Des

Simultaneous (nonperistaltic) contractions Repetitive (at least three peaks) Increased duration (>6 s) Spontaneous contractions Intermittent normal peristalsis Contractions may be of increased amplitude Nutcracker esophagus

Mean peristaltic amplitude (10 wet swallows) in distal esophagus > 180 mmHg Increased duration of contractions (>6 s) frequent Normal peristaltic sequences Hypertensive LES

LES pressure >45 mmHg but with normal relaxation

Normal esophageal peristalsis

Nonspecific esophageal motility disorders

No or decreased amplitude of peristalsis Normal LES pressure Normal LES relaxation Abnormal peristalsis, including any of the following: Abnormal waveforms Isolated simultaneous contractions Isolated spontaneous contractions Normal peristalsis sequence maintained LES normal

Vigorous achalasia

Repetitive simultaneous contractions in body of esophagus (as with DES) Partial or absent LES relaxation (as with achalasia)

Source: Reprinted with permission from Orringer MB. The esophagus: part III, disorders of esophageal motility. In Sabiston DC, Lyerly HK, eds., Textbook of Surgery: The Biological Basis of Modern Surgical Practice, 15th ed. Philadelphia, PA: W.B. Saunders, 1997: 722.

diverticulum or cricopharyngeal bar) and in the rest of the esophagus causing referred symptoms to the neck (such as distal esophageal tumor or GE reflux disease). Esophageal pH studies will also provide some information about the status of GE reflux and thus help guide the management of these patients. Endoscopy will not give the diagnosis of UES dysfunction, but it is important in ruling out the presence of tumor and esophagitis.

Treatment

Since there are many potential causes, including neurogenic, myogenic, structural, mechanical, and iatrogenic etiologies, the management of UES dysfunction depends of the individual case. In appropriate situations, a cervical esophagomyotomy is performed—an oblique, left neck incision is made, and a longitudinal incision of the muscularis layer, but not the submucosal and mucosal layers, of the proximal esophagus is made on the posterolateral aspect, from the level of the superior cornu of the thyroid cartilage to 1-2 cm behind the clavicle. Symptomatic relief has been obtained in 65-85 percent of the patients undergoing this procedure.

Achalasia

Definition and Clinical Presentations

The Greek translation of achalasia is failure of relaxation, and, in medical terms, achalasia refers to an inability of the LES to properly relax during the swallowing motion. The histopathologic basis of achalasia is that there is degeneration of the ganglion cells of Aurebach's plexus in the esophageal body and the LES. In South America, a parasitic infection by Trypanosoma cruzi (Chagas disease) is often the cause of the destruction of these ganglion cells; in Europe and North America, the etiology is less clear. The classic triad of symptoms includes dysphagia, regurgitation, and weight loss. Regurgitation of residual esophageal contents may lead to recurrent pneumonia and/or tracheobronchitis. Only a third of the patients will have substernal or epigastric pain, which is more typical of esophageal spasm. Esophageal cancer, characteristically a midesophageal squamous cell carcinoma, may be a late complication of achalasia, as one-tenth of patients with achalasia will develop this after 15-25 years.

Diagnostic Tests

The finding of bird's beak tapering of the distal esophagus on barium esophagogram is the classic hallmark of achalasia (Fig. 8-2). However, this radiographic appearance may vary depending on the chronicity of the disorder, from only a mild dilatation of the mid and proximal esophagus in early stage disease to sigmoid-shaped megaesophagus in advanced disease. Manometry typically shows an increased baseline LES pressure, the absence of LES relaxation normally seen with swallowing, and the lack of appropriate peristalsis throughout the rest of the esophagus. Endoscopy is performed

Figure 8-2 As shown in this barium esoph-agogram, achalasia is classically characterized radiographically by the smooth tapering of the distal esophagus, resembling the shape of a birdfs beak. (Source: Courtesy of Caroline Carrico, MD, and Anamaria Gaca, MD, Department of Radiology, Duke University Medical Center.)

Figure 8-2 As shown in this barium esoph-agogram, achalasia is classically characterized radiographically by the smooth tapering of the distal esophagus, resembling the shape of a birdfs beak. (Source: Courtesy of Caroline Carrico, MD, and Anamaria Gaca, MD, Department of Radiology, Duke University Medical Center.)

to rule out carcinoma (both in the distal esophagus and in the cardia of the stomach) and to evaluate the presence of any esophagitis or stricture.

