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GastroEsophageal Reflux

Disease
ANATOMY- Esophagus
 Tubular, elongated organ of the digestive system
which connects the pharynx to the stomach.
 Collapsed at rest

 Flat in upper 2/3 & rounded in lower 1/3

 It is 25 cm in length

 Commences from the lower border of the cricoid


cartilage.(C6)
 3 anatomical segments:
› Cervical: cricopharyngeus - suprasternal notch
› Thoracic: suprasternal notch - diaphragm
› Abdominal: diaphragm -fundus of the stomach

 Descends: front of the spine post. Mediastinum


through diaphragm T 10 Terminates: cardiac orifice of the
stomach T 11

 Two high-pressure zones


 The upper and
 The lower esophageal sphincter.
 UES: pharyngoesophageal
sphincter
 LES: cardiac
/cardioesophageal sphincter
 Vagus nerve and spinal nerves (T1 to
T10) via the thoracic and cervical
sympathetic trunk.
Gastroesophageal Reflux Disease
(GERD)
 Gastroesophageal reflux is a normal physiologic
phenomenon experienced intermittently by most
people, particularly after a meal.
 Gastroesophageal reflux disease (GERD) occurs
when the amount of gastric juice that refluxes
into the esophagus exceeds the normal limit,
causing symptoms with or without associated
esophageal mucosal injury.
 Prolonged reflux of hydrochloric acid and pepsin
in esophagus, oral cavity and respiratory system
 Chronic and relapsing condition
 Leads to esophagitis and other postinflammatory
conditions of intestinal and respiratory mucosa
 It is a common disease that accounts for
approximately 75% of esophageal pathology
 Now recognized as a chronic disease requiring
lifelong medical therapy.
Definition

Starting from the Genval Workshop (1999), through


Porto Consensus (2004) and Montreal definition of
GERD (2006), gastroenterologists tried to clarify
this vague and faded topic, develop a clear
definition of it, classify its manifestations in
esophageal and extra-esophageal (EE) syndromes,
and propose more definite pathophysiological
mechanisms.
 Montreal definition of GERD (a consensus document),
it is a condition that develops when reflux of stomach
contents causes troublesome symptoms and/or
complications. Heartburn-, regurgitation-, and reflux
related esophageal pain are the cardinal symptoms of
GERD.

 The Rome IV Conference definition of GERD is based


on dichotomous symptom correlation between
heartburn and reflux events, as recorded by pH
metry/impedance. It subclassified nonerosive disease
into true nonerosive disease, reflux hypersensitivity, and
functional heartburn.
 The Lyon Consensus conference focuses on the
“modern diagnosis of reflux disease,” it defines
parameters of esophageal testing based on which
one either establishes or excludes the diagnosis
of GERD. It concluded that future GERD
management strategies should focus on defining
individual patient phenotypes based on the level
of refluxate exposure,
Physiologic vs Pathologic
 Physiologic GERD  Pathologic GERD
› Postprandial › Symptoms
› Short lived › Mucosal injury
› Asymptomatic › Nocturnal sx
› No nocturnal sx
Causes
Most likely to occur in conditions that force abdominal contents
superiorly
 Loose lower esophageal sphincter (LES)
 Eating or drinking to Excess
 Extreme Obesity
 Pregnancy
 Running
 Lying flat after eating
 Hiatal hernia
 Smoking
*(HUNT study: smoking cessation improves GERD symptoms only in patients with normal BMI)
Pathophysiology
 Lower esophageal
sphincter
› Intrinsic muscle of distal
esophagus
› Sling fibers of cardia
› Diaphragm
› Transmitted pressure
of abdominal cavity

