chocolate, peppermint, alcohol, tobacco, or drugs soprazole (30 mg die), esomeprazole (20 mg), lan-
such as calcium channel blockers, nitrates, theophyl- soprazole (30 mg), omeprazole (20 mg),
line) can provide significant improvement in certain pantoprazole (30 mg), and rabeprazole (20 mg),
cases. Weight gain is often the trigger for GERD, taken in the morning at least 30 minutes before
and weight loss, although often difficult to achieve, breakfast, will control the symptoms of reflux
is likely the most useful “lifestyle” intervention. and heal reflux esophagitis in 80–90% of patients.
(b) Suppression of refluxed acid is currently the most Some individuals will benefit from a double dose
effective pharmacological method to stop symp- (administered once in the morning or preferably
toms of reflux (and secondary esophagitis). Differ- in divided doses 30 minutes before breakfast and
ent approaches are used. dinner). Recurrence of symptoms (or of esopha-
55 Antacids: These drugs typically contain buffer- gitis) when treatment is discontinued occurs in
ing agents such as bicarbonate, magnesium, and 2/3 of patients, and often a continuous therapy
aluminum, to neutralize gastric HCl. They are may be required. Maintenance therapy using PPI
available in liquid form (Maalox, Riopan, has been used for 20 years without significant side
Amphogel, Gaviscon, 15–30 ml q 1–2 h prn) or effects. It currently appears as the treatment of
tablets (Tums, Rolaids, etc.). Symptom relief is choice for most patients.
usually obtained rapidly within a few minutes,
but it is short-lived. Available over the counter in Reflux without esophagitis (NERD), given the absence
pharmacies, these agents are useful for self-treat- of complications, can be treated symptomatically and
ment of mild or occasional symptoms. High on demand. On the other hand, reflux esophagitis
doses of antacids may cause side effects (espe- should, even in the absence of symptoms, be managed,
cially diarrhea due to magnesium). most of the time, by a continuous maintenance treat-
55 H2 blockers: These (also called H2 receptor ment to minimize the chance of peptic or neoplastic
antagonists or H2RA)) suppress gastric H+ complications.
secretion by the parietal cells by blocking the his- (c) Reducing reflux material appears as a logical thera-
tamine stimulation. More powerful than antac- peutic strategy. It could, in theory, be obtained by
ids, they revolutionized the treatment of increasing the tone of the LES, by decreasing the
acid-related diseases when introduced in 1977. numbers of TILSR (transient inappropriate lower
Their ability to suppress acid is however limited sphincter relaxation), or by promoting gastric emp-
by, among other things, tachyphylaxis due to tying of gastric contents to the intestine in order to
The Esophagus
21 1
decrease the amount of material likely to backflow long term, to provide results superior to those obtained
into the esophagus. by chronic PPI treatment. In fact, 5–10 years after fun-
55 However, few drugs are available that decrease
the GE reflux. Domperidone (10 mg before
doplication was performed to avoid the need of chronic
PPI therapy, many patients will still require anti-reflux
1
meals and at bedtime), a gastrokinetic agent that pharmacotherapy. In the setting of “medical resistance”
increases gastric emptying and LES tone by act- (i.e., patients with persistent symptoms despite optimal
ing as an antidopaminergic, may be useful in a twice daily PPI therapy), fundoplication often leads to
small subset of patients, especially to decrease disappointing results. Its place in GERD therapy today
regurgitations poorly controlled by acid reduc- seems limited to patients where troublesome regurgita-
tion agents. tions resistant to medical treatment is the major issue, or
55 Reducing TILSRs appears as a logical for GERD patients who, for various reasons, prefer this
pharmacological target, given their important
intervention over chromic PPI therapy.
role in the pathophysiology of GERD. Agonists New techniques (e.g., magnetic sphincter augmenta-
of GABA (gamma-aminobutyric acid) are con- tion device implanted at the cardia) could offer in a near
sidered as therapeutic candidates; baclofen is future valid alternatives for GERD patients who desire
sometimes used. to discontinue medical therapy, or are not compliant or
55 Surgery can be used to decrease reflux (see are resistant to medical therapy.
below). (e) Endoscopic therapy: A variety of endoscopic tech-
(d) Anti-reflux surgery was, before the demonstrated niques aimed at correcting the sphincter barrier
efficacy of PPIs, the only valid treatment for GERD. defect have been developed. These include intragas-
The Nissen fundoplication not only corrects the hia- tric plication of the fundus, longitudinal plication
tal hernia but also wraps around the cardia a por- of the cardia, infiltration in the cardia with synthetic
tion of the gastric fundus to restore the “external” material(s), electro-fulguration of lower esophagus
sphincter (discussed in the anatomy 7 Sect. 1.1.1 of by radiofrequency (Stretta procedure), etc. The ben-
this chapter). Fundoplication is usually performed efit of these endoscopic maneuvers over the current
laparoscopically; it may involve different technical pharmacological or surgical treatments remains to
variations such as the classical Nissen procedure or be demonstrated.
the partial Toupet fundoplication. Fundoplication
decreases reflux by raising the basal tension of the (g) In Pediatrics:
LES while reducing TILSRs by incompletely under- 55 Gastroesophageal reflux disease (postprandial non-
stood mechanisms. Aside from the usual morbidity bilious food regurgitation) is physiological in infants
related to abdominal surgery, fundoplication can up to 18 months of age.
cause side effects in about 10% of subjects operated, 55 Only the occurrence of complications (peptic esoph-
including the following: agitis, growth retardation, or respiratory problems
55 Dysphagia: This may require dilatations to secondary to the reflux) should trigger additional
loosen up a too tight fundoplication. investigations and drug treatment.
55 Gasbloat: in the majority of the subjects oper- 55 GE reflux is not the cause of the unexplained crying
ated on, the new fundic valve will create a diffi- (“colic”) in infants.
culty with vomiting or belching. In some patients, 55 Peptic esophagitis is rare in children.
the inability to belch will cause abdominal dis- 55 Children at risks for peptic esophagitis include those
comfort by accumulation of gastric air. with chronic respiratory pathology (like cystic fibro-
55 Dyspepsia: Functional dyspepsia is often due to sis), previous surgery for esophageal atresia, or neu-
a poor accommodation of the gastric fundus rological disability (encephalopathy of neonatal
(see 7 Chap. 2). This motor dysfunction can ischemic origin, of metabolic or genetic origin).
obviously be enhanced by a fundoplication pro- 55 There is no correlation between symptoms and the
cedure compromising fundic anatomy and func- endoscopic aspect of the esophagus.
tion. The indication for fundoplication must 55 Barium meal is not indicated to establish the diagno-
therefore be considered very carefully in a patient sis of GERD in children.
with GERD and coexisting symptoms of func- 55 The barium meal can document anatomical abnor-
tional dyspepsia. malities that could generate regurgitations/vomiting
in infants such as an intestinal malrotation, an
In the case of “medical dependence” (i.e., patients who obstacle to gastric evacuation (pyloric stenosis also
cannot stop their PPIs without a relapse of symptoms), seen in ultrasound), and a congenital stenosis of the
surgical fundoplication does not seem, in the medium or esophagus.
1.8.2 Oropharyngeal (Transfer) Dysmotility toxin) of the UES can be done in some very
selected cases to reduce sphincter resistance and
1 (a) Symptoms. Proximal dysphagia perceived in the oro- then facilitate the passage of the bolus from the
oropharynx toward the esophageal lumen.
pharyngeal or cervical region is the predominant
symptom. It may be associated with symptoms of
nasal regurgitation, coughing, choking, and aspira-
tion pneumonia, related to misdirection of the swal- 1.8.3 Esophageal (Transport) Dysmotility
lowed food or fluid into the nasopharynx, larynx, or
trachea. Transport dysmotility along the esophagus, which usu-
(b) Pathophysiology. ally produces dysphagia or thoracic pain, can be due to
Damage to nerves (cranial nerves IX, X, and espe- hypo- or hypercontractility disorders of the smooth
cially XII) controlling the transfer motor function: muscles of the esophagus or of the lower esophageal
55 Brain stem nuclei damage by cerebral vascular sphincter (LES). These disorders are recognized mainly
stoke, tumors, Parkinson’s, etc. by measuring contractile pressure waves of the esopha-
55 Peripheral nerve damage by demyelinating dis- gus via intraluminal manometry (see . Fig. 1.13).
ease (multiple sclerosis) or others (sclerosis, amy- A. Hypomotility disorders. Absent contractility
otrophic lateral sclerosis, etc.). (as referred to in Chicago Classification) is most often
Damage to the striated muscles involved in transfer- due to scleroderma, a disease characterized by a collage-
ring the food bolus from the oropharynx to the esoph- nous fibrosing infiltration of skin tissues; it can also
agus by diseases such as myasthenia gravis (dysphagia affect the digestive tract, with the esophagus being the
often worsening with fatigue), oculopharyngeal dys- most common region affected. It is characterized mano-
trophy (hereditary dystrophy common in Quebec and metrically by esophageal contractile waves markedly
affecting pharyngeal and palpebral muscles), etc. decreased in amplitude (even not existing) and a lower
(c) Investigation. Radiology and endoscopy are both esophageal sphincter with a very weak tone (even absent).
useful to evaluate oropharyngeal dysmotility. Esophageal hypomotility can also be seen with neu-