Treatment

The goal of the treatment is to provide symptomatic palliation by relieving the functional obstruction at the LES. Medical therapy includes nitrates and calcium channel blockers. Balloon dilatation can be used in those who fail medical management and is a good first-line treatment, as the majority of patients (65-77 percent) obtain symptomatic relief, with only 1-5 percent risk of perforation.9 Repeat dilation procedures may be performed, but if the symptoms persist, then a distal esophagomyotomy (modified Heller myotomy) can be considered in appropriate situations. Approximately 15-20 percent of patients will require this operation,14 in which a longitudinal myotomy is performed, beginning from the level of the inferior pulmonary vein down across the LES and typically 1 cm onto the stomach. This operation can be performed through a left thoracotomy or an abdominal incision; it can also be done thoracoscopically or laparoscopically. Some surgeons favor performing an antireflux procedure with the myotomy to prevent problems with GE reflux. The risk of perforation in this operation is about 1 percent.9,14 In cases of sigmoid-shaped megaesophagus, symptoms of dysphagia and regurgitation can be relieved by esophageal resection, which would also effectively eliminate any possible risk of developing esophageal cancer.

Diffuse Esophageal Spasm

Definition and Clinical Presentations

In diffuse esophageal spasm (DES), repetitive, simultaneous, high-amplitude contractions of the esophagus lead to the classic symptoms of chest pain, dysphagia, or both. Patients with DES commonly have a history of irritable bowel syndrome, pylorospasm, spastic colon, and/or underlying psychiatric problems. DES is still a poorly understood esophageal hypermotility disorder and is often triggered by emotional factors, ingestion of cold substance, GE reflux, peptic ulcer disease, cholelithiasis, and pancreatitis.

Diagnostic Tests

Because of the clinical presentations, obtaining an accurate medical history is vital in making the diagnosis of DES. Since the classic symptoms of DES are similar to angina pectoralis from coronary artery disease, a cardiac workup is necessary. On barium esophagogram, curling or corkscrew esophagus, due to segmental and uncoordinated contractions of the circular muscle layer, is the hallmark of DES,9 although this radiographic finding is quite variable.9,14 Manometric findings include simultaneous, nonperistaltic, and spontaneous contractions that may be of increased amplitude. However, both barium esophagogram and manometry may be normal, since the episodes of esophageal spasm typically occur intermittently. Esophageal endoscopy should also be performed to rule out esophagitis, fibrosis, and an infiltrating tumor or other obstructing lesions distally.

Treatment

Since there is a psychiatric component in most cases of DES (documented psychiatric disorders are reported in more than 80 percent of patients with manometrically determined esophageal contraction abnormalities),14 many patients may respond therapeutically with psychiatric counseling or with simple reassurance that their chest pain is not due to a life-threatening problem such as myocardial infarction. The patient should be advised to avoid emotional stress or physiologic stressor such as food that might have a history of triggering DES symptoms in that individual. If present, associated problems such as GE reflux disease or cholelithiasis should be treated. Medications such as sublingual nitroglycerin, longer-acting nitrates, and calcium channel blockers may be effective in curtailing the symptoms of DES. Repeated esophageal dilation with smooth, tapered bougies may provide relief weeks to months at a time. Pneumatic dilatation is to be avoided due to the risk of creating a major tear with forceful expansion of a hypertonic and spastic esophagus. Although a long, thoracic esophagomyotomy (from the level of the aortic arch to the LES) is an option, it is not uniformly recommended as in severe achalasia, since long-term improvement is not frequently achieved with this operation in DES. In rare instances in which esophagomyotomy is performed for DES, antireflux procedures should be cautiously applied, and fundoplica-tion involving 360° wraps should not be used because of the already abnormal tone and contractions in the body of the esophagus.

Other Esophageal Motility Disorders

Related to DES is the nutcracker (super-squeeze) esophagus, in which the mean peristaltic amplitude exceeds 180 mmHg and at times reaches 225-430 mmHg.14 The duration of these progressive contractions are also frequently increased, but there are normal peristaltic sequences. The clinical presentations, the methods of diagnosis, and the treatment options are similar to DES. Patients who manifest clinical and manometric evidence of both DES (i.e., repetitive and simultaneous contractions of the esophageal body) and achalasia (i.e., partial or absent reflex LES relaxation) are categorized as having vigorous achalasia. Other primary esophageal motility disorders include hypertensive LES, hypotensive LES, and nonspecific esophageal motility disorders.

