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26 Braveman, Khitin, and Brams
Fig. 1. Barium swallow demonstrating “bird-beak” narrowing of esophagus typical of achalasia.
TREATMENT OPTIONS
It is impossible to restore normal peristaltic function of esophagus. The treatment of
achalasia focuses on relieving the distal esophageal obstruction at the lower esophageal
sphincter (LES). The most common methods include balloon dilation, botulinum toxin
(Botox) injection, and Heller myotomy.
Pneumatic balloon dilation is performed endoscopically with intravenous (iv) sedation. The muscle fibers of the distal esophagus are disrupted without causing perforation
of the mucosa. A volume-limited, pressure-controlled (Gruntzig-type) catheter is placed
across the gastroesophageal junction. The esophagus is then forcefully dilated to a
pressure of 300 Torr for 15 s. A contrast swallow is performed immediately following
to confirm the absence of a perforation
Most people report some symptomatic relief from pneumatic dilation. Approximately
60% of patients have relief of dysphagia and an additional 10% respond to a second
dilation. There is recurrence of dysphagia over time in 10% to 70% of patients requiring
redilation. The incidence of esophageal perforation following dilation is approx 4% with
a mortality of 0.5%. Gastroesophageal reflux occurs in 20 to 40% of patients (3).
Intrasphincteric injection of the LES with Botox through the flexible endoscope represents a newer modality for treating achalasia. The toxin blocks release of acetylcholine
from the presynaptic parasympathetic nerve endings in the smooth muscle producing a
Chapter 3 / Esophagectomy for Achalasia 27
denervation of the LES. The immediate results are excellent, with 70% to 100% of
patients experiencing relief within the first month. However, favorable results are
reported by 60% of patients by 6 mo, and by only 3 to 36% of patients at 1 yr. Repeat
treatments offer transient improvement, but beyond 6 mo, the results are negligible.
Although there are relatively few immediate complications with Botox injection, these
injections induce scarring and inflammation around the esophagus, making subsequent
surgical intervention more difficult (4).
SURGICAL MANAGEMENT
Heller esophagomyotomy is the optimal treatment of achalasia. This procedure
allows for the precise division of the longitudinal and circular muscles of the lower
esophagus, thus relieving the functional obstruction of distal esophagus. Although the
Heller myotomy was first performed transthoracically, the development of video-assisted
minimally invasive techniques has led to the development of a laparoscopic approach
that is equally effective but with minimal morbidity.
INDICATIONS
All patients who can tolerate general anesthesia and laparoscopy should be candidates
for surgery. In particular, patients under 40 yr of age have worse results with pneumatic
dilation, whereas Heller myotomy offers a 90% long-term success rate (5). Patients who
have failed other forms of therapy such as Botox injection or pneumatic dilation are
surgical candidates. These patients may have scarring in the distal esophagus increasing
the difficulty of the myotomy and increasing the mucosal perforation rate, but they have
equivalent outcomes with little additional morbidity (6).
CONTRAINDICATIONS
The surgery is contraindicated in patients with severe cardiopulmonary disease or
other morbidities that will put them at a higher risk for general anesthesia. These patients
may be treated with dilation or Botox injection. Patients with overwhelming cardiopulmonary risk may be treated with percutaneous endoscopically placed gastrostomy tube
for alimentation.
SURGICAL TECHNIQUE
The traditional approach to Heller myotomy is through a left thoracotomy in the
seventh intercostal space. The distal esophagus and proximal stomach are mobilized.
The longitudinal and circular muscles of the esophagus are incised from the inferior
pulmonary vein across the gastroesophageal junction completing the myotomy a variable distance onto the stomach. The muscle is dissected away from the mucosa allowing
the strong mucosal layer to protrude. A longer myotomy allows complete disruption of
the lower esophageal sphincter, relieving dysphagia but increasing the risk of reflux. To
optimize results, many surgeons add a partial fundoplication to a long myotomy. The
chest is closed with placement of chest tubes. Patients are hospitalized for 4–7 d.
