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ЗмістAssessment of esophageal function
Gastroesophageal reflux disease
Complications of Gastroesophageal Reflux
Principles of Surgical Therapy
Primary Antireflux Repairs
Transthoracic Nissen fundoplication
Outcome After Fundoplication
Atypical Reflux Symptoms
Motility disorders of the pharynx and esophagus
Motility Disorders of the Pharyngoesophageal Segment
Motility Disorders of the Esophageal Body and Lower Esophageal Sphincter
TABLE Esophageal Motility Disorders
Diffuse and Segmental Esophageal Spasm
Diverticula of the Esophageal Body
DISEASES OF GULLET
The esophagus is a muscular tube that starts as the continuation of the pharynx and ends as the cardia of the stomach. Manometrically, the length of the esophagus between the lower border of the cricopharyngeus and upper border of the lower sphincter varies according to the height of the individual. The musculature of the esophagus can be divided into an outer longitudinal and an inner circular layer. The upper 2.6 cm of the cervical esophagus contain only striated muscle fibers. From there on, smooth muscle fibers gradually become more abundant. When a surgical myotomy is indicated for a cricopharyngeal disorder, the myotomy incision needs to extend over this distance. Below this distance smooth muscle fibers gradually become more abundant. Most clinically significant esophageal motility disorders involve only the smooth muscle in the lower two thirds of the esophagus and the function of the cervical esophagus is normal. The lymphatics of the esophagus located in the submucosa of the esophagus are so dense and interconnected that they constitute a single plexus. There are more lymph vessels than blood capillaries in the submucosa. Lymph flow in the submucosal plexus runs in a longitudinal direction, and on injection of a contrast medium, the longitudinal spread is seen to be about 6 times that of the transverse spread. In the upper two-thirds of the esophagus the lymphatic flow is mostly cephalad, and in the lower third caudad. In the thoracic portion of the esophagus, the submucosal lymph plexus extends over a long distance in a longitudinal direction before penetrating the muscle layer to enter lymph vessels in the adventitia. As a consequence of this nonsegmental lymph drainage, a primary tumor can extend for a considerable length superiorly or inferiorly in the submucosal plexus. Consequently, free tumor cells can follow the submucosal lymphatic plexus in either direction for a long distance before they pass through the muscularis and on into the regional lymph nodes. The cervical esophagus has a more direct segmental lymph drainage into the regional nodes, and as a result, lesions in this portion of the esophagus have less submucosal extension and a more regionalized lymphatic spread.
The efferent lymphatics from the cervical esophagus drain into the paratracheal and deep cervical lymph nodes, and those from the upper thoracic esophagus empty mainly into the paratracheal lymph nodes. Efferent lymphatics from the lower thoracic esophagus drain into the subcarinal nodes and nodes in the inferior pulmonary ligaments. The superior gastric nodes receive lymph not only from the abdominal portion of the esophagus, but also from the adjacent lower thoracic segment.
A thorough understanding of the patient’s underlying anatomic and functional deficits prior to making therapeutic decisions is fundamental to the successful treatment of esophageal disease. The diagnostic tests as presently employed may be divided into five broad groups: (1) tests to detect structural abnormalities of the esophagus; (2) tests to detect functional abnormalities of the esophagus; (3) tests to detect increased esophageal exposure to gastric juice; (4) tests to provoke esophageal symptoms; and (5) tests of duodenogastric function as they relate to esophageal disease.
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. The simplest approach is to define the disease by its symptoms. However, symptoms thought to be indicative of GERD, such as heartburn or acid regurgitation, are very common in the general population, and many individuals consider them to be normal and do not seek medical attention. Even when excessive, 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. In addition, patients with GERD can present with atypical symptoms, such as nausea, vomiting, postprandial fullness, chest pain, choking, chronic cough, wheezing, and hoarseness. Furthermore, bronchiolitis, recurrent pneumonia, idiopathic pulmonary fibrosis, and asthma can be primarily because of GERD. To confuse the issue more, GERD can coexist with cardiac and pulmonary disease. Thus using clinical symptoms to define GERD lacks sensitivity and specificity. An alternative definition for GERD is 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 prescribed drug ingestion. In addition, the definition leaves undiagnosed those patients who have symptoms of gastroesophageal reflux but do not have endoscopic esophagitis. A third approach to defining GERD is to 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. The development of miniaturized pH electrodes and data recorders allowed measurement of esophageal exposure to gastric juice by calculating the %age of time the pH was less than 4 over a 24-h period. This provided an opportunity to objectively identify the presence of the disease.
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 because of repetitive reflux are esophagitis, stricture, and Barrett 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 (Table 1). The observation that a structurally defective sphincter occurs in 42 % of patients without complications (most of whom have one or two components failed) suggests that disease may be confined to the sphincter
because of compensation by a vigorously contracting esophageal body.
TABLE 1 Complications of Gastroesophageal Reflux Disease:
Complication No./ normal sphincter / defective sphincter
None 59 / 58% / 42%
Erosive esophagitis 47 /23% /77%a
Stricture 19 /11% /89%
Barrett esophagus 25/ 0%/ 100%
Grade more severe with defective cardia.
Before proceeding with an antireflux operation, several factors should be evaluated. First, 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. Patients with normal peristaltic contractions do well with a 360-degree Nissen fundoplication. When peristalsis is absent or severely disordered, or the amplitude of the contraction is below 20 mm Hg throughout the lower esophagus, a two-thirds partial fundoplication may be the procedure of choice. Second, anatomic shortening of the esophagus can compromise the ability to do an adequate repair without tension, and lead to an increased incidence 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 measures larger than 5 cm between the diaphragmatic crura and gastroesophageal junction on endoscopy. When esophageal shortening is present, a gastroplasty should be performed. In patients who have a global absence of contractility, and have dysphagia or a history of several failed previous antireflux procedures, esophageal resection should be considered as an alternative. Third, the surgeon should specifically query the patient for complaints of nausea, vomiting, and loss of appetite. In such patients, these symptoms may persist after an antireflux procedure, and patients should be given this information before the operation. In these patients, 24-h bilirubin monitoring and gastric emptying studies can be performed to detect and quantify duodenogastric abnormalities.