Radiological assessment of the swallowing process, romuscular disorders affecting the GI tract (rare condi-
using fluoroscopy during barium ingestion, will be cru- tions often leading to pseudo-obstruction syndrome; see
cial to identify and characterize the motor disorder. Its 7 Chap. 3) or, sometimes, be due to an inflammatory
diagnostic yield, however, is dependent upon the exper- response to esophagitis (peptic, caustic, etc.).
tise of the examiner.
The radiological assessment will also be used to iden- Symptoms Patients with scleroderma typically develop
tify Zenker’s diverticulum or an obstructive lesion of the severe GERD symptoms (heartburn, regurgitation)
hypopharynx or proximal esophagus that could give because of their defective LES pressure barrier and poor
clinical symptoms of high dysphagia. esophageal clearance secondary to weak or absent peri-
Endoscopy may be required to rule out a luminal stalsis. Dysphagia is also common, and, although partly
obstructing lesion. related to the absence of propulsive waves, is usually due
to the development of reflux esophagitis, often compli-
However, it must be remembered that the upper cated by peptic stricture formation. Overt or occult bleed-
localization of dysphagia reported by the patient can be ing from esophageal ulceration may also occur.
misleading since a middle or distal lesion may cause a
sensation of upper dysphagia (on the other hand, the Investigation Manometry of the esophagus is the deter-
lower localization of dysphagia is more reliable to iden- minant examination to identify the diagnosis.
tify the obstructing site since a sensation of a blockade Hypomotility profile is mostly due to scleroderma, but it
in the lower esophagus is never due to a proximal can be seen in rare infiltrative disorders such as amyloido-
lesion). sis or in chronic reflux esophagitis.
(d) Treatment of oropharyngeal dysmotility. Various Endoscopy is essential to assess the severity of esoph-
options are available: agitis.
55 Treatment of the causal pathology if possible
(e.g., myasthenia gravis). Treatment GERD can have severe consequences in
55 Diet adjustment and safe swallowing education patients with scleroderma esophagus (due to the absence
by specialists (occupational therapist, dieticians, of LES to block reflux and of esophageal contractions for
speech language pathologists, etc.). clearance of refluxed acid) and requires an aggressive
55 Surgical (or endoscopic) myotomy (or pharmaco- treatment. Suppression of acid reflux is essential. PPIs
logical relaxation by infiltration of botulinum can be given at high doses for optimal acid suppression.
The Esophagus
23 1
Swallow
Swallow Peristaltic
pressure Swallow Swallow Simultaneous 1
mmHg Simultaneous
Peristaltic
75 Peristaltic
0
75
Esophagus
0
75
LES 25
0
0 10 0 10 0 10 20 0 10 seconds
Normal Achalasia Diffuse spasm Nutcracker
.. Fig. 1.13 Esophageal manometry contractions recorded in various conditions of hypermotility. (Modified from Smout 1992)
They can be coupled with prokinetics to promote gastric Causes of achalasia Idiopathic primary achalasia is the
emptying (potentially affected by gastric hypomotility most common.
secondary to scleroderma infiltration of gastric smooth Achalasia can also be secondary to the following:
muscles). 55 Chagas disease due to the Trypanosoma cruzi para-
B. Hypermotility disorders. Hypermotility of the site, present mainly in South and Central America
esophagus is described under the following categories: and capable of attacking esophageal innervation.
1. Achalasia of the esophagus is a disease of the intrin- This parasite also frequently affects the innervation
sic innervation of the esophagus (infiltration of lym- of the heart resulting in fatal heart failure.
phocytes into the myenteric plexus leading to 55 A tumor of the gastric cardia infiltrating the enteric
destruction of neurons controlling LES relaxation nervous system in the region of the LES.
and esophageal peristalsis) and is classically charac- 55 A paraneoplastic manifestation (most often from
terized by the following contractile anomalies: lung cancer) affecting the motor function of the
55 Inadequate relaxation of the LES at the passage esophagus as well as the stomach (probably by anti-
of the food bolus. bodies against the enteric nervous system).
55 Increased basal tone of the LES.
55 Absence of peristaltic waves within the esopha-
geal body. Investigation of achalasia A barium swallow (see
55 Possibility of tertiary spastic waves of the esoph- . Fig. 1.11) can reveal a characteristic image of (1)
ageal body. esophageal dilation (mega esophagus), with possibly a
fluid level and food retention, and (2) narrowing of the
Symptoms Lower (transport) dysphagia, often for both esophagogastric junction mimicking the beak of a
liquid and solid foods, and regurgitations of undigested bird. Plain films of the lungs and abdomen may sug-
stagnant food from the esophagus are cardinal symptoms gest the diagnosis of achalasia by showing an enlarge-
of achalasia; chest pain is also reported by some patients. ment of the mediastinum due to the esophagus filled
Complications such as weight loss and aspiration pneu- with fluid, as well as an absence of the gastric air
monia (if nocturnal regurgitation is present) can occur. bubble.
During endoscopy, the LES is usually closed, and or DIC (distal integrated contraction of the peristaltic
some difficulty or resistance can be felt in passing the distal wave). Observations and concepts obtained by
1 endoscope through the cardia. Endoscopy is essential to
eliminate a tumoral infiltration of the cardia.
HRM are grouped together in the “Chicago
Classification,” a tool in perpetual development (a bit
Manometry is the definitive test to diagnose achala- like the DSM in psychiatry). Achalasia is now divided
sia of the esophagus. into three manometric types (I, II, III; . Fig. 1.15),
An example of conventional (or traditional) manom- suggesting the presence of differing pathophysiology
etry is presented in . Fig. 1.13 (characteristic motor (and/or stage) of disease and, possibly, the need for tar-
abnormalities were described above). Since the year geted adapted therapies.
2000, high-resolution manometry (HRM) has been used
to more precisely study the motor activity of the esopha- Treatment of achalasia. In order to alleviate dysphagia,
gus. Done with a nasogastric manometry catheter carry- the treatment aims to reduce the obstacle created by the
ing several electronic pressure sensors distributed every nonrelaxing sphincter. The therapeutic possibilities are as
centimeter (at least) along the esophagus and combined follows:
with sophisticated computer analysis of the obtained 55 Surgical myotomy of the LES, usually done laparo-
data, HRM allows a graphic representation of the scopically, and often with reconstruction by fundo-
esophageal transit and pressures (. Fig. 1.14), as well plication to avoid GE reflux secondary to the
as an objective quantitative analysis of the motor func- sphincter weakness induced by myotomy.
tion (with newly identified computerized parameters 55 Myotomy can also be performed endoscopically
such as IRP (integrated relaxation pressure of the LES) (POEM: per oral endoscopic myotomy).
.. Fig. 1.14 High-resolution esophageal manometry: examples of tracings with colors that identify a pressure gradient (green < yellow <
red). Left tracing: normal. (1) During swallowing, the upper esophageal sphincter (UES) relaxes; (2) a peristaltic contraction develops in the
esophageal body (3) the lower esophageal sphincter (LES) relaxes allowing the bolus to pass into the stomach. - Central tracing: achalasia
(type II). (1) After the relaxation of the UES, (2) no propulsive wave (here we have a diffuse luminal pressurization) occurs in the esophagus;
(3) the LES does not relax. - Right tracing: jackhammer esophagus. (1) normal relaxation of the UES; (2) a propulsive esophageal wave is
present, but it is of very large amplitude and prolonged duration in the distal region; (3) the LES relaxes normally. (Tracings from M. Bouin)
The Esophagus
25 1
.. Fig. 1.15 Achalasia of the esophagus according to MOHR (Chicago Classification 3.0, 2015). -Type I: absence of measurable contractions-
pressures in the esophageal lumen. -Type II (most common): no migratory contractions, but diffuse increase ( pressurization) of intra-esoph-
ageal pressure. -Type III (most difficult to treat): achalasia with spasmodic contractions of the esophageal muscle. The lower esophageal
sphincter (LES) is incapable of relaxation in all three types. (Tracings from M. Bouin)
55 Pneumatic dilatation of the LES by per oral dilata- tiary waves), often of excessive amplitude (. Fig.
tion balloons. It is a simple technique, performed 1.13).
under endoscopic and/or fluoroscopic visualization,
but having a significant risk of perforation (5–10% (a) Symptoms of DES. The primary symptoms are dys-
of procedures). phagia and chest pain. The latter occurs sporadically, is
55 Botulinum toxin endoscopic infiltration of the LES usually of short duration (seconds to minutes), and can be
is a simple technique, however, with short-lasting qualitatively similar to the pain of cardiac ischemia.
results (3–12 months, and can be repeated). It can be (b) Causes of DES. Diffuse spasm is rarely seen during
very helpful for nonsurgical candidates. manometry tests (mainly due to its intermittent schedule).
55 Pharmacological reduction of sphincter tone with It may be idiopathic or more often associated with achala-
calcium channel blocker drugs (nifedipine, etc.) or sia of the esophagus (and responsible for chest pains that
nitric derivatives (isosorbide, etc.) may help some may be experienced by patients suffering of achalasia).
patients. The term “esophageal spasm” is frequently used in
These treatments, by alleviating the sphincter obstacle, clinic to refer to constrictive chest pain of noncardiac
usually allow an adequate caloric feeding, but the swal- origin and that is attributed to presumed esophageal
