GASTROESOPHAGEAL
RELUX DISEASE
Gastroesophageal reflux disease (GERD) is the most common benign medical
condition of the stomach and esophagus.
PATHOPHYSIOLOGY :
Two Endogenous anti-reflux mechanisms include the
1. Lower esophageal sphincter (LES)
2. Spontaneous esophageal clearance.
GERD results from the failure of these endogenous antireflux mechanisms.
The LES has the primary role of preventing reflux of gastric contents into the
esophagus.
LES is a zone of high pressure located in the lower end of the esophagus. The
LES can be identified with esophageal manometry.
The LES is made up of four anatomic structures:
1. The intrinsic musculature of the distal esophagus is in a state of tonic
contraction. Within 500 milliseconds of the initiation of a swallow, these muscle fibers
relax to allow passage of liquid or food into the stomach, and then they return to a
state of tonic contraction.
2. Sling fibers of the gastric cardia are oriented diagonally from the cardia-fundus
junction to the lesser curve of the stomach the sling fibers contribute significantly to
the high-pressure zone of the LES.
3. The crura of the diaphragm surround the esophagus as it passes through the
esophageal hiatus. During inspiration, when intrathoracic pressure decreases relative
to intra-abdominal pressure, the anteroposterior diameter of the crural opening is
decreased, compressing the esophagus and increasing the measured pressure at the
LES.
Because of this fluctuation in LES pressure, it is important to measure the LES
pressure at midexpiration or end-expiration.
4.The gastroesophageal junction (GEJ) is firmly anchored in the abdominal cavity,
increased intra-abdominal pressure is transmitted to the GEJ, which increases the
pressure on the distal esophagus and prevents spontaneous reflux of gastric contents.
Gastroesophageal reflux (GER) occurs when intragastric pressure is greater than the high-
pressure zone of the distal esophagus.
This can develop under two conditions:
The LES resting pressure is too low (i.e., hypotensive LES); and
The LES relaxes in the absence of peristaltic contraction of the esophagus (i.e., spontaneous
LES relaxation).
Hypotensive LES is frequently associated with hiatal hernia because of displacement of the GEJ
into the posterior mediastinum.
The distinction between physiologic reflux (i.e., GER) and pathologic reflux (i.e., GERD) hinges on
the total amount of esophageal acid exposure, the patient’s symptoms, and the presence of
mucosal damage of the esophagus.
HIATUS HERNIA AND GERD
Hiatal hernias are often associated with GERD because their abnormal
anatomy compromises the efficacy of the LES.
Hiatal hernias are classified into four types (I to IV).
Type I hiatal hernia also called a sliding hiatal hernia, is the most common.
A type I hernia is present when the GEJ migrates cephalad into the posterior
mediastinum.
This occurs because of laxity of the phrenoesophageal membrane, a
continuation of the endoabdominal peritoneum that reflects onto the
esophagus at the hiatus.
A small sliding hernia does not necessarily imply an incompetent LES, but the
larger its size, the greater the risk for abnormal GER.
Many patients with small type I hiatal hernias do not have symptoms and do
not require treatment.
Hiatal hernia types II to IV, also referred to as PEH, are frequently
associated with gastroesophageal obstructive symptoms (e.g., dysphagia,
early satiety, and epigastric pain).
A type II hernia occurs when the GEJ is anchored in the abdomen, and the
gastric fundus migrates into the mediastinum through the hiatal defect.
A type III hernia is characterized by both the GEJ and fundus located in the
mediastinum.
A type IV hernia occurs when any visceral structure (e.g., colon, spleen,
pancreas, or small bowel) migrates cephalad to the esophageal hiatus and is
located in the mediastinum.
Clinical Presentation: Heartburn, regurgitation, and water brash are the
three typical esophageal symptoms of GERD.
Heartburn and regurgitation are the most common presenting symptoms.
Heartburn is specific to GERD and described as an epigastric or retrosternal
caustic or stinging sensation. Typically, it does not radiate to the back and is
not described as a pressure sensation, which are more characteristic of
pancreatitis and acute coronary syndrome, respectively.
The presence of regurgitation often indicates progression of GERD. In severe
cases, patients will be unable to bend over without experiencing an episode
of regurgitation.
Regurgitation of gastric contents to the oropharynx and mouth can produce a
sour taste that patients will describe as either acid or bile. This phenomenon
is referred to as water brash
Extraesophageal Symptoms of GERD :
Extraesophageal symptoms of GERD arise from the respiratory tract and include both
laryngeal and pulmonary symptoms
Two mechanisms may lead to extraesophageal symptoms of GERD.
