GERD – Schwartz 2004

Gastroesophageal reflux disease (GERD) is a common disease that accounts for

approximately 75% of esophageal pathology. Despite its high prevalence, it can be
one of the most challenging diagnostic and therapeutic problems in benign
esophageal disease. A contributing factor to this is the lack of a universally
accepted definition of the disease. 3 approaches are available

• Define the disease by its symptoms: these symptoms are not specific for
GERD, and can be caused by other diseases such as achalasia, diffuse spasm,
esophageal carcinoma, pyloric stenosis, cholelithiasis, gastritis, gastric or
duodenal ulcer, and coronary artery disease.

• the presence of endoscopic esophagitis. Using this criterion for diagnosis

assumes that all patients who have esophagitis have excessive regurgitation
of gastric juice into their esophagus. This is true in 90% of patients, but in
10% the esophagitis has other causes, the most common being unrecognized
chemical injury from drug ingestion.

• measure the basic pathophysiologic abnormality of the disease; that

is, increased exposure of the esophagus to gastric juice. In the past this was
inferred by the presence of a hiatal hernia, later by endoscopic esophagitis,
and more recently by a hypotensive LES pressure. measurement of
esophageal exposure to gastric juice by calculating the percentage of time
the pH was less than 4 over a 24-hour period.

PATHOPHYSIOLOGY OF GASTROESOPHAGEAL REFLUX

The human Antireflux mechanism consists of a pump, the esophageal body motor
function, and a valve, the LES.
GERD – Schwartz 2004

First the valve: GERD starts in the stomach (Fig. 24-37). It is caused by gastric
distention due to overeating or ingestion of fried foods, typical of the Western diet,
which delays gastric emptying. Gastric distention causes unfolding of the sphincter
as it is taken up by the distended fundus and exposure of the terminal squamous
epithelium within the sphincter to noxious gastric juice. Signs of injury to the
exposed squamous epithelium are erosions, ulceration, fibrosis, and columnar

metaplasia, with an inflammatory infiltrate or foveolar hyperplasia. Intestinal

metaplasia within the sphincter may result, as in Barrett's metaplasia of the
esophageal body. This process results in the loss of muscle function, and the
sphincter becomes mechanically defective, allowing free reflux with progressively
higher degrees of mucosal injury.

Structural damage to the components of the LES, such as loss of pressure,

inadequate overall length, or the loss of abdominal length—i.e., the portion
exposed to the positive-pressure environment of the abdomen as measured by
manometry—results in permanent failure of sphincter function. The probability of
increased exposure to gastric juice is 73% if one component of the sphincter is
abnormal, 74% if two components are abnormal, and 92% if all three are abnormal.
This indicates that the failure of one or two of the components of the sphincter may
be compensated for by the clearance of the esophageal body. Failure of all three
sphincter components inevitably leads to increased esophageal exposure to gastric
juice.

The second portion of the human antireflux mechanism is an effective esophageal

pump that clears the esophagus after physiologic reflux episodes. Ineffective
esophageal clearance can result in an abnormal esophageal exposure to gastric
juice in individuals who have a normal LES and gastric function, but fail to clear
physiologic reflux episodes. This situation is relatively rare, and ineffectual
GERD – Schwartz 2004

clearance is more apt to be seen in association with a structurally defective

sphincter, which augments the esophageal exposure to gastric juice by prolonging
the duration of each reflux episode.

Four factors important in esophageal clearance are gravity, esophageal motor

activity, salivation, and anchoring of the distal esophagus in the abdomen.

Manometry of the esophageal body can detect failure of esophageal clearance by

analysis of the pressure amplitude and speed of wave progression through the
esophagus.

Salivation contributes to esophageal clearance by neutralizing the minute amount

of acid that is left following a peristaltic wave. Return of esophageal pH to normal
takes significantly longer if salivary flow is reduced, such as after radiotherapy, and
is shorter if saliva is stimulated by sucking lozenges. Saliva production may also be
increased by the presence of acid in the lower esophagus. The patient experiences
excessive mucus in the throat. Clinically, this is referred to as "water brash."

A hiatal hernia can also contribute to an esophageal propulsion defect due to loss of
anchorage of the esophagus in the abdomen. This results in a reduction in the
efficiency of acid clearance (Fig. 24-39). Kahrilas has shown that complete
esophageal emptying without retrograde flow was achieved in 86% of test swallows
in control subjects without a hiatal hernia, 66% in patients with a reducing hiatal
hernia, and only 32% in patients with a nonreducing hiatal hernia. Impaired
clearance in patients with nonreducing hiatal hernias suggests that the presence of
a hiatal hernia contributes to the pathogenesis of GERD.