The primary goal of antireflux surgery is to safely restore the structure of the sphincter or to prevent its shortening with gastric distention, although preserving the patient’s ability to swallow normally, to belch to relieve gaseous distention, and to vomit when necessary. Regardless of the choice of the procedure, this goal can be achieved if attention is paid to five principles in reconstructing the cardia. First, the operation should restore the pressure of the distal esophageal sphincter to a normal level and its length to at least 3 cm. The fundoplication augments sphincter characteristics in patients in whom they are reduced prior to surgery and prevents unfolding of a normal sphincter in response to gastric distention. Second, 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 intraabdominal pressure. The permanent restoration of 1.5.2 cm of abdominal esophagus in a patient whose sphincter pressure has been augmented to normal levels will maintain the competency of the cardia over various challenges of intraabdominal pressure.
Third, the operation should allow the reconstructed cardia to relax on deglutition. In normal swallowing, a vagally mediated relaxation of the distal esophageal sphincter and the gastric fundus occurs. The relaxation lasts for approximately 10 s and is followed by a rapid recovery to the former tonicity. To ensure relaxation of the sphincter, three factors are important: (1) only the fundus of the stomach should be used to buttress the sphincter, because it is known to relax in concert with the sphincter; (2) 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, because the body of the stomach does not relax with swallowing; and (3) 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. Fourth, 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 fundoplication, and on the variation in intraabdominal pressure. A 360-degree gastric fundoplication should be no longer than 2 cm and constructed easily 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. Fifth, 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. Leaving the fundoplication in the thorax converts a sliding hernia into a paraesophageal hernia, with all the complications associated with that condition. Maintaining the repair in the abdomen under tension predisposes to an increased incidence of recurrence. This is likely to occur in patients who have a stricture or BE, and is because of shortening of the esophagus from the inflammatory process. This problem can be resolved by lengthening the esophagus with a Collis gastroplasty.
A laparoscopic approach is used in patients with normal esophageal contractility and length. Patients with questionable esophageal length may be best approached transthoracically, in which 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 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.
The most common antireflux procedure is the Nissen fundoplication. The procedure can be performed through an abdominal or a chest incision, and through a laparoscope. Rudolph Nissen described the procedure as a 360-degree fundoplication around the lower esophagus for a distance of 4.5 cm. Although this provided good control of reflux, it was associated with a number of side effects that have encouraged modifications of the procedure as originally described. These include using only the gastric fundus to envelop the esophagus in a fashion analogous to a Witzel jejunostomy, sizing the fundoplication with a 60F bougie, and limiting the length of the fundoplication to 1.2 cm. The essential elements necessary for the 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
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.
The laparoscopic approach. Laparoscopic fundoplication has become commonplace and has replaced the open abdominal Nissen fundoplication as the procedure of choice.
^ . The indications for performing an antireflux procedure by a transthoracic approach are as follows:
1. A patient who has had a previous hiatal hernia repair. In this situation, a peripheral circumferential incision in the diaphragm is made to provide simultaneous exposure of the upper abdomen. This allows safe dissection of the previous repair from both the abdominal and thoracic sides of the diaphragm.
2. A patient who has a short esophagus. This is usually associated with a stricture or BE. In this situation, the thoracic approach is preferred to allow maximum mobilization of the esophagus, and to perform a Collis gastroplasty to place the repair without tension below the diaphragm.
3. A patient with a sliding hiatal hernia that does not reduce below the diaphragm during a roentgenographic barium study in the upright position. This can indicate esophageal shortening, and again, a thoracic approach is preferred for maximum mobilization of the esophagus, and if necessary, the performance of a Collis gastroplasty.
4. A patient who has associated pulmonary pathology. In this situation, the nature of the pulmonary pathology can be evaluated and the proper pulmonary surgery, in addition to the antireflux repair, can be performed.
5. An obese patient. In this situation, the abdominal repair is difficult because of poor exposure, particularly in men, in whom the intraabdominal fat is more abundant.
Nearly all published reports of laparoscopic fundoplication show that this procedure relieves the typical symptoms of gastroesophageal reflux heartburn, regurgitation, and dysphagia.in greater than 90 % of patients. The incidence of persistent postoperative dysphagia has decreased to the 3.5 % range with increasing experience and attention to the technical details in constructing the fundoplication. Resting LES characteristics and esophageal acid exposure return to normal in nearly all patients. Morbidity after laparoscopic fundoplication is similar to that after open fundoplication, averaging 10.15 %. Unrecognized perforation of the esophagus or stomach is the most life-threatening complication. Perforations occur most often during hiatal and circumferential dissection of the esophagus, and their incidence is also related to the surgeon’s experience. Intraoperative recognition and repair are the keys to preventing a life-threatening complication.