Esophageal motility problems also occur secondary to various systemic illnesses such as diabetes, dermatomyositis, polymyositis, lupus erythematosus, and scleroderma. Esophageal dysmotility is especially prominent in sclero-derma, and it results from the weakening of distal esophageal tone and contraction due to progressive fibrosis and atrophy of the esophageal smooth muscle layers. Patients complain mostly of heartburn from GE reflux and regurgitation, and bleeding and dysphagia are occasionally seen. Treatment modalities are predominantly targeted to control the underlying systemic disease, although there is no known effective therapy for patients with sclero-derma. Symptomatic palliation can sometimes be achieved using antacids, standard antireflux medications, and head elevation during sleep. If there is stricture causing regurgitation, dysphagia, or odynophagia, esophageal dilatation procedures may provide symptomatic relief. Antireflux operations, specifically using the Collis gastroplasty-fundoplication technique, should be considered in patients who fail medical management. In advanced esophageal disease from scleroderma with intractable symptoms, transhiatal esophagec-tomy may offer significant relief from various complications of reflux.

Vascular Rings

Vascular rings are congenital anomalies that affect the esophagus and typically cause symptoms of dysphagia in young adulthood. Barium esophagogram or endoscopy demonstrates a more than usual narrowing of the esophagus at the level of the aortic arch and the great vessels. Because these vascular rings are frequently derived from aberrant vessels, angiography or magnetic resonance imaging (MRI) should be performed to demonstrate which vessels are involved. If the symptoms are severe enough, the treatment is surgical division of the vascular ring through a transthoracic approach.

Esophageal Webs Upper Esophageal Webs

The presence of upper or cervical esophageal webs is one of the manifestations of Plummer-Vinson syndrome, also known as Kelly-Patterson syndrome and sideropenic dysphagia. Plummer-Vinson syndrome typically afflicts White women older than 40 years of age, and the upper esophageal web is the presumed cause of the dysphagia. Other manifestations of the syndrome include iron-deficiency anemia, atrophic oral mucosa, glossitis, weight loss, and koilony-chias. The diagnosis of upper esophageal web is suspected in patients who fit this profile and is made when barium esophagogram demonstrates one or more webs above the level of the aortic arch. Upper endoscopy will confirm this diagnosis and usually is adequate to treat these characteristically thin, flimsy webs by rupturing them with or without esophageal dilatation. It is also important to improve the nutritional status and correct the iron-deficiency anemia as soon as the diagnosis is made, since early treatment decreases the risk of developing carcinoma of the hypopharynx, oral cavity, or esophagus, which has been known to occur in about 10 percent of these patients.

Lower Esophageal Webs

Most of the lower esophageal webs, or Schatzki rings, are discovered incidentally on barium esophagograms performed for unrelated reasons. Some patients have symptoms of dysphagia to solid foods if there is significant narrowing from the ring. These rings are focal, annular strictures that project perpendicular to the long axis of the esophagus at the esophagogastric junction; it is made up of mucosa and submucosa and not the muscles of the esophageal wall and histologically occurs at the squamocolumnar epithelial junction. The diagnosis of Schatzki ring indicates the presence of a hiatal hernia of the sliding type (see Hiatal Hernias and Gastroesophageal Reflux), but it does not necessarily mean that GE reflux or esophagitis exists. Besides the barium esoph-agogram, these rings can be diagnosed by endoscopy from their characteristic white, membranous narrowing in the lumen of the distal esophagus. Much like the upper esophageal web, Schatzki ring can easily be treated endoscop-ically or by balloon dilatation. Surgical resection of Schatzki ring is rarely necessary; however, when it is performed, the sliding hiatal hernia that is typically associated with this ring should also be repaired.

Diverticula

An esophageal diverticulum is an acquired condition in which all or a portion of the normal esophageal wall (mucosa, submucosa, and muscle) protrudes away from the lumen. Three specific types of esophageal diverticulum are discussed here, based on the location of the occurrence—pharyngoesophageal, midesophageal, and epiphrenic diverticula. Esophageal diverticula can also be classified according to the mechanism of development—pulsion-type diverticulum, created by a protrusion of only the mucosal and submucosal layers as a result of high-intraluminal pressure forcing these layers through a defect in the musculature of the esophageal wall, and traction-type diverticulum, formed by an outward traction or pulling of all three layers of the esophageal wall from inflammation and scarring at a site adjacent to the esophagus, such as a peribronchial lymph node.

