Managing gastroesophageal reflux disease (GERD) is difficult because it is a chronic relapsing disease. Surgical management of GERD is indicated only after medical management has failed. In patients who have the most advanced forms of GERD, surgical therapy is good for treating symptoms and healing esophagitis, but far from a gold standard. Freedom from symptoms, side effects, medical therapy, or reoperation cannot be guaranteed. Care must be taken when prescribing surgery for GERD, and it is best that an experienced surgeon at a specialty center participate in the patient’s lifelong care.
Is there a gold standard treatment for gastroesophageal reflux disease?
A gold standard is a model of highest excellence or perfection; in medicine, it refers to an ideal treatment or procedure that is definitive and curative, with perfect short- and long-term outcome. Medical therapy with proton pump inhibitors (PPIs) is 80% to 90% effective in long-term control of symptoms of gastroesophageal reflux disease (GERD). However, 10% to 20% of patients are refractory to this extended and expensive therapy. Current surgical therapy for GERD creates an obligate gastric volvulus, which also may be 80% to 90% effective in controlling symptoms, but can produce new, and not always transient, symptoms.
As with all hernia surgery, GERD surgery has a tendency to disrupt, fostered by the transitional environment between thorax and abdomen, resulting in breakdown of the surgical repair, return of the stomach to its herniated state, and reappearance of GERD. Thereafter, reoperation produces exponentially poorer outcomes with each successive surgery, culminating in an irreparable problem. Furthermore, surgery for GERD is irreversible, and if incorrectly prescribed or performed, it becomes a disease itself. Therefore, neither medical nor surgical therapies are definitive, perfect, or appropriate for all patients; rather, they are standard therapies for comparison but not gold standards.
Laparoscopic surgery for GERD has been incorrectly characterized as gold standard therapy. After first being reported in 1991, it was rapidly adopted and indiscriminately used in a broad spectrum of patients who were believed, correctly or incorrectly, to have GERD. Lessons previously learned from open surgery were ignored, forgotten, or unrecognized, only to be painfully relearned at patient expense, physicians’ professional reputations, and the status of GERD surgery. Declining use of surgery for GERD is evidence of an end to the laparoscopic frenzy and a return to appropriate use of both open and laparoscopic surgery in treating GERD.
Recognizing that no current therapy is a gold standard, an orderly exploration of definition, pathophysiology, natural history, and diagnosis and investigation of GERD, plus a review of operative techniques, postoperative care, special considerations, and surgical results, are necessary to elucidate the indications for surgical management of GERD.
Definition
GERD is defined as either symptoms or mucosal damage produced by abnormal reflux of gastric contents into the esophagus. This definition broadly and imprecisely characterizes the disease, setting the stage for inappropriate or unsuccessful therapy: neither presence of symptoms nor mucosal damage are rigorously classified or measured. Causation by reflux of gastric contents is not quantified beyond being abnormal, and means of assessment are not stated. This unusual and vague definition allows a wide spectrum of disorders to fall under one diagnosis and fosters misdiagnosis. The authors propose a more rigorous definition when surgery is considered for managing GERD: GERD is documented abnormal reflux of gastric contents into the esophagus, producing proven reflux-related symptoms or confirmed mucosal damage.
Definition
GERD is defined as either symptoms or mucosal damage produced by abnormal reflux of gastric contents into the esophagus. This definition broadly and imprecisely characterizes the disease, setting the stage for inappropriate or unsuccessful therapy: neither presence of symptoms nor mucosal damage are rigorously classified or measured. Causation by reflux of gastric contents is not quantified beyond being abnormal, and means of assessment are not stated. This unusual and vague definition allows a wide spectrum of disorders to fall under one diagnosis and fosters misdiagnosis. The authors propose a more rigorous definition when surgery is considered for managing GERD: GERD is documented abnormal reflux of gastric contents into the esophagus, producing proven reflux-related symptoms or confirmed mucosal damage.
Pathophysiology
GERD results from failure of the reflux barrier. This barrier has three components: (1) an intra-abdominal esophagus of adequate length, (2) an extrinsic sphincter, the esophageal hiatus, and (3) an intrinsic sphincter, the lower esophageal sphincter. Loss or breakdown of any of these elements, but typically all three, results in GERD.
Esophageal and gastric dysfunction independent of the reflux barrier may rarely cause GERD, but more commonly increases esophageal injury caused by reflux barrier failure. Upstream from the reflux barrier, esophageal dysmotility, which is sometimes secondary to GERD, inadequately clears gastric refluxate, heightening esophageal injury. Downstream from the reflux barrier, abnormal or delayed gastric emptying may overcome a marginal reflux barrier.
