GERD

• Gastroesophageal reflux disease (GERD) is a chronic gastrointestinal

disorder characterized by the regurgitation of gastric contents into the
esophagus
Etiology

• Motor abnormalities such as esophageal dysmotility causing impaired

esophageal acid clearance, impairment in the tone of the lower
esophageal sphincter (LES), transient LES relaxation, and delayed gastric
emptying are included in the causation of GERD .
• Anatomical factors like the presence of hiatal hernia or an increase in
intra-abdominal pressure, as seen in obesity are associated with an
increased risk of developing GERD.
• Other factors include :Age ≥50 years, low socioeconomic status, tobacco
use, consumption of excess alcohol, connective tissue disorders,
pregnancy, postprandial supination, and different classes of drugs E.g
benzodiazepines, NSAIDs, aspirin and calcium channel blockers.
EPIDEMIOLOGY
• GERD is one of the most common gastrointestinal disorders, with a
prevalence of approximately 20% of adults in western countries.
• A systematic review by El-Serag et al. estimated the prevalence of
GERD in the US between 18.1% to 27.8%. However, the true
prevalence of this disorder could be higher because more individuals
have access to over-the-counter acid, reducing medications.
• The prevalence of GERD is slightly higher in men compared to
women.
PATHOPHYSIOLOGY
• The pathophysiology of GERD is multifactorial and is best explained by
various mechanisms involved, including
• I)the influence of the tone of the lower esophageal sphincter,
• II)the presence of a hiatal hernia,
• III) esophageal mucosal defense against the refluxate and
• IV)esophageal motility.
ANATOMY

Three lower esophageal sphincter (LES) characteristics associated with gastro-

esophageal reflux disease (GERD) are, LES pressure = 6 mmHg, abdominal length
(AL) <1 cm and overall length (OL) <2 cm.
PATHOPHYSIOLOGY
Impaired Lower Esophageal Sphincter (LES) Function and Transient Lower Esophageal Sphincter Relaxations
(TLESRs)

• The LES is a 3-4 cm tonically contracted smooth muscle segment located at the
esophagogastric junction (EGJ) and, along with the crural diaphragm forms the
physiological EGJ barrier, which prevents the retrograde migration of acidic gastric
contents into the esophagus.
• LES maintains a high-pressure zone above intragastric pressures with transient
relaxation of the LES that occurs physiologically in response to a meal facilitating the
passage of food into the stomach.
• Patients with symptoms of GERD may have frequent transient LES relaxations
(TLESRs) not triggered by swallowing, resulting in exceeding the intragastric pressure
more than LES pressures permitting reflux of gastric contents into the esophagus.
• The LES tone and TLESRs are influenced by factors such as alcohol use, smoking,
caffeine, pregnancy, certain medications like nitrates, and calcium channel blockers
PATHOPHYSIOLOGY
HIATAL HERNIAS

• Hiatal hernia is frequently associated with GERD and plays a vital role in the
pathogenesis of GERD as it hinders the LES function.
• Patti et al. reported that patients with proven GERD with or without a small
hiatal hernia had similar LES function abnormalities and acid clearance.(Patti MG,
Goldberg HI, Arcerito M, Bortolasi L, Tong J, Way LW. Hiatal hernia size affects lower esophageal sphincter function, esophageal acid
exposure, and the degree of mucosal injury. Am J Surg. 1996 Jan;171(1):182-6.)