Pharyngoesophageal Diverticulum

Definition and Clinical Presentations

Pharyngoesophageal or Zenker diverticulum is the most common type of esophageal diverticulum and presents predominantly in patients over 60 years of age. It occurs at the junction of the pharynx and esophagus and specifically arises within the Killian triangle of the inferior pharyngeal constrictor, which is a point of weakness between the oblique fibers of the thyropharyngeus muscle and the horizontal fibers of the cricopharyngeus muscle (Fig. 8-3). Zenker diver-ticulum is a pulsion-type diverticulum, and its development is partly due to cricopharyngeal achalasia (UES dysfunction), a condition in which there is incomplete relaxation of the UES leading to elevated intraluminal pressure. As this diverticulum enlarges, it hangs over to the left side of the cricopharyngeus muscle inferiorly in the prevertebral space, an important point to understand when it comes to the surgical management of this problem.

Early in the development of Zenker diverticulum, patients are usually asymptomatic. When symptoms do surface, they complain of a sticking sensation in the throat, excessive salivation, intermittent cough, as well as intermittent dysphagia, typically with solids. As the diverticulum enlarges, more severe symptoms and signs may develop, such as regurgitation of undigested food, unusual gurgling sounds during swallowing, halitosis, voice change, retrosternal pain, and respiratory compromise from aspiration. Some patients develop various maneuvers, such as throat clearing, coughing, or massaging the neck, to help get the food past the upper esophagus.

Diagnostic Tests

Although clinical presentations may suggest the presence of the diver-ticulum, the diagnosis is made with barium esophagogram. Lateral view is important in demonstrating the diverticulum because the protrusion is initially directed posteriorly; anterior view will show that the diverticulum is, as discussed earlier, usually draped to the left side. Plain radiographic studies will sometimes reveal air-fluid level within the diverticulum. Manometric studies are typically unrevealing and are therefore not necessary when Zenker diverticulum is the only diagnosis being considered. In fact, the probe used for manometry may pose a risk of perforating the diverticulum. Computed

Figure 8-3 (A) Zenker (pharyngoesophageal) diverticulum occurs at the point of weakness between the oblique fibers of the thyropha-ryngeus muscle and the horizontal fibers of the cricopharyngeus muscle (short arrow). (B) The pharyngeal mucosa and (C) submu-cosa herniate through this area and typically expand caudally toward the left side into the superior mediastinum. (Source: Modified with permission from Zwischenberger JB, Alpard SK, Orringer MB. Esophagus. In Townsend CM, Beauchamp RD, Evers BM, et al., eds., Sabiston Textbook of Surgery: The Biological Basis of Modern Surgical Practice, 16th ed. Philadelphia, PA: W.B. Saunders, 2001: 715.)

Figure 8-3 (A) Zenker (pharyngoesophageal) diverticulum occurs at the point of weakness between the oblique fibers of the thyropha-ryngeus muscle and the horizontal fibers of the cricopharyngeus muscle (short arrow). (B) The pharyngeal mucosa and (C) submu-cosa herniate through this area and typically expand caudally toward the left side into the superior mediastinum. (Source: Modified with permission from Zwischenberger JB, Alpard SK, Orringer MB. Esophagus. In Townsend CM, Beauchamp RD, Evers BM, et al., eds., Sabiston Textbook of Surgery: The Biological Basis of Modern Surgical Practice, 16th ed. Philadelphia, PA: W.B. Saunders, 2001: 715.)

tomography (CT), MRI, and other radiographic studies also do not add much to the diagnosis or the management of Zenker diverticulum. Endoscopy should be performed only when filling defects or ulcers are seen on barium esophagogram, but the procedure must be performed with extra caution since there is a real risk in entering and perforating the diverticulum. It would not be inappropriate to delay the manometric and endoscopic studies after successful surgical treatment of the diverticulum.

Treatment

All symptomatic patients should undergo surgical treatment, regardless of the size of the diverticulum. The standard treatment of Zenker diverticulum is esophagomyotomy with concomitant resection of the diverticulum through a left cervical incision. Instead of resecting the diverticulum, an alternative approach is to perform diverticulopexy, a procedure in which the pouch is suspended with the mouth or neck in the most dependent position so that any food particle entering the diverticulum would easily drain out on its own. Another method of treating Zenker diverticulum is called pharyngoe-sophagotomy, or the Dohlman procedure, which entails endoscopically dividing the common wall between the diverticulum and esophageal wall. All of these approaches have excellent results with low rates of recurrence.