Epithelial and extramucosal mechanisms protect the esophageal mucosa from physiologic gastroesophageal reflux. Pathologic refluxate, either in amount or composition, overcomes these protective mechanisms, producing a characteristic but nonspecific injury of the esophageal mucosa. Microscopic review of reflux-induced esophagitis shows squamous hyperplasia and inflammatory infiltration of the mucosa by neutrophils, eosinophils, and lymphocytes. As injury progresses, mucosal erosion and eventual ulceration occurs. The reparative process may produce fibrous strictures. Metaplastic response to injury replaces esophageal squamous epithelium with specialized columnar epithelium (Barrett esophagus).
Natural history
GERD is chronic and relapsing. Because of its broad definition, it includes a wide spectrum of disease, from mildly symptomatic with no mucosal injury to irreversible esophageal damage regardless of symptoms, produced by scarring or malignant degeneration. In the United States, a 10,000-fold spread is present between the approximately 100 million patients who have at least weekly GERD symptoms to the tens of thousands of patients who have end-stage mucosal damage.
Although the natural history of the disease is poorly investigated and understood, it tends to persist and worsen with time. Unfortunately, which patients will develop unrelenting or uncontrollable symptoms or complications is unknown. Mortality is negligible for uncomplicated GERD, and small but significant for complicated GERD. Surgery for GERD remains controversial because the natural history of the disease is extremely variable, although progressive and relapsing.
Diagnosis and investigation
Diagnosis
Symptoms
GERD produces specific symptoms. A detailed history must be obtained from any patient who has suspected GERD, particularly one being considered for surgery. Its importance in decision making cannot be underestimated or overlooked. Typical GERD symptoms—heartburn and regurgitation—reflect dysfunction of the reflux barrier. Heartburn responding to aggressive PPI therapy is considered diagnostic of GERD. It is necessary to differentiate (1) heartburn (acid reflux) from regurgitation of stagnant, fermented food and saliva from an obstructed esophagus, such as occurs with achalasia, and (2) regurgitation (passive) from vomiting (active). Dysphagia is a third, less-specific, GERD symptom. It may be caused by GERD itself or stricture complicating GERD. GERD-related dysphagia must be differentiated from functional and mechanical dysphagia resulting from multiple other diseases that cause symptomatic esophageal obstruction.
Atypical GERD symptoms are cough, asthma, laryngitis, sore throat, chest pain, abdominal pain, and bloating. These symptoms in the absence of typical GERD symptoms point to diseases other than GERD. Careful investigation of alternative causes of atypical symptoms is necessary. Sophisticated testing, including impedance/pH monitoring, must be performed if GERD is believed to be the cause of atypical symptoms and surgery is being considered.
Mucosal injury
GERD may also produce esophageal injury. Esophagogastroduodenoscopy (EGD) with biopsy has replaced the upright air-contrast phase of the barium esophagram for mucosa evaluation. EGD and biopsy both diagnose and assess esophageal injury by visual and histopathologic mucosal examination. Visual assessment of esophageal injury is graded using the Los Angeles classification. Histopathologic findings, although nonspecific, are confirmatory in the clinical setting of GERD. The finding of specialized columnar epithelium (Barrett esophagus) in the tubular esophagus is secondary to GERD. In the absence of dysplasia, surveillance esophagoscopy and biopsy are required in patients who have Barrett esophagus, regardless of therapy.
EGD should be performed by the surgeon before surgery. The finding of a hiatal hernia identifies failure of two elements of the reflux barrier: loss of intra-abdominal esophagus and extrinsic sphincter. The following must be noted:
Measurements from incisor teeth to squamocolumnar junction, gastric rugal folds, and diaphragmatic hiatus
Length of hiatal hernia
Length of esophagus
Type of hiatal hernia
Presence of volvulus of the intrathoracic stomach
Mucosal abnormalities (strictures or rings)
Mural abnormalities (eg, submucosal tumors, leiomyoma)
Gastroesophageal reflux
The definition of GERD requires causation of symptoms or complications by abnormal reflux of gastric contents into the esophagus. Ambulatory pH monitoring performed off-medication both quantifies acid reflux and relates symptoms to acid exposure. It has evolved from an in-hospital test to an ambulatory wireless 48-hour study. Once reserved for diagnostic dilemmas, it is now essential before any proposed operation. It is invaluable in diagnosing GERD and documenting the preoperative state for later comparison.
Excessive acid exposure on pH testing is a surrogate for reflux of gastric contents into the esophagus, and in most patients it is adequate to diagnose GERD. In uncommon patients in whom duodenal reflux must be confirmed and quantified, ambulatory bilirubin monitoring is required. Similarly, in patients in whom non–acid reflux must be assessed, combined impedance and pH monitoring is necessary.
Investigations
The preoperative barium esophagram has been neglected, misused, and in some cases abandoned, with the advent of modern investigations of GERD. However, it provides valuable information about the mucosa, esophageal complications, reflux of gastric contents, reflux barrier, and esophageal function. It should, whenever possible, be ordered by the surgeon and performed by a radiologist who is experienced in preoperative assessment of GERD and is a member of the multidisciplinary treatment team.