lowing function may remain suboptimal due to the spasm. These spastic phenomena can be caused by the
absence of esophageal contractions for propulsion of ingestion of very cold or very hot food or occur during
the food down within the esophagus (many patients episodes of GE reflux. The manometric (or other) docu-
need to eat in upright position relying upon gravity for mentation of these episodes is difficult precisely because
food transit to the stomach). of their brief and intermittent nature.
2. Diffuse esophageal spasm (distal esophageal spasm, 3. Jackhammer esophagus is detected by HRM: LES
DES) is an abnormality characterized by nonperi- relaxation is normal, but the esophageal waves are
staltic, multiphasic, prolonged contractile waves (ter- markedly hypercontractile (DIC > 8000 mmHg) and
Another random document with
no related content on Scribd:
Dans ce pays de la passion, toute passion porte son excuse avec
elle, et il existe une adorable indulgence pour tous les écarts. La
duchesse soupira profondément et laissa paraître sur son visage
une expression de douleur contrainte.
—Dans notre pays, il se voit d’étranges choses, monsieur!
Vendramin vit d’opium, celui-ci vit d’amour, celui-là s’enfonce dans la
science, la plupart des jeunes gens riches s’amourachent d’une
danseuse, les gens sages thésaurisent; nous nous faisons tous un
bonheur ou une ivresse.
—Parce que vous voulez tous vous distraire d’une idée fixe
qu’une révolution guérirait radicalement, reprit le médecin. Le
Génois regrette sa république, le Milanais veut son indépendance, le
Piémontais souhaite le gouvernement constitutionnel, le Romagnol
désire la liberté...
—Qu’il ne comprend pas, dit la duchesse. Hélas! il est des pays
assez insensés pour souhaiter votre stupide charte qui tue
l’influence des femmes. La plupart de mes compatriotes veulent lire
vos productions françaises, inutiles billevesées.
—Inutiles! s’écria le médecin.
—Hé! monsieur, reprit la duchesse, que trouve-t-on dans un livre
qui soit meilleur que ce que nous avons au cœur? L’Italie est folle!
—Je ne vois pas qu’un peuple soit fou de vouloir être son maître,
dit le médecin.
—Mon Dieu, répliqua vivement la duchesse, n’est-ce pas acheter
au prix de bien du sang le droit de s’y disputer comme vous le faites
pour de sottes idées.
—Vous aimez le despotisme! s’écria le médecin.
—Pourquoi n’aimerai-je pas un système de gouvernement qui,
en nous ôtant les livres et la nauséabonde politique, nous laisse les
hommes tout entiers.
—Je croyais les Italiens plus patriotes, dit le Français.
La duchesse se mit à rire si finement, que son interlocuteur ne
sut plus distinguer la raillerie de la vérité, ni l’opinion sérieuse de la
critique ironique.
—Ainsi, vous n’êtes pas libérale? dit-il.
—Dieu m’en préserve! fit-elle. Je ne sais rien de plus mauvais
goût pour une femme que d’avoir une semblable opinion. Aimeriez-
vous une femme qui porterait l’Humanité dans son cœur?
—Les personnes qui aiment sont naturellement aristocrates, dit
en souriant le général autrichien.
—En entrant au théâtre, reprit le Français, je vous vis la
première, et je dis à Son Excellence que s’il était donné à une
femme de représenter un pays, c’était vous; il m’a semblé apercevoir
le génie de l’Italie, mais je vois à regret que si vous en offrez la
sublime forme, vous n’en avez pas l’esprit... constitutionnel, ajouta-t-
il.
—Ne devez-vous pas, dit la duchesse en lui faisant signe de
regarder le ballet, trouver nos danseurs détestables, et nos
chanteurs exécrables! Paris et Londres nous volent tous nos grands
talents, Paris les juge, et Londres les paie. Genovese, la Tinti, ne
nous resteront pas six mois...
En ce moment, le général sortit. Vendramin, le prince et deux
autres Italiens échangèrent alors un regard et un sourire en se
montrant le médecin français. Chose rare chez un Français, il douta
de lui-même en croyant avoir dit ou fait une incongruité, mais il eut
bientôt le mot de l’énigme.
—Croyez-vous, lui dit Émilio, que nous serions prudents en
parlant à cœur ouvert devant nos maîtres?
—Vous êtes dans un pays esclave, dit la duchesse d’un son de
voix et avec une attitude de tête qui lui rendirent tout à coup
l’expression que lui déniait naguère le médecin.—Vendramin, dit-elle
en parlant de manière à n’être entendue que de l’étranger, s’est mis
à fumer de l’opium, maudite inspiration due à un Anglais qui, par
d’autres raisons que les siennes, cherchait une mort voluptueuse;
non cette mort vulgaire à laquelle vous avez donné la forme d’un
squelette, mais la mort parée des chiffons que vous nommez en
France des drapeaux, et qui est une jeune fille couronnée de fleurs
ou de lauriers; elle arrive au sein d’un nuage de poudre, portée sur
le vent d’un boulet, ou couchée sur un lit entre deux courtisanes; elle
s’élève encore de la fumée d’un bol de punch, ou des lutines
vapeurs du diamant qui n’est encore qu’à l’état de charbon. Quand
Vendramin le veut, pour trois livres autrichiennes, il se fait général
vénitien, il monte les galères de la république, et va conquérir les
coupoles dorées de Constantinople; il se roule alors sur les divans
du sérail, au milieu des femmes du sultan devenu le serviteur de sa
Venise triomphante. Puis il revient, rapportant pour restaurer son
palais les dépouilles de l’empire turc. Il passe des femmes de
l’Orient aux intrigues doublement masquées de ses chères
Vénitiennes, en redoutant les effets d’une jalousie qui n’existe plus.
Pour trois swansiks, il se transporte au conseil des Dix, il en exerce
la terrible judicature, s’occupe des plus graves affaires, et sort du
palais ducal pour aller dans une gondole se coucher sous deux yeux
de flamme, ou pour aller escalader un balcon auquel une main
blanche a suspendu l’échelle de soie; il aime une femme à qui
l’opium donne une poésie que nous autres femmes de chair et d’os
ne pouvons lui offrir. Tout à coup, en se retournant, il se trouve face
à face avec le terrible visage du sénateur armé d’un poignard; il
entend le poignard glissant dans le cœur de sa maîtresse qui meurt
en lui souriant, car elle le sauve! elle est bien heureuse, dit la
duchesse en regardant le prince. Il s’échappe et court commander
les Dalmates, conquérir la côte illyrienne à sa belle Venise, où la
gloire lui obtient sa grâce, où il goûte la vie domestique: un foyer,
une soirée d’hiver, une jeune femme, des enfants pleins de grâce qui
prient saint Marc sous la conduite d’une vieille bonne. Oui, pour trois
livres d’opium il meuble notre arsenal vide, il voit partir et arriver des
convois de marchandises envoyées ou demandées par les quatre
parties du monde. La moderne puissance de l’industrie n’exerce pas
ses prodiges à Londres, mais dans sa Venise, où se reconstruisent
les jardins suspendus de Sémiramis, le temple de Jérusalem, les
merveilles de Rome. Enfin il agrandit le Moyen-âge par le monde de
la vapeur, par de nouveaux chefs-d’œuvre qu’enfantent les arts,
protégés comme Venise les protégeait autrefois. Les monuments,
les hommes, se pressent et tiennent dans son étroit cerveau, où les
empires, les villes, les révolutions se déroulent et s’écroulent en peu
d’heures, où Venise seule s’accroît et grandit; car la Venise de ses
rêves a l’empire de la mer, deux millions d’habitants, le sceptre de
l’Italie, la possession de la Méditerranée et les Indes!
—Quel opéra qu’une cervelle d’homme, quel abîme peu compris,
par ceux mêmes qui en ont fait le tour, comme Gall, s’écria le
médecin.
—Chère duchesse, dit Vendramin d’une voix caverneuse,
n’oubliez pas le dernier service que me rendra mon élixir. Après
avoir entendu des voix ravissantes, avoir saisi la musique par tous
mes pores, avoir éprouvé de poignantes délices, et dénoué les plus
chaudes amours du paradis de Mahomet, j’en suis aux images
terribles. J’entrevois maintenant dans ma chère Venise des figures
d’enfant contractées comme celles des mourants, des femmes
couvertes d’horribles plaies, déchirées, plaintives; des hommes
disloqués, pressés par les flancs cuivreux de navires qui s’entre-
choquent. Je commence à voir Venise comme elle est, couverte de
crêpes, nue, dépouillée, déserte. De pâles fantômes se glissent
dans ses rues!... Déjà grimacent les soldats de l’Autriche, déjà ma
belle vie rêveuse se rapproche de la vie réelle; tandis qu’il y a six
mois c’était la vie réelle qui était le mauvais sommeil, et la vie de
l’opium était ma vie d’amour et de voluptés, d’affaires graves et de
haute politique. Hélas! pour mon malheur, j’arrive à l’aurore de la
tombe, où le faux et le vrai se réunissent en de douteuses clartés qui
ne sont ni le jour ni la nuit, et qui participent de l’un et de l’autre.
—Vous voyez qu’il y a trop de patriotisme dans cette tête, dit le
prince en posant sa main sur les touffes de cheveux noirs qui se
pressaient au-dessus du front de Vendramin.
—Oh! s’il nous aime, dit Massimilla, il renoncera bientôt à son
triste opium.
—Je guérirai votre ami, dit le Français.
—Faites cette cure, et nous vous aimerons, dit Massimilla; mais
si vous ne nous calomniez point à votre retour en France, nous vous
aimerons encore davantage. Pour être jugés, les pauvres Italiens
sont trop énervés par de pesantes dominations; car nous avons
connu la vôtre, ajouta-t-elle en souriant.
—Elle était plus généreuse que celle de l’Autriche, répliqua
vivement le médecin.
—L’Autriche nous pressure sans rien nous rendre, et vous nous
pressuriez pour agrandir et embellir nos villes, vous nous stimuliez
en nous faisant des armées. Vous comptiez garder l’Italie, et ceux-ci
croient qu’ils la perdront, voilà toute la différence. Les Autrichiens
nous donnent un bonheur stupéfiant et lourd comme eux, tandis que
vous nous écrasiez de votre dévorante activité. Mais mourir par les
toniques, ou mourir par les narcotiques, qu’importe! n’est-ce pas
toujours la mort, monsieur le docteur?
—Pauvre Italie! elle est à mes yeux comme une belle femme à
qui la France devrait servir de défenseur, en la prenant pour
maîtresse, s’écria le médecin.
—Vous ne sauriez pas nous aimer à notre fantaisie, dit la