Midesophageal Diverticulum

Midesophageal or parabronchial diverticula are typically found near the tracheal bifurcation, are more commonly found on the right side, and usually have a wide neck. These diverticula are true diverticula, containing all three layers of the esophageal wall. Midesophageal diverticula have historically been attributed to mediastinal lymphadenitis and fibrosis from tuberculosis and histoplasmosis and are therefore traction-type diverticula. With a decline in the incidence of tuberculosis in recent decades, these postinflam-matory diverticula have decreased in number, and more midesophageal diverticula are considered to be that of the pulsion type today. For that reason, esophageal manometry is an important tool in evaluating patients with midesophageal diverticulum. However, just as in Zenker diverticulum, barium esophagogram establishes the diagnosis, and this study should be performed first. Endoscopy is important in ruling out other structural abnormalities and sometimes needed to pass the manometry probe safely into the stomach.

Epiphrenic Diverticulum

Definition and Clinical Presentations

Epiphrenic or supradiaphragmatic diverticula appear in the distal third of the esophagus. They are pulsion-type diverticula and, like midesophageal diverticula, occur more frequently on the right side. The size of the divertic-ulum usually does not dictate the severity or the type of symptoms, and patients who have symptoms such as dysphagia regurgitation, vomiting, chest and epigastric pain, and halitosis typically have associated motility disorders.

Diagnostic Tests

As in other types of esophageal diverticulum, epiphrenic diverticulum is diagnosed by barium esophagogram. Because underlying motor disorders are common in symptomatic patients, manometric studies are needed. Also, because a distal esophageal stricture or tumor can cause this type of diver-ticulum, endoscopic evaluation needs to be carried out.

Treatment

Patients with a small (less than 3 cm) epiphrenic diverticulum and with only mild symptoms do not require treatment. For those with severe symptoms or with anatomically dependent pouches that are enlarging, surgical treatment consisting of resection of the diverticulum and a long thoracic esophagomyotomy extending from the aortic arch to the GE junction is appropriate. Controversy exists due to the distal extent of the myotomy as well as due to the need for a concomitant antireflux procedure. If an antireflux procedure is performed, a partial fundoplication, as opposed to a 360° fundoplication, is recommended to reduce the risk of functional obstruction in the future. With proper esophagomyotomy, the recurrence of the diverticulum and the disruption of the suture line are rare.

Tears and Perforations2 Mallory-Weiss Syndrome

Bleeding from stomach or esophageal laceration as a result of forceful vomiting is known as Mallory-Weiss syndrome. This problem typically occurs after consuming large quantities of food and alcohol. Endoscopy will establish the diagnosis and the site of bleeding. Conservative management is usually adequate in most cases. Nasogastric lavage with ice water may slow down the hemorrhage. Intravenous vasopressin infusion may also be used to constrict the culprit vessels and control the bleeding. In cases in which surgical measure is required, an upper midline laparotomy or a left thoracotomy approach may be used to create a high gastrostomy in order to oversee the bleeding vessel under direct vision.

Boerhaave Syndrome

Boerhaave syndrome refers to spontaneous perforation of all layers of the esophageal wall, classically as a result of severe vomiting from heavy alcohol and food intake, but it can also occur with any event that rapidly raises the intraesophageal pressure while the UES is closed. After vomiting, patients present with epigastric and lower thoracic pain, which may radiate to the left shoulder due to diaphragmatic irritation. Dyspnea may develop because of the fluid in the pleural cavity. Most commonly, the perforation is located in the left, posterior aspect of the lower esophageal wall, approximately 3-5 cm above the GE junction. The next most common location of the perforation is on the right side of the midthoracic esophagus at the level of the azygos vein. Radiographic studies will demonstrate mediastinal air or hydropneumothorax. Water-soluble esophagogram or CT scan with oral contrast will confirm the diagnosis. Once the diagnosis is made, the initial line of therapy includes fluid resuscitation and broad-spectrum intravenous antibiotics. The mediastinal and pleural cavities are drained. If the perforation is significant (i.e., not microperforation), then operative management with primary closure, reenforced with a tissue flap, is preferred. The choices of tissue used for buttressing the primary repair include intercostal muscle bundle flap, pleural flap, pedicled pericardial fat, and omental flap. However, if the opening cannot be primarily closed due to friable and inflamed tissue, typically from a delay in diagnosis (traditionally defined as greater than 24 h), then the fundus of the stomach can be mobilized and be used as a Thal patch. Another option would be to perform esophageal exclusion proximal and distal to the perforation, drain the perforated area, create a cervical esophagostomy through the left side, and place a gastrostomy tube for nutritional support. A more extreme alternative would be to perform esophagectomy, especially if underlying esophageal cancer is suspected.