The condition whereby the tubular esophagus is lined with columnar epithelium rather than squamous epithelium was first described by Norman Barrett in 1950. He incorrectly believed it to be congenital in origin. It is now realized that it is an acquired abnormality, occurs in 7.15 % of patients with GERD, and represents the end stage of the natural history of this disease. It is also thought to be distinctly different from the congenital condition in which islands of gastric fundic epithelium are found in the upper half of the esophagus. The definition of BE has evolved considerably over the past decade. Traditionally, BE was identified by the presence of columnar mucosa extending at least 3 cm into the esophagus. It is now recognized that the specialized intestinal type epithelium found in the Barrett mucosa is the only tissue predisposed to malignant degeneration. Consequently, the diagnosis of BE is presently made given any length of endoscopically identifiable columnar mucosa that proves on biopsy to show intestinal metaplasia. Although long segments of columnar mucosa without intestinal metaplasia do occur, they are less uncommon today than they were previously. The hallmark of intestinal metaplasia is the presence of intestinal goblet cells. There is a high prevalence of biopsy-demonstrated intestinal metaplasia at the cardia, on the gastric side of the squamocolumnar junction, in the absence of endoscopic evidence of a columnar-lined esophagus. Evidence is accumulating that these patches of what appears to be Barrett in the cardia have a similar malignant potential as the longer segments, and may be the precursors for carcinoma of the cardia. The long-term relief of symptoms remains the primary reason for performing antireflux surgery in patients with BE. Healing of esophageal mucosal injury and the prevention of disease progression are important secondary goals. In this regard, patients with BE are no different than the broader population of patients with gastroesophageal reflux. They should be considered for antireflux surgery when patient data suggest severe disease or predict the need for long-term medical management. Most patients with BE are symptomatic. Although it has been argued that some patients with BE may not have symptoms, careful history taking will reveal the presence of symptoms in most, if not all, patients.
The typical complications in BE include ulceration in the columnar-lined segment, stricture formation, and a dysplasia -cancer sequence. Barrett’s ulceration is unlike the erosive ulceration of reflux esophagitis in that it more closely resembles peptic ulceration in the stomach or duodenum, and has the same propensity to bleed, penetrate, or perforate. The strictures found in BE occur at the squamocolumnar junction, and are typically higher than peptic strictures in the absence of BE. Ulceration and stricture in association with BE were commonly reported prior to 1975, but with the advent of potent acid suppression medication they have become less common. In contrast, the complication of adenocarcinoma developing in Barrett mucosa has become more common. Adenocarcinoma developing in Barrett mucosa was considered a rare tumor prior to 1975. Today it occurs in approximately one in every 100 patient-years of follow-up, which represents a risk 40 times that of the general population. Most if not all cases of adenocarcinoma of the esophagus arise in Barrett epithelium. Few studies have focused on the alleviation of symptoms after antireflux surgery in patients with BE. Those that are available document excellent to good results in 72.95 % of patients at 5 years following surgery. Farrell and associates also reported symptomatic outcome of laparoscopic Nissen fundoplication in 50 patients with both long- and short-segment BE. Mean scores for heartburn, regurgitation, and dysphagia all improved dramatically post-Nissen. Importantly, there was no significant decrement in symptom scores when 1-year results were compared to those at 2.5 years postoperatively. They did find a higher prevalence of anatomic failures requiring re-operation in patients with BE when compared to non-Barrett patients with GERD. Others have reported similar results. Taken together these studies document the ability of antireflux surgery to provide long-term symptomatic relief in patients with BE. Three relevant questions arise concerning the fate, over time, of the metaplastic tissue found in BE: (1) Does antireflux surgery cause regression of Barrett epithelium? (2) Does it prevent progression? and (3) Can the development of Barrett metaplasia be prevented by early antireflux surgery in patients
with reflux disease? The common belief that Barrett epithelium cannot be reversed is likely false. DeMeester and associates reported that after antireflux surgery, loss of intestinal metaplasia (IM) in patients with visible BE was rare, but occurred in 73 % of patients with inapparent IM of the cardia. This suggests that the metaplastic process may indeed be reversible if reflux is eliminated early in its process, that cardiac mucosa is dynamic, and that as opposed to IM extending several centimeters into the esophagus, IM of the cardia is more likely to regress following antireflux surgery. Recent evidence suggests that the development of BE may even be preventable. Although a very difficult hypothesis to study, Oberg and co-workers followed a cohort of 69 patients with short-segment, nonintestinalized, columnar-lined esophagus (CLE) over a median of 5 years of surveillance endoscopy. Forty-nine of the patients were maintained on PPI therapy and 20 had antireflux surgery. Patients with antireflux surgery were 10 times less likely to develop IM in these CLE segments over a follow-up span of nearly 15 years than those on medical therapy. This rather remarkable observation supports the two-step hypothesis of the development of BE (cardiac metaplasia followed by intestinal metaplasia), and suggests that the second step can be prevented if reflux disease is recognized and treated early and aggressively. There is a growing body of evidence to attest to the ability of fundoplication to protect against dysplasia and invasive malignancy. Three studies suggest that an effective antireflux procedure can impact the natural history of BE in this regard. Two prospective randomized studies found less adenocarcinoma in the surgically treated groups. Parrilla and associates reported that although the development of dysplasia and adenocarcinoma was no different overall, the subgroup of surgical patients with normal postoperative pH studies developed significantly less dysplasia and had no adenocarcinoma. Spechler identified one adenocarcinoma 11.13 years after antireflux surgery, compared to four following medical treatment. Most of these authors concluded that there is a critical need for future trials exploring the role of antireflux surgery in protecting against the development of dysplasia in patients with BE.
Chronic respiratory symptoms, such as chronic cough, recurrent pneumonias, episodes of nocturnal choking, waking up with gastric contents in the mouth, or soilage of the bed pillow, may also indicate the need for surgical therapy. Patients suffering from repetitive pulmonary aspiration secondary to gastroesophageal reflux often shows signs of pleural thickening, bronchiectasis, and chronic interstitial pulmonary fibrosis on their chest radiograph. If 24-h pH monitoring confirms the presence of increased esophageal acid exposure, and manometry shows normal esophageal body motility, an antireflux procedure can be done with an expected good result. However, these patients usually have a nonspecific motor abnormality of the esophageal body, which tends to propel the refluxed material toward the pharynx. In some of these patients, the motor abnormality will disappear after a surgical antireflux procedure. In others, the motor disorder will persist and contribute to postoperative aspiration of swallowed saliva and food. Consequently, the results of an antireflux procedure in patients with a motor disorder of the esophageal body are variable. Chest pain may be an atypical symptom of gastroesophageal reflux, and is often confused with coronary artery disease. Fifty % of patients in whom a cardiac cause of the chest pain has been excluded will have increased esophageal acid exposure as a cause of the episode of pain. An antireflux procedure provides relief of the chest pain more consistently than medical therapy. Dysphagia, regurgitation, or chest pain on eating in a patient with normal endoscopy and esophageal function studies can be an indication for an antireflux procedure. These symptoms are usually related to the presence of a large paraesophageal hernia, intrathoracic stomach, or a small hiatal hernia with a narrow diaphragmatic hiatus. A Schatzki ring may be present with the latter. All these conditions are easily identified with an upper GI radiographic barium examination done by a knowledgeable radiologist. These patients may have no heartburn, because the LES is usually normal and reflux of gastric acid into the esophagus does not occur. The surgical repair of the hernia usually includes an antireflux procedure because of the potential of destroying the competency of the cardia during the surgical dissection.