Laparoscopic Heller myotomy is the optimal procedure performed today, with excellent results and minimal morbidity. The procedure should be performed by surgeons
with advanced laparoscopic skills who have experience with this relatively unusual
28 Braveman, Khitin, and Brams
Fig. 2. Schematic of Heller esophagomyotomy. Longitudinal and circular esophageal muscles
are divided from distal esophagus and incision extended to proximal part of stomach and mucosal
layer is exposed.
Fig. 3. Partial fundoplication after myotomy.
disease. The surgery is performed under general anesthesia. Five laparoscopic trocars are
placed. The peritoneum overlying the distal esophagus is divided and the anterior esophagus
is exposed after inducing pneumoperitoneum. The anterior vagus nerve is identified and
protected. With laparoscopic magnification, the longitudinal and circular muscles are carefully divided, exposing the mucosal layer (Fig. 2). The myotomy is now extended proximally
6 cm from the G–E junction and distally 1 cm onto the proximal stomach. The muscle is
Chapter 3 / Esophagectomy for Achalasia 29
Fig. 4. Postoperative barium swallow.
dissected from the mucosa allowing the mucosa to protrude. Intraoperative flexible endoscopy is then performed to be certain there is no further distal obstruction. The myotomy can
be easily extended if necessary until the lower esophageal sphincter is ablated. Air is insufflated into the esophagus and the distended mucosa is assessed for evidence of perforation.
Once the myotomy is completed, an antireflux procedure is added. A 360°
fundoplication (Nissen) will cause dysphasia. Therefore, a partial fundoplication is
added. Some surgeons completely mobilize the G–E junction and perform a posterior
270° partial Toupet fundoplication. We favor an anterior 180° Dor fundoplication that
protects against reflux, yet does not require disruption of all the phrenoesophageal
attachments (Fig. 3). In the Dor fundoplication, the proximal fundus is sutured to the
hiatus and the divided esophageal musculature (Fig. 4).
The instruments and trocars are removed. The 0.5-cm to 1-cm incisions are closed
®
with absorbable sutures and Band-Aids
. Nasogastric tubes are not necessary. The patient
begins a liquid diet that evening and is discharged the following day. Dysphagia is
immediately improved. The postoperative pain, recovery, and return to work are similar
to that seen in elective laparoscopic cholecystectomy.
30 Braveman, Khitin, and Brams
COMPLICATIONS
Complications are uncommon with this procedure. Mucosal perforation occurs in
approx 4.5% of cases. If identified at the time of surgery, it is easily managed with simple
repair of the mucosa. Death is extremely uncommon, reported at 0.1%. Early complications occur in approx 5% of cases and include pneumonia, deep venous thrombosis,
urinary tract infection, paraesophageal hernia, subphrenic abscess, pleural effusion,
esophageal ulcer, and peptic ulcer.
Gastroesophageal reflux can occur after Heller myotomy. Pathologic reflux can be
subclinical in 50% of patients, but it can be shown on ambulatory pH testing. When
myotomy is performed without an antireflux procedure, reflux occurs in at least 25% of
patients, but it occurs in less than 10% of patients who have a concurrent antireflux
procedure. Reflux should be treated even if subclinical with acid-suppressive therapy to
avoid peptic ulceration and stricture.
Recurrent obstruction may occur as a result of several causes. The patient may have
had an inadequate myotomy or a fundoplication causing obstruction. The patient may
develop a peptic stricture if subclinical reflux occurs. The nature of the obstruction can
be investigated with barium swallow. Forceful dilation or reoperation may improve
these patients. In a few cases, esophagectomy may provide definitive management.
COST OF PROCEDURE
The cost for this procedure is approx $8000. This includes hospital charges for the
operating room, one night of hospitalization, and professional fees. There are few studies
comparing cost between pneumatic dilation, Botox, and Heller myotomy. These studies
are limited by their lack of extended follow-up, absence of quality-of-life assessment;
and changes in the hospitalization pattern for pneumatic dilation (fewer overnight
admissions). However, for a 5–7-yr period, laparoscopic Heller myotomy is the most
expensive option and the pneumatic dilation the least. Botox injection, in these studies,
is similar in cost to pneumatic dilation (7).