duchesse en souriant. Nous voulons être libres, mais la liberté que je
veux n’est pas votre ignoble et bourgeois libéralisme qui tuerait les
Arts. Je veux, dit-elle d’un son de voix qui fit tressaillir toute la loge,
c’est-à-dire, je voudrais que chaque république italienne renaquît
avec ses nobles, avec son peuple et ses libertés spéciales pour
chaque caste. Je voudrais les anciennes républiques aristocratiques
avec leurs luttes intestines, avec leurs rivalités qui produisirent les
plus belles œuvres de l’art, qui créèrent la politique, élevèrent les
plus illustres maisons princières. Étendre l’action d’un gouvernement
sur une grande surface de terre, c’est l’amoindrir. Les républiques
italiennes ont été la gloire de l’Europe au Moyen-âge. Pourquoi
l’Italie a-t-elle succombé, là où les Suisses, ses portiers, ont vaincu?
—Les républiques suisses, dit le médecin, étaient de bonnes
femmes de ménage occupées de leurs petites affaires, et qui
n’avaient rien à s’envier; tandis que vos républiques étaient des
souveraines orgueilleuses qui se sont vendues pour ne pas saluer
leurs voisines; elles sont tombées trop bas pour jamais se relever.
Les Guelfes triomphent!
—Ne nous plaignez pas trop, dit la duchesse d’une voix
orgueilleuse qui fit palpiter les deux amis, nous vous dominons
toujours! Du fond de sa misère, l’Italie règne par les hommes d’élite
qui fourmillent dans ses cités. Malheureusement, la partie la plus
considérable de nos génies arrive si rapidement à comprendre la
vie, qu’ils s’ensevelissent dans une paisible jouissance; quant à ceux
qui veulent jouer au triste jeu de l’immortalité, ils savent bien saisir
votre or et mériter votre admiration. Oui, dans ce pays, dont
l’abaissement est déploré par de niais voyageurs et par des poëtes
hypocrites, dont le caractère est calomnié par les politiques, dans ce
pays qui paraît énervé, sans puissance, en ruines, vieilli plutôt que
vieux, il se trouve en toute chose de puissants génies qui poussent
de vigoureux rameaux, comme sur un ancien plant de vigne
s’élancent des jets où viennent de délicieuses grappes. Ce peuple
d’anciens souverains donne encore des rois qui s’appellent
Lagrange, Volta, Rasori, Canova, Rossini, Bartolini, Galvani, Vigano,
Beccaria, Gicognara, Corvetto. Ces Italiens dominent le point de la
science humaine sur lequel ils se fixent, ou régentent l’art auquel ils
s’adonnent. Sans parler des chanteurs, des cantatrices, et des
exécutants qui imposent l’Europe par une perfection inouïe, comme
Taglioni, Paganini, etc., l’Italie règne encore sur le monde, qui
viendra toujours l’adorer. Allez ce soir à Florian, vous trouverez dans
Capraja l’un de nos hommes d’élite, mais amoureux de l’obscurité;
nul, excepté le duc Cataneo, mon maître, ne comprend mieux que
lui la musique; aussi l’a-t-on nommé ici il fanatico!
Après quelques instants, pendant lesquels la conversation
s’anima entre le Français et la duchesse, qui se montra finement
éloquente, les Italiens se retirèrent un à un pour aller dire dans
toutes les loges que la Cataneo, qui passait pour être una donna di
gran spirito, avait battu, sur la question de l’Italie, un habile médecin
français. Ce fut la nouvelle de la soirée. Quand le Français se vit
seul entre le prince et la duchesse, il comprit qu’il fallait les laisser
seuls, et sortit. Massimilla salua le médecin par une inclination de
tête qui le mettait si loin d’elle, que ce geste aurait pu lui attirer la
haine de cet homme, s’il eût pu méconnaître le charme de sa parole
et de sa beauté. Vers la fin de l’opéra, Émilio fut donc seul avec la
Cataneo; tous deux ils se prirent la main, et entendirent ainsi le duo
qui termine il Barbiere.
—Il n’y a que la musique pour exprimer l’amour, dit la duchesse
émue par ce chant de deux rossignols heureux.
Une larme mouilla les yeux d’Émilio, Massimilla, sublime de la
beauté qui reluit dans la sainte Cécile de Raphaël, lui pressait la
main, leurs genoux se touchaient, elle avait comme un baiser en
fleur sur les lèvres. Le prince voyait sur les joues éclatantes de sa
maîtresse un flamboiement joyeux pareil à celui qui s’élève par un
jour d’été au-dessus des moissons dorées, il avait le cœur oppressé
par tout son sang qui y affluait; il croyait entendre un concert de voix
angéliques, il aurait donné sa vie pour ressentir le désir que lui avait
inspiré la veille, à pareille heure, la détestée Clarina; mais il ne se
sentait même pas avoir un corps. Cette larme, la Massimilla
malheureuse l’attribua, dans son innocence, à la parole que venait
de lui arracher la cavatine de Genovese.
—Carino, dit-elle à l’oreille d’Émilio, n’es-tu pas au-dessus des
expressions amoureuses autant que la cause est supérieure à
l’effet?
Après avoir mis la duchesse dans sa gondole, Émilio attendit
Vendramin pour aller à Florian.
Le café Florian est à Venise une indéfinissable institution. Les
négociants y font leurs affaires, et les avocats y donnent des rendez-
vous pour y traiter leurs consultations les plus épineuses. Florian est
tout à la fois une Bourse, un foyer de théâtre, un cabinet de lecture,
un club, un confessionnal, et convient si bien à la simplicité des
affaires du pays, que certaines femmes vénitiennes ignorent
complétement le genre d’occupations de leurs maris, car s’ils ont
une lettre à faire, ils vont l’écrire à ce café. Naturellement les espions
abondent à Florian, mais leur présence aiguise le génie vénitien, qui
peut dans ce lieu exercer cette prudence autrefois si célèbre.
Beaucoup de personnes passent toute leur journée à Florian; enfin
Florian est un tel besoin pour certaines gens, que pendant les
entr’actes, ils quittent la loge de leurs amies pour y faire un tour et
savoir ce qui s’y dit.
Tant que les deux amis marchèrent dans les petites rues de la
Merceria, ils gardèrent le silence, car il y avait trop de compagnie;
mais, en débouchant sur la place Saint-Marc, le prince dit:—
N’entrons pas encore au café, promenons-nous. J’ai à te parler.
Il raconta son aventure avec la Tinti, et la situation dans laquelle
il se trouvait. Le désespoir d’Émilio parut à Vendramin si voisin de la
folie, qu’il lui promit une guérison complète, s’il voulait lui donner
carte blanche auprès de Massimilla. Cette espérance vint à propos
pour empêcher Émilio de se noyer pendant la nuit; car, au souvenir
de la cantatrice, il éprouvait une effroyable envie de retourner chez
elle. Les deux amis allèrent dans le salon le plus reculé du café
Florian y écouter cette conversation vénitienne qu’y tiennent
quelques hommes d’élite, en résumant les événements du jour. Les
sujets dominants furent d’abord la personnalité de lord Byron, de qui
les Vénitiens se moquèrent finement; puis l’attachement de Cataneo
pour la Tinti, dont les causes parurent inexplicables, après avoir été
expliquées de vingt façons différentes; enfin le début de Genovese;
puis la lutte entre la duchesse et le médecin français; et le duc
Cataneo se présenta dans le salon au moment où la conversation
devenait passionnément musicale. Il fit, ce qui ne fut pas remarqué
tant la chose parut naturelle, un salut plein de courtoisie à Émilio, qui
le lui rendit gravement. Cataneo chercha s’il y avait quelque
personne de connaissance; il avisa Vendramin et le salua, puis il
salua son banquier, patricien fort riche, et enfin celui qui parlait en ce
moment, un mélomane célèbre, ami de la comtesse Albrizzi, et dont
l’existence, comme celle de quelques habitués de Florian, était
totalement inconnue, tant elle était soigneusement cachée: on n’en
connaissait que ce qu’il en livrait à Florian.
C’était Capraja, le noble de qui la duchesse avait dit quelques
mots au médecin français. Ce Vénitien appartenait à cette classe de
rêveurs qui devinent tout par la puissance de leur pensée.
Théoricien fantasque, il se souciait autant de renommée que d’une
pipe cassée. Sa vie était en harmonie avec ses opinions. Capraja se
montrait sous les procuraties vers dix heures du matin, sans qu’on
sût d’où il vînt, il flânait dans Venise et s’y promenait en fumant des
cigares. Il allait régulièrement à la Fenice, s’asseyait au parterre, et
dans les entr’actes venait à Florian, où il prenait trois ou quatre
tasses de café par jour; le reste de sa soirée s’achevait dans ce
salon, qu’il quittait vers deux heures du matin. Douze cents francs
satisfaisaient à tous ses besoins, il ne faisait qu’un seul repas chez
un pâtissier de la Merceria qui lui tenait son dîner prêt à une certaine
heure sur une petite table au fond de sa boutique; la fille du pâtissier
lui accommodait elle-même des huîtres farcies, l’approvisionnait de
cigares, et avait soin de son argent. D’après son conseil, cette
pâtissière, quoique très-belle, n’écoutait aucun amoureux, vivait
sagement, et conservait l’ancien costume des Vénitiennes. Cette
Vénitienne pur-sang avait douze ans quand Capraja s’y intéressa, et
vingt-six ans quand il mourut; elle l’aimait beaucoup, quoiqu’il ne lui
eût jamais baisé la main, ni le front, et qu’elle ignorât complétement
les intentions de ce pauvre vieux noble. Cette fille avait fini par
prendre sur le patricien l’empire absolu d’une mère sur son enfant:
elle l’avertissait de changer de linge; le lendemain, Capraja venait
sans chemise, elle lui en donnait une blanche qu’il emportait et
mettait le jour suivant. Il ne regardait jamais une femme, soit au
théâtre, soit en se promenant. Quoique issu d’une vieille famille
patricienne, sa noblesse ne lui paraissait pas valoir une parole; le
soir après minuit, il se réveillait de son apathie, causait et montrait
qu’il avait tout observé, tout écouté. Ce Diogène passif et incapable
d’expliquer sa doctrine, moitié Turc, moitié Vénitien, était gros, court
et gras; il avait le nez pointu d’un doge, le regard satyrique d’un
inquisiteur, une bouche prudente quoique rieuse. A sa mort, on
apprit qu’il demeurait, proche San-Benedetto, dans un bouge. Riche
de deux millions dans les fonds publics de l’Europe, il en laissa les
intérêts dus depuis le placement primitif fait en 1814, ce qui
produisait une somme énorme tant par l’augmentation du capital que