 Reflux occurs when the high-pressure zone in


distal esophagus is too low or when sphincter
with normal pressure undergoes spontaneous
relaxation
Summary of Pathogenesis of GERD
1. Impaired lower esophageal
sphincter-low pressures or frequent
transient lower esophageal sphincter
relaxation
2. Hypersecretion of acid
3. Decreased acid clearance resulting
from impaired peristalsis or abnormal
saliva production
4. Delayed gastric emptying or
duodenogastric reflux of bile
Salts and pancreatic enzymes.
Symptoms
Symptom Predominance (%)
Heartburn 80
Regurgitation 54
Abdominal Pain 29
Cough 27
Dysphagia for solids 23
Hoarseness 21
Belching 15
Aspiration 14
Wheezing 7
Globus 4
Extraesophageal manifestations of
GERD
 Otolaryngeal:
› hoarsness/laryngitis
› Ch. Sore throat
 Other:
› Noncardial chest pain
Symptoms -- Heartburn
 Epigastric and retrosternal
 Caustic or stinging sensation
 Does not radiate to the back, is not pressurelike
 Can be confused with symptoms of PUD, bilary
colic, or CAD
Symptoms -- Regurgitation
 Indicates progression of disease
 Distinguish between digested and undigested
food
Hiatal Hernia
 Type I
› Not considered a true PEH
› Upward migration of the GE junction into the mediastinum
› Hernia sac consists of visceral peritoneum, paraesophageal
membrane, anterior wall of gastric cardia
 Type II
› Upward dislocation of fundus of stomach alongside a
normally positioned intraabdominal GE junction
 Type III
› Upward displacement of both GE junction and gastric
fundus
› More common than Type II
 Type IV – aka Giant
› Contains viscera other than stomach
95%

1%

4%
Type II Type III Type IV
Diagnostic Studies
 Empirical Therapy
 Upper Gastrointestinal Endoscopy (EGD)
 Upper Gastrointestinal Fluoroscopy with Barium
 24-hour pH testing
 Esophageal Manometry
EsophagoGastroDuodenoscopy

 Allows examination of the esophageal mucosa


 Identifies presence of esophagitis and grading of
severity
 Can identify other pathology, such as diverticula,
hiatal hernia, webs, rings, or strictures
 Tissue biopsies to screen for Barrett’s esophagus
Endoscopic grading of oesophagitis
A normal upper esophagoscopy
The Los Angeles Classification System for the
endoscopic assessment of reflux oesophagitis

GRADE A:
One or more mucosal breaks no
longer than 5 mm, non of which
extends between the tops of the
mucosal folds
The Los Angeles Classification System for the
endoscopic assessment of reflux oesophagitis

GRADE B:
One or more mucosal breaks
more than 5 mm long, none
of which extends between
the tops of two mucosal
folds
The Los Angeles Classification System for the
endoscopic assessment of reflux oesophagitis

GRADE C:
Mucosal breaks that extend
between the tops of two or more
mucosal folds, but which involve
less than 75% of the oesophageal
circumference
The Los Angeles Classification System for the
endoscopic assessment of reflux oesophagitis

GRADE D:
Mucosal breaks which
involve at least 75% of the
oesophageal circumference
Endoscopic view of GERD complications
24-hour pH test
 Gold Standard for
presence of pathologic
reflux
 Parameters measured
include: total # of
reflux episodes,
duration of longest
reflux episode,
percentage of time pH
is less than 4
Ambulatory pH testing – Recent Advances

 Combined impedance
and acid testing
› Allows for the
measurement of both
acid and nonacid
(volume) reflux.
› Important in pt with
persistent symptoms
despite an adequate
medical trial
Modified De Meester Scoring system
Features Grade
Heart Burn
None 0
Minimal- occasional episodes 1
Moderate- medical therapy visits 2
Severe- interferes daily activities 3
Regurgitation
None 0
Minimal- occasional episodes 1
Moderate-on position and straining 2
Severe- features of aspiration 3
Dysphagia
None 0
Minimal- occasional episodes 1
Needs fluid to clear 2
Causes food impaction 3
Ambulatory pH testing – Recent Advances
 Tubeless method– Bravo
System
› Allows a radiotelemetry
capsule to be attached to the
esophageal mucosa
› Decreases patient
discomfort, allows for
longer (48h) monitoring,
and may improve accuracy
by allowing the patient to
carry out their usual
activities
Esophageal Manometry

 Lower Esophageal Sphincter (LES)