First, proximal esophageal reflux and microaspiration of gastroduodenal contents
cause direct caustic injury to the larynx and lower respiratory tract; this is the most
common mechanism.
Second, distal esophageal acid exposure triggers a vagal nerve reflex that results in
bronchospasm and cough. The latter mechanism is due to the common vagal innervation of
the trachea and esophagus.
Acid is not the only underlying caustic agent resulting in laryngeal and pulmonary injury.
PPI therapy will suppress gastric acid production, but microaspiration of nonacid refluxate,
which contains caustic bile salts and pepsin, can cause ongoing injury and symptoms.
SYMPTOMS :
Heartburn
Regurgitation
Abdominal pain
Cough
Dysphagia for solids
Hoarseness
Belching
Bloating
Aspiration
Wheezing
Globus
EXTRAESOPHAGEAL SYMPTOMS
Laryngeal Symptoms of Reflux
Hoarseness or dysphonia
Throat clearing
Throat pain
Globus
Choking
Postnasal drip
Laryngeal and tracheal stenosis
Laryngospasm
Contact ulcers
Pulmonary Symptoms of Reflux Cough Shortness of breath Wheezing Pulmonary
disease (asthma, idiopathic pulmonary fibrosis, chronic bronchitis, and
Pulmonary Symptoms of Reflux :
Cough
Shortness of breath
Wheezing
Pulmonary disease (asthma, idiopathic pulmonary fibrosis, chronic bronchitis
Pulmonary Disease, GERD, and Antireflux Surgery :
GERD is a contributing factor to the pathophysiologic mechanism of several
pulmonary diseases. In these patients, the use of antisecretory medications is
associated with improved respiratory symptoms in only 25% to 50% of patients with
GERD-induced asthma
Antireflux surgery is associated with improvement in respiratory symptoms in
nearly 90% of children and 70% of adults with asthma and GERD. Idiopathic
pulmonary fibrosis (IPF) is a severe, chronic, and progressive lung disease that
generally results in death within 5 years of diagnosis. Proximal esophageal reflux
with microaspiration of acid and nonacid gastric contents has been implicated as
one possible cause of alveolar epithelial injury that can lead to IPF..
Medical treatment of GERD in patients with IPF is associated with longer survival
and slower pulmonary decline. PPI therapy does not prevent reflux which may
contribute to ongoing pulmonary injury in some patients. Therefore, in IPF patients
with significant GERD, LARS is more appropriate than PPI therapy. LARS appears to
be safe and to provide effective control of distal esophageal acid exposure, and it
may mitigate decline in pulmonary function.
Preoperative Diagnostic Testing :
Four diagnostic tests are useful to establish the diagnosis of GERD and to
identify abnormalities in gastroesophageal anatomy and function that may
have an impact on the performance of LARS.
Ambulatory pH and Impedance Monitoring
Ambulatory pH monitoring quantifies distal esophageal acid exposure and is
the “gold standard” test to diagnose GERD.
A 24-hour pH monitoring is conducted with a thin catheter that is passed
into the esophagus through the patient’s nares. The simplest catheter is a
dual-probe pH catheter, which contains two solid-state electrodes that are
spaced 10 cm apart and detect fluctuations in pH between 2 and 7. The
distal electrode must be placed 5 cm proximal to the LES; the location of the
LES is identified on esophageal manometry.
Alternatively, 48-hour ambulatory pH monitoring can be performed using an
endoscopically placed wireless pH monitor.
Ambulatory pH monitoring generates a large amount of data concerning
esophageal acid exposure, including total number of reflux episodes (pH < 4),
longest episode of reflux, number of episodes lasting longer than 5 minutes,
and percentage of time spent in reflux in the upright and supine positions.
A formula assigns each of these data points a relative weight according to its
capacity to cause esophageal injury, and the composite DeMeester score is
calculated.
Abnormal distal esophageal acid exposure is defined by a DeMeester score of
14.7 or higher. In addition to these objective data, the patient can keep
track of reflux-related symptoms by pressing a button on an electronic data
recorder.
Esophageal impedance monitoring identifies episodes of nonacid reflux. It is
performed with a thin, flexible catheter placed through the patient’s nares into the
esophagus. Impedance catheters use electrodes placed at 1-cm intervals to detect
changes in the resistance to flow of an electrical current (i.e., impedance).