par l’accumulation des intérêts. Cette fortune fut léguée à la jeune
pâtissière.
—Genovese, disait-il, ira fort loin. Je ne sais s’il comprend la
destination de la musique ou s’il agit par instinct, mais voici le
premier chanteur qui m’ait satisfait. Je ne mourrai donc pas sans
avoir entendu des roulades exécutées comme j’en ai souvent écouté
dans certains songes au réveil desquels il me semblait voir voltiger
les sons dans les airs. La roulade est la plus haute expression de
l’art, c’est l’arabesque qui orne le plus bel appartement du logis: un
peu moins, il n’y a rien; un peu plus, tout est confus. Chargée de
réveiller dans votre âme mille idées endormies, elle s’élance, elle
traverse l’espace en semant dans l’air ses germes qui, ramassés par
les oreilles, fleurissent au fond du cœur. Croyez-moi, en faisant sa
sainte Cécile, Raphaël a donné la priorité à la musique sur la poésie.
Il a raison: la musique s’adresse au cœur, tandis que les écrits ne
s’adressent qu’à l’intelligence; elle communique immédiatement ses
idées à la manière des parfums. La voix du chanteur vient frapper en
nous non pas la pensée, non pas les souvenirs de nos félicités, mais
les éléments de la pensée, et fait mouvoir les principes mêmes de
nos sensations. Il est déplorable que le vulgaire ait forcé les
musiciens à plaquer leurs expressions sur des paroles, sur des
intérêts factices; mais il est vrai qu’ils ne seraient plus compris par la
foule. La roulade est donc l’unique point laissé aux amis de la
musique pure, aux amoureux de l’art tout nu. En entendant ce soir la
dernière cavatine, je me suis cru convié par une belle fille qui par un
seul regard m’a rendu jeune: l’enchanteresse m’a mis une couronne
sur la tête et m’a conduit à cette porte d’ivoire par où l’on entre dans
le pays mystérieux de la Rêverie. Je dois à Genovese d’avoir quitté
ma vieille enveloppe pour quelques moments, courts à la mesure
des montres et bien longs par les sensations. Pendant un printemps
embaumé par les roses, je me suis trouvé jeune, aimé!
—Vous vous trompez, caro Capraja, dit le duc. Il existe en
musique un pouvoir plus magique que celui de la roulade.
—Lequel? dit Capraja.
—L’accord de deux voix ou d’une voix et du violon, l’instrument
dont l’effet se rapproche le plus de la voix humaine, répondit le duc.
Cet accord parfait nous mène plus avant dans le centre de la vie sur
le fleuve d’éléments qui ranime les voluptés et qui porte l’homme au
milieu de la sphère lumineuse où sa pensée peut convoquer le
monde entier. Il te faut encore un thème, Capraja, mais à moi le
principe pur suffit; tu veux que l’eau passe par les mille canaux du
machiniste pour retomber en gerbes éblouissantes; tandis que je me
contente d’une eau calme et pure, mon œil parcourt une mer sans
rides, je sais embrasser l’infini!
—Tais-toi, Cataneo, dit orgueilleusement Capraja. Comment, ne
vois-tu pas la fée qui, dans sa course agile à travers une lumineuse
atmosphère, y rassemble, avec le fil d’or de l’harmonie, les
mélodieux trésors qu’elle nous jette en souriant? N’as-tu jamais senti
le coup de baguette magique avec laquelle elle dit à la Curiosité:
Lève-toi! La déesse se dresse radieuse du fond des abîmes du
cerveau, elle court à ses cases merveilleuses, les effleure comme un
organiste frappe ses touches. Soudain s’élancent les Souvenirs, ils
apportent les roses du passé, conservées divinement et toujours
fraîches. Notre jeune maîtresse revient et caresse de ses mains
blanches des cheveux de jeune homme; le cœur trop plein déborde,
on revoit les rives fleuries des torrents de l’amour. Tous les buissons
ardents de la jeunesse flambent et redisent leurs mots divins jadis
entendus et compris! Et la voix roule, elle resserre dans ses
évolutions rapides ces horizons fuyants, elle les amoindrit; ils
disparaissent éclipsés par de nouvelles, par de plus profondes joies,
celles d’un avenir inconnu que la fée montre du doigt en s’enfuyant
dans son ciel bleu.
—Et toi, répondit Cataneo, n’as-tu donc jamais vu la lueur directe
d’une étoile t’ouvrir les abîmes supérieurs, et n’as-tu jamais monté
sur ce rayon qui vous emporte dans le ciel au milieu des principes
qui meuvent les mondes?
Pour tous les auditeurs, le duc et Capraja jouaient un jeu dont les
conditions n’étaient pas connues.
—La voix de Genovese s’empare des fibres, dit Capraja.
—Et celle de la Tinti s’attaque au sang, répondit le duc.
—Quelle paraphrase de l’amour heureux dans cette cavatine!
reprit Capraja. Ah! il était jeune, Rossini, quand il écrivit ce thème
pour le plaisir qui bouillonne! Mon cœur s’est empli de sang frais,
mille désirs ont pétillé dans mes veines. Jamais sons plus
angéliques ne m’ont mieux dégagé de mes liens corporels, jamais la
fée n’a montré de plus beaux bras, n’a souri plus amoureusement,
n’a mieux relevé sa tunique jusqu’à mi-jambe, en me levant le rideau
sous lequel se cache mon autre vie.
—Demain, mon vieil ami, répondit le duc, tu monteras sur le dos
d’un cygne éblouissant qui te montrera la plus riche terre, tu verras
le printemps comme le voient les enfants. Ton cœur recevra la
lumière sidérale d’un soleil nouveau, tu te coucheras sur une soie
rouge, sous les yeux d’une madone, tu seras comme un amant
heureux mollement caressé par une Volupté dont les pieds nus se
voient encore et qui va disparaître. Le cygne sera la voix de
Genovese s’il peut s’unir à sa Léda, la voix de la Tinti. Demain l’on
nous donne Mosè, le plus immense opéra qu’ait enfanté le plus beau
génie de l’Italie.
Chacun laissa causer le duc et Capraja, ne voulant pas être la
dupe d’une mystification; Vendramin seul et le médecin français les
écoutèrent pendant quelques instants. Le fumeur d’opium entendait
cette poésie, il avait la clef du palais où se promenaient ces deux
imaginations voluptueuses. Le médecin cherchait à comprendre et
comprit; car il appartenait à cette pléiade de beaux génies de l’École
de Paris, d’où le vrai médecin sort aussi profond métaphysicien que
puissant analyste.
—Tu les entends? dit Émilio à Vendramin en sortant du café vers
deux heures du matin.
—Oui, cher Émilio, lui répondit Vendramin en l’emmenant chez
lui. Ces deux hommes appartiennent à la légion des esprits purs qui
peuvent se dépouiller ici-bas de leurs larves de chair, et qui savent
voltiger à cheval sur le corps de la reine des sorcières, dans les
cieux d’azur où se déploient les sublimes merveilles de la vie
morale: ils vont dans l’Art là où te conduit ton extrême amour, là où
me mène l’opium. Ils ne peuvent plus être entendus que par leurs
pairs. Moi de qui l’âme est exaltée par un triste moyen, moi qui fais
tenir cent ans d’existence en une seule nuit, je puis entendre ces
grands esprits quand ils parlent du pays magnifique appelé le pays
des chimères par ceux qui se nomment sages, appelé le pays des
réalités par nous autres, qu’on nomme fous. Eh! bien, le duc et
Capraja, qui se sont jadis connus à Naples, où est né Cataneo, sont
fous de musique.
—Mais quel singulier système Capraja voulait-il expliquer à
Cataneo? demanda le prince. Toi qui comprends tout, l’as-tu
compris?
—Oui, dit Vendramin. Capraja s’est lié avec un musicien de
Crémone, logé au palais Capello, lequel musicien croit que les sons
rencontrent en nous-mêmes une substance analogue à celle qui
engendre les phénomènes de la lumière, et qui chez nous produit
les idées. Selon lui, l’homme a des touches intérieures que les sons
affectent, et qui correspondent à nos centres nerveux d’où
s’élancent nos sensations et nos idées! Capraja, qui voit dans les
arts la collection des moyens par lesquels l’homme peut mettre en
lui-même la nature extérieure d’accord avec une merveilleuse
nature, qu’il nomme la vie intérieure, a partagé les idées de ce
facteur d’instruments qui fait en ce moment un opéra. Imagine une
création sublime où les merveilles de la création visible sont
reproduites avec un grandiose, une légèreté, une rapidité, une
étendue incommensurables, où les sensations sont infinies, et où
peuvent pénétrer certaines organisations privilégiées qui possèdent
une divine puissance, tu auras alors une idée des jouissances
extatiques dont parlaient Cataneo et Capraja, poëtes pour eux seuls.
Mais aussi, dès que dans les choses de la nature morale, un homme
vient à dépasser la sphère où s’enfantent les œuvres plastiques par
les procédés de l’imitation, pour entrer dans le royaume tout spirituel
des abstractions où tout se contemple dans son principe et
s’aperçoit dans l’omnipotence des résultats, cet homme n’est-il plus
compris par les intelligences ordinaires.
—Tu viens d’expliquer mon amour pour la Massimilla, dit Émilio.
Cher, il est en moi-même une puissance qui se réveille au feu de ses
regards, à son moindre contact, et me jette en un monde de lumière
où se développent des effets dont je n’osais te parler. Il m’a souvent
semblé que le tissu délicat de sa peau empreignît des fleurs sur la
mienne quand sa main se pose sur ma main. Ses paroles répondent
en moi à ces touches intérieures dont tu parles. Le désir soulève
mon crâne en y remuant ce monde invisible au lieu de soulever mon
corps inerte; et l’air devient alors rouge et petille, des parfums
inconnus et d’une force inexprimable détendent mes nerfs, des
roses me tapissent les parois de la tête, et il me semble que mon
sang s’écoule par toutes mes artères ouvertes, tant ma langueur est
complète.
—Ainsi fait mon opium fumé, répondit Vendramin.
—Tu veux donc mourir? dit avec terreur Émilio.
—Avec Venise, fit Vendramin en étendant la main vers Saint-
Marc. Vois-tu un seul de ces clochetons et de ces aiguilles qui soit
droit? Ne comprends-tu pas que la mer va demander sa proie?
Le prince baissa la tête et n’osa parler d’amour à son ami. Il faut
voyager chez les nations conquises pour savoir ce qu’est une patrie
libre. En arrivant au palais Vendramini, le prince et Marco virent une
gondole arrêtée à la porte d’eau. Le prince prit alors Vendramin par
la taille, et le serra tendrement en lui disant:—Une bonne nuit, cher.
—Moi, une femme, quand je couche avec Venise! s’écria