Difficulty in swallowing (dysphagia) is the primary symptom of esophageal motor disorders. Its perception by the patient is a balance between the severity of the underlying abnormality causing the dysphagia, and the adjustment made by the patient in altering eating habits. Consequently, any complaint of dysphagia must include an assessment of the patient’s dietary history. It must be known whether the patient experiences pain, chokes, or vomits with eating; whether the patient requires liquids with the meal, is the last to finish, or is forced to interrupt a social meal; and whether he or she has been admitted to the hospital for food impaction. These assessments, plus an evaluation of the patient’s nutritional status, help to determine how severe the dysphagia is and evaluate the indications for surgical therapy. A surgical myotomy is designed to improve the symptoms of dysphagia caused by a motility disorder. The results can profoundly improve the patient’s ability to ingest food, but rarely return the function of the foregut to normal. The principle of the procedure is to destroy esophageal contractility to correct a defect in esophageal motility, resulting in improvement but never a return to normal function. To use a surgical myotomy to treat the problem of dysphagia, the surgeon needs to know the precise functional abnormality causing the symptom. This usually entails a complete esophageal motility evaluation. A clear understanding of the physiologic mechanism of swallowing, and identification of the motility abnormality giving rise to the dysphagia, are essential for determining if surgery is indicated and the extent of the myotomy to be performed. Endoscopy is necessary only to exclude the presence of tumor or inflammatory changes as the cause of dysphagia.
Disorders of the pharyngoesophageal phase of swallowing result from a discoordination of the neuromuscular events involved in chewing, initiation of swallowing, and propulsion of the material from the oropharynx into the cervical esophagus. They can be categorized into one or a combination of the following abnormalities: (1) inadequate oropharyngeal bolus transport; (2) inability to pressurize the pharynx; (3) inability to elevate the larynx; (4) discoordination of pharyngeal contraction and cricopharyngeal relaxation; and (5) decreased compliance of the pharyngoesophageal segment secondary to muscle pathology. The latter results in incomplete anatomic relaxation of the cricopharyngeus and cervical esophagus. Pharyngoesophageal swallowing disorders are usually because of acquired disease involving the central and peripheral nervous system. This includes cerebrovascular accidents, brain stem tumors, poliomyelitis, multiple sclerosis, Parkinson disease, pseudobulbar palsy, peripheral neuropathy, and operative damage to the cranial nerves involved in swallowing. Muscular diseases such as radiation-induced myopathy, dermatomyositis, myotonic dystrophy, and myasthenia gravis are less common causes. Rarely, extrinsic compression by thyromegaly, cervical lymphadenopathy, or hyperostosis of the cervical spine can cause pharyngoesophageal dysphagia. Zenker Diverticulum In the past, the most common recognized sign of pharyngoesophageal dysfunction was the presence of a Zenker diverticulum, originally described by Ludlow in 1769. The eponym resulted from Zenker classic clinicopathologic descriptions of 34 cases published in 1878. Pharyngoesophageal diverticula have been reported to occur in 0.1 % of 20,000 routine barium examinations, and classically occur in older adult, white males. Zenker diverticula tend to enlarge progressively with time because of the decreased compliance of the skeletal portion of the cervical esophagus that occurs with aging. Presenting symptoms include dysphagia associated with the spontaneous regurgitation of undigested, bland material, often interrupting eating or drinking. The symptom of dysphagia is due initially to the loss of muscle compliance in the pharyngoesophageal segment, later augmented by the presence of an enlarging diverticulum. On occasion, the dysphagia can be severe enough to cause debilitation and significant weight loss. Chronic aspiration and repetitive respiratory infection are common associated complaints. Once suspected, the diagnosis is established by a barium swallow. Endoscopy is usually difficult in the presence of a cricopharyngeal diverticulum, and potentially dangerous, owing to obstruction of the true esophageal lumen by the diverticulum and the attendant risk of diverticular perforation.