RESULTS OF HELLER MYOTOMY
Although there are no randomized prospective trials comparing surgical therapy with
medical therapy, there is data on the outcome of patients undergoing laparoscopic esophageal myotomy. Several excellent series have been published. Dysphagia was relieved
in more than 90% of patients with a follow-up of 2 yr (8). The largest published series
of 133 patients by Patti et al. reported excellent results in 90% of patients with a mean
follow-up of 28 mo (9).
SUMMARY
1. Achalasia is a neurological disease of the esophagus characterized by an aperistaltic body
and poor relaxation of LES.
2. Dysphagia and regurgitation with eventual weight loss are usual presenting complaints.
3. The diagnosis may be made with a barium swallow, but should be followed with upper
endoscopy and manometric studies.
4. Laparoscopic Heller myotomy with partial fundoplication is the optimal treatment for
patients with acceptable surgical risk. Ninety percent of patients report excellent results
with this minimally invasive procedure.
Chapter 3 / Esophagectomy for Achalasia 31
5. Pneumatic dilation and botulinum toxin injection are alternatives for patients who have
unacceptable surgical risk factors. In patients who are surgical candidates, these nonsurgical interventions should be avoided as first-line therapies because they increase the risk
of esophageal perforation if surgery is performed.
REFERENCES
1. Ellis FH, Olsen AM. Achalasia of the Esophagus. Major Problems in Clinical Surgery, Volume IX.
W.B. Saunders, Philadelphia, 1969.
2. Wong KH, Maydonovitch CL. Achalasia. In: The Esophagus. (Castell DO, Richter JE, eds.) Lippincott
Williams & Williams, Philadelphia, 1999, pp. 185–213.
3. Katz PO, Gilbert J, Castell DO. Pneumatic dilation is effective long-term treatment for achalasia. Dig
Dis Sci 1998;43:1973–1977.
4. Pasricha PJ, Ravich WJ, Hendrix TR, et al. Intrasphicteric botulinum toxin for the treatment of
achalasia. N Engl J Med 1995;332:774–778.
5. Spiess AE, Kahrilas PJ. Treating achalasia: from whalebone to laparoscope. JAMA 1998;280:638–642.
6. Hunter JG, Richardson WS. Surgical management of achalasia. Surg Clin N Am 1997;77:993–1015.
7. Richter JE. Comparison and cost analysis of different treatment strategies in achalasia. Gastrointest
Endosc Clin N Am 2001;11:359–370.
8. Zaninotto G, Costantini M, Molena D, et al. Treatment of esophageal achalasia with laparoscopic
Heller myotomy and Dor partial fundoplication: Prospective evaluation of 100 consecutive patients.
J Gastrointest Surg 2000;4:282–289.
9. Patti MG, Pellgrini CA, Horgan S, et al. Minimally Invasive Surgery for Achalasia: An 8-year expe-
rience with 168 patients. Ann Surg 1999;230:587–594.
32 Braveman, Khitin, and Brams
Chapter 4 / Surgery for GERD 33
4
Surgery for Gastroesophageal
Reflux Disease
Lev Khitin, MD and David M. Brams, MD
CONTENTS
INTRODUCTION
PATHOPHYSIOLOGY OF GERD
SYMPTOMS OF GERD
INDICATIONS FOR SURGERY
CONTRAINDICATIONS TO SURGERY
PREOPERATIVE EVALUATION
LAPAROSCOPIC FUNDOPLICATION: CONDUCT OF OPERATION
RESULTS AND COMPLICATIONS
ALTERNATIVE PROCEDURE
COST
SUMMARY
REFERENCES
INTRODUCTION
Gastroesophageal reflux disease (GERD) is one of the most common problems seen
in medical practice. Approximately 10% of the U.S. population experiences heartburn
daily, and 40% of the population has heartburn monthly. Seven percent of the population (40 million individuals) use over-the-counter antacids, H-2 receptor antagonists,
or proton pump inhibitors at least twice weekly to relieve GERD symptoms. Surgical
management of GERD is an effective alternative to medical management of GERD, and
it is being more commonly employed (1).