Vendramin.
En ce moment, le gondolier appuyé contre une colonne regarda
les deux amis, reconnut celui qui lui avait été signalé, et dit à l’oreille
du prince:—La duchesse, monseigneur.
Émilio sauta dans la gondole où il fut enlacé par des bras de fer,
mais souples, et attiré sur les coussins où il sentit le sein palpitant
d’une femme amoureuse. Aussitôt le prince ne fut plus Émilio, mais
l’amant de la Tinti, car ses sensations furent si étourdissantes, qu’il
tomba comme stupéfié par le premier baiser.
—Pardonne-moi cette tromperie, mon amour, lui dit la Sicilienne.
Je meurs si je ne t’emmène!
Et la gondole vola sur les eaux discrètes.
Le lendemain soir, à sept heures et demie, les spectateurs
étaient à leurs mêmes places au théâtre, à l’exception des
personnes du parterre qui s’asseyent toujours au hasard. Le vieux
Capraja se trouvait dans la loge de Cataneo. Avant l’ouverture, le
duc vint faire une visite à la duchesse; il affecta de se tenir près
d’elle et de laisser Émilio sur le devant de la loge, à côté de
Massimilla. Il dit quelques phrases insignifiantes, sans sarcasmes,
sans amertume, et d’un air aussi poli que s’il se fût agi d’une visite à
une étrangère. Malgré ses efforts pour paraître aimable et naturel, le
prince ne put changer sa physionomie, qui était horriblement
soucieuse. Les indifférents durent attribuer à la jalousie une si forte
altération dans des traits, habituellement calmes. La duchesse
partageait sans doute les émotions d’Émilio, elle montrait un front
morne, elle était visiblement abattue. Le duc, très-embarrassé entre
ces deux bouderies, profita de l’entrée du Français pour sortir.
—Monsieur, dit Cataneo à son médecin avant de laisser
retomber la portière de la loge, vous allez entendre un immense
poëme musical assez difficile à comprendre du premier coup; mais
je vous laisse auprès de madame la duchesse qui, mieux que
personne, peut l’interpréter, car elle est mon élève.
Le médecin fut frappé comme le duc de l’expression peinte sur le
visage des deux amants, et qui annonçait un désespoir maladif.
—Un opéra italien a donc besoin d’un cicérone? dit-il à la
duchesse en souriant.
Ramenée par cette demande à ses obligations de maîtresse de
loge, la duchesse essaya de chasser les nuages qui pesaient sur
son front, et répondit en saisissant avec empressement un sujet de
conversation où elle pût déverser son irritation intérieure.
—Ce n’est pas un opéra, monsieur, répondit-elle, mais un
oratorio, œuvre qui ressemble effectivement à l’un de nos plus
magnifiques édifices, et où je vous guiderai volontiers. Croyez-moi,
ce ne sera pas trop que d’accorder à notre grand Rossini toute votre
intelligence, car il faut être à la fois poëte et musicien pour
comprendre la portée d’une pareille musique. Vous appartenez à
une nation dont la langue et le génie sont trop positifs pour qu’elle
puisse entrer de plain-pied dans la musique; mais la France est
aussi trop compréhensive pour ne pas finir par l’aimer, par la cultiver,
et vous y réussirez comme en toute chose. D’ailleurs, il faut
reconnaître que la musique, comme l’ont créée Lulli, Rameau,
Haydn, Mozart, Beethoven, Cimarosa, Paësiello, Rossini, comme la
continueront de beaux génies à venir, est un art nouveau, inconnu
aux générations passées, lesquelles n’avaient pas autant
d’instruments que nous en possédons maintenant, et qui ne savaient
rien de l’harmonie sur laquelle aujourd’hui s’appuient les fleurs de la
mélodie, comme sur un riche terrain. Un art si neuf exige des études
chez les masses, études qui développeront le sentiment auquel
s’adresse la musique. Ce sentiment existe à peine chez vous,
peuple occupé de théories philosophiques, d’analyse, de
discussions, et toujours troublé par des divisions intestines. La
musique moderne, qui veut une paix profonde, est la langue des
âmes tendres, amoureuses, enclines à une noble exaltation
intérieure. Cette langue, mille fois plus riche que celle des mots, est
au langage ce que la pensée est à la parole; elle réveille les
sensations et les idées sous leur forme même, là où chez nous
naissent les idées et les sensations, mais en les laissant ce qu’elles
sont chez chacun. Cette puissance sur notre intérieur est une des
grandeurs de la musique. Les autres arts imposent à l’esprit des
créations définies, la musique est infinie dans les siennes. Nous
sommes obligés d’accepter les idées du poëte, le tableau du peintre,
la statue du sculpteur; mais chacun de nous interprète la musique au
gré de sa douleur ou de sa joie, de ses espérances ou de son
désespoir. Là où les autres arts cerclent nos pensées en les fixant
sur une chose déterminée, la musique les déchaîne sur la nature
entière qu’elle a le pouvoir de nous exprimer. Vous allez voir
comment je comprends le Moïse de Rossini!
Elle se pencha vers le médecin afin de pouvoir lui parler et de
n’être entendue que de lui.
—Moïse est le libérateur d’un peuple esclave! lui dit-elle,
souvenez-vous de cette pensée, et vous verrez avec quel religieux
espoir la Fenice tout entière écoutera la prière des Hébreux délivrés,
et par quel tonnerre d’applaudissements elle y répondra!
Émilio se jeta dans le fond de la loge au moment où le chef
d’orchestre leva son archet. La duchesse indiqua du doigt au
médecin la place abandonnée par le prince pour qu’il la prît. Mais le
Français était plus intrigué de connaître ce qui s’était passé entre les
deux amants que d’entrer dans le palais musical élevé par l’homme
que l’Italie entière applaudissait alors, car alors Rossini triomphait
dans son propre pays. Le Français observa la duchesse, qui parla
sous l’empire d’une agitation nerveuse et lui rappela la Niobé qu’il
venait d’admirer à Florence: même noblesse dans la douleur, même
impassibilité physique; cependant l’âme jetait un reflet dans le chaud
coloris de son teint, et ses yeux, où s’éteignit la langueur sous une
expression fière, séchaient leurs larmes par un feu violent. Ses
douleurs contenues se calmaient quand elle regardait Émilio, qui la
tenait sous un regard fixe. Certes, il était facile de voir qu’elle voulait
attendrir un désespoir farouche. La situation de son cœur imprima je
ne sais quoi de grandiose à son esprit. Comme la plupart des
femmes, quand elles sont pressées par une exaltation
extraordinaire, elle sortit de ses limites habituelles et eut quelque
chose de la Pythonisse, tout en demeurant noble et grande, car ce
fut la forme de ses idées et non sa figure qui se tordit
désespérément. Peut-être voulait-elle briller de tout son esprit pour
donner de l’attrait à la vie et y retenir son amant.
Quand l’orchestre eut fait entendre les trois accords en ut majeur
que le maître a placés en tête de son œuvre pour faire comprendre
que son ouverture sera chantée, car la véritable ouverture est le
vaste thème parcouru depuis cette brusque attaque jusqu’au
moment où la lumière apparaît au commandement de Moïse, la
duchesse ne put réprimer un mouvement convulsif qui prouvait
combien cette musique était en harmonie avec sa souffrance
cachée.
—Comme ces trois accords vous glacent! dit-elle. On s’attend à
de la douleur. Écoutez attentivement cette introduction, qui a pour
sujet la terrible élégie d’un peuple frappé par la main de Dieu. Quels
gémissements! Le roi, la reine, leur fils aîné, les grands, tout le
peuple soupire; ils sont atteints dans leur orgueil, dans leurs
conquêtes, arrêtés dans leur avidité. Cher Rossini, tu as bien fait de
jeter cet os à ronger aux tedeschi, qui nous refusaient le don de
l’harmonie et la science! Vous allez entendre la sinistre mélodie que
le maître a fait rendre à cette profonde composition harmonique,
comparable à ce que les Allemands ont de plus compliqué, mais
d’où il ne résulte ni fatigue ni ennui pour nos âmes. Vous autres
Français, qui avez accompli naguère la plus sanglante des
révolutions, chez qui l’aristocratie fut écrasée sous la patte du lion
populaire, le jour où cet oratorio sera exécuté chez vous, vous
comprendrez cette magnifique plainte des victimes d’un Dieu qui
venge son peuple. Un Italien pouvait seul écrire ce thème fécond,
inépuisable et tout dantesque. Croyez-vous que ce ne soit rien que
de rêver la vengeance pendant un moment? Vieux maîtres
allemands, Hændel, Sébastien Bach, et toi-même Beethoven, à
genoux, voici la reine des arts, voici l’Italie triomphante!
La duchesse avait pu dire ces paroles pendant le lever du rideau.
Le médecin entendit alors la sublime symphonie par laquelle le
compositeur a ouvert cette vaste scène biblique. Il s’agit de la
douleur de tout un peuple. La douleur est une dans son expression,
surtout quand il s’agit de souffrances physiques. Aussi, après avoir
instinctivement deviné, comme tous les hommes de génie, qu’il ne
devait y avoir aucune variété dans les idées, le musicien, une fois sa
phrase capitale trouvée, l’a-t-il promenée de tonalités en tonalités,
en groupant les masses et ses personnages sur ce motif par des
modulations et par des cadences d’une admirable souplesse. La
puissance se reconnaît à cette simplicité. L’effet de cette phrase, qui
peint les sensations du froid et de la nuit chez un peuple
incessamment baigné par les ondes lumineuses du soleil, et que le
peuple et ses rois répètent, est saisissant. Ce lent mouvement
musical a je ne sais quoi d’impitoyable. Cette phrase fraîche et
douloureuse est comme une barre tenue par quelque bourreau
céleste qui la fait tomber sur les membres de tous ces patients par
temps égaux. A force de l’entendre allant d’ut mineur en sol mineur,
rentrant en ut pour revenir à la dominante sol, et reprendre en
fortissimo sur la tonique mi bémol, arriver en fa majeur et retourner
en ut mineur, toujours de plus en plus chargée de terreur, de froid et
de ténèbres, l’âme du spectateur finit par s’associer aux impressions
exprimées par le musicien. Aussi le Français éprouva-t-il la plus vive
émotion quand arriva l’explosion de toutes ces douleurs réunies qui
crient:
O nume d’Israël!
Se brami in liberta
Il popol tuo fedel
Di lui, di noi pieta.
(O Dieu d’Israël, si tu veux que ton peuple fidèle sorte