Iatrogenic Perforations

Any diagnostic or therapeutic procedures or operations that involve the upper gastrointestinal tract have a chance of causing injuries to the esophagus. By sheer number of cases, the most common cause of iatrogenic perforation is diagnostic flexible esophagoscopy. The most frequent site of injury is in the cervical esophagus at the level of cricopharyngeus muscle near the upper sphincter, not uncommonly against a vertebral spur that is present posteriorly. Other frequent sites of iatrogenic perforation are the midthoracic esophagus at the level of the left mainstem bronchus and the lower esophagus at the diaphragmatic hiatus. The risk of iatrogenic perforation with diagnostic esophagoscopy is about 0.1 percent (0.09 percent for flexible fiber-optic esophagoscopy and 0.07 percent for rigid esophagoscopy).

On the other hand, the risks of perforation with therapeutic procedures vary with the types of procedures. For example, in treating achalasia, surgical esophagomyotomy carries a risk of only 1 percent, whereas pneumatic dilatation has a risk of 4 percent. That risk is significantly lower (0.5 percent) when using semiflexible bougies that are guided by an endoscopically placed wire.

Hiatal Hernias and Gastroesophageal Reflux3,4

Definition and Clinical Presentations

Hiatal hernia is a condition in which a variable portion of an abdominal organ, typically the stomach, becomes displaced above the diaphragm through the esophageal hiatus. When only the stomach is considered, there are essentially two types of hiatal hernias (Fig. 8-4). However, in a more elaborate classification system that includes the involvement of other abdominal organs, four have been described. In type I hiatal hernia (sliding or axial type), the GE junction is displaced above the level of the diaphragm through the esophageal hiatus. The LES, or the HPZ in the distal esophagus, is exposed to the negative pressure of the thoracic cavity, and this is presumed to predispose patients with type I hiatal hernia to problems with GE reflux. In type II hiatal hernia (paraesophageal or rolling type), a portion of the stomach her-niates into the mediastinum, but the GE junction remains below the level of the diaphragm, thereby keeping the LES within the positive pressure environment of the peritoneal cavity. In type III hiatal hernia, features from both

Type I

Type I

Figure 8-4 Involvement of the stomach in hiatal hernia can essentially be divided into two general types, based on the relative position of the GE junction. In type I hiatal hernia (sliding or axial type), the GE junction passes through the esophageal hiatus and is above the diaphragm. In type II hiatal hernia (parae-sophageal or rolling type), a portion of the stomach herniates through the esophageal hiatus but the GE junction remains within the abdominal cavity. (Source: Reprinted with permission from Jacobs DO. The esophagus. In Niederhuber JE, ed, Fundamentals of Surgery. Stamford, CT: Appleton and Lange, 1998: 279.)

Figure 8-4 Involvement of the stomach in hiatal hernia can essentially be divided into two general types, based on the relative position of the GE junction. In type I hiatal hernia (sliding or axial type), the GE junction passes through the esophageal hiatus and is above the diaphragm. In type II hiatal hernia (parae-sophageal or rolling type), a portion of the stomach herniates through the esophageal hiatus but the GE junction remains within the abdominal cavity. (Source: Reprinted with permission from Jacobs DO. The esophagus. In Niederhuber JE, ed, Fundamentals of Surgery. Stamford, CT: Appleton and Lange, 1998: 279.)

type I and type II are present; that is, both the GE junction and a part of the gastric fundus are above the esophageal hiatus. In type IV hiatal hernia, there is a large paraesophageal hernia that includes other organs such as the large or small intestine. Clinically, types II, III, and IV hiatal hernias should initially be considered together because of the mechanical problems that each one of these can create (e.g., incarceration and strangulation). However, because the GE junction is also displaced into the mediastinum in types III and IV, the GE reflux issues related to type I hiatal hernia should also be kept in mind.