If dysphagia is the predominant symptom and the diagnosis is in question, the examination should start as a timed barium esophagram. If not, the first phase of the barium esophagram is the upright air-contrast examination. Intended to evaluate esophageal mucosa for esophagitis, it is more importantly an excellent assessment of esophageal length and thus useful in diagnosing short esophagus. The second phase is a motility examination, performed with five sequential swallows separated by at least 30 seconds and video recorded. The third phase is the distended single-contrast examination, which identifies small reducible hiatal hernias, subtle strictures, rings, and other abnormalities of esophageal contour. The fourth phase involves provocative measures to identify reflux. The fifth phase is a solid-food examination using, for example, a barium tablet or barium-coated marshmallow to identify areas of obstruction. The final phase is the oropharyngeal examination, but this is not critical in patients who have GERD without cervical dysphagia. The barium esophagram report should describe each element of the examination:
- 1.
Emptying assessment in patients who have dysphagia (timed barium esophagram)
- 2.
Mucosal assessment
- 3.
Assessment of esophageal length
- 4.
Assessment of esophageal motility
- 5.
Presence and type of hiatal hernia
- 6.
Reducibility of hiatal hernia in upright position
- 7.
Identification of reflux, including maneuver, height of reflux, and time to clear reflux
- 8.
Presence of stricture or ring
Esophageal manometry excludes unsuspected motility disorders or motility disorders masquerading as GERD, confirms adequate esophageal peristalsis for GERD surgery, and quantifies preoperative resting pressure and relaxation of the lower esophageal sphincter for later comparison. High-resolution manometry is replacing conventional manometry because it provides a spatially enhanced dynamic representation of the esophageal body and reflux barrier. It isolates the esophageal hiatus from the lower esophageal sphincter (LES), increasing understanding of GERD and facilitating treatment decision-making. For modern GERD surgery, high-resolution manometry is invaluable and highly recommended.
If gastric emptying abnormalities are suspected by history or investigations, radionucleotide gastric emptying studies are warranted.
Surgical technique
Surgery for GERD rebuilds the three components of the reflux barrier. This requires three steps to address each main component.
Restoration of Intra-Abdominal Esophagus
Regardless of approach, the first step commences with dissection of the esophageal hiatus, which indirectly mobilizes the distal esophagus, esophagogastric junction, and gastric fundus. Hiatal dissection then permits intrathoracic mobilization of the esophagus into the posterior mediastinum, at least to the level of the inferior pulmonary veins. In many patients, this is sufficient to restore an adequate length of intra-abdominal esophagus. However, in certain patients, such as those who have the much-disputed diagnosis of short esophagus, this dissection alone is inadequate.
Short esophagus should be diagnosed preoperatively. It is suspected in patients who have a history of peptic stricture or repeated esophageal dilatation, long-segment Barrett esophagus, type I hiatal hernia (sliding) more than 4 cm long, type III hiatal hernia (rolling, giant paraesophageal), or nonreducible hiatal hernia on upright air-contrast barium esophagram ( Fig. 1 ). In these patients, adequate intra-abdominal length is obtained by adding a Collis gastroplasty. This procedure begins with dissection of the esophagogastric fat pad, which selectively vagotomizes the gastroplasty segment. A tube of stomach 3 to 6 cm in length is constructed along its lesser curve using surgical staplers. With adoption of laparoscopy, esophageal lengthening has evolved into a simple wedge gastroplasty, because of technical difficulties presented by laparoscopy and misunderstanding of the principles of constructing a Collis gastroplasty. Predictably, acid production in this unprepared gastric segment perpetuates GERD.
Failure to restore adequate intra-abdominal esophageal length produces a repair under tension that will eventually fail. In patients for whom GERD surgery failed, review of the operative report may identify inadequate restoration of the intra-abdominal esophagus as a reason for failure of the initial surgery.
Reconstruction of Extrinsic Sphincter
The esophageal hiatus, which serves as the extrinsic sphincter, is composed of a right and left crus arising from the right crus of the diaphragm ( Fig. 2 ). The right crus of the esophageal hiatus is nearly vertical and lies over the vertebrae, whereas the left crus of the esophageal hiatus is slightly more semicircular, slightly longer, and has no underlying support. Progressive herniation of the stomach into the posterior mediastinum results in minimal change of the right crus but bowing and further elongation of the left crus ( Fig. 3 ).
Suture closure of the esophageal hiatus to approximate its normal size is the essence of hiatal reconstruction. Deep suture bites into each crus, with slightly wider spacing on the left crus, constitutes standard reconstruction ( Fig. 4 ). For severely disrupted hiatus, a complex reconstruction is required. The left crus is plicated to normalize crural length, permitting a standard hiatal reconstruction ( Fig. 5 ).