d’esclavage, daigne avoir pitié de lui et de nous!)
—Jamais il n’y eut une si grande synthèse des effets naturels,
une idéalisation si complète de la nature. Dans les grandes
infortunes nationales, chacun se plaint longtemps séparément; puis
il se détache sur la masse, çà et là, des cris de douleur plus ou
moins violents; enfin, quand la misère a été sentie par tous, elle
éclate comme une tempête. Une fois entendus sur leur plaie
commune, les peuples changent alors leurs cris sourds en des cris
d’impatience. Ainsi a procédé Rossini. Après l’explosion en ut
majeur, le Pharaon chante son sublime récitatif de: Mano ultrice di
un dio! (Dieu vengeur, je te reconnais trop tard!) Le thème primitif
prend alors un accent plus vif: l’Égypte entière appelle Moïse à son
secours.
La duchesse avait profité de la transition nécessitée par l’arrivée
de Moïse et d’Aaron pour expliquer ainsi ce beau morceau.
—Qu’ils pleurent, ajouta-t-elle passionnément, ils ont fait bien
des maux. Expiez, Égyptiens, expiez les fautes de votre cour
insensée! Avec quel art ce grand peintre a su employer toutes les
couleurs brunes de la musique et tout ce qu’il y a de tristesse sur la
palette musicale? Quelles froides ténèbres! quelles brumes! N’avez-
vous pas l’âme en deuil? n’êtes-vous pas convaincu de la réalité des
nuages noirs qui couvrent la scène? Pour vous, les ombres les plus
épaisses n’enveloppent-elles pas la nature? Il n’y a ni palais
égyptiens, ni palmiers, ni paysages. Aussi quel bien ne vous feront-
elles pas à l’âme, les notes profondément religieuses du médecin
céleste qui va guérir cette cruelle plaie? Comme tout est gradué
pour arriver à cette magnifique invocation de Moïse à Dieu! Par un
savant calcul dont les analogies vous seront expliquées par Capraja,
cette invocation n’est accompagnée que par les cuivres. Ces
instruments donnent à ce morceau sa grande couleur religieuse.
Non-seulement cet artifice est admirable ici, mais encore voyez
combien le génie est fertile en ressources, Rossini a tiré des beautés
neuves de l’obstacle qu’il se créait. Il a pu réserver les instruments à
cordes pour exprimer le jour quand il va succéder aux ténèbres, et
arriver ainsi à l’un des plus puissants effets connus en musique.
Jusqu’à cet inimitable génie, avait-on jamais tiré un pareil parti du
récitatif? il n’y a pas encore un air ni un duo. Le poëte s’est soutenu
par la force de la pensée, par la vigueur des images, par la vérité de
sa déclamation. Cette scène de douleur, cette nuit profonde, ces cris
de désespoir, ce tableau musical, est beau comme le Déluge de
votre grand Poussin.
Moïse agita sa baguette, le jour parut.
—Ici, monsieur, la musique ne lutte-t-elle pas avec le soleil dont
elle a emprunté l’éclat, avec la nature entière dont elle rend les
phénomènes dans les plus légers détails? reprit la duchesse à voix
basse. Ici, l’art atteint à son apogée, aucun musicien n’ira plus loin.
Entendez-vous l’Égypte se réveillant après ce long
engourdissement? Le bonheur se glisse partout avec le jour. Dans
quelle œuvre ancienne ou contemporaine rencontrerez-vous une si
grande page? la plus splendide joie opposée à la plus profonde
tristesse? Quels cris! quelles notes sautillantes! comme l’âme
oppressée respire, quel délire, quel tremolo dans cet orchestre, le
beau tutti. C’est la joie d’un peuple sauvé! Ne tressaillez-vous pas de
plaisir?
Le médecin, surpris par ce contraste, un des plus magnifiques de
la musique moderne, battit des mains, emporté par son admiration.
—Bravo la Doni! fit Vendramin qui avait écouté.
—L’introduction est finie, reprit la duchesse. Vous venez
d’éprouver une sensation violente, dit-elle au médecin; le cœur vous
bat, vous avez vu dans les profondeurs de votre imagination le plus
beau soleil inondant de ses torrents de lumière tout un pays, morne
et froid naguère. Sachez maintenant comment s’y est pris le
musicien, afin de pouvoir l’admirer demain dans les secrets de son
génie après en avoir aujourd’hui subi l’influence. Que croyez-vous