Antireflux surgery was first performed in the 1950s. Diagnostic modalities and technical details evolved during the ensuing 30 yr, yielding superb results from antireflux
procedures. However, these procedures, which necessitated thoracotomy or laparotomy,
were usually only employed in the most severe cases refractory to medical management.
The advent of minimally invasive videoscopic surgery has revolutionized the surgical
management of GERD. The transabdominal Nissen fundoplication, which has a greater
than 90% effectiveness in treating GERD, became a laparoscopic procedure with equiva-
From: Clinical Gastroenterology: An Internist's Illustrated Guide to Gastrointestinal Surgery
Edited by: George Y. Wu, Khalid Aziz, and Giles F. Whalen © Humana Press Inc., Totowa, NJ
33
34 Khitin and Brams
lent results to the open Nissen, but with minimal postoperative pain and a rapid return
to normal activities. The minimally invasive laparoscopic Nissen fundoplication (LNF)
is now increasingly utilized in treating GERD (1,2).
LNF was initially performed only at referral centers. As experience with this procedure has grown, surgeons who perform advanced laparoscopy are routinely performing
LNF in community hospitals. As with many laparoscopic procedures, there is a learning
curve of 30 to 50 operations. When this curve is surmounted, operative times and complications decrease and long-term successful antireflux repair is achieved (2).
This chapter will discuss the pathophysiology of GERD, treatment options, indications for surgery, necessary preoperative evaluations, a description of LNF, alternative
antireflux procedures, and LNF’s results, complications, and costs.
PATHOPHYSIOLOGY OF GERD
Gastroesophageal reflux is multifactorial in etiology. The three major determinants
of GERD include transient lower esophageal sphincter (LES) relaxation with normal
resting LES pressure, anatomical disruption of gastroesophageal junction associated
with hiatal hernia, and hypotensive LES. The LES is not a discrete anatomic structure;
rather, it is a high-pressure zone that exists because of the anatomic relationships of the
distal esophagus, stomach, and diaphragm. The factors that contribute to the LES are as
follows: intrinsic esophageal and gastric musculature, relationship of the esophagus to
the gastric fundus, and relationship of the distal esophagus to the diaphragm (2,3).
The distal esophageal musculature is contracted in the resting state, but it completely
relaxes on swallowing. The orientation of the musculature of the cardia of the stomach
contributes to the LES. The relationship of the distal esophagus to the gastric fundus
(which compresses the distal esophagus when the stomach is distended) also contributes
to this high-pressure zone (4).
The relationship of the distal esophagus to the diaphragm stops reflux (Figs. 1–3).
Normally, the distal esophagus rests within the abdomen. As the esophagus traverses the
hiatus, the crura of the diaphragm compress the esophagus, increasing LES pressure.
This compression is maximal during inspiration, when intrathoracic pressure decreases
and risk of reflux is greatest. The intraabdominal pressure is also greater than that of the
thorax. This high-pressure zone is transmitted to the distal intraabdominal esophagus,
thus contributing to the LES pressure (4,5).
Pathologic reflux occurs if the elements contributing to the LES are dysfunctional. In
the absence of a primary esophageal motility disorder, the most common cause of reflux
and a low LES pressure is a Type I or sliding hiatal hernia (Fig. 4). A sliding hiatal hernia
develops when there is a laxity of the phrenoesophageal attachments. High intraabdominal
and negative intrathoracic pressures cause the distal esophagus and gastric cardia to
migrate into the chest, lowering the LES pressure and allowing reflux to occur (2,4,5).
Antireflux procedures augment the LES pressure by returning the distal esophagus to
abdomen. The relationship of the esophagus to the diaphragm and fundus is restored by
repairing the hiatus and performing a fundoplication.
SYMPTOMS OF GERD
GERD presents with symptoms related to exposure of gastric contents to the esophagus, pharynx, and lungs. Heartburn is the most common presenting symptom of GERD,
Chapter 4 / Surgery for GERD 35
Fig. 1. Normal anatomy of esophageal hiatus: coronal section.
Fig. 2. Normal anatomy of esophageal hiatus: overview.
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