The myotomy can be performed under local or general anesthesia through an incision along the anterior border of the left sternocleidomastoid muscle. The pharynx and cervical esophagus are exposed by retracting the sternocleidomastoid muscle and carotid sheath laterally, and the thyroid, trachea, and larynx medially. When a pharyngoesophageal diverticulum is present, localization of the pharyngoesophageal segment is easy. The diverticulum is carefully freed from the overlying areolar tissue to expose its neck, just below the inferior pharyngeal constrictor and above the cricopharyngeus muscle. It can be difficult to identify the cricopharyngeus muscle in the absence of a diverticulum. A benefit of local anesthesia is that the patient can swallow and demonstrate an area of persistent narrowing at the pharyngoesophageal junction. Furthermore, before closing the incision, gelatin can be fed to the patient to ascertain whether the symptoms have been relieved, and to inspect the opening of the previously narrowed pharyngoesophageal segment. Under general anesthesia, and in the absence of a diverticulum, the placement of a nasogastric tube to the level of the manometrically determined cricopharyngeal sphincter helps in localization of the structures. The myotomy is extended cephalad by dividing 1 to 2 cm of inferior constrictor muscle of the pharynx, and caudad by dividing the cricopharyngeal muscle and the cervical esophagus for a length of 4.5 cm. The cervical wound is closed only when all oozing of blood has ceased, because a hematoma after this procedure is common, and is often associated with temporary dysphagia while the hematoma absorbs. Oral alimentation is started the day after surgery. The patient is usually discharged on the first or second postoperative day. If a diverticulum is present and is large enough to persist after a myotomy it may be sutured in the inverted position to the prevertebral fascia using a permanent suture (i.e., diverticulopexy). If the diverticulum is excessively large so that it would be redundant if suspended, or if its walls are thickened, a diverticulectomy should be performed. Endoscopic stapled diverticulotomy recently has been described. The procedure uses aWeerda diverticuloscope with two retractable valves passed into the hypopharynx. The lips of the diverticuloscope are positioned so that one lip lies in the esophageal lumen and the other in the diverticular lumen. The valves of the diverticuloscope are retracted appropriately so as to visualize the septum interposed between the diverticulum and the esophagus. An endoscopic linear stapler is introduced into the diverticuloscope and positioned against the common septum with the anvil in the diverticulum and the cartridge in the esophageal lumen. Firing of the stapler divides the common septum between the posterior esophageal and the diverticular wall over a length of 30 mm, placing three rows of staples on each side. More than one stapler application may be needed, depending on the size of the diverticulum. The patient is allowed to resume liquid feeds either on the same day or the day after, and is usually discharged the day after surgery. Complications are rare and may include perforation at the apex of the diverticulum, and can be repaired with minimally invasive techniques.
Postoperative complications include fistula formation, abscess, hematoma, recurrent nerve paralysis, difficulties in phonation, and Horner’s syndrome. The incidence of the first two can be reduced by performing a diverticulopexy. Recurrence of a Zenker diverticulum occurs late, and is more common after diverticulectomy without myotomy, presumably because of persistence of the underlying loss of compliance of the cervical esophagus when a myotomy is not performed.
Disorders of the esophageal phase of swallowing result from abnormalities in the propulsive pump action of the esophageal body or the relaxation of the LES. These disorders result from either primary esophageal abnormalities, or from generalized neural, muscular, or collagen vascular disease (Table). The use of standard esophageal manometry techniques has allowed specific primary esophageal motility disorders to be identified out of a pool of non-specific motility abnormalities. These include achalasia, diffuse esophageal spasm, the so-called nutcracker esophagus, the hypertensive LES, and ineffectiveesophageal motility.
Primary esophageal motility disorders
Diffuse and segmental esophageal spasm
Hypertensive lower esophageal sphincter
Non-specific esophageal motility disorders
Secondary esophageal motility disorders
Collagen vascular diseases: progressive systemic sclerosis, polymyositis and dermatomyositis, mixed connective tissue disease, systemic lupus erythematosus, etc.
Chronic idiopathic intestinal pseudo-obstruction
Endocrine and metastatic disorders
The best known and best understood primary motility disorder of the esophagus is achalasia, with an incidence of six per 100,000 populations per year. Although complete absence of peristalsis in the esophageal body has been proposed as the major abnormality, present evidence indicates achalasia is a primary disorder of the LES. The observation that esophageal peristalsis can return in patients with classic achalasia following dilation or myotomy provides support that achalasia is a primary disease of the LES. The pathogenesis of achalasia is presumed to be a neurogenic degeneration, which is either idiopathic or because of inflammation. In experimental animals, the disease has been reproduced by destruction of the nucleus ambiguous and the dorsal motor nucleus of the vagus nerve. In patients with the disease, degenerative changes have been shown in the vagus nerve and in the ganglia in the Auerbach plexus of the esophagus itself. This degeneration results in hypertension of the LES, a failure of the sphincter to relax on deglutition, elevation of intraluminal esophageal pressure, esophageal dilatation, and a subsequent loss of progressive peristalsis in the body of the esophagus. The esophageal dilatation results from the combination of a nonrelaxing sphincter, which causes a functional retention of ingested material in the esophagus, and elevation of intraluminal pressure from repetitive pharyngeal air swallowing. With time, the functional disorder results in anatomic alterations seen on radiographic studies, such as a dilated esophagus with a tapering, beak-like narrowing of the distal end. There is usually an air-fluid level in the esophagus from the retained food and saliva, the height of which reflects the degree of resistance imposed by the nonrelaxing sphincter. As the disease progresses, the esophagus becomes massively dilated and tortuous.
Diffuse esophageal spasm is characterized by substernal chest pain and/or dysphagia. Diffuse esophageal spasm differs from classic achalasia in that it is primarily a disease of the esophageal body, produces a lesser degree of dysphagia, causes more chest pain, and has less effect on the patient’s general condition. True symptomatic diffuse esophageal spasm is a rare condition, occurring about 5 times less frequently than achalasia. The causation and neuromuscular pathophysiology of diffuse esophageal spasm are unclear. The basic motor abnormality is rapid wave progression down the esophagus secondary to an abnormality in the latency gradient. Hypertrophy of the muscular layer of the esophageal wall and degeneration of the esophageal branches of the vagus nerve have been observed in this disease, although these are not constant findings. Manometric abnormalities in diffuse esophageal spasm may be present over the total length of the esophageal body, but usually are confined to the distal two-thirds. In segmental esophageal spasm, the manometric abnormalities are confined to a short segment of the esophagus.
The classic manometric findings in these patients are characterized by the frequent occurrence of simultaneous waveforms and multipeaked esophageal contractions, which may be of abnormally high amplitude or long duration. Key to the diagnosis of diffuse esophageal spasm is that there remain some peristaltic waveforms in excess of those seen in achalasia. A criterion of 20 % or more simultaneous waveforms out of 10 wet swallows has been used to diagnose diffuse esophageal spasm. However, this figure is arbitrary and often debated. The LES in patients with diffuse esophageal spasm usually shows a normal resting pressure and relaxation on deglutition. In patients with advanced disease, the radiographic appearance of tertiary contractions appears helical, and has been termed corkscrew esophagus or pseudodiverticulosis. Patients with segmental or diffuse esophageal spasm can compartmentalize the esophagus and develop an epiphrenic or midesophageal diverticulum.