Full Ebook of The Digestive System From Basic Sciences To Clinical Practice 1St Edition Pierre Poitras Online PDF All Chapter

Uploaded by

Copyright:

Available Formats

You might also like

Full Ebook of The Digestive System From Basic Sciences To Clinical Practice 1St Edition Pierre Poitras Online PDF All Chapter

Uploaded by

Document Information

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Full Ebook of The Digestive System From Basic Sciences To Clinical Practice 1St Edition Pierre Poitras Online PDF All Chapter

Uploaded by

Copyright:

Available Formats

The Digestive System From Basic

Sciences to Clinical Practice 1st Edition

Testosterone From Basic to Clinical Aspects Alexandre

Tendinopathy From Basic Science to Clinical Management

Anatomy of the Digestive System Quick Study Academic

Neuroscience in the 21st Century From Basic to Clinical

DeGroot s Endocrinology Basic Science and Clinical

Polycystic Ovary Syndrome Basic Science to Clinical

Basic System Analysis 2nd Edition S. Palani

The Innate Immune System in Health and Disease from the

The Digestive System:

Marc Bilodeau • Mickael Bouin • Jean-Eric Ghia

ISBN 978-3-030-98380-2 ISBN 978-3-030-98381-9 (eBook)

I The Digestive Organs

3 The Small Intestine............................................................................................................................67

6 The Biliary Tree.....................................................................................................................................205

II Digestive Symptoms, Signs and Other

10 Nausea and Vomiting.......................................................................................................................311

11 Upper Gastrointestinal Bleeding (UGIB).............................................................................315

14 Abdominal Distension and Bloating......................................................................................331

23 Undernutrition and Nutritional Support............................................................................381

25 Genes and Digestive Cancers......................................................................................................397

27 Abnormal Liver Tests........................................................................................................................407

29 Diets and Digestive Diseases......................................................................................................417

Johane P. Allard, MD Division of Gastroenterology and Hepatology, Toronto General

Fernando Alvarez, MD Department of Gastroenterology, Hepatology and Nutrition, CHU

Christopher N. Andrews, MD Division of Gastroenterology & Hepatology, Foothills Medical

André Archambault, MD Department of Anesthesiology, Centre Hospitalier de l’Université de

Alan Barkun, MD Division of Gastroenterology, McGill University Health Center, Montreal,

Marc Bilodeau, MD Liver Unit, CHUM, Montreal, QC, Canada

Julien Bissonnette, MD Liver Unit, CHUM, Montreal, QC, Canada

Simon Bouchard, MD GI Unit, CHUM, Montreal, QC, Canada

Mickael Bouin, MD, PhD GI Unit, CHUM, Montreal, QC, Canada

Marc Bradette, MD Division of Gastroenterology, CHU Québec, Quebec, QC, Canada

Julie Carrier, MD Division of Gastroenterology, CHU Sherbrooke, Sherbrooke, QC, Canada

Hélène Castel, MD Liver Unit, CHUM, Montreal, QC, Canada

Louise D’Aoust, MD GI Unit, CHUM, Montreal, QC, Canada

Renée Déry, MD Department of Radiology, CHUM, Montreal, QC, Canada

Colette Deslandres, MD Department of Gastroenterology, Hepatology and Nutrition, CHU

Éric Drouin, MD Department of Gastroenterology, Hepatology and Nutrition, CHU

Christophe Faure, MD Department of Gastroenterology, Hepatology and Nutrition, CHU

Daphna Fenyves, MD Liver Unit, CHUM, Montreal, QC, Canada

Claire Fournier, MD Liver Unit, CHUM, Montreal, QC, Canada

Jean-Paul Galmiche, MD Professeur d’Hépatogastroentérologie, Institut des maladies de

Jean-Eric Ghia, PhD Department of Immunology, Internal Medicine (Gastroenterology),

Véronique Groleau, MD Department of Gastroenterology, Hepatology and Nutrition, CHU

Ugur Halac, MD Department of Gastroenterology, Hepatology and Nutrition, CHU

Frédéric-Simon Hould, MD Department of Digestive Surgery, University Institute of Cardiology

Geneviève Huard, MD Liver Unit, CHUM, Montreal, QC, Canada

Prévost Jantchou, MD, PhD Department of Gastroenterology, Hepatology and Nutrition,

Raymond G. Lahaie, MD GI Unit, CHUM, Montreal, QC, Canada

Michel Lemoyne, MD GI Unit, CHUM, Montreal, QC, Canada

Christiane Malo, PhD Professor of Physiology, Department of Physiology, Faculty of Medi-

Valérie Marchand, MD Department of Gastroenterology, Hepatology and Nutrition, CHU

Xavier Marchand, MD Emergency Medicine, CH Centre-de-la-Mauricie, Shawinigan-Sud,

Denis Marleau, MD Liver Unit, CHUM, Montreal, QC, Canada

Katarzyna Orlicka, MD GI Unit, CHUM, Montreal, QC, Canada

Benoit Panzini, MD GI Unit, CHUM, Montreal, QC, Canada

3 The Small Intestine............................................................................................................................67

6 The Biliary Tree.....................................................................................................................................205

10 Nausea and Vomiting.......................................................................................................................311

11 Upper Gastrointestinal Bleeding (UGIB).............................................................................315

14 Abdominal Distension and Bloating......................................................................................331

23 Undernutrition and Nutritional Support............................................................................381

25 Genes and Digestive Cancers......................................................................................................397

27 Abnormal Liver Tests........................................................................................................................407

29 Diets and Digestive Diseases......................................................................................................417

Abdel Karim Sermé, MD Gastroenterology Hospitalization Service, CHU Yalgado-Ouédraogo

FODMAP Fermentables, oligosaccharides, disaccharides, monosaccharides, and

Chapter 1 The Esophagus – 3

Chapter 2 The Stomach – 31

Chapter 3 he Small Intestine – 67

Chapter 4 The Colon – 125

Chapter 5 The Pancreas – 173

Chapter 6 The Biliary Tree – 205

Chapter 7 The Anorectum – 225

Chapter 8 The Liver – 249

1.1 Macroscopic Anatomy – 5

1.2 Microscopic Anatomy – 7

1.6 Inflammation Disorders – 11

1.7 Tumor Disorders – 15

1.8 Function Disorders – 17

The esophageal mucosa is made of a stratified squamous

the esophagus and the reddish columnar epithelium of 1.3 Embryology/Development

1.5.2 Esophageal (Transport) Motility

The overall therapeutic strategy is comparable for 1.8 Function Disorders