Type I hiatal hernia is common and is usually discovered incidentally on chest radiograph. It is considered by many not to be a true pathologic condition since the GE junction has been demonstrated to move above the level of the diaphragm in normal individual during a Valsalva maneuver. However, type I hiatal hernia is associated with GE reflux and subsequent reflux esophagitis; type I hiatal hernia is present in about 80 percent of patients with pathologic reflux. Only when the hiatal hernia is associated with GE reflux do patients become symptomatic. The typical symptoms include heartburn (80 percent) and regurgitation (54 percent). Other symptoms reported by a significant proportion (~30 percent) of patients with type I hiatal hernia are abdominal pain and cough. Types II, III, and IV hiatal hernias are not as frequently seen as type I, and they are rarely associated with GE reflux, but the herniated portion of the stomach is more likely to strangulate and infarct. They can be asymptomatic, even when a large portion of the stomach is involved; when present, predominant symptoms include epigastric, subcostal, and chest pain, dyspha-gia, and heartburn. Regurgitation, upper gastrointestinal bleeding, and hoarseness may occasionally occur if there are complications of the hernia. To avoid potentially catastrophic consequences, asymptomatic type II hiatal hernia should be surgically managed on an elective basis in patients with no contraindications; if symptoms do develop, they should be repaired emergently.

Diagnostic Tests

Radiographic studies such as barium esophagogram will help define the type of hiatal hernia present, but in GE reflux disease, other studies are needed to evaluate the presence of pathologic reflux. These include endoscopy to visualize the mucosa, endoscopic biopsy to document the mucosal and submu-cosal pathology, 24-h pH study to assess the extent of esophageal exposure to acid, and manometric recordings to evaluate any physiologic abnormalities in motor function.

Treatment

For GE reflux disease, the least aggressive and invasive treatment modalities should be attempted first. Initial recommendations might be to practice lifestyle changes such as cessation of smoking and avoidance of caffeine, fatty meals, or large meals before bedtime. The next level of treatment is medical management, which includes antacids, prokinetic agents, H2-blockers, and proton pump inhibitors. A 6-week trial of acid suppression therapy with a double dose of a proton pump inhibitor not only might relieve the symptoms but also helps confirm the diagnosis if the patient responds favorably.

Because of the tremendous success in the minimally invasive surgical techniques, operative management of GE reflux disease should be considered an alternative to medical therapy rather than the last resort. The underlying principle of any of the operative approaches is to reenforce the tone of the distal esophagus by partially or completely wrapping it with the fundus of the

Figure 8-5 There are three basic types of fundopli-cations: (A) Nissen fundoplication (360° wrap); (B) Thal and Dor fundoplications (partial anterior wrap); (C) Toupet fundoplication (partial posterior wrap). (Source: Reprinted with permission from Zwischenberger JB, Alpard SK, Orringer MB. Esophagus. In Townsend CM, Beauchamp RD, Evers BM, et al., eds, Sabiston Textbook of Surgery: The Biological Basis of Modern Surgical Practice, 16th ed. Philadelphia, PA: W.B. Saunders, 2001: 763.)

Figure 8-5 There are three basic types of fundopli-cations: (A) Nissen fundoplication (360° wrap); (B) Thal and Dor fundoplications (partial anterior wrap); (C) Toupet fundoplication (partial posterior wrap). (Source: Reprinted with permission from Zwischenberger JB, Alpard SK, Orringer MB. Esophagus. In Townsend CM, Beauchamp RD, Evers BM, et al., eds, Sabiston Textbook of Surgery: The Biological Basis of Modern Surgical Practice, 16th ed. Philadelphia, PA: W.B. Saunders, 2001: 763.)

Nissen Fundopli
Figure 8-5 (Continued)

stomach (fundoplication). The three basic types of fundoplications are: 360° wrap (Nissen fundoplication), partial anterior wrap (Thai and Dor fundoplications), and partial posterior wrap (Toupet fundoplication) (Fig. 8-5). In all of these approaches, the wrap is formed over a 2.5- to 3-cm distance. In general, the 360° wrap, Nissen fundoplication is used for patients with normal esophageal motility, and the partial fundoplications (the 180° anterior wrap or the 220-250° posterior wrap) are reserved for patients with abnormal esophageal mano-metric measurement, such as a distal esophageal pressure amplitude of less than 30 mmHg.

Reasons, Remedies And Treatments For Heartburns

Reasons, Remedies And Treatments For Heartburns

Find Out The Causes, Signs, Symptoms And All Possible Treatments For Heartburns!

Get My Free Ebook


Post a comment