Radiographic abnormalities such as segmental spasm, corkscrewing, compartmentalization, and diverticulum are the anatomic results of disordered motility function. Of these, the most persistent and easiest to demonstrate is an esophageal diverticulum. Diverticula occur most commonly with non-specific motility disorders, but can occur with all of the primary motility disorders. In the latter situation, the motility disorder is usually diagnosed before the development of the diverticulum. When present, a diverticulum may temporarily alleviate the symptom of dysphagia by becoming a receptacle for ingested food, and substitute the symptoms of postprandial pain and the regurgitation of undigested food. If a motility abnormality of the esophageal body or LES cannot be identified, a traction or congenital cause for the diverticulum should be considered. Because development in radiology preceded development in motility monitoring, diverticula of the esophagus were considered historically to be a primary abnormality, the cause, rather than the consequence, of motility disorders. Consequently, earlier texts focused on them as specific entities based on their location. Epiphrenic diverticula arise from the terminal third of the thoracic esophagus and are usually found adjacent to the diaphragm. They have been associated with distal esophageal muscular hypertrophy, esophageal motility abnormalities, and increased luminal pressure. They are pulsion diverticula, and have been associated with diffuse spasm, achalasia, or nonspecific motor abnormalities in the body of the esophagus. Whether the diverticulum should be surgically resected or suspended depends on its size and proximity to the vertebral body. When diverticula are associated with esophageal motility disorders, esophageal myotomy from the distal extent of the diverticulum to the stomach is indicated; otherwise, one can expect a high incidence of suture line rupture because of the same intraluminal pressure that initially gave rise to the diverticulum. If the diverticulum is suspended to the prevertebral fascia of the thoracic vertebra, a myotomy is begun at the neck of the diverticulum and extended across the LES. If the diverticulum is excised by dividing the neck, the muscle is closed over the excision site and a myotomy is performed on the opposite esophageal wall, starting at the level of diverticulum. When a large diverticulum is associated with a hiatal hernia, the diverticulum is excised, a myotomy is performed if there is an associated esophageal motility abnormality, and the hernia is repaired because of the high incidence of postoperative reflux when it is omitted. Midesophageal or traction diverticula were first described in the nineteenth century. At that time they were frequently noted in patients who had mediastinal lymph node involvement with tuberculosis. It was theorized that adhesions form between the inflamed mediastinal nodes and the esophagus. By contraction, the adhesions exerted traction on the esophagealwall and led to a localized diverticulum. This theory was based on the findings of early dissections, in which adhesions between diverticula and lymph nodes were commonly found. It is now believed that some diverticula in the midesophagus may also be caused by motility abnormalities. Most midesophageal diverticula are asymptomatic and incidentally discovered during investigation for nonesophageal complaints. In such patients, the radiologic abnormality may be ignored. Patients with symptoms of dysphagia, regurgitation, chest pain, or aspiration, in whom a diverticulum is discovered, should be thoroughly investigated for an esophageal motor abnormality and treated appropriately. Occasionally, a patient will present with a bronchoesophageal fistula manifested by a chronic cough on ingestion of meals. The diverticulum in such patients is most likely to have an inflammatory etiology. The indication for surgical intervention is the degree of symptomatic disability. Usually midesophageal diverticula can be suspended because of their proximity to the spine. If motor abnormality is documented, a myotomy should be performed similarly to that described for an epiphrenic diverticulum.
Long esophageal myotomy for motor disorders of the esophageal body. A long esophageal myotomy is indicated for dysphagia caused by any motor disorder characterized by segmental or generalized simultaneous waveforms in a patient whose symptoms are not relieved by medical therapy. Such disorders include diffuse and segmental esophageal spasm, vigorous achalasia, and nonspecific motility disorders associated with a mid- or epiphrenic esophageal diverticulum. However, the decision to operate must be made by a balanced evaluation of the patient’s symptoms, diet, lifestyle adjustments, and nutritional status, with the most important factor being the possibility of improving the patient’s swallowing disability. The symptom of chest pain alone is not an indication for a surgical procedure. Twenty-four-h ambulatory motility monitoring has greatly aided in the identification of patients with symptoms of dysphagia and chest pain who might benefit from a surgical myotomy. Ambulatory motility studies have shown that when the prevalence of effective contractions (i.e., peristalticwaveforms consisting of contractions with an amplitude above 30mmHg) drops below 50 % during meals, the patient is likely to experience dysphagia. This would
suggest that relief from the symptom could be expected with an improvement of esophageal contraction amplitude or amelioration of nonperistaltic waveforms. Prokinetic agents may increase esophageal contraction amplitude, but do not alter the prevalence of simultaneous waveforms. Patients in whom the efficacy of esophageal propulsion is severely compromised because of a high prevalence of simultaneous waveforms usually receive little benefit from medical therapy. In these patients, a surgical myotomy of the esophageal body can improve the patientsЃf dysphagia, provided the loss of contraction amplitude in the remaining peristaltic waveforms, caused by the myotomy, has less effect on swallowing function than the presence of the excessive simultaneous contractions. This situation is reached when the prevalence of effective waveforms during meals drops below 30 %, i.e., 70 % of esophageal waveforms are ineffective. In patients selected for surgery, preoperative manometry is essential to determine the proximal extent of the esophageal myotomy. Most surgeons extend the myotomy distally across the LES to reduce outflow resistance. Consequently, some form of antireflux protection is needed to avoid gastroesophageal reflux if there has been extensive dissection of the cardia. In this situation, most authors prefer a partial, rather than a full, fundoplication, in order not to add back-resistance that will further interfere with the ability of the myotomized esophagus to empty. If the symptoms of reflux are present preoperatively, 24-hour