Impedance increases in the presence of air and decreases in the presence of a liquid
bolus. Therefore, this technology can detect both gas and liquid movement in the
esophagus. Some impedance catheters also have one or more pH sensors, allowing the
simultaneous detection of acid and nonacid reflux.
When pH-impedance catheters are used, it is possible to determine the direction of
movement of esophageal acid exposures and therefore to differentiate between an
antegrade event (as in a swallow) and a retrograde event (as in GER).
There also exists a specialized pH-impedance catheter with a very proximal pH sensor
that detects pharyngeal acid reflux. This catheter can be useful in the evaluation of
patients with extraesophageal symptoms, such as cough, throat clearing, hoarseness,
and wheezing.
One disadvantage is that the automated analytic software is very sensitive and tends
to overestimate the number of nonacid reflux episodes, mandating that these studies
be manually reviewed and edited, which can be time-consuming.
Esophageal Manometry
Esophageal manometry is the most effective way to assess function of the
esophageal body and the LES. Standard esophageal manometry provides
linear tracings of pressure waves of the esophageal body and LES. High-
resolution esophageal manometry gathers data using a 32-channel flexible
catheter with pressure sensing devices arranged at 1-cm intervals, placed into
the esophagus through the nares; the study is conducted in approximately 15
minutes, during which time the patient performs 10 swallows.
A color-contour plot is generated and shows the response of the upper
esophageal sphincter and LES as well as of the esophageal body; time is on
the x-axis, esophageal length is on the y-axis, and pressure is represented by
a color scale. In patients undergoing evaluation for GERD, it can exclude
achalasia and identify patients with ineffective esophageal body peristalsis.
Repeated exposure of the esophagus to gastric reflux can lead to esophageal
motility disorders.
It also measures the LES resting pressure and assesses the LES for appropriate
relaxation with deglutition. Because the LES is the major barrier to GER, a
defective LES is common in patients with GERD.
Esophagogastroduodenoscopy :
It is an essential step in the evaluation of patients with GERD. The esophagus
should be examined for evidence of mucosal injury due to GER, including
ulcerations, peptic strictures, and Barrett esophagus.
Esophagitis can be reported according to several scoring systems, including
the Savary-Miller and Los Angeles (LA) classifications.
Endoscopic evaluation should also include an assessment of the GEJ flap
valve. To do this, the endoscope is retroflexed 180 degrees in the stomach to
visualize the GEJ from below.
The flap valve is graded 1 to 4, according to the length of the valve and how
tightly it adheres to the endoscope. The endoscopist should make note of the
presence of a hiatal hernia, and the hernia should be measured in both
cranial-caudal and lateral dimensions.
.
Barium Esophagram:
It provides a detailed anatomic evaluation of the esophagus and stomach. Of
particular importance are the presence, size, and anatomic characteristics of
a hiatal hernia or PEH. For ex :posterior mediastinum on esophagography can
suggest a more difficult operation that may require a more extensive
intrathoracic esophageal mobilization.
Additional gastroesophageal conditions that can be identified on barium
esophagram are esophageal diverticula, tumors, peptic strictures, achalasia,
dysmotility, and gastroparesis.
POTENTIAL CAUSES OF DYSPHAGIA IN
PATIENTS WITH GERD
Esophageal Obstruction
Peptic strictures
Schatzki ring
Malignant neoplasm
Benign neoplasm
Foreign body
Esophageal Motility Disorders
Diffuse esophageal spasm
Hypercontractile (“Jackhammer”) esophagus
Ineffective esophageal motility Achalasia
MANAGEMENT OF GERD
A. General measures—
Lifestyle changes
Control of obesity.
Stop smoking and alcohol.
Avoid tea, coffee and chocolate.
Propped up position.
Small frequent meals
B. Drugs
H2 antagonists; antacids.
Proton pump inhibitors (PPIs) are very effective .
-Omeprazole 20 mg—BD for 3–6 months.
– Lansoprazole 30 mg.
– Pantoprazole 40 mg.
– Esomeprazole 20 mg.
– Rabeprazole 20 mg,
-ilaprazole 10 mg
Prokinetic drugs –
Metoclopramide,
Domperidone 30 mg.
Cisapride, Mosapride.
Itopride 50 mg
Defoaming semethicone, alginic acid along with antacids.
Anticholinergic drugs—pirenzipine.
Mucosal protector drugs—sucralfate, colloid bismuth.