› Mean resting pressure
› Total length

 Esophageal Body
› To determine effectiveness of peristalsis
› Amplitude of esophageal wave
Esophagram
 Useful when operation is planned—shows
anatomy of esophagus and proximal stomach
 Demonstrates presence and size of hiatal hernia if
present
 Measurement of duodenogastric refux
› Bilitec 2000 recorder
› spectrophotometry

 Oesophageal impedance measurement


› Multiple Intraluminal Impedance
Complications of GERD

 Inflammation of the esophagus


 Bleeding or ulcers
 strictures
 Barrett's esophagus and adenocarcinoma
 Supraesophageal manifestations
› Asthma
› chronic cough
› pulmonary fibrosis
› ENT manifestations
Complications
 Erosive esophagitis
› Responsible for 40-60% of GERD symptoms
› Severity of symptoms often fail to match severity of
erosive esophagitis
Complications
 Esophageal stricture
› Result of healing of
erosive esophagitis
› May need dilation
Complications
8-15%

 Barrett’s Esophagus
› Intestinal metaplasia of the
esophagus
› Associated with the
development of
adenocarcinoma
Pathophysiology of Barrett’s Esophagus

› Acid damages lining of


esophagus and causes
chronic esophagitis
› Damaged area heals in a
metaplastic process and
abnormal columnar cells
replace squamous cells
› This specialized
intestinal metaplasia can
progress to dysplasia and
adenocarcinoma

Many patients with Barrett’s are asymptomatic


 The risk of cancer in Barrett's esophagus is
estimated to be 40 to 100 times
 Endoscopic surveillance is recommended for all
patients with Barrett's esophagus. Endoscopy is
performed every 2 years, and biopsies are taken
from the area of abnormal mucosa.
 If the biopsies reveal low-grade dysplasia, then
the frequency of endoscopies is increased.
 If high-grade dysplastic changes are seen and
confirmed by a second pathologist, then the risk
of subsequent adenocarcinoma is greater than
25%, and surgical resection should be
considered.
Summary
Treatment – Lifestyle Modification
 May benefit many patients with GERD, although
these changes alone are unlikely to control
symptoms in the majority of patients
 Elevation of the head of the bed, decreased fat
intake, cessation of smoking, avoiding
recumbency for 3 hr postprandially, avoidance of
certain foods (chocolate, peppermint)
 No data reflecting the efficacy of these
maneuvers
Treatment – Patient Directed
Therapy
 Antacids
 H2 receptor antagonists
 If symptoms persist, continuous therapy is
required, or alarm symptoms/signs develop – pt
should have additional evaluation and treatment
Treatment – Acid Suppression
 6-week course of acid-suppression therapy
 Double dose of a proton pump inhibitor
› Irreversible bind the proton pump in parietal cells of
the stomach
› Maximal effect 4 days after initiation of therapy and
lasts for the life of the parietal cell
› More effective than other antacid regimens
Treatment – Promotility Therapy
 May be used as an adjunct to acid suppression
therapy in patients with demonstrated defects in
esophagogastric motility (LES incompetence,
poor esophageal clearance, delayed gastric
emptying)
Surgical Therapy
 Indications
› Pt with evidence of severe esophageal injury (ulcer,
stricture, or Barrett’s)
› Incomplete resolution of symptoms or relapses while
on medical therapy
› Long duration of symptoms
› Younger patients
› Ideal patient: more than 10-year life expectancy and
are in need of lifelong therapy due to a mechanically
defective sphincter
Principles of Surgical Therapy
1. The operation should restore the pressure of the
distal esophageal sphincter to a level twice resting
gastric pressure, i.e., 12 mm Hg for a gastric
pressure of 6 mm Hg, and its length to at least 3
cm.
2. The operation should place an adequate length of
the distal esophageal sphincter in the positive
pressure environment of the abdomen.
3. The reconstructed cardia should relax with
swallowing.
4. The fundoplication should not increase the
resistance of the relaxed sphincter to a level that
exceeds the peristaltic power of the body of the
esophagus.
5. The operation should ensure that the
fundoplication can be placed in the abdomen
without undue tension and maintained there by
approximating the crura of the diaphragm above
the repair.
Primary Antireflux Repairs
 Nissen’s fundoplication- 3600 wrap
 Toupet’s partial 1800 posterior fundoplication
 Rosetti Hell anterior fundoplication
 Dor anterior fundoplication
 Watson’s anterolateral fundoplication (1200)
 Lind both anterior and posterior fundoplication
 Partial fundoplication with mesh wrap
Other Procedures
 Hill’s operation – Intraabdominal fixation of OG
junction
 Belsey Mark IV operation – Plication of
oesophagus to diaphragm with 2400 fundoplication
 Collis vertical gastroplasty – Vertical cut on
fundus to crate extra esophageal length
 Thal’s patch procedure – For strictures
 Narbona’s ligamentum teres cardiopexy
 Boerema operation – Fixing OG junction
 Oesophagogastrectomy
 Transhiatal oesophagectomy
The Nissen Fundoplication