pH monitoring is required to confirm its presence. The procedure may be performed either open or via thoracoscopy. The open technique is performed through a left thoracotomy in the sixth intercostal space. An incision is made in the posterior mediastinal pleura over the esophagus, and the left lateral wall of the esophagus is exposed. The esophagus is not circumferentially dissected unless necessary. A 2-cm incision is made into the abdomen through the parietal peritoneum at the midportion of the left crus. A tongue of gastric fundus is pulled into the chest. This exposes the gastroesophageal junction and its associated fat pad. The latter is excised to give a clear view of the junction. A myotomy is performed through all muscle layers, extending distally over the stomach 1.2 cm belowthe gastroesophageal junction, and proximally on the esophagus over the distance of the manometric abnormality. The muscle layer is dissected from the mucosa laterally for a distance of 1 cm. Care is taken to divide all minute muscle bands, particularly in the area of the junction. The gastric fundic tongue is sutured to the margins of the myotomy over a distance of 3.4 cm and replaced into the abdomen. This maintains separation of the muscle and acts as a partial fundoplication to prevent reflux. If an epiphrenic diverticulum is present, it is excised by dividing the neck and closing the muscle. The myotomy is then performed on the opposite esophageal wall. If a midesophageal diverticulum is present, the myotomy is made so that it includes the muscle around the neck, and the diverticulum is inverted and suspended by attaching it to the paravertebral fascia of the thoracic vertebra. The results of myotomy for motor disorders of the esophageal body have improved in parallel with the improved preoperative diagnosis afforded by manometry. Previous published series report between 40 and 92 % improvement of symptoms, but interpretation is difficult because of the small number of patients involved and the varying criteria for diagnosis of the primary motor abnormality. When myotomy is accurately done, 93 % of the patients have effective palliation of dysphagia after a mean follow-up of 5 years, and 89 % would have the procedure again if it was necessary. Most patients gain or maintain rather than lose weight after the operation. Postoperative motility studies show that the myotomy reduces the amplitude of esophageal contractions to near zero and eliminates simultaneous peristaltic waves. If the benefit of obliterating the simultaneous waves exceeds the adverse effect on bolus propulsion caused by the loss of peristaltic waveforms, the patient’s dysphagia is likely to be improved by the procedure. If not, the patient is likely to continue to complain of dysphagia and to have little improvement as a result of the operation. Preoperative motility studies are thus crucial in deciding which patients are most likely to benefit from a long esophageal myotomy. Myotomy of the lower esophageal sphincter. Second only to reflux disease, achalasia is the most common functional disorder of the esophagus to require surgical intervention. The goal of treatment is to relieve the functional outflow obstruction secondary to the loss of relaxation and compliance of the LES. This requires disrupting the LES muscle. When performed adequately (i.e., reducing sphincter pressure to<10mmHg), and done early in the course of disease, LES myotomy results in symptomatic improvement with the occasional return of esophageal peristalsis. Reduction in LES resistance can be accomplished intraluminally by hydrostatic balloon dilation, which ruptures the sphincter muscle, or by a surgical myotomy that cuts the sphincter. The difference between these two methods appears to be the greater likelihood of reducing sphincter pressure to less than 10 mm Hg by surgical myotomy as compared with hydrostatic balloon dilation. However, patients whose sphincter pressure has been reduced by hydrostatic balloon dilation to less than 10 mm Hg have an outcome similar to those after surgical myotomy. In performing a surgical myotomy of the LES, there are four important principles: (1) minimal dissection of the cardia, (2) adequate distal myotomy to reduce outflow resistance, (3) prevention of postoperative reflux, and (4) preventing
rehealing of the myotomy site. In the past, the drawback of a surgical myotomy was the need for an open procedure. With the advent of limited-access technology, the myotomy can now be performed laparoscopically. The therapeutic decisions regarding the treatment of patients with achalasia center around three issues. The first issue is the question of whether newly diagnosed patients should be treated with pneumatic dilation or a surgical myotomy. Long-term follow-up studies have shown that pneumatic dilation achieves adequate relief of dysphagia and pharyngeal regurgitation in 50.60 % of patients. Close follow-up is required, and if dilation fails, myotomy is indicated. For those patients who have a dilated and tortuous esophagus or an associated hiatal hernia, balloon dilation is dangerous and surgery is the better option. Whether it is better to treat a newly diagnosed esophageal achalasia patient by forceful dilation or by operative cardiomyotomy remains undecided. The outcome of the one controlled randomized study (38 patients) comparing the two modes of therapy suggests that surgical myotomy as a primary treatment gives better long-term results. There are several large retrospective series that report the outcome obtained with the two modes of treatment. Despite objections regarding variations in surgical and dilation techniques and the number of physicians performing the procedures, these collective data would appear to support operative myotomy as the initial treatment of choice, when performed by a surgeon of average skill and experience. The second issue is the question of whether a surgical myotomy should be performed through the abdomen or the chest. Myotomy of the LES can be accomplished via either an abdominal or thoracic approach. Recent data suggest that a transabdominal approach is preferable, particularly when done using minimally invasive techniques. The third issue.and one that has been long debated.is the question of whether an antireflux procedure should be added to a surgical myotomy. A recent preoperative randomized study supports the need for antireflux protection. Further support for an antireflux procedure is the fact that the development of a reflux-induced stricture after an esophageal myotomy is a serious problem, and usually necessitates esophagectomy for relief of symptoms. If an antireflux procedure is used as an adjunct to esophageal myotomy, a complete 360-degree fundoplication should be avoided. Rather, a 270-degree partial fundoplication or a Dor hemifundoplication should be used to avoid the long-term esophageal dysfunction secondary to the outflow obstruction afforded by the fundoplication itself.