C. Endoluminal therapies for GORD
Endoluminal suturing (Wilson-Cook)
Plexiglass microspheres (PMMA). Microsphere suspended in gelatin is injected
through endo scopic needle. Gelatin gets absorbed and spheres cause a tissue bulking.
Gatekeeper reflux repair system. Endoscopic delivery of preformed radiopaque
hydrogel into submucosa.
Stretta catheter. Flexible, soft, 6 mm sized, 65 cm length tube with balloon/basket
and 5.5 mm NITI electrode, irrigation and suction
Enteryx injection technique (estrinyl vinyl alcohol)
Endocinch technique
Endoscopic full thickness plication.
D. Surgery
Indications for surgical treatment
Failure of drug treatment
Sliding hernia
Barrett’s ulcer
Severe pain
Presence of complications like bleeding/stricture/ shortening, respiratory
problems
SURGERIES
Antireflux surgery is the only effective long-term beneficial therapy
ideally available and considered now.
Nissen’s posterior total fundoplication: Here after narrowing the crus
of diaphragm, mobilised posterior part of the fundus of the stomach is
wrapped totally 360° around the area of OG junction
Rudolph Nissen (1959) first did total fundoplication.
Opening the peritoneum over the oesophagus to mobilise the lower
end of esophagus.
Dissection of the diaphragmatic crura of the oesophagus.
Mobilisation of entire fundus by ligating short gastric vessels.
Vagi are preserved.
In Nissen’s, 60 French bougie wrap is ideal; after complete
mobilisation, only posterior part of the fundus is wrapped around after
crural repair
intra-abdominal length of 2 cm oesophagus is created
fundus of the stomach is known to relax in concert with oesophageal
sphincter so only fundus should be used to buttress the sphincter;
wrapping should be done only around sphincter oesophagus.
Crural repair is done using interrupted polypropylene sutures.
Fundoplication should prevent sphincter shortening/ unfolding during gastric
distension, should preserve normal swallowing ability, allow proper belching
and allow vomiting whenever needed.
Complications are—gas bloat syndrome (inability to belch); dysphagia;
inability to vomit; slippage, proximal migration; paraoesophageal hernia,
splenic injury. Floppy Nissen’s fundoplication reduces the incidence of gas
bloat syndrome.
Laparoscopic Nissen’s fundoplication is ideal and equally successful.
Transthoracic approach is used for Nissen’s fundoplication in patients who
had hiatus hernia repair earlier; who has short oesophagus; in patients who is
having sliding hiatal hernia that does not reduce below the diaphragm,
associated pulmonary disease, in obese, in patients who are having narrow
subcostal angle or barrel-shaped chest.
Toupet’s partial 180° posterior fundoplication: It is similar to Nissen’s
posterior fundoplication; it controls reflux alike Nissen’s but gas bloat is very
less. It is commonly done procedure now. Short gastric vessels are divided
completely or partially.
Rosetti Hell anterior fundoplication: Here anterior part of fundus of
stomach is used. Superomedial part of the fundus is brought around
oesophagus to suture into anterior part of fundus. Here short gastric vessels
are not ligated and much less fundus need to be mobilised.
Dor anterior fundoplication: Here right margin of the fundus is sutured to
left margin of the oesophagus; front part of fundus is sutured to right margin
of the oesophagus; 2nd row is also sutured to right crus.
Watson’s anterolateral fundoplication: 5 cm intraabdominal oesophagus is
created with blunt transhiatal dissection. 120° anterolateral fundoplication
augments the LOS function during stomach distension. Bougie insertion,
division of short gastric vessels are not needed here.
Lind both anterior and posterior fundoplication of 300°with 60° anteriorly
uncovered area is not routinely practiced now.
Partial fundoplication with mesh wrap around is also used. But complications
of mesh like erosion, stricture and adhesions are problems.
Fundoplications :
Nissens - total 360 posterior fundoplication.
Toupets -partial 180 posterior fundoplication.
Rosetti hell -total anterior fundal.
Dor - anterior partial
Watsons - anterolateral 120 partial
Lind - posterior and anterior
Other procedures :
Belsey Mark IV operation
Hill’s operation
Placement of Angelchik prosthesis
Collis’ vertical gastroplasty
Thal’s patch procedure
Narbona’s ligamentum teres cardiopexy
Boerema operation
Oesophagogastrectomy
Transhiatal oesophagectomy
Allison’s procedureo
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