 The most common antireflux procedure.


 Open and laparoscopic approach
 Principle elements:
1. Crural dissection, identification, and preservation of
both vagi.
2. Circumferential dissection of the esophagus.
3. Crural closure.
4. Fundic mobilization by division of short gastric
vessels.
5. Creation of a short, loose fundoplication by
enveloping the anterior and posterior wall of the
fundus around the lower esophagus.
Laparoscopic Nissen Fundoplication
 Success rate of greater than 90%
 Procedure of choice
Trocar Placement
› Midline—2/3 from xiphoid to
umbilicus, 10mm
 Laparascope
› Immediately below Xiphoid
Process, 5mm
 Grasping forceps
› Anterior Axillary Line just below
Costal Margin
 Right, 10mm
 Liver retractor around middle of
left lobe to retract ventrally
 Exposes anterior surface of the
proximal stomach near the
gastroesophageal junction
 Left, 5mm
 Grasping forceps, suction,
scissors
› Midclavicular Line, Left Upper
Quandrant, 5mm
 Dissecting and Suturing
Devices
Three types of fundoplication: 360-degree wrap (A), partial anterior fundoplication
(B), and partial posterior fundoplication (C).
 Transoral incisionless fundoplication (TIF) using the
Esophyx device (EndoGastric Solutions, Redmond,
WA)
 Endocinch procedure endoscopic placement of two
3 mm deep sutures in gastric mucosal folds
 Endoscopic anterior fundoplication using the
Medigus ultrasonic surgical endostapler (Medigus,
Omer, Israel).
Radiofrequency Thermal Therapy
-- Stretta
 Delivery of low-power, temperature-controlled
radiofrequency energy to the GEJ
 Two mechanisms

1. mechanically altering the GEJ


2. inducing the ablation of nerves that trigger
transient lower esophageal relaxation
Radiofrequency Thermal Therapy -- Stretta
The Stretta device was developed in
2000 and works by delivering thermal energy to the
LES, which is postulated to increase sphincter
thickness through scar tissue deposition, thereby
reducing reflux. However in a meta-analysis of
randomized controlled trials, Stretta treatment did not
reduce percentage of time when pH is less than 4 or
increase LES pressure or ability to stop PPIs
Injection/implantation techniques -- Enteryx
 Injectable biocompatible solution consisting of 8%
ethylene vinyl alcohol copolymer mixed in dimethyl
sulfoxide
 When injected into the LES, the solution interacts
with the surrounding fluid to become an inert
spongy solid mass
 Mechanism: may impart an alteration in the
compliance of tissues preventing sphincter
shortening and improving the barrier function of the
GEJ
Enteryx
The LINX® Reflux Management System
 It consists of a series of titanium beads, each with
a magnetic core, connected together with
titanium wires to form a ring shape.
 The LINX device is surgically implanted around
the lower end of the esophagus.
EndoStim Electrical Stimulation
Therapy
 involves attaching two small electrodes from the
lead to the lower esophagus. The lead is brought out
into a small pocket located under the abdominal
skin and connected to the stimulation device (IPG).
 EndoStim's proprietary technology uses
functional electrical stimulation (a type of
neuromodulation) to restore esophageal function,
thereby reducing GERD symptoms. Tiny pulses of
electric current are delivered to the LES without
causing any sensation.

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