COMPLICATIONS OF GASTROESOPHAGEAL REFLUX

The complications of gastroesophageal reflux result from the damage inflicted by

gastric juice on the esophageal mucosa or respiratory epithelium, and changes
caused by their subsequent repair and fibrosis. Complications due to repetitive
reflux are esophagitis, stricture, and Barrett's esophagus; repetitive aspiration may
lead to progressive pulmonary fibrosis. The severity of the complications is directly
related to the prevalence of a structurally defective sphincter

Complications of gastroesophageal reflux such as esophagitis, stricture, and

Barrett's metaplasia occur in the presence of two predisposing factors: a
mechanically defective LES and an increased esophageal exposure to fluid with a
pH of less than 4 and greater than 7.

The duodenal origin of esophageal contents in patients with an increased exposure

to a pH greater than 7 has been confirmed by esophageal aspiration studies.
GERD – Schwartz 2004

Studies have clarified and expanded these observations by measuring esophageal

bilirubin exposure over a 24-hour period as a marker for the presence of duodenal
juice. Direct measurement of esophageal bilirubin exposure as a marker for
duodenal juice has shown that 58% of patients with GERD have increased
esophageal exposure to duodenal juice, and that this exposure occurs most
commonly when the esophageal pH is between 4 and 7. Furthermore, it is
associated with more severe mucosal injury

The fact that the combination of refluxed gastric and duodenal juice is more noxious
to the esophageal mucosa than gastric juice alone may explain the repeated
observation that 25% of patients with reflux esophagitis develop recurrent and
progressive mucosal damage, often despite medical therapy. A potential reason is
that acid suppression therapy is unable to consistently maintain the pH of refluxed
gastric and duodenal juice above the range of 6. Lapses into pH ranges from 2 to 6
encourage the formation of undissociated, nonpolarized, soluble bile acids, which
are capable of penetrating the cell wall and injuring mucosal cells. To assure that
bile acids remain completely ionized in their polarized form, and thus unable to
penetrate the cell, requires that the pH of the refluxed material be maintained
above 7, 24 hours a day, 7 days a week, for the patient's lifetime. In practice this
would not only be impractical but likely impossible, unless very high doses of
medications were used. The use of lesser doses would allow esophageal mucosal
damage to occur while the patient was relatively asymptomatic. Antireflux
operative procedures re-establish the barrier between stomach and esophagus,
protecting the esophagus from damage in patients with mixed gastroesophageal
reflux.

MEDICAL THERAPY

The response to acid-suppressing medications predicts success and symptom relief

after surgery. In contrast to the widely held belief that failure of medical therapy is
an indication for surgery, a good response to proton pump inhibitors is desirable, as
it predicts that the symptoms are actually due to reflux of gastric contents.

When first seen with symptoms of heartburn without obvious complications,

patients can reasonably be placed on 8 to 12 weeks of simple antacids before
extensive investigations are carried out.

Patients should be advised to elevate the head of the bed; avoid tight clothing; eat
small, frequent meals; avoid eating their nighttime meal shortly before retiring; lose
weight; and avoid alcohol, coffee, chocolate, and peppermint, which may aggravate
the symptoms.

SUGGESTED THERAPEUTIC APPROACH

The traditional stepwise approach to the therapy of GERD should be re-examined in

view of a more complete understanding of the pathophysiology of gastroesophageal
reflux, the rising incidence of Barrett's esophagus, and the increasing mortality
GERD – Schwartz 2004

rates associated with end-stage reflux disease. The approach should be to identify
risk factors for persistent and progressive disease early in the course of the disease,
and encourage surgical treatment when these factors are present. The following
approach is suggested.
GERD – Schwartz 2004
GERD – Schwartz 2004

SELECTION CRITERIA OF PATIENTS FOR SURGERY

One should not be deterred from considering antireflux surgery in a

symptomatic patient with or without esophagitis or a defective sphincter, provided
the disease process has been objectively documented by 24-hour pH monitoring.
This is particularly true in patients who have become dependent upon therapy with
PPIs, or require increasing doses to control their symptoms. It is important to note
that a good response to medical therapy in this group of patients predicts an
excellent outcome following antireflux surgery.

Approximately 25 to 50% of the patients with GERD have persistent or

progressive disease, and it is this patient population that is best suited to surgical
therapy.

• Structurally defective LES: failure of medical ttt – surgery with or without

esophagitis or erosions

• Young patients with documented reflux disease with or without a

defective LES: cost-benefit ration in favor of surgery against life long ttt
(especially under 49 years)

• Complications:

o Stricture in a patient represents a failure of medical therapy.