• However, patients with large hiatal hernias were noted to have shorter and
weaker LES resulting in increased reflux episodes.
• It was also pointed out that the degree of esophagitis was worse in patients
with large hiatal hernias. A study evaluating the relationship between hiatal
hernia and reflux esophagitis by Ott et al. demonstrated the presence of hiatal
hernia in 94% of patients with reflux esophagitis.
PATHOPHYSIOLOGY
IMPAIRED ESOPHAGEAL MUCOSAL DEFENSE AGAINST THE GASTRIC REFLUXATE

• The esophageal mucosa comprises various structural and functional

constituents that function as a protective defense barrier against the
luminal substances encountered with GERD.
• This defensive barrier can be breached by prolonged exposure to the
refluxate, which consists of both acidic gastric contents (hydrochloric
acid and pepsin) and alkaline duodenal contents (bile salts and
pancreatic enzymes) leading to mucosal damage.
• It is believed that delayed gastric emptying contributes to GERD
symptoms due to gastric distention and increased exposure to the
gastric refluxate.
PATHOPHYSIOLOGY
DEFECTIVE ESOPHAGEAL PERISTALSIS

• Normally, the acidic gastric contents that reach the esophagus are
cleared by frequent esophageal peristalsis and neutralized by salivary
bicarbonate.
• In a prospective study by Diener et al., 21% of patients with GERD
were noted to have impaired esophageal peristalsis leading to
decreased clearance of gastric reflux resulting in severe reflux
symptoms and mucosal damage.(De Giorgi F, Palmiero M, Esposito I, Mosca F, Cuomo R. Pathophysiology of
gastro-oesophageal reflux disease. Acta Otorhinolaryngol Ital. 2006 Oct;26(5):241-6.)
HISTOPATHOLOGY

• The esophageal squamous

epithelium serves to function as a
protective defense barrier against
the retrograde migration of refluxate.
• Disruption of this epithelial defense
is a common phenomenon in GERD.
• The histopathologic diagnosis of
GERD is made based on an array of
microscopic findings that include
features of inflammation, basal cell
hyperplasia, papilla elongation, and
dilatation of intercellular spaces.
PRESENTATION
• The typical clinical presentation of GERD is heartburn and regurgitation.
• Other symptoms include dysphagia, odynophagia, belching, epigastric pain,
and nausea.
• Heartburn is defined as a retrosternal burning sensation or discomfort that
may radiate into the neck and typically occurs after the ingestion of meals or
when in a reclined position.
• Regurgitation is a retrograde migration of acidic gastric contents into the
mouth or hypopharynx.
• GERD presentation is considered to be atypical when patients present with
extra-esophageal symptoms such as chest pain, chronic cough, asthma,
laryngitis, dental erosions, dysphonia, and hoarseness, and globus sensation. 
INVESTIGATIONS
• ENDOSCOPY

• Able to visualize mild changes which include mucosal erythema,

edema, hyper- vascularity, friability, and blurring of the
SquamoColumnarJunction.

• The best validated and most widely used classification system

for reflux esophagitis now is the Los Angeles classification.
 ENDOSCOPY
Los Angeles classification.
• (a) Grade A is defined as mucosal breaks confined to the
mucosal fold, each no longer than 5 mm.
• (b) Grade B corresponds to at least one mucosal break longer
than 5 mm confined to the mucosal fold but
not continuous between two folds.
• (c) Grade C is characterized by mucosal breaks that are
continuous between the tops of mucosal folds but
not circumferential.
• (d) Finally, grade D is represented by extensive mucosal
breaks engaging at least 75% of the esophageal
circumference.
 BARIUM STUDY
• It is used to:
• Evaluate the entire anatomy of
esophagus,
•Document the presence and
size of a hiatal hernia,
• Stricture severity and location,
• Diverticula, esophageal
emptying, and the presence of
gastroesophageal reflux, both
spontaneously and induced by
provocative maneuvers.
ESOPHAGEAL MANOMETRY

• • Most accurate method to assess the coordination and

pressure of the lower esophageal sphincter (LES) and the
esophageal body.
• Findings in GERD is a defective LES or impaired esophageal
motility.
• It is an important component in the preoperative workup of
antireflux surgery.
• Excludes achalasia that may be occasionally misdiagnosed
as
GERD.
Characterizes the esophageal motility, and this information
will be used to determine the surgical approach (Nissen or
partial fundoplication).
Esophageal Reflux Testing