Laparoscopic esophageal myotomy. The laparoscopic approach is similar to the Nissen fundoplication in terms of the trocar placement and exposure. The procedure begins by division of the short gastric vessels in preparation for fundoplication. Exposure of the gastroesophageal junction (GEJ) via removal of the gastroesophageal fat pad follows. The anterior vagus nerve is swept right laterally along with the fat pad. Once completed, the GEJ and the left lateral 4-5 cm of esophagus should be bared of any overlying tissue. A left lateral esophageal myotomy is performed. It is generally easiest to begin the myotomy 1.2 cm above the GEJ. Either scissors or a hook-type electrocautery can be used to initiate the incision in the longitudinal and circular muscle. Distally,
the myotomy is carried across the GEJ and onto the proximal stomach along the greater curvature for approximately 3 cm. After completion, the muscle edges are separated bluntly from the esophageal mucosa for approximately 50 % of the esophageal circumference. An antireflux procedure follows completion of the myotomy. A left lateral partial fundoplication that augments the angle of His (Dor) or a posterior lateral partial fundoplication (Toupet) can be performed. The Dor type fundoplication is slightly easier to perform, and does not require disruption of the normal posterior gastroesophageal attachments (a theoretical advantage in preventing postoperative reflux). Outcome assessment of the therapy for achalasia. Critical analysis of the results of therapy for motor disorders of the esophagus requires objective measurement. The use of symptoms alone as an endpoint to evaluate therapy for achalasia may be misleading. The propensity for patients to unconsciously modify their diet to avoid difficulty swallowing is underestimated, making an assessment of results based on symptoms unreliable. Insufficient reduction in outflow resistance may allow progressive esophageal digitation to develop slowly, giving the impression of improvement because the volume of food able to be ingested with comfort increases. A variety of objective measurements may be used to assess success, including LES pressure, esophageal baseline pressure, and scintigraphic or time barium swallow assessment of esophageal emptying time. Esophageal baseline pressure is usually negative when compared to gastric pressure. Given that the goal of therapy is to eliminate the outflow resistance of a nonrelaxing sphincter, measurement of improvements in esophageal baseline pressure and transit time may be better indicators of success, but are rarely reported. Bonavina and colleagues reported good to excellent results with transabdominal myotomy and Dor fundoplication in 94 % of patients after a mean follow-up of 5.4 years. No operative mortality occurred in either of these series, attesting to the safety of the procedure. Malthaner and Pearson reported the long-term clinical results in 35 patients with achalasia, having a minimum follow-up of 10 years (Table 24-9). Twenty-two of these patients underwent primary esophageal myotomy and Belsey hemifundoplication at the Toronto General Hospital. Excellent to good results were noted in 95 % of patients at 1 year, declining to 68, 69, and 67 % at 10, 15, and 20 years, respectively. Two patients underwent early reoperation for an incomplete myotomy, and three underwent an esophagectomy for progressive disease. They concluded that there was a deterioration of the initially good results after surgical myotomy and hiatal repair for achalasia, which is because of late complications of gastroesophageal reflux.
Ellis reported his lifetime experience with transthoracic short esophageal myotomy without an antireflux procedure. One hundred seventy-nine patients were analyzed at a mean follow-up of 9 years, ranging from 6 months to 20 years. Overall 89 % of patients were improved at the 9-year mark. He also observed that the level of improvement deteriorated with time, with excellent results (patients continuing to be symptom free) decreasing from 54 % at 10 years to 32 % at 20 years. Both studies document nearly identical results 10.15 years following the procedure, and both report deterioration over time, probably because of progression of the underlying disease. The addition of an antireflux procedure if the operation is performed transthoracically has no significant effect on the outcome. The outcome of laparoscopic myotomy and hemifundoplication has been well documented. Two reports of over 100 patients have documented relief of dysphagia in 93 % of patients. Richter and coworkers reviewed published reports to date, including 254 patients with an average success rate of 93 % at 2.5 years. Conversion to an open procedure occurs in 0 - 5 % of patients. Complications are uncommon, occurring in less than 5 % of patients. Intraoperative complications consist largely of mucosal perforation, and have been more likely to occur after botulinum toxin injection.
|Diseases of gullet surgical anatomy|
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|Workshop 5 Topographic anatomy of the lateral part of the face. Surgical anatomy of parotid gland. Surgical anatomy of the facial nerve|
|Workshop 14 Surgical anatomy of posterior mediastinum. Anatomy and physiological particularities of surgical interventions on the esophagus||Workshop 16 Topography of the inguinal region. Surgical anatomy of the inguinal canal and its content. Surgical anatomy and treatment of inguinal hernia|
|Workshop 20 Surgical anatomy of small intestine. Resection of small intestine. Surgical anatomy of large intestine and appendix. Appendectomy. Formation of unnatural passage||Workshop 13 Surgical anatomy of heart and pericardium. Anatomy and physiological particularities of surgical interventions on the heart and pericardium|
|Workshop 6 Topographic anatomy of deep field of the face. Surgical anatomy of temporomandibular pterygopalatine, interpterygoid and parapharyngeal cellular interspaces.||Workshop 17 Surgical anatomy of peritoneum. Revision of organs of the abdominal cavity. Intestinal sutures. Surgical processing of wounds of hollow organs|
|Topographic anatomy of the neck. Boundaries, fascia, cellular interspaces and division into triangles. Topographic anatomy of submandibular and carotic triangles of the neck. Surgical anatomy of submandibular salivary gland||Тоpographic аnatomy of chest wall. Тоpographic аnatomy of subclavian region. Surgical anatomy of mammary gland. Surgical intervention into the mammary gland at suppurative mastitis, benign and malignant tumors.|
Тоpographic аnatomy of subclavian region. Surgical anatomy of mammary gland. Surgical intervention into the mammary gland at suppurative...