Malignancy and a drug-related etiology of the stricture should be
excluded, and the stricture progressively dilated up to a 60F bougie.
Then fundoplication is performed after manometry to assess
esophageal motility function.

o Barrett's columnar-lined esophagus. Patients with Barrett's

esophagus are at risk of progression of the mucosal abnormality up
the esophagus, formation of a stricture, hemorrhage from a Barrett's
ulcer, and the development of an adenocarcinoma. An antireflux
procedure may arrest the progression of the disease, heal ulceration,
resolve strictures and reduces the risk of progression to cancer. If
severe dysplasia or intramucosal carcinoma is found on mucosal
biopsy specimens, an esophageal resection should be done.

PREOPERATIVE EVALUATION

1. The propulsive force of the body of the esophagus should be

evaluated by esophageal manometry to determine if it has sufficient power
to propel a bolus of food through a newly reconstructed valve. Motility
disorders require partial fundoplication.

2. Anatomic shortening of the esophagus can compromise the ability

to do an adequate repair without tension, and lead to an increased incidence
GERD – Schwartz 2004

of breakdown or thoracic displacement of the repair. Esophageal shortening

is identified on a barium swallow roentgenogram by a sliding hiatal hernia
that will not reduce in the upright position, or that measure larger than 5 cm
between the diaphragmatic crura and gastroesophageal junction on
endoscopy.

3. The surgeon should specifically query the patient for complaints of

nausea, vomiting, and loss of appetite. They can be due to excessive
duodenogastric reflux or gastric pathology. This problem is most pronounced
in patients who have had previous upper gastrointestinal surgery,
particularly cholecystectomy. These symptoms may persist after an
antireflux procedure, and patients should be given this information before
the operation. 24-hour bilirubin monitoring and gastric emptying studies can
be performed to detect and quantify duodenogastric abnormalities.

4. Approximately 30% of patients with proven gastroesophageal reflux on

24-hour pH monitoring will have hypersecretion on gastric analysis, and
2 to 3% of patients who have an antireflux operation will develop a gastric or
duodenal ulcer. The presence of Helicobacter pylori should be assessed in
these patients and treated if present.

PRINCIPLES OF SURGICAL PROCEDURES

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 by a method that ensures its response to changes in intra-
abdominal pressure.

3. The operation should allow the reconstructed cardia to relax on

deglutition.

To ensure relaxation of the sphincter, three factors are important:

• Only the fundus of the stomach should be used to buttress the

sphincter, since it is known to relax in concert with the sphincter;

• The gastric wrap should be properly placed around the

sphincter and not incorporate a portion of the stomach or be placed
around the stomach itself, since the body of the stomach does not
relax with swallowing; and
GERD – Schwartz 2004

• Damage to the vagal nerves during dissection of the thoracic

esophagus should be avoided because it may result in failure of the
sphincter to relax.

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. The resistance of the relaxed sphincter depends on the
degree, length, and diameter of the gastric fundic wrap, and on the variation
in intra-abdominal pressure. A 360 degree gastric wrap should be no longer
than 2 cm and constructed over a 60F bougie. This will ensure that the
relaxed sphincter will have an adequate diameter with minimal resistance.
This is not necessary when constructing a partial wrap.

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.

PROCEDURE SELECTION

• A laparoscopic approach is used in patients with normal esophageal

contractility and length.

• Transthoracic approach is used for patients with questionable esophageal

length. where full esophageal mobilization serves as a lengthening
procedure.

• Those with a failed esophagus characterized by absent esophageal

contractions and/or absent peristalsis such as those with scleroderma are
best treated either medically or with a partial fundoplication in order to
avoid the increased outflow resistance associated with a complete
fundoplication.

• If the esophagus is short after it is mobilized from diaphragm to aortic arch, a

Collis gastroplasty is done to provide additional length and avoid placing
the repair under tension.

• In the majority of patients who have good esophageal contractility and

normal esophageal length, the laparoscopic Nissen fundoplication is the
procedure of choice for a primary antireflux repair

NISSEN FUNDOPLICATION

Modifications of the procedure as originally described. These include using only the
gastric fundus to envelop the esophagus in a fashion analogous to a Wetzel
jejunostomy, sizing the fundoplication with a 60F bougie, and limiting the length of
the fundoplication to 1 to 2 cm. The essential elements necessary for the
GERD – Schwartz 2004

performance of a transabdominal fundoplication are common to both the

laparoscopic and open procedures and include the following:

1. Crural dissection, identification, and preservation of both vagi, and the

anterior hepatic branch
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 placing the posterior fundic wall
posterior, and the anterior fundus anterior, to the esophagus, meeting at the
right lateral position

Step 4: Postoperative Care

• Clear liquids the night of surgery

• No bread, no meat, and no carbonated beverages the next morning;
maintained for 2 weeks postoperatively
• Antiemetics given at scheduled times for the first 24 hours, to avoid early
retching and early recurrence
• Discharged with prescription for antiemetics
• Swallow only if issues
• Follow up at 2 weeks postoperatively and liberalize diet