• • Ambulatory intraesophageal pH monitoring is still the

standard for establishing pathologic acid reflux.
• Ambulatory esophageal reflux monitoring can assess the
correlation of symptoms with abnormal acid exposure.
• It is indicated in medically refractory GERD and in patients
with extraesophageal symptoms suspicious for GERD.
• Ambulatory reflux (pH or in combination with impedance)
monitoring employs the utility of a telemetry pH capsule
or a transnasal catheter.
• It is the only available test that detects pathological acid
exposure, frequency of reflux episodes, and correlation of
symptoms with reflux episodes.
• Current practice guidelines recommend mandatory
preoperative ambulatory pH monitoring in patients
without evidence of erosive esophagitis
Empirical Trial of Acid Suppression

• • High PPI dose (e.g., omeprazole 40 to 80 mg/day), usually

• given for at least 2 weeks, and a positive response was
• defined as at least 50% improvement in heartburn.
• • Using this approach, the PPI empirical trial has a sensitivity of
68% to 83% but poor specificity for determining the presence
of GERD
However, a meta-analysis published literature by Numans et al. refuted
the accuracy of this empiric PPI trial diagnostic strategy(Numans ME, Lau J, de Wit NJ,
Bonis PA. Short-term treatment with proton-pump inhibitors as a test for gastroesophageal reflux disease: a meta-analysis of
diagnostic test characteristics. Ann Intern Med. 2004 Apr 06;140(7):518-27.)
TREATMENT
• The goals of managing GERD are to address the resolution of
symptoms and prevent complications such as esophagitis, BE, and
esophageal adenocarcinoma.
• Treatment options include lifestyle modifications, medical
management with antacids and antisecretory agents, surgical
therapies, and endoluminal therapies.
LIFESTYLE MODIFICATION
• Sleep and body position- Patients with nighttime GERD should begin the sleeping period with the left side
down. - Decrease in transient
lower esophageal sphincter relaxations (TLESRs) on the left side as compared to the right.
• • Refrain from eating within 2 to 3 hours of going to sleep as reflux is more frequent in the first half of the
sleep
•  Alcohol - Alcohol is a smooth muscle relaxant and reduces lower esophageal sphincter pressure (LESP).
Should be used judiciously.
• Studies have also shown improvement in GERD symptoms and pH monitoring studies with the elevation of the
head end of the bed.
• Diet modification with the elimination of chocolate, caffeine, and spicy foods, citrus, and carbonated
beverages in GERD is controversial and is not routinely recommended as per current ACG guidelines
• Smoking May increase esophageal sensitivity to acid by impairing intracellular regulation of pH.
Smoking cessation in individuals with GERD has been shown to reduce the number of upright reflux episodes.
• Weight gain has been associated with an increased risk of symptoms of GERD and weight loss associated with
a decrease in risk.
MEDICAL THERAPY
• H2 RECEPTOR ANTAGONISTS
• Antisecretory capabilities are best at night, with duration of acid
inhibition longer when the drug is taken in the evening or before
bedtime.
• • Esophagitis healing rates with H2RAs rarely exceeded 60% after up
to 12 weeks.
• •Grades I and II esophagitis heal in 60% to 90% of patients,
• • grades III and IV heal in only 30% to 50% despite high-dose
Proton Pump Inhibitor

• Superior efficacy compared with H2RAs on the basis of their

ability to maintain an intragastric Ph > 4 from 10 to 14 hours
daily compared with Approximately 6 to 8 hours daily with the
H2RAs
• Some patients need an increase in PPI dose because of
incomplete symptom relief, extra esophageal symptoms, or
Barrett esophagus.
• Healing of even severe ulcerative esophagitis after 8 weeks in
more than 80% of patients taking PPIs, compared with 51% on
H2RAs and 28% receiving placebo.
TREATMENT {CONTD)
• Alginates
• Alginic acid derivatives, or alginates, treat GERD via a unique mechanism by creating a
mechanical barrier that displaces the postprandial acid pocket.
• In the presence of gastric acid, they form a raft that localizes to the acid pocket in the proximal
stomach.
• Prokinetics
• • Although prokinetics may theoretically alleviate the pathophysiology of GERD by increasing
gastric and esophageal emptying, the evidence behind their clinical efficacy as add on therapy
over PPI is lacking.
• Transient Lower Esophageal Sphincter Relaxation Inhibitors
• Baclofen (5 to 20 mg 3 times daily) significantly reduces tLESRs, decreases both acid and
duodenal reflux, and improves symptoms in GERD patients treated for 4 weeks to several
months
SURGICAL MANAGEMENT
• ANTI REFLUX SURGERY
• Primary Indications for Antireflux Surgery
• (1) healthy patients with typical or atypical GERD symptom swell controlled on PPIs, desiring
alternative therapy because of drug expense, poor medication compliance, or fear of possible
long-term side effects;
• (2) patients with volume regurgitation and aspiration symptoms not controlled on PPIs
• (3) GERD complications such as peptic stricture, Barrett esophagus, or vocal cord injury

• Antireflux surgery reduces acid and nonacid GERD by

• Increasing basal LES pressure,
• Decreasing transient Lower Esophageal Sphincter Relaxations,
• Inhibiting complete LES relaxation
TYPES OF SURGERY
SURGICAL TECHNIQUE SELECTION
• Early uncomplicated disease :
• Trans-abdominal Nissen (laparoscopic) fundoplication. superior operation with better
long-term durability, but it causes more postoperative dysphagia and gas bloat symptoms.
• Decreased motility :
• Although surgery cannot directly influence esophageal motility in patients with GERD,
Nissen fundoplication can lead to improvement in esophageal contraction amplitude.
• Normal length but decreased motility :
• Complete fundoplication is discouraged. Toupet or Hill could be performed.
• Shortened esophagus :
• Collis (esophageal lengthening) gastroplasty combined with an intra-abdominal or
intrathoracic fundoplication.
Novel Endoscopic/Surgical Therapies

• The newest approach is the

transoral incisionless
fundoplication which recreates at
200- to 270-degree value using
polypropylene fasteners placed
endoscopically.
• Over time the fasteners tend to
dislodge, with a systematic review
reporting GERD symptom
recurrence in 60% of patients
with a similar rate back on PPIs.
COMPLICATIONS
• Erosive Esophagitis (EE)
• EE is characterized by erosions or ulcers of the esophageal mucosa.The degree of esophagitis is endoscopically
graded using the Los Angeles esophagitis classification system, which employs the A, B, C, D grading system based
on variables that include length, location, and circumferential severity of mucosal breaks in the esophagus .
• Esophageal Strictures
• Chronic acid irritation of the distal esophagus can result in scarring of distal esophagus leading to the formation of
a peptic stricture. Patients can present with symptoms of esophageal dysphagia or food impaction.
• ACG guidelines recommend esophageal dilation and continue PPI therapy to prevent the need for repeated
dilations .
• Barrett Esophagus
• This complication occurs as a result of chronic pathological acid exposure to the distal esophageal mucosa. It leads
to a histopathological change of the distal esophageal mucosa, which is normally lined by stratified squamous
epithelium to metaplastic columnar epithelium. Barrett's esophagus is more commonly seen in Caucasian males
above 50 years, obesity, and history of smoking and predisposes to the development of esophageal
adenocarcinoma. Current guidelines recommend the performance of periodic surveillance endoscopy in patients
with a diagnosis of Barrett's esophagus.
References
• -Schwartz’s principles of surgery.
• - .(De Giorgi F, Palmiero M, Esposito I, Mosca F, Cuomo R.
Pathophysiology of gastro-oesophageal reflux disease. Acta
Otorhinolaryngol Ital. 2006 Oct;26(5):241-6